Hypertension Flashcards

1
Q

What is the calculation for mean arterial BP?

A

SV x HR x TPR

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2
Q

Explain how blood pressure is controlled in the longer term

A

neurohumoral responses =

  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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3
Q

explain how blood pressure is controlled in the short term

A

baroreceptors reflex =

  1. adjust sympathetic and parasympathetic inputs to heart to alter CO,
  2. adjust sympathetic input to peripheral resistance vessels to alter TPR
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4
Q

Where are the baroreceptors found?

A

Aortic arch and carotid sinus = sensitive to stretch

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5
Q

Outline the baroreceptor reflex for high and low BP

A

Stretching = baroreceptors recognise higher BP = afferent signal to medulla centre = raise vagus stim + lower sympathetic stim = efferent signal to SA node to slow heart rate and vasodilation.

Low BP = less stretching = lower frequency afferent signals to medulla centre = lower vagus stim + raise sympathetic stim = efferent signal to SA = speed up HR, vasoconstriction

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6
Q

Why are baroreceptors not able to control longer term changes in BP?

A

Reflex resets normal to a higher BP - and maintains this new normal higher BP

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7
Q

Define the stages of hypertension

A

Stage 1 = >140/90mmHg.

Stage 2 = >160/100mmHG

Severe = >180/>110mmHg

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8
Q

Explain the impact of hypertension on organs and tissues in the body

A
Heart - L ventricle = hypertrophy. 
Kidney – nephrosclerosis and renal failure. 
Eyes - damaged vessels - retinopathy. 
Aneurysm
cerebrovascular disease = Stroke
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9
Q

What cells is renin released from?

A

granular cells of juxtaglomerular apparatus (JGA) in kidney

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10
Q

What factors stim renin release?

A

a) Reduced NaCl delivery to distal tubule
b) Reduced perfusion pressure in the kidney causes the release of renin (baroreceptors in afferent arteriole)
c) Sympathetic stimulation to JGA increases release of renin

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11
Q

What effect does angiotensin II have on the body?

A

Arterioles = vasoconstriction,

kidney = Na reabsorb,

sympathetic NS = release of NA,

adrenal cortex = release aldosterone,

hypothalamus = thirst

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12
Q

What effect does ACE have on bradykinin?

A

ACE is a kinase enzyme = breaks down bradykinin (vasodilator) = no vasodilation

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13
Q

What occurs after taking an ACE inhibitor?

A

Stops angiotensin I converting to angiotensin II = no effect on raising BP.

ACE can no longer break down bradykinin = vasodilation occurs = lowers BP

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14
Q

How does the sympathetic nervous system control BP?

A

Vasoconstriction in kidneys, decrease GFR = decrease Na excretion, stim renin prod = increased BP

Direct = baroreceptor reflex

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15
Q

How does atrial natriuretic peptide work?

A

Released from atria due to stretch = vasodilation + promotes Na excretion = water follows = lower circulating blood vol = lower BP

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16
Q

What is prostaglandin and its clinical effect?

A

Lipid compound =

1) enhance glomerular filtration and reduce Na+ reabsorption
2) inhibit platelets aggregation
3) buffer to excessive vasoconstriction by SNS and RAAS = vasodilation

17
Q

What are the causes of hypertension?

A

Primary = unknown cause.

Secondary = cause defined renovascular disease (occlusion = renal artery stenosis, decreased perfusion), chronic renal, hyperaldosteronism, cushings (excess glucocorticoid cortisol)

18
Q

Why is it important to treat hypertension?

A

Although hypertension may be asymptomatic, it can have unseen damaging effects on, heart and vasculature, can = heart failure, MI, stroke, renal failure and retinopathy

19
Q

How is hypertension treated?

A

Always recommend lifestyle changes

Primary = work out possible targets using: BP = SV x HR x TPR

Secondary = treat the primary cause

20
Q

How is hypertensions treated targeting the RAAS?

A

ACE inhibitors

Ang II antagonists

21
Q

How is hypertension treated via vasodilation?

A

L-type Ca channel blockers

alpha-1 receptor blocker

22
Q

How is hypertension treated using diuretics?

A

Thiazide diuretics = reduce circulating vol

23
Q

How is hypertension treated with beta blockers?

A

Blocking beta-1 receptors = reduce effect of sympathetic output = reduce ionotrophy and chronotropy

24
Q

What is bradykinin?

A

Peptide =

1) vasodilation = fall in BP