Acid/Base Disorders Flashcards

1
Q

What is the normal arterial blood pH

A

7.35-7.45

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

What is the most important buffering system?

A

The bicarbonate buffering system

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

Which organs play the largest roll in the bicarbonate buffering system?

A

Lungs (blow off CO2)

Kidneys (secrete acidic or alkaline urine)

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

What are the types of metabolic acidosis

A

High anion gap metabolic acidosis

Normal Anion gap metabolic acidosis

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

What are the types of metabolic alkalosis

A

Saline Responsive (hypovolemia aka contraction alkalosis)

Saline-non-responsive (euvolemic or hypervolemic)

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

In expected HC03 compensation for Respiratory Acidosis and Alkalosis, for every 10 mmHg increase in pCO2, what should the bicarb increase be for acute and chronic acidosis

A

Acute 1

Chronic 3.5

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

In expected HC03 compensation for Respiratory Acidosis and Alkalosis, for every 10 mmHg decrease in pCO2, what should the bicarb decrease be for acute and chronic alkalosis

A

Acute 2

Chronic 5

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

How many acid-base disturbances can be present at once

A

1-3

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

Outline the Acid-Base stepwise approach

A
  1. Determine if acidosis or alkalosis is present
  2. Determine if primary disturbance is metabolic or respiratory
  3. If metabolic calculate anion gap
    - -if hypoalbuminemia, corrected anion gap
    - - if HAGMA present calculate osmolar gap
    - - if HAGMA present consider delta-delta gap
  4. Calculate appropriate compensation for primary acid-base disorder
    - - if compensation is good, simple acid-base disorder present
    - - if compensation is bad, complex acid-base disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the normal HCO3 ABG value

A

24 mEq/L

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

What is the normal PCO2

A

40 mmHg

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

What is the normal Anion gap

A

12

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

What is the normal osmolality gap

A

10 mosm/kg

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

how do you calculate anion gap?

A

Na - (HCO3 + CL-)

normal value is 12 +/- 2

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

How do you calculate serum osmolality?

A

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

normal is 275-290

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

How do you calculate osmolar gap

A

Normal serum osmolality - Calculated

normal <10 -> screen for alcohol ingestion (HAGMA), ketoacidosis, lactic acidosis

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

When is the Delta-Delta gap useful

A

in patients with HAGMA to determine if there is a coexisting NAGMA

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

How do you calculate the Delta gap

A

Calculated AG - Normal AG

If measured HCO3 is = to [Normal HCO3 - (delta gap)] then no additional acid-base disturbance present

if measured HCO3 is greater than [] then there is Metabolic alkalosis + HAGMA

if measured HCO3 is less than [] then there is NAGMA in addition to HAGMA

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

What is the mnemonic for HAGMA

A

GOLD MARK

Glycols
Oxyproline (acetaminophen tox)
Lactic Acidosis
D- Lactic acidosis

Methanol
Aspirin
Renal Failure
Ketoacidosis

20
Q

What is the treatment of pyroglutamic (5-oxoproline) acidosis

A

Discontinue acetaminophen
IVF
N-acetylcysteine

Seen in women who are malnourished or critically ill

21
Q

What is the mnemonic for increased serum osmolality gap

A

MEDIE

Methanol
Ethanol
Diethylene Glycol
Isopropyl alcohol 
Ethylene Glycol
22
Q

What is the mnemonic for NAGMA

A

DURHAAM

Diarrhea*
Ureteral diversion 
RTA*
Hyperalimentation
Acetazolamide
Addison's Disease
Miscellaneous (toluene)
23
Q

What is the etiology of RTA

A

net acid excretion is impaired

Cannot be diagnosed in AKI

24
Q

What is type 1 RTA

A

decreased H+ ion secretion in distal tubules and collecting ducts

25
Q

What is type 2 RTA

A

decreased HCO3 reabsorption in proximal tubule

26
Q

What is RTA type 4

A

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

**MOST COMMON

27
Q

If you suspect RTA and have hyperkalemia, which RTA do you have?

A

Type 4 with positive urine anion gap

28
Q

If you suspect RTA and have hypokalemia with proximal tubular dysfunction, which RTA do you have?

A

Type 2 with or without urine anion gap

if you don’t have proximal tubular dysfunction you have type 1 with urine anion gap

29
Q

What is the function of measuring Urine Anion Gap

A

Differentiate Renal from non-renal NAGMA

30
Q

What is the equation for UAG

A

(UrineNa + UrineK) - Urine Cl

if negative - appropriate distal nephron acidification
if positive - inappropriate distal nephron acidification

31
Q

Describe RTA type 2

A

Proximal renal tubular acidosis

decreased capacity to resorb bicarb leading to low serum bicarb -> to eventual stabilization at lower bicarb level

32
Q

What are the clinical manifestations of Proximal RTA (type 2)

A

NAGMA with or without proximal tubular dysfunction

Hypokalemia (mild compared to RTA 1)

33
Q

What is the problem present in RTA type 1

A

unable to acidify urine

can be caused by amphotericin

34
Q

What is the main clinical manifestation of distal RTA (type 1)

A

Nephrolithiasis or nephrocalcinosis

NAGMA
Urine pH >5.5
Hypokalemia
UAG positive

35
Q

What are the two main etiologies of Hyperkalemic RTA (type 4)

A

Deficiency in circulating aldosterone)

Aldosterone resistance in collecting ducts

36
Q

What are the clinical manifestations of Hyperkalemic RTA (type 4)

A
Usually asymptomatic 
NAGMA 
Hyperkalemia 
Most pts in 50-70s with hx of DM or CKD
UAG positive
37
Q

Acidosis:Hyperkalemia::Alkalosis:

A

Hypokalemia

38
Q

What factors stimulate Na resorption, secondarily increase H+ secretion and thus stimulate HCO3 reabsorption leading to metabolic alkalosis

A
Hypokalemia
N/V
Diuretics 
Volume depletion 
Mineralocorticoid excess
39
Q

Whom does Bartter syndrome affect

A

Prenatal or neonatal pts

rare AR disease

40
Q

what are the clinical manifestations of Bartter syndrome

A

severe hypokalemia
metabolic alkalosis
Low to normal BP
Hypercalciuria and nephrocalcinosis

41
Q

Bartter syndrome types and their affected channels mnemonic

A

In order (1-4)

No - NKCC2
Regular - ROMK
Cock - CLC-Kb
Block - Barttin Mutation (3/4 same channel)

42
Q

Whom does gitelman syndrome affect

A

Late childhood or adulthood

AR more common than Bartter

43
Q

What are the clinical manifestations of Gitelman syndrome

A

Severe hypokalemia
Metabolic Alkalosis (saline non-responsive)
Low to normal BP
Hypocalciuria (opposite bartter syndrome)
Hypomagnesemia

44
Q

Whom is affected by liddle syndrome

A

young patients with HTN and electrolyte abnormalities

rare AD disease

45
Q

What are the clinical manifestations of Liddle syndrome

A

Resistant HTN
Hypokalemia
Metabolic Alkalosis (saline non-responsive)

46
Q

Describe the pathophysiology of liddle syndrome and the treatment

A

Mutation in the ENaC channel increasing their number

Treat with Amiloride or triamterene, low salt diet

don’t use spironolactone