HLK Week 6 Flashcards

1
Q

The most direct measurement of HCO3-:

A

Total venous CO2 (almost all CO2 is stored as HCO3-)

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2
Q

True or false: arterial and venous blood gases will equilibrate during cardiopulmonary arrest.

A

False: arterial blood samples should always be taken for the most accurate measure of pH and PCO2.

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3
Q

Respiratory alkalosis and its compensation:

A
  • Primary defect: PCO2 less than 40, pH greater than 7.4
  • Compensation (acute): 2 mEq decrease in HCO3- for every 10 mmHg drop in PCO2
  • Compensation (chronic): 5 mEq decrease in HCO3- for every 10 mmHg drop in PCO2
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4
Q

Respiratory acidosis and its compensation:

A
  • Primary defect: PCO2 greater than 40, pH less than 7.4
  • Compensation (acute): 1 mEq increase in HCO3- for every 10 mmHg increase in PCO2
  • Compensation (chronic): 3.5 mEq increase in HCO3- for every 10 mmHg increase in PCO2
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5
Q

Metabolic acidosis and its compensation:

A
  • Primary defect: HCO3- less than 24 mEq, pH less than 7.4

- Compensation: 1.3 mmHg drop in PCO2 for every 1 mEq drop in HCO3-

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6
Q

Metabolic alkalosis and its compensation:

A
  • Primary defect: HCO3- greater than 24 mEq, pH greater than 7.4
  • Compensation: 0.7 mmHg increase in PCO2 for every 1 mEq increase in HCO3-
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7
Q

True or false: in a mixed acid-base disorder, there can be multiple metabolic disorders but never more than one respiratory disorder.

A

True

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8
Q

Sources of acid in the body:

A
  • Diet and metabolism (e.g., protein from diet, CO2 from cells)
  • GI (upper gut produces acid, lower gut produces bicarb; net production of acid)
  • Non-volatile acids like HCl and lactic acid
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9
Q

Why does vomiting result in alkalosis, whereas diarrhea results in acidosis?

A

Acid is produced in the upper GI tract and is lost through vomiting. Bicarb is produced int he lower GI tract and is lost through diarrhea.

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10
Q

What makes a buffer good for regulating body acid?

A

The pK needs to be within one unit of the pH.

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11
Q

What regulates the concentration of HCO3- and CO2 in the body?

A
  • HCO3- is regulated by the kidneys

- CO2 is regulated by the lungs

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12
Q

Explain how acidosis produces a low bicarb level.

A

Bicarb is the buffer. As acid is produced it combines with bicarb, lowering bicarb levels.

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13
Q

Explain how a constant level of bicarb is maintained in the body.

A
  • Net renal bicarb regeneration (quantified as net acid excretion)

EQUALS

  • Bicarb lost buffering endogenously produced acid
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14
Q

How do the kidneys reabsorb bicarb, and where does it happen?

A

In the proximal tubule, they secrete H+ into the lumen via the sodium/hydrogen pump, this combines with filtered bicarb to produce carbonic acid, which dissociates into CO2 and water. These are reabsorbed into the renal tubular cells, where they recombine to form bicarb and H+. The bicarb exits into the interstitium, and the H+ is secreted back into the lumen to combine with more bicarb, starting the cycle over again.

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15
Q

Where does production of new bicarbonate occur?

A

In the distal nephron via protonation of phosphate

In the proximal tubule via production of ammonium

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16
Q

Explain how acidosis leads to secretion of ammonium

A

Acidosis stimulates the reuptake of filtered glutamine, which dissociates into bicarb and ammonium. Secreted ammonium lowers acidity.

17
Q

Production of new bicarb is tied to the secretion of which molecules in the kidney?

A
  • HPO4–

- NH4+

18
Q

Which type of casts indicates renal failure?

A

Broad casts

19
Q

Describe the morphology of broad casts:

A
  • Usually 2 - 6 times the size of normal casts

- Appear waxy, granular or cellular

20
Q

Name 2 things that cause alkaline urine:

A
  • Renal tubular acidosis

- UTI

21
Q

Causes of D- versus L-lactate anion gap acidosis:

A
  • D lactate is caused by bacterial overgrowth in the gut
  • L lactate comes from anaerobic respiration

Side note: L lactate acidosis occurs in sepsis because of tissue hypoxia leading to anaerobic respiration

22
Q

An important thing to remember about metabolic alkalosis:

A

Requires both a generation of metabolic alkalosis (loss of H+ through GI or kidneys) and maintenance of alkalosis (impairment in renal bicarb excretion).

23
Q

MOA for sulfonamides:

A

Folic acid synthesis inhibitor

24
Q

MOA for quinolones:

A

DNA topoisomerase II inhibitor

25
Q

MOA for nitrofurantoin:

A

Protein synthesis inhibitor via ribosomal inactivation

26
Q

Mnemonic for remembering the causes of anion gap acidoses:

A
- KUSSMAUL (Kussmaul respirations also seen with acidosis)
K = ketosis
U = uremia
SS = salicylate poisoning
M = methanol
A = alcohol (originally "aethylene")
U = uremia
L = lactic acidosis
27
Q

What would Bactrim be indicated for in the context of this class?

A

UTI

28
Q

What would quinolones be indicated for in the context of this class?

A
  • UTI

- Gonorrhea

29
Q

Mnemonic for causes of anion gap acidosis:

A
GOLDMARK
G = glycols
O = oxyproline
L = L-lactate
D = D-lactate
M = methanol
A = Aspirin
R = renal failure
K = ketosis
30
Q

Mnemonic for causes of respiratory acidosis:

A
CHAMPS
C = CNS diseases
H = hypoxia
A = anxiety
M = mechanical ventilation
P = progesterone
S = Salicylates/sepsis
31
Q

Mnemonic for causes of metabolic alkalosis:

A
CLEVER PD
C = contraction
L = licorice
E = endocrine
V = vomiting
E = excess alkali (GI)
R = refeeding alkalosis
P = post hypercapnia
D = diuretics
32
Q

Causes of leukocyturia:

A

Infxn, neoplasms, AIN, glomerular diseases, strictures, stones, interstitial cystitis

33
Q

Why do granular casts indicate intrinsic kidney disease?

A

They’re composed of degenerating tubular cells, which indicates necrosis.