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Internal medecin

Pulmonology
A patient with low grade fever and weight loss has poor excursion on the right
side of the chet with decresed fremitus ,flatness to percussion and decreses
breath sounds all on the right . the trachea is deviated to the left .which is mostly
likely diagnosis ?

Pulmonary TB:
Signs:
On PE, the patient appears chronically ill and malnourished

On chest examination, there are no physical findings specific

for tuberculosis infection

The examination may be normal or may reveal classic findings

such as post-tussive apical rales

Fibrotic changes will give rise to deviation of trachea,

dullness on percussion, reduced breath sounds and moist rales.

Tuberculosis pleural effusion will show physical findings like

dullness to percussion, decreased breath sounds etc.

Lab findings show anemia and leucocytosis.

 Diagnosis: Sputum culture ESR, CRP, Hemoglobin, TLC with
differential Tuberculin skin test CXR

Treatment: The goals of therapy are to eliminate all tubercle

bacilli from an infected individual while avoiding the emergence
of clinically significant drug resistance.

Drugs: Isoniazid, Rifampicin, Pyrazinamide, Ethambutol,

Streptomycin.

Multidrug-resistant tuberculosis (MDRTB) : are resistant to at

least Isoniazid and Rifampin and require a minimum of three
drugs to which the organism is susceptible.

1) COPD :
Case study
70 year old female ,Difficulty with breathing for
the past six months ,Wheezing
,Coughing ,Smokes one pack of cigarettes
for forty five years. No other medical
problems, No problems with her heart
,Does not drink alcohol or use drugs ,Her
husband smoked as well
1)Whats the Risk Factors for
COPD
1) Host Factors :
Genes (e.g. alpha1-antitrypsin deficiency)
Hyperresponsiveness
lung growth
2)Exposure
Tobacco smoke
Occupational dusts and chemicals
Infections
Socioeconomic status

Whats Key Indicators for COPD

Diagnosis:?

1) sign and symptom

Chronic cough : Present intermittently or every day often present throughout

the day; seldom only nocturnal

Chronic sputum production: Present for many years, worst in winters.

Initially mucoid becomes purulent with exacerbation.

Dyspnoea that is: Progressive (worsens over time),Persistent (present

every day),Worse on exercise, Worse during respiratory infections
Acute bronchitis: Repeated episodes.

History of exposure to risk factors: Tobacco smoke (including beedi)

occupational dusts and chemical smoke from home cooking and
heating fuel

2)Physical signs:
Inspection: check for barrel chest deformity, pursed-lips
breathing, chest/abdominal wall paradoxical movements and
use of accessory respiratory muscles

Percussion: check for decreased motion of the diaphragm and

tympanic sounds due to hyperinflation or bullae; in addition the
liver becomes easily palpable

Auscultation: adventitious rhonchi and wheezing

Auscultation of the heart: may show signs of cor pulmonale

3) lab tests:
1)Spirometry : pulmonary funtion test(pft)
irreversible obstructive pattern low FEV1
2) x-ray : hyperinflated lung ,flattened
3)ECG: Right-sided strain : often multiple
atrial tachycardia .
4)CT: shows loss of alveolar walls in
emphysema
 How Manage Stable COPD ?
Health education, exercise training
programs , pharmacotherapy.

*pharmacotherapy:
Bronchodilator medications (beta2-agonists,
anticholinergics, theophylline, and a combination
of these drugs
Glucocorticosteroids :
Mucolytics :
Oxygen therapy :

Flu shot ,Pneumovaxm ;Vaccinations help prevent

exacerbations!
 4)Differential Diagnosis: COPD
and Asthma.
COPD
Onset in mid-life
Symptoms slowly progressive
Long smoking history
Dyspnea during exercise
Largely irreversible airflow
Limitation

Asthma
Onset early in life (often childhood)
Symptoms vary from day to day
Symptoms at night/early morning
Allergy, rhinitis, and/or eczema also present
Family history of asthma
Largely reversible airflow limitation

Differential Diagnosis:
1) Asthma 2) Congestive heart failure 3)
Bronchiectasis 4) Tuberculosis
Others:
 Alpha1-Antitrypsin Deficiency
Bronchitis
Emphysema
Nicotine Addiction
Pulmonary Embolism

2) Asthma
Case study
This was one of very many emergency room visits for this
11-year-old boy for the past 6 years. The patient is a non-
smoker. He has frequent asthma attacks requiring care in
the emergency room. His asthma symptoms include chest
tightness, cough and wheezing. They are triggered by
upper respiratory infections, exposure to cigarette smoke
and perfume and exercise. His asthma symptoms have
been well-controlled on inhaled fluticasone at a dose of 44
mcg/puff taken 2 puffs twice a day through a spacer
device. Inhaled albuterol via a metered dose inhaler is
given as rescue medication for acute symptoms. The
patient sometimes misses his morning dose of inhaled
fluticasone One week ago, he developed a cough and
runny nose with a low-grade temperature. About 4 days
ago, he noted chest tightness and wheezing. He was
unable to run on the playground at school without
becoming short of breath. The night prior to presentation,
he required nebulized albuterol every 2 hours for relief of
his symptoms. His parents brought him to the emergency
room for further care Prior Significant or Chronic Medical
Illness: He has had eczema for the past 8 years

1)Risk Factors that Lead to Asthma Development

Predisposing Factors
Atopy

Causal Factors
Indoor Allergens ,Domestic mites ,Animal Allergens ,Cockroach
Allergens

Fungi ,Outdoor Allergens ,Pollens ,Fungi ,Occupational

Sensitizers

Contributing Factors
Respiratory infections ,Small size at birth ,Diet ,Air pollution

Outdoor pollutants ,Indoor pollutants ,Smoking ,Passive Smoking

Active Smoking

2)DIAGNOSIS OF ASTHMA
History and patterns of symptoms
Physical examination : Wheeze -Usually heard without a
stethoscope ,Dyspnea ,Rhonchi heard with a
stethoscope, Use of accessory muscles
Measurements of lung function : 1. Blood Finding (Blood
eosinophilia, elevated serum level of sIgE ), 2.
Radiographic finding (hyperinflation) 3.ECG 4. Peak
Flow Meter

Differential diagnosis
Chronic bronchitis
Heart failure (cardiac asthma)
Hypersensitivity pneumonia
Lung cancer

Treatment
Relievers : 1.Bronchodilator (beta2 agonist) Salbutamol

2.Anti-cholinergics: Ipratropium bromide

3.Xanthines :Theophylline
4.Adrenaline injections
 Preventers : 1. Corticosteroids: Prednisolone 2. Anti-
leukotrienes: Montelukast 3. Xanthines 4. Long acting 2
agonists : Bambuterol, Salmeterol 5. Mast cell stabilisers :
Sodium cromoglycate

Peak flow meter

Patient education

Treatment steps for achieving control

step1 As-needed rapid-acting 2-agonist

Step2 Low-dose inhaled ICS or leukotriene modifier

Step3 Low-dose inhaled ICS +long-acting 2-

agonist, medium-or-high-dose ICS, low-dose inhaled
ICS +leukotriene modifier, low-dose inhaled ICS
+sustained release theophylline

Step4 Medium-or-high-dose ICS plus (1)long-acting

2-agonist, (2) leukotriene modifier, (3) sustained
release theophylline

Step5 Oral glucocorticosteroid or anti-IgE treatment

Cardiology
Male patient 55 y old ,with history of hypertension
an DM, for 2 years ,the Bp of patient is normal
unders control of anti-hypertensive ,blood suger
can not be controled very well, patient after
activity feel chest pain ,which can be released
within 5 min by taking nitroglycerin .Recently the
patient complains chest pain happened more
frequncy .the symptoms as sim iler as previous
.this morning the chest pain with sweat ,nousesa
and vomiting .pain cant go by nitroglycerin ,EKG
show st segment elevation in leads 11 ,111,aVF.
Your diagnosis?

CORONARY HEART DISEASE

The term covers a group of clinical syndromes that
includes
1)Angina pectoris
2)Myocardial infarction
3)Sudden death
atherosclerosis
What Causes Coronary Artery Disease?
of the
Lifestyle riskcoronary
factors
arteries
that contribute to
heart disease artery
coronary
include
spasm

lack of exercise
embolis

high-fat stenosis
aortic diet
Whats the Risk factors ? emotional stress
hypertrophic
obstructive
having a "type
cardiomyopath
A" personality
 impatient,
normal
competitive)
coronary
arteries,
termed
syndrome X

A myocardial infarction is a serious condition where there

is complete blockage of blood supply to the heart. In
contrast, stable angina is chest pain or discomfort that
usually occurs with activity or stress resulting from poor blood
flow through the blood vessels in the heart.

Myocardial Stable Angina

Infarction

Causes Complete blockage of Decrease in blood supply to

blood supply to heart heart muscle --> myocardial
muscle. Secondary to ischemia
sudden and extended
obstruction of the
myocardial blood supply

Occurrence of pain Happen at anytime Occurs when doing physical

activity or due to emotional
 Myocardial Stable Angina
Infarction

stress

Symptoms Chest pain with damage to Chest pain with no damage to

the heart. Pain is sudden the heart. Pain is described as a
substernal chest pain tightness or pressure in the
radiates to left neck and chest, and may radiate to the
usually described as severe, neck, lower jaw, left arm, and
steady, and crushing. left shoulder.
Hypotension, weak rapid
pulse, and low grade fever

Outcome May be fatal Usually not fatal

Severity Serious condition. May Usually no permanent damage

cause permanent damage. to heart muscle. If blood flow is
If blood supply can be restored, no permanent
restored in the first 20 min damage.
irreversible damage may
be prevented.
Symptoms relieved by rest or
nitro within 10-15 minutes.
Symptoms persists after 15 Lack of relief indicates an
Relieving Factors minutes and not relieved by individual may be developing
 Myocardial Stable Angina
Infarction

rest or nitro. infarction.

Usually chest pain for less than

Duration Chest pain usually lasts for 15 minutes. Discomfort is
more than 15 minutes usually transient, lasting 3-5
min.

Not present

Serum cardiac Present

marker

INVESTIGATIONS
1)Biochemical Tests
hypercholesterolemia and other dyslipidemias

insulin resistance

C-reactive protein, lipoprotein Lp(a), and homocysteine

2)Physical Examination.
 It is often helpful to examine the heart during an episode of pain

a third heart sound and pulmonary rales ---- transient LV

dysfunction

transiently paradoxical splitting of the second heart sound

Transient apical systolic murmurs

3)Resting Electrocardiogram

4Exercise Electrocardiography
5) Nuclear Cardiology Techniques
6 Coronary Angiography
 Treatment
1)Increase the perfusion of coronary artery

2)Reduce the oxygen demand

3)Treatment of Risk Factors

Medical Therapy
General Measures : Bed rest, oxygen and EKG
monitoring ,Pain relief ,diamorphine 2.5-5mgIV
Anti-ischemic treatment : nitrates (should first be given
sublingually) beta blockers (Esmolol ) calcium channel
blockers ( verapamil or diltiazem)

Antithrombotic treatment : Anti-platelet therapy (aspirin,

clopidogrel) Anti-coagulant therapy (heparins ,GP IIb/IIIa
inhibitors )

Coronary revascularization : PCI ,coronary artery

bypass grafting

Others : ACE , Cholesterol-Lowering Medication

Hypertension
when systolic pressure is consistently greater
than 140 mm Hg or when diastolic pressure is
consistently 90 mm Hg or more
A 68-year-old woman is hospitalized with palpitations and
shortness of breath. She has a history of hypertension and
chronic atrial fibrillation, and her medications include
furosemide, candesartan, and warfarin. On physical
examination, the heart rate is 120 bpm with an irregularly
irregular rhythm, and blood pressure is 130/80 mm Hg; she has
an elevated jugular venous pulse, crackles in both lungs, and
marked lower extremity edema. Echocardiography shows left
ventricular hypertrophy,an ejection fraction of 70%, and no
significant valvular disease. She is treated with intravenous
diuretics, with improvement in her symptoms and resolution of
peripheral edema and of crackles on lung examination. Her heart
rate is now 99 bpm and her blood pressure is120/75 mm Hg.
Which of the following would be the most appropriate
medication to add?

A. Lisinopril

B. Spironolactone

C. Amlodipine

D. Metoprolol

E. Hydrochlorothiazide

2)40 years old male has recurrently suffered from

headache ,palpitation,.and not been treated his musered
 blood presure 3 times different time and his Bp are 220/126
mmhg ,180/120mmhg ,140/95mmhg.
Whats your diagnosis and treatment ?

Primary hypertension about 95%

Secondary Hypertension about 1- 5%

Secondary Hypertension

Coarctation of aorta

The Cushing syndrome

Primary aldosteronism

Pheochromocytoma

Renal vascular disease

Renal parenchymal disease

Parathyroid disorders

Thyroid disease
 \v Clinical Evaluation of hypertension
Other cardiovascular risk factors
and other clinical condition to
effect on prognosis
Evaluation of target
organ damage
Exclusion secondary
hypertension

Evaluation of
BP level
The diagnostic procedures comprise

1) repeated blood pressure measurements

2) medical history: family history ,past history ,medication
3) physical examination: (Funduscopy)
1) Secondary hypertension
2) organ damage
3) Visceral obesity
4) laboratory and instrumental investigations
 1) Routine tests

Fasting plasma glucose

Serum potassium

Serum total cholesterol, Serum LDL-cholesterol, Serum HDL-

cholesterol

Fasting serum triglycerides

Serum uric acid ,Serum creatinine, Estimated creatinine

clearance (Cockroft-Gault formula) or glomerular filtration rate
(MDRD formula)

Urinalysis (complemented by microalbuminuria via dipstick

test and microscopic examination)

Haemoglobin and haematocrit

Electrocardiogram

Management
Lifestyle changes

Durgs choices
Diuretics blocker

Other Durgs Calcium channel blocker

ACE inhibitor Angiotensin II receptor blocker

& Diuretics
Classification

Thiazide diuretics: Hydrochlorothiazide

Chlorothalidone
-blockers

Classification

Atenolol Metoprolol Propranolol Nebivolol Carvedilol

& Calcium channel blockerCCB)

Classification
1)Dihydropyridines: Nifedipine, Amlodipine
2)Non-dihydropiridine :Diltiazem , Verapamil
ACE inhibitor
Classification

Enalapril Fosinopri Lisinopril

Perindopril Quinapril Ramipril

& Angiotensin-receptor blocker (ARB)

Classification

Losartan Candesartan Irbesartan

gastrointestinal
& Upper gastrointestinal hemorrhage
(UGH)

WhereED/GI department

Whenmoring, march, 2012

Who:male,35y

Why: dizzy, melena,

PE: tenderness in upper abdomen, no regitity or rebound tenderness

History: long term, intermittent, recurrent epigastric pain

Question

What is most possible diagnosis

& Upper gastrointestinal hemorrhage (UGH)

GI bleeding is defined as blood loss from GI tract

Upper GI bleeding is caused by upper GI tract (esophagus,

stomach, duodenum, liver, bile duct, pancreas).

Not including blood from nose, oral cavity(), laryngeal

pharynx(), respiratory diseases (hemoptysis,)and false
occult blood test

Diagnosis
With or without

Ruled out:

Respiratory bleeding

Mouth, nose, throat bleeding

Food or drugs

Next gastrointestinal or UGH: Small intestine and colon

examination
Manifestation

Endoscopy

X ray

CTMRI

Selective arteriography
 Radionuclide-imaging

Treatment
Emergency: in bed, take oxygen, HR, BP, R, T, Urine should be
monitored

Infusion of fluids and blood

Medicine: vasopressin, somatostatin, H2 receptor antagonist,

omprazole(Losec)

Endoscopic treatment

Surgical treatment or Interventional therapy

Acute Pancreatitis
Causes :Gallstone, Alcohol, Hypertipidermia

Who :: male, 45y

Why: "complained of abdominal pain 4 hours after drinking and eating

high-fat high-protein foods abdominal pain appears as a knife-like
pain radiating to the left flank back, vomiting 1, for the examination of
stomach contents found in the abdomen. soft, epigastric tenderness,
no rebound tenderness. previous history of hyperlipidemia. "

Question:

What isAbdominal guarding

most possible diagnosis?

Abdominal Clinicaldistention
Manifestation
Abdominal
Abdominal
Pain : Uppertympany
abdominal pain rapidly increasing in
severity,
Decrease/absent
often within 60 minutes. The pain is Epigastric pain
and the patient has Diffuse abdominal pain with radiation to
bowel
back. The painsounds
is Restless and the patient Prefer to sit and

Severe AP:
peritoneal signs,
 ascites, jaundice,
palpable abdominal mass,
Grey Turners sign,
lean . Nausea Vomiting abdominal distention,
Cullens
Disturbance sign,
Water-Electrolyte acid-base balance,

signs of hypovolemic shock

A laboratory examination
pancreatic amylase: blood amylase> 500U/dL; urine amylase serum
lipase

Other: WBC, BG, blood Ca + +,

Abnormal liver function, blood gas analysis, DIC,

2 Imaging:. X-ray B ultrasound abdominal CT MRIMRCP

ERCP

Management
Fluid Management

Nutritional support

Rest gut

TPN
 Pain management

Supporting other organ systems

Treatment
IV replacement of fluids, proteins, and electrolytes
Fluid volume replacement and blood transfusions
Withholding food and fluids to rest the pancreas
NG tube suctioning
Drugs
Peritoneal lavage
Surgical drainage
Laparotomy to remove obstruction

Peptic ulcer
A major causative factor (60% of gastric and up to 90% of duodenal ulcers)
is chronic inflammation due to Helicobacter
pylori that colonizes the antralmucosa

Classification
Duodenum (called duodenal ulcer)
 Esophagus (called esophageal ulcer)

Stomach (called gastric ulcer)

Meckel's diverticulum (called Meckel's diverticulum ulcer; is very

tender with palpation)

Sign and symptoms

abdominal pain, classically epigastric strongly correlated to

mealtimes. In case of duodenal ulcers the pain appears about three
hours after taking a meal;

bloating and abdominal fullness;

waterbrash (rush of saliva after an episode of regurgitation to dilute

the acid in esophagus - although this is more associated
with gastroesophageal reflux disease);

nausea, and copious vomiting;

loss of appetite and weight loss;

hematemesis (vomiting of blood); this can occur due to bleeding

directly from a gastric ulcer, or from damage to the esophagus from
severe/continuing vomiting.

melena (tarry, foul-smelling feces due to presence of oxidized iron

from hemoglobin);

rarely, an ulcer can lead to a gastric or duodenal perforation, which

leads to acute peritonitis, extreme, stabbing pain,[4] and requires
immediate surgery.
A history of heartburn, gastroesophageal reflux disease (GERD) and use of
certain forms of medication can raise the suspicion for peptic ulcer.
Medicines associated with peptic ulcer include NSAIDs (non-steroid anti-
inflammatory drugs) that inhibit cyclooxygenase, and
most glucocorticoids (e.g. dexamethasoneand prednisolone).

Differential diagnosis
Gastritis

Stomach cancer

Gastroesophageal reflux disease

Pancreatitis

Hepatic congestion

Cholecystitis

Biliary colic

Inferior myocardial infarction

Referred pain (pleurisy, pericarditis)

Superior mesenteric artery syndrome

Diagnosis

1)esophagogastroduodenoscopy (EGD), a form of endoscopy, also

known as a gastroscopy. also endoscopy biopsy

2) blood test
3) barium x-ray

4) diagnosis of Helicobacter pylori can be made by: Urea breath test ,

Stool antigen test

Treatment

1) antacids or H2 antagonists
2) antibiotics
(e.g. Clarithromycin, Amoxicillin, Tetracycline,Metronidazole)
and 1 proton pump inhibitor (PPI)

3) surgical emergency: bleeding ulcers require endoscopy

urgently to stop bleeding with cautery, injection, or clipping.

Corhns disease and Ulcerative Colitis

Factor Crohns Disease Ulcerative Colitis

Distributio Affects small bowel and large Affects large bowel o

n bowel
Endoscopy Rectum frequently spared Rectum always aff ec
findings Inflammation not continuous Inflammation is unifo
(presence
of skip lesions) Bowel wall is thin with
Bowel wall is thickened and has a vascular pattern
cobblestoned appearance due to
deep ulcers and swelling of the
tissue

Radiology Strictures are common Strictures and fissure

Deep fissures and fistulae are much less common in
common Symmetrical inflamm
Asymmetrical inflammation

Histology Presence of granulomas are almost Granulomata absent

diagnostic Inflammation usually
Inflammation extends through the to mucosa
mucosa and muscle of the bowel
The increase in white cells tend to The increase in white
be lymphocytes to be polymorphs

Clinical Patients often thin and may be Weight loss usually re

appearance malnourished due to intestinal the severity of active
malabsorption of nutrients Bloody diarrhoea
Diarrhoea - only sometimes with Abdominal mass unc
blood
Abdominal mass common
 Endocrinology
Diabetes mellitus

the classic symptoms of untreated diabetes are weight

loss, polyuria (frequent urination), polydipsia(increased thirst),
and polyphagia (increased hunger)
 Comparison of type 1 and 2 diabetes[5]

Feature Type 1 diabetes Type 2 diabetes

Onset Sudden Gradual

Age at onset Mostly in children Mostly in adults

Body size Thin or normal[13] Often obese

Ketoacidosis Common Rare

Autoantibodies Usually present Absent

Normal, decreased
Endogenous insulin Low or absent
or increased

Concordance
50% 90%
in identical twins

Prevalence ~10% ~90%

 Diagnosis
Fasting plasma glucose level 7.0 mmol/l (126 mg/dl)
 Plasma glucose 11.1 mmol/l (200 mg/dL) two hours
after a 75 g oral glucose load as in a glucose tolerance test

Symptoms of hyperglycemia and casual plasma glucose

11.1 mmol/l (200 mg/dl)

Glycated hemoglobin (Hb A1C) 6.5%.

Management
1) Lifestyle change : good nutrition to achieve a normal body
weight, and sensible exercise,stop smoking ,control high
blood pressure,

2) Medications : Metformin (insulin)

3) Pancreatic transplantation
 Hyperthyroidism
Graves Disease (hyperthyroid) Case Stud Adam, age 27, is a
contractor and business owner who was diagnosed with graves
disease (hyperthyroidism). He had benign tumors in his breast
aglands. He could not work a full day because he was weak and
exhausted. Other symptoms were acne, constipation, blurred vision,
hot flashes, joint pain, weight loss, learning disabilities and back
problems. Psychological symptoms were mind racing, worrying,
irritable, mood swings, and obsessive compulsive. He was told by his
doctor that he had to have his thyroid removed and to take a
prescription drug the rest of his life. Adams first hair test revealed an
extremely slow oxidation rate which indicates weak cellular thyroid
effect in the body. He had a low Na/K ratio which indicates low vitality.
He was also showing very high levels of three amigos (iron,
manganese and aluminum). The amigos can irritate the tissues. His
zinc was elevated at 30mg% (15-16mg% is ideal) which indicates
hidden copper toxicity. Also he had high levels of lead, cadmium and
arsenic. He followed the slow oxidation plan, increased his distilled
water intake and took specific nutritional supplements 3 times a day.
His energy improved within a few weeks on the program. He did have
a few healing reactions of feeling hot for a couple of months and a
feeling of depression for a few days and then it pasted. Also had a few
cold sore flare ups and acne flared up for a few weeks. He stated that
he felt energetically and emotionally stronger. His second hair
analysis revealed a drop in the sodium and potassium levels. He was
now showing sympathetic dominance, a tendency to push himself.
The irritants (amigos) all came down within normal range which is
probably the reason why the sodium level came down. Lead,
cadmium and rsenic all came down . He was actively eliminating
selenium and mercury. At this time his tumors disappeared. He
indicated that he had not had this much energy in years. He even
decided to change careers and go into law enforcement. Hot flashes,
blurred vision, constipation and joint pain had also disappeared.
 What is hyperthyroidism?

Hyperthyroidism is a condition where the thyroid produces more

thyroxine than is needed by the body. It is also referred to as
thyrotoxicosis, or an over-active thyroid. It can occur if you have:

Graves disease - the most common cause

a toxic multinodular goitre (a goitre is an enlarged thyroid gland)

a solitary toxic thyroid adenoma (an adenoma is a clump of

cells)

thyroiditis (inflammation of the thyroid gland)

It can also occur when too much replacement thyroxine

(levothyroxine) is taken as a treatment for an under-active thyroid
(hypothyroidism).

What are the symptoms of hyperthyroidism?

Hyperthyroidism leads to an increase in the bodys metabolism
(energy production), often causing:

weight loss, despite an increased appetite

palpitations

sweating and heat intolerance

tiredness

nervousness and irritability

 shakiness

a rapid pulse

mood swings or aggressive behaviour

looseness of the bowels

weak muscles

warm, moist hands

thirst

passing larger than usual amounts of urine

itchiness

enlarged thyroid gland

Diagnosis
Hyperthyroidism is diagnosed using:

Medical history and physical exam. During the exam your

doctor may try to detect a slight tremor in your fingers when
they're extended, overactive reflexes, eye changes and warm,
moist skin

Blood tests. A diagnosis can be confirmed with blood tests

that measure the levels of thyroxine and TSH in your blood.
High levels of thyroxine and low or nonexistent amounts of
TSH indicate an overactive thyroid.

Radioactive iodine uptake test. For this test, you take a

small, oral dose of radioactive iodine (radioiodine). Over time,
 the iodine collects in your thyroid gland because your thyroid
uses iodine to manufacture hormones. after two, six or 24
hours and sometimes after all three time periods to
determine how much iodine your thyroid gland has absorbed.

A high uptake of radioiodine indicates your thyroid gland is

producing too much thyroxine. The most likely cause is either
Graves' disease or hyperfunctioning nodules. If you have
hyperthyroidism and your radioiodine uptake is low, you may
have thyroiditis.

Thyroid scan. During this test, you'll have a radioactive

isotope injected into the vein on the inside of your elbow or
sometimes into a vein in your hand. You then lie on a table
with your head stretched backward while a special camera
produces an image of your thyroid on a computer screen.

-Whsats the treatment and prevention ?

What treatment you need depends on your age,sex ,
history .etc.....

Radioactive iodine. Taken by mouth, radioactive iodine is

absorbed by your thyroid gland, where it causes the gland to
shrink and symptoms to subside, usually within three to six
months.

Anti-thyroid medications. (Tapazole).

Beta blockers.

Surgery (thyroidectomy).
 Differential Diagnoses
Euthyroid Hyperthyroxinemia
Goiter
Goiter, Diffuse Toxic
Graves Disease
Plummer-Vinson Syndrome
Struma Ovarii
Thyrotoxicosis

Nephrology
Urinary tract Infection

Urinary tract Infection (UTI) is an infection in any part of the urinary

system kidneys, ureters, bladder and urethra. Most infections
involve the lower urinary tract the bladder and the urethra.

Signs and symptoms

A) Kidneys (acute pyelonephritis): -Upper back and side (flank) pain

-High fever -Shaking and chills Nausea -Vomiting
B) Bladder (cystitis): -Pelvic pressure -Lower abdomen discomfort
-Frequent, painful urination -Blood in urine

C) Urethra (urethritis): -Burning with urination

Causes

The bacterial strains that cause UTIs include:

-Escherichia (E.) coli

-Staphylococcus saprophyticus

-Klebsiella, Enterococci , and Proteus mirabilis account for most of

remaining bacterial organisms that cause UTIs. They are generally
found in UTIs in older women.

-Rare bacterial causes of UTIs include Ureaplasma urealyticum and

Mycoplasma hominis

Treatment:

Antibiotics Sulfamethoxazole - trimethoprim

Amoxicillin

Nitrofurantoin

Ampicillin

Ciprofloxacin (Cipro)

Levofloxacin (Levaquin)