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Answer2985. #EXPLANATION According to the Rajiv Gandhi Shramik Kalyan Yojana (RGSKY) rules, an insured person who meets the eligibility criteria can claim the unemployment allowance for a maximum of 24 months. These 24 months do not have to be claimed continuously. The minimum duration for each spell of claiming the allowance is 1 month. #HIGHYIELD ⦁ The Rajiv Gandhi Shramik Kalyan Yojana (RGSKY), which provides unemployment allowance under the ESI scheme, came into effect on July 1, 2014. ⦁ Minimum Coverage: To be eligible for the unemployment allowance, the insured person must have been covered under the ESI scheme for at least two years and contributed for a minimum of 156 days in each contribution period. ⦁ Unemployment Due to: The unemployment must be due to closure of the factory/establishment, involuntary retrenchment, or permanent invalidity (not less than 40% arising out of non-employment injury). Benefits: ⦁ Allowance Amount: The unemployment allowance is equal to 50% of the last average daily wages for the first 12 months, and then 25% for the next 12 months, up to a maximum of 24 months during the insured person's lifetime. ⦁ Medical Care: During the allowance period, the insured person and their family are entitled to medical care at ESI hospitals/dispensaries. ⦁ Vocational Training: The ESIC may also provide vocational training to help the insured person find new employment. Claim Process: ⦁ Register for Unemployment: The insured person must register for unemployment within 30 days of losing their job at the nearest ESI branch office. ⦁ Submit Documents: Required documents include proof of employment, retrenchment order (if applicable), medical certificate (for permanent invalidity), and bank account details. ⦁ Verification and Approval: The ESIC will verify the documents and approve the claim if all eligibility criteria are met. ⦁ Disbursement: The allowance will be disbursed monthly through bank transfer or electronic clearing service. ⦁ Additional Points: The allowance can be availed in one spell or in different spells of not less than 1 month each. Other options: ⦁ Option A: The Rajiv Gandhi Shramik Kalyan Yojana (RGSKY), which provides unemployment allowance under the ESI scheme, came into effect on July 1, 2014, not April 1, 2015. ⦁ Option B: The unemployment allowance is equal to 50% of the last average daily wages for the first 12 months, and then 25% for the next 12 months, up to a maximum of 24 months during the insured person's lifetime. ⦁ Option C: During the allowance period, the insured person and their family are entitled to medical care at ESI hospitals/dispensaries. Reference: Park’s Textbook of Preventive & Social Medicine-27th Edition, Page No.769 Ans. D. The allowance can be availed in one spell or in different spells of not less than 1 month.

Answer2984. #EXPLANATION ⦁ The clinical history of the boy matches with datura poisoning and the alkaloids act through atropine and hyoscine blocking acetylcholine receptor producing sympathomimetic or parasympatholytic actions . CNS stimulation occurs in early phase , but depressed in later phases #HIGHYIELD: ⦁ Symptoms begin 30 to 60 minutes after ingestion and may continue for 24 to 48 hours because tropane alkaloids delay gastric emptying and absorption ⦁ All parts of the plant are poisonous with highest concentration of alkaloids found in roots and seeds SIGNS AND SYMPTOMS ⦁ Dryness of mouth ⦁ Dysphagia ⦁ Dysarthria ⦁ Dilatation of cutaneous blood vessels ⦁ Diplopia ⦁ Dry hot skin ⦁ Drunken gait ⦁ Delirium ⦁ Drowsiness ⦁ There can also be ⦁ diminished bowel sounds ⦁ distension of urinary bladder due to urinary retention ⦁ Rapid pulse which is full and bounding , later becomes weak and irregular ⦁ Increased respiration ⦁ Scarlatiniform rash over body ⦁ Amnesia , regarding ingestion is common ⦁ Physiological antidote: Physostigmine salicylate ( reversible acetylcholinesterase inhibitor) ⦁ Given as slow IV ( 0.5 - 1 mg over 5 minutes) with ECG monitoring OTHER OPTIONS: ⦁ Option B. In severe organophosphate toxicity, the prototypical patient may exhibit unresponsiveness, pinpoint pupils, muscle fasciculations, and diaphoresis. Additional symptoms can include emesis, diarrhea, excessive salivation, lacrimation, and urinary incontinence ⦁ Option C. Pollens of parthenium cause asthma (allergic bronchitis), especially in children playing outdoors and in adults and old-age persons. Contact of plant with the body causes dermatitis and the spread of the problem all over the body causes great discomfort ⦁ Option D. Symptoms of barbiturate toxicity commonly include difficulty thinking, decreased level of consciousness, bradycardia or rapid and weak pulse, poor coordination, vertigo, nausea, muscle weakness, thirst, oliguria, decreased temperature, and dilated or contracted pupils. Fatal cases are marked by coma, hypotension (low blood pressure), and respiratory depression (decreased efforts to breathe), evidenced by cyanosis and hypotension. EXTRA EDGE: ⦁ Fatal dose — 1 gm (100 to 125 seeds). ⦁ Fatal period — 24 hours. ⦁ Mydriatic test—The pupil dilates within half an hour, if datura is present ( a drop of solution is put into the eyes of the cat ). ⦁ A person suffering from delirium of datura is not criminally responsible for his acts Reference: Review Of Forensic Medicine And Toxicology ( Including Clinical And Pathological Aspects) , Gautam Biswas, 2nd Edition, Page No. 496 , 497 Reference: Ks Narayan Reddy , Essentials Of Forensic Medicine And Toxicology , 33rd Edition, Page No. 599 , 600 Ans. A. Datura poisoning

Answer2983. #EXPLANATION ⦁ Sevoflurane directly acts on the smooth muscle cells in the bronchioles, causing relaxation. This relaxation leads to dilation of the bronchioles, allowing for easier airflow in and out of the lungs. ⦁ Sevoflurane also inhibit neural activity in the airway, reducing the responsiveness of the airway smooth muscle to constrictive stimuli. By dampening neural signals that promote bronchoconstriction, sevoflurane indirectly promotes bronchodilation. #HIGHYIELD:  ⦁ Respiratory system ( Due to inhalational anesthetics )  ⦁ Ventilation  ⦁ All agents decrease tidal volume and increase the frequency ( respiratory rate) but with increasing doses , frequency also decreases , finally decreasing minute ventilation  ⦁ Ventilatory response are blunted with inhalational agents and maximum is seen with halothane  ⦁ Bronchial muscles:  ⦁ They are bronchodilators , by direct action on bronchial muscles and also by inhibiting central pathways for bronchoconstriction  ⦁ Bronchodilation achieved by inhalational anesthetics is by direct action on bronchial muscles and also by inhibition of central pathways for bronchoconstriction  ⦁ Hypoxic pulmonary vasoconstriction:  ⦁ All inhalational agents are vasodilators , thereby blunting HPV response worsening ventilation perfusion mismatch  ⦁ Nitrous oxide alone is pulmonary vasoconstrictor  ⦁ Ciliary activity: ⦁ All agents except ether decrease ciliary activity , thereby reducing capability of patient to cough out secretion in postoperative period  ⦁ Airway reflexes are depressed and this makes patient vulnerable to aspiration  #OTHER OPTIONS:  ⦁ Option D. Decreasing minute ventilation, has no role in bronchodilation  Reference: Short Textbook of Anesthesia by Ajay Yadav, 6th Edition, Page No 92 Ans: C. Both the above options

Answer2982. #EXPLANATION ⦁ Elevated triglyceride level but normal LDL and HDL cholesterol levels is seen in type I familial dyslipidemia. ⦁ It is due to lipoprotein lipase deficiency. #HIGHYIELD TYPE I DYSLIPIDEMIA ⦁ Type I dyslipidemia (or familial lipoprotein lipase deficiency) is caused by a deficiency of lipoprotein lipase. ⦁ This enzyme exists in capillary walls of adipose and muscle tissue and cleaves triglycerides into free fatty acids and glycerol. ⦁ The enzyme is activated by apolipoprotein C-II, which is found on VLDL cholesterol and chylomicrons. ⦁ Type I dyslipidemia is characterized by an accumulation of triglyceride-rich lipoproteins in the plasma. ⦁ Deficiency in apolipoprotein C-II produces a similar result. OTHER OPTIONS: ⦁ Option A - VLDL cholesterol remnants are removed from the circulation by apolipoprotein E receptors. Thus, apolipoprotein E deficiency (dysbetalipoproteinemia) results in an elevated VLDL cholesterol, triglyceride, and cholesterol levels. Often this disorder manifests with other conditions that cause hyperlipidemia such as diabetes. Xanthomas are often present. ⦁ Option B- LDL cholesterol receptor dysfunction is characteristic of familial hyperbetalipoproteinemia, also known as type II hyperlipidemia. In these cases, plasma LDL cholesterol levels rise, which causes an in- crease in plasma cholesterol; triglyceride levels remain normal. ⦁ Option D- Mixed hypertriglyceridemia (type V) is a dyslipidemia characterized by extremely high triglyceride levels and visibly foamy plasma. Unlike type I, type V is characterized by elevated VLDL cholesterol levels and is thought to be related to a VLDL cholesterol clearance problem. Reference- Harper’s Illustrated Biochemistry,31st Edition , Page No. 240 Ans. C. Lipoprotein lipase deficiency

Answer2981. #EXPLANATION ⦁ Glucose-6-phosphate is a pivotal compound in many pathways. ⦁ Immediately upon entering cells, blood glucose is phosphorylated to glucose-6-phosphate by hexokinase in most cells and by glucokinase in the liver. #HIGHYIELD ⦁ Glucose may only leave a cell in the dephosphorylated form produced by glucose-6-phosphatase, which is only found in liver. ⦁ Glucose-6-phosphate may be the starting point of glycolysis, glycogen synthesis, and the pentose phosphate pathway. ⦁ It can be considered the end point or switching point of glycogenolysis and gluconeogenesis. OTHER OPTIONS: ⦁ Option A- Galactose 1 phosphate is involved in galactose metabolism. ⦁ Option C- Uridine-diphosphoglucose (UDP-glucose) and UDP-galactose are high-energy forms of their respective sugars that are involved in converting galactose-I-phosphate to glucose-1-phosphate (the block in galactosemia) and in donating sugar groups to polysaccharides such as glycogen or glycosaminoglycans. ⦁ Option D- Fructose-6-phosphate is involved in glycolysis and gluconeogenesis. Reference- Harper’s Illustrated Biochemistry,31st Edition , Page No-137 Ans. B. Glucose-6-phosphate