Hypertension Flashcards

1
Q

What are the prime contributors to blood pressure?

A

CO = SV x HR

PVR (high PVR = high BP)

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2
Q

Aetiology of HPT

A

Polygenic: major genes and polygenes (obesity, race, BP)

Polyfactorial: environment, individual and shared (stress, oral contraceptive, physical inactivity)

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3
Q

What is Primary HPT

A

Idiopathic

  • Genetics
  • Obesity
  • Alcohol
  • Na intake
  • Stress
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4
Q

What is Secondary HPT

A

Occurs due to disease

  • Renal
  • Endocrine - Cushing’s syndrome, Conn’s syndrome
  • Congenital - coarctation of aorta
  • Pregnancy - pre-eclamsia
  • Drugs - oral contraceptive, steroids, NSAIDs
  • Sleep Apnoea
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5
Q

Symptoms

A

Usually asymptomatic but sustained HPT produces end organ damage to vessels, heart and kidney

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6
Q

Ideal BP

A

Between 120/80 - 140/90

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7
Q

Investigation to assess end-organ damage

A
ECG (LVH)
Echo (LVH)
Proteinuria
Renal ultrasound
Renal function
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8
Q

Risk factors

A
Previous MI stroke 
Smoking 
Diabetes Mellitus 
Hypercholesterolaemia 
Renal disease
LVH 
Male
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9
Q

What treatable causes should be screened for

A

Renal artery stenosis
Cushing’s syndromes
Conn’s syndrome
Sleep apnoea

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10
Q

First Treatment for under 55yrs

A

ACE Inhibitor/ARBs - not afrocaribbean or women of child bearing age

If single agent doesn’t control BP, then use two together

If child bearing age: CCB or Beta Blocker

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11
Q

First treatment of over 55yrs

A

CCB and to afrocaribbean of any age

If not suitable offer thiazide (diuretic) - oedema, intolerance, HF

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12
Q

Step 2 treatment

A

Add Diuretic - clortalidone or indapamide

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13
Q

Step 3 treatment

A

Add CCB, ACEi, Diuretic together

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14
Q

Step 4 treatment

A

For resistant HPT:
Low dose diuretic spironolactone (25mg) if K level < 4.5 mmol/l
or
High dose thiazide-like diuretic if K level > 4.5mmol/l

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15
Q

Mechanism of ACEi

A

I.e. Rampiril
Inhibits angiotensin converting enzyme (ACE) which converts angiotensin I -> angiotensin II (vasoconstrictor and hypertrophic agent)

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16
Q

Mechanism of CCB

A

I.e. amlodipine
Blocks L type Ca channels prevent Ca from entering myocytes and blood vessel walls - lower BP

Relax and widen blood vessels by affecting the muscle cells in the arterial walls - reduces TPR

17
Q

List possible complications of HPT

A

Stroke
LVH
MI
Renal failure

18
Q

Define Stage 1

A

Clinic BP: 140/90mmHg or higher

ABPM average: 135/85 mmHg or higher

19
Q

Define Stage 2

A

Clinic BP: 160/100mmHg or higher

ABPM average: 155/95 mmHg or higher

20
Q

Define sever HPT

A

Clinic systolic 180 mmHg or higher

Clinic diastolic 110 mmHg or higher

21
Q

Control of BP by the sympathetic nervous system

A

Vasoconstriction
Reflex tachycardia
Increased CO

All increase BP

22
Q

Control of BP by the renin-angiotensin-asdosterone system (RAAS)

A

Stimulated by :
Low BP (low MAP)
Low circulating volume
Low Na

Released by the juxtaglomerular and converts angiotensinogen to angiotensin I

Angiotensin I to angiotensin II by ACE

23
Q

Why are myocyte and smooth muscle hypertrophy poor prognostic factors?

A

Hypertrophy makes blood vessels stiff so that they can’t relax which increases bp and if the heart can’t relax, myocytes become ischaemic and start to fibres causing loss of function

24
Q

Action of Angiotensin II

A

Vasoconstriction
Anti-natriuretic peptide
Stimulator of aldosterone release from the adrenal glands
Hypertrophy of myocytes and smooth muscle

25
Q

Other causes of HPT

A

Over reactive resistance vessels - increases PVR due to defect in Na transporter of smooth muscle

Na effect - if kidneys unable to excrete Na, it builds up in vessels and fluid retained -> high BP

26
Q

Age effect in hypertension

A

BP rises with age due to decreased arterial compliance

27
Q

Environment effect in HPT

A

Mental and physical stress increase BP

28
Q

Genetic effect in HPT

A

FH of HPT common

29
Q

Sodium intake and diet effect in HPT

A

Reducing salt intake can reduce BP in hypertensive individuals

30
Q

Alcohol effect in HPT

A

Small amount of alcohol tend to decrease BP
Large amounts of alcohol tend to increase BP

If alcohol reduced, BP will fall over several days to weeks

31
Q

Weight effect in HPT

A

Weight reduction is most important non-pharmalogical measure - loss of weight will reduce BP

Lower birth weight, higher chance of developing HPT and heart disease

32
Q

Race effect in HPT

A

Caucasians have lower BP than black population in same environment
Rural living has lower BP than in towns
Black population genetically salt retainers, so are more sensitive to an increase in diet salt

33
Q

Treatment of Stage 1 HPT

A
Antihypertensive drug to people < 80yrs with ABPM > 135/85 with:
Target organ damage
CVD
Renal disease 
Diabetes
34
Q

Treatment of Stage 2 HPT

A

Drug treatment to any age with ABPM > 150/95

35
Q

Treatment of > 80yrs

A

Same drugs as people 55-80yrs, taking into account co-morbidities

BP target is different: < 145/85

36
Q

Contraindication to ACEI and drug-drug interactions

A

Renal artery stenosis
Renal failure - NSAIDs
Hyperkalaemia - Potassium supplements or potassium sparing diuretics

37
Q

Action of ARB

A

I.e. losartan, valsartan

Angiotensin II antagonists competitively block the actions of angiotensin II at the angiotensin AT1 receptor

38
Q

What drug do you add if combination of CCB, diuretic and ACEi cause incomplete effect?

A

Beta blocker

39
Q

HPT in pregnancy

A

During normal pregnancy, BP falls but if patient has existing HPT it can cause primary HPT -pre-eclampsia

Do not treat with ARB or ACEi, use: nifedipine MR, methyl dopa, atenolol

then add diuretic and/or amlodipine