Undeleted > HT > Flashcards

HT Flashcards

(75 cards)

Study These 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 stages of HT

A
  1. 140-159/90-99

2. >160/100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 cat. of HT

A
  1. systolic/diastolic
    - 95% idiopathic
    - the rest secondary
  2. systolic only
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 epi features of essential HT

A
  1. onset 25-45
  2. usually fam Hx
  3. both elevated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pathogenetic factors involved

A
  • genes
  • race
  • hemodynamics
  • SNS activation
  • endothelial dys
  • renal contribution
  • obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is role of genes

A

polygenic, but related to fams and twins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is race factor

A

blacks

  • SES - salt, poor materanl nut
  • genetics - APO-L1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 issues with endothelial dysfunction

A
  1. NO
    - may be low due to angiotensin2 related oxidant stress
  2. endothelin (vasoconstrictor) elevated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is renal contribution

A
  • not exreting Na
  • may be due to congenically low nepron
  • SNS and RAAS activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is effect of obesity

A

peripheral insulin resistant

  1. direct HT effect
  2. increases insulin secretion>hyperinsulinemia>HT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

2 main causes of renal A stenosis

A
  1. young- fibromusclualr
  2. old - athero
  • both activate RAAS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when to suspect renal A sten

A
  • young person with HT
  • older person with new diastolic HT
  • refractiry HT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Dx for stenosis

A

imaging - only if a cand. for revasc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tx for stenosis

A
  • limited benefit for revasc

- meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3 major endo dysfunctions that can lead to HT

A
  1. hyperaldosteronism (conns)
  2. pheo
  3. cushings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what happens in coarctation

A
  • narrowing in aorta where ductus connects

- HT in arms, hypo in legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what drugs can lead to HT

A 
prescribed
- OCP
- NSAIDS
- steroid
- EPO
- cyclosporine, tacrolimus
other
- cocaine
- EtOH
- licorice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
2 main types of vascular lesions
1. large As - athero 2. small As - chronic - arteriolar sclerosis - acute - fibrinoid necrosis
26
what are cardiac cons. of HT
1. high afterload - LVH 2. leads to diastolic dysfucntion - heart is stiff - pulm edema 3. leads to systolic dysfunction - most common cause of CHF
27
3 neuro cons.
1. encephalopathy 2. dementia 3. stroke - ischemic and hemmoragic
28
what is renal effect of HT
- faster progression of all renal disease | - kidney disease causes HT
29
4 stages of retina effects
1. focal arteriolar spasm 2. diffuse spasm 3. soft exudates of flame hemo 4. papilledema
30
4 parts of assessement of HT PT
1. confirm HT 2. evidence of target organ damage 3. other CV risks 4. secondary causes
31
how to office measure
if over 140/90, do twice more and discard 1st
32
2 other monitors for PT
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
what are 2 options to true HT and normotension
- white coat - false pos | - masked HT - false neg
34
features of white coat
20% of PTs in office - anxiety - more common in women, elderly, smokers - less likely if by nurse, stage 2 or repeastedly high
35
features of masked
- p to 10% of pop - more common in young men, smokers, alc, obese - provoked by steress, anxiety
36
3 ways to test for end organ damage
1. Hx - angina, MI, stroke 2. PHx - LVH - CHF - prior stroke - fundoscopy 3. lab tests - renal - cardiac
37
how do CV risk factors and HT interact
synergistic | - when have a high baseline risk, Tx that cuts in half has a better absoulte risk reduction
38
4 things to consider if refractory HT
1. renal A sten 2. renal parencymal disease 3. hyperaldo 4. pheo
39
6 non-pharma mgmt things to do
1. salt resticton 2. diet - DASH 3. weight loss - at least 10lbs 4. tobacco 5. EtOH 6. excercise - FITT goals
40
what is FITT
Freq Intensity Time Type
41
5 major cats
ABCDE 1. ACEi and ARB 2. BBlock 3. CCBs 4. Diuertics 5. Eerthing else
42
Agents, MOA, SE, roles for ACEis
``` Agents - prils MOA - reduce angiotensin 2 - vasodilation and naturesis - also antifibrotic and antiproliferative SE - cough - hyperkalemia - teratogenic Role - first line ```
43
what is effect of ACEi on kidney
some patients have rapid drop in GFR and need to be stopped, most have short drop and evens out pretty quick
44
Agents, MOA, SE, roles for ARBs
``` Agents - sartans MOA - antagonize angiotensin 2 R SE - hyperkalemia - teratogenic Role - DM - sub for ACE if intolerant ```
45
what is other RAAS drug
aliskiren | - direct renin inhib
46
Agents, MOA, SE, roles for Bblockers
``` 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
2 types of solubility
water - renal elim - once daily, less CNS effects lipid - liver elim
48
Agents, MOA, SE, roles for CCBs
``` 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
Agents, MOA, SE, roles for diuretics
``` 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
2 main not-K sparing
1. thiazide - DCT | 2. furosemide - ALOH
51
2 main K-sparing
1. spironolactone | 2. aminolride
52
Agents, MOA, SE, roles for A-blockers
``` Agents - -azosin MOA - A r blocker - vasodilation SE - ortho hypo - first dose hypo Role - not first line, but 3 or 4 ```
53
Agents, MOA, SE, roles for direct vasodilators
``` agent - hydrazine - minoxidil MOA - directly act with smooth muscle - very potetnet SE - reflex tachy - SLE - minoxidil - hair growth Role - refractory HT ```
54
Agents, MOA, SE, roles for central sympatholytics
``` agent - clonidine - methyldopa MOA - stim PRE-synaptic A-2 R - inhib SNS outflow SE - sedation - ortho hypo Role - preganccy for methydopa ```
55
how to use meds
- start low dose of one med | - one med to treat 2 probs when possible
56
what is main goal of Tx
BOTH 140 and 90
57
other goals to consider
DM - 130/85 >80yo - 150/90 renal disease - 130/80
58
what is too low
no benefit to 120/70 | lowering
59
4 things to do if not at goal
1. optimize dose 2. if NO response, swtich class 3. add a second agent 4. consider causes of refractory HT
60
ways to improve adherence
- shared, clear goals - empathic approach - address cost - written direactions - once daily, blister packs
61
how to monitor once stable
1. office - 3-6 months 2. regular home BP monitoring 3. 24-hour ambulatory - is hypo - if fluctuating readings
62
2 other therapies to consider
1. ASA | 2. statins
63
5 factors that reduce the NNT
1. high baseline risk 2. higher initial BP 3. longer duration of Tx 4. greater magnitude of BP fall 5. other interventions
64
what is hypertensive crisis
situation that needs to be lowered NOW | - S>200 or D over 120
65
what is HT emergency
needs to be lowered in 60 min
66
what is malig. HT
V high BP with papiledema
67
5 systems that can cause HT emergency
1. brain 2. CV 3. catecholamine excess 4. severe eclampsia/preeclampsia 5. accelerated-malignant HT
68
what is cerebral autoregulation
- brain keep perfusion pressure between 50-150
69
what is HT encephalopathy
- diffuse brain dysfucntion - not focal - cerebral edema - rare
70
what is catechalime excess syndrome
- intox with cocaine, amphetamines - withdrawal from anti-HT, sedatives - MOAis - pheo
71
what is eclampsia or pre
- acute sustained raise in BP >160 or 110 - need to lower ASAP - be careful with meds
72
3 cats. of HT urgencies
1. severe asymptomatic (>200/120) 2. accelerated-malignant HT with no end organ damage 3. pre and post operative HT d>110
73
3 issues of HT in operative setting
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
4 steps to PT with severe HT
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
5 major drugs for HT emergencies
1. nitroprusside 2. labetalol 3. nitroglycerine 4. phentolamine 5. hydrailine
Undeleted
flashcards
Decks in class (589)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions