6. Control Of BP And Hypertension Flashcards

1
Q

How do you calculate mean arterial BP?

A

Cardiac output * total peripheral resistance

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2
Q

How do you calculate cardiac output?

A

Stroke volume * heart rate

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3
Q

What is responsible for short term regulation of blood pressure?

A

Baroreceptor reflex

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4
Q

What are the 4 neurohumoral pathways which control BP long term

A

Renin-angiotensin-aldosterone system
Sympathetic nervous system
Antidiuretic hormone (ADH)
Atrial natriuretic peptide (ANP)

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5
Q

What is the main aim of the mechanisms for long term control of BP?

A

Controlling Na+ balance, and therefore extracellular fluid volume (including plasma)

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6
Q

What cells is renin released from?

A

Granular cells of juxtaglomerular apparatus (JGA) in the kidney

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7
Q

What 3 factors stimulate renin release?

A

Reduced NaCl delivery to distal tubule.
Reduced perfusion pressure in the kidney (detected by baroreceptors in afferent arteriole in kidney).
Sympathetic stimulation to JGA.
(SO DECREASED CIRCULATING VOLUME)

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8
Q

What are the 3 steps in the renin-angiotensin-aldosterone system?

A

Release of renin, reacts with angiotensinogen which is a plasma protein, to produce angiotensin I. ACE then converts this into angiotensin II

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9
Q

What 3 affects does angiotensin II have to increase BP

A

Vasoconstriction
Stimulates Na+ reabsorption at kidney
Stimulates aldosterone secretion from adrenal cortex

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10
Q

What are the 2 types of angiotensin II receptors, and which is the main actions via? What type of receptor are they?

A

AT1 and AT2
Main actions via AT1
GCPR

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11
Q

Give 3 sites of angiotensin II receptors, and their action

A

Arterioles - vasoconstriction
Kidney - stimulates Na+ reabsorption
Adrenal cortex - stimulates release of aldosterone

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12
Q

What cells does aldosterone mainly act on?

A

Principle cells of collecting ducts

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13
Q

What 3 things does aldosterone stimulate/activate?

A

Stimulates Na+ and water reabsorption.
Activates apical Na+ (re uptake) and apical K+ channels (secretion)
Increases basolateral Na+ extrusion via Na/K/ATPase

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14
Q

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

A

Breaks down bradykinin, which has vasodilator actions, so this also works to help increase BP

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15
Q

What 2 drugs act of the RAAS system to reduce hypertension?

A

ACE inhibitors

Ang II receptor antagonists

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16
Q

How does sympathetic nervous system stimulation on the kidneys help to maintain BP?

A

Acts on arterioles to reduce renal blood flow and decrease GFR, so decrease Na+ excretion.
Stimulated renin release via RAAS.
Stimulated Na+ reabsorption from PCT.

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17
Q

What is the main role of antidiuretic hormone in maintaining BP? In what other ways does it also do this?

A

Formation of concentrated urine by retaining water to control plasma osmolarity - increases water reabsorption in distil nephron.
Stimulates Na+ reabsorption and causes vasoconstriction.

18
Q

What 2 things stimulate ADH release?

A

Increases in plasma osmolarity

Severe hypovolaemia

19
Q

What does atrial natriuretic peptide promote?

A

Vasodilation of afferent arteriole
Increased glomerular filtration rate
Inhibits Na+ reabsorption along nephron
So Na+ excretion

20
Q

Where is atrial natriuretic peptide synthesised and stored?

A

Atrial myocytes

21
Q

When is atrial natriuretic peptide released?

A

From atrial cells in response to stretch

22
Q

Is atrial natriuretic peptide released to increase or decrease BP?

A

Decrease, so reduced effective circulating volume inhibits the release of ANP to support BP

23
Q

What do prostaglandins do?

A

Act as vasodilators.
Enhance glomerular filtration and reduce Na+ reabsorption.
Act as a buffer to excessive vasoconstriction produced by SNS and RAAS, so are important when levels of Ang II are high.

24
Q

Where is dopamine formed and what is it formed from?

A

In the kidney, from circulating L-DOPA

25
Where are dopamine receptors present?
Renal blood vessels and cells of proximal convoluted tubule and thick ascending limb of the loop of Henle
26
What does dopamine cause to happen?
Vasodilation in kidneys | Reduced reabsorption of NaCL
27
What is the definition of hypertension? What different stages can this be?
Sustained increase in BP | Stage I, II or severe
28
What is primary hypertension?
Cause is unknown
29
What is secondary hypertension?
Cause can be defined eg chronic renal disease, Cushing's syndrome
30
What is renovascular disease?
Occlusion of the renal artery (stenosis)
31
How does renovascular disease lead to secondary hypertension?
``` Occlusion of renal artery Fall in perfusion pressure in kidney Increased renin production Activation of RAAS Vasoconstriction and Na+ retention in other kidney ```
32
How does renal parenchyma disease (caused by chronic kidney disease) lead to secondary hypertension?
Early stage - loss of vasodilator substances. | Later stage - Na+ and water retention due to inadequate glomerular filtration (volume dependant hypertension).
33
Give one adrenal cause of secondary hypertension and how it causes hypertension
Cushing's syndrome - excess secretion of glucocorticoid cortisol, which at high concentrations acts on aldosterone receptors, leading to Na+ and water retention
34
Hypertension leads to increased afterload (pressure on wall of LV during ejection). What does this result in?
LV hypertrophy - heart failure | Increased myocardial oxygen demand - myocardial ischaemia and MI
35
Hypertension leads to arterial damage. HWat does this cause?
Atherosclerosis and weakened vessels - cerebro-vascular disease stroke, aneurysm, nephro-sclerosis and renal failure, retinopathy
36
What target organs should be assessed in hypertension?
Brain, eyes, heart, kidneys, arteries
37
In primary hypertension what can be used to work out possible targets for treatment?
Equation for mean arterial BP
38
Give 3 non-pharmacological approaches for treating hypertension
Exercise Reduced Na+ intake Reduced alcohol intake Diet
39
What could limit the effectiveness of antihypertensive therapy?
Failure to implement lifestyle changes
40
Give two types of vasodilators and how they work to treat hypertension
L-type Ca channel blockers - reduce Ca2+ entry to vascular smooth muscle cells, so relaxation. Alpha1 receptor blockers - reduce sympathetic tone, but can cause postural hypotension.
41
What is the main group of diuretics given to treat hypertension, and how do they work?
Thiazide diuretics - reduce circulating volume by inhabiting Na+ reabsorption in distal tubule
42
What do beta blockers do?
Block beta1 receptors in the heart, to reduce effects on sympathetic output, thus reducing heart rate and contractility. Only used if other indications such as previous MI