Jan15 M1,2-Hypertension Flashcards by Django E.

htn is the leading risk factor for __ and __

cardiac disease and strok

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lifetime risk of developing htn

90%

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determinants of BP

SV, HR, TPR and hormones that modulate all that + SS

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in perfect kidney, why does htn not occur

pressure natriuresis of Na and water

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consequence of repeated exposure to high BP in patients with chronic htn

pressure natriuresis is blunted

- bad RAAS response (is activated)

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chronic htn consequence on the kidney

microvascular and tubulointerstitial damage

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ctly high BP consequence on heart+circulation

increased afterload

- damage to arterial system from mechanical shear stress

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name for complications from htn

target organ damange

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target organ damage in brain, eye, circulation, kidneys, heart

brain: TIA, stroke
eye: retinopathy
vessels: peripheral vascular disease
kidneys: hypertensive nephrosclerosis and renal failure
heart: LVH, CHD, HF

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how BP affects CV risk

every increase in 20/10 above 120 doubles CV death risk

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how target organ damage risk varies with BP

higher BP = higher risk

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other risk factors that htn clusters with (4)

hyperlipidemia
diabetes
obesity
smoking

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2 types of htn and %

essential (95%)

secondary (5%)

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cause of essential htn

complex and multifactorial (genetics, RAAS dysfct, SS response, etc.)

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what proportion of patients with htn have essential + what proportion require secondary htn workup

majority have essential

majority doesn’t require 2ndary htn workup

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causes of secondary htn with main one

primary hyperaldo*, CKD, RAS, thyroid disease, sleep apnea, meds, cushing, coarctation of the aorta

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primary hyperaldo cause

adenoma or hyperplasia of adrenals

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primary hyperaldo: renin level, K level, Na level, H+ level

renin is low (suppressed)
Na is high
K is low
H is low (alkalosis)

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why alkalosis in hyperaldo

aldo revs up the Na-H exchanger in the PCT

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2 factors that contribute to htn in CKD

rise in AT2 happens, causing vasoconstriction

- retention of Na and water

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RAS causes (2)

ats or fibromuscular dysplasia

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RAS: why causes htn

kidney senses low flow and activates RAAS

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how htn due to RAS detected

abdominal bruit
hypoK (bc of high aldo)
AKI happens after giving an ACEi or an ARB

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ACEi/ARBs in bilateral vs unilateral RAS

NO in bilateral bc precipitates renal failure: even lower flow to kidneys
YES in unilateral bc inactivate AT2 (RAAS) and other kidney can compensate

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2 hormones causing htn in RAS

AT2 and aldo

thyroid diseases that can cause htn

hypo and hyperthyroidism

how hypothyroidism causes htn

cardiac hyperactivity occurs (CO = SV x HR is now greater)

how hyperthyroidism causes htn

increase in peripheral resistance occurs

how to check for thyroid disease if suspect it as cause of htn (in 2ndary htn workup)

other symptoms + blood test (easy to check)

sleep apnea def

intermittent hypoxia during sleep

3 abnormal things in sleep apnea

- SS overactivity - oxidative stress - lack of nocturnal declne in BP

how to check for sleep apnea

snoring, daytime sleepiness, obesity

why meds can cause htn (what meds)

NSAIDs, glucocorticoids, RBC stimulating agents (increase blood viscosity), alcohol, cocaine, licorice root, calineurin inhibitors (anti rejection agent)

pheochromocytoma as cause of htn: def

adrenal tumor where high catecholamine (E, NE) secretion

symptoms of pheochromocytoma as cause of htn

high SS activity: htn, tachy, headache, anxiety, sweating

pheochromocytoma as cause of htn: labs

high catecholamines in the blood

coarctation of the aorta as cause of htn def

narrowing distal to subclavian artery: higher BP in upper extremities

hormones activated in coarctation of the aorta

RAAS bc low flow to the kidneys

how to check for coarctation of the aorta on physical exam and name for that

radial femoral delay (check BPs diff)

criteria for 2ndary htn screening (5)

- extremes of age (-20 and +50) - sudden onset of htn - resistant htn - family history - specific labs/physical

what labs/physical exam hints lead us to testing for 2ndary htn

hypoK, abdominal bruit, radial femoral delay, OSA, drop in GFR after starting ACEi/ARB

hypertensive crisis def

severe elevation of BP (over 200/120) with acute or chronic end organ damage

causes of hypertensive crisis (2)

untreated htn | acute illness superimposed on htn

treatment of hypertensive crisis

rapid lowering of BP

normal circulatory changes in pregnancy

higher: blood volume, SV, HR, CO, lower TPR due to increased resistance to AT2 and NE and increased vasodilators

how BP changes in pregnancy from trimester to trimester

drops. 1st trimester drop 2nd trimester: peak low 3rd trimester: back to nromal slowly

4 htn disorders in pregnancy

1. pre-existing chronic htn 2. transient htn in pregnancy 3. preeclampsia-eclampsia 4. preeclampsia superimposed on chronic htn

if pregnancy is before 20 weeks (first half), what's the cause

had chronic htn before

ddx if htn after 20 weeks of pregnancy (3)

1. preeclampsia | 2. gestational htn (transient htn or will lead to preeclampsia)

most serious pregnancy associated htn disorder

preeclampsia

preeclampsia def

presence of htn + proteinuria/other organ damage in the mother

preeclampsia cause

abnormal placental vasculature dev so substances circulating lead to endoth damage and vasoconstriction

transient htn treatment

resolves by itself. BP meds if BP too high (prevent stroke)

preeclampsia effect on the mother

hemolytic anemia, thrombocytopenia, high liver enzymes, renal failure, pulm edema

preeclampsia effect on the baby

growth restriction, premature delivery, maybe death

risk factors for preeclampsia

-primigravidy or primipaternity (first baby) -extremes of maternal age (18- 35+) -chronic htn -diabetes etc.

preeclampsia treatment

delivery of the baby | BP meds

pregnancy htn approach

1. rule out preeclampsia (check organ damage) | 2. dx is chronic htn, transient htn or ealy stage of preeclampsia

Canadian guidelines htn def (when to initiate therapy)

140/90 most pts 130/80 diabetics 130 for certain pts 160/100 in low risk pts

target BP with OBPM (office BP measurement: manual)

below 120 for high risk below 130/80 for diabetics below 140/90 for others

target BP with AOBP (automated office BP)=BP true

135/85

pregnancy htn: treat over what

150/100

pregnancy htn treatment target no comorbidities patient vs comorbidities

no comorb: aim 130/80 | comorb: aim 140/90

key things for pregnancy htn

history, physical exam (some things can show previous htn so chronic. like foot ulceR), labs, ECG, risk factors

2 home BP measurements

ABPM (24 hrs): ambulatory monitor | HBPM: home monitor

key thing for using the BP guidelines and numbers

must do proper technique

best method for office BP measuremnet

AOBP

key point on htn dx

not made on first visit - need out of office repeated measurements - need to check white coat htn and masked htn

3 kinds of htn

masked, true, white coat (false htn)

only way you would dx htn on first measurement

BP over 180/110

why out of office BPM is better

correlates better with end organ damage

types of htn : worst to best

masked, uncontrolled, white coat

2 steps in htn treatment

lifestyle changes | meds

lifestyle changes to treat BP and main one

``` reduce salt* (less 2g a day) weight loss physical activity stop smoking less 2 drinks a day ```

major Na source in our diet

processed foods

5 first line BP meds

``` thiazide ACEi ARB CCB (long-acting) single pill combination (ACE or ARB + CCB or diuretic) ```

key point on BP meds

monotherapy is often not enough

what determines first line BP med chosen (2)

- special indications | - side effects

main side effect of ACEi and of CCB

ACEi: cough CCB: edema (but otherwise it's a very good med)

what meds to use in pregnancy and main one

- CCB (nifepidine**) - methyldopa (alpha 2 agonist so less SS) - hydralazine (vasodilator) - labetalol (beta blocker)

what meds not to use in pregnancy

ACEi/ARB (associated with fetal renal abnormalities)

after treating BP, important thing to remember

must act on other risk factors

how to choose if non pharma or pharma treatment

non pharma if only 1 risk factor + no evidence of end organ damage: then give 6 months max for change

important thing to consider in choosing BP med

electrolyte abnormalities. can't give diuretic if hypoK patient