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CVS 2023 > Control of BP > Flashcards

Control of BP Flashcards

1
Q

What is hypertension?

A

Sustained increase in BP

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2
Q

What is BP measured in?

A

mmHg (millimetres of mercury)

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3
Q

Normal BP

A

90/60mmHg –> 120/80mmHg

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4
Q

Stage 1 hypertension

A

> 140/90mmHg

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5
Q

Stage 2

A

> 160/100mmHg

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6
Q

severe hypertension

A

> 180 systolic or >110 diastolic

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7
Q

Primary hypertension

A

Cause unknown (90%)

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8
Q

Secondary hypertension

A

Cause known eg:

Renovascular disease, chronic renal, hyperaldosteronism, cushings

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9
Q

Treatment for secondary hypertension

A

Treat underlying cause!!!

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10
Q

Why is hypertension known as silent killer?

A

No symptoms until BP is measured

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11
Q

What effect does hypertension have on body?

A

Damages heart and vasculature

lead to heart failure, MI, stroke, renal failure and retinopathy

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12
Q

arterial damage hypertension

A

Atherosclerosis/weakened vessels

= stroke, aneurysm, nephrosclerosis/renal failure, retinopathy

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13
Q

Increase afterload from hypertension (amount of force needed to eject blood)

A

LV hypertrophy and Increased myocardial oxygen demand

= heart failure, myocardial ischaemia, MI

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14
Q

Target organ damage for cardiovascular disease

A 
Brain (ischaemia/haemorrhage)
Eyes (retinopathy)
Heart (LV hypertrophy, MI)
Kidneys (atrophy from damaged vessels)
Arteries (calcified atheroma)
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15
Q

Exams for CVD

A 
Check back of eyes (retinopathy?)
Listen for heart murmurs
Urine sample
Palpate kidneys (atrophy?)
ECG
Palpate arteries/listen for bruit
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16
Q

What does intervention achieve?

A 
Reduced risk of:
Coronary heart disease (17%)
Stroke (27%)
Heart failure (28%)
All-cause mortality (13%)
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17
Q

Blood pressure equations

A

BP = CO x TPR

CO = SV x HR

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18
Q

Medium and long term control of blood pressure

A

Neurohumoral response

Controlling of sodium balance

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19
Q

How is blood pressure controlled with Na+?

A

Water follows Na+
If increase Na+, increase plasma volume

(then increase stroke volume)

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20
Q

4 neurohumoral pathways controlling BP

A

RAAS (renin-angiotensin-aldosterone system)
SNS (Sympathetic nervous system)
ADH (Antidiuretic hormone)
ANP (anti natriuretic peptide)

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21
Q

where is renin released from?

A

Kidneys - granular cells of juxtaglomerular apparatus (JGA)

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22
Q

What stimulates renin release?

A

Reduced salt (NaCl) delivery to distal tubule
Reduced perfusion pressure to kidney (baroreceptors)
Sympathetic stimulation to JGA

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23
Q

what does renin do?

A

Cleaves angiotensinogen to angiotensin 1

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24
Q

What happens to angiotensin 1?

A

Cleaved to angiotensin 2 by ACE (angiotensin converting enzyme)

25
Q

What effects does angiotensin 2 have?

A 
Vasoconstriction
Na+ reabsorption in kidney
Increase aldosterone release 
Increase thirst sensation (hypothalamus)
Increase NA release (sympathetic NS)
26
Q

what does angiotensin 2 act on?

A

Angiotensin 2 receptors (AT1 and AT2)

Main action on AT1

27
Q

What does aldosterone do?

A

Stimulates Na+ reabsorption in collecting ducts (so water too)

Activates Na+ channel (epithelial Na+ channel ENaC) and apical K+ channel

Increases Na+ extrusion via Na+K+ATPase

28
Q

What other effects does ACE (angiotensin converting enzyme) have?

A

Breaks down bradykinin (vasodilator) into peptide fragments

29
Q

What happens if using an ACE inhibitor?

A

Angiotensin 1 is not cleaved into angiotensin 2

Bradykinin not broken down = vasodilation

30
Q

What can occur if there is accumulation of bradykinin?

A

Dry cough (in lungs)

31
Q

examples of ACE inhibitors

A

Captopril
Lisinopril
Perindopril

32
Q

effects of sympathetic nervous system

A

Vasoconstriction
= reduced renal blood flow
= Decrease GFR (decrease Na+ excretion)

Stimulates renin release

activates Na+ H+ exchanger and Na+K+ATPase

33
Q

ADH stimulated by

A

Increases in plasma osmolarity

Severe hypovalaemia

34
Q

ADH function

A

Form concentrated urine

Retain water in body

35
Q

What does ADH also stimulate

A

Na+ reabsorption (Na/K/Cl cotransporter in thick ascending limb)

Vasoconstriction

36
Q

Atrial Natriuretic peptides function (ANP)

A

Counteract other methods

Promotes Na+ excretion

37
Q

Where is ANP synthesised and stored?

A

Atrial myocytes

38
Q

When is ANP released?

A

In response to stretch (high BP so needs to lower BP)

39
Q

What inhibits ANP?

A

Reduced effective circulating volume

reduced filling = reduced stretch = less ANP

40
Q

Actions of ANP

A

Vasodilation

Increased blood flow increases GFR

Inhibits Na+ reabsorption = natriuresis (loss of Na+ in urine)

41
Q

Prostaglandins

A

Vasodilators

enhance GFR = reduced Na+ reabsorption

42
Q

When are prostaglandins important?

A

Buffer excess vasoconstriction from SNS/RAAS
When Angiotensin 2 levels are HIGH

= protect

43
Q

Dopamine

A

Vasodilation and increase renal blood flow
(receptors present on renal BV, PCT cells)

Reduces reabsorption of NaCl

44
Q

How doe dopamine reduce absorption of NaCl?

A

Inhibits NH exchanger and Na+K+ATPase in PCT

45
Q

How does renovascular disease cause hypertension?

A

Occlusion of renal artery (renal artery stenosis)
Lower perfusion to kidney
Increased renin production

=RAAS system activated (Vasoconstriction and Na+ retention)

46
Q

How does renal parenchymal disease cause hypertension?

A

Loss of vasodilator substances (eg dopamine)

Na+ and water retention due to low GFR

47
Q

Adrenal causes of hypertension

A

Conns syndrome
Cushings
Phaechromocytoma

48
Q

Conns syndrome cause of hypertension

A

Aldosterone secreting adenoma
= hypertension and hypokalaemia

(Na+ reabsorbed, K+ secreted out)

49
Q

Cushings causing hypertension

A

High levels of glucocorticoid cortisol

At high concentrations, acts on aldosterone receptors

50
Q

Phaeochromocytoma cause of hypertension

A

Tumour of adrenal medulla
secretes catecholamines (noradrenaline and adrenaline)
= surge in BP via SNS

51
Q

Treating hypertension non pharmacological

A 
Exercise
Diet
Reduced Na+ intake
Reduced alcohol
(failure to implement = drugs work less effectively)
52
Q

Drug targets for RAAS

A

Ace inhibitors
Angiotensin 2 receptor antagonists
= diuretic and vasodilator effects

53
Q

Angiotensin receptor blockers example

A

Losartan, Valsartan

54
Q

Vasodilator treatments

A

L type Ca2+ blockers (Ca2+ cannot enter smooth muscle cells = no contraction)

a1 receptor blockers (reduces sympathetic tone = relaxation of smooth muscle cells lower BP)

55
Q

L type Ca2+ blockers eg

A

Verapamil, Nifedipine

56
Q

a1 receptor blocker example

A

Doxazosin

57
Q

Diuretics treatment

A

Thiazide diuretics = reduce circulating volume
(inhibits Na/Cl cotransporter)

Aldosterone antagonists (spironolactone)

58
Q

Beta blockers treatment

A

Blocking b1 receptors reduces sympathetic output
reduce HR and force of contraction

Not usually used (only if previous MI)

59
Q

Main drug types for hypertension

A 
Renin inhibitors
ACE inhibitors
Angiotensin 2 antagonists 
Aldosterone antagonists 
Beta blockers

CVS 2023 (26 decks)

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