16 - Acid-base disorders Flashcards

1
Q

Henderson-hasselbalch equation

A

H + HCO3 -> H2CO3 -> CO2 + H2O

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2
Q

Tissue gas exchange

A

Cl- in put into an RBC when CO2 is reacted with hydrogen in order to maintain charge

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3
Q

What happens when you shift to the right on the O2-Hb dissociation curve

A

Increased 2,3 diPG
Acidosis (H+)
Increased Temperature

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4
Q

To maintain charge in kidneys what in inputed

A

Na+ with HCO3-

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5
Q

Mineralocorticoid action in the kidney

A

K+/H+ go in at distal renal tubule and Na+ goes out

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6
Q

Acid-base in the GI tract

A

H+ goes to stomach

Hydrogen carbonate goes to pancreas

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7
Q

Acid-base balance and the liver

A

Dominant site of lactate metabolism

Only site of urea synthesis

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8
Q

Acid-base balance - liver rxns

A

1: proteins catabolised to NH4+ and HCO3-
2: Average proteins produce a slight XS NH4+ (balance of dicarboxylic, dibasic, neutral a/a)
3: role of urea cycle is to combine NH4+ and CO2 to neutralise HCO3 - from protein catabolism

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9
Q

Acid-base balance - severe liver failure

A

NH4 + oxo-glutarate cannot form glutamine

NH4 and CO2 cannot form urea

Metabolic alkalosis with ammonium toxicity

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10
Q

Why is it metabolic alkalosis in severe liver failure?

A

2NH4 + HCO3 -> (NH2)2CO + H+

LHS is acid
RHS is base

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11
Q

Compensatory mechanisms for acid-base balance

A

Resp.
Renal bicarb regen
Hepatic shift between urea synthesis and ammonia excretion

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12
Q

Metabolic acidosis - what happens

A

Increased H+ formation
Acid ingestion
Reduced renal H+ excretion
Loss of bicarb

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13
Q

Metabolic acidosis - blood gas affects

A

[H+] up
pCO2 down
pO2 up

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14
Q

Metabolic alkalosis - what happens

A

generation of bicarb by gastric mucosa
Renal generation of HCO3- in hypokalaemia
Administration of bicarb

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15
Q

Metabolic alkalosis - blood gas affects

A

[H+] down
pCO2 up
pO2 down

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16
Q

Metabolic alkalosis - consequences

A

K+ goes into cells and urine
PO4 goes into cells
Resp. suppression

17
Q

Resp. acidosis - what happens

A

CO2 retention due to:
inadequate ventilation
parenchymal lung disease
inadequate perfusion

18
Q

Resp. acidosis - blood gas effects

A

[H+] up
pCO2 up
pO2 down

19
Q

Resp. alkalosis - what happens

A

Increased CO2 excretion due to excessive ventilation producing alkalosis

20
Q

Resp. alkalosis - blood gases

A

[H+ down]
pCO2 down
pO2 up

21
Q

Metabolic acidosis causes

A

increased H+ formation
Acid ingestion
Reduced renal H+ excretion
Loss of bicarbonate

22
Q

Causes of increased [H+]

A

ketoacidosis, diabetic or alcoholic
lactic acidosis
poisoning
inherited organic acidoses

23
Q

Diabetic ketoacidosis

A

Hyperglycaemia
Osmotic diuresis -> pre-renal uraemia
Hyperketonaemia
Increased FFA -> all lead to acidosis

24
Q

Lactic acidosis types

A

Type a = shock

Type b = metabolic and toxic causes

25
Q

Acidosis in an alcoholic

A
NAD+ depletion (thiamine)
Thiamine deficiency (PDH co-factor)
Enhanced glycolysis for ATP formation
Keto-acids secondary to counter-regulatory hormones
CAUSES PROFUSE VOMITING
26
Q

Does high lactate = lactic acidosis? In alkalosis

A

Increased glycolysis
Reduced O2 delivery due to shift in O2 dissociation curve
Lactate induced vasoconstriction
Impaired mitochondrial resp.

27
Q

Does high lactate = lactic acidosis? O2 debt to #2

A

Further anaerobic lactac
te production
Hyperventilation

28
Q

Renal failure effects

A
Reduced volume of nephrons
Increased bicarb loss
Reduced NH4+ excretion
NH4 to liver for urea + H+ synthesis
Only fraction of NH4+ derived from glutamine