NBME#2 block 1 Q1-----------Q50 - maryam2009

[ArchivalUser]

Q20.C
Natural killer activity enhanced by IL2,INF beta,INF alpha

Q21.D

The most common sources of embolism are proximal leg deep venous thrombosis (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs. The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).

The development of thrombosis is classically due to a group of causes named Virchow's triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

Alterations in blood flow: immobilization (after surgery, injury or long-distance air travel), pregnancy (also procoagulant), obesity (also procoagulant), cancer (also procoagulant)
Factors in the vessel wall: of limited direct relevance in VTE
Factors affecting the properties of the blood (procoagulant state):
Estrogen-containing hormonal contraception
Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders)
Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)
Cancer (due to secretion of pro-coagulants)

The main indication for thrombolysis is in submassive PE where right ventricular dysfunction can be demonstrated on echocardiography, and the presence of visible thrombus in the atrium.

[ArchivalUser]

Q22. A
ACE inhibitors- side effects/toxicity- cough, angioedema, hyperkalemia, protenuria, rash, increased renin

[ArchivalUser]

22.A

The adverse effect of using ACEI...captopril,Enalopril,fosinopril vauses is cough due to the prevention of Bradykinin degradation .
these agents also can cause electrolyte imbalances...hyperkalemia,mild hyponatriemia.
angioedema,taste changes,
contraindication: the pregnant women......fetal renal damage

clinical use
ACE inhibitors are used primarily in the treatment of hypertension, though they are also sometimes used in patients with cardiac failure, renal disease or systemic sclerosis. ACEIs can also be used to treat diabetic nephropathy and left ventricular hypertrophy.

EffectsACE inhibitors block the conversion of angiotensin I to angiotensin II.[2] They, therefore, lower arteriolar resistance and increase venous capacity; increase cardiac output, cardiac index, stroke work, and volume; lower renovascular resistance; and lead to increased natriuresis (excretion of sodium in the urine). Renin will increase in concentration in the blood due to negative feedback of conversion of AI to AII. Angiotensin I will increase for the same reason. AII will decrease. Aldosterone will decrease. Bradykinin will increase due to less inactivation that is done by ACE enzyme.

Under normal conditions, angiotensin II will have the following effects:

vasoconstriction (narrowing of blood vessels), which may lead to increased blood pressure and hypertension
– constriction of the efferent arterioles of the kidney, leading to increased perfusion pressure in the glomeruli.
Contribute to ventricular remodeling and ventricular hypertrophy of the heart.
stimulation of the adrenal cortex to release aldosterone, a hormone that acts on kidney tubules to retain sodium and chloride ions and excrete potassium. Sodium is a "water-holding" molecule, so water is also retained, which leads to increased blood volume, hence an increase in blood pressure.
stimulation of the posterior pituitary to release vasopressin (also known as anti-diuretic hormone (ADH)), which also acts on the kidneys to increase water retention.
decrease renal protein kinase C.
With ACE inhibitor use, the effects of angiotensin II are prevented, leading to decreased blood pressure.

Epidemiological and clinical studies have shown that ACE inhibitors reduce the progress of diabetic nephropathy independently from their blood pressure-lowering effect. This action of ACE inhibitors is utilised in the prevention of diabetic renal failure.

Wikipedia

[ArchivalUser]

23= AA==
clostridium perfringes -gram positive ;spore forming rods ;nonmotile
Anaerobic
double zone beta hemolysis
pathgnesis by Alpha toxin aka phospholipase which is a lecithinas which disrupts membranes of RBcs ;platelest neutrophills ;wbcs and endothelial cells producing massive necrosis and hamorrhage
Detected by naeglers reaction -egg yolk agar plate
Other toxin is enterotoxin --producesd in intestine in food poisoning ;disrupts ion transport leading to watery diarrhea and cramp

[ArchivalUser]

24-bb calcium salts
80% stones are ca oxalate stones
Risk factors
Hypercalciuria in the absence of hypercalcemia
Most common metabolic abnormality
Due to increased gastrointestinal reabsorption of calcium
Decreased urine volume concentrates the urine
Reduced urine citrate---Citrate normally chelates calcium
Primary hyperparathyroidism
Diets high in dairy products (contain phosphate) or oxalates

Clinical and laboratory findings
Ipsilateral colicky pain in the flank with radiation to the groin
Gross and microscopic hematuria
Majority of stones contain calcium (∼80% of cases).
Often visualized on a routine radiograph
Renal ultrasound and IVP detect stones that do not visualize

** other types of stones

2=Magnesium ammonium phosphate
"Staghorn calculus" or struvite stone
Associated with urease producers (e.g., Proteus)
Urine is alkaline and smells like ammonia.
3=Uric acid, cystine

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25 Aa aortic dissection
clues- HTN ;TEARING chest pain radiating to shoulder or back ;widening of mediastenum

http://en.wikipedia.org/wiki/File:AoDiss_ChestXRay.jpg

http://en.wikipedia.org/wiki/File:DissectionCT.png

[ArchivalUser]

25. A.

Aortic dissection:
pts with aortic dissection have chest pain which may look like MI (radiating to the left shoulder).
increased BP and heart rate don't really help us differentiate the 2 conditions.

but, distant heart sound and pulsus paradoxus along with low voltage on EKG make the difference.

X-ray: widening the mediastinum also helps.

..................

please note: pulsus paradoxus is also seen with severe COPD/Asthma, tension pneumothorax, etc

distant heart sound is also seen with severe LV dysfunction.

decreased EKG voltage could be seen with LV dysfunction.

Mediastinum widening is also seen with mediastinitis (esophageal rupture), bacillus anthracis infection .. etc.

[ArchivalUser]

sorry drona99 for repeating the Q.

[ArchivalUser]

26- biotin=
carboxylase reaction needs ABC
A-ATP
B-BIOTIN
C-CO2
not sure abt diagnosis here if anyone has idea?

[ArchivalUser]

hey fcbarcelone ur welcome ..thanks for adding so impo points