Flashcards in Dx and Tx HTN Deck (60)
What is essential/primary and secondary HTN?
-Primary: chronic elevation in blood pressure without evidence of other disease
-Secondary: elevation in blood pressure from other disorder.
When do you start thinking about secondary causes of HTN?
-when you cannot get their BP under control alone with medications, if there is a sudden onset or if they start developing sx, if its episodic. Previously well controlled HTN develops sudden increase in BP.
ex: pheochromocytoma, renal artery stenosis, cushings, kidney failure, sleep apnea, birth control, NSAIDS.
What are some environmental factors that play a role in essential htn? Non-environmental factors?
-Gender (generally greater than 65 but becoming more common in children and teenagers)
Sx of Essential HTN
asymptomatic, HA, end organ damage in long term undiagnosed or untreated htn.
Risk factors for HTN
-Cigarettes and Coffee
-stress, anxiety, depression
-Oral Contraceptives (estrogen and progesterone)
Complications of HTN
**END ORGAN DAMAGE**
-TIA, stroke, vascular dimentia
-Heart failure, LVH
-Diabetic Retinopathy (cotton wool spots, neuovascularization, flame hemmorhages, av nicking, silver wiring)
-Renal impairment, proteinuria
what is isolated systolic htn?
-elevated systolic pressure when the diastolic is normal. May pose significant danger for heart events and stroke.
**this increases pulse pressure**
What is pulse pressure? What are some effects of high pulse pressure?
-the difference between systolic and diastolic BP.
-High pulse pressure produces greater stretch of the arteries causing damage to the elastic elements of the vessel
What are the two main types of Secondary HTN?
--renal artery stenosis
-Adrenal causes of HTN
What % of all cases of HTN are primary? secondary?
95% primary HTN
5% secondary HTN
What medications may cause HTN?
-OTC cold remedies containing ephedrine or sympathomimetics
What is the most common cause of 2ndry HTN? Explain why.
-Renal artery stenosis; narrowing of renal artery, kidney senses low O2 when the renal artery is blocked. Renin is then sent from the JG cells out to the blood stream into the lungs where Angiotensin I is converted to AngiotensinII via ACE. AngioII tells the adrenals to release aldosterone, arterioles to constrict, pituitary to release ADH/vassopressin, and renal tubules to absorb Na, Cl and excrete K. Aldosterone retains sodium and therefore water. Volume is increased.....increased BP.
are ACE inhibitors protective or harmful to the kidneys? how?
harmful! they will kill the kidneys if you let them!
-AngioII causes vasoconstriction of the efferent glomerular arterioles, which increases perfusion pressure and GFR.WIth stenosed renal arteries afferent flow cannot be increased and efferent arteriole constriction is crucial for maintaining some degree of filtration. ACE inhibitors prevent conversion of Angio 1 to Angio II and therefore remove the kidneys only remaining regulatory mechanism as well as cutting the perfusion pressure and eliminating what little renal function remains.
What are the two processes of Renovascular hypertension?
-Atherosclerotic renal artery disease; common in older men, often bilateral proximal aspect of renal artery.
-Fibromuscular dysplasia: fibrosis and aneurysm formation in the middle and distal renal arteries, common in young women.
What are some clinical clues of renovascular htn?
-sudden onset w/o FHX
-drug resistant HTN
-worsening renal function after ACE inhib.
Dx: renal functions: BUN, creatinine
-plasma renin levels
Tx: -balloon angioplasty, surgery with stent
-what is this?
-unilateral adrenal adenoma (most common in women)
-bilateral adrenal hyperplasia (most common in men)
What is this?
-increased aldosterone, stimulates excessive renal Na+ retention with resultant volume expansion and htn.
-increased intravascular volume augments renal perfusion, thereby renin secretion is suppressed.
-serum renin level (low)
-urine aldosterone levels
-increased serum aldosterone level that does not suppress after saline-induced volume expansion
-CT to differentiate between adrenal adenomas and hyperplasia, make sure its at the level of the kidney and not in the pituitary.
-adrenal tumors are resected
-adrenal hyperplasia: Spironolactone (diuretic, K+ sparing)
-signs and sx
Signs and Sx:
-HA, sweating, palpitations, tachycardia, n/v, cyclic HTN
dx: 24hr urine catecholamine and metanephrines (biproduct of catecholamine)
-Surgical resection: alpha and beta blockage and volume expansion before surgery.
-chronic therapy with phenoxybenzamine (alpha adrenergic blocker)
-what is this?
-what is paradoxical about this?
-what: narrowing of the aorta, just distal of the left subclavian artery. congenital defect that obstructs aortic outflow leading to elevated pressures proximal to the coarctation.
-distal pressures are not reduced as would be expected, reduced systemic blood flow and in particular reduced renal blood flow leads to an increase in the release of renin and the activation of the RAAS.
* expect aortic coarctation if diff pressures in arms vs legs, right arm vs left arm on a child!!!
How does aortic coarctation effect the barroreceptors?
-baroreceptor reflex is blunted due to structural changes in the walls of the vessels, over time they become desensitized to chronic elevation in pressure and become "reset" to the higher pressure.
HTN medication of choice for black Americans?
-calcium channel blockers
**ARBS AND ACEI are CI!!!!!
JNC VIII adult blood pressure classification
Normal: less than 120mmhg systolic, less than 80mmhg diastolic
prehypertension: less than 120mmhg systolic, 80-89mmhg diastolic
HTN 1: 140-159mmhg systolic, 90-99mmhg diastolic
HTN 2: greater than or equal to 160mmgh systolic, greater than or equal to 100mmhg diastolic
Sx of Hypertensive end organ damage
-cerebral vascular disease
Evaluation of pt with HTN
-BP in both arms and compared with pressure in legs
-funduscopic exam: retinal changes, AV nicking, copper wire, retinal hemorrhages and exudates
-heart exam: S4 and S4
-vascular exam: carotid bruits, PVD, abdominal bruits
-neuro exam for evidence of prior strokes
-CMP; renal function, glucose, and electrolytes
-CBC (hemochromotosis=iron over load, anemia)
Goal of HTN Tx
-reduce risk factors and prevent end organ damage!!!!!
beginnig at 115/75mmhg, CVD risk doubls for each increment of _______.
When do you begin treating HTN?
-a patient shouldnt be labeled as having HTN unless the BP is persistently elevated after three to six visits over a several month period.
*medications should begin if systolic pressure is persistently greater than 140/90 despite attempted nonpharmacologic therapy.
primary htn are generally treated with drugs that aim to...
Patients with 2ndry htn are best tread by.....
1. reduce blood volume
2. reduce systemic vascular resistance
3. reduce cardiac output by depressing heart rate and stroke volume.
-2ndry are best treated by controlling or removing the underlying disease or pathology