Pharm Exam 3: Anti-Hypertensives 1/2 Flashcards
(98 cards)
1
Q
________ is the most common CV disease
A
HTN
2
Q
less than ______% of pts with HTN are well controlled
A
50
3
Q
pts with HTN have an increased incidence of what other diseases?
A
- renal failure
- CAD
- heart failure
- stroke
- dementia
4
Q
T/F: risk of end organ damage is proportional to the extent of HTN
A
True
5
Q
normal BP
A
< 120 / < 80
6
Q
elevated BP (pre-htn)
A
120-129/<80
7
Q
stage 1 htn
A
130-139 or 80-89
8
Q
stage 2 HTN
A
> 140 and/or > 90
9
Q
BP = ______________
A
CO x Peripheral VR
10
Q
________________ accounts for 95% of HTN cases
A
primary
11
Q
what is primary htn?
A
no universally established cause
12
Q
primary htn is aka ___________________
A
essential HTN
13
Q
secondary htn
A
is HTN secondary to other potentially rectifiable conditions/causes
14
Q
common causes of 2ndary htn
A
- intrinsic renal dz
- renovascular dz (renal artery stenosis)
- mineralcorticoid excess
- sleep apnea
15
Q
what are uncommon causes of secondary htn
A
- pheochromocytoma
- glucocorticoid excess
- corarctation of the aorta
- hyper/hypothyroidism
16
Q
causes of perioperative HTN
A
- inadequate anesthesia
- airway manipulation
- hypoxia/hypercarbia
- pharmacologic adjuncts
- urinary distension
- aortic cross clamping
- hypervolemia
- hypothermia/shivering
- tourniquet pain
- poor medication compliance
- disease related factors
17
Q
what are disease related factors that can be etiology of HTN perioperatively
A
- pheochromocytoma
- hyperthyroid
- hyperreflexia
- MH
- intracranial HTN
- renovascular HTN
18
Q
what two drugs do we give on induction to blunt the SNS response –> i.e. prevent HTN
A
lidocaine and fentanyl
19
Q
what are your anatomic sites of BP control ?
A
- arterioles (AL)
- venous capacitance vessels (PL)
- heart (HR, CO)
- kidney (RAAS)
20
Q
______________ are your capacitance vessels; while _______________ is your resistance vessels
A
veins; arteries
21
Q
what is your humoral mechanism of blood pressure control
A
RAAS
22
Q
what vascular substances are involved in the regulation of Blood pressure?
A
NO- dilates blood vessels
Endothelin 1 - constricts blood vessels
23
Q
which system is responsible for moment-to-moment regulation of BP
A
baroreceptors
24
Q
what system is responsible for long term regulation of BP
A
kidneys
25
what is the neurogenic control center of BP regulation
vasomotor center of the medulla
26
how is local nitrous oxide DIRECTLY released
by endothelium
27
how is local nitrous oxide INDIRECTLY released
from sodium nitroprusside
28
local NO is created in the _______________ cells and then pushed into ________________
endothelial; smooth muscle
29
how do sympathoplegics (sympatholytics) function (in general) as anti-htn
decrease PVR, decrease Heart fx, increase venous capacitance
30
how do diuretics (in general) act as anti-htn
decrease sodium and blood volume
31
how do direct vasodilators function in tx of htn
decrease PVR by relaxing vascular smooth muscle
32
if you use a vasodilator alone in the tx of HTN why would a diuretic and beta blocker need to be added as well ?
VD will cause decrease in PVR --> reflex tachycardia + sodium and water retention.
add beta blocker to prevent tachycardia and add diuretic to prevent salt and water retention
33
most patients with moderate to sever htn require __________ or more anti-htn meds
2
34
what anti-htn drugs can be used as initial drug therapy d/t reduction of complications?
1. thiazide diuretics
2. ACE-I
3. ARB
4. CCB
35
why are diuretics not commonly used as first line agent in the tx of htn
they can increase serum lipid profile and/or impair glucose tolerance --> risk of CAD
36
_____________ are less effective at reducing cardiovascular event, and are currently not recommended as first line tx for uncomplicated htn
beta blockers
37
you know someone's HTN is poorly controlled if they are on _______+ anti-hypertensives
4
38
under what condition can a diuretic be used as the sole agent in htn treatment?
mild htn - only need reduction of BP by 10-15 mmHg
39
which diuretic is the preferred agent as an antihtn agent?
thiazide diuretics - specifically chlorthalidone
40
adverse effects of diuretics
1. hypokalemia
2. magnesium depletion
3. impair glucose tolerance
4. increase serum lipid concentration
5. increase uric acid --> gout
41
what is the purpose of using a diuretic + a potassium sparing diuretic?
reduces blood pressure without causing hypokalemia/hypomagnesmia
42
what is the purpose of using a diuretic + Beta blocker
counteracts the water retaining effects of the beta blocker
43
what is the purpose of using ACEI + diuretic
thiazide diuretic can activate RAAS, ACE-I will counteract this effect
44
what is the purpose of using ARB + diuretic
thiazide diuretic can activate RAAS, ARB will counteract this effect and not cause the dry cough that ACE-I do
45
what are the 2 physiological actions that diuretics do allowing them to fx as anti-htn
1. decrease intravascular volume
2. cause direct arterial vasodilation
46
under what condition, would a thiazide drugs diuretic effect be less effective
with renal insufficiency
47
why are loop diuretics not used as a first line agent for htn
short duration of action
48
when is a potassium sparing diuretic useful in the tx of htn
htn caused by hyperaldosteronism
49
of pts with primary HTN, _____% have too high plasma renin, and _______% have too low
20; 20
50
renin is released when:
1. decreased renal arterial bp
2. SNS neural stimulation
3. reduced sodium delivery
4. increased sodium in the distal renal tubule
51
angiotensin II has ________________ and _____________ activity
vasoconstrictor; sodium retaining.
52
angiotensin II and III both stimulate _____________ release
Aldosterone
53
drug classes that act on RAAS
1. ACE-I
2. ARBs
3. Renin antagonist
4. aldosterone receptor inhibitors
54
___________ are drugs that do not act on RAAS, but can reduce renin secretion
beta blockers
55
what drug is a renin inhibitor
aliskiren
56
physiologic response of aliskiren, a renin-inhibitor
1. vasodilation (arterial and venous)
2. decreases blood volume
3. decreases SNS
4. inhibits cardiac and vascular hypertrophy
57
how do ACE-I work?
1. inhibit the enzyme that converts ang I to ang II
2. stimulates the kallekrein-kinin system by inhibiting the breakdown of bradykinin
58
__________________ do NOT cause reflex SNS activation, therefore they are safe to use in pts with ischemic heart disease.
ACE-inhibitors
59
which specific drug do you have to use caution with, when also using a NMBA d/t synergistic effects
lisinopril
60
what class of drugs may reduce the incidence of DM in pts with high cardiovascular risk
ACE - I
61
what class of anti-htn drugs, is useful in treating patients with CKD, d/t its ability to diminish proteinuria and stabilize renal fx
ACE-I
62
all ACE-I are prodrugs except
lisinopril
63
what is the most common side effect with ACE-I
dry cough
64
what causes the dry cough s/e in 10% of pts on an ACE-I
increase in bradykinin (d/t inhibition of bradykinin metabolism)
65
what are the common side effects with ACE-I
1. dry cough
2. hypotn with hypovolemia
3. hyperkalemia
4. angioedema
66
ACE-I are contraindicated with ____________ & ___________
pregnancy; bilateral renal artery stenosis
67
why are ACE-I contraindicated with pregnancy
1. fetal hypotension
2. anuria
3. renal failure.
68
it is acceptable for Cr to increase up to ____________% while using ACE-I, as long as do not have sudden leaps
30%
69
before being put on an ACE-I, baseline Cr must be < _________, and serum K should be less than ________
2.5; 5.2
70
what is a common effect of patients with heart failure if put on an ACE-I
develop hypotension and worsening renal fx
71
T/F: ACE-I have a relatively low incidence of side effects and are well tolerated
true
72
patients with bilateral renal artery stenosis can go into renal failure if __________ is administered
ACEI or ARB
73
if you use K+ supplements or K+ sparing diuretics with ACE-I what is the result
hyperkalemia
74
what is the effect if you use NSAIDs with ACEI ?
block bradykinin-mediated vasodilation
75
what is the only ARB approved for post-myocardial infarction
valsartan
76
what drugs inhibit cardiac and vascular remodeling associated with chronic HTN, heart failure, and MI
ACEI and ARB
77
physiological response of ARBs for HTN
1. dilate arteries and veins
2. down regulate SNS activity by blocking the effect of ang II on SNS
3. promote renal excretion of sodium and water by blocking AngII
78
T/F: s/e are more rare with ACE-I than ARB
false; more rare with ARB
79
which drug class has a more complete inhibition of angII - ACEI or ARB?
ARB
80
why do ARBs not have as big of a risk with dry cough and/or angioedema when compared to ACEI
no effect on bradykinin metabolism
81
if using an ARB, when do hypotensive effects increase?
diuretic use
vasodilators
anesthetic drugs
82
if a patient comes in on an ARB, and has intraoperative hypotension, how should you treat it?
fluids & vasopressors (esp vasopressin)
83
anesthetic considerations with ARBs
1. hypotensive effects with diuretic use, hypovolemia, VD, and anesthesia
2. interoperative hypotn tx with fluids and vasopressors (incl vasopressin)
3. risk of hyperkalemia with potassium containing solutions
4. increase muscle relaxant effects of non-depolarizing muscle agents
84
contraindications with ARBS
pregnancy & Bilateral renal artery stenosis
85
if a patient is unable to tolerate ACE-I, they are often switched to a _________
ARB
86
potassium sparing diuretics are aka _____________ and/or ________________
aldosterone receptor inhibitors; mineralcorticoid receptor antagonist
87
what are your aldosterone receptor inhibiting drugs
1. eplerenone (inspra)
2. spirinolactone (aldactone)
88
which diuretic might be useful in a patient with a pericardial effusion
aldosterone receptor inhibitors (k-sparin)
89
K - sparing diuretics (aldosterone receptor inhibitors) may cause what electrolyte imbalance?
hyperkalemia
90
are vasodilators a good single tx method for htn?
no d/t compensatory reflexes --> increased HR, blood volume, sodium
91
if you are using a vasodilator to tx htn, adding a beta blocker will stop what 3 compensatory mechanisms from counteracting the VD?
1. block increased renin release
2. block increase in HR
3. block increased cardiac contractility
92
The risk of CV disease doubles for every ____/____ increase in BP.
20/10
93
A primary autonomic mechanism that involves sensory input from the carotid sinus and the aorta to the vasomotor center (Neurogenic Control) and output via the PNS and SNS motor nerves.
Baroreceptors
94
Activation (Stretch) of these inhibits central sympathetic discharge.
Baroreceptors
95
Decreased stretch on the baroreceptors decreases their activity. This leads to a RAPID increase in SNS outflow, leading to:
-Increased PVR (via constriction of arterioles)
-Increased CO (via direct stimulation of the heart and constriction of capacitance vessels to increase venous return)
Restoring normal BP
96
What stimulates the release of Renin?
-Reduction in renal blood flow (decreased pressure in renal arterioles)
-Sympathetic neural activity (via Beta receptors)
97
What does Angiotensin 2 cause?
1) Direct constriction of resistance vessels
2) Stimulation of aldosterone synthesis in the adrenal cortex
98
An arterial dilator used for HTN crisis
-Only IV agent that improves renal perfusion
-D1 agonist
-Dilates peripheral arteries and causes natriuresis
-SE: Reflex tachycardia, increases IOP (beware in glaucoma)
Fenoldopam
