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14 Cards in this Set

  • Front
  • Back
Made by C cells of thyroid:

Chief cells of parathyroid gland make:

Anatomic location of thyroid:

Origin of superior/inferior thyroid arteries:

Each lobe consists of:
calcitonin

PTH

tracheal cartilage 2-3

superior - common carotid
inferior - thyrocervical trunk

follicles filled with colloid
Thyroid follicle produces:

Explain exocrine synthesis of TGB:

Anti-thyroid drugs block what?
thyroglobulin - TGB

AA's/iodine uptake into cell --> TGB synthesized on RER --> iodide/tyrosine residues attach --> exocytosis

addition of iodide/tyrosine to TGB
Step of endocrine portion/secretion:

Which is more potent, T3 or T4?
1a. endocytosis/digestion of colloid from TSH stimulus
1b. colloid fuses w/ lysosomes
1c. digestive enzymes release T3, T4, iodine
2. T3/T4 diffuse through membrane into capillary - transport facilitated by thyroxine-binding protein

T3 - 3-4x more potent
Function of thyroid hormone:

Found in isolated clusters between follicles or in follicular epithelium, produce calcitonin:

Function of calcitonin:
stimulates metabolic rate
augments thermogenesis
augments glucose production
required for normal CNS development

parafollicular (C) cells

acts to decrease Ca++ by inhibiting bone resorption - binds to osteoclast
Explain formation of thyroid gland:

Common abnormalities of development:
endoderm invaginates into mesoderm --> creates thyroid diverticulum on tongue --> grows inferiorly between 2nd/3rd pharyngeal arches --> migrates to anterior trachea

lingual thyroid, pyramidal lobe, thyroglossal cyst/fistula, congenital hypothyroid (cretinism)
Common causes of hyperthyroid:

Cause of Grave's disease:

exophthalmos is due to what?

Tx?
excessive TSH - from pituitary, Grave's, ingestion of T4 (weight loss)

TSI attached to TSH receptor --> increased thyroid hormone

collagen deposition behind eyeball

surgical removal, radioactive iodine
symptoms of hypothyroid:

Causes:

Tx:
cold intolerance, low metabolic rate, weight gain, photophobia

decreased iodine intake, loss of pituitary stimulation, autoimmune destruction

oral thyroid meds
Endemic goiter is due to:

S/S of cretinism:
iodine deficiency

poor growth
bone maturation and puberty delayed
poor ovulation/infertility
neurologic impairment
mild-severe retardation
Structure/development of parathyroid:

Secretes PTH:

PTH function:

Role of Vitamin D?
3rd (PT 4)/4th (PT 3) pharyngeal pouches

chief cells

regulates Ca/Phosphate --> promotes osteoclasts --> increased serum Ca++
acts on kidney to resorb Ca++

stimulates GI mucosal cells to absorb Ca and synthesize calbindin (carrier protein)
Explain pathway of 7-DHC in skin to intestine:

PTH activity is balanced by what hormone?

Explain blood/bone calcium in hypoPTH:
7-DHC --> (UV) --> Vitamin D3 --> liver --> 25-hydroxycholecalciferol --> kidney --> PTH --> calcitrol --> intestine --> increased Ca++ absorption

calcitonin

low blood Ca++, bone Ca++ not released --> tetany
Hyper-PTH causes what?

Cell lineage of osteoblasts:

Primary function:

Osteoblasts have surface receptor for:
high serum Ca++, bone loss (osteomalacia), abnormal Ca++ deposition in kidneys, arteries

osteoprogenitor cells --> osteoblasts

deposition/mineralization of osteoid --> new bone formation

PTH
Osteoblasts secrete what for bone mineralization?

Mediates osteoblast binding to ECM:

induces preosteoclasts --> osteoclasts:

involved in osteoclast development:

mediates formation of sealing zone:
osteocalcin, osteonectin

bone sialoprotein

OPG - osteoprotegerin

RANKL

osteopontin
Osteoclast cell lineage:

Do osteoclasts have PTH receptors?

3 signaling molecules crucial to osteoclast development:
monocytes --> macrophages --> resting osteoclast --> functional osteoclast

no - response to cytokines released from osteoblasts

MCS-F - binds to macrophages --> osteoclast precursors
RANK-L - cell membrane protein - induces final differentiation
OPG - keeps osteoclasts in resting mode until needed
How do osteoclasts function?

Calcitonins effect on osteoclasts:
develop ruffled borders at resorption sites
resorption lacuna form - sealed EC compartment
produce H+/HCO3-, lysosomal hydrolases released
bone matrix degraded, releasing minerals

calcitonin inhibits activity