HTN Flashcards
AHA HTN classifications
normal: <120/80
elevated: 120-129/<80
Stage 1: 130-139 or 80-89
Stage 2: 140+ or 90+
HTN crisis: >180 and/or >120 (concern for end organ damage)
What age ranges are there more complications with diastolic or systolic HTN
-diastolic HTN has more complications in pt <50yo
-systolic HTN has more complications in pt >60yo
epidemiology of HTN
-more common in Blacks than Whites
-more common in economically disadvantaged
-75% of pt >70yo have HTN
Requirements for diagnosis HTN
elevated BP on at least 2 office visits with at least 2 BP measurements each time
-ambulatory BP monitoring (at home) to r/o white coat HTN
-ID lifestyle factors
-Assess target organ injury or clinical CV dz (heart, lungs, kidneys, eyes)
-primary HTN is MC
when to consider secondary HTN
-if pt is <30 or >50yo
-BP >180/110 at dx
-significant target organ injury at dx
-renal insufficiency
-LVH
-poor response to multi-drug regimen
Possible sx and hx associated with HTN
*most are asymptomatic
-HA is MC
-FH
-lifestyle habits (sedentary, high Na, alcohol, tobacco)
-sx that suggest end organ dx (angina, edema, TIA)
-review meds
-hx of prior BP meds
HTN: PE
-at least 2 BP measurements
- BMI
-waist circumference
-retinal exam (AV nicking, “wiring”, hemorrhages)
-edema
HTN labs/imaging
-CBC
-lipid panel (common comorbidity is HLD)
-serum creatinine, fasting blood sugar, BUN, uric acid, K, Ca (meds can affect K & Ca levels)
-UA
-Renal fxn
-TSH (concern for hyperthyroidism, TSH would low)
-EKG
-CXR (heart enlargement, LVH)
HTN tx goal is
<130/80
nonpharm tx for HTN
-wt loss (most significant effect)
-exercise
-decrease Na
-increase K (dietary, NOT supplement)
-decrease alcohol
-decrease tobacco
when to initiate medication to tx HTN
-individualized to each pt
-pt w/ out-of-office BP > or = 135/85
-pt w/ avg office BP > or = 140/90
-pt w/ out-of-office or in-office BP > or = 130/80 who have 1 or more of the following features: established CVD, T2DM, CKD, 65yo+, estimated 10yr risk of atherosclerotic CVD of at least 10%
ACEI/ARBs
-more effective in younger (<60yo) whites
-less effective in Blacks and older patients
-drug of choice in DM/CKD
-check K and Cr prior to starting; recheck 2 weeks
-ACEI/ARB will vasodilate efferent arteriole
When should you avoid ACEI/ARBs
-Blacks and elderly
-any pt who has renal a. stenosis (ACEI will decrease BF to kidney)
ACEI side effects (CAPTOPRIL)
Cough (MC)
Angioedema (like hives of oral mucosa in airway)
Pregnancy problems (teratogenic)
Taste changes
Other (Rash, fatigue)
Proteinuria
Renal insufficiency
Increased K
Low BP
How does aldosterone affect K and Na
aldosterone increases Na and decreases K
Renin inhibitors
-Aliskiren is rarely used; often unavailable
-lowers BP, reduces albuminuria, and limits LVH
-do NOT combine renin inhibitors with ACEI/ARBs in DIABETICS
Ca Ch blockers
-equally effective in all ages and demographic groups
-preferable to ACEI/ARBs in Blacks and elderly
-MOA: prevent vasoconstriction by blocking Ca channels
MC se: HA, peripheral edema, bradycardia, constipation
ex. Amlodipine, nifedipine (Dihydropyridines end in “ine and non-dihydropyridines don’t)
can combine w/ thiazide diuretics
Diuretics to tx HTN
-often used in mild-moderate HTN
-more effective in Blacks, elderly, obese
-SE: hypokalemia, hyponatremia, increased urate (uric acid reabsorption so avoid in pt w/ gout)
-Thiazides (chlorthialidone, HCTZ, indapamide) are superior to loop diuretics
MOA of diuretics
decreases total volume
keeps Ca out of kidneys and in the body (can prevent kidney stones, good for pt w/ osteoporosis or at risk of osteoporosis)
Aldosterone Receptor Blockers
-spironolactone and eplerenone
-mostly used in pts w/ CHF
-SE: gynecomastia; hyperkalemia
Beta blockers
-decrease HR and CO
-most commonly used post-MI
-SE: bradycardia and hypotension are MC
Alpha blockers
-relaxes arteries, lowers peripheral vascular resistance
-may use in pts with BPH
-orthostatic hypotension is a concern (so have pt take medication before bedtime)
-ex. prazosin, terazosin, doxazosin
What is a drug that reduces sympathetic outflow in CNS and is the first choice HTN drug in pregnancy (works on sympathetic NS)
Methyldopa
When should you initiate 2 HTN drugs and how to decide drugs
when BP is >20mmHg above goal
-drugs must be from DIFFERENT classes
-usually some combination of an ACEI, CCB, or thiazide
-single pills are idea; no single pill for CCB + thiazide available
when should you reassess BP after initiating BP medication
2-4 weeks
types of hypertensive crisis
hypertensive emergency and hypertensive urgency
Hypertensive Emergency
-BP >180/120 WITH organ injury
-hemorrhages, exudates, and papilledema on retinal exam
-encephalopathy (i.e. HA, confusion, somnolence, stupor, visual loss, focal neurologic deficits, seizure, coma)
-oliguria (decreased urine) & azotemia (waste build up in kidneys)
-N/V
-Chest pain
-Back pain (could be aortic dissection)
PE findings of hypertensive crisis
similar to CHF
HTN Crisis: Labs/imaging
-CBC
-blood smear to look for fragmented RBCs
-serum creatinine and BUN
-UA
-serum Na, K, glucose
-CXR
-EKG
Hypertensive Urgency
BP >180/120 WITHOUT organ injury
Tx of Hypertensive Urgency
-lower pressure to <160/100 over hours/days (long term goal is lower)
-provide a quiet room
-Clonidine, captopril
Tx of Hypertensive Emergency
-depends on particular emergency (stroke - TPA, aortic dissection - surgery)
most common cause of secondary HTN
renovascular HTN
Renovascular HTN
-stenosis lesion of renal circulation
-stimulates RAAS (renin-angiotensin-aldosterone system)
when should you suspect renovascular HTN
-onset before age 20 or after age 50
-HTN resistant to 3 or more drugs
-abdominal bruits
-atherosclerotic dz of the aorta or peripheral arteries
-abrupt increase in creatinine >25% after taking ACEI
-episodes of pulmonary edema assoc w/ abrupt surges in BP
Imaging to dx renovascular HTN and what is gold standard
-duplex renal US
-MRA (with renal disease exposure to gadolinium may lead to nephrogenic systemic fibrosis)
-spiral CT angiography
*gold standard is renal angiograms
Causes of secondary HTN
Renovascular HTN
Primary aldosteronism
Pheochromocytoma
Cushing syndrome
Coarctation of the aorta
pheochromocytoma (SE)
tumors of adrenals
-produce catecholamines (epi stimulates sympNS)
-SE: HA, diaphoresis, palpitation, and pallor associated with HTN
S/S of Cushing syndrome
-Central obesity
-skin atrophy
-striae
-acne
-slow wound healing
-proximal m. wasting and weakness
-osteoporosis
-menstrual irregularity
-hyperpigmentation
-glucose intolerance
-hypokalemia
-HTN
Sx and PE findings of coarctation of the aorta
-Sx: HA, cold feet, claudication
-PE findings: >20mmHg difference in BP btwn arms and legs; weak pulses in the legs
*constriction along aorta (s/s will depend on where constriction is)
