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CSI > HTN > Flashcards

HTN Flashcards

1
Q

damage from HTN

A 
stroke
retinopathy, blindness
MI
HF
kidney failure
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2
Q

180/110

A

HTN emergency

see slide 4

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3
Q

consistently above 140/90 check for

A

end organ damage
if yes: tx for HTN

if not, diet and exercise

(home BP: 135/85)

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4
Q

HTN values

A

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

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5
Q

how to perform BP

A

slide 7, 8

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6
Q

long standing HTN

A

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

if untx dev. ESRD

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7
Q

etiology of HTN: primary (95%)

A

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)

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8
Q

Secondary Hypertension

Who should be screened?

A

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

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9
Q

Genetic causes of secondary HTN

A

Liddle syndrome
hyperaldo
HTN in pregnancy

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10
Q

Renal/renovascular causes of secondary HTN

A

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

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11
Q

pheochromocytoma

A

paroxysmal elevations in BP

triad of pounding ha, palps, sweating

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12
Q

primary aldosteronism

A

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

tx: spironalactone: aldosterone inhib

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13
Q

cushings

A

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

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14
Q

sleep apnea

A

primarily in obese men, snore loudly

daytime somnolence, fatigue, morning confusion

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15
Q

coarctation of aorta

A

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)

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16
Q

hypothyroidism

A

symptoms of hypothyr.

elevated TSH

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17
Q

primary hyperparathyroidism

A

elevated serum calcium

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18
Q

complications

A

If untreated can lead to acute complications

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

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19
Q

HTN: Silent killer

A

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

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20
Q

Pheochromocytoma will have

A

episodic presentation

Anxiety, palpitations, profuse perspiration, tremor, HA

21
Q

Optho exam

A

Cotton wool spots, AV nicking, hemorrhage, *papilledema

22
Q

other tests/imaging

A

ECG, ECHO, radial-femoral delay

23
Q

EKG

A

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)

24
Q

pics: heart on LVH

A

slide 24

25
Q

lifestyle mods

A

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

26
Q

who should be treated?

A

All receive lifestyle modification

Controversial…
Persistently > 140 SBP (if younger than 60)
Persistently > 150 SBP (if older than 60)
Persistently > 90 DBP

27
Q

HTN meds to start with

Afr. American with ISOLATED HTN: ??

White ??

Afr. Am. pt with DM ??

A

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

28
Q

systolic HF meds

A

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

29
Q

postMI

A

ACE-I
B-blocker
ARB
ald antag

30
Q

proteinuria

A

ACE-I

ARB

31
Q

angina

A

B-blocker

CCB

32
Q

a fib

A flutter

A

B block, nondihydorpyridine

CCB

33
Q

more drugs for comorbs

A 
benign protastic hyperplasia: a-blocker
essential tremor: B-blocker (noncardiosel)
hyperthyroidism: B-blocker
migraine: B-blocker, CCB
osteoporosis: thiazide diuretic
Raynaud's: dihydropyridine CCB
34
Q

contraindications

A

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

35
Q

Diuretics

how they work

A

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

36
Q

B-blockers

A

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

37
Q

B-blocker complications

A

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

38
Q

Renin inhibitors

A

Lack efficacy data over ACE-I/ARB

39
Q

ACE-I

A

Inhibits RAAS, prevents degradation of bradykinin

40
Q

ARB

A

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

41
Q

Aldosterone receptor blockers

A

CHF, cirrhosis

Can lead to gynecomastia, hyperkalemia, breast pain

42
Q

CCB

A

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

43
Q

Alpha blockers

A

Lower PVR; useful with BPH

First-dose hypotension (start slow, start at night), caution in CHF
can’t use if EF is too low

44
Q

Central sympatholytic (clonidine, methyldopa)

A

Stimulate alpha in CNS thus reducing efferent peripheral SNS outflow

adverse: ED, rebound HTN, dry mouth, caution in pregnancy with methyldopa

45
Q

Direct vasodilators

A

Hydralazine/minoxidil

hydrazine with nitrates in Afr. Am: reduces mortality

46
Q

Peripheral Sympathetic Inhibitors

A

Reserpine

adverse: depression

47
Q

HTN urgencies

A

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

48
Q

OMM

A

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

49
Q

certain antiHTN drugs may have adverse effects on comorbid conditions:

A

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

CSI (75 decks)

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