Drugs Acting on Central Nervous System

• Clinical Pathology of Enteric Inflammation:
• Enteritis is inflammation of the intestinal mucosal lining caused by infectious agents (rotavirus, coronavirus, Salmonella, E. coli, coccidia) or dietary irritants.
• Disruption of the mucosal architecture (villous atrophy, crypt hyperplasia, and loss of brush-border disaccharidases) results in malabsorption and hypersecretion.
• The direct, hallmark clinical manifestation of this fluid and electrolyte transport failure is profuse Diarrhea (scours), accompanied by dehydration and metabolic acidosis.
• nalysis:
• (Diarrhea): Correct primary clinical sign.

Correct option: (2) Diarrhea

• Mechanisms of Jaundice (Icterus):
• Hemolytic (Pre-Hepatic) Jaundice: Arises from excessive intravascular or extravascular breakdown of erythrocytes, overwhelming the hepatic capacity for bilirubin conjugation:
• Caused by hemoparasites (Babesia, Anaplasma), isoimmune hemolytic anemia, and Bacterial toxins (e.g., Clostridium perfringens type A alpha-toxin phospholipase C, Leptospira interrogans hemolysins) that directly lyse erythrocyte cell membranes.
• Biliary calculi cause post-hepatic obstructive jaundice; hepatic fibrosis causes hepatic jaundice.
• nalysis:
• (Bacterial toxins): Correct cause of hemolytic icterus.

Correct option: (3) Bacterial toxins

• Ruminal Metabolism and Toxic Activation:
• Cyanogenic Glycosides (e.g., dhurrin in immature sorghum/jowar, linamarin in linseed/flax):
• Intact cyanogenic glycosides are relatively non-toxic when consumed.
• In the rumen, microbial $\beta$-glucosidase and hydroxynitrile lyase enzymes rapidly hydrolyze the glycosides, liberating free, lethal Hydrocyanic Acid (HCN / Cyanide):

• Free cyanide binds ferric iron ($Fe^{3+}$) in cytochrome oxidase, arresting cellular respiration. Hence, ruminal metabolism directly intensifies its toxicity.
• nalysis:
• (Cyanogenic glycosides): Correct.

Correct option: (3) Cyanogenic glycosides