Drugs to treat Hypertension Flashcards
(121 cards)
1
Q
define sympathoplegic
A
drugs used to treat HTN and anxiety which inhibit the postsynaptic transmission of SNS signaling
2
Q
General MOA’s for drugs used to treat HTN
A
Diuretics, Sympathoplegics, Vasodilators, Angiotensin agonists, Renin inhibitor
3
Q
Name the categories of Sympathoplegics
A
Drugs which inhibit CNS sympathetic outflow (Clonidine) Ganglionic blockers (trimethaphan and hexamethonium) Drugs that act at nerve terminals (guanethidine) Alpha and beta antagonists (prazosin, propranolol)
4
Q
Name the vasodilators
A
hydralazine , caclium channel blockers (nefidipine and verapamil) parenteral vasodilators (nitroprusside)
5
Q
name the diurectics
A
Thiazides–>HCTZ–>good for mild HTN Loop diuretics–> Furosemide (lasix)–>used in mod/severe and HTN emergencies
6
Q
name the angiotensin antagonists
A
Ace inhibitors ARB’s
7
Q
name the renin inhibitor
A
aliskiren tekamlo (aliskiren and amlodipine)
8
Q
Compensatory response to diuretics
A
minimal
9
Q
COmpens. response to beta blockers
A
minimal
10
Q
Compensatory response to alpha1-ganglionic blockers-clonidine-methyldopa
A
salt and water retension *slight tachycardia with alpha 1 blockers (prazosin, tarazosin, doxazosin)
11
Q
Compens. mechanism to hydralazine
A
salt and water retention, mild tachycardia
12
Q
compensatory mechnanism to minodoxil
A
marked water and salt retention, marked tachycardia
13
Q
compensaotry change to nefidipine and verapamil
A
minor salt and water retention
14
Q
compensatory change to nitroprusside
A
salt and water rentention
15
Q
compensatory change to ACE/ARB’s
A
minimal
16
Q
Sympathoplegics all work by reducing what
A
- venous tone (increasing compiance) 2. Heart rate 3 contractility 4. CO. 5. TPR
17
Q
most patients with HTN have normal CO, therefore their HTN rests
A
on increases TPR
18
Q
Drugs that act at the baroreceptor site
A
WE CURRENTLY HAVE NONE
19
Q
CNS active agents
A
clonidine and methyldopa
20
Q
Clonidine and Methyldopa MOA
A
–>decreasing CO and TPR –>activation of alpha 2 receptors quickening the onset of negative feedback control and inhibiting NE release
21
Q
Methyldopa active form
A
methyl-norepinephrine converted in the brain
22
Q
sudden discontinuation of clonidine can cause
A
rebound HTN
23
Q
tx of rebound HTN from clonidine withdrawl
A
clonidine reintroduction addisiotn of alpha 2 blocker–>phentolamine
24
Q
drugs that depletes NE sotres
A
resperidine–>contraindicated in pregnancy
25
drugs that deplete stores and inhibit release
guanethidine guanadrel
26
name the alpha 1 receptor blockers
prazosin tarazosin doxazosin \*moderately effective
27
name the non-selective alpha blockers
phentolamine phenoxybenzamine
28
phenoxybenzamine and phentolamine are of no use in tx of chronic HTN bc
they have a large risk of CV stimulation --\>they are non-specicific--\>ALPHA 1 BLOCKADE AND ALPHA 2 INHIBIBITON INCREASES SYMPATHETIC TONE AND PREVENTS THE NEGATIVE FEEDBACK OF THE ALPHA 2 RECEPTOR
29
MAJOR PROBLEM with alpha 1 antagonists
ist done orthostatic hypotension \*also useful to treat BPH
30
vasodilators act via 4 mechanisms
1. release of NO 2. opening of potassium channels resulting in hyperpolarization 3. binding to D1 (dopaminergic) 4. blockage of calcium channels
31
Name the memprane stabalizing beta blockers
Propranolol Acetobutalol Carvedilol
32
Name the beta blockers with ISA
Propranolol Acetabutalol Pindolol \*partial beta 1 agonist
33
non-specific beta blockers
NPPPT +carteolol
34
Specific Beta Blockers
A-N \*except carteolol
35
Beta blockers initially decrease cardiac output but eventually decrease TPR via what likley mechanism
inhibit renin release from JGS cells which are beta 1 receptor dependent for activation
36
Hydralazine and Minidoxil are more effective on
veins rather than arteries (therfore would have a greater effect on edema than the the others)
37
Hydralazine MOA
secretion of NO (EDGFR) \*never used at high doses
38
Hydralazine can cause what side effect
Hydralazine Induced Systemic Lupic Erythematous--\>subsides with attenuation of drug
39
Minidoxil MOA
extremely efficacious--\>used in severe HTN --\>prodrug that its metabolite (minidoxi sulfate) inhibits potassium channel opening--\>hyperpolarizes and relaxes smooth muscle
40
compensation for minidoxil requires
concurrent beta blocker treatment \*can cause hirsutism
41
Ca channel blockers (L-type)
Nefidipine Verapamil DIltizem
42
prototypical dihydroproline channel blockers
nefidipine \*others include amlodipine, felodipine, isradipine
43
DHP channel blockers MOA
reduce cardiac output by inhibiting calcium influx during depolarization--\>slower HR, less contractility
44
why are CA channel blockers preferred over Minidoxil and Hydralazine
less side effects---\> fewer compensatory changes
45
Parenteral vasodilator used in HTN emergencies
nitroprusside
46
nitroprusside MOA
release of NO from the drug molecule itself leading to vessel relaxation and rapid decrease in BP \*half life is in minutes so must be consinuously infused
47
MInidoxil must be administered with
a beta blocker bc it causes severe tachycardia
48
third generation specific beta blocker
nebivolol and bisoprolol
49
name the direct vasodilators
minidoxil
nitroprusside
diazoxide
fenoldapam
50
51
pharmacologic effects of alpha 1 blockers
decrease tpr
reduce bp
relieve symptoms of BPH (relax bladder and prostate)
increase HDL
lower HDL
beneficial in insulin resistance
52
side effects of alpha one blockers
first fose postural hypotension
53
are alpha 1 blockers recommended as first line tx of HTN according to ALLLHAT
NO
54
Beta blockers with MSA
PAC-M
propranolol
acebutolol
carvedilol
metoprolol
55
beta blockers with ISA
APT-T
prindolol
propranolol
timolol
acebutolol
56
may be useful in pt.'s with severe brady cardia
ISA agents
partial beta1 agonist
--\>acts as a antagonist and agonist simultaenously (concentration dependent effect)
57
cardioselectivity beta blockers
A-N
atenolol, metoprolol (mentioned specifically)
58
non selective beta blockers
tomolol
pindolol
proprnaolol
59
MOA for a beta blocker with no ISA
block beta-1 adrenergic recpetors
decrease heart rate and contractility--\>decrease CO
block beta 1 AR in JGA--\>decrease renin output
60
this class of drugs works well in pt.'s with TN and hihg renin output
beta blockers with no ISA
61
"provides effective therapy for all grades of HTN"
beta blockers with no ISA effect
62
do beta blockers cause salt retention
NO--\>can be administered without a diuretic
BB + diuretic is additive effect
63
compelling indications of use for BB's
CHF and MI, Ischemic Heart Disease
64
preferred Hypertensive in pt.'s with hyperthyroidism and migraines
beta blockers
65
Side effects of beta blockers
cold extremities--\>worsens periph. arterial insuff.
bradycardia--\>will slow it down too much, slows AV nodal condunction
bronchospasm --\>need beta 2 to be agonized in asthma
bad dreams/depression
Hypoglycemia--\>only seen in NSBB's
Blocks HSL in lipocytes--\> increases LDL, Reduces HDL increases Trigs
66
Prolonged beta blocker and abrupt cessation of therapy will cause
Tachycardia--\> use increases beta adrenergic receptor density--\>stoppage of therapy will cause a large increase in CO
\*withdraw slowly
67
3rd generation beta blockers with Beta and Alpha blocking ability
LCN
Labetalol
Carvedilol
Nebivolol
68
non-selective beta and alpha1 antagonist
labetolol
carvedilol
69
beta blocker given IV for HTN emergencies
labetolol
70
71
highly selective beta1 antagonist with NO mediated vasodilation
nebivolol
72
useful in HTN with metabolic syndrome
nebivolol
--\>antioxidant activity with increased carb and lipid metabolism
IncreasesSV
maintains CO and systemic blood flow
73
3rd generation beta blocker useful for CHF and HTN
carvedilol
74
decreases mortality and morbity in patients with CHF and HTN
carvedilol
75
3rd gen. BB which protects membranes from lipid peroxidation
carvedilol
--\>antioxidant, binds and scavenges ROS's
76
dry cough from ACEI is caused by
inibition of bradykinin breakdown
--\>there are bradykinin recptors which become overstimulated in the nasopharynx
77
ace inhibitors on the kidney
increase renal blood flow without increasing GFR
78
ACE-I which is renoprotective in diabetics
captopril
-\>increases syntheis of prostaglandins--\>deleays progression of renal disease in Diabetics
79
is posutral hypertension associated with ace inhibitors
no--\>they leave the baroreceptor reflex intact
-
80
most powerful vasocontrctor known
ATII
81
side effects of ACE-I
exacerbate hypotension in volume depleted/sodium depleted pt.'s
HYPERKALEMIA--\>avoid potassium sparing diuretics
dry cough--\>brady
angioedema--\>brady (vasodilator)
fetotoxicity (so are statins and arbs)
82
MOA for ARB's
selectively block ATII type I receptors which are responsible for all the effects of ATII
cause vasodilation and increase Na/Water retention
(thus decrease TPR, plasma volume, CO, and BP)
no effect on bradykinin breakdown
83
pt. on ACE-I develops intolerable cough
put him on a ARB's
84
ARB-prodrug metabolized into an active roduct
LOSARTAN
85
MOA for Losartan
competitive inhibitor of TXA2 receptor (therfore inhibitor of platelet aggrgation)
increases uric acid secretion
\*irbesartan, valsartan, temlasartan do NOT increase uric acid secretion
86
ARB useful in tx of gout
losartan
87
main side effect of ARB's
fetotoxicity
88
89
name the three classes of L type caclium channel blockers
Phenylalkylamines (Verapamil)
Benzothiazepines (diltizem)
Dihydropirines (nefidipine, amlodipine)
90
CLASS/DRUG relatively selective for myocardium--\>less effective at vasodilation
verapamil (phenyalkamine)
91
CLASS/DRUG intermediate between phenyalkyamines and dihydropyridines for myocardial antagonist/vasodilaition
Diltiazem: Benzothiazepines
92
CCB most specific for vasodilation
Amlodipine, Nefidipine (dihydropyridines)
--.selectively block L-type Ca2+ channels in the vasculature
(they are unable to depolarize..unabe to contract--\>therfore they are vasodilated)
decrease TPR and arterial pressure
93
94
does nefidipine cause postural HTN
NO, baroreceptor relfex is left intact
95
drugs most useful in pt.'s with HTN and LOW RENIN output
such as the elderly and AA's
nefidipine and amlodipine
dihydropyridines
96
MOA for alpha 2 selective AGONISTS
clonidine, guanfacine
* decreases sympathetic impulses from RVLM to heart & blood vessels.
* decrease in peripheral vascular resistance and decrease in HR.
--\>the nerve terminal becomes negatively feedback inhibited quicker
97
side effects of alpha 2 agonists
sedtion , drowsiness, fatigue,
98
clonidine withdrawl leads to
severe HTN
\*withdraw slowly
99
MOA for hydralazine
selective arteriolar smooth muscle relaxer
\*triggers baroreflexive sympathetic output--\> tachycardia and renin release
100
uses of hydralazine
IV in eclampsia
101
side effects in hydralazine
Autoimmune hemolytic anemia
angina
tachycardia
palpitations
102
103
hydralazine is usually used with
BB and diuretics
104
minodoxil MOA
relaxes arteriolar smooth muscle by OPENING K-atp channels
dilates arterioles but not veins--\>causes reflex tachy and activates renin secretion
--\>stuck in the inactive-open stage
--\>depolarazation cannot happen
105
side effect of minodoxil
hirsutism
increased renin
106
MOA for nitroprusside
given IV for Malignant HTN
--\>forms NO with stimulates smooth muscle production fo cGMP
--\>CAUSES RELAXATION AND DECREASE IN BP
107
direct dilator that dilates veins and arteries
nitroprusside--increases venous pooling
decreases afterload--\>increases CO in CHF due to left heart failure
\*\*hydralazine is specific to the arteriolar circulation
108
109
augments the action of ALL anti-HTN's
diuretics
with BB's decreases mortality in pt.'s with HTN
110
which pt.'s show better response to thiazides
pt.s with volume dependent HTN (with low renin levels)
111
HTN drug that has secondary protective effect in CAD
beta blockers
\*useful in pt.'s with HTN, tachycardia, HIGH CO, and/or high renin
--\>less effective in african americans and elderly
hyperthyroidism, migraine glaucoma
112
considered standard tx option used with diuretics and ACEI
bisoprolol
--\>34%mortality benefit
113
114
ACE-i's and ARB's work best in
young ppl with htn due to high renin output
115
ace inhibitor with someone who has low renin outut
elderly and AA's
requires what
co-admin with diuretic
116
should be initial antihypertensive drug in Diabetic pt.'s with HTN
ACE-I or ARB
then CCB in 2nd drug needed
117
HTN drug choice in pt's with non-diabtic nephroathy
captopril
118
pt.'s prone to CHF should be prescribed
ACE-I or ARB
119
specific for relaxation of coronary vessels
dihyropyridines
120
very useful in low-renin output HTN pt.'s
CCB's
121
can CCB's be safely used in DM pt.'s
yes
