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Semester 3 - Urinary > Session 4 - Changes in Plasma Volume (Hormonal control) > Flashcards

Session 4 - Changes in Plasma Volume (Hormonal control) Flashcards

1
Q

Where does medium and long term control of blood pressure stem from?

A

• Neurohumoral responses

Directed at controlling sodium balance and thus extracellular fluid volume

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2
Q

How does modification of ECF modify BP?

A
  • Blood plasma part of ECF

* Modifying ECF volume modifies volume of blood

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3
Q

What are the four parallel pathways which control BP?

A
  • Renin-angiotensin-aldosterone system
    • Sympathetic nervous system
    • Antidiuretic hormone (ADH)
    • Atrial natriuretic peptide (ANP)
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4
Q

Where is renin released form?

A

• Granular cells of juxtaglomerular apparatus

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5
Q

What three factors control renin release?

A
  • Reduced NaCl delivery to distal tubule (reduced perfusion, low GFR)
    • Reduced perfusion pressure in the kidney causes the release of renin (baroceptors in afferent arteriole cause release from granluar cells of JGA)
    • Sympathetic stimulation to JGA increases release of renin
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6
Q

What does the sympathetic system stimulate to cause renin release?

A

• B adrenergic receptors of granular cells of JGA

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7
Q

How is renin released by JGA as a result of decreased GFR?

A
  • Less NaCl detected by macula densa cells in JGA
    • Stimulates granular cells to release prostaglandin PGI2
    • PGI2 acts on granular cells to cause renin release
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8
Q

How is renin released by granular cells as a result of reduced perfusion pressure ?

A

• Decreased pressure decreases wall tension at granular cells, which stimulates renin release

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9
Q

What does renin do?

A
  • Enzyme released by juxtaglomerular granular cells
    • converts angiotensinogen to angiotensin 1
    • ACE converts angiotensin 1 to angiptensin 2
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10
Q

Where is ACE found?

A

• On the endothelium of cells, especially in lung

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11
Q

How does angiotensin 2 cause increase in BP?

A
  • Vasoconstriction - arterioles
    • Stimulates Na+ reabsorption - kidney
    • Sympathetic nervous system - Increased release of NA
    • Aldosterone release - adrenal cortex (revise effects) (Na+ reabsorption)
    • Releases ADH - Hypothalamus, stimulated by thirst receptors
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12
Q

What two receptors does Ang 2 act on?

A

• AT1 and AT2

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13
Q

What is the main receptor Ang 2 acts on?

A

• AT1

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14
Q

What type of receptors AT1 and AT2

A

• G protein couples

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15
Q

What five places does angiotensin effect?

A
  • Arterioles
    • Kidney
    • Sympathetic NSAdrenal cortex
    • Hypothalamus
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16
Q

Outline what angiotensin 2 does to the following-Arterioles

A
  • Vasoconstriction

* Vasoconstricts afferent and efferent arterioles

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17
Q

Outline what angiotensin 2 does to the following

Kidney

A

• Stimulates Na+ reabsorption at the kidney

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18
Q

What does angiotension 2 do to the hypothalamus?

A

• Stimulates ADH release

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19
Q

Outline what angiotensin 2 do in the nephron

A
  • Vasoconstriction of afferent and efferent arterioles

* Enhanced Na+ reabsorption at the PCT in apical membrane

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20
Q

What does aldosterone do?

A
  • Stimulates Na+ and water reabsorption
    • Acts on principal cells of collecting duct
    • Activates/increases expression apical Na+ channel (ENaC) and apical K+ channel
    • Also increases basolateral Na+ extrusion via activation/increased expression Na/K/ATPase
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21
Q

What inhibits aldosterone?

A

• Spironolactone

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22
Q

What does ACE do other than its direct effects?

A

• Breaks down bradykinin -> Peptide fragments

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23
Q

Why do ACE inhibitors cause a cough?

A
  • Reduce breakdown of bradykinin
    • More bradykinin, more vasodilation
    • Also causes cough in lungs
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24
Q

Give three ways sympathetic nervous system effects BP

A

• High levels of sympathetic innervation reduces renal blood flow (Decreased GFR/Decreased Na+ excretion)
• Activates apical Na/H-exchanger and basolateral Na/K ATPase in PCT
• Stimulates renin release from Jgcells
○ Leads to increased Ang 2 levels

Increased aldosterone

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25
Q

How does sympathetic stimulation effect the nephron?

A
  • Acts on arterioles to reduce renal blood flow
    • Stimulates granular cells of afferent arteriole to release renin
    • Stimulates Na+ reabsorption from PCT via renin-ang-aldosterone axis
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26
Q

What is the main role of ADH?

A

• Formation of concentrated urine by retaining water and controlling plasma osmolarity

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27
Q

What is ADH release triggered by?

A

• Stimulated by increases in plasma osmolarity or severe hypovolaemia

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28
Q

How does ADH generate concentrated urine?

A
  • Addition of aquaporin to collecting duct

* Stimulates apical Na/K/Cl co-transporters in thick ascending limb, increasing water reabsorption down conc gradient

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29
Q

How does addition of aquaporin by ADH to collecting duct effect blood volume?

A
  • Re-absorption of water

* Forms concentrated urine

30
Q

How does stimulation of Na/K/Cl co-transporter in the thick ascending limb increase reabsorption of water?

A

• Less Na+ moves out into the medulla, reduced osmotic

31
Q

What occurs after a 5-10% drop in blood pressure?

A
  • Low pressure baroreceptors in the atria and pulmonary vasculature send signals to the brainstem via the vagus nerve
    • This activity modulates both sympathetic nerve outflow, secretion of ADH and a reduction in ANP release
32
Q

What occurs after a 5-150% drop in blood pressure?

A
  • High pressure baroceptors (carotid sinus/aortic arch)
    • Impulses sent via vagus and glossopharyngeal nerves
    • Increase sympathetic nerve activity and secretion of ADH
33
Q

What is the role of atrial natriuretic peptide?

A
  • Promotes Na+ excretion

* Released from atrial cells in response to stretch (high BP)

34
Q

How is release of ANP inhibited?

A
  • Synthesised and stored in atrial myocytes

* Low pressure sensors in atria can inhibit release if detect low pressure

35
Q

What does ANP do?

A
  • Vasodilation of afferent arteriole of kidney
    • Increased blood flow increase GFR
    • Inhibits Na+ reabsorption along the nephron
    • Acts in opposite direction to the other neurohumoral regulators
36
Q

What is the main role of prostaglandins?

A
  • Act as vasodilators
    • Locally acting prostaglandins enhance glomerular filtration and reduce Na+ reabsorption
    • Act as a buffer to excessive vasoconstriction produced by SNS and RAA system
    • Important when levels of Ang 2 are high
37
Q

What is an NSAIDs?

A

• Non-steroidal anti-inflammatory drug

38
Q

How do NSAIDs effect prostaglandins?

A

• Inhibit cyclo-oxygenase (COX-1) pathway involved in formation of prostaglandins

39
Q

Why would it be a terrible idea to administer NSAIDs when patient’s renal perfusion compromised?

A

• Further decrease GFR -> acute renal failure

40
Q

Why should NSAID’s not be given to heart failure or hypertensive patients

A

• Can exacerbate the condition by increasing NaCl and water retention

41
Q

How do you calculate mean arterial BP?

A

• CO x TPR

42
Q

How do you calculate CO?

A

• SVxHR

43
Q

What is hypertension?

A
  • Sustained increase in BP

* Hypertension - 140/90 +

44
Q

What is mild hypertension

A

• 140-159/90-99

45
Q

What is moderate hypertension?

A

• 160-179/100-109

46
Q

What is severe hypertension

A

• >180/>110

47
Q

What is the most common type of high blood pressure?

A

Essential hypertension (cause unknown

48
Q

What do you call hypertension where cause can be defined?

A

• Secondary hypertension

49
Q

Give four possible causes of secondary hypertension

A
  • renovascular disease
    • chronic renal disease
    • aldosteronism

Cushing’s syndrome

50
Q

Give two possible causes of essential hypertension

A
  • Genetic

* Environmental

51
Q

What is renovascular disease and how does it cause secondary hypertension?

A
  • Occlusion of the renal artery causes fall in perfusion pressure
    • Decreased perfusion pressure leads to increased renin production
    • Activation of RAAS
    • Vasoconstriction and Na+ retention at other kidney
52
Q

What is renal parenchymal disease?

A
  • Loss of vasodilator substances

* Causes Na+ and water retention due to inadequate filtration

53
Q

Give three adrenal causes of secondary hypertension

A
  • Conn’s syndrome
    • Cushing’s syndrome
    • Tumour of the adrenal medulla
54
Q

What is conn’s syndrome?

A

• Aldosterone secreting adenoma

○ Causes hypertension and hyperkalaemia

55
Q

What is Cushing’s syndrome and how does it cause high BP (get this wrong and you’re a disgrace)

A
  • Excess secretion of cortisol

* At high conc acts on aldosterone

56
Q

How can a phaeochromocytoma cause secondary hypertension?

A

• Secretes catacholamines which increase BP

57
Q

Why is it important to treat hypertension?

A
  • Damages heart and vasculature

* Can lead to heart failure, Mi, stroke, renal failure and retinopathy

58
Q

Give the two main effects of hypertension?

A
  • Increased afterload

* Increased arterial damage

59
Q

What does increased afterload cause?

A
  • Left ventricular hypertrophy -> Heart failure

* Increased myocardial oxygen demand -> Myocardial ischaemia and MI

60
Q

Give two forms of arterial damage

A

• Atherosclerosis

Weakened vessel

61
Q

What are the results of arterial damage?

A
  • Myocardial ischaemia and MI
    • Cerbro-vascular disease and stroke
    • Aneurysm
    • Nephro-sclerosis and renal failure
    • Retinopathy
62
Q

Give five ways of treating hypertension

A
  • ABCDE
    • ACE-inhibitors
    • Beta blockers
    • Calcium ion channel blockers (vasodilators)
    • Diuretic (Thiazide and loop)
    • Exercise and other lifestyle factors
63
Q

What do ace inhibitors do?

A
  • Block production or action of Ang 2

* Vasodilation, reduced aldosterone

64
Q

What do diuretics do?

A

Reduce circulating volume of fluid

65
Q

Name a diuretic

A

• Thiazide diuretic

Inhibits Na/Cl co-transporter on apical membrane of cells in distal tubule

66
Q

Name an aldosterone inhibitor

A

Spironolactone

67
Q

Name two types of vasodilators

A

• L-type Ca channel blockers
○ Reduces Ca2+ entry to vascular smooth muscle cells
○ Relaxation of vascular smooth muscle
• A1 receptor blockers

Reduces sympathetic tone (relaxation of vascular smooth muscle

68
Q

What do Beta Blockers do?

A
  • Reduce heart rate and contractility

* Not used in first line treatment

69
Q

Give four non-pharmacological approaches to reducing BP

A
  • Exercise
    • Diet
    • Reduced Na+ intake
    • Reduced alcohol intake
70
Q

What is responsible for short term regulation of BP?

A

• Baroceptor reflex

71
Q

Outline the baroceptor reflex

A
  • High mean arterial pressure detected by Baroceptors
    • Afferent pathway to medulla
    • Medulla processes response
    • Efferent pathway to heart and blood vessels
    • Bradycardia and vasodilation modify BP
72
Q

Why are the baroceptors not suited to longer term control?

A

• Baroceptors firing recents and adapts to blood pressure

Semester 3 - Urinary (33 decks)

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