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4GHM > L8 thyroid parathyroid > Flashcards

L8 thyroid parathyroid Flashcards

1
Q

anatomy of thyroid gland

A
  • butterfly shaped, two lobes joined at the front by an isthmus
  • located in the front of neck, around larynx cartilage
  • each lobe 5x3x2cm
  • one of the largest endocrine glands, 20-60g
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2
Q

microscopic anatomy of thyroid gland

A
  • a follicle is the functioning unit
  • follicular cells: secrete thick colloid that fills lumen and iodine
  • colloid made of thyroglobulin (Tg) (high molecular weight protein)
  • Tg facilitates assembly of thyroxine (T4) and triiodothyronine (T3) in lumen
  • colloid: gelatinous protein
  • c cells: secrete calcitonin
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3
Q

TSH

A

thyroid stimulating hormone,
- prod by anterior pituitary to stimulate thyroid gland to secrete T3, T4 into bloodstream
- done by follicular cells reabsorbing iodinated Tg and degrading it.

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4
Q

T3 T4 uses

A

homeostasis of all cells
influences cell differentiation, growth, metabolism
major metabolic hormone as it targets almost all cells

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5
Q

iodide trapping

A
  • follicular cells have sodium-iodide symporter (NIS) on their cell membrane
  • NIS transport iodide along with sodium, using the sodium’s concentration gradient (maintained by NaK pump)
  • inside cell, iodide ions are transported across the cell towards the apical membrane, where pendrin facilitates the efflux of iodide into the lumen
  • the iodide ions are oxidized and incorporated into Tg, leading to the formation of thyroid hormones T3 and T4
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6
Q

sources of iodine

A

food - seafood, kelp, eggs, bread, dairy, salt
supplements

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7
Q

recommended daily intake of iodine

A

~150ug

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8
Q

TPO

A

thyroperoxidase
- exists on lumen-facing membrane of follicular cells
- catalyses oxidation of iodide ions in the presence of H2O2, converting iodide into its more reactive form, iodine, which is essential for the iodination process.
- iodine undergoes a reaction with tyrosine which results in the formation of monoiodotyrosine (MIT) and diiodotyrosine (DIT). MIT and DIT serve as precursors for the formation of the thyroid hormones T3 and T4.

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9
Q

proteolysis of Tg

A

Tg is phagocytoses into follicular cell, fuses with lysosome to form phagolysosome. Tg is them hydrolyses to T3 and T4, which are them secreted into circulation

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10
Q

T4

A

primary secretory product of thyroid gland, 70-90ug produced per day

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11
Q

T3

A

15-30ug produced per day, from two sources
1) 80% from de-iodination of T4 in peripheral tissue
2) 20% from thyroid secretion

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12
Q

enzymes that deiodinate T4

A

monodeiodinase
type I: in liver, kidney, thyroid, pituitary, 80% of the process
type II: in CNS, pituitary, brown adipose tissue, heart
type III: in placenta and CNS, converts to rT3 which is inactive

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13
Q

what is 5’ deiodination

A

the iodine atom is removed from the 5’ position of the outer ring of T4.

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14
Q

why does T4 need to be converted to T3

A

more biologically active and has a higher affinity to bind to nuclear receptors, regulating gene expression and metabolic processes in target cells

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15
Q

T4 and T3 roles in growth and development

A
  • increase formation of protein
  • increase utilization of O2 and ATP synthesis
  • increase heat production
  • increase fat metabolism
  • decrease fat store
    -essential for normal brain development
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16
Q

metabolic effects of T3

A
  • stimulates lipolysis and release of free fatty acids and glycerol
  • stimulates cholesterol metabolism into bile acids
  • facilitate rapid removal of LDL from plasma
  • stimulates carbohydrate metabolism and protein degradation
17
Q

types pf hypothyroidism

A

1) primary: from thyroid destruction
2) secondary: deficient TSH secretion due to lesions in pituitary eg tumour
3) tertiary/ central: deficit in stimulation of TSH release

18
Q

primary hypothyroidism

A

Hashimoto’s thyroiditis, autoimmune antibodies against TPO. inflamed gland, fatigue, muscle weakness, weight gain, high TSH, low T3/4

19
Q

secondary hypothyroidism

A

low TSH, due to compressing lesions, surgery/ radiation to pituitary, iron overload due to thalassemia

20
Q

tertiary/ central hypothyroidism

A

congenital due to deficit iodine during pregnancy. require daily dose of thyroxine

21
Q

hyperthyroidism

A

graves disease
- affects more female than male
- autoimmune disorder, antibodies bind to and activate TSH receptor
- exophthalmos – inflammation of the periorybital connective tissue and extraocular muscle
- radioiodine, surgery, antithyroid drug

22
Q

thyroid hormone carriers

A

> 99% of T3/4 is bound to plasma carrier proteins
- TBG (thyroxine-binding globulin) binds 75%
- TTR/TBPA (transthyretin/ thyroxine-binding prealbumin) binds 10-15% T4
- Albumin binds 7%
- HDL (high-density lipoproteins bind 6% t3 and 3% T4

23
Q

free hormone hypothesis

A

only free/unbound hormones has metabolic activity – around 0.3% of T3 and 0.03% of T4
HOWEVER, the concept is only partially correct

24
Q

total hormone concentration

A
  • normally kept proportional to the concentration of carrier proteins
  • kept appropriate to maintain constant red hormone level
  • metabolic state correlates more to concentration of free hormone rather than the total hormone in circulation
25
Q

drugs that increase T3/4 by increasing TBG

A

oral contraceptives, methadone, clofibrate, heroin

26
Q

conditions that increase T3/4 by increasing TBG

A

pregnancy, chronic active hepatitis, HIV, biliary cirrhosis

27
Q

drugs that decrease T3/4 by decreasing TBG

A

glucocorticoids, androgens, salicylates, antiseizure drugs

28
Q

conditions that decrease T3/4 by decreasing TBG

A

genetic factors, acute or chronic illness

29
Q

parathyroid glands

A

usually 4 small glands on posterior surface of the thyroid
- upper pair are superior parathyroid glands
- lower pair are inferior parathyroid gland

30
Q

microscopic anatomy of the parathyroid

A

chief cells and oxyphil cells
- oxyphil cells are derived from the chief cells and it increases in number with age
- adipose cells may appear with age
- many blood capillaries

31
Q

parathyroid hormone

A
  • secreted by chief cells
  • regulates blood calcium levels
  • synthesized as preparathyroid hormone in the gland
  • cleaved to form proparathyroid, then again to the 84-AA-PTH
  • half life = 2-4 min
32
Q

regulation of plasma calcium levels

A

PTH and calcitonin regulate by controlling GI absorption, renal excretion and bone calcium flux
- CaSR (calcium sensing receptor) is a GPCR that is expressed on the surface of the parathyroid cells which senses fluctuations int he concentration of extracellular Ca
- binding of Ca to the receptor inhibits secretion of PTH

33
Q

calcium homeostasis (Ca levels too low)

A
  • PTH secretion increase
  • stimulates increased Ca absorption in intestine
  • inhibits Ca excretion at kidneys
  • increases osteoclasts (bone cell) activity releases calcium from bones
  • increases rate of release of phosphate by kidneys
34
Q

calcium homeostasis (Ca too high)

A
  • calcitonin secretion increase from c cells –– stimulates uptake of calcium by bone and reduces Ca uptake in kidneys
  • gastrin is released when Ca is ingested, gastrin then stimulates release of calcitonin, and calcitonin stops gastrin release (neg feedback)
35
Q

vitamin D in Ca homeostasis

A

(formed in skin when cholesterol precursor is in contact with UV light)
- liver converts vit D into 25-hydroxyvitamin D
- PTH converts that into 1,25-dihydroxyvitamin D3 (most active form) via 1-hydroxylase in the proximal tubes of the kidney
- this form of vitamin D promotes absorption of Ca from gut by intestinal epithelial cells

36
Q

hyperparathyroidism

A

too much PTH secreted due to cancer
- bones are weak and deforms/ break easily
- excessive calcium levels in blood
- calcium phosphate – kidney stones
- painful bones
- depression, anxiety, fatigue
treatment by surgery of gland

37
Q

hypoparathyroidism

A

too little PTH due to surgical trauma, magnesium deficit, autoimmune, CaSR deficit
- impaired nerve and muscle function
- muscle spasm and tetany (cramp, numbness, twitching, tingling)
- can be fatal
treated by calcium injection and hormone replacement

38
Q

history that suggests hypocalcemia (newborn and adult)

A

Newborns
- may be asymptomatic
- lethargy
- poor feeding
- vomiting
- abdominal distention
Children/adult
- seizure
- twitch
- cramping
- laryngospasm (vocal cord spasm, breathing impaired)

4GHM (8 decks)

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