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Cardiovascular system > Lecture 11- Control of blood pressure > Flashcards

Lecture 11- Control of blood pressure Flashcards

1
Q

Why is hypertension so dangerous?

A

Hard to notice

  • Could be anyone of us… ‘the silent killer’- no symptoms until cardiovascular event
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2
Q

What is hypertension?

A

Sustained increase in BP

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3
Q

Ideal adult pressure is considered to be between

A

90/60 mmHg and 120/80 mmHg

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4
Q

how many stages of hypertension

A

3

  • stage 1
  • stage 2
  • severe
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5
Q

stage 1 hypertension BP

A

>140/90 mmHg

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6
Q

stage 2 hypertension BP

A

160/100 mmHg

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7
Q

severe hypertension BP

A

>180 systolic or >110 diastolic

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8
Q

stage 1 is also called

A

pre-hypertension

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9
Q

What causes hypertension?

A
  • In around 95% of cases the cause is unknown- ‘essential’ or primary (idiopathic) hypertension
  • Where the cause can be defined it is referred as secondary hypertension
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10
Q

causes of secondary hypertension

A
  • Renovascular disease
  • Chronic renal disease
  • Hyperaldosteronism
  • Cushing’s syndrome
    • Important to identify and treat the underlying cause
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11
Q

Why is it important to treat hypertension?

A
  • Silent killer
  • Although hypertension may be asymptomatic- it can have unseen damaging effects on
    • Heart and vasculature
    • Potentially leading to heart failure, MI, stroke, renal failure and retinopathy
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12
Q

HBP affects how many adults in england

A

1 in 4

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13
Q

how many hearts attacks and strokes are associated with high BP

A

at least half

also a major risk factor for chronic kidney disease, heart failure and dementia

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14
Q

Diseases attributable to hypertension- vascular diseases

A
  • Stroke
  • Heart failure
  • Cerebral haemorrhage
  • Chronic kidney failure
  • Hypertensive encephalopathy
  • Retinopathy
  • Peripheral vascular disease
  • Aortic aneurysm
  • Left ventricular hypertrophy
  • MI
  • Coronary heart disease
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15
Q

how does hypertension lead to vascular diseases

A

increases both afterload and arterial damage

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16
Q

increased afterload can lead to

A
  1. left ventricular hypertropy –> heart failure
  2. increased myocardial oxygen demnad –> MI and ischaemia
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17
Q

arterial dmaage can cause ….. and ….. leading to :

A

atheroscleorsis and weakened vessels :

  • MI
  • Cerebrovascular disease stroke
  • aneurysm
  • nephorclerosis and renal failure
  • retinopathy
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18
Q

how to examine targte organ damage/ clinical CVD

A

e. g. ask them anbout signs of ischaemia e.g. chest pain
e. g. feel for aneursysm
e. g. listen to peripheral pulses

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19
Q

left ventiruclar hypertrophy due to

A

increased afterload

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20
Q

hypertensive retinopathy

A
  • Hard parts- hard exudate (white parts)
  • Red haemorrhages
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21
Q

atheroscelerosis

A

becomes heavilty calcified due to arterial damage

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22
Q

ischaemic stroke

A
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23
Q

chronic kidney disease

A

kidney reduces in size due to hypoxia

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24
Q

Effect of intervention

A
  • Interventions show a significant reduction in mortality
  • Any intervention which reduced blood pressure reduces all-cause mortality
  • Every 10mmHg reduction in BP results in
    • 17% reduction in CHD
    • 27% reduction for stroke
    • 28% reduction for heart failure
    • 13% reduction in all-cause mortality
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25
Q
A
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26
Q

how is BP regulated

A

by borth short term and long term regulation

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27
Q

BP

mean arterial BP=

A

BP= CO x TPR

mean arterial BP= SBP+ (2x DBP)/ 3

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28
Q

CO=

A

SV X HR

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29
Q

short term regulation

A

baroreceptor reflex

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30
Q

long term regulation

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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31
Q

baroreceptor reflxes

A
  • Sense high pressure
    • Baroreceptors found in carotid sinus and aortic arch
      • Sense stretch of the elastic blood vessels
      • Increased stretch (during increased BP) stimulates receptor
      • Sends message to medulla in the brain
      • Sends efferent messages back to alter BP
        • negative chronotropy and dilate peripheral blood pressure reduce BP
  • Also sense low BP
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32
Q

baroreceptors are found in

A

the carotid sinus and aortic arch

33
Q

e.g. if BP drops (if you are bleeding to death)

A

your body needs to compensate

  • Adjusts sympathetic and parasympathetic inputs to the heart to alter cardiac output
  • Adjust sympathetic input to peripheral resistance vessels to alter TPR
34
Q

Medium and longer term control of BP

A
  • Complex interaction of neurohumoral responses
  • Directed at controlling sodium balance and thus extrasellar fluid
35
Q

4 parallel neurohumoral pathways control circulating volume and hence BP

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
36
Q

1. Renin-angiotensin-aldosterone system

A
  • Renin released by granular cells of the juxtaglomerular apparatus (JGA) in response to:
    • Reduced NaCl delivery to distal tubule
    • Reduced perfusion pressure in the kidney causes the release of renin (detected by baroreceptors in afferent arteriole
    • Sympathetic stimulation to JGA increases release of renin
  • Renin converts angiotensinogen to angiotensin I
  • Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II
    • Angiotensin II
      • Powerful vasoconstrictor
      • Stimulates Na+ reabsorption and therefore water reabsorption in the kidney  increasing BP
      • Stimulates aldosterone release from the adrenal cortex:
        • Act on principle cells of collecting duct
        • Stimulates Na+ and therefore water reabsorption
        • Activates apical Na+ channel and apical K+ channels
        • Increases basolateral na+ extrusion via Na/K/ATPase
37
Q

action of angiotensin II

A

​

  1. Powerful vasoconstrictor
  2. Stimulates Na+ reabsorption and therefore water reabsorption in the kidney –>increasing BP
  3. Stimulates aldosterone release from the adrenal cortex
38
Q
A
39
Q

aldosterone

A
  • Act on principle cells of collecting duct
  • Stimulates Na+ and therefore water reabsorption
  • Activates apical Na+ channel and apical K+ channels
  • Increases basolateral na+ extrusion via Na/K/ATPase
40
Q

angiotensin II receptors

A

2 types: AT1 (main action) and AT2

-GPCRs

41
Q
A
42
Q

angiotensin II affect on different tissue

A

* hypothalamus- stimulates thirst

43
Q

RAAS interacts with many other systems including ………. pathway

A

bradykinin

44
Q

bradykinin is a

A

vasodilator

45
Q

ACE and bradykinin

A

ACE breaks it down

The vasoconstriction effects of AngII are further augmented because ACE is also one of the kininase enzymes which breaks down the vasodilator bradykinin

46
Q

ACE inhibitors are given to people with

A

high bp

47
Q

ACE inhibitors

A

block the affect of ACE- block conversion of AT1-2, allow brady kinin to build up slowly (vasodilator)

  • Heart failure
  • Post MI
48
Q

sympatheric nervous system and renal blood flow

A

High levels of stimulation reduce renal blood flow

  • Vasoconstriction of arterioles
  • Decrease GFR- Decrease Na excretion
  • Activates apical Na/H-exchanger and basolateral Na/K ATPase in PCT
  • Stimulated JG cell to release renin
49
Q

Renin

A
  • Stimulating RAAS
    • Increase in Ang II
    • Increase aldosterone
    • Increase sodium reabsorption
50
Q

ADH

A
  • Main role in formation of concentrated urine by retaining water to control plasma osmolarity
    • Increases water reabsorption in distal nephron (AQP2)
51
Q

ADH release is stimulated by

A
  • Increases in plasma osmolarity
  • Severe hypovolaemia
52
Q

ADH stimulates

A
  • Stimulates Na+ reabsorption
    • Acts on thick ascending limb
    • Stimulates Na/L/Cl co-transporter
  • Causes vasoconstriction
53
Q

name the natriuretic peptides

A

ANP and BNP

Atrial natriuretic peptides

Brain-like natriuretic peptides

54
Q

both ANP and BNP promote

A

Na+ excretion

55
Q

what stimulates ANP release

A
  • ANP released in the atria in response to stretch
  • Low pressure volume sensors in the atria
56
Q

what inhibits release of ANP

A
  • Reduced effective circulating volume inhibits the release of ANP to support BP
    • Reduced filling of the heart
    • Less stretch
    • Less ANP released
57
Q

effect of ANP

A
  • Causes vasodilation of the afferent arteriole
  • Increased blood flow increases GFR
  • Inhibits Na+ reabsorption along the nephron
  • Causes natriuresis (loss of sodium into urine)
  • If circulating volume is low ANP release is inhibited
58
Q

other systems invovled in BP

A

prostaglandins

dopamine

59
Q

prostaglandins

A
  • Local mediator of vasodilation
  • More important clinically than physiologically
  • Locally acting prostaglandins (PGE2)enhance glomerular filtration and reduce Na+ reabsorption
  • May have important protective function
  • Act as a buffer to excessive vasoconstriction produce by Sympathetic NS and RAA system
  • Important when levels of Ang II are high
60
Q

Dopamine

A
  • Formed locally in the kidney from circulating L-DOPA
  • Dopamine receptors are present on renal blood vessels and cells of PCT and TA
    • DA causes vasodilation and increases renal blood flow
    • DA reduces reabsorption of NaCL
      • Inhibits NH exchanger and Na/K ATPase in principal cells of PCT and TAL
61
Q

Secondary hypertension: renovascular disease

A
  1. Occlusion of the renal artery (renal artery stenosis) causes a fall in perfusion pressure in that kidney
  2. Decreased perfusion pressure leads to increased renin production
  3. Activation of RAAS
  4. Vasoconstriction and sodium retention at other kidney
62
Q

Secondary hypertension: renal parenchymal disease

A
  1. Earlier stage may be loss of vasodilator substance
  2. In later stage Na+ and water retention due to inadequate glomerular filtration
    • Volume-dependent hypertension
63
Q

Secondary hypertension: Adrenal causes

A
  • Conns syndrome
  • Cushings syndrome
  • Tumour of the adrenal medulla
64
Q

Conn’s syndrome

A

aldosterone secreting adenomas

  • Hypertension and hypokalaemia
65
Q

Cushing’s syndrome

A
  • excess secretion of glucocorticoid cortisol
  • At high conc will act on aldosterone receptors- Na+ and water retention
66
Q

Tumour of the adrenal medulla

A

phaeochromocytoma- secretes catecholamine (NA and A)

67
Q

most cases pof HP are

A

primary- no identifiable cause

68
Q

Treating hypertension: Non-pharmacological approaches

A
  • Exercise
  • Diet
  • Reduced Na+ intake
  • Reduced alcohol intake
  • Lifestyles changes above can have limited effect
  • Failure to implement lifestyle changes can limit the effectiveness of antihypertensive therapy
69
Q

drugs :treating hypertesnion

A
  • ACE inhibitors
  • Ang II receptor antagonists
  • Vasodilators
  • Diuretics
  • B blockers
70
Q

ACE inhibitors

A

prevent conversion of Ang I –> Ang II–> reduce retention of sodium

71
Q

side effect of ACE inhibitors

A
  • However bradykinin will increase
    • Will cause vasodilation in the lungs
      • Cause a dry cough (major side effect of ACE inhibitor)
72
Q

Ang II receptors antagonists

A
  • Ang II is a powerful vasoconstrictor- direct action on the kidney and promotes release of aldosterone, leading to NaCL and water retention
  • Blocking production of Ang II has diuretic and vasodilator effects
73
Q

treating hypertension with vasodilators

A
  • L-type Ca channel blockers (e.g. verapamil, Nifedipine)
  • Alpha1 receptor blockers (doxazosin)
74
Q

L-type Ca channel blockers (e.g. verapamil, Nifedipine)

A
  1. Reduced Ca2+ entry to vascular smooth muscle cells
  2. Relaxation of vascular smooth muscle
75
Q

Alpha1 receptor blockers (doxazosin)

A
  • Reduce sympathetic tone (relaxation of vascular smooth muscle)
  • Can cause postural hypotension
76
Q

Diuretics

A
  • Thiazide
    • Reduce circulating volume
    • Inhibits Na/CL co-transporter on apical membrane of cells in distal tubule
  • Other diuretic e.g. aldosterone antagonists (spironolactone) will lower BP
    • Not first line of choice
77
Q

Beta blockers

A
  • Block SNS
  • Less commonly used to treat hypertension
  • Blocking B1 receptors in the heart will reduce effects of sympathetic output
    • Reduce HR and contractility
    • Not used in hypertension alone
    • Would only be used if there are other indications such as previous MI
78
Q

summary of targets of action of commonly used antihypertensives

A

Cardiovascular system (30 decks)

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