Renal 1 Flashcards

1
Q

what are the 3 main regulations 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

how much urine is made per min

A

1mL

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5
Q

what is the functional unit of the kidney

A

nephron

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6
Q

what are the two layers of the kidney

A

cortex and medulla (inside more)

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7
Q

how many nephrons in each kidney

A

bout a million’

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8
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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9
Q

what are glomerular capillaries permeable and not permeable to

A

permeable to water and many things, just impermeable to plasma proteins

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10
Q

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

A

hydrodynamic force

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11
Q

what are diuretics

A

increased excretion of Na and Cl that causes a secondary loss of water

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12
Q

what are the main uses of diuretics (1)

A

alter the volume or composition of body fluids

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13
Q

how do diuretics act directly

A

on cells of the nephron in the kidney

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14
Q

how do diuretics act indirectly

A

modifying the content of the filtrate

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15
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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16
Q

are ostmotic diuretics direct or indirect and why

A

indirect because they change the content of the filtrate

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17
Q

what kind of agent are osmotic diuretics (pharmacological role)

A

they are actually inert, they pass through filter in glomerulus with limited reabsprtption

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18
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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19
Q

how do osmotic diuretics reduce water reabsorption

A

due to osmotic force of solute within the tubule

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20
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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21
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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22
Q

what are therapeutic uses for osmotic diuretics

A

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

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23
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

24
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)

25
can osmotic diuretics cause dehydration
yes
26
where does the majority of filtered Na+ and HCO3- reabsorption happen
early proximal tubule
27
how does Na+ enter the proximal tubule
Na+/H+ exchanger
28
how does Na+ enter the blood (proximal tubule)
Na+/K+ ATPase
29
what does carbonic anhydrase do in the lumen
turns H2CO3 into H2O and CO2
30
how is H2CO3 made in the lumen
HCO3- +H+
31
how does CO2 get into the early proximal tubule
diffusion
32
how is carbonic acid made in the proximal convoluted tubule
CO2 +H2O --> H2CO3 which is catalyzed by carbonic anhydrase
33
which reactions does carbonic anhydrase catalyze
H2CO3 --> CO2 +H2O and CO2 +H2O --> H2CO3
34
how does HCO3- exit the proximal tubule and into the blood
basolateral Na+/HCO3- co transporter
35
what happens in the late proximal tubule to HCO3-
low levels
36
what is the result of low levels of HCO3- in the lumen of late proximal tubule
H+ has no where to bind so the lumen is acidified
37
what happens when the lumen is acidic in the late proximal tubule
Cl-/base exchanger brings base to neutralize acid and Cl- enters the tubule
38
where do carbonic anhydrase inhibitors act on
proximal tubule
39
what does carbonic anhydrase inhibitors do to HCO3- reabsorption into blood
decrease
40
what do carbonic anhydrase inhibitors do to metabolic pH and how
decrease, causes metabolic acidosis because decreases HCO3- reabsorption into blood
41
what do carbonic anhydrase inhibitors do to Na+ reabsorption and how
decreases, because decreases supply of H+ for NHE3 (CA inhibitors prevents H2CO3 formation so H2CO3 cant be broken down into H+ and HCO3-)
42
what happens to water reabsorption with carbonic anhydrase inhibitors and how
decrease water reabsorption because there is decreased Na+ reabsorption (NHE3 not as active)
43
what happens to the pH of urine with carbonic anhydrase inhibitors
increases, becomes alkaline
44
what are 3 theraputic uses for carbonic anhydrase inhibitors
glaucoma urinary alkalinisation metabolic alkalosis
45
why are carbonic anhydrase inhibitors good for glaucoma
because carbonic anhydrase regulates formation of aqueous humor)
46
why are carbonic anhydrase inhibitors good for urinary alkalinisation treatment
because it increases the solubility of uric acid, good for gout (want urine alkaline for this)
47
what are some adverse effects of carbonic anhydrase inhibitors (3)
metabolic acidosis renal stones renal K+ wasting
48
how does carbonic anhydrase inhibitors cause metabolic acidosis
less HCO3- absorbed into blood
49
carbonic anhydrase inhibitors cause renal stones
Ca2+ and other salts precipitate in alkaline pH
50
how do carbonic anhydrase inhibitors cause renal K+ wasting
increased Na+ in collecting tubes causes increased K+ excretion
51
what does the SGLT2 do
reabsorb glucose and Na+ into tubule
52
where are the SGLT2 cotransporters
apical membrane of proximal convoluted tubule
53
what do SGLT2 inhibitos do
reduce absorption of glucose and Na+
54
when can SGLT2 inhibitors be used therapeutically
for diabetes type 2 because it reduces glucose reabsorption so its good to reduce glu in blood
55
do SGLT2 inhibitors have diuretic properties
yes but its not the main use. main use is for diabetes