Kidney Flashcards

(52 cards)

1
Q

how many nephrons do humans have

A

500 thousand to 1 million

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2
Q

the nephron

A

afferent arteriole, (glomerulus/bowmans capsule) efferent arterole, proximal convoluted tubule, loop of henle, distal convoluted tubule

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3
Q

which are the specialised cells and where are they

A

podocytes - specialised epithelial cells - between the basement membrane the the urinary space

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4
Q

glomerular filtration barrier

A

blood - fenestrated endothelium - basement membrane - podocytes - urinary space

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5
Q

what kind of permeability - and what passes

A

selective permeability - H2O, electrolytes pass

Not proteins

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6
Q

why don’t proteins pass through the membrane?

A

they are negatively charged, and so is the basal membrane - proteins are maintained on the blood side

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7
Q

what is the primary urine

A

pressure coming to of the bowman capsule - efferent arteriole

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8
Q

loop of hence permeability

A

defending - v permeable to water
ascending (thick limb) no permeable to water but permeable to salts (sodium, potassium and 2 chloride ions) - 90% sodium is reabsorbed

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9
Q

how is water reabsorbed in DCT?

A

through aquaproins

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10
Q

what is th concentration gradient important for?

A

urea recycling

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11
Q

approximately how much Na is filtered each day?

A

25 000 mEq

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12
Q

approximately how much H2O is filtered each day?

A

180 litres

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13
Q

how much Na is excreted each day?

A

150 mEq

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14
Q

how much H2O is excreted each day?

A

1.5 litres

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15
Q

what % of the sodium and water is reabsorbed?

A

more than 99%

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16
Q

why would you filter and reabsorb that much?

A

to remove wate and toxin

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17
Q

what are the 5 groups of diuretics?

A
  • osmotic
  • carbonic anhydrase inhibitors
  • loop
  • thiazides
  • potassium sparing
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18
Q

what % of the top 200 drugs in the US are diuretics?

A

10%

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19
Q

what are diuretics?

A

drugs that increase urine output by the kidney

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20
Q

when would you use diuretics

A

oedema of any origin, congestive heart failure, hypertension

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21
Q

when would you use diuretics

A

oedema of any origin, congestive heart failure, hypertension

22
Q

how do most diuretics work?

A

inhibit reabsorbtion of sodium at different levels of the renal tubular system

more sodium excreted, more water excreted

23
Q

what is a synergistic effect

A

when a combination of therapies are used

24
Q

where do osmotic diuretics act?

A

on the first part of the glomerulus

25
glomerular capillary permeability
high permeability to water and electrolytes
26
what % of plasma is filtered into Bowman space and PCT
20%
27
which pump is the first part os the PCT/glomerulus
H+/Na exchange - Na out (reabsorbed) and H in
28
an example of an osmotic diuretic
mannitol
29
what pharmacological value does mannitol have
pharmacologically inert doesn’t bind to a receptor and doesnt interfere with any channel
30
how does mannitol work?
- increases plasma osmolarity - filtered at glomerulus and poorly reabsorbed - increases osmotic pressure in glomerular filtrate - decreases H2O reabsorption from nephron - stays in the tubule - water moves into tubule and is excreted
31
why can't salt or glucose be used as osmotic diuretics?
they are osmotic substances that are reabsorbed and taken up into cells - we don't want the diuretic to be reabsorbed
32
why would you give mannitol with a slow infusion?
too fast you will drag water from inside the cells – bad - dehydrate the own cells suffer even more
33
what os glaucoma and which diuretic would you use?
accumulation of liquid in the eye mannitol
34
where does mannitol enter and where does it draw liquid from?
does not enter the brain or eye - draws liquid from tissues
35
what would you use mannitol for?
forced diuresis e.g. in poisonings acute glaucoma cerebral oedema
36
how would you administer mannitol
slow IV. Infusion of 5 – 20% solution
37
what is reabsorbed in the PCT?
sodium, water and bicarbonate
38
what % of sodium is reabsorbed in the PCT?
65-70% | 2/3
39
what does carbonic anhydrase do?
catalyses the dissociation reaction H2CO3 --> CO2 + H2O
40
formula for carbonic acid
H2CO3
41
which exchanger is used between PCT and epithelial cells
Exchanger for sodium and hydrogen Exhange hydrogen ion – sodium into the blood – atpase
42
what happens if you inhibit the carbonic anhydrase?
don’t form the hydrogen ion – sodium doesn’t have anything to exchange with – doesn’t get into the cell so then doesn’t get into the blood – sodium and the water stay in the tubule - excretion
43
where does carbonate come from and where does it diffuse into?
comes from the dissociation of NaHCO3 or H2O +CO2 joining - diffuses into the blood
44
what is crucial about Carbonic anhydrase inhibitor diuretics?
the H+ isn't forms anymore
45
why would carbonic anhydrase be slightly redundant?
So many mechanisms to regulate hydrogen ions – that the H ions still apear in the cell – so is redundant
46
what sort of drug is Acetazolamide?
Carbonic anhydrase inhibitor
47
what effect would Acetazolamide have on the urine? why?
cause mildly alkaline urine - increase excretion of HCO3-
48
What does Acetazolamide do?
Suppresses H+ production and thus reduce Na+-H+ exchange – less Na+ reabsorption Increases excretion of HCO3- (accompanied by Na+, K+ and H2O) – causes mildly alkaline urine – metabolic acidosis Effect is self-limiting
49
what are the uses for Acetazolamide?
Glaucoma – inhibits CA in eyes to reduce the formation of aqueous humour - Adjunct therapy in metabolic alkalosis (inc. excretion of bicarbonate (acidosis)) Prophylaxis (treatment) of altitude sickness
50
what are the adverse effects of Acetazolamide?
Dizziness and light headache Blurred vision Loss of appetite and stomach upset
51
why do you get altitude sickness?
Less oxygen, saturation blood oxygen needs to be constant, hyperventelate, eliminate too much co2, metabolic alkilosis - hangover sensation
52
how does acetazolamide help altitude sickness?
increases the excretion of bicarbonate