lecture 13 - renal system 3 Flashcards

(43 cards)

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
what does renin do?
converts angiotensinogen to angiotensin I
26
what does ACE do?
converts angiotensin I to angiotensin II - the more active agent
27
what does angiotensin II do?
causes release of aldosterone from the adrenal cortex
28
what does aldosterone do?
causes an increase in Na+ reabsorption in the DCT and CD this increases extracellular fluid this restores volume renin no longer produced
29
how does the renin-angiotensin-aldosterone axis work?
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
cellular action of aldosterone
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
what are principal cells?
aldosterone can diffuse into these and find a steroid hormone receptor in the cell (nucleus)
32
what are ENaC?
epithelial sodium channels
33
what are ROMK?
renal outer medulla potassium channels
34
what is aldosterone?
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
angiotensin II
* 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
what is ANP?
atrial natriuretic peptide
37
where is ANP produced?
by the atria in response to stretch - increases blood volume / BP
38
what does ANP do?
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
what is micturition?
the action of urinating
40
what is urine?
fluid that leaves the collecting duct flows through the ureter to the bladder
41
what is the bladder?
hollow organ that can expand to hold 500ml smooth muscle wall neck of bladder continuous with urethra has 2 rings of sphincter muscles
42
what are the 2 rings of sphincter muscles in the bladder?
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
mechanism of micturition
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