(2.1) Acid/Base Disorders [DSA-Selby] Flashcards

1
Q

Bicarbonate reaction

A

CO2 + H2O <=> H2CO3- via carbonic anhydrase

H2CO3- <-> H+ + HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the Henderson Hasselbach equation? What is the relationship between pH and PCO2?

A

HCO3- and pH directly related

PCO2 and pH inversely related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do the lungs regulate pH?

A

Control concentration of PCO2 by increasing or decreasing respiratory rate

Inc RR = more CO2 blown off

Dec RR= less CO2 blown off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do the kidneys regulate pH?

A

Excreting acidic or alkaline urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is acid excreted by the kidneys?

A

Renal epithelial cells secrete large amounts of H+ into the tubular lumen => acid removed from ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 acid-base disturbances and their relationship to the buffer system?

A

Metabolic Acidosis
– Low serum HCO3-
Metabolic Alkalosis
– High serum HCO3-
Respiratory Acidosis
– High PCO2

Respiratory Alkalosis
– Low PCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Normal anion gap metabolic acidosis (NAGMA) is also referred to as _____ acidosis

A

Hyperchloremic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is base excreted by the kidneys?

A

Large amounts of HCO3- continuously filtered into the urine

If not reabsorbed, will be excreted => base removed from ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are the acid-base disturbances compensated

A

Lung compensates for kidney disturbance

Kidney compensates for lung disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Compensation formula for metabolic acidosis

A

Winter’s formula: PCO2 = 1.5[HCO3-] + 8 +/- 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Compensation formula for metabolic alkalosis

A

Dr. Karius’s formula: pCO2 = 0.7 [HCO3-24] + 20 mmHg ± 5

Dr. Selby: PCO2 increases by 0.7 mmHg for ever 1.0 mEq/L increase in HCO3- from normal (normal HCO3- is 24)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Compensation formula for:

Acute respiratory acidosis

Chronic respiratory acidosis

A

Dr. Karius:

Acute: [HCO3-] = PCO2/10 +/- 3

Chronic: 24 + (PCO2 - 40)/10 = [HCO3-]

Dr. Selby:

Acute: HCO3- increases by 1 mEq/L for every 10 mmHg increase in PCO2 from normal (normal is 40)

Chronic: HCO3- increases by 3.5 mEq/L for every 10 mmHg increase in PCO2 from normal (40)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Compensation formula for:

Acute respiratory alkalosis

Chronic respiratory alkalosis

A

Dr. Karius:

Acute: 24 - 2(40 - PCO2)/10 = [HCO3-]

Chronic: 24 - 5(40 - PCO2)/10 = [HCO3-]

Dr. Selby:

Acute: HCO3- will decrease by 2 mEq/L for every 10 mmHg decrease in PCO2 from normal (normal is 40)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How many acid-base disturbances can someone have at one time?

A

3

(4 is impossible, cannot breathe fast and slow simultaneously)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the anion gap equation?

A

AG = Na+ - (HCO3- + Cl-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a normal anion gap?

A

Normal AG = 12 +/- 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why does the anion gap remain normal in NAGMA?

A

H+ is buffered by HCO3-, which drops HCO3- =>

Cl- levels rise and offset HCO3- => normal AG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does hypoalbuminemia affect anion gap? How is this corrected?

A

Hypoalbuminemia falsely lowers AG

For every 1 g/dL drop in albumin, calculated AG decreases by 2.5 mEq/L and may mask an elevated AG

Correct by adding back the deficit to get the correct AG

Albumin-Corrected Anion Gap = Anion Gap + 2.5 x ([Normal Albumin] - [Observed Albumin])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the serum osmolality equation? What is the normal?

A

Calculatedulated serum osmolality = 2(Na) + (Glucose/18) + (BUN/2.8)

Normal = 275 - 290 mosm/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the osmolar gap? What is the normal?

A

Osmolar gap = Measured serum osmolality - calculated serum osmolality

Normal osmolar gap < 10 mosm/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If osmolar gap >10 mosm/L, what is that suggestive of?

A

Additional solutes in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What level of anion gap is highly suspicious for alcohol ingestion?

A

AG >20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is osmolar gap most clinically useful for?

A

Screening for alcohol ingestion, particularly in HAGMA

(can also screen ketoacidosis and lactic acidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the Delta-Delta gap used for?

A

Used in pts with HAGMA to determine if there is coexistent NAGMA or metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you calculate the Delta-Delta Gap?

A

Every increase in AG, there should be an equal decrease in serum HCO3-

Delta gap = calculated AG - normal AG (12)

Delta HCO3- = normal HCO3- (24) - Delta gap

26
Q

What is the range for normal pH?

A

7.35-7.44

27
Q

Normal HCO3-?

A

24 mEq/L

28
Q

Normal PCO2?

A

40 mmHg

29
Q

Preferred Ddx for HAGMA?

A

GOLD MARK (previously MUDPILES)

Glycols (ethylene and propylene)

Oxoproline (Pyroglutamic acid), tylenol toxicity

L-Lactic acidosis

D-Lactic Acidosis - only seen with colonic metabolization

Methanol

Aspirin

Renal failure

Ketoacidosis (alcoholic, diabetic, starvation)

30
Q

45 yo female presents to the ED. Upon examination, she appears malnourished and weak. Pt states that she takes acetaminophen daily for headaches. What kind of acid-base disturbance might you see?

A

Pyroglutamic (5-oxoproline) acidosis

(Seen more in women who are malnourished or critically ill)

31
Q

What mechanism is responsible for pyroglutamic acidosis?

A

Acetaminophen depletes glutathione =>

Increased formation of pyroglutamic acid and accumulation

32
Q

What diagnostic test would you order for pyroglutamic (5-oxoproline) acidosis?

A

Urinary organic acid screen

33
Q

What is the treatment for pyroglutamic (5-oxoproline) acidosis?

A

Discontinue acetaminophen

IVF

N-acetylcysteine

34
Q

Ddx for increased osmolar gap?

A

ME DIE (same…)

Methanol

Ethanol

Diethylene glycol - Mannitol diuretic

Isopropyl alcohol (rubbing alcohol)

Ethylene glycol

(also propylene glycol, ketoacidosis, and lactic acidosis)

35
Q

If a patient has metabolic acidosis, association of which alcohol can be ruled out?

A

Isopropyl alcohol (NOT associated with metabolic acidosis)

36
Q

What is the relationship between acidosis and serum potassium?

A

Acidosis is associated with hyperkalemia

(H+ enter cells, K+ exit)

37
Q

What is the relationship between alkalosis and serum potassium?

A

Alkalosis is associated with hypokalemia

(H+ exits the cells, K+ enter)

38
Q

Ddx for normal anion gap metabolic acidosis (NAGMA)?

A

DURHAM

Diarrhea

Ureteral diversion (ileal conduit) or fistula

Renal tubular acidosis (RTA)

Hyperalimentation (Enteral nutrition)

Acetazolamide (carbonic anhydrase inhibitor)

Addison’s disease (adrenal insufficiency)

Miscellaneous (toulene toxicity - glue sniffing)

39
Q

Type 2 RTA has decreased capacity in the ____ to reabsorb ____

A

Decreased capacity in the PT to reabsorb HCO3-

(results in low serum HCO3-, will eventually stabilize at the lower level)

40
Q

Where is the majority of HCO3- reabsorbed in the kidney?

A

Proximal tubule (80-90%)

41
Q

8 year old patient presents with type 2 RTA, what is their most likely diagnosis?

A

Cystinosis

(Most common cause of Type 2 RTA in children)

42
Q

An adult presenting with type 2 RTA likely has what etiology? With what secondary cause?

A

Fanconi syndrome with secondary Multiple Myeloma

43
Q

A patient with proximal RTA may present with what clinical manifestations?

A

(Type 2 RTA)

NAGMA w/ or w/o PT dysfunction

Hypokalemia (milder than Type 1)

44
Q

How do you diagnose a proximal (Type 2) RTA?

A

Urine pH high or low depending on serum HCO3-

Can have urine pH <5.5 when in new steady state (normal H+ secretion in distal nephron)

Urine anion gap positive or negative

45
Q

What is the urine anion gap (UAG) clinically used for?

A

Clinically used to differentiate renal from non-renal causes of NAGMA

46
Q

What is the difference between a positive and a negative urine anion gap?

A

Negative = appropriate distal nephron urinary acidification

Positive = inappropriate distal nephron acidification

47
Q

What is urine anion gap a marker of?

A

NH4Cl (ammonium chloride) excretion => appropriate urinary acidification

(will increase in the setting of metabolic acidosis)

48
Q

What are the two main causes of distal (Type 1) RTA?

A

Unable to acidify urine due to:

1) Decreased H+ ion secretion due to channel defects
2) Gradient defect: abnormally permeable distal tubule and collecting duct allows H+ ions to flow back into tubular cell

(lack of H+ ion secretion prevents urinary acidification and excretion of ammonium)

49
Q

A patient taking amphotericin may be at risk for what type of RTA?

A

Distal (Type 1) RTA

(May cause gradient defect)

50
Q

What clinical manifestations may be seen with distal (Type 1) RTA?

A

Nephrolithiasis

Nephrocalcinosis

51
Q

Which RTA presents with systemic disease?

A

Distal (Type 1 RTA)

(usually presents with Sjogren’s disease)

52
Q

Which RTA can be caused by glue sniffing?

A

Type 1 (Distal) RTA due to toulene

53
Q

What diagnostic criteria may present for Type 1 (distal) RTA?

A

NAGMA

Unable to acidify urine pH <5.5

Hypokalemia (severe)

UAG positive

54
Q

Type 4 RTA is also known as _____ RTA

A

Hyperkalemic

Characterized by distal nephron dysfunction from impaired H+ and K+ excretion => NAGMA and hyperkalemia

55
Q

What are the two main theories of hyperkalemic RTA?

A

Deficiency of circulating aldosterone (DM, NSAIDS, Bblockers, ACEi/ARB, high dose heparin)

Aldosterone resistance in collecting ducts (interstitial renal disease, K+ sparing drugs)

56
Q

60 yo male w/ hx of DM presents for a wellness check. Upon lab study, pt has NAGMA and hyperkalemia but does not appear symptomatic. What type of RTA is this pt likely to have?

A

Type 4 (hyperkalemic)

(most pts in 50s-70s w/ hx of DM or CKD)

57
Q

What diagnostic presentations might a patient with Type 4 RTA have?

A

Variable urine pH >5.5

Positive UAG

58
Q

In general, what factors may lead to a metabolic alkalosis?

A

Factors that stimulate Na+ reabsorption

Increase H+ secretion and stimulate HCO3- reabsorption

59
Q

Ddx for metabolic alkalosis?

A

Hypokalemia

Vomiting/nasogastric tube suctioning

Diuretics (loop and thiazide)

Volume depletion (Contraction alkalosis)

Mineralocorticoid excess (appropriate or inappropriate)

60
Q

Contraction alkalosis would occur in what setting?

A

Volume depletion in the setting of Cl- depletion => RAAS activation and aldosterone secretion

61
Q

What is the relationship between an alpha-intercalated cell and a beta-intercalated cell?

A

Beta-intercalated cell is a mirror image of alpha-intercalated

HCO3- exits into tubular lumen

In contraction alkalosis, must replete Cl- to help HCO3- secretion