Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medical Physiology > Hypothalamic Thyroid Axis > Flashcards

Hypothalamic Thyroid Axis Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

how does TRH binding cause TSH binding

A

TRH binds Gq. Gq –>PKC–>IP3 binds to SR to release Ca

DAG –>PKC–>P proteins make TSHalpha,beta mRNA–>TSHa,b–>TSH released to blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what occurs with TSH binding

A

binds to dimeric glycoprotein alpha and beta, causes increase in Ca, Phosphoinositide, and cAMP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what growth is increased by increased Ca, phosphoinositide, cAMP with TSH

A

increased thyroid: DNA, RNA, protein and phospholipids

increased thyroid: cell size, number, and follicle formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is increased with increased Ca, PI, cAMP with TSH?

A

increased: trapping I, iodination, coupling, endocytosis of colloid, proteolysis of thyroglobulin
increased: glucose oxidation, NADPH generation

for synthesis of thyroid hormone T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what thyroid hormone is active in target tissues

A

T3 but T4 has longer half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when is TSH released

A

in response to stress, and is sensitive to T3 and T4 levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is thyroglobulin

A

precursor to MIT and DIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what allows iodine to enter the cell from the blood

A

Na/I symporters.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what allows iodine to leave the cell to enter the follicle colloid

A

pendrin channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what occurs once the iodine is in the follicle

A

it is oxidized and conjugated onto thyroglobulin by TPO (thyroid peroxidase)

MIT and DIT or 2 DITs added to thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is DIT

and MIT

A

diiodotyrosine and monoiodotyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what occurs once iodine is conjugated

A

thyroglobulin with MIT and DIT are endocytosed into the thyroid follicular cell. proteolysis clips the thyrosine and thriiodothyronine off the thyroglobulin and THYRG and unused MIT and DIT are recycled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how are T3 and T4 released into the blood

A

Monocarboxylate transporter 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is tyrosine a precursor for

A

dopamine, NE, epinephrine, thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do thyroid hormones circulate

A

most are bound (0.23% and 0.025% are free)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

similarities of thyroid hormones

A
  1. synthesized by enzymatic pathway
  2. require thyroglobulin, tyrosine, inorganic iodine
  3. lipid soluble so have intracellular receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are thyroid hormones bound to

A
  1. thyroid binding globulin (TBG)
  2. thyroid hormone binding pre-albumin
  3. albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how are the thyroid hormones eliminated

A

conjugated glucuronic acid or sulfate for elimination via liver and kidney – into urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

does thyroglobulin circulate

A

yes, but is only active in the thyroid follicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is useful to detect differentiated thyroid tumors?

A

thyroglobulin Ab because is produced in follicular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3 steps of thyroid hormone production

A

iodine dependent

  1. uptake
  2. incorporation
  3. coupling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how much iodine is used for thyroid hormones or other tissues

A

the majority is excreted right away into the urine.
most that is actually used is by other tissues.
only 13% is actually used for thyroid hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe iodine uptake

A

I2 eaten–>GI tract–>reduction (intestinal absorption–>inorganic iodine–>blood–>ACTIVE TRANSPORT BY THYROID NA/I SYMPORTER–>into the follicle via pendrin receptor–>into the colloid—>oxidation in the colloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

where is iodine incorporated on the thyroglobulin

A

on tyrosine residues ON the thyroglobulin

25
Q

what is iodine coupling?

A

when MIT and DIT are coupled together by thyroid peroxidase enzyme

2DIT or 1 MIT and 1 DIT

26
Q

what is reverse T3?

A

when the iodine is clipped off of the 5 carbon instead of the 5’ carbon (5-deiodinase)
is not active, and is usually produced elsewhere

27
Q

how are T3 and T4 released

A

deiodinase clips T3 and T4 off TG

28
Q

what enzyme assists with coupling

A

thyroid peroxidase

29
Q

what stimulates thyroid hormones

A
  1. TSH
  2. thyroid stimulating immunoglobulins
  3. increased thyroglobulin levels (in pregnancy)
30
Q

what inhibits thyroid hormones

A
  1. iodine deficiency
  2. deiodinase deficiency (not recycled)
  3. excessive I intake (suppresses thyroid) (wolff chaikoff effect)
  4. perchlorate;thiocyanate (inhibit Na/I symport)
  5. propylthiouracil (inhibits peroxidase)
  6. decreased TBG levels (liver disease)
  7. circulating T3 T4
31
Q

what foods are rich in iodine

A

anything that is grown in salt water like seaweed, scallops, cod

32
Q

how is T4 made to T3

A

5’ iodinase clips an iodine and makes it T3

33
Q

what effects does T3 have on CNS

A

maturation

34
Q

effects of T3 on growth

A

bone maturation, growth formation

35
Q

effects of T3 on BMR

A
  1. increased Na/K ATPase
  2. increased oxygen consumption
  3. increased heat production
  4. increased BMR
36
Q

effects of T3 on metabolism

A
  1. increased glucose absorption
  2. increased glycogenolysis
  3. increased gluconeogenesis
  4. increased lipolysis
  5. increased protein synthesis and degradation (net is catabolic)
37
Q

effects of T3 on CV

A

increased CO

38
Q

what occurs once T3 binds to the intranuclear receptor

A

the corepressor is removed and a coactivator is added, then transcription can occur

39
Q

blood response to thyroid hormones

A
  1. increases glucose (gluconeo, glycogenolysis)
  2. increases FFA (increased lipolysis)
  3. decreased free AA (growth, protein synthesis)
40
Q

what occurs to AA if hypothyroid?

A

increased free AA (because net is catabolism, increased levels in blood)

41
Q

other T3/T4 functions

A
  1. growth and development (insulin, GH, IGF)
  2. nervous system
  3. hair follicles
  4. teeth eruption
  5. vitamin A production
  6. neurotransmitters maybe
42
Q

what is goiter

A

can be caused by hyperthyroidism, iodine deficiency, increased TSH, or thyroid hypertrophy

43
Q

what is graves disease

A

Ab against TSH receptors, so TSH just keeps getting released. causes high BMR and exopthalmos d/t glycosaminoglycans by TSHr positive fibroblasts.
increased ventilation, sweating, appetite, weight loss, tachycardia, increased CO, tremors, restlessness, nervousness

44
Q

what can cause hyperthryoidism

A
  1. goiter
  2. graves disease
  3. toxic goiter
  4. thyroid cell tumors
45
Q

what is toxic goiter?

A

acute excess of T3/T4 without stimulation from TSH due to possible toxins like thiocyanate

46
Q

what does thiocyanate do

A

decreases iodide transport via Na/I symporter into the follicle
(may have enough, but not enough in usable form)

47
Q

what can cause hypothyroidism?

A
  1. diffuse goiter
  2. hashimotos thyroiditis
  3. iodine deficiency (leads to thyroid cell destruction)
  4. neonate cretinism
  5. adult myxedema
48
Q

what causes hashimotos

A

Ab against thyroid peroxidase enzyme and thyroglobulin, so no T3 or T4 is made.

49
Q

symptoms of cretininsm

A

mental/physical development is slow, secondary sex characteristics don’t develop. low body temp, poor teeth, leathery/thick skin, decreased muscle tone, low BP, HR and BMR

50
Q

symptoms of myxedema

A

mental ability is suppressed, personality changes, lethargy, obese, dry skin, hair falls out, low BP, low HR, low BMR

51
Q

sx of hashimotos

A

lethargy, weight gain, cold intolerance, constipated, depression, bradycardia, emotional stress, irregular menstruation, memory problems

52
Q

what occurs in cretinism

A

decreased long bone growth and the epiphyseal plate doesn’t complete

obese and puffy face

53
Q

what lab findings in myxedema?

A

hypoglycemia, hyponatremia, hypoxemia, hypercapnea, prolonged QT and low voltage, pericardial effusion

54
Q

what is seen in both hyper and hypothyroidism

A

goiter!

55
Q

how to treat hyperthyroidism

A

thyroidectomy or radioactive iodine (destroys thyroid)

56
Q

what is secondary hypothyroidism?

A

an issue with the hypothalamo-pituitary axis (no TSH) or end organ resistance (target organs don’t have thyroid receptors)

57
Q

what is primary hypothyroidism

A

issue with thyroid itself not releasing T3, T4. will have increased TSH.
cretinism or myxedema

58
Q

what is secondary hyperthyroidism

A

Ab to TSH receptor cause no negative feedback, or TSH is released from somewhere in the body to produce T3,T4 (negative feedback from hypothalamus doesn’t matter)

59
Q

what is primary hyperthyroidism

A

an adenoma or carcinoma is causing the thyroid itself to release T3/T4

Medical Physiology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions