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medicine 2 > Week 7 - Thyroid > Flashcards

Week 7 - Thyroid Flashcards

1
Q

What hormones does the thyroid produce?

Where are these hormones produced?

A

T3 and T4

Calcitonin

By follicular cells and parafollicular cells

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2
Q

What is the parathyroid composed of?

What is secreted here?

A

4 parathyroid glands on posterior thyroid

Can be up to 8 glands

Secrete parathyroid hormone

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3
Q

What are the roles of parathyroid hormones?

A
  • Calcium homeostasis
  • Raise serum calcium
  • Stimulate osteoclast reabsorption of bone
  • Increase calcium reabsorption in kidney
  • Increase calcium uptake in gut
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4
Q

What are pathology related to thyroid gland?

A
  • Hyperplasia (from overstimulation of gland producing TSH)
    • Grave’s disease
    • Tumour nodules
  • Thyroid cancer
  • Goitre
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5
Q

What are pathology related to parathyroid gland?

A
  • Hyperparathyroidism
  • Primary = tumour
  • Secondary = kidney failure
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6
Q

What are T3 and T4?

What is their role?

A

Iodine-containing low molecular weight hormones

  • Regulate BMR and growth maturation
  • Secretion regulted by TSH from anterior pituitary
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7
Q

What is calcitonin?

What is its role?

A

Polypeptide hormone

  • Lowers blood calcium
  • PTH antagonist
  • Produced by parafollicular cells
  • Contain neuroendocrine granules
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8
Q

What is required for thyroid hormone synthesis?

What catalyses this process?

A
  • Source of iodine
  • Source of tyrosine residues
  • Thyroglobulin for site of synthesis

Thyroid peroxidase

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9
Q

What are the actions of thyroid hormones?

A
  • Increase body metabolism
      • carb, protein, and fat metabolism
      • O2 consumption and heat production
  • Stimulate growth and development
  • Synergistic with actions of SNS / catecholamines
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10
Q

What happens during the process of iodination of tyrosine residues on thyroglobulin?

A
  • Tyrosine iodinated at 3’ ring –> MIT formed
  • Tyrosine iodinated at 3’ and 5’ ring –> DIT formed
  • DIT + DIT = T4
  • MIT + DIT = T3
  • DIT + MIT = reverse T3 = biologically inactive
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11
Q

What is the role of reverse T3?

A

Anatgonist at T3 receptors

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12
Q

What happens to T3,T4, and TSH levels in primary and secondary hypothyroidism and in lack of dietary iodine?

A

Primary = - T3 and T4, + TSH

Secondary = - T3 and T4, - TSH

Lack of iodine = - T3 and T4, + TSH

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13
Q

What happens to T3, T4, and TSH levels in primary and secondary hyperthyroidism, and hyper-secreting thyroid tumour?

A

Primary = + T3 and T4, - TSH

Secondary = + T3 and T4, + TSH

Tumour = + T3 and T4, - TSH

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14
Q

What are the main, primary, and secondary causes of hypothyroidism?

A
  • Autoimmunity
  • Lack of dietary iodine
  • Drug-induced
  • Thyroid hormone resistance

Primary = failure of thyroid gland

Secondary = anterior pituitary failure

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15
Q

What are the main causes of hyperthyroidism?

A
  • Hyper-secreting thyroid tumour
  • Latrogenic causes
  • Grave’s disease
  • Abnormal TSI
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16
Q

What are the symptoms of hypothyroidism?

A
  • Weight gain
  • Dry skin
  • Hoarse voice
  • Menstrual changes
  • Cold intolerance
  • Constipation
  • Low HR/BR
  • Depression, confusion, poor memory
  • Myoxoedema (puffy appearance)
  • Reduced BMR
17
Q

What is cretinism?

A

Neonate

Dwarfism and mental retardation

Every newborn tested for TSH and T4

18
Q

How can you treat hypothyroidism?

What are some issues though?

A
  • Synthetic thyroid hormones
  • Levothyroxine (T4)
      • drug of choice, can worsen angina
  • Liothyronine (T3)
      • rapid onset can induce heart failure, used in severe hypothyroid state
19
Q

What are the symptoms of hyperthyroidism?

A
  • Weight loss
  • Sweating
  • Heat intolerance
  • Palpitations
  • Tremor
  • Nervousness
  • Diarrhoea
  • Goitre and exopthalmos
20
Q

How do you diagnose hyperthyroidism?

A
  • Thyroid function test
  • If Grave’s suspected, test for thyroid-stimulating antibodies
  • Perform thyroid uptake test for thyroid tumours
21
Q

How can you treat hyperthyroidism?

A
  • Anti-thyroid drugs
    • Thionamides - carbimazole + PTU
  • Radioiodine
  • Surgery
22
Q

How do anti-thyroid drugs work?

A
  • Decrease production of thyroid hormones by inhibitng iodination and coupling processes
  • Blockage of T4 to T3 deiodination
  • Non-selective beta blockers reduce actions of catecholamines
  • 12-18 month restoration
23
Q

When is radioiodine used?

A
  • Used in older patients with nodular goitres and hyperthyroidism
  • Used when thyroxicosis recurs after anti-thyroid drug therapy
  • 2-4- max effect
24
Q

How does + adipose tissue cause increase in CVD?

A

Adipose tissue secretes cytokines and inflammatory factors

25
Q

What genetic factor can lead to obesity?

A
  • POMC mutation
  • Reduction in leptin
  • Reduction in appetite suppression
    • copies of FTO gene = + weight gain
  • FTO controls neural regulation of appetite
26
Q

What medications are used to treat obesity?

A

Orlistat - intestinal lipase inhibitor

Saxenda - GLP-1 analogue

27
Q

What is the role of the arcuate and paraventricular nucleus?

A

Arcuate:

  • NPY, AgRp and POMC, CART neurotransmitter release
  • Stimulation or inhibition of food intake
  • Reward circuit stimulated

Paraventricular:

  • Involved in stimulation / inhibition of reward centre
28
Q

What hormones are released upon gastric distention?

What is their role?

A
  • CCK
  • GLP-1
  • Oxytonmodulin
  • Peptide YY
  • Apolipoprotein A-IV
  • Enterostatin

All inhibit food intake

29
Q

What is leptin and its role?

A
  • Peptide hormone secreted from adipose
    • food intake = - leptin
    • food = + leptin = appetite suppression
  • Production correlates with amount of adipose tissue
30
Q

What is ghrelin and how does it act?

A
  • Produced from GIT
  • Secretion when food anticipated
  • Acts centrally at ARC or brain stem to stimulate food intake
    • Acts via NPY and AgRP
    • ghrelin at certain times of day
31
Q

What is PYY and how does it work?

A
  • Secreted from distal GIT dependent on nutrient intake
  • Stimulated by CCK, gastric acid, and bile
  • Inhibits food intake
  • PYY1-36 = cleaved to PYY3-36
    • Acts at NPY Y2 receptor
    • Inhibits release of NPY = less food intake
  • PYY stays elevated for 12 hours post-meal
32
Q

Which reward centres are stimulated upon food intake?

What is bupropion and how does it work?

A

Opioid receptors, Cannabinoid receptors, Dopamine

Bupropion = dopamine reuptake inhibitor

    • dopamine in synapse
  • Prolonged activation of dopamine receptor
33
Q

How does orlistat work and how do you take?

Side effects?

Dosing?

A
  • Inhibits gastric and pancreatic lipase
  • Take before each meal
  • Combine with low-fat diet
  • Only give when obese or + risk factors
  • SE = steatorrhea, fat soluble vitamin deifciency
  • Dosing = 120mg at meal time, 360mg max.
34
Q

How does saxenda work and what are problems with it?

A
  • Glucagon-like peptide receptor agonist
  • Subcutaneous injection
  • Appetite suppression from + POMC/CART secretion
  • Suppresses dopamin signalling
  • Problems = + expensive and + similar to orlistat

medicine 2 (29 decks)

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