Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Pharm > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

thiazide
potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the most common diuretic for HTN treatment?

A

Thiazides
- hydrochlorothiazide
- chlorothiazide
- chlorthalidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A
  • angiotensin-converting enzyme inhibitors (ACE)
  • angiotensin II receptor blockers (ARBS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what do bradykinins cause?

A

vasodilation (increasing bradykinin levels = increases vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

propranolol

A

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
Q

labetalol

A

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
Q

carvedilol

A

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
Q

metoprolol

A

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
Q

atenolol

A

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
Q

doxazosin

A

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
Q

terazosin

A

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
Q

prazosin

A

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
Q

clonidine

A

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
Q

amlodipine

A

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
Q

felodipine

A

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
Q

nifedipine

A

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
Q

diltiazem

A

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
Q

verapamil

A

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
Q

hydralazine

A

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
Q

ACE Inhibitors

A
  • quinapril
  • captopril
  • benazepril
  • lisinopril
  • enalapril
41
Q

ARBs

A
  • losartan
  • valsartan
42
Q

non-selective BB

A
  • propranolol
  • labetalol
  • carvedilol
43
Q

A1 Blockers

A
  • doxazosin
  • terazosin
  • prazosin
44
Q

anti-angina: BB MOA

A
  • decrease heart rate/ contractility
  • reduces work of heart
  • decreases the oxygen demand of the heart
45
Q

anti-angina: non-dihydropyridine calcium channel blockers MOA

A
  • decrease heart/ contractility
  • reduces work of heart
  • decreases the oxygen demand of the heart
46
Q

anti-angina organic nitrodilators: nitroglycerin

A
  • 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
Q

aspirin

A

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
Q

dipyridamole

A

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
Q

cilostazol

A

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
Q

aspirin & dipyridamole

A

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
Q

clopidogrel

A

anti-platelet
MOA
- inhibit adenosine diphosphate (ADP) P2Y12 receptors
- irreversibly inhibit platelet aggregation
* lasts the life of platelets

52
Q

ticlopidine

A

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
Q

warfarin

A

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
Q

apixaban

A

anti-coagulant
direct-acting oral anti-coagulant (DOAC)
- works immediately
- no blood test monitoring
- no diet concerns

MOA: directly inhibits factor x

55
Q

aminocaproic acid (amicar)

A

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
Q

“statin”
lovastatin
simvastatin
atorvastatin
fluvastatin
rosuvastatin
pravastatin

A

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
Q

cholestyramine

A

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
Q

ezetimibe

A

anti-hyperlipidemia drug
* lowest LDL

MOA
- blocks transport of dietary cholesterol in GI tract - no transport of dietary cholesterol in body

59
Q

niacin (nicotinic acid, vitamin B3)

A

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
Q

fenoFIBrate
gemFIBrozil

A

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
Q

omega - 3 acid ethyl esters (fish oil)

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions