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HT Flashcards

1
Q

def. HT

A

present when the benefits of Tx outweigh the SE
- generally 140/90
25% of adult pop, 70% by age 80

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2
Q

2 stages of HT

A
  1. 140-159/90-99

2. >160/100

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3
Q

2 cat. of HT

A
  1. systolic/diastolic
    - 95% idiopathic
    - the rest secondary
  2. systolic only
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4
Q

patho of isolated systolic

A
  1. age + athero>
  2. change in wall of aorta (calc, collagen, less elastin)>
  3. low compliance>
  4. high systolic BP
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5
Q

3 epi features of essential HT

A
  1. onset 25-45
  2. usually fam Hx
  3. both elevated
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6
Q

pathogenetic factors involved

A
  • genes
  • race
  • hemodynamics
  • SNS activation
  • endothelial dys
  • renal contribution
  • obesity
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7
Q

what is role of genes

A

polygenic, but related to fams and twins

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8
Q

what is race factor

A

blacks

  • SES - salt, poor materanl nut
  • genetics - APO-L1
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9
Q

what causes MAP to increase

A
  • either high CO or high resitance - most often resistance
  • neurohormonal factors
  • autoreg in response to CO
  • blood vessel changes
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10
Q

2 main systems that get activated and what activates them

A
  1. SNS
    - stress
    - smoking
    - acl
    - obesity
    - baroreceptor dys
  2. RAAS
    - genes
    - SNS activation
    - sub pop of ischemic nephrons
    - OCPs
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11
Q

2 issues with endothelial dysfunction

A
  1. NO
    - may be low due to angiotensin2 related oxidant stress
  2. endothelin (vasoconstrictor) elevated
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12
Q

what is renal contribution

A
  • not exreting Na
  • may be due to congenically low nepron
  • SNS and RAAS activation
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13
Q

what is effect of obesity

A

peripheral insulin resistant

  1. direct HT effect
  2. increases insulin secretion>hyperinsulinemia>HT
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14
Q

what are vessel wall changes

A
  1. initial resistance is dynamic
  2. sustained HT
    - arteioles can be lost
    - vasc. smooth muscle can be affected by angio2 - hypertrophy, extracell matrix
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15
Q

*** 5 causes of secondary HT

A
  1. renal
    - renal parenchymal
    - renal A stenosis
  2. endocrine
    - adrenal - cushings
    - other
  3. drug
    - Rx
    - licorice
  4. sleep apnea
  5. carctation of aorta
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16
Q

what is effect of renal parenchymal probs

A
  • acute and chronic renal diease
  • get ECF vol expansion
  • abnormal RAAS
  • need to control BP and antag. RAAS
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17
Q

2 main causes of renal A stenosis

A
  1. young- fibromusclualr
  2. old - athero
  • both activate RAAS
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18
Q

when to suspect renal A sten

A
  • young person with HT
  • older person with new diastolic HT
  • refractiry HT
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19
Q

Dx for stenosis

A

imaging - only if a cand. for revasc

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20
Q

Tx for stenosis

A
  • limited benefit for revasc

- meds

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21
Q

3 major endo dysfunctions that can lead to HT

A
  1. hyperaldosteronism (conns)
  2. pheo
  3. cushings
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22
Q

what happens in coarctation

A
  • narrowing in aorta where ductus connects

- HT in arms, hypo in legs

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23
Q

what drugs can lead to HT

A 
prescribed
- OCP
- NSAIDS
- steroid
- EPO
- cyclosporine, tacrolimus
other
- cocaine
- EtOH
- licorice
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24
Q

2 main reasons HT is bad for you

A
  1. ather risk factor
    - coronary
    - stroke
    - AAA
  2. endo organ damage
    - heart
    - brain
    - kidney
    - eye
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25
Q

2 main types of vascular lesions

A
  1. large As
    - athero
  2. small As
    - chronic - arteriolar sclerosis
    - acute - fibrinoid necrosis
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26
Q

what are cardiac cons. of HT

A
  1. high afterload - LVH
  2. leads to diastolic dysfucntion - heart is stiff
    - pulm edema
  3. leads to systolic dysfunction
    - most common cause of CHF
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27
Q

3 neuro cons.

A
  1. encephalopathy
  2. dementia
  3. stroke
    - ischemic and hemmoragic
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28
Q

what is renal effect of HT

A
  • faster progression of all renal disease

- kidney disease causes HT

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29
Q

4 stages of retina effects

A
  1. focal arteriolar spasm
  2. diffuse spasm
  3. soft exudates of flame hemo
  4. papilledema
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30
Q

4 parts of assessement of HT PT

A
  1. confirm HT
  2. evidence of target organ damage
  3. other CV risks
  4. secondary causes
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31
Q

how to office measure

A

if over 140/90, do twice more and discard 1st

32
Q

2 other monitors for PT

A
  1. home
    - cuff at home bid for 7 days
    - discard first day
    - HT >135/85
  2. ambulatory
    - takes all the time
    - HT if 24 hour > 130/80 or day is 135/85
33
Q

what are 2 options to true HT and normotension

A
  • white coat - false pos

- masked HT - false neg

34
Q

features of white coat

A

20% of PTs in office

  • anxiety
  • more common in women, elderly, smokers
  • less likely if by nurse, stage 2 or repeastedly high
35
Q

features of masked

A
  • p to 10% of pop
  • more common in young men, smokers, alc, obese
  • provoked by steress, anxiety
36
Q

3 ways to test for end organ damage

A
  1. Hx
    - angina, MI, stroke
  2. PHx
    - LVH
    - CHF
    - prior stroke
    - fundoscopy
  3. lab tests
    - renal
    - cardiac
37
Q

how do CV risk factors and HT interact

A

synergistic

- when have a high baseline risk, Tx that cuts in half has a better absoulte risk reduction

38
Q

4 things to consider if refractory HT

A
  1. renal A sten
  2. renal parencymal disease
  3. hyperaldo
  4. pheo
39
Q

6 non-pharma mgmt things to do

A
  1. salt resticton
  2. diet - DASH
  3. weight loss - at least 10lbs
  4. tobacco
  5. EtOH
  6. excercise - FITT goals
40
Q

what is FITT

A

Freq
Intensity
Time
Type

41
Q

5 major cats

A

ABCDE

  1. ACEi and ARB
  2. BBlock
  3. CCBs
  4. Diuertics
  5. Eerthing else
42
Q

Agents, MOA, SE, roles for ACEis

A 
Agents - prils
MOA
- reduce angiotensin 2
- vasodilation and naturesis
- also antifibrotic and antiproliferative
SE
- cough
- hyperkalemia
- teratogenic
Role
- first line
43
Q

what is effect of ACEi on kidney

A

some patients have rapid drop in GFR and need to be stopped, most have short drop and evens out pretty quick

44
Q

Agents, MOA, SE, roles for ARBs

A 
Agents - sartans
MOA
- antagonize angiotensin 2 R
SE
- hyperkalemia
- teratogenic
Role
- DM
- sub for ACE if intolerant
45
Q

what is other RAAS drug

A

aliskiren

- direct renin inhib

46
Q

Agents, MOA, SE, roles for Bblockers

A 
Agents - -olols
MOA
- reduce HR and contractility 
- reduce renin
SE
- bronchospasm
- bradycard
- heart block
- CNS
Role
- less common for just HT
- more for CAD, CHF, Afib, anxiety
47
Q

2 types of solubility

A

water
- renal elim - once daily, less CNS effects
lipid
- liver elim

48
Q

Agents, MOA, SE, roles for CCBs

A 
Agents - -dipines
MOA
- arteriolar vasodilation - no CA into smooth muscle of cell
SE
- peripheral edema
- flushing HA
Role
- very common, may be first choice
49
Q

Agents, MOA, SE, roles for diuretics

A 
Agents - you know them
MOA
- renal tubular reduce Na reabsorbtion
- anti-HT
SE
- hypokalemia, hyernatremia
- ECF vol. depletion
- gout
- ED
Role
- very common, espeically blacks
- edema
- prevent Ca stones
50
Q

2 main not-K sparing

A
  1. thiazide - DCT

2. furosemide - ALOH

51
Q

2 main K-sparing

A
  1. spironolactone

2. aminolride

52
Q

Agents, MOA, SE, roles for A-blockers

A 
Agents - -azosin
MOA
- A r blocker - vasodilation
SE
- ortho hypo
- first dose hypo
Role
- not first line, but 3 or 4
53
Q

Agents, MOA, SE, roles for direct vasodilators

A 
agent
- hydrazine
- minoxidil
MOA
- directly act with smooth muscle
- very potetnet
SE
- reflex tachy
- SLE
- minoxidil - hair growth
Role
- refractory HT
54
Q

Agents, MOA, SE, roles for central sympatholytics

A 
agent
- clonidine
- methyldopa
MOA
- stim PRE-synaptic A-2 R
- inhib SNS outflow
SE
- sedation
- ortho hypo
Role
- preganccy for methydopa
55
Q

how to use meds

A
  • start low dose of one med

- one med to treat 2 probs when possible

56
Q

what is main goal of Tx

A

BOTH 140 and 90

57
Q

other goals to consider

A

DM - 130/85
>80yo - 150/90
renal disease - 130/80

58
Q

what is too low

A

no benefit to 120/70

lowering

59
Q

4 things to do if not at goal

A
  1. optimize dose
  2. if NO response, swtich class
  3. add a second agent
  4. consider causes of refractory HT
60
Q

ways to improve adherence

A
  • shared, clear goals
  • empathic approach
  • address cost
  • written direactions
  • once daily, blister packs
61
Q

how to monitor once stable

A
  1. office - 3-6 months
  2. regular home BP monitoring
  3. 24-hour ambulatory
    - is hypo
    - if fluctuating readings
62
Q

2 other therapies to consider

A
  1. ASA

2. statins

63
Q

5 factors that reduce the NNT

A
  1. high baseline risk
  2. higher initial BP
  3. longer duration of Tx
  4. greater magnitude of BP fall
  5. other interventions
64
Q

what is hypertensive crisis

A

situation that needs to be lowered NOW

- S>200 or D over 120

65
Q

what is HT emergency

A

needs to be lowered in 60 min

66
Q

what is malig. HT

A

V high BP with papiledema

67
Q

5 systems that can cause HT emergency

A
  1. brain
  2. CV
  3. catecholamine excess
  4. severe eclampsia/preeclampsia
  5. accelerated-malignant HT
68
Q

what is cerebral autoregulation

A
  • brain keep perfusion pressure between 50-150
69
Q

what is HT encephalopathy

A
  • diffuse brain dysfucntion - not focal
  • cerebral edema
  • rare
70
Q

what is catechalime excess syndrome

A
  • intox with cocaine, amphetamines
  • withdrawal from anti-HT, sedatives
  • MOAis
  • pheo
71
Q

what is eclampsia or pre

A
  • acute sustained raise in BP >160 or 110
  • need to lower ASAP
  • be careful with meds
72
Q

3 cats. of HT urgencies

A
  1. severe asymptomatic (>200/120)
  2. accelerated-malignant HT with no end organ damage
  3. pre and post operative HT d>110
73
Q

3 issues of HT in operative setting

A
  1. pre-op -safe to operate?
  2. post-op - increased bleeding, may be due to pain or anxiety
  3. may be NPO - need to use paraenteral meds
74
Q

4 steps to PT with severe HT

A
  1. rule out acute target organ damage
  2. considr secondary causes
  3. decide on goal of Tx and drug
  4. decide on dispostion - home, ward, ICU
75
Q

5 major drugs for HT emergencies

A
  1. nitroprusside
  2. labetalol
  3. nitroglycerine
  4. phentolamine
  5. hydrailine

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