Chapter 12a (cardiovascular drugs) Flashcards

(73 cards)

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
lipid carrier molecules order of density
chylomicron, VLDL, IDL, LDL, and HDL
26
lipid carrier molecules
allow lipids to be soluble in blood
27
HDL
high-density lipoprotein; carries wayward fats from BVs back to liver
28
LDL
low-density lipoprotein; carries cholesterol to cells
29
VLDL
very low-density lipoproteins; most of triglycerides are carried here
30
lipid ratio risk levels
goal is to have LDL/HDL ratio less than 3.5. Would probably treat anything higher than 4.5
31
HTN step 1 treatment
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
hypertensive urgency
BP around 190/120. Requires immediate help. Headaches, bloody noses
33
hypertensive crisis
BP around 190/120 so high that it changes mental status (obtunded)
34
first-line drug therapy for HTN
second step therapy overall; diuretics, ACEi, ARBs, and CCBs
35
second-line drug therapy for HTN
third step therapy overall; combination therapy, B-blockers (not used as monotherapy) Often use ACE inhibit/ARB and a CCB
36
third-line drug therapy for HTN
4th step therapy overall; direct vasodilators
37
initial drug therapy for HTN for black patients
CCB or diuretic (often combined in one pill)
38
initial drug therapy for HTN for white patients
ACE-inhib or ARB
39
loop diuretics
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
thiazide diuretics
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
potassium sparing diuretics
work on the late part of the DCT and collecting ducts; cause rise in K blood levels
42
low-ceiling diuretics
thiazide diuretics and K sparing diuretics; used for treating HTN
43
high-ceiling diuretics
loop diuretics; used for treating CHF (very powerful diuretics)
44
HCTZ
hydrochlorothiazide; prototype thiazide diuretic
45
chlorathalidone
prototypical thiazide-like diuretic
46
thiazide and loop diuretic long-term mechanism
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
Lasix
furosemide; loop diuretic
48
K supplements
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
Dyrenium
triamterene; potassium sparing diuretic
50
Inderal
propranolol; non-selective B blocker
51
Coreg
carvedilol; B-1 blocker (cardioselective)
52
cardioselective B blockers
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
CCBs
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
Calan
verapamil; CCB
55
Norvasc
amlodipine; most commonly used CCB b/c of long lasting effect
56
ACE-I
ace-inhibitors; inhibit ACE to stop formation of angiotensin 2 to lower BP, cause cough
57
RAS
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
Capoten
captopril; first ACE-I
59
Zestril
lisinopril; ACE-I go to, often combined with diuretic
60
ARBs
angiotensin 2 receptor blockers; directly block angiotensin 2 rc, work like ACE-I but do not produce cough
61
ACE-Is and ARBs
RASi; renin-angiotensin-[aldosterone]-systemic inhibitors
62
Cozaar
losartan; ARB
63
irbesartan
ARB
64
Tenormin
atenolol; selective B1 blocker
65
Lopressor
metoprolol
66
Tenoretic
atenolol and a thiazide diuretic combination; combos of B-blockers and thiazides are 3rd step HTN therapy
67
NO
nitroglycerine; used for angina mostly but also for severe HTN as step 4 therapy
68
Apresoline
hydralazine; direct arterial vasodilator; used for HTN | Often black males will respond better to this
69
BilDil
NO and hydralalzine combination; a race-based drug for black males with CHF or HTN
70
Rogaine
minoxidil; topical K-channel opener vasodilator with too many side effects for systemic use routinely, but used as hair loss treatment OTC
71
Capozide
captopril, ACE-I, diuretic, and HCTZ combination; for HTN
72
most common HTN combination therapy
K wasting and K sparing diuretic or diuretic plus ACE-I, ARB, or CCB
73
zestoretic
denotes combination of Zestril and mild diuretic (thiazide)