Hypertension Flashcards

1
Q

What is the rationale for treating hypertension with diuretics?

A
  • Hypertension is caused by an increase in blood volume.
  • Diuretics decrease the amount of water retained in the body.
  • More body water is excreted, thus reducing the blood volume, leading to decreased blood pressure.
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2
Q

Which types of diuretics are most effective?

A

Loop diuretics, such as Frudemide

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3
Q

In advanced heart failure, the extracellular fluid volume is expanded and yet the renin-angiotensin-aldosterone system is active. Explain.

A
  • Normally, if the extracellular fluid volume increased, RAAS activity would decrease.
  • In heart failure, decreased perfusion of the organs.
  • With decreased blood flow, the kidneys sense this and release more renin in an attempt to increase renal blood volume.
  • RAAS will remain active.
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4
Q

What is blood pressure?

A

Pressure exerted by the blood on the blood vessels.

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5
Q

What is the short-term means of blood pressure regulation?

A

Baroreceptors

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6
Q

What are the long-term means of blood pressure regulation?

A

Via hormones and Na+ balance, eg. ECFV, degree of vasoconstriction

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7
Q

How can high blood pressure arise?

A
  • an increase in ECFV
  • an increase in vasoconstrictor agents
  • a reduction in vasodilator agents
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8
Q

What are the two types of hypertension?

A
  • PRIMARY HYPERTENSION ( >90% of cases): has an unknown cause
  • SECONDARY HYPERTENSION (~10% of cases): has an identifiable cause
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9
Q

What can hypertension be caused by?

A
  • renal diseases (eg. glomerulonephritis, diabetic nephropathy)
  • vascular causes (eg. renal artery stenosis)
  • hormonal abnormalities (eg. Conn’s syndrome, Cushing’s syndrome)
  • drugs (eg. contraceptive pill)
  • pregnancy (eg. pre-eclampsia)
  • monogenic genetic diseases (eg. Liddle’s)
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10
Q

Describe essential hypertension

A
  • More prevalent in urban areas
  • Caused by a combination of genetic and environmental factors
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11
Q

Why do we need to treat hypertension?

A

Reduces the chances of heart attacks by 16%
Reduces vascular mortality by 21%

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12
Q

What are the goals of anti-hypertensive treatment?

A
  • adequate blood pressure control
  • prevention of organ damage
  • controlling other cardiovascular risk factors
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13
Q

What are the three main treatment pathways for hypertension?

A
  • non-pharmacological (eg. lifestyle modifications)
  • pharmacological treatment
  • surgical treatment
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14
Q

List some non-pharmacological treatments for hypertension.

A
  • quit smoking (if applicable)
  • weight control
  • eat less salt
  • regular exercise
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15
Q

List some pharmacological treatments for hypertension

A
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • diuretics
  • vasodilators
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16
Q

What are some side effects of ACE inhibitors (caused by the decreased Angiotensin II effects)?

A
  • cough (common) - due to bradykinin breakdown
  • angioedema (rare) - due to bradykinin breakdown (very serious, prevents breathing)
17
Q

What are some side effects of ACE inhibitors and AT1 receptor blockers?

A

hyperkalemia - due to decreased aldosterone, which leads to decreased Na reabsorption and hence decreased K excretion

18
Q

When are ACE inhibitors and AT1 receptor blockers contraindicated?

A

contraindicated in pregnancy - foetal problems
contraindicated in renal stenosis

19
Q

Why are ACE inhibitors contraindicated in renal stenosis?

A
  • Decreased efferent renal arteriole constriction
  • Decreases the pressure gradient across the Bowman’s capsule
  • Decreased GFR
20
Q

What are the consequences of sympathetic nerve stimulation of the CVS?

A

β1 - increase HR and contractility, which increases CO, which increases BP
α1 - vasoconstriction, which increases TRP, which increases BP

21
Q

How would you decrease sympathetic activity?

A

CNS: α2 adrenoreceptor agonists (eg. Clonidine, used in hypertensive crisis)
Ganglion blockers: NIC blockers (eg. Trimethapan, used in hypertensive crisis)
Synaptic blockade (eg. Reserpine)

22
Q

List some adrenoceptor blockers.

A

α1 blockers: cause the relaxation of vascular smooth muscle, eg. prazosin
β1 blockers: cause a reduction in CO and renin release (eg. atenolol)

23
Q

Describe K channel openers as vasodilators.

A
  • Increased K+ efflux from the cells.
  • Causes vascular smooth muscle hyperpolarisation.
  • Reduction in VGCC activity
  • Reduction in intracellular [Ca].
  • Reduced MLCK activity
  • Increased relaxation - vasodilation.
24
Q

Describe voltage-dependant Ca2+ channel blockers as vasodilators.

A
  • Block VGCC activity in vascular smooth muscle cells.
  • Reduction in intracellular [Ca].
  • Reduced MLCK activity
  • Increased relaxation - vasodilation.
25
Q

Give an example of a voltage-dependant Ca2+ channel blocker.

A

Dihydropyridines e.g amlodipine

26
Q

What issues do you need to consider in selecting drug therapy?

A
  • essential vs. secondary hypertension
  • side effects of the drugs
  • drug interactions
  • co-existing diseases
  • quality of life
27
Q

What are 3 possible mechanisms for essential hypertension?

A

→ Increased sympathetic nervous system
→ Increased RAAS
→ endothelial dysfunction

28
Q

What are 2 possible defects in essential hypertension?

A

→ Vascular smooth muscle contraction
→ Na+ handling and excessive salt intake

29
Q

What are 4 risk factors for essential hypertension?

A

→ Obesity
→ Age
→ Ethnicity

30
Q

What is hypertension a risk factor for?

A

→ Stroke
→ Ischaemic heart disease
→ Left ventricular hypertrophy and heart failure

31
Q

What is the criteria for hypertension?

A

140/90 mmHg