Parathyroid & Adrenal Gland Disorders

• These notes cover parathyroid disorders, adrenal gland disorders, Cushing's syndrome, and pheochromocytoma

Parathyroid Disorders

• Involves hyperfunction and hypofunction of the parathyroid glands (PTG)
• There are four PTGs situated in the neck on the posterior side of the thyroid
• PTGs produce parathormone/parathyroid hormones (PTH), which regulate calcium and phosphorus

Role of PTH

• Increased PTH increases calcium absorption and serum calcium
• PTH's action is influenced by vitamin D, which promotes its function
• Decreased PTH decreases Phosphorus
• Increased calcium lowers PTH secretion via negative feedback
• Calcitonin is released when calcium levels increase, opposing PTH's action

Hyperparathyroidism

• Overproduction of PTH leading to hypercalcemia
• Causes bone decalcification and renal calculi (kidney stones containing calcium)
• Primary hyperparathyroidism: PTG secretes excessive parathormone
• Secondary hyperparathyroidism: caused by chronic kidney failure and renal rickets
• Renal Rickets causes CKD and bone deformity (softening) d/t potassium retention, increased stimulation of PTG, and increased parathormone secretion

Hyperparathyroidism Clinical Manifestations

• Neurological symptoms from direct calcium action on the brain and nervous system
• Increased calcium decreases nerve and muscle tissue excitation
• Neurosis, psychosis, psychomotor, and personality disturbances
• Presence of memory loss, depression, stupor, or coma
• GI symptoms include abdominal pain, anorexia, N&V, dyspepsia, constipation
• Neuromuscular and musculoskeletal symptoms: fatigue, muscle weakness/atrophy, lower back pain, fractures, bone/joint pain from demineralization/tumors
• Renal symptoms: nephrolithiasis with stone formation in one or both kidneys

Hyperparathyroidism: Condition Specific Symptoms

• Condition relates to increased excretion of renal calculi and phosphorus
• Can lead to renal insufficiency from calcium phosphate precipitation in renal pelvis/parenchyma

Hyperparathyroidism: Diagnostic Tests

• Increased serum calcium and decreased PO4 levels
• Radioimmunoassay differentiates primary hyperparathyroidism using antigen-antibody binding and radioactive iodine
• X-rays show bone changes, cysts, and erosions from demineralization
• Bone scans are for advanced cases
• Double-Ab PTH test distinguishes it from hyperparathyroidism caused by malignancy
• UTZ, MRI, Thallium scan, FNB evaluate PTG function and localize cysts, adenoma, and hyperplasia

Hyperparathyroidism: Medical Management

• Parathyroidectomy: surgical removal of abnormal parathyroid tissues and in some cases, only a single diseased gland is removed
• Hydration: encourages daily fluid intake of 2000 ml+ to prevent calculus formation, and patients should report calculi symptoms
• Avoid diuretics, which decrease calcium excretion, and avoid dehydration

Hyperparathyroidism: Hypercalcemic Crisis Prevention

• Prevent extreme elevation of serum calcium levels
• Normal calcium: 8.8 – 10.4 mg/dL; over 13 mg/dL causes life-threatening neurological, cardiovascular, and renal symptoms
• Manage the crisis with rapid hydration using IV isotonic solution to maintain urine output of 100-150 mL; administer calcitonin to promote renal excretion and reduce bone resorption
• Immediate consultation is needed for dehydration symptoms
• Encourage mobility for immobile clients at risk for renal calculi
• Restrict calcium intake and administer loop diuretics (furosemide, ethacrynic acid), oral calcitonin, and bisphosphonates
• Emergency treatments include mithramycin (cytotoxic), calcitonin, and dialysis

Hyperparathyroidism: Nursing Management

• Detect tetany symptoms early post-op

Hypoparathyroidism

• Deficiency in parathormone
• Results in hypocalcemia and Hyperphosphatemia
• It is caused by decreased intestinal calcium absorption and decreased bone resorption
• Results in hypophosphaturia and decreased renal secretion of phosphorus

Hypoparathyroidism: Causes

• Congenital absence, autoimmune disease, removal of PTG, S/P thyroidectomy, massive thyroid radiation therapy, and low serum calcium from PTH deficiency
• Can cause neuromuscular irritability, leading to hypocalcemia manifestations

Hypoparathyroidism: Hypocalcemia Symptoms

• Tetany occurs, indicated (+) Chvostek's and Trousseau's sign tests
• General muscle hypertonia (increased resistance to manual movement = increased stiffness), tremors, spasms (a/w uncoordinated contraction w/ or w/o efforts to make voluntary movement)
• Latent symptoms present which include Numbness, tingling, cramps in the extremities, hands and feet stiffness
• Overt symptoms present which include Bronchospasm, Laryngeal spasm, and Carpopedal spasm

Hypoparathyroidism: Overt Symptom Specifics

• Flexion of the elbows, wrist
• Extension of carpophalangeal joints
• Dorsiflexion of feet
• Dysphagia
• Cardiac arrhythmias, hypotension, ECG changes
• Seizures
• Anxiety, irritability, depression, and delirium

Hypoparathyroidism: Diagnosis

• (+) Chvostek’s and Trousseau’s sign are observed
• Diagnosing is difficult due to vague symptoms
• Very low serum calcium
• Elevated serum PO4
• X-ray may reveal increased bone density and calcification of subcutaneous paraspinal basal ganglia of brain
• ECG shows prolonged QT intervals, QRS complex, and ST segment changes

Hypoparathyroidism: Medical Management

• Increase serum Ca to 9-10 mg/dL (or 2.2-2.5 mmoL)
• Eliminate sx of hypoparathyroidism and hypocalcemia
• Medical intervention is Calcitriol (Vit. D), Supplemental Ca & Mg, and Thiazides
• Recombinant PTH is not for hypoparathyroidism
• IV Calcium Gluconate indicated for life threatening hypocalcemia following thyroidectomy

Hypoparathyroidism: Continued Medical Management

• Uses Sedatives and anti-convulsant (Phenobarbitals) for seizures. Also include Oral Calcium, and Aluminum hydroxide, and aluminum carbonate
• Tracheostomy is needed for respiratory support during occurrences
• Keep the environment free of noise, bright lights, and sudden movement to avoid neuromuscular irritability
• Diet should consist of High Ca, low PO4 and avoid milk, milk products, egg yolk and spinach

Hypoparathyroidism: Nursing Management

• Maintain a patent IV line and Keep Ca gluconate available
• Look out for hypocalcemia symptoms and anticipate signs of tetany as well as respiratory difficulties
• Precaution for seizures, administer sedatives, and anticonvulsants
• Encouraging high Ca, low PO4 diet with tracheostomy set and ET tube available

The Adrenal Glands

• Separate and independent functions attached to the upper portion of the kidney
• The Adrenal Cortex (outer layer) is where steroid hormones are secreted
• Cortisol(glucocorticoids), Aldosterone(mineralocorticoids), Androgen(sex hormone) are secreted here
• Adrenal medulla (center) secretes catecholamines with Epinephrine and norepinephrine

The Adrenal Cortex: Secretions

• Secretion is regulated by the hypothalamus-pituitary-adrenal glands axis, as well as negative feedback mechanism-release of CRH
• Cortisol acts as Glucocorticoid: in glucose as well as CHO, CHON, and fat metabolism
• Regulates body response to stress, affects emotion stability
• Also serves A role in immune system
• Aldosterone serves a Mineralocorticoid
• Secreted when Angiotensin IIis present and acts on renal tubules/GIT to Increase Na absorption
• Increasing aldosterone helps regulate BP

The Adrenal Glands: Notes

• Note: There is also increase of Aldosterone release in the presence of hyperkalemia
• Androgens - controlled by ACTH affect male sex hormones and have minor effects

The Adrenal Medulla: Notes

• Functions as part of ANS, where secretes hormones through stimulation of the SNS
• Releases catecholamines like Epinephrine (Adrenaline) which serves 90% for Fight-flight response
• Secretion leads to reduced blood flow to unnecessary tissues but increased blood flow to necessary tissues
• Also induces release of free-fatty acids and glucose levels with Increased BMR
• Norepinephrine increases alertness/arousal, regulates BP during stress, and acts a major neurotransmitter

Adrenocortical Insufficiency (Addison’s Disease)

• Dysfunction of the hypothalamus-pituitary-adrenal Loop causes insufficient adrenal secretions
• rare condition

Adrenocortical Insufficiency (Addison’s Disease): Causes

• Autoimmune (70-90%)
• TB and histoplasmosis (fungal infection)
• Histoplasmosis damages adrenal tissues and included diagnostic workup
• Surgery and medications such as Rifampicin, Barbiturates, Ketoconazole, and Tyrosine Kinase Inhibitors and some Cancers
• Tx of corticosteroids for 2-4 wks suppresses’ fxn

Adrenocortical Insufficiency (Addison’s Disease): Clinical Manifestations

• Key concept: Know hormone functions
• Glucocorticoids promote sodium/water reabsorption and potassium excretion
• Loss of aldosterone can lead to Increased secretion of sodium/water, retain pottasium which lead to fluid deficiency hence reducing cardiac output
• Increase in ACTH causes bronze like pigmentation to knuckles, knees, etc.

Adrenocortical Insufficiency (Addison's Disease): Negative Affects

• Negative affects result from failure of hypothalamus-pituitary-adrenal gland loop/feedback system resulting in Addisonian crisis
• Addisonian crisis: severe Hypotension/Cyanosis/Fever, signs of Shock
• Medical treatment includes IV hydrocortisone followed by 3-4L of PNSS or 5% dextrose, and vasopressors
• Can also be used for infection or to manage Gl/Fluid losses

Adrenocortical Insufficiency (Addison's Disease): Clinical Diagnosis

• Diagnose through serum cortisol/plasma ACTH and Hypovolemia
• Other means of diagnosis include electrolyte imbalance due to sodium/potassium excretion
• Administer HRT (hormone replacement therapy)
• The primary Glucocorticoid is Cortisone/Hydrocortisone and for early morning at doses a third of which stimulate diurnal rhythm
• Mineralocorticoids includes Fludrocortisone acetate
• Monitor patients BP, and perform skin checks

Cushing's syndrome

• Results from adrenal cortex hyper function, leading to excessive secretion
• Specifically affects Mineralocorticoids, Glucocorticoids and Androgens

Cushing's Syndrome: Causes

• Prolonged use of corticosteroid therapy (most common)
• Excessive glucocorticoid production from hyperplasia of adrenal cortex or Pituitary gland tumor

Cushing's Syndrome: Clinical Manifestations

• Commonly affects women between ages 20-40
• It triggers central-type of obesity and results in Fatty “buffalo hump”

Cushing's Syndrome: Skin Related Symptoms

• Commonly leads to skin conditions related to easy wounding, purple striae on trunk as well as thin extremities
• Sodium and water retention and sleep disturbance is also expected

Cushing's Syndrome: Diagnostic Test

• Perform tests with high focus on urine analysis and cortisol level analysis as well as the Urinary cortisol,
• A common tool for analysis includes Low-dose dexamethasone suppression test

Pheochromocytoma

• A rare tumor stemming from the chromaffin cells. Leads to excessive epinephrine/norepinephrine secretion that induces hypertension, headache, hyperhidrosis
• Use the hormone that originates from adrenal medulla during excessive secretion
• Hypertension is a common hallmark with 5'HS
• Use urine or plasma levels test for direct conclusive test and avoid Coffee/Tea to prevent any change.
• Use the medical/nursing managements to reduce the cause.