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Bloc E - GI & Metabolism > Feb2 M1,2-Thyroid > Flashcards

Feb2 M1,2-Thyroid Flashcards

1
Q

structures near thyroid

A

parathyroid glands

recurrent laryngeal nerve

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2
Q

composition of thyroid on histology

A

follicles made of single layer of epith cells (follicular cells or thyrocytes)

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3
Q

content of follicle cavities

A

colloid. amorphous eosinophilic material

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4
Q

active vs inactive thyrocytes

A 
active = tall and columnar
inactive = flat and cuboidal
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5
Q

species that have thyroid gland

A

all vertebrates (poikilotherms = cold blooded and homeotherms = warm blooded)

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6
Q

thyroid gland role in cold blooded vs warm blooded vertebrates

A

cold blooded = growth and development only

warm blooded = growth and dev + thermogenesis and metabolic effects

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7
Q

congenital hypothyroidism: main reason to treat as quick as possible

A

avoid developmental problems

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8
Q

why thyroid hormone said to not work in isolation

A

works with growth axis and reproductive (gonad) axis

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9
Q

hypothyroidism effect on puberty

A

puberty and growth retarded by a couple years (hockey stick sign)

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10
Q

how thyroid hormone influences BMR in homeotherms vs poikilotherms and how can be measured

A

homeotherms: increased O2 consumption. higher BMR
poikilotherms: same O2 consumption as no TH.

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11
Q

thyroid hormone molecule backbone + name without the iodine atoms

A

two benzene rings with ether linkage between them: called thyronine when no iodine atoms

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12
Q

T4 vs T3 vs rT3

A

T4: I on 3’5’ (outer ring) and 3,5 (inner ring) = 3,5,3’,5’ tetraiodothyronine
T3: 3,5,3’ triiodothyronine (lack 5’ I in outer ring)
rT3: 3,3’,5’ triiodothyronine (lack 5 I in inner ring = bio inactive)

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13
Q

other name for T4 (when 4 iodines)

A

thyroxine

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14
Q

2 atoms important in thyroid hormone synthesis

A

iodine and selenium

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15
Q

3 pools of iodine in the body

A
  1. exchangeable (plasma inorganic I)
  2. Organic pool (I attached to T3 and T4 and to TGB: thyroglobulin)
  3. Stored in thyroid (most of iodine)
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16
Q

how to determine if someone is iodine deplete

A

urine iodine. if too low, means I deficient

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17
Q

iodine conc in thryoid vs plasma

A

200x more

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18
Q

transporter on basolateral surface of thyrocytes + fct

A

NIS (sodium-iodine cotransporter). Na+ and I-

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19
Q

what drives energy of NIS (Na I Symporter)

A

Na K ATPase

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20
Q

4 ions that can compete with iodine on NIS

A

perchlorate, pertechnetate, thiocyanate or fluoride

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21
Q

why iodine makes its way to apical surface of the thyrocytes

A

can’t remain in the cell. hallogens are very reactive and corrosive so need way to store it and not destroy the cell

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22
Q

What makes iodine exits thyrocytes on apical surface

A

pendrin: an iodine-chloride exchanger

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23
Q

inside what large protein is TH produced

A

thyroglobulin (TGB)

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24
Q

3 functions of TGB

A
  • Storage
  • template for TH synthesis
  • autoregulates TH synthesis
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25
Q

TGB protein structure

A

dimers. 330 000 kDa

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26
Q

TGB produced where and stored where

A

prod in thyrocytes

stored in colloid of follicles

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27
Q

TGB: relative amount of tyrosine

A

not that much

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28
Q

TGB tyrosine residues where and name for that site

A

strategic sites (close to each other) so that enzymatic rxs are efficient: called hormogenic sites

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29
Q

hormogenic sites fct (sites where tyrosine residues strategically placed)

A

serve as template for TH synthesis

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30
Q

other name for hormogenic site of TGB with the tyrosine residues

A

tyrosyl residues

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31
Q

iodine vs iodide

A 
iodine = I
iodide = I- (think d = deficient = negative)
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32
Q

3 first steps of TH synthesis

A
  • iodide conc into the cell (NIS)
  • moves to apical surface (unknown mech)
  • iodide conc in colloid (by pendrin)
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33
Q

tyrosyl vs tyrosine

A

tyrosyl is the radical, or a.a residues, of the a.a tyrosine

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34
Q

next step after iodine conc in colloid (2)

A

TPO (tyroperoxidase) does 2 things

  • oxidize iodide to iodine
  • attach iodine covalently to tyrosyl residues to make MIT (monoiodotyrosyl) or 2 iodines to make DIT
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35
Q

Importance of TPO step

A

is a rate limiting enzyme

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36
Q

What TPO does after it has created DIT and MIT

A

attaches them together
MIT + DIT = T3
DIT + DIT = T4

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37
Q

where is the TH formed from DIT and MIT and why

A

it is in TGB and is stored in TGB (all steps to its synthesis were done on TGB. TGB = template)

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38
Q

how much reserve ot thyroid

A

for 4-6 weeks

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39
Q

How T3 and T4 move from colloid to blood stream

A

thyrocytes endocytose pieces of colloid. phagosome fuses with lysosome to make phagolysosome. T3 and T4 then secreted in blood stream

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40
Q

how does body avoid losing iodine stores

A

MIT and DIT are not secreted (tyrosyl residues) but are recycled

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41
Q

T4 (thyroxyl) produced where

A

thyroid gland only

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42
Q

T3 produced where and how

A

30 ug daily
20% (6 ug in thyroid)
80% (24 ug in liver or kidney from conversion of T4 to T3)

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43
Q

what proteins convert T4 to T3 and give 2 of them

A

selenoproteins: deiodinase type 1 and type 2

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44
Q

deiodinase type 1 location

A

liver and kidney

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45
Q

deiodinase type 2 location

A

brain (hypothalamus included) and brown adipose tissue

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46
Q

which protein can deactivate T4 and is responsible for the load of rT3 in the blood + what it does

A

type 1 deiodinase (can both activate and deactivate T4 therefore: to T3 or rT3)
remove I on pos 5

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47
Q

metabolic pathway (of thyroid hormone desactivation or elimination) other than conversion to rT3 + when it happens

A

conjugation via enterohepatic pathway. (decrease amount of T3 T4 returning to circulation)
in hyperthyroidism for ex

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48
Q

T4 vs T3 + which is responsible for most of the activity of thyroid secretions

A
  • T3 10x more affinity for nuclear R than T4
  • T3 10x more potent than T4 (active = T3, prohormone = T4)
  • T3 10x more abundant on nuclear R than T4
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49
Q

what stimulates thyroid to release its hormones

A

thyrotropes of anterior pit release TSH (or thyrotropin)

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50
Q

group of pituitary hormones that have similar structures and that TSH is included in

A

TSH, FSH, LH, CG

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51
Q

TSH, FSH, LH, CG: things in common

A

glycoproteins

alpha subunit in common

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52
Q

TSH, FSH, LH, CG: what makes them different

A

beta subunit specific to each: responsible for ligand-R interaction

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53
Q

TSH-R vs TH-R

A

TSH-R is on cell (thyrocyte) surface

TH-R is a nuclear R

54
Q

what is really responsible for the activity of TSH + what makes it

A

its carbohydrate moiety group (CHO moiety). TRH of hypothalamus responsible for glycosylation of TSH

55
Q

TSH amount if hypothalamus damaged

A

normal amount but is inactive (no TRH)

56
Q

problem in immune assays detecting TSH

A

detect beta subunit but can’t detect degree of glycosylation (and therefore how much TSH is active)

57
Q

what determines TSH’s half life

A

CHO moiety

58
Q

what exactly produced TRH

A

paraventricular nuclei of the hypothalamus

59
Q

can you have hypothyroidism if normal TSH levels?

A

yes, if hypothalamus is damaged, will detect normal TSH levels with immune assay but in fact TSH inactive bc no CHO moiety

60
Q

how TSH transmits signal to thyrocytes for TH release

A

binds membrane R and activates 2 downstream GPCRs

61
Q

earliest effect of TSH on thyroid gland

A

(release of preformed hormones)

  • TGB endocytosis
  • degradation and release of iodo a.a
  • intrathyroidal deiodination of iodotyrosines
62
Q

TSH effects on steps on TH synthesis (which stim and which are not)

A

increases NIS activity, iodide oxidation to iodine and organification, coupling of DITs and MITs,, TGB synthesis and procesing
DOESN’T increase pendrin activity (iodide-Cl exchanger)

63
Q

what is believed to upregulate pendrin (even though real mech is unknown)

A

TGB (bc remember it has TH synthesis regulation fct so may act to upregulate pendrin on apical surface)

64
Q

why moderate levels of hypothyroidism look normal

A

will see normal T3 in the blood bc high TSH from low TH stimulated thyrocytes to prod more TSH AND TO CONVERT T4 TO T3 IN THE THYROID

65
Q

how TSH works to stimulate more conversion of T4 to T3 WITHIN the thyroid

A

upregulates (increases expression of deiodinase)

66
Q

hypothalamus (paraventricular nuclei) 2 roles in HP-thyroid axis

A
  • make TRH

- has deiodinase type 2 converting T4 to T3

67
Q

feedback loops in TH and relative importance

A

T4 and T3 feedback on pit and hypot

hypoth feedback is even more important

68
Q

why thyroid test complicated

A

other influences on HP-thyroid axis like neuropeptides, ntrs and hormones

69
Q

external players doing positive regulation on HPT axis and where they act

A

cold, catecholamines (NE, E,..), CART, hormone leptin. act on hypothalamus

70
Q

external players doing negative regulation on HPT axis and where they act

A
  • cortisol and dopamine on hypothalamus

- somatostatin and dopamine on pituitary

71
Q

sick euthyroid hormone syndrome def

A

abnormal thyroid fct test (TSH, T3, T4) but HPT axis seems to work normally bc of these external regulators

72
Q

symptoms of hypothyroidism

A

sensitive to cold, slow mental process, low memory, weak slow heart, muscle weaknes, fatigue, constipation, thick and puffy skin, goiter sometimes*

73
Q

possible complication of extreme case of hypothyroidism

A

pneumonia, can lead to myxedema coma

74
Q

skin manifestation (important) in hypothyroidism

A

yellowish, thick, swollen, edematous (but not bc of fluid. it’s not edema)
all that bc deposition of mucopolysaccharides in dermis and subcutaneous tissue

75
Q

hyperthyroidism symptoms

A

good appetite but weight loss, restless, anxious, hard to sleep, tremor, fast and strong heart, goitre

76
Q

4 systems impacted by hypo or hyper T

A
  • brown adipose tissue (thermogenesis)
  • brain and cognition
  • CVS
  • Digestive system
77
Q

thermometer area of the hypothalamus + how it controls temperature

A

preoptic area. has body projections to contorl tissues and organs responsible for heat prod and dissipation

78
Q

normal response to cold

A

vasoconstriction, shivering

79
Q

main mechanism of heat production and what controls it

A

brown adipose tissue (very active organ). thyroid controls it

80
Q

main mechanisms of heat dissipation

A

perspiration, hyperventilation, vasodilation

81
Q

2 components of BMR

A
  1. obligatory constant minimal energetic cost of living (breathing, heart beat, etc.)
  2. variable energy expenditure
82
Q

thermoneutrality def

A

state where mechanisms of heat prod and heat dissipation are equal (is at 23 C)

83
Q

temperature at which thermoneutrality is reached

A

23 c

84
Q

name of mechanism that kicks in below temp of 23 to increase heat production

A

facultated or adaptive thermogenesis (includes shivering)

85
Q

FT or AT (facultative or adaptive thermogenesis) is what % of BEE (basal energy expenditure)

A

0-15%

86
Q

why body naturally produces heat

A
  • lot of energy invested to make ATP lost as heat

- ATP conversion into work: heat loss there too

87
Q

facultative (or adaptive) thermogenesis def

A

ability to render our thermodynamic system inefficient (lose more E to heat and less serves to make ATP)

88
Q

how TH allows facultative (adaptive) thermogenesis in brown adipose tissue

A
  1. more ATP consumption and turnover

2. facultative thermogenesis (more E lost in heat)

89
Q

when brown adipose tissue is metabolically upregulated

A

when need important heat production (like when in the cold) and not being an obese person

90
Q

thyroid hormone exact mechanism of action on brown adipose tissue (and which TH)

A

T3 mostly (bc is the active hormone): upregulates uncoupling protein which goes in IMM and lets H+ flow down conc gradient passively

91
Q

other term for hyperT

A

thyrotoxicosis

92
Q

how minimal energy for living and BEE vary in hyper and hypoT compared to normal

A

same minimal E used for living

greater or lower BEE.

93
Q

why hyperT complain of heat intolerance exam

A

are more comfortable at 18C because more of their E is lost to heat

94
Q

why hypoT complain of feeling cold exam

A

generate less heat. more comfortable at 25C (use UCP less)

95
Q

how brain affected by thyroid problems (in hypoT for ex)

A

memory problems, low ambition, depression. myxedema (or myxedema coma), accum of polysaccharides under the tongue so prob of speech

96
Q

myxedema definition

A

synonym of hypoT that also includes the dermato features (of mucopolysacch deposition)

97
Q

effects of hyperT on the brain young vs old adults

A

young: hyperactivity, insomnie, tremors
old: low appetite, weight loss, dyspnea

98
Q

why old adults have apathy as consequence of hyperT and name for that

A

apathetic thyrotoxicosis. TH downregulates catech. (serotonin is one) in CNS

99
Q

TH effect on CVS: heart itself

A

TH increases chronotropy and inotropy

100
Q

TH effect on CVS: circulation

A 
hyperT = vasodilation (get blood to brown adipose tissue)
hypoT = vasoconstriction
101
Q

hyperT vs hypoT effect on hemodynamics and CO

A 
hyperT = less BP, less afterload. high CO
hypoT = high BP, high afterload. low CO
102
Q

hypoT important effect on vessels + consequence

A

ats bc of high BP, high serum cholesterol (but ats has no effect bc low O2 demand)

103
Q

danger in treating hypoT too quickly

A

can precipitate MI

104
Q

hypoT possible defect in the heart

A

pericardial effusion bc of leaky capillaries and vasodilation

105
Q

hyperT effect on the heart

A

hyperdynamic. can get dyspnea from increased O2 demand

106
Q

hyperT possible disease it can cause to heart and treatment

A

high output HF with pulm edema

give furosemide

107
Q

hyperT effects on digestive system (2)

A
  • diarrhea (frequent passage of stool)

- elevated liver enzymes

108
Q

hypoT effects on digestive system (4)

A
  • NAFLD (high cholesterol so try to pack it in liver)
  • metab syndrome
  • ascites (leaky capillaries)
  • constipation
109
Q

bowel complication of hypoT

A

Ogilvy syndrome. bowel distension bc of paralysis of intestinal wall (paralitic ileus)

110
Q

test to dx thyroid function

A

TSH and T4 levels

111
Q

high TSH low T4 shows what

A

primary hypoT (problem in thyroid)

112
Q

low TSH high T4 shows what

A

primary hyperT (and suppresses hyp TRH and pit TSH)

113
Q

high TSH high T4 shows what

A

secondary hyperT (pit adenoma producing unregulated TSH)

114
Q

low TSH low T4

A

central hypoT (secondary if pit, tertiary if hypothalamus) hypoT (something injured pit or hypothalamus)

115
Q

why TSH best test for thyroid function

A

very sensitive and responds a lot to TH levels. can have normal T4 and high TSH, showing pre hypoT

116
Q

subclinical hypoT def vs overt hypoT

A

normal T4, high TSH.

overt hypoT is low T4 high TSH

117
Q

treatment for overt hypoT

A

give levothyroxine (T4)

118
Q

subclinical vs overt hyperT

A

subclinical: normal T4 low TSH

overt hyperT: high T4 low TSH

119
Q

how quickly T4 and TSH normalize after treating hypoT or hyperT and how to follow up

A

T4 normal quickly. TSH 4-6 weeks.
Ask for side effects after 10 days.
wait 6 weeks to check if dosage correct

120
Q

2 tests for hypoT other than lab

A
  • ultrasound to check for lobulated bossylated enlarged thyroid
  • serum TPO Abs to check if they have been released after an autoimmune (cellular, T cells) killing of thyrocytes
121
Q

Grave’s vs Hashimoto thyroiditis

A 
Grave's = specific disease where autoimmune agaisnt TSH-R makes gland hyperT
Hashimoto = autoimmune killing of thyrocytes (give hypoT)
122
Q

hyperT test

A

thyroid synthygraphy give iodide isotope to check where it is present and identify the overactive cells (it will enter through NIS)

123
Q

diseases included in Grave’s disease (autoimmune hyperT)

A
  • diffuse homogenous hyperactivity
  • toxic adenoma (benign tumor producing TH independently)
  • toxic multinodular Goiter
124
Q

toxic adenoma of thyroid (hyperT) pathophgy

A

gain of fct mutation in TSH-R. benign tumor makes TH all the time

125
Q

Grave’s disease pathophgy

A

Abs to TSH-R. (makes R think there’s TSH binding it). always producing TH

126
Q

central hypoT usual cause and treatment

A
  • cause: non functioning microadenoma (thyrotropes in pituitary destroyed)
  • treat: TH for life
127
Q

3 stages of thyroiditis

A

thyrotoxic (hyperT), hypoT, recovery

128
Q

thyrotoxic stage of thyroiditis

A

initial destruction of thyroid allows release of large reserve of TH (hyperT for 6 weeks to 1 year max)

129
Q

hypothyroid stage of thyroiditis

A

hypoT bc no more TH (destruction of thyrocytes) until recovery. can last a year

130
Q

recovery stage of thyroiditis and what if it doesn’t happen

A
  • may get recovery of thyroid and recovery of TH synthesis.

- if it doesn’t happen: years-lasting thyroiditis

Bloc E - GI & Metabolism (58 decks)

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