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
