HTN

Question 1

damage from HTN

Answer 1

stroke
retinopathy, blindness
MI
HF
kidney failure

Question 2

180/110

Answer 2

HTN emergency

see slide 4

Question 3

consistently above 140/90 check for

Answer 3

end organ damage
if yes: tx for HTN

if not, diet and exercise

(home BP: 135/85)

Question 4

HTN values

Answer 4

Normal: less than 120/80
pre-HTN: 120-139/80-89
stage 1: 140-159/90-99
stage 2: greater than 160/greater than 100

Question 5

how to perform BP

Answer 5

slide 7, 8

Question 6

long standing HTN

Answer 6

develop LVH–>higher rate of CV events
tx pressure, mass will decrease

if untx dev. ESRD

Question 7

etiology of HTN: primary (95%)

Answer 7

Overactivitation of SNS and RAAS
Blunting of pressure-natriuresis relationship
Variation in CV/renal development
Elevated intracellular Na+/Ca+
Exacerbating factors (too much salt, meds: NSAIDS, cocaine, smoking, etOH, sleep apnea, OCPs)

Question 8

Secondary Hypertension

Who should be screened?

Answer 8

Severe or resistant HTN: Persistent HTN despite use of adequate doses of three antiHTN from different classes
Acute rise in BP in a patient with previously stable values
Age less than 30 in non-obese, non-African American pt w. negative fam hx
malignant/accelerated HTN (severe HTN and evidence of end-organ damage)
age of onset before puberty

Question 9

Genetic causes of secondary HTN

Answer 9

Liddle syndrome
hyperaldo
HTN in pregnancy

Question 10

Renal/renovascular causes of secondary HTN

Answer 10

FMD (fibromuscular dysplasia) in young women (rev)
Refractory HTN
Bruits, PAD
Cr increase with ACE-I (bilat renal artery stenosis)
Pulmonary edema

slide 17
flash pulmonary edema

Question 11

pheochromocytoma

Answer 11

paroxysmal elevations in BP

triad of pounding ha, palps, sweating

Question 12

primary aldosteronism

Answer 12

unexplained hypokalemia with Ur K+ wasting (but more than 50% are normokalemic)

tx: spironalactone: aldosterone inhib

Question 13

cushings

Answer 13

cushingoid facies, central obesity, prox musc wkness and ecchymoses
may have hx glucocorticoid use

Question 14

sleep apnea

Answer 14

primarily in obese men, snore loudly

daytime somnolence, fatigue, morning confusion

Question 15

coarctation of aorta

Answer 15

HTN in arms, diminished/delayed femoral pulses and low/unobtainable BP in legs
left brachial pulse diminished and equal to femoral pulse if origin of the left subclavian artery is distal to the coarctation

*bicuspid aortic valve, assoc. with aortapathies (tx: stent)

+ coarc. check for intracranial aneurysms if both! (MRI)

Question 16

hypothyroidism

Answer 16

symptoms of hypothyr.

elevated TSH

Question 17

primary hyperparathyroidism

Answer 17

elevated serum calcium

Question 18

complications

Answer 18

If untreated can lead to acute complications

Chronic complications:
Hypertensive heart disease
Hypertensive cerebrovascular disease and dementia
Hypertensive kidney disease

Question 19

HTN: Silent killer

Answer 19

Silent killer
Mostly asymptomatic; headache
If severe can cause encephalopathy with N/V, confusion, vision changes

Question 20

Pheochromocytoma will have

Answer 20

episodic presentation

Anxiety, palpitations, profuse perspiration, tremor, HA

Question 21

Optho exam

Answer 21

Cotton wool spots, AV nicking, hemorrhage, *papilledema

Question 22

other tests/imaging

Answer 22

ECG, ECHO, radial-femoral delay

Question 23

EKG

Answer 23

look for LVH

S wave in V3
+ R wave in AVL:
if 23 in female, 28 in male
it’s HTN

S wave in V1 of V2 + R wave in V4 or V5: >35 is HTN

ST depression and asymmetrical T wave inversion

LA enlargement (HTN HD)

Question 24

pics: heart on LVH

Answer 24

slide 24

Question 25

lifestyle mods

Answer 25

diet, exercise every 10 k weight lost BP drops 5-20 more slide 25

Question 26

who should be treated?

Answer 26

All receive lifestyle modification Controversial… Persistently > *140 SBP* (if younger than 60) Persistently > 150 SBP (if older than 60) Persistently > 90 DBP

Question 27

HTN meds to start with Afr. American with ISOLATED HTN: ?? White ?? Afr. Am. pt with DM ??

Answer 27

AA: CCB and thiazide White: ACE-I and BB However, many pts have comorbidities which should prompt targeted therapy ie: Afr. Amer pt with DM should receive ACE-I first

Question 28

systolic HF meds

Answer 28

ACE-I (red. RAS, prev. breakdown of bradykinin (inflamm)) ARB (help with cough from ACE-I) B-blocker (if used before: metoprolol succinate, carvedilol) diuretic aldosterone antag

Question 29

postMI

Answer 29

ACE-I B-blocker ARB ald antag

Question 30

proteinuria

Answer 30

ACE-I | ARB

Question 31

angina

Answer 31

B-blocker | CCB

Question 32

a fib | A flutter

Answer 32

B block, nondihydorpyridine | CCB

Question 33

more drugs for comorbs

Answer 33

``` benign protastic hyperplasia: a-blocker essential tremor: B-blocker (noncardiosel) hyperthyroidism: B-blocker migraine: B-blocker, CCB osteoporosis: thiazide diuretic Raynaud's: dihydropyridine CCB ```

Question 34

contraindications

Answer 34

angioedema: don't use ACE-inhib. Bronchospasticity: DON'T USE B-blocker depression: DON'T USE reserpine liver disease: DON'T USE methyldopa (used during preg) preggos: DON'T USE ACEinh, ARB, renin inhib 2nd/3rd degree heart block: DON'T USE B-block, nondihydropyridine CCB

Question 35

Diuretics | how they work

Answer 35

Initially lower plasma volume but decrease SVR long-term electrolytes, gout, ED, hyperkalemia Thiazides: hydrochlorothiazide best for long-term (give lasix initially) porthaladone: longer half-life loop: not as good for 1st or 2nd line

Question 36

B-blockers

Answer 36

not 1st line for BP anymore Decrease HR and CO, decrease renin levels Carvedilol decrease PVR thru alpha-blockade Nebivolol increases endogenous NO release-->vasodilation may cause bronchospasm, bradycardia, fatigue, ED

Question 37

B-blocker complications

Answer 37

Do not use alone for tx of HTN from cocaine or for pheo unless alpha blockade (unopposed alpha is bad)

Question 38

Renin inhibitors

Answer 38

Lack efficacy data over ACE-I/ARB

Question 39

ACE-I

Answer 39

Inhibits RAAS, prevents degradation of bradykinin

Question 40

ARB

Answer 40

Inhibit RAAS Olmesartan can be a/w a sprue-like syndrome Caution for ACE-I/ARB if Cr worsens > 25%, could be due to renal artery stenosis

Question 41

Aldosterone receptor blockers

Answer 41

CHF, cirrhosis | Can lead to gynecomastia, hyperkalemia, breast pain

Question 42

CCB

Answer 42

Peripheral vasodilation with less reflex tachy/fluid retention do not use nondihydropyridine CCB in systolic HF (can only use norovast, amlodipine) Caution in CHF

Question 43

Alpha blockers

Answer 43

Lower PVR; useful with BPH *First-dose hypotension* (start slow, start at night), caution in CHF can't use if EF is too low

Question 44

Central sympatholytic (clonidine, methyldopa)

Answer 44

Stimulate alpha in CNS thus reducing efferent peripheral SNS outflow adverse: ED, rebound HTN, dry mouth, caution in pregnancy with methyldopa

Question 45

Direct vasodilators

Answer 45

Hydralazine/minoxidil hydrazine with nitrates in Afr. Am: reduces mortality

Question 46

Peripheral Sympathetic Inhibitors

Answer 46

Reserpine adverse: depression

Question 47

HTN urgencies

Answer 47

Treat when acute end-organ damage or BP > 220/125 Reduce ~ 25% in first 1-2 hrs and then target less than 160/100 within 2-6 hrs using Nicardipine, labetalol, nitroprusside, NTG

Question 48

OMM

Answer 48

OA Release: increase Vagal output Rib Raising: inhibitory (attenuate facilitation) Cervicals: carotid baroreceptors, cervical ganglions Thoracolumbar junction: renals and RAS Chapman’s Reflexes: myocardium, adrenals CV4: fluid homeostasis and decrease stress Myofascial Trigger Points: mobilize fluids

Question 49

certain antiHTN drugs may have adverse effects on comorbid conditions:

Answer 49

depression: BB, central a2 agonist gout: diuretic hyperkalemia: aldo anta, ACEi, ARB, renin inhib hyponatremia: thiazide diuretic renovascular disease: ACEi, ARB, renin inhib.