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Semester 2-CVS > Session 5-Control Of Blood Pressure > Flashcards

Session 5-Control Of Blood Pressure Flashcards

1
Q

What is the equation for cardiac output?

A

CO=SV x HR

Cardiac output=stroke volume x heart rate

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2
Q

What is the mechanism for short term regulation of blood pressure?

A

Baroreceptor reflex

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3
Q

Which nerve endings are sensitive to stretch?

A

Those in the carotid sinus and aortic arch

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4
Q

True or false: decreased arterial pressure stretches baroreceptors

A

FALSE - increased pressure stretches

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5
Q

True or false: baroreceptor reflex works well to control acute changes in BP (up to 15 minutes)

A

TRUE

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6
Q

Why does the baroreceptor reflex not control sustained changes in BP?

A

The threshold for baroreceptor firing resets

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7
Q

What are medium and longer term controls of BP directed at?

A

Controlling sodium balance and thus extracellular fluid volume

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8
Q

What controls plasma volume?

A

Control of extracellular fluid volume - water follows sodium therefore controlling total body sodium levels controls plasma volume

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9
Q

What are the four neurohumoral pathways controlling circulating volume and therefore BP?

A

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

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10
Q

Which cells release renin?

A

Granular cells of juxtaglomerular apparatus (JGA)

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11
Q

Which factors stimulate renin release? (3)

A

1) reduced NaCl delivery to distal tubule
2) reduced perfusion pressure in kidney causes release of renin
3) sympathetic stimulation to JGA increases release of renin

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12
Q

Which reaction does renin catalyse?

A

Angiotensinogen -> angiotensin

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13
Q

Which enzyme catalyses the conversion of angiotensin I to angiotensin II?

A

Angiotensin converting enzyme (ACE)

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14
Q

How does angiotensin II affect the body? (3)

A

1) vasoconstriction
2) stimulates Na+ reabsorption at kidney
3) stimulates aldosterone from adrenal cortex which then stimulates no. 2)

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15
Q

What are two types of angiotensin II receptors?

A 
Angiotensin 1 (AT1)
Angiotensin 2 (AT2)
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16
Q

True or false: the main actions are via AT1 receptor which is a GPCR

A

TRUE

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17
Q

What action do the angiotensin II receptors have at the following sites:

1) sympathetic nervous system
2) hypothalamus

A

1) vasoconstriction

2) increases thirst sensation (stimulates ADH release-antidiuretic)

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18
Q

What are the actions of aldosterone? (4)

A

1) acts one principal cells of collecting ducts
2) stimulates Na+ and therefore water reabsorption
3) activates apical Na+ channel and apical K+ channel
4) increases basolateral Na+ extrusion via Na/K ATPase

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19
Q

What is the apical Na+ channel called?

A

ENaC (Epithelial Na Channel)

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20
Q

True or false: bradykinin, found in the lung, has vasoconstrictor actions

A

FALSE - vasodilator

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21
Q

What does angiotensin converting enzyme break bradykinin into?

A

Peptide fragments

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22
Q

What effect does the breakdown of bradykinin have?

A

Vasoconstriction effects of angiotensin II are augmented because ACE breaks bradykinin down (has vasodilator effects)

23
Q

What is a side effect of ACE inhibitors?

A

Dry cough

24
Q

Complete the sentence:

High levels of sympathetic stimulation ___________ renal blood flow as there is ___________________ of arterioles. It also ________ glomerular filtration rate (GFR).

A

Reduces
Vasoconstriction
Decreases

25
Q

What does stimulation of the sympathetic nervous system release and what does this lead to?

A

Renin from juxtaglomerular cells

Increased angiotensin II levels and therefore increased aldosterone levels

26
Q

What is the main role of antidiuretic hormone? (ADH)

A

Formation of concentrated urine by retaining water to control plasma osmolarity

27
Q

What stimulates the release of antidiuretic hormone (ADH)? (2)

A

1) Increases in plasma osmolarity

2) Severe hypovolaemia

28
Q

True or false: ADH also stimulates Na+ reabsorption

A

TRUE

29
Q

What does atrial natriuretic peptide (ANP) promote?

A

Na+ excretion

30
Q

Complete the sentences:

Atrial natriuretic peptide (ANP) is synthesised and stored in _________ _____________ and are released in response to ________. Reduced circulating blood volume ___________ the release of ANP as there is less _________.

A

Atrial myocytes
Stretch
Inhibits
Stretch

31
Q

What are the actions of atrial natriuretic peptide (ANP)? (4)

A

1) vasodilation of afferent arteriole
2) increases blood flow (increases glomerular filtration rate)
3) inhibits Na+ reabsorption along nephron
4) causes natriuresis (loss of sodium in urine)

32
Q

What do prostaglandins act as?

A

Vasodilators

33
Q

True or false: prostaglandins act as a buffer to excessive vasoconstriction produced by parasympathetic nervous system and RAAS

A

FALSE - sympathetic nervous system, not parasympathetic

34
Q

What does dopamine cause? (3)

A

1) Vasodilation
2) Increases renal blood flow
3) Reduces reabsorption of NaCl

35
Q

What is hypertension?

A

Sustained increase in blood pressure

36
Q

What BP measured in a clinic is classified as stage 1 mild hypertension?

A

> /= 140/90 mmHg

37
Q

What BP measured in a clinic is classified as stage 2 moderate hypertension?

A

> /= 160/100 mmHg

38
Q

What BP measured in a clinic is classified as severe hypertension?

A

> /= 180/110 mmHg

39
Q

What is the difference between primary and secondary hypertension?

A

Where the cause of hypertension can be defined, it is referred to as secondary hypertension. Where the cause is unknown, it is referred to as primary hypertension

40
Q

What are some causes of hypertension?

A

Renovascular disease
Chronic renal disease
Hyperaldosteronism
Cushing’s syndrome

41
Q

How can renovascular disease cause secondary hypertension?

A

Occlusion of renal artery (renal artery stenosis) abuses fall in perfusion pressure in kidney -> increased renin production -> activation of RAAS -> vasoconstriction and Na+ retention at other kidney

42
Q

What can happen in later stages of renal parenchymal disease?

A

Na+ and water retention due to inadequate glomerular filtration

43
Q

How can Cushing’s syndrome lead to hypertension?

A

Excess secretion of glucocorticoid cortisol - at high concentration acts on aldosterone receptors -> Na+ and water retention

44
Q

How can phaeochromocytoma lead to hypertension?

A

Tumour of adrenal medulla -> secretes catacholamines (noradrenaline, dopamine and adrenaline)

45
Q

What can hypertension lead to?

A

Heart failure
MI
Stroke
Renal failure

46
Q

How can hypertension lead to heart failure?

A

Increases afterload -> LV hypertrophy

47
Q

How can hypertension lead to myocardial ischaemia and MI?

A

Increased afterload -> increased myocardial oxygen demand

OR

Arterial damage -> atherosclerosis

48
Q

How can hypertension lead to cerebro-vascular disease/stroke, aneurysm, renal failure and retinopathy?

A

Arterial damage -> atherosclerosis and weakened vessels

49
Q

How is secondary hypertension treated?

A

Treat primary cause

50
Q

What are the non-pharmacological approaches to treating hypertension?

A

Exercise
Diet
Reduced Na+ intake
Reduced alcohol intake

51
Q

How can the RAAS be targeted to treat hypertension?

A

1) ACE inhibitors

2) Angiotensin II receptor antagonists -> vasodilator and diuretic effects

52
Q

True or false: L-type Ca channel blockers can be used to treat hypertension

A

TRUE - reduce Ca2+ entry to vascular smooth muscle cells so they relax

53
Q

How can beta blockers be used to treat hypertension?

A

Block beta1 receptors in the heart, reducing effects of sympathetic output and reduce heart rate and contractility

Semester 2-CVS (18 decks)

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