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

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

Flashcards in Session 4 - Changes in Plasma Volume (Hormonal control) Deck (72):
1

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

• Neurohumoral responses

Directed at controlling sodium balance and thus extracellular fluid volume

2

How does modification of ECF modify BP?

• Blood plasma part of ECF
• Modifying ECF volume modifies volume of blood

3

What are the four parallel pathways which control BP?

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

4

Where is renin released form?

• Granular cells of juxtaglomerular apparatus

5

What three factors control renin release?

• 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

6

What does the sympathetic system stimulate to cause renin release?

• B adrenergic receptors of granular cells of JGA

7

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

• 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

8

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

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

9

What does renin do?

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

10

Where is ACE found?

• On the endothelium of cells, especially in lung

11

How does angiotensin 2 cause increase in BP?

• 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

12

What two receptors does Ang 2 act on?

• AT1 and AT2

13

What is the main receptor Ang 2 acts on?

• AT1

14

What type of receptors AT1 and AT2

• G protein couples

15

What five places does angiotensin effect?

• Arterioles
• Kidney
• Sympathetic NS Adrenal cortex
• Hypothalamus

16

Outline what angiotensin 2 does to the following-Arterioles

• Vasoconstriction
• Vasoconstricts afferent and efferent arterioles

17

Outline what angiotensin 2 does to the following

Kidney

• Stimulates Na+ reabsorption at the kidney

18

What does angiotension 2 do to the hypothalamus?

• Stimulates ADH release

19

Outline what angiotensin 2 do in the nephron

• Vasoconstriction of afferent and efferent arterioles
• Enhanced Na+ reabsorption at the PCT in apical membrane

20

What does aldosterone do?

• 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

21

What inhibits aldosterone?

• Spironolactone

22

What does ACE do other than its direct effects?

• Breaks down bradykinin -> Peptide fragments

23

Why do ACE inhibitors cause a cough?

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

24

Give three ways sympathetic nervous system effects BP

• 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

25

How does sympathetic stimulation effect the nephron?

• 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

26

What is the main role of ADH?

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

27

What is ADH release triggered by?

• Stimulated by increases in plasma osmolarity or severe hypovolaemia

28

How does ADH generate concentrated urine?

• Addition of aquaporin to collecting duct
• Stimulates apical Na/K/Cl co-transporters in thick ascending limb, increasing water reabsorption down conc gradient

29

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

• Re-absorption of water
• Forms concentrated urine

30

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

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

31

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

• 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

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

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

33

What is the role of atrial natriuretic peptide?

• Promotes Na+ excretion
• Released from atrial cells in response to stretch (high BP)

34

How is release of ANP inhibited?

• Synthesised and stored in atrial myocytes
• Low pressure sensors in atria can inhibit release if detect low pressure

35

What does ANP do?

• 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

What is the main role of prostaglandins?

• 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

What is an NSAIDs?

• Non-steroidal anti-inflammatory drug

38

How do NSAIDs effect prostaglandins?

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

39

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

• Further decrease GFR -> acute renal failure

40

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

• Can exacerbate the condition by increasing NaCl and water retention

41

How do you calculate mean arterial BP?

• CO x TPR

42

How do you calculate CO?

• SVxHR

43


What is hypertension?

• Sustained increase in BP
• Hypertension - 140/90 +

44

What is mild hypertension

• 140-159/90-99

45

What is moderate hypertension?

• 160-179/100-109

46

What is severe hypertension

• >180/>110

47

What is the most common type of high blood pressure?

Essential hypertension (cause unknown

48

What do you call hypertension where cause can be defined?

• Secondary hypertension

49

Give four possible causes of secondary hypertension

• renovascular disease
• chronic renal disease
• aldosteronism

Cushing’s syndrome

50

Give two possible causes of essential hypertension

• Genetic
• Environmental

51

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

• 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

What is renal parenchymal disease?

• Loss of vasodilator substances
• Causes Na+ and water retention due to inadequate filtration

53

Give three adrenal causes of secondary hypertension

• Conn's syndrome
• Cushing's syndrome
• Tumour of the adrenal medulla

54

What is conn's syndrome?

• Aldosterone secreting adenoma
○ Causes hypertension and hyperkalaemia

55

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

• Excess secretion of cortisol
• At high conc acts on aldosterone

56

How can a phaeochromocytoma cause secondary hypertension?

• Secretes catacholamines which increase BP

57

Why is it important to treat hypertension?

• Damages heart and vasculature
• Can lead to heart failure, Mi, stroke, renal failure and retinopathy

58

Give the two main effects of hypertension?

• Increased afterload
• Increased arterial damage

59

What does increased afterload cause?

• Left ventricular hypertrophy -> Heart failure
• Increased myocardial oxygen demand -> Myocardial ischaemia and MI

60

Give two forms of arterial damage

• Atherosclerosis

Weakened vessel

61

What are the results of arterial damage?

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

62

Give five ways of treating hypertension

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

63

What do ace inhibitors do?

• Block production or action of Ang 2
• Vasodilation, reduced aldosterone

64

What do diuretics do?

Reduce circulating volume of fluid

65

Name a diuretic

• Thiazide diuretic

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

66

Name an aldosterone inhibitor

Spironolactone

67

Name two types of vasodilators

• 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

What do Beta Blockers do?

• Reduce heart rate and contractility
• Not used in first line treatment

69

Give four non-pharmacological approaches to reducing BP

• Exercise
• Diet
• Reduced Na+ intake
• Reduced alcohol intake

70

What is responsible for short term regulation of BP?

• Baroceptor reflex

71

Outline the baroceptor reflex

• 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

Why are the baroceptors not suited to longer term control?

• Baroceptors firing recents and adapts to blood pressure