6. Control Of BP And Hypertension Flashcards

1
Q

How do you calculate mean arterial BP?

A

Cardiac output * total peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do you calculate cardiac output?

A

Stroke volume * heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is responsible for short term regulation of blood pressure?

A

Baroreceptor reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What cells is renin released from?

A

Granular cells of juxtaglomerular apparatus (JGA) in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What cells does aldosterone mainly act on?

A

Principle cells of collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

ACE inhibitors

Ang II receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Where are dopamine receptors present?

A

Renal blood vessels and cells of proximal convoluted tubule and thick ascending limb of the loop of Henle

26
Q

What does dopamine cause to happen?

A

Vasodilation in kidneys

Reduced reabsorption of NaCL

27
Q

What is the definition of hypertension? What different stages can this be?

A

Sustained increase in BP

Stage I, II or severe

28
Q

What is primary hypertension?

A

Cause is unknown

29
Q

What is secondary hypertension?

A

Cause can be defined eg chronic renal disease, Cushing’s syndrome

30
Q

What is renovascular disease?

A

Occlusion of the renal artery (stenosis)

31
Q

How does renovascular disease lead to secondary hypertension?

A
Occlusion of renal artery 
Fall in perfusion pressure in kidney
Increased renin production
Activation of RAAS
Vasoconstriction and Na+ retention in other kidney
32
Q

How does renal parenchyma disease (caused by chronic kidney disease) lead to secondary hypertension?

A

Early stage - loss of vasodilator substances.

Later stage - Na+ and water retention due to inadequate glomerular filtration (volume dependant hypertension).

33
Q

Give one adrenal cause of secondary hypertension and how it causes hypertension

A

Cushing’s syndrome - excess secretion of glucocorticoid cortisol, which at high concentrations acts on aldosterone receptors, leading to Na+ and water retention

34
Q

Hypertension leads to increased afterload (pressure on wall of LV during ejection). What does this result in?

A

LV hypertrophy - heart failure

Increased myocardial oxygen demand - myocardial ischaemia and MI

35
Q

Hypertension leads to arterial damage. HWat does this cause?

A

Atherosclerosis and weakened vessels - cerebro-vascular disease stroke, aneurysm, nephro-sclerosis and renal failure, retinopathy

36
Q

What target organs should be assessed in hypertension?

A

Brain, eyes, heart, kidneys, arteries

37
Q

In primary hypertension what can be used to work out possible targets for treatment?

A

Equation for mean arterial BP

38
Q

Give 3 non-pharmacological approaches for treating hypertension

A

Exercise
Reduced Na+ intake
Reduced alcohol intake
Diet

39
Q

What could limit the effectiveness of antihypertensive therapy?

A

Failure to implement lifestyle changes

40
Q

Give two types of vasodilators and how they work to treat hypertension

A

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
Q

What is the main group of diuretics given to treat hypertension, and how do they work?

A

Thiazide diuretics - reduce circulating volume by inhabiting Na+ reabsorption in distal tubule

42
Q

What do beta blockers do?

A

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