Hypertension Flashcards
Hypertension
primary or essential
secondary
idiopathic
Causes of primary or essential hypertension
exact cause unknown, possible:
environmental factors (excess salt, obesity, sedentary lifestyle)
genetic factors (overactive renin-angiotensin-aldosterone system and/r overactive sympathetic nervous system)
secondary to aorta artery stiffening secondary to aging AKA high SBP with normal DBP, usually in geri pt, “isolated hypertension”
Causes of secondary hypertension
cause identified, usually has to do with other disease process:
CKD (anemia, low GFR, small kidney)
hypothyroidism (elevated TSH)
hyperparathyroidism (elevated calcium)
pheochromocytoma (hormone-secreting tumor that causes adrenal glands to produce too much hormone causing HTN, sweating, HA)
OSA
renovascular hypertension (abd bruit, elevated plasma renin activity, >30% elevation of creatinine when starting HTN-lowering Rx) renovascular hypertension is high blood pressure due to narrowing of the arteries that carry blood to the kidneys. This condition is also called renal artery stenosis.
primary aldosteronism (hypokalemia, aldosterone/plasma renin activity ratio >35:30)
RX causing HTN
oral contraceptives
nicotine
steroids
appetite suppressants
tricyclic antidepressants
anti-depressant venlafaxine (Effexor)
cyclosporine (sandimmune)
NSAIDs
nasal decongestants
herbs like capsicum, goldenseal, licorice root, ma huang (Ephedra), Scotch broom, witch hazel, and yohimbine
ambulatory BP monitoring
TX pt with suspected variable BP, which could be caused by:
white coat hypertension
episodic hypertension
hypertension resistant to increasing RX regimens
hypotensive symptoms while taking antihypertensive RX
autonomic dysfunction
Role of the renal system in blood pressure control
RAAS regulates sodium, potassium, and fluid balance in the body.
In response to BP changes (low BP) due to reduced renal perfusion, decreased intravascular volume, or increased circulation of catecholamines, kidney secretes the renin enzyme.
renin converts angiotensinogen to angiotensin 1,
angiotensin-converting enzyme (ACE) converts angiotensin 1 to potent vasoconstrictor angiotensin 2,
angiotensin 2 causes vasoconstriction, stimulates the sympathetic nervous system, stimulates adrenal gland to release aldosterone (increase aldosterone causes retention of sodium and water), BP increases.
in normal physiology, angiotensin 2 inhibits further release of renin through a negative feedback system.
IN OTHER WORDS:
The renin-angiotensin system or RAS regulates blood pressure and fluid balance in the body. When blood volume or sodium levels in the body are low, or blood potassium is high, cells in the kidney release the enzyme, renin. Renin converts angiotensinogen, which is produced in the liver, to the hormone angiotensin I. An enzyme known as ACE or angiotensin-converting enzyme found in the lungs metabolizes angiotensin I into angiotensin II. Angiotensin II causes blood vessels to constrict and blood pressure to increase. Angiotensin II stimulates the release of the hormone aldosterone in the adrenal glands, which causes the renal tubules to retain sodium and water and excrete potassium. Together, angiotensin II and aldosterone work to raise blood volume, blood pressure and sodium levels in the blood to restore the balance of sodium, potassium, and fluids. If the renin-angiotensin system becomes overactive, consistently high blood pressure results.
Types of antihypertensive agents
thiazide diuretics
loop diuretics
potassium-sparing diuretics
beta-adrenergic blockers
ACE inhibitors
angiotensin 2 receptor blockers
renin inhibitors
calcium channel blockers
peripheral alpha-1 receptor blockers
central alpha-2 receptor agonists
direct vasodilators
adrenergic antagonists
thiazide diuretics
thiazide diuretics MOA works by increasing urine excretion of sodium, chloride, potassium, bicarbonate AND increase calcium and uric acid retention
RX
!! if potassium level is <4, effects of digoxin is potentiated with thiazide !!
hydrochlorothiazide (Microzide)
chlorthalidone
indapamide (Lozol)
metolazone (Zaroxolyn)
AX/SE -hypokalemia -hyponatremia -hypomagnesemia *hypercalcemia *hyperuricemia *hyperglycemia tinnitus paresthesia abd cramps n/v/d muscle cramps weakness sexual dysfunction renal dysfunction
CX
- impaired renal function
- thiazides or sulfonamides sensitivity
- gout
loop diuretics
loop diuretics MOA is inhibiting reabsorption of sodium and chloride
TX loop should be used for edema due to CHF, cirrhosis, renal disease.
loop diuresis greater than thiazides, especially in normal renal pt
RX bumetanide (Bumex) furosemide (Lasix) torsemide (Demadex) ethacrynic acide (Edecrin)
AX/SE -hypocalcemia -hyponatremia -hypokalemia *hyperlipidemia (in high doses only) *hyperglycemia (in high doses only) renal dysfunction
CX
anuric pt
sulfonylureas hypersensitivity (sulfonylureas found in anti-diabetic drugs)
hepatic coma
potassium-sparing diuretics
potassium-sparing diuretics TX best benefits Heart Failure, then also HTN
RX spironolactone (Aldactone) amiloride (Midamor) eplerenone (Inspra) triamterene (Dyrenium)
AX/SE
-hyponatremia
*hyperkalemia
^^especially in pt with diabetes, renal insufficiency, concurrent ACE inhibitor, NSAIDs, potassium supplements, potassium serum level >5
gynecomastia
hirsutism
menstrual insufficiency
What does ACE inhibitors target?
ACE inhibitors target angiotensin-converting enzyme, stopping it from converting angiotensin 1 to angiotensin 2
What do diuretics target?
Diuretics (loop, thiazide, potassium-sparing) target the effects caused by angiotensin 2
(1)systemic vasoconstriction, and (2)renal sodium reabsorption
AND (3)the effect of renal sodium reabsorption from release of aldosterone
What do angiotensin receptor blockers (ARBs) target?
Angiotensin receptor blockers (ARBs) block angiotensin 2 from exerting efforts, so
(1) no release of aldosterone from adrenal gland
(2) no systemic vasoconstriction and (3)renal sodium reabsorption
ACE inhibitors (angiotensin converting enzyme inhibitors)
ACEi MOA inhibiting angiotensin-converting enzyme from converting angiotensin 1 to angiotensin 2;
also inhibit degradation of bradykinin;
also increase synthesis of vasodilating prostaglandins
RX lisinopril (Zestril, Prinivil) benazepril fosinopril captopril (Capoten) enalapril (Vasotec)
ACE inhibitors work well for CHF, post-MI, systolic dysfunction, does not work well in AA pt
AX/SE dry cough renal dysfunction rash (with captopril) dizziness angioedema in AA pt laryngeal edema *hyperkalemia in pt with renal disease / diabetes
CX pregnancy renal stenosis of any kind concurrent ARBs concurrent renin inhibitors ^^any agents already working on the RAAS system
renin inhibitors
renin inhibitors MOA blocks the conversion of angiotensinogen to angiotensin 1
RX
aliskiren (Tekturna)
AX/SE
diarrhea/GI stuff
angioedema
CX
concurrent with ACEi
concurrent with ARB
pregnancy
hypertensive emergency
S/SX
ches pain
dyspnea
neurologic deficits
EXAM serial BP in both arms lung and heart auscultation renal artery auscultation neurologic evaluation funduscopic evaluation imaging studies if chest/back pain and unequal pulses in upper extremities
if untreated/delayed TX, can cause arteriolar fibrinoid necrosis, endothelial damage, platelet and fibrin deposition inside smooth muscle, loss of auto-regulatory function, the following may occur: encephalopathy MI unstable angina pulmonary edema eclampsia stroke intracranial hemorrhage arterial bleeding aortic dissection
TX
IV antihypertensive agents
what do calcium channel blockers target?
CCB target movement of calcium ions, blocking them from crossing into the cell membrane, thus relaxing the smooth muscles and causing vasodilation
non-dihydropyridine calcium channel blockers
non-dihydropyridine CCBs MOA is to reduce heart rate, to reduce contractility and to reduce cardiac output, to reduce cardiac conduction at the AV node
RX
verapamil (Calan)
diltiazem (Cardizem)
!! do not non-dihydropyridine CCBs to pt with 2nd or 3rd degree block, or to pt with left ventricular (systolic) dysfunction when EF is <45%)
AX/SE low cardiac output bradycardia GI stuff like constipation (think slowed smooth muscle) peripheral edema hypotension
dihydropyridine calcium channel blockers
dihydropyridine CCBs MOA is to block systemic vasoconstrictions
RX amlodipine (Norvasc) felodipine (Plendil) nifedipine (Procardia XL) -- !! nifedipine is known for causing reflex tachycardia and for causing inconsistent fluctuations of BP !! nicardipine (Cardene SR) nisoldipine (Sular) isradipine (DynasCirc)
dihydropyridine calcium channel blockers are great for AA pt and for pt with ischemic heart disease
AX/SE (think S/SX of vasoconstriction:) HA flushing palpations lower extremities/peripheral edema
angiotensin 2 receptor blockers (ARBs)
ARBs MOA blocks vasoconstriction and aldosterone-secreting effects of angiotensin 2 by blocking the binding of angiotensin 2 to angiotensin 2 receptor found in many tissues.
ARBs are used in pt with HTN, DM2 neuropathy, HF, and those who can’t handle ACEi.
RX losartan (Cozaar) valsartan (Diovan) candesartan (Atacand) telmisartan (Micardis) eprosartan (Teveten) olmesartan (Benicar) irbesartan (Avapro)
AX/SE dizziness *hyperkalemia angioedema upper respiratory tract infections/sinuitis/rhinitis/pharyngitis/bronchitis/cough viral infection fatigue diarrhea
CROSS-REACTIVITY between ACEi and ARBs so if angioedema occurs in ACEi then risk for angioedema to occur in ARBs also present
CX renal and hepatic impaired pt pregnancy concurrent ACEi concurrent renin inhibitors
beta-adrenergic blockers (beta blockers)
beta blockers MOA is to block central and peripheral beta receptors–>resulting in decreased cardiac output and sympathetic outflow
TX hypertension
RX cardioselective beta blockers bind to beta-1 receptors, they are safer (in lower doses) for COPD, asthma, and peripheral vascular disease pt: metoprolol tartrate (Lopressor) metoprolol succinate (Toprol-XL) atenolol (Tenormin) nebivolol (Bystolic) bisoprolol (Zebeta)
RX non-cardioselective beta blockers bind to beta-1 and beta-2 receptors.
RX beta blockers decrease sympathetic activity in HF pt, decrease mortality rates in HF pt and decrease ventricular remodeling in LVH pt: carvedilol (Coreg) metoprolol succinate (Toprol-XL)
RX beta blockers that possess intrinsic sympathomimetic activity (ISA), which reduce heart rate and contractility during excessive sympathetic outflow, and maintain heart rate and contractility during resting states:
pindolol (Visken)
acebutolol (Sectral)
!! Beta blockers should only be used in pt with STABLE CHF and should be temporarily discontinued if pt has acute decompensation !!
!! Beta blockers should be tapered gradually over 2 weeks to prevent withdrawal symptoms, which include unstable angina, MI, or death in cardiac pt !!
!! pt with CAD may experience tachycardia, palpations, increased sweating, and fatigue !!
AX/SE fatigue drowsiness dizziness bronchospasm n/v bradycardia atrioventricular (AV) conduction abnormalities development of CHF **masks SX of hypoglycemia with exception of sweating
CX
pt with sinus bradycardia
2nd/3rd degree heart block
overt cardiac failure
Non-ISA beta blockers are preferred for HTN pt with CAD, especially after MI
beta-1 receptors, what do they do?
beta-1 receptors are found in the heart and kidney
regulate heart rate, renin release, and cardiac contractility
beta-2 receptors, what do they do?
beta-2 receptors are found in the lungs, liver, pancreas, and arteriolar smooth muscle
regulate bronchodilation and vasodilation
direct vasodilators
direct vasodilators MOA is to relax arteriolar smooth muscle
TX hydralazine for HTN, CHF, pre-eclamsia
TX minoxidil for HTN in oral form, alopecia as topical
RX
hydralazine (Apresoline)
minoxidil (Loniten)
^^hydralazine and minoxidil can cause fluid retention and reflex tachycardia, to treat fluid retention and reflex tachycardia that may come with hydralazine and minoxidil, give pt TX concurrent diuretic and a beta-blocker OR non-hydropyridine CCB (diltiazem or verapamil) OR central alpha-2 receptor agonist (clonidine)
AX/SE
hydralazine can cause lupus-like syndrome for dosage >300mg/day (muscle/joint pain aka myalgia/arthralgia, fatigue, dermatitis, drug fever, peripheral neuropathy)
other SE of hydralazine, n/v/d, dizziness, tachycardia/palpitations
AX/SE
minoxidil can cause hirsutism, dizziness, angioedema, fatigue
CX of hydralazine:
CAD
mitral valvular rheumatic heart disease
CX of minoxidil:
pheochromocytoma
acute MI
dissecting aortic aneurysm
central alpha-2 receptor agonists
MoA
central alpha-2 receptor agonists stimulate alpha-2 adrenergic receptors in the brain, resulting in decreased sympathetic outflow, decreased cardiac output, decreased peripheral resistance
AX/SE fluid retention sedation dry mouth possible first-dose effect of dizziness and syncope
CX avoid abrupt cessation recent MI renal failure cerebrovascular disease condution disturbances severe coronary insufficiency
RX (should combine with a diuretic due to SE of fluid retention) clonidine (Catapres) methyldopa (Aldomet) guanabenz (Wytensin) guanfacine (Tenex)
adrenergic antagonists
adrenergic drug mimics epinephrine (works on both beta and alpha) and norepinephrine (works on alpha receptors only) actions which stimulates the central nervous system for flight or fight actions.
adrenergic antagonists MOA is to inhibit the sympathetic system by depleting norepinephrine stores in the central nervous system, resulting in decrease in peripheral vascular resistance (adrenergic antagonist relaxes)
RX
reserpine (Serpasil)
guanethidine (Ismelin)
guanadrel (Hylorel)
AX/SE Depression (due to decreased catecholamine and serotonin levels in the CNS) Impotence Diarrhea Bradycardia Drowsiness Nasal stuffiness Orthostatic hypotension Syncope
peripheral alpha-1 receptor blockers
MoA
TX benign prostatic hypertrophy (BPH)
not usually solely for HTN
peripheral alpha-1 receptor blockers dilate arterioles and veins, causing relaxation of smooth muscle
AX/SE
first-dose phenomenon–>dizziness/faintness, palpitations, syncope
!! start at bedtime and dosage adjusted slowly !!
vivid dreams
depression
fluid retention in chronic administration so give with a diuretic
CX
AVOID if pt has cardiovascular disease
concurrent use of tadalafil (Cialis), sildenafil (Viagra), vardenafil (Levitra) (because of increased risk of symptomatic hypotension)
IF both are prescribed, washout window of at least 4-6 hours recommended
RX
doxazosin (Cardura)
prazosin (Minipress)
terazosin (Hytrin)
different pt populations for TX HTN
DIABETIC PT
HTN increases CV risks in DM pt
ACEi and ARBs are gold standard (not given together though)
!! CX do NOT give 2 RAAS blockers or combine ACEi and ARBs together de to renal risk, hypotension, and hyperkalemia !!
CKD PT
ACEi or ARBs (with/without diabetes)
AA PT
thiazides or CCB are preferred with/without diabetes
more responsive to monotherapy over combination
thiazides and CCB (amlodipine) > ACEi
!! CX do NOT give alpha blockers as initial monotherapy
WOMEN PT
women pt diagnosed with HTN before pregnancy should continue taking antihypertensive RX throughout pregnancy.
-methyldopa is recommended for pregnant HTN pt
!! CX Avoid ACEi, renin inhibitors, and ARBs during pregnancy, also avoid beta-blockers during early pregnancy !!
GERI PT
IF taking beta-blockers, take nebivolol or carvedilol for better outcome
FOR isolated systolic hypertension, start with diuretic if renal okay, and can take non-dihydropyridine CCB okay too
PEDI PT
DO NOT follow adult HTN TX guidelines
IF a diuretic is chosen, the longer acting and more potent chlorthalidone should be considered as 1st-line
beta-blockers more effective IF pt has ischemic heart disease
beta-blockers inferior IF prevention of stroke
ACEi + CCB (benazepril + amlodipine) > ACEi + thiazide (benazepril + hydrochlorothiazide)
ACEi + ARB together are not more effective than monotherapy, in fact, together they had worser renal outcomes
start with 1 drug
1 month later if not working well, add a 2nd drug
1 month later if not working well, add a 3rd drug
if still not working well, then consider pt has resistant hypertension
