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Free STEP1 Exam Braindumps (page: 68)

Page 67 of 213
PDF with 845 Questions

The statin class of drugs that are currently used to control hypercholesterolemia function to lower circulating levels of cholesterol by which of the following mechanisms?

  1. increasing the elimination of bile acids, leading to increased diversion of cholesterol into bile acid production
  2. increasing the synthesis of apolipoprotein B-100 (apo ), resulting in increased elimination of cholesterol through the action of low-density lipoprotein (LDL) uptake by the liver
  3. decreasing the absorption of dietary cholesterol from the intestines
  4. inhibiting the interaction of LDLs with the hepatic LDL receptor
  5. inhibiting the rate-limiting step in cholesterol biosynthesis

Answer(s): E

Explanation:

The statin class of cholesterol-lowering drugs all exert their effects on the activity of HMG-CoA reductase.
This enzyme carries out the rate-limiting step in cholesterol biosynthesis. The cholestyramine-based resins are used therapeutically to bind up intestinal bile salts, which increases the excretion of bile (choice A). The net effect of increased bile excretion is increased diversion of cholesterol into bile acid synthesis, thereby lowering circulating cholesterol levels. No current therapy targets synthesis of apolipoprotein synthesis (choice B), decreasing intestinal absorption of cholesterol (choice C), or inhibition of LDL-receptor interactions (choice D).



Which of the following represents the enzyme deficiency that leads to "essential fructosuria"?

  1. fructose-1-phosphate aldolase (aldolase B)
  2. fructose-1, 6-bisphosphate aldolase (aldolase A)
  3. fructokinase
  4. hexokinase
  5. 6-PFK-1

Answer(s): C

Explanation:

Essential fructosuria is an autosomal recessive disorder manifesting benign asymptomology due to a lack of fructokinase. The principal clinical signs of essential fructosuria are hyper-fructosemia and fructosuria.
Deficiency in aldolase B (choice A) results in the clinically severe disorder, hereditary fructose intolerance.
Symptoms include severe hypoglycemia and vomiting after ingestion of fructose. Prolonged fructose ingestion by infants with this disorder will lead to poor feeding, hepatomegaly, vomiting, jaundice, and eventually hepatic failure and death. Aldolase A deficiency (choice B) is very rare and has only been observed associated with erythrocytes and fibroblasts and leads to hemolytic anemia. Hexokinase deficiency (choice D) is also rare and associated with erythrocyte disfuction leading to chronic hemolytic anemia. Deficiency in PFK-1 (choice E) results in the glycogen storage disease known as Tarui disease.
Symptoms of PFK-1 deficiency include exercise-induced cramping and pain, myoglobinuria, and hemolytic anemia.



Clinical evidence indicates aspirin is effective in the control of numerous chronic conditions such as atherosclerosis. The principal cardiovascular benefit from aspirin is due to its ability to reduce the incidence and severity of thrombotic episodes. The anticoagulant effect of aspirin occurs through its ability to inhibit which of the following activities?

  1. cyclooxygenase
  2. fibrin cross-linking by factor XIIIa
  3. phospholipase
  4. thrombin binding to activated platelets
  5. von Willebrand factor

Answer(s): A

Explanation:

The synthesis of the cyclic eicosanoids (the prostaglandins and the thromboxanes) begins with the cyclization of arachadonic acid. This reaction is carried out by the enzyme prostaglandin endoperoxide synthetase. This enzyme has two distinct activities, cyclooxygenase and a peroxidase. The activity of the cyclooxygenase domain is inhibited by a class of compounds referred to as the NSAIDs. Aspirin is of this class of drug and, therefore, inhibits the cyclooxygenase activity. The inhibition of prostaglandin synthesis has a negative effect on the process of coagulation through a reduction in the production of , a potent activator of platelet function. Aspirin also reduces the production of prostacyclin by endothelial cells. is a vasodilator and an inhibitor of platelet aggregation. Since endothelial cells regenerate active cyclooxygenase faster than platelets, the net effect of aspirin is more in favor of endothelial cellmediated inhibition of the coagulation cascade. The action of the steroidal anti- inflammatory drugs occurs through the inhibition of phospholipase (choice C), and inhibition of this enzyme has no direct effect on the coagulation process. The other choices (B, D, and E) are not targets for the action of aspirin.



Gluconeogenesis is an extremely important reaction carried out in hepatocytes allowing for glucose homeostasis in the blood. The primary positive control of hepatic gluconeogenesis is exerted by which of the following?

  1. high acetylcoenzyme A (acetyl-CoA) levels
  2. high adenosine triphosphate (ATP) levels
  3. high citrate levels
  4. low ATP levels
  5. low citrate levels

Answer(s): A

Explanation:

The first step in gluconeogenesis is the formation of oxaloacetate from pyruvate. The enzyme controlling this step is pyruvate carboxylase, an allosteric enzyme that does not function in the absence of its primary effector, acetyl-CoA, or closely related acyl-CoA. Thus, a high level of acetyl-CoA signals the need for more oxaloacetate. If there is a surplus of ATP, oxaloacetate will be used for gluconeogenesis. Under conditions of low ATP, oxaloacetate will be consumed in the citric acid cycle. Citrate is the primary negative effector of glycolysis and the primary positive effector of fatty acid synthesis. High levels of citrate (choice C), but not low levels (choice E), do positively affect the activity of fructose-1, 6-bisphosphatase, one of the bypass enzymes of gluconeogenesis, but this is not the primary site of control, since the carbon atoms must first go through the pyruvate carboxylase reaction. Low ATP levels (choice D) would be reflected in an elevation in ADP levels, and ADP negatively affects the activity of pyruvate carboxylase. High ATP levels (choice B) are necessary in order for gluconeogenesis to proceed, and will negatively affect glycolysis at the level of PFK-1, allowing for an increased net flow of carbon into glucose. However, increased levels of ATP do not directly regulate the enzymes of gluconeogenesis.






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