Endocrine System Study Guide

Diabetes Mellitus

Types of Diabetes

• Type 1: Autoimmune destruction of beta cells, absolute insulin deficiency
• Type 2: Insulin resistance + relative insulin deficiency, most common
• Gestational: Develops during pregnancy
• Secondary: Medications (steroids), pancreatitis, other conditions

Diagnostic Criteria

• Fasting plasma glucose ≥126 mg/dL
• Random glucose ≥200 mg/dL with symptoms
• HbA1c ≥6.5%
• 2-hour OGTT ≥200 mg/dL
• Target glucose in ICU: 140-180 mg/dL

Insulin Management

• Rapid-acting: Lispro, Aspart, Glulisine (onset 15 min)
• Short-acting: Regular insulin (onset 30-60 min)
• Intermediate: NPH (onset 2-4 hours)
• Long-acting: Glargine, Detemir (onset 2-4 hours, 24-hour coverage)
• IV insulin: For DKA, HHS, perioperative, and critical illness

Hypoglycemia

• Definition: Blood glucose <70 mg/dL
• Severe: <54 mg/dL or requiring assistance
• Symptoms: Tremor, diaphoresis, tachycardia, confusion, seizures, coma
• Treatment: 15-20g fast-acting carbs if conscious
• If unconscious: IV dextrose (D50) or glucagon

DKA & HHS

DKA Overview

• Common in Type 1 diabetes, absolute insulin deficiency
• Triad: Hyperglycemia, Ketosis, Metabolic acidosis
• Glucose typically 300-800 mg/dL
• pH <7.3, Bicarbonate <18 mEq/L
• Anion gap elevated (often >20)
• Ketones present in blood and urine
• Rapid onset: Usually develops within 24 hours

HHS Overview

• Common in Type 2 diabetes, elderly patients (>65 years)
• Glucose markedly elevated: Often >1000 mg/dL
• Serum osmolality severely elevated (>320 mOsm/kg)
• Minimal or no ketoacidosis (pH usually >7.3)
• More profound dehydration than DKA (fluid deficit 8-10L)
• Slow, insidious onset: Develops over several days
• Higher mortality rate than DKA

DKA vs HHS Comparison Table

• Age: DKA younger (<65) | HHS older (>65)
• Diabetes type: DKA = Type 1 | HHS = Type 2
• Onset: DKA rapid (<24 hrs) | HHS gradual (days)
• Glucose: DKA 300-800 | HHS >600-1000 mg/dL
• pH: DKA <7.3 (acidosis) | HHS usually >7.3
• Ketones: DKA present | HHS minimal/absent
• Osmolality: DKA variable | HHS >320
• Anion gap: DKA >20 | HHS often normal

Clinical Presentation Differences

• DKA presentation: Kussmaul respirations (deep, rapid breathing to blow off CO2)
• DKA: Fruity (acetone) breath odor from ketone production
• DKA: Abdominal pain, nausea, vomiting common
• HHS presentation: Profound neurological changes predominate
• HHS: Lethargy, confusion, seizures, coma (from hyperosmolarity)
• HHS: Focal neurological deficits may mimic stroke
• Both: Polyuria, polydipsia, dehydration signs

Fluid Loss Comparison

• DKA: Urine output typically >5 liters due to osmotic diuresis
• HHS: Urine output even greater (>9 liters) with severe hyperosmolarity
• Both conditions cause significant electrolyte depletion
• Total body potassium depleted despite possible initial hyperkalemia
• Aggressive fluid resuscitation is cornerstone of treatment

Treatment Principles

• Fluids FIRST: Aggressive NS initially (1-2L in first hour)
• Switch to 0.45% NS when volume replete or Na >135
• Add dextrose when glucose <200-250 mg/dL (prevents hypoglycemia)
• Insulin: IV regular insulin drip AFTER initial fluid bolus
• DKA: Continue insulin until anion gap closes (not just glucose)
• HHS: Slower glucose correction to prevent cerebral edema
• Potassium: Replace when K <5.3 and patient voiding
• Monitor: Glucose hourly, BMP every 2-4 hours
• Transition to SQ insulin when eating and stable

Adrenal Disorders

Adrenal Gland Hormones

• Cortex produces: Cortisol, Aldosterone, Androgens
• Medulla produces: Catecholamines (epi, norepi)
• Cortisol: Stress response, glucose regulation, anti-inflammatory
• Aldosterone: Na retention, K excretion, BP regulation

Adrenal Insufficiency (Addison's)

• Primary: Destruction of adrenal glands (autoimmune, infection, hemorrhage)
• Secondary: Pituitary failure, chronic steroid use (suppressed HPA axis)
• Symptoms: Fatigue, weight loss, hyperpigmentation (primary only)
• Labs: Hyponatremia, Hyperkalemia, Hypoglycemia

Adrenal Crisis

• Life-threatening emergency
• Triggers: Stress, surgery, infection in patient with adrenal insufficiency
• Presentation: Severe hypotension, shock, altered mental status
• Treatment: IV fluids (NS or D5NS), Hydrocortisone 100mg IV bolus
• Stress-dose steroids: Hydrocortisone 50-100mg every 6-8 hours
• Do not wait for lab confirmation to treat

Thyroid Disorders

Thyroid Hormone Physiology

• TSH from pituitary stimulates thyroid
• T4 (thyroxine): Main secreted hormone, converted to T3
• T3 (triiodothyronine): Active hormone
• Negative feedback: High T3/T4 suppresses TSH

Hyperthyroidism

• Causes: Graves disease (most common), toxic nodule, thyroiditis
• Symptoms: Tachycardia, weight loss, heat intolerance, tremor, anxiety
• Graves: Exophthalmos, goiter, pretibial myxedema
• Labs: Low TSH, High T3/T4
• Treatment: Beta blockers, PTU/Methimazole, radioactive iodine, surgery

Thyroid Storm

• Life-threatening hyperthyroidism
• Triggers: Surgery, infection, trauma, iodine load in untreated hyperthyroidism
• Signs: Fever >104°F, severe tachycardia (>140), altered mental status
• Hypertension, then hypotension and shock
• Treatment: Beta blockers (control HR), PTU (blocks synthesis)
• Iodine (after PTU - blocks release), Glucocorticoids
• Cooling measures, treat precipitant

Hypothyroidism

• Causes: Hashimoto thyroiditis (autoimmune), iodine deficiency, post-treatment
• Symptoms: Fatigue, cold intolerance, weight gain, constipation, bradycardia
• Labs: High TSH, Low T4
• Treatment: Levothyroxine (T4) replacement

Myxedema Coma

• Severe, decompensated hypothyroidism
• Triggers: Cold exposure, infection, sedatives in untreated hypothyroidism
• Signs: Hypothermia, bradycardia, hypotension, altered mental status
• Hyponatremia, hypoglycemia, hypoventilation
• Treatment: IV thyroid hormone (T4 +/- T3), Glucocorticoids
• Supportive care: Warming, ventilatory support, fluids
• High mortality even with treatment

Hypo vs Hyperthyroidism Comparison

Laboratory Findings

• HYPERTHYROIDISM: TSH ↓ (suppressed), T3+T4 ↑ (elevated)
• HYPOTHYROIDISM: TSH ↑ (elevated), T4 ↓ (decreased)
• TSH is the most sensitive indicator of thyroid function
• Primary thyroid disease: TSH moves opposite to T3/T4
• Secondary (pituitary) disease: TSH moves same direction as T3/T4

Cardiovascular Signs

• HYPERTHYROIDISM: Tachycardia, hypertension, palpitations, atrial fibrillation
• HYPOTHYROIDISM: Bradycardia, hypotension, pericardial effusion
• Think: HYPER = heart racing | HYPO = heart slowing

Metabolic & Thermoregulation

• HYPERTHYROIDISM: Heat intolerance, diaphoresis, weight loss despite increased appetite
• HYPOTHYROIDISM: Cold intolerance, dry skin, weight gain, constipation
• Think: HYPER = running hot | HYPO = running cold

Neurological & Psychiatric

• HYPERTHYROIDISM: Anxiety, tremors, restlessness, insomnia, hyperreflexia
• HYPOTHYROIDISM: Depression, fatigue, lethargy, slowed cognition, hyporeflexia
• Think: HYPER = revved up | HYPO = slowed down

Physical Exam Findings

• HYPERTHYROIDISM: Exophthalmos (Graves), goiter, warm moist skin, fine tremor
• HYPOTHYROIDISM: Myxedema (non-pitting edema), coarse dry skin, hair loss, hoarse voice
• Both may present with goiter depending on cause

Life-Threatening Complications

• HYPERTHYROIDISM: Thyroid Storm - fever >104°F, severe tachycardia, AMS, cardiovascular collapse
• HYPOTHYROIDISM: Myxedema Coma - hypothermia, bradycardia, hypotension, coma, respiratory failure
• Both are medical emergencies requiring immediate intervention

Treatment Approaches

• HYPERTHYROIDISM: Beta blockers (symptom control), PTU/Methimazole (synthesis), Iodine, Hydrocortisone
• HYPOTHYROIDISM: Levothyroxine PO daily (before breakfast for absorption)
• THYROID STORM: Add IV fluids, cooling measures, treat precipitant
• MYXEDEMA COMA: IV T4 + T3, IV hydrocortisone, passive warming, ventilatory support

SIADH & Diabetes Insipidus

SIADH (Syndrome of Inappropriate ADH)

• Excess ADH secretion → water retention → dilutional hyponatremia
• Causes: CNS disorders, malignancy (small cell lung), pulmonary disease, medications
• Labs: Serum Na <135, Serum Osm <275, Urine Osm >100, Urine Na >40
• Euvolemic or mildly hypervolemic
• Treatment: Fluid restriction, Hypertonic saline if severe/symptomatic
• Correct Na slowly: 8-10 mEq/L per 24 hours max

Diabetes Insipidus (DI)

• Insufficient ADH effect → massive water loss → hypernatremia
• Central DI: Brain doesn't produce ADH (trauma, surgery, tumors)
• Nephrogenic DI: Kidneys don't respond to ADH (lithium, hypercalcemia)
• Symptoms: Polyuria (5-15 L/day), extreme thirst, dilute urine
• Labs: Serum Na >145, Serum Osm >295, Urine Osm <200, Specific gravity <1.005

DI Treatment

• Central DI: DDAVP (synthetic ADH)
• Nephrogenic DI: Thiazide diuretics (paradoxical effect), treat underlying cause
• Free water replacement: Calculate water deficit
• Monitor serum sodium closely
• In ICU: Often see central DI post-neurosurgery or with brain death

SIADH vs DI Comparison Table

• Serum ADH: SIADH = HIGH | DI = LOW
• Urine Output: SIADH = LOW (<0.5 mL/kg/hr) | DI = HIGH (up to 15 L/day)
• Serum Sodium: SIADH = LOW (<135) | DI = HIGH (>145)
• Serum Osmolality: SIADH = LOW (<275) | DI = HIGH (>295)
• Urine Osmolality: SIADH = HIGH (>100) | DI = LOW (<200)
• Urine Specific Gravity: SIADH = HIGH (>1.020) | DI = LOW (<1.005)
• Urine Sodium: SIADH = HIGH (>40) | DI = LOW (<20)

Clinical Pearl: Quick Differentiation

• SIADH = "Soaking wet inside" - retaining water, diluting everything
• DI = "Drying out" - losing water, concentrating everything
• Both can cause altered mental status but from opposite causes
• SIADH risk: Cerebral edema from hyponatremia → seizures
• DI risk: Severe dehydration → hypernatremia → CNS dysfunction