Renal III Flashcards

1
Q

CKD cycle

A
damage glomerulus
less NaCl in macula densa
TGFeedback increases renin
ang II causes EA constr.
can cause more damage
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2
Q

what diseases can magnify CKD?

A

hypertension

diabetes

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3
Q

what type of acid base imbalance is caused by CKD?

A

metabolic acidosis

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4
Q

waste products are dependent on what to be filtered?

A

GFR

as GFR decreases more waste products will build up in the plasma

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5
Q

phosphate and H+ are maintained at normal filtration UNTIL?

A

GFR falls under 30% of normal

bc the kidney has high baseline excretion rates and hormonal influence

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6
Q

electrolytes are maintained UNTIL?

A

renal failure

dialysis is used to maintain function

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7
Q

what does metabolism of macronutrients produce?

A

significant volatile acid load (CO2) ~15,000 mEq/d
small nonvolatile acid load
~70mEq H+/d

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8
Q

what are the 3 systems used to buffer the acid produced daily?

A

rapid ECF buffer by HCO3- and phosphate
rapid pulm exhalation
slow renal excretion of H+

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9
Q

what does the kidney use to buffer H+?

A

NH3 and Phosphate

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10
Q

normal H+ value

A

40mEq/L

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11
Q

what detects changes in pH?

A

peripheral chemoreceptors in carotid and aortic bodies

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12
Q

what alters respiratory control centers in medulla?

A

PaO2 and PaCO2

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13
Q

as you increase alveolar ventilation by 2 how much does that increase pH

A

.2 increase in pH

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14
Q

why are there two systems working here?

A

compensation

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15
Q

acute disturbances

A

less time and less compensation

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16
Q

chronic disturbance

A

more time and more compensation

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17
Q

what does compensation do?

A

helps normalize pH but does NOT correct the original disturbance

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18
Q

3 major acid-base functions of the kidney

A

excretion of fixed metabolic acids
regulation of plasma HCO3-
protect from bad buffering

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19
Q

what is bad buffering?

A

proteins can buffer but it alters their function

20
Q

what % of filtered load of bicarb is excreted in the urine?

A

0%

21
Q

how much bicarb is filtered and reabsorbed?

A

4320mEq

22
Q

what promotes H+ secretion/HCO3- reabsorption?

A

acidosis
hypokalemia
aldosterone or ang II
decrease in ECF volume (more Na/H activity)

23
Q

what is the pH of normal urine

A

6 or less

24
Q

what does Ang II do to the Na/H transporter

A

increased activity

25
Q

what does increased acid load do to HCO3 transporters?

A

increases the amount of transporters

unknown mechanism

26
Q

where is the majority of H+ secretion happen

A

PT

27
Q

what parts or cells are used for H+/HCO3- management during normal to acidosis?

A

PT, TAL, DT, CD

type A cells

28
Q

what type of cells or parts are used for H+/HCO3- management during alkalosis?

A

DT, CCD

type B cells

29
Q

when there is more K in the lumen what does the type A cell do

A

takes up more K and secretes more H+ and can put you at risk for alkalosis in the blood

30
Q

what do type B cells do

A

bicarb secreted via HCO3-/Cl- exchanger

renal H+ reabsorb

31
Q

can type A turn into type B cell when in sustained alkalosis?

A

yes evidence to support this

32
Q

A low and normal dose of Diamox (acetazolamide) blocks Carbonic Anhydrase (mostly in the PT) and is commonly Rx’d to treat glaucoma. Will the urine be acidic or alkaline?

A

alkaline

33
Q

why can alkalosis cause hypokalemia

A

because the HCO3- in the lumen causes the K+ channels to be open & establishes an electrochemical gradient
more K+ is secreted or excreted

34
Q

what does acute acidosis decrease

A

all ATPase transporter activity

the open probability of the K+ channels (hyperkalemia?)

35
Q

what does chronic acidosis increase?

A

-sk.m. H+/K+ exchanger (increase [plasma K+]
-reduce Na/KATPase acticity (lowers ECFV)
-both of above increase aldosterone
-higher flow rates and aldosterone promote K+ secretion
HYPOkalemia!!

36
Q

where has most of the H+ in the tubular lumen come from

A

built up from tubular secretion

37
Q

can bicarb serve as the renal base?

A

no bc we need to reabsorb it

38
Q

what is the maximal free H+ of the urine?

A

0.03mmol/L

39
Q

what are the primary filtered renal buffers?

A

phosphate and ammonia

40
Q

what are large acid loads excreted mainly in the form of?

A

ammonium

41
Q

which renal buffer can adapt to meet demand?

A

ammonia

phosphate stays around the same level (increases slightly)

42
Q

where is glutamine synthesized

A

the liver from NH4 and bicarbonate

43
Q

what happens to glutamine when it reaches the proximal tubule?

A

converted into 2 new bicarbs and 2 NH4

44
Q

where is ammonium reabsorbed?

A

the TAL by NKCC

45
Q

what happens to ammonium in the CCD?

A

it is secreted from the interstitial fluid via NaK pump and HATPase