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ACID BASE DISORDERS > ACID BASE DISORDERS > Flashcards

ACID BASE DISORDERS Flashcards

1
Q

What is the bodily PH ?

A

7.4

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2
Q

What are acid base disorders ?

A

Metabolic acidosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis

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3
Q

What is acid base physiology associated with?

What is the rel between H+ and ph?

A

Hydrogen ion balance
ph= -log(H+)
inverse and non linear

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4
Q

What occurs when there is a change in PH?

A

When there is a change of 0.3 units of PH, a change by a factor of 2 occurs in H+

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5
Q

What is the net acid production ?

A

100mmol/day

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6
Q

Types of buffering

A

Good buffering- carbonic anhydrase

Bad buffering-bone, Hgb and plasma proteins

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7
Q

What occurs when the PH is 6.8

A

grand mal seizure or ischaemic bowl disease

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8
Q

Describe the rel of Ph to bicarbonate and Co2

A

Henderson Hesselback’s equation PH = bicarb/c02

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9
Q

Features of metabolic acidosis

A

increase in fixed acids (lactate, acetoacetate and beta hydroxybuturate) in blood
Must occur in same direction
so decrease in plasma

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10
Q

What causes a decrease in plasma bicarbonate?

A

gain in strong acid via endogenous sources; ketoacids

loss of base via kidneys/diarrhea

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11
Q

What can metabolic acidosis be classified into?

A

increased anion gap

normal anion gap

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12
Q

Define anion gap and normal AG ?

A

Cations (sodium plus potassium) minus anions (bicarbonate plus chloride). If
hydrogen ions accumulate, the hydrogen ion is not accounted for on the cation side, but the
decrease in bicarbonate buffer compensation would appear as a bicarb deficit, and the anion
gap would increase

normal AG - 8-12. This is used to diagnose metabolic acidosis

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13
Q

What accounts for a high anion gap?

A

P04, IgA, albumin, lactate
high Anion gap accounts for above (these are the unmeasured anion and cations)
normal anion gap if Cl and HCO3 are the only anions that are elevated

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14
Q

Causes of NAGMA

A

Cl intoxification

  • Cl gas intoxification
  • Hcl intoxification
  • early renal failure
  • dilutional acidosis

Gi loss of HCo3

  • diarrhea
  • surgical drains
  • fistulas
  • uterosigmoidostomy
  • obstructed uteroileostomy
  • cholestyramine

Renal loss of HCO3
-RTA ; proximal distal , hypoaldosteronism

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15
Q

What are the differiental diagnosis of raised anion gap metabolic acidosis?

A
  • lactic acidosis
  • ketoacidosis
  • renal failure
  • poisonings
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16
Q

When does lactic acidosis occur?

A

When there is increased production of lactate by tissues

When there is decreased hepatic metabolism of lactate

17
Q

What are the two types of lactic acidosis and what are their mechanism?

A

A- due to lack of oxygen delivery to tissue i.e tissue hypoxia. This slows mitochondial metabolism and pyruvate is converted to lactate

  • shock - septic,haemorrhagic,neurogenic,cardiogenic
  • resp failure
  • anemia
  • Co poisoning

B- no evidence of tissue hypoxia; carbohydrate metabolism is disabled and excess pyruvate is made
This is typically seen in mitochondial failure which occurs w/ cyanide, thiamine deficiency, malignancy, medications- anti HIV, metformin and aspirin

18
Q

How does lactate form in septic shock?

A

This is driven by endogenous adrenaline that stimulates B2 receptors for aerobic glycolysis. Also seen in extreme exercise

19
Q

Describe renal failure in metabolic acidosis?

A

failure to excrete daily acid intake of 1mmol/kg
acute acidosis occurs
raised AG due to retention of multiple anions

20
Q

What is ketoacidosis?

A

raised anion gap metabolic acidosis due to increase in ketone bodies. This ketone body production occurs due to altered hepatic metabolism of lipids to cause ketogenesis (via beta oxidation of fatty acids)

21
Q

Where can each type of ketone body be found?

A

beta hydroxybutyrate- plasma
acetone- lungs
acetoacetate- kidney – detected by urinary stick tests

22
Q

What causes alcoholic ketoacidosis

A

person who binge drinks then ceases. Ethanol and starvation (due to lack of nutrition as excessive vomiting occurs) are the mainstay of this illness

23
Q

What is the pathophysiology of alcoholic ketoacidosis

A

Due to decreased nutrition, glycogen stores used up and there is a decrease in insulin and increase in glucagon.
Ethanol is converted to acetate in the liver w/ help is NAD+(depletion of this store). The NADH/NAD ratio inhibits gluconeogenesis (thus hypoglycaemia and thus no insulin secretion) and favors production of beta hydroxybutyrate.

The decreased ratio of insulin to glucagon causes altered hepatic metabolism of lipids (beta oxidation of lipids) to form ketone bodies –> acetoacetate via acetyl CoA.

24
Q

What other manifestations occur w alcoholic ketoacidosis

A 
Gi symtoms; haematemesis, maelena, ab pain. nausea 
acidemia may occur
Volume depletion common 
Glucose level low
increased FFA common
25
Q

How do you treat a pt with alcoholic ketoacidosis?

A

Glucose, B vitamins

26
Q

Is insulin used to treat a patient with alcoholic ketoacidosis?

A

NO

27
Q

Explain poisonings

A

These contain ethylene glycol which causes pt to feel intoxicated and leads to acid production(glycolic acid, glyoxalic acid, oxalic acid) -> pt crashes due to circulatory collapse. Essentially alcoholic ketoacidosis occurs

28
Q

What is the basis for treatment of poisonings

A

dialysis used to remove toxic compounds like oxalic acid and B vitamins used to break down toxic compounds

29
Q

What B vitamin is used to breakdown glycolic acid?

A

Thiamine

30
Q

What B vitamin is used for oxalic acid

A

pyridoxine (B6)

31
Q

What is used for formic acid?

A

Folate - B9

32
Q

What are the management principles for poisonings

A

•Clinical suspicion is key.
•Coma, seizures, shock mean generated toxic acids.
•Don’t treat if patient is drunk.
•Don’t just treat a small OG or AG on their own.
•Treatment:
–Isotonic NaHCO3 to keep pH > 7.35 (1C).
–Fomepizole if osmolar gap.
–Dialysis if elevated toxic alcohol, severe acid base disorder or target organ damage.
–B vitamins.

ACID BASE DISORDERS (1 decks)

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