Renal Regulation of Water and Acid-Base Balance Flashcards

1
Q

Equation for osmolarity

A

concentration x no of dissociated particles

units Osm/L or mOsm/l

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2
Q

List examples of unregulated water loss.

A

sweat
faeces
vomit
water evaporating from resp lining and skin

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3
Q

List an example of regulated water loss.

A

urine production

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4
Q

What percentage of water is reabsorbed in the proximal convoluted tubule?

A

67%

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5
Q

What condition is required for water to be reabsorbed into the loop of Henle and collecting duct?

A

medullary interstitium must be hyperosmotic to provide a gradient

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6
Q

By what mechanism does the loop of Henle concentrate urine?

A

countercurrent multiplication

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7
Q

urea recycling

A

SLIDE

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8
Q

Amino acid length of ADH

A

9

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9
Q

another name for ADH?

A

vasopressin

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10
Q

main function of ADH

A

promote water reabsorption from collecting duct

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11
Q

where is ADH produced?

A

hypothalamus

neurons in supraoptic and paraventricular nuclei

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12
Q

where is ADH stored?

A

posterior pituitary

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13
Q

how are changes in plasma osmolarity detected?

A

osmoreceptors in hypothalamus

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14
Q

normal plasma osmolarity in a healthy adult?

A

275-290 mOsm/kg

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15
Q

What % change is required for detection by baroreceptors?

A

5-10

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16
Q

stimulatory factors that influence ADH production and release

A
^ plasma osmolarity
decreased BP
hypovolaemia
nausea
angiotensin II
nicotine
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17
Q

inhibitory factors that influence ADH production and release

A
decreased plasma osmolarity
hypervolemia
^ BP
ethanol
atrial natruiretic peptide
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18
Q

mechanism of action of ADH

A

ADH acts on a G-protein coupled receptor > (adenylate cyclase > cAMP > pkA) > ^transcription + insertion Aquaporin–2 channels to apical membrane of the DCT + CD > ^ permeability to water > water moves out of nephron > into blood stream

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19
Q

list examples of ADH-related clinical disorders

A

central diabetes insipidus
nephrogenic diabetes insipidus
syndrome of inappropriate ADH secretion

20
Q

cause of central diabetes insipidus

A

decreased/negligent production and release of ADH

21
Q

clinical features of central diabetes insipidus

A

polyuria

polydipsia

22
Q

treatment for central diabetes insipidus

A

external ADH

23
Q

cause for SIADH

A

increased production and release of ADH

24
Q

clinical features of SIADH

A

hyperosmolar urine
hypervolemia
hyponatremia

25
Q

treatment for SIADH

A

non-peptide inhibitor of ADH receptor (conivaptan & tolvaptan)

26
Q

cause of nephrogenic diabetes insipidus

A

less/mutant AQP2

mutant V2 receptor

27
Q

symptoms of nephrogenic diabetes insipidus

A

polyuria

polydipsia

28
Q

treatment for nephrogenic diabtes insipidus

A

thiazide diuretics and NSAIDs

29
Q

role of kidneys in acid base balance

A

secretion and excretion of H+
reabsorption of HCO3-
production of new HCO3-

30
Q

what enzyme catalyses the reaction between CO2 and H20?

A

carbonic anhydrase

31
Q

majority of HCO3- is reabsorbed where?

A

PCT

32
Q

how is HCO3- reabsorbed in PCT?

A

CO2 diffuses in > catalysed by carbonic anhydrase with H20 > H+ + HCO3- > via NA+ - HCO3- symporter to blood stream

33
Q

function of alpha intercalated cell

A

HCO3- reabsorption & H+ secretion

34
Q

function of beta intercalated cell

A

HCO3- secretion & H+ reabsorption

35
Q

production of NEW bicarbonate ion in the PCT

A

glutamine broken down into 2NH4+ and A2- > A2- to 2HCO3- > absorbed into blood
NH4+ removed via Na+ antiporter or NH3 removed over membrane and H+ via Na+ antiporter

36
Q

production of NEW bicarbonate ion in the DCT + CD

A

in alpha intercalated cell

water + CO2 > H+ + HCO3- > transported via Cl- - HCO3- antiporter

37
Q

characteristics of metabolic acidosis

A

decreased HCO3-

decreased pH

38
Q

characteristics of metabolic alkalosis

A

increased HCO3-

increased pH

39
Q

characteristics of respiratory acidosis

A

increased pCO2

decreased pH

40
Q

characteristics of respiratory alkalosis

A

decreased pCO2

increased pH

41
Q

compensatory response for metabolic acidosis

A

increased ventilation to blow off CO2

^ [HCO3-] reabsorption and production

42
Q

compensatory response for metabolic alkalosis

A

decreased ventilation

^ [HCO3-] excretion

43
Q

compensatory response for acute respiratory acidosis

A

intracellular buffering

44
Q

compensatory response for chronic respiratory acidosis

A

^ [HCO3-] reabsorption and production

45
Q

compensatory response for acute respiratory alkalosis

A

intracellular buffering

46
Q

compensatory response for chronic respiratory alkalosis

A

decreased [HCO3-] reabsorption and production