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Medicine Unit 8 > Renal physiology > Flashcards

Renal physiology Flashcards

1
Q

filtrate definition

A

liquid that has passed through a filter

urine in this case

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2
Q

lumen definition

A

inside space of a tubular structure

urinary space= tubular space

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3
Q

paracellular definition

A

between the cells

absorption between cells of the tubule

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4
Q

basolateral definition

A

surface below/to the side

surface of the tubular cell next to the bloodstream

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5
Q

osmolality definition

A

concentration of a solution

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6
Q

diffusion definition

A

movement of molecules from high to low concentration

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7
Q

reabsorption definition

A

movement of substance from tubular lumen into the blood

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8
Q

secretion definition

A

movement of substance from blood into tubular lumen

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9
Q

concentration of the filtrate

A

osmolality and movement of molecules along concentration gradient
also movement of molecules by active transport facilitated by transporters

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10
Q

structure of the kidneys

A

retroperitoneal
T12-L3
blood supply= renal arteries directly from aorta
25% of circulating blood
right lower than the left of to the weight of the liver

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11
Q

cross section of the kidney

A
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12
Q

functional unit/ nephron

A
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13
Q

functions of the kidney

A

filtering
reabsorption
secretion

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14
Q

what is each nephron comprised of

A

afferent arteriole
glomerulus
efferent arteriole
macula densa
PCT loop
DCT
collecting duct

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15
Q

2 types of nephron

A

cortical
juxtaglomerular

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16
Q

cortical nephron

A

glomerulus that sits high in the cortex
loop that enters medullar superficially

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17
Q

juxtaglomerular nephron

A

low lying glomerulus in cortex
loops that extend deep into the medulla

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18
Q

label the image

A

purple is glomerulus
gold is arteiroles

tight proximity of glomeruli

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19
Q

3 main functions of the kidney

A

homeostatic function
hormonal influence
protein catabolism and gluconeogenesis

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20
Q

homeostatic function

A

blood pressure
urine production, filtering reabsorption of sodium and water
osmolality, salt and water balance

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21
Q

hormonal influence

A

rennin
angiotensin 2
PG-E
endothelia
bradykinin
EPO
calcitriol

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22
Q

how much filter does the kidney receive daily and then how much urine is produced

A

180L
but reabsorb 99% filtrate so urine 1-2L per day

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23
Q

summary of actions in the connecting segment and cortical collecting duct

A

aldosterone mediated potassium secretion by principal cells
hydrogen ion secretion by alpha intercalated cells
potassium reabsorption by alpha intercalated cells
ADH-mediated water reabsorption

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24
Q

summary of actions in the medullary collecting duct

A

potassium reabsorption or secretion
final NaCl reabsorption
ADH-mediated water ad urea reabsorption
hydrogen ion and Nh3 secretion

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25
Q

summary of actions in the distal tubule

A

small amount of NaCl reabsorbed
active regulation of calcium excretion

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26
Q

summary of actions in the loop of henle

A

countercurrent multiplier
reabsorption of 15-25% of filtered NaCl
active regulation of magnesium excretion

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27
Q

summary of actions in the proximal tubule

A

isosmotic reabsorption of 65-70% filtered water and NaCl
reabsorption of 90% of filtered HCO3
major site of NH3 production
reabsorption of almost all filtered glucose and amino acids
reabsorption of potassium, phosphate, calcium, magnesium, urea and irate

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28
Q

=summary of actions in the glomerulus

A

filtratio

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29
Q

cells in each part of nephron

A

specialised tubular cells
designed to optimise function at each stage

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30
Q

afferent and efferent arterioles basic

A

control flow of blood through glomerulus
afferent= arriving
efferent= exiting

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31
Q

afferent and efferent arterioles functions

A

able to constrict and relax
repsinsbile for controlling and influencing interglomerular flow, pressure and filtration

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32
Q

what are afferent and efferent arterioles controlled by

A

starling forces

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33
Q

blood pressure too low, arterioles

A

constrict efferent arteriole to increase flow and pressure
RAAS

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34
Q

blood pressure too high, arterioles

A

constriction of afferent to reduce hydraulic pressure in the glomerulus

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35
Q

intrinsic mechanisms for renal auto regulation

A

Renal autoregulation - the kidney itself can adjust the dilation or constriction of the afferent arterioles, which counteracts changes in blood pressure. Thisintrinsicmechanism works over a large range of blood pressure, but can malfunction if you have kidney disease includes arteriole myogenic mechanism and tubular glomerular feedback (more later)

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36
Q

extrinsic mechanism nervous control

A

nervous system and hormonal control can override renal auto regulation ad decrease the glomerular filtration rate when necessary
large drop in BP: nervous system stimulate contraction of afferent arteriole sympathetic vasoconstriction due to epinephrine and constriction of afferent reducing urine production
can also activate RAAS

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37
Q

extrinsic mechanism hormonal control

A

atrial natriuretic peptide is a hormone that can increase glomerular filtration rate
hormone produced heart
secreted when plasma volume increases
increasing urine production

38
Q

decreased resistance in afferent

A

increased RBF increased GFr
use CCB or alpha 1 blockade

39
Q

increased resistance in afferent

A

decreased RBF and GFR
use NSAIDs via PG inhibition

40
Q

decreased resistance in efferent

A

increased RBF and decreased GFR
use ACEi or ARB

41
Q

increased resistance in efferent

A

decreased RBF and increased GFR
RAAS activation

42
Q

RAAS system

A
43
Q

effects of AT2

A

constrict efferent arteriole to maintain glomerular blood flow
stimulation of ADH secretion from pituitary to reabsorb more water in collecting ducts
stimulates aldosterone secretion from adrenals
acts on DCT to reabsorb more water and sodium
net effect is increase in BP

44
Q

macula densa

A

area of closely packed specialised cells lining the wall of the distal tubule
cells sense sodium chloride concentration in distal convoluted tubule

45
Q

tubuloglomerular feedback

A

decreased sodium to the macula densa

46
Q

decreased sodium to macula densa tubuloglomerular feedback

A

relaxes afferent arteriole
increases renin from juxtaglomerular cells

47
Q

increases renin from juxtaglomerular cells tubuloglomerular feedback

A
48
Q

relaxes afferent arteriole tubuloglomerular feedback

A

Increases glomerular hydrostatic pressure
Helps increase GFR

49
Q

relaxes afferent arteriole tubuloglomerular feedback

A

Increases glomerular hydrostatic pressure
Helps increase GFR

50
Q

increases renin from juxtaglomerular cells tubuloglomerular feedbakc

A

Activation of RAAS
Vasoconstriction of efferent arteriole
Increased intraglomerular hydrostatic pressure
Sodium and water reabsorption downstream

51
Q

3 layers to filter from blood to Bowmans space

A

Endothelium
Basement membrane
Podocytes (epithelium)

52
Q

endothelium in filter

A

negatively charged layer with fenestrations

53
Q

basement membrane in the filter

A

produced by endothelium and podocytes
negatively charged collagenous and non collagenous matrix with channels

54
Q

podocytes in the filter

A

“interdigitating foot processes” that prevent large molecules from entering urinary space; phagocytic function  engulf macromoleclues trapped in slits.

55
Q

mesangium in the filter

A

not a layer; but filler tissue which anchors the whole structure from the arterioles to the peritubular capillaries.

56
Q

Bowmans capsule

A

collects urine

57
Q

glomerular filtration

A

water freely filtered
small charged particles freely filtered (Na+, K+, Cl-, glucose, urea)
large particles not filtered, red blood cells
minimal filtration of smallish negatively charged particles e.g. albumin. this barrier repels negatively charged proteins

58
Q

why is the control of intraglomerular pressure crucial

A

too much
too little
causes problems

59
Q

too much hintraglomerular pressure

A

breakdown of the filter
leaking of larger molecules into Bowman’s space inc. blood and protein
Haematuria and proteinuria

60
Q

too little intraglomerular pressure

A

Not enough flow
Fall in filtration and GFR

61
Q

drugs we use in glomerulus

A

ACE inhibitors and Angiotensin 2 Receptor Blockers
ACE is the enzyme to convert AT1 to AT2
AT2 causes efferent vasoconstriction to increase pressure and filtration in the glomerulus
ACEi  no AT2  no effect on efferent arterioles, and also no knock-on BP
Reduction in intraglomerular pressure -> reduction in GFR
Long term protective effect and preservation of renal function

62
Q

measuring GFR

A

Creatinine isproduct of creatine muscle metabolism
Almost constant rate of production
Freely filtered
Minimally reabsorbed and secreted
Allows estimation of GFR when adjusted for muscle mass, age and sex
CKD EPI – eGFR

63
Q

proximal convoluted tubule, how to think pf it

A

as heavy lifter of the nephron
receives 180L per day of filtrate that is iso-omotic with plasma
no RBC’s
virtually no protein

64
Q

iso-osmotic

A

approx same number of small molecules and ions

65
Q

proximal convoluted tubule

A

Bulk of the reabsorption (60%) of the filtrate
90-100% reabsorption of glucose and aminoacids
Transporters (sodium – glucose, sodium – phosphate, sodium –amino acid)
Paracellular reabsorption
Reabsorption AND secretion, e.g. Sodium – hydrogen antiporter
Na/H antiporter aids in bicarbonate reabsorption

66
Q

glucose handling in the kidney

A

early proximal tubule
late proximal tubule

67
Q

early proximal tubule

A

High capacity-low affinity Na-Glu symporter – SGLT2
Reabsorbs most of filter glucose
Diffusion out of cell across basolateral membrane via GLUT2 transporter

68
Q

late proximal tubule

A

Low capacity-high affinity Na-Glu symporter - SGLT21
Reabsorbs remaining glucose
Diffusion out of cell across basolateral membrane via GLUT1 transporter

69
Q

glycosuria and diabetes

A

Glucose is freely filtered at glomerulus and reabsorbed in PCT
High plasma glucose levels (10-12 mmol/L) saturates SGLT transporters
Overspill of glucose into urine
Osmotically active particle
Diuresis (increased urine production)

70
Q

water reabsorption in the PCT

A

Interstitium now hyperosmotic
Osmotic movement of water across tight junctions and aquaporins
Hydrostatic pressure in interstitium increases
High oncotic pressure within peritubular capillaries (proteins)
Push and drag of water into capillaries
Fluid in PCT is now iso-osmotic with plasma again

71
Q

polyuria

A

excessive urination

72
Q

polydypsia

A

excessive thirst

73
Q

loop of henle how to think of it

A

engine of the nephron
descending into the medulla
hairpin turn back out and into the cortex

74
Q

loop of henle function

A

Starts at end of PCT and finishes at the macula densa.
Remaining 40-45% of filtrate not handled by PCT
Reabsorptionof 25-35% of Na⁺ and Cl⁻
First time we’re seeing salt and water reabsorption separated
Water is passive in the descending limb, sodium is active in the ascending limb

75
Q

loop of henle NKCC

A

The main channel in the Loop used to reabsorb Na⁺, K⁺ and Cl⁻
1. Na⁺, K⁺, 2Cl⁻ enter
2. K⁺ spat back out
3. Paracellular transport

76
Q

recycling ROMK channel

A

that spits potassium back into the tubule creating a negative change within the cell and a positive charge inside the tubule allowing the paracellular reabsorption of positively charged sodium, calcium and magnesium

77
Q

counter current mechanism in the loop of henle

A

steep concentration ngradient
maximise Na+ reabsorption
filtrate leaving the loop of henle is hypo-osmotic with plasma

78
Q

drugs used in loop of henle

A

Loop diuretics (as the name suggests)
Furosemide
Bumetanide
Act on the NKCC to inhibit reabsorption of Na⁺, K⁺ and Cl⁻
Increases the osmolality of the filtrate
Reduced concentration gradient less water reabsorbed by diffusion
diuresis and natriuresis.

79
Q

what to think of the distal convoluted tubule as

A

nephron site of intelligent and qualitative sodium and water reabsorption for what is beneficial to the body

80
Q

distal convoluted tubule function

A

Starts from the macula densa and ends at connecting segment
“Fine tuning” of remaining 5% of Na⁺ and Cl⁻
Sodium-chloride co-transporter (NCCT)
Na⁺/H⁺ exchanger and Cl⁻/HCO₃⁻ exchanger
NO water reabsorption here

81
Q

transport mechanisms in the distal convoluted tubule

A

NCCT – does exactly what it says on the tin
- Also powered by Na⁺K⁺ATPase
- Blocked by thiazide diuretics e.g. bendroflumethiazide, indapamide
Na⁺/H⁺ exchanger = Na⁺ in, H⁺ out
Cl⁻/HCO₃⁻ exchanger = Cl⁻ in, HCO₃⁻ out
H⁺ + HCO₃⁻ = H₂CO₃ ⇌ H₂O + CO₂
10-15% of calcium reabsorption occurs here under influence of PTH and vitamin D (mostly in Loop)

82
Q

distal convoluted tubule Na+

A

Low intracellular Na+
NCCT takes up sodium
Impermeable to water
Filtrate leaving the DCT becomes more dilute -50 mosm/L

83
Q

brief function of collecting ducts

A

fine tuning reabsorption and secretion

84
Q

2 main segments of collecting dust

A

cortical
medullary

85
Q

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)

86
Q

water reabsorption in CD

A

Tubular side is impermeable to water
BUT Permeabilitycan be increased
Insertion of aquaporins (water channels) into tubular 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

87
Q

ENaC function

A

reabsorb sodium and water inresponse to aldosterone-> potassium secretion

88
Q

drugs used in collecting ducts

A

Mineralocorticoid antagonists (MRAs) e.g. spironolactone reduce sodium and water reabsorption in the distal nephron  drop in BP
MRAs cause hyperkalaemia

89
Q

overexpresison of ENaC

A

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

90
Q

diabetes insipidus

A

Non-response of ADH to V2 receptors = Nephrogenic diabetes insipidus
Reduced production of ADH = Cranial diabetes insipidus

Medicine Unit 8 (24 decks)

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