Endocrine Function Alterations Lecture

Endocrine Function Alterations

• This lecture covers alterations in endocrine function, focusing on the pancreas, acute pancreatic dysfunction, acute endocrine dysfunction, diabetes, diabetic ketoacidosis (DKA), and hyperglycemia hyperosmolar state (HHS).

Topics for This Lecture

• Structure and function of the pancreas
• Acute pancreatic dysfunction (including acute pancreatitis)
• Acute endocrine dysfunction
• Diabetes
• Diabetic ketoacidosis (DKA)
• Hyperglycemia hyperosmolar state (HHS)

By the End of This Lecture

• Students will be able to critically reflect on the endocrine system's anatomy and physiology and how dysfunction causes systemic changes.
• Students will be able to explain the pathophysiology and effects of acute pancreatitis, diabetes (DKA and HHS), on the body.
• Students will begin to prioritize patient conditions related to nursing assessment of clinical manifestations and how it relates to other systems.

Objectives for This Lecture

• Identify at least two causes of pancreatitis and its effects on the body.
• Verbalize the pathophysiology of type 1 and type 2 diabetes.
• Differentiate between diabetic ketoacidosis (DKA) and hyperglycemia hyperosmolar state (HHS).

Pancreatic Dysfunction

Pancreas, Structure, and Function

• Has both endocrine and exocrine functions.
• Endocrine: secretes hormones such as insulin, glucagon, somatostatin, and pancreatic polypeptide.
• Exocrine: acinar cells secrete enzymes, and duct networks secrete alkaline fluids crucial for digestion.
• Aqueous secretions contain potassium, sodium, bicarbonate, and chloride.
• Alkaline pancreatic juice neutralizes acidic chyme, enabling digestive enzyme function and intestinal fat absorption.
• Pancreatic enzymes (proteases, amylases, lipases) hydrolyze proteins, carbohydrates, and fats.
• Secretion is hormonally and vagally stimulated.
• Secretin stimulates bicarbonate-rich fluid secretion for chime neutralization and digestion.
• Cholecystokinin and acetylcholine stimulate enzymatic secretion.

Acute Pancreatitis

• Risk Factors: Obstructive biliary tract disease (cholelithiasis), alcoholism, obesity, peptic ulcers, trauma, hyperlipidemia, hypercalcemia, smoking, and genetic factors.
• Pathophysiology: Usually mild but can be necrotizing or hemorrhagic, developing due to pancreatic duct obstruction (e.g., gallstones). Leads to autodigestion of pancreatic cells, causing vascular damage, coagulation necrosis, fat necrosis, and edema. Ethanol metabolism in acinar cells creates toxic metabolites, leading to acinar cell injury and enzyme release. Chronic alcohol use can cause protein plug formation and sphincter of Oddi spasm, further obstructing pancreatic ducts and leading to inflammation and pancreatitis.
• Pathophysiology (continued): Severe acute pancreatitis involves pro-inflammatory cytokines activating leukocytes, injuring vessel walls, and leading to abnormal coagulation in lungs and kidneys. Paralytic ileus, gastrointestinal bleeding (GI bleed), and systemic inflammatory response syndrome (SIRS) can occur.
• Clinical Manifestations: Mid-epigastric or LUQ pain with nausea and vomiting (paralytic ileus), jaundice, fever, and leukocytosis. Patients may exhibit abdominal distention, hypovolemia, hypotension, tachycardia, myocardial insufficiency, and shock. Severe acute pancreatitis can manifest as tachypnea, hypoxemia, pulmonary edema, atelectasis, pleural effusions, hypovolemia, renal failure (acute tubular necrosis), tetany due to hypocalcemia, and transient hyperglycemia.

Acute Pancreatitis - Nursing Assessment

• GI assessment: Bowel sounds, distension, nausea, vomiting, and guarding.
• Respiratory assessment
• Cardiovascular assessment.
• Renal assessment: Hyperlipidemia, hyperglycemia, and hypocalcemia
• Lab Values: Lipase and amylase are often elevated (may be 3x normal), along with WBC, bilirubin, sodium, potassium, creatinine, BUN, lipids (TC, TG, HDL, LDL), calcium, troponin, and ABGs.

Endocrine Dysfunction

Regulation of Blood Glucose

• ...

Diagnosing Diabetes and Prediabetes

• Prediabetes: Impaired fasting glucose and/or impaired glucose tolerance seen on two separate tests.

Types of Diabetes Mellitus

• Type 1
• Type 2
• Other
• Gestational

Classification of Diabetes

• Type 1 diabetes: Primarily results from pancreatic beta-cell destruction, leading to insulin deficiency and a high risk of ketoacidosis. This form includes autoimmune cases and cases with unknown cause.
• Type 1 diabetes includes latent autoimmune diabetes in adults (LADA).
• Type 2 diabetes: Ranges from predominant insulin resistance to a predominant secretory defect, often with insulin resistance. Ketosis isn't as common as in type 1.
• Gestational diabetes mellitus: Glucose intolerance with onset during pregnancy.

So... What's Your Type?

• Type 1: Pancreas doesn't produce insulin, complete loss of beta cell function, unknown etiology potentially autoimmune or idiopathic, requires exogenous insulin — 10% of population
• Type 2: Pancreas produces insufficient insulin or there is insulin resistance, progressive loss of beta cell function, usually diagnosed in adults — 90% of population
• Other Specific Types: Genetic defects of beta-cell function, genetic defects in insulin action, diseases of the exocrine pancreas, endocrinopathies, drug or chemical-induced beta-cell dysfunction, infections, uncommon forms of immune-mediated diabetes, other genetic syndromes associated with DM.
• Gestational: Insulin resistance combined with inadequate insulin secretion, common in women who are obese, older, or have a family history of diabetes —↑risk in women of certain ethnicities.

Etiology - Type 1 DM

• Accounts for 10% of diabetes cases.
• Diagnosed in childhood, adolescence, or early adulthood.
• Absolute lack of insulin.
• Etiology: autoimmune (genetic and environmental trigger) or idiopathic.

Etiology - Type 2 DM

• Accounts for 90% of diabetes cases.
• Common over 2004 Canadian >45
• Genetic, metabolic syndrome, insulin receptor substrate protein abnormalities in some young adults.
• Sedentary lifestyle, visceral obesity.
• Preventable.

Gestational DM

• Affects about 1-2% of pregnancies
• Gestational age 24-28 weeks: hormonal changes from placenta causing insulin resistance.
• Diagnosis: 50g oral glucose screen.
• Often resolves after pregnancy, 97% will not have it again, but a higher risk for postpartum type II.
• Offspring have increased risk for DM and obesity.

Complications Associated with Diabetes

• Macrovascular:
  • Cardiac ischemia
  • CAD/ACS
  • Angina
  • MI
  • Peripheral Arterial Disease
  • Cerebrovascular/Carotid Disease
  • TIA
  • Stroke
• Microvascular:
  • Retinopathy
  • Neuropathy
  • Nephropathy
  • CKD

Hypoglycemia

• Symptoms: autonomic (trembling, palpitations, sweating, anxiety, hunger, nausea, tingling) and neuroglycopenic (difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, headache, dizziness).
• Severity categories: Mild (autonomic symptoms, self-treatable); Moderate (autonomic and neuroglycopenic symptoms, self-treatable); Severe (individual requires assistance, unconsciousness may occur, plasma glucose typically < 2.8 mmol/L).

Diabetic Ketoacidosis (DKA)

• Hyperglycemia, gluconeogenesis, glycogenolysis (use of glucose by liver, muscle, and fat)
• Serum glucose concentration may be >27.8-44 mmol/L.
• Anion gap and metabolic acidosis.
• Ketonemia.
• Develops within 1-24 hours.
• Pathogenesis: Relative insulin deficiency, fasting/starvation, and stress hormone excess contribute to the development of DKA.
• Clinical Presentation: Dehydration (hypotension, shock), tachycardia, Kussmaul respirations, fruity breath, altered mental status, signs of precipitating cause, dry mouth, thirst, weakness, nausea, vomiting.

Diagnosis and Management

• Lab tests: Glucose, CBC with differential, electrolytes (to calculate anion gap), serum creatinine, venous blood gas, and urine for glucose and ketones.
• Other considerations: Airway management, cerebral edema, increased thrombotic event incidence, anticoagulation, phosphate, and magnesium.

Hyperglycemia Hyperosmolar State (HHS)

• Hyperglycemia: Serum glucose concentration > 56 mmol/L.
• Endogenous insulin present but ineffective.
• Severe dehydration; hyperosmolarity.
• Neurologic abnormalities; coma.
• Little to no ketosis.
• More common in elderly.
• Develops over days.

Priorities to Be Addressed in the Management of Adults Presenting With Hyperglycemic Emergencies

Key Points to Remember

• Assess renal and endocrine function, linking anatomy, physiology to endocrine system function.
• Explain the underlying "why" of endocrine assessments and their connections to other systems.
• Apply concepts of normal endocrine function and understand the pathophysiology, clinical manifestations, and nursing assessment related to acute pancreatitis and diabetes—including DKA and HHS.