REVALIDA MUST KNOW TOPICS

Integumentary Hematopoietic 10. Muscles of mastication

1. Layers 1. CBC normal values 11. GI metabolism
2. Layers traversed by an injection 2. IVF 12. Alcoholic liver disease
3. Layers of the scalp 3. ECF vs ICF
4. Burns 4. Bacterial vs. viral infection GUT
5. Layers of lumbar puncture 5. RBC components 1. Renal blood floz/ circulation
6. Layers- pericardiocentesis 6. Blood component therapy- 2. Urine formation
7. Layers- thoracentesis components and functions 3. Urea cycle
7. Anemias 4. Kreb’s cycle
Musculoskeletal 8. Peripheral blood smear 5. Urinalysis normal values
1. Physiology of muscle contraction 9. Reye’s syndrome 6. Renal syndromes
2. Carpal and tarsal bones 7. BUN
3. Trauma Cardiovascular 8. Renal functions – filtration,
4. Physiology of smile 1. Heart blood supply reabsorption, secretion
5. Muscles of mastication 2. Blood circulation – upper and lower
6. Rotator cuff muscles 3. Cardiac cycle Endocrine
7. Hamstring muscle 4. ECG tracing 1. Thyroid storm
8. Diagnostic criteria for rheumatoid 5. Murmurs- types and grading 2. Thyroid hormone synthesis
arthritis 6. Fetal circulation 3. Hypertensive vs. DM retinopathy
7. Shock – types and parameters 4. DM and GDM
Nervous 8. Layers- pericardiocentesis 5. Insulin preparation
1. CSF flow 9. DVT treatment
2. CNS infection – bacterial, viral, 10. CHF criteria Reproductive
fungal, parasitic 11. Jones criteria 1. Menstrual cycle
3. Parts of brain and basic function 12. Advantages of enoxaparin vs. 2. HPO axis
4. Spinal nerves heparin 3. Breast CA
5. Cranial nerves exits 13. Warfarin/heparin overdose 4. Lactation
6. Brachial plexus treatment 5. Drugs safe in pregnancy
7. Sympathetic and parasympathetic 6. Leopold’s maneuver
nervous system Respiratory
8. Cavernous sinus thrombosis 1. Physiology of breathing Pediatrics
9. Lumbar puncture analysis 2. Cough and sneeze reflex 1. EPI vaccines
10. Neurotransmitter 3. Muscles of respiration 2. Developmental milestones
11. Circle of Willis 4. CART program for pneumonia 3. SMR staging
12. Pain pathway 5. Transudate vs. exudates
13. Benign febrile seizures 6. PTB –clinical and radiologic Surgery
14. Substance abuse disorder classification, treatment 1. Trauma
15. Schizophrenia 7. Upper vs. lower respiratory tract 2. Burns
16. OC disorder infection 3. Inflammation and repair
8. Layers- thoracentesis 4. Surgical nutrition
Special Senses 9. Common mediastinal tumors 5. Wound classification
1. Principles of accommodation 10. Endotracheal intubation indications
2. Waldeyer’s ring Pharmacology
3. Pathway of tearing GIT 1. H1 and H2 histamines
4. Visual pathway 1. Physiology of digestion – CHO, 2. Steroids
5. Auditory pathway CHON, fats 3. Antibiotics
6. Sinuses 2. Vomiting reflex
7. Papilledema vs. papillitis 3. Swallowing reflex Infectious diseases
8. Ocular hypertension 4. TCA (Kreb’s cycle) 1. Malaria life cycle
9. Layers of retina 5. Upper vs. lower bleeding 2. Bacterial vs. viral infection
10. Layers of cornea 6. Diarrhea treatment
7. Layers of abdominal wall Bioethics
8. Fecalysis normal values 1. principles
9. Bilirubin metabolism

RESPIRATORY
4. CART(?) program for pneumonia  Decreased tactile fremitus and dullness on chest percussion may result from
Community-acquired pneumonia (CAP): pleural effusion (usually due to H influenzae infection) or empyema
Lower respiratory infection involving the pulmonary parenchyma, results from
proliferation of microbial pathogens at the alveolar level and subsequent DX: Chest radiograph: predominantly focal segmental or lobar distribution of
immunologic response mounted by the host infiltrates
Sputum gram stain, blood culture
Most common: Streptococcus pneumoniae, Haemophilus
influenzae, and Moraxella catarrhalis DDX: Acute bronchitis, Acute exacerbation of chronic bronchitis, Myocardial
infarction, Congestive heart failure and pulmonary edema, Pulmonary fibrosis
 Purulent sputum is characteristic
 Rales are heard over the involved lobe or segment TX: Effective monotherapy antibiotics include doxycycline or respiratory
quinolones
 Increased tactile fremitus, bronchial breathing, and E-to-A change may be
Combination therapy usually consists of ceftriaxone plus
present if consolidation has occurred
doxycycline, azithromycin, or a respiratory quinolone
CURB-65, also known as the CURB criteria, is a clinical prediction rule that has
been validated for predicting mortality in community-acquired pneumonia. The
risk of death at 30 days increases as the score increases

0-1: Treat as an outpatient

2-3: Consider a short stay in hospital or watch very closely as an outpatient
4-5: Requires hospitalization with consideration as to whether they need to be in
the intensive care unit

6. PTB -clinical and radiologic classification, treatment
-Caused by mycobacterium tuberculosis
-Most commonly transmitted from a person with infectious pulmonary TB to
others by droplet nuclei, which are aerosolized by coughing, sneezing, or speaking
-The most infectious patients have cavitary pulmonary disease and laryngeal TB
REGISTRATION GROUP
New- a patient who has never had treatment for TB or who has taken ant-TB drugs
for less than one month
Relapse- a patient previously treated for tuberculosis, who has been declared
‘cured’ or ‘treatment completed,’ and is now diagnosed with bacteriologically
positive (smear or culture) tuberculosis
Failure- a patient who, while on treatment, is sputum smear positive at 5 months
or later during the course of treatment
Return after Default- a patient who returns to treatment with positive
bacteriology (smear or culture), following interruption of treatment for two
months or more
Transfer-in-a patient who has been transferred from another facility with proper
referral slip to continue treatment
Clinical manifestations:
-Cough of 2 weeks or more
-Night sweats, weight loss, anorexia, unexplained fever and chills, chest pain,
fatigue, body malaise
Radiologic: Chest and spine radiographs may show old or active pulmonary
tubercular (TB) lesions. However, in 50% of patients, chest radiographic findings
are negative.
Kidney, ureter, and bladder (KUB) radiographs reveal calcifications in the kidney
and ureter in approximately 50% of patients. Calcifications are intraluminal, as
opposed to schistosomiasis cases, which produce intramural calcifications.
Calcifications in the bladder are uncommon.
Plain abdominal radiography is useful to search for evidence of renal or ureteral
tuberculosis (ie, renal or ureteral calcifications).
MX: Isoniazid (H) - 5mg/kg
Rifampicin (R) - 10mg/kg
Pyrazinamide (Z) - 25mg/kg
Ethambutol (E) - 15mg/kg
Streptomycin (S) - 15mg/kg
Treatment regimen:

DX: AFB Sputum microscopy, Sputum TB Culture, Chest radiograph, TB-PCR


7. Upper vs. lower respiratory tract infection
Upper respiratory tract infections (URI or URTI) are the illnesses caused by an
acute infection which involves the upper respiratory
tract: nose, sinuses,pharynx or larynx. This commonly includes:
tonsillitis, pharyngitis, laryngitis,sinusitis, otitis media, and the common cold.
Common URI terms are defined as follows:
 Rhinitis - Inflammation of the nasal mucosa
 Rhinosinusitis or sinusitis - Inflammation of the nares and paranasal sinuses,
including frontal, ethmoid, maxillary, and sphenoid
 Nasopharyngitis (rhinopharyngitis or the common cold) - Inflammation of
the nares, pharynx, hypopharynx, uvula, and tonsils
 Pharyngitis - Inflammation of the pharynx, hypopharynx, uvula, and tonsils
 Epiglottitis (supraglottitis) - Inflammation of the superior portion of the
larynx and supraglottic area
 Laryngitis - Inflammation of the larynx
 Laryngotracheitis - Inflammation of the larynx, trachea, and subglottic area
 Tracheitis - Inflammation of the trachea and subglottic area
Lower respiratory tract infection, while often used as a synonym for pneumonia,
can also be applied to other types of infection including lung abscess and acute
bronchitis. Symptoms include shortness of breath, weakness, high fever, coughing
and fatigue.
Bronchitis can be classified as either acute or chronic. Acute bronchitis can be
defined as acute bacterial or viral infection of the larger airways in healthy
patients with no history of recurrent disease. It consists of transient inflammation
of the major bronchi and trachea. Most often it is caused by viral infection and
hence antibiotic therapy is not indicated in immunocompetent individuals. There
are no effective therapies for viral bronchitis. Acute Exacerbations of Chronic
Bronchitis (AECB) are frequently due to non-infective causes along with viral ones.
50% of patients are colonised with Haemophilus influenzae, Streptococcus
pneumoniae or Moraxella catarrhalis. Antibiotics have only been shown to be
effective if all three of the following symptoms are present:- increased dyspnea,
increased sputum volume and purulence. In these cases 500 mg of Amoxicillin
orally, every 8 hours for 5 days or 100 mg doxycycline orally for 5 days should be
used
Pneumonia occurs in a variety of situations and treatment must vary according to
the situation. It is classified as either community or hospital acquired depending
on where the patient contracted the infection. The most common treatment is
antibiotics and these vary in their adverse effects and their effectiveness. The
most common cause of pneumonia is pneumococcal bacteria, Streptococcus
pneumoniae accounts for 2/3 of bacteremic pneumonias. For optimal
management of a pneumonia patient the following must be assessed;-
pneumonia severity (including where to treat e.g. Home, hospital or intensive
care), identification of causative organism, analgesia of chest pain, the need for
supplemental oxygen, physiotherapy, Hydration, bronchodilators and possible
complications of emphysema or lung abscess.
9. Common mediastinal tumors
The mediastinum is the cavity that separates the lungs from the rest of the chest.
It contains the heart, esophagus, trachea, thymus, and aorta. The mediastinum
has three main parts: the anterior mediastinum (front), the middle mediastinum,
and the posterior mediastinum (back)
The most common mediastinal masses are neurogenic tumors (20% of
mediastinal tumors), usually found in the posterior mediastinum, followed
bythymoma (15-20%) located in the anterior mediastinum
Masses in the anterior portion of the mediastinum can include thymoma,
lymphoma, pheochromocytoma, germcelltumors including
teratoma, thyroid tissue, and parathyroid lesions. Masses in this area are more
likely to be malignant than those in other compartments
Masses in the posterior portion of the mediastinum tend to be neurogenic in
origin, and in adults tend to be of neural sheath origin including neurilemomas
and neurofibromas.
Lung cancer typically spreads to the lymph nodes in the mediastinum Mouth &
Moist Dry Very Dry
Tongue
Thymoma is a tumor originating from the epithelial cells of the thymus. Thirst Drinks normally Thirsty Drinks poorly
Thymoma is an uncommon tumor, best known for its association with the Skin Goes Back Quickly <2 secs Slowly >2 secs Very slowly
neuromuscular disorder myasthenia gravis. Once diagnosed, thymomas may be >2 signs =
removed surgically. In the rare case of a malignant tumor, chemotherapy may be No Signs of >2 signs = Some
Severe
used. Dehydration Dehydration
Dehydration

Lymphoma is a type of blood cancer that occurs when B or T lymphocytes, Plan A

the white blood cells that form a part of the immune system and help protect the  More fluids than usual  prevent dehydration
body from infection and disease, divide faster than normal cells or live longer  Plenty of food  prevent undernutrition
than they are supposed to. Lymphoma may develop in the lymph  Take child to health worker if child does not get better in 3 days
nodes, spleen,bone marrow, blood or other organs[2] and eventually they form
 ORS solution at home if been on Plan B or C, diarrhea gets worse
a tumor.
Age After Each Loose Stool Use at home
<2yrs 50-100 mL 500 mL/day
GASTROINTESTINAL
2-10 yrs 100-200 mL 1000 mL/day
6. Diarrhea treatment
>10 yrs As much as wanted 2000 mL/day
Definition
 Diarrhea Plan B
o Passage of 3 or more liquid stools in a 24 hour period. Amount of ORS in First 4 hours
o Acute = few hours or days, Persistent = lasting > 2 weeks Age Weight mL
o Dysentery – bloody diarrhea <4 mos < 5 kg 200-400
 Dehydration 1-11 mos 5-7.9 kg 400-600
o Loss of fluid without loss of supporting tissues 12-23 mos 8-10 kg 600-800
o Contraction of extracellular volume in relation to cell mass. 2-4 years 11-15.9 kg 800-1200
5-14 years 16-29.9 kg 1200-2200
>15 years > 30 kg
 Secretory: Secretory diarrhea means that there is an increase in the active  After 4 hours, reassess the child  A,B,C
secretion, or there is an inhibition of absorption. There is little to no structural
damage. The most common cause of this type of diarrhea is a cholera toxin that Plan C
stimulates the secretion of anions, especially chloride ions.  Start IV fluids  100 mL/kg Ringer’s Lactate Solution
 Osmotic: Osmotic diarrhea occurs when too much water is drawn into the o < 1 year – 30 mL/kg for 1 hour, 70 mL/kg for 5 hours
bowels. If a person drinks solutions with excessive sugar or excessive salt, these o Older – 30 mL/kg for 30 mins, 70 mL/kg for 2.5 hours
can draw water from the body into the bowel and cause osmotic diarrhea.  Repeat if radial pulse is weak
Osmotic diarrhea can also be the result of maldigestion (e.g., pancreatic disease  Give ORS as soon as the patient can drink
or Coeliac disease), in which the nutrients are left in the lumen to pull in water.  If no IV fluids available  Give ORS 20 mL/kg/hour for 6 hours by NGT.
Or it can be caused by osmotic laxatives (which work to alleviate
constipation by drawing water into the bowels). In healthy individuals, too Other Problems
much magnesium or vitamin C or undigested lactose can produce osmotic  Blood in stool  treat Shigella  TMP-SMX for 5 days
diarrhea and distention of the bowel. A person who has lactose intolerance can  Diarrhea >14 days  refer if <6 mos old, dehydration is present  teach
have difficulty absorbing lactose after an extraordinarily high intake of dairy mother to feed child with Plan A  Tell mother to bring the child back after 5
products. days if diarrhea has not stopped
 Exudative: Exudative diarrhea occurs with the presence of blood and pus in the  Severe malnutrition  refer to hospital, provide ORS
stool. This occurs with inflammatory bowel diseases, such as Crohn's Cause Drug of choice Alternative
disease or ulcerative colitis, and other severe infections such as E. coli or other Furazolidone, TMP-
Cholera Tetracycline
forms of food poisoning. SMX
 Motility-related: Motility-related diarrhea is caused by the rapid movement of Shigella TMP-SMX Nalidixic Acid
food through the intestines (hypermotility). If the food moves too quickly Amoebiasis Metronidazole
through the gastrointestinal tract, there is not enough time for sufficient Giardiasis Metronidazole Quinacrine HCl
nutrients and water to be absorbed. This can be due to a vagotomy or diabetic
neuropathy, or a complication of menstruation. Hyperthyroidism can produce 8. Fecalysis normal values
hypermotility and lead to pseudodiarrhea and occasionally real diarrhea. Under normal circumstances, the results of fecalysis will show no presence of
Diarrhea can be treated with antimotility agents (such as loperamide). parasites. If a person does show the presence of parasites, then the type of
Hypermotility can be observed in people who have had portions of their bowel parasite will need to be addressed.
removed, allowing less total time for absorption of nutrients. color: brown
 Inflammatory: Inflammatory diarrhea occurs when there is damage to the consistency: soft
mucosal lining or brush border, which leads to a passive loss of protein-rich parasites: no parasites or ova seen
fluids and a decreased ability to absorb these lost fluids. Features of all three of muscle fibers: none
the other types of diarrhea can be found in this type of diarrhea. It can be vegetables cells: none
caused by bacterial infections, viral infections, parasitic infections, or rbc: 0-1/hfp
autoimmune problems such as inflammatory bowel diseases. It can also be pus cells: 0-1/hpf
caused by tuberculosis, colon cancer, and enteritis. macrophage: none
 Dysentery: Generally, if there is blood visible in the stools, it is not diarrhea, bacteria: none
but dysentery. The blood is trace of an invasion of bowel tissue. Dysentery is a fat globules: none
symptom of, among others, Shigella, Entamoeba histolytica, and Salmonella.
12. Alcoholic liver disease
Dehydration Assessment:
Encompasses the hepatic manifestations of alcohol overconsumption,
A B C
including fatty liver, alcoholic hepatitis, and chronic hepatitis with hepatic
Eyes Normal Sunken Very Sunken
fibrosis or cirrhosis
Tears Normal Absent Absent
Threshold for developing alcoholic liver disease
Men: >60-80g/day alcohol for 10 years
Women: 20-40g/day
The following contain ~12g of alcohol
-one bottle of beer
-four ounces of wine
-one ounce of 80% spirits

LABORATORY RESULTS
Alcoholic hepatitis:
AST or ALT increased 2 to 7 fold
AST/ALT ratio >1
Increased bilirubin -The first step in urine formation is the filtration of blood in the kidneys. In a
healthy human the kidney receives between 12 and 30% of cardiac output, but it
Alcoholic cirrhosis: averages about 20% or about 1.25 L/min.
Low albumin -The basic structural and functional unit of the kidney is the nephron. Its chief
Prolonged PT function is to regulate the concentration of water and soluble substances like
Increased bilirubin sodium salts by filtering the blood, reabsorbing what is needed and excreting the
Thrombocytopenia (due to portal HPN + hypersplenism) rest as urine.
CT/UTZ: nodular liver, splenomegaly, venocollaterals -In the first part of the nephron, the renal corpuscle blood is being filtrated from
the circulatory system into the nephron. A pressure difference between forces
MX: Complete abstinence is cornerstone of treatment the filtrate from the blood across the filtration membrane. The filtrate includes
Glucocorticoids may be used for severe alcoholic hepatitis defined as: water, small molecules and ions that easily pass through the filtration membrane.
Discriminant function >32, MELD score >20 However larger molecules such as proteins and blood cells are prevented from
passing through the filtration membrane.
GENITOURINARY SYMPTOM -The amount of filtrate produced every minute is called the glomerular filtration
rate or GFR and amounts to a staggering 180 liters per day. About 99% of this
2. Urine Formation filtrate is then reabsorbed as it passes through the nephron and the remaining 1%
-Average urine production in adult humans is 1 – 2 L per day, depending on state becomes urine.
of hydration, activity level, environmental factors, weight, and the individual's The urinary system is regulated by the endocrine system by hormones such
health. as antidiuretic hormone, aldosterone, and parathyroid hormone.
-Polyuria is a condition of excessive production of urine (> 2.5 L/day)
-Oliguria when < 400 mL per day
-Anuria when < 100 mL per day Regulation of concentration and volume:

The urinary system is under influence of the blood pressure, nervous

system and endocrine system.
-Antidiuretic hormone (ADH) is a neurohypophysial hormone found in
most mammals. Its two primary functions are to retain water in the body and to
constrict blood vessels.
-Vasopressin regulates the body's retention of water by acting to increase water
absorption in the collecting ducts of the kidney nephron. Vasopressin increases
water permeability of the kidney's collecting duct and distal convoluted tubule by
inducing translocation of aquaporin-CD water channels in the kidney nephron
collecting duct plasma membrane.[4]
5. Urinalysis normal values
-Normal: None
-Abnormal: Blood in the urine is an abnormal finding. However, it is not possible
to determine the cause of the bleeding without further testing. Common causes
include infection, trauma, kidney stones, cancer, surgery on an area of the urinary
tract, kidney disease, trauma related to the insertion of a urinary catheter.

PHYSICAL CHARACTERISTICS: Bilirubin

Color -Normal: None
-Normal: Pale to dark yellow -Abnormal: Increased levels due to biliary tract disease, cirrhosis, gallstones,
-Abnormal: No color - kidney disease/diabetes, Red - blood in the urine hepatitis, liver disease
Transparency
-Normal: Clear Nitrite
-Abnormal: Cloudy (pus, WBC, RBC, sperm, bacteria, yeast)
-Normal: None
-Abnormal: Bacteria that cause a UTI make an enzyme that changes urinary
nitrates to nitrites. Nitrites in urine show a UTI is present.

Ketones
-Normal: None
-Abnormal: Ketones in the urine can mean uncontrolled diabetes, a very low-
carbohydrate diet, starvation or eating disorders, or alcoholism. Ketones are often
found in the urine when a person does not eat (fasts) for 18 hours or longer. This
may occur when a person is sick and cannot eat or vomits for several days.

Urobilinogen
-Normal: None
-Abnormal: Formed by the breakdown of bilirubin and passed from the body in
stool. Can be a sign of liver disease (cirrhosis,hepatitis) or that the flow of bile
from the gallbladder is blocked.

MICROSCOPIC FINDINGS (CAST):

Hyaline, Granular, Waxy
-Normal: None
CHEMICAL TEST:
-Abnormal: Depending on the type, casts can mean inflammation or damage to
pH
the tiny tubes in the kidneys, poor blood supply to the kidneys, metal poisoning
-Normal: 4.6-8.0
(such as lead or mercury), heart failure, or bacterial infection
-Abnormal: High (alkaline) = severe vomiting, kidney disease, some UTI, asthma.
A cast, which may be referred to as a red, white, or hyaline cast, typically looks
Low (acidic) = emphysema, uncontrolled diabetes, severe diarrhea, dehydration,
like a small clump of egg white suspended in the urine. The presence of casts is
starvation
not normal and may be suggestive of kidney issues.

CELLS:
Specific Gravity (urine concentration)
-Normal: 1.005-1.030  RBC, Pus, Yeast, Squamous, Renal, Transitional, Epithelial, Bacteria, Mucus
-Abnormal: High = very concentrated urine, either from fluid loss or kidney Thread
problem, with substances (sugar/protein) in the urine. Low = dilute urine, from  -Normal: Few/None
too much fluid, severe kidney disease, diuretic use  -Abnormal: Bacteria, yeast cells = UTI
 Very few or no WBCs should be present in the urine. Significant numbers
Albumin typically indicate the presence of infection.
-Normal: None  Like white blood cells, there should be very few or no red blood cells found
in the urine.
-Abnormal: Possible kidney damage, infection, cancer, hypertension, diabetes,
SLE, glomerulonephritis, heart failure  The presence of bacteria may indicate an infection or contamination of the
sample.
Sugar  Squamous/Epithelial cells may mean that the sample is not as pure as it
-Normal: None needs to be. New sample needed.
-Abnormal: Uncontrolled diabetes, adrenal gland problem, liver damage, brain
injury, some types of kidney diseases CRYSTALS:
Amorphous urate, Uric acid, Calcium oxalate, Amorphous phosphate, Triple
Leukocytes phosphate
-Normal: Few/None. -Normal: Few
-Abnormal: Leukocytes in the urine typically indicate a past or current infection in -Abnormal: Large amounts of crystals, or certain types of crystals, can mean
the urinary tract. kidney stones, damaged kidneys, or problems with metabolism. Some medicines
and UTI can increase the number of crystals in urine.
Erythrocytes
6. Renal syndromes

Acute Kidney Injury

Acute kidney injury is a syndrome in which glomerular filtration declines over a
period of hours to days. The patient with acute renal failure is approached best
by evaluation for prerenal, renal, and postrenal causes.

Generally it occurs because of damage to the kidney tissue caused by

decreased renal blood flow (renal ischemia) from any cause (e.g. low blood
pressure), exposure to substances harmful to the kidney, aninflammatory process
in the kidney, or an obstruction of the urinary tract which impedes the flow of
urine.

AKI is diagnosed on the basis of characteristic laboratory findings, such as

elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce
sufficient amounts of urine.

BUN is an indication of renal health. Normal ranges 8-20 mmol/L. If Glomerular

Filtration Rate (GFR) and blood volume decrease (hypovolemia) then BUN will
increase. Other factors responsible for its increment are fever,
increased catabolism, high-protein diet and gastrointestinal bleeding.

Serum creatinine is an important indicator of renal health because it is an easily

measured byproduct of muscle metabolism that is excreted unchanged by the
kidneys. The typical human reference ranges for serum creatinine are 0.5 to
1.0 mg/dl for women and 0.7 to 1.2 mg/dl for men.

BUN-to-creatinine ratio:

KDIGO STAGING OF AKI

STAGE CREATININE URINE OUTPUT
RIFLE criteria - For staging of AKI 1 1.5–1.9 times baseline <0.5 ml/kg/h for 6–12
OR hours
>/=0.3 mg/dl (>/= 26.5
 Risk: GFR decrease >25%, serum creatinine increased 1.5 times or urine mmol/l) increase
production of < 0.5 ml/kg/h for 6 hours
2 2.0–2.9 times baseline <0.5 ml/kg/h for >/=12
 Injury: GFR decrease > 50%, doubling of creatinine or urine production hours
< 0.5 ml/kg/h for 12 hours
3 3.0 times baseline <0.3 ml/kg/h for >/=24
 Failure: GFR decrease > 75%, tripling of creatinine or creatinine OR hours
> 355 μmol/l (with a rise of > 44) (> 4 mg/dl) OR urine output below Increase in serum OR
0.3 ml/kg/h for 24 hours or anuria for 12 hours. creatinine to >/=4.0 Anuria for X>/=2 hours
 Loss: persistent AKI or complete loss of kidney function for more than 4 mg/dl (>/=353.6
weeks mmol/l)
 End-stage renal disease: need for renal replacement therapy (RRT) for more OR
than 3 months Initiation of renal
replacement therapy
OR, In patients <18
years, decrease in eGFR
to <35 ml/min per 1.73
m2

Chronic Kidney Disease (CKD)

-Abnormal kidney function and progressive decline in glomerular filtration rate
(GFR) brought about by various etiologies.
-Generally defined as kidney damage >=3months with GFR<60mL/min and
structural or functional abnormalities in the kidney
-Leading causes: diabetic glomerular disease, glomerulonephritis, hypertensive
nephropathy

Clinically manifested by Uremia: in kidney failure, urea and other waste products,
which are normally excreted into the urine, are retained in the blood. Early
symptoms include anorexia and lethargy, and late symptoms can include
decreased mental acuity and coma. Other symptoms include fatigue, nausea,
vomiting, cold, bone pain, itch, shortness of breath, and seizures.
 Stage 1: Slightly diminished function; kidney damage with normal or
relatively high GFR (≥90 mL/min/1.73 m2). Kidney damage is defined
as pathological abnormalities or markers of damage, including
abnormalities in blood or urine test or imaging studies.
 Stage 2: Mild reduction in GFR (60–89 mL/min/1.73 m2) with kidney
damage. Kidney damage is defined as pathological abnormalities or
markers of damage, including abnormalities in blood or urine test or
imaging studies.
 Stage 3: Moderate reduction in GFR (30–59 mL/min/1.73 m2). British
guidelines distinguish between stage 3A (GFR 45–59) and stage 3B
(GFR 30–44) for purposes of screening and referral.
 Stage 4: Severe reduction in GFR (15–29 mL/min/1.73 m2) Preparation
for renal replacement therapy
 Stage 5: Established kidney failure (GFR <15 mL/min/1.73 m2,
permanent renal replacement therapy (RRT), or end stage renal
disease (ESRD)
Nephritic Syndrome
The acute nephritic syndrome is an uncommon but dramatic presentation of an
acute glomerulonephritis The hallmark of the acute nephritic syndrome is the
presence of dysmorphic RBCs and RBC casts, but their absence does not exclude
the syndrome. The acute nephritic syndrome can be caused by any of the rapidly
progressive glomerulonephropathies, all of which warrant urgent and usually
inpatient evaluation.
-1-2g/24h proteinurea
- Hematuria with RBC casts
- Pyuria, Hypertension, Fluid retention, Rise in serum creatinine
Nephrotic Syndrome
The nephrotic syndrome is characterized by the presence of proteinuria of greater
than 3.5 g/day, hypoalbuminemia (<30g/L), with accompanying edema,
hypertension, and hyperlipidemia. In general, the diseases associated with
nephrotic syndrome do not cause acute kidney injury, although acute kidney
injury may be seen with minimal change disease, HIV-associated nephropathy,
and bilateral renal vein thrombosis. The causes of primary idiopathic nephrotic
syndrome, in decreasing order of prevalence, are focal and segmental
glomerulosclerosis, membranous nephropathy, minimal change disease, and
membranoproliferative glomerulonephritis. Secondary causes of the nephrotic
syndrome include diabetic nephropathy, amyloidosis, and SLE with membranous
nephropathy.
- >3gram/24 hour proteinurea
-Hypertension, Hypercholesterolemia, Hypoalbuminemia, Edema/anasarca,
microscopic hematuria
Nephrolithiasis (kidney stones)
-One of the most common urologic problems
-Calcium (75-85%), salts, uric acid, cysteine, and struvite make up most kidney
stones
-Common cause of isolated hematuria
-Pain gradually increases in severity as stone traverses ureter
-DX: Helical CT scan
-MX: alpha-blockers, nephrolithotomy, ureteroscopy
Renal Tubular Acidosis
-Disorder of renal acidification out of proportion to the reduction in GFR
-Characterized by hyperchloremic metabolic acidosis with normal anion gap
-Type 1 Distal, Type 2 Proximal, MX: alkali supplementation
-Type 4 most common, with impaired secretion of distal H+ and K+ ions ->
hyperchloremic acidosis with hyperkalemia. MX: correct hyperka
7.BUN
Reference Range
 Blood urea nitrogen (BUN) testing is commonly part of the basic metabolic
panel (BMP) or comprehensive metabolic panel (CMP), which is commonly
obtained as part of a routine medical examination. It is also obtained in
patients in emergency or urgent care settings, as it can provide valuable
information that may provide clues to various clinical presentations that
may be caused by chemical imbalances in the body that require prompt and
immediate attention.
 Urea production occurs primarily in the liver (urea cycle, also referred to as
the ornithine cycle) and is regulated by N-acetylglutamate. Urea is found
dissolved in blood and is excreted by the renal tubules. In addition, a small
amount of urea is also excreted in sweat. Therefore, the BUN level may
reflect functioning of the liver and/or kidneys.
 The reference range of the BUN level is 3-20 mg/dL. Individual laboratories
may have different reference ranges, since the procedure may vary.
Interpretation
 As with serum creatinine, the BUN level varies inversely with the glomerular
filtration rate (GFR).[1] However, certain conditions can result in elevated
BUN levels that may not truly reflect renal functioning.[2]
 The rate of urea production is not constant. It is elevated in those who
consume a diet fairly high in protein and in conditions characterized by
enhanced tissue breakdown (eg, hemorrhage, trauma, glucocorticoid
therapy). Certain antibiotics, such as tetracyclines, may interfere with
protein synthesis and tend to be catabolic, thereby also increasing BUN
levels. On the other hand, a low-protein diet or liver disease can decrease
the BUN level without affecting GFR or renal function.[3]
 Liver disease may be associated with near-normal values of both BUN (due
to decreased urea production) and serum creatinine (due to muscle
wasting), despite a significant decline in renal function manifested by
decreased GFR.[4]
 Approximately 40%-50% of the filtered urea undergoes passive
reabsorption in the proximal tubule. In states of intravascular volume
 depletion, proximal sodium and water reabsorption increases, coupled with
a parallel increase in the reabsorption of urea. This results in a
disproportionate rise in BUN levels relative to any change in serum
creatinine levels. This elevation in the BUN-to-creatinine ratio is one of the
laboratory indicators of decreased renal perfusion. The ratio is indicative of
prerenal injury when the BUN-to-creatinine ratio is greater than 20.

 The ratio is may also be useful for diagnosing gastrointestinal bleeding in

some patients who do not present with overt blood loss. In children, a BUN-
to-creatinine ratio of 30 or greater has a sensitivity of 68.8% and a specificity
of 98% for upper gastrointestinal bleeding.

 The value of this ratio is limited by other factors that can affect BUN
independently, such as various drugs.

Drugs that can increase BUN levels include the following:

 Allopurinol  Methicillin
 Aminoglycoside  Methotrexate
antibiotics  Methyldopa
 Amphotericin B  Neomycin
 Aspirin (high doses)  Penicillamine
 Bacitracin  Polymyxin B
 Carbamazepine  Probenecid
 Cephalosporins  Propranolol
 Chloral hydrate  Rifampin
 Cisplatin  Spironolactone
 Colistin  Tetracyclines
 Furosemide  Thiazide diuretics
 Guanethidine  Triamterene
 Indomethacin  Vancomycin

The following drugs can decrease BUN levels:

 Chloramphenicol
 Streptomycin

BUN levels tend to increase with age. In infants and children, BUN levels are about
two thirds of those found in healthy young adults, while levels in adults older than
60 years are slightly higher than those in younger adults. They are also slightly
higher in males than in females, probably reflective of the lower muscle mass in
the latter. During pregnancy, physiologic changes in blood flow can also lower
BUN levels.
8.Renal Functions – filtration, reabsorption, secretion
 ENDOCRINE
1. Thyroid Storm
Definition: Thyroid storm refers to the heightened and life-threatening
manifestations of thyroid hyperactivity.
Etiology/Pathophysiology
In the past, thyroid storm classically began a few hours after a thyroidectomy
performed on a patient taken too soon to surgery. Most cases of thyroid storm
are secondary to toxic diffuse goiter (Graves’ disease). Precipitating factors
associated with thyroid storm include infections, stress, trauma, thyroidal or non-
thyroidal surgery, diabetic ketoacidosis, labor, heart disease and RAI treatment
due to RAI thyroiditis. The mechanism by which such factors worsen
thyrotoxicosis may be related to cytokine release and acute immunologic
disturbance caused by the precipitating condition.
Clinical manifestations
Clinical features are similar to those of thyrotoxicosis, but more exaggerated.
Fever is almost invariable and may be severe; sweating is profuse. Marched
tachycardia of sinus or ectopic origin and arrhythmias may be accompanied by
pulmonary edema or CHF. Early on, tremulousness and restlessness are present;
delirium or frank psychosis may supervene. N/V, and abdominal pain occur early
in the course. As the disorder progresses, apathy, stupor, and coma may
supervene. Coma and death may ensue in up to 20% of patients.
Diagnostic tests
The serum thyroid hormone levels in crisis are not appreciably greater than those
in uncomplicated thyrotoxicosis. Therefore thyroid storm is primarily a clinical
diagnosis. Electrolytes, BUN, blood sugar, LFT and plasma cortisol should be
monitored. The diagnosis of thyroid storm is incomplete until a search for some
cause of the crisis, especially infection, has been made.
Management of Thyroid Storm
Inhibition of thyroid hormone formation and secretion
PTU
Sodium iodide
Sympathetic blockade
Propranolol
Glucocorticoid therapy
hydrocortisone
Supportive therapy
IV fluids
Temperature control (cooling blankets, paracetamol)
O2 if needed
Digitalis for congestive failure and to slow ventricular response
Treatment of precipitating event (e.g. infection)
Sedation and nutrition
Prevention of thyroid storm
 Patients should be rendered euthyroid to mild hyperthyroidism before
RAI treatment or surgery
 Patients should be educated on the importance of compliance with
antithyroid medications
2. Thyroid hormone synthesis
(1) Thyroglobulin is synthesized from tyrosine in the thyroid follicular
cells, packaged in secretory vesicles, and extruded into the follicular
lumen (step 1).
(2) The iodide (I-) pump, or Na+ I- cotransport
 Is present in the thyroid follicular epithelial cells
 Actively transports I- into the thyroid follicular cells for
subsequent incorporation into thyroid hormones (step 2)
 Is inhibited by thiocyanate and perchlorate anions
(3) Oxidation of I- to I2
 Is catalyzed by a peroxidase enzyme in the follicular cell
membrane (step 3)
 I2 is the reactive form , which will be “organified” by
combination with tyrosine on thyroglobulin
 The peroxidase enzyme is inhibited by propylthioruacil,
which is used therapeutically to reduce thyroid hormone
synthesis for the treatment of hyperthyroidism
 The same peroxidase enzyme catalyzes the remaining
organification and coupling reactions involved in the
synthesis of thyroid hormones
(4) Organification of I2
 At the junction of the follicular cells and the follicular
lumen, tyrosine residues of thyroglobulin react with I2 to
form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
(step 4)
 High levels of I- inhibit organification and, therefore, inhibit
synthesis of thyroid hormone (Wolff-Chaikoff effect)
(5) Coupling of MIT and DIT
 While MIT and DIT are attached to thyroglobulin, 2 coupling
reactions occur (step 5)
 When two molecules of DIT combine, thyroxine (T4) is
formed
 When one molecule of DIT combines with one molecule of
MIT, triiodothyronine (T3) is formed
 More T4 than T3 is synthesized, although T3 is more active
 Iodinated thyroglobulin is stored in the follicular lumen
until the thyroid gland is stimulated to secrete thyroid
hormones
(6) Stimulation of thyroid cells by TSH
 When thyroid cells are stimulated, iodinated thyroglobulin
is taken back into the follicular cells by endocytosis (step 6).
Lysozomal enzymes then digest thyroglobulin, releasing T4
and T3 into the circulation (step 7).
 Leftover MIT and DIT are deiodonated by thyroid
deiodinase (step 8). The I2 that is released is reutilized to
synthesize more thyroid hormones. Therefore, deficiency
of thyroid deiodinase mimcs I2 deficiency.
(7) Binding of T3 and T4
  In the circulation, most of the T3 and T4 is bound to the
thyroxine-binding globulin (TBG)
 In hepatic failure, TBG levels decrease, leading to a
decrease in total thyroid hormone levels, but normal levels
of free hormone
 In pregnancy, TBG levels increase, leading to an increase in
total thyroid hormone levels, but normal levels of free
hormone (i.e. clinically euthyroid)
(8) Conversion of T4 to T3 and reverse T3 (rT3)
 In the peripheral tissues, T4 is converted to T3 by 5’-
iodinase (or to rT3)
 T3 is more biologically active than T4
 rT3 is inactive
3. Hypertensive vs. DM retinopathy
Diabetic Retinopathy
Clinical stages
a) Background or nonproliferative DM reninopathy
 Microaneurysms, dot blot hemorrhage, flame shaped
hemorrhages, hard exudates (outer plexiform layer)
b) Pre-proliferative DM retinopathy
 Cotton wool spots (soft exudates, nerve fiber layer)
c) Proliferative DM retinopathy
 Neovascularization into vitreous and optic disc, vitreous
hemorrhage, tractional RD
Tx: Panretinal photocoagulation (principle: destruction of
ischemic retina to reduce O2 demand hence reduce angiogenic
stimulus for neovascularization)
Hypertensive Retinopathy
Scheie Grading
I – Slight generalized attenuation retinal arterioles
II – Obvious attenuation/further narrowing
III – Changes in I and II + exudates and hemorrhages
IV – I, II, III + optic disc edema
Tx: BP control, PRP if necessary
4. DM and GDM
TYPE 1 DIABETES MELLITUS
Type 1 diabetes is a chronic illness characterized by the body’s inability to
produce insulin due to the autoimmune destruction of the beta cells in the
pancreas. Onset most often occurs in childhood, but the disease can also
develop in adults in their late 30s and early 40s.
Signs and symptoms
The classic symptoms of type 1 diabetes are as follows:
 Polyuria
 Polydipsia
 Polyphagia
 Unexplained weight loss
Other symptoms may include fatigue, nausea, and blurred vision.
The onset of symptomatic disease may be sudden. It is not unusual for
patients with type 1 diabetes to present with diabetic ketoacidosis (DKA).
Diagnosis
Diagnostic criteria by the American Diabetes Association (ADA) include the
following :
 A fasting plasma glucose (FPG) level ≥126 mg/dL (7.0 mmol/L), or
 A 2-hour plasma glucose level ≥200 mg/dL (11.1 mmol/L) during a 75-
g oral glucose tolerance test (OGTT), or
 A random plasma glucose ≥200 mg/dL (11.1 mmol/L) in a patient with
classic symptoms of hyperglycemia or hyperglycemic crisis
Lab studies
 A fingerstick glucose test is appropriate for virtually all patients with
diabetes
 HbA1c assay for diagnosing type 1 diabetes only when the condition is
suspected but the classic symptoms are absent
Management
Glycemic control
Benefits of tight glycemic control include not only continued reductions in
the rates of microvascular complications but also significant differences in
cardiovascular events and overall mortality.
Self-monitoring
Self-monitoring of blood glucose levels allows rational adjustments in insulin
doses. All patients with type 1 diabetes should learn how to self-monitor
and record their blood glucose levels with home analyzers and adjust their
insulin doses accordingly.
Insulin therapy
Patients with type 1 diabetes require lifelong insulin therapy. Most require
2 or more injections of insulin daily, with doses adjusted on the basis of self-
monitoring of blood glucose levels. Insulin replacement is accomplished by
giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is
either long-acting (glargine or detemir) or intermediate-acting (NPH). The
preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-
acting (regular).
Diet and activity
 Daily caloric intake prescription
 Recommendations for amounts of dietary carbohydrate, fat, and
protein
 Instructions on how to divide calories between meals and snacks
 Exercise
TYPE 2 DIABETES MELLITUS
Type 2 diabetes mellitus consists of an array of dysfunctions characterized
by hyperglycemia and resulting from the combination of resistance to
insulin action, inadequate insulin secretion, and excessive or inappropriate
glucagon secretion.
Signs and symptoms
Many patients with type 2 diabetes are asymptomatic. Clinical
manifestations include the following:
 Classic symptoms: Polyuria, polydipsia, polyphagia, and weight loss
 Blurred vision
 Lower-extremity paresthesias
 Yeast infections (eg, balanitis in men)
Diagnosis
 A fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or
higher, or
 A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher
during a 75-g oral glucose tolerance test (OGTT), or
 A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a
patient with classic symptoms of hyperglycemia or hyperglycemic
crisis
Whether a hemoglobin A1c (HbA1c) level of 6.5% or higher should be a
primary diagnostic criterion or an optional criterion remains a point of
controversy.
Management
Goals of treatment are as follows:
 Microvascular (ie, eye and kidney disease) risk reduction through
control of glycemia and blood pressure
 Macrovascular (ie, coronary, cerebrovascular, peripheral vascular) risk
reduction through control of lipids and hypertension, smoking
cessation
 Metabolic and neurologic risk reduction through control of glycemia
The European Association for the Study of Diabetes (EASD) and the
American Diabetes Association (ADA) position statement contains 7 key
points:
1. Individualized glycemic targets and glucose-lowering therapies
2. Diet, exercise, and education as the foundation of the treatment
program
3. Use of metformin as the optimal first-line drug unless contraindicated
4. After metformin, the use of 1 or 2 additional oral or injectable agents,
with a goal of minimizing adverse effects if possible
5. Ultimately, insulin therapy alone or with other agents if needed to
maintain blood glucose control
6. Where possible, all treatment decisions should involve the patient,
with a focus on patient preferences, needs, and values
7. A major focus on comprehensive cardiovascular risk reduction
Approaches to prevention of diabetic complications include the following:
 HbA1c every 3-6 months
 Yearly dilated eye examinations
 Annual microalbumin checks
 Foot examinations at each visit
 Blood pressure < 130/80 mm Hg, lower in diabetic nephropathy
 Statin therapy to reduce low-density lipoprotein cholesterol
Gestational Diabetes
Gestational diabetes mellitus is defined as glucose intolerance of variable
degree with onset or first recognition during pregnancy. Infants of mothers
with preexisting diabetes mellitus experience double the risk of serious
injury at birth, triple the likelihood of cesarean delivery, and quadruple the
incidence of newborn intensive care unit (NICU) admission.
Maternal-Fetal Metabolism in Normal Pregnancy
In the pregnant woman, each meal sets in motion a complex series of
hormonal actions, including a rise in blood glucose and the secondary
secretion of pancreatic insulin, glucagon, somatomedins, and adrenal
catecholamines. These adjustments ensure that an ample, but not
excessive, supply of glucose is available to the mother and fetus.
Compared with nonpregnant subjects, pregnant women tend to develop
hypoglycemia (plasma glucose mean = 65-75 mg/dL) between meals and
during sleep. This occurs because the fetus continues to draw glucose across
the placenta from the maternal bloodstream, even during periods of fasting.
Interprandial hypoglycemia becomes increasingly marked as pregnancy
progresses and the glucose demand of the fetus increases.
Levels of placental steroid and peptide hormones (eg, estrogens,
progesterone, and chorionic somatomammotropin) rise linearly throughout
the second and third trimesters. Because these hormones confer increasing
tissue insulin resistance as their levels rise, the demand for increased insulin
secretion with feeding escalates progressively during pregnancy. By the
third trimester, 24-hour mean insulin levels are 50% higher than in the
nonpregnant state.
Maternal-Fetal Metabolism in Diabetes
 If the maternal pancreatic insulin response is inadequate, maternal and,
then, fetal hyperglycemia results. This typically manifests as recurrent
postprandial hyperglycemic episodes. These postprandial episodes are the
most significant source of the accelerated growth exhibited by the fetus.
 Surging maternal and fetal glucose levels are accompanied by episodic fetal
hyperinsulinemia. Fetal hyperinsulinemia promotes excess nutrient storage,
resulting in macrosomia. The energy expenditure associated with the
conversion of excess glucose into fat causes depletion in fetal oxygen levels.
 These episodes of fetal hypoxia are accompanied by surges in adrenal
catecholamines, which, in turn, cause hypertension, cardiac remodeling and
hypertrophy, stimulation of erythropoietin, red cell hyperplasia, and
increased hematocrit. Polycythemia (hematocrit >65%) occurs in 5-10% of
newborns of diabetic mothers. This finding appears to be related to the level
of glycemic control and is mediated by decreased fetal oxygen tension. High
hematocrit values in the neonate lead to vascular sludging, poor circulation,
and postnatal hyperbilirubinemia.
 During a healthy pregnancy, mean fasting blood sugar levels decline
progressively to a remarkably low value of 74 ± 2.7 (standard deviations
[SD]) mg/dL. However, peak postprandial blood sugar values rarely exceed
120 mg/dL. Meticulous replication of the normal glycemic profile during
pregnancy has been demonstrated to reduce the macrosomia rate.
Specifically, when 2-hour postprandial glucose levels are maintained below
120 mg/dL, approximately 20% of fetuses demonstrate macrosomia. If
postprandial levels range up to 160 mg/dL, macrosomia rates rise to 35%.
Screening for diabetes mellitus during pregnancy
Gestational diabetes
The following 2-step screening system for gestational diabetes is currently
recommended in the United States:
 50-g, 1-hour glucose challenge test (GCT)
 100-g, 3-hour oral glucose tolerance test (OGTT) - For patients with an
abnormal GCT result
Postdiagnostic testing
Once the diagnosis of diabetes is established in a pregnant woman,
continued testing for glycemic control and diabetic complications is
indicated for the remainder of the pregnancy.
First-trimester laboratory studies
 HbA1C
 Blood urea nitrogen (BUN)
 Serum creatinine
 Thyroid-stimulating hormone
 Free thyroxine levels
 Spot urine protein-to-creatinine ratio
 Capillary blood sugar levels
Second-trimester laboratory studies
  Spot urine protein-to-creatinine study in women with elevated value suspension /
in first trimester 50% insulin
lispro injection
 Repeat HbA1C
(Humalog mix
 Capillary blood sugar levels 50/50) (4)
70% insulin 5-15 min Dual 10-16 h
Ultrasonography aspart
protamine
 First trimester - Ultrasonographic assessment for pregnancy dating suspension /
and viability 30% insulin
 Second trimester - Detailed anatomic ultrasonogram at 18-20 weeks aspart injection
and a fetal echocardiogram if the maternal glycohemoglobin value was (Humalog mix
elevated in the first trimester 70/30) (4)
 Third trimester - Growth ultrasonogram to assess fetal size every 4-6 70% NPH / 30% 30-60 mins Dual 10-16 h
weeks from 26-36 weeks in women with overt preexisting diabetes; regular
perform a growth ultrasonogram for fetal size at least once at 36-37
weeks for women with gestational diabetes mellitus Indications for Insulin
Management  Persons with Type 1 (insulin dependent) diabetes or post-
pancreatectomy diabetes
Diet  Acutely decompensated diabetes (with diabetic ketoacidosis or
hypersomolar, hyperglycemic coma)
The goal of dietary therapy is to avoid single large meals and foods with a  Hyperglycemic pregnant diabetic not controlled by diet alone
large percentage of simple carbohydrates. The diet should include foods  Short-term treatment of type 2 or impaired glucose tolerance during
with complex carbohydrates and cellulose, such as whole grain breads and intercurrent events (operations, infections, myocardial infarction)
legumes.  Persons with Type 2 diabetes, but good blood glucose control cannot
be achieved/maintained by diet, exercise, oral hypoglycemic
Insulin
 Emergency treatment of hyperkalemia. Insulin is given with glucose to
lower ECF K+ via distribution into cells
The goal of insulin therapy during pregnancy is to achieve glucose profiles
similar to those of nondiabetic pregnant women. In gestational diabetes,
Characteristics of Insulin Preparation
early intervention with insulin or an oral agent is key to achieving a good
Rapid Acting Insulin
outcome when diet therapy fails to provide adequate glycemic control.
 Very fast onset, short duration
Glyburide and metformin Insulin Analogs
1. Insulin Lispro
The efficacy and safety of insulin have made it the standard for treatment  Same AA as human insulin except B28 contains lysine and B29
of diabetes during pregnancy. Diabetic therapy with the oral agents contains proline
glyburide and metformin, however, has been gaining in popularity. Trials  Switching results in insulin molecule that resists formation of
have shown these 2 drugs to be effective, and no evidence of harm to the hexamers and tends to remain monomeric, thus promoting a
fetus has been found, although the potential for long-term adverse effects more rapid rate of absorption for SC injection. Shorter duration
remains a concern.[6] of action (2-4 hours)
 Injection immediately before a meal affords hypoglycemic
5. Insulin preparation control similar to regular insulin given 30 minutes before the
meal
Pharmacokinetics of Available Insulin Preparations 2. Insulin Aspart
Onset Peak Effective  Substitution of the B28 proline with aspartic acid
Duration  The modification reduces ProB28 and GlyB23 monomer-
Rapid Acting monomer interaction inhibiting self-aggregation
Insulin aspart 5-15 mins 30-90 mins <5h  Rapidly breaks into monomers after SC injection
injection  Absorption and activity profile similar to insulin lispro
Insulin lispro 5-15 mins 30-90 mins <5h 3. Insulin Glusine
injection  Asparagine is substituted for lysine at B3 and glutamic acid for
Insulin glutisine 5-15 mins 30-90 mins <5h lysine at B29
injection
Slow Acting Short Acting Insulin
Regular 30-60 min 2-3 h 5-8 h 1. Regular or Soluble Crystalline Zinc Insulin
Intermediate, basal  Predominantly dimeric and hexameric causing delay in onset and
NPH 2-4 h 4-10 h 10-16 h prolonging time to peak action
Long Acting  Given 30 mins SC before a meal to control postprandial
Insulin glargine 2-4 h No peak 20-24 h hyperglycemia
injection  Preparation of choice for IV therapy during surgery, acute
Insulin detemir 3-8 h No peak 5.7-23.2 h infections, diabetic ketoacidosis
injection
Intermediate Acting Insulin
Premixed
1. NPH
75% insulin 5-15 min Dual 10-16 h
 Mixes insulin and protamine in an equal ratio and neurtral pH
lispro protamine
with small amount of zinc
suspension /
 Converts the normally rapidly absorbed insulin to a preparation
25% insulin
lispro injection with longer duration of action
(Humalog mix
75/25) Long Acting Insulin
1. Insulin Glargine
50% insulin 5-15 min Dual 10-16 h
 Insulin analog
lispro protamine
  Provides constant basal insulin supply and mimics physiological  Basal body temperature increases because of the effect of
post-absorptive basal insulin secretion progesterone on the hypothalamic thermoregulatory center
 Used in conjunction with short-acting insulin  If fertilization does not occur, the corpus luteum regresses at the
 Lowers post-absorptive plasma glucose but reduces the risk of end of the luteal phase. As a result, estradiol and progesterone
nighttime hypoglycemia levels decrease abruptly.
2. Insulin Detemir (4) Menses (days 0-4)
 Terminal threonine is dropped from B30 and myristic acid is  The endometrium is sloughed because of the abrupt withdrawal
attached to the terminal B29 lysine of estradiol and progesterone
 This modification prolongs the availability of the injected analog
by increasing both self-aggregation in SC and reversible albumin
binding
 Dose dependent onset of action of 1-2 h and duration of action
for more than 24 h
Insulin Mixtures
 Combination of intermediate acting and rapid or short acting
insulin in premixed ratio
 Useful for patients with physical impairments (visual or manual)
who are on mixed insulin regimens
 Not ideal for most diabetics who may achieve better control by
separately mixing short-acting and intermediate acting insulins
to arrive at a ratio that is better suited to manage their diabetes

Degree of Control of Plasma Glucose is Modified By

 Changes in insulin absorption
 Factors that alter insulin absorption
 Diet and exercise

Factors that Affect the Absorption of Insulin

 Site of injection – abdominal wall > arm > buttocks > thigh
 Type of insulin
 Subcutaneous blood flow
 Regional muscular activity at site of injection
 Depth of injection
 Species source – human insulin absorbed faster

Complications of Insulin Therapy

 Hypoglycemia
 Weight gain
 Insulin lipodystrophy (atrophy and/or hypertrophy)
 Insulin allergy and resistance
 hypokalemia

REPRODUCTIVE
1. Menstrual cycle 2. HPO Axis
(1) Follicular phase (days 0-14)
 A primordial follicle develops to the graafian stage, with atresia (Hypothalamic-Pituitary Gonadal Axis, or
of neighboring follicles Hypothalamic-Pituitary Ovarian Axis)
 LH and FSH receptors are upregulated in theca and granulosa
cells Hypothalamic control – GnRH
 Estradiol levels increase and cause proliferation in the uterus
 FSH and LH levels are suppressed by negative feedback effect of
 Pulsatile GnRH stimulates the anterior pituitary to secrete FSH and LH
estradiol on the anterior pituitary Anterior lobe of the pituitary – FSH and LH
(2) Ovulation (day 14)
 Occurs 14 days before menses, regardless of cycle length. Thus, FSH and LH stimulate the following in the ovaries:
in a 28-day cycle, ovulation occurs on day 14; in a 35-day cycle,
 Steroidogenesis in the ovarian follicle and corpus luteum
ovulation occurs on day 22
 Follicular development beyond the antral stage
 A burst of estradiol synthesis at the end of the follicular phase
 Ovulation
has a positive feedback effect on the secretion of FSH and LH (LH
 Lutenization
surge)
 Estrogen levels decrease just after ovulation (but rise again
during the luteal phase)
 Cervical mucus increases in quantity; it becomes less viscous and
more penetrable by sperm

(3) Luteal phase (days 14-28)

 The corpus luteum begins to develop, and synthesizes estrogen
and progesterone
 Vascularity and secretory activity of the endometrium increase
to prepare for receipt of a fertilized egg
 Stage T N M

IA T1 N0 M0

IB T0 N1mi M0

T1 N1mi M0

IIA T0 N1 M0

T1 N1 M0

T2 N0 M0

IIB T2 N1 M0

T3 N0 M0

IIIA T0 N2 M0

T1 N2 M0

T2 N2 M0
3. Breast Cancer
T3 N1 M0
Breast Cancer Staging
T3 N2 M0
Primary tumor (T)
IIIB T4 N0 M0

T0 No evidence of primary tumor T4 N1 M0

T4 N2 M0
T1 Tumor ≤ 20 mm in greatest dimension
IIIC Any T N3 M0
T2 Tumor > 20 mm but ≤ 50 mm in greatest dimension IV Any T Any N M1

T3 Tumor > 50 mm in greatest dimension Pathophysiology

The current understanding of breast cancer etiopathogenesis is that invasive
T4 Tumor of any size with direct extension to the chest wall and/or to the skin cancers arise through a series of molecular alterations at the cell level. These
(ulceration or skin nodules) alterations result in breast epithelial cells with immortal features and
uncontrolled growth.
Regional lymph nodes (N)
Genomic profiling has demonstrated the presence of discrete breast tumor
subtypes with distinct natural histories and clinical behavior. The exact number of
Clinical disease subtypes and molecular alterations from which these subtypes arise
remains to be fully elucidated, but these generally align with the presence or
absence of estrogen receptor (ER), progesterone receptor (PR), and human
N0 No regional lymph node metastasis
epidermal growth factor receptor 2 (HER2).

N1 Metastasis to movable ipsilateral level I, II axillary lymph node(s)

N2 Metastases in ipsilateral level I, II axillary lymph nodes that are clinically fixed
or matted or in clinically detected* ipsilateral internal mammary nodes in
the absence of clinically evident axillary lymph node metastasis

N3 Metastases in ipsilateral infraclavicular (level III axillary) lymph node(s), with

or without level I, II axillary node involvement, or in clinically
detected * ipsilateral internal mammary lymph node(s) and in
the presence of clinically evident level I, II axillary lymph node metastasis; or
metastasis in ipsilateral supraclavicular lymph node(s), with or without
axillary or internal mammary lymph node involvement

Distant metastasis (M)

M0 No clinical or radiographic evidence of distant metastasis

M1 Distant detectable metastases as determined by classic clinical and

radiographic means and/or histologically proven > 0.2 mm
 Evaluation of breast cancer includes the following:

 Clinical examination
 Imaging
 Needle biopsy

Physical examination

If a palpable lump is found and possesses any of the following features, breast
cancer may be present:

 Hardness
 Irregularity
 Focal nodularity
 Fixation to skin or muscle

Screening

Early detection remains the primary defense in preventing breast cancer.

Screening modalities include the following:

 Breast self-examination
 Clinical breast examination
 Mammography
 Ultrasonography
 Magnetic resonance imaging

Biopsy

Core biopsy with image guidance is the recommended diagnostic approach for
newly diagnosed breast cancers. This is a method for obtaining breast tissue
without surgery and can eliminate the need for additional surgeries. Open
excisional biopsy is the surgical removal of the entire lump.

Differential Diagnoses
Etiology
 Breast Abscess and Masses
Risk factors for breast cancer:  Breast, Fibroadenoma
 Increasing age and female sex
 Family history of breast cancer Management
 Family history of BRCA1 and BRCA2 mutations
Surgery
 Late age at first pregnancy, nulliparity, early onset of menses, and late
age of menopause Surgery is the primary treatment for breast cancer. Lumpectomy or total
 Obesity, sedentary lifestyle mastectomy may be indicated.
 Dietary (eg, charred and processed meats)
Radiation therapy may follow surgery in an effort to eradicate residual disease
 Regular, moderate consumption of alcohol (3-5 alcoholic beverages
while reducing recurrence rates. Adjuvant treatment for breast cancer involves
per week)
radiation therapy and a variety of chemotherapeutic and biologic agents. There
 Tobacco smoke (both active and passive exposure) are 2 general approaches for delivering radiation therapy:
 Environmental carcinogens (eg, exposure to pesticides, radiation, and
environmental and dietary estrogens)  External-beam radiotherapy (EBRT)
 Partial-breast irradiation (PBI)
Signs and symptoms
 Surgical resection with or without radiation is the standard treatment
Early breast cancers may be asymptomatic, and pain and discomfort are typically for ductal carcinoma in situ.
not present. If a lump is discovered, the following may indicate the possible
presence of breast cancer: Pharmacologic agents

 Change in breast size or shape Hormone therapy and chemotherapy are the 2 main interventions for treating
metastatic breast cancer. Common chemotherapeutic regimens include the
 Skin dimpling or skin changes
following:
 Recent nipple inversion or skin change, or nipple abnormalities
 Single-duct discharge, particularly if blood-stained  Docetaxel
 Axillary lump  Cyclophosphamide
 Doxorubicin
Diagnosis
 Carboplatin
Breast cancer is often first detected as an abnormality on a mammogram before  Methotrexate
it is felt by the patient or health care provider.
 Trastuzumab
 Hep B 6 weeks or at 0.5 ml (3) IM,
Two selective estrogen receptor modulators (SERMs), tamoxifen and raloxifene, birth – 0, 1 & 6 anterolateral
are approved for reduction of breast cancer risk in high-risk women. months aspect of thigh

4. Lactation Measles 9 mos; 6 mos if 0.5 ml (1) SC, outer part

epidemic of thigh
 Estrogens and progesterone stimulate the growth and development of
the breasts throughout pregnancy BCG 2 At school 0.1 ml (1) ID, deltoid L
 Prolactin levels increase steadily during pregnancy because estrogen entry, whether arm
stimulates prolactin secretion from the anterior pituitary or not child
 Lactation does not occur during pregnancy because estrogen and has BCG scar
progesterone block the action of prolactin on the breast Tetanus Women of 0.5 ml (5) IM, deltoid TT1 at
 After parturition, estrogen and progesterone levels decrease abruptly Toxoid childbearing region first
and lactation occurs age contact
 Lactation is maintained by suckling, which stimulates both oxytocin
and prolactin secretion TT2 at
 Ovulation is suppressed as long as lactation continues because least 4
prolactin has the following effects weeks
a. Inhibits hypothalamic GnRH secretion after
b. Inhibits the action of GnRH on the anterior pituitiary, and
TT3 6
consequently inhibits LH and FSH secretion
weeks
c. Antagonizes the actions of LH and FSH on the ovaries
after
PEDIATRICS
TT4 at
1. EPI vaccines least 1
Expanded Program on Immunization – Philippines year after
 Immunization is the process of inducing immunity against a specific
TT5 at
disease least 1
 Immunity can be induced either passively through administration of year after
preformed antibodies or actively through administration of a vaccine
or toxoid

Active immunization BCG Vaccine

 Involves administration of whole or parts of a microorganism or a  Live attenuated vacterial vaccine
modified product of that microorganism (toxoid, purified antigen)  At birth or anytime after birth
 This will evoke an immunologic response mimicking that of the natural  0.05 ml ID from birth to 4 weeks, 0.1 ml ID beyond 1 month at right
infection upper deltoid
 Usually presents little or no risk to the recipient
 Vaccines can consist of: Hepatitis B Vaccine
a. Live attenuated virus – measles, MMR, OPV, varicella,  Inactivated viral antigen
rotavirus vaccines  0,1 & 6 months
b. Live attenuated bacteria – BCG  If mother is HBsAg (+), give HIBG and Hep B vaccine within 12 hours of
 Contraindication to ALL VACCINES birth
a. Serious allergic reaction (anaphylaxis) after a previous  After birth, the 2nd dose should be given at age 1-2 months
vaccine dose  The 3rd dose should be given at 6 months
b. Serious allergic reaction to a vaccine component  Dose: up to 19 years old – 10 mcg (0.5 ml)
 Contraindications to ALL LIVE VACCINES 19 years odl and above – 20 mcg (1 ml)
a. Immunocompromised patients
b. Patients given immunoglobulin and blood products for the Diphtheria, Tetanus and Pertussis (DTP) Vaccine
past 3 months DTap
c. Pregnancy and possibility of getting pregnant within 3  DT are toxoids
months  aP is killed/inactivated acellular pertussis
d. Household contacts of immunocompromised patients (for DTP or DTwP
OPV only)  DT are toxoids
 P is killed/inactivated whole cell pertussis
Vaccine Minimum Age Dose Route and Site Min  DTP/DTaP vaccine usual side effect: fever up to 72 hours
(No) of Admin interval
b/w Poliomyelitis Vaccine
doses  6 weeks, then at least 4 week intervals
BCG 1 Birth; or any 0.05 ml ID, deltoid R  Inactivated or killed polio vaccine (IPV) – 0.5 ml, IM
time after for NB; arm
birth 0.1 ml for Measles vaccine
infants  live attenuated
(1)  0.5 ml SC
 Recommended at age 9 months but may be given as early as 6 months
DTP 6 weeks 0.5 ml (3) IM, upper outer 4 weeks when there is an epidemic
portion of thigh
Hemophilus influenzae b (Hib) Vaccine
OPV 6 weeks 2 drops PO, mouth 4 weeks  0.5 ml IM given at 2, 4, 6, and 12-15 months old
(3)
Measles, Mumps, Rubella (MMR) Vaccine
 Live attenuated viral vaccine
 0.5 ml SC  PCV is given at 2, 4, 6 and 12-15 months or 1 dose at 2 years of age
 Given at 12-15 months, a booster dose is recommended at 4-6 years  PPV is given for children 2 years and above
old  0.5 ml IM

Varicella Vaccine
 live attenuated vaccine Influenza Vaccine
 0.5 ml SC  Inactivated vaccine
 Routinely given at age 12 months and up but can be given as early as  Dose for 3 years and above: 0.5 ml IM or SC
9 months 6-36 months: 0.25 ml IM or SC
 Dose: single dose for ages 1-12 years; a booster dose is recommended  Indications:
at 4 to 6 years old - Prophylaxis in children older than 6 months and adult over 60
 2 doses 6-10 weeks apart in children >13 years years
- CV or metabolic disease, cystic fibrosis, chronic respiratory
Hepatitis A Vaccine disease, chronic renal insufficiency
 Inactivated viral antigen
 Given to children 1 years and above in 2 doses 6 to 12 months apart Rotavirus Vaccine
 Dose for 1-18 years old: 0.5 ml IM  Inactivated vaccine
>19 years old: 1ml IM  Given at 2, 4 and 6 months
 Indications  0.5 ml IM
- Persons travelling to areas with high prevalence of Hep A
- Occupational hazards Human Papilloma Virus Vaccine
- Hemophiliacs – contacts of infected persons  Inactivated vaccine
 Given from 9-45 years old at 0, 1, and 4 months; or 0, 2, and 6 months
 0.5 ml IM
Pneumococcal Vaccine

 Head lags on pull to sit

2. Developmental milestones 3 months
 Visually tracks objects well
Newborn period (1st 4 weeks)
 Begins to have hand regard
 Lies in flexed position, turns head side to side
 Good head control on prone and looks around
 Head lags on ventral suspension
 Improved head control on sitting position
 May fixate face on light in line of vision
 Sustained smiling and cooing
 Doll’s eye movement of eye when turning body
4 months
 Visual preference for human face
 Begins to reach for toys symmetrically
1 month
 Regards toys and puts them into mouth
 Spontaneous motor activity
 Removes diaper on face
 Lifts head momentarily on prone
 Good head control on sitting position
 Head lags when pulled to sit
 Midline regard (plays with hands)
 Begins to regard surroundings
 Laughs
 Follows objects to midline
6 months
2 months
 Reaches with either hand
 Motor activity generalized
 Chest up when prone
 Smiles and coos socially
 Rolls over
 Follows objects past midline
 May sit briefly when placed
  Laughs and plays with examiner  Draws person with head, trunk, arms or legs
 Imitates speech sounds  Counts 3 objects
8 months  Draws a triangle, copies a square
 Sits alone  Names one or more colors
 Begins to creep  Sings songs
 Regards self in mirror  Toilet trained
 Babbles  Role plays
 Crude prehension 5 years
 Transfer object from 1 hand to the other  Skips
 Says papa and mama indiscriminately  Draws a person
 Responds to commands of “no”  Dresses / undresses unaided
10 months  Names 4 or more colors
 Crawls and pulls to stand  Counts > 10
 Begins to cruise around the crib or furniture  Ties shoelaces
 Better prehension (thumb and forefinger opposition)  Asks meaning of words
 Utters “mama” or “dada” 6 years
 Holds bottle  Draws a person with hands and clothes
 Feed self with crackers  Repeats 4-5 digits forward
 Waves bye-bye  Knows morning and afternoon
 Gesture language  Knows right and left sides
12 months  Copies a diamond
 Walks alone with one hand held
 Stands alone 3. SMR Staging
 2 words other than mama and dada
 Beings to feed with fingers Classification of Sex Maturity States in Girls
 Kisses on request :* SMR Stage Pubic Hair Breasts
 Releases object on request
1 Preadolescent Preadolescent
 Obeys commands with gestures
15 months 2 Sparse, lightly Breast and papilla
 Independent walking pigmented, medial elevated as small
 Creeps upstairs border of labia mound; diameter of
 3-4 words other than mama, dada areola increased
 Drinks from cup
3 Darker, beginning Breast and areola
 Begins to feed with spoon
to curl, increased enlarged, no contour
 Vocalizes and points to something
amount separation
 Obeys simple commands without gesture
18 months 4 Coarse, curly, Areola and papilla form
 Walks well abundant, but less secondary mound
 Throws a ball than in adult
 Stacks 3-4 blocks
 10 word vocabulary
5 Adult feminine Mature, nipple projects,
 Pulls toy on string
triangle, spread to areola part of general
2 years
medial surface of breast contour
 Runs well, jumps thighs
 Uses pronouns and produces 3 word sentences
 Feeds self with spoon Classification of Sex Maturity in Boys
 Toilet-trained by day SMR Pubic hair Penis Testes
 Removes clothes
 Points to body parts 1 None Preadolescent Preadolescent
2 ½ years
2 Scanty, long, Minimal Enlarged
 Partially undresses self
slightly change or scrotum, pink,
 Draws vertical and horizontal lines
pigmented enlargement texture altered
 Knows full name, uses “I”
 Helps to put things away 3 Darker, Lengthens Larger
3 years starting to
 Alternate feet in climbing stairs curl, small
 Pedals a tricycle amount
 Builds a tower of 6-8 blocks 4 Resembles Larger, glans Larger, scrotum
 Plays simple games adult type but and breadth dark
 Names drawing less quantity, increase size
 Copies a circle, later a cross coarse, curly
 Uses plurals and obeys prepositional commands 5 Adult Adult size Adult size
 Knows age and sex distribution,
 Buttons and unbuttons spread to
 Puts on shoes medial surface
 Counts 1-10 of thighs
4 years
 Runs and climbs well
 Descends stairs on alternate feet
 Hops on one foot
 Throws ball overhead
 SURGERY

1. Trauma
1. Primary survey –identification of life threatening condition and
managing it
A-Airway
Problem recognition:
- Tacchypnea
- Altered level of conscsiousness
- Trauma to the face
- Refuse to lie down
Objective signs:
- Agitated (hypoxia), obtunded (hypercarbia) or
cyanosis (hypoxemia)
- Abnormal sounds. Noisy breathing is obstructed
breathing. Snoring, gurgling and stridor is partial
occlusion of pharynx or larynx
- Feel for movement of air
Management:
- Protect cervical spine. Head and neck in neutral
position
- Airway maintenance technique:
o Chin lift
o Jaw thrust
o Oropharyngeal airway
o Nasopharyngeal airway
- Definitive airway – tube in trachea connected to O2
supply
Indications:
o Apnea
o Inability to maintain patent airway
o Protection from blood or vomitus
o Impending or potential compromise of
airway
o Close head injury
o Failure to maintain adequate oxygenation
by facemask
Types
o Orotracheal intubation
o Nasotracheal intubation
o Surgical airways (surgical
cricothyroidotomy)
B-Breathing and ventilation
Pronblem Recognition
- Auscultation to assure air exchange
- Percussion to reveal presence of blood or air in chest
- Visual inspection and palpatioin to reveal chest wall
injuries
- Presence of tension pneumothorax, flail chest with
pulmonary contusion and open pneumothorax
Management
- Pneumothorax – relieved by needling until chest tube
is inserted
- Hemothorax – chest tube
- Flail chest, fracture ribs and pulmonary contusion –
positive pressure ventilation
- Oxygenation –facemask at 10-2lpm
- Ventilation – mouth to face mask or bag valve face
mask
C-Circulation
Problem recognition
- Level of consciousness
- Skin color
- Pulse
- Bleeding
Management
- 2 large caliber IV catheter
- Ringer’s lactate solution
- Typed specific blood (pRBC)
- Warm blood products or IV solution
D-Disability (neurologic evaluation)
- LOC and pupillary size and reaction
 - GCS
Patient categorization First Only the epidermis
- Coma – GCS >8 Degree Mild sunburn
- Head injury severity Not included in the calculation of total body surface area
o Severe GCS>8 Second Superficial
o Moderate GCS 9-12 Degree - Only the epidermis and part of the dermis
o Minor GCS 13-15 - Wounds are red and moist with blister formation
- Secure airway and hyperventilate - Intact tactile and pain sensors
E-Exposure - Heal 14-21 days with minimal scarring
- Completely undress Deep
- Cover the patient - Entire epidermis and dermis, leaving only the skin
- Warm fluids appendages intact
2. Resuscitation - Motted appearance and areas of waxy white injury
- Insertion of catheters (urinary, gatric) - Surface is dry and anesthetic
- Xrays - Heal 4-6 weeks
o Blunt trauma patient - if unstable epithelium  late hyperthropic scarring
 Cervical spine and contracture formation
 AP chest - Tx: excision and skin grafting
 AP pelvis Third Involves the entire skin and underlying subcutaneous tissue
3. Secondary survey Degree Wound is white or cherry and/or black
- Head to toe evaluation, history and VS Thrombotic blood vessels may be visible, wound is dry with
- Complete neuro exam leathery textyre
- Xrays and Special procedures(CT, labs..) Do not heal spontaneously and require skin graftin
- AMPLE (allergies, meds, past illness, last meal,
event/environment r/t injury) Management:
SCENE OF THE ACCIDENT:
1. Eliminate heat source. Stop patient from running if his clothes are on
fire
2. Controversial: cooling burn wounds which only last for 2-3 minutes 
prolonged edema & impaired healing  partial thickness to full
thickness. PREFERRED: tepid water
3. Irrigate chemical burns with water

EMERGENCY ROOM
1. Burn chart to estimate affected body surface
*subtract 1% per year of age
** add 0.5% per year of age
Extent is not evaluated in first degree
2. History should elicit possible smoke inhalation, pertinent past medical
history, other associated injuries
Hospital admission: >10% children/ >15% adult; involvement of face,
4. Continued re evaluation neck, BOTH hands, BOTH feet, perineum; electrical and chemical
5. Definitive treatment burns; associated injuries, complicating medical problems suspected
2. Burns child abuse or neglect; self inflicted; psycho problem
Outpatient: KEEP THE WOUND CLEAN!
 Frequently affects children and young adults Wash, trim debris, shave hair at least 2.5cm AROUND the burn area
 Most common: open flame and hot liquids Blisters: allow to heal spontaneously (leave intact)/ evacuate blister
 Less common: contact with hot meals, toxic chemicals and high fluid without removing overlying skin/ debride blister (only for GROSS
voltage electrical current CONTAMINATION
 Mechanism: Transfer of heat from higher to lower temperature  Topical chemotherapeutic: to delay wound healing; overtreatment is
tissue destruction the most common cause of complications; sometimes petrolatum
 Speed of heat transfer is critical would do
 Cell injury: 45-50°C Bulky dressing: reduce pain but potential danger for bacterial
 Protein denaturation: >50°C overgrowth
 Cell death (protein coagulation): > 65°C
3. Fluid replacement
Most popular: LRS
Chemical burn Thermal injury Electrical injury
Parkland formula (4mL/kg/%burn) ½ to be given in the first 8h then
Cell destruction Coagulation necrosis Minimal destruction of the skin
the remainder for the next 16hrs then for the 2nd day give colloids (0.3-
depends on the of variable depth w/ Impt is the amount of current
0.5mL/kg/%burn) + D5W based on UO
length of varying degree of that passes between entrance
FOR THE FIRST 24h: ^ht and wt should be considered for total body
contact until vascular thrombosis and exit points
surface area; ^^ volume is higher in children due to high surface area
neutralization Require topical Least resistant: nerve, blood
Burn related losses: 5L/m2 body surface burned/24 hr
antimicrobials for and muscle
Maintenance fluid: 2L/m2 total body surface/24hr
adequate
FOR THE 2nd AND SUBSEQUENT days
concentration on
3.75L/m2 body surface area/d PLUS 1.5L/m2 total body surface
wound surface
area/day
4. Monitoring: VS, PE, Labs (Hct, BUN, UUN, ABG, serum and urine osmol,
Depth of skin destruction:
serum and urine electrolytes, urine SG), fluid loses (gastric, urine,
- Dependent upon the thickness of the skin at the local area and the
stool)
presence and degree of development of skin appendage (sweat
5. Wound care
glands, hair follicle) and dermal papillae
Exposure therapy- light and cool environment without topical antibiotics
- Defining depth- important in treatment and prognosis
after debridement, for superficial burn wounds involving face and perineum
 Open dressing  Injury may accompany normal, beneficial inflamatory reactions
Occlusive dressing- close method, circumferential burn and those requiring  Pathology may become the dominant features if a rreaction si very
transport w/w/o topical antibiotics strong (i.e. severe infection), prolonged (eliciting agent resists
Excisional therapy- most demanding, remove all non-viable tissues readication), or inappropriate (e.g. directed against self-antigens -in
immediate wound coverage, 2nd-5th post burn days auto-immune diseases
Laser Doppler velocimetry- most promising in detecting depth by measuring  Cells and molecules of host defense normally circulate in the blood,
degree of blood flow and the goal of the inflammatory reaction is to bring them to the site
Escharotomy/fasciotomy- circumferential & constricting burns of infection or tissue damage
Escharotomy- skin and subcutaneous tissue are constricting  These include blood leukocytes and plasma proteins, cells of vascular
Fasciotomy- deep compartment hypertension walls, and cells and extracellular matrix (ECM) of the surrounding
Skin grafting- remains unhealed by the end of the 4th week connective tissue (see figure above)
 Inflammation can be acute or chornic:
- Acute inflammation: rapid in onset, short duration. Lasts
Commonly used topical antimicrobials for a few minutes to a few days. Characterized by fluid and
Silver sulfadiazine (silvadene) Ca nitrate- silver plasma exudation, and predominantly neutrophilic
sulfadiazine leukocyte accumulation
Povidone iodine Nitrofurazone - Chronic inflammation: more insidious, longer duration.
Chlorhexidine gluconate Gentamicin Lasts for days to years. Typified by influx of lymphocytes
and macrophages with vascular proliferation and fibrosis
(scarring)
 When a host encoungers an injurious agent (i.e. microbe) or dead cells,
phagocytes try to eliminate these agents
 Phagocytes and other host cells react to foreign or abnormal
substance by liberating protein and lipid molecules that function as
chemical mediators of inflammation
 Mediators are also made from plasma proteins that react with
microbes or injured tissues
 Mediators promote efflux of plasma and recruitment of circulating
Adult Child leukocytes to site where offending agent is located
<10y/o  Activated leukocytes try to remove offending agent by phagocytosis
Head & neck 9% 19%*  Unfortunate side effect of activation of leukocytes may be
Ant trunk 18% 18% damage to normal host tissues
Post trunk 18% 18%
Five cardinal signs
R UE 9% 9%
L UE 9% 9%
 Dolor (pain)
R LE 18% 13%**
 Calor (heat)
L LE 18% 13%**
 Rubor (redness)
Perineum 1% 1%
 Tumor (swelling)
Total 100%
 Functio laesa (loss of function)

Stimuli for Acute Inflammation

 Infections (bacterial, viral, fungal, parasitic) – most common and
medically important causes of inflammation
3.Inflammation and repair  Trauma (blunt and penetrating) and physical and chemical agents
(thermal injury e.g. burns, frostbite; irradiation; environmental
chemicals) injure host cells and elicit inflammatory reactions
 Tissue necrosis (from any cause), including ischemia (i.e. myocardial
infarct) and physical/chemical injury
 Foreign bodies (splinters, dirt, sutures)
 Immune reactions (also called hypersensitivity reactions) against
environmental substances or against self tissues

Leukocyte Recruitment

 Inflammation is a protective response intented to eliminate the intial

cause of cell injury as well as the necrotc cells and tissues resuling from
the original insult
 Inflammation accomplishes its protective mission by diluting,
destroying, or neuralizing harmful agents (i.e. microbes and toxins)
 It sets into motion events that heal and repair sites of injury
 Although inflammation helps clear infections and other noxious stimuli
and initiates repair, the inflammatory reaction and subsequent repair
process can cause considerable harm
  Sequence of events in recruitment of leukocytes from the vascular
lumen to the extravascular space:
(1) Margination, adhesion to endothelium, rolling along vessel wall
(2) Firm adhesion to the endothelium
(3) Transmigration between endothelial cells
(4) Migration in interstitial tissues toward a chemotactic stimulus The Harris-Benedict equations are suitable for estimating energy requirements in
the majority of hospitalized patients. It has been demonstrated that the provision
Margination and Rolling of 30 kcal/kg per day will adequately meet energy requirements in most
postsurgical patients, with a low risk of overfeeding. After trauma or sepsis,
 As blood flows from capillaries into postcapillary venules, circulating energy substrate demands are increased, necessitating greater nonprotein
cells are swept by laminar flow against the vessel wall calories beyond calculated energy expenditure.
 Leukocytes are pushed out of the central axial column and thus have a
better opportunity to interact with lining endothelial cells
 Margination – leukocyte accumulation at the periphery of vessels
 Rolling - leukocytes tumble on the endothelial surface, transiently
sticking along the way
 Weak and transient adhesions involved in rolling are mediated by the
selectin family of adhesion molecules
 E selectin – expressed on endothelial cells
 P selectin – present on endothelium and platelets
 L selectin – on surface of most leukocytes
 Selectins bind sialylated oligosaccharides (i.e. sialyl-Lewis X on
leukocytes) attached to mucin-like glycoproteins on various cells
 Selectins are upregulated after stimulation by specific mediators An appropriate nonprotein-calorie:nitrogen ratio of 150:1 (e.g., 1 g N = 6.25 g
 Binding of leukocytes is restricted to endothelium at sites of infection protein) should be maintained, which is the basal calorie requirement provided
and/or tissue injury to limit the use of protein as an energy source.

Adhesion and Transmigration 5. Surgical Wound Classification

 Adhesion of leukocytes to endothelial surfaces is mediated by

integrins expressed on leukocyte cell surfaces interacting with ligands
on endothelial cells
 Chemokines – chemoatractant cytokines secreted by many cells at
sites fo inflammation. They are displayed bound to proteoglycans on
the endothelial surface
 When adherent leukoytes encounter displayed chemokines, cells are
activated, and their integrins undergo conformational changes and
cluster together, thus converting to a high affinity form.
 TNF and IL-1 activate endothelial cells to increase their expression of
ligands for integrins
 Net result of cytokine-stimulated increased integrin affinity and
increased expression of integrin ligands is table attachment of
leukocytes to endothelial cells at sites of inflammation
 After being arrested on the endothelial surface, leukocytes migrate I. Clean:
throught he vessel wall by squeezing between cells at intercellular - Uninfected, no inflammation
junctions. This movement of leukocytes is called diapedesis
 - Resp, GI, GU tracts not entered
Chemotaxis

 After extravasating from the blood, leukocytes migrate twoard sites of

 - Closed primarily
infection or injury along a chemical gradient by chemotaxis
 Exogenous and endogenous substances can be chemotactic for Examples: Ex lap, mastectomy, neck dissection, thyroid, vascular, hernia,
leukocytes, including (1) bacterial products, (2) cytokines, (3) splenectomy
compotnents of the complement system, and (4) products of the
lipoxygenase pathway of arachidonic acid metabolism  II. Clean-contaminated:
 These mediators are produced in response to infections and tissue - Resp, GI, GU tracts entered, controlled
damage and during immunologic reactions
 Leukocytes move by extending pseudopods that anchor to the ECM - No unusual contamination
and pull the cell in the direction of the extension
 The type of emigrating leukocyte varies with age of the inflammatory Examples: Chole, SBR, Whipple, liver txp, gastric surgery, bronch, colon surgery
response and with the type of stimulus
- Neutrophils predominate in the inflammatory infiltrate in
 III: Contaminated:
the first 6-24 hours
- Monocyes replace them in 24-48 hours  - Open, fresh, accidental wounds
-
4. Surgical Nutrition  - Major break in sterile technique

The goals of nutritional support in the surgical patient are to prevent or reverse - Gross Spillage from GI tract
the catabolic effects of disease or injury and meet substrate requirements for
protein synthesis. Failure to provide adequate nonprotein energy sources will - Acute nonpurulent inflammation
lead to consumption of lean tissue stores.
 Examples: Inflamed appy, bile spillage in chole, diverticulitis, Rectal surgery, 2. Steroids
penetrating wounds
 Corticosteroids bind to cytosolic receptors and the complexes formed
 IV: Dirty: undergo dimerization and then enter the cell nucleus. There they alter gene
expression by binding to tissue specific nuclear response elements.
 - Old traumatic wounds, devitalized tissue  Metabolic effects: Glucocorticoids increase gluconeogenesis, insulin
secretion, liogenesis, lipolysis. Catabolic effects nclude muscle and lymphoid
 - Existing infection or perforation tissue wasting, osteoporosis and growth inhibition. Mineralocorticoids
increase synthesis of ion transporters and sodium channels in renal
 - Organisms present BEFORE procedure collecting tubules.
 Immunosuppressive and anti-inflammatory actions: High doses of
 Examples: Abscess I&D, perforated bowel, peritonitis, wound debridement, glucocorticoids result in decreased synthesis of prostaglandins and
positive cultures pre-op leukotrienes. There is also decreased leukocyte migration, phagocytosis,
lymphocyte proliferation and activity.
PHARMACOLOGY
Natural corticosteroids
1. H1 and H2 Histamines
 Histamine is neurotransmitter and mediator of allergic responses.  Cortisol – major natural glucocorticoid – rapidly metabolized, short,
 Synthesized from histidine and stored in vesicles in mast cells, duration of action
basophils and some nerve endings  Aldosterone – major natural mineralocorticoid
 Histamine’s effects are mediated by three G-protein coupled receptors
Synthetic corticosteroids – longer duration of action, less mineralocorticoid
Receptor G protein Location Function effect
H1 Gq Smooth, muscle, Increased IP3
gland cells, some and DAG,  Prednione, triamcinolone and dexamethasone (in order of increasing DOA)
nerve endings smooth muscle  Fludrocortisone – synthetic mineralocorticoid
contraction
(except vessels); Clinical uses
increased
secretion  Adrenal dysfunction – replacement therapy in Addison’ disease and as
H2 Gs Parietal cells Increased cAMP, supplementation in acute adrenal insufficiency states (infection,
(stomach), heart increased acid shock, trauma)
secretion,  Nonendocrine uses – use in inflammatory and immune disorders
cardiac
stimulation Toxicities
H3 ? Nerve endings Modulation of
transmitter a) Suppression of ACTH – adrenocortical atrophy
release b) Cushingoid state – fat deposition and muscle atrophy
c) Metabolic effects – hyperglycemia, increased insulin demand, osteoporosis,
aseptic hip necrosis, decreased skeletal growth in children;
H1 blocking drugs (traditional antihistamines) fall into three groups mineralocorticoid – electrolyte imbalance, edema, hypertension
d) Other toxicities – GI ulcers, decreased wound healing, cataract formation,
Group Examples Uses Toxicities glaucoma, increased infections, mental dysfunction
1st Generation Diphenhydramine Allergy, sleep Strong alpha
aid, motion and Corticosteroid Antagonists
sickness, muscarinic
nausea of block; Receptor antagonists
chemotherapy strongly
sedative Spironolactone Blocks aldosterone receptors
1st Chlorpheniramine Allergy Much Mifepristone Blocks glucocorticoid receptors
generation, reduced Synthesis inhibitors
newer sedative and
ANS effects Ketoconazole – inhibits both corticosteroids and gonadal receptors
2nd Fexofenadine, Allergy Negligible
Generation loratidine, CNS and ANS 3. Antibiotics
desloratidine, effects
cetirizine Inhibitors of cell wall synthesis: Penicillin
H1 blockers are used in the treatment of urticarial, hay fever and other IgE
mediated allergic reactions. Toxicities reflect ther ANS and CNS effects. Bactericidal antibiotics that contain a Beta lactam ring necessary for antimicrobial
activity.
H2 blockers
Subclasses
 Cimetidine
 Famotidine Penicillinase-susceptible Pen G, Pen V
 Nizatidine narrow spectrum
 Ranitidine Penicillinase-resistant narrow Methicillin, nafcillin
spectrum
H2 blockers are used for acid peptic ulcer disease, especially heartburn and peptic Penicillinase-susceptible broad Ampicillin, amoxicillin,
ulcer. Toxicities include inhibition of hepatic cytochrome P450, drug metabolizing spectrum ticarcillin
enzymes and an antiandrogenic action.

*most H2 toxicities are from Ranitidine

MOA: bind to specific proteins (penicillin binding proteins, PBPs) and inhibit
transpeptidation, the final step in cell wall synthesis and also activate autolytic
enzymes which cause lesions in th bacterial cell membrane
MOR:
Imipenem and meropenem are bactericidal, penicillinase resistant antibiotics
with wide activity against gram (+) and gram (-), including anaerobes.
Carbapenems are IV agents eliminated by the kidney; imipenem is given with
cilastatin, which blocks its metabolism.
Toxicities – nausea, diarrhea, skin rash, seizures

 Formation of penicillinases (staph, gram-negative bacilli) Vancomycin

 Changes in PBP structure prevent binding (MRSA, NRSA)
 Changes in porin structure prevent access to the cytoplasmic
membrane (pseudomonas resistant to ticarcillin)
Pharmacokinetics
MOA: Bactericidal inhibitor of cell wall synthesis by inhibiting glycosylation
reactions. Resistance involves decreased binding of the drug.
Pharmacokinetics: renal elimination
Clinical use: DOC for MRSA and for pseudomembranous colitis
Toxicities – fever, chills, potential ototoxicity and nephrotoxicity

Oral bioavailability: Gastric acids inactivates some penicillins (Pen G)

Elimination: Most are eliminated via active tubular secretion; nafcillin is

eliminated in bile and ampicillin undergoes enterohepatic cycling

Clinical Uses

Pen G Strep, pneumococci,

enterococci, meningococci,
Treponema pallidum,
spirochetes
Nafcillin, oxacillin, related drugs Known or suspected staph
Inhibitors of Protein synthesis: Macrolides, Clindamycin, Tetracycline and
infections (not MRSA)
Chloramphenicol
Amoxicillin and ampicillin Streptococci, E coli,
Haemophilus influenza, MOA and Resistance: All are bacteriostatic inhibitors of protein synthesis at the
Moraxella catarrhalis, Listeria ribosomal level.
monocytogenes, H pylori
Ticarcillin and related drugs Gram negative bacilli including Macrolides Binds to 50s subunit to block
Pseudomonas aeruginosa translocation
Clindamycin
(synergy with aminoglycosides)
Chloramphenicol Binds to 50s subunit but
prevents transpeptidation by
preventing binding of
*certain penicillins are enhanced by the addition of clavulanic acid and sulbactam
aminoacyl moiety of charged
– inhibit bacterial penicillinases tRNA
Tetracyclines Bind to 30s subunit to prevent
Inhibitors of cell wall synthesis: Cephalosporins, carbapenems, vancomycin
binding of charged tRNA to the
acceptor site of the ribosomal
Cephalosporins
mRNA complex
MOA: bactericidal B-lactams similar to penicillins. Resistance may occur via B-
Resistance – in gram (+) cocci, resistance to macrolides involves methylation of
lactamase formation and changes in PBP
the 50s receptor, preventing binding of the antibiotics; chloramphenicol –
formation of acetyltransferases that inactivate the drug; tetracycline – decreased
1st gen Gram-positive cocci (not MRSA) E coli, Klebsiella pneumonia intracellular accumulation
and some Proteus species
2nd gen Gram negative bacilli including Bacteroides fragilis (cefotetan); Macrolide antibiotics
Haemophilus influenza and Moraxella catarrhalis (cefaclor) Erythromycin, azithromycin, clarithromycin
Good oral bioavailability
3rd gen Gram (+), gram (-) cocci and gram (-) bacilli including B- Erythromycin (biliary excretion) and clarithromycin (metabolism and renal
lactamase forming strains including Pseudomonas clearance) have half-lives of <5 hours.
(ceftazidime), anaerobes (ceftizoxime) and gonococci Azithromycin accumulates in the tissues and undergoes renal elimination with a
(ceftriaxone, cefixime) half-life of >3days.
Clinical Uses: Gram (+) cocci, Mycoplasma pneumonia, chlamydial species,
4th gen Cefipime
ureaplasma urealyticum, Legionella pneumophilia
*none of the cephalosporins has clinically useful activity in the treatment of
Azithromycin - Haemophilus influenza and Moraxella catarrhalis
infections caused by methicillin-resistant staph, Listeria species, enterococci,
Clarithromycin – H pylori
Mycoplasma pnumoniae, chlamydia
Toxicities: Erythromycin causes GI distress, cholestasis (avoid in pregnancy). Both
eryhthromycin and clarithromycin inhibit Cytochrome P-450 – may enhance
Toxicities carbamazepine, theophylline, warfarin. Azithromycin does not inhibit drug
metabolism and is safe in pregnancy.
Allergic reactions
Clindamycin
 Complete cross allergenicity between different cephalosporins Pharmacokinetics: Effective orally, eliminated by metabolism, biliary and renal
 Partial cross allergenicity with penicillin and cephalosporins clearance.
Clinical Uses: Gram (+) cocci and anaerobes including Bacteroides strains. It is
Other effects – nausea, diarrhea, and opportunistic infections; prophylactic against enterococcal endocarditis in penicillin-allergic patients and is
hypoprothrombinemia (cefotetan) and disulfiram like reactions with ethanol back up drug for Pneumocystis Carnii and Toxoplasma gondii.
Toxicities: Gi distress, skin rash, opportunistic infections including
Carbapenems pseudomembranous colitis.
Tetracyclines
Tetracyclines and doxycycline
Pharmacokinetics: Good oral bioavailability (avoid antacids); eliminated via the
kidney but a large fraction of doxycycline appears in the feces.
Clinical Uses: Vs Mycoplasma pneumonia, chlamydial species, Rickettsia, and
Vibrio.
Tetracyclines – used in H pylori, back up in syphilis, prophylactically in chronic
bronchitis and acne
Doxycycline – DOC in Lyme disease
Toxicities: GI disturbances, tooth enamel dysplasia and bone growth irregularities
in children
Chloramphenicol
Pharmacokinetics: Orally effective, metabolized by glucoronosyltransferase
Clinical Uses: back up drug in bacterial meningitis, typhoid fever, rickettsial
disease and Bacteroides infections.
Toxicities: opportunistic infections, bone marrow suppression, aplastic anemia,
gray baby syndrome – neonates with inadequate glucoronosyltransferase
Inhibitors of Protein synthesis: Aminoglycosides, Streptogramins, Linezolid
Aminoglycosides
MOA: Aminoglycosides – bacterial inhibitors of protein synthesis
Intracellular accumulation is oxygen dependent – anaerobes resistant
Bind to 30s ribosomal subunit and cause misreading of mRNA
Streptogramins are also bactericidal, binding to a site on the 50s subunit extrusion
of nascent polypeptides; also inhibit tRNA synthetase
Linezolid (bacteriostatic) binds to 50s and blocks initiation
MOR: Resistance to aminoglycosides in gram (+) bacteria via formation of
inactivating transferases.
Pharmacokinetics of aminoglycosides
Absorption – not absorbed orally, needs parenteral administration
Elimination – renal clearance is proportional to GFR, half-life 2-3 hours.
*despite short half-life, once daily dosing is effective
*killing is concentration dependent but nephrotoxicity is dependent on both time
and dosage
Gentamicin, tobramycin and amikacin: aminoglycosides are used for gram (-)
bacilli, E coli, Enterobacter, Klebsiella, Proteus, Pseudomonas and Serratia
*synergism with penicillins against enterococci and Pseudomonas strains
Streptomycin and neomycin: Streptomycin is used for tuberculosis, cholera, and
tularemia. Neomycin is only used topically due to toxicity
Toxicities of aminoglycosides
Nephrotoxicity – ATN
Ototoxicity – auditory or vestibular function which may not be fully reversible
Contact dermatitis – frequent with neomycin
Streptogramins and Linezolid
Streptogramin combination of quinupristin and dalfopristin – IV for MRSA,
vancomycin resistant Staph aureus and enterococcus.
Linezolid – similar clinical indication and active against penicillin resistant
pneumococci
Toxicities: Streptgramins – arthralgia and myalgia, inhibitors of CP-450
Inhibitors of Folic Acid synthesis: Sulfonamides and Trimethoprim
MOA
Sulfonamides: inhibit dihydropteroate synthase (1st step in folic acid synthesis)
Trimethoprim: analog of dihydrofolic acid, inhibits the dihydrofolate reductase in
bacteria
Sequential blockade: combo of sulfamethoxazole and trimethoprim cause
sequential blockade of folic acid synthesis
MOR
Sulfonamides: changed sensitivity of dihydropteroate synthase, increased
production of PABA and decreased intracellular accumulation of the drugs.
Trimethoprim: change in sensitivity of DHFR.
Pharmacokinetics
Most sulfonamides are effective orally
 Eliminated via the kidney – may cause crystalluria in acidic urine
 Sulfonamides bind to plasma proteins and can displace other drugs
(phenytoin and warfarin) and bilirubin
Trimethoprim is well absorbed orally and excreted largely unchanged by the
kidney
Clinical use: UTI, ocular chlamydial infections, burn dressings, ulcerative colitis
Trimethoprim-sulfamethoxazole (TMP-SMX), UTI, respiratory, ear, sinus
infections including those due to Haemophilus influenza and Moraxella
catarrhalis. DOC for prevention and tx of Pneumocystis carinii.
Toxicities
Sulfonamides: hypersensitivity reactions, nausea, diarrhea, hemolysis in G6PD
deficiency, phototoxicity, crystalluria and drug interactions.
TMP-SMX: sulfonamides AE along with anemia and granulocytopenia
Inhibitors of Nucleic Acid synthesis: Fluoroquinolones
Norfloxacin and ciprofloxacin are prototypes
MOA
Fluoroquinolones are bactericidal inhibitors of nucleic acid synthesis. Inhibit both
topoisomerase II and IV, preventing separation of the replicated DNA.
MOR
Resistance is increasing in gram (+) cocci.
 Mechanisms include decreased intracellular accumulation of drug
 Changes in sensitivity to inhibition of the topoisomerases
Pharmacokinetics
 Antacids may interfere with oral bioavailability
 Renal clearance
Clinical uses
General: wide spectrum of activity associated with GU, GI and URTI.
Specific: Ciprofloxacin and ofloxacin – gonorrhea; Levofloxacin and sparfloxacin –
Mycoplasma pneumonia, CAP; Moxifloxacin and trovafloxacin - Mycoplasma
pneumonia, anaerobes, Chlamydia
Toxicities
Common to all – GI distress, skin rash, tendinitis, headache, dizziness
*seizures have occurred in high doses
*not for use on pregnancy due to effects on collagen metabolism
Antimycobacterial drugs
HRZES
H and R are used for prophylaxis and latent tuberculosis infection
INH
MOA and resistance: drug is converted to a metabolite that inhibits mycolic acid
synthesis
 High level of resistance – involves deletions in the katG gene that codes
for catalase
 Low-level of resistance – involves deletions in the inhA gene that codes
for the target acyl carrier protein
Pharmacokinetics: INH is metabolized by N-acetyltransferase
Toxicities – neurotoxicity (tx-B6), hepatitis, hemolysis in G6PD deficiency
Rifampicin
MOA and resistance: inhibits DNA-dependent RNA polymerase. Resistance occurs
via changes in polymerase sensitivity to inhibition.
Pharmacokinetics: undergoes hepatic metabolism with red-orange metabolites
Toxicities: GI distress, rash, decreases effect of other drugs including
anticonvulsants and warfarin

Ethambutol and Pyrazinamide
 Ethambutol – inhibits synthesis of arabinogalactan (component of cell
walls); AE – retrobulbar neuritis
 Pyrazinamide – requires bioactivation for activity, target is unknown;
hyperuricemia, phototoxicity, exacerbation of porphyria
Drugs for Mycobacterium avium-intracellulare
Prophylaxis – azithromycin or clarithromycin
Tx – Clarithromycin + ethambutol with or without rifampicin
Drugs for Leprosy
Dapsone – DOC for M leprae and back up for Pneumocystis carinii
Toxicities – Gi irritation, methemoglobinemia and hemolysis in G6PD deficiency
Alternatives – rifampicin, clofazimine
Antibiotics to be avoided in Pregnancy
Aminoglycosides – ototoxicity in developing fetus
Clarithromycin – embryotoxic
Erythromycin estolate – cholestasis in pregnant px
Fluoroquinolones – deleterious effects on collagen metabolism
Tetracyclines – interferes with bone and tooth formation
Sulfonamides – may cause kernicterus when used in 3rd trimester
Metronidazole – mutagenic in Ames test
MISC Antimicrobials
Metronidazole
MOA – forms metabolite that interferes with nucleic acid synthesis
Clinical Use – DOC in amoebiasis, giardiasis, trichomoniasis, Bacteroides fragilis,
Clostridium deficile, Gardnerella vaginalis, H pylori
Toxicity – GI irritation, headache, disulfiram like reactions with ethanol
Fosfomycin
MOA and resistance – inhibits enopyruvate transferase, preventing formation of
N-acetylmuramic acid needed for cell wall synthesis
Urinary antiseptics
Nitrofurantoin – eradication of most urinary pathogens except Proteus and
Pseudomonas; toxicity - Gi irritation, and hemolysis in G6PD deficiency
Nalidixic acid – quinolone with activity similar to nitrofurantoin; toxicity –
glycosuria, skin rash, phototoxicity and ocular dysfunction
Methenamine – urinary acidifier that releases formaldehyde below pH 5.5

RBC's hemoglobin and has grown to occupy most of the cell. It is now called a
schizont. Multiple nuclear divisions have taken place (schizogony or merogony),
INFECTIOUS DISEASES and the RBC then ruptures to release 6–30 daughter merozoites, each potentially
capable of invading a new RBC and repeating the cycle.
1. Malaria
In P. vivax and P. ovale infections, a proportion of the intrahepatic forms do not
Malarial life cycle divide immediately but remain dormant for a period ranging from 3 weeks to a
year or longer before reproduction begins. These dormant forms, or
Human infection begins when a female anopheline mosquito inoculates hypnozoites, are the cause of the relapses that characterize infection with these
plasmodial sporozoites from its salivary gland during a blood meal. These two species.
microscopic motile forms of the malarial parasite are carried rapidly via the
bloodstream to the liver, where they invade hepatic parenchymal cells and begin
a period of asexual reproduction. The swollen infected liver cell eventually bursts,
discharging motile merozoites into the bloodstream. These merozoites then
invade the red blood cells (RBCs) and multiply six- to twentyfold every 48–72 h.
When the parasites reach densities of 100 million parasites in the blood, the
symptomatic stage of the infection begins. After entry into the bloodstream,
merozoites rapidly invade erythrocytes and become trophozoites. Attachment
is mediated via a specific erythrocyte surface receptor. In the case of P. vivax, this
receptor is related to the Duffy blood-group antigen Fya or Fyb. By the end of the
48-h intraerythrocytic life cycle (24 h for P. knowlesi, 72 h for P. malariae), the
parasite has consumed two-thirds of the
 BIOETHICS PRINCIPLES

1. Respect for autonomy

Respect for the autonomy of the patient would, in common parlance,
imply that the patient has the capacity to act intentionally, with
understanding, and without controlling influences that would mitigate
against a free and voluntary act. This principle is the basis for the
practice of "informed consent" in the physician/patient transaction
regarding health care.

2. Nonmaleficence
Nonmaleficence requires of us that we not intentionally create a harm
or injury to the patient, either through acts of commission or omission.
In common language, we consider it negligent if one imposes a
careless or unreasonable risk of harm upon another. Providing a
proper standard of care that avoids or minimizes the risk of harm is
supported not only by our commonly held moral convictions, but by
the laws of society as well.

3. Beneficence
Health care providers have a duty to be of a benefit to the patient, as
well as to take positive steps to prevent and to remove harm from the
patient. This principle is at the very heart of health care implying that
a suffering supplicant (the patient) can enter into a relationship with
one whom society has licensed as competent to provide medical care,
trusting that the physician’s chief objective is to help.

4. Justice
A form of fairness or as Aristotle once said, "giving to each that which
is his due." This implies the fair distribution of goods in society and
requires that we look at the role of entitlement.