Hypertension Pharm Flashcards
(76 cards)
1
Q
predominant alpha receptor on vascular smooth muscle?
A
alpha1 receptors
2
Q
stimulation of alpha 1 receptors causes
A
vasoconstriction
3
Q
beta 2 receptor stimulation causes
A
vasodilation
4
Q
alpha 2 receptor stimulation
A
inhibits release of norepinephrine
**don’t use an alpha2 blocker as 1st line
5
Q
alpha 1 antagonists
A
result invasodilation
used to tx hypertension
6
Q
alpha agonists
A
- aren’t used in many cardiac conditions
- can be linked to causing cardiac sx
- ex: pseudoephedrine stimulates alpha receptors but is used as decongestant
- commonly cause PVC’s
7
Q
primary hypertension
A
90-95% of cases
no identifiable underlying cause
Tx w/ drugs and lifestyle mod
8
Q
secondary hypertension
A
5-10% of cases
identifiable underlying condition»_space;
renal artery stenosis, pheochromocytoma, thyroid, gravid state
9
Q
Hypertension tx approach
A
controlling high BP #1
BP< 140/90 mmHg = significant decrease in CVD complications
combination therapy 2+ drugs for long term control
Tx SYSTOLIC BP»_space; diastolic will follow
10
Q
aggressive BP reduction
A
can cause myocardial and cerebral ischemia & or infarction
11
Q
Primary HTN drugs
A
reduce CO by:
a. reducing BV or preload (diuretics)
b. reducing HR (B-blockers, CCB)
c. reducing SV (cardioinhibitory drugs & diuretics)
12
Q
dilating systemic vasculature
A
reduce systemic vascular resistance/afterload
13
Q
Diuretics
A
reduce preload»_space; increase urine output
14
Q
thiazide diuretics
A
hydrochlorothiazide HCT
reduces preload»_space; lowers: BVol, CO, SVR (systemic vascular resistance)
used in hypertension Tx
15
Q
aldosterone blocking diuretics
A
spironolactone
potassium-sparing
Tx 2ndary HTN caused by hyeraldosteronism
sometimes as adjunct to thiazide to prevent hypokalemia
16
Q
electrolyte imbalances w/ diuretics
A
*hypokalemia»_space; prob w/ other drugs» potentiates digitalis toxicity
*corticosteroids enhance hypokalemia from loop d’s
*Loop D’s can leed to hypomagnesemia
*hyperglycemia in DM
hyperuricemia
17
Q
Beta Blockers
A
1st line for many d/orders
used extensively for those w/ comorbidities
HF, post-MI, angina»_space; doc decrease in mortality & morbid
18
Q
two classes of beta blockers
A
- non-selective»block b1 & b2 receptors
2. relatively selective b1 blocker»cardioselective
19
Q
B-blocker MOA
A
bind to beta-adrenoceptors & block binding of norepinephrine & epinephrine
- sympatholytic
- decrease contractility, HR, conduction velocity
- prevents remodeling of the hearth
20
Q
Beta-blockers partial agonists
A
partially activate receptor while blocking binding to epi, & norepi
- lower effect on CO and HR reduction
- possess “intrinsic sympathomimetic activity (ISA)
- may be useful for asthmatics
- NOT useful in pts w/ recent MI/HF
21
Q
non-selective beta blockers & asthma
A
beta 2 promotes vasodilation in airway & smooth mm
-using a non-selective may cause harm for those w/ asthma or who have vasospasms
22
Q
membrane stabilizing activity (MSA) of B-blocker
A
makes nerve cells less excitable
occurs @ doses higher than HTN therapeutic range
-benefits some w/ arrhythmias - not clinically significant w/ treating HTN
EX: propranolol (used for mental health issues “chill pill”) & metroprolol
23
Q
alpha & beta inhibitory meds
A
Labetalol & carvedilol
- added alpha blockage»_space; aids in reducing peripheral vascular resistance
- Tx essential HTN, CHF
24
Q
ACEI ARBS & B-blockers less effective for:
A
black and or elderly patients
25
In post MI pts beta blockers
limit infarct size
26
Beta blockers & prinzmetal angina
should be avoided
| coronary vasospasm can be exacerbated by b2 blockade
27
anti arrhythmia properties of beta blockers
inhibit sympathetic influences on cardiac electrical activity
sympathetic stimuli can activate ectopic foci > shut it down w/ a b-block
28
B1 -blockers & adrenoceptors
```
decrease sinus rate
decrease conduction velocity
inhibit aberrant pacemaker activity
>>major role in blocking arrhythmias caused by reentry
do NOT prolong QT interval
```
29
systolic disfunction HF
the contractile fxn of the heart is depressed >>loss of inotropy
30
Beta blockers & systolic d/fxn
improve cardiac fxn and reduce mortality
- reduce deleterious cardiac remodeling that occurs in chronic HF
- carvedilol>>reverses remodeling process by reducing LV volumes & improving systolic fxn
31
Beta blocker general ADR's
contraindicated for sinus bradycardia & partial AV block
nonselective BB's contraindicated for asthma & COPD
-caution w/ cardioselective CCB's (verpamil) >additive effects
-orthorstatic HTN generally NOT a problem unless DDI
-dislipidemias > elevation in triglycerides
-aggravation of hypoglycemia > DM pmts (esp non-selective BB's)
-bronchoconstriction >nonselective BB's
-use cautiously w/ DM pts >>masks insulin-induced hypoglycemia TACHYCARDIA
-exacerbation of prinzmetal angina, peripheral vascular dz, & raynaud's >> cold extremities
-CNS disturbances (common w/ propranolol & carvedilol, NOT common w/ atenolol)
32
BB's general DI's
CYP450 system
NSAIDS + BB = increased risk Acute Kidney Injury (reduction in prostaglandin production)
cardioinhibitory drugs + BB's = increased risk hypOtension
avoid alcohol
33
Calcium Channel Blockers MOA
- bind to L-type calcium channels on vascular smooth mm, cardiac monocytes, & cardiac nodal tissue (SA, AV)
- regulate influx of Ca into mm cells>stimulating contraction
- vascularsmooth mm relaxation (vasodilation),
- decreased myocardial force (-) inotropy,
- decrease HR (chronotropy),
- decreased conduction velocity (-) dromotropy
34
Long acting CCB's
beneficial in Tx most cardiac conditions
35
dihydropyridine CCB's
```
vasodilators
primarily affect vascular smooth mm
used to reduce systemic resistance & HTN (arterial P)
*Not used for unstable angina
ex amlodipine (dipines)
```
36
non-dihydropyridine CCB's
mostly cardioinhibitory w/ some vasodilitory components
primarily affect myocytes & nodal tissue, lesser extent vascular smooth mm
Tx angina & arrhythmias
ex: diltiazem & verapamil
37
dihydropyridine CCB's & angina
vasodilation & hypotension can lead to reflex tachycardia>>increasing myocardial O2 demands >>worsening angina sx potentially tipping to infarct
38
diltiazem
intermediate btn verapamil & dihydropyridines in selectivity for vascular CC's
-used for HTN
-angina
-arrhythmias
has both cardiac depressant & vasodilator actions
-able to reduce arterial P w/out producing reflex cardiac stimulation
39
CCB's & heart failure
drugs decrease electrical activity/conduction velocity through AV node
>>Increasing mortality risk when treating HF pts w/ LV disfxn
40
CCB's & DM Type II
appear to do better than those tx w/ diuretics (which have adverse effects on blood glucose or lipid metabolism)
41
amlopidine & asthma
CCB dihydropyridine
vasodialator
Yes for asthmatics
42
Diltiazem (cardizem)
nondihydropyrine (cardioselective) + vasodilator
Tx: HTN, chronic stable angina, prinzmetal variant angina, arrhythmias
*slows the heart & vasodilates
*can induce bradycardia & partial AV block
*liver metabolism excreted n urine
43
Amlodipine (norvasc)
dihydropyridine >> peripheral vasodilator
Tx HTN & chronic stable angina
long acting
*useful for pts not tolerating diuretics or BB's (DM, COPD, Asthma)
*elderly pts w/ isolated systolic hypertention
*liver metabolism (CYP450 3A4 isoenzyme) >urine excr.
44
Verapamil (Vovera-HS)
nondihydropyridine >>cardioselective
* slow myocardial conduction & vasodilator
* Tx HTN, chronic stable agnina, prnzmetal variant angina & arrhythmias
* less vasodilation than diltiazem
* Titrate*
45
CCB's may be preferred in pts w/
```
asthma
COPD
Pulm HTN (don't want beta 2 blockage)
Peripheral vascular dz
Raynaud's phenomenon
SVT (verapamil is as effective as adenosine)
```
46
CCB's primarily effect which vessels
arterial resistance vessels, minimal effect on venous capacitance vessels
47
CCB pros
lowers BP in pts regardless of :
age, sex or race
*do not promote dyslipidemias, DM issues or aggravation of Peripheral Vascular Dz
48
CAD Anti-anginal effects of CCB's
derived from vasodilator and cardiopressant actions
49
Systemic vasodilation causes
reduction in arterial P >> reduces ventricular AFTERload >> decreasing O2 demands
-The more cardioselective options (nondihydropyridines: verapamil & diltiazem) >> excellent angina Tx
50
coranary arteries & CCB's
CCB's dilate coronary arteries & prevent or reverse coronary vasospasm (which occurs in printzmetal's variant angina) >> increasing O2 SUPPLY to myocardium #win
51
amlodipine & chronic stable angina
it's used, especially when exercise induced b/c it doesn't reduce exercise capability
**But NOT recommended for unstable angina
52
which CCB to use for arrhythmias?
diltiazem & verapamil
ability to decrease firing rate of aberrant pacemaker sites w/in the heart
-especially at the AV node >> helps block reentry mechanisms which can cause SVT
-decrease conduction velocity & prolong repolarization
***Not for Wolfe-Parkinson-White assoc A. Fib (it exacerbates the condition
53
dihydropyridine CCB ADR's (vascular selective)
```
constipation w/ decreases in peristalsis
flushing,
HA
Hypotension
Edema
reflex tachycardia
```
54
non-dihydropyridine CCB's (cardiac selective)
bradycardia
impaired electrical conduction (AV block)
depressed contractility
>>can also have the vasodilation ADR's just not as potent as the dihydropyridines
55
CCB pregnancy category
C for all of them
56
CYP450 & CCB's
involved in all metabolism
all CYP450 inhibitors too (especially verapamil)
could increases digoxin levels
*grapefruit inhibits metabolism of CCB's
57
BB's + nondihydropyridine CCB's
potentiate cardiac electircal & mechanical activity depression (but can be done)
58
Alpha 2 receptors
inhibit neurotransmitter release from presynaptic neurons
59
centrally acting (presynaptic) alpha2
sympatholytics block by binding to alpha2 adrenoceptors
-reduces sympathetic outflow to the heart > decrease HR & contractility>>decreasing CO
-decreases arterial pressure
inhibits neurotransmitter release from presynaptic neurons>>inhibiting the sympathetic signal from continuing
60
A2 MOA
decrease norepinephrine release in the brain > in arterial blood pressure centers
- decreases norepinephrine release peripherally too
- reduces CO & vascular resistance (clonidine >methyldopa)
61
A2 indications
alternative HTN Tx (rarely 1st line)
- Methyldopa is preferred Anti-HTN for PREGOS
- Clonidine preferred for pts undergoing w/drawl related HTN from tobacco or other drugs
- Clonidine does not lower exercise tolerance like BBs
- combo'ed w/ diuretics to prevent fluid accumulation
- pts w/ renal concerns + HTN
62
A2 ADR's
abrupt d/c of drug associated w/ high risk of HTN crisis or rebound hypertension (mortality). *MUST TAPER*
dry mouth, orthostatic hypotension, bradycardia, vision disturbances, and CNS depression
63
A2 DI's
BB's>>decrease/reverse antiHTN effects
| Tricyclic antidepressants/SSRI/SNRI: block antiHTN evicts & increase risk for rebound HTN
64
Alpha1 antagonists (vasodilators) MOA
bind to alpha-adrenoceptors located on vascular smooth muscle>>vasodilation
65
Prazosin (minipress)
Tx Primary HTN & BPH
metabolized in liver
titration needed
ADR: nasal congestion (dilation of nasal mucosal arterioles), reflex tachycardia (minimize w/ bedtime admin),
dizzy, orthostatic hypotension (loss of reflex vasoconstriction upon standing), fluid retention (add diuretic)
DI's: w/ other antiHTN >>increase risk of hypotension, ETOH
66
ACE inhibitors (lisinopril, enalapril, ++) MOA
MOA: prodrugs (except lisinopril) inhibit the formation of angiotensin II by competing w/ angiotensin I for binding w/ ACE
67
ACE inhibitors (lisinopril, enalapril, ++)
vasodilator >>blocks the breakdown of bradykinins which are vasodilators so the stay in circulation longer
68
ACE inhibitors (lisinopril, enalapril, ++) actions
dilate arteries & veins
reducing arterial P, preload & afterload on the heart
down regulate sympathetic adrenergic activity >>sympatholytic
promotes renal excretion of Na+ & H2O
-inhibits cardiac & vascular remodeling associated w/ chronic HTN, HF, MI
69
Lisinopril
fair absorption
| no metabolism, excreted unchanged in urine
70
enalapril
good absorption
| prodrug, activated in liver to "enalaprilat"
71
ACEI (lisinopril & enalapril)
indications: primary HTN,
less effective in African American's but you want to use still, add a diuretic
-decrease urinary protein excretion & slow diabetic proteinuric dz
-decreases interglomerular pressure>>inhibits efferent constriction
**conditions which glomerular filtration critically dependent on angiotensin II, ACEI can induce acute renal failure>>reversible once drug stopped
often used w/ a diuretic
72
what labs to check prior to ACEI or ARB
BUN & Cratinine >> need to check status of GFR
73
ACEI & heart failure
reduced afterload >>enhances ventricular SV & ejectionF%
reduced preload>>decreases pulm & systemic congestion
reduced sympathetic activation>>
improving O2 supply/demand ratio>>decreasing demand
Prevents angiotensin II from triggering deleterious cardiac remodeling
*often used w/ diuretic
74
ACEI post MI
help reduce deleterious remodeling that occurs post MI
| useful in pts at risk of MI b/c CAD >>esp. diabetics even if signs not there yet
75
ACEI ADR's
```
well tolerated
dry cough
Hypotension in HF pts
angioedema
PREGO CATEGORY D
```
76
ACEI DI's
```
ETOH
diuretics
antiHTN's
K+ containing meds & foods or meds that increase K+ levels
high salt diet>>lowers effectiveness
```
