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22 Cards in this Set
- Front
- Back
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Parathyroid gland
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*CHIEF CELLS: polygonal, central round nuclei. Contain GLYCOGEN & SECRETORY GRANULES that contain parathyroid hormone.
*OXYPHIL CELLS: singly/clusters, larger w/ inc mito w/ no secretory granules. *amount of fat at max of 25% of gland at age 25. *regulated by level of free/ionized Ca+ in blood. Dec serum Ca+ stim synth & secretion of PTH |
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Parathyroid Hormone
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*inc renal tubular reabsorption of Ca++,
*conversion of VitD-->active form in kidneys, *inc urinary phosphate exretion--> dec serum P levels *inc GI Ca+ absorption * NET RESULT = INCREASE level free Ca+--> inhib PTH secretion |
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Hypercalcemia
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*caused by inc levels of PTH, usu malignancies, esp advanced lesions due to bone resorption
*solid tumors secret PTH RELATED PROTEIN (PTHrP)--> espression of receptor activator of NUCLEAR FACTOR KAPPA BETA LIGAND (RANKL) *RANKL =on osteoblasts, osteoclast differentiation factor which binds RANK on surface of osteoclast progenitor cells--> differentiation --> mature osteoclasts *OSTEOPROTEGRIN: decoy receptor of RANKL, removes excess ligand & prevent unbalanced bone resorption. secreted by osteoblasts & inhibited by RANKL--> alter RANKL/OSTEOPROTEGRIN RATIO TO FAVOR OSTEOCLASTOGENESIS |
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Primary Hyperparathyroidism
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*common, esp F, causes hypercalcemia
*CAUSE: adenomas, primary hyperplasia, parathyroid carcinoma, & solitary parathyroid adenoma in a sporadic setting. *familial kind assoc w/ MEN1 &MEN 2 & familial hypocalciuric hypercalcemia |
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Familial Primary Hyperthyroidism
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*MEN-1: inactivated MEN1 gene on chr 11q13 in parathyroid adenomas & parathyroid hyperplasia
*MEN2: caused by activ mutations in tyrosine kinase-R RET on chr 10q, assoc w/ parathyroid hyperplasia *FAMILIAL HYPOCALCIURIC HYPERCALCEMIA: autosomal dominant, assoc w/ enhance parathyroid fxn due to dec sensitivity to extracell Ca from inactive mut in parathyroid Ca sensing receptor gene (CASR) on chr 3q |
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Sporadic parathyroid adenomas
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* Caused by 2 molec defects:
1. CYCLIN D1 GENE INVERSION: cylcin prot overexpressed--> cell prolif 2. MEN 1 MUTATION: including ones not assoc w/ MEN syndrome. |
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Parathyroid Adenoma
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*Usu solitary, well circ, soft, tan red/brown nodule w/ capsule. Glands outside of adenoma normal/slight shrink.
*uniform cheif cells w/ polygonal shape & small central nuclei. Dec Fat. *pleomorphic cells, but benign. Nests of large oxyphil cells. *OXYPHIL ADENOMA: entire adenoma composed of oxyphils |
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Primary hyperplasia
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*occur sporadically, or w/ MEN syndome.
*all 4 glands usu involv but occas just one or 2 *cheif cell hyperplasia, diffuse or multinodular. Dec fat. |
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Skeletal Changes in hyperparathyroidism
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* inc # of osteoclasts: erode bone matrix to mobilize Ca+ salts esp in metaphyses of long bones.
*bone resorption-->inc osteoblast activ & form new boney trabeculae *OSTEITIS FIBROSA CYSTICA: thin cortex w/ marrow containing inc amounts of fibrous tissue w/ foci of hemorrhage & cyst formation. *BROWN TUMORS: aggs of oclasts, hemorrhage & giant cells resembling neoplasms. *Hypercalcemia--> renal stones, calcification of renal tubules/interstitium. Met calcification of stomach, lungs, myocardium, & BV |
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Parathyroid Carcinoma
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*circumscribed, appear similar to adenomas, clearly invasive.
*involve one parathyroid w/ irreg mass, >10cm *uniform cells, resemble normal cells. trabecular pattern w/ dense capsule. *for dx of malig: must invade surrounding tissue/met |
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Asymp hyperparathyroidism
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*Cause: primary hyperthyroidism.
*detected during routine blood work as hypercalcemia. *classic manifests of hyperparathyroid not always seen if identified early |
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Parathyroid Hormone Studies
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* Non parathyroid tumors: secrete PTHrP
*inc in PTH assoc w/ hypophosphatemia, inc urinary secretion of P. *secondary renal dz-->P retention & normalization of P serum levels |
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Symptomatic Primary Hyperparathyroidism
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*signs & sx reflect effects of inc PTH secretion & hypercalcemia
*Bone dz: bone pain w/ fracture of bones weakened by OSTEOPOROSIS OR OSTEITIS FIBROSA CYSTICA *nephrolithiasis: w/ pain & obstructive uropathy *GI: constipated, N, peptic ulcer, pancreatitis, gallstones *CNS: depression lethargy, seizures *neuromusc: weak, fatigue *cardio: calcificationon aortic * mitral valves |
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Secondary Hyperparathyroidism
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*arise from chronic hypocalcemia, compensartory overactivity of parathyroid gland
*RENAL FAIL IS MOST COMMON CAUSE also dec dietary Ca+, malabsorption w/ steatorrhea, VitD def *parathyroid glands hyperplastc, assymetric. inc # chief cells. Fat cells dec. *bone changes similar to primary hyperparathyroidism. *met calcifications in lung, heart, stomach, BV. *Sx dominated by chronic renal fail. *ischemia from vascular calcification *TERTIARY HYPERPARATHYROIDISM: parathyroid activ becomes autonomous & excessive--> hypercalcemia |
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Chronic renal fail
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* dec P excretion --> hyperphosphatemia
* inc P--> dec serum Ca+ & +parathyroid activity *loss of renal parenchyma--> dec availabilty of alpha-1hydroxylase (needed for synth of active Vit D)-->dec int absorp Ca+ *vit D def compounds hyperparathyroidism |
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Hypoparathyroidism
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*less common. usu from removal of glands.
*Types: APS1, autosomal dominant hypoparathyroidism, familial isolated, congenital absence of glands |
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AUTOIMMUNE POLYENDOCRINE SYNDROME TYPE 1 (APS1):
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assoc w/ mucocutaneous candidiasis & primary adrenal insufficiency
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AUTOSOMAL DOMINANT HYPOPARATHYROIDISM
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gain of fxn mutations in Ca+sensing receptor (CASR) gene which suppresses PTH--> hypocalcemia & hypercalcuria
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FAMILIAL ISOLATED HYPOPARATHYROIDISM
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rare
autosomal dominant or recessive |
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CONGENITAL ABSENCE OF PARATHYROID GLAND
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may occur in conjunction w/ other malformations such as thymic dysplasia (DiGeorge Syndrome) or cardiac defects.
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clinical manifestations of hypoparathyroidism
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*TETANY:neuromusc irritability due to dec serum ionized Ca+ conc w/ numbness, laryngospasm, seizures
*CHVOSTEK SIGN: tapping of facial nerve--> contraction of eye, nose, mouth *TROUSSEAU SIGN: carpal spasm from occlusion of circ to forearm & hand w/ BP cuff for few minutes *MENTAL STATUS CHANGE: emotional instability, anxiety, depression, psychosis, hallucinations *INTRACRANIAL MANIFESTATIONS: calcifications of basal ganglia due to inc in P levels--> tissue deposits of locally prod Ca+, parkinson like movement, inc ICP *OCULAR DZ: calcification of lens w/ cataract formation *CARDIOVASCULAR MANIFESTATIONS: conduction defect w/ prolongation of QT interval. *DENTAL ABNORMALITIES: dental hypoplasia, fail of teeth eruption, defective enamal, caries |
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pseudohypoparathyroidism
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*end organ resistance to actions of PTH
*PTH levels normal/elevated *Defects in G-prot triggered 2nd messengers. *px as hypocalcemia, hyperphosphatemia, & inc PTH |
