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endocrine > thyroid pathology > Flashcards

thyroid pathology Flashcards

1
Q

what are embryological abnormalities of the thyroid?

A

Failure of descent – lingual thyroid
Excessive descent – retrosternal location in mediastinum
Thyroglossal duct cyst

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2
Q

where does the thyroid arise from?

A

Develops from evagination of pharyngeal epithelium
Descent from foramen caecum to normal location in anterior neck below larynx along thyroglossal duct

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3
Q

what is the thyroid made of?

A

Composed of lobules defined by thin fibrous septa each containing follicles. Each follicle surrounded by flat to cuboidal follicular epithelial cells. Within the centre of each follicle is dense amorphous pink material containing thyroglobulin. also has scattered larger C cells.

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4
Q

what does TSH bind to?

A

TSH receptor on the surface of the thyroid epithelial cells

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5
Q

what activates G proteins?

A

conversion of GTP to GDP and production of cAMP

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6
Q

what does cAMP do?

A

increases production of T3 and T4 which circulate in bound (to their target cells) and free forms

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7
Q

what stimulates the release of TSH from the anterior pituitary gland?

A

TRH from the hypothalamus

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8
Q

what are autoimmune causes of thyroiditis?

A

hashimoto’s thyroiditis and grave’s disease

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9
Q

how does hashimoto’s thyroiditis occur?

A

gradual failure of thyroid function due to autoimmune destruction of thyroid tissue
more common in females age 45-60

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10
Q

what is the pathology of hashimoto’s?

A

Anti-thyroid antibodies
Anti-thyroglobulin and anti-peroxidase
When bound cause antibody dependent cell mediated cytotoxicity
CD8 +ve cells may mediate destruction of thyroid epithelium
Cytokine mediated cell death
- g interferon from T cell activation recruits macrophages that may damage thyroid follicles

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11
Q

what is the presentation of hashimoto’s?

A

Thyroid may be diffusely enlarged
Prominent lymphoid infiltrate
Lymphocytes, plasma cells and reactive follicles with germinal centres
Thyroid follicles atrophy
Follicular cells have abundant eosinophilic cytoplasm (Hurthle cells)
May see progressive fibrosis within the gland

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12
Q

how does hypothyroidism occur?

A

low levels of T3 and T4
majority of cases are due to hashimoto’s
can also be caused by iodine deficiency, drugs, congenital abnormalities
rarely result of secondary (pituitary) or tertiary (hypothalamic) pathology

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13
Q

what are people with hashimoto’s thyroiditis at increased risk of?

A

other autoimmune diseases
developing B cell non-hodgkin’s lymphoma (NHL) in the thyroid gland

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14
Q

how does hyperthyroidism occur?

A

excess T3 and T4
85% due to grave’s disease
can also be caused by hyperfunctioning nodules & tumours, thyroiditis, ectopic production and exogenous intake

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15
Q

what are the symptoms of grave’s disease?

A

Triad of features
Hyperthyroidism with diffuse enlargement of the thyroid
Eye changes (exophthalmos)
Pretibial myxoedema.
The eye changes result from fibroblasts etc expressing TSH receptors

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16
Q

what is goitre?

A

any enlargement of the thyroid gland

17
Q

describe diffuse goitre

A

Endemic - >10% population affected
Iodine deficiency &/or goitrogenic substances
Sporadic – F > M, puberty and young adults
Ingestion of substances limiting T3/T4 production
Inborn errors of metabolism (dyshormonogenesis)
Most cases – cause unknown
Usually euthyroid – present with mass effects
T3 / T4 normal but TSH high or upper limit of normal
In children dyshormonogenesis may cause cretinism

18
Q

how does multi-nodular goitre arise and what are the risks?

A

evolves from long standing simple goitre
variation of response of follicular cells to external stimuli
risk of rupture, haemmorhage, scarring, calcification
mass effects- cosmetic, airway obstruction, dysphagia, compresses vessels
may develop autonomous nodule

19
Q

what is the main type of benign thyroid tumour?

A

follicular adenoma

20
Q

what are the most common malignant thyroid tumours?

A

carcinomas- most common papillary, then follicular, anaplastic, medullary

21
Q

describe thyroid adenomas

A

Discrete solitary mass
Incidental finding
If large local symptoms eg dysphagia
Encapsulated by a surrounding collagen cuff
Composed of neoplastic thyroid follicles i.e. Follicular Adenoma

22
Q

what do adenomas get mixed up with?

A

dominant nodule in multinodular goitre
follicular carcinoma

23
Q

what are the most common causes of thyroid malignancy?

A

ionising radiation, iodine deficiency

24
Q

describe papillary carcinoma

A

usually solitary nodule in thyroid, can be multifocal and often cystic. can also be calcified- called psammoma bodies
can have lymph node metatstasis

so if thyroid tissue or psammoma bodies are found in lymph nodes always look for thyroid papillary carcinoma

25
Q

what are the symptoms of papillary carcinoma?

A

Lesion in thyroid gland or cervical lymph node mass (metastasis)
Local effects
Hoarseness
Dysphagia
Cough
Dyspnoea
All suggest locally advanced disease

26
Q

describe follicular carcinoma

A

Usually single nodule
Slowly enlarging, painless, non-functional

Rarely lymphatic spread but propensity for haematogenous spread

Bone, lungs, liver

27
Q

what is the prognosis of follicular carcinoma?

A

Prognosis depends on
Extent of invasion and stage at presentation
High stage at presentation
50% mortality at 10yrs
Minimally invasive lesions - >90% survival at 10yrs

28
Q

describe medullary thyroid carcinoma (MTC)

A

Relatively rare tumour
Derived from C-Cells (neuroendocrine)
Can secrete calcitonin
Can be:
Sporadic (70%)
Associated with Multiple Endocrine Neoplasia (MEN IIA or IIB)
Familial medullary carcinoma
MEN cases can arise in very young patients
Sporadic and familial cases are seen in adults (40s – 50s)

29
Q

what is the difference between sporadic and familial medullary carcinoma?

A

Sporadic cases – solitary nodule
Familial cases – bilateral / multicentric - C cell hyperplasia
Composed of spindle or polygonal cells arranged in nests, trabeculae or follicles
Associated Amyloid deposition (amyloid represents deposition of an abnormally folded protein – in this case calcitonin)

30
Q

what is the presentation of medullary carcinoma?

A

Neck mass with local effects (dysphagia, hoarseness, airway compromise)
Paraneoplastic syndrome
Diarrhoea (VIP production)
Cushings (ACTH production)

31
Q

what is the treatment of medullary carcinoma?

A

total thyroidectomy

32
Q

describe anaplastic carcinoma

A

Undifferentiated and aggressive tumours

Usually older patients

May occur in people with a history of differentiated thyroid cancer

Rapid growth and involvement of neck structures and death

endocrine (25 decks)

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