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CPR II Exam 3 > Clinical Approach to Acid-Base Disorders (Selby) > Flashcards

Clinical Approach to Acid-Base Disorders (Selby) Flashcards

1
Q

What enzyme is responsible for producing bicarbonate in the Bicarbonate Buffer System?

Where is it located?

A

Carbonic Anhydrase

  • located in both lung alveoli and tubular epithelial cells
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2
Q

What are the 4 major acid-base disturbances and what are they characterized by?

A

Metabolic ACIDosis = low serum HCO3

Metabolic ALKAlosis = high serum HCO3

Respiratory ACIDosis = high PCO2

Respiratory ALKAlosis = low PCO2

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3
Q

How is each of the 4 metabolic disturbances compensated for?

A

Metabolic Acidosis –> Respiratory Alkalosis
- dec. HCO3 –> dec. PCO2 (inc. RR)

Metabolic Alkalosis –> Respiratory Acidosis
- inc. HCO3 –> inc. PCO2 (dec. RR)

Respiratory Acidosis –> Metabolic Alkalosis
- inc. PCO2 –> inc. HCO3 (inc. reabsorption)

Respiratory Alkalosis –> Metabolic Acidosis
- dec. PCO2 –> dec. HCO3 (dec. reabsorption)

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4
Q

How does HCO3 change during Acute/Chronic Respiratory Acidosis and Acute/Chronic Alkalosis?

A

Respiratory Acidosis

  • A: inc. 1 mEq/L for every 10 mmHg inc in pCO2
  • C: inc. 3.5 mEq/L for every 10 mmHg inc in pCO2

Respiratory Alkalosis

  • A: dec. 2 mEq/L for every 10 mmHg dec in pCO2
  • C: dec. 5 mEq/L for every 10 mmHg dec in pCO2
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5
Q

Acid-Base Stepwise Approach

What are the 4 steps in the approach to pts. with metabolic disturbances?

A
  1. determine if acidosis or alkalosis is present
  2. determine if disturbance is metabolic/respiratory
  3. if metabolic acidosis –> calculate anion gap
    • hypoalbuminemia –> osmolar gap
    • HAGMA –> osmolar gap and delta-delta gap
  4. calculate appropriate compensation
    • compensation appropriate - simple disorder
    • compensation inappropriate - mixed
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6
Q

What are these normal value ranges:

  1. pH in the body
  2. HCO3
  3. PCO2
  4. Anion Gap
  5. Osmolality Gap
A
  1. 7.35 - 7.44
    • acidosis: pH < 7.35
    • alkalosis: pH > 7.44
  2. 24 mEq/L
  3. 40 mmHg
  4. 12
  5. 10 mOsm/kg
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7
Q

How is the Anion Gap calculated and what does it help differentiate?

A

AG = Na - (HCO3 + Cl)
- normal AG = 12 +/- 2

  • clinically used to differentiate HAGMA vs NAGMA
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8
Q

How is the Osmolar Gap calculated?

What is it useful for screening for?

A
  1. calculate serum osmolality (normal = 275-290)
    • 2 (Na) + (Glucose/18) + (BUN/2.8)
  2. calculate osmolar gap
    • measured serum - calculated serum osmolality
    • normal gap < 10 mOsm/kg
    • > 10 mOsm/kg = additional solutes in blood

useful for alcohol ingestion screening –> if AG > 20, be highly suspicious of alcohol ingestion

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9
Q

How is the Delta-Delta Gap calculated?

Why is it performed and what does measuring HCO3 mean?

A
  • used in pts. with HAGMA to determine if coexistent NAGMA or metabolic alkalosis present
  1. Delta Gap = calculated AG - normal AG (12)
  2. Delta HCO3 = normal HCO3 (24) - delta gap
  • HCO3 close to 16 = no additional disturbances
  • HCO3 > 16 = metabolic alkalosis with HAGMA
  • HCO3 < 16 = NAGMA with HAGMA
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10
Q

HAGMA differential diagnosis

What does the GOLD MARK mneumonic mean?

A

G - glycols (ethylene and propylene)
O - oxoproline (acetaminophen toxicity)
L - L lactic acidosis (NORMAL)
D- D lactic acidosis (BACTERIA) must request this

M - methanol
A - aspirin
R- renal failure
K - ketoacidosis (alcohol, diabetes, starvation)

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11
Q

How is Acetaminophen Toxicity diagnosed in pts with HAGMA and how is it treated?

A

Dx: urinary organic acid screen

Tx: discontinue drug, IVF, N-acetylcysteine

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12
Q

What is the differential diagnosis for Increased Osmolar Gap and why are they important to look for?

MEDIE

A

M - methanol
E - ethanol

D - diethylene glycol (diuretics - mannitol)
I - isopropyl alcohol (RUBBING ALCOHOL)
NOT ASSOCIATED WITH METABOLIC ACIDOSIS
E - Ethylene Glycol (ANTIFREEZE)

important because these will KILL YOU if not treated

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13
Q

What does Alcohol Dehydrogenase convert Methanol and Ethylene Glycol into and what clinical issues does this lead to?

A

Methanol –> Formic Acid = BLINDNESS

Ethylene Glycol –> Oxalic Acid = RENAL FAILURE
- crystalize in the urine

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14
Q

What are the two major causes of Normal Anion Gap Metabolic Acidosis (NAGMA)?

A

Diarrhea and Renal Tubular Acidosis

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15
Q

What is Renal Tubular Acidosis and when can it NOT be diagnosed?

What are the 3 classifications of RTA?

A
  • condition where net acid excretion by the kidneys is impaired that CANNOT be diagnosed in the setting of Acute Kidney Injury (AKI)

RTA Type 1 (Distal)
- dec. net H secretion in distal tubules and CDs
RTA Type 2 (Proximal)
- dec. HCO3 reabsorption in proximal tubules
RTA Type 3 (Hyperkalemic RTA) = MOST COMMON
- dec. aldosterone secretion or resistance
- dec. net H/K secretion in collecting duct (CD)

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16
Q

How is the Urine Anion Gap calculated and what is it used to differentiate between?

A

UAG = (UrineNa + UrineK) - UrineCl

  • (-) = appropriate distal nephron urine acid. (Type 2)
  • (+) = inappropriate distal nephron (Type 1 or 4)
  • differentiates renal from non-renal causes of NAGMA and is a marker of NH4Cl excretion
17
Q

Proximal RTA (Type 2)

How does it clinically manifest and what are two ways it is diagnosed?

A

C: NAGMA with or without proximal tubular dysfunction and HYPOkalemia (mild compared to Type 1)

Dx: Urine pH can be high or low (pH < 5.5 when in new steady state) and UAG that is NEGATIVE

18
Q

Distal RTA (Type 1)

What is it, what does it lead to, and what are two conditions that can lead to it other than inherited? (S/T)

A
  • due to dec. net H ion secretion in the distal nephron (H/K ATPase or H ATPase defects) or gradient defect allowing H ions to flow back into tubular cells
    • Amphotericin/fungal infections
  • lack of net H ion secretion prevents urinary acidification and excretion of ammonium
  • can be seen in pts. with Sjogren’s Syndrome and pts. that sniff GLUE (due to Toluene)
19
Q

Distal RTA (Type 1)

How does it clinically manifest and what are 3 ways it is diagnosed?

A

C: nephrolithiasis (kidney stones) and nephrocalcinosis (calcium deposits in parenchyma)

Dx: NAGMA, unable to acidify urine pH < 5.5, HYPOkalemia (SEVERE), (+) UAG

20
Q

Hyperkalemic RTA (Type 4)

What is it and what two things usually cause it?

A
  • distal nephron dysfunction from impaired renal excretion of H and K causing NAGMA and HYPERkalemia
    • deficient circulating aldosterone
    • aldosterone resistance in collecting ducts
  • either above case results in impaired Na reabsorption by principle cells
21
Q

Hyperkalemic RTA (Type 4)

How does it clinically manifest and what are two ways it is diagnosed?

A

C: NAGMA with HYPERKALEMIA (usually asymptomatic though)
- most pts. in 50-70s with Hx of diabetes/CKD

Dx: variable urine pH (usually > 5.5) and (+) UAG

22
Q

What are 5 common causes of Metabolic Alkalosis? (H/V/D/VD/ME)

A 
Hypokalemia
Vomiting or Nasogastric Tube Suction
Diuretics (thiazide or loop diuretics)
Volume Depletion (contraction alkalosis)
Mineralocorticoid Excess

**factors that stimulate Na reabsorption, secondarily inc. H secretion (simulating HCO3 reabsorption leading to metabolic alkalosis)

23
Q

Bartter Syndrome

What is it caused by, what are its 4 clinical manifestations, and how does pathophysiologically develop?

A
  • caused by Auto Recessive disease in PRENATAL/NEONATAL pts (usually death)

C: hypokalemia, metabolic alkalosis (saline NON-responsive), low BP, HYPERcalciuria and nephrocalcinosis

PP: inactivating mutations of Thick-Ascending Loop transporters
- NaCl loss –> volume depletion –> 2nd hyperaldosteronism

24
Q

What are these types of Bartter Syndrome caused by:

Type 1 (N)
Type 2 (R)
Type 3 (C)
Type 4 (B)

What is their net result similar to?

A
  1. NKCC2 mutation
  2. ROMK mutation
  3. CLC-Kb mutation
  4. Barttin mutation

net result is similar to LOOP DIURETIC use

25
Q

Gitelman Syndrome

What is it caused by, how does it manifest clinically (5), and how does it pathophysiologically develop?

What is its net result similar to?

A
  • caused by Auto Recessive disorder and is seen in late childhood/adulthood (MORE COMMON than Bartter)

C: hypokalemia, metabolic alkalosis (saline non-responsive), low BP, HYPOCALCIURIA (opposite of Bartter), HYPOmagnesemia

PP: inactivating mutations of NaCl cotransporter in Distal Convoluted Tubule

net result similar to THIAZIDE DIURETIC use

26
Q

Liddle Syndrome

What is it caused by, how does it clinically manifest (3), and how does it pathophysiologically develop?

A
  • caused by Auto DOMINANT with pts. presenting at young age with hypertension and electrolyte abnormalities

C: RESISTANT HYPERTENSION (on at least 3 agents), hypokalemia, metabolic alkalosis (saline non-responsive)

PP: mutations of ENaC channels in collecting duct of nephron (prevent degradation and removal from luminal surface) –> inc. number of ENaC with inc. urine Na and urine K/H secretion

27
Q

Liddle Syndrome

How is it diagnosed and what is its treatment?

A

Dx: genetic testing and low aldosterone/renin lvls

Tx: amiloride or triamterene (block sodium channels) and low salt diet

CPR II Exam 3 (12 decks)

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