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USMLE Preparation > USMLE-Rx Review > Flashcards

USMLE-Rx Review Flashcards

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USMLE® Step 1 flashcards
1
Q

What side-effects are associated with Digoxin?

What is its MOA?

What is the biggest concern when this drug becomes toxic?

A

Nausea, dizziness and blurry vision with a yellowish hue. There is a very narrow therapeutic index.

Inhibition of the Na+/K+ pump, which leads to increased intracellular [Na+] and increased extracellular [K+]. The increased [Na+] inhibits the Na+/Ca++ pump, which increases intracellular [Ca++]. This increases contractility.

The induced hyperkalemia can cause fatal arrhythmias.

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2
Q

What is Phenoxybenzamine used for?

What is its MOA?

A

First-line therapy of in a patient with a Pheochromocytoma. Without adequate alpha-receptor blockade, patients are at a risk for intraoperative hypertensive crisis.

Irreversible antagonism of a-1 and a-2 receptors.

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3
Q

In terms of treating a Pheochromocytoma, when should Propanolol be given? Why?

What is its MOA?

A

It should be given after administration of an alpha-receptor antagonist. This must be done secondly, because if it is done first, it can result in a further spike in BP due to blockade of the beta2-receptor-mediated vasodilation.

Non-selectively blocks beta-receptors.

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4
Q

What is the MOA of Labetalol?

A

It blocks both alpha and beta receptors.

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5
Q

What is the MOA of Octreotide?

What is its indication?

A

It is a synthetic analog of somatostatin.

Used to manage symptoms of carcinoid tumors.

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6
Q

What is the confidence interval?

What is the variance?

What is the standard deviation?

A

Confidence interval: a range of values where the mean is expected to fall.

Variance: helps describe the variability within a population, but does not draw any conclusions regarding the range within the mean can be found.

Standard deviation: shows the variability existing among a range values typically centered around the mean.

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7
Q

What is the MOA of Lidocaine?

When should it be given?

A

It is a class-1B anti-arrhythmic and blocks inactivated Na+ channels.

It is used to treat ventricular arrhythmias after an MI.

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8
Q

What causes an SVT?

What are the 2 general mechanisms by which they arise?

A

Either the atria or AV node causes an abnormally fast HR.

Increased automaticity - AV node re-entry tachycardia (AVNRT).
Re-entry - AV re-entry tachycardia (AVRT).

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9
Q

In addition to conservative measures (carotid massage, etc.), what is the first-line pharmacological therapy used to treat SVTs?

How does it cause effects?

What are side-effects?

A

IV adenosine.

It has a short half-life and acts by slowing the conduction velocity and increasing the refractory period at the AV node.

Flushing, hypotension and chest pain.

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10
Q

What are the indications for the following:

Amiodarone
Amlodipine
Procainamide

A

Amiodarone: VT and Afib.

Amlodipine: to reduce SVR and arterial pressure. It is a CCB and does not effect the myocardium.

Procainamide: atrial and ventricular arrhythmias.

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11
Q

What is the classic sign of an SVT on an ECG?

A

Narrowed QRS complexes

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12
Q

What are the treatment options for Digoxin toxicity?

A

Normalization of electrolytes
Lidocaine
Digoxin immune Fab
Mg++

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13
Q

Which types of diuretics may cause hypercalcemia?

A

Thiazide diuretics

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14
Q

Which bacteria is associated with Guillan-Barre syndrome?

A

C. jejuni

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15
Q

What kind of bug is C. jejuni?

How is it transmitted?

What are symptoms of an infection?

What is the progression of the infection?

A

G- motile rod.

Consumption of unpasteurized milk, untreated water or under-cooked poultry. It is also a zoonotic that can be transmitted by animals (dogs, cats, pigs, etc.)

Bloody diarrhea, abdominal pain, fever, emesis.

Typically is self-limiting.

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16
Q

What food is B. cereus associated with?

A

Reheated rice

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17
Q

What is a case-control study?

What are they used for?

A

Compares people with a disease to a gruop of people without the disease to determine the odds of prior exposure or risk factors.

They are cheap and are used in a preliminary fashion, due to the fact that they are observational in nature and are low in the hierarchy of evidence.

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18
Q

What is a randomized control study?

What are the advantages and disadvantages of this study?

A

A study where one group gets a medicine and the other gets a placebo, and neither the patients nor the researchers know which is which.

Advantages: most reliable form of scientific evidence, as they reduce spurious causality and bias.
Disadvantages: expensive, requires a lot of time, conflicts of interest and ethical concerns.

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19
Q

What is a cohort study?

A

They compare a group with a given exposure or risk factor to a group without it.

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20
Q

What is a case-series?

A

A type of clinical research study where subjects with known exposure are tracked and their outcomes are measured and compared.

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21
Q

What is an open-label trial?

A

A study where participants and researchers are aware of the study arm in which participants are allocated. There is no blinding or masking of participants or researchers.

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22
Q

Which IBD is associated with acute cholecystitis?

A

Crohn disease

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23
Q

What is a classic feature of Crohn disease?

What part of the GI does it usually affect? What is the consequence of this?

A

Transmural skip lesions, which may lead to strictures.

Terminal ileum. This leads to decreased bile acid reabsorption, which causes formation of cholesterol stones (acute cholecystitis).

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24
Q

What kind of stones are caused by hemolysis of RBCs?

A

Pigment stones, which can obstruct the Gb.

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25
Q

What is a gallstone ileus?

A

A passage between the SI and the Gb that a gallstone can enter and cause obstruction in the SI. This would present with symptoms similar to a SBO.

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26
Q

What are the symptoms of ascending cholangitis?

A

Fever, jaundice and abdominal pain, which may progress to shock, altered mental status and/or death.

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27
Q

What are the major side-effects of calcium carbonate?

A

Hypercalemia - fatigue, muscle weakness, depression and constipation.

Hypokalemia

Hypophosphatemia

*Milk-alkali syndrome

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28
Q

What is electrolyte abnormality is associated with magnesium hydroxide?

A

Hypokalemia

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29
Q

What is the major side-effect of aluminum hydroxide?

What are electrolyte abnormalities?

A

Constipation

Hypokalemia and hypophosphatemia

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30
Q

What is the effect of Digoxin on EF and HR?

A

Increased EF, increases HR due to increased vagal tone (because of inhibition of AV node).

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31
Q

What is the major side-effect of Metformin?

What is its MOA?

What are its main effects?

A

Lactic acidosis (usually only in patients w/ concomitant RF): SOB, abdominal pain, altered mental status, hypotension, and HAGMA in the setting of RF.

Inhibits hepatic mitochondrial enzymes which inhibit gluconeogenesis.

Increases glucose sensitivity in peripheral tissues and increases peripheral glucose utilization.

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32
Q

What are features of Pompe disease?

What is the cause of death in infants with this disease?

What kind of disease is it?

What is a classic histological finding?

A

Glycogen buildup in the liver, heart and skeletal muscle which lead to cardiomegaly.
Weakness/hypotonia.

Cardiorespiratory failure.

Lysosomal a-glucosidase deficiency. It is a type 2 glycogen storage disease.

PAS-positive (glycogen within lysosomes).

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33
Q

Which enzyme deficiencies and symptoms are associated withe the following glycogen storage diseases:

Cori disease

Von Gierke

Galactose-1-phosphate uridyltransferase deficiency

McArdle disease:

A

Cori disease: a-1,6-glucosidase deficiency; hypoglycemia.

Von Gierke: glucose-6-phosphatase; severe hypoglycemia (> Cori disease).

Galactose-1-phosphate uridyltransferase deficiency; infantile cataracts.

McArdle disease: myoglycogen phosphorylase deficiency; MSK symptoms (myalgias, etc.).

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34
Q

What is the MOA of adenosine?

A

Binds to A1 receptors in cardiac cells and leads to K+ channel activation and inhibition of L-type Ca++ channels, which causes a conduction delay through the AV node (reason it is given for arrhythmias).

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35
Q

What the effect of using a PDE3 inhibitor?

What is the MOA?

What are some examples?

A

Increased cardiac contractility and decreased PVR.

Inhibits the breakdown of cAMP in myocardial and smooth muscle cells.

Milrinone, anagrelide, cilostazol.

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36
Q

What is the effect of Carvedilol on cardiac contractility and PVR?

A

It decreases contractility and PVR.

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37
Q

What are symptoms of PAN?

What is the pathophysiology?

Which antibodies are negative?

What kind of hypersensitivity is it?

A

Hep. B, fever, weight loss, abdominal pain, melena, HTN, renal damage.

Immune-complex mediated vasculitis of medium-sized arteries (renal aa., etc.).

ANCA-negative

Type III hypersensitivity.

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38
Q

What are the ANCA+ vasculitities?

A

Microscopic polyangiitis
Granulomatosis with polyangiitis (Wegener’s)
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

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39
Q

What becomes oxidized in tissues with iron overload?

A

Tyrosine in melanocytes

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40
Q

What is a Mallory-Weiss tear?

A

A longitudinal laceration of the mucosa at the GEJ. Painful hematemesis follows prolonged episodes of vomiting and retching, and generally resolves spontaneously. Less severe than Boerhaave’s syndrome.

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41
Q

What comes from the 1st pharyngeal arch?

What comes from the 2nd pharyngeal arch?

What comes from the 3rd pharyngeal arch?

What comes from the 4th pharyngeal arch?

What comes from the 5th pharyngeal arch?

What comes from the 6th pharyngeal arch?

A

1st - muscles of mastication.

2nd - numerous facial muscles.

3rd - stylopharyngeus m. and hyoid.

4th - most of the pharynx.

5th - rudimentary; no structures.

6th - arytenoid cartilages and intrinsic muscles of larynx. Fuses with the 4th PA.

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42
Q

What occurs in laryngomalacia?

It occurs due to a defect of which PA?

A

Bulky arytenoid cartilages prolapse anteromedially on inspiration, resulting in stridor.

PA 6.

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43
Q

Which malignancy is associated with SIADH?

A

Small cell lung carcinoma

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44
Q

Do “cold” or “hot” thyroid nodules sugest excessive TH from an overactive thyroid?

A

Cold nodules

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45
Q

What causes thyrotoxicosis factitia?

What are the TSH, T3 and T4 levels?

What is the outcome of the radioactive iodine uptake (RAIU) test?

A

Ingestion of exogenous levothyroxine, usually in an effort to lose weight (not realizing the adverse effects).

Low TSH; high T3/4.

Little to no uptake on RAIU test.

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46
Q

What kind of drug is Verapamil?

A

A CCB that blocks phase 0 (VG Ca++ channels) decreasing conduction through the AV nodes.

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47
Q

What is the MOA of Atropine?

A

Muscarinic antagonist that increases HR, but has no inotropic effects on the heart.

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48
Q

What is the MOA of NIfedipine?

A

DHP Ca++ channel blocker which causes signififcant vasodilation, with little effect on pacemaker APs.

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49
Q

What is the MOA of Procainamide?

A

Blocks Na+ and K+ channels

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50
Q

What is the MOA of Gemfibrozil?

What is a common side-effect?

A

It is a fibrate and acts on PPAR-a to increase TG clearance.

Gallstone formation, due to reduced cholesterol solubility via inhibition of 7a-hydroxylase.

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51
Q

What are side-effects of Statins?

A

Hepatotoxicity and myopathy

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52
Q

What are side-effects of Exetimibe?

A

Hepatotoxicity or diarrhea.

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53
Q

What metabolic changes occur after Niacin use?

What are some side-effects?

A

Increased HDL and decreased LDL and TGs.

Flushing, hyperglycemia and hyperuricemia.

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54
Q

What kind of virus is Coxsackie B?

What ECG findings might be associated with an infection?

A

Single-stranded, naked. icosahedral RNA virus

ST-elevation and PR segment depression (Myocarditis)

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55
Q

Which nodes are common to be seen in gastric cancer?

A

Periumbilical node (Sister Mary Jospeh node) and supraclavicular lymphadenopathy (Virchow’s node)

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56
Q

PDE-5 inhibitors are contraindicated in which patients?

What’s the MOA?

A

Patients who take nitrates for chest pain.

Inactivation of second messengers, like cGMP.

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57
Q

Where is iron absorbed?

A

Duodenum

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58
Q

What changes would you expect to see for MCV in a patient with iron or vitamin B12 deficiencies?

A

Low MCV - microcytic anemia by iron deficiency (duodenum)

High MCV - macrocytic anemia by vitamin B12 deficiency (ileum)

59
Q

Where is folate absorbed?

A

Jejunum

60
Q

What is intestinal atresia associated with?

What is the presentation?

A

Down syndrome.

Intractable emesis shortly after birth.

Failed recanalization of the GI tract in embryogenesis.

61
Q

What is mutated in HOCM?

A

Beta-myosin heavy chain

62
Q

What is the major predisposing factor of Budd-Chiari syndrome?

What are other minor risk factors?

A

Polycythemia vera

Thrombotic diasthesis: antiphospholipid syndrome, factor V leiden.
Pregnancy/OCP use
Intra-abdominal neoplasms

63
Q

What occurs in Wolff-Parkinson-White syndrome?

How does it appear on an ECG?

A

Development of an AV accessory tract that bypasses the AV node (goes straight from atria to ventricles).

Short PR intervals, long QRS complexes, and an “upsloping” delta wave of the QRS complex.

64
Q

“Disordered myofibril hypertrophy” should make you think of what?

A

HOCM

65
Q

What are the 1st-line treatments for black men with HTN?

A

Thiazide diuretics (HCTZ) or CCBs (Amlodipine), because HTN tends to be more volume-dependent than to do with renin in AA patients.

66
Q

What causes acute mesenteric ischemia?

What are symptoms of this condition?

A

Usually an arterial thrombus that develops from Afib that was not properly managed by anti-coagulation therapy, which gets lodged in the SMA (supplies midgut structures).

Poorly localized extreme abdominal pain.

67
Q

What do the following supply:

Celiac trunk
SMA
IMA

A

Celiac trunk - foregut
SMA - midgut
IMA - hindgut

68
Q

Which is more acute: thrombus or embolus?

A

Emboli are acute, while thrombi tend to be more subacute/chronic.

69
Q

Excessive Nitroprusside therapy can cause what?

What does that lead to?

What features would you expect to see in a patient?

A

CN toxicity, which leads to binding of cytochrome C and inhibition of mitochondrial cytochrome C oxidase (last step in ETC).

HA, confusion, cherry-red lips, mucous membranes, seizures, vomiting, etc.

70
Q

Which side-effects are associated with DPP-4 inhibitors (Gliptins)?

A

Nasopharyngitis and pancreatitis

71
Q

What side-effects are associated with Glitazones?

A

Fluid retention, HF and weight gain

72
Q

What side-effects are associated with SGLT-2 inhibitors (Gliflozins)?

A

UTIs, yeast infections, KA

73
Q

What is the role of acetyl-CoA carboxylase?

What will a deficiency lead to?

A

To catalyze the production of Malonyl-CoA (with the cofactor of biotin), which is involved in FA synthesis.

Poor growth, myopathy and hypotonia.

74
Q

What are symptoms of microscopic polyangiitis?

Which antibodies are positive?

A

Palpable purpura, hematuria and hemoptysis. Often there will be necrotizing vasculitis.

+ANCA

75
Q

What diseases are associated with the following:

Anti-epithelial cell antibodies:
Anti-dsDNA antibodies:
Anti-microsomal antibodies:
Anti-mitochondrial antibodies:

A

Anti-epithelial cell antibodies: Pemphigus vulgaris
Anti-dsDNA antibodies: Lupus
Anti-microsomal antibodies: Hashimoto’s thyroiditis
Anti-mitochondrial antibodies: Primary biliary cirrhosis

76
Q

What hematologic lab value is depressed in a patient with cirrhosis (Hep. C, alcoholism, etc.)?

What are the values of the PT and PTT?

A

Low platelets, due to the hypersplenism seen in cirrhosis.

Elevated clotting times, due to failure to produce adequate clotting factors.

77
Q

“Collagen synthesis around central hepatic veins” should make you think of:

A

Alcoholic liver disease

78
Q

Which gene is mutated in hereditary hemochromatosis?

What symptoms would you find in a patient with the disease?

A

HFE gene -> excess absorption of iron.

Hyperpigmentation, T1DM, liver disease (micronodular cirrhosis).

79
Q

What is the cause of extreme excess of BR in neonates?

What is the albumin-BR binding affinity?

What is the relative solubility of BR?

What is the [serum albumin]?

A

Increased EH circulation of BR.

Decreased albumin-BR binding affinity/capacity.

Decreased BR solubility.

[serum albumin] is decreased.

80
Q

What is the 2-fold effect of an AV fistula on the CVS?

A
  1. Shunting blood from the arterial to venous systems increases venous return, increasing preload.
  2. Bypassing the arterioles decreases total peripheral resistance, thereby decreasing afterload.

This means there is increased EDV and decreased ESV.

81
Q

What would you expect to see in a cardiac pressure-volume loop in a patient taking meds to increase the contractility of the heart (B1-agonists, Digoxin, etc.)?

A

A leftward expansion, meaning there is decreased ESV.

There would be normal LV pressure and EDV.

82
Q

What is the MOA of Phenoxybenzamine?

A

Blocks a-1 and a-2 receptors.

83
Q

Why does a patient with Graves’ disease have an increased risk for fractures?

A

They have a risk of osteoporosis, due to thyroxine’s activation of osteoclasts.

84
Q

How does Anorexia Nervosa cause amenorrhea?

A

It causes hypothalamic dysfunction.

85
Q

What are symptoms of catecholamine deficiency?

A

Weakness, fatigue, syncope and orthostatic hypotension.

86
Q

A deficiency of DA beta-hydroxylase will lead to a decrease in what?

A

Catecholamines

87
Q

Low tyrosine levels are seen in which disease?

What is defective in this disease?

A

PKU

PAH enzyme

88
Q

What is the MOA of Esmolol?

What makes it unique?

A

Beta-1 antagonist

It is short-acting

89
Q

What are side-effects of Cimedtidine?

A

Gynecomastia, thrombocytopenia and inhibition of CYP450s.

90
Q

What drug interacts with Levofloxacin?

A

Calcium carbonate for GERD

91
Q

Omega-3 FAs might help with what (in terms of lipid prolifes)?

A

Decreased VLDL and apolipoprotein B

92
Q

What are the side-effects of SURs?

A

Hypoglycemia

93
Q

What is the indication for Orlistat?

What are the side-effects?

A

Weight loss

GI-related and malabsorption of fat soluble vitamins (ADEK).

94
Q

What are symptoms of Kawasaki disease?

What is the progression of the disease?

What is the classic histopathological sign?

What cardiac defect is associated with it?

A

Conjunctivitis, mucosal erythema, hand/foot edema, adenopathy.

Self-limiting.

“Acute necrotizing vasculitis of medium-sized aa.”

Coronary a. aneurysms and occasional MI.

95
Q

What is the main action of Nitroprusside?

What is it known as the 1st-line treatment of?

A

Decrease afterload*, venous return and CO.

Cardiogenic shock

96
Q

How is Sensitivity calculated?

A

Sensitivity = TP/(TP + FN)

97
Q

What are symptoms of Bartonella hensleae?

What is the classic feature?

A

Regional lymphadenopathy, splenomegaly, fever.

Bacillary angiomatosis.

98
Q

What are the symptoms of Brucella melitensis?

How can it be contracted?

A

Undulant fever, nightsweats, weight loss, fatigue, muscle/joint pain, foul smelling and HSM.

Contaminated milk or livestock.

99
Q

What does a Pasturella multocida infection cause?

A

Cellulitis post dog or cat bite.

100
Q

What does a Borrelia recurrentis cause?

A

Relapsing fever and hepatic injury (like jaundice).

101
Q

What cell type is overactive in ZE syndrome?

A

G cells, which secrete Gastrin to act on Parietal cells to increase H+ production.

102
Q

What do I cells secrete?

A

CCK

103
Q

What cardiac defect is seen in a child whose mother had a rubella infection in vivo?

What does it come from during development?

A

PDA

Left 6th aortic arch.

104
Q

What are the TORCHES infections?

A 
T - toxoplasmosis
o
R - rubella
C - CMV
H - Herpes, HIV
S - syphilis

These infections can cross the placenta.

105
Q

What are signs of a Rubella infection?

A

Maculopapular rash beginning on the face and traveling to the rest of the body, with fever, arthralgias and lymphadenopathy.

106
Q

Greatest risk factor for pancreatic carcinoma?

A

Smoking

107
Q

What kind of bacteria is S. viridans?

What does it cause?

A

G+, catalase-positive, alpha-hemolytic and optochin resistance.

Endocarditis post dental work.

108
Q

What kind of bug is S. aueus?

A

G+, catalase-positive

109
Q

What is the treatment for chronic pancreatitis?

Why?

A

Octreotide - a somatostatin analog.

It is inhibits secretion of hormones in the GI tract.

110
Q

What disease is associated wit a mutation in collagen III?

A

Ehlers-Danlos syndrome

111
Q

What is the treatment of achalasia?

What if it is due to cancer?

A

CCB to cause SM relaxation

5-fluorouracil (blocks synthesis of thymidine)

112
Q

What is the treatment of Chaga’s disease?

A

Benznidazole - works by production of free radicals.

113
Q

Which receptors does NE affect?

A

a-1 > a-2 > beta-1

114
Q

What problem does the toxin from Amanita phalloides (mushroom) cause?

What’s it called?

A

Inhibition of RNA II and III

a-amantin

115
Q

What can exposure to polycyclic hydrocarbons cause?

A

Lung and bladder cancer

116
Q

What can exposure to vinyl chloride cause?

A

Hepatic angiosarcoma

117
Q

What can exposure to aflatoxin-B1 cause?

What else can cause this malignancy?

A

Hepatocellular carcinoma

AAT deficiency

118
Q

What occurs in Peyer’s patches?

A

Antigens are presented to B cells.

119
Q

What is the mnemonic for infective endocarditis?

A

Fever
Roth’s spots - retina
Osler nodes - raised lesions on fingers and toes
Murmur

Janeway lesions - raised lesions on palms and soles
Anemia
Nail hemorrhages (splinter hemorrhages)
Emboli

120
Q

What is the most common cause of IE in most people?

What is the exception?

A

Viridans streptococci (S. mutans, S. sanguinis, S. oralis, S. mitis).

S. aureus in IVDU.

121
Q

Peutz-Jeghers syndrome includes which clinical signs?

What is found on endoscopy?

What is the mutation associated?

Patients are at an increased risk for what types of cancers?

A

Abdominal pain, stools with blood and mucous (currant jelly stools) and hyperpigmented macules on lips.

Hamartomatous polyps.

AD STK11 mutation.

GI and breast CA.

122
Q

What is Gardner syndrome?

What is Turcot syndrome?

A

A subtype of FAP where patients also have osseous and soft tissue tumors, supernumerary teeth and retinal hypertrophy.

A subtype of FAP where patients have CNS tumors.

123
Q

What kind of mutation (in terms of heredity type) occurs in dopamine-b-hydroxylase deficiency?

A

AR mutation

124
Q

Metabolic alkalosis is characterized by:

A

pH > 7.4 and high HCO3- (and pCO2)

125
Q

What is the major pathological sign in acute cholecystitis?

Where is the blockage?

What mnemonic is applicable?

A

Gb wall thickening, with muldly elevated or normal LFTs.

At the cystic duct.

4 F’s: female, forty, fat and fertile.

126
Q

Hep. A and Hep. E are what kind of viruses?

What symptoms ensue?

What is the unique concern in a Hep. E infection?

A

Linear ssRNA genome transmitted via F-O route.
HAV is a picornavirus and HEV is a hepevirus.

Jaundice and systemic symptoms (abdominal pain, N/V, fatigue, etc.) with recovery within a few months.

Hep. is associated with fulminant hepatic failure in pregnant women.

127
Q

What artery can be implicated in a AAA operation?

What structures can become ischemic as a result?

A

IMA

Sigmoid colon (hindgut structures)

128
Q

What is the treatment for acromegaly?

A

Octreotide (somatostatin analog)

129
Q

How WBCs kill parasites?

A

Antibody-dependent cell-mediated cytotoxicity and associated release of major basic protein (MBP).

130
Q

What enzyme is deficient in hereditary fructose intolerance? What accumulates as a result?

What symptoms ensue?

A

Aldolase B; fructose-1-phosphate.

Hypoglycemia, acute liver disease, jaundice and vomiting.

131
Q 
FA oxidation (breakdown) occurs where?
FA synthesis occurs where?

What specific enzyme is found in the mitochondria?

A

FA oxidation - mitochondria
FA synthesis - cytosol

Acyl-CoA dehydrogenase

132
Q

What are the functions of the following transporters:

GLUT2

GLUT4

GLUT5

SGLT1 (sodium-dependent glucose transporter)

A

GLUT2 - imports Glu, Gal, Fru

GLUT4 - insulin-dependent receptor in muscle and adipose tissue

GLUT5 - imports Fru only

SGLT1 - imports Glu and Gal

133
Q

What is the pathogenesis of poststreptococcal GN and acute RF?

What hug causes it?

What unique symptom is associated?

A

Type 2 hypersensitivity resulting in an M protein cross-reaction with host antigens (molecular mimicry).

Strep. pyogenes (Grp. A beta-hemolytic)

Sydenham chorea.

134
Q

At what point of luminal narrowing does temporary cardiac ischemia ensue?

A

> 70%

135
Q

In children, what is the most common cause of acute appendicitis?

A

Lymphoid hyperplasia commonly due to a viral infection or vaccine.

136
Q

What are the symptoms/lab findings of the following:

Obstruction of ampulla of Vater
Obstruction of the common bile duct

A

Obstruction of ampulla of Vater - both biliary and pancreatic involvement.

Obstruction of the common bile duct - elevated BR and elevated ALP levels.

137
Q

Obstruction of the biliary tract with a BR stone is associated with:

A

Sickle cell disease

138
Q

Fatty changes and “Mallory bodies w/ neutrophilic infiltrates” should make you think of…

A

Alcohol-induced hepatitis

139
Q

Which sex is more likely to have Primary SClerosing Cholangitis?

What is the disease association?

What lab changes are seen?

What antibodies are positive?

A

Male

UC

Elevated ALP

p-ANCA (perinuclear)

140
Q

What is the MAO of Hydralazine?

What is the classic side-effect?

A

Direct dilation of arterioles

Drug-induced SLE w/ malar rash

141
Q

What is a Curling ulcer?

A

A stomach ulcer that occurs after severe burns. Treated with prophylactic Omeprazole.

142
Q

How long does it take for troponins and CK-MB to increase post MI?

What should be ordered first if MI is suspected?

A

4-6 hrs.

Should order ECG.

143
Q

What drug regimen should patients with familial hypercholesterolemia be on?

A

Statins and Ezetimibe and/or PCSK9 inhibitors synergistically.

USMLE Preparation (7 decks)

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