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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
What effects does angiotensin 2 have?
``` Vasoconstriction Na+ reabsorption in kidney Increase aldosterone release Increase thirst sensation (hypothalamus) Increase NA release (sympathetic NS) ```
26
what does angiotensin 2 act on?
Angiotensin 2 receptors (AT1 and AT2) | Main action on AT1
27
What does aldosterone do?
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
What other effects does ACE (angiotensin converting enzyme) have?
Breaks down bradykinin (vasodilator) into peptide fragments
29
What happens if using an ACE inhibitor?
Angiotensin 1 is not cleaved into angiotensin 2 | Bradykinin not broken down = vasodilation
30
What can occur if there is accumulation of bradykinin?
Dry cough (in lungs)
31
examples of ACE inhibitors
Captopril Lisinopril Perindopril
32
effects of sympathetic nervous system
Vasoconstriction = reduced renal blood flow = Decrease GFR (decrease Na+ excretion) Stimulates renin release activates Na+ H+ exchanger and Na+K+ATPase
33
ADH stimulated by
Increases in plasma osmolarity | Severe hypovalaemia
34
ADH function
Form concentrated urine | Retain water in body
35
What does ADH also stimulate
Na+ reabsorption (Na/K/Cl cotransporter in thick ascending limb) Vasoconstriction
36
Atrial Natriuretic peptides function (ANP)
Counteract other methods | Promotes Na+ excretion
37
Where is ANP synthesised and stored?
Atrial myocytes
38
When is ANP released?
In response to stretch (high BP so needs to lower BP)
39
What inhibits ANP?
Reduced effective circulating volume | reduced filling = reduced stretch = less ANP
40
Actions of ANP
Vasodilation Increased blood flow increases GFR Inhibits Na+ reabsorption = natriuresis (loss of Na+ in urine)
41
Prostaglandins
Vasodilators | enhance GFR = reduced Na+ reabsorption
42
When are prostaglandins important?
Buffer excess vasoconstriction from SNS/RAAS When Angiotensin 2 levels are HIGH = protect
43
Dopamine
Vasodilation and increase renal blood flow (receptors present on renal BV, PCT cells) Reduces reabsorption of NaCl
44
How doe dopamine reduce absorption of NaCl?
Inhibits NH exchanger and Na+K+ATPase in PCT
45
How does renovascular disease cause hypertension?
Occlusion of renal artery (renal artery stenosis) Lower perfusion to kidney Increased renin production =RAAS system activated (Vasoconstriction and Na+ retention)
46
How does renal parenchymal disease cause hypertension?
Loss of vasodilator substances (eg dopamine) | Na+ and water retention due to low GFR
47
Adrenal causes of hypertension
Conns syndrome Cushings Phaechromocytoma
48
Conns syndrome cause of hypertension
Aldosterone secreting adenoma = hypertension and hypokalaemia (Na+ reabsorbed, K+ secreted out)
49
Cushings causing hypertension
High levels of glucocorticoid cortisol | At high concentrations, acts on aldosterone receptors
50
Phaeochromocytoma cause of hypertension
Tumour of adrenal medulla secretes catecholamines (noradrenaline and adrenaline) = surge in BP via SNS
51
Treating hypertension non pharmacological
``` Exercise Diet Reduced Na+ intake Reduced alcohol (failure to implement = drugs work less effectively) ```
52
Drug targets for RAAS
Ace inhibitors Angiotensin 2 receptor antagonists = diuretic and vasodilator effects
53
Angiotensin receptor blockers example
Losartan, Valsartan
54
Vasodilator treatments
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
L type Ca2+ blockers eg
Verapamil, Nifedipine
56
a1 receptor blocker example
Doxazosin
57
Diuretics treatment
Thiazide diuretics = reduce circulating volume (inhibits Na/Cl cotransporter) Aldosterone antagonists (spironolactone)
58
Beta blockers treatment
Blocking b1 receptors reduces sympathetic output reduce HR and force of contraction Not usually used (only if previous MI)
59
Main drug types for hypertension
``` Renin inhibitors ACE inhibitors Angiotensin 2 antagonists Aldosterone antagonists Beta blockers ```

CVS 2023 (26 decks)

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