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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

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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
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

Semester 3 - Urinary (33 decks)

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