S2: Treatment of Hypertension Flashcards

1
Q

What is blood pressure?

A

Pressure exerted by blood on blood vessels

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

What is the short term and long term regulation of blood pressure?

A

Short term - Neural systems e.g. baroreceptors

Long term - Hormones, Na+ balance e.g. ECFV, degree of vasocontriction

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

What can cause high blood pressure?

A
  • Increase in ECFV
  • Increase in vasoconstrictor agents
  • Reduction in vasodilator agents e.g. NO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Limits for hypertension

A

Hypertension is defined according to increased risk
· - 140/90 mmHg < 50 years
·- 160/95 mmHg for older individuals

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

What is hypertension a risk factor for?

A
· Stroke
· Ischemic heart disease
· Renal failure
· Retinopathy
· Left ventricular hypertrophy (increased afterload)
Heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is isolated systolic hypertension?

A

With age, there is reduced aorta compliance which increases pressure in aorta during ejection. This causes isolated systolic BP

  • High systolic
  • Normal Diastolic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of secondary hypertension (identifiable cause)

A

· Renal diseases e.g. glomerulonephritis, diabetic nephropathy
· Vascular causes e.g. renal artery stenosis
· Hormonal abnormalities e.g. Conn’s syndrome, Cushing’s syndrome, phaechromocytoma
· Drugs e.g. contraceptive pill
· Pregnancy e.g. pre-eclampsia
Monogenic genetic diseases e.g. Liddle’s

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

Risk fir essential hypertension (no known cause)

A
  • Prevalent in urban based populations

Genetic pre-disposition and environments factors are proposed to cause essential hypertension through many mechanisms

· Increased sympathetic nervous system (SNS)
· Increased renin-angiotensin-aldosterone system (RAA)
· Obesity / Insulin resistance
· Endothelial dysfunction
· Defect in vascular smooth muscle contraction
· Defects in renal Na handling, increased salt intake
· Age
Ethnicity, e.g. more common in Afro-Caribbean groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What consequences does reduction in BP reduce?

A

· 5 mmHg drop in diastolic BP for 5 yrs
· Reduce strokes by 42%
· Reduce heart attacks by 16%
Reduce vascular mortality by 21%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the goals in anti-hypertensive treatment?

A

· Adequate blood pressure control - < 140/90 mmHg, alter relative risk
· Prevention of target organ damage
Controlling other cardiovascular risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the three main treatment pathways?

A

· Non-pharmacological, e.g. Life-style modifications
· Pharmacological treatment
Surgical, e.g. Conn’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List some lifestyle changes that can help manage hypertension

A
  • Quit smoking
  • Weight control - high fat foods
  • Eat less salt
  • Regular exercise
  • Reduce alcohol intake
  • Behavioural therapies e.g. CBT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the major classes of hypertensive drugs?

A
· ACE inhibitors
· Angiotensin II receptor blockers
· Diuretics
· Drugs acting on Sympathetic Nervous System
Vasodilators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What for ACE inhibitors and AT1 receptor blockers do?

A

Reduce RAAS system but in different ways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give an example of ACE inhibitors

A

Enalapril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give an example of AT1 Receptor Blockers

A

Losartan

17
Q

Side effects/contraindications of ACE inhibitors caused by decreased Ang II effects

A

ACE is also an enzyme that breaks down bradykinin (inflammatory mediator) as well as converting Ang I to Ang II

  • Cough (common) - so ACE inhibitor decreases bradykinin breakdown. This causes a dry cough due to small stimuluses causing inflammation as there is increased bradykin
  • Angioderma (rare) - can prevent breathing if oedema is around face due to increased brakykinin
18
Q

Side effects/contraindications of ACE inhibitors and AT1 Receptor blockers

A
  • Hyperkalaemia (due to decreased aldosterone, Na+ reabsorption and hence decreased K+ excretion and it builds up)
  • Contraindicated in pregnancy - foetal problems
  • Contraindicated in renal stenosis as Ang II causes vasoconstriction (decreased efferent renal arteriole constriction and decreased pressure gradient across bowman’s capsule which decreases GFR)
19
Q

What do diuretics do?

A
  • Increase in sodium and water excretion

- Reduce blood volume - reduces CO - reduce BP (BP= CO x TPR)

20
Q

3 types of diuretic

A
  • Loop diuretics
  • Thiazides
  • Potassium sparing
21
Q

Major side effects of diuretics

A
  • Hypokalaemia (loop and thiazide diuretics but not K+ sparing diuretics
  • Lipid abnormalities
  • Glucose intolerance/hyperglycermia due to decrease in insulin release
22
Q

What effect does stimulating the B1 and a1 receptors have?

A

B1 - increase HR and contractility - increase CO - increase BP
a1 -vasoconstriction - increase TPR - Increase BP

23
Q

Name 3 type of drugs that decrease sympathetic activity

A

CNS: a2 adrenoreceptor agonists e.g. Clonidine (hypertensive crisis)

Ganglion blockers: Nicotinic blockers e.g. Trimethapan

Synaptic blockade: e.g. reserpine - reduces release of NA to try and reduce BP

24
Q

Describe what a1 and B1 blockers do

A

· α1 blockers : relaxation of vascular smooth muscle, e.g. prazosin (hypertensive crisis)
β1 blockers : reduction in CO and renin release, e.g. atenolol

25
Q

Give the mechanism of K+ channel openers

e.g. minoxidil, diazoxide

A

Vasodilators

  • VGK channels open, K+ efflux
  • VSM hyperpolarisation inside cell
  • Reduction in VGCa2+ activity (further away from threshold to activate these)
  • Reduction in [Ca2+] i
  • Less MLCK
  • increased relaxation
  • Vasodilation
26
Q

Give the mechanism of voltage dependent Ca2+ blockers

e.g. dihydropyridines (amlodipine)

A

Vasodilators

  • Block VGCa2+ activity is VSMCs
  • Reduction in [Ca] i
  • Less MLCK activity
  • Increased relaxation
  • Vasodilation
27
Q

Which is more vascular selective?

K+ channel openers
Voltage dependent Ca+ blockers

A

Voltage dependent Ca+ blockers

28
Q

Problems with Voltage dependent Ca+ blockers

A

Constant decrease in BP affects baroreceptor reflex - reflex tachycardia and overtime threshold changes.

With increased vasodilation blood can also pool in extremities

29
Q

What factors need to be taken into consideration when choosing a drug?

A
· Essential vs. secondary hypertension
· Evidence of efficacy
· Side effects of drug
· Drug interactions
· Individual demographics
· Co-existing diseases
· Quality of life
· Economic considerations

Complicated – so there are guidelines
NICE – National Institute for Health and Clinical Excellence