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Z MD1 Renal block > Physiology > Flashcards

Physiology Flashcards

0
Q

what is uremia

A

the accumulation of dozens of toxic metabolites (not only urea)

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1
Q

main functions of the kidneys (7)

A
  • water and sodium homeostasis
  • acid/base balance
  • control of ECF Ion conc
  • excretion of waste products and xenobiotics
  • endocrine functions
  • formation of concentrated urine
  • formation of dilute urine
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2
Q

which hormones do the kidneys make

A

EPO
renin
Vitamin D3
PGI2

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3
Q

what is the difference between superficial cortical glomeruli and juxtamedullary glomeruli

A

SCG - LOP penetrates only a short distance into the medulla and their efferent arterioles give rise to cortical capillaries surrounding the PCT and DCTs
JMG - LOP penetrates deep into the medulla and their efferent arterioles become the vasa recta that also penetrate deep into the medulla parallel to the LOH

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4
Q

what is the proportion between SCG and JMG?

A

JMG only make up 10% of glomeruli

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5
Q

main function of JMG

A

give the greatest responsibility to concentrating the urine - increase the osmolarity of the urine

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6
Q

what are the two parts of the proximal tubule

A

pars recta and PCT

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7
Q

what is the difference in the thin and thick parts of the ascending limb of the LOH between SCG and JMG?

A

SCG - thin is very short

JMG - thin is very long

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8
Q

how many nephrons do we have

A

2 million (1 million in each kidney)

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9
Q

what is the filtration fraction at the kidney

A

20% of the renal plasma flow

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10
Q

what is the GFR?

A

125ml/min

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11
Q

what is the volume of fluid that is passed through the kidneys a day

A

180L

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12
Q

at what point do you start to get problems if your GFR starts to drop

A

when it drops down to 30-40ml/min

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13
Q

where are the macula densa cells

A

epithelial cells of the thick ascending that lie against the afferent and efferent arterioles

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14
Q

what are the 2 components of renal autoregulation

A

myogenic response

tubuloglomerular reflex

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15
Q

what what range of MAP can the nephron keep the pressure constant in the glomerulus

A

70-180mmHg

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16
Q

How do macula densa cells participate in renal autoregulation

A

sense the NaCl that is delivered to it (if pressure too high, NaCl will be higher) –> releases adenosine and thromboxane to constrict the afferenent arteriole

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17
Q

what is the pressure in the glomeruli kept at

A

50mmHg

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18
Q

where are the cells that make renin?

A

they are the granular cells lining the afferent arteriole

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19
Q

three parts of the filtration complex of the glomerulus

A

fenestrations
basal lamina
slits between foot processes of podocytes

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20
Q

what stops most proteins moving through the glomerulus

A

their negative charge is repelled by the negative charge on the basal lamina and fenestrations

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21
Q

why in diabetes, does the amount of albumin increase in the urine

A

because in the diabetes the negative charge of the basal lamina is lost and so a disproportionate amount of albumin is allowed through the glomerulus and lost in the urine

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22
Q

what are the normal values of the forces acting towards filtration at the glomerulus

A

hydrostatic pressure in the glomerular capillary = 50mmHg
hydrostatic pressure in the bowmans capsule = 10mmHg
Oncotic pressure in the glomerular capillary = 25-40mmHg
oncotic pressure in the Bowmans capsule = 0mmHg

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23
Q

what is the net filtration pressure at the glomerules

A

10-15mmHg

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24
Q

what happens to GFR when the afferent arteriole is constricted? What about the efferent arteriole?

A

afferent - GFR decreases due to decreased hydrostatic pressure
efferent - GFR increases due to increased hydrostatic pressure

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25
Q

where does angiotensin 2 act in the kidney primarily

A

primarily on the efferent arteriole - constricts them (supporting filtration)

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26
Q

Ang2 inhibitors and their effect on the kidney

A

dilation of the efferent arteriole - decreases GFR

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27
Q

what is the equation for renal blood flow

A

change in pressure from renal artery to capillary / resistance of the afferent and efferent arterioles

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28
Q

what is the myogenic response

A

afferent arteriole constricts in response to stretch by increased pressure

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29
Q

three things that can cause renin release

A
  • sympathetic activation
  • decreased BP in afferent arteriole
  • decreased NaCl delivery at the macula densa
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30
Q

what is the equation for renal clearance of a substance

A

urine volume x urine concentration / conc in blood

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31
Q

the clearance of substance x is equal to

A

the volume of plasma cleared of X per time

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32
Q

how much of the creatinine we produce is cleared

A

all of it

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33
Q

explain the renal clearance of penicillin

A

clearance is greater that filtration as extra is secreted into the urine

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34
Q

where is potassium, Ca and phosphate reabsorbed

A

primarily PT

DT to some extent

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35
Q

what controls the absorption of Ca

A

PTH and vitamin D3

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36
Q

how is phosphate absorbed

A

cotransported across with Na

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37
Q

which solvent is excreted completely

A

urea

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38
Q

which solvent is completely reabsorbed

A

glucose

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39
Q

how much water and salt is reabsorbed

A

water - 99%

Na - 99.5%

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40
Q

what is the osmolarity of the filtrate at the beginning of the nephron

A

~300mOsM

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41
Q

what is the max osmolarity that urine can get to

A

1200mOsM

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42
Q

what is absorbed in the descending LOH

A

water

43
Q

what is absorbed in the thin ascending LOH

A

favours movement of NaCL into the ECF (passive reabsorption through PARACELLULAR junctions)

44
Q

how is the filtrate in the lumen of the nephron dilute by the time it gets to the DT

A

because more Na is reabsorbed compared to water by this point

45
Q

what causes the movement of water out of the descending LOH

A

urea conc in the ECF

Na conc in the ECF from the ascending LOH

46
Q

what is the osmolarity of the urine by the end of the LOH

A

100mOsM

47
Q

what is the range of osmolarity of the urine at the end of the collecting duct

A

50-1200mOsM

48
Q

how is the amount of water reabsorbed regulated

A

by insertion of aquaporins in the CD

49
Q

what is the mainstay cellular transport mechanism in the nephron?

A

3Na/2K ATPase on basolateral membrane

50
Q

how is Na reabsorbed in the PT

A

by active transport by Na/K ATPase

51
Q

what channels are on the apical membrane of the PT

A

Na cotransporter

Na/H+ exchanger

52
Q

what types of substances does the Na cotransporter cotransport

A

glucose
amino acids
phsophate

53
Q

how is Cl- ions absorbed in the PT

A

the movement of Na absorption leaves a negative charge in the lumen and therefore anions move along gradient through paracellular spaces and transcellularly

54
Q

how does HCO3- get absorbed

A

due to Na/HCO3 transporter in the PT on the basolateral membrane. Gradient set up by Na/H+ exchanger on apical membrane
moves TRANSCELLULARLY

55
Q

how is water reabsorbed in the PT

A

moves by osmosis following gradient both paracellularly and transcellularly

56
Q

what is solvent drag

A

the gradient that pulls water across the cells of the PT also pulls other things that are dissolved in it
(K+, Ca+, )

57
Q

between Cl and HCO3 which is preferentially reabsorbed in the early PT and what does this cause

A

HCO3 - causes conc of Cl to rise and by the late PT we have high Cl –> causes Cl reabsorption in the late PT paracellularly

58
Q

what does the movement of Cl in the late PT lead to…

A

change in electrochemical gradient (now +3mV in lumen) –> Na reabsorption both paracellularly and transcellularly

59
Q

what is absorbed in the thin LOH and how

A

Na by passive diffusion through tight junctions of paracellular pathway. No water

60
Q

what is absorbed in the thick LOH and how

A

Na - by active reabsorption. No water

61
Q

what is the transporter on the thick LOH apical membrane

A

Na/K/2Cl cotransporter

62
Q

which drug inhibits the Na/K/Cl cotransporter

A

frusemide

63
Q

what is the transporter on the DCT on the apical side

A

Na/Cl

64
Q

which drug inhibits the Na/Cl transporter in the DCT

A

thiazide diuretics

65
Q

which channels are on the apical side of the CD

A

K and Na channels (not active)

aquaporins if present

66
Q

what is the definition of acute renal failure

A

urine flow less than 500ml/day

67
Q

what is the definition of chronic renal failure

A

glomerular flow <72L/day

- typically occurring over a long time

68
Q

how can you get glomerular disease and tubular disease of acute renal failure

A

can have just a loss of GFR with only minor impairment of tubular function, or can have minor loss of GFR with great impairment of tubular function

69
Q

what are the endocrine sequalae that occurs with chronic renal failure

A
  • excessive activation of RAS –> vasoconstriction
  • vitamin D activation
  • erythropoeitin decreases –> anaemia
70
Q

why is plasma urea a poor guide to GFR

A

very variable in reabsorption (diet dependent)

71
Q

what is the normal plasma clearance of creatinine

A

50-120microM/L

72
Q

formula for working out creatinine clearance and therefore GFR

A

UV/P

73
Q

how does a drop in systemic pressure to the kidneys result in acute renal failure

A

drops below 70mmHg –> kidney autoregulation fails –> decreased GFR –> anoxia and stasis –> formation of casts and death of tubular cells –> necrosis

74
Q

what conditions are associated with anuria

A 
ARF
heroin overdose
HSV2
prostatic malignancy
mechanical obstruction
drugs
75
Q

pre-renal causes of ARF

A 
shock
sepsis
haemolysis
rhabdomyolysis
nephrotoxic drugs
76
Q

how does rhabdomylosis cause ARF

A

breakdown of skeletal muscle releases myoglobin –> toxic to the nephron –> necrosis

77
Q

what are the causes of intrinsic ARF

A

glomerular disease
interstitial nephris
tubular damage

78
Q

what do you have to be careful about in a patient with ARF

A

acidosis and hyperkalaemia

79
Q

most common cause of post renal ARF

A

prostatic malignancy

80
Q

what happens to the nephrons in chronic renal failure

A

remaining nephrons hypertrophy and are able to undergo hyperfiltration to try and compensate for the loss of the damaged nephrons

81
Q

why is glomerula hypertrophy and hyperfiltration a bad thing during chronic renal failure

A
  • because the tubules are not able to keep up with the filtrate and therefore the filtrate is not modified in the way it should be
  • causes glomerular hypertension –> further damage
82
Q

presentation of a patient with chronic renal failure

A 
fatigue
loss of appetite
skin pigmentation
dehydration
itchiness
bleeding
83
Q

what will the dipstick show in someone with CRF

A

specific gravity will be close to plasma (1.010)

84
Q

common causes of CRF

A

diabetes
hypertension
chronic glomerulonephritis
cystic disease

85
Q

what are the consequences in salt and water imbalances with CRF predominately glomerular or predominantly tubular

A

glomerular - sodium retention and hypertension

tubular - sodium loss and low BP, impaired conc ability

86
Q

why does acidosis occur during renal failure

A

due to the loss of tubular function - ammonia production by the kidney fails and you are not able to excrete H ions at the normal rate

87
Q

what happens to the levels of Ca and PO4 during renal failure

A

rise in PO4 (due to reduced excretion)

reduction in Ca

88
Q

why do you get bone disease with chronic renal failure

A

due to loss of Vit D3 and high PTH

89
Q

normal value of HCO3

A

24mmol/L

90
Q

normal value for pCO2

A

40mmHg

91
Q

what can cause challenges to pH

A

pCO2, metabolism, gastrointestinal secretions, renal function

92
Q

what acids are created in the body

A
  • sulphuric and phsophoric acids from proteins and lipids
  • lactic acid anaerobic metabolism
  • keto acids from FAs
93
Q

what would cause metabolic acidosis

A

chronic renal failure
chronic diarrhoea (loss of bicarbonate)
starvation

94
Q

what can high levels of HCO3 mean

A 
metabolic alkalosis
respiratory acidosis (compensation)
95
Q

what can low levels of HCO3 mean

A 
metabolic acidosis
respiratory alkalosis (compensation)
96
Q

why does metabolic acidosis cause hyperkalemia

A

because the kidney swaps K for H when trying to excrete the excess H+ into the urine

97
Q

how do you calculate the anion gap

A

(Na+ + K+) - (HCO3 + Cl-)

98
Q

normal anion gap

A

12mmol/L

99
Q

what is the major contributor to the anion gap

A

albumin

100
Q

what conditions give acidosis with a high anion gap

A

lactic acidosis
diabetic ketoacidosis
renal failure

101
Q

what happens as a result of alkalosis in regards to ion transport

A

type 2 intercalated cell:
- excretion of HCO3 via antitransportation with Cl- in type 2 intercalated cell
- H+ reabsorbed through antiporter with K+ and through its own ATP pump
PCT
- decreased HCO3 reabsorption in PCT (cotransporter with Na)
- decreased H+ excretion (cotransporter with Na)

102
Q

match up acidosis, alkalosis, hypokalaemia and hyperkalaemia

A 
acidosis = hyperkalaemia
alkalosis = hypokalaemia
103
Q

what is the most important thing in defining renal failure

A

level of glomerular filtration rate

104
Q

what can cause anuria

A

outlet obstruction eg. prostatic malignancy

renal artery occlusion

105
Q

explain the water and Na problems that arise from chronic renal failure of predominantly glomerular basis and tubular basis

A

glomerular - Na retention and HT

tubular - Na wasting and low BP

106
Q

response to acidosis

A

Type A intercalated cell
- H+ pumped into the lumen by exchange of K+ and by own ATPase transporter
-HCO3 pumped into interstitium by exchange of Cl
PCT
- excretion of NH4+ through glutamine excretion
- excretion of phosphate

Z MD1 Renal block (8 decks)

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