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M2 Pathology > Thyroid Pathology > Flashcards

Thyroid Pathology Flashcards

1
Q

symptoms of hyperthyroidism

A
  1. loss of weight
  2. thin
  3. increased appetite
  4. diarrhoea
  5. oligomenorrhea
  6. heat intolerance
  7. irritable state
  8. starring gaze, lid lag (exophthalmos)
  9. pretibial myxoedema
  10. warm and sweaty
  11. tachycardia, AF
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2
Q

symptoms of hypothyroidism

A
  1. gain of weight
  2. mildy obese
  3. (possibly) poor appetite
  4. constipation
  5. oligomerrhea/menorrhagia
  6. cold intolerance
  7. mental slowness
  8. peaches and cream skin
  9. proximal myopathy
  10. dry and cool
  11. bradycardia, pericardial effusion
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3
Q

state the pathologies linked to DIFFUSE GOITRE. (4)

A
  1. grave’s disease
  2. hashimoto’s thyroidits
  3. granulomatous (DeQuervain) thyroiditis
  4. simple goitre
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4
Q

state the simple pathologies linked to LOCALISED SWELLING (goitre). (3)

A
  1. nodular goitre
  2. neoplasms
  3. thyroidits (hashi/deq)
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5
Q

state the common pathologies linked to hyperthyroidism. (4)

A
  1. grave’s disease
  2. hyperplasia
  3. nodular goitre
  4. neoplasms
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6
Q

state the common pathologies linked to euthyroidism. (2)

A
  1. nodular goitre
  2. neoplasms
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7
Q

state the common pathologies linked to hypothyroidism. (2)

A
  1. hashimoto’s thyroiditis
  2. congenital anomalies
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8
Q

state the 2 commonest congenital pathologies.

A
  1. thyroglossal duct cyst
  2. abnormal development of thyroid gland
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9
Q

features of thyroglossal duct cyst

A
  • embryonal vestige (retention of underdeveloped parts)
  • midline neck cyst
  • complicated by infection & malignant change
  • treat by complete excision
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10
Q

features of abnormal development of thyroid gland

A
  • associated with aplasia & hyperplasia
  • severe intellectual disability
  • short stature
  • coarse facial features
  • protruding tongue
  • umbilical hernia
  • CRETINISM
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11
Q

where can ectopic thyroid tissue develop?

A
  1. upper GI tract
  2. upper respi tract
  3. soft tissues of neck
  4. CVS
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12
Q

state the pathogenesis of diffuse and MNG

A

can be endemic or sporadic
- endemic -> iodine deficiency -> decreased thyroid hormone production
- sporadic -> dyshormogenetic goitre

THERE WILL BE COMPENSATORY INCREASE IN TSH
1. if HYPERTROPHY AND HYPERPLASIA OF FOLLICULAR CELLS -> ENLARGEMENT OF THYROID GLAND -> simple goitre
2. if RECURRENT (1) -> mng

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13
Q

expand on the morphology of simple (diffuse) goitre

A

hyperplastic stage -> colloid involution stage

  1. hyperplastic stage
    - diffuse mild enlargement
    - crowded columnar cells, pseudopapillae
  2. colloid involution stage
    - flattened cuboidal epithelium
    - abundant colloid
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14
Q

expand on the morphology of multinodular goitre

A
  • extreme, irregular enlargement
  • COMMONEST CAUSE OF GOITRE
  • mimics neoplastic disease
  • can lead to mass effects (hoarseness of voice, vocal cord palsy, dysphagia)
  • toxic goitre -> hyperthyroidism
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15
Q

state the common autoimmune conditions. (4)

A
  1. hashimoto thyroiditis
  2. grave’s disease
  3. granulomatous thyroiditis
  4. IgG4 related thyroiditis
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16
Q

HASHIMOTO THYROIDITIS

State pathogenesis of disease and its features.

A

Pathogenesis:
destruction of self-tolerance to thyroid Ag through…
1. cytotoxic CD8+ T cell mediated apoptosis
2. cytokine-mediated cell-mediated apoptosis
3. sensitisation of CD4+ Th cells to thyroid antigens
4. antibody-dependent cell-mediated cytotoxicity

Features:
- old women disease
- familial marker: HLA-DR3, DR5

17
Q

HASHIMOTO THYROIDITIS

State the clinical features, macro and micro features and complications.

A

Clinical features:
1. painless diffuse/localised goitre
2. hypothyroidism
3. preceding transient thyrotoxicosis
4. anti-TPO, anti-TSH, anti-Tg Ab

Macro:
- pale enlarged diffuse gland
- pale yellow firm cut surface

Micro:
- infiltrates: lymphocytes, plasma cells, lymphoid follicles
- fibrosis
- thyroid follicles: hurthle (oncocytic) cell change

Complications:
- high risk of MALT lymphoma
- high risk of other autoimmune disease (type 1 DM, SLE)

18
Q

GRAVES’ DISEASE

State the pathogenesis of disease and its features.

A

Pathogenesis:
(Breakdown in Th cell tolerance)
TRAb (TSH receptor autoantibodies) bind to TSH receptor to mimic TSH action and increase release of TH + thyrotropin/TSH-binding inhibitor immunoglobulins (TBII) stimulate thyroid to increase release of TH

Features:
- young and middle aged women
- familial HLA-B8, DR3
- anti-TPO, anti-Tg

19
Q

GRAVES’ DISEASE

State the clinical features, macro and micro features of the disease.

A

Clinical features:
- pretibial myxoedema
- infiltrative ophthalmopathy (exolphthalmos)
- hyperthyroidism
- diffuse goitre
- bruit
- wide starring gaze with lid lag
- thyrotoxicosis

Macro:
- symmetric diffuse enlargement
- soft reddish meaty cut surface

Micro:
- lymphoid infiltrate (less than hashi)
- follicular cells tall columnar and crowded
- pale and scalloped colloid

20
Q

GRANULOMATOUS (DeQuervain) THYROIDITIS

State the pathogenesis of the disease and its features.

A

Pathogenesis:
Virus induced cytotoxic T lymphocyte response to thyroid antigen -> damage follicular cells

Features:
- short history
- self limiting
- middle-aged women

21
Q

GRANULOMATOUS (DeQuervain) THYROIDITIS

State the clinical features, macro, and micro features of the disease.

A

Clinical features:
- pain in the neck, goitre
- mild hyperthyroidism -> hypothyroidism -> euthyroid
- recent URTI

Macro:
- Enlarged firm gland
- Patchy film pale yellowish areas with intervening normal parenchyma

Micro:
- Lymphocytes, Histiocytes
- Multinucleated giant cells (loss of nuclei, engulf colloid)
- Destruction of follicles, neutrolphils, microabscesses

22
Q

Ig-G4-RELATED THYROIDITIS

State the clinical features, treatment and morphology of the disease.

A

Clinical features:
- progressive fibrosis
- enlargement and adherence to neck structures
- serum lgG4 raised

Treatment:
- corticosteroid therapy

Morphology:
- lymphoplasmacytic infiltration

23
Q

State the follicular origin benign neoplasms. (2)

A
  1. Follicular adenoma
  2. Oncocytic adenoma
24
Q

State the follicular origin malignant neoplasms. (5)

Hint: PF, PD, A

A

Poor grade:
1. Papillary thyroid carcinoma
2. Follicular carcinoma

High grade:
1. Poorly differentiated thyroid carcinoma
2. Differentiated high grade thyroid carcinoma

Undifferentiated:
1. Anaplastic thyroid carcinoma

25
Q

State the non-follicular cell origin neoplasms. (2)

A
  1. Medullary carcinoma
  2. Lymphoma
26
Q

BENIGN NEOPLASMS!

State the clinical features, macro and micro features of these conditions.

A

Clinical features:
- solitary painless nodule

Macro:
- rounded encapsulated nodule
- intact capsule

Micro:
- no capsular invasion
- no vascular invasion
(follicular adenoma): uniformed microfollicles distinct from surrounding parenchyma

(oncocytic adenoma): cells show oncocytic change + features of FA

27
Q

state the genetic aberrations of the malignant neoplasms.

A
  1. follicular carcinoma (low grade)
    - RAS mutation, PPAR-y/PAX8
  2. papillary thyroid carcinoma (low grade)
    - RET/PTC rearrangements, BRAF mutation
  3. medullary carcinoma (non-follicular)
    - RET mutation (MEN2 syndrome)
  4. poorly differentiated (high grade) and anaplastic thyroid carcinoma (undifferentiated)
    - TP53 mutation, TERT receptor mutation
28
Q

FOLLICULAR CARCINOMA

State the morphology and clinical features of this malignancy.

A

Morphology:
- vascular invasion and/or capsular invasion
- widely invasive rarely - gross extension into extrathyroidal tissues (not well circumscribed, no full capsule around tumour)

Clinical features:
- slow growing painless cold nodule
- metastasises through bloodstream (lungs and bone)

29
Q

PAPILLARY THYROID CARCINOMA

State the clinical features, prognosis, types of variants, macro and micro features of the malignancy.

A

Clinical features:
- painless nodule
- lymphatic spread -> enlarged cervical lymph nodes
- young adults and children
- hoarseness of voice, cough, dysphagia

Prognosis:
- >95% 10 year survival

Types of variants:
- classical PTC
- follicular variant (infiltrative & invasive encapsulated)
- encapsulated classic PTC
- tall cell variant

Macro:
- solitary and multifocal
- encapsulated
- whitish nodules
- cystic changes, calcification, fibrosis

Micro:
- nuclear features even in the presence of papillae
- finely dispersed chromatin
- nuclear grooves
- pseudoinclusions

30
Q

Name 5 features of classic PTC.

A
  • branching well formed papillae with fibrovascular cores
  • uniform, cuboidal cells with diagnostic nuclear features
  • psammoma bodies
  • lymphatic invasion
31
Q

What are the two subtypes of follicular variant PTC.

A

Infiltrative follicular variant PTC

Invasive encapsulated follicular variant PTC

32
Q

What are the features of each subtype of follicular variant PTC?

A

INFILTRATIVE FOLLICULAR VARIANT PTC
- non-encapsulated infiltrative growth pattern
- BRAF V600E mutation, RET translocation

INVASIVE ENCAPSULATED FOLLICULAR VARIANT PTC
- encapsulated, circumscribed with capsular or vascular invasion
- RAS mutation, PPAR-y/PAX8 rearrangements
- differential = follicular carcinoma

M2 Pathology (20 decks)

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