a. ↓ Bicarb b. ↑K c. Ketonuria d. pH 7.5
Probable Answer: pH 7.5 Explanation: See also next page pH > 7.45 → alkalaemia
< 7.35 → acidaemia
PaCO2 > 40 mmHg – respiratory acidosis
< 40 mmHg – respiratory alkalosis HCO3- < 24 mmol l-1 – metabolic acidosis
> 24 mmol l-1 – metabolic alkalosis.
In metabolic alkalosis potassium is decreased.
99. ↓pO2 +↑pCO2 occur in a. Pulmonary edema.
b. CHF.
c. Pneumonia
d. Salicylate poisoning e. High attitude.
Probable answer: Pulmonary edema
PaO2 is indicator of Oxygenation and Pa CO2 is indicator of Alveolar Ventilation.
Thus, a low pO2 indicates hypo-oxygenation and a high pCO2 indicates hypoventilation (or respiratory acidosis). This occurs in causes of respiratory acidosis (see next page)
CHF and pneumonia cause respiratory alkalosis.
Salicylate poisoning causes metabolic acidosis with stimulation of respiratory center and ↓pCO2 → compensatory alkalosis.
High attitude cause hypoxia but not hypercapnia.
Acid Base and ABG
c. Respiratory acidosis.
d. Respiratory alkalosis.
e. Thiazide diuretics.
Probable answer: Laxative abuse
↓ K + ↓bicarbonate → Chronic laxative abuse can cause Low potassium with metabolic acidosis
↓ K + ↑bicarbonate → excessive frusemide therapy
In renal failure K is high due to retention
Thiazides: Excessive use of furosemide will most likely lead to a metabolic alkalosis due to hypochloremia and hypokalemia.
101. If arterial blood is left at room temperature, pH changes by temperature about:
a. Decreases 0.02 -0.03 unit PH per hour
b. Increases 0.02-0.03 units pH per hour.
c. Doesn’t change.
d. Decreases 0.2-0.3 units pH per hour.
e. Increases 0.2-0.3 units pH per hour.
Probable answer: 0.02 -0.03 unit PH per hour Explanation:
Turnaround time for ABG sample:
- Turnaround time: < 15 min
- If delay is anticipated, the syringe or tube containing the blood should be immersed in a mixture of ice and water until analysis.
Effects of delay on ABG results:
In freshly drawn blood with a normal PO2 that is maintained anaerobically, cell respiration causes:
at 2 - 4 oC At RT at 37°C
↓PO2 ↓2 mmHg/h ↓5 - 10
mmHg/h
↑PCO2 ↑0.5 mmHg/h ↑1 mmHg/h ↑5 mmHg/h
↓pH (accompanied by ↓glucose ↑
102. Respiratory acidosis occurs in:
a) Pulmonary fibrosis.
b) Lactic acidosis.
c) Pneumonia, d) Pulmonary emboli,
Probable answer: Pulmonary fibrosis Causes of respiratory acidosis include:
Respiratory center depression
Respiratory tract Others
- Drugs, - CNS tumors,
- Infections, trauma of CNS e.g. encephalitis, CVA, - 1ry central
- Pulmonary infections, - Effusion,
Lactic acidosis causes metabolic acidosis. Pneumonia and pulmonary emboli cause respiratory alkalosis.
103. In acidosis the following never occurs:
a) Hypokalemia b) Hyperkalemia.
c) Hyponatremia.
d) Hypernatremia.
Probable answer: Hypokalemia.
In acidosis, H+ shifts intracellularly and K+ shifts outwards to maintain electrical neutrality → K+ concentration rises 1.2 to 1.7 mmol/L for every 0.1 unit drop in pH.
Acid Base and ABG
C
hemistryMETABOLIC ACIDOSIS RESPIRATORY ACIDOSIS RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS
Causes:
- H+ excretion - H+ production - Bicarbonate loss.
- Bicarbonate dilution.
Types :
Normal AG metabolic acidosis:
Loss of HCO3
or ingestion of acid, e.g.
- Diarrhea, pancreatic fistula.
- RTA.
- Addison's disease.
- Drugs, e.g. carbonic anhydase inhibitors
Raised AG metabolic acidosis:
Accumulation of acids, e.g.:
- DKA
- Lactic acid, e.g. shock, infection.
- Drugs/toxins, e.g. salicylates, ethylene glycol, methanol.
Causes:
Respiratory center depression:
- Drugs, - CNS tumors,
- Infections, trauma of CNS e.g.
encephalitis, CVA, - 1ry central hypoventilation.
Respiratory tract:
- COPD,
- Pulmonary fibrosis, - Status asthmaticus, - Tumour,
- Pulmonary infections, - Effusion,
- ARDS,
- Chest wall diseases.
Others:
- Abdominal distention e.g. extreme obesity, ascites
- Sleep apnea.
Causes:
Nonpulmonary stimulation of respiratory center - Anxiety,
- Febrile states, - Gram--ve septicaemia, - Metabolic encephalopathy.
- CNS infections - Hypoxia, - Salicylates,
- Progesterone; pregnancy - Hyperthyroidism
Pulmonary disorders - Pneumonia,
- Asthma,
- Pulmonary emboli, - Interstitial lung disease, - Congestive HF
Ventilator-induced hyperventilation - Respiratory compensation after
correction of metabolic acidosis.
Causes:
1. Addition of HCO3- to the blood.
2. Loss of HCl, K+ or Cl -3. Cl- deficiency.
4. Volume depletion – post operative diuresis
5. Mineralocorticoid excess
6. Transfusion of large volumes of packed RBCs (Citrate metabolized to
bicarbonate)
CI responsive metabolic alkalosis
Prolonged vomiting or nasogastric suction.
Pyloric or upper duodenal obstruction.
Prolonged loop diuretic therapy.
Villous adenoma (unregulated secretion of HCI).
CI resistant metabolic alkalosis
Mineralocorticoid or glucocorticoid:
- 1ry or 2ry hyperaldosteronism.
- Bilateral adrenal hyperplasia - ACTH-producing adenoma
(Cushing's disease).
- 1ry adrenal adenomas producing glucocorticoids (Cushing's syndrome) or aldosterone.
Metabolic Acidosis Respiratory acidosis with renal compensation
HCO3- 23-30 m Eq /L
Respiratory alkalosis with renal
compensation Metabolic Alkalosis
<24 24 >24 <24 24 >24
Metabolic with respiratory
compensation Respiratory Acidosis
pCO2
35-48 mmHg
Respiratory Alkalosis Metabolic with renal compensation
<40 40 >40 <40 40 >40
Panic acidosis Acidosis pH
7.39 - 7.41 Alkalosis Panic alkalosis
7.2 7.35 7.4 7.45 7.6
Liver
C
hemistryLiver
104. An obese middle aged female is complaining with acute right hypochondrial pain with jaundice, what to do first?
a. Albumin b. CBC c. LFT
d. PT and PTT.
e. Stool.
f. Urine analysis.
Probable answer: urine analysis.
Fatty middle aged female, with acute severe pain in right
hypochondrium and jaundice is most probably suffering of CBD stones
CBC showing ↑WBCs may be more relevant with acute appendicitis.
Urine in CBD stones is +ve for bilirubin (presence of conjugated bilirubin) and negative for urobilinogen. Although urine dipsticks do not measure –ve urobilinogen levels & only measure normal or elevated amounts (only measured by quantitative test), however, a case of jaundice associated with high bilirubin and is not associated with increased urobilinogen is most probably obstructive.
Stool analysis shows steatorrhea which is not diagnostic for the case.
Liver function tests is another choice:
1. Bilirubin: ↑ with 75% conjugated
2. GGT: Most significantly elevated by obstructive disease and its specificity to obstruction is increased with increased ALP.
3. ALP: is elevated to 2x – 4x in diseases or damage of the ducts with cholestasis.
4. AST & ALT: elevated with both intra- & extra- hepatic cholestasis.
PT is prolonged if cholestasis is prolonged and not early.
105. Which test is increased in the preecteric period of viral hepatitis,?
a. Serum bilirubin.
b. Urinary bilirubin c. ALP
d. Albumin e. GGT
Probable answer: Urinary bilirubin
The clinical course of acute viral hepatitis has three major phases: