Muster - Loop of Henle, Distal Tubule & Cortical Collecting Duct Flashcards

1
Q

what type of cancer is known for causing a proximal tubular dysfuction

A

Multiple Myeloma

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2
Q

what is one classic finding (classical diagnostic tool) in someone with proximal tubule dysfunction

A

spilling of bicarbonate into the urine until it hits an equilibrium

then if you give them bicarb, it throws off the equilibrium and the pH in the urine starts to rise

can also look for elevated urine glucose in a person with normal blood glucose, can also look for AAs

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3
Q

Ingestion of this can cause proximal tubule dysfuciton

A

lead

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4
Q

what is the best equation for estimating creatinine clearance

A

Cockcroft-Gault

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5
Q

orthostatic hypotension is a sign of what

A

volume depletion

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6
Q

key function of the ascending loop of henle

A

reabsorbs sodium without resorbing water

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7
Q

what part of the renal tubule is ONLY permeable to water

A

descending limb

so the osmolality is greatest in the lowest part of the medullary space at around 1400mOms

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8
Q

cells in the ascending limb look like

A

big and simple cuboidal

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9
Q

part of the renal tubule that is not permeable to water

A

ascending limb

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10
Q

where are the NKCC pumps in the renal tubule

what ion is moving down its EC gradient

A

lumen side in the cells of the ascending limb

sodium is moving down its electrochemical gradient

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11
Q

about a third of the sodium that is reabsorbed in the ascending limb moves through the _____

how

A

pericellular space

its because the Cl- attracts it there (Cl- pumped over via the NKCC pump)

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12
Q

bartter syndrome

A

nonfunctional NKCC pump (lisinopril blocks this)

mental retardation
volume depletion
hypokalemia
metabolic alkalosis
hypercalcURIA
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13
Q

where are the NaCl channels in the renal tubule

A

in the distal tubule (in the cortex)

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14
Q

Gitleman syndrome

A

genetic mutation in the NaCl transporter (HCTZ, chlortalidone block this)

normal BP
metabolic alkalosis
hypocalcURIA
hypomagnesemia
hyopkalemia
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15
Q

what is a potassium sparing diuretic

two classes and two examples from each

A

CLASSICLY:
epithelial sodium channel (ENac) blockers:
Amiloride
Triamterene

or

an aldosterone antagonist (don’t work on just ENac):
Spironolactone
Eplerenone

K STAys
Spironolactone, Triamterine, Amiloride

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16
Q

what can happen after you are taken off a diuretic

A

when you are on the diuretic, your kidney recognizes it as a drop in volume.

When taken off the diuretic the kidney freaks out and takes up even more sodium than you got them off of with your diuretic.

AKA the pendulum swings back too far

17
Q

What is the best time to give a diuretic

A

after a bid salt meal.

if their diuretic wears off just before they eat a lot of salt, the rebound effect will cause an even greater retention of sodium

18
Q

where is the only place in the kidney that you can have variable and controllable sodium reabsorption

A

collecting tube

19
Q

epithelial sodium channel

faces what side of cell - lumen or vessel

(ENac)

A

lumen

20
Q

Renal outer medularry potassium channel

ROMK

A

just allows potassium to flow back into the lumen of the renal tubule (as the K concentration increases in the tubule cell from the activity of the Na/K antiporter

21
Q

fixed amount of sodium that we resorb

A

95%

(can only control 5% of your filtered load)

you can maximally get rid of about 5% (50g) of this per day, 95% is always absorbed

22
Q

filtered load equation and normal value for sodium

A

GFR * [Na]plasma

around 25,000mM/day. (1Kg/day)

1g=25mM

23
Q

juxtaglomerular cells release what

A

renin

they are in the afferent arteriole

24
Q

why does the distal tubule come back and run next to the afferent arteriole

A

so that the juxtaglomerular cells can detect:

distal flow rate
Na and Cl delivery

so that they juxtaglomerular cells can tell the distal tubule if they are receiving less stretching. this causes production of renin

25
Q

where does aldosterone cause resorption of sodium in the renal tubule

how does it do it mechanisticly

A

in the collecting tubule

stimulated by low sodium or high potassium

aldosterone binds steroid response elements, causing an increase in the transcription, translation, and insertion of the Na/K transporter, and the ENac and ROMK channels

26
Q

what happens if you have an upregulation of ENac

A

going to get more sodium absorption

called “little’s syndrome”

present with salt sensitive hypertension

27
Q

type I pseudo hypoaldosteronism

A

get a loss of ENac function

you have enough aldosterone, it just doesn’t work on ENac function

get: sodium wasting, fluid wasting