Answer: Alcohol is metabolized in liver to acetaldehyde (toxic), causing oxidative stress, fatty liver (steatosis), inflammation (alcoholic hepatitis), and eventually scarring (cirrhosis).
- A Alcohol consumption is understood by hepatologists to have essentially little measurable toxic effect on liver cell function, even after decades of sustained, heavy daily consumption by the patient
- B Alcohol is metabolized in liver to acetaldehyde (toxic), causing oxidative stress, fatty liver (steatosis), inflammation (alcoholic hepatitis), and eventually scarring (cirrhosis)
- C Alcohol is understood to exert its primary toxic effects mainly on brain tissue, largely sparing liver cell function, with hepatocytes remaining structurally and functionally normal indefinitely
- D Liver damage caused by chronic, long-term alcohol consumption is usually largely reversible, generally by abstaining from alcohol for a short period of time
Correct answer: B. Alcohol is metabolized in liver to acetaldehyde (toxic), causing oxidative stress, fatty liver (steatosis), inflammation (alcoholic hepatitis), and eventually scarring (cirrhosis)
Explanation: Alcohol metabolism pathway: ethanol → acetaldehyde (alcohol dehydrogenase) → acetate (aldehyde dehydrogenase). Acetaldehyde is highly toxic: forms protein adducts, causes oxidative stress, mitochondrial damage, activates hepatic stellate cells. Progression: fatty liver (reversible) → alcoholic hepatitis → cirrhosis (irreversible scarring) → liver failure/hepatocellular carcinoma.
The Plasmodium parasite needs both hosts: the female Anopheles mosquito injects sporozoites while biting (infecting the human liver and RBCs, causing the malaria fever cycle), then picks up gametocytes from an infected person's blood, completing the parasite's sexual stage inside the mosquito.
Concept context
Pathogens, infectious diseases, non-infectious diseases, drugs, cancer, and public health. High NEET importance.