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CVS A > Session 5 Lecture 1 > Flashcards

Session 5 Lecture 1 Flashcards

1
Q

What is the short term regulation for blood pressure?

A

Baroreceptor reflex

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2
Q

What is the mean arterial blood pressure?

A

CO x TPR

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3
Q

What works well to control acute changes in BP?

A

Baroreceptor reflex

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4
Q

What does the baroreceptor reflex do?

A

Produces rapid response to changes in BP - does not control sustained increases

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5
Q

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

A

Because the threshold for baroreceptor firing resets

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6
Q

How does the baroreceptor reflex alter cardiac output?

A

Bu adjusting sympathetic and parasympathetic inputs to the heart

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7
Q

How does the baroreceptor reflex adjust TPR?

A

Adjusts sympathetic input to peripheral resistance vessels

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8
Q

How is the baroreceptor reflex initiated?

A

Nerve endings in the carotid sinus and aortic arch are sensitive to stretch

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9
Q

How is an increase in arterial pressure detected?

A

Stretched the receptors in the carotid sinus and aortic arch

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10
Q

What effect counteracts increased mean arterial pressure?

A

Bradycardia and vasodilation

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11
Q

What are the medium and longer term control mechanisms of blood pressure?

A

Complex interaction of neurohumoral responses

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12
Q

What are the medium and longer term controls of blood pressure aiming to do?

A

Directed at controlling sodium balance and thus extracellular fluid.

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13
Q

How can you control plasma volume?

A

Water follows Na+ therefore controlling total body Na+ controls plasma volume

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14
Q

How many parallel neuroheumeral pathways control circulating volume and hence BP?

A

Four

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15
Q

What are the different neurohumoral pathways that control circulating volume and therefore BP?

A
  1. RAAS
  2. Sympathetic nervous system
  3. ADH
  4. Atrial natriuretic peptide
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16
Q

How do these neurohumoral pathways control BP?

A

Control BP in part by controlling sodium balance and extracellular fluid volume

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17
Q

What does RAAS stand for?

A

Renin-angiotensin-aldosterone system

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18
Q

Where is renin released from?

A

Granular cells of juxtaglomerular apparatus (JGA)

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19
Q

What factors stimulate renin release?

A
  • Reduced NaCl delivery to distal tubule
  • Reduced perfusion pressure in the kidney
  • Sympathetic stimulation to JGA
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20
Q

How does decreased circulating volume stimulate renin release?

A
  • Decreased NaCl delivery to the macula densa
  • Sympathetic stimulation to juxtoglomerular apparatus
  • Decreased renal perfusion pressure (sensed by renal baroreceptors).
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21
Q

What is the function of renin?

A

Converts angiotensinogen into angiotensin I

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22
Q

How does angiotensin I get converted to angiotensin II ?

A

By the angiotensin converting enzyme (ACE)

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23
Q

What effects does angiotensin II have?

A

Vasoconstriction
Stimulates Na+ resorption at kidney
Stimulates aldosterone

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24
Q

How many receptors are there for angiotensin II?

A

two types of receptors - AT1 and AT2

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25
Q

What receptor is responsible for the main action of angiotensin II ?

A

Main actions via AT1 receptor

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26
Q

What is the action of angiotensin II in the arterioles?

A

Vasoconstriction

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27
Q

What is the action of angiotensin in the kidney?

A

Stimulate Na+ resorption at the kidney

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28
Q

What is the action of angiotensin II in the sympathetic nervous system?

A

Increased released of NA

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29
Q

What is the action of angiotensin II in the adrenal cortex?

A

Stimulates release of aldosterone

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30
Q

What is the action of angiotensin II in the hypothalamus?

A

Increases thirst sensation (stimulates ADH release)

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31
Q

What is the action of aldosterone on the kidney?

A
  • Sitmulates Na+ and therefore water reabsorption
  • Activates apical Na+ channel and apical K+ channel
  • Increases basolateral Na+ extrusion vie Na/K/ATPase
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32
Q

What is angiotensin converting enzyme also known as?

A

Kininase II

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33
Q

Why are the vasoconstriction effects of Ang II further augmented?

A

Because ACE is also one of the kininase enzymes which breaks down the vasodilator bradykinin

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34
Q

Give some examples of ACE inhibitors

A

Captopril, lisinopril, perindopril and enalapril

35
Q

Why do most people on ACE inhibitors develop a dry cough?

A

Because you get an accumulation of bradykinin which causes a dry cough

36
Q

What effects can high levels of sympathetic stimulation have on renal blood flow?

A

Reduces renal blood flow because of vasoconstriction of arterioles

37
Q

How does the sympathetic nervous system affect sodium balance?

A
  • Decreases GFR - decrease Na+ excretion
  • Activates apical Na/H exchanger and basolateral Na/K ATPase in PCT.
  • Stimulates renin release from JGcells
38
Q

What is the main role of Antidiuretic hormone?

A

Formation of concentrated urine by retaining water to control plasma osmolarity

39
Q

What stimulates ADH release?

A

Increases in plasma osmolarity

Or sever hypovolaemia

40
Q

What is another name for antidiuretic hormone?

A

Arginine vasopressin

41
Q

What are the actions of ADH?

A
  • Stimulates Na+ reabsorption

- Causes vasoconstriction

42
Q

What is the function of atrial natriuretic peptide (ANP)?

A

Promotes Na+ excretion

43
Q

Where are atrial natriuretic peptides synthesised and stored?

A

Atrial myocytes

44
Q

When are atrial natriuretic peptides released?

A

Released from atrial cells in response to stretch. There are low pressure volume sensors in the atria

45
Q

What inhibits the release of ANP?

A

Reduced effective circulating volume inhibits the release of ANP to support BP

46
Q

Why does reduced effective circulating volume inhibit release of ANP?

A

Reduced filling of the heart therefore less stretch and less ANP released

47
Q

What are the actions of ANP?

A

Causes vasodilation of the afferent arterioles
Inc blood flow and GFR
Inhibits Na+ reabsorption
Causes natriuresis

48
Q

What is the function of protaglandins?

A

Act as vasodilators and act as a buffer to excessive vasoconstriction produced by SNS and RAAS.

49
Q

When are prostaglandins important?

A

When levels of Ang II are high

50
Q

Where is dopamine formed?

A

Locally in the kidney from circulating L-DOPA

51
Q

Where are dopamine receptors present?

A

On renal blood vessels and cells of PCT and TAL

52
Q

What effects does dopamine have?

A

Causes vasodilation and increases renal blood flow

Reduces reabsorption of NaCl

53
Q

What is hypertension?

A

Sustained increase in blood pressure

54
Q

What is stage 1 hypertension?

A

Mild

>140/90 mmHg in clinic

55
Q

What is stage 2 hypertension?

A

Moderate

>160/100 mmHg in clinic

56
Q

What is severe hypertension?

A

> 180 systolic or >110 diastolic in clinic

57
Q

Is blood pressure high or lower in clinic compared to home?

A

At home blood pressure lower

58
Q

What causes hypertension?

A

In most cases, the cause is not known - this is referred to primary hypertension

59
Q

What is secondary hypertension?

A

This is when the discrete cause can be found

60
Q

Give examples of causes is secondary hypertension

A

Renovascular disease
Chronic renal disease
Hyperalsdosteronism
Cushing’s syndrome

61
Q

What is ‘essential’ or primary hypertension?

A

No definable cause - may be genetic factors, environmental factors etc

62
Q

What is important to take into consideration when dealing with secondary hypertension?

A

Treat the primary cause

63
Q

How does renovascular disease cause hypertension?

A

Renal artery stenosis causes fall in perfusion pressure in that kidney. Inc renin production. Activation of RAAS. Vasoconstriction and Na+retention

64
Q

How does renal parenchyma disease lead to secondary hypertension?

A

Earlier stage - loss of vasodilator substances

Later stage - Na+ and water retention due to inadequate glomerular filtration

65
Q

What adrenal causes can lead to secondary hypertension?

A

Conn’s syndrome
Cushing’s syndrome
Tumour of adrenal medulla - phaeochromocytoma

66
Q

How does Conn’s syndrome lead to secondary hypertension?

A

Aldosterone secreting adenoma

67
Q

How does Cushing’s syndrome lead to secondary hypertension?

A

Excess secretion of glucocorticoid cortisol

68
Q

How does a tumour of the adrenal medulla lead to secondary hypertension?

A

Secretes catecholamines (adrenaline and noradrenaline)

69
Q

Why is it important to treat hypertension?

A

Silent killer. Has damaging effects on heart and vasculature.

70
Q

What can hypertension potentially lead to?

A

Heart failure, MI, stroke, renal failure and retinopathy

71
Q

What disease attributable to hypertension?

A

CHD, heart failure, stoke, cerebral haemmohharge, kidney failure, MI - basically lots of vascular disease

72
Q

Where do you examine when looking for damage caused by hypertension?

A

Eyes, brain, heart, kidneys and arteries.

73
Q

What is the blood pressure equation?

A

BP = CO x TPR

74
Q

What are the non-pharmacological approaches to treating hypertension?

A

Exercise, diet, reduced Na+ intake, reduced alcohol intake, lifestyle changes

75
Q

Give example of methods to treat hypertension by targeting the RAAS?

A

ACE inhibitors

Ang II receptor antagonist

76
Q

What effects does blocking the production or action of Ang II have?

A

Has diuretic and vasodilator effects

77
Q

Give examples of vasodilators that can be used to treat hypertension?

A

L-type Ca channel blockers

Alpha 1 receptor blockers

78
Q

How do L -type Ca channel blockers treat hypertension?

A

Reduce Ca2+ entry to vascular smooth muscle cells

Relaxation of vascular smooth muscle

79
Q

How can alpha 1 receptor blockers be used to treat hypertension?

A

Reduce sympathetic time (relaxation of vascular smooth muscle) and can cause postural hypotension

80
Q

Give examples of diuretics that can be used to treat hypertension

A

Thiazide diuretics - reduce circulating volume

81
Q

Give examples of other diuretics that will also lower BP?

A

Aldosterone antagonists (spironolactone)

82
Q

How do thiazide diuretics reduce circulating volume?

A

Inhibit Na/Cl co-transporter on apical membrane of cells in signal tubule

83
Q

How can beta blockers be used to treat hypertension?

A

Block beta 1 receptors in the heart therefore reduce effects of sympathetic output therefore reduce heart rate and contractility

84
Q

When are beta blockers used to treat hypertension?

A

No used in hypertension alone, would only be used if there are other indications such as previous MI

CVS A (18 decks)

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