Podcast
Questions and Answers
What is the primary cause of gestational diabetes?
What is the primary cause of gestational diabetes?
Which of the following is NOT a risk factor for gestational diabetes?
Which of the following is NOT a risk factor for gestational diabetes?
What is the purpose of the Oral Glucose Tolerance Test (OGTT) in diagnosing gestational diabetes?
What is the purpose of the Oral Glucose Tolerance Test (OGTT) in diagnosing gestational diabetes?
What is the typical weight range for babies born to mothers with gestational diabetes who do not manage their condition?
What is the typical weight range for babies born to mothers with gestational diabetes who do not manage their condition?
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Which of the following is NOT a potential complication for babies born to mothers with gestational diabetes?
Which of the following is NOT a potential complication for babies born to mothers with gestational diabetes?
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Which of the following is a potential complication for mothers who have experienced gestational diabetes?
Which of the following is a potential complication for mothers who have experienced gestational diabetes?
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What is the most likely reason behind the increasing incidence of gestational diabetes in the US?
What is the most likely reason behind the increasing incidence of gestational diabetes in the US?
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Compared to Caucasians, which of the following ethnic groups are at a higher risk of developing gestational diabetes?
Compared to Caucasians, which of the following ethnic groups are at a higher risk of developing gestational diabetes?
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What is the primary effect of decreased insulin activity in the context of diabetes?
What is the primary effect of decreased insulin activity in the context of diabetes?
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How does glucagon contribute to hyperglycemia?
How does glucagon contribute to hyperglycemia?
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What is the role of GLUT4 in glucose transport?
What is the role of GLUT4 in glucose transport?
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Which hormone is responsible for breaking down glycogen and stimulating gluconeogenesis, leading to elevated glucose levels?
Which hormone is responsible for breaking down glycogen and stimulating gluconeogenesis, leading to elevated glucose levels?
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What is the main mechanism by which SGLT2 inhibitors lower blood glucose?
What is the main mechanism by which SGLT2 inhibitors lower blood glucose?
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What is the major physiological consequence of untreated diabetes?
What is the major physiological consequence of untreated diabetes?
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Which of the following is NOT a direct consequence of hyperglycemia?
Which of the following is NOT a direct consequence of hyperglycemia?
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What is a major metabolic change that contributes to diabetic ketoacidosis?
What is a major metabolic change that contributes to diabetic ketoacidosis?
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Which of the following is NOT a symptom of diabetes?
Which of the following is NOT a symptom of diabetes?
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What is the primary cause of accelerated atherosclerosis in individuals with diabetes?
What is the primary cause of accelerated atherosclerosis in individuals with diabetes?
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How does diabetic neuropathy affect patients?
How does diabetic neuropathy affect patients?
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Which of the following is a mechanism by which reactive oxygen species contribute to diabetic complications?
Which of the following is a mechanism by which reactive oxygen species contribute to diabetic complications?
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What is the effect of formation of sugar alcohols (e.g., sorbitol) in diabetic tissues?
What is the effect of formation of sugar alcohols (e.g., sorbitol) in diabetic tissues?
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What is the role of nitric oxide in maintaining healthy blood flow?
What is the role of nitric oxide in maintaining healthy blood flow?
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How do advanced glycation end products (AGEs) contribute to diabetic complications?
How do advanced glycation end products (AGEs) contribute to diabetic complications?
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Which of the following is NOT a significant factor contributing to poor blood flow in individuals with diabetes?
Which of the following is NOT a significant factor contributing to poor blood flow in individuals with diabetes?
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What is the primary reason for the increased risk of diabetic ketoacidosis (DKA) in individuals with type 1 diabetes compared to those with type 2 diabetes?
What is the primary reason for the increased risk of diabetic ketoacidosis (DKA) in individuals with type 1 diabetes compared to those with type 2 diabetes?
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Which of the following is NOT a direct consequence of increased lipolysis in the context of diabetic ketoacidosis?
Which of the following is NOT a direct consequence of increased lipolysis in the context of diabetic ketoacidosis?
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What is the primary mechanism by which alcohol increases the risk of hypoglycemia?
What is the primary mechanism by which alcohol increases the risk of hypoglycemia?
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A patient taking glyburide experiences symptoms of hypoglycemia after exercising. Which of the following statements best explains this phenomenon?
A patient taking glyburide experiences symptoms of hypoglycemia after exercising. Which of the following statements best explains this phenomenon?
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Which of the following is NOT a symptom commonly associated with both hyperglycemia and hypoglycemia?
Which of the following is NOT a symptom commonly associated with both hyperglycemia and hypoglycemia?
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Which of the following statements accurately describes the role of insulin in glucose metabolism?
Which of the following statements accurately describes the role of insulin in glucose metabolism?
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What is the primary metabolic consequence of insulin deficiency in diabetic ketoacidosis?
What is the primary metabolic consequence of insulin deficiency in diabetic ketoacidosis?
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What is the primary mechanism by which Kussmaul breathing helps to alleviate diabetic ketoacidosis?
What is the primary mechanism by which Kussmaul breathing helps to alleviate diabetic ketoacidosis?
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Which of the following situations can predispose a diabetic patient to developing diabetic ketoacidosis (DKA)?
Which of the following situations can predispose a diabetic patient to developing diabetic ketoacidosis (DKA)?
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Which of the following accurately describes the relationship between epinephrine and cortisol in glucose metabolism?
Which of the following accurately describes the relationship between epinephrine and cortisol in glucose metabolism?
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Flashcards
Gestational Diabetes
Gestational Diabetes
A type of diabetes that occurs during pregnancy due to insulin resistance.
Oral Glucose Tolerance Test (OGTT)
Oral Glucose Tolerance Test (OGTT)
A test where a patient drinks a glucose solution to diagnose gestational diabetes.
Risk Factors for Gestational Diabetes
Risk Factors for Gestational Diabetes
Factors that increase the likelihood of developing gestational diabetes, including age, obesity, and family history.
Macrosomia
Macrosomia
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Complications for Babies
Complications for Babies
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Complications for Mothers
Complications for Mothers
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Epidemiology of Gestational Diabetes
Epidemiology of Gestational Diabetes
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Pathophysiology of Diabetes
Pathophysiology of Diabetes
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Insulin's role
Insulin's role
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Anabolic vs. Catabolic
Anabolic vs. Catabolic
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Glucagon
Glucagon
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SGLT2 Inhibitors
SGLT2 Inhibitors
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Hyperglycemia Symptoms
Hyperglycemia Symptoms
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Diabetic Retinopathy
Diabetic Retinopathy
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Glycosylation
Glycosylation
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Reactive Oxygen Species (ROS)
Reactive Oxygen Species (ROS)
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Ketone Production
Ketone Production
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Diabetic Neuropathy
Diabetic Neuropathy
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Microalbuminuria
Microalbuminuria
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Diabetic Nephropathy
Diabetic Nephropathy
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Cortisol Effects
Cortisol Effects
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GLUT4 Transporter
GLUT4 Transporter
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Symptoms of Weight Loss
Symptoms of Weight Loss
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Microvascular Complication
Microvascular Complication
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Diabetic Ketoacidosis (DKA)
Diabetic Ketoacidosis (DKA)
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Kussmaul Breathing
Kussmaul Breathing
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Glycogenesis
Glycogenesis
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Glycogenolysis
Glycogenolysis
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Lipolysis
Lipolysis
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Diabetic Hyperglycemia Symptoms
Diabetic Hyperglycemia Symptoms
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Risk Factors for Hypoglycemia
Risk Factors for Hypoglycemia
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Study Notes
Gestational Diabetes Overview
- Gestational diabetes is glucose intolerance developing during pregnancy, mainly caused by insulin resistance.
- Testing is typically done in the third trimester using an Oral Glucose Tolerance Test (OGTT).
- The OGTT involves a 75-gram glucose drink and subsequent glucose level checks.
- A diagnosis is made if the patient fails to meet specific criteria during the OGTT.
- Approximately 9% of pregnant women in the US have gestational diabetes, and the prevalence is increasing.
- Obesity is a strong risk factor (60-80% of cases).
- Other risk factors include age, family history of type 2 diabetes, prior gestational diabetes, and ethnicity (higher incidence in Asian, Hispanic, and African Americans compared to Caucasians).
- Lack of exercise is also a risk factor.
Complications of Gestational Diabetes
- Maternal: Difficult labor (increased chance of C-section), increased risk of developing type 2 diabetes after delivery, and increased risk of type 2 diabetes later in life for the offspring.
- Fetal: Macrosomia (high birth weight), stillbirth, neonatal hypoglycemia, respiratory problems, and birth defects (e.g., heart problems).
Patient Case Example
- A 32-year-old woman (TM) experienced gestational diabetes, delivering a 9-pound baby via C-section.
- Her 2-hour OGTT glucose level was 219 mg/dL.
- Treatment involved diet control and follow-up appointments.
Pathophysiology of Diabetes (General)
- Reduced glucose entry into target tissues (adipose, muscle, heart) increases blood glucose levels.
- Reduced amino acid entry into muscle impedes storage.
- Decreased triglyceride synthesis in fat tissue.
- Increased lipolysis (fat breakdown).
- Decreased anabolic function due to reduced insulin activity.
- Increased "bad" cholesterol (VLDL and LDL).
- Increased liver glucose release into bloodstream and reduced glycogen storage.
- Increased gluconeogenesis (new glucose production).
- Shift of stored glucose into blood, further raising blood glucose.
Effects of Untreated/Uncontrolled Diabetes
- Reduced anabolic effects from lack of insulin.
- Increased glucagon effects (promoting gluconeogenesis and glycogen breakdown).
- Instead of forming storage molecules, glycerol and free fatty acids undergo gluconeogenesis, generating more glucose.
- Amino acids are also used for gluconeogenesis instead of protein formation.
- Reduced glucose uptake into tissues, increased liver glucose production, and decreased glucose utilization for storage.
- Shift from anabolic to catabolic function, increased ketone production (can lead to ketoacidosis).
Glucose Transporters
- SGLT: Sodium-Glucose Co-transporter
- SGLT1: In small intestine and renal tubules, absorbs glucose.
- SGLT2: In proximal convoluted tubule, reabsorbs glucose.
- Hyperglycemia (glucose > 180 mg/dL): SGLT2 cannot reabsorb all glucose, leading it to be present in the urine. SGLT2 inhibitors eliminate glucose via urine.
- GLUT: Glucose Transporter
- GLUT2: On beta cells, facilitates glucose entry and insulin secretion.
- GLUT4: On muscle cells, facilitates glucose entry, primarily during exercise (insulin-independent).
Hormones Increasing Glucose Levels
- Glucagon: From pancreatic alpha cells, breaks down glycogen and stimulates gluconeogenesis.
- Higher insulin:glucagon ratio: Favors anabolic functions (storage).
- Lower insulin:glucagon ratio: Favors catabolic functions (breakdown).
- Thyroid Hormone: Increases glucose absorption, potentiates catecholamine effects, causes glycogen depletion, and accelerates insulin degradation.
- Cortisol: Reduces glucose tolerance, increases protein catabolism and gluconeogenesis, increases ketone production, and decreases peripheral glucose utilization.
- Growth Hormone: Has lipolytic and ketogenic effects, reduces glucose uptake, increases liver glucose release, and raises overall glucose levels.
Diabetes Symptoms
- Hyperglycemia: High blood glucose.
- Glucosuria: Glucose in urine.
- Polyuria: Frequent urination from osmotic diuresis.
- Polydipsia: Excessive thirst due to water loss.
- Protein depletion: Due to lack of insulin's anabolic function.
- Weight loss: Inefficient glucose utilization.
- Susceptibility to infections: High glucose allows for pathogen proliferation.
- Other Symptoms: Weight loss, fatigue, blurry vision, and increased thirst.
Diabetes Complications
- Microvascular:
- Diabetic retinopathy: Eye problems, potential blindness.
- Diabetic nephropathy: Kidney problems, leading cause of end-stage renal disease (ESRD) in US.
- Microalbuminuria: Protein in urine indicates kidney damage.
- Macrovascular:
- Accelerated atherosclerosis in blood vessels.
- Increased risk of heart attack, stroke, and peripheral vascular atherosclerosis.
- Increased blood pressure due to reduced blood vessel diameter from fat deposits.
- Neuropathic: Diabetic neuropathy affecting both autonomic and peripheral nervous systems, causing pain and numbness, especially in lower extremities, sensory loss, and increased risk of injury/infection.
Mechanisms of Diabetic Complications
- Increased Reactive Oxygen Species (ROS) damage.
- Sugar alcohol formation (e.g., sorbitol), leading to tissue damage.
- Decreased Glutathione and NADPH, reducing ROS reduction capacity.
- Decreased Nitric Oxide.
- Glycosylation, forming Advanced Glycation End products (AGEs) causing inflammation and tissue damage.
- Poor blood flow from lack of nitric oxide, leading to tissue ischemia (reduced blood supply).
Diabetic Ketoacidosis (DKA)
- Most common in type 1 diabetes, less common in type 2.
- Ketones become energy source in insulin deficiency, causing metabolic acidosis.
- Characterized by Kussmaul breathing, acidic urine, severe electrolyte loss, and dehydration.
- Severe can cause coma.
- Stressful conditions can trigger DKA by raising glucose.
Glucose Metabolism
- Glucose conversion to glucose-6-phosphate, glucose-1-phosphate, pyruvate, acetyl CoA, and TCA cycle.
- Glycogenesis: Glucose storage as glycogen (stimulated by insulin).
- Glycogenolysis: Glycogen breakdown to glucose (accelerated by epinephrine and cortisol).
- Lipolysis: Triglyceride breakdown to fatty acids (stimulated by epinephrine and cortisol).
- Ketogenesis: Fatty acid conversion to ketones (accelerated by epinephrine and cortisol).
Ketone Production
- Decreased insulin reduces glucose uptake, increases hyperglycemia, glucosuria, osmotic diuresis, and electrolyte depletion.
- Increased protein catabolism raises amino acids.
- Increased lipolysis produces more fatty acids, converted to ketones.
- Major ketones: acetoacetate, acetone, and beta-hydroxybutyrate.
Diabetic Hypoglycemia
- Hypoglycemia related to diabetes treatment, not the disease itself.
- Insulin overdose, alcohol (inhibits gluconeogenesis), and exercise increase hypoglycemia risk.
- Symptoms generally occur below 70 mg/dL, but can vary in chronically hypoglycemic patients.
- Symptoms include pallor, sweating, tachycardia, hunger, headache, visual disturbances, seizures, and coma.
- Repeated episodes can impair hypoglycemia recognition.
Hyperglycemia and Hypoglycemia Symptoms - Summary Table
Symptom Category | Hyperglycemia | Hypoglycemia |
---|---|---|
Urination | Frequent urination (polyuria) | |
Thirst | Excessive thirst (polydipsia) | |
Vision | Blurred vision | Blurred vision |
Energy | Fatigue | |
Head | Headache | Headache |
Smell | Fruity-smelling breath (DKA) | |
Gastrointestinal | Nausea, vomiting | Feeling hungry |
Respiratory | Shortness of breath | |
Mental | Confusion | Shakiness, nervousness, anxiety, irritability, confusion, dizziness |
Other | Sweating, tachycardia | Sweating, tachycardia, seizures, unconsciousness, coma |
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Description
This quiz covers the key aspects of gestational diabetes, including its causes, testing methods, and associated risks. Learn about the Oral Glucose Tolerance Test and the complications it can pose for both mother and child. Understand the prevalence and various risk factors tied to this condition.