B4-102 CBCL: Hypertension and Treatment Flashcards
inhibit NaCl reabsorption in distal convoluted tubule
thiazides
preferred antihypertensive drugs in elderly
- thiazides
- Ca+ channel blockers
preferred thiazide due to long half life and proven reduction of CVD
chlorthalidone
uses for thiazides
* hypertension
* congestive heart failure
* nephrolithiasis
* nephrogenic diabetes insipidus
adverse effects: thiazides
- hypokalemic metabolic acidosis
hyponatremia - hypergluc
glycemia
lipidemia
uricemia
calcemia
potassium sparing diurectics
Keep your SEAT
Spironolactone
Eplerenone
Amiloride
Triamterene
used to counteract hypokalemia caused by loop or thiazide diuretics
potassium sparing diuretics
end in -pril
ACE inhibitors
how do ACE inhibitors lower bp?
reduced angiotensin and increased bradykinin cause vasodilation
adverse effects: ACE inhibitors
Captopril’s CATCHH
cough
angioedema
teratogen
creatinine (increased)
hyperkalemia
hypotension
first choice of treatment for hypertensive patients with
* diabetes
* chronic renal disease
* left ventricular hypertrophy
ACE inhibitors
lower BP without compromising blood supply to heart, brain, or kidneys
ACE inhibitors
do not use in combination with ARBs or direct renin inhibitor
ACE inhibitor
end in -sartan
angiotensin receptor antagonists
how do angiotensin receptor antagonists differ from ACE inhibitors?
- more specific- no bradykinin increase
- more complete inhibition
adverse effects: ARBs
- hyperkalemia
- decreased GFR
- hypotension
- teratogen
similar to ACE, without coughing/bradykinin induced effects
reduced intracellular Ca+ causing arteriolar smooth muscle relaxation
Ca+ channel blockers
do not cause reflex tachycardia
verapamil and diltiazem
verapamil
diltiazem
-dipines
Ca+ Channel blockers
- strongest vasodilators
- most likely to produce reflex tachycardia
dihyropyridines
-dipines
adverse effects: dihydropyridines
peripheral edema
flushing
dizziness
adverse effects: nondihydropyridines
verapamil and dilitiazem
- cardiac depression
- bradycardia
- AV block
- constipation
- orally active
- dose-dependent reduction of plasma renin
- dose dependent reduction of blood pressure
aliskiren
contraindications: aliskiren
- pregnancy
- do no combine with ACE inhibitors or ARB
- reduction in renal sympathetic nerve activity
- may also exert direct renal activity
clonidine
direct renin inhibitor
aliskiren
drugs that block renin secretion
clonidine
beta blockers
block intra and extra renal receptors involved in neural control of renin secretion
beta blockers
block adrenergic receptors at nerve endings
peripheral antagonists
stimulates medullary adrenergic receptors
central agonists
beta-1 selective blockers
4
- atenolol
- betaxolol
- bisoprolol
- metoprolol
beta-1 selective blockers
4
- atenolol
- betaxolol
- bisoprolol
- metoprolol
b1 selective and vasodilatory beta blockers
1
nebivolol
non selective beta blockers
2
- nadolol
- propranolol
beta blockers- intrinsic sympathomimetic activity
4
- acebutolol (b1 selective)
- penbutolol (non selective)
- pindolol (non selective)
- carteolol (non selective)
beta blockers- combined a and b receptors
2
- carvedilol (a1 antagonist, nonselective)
- labetalol (a1 antagonist, nonselective)
beta blockers lower BP by 3 mechanisms:
- reduce CO
- reduce renin secretion
- reduce sympathetic vasomotor tone
more effective in caucasian and young hypertensives
beta blockers
long term benefits on mortality and CVD when used in people with heart failure or acute MI
beta blockers
pose a significant risk of new-onset diabetes
beta blockers
can worsen symptoms of
* reduced myocardial reserve
* asthma
* peripheral vascular neuropathy
* diabetes
beta blockers
a1 antagonists
-zosins
mechanism of action: a1 antagonists
BP falls due to decreased TPR
centrally acting sympatholytic drugs
3
- clonidine
- methyldopa
- guanfacine
sudden withdrawal causes hypertensive crisis, headache, tremor, abdominal pain
clonidine
limited to pregnancy
methyldopa
orally active direct vasodilators
2
hydralazine
minoxidil
IV direct vasodilators
5
- sodium nitroprusside
- diazoxide
- fenoldopam
- enalprilat
- nicardipine
IV direct vasodilator used for eclampsia
hydralazine
when would you use IV vasodilators?
hypertensive emergencies
dilate arteries selectively without affecting venous smooth muscle
3
- hydralazine
- minoxidil
- diazoxide
dilates arteries by acting as a D1 agonist
fenoldopam
dilates both arteries and veins
sodium nitroprusside
adverse effects: vasodilators
- relex tachycardia
- increased renin secretion
may cause lupus like syndrome
hydralazine
causes hypertrichosis
minoxidil
still hypertensive with two drugs
resistant hypertension
recommendations for treatment in pregnancy
4
New Moms Love Hugs
nifedipine
methyldopa
labetalol
hydralazine
classes for treatment of primary hypertension
- thiazide diuretics
- ACE inhibitors
- ARBs
- dihydropyridine
- Ca+ channel blockers
classes of treatment of hypertension with heart failure
- diuretics
- ACE inhibitors
- ARBs
- beta blockers
- aldosterone antagonists
classes for treatment of hypertension in diabetes mellitus
- ACE/ARBs
- Ca channel blockers
- thiazide diuretics
- beta blockers
classes for treatment of hypertensions with asthma
- ARBs
- Ca channel blockers
- thiazides
- cardioselective beta blockers
should be avoided in patients with hypertension and asthma
- nonselective beta blockers
- ACE inhibitors
can mask hypoglycemia symptoms
beta blockers
protective against diabetic neuropathy
ACE/ARBs
definition of hypertension
persistent systolic BP > 130 and/or
diastolic >80
risk factors for hypertension
- age
- obesity
- diabetes
- sedentary
- high sodium diet
- excess alcohol intake
- smoking
- family hx
primary hypertension is related to
- increased CO or
- increased TPR
secondary hypertension is related to
renal/renovascular diseases
severe hypertension without acute end-organ damage
hypertensive urgency
severe hypertension with evidence of end organ damage
hypertensive emergency
hypertension predisposes risk to
- CAD
- LVH
- HF
- a fib
- aortic dissection/aneurysm
- stroke
- retinopathy
life course points of intervention: genes and early life
- genetic susceptibility
- prenatal exposures
life course points of intervention: life course contributors
- diet, exercise, sleep, stress
- housing policy
- environmental exposures
life course points of intervention: treatment
- diagnosis of hypertensions
- access to treatment, follow up, adequate control
- sustained control or end organ damage
common environmental exposures
- lead
- combustion products
fetal and early life exposures are heavily associated with
heavy metals and organics
first line treatment for hypertension
- thiazides
- ACE
- ARB
- calcium channel blockers
second line treatment for hypertension
- beta blockers
- direct renin inhibitors
- alpha blockers
- centrally acting agents
- vasodilators
examples of end organ damage by hypertension
- brain anuerysm
- dementia
- MI
- heart failure
- kidney disease
- stroke
- vision loss
should be avoided in patients with sulfa allergies
thiazides
social stress causes hypertension through:
- increased sympathetic tone
- vasoconstriction
- oxidative stress
can lead to significant loss of potassium and may have to be paired with a potassium sparing agent
chlorthalidone
could lead to hyperkalemia through decreased aldosterone levels
ACEs/ARBs
- beta 1 selective
- used for patients with asthma
acebutolol
can worse diabetes and increase plasma lipids
beta blockers
contraindicated in pregnancy
ACEs
ARBs
can cause reflex tachycardia
nifedipine
can result in bradycardia
verapamil, dilitiazem
first line treatment for patients with hypertension and diabetes
ACE inhibitors
do ACE inhibitors affect the lipid profile?
no
can lead to hyperglycemia and hyperlipidemia
thiazides
can precipitate diabetes
beta blockers
should not be used with ARBs or direct renin inhibitors
ACEs
potassium sparing agent for hypokalemia
spironolactone
can lead to hyperkalemia
ACEs
**cannot combine with spironolactone
should not be used in patients with suldonamide allergies
thiazides
definition of hypertension in screening and treatment guidelines
.>130 systolic OR >80 diastolic
hypertension is more common in
african american individuals
how is race defined in health surveys and reasearch
patient self identifies
DOC in elderly
thiazides or CCB
may worsen CVD outcomes in elderly
beta blockers
not as effective in elderly
ACEs
ARBs
prevent degradation of bradykinin
ACEs
can lead to angioedema
ACE inhibitors
inhibit renin secretion
beta blockers
can result in dry hacking cough
ACE inhibitors
direct renin inhibitor
aliskiren
work downstream of renin secretion but do not affect its activity directly
ACEs
ARBs
do ACEs affect blood glucose concentrations?
no
most common side effect is constipation
verapamil
may cause hypokalemia
thiazides
may cause hyperkalemia
ACEs
ARBs