Physiology Acid/Base from Vanders and FA

Question 1

Type 1 RTA

Answer 1

Defect in ability of Alpha intercalated cells to secrete H+. New HCO3- not generated–>Metabolic acidosis with Hypokalemia

Question 2

Causes of Type 1 RTA

Answer 2

Amphotericin B toxicity, Analgesic nephropathy, multiple myeloma (light chains) and congenital anomilies of Urinary tract

Question 3

Type 2 RTA

Answer 3

Defect in proximal HCO3- reabsorption results in increase excretion of HCO3- in urine and subsequent metabolic acidosis.

Urine is acidified by alpha intercalated cells in collecting tubule, associated with hypokalemia, increase risk of hypophosphatemic rickets

Question 4

Causes of Type 2 RTA

Answer 4

Fanconi syndrome, chemicals toxic to proximal tubule, and carbonic anhydrase inhibitors

Question 5

Type 4

Answer 5

Hypoaldosteronism, aldosterone resistance, or K+sparing diuretics

Hyperkalemia impairs ammoniagenesis in the proximal tubule–>Decrease buffering capacity and Decrease H+ excretion into urine

Question 6

Type 1 RTA, where and pH

Answer 6

Distal tubule, pH>5.5

Question 7

Type 2 RTA where and pH

Answer 7

Proximal tubule <5.5

Question 8

Type 4 RTA pH

Answer 8

Hyperkalemic, pH <5.5

Question 9

Normal gas values for: 
pH
pCO2
PO2
HCO3

Answer 9

pH: 7.35-7.45
pCO2: 35-45
PO2>90
HCO3: 22

Question 10

Causes of Metabolic acidosis w/ increase anion gap

Answer 10

MUDPILES 
Methanol 
Uremia 
Diabetic ketoacidosis 
Propylene glycol 
Iron Tablets or INH
Lactic acidosis 
Ethylene glycol (oxalic acid) 
Salicylates (Late)

Question 11

Causes of Metabolic acidosis w/ Normal anion gap

Answer 11

HARD-ASS
Hyperalimentation 
Addisons disease 
Renal tubular acidosis 
Diarrhea 
Acetazolamide
Spironolactone 
Saline Infusion

Question 12

Calculation for anion gap

Answer 12

Anion gap=Na+- Cl+HCO3-

Question 13

Buffers of ECF

Answer 13

Phosphate and albumin

Question 14

Most important buffer

Answer 14

Bicarbonate

Question 15

Alpha intercalated cells vs. Beta intercalated cells

Answer 15

Both in the distal tubule
Alpha intercalated cells: Secrete H+
K+ in cell H+ out into lumen. Reabsorbs all remaining filtered becarb as well as any secreted. Produces titratable acid

B-Intercalated cells: Secretion of bicarb. Reabsorb K+

Question 16

Where is bicarb reabsorbed in the nephron?What transporters

Answer 16

Proximal Tubule: Basolateral Na-HCO3 symport and Cl-HCO3 antiport

Thick ascending limb

Distal: Alpha intercalated can reabsorb to balance

Question 17

What cells secrete bicarb

Answer 17

B-intercalated cells

Question 18

How is H+ excreted in urine?

Answer 18

Bind with buffer such as HCO3- or more commonly NH3–>Excreted known as diffusion trapping

Question 19

Most important filtered buffer

Answer 19

Phosphate, H2PO3

Question 20

Explain H+ Excretion on Ammonium

Answer 20

Glutamine released in liver and taken up by the proximal tubule–>prox tub converts glutamine back to HCO3- and NH4–>NH4 enters the lumen and HCO3 exits blood–>NH4 is broken down into NH3+ H–>NH3 enters lumen by diffusion and H+ enters lumen by Na+/H+antiporter–>NH3 binds with H+ and excreted as NH4; can be reabsorbed by transports (Na-NH4-2Cl at TAL) if there is a lot of NH4

Question 21

When the body is acidic, low pH what is going on with glutaminase?

Answer 21

Glutaminase will increase to break down Glutamine to make more HCO3- to buffer the ECF

Question 22

How can New HCO3 in blood be measured

Answer 22

measuring the NH4 excreted in urine

Question 23

If there is high glutamine in the liver what is the body pH?

Answer 23

Acid, low pH

Question 24

In acidosis, why is lactated ringers given?

Answer 24

Mixture of salts that contain lactate which is conjugate base–>Co2+H2o–>Lactic acid take H+ from body leaves HCO3–>Increasing pH

Question 25

Resp acidosis

Answer 25

Low pH, High PCO2

Compensation: Increase in bicarb from kidneys through increase NH4 production and excretion

Question 26

Renal failure results in acidosis or alkalosis

Answer 26

Metabolic acidosis, H+ can’t be excreted

Question 27

Diarrhea

Answer 27

Metabolic acidosis by direct loss of HCO3-
Characteristics–>low plasma HCO3-, low pH, reduced PCO2 due to resp compensation. Anion gap normal, and Cl- conc elevated

Question 28

Factors that cause kidney to generate or maintain metabolic alkalosis

Answer 28

HCO3 in plasma in increased–>Problem with regulation of HCO3-

1. Volume contraction–>Activate RAA–>aldosterone increase–>Increase H+secretion–>More HCO3- reabsorbed
2. Cl- depletion–> H+ secretion stimulated–>HCO3- excretion. (Chronic vomiting,heavy diuretic use)
3. Aldosterone excess and K+Depletion: Aldosterone increase H+Secretion. K+ depletion resutls in H+ secretion and NH4+ production (excessive diuretic use)

Question 29

Primary Aldosteronism: pH HCO3, PCO2, Na, Cl-

Answer 29

Metabolic alkalosis

Increase pH; Increase HCO3-; increase pCO2; Normal anion gap, slight reduction in Cl-

Question 30

Given Carbonic Anhydrase inhibitor: pH, HCO3, pCO2, Na, Cl-

Answer 30

Metabolic acidosis. Secretion of H+ decreased, reabsorption of HCO3- would decrease–>Increased excretion of HCO3–>Metabolic acidosis

Question 31

Characteristic of Diabetic Ketoacidosis (HCO3,pH, pCO2, anion gap)

Answer 31

Decrease HCO3
Decrease pH
Decrease pCO2
Increase Anion gap due to accumulation of B-OH butyric acid and acetoacetic acid

Question 32

What part of the loop of henle is impermeable to water?

Answer 32

Thin Ascending limb is impermable to water, permeable to Na+

Thin Descending limb opposite permeable to water, and impermeable to Na+

Question 33

Factors that shift K+ into cells, Hypokalemia

Answer 33

Insulin
Aldosterone
B-adrenergic stimulation
Alkalosis

Question 34

Factors that shift K+out of cells, Hyperkalemia

Answer 34

Insulin deficiency (DM)
Aldosterone deficiency (Addison's disease)
B-adrenergic blockade 
Acidosis
Cell lysis 
Strenous exercise
Increased extracellular fluid osmolarity

Question 35

Where does ADH act on?

Answer 35

Distal medullary and cortical collecting tubule

Binds to receptor on basolateral side, and adds AQ2 to apical side

Question 36

What diuretics cause acidemia?

Answer 36

Carbonic anhydrase inhibitors

K+ sparing-aldosterone (Hyperkalemia causes K+ to enter all cells via H+K+exchanger–>Acidosis)

Question 37

What diuretics cause Alkalosis?

Answer 37

Loop diuretics
thiazides
Volume contraction–>Increase ATII–>Increase Na/Hexchanger at Prox tub–>Increase HCO3 reabsorption
Decrease in K+ leads to K+ leaving a cell H+ enters cell

Question 38

Equation for reabsorption

Answer 38

reabsorption= Filter load- Excretion rate

Filtered load= GFRplasma conc
Excretion rate= UV

Question 39

Free water clearance

Answer 39

Ch2o=V-Cosm

Positive: Absence of ADH, free solute free water is excreted
Negative: Presence of ADH this solute-free water is NOT excreted

Question 40

What is the charge of the glomerular capillary?

Answer 40

Negative due to heparin sulfate

Question 41

What is Liddle’s Syndrome?

Answer 41

Acts at the collecting duct on the Na+ channels. Tx with amiloride

Excessive activity of the amiloride-sensitive sodium channel in the collecting tubules would cause a transient decrease in sodium excretion and expansion of extracellular fluid volume, which in turn would increase arterial pressure and decrease renin secretion, leading to decreased aldosterone secretion.

Question 42

What is Conn’s Syndrome? Common lab findings?

Answer 42

Primary excessive secretion of aldosterone (Conn’s syndrome) would be associated with marked hypokalemia and metabolic alkalosis (increased plasma pH).

Question 43

Volume equation?

Answer 43

Volume= amount/concentration

Question 44

3 Non-volatile (fixed) acids

Answer 44

Non-volatile (fixed) acids are all acids produced from sources other than CO2 and include:

    Sulfuric acid (H2SO4)
    Phosphoric acid (H3PO4)
    Lactic acid