Diabetes and Metabolism Quiz

Question 1

• A patient with type 1 diabetes takes insulin before dinner but doesn't eat.
• After 3 hours, the patient feels shaky, sweaty, and confused.
• This is due to low blood glucose levels.

Question 2

• A patient with type 1 diabetes falls asleep before recognizing symptoms.
• Paramedics are called, and administration of insulin will reverse the effect of unconsciousness.

Question 3

• Caffeine is an inhibitor of cAMP phosphodiesterase.
• Drinking strong espresso coffee results in a prolonged response to glucagon in the liver.

Question 4

• A mutation in pancreatic glucokinase can lead to MODY (maturity-onset diabetes of the young).
• This is due to a reduced ability to raise ATP levels in pancreatic beta cells.

Question 5

• The brain has the highest demand for glucose as fuel.

Question 6

• Glucagon release doesn't affect muscle metabolism because muscle cells lack the specific glucagon receptor.

Question 7

• Tremors, sweating, and rapid heartbeat indicate the release of epinephrine.

Question 8

• A high-carbohydrate meal will result in the lowest level of circulating glucagon shortly after consumption.

Question 9

• To determine if a patient with severe hyperglycemia has type 1 or type 2 diabetes, a C-peptide level should be tested.

Question 10

• High blood glucose levels can lead to cerebral dysfunction due to dehydration.

Question 1

• The primary transporter for fructose from blood to cells is GLUT 5.

Question 2

• A patient with alcoholism and pancreatitis has difficulty digesting starch.

Question 3

• If a type 1 diabetic patient skips insulin injections, red blood cells will be primarily affected.

Question 4

• Digesting flour, milk, and sucrose leads to absorption of glucose, fructose, and galactose into the bloodstream.

Question 5

• A patient with a genetic defect in intestinal epithelial cells will have higher levels of lactose, sucrose, and maltose in the stool after consuming milk and table sugar.

Question 6

• Amylopectin is a carbohydrate containing a-1,6 glycosidic bonds.

Question 7

• Increased fiber intake causes abdominal cramping, bloating, and increased flatulence due to bacterial fermentation of fiber in the colon.

Question 8

• Glucose is the primary carbohydrate form in a diet containing fruits, fruit drinks, milk, honey, and vegetables.

Question 9

• A 10-year-old experiencing diarrhea after a viral gastroenteritis and milk intolerance should temporarily eliminate milk products.

Question 10

• A runner looking for a high glycemic index food choice should select ice cream or malted milk balls.

Question 11/1

• Glucose is the body's primary fuel source for virtually all tissues
• Glycolysis generates energy for cellular survival.

Question 11/2

• Oxidizing one molecule of glyceraldehyde 3-phosphate and forming pyruvate results in two molecules of ATP and two molecules of NADH.

Question 11/3

• Glycolysis generates 2 ATP and 2 NADH, starting with glucose 1-phosphate and producing pyruvate.

Question 11/4

• Glycolysis occurs in all human cells.
• ATP is produced through oxidative phosphorylation.

Question 12/1

• The primary high-energy product of glycolysis is fructose 1,6-bisphosphate.

Question 12/2

• When glycogen is degraded, the resultant glucose 1-phosphate is isomerized to glucose 6-phosphate.

Question 12/3

• Oxidizing glucose 1-phosphate to pyruvate results in 3 ATP and 4 NADH.

Question 12/4

• Glycolysis is central to cellular energy production.
• Pyruvate kinase is the rate-limiting enzyme in glycolysis.

Question 13/1

• The matrix of the mitochondria is the site of most of the reactions in the citric acid cycle.

Question 13/2

• Fructose metabolism and glycolysis share glyceraldehyde 3-phosphate (G3P).

Question 13/3

• A four-week-old infant with frequent vomiting, abdominal tenderness, enlarged liver, and hints of cataracts likely has a positive urine reducing sugar test, indicating a possible deficiency in glucose-6-phosphate dehydrogenase.

Question 13/4

• Measuring intracellular fructose 6-phosphate would help in determining the underlying enzyme deficiency.

Question 13/8

• Metformin reduces hepatic gluconeogenesis.
• Lactic acidosis is not a common complication when using metformin due to the Cori cycle overcoming lactate buildup in the liver.

Question 13/9

• Glucose to glucose 6-phosphate is the step that commits glucose to the glycolytic pathway.

Question 13/10

• Red blood cells produce energy through substrate-level phosphorylation, generating ATP without the use of oxygen.

Question 14/1

• Lactic acidemia can result from a deficiency in the E1 subunit of pyruvate dehydrogenase.

Question 14/2

• Thiamine deficiency can lead to pyruvate buildup and subsequent accumulation of lactic acid.

Question 14/3

• In the TCA cycle, succinate dehydrogenase is unique in that it is directly embedded within the mitochondrial membrane.

Question 15/1

• An individual with reduced activity in a-ketoglutarate dehydrogenase typically has a reduced rate of TCA cycle activity.

Question 15/2

• To maintain electrochemical gradients across the membrane, red blood cells require ATP.

Question 15/3

• Inhibition of the TCA cycle reduces ATP due to a lower rate of electron transport.

Question 16/1

• Loss of Complex III leads to minimal oxygen consumption in isolated mitochondria during electron flow.

Question 16/2

• Use of valinomycin with potassium in the mitochondria eliminates proton gradient formation from malate oxidation.

Question 16/3

• Dinitrophenol (DNP) uncouples oxidative phosphorylation by allowing protons to cross the inner mitochondrial membrane instead of through ATP synthase.

Question 17/1

• Low iron stores cause fatigue and anemia because iron is essential for electron transfer in the electron transport chain.

Question 17/2

• Elevated NADH : NAD+ ratio is observed in OXPHOS defects.

Question 17/3

• Lead interferes with heme synthesis, impacting proteins such as hemoglobin and myoglobin but not complex III.

Question 18/1

• Rotenone is a potent inhibitor of electron transfer involving NADH dehydrogenase or complex I, leading to a significant reduction in ATP production by inhibiting electron flow to downstream complexes.

Question 18/2

• Oxidative phosphorylation relies on NADH and FAD (FADH2) for electrons.
• Oxidative phosphorylation's process generates ATP through electron transfer to oxygen, which is the final electron acceptor in the mitochondria.

Question 19/1

• Complex III has a crucial role as a mediator in the electron transfer chain, particularly in the transport of electrons.

Question 19/2

• Mitochondrial uncoupling proteins (UCPs) can increase body temperature by decreasing the efficiency of ATP production, without affecting the electron transport chain directly.

Question 19/3

• Vitamin E, a powerful antioxidant, protects against radical damage by stabilizing radicals, preventing the damage to macromolecules.

Question 20/1

• Superoxide dismutase catalyzes superoxide radicals into hydrogen peroxide.

Question 20/2

• Vitamin E's antioxidant action involves stabilizing radicals through covalent bonding to neutralize radicals.

Question 20/3

• Iron plays a key role in catalyzing the conversion of hydrogen peroxide to hydroxyl radicals.

Question 21/1

• Mitochondrial DNA has a higher susceptibility to oxidative damage (10 times that of nuclear DNA due to ROS). The absence of histones and increased membrane permeability to reactive oxygen species are responsible for this greater susceptibility.

Question 21/2

• A chronic granulomatous disease patient will have an impaired ability to produce superoxide.

Question 21/3

• Oxidized glutathione is an important aspect for detoxifying in diseases like ALS, where oxidative stress is a major factor.

Question 22/1

• Nitric oxide (NO) is a potent vasodilator. It is involved in ischemic heart disease, infertility, viral infections, and fungal diseases.

Question 22/2

• Ingesting xenobiotics can increase risk for free radical injury through various mechanisms.

Question 22/3

• Foreign materials' metabolic breakdown produces hazardous byproducts like hydrogen peroxide due to the presence of enzymes such as cytochrome P450. These factors can increase free radical injury.

Question 23/1

• The degradation of liver glycogen under glucagon release conditions leads to more glucose 1-phosphate than glucose produced.

Question 23/2

• The shorter-than-normal branches in the liver glycogen of a patient indicates a dysfunction in glycogen phosphorylase.

Question 24/1

• A deficiency of muscle phosphorylase activity would lead to lower lactate levels and preserved glycogen levels in the forearm muscles of patients challenged by exertion.

Question 24/2

• A normal glucose tolerance test will lead to higher glycogen synthase activity, increased ratio of glycogen phosphorylase a to b, etc.

Question 25/1

• Muscle glycogen degradation is triggered by conditions involving high levels of intracellular calcium and increased intracellular glucose-6-phosphate in the event of muscle exercise.

Question 25/2

• The liver and glucose 6-phosphatase control circulating glucose levels under various conditions.

Question 26/1

• Glycogen synthesis and degradation involve different enzyme pathways, so they aren't directly reversible processes. Glycogen synthesis is catalyzed by glycogen synthase, whereas degradation is primarily done through glycogen phosphorylase. Both use UDP-glucose as an intermediate.

Question 26/2

• Glycogen storage diseases generally involve enzyme defects causing conditions like abnormally increased glycogen deposits in various tissues, including the liver.

Question 27/1

• Normal glucose levels in the first two hours after birth generally suggest a normal physiological process.