Parathyroid Pathology Flashcards
Parathyroid Histology
Cells (3) with Features, Aging Effects (2)
Chief Cells: Secretory granules with PTH
Oxyphil Cells: Mitochondria packed, Glycogen granules
Adipocytes
Infancy/Childhood: mostly made of chief cells
Adulthood: Stromal fat increases (to 30% of gland tissue)
Parathyroid Hormone
Stimulation and Effects
Bone, Kidneys (3), Small Intestine
Stimulated by decreased serum free Calcium
Bone: Stimulate osteoclasts to increase bone resorption
Kidneys: Increase Ca2+ reabsorption, Decrease PO4 reabsorption, Convert Vit D to Dihydroxy Vit D
Small Intestine: Increase Ca2+ absorption
Primary Hyperparathyroidism
Etiologies (3) and Clinical Features (5)
Parathyroid Adenoma (most common)
Primary Hyperplasia
Parathyroid Carcinoma
Bones: Osteoporosis, Osteitis Fibrosis Cystica
Renal Stones
Abdominal Groans: Constipation, Gallstones
Psychiatric Moans: Depression
Parathyroid Adenoma Molecular Defects (2), Morphology (3) and Diagnosis
Cyclin D1 inversion causing overexpression
MEN1 gene mutations (mostly somatic mutations)
Solitary tumor - one PT gland affected
Chief cells mostly
Rim of normal tissue surrounding tumor
Dx via Technetium scan
Parathyroid Hyperplasia
Morphology (4) and Possible Etiology
All 4 parathyroid glands usually affected
Mostly chief cell hyperplasia
Absence of adipocytes
Water-clear cell hyperplasia less common
MEN syndromes
Parathyroid Carcinoma
Signs (4)
PTH that doesn’t decrease after surgery
Adjacent tissue invasion
Vascular invasion
Metastasis
Hypercalcemia Etiologies Elevated PTH (2) and Decreased PTH (5)
Elevated:
Hyperparathyroidism
Familial hypocalciuric hypercalcemia
Decreased: Malignancy Vitamin D Toxicity Immobilization Thiazide Diuretics Sarcoidosis
Hypercalcemia of Malignancy Pathogenesis PTHrP Related (2), Vitamin D Related (2) and Osteolytic (3)
PTHrP: released by Squamous Carcinomas, acts on bone, kidneys and intestines same as PTH
Vit D: elevated by Lymphomas, stimulates bone resorption and intestinal absorption
Osteolytic: Breast carcinoma and Myeloma cause osteoclast activation
Secondary Hyperparathyroidism
Description (2), Etiology,
Clinical Features (2) with Descriptions
Chronic hypocalcemia causing compensatory parathyroid hyperplasia
Renal failure is the main cause
Renal Osteodystrophy: dissecting osteitis, Rugger Jersey Sign
Calciphylaxis: Metastatic calcification of vessels (ischemia), lungs, heart, stomach
Tertiary Hyperparathyroidism
Pathogenesis (3)
Chronic hypocalcemia
Parathyroid begins to function autonomously and excessively
Resultant hypercalcemia
Hypoparathyroidism Clinical Features (4) and Physical Exam Findings (3)
Behavioral disturbance/stupor
Paresthesias
Muscle tetany and cramps
Convulsions
(+) Trosseau sign
(+) Chvostek sign
Prolonged QT on EKG
Hypoparathyroidism
Etiologies with Descriptions
Acquired (2) and Congenital (3)
Iatrogenic (parathyroidectomy)
Autoimmune conditions
DiGeorge Syndrome: 3rd/4th pharyngeal pouch defect, absence of PT glands
CASR Activation Mutation: Autosomal dominant hypoparathyroidism, causes hypersensitive Ca2+ receptors
Familial Isolated Hypoparathyoidism
Precursor PTH can’t become functional
CASR Gene Mutations
Inactivating and Activating
Associated Disease and Pathogenesis
Inactivating:
Familial Hypocalciuric Hypercalcemia
PTH increased causing increased calcium with decreased excretion by kidneys
Activating:
Autosomal dominant Hypoparathyroidism
PTH decreased causing Hypercalciuria and Hypocalcemia
DiGeorge Syndrome
Etiology and Clinical Features (4)
22q11.2 chromosome deletion
Thymic hypoplasia (immune deficiency) Truncus arteriosus (cyanosis) Tetralogy of Fallot (cyanosis) Parathyroid hypoplasia (tetany)
Pseudohypoparathyroidism Pathogenesis (2) and Lab Findings (3)
Defective GPCR causing end organ PTH resistance
Normal/Elevated PTH
Hyperphosphatemia
Hypocalcemia