Parathyroid Pathology Flashcards

1
Q

Parathyroid Histology

Cells (3) with Features, Aging Effects (2)

A

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)

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2
Q

Parathyroid Hormone
Stimulation and Effects
Bone, Kidneys (3), Small Intestine

A

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

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3
Q

Primary Hyperparathyroidism

Etiologies (3) and Clinical Features (5)

A

Parathyroid Adenoma (most common)
Primary Hyperplasia
Parathyroid Carcinoma

Bones: Osteoporosis, Osteitis Fibrosis Cystica
Renal Stones
Abdominal Groans: Constipation, Gallstones
Psychiatric Moans: Depression

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4
Q
Parathyroid Adenoma
Molecular Defects (2), Morphology (3) and Diagnosis
A

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

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5
Q

Parathyroid Hyperplasia

Morphology (4) and Possible Etiology

A

All 4 parathyroid glands usually affected
Mostly chief cell hyperplasia
Absence of adipocytes
Water-clear cell hyperplasia less common

MEN syndromes

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6
Q

Parathyroid Carcinoma

Signs (4)

A

PTH that doesn’t decrease after surgery
Adjacent tissue invasion
Vascular invasion
Metastasis

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7
Q
Hypercalcemia Etiologies
Elevated PTH (2) and Decreased PTH (5)
A

Elevated:
Hyperparathyroidism
Familial hypocalciuric hypercalcemia

Decreased: 
Malignancy
Vitamin D Toxicity
Immobilization
Thiazide Diuretics
Sarcoidosis
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8
Q
Hypercalcemia of Malignancy Pathogenesis
PTHrP Related (2), Vitamin D Related (2) and Osteolytic (3)
A

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

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9
Q

Secondary Hyperparathyroidism
Description (2), Etiology,
Clinical Features (2) with Descriptions

A

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

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10
Q

Tertiary Hyperparathyroidism

Pathogenesis (3)

A

Chronic hypocalcemia
Parathyroid begins to function autonomously and excessively
Resultant hypercalcemia

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11
Q
Hypoparathyroidism
Clinical Features (4) and Physical Exam Findings (3)
A

Behavioral disturbance/stupor
Paresthesias
Muscle tetany and cramps
Convulsions

(+) Trosseau sign
(+) Chvostek sign
Prolonged QT on EKG

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12
Q

Hypoparathyroidism
Etiologies with Descriptions
Acquired (2) and Congenital (3)

A

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

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13
Q

CASR Gene Mutations
Inactivating and Activating
Associated Disease and Pathogenesis

A

Inactivating:
Familial Hypocalciuric Hypercalcemia
PTH increased causing increased calcium with decreased excretion by kidneys

Activating:
Autosomal dominant Hypoparathyroidism
PTH decreased causing Hypercalciuria and Hypocalcemia

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14
Q

DiGeorge Syndrome

Etiology and Clinical Features (4)

A

22q11.2 chromosome deletion

Thymic hypoplasia (immune deficiency)
Truncus arteriosus (cyanosis)
Tetralogy of Fallot (cyanosis)
Parathyroid hypoplasia (tetany)
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15
Q
Pseudohypoparathyroidism
Pathogenesis (2) and Lab Findings (3)
A

Defective GPCR causing end organ PTH resistance

Normal/Elevated PTH
Hyperphosphatemia
Hypocalcemia

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