lecture 13 - renal system 3 Flashcards

1
Q

what is diuresis?

A

the removal of excess water in urine

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2
Q

what are diuretics?

A

drugs that promote urine excretion

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3
Q

what does ADH do?

A

vasopressin

controls permeability of cells in the collecting duct to water
• makes collecting duct more permeable
• results in conc urine and water conservation

can also have cardiovascular effects - causes vasoconstriction

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4
Q

what are water pores also called?

A

aquaporins

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5
Q

action of ADH

A

1) ADH binds to receptor on basolateral cell surface
2) stimulates adenyl cyclase to generate cAMP and activates protein kinases
3) increases insertion of aquaporin 2 into apical membrane
4) increases water permeability
5) increases water absorption
6) produces concentrated urine
7) water conservation

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6
Q

what are the 2 main mechanisms of ADH release?

A

osmoreceptors are the main controllers of ADH

cardiovascular effects - decreased blood volume or pressure can stimulate ADH release

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7
Q

where is ADH produced?

A

by cells in the supraoptic and paraventricular nuclei of the hypothalamus

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8
Q

where is ADH stored?

A

in vesicles in the posterior pituitary gland

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9
Q

what do osmoreceptors detect?

A

changes in plasma osmolarity

increased plasma osmolarity = increased ADH

decreased plasma osmolarity = decreased ADH

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10
Q

how is ADH removed?

A

by the liver and kidney

quickly metabolised

half life of 15 minutes

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11
Q

osmolar control of ADH secretion

A

when osmolarity is low there is little plasma ADH

set point = 280mOsm

steep relationship

when you get to 300mOsm there is no further increase

full range over 20mOsm increase is osmolarity

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12
Q

non-osmolar control of ADH secretion

A

need atleast a 10% reduction in blood volume before any ADH is released

causes a larger amount of ADH to be released

ADH is a potent vasoconstrictor

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13
Q

physiological stimuli for ADH release

A
  • heightened emotions
  • stress
  • high temperature
  • exercise
  • pain

alcohol inhibits ADH release

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14
Q

inappropriate secretion of ADH

A
  • post operative pain
  • intracranial disease/injury
  • ectopic ADH production - tumours
  • opiates
  • chloropropamide, MDMA - ecstasy
  • pneumonia
  • TB
  • pulmonary disease
  • nicotine
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15
Q

why do you get nocturnal enuresis (bed-wetting)?

A

delay in the development of normal circadian rhythm of ADH

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16
Q

how does MDMA dramatically alter fluid balance?

A

can result in increased circulating volume and hyponatremia (low Na concentration in the blood)

it triggers thirst reflex so increases fluid in but also increases ADH secretion so decreases fluid out

can result in people drowning internally

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17
Q

ADH deficiency

A

diabetes insipidus

polyuria due to deficiency of ADH or its action

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18
Q

what is polyuria?

A

excessive urine production

19
Q

what are the 2 types of diabetes insipidus?

A

central

nephrongenic

20
Q

central diabetes insipidus?

A

deficiency of ADH secretion

21
Q

nephrogenic diabetes insipidus?

A

nephrons do not respond to ADH

22
Q

how do you increase Na+ reabsorption in the nephron?

A

activate the renin-angiotensin-aldosterone axis activated to increase Na+ reabsorption

23
Q

what stimulates renin release?

A

decreased NaCl at macula dense

stretch receptors in afferent arteriole sense decrease in BP

increases sympathetic nerve simulation due to central decrease in BP

24
Q

what is ACE?

A

angiotensin converting enzyme

25
Q

what does renin do?

A

converts angiotensinogen to angiotensin I

26
Q

what does ACE do?

A

converts angiotensin I to angiotensin II - the more active agent

27
Q

what does angiotensin II do?

A

causes release of aldosterone from the adrenal cortex

28
Q

what does aldosterone do?

A

causes an increase in Na+ reabsorption in the DCT and CD

this increases extracellular fluid
this restores volume

renin no longer produced

29
Q

how does the renin-angiotensin-aldosterone axis work?

A

1) renin converts angiotensinogen to angiotensin I
2) ACE converts angiotensin I to angiotensin II – the more active agent
3) this travels to the adrenal cortex & causes the release of aldosterone
4) aldosterone causes increased Na+ reabsorption in the DCT & CD
5) this increases extracellular fluid
6) restoration of volume
7) renin no longer produced

30
Q

cellular action of aldosterone

A

1) aldosterone binds to receptor in cytoplasm of principal cell
2) initiates transcription
3) increases number of ENaC channels in apical surface
4) increases Na+/K+ pump
5) Na+ reabsorption, Cl- follows
6) K+ secretion by ROMK

31
Q

what are principal cells?

A

aldosterone can diffuse into these and find a steroid hormone receptor in the cell (nucleus)

32
Q

what are ENaC?

A

epithelial sodium channels

33
Q

what are ROMK?

A

renal outer medulla potassium channels

34
Q

what is aldosterone?

A

a steroid hormone synthesised in the adrenal cortex following stimulation by angiotensin II

promotes reabsorption of Na+ by principal cells in DCT and CD

overall effect:
• decreased NaCl and H2O secretion
• increased blood volume

35
Q

angiotensin II

A
  • stimulates release of aldosterone from the adrenal cortex
  • acts on the brain to create the sensation of thirst
  • powerful vasoconstrictor
  • inhibits the baroreceptor reflex and increases the release of norepinephrine from the sympathetic postganglionic fibres

overal effect:
• decreased NaCl and H2O secretion
• increased blood volume and BP

36
Q

what is ANP?

A

atrial natriuretic peptide

37
Q

where is ANP produced?

A

by the atria in response to stretch - increases blood volume / BP

38
Q

what does ANP do?

A

regulation of plasma volume and [Na+]

increases renal water and Na+ excretion

opposite actions to ADH and aldosterone

inhibits thirst, ADH, aldosterone, and renin release

overall effect:
• increased NaCl and H2O excretion
• decreased blood volume and BP

39
Q

what is micturition?

A

the action of urinating

40
Q

what is urine?

A

fluid that leaves the collecting duct

flows through the ureter to the bladder

41
Q

what is the bladder?

A

hollow organ that can expand to hold 500ml

smooth muscle wall

neck of bladder continuous with urethra

has 2 rings of sphincter muscles

42
Q

what are the 2 rings of sphincter muscles in the bladder?

A

internal
• smooth muscle
• has normal tone that keeps in contracted

external
• skeletal muscle controlled by somatic motor neurones
• tonic stimulation from CNS maintains contraction

43
Q

mechanism of micturition

A

1) stretch receptors fire
2) parasympathetic neurones fire
3) motor neurones stop firing
4) smooth muscle contracts
5) internal sphincter passively pulled open
6) external sphincter releases