Mod 2: Acid Base Flashcards

1
Q

Drop in 1pH=

A

NaKpump function 50% dysfunction

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2
Q

Acid enters blood from 5 sources

A
Carbonic acid
Lactic acid
Sulfuric acid
Phosphoric acid
Ketone bodiesmk
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3
Q

Lactic acid byproduct of

A

Anaerobic metabolism of glucose

Caused by poor perfusion /AIDS medication

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4
Q

Sulfuric acid results from

A

Oxidation of sulfur containing amino acids

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5
Q

Phosphoric acid results from

A

Metabolism of phosphoproteins and ribonucleotides

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6
Q

Chemical buffer systems (4)

A

Bicarbonate
Phosphates
Proteins
HGB

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7
Q

Kidneys role in balance (3)

A

Reabsorb bicarbonate
Excrete H
Excrete H as ammonium

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8
Q

Phosphates (buffer)
Inorganic
Organic

A

Inorganic-ECF buffer
HPO4/H2PO4
Organic-ICF Buffers: ATP,ADP, AMP, Glucose1phosphate, 2,3DPG

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9
Q

Proteins as buffers

A

ECF buffers bc negative and bind to hydrogen =hypercalcemia

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10
Q

Hgb as buffer

A

IMPORTANT ICF buffer
H20, co2 on RBC=Carbonic acid=H,HCO3 H is buffered by Hgb
CO2 carried to lungs and expired

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11
Q

Acetazolamide site of action

A

Carbonic anhydrase inhibitor in lumen, blocks reabsorption of hco3, stays carbonic acid cannot go back to cell

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12
Q

When is bicarbonate excreted

A

Plasma bicarbonate reaches 40mEq/L-saturated

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13
Q

Expanded ECF volume affect on HCO3 reabsorption

A

Inhibited=acidic

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14
Q

Depleted ECF affect on bicarbonate absorption

vECF Stimulates what

A

Increased=alkalotic

RAAS stimulated
Angiotensin2 stimulates NAH exchanger in proximal tubule=^reabsorbtion=alkalosis (contraction alkalosis) 2` volume depletion like w loop/thiazide diuretics

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15
Q

Excretion of H as titrateable acid

A

In distal and collecting ducts are H-ATPase and H-K-ATPase
H->Lumen->binds w HPO4(monohphos)= dihydrogenphosphate->
Excreted
1Hgone=1bicarb abosrbed

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16
Q

Excretion of H as ammonium

A

Proximal tubule, ascending loop, collecting ducts
Glutamine+glutaminase= NH4+glutamate
Glutamate->a-Ketoglutarate->CO2+H2O
Eventually into HCO3=reabsorbed

17
Q

Excretion of H as ammonium

NH3 NH4

A

NH3 diffuses, NH4->lumen by NaH exchanger
NH3+H =NH4(excreted or reabsorbed by asc loop->interstitial kidney fluid by substituting for K on NaK2CL transporter
(Inhibited by hyperK)

18
Q

Metabolic acidosis effect on on reabsorption of NH4

A

Enhance

19
Q

NH3 concentration gradient

A

Greater in Kidney interstium than collecting duct lumen, flows into tubule and binds with NH4=excreted

20
Q

Excretion of NH4 Increases as urine pH ____

Helpful when

A

Decreases

When in acidic state

21
Q

CO2 (indirect HCO3)

A

Acid 23-30 alk

22
Q

Hco3

A

21-28

23
Q

Base excess/Deficit

A

Negative =metabolic acidosis

Positive= metabolic alk or resp acidosis compensation

24
Q

Bicarbonate loss from

A

Diarrhea, renal tubular necrosis 2(cant reabsorb)

25
Q

Diminished acid excretion from

A

CKD, Tubular necrosis 1

26
Q

Academia effects

A

vCardiac contractility/output,vBP, ^K

27
Q

High anion gap acidosis=

A

Lactic,keto,acidosis, renal failure

28
Q

Normal anion gap acidosis

A

Hyperchloremic acidosis

GI loss, ^saline, NSAIDS, ACEi, tremthoprim

29
Q

Metabolic alk

A

Hypocal, hypoK,hypoventilation ^pCO2