Renal - 03 - Acid Base

Front 1

causes of metabolic acidosis

Back 1

exogenous acids (salicylate, methanol, ethelyene glycol)

endogenous acid production (ketoacids, lactic acids)

decreased renal excretion (renal failure, distal renal tubular acidosis)

loss of alkali (diarrhea, proximal renal tubular acidosis)

Front 2

metabolic alkalosis causes

Back 2

exogenous alkali (NaHCO3 administration)

loss of acid (vomiting, excess renal HCO3- production)

Front 3

which part of nephron is new bicarbonate is produced

Back 3

medullary collecting tubule

alpha intercalted cells

Front 4

bicarb reabsorption in the proximal tubule is new or old bicarbonate

Back 4

old

proximal tubule recycles/reclaims bicarbonate - not made new

Front 5

reclaimation of HCO3- in the proximal tubule is done through

Back 5

Na+/H+ exchanger - controlled by ATII

H+ is put into the tubule lumen to titrate HCO3- to H2CO3 (no net secretion of H+)

H2CO3 is converted to CO2 and H2O via carbonic anhydrase

CO2 is reabsorbed through tubule membrane and converted back into HCO3- and H+

H+ is recycled and the HCO3- is pumped into the blood

Front 6

principle cell's purpose in acid-base physiology

Back 6

reabsorption of Na+ creates a negative lumen that draws Cl- out of the tubule paracellularly

creation of negative lumen enhances H+

Front 7

alpha intercalated cell

Back 7

H+ ATPase - regulated by aldosterone

transport of H+ which is created by conversion of H2CO3 -> HCO3- and H+

allows new HCO3-

Front 8

purpose of H+ secretion in cortical collecting tubule

Back 8

reabsorb bicarb that wasnt absorbed in the proximal

lower ph allows titration of filtered buffers like HPO4

HN3 -> HN4+ (but this is mostly medullary)

Front 9

beta intercalated cells

Back 9

oppsite of alpha intercalated cell

secretes bicarb into lumen

only used when blood is alkalotic

Front 10

purpose of medullary collecting tubule

Back 10

ammonia trapping

NH3 -> HN4+

during metabolic acidosis - see NH4+ increase to pee out acid

Front 11

T/F hydrogen ion secretion is controlled by aldosterone in the proximal tubule

Back 11

False - ATII controls hydrogen ion secretion in the proximal tubule

aldosterone controls the hydrogen ion secretion the distal tubule/collecting duct (alpha intercalated cell)

Front 12

serum anion gap

Back 12

Na - (HCO3- + Cl-)

normal = 12

elevated when you have acid other than HCl in the plasma

causes: MUDPILES

methanol
uremia
diabetic ketoacidosis
propylene glycol
isoniazid
lactic acidosis
ethylene glycol

Front 13

hypercholeremic metabolic acidosis - causes

Back 13

normal anion gap

causes:
RTA
Renal failure
GI loss of bicarb - diarrhea

addition of hcl to body
dilution of extracellular buffer stores with solution lacking bicarb

Front 14

how does diarrhea cause bicarb loss

Back 14

sodium bicarb is normally secreted into the GI to neutralize acid

in diarrhea you get excess secretion of bicarb which is expelled from the body

Front 15

urine anion gap

Back 15

urine Na + K - Cl

negative value = normal renal tubular acidification (suggets high NH4+)

positive value = RTA (suggests low NH4+)

Front 16

clinical evaluation of RTA

Back 16

1. look at potassium

2. look at urinary pH during acidosis

3. look at aldosterone

4. look at cortisol

Front 17

type I RTA

Back 17

hypokalemic (RTA 1 and 2 are both hypokalemic)

distal tubule

problem with ability to pump H+ ions

Front 18

type II RTA

Back 18

hypokalemic (RTA 1 and 2 are both hypokalemic)

proximal tubule

defective bicarb reabsorb

Front 19

type III RTA

Back 19

normokalemic

disorder of ammonia or phosphate delivery due to decrease in GFR

Front 20

type IV RTA

Back 20

hyperkalemic (RTA 4,5,6 are all hyperkalemic)

aldosterone deficiency

Front 21

type V RTA

Back 21

hyperkalemic (RTA 4,5,6 are all hyperkalemic)

aldosterone resistance

Front 22

type VI RTA

Back 22

hyperkalemic (RTA 4,5,6 are all hyperkalemic)

voltage dependent RTA, due to defect in Na+ reabsorption distally

Front 23

potassium > 6.5
urine pH < 5.5
low plasma aldosterone
normal plasma cortisol

what kind of RTA

Back 23

Type IV RTA

Front 24

K < 4.5
urinary pH > 5.5

what kind of RTA

Back 24

type I RTA

Front 25

K < 4.5
urinary pH< 5.5

what kind of RTA

Back 25

type II RTA

Front 26

K > 6.5
urinary pH > 5.5

what kind of RTA

Back 26

type VI RTA

Front 27

K > 6.5
urinary pH < 5.5
normal aldosterone

what kind of RTA

Back 27

type V RTA

Front 28

metabolic alkalosis (general causes)

Back 28

loss of acid - vomitting, small bowel obstruction, volume depletion

gain of HCO3-

loss of chloride more so than HCO3- (diuretics)

Front 29

how does loss of cholride cause metabolic alkalosis

Back 29

less chloride means less Na absorbed via NaCl cotransport in the distal tubule

thus higher load of Na+ reaches the cortical collecting ducts where Na/H transporters take up the Na in exchange for H+ (more H+ lost -> alkalosis)

Front 30

how does volume depletion cause metabolic alkalosis

Back 30

increased aldosterone means more Na/H exchange to retain water/sodium - means more H+ released

Front 31

how does high CO2 cause metabolic alkalosis

Back 31

increased CO2 in intercalated cells combines with OH- to form new HCO3-

Front 32

how does low K cause metabolic alkalosis

Back 32

more K in the distal tubule -> more uptake via K/H transporter in the alpha intercalated cell -> increased H+ excretion