Hypertension Flashcards

1
Q

How is blood pressure regulated? Give relevant equations

A
Pressure = flow x resistance
mABP = CO x TPR
CO = SV x HR
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2
Q

How is blood pressure managed in the short term?

A

Baroreceptor reflex-stretch receptors in aortic arch and carotid sinus. Issue is, it resets to a new set point after 15 minutes (as threshold for firing changes)

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3
Q

When is renin released?

A

Renin is released from granular cells of afferent arterioles (granular cells of juxtaglomerular apparatus) in response to reduced perfusion pressure.

Factors that stimulate renin release are:

a) reduced NaCl delivery to distal tubule (macula densa)
b) reduced perfusion pressure in kidney (baroreceptor reflex)
c) sympathetic stimulation to JGA increases release of renin

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4
Q

How is angiotensin converted into its active form?

A

Angiotensinogen is converted into angiotensin 1 with renin.

Angiotensin 1 is converted into Angiotensin 2 via ACE.

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5
Q

What are the main actions of Angiotensin 2.

A

Mainly acting via AT1 receptors:

Arterioles= Vasoconstriction
Kidney= Na+ reabsorption
SNS= Increased NA release (positive feedback)
Adrenal cortex= aldosterone release
Hypothalamus= ADH release
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6
Q

What are the actions of aldosterone?

A

acts on principle cells of collecting ducts.

  • Stimulates Na+ (and therefore water reabsorption)- via ENaC and
  • increases basolateral Na+ extrusion via Na+K+ATPase
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7
Q

How does ACE interact with bradykinin?

A

Bradykinin has vasodilatory actions. ACE causes it to break down into peptide fragment. So ACE inhibitors cause dry cough as bradykinin accumulates.

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8
Q

What is the significance of the SNS in blood pressure regulation?

A

Increased sympathetic stimulation means decreased renal blood flow (vasoconstriction of arterioles, decreased GFR, decreased Na+ excretion and activation of Ang2 system)

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9
Q

What does Anti Diuretic Hormone do?

A

It increases water reabsorption in distal nephron (via AQP2) and release is stimulated by increased plasma osmolarity and severe hypovolemia. It increases sodium reabsorption in thick ascending limb via apical Na+/K+/Cl-.

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10
Q

What are natriuretic peptides?

A

peptides synthesised and stored in atrial myocytes that ar released in response to stretch. Increased filling means increased stretch and more ANP released.

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11
Q

What does ANP do physiologically?

A

Supports blood pressure:

  • vasodilation of afferent arterioles
  • increased GFR
  • Inhibition of Na+ reabsorption
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12
Q

What effect do prostaglandins have?

A

They act as vasodilators. They are locally acting and have a short half life.

  • PGE2 mainly enhances glomurelar filtration and reduces Na+ reabsorption.
  • hypothesised that they may have important protective function (i.e. a buffer to excessive vasoconstriction from SNS and RAAS) so important when Ang2 levels high
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13
Q

How does dopamine affect blood pressure?

A
  • locally formed in kidney from L-DOPA.
  • dopamine receptors on renal blood vessels and PCT and TAL cells cause vasodilation and increased NaCl reabsorption.
  • therefore Parkinson’s treatment side effects can include low blood pressure and fainting etc
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14
Q

How are the different stages in hypertension defined?

A

Stage 1= above 140/90 (in clinic) and above 135/85 (ABPM/HBPM)

Stage 2= above 160/100 (in clinic) and above 150/95 (ABPM/HBPM)

Severe= above 180 systolic or 110 diastolic

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15
Q

How can renovascular disease cause hypertension?

A
  • renal artery stenosis causes fall in perfusion pressure in that kidney
  • decreased perfusion pressure- increased renin production, increased RAAS activation, vasoconstriction and sodium retention at other kidney
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16
Q

How renal parenchymal disease cause hypertension?

A
  • earlier stages may be characterised by loss of vasodilator substances
  • later stages, sodium and water retention due to inadequate glomerular filtration (volume dependent hypertension)
17
Q

Outline the adrenal causes of hypertension

A

Conn’s Syndrome- Aldosterone secreting adenoma, causing hypertension and hyperkalemia

Cushing’s Syndrome- excess secretion of glucocorticoid (cortisol) at high concentrations which acts on aldosterone receptors (causes sodium and therefore water retention)

Phaeocytochroma- Catecholamine secretion- catecholamine secretion (NA and adrenaline stimulating sympathetic nervous system)

18
Q

How can hypertension lead to heart failure?

A
  • increased after load

- leading to LV hypertrophy

19
Q

How can hypertension be treated non pharmacologically?

A
  • exercise
  • diet
  • reduced sodium intake
  • reduced alcoholl intake
  • failure to implement lifestyle changes could limit effectiveness of antihypertensive therapy

Note, smoking does not cause hypertension

20
Q

How can hypertension be treated pharmacologically?

A
  • ACE Inhibitors
  • ANG2 Receptor Antagonists
  • Diuretics
  • Beta blockers
  • A1 receptor blockers
  • L Type Ca2+ channel blockers