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PMCOL 343 > Renal 1 > Flashcards

Renal 1 Flashcards

1
Q

what are the 3 main roles of the kidney

A

fluid, acid-base, electrolyte imbalance

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2
Q

what % of cadiac output goes to the kidneys

A

20%

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3
Q

what % of glomerular ultrafiltrate is reabsorbed

A

more than 99%

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4
Q

what is the functional unit of the kidney

A

nephron

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5
Q

how many nephrons in each kidney

A

bout a million’

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6
Q

what are the 5 main sections to the nephron

A

glomerulus, proximal tubule, loop of henle, distal convoluted tubule, collecting duct

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7
Q

what are glomerular capillaries permeable and not permeable to

A

permeable to water and many things, just impermeable to plasma proteins (eg. albumin)

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8
Q

how does the protein-free glomerular filtrate enter the bownmans capsule

A

hydrodynamic force

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9
Q

what do diurectics cause excretion of?

A

increased excretion of Na and Cl, causing a secondary loss of water

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10
Q

what are the main uses of diuretics (1)

A

alter the volume or composition of body fluids

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11
Q

where do diuretics act directly

A

on cells of the nephron in the kidney

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12
Q

where do diuretics act indirectly

A

by modifying the content of the filtrate

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13
Q

what are 6 classes of diuretics

A

osmotic diuretics, carbonyl anhydrase inhibitors, loop diuretics, thiazides, potassium sparing diuretics, antidiuretic hormone antagonists

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14
Q

what happens to osmotic diuretics when they pass through the nephron

A

they are not absorbed (if any, very minimal)

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15
Q

how do osmotic diuretics reduce water reabsorption

A

due to osmotic force of solute within the tubule

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16
Q

where do osmotic diuretics act

A

proximal tubule, descending loop of henle and collecting duct (where the nephron is most permeable to water)

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17
Q

what is the net effect of osmotic diuretics

A

increase in urine volume and urine flow rate, reduced Na+ reabsorption

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18
Q

what are therapeutic uses for osmotic diuretics

A

reduce intracranial pressure (brain injury or cerebral edema) or glaucoma

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19
Q

how/why can osmotic diuretics be used for brain injury and glaucoma

A

because they increase plasma osmotic pressure, which causes extraction of water from brain and eye

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20
Q

what is a serious adverse effect of osmotic diuretics and how can it happen

A

heart failure due to transient increase in extracellular fluid volume (sudden increase due to water leaving cells to follow osmotic force of blood-makes heart pump so hard)

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21
Q

can osmotic diuretics cause dehydration

A

yes

22
Q

where does the majority of filtered Na+ and HCO3- reabsorption happen

A

early proximal tubule

23
Q

how does Na+ enter the proximal tubule

A

Na+/H+ exchanger

24
Q

how does Na+ enter the blood (proximal tubule)

A

Na+/K+ ATPase

25
Q

what does carbonic anhydrase do in the lumen

A

turns H2CO3 into H2O and CO2

26
Q

how is H2CO3 made in the lumen

A

HCO3- +H+

27
Q

how does CO2 get into the early proximal tubule

A

diffusion

28
Q

how is carbonic acid made in the proximal convoluted tubule

A

CO2 +H2O –> H2CO3 which is catalyzed by carbonic anhydrase

29
Q

which reactions does carbonic anhydrase catalyze

A

H2CO3 –> CO2 +H2O

and

CO2 +H2O –> H2CO3

30
Q

how does HCO3- exit the proximal tubule and into the blood

A

basolateral Na+/HCO3- co transporter

31
Q

what happens in the late proximal tubule to HCO3-

A

low levels

32
Q

what is the result of low levels of HCO3- in the lumen of late proximal tubule

A

H+ has no where to bind so the lumen is acidified

33
Q

what happens when the lumen is acidic in the late proximal tubule

A

Cl-/base exchanger brings base to neutralize acid and Cl- enters the tubule

34
Q

where do carbonic anhydrase inhibitors act on

A

proximal tubule

35
Q

what does carbonic anhydrase inhibitors do to HCO3- reabsorption into blood

A

decrease

36
Q

what do carbonic anhydrase inhibitors do to metabolic pH and how

A

decrease, causes metabolic acidosis because decreases HCO3- reabsorption into blood

37
Q

what do carbonic anhydrase inhibitors do to Na+ reabsorption and how

A

decreases, because decreases supply of H+ for NHE3 (CA inhibitors prevents H2CO3 formation so H2CO3 cant be broken down into H+ and HCO3-)

38
Q

what happens to water reabsorption with carbonic anhydrase inhibitors and how

A

decrease water reabsorption because there is decreased Na+ reabsorption (NHE3 not as active)

39
Q

what happens to the pH of urine with carbonic anhydrase inhibitors

A

increases, becomes alkaline

40
Q

what are 3 theraputic uses for carbonic anhydrase inhibitors

A

glaucoma
urinary alkalinisation
metabolic alkalosis

41
Q

why are carbonic anhydrase inhibitors good for glaucoma

A

because carbonic anhydrase regulates formation of aqueous humor)

42
Q

why are carbonic anhydrase inhibitors good for urinary alkalinisation treatment

A

because it increases the solubility of uric acid, good for gout (want urine alkaline for this)

43
Q

what are some adverse effects of carbonic anhydrase inhibitors (3)

A

metabolic acidosis
renal stones
renal K+ wasting

44
Q

how does carbonic anhydrase inhibitors cause metabolic acidosis

A

less HCO3- absorbed into blood

45
Q

carbonic anhydrase inhibitors cause renal stones

A

Ca2+ and other salts precipitate in alkaline pH

46
Q

how do carbonic anhydrase inhibitors cause renal K+ wasting

A

increased Na+ in collecting tubes causes increased K+ excretion

47
Q

what does the SGLT2 do

A

reabsorb glucose and Na+ into tubule

48
Q

where are the SGLT2 cotransporters

A

apical membrane of proximal convoluted tubule

49
Q

what do SGLT2 inhibitos do

A

reduce absorption of glucose and Na+

50
Q

when can SGLT2 inhibitors be used therapeutically

A

for diabetes type 2 because it reduces glucose reabsorption so its good to reduce glu in blood

51
Q

do SGLT2 inhibitors have diuretic properties

A

yes but its not the main use. main use is for diabetes

PMCOL 343 (31 decks)

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