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Phase 2a Medicine > ENDO - THYROIDISMS > Flashcards

ENDO - THYROIDISMS Flashcards

1
Q

Where is the thyroid located?

A

in the anterior neck between C5-T1 vertebrae.
Divided into 2 lobes connected by an isthmus.

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2
Q

Name 4 effects of T3/T4

A
  1. BMR: increases basal metabolic rate.
  2. METABOLISM : anabolic effects at low serum levels and catabolic effects at higher levels.
  3. GROWTH: increases release and effect of GH and IGF-1
  4. CARDIOVASCULAR: increases heart rate and contractility through increasing sensitivity to catecholamines
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3
Q

Explain the physiology of thyroid hormone production.

A
  • Within the thyroid gland are numerous follicles composed of an enclosed sphere of follicular cells surrounding a core containing protein-rich material called COLLOID.
  • synthesis starts when circulating iodide is actively cotransported with Na+ ions across basolateral membranes of the follicular cells- IODIDE TRAPPING. Na+ pumped back out of cell na+/k+- atpases
  • negatively charge iodide ions diffuse to the apical membrane of the follicular cells and are transported into the colloid.
  • colloid of follicules contain large amount of protein called thyroglobulin.
  • once inside the colloid iodide is rapidly oxidised to iodine which then bind to tyrosine residues on the thyroglobulin (produced by follicular cells) under the action of thyroid peroxidase. the tyrosine may either bind to 1 iodine molecule - T1 OR 2 T2.
  • when the thyroid is stimulated to produce thyroid hormone, the T1 and T2 are cleaved from their tyrosine backbone but are still attached to the thyroglobulin and join to create T3 (t1+2) or t4 (t2+t2).
  • for thyroid hormone to be secreted into blood, extensions of colloid-facing membranes of the follicular cells engulf portion of the colloid (with its iodinated thyroglobulin) by endocytosis.
  • TSH stimulates movement of t3 and t4 containing colloid into secretory cells.
  • the iodated thyroglobulin is then brought into contact with lysosomes in the cell interior.
  • protelysis of the thyroglobulin = release of t3 and t4 diffuse out of follicular cells into interstitial fluid into blood.
  • there is sufficient iodinated thyroglobulin stored within the follicles of the thyroid to provide thyroid hormone for several weeks even in the absence of fdietary iodoine - this is unqieu amongst endocrine glands.

the thyoid produces more t4 than t3 - t3 is more active and is produced peripherally from the conversion of t4. more t4 is produced by t3 is more active.

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4
Q

which cells produce thyroglobulin?

A

follicular cells

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5
Q

Define Hyperthyroidism

A
  • overactive thyroid gland causing excess thyroid hormone and thyrotoxicosis.
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6
Q

Define thyrotoxicosis:

A
  • excess of thyroid hormone, overactive thyroid gland isn’t a prerequisite (Eg consumption of thyroid hormone)
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7
Q

Give some epidemiology of hyperthyroidism

A

affects 2-5% of women at some time - 20-40 yrs

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8
Q

What are the primary causes of hyperthyroidism?

A
  1. Graves - most common. anti-tsh antibodies stimulating the thyroid gland. DIFFUSE GOITRE AND THYROID EYE SIGNS.
  2. Toxic multinodular goitre - iodine deficiency leads to compensatory TSH secretion and hyperstimulation = nodular goitre formation. These nodules could become TSH-independent and secrete thyroid hormones.
  3. Toxic Adenoma - A single autonomous functional nodule secreting thyroid hormone.
  4. Subclinical hyperthyroidism : normal T3/T4 but low TSH. usually due to toxic multinodular goitre or graves.
  5. Thyroiditis : in initial stages of thyroiditis, transient hyperthyroid state followed by hypothyroid state.
  6. Drugs: Amiodarone : can cause both hyper and hypo thyroidisms.
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9
Q

Name some secondary causes of hyperthyroidism

A
  1. Pituitary Adenoma : TSH-secreting pituitary adenoma
  2. Ectopic Tumour: such as hCG-secreting tumours eg: choriocarcinoma
  3. Hypothalamic Tumour : = excessive TRH secretion : very rare cause of hyperthyroidism
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10
Q

Name some other rarer causes of hyperthyroidisms

A

beta-HCG related: mimics TSH action - causes thyroid hormone synthesis and release. occurs in state of elevated beta-HCG ie pregnancy, choriocarcinoma.

ectopic thyroid tissue - thyroid tissue found elsewhere that produces thyroid hormone.

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11
Q

What are the risk factors for hyperthyroidism?

A

family history

autoimmune disease eg : vitiligo, t1dm, addisons

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12
Q

Name the key presentations for hyperthyroidism

A

THYROIDISM

Tremor
Heart rate increases
Yawning
Restless
Oligomenorrhoea
Irritability
Diarrhoea
Intolerance to heat
Sweating
Muscle wasting (wt loss)

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13
Q

What are the signs of hyperthryoidism?

A

postural tremor
palmar erythema
hyperreflexia
sinus tachycardia/arrhythmia
goitre
lid lag and retraction

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14
Q

Signs of hyperthyroidism specific to GRAVES disease

A
  1. thyroid acropachy
  2. thyroid bruit
  3. pretibial myxoedema
  4. eye signs:
  5. exophthalmos (bulging of the eye)
  6. ophthalmoplegia (paralysis or weakness of the eye muscles)
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15
Q

Symptoms of hyperthyroidism

A
  • weight loss
  • anxiety
  • fatigue
  • reduced libido
  • heat intolerance
  • palpitations
  • menstrual irregularity
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16
Q

what are the 1st line investigations for hyperthyroidism?

A

THYROID FUNCTIONS TESTS (TFTS)

interpretation:
low tsh , high t4 : primary hyperthyroidism eg graves

low tsh and normal t4: subclinical hyperthyroidism

high tsh and t4 / normal tsh and high t4 : secondary hyperthyroidism: eg tsh-secreting pituitary adenoma

17
Q

After 1st line tfts, what other investigations do you do for hyperthyroidism?

A

Antibodies: anti-tsh receptor antibodies positive in 95% of pts with Graves.

Anti-TPO (thyroid peroxidase) and anti-thyroglobulin antibodies might be positive.

18
Q

what autoantibody are u likely to see in Hashimoto’s thyroiditis?

A

anti-tpo

30-50% chance - anti-thyroglobulin

19
Q

What autoantibody are u likely to see in Graves?

A

anti-tsh receptor, anti-tpo

20-40% chance of anti-thyroglobulin

20
Q

Other non 1st line investigations to consider for hyperthyroidism

A
  1. thyroid USS: offered to patients with thyrotoxicosis if they have a PALPABLE thyroid nodule or in pts with normal thyroid function when malignancy is suspected
  2. Technetium radionuclide scan: if anti-tsh antibodies are negative. shows diffuse uptake in graves, unlike in toxic adenoma or toxic multinodular goitre
  3. glucose : hyperthyroid associated with hyperglycaemia
  4. ecg : hyperthyroid associated with AF
21
Q

differentials of hyperthyroid

A

usually clinically obvious

  • differentiation of mild cases from anxiety can be difficult look for:
    1. eye signs eg : lid lag and stare
    2. diffuse goitre
    3. proximal myopathy and wasting
22
Q

what is the 1st line management for hyperthyroidism/GRAVES?

A

Phase 2a Medicine (22 decks)

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