HTN treatment lecture Flashcards
1
Q
essential (primary) HTN
A
unknown cause (90%)
2
Q
secondary HTN
A
identifiable cause (disease, drug, CKD, NSAIDs) (5-10%)
3
Q
white coat HTN
A
BP increases in a clinical setting, normal or low at home
4
Q
pseudohypertension
A
BP falsely elevated due to rigid calcified brachial artery
5
Q
osler’s maneuver
A
used to test for pseudohypertension.
BP cuff inflated above peak SBP, if radial artery remains palpable + osler’s (pseudohypertension)
6
Q
isolated systolic HTN
A
only systolic is high
DBP is normal or low
7
Q
resistant HTN
A
not at goal BP but on max dose of at least 3 drugs; one of which includes a diuretic
8
Q
hypertensive crisis
A
> 180/120
Emergency if TOD- goal DBP<110 over min-hours with IV agents
urgency if no TOD- can use PO agents to decrease BP to stage 1 values over several hours
9
Q
diagnosis of HTN is based on
A
2 reading taken on separate occasions
10
Q
home readings over 5-7 days greater than ____ are abnormal
A
> 130/85
11
Q
ambulatory BP monitoring (ABPM)
A
checks BP every 15 minutes over 24 hours
- should drop 10-20% during sleep
- > 130/85 abnormal
12
Q
normal BP
A
<120/80
13
Q
prehypertension
A
SBP 120-139 ot DBP 80-89
14
Q
Stage 1
A
SBP 140-159 or DBP 90-99
15
Q
stage 2
A
SBP >160 or DBP>100
16
Q
major cardiovascular risk factors
A
HTN, obesity, dyslipidemia, DM, smoking, inactivity, albuminuria (GFR55 men, >65 women), family history
17
Q
identifiable causes of HTN
A
sleep apnea, drug induced, primary alosteronism, renovascular disease, cushing syndrome, steroids, pheochomacytoma, CKD, thyroid/parathyroid disease, coarctation of aorta
18
Q
diagnostic work up steps
A
- assess risk factors & co-morbidities
- reveal identifiable causes
- assess presence of target organ damage
- history & physical exam
5/ baseline lab tests
19
Q
lifestyle modification
A
- weight reduction (normal BMI 18.5-24.9)
- Dash diet
- Na restriction (< 2400mg; <1 drink in women
20
Q
BP goal for most patients
A
<140/90
21
Q
BP goal for >80 & 60-80 who are frail
A
<150/90
22
Q
BP goal for anyone who has DM or CKD
A
<140/90
23
Q
compelling indications
A
- left ventricular dysfunction
- post MI
- coronary artery disease
- DM
- CKD
- recurrent stroke prevention
24
Q
stage 1 therapy w/ no compelling indicators
A
monotherapy using ACEI, ARB, CCB, or thiazide
25
stage 1 black patients w/ no compelling indicators should be started on
CCB or thiazide
26
stage 2 therapy w/ no compelling indicators
2 drug combo for most
| thiazide or CCB + ACEI or ARB
27
primary anihypertensives
ACEI, ARBs, thiazides, CCBs
28
alternative antihypertensives
beta-blockers, direct renin inhibitors, alpha-blockers (peripheral), central alpha2-agonst, adrenergic inhibitors, vasodilators
29
ALLHAT conclusions
1. no difference in primary outcome or all-cause mortality
2. ACEI less effective in black patients to decrease BP & CV outcomes (as mono therapy)
3. chlorthalidone was the drug of choice bc decreased secondary outcomes & at the same time was least expensive
4. more than 1 agent was required to control BP in most patients
30
diuretics have synergistic effect w/ other agents. esp:
ACEI/ARBs & beta-blockers
31
diuretic early BP decrease due to
diuresis
32
diuretic chronic BP decrease due to
decreased PR
33
1st generation thiazides not effective in
significant renal impairment (SCr >2.5, CrCl <30)
34
thiazides may be considered 1st line, esp in
blacks & elderly
35
thiazide most common side effects
hypokalemia, hypo-Mg, hyperuricemia
36
thiazide clinical pearls
1. diuretic decreases w/ time
2. takes 2-3 weeks to see max benefit
3. chlrthalidone is ~1.5X more potent than HCTZ & has longer T1/2
4. increase dose leads to increased electrolyte problems. generally limit HCTZ dose to 25mg/day
37
thiazide diuretics
HCTZ & chlorthalidone
38
Thiazide-like diuretics
indapamide & metolazone
39
loop diuretics
furosemide, torsemide, bumetamide
40
loop diuretics may be considered in uncomplicated HTN in patients with
significant renal dysfunction not responsive to thiazides
41
loop diuretic clinical pearls
limited routine use
biggest role is resistant HTN in presence of renal dysfunction
significant diuresis & electrolyte problems
42
potassium-sparing diuretic clinical pearls
primarily used with thiazides to decrease hypokalemia
| may cause hyperkalemia, esp. in combo w/ ACEI/ARB
43
aldosterone antagonists (K-sparing) drugs
eplerenone & spironolactone
44
k- sparing drugs (Na channel)
amiloride, trimterene
45
aldosterone antagonists contraindications
1. spironolactone should be avoided in CrCl 1.8 (women), >2(men), & T2DM w. albuminuria
46
aldosterone antagonist clinical pearls
may cause significant hyperkalemia, esp. w/ ACEI/ARB or K supplements
47
monitoring therapy for diuretics
1. Chem7 (esp. Na, K, BUN, SCr, Glu)
| 2, base line, then in 1-2 weeks, then Q6-12 months or after initiating other agents
48
ACEI affect on SCr
modest elevation (up to 35% normal)
49
why pick ACEI first?
DM, CKD, HF, stroke, MI
50
ACEI ADE
dry cough, angioedema, hypotension, renal dysfunction, hyperkalemia
51
ACEI contraindications
prego (category C)
bilateral renal artery stenosis
avoid concurrent NSAID use if possible
52
ACEI clinical pearls
1. decrease or stabilize albuminuria-protective in DM
2. chronic renal insufficiency is NOT a CI- start low and go slow
3. monitor renal function & K
4. limit salt intake
53
NSAID effects
- decrease GFR
| - block prostaglandins that vasodilate afferent arteriole-> block afferent (ACEI/ARBs block efferent)
54
ARB clinical pearls
1. no cough & decreased risk of angioedema
2. similar outcomes & ADE as ACEI
3. renal data available in DM & CKD
4. typically more expensive than ACEI
5. do not use in combo with another RAS inhibitor
55
DHP CCBs
- may cause reflex tachyradia
- pedal edema most common SE
- peripheral vasodilatory effects
56
non-DHP CCBs
- cardiac effects
- useful for supraventricular tachyarrhythmias
- good coronary vasodilators
- most common ADE: bradycardia & heart block
57
non-DHP drugs
verapamil & diltiazem
58
heart block
can go from bradycardia to a disease in the electrical system of the heart.
59
DHP drugs
-pine
| nifedipine, nicardipine, amlodipine, isradapine, felodipine, nisoldipine
60
CCB clinical pearls
1. may use DHP + nonDHP together
2. constipation, esp. verapamil
3. bc of cardiac effects, caution in cobo w/ beta-blockers & nonDHP
4. avoid short-acting DHP
5. watch for interactions (CYP450), esp. with verapamil & diltiazem
61
can consider beta-blockers first line in what compelling indications
MI, heart failure, angina
| high renin-hypertensives, arrhythmias, migraines, tremors, anxiety, thyrotoxicosis
62
beta-blockers are less effective in
black patients
63
beta1 selective beta-blockers
```
atenolol
betaxolol
bisoprolol
metoprolol tartrate
metoprolol succinate
nevibolol
```
64
nonselective beta-blockers
nadolol
propranolol
timolol
65
intrinsic sympathomimetic beta-blockers
acebutolol
carteolol
penbutolol
pindolol
66
mixed alpha & beta blockers
carvedilol
| labetolol
67
ADE of nonselective beta blockers (Beta 1)
bradycardia, heart block, acute heart failure
68
ADE for B2 blocking
bronchospasms in asthma/COPD
| cold extremities or aggravation of intermittent claudication or Raynaud's phenomenon
69
beta-blocker clinical pearls
1. all lower BP to a similar extent
2. cardio-selectivity is dose dependent & varies from patient to patient
3. use selective agents in those w/ COPD/asthma- BAM (bisopropol, atenolol, metoprolol)
4. do not abruptly withdraw
5. use with extreme caution if also on a nonDHP- big time risk for bradycardia & potential heart block
70
direct renin inhibitor
aliskiren
71
direct renin inhibitor ADE & CIs
same as ACEI & ARBs
72
direct renin inhibitor clinical pearls
1. equally effective as ACEI & ARBs
2. do not`want to use them with another RAS inhibitor (ACEI/ARB)
3. no hard outcomes data
73
alpha1 blocker MOA
block alpha1 receptors on blood vessels which causes vasodilation in periphery
74
alpha1 blockers are
alternative agents which should be used in combo
75
alpha1 blocker ADE
orthostatic hypotension, dizziness, palpitations
76
alpha1 blocker drugs
doxazosin
prazosin
terazosin
77
alpha1 blocker clinical pearls
1. useful in mean with benign prostate hyperplasia (BPH)
2. take 1st dose at bedtime
3. may cayse Na-H2O retention- most effective when given with a diuretic
78
alpha2 agonist clinical effects
decr. sympathetic tone, incr. PS activity-> < in HR, CO, PR, renin & barareceptor reflexes
79
alpha2 receptors are mostly found where?
in the brain
80
alpha 2 agonist drugs
clonidine
guanfacine
guanebenz
methyldopa
81
alpha2 agonist ADE
1. sedation & dry mouth
2. CNS effects- depression, dizziness, orthostatic hypotension, anticholinergic effects (clonidine)
3. Na-H2O repention (methyldopa)
82
alpha2 agonist clinical pearls
1. generally avoid when possible esp, in elderly bc of central effects
2. methyldopa should be given w/ diuretic except in prego
3. do not abruptly withdraw
4. methyldopa may cause hepatitis or hemolytic anemia
83
reserpine ADE
1. significant Na/H2O retention
2. may incr. nasal stuffiness, gastric acid secretion, diarrhea, & bradycardia due to incr. PS activity
3. associated w/ incr. depression
84
reserpine clinical pearls
1. use with a diuretic
| 2. very inexpensive
85
direct arterial vasodilator drugs
hydralazine & minoixil
86
direct arterial vasodilator MOA
cause direct arterial SM relaxation. may activate barorecptors & incr. sympathetic outflow (> HR, CO, renin,
87
direct arterial vasodilator ADE
1. Na-H2O retention
2. reflex tachycardia
3. drug-induced lupus-like syndrome (hyralazine)
hirsutism (minoxidil)
88
direct arterial vasodilator clinical pearls
1. use w/ beta blocker & diuretic- due to compensatory mechanisms
2, monotherapy can precipitate angina-reflex tachycardia
3. reserved for dificult to control HTN
89
about what % of patients achieve goal BP with monotherapy?
<50%
90
synergistic combinations
block compensatory mechanisms
91
synergistic combinations
1. RAS inhibitor + diuretic
| 2. CCB + RAS inhibitor
92
additive combinations
1. beta-blockers + diuretic
2. beta-blocker + DHP CCB
3. nonDHP +DHP
93
less effective combinations
1. diuretics + DHP CCB
| 2. beta-blockers + RAS inhibitors
94
diuretics & DHP CCBs both
decrease PR
95
beta-blockers & RAS inhibitors both
inhibit renin releae
96
HTN in elderly is often
ISH (lead pipe syndrome)
| - systolic is high, but diastolic is normal
97
avoid what drugs in the elderly?
central acting agents & alpha blockers
98
preeclampsia
increased BP with proteinuria
99
most common drugs used in preeclampsia
methyldopa or labetolol
| - beta-blockers, CCB, diuretics probably ok- not a lot of data
100
Contraindicated in prego
ACEI, ARBs, direct Renin inhibitors
101
standard for monitoring HTN
clinic BP monitoring
102
BP response should be evaluted
2-4 weeks after initiating or changing therapy
| -thiazides take 2-3 weeks to see max benefit
103
diuretic monitoring
BP, BUN/SCr, electrolytes (k, Mg, Na)
104
aldosterone antagonist monitoring
BP, BUN/SCr, K
105
Beta-blocker monitoring
BP, HR
106
ACEI/ARB/Renin inhibitor monitoring
BP, BUN/SCr, K
107
CCB monitoring
BP, HR
108
Possible 2* causes of resistant HTN
1. non-adherence
2. lifestyle & non-pharmacological modalities
3. other meds
4. other diseases
109
medication considerations in unknown causes
1. use synergistic or additive combos
2. consider changing to loop
3. add spionolactone
4. combined alpha-beta blockers
5. centrally acting agents
110
renal parenchymal disease
ACEI/ARB+ loop;BB; CCB
111
renal artery disease
angioplasty with stenting in unilateral disease & selected pts
112
aldosteronism
aldosterone antagonists; ACEI/ARB; surgery for adenoma
113
pheochromocytoma
alpha-adrenergic inhibitor; BB; surgical removal
114
cushing's syndrom
surgery
115
hyper/hypo-thyroidism
treat underlying condition
116
sleep apnea
weight loss; CPAP; possibly aldosterone antagonist
117
coarctation of aorta
surgey
