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Cardiovascular System Flashcards

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1
Q

hydrochlorothiazide

A

drug class: diuretics
location: DCT
MOA:
- inhibits the Na/Cl transporter in the distal tubule
- increase excretion of Na and water
- promoting diuresis
side effects
- decrease serum k+ (hypokalemia)
- decrease serum Na+ (hyponatremia)
- decrease serum H+ (metabolic alkalosis)

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2
Q

chlorothiazide

A

drug class: diuretics
location: DCT
MOA:
- inhibits the Na/Cl transporter in the distal tubule
- increase excretion of Na and water
- promoting diuresis
side effects
- decrease serum k+ (hypokalemia)
- decrease serum Na+ (hyponatremia)
- decrease serum H+ (metabolic alkalosis)

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3
Q

chlorthalidone

A

drug class: diuretics
location: DCT
MOA:
- inhibits the Na/Cl transporter in the distal tubule
- increase excretion of Na and water
- promoting diuresis
side effects
- decrease serum k+ (hypokalemia)
- decrease serum Na+ (hyponatremia)
- decrease serum H+ (metabolic alkalosis)

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4
Q

furosemide

A

drug class: diuretics
location: loop of Henle

MOA:
- inhibits the Na/K/Cl cotransporter in the thick ascending limb of the loop of Henle
- increase excretion of Na and water
- promoting diuresis

side effects
- decrease serum k+ (hypokalemia)
- decrease serum Na+ (hyponatremia)
- decrease serum H+ (metabolic alkalosis)
- ototoxicity (tinnitus, hearing impairment)

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5
Q

spironolactone

A

drug class: diuretics (weak diuretic)
location: DCT
* used more in congestive heart failure

MOA:
- inhibits aldosterone’s actions on the Na/K/H pump in DCT
- increase the excretion of Na and water
- promoting diuresis

side effects:
- blocking aldosterone receptors also blocks androgen receptors = anti-testosterone/ anti-androgenic effect: gynecomastia, sexual dysfunction (M), menstrual irregularities (W)
- increase serum k+ (hyperkalemia)
- decrease serum Na+ (hyponatremia)
- increase serum H+ (metabolic acidosis)

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6
Q

triamterene

A

drug class: diuretics (weak diuretic - not a first line)
location: DCT

MOA
- directly inhibit NA/K/H pump in the DCT
- increase the excretion of Na and water
- promoting diuresis

side effects
- increase serum k+ (hyperkalemia)
- decrease serum Na+ (hyponatremia)
- increase serum H+ (metabolic acidosis)

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7
Q

what are 3 adverse effects of ALL diuretics

A
  • dehydration: dizziness, hypotension, fainting, dry eyes
  • electrolyte imbalance (Na, K, H)/ muscle cramps
  • frequent urination
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8
Q

triamterene + ________ improves blood ________ levels if thiazide is making it too low

A

thiazide
potassium

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9
Q

t/f: potassium-sparing drugs do not cause hypokalemia

A

true

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10
Q

what is the most effective diuretic, and why?

A

furosemide (loop diuretic) because it blocks more Na absorption
- more commonly used to improve edema (seen in congestive heart failure)

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11
Q

what is the most common diuretic for HTN treatment?

A

Thiazides
- hydrochlorothiazide
- chlorothiazide
- chlorthalidone

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12
Q

define idiosyncratic drug reaction.
what two subclasses of diuretics can cause this reaction?

A

(from sulfa chemical) abnormal, unpredictable response
- thiazides; DCT
- loop diuretics; loop of henle

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13
Q

name two drug classes that inhibit the renin-angiotensin-aldosterone system.

A
  • angiotensin-converting enzyme inhibitors (ACE)
  • angiotensin II receptor blockers (ARBS
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14
Q

quinapril

A

drug class: ACE

MOA
- prevent the formation of angiotensin II by inhibiting ACE; causes vasodilation and sodium/water excretion in urine (reduces blood volume in the body)
- inhibiting ACE also blocks the metabolism of bradykinins

side effects
- dry cough due to increased bradykinin levels
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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15
Q

captopril

A

drug class: ACE

MOA
- prevent the formation of angiotensin II by inhibiting ACE; causes vasodilation and sodium/water excretion in urine (reduces blood volume in the body)
- inhibiting ACE also blocks the metabolism of bradykinins

side effects
- dry cough due to increased bradykinin levels
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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16
Q

benazepril

A

drug class: ACE

MOA
- prevent the formation of angiotensin II by inhibiting ACE; causes vasodilation and sodium/water excretion in urine (reduces blood volume in the body)
- inhibiting ACE also blocks the metabolism of bradykinins

side effects
- dry cough due to increased bradykinin levels
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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17
Q

lisinopril

A

drug class: ACE

MOA
- prevent the formation of angiotensin II by inhibiting ACE; causes vasodilation and sodium/water excretion in urine (reduces blood volume in the body)
- inhibiting ACE also blocks the metabolism of bradykinins

side effects
- dry cough due to increased bradykinin levels
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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18
Q

enalapril

A

drug class: ACE

MOA
- prevent the formation of angiotensin II by inhibiting ACE; causes vasodilation and sodium/water excretion in urine (reduces blood volume in the body)
- inhibiting ACE also blocks the metabolism of bradykinins

side effects
- dry cough due to increased bradykinin levels
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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19
Q

are ACE or ARBS used in HTN first-line treatment?

A

ACE inhibitors - if the patient experiences a bothersome cough (they are switched to ARB)

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20
Q

what do bradykinins cause?

A

vasodilation (increasing bradykinin levels = increases vasodilation)

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21
Q

losartan

A

drug class: ARB

MOA: inhibit angiotensin II from binding to AT1 receptors on kidneys and blood vessels
- causes vasodilation
- causes sodium/water excretion in urine (reduces blood volume in the body)

side effects
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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22
Q

valsartan

A

drug class: ARB

MOA: inhibit angiotensin II from binding to AT1 receptors on kidneys and blood vessels
- causes vasodilation
- causes sodium/water excretion in urine (reduces blood volume in the body)

side effects
- hyperkalemia: decrease in aldosterone effects on kidney
- angioedema (RARE but life-threatening swelling of lips, tongue, throat, impaired breathing, swelling of eyes)

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23
Q

t/f: ARBs avoided as well if patient has angioedema with ACE inhibitors

A

true

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24
Q

t/f: ACE + ARBs are very common meds used in first-line HTN treatment (like thiazides diuretics)

A

true (patient will NOT be on both ACE and ARB)

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25
propranolol
drug class: non-selective beta blocker MOA: inhibit B1 & B2 receptors - B1 inhibition reduces heart rate/ construction - B2 inhibition on lungs = bronchoconstriction side effects: - bradycardia: dizziness, fainting, blurring/ fading vision, fatigue, lack of concentration, nausea (contraindicated in patients w/ bradycardia; HR <60 bpm) - tiredness, depression - bronchospasm/ constriction (non-selective BB, wheezing SOB) (contraindicated in patients with respiratory diseases; asthma or COPD) - masks symptoms of hypoglycemia in diabetes (won't get racing heart rate; first sign if blood sugar is too low)
26
labetalol
drug class: non-selective beta blocker MOA: inhibit B1 & B2 receptors - B1 inhibition reduces heart rate/ construction - B2 inhibition on lungs = bronchoconstriction side effects: - bradycardia: dizziness, fainting, blurring/ fading vision, fatigue, lack of concentration, nausea (contraindicated in patients w/ bradycardia; HR <60 bpm) - tiredness, depression - bronchospasm/ constriction (non-selective BB, wheezing SOB) (contraindicated in patients with respiratory diseases; asthma or COPD) - masks symptoms of hypoglycemia in diabetes (won't get racing heart rate; first sign if blood sugar is too low)
27
carvedilol
drug class: non-selective beta blocker MOA: inhibit B1 & B2 receptors - B1 inhibition reduces heart rate/ construction - B2 inhibition on lungs = bronchoconstriction - a1 inhibition = vasodilation side effects: - bradycardia: dizziness, fainting, blurring/ fading vision, fatigue, lack of concentration, nausea (contraindicated in patients w/ bradycardia; HR <60 bpm) - tiredness, depression - bronchospasm/ constriction (non-selective BB, wheezing SOB) (contraindicated in patients with respiratory diseases; asthma or COPD) - masks symptoms of hypoglycemia in diabetes (won't get racing heart rate; first sign if blood sugar is too low)
28
metoprolol
drug class: cardioselective beta blocker MOA: inhibit B1 - B1 inhibition reduces heart rate/ construction side effects: - bradycardia: dizziness, fainting, blurring/ fading vision, fatigue, lack of concentration, nausea (contraindicated in patients w/ bradycardia; HR <60 bpm) - tiredness, depression - bronchospasm/ constriction (non-selective BB, wheezing SOB) (contraindicated in patients with respiratory diseases; asthma or COPD) - masks symptoms of hypoglycemia in diabetes (won't get racing heart rate; first sign if blood sugar is too low)
29
atenolol
drug class: cardioselective beta blocker MOA: inhibit B1 - B1 inhibition reduces heart rate/ construction side effects: - bradycardia: dizziness, fainting, blurring/ fading vision, fatigue, lack of concentration, nausea (contraindicated in patients w/ bradycardia; HR <60 bpm) - tiredness, depression - bronchospasm/ constriction (non-selective BB, wheezing SOB) (contraindicated in patients with respiratory diseases; asthma or COPD) - masks symptoms of hypoglycemia in diabetes (won't get racing heart rate; first sign if blood sugar is too low)
30
doxazosin
drug class: alpha 1 blocker MOA: inhibit A1 receptors on blood vessels = vasodilation - usually not first-line to treat HTN unless the patient has benign prostatic hyperplasia side effects: - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out)
31
terazosin
drug class: alpha 1 blocker MOA: inhibit A1 receptors on blood vessels = vasodilation - usually not first-line to treat HTN unless the patient has benign prostatic hyperplasia side effects: - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out)
32
prazosin
drug class: alpha 1 blocker MOA: inhibit A1 receptors on blood vessels = vasodilation - usually not first-line to treat HTN unless the patient has benign prostatic hyperplasia side effects: - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out)
33
clonidine
drug class: sympathetic nervous system inhibitor (centrally acting sympathetic agonist) MOA - inhibit A2 receptors in the brain - reduces sympathetic outflow to the heart (decreases heart rate) and blood vessels (vasodilation) side effects - sedation - bradycardia - impotence - sudden discontinuation can result in severe rebound HTN (due to excess sympathetic activity rebounding) * so many side effects are the reason why clonidine is NOT used the first line or alone * usually reserved for hypertension that is DIFFICULT to control
34
amlodipine
drug class: vasodilator; dihydropyridine calcium channel blocker MOA: - inhibit L type calcium channels, decreasing the influx of calcium in the smooth muscle blood vessels (vasodilation) side effects - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out) - peripheral edema - headache due to vasodilation - flushing due to vasodilation
35
felodipine
drug class: vasodilator; dihydropyridine calcium channel blocker MOA: - inhibit L type calcium channels, decreasing the influx of calcium in the smooth muscle blood vessels (vasodilation) side effects - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out) - peripheral edema - headache due to vasodilation - flushing due to vasodilation
36
nifedipine
drug class: vasodilator; dihydropyridine calcium channel blocker MOA: - inhibit L type calcium channels, decreasing the influx of calcium in the smooth muscle blood vessels (vasodilation) side effects - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out) - peripheral edema - headache due to vasodilation - flushing due to vasodilation
37
diltiazem
drug class: vasodilator; non-dihydropyridine calcium channel blocker MOA: - inhibit L type calcium channels, decreasing the influx of calcium into cardiac myocytes and SA/VA node (reduced heart rate) - less effective on blood vessels: inhibit L type calcium channels, decreasing the influx of calcium in the smooth muscle blood vessels (vasodilation) side effects - bradycardia and heart failure (can occur especially if combined with BB) - risk of lowering HR too much if using both CBB + BB since both work directly on the heart - contraindicated in bradycardia and heart failure - HIGH RISK FOR BRADYCARDIA/ HF IF PT. ON TIMOLOL AND NON-DYHYDRIPYRIDINE
38
verapamil
drug class: vasodilator; non-dihydropyridine calcium channel blocker MOA: - inhibit L type calcium channels, decreasing the influx of calcium into cardiac myocytes and SA/VA node (reduced heart rate) - less effective on blood vessels: inhibit L type calcium channels, decreasing the influx of calcium in the smooth muscle blood vessels (vasodilation) side effects - bradycardia and heart failure (can occur especially if combined with BB) - risk of lowering HR too much if using both CBB + BB since both works directly on the heart - contraindicated in bradycardia and heart failure - HIGH RISK FOR BRADYCARDIA/ HF IF PT. ON TIMOLOL AND NON-DIHYDROPYRIDINE
39
hydralazine
drug class: vasodilator; direct acting vasodilator MOA: UNCLEAR - does a ton of things on vascular smooth muscle - opening k+ channels on smooth muscle - inhibit calcium release from muscle - simulated nitric oxide release from vascular endothelial leading cGMP release (strong vasodilation) side effects: - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out) - peripheral edema - headache due to vasodilation - flushing due to vasodilation
40
ACE Inhibitors
- quinapril - captopril - benazepril - lisinopril - enalapril
41
ARBs
- losartan - valsartan
42
non-selective BB
- propranolol - labetalol - carvedilol
43
A1 Blockers
- doxazosin - terazosin - prazosin
44
anti-angina: BB MOA
- decrease heart rate/ contractility - reduces work of heart - decreases the oxygen demand of the heart
45
anti-angina: non-dihydropyridine calcium channel blockers MOA
- decrease heart/ contractility - reduces work of heart - decreases the oxygen demand of the heart
46
anti-angina organic nitrodilators: nitroglycerin
- nitroglycerin (sublingual) for relief of acute angina - nitroglycerin (topical/ transdermal patch) for prevention of angina MOA - turns nitric oxide in the body - activates cGMP in blood vessel smooth muscle wall - inhibits Ca entry into the cell - strong vasodilation in coronary arteries - more oxygen to the heart and improves coronary artery vasospasm - improves oxygen supply to the heart side effects - sympathetic NS tries to compensate for the vasodilation of the blood vessels (reflexively increase HR = reflex tachycardia) - orthostatic HTN (loss of reflex vasoconstriction upon standing, dizziness, vision may blur out, pass out) - peripheral edema - headache due to vasodilation - flushing due to vasodilation
47
aspirin
anti-platelet MOA - inhibits cox 1 (thus inhibiting the production of thromboxane A2) - irreversibly (covalently) inhibits platelet aggregation ** lasts the lifetime of a platelet (5-7 days) AE - cox1 enzyme produces protective factors (gastric mucus in the stomach) - dyspepsia - GI bleeding - eyes: subconjunctival heme - tinnitus
48
dipyridamole
anti-platelet: weaker than aspirin MOA - inhibit phosphodiesterase (which usually breaks down cAMP) - increased cAMP in the platelet + blood vessels - inhibit platelet aggregation + adhesion into the blood vessels - vasodilates coronary arteries AE: vasodilation causes headaches
49
cilostazol
anti-platelet: weaker than aspirin MOA - inhibit phosphodiesterase (which usually breaks down cAMP) - increased cAMP in the platelet + blood vessels - inhibit platelet aggregation + adhesion into the blood vessels - vasodilates coronary arteries AE: vasodilation causes headaches
50
aspirin & dipyridamole
anti-platelet: weaker than aspirin MOA - inhibit phosphodiesterase (which usually breaks down cAMP) - increased cAMP in the platelet + blood vessels - inhibit platelet aggregation + adhesion into the blood vessels - vasodilates coronary arteries AE: vasodilation causes headaches
51
clopidogrel
anti-platelet MOA - inhibit adenosine diphosphate (ADP) P2Y12 receptors - irreversibly inhibit platelet aggregation * lasts the life of platelets
52
ticlopidine
anti-platelet MOA - inhibit adenosine diphosphate (ADP) P2Y12 receptors - irreversibly inhibit platelet aggregation * lasts the life of platelets AE - severe neutropenia (severely reduced WBC, i.e., neutrophils) - needs blood work to monitor blood cells periodically
53
warfarin
anti-coagulant MOA - inhibits vitamin k - decreased production of vitamin k dependent clotting factors produced in the liver - reduced fibrin formation/ thrombus SE - lots of drugs interaction - takes 4-5 days to take effect - 4-5 days to stop seeing effects - need a consistent vitamin K diet - requires blood test (INR); too high = increased bleeding; too low = increased clotting
54
apixaban
anti-coagulant direct-acting oral anti-coagulant (DOAC) - works immediately - no blood test monitoring - no diet concerns MOA: directly inhibits factor x
55
aminocaproic acid (amicar)
the antidote to t-pa toxicity - intravenous or oral to control bleeding for excessive plasmin activation MOA: competitively inhibits t-pa = blocks t-pa from binding to plasminogen AE: can cause thrombosis **t-pa: IV, breaks up clots causing MI, stroke, and pulmonary embolism to restore blood flow; given within hours - t-pa are enzymes that convert plasminogen to plasmin -plasmin breaks down fibrin + fibrinogen - break up clot SE: increased bleeding & intracranial heme
56
"statin" lovastatin simvastatin atorvastatin fluvastatin rosuvastatin pravastatin
anti-hyperlipidemia drug HMG CoA reductase inhibitors MOA - inhibit HMG CoA reductase (an enzyme used to convert HMG CoA into mevalonate) - rate-limiting step in cholesterol biosynthesis AE - muscle pain/myalgia - rhabdomyolysis: break down of muscle proteins - ends up in urine 'coca cola' urine and muscle loss - hepatotoxicity (liver toxicity) - sclera turns yellow - rare ocular: diplopia & ptosis
57
cholestyramine
anti-hyperlipidemia drug bile acid-binding resins MOA: - bind bile acids in the gut, which contain cholesterol - prevent absorption - less free fatty acid in the bloodstream - liver synthesizes more bile acid from cholesterol - results: reduced cholesterol (mostly LDL)
58
ezetimibe
anti-hyperlipidemia drug * lowest LDL MOA - blocks transport of dietary cholesterol in GI tract - no transport of dietary cholesterol in body
59
niacin (nicotinic acid, vitamin B3)
anti-hyperlipidemia drug - requires a large dose MOA: - inhibits VLDL secretion - reduces LDL + triglycerides - increase HDL (unknown mechanism) AE Ocular - CME that does not leak on FA (swelling in the macula) Systemic - flushing + itching (urticaria) - increase blood glucose - increase uric acid (gout) - hepatotoxicity
60
fenoFIBrate gemFIBrozil
anti-hyperlipidemia drug fibric acid derivative MOA - binds to peroxisome proliferator-activated receptor (PPAR -alpha) - increases lipoprotein lipase activity to breakdown VLDL - works well to decrease VLDL + triglycerides SE - hepatotoxicity - muscle pain (myalgias)
61
omega - 3 acid ethyl esters (fish oil)
anti-hyperlipidemia drug * lovaza is Rx only MOA - unknown; may reduced synthesis of triglycerides in the liver - may increase LDL SE: fish burps (refrigerating decreases)

General Pharm (6 decks)

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