HTN Flashcards
1
Q
preload
A
volume of blood in heart after diastole (filling)
2
Q
afterload
A
amt of resistance the left ventricle must overcome to pump blood out of heart and to the body
3
Q
diuretics work primarily on ____ _____ (broad)
A
blood volume
4
Q
what will we see with dual therapy with anti-hypertensive and diuretic?
A
enhanced therapeutic effects :)
5
Q
3 types of diuretics + their prototype
A
- loop - Lasix
- thiazide - hydrochlorothiazide
- potassium-sparing - spironolactone
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
7
Q
what is known as the superhero of diuretics? + what’s the prototype?
A
loop diuretics - Lasix
8
Q
what diuretic would we use for acute pulmonary edema?
A
furosemide
9
Q
MOA of loop diuretics (furosemide)
A
inhibits Na and Cl reabsorption @ LOOP of henle –> decreased blood volume
10
Q
what is onset for PO furosemide + how long does it last
A
1 hour onset; lasts 8 hours
11
Q
what is onset for IV furosemide? knowing this, what is your main nursing consideration?
A
5 minutes –> GET BED PAN READY!
12
Q
SE of furosemide (3)
A
- electrolyte imbalances (Na, Cl, K)
- hypotension
- ototoxicity (if too quick IV or dose too big)
13
Q
with furosemide we see an increased risk of what? (3)
A
- digoxin toxicity
- lithium toxicity
- gout exacerbations
14
Q
MOA of thiazide diuretics
A
reduces blood volume @ distal tubule
15
Q
prototype for thiazide diuretics
A
hydrochlorathiazide (HCTZ)
16
Q
onset for HCTZ + how long does it last?
A
onset 2 hours; lasts 12
17
Q
what is the most widely used diuretic?
A
HCTZ
18
Q
SE of HCTZ (3)
A
- electrolyte imbalances (K+ loss not as extreme as in loop diuretics)
- hypovolemia
- hyperglycemia
19
Q
with HCTZ use, we see increased risk of what? (3)
A
- digoxin toxicity
- lithium toxicity
- gout exacerbations
20
Q
what is the prototype for potassium-sparing diuretics?
A
spironolactone
21
Q
what is the MOA of K+ sparing potassium diuretics?
A
BLOCKS aldosterone @ distal tubule –> fluid loss, but K+ remains
22
Q
SE of spironolactone
A
- hyperkalemia
2. endocrine effects (gynecomastia)
23
Q
onset of action for spironolactone
A
48 hrs (NOT a go-to/rescue drug)
24
Q
patient education points when using spironolactone
A
avoid salt substitutes (contain K+ and risk of hyperkalemia is increased)
25
which diuretics put a pt at risk of hypokalemia?
1. loop
| 2. thiazide
26
which diuretic puts a pt at risk of hyperkalemia?
potassium sparing
27
potassium-sparing drugs are usually NOT given with which other antihypertensive drug class?
RAAS drugs
28
when monitoring hydration status with diuretic use, what things are we monitoring?
I+O, daily weights
29
prototype for alpha 1 adrenergic antagonist
prazosin (minipress)
30
MOA of prazosin
blocks SNS activity on arterioles + veins --> vasodilation
31
what effect would prazosin have on a person with BPH?
relaxation of smooth muscles in bladder + prostatic capsule
32
SE of prazosin (3)
1. orthostatic hypotension
2. reflex tachycardia (b/c of drop in BP, body is compensating)
3. nasal congestion (b/c of vasodilation in nose)
33
which medication is associated with 1st dose orthostatic hypotension?
prazosin
34
what is the prototype for alpha 2 adrenergic agonist?
clonidine (Catapres)
35
MOA of clonidine?
CENTRALLY ACTING (CNS) - decreases amount of neurotransmitter NE, which decreases SNS stimulation
--> leads to vasodilation, decreased BP, decreased CO
*alpha 2 = BRAIN*
36
SE of clonidine
*hint: think of MOA of this drug to determine your SE*
drowsiness, sedation, dry mouth, rebound HTN (if stopped cold turkey)
*working on CNS, so you'll see CNS effects*
37
which drug will you see rebound HTN with if stopped cold turkey?
clonidine (b/c of the rebound SNS stimulation)
38
routes for clonidine
oral + patch (change q 7 days)
39
prototype for cardioselective beta blocker
metoproLOL
*cardio selective = only acting on beta 1 (heart)*
40
MOA of metoprolol
1. decreased HR
2. decreased conduction
3. deceased force of contraction
41
SE of metoprolol
*hint: SE r/t work on heart + SE r/t decreased BP*
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
which type of beta blocker would we want diabetic patients on? why?
cardioselective; b/c with nonselective, beta 2 is blocked which blocks glycogenolysis --> hypoglycemia
43
re: beta blockers, what do we need to tell our patients with DM?
this can mask s+s of hypoglycemia (b/c SNS is blocked) --> monitor BG very closely!
44
what VS should we check before admin of beta blocker?
BP+HR (apical) - hold if <60
45
what patient teaching is important with beta blockers?
1. don't stop cold turkey!
2. watch for s+s of hypoglycemia
3. watch for s+s of HF (can decrease CO)
46
prototype for alpha/beta blockers
carvedilol
47
MOA of carvedilol
blocks alpha 1 + beta 1 + beta 2
48
based on MOA of carvedilol, what effect would we see on the receptors?
vasodilation (alpha 1)
decreased HR, contractility, conduction (beta 1)
bronchoconstriction (beta 2)
49
SE of carvedilol
1. hypotension
2. AV heart block
3. bradycardia
4. bronchoconstriction
50
calcium channel blockers don't work on ______
VEINS
| arteries, arterioles only
51
mnemonic to remember CCB + what are the prototypes?
Very Nice Drugs
1. verapamil
2. nifedipine
3. diltiazem
52
MOA of CCBs (dipines + non dipines)
BOTH types: prevents muscle contraction --> smooth muscle relaxes --> vasodilation
non-dipines: verapamil + diltiazem: decreases HR, contractility, conduction
53
we should not have patients on which 2 drug classes at the same time?
Calcium channel blockers + beta blockers (b/c both acting on heart)
54
2 types of CCBs + the prototypes + which act on the heart
1. dipines: nifedipine (only vessels)
| 2. nondipines: verapamil + diltiazem (vessels and HEART) "vera and dilt are sweethearts, they're always together"
55
out of the CCBs, which one would you see reflex tachycardia with? what other medication can we give to decrease the effects of this?
nifedipine - give with BB to decrease reflex tachycardia effects
56
SE of nifedipine
*hint: think of mechanism of action*
- reflex tachycardia
- flushing
- hypotension
- peripheral edema
57
calcium channel blockers mainly work on increasing ______ ______
coronary perfusion
58
route for verapamil
PO
| IV
59
SE of verapamil
*hint: SE r/t vasodilation + SE r/t work on heart*
-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
which CCB has a drug-food interaction? what is it?
verapamil + grapefruit
"old vera loves her grapefruit"
61
4 drug classes for HTN in the RAAS system
1. ACE inhibitors
2. ARBs
3. direct renin inhibitors
4. aldosterone receptor blockers
62
angiotensin 2 is known as a _______ _________
potent vasoconstrictor !!
63
what are our * GOLD STAR* drugs in the RAAS system (best at stopping Angie)
ACE inhibitors
| angiotensin converting enzyme
64
MOA of ACE inhibitors (3 things - think sequence of events)
1. prevent conversion of angie 1 to angie 2 --> vasodilation
2. blocks aldosterone (prevents reabsorption of Na and Cl)
3. increases bradykinin
65
what is recommended re: ACE inhibitor + patients with DM?
that they take a ACE inhibitor even BP is normal to prevent diabetic nephropathy (increases vasodilation in glomerulus)
66
SE of ACE inhibitors (4)
- dry cough*** (will improve with SOME patients after a few weeks)
- angioedema
- hyperkalemia (b/c blocking aldosterone)
- 1st dose hypotension
67
MOA of ARBs
block binding of angie 2 at receptors --> vasodilation
68
SE of ARBs
decreased risk of cough / some cross sensitivity with ACE for angioedema
69
are the RAAS drugs OK to use in preggos?
NOPE!
70
prototype for ARBs
valsartan
71
prototype for direct renin inhibitors
aliskiren (Tekturna)
72
SE of aliskiren (Tekturna)
- cough
- angioedema
- diarrhea
73
drug-food interaction with aliskiren
avoid with high fat meal - can decrease absorption
no LIS with the LIPASE
74
prototype for aldosterone receptor blocker for HTN drug
spironolactone (blocks aldosterone + prevents reabsorption of Na and Cl, but hangs onto K)
75
prototypes (2) of direct vasodilators
1. hydralazine (Apresoline)
| 2. nitroprusside
76
MOA of hydralazine
direct relaxation of smooth muscle of vessels
77
SE of hydralazine (3)
- reflex tachycardia
- increased blood volume
- SLE syndrome (butterfly rash like lupus - iatrogenic disease)
78
hydralazine is primarily used for what?
emergency situations to rapidly decrease BP (IV)
79
AE of hydralazine
severe hypotension
| reflex tachycardia
80
MOA of nitroprusside
venous and arteriolar dilation
81
what is the DOC for HTN emergency? and what are the diastolic indications?
nitroprusside (IV)
diastolic >120
"NITRO = fast"
82
which drug r/t HTN should we not use longer than 72 hours b/c of risk of toxic accumulation
nitroprusside
| like cyanide toxicity
