Acid Base Disorders Flashcards

1
Q

What is metabolic acidosis?

A

low serum HCO3

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2
Q

What is metabolic alkalosis?

A

high serum HCO3

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3
Q

What is respiratory acidosis?

A

high PCO2

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4
Q

What is respiratory alkalosis?

A

low PCO2

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5
Q

What are the types of metabolic acidosis?

A

HAGMA and NAGMA

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6
Q

What are the types of metabolic alkalosis?

A

Saline responsive and saline non responsive

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7
Q

What are the types of respiratory acidosis and alkalosis?

A

acute or chronic

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8
Q

How is metabolic acidosis compensated?

A

Through respiratory alkalosis (decreased PCO2 via increased RR)

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9
Q

How is metabolic alkalosis compensated?

A

Through respiratory acidosis (increased PCO2 via decreased RR)

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10
Q

How is respiratory acidosis compensated?

A

Through metabolic alkalosis (increased HCO3 via increased kidney reclamation and generation of new HCO3)

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11
Q

How is respiratory alkalosis compensated?

A

Through metabolic acidosis (decreased HCO3 via decreased kidney reclamation and generation of new HCO3)

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12
Q

For every 10mmHg increase in PCO2, HCO3 should what?

A

Increase by 1 (acute) or 3.5 (chronic) in respiratory acidosis

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13
Q

For every 10mmHg decrease in PCO2, HCO3 should what?

A

Decrease by 2 (acute) or 5 (chronic) in respiratory alkalosis

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14
Q

What is the normal pH of blood?

A

7.4

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15
Q

Acidosis is defined as a pH of what?

A

<7.35

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16
Q

Alkalosis is defined as a pH of what?

A

> 7.45

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17
Q

What is the normal value for PCO2?

A

40mmHg (+/- 5…35-45)

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18
Q

What is the normal value for HCO3?

A

24 (+/- 2…22-26)

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19
Q

What is the normal value for anion gap?

A

10 (+/- 5 or 6…5-16)

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20
Q

What is the normal value for osmolality gap?

A

10-15 mosm/Kg

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21
Q

What is the formula for calculating anion gap?

A

Na - (HCO3 + Cl)

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22
Q

When is anion gap clinically used?

A

To differentiate between etiologies of metabolic acidosis (NAGMA vs HAGMA), diagnose paraproteinemias (low AG values), diagnose lithium, bromide or iodide intoxications (low or negative AG values), for quality control monitoring in chemical labs

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23
Q

What is the formula to calculate serum osmolality?

A

2(Na) + (Glucose/18) + (BUN/2.8)

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24
Q

How do you determine osmolar gap?

A

measured serum osmolality - calculated serum osmolality

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25
Q

What is the normal osmolar gap?

A

<10, if it is above 10 then additional solutes are present in the blood

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26
Q

When is osmolar gap clinically useful?

A

Screening for alcohol ingestions, particularly in HAGMA cases (although not all alcohols produce an acidosis), screening for ketoacidosis and lactic acidosis

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27
Q

If AG is above 20 you should be highly suspicious of what?

A

alcohol ingestion

28
Q

When is the delta-delta gap used?

A

In pts with HAGMA to determine if there is a coexistent NAGMA or metabolic alkalosis present

29
Q

For every increase in AG there should be an equal decrease in what?

A

serum HCO3

30
Q

How is the delta gap determined?

A

calculated AG - normal AG

31
Q

How is delta HCO3 determined?

A

normal HCO3 - delta gap

32
Q

If the measured delta HCO3 was close to 16, what does this suggest?

A

no additional acid base disorders present

33
Q

If the measured delta HCO3 was >16, what does this suggest?

A

a metabolic alkalosis is present in addition to the HAGMA

34
Q

If the measured delta HCO3 was <16, what does this suggest?

A

a NAGMA is present in addition to the HAGMA

35
Q

What are the MUDPILES ddx for HAGMA?

A

Methanol, uremia, diabetic keotacidosis, paraldehyde, iron and isoniazid, lactic acidosis, ethanol/ethylene glycol, salicylates

36
Q

What is the GOLD MARK ddx for HAGMA?

A

Glycols (ethylene and propylene), oxoproline (pyroglutamic acid; acetaminophen toxicity), L-lactic acidosis, D-lactic acidosis (colonic metabolization of glucose, starch, other carbs by bacteria, seen in short bowel syndromes), methanol, aspirin, renal failure, ketoacidosis (diabetic, alcoholic, starvation)

37
Q

What is the ddx for increased osmolar gap? (MEDIE)

A

methanol, ehtanol, diethylene glycol (diuretic [mannitol]), isopropyl alcohol (or isopropanol aka rubbing alcohol), ethylene glycol

38
Q

What is the ddx for NAGMA (DURHAAM)? Or HARDASS

A

Diarrhea, ureteral diversion (ileal conduit) or fistula, renal tubular acidosis, hyperalimentation (i.e. enteral nutriton or total parenteral nutrition, TPN), acetazolamide (carbonic anhydrase inhibitor), Addison’s disease (adrenal insufficiency), Misc (toluene toxicity-glue sniffing, pancreatic fistula, meds)

39
Q

What is renal tubular acidosis?

A

A condition in which net acid excretion by the kidneys is impaired which results in NAGMA; cannot be diagnosed in the setting of AKI

40
Q

Which two renal tubular defects can lead to RTA?

A

impaired H ion secretion, impaired HCO3 reabsorption

41
Q

What does RTA type 1 result from (aka distal RTA)?

A

decreased net H ion secretion in distal tubules and collecting duct

42
Q

What does RTA type 2 (aka proximal RTA) result from?

A

Decreased HCO3 reabsorption in the proximal tubule

43
Q

What does RTA type 4 (aka hyperkalemic RTA) result from?

A

Decreased aldosterone secretion or aldosterone resistance; leads to decreased net H and K secretion in collecting duct

44
Q

Which types of RTA have a positive urine anion gap?

A

Type 1 and 4 (type 2 can be positive)

45
Q

What is urine anion gap (UAG)?

A

clinically used to differentiate between renal and non-renal causes of NAGMA; it is a marker of NH4Cl excretion which indicates appropriate urinary acidification

46
Q

What does a negative UAG indicate?

A

appropriate distal nephron urinary acidification

47
Q

What does a positive UAG indicate?

A

inappropriate distal nephron urinary acidification

48
Q

How is UAG calculated?

A

(UrineNa + UrineK) - UrineCl

49
Q

What is the MCC of proximal RTA in children?

A

cystinosis

50
Q

What are the clinical manifestations of proximal RTA?

A

NAGMA with or without proximal tubular dysfunction and hypokalemia (mild compared to distal RTA)

51
Q

How is proximal RTA diagnosed?

A

Urine pH can be high or low depending on serum HCO3 level (can have urine <5.5 when in new steady state), UAG is negative

52
Q

Unlike proximal RTA, distal RTA pts are unable to what?

A

acidify their urine (which also prevents excretion of ammonium)

53
Q

What is the etiology for distal RTA?

A

Can be primary (idiopathic or inherited) vs acquired; commonly seen with Sjogren’s syndrome; glue sniffing is another common cause due to toluene

54
Q

What is the clinical manifestation of distal RTA?

A

associated with nephrolithiasis and nephrocalcinosis

55
Q

How is distal RTA diagnosed?

A

NAGMA, unable to acidify urine (pH >5.5), hypokalemia (usually severe), UAG is positive

56
Q

What is hyperkalemic RTA characterized by?

A

distal nephron dysfunction from impaired renal excretion of H and K causing a NAGMA and hyperkalemia; due to deficiency of circulating aldosterone or aldosterone resistance in the CD

57
Q

What can cause deficiency or circulating aldosterone?

A

DM and drugs (NSAIDs, beta blockers, ACEi/ARBs, high dose heparin, etc)

58
Q

What can cause aldosterone resistance in the CD?

A

Interstitial renal dz (sickle cell nephropathy, obstructive uropathy, lupus, etc), drugs such as amiloride, triamterene, spironolactone, trimethoprim

59
Q

What is the clinical manifestation of hyperkalemic RTA?

A

usually asx, NAGMA, hyperkalemia, most pts are in their 50-70s with a hx of DM or CKD

60
Q

How is hyperkalemic RTA diagnosed?

A

variable urine pH but usually >5.5, UAG+

61
Q

Acidosis is associated with what?

A

hyperkalemia and vice versa

62
Q

Factors that simulate Na reabsorption, secondarily increase H secretion and thus stimulate hwat?

A

HCO3 reabsorption potentially leading to a metabolic alkalosis

63
Q

What is the Ddx for metabolic alkalosis?

A

Hypokalemia, vomiting or NG tube suctioning (GI loss of HCl), diuretics, volume depletion, mineralocorticoid excess, Bartter, Gitelman syndrome, Liddle syndrome, postyhypercapnic alkalosis, hypercalcemia/milk-alkali syndrome, diarrhea

64
Q

What is the Ddx for respiratory alkalosis? (PAST PH)

A

anything that increases RR or TV including PNA, PE, pulmonary edema, PTX, pregnancy, sepsis, CHF, anxiety, pain, fever, meds (salicylates), elevated altitude, exercise, trauma, inappropriate ventilator settings

65
Q

What is the ddx for respiratory acidosis? (AS A COW)

A

Anything that lowers RR/TV, increases dead space or worsens obstruction including respiratory muscle weakness, hypo or hyperkalemia, ALI/ARDS, PNA, PE, ILD, fractured ribs, COPD, asthma, drugs; inadequate ventilator setting sand increases in CO2 production (increased carb diet, hyperthermia, seizures)