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Questions and Answers
What is the most common cause of nontraumatic lower extremity amputation in diabetes patients?
Which sign is commonly associated with diabetic retinopathy?
What condition can arise due to poor circulation and lack of care in diabetic patients?
What is a psychological aspect commonly seen in individuals with Type 2 diabetes?
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What skin condition can develop at the site of insulin injections?
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In diabetic patients, which factor is crucial to decrease the risk of complications?
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Microalbuminuria is an indication of damage to which structure in diabetic patients?
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What change in vaginal pH can promote Candida proliferation in diabetes?
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What characterizes Type 1 Diabetes Mellitus (T1DM)?
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What is a common cause of Type 2 Diabetes Mellitus (T2DM)?
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Which complication is most likely to occur in patients with uncontrolled diabetes?
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Which physiological response does glucagon initiate when blood glucose levels are low?
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What is the primary result of ketone formation in diabetes?
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What does the presence of C-peptide in a patient's test results indicate?
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What is the main feature of diabetic ketoacidosis (DKA)?
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What does hyperosmolar hyperglycemic syndrome (HHS) primarily indicate?
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What factor may exacerbate the Somogyi effect in diabetes management?
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In the context of diabetes, what does the term 'autonomic neuropathy' refer to?
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What is a common feature that characterizes the classic symptoms of diabetes mellitus?
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Why might patients with diabetes be more susceptible to infections?
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What is a characteristic of gestational diabetes mellitus (GDM)?
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Study Notes
Diabetes Mellitus (DM)
- Disorder of carbohydrate metabolism characterized by high blood glucose levels
- Body cannot produce or properly utilize insulin
- Contributes to increased morbidity and mortality
- Increases the risk of CVD, renal damage, peripheral vascular disease, neurological disorders, blindness and amputation
Four Major Categories of DM
- Type 1 DM (T1DM): - Characterized by a lack of insulin production - Beta cells of pancreas are destroyed - Requires insulin treatment
- Type 2 DM (T2DM): - Represents 90% of cases - Characterized by insulin resistance
- Gestational DM (GDM): - Develops during pregnancy due to hormone-induced insulin resistance - Can lead to macrosomia (large babies)
- Other: - Caused by factors like pancreatitis, cystic fibrosis, or neonatal conditions
Epidemiology of DM
- Affects over 30 million individuals in the US
- Prevalence increasing parallel to obesity rates and sedentary lifestyles
- Prevalence increases with age
- DM is a polygenic disorder with environmental triggers
Etiology of DM
- Type 1 DM: - Autoimmune destruction of beta cells - Antibodies present - No insulin production by the body
- Type 2 DM: - More gradual onset - Insulin resistance - Insulin is produced but not utilized effectively - Associated with sedentary behavior and obesity
Insulin and Carbohydrate Ingestion
- Insulin: - Produced by beta cells - Facilitates glucose movement from blood to cells
- Carbohydrate ingestion: - Simultaneous rise and fall of blood glucose and insulin levels - Insulin levels rise in response to the increase in blood glucose
Insulin Facilitates Glucose Uptake
- Insulin promotes glucose uptake in: - Muscle: Glycogenesis (glucose storage) - Liver: Glycogenesis and gluconeogenesis (glucose production) - Adipose tissue: Reduced lipolysis (fat breakdown)
Carbohydrate Metabolism Overview
- Glucose is used for energy, glycogen storage, and lipid (fat) synthesis
- Glycogenesis: Glucose to glycogen (storage) in liver and muscle
- Glycogenolysis: Glycogen to glucose (release) when blood glucose is low
- Gluconeogenesis: Non-carbohydrate sources like amino acids and glycerol are converted to glucose in the liver and kidneys
Ketone Formation and Diabetic Ketoacidosis (DKA)
- DKA primarily occurs in Type 1 DM
- Ketones are produced when glucose cannot be utilized for energy
- Accumulation of ketones can lead to metabolic acidosis (DKA)
Blood Glucose Levels
- Normal Blood Glucose: 70–100 mg/dL (fasting)
- Hypoglycemia: BG < 70 mg/dL
- Impaired Glucose Tolerance (IGT) / "Prediabetes": Fasting BG: 100–125 mg/dL
- Diabetes: Fasting BG: >126 mg/dL
- Postprandial BG: - Glucose levels after eating - > 200 mg/dL indicates diabetes
Role of Insulin
- Insulin: An anabolic hormone that facilitates glucose uptake and utilization
- Hyperinsulinism: Elevated insulin levels which may occur in early T2DM, attempting to overcome insulin resistance
- Hypoglycemia: Too much insulin leads to low blood glucose levels
Other Glucose-Regulating Hormones
- Glucagon: Released by alpha cells of the pancreas; raises blood glucose (injectable form for severe hypoglycemia)
- Somatostatin: Released by delta cells of pancreas; diminishes insulin and glucagon secretion, slows GI activity
- Incretins: GI hormone that stimulates insulin release and slows GI motility (includes GLP-1 and GIP)
- Cortisol: Released by adrenal cortex; a steroid hormone that increases blood glucose
Glucose-Regulating Signals from Pancreas
- Pancreatic cells release hormones (like insulin and glucagon) in response to blood glucose levels
T1DM: Pathological Mechanism
- Autoimmune destruction of beta cells mediated by T-cells
- Genetic predisposition
- Initial presentation is often DKA
- Symptoms: Polyuria (increased urination), polydipsia (increased thirst), polyphagia (increased hunger)
T2DM: Pathological Mechanism
- Insulin resistance with increased insulin levels
- Molecular mechanisms: Oxidative stress, inflammation, insulin receptor mutation, mitochondrial dysfunction
- Associated with metabolic syndrome (HTN, dyslipidemia, hyperinsulinism, central obesity)
- Hyperosmolar Hyperglycemic State (HHS): Hyperglycemia with dehydration, usually occurs in type 2 DM and progresses slowly
Gestational Diabetes Mellitus (GDM)
- Develops during pregnancy due to pregnancy-induced insulin resistance
- Complications: Fetal defects, premature delivery, newborn hypoglycemia, macrosomia
- Screening: 2nd trimester oral glucose tolerance test (OGTT)
- GDM typically resolves after delivery but can increase the risk of T2DM
Diabetes Tests
- Blood Glucose: Fasting and random blood glucose measurements
- Oral Glucose Tolerance Test (OGTT): 75g glucose ingested, blood sugar is measured
- Glycated Hemoglobin (A1c): Indicates average blood sugar levels over 3 months
- eAG: Average blood glucose over the last few months
- Islet Cell Autoantibodies (ICAs): Present in T1DM
- C-Peptide Test: Measures endogenous insulin production, helps differentiate between T1DM and T2DM
Diabetes Tests: Urinalysis
- Glucosuria: Elevated blood glucose levels lead to glucose in urine
- Ketonuria: Ketones in urine are associated with DKA and increased ketone production
Complications of DM
- Both acute and long-term complications
- Acute: Hypoglycemia, hyperglycemia, DKA (T1DM), HHS (T2DM)
- Long-term systemic: Blindness, kidney failure, neuropathy, cardiovascular disease, amputation
Hypoglycemia
- Blood Glucose less than 70 mg/dL
- Causes: - Excessive exogenous insulin - Inadequate food intake - Excessive physical activity - Infection, illness, drug interaction
- Compensatory response: Activation of the sympathetic nervous system: Sweating, hunger, dizziness, headache, heart palpitations, confusion
- Management: - Rapid acting carbohydrates (15 grams) - Avoid fats (delay glucose absorption) - If BG >70 mg/dL, provide a meal or snack - IV glucose or subcutaneous glucagon injection
- Repeated hypoglycemia can blunt the compensatory response, potentially leading to autonomic neuropathy
Somogyi Effect and Dawn Phenomenon
- Somogyi Effect: - Morning hyperglycemia due to hypoglycemia during sleep often caused by excessive insulin dosage - Adjust insulin dosage
- Dawn Phenomenon: - Morning hyperglycemia without hypoglycemia during sleep - Adjust medication, exercise, and eating patterns
Classic Signs of Diabetes Mellitus
- Polydipsia (increased thirst): High blood glucose increases plasma osmolarity, leading to fluid shifts and dehydration, stimulating thirst
- Polyphagia (increased hunger): Cells cannot utilize glucose effectively due to lack of insulin, increasing appetite
- Polyuria (increased urination): Increased renal glucose filtration and osmotic diuresis lead to increased urination
Fluid Shifts and Glucose in Urine
- Glucose and fluid are excreted in urine due to the kidney's inability to reabsorb them efficiently
Additional Signs of DM
- Blurred vision: Glucose accumulation in aqueous fluid alters light refraction
- Fluid/Electrolyte Imbalance: - Intracellular (ICF) to extracellular fluid (ECF ) shifts can lead to dilutional hyponatremia - Electrolyte shifts: Potassium (K+) shifts out of cells
Diabetic Ketoacidosis (DKA)
- Occurs when insulin is lacking (primarily in T1DM)
- Insulin prevents lipolysis and ketone formation
- Ketone buildup leads to metabolic acidosis (DKA)
- Diagnostic criteria: - BG > 250 mg/dL - pH < 7.3 - HCO3− < 18 mEq/L - Blood osmolarity > 20 mOsm/L
- Presentation: Nausea, vomiting, abdominal pain, deep rapid breathing (Kussmaul breathing), fruity breath odor
Hyperosmolar Hyperglycemic State (HHS)
- Hyperglycemia: Inability to facilitate glucose uptake, contributing to increased blood sugar
- Hyperosmolarity: Elevated blood glucose leads to osmotic diuresis and dehydration
- Clinical progression: Can develop slowly over days to weeks
- Presentation: Weakness, dehydration, tachycardia, thready pulse, confusion, coma
- Causes: Infection, trauma, non-compliance with DM management
- Treatment: Fluids (first) followed by insulin
Long-Term Complications of DM
- Arteriosclerosis (damaged blood vessels): Hyperglycemia damages endothelial cells, leading to plaque formation
- Peripheral angiopathy (poor circulation): Damage to blood vessels in the extremities
- Diabetic retinopathy (damaged eye vessels): Can lead to blindness
- Diabetic neuropathy (nerve damage): Affects nerves, particularly in the feet, causing numbness, tingling, and pain
- Autonomic neuropathy: Disrupts autonomic nervous system function
- Diabetic nephropathy (kidney damage): Can lead to kidney failure
- Poor wound healing: Reduced blood flow and high sugar levels impair the healing process
- Immunosuppression: Weakened immune response
DM and Atherosclerosis
- Increases risk of acute cardiac events (MI)
- Atherosclerosis affects both large and small arteries
- Hyperglycemia leads to oxidative stress, contributing to vascular damage
DM and Peripheral Neuropathy
- Distal, symmetric polyneuropathy: Damage to neural arteries begins in the feet, progresses upwards
- Effects: Burning, tingling, impaired sensation, pain perception, motor weakness, gait abnormalities, charcot joints
DM and Autonomic Neuropathy
- Affects various systems: - Cardiac: Tachycardia, hypotension - GI: Gastroparesis, gastric emptying abnormalities, anorexia, nausea, bowel dysfunction - Urinary: Increased UTI risk - Reproductive: Erectile dysfunction - Temperature regulation: Decreased sweating, hyperthermia, dry skin - Glycemic control: Hypoglycemia, impaired awareness of warning signs
DM and Susceptibility to Infection
- Impaired WBC function increases the risk of infections like staphylococcus aureus and candida (yeast)
- High glucose levels alter vaginal pH, promoting candida proliferation
DM and Amputation
- Leading cause of non-traumatic limb amputations
- Peripheral neuropathy, poor circulation, and immune suppression increase infection risk, potentially leading to gangrene and amputation
DM and Foot Care
- Regular foot examination is essential for early detection of injuries, ulcers, and infections
DM and Retinopathy/Blindness
- Leading cause of blindness in adults
- Retinal circulatory damage: Microaneurysms, macular edema, "cotton wool spots" (infarcted areas)
- Proliferative retinopathy: New vessel growth, fragile and prone to rupture, retinal detachment
- Regular eye exams are crucial
DM and Nephropathy
- Can lead to renal failure
- Damage to glomerular capillaries leading to microalbuminuria (protein in the urine)
- Thickening of the glomerular basement membrane due to glycosylation
- Activation of the RAAS (renin-angiotensin-aldosterone system) exacerbates blood pressure issues
DM and Dermatological Changes
- Prolonged wound healing and ulcer formation
- Diabetic skin spots: Hyperpigmented areas
- Acanthosis nigricans: Tiny, hyperpigmented macular lesions
- Lipoatrophy: Can occur at insulin injection sites
DM and Psychological Resistance
- Depression is more common in individuals with DM
- Guilt, discouragement, self-blame
- Anxiety regarding disease management
- Denial and non-compliance
- Psychological insulin resistance: Refusal to comply with insulin management
DM and Eating Disorders
- Young women with T1DM are at risk for eating disorders
- Insulin purging: Restricting or skipping insulin to stimulate lipolysis and weight loss
- Suspect eating disorder in patients with: - Recurrent DKA - Chronically poor glycemic control
DM Treatment Overview
- Blood glucose control: Both hyperglycemia and hypoglycemia need to be managed
- Glycemic control: Primary treatment goal to minimize the risk of complications
- Reduce CVD risk: Lipid panels, LDL < 60 mg/dL, Trigylcerides under control
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Description
Explore the complexities of Diabetes Mellitus, including its impact on carbohydrate metabolism, insulin production issues, and the associated health risks. This quiz examines the four major categories of DM and their distinct characteristics. Test your knowledge on the epidemiology and implications of diabetes in today's society.
