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CVS * > S5 Control Of Blood Pressure > Flashcards

S5 Control Of Blood Pressure Flashcards

1
Q

What is hypertension?

A

A sustained increase in blood pressure

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2
Q

What is blood pressure measured in?

A

mmHg

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3
Q

What is the normal/ideal blood pressure range?

A

Between 90/60 mmHg and 120/80 mmHg

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4
Q

What is the blood pressure for someone with stage 1 hypertension (in clinic, ambulatory monitoring and at home monitoring)?

A

In clinic - 140/90 mmHg or above

Ambulatory/home monitoring - average of 135/85 mmHg or above

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5
Q

What is the blood pressure for someone with stage 2 hypertension (in clinic, ambulatory monitoring and at home monitoring)?

A

In clinic - 160/100 mmHg or above

Ambulatory/home monitoring - 150/95 mmHg or above

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6
Q

What is the blood pressure for someone with severe hypertension (in clinic)?

A

180 or above systolic

110 or above diastolic

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7
Q

What causes hypertension?

A

Primary/essential - cause unknown (95% cases)

Secondary - caused by e.g. renovascular disease, chronic renal disease, hyperaldosteronism, Cushing’s syndrome

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8
Q

Why is it important to treat hypertension?

A

Can be asymptomatic, it can have unseen damaging effects on the heart and vasculature

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9
Q

What are 11 diseases that can occur due to hypertension?

A

VASCULAR DISEASES

  1. Stroke
  2. Heart failure
  3. Coronary heart disease
  4. MI
  5. Left ventricular hypertrophy
  6. Aortic aneurysm
  7. Peripheral vascular disease
  8. Retinopathy
  9. Hypertensive encephalopathy
  10. Chronic kidney failure
  11. Cerebral haemorrhage
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10
Q

What does hypertension do to the afterload? What are the effects of this?

A

Increases afterload

  • left ventricular hypertrophy which leads to heart failure
  • increased myocardial oxygen demand leads to myocardial ischaemia and MI
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11
Q

Hypertension causes arterial damage, what does this lead to?

A
  • atherosclerosis causes myocardial ischaemia and MI, cerebrovascular diease e.g. stroke, aneurysm, nephrosclerosis and renal failure, retinopathy
  • weakened vessels causes cerebrovascular diease e.g. stroke, aneurysm, nephrosclerosis and renal failure, retinopathy
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12
Q

What are the 5 main organs damaged by hypertension?

A
  1. Brain
  2. Eyes
  3. Heart
  4. Kidneys
  5. Arteries
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13
Q

How does chronic kidney disease caused by hypertension look?

A

One shrunken kidney due to a lack of blood supply (e.g. due to arterial damage)

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14
Q

What are the white patches on retina imaging of someone with hypertension?

A

Hard exudates of lipids that have been squeezed out of blood vessels due to high pressures

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15
Q

What is short term regulation of blood pressure? How do you alter CO and TPR?

A

Baroreceptor reflex

  • adjust sympathetic and parasympathetic inputs to the heart to alter cardiac output
  • adjust sympathetic input to peripheral resistance vessels to alter TPR
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16
Q

How do you calculate mean arterial pressure?

A

CO x TPR

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17
Q

What is medium and long term control of blood pressure?

A

Interaction of neurohumoral responses - control sodium balance and so extracellular fluid volume e.g. plasma

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18
Q

What are the four neurohumoral pathways that controls circulating volume and hence blood pressure?

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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19
Q

Where is renin released from?

A

Granular cells of the juxtaglomerular apparatus (JGA) in the afferent arteriole of the kidney

20
Q

What factors stimulate renin release?

A
  • reduced NaCl delivery to the distal tubule
  • reduced perfusion pressure in the kidney (detected by baroreceptors)
  • sympathetic stimulation to juxtaglomerular apparatus (JGA)
21
Q

What does renin cause?

A

Conversion of angiotensinogen to angiotensin I

22
Q

What enzyme converts angiotensin I to angiotensin II?

A

ACE - angiotensin converting enzyme

23
Q

What does angiotensin II do?

A
  • increases vasoconstriction
  • stimulates Na+ reabsorption at the kidney
  • stimulates aldosterone release from the adrenal cortex

Increases blood pressure

24
Q

What are the two types of angiotensin II receptors?

A

AT1 (main actions via this) an AT2

GPCRs

25
Q

What does binding of angiotensin II to it’s receptors cause in arterioles, kidneys, sympathetic nervous system, adrenal cortex, hypothalamus?

A

Arterioles - vasoconstriction
Kidney - stimulated Na+ reabsorption at the kidney
Sympathetic nervous system - increased NA release
Adrenal cortex - stimulates release of aldosterone
Hypothalamus - increases thirst sensation (stimulates ADH release)

26
Q

What is the action of aldosterone on the kidney?

A
  • acts on principal cells of collecting ducts
  • stimulates Na+ and so water reabsorption
  • activates apical Na+ channel (ENaC - epithelial Na channel) and apical K+ channel
  • increases basolateral Na+ extrusion via Na/K/ATPase
27
Q

Does an acute bradykinin build up lead to vasodilation or vasoconstriction?

A

Vasodilation

28
Q

What effect does ACE have on bradykinin?

A

Break it down (into peptide fragments)

29
Q

What would be the benefit of inhibiting ACE?

A
  • prevents conversion of angiotensin I to angiotensin II

* prevents break down of bradykinin so vasodilation can occur

30
Q

Give 4 examples of ACE inhibitors.

A
  1. Captopril
  2. Lisinopril
  3. Perindopril
  4. Enalapril
31
Q

How does the sympathetic nervous system affect hypertension?

A
  • high levels of sympathetic stimulation reduce renal blood flow (vasoconstriction of arterioles)
  • activates apical NHX and basolateral Na/K/ATPase in the PCT
  • stimulates renin release from JGA (increase in angiotensin II levels, increase in aldosterone levels - increase Na+ reabsorption)
32
Q

How does ADH affect hypertension?

A
  • release is stimulated by increases in plasma osmolarity/severe hypovolaemia
  • stimulates Na+ reabsorption (via apical Na/K/Cl cotransporter)
33
Q

How do natriuretic peptides affect hypertension?

A
  • promote Na+ excretion and inhibits Na+ reabsorption so decrease hypertension
  • cause vasodilation of afferent arteriole - increases blood flow, increases glomerular filtration rate
34
Q

Where are natriuretic peptides synthesised and stored?

A

Atrial myocytes

35
Q

When are they released from atrial cells?

A

In response to stretch

36
Q

When are ANPs inhibited?

A

When circulating volume is reduced

37
Q

What do prostaglandins act as? What do they do?

A

Vasodilators

Enhance glomerular filtration and reduce Na+ reabsorption

Act as a buffer to excessive vasoconstriction produced by the sympathetic nervous system and renin-angiotensin-aldosterone system

38
Q

What does dopamine cause?

A

Vasodilation and increases renal blood flow

And reduced reabsorption of NaCl

39
Q

How does renovascular disease cause secondary hypertension?

A
  1. Renal artery stenosis
  2. Fall in perfusion pressure in that kidney
  3. Increased renin production
  4. Activation of RAA system
  5. Vasoconstriction and Na+ retention occurs at other kidney
40
Q

How does renal parenchymal disease cause secondary hypertension?

A
  1. Loss of vasodilator substances

2. Na+ and water retention due to inadequate glomerular filtration

41
Q

How do adrenal causes cause secondary hypertension?

A
  • Conn’s syndrome - aldosterone secreting adenoma - Na+ and water retention - hypertension and hypokalaemia occurs
  • Cushing’s syndrome - excess secretion of glucocorticoid cortisol (at high concs, acts on aldosterone receptors) - Na+ and after retention
  • Tumour of the adrenal medulla - secretes catecholamines - stimulates sympathetic nervous system
42
Q

How do you treat hypertension non-pharmacologically?

A
  • exercise
  • diet
  • reduce Na+ intake
  • reduce alcohol intake
43
Q

How do you treat hypertension by targeting the RAA system?

A
  • ACE inhibitors

* angiotensin II antagonists - lorsatan, valsartan, temisartan

44
Q

How do you treat hypertension with vasodilators?

A
  • L-type Ca2+ channel blockers - verapamil, nifedipine - reduce Ca2+ entry to vascular smooth muscle cells, relaxation of vascular smooth muscle
  • alpha-1 receptor blockers - doxazosin - reduce sympathetic tone, relaxation of vascular smooth muscle
45
Q

How do you treat hypertension with diuretics?

A
  • thiazides diuretics
  • inhibit Na/Cl cotransporter on apical membrane of cells in distal tubule
  • aldosterone antagonists (not common)
46
Q

How do you treat hypertension with beta blockers?

A

Block beta-1 receptors in the heart - reduces effects of sympathetic output (not common)

CVS * (17 decks)

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