Iodine Flashcards

1
Q

role of I in thyroid metabolism

A

T3 = triiodothyronine (contains 3 I) = active hormone in cells
T4 = thyroxine (4 I) = transport or prohormone form in plasma

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2
Q

where is iodine found

A

oceans and deposited in soil
plant sources= amount depends on soil
animal sources= amount depends on plants eaten, water, how and were animals were fed
SEAFOODS= rich source

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3
Q

precursors of iodine hormone

A

MIT and DIT

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4
Q

active form of I hormone

A

T3= triiodothyronine

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5
Q

transport/prohormone form of I hormone

A

T4= thyroxine

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6
Q

Iodide absorption

A

constant supply to replace losses (urine, sweat)

**UNLIKE MOST MICORMINS significant excretion of I (controlled) BUT no controlled absorption

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7
Q

where do humans store I

A

thyroid gland

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8
Q

GI absorption of I

A

almost 100% (not regulatory site)
absorption in stomach and small intestine

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9
Q

small intestine I absorption

A

absorb thyroid hormones as T3 and T4, so these are given directly as medication

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10
Q

6 steps of thyroid hormone synthesis

A
  1. I enters thyroid cell by active transport (95mcg per day taken up= EAR)
  2. I added to thyroglobulin (Thg) at a a tyrosine -> monoiodotyrosine (MIT)
    - Fe-dependent thyroid peroxidase
    - complex is called Thg-MIT
    - Thg is protein made in thyroid cell
  3. another I added to Thg-MIT=Thg-DIT
  4. (IN COLLOID) Thg-DIT + Thg-DIT = (condense) Thg-T4
  5. Thg-DIT +Thg-MIT = (condense) Thg-T3 and Thg-rT3 *reverse
  6. (BACK TO THYROID CELL) T3, T4 removed/cleaved from Thg complex and released into plasma
    -all unused I recycled
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11
Q

in thyroid hormone synthesis, when is H2O2 used

A

steps 2 and 4
NADPH oxidase
thyroid peroxidase and thyroperoxidase

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12
Q

in thyroid hormone synthesis, which reactions occur in protein Thg

A

step 3, 4, and 5
3. MIT + I = DIT
4. DIT + DIT = T4
5. MIT + DIT = T3

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13
Q

what happens in step 6 in thyroid hormone synthesis

A

Thg removed by degrading to amino acids

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14
Q

how is most T3 made

A

minor: condense Thg-DIT+Thg-MIT
major: in bloodstream made by deiodination of T4 (prohormone)

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15
Q

deiodinases

A

T4 = T3 or rT3 (inactive)
5’-deiodinase = T3
5-deiodinase = rT3
both require Se

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16
Q

control of thyroid hormone production

A

pituitary gland releases thyroid stimulating hormone (TSH)-thyrotropin
-> promotes I uptake and protein synthesis by the thyroid gland
low T3 = more TSH = more I into gland
high T3= less TSH = prevent further I uptake

17
Q

what happens if TSH stimulated during I deficiency

A

hyperplasia of thyroid gland “goitre”
neck swells bc more Thg is being made in anticipation of making T4

18
Q

goitre common in? treatment?

A

developing countries, low iodine
shrink when given iodine or thyroxine

19
Q

transport of T3 and T4

A

most plasma thyroid hormone is T4
both bind to transport proteins
T4= thyroxine binding globulin
T3= albumin
transthyretin- cotransports with RBC/retinol
small amount T3 and T4 unbound
bind receptors and enter cells to exert hormone actions

20
Q

function of T3 in cells

A

in cells T4 (5’deoidonase) = T3
in cells of tissues (liver, brain, pituitary, brown adipose, muscle)
- T3 binds nuclear receptors = influence transcription by increase mRNA selected genes

21
Q

function of T3 in cytosol of tissue cells

A

influence cell metabolism by activating phosphatidylinositol 3-kinase (PI3K) (signaling pathway)

22
Q

overall function of T3

A

increase BMR, O2 consumption, heat production
- hypothyroidism: gain wt, fatigue, cold

CNS development

linear growth

23
Q

effect of T3 on adipose tissue

A

enhance lipolysis

24
Q

effect of T3 on muscle

A

enhance contraction

25
Q

effect of T3 on bone

A

promote anabolism (growth and development)

26
Q

effect of T3 on CV

A

increase heart rate

27
Q

effects of T3 on GI

A

stimulate nutrient digestion and absorption

28
Q

effect of T3 on metabolism

A

stimulate metabolic rate, oxygen consumption in metabolically active tissues

29
Q

EAR I

A

EAR set to meet requirements for uptake by thyroid gland= 95mcg/day

maintain balance of I through reuse/recycled I and replace losses with diet

30
Q

RDA I

A

150mcg
2SD = 20%

pregnancy = higher 220mcg
lactation = higher 290mcg

thyroidectomy (removed by surgery, or ablation with radioactive I)
if complete: prescribe T3/T4 and dietary I unnecessary
if incomplete: RDA would supply sufficient for capacity of gland, supplementation may or may not be necessary

31
Q

food sources I

A

seafood
dairy/eggs

32
Q

IDDs

A

iodine deficiency disorders
goitre and cretin
both put region/country at risk for low productivity, poor quality of life

33
Q

goitre

A

attempt by thyroid gland to synthesize thyroid hormones
= overstimulated by TSH
hyperplasia of gland (increase number of cells in gland)
if pop prevalence exceeds 10%= endemic goitre
symptoms: hypothyroidism = low BMR = wt gain, poor growth in children bc can’t produce enough hormone

34
Q

cretin

A

child of mother deficient during pregnancy
hypothyroidism in the fetus/young children prevents CNS development =
- permanent mental retardation
- neurological effects
- growth abnormalities known as cretinism

35
Q

2 main causes of IDDs

A
  1. lack of I in food or water due to soil levels, lack access to seafoods
    - usually mountainous areas
    and/or:
  2. consumption of goitrogens = foods that inhibit iodine metabolism
    ex) generate SCN- (thiocyanate) which interferes with uptake of I by thyroid gland
    foods of cabbage species (eastern europe), some types of cassava (philippines, africa)
    *diff countries have diff I medications, Can only T4 bc soil levels/ food levels are high

ALSO: when Se (need for T3->T4), Vit A, and/or Fe low, then problem is worsened for I deficiency

36
Q

IDD prevalent areas globally

A

andes: mountains (South America)
Eastern Europe: cabbage
Nepal: Himalayas
Ethiopia: high altitude = low I in soil, don’t eat seafood

37
Q

Prevention of IDDs

A

fortification of a staple (salt or sugar) with KI, iodization is effective

in Can, mandatory to add 76mcg/g table salt (2g meets RDA)
*none in pickling salt, sea salt, fleur de sel, Himalayan pink salt

As ppl use less table salt, I intake is falling
in New Zealand manufacturers now required to use iodized salt in making processed foods

38
Q

UL for I

A

= 1100mcg all sources
LOAEL= 1700mcg, UF= 1.5
UL based on having elevated serum TSH and goitre-like symptoms (hypothyroidism) with too much I
*paradoxical, hit, unexplained wt loss, hyperthyroid

Norhtern Japan- high consumption of seafoods and seaweeds leads to I toxicity
(dried seaweed = 3000mcg/g or higher)