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Pharm 323 Spring 22 > HTN > Flashcards

HTN Flashcards

1
Q

preload

A

volume of blood in heart after diastole (filling)

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2
Q

afterload

A

amt of resistance the left ventricle must overcome to pump blood out of heart and to the body

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3
Q

diuretics work primarily on ____ _____ (broad)

A

blood volume

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4
Q

what will we see with dual therapy with anti-hypertensive and diuretic?

A

enhanced therapeutic effects :)

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5
Q

3 types of diuretics + their prototype

A
  1. loop - Lasix
  2. thiazide - hydrochlorothiazide
  3. potassium-sparing - spironolactone
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6
Q

which diuretic is MOST efficacious?

A

furosemide (Lasix)

action is earlier on within nephron transport –> larger # of solutes to act on –> more diuresis

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7
Q

what is known as the superhero of diuretics? + what’s the prototype?

A

loop diuretics - Lasix

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8
Q

what diuretic would we use for acute pulmonary edema?

A

furosemide

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9
Q

MOA of loop diuretics (furosemide)

A

inhibits Na and Cl reabsorption @ LOOP of henle –> decreased blood volume

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10
Q

what is onset for PO furosemide + how long does it last

A

1 hour onset; lasts 8 hours

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11
Q

what is onset for IV furosemide? knowing this, what is your main nursing consideration?

A

5 minutes –> GET BED PAN READY!

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12
Q

SE of furosemide (3)

A
  1. electrolyte imbalances (Na, Cl, K)
  2. hypotension
  3. ototoxicity (if too quick IV or dose too big)
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13
Q

with furosemide we see an increased risk of what? (3)

A
  1. digoxin toxicity
  2. lithium toxicity
  3. gout exacerbations
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14
Q

MOA of thiazide diuretics

A

reduces blood volume @ distal tubule

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15
Q

prototype for thiazide diuretics

A

hydrochlorathiazide (HCTZ)

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16
Q

onset for HCTZ + how long does it last?

A

onset 2 hours; lasts 12

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17
Q

what is the most widely used diuretic?

A

HCTZ

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18
Q

SE of HCTZ (3)

A
  1. electrolyte imbalances (K+ loss not as extreme as in loop diuretics)
  2. hypovolemia
  3. hyperglycemia
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19
Q

with HCTZ use, we see increased risk of what? (3)

A
  1. digoxin toxicity
  2. lithium toxicity
  3. gout exacerbations
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20
Q

what is the prototype for potassium-sparing diuretics?

A

spironolactone

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21
Q

what is the MOA of K+ sparing potassium diuretics?

A

BLOCKS aldosterone @ distal tubule –> fluid loss, but K+ remains

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22
Q

SE of spironolactone

A
  1. hyperkalemia

2. endocrine effects (gynecomastia)

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23
Q

onset of action for spironolactone

A

48 hrs (NOT a go-to/rescue drug)

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24
Q

patient education points when using spironolactone

A

avoid salt substitutes (contain K+ and risk of hyperkalemia is increased)

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25
Q

which diuretics put a pt at risk of hypokalemia?

A
  1. loop

2. thiazide

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26
Q

which diuretic puts a pt at risk of hyperkalemia?

A

potassium sparing

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27
Q

potassium-sparing drugs are usually NOT given with which other antihypertensive drug class?

A

RAAS drugs

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28
Q

when monitoring hydration status with diuretic use, what things are we monitoring?

A

I+O, daily weights

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29
Q

prototype for alpha 1 adrenergic antagonist

A

prazosin (minipress)

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30
Q

MOA of prazosin

A

blocks SNS activity on arterioles + veins –> vasodilation

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31
Q

what effect would prazosin have on a person with BPH?

A

relaxation of smooth muscles in bladder + prostatic capsule

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32
Q

SE of prazosin (3)

A
  1. orthostatic hypotension
  2. reflex tachycardia (b/c of drop in BP, body is compensating)
  3. nasal congestion (b/c of vasodilation in nose)
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33
Q

which medication is associated with 1st dose orthostatic hypotension?

34
Q

what is the prototype for alpha 2 adrenergic agonist?

A

clonidine (Catapres)

35
Q

MOA of clonidine?

A

CENTRALLY ACTING (CNS) - decreases amount of neurotransmitter NE, which decreases SNS stimulation

–> leads to vasodilation, decreased BP, decreased CO

alpha 2 = BRAIN

36
Q

SE of clonidine

hint: think of MOA of this drug to determine your SE

A

drowsiness, sedation, dry mouth, rebound HTN (if stopped cold turkey)

working on CNS, so you’ll see CNS effects

37
Q

which drug will you see rebound HTN with if stopped cold turkey?

A

clonidine (b/c of the rebound SNS stimulation)

38
Q

routes for clonidine

A

oral + patch (change q 7 days)

39
Q

prototype for cardioselective beta blocker

A

metoproLOL

cardio selective = only acting on beta 1 (heart)

40
Q

MOA of metoprolol

A
  1. decreased HR
  2. decreased conduction
  3. deceased force of contraction
41
Q

SE of metoprolol

hint: SE r/t work on heart + SE r/t decreased BP

A

r/t work on heart:

  • bradycardia
  • AV heart block
  • decreased CO (watch for HF!)
  • rebound excitation

r/t BP:

  • hypotension
  • fatigue
  • drowsy
  • dizzy
  • headache
  • depression

“BLAH FEELING” :(

42
Q

which type of beta blocker would we want diabetic patients on? why?

A

cardioselective; b/c with nonselective, beta 2 is blocked which blocks glycogenolysis –> hypoglycemia

43
Q

re: beta blockers, what do we need to tell our patients with DM?

A

this can mask s+s of hypoglycemia (b/c SNS is blocked) –> monitor BG very closely!

44
Q

what VS should we check before admin of beta blocker?

A

BP+HR (apical) - hold if <60

45
Q

what patient teaching is important with beta blockers?

A
  1. don’t stop cold turkey!
  2. watch for s+s of hypoglycemia
  3. watch for s+s of HF (can decrease CO)
46
Q

prototype for alpha/beta blockers

A

carvedilol

47
Q

MOA of carvedilol

A

blocks alpha 1 + beta 1 + beta 2

48
Q

based on MOA of carvedilol, what effect would we see on the receptors?

A

vasodilation (alpha 1)
decreased HR, contractility, conduction (beta 1)
bronchoconstriction (beta 2)

49
Q

SE of carvedilol

A
  1. hypotension
  2. AV heart block
  3. bradycardia
  4. bronchoconstriction
50
Q

calcium channel blockers don’t work on ______

A

VEINS

arteries, arterioles only

51
Q

mnemonic to remember CCB + what are the prototypes?

A

Very Nice Drugs

  1. verapamil
  2. nifedipine
  3. diltiazem
52
Q

MOA of CCBs (dipines + non dipines)

A

BOTH types: prevents muscle contraction –> smooth muscle relaxes –> vasodilation

non-dipines: verapamil + diltiazem: decreases HR, contractility, conduction

53
Q

we should not have patients on which 2 drug classes at the same time?

A

Calcium channel blockers + beta blockers (b/c both acting on heart)

54
Q

2 types of CCBs + the prototypes + which act on the heart

A
  1. dipines: nifedipine (only vessels)

2. nondipines: verapamil + diltiazem (vessels and HEART) “vera and dilt are sweethearts, they’re always together”

55
Q

out of the CCBs, which one would you see reflex tachycardia with? what other medication can we give to decrease the effects of this?

A

nifedipine - give with BB to decrease reflex tachycardia effects

56
Q

SE of nifedipine

hint: think of mechanism of action

A
  • reflex tachycardia
  • flushing
  • hypotension
  • peripheral edema
57
Q

calcium channel blockers mainly work on increasing ______ ______

A

coronary perfusion

58
Q

route for verapamil

59
Q

SE of verapamil

hint: SE r/t vasodilation + SE r/t work on heart

A

-CONSTIPATION*** (Very common)

r/t relaxation of vascular smooth muscle:

  • hypotension
  • dizziness
  • flushing
  • edema

r/t work on heart:

  • bradycardia
  • AV heart block
  • HF (in compromised heart)
60
Q

which CCB has a drug-food interaction? what is it?

A

verapamil + grapefruit

“old vera loves her grapefruit”

61
Q

4 drug classes for HTN in the RAAS system

A
  1. ACE inhibitors
  2. ARBs
  3. direct renin inhibitors
  4. aldosterone receptor blockers
62
Q

angiotensin 2 is known as a _______ _________

A

potent vasoconstrictor !!

63
Q

what are our * GOLD STAR* drugs in the RAAS system (best at stopping Angie)

A

ACE inhibitors

angiotensin converting enzyme

64
Q

MOA of ACE inhibitors (3 things - think sequence of events)

A
  1. prevent conversion of angie 1 to angie 2 –> vasodilation
  2. blocks aldosterone (prevents reabsorption of Na and Cl)
  3. increases bradykinin
65
Q

what is recommended re: ACE inhibitor + patients with DM?

A

that they take a ACE inhibitor even BP is normal to prevent diabetic nephropathy (increases vasodilation in glomerulus)

66
Q

SE of ACE inhibitors (4)

A
  • dry cough*** (will improve with SOME patients after a few weeks)
  • angioedema
  • hyperkalemia (b/c blocking aldosterone)
  • 1st dose hypotension
67
Q

MOA of ARBs

A

block binding of angie 2 at receptors –> vasodilation

68
Q

SE of ARBs

A

decreased risk of cough / some cross sensitivity with ACE for angioedema

69
Q

are the RAAS drugs OK to use in preggos?

70
Q

prototype for ARBs

71
Q

prototype for direct renin inhibitors

A

aliskiren (Tekturna)

72
Q

SE of aliskiren (Tekturna)

A
  • cough
  • angioedema
  • diarrhea
73
Q

drug-food interaction with aliskiren

A

avoid with high fat meal - can decrease absorption

no LIS with the LIPASE

74
Q

prototype for aldosterone receptor blocker for HTN drug

A

spironolactone (blocks aldosterone + prevents reabsorption of Na and Cl, but hangs onto K)

75
Q

prototypes (2) of direct vasodilators

A
  1. hydralazine (Apresoline)

2. nitroprusside

76
Q

MOA of hydralazine

A

direct relaxation of smooth muscle of vessels

77
Q

SE of hydralazine (3)

A
  • reflex tachycardia
  • increased blood volume
  • SLE syndrome (butterfly rash like lupus - iatrogenic disease)
78
Q

hydralazine is primarily used for what?

A

emergency situations to rapidly decrease BP (IV)

79
Q

AE of hydralazine

A

severe hypotension

reflex tachycardia

80
Q

MOA of nitroprusside

A

venous and arteriolar dilation

81
Q

what is the DOC for HTN emergency? and what are the diastolic indications?

A

nitroprusside (IV)

diastolic >120

“NITRO = fast”

82
Q

which drug r/t HTN should we not use longer than 72 hours b/c of risk of toxic accumulation

A

nitroprusside

like cyanide toxicity

Pharm 323 Spring 22 (18 decks)

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