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USMLE Step 1 Pharmacology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. Ca2+ channel blockers - site of action?
Cell membrane Ca2+ channels of cardiac sarcomere
Inhibit steroid synthesis - used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
Doxycycline - because it is fecally eliminated
collecting ducts

2. MOA: Disrupt bacterial/fungal cell membranes
nausea - headache - lupus - like syndrome - reflex tachycardia - angina - salt retention
Prophylaxis for Influenza A - Rubella; Parkinson's disease
Polymyxins
With supplemental Folic Acid

3. Name two bile acid resins.
1) Chloramphenical = bacteriostatic 2) Erythromycin = bacteriostatic 3) Lincomycin = bacteriostatic 4)cLindamycin = bacteriostatic
fetal renal damage - hyperkalemia - Cough - Angioedema - Proteinuria - Taste changes - hypOtension - Pregnancy problems - Rash - Increased renin - Lower Angiotensin II (CAPTOPRIL)
cholestyramine - colestipol
The PT.

4. What is the only depolarizing neuromuscular blocking agent?
Succinylcholine
Cryptococcal meningitis in AIDS patients and Candidal infections of all types
edrophonium (extremely short acting anticholinesterase)
AZT - to reduce risk of Fetal Transmission

5. What is the receptor affinity and clinical use of isoproterenol?
It affects beta receptors equally and is used in AV heart block (rare).
NO HYPERURICEMIA - NO SULFA AllERGY; same as furosemide otherwise
GI side effects. (Indomethacin is less toxic - more commonly used.)
Blocks Peptide Bond formation at the 50S subunit - Bacteriostatic

6. What are two processes Corticosteroids inhibit leading to decreased inflammation?
Botulinum
Chagas' disease - American Trypanosomiasis (Trypanosoma cruzi)
Receptors = D1=D2>beta>alpha - thus increasing heart rate (beta) and blood pressure (alpha vasoconstriction) while maintaining kidney perfusion (dopamine receptors)
1. Phospholipase A2 is prevented from releasing arachidonic acid 2. Decreases protein synthesis thus lowering amount of Cyclooxygenase enzymes

7. Amiodarone - toxicity?
pulmonary fibrosis - corneal deposits - hepatotoxicity - skin deposits resulting in photodermatitis - neurologic effects - consitpation - CV (bradycardia - heart block - CHF) - and hypo - or hyperthyroidism.
Vibrio cholerae Acne Chlamydia Ureaplasma Urealyticum Mycoplasma pneumoniae Borrelia burgdorferi (Lyme's) Rickettsia Tularemia
1. Better bioavailability 2. 2 to 4 times longer half life 3. Can be administered subcutaneously 4. Does not require laboratory monitoring
Benzodiazepine.

8. What are the side effects of Rifampin?
thiazides - amiloride
Minor hepatotoxicity - Drug interactions (activates P450)
atropine - homatropine - tropicamide
GI intolerance (nausea - diarrhea) - Hyperglycemia - Lipid abnormalities - Thrombocytopenia (Indinavir)

9. What physiological effects was the Anes using Atropine to tx
proarrhythmic
Pregnant women - Children; because animal studies show Damage to Cartilage
SLUD (salivation - Lacrimation - urination - Defecation)as well as airway secretion - GI motility - acid secretions
Antifungal.

10. Adverse effects of Nifedipine - verapamil?
INH: Injures Neurons and Hepatocytes
Rare.
dizziness - flushing - constipation (verapamil) - nausea
- Isoniazid

11. Beta Blockers - BP?
loop diuretics - spironolactone
Penicillin - Ampicillin - Ticarcillin - Pipercillin - Imipenem - Aztreonam - Cephalosporins
decrease
Depolymerizes microtubules - impairing leukocyte chemotaxis and degranulation.

12. MOA: Disrupt fungal cell membranes
atropine - homatropine - tropicamide
GI upset
Amphotericin B - Nystatin - Fluconazole/azoles
Scopolamine

13. What is the mechanism of Tacrolimus (FK506)?
AV nodal cells
Ototoxicity - Hypokalemia - Dehydration - Allergy (sulfa) - Nephritis (interstitial) - Gout
is resistant
Similar to cyclosporine; binds to FK- binding protein - inhibiting secretion of IL-2 and other cytokines.

14. What is the MOA for Clindamycin?
Foscarnet = pyroFosphate analog
Benzodiazepine.
Blocks Peptide Bond formation at the 50S subunit - Bacteriostatic
alpha -1 > alpha -2; used as a pupil dilator - vasoconstrictor - and for nasal decongestion

15. Antimicrobial prophylaxis for Gonorrhea
Acute (hours)
Interferes with microtubule function - disrupts mitosis - inhibits growth
Ototoxicity - Hypokalemia - Dehydration - Allergy (sulfa) - Nephritis (interstitial) - Gout
Ceftriaxone

16. What are nine findings of Iatrogenic Cushing's syndrome caused by glucocorticoid therapy?
1. Reliable (<1% failure) 2. Lowers risk of endometrial and ovarian cancer 3. Decreased incidence of ectopic pregnancy 4. Lower risk of pelvic infections 5. Regulation of menses
1. Aluminum hydroxide: constipation and hypophosphatemia 2. Magnesium hydroxide: diarrhea 3. Calcium carbonate: Hypercalcemia - rebound acid increase - All may cause hypokalemia
1. Buffalo hump 2. Moon facies 3. Truncal obesity 4. Muscle wasting 5. Thin skin 6. Easy bruisability 7. Osteoporosis 8. Adrenocortical atrophy 9. Peptic ulcers
Succinylcholine

17. What is the MOA of Isoniazid (INH)?
- Estrogen receptor antagonist - Breast CA - increased endometrial CA risk
Meningitis (H. influenza - N. meningitidis - S. pneumoniae) - Conserative treatment due to toxicities
Early myocardial infarction.
Decreases synthesis of Mycolic Acid

18. For Warfarin What is the Ability to inhibit coagulation in vitro
- Dimercaprol - succimer
Dermatophytes (tinea - ringworm)
No
G6PD deficient individuals

19. What is the category - desired effect - and adverse effect of Isoproterenol in the treatment of Asthma?
severe orthostatic hypotension - blurred vision - constipation - sexual dysfunction
Inhibits Viral DNA polymerase
Nonspecific beta - agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Adverse effect is tachycardia (Beta 1).
Sucralfate cannot work in the presence of antacids or H2 blockers because it requires an acidic environment to polymerize.

20. What drug is used to diagnose myasthenia gravis?
CL= (rate of elimination of drug/ Plasma drug conc.)
1)Binds penicillin - binding proteins 2) Blocks transpeptidase cross - linking of cell wall 3) Activates autolytic enzymes
edrophonium (extremely short acting anticholinesterase)
Hypersensitivity reactions

21. What are three clinical uses of the Leuprolide?
1. Antipyretic 2. Analgesic 3. Anti - inflammatory 4. Antiplatelet drug.
all except the K+ sparing diuretics Spironolactone - Triamterene - Amiloride
1. Infertility (pulsatile) 2. Prostate cancer (continuous: use with flutamide) 3. Uterine fibroids
Protease inhibitor.

22. What are three types of antacids and the problems that can result from their overuse?
Penicillin - Cephalosporins - Vancomycin - Aminoglycosides - Fluoroquinolones - Metronidazole
Same as penicillin. Extended spectrum antibiotics
Edrophonium
1. Aluminum hydroxide: constipation and hypophosphatemia 2. Magnesium hydroxide: diarrhea 3. Calcium carbonate: Hypercalcemia - rebound acid increase - All may cause hypokalemia

23. List the mechanism - clinical use - & toxicity of Cyclophosphamide.
- Alkalating agent - NHL - Breast - ovary - & lung. - Myelosuppression - & hemorrhagic cystitis.
CMV Retinitis in IC pts When Ganciclovir fails
Epinephrine
1. Weight gain 2. Hepatotoxicity (troglitazone)

24. MOA: Bactericidal antibiotics
Doxycycline - because it is fecally eliminated
Penicillin - Cephalosporins - Vancomycin - Aminoglycosides - Fluoroquinolones - Metronidazole
sedation - sleep alterations
Gentamicin - Neomycin - Amikacin - Tobramycin - Streptomycin

25. What neurotransmitter does Amantadine affect? How does it influence this NT?
Activates cholinergic receptors on bladder and bowel smooth muscle - alleviating post - op and neurogenic ileus and urinary retention.
AZT - to reduce risk of Fetal Transmission
Dopamine; causes its release from intact nerve terminals
Beta lactams - inhibit cell wall synthesis - Bactericidal

26. Why are the Sulfonylureas inactive in IDDM (type -1)?
troponin - tropomyosin system
torsade de pointes
Because they require some residual islet function.
Cimetidine is a potent inhibitor of P450; it also has an antiandrogenic effect and decreases renal excretion of creatinine. Other H2 blockers are relatively free of these effects.

27. Why is there a drop in systolic - mean - and diastolic bp with infusion of isoproterenol?
Stimulating beta receptors stimulates heart rate - but beta receptor induced vasodilation reduces peripheral resistance.
Local anesthetic.
Giardiasis - Amoebic dysentery (E. histolytica) - Bacterial vaginitis (Gardnerella vaginalis) - Trichomonas
1. In liver - increases storage of glucose as glycogen. 2. In muscle - stimulates glycogen and protein synthesis - and K+ uptake. 3. In adipose tissue - facilitates triglyceride storage.

28. What are are the Sulfonylureas (general description) and What is their use?
Finasteride inhibits 5 Alpha - reductase - this decreases the conversion of testosterone to dihydrotestosterone - useful in BPH
Sulfonylureas are oral hypoglycemic agents - they are used to stimulate release of endogenous insulin in NIDDM (type -2).
Vibrio cholerae Acne Chlamydia Ureaplasma Urealyticum Mycoplasma pneumoniae Borrelia burgdorferi (Lyme's) Rickettsia Tularemia
Antimetabolite derivative of 6- mercaptopurine that interferes with the metablolism and synthesis of nucleic acid.

29. Where does Griseofulvin deposit?
pulmonary edema - dehydration
Choline acetyltransferase
Keratin containing tissues - e.g. - nails
carbonic anhydrase inhibitors - K+ sparing diuretics

30. What are the clinical uses for 1st Generation Cephalosporins?
When pts have Low CD4+ (< 500 cells/cubic mm) or a High Viral Load
Large anionic polymer - acidic
Gram + cocci - Proteus mirabilis - E. coli - Klebsiella pneumoniae (PEcK)
Can affect absorption - bioavailability - or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.

31. Name two classes of drugs for HIV therapy
Protease Inhibitors and Reverse Transcriptase Inhibitors
decrease the slope of phase 4 - increase PR interval (the AV node is particularly sensitive)
competitive inhibirot of aldosterone in the cortical collecting tubule
Neomycin

32. These drugs acts indirectly by releasing strored catecholamines in the presynaptic terminal
all of them
Amphetamine and Ephedrine
sedation - sleep alterations
fetal renal damage - hyperkalemia - Cough - Angioedema - Proteinuria - Taste changes - hypOtension - Pregnancy problems - Rash - Increased renin - Lower Angiotensin II (CAPTOPRIL)

33. MOA: Block cell wall synthesis by inhib. Peptidoglycan cross - linking (7)
proximal convoluted tubule
Treatment of hypertension - especially with renal disease (lowers bp centrally - so flow is maintained to kidney).
scopolamine
Penicillin - Ampicillin - Ticarcillin - Pipercillin - Imipenem - Aztreonam - Cephalosporins

34. What are three possible toxicities of NSAID usage?
cholestyramine - colestipol
Botulinum
Nephrotoxicity
1. Renal damage 2. Aplastic anemia 3. GI distress

35. Toxic side effects of the Azoles?
- Shifts the curve down - reduces Vmax
hypertension - angina - arrhythmias
1. Predisposes to viral infections and lymphoma 2. Nephrotoxic (preventable with mannitol diuresis)
Hormone synthesis inhibition (Gynecomastia) - Liver dysfunction (Inhibits CYP450) - Fever - Chills

36. What are five toxicities associated with Tacrolimus (FK506)?
Gentamicin - Neomycin - Amikacin - Tobramycin - Streptomycin
1. Significant: nephrotoxicity 2. Peripheral neuropathy 3. Hypertension 4. Pleural effusion 5. Hyperglycemia.
Blocks viral penetration/uncoating; may act to buffer the pH of the endosome
1. Renal damage 2. Aplastic anemia 3. GI distress

37. How do we stop angina?
decrease myocardial O2 consumption by: 1- decreasing end diastolic volume 2- decreasing BP 3- decreasing HR 4- decreasing contractility 5- decreasing ejection time
blocks SR Ca2+ channels
Vibrio cholerae Acne Chlamydia Ureaplasma Urealyticum Mycoplasma pneumoniae Borrelia burgdorferi (Lyme's) Rickettsia Tularemia
Imipenem

38. Which drug(s) cause this reaction: P450 inhibition(6)?
Binds ergosterol - Disrupts fungal membranes
edrophonium (extremely short acting anticholinesterase)
Penicillin.
- Cimetidine - ketoconazole - grapefruit juice - erythromycin - INH - sulfonamides

39. What is the effect of guanethidine on adrenergic NE release?
It inhibits release of NE.
AZT - to reduce risk of Fetal Transmission
all except the K+ sparing diuretics Spironolactone - Triamterene - Amiloride
Ciprofloxacin - Norfloxacin - Ofloxacin - Grepafloxacin - Enoxacin - Nalidixic acid

40. What are the clinical uses for Aztreonam?
Gram - rods: Klebsiella species - Pseudomonas species - Serratia species
Lipoxygenase
troponin - tropomyosin system
HTN - CHF - calcium stone formation - nephrogenic DI.

41. ___________ are Teratogenic
- Nitrate - hydroxocobalamin thiosulfate
Aminoglycosides
osmotic diuretic - increase tubular fluid osmolarity - thereby increasing urine flow
impotence - exacerbation of asthma - CV effects - CNS effects - may mask hypoclycemia

42. Describe the MOA of Interferons (INF)
Glycoproteins from leukocytes that block various stages of viral RNA and DNA synthesis
Saquinavir - Ritonavir - Indinavir - Nelfinavir
As an anticholinesterase it increases endogenous ACh and thus increases strength.
Prefers beta's at low doses - but at higher doses alpha agonist effects are predominantly seen.

43. What is the mechanism of action of the Alpha - glucosidase inhibitors?
Large anionic polymer - acidic
Inhibit intestinal bursh border Alpha - glucosidases; delayed hydrolysis of sugars and absorption of sugars leading to decresed postprandial hyperglycemia.
Aplastic anemia (dose independent) - Gray Baby Syndrome
Antileukotriene; blocks leukotriene receptors.

44. Adverse effects of beta - blockers?
impotence - asthma - CV effects (bradycardia - CHF - AV block) - CNS effects (sedation - sleep alterations)
Cyclooxygenases (COX I - COX II).
- Sulfonamides - furosemide - methicillin - rifampin - NSAIDS (ex. ASA)
It inhibits release of NE.

45. Resistance mechanisms for Aminoglycosides
Theoretically it could be used to block the cephalic phase of acid secretion (vagal stimulation).
Epinephrine to treat anaphylaxis. Also useful if you have open angle glaucoma - asthma - or hypotension.
Modification via Acetylation - Adenylation - or Phosphorylation
Nonspecific beta - agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Adverse effect is tachycardia (Beta 1).

46. Beta Blockers - CV toxicity?
bradycardia - AV block - CHF
Bactericidal for: Gram + rod and cocci - Gram - cocci - and Spirochetes
troponin - tropomyosin system
Terminal D- ala of cell wall replaced with D- lac; Decreased affinity

47. What is the memory key for the effect of aluminum hydroxide overuse?
YES
Anaerobic infections (e.g. - B. fragilis - C. perfringens)
AluMINIMUM amount of feces.
Indirect agonist - uptake inhibitor

48. What are common toxicities associated with Macrolides? (4)
GI discomfort - Acute cholestatic hepatitis - Eosinophilia - Skin rashes
Warfarin interferes with the normal synthesis and gamma - carboxylation of vitamin K- dependent clotting factors II - VII - IX - and X - Protein C and S via vitamin K antagonism.
hypertension - CHF - diabetic renal disease
collecting ducts

49. What is the MOA for Metronidazole?
Intrathecally
Acetaminophen has antipyretic and analgesic properties - but lacks anti - inflammatory properties.
Forms toxic metabolites in the bacterial cell - Bactericidal
Initially vasoconstriction would increase bp - but then it acts on central alpha -2 receptors to decrease adrenergic outflow resulting in decreased bp.

50. What microorganisms are Aminoglycosides ineffective against?
aPTT (intrinsic pathway)
Blocks viral penetration/uncoating; may act to buffer the pH of the endosome
Anaerobes
Vd= (Amt. of drug in body/ Plasma drug conc.)