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Renal system > kidney as a regulator, excretor and producer > Flashcards

kidney as a regulator, excretor and producer Flashcards

1
Q

what are the roles of the kidney?

A

excretor
producer
regulator

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2
Q

what does the kidney produce?

A

erythropoietin

vitamin D

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3
Q

Erythropoietin (EPO)

A

secreted by the kidney

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4
Q

what produces EPO?

A

peritubular cells of kidney

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5
Q

what causes EPO production?

A

fall in oxygen level in renal tissues

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6
Q

what does EPO do?

A

stimulates precursors in bone marrow and their differentiation to RBCs

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7
Q

untreated chronic kidney disease

A

likely to cause anaemia due to EPO deficiency

hypocalcaemia

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8
Q

formation of vitamin D

A

skin and UV light
cholecalciferol produced from dietary precursors
converted to 25-hydroxycholecalciferol in liver
converted to 1,25-dihydroxycholecalciferol in kidney

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9
Q

what does vitamin D do?

A

raises serum calcium by:
promotes GI absorption
decreasing renal excretion - increased reabsorption
stimulating bone reabsorption

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10
Q

overall renal function

A

high volume filtration - majority is reabsorbed
multiple mechanisms for selective, adjustable reabsorption or secretion
variable intercellular junctions act as selective barriers to passage of small molecules

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11
Q

tubular cells

A

tight junction between tubular cells - selective and variable barrier to small molecules

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12
Q

capillaries

A

capillary wall junctions allow easy movement of ions and water

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13
Q

Na+/K+ ATPase

A

pump
maintains the low Na+ concentration intracellularly
it is the main active process in Na+ reabsorption

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14
Q

passive conductance

A

water and K+ can leave the tubular cells passively into the interstitial fluid and capillary

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15
Q

tight junctions

A

fusion of adjacent cell membranes to crease a barrier to passage of water and dissolved particles
the extent is variable

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16
Q

variable tight junctions in kidney

A

PCT - loose/ leaky
DCT - tight
CD - very tight

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17
Q

standard capillary tight junctions

A

large gaps between cells allowing water and electrolytes to pass easily

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18
Q

afferent arteriole

A

goes into glomerulus

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19
Q

efferent arteriole

A

goes out of the glomerulus - takes the blood out

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20
Q

order of nephron structure

A 
glomerulus
PCT
Loop of Henle
DCT
collecting duct
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21
Q

what does the glomerulus do?

A

produces filtrate

120ml/min

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22
Q

how does the glomerulus work?

A

high pressure filtration of blood
podocytes covering the ball of glomerular capillaries have filtration channels which are negatively charged and so cations and uncharged particles can more easily move through

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23
Q

podocytes

A

loss

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24
Q

proteins

A

most cannot get through the glomerulus - small ones can. Albumin is the cut off, so if albumin is present there may be pathology

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25
Q

what is filtered through the glomerulus?

A 
glucose
Na+
HCO3-
water
other ions
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26
Q

loss of filtrate

A

leads to a rise in oncotic pressure in efferent arteriole which is useful to increase reabsorption as it increases the gradients

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27
Q

what influences filtration?

A

hydrostatic pressure gradient pushing water out
oncotic pressure gradient pushing in
net filtration pressure - 14mmHg out into bowman’s capsule

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28
Q

filtration fraction

A

the proportion of plasma that goes through the kidney - that becomes filtrate - 15-20%

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29
Q

glomerular filtration rate (GFR)

A

useful measure of renal function as this is generally what is affected by pathology

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30
Q

marker of GFR

A

readily filtered

not metabolised, reabsorbed or secreted

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31
Q

how to measure GFR?

A

rate of filtration = rate of excretion (mg/min)

filtrate flow x filtrate concentration

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32
Q

calculate GFR

A

filtrate flow x filtrate concentration = urine flow x urine concentration
GFR = filtrate flow
the others can be measured
filtrate conc = plasma conc

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33
Q

what are the GFR markers?

A

creatinine

cystatin C - more accurate but more difficult to measure

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34
Q

creatinine

A

product of muscle metabolism
minor tubular secretion - overestimation slightly
has to be measured at resting state

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35
Q

cystatin C

A

small protein produced by most cells

no tubular secretion

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36
Q

Inulin

A

plant extract - has to be infused so not natural

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37
Q

GFR =

A

UFR x urine conc/ plasma conc

UFR = urine flow rate

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38
Q

GFR is

A

inversely proportional to plasma concentration of creatinine in a steady state

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39
Q

creatinine variability

A

normally production is constant but age and race influence this
older = less production
black people = larger production
need to be factored in when measuring GFR using creatinine

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40
Q

detection of early kidney damage

A

GFR has to fall substantially before a noticeable rise in plasma creatinine is seen so difficult to detect early damage
severity is based on creatinine levels (5 stages)

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41
Q

stage 5 renal impariment

A

renal failure - need dialysis

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42
Q

what is autoregulation?

A

keeping the flow constant despite pressure changes

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43
Q

what needs autoregulation in the kidney?

A

renal blood flow
glomerular filtration rate
both have mechanisms

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44
Q

MAP for kidney

A

70-160mmHg

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45
Q

drop in afferent blood pressure

A

fall in renal blood flow via efferent arteriole and GFR

46
Q

Autoregulation 1

A

to maintain renal blood flow

afferent arteriole dilates which improves renal blood and lowers pressure

47
Q

Autoregulation 2

A

to maintain GFR
efferent arteriole constricts
improves GFR but at a lower renal blood flow
filtration fraction increases

48
Q

mechanisms of autoregulation

A

myogenic

tubulo-glomerular feedback

49
Q

tubulo-glomerular feedback

A

adenosine
angiotensin II
PGE2

50
Q

Adenosine

A

produced in hydrated state
constricts afferent arteriole
reduces GFR
inhibits renin release

51
Q

what switches off adenosine?

A

reduced filtrate flow

52
Q

Angiotensin II

A

produced from RAAS
constricts efferent arteriole selectively to maintain glomerular capillary pressure and raise GFR
beware of inhibition of this in BP treatment (ARBs and ACEi) in hypovolaemia as kidneys are not protected by autoregulation

53
Q

when is PGE2 released?

A

produced in DCT in response to decreased filtrate flow

54
Q

what does PGE2 do?

A

dilates afferent arteriole to maintain renal blood flow
cytoprotective to tubule
antagonises vasopressin
beware of NSAIDs in hypovolaemia/ hypotension - loss of autoregulation 2

55
Q

PCT main role

A

conservation of the majority of the useful filtrate components

56
Q

what happens in the PCT?

A

reabsorption of Na+
and same amount of water
HCO3- reabsorption and glucose reabsorption completely

57
Q

fluid composition after PCT

A

Na+ conc same as plasma due to reabsorption of water and sodium in equal amounts
no glucose
no HCO3-

58
Q

how is Na+ reabsorbed in the PCT?

A

antiporter - H+/Na+ - 1 for 1 exchange

Na+/ glucose symporter

59
Q

antiporter H+/Na+

A

1 H+ secreted and 1 Na+ reabsorbed with HCO3- from acid/ base buffering

60
Q

Na+/ glucose symporter

A

cotransport of Na+ and glucose into tubular cell

Na+ into blood by Na+/K+ pump

61
Q

leaky junctions

A

allows passage of water into blood from tubule lumen

follows Na+

62
Q

Cl- reabsorption

A

water follows sodium reabsorption
increases tubular conc of Cl- so it can then be reabsorbed down a conc gradient via para-cellular route
makes charge in tubular lumen - creating an electrochemical gradient which drives sodium reabsorption

63
Q

paracellular router

A

between tubular cells - cell junctions

64
Q

glucose reabsorption

A

transport maximum = 2mmol/min

if GFR and glucose conc in blood increases glucose will be excreted into the urine

65
Q

exceeding transport maximum (Tm)

A

glycosuria and osmotic diuresis

66
Q

role of Loop of Henle

A

producing hypotonic tubular fluid and hypertonic interstitial fluid
some reabsorption of Na+, K+, Cl-

67
Q

how does the loop of henle work?

A

selective permeabilities to ions and water in ascending and descending limbs
countercurrent multiplier

68
Q

ascending limb of LoH

A

impermeable to water

permeable to ions

69
Q

what happens in ascending limb

A

Na+, Cl-, K+ ions pumped out
water unable to leave
water cannot escape due to very tight cell junctions

70
Q

cortex

A

as ions are lost and water retained tubular fluid becomes more dilute and cortex medullary fluid/ interstitial fluid more concentrated

71
Q

how are Na+/ K+/ Cl- reabsorbed?

A

NKCC cotransporter into tubular cell
K+ passively diffuses into bloof
sodium potassium pump moves sodium into blood

72
Q

descending limb of LoH

A

water permeable

impermeable to Na+, K+ and Cl-

73
Q

what happens at the bottom of the loop of Henle?

A

interstitial fluid very concentrated due to descending limb

74
Q

countercurrent multiplier purpose

A

reabsorbed water and electrolytes need to be removed without disrupting the osmotic gradients

75
Q

countercurrent flow

A

returning blood in contact with descending LoH and arriving blood in contact with ascending LoH

76
Q

what happens in countercurrent multiplier?

A

electrolytes pass from ascending LoH to descending limb of vasa recta
water passes from descending LoH to ascending limb of vasa recta

77
Q

blood flow around LoH

A

vasa recta

78
Q

vasa recta

A

become hypermolar in medulla but returned to normal by the time they return to the blood supply

79
Q

hypertonic environment in medulla

A

allows highly efficient water reabsorption in the collecting duct

80
Q

DCT

A

final regulation of extent of Na+, K+ and H+ excreted in urine

81
Q

what cells are involved in DCT?

A

principal

intercalated

82
Q

principal cells

A

reabsorb Na+
secrete K+
controlled by aldosterone
by ENaC

83
Q

Intercalated cells

A

reabsorb K+
secrete H+
driven by ATPase
H+/K+ pump

84
Q

fluid composition after DCT

A

determined by body volume state, acidosis and K+ conc

85
Q

ENaC

A

epithelial sodium channel

86
Q

what stimulates ENaC?

A

aldosterone
alkalosis
increased K+ conc

87
Q

H+/K+ pump

A

active transport
secretes H+ and reabsorbs K+
involved in acid/ base balance

88
Q

what stimulates the H+/K+ pump?

A

acidosis

decreased K+ conc

89
Q

main role of collecting duct

A

final regulation of water excretion - urine conc

90
Q

how does collecting duct work?

A

normally impermeable to everything but becomes water permeable by insertion of aquaporins into luminal membrane

91
Q

regulation of collecting duct

A

ADH

controlled by osmoreceptors

92
Q

aquaporins

A

trans-membrane proteins with narrow hour-glass shaped and charged walls
only allow water to pass through
without them water moves slowly by osmosis

93
Q

types of aquaporins

A

more than 8
4 in kidney (1-4) - 3 constantly present and don’t vary
AQP2 inserted in response to ADH so variable

94
Q

AQP1

A

PCT
descending LoH
basal membrane
constant

95
Q

AQP3

A

collecting duct basal membrane

constant

96
Q

AQP4

A

collecting duct basal membrane

constant

97
Q

AQP2

A

collecting duct
luminal membrane
inserted in response to ADH
variable water reabsorption

98
Q

what allows AQP2 to work?

A

hypertonicity of interstitium

99
Q

ADH

A

small polypeptide

3 types of receptors

100
Q

ADH receptos

A

GPCR
V1a
V2
V3/ B1b

101
Q

V1a receptor

A

peripheral circulation

vasoconstriction

102
Q

V2 receptor

A

collecting duct endothelium
AQP2 insertion
clotting factor release

103
Q

V3/ V1b

A

CNS

ACTH release

104
Q

where is H+ secretion mainly done?

A

PCT and HCO3- reabsorption

final urine acidity determined in DCT by intercalated cells

105
Q

BP control in kidney

A

juxta-glomerular apparatus

106
Q

juxta-glomerular apparatus location

A

between afferent arteriole and DCT allows input from both in terms of pressure supplying kidney and if Na+ flow is low in tubules

107
Q

what does juxtaglomerular apparatus detect?

A

drop in kidney blood pressure

drop in sodium conc of tubules by macula densa

108
Q

macula densa

A

stores granules of renin

109
Q

drop in Na+ or blood flow detected by juxtaglomerular apparatus

A

dilation of afferent arteriole by adenosine drop or PGE2 increase
releases renin from granular cells

110
Q

renin release

A

triggered by sympathetic NS directly from B1 receptors as well

111
Q

role of kidney in response to hypovolaemia

A

Drop in Na+/ flow/ BP detected by juxtaglomerular apparatus causing renin release
turns angiotensinogen into angiotensin I in plasma
ACE forms angiotensin II in lungs

112
Q

what does angiotensin II do?

A

vasoconstriction
autoregulation in kidney
negative feedback
aldosterone release - sodium reabsorption
release of ADH - retains water and causes vasoconstriction
works with neural baroreceptors causing vasoconstriction, increased Heart rate and more renin release

Renal system (17 decks)

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