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

Lecture 11- Control of blood pressure Flashcards

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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
26
how is BP regulated
by borth short term and long term regulation
27
BP mean arterial BP=
BP= CO x TPR mean arterial BP= SBP+ (2x DBP)/ 3
28
CO=
SV X HR
29
short term regulation
baroreceptor reflex
30
long term regulation
1. Renin-angiotensin-aldosterone system 2. Sympathetic nervous system 3. Antidiuretic hormone (ADH) 4. Atrial natriuretic peptide (ANP)
31
baroreceptor reflxes
* **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**
32
baroreceptors are found in
the carotid sinus and aortic arch
33
e.g. if BP drops (if you are bleeding to death)
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
**Medium and longer term control of BP**
* Complex interaction of **neurohumoral** responses * Directed at controlling sodium balance and thus extrasellar fluid
35
**4 parallel neurohumoral pathways control circulating volume and hence BP**
1. Renin-angiotensin-aldosterone system 2. Sympathetic nervous system 3. Antidiuretic hormone (ADH) 4. Atrial natriuretic peptide (ANP)
36
**1. Renin-angiotensin-aldosterone system**
* 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
action of angiotensin II
​ 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
39
aldosterone
* 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
angiotensin II receptors
2 types: AT1 (main action) and AT2 -GPCRs
41
42
angiotensin II affect on different tissue
\* hypothalamus- stimulates thirst
43
**RAAS interacts with many other systems including .......... pathway**
**bradykinin**
44
bradykinin is a
vasodilator
45
ACE and bradykinin
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
ACE inhibitors are given to people with
high bp
47
**ACE inhibitors**
block the affect of ACE- block conversion of AT1-2, allow brady kinin to build up slowly (vasodilator) * Heart failure * Post MI
48
sympatheric nervous system and renal blood flow
**H**igh 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
Renin
* Stimulating RAAS * Increase in Ang II * Increase aldosterone * Increase sodium reabsorption
50
ADH
* Main role in formation of concentrated urine by retaining water to control plasma osmolarity * Increases water reabsorption in distal nephron (AQP2)
51
ADH release is stimulated by
* Increases in plasma osmolarity * Severe hypovolaemia
52
ADH stimulates
* Stimulates Na+ reabsorption * Acts on thick ascending limb * Stimulates Na/L/Cl co-transporter * Causes vasoconstriction
53
name the natriuretic peptides
ANP and BNP Atrial natriuretic peptides Brain-like natriuretic peptides
54
both ANP and BNP promote
Na+ excretion
55
what stimulates ANP release
* ANP released in the atria in response to stretch * Low pressure volume sensors in the atria
56
what inhibits release of ANP
* Reduced effective circulating volume inhibits the release of ANP to support BP * Reduced filling of the heart * Less stretch * Less ANP released
57
effect of ANP
* 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
other systems invovled in BP
prostaglandins dopamine
59
prostaglandins
* 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
**Dopamine**
* 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
**Secondary hypertension: renovascular disease**
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
**Secondary hypertension: renal parenchymal disease**
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
**Secondary hypertension: Adrenal causes**
* Conns syndrome * Cushings syndrome * Tumour of the adrenal medulla
64
**Conn’s syndrome**
aldosterone secreting adenomas * Hypertension and hypokalaemia
65
**Cushing’s syndrome**
* excess secretion of glucocorticoid cortisol * At high conc will act on aldosterone receptors- Na+ and water retention
66
**Tumour of the adrenal medulla**
phaeochromocytoma- secretes catecholamine (NA and A)
67
most cases pof HP are
primary- no identifiable cause
68
**Treating hypertension: Non-pharmacological approaches**
* 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
drugs :treating hypertesnion
* ACE inhibitors * Ang II receptor antagonists * Vasodilators * Diuretics * B blockers
70
ACE inhibitors
prevent conversion of Ang I --\> Ang II--\> reduce retention of sodium
71
side effect of ACE inhibitors
* However bradykinin will increase * Will cause vasodilation in the lungs * Cause a dry cough (major side effect of ACE inhibitor)
72
**Ang II receptors antagonists**
* 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
treating hypertension with vasodilators
* **L-type Ca channel blockers (e.g. verapamil, Nifedipine)** * **Alpha1 receptor blockers (doxazosin)**
74
L-type Ca channel blockers (e.g. verapamil, Nifedipine)
1. Reduced Ca2+ entry to vascular smooth muscle cells 2. Relaxation of vascular smooth muscle
75
Alpha1 receptor blockers (doxazosin)
* Reduce sympathetic tone (relaxation of vascular smooth muscle) * Can cause postural hypotension
76
**Diuretics**
* **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
**Beta blockers**
* 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
summary of targets of action of commonly used antihypertensives

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