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REM Exam 2 > Physiology Acid/Base from Vanders and FA > Flashcards

Physiology Acid/Base from Vanders and FA Flashcards

1
Q

Type 1 RTA

A

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

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2
Q

Causes of Type 1 RTA

A

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

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3
Q

Type 2 RTA

A

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

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4
Q

Causes of Type 2 RTA

A

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

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5
Q

Type 4

A

Hypoaldosteronism, aldosterone resistance, or K+sparing diuretics

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

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6
Q

Type 1 RTA, where and pH

A

Distal tubule, pH>5.5

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7
Q

Type 2 RTA where and pH

A

Proximal tubule <5.5

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8
Q

Type 4 RTA pH

A

Hyperkalemic, pH <5.5

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9
Q 
Normal gas values for: 
pH
pCO2
PO2
HCO3
A

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

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10
Q

Causes of Metabolic acidosis w/ increase anion gap

A 
MUDPILES 
Methanol 
Uremia 
Diabetic ketoacidosis 
Propylene glycol 
Iron Tablets or INH
Lactic acidosis 
Ethylene glycol (oxalic acid) 
Salicylates (Late)
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11
Q

Causes of Metabolic acidosis w/ Normal anion gap

A 
HARD-ASS
Hyperalimentation 
Addisons disease 
Renal tubular acidosis 
Diarrhea 
Acetazolamide
Spironolactone 
Saline Infusion
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12
Q

Calculation for anion gap

A

Anion gap=Na+- Cl+HCO3-

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13
Q

Buffers of ECF

A

Phosphate and albumin

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14
Q

Most important buffer

A

Bicarbonate

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15
Q

Alpha intercalated cells vs. Beta intercalated cells

A

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+

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16
Q

Where is bicarb reabsorbed in the nephron?What transporters

A

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

Thick ascending limb

Distal: Alpha intercalated can reabsorb to balance

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17
Q

What cells secrete bicarb

A

B-intercalated cells

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18
Q

How is H+ excreted in urine?

A

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

19
Q

Most important filtered buffer

A

Phosphate, H2PO3

20
Q

Explain H+ Excretion on Ammonium

A

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

21
Q

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

A

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

22
Q

How can New HCO3 in blood be measured

A

measuring the NH4 excreted in urine

23
Q

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

A

Acid, low pH

24
Q

In acidosis, why is lactated ringers given?

A

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

25
Q

Resp acidosis

A

Low pH, High PCO2

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

26
Q

Renal failure results in acidosis or alkalosis

A

Metabolic acidosis, H+ can’t be excreted

27
Q

Diarrhea

A

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

28
Q

Factors that cause kidney to generate or maintain metabolic alkalosis

A

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)
29
Q

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

A

Metabolic alkalosis

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

30
Q

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

A

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

31
Q

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

A

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

32
Q

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

A

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

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

33
Q

Factors that shift K+ into cells, Hypokalemia

A

Insulin
Aldosterone
B-adrenergic stimulation
Alkalosis

34
Q

Factors that shift K+out of cells, Hyperkalemia

A 
Insulin deficiency (DM)
Aldosterone deficiency (Addison's disease)
B-adrenergic blockade 
Acidosis
Cell lysis 
Strenous exercise
Increased extracellular fluid osmolarity
35
Q

Where does ADH act on?

A

Distal medullary and cortical collecting tubule

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

36
Q

What diuretics cause acidemia?

A

Carbonic anhydrase inhibitors

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

37
Q

What diuretics cause Alkalosis?

A

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

38
Q

Equation for reabsorption

A

reabsorption= Filter load- Excretion rate

Filtered load= GFRplasma conc
Excretion rate= UV

39
Q

Free water clearance

A

Ch2o=V-Cosm

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

40
Q

What is the charge of the glomerular capillary?

A

Negative due to heparin sulfate

41
Q

What is Liddle’s Syndrome?

A

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.

42
Q

What is Conn’s Syndrome? Common lab findings?

A

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

43
Q

Volume equation?

A

Volume= amount/concentration

44
Q

3 Non-volatile (fixed) acids

A

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

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

REM Exam 2 (10 decks)

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