Kaplan: Pharm - General Cvs And Ddx

Front 1

Drugs that cause pulmonary fibrosis

Back 1

Amioderone (antiarrhythmetic)

Bleomycin (chemo)

Front 2

Drugs that cause gingival hyperplasia

Back 2

Phenytoin

Cyclosporine

"-dipines" (dihydropyridine CCBs)

Front 3

Drugs that cause ototoxicity

Back 3

Loop diuretics

Amingoglycosides (classic interaction w/ Loops)

Vancomycin

Front 4

Drugs w/ a disulfram-like reaction

Back 4

Disulfram
Metronidazole
Cefoperazone
Cefotetan
Chlorpropamide
Griseofulvin

Front 5

CV: Patient is on OCs, starts Drug X and becomes pregnant. What does this tell you about Drug X?

Back 5

Drug X is a p450 inducer

Front 6

Major inducers of p450

Back 6

*Rifampin*

Anticonvulsants

Front 7

Drugs that DO NOT need to be adjusted in renal failure

Back 7

Nafcillin
Erythromycin
Ceftriaxone
Doxycycline
(eliminated via liver)

Front 8

Microtubule Inhibitors

Back 8

Griseofulvin
Colchicine
Vincristine
Vinblastine
Paclitaxel
(Mabendizol)

Front 9

Drugs that cause phototoxicity

Back 9

Tetracyclines

Sulfanamides

Quinolones

Amiodarone

Front 10

Drugs that cause SIADH

Back 10

Vincristine
Vinblastine
Carbamazepine

Front 11

Drugs that cause Stevens-Johnson Syndrome

Back 11

Lamotragine
Folic Acid inhibitors (sulfonamides, trimethoprim, pyrimethoprim)
"-quines" - Malaria drugs

Sulindac (NSAID)

Front 12

Drugs that cause drug-induced SLE

Back 12

"It's HIP to have SLE!"

Hydralazine
Isoniazid (INH)
Procainamide

Front 13

Drugs that cause nephrotoxicity

Back 13

Aminoglycosides
Cisplatin
Amphotericin B

Front 14

Drugs that induce hemolytic anemia is patients w/ G6PD deficiency

Back 14

"Quines" - antimalarials
Sulfasalazine (RA drug)

Front 15

Thiazides, loops, penicillins, cephs, aspirin

Weak acids or bases?

Back 15

Weak acids

Front 16

Morphine, local anesthetics, amphetamines, PCP

Weak acids or bases?

Back 16

Weak bases

Front 17

Natual pH of:
Stomach
Small inestine
Blood
Urine

Back 17

Stomach = 1-2
Small intestine = 6
Blood = 7.4
Urine = 5-8

Front 18

Pt ODs on aspirin, a weak acid. Since there is no antidote, what is the best Tx?

Back 18

Alkalinize urine to facilitate excretion (could use NaHCO3)

Front 19

CV: Sjogren's Dz + pilocarpine = ?

Back 19

Pilocarpine (muscarinic agonist) increases systemic SE

*Sjogren's Dz = AI Dz, lymphatic infiltration of lacrimal & salivary glands; female age 35-45

Front 20

DDx: Patient presents with weakness in facial and other small muscles. Weakness increases with use, but recovers w/ rest.

How do you distinguish between myasthenia and cholinergic crisis?

Back 20

Use edrophonium

If MG, temporary improvement in Sx

If cholinergic crisis, no change or slight worsening of Sx

Front 21

Describe AChE inhibitor poisoning

Back 21

DUMBBELSS

Diarrhea, Urination, Miosis, Bradycardia (M2), Bronchoconstriction, Excitiation of Muscle and CNS (Nm), Lacrimation, Salivation, Sweating

*Mostly M3 stimulation*

Tx: Atropine - treats muscarinic effects
pralidoxime (2-PAM) - Regeneration of AChE (time dependent aging)

Front 22

Drugs that cause flushing

Back 22

Isoproterenol
Vasodilators
Niacin
Histamine release (Vancomycin - Red Man Syndrome, Morphine, Amphotericin B)

Front 23

Pt with pheochromocytoma develops HTN. By what mechanism and how to you treat it?

Back 23

Increased levels of Epi --> HTN

Tx w/ a1 blocker (i.e. phenylephrine, methoxamine) --> can cause hypoTN

Front 24

CV: Pt w/ hypertension + BPH. What drug should you use?

Back 24

a1 blocker

"-osin"
Prazosin, doxazosin, terazosin, tamulosin

Front 25

Why do nonselective alpha blockers cause more reflex tachycardia than a1 selective blockers?

Back 25

a1 blockers only target a1 receptors on blood vessels.

Nonselective a blockers also stimulate a2 receptors on nerve innervating the heart.

Front 26

Pt on long-term beta blocker Tx has a second CV drug added to regimen. The patient develops severe bradycardia and dies. What was the added drug?

Back 26

Calcium channel blocker

probably verapamil (more selective for the heart)

Front 27

Effect of B2 blockade on blood glucose?

Back 27

B2 blockage decreases insulin release from beta islet cells --> blocks GNG and glycogenolysis --> decreases blood glucose

Front 28

Glucagon's effect on the heart and MOA?

Back 28

Positive inotropic and chronotropic

Uses glucagon receptors that are G-protein linked to adenylyl cyclase. This is the basis for its use in beta-blocker OD.

Front 29

CV: Pt w/ HTN + glaucoma. Which drug should you use?

Back 29

Timolol

Unlike most BB, timolol doesn't have a local anesthetic effect on the eye

Front 30

Tx of open-angle glaucoma

Back 30

BB to decrease formation of aqueous humor by ciliary epithelial cells

Muscarinic agonists to improve drainage through the canal of Schlemm

Front 31

Tx for closed-angle glaucoma

Back 31

*Drug management only to get by til emergency surgery*

Cholinomimetics, carbonic anhydrase inhibitors, and/or mannitol

Front 32

CV: warfarin + sulfonamide = ?

Back 32

Increase in warfarin toxicity.
Warfarin is highly plasma protein bound -> Sulfonamide displaces warfarin -> Increased free warfarin -> Increased warfarin tox

Front 33

CV: Neonate w/ unconjugated bilirubin is given a sulfonamide. What happens?

Back 33

Kernicterus and/or bilirubin encephalopathy

Front 34

CV: Butterfly rash + positive ANA = (2)

Back 34

1. Primary SLE

2. drug-induced SLE (antihistones will be present and Sx disappear when drug is stopped)
- HIP: hydralazine, INH, procainamide

Front 35

CV: Smoker on theophylline. How does this affect dosing?

What if a macrolide is added?

Back 35

Must increase dose of theophylline (metab via CYP 3A4) to compensate for CYP 3A4 induction from smoking.

Macrolides are 3A4 inhibitors. Will see theophyllin tox if dose not reduced.

Front 36

CV: Chloramphenicol given to a new born = ?

Back 36

Grey baby syndrome.

Newborn has impaired glucuronidation ability. Chloramphenicol (and morphine) metab via Phase II glucuronidation

Front 37

Tyrosine kinase pathway activated by what proteins?

Uses what second messengers?

Back 37

Cytokines (erythropoietin, somatotropin, interferons)

JAK-STAT pathway

Front 38

How do bradykinin and histamine signal via the second messanger cGMP?

Back 38

NO --> activates guanylyl cyclase --> increase cGMP in smooth muscle --> cGMP facilitates dephosphorylation of myosin light chains in vascular smooth muscle --> prevents interaxn w/ actin --> vasodilation

Front 39

Which 2 classes of antiarrhythmic drugs prolong the PR interval?

Back 39

Ca-channel blockers
Beta blockers

Front 40

Drugs that cause Torsades

Back 40

Quinidine

Front 41

CV: Pt presents with digoxin toxicity. What drug is used as the antidote?

Back 41

Lidocaine (Class 1B Na channel blocker)

Front 42

Which antiarrhythmic drug has least cardiotoxicity?

Back 42

Lidocaine (Class 1B Na-channel blocker)

Front 43

CV: 1st line Tx for A-fib?

Back 43

Warfarin + SVT drugs [Class II (beta blockers) & IV (CCBs) antiarrhythmics, adenosine, digoxin]

Front 44

Drugs that cause Torsades

Back 44

K-channel blockers (Class 1A and Class III)

Antipsychotics (thioridazine)

Tricyclic antidepressants

Tx: Magnesium

Front 45

CV: Patient on drug therapy for HTN and angina presents with methemoglobinemia. What caused this and how to you treat it?

Back 45

Nitrites, like nitroprusside and nitroglycerine, cause methemoglobinemia.

Tx with methylene blue

Front 46

CV: Patient on nitroprusside Tx for 24 hours develops cyanide poisoning. How do you treat it?

Back 46

Administer Na nitrite or amyl nitrite. --> promote formation of methemaglobin, which binds the CN-
--> prevents inhibitory action on complex IV of ETC
--> Finally Tx w/ Na thiosulfate to make less toxic thiocynate (SCN-)

Front 47

Pt w/ high cholesterol and TGs is being treated for HTN. Which drug should you use?

A. Propanolol
B. Lisinopril
C. Hydrochlorothiazide

Back 47

B. Lisinopril

Beta blockers and thiazides can increase blood lipids and shouldn't be used in patients w/ dyslipidemia.

Front 48

ACEi and ARBS (increase/decrease) renin?

Back 48

Increase

Front 49

What 4 classes of drugs are used in the Tx of chronic HTN

Back 49

Diuretics (1st line)

ACE/ARB

Beta blockers

Ca-channel blockers

Front 50

Pt w/ HTN + Angina. What drug do you use?

Back 50

Beta blockers or CCBs

Front 51

Pt w/ HTN + Diabetes. What drug do you use?

Back 51

ACEIs/ARBs

Beta-blockers (esp. non-selective) would block insulin secretion from B2 on pancreatic islet cells.

Front 52

Pt w/ HTN + CHF. What drug do you use?

Back 52

ACEIs/ARB or beta blockers

Front 53

Post-MI pt w/ HTN. What drug do you use?

Back 53

Beta blocker

Front 54

Pt w/ HTN + BPH. What drug do you use?

Back 54

alpha blockers

Front 55

Pt w/ HTN + dyslipidemia. What drug do you use?

Back 55

Alpha blockers, CCBs, ACEIs/ARBs

Don't use BB or thiazides b/c they increase lipids

Front 56

Tx for Wolf-Parkinson-White Syndrome

Back 56

Class IA (Na-channel blocker; procainamide) or Class III (K-channel blocker; amioderone). These drugs block the accessory pathway

Don't use digoxin, BB, CCBs, or adenosine --> They show AV conduction

Front 57

Drugs used in Class/stable angina? (3 classes)

Back 57

Nitrates

Beta blockers

CCBs

Front 58

Drugs used in vasospastic/Prinzmetal angina

Back 58

Nitrates

CCBs

Front 59

Post MI Tx

Acute?

Chronic?

Back 59

Acute = O2, nitroglycerin, aspirin

Chronic = BB, ACEI, Statins

Front 60

DOC for Raynaud's Dz

Back 60

Nifedipine

Front 61

Pt with severe peripheral edema, has a sulfa allergy. Which diuretic do you use?

Back 61

Ethacrynic acid (loop diuretic)

Most diuretics, and all other loop diuretics, are sulfa drugs

Front 62

Relationship between K+ and:

H+?

Insulin?

Back 62

H+: K generally travels w/ H+, so hypokalemia and alkalosis generally go together (and vice versa)

↑ K <--> ↑ insulin
(and vice versa)

Front 63

Most common cause of hypokalemia and metabolic alkalosis?

Back 63

Loop and thiazide diuretics

Front 64

Most common cause of hyperkalemia?

Back 64

Renal failure

Front 65

What is nephrogenic diabetes insipidus and how is it treated?

Back 65

It's caused by an uncoupled V2 receptor

Tx: HCTZ (↓ plasma volume --> ↓ GFR --> ↑ tubule resorption of Na

Front 66

What is central diabetes insipidus and how is it treated?

Back 66

It's caused by ↓ ADH levels

Tx: Desmopressin