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Kidneys > Treatment of hypertension > Flashcards

Treatment of hypertension Flashcards

1
Q

What is blood pressure?

A

The pressure exerted by blood on the blood vessels

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2
Q

How is blood pressure regulated in the short term?

A
  • use of baroreceptors

- sympathetic and parasympathetic outflow

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3
Q

How is blood pressure regulated in the long term?

A
  • hormonal control

- degree of vasoconstriction

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4
Q

How does hormonal control regulate blood pressure in the long term?

A
  • Through the control of blood volume, via the ECFV
  • ECFV is controlled indirectly by the kidneys, but it is the amount of Na that is controlled, not the concentration
  • If ECFV drops, there is more sodium retention by the kidneys which brings water with it, therefore restoring ECFV
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5
Q

How is Mean Arterial Blood Pressure (MABP) calculated?

A

MABP = CO x TPR

CO= Cardiac output 
TPR= Total peripheral resistance
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6
Q

What is hypertension?

A

High blood pressure:
defined as having a BP reading of more than 140/90 mmHg over a number of weeks

(currently hypertension is defined as a threshold)

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7
Q

Stage 1 hypertension

A

BP greater than or equal to 140/90 mmHg

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8
Q

Stage 2 hypertension

A

BP greater than or equal to 160/100 mmHg

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9
Q

Severe hypertension

A

BP greater than or equal to 180/110 mmHg

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10
Q

Healthy BP

A

120 systolic or lower

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11
Q

What is hypertension a risk factor for?

A
  • Stroke, Ischaemic heart disease
  • Left ventricular hypertrophy, heart failure
  • Renal failure
  • Retinopathy
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12
Q

What are the two main causes of hypertension?

A
  1. Primary or essential (when there is an unknown cause)

2. Secondary (when there is an identifiable cause)

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13
Q

What percentage of hypertension cases are primary?

A

> 90%

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14
Q

What percentage of hypertension cases are secondary?

A

<10%

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15
Q

What is primary hypertension?

A

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

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16
Q

List some examples of how secondary hypertension can occur?

A
  • Renal disease
  • Vascular, e.g. renal artery stenosis
  • Hormonal, e.g. Conn’s syndrome, Cushing’s syndrome
  • Monogenic genetic diseases, e.g. Liddle’s
17
Q

List possible mechanisms and risk factors that are involved with essential hypertension?

A
  • Increased SNS
  • Increased RAAS
  • Endothelial dysfunction
  • Defect in vascular smooth muscle contraction
  • Defects in renal Na handling, increased salt intake
  • Obesity/insulin resistance
  • Age (Increases with age)
  • Ethnicity, e.g. more common in Afro-Caribbean groups
  • Family history
18
Q

What are the three main reasons why we should treat hypertension?

A
  1. Risk reduction
  2. Goals of anti-hypertensive treatment
  3. Treatment pathways
19
Q

How lifestyle can be adapted to minimize risk of developing hypertension?

A
  • Quit smoking
  • Weight control
  • Eat less salt
  • Regular exercise
  • Reduce alcohol intake
  • Behavioural therapies, e.g. CBT
20
Q

What are the major classes of anti-hypertensive drugs?

A
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Diuretics
  • Drugs acting on SNS
  • Vasodilators
21
Q

Describe the mechanism of action of ACE (Angiotensin Converting Enzyme):

A
  • Angiotensionogen is first converted by Renin in the kidney to Angiotensin 1
  • Angiotensin 1 is converted by ACE (found in high conc in the lungs) into active form Angiotensin 2
  • This acts on Angiotensin 1 receptors
  • The two major effects being strong vasoconstriction and aldosterone secretion
22
Q

How do ACE inhibitors and AT1 receptor blockers treat hypertension?

A

Decrease in vasoconstriction and aldosterone secretion to reduce blood pressure

23
Q

What are the side effects of ACE inhibitors?

A
  • Cough (common) due to decrease in bradykinin breakdown
  • Angiodema (rare but serious)
  • if patient suffers from these symptoms, AT1 RBs are used instead
24
Q

What are the side effects of both ACEi and ARBs?

A

Hyperkalaemia (K+ level in blood higher than normal)

25
Q

How do diuretics treat hypertension?

A
  • Increase in sodium and water excretion
  • Reduce blood volume -> reduces CO -> reduce BP
    (BP ~ CO x TPR)
26
Q

Describe sympathetic neural effects on CVS:

A

B1: increases heart rate and contractility - increases cardiac output - increases blood pressure

a1: vasoconstriction - TPR - increases BP

Beta blockers (B1 blockers, e.g. atenolol): reduction in CO and renin release

27
Q

Mechanism of action of vasodilators?

A

K+ channel openers

28
Q

Structural features of arterioles that make them a good target for vasodilators?

A

Arterioles normally have significant smooth muscle tone: scope for relaxation

29
Q

Examples of vasodilators (K channel openers)

A

Minoxidil, Diazoxide

30
Q

Action of vasodilators (K channel openers)

A
  • Increased outward K current
  • Hyper-polarization
  • Reduced VGCC activity
  • Reduced [Ca]i
  • Less MLCK activity -> increased relaxation (vasodilation)
31
Q

Action of vasodilators (voltage-dependent Ca2+ channel blocker)

A
  • Block VGCC activity in VSMCs
  • Reduced [Ca]i
  • Less MLCK activity -> increased relaxation (vasodilation)
32
Q

Example of a voltage-dependent Ca2+ channel blocker vasodilator?

A

Nifedipine

33
Q

What are the factors that need to be taken into consideration when deciding which drug to use?

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

Kidneys (6 decks)

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