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17 Cards in this Set

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What is the primary job of the PT re: acid-base regulation?
reabsorb the filtered HCO3-
What are the three primary mechanisms thru which metabolic acidosis occurs?
1. loss of bicarb (diarrhea, PT dysfuntion)
2. decreased renal excretion of H+ (distal renal tubular acidosis, acute/chronic kidney injury)
3. Excess acid intake/production (lactic acidosis, ketoacidosis, etheylene glycol, etc.)
What is the primary mechanism of respiratory acidosis? alkalosis?
primary decrease in minute ventilation --> increase in CO2 i/ the blood --> shifts the equilibrium towards more H+ --> respiratory acidosis

increase in minute ventilation, drop in primary CO2, shift towards consumption of protons --> systemic alkalosis.
What are the two primary mechanisms causing metabolic alkalosis?
- Which mechanism is dependent on the copresentation of impaired renal excretion?
Loss of acid (vomiting, or thru kidney (hyperaldosteronism)

Excess bicarb (NaBiCarb or Citrate admin) --> also requires impaired renal excretion to cause alkalosis
In vomiting, do you lose HCl or Bicarb? diarrhea?
HCl, Bicarb.
Can renal compensation ever return the pH to completely normal in a pt with a primary acid-base dz?

what is going on if you do see a normal pH in a pt with a primary acid-base dz?
No.

There must be another primary dz present.
What is the a) site and b) method of compensation for the following dz:
Met acidosis
Met alkalosis
Resp acidosis
Resp alkalosis
- medulla, increase minute Vent.
- medulla, decrease minute Vent.
- Type A intercalated cells, increase H+ secretion
+ also sensed in the PT, which incrase Bicarb reabsorption.
- Type B ICs, increased HCO3- secretion
What is an equation that can be used to estimate expected pCO2 associated with a given HCO3- decrease?

How about the association worded statement for the same effect for pCO2 < and > 24?
pCO2 = HCO3 + 15

pCO2 = 1.5 x HCO3 + 8(+/-2)
"Winter's equation"

~1.2 mmHg decrease in pCO2 for each 1 meQ/L fall in HCO3- below 24 mEq/L.

0.7 increase in pCO2 for every meQ/L >24
What are the two stages/components of the metabolic response to respiratory alkalosis/acidosis? Timescale for them?
Acute and Chronic
Chronic is 3-5 days after event.
When we measure venous electrolytes, what are the main things we measure? What is the anion gap? Equation?

***What is the normal value?
Sodium, Chloride, and bicarbonate

The amount of anions that aren't actually measured (what Cl and bicarb don't account for)

AG = Na - (Cl + HCO3)

12 mEq/L --> we have to know this
What's on the differential for increased anion gap Metabolic Acidosis?
MUD PIES

Methanol
Uremia
Diabetic ketoacidosis
Pyroglutamic acidosis
Ischemia-Lactate
Ethylene glycol
Salicylate toxicity
What is the basic pathogenesis of Diabetic ketoacidosis?
Insulin deficiency and increase in glucagon --> increased G in blood --> increased liver G production --> adipose tiss breakdown --> met by liver to ketoacids --> metabolic ketoacidosis
What are the types of lactic acidosis and some associated causes?
Type A - hypoperfusion / hypoxia (shock, sepsis, CO poisoning, anemia)

Type B - absense of hypoperfusion / hypoxia (drugs, systemic dz)
What is the Osmolal Gap? If it is high along with a high AG, which etiologides of MUD PIES should be strongly considered?
= MeasuredOsm - CalculatedOsm (the thing about 2xNa(plas) + G/18 + BUN/2.8 from smallgroup)

Methanol & Ethylene glycol
What is the tx for metabolic acidosis caused by ethylene glycol and methanol poisoning?
hemodialysis + compound to inhibit the metabolism of the offending agent.
If you see a pt with metabolic acidosis with a normal AG, what might you think?
renal tubular acidosis
diarrheal state
What is the expect pCO2 used to help calculate?
If you see something like metabolic acidosis, and you want to figure out if there is a concurrent primary respiratory dz (or if the respiratory compensation is normal), use those equations for expected pCO2. If it's around expected, it's probably just normal compensation.