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Pharm - Kaplan Flashcards

1
Q

Anti-GAD (glutamic acid decarboxylase deficiency)

Treatment?

A

DM type 1

Insulin

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2
Q

Enoxaparin…MoA?

Use?

A

Binds AT3, inhibits thrombin and factor Xa

DVT (treatment and prophylaxis)

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3
Q

HLA-DR3, DR4, DR3/4

A

Type 1 DM (anti-GAD antibodies)

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4
Q

HLA-DR5

Treatment?

A

Hashimoto’s thyroiditis

Levothyroxine

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5
Q

Functions of angiotensin 2

Thus, functions of ACEIs/ARBs

A
  • Stimulate aldosterone (increase Na/H2O retention)
  • Vasoconstrict (increase TPR)

Diuresis, vasodilation

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6
Q

Drugs causing oxidative stress, thus affecting G6PD

What does this mean?

A 
TMP-SMX
Nitrofurantoin
Fluoroquinolones
Isoniazid
Dapsone
Primaquine
Quinine

Meaning = buildup of H2O2

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7
Q

Inhibitor of ergosterol synthesis via squalene epoxidase

Use?

A

Terbinafine

Dermatophytes – esp. tinea corporis

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8
Q

Inhibitor of beta glucan synthesis

Use?

A

Echinocandins (Caspofungin)

Invasive or resistant oral candidiasis

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9
Q

Anti-fungal w/ mitotic spindle function inhibition

Use?

A

Griseofulvin

Dermatophytes (oral)

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10
Q

How to remember which organs have which muscarinic receptors?

A

Most important organ (M1) = Brain
2nd most important (M2) = Heart
EVERYTHING ELSE = M3 (except glands - M1)

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11
Q

Anti-fungal that inhibits thymidylate synthetase

Use?

A

Flucytosine

Cryptococcus (but NOT in HIV – BM suppression)

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12
Q

Inhibitor of egosterol synthesis via lanosterol 14-alpha-demethylase

Use?

A

-azoles (antifungal)

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13
Q

Anti-fungal that binds to egosterol

A

Amphotericin B

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14
Q

A patient is treated for a UTI while taking an antacid. The UTI continues to get worse. What drug class was given?

Why did it get worse?

A

Fluoroquinolones

Iron and calcium inhibit the absorption of fluoroquinolones

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15
Q

Drugs for heart failure that improve mortality

Why?

A

ACEI’s, ARBs, Aldosterone antagonists, Beta blockers

Ang 2 is involved in heart remodeling during CHF

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16
Q

Prevention of uric acid crystals in tumor lysis syndrome

A

Allopurinol

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17
Q

A man taking a drug for depression starts having sweating, tachycardia, and headache after eating pizza. Explain.

A

Taking a MAO + eating tyramine foods (cheese, beer, wine) –> tyramine displaces NE from nerves and blocks its metabolism –> SYMPATHETIC CRISIS

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18
Q

Side effects of TCAs

A

3 C’s: Coma, Cardiotoxicity, Convulsions

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19
Q

Activation of PPAR-alpha

Side effect?

A

Fibrates (Gemfibrozil, Fenofibrate, Clofibrate)

Gallstones (increases cholesterol in bile)

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20
Q

Bile acid sequestrants

Side effect?

A

Cholestyramine, Colestipol

Constipation

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21
Q

Flushing, hyperglycemia, hyperuricemia…drug?

A

Niacin

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22
Q

Rhabdomyolysis…drug?

A

Statin

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23
Q

PPAR-gamma activators

Functions?

Side effects?

Contraindication?

A

Thiazolidinediones (-glitazone)

Increase insulin sensitivity, decrease gluconeogenesis
Decrease TGs, increase HDL, decrease CRP, decrease Glc

Hepatotoxicity, heart failure

Class 3-4 Heart Failure

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24
Q

A patient is given fentayl and midazolam for anesthesia. What is the best combo of drugs to fight the respiratory depression in this patient?

A

Naloxone (for the fentanyl) + Flumazenil (for the benzo)

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25
Q

Alkylating agent that attacks guanine N7

Side effect to note

Treatment? MoA?

A

Cyclophosphamide

Hemorrhagic cystitis

Mesna (traps acrolein in bladder)

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26
Q

Alkylating agent that cross-links DNA strands

Side effects

Treatment for the one?

A

Cisplatin

Nephrotoxic, Neurotoxic (deafness)

Amifostene (for nephrotoxicity)

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27
Q

Alkylating agent used in Hodgkin’s lymphoma

A

Procarbazine

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28
Q

Intercalating agent that causes DNA strand breakage

Side effect?

Treatment? MoA?

A

Anthracyclines (Doxorubicin)

Delayed CHF

Dexrazoxane - Prevents formation of free radicals

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29
Q

Treatment of methotrexate BMS? MoA?

A

Leukovorin - Folinic acid rescue

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30
Q

Pyrimidine antimetabolite that inhibits thymidylate synthetase (2)

A

5-FU, Capecitabine

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31
Q

Purine antimetabolite activated by HGPR transferase

A

6-mercaptopurine

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32
Q

Complexes with Fe and O2 to cause DNA strand scission

What cell cycle phase?

Side effects?

A

Bleomycin

G2

Pulmonary fibrosis, pneumonitis

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33
Q

Inhibitor of microtubule polymerization (2)

Side effect to note?

A

Vincristine, Vinblastine

Neurotoxicity

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34
Q

How to remember how beta blockers work?

A 
A-M = beta-1 selective (EXCEPT C and L)
N-Z = beta non-selective

**Carvedilol and Labetolol = beta-1, beta-2, and alpha-1

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35
Q

What do beta blockers do to blood pressure?

A

DECREASE it (prevents glycogenolysis by skeletal muscle and liver)

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36
Q

Dopamine…

  • Low dose?
  • Medium dose?
  • High dose?
A 
Low = D1 (renal artery dilation)
Medium = Beta-1 (heart)
High = alpha-1 (vessels, etc.)
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37
Q

Which are more sensitive to stimulation: alpha or beta?

A

BETA (beta response predominant at low dose, alpha response predominant at high dose)

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38
Q

Phenylephrine…MoA

A

Alpha-1 agonist

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39
Q

How to remember the alpha-2 agonist drugs?

A

A = MC^2

A = alpha
^2 = alpha-2
M = methyldopa
C = clonidine
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40
Q

Beta-1 selective agonist

Beta-2 selective agonists (3)

A

Dobutamine

Salmeterol, albuterol, terbutaline

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41
Q

In a sympathetic BP/HR tracing, an increase in BP = ?

An increase in pulse pressure = ?

Bradycardia?

A

Alpha-1

Beta-1

Reflex

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42
Q

Epinephrine…

  • Low dose
  • Medium dose
  • High dose
A 
Low = beta-1 and beta-2 (like isoproterenol)
Medium = beta-1 only (alpha-1 and beta-2 cancel out)
High = alpha-1, beta-1, beta-2 (looks like norepinephrine)
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43
Q

Differentiating NE vs. High Dose Epinephrine

A

Give alpha-1 blocker…

  • NE – BP goes back to normal
  • Epi – BP drops below normal (beta-2 effect)
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44
Q

Selegiline…MoA

Use?

Can you get tyramine hypertension w/ this?

A

Inhibition of MAO type B (brain – blocks dopamine metab.)

Parkinson’s

NO – tyramine is metabolized by MAO-A only

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45
Q

A patient has Horner’s syndrome. What is the difference between putting cocaine in the eye, vs. putting amphetamine in the eye?

A

Cocaine – prevents re-uptake – will work if NE is already being released

Amphetamine – promotes release – will work as long as that last nerve in the pathway is in tact

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46
Q

Phenoxybenzamine vs. Phentolamine

A 
Phentolamine = competitive alpha antagonist
Phenoxybenzamine = non-competitive alpha antagonist
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47
Q

Alpha-1 selective antagonists

Use?

How is tamsulosin different than the rest?
Benefit of it?

A

Prazosin, Terazosin, Tamsulosin, etc.

BPH, other things

No Z in the name = alpha-1A selective = prostate (BPH)
Does NOT affect the BP like the others do

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48
Q

Alpha-2 selective antagonist

Use?

A

Mirtazepine

Antidepression

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49
Q

Treatment for pheochromocytoma

A

Phenoxybenzamine (BOTH HAVE 16 LETTERS)

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50
Q

When is blocking beta-2 beneficial?

A

Glaucoma (reduced aqueous humor production)

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51
Q

Side effect of beta blockers

A

Dyslipidemias

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52
Q

Beta blockers with partial agonist activity (ISA)

A

Acebutolol, Pindolol

53
Q

Most and least sedating beta blockers

A 
Most = propranolol
Least = atenolol
54
Q

Sotalol…MoA

A

Beta-blocker + K+ channel blocker

55
Q

Being treated for asthma, develops tremor, tachycardia, and seizure…possible cause?

MoA?

A

Theophylline toxicity

Phosphodiesterase inhibitor

56
Q

Alpha-1 agonist vs. muscarinic antagonist…which one can cause cycloplegia?

Why?

A

Muscarinic antagonist

Accommodation = M3 on ciliary muscle = PARASYMP ONLY

57
Q

Open-angle glaucoma…treatments of choice?

Is this a slow or fast onset of disease?

A
  • *Latanoprost (PG analog – increases outflow)
  • *Beta-blockers (Timolol) (inhibit production)

Slow

58
Q

Closed-angle glaucoma…treatments of choice?

Is this a slow or fast onset of disease?

A

**Acetazolamide (decreases production)
Mannitol (increases drainage)
Pilocarpine (increases drainage)

Fast

59
Q

Pupil constriction
Airway constriction
BV dilation

A

Muscarinic agonism (ex. Pilocarpine)

60
Q

Mecamylamine

A

Ganglion blocker

61
Q

Major drugs with a side effect of hyperuricemia (3)

Why?

A

Aspirin, loop diuretics, thiazide diuretics

Compete for weak acid secretion at the PCT w/ urate

62
Q

Potassium sparing diuretics

A

Amiloride, Triamterene

63
Q

Aldosterone receptor antagonists

A

Spironolactone, eplerenone

64
Q

Renal side effect of Lithium

How?

Treatment? Why?

A

Nephrogenic diabetes insipidus

Enters principal cells via NAC, then block V2 receptors

Amiloride - blocks uptake through NAC

65
Q

Spironolactone vs. Eplerenone - side effects

A

Spironolactone - hirsutism/gynecomastia (AR agonist)

Eplerenone - no androgen side effects

66
Q

Patient with tinnitus or fullness sensation in ear. Recently started being treated for heart failure. Drug class?

Drugs that increase this risk?

A

Loop diuretics

Aminoglycosides

67
Q

Calcineurin inhibitor

How does it work?

Side effects?

A

Cyclosporin

Binds cyclophilin and inhibits IL-1 and IL-2 production and T-cell activation

Nephrotoxicity, severe hypertension, gingival hyperplasia, hyperlipidemia, hyperglycemia

68
Q

Ulcerative stomatitis side effect…cancer drug?

A

Methotrexate

69
Q

Nephrogenic DI…drug of choice?

Explain

A

Thiazides

Decrease Na+ levels in the blood –> compensatory increase in reabsorption in the proximal tubular –> water follows

70
Q

Function of thiazides on vessels and insulin

A

**Hyperpolarize SM –> vasodilation (long term)

Hyperpolarize beta cells –> decreased insulin

71
Q

MoA…

  • Flutamide
  • Leuprolide
  • Octreotide
  • Finasteride
A

Flutamide = androgen receptor competitive antagonist

Leuprolide = GnRH analog

Octreotide = somatostatin analog

Finasteride = 5-alpha reductase inhibitor (BPH)

72
Q

Why do thiazides cause hyperglycemia (part of hyperGLUC)?

Can loop diuretics do this?

A

Hypokalemia –> decreased insulin secretion –> increased blood glucose

Yes, but not as much

73
Q

Aliskiren..MoA

A

Renin antagonist

74
Q

6-mercaptopurine…activated into what?

2 enzymes needed for metabolism of these drugs?

So?

What is contraindicated in these patients?

A

Azathioprine

HGPRT, X.O.

Must reduce dose if taking allopurinol or febuxostat

Live virus vaccines (b/c decreased T-cell immunity)

75
Q

Binds to 30S ribosome and inhibits binding of aminoacyl-tRNA

Uses?

A

Tetracyclines

Cholera, lyme disease, acne, Rickettsia, others…

76
Q

Prevention of initiation complex, causing mRNA misreading and inhibiting protein synthesis

Side effects?

A

Aminoglycosides

Nephrotoxic, ototoxic, teratogen

77
Q

Inhibition of DNA gyrase (topoisomerase 2), preventing negative supercoils

Side effects?

A

Fluoroquinolones

Tendon rupture, arthropathy, phototoxic, CNS stimulation

78
Q

When are ACEI’s and ARB’s BAD for the kidney?

A

Renal artery stenosis –> decreased GFR –> renal failure

79
Q

Calcium channel blockers…how to remember?

How to remember where these work?

A

“VD Dipines” – Verapamil, Diltiazem, Amlodipine

In order of HEART –> VESSELS

  • Verapamil = most cardiac
  • Dipines = most vascular
80
Q

Gingival hyperplasia…drugs?

A
  • Cyclosporin
  • Phenytoin
  • Dipines (CCBs)
81
Q

Functions of alpha-1 antagonists (-zosin)

A
  • Arteriolar dilation

- VENOUS dilation

82
Q

Side effects of alpha-1 blockers (3)

A
  • First dose syncope
  • Orthostatic hypotension (bc of VENOUS dilation)
  • Urinary incontinence
83
Q

Function of alpha-2 agonists

Uses? (3)

A

DECREASE sympathetic outflow (POWERFUL)

  • HTN
  • Opiate withdrawal (clonidine)
  • HTN management in pregnancy (methyldopa)
84
Q

Side effect of methyldopa

A

Hemolytic anemia (positive Coombs test)

85
Q

Function of Hydralazine

MoA?

Side effect?

A

ARTERIOLAR dilation ONLY

Via N.O.

Drug-induced SLE

86
Q

Functions of Nitroprusside

MoA?

Use?

Side effect?

A

Arteriolar AND venule dilation

Via N.O.

HTN emergencies

Cyanide poisoning

87
Q

Minoxidil, Diazoxide

A

K+ Channel agonists –> ARTERIAL dilation ONLY

88
Q

Side effects of minoxidil and diazoxide (useful ones)

A
  • Hypertrichosis (minoxidil – used for baldness)

- Hyperglycemia (diazoxide – used for insulinoma)

89
Q

Angina + HTN…drugs to use?

A

Beta blockers, CCBs

90
Q

Diabetes + HTN…drugs to use?

A

ACEIs, ARBs

91
Q

HF + HTN…drugs to use?

A

ACEIs, ARBs, Beta blockers

92
Q

Post-MI + HTN…drugs to use?

A

Beta blockers

93
Q

BPH + HTN…drugs to use?

A

Alpha blockers

94
Q

**HTN drugs contraindicated in dyslipidemias

A

Beta blockers, thiazides (both raise lipid levels)

95
Q

Treatment mechanism for pulmonary hypertension

Drugs and mechanisms? (3)

A

Vasodilation

  • Bosentan (endothelin blocker)
  • Epoprostenol (PGI2)
  • **Sildenafil (PDE-5 inhibitor)
96
Q

5 strategies to treating heart failure

A
  • Decrease sympathetics (control it)
  • Decrease afterload (ACEIs, ARBs, arterial dilators)
  • Decrease preload (diuretics, ACEIs, ARBs, venodilators)
  • Increase contractility (Digoxin, beta agonists)
  • **Stopping cardiac remodeling (ACEI’s, ARBs, Spironolactone, beta blockers)
97
Q

How to substitute if you can’t take ACEIs/ARBs?

A

Hydralazine (arteriolar dilation) + Nitrate (venous dilation)

98
Q

MoAs of Metoclopramide

Contraindicated in who?
What else is contraindicated in these people? (3)

A
  • Sensitizes tissues to acetylcholine (ex. GI smooth muscle)
  • Blocks dopamine receptors (anti-emesis)

Mechanical GI obstruction
Senna (GI stimulants), CCBs (Verapamil), anticholinergics

99
Q

Function of dopamine and dobutamine on the heart?

Use?

Side effect?

A

Activates beta-1 receptors –> opening of Ca++ channel –> increase contractility

ACUTE heart failure ONLY

Tachyphylaxis (quick loss of response)

100
Q

What type of PDE functions in the heart?

Drugs that block that?

A

PDE type 3

Inamrinone, Milrinone

101
Q

2 functions of Digoxin
Benefits of each?

Side effects to note?

A
  • DIRECT = increase heart contractility (CHF)
  • INDIRECT = increase vagal output (SVTs)

Blurry yellow vision, halos around lights, bad arrhythmias

102
Q

Intermittent claudication…drug to use?

MoA?

Contraindication?

A

Cilostazol

PDE3 inhibitor

CHF – increased mortality

103
Q

Drugs that work on the ventricular action potential (MoAs)

Which parts of the EKG do they control?

Used for what types of arrhythmias?

A

Na+ channel blockers – prolong phase 0 – prolong QRS
K+ channel blockers – prolong phase 3 – prolong QT

For VENTRICULAR arrhythmias

104
Q

See “rhythm control” drugs…think what?

A

Ventricular control (Na+ or K+ channel blockers)

105
Q

Drugs that work on the SA/AV node action potential (MoAs)

Which part of the EKG do they control?

Used for what type of arrhythmias?

A

Calcium channel blockers – prolong phase 4
Beta blockers – prolong phase 4

PR interval

SVTs

106
Q

Function of carotid massage and valsalva on the heart

A

Increase vagal firing –> PSNS on the heart –> slow SVTs

107
Q

Polymorphic ventricular tachycardia…other name?

Caused by what?

Drugs that do this?

A

Torsades de pointes

Prolonging the QT

K+ channel blockers

108
Q

Quinidine…

  • Class?
  • Additional bad effects?

Side effects?

A

Class 1A – Na+ and K+ channel blockers

  • Muscarinic block –> increased HR
  • Alpha-1 block –> reflex tachycardia
  • Displaces digoxin, increasing its toxicity
  • Cinchonism (GI, **tinnitus, ocular issues, CNS excitation)
  • Hypotension (alpha-1 block)
  • Torsades (increased QT)
109
Q

MoAs of Class 1B antiarrhythmics

Do NOT cause what?

Classic drug?

A
  • Block inactivated Na+ channels in hypoxic/ischemic tissue
  • Block slow Na+ channels in phase 4, increasing recovery

NO TORSADES (unlike Class 1A)

Lidocaine

110
Q

Use for Lidocaine

Oral version?

A

V tach

Mexiletine

111
Q

MoA of Class 1C antiarrhythmics

Drug?

Use?

Contraindication?

A

Block fast Na+ channels in His-Purkinje tissues

Flecainide

A-fib – RHYTHM control (not rate)

Ventricular tachycardia

112
Q

Class 2 antiarrhythmics

Use?

Unique one?

A

Beta blockers

SVTs (prolong PR interval)

Esmolol - super short - used for ACUTE treatment only

113
Q

Class 3 antiarrhythmics

MoA?

Why do they prolong the effective refractory period?

A

K+ channel blockers

Prolong phase 3 repolarization –> prolong QT interval

Prevent voltage-gated Na+ channel re-opening b/c preventing repolarization

114
Q

Amiodarone - class?

MoA?

Use?

Side effects? (5)

A

Class 3 (K+ channel blockers)

Mimics ALL classes (Na, Ca, K, and beta blocker)

ALL ARRHYTHMIAS

Pulmonary fibrosis, hepatic necrosis, thyroid dysfunction, blue skin, corneal deposits

115
Q

Benefits of Dronedarone over Amiodarone

A

No iodine = no blue skin or thyroid problems

116
Q

Sotalol - class?

MoAs?

Side effect?

A

Class 3 (K+ channel blockers)

Beta blocker w/ K+ channel blocker too – slows phase 3 and HR and AV conduction

TORSADES (MOST likely)

117
Q

Class 4 – MoA

Results?

Drugs?

Use?

A

Ca++ channel blockers

Slow phase 0, phase 4, SA and AV nodal conduction

Verapamil, Diltiazem

SVTs

118
Q

Adenosine - MoA

Half life?

Use? What else can be tried first?

A

Activates adenosine receptors in SA/AV NODES – Gi causes K+ efflux and hyperpolarization

10 seconds

Paroxysmal SVTs – carotid sinus and valsalva first

119
Q

SVTs - drugs?

VTs - drugs?

A

Class 2, Class 4, Adenosine, Digoxin

Class 1, Class 3

120
Q

A. fib - treatments

Rhythm control?

A
  • Rate control
  • Anticoagulation

Flecainide (1C)

121
Q

Wolff-Parkinson-White…treatment idea?

A

Slow the fast muscle action potential (class 1)

122
Q

Treatments for stable angina

A

Nitrates - vasodilation (BUT reflex tachycardia)
**Beta blockers – slow heart, reduce oxygen demand rise
CCBs (VD) – slow heart, reduce oxygen demand rise

123
Q

Treatments for vasospastic angina

A

Nitrates - vasodilation

CCBs (DIPINES) - vasodilation

124
Q

Drugs used in stable angina NOT used in vasospastic

A

Beta blockers (don’t vasodilate, might vasoconstrict)

125
Q

Why do M3 receptors cause RELAXATION of vessels?

A

Coupled to N.O. synthase, which causes NO to go into the muscle, cause cGMP rise, causing muscle relaxation

126
Q

How to prophylax for attacks of stable angina?

MoA?

A
  • Transdermal nitroglycerine
  • Isosorbide nitrates

NO –> cGMP –> dephosphorylation of MLC (inactivation)

127
Q

How do PDE5 inhibitors work?

Why not take with nitrates?

A

Decrease inactivation of cGMP –> more dephosphorylation of MLCK –> more vascular relaxation

Nitrates work the SAME way

128
Q

Angina drug that is contraindicated in long QT

A

Ranolazine

129
Q

Why does cAMP cause SM relaxation?

Why does cGMP cause SM relaxation?

Why do CCBs cause SM relaxation?

A

PKA –> phosphorylated MLCK –> can’t activate MLC

PKG –> phosphatase –> dephosphorylate MLC –> inactive

No Ca+ –> no Ca-Calmodulin –> no MLCK activation

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