Diabetes Management and Physiology Quiz
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Questions and Answers

A patient with type 1 diabetes mellitus takes an insulin injection before eating dinner but then gets distracted and does not eat. Approximately 3 hours later, the patient becomes shaky, sweaty, and confused. These symptoms have occurred because of which one of the following?

  • Increased glucagon release from the pancreas
  • Decreased glucagon release from the pancreas
  • Elevated ketone-body levels
  • High blood glucose levels
  • Low blood glucose levels (correct)
  • Concerning our patient in question 19.1, if the patient had fallen asleep before recognizing the symptoms, the patient could lose consciousness while sleeping. If that were to occur and paramedics were called to help the patient, the administration of which one of the following would help to reverse this effect?

  • Epinephrine (correct)
  • Triglycerides
  • Insulin
  • Normal saline
  • Short-chain fatty acids
  • Caffeine is a potent inhibitor of the enzyme cAMP phosphodiesterase. Which one of the following consequences would you expect to occur in the liver after drinking two cups of strong espresso coffee?

  • A prolonged response to glucagon (correct)
  • A reduced rate of glucose export to the circulation
  • An enhancement of glycolytic activity
  • A prolonged response to insulin
  • An inhibition of PΚΑ
  • Assume that an increase in blood glucose concentration from 5 to 10 mM would result in insulin release by the pancreas. A mutation in pancreatic glucokinase can lead to MODY because of which one of the following within the pancreatic ẞ-cell?

    <p>A reduced ability to raise ATP levels (E)</p> Signup and view all the answers

    Flashcards

    Glycogen Degradation in Liver

    When glucagon is released, glycogen breakdown in the liver predominantly produces glucose, not glucose 1-phosphate.

    Glycogen Branching Defect

    A deficiency in amylo-1,6-glucosidase (debranching enzyme) would disrupt the normal branching pattern of glycogen, leading to shorter branches.

    Muscle Phosphorylase Deficiency

    Muscle phosphorylase deficiency impairs glycogen breakdown in muscle, leading to lower glycogen levels during exercise.

    Glucose Tolerance Test

    After a glucose load, a normal individual exhibits enhanced glycogen synthase activity in the liver, promoting glycogen synthesis.

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    Type 1 Diabetes and Glycogen Metabolism

    In prolonged insulin deficiency and lack of food intake, hepatic glycogen breakdown is activated, and the liver is actively releasing glucose to maintain blood sugar.

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    Muscle Glycogen Breakdown

    Muscle glycogen breakdown is typically triggered by high levels of intracellular calcium, signaling muscle contraction and energy demand.

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    Liver Glucose 6-phosphatase

    Liver glucose 6-phosphatase is essential for maintaining normal blood glucose by converting glucose 6-phosphate back into glucose.

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    Glycogen Synthesis Energetics

    Glycogen synthesis requires energy (ATP) to fuel UDP-glucose formation, a key precursor for glycogen synthesis.

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    Glycogen Storage Diseases

    Glycogen storage diseases often involve the liver and can cause hepatomegaly (enlarged liver).

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    Normal Newborn Blood Glucose

    A baby's blood glucose levels at 1 and 2 hours after birth are within the normal range for a healthy newborn.

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    Insulin Deficiency and Glycogen Metabolism

    A patient with type 1 diabetes, who has neglected to take insulin, will have increased levels of glucagon and decreased levels of insulin. This leads to increased glycogen breakdown by the liver. The absence of insulin will inhibit glucose uptake by cells, which will result in a very low level of blood glucose. This can lead to the ketoacidosis that is another hallmark of diabetic ketoacidosis. The metabolic consequences of insulin deficiency will include the stimulation of glycogen breakdown in the liver to increase glucose levels in the blood, and the stimulation of gluconeogenesis in the liver to generate new glucose as well.

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    Glycogen Synthesis Initiation

    The enzyme responsible for the initiation of glycogen synthesis, glycogenin, forms a primer for the addition of glucose residues.

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    Glycogen Debranching

    The final step in glycogen degradation, catalyzed by amylo-1,6-glucosidase, removes glucose residues attached by α-1,6 linkages.

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    Insulin and Glycogen Metabolism

    Insulin stimulates glycogen synthesis by activating glycogen synthase and inhibiting glycogen phosphorylase.

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    Glucagon and Glycogen Metabolism

    Glucagon acts as a signaling molecule that activates protein kinase A (PKA), leading to phosphorylation of glycogen phosphorylase and its activation.

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    Glycogen Phosphorylase Forms

    Glycogen phosphorylase a is the active form of the enzyme, while glycogen phosphorylase b is inactive.

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    Glucose 6-Phosphatase

    The enzyme glucose 6-phosphatase is responsible for converting glucose 6-phosphate back into glucose, allowing its release from the liver into the bloodstream.

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    Liver's Role in Glucose Homeostasis

    The liver's ability to release glucose into the bloodstream is crucial for maintaining normal blood glucose levels.

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    Glycogen Regulation

    Glycogen synthesis and degradation are tightly regulated to ensure appropriate glucose levels in the body.

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    Glycogen Storage Diseases

    The glycogen storage diseases are caused by defects in various enzymes involved in glycogen metabolism, leading to abnormal glycogen accumulation or breakdown.

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    Glycogen Storage Disease Symptoms

    Glycogen storage diseases can result in a variety of symptoms, including hypoglycemia, hepatomegaly, and muscle weakness, depending on the specific enzyme affected.

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    Key Enzymes in Glycogen Metabolism

    Glycogen synthase activity is critical for glycogen synthesis, while glycogen phosphorylase activity is important for glycogen breakdown.

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    Liver and Blood Glucose Regulation

    The liver plays a major role in maintaining blood glucose homeostasis, through glycogen storage and release, and gluconeogenesis.

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    Insulin and Glucagon

    Both insulin and glucagon are key hormones in regulating blood glucose levels, with insulin promoting storage (glycogen synthesis) and glucagon promoting breakdown (glycogenolysis).

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    Gluconeogenesis: Making New Glucose

    The liver's ability to synthesize glucose from non-carbohydrate sources, such as lactate and amino acids, through gluconeogenesis, is crucial for maintaining blood glucose levels during fasting.

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    Glucose 6-Phosphate Metabolism

    Glucose 6-phosphate, a product of glycogen breakdown and glycolysis, can be further metabolized to enter the pentose phosphate pathway or be converted to glucose by glucose 6-phosphatase.

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    Cori Cycle: Recycling Lactate

    The Cori cycle refers to the interconversion of lactate and glucose between muscle and liver, enabling the replenishment of glucose stores in the liver.

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    Glycogen Breakdown: Signaling

    Glycogenolysis, the breakdown of glycogen, is stimulated by glucagon and epinephrine. These hormones activate protein kinase A (PKA), which phosphorylates and activates glycogen phosphorylase, leading to the release of glucose from the liver into the bloodstream.

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    Glycogen Storage Diseases: Overview

    Glycogen storage diseases are a group of inherited metabolic disorders caused by defects in enzymes involved in glycogen metabolism. These defects can lead to the accumulation of abnormal glycogen in various tissues, resulting in a variety of clinical symptoms.

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    Glycogen Storage Diseases: Tissues Affected

    The glycogen storage diseases can affect different tissues, including the liver, muscles, and heart, depending on the specific enzyme defect. These diseases can cause hypoglycemia, hepatomegaly, muscle weakness, and other clinical manifestations.

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    Glycogen Metabolism: Regulation

    Glycogen synthesis and degradation are tightly regulated processes involving a complex interplay of enzymes, hormones, and signaling pathways. This regulation ensures that blood glucose levels remain within a normal range for optimal cellular function.

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    Study Notes

    Question 1 Summary

    • A patient with type 1 diabetes who skips dinner and then experiences symptoms like shakiness, sweating, and confusion after 3 hours, is likely due to low blood glucose levels.
    • Elevated ketone body levels are also a possibility, but the initial symptoms suggest low blood sugar.

    Question 2 Summary

    • If a type 1 diabetic patient, who falls asleep before recognizing symptoms of low blood sugar (hypoglycemia), experiences loss of consciousness, intravenous fluids such as normal saline could be used to help reverse the hypoglycemic effect.
    • Administering insulin is the correct choice for treating hypoglycemia.

    Question 3 Summary

    • Caffeine inhibits the enzyme cAMP phosphodiesterase.
    • Consuming two cups of strong espresso coffee would likely lead to a prolonged response to glucagon in the liver.

    Question 4 Summary

    • A mutation in pancreatic glucokinase can cause Maturity-Onset Diabetes of the Young (MODY).
    • A reduced ability to raise cAMP levels within pancreatic beta cells is a possible cause.

    Question 5 Summary

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

    Question 6 Summary

    • Glucagon does not affect muscle metabolism because muscle cells lack the glucagon receptor.

    Question 7 Summary

    • Tremors, sweating, and rapid heartbeat in a male patient with fasting hypoglycemia are symptoms of low blood sugar.
    • These symptoms suggest a release of epinephrine (adrenaline).

    Question 8 Summary

    • A meal high in carbohydrates (e.g., high-carbohydrate meal) results in lower levels of circulating glucagon because of a reduced rate of protein breakdown and gluconeogenesis.
    • A high-carbohydrate meal leads to relatively lower levels of circulating glucagon.

    Question 9 Summary

    • In a patient admitted to the hospital for a coma caused by severe hyperglycemia (high blood sugar), testing the C-peptide level can help differentiate between type 1 and type 2 diabetes.

    Question 10 Summary

    • High blood glucose can result in cerebral dysfunction, often because of dehydration-related factors.

    Question 1 Summary

    • A high blood glucose concentration (5 to 10 mM) in the pancreas likely triggers insulin release.

    Question 1 Summary

    • The facilitative transporter responsible for fructose transport from blood to cells is GLUT5.

    Question 2 Summary

    • Patients with alcoholism who exhibit discomfort after high-carbohydrate meals and impaired exocrine pancreatic function likely have a reduced ability to digest starch.

    Question 3 Summary

    • After digesting flour, milk, and sucrose, the primary carbohydrate products entering the bloodstream are glucose, fructose, and galactose.

    Question 4 Summary

    • Patients with a genetic defect leading to impaired disaccharidase activity will exhibit higher levels of undigested sugars (maltose, sucrose, and lactose) in their stool after consuming a bowl of oatmeal, milk, and table sugar.

    Question 5 Summary

    • Amylopectin, a type of starch, is characterised by having a-1,6 glycosidic bonds.

    Question 6 Summary

    • When a patient increases the fiber intake in their diet, abdominal cramping, bloating, and flatulence could be caused by the presence of bacteria in the colon which convert fiber into gases such as CO2 and methane.

    Question 7 Summary

    • Increased dietary fiber consumption can lead to increased flatulence due to bacterial fermentation in the colon.

    Question 8 Summary

    • A patient with diabetes who limits simple sugars, but consumes fruits, fruit juices, and milk (sources of fructose/glucose) will primarily be consuming glucose.

    Question 9 Summary

    • A 10-year-old patient experiencing nausea, abdominal pain, and flatulence after consuming milk is likely suffering from lactose intolerance.
    • The best advice for the patient is to avoid milk products for a period to observe for improvement. If symptoms persist, further testing and advice from a doctor are required.

    Question 10 Summary

    • Foods high in glycemic index, like ice cream and malted milk balls, provide a quick source of glucose for the runner's "carb loading" efforts (pre-race energy boost).

    Question 1 Summary

    • Glycolysis is the breakdown of glucose. The main role is to produce energy (ATP and NADH) essential for cellular function.

    Question 2 Summary

    • Glyceraldehyde-3-P reacts with inorganic phosphate and NAD+ to form 1,3-bisphosphoglycerate and NADH.
    • The net yield of ATP and NADH at the end of glycolysis is 2 ATP and 2 NADH.

    Question 3 Summary

    • The net yield of ATP during glycolysis when starting with glucose 1-P and ending with two molecules of pyruvate is 2 ATP and 2 NADH.

    Question 4 Summary

    • Glycolysis, a metabolic pathway, is used by all human cells for energy production.
    • ATP molecules are formed during glycolysis by substrate-level phosphorylation.

    Question 5 Summary

    • Glyceraldehyde 3-P is a substance found in the fructose metabolic pathway and glycolytic pathway.

    Question 6 Summary

    • A four-week-old child with vomiting, abdominal tenderness, and a hint of cataracts, along with a positive urine reducing sugar test but slightly below normal glucose levels, likely has galactosemia.

    Question 7 Summary

    • Measuring the concentration of galactose-1-phosphate inside the cell can identify a specific enzymatic deficiency involved in galactose metabolism.

    Question 8 Summary

    • Metformin, a type 2 diabetes medication, reduces hepatic gluconeogenesis.
    • This medication does not cause lactic acidosis as a significant side effect due to Cori cycle activity.

    Question 9 Summary

    • Glucose converting to glucose-6-phosphate is an important step in committing glucose to enter the glycolysis pathway.

    Question 10 Summary

    • Red blood cells rely mainly on glycolysis to produce ATP, which is needed for maintaining ion gradients across their membranes. If these gradients are disrupted, the cells can swell and burst, causing hemolytic anemia.

    Question 1 Summary

    • An individual with lactic acidemia and reduced activity of alpha-ketoglutarate dehydrogenase likely has a mutation in the E1 subunit of pyruvate dehydrogenase.

    Question 2 Summary

    • Pyruvic acid is a likely metabolic acid that accumulates in thiamine deficiency.

    Question 3 Summary

    • Succinate dehydrogenase is the only enzyme in the TCA cycle embedded in the inner mitochondrial membrane.

    Question 4 Summary

    • Increased NADH is a key regulator of the TCA cycle, and high NADH levels typically slow the process down, whereas low levels, as occurs during exercise, accelerate it.

    Question 5 Summary

    • A deficiency in Pantothenate can result in an inability to produce coenzyme A.

    Question 6 Summary

    • The compound that provides net eight electrons to the cofactors during the citric acid cycle is acetyl coenzyme A.

    Question 7 Summary

    • High levels of oxygen consumption by the mitochondria, a process facilitated by the addition of valinomycin and potassium, indicate that the electron transport chain is functioning properly.

    Question 8 Summary

    • Uncouplers like Dinitrophenol (DNP) disrupt the proton gradient (proton motive force) across the inner mitochondrial membrane, thereby inhibiting/disrupting oxidative phosphorylation.

    Question 9 Summary

    • In a high salt solution, pyruvate and oxygen are added to trigger electron flow but minimal oxygen consumption occurs when an important component in the electron transport chain (like cytochrome C) is missing.

    Question 10 Summary

    • UCPs (uncoupling proteins) facilitate the uncoupling of ATP formation/oxidative phosphorylation, leading to more energy as heat instead of ATP, which can result in an increase in body temperature.

    Question 1 Summary

    • Superoxide dismutase catalyzes the conversion of superoxide radicals (O2-) to hydrogen peroxide (H2O2) and oxygen (O2).

    Question 2 Summary

    • The mechanism of vitamin E's antioxidant action involves stabilization of free radicals by preventing the formation of covalent bonds with these radicals.

    Question 3 Summary

    • Iron is the metal that is involved in the conversion of hydrogen peroxide to other reactive oxygen species (free radicals).

    Question 4 Summary

    • The level of oxidative damage to mitochondrial DNA is 10 times greater than to nuclear DNA because of the lack of a protective barrier, such as histones or a membrane around the mitochondrias DNA.

    Question 5 Summary

    • A lack of NADPH production in chronic granulomatous disease results in an inability for neutrophils to effectively kill and digest pathogens.

    Question 6 Summary

    • Patients with chronic granulomatous disease primarily lack the ability to produce superoxide.

    Question 7 Summary

    • Patients with a family history of amyotrophic lateral sclerosis (ALS) mutations may have difficulties in detoxification pathways, specifically the processing or removal of oxidized glutathione.

    Question 8 Summary

    • Nitric oxide (NO), a potent vasodilator, exists as an example of a reactive nitrogen-oxygen species (rNOS) capable of producing damage if excessive.

    Question 9 Summary

    • Foreign chemicals (xenobiotics), including alcohol and medications, can increase the risk of free-radical injury by inducing enzymes that create harmful reactive oxygen species.

    Question 10 Summary

    • Citrus fruits are a food source rich in antioxidants.

    Question 1 Summary

    • Under conditions of glucagon release, liver glycogen degradation primarily produces glucose 1-phosphate (with a significant excess relative to glucose alone).

    Question 2 Summary

    • Abnormalities in glycogen branching, in a patient with abnormally high liver glycogen after fasting, may result from defects in glycogen phosphorylase or its related proteins/activities.

    Question 3 Summary

    • A deficiency in muscle phosphorylase results in lower lactate levels as compared to normal individuals exercising. This is because of reduced glycogen breakdown and subsequent lactate production during forearm exercise.

    Question 4 Summary

    • In a normal glucose tolerance response, the enhanced increase in glycogen synthases within the liver in response to a high glucose load will aid in producing glycogen for storage.

    Question 5 Summary

    • In a diabetic patient who skips insulin injections, high blood sugar (hyperglycemia) may result, which is likely a result of glycogen degradation in the liver.

    Question 6 Summary

    • Conditions of severely hypoxic muscle cells are usually marked by an accumulation of calcium and then subsequent glycogen breakdown.

    Question 7 Summary

    • Muscle glycogen degradation when protein kinase A is unable to respond correctly to high cAMP levels would likely be limited to a situation when there are low levels of intracellular calcium.

    Question 8 Summary

    • The maintenance of normal blood glucose levels depends on liver glucose-6-phosphatase to synthesize glucose for release into the bloodstream when needed.

    Question 9 Summary

    • All glycogen storage diseases (except for type O) involve liver dysfunction as a frequent associated condition.

    Question 10 Summary

    • Normal blood glucose levels (ranging from 50 to 80 mg/dL in the first two post-birth hours) after normal delivery indicate that the process is a normal physiological change.

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    Description

    Test your understanding of diabetes management, particularly in type 1 diabetes cases, along with the physiological effects of caffeine and mutations that lead to MODY. This quiz covers critical symptoms, treatments, and biological mechanisms relevant to diabetes care.

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