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Bloc D - Renal > Jan15 M1,2-Hypertension > Flashcards

Jan15 M1,2-Hypertension Flashcards

1
Q

htn is the leading risk factor for __ and __

A

cardiac disease and strok

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2
Q

lifetime risk of developing htn

A

90%

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3
Q

determinants of BP

A

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

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4
Q

in perfect kidney, why does htn not occur

A

pressure natriuresis of Na and water

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5
Q

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

A
  • pressure natriuresis is blunted

- bad RAAS response (is activated)

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6
Q

chronic htn consequence on the kidney

A

microvascular and tubulointerstitial damage

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7
Q

ctly high BP consequence on heart+circulation

A
  • increased afterload

- damage to arterial system from mechanical shear stress

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8
Q

name for complications from htn

A

target organ damange

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9
Q

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

A

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

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10
Q

how BP affects CV risk

A

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

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11
Q

how target organ damage risk varies with BP

A

higher BP = higher risk

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12
Q

other risk factors that htn clusters with (4)

A

hyperlipidemia
diabetes
obesity
smoking

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13
Q

2 types of htn and %

A

essential (95%)

secondary (5%)

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14
Q

cause of essential htn

A

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

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15
Q

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

A

majority have essential

majority doesn’t require 2ndary htn workup

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16
Q

causes of secondary htn with main one

A

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

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17
Q

primary hyperaldo cause

A

adenoma or hyperplasia of adrenals

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18
Q

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

A

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

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19
Q

why alkalosis in hyperaldo

A

aldo revs up the Na-H exchanger in the PCT

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20
Q

2 factors that contribute to htn in CKD

A
  • rise in AT2 happens, causing vasoconstriction

- retention of Na and water

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21
Q

RAS causes (2)

A

ats or fibromuscular dysplasia

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22
Q

RAS: why causes htn

A

kidney senses low flow and activates RAAS

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23
Q

how htn due to RAS detected

A
  • abdominal bruit
  • hypoK (bc of high aldo)
  • AKI happens after giving an ACEi or an ARB
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24
Q

ACEi/ARBs in bilateral vs unilateral RAS

A
  • 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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25
Q

2 hormones causing htn in RAS

A

AT2 and aldo

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26
Q

thyroid diseases that can cause htn

A

hypo and hyperthyroidism

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27
Q

how hypothyroidism causes htn

A

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

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28
Q

how hyperthyroidism causes htn

A

increase in peripheral resistance occurs

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29
Q

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

A

other symptoms + blood test (easy to check)

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30
Q

sleep apnea def

A

intermittent hypoxia during sleep

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31
Q

3 abnormal things in sleep apnea

A
  • SS overactivity
  • oxidative stress
  • lack of nocturnal declne in BP
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32
Q

how to check for sleep apnea

A

snoring, daytime sleepiness, obesity

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33
Q

why meds can cause htn (what meds)

A

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

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34
Q

pheochromocytoma as cause of htn: def

A

adrenal tumor where high catecholamine (E, NE) secretion

35
Q

symptoms of pheochromocytoma as cause of htn

A

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

36
Q

pheochromocytoma as cause of htn: labs

A

high catecholamines in the blood

37
Q

coarctation of the aorta as cause of htn def

A

narrowing distal to subclavian artery: higher BP in upper extremities

38
Q

hormones activated in coarctation of the aorta

A

RAAS bc low flow to the kidneys

39
Q

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

A

radial femoral delay (check BPs diff)

40
Q

criteria for 2ndary htn screening (5)

A
  • extremes of age (-20 and +50)
  • sudden onset of htn
  • resistant htn
  • family history
  • specific labs/physical
41
Q

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

A

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

42
Q

hypertensive crisis def

A

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

43
Q

causes of hypertensive crisis (2)

A

untreated htn

acute illness superimposed on htn

44
Q

treatment of hypertensive crisis

A

rapid lowering of BP

45
Q

normal circulatory changes in pregnancy

A

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

46
Q

how BP changes in pregnancy from trimester to trimester

A

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

47
Q

4 htn disorders in pregnancy

A
  1. pre-existing chronic htn
  2. transient htn in pregnancy
  3. preeclampsia-eclampsia
  4. preeclampsia superimposed on chronic htn
48
Q

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

A

had chronic htn before

49
Q

ddx if htn after 20 weeks of pregnancy (3)

A
  1. preeclampsia

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

50
Q

most serious pregnancy associated htn disorder

A

preeclampsia

51
Q

preeclampsia def

A

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

52
Q

preeclampsia cause

A

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

53
Q

transient htn treatment

A

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

54
Q

preeclampsia effect on the mother

A

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

55
Q

preeclampsia effect on the baby

A

growth restriction, premature delivery, maybe death

56
Q

risk factors for preeclampsia

A

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

57
Q

preeclampsia treatment

A

delivery of the baby

BP meds

58
Q

pregnancy htn approach

A
  1. rule out preeclampsia (check organ damage)

2. dx is chronic htn, transient htn or ealy stage of preeclampsia

59
Q

Canadian guidelines htn def (when to initiate therapy)

A

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

60
Q

target BP with OBPM (office BP measurement: manual)

A

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

61
Q

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

A

135/85

62
Q

pregnancy htn: treat over what

A

150/100

63
Q

pregnancy htn treatment target no comorbidities patient vs comorbidities

A

no comorb: aim 130/80

comorb: aim 140/90

64
Q

key things for pregnancy htn

A

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

65
Q

2 home BP measurements

A

ABPM (24 hrs): ambulatory monitor

HBPM: home monitor

66
Q

key thing for using the BP guidelines and numbers

A

must do proper technique

67
Q

best method for office BP measuremnet

A

AOBP

68
Q

key point on htn dx

A

not made on first visit

  • need out of office repeated measurements
  • need to check white coat htn and masked htn
69
Q

3 kinds of htn

A

masked, true, white coat (false htn)

70
Q

only way you would dx htn on first measurement

A

BP over 180/110

71
Q

why out of office BPM is better

A

correlates better with end organ damage

72
Q

types of htn : worst to best

A

masked, uncontrolled, white coat

73
Q

2 steps in htn treatment

A

lifestyle changes

meds

74
Q

lifestyle changes to treat BP and main one

A 
reduce salt* (less 2g a day)
weight loss
physical activity
stop smoking
less 2 drinks a day
75
Q

major Na source in our diet

A

processed foods

76
Q

5 first line BP meds

A 
thiazide
ACEi
ARB
CCB (long-acting)
single pill combination (ACE or ARB + CCB or diuretic)
77
Q

key point on BP meds

A

monotherapy is often not enough

78
Q

what determines first line BP med chosen (2)

A
  • special indications

- side effects

79
Q

main side effect of ACEi and of CCB

A

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

80
Q

what meds to use in pregnancy and main one

A
  • CCB (nifepidine**)
  • methyldopa (alpha 2 agonist so less SS)
  • hydralazine (vasodilator)
  • labetalol (beta blocker)
81
Q

what meds not to use in pregnancy

A

ACEi/ARB (associated with fetal renal abnormalities)

82
Q

after treating BP, important thing to remember

A

must act on other risk factors

83
Q

how to choose if non pharma or pharma treatment

A

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

84
Q

important thing to consider in choosing BP med

A

electrolyte abnormalities. can’t give diuretic if hypoK patient

Bloc D - Renal (32 decks)

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