Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology > 4.2 Food intake and thyroid gland > Flashcards

4.2 Food intake and thyroid gland Flashcards

1
Q

thyroid gland:
- ________ organ specialized for ________ production
- weight?
- _______ shape (2 ______) and located below ________
- blood supply?
- innervated by what nerves?
- how is it regulated? ish

A
  • endocrine organ specialized for hormone production
  • 15-20 g
  • butterfly shape (2 lobes) located below larynx
  • large blood supply
  • innervated by sympathetic nerves
  • through thyroid stimulating hormone (TSH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  • functional unit of thyroid gland? describe
  • how many functional units per gland?
  • which cells are a source of another hormone?
A
  • thyroid follicles –> produce thyroid hormone
  • consisting of a single layer of epithelial cells/thyrocytes surrounding a lumen that contains a colloid (highly proteinaceous)
  • few thousand follicles per gland
  • parafollicular cells (C-cells) = source of calcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • function of thyroid gland?
  • ___A___ ___A___ regulates thyroid hormone release? ___A____ ____A_____ affects the delivery of (3)
  • what nerves control the ___A____ ____A_____ through the gland?
A
  • secrete thyroid hormones
  • blood flow regulates thyroid hormone release by affecting the delivery of TSH, iodine and nutrients
  • postganglionic sympathetic nerves control the blood flow through the gland + fct of thyroid follicles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe underactive vs overactive thyroid follicle

A

UNDERACTIVE:
- cells are smaller + colloid space is really big
OVERACTIVE:
- really big cells + smaller colloid

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

describe:
- 5-monoiodotyrosine
- 3-5 diiodotyrosine
- thyroxine
- 3,5,3’-triiodothyronine
- 3,3’-diiodothyronine
- 3,3’,5’-triiodothyronine

*which one is T3, T4, T2 and rT3?

A
    • 5-monoiodotyrosine: 1 benzene ring, iodine on 5th C
  • 3-5 diiodotyrosine: 1 benzene ring, iodines on 3rd and 5th C
  • thyroxine: 2 benzene rings! 4 iodines: two on 3 and 5 and two on 3’ and 5’ –> T4!!
  • 3,5,3’-triiodothyronine: 2 benzene rings –> iodines on 3, 5 and 3’ –> T3
  • 3,3’-diiodothyronine: 2 benzene rings –> one iodine on each at 3 position –> T2
  • 3,3’,5’-triiodothyronine: 2 benzene rings –> 2 iodines on 3’ and 5’ + 1 iodine on 3 –> reverse T3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which iodothyronines biologically active?

A
  • T3 (3,5,3’ triiodothyronine) and T4 (thyroxine) are the 2 biologically active forms
  • rT3 (3,3’,5’-triiodothyronine) and T2 (3,3’ diiodothyornine) are inactive and formed in peripheral tissues (outside of thyroid gland, as metabolites of T3 and T4)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe the 5 general steps of synthesis of T3/T4. + extra

A
  1. trapping: uptake/active transport of iodine into thyroid cell using sodium iodine-symporter (NIS) (and NA/K+ ATPase pump)
  2. organification: oxidation of iodide and iodination of tyrosyl residues in thyroglobulin (ie add iodine (organic compound) to a Tyr on a protein
  3. coupling: linking pairs of iodotyrosines in thyroglobulin to form T3 and T4
  4. proteolysis of Tf to release T3 and T4 (to detach T3 and T4 from protein)
  5. deiodination of iodotyrosines and recycling of I-
    *intrathyoidal 5’ deiodination of T4 to T3 –> convert T4 to T3 if too many T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

is the transport of iodine from capillary to thyroid cell an active transport?

A

yes! even though the sodium-iodide symporter is a passive transporter (sodium goes down concentration gradient = provides energy to transport I- against its [] gradient), Na/K ATPase pump is used to maintain the sodium gradient = needs energy = transport of iodine is an active process

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

where does iodination occur?

A

in colloid!w

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

which transporter carries T3 and T4 out of cell into capillary?

A
  • monocarboxylate transporter 8 (MCT8 or MCT10)
    *but T3 and T4 can also just diffuse through the membrane bc they’re lipophilic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the role of DUOX?
- vs thyroid peroxidases

A
  • DUOX = dual oxidases –> makes hydrogen peroxide necessary for organification
  • thyroid peroxidases: (TPO) –> catalyzes organification & coupling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

recommended dietary iodine intake:
- adults
- pregnancy
- children
- typical iodine intakes in NA?
- why intake differs in different countries?

A
  • adults: 150 ug
  • pregnancy: 200 ug
  • children: 90-120 ug
  • typical iodine intakes in NA: 75-300 ug
  • bc of different iodination of food products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NIS: what is it?
- stimulated and regulated by what?
- role?

A
  • Na/I symporter
  • stimulated and regulated by TSH
  • transport of iodine against steep concentration gradient ([iodine] in blood plasma is extremely low –> 30-40 fold difference btw ECF and cytoplasm) –> iodine transport is via a symport (co-transport of Na+ and I- driven by Na+ gradient) –> Na+ gradient is maintained by ATP driven Na+/K+ ATPase = active transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • what can block uptake of iodine through NIS? –> useful?
  • what (2) are competitive inhibitors of NIS? –> causes what?
  • what can be used to destroy thyroid tissue?
A
  • anions like ClO4- block uptake of iodine (bc the anions are uptaken by NIS) –> perchlorate/chloridetetroxide can be used to block hyperthyroidism
  • bromide (Br-) and nitrite NO2-) are competitive inhibitors –> present in diet –> can cause apparent iodine deficiency in some areas of world (enough I- in diet/blood but not enough get into cells)
  • radioactive iodine (oral I^131) –> destroy tissue in case of cancer or hyperthyroidism (radical therapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

thyroglobulin
- large _________
- dimer? monomer? multimer?
- each Tg contains ____ tyrosine residues
- what stimulates its transcription/translation/post-translational mods/transport in follicular cells of thyroid?
- extensively _______ in Golgi (10% _____ by weight)
- stored?

A
  • large glycoprotein (MW 660 kD)
  • dimer! (homodimer)
  • 140 tyrosine residues
  • TSH!
  • glycosylated –> 10% CHO by weight
  • packaged into vesicles, exocytosed into lumen of follicle (colloid) –> also under influence of TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • iodination of Tg is carried out by which enzyme?
  • this enzyme is packaged in an inactive form together with what into vesicles in the _______
  • this enzyme is activated at _______ membrane by which cofactor? –> this cofactor is produced by which enzyme?
A
  • thyroid peroxidase (TPO)
  • with thyroglobulin into vesicles in Golgi
  • activated at apical membrane by co-factor H2O2 (produced by DUOX: dual oxidase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is TPO+I-TG-PROTEIN formed?

A

TPO + I- + TG PROTEIN –> requires H2O2 (that becomes 2 OH-) –> becomes I.TPO.TG-PROTEIN complex –> becomes TPO+I-TG-PROTEIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  • which enzyme is the target for many drugs to reduce thyroid hormone production?
  • several inhibiting compounds (_________) are present in foods (2 ex)
  • why does blocking iodination result in hyperplasia and goiter?
A
  • thyroid peroxidase!
  • goitrogens (inhibit TPO + cause goiter) –> ie milk from cows fed certain plants, brassicae
  • block iodination = decrease negative feedback = increase TSH production = increase thyroid gland size = goiter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  • only which tyrosine residues of Tg become iodinated? what fraction?
  • iodination causes ______ changes which leads to the formation of (2) within the structure of thyroglobulin –> what catalyzes this step? what is this step called?
  • ____ + _____ = T3
  • ____ + _____ = T4
A
  • only tyrosine residues on surface of Tg (1/3)
  • causes structural changes –> formation of triiodothyronin (T3) and thyroxine (T4) –> TPO catalyzes coupling
  • MIT + DIT –> T3
  • DIT + DIT –> T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

thyroid hormone prod:
- which 2 steps occur together?
- what can happen to the peptide during reaction?
- maximum of ___ T3 and/or T4 hormones within each Tg molecule are formed
- the _______ is such that it keeps the level of ___ (____ form of thyroid hormone) steady despite fluctuations in dietary intake of iodine)

A
  • coupling + iodination –> both are catalyzed by TPO
  • peptide may be broken during coupling –> thats why not a lot of coupling happens
  • max of 4 within each Tg molecule
  • kinetics –> keep level of T3 (active form) steady in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

overall regulation of iodination and coupling is based on what?

A

levels of T3 in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  • what type of hormone are thyroid hormones?
  • are they stored?
  • what happens after? (5 steps ish)
A
  • lipophilic! –> generally not stored
  • thyroid hormones are stored bc T3 and T4 are synthesized on top of Tg
    1. Tg is internalized/endocytosed into colloid droplets
    2. remain there until lysosomes bring in proteases and deiodonases
    3. proteases detach T3/T4 and MIT/DIT from Tg
    4. deiodonases detach I- from MIT/DIT to recycle iodine
    5. T3/T4 are diffused out of membrane OR use MCT8/MCT10 (transporters) to exit basal membrane of thyroid cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  • which thyroid hormones are biologically active?
  • what is the sick euthyroid syndrome?
A
  • T4 and T3 –> some inactive derivatives are found in serum
  • sick euthyroid syndrome –> high levels of r-T3 in conjunction with low levels of T3 –> thyroid normal function but some other metabolic condition (ie anorexia, cancer) converts T3 into rT3 –> hypothyroidic condition
24
Q
  • thyroid hormones bound to which 3 carrier proteins? –> carrier proteins are synthesized where?
  • what can causes elevation of free T3/T4? examples
A
  • thyroxine binding protein (TBG) + transthyretin (thyrosine-binding prealbumin) + albumin –> synthesized in liver (99%)
  • some drugs compete with binding to carrier protein –> causes hyperthyroidism bc more free T3/T4 –> examples are some drugs for treating epilepsy and inflammation
25
Q

properties of T3/T4:
- Half-life: T3 vs T4 vs rT3
- does T3 or T4 have more affinity to binding protein?
- is T3 or T4 more active?
- is T3 or T4 synthesized more?
- total T3 = ___% of T4 –> free concentration of T3 = ___% of free T4
- is T3 or T4 more improtant?

A
  • T3 (1-3 days), T4 (5-7 days bc more affinity to BP), r-T3 (5h)
  • T4 has more affinity!
  • T3 is 2-10 times more active than T4
  • T4 is synthesized more
  • total T3 = 2% of T4 –> however, stronger binding of T4 makes that the free concentration of T3 is about 30% that of free T4
  • overall serum T3 and T4 are equally important (not counting tissue specific conversion)
26
Q
  • cells can only take up _____ thyroid hormones, not the ______ _______ –> what concentration is important?
  • what determines this concentration?
A
  • free thyroid hormones! not carrier proteins –> free hormone concentration is important
  • determined by level of binding proteins (influences half life and bioactivity of hormone)
27
Q

high binding protein vs low binding protein
- effect on total hormone required to maintain free hormone level
- effect on thyroid gland
- happens in what situations?

A

HIGH BINDING PROTEIN:
- more total hormone required to maintain free hormone level = thyroid gland has to work more
- pregnancy, oral contraceptives (E2), cirrhosis, hepatitis
LOW BINDING PROTEIN:
- less total hormone required to maintain free hormone level –> thyroid gland works less
- starvation, liver disease, androgens, high dose glucocorticoids

28
Q

describe the 3 types of deiodinases

A

TYPE 1:
- T4 –> T3
- liver, kidney, muscle –> peripheral conversion
TYPE 2:
- T4 –> T3
- brain, pituitary –> key for feedback on TRH and TSH (bc T3 is negative feedback to regulate TSH secretion)
TYPE 3:
- T3 –> rT3/T2 –> inactivation if T3 is in excess

29
Q

all 3 deiodinases contain _______ in the form of rare aa ___A____, the ___ aa (codon = _____)
- only 25 ____A_______ containing protein have been identified –> 11 in _______

A
  • contain selenium in form of rare aa selenocysteine: 21st aa (codon UGA (sense codon: codes for STOP and selenocysteine))
  • only 25 selenocysteine –> 11 in thyrocytes/follicular thyroid cells
30
Q

what are the 2 general effects of thyroid hormone?
- what is the primary mode of thyroid function?
- interaction with other _______ ______ provides what?

A
  1. growth and development
  2. maintenance of basal metabolic rate (metabolic regulation)
    - receptors are activated by T3-T4 –> modulate transcription (T3 more biologically active than T4)
    - integration with other transcription factors provides tissue specificity (corregulation)
31
Q
  • thyroid receptor is what type of receptor?
  • localization? (2)
  • may activate or inactivate what (ex)
  • receptor acts as (3)
  • what is its most common heterodimer partner?
  • which 2 genes encode T3/T4 receptors? –> each gives rise to what?
A
  • nuclear receptor! (ligand dependant transcription factor)
  • nuclear (class II NR) and also in mitochondria
  • may activate or inactivate transcription (ie activate GH transcription, inactivate TSH transcription) –> depends on corepressor/co TF)
  • acts are monomer, homodimer, heterodimer
  • RXR
  • THRA (NR1A1) and THRB (NR1A2) –> each gives rise to 2 receptor isoforms (a and b) by alternative splicing
32
Q

what is the typical mechanism of action of thyroid hormones in nucleus?

A

thyroid hormone (ie T3) enters cytoplasm + enters nucleus –> binds to receptor –> dimerization –> TF acts as activator or inhibitor –> gene expression (or inactivation)

33
Q

what is the typical mechanism of action of thyroid hormones in mitochondria? (3)

A
  1. T3 inactivated by deiodinase 3 into T2 –> T2 binds to cytochrome c (e- transport chain protein in ox phos) to increase oxidative phosphorylation
  2. T3 binds to uncoupling proteins (UCPs) to increase thermogenesis (T3 = positive regulator of UCP)
  3. T3 binds to THR to increase mitochondrial transcription (act normally just like in nucleus)
34
Q

is T2 biologically active?

A

not biologically active bc doesn’t bind to thyroid receptor

35
Q

overall physiological effects of thyroid hormones on:
- heart
- adipose

A

HEART:
- chronotropic (increase heart beat) –> increase number of b-adrenergic receptors and response to catecholamines (indirect action)
- inotropic (increase strength of each heart beat) –> increase myosin heavy chain (high ATPase activity) –> direct action
ADIPOSE:
- catabolic –> stimulates lipolysis (removal of TG from fat)

36
Q

overall physiological effects of thyroid hormones on:
- muscle
- bone
- gut
- liver

A

MUSCLE:
- catabolic and development –> increases protein metabolism + slow twitch fibres + increase oxygen consumption
BONE:
- development –> promote growth
GUT:
- metabolic –> promote CHO absorption
LIVER:
- metabolic –> stimulate LDL receptor expression (involved in cholesterol metabolism)

37
Q

effects of thyroid hormones on growth and tissue development:
- thyroid hormones increase/ decrease growth & maturation of (4)
- increase _____ and _______ of skeletal muscle contraction
- inhibits synthesis and increases degradation of what? –> consequence?

A
  • increase growth and maturation of bone, epidermis, hair follicles and nails
  • increase rate and force of skeletal muscle contraction
  • inhibits synthesis and increases degradation of mucopolysaccharides (play a role in skin elasticity) in subcutaneous tissue –> hypothydroidism may have myxodema (puffiness in body/face associated with mucopolysaccharides accumulation under skin)
38
Q

what are the effects of thyroid hormone on CHO metabolism (1) and cholesterol metabolism (1)?

A

CHO met:
- increase absorption of CHO from GI tract
CHOLESTEROL met:
- decrease cholesterol levels in circulation independent of calorigenic action –> due to increase of LDL receptors in liver = increase hepatic clearance/absorption/recycling of cholesterol

39
Q
  • explain the calorigenic action of thyroid hormones
  • exceptions?
  • some calorigenic effects are also due to (2)
A
  • generally increases O2 consumption and heat production in metabolically active tissues = promote metabolic activity = generation of ATP/Energy
  • exceptions are adult brain, testes, uterus, lymph nodes, spleen, anterior pituitary –> not involved in metabolic regulation so no increase in calorigernic activity
  • due to FA mobilization (increase lipolysis) and increase in Na+/K+ ATPase activity
40
Q

does T3 or T4 elicit a bigger increased O2 consumption depending on the dose? (figure)
- which one is used in treatment?

A
  • T3 is more active! smaller dose will lead to bigger increase metabolism/O2 consumption
  • T4 is used in treatment bc it has a longer half-life + it has a more sustained impact on O2 consumption!
    *T4: measurable effect in several hours, lasts for 6 days or more
41
Q

effects of thyroid hormones on cardiovascular system:
- which genes are turned on (6)
- vs which genes are inhibited (4)

A

TURNED ON:
1) a-myosin heavy chain (high ATPase activity = increase ATP consumption = increase cardiac contraction rate and force of contraction
2) sarcoplasmic reticulum Ca2+ ATPase
3) b-adrenergic receptor!! = modulates adrenergic response
4) G-proteins
5) Na+-K+ ATPase
6) some K+ channels
INHIBITED:
a) b-myosin heavy chain (low ATPase activity) –> = leads to increased ATP consumption by a-myosin chains
b) 2 types of adenyl cyclase
c) T3 nuclear receptor
d) Na+-Ca2+ exchanger

42
Q
  • which thyroid hormone triggers action on heart myocytes?
  • what is the net result of thyroid hormones on cardiovascular system?
A
  • T3! from circulation since myocytes lack deiodinase to form T3 from T4
  • increased heart rate and force of contraction (by increase muscle fibers that use more ATP and decrease muscle fibers that use less ATP) (direct action on cardiac myocytes) + indirectly modulate adrenergic response by way of increase b-adrenergic receptors
43
Q
  • what are catecholamines?
  • do catecholamines have similar effects as T4/T3? explain/give examples
  • blocking b-adrenergic receptors enhances/reduces action of T3/T4? –> explain
A
  • catecholamines = norepinephrine or epinephrine –> comes from adrenal medulla
  • yes! but of shorter duration –> increase in metabolic rate, stimulation of nervous system, cardiovascular effects
  • REDUCES action of thyroid hormone –> no adrenergic receptor = cut off indirect action of T3/T4
44
Q
  • what is a thyroid storm?
  • what can be used to treat it?
A
  • sudden increase in thyroid hormone = thyroid hormone toxicity –> induced by infection, trauma, drugs etc. –> molecular mechanisms unclear but high temp (106F) + heart rate (200 bpm) –> may be lethal if not treated immediately
  • beta-blockers!
45
Q

effect of thyroid hormones on nervous system:
- __________ convert T4 to T3
- effect?
- lack of T3/T4 during early development –> 3 consequences = __________

A
  • astrocytes (nursing cells of neurons)
  • indirectly increased responsiveness of neurons to catecholamines
  • mental retardation + motor rigidity + deaf mutism = cretinism
    *cretinism = thyroid hormone deficiency in fetal/infant -> negative impact on nervous system development and muscular development
46
Q

hyperthyroidism vs hypothyroidism effects on skeletal muscle?
- in both cases, relationship btw ______ and _________ _______ are unclear

A

HYPER: muscle weakness due to increased protein catabolism (T3/T4 will increase protein degradation in muscle
HYPO: muscle weakness, cramps, stiffness due to reduced metabolic rate (decreased O2 consumption)
- in both cases, relationship btw myopathy and thyroxine levels are unclear

47
Q

effects of thyroid hormones on reproductive system
- females (3)
- males (1)

A

FEMALES:
- required for normal follicular development + ovulation
- required for normal maintenance of pregnancy
MALES:
- required for normal spermatogenesis

48
Q

4 types of hypothyroidism (causes)

A
  1. primary: thyroid gland failure/not functional –> most common cause
  2. secondary: pituitary failure (TSH deficiency/no stimulation)
  3. tertiary: hypothalamic failure (TRH deficiency/no stimulation)
  4. peripheral resistance to action of thyroid hormones –> tissue has response deficiency –> receptor OR deiodinase deficiency/problem
49
Q
  • hypothyroidism results in what (general)
  • symptoms (5)
  • signs (physical ish) (4)
  • infants and children (4)
  • treatment?
A
  • results in slowing down metabolism
  • symptoms = fatigability/weakness, coldness, weight gain, constipation, low voice
  • signs = cold and dry skin, swelling of face/hands/legs, slow reflexes, myxedema
  • infants and children: retardation, short stature, swelling of face/hands, possible deafness –> cretinism
  • treatment: levothyroxine (T4 replacement therapy) due to longer half-life (vs T3)
50
Q
  • iodine deficiency at <____ ug/day can cause _______ _______
  • what can also cause apparent iodine deficiency?
  • consequences of iodine deficiency, explain
A
  • <50ug/d can cause endemic goiter
  • apparent iodine deficiency can also be caused by perchlorates and other treatments (competitive inhibitor)
  • iodine deficiency = less T3/T4 = decreased negative feedback = elevated TSH = enlargement of thyroid = less T3/T4
51
Q

iodine deficiency in pregnancy results in what damage?
- ________ = (3 symptoms)
- large doses of iodine may inhibit/activate synthesis and excretion of thyroid hormones

A
  • neurological damage
  • cretinism = intellectual impairment, deafness, paralysis
  • INHIBIT synthesis and excretion of thyroid hormones –> increase Iodine can have negative effect on thyroid hormone synthesis
52
Q
  • 3 consequences/symptoms of hypothyroid children
  • T3/T4 potentiates the effect of _____ on tissues
  • if iodine deficiency occurs in newborn infants, more severe effects including (3)
A
  • slowed bone growth + delay of epiphysial closure (bent bones) + GH secretion is depressed
  • GH!
  • mental retardation, stunted growth, delayed puberty
53
Q
  • currently, how many children are mentally retarded due to iodine deficiency?
  • mostly where in the world? (2)
  • solution?
A
  • 20 million
  • sub-saharan Africa + South Asia
  • food policy! to iodize salt! knowledge of endocrinology can be implemented in policy
54
Q
  • why can elderly gradually develop hypothyroidism? also called ___________
  • more susceptible when?
  • untreated hypothyroidism during that period of time can cause (5)
A
  • bc T4 levels gradually decrease by as much as 50% in elderly –> thyropause (like menopause)
  • during winter!
    1. progressive weakness
    2. hypoventilation
    3. hypoglycemia
    4. hypothermia (especially bad during winter!)
    5. progressing to come and death
55
Q
  • what is the major cause of hypothyroid disorders in areas of iodine sufficiency? (ie Canada)
  • what type of disease?
  • causes goiter?
  • what happens?
  • lab values to measure (4)
  • treatment?
A
  • Hashimoto’s disease
  • autoimmune disease
  • goiter in younger patients, no goiter in older patients
  • autoimmune response is against TPO and/or Tg –> decreased function of both proteins
  • high TSH (bc no neg. feedback) + low T4 (measured bc longer half-life) + anti-TPO Ab, anti-TG ab
  • treat with levothyroxine (T4)
56
Q

HYPERTHYROIDISM
- symptoms (6) –> all bc of what?
- signs (3)
- most common cause?

A
  • palpitations, nervousness, fatigue, diarrhea, sweating, heat intolerance –> bc of accelerated metabolism
  • thyroid enlargement + tremor + exophthalmos (bulging eyes)
  • Grave’s disease!
57
Q

Grave’s disease
- what type of disease?
- explain what happens?

A
  • autoimmune disease
  • immune system produces anti-TSH receptor antibodies: extracellular domain of TSH receptor is cleaved off and enters circulation where antibodies are generated (bc system thinks its a foreign protein) –> these antibodies can bind to extracellular domains of intact TSH receptors –> induces signal transduction of TSH pathway resulting in T4/T3 production without TSH!
  • T4 suppresses TSH release from pituitary (negative feedback) –> decrease TSH levels in those patients

Endocrinology (14 decks)

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