Week 3 (Endocrine)

-Hashimoto's: autoimmune destruction of thyroid tissue
-Iodine deficiency: insufficient raw material for hormone production
-Post-Thyroidectomy: surgical removal of thyroid gland
-Medications: lithium, amiodarone can impair thyroid function

-Unexplained weight gain
-Swelling around the eyes
-Dry skin with less sweating, hair loss, brittle nails with ridges, and feeling unusually cold
-Bradycardia
-High blood pressure, reduced heart output
-Cognitive changes: memory impairment, slowed thinking, difficulty concentrating

-Elevated TSH
-Low T4
-Elevated lipids, CK, liver enzymes

Levothyroxine

-Hyperthyroidism
-Untreated adrenal insufficiency
-Untreated cardiac arrhythmia
-Myocardial infarction
-Inflammatory cardiac process

-Dosing is weight based
-Given by mouth or IV
-Take one hour before meal or three hours after a meal

-Thyroid overproduces T3 and T4 hormones
-Body systems function at increased rates
-Negative feedback inhibits pituitary TSH production

-Graves' disease: Autoimmune disorder where antibodies mimic TSH causing unregulated thyroid hormone production
-Toxic nodular goiter: Multiple autonomous hyperactive nodules develop in the thyroid
-Thyroiditis: Inflammation causes release of preformed thyroid hormones creating temporary hyperthyroidism lasting 2-6 months, often followed by hypothyroidism
-TSH-secreting pituitary tumors: <1% of cases

-Metabolic: weight loss despite increased appetite, heat intolerance, sweating
-Cardiovascular: tachycardia, palpitations, hypertension, atrial fibrillation
-Neurologic: anxiety, tremors, hyperreflexia, insomnia
-Gastrointestinal: frequent bowel movements, diarrhea, nausea
-Ocular (Graves'): exopthalmos, lid lag, periorbital edema

-Decreased TSH
-Increased free T3 and free T4
-Thyroid stimulating immunoglobulin: positive in Graves' disease
-TRH stimulation test: absent TSH response in primary hyperthyroidism; helpful in differentiating from secondary causes

Methimazole and PTU inhibit thyroid hormone synthesis
*Usually first-line for new diagnosis or mild cases

-Treatment for hyperthyroidism
-Destroys thyroid cells that take up iodine
-Often leads to hypothyroidism requiring replacement

-Surgical removal of part or all of the thyroid
-Used to treat hyperthyroidism
-Used for large goiters or when other treatments fail

-Beta-blockers: propranolol, metoprolol, atenolol; controls heart rate, tremors, and anxiety
-Benefits: rapid symptom relief; reduced cardiac workload; improves quality of life
-Monitoring: heart rate and BP; signs of bronchospasm; hypoglycemia masking

*MEDICAL EMERGENCY
-High fever: life-threatening hyperthermia requires immediate cooling
-Extreme tachycardia: HR may exceed 180 bpm with arrhythmias
-30% mortality rate, even with treatment

-Cardiovascular monitoring: check heart rate, rhythm, and blood pressure frequently
-Nutritional support: offer high-calorie, high-protein diet with frequent small meals
-Temperature regulation: provide cool environment and light clothing
-Eye care: apply lubricating drops for exophthalmos and lid lag

-Airway management
-Voice assessment: check for hoarseness indicating potential recurrent laryngeal nerve damage during surgery
-Calcium monitoring: assess for signs of hypocalcemia due to inadvertent parathyroid gland injury or removal
-Incision care: monitor surgical site for bleeding, infection, and ensure proper wound healing

-Decreased PTH
-Hypocalcemia: reduced calcium resorption from bone and kidneys
-Hyperphosphatemia: decreased phosphate excretion by kidneys
-Neuromuscular irritability: calcium imbalance causes nerve and muscle dysfunction

-Surgical damage is the most common cause
-Autoimmune destruction of parathyroid tissue
-Genetic: DiGeorge syndrome or other genetic disorders affecting development

-Neuromuscular: tetany, muscle cramps, paresthesias, seizures
-Dermatological: dry skin, brittle nails, hair loss, candidiasis
-Cardiovascular: prolonged QT interval, heart failure, arrhythmias
-Neurological: seizures, cognitive impairment, basal ganglia calcifications

-Decreased PTH
-Decreased calcium
-Elevated phosphorus
-Slightly decreased magnesium

-Acute management: IV calcium gluconate for severe symptoms; monitor cardiac function during administration
-Long-term therapy: oral calcium supplements (calcium carbonate or citrate); active vitamin D (calcitriol) to enhance calcium absorption
-Emerging therapy: recombinant human PTH (Natpara) for refractory cases; may reduce calcium and vitamin D requirements

-Seizure Precautions: maintain safe environment with padded side rails; keep emergency medications readily available
-Airway management: monitor for laryngospasm and respiratory distress; keep emergency airway equipment accessible
-Cardiac monitoring: observe for QT prolongation and arrhythmias; monitor vital signs frequently

-Increased PTH Secretion: often from parathyroid adenoma
-Enhanced Bone Resorption: calcium is released from bones, leading to osteoporosis
-Altered Renal Handling: increased calcium reabsorption and phosphate excretion

*Bones, stones, groans, and psychiatric overtones*
-Skeletal Manifestations: bone pain and increased risk of fractures due to osteoporosis
-Renal Manifestations: kidney stones
-Gastrointestinal Manifestations: abdominal complaints including constipation, nausea, and peptic ulcers
-Neuropsychiatric Manifestations: mental status changes including fatigue, depression, and cognitive dysfunction

-Primary: intrinsic parathyroid gland disorder (adenoma, hyperplasia, carcinoma)
-Secondary: compensatory response to hypocalcemia (Vitamin D deficiency, CKD, malabsorptioin)
-Tertiary: autonomous function after long-standing secondary (renal transplant patients, advanced renal disease)

-Surgical approach: parathyroidectomy
-Medication management: cinacalcet (calcimimetic) reduces PTH secretion; biphosphonates protect bone density
-Supportive care: hydration to prevent kidney stones; dietary calcium in moderation

-Central DI: insufficient ADH production by hypothalamus
-Nephrogenic DI: kidney resistance to ADH action
-Water Regulation: inability to concentrate urine
-Resule: polyuria and fluid imbalance

-Head trauma
-Neurosurgery
-Brain tumors
-Autoimmune

-Medications (lithium)
-CKD
-Hypercalcemia
-Genetic mutations

-Massive daily urine production (polyuria)
-Urine gravity <1.005: extremely dilute urine, clear as water
-Extreme thirst (polydipsia) compensates for losses

-Desmopressin (DDAVP): first-line therapy administered as intranasal spray
-Careful titration required to prevent hyponatremia, especially in elderly patients
-Monitor serum sodium levels 1-2 weeks after initiation and dose adjustments

-Thiazide diuretics paradoxically reduce urine output by promoting proximal tubular water reabsorption
-Dietary sodium restriction
-NSAIDs like indomethacin may reduce GFR and increase water reabsorption in resistant cases
-Amiloride for lithium-induced nephrogenic DI

-Fluid management: strict intake and output monitoring; daily weight measurements
-Electrolyte monitoring
-Medical Alert: encourage patients to wear medical identification; ensure emergency plan is in place

-MOA: Synthetic T4 hormone that converts to T3 in the body
-Indications: Primary or secondary hypothyroidism; post-thyroidectomy replacement

-Side Effects: palpitations, tachycardia, insomnia, weight loss, anxiety
-Nursing Care: monitor TSH and free T4 levels; check heart rate and blood pressure

-MOA: blocks iodine incorporation
-First-line treatment for most hyperthyroidism cases

-Avoid in first trimester pregnancy
-Monitor for rash, agranulocytosis

-MOA: blocks T4 to T3 conversion
-Preferred treatment in thyroid storm and pregnancy

-Higher risk of hepatotoxicity
-Monitor liver function tests

Examples: methimazole (tapazole), propylthiouracil (PTU)
-Report fever or sore throat immediately
-Takes weeks for full effect
-Never stop suddenly

-Administration: administer slowly via IV; monitor ECG continuously during infusion
-Indications: tetany and seizures from hypocalcemia; calcium channel blocker overdose
-Adverse effects: flushing, hypotension, cardiac dysrhythmias with rapid administration
-Monitoring: check calcium, magnesium, phosphorus levels; watch IV site for infiltration

-Potent form of vitamin D3 that doesn't require kidney activation
-Increases calcium absorption from GI tract and mobilizes bone calcium

-Regular calcium and phosphate checks; watch for hypercalcemia signs
-Promotes calcium reabsorption in kidneys; vital in renal osteodystrophy

-MOA: Increases sensitivity of calcium-sensing receptors; decreases PTH without raising calcium levels
-Indications: Secondary hyperparathyroidism in end-stage renal disease; alternative to a parathyroidectomy in some cases

-Monitoring: check calcium and PTH levels regularly. Watch for hypocalcemia symptoms. Monitor ECG for QT prolongation
-Education: take with food to minimize nausea. Report muscle cramps or tingling immediately. Regular lab work is essential.

MOA: Synthetic ADH analog enhances renal water reabsorption

-Can cause water intoxication if overdosed
-Track fluid intake/output and sodium levels

-MOA: Creates mild hypovolemia to increase proximal tubule reabsorption; diuretic that paradoxically reduces urine output in NDI
-Monitoring: Monitor for hypokalemia and hyponatremia

Take on an empty stomach. Space from calcium/iron by 4 hours

Report fever immediately. Never stop suddenly.

Check pulse before doses. Rise slowly from sitting.

Take with calcium supplements. Maintain hydration.

Monitor for headaches. Avoid excessive fluid intake.