Viva Questions of Water-Electrolyte & Acid-Base Balance

Correlation:

Q: Mention the routes of water excretion in human body. (Topic: Water-electrolyte balance)

A: Urine: 1-2 Ltr/day Skin: Perspiration- 450 ml/day, Lungs: Respiration- 400 ml/day,

Feces: GI tract-150 ml/day

Q: Urine output is controlled by? (Topic: Water-electrolyte balance)

A: Urine output is the Major route of water excretion: controlled by ADH (posterior pituitary hormone). ↑ Plasma osmolality: promotes ADH secretion:  ↑ Water Re-absorption from renal tubules: Less Urine Output.

Q: Plasma osmolality depends on which mineral? (Topic: Minerals)

A: Plasma osmolality depends on sodium concentration; hence Sodium indirectly controls amount of water in the body.

Q: Regulation of water electrolyte balance is function of which organ? (Topic: Organ function Tests)

A: Kidney

Q: Describe role of Renin-angiotensin system in water and electrolyte balance. (Topic: Water-electrolyte balance)

A: Decrease in BP (fall in ECF volume) → Renin (juxtaglomerular apparatus of Nephrons) → Angiotensinogen   → Angiotensin I → Angiotensin II          → Aldosterone.

Interrelationship between renin, Angiotensin and Aldosterone plays an important role in regulation of Na+ Reabsorption. Aldosterone & ADH coordinate together to maintain normal fluid and electrolyte balance.

Q: Angiotensin I & II belongs to? (Topic: Amino Acids & Proteins)

A: Both belongs to biologically important peptides.

Angiotensin I- Decapeptide and Angiotensin II- Octapeptide

Q: Mention other biologically important peptides involved in water-electrolyte balance? (Topic: Amino Acids & Proteins)

A: Bradykinin & kallidin: Nonapeptide and Decapeptide respectively

  • Activated when IVV is increased
  • Causes Natriuresis & Diuresis
  • Action opposite to ADH & Aldosterone.

Q: Mention Polypeptide hormone secreted by Right Atrium of Heart in response to increase IVV, which causes Natriuresis. (Topic: Water-electrolyte balance)

A: ANP Atrial Natriuretic Peptide

 

Correlation:

Q: Mention the first line of defense against pH change? (Topic: Acid-Base Balance)

A: Buffer system

Q: Which is the predominant buffer system of ECF? (Topic: Acid-Base Balance)

A: Bicarbonate buffer

Q: Which is the predominant buffer system of ICF? (Topic: Acid-Base Balance)

A: Phosphate buffer

Q: Mention the minerals which acts as buffers? (Topic: Minerals)

A: Sodium regulates the body’s acid–base balance along with chloride and bicarbonate. It is involved in forming a bicarbonate buffer system (NaHCO3–H2CO3) and a phosphate buffer system (NaH2PO4–Na2HPO4). These buffer systems play an important role in the acid–base balance.

Q: Name the plasma protein which acts as buffer? (Topic: Amino Acids & Proteins)

A: Albumin: Maximum buffering capacity.

Q: Name the amino acid which acts as buffer. (Topic: Amino Acids & Proteins)

A: Imidazole group of Histidine

Q: Define buffer. How it acts? (Topic: Acid-Base Balance)

 

A: Buffers are the solutions which resist change in pH by the addition of small amounts of acids or bases. Any substance that can reversibly bind hydrogen ions can be labelled as a buffer.  Buffers can neither remove H+ ions from the body nor add them to it. They can only keep H+ ions in a temporarily suspended form. Results in a much smaller pH change. Buffer acts quickly but not permanently.

 

Correlation:

Q: Second line of defense against pH Change which acts by CO2 excretion? (Topic: Acid-Base Balance)

A: Respiratory mechanism

Q: What is chloride shift? (Topic: Acid-Base Balance)

A: As concentration of HCO3- increases in RBC, it diffuses into plasma along concentration gradient, in exchange for Cl-, to maintain electrical neutrality- Chloride shift

Q: What is Isohydric Transport? (Topic: Acid-Base Balance)

A: At tissue level, Hb binds H+ ions and helps to transport CO2 as HCO3- with a minimum change in pH. In the lungs, Hb combines with O2, H+ ions are removed which combine with HCO3- to form H2CO3. (CO2 exhaled.)

Q: Mention the Factors affecting Oxygen Dissociation Curve. (Topic: Hemoglobin)

A: Small molecules that influence the O2 binding capacity of Hb are called effectors/modulators.

Negative effectors: 2,3-BPG, CO2, H+, Cl-

Positive effectors: O2

Q: Mention the pathway in which 2,3 BPG is synthesized? (Topic: Carbohydrates)

A: Rapaport-Leubering Cycle: Shunt pathway to glycolysis.

Q: Mention the clinical significance of 2,3 BPG. (Topic: Hemoglobin)

A: Stabilizes deoxygenated Hb by cross linking β- chains. Normally present in RBCs and shift the O2 dissociation curve to the right Favors the O2 dissociation and its supply to tissues. In Hypoxia (high altitude, COPD), Anemia: 2,3 BPG levels are elevated, so increased supply of O2 to tissues.

Q: What is Bohr effect? (Topic: Hemoglobin)

A: Influence of pH and pCO2 to facilitate oxygenation of Hb in lungs and deoxygenation at the tissues is known as Bohr Effect.  Bohr effect causes a shift in the oxygen dissociation curve to the right.

 

Correlation:

Q: Second line of defense against pH Change which acts by H+ excretion? (Topic: Acid-Base Balance)

A: Renal mechanism

Q: Mention the basic mechanisms of renal regulation of pH. (Topic: Acid-Base Balance)

A:

  • Reabsorption of bicarbonate
  • Addition of new bicarbonate to the plasma
  • Excretion of ammonium ions (Half to two-thirds of body acid load is eliminated)
  • Excretion of free H+ ions

Q: Half to two-thirds of body acid load is eliminated in the form of? (Topic: Acid-Base Balance)

A: Excretion of ammonium NH4+ ions

Q: Ammonium NH4+ ions and bicarbonate HCO3- ions are eliminated in the form of? (Topic: Amino Acids & Proteins)

A: As Urea-by-Urea cycle

Q: Mention the significance of urea cycle in pH regulation. (Topic: Amino Acids & Proteins)

A: Detoxification of NH3    

Disposes off two waste products—NH3 & HCO3

Participates in blood pH regulation

Q: Detoxification of ammonia as urea is function of which organ? (Topic: Organ function Tests)

A: Liver function

 

Correlation:

Q: What is anion gap? (Topic: Acid-Base Balance)

A: Unmeasured anions in the plasma (A-); Proteins, phosphate, sulfate, urate.

Q: Mention causes of High Anion Gap Metabolic Acidosis. (Topic: Acid-Base Balance)

A: Lactic acidosis

Keto acidosis (Diabetes, Alcohol, Starvation)

Toxins (Ethylene Glycol, Methanol, Salicylates)

Renal Failure

Q: Mention the mechanism of ketogenesis in starvation & uncontrolled diabetes. (Topic: Integration)

A: Carbohydrate is either unavailable (starvation) or underutilized (diabetes)- Oxaloacetate is unavailable for combining with acetyl CoA Impaired TCA cycle- Acetyl CoA is diverted for KB synthesis.

Q: Mention the mechanism of diabetic ketoacidosis. (Topic: Carbohydrates)

A: Diabetic Ketoacidosis: Acetoacetate & β- hydroxybutyrate: strong acids.

Increase in their blood concentration, lowers the blood pH, leading to condition of Metabolic acidosis called as Diabetic ketoacidosis (DKA).

Q: Mention the biochemical picture in metabolic acidosis. (Topic: Acid-Base Balance)

A: Decrease in bicarbonate (HCO3-), Increase in H+ ions, Decrease in pH

Q: Mention the mechanism of compensation in metabolic acidosis. (Topic: Acid-Base Balance)

A: Respiratory- Hyperventilation (elimination of CO2): H2CO3

Renal excretion of H+ ions.

 

 

 

Correlation:

Q: Mention the biochemical picture in metabolic alkalosis. (Topic: Acid-Base Balance)

A: Increase in bicarbonate (HCO3-), Decrease in H+ ions, Increase in pH

Q: Mention the causes of Metabolic alkalosis. (Topic: Acid-Base Balance)

A: Sustained vomiting, Bicarbonate administration for prolonged periods, Overdose of diuretic drugs, Mineralocorticoids excess (Cushing’s syndrome, Conn’s syndrome)

Q: Mention the effect of Mineralocorticoids excess (Cushing’s syndrome) on serum sodium and potassium levels. (Topic: Minerals)

A: Cushing’s syndrome leads to hypernatremia (Increase in serum sodium levels) and hypokalaemia (decrease in serum potassium levels)

Q: Mention the effect of Mineralocorticoids excess (Cushing’s syndrome) on BMR levels. (Topic: Nutrition)

A: BMR elevated in Cushing’s syndrome

Q: Mention other causes of increase in BMR. (Topic: Nutrition)

A: Fever, Infections, Leukemia, polycythemia, anemia, Cardiac failure, hypertension, dyspnea, Acromegaly (Increased cellular activity), Hyperthyroidism

Q: Mention causes of decreased BMR. (Topic: Nutrition)

A: Addison’s disease (adrenal insufficiency), Hypothyroidism

Q: Mention the mechanism of compensation in metabolic alkalosis. (Topic: Acid-Base Balance)

A: Respiratory compensation– hypoventilation to retain CO2 (hence H2CO3 ↑).

Renal mechanism excretes more HCO3– and retains H+.

 

Correlation:

Q: Mention the biochemical picture in respiratory acidosis. (Topic: Acid-Base Balance)

A: Increase in carbonic acid (H2CO3), Increase in H+ ions, Decrease in pH

Q: Mention the causes of respiratory acidosis. (Topic: Acid-Base Balance)

A: Causes: Chronic

  • Depression of respiratory center – drugs opiates or head trauma
  • Paralysis of respiratory or chest muscles
  • Emphysema, asthma, pneumonia, COPD

Causes: Acute: ARDS, pneumothorax

Q: Name the enzyme used in treatment of emphysema. (Topic: Enzymes)

A: Antitrypsin α-1

Q: Mention the role of eicosanoids (prostaglandin) in treatment of asthma. (Topic: Lipids)

A: PGE- Acts as a bronchodilator; PGF- acts as a bronchoconstrictor.

PGE useful in treatment of bronchial asthma.

Q: Deficiency of which lipid leads to respiratory distress syndrome (RDS).

A: Deficiency of Dipalmitoyl lecithin (Phospholipid) leads to RDS

Q: Mention the mechanism of compensation in respiratory acidosis. (Topic: Acid-Base Balance)

A: Kidneys: excrete hydrogen ion & titratable acidity,

Retain bicarbonate ion and ads up to the alkali reserve of the body.

 

Correlation:

Q: Mention the biochemical picture in respiratory alkalosis. (Topic: Acid-Base Balance)

A: Decrease in carbonic acid (H2CO3), Decrease in H+ ions, Increase in pH

Q: Mention the causes of respiratory alkalosis. (Topic: Acid-Base Balance)

A:

  • Hyperventilation resulting from hysteria and anxiety states cause respiratory alkalosis.
  • Raised intracranial pressure and brain stem lesions cause hyperventilation by stimulating the respiratory centre. Ingestion of certain drugs (Salicylate)
  • Hypoxia occurring in high altitudes, severe anaemic conditions and pulmonary disease.

Q: Mention the role of 2,3 BPG in high altitude/hypoxic conditions. (Topic: Carbohydrates)

A: Role in hypoxia- In presence of 2,3 BPG shifts oxyhemoglobin dissociation curve to right, so oxyhemoglobin unloads more oxygen to tissues. At high altitude, hypoxic conditions, anemia, fetal tissue: 2,3-BPG increases: Enhance the supply of oxygen to tissues.

Q: Mention the factors, which shift oxygen dissociation curve to right. (Topic: Hemoglobin)

A: High 2,3-BPG, High H+, High CO2, High Temperature, HbS

Q: Mention the relation between high altitude and iodine content. (Topic: Minerals)

A: Iodine content in the soil and water is very low in high altitudes.

Q: Mention the mechanism of compensation in respiratory alkalosis. (Topic: Acid-Base Balance)

A: Compensation: Kidneys: conserve hydrogen ion & Excrete bicarbonate ion.

Q: Which is the most common acid-base balance? (Topic: Acid-Base Balance)

A: Respiratory Acidosis

 

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