Metabolism Flashcards

1
Q

Functions of thyroid hormones

A

Normal growth development
Metabolic activity and oxygen requirements
Lipid and carb metabolism

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2
Q

Embryology of thyroid

A

Week 4: thyroid appears from endodermal tissue
Week 5: thyroglossal duct breaks down and gland decends
Week 7: thyroid migrates anterior to trachea
Week 10: thryoglossal duct disappears
Week 12–20: thyroid functional
Week 20–26: thyroid independent

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3
Q

Lingual thyroid

A

Failure of thyroid to migrate during development

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4
Q

Thyroglossal cyst

A

Remnant of thyroglossal duct that didn’t break down

Can be seen moving up when patient protrudes tongue

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5
Q

Anatomy of thyroid

A

Deep to sternohyoid
Anterior to recurrent laryngeal nerve and trachea cartilage rings 2 and 3
Right to oesophagus

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6
Q

Blood supply of thyroid

A

Superior thyroid artery from external carotid artery

Inferior thyroid artery from subclavian artery (thyrocervical trunk)

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7
Q

Medullary thyroid cancer

A

Aggressive cancer that secretes calcitonin

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8
Q

Thyroglobulin

A

Storage form of T3/4 found in colloid of the thyroid

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9
Q

Describe the process of T3/4 release

A

1) Iodine uptake into bloodstream is oxidised to iodide
2) Iodide rapidly incorporated into tyrosine molecules in follicular cells, then into thyroglobulin
3) At lumen interface, remaining iodide is catalysed to MIT and DIT by thyroid peroxidase (which required H2O2) and is stored in colloid as thyroglobulin
4) TSH from AP reaches follicular cell membrane which scallops in to allow endocytosis of “colloid drops” containing thyroglobulin and releases T4/3 into capillary

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10
Q

Locations of NIS

A
Breast
Salivary glands
Ciliary body of eye
Gastric mucosa
Differentiated thyroid cancer cells
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11
Q

Symptoms of thyrotoxicosis

A
Nervousness
Sweating
Weight loss
Heat sensitivity
Tachycardia
Weakness
Goitre
Skin changes
Tremor
Eye signs e.g., in Graves
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12
Q

Causes of thyrotoxicosis

A
Thyroiditis
Graves
Amiodarone
Iodine
Thyroxine
Toxic nodule
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13
Q

TSH and T4 levels in primary hypothyroidism

A

TSH will be high and T4 will be low

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14
Q

TSH and T4 levels in secondary hypothyroidism

A

TSH will be normal or low and T4 will be low

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15
Q

TSH and T4 levels in primary hyperthyroidism

A

TSH will be low and T4 will be high

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16
Q

TSH and T4 levels in secondary hyperthyroidism

A

TSH will be high and T4 will be high

17
Q

NIS

A

Sodium iodine transporter
Iodide concentration in plasma is extremely low so it is “trapped” by NIS
Active transporter that exchanges 2 sodium ions for 1 iodide ion against its concentration gradient

18
Q

Parathyroid hormone functions

A

Stimulates osteoclastic bone resporption
Stimulates renal tubular reabsorption of calcium
Stimulates gut absorption of calcium by acting on the kidney to convert calcidiol to calcitriol

19
Q

3 things that can regulate PTH release

A

Serum ionized calcium
Serum phosphate
Serum 1,25 dihydroxyvitamin D

20
Q

ECF calcium

A

45% ionised, bioactive
10% complexed with anions
45% protein-bound

21
Q

Describe how PTH is released into the ECF

A

Calcium present in food enters the stomach. Magnesium acts as a cofactor to uptake calcium via the transmembrane calcium receptor. Calcium is uptaken into the parathyroid chief cell which activates PTH to be released into the ECF.

22
Q

Basic vitamin D metabolism

A

Sunlight absorbed by skin, which makes calciferol (also from diet)
Calcirefol is hydroxylated by the liver to make calcidiol
Calcidiol moves to the kidney where it is metabolised via PTH to calcitriol
Calcitriol uptaken by the kidney tubules, increasing calcium and phosphate absorption

23
Q

Parathyroid hormone-related peptide

A

Important paracrine regulator of breast, skin and bone

Produced in excess by some cancers, leading to hypercalcaemia (acts very similarly to PTH)

24
Q

Primary hyperparathyroidism

A

Overactive parathyroid gland causing bone breakdown and increased reabsorption of calcium
Causes PTH-dependent hypercalcemia

25
Q

Examples of vitamin-D dependent causes of hypercalcaemia

A

Sarcoidosis – granulomas express high levels of 1α-hydroxylase, the enzyme that catalyzes the hydroxylation of 25-OH vitamin D to its active form which increases calcium and phosphate reabsorption
Vitamin D intoxication

26
Q

Hypoparathyroidism

A

Causes hypocalcaemia due to reduced release of PTH and therefore decreased absorption and resorption of calcium
Can be caused by many things, including surgery, radiation, autoimmune disease, infiltrative diseases etc.

27
Q

Pseudohypoparathyroidism

A

Parathyroid hormone resistance

PTH levels will be high, calcium levels low and phosphate levels high

28
Q

Causes of hypoparathyroidism due to abnormalities of vitamin D metabolism

A

Vitamin D deficiency/resistance
Renal failure
Deficient
1α-hydroxylation

29
Q

PTH influence on phosphate

A

Promotes excretion of phosphate in urine and pulls it out of bone along with calcium

30
Q

Phosphatonins

A

Specifically regulate renal handling of phosphate, therefore causes phosphate wasting

31
Q

Causes of hyperphosphataemia

A

Increased input e.g. IV phosphate, cell death

Decreased excretion e.g. renal failure, PTH deficiency

32
Q

Causes of hypophosphataemia

A

Inadequate GI absorption e.g. due to vitamin D deficiency
Respiratory alkalosis
Renal loss

33
Q

How do phosphatonins contribute to hypophosphataemia?

A

FGF23 (derived from bone) inhibits the hydroxylation of inactive form of vitamin D and decreases sodium phosphate reabsoprtion in the kidney
Together, there is an overall decrease in phosphate absorption leading to hypophosphataemia

34
Q

Osteomalacia

A

Failure of bone to mineralise
Accumulation of unmineralised osteoid
Can be calciopenic, phosphopenic or due to osteoblast dysfunction

35
Q

Autosomal Dominant Hypercalciuric Hypocalcaemia

A

Constitutive activation of calcium sensing receptor
Parathyroids read plasma ionised calcium level as being higher than it really is, so PTH level is inappropriately low for a given calcium level
No real treatment, can give small doses of vitamin D if recurrent symptoms are present