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CPR Final > Clin Med approach to Acid Base Disorders > Flashcards

Clin Med approach to Acid Base Disorders Flashcards

1
Q

Low serum HCO3- corresponds with what?

A

Metabolic acidosis

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2
Q

High serum HCO3- corresponded with what?

A

Metabolic alkalosis

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3
Q

High PCO2 corresponds with what?

A

Respiratory acidosis

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4
Q

Low PCO2 corresponds with what?

A

Respiratory alkalosis

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5
Q

What are the two types of metabolic acidosis?

A
  1. High anion gap metabolic acidosis

2. Non anion gap metabolic acidosis (hyperchloremic acidosis)

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6
Q

What are the two types of metabolic alkalosis?

A
  1. saline responsive (hypovolemia/ contraction alkalosis)

2. Saline non responsive - euvolemia or hypervolemia

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7
Q

What is the compensation for metabolic acidosis?

A

Winter’s formula : PCO2 =1.5(HCO3-) +8 +/- 2

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8
Q

What is compensation for metabolic alkalosis?

A

PCO2 will increase by 0.7mmHg for each 1.0mEq/L increase in HCO3 from normal

(normal HCO3 is 24)

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9
Q

What is compensation for acute respiratory acidosis?

A

HCO3 will increase by 1mEq/L for every 10 mmHg increase of PCO2 from normal

normal PCO2 is 40mmHg

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10
Q

What is the compensation for Chronic respiratory acidosis?

A

chronic acidosis will show HCO3 will increase of 3.5 mEq/L for every 10 mmHg increase of PCO2 from normal of 40mmHg

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11
Q

What is the compensation for acute respiratory alkalosis?

A

HCO3 will decrease by 2mEq/L for every 10 mmHg decrease in PCO2 from normal

normal PCO2 is 40 mmHg

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12
Q

What is the compensation for chronic respiratory alkalosis?

A

HCO3- will decrease by 5 mEq/L for every 10 mmHg decrease in PCO2 from normal

normal PCO2 is 40 mmHg

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13
Q

What is normal pH of ABG?

A

pH 7.35-7.44

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14
Q

What is the normal HCO3- concentration in ABG?

A

24 mEq/L

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15
Q

What is the normal PCO2 concentration in ABG

A

40mmHg

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16
Q

What is the normal anion gap in ABG?

A

12 +/- 2

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17
Q

What is the normal osmolarity gap in ABG?

A

10mosm/kg

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18
Q

What is the anion gap formula?

A

(Na+) - (HCO3- +CL-)

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19
Q

what is normal serum osmolality?

A

275-290mosm/kg

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20
Q

What is osmolar gap?

A

measured serum osmolality -calculated serum osmolality

normal <10mosm/kg

if osmolar gap>10mosm/kg –> consider additional solutes in the blood

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21
Q

Why would an osmolar gap calculation be used clinically?

A
  1. screen for alcohol ingestion (AG>20) – esp in HAGMA
  2. Screen for ketoacidosis
  3. screen for lactic acidosis
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22
Q

What is the use of the Delta-Delta gap?

A

Delta-delta gap is used in patients with HAGMA to determine if there is a coexistent NAGMA

-every increase in AG should correspond with an equal decrease in serum HCO3

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23
Q

What is GOLD MARK?

A

DDX for HAGMA

Glycols
Oxoproline (pyroglutamic acid- acetaminophen toxicity)
L - L -lactic acidosis
D D-lactic acidosis (seen in short bowels syndrome from bacteria colonies)

Methanol
Aspirin
Renal Failures
Ketoacidosis (alcoholic, diabetic, starvation)

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24
Q

What is ME DIE

A

DDX of increased osmolar gap— these will kill you if not fixed

M- methanol
E-Ethanol

D-Diethylene glycol
I- Isopropyl alcohol
E-ethylene glycol

Propyleny glycol, keto acidosis, and lactic acidosis also included

25
Q

Methanol is concerted to what?

A

Methanol is converted to formic acid which can cause blindness (optic disk damage)

26
Q

What is the ethylene glycol metabolism?

A

ethylene glycol–> glycolic acid –> glyoxylic acid–> renal failure, oxalic acid, and glycine

27
Q

What is DURHAAM?

A

DDX for Normal anion gap metabolic acidosis (NAGMA)

D- diarrhea **
U-uretal diversion
R- renal tubular acidosis ***
H-hyperalimentation (parenteral nutrition
A-acetazolamide (carbonic anhydrase inhibitor)
A-addisions disease
M-miscellaneous

28
Q

What occurs when net excretion by the kidneys is impaired and results in NAGMA?

A

Renal tubular acidosis

29
Q

What cannot be diagnosed in the setting of AKI?

A

RTA

30
Q

Results from decreased net H+ ion section in distal tubules and collecting duct

A

RTA 1 (Distal RTA)

31
Q

Results from decreased HCO - reabsorption in the proximal tubule

A

RTA 2 (Proximal RTA)

32
Q

Results from decreased aldosterone secretion or aldosterone resistance

A

RTA 4 - Hyperkalemic RTA

-leads to decreased net H+ and K+ section in the collecting duct
hyperkalemia-> decreased NH3 synthesis in PCT-> decreased NH4 secretion

33
Q

What is the most common RTA seen in DM2 or CKD?

A

Type 4 RTA (shows hyper kalmia and + urine anion gap

34
Q

What has amionaciduria, phosphaturia, glycosuria, Bicarbonaturia, tubular proteinuria, uricosuria?

A

Proximal tubular dysfunction - Fanconi syndrome

  • may lead to metabolic acidosis, hypophosphateimia, osteopenia
35
Q

What is the Urine anion gap used for?

A

differentiate renal from non-renal causes of NAGMA

-marker of NH4CL exertion

UAG = (UrineNa+ + Urine K+) – UrineCl- Mproximl
• If UAG is negative, it indicates appropriate distal nephron urinary acidification
• If UAG is positive, it indicates inappropriate distal nephron urinary acidification

36
Q

What ion is produce from glutamine metabolism in proximal tubule cell?

A

NH4+

37
Q

What is permeable? NH3 or NH4+?

A
  • AmmoNIA (NH3) is highly permeable and can cross the cell membrane of tubular cells easily
  • AmmoNIUM (NH4+) is impermeable and needs transporter help to move in and out of tubular cells
  • Once a H+ ion bind to NH3 in the collecting duct forming NH4+, it is trapped within the tubular lumen and is ultimately excreted in urine
38
Q

Why is urine Cl- the surrogate marker of ammonium excretion?

A

NH4+ is bound to Cl- to become NH4Cl-

39
Q

Cystinosis in children and Fanconi syndrome in adults (secondary multiple myeloma) , and carbonic anhydrase inhibitors can cause what?

A

Proximal RTA - type 2

-Increased risk of hypophosphotemic rickets

40
Q

NAGMA with or without proximal tubular dysfunction and Hypokalemia are clinical manifestations of what?

A

RTA 2–> Hypokalemia is Mild compared to distal RTA (type 1)

RTA 2 is defect in HCO3 reabsorption in PCT causes increased HCO3 in urine and metabolic acidosis

41
Q

Patients with this RTA cannot acidify urine

A

RTA 1 (distal RTA)

Results from decreased net H+ ion secretion in the distal nephron:

  1. Decreased H+ ion secretion
    • H+/K+-ATPase or H+-ATPase defect
  2. Gradient defect
    • Abnormally permeable distal tubule and collecting duct allows secreted H+ ions to flow back into tubular cell
    – Can be caused by Amphotericin for fungal infections

• Lack of net H+ ion secretion prevents urinary acidification and excretion of ammonium
– Also prevents some HCO - reabsorption in the distal tubule 3

42
Q

What RTA could be seen with Sjogrens or Glue sniffing (Toulene)

A

Distal RTA (RTA type 1)

43
Q

What RTA is associated with nephorlithisasis or nephrocalcinosis?

A

Distal RTA- RTA 1

-decreaed H+ excretion from distal nephron and can’t acidify urine so ammonium is not excreted

44
Q

Acidosis is associated with?

A

hyperkalemia

45
Q

alkalosis is associated with?

A

hypokalemia

46
Q
  1. Hypokalemia
  2. Vomiting/nasogastric tube suctioning
  3. Diuretics
  4. volume depletion
  5. mineralocorticoid excess

can all cause what?

A

Metabolic alkalosis

47
Q

NKCC2 mutation

A

Bartter syndrome type 1

48
Q

ROMK mutation

A

Bartter syndrome type 2

49
Q

CLC-Kb mutation

A

Bartter syndrom type 3

50
Q

Barttin mutation

A

Bartter syndrome type 4

51
Q

What is net result of Bartter Syndrome similar to?

A

loop diuretic

52
Q

– Severe hypokalemia
– Metabolic alkalosis (saline non-responsive)
– Low to normal blood pressure
– Hypercalciuria and nephrocalcinosis

are clinical sx of?

A

Bartter Syndrome

53
Q

– Severe hypokalemia
– Metabolic alkalosis (saline non-responsive)
– Low to normal blood pressure
– Hypocalciuria (opposite of Bartter Syndrome, helpful distinguishing tool)
• Like seen with thiazide diuretics – Hypomagnesemia

are clinical symptoms of?

A

Gitelman Syndrome

54
Q

Inactivating mutations in TAL transporters causes?

A

Bartter’s syndrome (rare)

55
Q

Inactivating mutations in Na-Cl co-transporter NCCT causes?

A

Gitleman sundrome

56
Q

Net result of Gitleman syndrome is similar to?

A

Thiazide Diuretic use

57
Q

Resistant Hypertension
– Hypokalemia
– Metabolic alkalosis (saline non-responsive)

are seen in ?

A

Liddel Syndrome

58
Q

Mutations in epithelial Na+ channels in the collecting duct of the nephron causes what?

A

Liddle syndrome

59
Q

What is tx of liddle syndrome?

A
  • Amiloride or triamterene

CPR Final (2 decks)

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