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Anemia ............................................................................. 15
- SUMMARY - Digestive Bleeding ............................................................... 15
GASTRO ................................................................................... 2 Clinical Classification ............................................................ 15
1 - Liver ................................................................................ 2
Generality ........................................................................... 2 8 - Acute Abdomen .............................................................. 16
Laboratory tests: .................................................................. 2 Acute Abdomen .................................................................. 16
Specific tests for the virus ....................................................... 2 Diagnosis through the pain .................................................... 16
Instrumental Investigations ..................................................... 2 Abdominal pain .................................................................. 16
fatty liver ............................................................................ 2 ENDO ..................................................................................... 17
Acute Hepatitis .................................................................... 2 9 - Diabetes......................................................................... 17
Chronic Hepatitis .................................................................. 3
Glucose Metabolism ............................................................ 17
Hepatic Fibrosis .................................................................... 3
Insulin .............................................................................. 17
Liver Cirrhosis ...................................................................... 3
Glucagon .......................................................................... 17
Child-Pugh score................................................................... 3
incretins ........................................................................... 17
MELD Score ......................................................................... 4
Diabetes ........................................................................... 17
hemochromatosis ................................................................. 4
Cardiovascular Complications of Diabetes ................................. 18
Wilson's Disease ................................................................... 4
Therapy ............................................................................ 19
Budd-Chiari syndrome (SBC) .................................................... 4
Adjusted and Not Compensated Cirrhosis ................................... 4 10 - Obesity and Metabolic Syndrome .................................. 19
Complications of Cirrhosis....................................................... 4 Obesity ............................................................................. 19
Criteria Milan ...................................................................... 5 Metabolic Syndrome ............................................................ 19
Criteria for Barcelona............................................................. 5 Family Hypercholesterolemia ................................................. 19
NAFLD and NASH .................................................................. 5
11 - Neuroendocrinology ..................................................... 20
2 - Gallbladder and Biliary tract.............................................. 6 Pituitary gland .................................................................... 20
Jaundice ............................................................................. 6 hypopituitarism .................................................................. 20
cholestasis .......................................................................... 6 craniopharyngioma.............................................................. 20
Biliary Tree.......................................................................... 6 pituitary tumors.................................................................. 20
Lithiasis gallbladder ............................................................... 7 Acromegaly ....................................................................... 21
Lithiasis duct stones .............................................................. 7 prolactinomas .................................................................... 21
NET (Neuro-Endocrine Tumor) ............................................... 21
3 - Pancreas .......................................................................... 7
Pancreatic NET ................................................................... 21
Acute Pancreatitis ................................................................. 7
Chronic Pancreatitis .............................................................. 8 12 - Thyroid ........................................................................ 22
Pancreatic cyst ..................................................................... 8 Hyperthyroidism ................................................................. 22
Therapies for hyperthyroidism ............................................... 22
4 - Esophagus ....................................................................... 8
thyroiditis ......................................................................... 22
Achalasia ............................................................................ 8
Thyroid Cancer ................................................................... 22
Gastroesophageal reflux ......................................................... 8
Hypothyroidism .................................................................. 23
Barrett's Esophagus............................................................... 9
Congenital Hypothyroidism ................................................... 23
Esophageal Adenocarcinoma ................................................... 9
Acquired Hypothyroidism ...................................................... 23
squamous Cell carcinoma ....................................................... 9
Subclinical Hypothyroidism .................................................... 23
esophageal cancer therapy ..................................................... 9
esophageal diverticula ........................................................... 9 13 - Parathyroid .................................................................. 23
hypercalcemia .................................................................... 23
5 - Stomach .......................................................................... 9
Hypocalcemia..................................................................... 24
Gastritis ............................................................................. 9
pseudohypoparathyroidism ................................................... 24
Acute Gastritis ..................................................................... 9
Chronic gastritis ................................................................... 9 14 - Osteoporosis ................................................................ 24
ulcer Peptide ..................................................................... 10 Endocrine Diseases associated with Osteoporosis ....................... 24
Gastric Adenocarcinoma....................................................... 10
15 - Adrenal ........................................................................ 25
Gastritis Alkaline ................................................................ 10
adrenal ............................................................................. 25
Dyspepsia ......................................................................... 11
Aldosteronism .................................................................... 25
Hiatal hernia...................................................................... 11
Cushing's Syndrome............................................................. 25
6 - Intestine ........................................................................ 11 Addison's Disease................................................................ 26
Irritable Bowel Syndrome ..................................................... 11 Congenital Adrenal Hyperplasia (CAH) ...................................... 26
SIBO ................................................................................ 11 incidentaloma .................................................................... 27
Diverticula of the Colon ........................................................ 11 Pheochromocytoma ............................................................ 27
malabsorption ................................................................... 12
16 - Multiple Endocrine Neoplasia (MEN) .............................. 27
Lactose intolerance ............................................................. 12
Diarrhea ........................................................................... 12 17 - Female gonadal disorders .............................................. 28
Celiac disease .................................................................... 13 amenorrhea....................................................................... 28
Crohn's disease .................................................................. 13 early menopause ................................................................ 29
Ulcerative Colitis (UC) .......................................................... 13
Differential Diagnosis between "Crohn's disease" and "RCU" ......... 13 18 - Puberty ........................................................................ 29
Instrumental investigations to diagnose IBD .............................. 13 pubertal development .......................................................... 29
Polyps .............................................................................. 14 early puberty ..................................................................... 29
Colon-Rectal Cancer ............................................................ 14 19 - Men gonadal disorders .................................................. 29
Surgical Therapies for Colon-Rectal diseases.............................. 14
male Hypogonadism ............................................................ 29
MIN CIN & ........................................................................ 14
erectile Dysfunction ............................................................. 30
Adenocarcinoma Colorectal .................................................. 14
premature ejaculation .......................................................... 30
7 - digestive haemorrhages.................................................. 15
Specific tests for the virus: Viruses that damage liver disease are
GASTRO classified into minor (cytomegalovirus, Epstein-Barr Virus) and
higher (HAV, HBV, HCV).
1 - Liver
- Virus minorThese viruses heal on their own, without
Generality: Is the largest gland in the body, weighing 1.2-1.5 Kg. The treatment, in less than six months. To search for a minor virus
inflow of blood is ensured by the hepatic artery and the portal vein, makes the analysis of the immunoglobulins IgM and IgG: IgM
which collects the effluent blood from the intestine, while the hepatic are the expression of ongoing infections, while the IgG of past
veins that drain the organ, flow into the inferior vena cava. The liver infection. If you have a history of elevated aminotransferase
capillaries (sinusoids) are equipped with large fenestrations that, in levels for more than six months it is useless to search for minor
the event of liver damage, tend to disappear (the capillarity virus.
phenomenon) thus losing the ability to exchange the nutrient material - Virus more Included in this category, the only one that does
with the parenchyma. The cells are: not tend to has become chronic HAV: rarely fatal virus that gives
- Hepatocytes (60%): cells able to replicate rapidly after acute lifelong immunity and healing; often it is contracted by ingestion
toxic insults or resections (liver regeneration). of raw seafood. The main viruses that more have become chronic
- endothelial cells (20%). HBV and HCV. To ensure the presence of these viruses seek
respectively HBsAg and HCVAb. Once confirmed the presence of
- Kupffer cells (15%): "scavengers" macrophages which eliminate
the virus, we need to ensure if the virus is replicating or less: We
toxic substances and secrete inflammatory cytokines (TNF). They
are looking for HBV DNA polymerase and RNA polymerase for
can also store the iron in the form of ferritin and hemosiderin. HCV.
- stellate cells or Ito (5%): important because they are able to
produce growth factors that initiate the phenomenon of Instrumental Investigations:
fibrogenesis. - Fibroscan: Apparatus similar to an ultrasound system that
evaluates the hardness of the liver using a probe that sends
Laboratory tests: elastic waves and analyzes the speed of propagation of the
- ALT (9-60 IU / L): alanine aminotransferase, an enzyme present same in the liver tissue.
in the mitochondria of liver cells, involved in protein synthesis. A - Ultrasound: investigation that allows us to analyse the size and
lesion dell'epatocita determines the leakage of this enzyme structure of the liver, borders and margins, the portal blood
which increases its concentration in blood. So the values increase flow (Doppler of the portal vessels), if there is a reduced
in cases of acute viral hepatitis, chronic or fulminant. Among circulation, if there is cirrhosis, if there is splenomegaly ( index
other possible causes of elevated aminotransferase there are of liver fibrosis, in fact, the blood cannot get through the liver
Celiac (NB), and autoimmune hepatitis. goes to congest the spleen), if there is the presence of a
- AST: (10-40 IU / L), aspartate transaminase, another gallbladder disease.
mitochondrial enzyme but is also present in other tissues (heart). - gastroscopy: To see if there are signs of portal hypertension
It follows that in myocardial infarction the ALT levels increase to (complication of hepatic cirrhosis), such as esophageal varices
a lesser extent than those of AST. The AST / ALT ratio under and varices of the gastric fundus.
physiological conditions is generally> 1
- liver Biopsy: It allows you to make a morphologic diagnosis
However: (Grading and Staging) and follow the disease over time. Although
 Values <1 (Inverted ratio) are associated with the most part the gold standard, it is best avoided in case of advanced cirrhosis.
of liver diseases (acute hepatitis, chronic, electrocuting) - gastroscopy: Check if there are esophageal varices to
 Values > 2 They are associated with myocardial infarction understand the degree of portal interdiction.
it's at alcoholic hepatitis (In this case also it increases GGT).
fatty liver: Accumulation of fat due to a decrease in exports of fats
- Gamm-GT range: (0-51 IU / L) enzyme involved in detoxification
from the liver, altered to oxidation or to an increased synthesis of
mechanisms of oxidative damage. It is therefore used as a marker
fatty acids. There are 3 forms of steatosis:
for the in-take of ethanol. An increase indicates damage from
alcoholism. - Macrovesicular: Alcohol, obesity, diabetes. Macrovesicular
because the lipid accumulation is present in the cell in the form
- ALP: (30-120 IU / L) alkaline phosphatase, an enzyme contained
of a single large drop.
in the cells lining the intrahepatic bile ducts. An increase in this
- Microvesicular: HCV.
value is indicative of obstruction of the biliary tract. If the patient
- Mista: NAFLD (Non-Alcoholic Fatty Liver Disease).
also reports pain, it is very likely that this is gallstones.
- Alb: (3.9 - 5.0 g / dL), albumin, synthesized by the liver. His values Acute Hepatitis: Condition of elevated aminotransferase levels (10-
decrease in case of chronic liver diseases, such as cirrhosis, fold increase compared to the normal value) with prominent
because of reduced synthesis. inflammation for a period of less than six months. It can be caused
- Bilirubin: (0.3 - 1.0 mg / dL) is a product of EME degradation. Once by viruses, drugs or toxic chemicals. If the inflammation affects the
synthesized (indirect bilirubin or "unconjugated") is made water- entire liver (hepatitis massive) we may find ourselves in front of
soluble at the hepatic level (direct bilirubin or "conjugated") and fulminant hepatitis: liver can weigh 500-700gr., Resulting in flaccid
secreted into the bile. High levels of bilirubin in the blood may with a capsule that, unable to adapt to the sharp decrease in
reflect liver problems or extra-hepatic: volume, becomes wrinkled and opaque. Histologically we have the
formation of characteristic bodies, which allow you to make
o Bilirubin Ind: (0.2 - 0.8 mg / dL) increases in case of differential diagnosis between viral and alcoholic hepatitis:
damage intrahepatic.
o Bodies of Councilman: Typical of viral hepatitis,
o Bilirubin Dir: (0.1 - 0.3 mg / dL) increases in case of spheroidal bodies are made up of hepatocyte apoptosis.
damage extrahepatic, For example due to obstruction
o Bodies of Mallory: Typical of alcoholic hepatitis and
of the bile ducts.
alcoholic cirrhosis, eosinophilic cytoplasmic inclusions are
composed of damaged intermediate filaments.
Chronic hepatitis: hypertransaminasemia and necrotic strange) or flapping tremor (tremor flutter), jaundice. From the
inflammatory lesion for a period of at least 6 months. laboratory analysis note: increased transaminases, decreased plasma
The main causes are: viral hepatitis, autoimmune hepatitis, proteins (hypoalbuminemia), decrease of prothrombin (hence decrease
inherited metabolic liver disease, drug hepatitis. Macroscopically: in PT: prothrombin time) and, if there is cholestasis, we also increased
the liver is smaller in size as fibrosis progresses It evolves. If left bilirubin.
untreated it evolves into cirrhosis 
- Pathogenesis: Hepatocyte necrosis The cells secrete cytokines that
The main causes are: viral hepatitis, autoimmune hepatitis, inherited 
activate genes involved in fibrogenesis in Ito cells formation of fibrous
metabolic liver disease, drug hepatitis. Macroscopically: the liver is 
septa (3 events)
smaller in size as fibrosis progresses 
It evolves. If left untreated it evolves into cirrhosis. entrapment of a liver parenchyma area: the extent of
hepatic parenchyma in space by fibrotic phenomena gives
- Chronic Viral Hepatitis: rise to nodules. The ischemic necrosis of these nodules
o HBV: The virus HBV entering nell'epatocita does not direct invokes inflammatory infiltrates and induces progressive
cytopathic action, ie not destroys the cell (as does the HAV), hepatocyte
 death with further fibrosis and nodular
but is inserted into the host DNA to replicate and to produce  growth.
viral particles. The cell tolerate the virus, but still a reaction 
intrasettali formation of vessels that bypass the sinusoids.
against HBV proteins which considers as foreign: it has The latter lose their natural fenestration (capillarity of
production of antibodies against these cells expressing the  sinusoidal waves) with severe vascularity.
HBV antigen. The immune reaction that damages the liver 
cholestasis: The destruction of the interface between the
cells, but is not effective enough to eradicate the virus (for parenchyma
  and portal tracts may occlude in turn the
this reason, becomes chronic hepatitis). In some cases we bile ducts.
may have inactive chronic infection: the virus has integrated - Types of Cirrhosis:
its genome into the cellular DNA, but remains silent (healthy O Viral (57.3%): evolution of a chronic viral hepatitis (HBV
carrier) and can be reactivated during immunosuppressive in 7.1% of cases and 50.2% in HCV). It is characterized
therapy. by the presence of macronodules (nodules> 1 cm) and
has a greater tendency to the development of
o HCV: It differs from the HBV virus as HCV is a RNA hepatocellular carcinoma. It is more frequent in
virus, meaning that healing always involves the Campania.
elimination of the virus and there is no possibility of a O alcoholic (16.4%): determined by chronic use of large
reactivation. Furthermore, the HCV by a subtle damage amount of alcohol (ethanol acts as a hepatotoxic agent).
from oxidative stress which does not entail significant It is characterized by the presence of Micronodules
(nodules <3-5 mm). Before we get to the true cirrhosis
increase in transaminases (cytolysis is reduced). They
and its
make frequent lymphoid aggregates in the portal tracts. we have various developmental stages of the disease:
- Grading and Staging of Viral Hepatitis: There are various steatosis
systems to carry Grading (evaluation necrotic-inflammatory  
hepatic alcoholic steatohepatitis alcoholic
activity) and Staging (evaluation state of fibrosis). The main cirrhosis. It is more frequent in Lombardy.
ones are those of Metavir Ishak and evaluating, through a liver O Alcohol + Virus (18.6%).
biopsy, the degree of liver fibrosis. O Other (7.7%): from autoimmune diseases (Chronic
O Metavir: F0 = no fibrosis; F1 = mild fibrosis; F2 = f. hepatitis autoimmune, primary biliary cirrhosis,
average; F3 = f. strict; F4 = cirrhosis. primary sclerosing cholangitis); metabolic diseases
o Ishak: In addition to assessing fibrosis, also assesses
(hemochromatosis, Wilson's disease); stasis liver
other histological features such as the presence of
nodules, confluent necrosis and portal inflammation. (barrier to blood flow that creates congestion, can be
generated by a heart failure or Budd-Chiari syndrome);
Hepatic Fibrosis: Connective tissue accumulation in the liver, typical surgeries; drugs.
of chronic liver disease (especially cirrhosis) and generally resulting [NB these diseases in bold was requested oral and are
in inflammatory-necrotic phenomena. Over the inflammatory explained in the pages].
process is invasive, more disrupts the structure of the liver lobule. It
has formation of fibrotic septa scratch: these septa arise from the Classification Child-Pugh score: This classification evaluates the
new formation of collagen which replaces the lost parenchyma. severity of the dividing cirrhosis in 3 stages (CHILD A, B and C): the
Finally, because of fibrotic damage to the liver parenchyma, it pieces which is in Child A is a well-balanced pcs, which has a
undergoes cirrhosis. serious liver disease, but whose function is still perfectly
preserved ( compensated cirrhosis); A patient in Child C instead
Liver Cirrhosis: Fatal disease process, expression of a chronic advanced has a severe decompensated cirrhosis, which means that the
liver damage. We have a strong liver architecture alteration to fibrosis patient has a few weeks old. The final score for the division into
and formation of parenchymal nodules (proliferating hepatocytes stages is obtained by analysing parameters 5 (2 and 3 clinical
surrounded by fibrous tissue). The main causes are viral hepatitis, laboratory):
alcohol and metabolic liver diseases. Its complications: portal - Encephalopathy: (1 = None; 2 = Mild; Refractory = 3) buy in
hypertension, progressive liver failure and development of HCC. The case of hepatic impairment and in case of "porto-systemic
clinical signs that evaluate through the E.O are: hepatosplenomegaly, shunt" (intestinal toxic substances do not pass through the
caput medusae (sign of portal hypertension), spider nevi (or stellar liver, but they enter directly into the circulation systemic).
angioma, is a skin lesion in the shape of typical cobweb of the patient - Ascites: (1 = None; 2 = Trattabile; Refractory = 3) expresses
suffering from Liver Cirrhosis), ascites (a sign of dx heart failure), the the entity of portal hypertension, but also the protein-
state of consciousness disorders (behaviors synthetic activity of the liver.
- Albumin: (1 => 3.5; 2 = 2.8-3.5; 3 = <2.8) protein from
important oncotic capacity.
- Bilirubin: (1 = <2; 2 = 2-3; 3 => 3) index of cholestasis.
- prothrombin activity: (1 => 70%; 2 = 40-70%; 3 = <40%) (Initially mainly splanchnic). Hence: blood splenic
index of protein-synthetic capacity of the liver 
sequestration baroreceptor activation and osmoreceptors
MELD Score: The Model of End-Stage Liver Disease is an index to decide
 
activation of the Renin-Angiotensin System (SRA)
whether or not to liver transplantation to patients with cirrhosis CHILD 
increased retention of Na and water increase in blood
B and C. The Currency score 3 parameters: bilirubin, prothrombin time volume, venous return to the heart and, therefore, further
and creatinine. The score obtained from this assessment generates portal influx which exacerbates hypertension.
progressive levels of mortality at three months of patient values <9 = The portal hypertension complications are:
1.9% mortality; 10-19 = 6.0%; 20-29 = 19.6%; 30-39 = 52.6%; > 40 = o Formation of shunt porto-systemic collateral circulation
71.3%. The ideal score for a transplant is around 15-16, but the decision and, as a compensatory mechanism to lower the intra-portal
must be made also according to the availability of organs, with priority pressure, however, causing an overall increase of the
to patients with the highest score. resistances. They manifest with
caput medusae.
hemochromatosis: AR disease characterized by accumulation of
o splenomegaly: The splenic vein fails to empty and the
iron (in the form of hemosiderin) due to the mutation of a gene
blood returns to the spleen, ingrossandola.
involved in its absorption in the intestine. Iron has direct toxicity
on host tissues: determine lipid peroxidation stimulates collagen o esophageal varices and the gastric fundus: these varices
formation, accentuates the ROS mediated DNA damage. In the can rupture (for gastro-esophageal reflux erosion, or to
liver it leads to a slow development of fibrous septa (which can increase pressure) causing digestive bleeding with a
evolve into micronodular cirrhosis). To slide the hepatocyte mortality rate of 10% on the first episode, 30-40% at the
appears rich blue granules of hemosiderin coloration: Prussian second episode and> 60-70% on the third episode.
blue). Varicose veins are distinguished on the basis of risk,
thanks to the parameters: extension of varicose veins, if
Wilson's Disease: AR disease characterized by copper they occupy less or more than 1/3 of the lumen, based
metabolism dysfunction. The ceruloplasmin (formed by copper on the color (white or blue) and the shape (straight,
and α2-globulin) is not able to leave the liver to merge in a circle.
It has hepatic copper accumulation -> toxic liver damage by tortuous, broad), in by the presence of red marks (points
   to give us a level of intimate vessel), bleeding and
ROS focal necrosis steatosis inflammation with acute erosions. The treatment consists in ligation with elastic
  bands to stop the bleeding.
hepatitis chronic hepatitis cirrhosis.
Budd-Chiari syndrome (SBC): Is a clinical picture o Ascites and Encephalopathy.
by ascites, jaundice, hepatomegaly, splenomegaly and hypertension - Ascites: Extracellular fluid accumulation, free in the cavity
portal, caused by occlusion of the hepatic veins (at least 2 abdominal, between the peritoneal layers. It occurs in 50% of
3). The clinical picture of patients may progress over time cirrhotic patients. It is detectable if EO> 1500ml. In
Cirrhosis. Occlusion of the hepatic veins can be caused by: Following the first episode of ascites, there is a change in the
thrombosis, cancer, pregnancy, infection. Survival of pieces: more than 50% die within two years. ascites
defines itself not complicated when it is not associated with
Adjusted and Not Compensated Cirrhosis: The residual functionality
infections (spontaneous bacterial peritonitis) or to failure
a cirrhotic liver depends on the number of hepatocytes that work,
Renal Syndrome (Hepatorenal). Then analyze the
so when you reduce excessively, it goes towards
content of ascites: if the protein content
liver failure. Not all cirrhosis, for this leads to
<2.5gr / dl we talk about exuding, if it is> 2.5 g / dl
failure: a patient with cirrhosis "offse/compensata" has no symptoms
we speak of exudate (in the case of infectious overlap or
clinically relevant, in addition to those due basic etiology,
neoplasms). Only 15% of ascites recognize a different cause
as: itching (in cholestatic forms), fever (in the forms from the cirrhotic: cancer, peritoneal infection, congestive
heart failure
autoimmune) and asthenia (in viral forms). The compensated phase can
cardiac, renal failure with nephrotic, disease syndrome
last for many years. When cirrhosis begins to deteriorate,
it is said that "decompensates" when complications occur of
O Treatment The first thing to do in a pc with ascites
cirrhosis, such as portal hypertension and significant reduction of
place it in the supine position to facilitate the venous
Liver function (hypoalbuminemia, coagulopathy, subittero). There
then proceed with a low-salt diet and diuretics (these
10-year survival is 70% in compensated cirrhosis and
the last in the long run, to a worse prognosis
20-30% in decompensated cirrhosis.
resulting in renal failure). The ascites is defined
Complications of Cirrhosis: refractory When not responding to therapy (which
- portal hypertension: Normally the portal system is It includes a healthy lifestyle, and food hygiene
diuretic therapy is not extended): the pieces no longer
low resistance and high flow, with flow 1000-1200 urine and increase the renal function tests (increase
ml / min and a pressure of 7mmHg. In hypertension portal,
pressure reaches values of 13-15mmHg. hypertension creatinine and serum potassium, whereas decreases
portal is developed in two different phases: BUN). Ascites negotiable has a mortality rate of 4% to
O Initial phase: Hypertension is due to an increase Two years, while the intractable is> 50% (if associated
of the resistors in the liver for the formation of in PBS is> 70%).
nodules of degeneration, the capillarity of o Theories on the origin of ascites:
sinusoids, for contractile activity of the cells and Ito ▪ Under-filling: Insufficient liver does not synthesize
Kupffer. more albumin, thus decreasing the pressure
oncotic. In the meantime, however, it increases the
O systemic Phase: The phenomena of the initial phase determine pressure
local hypoxia and release of VEGF and NO with consequent hydrostatic due to portal hypertension. All the
Local angiogenesis and peripheral vasodilatation. blood is conveyed to the splanchnic

(Splenomegaly), so that returns to the heart is little cirrhosis as a result of HBV infection is less than the incidence
 that occurs between those who are infected with HCV. HBV
the heart pump less less blood reaches the kidneys
 has oncogenic properties with direct integration into the host
It activates the SRA which induces retention of Na
 genome and regulation of cell growth and proliferation. HCV
and water further increase of the hydrostatic
pressure. This alteration of the forces of Starling leads produces proteins capable of regulating p53. Of infected with
to sweating intraperitoneal. HCV: 70% tends to become chronic, 30% goes to cirrhosis and
▪ 3% goes towards hepatocellular carcinoma. Hepatocellular
Over-flow: According to this theory, the initial carcinoma develops more frequently in men (incidence in Italy
event in the formation of ascites is a primitive salt for men is 7.1 per 100,000, while for women it is 2.7). The
and water retention of sodium and water by the most effective treatment is surgery (lobectomy and, when
kidney, "primitive" in the sense that in the cirrhotic
possible, transplantation), while chemotherapy and
occurs independently of any volumetric stimulus.
This in turn would lead to a progressive expansion radiotherapy are not very effective. macroscopically,
of plasma volume, and since this phenomenon
Criteria Milan: Indicate the eligibility for transplantation in cases of
occurs in the context of an alteration of the Starling
hepatocellular carcinoma, or those conditions that guarantee a
forces at the level of the splanchnic and
intrahepatic compartment, sooner or later the post-transplant survival to 5 years equal to or greater than 70%.
excess of circulating liquid pours These criteria should be used because there is great availability of
( "Overflow") in the peritoneal cavity forming livers for transplantation, so we can not perform a transplant in
ascites. patients then die after one year. The criteria are:
- Presence of 1 nodule only by the maximum size of 5 cm in
▪ diameter.
Theory of peripheral arterial vasodilation:
According to this hypothesis, the fundamental - Presence at the maximum of 3 nodules, each of which ≤3 cm.
moment in the pathogenesis of ascites is a
peripheral arteriolar vasodilation, which occurs as Criteria for Barcelona (BCLC: Barcelona Clinic Liver Cancer): allows you
a result of portal hypertension. to classify patients into five groups based on performance status (the
- Encephalopathy: Altered consciousness, personality, performance status is a score that assesses: patient's level of activity,
neuromuscular functions (flapping tremor) and the sleep- occupational or physical limitations, personal care skills, constriction
wake cycle. It occurs in 20% of patients and occurs due to the bed or chair more or less than 50% of the day), Child-Pugh and
presence of toxic metabolites (not disposed of by the liver) in characteristics of the tumor.
the CNS. Among the causes we have the ammonia (ammonia - Very Early Stage (0): includes patients with a single tumor
produced in the intestine by bacteria and mucosal diameter <2cm, with compensated liver function (Child-Pugh
deaminase), and the imbalance between aromatic amino A), and no symptoms related to cancer.
acids (which increase) and branched chain amino acids (which - Early Stage (A): includes patients with a single HCC or number
decrease) that creates a cerebral level a shift towards weak of nodules ≤ 3, each with a diameter ≤ 3cm, with preserved
neurotransmitters. A hallmark is a asterixis (or asterixi): hepatic impairment (Child-Pugh A and B).
asking the subject to put your arms straight in front of him - Intermediate Stage (B) includes patients with multinodular
with his wrists in dorsiflexion and fingers like a fan, you can tumors (> 3 nodules in diameter> 3 cm), with no evidence of
detect a gross tremor shook large arrhythmic called a vascular invasion or extrahepatic localization, in good
"butterfly heartbeat" (flapping) functional compensation (Child-Pugh A and B).
- PBS (Spontaneous bacterial peritonitis): contamination of the - advanced Stage (C) includes patients who experience disease-
ascites by bacteria (E. Coli) occurs because in subject cirrhotic related symptoms, with vascular invasion and / or extrahepatic.
bilirubin is very low, but the bile salts cause vascular damage, - Terminal Stage (D): includes patients in end stage, with
which, together with altered motility, favor the bacterial impaired hepatic function (Child-Pugh C) and severe disability
overgrowth in the gut, causing loss of bowel function. In this way related to neoplastic disease.
the tight junctions are opened and the bacteria pass into the
liquid. To confirm the suspicion of PBS do an exploratory NAFLD and NASH: Non-Alcoholic Fatty Liver Disease, encompasses a
paracentesis. wide spectrum of liver disease (including NASH) characterized by
- Hepatorenal Syndrome: Irreversible renal failure leading to accumulation of fat and triglycerides in hepatocytes, developed in
death if not diagnosed very quickly. The most popular theory individuals in which the intake ethyl is zero or negligible. As part of
is that the systemic vasodilation NAFLD there are a wide variety of forms, ranging from mild
(Especially splanchnic) and reactive hypovolemia cause steatosis, with a simple inflammatory damage, up to the full-blown
vasoconstriction in compensatory cortical nephrons, with cirrhosis due to chronic persistence of the inflammatory
functional impairment renal hemodynamics. The treatment phenomenon. NAFLD may be caused by metabolic syndrome, in this
involves albumin injections, elimination of diuretics. case we talk about primary NAFLD, or by other conditions such as
the intake of drugs, surgical maneuvers, genetic alterations or
- Hepatocellular carcinoma (HCC) is the 5to most frequent cancer
concomitant diseases (eg. Celiac disease), which determine
in the world and accounts for 6% of all cancers with
secondary NAFLD. NASH (Non-Alcoholic steatohepatitis) is nothing
approximately 500,000 cases per year. It is believed that the
but a steatosis accompanied by inflammatory events and, in some
disease-causing connection between chronic / hepatitis cirrhosis
cases, even by fibrosis. Inflammation can be caused by damage to
and HCC are repeated cycles of necrotic-inflammatory processes
and regenerative processes (chronic hepatocellular damage); 5
especially oncogenesis driver genes that go more often to meet
mutation are K-RAS and p53. It can present as a single large
mass, or as widely distributed multifocal nodules. The incidence
of HCC among those who developed
cell membranes caused by lipid peroxidation. These changes can bilirubin. In this case hyperbilirubinemia is mixed because a
stimulate the stellate cells of Ito causing fibrosis. If advanced, NASH portion of the liver parenchyma still works.
can lead to cirrhosis. o Pre-hepatic jaundice: Caused by hyperhemolysis
(spherocytosis, G6PDH deficiency, autoimmune diseases)
Metabolic Syndrome (Appreciation): pathological condition
or ineffective erythropoiesis. These conditions lead to an
characterized by central obesity in conjunction with at least two of
increase in indirect bilirubin due to the increased blood
the following factors: dyslipidemia (evaluated as a low value of HDL),
catabolism of damaged red blood cells. The liver continues
fasting hyperglycemia (> 110 mg / dl), arterial hypertension, fatty
to successfully carry out its work, although a small portion
liver, whose prime mover is given insulin resistance. [More details in
of indirect bilirubin in the blood poured eludes capture.
the ENDO].
cholestasis: Hyperbilirubinemia is not, but it is a multiple etiology
syndrome characterized by retention in the liver and in the blood
2 - Gallbladder and Biliary tract compartment of one or more substances normally secreted in the
bile, due to either a deficiency of biliary secretion or in the presence
Jaundice: Yellowing of the skin, sclera and visible mucous
of biliary tree obstruction, of whose jaundice is one of the
membranes that occurs when bilirubin reaches concentrations> 2.5-
3 mg / dl. In a black man jaundice recognize only the sclera. An event manifestations. There can be no jaundice cholestasis and cholestasis
that always occurs before jaundice is the subittero, only visible in the without jaundice. The hepatobiliary ultrasound is very useful to
sclera, when the bilirubin is> 1.5 mg / dl. evaluate the diameter of the common bile duct (physiologically 3-
- Laboratory AnalysisIt is useful to study the type of bilirubin 4mm). The ultrasound gives us information on the expansion, but
not the kind of obstacle to see the obstruction use the CPRM
(Direct or indirect) that increases blood. If the increase regards
(resonance cholangiopancreatography). The type of branching that
indirect (unconjugated), we alterations upstream dell'epatocita
is affected, we have:
(pre-hepatic), if it increases the direct (conjugated) have post-
hepatic abnormalities. - intrahepatic cholestasis: Affects the bile ducts within the liver
- Types of jaundice: parenchyma, so the canals, the duttoli and scholars. The causes
or Post-hepatic jaundice (or cholestatic): Also called
or Primary biliary cirrhosis (CBP): most frequent cause, it is
obstructive, It is a condition in which the liver plays its
function properly, but the flow of bile into the intestine is a autoimmune chronic liver disease caused by the
prevented. We increased direct bilirubin because there is destruction of interlobular bile ducts. In 95% of patients
have positive for anti-mitochondrial antibody (AMA-
an obstacle to its excretion (biliary stones, cancer of the
positive). It is much more common in middle-aged
pancreatic head, etc.). The symptoms are characteristic:
women. The main symptoms are: itching (initial
white stools (bilirubin does not enter the intestine, so it
symptom), abdominal pain, portal hypertension
can not be converted to urobilinogen and stercobilin by
(cirrhosis), malabsorption and effort.
intestinal bacteria), urine color marsala (or Coca-Cola
colored, because the direct bilirubin is water soluble, and or Cholangitis primary sclerosing (CSP): cholestatic liver
can be eliminated in the urine), itching (in bile are the bile disease Chronic liver of unknown etiology characterized
salts, which when they go into circulation tend to settle by involvement of the bile ducts intra- and / or
extrahepatic with inflammatory lesions fibro-obliterative.
at the cutaneous level, in fact by giving an intense
It is more common in males 30 to 40 years.
or Cholestasis of pregnancy.
or Jaundice intra-hepatic (or hepatocellular): Linked to
or Hepatitis, cancer, post-liver transplant.
reduced functionality of liver cells and is characterized
- extrahepatic cholestasis: Affects the bile ducts outside the
by the increase in indirect bilirubin levels in the
bloodstream. It can be caused by congenital hepatic parenchyma: right hepatic duct, the left hepatic duct,
abnormalities or uptake of bilirubin metabolism: common hepatic duct, cystic duct, common bile duct. The
causes are:
▪ or Lithiasis of the common bile duct: Calculations blocking
Gilbert's Syndrome: AD incomplete penetrance; It
consists of a defect in uptake of indirect bilirubin, which the flow bile (more details later).
determines a slowing of conjugation. It is very common, or Benign stenosis: for example, after an inflammation that
it affects 3-10% of the population, and made his debut It caused a retraction of the biliary tract.
in 15-18 years.
or malignant stenosis: cholangiocarcinoma, pancreatic
▪ tumors.
Crigler syndrome-Najjar: AR neonatal-onset; It
consists of a defect in the conjugation of bilirubin for Biliary Tree: Image.
a decrease in enzyme GT (glucouronosiltransferasi).
In newborns, bilirubin in high concentrations can
cross the blood-brain barrier, which is still not well-
formed, causing damage to the CNS: this condition is
called Kernicterus (or bilirubin encephalopathy) and
is treated using ultraviolet rays for
oxidize bilirubin and make lower levels. The intra-
hepatic jaundice can also be caused by acquired
disorders, such as acute hepatitis and cirrhosis, which
may impede the uptake or outflow of

Lithiasis gallbladder: Very common condition that affects 300,000 o Biliary Pancreatitis: The calculation may become stuck in
new people every year. It involves deposition of gallstones in the a 'of the switch level of Vater causing an reflux of bile into
gallbladder. the pancreas resulting in inflammation. Increased GGT
- Types of calculationsIf the bile acids and phospholipids are and alkaline phosphatase. The pc has jaundice.
superior to cholesterol have stable micelles; if the relationship - Therapy: To relieve colic immediately we administer an anti-
is no longer maintained (increased cholesterol and decrease in inflammatory antispasmodic + (the pain of colic stems from
other two components), we unstable vesicles that induce spasm of the muscle that runs out gradually). It is advisable to
crystallization and the formation of the calculation. carry out an ultrasound scan as soon as possible to confirm the
O Detective stories: Consist cholesterol and have a presence of stones. Confirmed diagnosis, pz may decide
consistency crystal clear, the vast majority of the whether to proceed with surgical removal of the gallbladder
calculations in industrialized countries. They can be very (cholecystectomy) in laparoscopy, or if they do not perform any
large (2-3 cm) and x-ray appear transparent. They are operation: one must not forget that the majority of patients are
associated with metabolic abnormalities and high-fat asymptomatic and that after the first colic, more than 50% the
diets. pieces will have no other colic in the future (especially if you
O blacks: Consist calcium carbonate is calcium phosphate, follow a low fat diet); But it is also true that a symptomatic
They have hard consistency. We find them in people who gallstones should also operate on her to prevent cholecystitis.
have hemolytic anemia. They have very small (3-6 mm) When the calculation is < 2cm We can also evaluate a medical
and radiography appear dull. therapy is the administration of drugs capable of reversing the
O Brown: Consist bilirubinate-Ca is palmitate-Ca, They ratio of bile salts and cholesterol. There is also the endoscopic
have a soft consistency and appear transparent to therapy: this involves the use of a side-viewing endoscope
radiography. They are the result of infectious processes. which presents a scalpel capable of affecting the sphincter of
- Pathogenesis of calculations: Some calculations may form Oddi. The extraction is carried out with the calculations of
both an increase in cholesterol and saturated other "cestellini", or balloons.
components crystallizes (yellow stones), is due to hemolytic
diseases (blacks calculations), is due to infection (brown Lithiasis duct stones: When the calculation escapes from the gallbladder
stones). Besides the causes already mentioned, we have and goes to occlude the common bile duct. Generally present in the
implication of three organs:or Gallbladder: Impaired elderly. It can also happen during an intervention, when the surgeon
motility. If the gallbladder empties who was going to operate the gallbladder did have a passage of
calculations in cystic: immediately after the intervention this calculation
Frequently, I will go away content and therefore do not
allow the precipitation of calculations. The moved and returned to the patient the colic. Complications are:
Cholecystokinin (CCK) is a hormone secreted in the cholangitis, fever, jaundice. The therapy involves a reclamation of the
intestine that causes contraction of the gallbladder. biliary tract through ERCP (endoscopic retrograde
O Liver: Alteration of the production of bile salts. cholangiopancreatography).
O Intestine: Alteration of the entero-hepatic circle of Sali
Bile: If the bile salts are reabsorbed entering this circle,
they will be deleted. So we have a depletion of the pool 3 - Pancreas
of bile salts. The liver can increase production, but it can Acute Pancreatitis: Acute necrotic inflammation charged to the
not compensate for the loss. pancreatic parenchyma. It is a reversible condition. The main
- Symptoms: The only symptom attributable to the disease has changes are: microvascular damage that causes edema,
colic, although in 2/3 of the cases the patient is completely steatonecrosis, acute inflammation, proteolytic destruction of the
asymptomatic. Colic is an acute painful episode located right pancreatic parenchyma, destruction of vessels resulting interstitial
hypochondrium and epigastrium (radiated back to the back and hemorrhage. The complications are: hemorrhage and formation of
right shoulder) that lasts at least half an hour and that is usually pancreatic cysts. The main clinical feature
seen in the evening after meals. The gallbladder begins to è the continuous and intense pain, almost numbing, localized in the
contract for the stimulation of CCK, but then you fail to contract epigastrium with radiation to the rear center of the back, insensitive to
more: but rather stretches and swells because that calculation antispasmodics but sensitive to painkillers. For a correct diagnosis we
has occupied the infundibulum: are then stimulated nerve must be dosed amylase and lipase in serum and urine (pain + =
endings. hyperamylasemia acute pancreatitis). We may have a mild form (only
or DD with Renal ColicWhile biliary colic radiating to interstitial edema, little necrosis, does not give organ deficiency or
shoulder, renal radiates inside thigh and testicles. In addition, systemic involvement) and a severe form
the renal colic may occur at any time (and not necessarily (Type necrotizing, associated with organ failure, requires intensive
after meals).or DD with acute cholecystitis: In therapy, may result in the death of pcs). It has an incidence of 5.6
cholecystitis there is high fever. cases per 100,000 inhabitants and is most common between 40 and
O DD with Pancreatitis: Pancreatitis pain is much more 60 years. It is caused by activation of the digestive enzymes
rending and radiates back to the bar. abnormal intrapancreatic for:
O DD with acute appendicitis: the most important element - obstruction of the pancreatic duct: Gallstones, trauma or protein
is the age. Acute appendicitis occurs in the young, while precipitates can hinder the flow of pancreatic juice
the lithiasis is more common in the elderly. determining its stagnation interstitial environment. Here
- Complication lipases (enzymes that are secreted already in active form)
cholecystitis: Inflammation of the gallbladder, which is steatonecrosis and cause damage to cell membranes, with
filled with white liquid and becomes palpable EO positive consequent activation of all other enzymes.
Murphy and fever. - damage of acinar cells: Are cells of the exocrine pancreas that
s:or secrete the zymogen granules, inactive proenzymes that

constitute the pancreatic juice. They can be damaged by  Endoscopic: We operate a pneumatic dilation using a balloon
viruses, drugs, alcohol, or other factors. catheter in the middle of the cardia. Dilate the cardia for 2-3
- defective intracellular transport of pro-enzymes within the minutes so as to have a tearing of the fibers is not associated with
acinar cells. breakage. Alternatively we can use botulinum toxin (1 cc of toxin in
4 quadrants of the circumference) to determine flaccid
Chronic Pancreatitis: Inflammation with destruction of the exocrine
muscle paralysis. It should be repeated several times.
pancreas, fibrosis and, in the final stages, the destruction of the
 surgical: Invasive and costly procedure.
endocrine component (initially the islets of Langerhans are blended
together and may appear enlarged, but eventually they disappear). Gastroesophageal reflux (GERD: reflux disease Gastro-
It differs from the acute form because there is an irreversible ISsofageo; or GERD: Gastro-Esophageal Reflux Disease):
deterioration of pancreatic function. It can be caused by chronic hypomotility pathology that affects the esophagus, is a chronic
alcoholism or chronic acute pancreatitis (repeat episodes of relapsing condition and, precisely due to the reflux of gastric
parenchymal fibrosis and loss). Even here pcs reports a strong contents into the esophagus (thus also bile, pancreatic enzymes and
continuous epigastric pain. Exocrine insufficiency means reduction gastric juices). It is caused by failure of the SEI seal. It is a condition
in our ability to digest food, especially fatty ones: one of the clinical frequently associated hiatal hernia, or to the ascent of a portion of
manifestations the stomach from the abdomen to the chest, through the diaphragm
è In fact, steatorrhea, namely the presence of oily stool. hole (above the angle of His). It is a complex disease: the
The main endocrine insufficiency is obviously deficient secretion of predisposing factors can be genetic, demographic and behavioral.
insulin, leading to diabetes. The diagnosis of chronic pancreatitis is The most common risk factors are smoking and obesity.
anamnesis: if I find myself in front of a person with recurring pain - Symptoms most common are heartburn and regurgitation
characteristic and is an alcoholic, the tentative diagnosis is likely. It (retro-sternal burning).
proceeds with a CT abdomen that often reveals calcification in - Pathogenesis: May be due to: increase in esophageal clearance
pancreatic. Therapy: The patient must be put in pancreatic rest, then (of esophageal emptying time); decrease in the SEI pressure;
fed only by parenteral route. If there is diabetes, insulin is alteration of cell turnover; duodeno-biliary reflux; increased
administered. secretion of hydrochloric acid and pepsin; reduction of gastric
Pancreatic cyst: When rinveniamo a cystic lesion there may be two
- Diagnosis: It shall be effected by:
possibilities: either is a pseudocyst (collection of fluid in a cavity not
or Endoscopy: To evaluate the epithelial damage.
lined with epithelium, but bounded by inflammatory fibrous tissue),
or pHmetry: Esophageal pH should be> 4.
or is a tumor cysts (which may be benign, cystadenoma, or
malignant, cystadenocarcinoma). or manometry: SEI to assess the tone and peristalsis.
- Therapy: Using prokinetic drugs, which stimulate the
esophageal peristalsis, increasing the tone of the SEI and
promoting gastric emptying. To reduce the acidity are used
4 - Esophagus proton pump inhibitors (PPIs). The cases not responsive to this
Achalasia: Pathological condition determined by the non-relaxation therapy should be treated with a surgical technique known as
of the lower esophageal sphincter (SEI, or LES in English) that occurs plastic antireflux according Nissen-Rossetti: you run into
hypertonic, and the absence of peristalsis of the body of the laparoscopy and consists of the plication (winding) of the
esophagus (example of hypomotility). The incidence is 1 in 100,000. gastric fundus around the lower esophagus and suture in situ.
The peak is between 40 and 60 years. This leads to a pressure increase in the slope esophageal
- CausesThey are multiple. We have 4 pathogenetic hypothesis: sphincter, with improvement in symptoms.
myogenic (deficit of beta receptors and increase in alpha), - Classification of MontrealWe divide the GERD:
hormone (excess gastrin), Congenital (AR), Neurogenic (most or esophageal syndromes: Which in turn can be:
accepted theory, it may be due to a ganglion cell deficiency of Symptomatic syndromes:
inhibitory neurons, or for degeneration of the vagal center or ✓
Chest Pain Reflux
vagal fibers). ✓
typical reflux
- Symptoms: Dysphagia, which can become odynophagia (pain in ▪
Syndromes associated with Injuries:
the passage of food), and paradoxical as it applies to liquids as ✓
Barrett's Esophagus
well as solids. 90% of the food stops at the level of the Lower

Esophageal Sphincter. In 40% of cases have pain for not Esophageal Adenocarcinoma

peristalsis and relaxation of the organ. The dilation of the Reflux oesophagitis
esophageal wall is defined by the term megaesophagus. In 6% ✓
stenosis peptide
of cases there is regurgitation (passage through the Upper o Extra syndromes-esofagee:
Esophageal Sphincter of material that has not yet reached the ▪
Associations Confirm:
stomach) to the esophagus stagnation of what we swallowed.

- Diagnosis: Manometry is the gold standard. The pressure of the Cough reflux

SEI gets to be> 40 mmHg (normal is <25 mmHg). Reflux Laryngitis
Endoscopy is useful to rule out the possibility of a tumor. ✓
Asthma Reflux
- Therapy: could be: ✓
Dental Erosion reflux
or medical: use nitrates is calcium channel blockers for ▪
Associations Proposals:
induce vasodilation, and then allow the opening of the SEI

arrival of the bolus. The effectiveness of this therapy Pharyngitis
declines rapidly (within one week, one month maximum). ✓

Ear infection

pulmonary fibrosis
- Classification of Oesophagitis according to endoscopy: lymphatic vessels are located in the submucosa, and then an
or Not erosive esophagitis (NERD): more than 60% of all advanced form is more likely to give metastases compared to an
oesophagitis, are associated with atypical symptoms, early form. Esophagus and stomach, lymphatic vessels are already in
extra-esophageal and absence of lesion. It can be the lamina propria. [The anatomical order of esophageal robes, from
determined by both a pathological acid reflux, both from the lumen outward, is as follows: mucosa (epithelium
a hypersensitivity of the esophagus (the condition in    
lamina propria muscularis mucosa) submucosa muscularis].
which the pH is normal).
If the tumor has not yet given nodal or distant metastases, we can
or erosive esophagitis (ERD): injuries are divided by proceed with a call EMR therapy (EMR), which provides for the
the classification of Los Angeles: 
endoscopic mucosal resection (that is "detached" from the submucosa).
. GRADE A: Lesions <5 mm without confluence. This technique is intended to remove the pre-cancerous lesions or early
. GRADE B: Lesions> 5mm without confluence.  
stage and is a viable alternative to surgery.
. Grade C:> 5mm, confluent, involvement of the Another approach is that of the radiotherapy which can be both external
esophageal circumference <75%. and internal: external beam radiation therapy involves the use of a large
. GRADE D:> 5mm, confluent, involvement of the machine outside the body that sends radiation in the affected area; the
esophageal circumference> 75%. internal radiation therapy (also called brachytherapy) involves the use
o Esophagitis Complicated (CRD): forms with possible of a tube which is inserted into the esophagus and emits radiation
ulcers, Barrett's esophagus or cancer. constantly. One of the isotopes used in this therapy is yttrium (Silvero

Barrett's Esophagus: Condition of metaplasia in which 1/3 of the
epithelium of the lower esophagus, which is normally squamous esophageal diverticula: They are saccular protrusions, similar to the
multilayered, it becomes simple cylindrical with goblet cells. It is believed bags or pockets, which are formed in the wall of the esophagus. The
that the main cause is the chronic acid exposure from reflux esophagitis. causes which determine the onset include the increase of pressure
It is reversible (especially in children) can be treated with antacids, within the esophagus, weakness on the wall, and to load cicatricial
balancers and motility pump inhibitors. Barrett's esophagus is a phenomena of periesophageal tissues (that surround the
precancerous condition because it increases the risk of developing esophagus). The bolus stagnation within these diverticula can lead
adenocarcinoma (30/40 times if the lesion> 3cm). Dysplasia is found in to episodes of regurgitation and associated with complications such
0.2-2% of patients if dysplasia is present, the patient will have to do the as inflammation and perforation of the bowel. The diverticula may
follow-up to 3 years; If dysplasia is mild it will make follow-up to 1 year; be formed at any level of the esophagus, but mainly involving the
If dysplasia is severe will follow-up at 6 months (odds of transformation distal portion of the cervical and thoracic what tract.
is 5-6% per year). macroscopically: presence of red mucosa patches
which extend above the gastroesophageal junction. Depending on the
extent of these spots we can be classified in the Barrett: Barrett
Ultrashort (<2cm), Short Barrett (2-3 cm), Barrett Long (> 3 cm). For a
5 - Stomach
correct diagnosis it is necessary to identify the slide goblet cells (pale Gastritis: Inflammatory process that affects the gastric mucosa. We
blue with hematoxylin-eosin) can diagnose gastritis only when histological examination showed
an inflammatory infiltrate of the superficial layers of the gastric
mucosa. Therefore the diagnosis of gastritis is only and only
Esophageal Adenocarcinoma: Cancer that forms in the lower third histological.
of the esophagus and may invade the cardia. It can develop in
patients with Barrett's esophagus: when this injury is very large and Acute Gastritis: Transient inflammation (1-2 weeks). It may be
exceeds 3cm extension along the esophageal axis, the possibility of asymptomatic, but in the most serious cases there may be erosion
conversion reaches 39%. Other risk factors are: gastro-esophageal of the mucosa, ulceration and hemorrhage that determine degrees
reflux and obesity. diagnostic examination with EGD, the tumor of epigastric pain variables. The pathogenesis depends etiological
occurs initially in the form of flat or revealed patchy, to then form agent: NSAIDs (inhibition of cyclooxygenase: reduction of
larger masses> 5cm. To confirm the diagnosis, do a biopsy and are production of prostaglandins that, at the gastrointestinal level,
looking for the presence of Barrett esophagus in the vicinity of the stimulate the production of mucus and bicarbonate), alcohol,
tumor. trauma (which increase the secretion of gastric juice to vagal
stimulation) and hypoxia.
squamous Cell carcinoma: Attributable to alcohol and tobacco
Chronic gastritis: Less severe and more persistent symptoms
consumption. Unlike adenocarcinoma, this cancer tends to develop
compared to the acute gastritis, chronic gastritis also exposes the
in the medium 1/3 or 1/3 in the upper esophagus. Start with a lesion
epithelium to damage by free radicals (related to inflammation) and
in situ called "dysplasia scaly" which then evolves into polypoid
proliferative stimuli that, over time, can determine genetic
tumor masses that protrude toward the lumen obliterandolo
alterations and dysplasias (for this reason it is fundamental perform
(dysphagia). At the time of diagnosis (EGD) symptomatic tumors are
endoscopy with biopsy to evaluate the state of the mucosa and to
already very large and have invaded the wall of the esophagus. The
exclude the possible presence of precancerous lesions). The major
rich network of lymphatic submucosa facilitates the spread of the
chronic gastritis are:
tumor nodules often occur to several centimeters from the main
mass. - Gastritis Helicobacter Pylori: 95% of all chronic gastritis, infection
causes an increased production of acids and the rupture of the
esophageal cancer therapy: Neoplasms of the digestive tract can be normal protective mechanisms of the stomach and duodenum. It
divided into two broad categories based on the degree of tumor consists predominantly antral, although in some patients
infiltration. We have: early tumors, which have not passed the progresses to involve the body and gastric fundus. It can develop
muscularis mucosa, and advanced forms, which have passed the into intestinal metaplasia with increased risk
muscularis mucosa. In the majority of the digestive system (except
the esophagus and stomach) i 9
gastric adenocarcinoma. The diagnosis is made through a non- dyspepsia (digestive), dysphagia. If the disease is in an advanced
invasive test called Urea Breath Test (breath test) which is based stage, we note EO: palpable mass, left supraclavicular
on the ability of H. pylori to quickly metabolize the urea lymphadenopathy, periumbilical subcutaneous nodules,
administered by mouth, to obtain ammonia and carbon dioxide. hepatomegaly. In all countries, both the incidence and mortality are
2-fold higher in males. The main cause that determines the
The CO2produced by urease of H. pylori it is absorbed by the gastric development of adenocarcinoma is the H. Pylori infection: in 20% of
walls, and then conveyed in the blood and rapidly excreted in the cases the infection develops into gastric ulcer and / or duodenal
expired air. The Urea Breath Test is only able to assess the presence ulcers, while in 3% of cases can give rise to a gastric carcinoma. In
or absence of the bacteria, but not the state of the mucous industrialized countries, the prevalence of infection is around 30%,
while in Japan, Asia, Africa and South America the prevalence is
membrane: Whereas we find ourselves in front of a chronic
growing, so much so that almost all of the population has the
gastritis, we must also investigate the possible presence of infection. The H. Pylori manages to survive in the environment of the
precancerous lesions by using the EGD. Through endoscopy it is stomach acid due to its urease which neutralizes the gastric acid in
necessary to make 5 biopsies (antral 2, in the small and in the large the immediate vicinity, creating an alkaline microenvironment in
curvature), 1 nell'angulus, 2 to level of the body and of the bottom, which the bacterium manages to live. The events that follow are:
always in correspondence with the small and the large curvature): 
inflammation and immune release of cytokines and chemokines
in this way it has a global overview of the status of all of the
stomach mucosa.
 
ranging in block somatostatin (hormone that inhibits gastrin)
increase gastrin values
- autoimmune Gastritis: AD hereditary disease that   
gastric acid hypersecretion gastritis mucosal atrophy and
predominantly affects women (ratio 3: 1). It represents 1-3% of
 
all atrophic gastritis and are found mainly in Northern Europe. intestinal metaplasia dysplasia gastric adenocarcinoma. Surgery is
We identify in serum and in gastric secretions of antibodies the only real chance of recovery. Depending on the extent of the tumor
directed against the parietal cells, delegated to the HCl can make a total gastrectomy or distal: in the latter case we leave the
(hydrochloric acid production) and factor gastric fundus and only take away the distal portion. It is important to
intrinsic: remind the patient who underwent gastrectomy to avoid simple sugars
  because they are absorbed quickly and cause an increase in insulin
or Deficit HCL: decrease secretion HCL increase gastrin
resulting in hypoglycemia [Prof. Question. Sarnelli]. It is also important
hypergastrinemia and hyperplasia of antral G cells.
to make a total body CT scan with contrast medium to investigate
or Deficiency of intrinsic factor: determines failure Vitamin 

possible metastases. We distinguish three types of adenocarcinomas:
B12 resulting in pernicious anemia.
- diffuse type: Mainly affects women, under the age of 50 years.
ulcer Peptide: Unlike erosion (superficial lesion, which does not People with blood type A have a higher risk of developing
exceed the muscularis mucosae), the peptide ulcer is a chronic lesion cancer (there are no known reasons for this association).
of the mucosa and submucosa of the stomach (gastric ulcers) and Carcinogenesis is triggered by infection with H. pylori. It is
the duodenum (duodenal ulcer) that extends to the muscularis and, more aggressive bowel isotype, but less aggressive than
in more severe cases, it can also determine the perforation of the undifferentiated. Histologically we have cells with large
organ concerned. It is very common: 10% of the population suffers. vacuoles mucinous that expand the cytoplasm and push the
It can be caused by H. pylori infection (90% of cases), use of NSAIDs,  core toward the periphery (for signet ring cell).
gastric cancer. In the case of H. pylori ulcers proceed with antibiotic - intestinal type: Most frequent, form bulky tumors with glandular
therapy. The most common symptom is heartburn, which increases structure. It is so called because it is associated with intestinal
on an empty stomach. The complications are perforation and metaplasia: gastric epithelial transformation into epithelium
gastrointestinal bleeding that occurs with live blood issue with similar to the bowel. It tends to develop after age 65, there
vomiting (vomiting blood) and black stools (melena). Endoscopic are no correlations with the blood group. More common in
treatment of bleeding lesions involves the use of Clips, metal clips men. Carcinogenesis is triggered by infection with H. pylori. It

capable of exerting a substantial compressive force, such as to  has a relatively good prognosis.
determine a mechanical hemostasis on treated vessels. There are - undifferentiated type More severe form that often gives
several types, one of the most recent is the triclip, characterized by metastases to non-gastric lymph nodes. It could introduce
3 tips that eliminate the need of the rotational movements which activating HER2 mutation that worsens the prognosis, but
are instead necessary with the clips to two metal arms.  makes this cancer eligible for targeted therapy (trastuzumab).
If the cancer is diagnosed in the early stages it is called Early Gastric
Gastric Adenocarcinoma: Most common malignancy of the stomach 20
Cancer: in this case the cancer is only present in the mucosa and
times more frequent in Japan. The disease is related in 95% of cases to
submucosa and has greater chance of recovery (patients treated with
environmental factors, it is seen that a Japanese who emigrated to the
total gastrectomy and removing all surrounding lymph nodes a
USA (first generation) had a risk of developing cancer equal to that of the
probability of 5-year survival> 90%). If not detected early it can evolve
Japanese remained at home, while his son (second generation, as born
in America) he had the same risk of the US population and not the into an advanced stage that approfonda in the lower cowls and can give

metastases (5-year survival <20%).
Japanese. It Represents 5tocause of death from cancer since it is a type
of very difficult cancer to diagnose early on: the pc is the attention Gastritis Alkaline: Disease related to reflux of bile material from the
oncologist if symptoms occur. It reports a dull ache and constant duodenum. It is not uncommon to encounter this reflux pcs gastrectomy
epigastric. The pain radiating posteriorly is indicative of neoplastic or cholecystectomy. The cause of the damage to the mucosa
extragastric encroachment, often with pancreatic infiltration. Other
symptoms include weight loss, anemia, 10
gastric is determined by the action of detergent bile acids, contained o Alterations in gut motility.
in the refluxed liquid that reaches the gastric wall. - Therapy: Varies depending on the dominant symptom. They
are all symptomatic and non-curative treatments. The only
DyspepsiaIt is a symptom of the upper digestive tract that includes: curative treatment that could work involves the use of
early satiety, bloating, epigastric pain, nausea, vomiting, belching probiotics.
and heartburn. At the end of the diagnostic path (whose o In pc with bowel constipated: high fiber diet and mild
examination prince is gastroscopy) the pieces will be classified into laxatives
two broad categories: osmotic (lactulose).
- Dyspepsia Organic (40%) secondary to another disease of the GI o In pz with bowel diarrhea: antidiarrheal (loperamide).
tract such as ulcers peptide (17%) and gastric cancer
o In pz with pain: antispasmodics (debrilat, spasmex),
(1%). muscle relaxants, calcium channel blockers.
- Functional Dyspepsia (60%): that is not associated with any Differential Diagnosis: the main pathologies to be excluded
organic lesion but functional disorders. We have: motility before diagnosing an IBS are: celiac disease, intolerance to
disorders (administer prokinetics), sensitivity disorders or lactose, hemorrhage, familial cancer or polyposis, processes
microbiological changes (H. Pylori). inflammatory (MICI), changes in metabolism. The diagnosis of
IBS is essentially done by exclusion. The exams are:
Hiatal hernia: It is caused by the passage of a portion of the stomach
o Search for occult blood in the stool.
into the thorax from the abdomen, through the iris hole. It is a rather
o Colonoscopy.
widespread disease that affects about 15% of the Italian average.
There are 3 types of hiatal hernia: o Lactose break test.
o Markers for celiac disease.
- From Sliding: Is the most frequent (90%). The gastroesophageal
junction is pushed upward causing in many cases a
SIBO (Small Intestine Bacterial Overgrowth): Syndrome Bacterial
gastroesophageal reflux. This step is sometimes reversible and
overgrowth in the small intestine where they occur both bacterial
particularly sensitive to abdominal pressure fluctuations
growth events, both modification of the strains which tend to
(swallowing, excessive exertion, coughing).
resemble those of the colon. The peristalsis, in addition to
- From rolling (O Paraesophageal): the gastroesophageal junction determining the progression of the substances inside the intestine,
remains in its natural seat, while the bottom of the stomach passes
keeps the lumen "clean" by an excess of bacteria pushing them away
into the thorax. The greatest risk in this case
with mechanical action. The presence of a high amount of bacteria
It is that the hernia ends up choking between the esophagus in the small intestine causes a direct damage on enterocytes and a
and the hiatus or may seriously compromise the blood supply modification of the bile acids (resulting in malabsorption of dietary
to the stomach.
- Mista: Has the characteristics of both of the above forms.
- Causes of SIBO are all those diseases which can interfere with
peristalsis: neurological / muscular diseases, diabetes mellitus,
diverticula of the small intestine, Crohn's disease, surgical
- Symptoms: I am very lacking specificity. We may have
abdominal symptoms (bloating, abdominal pain, diarrhea,
dyspepsia) and extra-intestinal symptoms (malabsorption;
weight loss; pernicious anemia from vitamin B12 deficiency,
osteoporosis or for tetany hypocalcemia by vitamin D
- Diagnosis:
o Poll jejunal (Invasive): It provides the suction, with a
6 - Intestine tube introduced into the jejunum (via the endoscope),
Irritable Bowel Syndrome (IBS: Irritable Bowel Syndrome): intestinal juice on which you run the bacterial count.
intestinal disorder in which the subject has abdominal pain or physiological values are <10,000 bacteria / ml.
discomfort associated with alterations of (constipation or diarrhea). o Breath Test (Non-invasive): detects the amount of hydrogen
This syndrome is prevalent in women (especially the stiptica shape) nell'espirato (after administration of glucose) due to premature
and has a strong social and economic impact: involves a reduced fermentation by bacteria of the small intestine.
quality of life and is the 2 cause of absenteeism from work. - Therapy: Antibiotics for 7-10 days.
- Classification: IBS divide into 3 subgroups based on stool
frequency: Diverticula of the Colon: Extroflexions saccular wall of the colon through
o stiptica Form: <3 bowel movements per week the circular muscle layer. They are formed in the wall areas with less
o diarrheal Form:> 3 bowel movements per day resistance, namely those in which it passes the perforating arteries. The
o Form mixed: Alternating periods of diarrhea and mechanism that causes the formation of diverticula is the increased
constipation. endoluminal pressure (especially at the level of the descending colon
- Causes: and sigmoid). Risk factors that determine this pressure increase were:
o Psychological factors: Documented in more than 80% of constipation, low-fiber diet, lack of physical activity. In the elderly
IBS patients. The main factors are: stress, anxiety, diverticula are the leading cause of rectal bleeding (rectal bleeding).
depression. When they increase the contractions of the Diagnostic examinations are: abdominal CT and pelvis with contrast
colon speak of diarrheal variant of IBS, while the stiptica (very useful in an emergency, helps us to investigate whether the
variant involves a slow intestinal transit and a reduced presence of diverticula, both on the presence of complications such as
number of contractions. abscesses and perforations), intestinal X-ray, exam endoscopy
o visceral Hypersensitivity. (Warning : if you are a senior with diverticula and rectal bleeding you
can not proceed with a colonoscopy or you might cause him a
perforation). Diverticula of the colon can be divided into:

- diverticulosis (75%): When diverticula are asymptomatic. ▪
InflammatoryIf the inflammation is localized to the
- Diverticular disease (25%): When diverticula are symptomatic.
small intestine we also have malabsorption. In
This is the case of diverticulitis which is an inflammation of the addition, the stool volume is large because all the
diverticulum. It can be determined, for example, because of food is digested and absorbed. The pieces should be
stagnating in the diverticulum of food residues. The main placed on an empty stomach.
symptom is continuous pain (sometimes more last up to 12-24 ▪
hours), more or less localized, that does not change with the secretory: The infectious agent or drugs stimulate the
formation of second messengers that increase the
evacuation. It may be associated with chills and fever. The
conductance on the apical membrane of the chlorine at
diverticulitis can be uncomplicated (20%) or complicated (5%).
the output (is secreted into the lumen against gradient).
When complicated the only survey that we can do is the TAC (to The chlorine in the lumen draws Na and K, and then
avoid further complications). The disease involves complicated: water, which pass and determine the formation of
o Abscesses: determine ache local. If they are well watery diarrhea. This diarrhea persists during fasting
localized can be drained. and intense and dehydrating. At exams it is seen acidosis
o Fistula: Communication between the colon and another and hypokalemia, so if potassium is administered within
organ that It occurs as a result of erosion of the 24 hours you risk the death of pcs.
mucosa. An example is the fistula colon-bladder which ▪
is an urgency because the presence of fecal material osmotic: The presence in the intestinal lumen of
into the bladder from a urinary infection important. osmotically active substances that attract fluids from
the plasma according to an osmotic gradient. This
o Drilling: You create a route towards the cavity peritoneal diarrhea we find it in case of malabsorption (celiac
resulting peritonitis (acute abdomen and positivity to disease, bacterial contamination), maldigestion
maneuver Blumberg). The perforation is a surgical (lactase deficiency, pancreatic insufficiency) or
emergency. administration of laxatives. Clinically manifested by
O Bowel obstruction: Thickening of the wall Intestinal steatorrhea (presence of fatty substances or
with reduction of lumen caliber and stenosis. undigested in stool) and diarrheal episodes decrease
For more information I suggest you watch this video with fasting.

lesson by Prof. Nardone: impaired motility. o Features of feces: Aqueous, blood, Grasse.
- Criteria Kaplan: They are used for differential diagnosis
Malabsorption: Indicates the deficit passage of one or more between viral or bacterial diarrhea. If the following parameters
products of digestion from the gastrointestinal tract into the are all positive, then the diarrhea is almost certainly caused by
blood. It can be selective (relative to a single nutrient, such as viruses:
lactose intolerance), partial (relative to a part more or less wide of o Associated with vomiting> 50% of affected individuals.
nutrients) or total (typical of celiac disease and other conditions o Incubation of 1-2 days.
that damage the mucosa of the small intestine) . In order to o Average duration of 12-60 h.
attend, the main causes of malabsorption are: celiac disease o Examination of culture negative stool.
→Crohn→ pancreatitis (to assess the functionality of the pancreas - diagnostic algorithm, To assess the presence or absence of
were metered trypsin and chymotrypsin in stool) →infectious. blood
Lactose intoleranceIt can be of three types: e leukocytes in the stool. If there are, diarrhea is
inflammatory. If they are absent:
- Primary: Physiological deficiency in lactase, an enzyme
present at birth, but then is lost. It affects more than 50% o If stool volume <500cc and diarrhea disappears with
fasting diarrhea altered motility.
of adults.
o If the volume of stools is plentiful (500-1000cc) and
- Secondary: Inflammation of the intestine, enzymes of the
diarrhea disappears with fasting osmotic diarrhea.
brush and I malabsorption are destroyed.
o If stool volume> 1000 cc, diarrhea persists despite fasting
- Congenital: AR form, very rare. As soon as the baby takes secretory diarrhea.
milk has an important diarrhea, if we do not recognize the
- Giardia lambliaIt is a common pest in Brazil that is established in
baby dies.
the small intestine. Do not invade the mucosa, or destroys the cells,
Diarrhea: Is an increase in the number of bowel movements (> 3 / so endoscopic examination do not notice anything. Giardiasis can
day) and decreased stool consistency than regular habits and the cause acute diarrhea in 50% of cases or become chronic in 30% of
geographical area where you live. symptomatic pcs. Some conditions predispose to infection, such as
- Classification: the use of proton pump inhibitors, which reduce gastric acidity and
o Duration: therefore remove the block toward the microbes that come from
▪ outside. The main symptoms are: nausea, vomiting, acute watery
Acute: <2 weeks. It is usually caused by inflammation,
caused by bacterial, viral or parasitic. diarrhea debilitating, malabsorption and weight loss. It is
▪ important to make a differential diagnosis with Celiac doing a
Persistent: 2-4 weeks. It is typical of childhood and is cultural examination of the feces, which must be repeated for at
caused by viral infections (rotavirus).
▪ least 3 consecutive days due to intermittent excretion of the
Chronic:> 4 weeks.
o Basic Pathology: Functional, Organic, Post-surgical. or
Office Pathology: Small Intestine, Colon, Pancreas.
O Pathophysiology: (See "Diagnostic Algorithm" later) - Whipple's Disease: Is a malabsorption syndrome caused by the
bacterium Tropheryma whippelii. The four cardinal symptoms are:
arthritis, weight loss, abdominal pain and diarrhea. The diagnosis
is made by means of the small intestine biopsy
e The therapy involves the intake of long-term antibiotics
(because the disease may recur).

Celiac disease: Immune-mediated disorder of sensitivity to gluten, Stricturoplastica: The latter is a plastic enlargement of the intestinal wall
which damages the intestinal mucosa and consequent malabsorption.
It has an increase of lymphocytes T and B, with production of IgA and that consists in making a longitudinal incision in the bowel wall extended
IgG  enterocytes are destroyed regenerative  hyperplasia of the along the entire length of the narrowed segment and then close it
crypts. The autoimmune response may spread to the liver, pancreas, transversely.
skin, thyroid and joints.
- Symptoms Diarrhea, weight loss (malabsorption) and fatigue. In Ulcerative Colitis (RCU): inflammatory and ulcerative chronic disease
children, we also notice a delay nell'accrescimento treatable with that occurs in the colon mucosa, with constant involvement of the
diet. In adults it is also possible to find iron deficiency anemia from rectum, and is characterized most often by a mucus-bloody diarrhea
lack of iron absorption and 4% of infertility in women with celiac (blood and mucus in the stool). Bleeding is the most common local
disease. complication. The inflammation is continuous and localized at the level
of the mucosa and submucosa of the organ. Another complication is
- Diagnosis:
particularly serious toxic colitis, which occurs when the inflammation
o There HLA typing (Human Leukocyte Antigen) inCeliac makes you lose muscle tone paralysis  gas accumulation dilation
disease is a genetic susceptibility test that evaluates the (toxic megacolon: diameter of the transverse colon> 6cm). The
greater or lesser susceptibility of an individual to develop incidence of colorectal cancer has increased. The disease usually begins
the disease and has especially a negative predictive value, in the rectosigmoid portion and then extend as far as to affect the entire
as the absence of risk alleles colon. The main symptoms include diarrhea, bloody-mucus, slight
(DQ2 and DQ8) makes unlikely the development of the abdominal pain, rectal tenesmus (painful spasms of the anus which is
disease. accompanied by urgency of evacuation, caused by inflammation of the
rectum). Unlike Crohn's disease do not develop granulomas, or
o Classification of Marsh: Classification of Marsh
thickening of the wall or stenosis (critical for DD between Crohn
through EGDS, let's make one
infiltrating the colon, and ulcerative colitis). Surgery is curative and is
biopsy in the second or third portion of the duodenum and
performed in 20-30% of patients (colectomy or J-Pouch).
we analyze the tissue histologically:

▪ Marsh 0: normal mucosa Differential Diagnosis between "Crohn's disease" and "RCU":
Marsh I: Interstitial infiltrate of lymphocytes (plasma) without atrophy and These are the two IBD (inflammatory bowel disease) most
without crypt hyperplasia. important. The differential diagnosis is essential:

Marsh II: + Infiltrated hyperplasia of the crypts of Lieberkuhn (which - Crohn's disease:
compensates for the lack of height of the villus; o It develops granulomas noncaseating
Repair) attempt. o It approfonda through the wall of the mucosa
▪ o It's an illness segmental: Affects the colon jumps
Marsh III: Mild atrophy of the villi (a), moderate (b) or severe (c).
o It is a systemic disease may localize in colon is ileum

Marsh IV: Total villous atrophy and cryptic hypoplasia. o Complications are: stenosis is fistulas
- Complications: The most common complication of celiac disease or There is no baseline plasmacytosis
- Ulcerative Colitis:
T-cell lymphoma (5-10%): if a pc celiac disease no longer o It develops granulomas
responds to treatment can it be lymphoma.
o It extrinsic superficially Mucosal or It is a disease
- Refractory Celiac Disease: A small minority of patients are widespread morphology and not segmental or It
suffering from refractory celiac disease, which means they do not consists predominantly localized in rectosigmoid
improve despite a gluten-free diet: This probably happens o Complications are: toxic megacolon is cancer
because the disease has been present for so long that the
o Is present plasmacytosis baseline (At least 5 plasma cells
intestines are no longer able to heal or because the patient does
at the base of the Crypt).
not fully adhere to the diet.
Instrumental investigations to diagnose IBD:
Crohn's disease: Chronic inflammatory bowel disease that can affect any
- Ultrasound bowel: It allows to highlight a thickening of the wall
part of the gastrointestinal tract. It is considered an autoimmune disease,
due to inflammation. The intestine, when normal, you can not
and there is evidence of a genetic predisposition to it. The diseased bowel
see by ultrasound, but when it is inflamed, the walls are
segments are typically well demarcated from adjacent normal bowel
thickened and lose their physiological stratification (usually in
segments (skip lesions), hence the name of regional enteritis. In most
a normal intestine of the layers we see, that when there is
cases we have an ileal involvement (ileus = only 25% of cases; ileum colon
inflammation is lost) . It is a survey simple, economical,
+ = 75% of cases). The symptoms are different depending on the affected
repeatable and non-invasive.
region in the bowel causes diarrhea, malabsorption and pain; in the colon
- Enterorisonanza: MRI of the small intestine. It introduces a
causes diarrhea, rectal bleeding, pain; in the stomach causes indigestion
contrast medium for intravenous injection, that is going to
and pain. The most frequent complications are: obstruction (intestinal
localize at the level of the intestinal wall, and this allows to
stenosis), fistula formation (pathological communication between two
evaluate inflammation.
intestinal cavity), abscesses, intestinal perforation, bleeding, cancer. The
- ColonoscopyIt is a survey that allows you to see
complexity of the disease causes a marked risk of mortality, especially in
directly injuries. [Oral Question: If you have a patient with
the 2 years following diagnosis. At least 50% of pc requires surgical
Crohn's doing a colonoscopy and it is negative, you can use the
treatment in the first 10 years of the disease, 70-80% of pcs require surgery
pill for the small intestine? No, because one of the
later in life. Surgery is not curative because pariamo a segmental disease,
complications of Crohn's strictures, then the pill risk of causing
thus eliminating the damaged portion, can appear other injuries. The
intestinal obstruction].
surgeries performed on small bowel in Crohn's disease are bowel resection
is the 70-80% of pcs require surgery later in life. Surgery is not curative
because pariamo a segmental disease, thus eliminating the damaged
portion, can appear other injuries. The surgeries performed on small 13
bowel in Crohn's disease are bowel resection is the 70-80% of pcs require
surgery later in life. Surgery is not curative because pariamo a segmental
disease, thus eliminating the damaged portion, can appear other injuries.
The surgeries performed on small bowel in Crohn's disease are bowel
resection is the
- histological examination: After a biopsy by endoscopy, we cause rectal bleeding and anemia. To make a
histological survey to learn more about the nature of the injury. diagnosis of at least 100 FAP polyps (numbers are needed
comprised between 10 and 100 are found in a variant
Polyps: Small reliefs of the mucosa. They can be pedunculated TOttenuata and less aggressive called AFAP). The diagnosis is
(protrude from the intestinal wall as a fungus) or sessile (without
confirmed by genetic testing, in fact, the FAP is transmitted
peduncle, coated on the wall of the bowel). They have different
AD mode and is caused by APC: APC mutations is a
- not Neoplastic: For benign reasons. They are 90% of colon negative regulator of B-catenin; If APC is mutated, B-
polyps. After the age of 60 are present in 50% of subjects. They
catenin accumulates and goes into the nucleus where it
have a tendency to develop into cancer. They are divided into:
activates the promoters of
o inflammatory polypsThey are not polyps but occur as such cyclin D1 and MYC. A series of mutations determine the
in the course of inflammatory diseases such as Crohn's transition from initial adenoma (APC mutated), for adenoma
disease, RCU and infectious colitis. They are characterized
advanced (K-RAS mutated) to invasive cancer (mutated p53).
by infiltration of inflammatory cells.
- HNPCC(Colon-Rectal Cancer Hereditary non-polyposis or
Polyps hamartomatous: The hamartoma is a lesion not
Lynch syndrome) tumors tend to appear at a younger age
precancerous with alteration of the mucosal epithelium
than the FAP, and are also located in other locations,
growth (in particular of smooth muscle cells of the wall and
especially in the right colon. The Lynch syndrome is caused by
goblet cells). They are red lesions with peduncles and a
smooth surface, that in 80% of cases are localized in mutations in genes responsible for the shelter of the defects
therectum (especially in juvenile polyposis). of DNA base pairing (DNA mismatch repair, MMR), that is,
those errors that occur during DNA replication. Other
O hyperplastic polyps: Very frequent lesion (especially in the
mutations increase expression of MSH2 and MLH1 genes.
elderly). They are sessile polyps, typically of size equal to
They can be carried out immuno-histochemical investigations
5mm, single or multiple, smooth and mushy. It is mainly
of the tumor tissue with antibodies directed against different
localized in the sigmoid colon and rectum. The cells are
proteins of the MMR, so as to identify which proteins are not
morphologically normal, but have microsatellite instability
expressed correctly. One consequence of inactivation of the
(and therefore are potentially malignant).
MMR is microsatellite instability (MSI):
The delayed exfoliation of these cells (slow cell turnover)
determines a crowding that creates the tight surface Surgical Therapies for Colon-Rectal diseases: In case of drug
architecture feature of these lesions. therapy does not give any response, it proceeds surgically:
- neoplastic: Stem from the proliferation of dysplastic cells - colectomy: Surgical removal of the colon or part of it. It
or adenomatous polyps (or adenomas) Are real neoplasms must be total in all those cases in which the disease may
that if left in situ infiltrate in 100% of cases. The larger the recur or be extended to the remaining part of the organ
size is increased risk of developing a cancer (of magnitude (RCU insensitive to drugs).
larger lesions are highly dysplastic). They have a diameter - J-Pouch: It is to mend the last ileal loop directly to the anus.
of 0.3 to 10 cm and can be pedunculated or sessile. They So they removed both the Colon, Rectum both. It is a
are classified according to their architecture: tubular (90%), procedure used in UC, Crohn's, Colon Cancer, FAP and
tubulo-villous and villous. HNPCC, toxic megacolon.
or Adenoma tightened sessile: Histologically identical polyps - Ano Artificial: To be considered as a last resort, because such
hyperplastic, but have two important differences for the a state would be humiliating for the patient. This surgery can
differential diagnosis: are predominantly located in the right also cause erectile dysfunction as a result of the termination
colon and have an architecture tightened throughout the of erectile nerves.
length of the glands, including the base of the crypt
(While the hyperplastic polyps have tightened architecture MIN CIN &They are two distinct pathways that lead to
confined to the surface). The word means tight 'tumorigenesis in sporadic Colon-Rectal Cancer.
"Serrated" because the glands have a serrated lumen - The pathway of MIN, which is characterized by a widespread
rather than linear. microsatellite instability due to problems in the MMR, represents
15% of all cases of sporadic colorectal cancer.
Colon-Rectal CancerThey represent the most frequent cause of death - The pathway of CIN is characterized by a phenotype of
in the context of visceral malignancies that affect both sexes. The main Chromosome Instability and represents 85% of cases of
risk factors include: diet high in red meat, fats and simple sporadic colorectal cancer.
carbohydrates, smoking and lack of physical activity. Screening using
different tests, such as searching for occult blood in the stool and Adenocarcinoma Colorectal: An adenocarcinoma is a malignant
colonoscopy. The main symptoms caused by intestinal obstruction tumor that originates from glandular epithelium cells that, in this
caused by the tumor mass, are: abdominal pain, vomiting and specific case, originates from the mucosa lining of the colon (which in
constipation. Most of the times are sporadic (occur after age 50), but fact has properties secretory). APC is mutated on both alleles, also
such cases are associated with familial syndromes (which have higher there is correlation with MMR and microsatellite instability. The
incidence below 40 years), such as FAP and HNPCC: adenocarcinomas are distributed fairly evenly along the entire length
of the colon with a few differences between the proximal and distal
- FAP (FAP): characterized by the appearance of hundreds or
colon. In the proximal colon accrue as polypoid masses, while in the
thousands of polyps (adenomas) in the rectum and colon. Many
distal colon
patients are asymptomatic for years, until adenomas become
so large and numerous that
grow in a circumferential annular and produce stenosis and rectum. They identify with colonoscopy. It occurs 20
luminal narrowing, up to the occlusion. cases per 100,000 inhabitants.
- Diagnosis: We use first endoscopic investigations to identify
the source of bleeding. If you can not locate the seat, then we
7 - digestive haemorrhages talk about the occult origins hemorrhages, which account for 2-
3% of cases.
AnemiaIt is a major alarm bell that should make us suspect the
- Types of bleeding:
presence of digestive bleeding. It is important to make a proper
medical history to assess the presence of familiar diseases or hematemesis: Bleeding from the mouth, which in most
(thalassemia, spherocytosis, sickle cell anemia, etc.). cases, is due to rupture of esophageal varices. Could be:
- Laboratory parameters: ▪
bright red: Condition worse because it means that
or Hb: Hemoglobin. It has anemia when the concentration of there has been so excessive bleeding to fill the
Hb falls below 13 g / dl in men or 12 g / dl in women not stomach and cause vomiting.

in pregnancy. The anemia can be mild (10-12 g / dL), Dark red: A coffee beans background. The blood is dark
moderate (8-10 g / dl) or severe (<8 g / dl; blood
It has long been in the stomach and Hb was
transfusion required).
converted into heme dall'HCl.
or reticulocytesThey are index of erythropoietic activity o HemoptysisATTENTION, it's not blood coming
from the digestive tract! It comes from the bronchi or lungs.
or Hematocrit: Percentage of blood volume occupied from It is bright red blood that is emitted by coughing.
erythrocytes, 37-47% in women and 42-52% in men.
o Melena: Blood from the anus issue digested with feces,
or MCH: Media corpuscular hemoglobin.
which then appear black, shiny, sticky and strongly
or MCV: Mean corpuscular volume.
smelling. This blood can derive from the tract
- Classification of basic pathophysiological: It depends on the
upper digestive and from that lower because the black
mechanism responsible dell'anemizzazione.
color is due to the action of bacterial flora.
or by insufficient erythropoiesis: Iporigenerativa anemia,
o rettorragia (Or hematochezia): bright red bleeding from
decreased reticulocytes.
the anus. It is one of the most common symptoms of
or by increased hemolysisRegenerative anemia, increase hemorrhoidal disease, but may be indicative of other
reticulocytes. diseases more
- Classification based on morphology: This classification takes severe as diverticula and some forms of cancer.
into consideration the values of MCV and MCH.
o haematochezia: Emission of feces mixed with bright red
or normochromic normocytic anemiaWhen the values of blood. It differs from Melena which is instead the black stools
MCH and MCV are normal. It is typical of chronic disease: emission. It differs from rectorragy because the latter refers
IBD (inflammatory bowel disease, or Crohn's and UC), to a larger amount of
cancer, cirrhosis. blood in faeces.
or hypochromic microcytic anemia: MCH <27pg + MCV
o Occult bleeding in stool: Feces appear normal, neither
<80fl. The most widespread is the iron-deficiency black nor red, but if you go to analyze the composition we
anemia, characterized by shortage of iron (absorbed in find the presence of blood.
the duodenum-jejunum level). We find it in: celiac
disease (is immediately screened for celiac disease; if the Clinical ClassificationThe first thing to do is to assess the extent of
test is negative we proceed to investigate other causes the bleeding and if there are problems of hypovolemic shock. It is
through gastroscopy), inflammatory processes duodenal- also important to assess how much time there was this blood loss: if
jejunal (Crohn's disease), colon cancer, gastric cancer, it occurred in a short time, the pieces will hypovolemic shock; if it
menstrual cycle. occurred in the course of months or years, the pieces will also
or hyperchromic macrocytic anemia: MCH> 32pg + MCV> appear asymptomatic.
94fl. It is caused by vitamin B12 or folate deficiency, so - Classification hemorrhagic: Evaluate the amount of bleeding
you have to investigate the possible presence of in 4 stages:
intestinal diseases associated with malabsorption (celiac or Stage I: Blood loss 15% (500-750 ml of blood). The
disease). patient is in good health, it may be asymptomatic (circle
of compensation guaranteed by vasoconstriction).
Digestive Bleeding: ▪
HR <100
- Categories: Divide according to the site of bleeding: ▪ PA normal
or Bleeding digestive tract of the upper: over the
▪ Urinary Flow> 30 ml / h
ligament of Treitz (or suspensory ligament of the
▪ Mental state: anxiety
duodenum). They affect the esophagus, stomach and
▪ Cute: Normal
duodenum. They identify with the EGD. They occur 100
cases o Stage II: Blood loss 15-30% (up to 1.5 liter of blood).

100,000 inhabitants. FC> 100
Causes: Ulcers, esophageal varices, esophagitis, ▪ PA normal
▪ cancer ▪ Urinary flow 20-30 ml / h
esophageal, gastric cancer, peptic peptide, ▪ Mental state: agitation
Mallory-Weiss tears (when there is an effort ▪ Cute: wet
vomiting with retching there are movements o Stage III: Blood loss 30-40%
Antiperistaltic that can tear the lower third ▪
FC> 120
esophagus. It happens mostly in alcoholics). ▪ PA reduced
or Bleeding of the lower digestive tract: under the ▪ Urinary Flow 5-15ml / h
ligament of Treitz. They affect the small intestine, the ▪ Mental state: confusion
colon and the

Skin: sweaty compression of sensory nerve trunks). Depending on the source of the
o Stage IV: Blood loss greater than 40% painful stimulus, we can distinguish three types of abdominal pain:

FC> 140 - pure visceral pain: Poorly discriminated, the pc can not give a
▪ PA reduced precise topographical connotation. Origin from deep tissues
▪ Urinary Flow <5 ml / h and is often accompanied by restlessness and psychomotor
▪ Mental state: lethargy symptoms autonomic reflexes (nausea, vomiting, tachycardia,
▪ Skin: cold and cyanotic tachypnea, sweating). The most frequent cause is the spasm of
- Shock Index: Heart Rate / Systolic Hypertension. This parameter smooth muscle (eg. Hyperperistalsis of the gastroenteritis).
should be checked for about 1 hour. The pieces can be defined as - parietal Pain: Very intense and well localized pain, which
non-decompensated if the value is <1 for at least 2 hours. occurs when the stimulus directly affects the dolorifiche
- In the elderlyWhen a senior has a hypovolemic shock we are in a endings of the parietal peritoneum. The pc is always presented
serious situation because of the rigidity of the vessels. As there is with abdomen contract. The maneuver Blumberg evokes a
no correspondence between the elderly lost blood volume and sharp pain in the pc.
cardiovascular signs (rate, blood pressure) do not experience any - referred pain (Visceral-parietal): a starting visceral pain that is
cardiovascular adaptation, related to a muscle-cutaneous parietal area for convergence, in
a Unlike the young subject in which the loss of blood volume medullary layer, visceral afferent neurons on the same surface
causes vasoconstriction. charge of painful sensitivity. An example is that of biliary colic,
whose pain is reported in the scapular region dx (transmitted
EXAMINATION OF APPLICATIONS"You're in the emergency room by diaphragmatic phrenic nerve endings).
and you get a pc in shock with a hemorrhage of the lower digestive
tract, what do you do in the first three minutes?"
1) Venous access Central: To infuse solutions quickly and
2) Nasogastric.
3) Urinary catheter: Connecting to a device for measuring hourly
4) Collect a venous blood sample: For the CBC and for the
identification of blood group. It uses the existing venous access.
5) Heart rate + Beat.
6) Physical Examination.

Between blood tests blood count and INR ALWAYS ask because you
may also need to transfuse platelets or plasma in addition to red
blood cells. Also if the patient suffered fluid infusion comes in early
shock and ask directly to the blood.

8 - Acute Abdomen
Acute AbdomenIt is a syndrome characterized by abdominal pain
with sudden onset and high intensity. It lasts for at least 6 hours.
Possible causes include:
- Relaxing or spasm of a hollow viscus.
- Relaxing capsule of parenchymal organs (liver, spleen,
- Traction of the mesentery or peritoneum.
- Neoplastic infiltration or compression of hollow viscera.
- Compression of sensory nerves.
- Ischemia through the production of catabolites.

Diagnosis through the painIt is possible to hypothesize the cause

(which will need to continue with further investigation) evaluating
the onset, intensity and change in pain:
- continuous pain with violent onset: acute pancreatitis,
perforation, mesenteric embolism, ruptured aortic aneurysm.
- Pain that increases gradually: Type suppurative disease
(appendicitis, peritonitis).

Abdominal pain: There are different mechanisms that can

determine this pain: chemical stimuli (inflammation, variation of the
pH, ischemia, necrosis) and mechanical stimuli (distension of the
capsule of parenchymatous organs, wall distension of hollow
viscera, smooth muscle spasm,

organs, in fact you are evaluating the use of GLP-1 or its receptor
ENDO antagonists for the treatment of diabetes type 2:
o cells α pancreas inhibiting secretion glucagon.
9 - Diabetes o cells β pancreas stimulating secretion Insulin.
Glucose Metabolism: Blood sugar typically has values that fall within o Stomach: slows gastric emptying, as well as to more slowly in the
a very narrow range, ranging from 70 mg / dl to 120-140 mg / dl intestinal absorption of glucose.
(after lunch). Glucose is produced by the liver through a fine balance o SNC: the hormone is within the satiety mechanisms.
between the two main hormones of glucose metabolism, which are o Skeletal Muscle: promotes glucose uptake.
insulin and glucagon. The relationship between insulin and glucagon
- GIP (Glucose-dependent insulinotropic peptide): A hormone
in the liver is important for the activation of some metabolic
produced by the K cells of the duodenum. Its main role is to
pathways and inhibition of other.
stimulate the secretion of insulin, but it has been discovered that
- During fastingLow insulin, glucagon high. The liver, after it has also carries antiapoptotic action by increasing the expression of
finished its glycogen reserves, can no longer produce glucose Bcl-2 (anti-apoptotic) and decreasing the expression of Bax
through glycogenolysis, but must draw on other energy (proapoptotic) in β cells of the pancreas .
reserves activating gluconeogenesis. Gluconeogenesis is the
synthesis of glucose from non-carbohydrate substances, such Diabetes: Syndrome characterized by hyperglycemia.
as glycerol from the lipolysis of the adipose tissue and - Types of diabetes:
glucosintetici amino acids from the proteolysis of muscle tissue. o Diabetes mellitus type 1: It appears as a disease
The production of glucose then continues through autoimmunethat affects the β cells of the pancreas that
gluconeogenesis, while the peripheral organs are trying to secrete insulin (insulin deficiency). Debut <30 years
minimize the uptake of glucose, just to preserve it for the noble o Diabetes mellitus type 2: It appears as a disease
organs such as the brain. metabolic in a context of insulin resistance.
- After lunch: During the glucose, which is absorbed from the It represents 90% of cases and affects the adult. Obesity is the
intestine, goes into the portal circulation and is picked up by the leading cause in people who are genetically predisposed to the
liver was postprandial (first 4-6 hours after lunch). Insulin salt disease. Obesity creates a certain degree of insulin resistance,
because your blood sugar tends to rise, whereas glucagon is but at the beginning does not develop diabetes because the β
suppressed. The liver completely suppresses its production of cells compensate by secreting more insulin (hyperinsulinemia).
glucose due to increasing levels of insulin. At some point these cells are no longer able to compensate
The insulin activates glucose uptake at the level of other organs, and diabetes occurs.
such as skeletal muscle (which must rebuild glycogen stores), O Secondary DiabetesIt is secondary to endocrine
preventing an excessive increase in blood sugar in the blood. These disorders (Cushing's disease), drug-induced pancreatitis
mechanisms are altered in diabetes type 2. In addition, when there or neuroendocrine tumors.
is a condition of insulin resistance, the muscle does not picks up o MODY (Maturity Onset Diabetes of Young): AD disease
and develops hyperglycemia. autoimmune not due to genetic defects in β cells.
The age of onset is less than 25 years.
Insulin: Peptide hormone secreted by the β cells of the pancreatic O SHE GIVES IT (Late Autoimmune Diabetes of Adult):
islets of Langerhans. It has hypoglycemic action (lowers blood the pieces, initially defined as a Type 2 diabetic, it is
glucose by facilitating the passage of glucose from the blood to the actually suffering from a form of autoimmune diabetes in
cells), it promotes glycogen synthesis in the liver (accumulation of slow evolution. It develops in adulthood.
glucose in the form of glycogen) and inhibits glycogenolysis O Gestational Diabetes: Metabolic disturbance glucose that
(breakdown of glycogen to glucose). He also liposintetica action and occurs only during pregnancy due to hormonal
acts centrally by blocking the feeling of hunger. Insulin is an imbalances. It can be controlled with diet and, in extreme
exceptional molecule because besides performs metabolic cases, the use of insulin.
functions, it also effects the growth and gene expression stimulation. - Symptoms:
Oral Question: "What is the hormone responsible for essential o polyuria is polydipsia When glucose exceeds the threshold
hypertension?" Insulin because it is a growth factor that also acts on renal (180mg / dl), appears in the urine and being osmotic
the endothelium. In addition it is noteworthy that the insulin attracts water and by polyuria (and consequently
resistance only affects the metabolic effects of this hormone, while polydipsia, or a feeling of intense thirst).
those of growth remain unchanged. This means that the increase in o polyphagia: Fails the inhibitory effect on the center hunger
insulin concentration, next to insulin resistance, helps to determine (CNS) normally exercised by insulin.
a framework high pressure accompanied by the synthesis of small, O Itching genital: Glucose in the urine means habitat
dense LDL (all cardiovascular risk factors). proliferative for bacteria and fungi.
O visual disturbances: Linked osmotic effect of glucose also
Glucagon: Peptide hormone secreted by the α cells of the pancreatic
exercised at the level of the vitreous humor. The
islets of Langerhans. It is the antagonist of insulin and its action
statistically significant glycemic threshold for
promotes glycogenolysis in the liver (production of glucose from
retinopathy is a fasting blood glucose> 116 (after which
glycogen), inhibits glycogen synthesis and stimulates
gluconeogenesis. it is only a matter of time for the appearance of the
incretins: Hormone secreted after meals that are intended to o Fatigue and impaired healing.
control blood sugar in several ways. - Diagnosis: To confirm the diagnosis, you have to use more than
- GLP-1 (Glucagon-like Peptide 1): A hormone secreted from L one test and associate them with symptomatic manifestations of.
cells in the ileum after a meal. It works on many levels - Fasting blood glucose:

Blood glucose <100: normal.
▪ o hypoglycemic syndrome: Excessive fall in blood glucose
Glucose 100-126: individual at risk (prediabetic) with
susceptibility to cardiovascular complications. levels, up to concentrations equal to or below 50 mg / dl. The
▪ causes are: not taking meals, reduced carbohydrate intake,
Blood glucose> 126: provisional diagnosis of diabetes.
alcohol use, physical activity, erroneous or excessive insulin,
o Glycemic curve - tolerance test OGTT (OGTT): measuring the
concentration of glucose before and after the oral insulinoma (NET). To speak of hypoglycemia should be all 3
administration of sugar solution. components of Whipple's triad: blood glucose <50 ml / dl,

Subject normal: blood glucose <140 to 2 hours from the typical symptoms and regression of the symptoms with the
load. intake of glucose. Typical symptoms are of two categories:
▪ Subject to Risk: 140-200 blood sugar. ▪
Symptoms adrenergic: Manifest themselves first,

Provisional diagnosis of diabetes: blood glucose> 200.
when the blood glucose <50-60. The pc has:
o Glycosylated Hemoglobin (HbA1c): also known as
palpitations, shakiness, rapid heartbeat, anxiety and
hemoglobin "Glycated", it is to form hemoglobin prolonged
feelings of hunger.
exposure to plasma glucose. Optimal values are <6.3%. ▪
Symptoms neuroglycopenic: When glucose values
- Complications:
reach critical levels (<40). They are: headache,
o diabetic ketoacidosisIt is the most frequent endocrine
dizziness, impairment of consciousness, abnormal
emergency. It is a metabolic complication of Diabetes Mellitus
behavior, drowsiness, unconsciousness, coma.
type 1 characterized by this triad: hyperglycemia,
hyperketonemia, metabolic acidosis. For the development of Cardiovascular Complications of Diabetes: A diabetic has a greater
ketoacidosis is the basis of absolute insulin deficiency cardiovascular risk than those who did not have diabetes. The main
associated with increased counter-regulatory hormones. cardiovascular risk factors: high cholesterol, smoking, hypertension,
These controinsulari hormones cortisol, adrenaline, Gh. You low HDL levels. The chronic complications of diabetes can be divided
will have a mix of lipolysis, proteolysis and Glycogenesis. into:
Lipolysis (ie fatty acid release) + absolute insulin deficiency (ie - Microvascular Complications: Is an alteration of the capillaries,
inability to use glucose as an energy source) = cells use fatty which produces its most important consequences of the kidney
acids as an energy source. Their use leads to the formation of level (diabetic nephropathy), the retina (diabetic retinopathy)
ketone bodies accumulate in the blood (hyperketonemia) and of the peripheral and autonomic nervous system (diabetic
and, because of their acidity, the alkaline reserves dry up neuropathy). These phenomena arise from glycation of several
causing acidosis. proteins essential for the integrity of the capillaries, leading to
▪ thickening of the basement membrane of the wall of the latter
Symptoms: We polyuria, polydipsia, dehydration (with
tachycardia and hypotension), acidosis (breath acetone), and a slowdown of the internal blood flow, with negative
water / electrical imbalances (muscle cramps, abdominal repercussions on oxygenation logic and the nourishment of the
pain). tissues involved. The loss of elasticity is due to the formation of
▪ glucose bridges between the elastic fibers. Chemical compounds
Diagnosis: Is made with next generation blood glucose born from glycation are called AGE (Advanced Glication End-
meters which not only measure blood glucose on your
finger, also measure the ketone. The dosage of the products): This acronym refers to the phenomenon of vascular
ketone should be performed every time the blood sclerosis, which usually occurs in older people, while in diabetic
glucose rises above 300 mg / dl. patients occurs very early age. The major microvascular
▪ complications are:or diabetic retinopathy: Damage at the level
Therapy: (For hyperglycemia and hyperketonemia) is
administered insulin, a good deal of of capillaries
liquids (dehydration), potassium (for the electrolyte retina that occurs in 85% of diabetics pcs. We have an
deficiency) and bicarbonate (for acidosis). initial phase characterized by the formation at the
o hyperglycaemic- hyperosmolar syndrome: Is a metabolic expense of retinal capillaries, small aneurysms that can
complication of Diabetes Mellitus type 2 characterized by this rupture and cause bleeding in the retina. The next phase,
triad: severe hyperglycaemia, marked dehydration, called proliferative phase, is characterized by the
hyperosmolarity. It differs from diabetic ketoacidosis because in occlusion of some ischemic retinal capillaries with
this case is not stimulated lipolysis (so no ketogenesis with formation of new capillaries. Being very fragile, newly
formation of ketone bodies) and we acidosis, also the insulin formed capillaries tend to break with ease and this
deficiency is not absolute, but relative. What characterizes this continues rupture determines scarring phenomena that
syndrome is a marked hyperglycemia (increased production of compromise the patient's vision.
hepatic glucose) that is associated with a strong osmotic diuresis o diabetic nephropathy: Disease that involves damage to
with severe dehydration. The glucose levels can exceed 600 mg / load of the extensive network of capillaries constituents
dl. It has a very high mortality, probably because it mainly affects kidney glomeruli (glomerulosclerosis). It is the second
older people between 60 and 70 years. The root causes are all most common cause of chronic renal failure.
those acute processes that increase your insulin needs and o diabetic neuropathy: Give more or less extended charged
increase counter-regulatory hormones: infections, myocardial the peripheral nervous system. Can it relate to many
infarction, stroke, surgery, drugs (diuretics, corticosteroli, beta- different nerves (polyneuropathy), or a single nerve
blockers). The therapy requires urgent rehydration pcs + insulin. (mononeuropathy). Symptoms depend on the type of
nerve affected:

If it is a motor nerve complains spasms, muscle
cramps, weakness and / or muscle paralysis, difficulty
to hold an object, posture and gait disorders (foot
▪ blood pressureand the lipid profile (LDL <100; total cholesterol
If it is a sensory nerve complains: pins and needles,
tingling, numbness, pain, balance deficits, loss of <150-160; triglycerides <150). This multifactorial approach
coordination. achieves a reduction in cardiovascular events by 53%, while
▪ only deal with the sugar we get to 15%.
If it is a nerve of the autonomic nervous system:
constipation or diarrhea, malaise, abdominal
bloating, vomiting, orthostatic hypotension, resting
tachycardia, excessive sweating or absent, sexual
dysfunction, difficulty of complete emptying of the 10 - Obesity and Metabolic Syndrome
bladder, incontinence, dysphagia. [Sarnelli Question:
"what is the molecular mechanism of gastroparesis in ObesityThey speak of obesity when the BMI (body mass index)
diabetic neuropathy of the autonomic nervous è > 30. The BMI is calculated by dividing weight in kilograms by
system?". The answer is: which affects the Nitrogen
Monoxide Synthase. Hyperglycemia compisce in height2. In Italy, the prevalence of obesity is 10%. The 5% of cases
particular neurons producing NO, which inhibit the neuroendocrine causes, which can be: hypothyroidism, syndrome
contraction of the sphincters. In gastroparesis we Prader Willi syndrome, polycystic ovary syndrome (PCOS), Cushing's
have therefore a continued contraction of the
sphincter of the stomach delaying gastric emptying. syndrome. The problem of obesity is related to the problem of
delaying/slow down visceral fat which is associated with reduced insulin sensitivity that
- Macrovascular complicationsThey are the leading cause of predisposes to diabetes, cancer and cardiovascular disease. This is
death of diabetic pcs (80%). Unlike microvascular because this fat produces FFA (Free Fatty Acid, English Free Fatty
complications, which occur only in pieces with overt diabetes, Acids), TNF alpha, inflammatory cytokines.
macrovascular complications can also occur in pieces pre- Metabolic Syndrome: Also known as "Syndrome X" or "insulin
diabetic. This is because the pathogenesis is multifactorial and resistance syndrome", is a clinical situation in which several factors
is mainly based on three pillars: a pillar hyperglycemia (with all related to each other combine to increase the possibility of
the associated damage), the second pillar is represented by developing diabetes (increased risk of 5 times) and circulatory
other risk factors (hypertension, smoking, LDL), the third and It pathologies .
is the last pillar of growth factors. Recall that insulin exerts its - Diagnosis: The pieces must have at least three of the
action through two ways, the metabolic and proliferative that: following conditions:
a pc with insulin resistance may have increased levels of insulin - o abdominal circumference> 102cm man; > 88cm woman.
in the blood, and this increase of insulin causes vascular - o Triglycerides> 150-200 mg / dl
proliferation (with an increase of blood pressure). o Circulating HDL <40mg in humans; <50mg in women.
o ischemic heart disease. o Pressure> 130/85
o Cerebral vascular disease. o Fasting blood glucose> 100 mg / dl
o peripheral arterial Disease: Especially in the limbs lower - Therapy: It is preferred to follow a non-pharmacological
(diabetic foot). intervention in order to act on several parameters simultaneously.
Therapy: in case of: We recommend the subject to practice a bit 'of exercise for 30
- Pz with Type 1 Diabetes: The main thing is to control your blood minutes three times a week, so I have a series of small benefits that
sugar and preserve the health status over time. If the it is young reduce all risk factors: it reduces blood pressure, reduce
our therapeutic approach will be more intense and focused to triglycerides and cholesterol , you lose a few pounds. With a non-
achieve a level of glycosylated hemoglobin <6.5%: in this way we pharmacological intervention is to prevent cases of diabetes 2 to 3.
reduce to the minimum the possibility that our pc may in the future Pharmacological interventions are not recommended because
develop vascular disease. They use of insulin pumps, or systems they act on the single factor: a drug for the pressure, one for
capable of infusing insulin in a continuous manner (the incidence cholesterol, etc.
of retinopathy is 5 times lower than the conventional therapy of 3- - Cholesterol Levels: There is an association between cholesterol
4 insulin injections per day). If the pieces are elderly rather we must levels and mortality, which is equal to the incidence of
have a more cautious approach. Some studies have shown that cardiovascular disease. The lower the value of cholesterol, the
intensive therapy in elderly patients increased the risk of death better. Optimal values are <140 mg / dl.
from hypoglycemia.
Family HypercholesterolemiaWhen cholesterol values remain high,
This is because the elderly is more likely that the arterial tree is despite proper diet and regular exercise, it is called familial
compromised. At the first hypo, your body responds with a hypercholesterolemia. This disease is linked to a problem of the hepatic
surge of adrenaline that causes vasoconstriction in coronary if LDL receptor, which determines a reduced catabolism of the same and
the coronary arteries were already compromised by occlusion, an increased production of cholesterol: the liver does not remove LDL
the subject will have a condition that will lead to cardiac death. from the circulation in adequate amount, or rather perceives a reduced
Ultimately, our therapeutic approach in the elderly must availability of cholesterol and then synthesizes it. It is not a rare
prevent by all means hypoglycemia. condition: 1 in 500 has the disease heterozygous. One must be able to
- Pz with Type 2 Diabetes: To reduce cardiovascular events, we must recognize these pieces because they have a higher risk of developing a
not only monitor glycated hemoglobin, fasting plasma glucose and heart attack at age 40, then a malignant disease. If two people with
postprandial one, but also the familial hypercholesterolemia are combined, the risk of having a
child with the disease in homozygosity is high and this condition is
incompatible with life. These children die before age 10, the only
thing you can do is liver transplantation, because the liver to
synthesize lipoproteins.

11 - Neuroendocrinology feedback is produced CRH (corticotropin), which, in addition
to stimulating the production of ACTH, also stimulates that
Pituitary glandIt is an endocrine gland located at the base of the skull. of MSH.
It is divided into: o Deficiency of TSH: Results in hypothyroidism, with low levels of
- Adenohypophysis (Or anterior pituitary): thyroid hormones. The subject will present fatigue,
o ACTH (Corticotropin): the targets adrenal cortex which is sensitivity to cold, Constipation, dry skin, weight gain, prolonged
divided into 3 parts: sleepiness, bradilalia.
 Glomerular zone: production of mineralocorticoids,
especially aldosterone o GH deficiency: It leads to dwarfism in children, while in adults it
has an impairment of muscle tone and cardiac function. The
▪ collated Zone: Production of glucocorticoids, especially cortisol.
main clinical features are: presence of central obesity (GH is a
▪ reticulated Zone: Production of androgens and estrogens. major lipolytic), the muscles are atopic with asthenia, there is a
o TSH (Thyrotropin): stimulates the synthesis of thyroid reduction of hair growth, small jaw, biventricular hypokinesia,
hormones and acts on the trophism of the thyroid. delay in bone development.
o GH (Somatotropin or growth hormone). ▪ Diagnosis: The most widely used tests are the insulin
hypoglycemia test (ITT) and the GHRH + Arginine.
o FSH and LH (gonadotropin): stimulates the production of
o Deficit of FSH and LH Determines hypogonadism
gonadal steroid and gametogenesis.
hypogonadism and amenorrhea (absence of menstruation)
o PRL (PRL): stimulates maturation of mioepitelio of mammary
in women, while we hypogonadism in humans.
- neurohypophysis (Or posterior pituitary): o Deficit ADH: Because diabetes insipidus and is manifested
by polyuria and polydipsia (increased thirst). The urine are
o ADH (Or Vasopressin Antidiuretic Hormone): adjusts the
very abundant (> 2.5-3 liters / 24h) but little concentrated
permeability of water, Na, Cl and K at the level of tubule
(hypotonic). There are 3 types of diabetes insipidus:
renal manifold. ▪ Central: Quantitative defect ADH.
o Oxytocin: It has as target organ the myometrium and the ▪
nephrogenic: Resistance of the ADH receptors in the
mioepitelio of the mammary glands, is therefore involved in kidney. The DD with the central one is made by ADH test: if
the patient responds to the administration of ADH, then it is
the delivery mechanisms and nell'eiezione milk. "central."

primary polydipsia More common, it is a transitional form
hypopituitarism: Failure that involves the pituitary functions,
and psychogenic. In this case you make the thirst tests,
characterized by the reduction of the secretion of one or more which do not do drink pcs (to be monitored) and evaluate
hormones. It can be: partial, full, front or rear. how concentrated the urine in liquid deficiency: the
• Causes: Pituitary tumors and their treatment (surgery or radiotherapy, nephrogenic and neurogenic (central) fail to concentrate
the urine, while the form of primary polydipsia concentrates
necrosis, infections, immunological disorders, trauma (1/3 cranial the urine.
trauma causes hypopituitarism), subarachnoid hemorrhage, anorexia
or obesity, damage from birth, genetic mutations, pregnancy (when Craniopharyngioma: Is 1.2 to 4% of all brain tumors and 6-9% of those in
the pituitary pregnancy undergoes a considerable increase in the children. He incidence peaks between 5-10 years and between 40-60 years.
production of adaptive They are slow-growing tumors become symptomatic only after reaching
large. The symptoms depend on the affected region and the age of the pc:
PRL that will serve then-feeding), Empty Sella Syndrome (a ventricle
- In adults: Endocrine hypertension, impaired vision, diabetes insipidus,
arachnoid creeps in the front cable and pushes down the pituitary decreased libido (gonadotropin deficiency).
gland leading to a reduction of function). - In children: Growth alterations (GH deficiency), delayed puberty
• Symptoms: The pituitary insufficiency depend tropine is lacking, but (gonadotropin deficiency), diabetes insipidus.
the weakness is present in almost all of these deficits.
Pituitary tumors:
O ACTH deficiency determines hypoadrenocorticism that you
expressed with a deficiency of glucocorticoids (cortisol) and - Classification: They can be divided into primary or secondary, a
mineralocorticoid (aldosterone). Of all the hormones produced by the malignant or benign biological behavior, secreting or non-
secreting. They can be divided into:
pituitary, ACTH is that when deficit, gives the earliest
O Prolactinomas (30%) the most frequently.
O GH-omi (14%): GH-secreting tumours that determine acromegaly
▪ and gigantism.
Symptoms: The presents of hypotensive (primary
symptom). O Secreting adenomas mixed (5%): produces and GH Prolactin.
Other symptoms include fatigue, pallor, anorexia, O Non-secreting adenomas: Do not produce any hormone.
weight loss, hypoglycemia, hyponatremia. They can form voluminous masses causing compression
▪ symptoms.
Therapy: Follow for life and is designed to replace the
missing hormone. It can be direct (pituitary hormone O ACTH-secreting adenomas (4%): they are usually small,
administration) or indirect (hormone administration of but can result in a very imposing symptoms
the target gland). O Adenomas gonadotropic.

Diagnosis Dynamic tests for various hormones. Consists in
ACTH administered per piece: if the patient responds means
that the adrenal gland works fine, but what does not work is the 20
ACTH. If the pc is not responding it could also be of Addison's
disease. The DD between these two diseases is done by
evaluating melasma, present only in Addison's disease: in
Addison's disease have too MSH (melanocyte-stimulating
hormone) because there is cortisol, and
o TSH-secreting adenomas (1%): cause hyperthyroidism. When there is a NET is important to recognize the lesion if the lesion
Unlike primitive hyperthyroidism, in which the TSH is is localized in the pancreas has a worse prognosis than an intestinal
lowered to negative feedback, in this case the TSH is high. lesion. Also can come in two forms: a sporadic (in this case we have
Obviously it made a CT scan to check if there is an to fight a single cancer) and hereditary (which may be more
adenoma and you have to make a DD for peripheral associated lesions, as in the case of MEN). NET can be divided into
resistance to thyroid hormones. two categories:
Acromegaly: Primary adenomas Disproportionate increase in the - NET Function (30%) with production of a substance that has
volume of hands, feet and skull. It is determined by alterations of specific effects, as in NET of the pancreas (insulinoma and
GH secretion, Excessive GH gastrinoma) and pheochromocytomas. For the diagnosis
- Symptoms: Compression of the optic chiasm, with deterioration of looking for the presence in the blood of specific
visual acuity (vision), joint pain, arthritis, carpal tunnel syndrome, immunohistochemical markers: proteins produced
cardiac hypertrophy, ventricular arrhythmias, visceromegaly (in physiologically by neuroendocrine cell even in the absence of
particular of the thyroid, which determines the presence of tumor, but whose concentration increases in the presence of
nodular goiter), macroglossia (which may obstruct the airway), neoplasia (eg. Insulin).
colon polyps, hyperglycaemia (for insulin resistance mediated by - NET Function (70%), we can not study them with markers and
GH). therefore are diagnosed late, when there are already metastases.
- Diagnosis: The patient needs eye exam to evaluate They occur in young subjects and are of considerable size and high
compressive phenomena. The diagnosis is made through the rate of malignancy. As there is no specific markers, the only way to
dosage of GH and IGF-1. Another test to be performed is the diagnose them is by making use of non-specific markers (always
OGTT produced by neuroendocrine cells, but which can be found in high
concentrations even in non-neoplastic conditions):
- OGTT: is a GH suppression test which exploits the blood
O chromogranins: They are soluble acidic glycoprotein in water,
glucose feedback on GH (if blood glucose increases there is an
inhibition of GH), so if by feeding sugar to the values of GH distributed in elettrodensi granules of all neuroendocrine cells
pieces do not fall, then we can confirm the diagnosis. and play an essential role in calcium-dependent exocytosis.
Chromogranin A (CgA) It is the most important one used in
- Therapy: We intervene surgically reaching the sella turcica
clinical practice.
through the nasal cavity. The tumor is removed, trying to
preserve pituitary function and preventing recurrence. Drug o Neuron Specific Enolase: Is not a marker of active secretion,
therapy involves the use of summation antagonists of GH but increases for cytolysis and necrosis, which are very
receptor (GH analogue, but with a modification that does present in the most aggressive forms of cancer.
prevent dimerization). o synaptophysin.

Prolactinomas: There is a positive correlation between the size of Pancreatic NET: Most of these tumors is not functional. Among those
the prolactinoma and serum PRL levels. functional the most frequent is the insulinoma (17%) of which the most
- DD with hyperprolactinemiaIt is a condition characterized by obvious clinical sign is hypoglycaemia. Afterwards we gastrinoma (9%),
the increase, blood levels of prolactin. This may be physiological NET evil borne by Delta pancreatic cells (secreting gastrin, which
(pregnancy) or drug induced: the drug history is important stimulates the production of HCl by parietal cells of the stomach). The
because drugs such as antidepressants do Plasil and raise problem is of hypergastrinemia secondary hypersecretion of gastric
prolactin at very high levels. hydrochloric acid, with abdominal pain and diarrhea are the most
important clinical manifestations because it ulcer occurs in 80% of cases
- Symptoms: In women the symptoms are galactorrhoea (milky
(proximal duodenum). We see in particular the two NET:
secretion from the nipple that occurs outside the lactation
period), hypogonadism and amenorrhea. In men have low - Insulinoma: The characteristic clinical feature is the
sperm counts, decreased libido, impotence. hyperinsulinemic hypoglycemia, which prevail over those
- Diagnosis: This is done with the EO by looking for signs of symptoms neuroglycopenic adrenergic, it caused precisely by
hypogonadism and by squeezing the nipple. It also carries a the production of insulin in excessive quantities and not
dosage of prolactin. For greater diagnostic accuracy, the pieces proportionate in relation to meals. Since insulin has
may undergo MRI or CT scan to search for any pituitary liposintetico effect, it is often associated with obesity. It is more
adenoma. common in women (ratio 2: 1) and occurs between 40 and 60
years. In 80% of cases the adenoma is single and is localized in
- Therapy: Necessary if the amenorrhea persists for more than six
the queue level.
months, because it can cause infertility. Among the most widely
used drugs, dopamine antagonists are the preferred therapy: o Diagnosis: You make of the Fast Test to assess whether
taking these drugs seems to quickly reduce the levels of prolactin the insulin secretion rather than shut down in consideration
in the blood. In patients who do not respond to this therapy, it is of the fasting, continues to be maintained. They make
recommended that the after radiotherapy (to reduce tumor size) withdrawals every two hours (if the blood sugar falls too
or surgery. quickly, the time between one sample and another
decreases). We suspend the test at the onset
NET-(Neuro-Endocrine-Tumor): Cancers that affect the specific symptoms with glucose 40 45 mg /dl.
neuroectodermal cells. They appoint according to the hormone that Surgical removal of insulinns
produce, adding the suffix -OMA (eg. Gastrinoma). It is essential to - Gastrinoma (O Zollinger-Ellison syndrome): excess or
know the grading, which in the case of NET is mainly based on two deficiency of gastrin. It affects mainly males, with age of onset
indicators: the number of mitosis and Ki-67 (nuclear protein of about 40 years. The gastrinoma is confined to 80% of cases
required for cell proliferation). in the triangle of gastrinoma (delimited by the head of the
- NET 1st grade (Well differentiated): n ° mitosis <2-10 and Ki 67
pancreas, from 1to and 2to portion of the duodenum and the
<3% ً
- ◌
- NET 2nd degree (Moderately differentiated): n ° mitosis from
2 to 20 and Ki-67 from 3% to 20%
- NET 3rd degree (Poorly differentiated): Ki-67> 20%.
 Blurry or double vision
Whipple Trial: Whipple procedure — also known as a
pancreaticoduodenectomy — is a complex operation to  Drowsiness
remove the head of the pancreas, the first part of the small  Confusion
intestine (duodenum), the gallbladder and the bile duct  Convulsions or seizures
 Unconsciousness
 Death
 Surgery for tumors or disorders in the body and tail of
the pancreas. Surgery to remove the left side (body
and tail) of the pancreas is called a distal
pancreatectomy. With this procedure, your surgeon
may also need to remove your spleen.

 Surgery to remove the entire pancreas. This is called

total pancreatectomy. You can live relatively normally
without a pancreas but will need lifelong insulin and
enzyme replacement.

 Surgery for tumors affecting nearby blood

vessels. Many people are not considered eligible for
the Whipple procedure or other pancreatic surgeries
if their tumors involve nearby blood vessels. At a very
few medical centers in the United States, highly
specialized and experienced surgeons will safely
perform these operations in select patients. The
procedures involve also removing and reconstructing
parts of blood vessels.

Early warning signs and symptoms

Early signs and symptoms of diabetic hypoglycemia


Irritability or moodiness
Anxiety or nervousness
Nighttime symptoms
Diabetic hypoglycemia can also occur while you sleep.
Signs and symptoms, which can awaken you, include:
 Damp sheets or bedclothes due to perspiration
 Nightmares
 Tiredness, irritability or confusion upon waking
Severe symptoms
If diabetic hypoglycemia goes untreated, signs and
symptoms of severe hypoglycemia can occur. These
 Clumsiness or jerky movements
 Muscle weakness
 Difficulty speaking or slurred speech
point of confluence of the cystic duct with the common bile thyroiditis: Inflammatory disease of the thyroid.
duct). It affects the pancreatic cells D1, gastrin secreting, with - Autoimmune thyroiditis Hashimoto: Thyroiditis is the most
the formation of gastric and duodenal ulcers. The marker is common, characterized by the damage of the thyroid
gastrin, which is very high. parenchyma due to the presence of antibodies anti-TBG
(Thyroxine-binding globulin) and anti-microsomal. thyroid
o Diagnosis: Making the Test of secretin which provides for
appears to increased volume, hypothyroidism develops
the measurement seriata gastrin after intravenous
progressively. The ratio F: M = 18: 1. Under the microscope we
infusion of secretin. In the case of the blood gastrin see a mononuclear inflammatory infiltrate composed of small
Gastrinoma exceeds 200 pg / dl within 2-10 min after lymphocytes, plasma cells and germinal centers. Hashimoto's
infusion of secretin. Having established the presence of thyroiditis may regress spontaneously, but in most cases it
gastrinoma, we proceed with EGDS for ricercarne the tends to become chronic. In the initial phase it can manifest as
seat. a thyrotoxicosis.
o Diagnosis: Peak blood anti-TBG and anti-microsomal. If
present it proceeds with Needle biopsy ultrasound-
12 - Thyroid guided.
Hyperthyroidism: Condition of increased production of thyroid o Therapy: Action is taken when administering thyroxine
hormones. The main clinical manifestations are: increased metabolism, necessary. The patients who require higher doses are
sweating, anxiety, nervousness, motor agitation, tremor, children and pregnant women, because TSH values> 2.4,
hypocholesteremia, weight loss, diarrhea, tachycardia up to atrial which increases to a lack of thyroid hormone feedback,
fibrillation, menstrual disorders, nocturia. can cause abortion or intrauterine death.
- Graves-Basedow's disease: Characterized by an increased - De Quervain's thyroiditis (Or subacute granulomatous
production of antibodies against the TSH receptor. These antibodies thyroiditis) caused by viral infection. The gland appears
increased in size mono- or bilaterally, with hard consistency
mimic the action of TSH and trigger the synthesis and release of
and white / yellow color. F: M = 3: 1. The pc feels sharp pain on
thyroid hormones. It occurs in young (25-40 years), and the ratio F:
M (Female-Male) = 5: 1. We have a triad of symptoms: goiter,
exophthalmos, and myxedema (thickening of the dermis by pre-tibial Thyroid Cancer:
due to the autoimmune process directed against components of the - Follicular adenoma: Swelling lonely, resulting follicular
dermis). epithelium, moving in swallowing. It differs from a goitre since
the adenoma presents a well-defined capsule (not present in
Diagnosis: You make Test to TRH. This test involves the the goiter). In addition, the crop has many nodules (although
administration of TRH per piece: serum TSH levels do not increase in one can be dominant), whereas the adenoma has only one.
suffering from Graves-Basedow for it suppressed by excess hormone. The latter appears to scan cold (low uptake of radioactive
- Plummer's disease: Is due to the presence of a hyperfunctioning benign iodine) and not working. These adenomas have an excellent
tumor which may be single (toxic adenoma, toxic because the thyroid prognosis.
hormones produced in excess are toxic), or multiple (multinodular toxic - o nodule single.
goiter). In most cases we have activating mutations in the TSH receptor o well evident capsule.
(TSH-R). It is more common after age 50 with a ratio F: M = 5: 1. The o Low mitotic activity.
symptoms are less pronounced than in Basedow-Graves (we - Follicular carcinoma: Caused by RAS mutations. Depending on
exophthalmos) because the production of thyroid hormones the degree of invasion of the capsule or of the blood vessels,
è lower. A correct diagnosis of Plummer's disease presents 3 main some pathologists classify this cancer as minimally invasive or
features: highly invasive.
o TSH is low The activity of the thyroid gland completely o nodule single, Circumscribed or infiltrating.
independent from TSH. o It may be or not equipped with a capsule.
o thyroid hormones are high. o Intense mitotic activity with areas of
o presence of hot thyroid nodule: making scintigraphy (With necrosis.
injection of iodinated contrast material) is detected one or O The metastasis not only they can spread to the lymph nodes
more metabolically active nodules. They are distinct from cold regional, but also to the bones, lungs, kidneys and skin.
those who are not active and do not produce hormones. - Papillary carcinoma (Real) it is the most frequent (75%). It is
caused by mutations in B-RAF (V600E). The follicular cells
Therapies for hyperthyroidism: In order of effectiveness, we have: proliferate to form buds. They have typical characteristics:
- ablative therapy Radioiodine I131: Radioactive iodine is used with much psammoma bodies (small soccer balls that are expressions of
higher dose than you give to make scintigraphy. death papillae, degenerating, free cellular substance which
- I131 concentrates in hypercaptative tissue and destroys it from the then calcific) and optically empty cores (so-called orphan
- functional point of view. It should not be used in case of Annie eyes).
pregnancy or breastfeeding. It can determine hypothyroidism. o The nodule can be single or multiple.
- Pharmacological therapy: Administering the thionamides, o Only in 10% of cases have a capsuleoften incomplete.
substances which inhibit the conversion of T4 to T3. o The metastasis They are often limited to the neck lymph
- Surgical therapy: Thyroidectomy or lobectomy. There are risks
or There are the psammoma body.
associated with the passage of the recurrent laryngeal nerve in
thyroid lobes, which could be cut during surgery resulting in paralysis - Papillary carcinoma (Follicular variant): it has all the
of the vocal cords. characteristics of a papillary carcinoma, but does not produce
buds and has the same architecture of a follicular carcinoma.
- Medullary carcinoma (MTC: Medullary Thyroid Carcinoma)
(5-10%): C occur within the cells (or para-follicular) that
produce calcitonin. It is a solid neoplasm, not capsulated,
infiltrating the surrounding structures. Under the microscope, in a deficiency of thyroid hormones into the circulation. The main
we notice deposits of amyloid (which is precisely the calcitonin symptoms are: fatigue, asthenia, cold intolerance, exertional
impaired). The most frequently mutated RET gene. In 25% of dyspnea, weight gain, slowing of intellectual functions, constipation,
cases it is associated with MEN 2: in this case the age of onset dry skin, myxedema (edema in subcutis), depression, alteration of
is certainly anticipated. the menstrual cycle, bradilalia, bradycardia, movements slowed.
o Diagnosis: Just set the levels of serum calcitonin. For - Classification:
better diagnostic certainty can we get examining a needle o Primary Hypothyroidism (Or primary): dysfunction
biopsy by immunohistochemistry showed that amyloid thyroid. It can be caused by: thyroidectomy, dysgenesis,
deposits. Still, you can make genetic testing for RET: can
congenital enzyme defects, iodine deficiency, drugs or
be changed throughout the body (familiar form) or only in
tumor cells (sporadic form). toxic substances.
o Symptoms: diarrhea is skin flush. o Secondary hypothyroidism: bound to dysfunctions
hypothalamic or pituitary.
- Anaplastic carcinoma ( undifferentiated): solid nodular lesion
o Tertiary Hypothyroidism: Syndrome peripheral resistance
in indefinite margins that grows rapidly and that infiltrates the
tissue to thyroid hormones.
surrounding structures thyroid (larynx and esophagus) causing
dysphagia. There are frequent vascular tumor invasion, which - Therapy: Using a medicine called L-thyroxine (L-T4), which is
determine metastasis. Survival to 10 years: 5%. In principle, it administered orally (so it's easy to use) and has a half-life of
is not recommended surgery because the prognosis does not approximately 7 days (so if the patient forgets the tablet the
exceed 6 months. It makes palliative chemo and radio to reduce blood concentration is altered). Side effects are very rare. The
growth. effectiveness of the therapy is measured by measuring the
values of TSH: normal values are 0.35-4.5 μU / ml.
The SIAPEC (Italian Society of Pathology and Cytology Diagnostics
Anatomy) released a system to classify thyroid lesions based on the Congenital Hypothyroidism: AR metabolic disease more common in
results obtained from a sample with fine-needle aspiration: infants absolute (1 in 3,000-5,000 live births). The two main clinical
features of the disease are cretinism and short stature. The ratio F:
- TIR 1: Inadequate sample (blood contamination or artifacts),
repeat sampling. M = 6: 1. Depending on the cause it is divided into:
- TIR 1C: Cystic lesions, that is not diagnostic for non inadequacy - (80%) Thyroid dysgenesis: we can have agenesis (thyroid
of the levy, but the characteristics of the nodule. The levy primitive cell populations begin to proliferate but then, for
should be repeated only in certain clinical settings. The risk of some reason, are locked and do not form the thyroid) or
malignancy is extremely low. defects in migration in the pharynx.
- (20%) of production block: the thyroid is formed and migrates
- TIR 2: Benign, non-neoplastic lesions (hyperplastic nodules of
correctly, but for some reason (eg. Block in the iodine transport)
the thyroid goiter and thyroiditis). The presence of colloid is a
benign sign (as it indicates that the nodule is still well- does not produce thyroid hormones. It can increase volume for
differentiated). Risk of malignancy <3%. Follow up. generating goiter overstimulation of TSH.
- (<1%) of the hypothalamic-pituitary origin.
- TIR 3: Degree of uncertain malignancy. The cytological criteria
are not sufficient, alone, to determine whether the lesion is Acquired Hypothyroidism: It is found in endemic goiter, in which
malignant or benign.
we have an iodine deficiency; for this reason the thyroid is placed
It is divided into two categories according to the histological continuously under the stimulus of TSH, but because it lacks iodine
analysis results: for example in follicular neoplasms let's see if fails to produce sufficient amounts of thyroid hormones and tends
there is capsular and vascular invasion.
to swell. You can have the lumps because the thyroid is over-
O TIR 3A: There is no invasion. 5-10% risk of malignancy. stimulated by TSH and cells tend to proliferate, so the probability
Follow-up six months. [Examination Question: "in that that there are point mutations in genes that control cell growth is
class end thyroid adenomas?". Answer: TIR 3A] very high. There are also some foods, said goitrogens foods, which
o TIR 3B: There is invasion. 15-30% risk of malignancy. bring substances able to interfere with the metabolism of iodine:
- TIR 4: Suspicion of malignancy 60-80%, we proceed with broccoli, cabbage, turnips, spinach, soybean, lettuce, nitrates
surgery. present in meat and preserved fish.
- TIR 5: Evil 100% (papillary carcinoma). The false positive is very
rare. It proceeds with total thyroidectomy peritiroidei with removal Subclinical Hypothyroidism: Condition in which the pieces have
of lymph nodes for staging of the tumor. normal levels of thyroid hormones in a circle, but substantially
elevated TSH. It is very common, especially in the elderly.
Rule-Out and Rule-In: It is used in tests for the detection of genetic
alterations seen in thyroid tissue. What happens in the laboratory to
thyroid aspirates doubt is the sequencing of the DNA with a panel of
50 genes trading, the most frequently mutated in human cancers, 13 - Parathyroid
called Cancer Hotspot Panel. The Parathyroid glands are producing Parathyroid hormone (PTH),
- Rule-Out: Benign markers are sought to rule out the possibility the main regulator of calcium-phosphoric metabolism (other
of a malignant tumor. It is used in the case of TIR 3B. In the case regulators are vitamin D and calcitonin). Serum calcium levels have
of TIR 3A in Italy it is preferred to repeat sampling without a very narrow range, 8.5 to 10.4 mg / dl.
making the Rule-Out (because this is an expensive technique).
hypercalcemia: Characterized by high levels of calcium in the blood
- Rule-In: you search for markers of malignancy to avoid and can be mild (<12 mg / dl), moderate (12-14 mg / dl) or severe (>
unnecessary surgery. It is used in the case of TIR 4. 14 mg / dl).
Hypothyroidism: Very common medical condition that affects, in - Classification:
its subclinical form, 8-10% of the population. It takes the form 23
o Primary Hyperparathyroidism: Due to an adenoma in old age. It is a silent disease, which gives news of him only when
hypersecreting. The size of the adenoma is correlated to the there is pain, but when the pieces feel pain microfracture have
serum calcium levels. The 85-90% of cases are sporadic. already occurred, not after major traumatic events. It must
Familial forms are associated with MEN1 (present in over differentiate dall'osteopenia, which is a modest bone
90% of pcs with this syndrome) or MEN 2A (50% of pcs). demineralization (alarm bells). The bones are composed for 70% of
o Secondary Hyperparathyroidism: Due to chronic renal failure, mineral substance (calcium, phosphorus, etc.) That gives rigidity,
intestinal malabsorption, deficiency or resistance to vitamin D, and 30% from organic substances (collagen, cells) that gives
drugs (AEDs). elasticity and nutrition.
- SymptomsThey are subdivided into Acute and Chronic: - Classification:
o Acute : Fluctuating blood calcium, with peaks of> 14mg / dl or Osteoporosis PrimitivaMore frequent in women. You can
▪ Gastro-Intestinal: Anorexia, nausea, vomiting.

Kidney Polyuria, polydipsia.

Neuro-Muscular Why Ca is important in PdA, we ▪
type 1: Post-menopausal. The physiological
depression, confusion, coma. deficiency of estrogen, at this stage, exposes women
▪ cardiac: Bradycardia, AV block (AV block).
to a more premature depletion of bone mass
o chronic: Stable serum calcium, <14mg / dl. compared to males. This is because estrogens have a
▪ Gastro-Intestinal: Dyspepsia, pancreatitis (for calcium specific task in the activation of vitamin D.
saponification). ▪
▪ kidney: Nephrolithiasis (kidney stones). type 2: Senile. physiological shape.
▪ ▪
Neuro-Muscular: Muscle weakness. Youth: A genetic form.

cardiac: Hypertension, calcification of arteries and o Secondary OsteoporosisMore common in men. It is
heart valves. secondary to endocrine disorders (hyperthyroidism,
▪ Bone manifestations: due to the hyperactivity of the Cushing's syndrome, hyperprolactinemia), metabolic
osteoclasts, we have vertebral collapses and fractures. disorders, obesity (leptin and adiponectin are negative
- Therapy: Calcium levels are recognized by specific receptors in
regulators of vitamin D), smoking, anemia, rheumatic
parathyroid hormone level, CaSR (Calcium Sensing Receptor),
diseases, gastro-enteric (celiac disease), kidney disease,
capable of regulating PTH production. The drug Cinacalcet is a
drugs (particularly glucocorticoids)
calcimimetic acting on these receptors.
- Diagnosis: It is done via MOC (Mineralometria Bone
Hypocalcemia: Deficiency or complete absence of PTH, from surgical Computed), a test that measures bone mineral mass (BMC) and
causes, autoimmune, idiopathic or (rarely) family. It comes in transient bone mineral density (BMD) by means of a special RX. The two
form (<6 months, by reversible damage) in 20-30% of cases. A clinical main parameters are:
sign that we find very often is the nell'ipocalcemia Trousseau sign: we o T-score: Evaluates how much the value in question
measure the pieces of blood pressure, and after we see How long we differs from that of the reference sample (healthy
keep him sidelined sphygmomanometer of that pressure: If there is subject).

hypocalcemia, the pieces began to contract my fingers up to have just Subject healthy: Values between +1 and -1

Osteopenia: Values between -1 and -2.5
the classic hand is characterized by spastic contractions of the hand. ▪
Osteoporosis: Values <-2.5
- Symptoms:
or muscle: cramps, muscle spasms, arrhythmias is failure o Z-score: Specifies how much the value in question differs
cardiac from that of a healthy population of reference, composed
of persons of the same sex and the same age as the subject
or No muscle: cataract (Subcapsular) dry skin fragile,
under consideration. Because of this feature it is
Dermatitis (impetigo herpetiformis).
particularly suitable for children and adolescents.
- Therapy: Using the Teriparatide, a synthetic polypeptide containing
the first 34 amino acids of the N-terminal sequence (biologically
- Therapy: In the past we have used a basic therapy of estrogen,
active part) of Parathyroid. Similarly to the PTH, the Teriparatide
but then it is seen that an increase of estrogen is related to an
stimulates bone formation going to act on osteoblasts, increases the increased incidence of certain types of cancer. Now they use
absorption of Ca in the intestine and increases its tubular diphosphonates (which reduce the incidence of fractures
reabsorption. because they improve the status of bone mineralization) and
recombinant PTH and inhibitors of RANK-L (ligand that
pseudohypoparathyroidism: Heterogeneous group of inherited activates osteoclasts). Drug therapy is associated with a diet
diseases that have in common the peripheral resistance to parathyroid rich in calcium (800mg / day between 30-60 years), phosphorus
hormone, resulting in hypocalcemia and hyperphosphatemia. and Vitamin D.
Endocrine Diseases associated with Osteoporosis:
- Hyperthyroidism: It depends on the action of TSH on osteoclasts.
14 - Osteoporosis In the last few years it has demonstrated that TSH has a major
[Asked very topic in recent exams] effect on osteoclasts. Primary hyperthyroidism you have
osteoporosis and initially it was thought that they were the cause
Osteoporosis is a systemic skeletal disease that is characterized by:
of thyroid hormones, but then it turned out that the TSH is to act
low bone mass; alteration of microarchitecture; increased fragility.
with inhibitory effect on osteoclasts. The primary hyperthyroidism
These conditions lead to a high risk of fracture. In Campania 12% of
leads to a decrease of TSH secretion via a negative feedback
women and 4% of men are affected by this disease. It is more frequent
mechanism, so the inhibition of TSH is less on osteoclasts and
increases bone resorption.
- Cushing's Syndrome: Glucocorticoids act directly on
osteoclasts, reducing apoptosis and increasing proliferation.

- Hyperparathyroidism: Also the increase of PTH is able to o Hypokalemia: Potassium regulates many functions, such
modulate bone absorption by activating osteoclasts. as the contractile activity of the myocardium. One of his
- hyperprolactinaemia: The increase of prolactin causes a deficiency can cause myopathy, severe disorders cardio-
reduction of the production of estrogen, which is responsible circulatory and neurological damage.
in turn of bone demineralization.
Cushing's Syndrome: Overproduction of glucocorticoids (cortisol)
by the adrenal gland. Glucocorticoids are hyperglycaemic hormone,
or increase the availability of glucose; this effect also occurs through
15 - Adrenal neoglucogenesis, with transformation of the proteins in
Adrenal: Is an endocrine gland comprised of two separate carbohydrates.
portions: - Classification:
- Cortical: Is divided into 3 areas: o Primary (ACTH-dependent): not only stimulates
o glomerular area: External, mineralocorticoid glucocorticoids, but also mineralocorticoid and
(Aldosterone). androgens.
O zona fasciculata: Intermediate, glucocorticoids (cortisol).  pituitary adenoma: The pituitary secretes more
ACTH (which stimulate the adrenal glands to
O netted area. zone reticlate: Internal, sex hormones
produce more cortisol). It occurs in 68% of all cases
(androgens, Estrogen).
of Cushing's syndrome.
- medullary: Produces Norepinephrine (20%) and adrenaline ▪ adenoma hypothalamic: The hypothalamus secretes
(80%). more CRH (which stimulate the pituitary gland to
release more ACTH).
Aldosteronism: Disease characterized by hypersecretion of
mineralocorticoid (aldosterone) by the adrenal gland. Aldosterone ▪ ectopic ACTH syndrome: ACTH is produced in
is a hormone that increases the reabsorption of Na+ and H2O at the several other pituitary tissues to cause cancer. It
occurs in 12% of all cases of Cushing's syndrome.
level of ENaC channels of the manifold distal tubule and increases 
the excretion of K+, With consequent hypernatremia and ectopic CRH syndrome.
hypokalemia. o Secondary (ACTH-independent): in this case the ACTH levels
- Classification: are low for the negative feedback on the hypothalamus.
O Primary: Also known as Conn's syndrome, is due to Recently it was discovered that these patients have the
internal causes the adrenal gland. The renin levels are L206R mutation (Leucine in position 206 replaced with
very low, suggesting that the feedback is working. There Arginine) that alters the binding between the catalytic
diagnosis it is based on the aldosterone / renin ratio: if> sub-units and sub-units of the regulatory PRKACA causing
25 suspected; if> 50 diagnostic. It is divided into: hyperactivity.
▪ aldosterone-secreting adrenal adenoma (70%).  adrenocortical adenoma: Benign tumor of the cortex.
▪  adrenocortical carcinoma: Cortical malignancy.
Bilateral adrenal hyperplasia (25%).
▪ - clinical picture: Cortisol has effects on different organs and
aldosterone secreting adrenal carcinoma (4%).

glucocorticoid suppressible aldosteronism (1%): a o Osteoporosis and vertebral fracture: By the action of
family disease AD. In the presence of this chimeric gene, glucocorticoids on osteoclasts.
we are faced with a situation in which the Aldosterone is o Hypertension.
under the control of ACTH; ACTH therefore not only
regulates the release of cortisol, but also aldosterone. To o Hypokalemia: Cortisol, when it is in excess, it can activate
treat aldosterone receptors by determining this typical
situation hyperaldosteronism.
affected individuals, cortisol is administered from the
outside so that, via negative feedback, to lower the o mood Changes: The pc is very delicate, often crying and
levels of ACTH and thus transcription has difficulty following therapy
aldosterone. o Reduction of muscle mass and lipid: Due to the catabolic
cortisol. Lipids are put into circulation per share (probably)
o Secondary It is rather due to hyperactivity of the renin-
local enzymes that operate under the stimulation of
angiotensin-aldosterone system. In these cases the
feedback is no longer functioning and levels of renin and cortisol, leading to accumulation of fat in only a few
angiotensin are high. It can occur in the case of: points:
o Renal artery obstruction or heart failure: the blood does  On the face: moon face. Face widened with
not arrive correctly to the kidney then the blood pressure hypertrophy and erythrosis (redness) of the
is perceived lower than the real one and is fed into the cheekbones.
▪ On the back: buffalo hump.
circulating renin, resulting in an increased release of ▪
On the abdomen: protruding abdomen, with Rubre
aldosterone. striae (stretch marks in red).
nephrotic syndrome In fact when the kidney undergoes o plethora facial: Red high color on the skin.
damage and will begin losing proteins from the plasma to o bruising and petechiae: Caused by fragile vessels
the urine, we may have to give compensatory
hypersecretion of renin. due to the catabolic effects of cortisol. The skin becomes

reninomi: Juxtaglomerular cells of tumors, namely thin, you see the capillaries that are much more fragile and
the renin-secreting cells. also has difficulties in repairing wounds.
- Symptoms: The clinical picture is determined by: o carbohydrate intolerance: Corticosteroids act on
o hypernatremia: Reabsorption of Na, for its carbohydrate metabolism.
"Atmosphere of solvation", also involves a reabsorption o hyperandrogenism: Excessive production of androgen
of H2O such as to determine arterial hypertension. hormones in women accompanied by hirsutism (abnormal
hair growth in locations where they normally

They are absent). It also determines acne and menstrual dysfunction. a particular tissue-tropism for the adrenal gland.
- Diagnosis: the diagnosis of Cushing's syndrome is confirmed O Adrenoleukodystrophy X-linked (X-ADL) (10-20%).
by the presence of high levels of cortisol, which can be dosed O rare forms (2-5%).
in the blood, in urine collected in 24 hours or in saliva. - Diagnosis: Dosiamo cortisol levels (at 8:00 am). If you are very
In the latter case the sample is collected towards the midnight, low (<3μg / dl) then we have a good chance that there is a deficit
time of day when cortisol levels in healthy people they are in its production. We continue by performing an ACTH
quite low. Clinical tests they are also performed after the stimulation test: if administering ACTH does not occur any
administration of suppressors, such as dexamethasone, cortisol response, then we can confirm the diagnosis. We can also
or hormonal stimulators (like ACTH); it is also possible to dose ACTH levels in Addison's disease are high.
evaluate the plasma levels of adrenocorticotropic hormone to - Therapy: It is based on the use of hydrocortisone (30mg daily),
highlight the forms caused from ACTH hypersecretion. In which compensates for the glucocorticoid deficiency. In the
addition to clinical tests, they are made often necessary forms with mineralocorticoid deficiency it may be necessary to
instrumental investigations, such as a CT scan or an MRI scan add fluoroidrocortisone (has high mineralocorticoid activity).
to evaluate the appearance of the adrenal glands and the
pituitary gland (there may be very small adenomas, even 2 Congenital Adrenal Hyperplasia (CAH): It represents a group of
mm).' hereditary metabolic defects autosomal recessive, each of which is
characterized by the reduction or absence of a particular enzyme
- Therapy: The treatment is subject to a correct identification of its
necessary for the development of cortical steroids, principally
origins (ACTH-dependent or ACTH-independent pituitary /
ectopic tumor). The forms of tumor origin can be resolved by cortisol. The cortisol deficiency leads to increased secretion of ACTH,
surgery or radiation therapies. In some pieces in which surgical which causes adrenal hyperplasia. The steroidogenesis is then
option is not viable, it is necessary the use of drugs that reduce channeled in other ways, with increased production of androgens
the production of cortisol. They come in three classes: (especially testosterone), which are responsible for virilization
1. Modulators of ACTH secretion. (aberrant sexual differentiation with alteration of the development of
secondary sexual organs).
2. Inhibitors of adrenal steroidogenesis.
3. Antagonists of the cortisol receptor. - clinical picture: The girl initially normal development of sexual
- Difference between syndrome and Cushing's disease: characteristics, but when it takes over the excess of androgens
O Cushing's Syndrome: Clinical condition characterized excess has the development of male sexual characteristics. Actually this
glucocorticoid hormones in the bloodstream. When the is not true, and their male sexual organs, because the testicles
body produces too much cortisol, no matter what is the are absent, but simply have a clitoral hypertrophy which makes it
cause, we are in the presence of Cushing's Syndrome. look like a peniero organ.
o Cushing's Disease It is the most common cause of the - Pathogenesis: You have the mutation of one of the five enzymes
homonymous syndrome. It is an endocrine disease, due to involved in the synthesis of cholesterol. The mutation of one of
hypersecretion of chronic pituitary ACTH caused by a these leads to a reduced production of glucocorticoids and
pituitary adenoma corticotroph. mineralocorticoids, with a consequent increase of androgens. In
90-95% of cases the enzyme affected is the 21-hydroxylase
Addison's Disease (Chronic Adrenal Insufficiency) is a bit 'the opposite (encoded by the gene CYP-21), which normally catalyzes the
of Cushing's disease. It has deficits in the production of glucocorticoid conversion of 17-hydroxy-progesterone in 11-deoxycortisol,
and mineralocorticoid for alteration or destruction of the adrenal precursor of cortisol.
cells. - Clinical variants: The severity of the disease varies depending on
- Symptoms: It is expressed by a classical triad. the residual activity of 21-hydroxylase in the following mutation:
o melanodermia (90-100%): hyperpigmentation of the skin. O classic form: Occurs in the neonatal period or in early stages
If there is a block of the adrenal gland does overproduction of of childhood. It can be of two types:
pituitary ACTH. Given that the precursor of ACTH, POMC, also  with salt loss: Total enzyme deficiency. It is produced either
originates the MSH hormone (which determines the cortisol or aldosterone. If not effectively treated leads to death.
proliferation of melanocytes), it is also Clinical symptoms are: deterioration in cardiac function,
reduced glomerular filtration, vomiting, diarrhea, weight loss,
MSH itself increased production. The hyperpigmentation
dehydration, hyponatremia, hyperkalemia, hypotension and
also affects the mucous membranes, in particular oral,
masculinization in girls.
gingival, vaginal and rectal.
 simple virilization: Do not make enough cortisol, but you have
O Slimming is asthenia (90%): for the lack of action cortisol adequate amounts of Aldosterone. It has, however virilization.
on cellular metabolism (hypoglycemia, gluconeogenesis
o non-classical form: il difetto non è totale, ma parziale. In
deficit, deficit lipolysis).
genere è asintomatica o associata a pochi segni di
O low blood pressure is hyperkalemia (70%): for deficit iperandrogenismo. In genere si manifesta tardivamente.
aldosterone. [Examination Question: "What is the most Può essere di due tipi:
common cause of hyperkalemia in endocrinology?".  ad insorgenza tardiva: sintomatica, si verificano condizioni quali
Answer: "Addison's disease"] pubertà precoce, acne, irsutismo,
- Classification: 26
O Autoimmune form (65-70%): it is observed the presence of
autoimmune inflammatory infiltrate.
 post-tuberculosis (20-25%) is via a spread linfoematogena
Mycobacterium tuberculosis, which has
menstrual abnormalities, azoospermia (absence of 16 - Multiple Endocrine Neoplasia (MEN)
sperm in the semen), oligospermia, infertility. The MEN describe a group of 3 autosomal dominant hereditary
▪ syndromes (MEN1, MEN 2A, MEN 2B) characterized by onset of
cryptically: Asymptomatic. Prevail clinical signs
associated with a condition of mild-moderate malignant proliferative processes at the expense of some endocrine
hyperandrogenism. glands. The onset occurs in at least 2 glands and can be synchronous
- prenatal therapy It is recommended to do the genetic analysis (simultaneously) or metachronous (at two different times).
of the gene CYP-21 to determine if you are disabled or
- MEN1: Also known as the "syndrome of 3 p" (parathyroid,
suffering from this disease. If the unborn child is suffering are
pancreas, pituitary), but in 40% of cases there is also concern
administered in pregnant women low-dose dexamethasone
with adrenal hypercortisolism (Cushing). AD is linked to
(analogue of cortisol, to determine a reduction in ACTH).
Depending on the child's sex is so decided to suspend (male) mutations of the MEN1 gene (tumour suppressor). It occurs
or to continue (female) therapy. If the disease is in the late between 30 and 40 years.
phase, it may be associated with any corrective surgical o Target Organs:
▪ (90%) Parathyroid (hyperplasia or neoplasia):
hypercalcemia, osteopathy.
incidentaloma: Adrenal tumor discovered accidentally during the ▪ (50-80%) Pancreas (adenoma): gastrinoma,
course of investigation moves from other causes, such as an insulinoma.
▪ (50%) Pituitary (adenomas dell'adenoipofisi):
ultrasound of the abdomen in a patient with gallstones. Very often,
prolactinoma, ACTH-oma, GH-oma.
when we are faced with a neoplastic lesion, it is a benign lesion and ▪ (40%) Adrenal gland (adenoma of the adrenal
non-secretory. We must therefore make endocrinological cortex): Cushing.
examination and determine whether treatment. o Diagnosis The first thing to do is set the levels of calcium
and PTH. To confirm the suspicion dosiamo also: insulin,
Pheochromocytoma: Is a tumour originating from the chromaffin
glucagon, somatostatin, chromogranin, serotonin and
cells of the adrenal medulla. It is a rare tumour, which can be gastrin. Important in these conditions the use of CT scans,
suspected when the pc that is good has suddenly of hypertensive resonance and histological analysis of the sentinel lymph
crisis, or when suffering from chronic resistant hypertension, or nodes.
when we have a incidentaloma. It can be sporadic or familial (MEN o Therapy The choice of therapy depends on the location of
2A and MEN 2B). If we find a pheochromocytoma in a patient, we tumours, very often we resort to surgery. There are
also suspect the presence of other cancers, such as dependents of currently treatments that can eliminate the mutation,
the thyroid and parathyroid. however, you can control the symptoms with drugs
- Rule of 10%: 10% is headquartered than adrenal, 10% is specifically.
bilateral, 10% develops in familial syndromes (MEN 2A and 2B), - MEN 2A: AD has a transmission. The gene involved in the
the 10% spread in the pediatric age, 10% are malignant. This pathogenesis is what RET encodes a tyrosine kinase membrane
rule is now partially refuted: according to the latest estimate,
receptor. It is a receptor for growth factors. This receptor is also
the percentage of family pheochromocytomas is 25%.
important for the development of certain peripheral nerve
- Symptoms: In addition to arterial hypertension (90%), the elements, such as intestinal ganglia: inactivating mutations
classic symptom triad is given by headache (80%, refractory to block the development plexus of Auerbach and Meissner and
anti-inflammatory since due to vascular effects), sweating
patients have problems in the intestinal peristalsis. In MEN 2A
(71%) and palpitation (by excess catecholamines).
mutation affecting a cysteine residue in the extracellular
- Diagnosis: There were metered urinary catecholamines that domain. Genetic testing should be done in all patients with
both serum (after a proper diet to avoid the introduction of
medullary thyroid carcinoma (MTC).
foods that may interfere with an appropriate dosage). It
o Target Organs:
proceeds with CT or scintigraphy. ▪ Medullary Thyroid (90-100%): TCM.

- Therapy: It is essentially surgical (unilateral in sporadic forms, ▪ adrenal (40-50%): pheochromocytoma (often bilateral).
▪ Parathyroid (10-25%): parathyroid adenomas.
bilateral in familiar ones). In the case of malignant forms it is
- MEN 2BEven in this case, the mutation affects RET, however,
also used to radiotherapy or chemotherapy. Medical therapy
to be changed is an intracellular domain of methionine. It has a
involves administering ALFA-blockers. beta-blockers It is
more severe phenotype of MEN 2A, but is less frequent. If the
important NOT given to this pc (often doctors can make
genetic test is positive for this mutation, the treatment includes
mistakes and give beta-blockers to a pc that does not know,
a prophylactic thyroidectomy within the first year of life (within
which refers hypertension and tachycardia): This would fail
the first 5 in the case of MEN 2A) + surgical removal of the
because the vasodilatory effects of beta-blockers and this it
tumours identified. The distinguishing feature is the marfanoid
could cause a hypertensive crisis difficult to control. The ALFA-
habitus: the pieces are tall, thin, with long arms and fingers,
blockers should be used for at least 15 days before holding the
ligamentous laxity (thumb that can fold on the back of the
pieces surgery (After these 15 days you are also used beta-
hand) and faired chest, but do not have alterations in the
blockers and then we proceed with the operation).
crystalline and aorta such as individuals suffering from Marfan
o Target Organs: MEN 2B usually presence without
hyperparathyroidism. The main organs affected are:
▪ Medullary Thyroid (100%): MTC.
▪ Adrenal: Pheochromocytoma.

17 - Female gonadal disorders to cover the cornea), a chest armor, infantilism of the genitalia
characters, small jaw, a number of melanocytic nevi.
amenorrhea: No flow at least 6 months. Could be:
- primary: Absence of menarche (first menstruation) at age 16. 3XX pure gonadal dysgenesis: Baby girls are girls without genital
Diagnosis is based on secondary sexual characteristics:
ambiguity. However, during adolescence or early adulthood, exhibit
o if the external genitalia are virilization Then we have a delay or absence of puberty with amenorrhea. The development of
case female pseudohermaphroditism. the internal and external genitalia is normal. The ovarian dysgenesis
o if the external genitalia are absent or recently formed, is due to genetic defects of ovarian development, such as mutations
then let's look at the levels of FSH and LH: which inactivate the FSH-R receptor. So the ovary is resistant to
▪ gonadotropin stimulation.
if levels are reduced we associate them:
✓ 4Resistant Ovarian SyndromeEven in this case the ovary is resistant
Organic causes of hypogonadotropic
hypogonadism: Masses hypothalamic or to gonadotropin stimulation, but there are no genetic mutations in
pituitary due to inflammation or tumors. the same or its receptors. It is likely that the obstacle is due to the

Kallman syndrome1: Failure of Gn-RH presence of anti-gonadotropin receptor antibodies.

if the levels are normal associate them: 5Androgen
✓ insensitivity syndrome (Morris) (Testicular
functional amenorrhea: Stress, slimming,
competitive sport. feminization): the karyotype was 46XY, is characterized by abnormal
✓ androgen receptor (remember: the main androgen is testosterone).
Delayed puberty Constitutional.
▪ The testes are there but testosterone does not work in peripheral
if levels are increased we evaluate the karyotype:

45 X0: Turner Syndrome2. tissues, so the subject will look feminine. A patient is very famous
✓ Marilyn Pauline Novak (known by the name of Kim Novak).
46 XX: pure gonadal dysgenesis3 (Condition
linked to the resistance to ovarian stimulation of
gonadotropins) or deficit of steroidogenesis. 6Polycystic Ovarian Syndrome (PCOS): Iperandrogenitismo ovarian

46 XX: Resistant Ovarian Syndrome4.
o if the external genitalia are present we evaluate: syndrome. It is the most common gynecological disorder in women

anatomical abnormalities. of reproductive age (prevalence 6-7%) and is the leading cause of

if the uterus is absent: we evaluate the karyotype. female infertility. Historically, it was known under the name of Stein-

46 XY: androgen insensitivity syndrome5 Leventhal syndrome: this syndrome necessarily demanded the
(Testicular feminization). presence of multi-cystic ovaries, while today it is no longer an

46 XX: agenesis of the Muller ducts. essential criterion. Today it is believed that it is a real metabolic
- secondary: Girl who has experienced menarche, but for at least syndrome.
6 months no longer had the cycle. We assess whether the - clinical picture: The main manifestations of the disease are:
patient is pregnant dosing the βhCG (beta-human Chorionic o infertility.
Gonadotrophin). This hormone has the task of preventing the o hyperandrogenism: Excess androgens which cause:
disintegration of the corpus luteum in the ovary and to ▪
acne, hirsutism and elevated sebaceous secretion.
maintain the production of progesterone, which is crucial for ▪
oligomenorrhea (60%) or amenorrhea (30%).
the continued pregnancy.
o polycystic ovaries magnified: Through pelvic ultrasound
o the patient is pregnant.
is You can observe more than 12 pelvic follicles. The
o the patient is not pregnant:
 increase in FSH and LH decrease of oestrogen. ovary has a volume higher than 8 cm3.
 FSH and LH normal and normal oestrogen: polycystic o altered ratio LH / FSH: More LH FSH (see theory 1).
ovary syndrome6, Thyroid disease, Cushing's disease, o obesity and insulin resistance: To dysfunction of adipose
Addison's disease (diseases involving the steroid tissue (see theory 3).
metabolism). - Pathogenesis3 assumptions have been made:
1. hypothalamic dysfunction: Entails of Gn-RH secretion
1Kallman syndrome: In this syndrome does not occur pubertal
peaks more accelerated with an increase in the secretion
development because of lack of hypothalamic neurons secreting Gn- of gonadotropins (with a ratio in favor of LH). The
RH. It has a prevalence of 1 / 8,000 males and 1 / 40,000 for females. increased LH stimulates ovarian theca to produce more
It is associated with anosmia (loss of smell) or hyposmia (decreased androgens, for which a fundamental characteristic of this
olfactory sensitivity). We will find LH-FSH low and alterations of the pathology is the excess androgenic
olfactory bulb.
(Hyperandrogenism) which has two fundamental
2Turner Syndrome (TS) is the only monosomy compatible with life, consequences: irutismo and alteration of the regulatory
although 98% of fetuses go against spontaneous death. It depends mechanisms of folliculogenesis (not the follicle regresses
on a meiotic nondisjunction that occurs during spermatogenesis in to corpus luteum and then disappear, but remains under
80% of cases but is not correlated with the age of the parents have arrest, for which accumulate these follicles not erupted
a child with TS does not increase the risk of having another affected. properly and form cysts).
The 1to cause of death in a patient affected by TS is the aortic 2. The second hypothesis says that hyperandrogenism is of
coarctation. ovarian origin, but of adrenal origin.
- Phenotype: Short stature (useful diagnostic criterion), 3. To date, it is identified as the main cause of PCOS and
pterygium (formation of a fibrovascular membrane at the level unique insulin resistance (IR). The hyperinsulinism
of the scleral conjunctiva which may extend progressively until induces the secretion of ovarian androgen levels, which
stimulate the growth of adipose tissue with visceral fat
formation, which in turn induces activation of the TNF-
alpha secretion, leptin, IL6 and reduction of

adiponectin, which increase the phenomenon of insulin o In humansThe first sign is the increase in testicular
resistance (vicious circle). There are several evidences that volume, followed by the development of pubic hair and
show that the IR may be the cause, as insulin: axillary and increased penis length. The first ejaculation
 It directly stimulates the secretion of ovarian occurs around 13-14 years and spermatogenesis begins at
androgen level. the age of 11-15 years. There may be the appearance of
▪ gynecomastia, ie a volume increase of the glandular
It reduces the amount of SHBG (Sex Hormon Binding portion of the human breast. In some cases it is
Globulin), the protein that regulates the amount of
free androgens: alterations of this protein result in an pathological, since index of an excessive amount of
increase of the free portion of hormones. estrogen, while in puberty is physiological.
▪ - What affect pubertal development: The greater consumption
Increase the LH receptor expression in ovarian level, of proteins and a greater caloric intake are connected to an
so that the ovary is more sensitive to stimulation by
LH with promotion of the growth of cysts and ovarian early menarche. The sport seems to anticipate pubertal
androgen production. development without comportarne a modification of the
▪ significant parameters in the male. Unlike females who practice
It stimulates the production of androgens at the
level of the adrenal gland with further increase. sport at a competitive level show a slowing in the progression
of mammary development, delay seems to increase in athletes
o Diagnosis: It is based on the revised Rotterdam criteria
with low body weight.
(2003), which are the most current, used and recognized.
The diagnosis is confirmed if there are 2 of the following 3 early puberty (PP) is divided into:
conditions: - pp true (Or central): condition caused by axis premature
irutismo; presence of polycystic ovaries; menstrual activation of the hypothalamic-pituitary-gonadal axis. You Gn-
disorders (basically oligomenorrhea). RH dependent. It is characterized by the appearance of
o Therapy: We must aim at improving insulin sensitivity. This secondary sexual characteristics at an age not physiological. In
objective can be achieved with proper food hygiene and this case a non-synchronization of sex hormones with GH
practicing physical activity (which is also the most effective causes a premature fusion of the cartilages, then the children
drug). If diet and exercise do not work (80% of the time is are in a higher early stage, but the final height is lower than the
the pcs not to respect them), drugs that are used: average.

They reduce the production of androgens by the - early pseudopubertà (Or peripheral): simulates what happens
ovary. in puberty, but there is no axis activation, indeed there is a
▪ They block their action on cell receptors. secretion of sex steroids which does not depend on this
▪ They increase the secretion of FSH. activation. This condition can be generated by secreting
early menopause: The physiological menopause occurs at 50-55
years, while that early is anticipated at 40-45 years. It can be caused
by cigarette smoke and were undernourished. It is also important to 19 - Men gonadal disorders
investigate the age of the mother of menopause.
male Hypogonadism: The testis is a gland that does two things: on
the one hand produces testosterone, which we need for secondary
sexual characteristics and normal sexual activity, the other takes
18 - Puberty care of spermatogenesis, which is necessary for fertility. We
pubertal development: Secretion of gonadotropins is adjusted in a hypogonadism when one or both of these functions are to be
manner pulsatine from GnRH. The center of the pulsatility generator deficient.
è It located in the hypothalamus at the level of the arcuate nucleus. - Classification:
This pulse generator is active both in fetal life that in early childhood or Primary Hypogonadism: also called hypergonadotropic
(first 2 years of life), then is reduced to what is termed "juvenile because the defect is in the testicles.
▪ Klinefelter's syndrome7
pause" and resumes in the stage of puberty. What characterizes this ▪ Infections (orchitis), testicular cancer, trauma,
juvenile pause hypothalamus is a high sensitivity to the negative testicular torsion.
▪ Anorchia true: the complete absence of testicles.
feedback exerted by sex hormones. In the fetal period FSH and LH ▪ Cryptorchidism: the testes are there but are stuck in
are elevated, then a decline occurs with the birth; then they rise and the inguinal canal or abdomen.
remain high in the first two years of life and then fall in youth break.
o Secondary Hypogonadism: Said hypogonadism because it
- What influences the age of puberty: Gender (female 8-13 years; affects the hypothalamic-pituitary region. The defect is in
men 9-14 years), nutritional status, genetic characteristics, the production of gonadotropins and not in that of
correct functioning of the endocrine glands. testosterone.
- What are the symptoms: ▪ Kallman syndrome1
▪ hypopituitarism: The pituitary gland is affected by
O In women: The appearance of aging signs Sexual is realized infectious processes / infiltrative / tumor / trauma.
with the thelarche (breast development), the adrenarche ▪ hyperprolactinaemia: Produces hypogonadism for 2
(development of pubic hair), with the increase in the reasons, both because of the high PRL levels have
volume of the reproductive organs, and finally with inhibitory action on testosterone, both because the
menarche. The development of the mammary gland is prolactinoma crushing the pituitary induces a
secondary hypogonadism.
principally controlled by the estrogen produced by the
ovary, while the development of pubic and axillary hair is
controlled by androgens (secreted by the adrenal gland
and ovary).
o Hypogonadism Combined or Mixed: Late hypogonadism, gonadotropins (low or absent in Kallmann syndrome) and the onset
in part due to a hypothalamic-pituitary defect, in part of hyposmia or anosmia (always in S. Kallman).
also due to the testicle.
Erectile Dysfunction: Chronic inability to achieve or maintain an
o Hormone resistance peripheral: Deficit of 5-alpha-
erection sufficient and lead a satisfactory sexual intercourse. Stress,
reductase, an enzyme necessary for the conversion of
depression and nervousness are risk factors. 13% of men suffer from
testosterone to dihydrotestosterone (active form). It can
this condition. An erection requires several effective systems: on the
also be caused by defects in the androgen receptor. The
one hand we have the sexual stimulation that activates the nerve
phenotype is the syndrome Morris5.
centers (SNC) and from there is transmit to the smooth muscle cells
- Symptoms: 3 hinges male hypogonadism include: reduced
of the corpora cavernosa, on the other we have the mechanism of
frequency of spontaneous erections in the morning; erectile
the bodies cavernosa itself that trap blood preventing venous return
dysfunction or difficulty in maintaining an erection solid
throughout sexual intercourse; reduced sexual thoughts. as long as the stimulus lasts. So the etiology of erectile dysfunction
can be: psychogenic, neurogenic, endocrine, vascular or hollow. We
The ipogonadico reached, as mentioned in the jargon, the
have to investigate each of these possible causes to identify and
"peace of mind." Other symptoms include lack of libido or
solve the problem.
desire, loss of body hair, breast sensation of discomfort - diagnostic procedure: Medical history to identify risk factors
(accompanied by gynecomastia), loss of body hair, reduced EO to assess whether there is hypogonadism, vascular
testicular volume. Warning: the reduction of testicular volume damage, prostate or deformations peniere  echo-doppler flaccid
penis or with induced erection (prostaglandins injected into
can also be caused by the use of anabolic steroids.
corpora cavernosa) to assess vascular peakslaboratory tests.
- Risk factors: Alcohol is a major inducer of hypogonadism. Another diagnostic method involves the use of rings to be
Corticosteroids inhibit both directly the production of applied to the penis before falling asleep: if an erection occurs
testosterone, is the production of gonadotropins (then acting the ring is stretched and the event is logged by an appliance.
on two levels). - Diseases associated: This disease is often a symptom of other
- protective factors: A good sexual activity stimulates the release more serious diseases, such as cardiovascular disease or
of LH, which is to stimulate the production of testosterone. diabetes. It found that men with erectile dysfunction have a
higher risk of dying from stroke or heart attack.
So sexual activity helps maintain toned testosterone levels.
- Diagnosis: Dosiamo testosterone. Physiologic are> 350ng / dl. Premature Ejaculation: Reduction of the ejaculatory latency, or the
Pathological values are <230ng / dl. To measure the volume time between penetration and ejaculation. There are no precise
testicular we use a tool called orchidometer, which uses timing, you can typically occur within 2-5 minutes from the
indicators from 1 to 25 ml of volume ranging compared with penetration. The factors usually linked to premature ejaculation are:
the testicle of pcs. An adult must be at least 12 ml (width x performance anxiety, prostatitis, sexual immaturity. It creates stress
length 2.5-3.5cm 4.1-5.5cm). Lower values are indicative of and affects the sexual health of a couple. It is a multidimensional
hypogonadism. disease (biological and psychological) that involves 30% of men. The
- Therapy: Therapies are different depending on the problem. In history is important to understand if there are problems
most cases it is externally administered androgens, but it is also psicorelazionali.
possible to use a gonadotropin-based therapy (if, for example, - Classification:
we want to stimulate spermatogenesis) directly. It depends on o PrimaryIs anyone have it forever.
the patient's needs and by his age: o Secondary: Born after some newly arisen reason
o If a ipogonadico give testosterone, not I preserve fertility, (Acquired).
indeed give him a further inhibition on FSH and LH It can also be classified into: anteportam or intramoenia
then on the endogenous production of the testis, (before or after penetration; situational or absolute (not
however, it preserves the sexuality and the secondary depend on any situation); simple or complicated (with erectile
sexual characteristics. dysfunction).
O If I want instead to preserve fertility, I will have to administer - Root causes:
gonadotropins (and non-androgens). It is also true that we or Hypersensitivity peniera: Neurological problem where
can not somministrargliele for life, are subcutaneous glans is particularly rich in sensitive afferents. or
injections that can be uncomfortable for the pc: why it Foreskin overabundant or short frenulum.
alternates a testosterone-based therapy to a O prostatitis: Due to a sedentary lifestyle, but they can be
gonadotrophin (when she wants to have children). If the due to going by bike or motorbike.
pc is very young it is advisable to alternate cycles of 3-6 o endocrine problems: Such as hyperthyroidism and diabetes
months of gonadotropins and then testosterone, as well mellitus.
as to prevent the testicular volume can be reduced too. - Therapy If we have organic causes (redundant prepuce or
7Klinefelter's syndrome (47 XXY) is a genetic disorder that affects
short frenulum) can act with circumcision or affecting the
frenulum. You can use creams retardants (local anesthetic) to
only males. What characterizes this disease is the presence of an the glans level. Drug therapy should be used as a last option:
extra X chromosome. Such a chromosome does not allow, during There are medications that elevate serotonin levels which
puberty, the normal development of male sexual characteristics. were previously used as antidepressants. The higher the
Clinically shows two important characteristics: disproportionate arts
proportion of serotonin in the CNS/SNC, the more time it
and hard testicles (as well as small and considered). The testicles are
takes to ejaculate.
hard consistency to the tubules in involution sclerosis-ialinotica. The
DD with Kallman syndrome in the levels of 330