Renal Exam 1: Acid-Base Disorders

Front 1

How much acid is produced each day from ingested protein?

Back 1

50-100 mEq/d

Front 2

How much acid is excreted each day by the kidney?

Back 2

1 mEq/kg body wt

Front 3

Where does excess base come from (dietary)?

Back 3

fruits & veggies --> citrate --> HCO3

Front 4

acidemia --> (high/low) citrate

Back 4

low

Front 5

alkalemia --> (high/low) citrate

Back 5

high

Front 6

What is the main role of the proximal tubule?

Back 6

reclaim bicarb! 4000 mEq/day filtered and reabsorbed

Front 7

What is the mechanism by which bicarb is reabsorbed in the proximal tubule?

Back 7

Shuttling.

Front 8

Reabsorption of bicarb in the proximal tubular lumen: NaHCO3 filtered at glomerulus. __ is exchanged for __ which combines w/ HCO3 to form __. __ breaks this down to __ and __ which re-enter the cell where __ and __ combine to form bicarb which moves into the __ via __-transport with __. The __ gradient is maintained by the __.

Back 8

NaHCO3 filtered at glomerulus. Na+ is exchanged for H+ which combines w/ HCO3 to form H2CO3. CA breaks this down to CO2 and H2O which re-enter the cell where OH- and CO2 combine to form bicarb which moves into the PERITUBULAR CAPILLARY via CO-transport with Na+. The Na+ gradient is maintained by the Na/K-ATPase.

Front 9

What is the minimal urine pH? What does this mean in terms of urinary excretion of H+?

Back 9

Minimal pH is 4.5. Means you could only secrete 40-80 mmol/d of free H+. We use buffers (NH3 & HPO4--) to bind the rest and aid in excretion.

Front 10

Type-A intercalated ducts help us get rid of __ and Type-B cells help get rid of __.

Back 10

Type-A get rid of ACID
Type-B get rid of BASE

Front 11

In what cells of the nephron does HPO4-- bind protons (and how do the protons get into the lumen)?

Back 11

Proximal tubule via Na+/H+ exchanger
Type-A intercalated cell via H+ ATPase

Front 12

What is meant by Ammonium Trapping in the CCD?

Back 12

NH3 crosses from the peritubular capillary across the cell into the tubular lumen where it combines w/ a H+ (from the H+ pump) forming NH4+. This NH4+ is now trapped in the lumen and will be excreted in the urine.

Front 13

Where is NH3 synthesized?

Back 13

in the proximal tubule

Front 14

In the setting of acidosis, NH3 synthesis __

Back 14

increases

Front 15

In the setting of diarrhea, what would you expect to happen to NH3 production?

Back 15

It should increase to get rid of the extra H+

Front 16

Under physiological conditions, what should be the urine pH?

Back 16

6

Front 17

In the setting of systemic acidosis, what would you expect the urine pH to be?

Back 17

< 5.5

Front 18

If systemic acidosis and urine pH > 5.5 one of 3 things is happening, what are they?

Back 18

1. increased delivery of bircarb
2. decreased excretion of H+
3. urea splitting organism (Proteus)

Front 19

What are the 3 primary mechanisms that lead to metabolic acidosis?

Back 19

1. loss of HCO3
2. Decreased renal excretion of H+
3. Excess acid

Front 20

What are the main etiologies of a loss of HCO3 leading to metabolic acidosis?

Back 20

1. In the GI tract (DIARRHEA)
2. In the kidney (proximal renal tubular acidosis -- failure of prox tubule to reabsorb bicarb)

Front 21

What are the main etiologies of decreased renal excretion of H+ that lead to metabolic acidosis?

Back 21

1. Distal renal tubular acidosis (H+-ATPase defect)
2. Acute and Chronic Kidney Injury (no buffer)

Front 22

What are the main etiologies of excess acid that lead to metabolic acidosis?

Back 22

1. Endogenous: Lactic Acidosis or Ketoacidosis
2. Exogenous: Ethylene Glycol, Methanol, Salicylates

Front 23

Explain the etiology of respiratory acidosis

Back 23

hypoventilation --> primary increase in CO2 --> increase in H+ --> RA
Remember: pH = HCO3/CO2

Front 24

What is the primary problem in metabolic alkalosis?

Back 24

increase in HCO3 concentration

Front 25

What are the 2 primary mechanisms that lead to metabolic alkalosis?

Back 25

1. Loss of acid
2. Excess bicarb

Front 26

What are the main etiologies of acid loss that lead to metabolic alkalosis?

Back 26

1. GI tract (VOMITING)
2. Kidney (HYPERALDOSTERONISM)

Front 27

How does hyperaldosteronism lead to acid wasting and metabolic alkalosis?

Back 27

increase in lumen negativity b/c ENaC sucks up Na+ --> H+ excretion and HCO3 reabsorption

Front 28

True or False: All pts given exogenous citrate or bicarb will develop metabolic alkalosis

Back 28

False. This will only happen if they have underlying defect in HCO3 excretion such as decreased GFR.

Front 29

What is the mechanism causing respiratory alkalosis?

Back 29

increased minute ventilation (hyperventilation).

Front 30

What is the compensatory response to a primary metabolic acidosis?

Back 30

hyperventilate to decrease CO2

Front 31

What is the compensatory response to a primary metabolic alkalosis?

Back 31

hypoventilate to increase CO2

Front 32

For which disorder is the compensation mechanism greatest: metabolic acidosis or alkalosis? Why?

Back 32

Greater in metabolic acidosis b/c you can increase your breathing rate a lot. In alkalosis, you can only hypoventilate so much before you pass out.

Front 33

What is the main compensatory mechanism in resp. acidosis?

Back 33

decreased pH sensed in proximal tubule --> increased HCO3 reabsorption

Front 34

What is the main compensatory mechanism in resp. alkalosis?

Back 34

decreased HCO3 reabsorption

Front 35

What is the primary disturbance in metabolic acidosis?

Back 35

decrease in HCO3

Front 36

What is the primary disturbance in metabolic alkalosis?

Back 36

increase in HCO3

Front 37

what is the primary disturbance in resp acidosis?

Back 37

increase in CO2

Front 38

What is the primary disturbance in resp alkalosis?

Back 38

decrease in CO2

Front 39

What is the expected compensation (CO2) in metabolic acidosis?

Back 39

LOTS OF WAYS TO CALCULATE THIS:
1. E[pCO2] = 1.5(HCO3) + 8 +/- 2 (Winter's eqn)
2. E[pCO2] = HCO3 + 15
3. 1.2 mmHg fall in pCO2 for each 1 mEq/L fall in HCO3 below 24 mEq/L

Front 40

What is the expected compensation (CO2) in metabolic alkalosis?

Back 40

pCO2 increases by 0.7 for each mEq/L HCO3 above 24 mEq/L

Front 41

What is the expected compensatory change in HCO3 in acute resp acidosis?

Back 41

HCO3 increase by 1 for each 10 mmHg rise in pCO2 (above 40)

Front 42

What is the expected compensatory change in HCO3 in chronic resp acidosis?

Back 42

HCO3 increase by 3.5 for each 10 mmHg rise in pCO2 (above 40)

Front 43

What is the expected compensatory change in HCO3 in chronic resp alkalosis?

Back 43

HCO3 decrease by 5 for each 10 mmHg fall in pCO2 (below 40)

Front 44

What is the expected compensatory change in HCO3 in acute resp alkalosis?

Back 44

HCO3 decrease by 2 for each 10 mmHg fall in pCO2 (below 40)

Front 45

How do you calculate the anion gap?

Back 45

AG = Na - (Cl + HCO3)

Front 46

What is the differential for increased AG metabolic acidosis?

Back 46

GOLDMARK
Glycols
Oxoproline
L-lactate (endogenous)
D-lactate (bacterial overgrowth of gut)
Methanol poisoning
Aspirin toxicity
Renal failure
Ketoacidosis (DM, EtOH, starvation)

Front 47

What characterizes Type A lactic acidosis and what are some etiologies?

Back 47

Due to hypoperfusion or hypoxia
Causes:
Shock (septic, cardiac, hemorrhagic)
Acute hypoxia
CO poisoning
Severe anemia

Front 48

What characterizes Type B lactic acidosis and what are some etiologies?

Back 48

Absence of hypoperfusion and hypoxia
Causes:
Drugs (metformin, Cyanide, Linezolid, Propofol)
System disease (Liver failure, malignancy)
NOTE: These all are due to disruptions in oxidative phophorylation

Front 49

What are some causes of D-lactic acidosis?

Back 49

Jejunoileal bypass
Small bowel resection
Sx: slurred speech, ataxia, cerebellar sx

Front 50

What is a normal osmolal gap?

Back 50

5

Front 51

How do you calculate the osmolal gap?

Back 51

MeasuredOsm - CalculatedOsm
Where CalcOsm = 2*plasma Na + glucose/18 + BUN/2.8
> 10 is considered abnormal

Front 52

What is considered an abnormal osmolal gap?

Back 52

values > 10 (normal is 5)

Front 53

What are some causes of increased AG met acidosis w/ elevated osmolal gap?

Back 53

MUST BE A SUBSET OF GOLDMARK:
Glycols, Methanol, Ketoacidossis, Lactic acidosis. Also formaldehyde poisoning

Front 54

What are some causes of elevated osmolal gap w/o metabolic acidosis?

Back 54

Isopropyl alcohol poisoning
Mannitol
Dextran-40

Front 55

How do you treat ethylene glycol and methanol poisoning?

Back 55

fomepazole (or EtOH, dialysis if really bad).

Front 56

What causes oxoproline (pyroglutamic) acidosis?

Back 56

depleted glutathione stores
1. CHRONIC tylenol use
2. pregnancy
3. vegetarian diet
4. liver disease

Front 57

What is you DDx of normal anion gap metabolic acidosis?

Back 57

1. Diarrhea (bicarb lost in stool)
2. Renal Tubular Acidosis (bicarb lost in urine or decreased H+ excretion)