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Pre-pharmacology > Chapter 12a (cardiovascular drugs) > Flashcards

Chapter 12a (cardiovascular drugs) Flashcards

1
Q

high blood pressure defined by

A

130/80 strictly, but definite at 140/90

normal is 120/80

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2
Q

idiopathic/essential hypertension

A

unknown mechanism that brought about the disease

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3
Q

known causes of hypertension

A

renal, endocrine, weight, or diabetic problems, sleep apnea, or pregnancy
Less than 10% of cases have known causes

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4
Q

HTN

A

hypertension

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5
Q

risk factors for HTN

A

smoking, high weight, diet, and genetic

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6
Q

high genetic load

A

you are more at risk for a disease because of genetics

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7
Q

ASVD

A

atheroslcerotic vascular disease; plaque build up on body’s arteries

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8
Q

CAD

A

coronary artery disease; aka coronary heart disease (CHD); narrowing of small BVs that supply oxygen to heart

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9
Q

angina pectoris

A

episodic heart pain that goes away; manifestation of CAD; from lack of oxygen to heart

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10
Q

MI

A

myocardial infarction; permanent loss of heart muscle, leading cause of death in US

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11
Q

silent heart attacks

A

those that people didn’t even know they had

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12
Q

risk factors for CAD

A

smoking, genetics, high weight, high BP, and angina is RF for MI

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13
Q

HF

A

heart failure; heart fails to pump adequate amounts of blood (so fluid often accumulates in body; edema; and in lungs so breathing is restricted)
Blood often stagnates in body, backs up in lungs, and people have symptoms from poor oxygen delivery (muscle weakness from poor delivery in muscles, confusion from poor delivery in brain, etc.)

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14
Q

risk factors for HF

A

high BP, CAD (so indirectly smoking), previous MI, poor diet, alcohol consumption (binging), viral illness, pregnancy (post-partum cardiomyopathy)

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15
Q

orthopnea from HF

A

fluid backs up even more in lungs when lying down so they cannot breathe when lying down

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16
Q

dysrhythmia

A

anything but normal sinus rhythym

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17
Q

arrhythmia

A

absence of heart rhythym

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18
Q

atrial fibrillation

A

patients require anti-coagulants to prevent blood pooling in atria that isn’t contracting correctly

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19
Q

tachycardia

A

fast heart rate

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20
Q

bradycardia

A

slow heart rate

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21
Q

dyslipidemia

A

disorders with cholesterol, triglycerides, and lipid carrier molecules

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22
Q

lipid profile

A

describes cholesterol, triglyceride, and lipid carrier molecules in blood; very important for controlling for other CV diseases

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23
Q

risk factors for dyslipidemias

A

poor diet and genetics

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24
Q

most important factors for improving CV health

A

lose weight, healthy lipid profile (first by diet, then pharmacology), increase exercise, decrease stress, and limit smoking and alcohol use

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25
Q

lipid carrier molecules order of density

A

chylomicron, VLDL, IDL, LDL, and HDL

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26
Q

lipid carrier molecules

A

allow lipids to be soluble in blood

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27
Q

HDL

A

high-density lipoprotein; carries wayward fats from BVs back to liver

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28
Q

LDL

A

low-density lipoprotein; carries cholesterol to cells

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29
Q

VLDL

A

very low-density lipoproteins; most of triglycerides are carried here

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30
Q

lipid ratio risk levels

A

goal is to have LDL/HDL ratio less than 3.5. Would probably treat anything higher than 4.5

31
Q

HTN step 1 treatment

A

non-drug therapy; salt reduction, weight loss, exercise, and smoking cessation. Patients often don’t take this seriously and then drug therapy is required

32
Q

hypertensive urgency

A

BP around 190/120. Requires immediate help. Headaches, bloody noses

33
Q

hypertensive crisis

A

BP around 190/120 so high that it changes mental status (obtunded)

34
Q

first-line drug therapy for HTN

A

second step therapy overall; diuretics, ACEi, ARBs, and CCBs

35
Q

second-line drug therapy for HTN

A

third step therapy overall; combination therapy, B-blockers (not used as monotherapy)
Often use ACE inhibit/ARB and a CCB

36
Q

third-line drug therapy for HTN

A

4th step therapy overall; direct vasodilators

37
Q

initial drug therapy for HTN for black patients

A

CCB or diuretic (often combined in one pill)

38
Q

initial drug therapy for HTN for white patients

A

ACE-inhib or ARB

39
Q

loop diuretics

A

inhibit Na/water reabsorption in the ascending loop of Henle; cause huge loss of K, must be given with K supplement. Used for CHF

40
Q

thiazide diuretics

A

sulfa drugs; work on the early part of the DCT; cause moderate K loss
Often combined with K sparing to even out K balance

41
Q

potassium sparing diuretics

A

work on the late part of the DCT and collecting ducts; cause rise in K blood levels

42
Q

low-ceiling diuretics

A

thiazide diuretics and K sparing diuretics; used for treating HTN

43
Q

high-ceiling diuretics

A

loop diuretics; used for treating CHF (very powerful diuretics)

44
Q

HCTZ

A

hydrochlorothiazide; prototype thiazide diuretic

45
Q

chlorathalidone

A

prototypical thiazide-like diuretic

46
Q

thiazide and loop diuretic long-term mechanism

A

change Na balance in walls of vasculature of kidneys that eventually leads to relaxation of arteries and decrease in resistance of arteries to decrease BP; short term they just reduce volume in serum

47
Q

Lasix

A

furosemide; loop diuretic

48
Q

K supplements

A

K-Lyte; Slow-K; given to patients on loop diuretics to avoid hypokalemia. Given orally unless in emergency then IV. Rx preparations have 10x more absorb-able K than a banana (formulated in 8-20 mEq/dose)

49
Q

Dyrenium

A

triamterene; potassium sparing diuretic

50
Q

Inderal

A

propranolol; non-selective B blocker

51
Q

Coreg

A

carvedilol; B-1 blocker (cardioselective)

52
Q

cardioselective B blockers

A

selectively block B-1 to slow down heart and sympathetic output to not make people as sweaty or as excitable; good for CHF or HTN
Often combined with diuretics; not used for monotherapy
Black males often do not respond well to this treatment

53
Q

CCBs

A

calcium channel blockers; block Ca channels in walls of heart and BVs. Relax smooth muscle in BVs to decrease BP and increase BF
Good for those with CAD or HTN

54
Q

Calan

A

verapamil; CCB

55
Q

Norvasc

A

amlodipine; most commonly used CCB b/c of long lasting effect

56
Q

ACE-I

A

ace-inhibitors; inhibit ACE to stop formation of angiotensin 2 to lower BP, cause cough

57
Q

RAS

A

renin-angiotensin-aldosterone-system; Low BP stimulates juxtaglomerular cells in kidney releases renin which converts angiotensinogen (from liver) to angiotensin 1, then ACE in lungs converts angiotensin 1 to 2. Angiotensin 2 is a potent vasoconstrictor and causes aldosterone secretions which increases reabsorption of slat and water.

58
Q

Capoten

A

captopril; first ACE-I

59
Q

Zestril

A

lisinopril; ACE-I go to, often combined with diuretic

60
Q

ARBs

A

angiotensin 2 receptor blockers; directly block angiotensin 2 rc, work like ACE-I but do not produce cough

61
Q

ACE-Is and ARBs

A

RASi; renin-angiotensin-[aldosterone]-systemic inhibitors

62
Q

Cozaar

A

losartan; ARB

63
Q

irbesartan

A

ARB

64
Q

Tenormin

A

atenolol; selective B1 blocker

65
Q

Lopressor

A

metoprolol

66
Q

Tenoretic

A

atenolol and a thiazide diuretic combination; combos of B-blockers and thiazides are 3rd step HTN therapy

67
Q

NO

A

nitroglycerine; used for angina mostly but also for severe HTN as step 4 therapy

68
Q

Apresoline

A

hydralazine; direct arterial vasodilator; used for HTN

Often black males will respond better to this

69
Q

BilDil

A

NO and hydralalzine combination; a race-based drug for black males with CHF or HTN

70
Q

Rogaine

A

minoxidil; topical K-channel opener vasodilator with too many side effects for systemic use routinely, but used as hair loss treatment OTC

71
Q

Capozide

A

captopril, ACE-I, diuretic, and HCTZ combination; for HTN

72
Q

most common HTN combination therapy

A

K wasting and K sparing diuretic or diuretic plus ACE-I, ARB, or CCB

73
Q

zestoretic

A

denotes combination of Zestril and mild diuretic (thiazide)

Pre-pharmacology (27 decks)

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