Endocrine System & Diabetes

Overview

Module on the endocrine system with emphasis on glucose regulation and diabetes. Covers glands, hormones, blood glucose control, diabetic emergencies, and chronic complications.

Endocrine Glands: Organs and Functions

• Nine main glands: hypothalamus, pineal, pituitary, thyroid, parathyroid, thymus, pancreas, adrenal, testes/ovaries.
• Hormones travel via bloodstream and regulate growth, reproduction, metabolism.
• Many disorders arise from too much, too little, or resistance to hormones.

Hypothalamus

• Small, almond-sized brain region above brainstem and below thalamus.
• Integrates nervous and endocrine systems to maintain homeostasis.
• Controls pituitary; synthesises ADH and oxytocin released by posterior pituitary.

Pituitary Gland

• Pea-sized, below hypothalamus; “master gland” regulating other glands.
• Two lobes with distinct roles; releases nine hormones.
• ADH: released with low volume/pressure; increases water reabsorption and vasoconstriction.

Adrenal Glands

• Sit atop kidneys; cortex (outer, yellow) and medulla (inner, dark red/brown).
• Cortex: aldosterone (salt-water balance, BP), cortisol (stress, metabolism, anti-inflammatory).
• Medulla: adrenaline, noradrenaline; drive tachycardia, hypertension, tachypnoea, cool sweaty skin.
• Hypoadrenal shock (adrenal crisis): inadequate cortisol under stress; follow patient plans and CPGs.

Thyroid Gland

• Butterfly-shaped, anterior to trachea, below thyroid cartilage.
• Regulates metabolism; hypothyroidism (thyroxine), hyperthyroidism managed medically/surgically.

Blood Glucose Regulation

• Normal non-fasting BGL: 3.5–9 mmol/L.
• Pancreas: ~98% exocrine (digestive enzymes); ~2% endocrine islets (alpha, beta cells).
• Alpha cells: glucagon increases blood glucose via hepatic glycogenolysis and gluconeogenesis.
• Beta cells: insulin decreases blood glucose; promotes cellular uptake and glycogenesis in liver/muscle.
• Negative feedback between insulin and glucagon maintains homeostasis.
• Skeletal muscle stores significant glycogen for its own use; not exported to blood.
• Brain relies on continuous blood glucose; transport via GLUT-1 across blood-brain barrier; no insulin needed.

Key Processes and Terms

• Glycogenolysis: breakdown of glycogen to glucose in liver.
• Gluconeogenesis: creation of new glucose from fats and proteins during fasting.
• Glycogenesis: storage of glucose as glycogen in liver and skeletal muscle.

Diabetes Mellitus: Types and Pathophysiology

• Causes: absolute insulin lack, impaired insulin release, inactive insulin, receptor dysfunction.
• Result: hyperglycaemia, osmotic diuresis (polyuria), dehydration, fat breakdown, ketone production.

Type 1 Diabetes

• Usually childhood/adolescence; sudden onset; autoimmune beta-cell destruction.
• Causes: genetic predisposition, environmental triggers, lymphocyte-mediated hypersensitivity; 5–10% idiopathic.
• Absolute insulin deficiency; requires insulin therapy; risk of DKA.

Type 2 Diabetes

• More common; typically adults >30, often with obesity; can occur in children.
• Insufficient insulin and/or insulin resistance; beta-cell exhaustion over time.
• Treated with oral hypoglycaemics (e.g., Metformin, Gliclazide, Glipizide); many progress to insulin.
• Comorbidities: ischaemic heart disease, peripheral vascular disease, renal impairment.
• HbA1c reflects average glucose over 2–3 months; used for diagnosis.

Acute Complications of Diabetes

• Hyperglycaemia often due to non-compliance, illness, injury, medicines; main risk is dehydration.
• Treatment focus: correct hypovolaemia; request higher-level support if poor perfusion or shock.

Diabetic Ketoacidosis (DKA)

• Almost exclusively type 1; severe insulin lack; fat/muscle breakdown → ketones → metabolic acidosis.
• Signs: BGL >20 mmol/L, dehydration, hypotension, tachycardia, fatigue, reduced intake, N/V, abdominal pain.
• Breath may smell fruity; Kussmaul respirations; decreased level of consciousness.

Hyperosmolar Non-Ketosis (HONK/HHS)

• Usually type 2; gradual onset days to weeks; some insulin prevents ketosis.
• Signs: polyuria, polydipsia, fatigue, dehydration, tachycardia, hypotension.

DKA vs HONK/HHS

Hypoglycaemia

• Defined as BGL <3.5 mmol/L; rapid onset; often with insulin/oral agents.
• Causes: medication overdose, inadequate intake, dose changes, renal failure, liver failure, sepsis (children).
• Neonates: hypoglycaemia <2.5 mmol/L; check if activity not normal.

Clinical Features

• Cerebral: headache, confusion, impaired problem-solving, abnormal behaviour, slurred speech, reduced consciousness.
• Sympathetic: anxiety, tachycardia, hypertension, sweating, peripheral vasoconstriction.

Treatment

• Aim: raise blood glucose level.
• EMT scope: oral glucose, carbohydrates, IM glucagon; request IV glucose support as needed; follow CPGs.

Chronic Complications of Diabetes

• Cardiovascular disease: increased risk of MI, stroke, slower wound healing, infections.
• Retinopathy: retinal vessel damage; leading cause of blindness in developed countries.
• Neuropathy: nerve and microvascular damage, commonly feet/legs; ulcers, infection, amputation risk.
• Nephropathy: kidney microvascular and nephron damage; proteinuria; reduced waste elimination.

Measuring Blood Glucose Levels (BGL)

• Use ambulance-approved glucometers; review device history for trends.
• Not routine for all patients; take in indicated groups per CPGs.

Special Diabetes Types

Gestational Diabetes Mellitus (GDM)

• Diabetes first detected in pregnancy; usually resolves postpartum; ~4000 cases/year in NZ.
• Cause: pregnancy hormones and altered glucose metabolism; pancreas must triple insulin output.
• Risk factors: Māori, Pacific, Indian, Asian ethnicity; age >35; family history; prediabetes; prior GDM; large baby; obesity; PCOS.
• Maternal complications: pre-eclampsia, pre-term labour, delivery issues.
• Fetal/neonatal complications: pre-term with respiratory distress, post-delivery hypoglycaemia, excessive birth weight.

Diabetes Insipidus

• Rare; impaired ADH production/secretion causing impaired renal water reabsorption.
• Not related to sugar regulation; routine BGL not required.
• Lifelong; managed with ADH-replacing medicines; ambulance care focuses on dehydration and shock signs.

Key Terms & Definitions

• Homeostasis: maintenance of internal balance by regulatory systems.
• ADH (antidiuretic hormone): reduces renal water loss; increases vasoconstriction.
• Aldosterone: regulates salt and water; maintains blood pressure.
• Cortisol: stress hormone; metabolism regulation; anti-inflammatory effects.
• Catecholamines: adrenaline and noradrenaline; mediate sympathetic responses.
• Polyuria: excessive urination with water and electrolyte loss.
• Polydipsia: excessive thirst due to dehydration.
• Ketosis: normal state where ketones supply part of energy.
• Ketoacidosis: dangerous acid buildup from ketones, typically in type 1.
• Kussmaul respirations: deep, rapid breathing in metabolic acidosis.
• HbA1c: average blood glucose over 2–3 months; diagnostic test.

Action Items / Next Steps

• Follow CPGs for assessment and treatment of hyperglycaemia and hypoglycaemia.
• Correct hypovolaemia promptly in hyperglycaemia; escalate if shock signs present.
• Treat hypoglycaemia with oral glucose/carbohydrates or IM glucagon; request IV glucose if required.
• In suspected adrenal crisis or diabetes insipidus with dehydration, follow patient plans and seek clinical support.