Chapter 25_2 flashcards
(26 cards)
Type 1 Diabetes (T1DM): Pathophysiology
An autoimmune disease where T-cells attack and destroy the insulin-producing beta cells of the pancreas, leading to an absolute insulin deficiency. Patients have no insulin.
T1DM: Clinical Presentation
Often presents with the classic 3 P’s (Polyuria, Polydipsia, Polyphagia), weight loss despite increased appetite, fatigue, and frequently, diabetic ketoacidosis (DKA) is the first sign.
Type 2 Diabetes (T2DM): Pathophysiology
The body’s cells become resistant to insulin’s effects (insulin resistance). The pancreas tries to compensate by producing more insulin (hyperinsulinism) but eventually becomes exhausted, leading to hyperglycemia.
T2DM: Major Risk Factors
Obesity and sedentary lifestyle are major risk factors. It is also a key component of Metabolic Syndrome.
Metabolic Syndrome: Components (Box 25-2)
A cluster of conditions increasing CVD and T2DM risk. Must have >=3 of the following: Elevated waist circumference, elevated triglycerides (>=150), reduced HDL (<40 men, <50 women), elevated BP (>=130/85), elevated fasting glucose (>=100).
Gestational Diabetes Mellitus (GDM): Cause & Risks
Diabetes diagnosed during pregnancy, likely due to hormones causing insulin resistance. Risks to infant include macrosomia (large baby), neonatal hypoglycemia, and higher risk for developing T2DM later in life.
Acute Complication: Diabetic Ketoacidosis (DKA)
A life-threatening complication, mainly in T1DM, due to absolute insulin deficiency. The body breaks down fat for energy -> produces excess ketones (acids) -> metabolic acidosis.
DKA: Diagnostic Criteria & Symptoms (Box 25-6)
Criteria: Blood glucose >= 250 mg/dL, arterial pH < 7.3, serum bicarbonate < 18 mEq/L, ketonemia, and ketonuria. Symptoms: Nausea/vomiting, dehydration, Kussmaul’s respirations (rapid, deep breathing), fruity breath odor, confusion.
DKA: Management
Fluid replacement (IV fluids FIRST), followed by IV insulin until blood glucose is < 250 mg/dL. Careful monitoring and replacement of electrolytes, especially potassium, is critical.
Acute Complication: Hyperosmolar Hyperglycemic Syndrome (HHS)
Life-threatening complication of T2DM. Characterized by severe hyperglycemia (BG > 600 mg/dL), extreme dehydration, and high blood osmolarity, but with minimal or no ketone formation because some insulin is present.
HHS: Symptoms & Treatment
Symptoms: Profound dehydration, rapid/thready pulse, hypotension, confusion, stupor, seizures, coma. Treatment: IV rehydration FIRST to stabilize osmolarity, then IV insulin and electrolyte replacement.
Somogyi Effect vs. Dawn Phenomenon
Both cause morning hyperglycemia. Somogyi Effect: Nocturnal HYPOglycemia triggers a rebound hormonal response that raises blood sugar by morning. Dawn Phenomenon: Nocturnal elevations of growth hormone cause blood sugar to rise overnight, WITHOUT nighttime hypoglycemia.
Long-Term Complication: Chronic Hyperglycemia & Vascular Damage
Chronic high blood glucose damages the endothelial lining of arteries (angiopathy), leading to widespread atherosclerosis. This affects both large arteries (macrovascular) and small arteries (microvascular).
Long-Term Complication: Diabetic Retinopathy
Damage to retinal arteries from chronic hyperglycemia, leading to microaneurysms, hemorrhages, and “cotton wool spots”. It is a leading cause of blindness in adults.
Long-Term Complication: Diabetic Nephropathy
Damage to the glomerular capillaries, causing them to become hyperpermeable and leak protein (microalbuminuria). It is a leading cause of end-stage renal disease.
Long-Term Complication: Peripheral Neuropathy
Damage to sensorimotor nerves, typically in the feet, due to poor circulation. Causes loss of sensation, burning, tingling, and pain. It greatly increases the risk for foot ulcers and amputation.
Long-Term Complication: Autonomic Neuropathy
Dysfunction of the sympathetic and parasympathetic nervous systems. Can cause postural hypotension, gastroparesis, bladder problems, and “hypoglycemia unawareness” (blunting of warning signs).
Diabetes & Foot Care
Peripheral neuropathy, poor circulation, and immunosuppression create a high risk for foot ulcers, infection, gangrene, and amputation. Daily foot inspection and podiatric care are essential.
Goal for Glycemic Control (ADA)
A1c: <= 7%. Preprandial (before meal) glucose: 80-130 mg/dL. Postprandial (after meal) glucose: <= 180 mg/dL.
Basal-Bolus Insulin Regimen
A common therapy approach that mimics the body’s natural insulin pattern. It uses a once-daily injection of a long-acting insulin (basal) and boluses of a rapid-acting insulin with meals (prandial).
Insulin Analogs vs. Conventional Insulins
Insulin Analogs (e.g., lispro, glargine) have been modified to more closely mimic the body’s natural insulin secretion patterns, with very rapid or very long, flat action profiles. Conventional Insulins (e.g., Regular, NPH) are older forms.
T2DM Treatment: First-Line Oral Agent
Metformin (a Biguanide) is the recommended initial medication for T2DM when lifestyle changes are insufficient. It works by decreasing liver glucose production and increasing insulin sensitivity in body cells.
Classes of Oral Antidiabetic Agents: Sulfonylureas & Meglitinides
These are insulin secretagogues, meaning they stimulate the pancreas to secrete more insulin.
Classes of Oral Antidiabetic Agents: Thiazolidinediones (TZDs)
Act by sensitizing skeletal muscle and adipose tissue to insulin and blocking glucose production by the liver. Example: Pioglitazone (Actos).
