kidneys 2 Flashcards

1
Q

what order does plasma go through kidney?

A

bowmanns capsule, proximal tubule, loop of henle, distal tubule, collecting duct

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2
Q

what is filtered in glomerular filtration?

A

blood plasma (20% removed)

permits H20 and small molecules
restricts blood cells and proteins

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3
Q

what does ultrafiltrate consist of?

A

protein free plasma
(1% protein filtered- albumin)
conc of Na in bowmanns capsule is same that is in plasma

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4
Q

what is difference between trancellular and paracellular transport ?

A

transcellular is through cell (requires membrane transport proteins)
paracellular is between cells

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5
Q

what does proximal tubules reabsorb?

A

70% filtrate
70% H2O and NA
~100% glucose and amino acids
90% HCO3- (bicarbonate)

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6
Q

give transport proteins on apical side

A

SGLT1, SGLT2, NaPiII

NHE3?

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7
Q

what happened in NaPiII knockout mice?

A

less phosphate in serum (less reabsorbed) (more in urine)

low phsophate = less dense bone

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8
Q

what is apical and basolateral ?

A

apical is lumen of tubules, baslateral is peritubular capillaries

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9
Q

what is SGLT1 and SGLT2 structure?

A

1-664 aa (14 TMD)
2-672 aa

(glocose and sodium reabsorbtion)

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10
Q

what happens in familial renal glycosuria?

A

increase in urinary glucose
normal plasma glucose
(due to 21 mutations in SGLT2)

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11
Q

what happens in NHE3 knockout mice ?

A

lower plasma HCO3-
plasma PH decreases (more acidic)
BP decreases

(inhibition of H+ secretion ) causes inhibitions of Na and Hco3- transport

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12
Q

what does loop henle do?

A

regulates urine conc
reabsorbs Na+, Cl-, and H2O
reabsorbs Ca2+ and Mg2+

site of action of loop diuretics

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13
Q

what are structures of loop diuretics and what do they do?

A

thin descending limb (reabs of H2O)
thin ascending limb (reabs of Na+, Cl-)+ urea (not permeable to water)
thick ascending limb (reabs Na+ Cl-) (extremely impermeable to H2O)

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14
Q

what are thick ascending limb carriers?

A

NKCC2, ROMK (apical)

CLCK with Barttin (basolateral)

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15
Q

what is bartters syndrome?

A
genetic inheritance - recessive 
slat wasting and polyuria 
hypotension
hypokalaemia
higher PH
hypercaluciuria
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16
Q

what is mutated in bartters syndrome?

A
barttin mutated (CLCK doesnt work) 
this causes increased cellular Cl-, NKCC2 diesnt work
17
Q

what happens in ROMK mouse ?

A

polyuria, salt wasting, BUT plasma PH lower than n bartters (acidosis) little/no diff in K+ (no hypokalaemia)

18
Q

what does early distal tubule do?

A

reabsorb Na+ and Cl-
Reabsorption Mg2+
is sensitiv to thiazide diuretics

19
Q

what are carriers on early DT?

A

apical - NCC + Mg

basolateral - CLCK, an barttin (+na k pump)

20
Q

what is gitelmans syndrome?

A
inherited - recessive, 
salt wasting + polyuria 
hypotension 
hypokalaemia 
higher PH
hypocalciura
(same as battins expect hypocalciuria)
21
Q

what causes gitelmans?

A

loss of function mutation in NCC (less Na and H2O reabsorbed)

22
Q

what can chlorothiazide do?

A

can be used to treat high blood pressure
similar syptom to gitelmans
acts on DT

23
Q

what does late DT , connecting tubules and collecting duct do?

A

concentrated urine
rabsorption of Na and H2O
secretion of K+ and H+

24
Q

what are cells types in LDT and CCD?

A

principle - Na+ and H2O reabsorption.
K+ and H+ secretion

intercalated- alpha and beta
H+ secrestion and reabsorption
HCO3- reabsorption and secretion

25
Q

what do alpha and beta intercalated cells do?

A

alpha - H+ secretion and HCO3- reabsorption

beta - HCO3- secretion and Cl and H+ reabsorption

26
Q

what does medullary CD do?

A

low Na+ permeability

high H2O and urea permeability in prescence of vasopressin

27
Q

what is rhabdomyolysis

A

release myoglobin from damaged muscle - can cause tubule damage