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- 17. Accumulation of high levels of chloramphenicol in newbom that leads to a gray baby syndrome is due to он H .CHCI2 O,N- но chloramphenicol A. Lack of UDP-glucuronosyltransferase B. Renal uptake of metabolized product C. High lipophilicity of chloramphenicol D. Poor absorption of chloramphenicol 16Alpha-glucosidase inhibitors are contraindicated in all of the following cases, except:A. Diabetic ketoacidosisA. Liver cirrhosisB. HypertensionC. Large abdominal herniasD. Ulcerative colitis1. Select the INCORRECT statement about Glutamate dehydrogenase : a. Catalyzes the removal of NH4+ into glutamate b.Catalyzes the incorporation of NH*4 into a-ketoglutarate c. Catalyzes the removal of NH*4 from glutamate C d. Catalyzes the incorporation of NH'4 into a-keto acid
- A deficiency in sorbitol dehydrogenase cause all of the following except: Select one: O a. pathologic alternations related to Diabetes mellitus b. no lactose synthesis O c. lack of sperm motility O d. no fructose synthesis5. Richner-Hanhart syndrome is associated with a defect in which of the following? A. Fumarylacetoacetate hydrolase B. Tyrosine aminotransferase C. p-hydroxyphenylpyruvate hydroxylase D. Homogentisate oxidaseA patient presenting in musty odour and hypopigmentation has also presented with high levels of phenyl pyruvate in their blood. Which enzyme is upregulated? A. Phenylalanine dehydrogenase B. Phenylalanine hydroxylase C. Transaminase D. Arginase
- An infant with corneal clouding has dermatan sulfate and heparan sulfate in his urine. Decreased activity of which of the enzymes listed below would confirm the suspected diagnosis of Hurler syndrome? * A. α-Glucuronidase B. Glycosyltransferase C. α-L-Iduronidase D. Iduronate sulfatase E. None of the given optionsShaded in black-white trait (Glucose-6-phosphate dehydrogenase deficiency) 1. How many males are there? 2. What could be the phenotype of the daughter at III-4? a. does not have the disorder b. carrier c. cannot be determined d. has the disorder 3. What is the probability of having a female offspring with G-6-P dehydrogenase deficiency if the proband marries a woman who is a carrier of the disorder? (Answer in percentage)Match the each enzyme deficiency with their corresponding disease β-hexosaminidase A α -galactosidase Sphigomyelinase β-glucosidase A. Fabry disease B. Tay-Sachs disease C. Niemann-Pick disease D. Gaucher disease
- Indicate what will happen ( increase, decrease or no effect) tothe activity of the enzyme or rate of the metabolic pathway in the given conditions a. release of glucagon in the blood to the activity of carnitine acyl transferase 1 b. high malonyl CoA to the activity of carnitine acyl transferase I C. Epinephrine to the activity og glycogen synthase d. high citrate to the activity of acetyl CoA carboxylase e. high acetyl CoA to ketogenesis1. There are two metabolic routes for the conversion of oxaloacetate to phosphoenolpyruvate (PEP). What factors likely indicate which route is used? Do the two routes have different requirements for cellular energy (e.g. ATP)? 2. Compare the export of glucose from hepatocytes to the import into hepatocytes. 3. Would you expect anaplerotic reactions to be active in the postprandial hepatocyte? Why?1. Briefly explain why an individual with Aldolase B deficiency will suffer from hypoglycemia upon ingestion of fructose. Make sure to mention the affected pathways and explain why these are affected. 2. Briefly explain the mechanism involved when an individual with glucose 6-phosphate dehydrogenase deficiency develops an episode of hemolytic crisis after eating fava beans. Make sure to mention pathways and enzymes involved.