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Molecular Basis Of Disease > Trace Elements (Iodine, Copper, Selenium and Aluminium)) > Flashcards

Trace Elements (Iodine, Copper, Selenium and Aluminium)) Flashcards

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1
Q

How much iodine is required daily?

A

about 150 micrograms

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2
Q

What is the function of iodine in the body

A

substrate used for thyroid hormone synthesis

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3
Q

Where is iodine primarily found and what foods are a good source of iodine?

A

primarily found in ocean (seafood and kelps)

food sources:
- fairy products
- seafood
- seaweed
- eggs
- bread
- some vegetables

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4
Q

Due to iodines low environmental levels it is the number one cause of

A

preventable intellectual disability in children

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5
Q

What are the 2 thyroid hormones?

A
  1. thyroxine (T4) prohormone
    - transport from cell to cell form
    - longer half life and more stable
  2. triiodothyronine (T3)
    - active form
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6
Q

Where is the thyroid gland located

A

on trachea
- 2 lobes joined by narrow isthmus

filled with major thyroid secretory cells around in hollow spheres (follicles)

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7
Q

What is the structure of the follicles in the thyroid gland

A

secretory cells (follicular cells) form rings around inner lumen (colloid) with a C cell in the connective tissue associated with the follicle
- colloid serves as the extracellular storage and production site of thyroid hormones
- C cells secrete calcitonin which regulates blood calcium levels and stops the breakdown of bone by releasing osteoclasts by releasing Ca2+

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8
Q

Where are thyroid hormones mostly found other than the thyroid gland

A

circulating in plasma:
- most complexed to T4 binding globulin
- small amount free active T3

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9
Q

How are thyroid hormone regulated

A
  1. thyrotropin-releasing hormone (TRH) secreted by the hypothalamus
  2. TRH stimulates thyroid stimulating hormone (TSH) produced by the anterior pituitary gland
  3. TSH regulates T3 and T4 synthesis in the thyroid gland
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10
Q

What is the first step in thyroid hormone synthesis

A

thyroglobulin (Tg) is synthesised in the rough ER and enters the colloid by exocytosis

meanwhile a sodium/iodide symporter (Na/I) pumps iodide actively into the cell

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11
Q

What is the second step in thyroid hormone synthesis

A

Iodide enters the colloid from cytoplasm by pendrin transporter and TPO (thyroperoxidase) converts iodide into active iodine

iodine iodinates Tg at tyrosyl residues causing the adjacent iodinated tyrosyl residues to be paired together forming MIT (monoiodotyrosine) and DIT (diiodotyrosine)

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12
Q

What is the third step in thyroid hormone synthesis

A

Tg then re-enters the follicular cell by endocytosis where lysosomes fuse and proteolysis occurs which liberates T3 and T4 molecules

T3 and T4 in cytoplasm then enter the colloid

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13
Q

What is the function of TSH other than stimulating the production of thyroid hormones

A
  1. stimulates expression of transporters and enzymes involved in T3 and T4 production (and endocytosis of Tg)
  2. also stimulates growth of thyroid gland
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14
Q

What happens when is no or excess TSH

A

no TSH = thyroid atrophies (shrinks)
- hypothyroidism
- hormones released at very low rate

too much TSH = thyroid hypertrophies
- hyperthyroidism

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15
Q

What is the consequence of iodine deficiency during pregnancy

A

stillbirth
spontaneous abortion
congenital abnormalities

if child is born can result in:
- stunted growth
- diminished intelligence
- retardation

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16
Q

Where is iodine deficiency most prominent

A

developing countries
- himalayas
- andes
- africa

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17
Q

How was iodine deficiency improved in australia?

A

iodised salt
iodised water
bread made with iodised salt
- provides enough iodine to avoid low thyroid activity for most people

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18
Q

What are the effects of long term iodine deficiency

A

thyroid gland adapt to insufficient supply of iodine by increasing trapping
- Goitre occurs (increase size of thyroid gland)
- hypothyroidism occurs (not enough thyroid hormones produced)

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19
Q

What are the symptoms of long term iodine deficiency

A

dry skin
hair loss
decreased metabolic rate
- fatigue/ lethargy
slowed reflexes
constipation

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20
Q

How is the negative feedback loop for thyroid hormone stimulation affected in hypothyroidism

A

due to lack of T3 and T4 being released from thyroid the hypothalamus keeps secreting TRH and in turn TSH.

As TSH keeps being secreted a goiter occurs

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21
Q

Are goiters found in iodine deficient children

A

no just adults

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22
Q

What is the symptoms of iodine toxicity

A

burning of mouth, throat and stomach
fever
nausea
vomiting
diarrhea
weak pulse
cyanosis
coma

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23
Q

What can cause iodine toxicity

A
  1. iodine supplementation programmes in iodine deficient populations
    - can result in iodine induced hyperthyroidism (especially if goiter present)
  2. excess iodine intake in healthy individuals
    - elevated blood concentrations of TSH but inhibits thyroid hormone production
    - leads to hypothyroidism and goiter (but not known how)
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24
Q

Iodine toxicity leads to Wolff Chaikoff effect. What is this effect?

A

reduction of thyroid hormone levels caused by ingestion of large amounts of iodine by rejecting the large amounts of iodine

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25
How much copper is required per day? does this differ from the amount a regular diet provide?
required: about 900 micrograms regular diet: 1-1.5 micrograms per day
26
What are good food sources for copper?
oysters and shellfish seeds and nuts meats (high in kidney and liver) whole grains
27
What key enzymes in the body is copper essential in?
1. superoxide dismutase - removes superoxides by converting them into hydrogen peroxide 2. lysyl oxidase (extracellular copper enzyme) - needed for collagen and elastin synthesis 3. cytochrome c oxidase - last enzyme in the electron transport chain
28
Where in the process of collagen synthesis and secretion is lysyl oxidase needed?
After tropocollagen is formed Cu dependant lysyl oxidase deaminates lysine and hydroxylysine residues to form aldehyde groups which forms cross links - turns tropocollagen into final collagen product
29
Where in the electron transport chain does cytochrome c oxidase (complex IV) used and what is its function?
1. sugars and fatty acids are oxidised to acetyl CoA 2. acetyl CoA oxidised to generate NADH 3. electrons from NADH are passed down the electron transport chain which creates energy to generate a proton gradient across the mito inner membrane 4. cytochrome c oxidase is the last enzyme in this chain which oxidises 3 cytochrome c molecules (reducing O2 to 2H20)
30
What does copper deficiency cause
1. decreased cross linking of collagen and elastin (lack of lysyl oxidase) 2. poor bone formation and strength 3. hyperextensible skin and weak ligaments 4. increased occurrence of aortic aneurysms 5. increase ROS (lack of SOD) 6. loss of complex IV activity/ATP generation (lack of cytochrome c oxidase)
31
What is the most common cause of copper deficiency
malabsorption of copper or zinc toxicity (zinc competitively binds to MET in gut enterocytes)
32
What is a copper deficiency genetic disease and what is the genetic basis of the disease
Menkes disease - X linked recessive disorder (congenital)
33
When does Menkes disease onset occurs and what does it result in?
onset: during infancy result: growth failure and nervous system deterioration
34
What is the molecular basis of Menkes disease
causes a defect in ATP7A (transporter expressed on most tissues except the liver) - defect in copper transporting protein in trans-golgi network which impaires copper absorption in gut - low copper in many tissues which accumulates in kidneys
35
What are the symptoms of copper toxicity
yellowing of eye (Kayser Fleischer rings) metallic taste anaemia vomiting, nausea, abdominal pain no urine production diarrhea yellowing of skin muscle weakness chills, fever and systemic pain
36
What is excess copper in the body known as and what does it occur from?
copperiedus occurs from: - ingesting acidic foods cooked in uncoated copper cookware - exposure to excess copper in drinking water or other environmental sources
37
Wilson's disease is a genetic disease causing copper toxicity. What is the molecular basis of this disease?
defect in transporter ATP7B - expressed in brain, liver and kidney - involved in copper export out of cell A defect in this transporter leads to copper levels building up in the liver which then overflow and cause a build up in brain and kidneys
38
What is a major consequence of copper toxicity in Wilson's disease
high amounts of copper leads to the Fenton reaction occuring more than normal leading to increased ROS production
39
How is Wilson's disease treated
treated with chelators and or zinc
40
What is the main symptom of Wilsons disease
Keyser-Fleischer rings around iris
41
What is the difference between Menkes and Wilsons
Menkes - affects ATP7A transporter so copper cannot get into the cell Wilsons - affects ATP7B transporter so copper cannot get out of the cell
42
What kind of element is Selenium and what is its function in the body
non metal found in minerals function: incorporated into proteins to form selenoproteins which contain selenocysteine residues
43
What are some examples of selenoproteins
1. selenoprotein P - found in blood plasma - may be an antioxidant 2. glutathione peroxidase (GPx) 3. Iodothyronine deiodinases
44
What is the role of glutathione peroxidase
reacts with glutathione and hydrogen peroxidase which reduces hydrogen peroxidase to water and produces oxidised glutathione (GSSG)
45
What is the role of Iodothyronine deiodinases in thyroid hormone synthesis?
iodine removed from MIT and DIT through this selenoproteins - this allows iodine to be recycled
46
What are good food sources for selenium?
nuts (brazil nuts especially) cereals meat mushrooms fish eggs
47
What is the optimal dietary daily intake of selenium?
40 micrograms per day
48
What disease does Selenium deficiency cause?
Keshan disease
49
What does Keshan disease cause
cardiomyopathy (white muscle disease) - due to defects in GPx leads to bleaching by peroxides and hydroperoxides
50
Can Keshan disease be reversed by selenium supplements
no
51
How much selenium per day can cause selenosis (selenium toxicity)
400 micrograms per day
52
What is the most common way to be exposed to toxic amounts of selenium
exposure to smoke of burning coal containing Se
53
What are the symptoms of Se poisoning
garlic odour breath gastrointestinal disorders hair loss and sloughing of nails fatigue and irritability neurological damage cirrhosis of the liver pulmonary edema
54
There were 3 major outbreaks of Se poisoning in the last 25 years. What were they all due to?
errors in formulation of nutritional supplements - ranging from 180-1000 times the amount indicated on the bottle
55
Aluminium is insoluble. What can make it soluble?
decrease in pH (acidic environment)
56
how much aluminium is ingested daily and how much of it is actually absorbed?
ingested = 3-5 mg absorbed = 0.02-0.1%
57
Aluminium is absorbed into the body by what sources
food/water additives utensils medicines - antacids - astringents - buffered aspirin cosmetics/ deodorant
58
How is aluminum excreted from the body
majority from faeces however a small amount enters the bloodstream but leaves quickly in the urine
59
what is the concentration of aluminum in water and how does aluminum get into the water supply
concentration = low aluminum sulphate is used as a flocculant in water (a substance which promotes clumping of particles to clean water supply)
60
The uptake of aluminum in the gut depends on what environmental factor
pH
61
When gut pH changes what changes about the uptake of aluminum
different forms of hydroxylated forms of aluminum lower pH = soluble forms of Al absorbed higher pH = insoluble forms of Al absorbed
62
Is Al uptake paracellular or transcellular
not known
63
polyvalent cations of Al is chemically similar to what other ion?
Calcium and iron
64
What implications do the chemical similarities between Al and calcium cause?
Al may interact with multiple types of voltage gated Ca2+ channels - Al can inhibit/ block Ca2+ uptake in gut - can disrupt signal transduction pathways Ca2+ is needed for
65
What implications do the chemical similarities between Al and iron cause?
in plasma Al can bind to transferrin instead of Fe - taken up by peripheral tissues (through receptor mediated endocytosis) ann can accumulate in brain, liver, spleen, kidney, bone
66
What symptoms is aluminum toxicity associated with
renal failure neuronal cell death
67
What are the symptoms of Al toxicity
motor disturbances (tremors) seizures visual hallucinations dementia coma and death
68
What are some non-specific symptoms of Al toxicity
muscle weakness bone pain, osteomalacia (soft bones), fractures, premature osteoporosis multiple non-healing issues
69
What is a common medical treatment which can cause Al toxicity
haemodialysis 1. can expose patient to dialysate (dialysis fluid) which is high is high in aluminum as they are used as phosphate binders (to reduce the absorption of phosphate) - drinking contaminated water after exposure can lead to Al toxicity 2. if dialysis does not effectively remove excess Al from body it can build up over time
70
If serum level is above 60 mg/L what is the treatment for Al toxicity
desferrioxamine treatment or another chelating agents - binds excess Al and will remove it through faeces or urine

Molecular Basis Of Disease (17 decks)

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