Hypertension Flashcards

1
Q

Name the four main groups of aetiology of primary/essential hypertension

A

Major genes, Polygenes, Environment, Individual factors

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2
Q

List major genes contributing to hypertension

A

Angiotensinogen mutation, Diabetes, Hyperlipidemia

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3
Q

List polygenetic factors in hypertension

A

OBESITY, Race - particularly afro-caribbean, Familial history

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4
Q

Environmental causes of hypertension

A
AGE - reduced arteriolar compliance
DIET - high fat, salt, calorie
High alcohol intake
SMOKING - adds 20/10
High caffeine consumption
Oral contraceptive
Low exercise
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5
Q

List individual factors contributing to hypertension

A

Previous MI, Male (2x MI risk), LV hypertrophy (2x MI risk), Stress, Low birthweight

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6
Q

What are the two likely mechanisms of primary hypertension

A

increased arteriolar reactivity and constriction, caused by genetic defects and/or environmental factors, causing increased TPR.

Impaired ability to secrete appropriate amounts of Na at any conc. resulting in retention and increased plasma volume.

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7
Q

List the categories of the main causes of 2ndry hypertension

A
Renal disease
Endocrine causes
OSAD
Drug induced - oral contraceptive, NSAIDs
Pregnancy - preeclampsia 
Vascular  - coarctation of aorta
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8
Q

List renal causes of 2ndry hypertension

A

Chronic pylonephritis
Polycystic kidney disease
Renal artery stenosis
Fibromuscular dysplasia

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9
Q

Common endocrine causes of 2ndry hypertension

A

Conn’s disease - adrenal gland disease causing hyoeraldesteronism
Cushings syndrome - hypercortisolism
Acromegaly
Hypo and Hyperthryroidism

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10
Q

Outline stages of hypertension

A

Stage one: clinic BP 140/90 or ABPM 135/85

Stage 2: Clinic BP 160/100 or ABPM 150/95

Stage 3: Clinic BP systolic >/= 180 or diastolic >/=110

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11
Q

Outline the effects of untreated hypertension

A

Cognitive effects - Increased likelihood of stroke, more rapid cognitive decline

MI, LVF, Coronary heart disease, Congestive heart failure,

Renal damage, causing proteinuria - requiring dialysis, transplant

Peripheral vascular disease - intermittent claudication

Retinopathy

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12
Q

Outline investigation and diagnosis of HT

A
  1. Clinic or ABPM
    If patient is 55 or older, or of afro-caribbean descent, begin treatment,
  2. If patient is younger than 55, refer to specialist to investigate
    - end organ damage - renal, cognitive, cardiac, vascular
    - secondary causes - Cardio, renal, endocrine, vascular, OSAD
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13
Q

Outline treatment of hypertension in >55 and people of afro-caribbean descent

A
  1. CCB. if not tolerated/effective thiazide like diuretic
  2. CCB+TLD.
    ACEI or ARB if TLD not tolerated/already in use
  3. CCB+TLD+ACEI/ARB
  4. Consider further diuretic therapy
    - if K conc.4.5mmol consider higher conc. TLD use

If further diuretic use is contradicted/not tolerable - a/B blocker

  1. If hypertension still uncontrolled trial less commonly used agent: Central acting, alpha adrenoreceptor
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14
Q

Outline treatment of hypertension in patients >55

A
  1. ACEI or ARB
  2. above + CCB or TLD
  3. ACEI/ARB+CCB+TLD
  4. Consider further diuretic therapy
    - if K conc.4.5mmol consider higher conc. TLD use

If further diuretic use is contradicted/not tolerable - a/B blocker

  1. If hypertension still uncontrolled trial less commonly used agent: Central acting, alpha adrenoreceptor
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15
Q

name 2 commonly used ACEI and their action

A

Ramipril and Perondipril

Inhibit conversion of Angiotensin I to II by ACE.

Angiotensin II acts on AT1 receptors and is a potent stimulator of vasoconstriction, vascular and LV hypertrophy, vascular and myocardial fibrosis.

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16
Q

Contraindications of Ramipril and Perondipril use

A

Renal failure/artery stenosis

hyperkalemia

17
Q

Possible ADRs of Ramipril and Perondipril

A

COUGH
Renal impairment/damage
first dose hypotension

18
Q

Drug-drug interactions of Ramipril and Perondipril

A

NSAIDs - renal damage/failure

TLD - hyperkalemia

19
Q

List the 4 commonly used Angiotensin II antagonsists, outline action

A

SARTANs - Losartan, Valsartan, Irbesartan, Candesartan.

Binding A1 angiotensin receptors, prevents vasoconstriction, LVH, vascular and myocardial hypertrophy and fibrosis.

20
Q

Types of CCB’s and examples

A

Vascular specific - Nifedipine, Amlodipine. Reduce contractility/TPR

Cardiac specific - Verapamil, Diltiazem. Reduce rate and contractility, therefore CO

Both act on L type calcium channels

21
Q

what is the advantage of ARB use over ACEI

A

no cough, better compliance

22
Q

List advantages, contraindications and ADRs of CCB’s

A

Advantages- high compliance, low side effects

Contra’s - MI, Heart failure, bradycardia (rate limiting CCBs)

ADR – Headache, Ankle oedema, Indigestion and reflux oesophagitis, constipation.

23
Q

What are Chlortalidone and Indapamide

A

Thiazide like Diuretics

24
Q

Describe mech of TLD’s

A

Block reabsorption of Na, increase diuresis

25
Q

List less commonly used agents i.e. step 5

A

Central acting - Methyldopa: Acts on CNS alpha receptors, reduces sympathetic outflow

Alpha-adrenoreceptor antagonist - Doxasosin. Prevents vasoconstriction

26
Q

name the types of HT in pregnancy

A

pre-existing, gestational, pre-eclampsia

27
Q

Outline treatment of HT in pregnancy

A

DO NOT USE ACEI/ARB - both teratogenic
TLD -

  1. CCB - Slow release Nifedipine.
  2. Thiazide like diuretic
  3. B-blocker or central acting agent - possibly further diuresis.

If Preeclampsia: As above plus IV Beta blocker and Vasodilator Hydralizine