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Medicine Unit 8 > Renal physiology 2 > Flashcards

Renal physiology 2 Flashcards

1
Q

body composition female

A

45% solids
55% fluids

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2
Q

body composition male

A

40% solids
60% fluids

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3
Q

composition of total body fluid

A

2/3 intracellular fluid
1/3 extracellular fluid

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4
Q

composition of extracellular fluid

A

80% interstitial
20% plasma

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5
Q

why are there differences in body composition male and females

A

higher proportion of body fat in females

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6
Q

water Balance

A

what goes in must come out
amounts will vary significantly
regulated intake and output from thirst and ADH

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7
Q

gaining water

A

from drinking
from food via oxidative metabolism

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8
Q

how is water lost

A

expired gas saturated with water vapour e.g. breathing

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9
Q

sweat

A

hypotonic
body fluid can become hypertonic if you sweat a lot

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10
Q

why osmoregulate

A

changes in volume of ECF will change the osmolality
can affect size of cells due to changes in tonicity

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11
Q

tonicity

A

solutes effect on cells volume

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12
Q

what happens if the body fluid becomes hypotonic

A

cells will swell
kidneys excrete filter urine to restore homeostasis

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13
Q

what happens if the body fluid becomes hypertonic

A

cells shrink
kidneys excrete concentrated urine to restore homeostasis

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14
Q

osmolarity

A

number of particles in solution
usually referred to in comparison to another compartment
quantitive measure

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15
Q

central pontine myelinolysis

A

destruction of the myelin sheath in the pons
causes rapid osmotic changes

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16
Q

plasma osmolality

A

280-300 mOsm/kg-1 H2O

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17
Q

urine volume

A

0.5 – 18L/day-1

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18
Q

urine osmolality

A

1200-50 mOsm/kg-1 H2O
(normally 300-500 mOsm/kg-1 H2O )

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19
Q

what are plasma and urine osmolality and urine volume regulated by

A

ADH
from posterior pituitary

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20
Q

osmolality of ECF control

A

primarily controlled by regulating amount of water in the body
not NaCl

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21
Q

volume of ECf control

A

regulating NaCl in body
not water

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22
Q

osmoregulation dominates what

A

volume regulation

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23
Q

loop of henle

A

starts at the end of PCT and finishes at the macula densa
remaining 40-45% of filtrated isn’t handled by PCT
25-35% of Na+ and Cl-
salt and water reabsorption are separated
water passive in descending limb
salt is active in ascending limb

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24
Q

what is the main channel in the loop of henle used to absorb

A

Na+
K+
Cl-

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25
Q

NKCC loop of henle

A

Na+, K+ and 2Cl- enter
K+ removed
paracellular transport

26
Q

purpose of the loop of henle counter current

A

maximise reabsorption of water and sodium
reabsorbed separately
as the ascending loop is impermeable to water
reabsorption in ascending loop affects the descending loop

27
Q

counter current in LOH

A
  1. ascending limb NKCC
  2. interstitial osmolality increases
  3. descending limb surrounded by the same interstitium
  4. water moves out of the descending limb
  5. urine moves down the limb and ascends counter current to teach other
    concentrated reaches thick ascending limb
    NKCC does job
28
Q

urine osmolality entering and leaving the loop

A

the same

29
Q

why is loop anatomy crucial

A

limbs tightly packed together
change in interstitial osmolality in ascending limb directly affects the descending limb

30
Q

urea reabsorption

A

in the collecting ducts
contributes to interstitial osmolality

31
Q

what does reabsorption of solutes in the ascending limb do

A

increase interstitial osmolality
more water reabsorption in descending limb due to close proximity
urine osmolality increases down the limb as more water is reabsorbed
when urine travels up ascending limb there’s a lot of salt to reabsorb via NKCC
limbs/ urine move counter current

32
Q

loop diuretics

A

furosemide
bumetanide

33
Q

action of loop directs

A

act on NKCC to inhibit reabsorption of Na+, K+ and Cl-
increases osmolality in urine
reduced concentration gradient
less water reabsorbed by diffusion
diuresis and natriuresis

34
Q

production of concentrated urine in presence of max ADH

A

isosmotic fluid enters proximal tubule
isosmotic reabsorption occurs
descending limb is highly permeable to water so water leaves by osmosis
until equilibrium of interstitial fluid
ascending thin limb permeable to solute so solute passively diffuses out
solute actively pumped out of thick ascending limb to maintain horizontal gradient as part of countercurrent mechanism
maintains corticomedullary osmotic gradient
early distal tubule impermeable to water so active dilution continues as NaCl is actively reabsorbed
later distal tubule and CD are permeable in ADH presence
water moves from tubule to intersittium by osmosis
drive by the osmotic pressure difference of fluid in tubule and interstitium
max ADH, small volume of high osmolarity urine is produced
reabsorbed water enters capillaries
returns to circulation
decreases plasma osmolarity

35
Q

urea trapping/recycling

A

tubule impermeable to urea except in medulla
urea concentration increases as fluid flows along nephron and water reabsorbed
medullary collecting duct urea concentration and permeability is high
urea diffuses out of tubule down conc grad
into the medullary intersittium
increases osmolarity
Medullaryurea concentration increases (1)
Some urea diffuses into loop ofHenlein the medulla (2)
Urea trapped in tubule as fluid leaves loop ofHenle(3) and entersCD (4)
Urea recycles fromnephrontointerstitium, back tonephron
Urea accumulates inmedullaryinterstitiumto help maintaincortico-medullaryosmotic gradient (50% is excreted, 50% recycled)
Urea excretion is minimal when water needs to be conserved

36
Q

distal convoluted tubule

A

macula densa to connecting segment
fine tuning of remaining Na+ and Cl-
sodium chloride co transporter
Na+/H+ and Cl-/HCO3- exchangers
no water reabsorption

37
Q

NCCT

A

Also powered by Na⁺K⁺ATPase Blocked by thiazide diuretics e.g. bendroflumethiazide, indapamide

38
Q

Na+/H+ exchanger

A

Na+ in
H+ out

39
Q

Cl-/HCO3- exchanger

A

Cl- in
HCO3- out

40
Q

H+ and HCO3-

A

H⁺ + HCO₃⁻ = H₂CO₃ ⇌ H₂O + CO₂

41
Q

calcium reabsorption in DCT

A

10-15%
under influence of PTH and vitamin D

42
Q

composition in DCT

A

low intracellular Na+
NCCT takes up the sodium
impermeable to water
filtrate leaving the DCT will become more dilute

43
Q

main segments of the collecting duct

A

cortical
medullary

44
Q

main functions of the collecting ducts

A

Potassium excretion and sodium reabsorption (ENaC and Na,K,ATPase) – principle cells
Acid-base handling – intercalated cells
Hormonal influence – aldosterone and ADH
Urea reabsorption via UT-A1 and UT-A3 (urea recycling)

45
Q

intercalated and principle cells

A

potassium secretion

46
Q

water reabsorption in the CD

A

Apical membrane (tubular side) is impermeable to water
BUT Permeabilitycan be increased
Insertion of aquaporins (water channels) into apical membrane
Under ADH influence
Basolateral surface is permeable
Water moves into the interstitium via osmosis
This osmotic gradient has been set up by the LoH countercurrent multiplier

47
Q

action of ADH over hydration

A

Little/no ADH released
Few/no water channels inserted
Water channels are internalised into vesicles, away from membrane
Tubule impermeable to water
Water is lost in high flow-rate, dilute urine

48
Q

action of ADH dehydration

A

ADH released from posterior pituitary
Insertion of water channels on apical membrane
Vesicles fuse with membrane
Water is reabsorbed back into the bloodstream
Small volume of concentrated urine lost

49
Q

what is ADH regulated by

A

hypothalamic osmoreceptors in response to changes in plasma osmolarity

50
Q

ADH release

A

cells swell or shrink
ADH synthesised and packaged into granules in neurons in hypothalamus
transported down the axon and stored and released from nerve terminals into the posterior pituitary
released into the blood stream

51
Q

effect of plasma osmolality on ADH secretion

A

as plasma osmolality increases the ADH increases
rapidly
if <280 mOsm/kg (dilute) no ADH release

52
Q

as plasma osmolarity increases

A

ADH secretion increases
Water channels insertedinto LDT & CD
Water reabsorbed byosmosis
Urine flow rate decreases
Urine osmolarity increases(removed water from it)
Plasma osmolaritydecreases back to normallimits
No change in total soluteexcretion

53
Q

high osmolality, negative feedback

A

High plasma osmolality (egdehydration) detected by hypothalamic osmoreceptors
Secretion of ADH from posterior pituitary
Increased aquaporins in LDT & CD
Conservation of water by the kidney (concentrated urine)
Water reabsorbed back into blood
Reduction in plasma osmolality

54
Q

low plasma osmolality negative feedback

A

Low plasma osmolality (egover-hydrated)
Less/no ADH
Less/no aquaporins in LDT and CD
Removal of water by the kidney (large volume, dilute urine)
Increase in plasma (and hence ECF) osmolality

55
Q

nephrogenic diabetes insipidus

A

Non-response of ADH to V2 receptors

56
Q

cranial diabetes insipidus

A

Reduced production of ADH

57
Q

drugs used to target collecting ducts

A

Mineralocorticoid antagonists (MRAs) e.g. spironolactone, stop salt and water retention in the distal nephron  drop in BP.
MRAs cause hyperkalaemia

58
Q

over expression of ENaC

A

Liddle’s syndrome (Autosomal dominant cause of hypertension associated with hypokalaemia)

59
Q

diabetes insipidus, cranial and ADH

A

Diabetes insipidus
Insufficient ADH secretion (cranial DI)
Idiopathic (characterised by degeneration of hypothalamic ADH secreting cells)
Caused by head trauma, infection or brain surgery
Familial (ADH gene mutation)
tment with synthetic ADH (Desmopressin)

60
Q

failing to respond to ADH in NDI

A

Failure to respond to ADH (nephrogenic DI)
Kidney damage from certain drugs, or inherited
Dietary management, diuretics (to reduce GFR) and NSAIDS
Up to 18L/day urine output

61
Q

alcohol and ADH

A

Inappropriately inhibits ADH
Beating a hangover

Medicine Unit 8 (24 decks)

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