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Pharm 1 Jack > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

enteral

A

absorbed through the GI tract

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2
Q

parenteral

A

given outside of the GI tract

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3
Q

PO

A

oral

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4
Q

PR

A

rectal

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5
Q

SL

A

sublingual

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6
Q

IV

A

intravascular or intravenous

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7
Q

IM

A

intramuscular

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8
Q

SC or SQ

A

subcutaneous

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9
Q

advantage of parenteral route

A

more rapid and predictable absorption, useful in unconscious or vomiting person

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10
Q

disadvantage of parenteral admin

A

needs to be aseptic, could cause pain/irritation, can’t give insoluble drugs via IV, much harder to “take back” a dose once given

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11
Q

what sort of drug will more readily cross plasma membranes

A

small, non-ionized, lipid soluble drugs

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12
Q

when a drug is absorbed via GI tract what does it go through before entering the systemic circulation

A

portal circulation aka first pass hepatic metabolism

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13
Q

what happens if a drug is rapidly metabolized in the liver

A

a smaller amount of the drug in the original unchanged state will reach the target tissues

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14
Q

what kind of drug can the kidney not efficiently eliminate

A

lipid soluble, so they are reabsorbed from kidney back into systemic circulation

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15
Q

Phase I drug metabolism involves

A

converting lipid soluble molecules into water soluble by introducing or unmasking a polar group (-OH or -NH2)

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16
Q

Phase I reaction are most frequently catalyzed by

A

cytochrome P450

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17
Q

Phase II reactions consist of

A

conjugation, wherein an endogenous polar group is added to a drug molecule (ex: glucuronic acid, sulfuric acid, acetic acid, amino acid) so that it can be excreted from the kidney

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18
Q

bioavailability is

A

fraction of administered drug that reaches systemic circulation in an unchanged form…(if 100 mg of a drug is taken orally and 70 mg of the drug is absorbed unchanged, then the bioavailability of that drug is 70%)

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19
Q

half life is

A

the amount of time required for the plasma concentration of a drug to decrease by 50% after discontinuation of a drug

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20
Q

a loading dose is

A

an initial dose of drug that is higher then subsequent doses for the purpose of rapidly achieving therapeutic drug concentrations in the serum.

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21
Q

efficacy refers to

A

the degree to which a drug is able to induce maximal therapeutic effects. Efficacy is a term often used to compare drugs of different classes.

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22
Q

potency is

A

the amount of drug required to produce 50% of the maximal response that the drug is capable of inducing. Potency is a term more frequently used to compare drugs of a similar class.

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23
Q

the EC50 or effective concentration 50 is

A

the concentration or dosage of an agent which induces a specified clinical effect in 50% of the subjects to which the drug has been administered.

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24
Q

LD50 or lethal dose 50 is

A

the concentration or dosage of an agent or drug which causes death in 50% of the subjects to which that agent or drug has been administered.

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25
Q

therapeutic index (TI) is

A

a ratio of the dose of a drug that produces toxicity relative to the dose of the same drug that produces a clinically desired response. Looked at as an equation, this would be T.I. = LD50 / EC50…thus a measure of the drug’s safety. A large value indicates that there is a wide margin between an effective dose and a toxic dose.

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26
Q

competitive antagonists

A

interact with the receptors at the same site as the agonist and thus compete for binding with the agonist. (May be reversible or irreversible)

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27
Q

noncompetitive antagonists

A

bind to a site other then the agonist binding domains. (Effects generally irreversible)

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28
Q

physiologic antagonism

A

refers to two agonists in unrelated reactions which cause opposite effects.

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29
Q

neutral antagonism

A

refers to a process in which two drugs bind to one another which serves to inactivate or partial inactivate each of the drugs.

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30
Q

CI drug

A

no approved medical use

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31
Q

CII drug

A

high potential for abuse

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32
Q

CIII drug

A

moderate potential for abuse

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33
Q

CIV drug

A

low potential for abuse

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34
Q

X drug

A

contraindicated in pregnancy

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35
Q

q

A

every

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36
Q

qH

A

every hour

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37
Q

qAM

A

every morning

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38
Q

qPM

A

every evening

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39
Q

qHS

A

every bedtime

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40
Q

qD

A

every day

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41
Q

qOD

A

every other day

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42
Q

BID

A

two times a day

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43
Q

TID

A

three times a day

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44
Q

QID

A

four times a day

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45
Q

_xD

A

_ times a day

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46
Q

qWK

A

every week

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47
Q

qMO

A

every month

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48
Q

PRN

A

as needed

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49
Q

Stage 2 HTN

A

160-179/100-109

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50
Q

Stage 3 HTN

A

> 180/110

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51
Q

Most common cause of chronic renal disease

A

HTN

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52
Q

Primary HTN etiology

A

unknown

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53
Q

What catalyzes angiotensinogen to angiotensin I

A

renin, a proteolytic enzyme formed in the granules of juxtaglomerular cells

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54
Q

Angiotensin I goes to Angiotensin II by being cleaved by

A

ACE (angiotensin converting enzyme) which is found mostly in the lungs but also the kidneys and brain and elsewhere

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55
Q

most potent vasoconstrictor produced by the body

A

angiotensin II

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56
Q

in response to HTN the smooth muscle cells surrounding and within arterioles develop

A

hypertrophy and hyperplasia which causes artery lumen size to decrease

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57
Q

most common side effect of hypertensive drugs is

A

hypotension

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58
Q

two/three classifications of diuretics

A

potassium wasting, potassium sparing, combination of the two

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59
Q

how do thiazide diuretics work

A

increase sodium and water excretion into urine by inhibiting sodium and chloride reabsorption in the cortical thick ascending limb and early distal tubule

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60
Q

side effect on minerals when taking thiazide diuretics

A

can cause calcium and uric acid to be reabsorbed by proximal tubule in increased amounts…so serum levels of calcium and uric acid rise

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61
Q

thiazide diuretics are best used for

A

initial treatment of mild HTN, particularly in the setting of chronic edema

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62
Q

how are thiazide diuretics delivered

A

oral route

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63
Q

onset of action for thiazide diuretics

A

1 hour

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64
Q

thiazide diuretics are often used in conjunction with

A

other HTN meds like beta blockers and ACE inhibitors

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65
Q

side effects of thiazide diuretics

A

hypotension, weakness, dizziness, hyponatremia, hypokalemia, hypercalcemia, hyperuricemia, glucose intolerance, hypercholesterolemia, and hypertriglyceridemia

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66
Q

Primary thiazide diuretic

A

hydrochlorthiazide (HCTZ)/hydrodiuril

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67
Q

indication for hydrochlorthiazide/hydrodiuril

A

HTN, chronic edema, hypocalcemia when due to excessive urinary loss of calcium

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68
Q

MOA of hydrochlorthiazide/hydrodiuril

A

inhibition of sodium and chloride reabsorption in ascending limb and distal tubule

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69
Q

Char of hydrochlorthiazide/hydrodiuril

A

PO, rapid absorption

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70
Q

dose for hydrochlorthiazide/hydrodiuril

A

25-100 mg per day in single or divided doses

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71
Q

what supplement is generally recommended when taking hydrochlorthiazide/hydrodiuril

A

potassium

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72
Q

hydrochlorthiazide/hydrodiuril should not be used by

A

patients with a sulfa allergy, they contain a sulfonamide moiety

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73
Q

thiazide diuretics are not effective in patients with

A

renal failure

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74
Q

main loop diuretic

A

furosemide/lasix

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75
Q

what do loop diuretics do

A

inhibit chloride reabsorption in the ascending loop of Henle by blocking the Na+/K+/Cl- co-transporter system

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76
Q

stronger diuretic: loop diuretics or thiazide

A

Milligram for milligram, thiazides have a lesser diuretic action than the loop diuretics…This is because the loop of Henle plays a greater role in sodium resorption than does the thick ascending limb and distal tubule

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77
Q

what happens at the thick ascending limb

A

thick ascending limb is a major site of calcium and magnesium reabsorption, processes which are dependent on normal sodium and chloride reabsorption

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78
Q

loop diuretics can increase the loss of

A

sodium, potassium, calcium, and magnesium

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79
Q

the use of a loop diuretic can potentially cause electrolyte abnormalities such as

A

hyponatremia, hypokalemia, hyperglycemia (presumed due to impaired insulin release), hypocalcemia, hypomagnesemia and hyperuricemia

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80
Q

initial onset of action for loop diuretics

A

20-30 min (half life of 1-1.5 hours)

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81
Q

loop diuretics are the prefered diuretic in patients with

A

renal disease (low GFR) and in hypertensive emergencies

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82
Q

loop diuretics are useful in conditions that are refractory to less potent diuretic, for example

A

CHF, renal insufficiency, and nephrotic syndrome…can also be used to treat hypercalcemia since they increase calcium excretion

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83
Q

who should loop diuretics be used with caution in

A

patients who are more likely to be susceptible to volume contraction (hypovolemia) and patients prone to dehydration

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84
Q

indication for furosemide/lasix

A

HTN, acute or chronic edema, hypercalcemia. Preferred diuretic in hypertensive patients with renal disease.

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85
Q

MOA of furosemide/lasix

A

inhibition of sodium and chloride reabsorption in the loop of henle

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86
Q

char of furosemide/lasix

A

PO/IV rapid absorption

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87
Q

side effects of furosemide/lasix

A

may potentiate orthostatic hypotension, contains a sulfonamide moiety and shouldn’t be used with patients who have sulfonamide allergies. Not effective in patients with renal failure.

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88
Q

average dose for potassium replacement

A

10 mEq which is equal to 750 mg of microencapsulated potassium chloride, USP.

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89
Q

what do potassium sparing diuretics do

A

increase sodium excretion and inhibit potassium secretion in the distal convoluted tubule

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90
Q

examples of disease states the potassium sparing diuretics should not be used with

A

severe renal insufficiency, poorly controlled DM, and multiple myeloma

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91
Q

drugs that can cause hyperkalemia

A

ACE inhibitors and Angiotensin II receptor blockers

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92
Q

primary potassium sparing diuretic

A

spironolactone/aldactone

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93
Q

indication for spironolactone/aldactone

A

HTN, chronic edema, hypercalcemia. May be used in patients with renal disease but not anuric patients. Used to treat hyperaldosteronism. Has anti-androgenic properties and is thus used to treat hirsutism and PCOS

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94
Q

MOA of spironolactone/aldactone

A

inhibits sodium and chloride reabsorption while promoting potassium reabsorption in the distal tubule…also a direct antagonist of aldosterone so it helps increase urinary sodium loss and reduce vascular volume

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95
Q

Char of spironolactone/aldactone

A

takes up to 1 to 2 days before increased diuresis (half life 1-1.5). Can’t be given with other classes of diuretics. Not effective in patients with renal failure.

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96
Q

Side effects of spironolactone/aldactone

A

hyperkalemia, avoid with patients on potassium supplementation/ACE inhibitors/ARBs

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97
Q

beta blockers reduce blood pressure by

A

reducing adrenergic receptors in the heart (B1) thereby decreasing cardiac output. Non-selective beta blockers also diminish peripheral vasoconstriction by reducing adrenergic input at B-2 receptor sites on smooth muscle surrounding the peripheral vasculature.

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98
Q

prototype B-blocker

A

propranolol/inderal

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99
Q

propranolol acts at

A

B-1 and B-2 receptor sites

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100
Q

beta blocker atenolol/tenormin acts at

A

B-1 receptors (selective)

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101
Q

selective B-1 receptor blockage helps to avoid

A

potential for bronchospasm that may result when B-2 receptors are blocked

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102
Q

even cardioselective B-blockers are contraindicated in patients with

A

severe asthma or COPD who are known to have a prominent bronchospastic component that is sensitive to beta blockade

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103
Q

disadvantage of B-blockers include

A

high incidence of adverse CNS affects, sexual dysfunction in men/women, and bradycardia

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104
Q

contraindications of beta blockers include

A

certain cardiac conduction abnormalities, severe asthma, and severe COPD

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105
Q

abrupt withdrawal of beta blockers can result in

A

rebound HTN and/or rebound tachycardia, probably due to up-regulation of beta receptors during treatment…can result in MI or stroke

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106
Q

overdose of a beta blocker can result in

A

bradycardia and heart block

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107
Q

treatment of choice to reverse bradycardic effects of a beta blocker is

A

the hormone glucagon

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108
Q

MOA for glucagon to reverse B-blocker

A

increase of cAMP in myocardium, effectively bypassing the B-adrenergic second messenger system

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109
Q

class of propranolol/inderal

A

non-selective beta blocker (B-1 and 2)

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110
Q

indication of propranolol/inderal

A

HTN, angina and acute MI, tachyarrhythmias, migraine headache prophylaxis, essential tremors

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111
Q

MOA of propranolol/inderal

A

adrenergic blockage at beta receptors

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112
Q

Char of propranolol/inderal

A

PO, IV. There’s also oral time-released form that is longer acting i.e. Inderal LA.

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113
Q

Side effect of propranolol/inderal

A

may potentiate orthostatic hypotension especially if mixed with alcohol or narcotic analgesics. Weakness, fatigue, depression, sexual dysfunction.

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114
Q

Atenolol/tenormin class

A

Beta 1 blocker (cardioselective)

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115
Q

indication of atenolol/tenormin

A

HTN, angina and acute MI, and several forms of tachyarrhythmia. Atenolol is indicated in the management of hemodynamically stable patients with definite or suspected acute MI to reduce cardiovascular mortality.

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116
Q

MOA of atenolol/tenormin

A

adrenergic blockage at the beta 1 receptor sites

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117
Q

Char of atenolol/tenormin

A

PO, IV. Peak blood levels are usually reached between 2 and 4 hours after ingestion. Follow pulse rate.

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118
Q

side effects of atenolol/tenormin

A

cardioselective effect is not absolute and at higher doses, blockage of beta 2 receptors can occur. Contraindicated in certain arrhythmias and heart blocks. Use cautiously in combo with calcium channel blockers.

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119
Q

first line treatment of HTN by the books

A

diuretics

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120
Q

first line treatment of HTN in conventional clinical practice

A

ACE inhibitors and calcium channel blockers

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121
Q

two ways asthma meds work

A

relax bronchial smooth muscle, reduce inflammation

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122
Q

sympathetic (adrenergic) tone causes ___ in the lungs

A

bronchodilation

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123
Q

parasympathetic (cholinergic) tone causes ___ in the lungs

A

bronchoconstriction

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124
Q

treatment for acute asthmatic attacks that are unresponsive to other medications

A

epinephrine (adrenalin)

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125
Q

how does epinephrine work

A

non-selective adrenergic agonist that binds to alpha, beta-1, and beta-2 receptors. Causes cardiac stimulation via beta-1 receptors resulting in possible tachycardia, palpitations, and potential arrhythmias.

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126
Q

class of epinephrine

A

adrenergic agonist

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127
Q

indication of epinephrine

A

emergent treatment of asthma, status asthmaticus, anaphylaxis

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128
Q

MOA of epinephrine

A

Powerful β-2 agonist activity results in increased cAMP. Increased cAMP causes immediate relaxation of bronchial smooth muscle cells and resultant bronchodilation

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129
Q

Char of epinephrine

A

SQ, IV, IM, inhalation, endotracheal tube administration. Rapid onset of action but brief duration of action.

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130
Q

what is primatene mist

A

OTC preparation containing a very low dose of epinephrine

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131
Q

side effects of epinephrine

A

tachycardia, increased cardiac demand, anxiety, dry mouth (alpha 1 effect) and hyperglycemia

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132
Q

class of albuterol/ventolin, proventil

A

beta 2 agonist

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133
Q

indication of albuterol/ventolin, proventil

A

treatment of acute, uncomplicated asthma symptoms

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134
Q

MOA of albuterol/ventolin, proventil

A

Bronchodilation via β2 adrenergic receptor stimulation, increased cAMP levels and resultant bronchial smooth muscle relaxation

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135
Q

Char of albuterol/ventolin, proventil

A

Inhaled route results in onset of action in ~15 minutes with a duration of action of 3-4 hours. PO route has onset of action of ~ 30 minutes and a duration of action of 4-8 hours. Average dose is 2 puffs orally, 3 to 4 times a day

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136
Q

side effects of albuterol/ventolin, proventil

A

Although promoted as a β-2 selective agonist, β-1 agonist activity is also reported with predictable potential side effects of tachycardia, palpitations, anxiety, etc. Beta blockers inhibit activity. No anti-inflammatory effects.

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137
Q

class of salmeterol/severent

A

long acting beta 2 agonist

138
Q

indication of salmeterol/severent

A

chronic treatment of asthma or bronchospasm. Not for treatment of acute asthma.

139
Q

MOA of salmeterol/severent

A

bronchodilation via Beta-2 adrenergic receptor stimulation

140
Q

Char of salmeterol/severent

A

inhaled only. Onset of action about 20-30 min with a duration of action of 12 hours. Usually dosed twice daily.

141
Q

Side effects of salmeterol/severent

A

headache, cough,. Beta blockers inhibit activity.

142
Q

how do anticholinergic drugs work

A

competitive antagonists at muscarinic acetylcholine receptor sites. Antagonism results in unopposed sympathetic tone in the airways with resultant smooth muscle relaxation and bronchodilation.

143
Q

when are anticholinergic drugs typically indicated

A

generally not indicated for acute asthma attacks but rather for maintenance therapy in asthma patients who cannot tolerate treatment with a beta agonist

144
Q

primary anticholinergic drug

A

ipratropium/atrovent

145
Q

what do leukotriene inhibitors do

A

antagonism of leukotriene receptor sites in bronchial wall smooth muscle

146
Q

class of zafirlukast/accolate

A

leukotriene receptor antagonist

147
Q

indication of zafirlukast/accolate

A

prophylaxis and treatment of chronic asthma

148
Q

MOA of zafirlukast/accolate

A

Competitive antagonism of leukotriene D4 and E4 receptors result in inhibition of bronchoconstriction and inflammation. Not indicated for reversal of bronchospasm in acute asthma attacks

149
Q

Char of zafirlukast/accolate

A

PO. Well absorbed. Peak levels in 3 hours. Inhibits cytochrome P450 enzymes. Effects are somewhat similar to those expected with Cromolyn

150
Q

Side effects of zafirlukast/accolate

A

headache, GI distress, diarrhea, older patients may have increased incidence of respiratory infections

151
Q

how do corticosteroids work

A

inhibition of phospholipase A2 blocks release of arachadonic acid, the precursor of the prostaglandins and leukotrienes from membrane bound phospholipids. Histamine release and kinin activity is also suppressed by glucocorticoids.

152
Q

side effects of glucocorticoides include

A

reduced resistance to infections, hyperglycemia, severe bone loss, avascular necrosis, cataracts, myopathy, thinning of skin, diminished wound healing, insomnia and mental status changes

153
Q

primary inhaled steroid

A

beclomethasone/beclovent, vanceril

154
Q

class of beclomethasone/beclovent

A

corticosteroid

155
Q

indication of beclomethasone/beclovent

A

asthma not controlled by sympathomimetics (bronchodilators) alone

156
Q

MOA of beclomethasone/beclovent

A

decreased inflammation and edema in the respiratory tract via reduction in number and activity of macrophages, eosinophils, and T-lymphocytes. Mucosal edema reversed by decreasing the permeability of capillaries and inhibiting the release of leukotrienes. No direct effect on airway smooth muscle.

157
Q

Char of beclomethasone/becolvent

A

Similar to the beta adrenergic drugs, the inhaled route of steroids allows for fewer systemic side effects. However, it is also common for ~90% of total amount inhaled to be deposited in mouth and larynx and only ~10% directly deposited in airways. Placement of “spacer” may allow for improved delivery

158
Q

Side effects of beclomethasone/beclovent

A

Inhaled steroids generally have fewer side effects then P.O. steroids. Oropharyngeal yeast infection or thrush can occur. Rinsing mouth after inhaler use can help to reduce incidence of thrush. The potential for adrenal suppression is small but does exist

159
Q

Class of prednisone/deltasone

A

corticosteroid

160
Q

indication for prednisone/deltasone

A

COPD, worsening asthma

161
Q

MOA of prednisone/deltasone

A

decrease inflammation and edema in respiratory tract

162
Q

Char of prednisone/deltasone

A

PO, (IV and IM corticosteroids are also available). Steroids must be considered as adjunct therapy and discontinued as soon as possible. Dose 10 to 100 mg 1 to 2 times daily

163
Q

side effects of prednisone/deltasone

A

Salt and water retention, fat gain and redistribution, hyperglycemia and diabetes, osteoporosis and pathologic fractures, adrenal suppression. Abrupt withdrawal of prednisone or other drugs with corticosteroid properties may result in severe and potentially life threatening hypofunction of the adrenal glands, also known as Addisonian crisis.

164
Q

What’s significant about theophylline/theo-dur

A

bad TI, lethal dose is not far from effective dose

165
Q

class of theophylline/theo-dur

A

xanthine or methylxanthine bronchodilators

166
Q

MOA of theophylline/theo-dur

A

no exactly known but one mechanism is the inhibition of phosphodiesterase, the enzyme which breaks down cAMP

167
Q

two narcotic analgesic antitussives

A

codeine and hydrocodone…decrease sensitivity of response in cough centers that exist within CNS

168
Q

class of codeine

A

narcotic analgesic and cough suppressant

169
Q

indication for codeine

A

pain relief, cough suppression

170
Q

MOA of codeine

A

suppresses the sensitivity of CNS cough centers in the medulla

171
Q

Char of codeine

A

PO. Onset of action generally within 30 to 60 min. Often formulated with an antihistamine in a syrup. Usual dose 1 to 2 tsp every 4-6 hours.

172
Q

Side effects of codeine

A

drowsiness, constipation, GI upset, potential for drug dependence

173
Q

Class of dextromethorphan

A

synthetic derivative of morphine

174
Q

indication of dextromethorphan

A

cough suppression

175
Q

MOA of dextromethorphan

A

suppresses the sensitivity of CNS cough centers

176
Q

Char of dextromethorphan

A

PO. Onset of action 30-60 minutes. No analgesic or addictive potential. Less constipating then the narcotic based antitussives. Often formulated with an antihistamine in a syrup. Usual dose 1 to 2 tsp every 4 to 6 hours.

177
Q

class of diphenhydramine/benadryl

A

antihistamine

178
Q

indication of diphenhydramine/benadryl

A

allergic rhinitis and conjunctivitis, urticaria, pruritis, often to induce sleep

179
Q

MOA of diphenhydramine/benadryl

A

H1 receptor site blockage. The production and release of histamine is not blocked.

180
Q

Char of diphenhydramine/benadryl

A

PO, dose 25-100 mg every 6-8 hours. Readily crosses the blood brain barrier.

181
Q

side effects of diphenhydramine/benadryl

A

Variable degrees of sedation (recall that this drug class exhibits ready passage through the BBB), drying and thickening of secretions (which may actually worsen symptoms of asthma or sinusitis) and possible urinary retention…Think of this side effect profile whenever a pharmacologic agent is described as being anti-cholinergic.

182
Q

primary non-sedating antihistamine

A

loratadine/claritin

183
Q

class of loratadine/claritin

A

non-sedating antihistamine

184
Q

indication of loratadine/claritin

A

seasonal allergic rhinitis, hay fevere

185
Q

MOA of loratadine/claritin

A

H1 receptor antagonist

186
Q

Char of loratadine/claritin

A

Does not readily cross the BBB, thus little to no sedation. Usual dose is once a day.

187
Q

Side effects of loratadine/claritin

A

drying of secretions. Dry mouth is common.

188
Q

alpha agonist nasal spray (decongestants) often significant

A

rebound effects…so there is a high incidence of “dependence” (rhinitis medicosum)

189
Q

Smoking cessation meds in order of least to most effective

A

gum, lozenges, transdermal patches, oral, nasal spray

190
Q

Mechanisms of varenicline/chantix

A

partial agonist of alpha 4/beta 2 nicotinic acetylcholine receptor sites

191
Q

side effects of varenicline/chantix

A

increasing reports of neuro-psychiatric symptoms that range from nightmares or insomnia to depression and suicidal ideations to increased agitation and rage

192
Q

stimulation of alpha adrenergic receptors in the peripheral vasculature results in

A

vascoconstriction

193
Q

blockade of alpha blockers results in

A

reduced sympathetic tone, thereby causing vasodilation and decreased peripheral resistance

194
Q

alpha blockers also block alpha 1 receptors in the smooth muscle of the bladder neck and prostate so they help improve urine flow in people with

A

BPH

195
Q

primary alpha blocker

A

prazosin/minipress (alpha 1)

196
Q

class of prazosin/minipress

A

alpha 1 adrenergic blocker

197
Q

indication of prazosin/minipress

A

HTN, BPH

198
Q

MOA of prazosin/minipress

A

blockage of alpha 1 receptors

199
Q

Char of prazosin/minipress

A

PO. Vasodilation. Can relax tone in bladder neck.

200
Q

Side effects of prazosin/minipress

A

dizziness, H/A, orthostatic hypotension, impotency

201
Q

calcium channel blockers cause

A

dilation of both cardiac and peripheral vessels (mainly arterioles)

202
Q

calcium channel blockers are used for

A

treatment of HTN, angina, and cariac arrhythmias. Also used as prophylaxis of migraine headache and for Raynaud’s syndrome

203
Q

3 main classes of calcium channel blockers

A

Benzothiazepine, Diphenyl alklamine, Dihydropyridine

204
Q

Most common side effects of calcium channel blockers include

A

hypotension, dizziness, headache, and flushing of skin

205
Q

calcium channel blockers should be used with more caution in patients with

A

bradycardia or severe CHF

206
Q

class of verapamil/isopten

A

calcium channel blocker

207
Q

indication of verapamil/isopten

A

HTN, angina–especially vasospastic angina, CHF

208
Q

MOA of verapamil/isopten

A

blocks calcium influx with resultant peripheral vasodilation and improved myocardial tone

209
Q

Char of verapamil/isopten

A

PO, slow onset of action. Effects of peripheral vasodilation often useful in reducing both preload and afterload

210
Q

side effects of verapamil/isopten

A

Flushing, H/A, hypotension. Caution when using concurrently with beta blockers in terms of potential increased risk for bradycardia and possible arrhythmias. Upon the discontinuation of a calcium channel blocker, there is generally less risk for rebound hypertension then when discontinuing a beta blocker.

211
Q

long term use of calcium channel blockers is associated with increased risk for

A

developing breast cancer

212
Q

ACE inhibitors reduce BP by

A

interfering with the generation of Angiotensin II from Angiotensin I…also inhibit the degradation of bradykinins, allowing for another mechanism by which peripheral vascular resistance can be reduced

213
Q

ACE inhibitors are excellent first line agent in hypertensive patients with

A

congestive heart failure as well as hypertensive patients with diabetes

214
Q

what drug is considered least likely of the antihypertensive drugs to cause sexual dysfunction in males

A

ACE inhibitors

215
Q

How do ACE inhibitors affect serum lipids, glucose or uric acid levels

A

ACE inhibitors do not adversely affect

216
Q

ACE inhibitors can potentially increase serum

A

potassium

217
Q

ACE inhibitors are often the drug of choice in treating HTN patients with

A

diabetes…demonstrated an ability to slow development of diabetic nephropathy

218
Q

With ACE inhibitors, avoid concurrent use of

A

potassium sparing diuretic…but potassium wasting diuretics are quite commonly used in conjunction

219
Q

All ACE inhibitors have potentially adverse side effect of

A

dry irritating cough

220
Q

ACE inhibitors and pregnancy

A

contraindicated in pregnancy due to fetal pulmonary and developmental abnormalities

221
Q

Rare potential adverse effect of all ACE inhibitors that can be life threatening

A

Angioedema, life threatening when it involves the tongue and oropharyngeal area

222
Q

Primary ACE inhibitor

A

Lisinopril/Prinivil or Zestril

223
Q

Class of Lisinopril/Prinivil or Zestril

A

ACE inhibitor

224
Q

indication of

A

HTN, shown to improve mortality and morbidity in post-MI patients

225
Q

MOA of Lisinopril/Prinivil or Zestril

A

Blocks conversion of angiotensin I to angiotensin II, resulting in significant decrease in peripheral vascoconstriction

226
Q

Char. of Lisinopril/Prinivil or Zestril

A

often used concurrently with a potassium wasting diuretic

227
Q

Side effects of Lisinopril/Prinivil or Zestril

A

hypotension, potential hyperkalemia, contraindicated in pregnancy (category X). May cause dry, irritating cough. May cause severe and life threatening angioedema in susceptible patients.

228
Q

Angiotensin II receptor blockers are an excellent first line agent in HTN patients with

A

CHF as well as HTN patients with DM

229
Q

Do Angiotensin II receptor blockers block the degradation of bradykinins?

A

No

230
Q

Do Angiotensin II receptor blockers cause cough and angioedema?

A

Yes, although their potential to do so is less than ACEI

231
Q

Do Angiotensin II receptor blockers cause hyperkalemia?

A

Yes

232
Q

Precautions for use of ACE inhibitors

A

patients with hyperkalemia, hypovolemia, or severe renovascular disease. Strictly contraindicated in pregnant patient (category X)

233
Q

primary Angiotensin II receptor blocker

A

Losartan/Cozaar

234
Q

Class of Losartan/Cozaar

A

Angiotensin II receptor antagonist

235
Q

indication of Losartan/Cozaar

A

HTN, diabetic nephropathy with proteinuria

236
Q

MOA of Losartan/Cozaar

A

blocks the effects of Angiotensin II resulting in significant decrease in peripheral vasoconstriction

237
Q

Char. of Losartan/Cozaar

A

PO, often used along with a non-potassium sparing diuretic

238
Q

side effects of Losartan/Cozaar

A

hypotension, potential hyperkalemia, contraindicated in pregnancy. Persistent dry cough. Angioedema

239
Q

how do centrally acting alpha agonists work

A

stimulate the presynaptic alpha 2-adrenergic receptors in the CNS

240
Q

side effects of centrally acting alpha agonists

A

marked sedation, fatigue, orthostatic hypotension

241
Q

how do direct vasodilators work

A

cause arterial dilation by opening K+ channels in vascular smooth muscle cells

242
Q

example of a direct vasodilator

A

Minoxidil/Loniten

243
Q

Minoxidil is generally reserved for

A

severe hypertension, resistant to previous antihypertensive treatment attempts

244
Q

What is the more potent direct vasodilator: Minoxidil or Hydralazine?

A

Minoxidil is more potent than Hydralazine but it is associated with more adverse effects, including potential for marked sodium and water retention and hirsutism

245
Q

Unique side effect of minoxidil

A

hirsuitism

246
Q

hydralazine is generally reserved for

A

severe HTN resistant to previous antihypertensive treatment attempts

247
Q

Hydralazine can result in the side effect known as

A

drug induced lupus syndrome

248
Q

first drug FDA approved in new antihypertensive drug class known as direct renin inhibitors

A

Aliskiren (Tekturna)

249
Q

side effects of Aliskiren (Tekturna)

A

hypotension, headache, diarrhea, hyperkalemia, and angioedema

250
Q

principal action of IV nitroglycerin

A

vasodilation of both arteries and veins (veins more so)

251
Q

indication for IV nitroglycerin

A

manage HTN during and after coronary bypass, heart failure, acute MI, unstable angina pectoris and acute pulmonary edema

252
Q

What is IV sodium nitroprusside converted to in the body?

A

nitric oxide

253
Q

MOA of IV Labetalol

A

alpha-1 and beta adrenergic blocker

254
Q

the oral form of labetalol is indicated in

A

treatment of pregnancy induced HTN

255
Q

Prinzmetal angina occurs at

A

rest, rather than exertion

256
Q

three main classes of drugs that have proven very effective in treating patients with stable angina pectoris

A

nitrates, beta blockers, calcium channel blockers

257
Q

Nitric oxide, derived from nitrates, activate ___

A

guanyl cyclase and increase the intracellular cyclic GMP which results in vascular smooth muscle relaxation

258
Q

two main classes of nitrate drugs

A

nitroglycerin (ntg)/nitrostat and isosorbide dinitrate/isordil

259
Q

class of nitroglycerin/nitrostat

A

nitrate vasodilator

260
Q

indications of nitroglycerin/nitrostat

A

all forms of angina. may be used for acute relief of angina or prophylaxis of angina prior to increased exertional activtiy

261
Q

MOA of nitroglycerin/nitrostat

A

immediate vasodilation via production of nitric oxide. dilation of myocardial arteries increases blood supply to the myocardium. preload is reduced by reducing peripheral venous tone.

262
Q

Char. of nitroglycerin/nitrostat

A

SL, oral spray, topical paste, transdermal patch and I.V. routes. SL doses of reach peak levels in 1 to 2 minutes and have a duration of 30 to 60 minutes. Topical paste has onset of action in 30 to 60 minutes and a duration of 2 to 12 hours. Transdermal NTG reaches peak activity in 30 to 60 minutes and has a duration of action of 24 hours. IV NTG has an onset of action in 1 to 2 minutes and has a duration of action of 3 to 5 minutes.

263
Q

side effects of nitroglycerin/nitrostat

A

Headache, hypotension, rebound tachycardia. Alcohol, antihypertensives and vasodilators increase the risk of orthostatic hypotension. Use with Silendafil (Viagra) is contraindicated due to potential for causing severe hypotension.

264
Q

class of isosorbide dinitrate/isordil

A

long acting nitrate vasodilator

265
Q

indication of isosorbide dinitrate/isordil

A

angina, prophylaxis of angina

266
Q

MOA of isosorbide dinitrate/isordil

A

similar to NTG

267
Q

Char. of isosorbide dinitrate/isordil

A

SL, Oral. SL has onset of action by 5 min. with duration of action of 1 to 4 hours. Oral form has onset of action in 30 minutes with duration of 4 to 6 hours, up to 8 hours with sustained released forms. Not readily metabolized by the liver. Lower potency than nitroglycerin in relaxing vascular smooth muscle.

268
Q

Side effects of isosorbide dinitrate/isordil

A

headache, hypotension, rebound tachycardia. Concurrent use of alcohol, antihypertensives and vasodilators increase the risk of orthostatic hypotension. Concurrent use of Silendafil (viagra) and Isosorbide is contraindicated due to the potential for severe hypotension.

269
Q

beta blockers diminish cardiac oxygen demand by

A

decreasing both cardiac contractility and cardiac rate

270
Q

the occupation of cardiac beta 1 receptor sites by a beta blocking agent also acts to protect the heart from full effects of

A

sympathetic (nor-epinephrine and epinephrine) stimulation

271
Q

in patients with acute myocardial infarction, beta blockers have been shown to

A

decrease the size of the infarct

272
Q

the treatment of choice to reverse the bradycardic effects of a beta blocker is

A

hormone glucagon…likely mechanism is increase in cAMP in the myocardium, effectively bypassing the Beta-adrenergic second messenger system

273
Q

Class of propranolol/inderal

A

non-selective beta blocker

274
Q

indication of propranolol/inderal

A

angina, status-post myocardial infarction, hypertension, panic attacks, migraine headache

275
Q

MOA of propranolol/inderal

A

blocks adrenergic stimulation which serves to decrease heart rate and myocardial oxygen demand and also decreases renin release

276
Q

Char. of propranolol/inderal

A

PO, IV non selective beta blockade with potential for bronchoconstriction via antagonism of Beta 2 receptors in bronchi

277
Q

side effects of propranolol

A

Bronchoconstriction, hypotension, bradycardia, fatigue, impotence. Abrupt discontinuation may cause rebound hypertension and tachycardia with subsequent increase in myocardial oxygen demand. Abrupt discontinuation increases the risk of arrythmias, stroke, angina and M.I. Can increase the effects of calcium channel blockers.

278
Q

class of atenolol/tenormin

A

selective beta blocker

279
Q

indication of atenolol/tenormin

A

angina, HTN, MI

280
Q

MOA of atenolol/tenormin

A

decrease heart rate and myocardial oxygen demand by selective B1 adrenergic blockade

281
Q

Char. of atenolol/tenormin

A

PO and IV, PO decreased risk bronchoconstriction relative to non-selective beta blockers

282
Q

Side effects of atenolol/tenormin

A

similar to propranolol with less risk for bronchoconstriction

283
Q

treatment of choice to reverse the symptomatic effects of bradycardia of a calcium channel blocker is

A

calcium gluconate…but glucagon can be given if calcium gluconate increases pulse rate

284
Q

class of amlodopine/norvasc

A

calcium channel blocker

285
Q

indication of amlodopine/norvasc

A

angina–especially variant or vasospastic angina, HTN

286
Q

MOA of amlodopine/norvasc

A

blocks calcium influx with resultant vasodilation of ardiac and peripheral arteries. diminishes sympathetic induced coronary artery spasm

287
Q

Char of amlodopine/norvasc

A

PO, slow onset of action, 3 to 6 hours

288
Q

side effects of amlodopine/norvasc

A

flushing, headache, hypotension. calcium channel blockers can act synergistically with beta blockers with a resultant increased risk for hypotension and bradycardia

289
Q

what do you do with someone with unstable angina

A

administer MONA = morphine, oxygen, nitrate, aspirin

290
Q

standard analgesic in cases of unstable angina and/or myocardial infarction

A

morphine sulfate via IV

291
Q

how do you reverse morphine

A

Naloxone

292
Q

class of morphine sulfate

A

analgesic

293
Q

indication of morphine sulfate

A

pain relief, especially in setting of unstable angina or MI

294
Q

MOA of morphine sulfate

A

opiate receptor agonist

295
Q

Char of morphine sulfate

A

PO, IV, IM, SQ, PR. Mild vasodilator. Potent analgesis. Anxiolytic.

296
Q

Side effects of Morphine Sulfate

A

Potential for respiratory depression must be monitored. Potential for severe hypotension.

297
Q

class of aspirin/ASA

A

salicylate with anti-inflammatory analgesic and antipyretic properties

298
Q

indication for aspirin/ASA

A

Reduces the risk of M.I. in patients with unstable angina or prior infarction. Reduces risk of recurrent transient ischemic attacks and stroke.

299
Q

MOA for aspirin/ASA

A

Irreversibly inhibits cyclooxgenase enzyme. Inhibition of cyclooxgenase prevents the formation of thromboxane A2 and prostaglandins with resultant diminished platelet aggregation.

300
Q

Char of aspirin/ASA

A

P.O., adult dose - 325 mg, children’s dose - 81 mg. Aspirin is well absorbed in upper small intestine, Metabolized in liver

301
Q

side effects of aspirin/ASA

A

G.I. ulceration, bleeding, salicylism with hyperventilation, tinnitus, dizziness, nausea and vomiting. Markedly increased risk for the development of Reye’s syndrome in children with fevers due to viral conditions such as mumps or chickenpox.

302
Q

ADP receptor antagonists can be used in patients who are

A

intolerant or allergic to aspirin

303
Q

class of Clopidogrel/ Plavix

A

platelet aggregation inhibitor

304
Q

Indication of Clopidogrel/ Plavix

A

reduces thrombotic events. Shown to decrease incidence of MI and stroke

305
Q

MOA of Clopidogrel/ Plavix

A

ADP receptor blockade results in diminished platelet aggregation

306
Q

Char. of Clopidogrel/ Plavix

A

generally preferred over Ticlopidine (Ticlid) because it more rapidly inhibits platelets and appears to have a more favorable safety profile

307
Q

side effects of Clopidogrel/ Plavix

A

Bleeding, nausea, headache, neutropenia. Contraindicated in patients with active bleeding i.e. a bleeding peptic ulcer. The anti-platelet activity of these drugs is considered to be “irreversible”, that is, the effect generally lasts for the life of the affected platelet. Use cautiously, if at all, when a patient is taking Coumadin.

308
Q

what do Glycoprotein IIB/IIIA inhibitors do

A

prevent the binding of fibrinogen, thereby blocking platelet aggregation.

309
Q

class of Abciximab/ ReoPro

A

glycoprotein IIB/IIIA inhibitor

310
Q

indcation of Abciximab/ ReoPro

A

Reduces risk of M.I. Abciximab has been approved for use in elective/urgent/emergent percutaneous coronary intervention.

311
Q

MOA of Abciximab/ReoPro

A

Inhibition of Glycoprotein IIB/IIIA receptor sites on platelets prevents the binding of fibrinogen and Von Willebrand’s factor to activated platelets, resulting in decreased platelet aggregation.

312
Q

Char. of Abciximab/ReoPro

A

IV administration only. Abciximab is a monoclonal antibody fragment. The platelet anti-aggregation effects from a single dose will last for 24 – 48 hours.

313
Q

Side effects of Abciximab/ReoPro

A

Increased bleeding, strictly contraindicated in patients with active internal bleeding, a history of intracranial hemorrhage, head trauma or history of stroke within the previous 30 days.

314
Q

how does regular weight heparin act as an anti-coagulant

A

Regular weight heparin acts as an anti-coagulant by binding to antithrombin III. The heparin-antithrombin III complex then binds to and inactivates activated factor X (Xa) and factor II (thrombin).
Heparin ultimately acts to prevent conversion of fibrinogen to fibrin.
Heparin does not actively lyse clots but is able to inhibit further thrombogenesis.

315
Q

How is Heparin given

A

parenterally–IV or SQ

316
Q

Indications for Heparin

A

Heparin has been widely used an anticoagulant for unstable angina, acute M.I, atrial fibrillation and post-P.E. due to D.V.T., however in this country, low-molecular weight heparin has largely replaced regular weight heparin because of it’s better side effect profile.

317
Q

What reverses the effects of heparin

A

Protamine sulfate

318
Q

how does low molecular weight heparin act

A

directly inactivates factor X (Xa) in the clotting cascade…proven to be as effect as regular weight Heparin but with fewer reported side effects

319
Q

low molecular weight heparin has been show to reduce

A

cardiac ischemic events and death by as much as 15% in patients with unstable angina

320
Q

class of Enoxaparin/ Lovenox

A

low molecular weight heparin

321
Q

indication of Enoxaparin/ Lovenox

A

unstable angina, acute MI, prophylaxis and treatment of DVT and PE

322
Q

MOA of Enoxaparin/ Lovenox

A

binds to and inactivates activated factor X (Xa)

323
Q

Char of Enoxaparin/ Lovenox

A

therapeutic anticoagulant effects are notes when clotting time is 2 to 2.5 times longer than normal clotting time
Char: SQ/IV , Rapid onset of action. Anticoagulant effects of low molecular weight heparin may be reversed with Protamine sulfate, a heparin antagonist.
Heparin and low dose heparin can be administered to pregnant women.
Labs: Follow serum levels of clotting factor Xa, aPTT, CBC and platelet count.

324
Q

side effects of Enoxaparin/Lovenox

A

Hemorrhage, caution in patients with liver disease, bleeding disorders such as G.I. bleed. Discontinue if sign of bleeding are noted. Life threatening thrombocytopenia - known as Heparin induced thrombocytopenia (HIT) syndrome can occur. Discontinue Enoxaprin if the patient’s platelet count falls below 100,000/mm3.

325
Q

Class of Warfarin/Coumadin

A

oral anticoagulant

326
Q

indication of Warfarin/Coumadin

A

Prophylaxis and treatment of DVT, PE and thromboembolic events associated with atrial fibrillation and/ or cardiac valve replacement.

327
Q

MOA of Warfarin/Coumadin

A

Antagonizes vitamin K. This interferes with the synthesis of vitamin K dependent clotting factors (factors II, VII, IX, and X).

328
Q

Char. of Warfarin/Coumadin

A

PO only. Very well absorbed. Metabolized by liver, half life approx. 37 hours

329
Q

Side effects of Warfarin/Coumadin

A

Bleeding. Check Protime (PT) or INR (International Normalized Ratio) to maintain optimal blood levels.

330
Q

Anti-coagulant effects of Coumadin may be reversed with

A

Vitamin K, often administered IV in an emergent situation

331
Q

Coumadin should not be used by

A

Pregnant women–category X

332
Q

class of Rivaroxaban/ Xarelto

A

anticoagulant

333
Q

indication of Rivaroxaban/ Xarelto

A

Prophylaxis of deep vein thrombosis which may lead to pulmonary embolism in adults undergoing hip and knee replacement surgery as well as stroke prophylaxis in patients with non-valvular disease induced atrial fibrillation.

334
Q

MOA of Rivaroxaban/Xarelto

A

direct inhibiton of factor Xa

335
Q

Char of Rivaroxaban/Xarelto

A

PO only

336
Q

side effects of Rivaroxaban/Xarelto

A

Bleeding. Clinical trial data have shown that Xarelto allows for predictable anticoagulation with no need for dose adjustments and routine coagulation monitoring. However, these trials have excluded patients with liver disease and end-stage liver disease; therefore, the safety of Rivaroxaban in these populations is unknown.

337
Q

class of streptokinase

A

Thrombolytic (clot buster)

338
Q

indication of streptokinase

A

acute myocardial infarction, acute ischemic (non-hemorrhagic) stroke, acute D.V.T. or P.E.

339
Q

MOA of streptokinase

A

Activates plasminogen to plasmin. Plasmin digests fibrin and fibrinogen forming degradation products.

340
Q

Char. of streptokinase

A

Isolated from Streptococcus species - group C beta-hemolytic strep. I.V. administration only, half life ~1 hour….Strict inclusion and exclusion criteria must be met before Streptokinase or any of the thrombolytic agents can be used.
Exclusionary criteria include the amount of time passed since M.I. or stroke and such conditions as active internal bleeding, a history of intracranial hemorrhage, a intracranial neoplasm and head trauma within the previous 30 days. (Additional exclusion criteria exist.)

341
Q

Side effects of streptokinase

A

Bleeding. Enhances risk of bleeding caused by aspirin, NSAIDs heparin, Coumadin and the anti-platelet agents.

342
Q

Antidote to bleeding in the class of drugs known as “clot busters” (streptokinase)

A

Aminocaproic acid (Amicar) is a plasmin in-activator and antifibrinolytic. It is utilized for bleeding that occurs as a result of streptokinase and other agents in this class of drugs referred to as the “clot busters”.

Pharm 1 Jack (8 decks)

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