endocrine- thyroid gland

Question 1

where is the thyroid gland located?

Answer 1

• in the neck

- releases thyroid hormones (TH) made from thyroglobulin (protein) and contain iodine

Question 2

T3=

Answer 2

triiodothyronine

Question 3

T4=

Answer 3

thyroxine

Question 4

T4 is converted to

Answer 4

T3, T3 is the biologically active form of TH

Question 5

T3 and T4 target most cells in body to…

Answer 5

increase metabolic rate (increase protein/fat/CHO metabolism, heat production, HR—> tachycardia)

Question 6

too much TH=

Answer 6

hyperthyroidism, grave’s disease

Question 7

too little TH=

Answer 7

possible dietary iodine deficiency, congenital

Question 8

what cells secrete TH?

Answer 8

follicle cells

Question 9

goiter=

Answer 9

enlarged thyroid gland d/t hyper or hypothyroidism

Question 10

toxic goiter=

Answer 10

hyperfunction, excess production of thyroid hormones that do not rely on stimulation fromTSH
-gland appears NODULAR (bumps)

Question 11

endemic goiter=

Answer 11

hypofunction, due to defiency of iodine (iodide is taken up and converted to iodine, which is needed for the synthesis of thyroid hormone), with a deficiency, TH is made but has decreased function— stimulates anterior pituitary to release TSH, causing hyperplasia and hypertrophy

Question 12

hyperthyroidism is usually d/t? example is?

Answer 12

autoimmunity

-GRAVES disease (85% of all hyperthyroidism)

Question 13

graves has higher rates in?

Answer 13

women, onset is 20-40 years in age

Question 14

hallmarks of graves disease?

Answer 14

1. hyperthyroidism (seen in lab values)
2. goiter
3. exopthalmos- protruding eyeball d/t fluid accumulation in fat pads and orbitus muscle in the eye

Question 15

what normally happens in thyroid?

Answer 15

NORMALLY:
hypothalamus releases TRH (thyroid releasing hormone)
-triggers anterior pituitary to release TSH, which binds to TSH receptors on thyroid gland
-this stimulates the production of T3 and T4
-once T3 and T4 exist in sufficient quantities, negative feedback occurs and hypothalamus and anterior pituitary are told to STOP releasing TSH

Question 16

pathology of graves? what is happening??

Answer 16

-process still occurs (the normal process) BUT the thyroid stimulating antibodies are released as an autoimmune process (TsAbs)
-TsAbs have same action of TSH and result in production of T3 and T4 which inhibit TSH via negative feedback
-although TSH inhibited, TsAbs continue to be produced and bind to TSH receptors to continue production of thyroid hormone
SO, OVERPRODUCTION of T3 and T4 and HYPERFUNCTION and HYPERTROPHY of thyroid
OVERSTIMULATION of metabolism
-abnormal thyroid stimulation!!

Question 17

thyroid stimulating immunoglobulins are also known as

Answer 17

tsAbs

Question 18

what is thyrotoxicosis?

Answer 18

a complication of hyperthyroidism

• only seen if pt is not treated for hyperthyroidism or not diagnosed
• what graves disease will present as
• may be precipitated by stress (ex. resp infection, DKA, thyroidectomy)

Question 19

manifestations of graves?

Answer 19

• fever (increased metabolism—> production of ATP and heat, intolerance to increased heat
• compensation is maxed out even at normal temperature
• severe CV and CNS problems
• increased metabolic rate—> use up CHO stores leads to increased protein and lipid catabolism (break down)
• demand for O2 and waste material—> increased HR and CO
• angina (heart needs oxygen too!)
• CNS: delirium, agitation, insomnia, irritability (cannot handle increased heat!), indirectly related
• increased mortality rate (fairly high if not treated)

Question 20

treatment for graves? (what drug!!)

Answer 20

• TAPAZOLE- decrease TH (t3,t4) synthesis it is a antithyroid drug; first line approach
• radioactive iodine therapy (provides iodine but when it binds to thyroid cells it emits radiation and forms free radicals, given to decrease overproduction, low dose, not irreversible which is good)
• surgery: remove part of thyroid gland (u can quickly become HYPO tho!!)

Question 21

primary hypothyroidism=

Answer 21

to do with thyroid itself (95%)

Question 22

secondary hypothyroidism=

tertiary hypothyroidism=

Answer 22

2. to do with anterior pituitary

3. to do with hypothalamus

Question 23

etiology of HYPOthyroidism…

Answer 23

autoimmunity

and iatrogenic!!! treatment can quickly lead to hypofunctioning!

Question 24

what is hashimotos thyroiditis?

Answer 24

most common HYPOthyroidism
autoimmunity targeting gland (abs and t cells)–> inflammation
-antithyroid antibodies block TSH binding (produced d/t autoimmunity)
-lymphocyte infiltrates DESTORY gland! induce ATROPHY! and fibrosis

Question 25

90% of people with hashimotos are?

Answer 25

middle aged women!

Question 26

manifesations of hashimotos?

Answer 26

• hypometabolic state
• myxedema (mucoid secretion in dermis of skin causing swelling of skin—>waxy appearance, carbs that cant be metabolized cause this)
• cold sensitivity (d/t decreased heat production–> normally fixed by thyroid hormones)
• decreased CO (cardiac muscles do not have required ATP)
• fatigued (d/t decrease AP)
• weak muscle action
• increased weight loss (not metabolizing nutrients, put into storage–> usually glucose converted into glycogen and stored in liver)

Question 27

treatment of hashimotos thyroiditis?

Answer 27

-replacement therapy (T4 daily) !!!!
T4 is naturally converted to T3 in your body (when t4 ccmes in contact w other blood cells, it removes its iodine and becomes T3)
—> giving T4 allows natural processes to occur in body and has a longer half life than T3