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Renal > acid-base physiology > Flashcards

acid-base physiology Flashcards

1
Q

P02, PCO2, HCO3-, ph - normal ranges

A

PO2: 75-105 mm Hg
PCO2: 33-44 mm Hg
HCO3-: 22-28 mEq/L
pH: 7.35-7.45

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2
Q

Metabolic acidosis - HCO3-, PCO2, ph, compensatory response

A

ph –> decreased
PCO2 –> decreased
HCO3- –> decreased
compensatory response –> immediate hyperventilation

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3
Q

Metabolic alkalosis - HCO3-, PCO2, ph, compensatory response

A

ph –> increased
PCO2 –> increased
HCO3- –> increased
compensatory response –> immediate hypoventilation

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4
Q

Respiratory acidosis - HCO3-, PCO2, ph, compensatory response

A

ph –> decreased
PCO2 –> increased
HCO3- –> increased
compensatory response –> increased renal HCO3- reabsorption (delayed)

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5
Q

Respiratory alkalosis - HCO3-, PCO2, ph, compensatory response

A

ph –> increased
PCO2 –> decreased
HCO3- –> decreased
compensatory response –> decreased renal HCO3- reabsorption (delayed)

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6
Q

Henderson-Hasselbalch equation

A

6.1 + log (HCO3-)/0.03PCO2

ph=pk+log(A-/HA)

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7
Q

Winters formula is a formula used to evaluate

A

respiratory compensation in a metabolic acidosis

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8
Q

Winters formula - equation

A

PCO2=1.5 (HCO3-) + 8 +/- 2

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9
Q

Winters formula - explanation

A

If measured PCO2 is bigger than predicted PCO2 –> concominant respiratory acidosis
If measured PCO2 is smaller than predicted –> concomitant respiratory alkalosis

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10
Q

diagnosis if acidemia or alkalemia

A

check artrial ph:

a. if more than 7.45 –> alkalemia
b. if less than 7.35 –> acidema

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11
Q

alkalemia - respiratory or metabolic alkalosis ?

A
  1. if PCO2 less than 36 –> Respiratory alkalosis

2. if HCO3- more than 28 meq/L –> metabolic alkalosis

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12
Q

Metabolic alkalosis - DDx

A
  1. loop diuretics
  2. vomiting
  3. antiacids
  4. hyperaldosteronism
  5. thiazide use
  6. Hypokalemia
  7. several renal tubular defects
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13
Q

Respiratory alkalosis - DDx

A

Hyperventilation:

  1. Hysteria
  2. Hypoxemia (eg. high altitude)
  3. Pulmoary embolism
  4. Tumor
  5. salicylates (early)
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14
Q

acidemia - respiratory vs metabolic alkalosis?

A

PCO2 more than 44 mm Hg –> respiratory acidosis

HCO3- less than 20 meg/L –> metabolic acidosis

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15
Q

Respiratory acidosis - DDx

A

Hypoventilation:

  1. Airway obstruction
  2. Acute lung disease
  3. Chronic lung disease
  4. Opioids/sedatives
  5. weakening of respiratory muscles
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16
Q

Metabolic acidosis - next step

A

Check anion gap = Na+ - (CL+HCO3-):
more than 12 –> anion gap metabolic acidosis
8-12 –> normal anion gap metabolic acidosis

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17
Q

anion gap metabolic acidosis - DDx

A
  1. Methanol (formic acid)
  2. Uremia
  3. Diabetic ketoacidosis
  4. Propylene glycol
  5. Iron tablets
  6. ISONIAZIDE
  7. Lactic acidosis
  8. Ethylene glycol (–> oxalic acid)
  9. Salicilates (late)
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18
Q

normal anion gap metabolic acidosis - DDx

A
  1. Hyperalimentation (artificial supply of nutrients, typically intravenously)
  2. Addison disease
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamide
  6. Spironolactone
  7. saline infusion
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19
Q

Renal tubular acidosis - definition

A

disorder of the renal tubules that leads to normal annion gap (hyperchloremic) metabolic acidosis

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20
Q

Hyperchloremic acidosis is

A

a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma HCO3- concentration, and an increase in plasma CL- concentration

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21
Q

Renal tubular acidosis - types

A
  1. Distal tubular acidosis (type 1)
  2. Proximal renal tubular acidosis (type 2)
  3. Combined proximal and distal renal tubular acidosis (type 3)
  4. Hyperkalemic renal tubular acidosis (type 4)
22
Q

Distal tubular acidosis (type 1) - mechanism

A

defect in ability of α intercaleted cells to secrete H+ –> no new HCO3 is generated (CL/HCO3- exchanger in the basolateral membrane) –> metabolic acidosis and urine ph more than 5.5

23
Q

Distal tubular acidosis (type 1) is associated with (an mechanism)

A
  1. hypokalemia (α-cell cannot secrete H+, and cannot reabsorb K+, maybe because H+/K+ pump)
  2. high risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover
24
Q

causes of Distal tubular acidosis (type 1)

A
  1. amphotericin B toxicity
  2. analgesic nephropathy
  3. congenital anomalies (obstruction of urinary tract)
25
Q

Proximal renal tubular acidosis (type 2) - mechanism

A

defect in PCT HCO3 reabsorption –> increased excretion HCO3- in urine and subsequent metaboli acidosis. Urine is acidified by α-intercalated cells in collecting tubule (urine ph less than 5.5)

26
Q

causes of Proximal renal tubular acidosis (type 2)

A
  1. Fanconi syndrome

2. carbonic anhydrase inhibitors

27
Q

Proximal renal tubular acidosis (type 2) is associated with

A
  1. hypokalemia

2. high risk for hypophosphatemic rickets (low phosphate - maybe from Fanconi)

28
Q

Hyperkalemic renal tubular acidosis - mechanism

A

Hypoadlosterinism –> hyperkalemia –> low NH3 synthesis in PCT –> low NH4+ excretion –> urine ph less than 5.5

29
Q

causes of Hyperkalemic renal tubular acidosis (generally)

A
  1. low aldosterone production

2. aldosterone resistance

30
Q

example of low aldosterone production causes

A
  1. diabetic hyporeninism
  2. ACE inhibitors
  3. angiotensin receptor blockers
  4. NSAID
  5. heparin
  6. cyclosprorine
  7. adrenal insufficiency
31
Q

example of aldosterone resistance causes

A
  1. K+ sparing dieuretics
  2. nephropahty due to obstruction
  3. TMP/SXM
32
Q

Renal tubular acidosis - types/urine ph/potasium/concentration

A
  1. Distal tubular acidosis (type 1) - urine ph more than 5.5 - hypokalemia
  2. Proximal renal tubular acidosis (type 2) - urine ph less than 5.5 - hypokalemia
  3. Hyperkalemic renal tubular acidosis (type 4) - urine ph less than 5.5 - hyperkalemia
33
Q

Renal tubular defects that cause metabolic alkalosis

A
  1. Syndrome of apparent Mineralocorticoid Excess
  2. Liddle syndrome
  3. Gitelman syndrome
  4. Bartter syndrome
34
Q

Aspirin - pH disturbances

A

respiratory alkalosis early (hyperventilation)

transition to mixed metabolic acidosis-respiratory alkalosis

35
Q

Why does infusion of normal saline cause metabolic acidosis?

A

The bicarbonate ions are diluted by the isotonic fluid, and acidosis occurs as a resul

36
Q

Renal tubular acidosis - causes of every type

A

Distal (type 1) –> a. amphotericin B toxicity b. analgesic nephropathy c. congenital anomalies (obstruction) of urinary tract
Proximal (type 2) –> a. Fanconi syndrome b. carbonic anhydrase inhibitors
Hyperkalemic (type 4) –> decreased aldosterone production (diabetic hyporeninism, ACE inhibitors, ARB, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance ( K+-sparing diuretics, nephropathy due to pbstruction, TMP/SXM)

37
Q

weak acids - renal diffusion (mechanism and example)

A
  • 2 FORMS: HA + A-
  • only HA form diffuse
  • in acidic urine –> HA predominates –> more back diffusion and decreased excretion
  • in alkaline urine –> A- predominates –> less back diffusion and increased excretion
    example: the excetion of salicylic acid can be increased in by alkalinizing the urine
38
Q

weak bases - renal diffusion (mechanism and example)

A
  • 2 FORMS: BH+ and B form
  • only B form diffuse
  • in acidic urine –> BH+ predominates –> less back diffusion –> increased excretion
  • in alkaline urine –> B predominates –> more back diffusion –> decreased excretion
39
Q

Types of acid in the body (and which)

A
  1. Volatile –> CO2

2. Nonvotalie (fixed) –> sulfuric, phosphoric, ketoacids, lactic acids, salicylic acid

40
Q

Buffers of the body (and pK)

A

Extracellular –> HCO3 (6.1), phosphate (6.8)

Intracullular –> Organic phosphates, Protein (esp Hb)

41
Q

according to Henderson Hasselbalch equation, when the ph equals the pK –> ….

A

conentration of HA and A- are equal

42
Q

H+ is renal excreted as

A
  1. H2PO4- (titratable acid)

2. NH4+

43
Q

renal NH4+ production - regulation

A
  1. acidosis –> adaptive increase in NH3 synthesis

2. hyperkalemia –> inhibits NH3 synthesis (hyperkalemic renal tubular acidosis)

44
Q

Compensation of chronic metabolic acidosis

A

adaptive increase in NH3 synthesis (beside hyperventilation)

45
Q

metabolic alkalosis accompanied by ECF (eg. vomiting)

–>

A

renin - angiotensinin axon –> increased reabsorption of HCO3 increases, worsening the metabolic alkalosis

46
Q

Respiratory alkalosis -symptoms of …… may occur because

A

hypocalcemia
because H+ and Ca2+ compte for binding sites on plasma proteins –? decreased protein binding causes increased protein binding of Ca2+ and decreased free Ca2+

47
Q

Metabolic acidosis - predicted compensatory response

A

1 meq/L decrease in HCO3- –> 1.3 mmHg decrease in PCO2

48
Q

Metabolic alkalosis - predicted compensatory response

A

1 meq/L increase in HCO3- –> 0.7 mmHg increase in PCO2

49
Q

Respiratory acidosis - predicted compensatory response

A

acute: 1 mmHg increase in PCO2 –> 0.1 meg/L increase in HCO3-
chronic: 1 mmHg increase in PCO2 –> 0.4 meq/L increase in HCO3-

50
Q

Respiratory alkalosis - predicted compensatory response

A

acute: 1 mmHg decrease in PCO2 –> 0.2 meq/L decrease in HCO3-
chronic: 1mmHg decrease in PCO2 –> 0.4 meg/L decrease in HCO3-

Renal (15 decks)

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