treatment of hypertension Flashcards

1
Q

explain short term and long term blood pressure regulation

A

short term

  • baroreceptors
  • starlings law
  • sympathetic and parasympathetic outflow

long term

  • Na+ balance
  • ECFV
  • degree of vasoconstriction
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2
Q

high blood pressure can arise from…

A

increase in vasoconstrictor agents

decrease in vasodilator agents

increase in the ECFV

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3
Q

hypertension =

A

high blood pressure

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4
Q

hypertension ______ with age

A

increases

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5
Q

hypertension is a strong risk factor for….

A

Stroke, Ischemic heart disease, Renal failure, Retinopathy,

Left ventricular hypertrophy, Heart failure

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6
Q

what is the difference between primary/essential hypertension and secondary hypertension

A

secondary hypertension has an identifiable cause

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7
Q

causes of secondary hypertension:

A
  • vascular causes (renal artery stenosis- obstruction in one of the renal arteries will lead to reduction in blood flow to that kidney, and hence activation of the RAAS system)
  • renal diseases (glomerulonephritis, diabetic nephropathy)
  • hormonal abnormalities (conn’s syndrome)
  • drugs (contraceptive pill)
  • genetic diseases (liddles syndrome, overproduction of ENAC channels, excess Na+ retention)
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8
Q

essential hypertension causes

A

increased sympathetic nervous system

increased RAAS

endothelial dysfunction - decreased ability of endothelial cells to release local vasodilators, increasing vasoconstrictors and TPR

defect in vascular smooth muscle contraction

defects in renal Na handling, increased salt intake

age

ethnicity, e.g. more common in Afro-Caribbean groups

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9
Q

why treat hypertension?

A

lowering blood pressure will reduce the risk of consequences (strokes, heart attacks, blood vessels damage)

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10
Q

what are goals of hypertension treatment?

A

control of BP
prevention of organ damage
controlling other CVS risk factors

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11
Q

3 main treatment pathways

A

(progress through the 3 main treatment pathways if the one above doesn’t work)

  1. Non-pharmacological, e.g. Life-style modifications
  2. Pharmacological treatment
  3. Surgical, e.g. Conn’s syndrome
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12
Q

non-pharmacological treatment – lifestyle changes

A

Quit smoking – What help is available? Unknown dangers with vaping

Weight control – Can you name high / low calorie foods? Obesity associated with high BP

Eat less salt – Can you name high / low salt foods?

Regular exercise – How much is sufficient?
Exercise improves BP

Reduce alcohol intake – What are the recommended levels?

Behavioural therapies – CBT, reduce stress, mindful meditation

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13
Q

Pharmacological treatment

A

Major Classes of Anti-hypertensive Drugs:

ACE inhibitors - antagonise the RAAS

Angiotensin II receptor blockers - target the RAAS

Diuretics - increase the electrolyte and fluid loss through the kidneys, reducing ECFV

Drugs acting on Sympathetic Nervous System - beta blockers

Vasodilators

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14
Q

ACE inhibitors (enalapril) + AT1 receptor blockers (losartan)

A

Inhibiting this enzyme will decrease the angiotensin levels
Leads to less vasoconstriction and less aldosterone secretion – both which work together to lower BP

Some people cannot take this, so they are given inhibitor of the angiotensin II receptor, so it cannot bind to the AT1 receptor and cause vasoconstriction and aldosterone secretion

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15
Q

side effects of ACE inhibitors/ AT1 receptor blockers

A

Side effects: ACEi

Cough (common) due to decrease in bradykinin breakdown
Angioedema (rare but serious)

Side effects: both ACEi and ARBs

Hyperkalaemia, because aldosterone isn’t secreted, so sodium isn’t reabsorbed, so potassium isn’t secreted, build up of K+ levels

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16
Q

diuretics

A

Increase in sodium and water excretion

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

Loop diuretics - the most powerful, given in emergency hypertension to lower the increased concentration gradient in the interstitium medulla, lowering the osmolality and lowering the reabsorption of water here

Thiazides

Potassium-sparing

major side effects = hypokalaemia (Loop and thiazide diuretics but not K sparing diuretics)

hyperglycemia due to
decreased insulin release

17
Q

why are beta-blockers given?

A

because β1 – increase HR and contractility → increase CO → increase BP

also α1 – vasoconstriction of VSMC → TRP → increase BP

18
Q

vasodilators

A
  1. K+ channel openers
  • VGKC open, K+ efflux
  • Hyperpolarization
  • Reduction in VGCC activity
  • Reduction in intracellular [Ca]
  • Less MLCK activity
  • Increased relaxation
  • Vasodilatation
  1. VGCC blockers
    - Block VGCC activity in VSMCs
    - Reduced [Ca]i
    - Less MLCK activity
    - Increased relaxation
    - Vasodilatation
19
Q

Key issues to consider in selecting Drug Therapy

A
Evidence of efficacy
Side effects of drug
Drug interactions
Individual demographics
Co-existing diseases
Quality of life
Economic considerations