Pathology Flashcards

1
Q

Hyper pituitary

A

Adenoma in ant lobe
Hyperplasia
Carcinoma
Ectopic
Hypothalamus

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2
Q

Classification of pituitary adenoma

A

On the basis of hormones produced by neoplastic cells

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3
Q

Somatostatin

A

Inhibits GH and TSH
Analogs are used to treat acromegaly

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4
Q

Pathogenesis of pituitary adenoma

A

1- mutation in GNAS abrogates the activity of Gsa of GTPase leading to constitutive activation of Gsa , cAMP is produced continuously and unchecked cellular proliferation
2- MEN1, CDKN1B, PRKAR1A & AIP gene
3- cell cycle : CD1 overexpression, mutations TP 53, epigenetic silencing of RB gene, RAS oncogene.

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5
Q

Somatotroph adenomas

A

GH +++IGF1~ overgrowth of bones n muscle
In child before epiphysis close: increase in body size, disproportionately long arms and legs.

After closure of epiphysis: growth of soft tissue, skin, viscera, bones of face.
Prognathism: lower jaw grows
Teeth separate
Sausage like fingers, ACROMEGALY
Diabetes mellitus: GH induced peripheral insulin resistance.

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6
Q

Test for acromegaly

A

GH is not suppressed in response to oral load of glucose.

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7
Q

Morphology of pituitary adenoma

A

May compress ,erode and extend in optic chiasm nd adjacent structure
Uniform polygonal cells arranged in sheets,cords and papillae
* cellular monomorphism and absence of reticulin in neoplastic adenomas

Atypical adenoma: TP53 mutations, high mitotic activity, aggressive,

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8
Q

Genes in Marfan syndrome

A

Fibrillin 1
TGFBR in MFS Type II
ACTA2
MYTH11

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9
Q

How to see if thyroid nodule is neoplastic?

A

Solitary nodules
In ver young or very old
Males
Radiation exposure history
Cold nodules that do not take up radioactive iodine

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10
Q

Thyroid adenomas (painless) (cold)

A

Derived from follicular epithelium

Less common toxic adenomas that cause thyrotoxicosis
Pathogenesis =
Gain of function mutations in TSHR and GNAS
Thyroid autonomy
Over abundance of thyroid hormone = hyperthyroidism (HOT NODULE)

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11
Q

Morphology of thyroid adenomas

A

Solitary
INTACT CAPSULE, well defined
Oxyphil change: bright eosinophilic granular cytoplasm
Nuclear pleomorphism,atypia and prominent nuclei

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12
Q

Thyroid carcinoma pathogenesis

A

Female predominance
ionizing radiation in first 2 decades of life.

PAPILLARY: +MAP kinase pathway > rearranged tyrosine kinase RET and NTRK1 , point mutation in BRAF

FOLLICULAR: driver mutations in RAS or PI3K/AKT (GOF) , LOF mutations in PTEN, PAX8 , PPARG

ANAPLASTIC: RAS, TP53
These are derived from follicular epithelium.
MEDULLARY: arise from parafollicular C cells. In MEN 2
RET mutations in tyrosine kinase receptor

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13
Q

Papillary carcinoma thyroid

A

Presents as painless mass in thyroid or neck when metastases to lymph nodes.

Poor prognosis in elderly.

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14
Q

Encapsulated,Papillae with multiple layers of cuboidal epithelial cells, orphan annie eye nuclei due to dispersed chromatin, pseudo inclusions, psamomoma bodies present. What is it?

A

Papillary carcinoma of thyroid

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15
Q

Presents as solitary cold nodule , no nodal metastases but to lungs,bone,liver, in a female above 40-60, resembling the follicles of normal thyroid, infiltrates thyroid parenchyma,hurthle cells are seen. No capsule, What is it?

A

Exclude capsule✅
Vascular invasion ✅
This is follicular carcinoma (not adenoma)
Widely invasive

A follicular variant of papillary carcinoma may progress to follicular carcinoma.

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16
Q

Presents as bulky mass in neck age 65 with history + .
Highly anaplastic undifferentiated pleomorphic / spindle shaped cells
What is it.

A

Anaplastic carcinoma
Poor prognosis due to extensive growth and compromising neck structures.

17
Q

Neuroendocrine tumor that secretes calcitonin and other pp hormones. Patient has MEN 2. Patient is young child. He has dysphagiA / hoarseness,
Symptoms like diarrhoea due to VIP.
Elevated calcitoninlevels.

A

Medullary carcinoma

Morphology = both lobes, amyloid deposits, multicentricity , polygonal or spindle cells,calcitonin in cytoplasms,
Familial: multicentric C cell hyperplasia
Arise from focal hyperplasia

18
Q

3 causes of thyrotoxicosis

A

Graves’ disease: hyperplasia, autoimmune
Hyper functioning: multi nodular goiter
And adenoma of thyroid.

19
Q

Radioactive iodine determines etiology

A

Graves’ disease and toxic adenoma: increased uptake
Thyroditis: decreased uptake

20
Q

Causes of hypothyroidism

A

Thyroid dysgenesis
Deficiency of iodine (enlarged thyroid)
Hashimoto thyroiditis (enlarged thyroid)
Iatrogenic

21
Q

Baby presents after 18 day with impaired development of skeleton nd CNS , mental retardation, short stature, coarse facial features, protruding tongue, umbilical hernia. Diagnosis.

A

Cretinism

22
Q

Pathogenesis of myxedema

A

Decreased cardiac output: thyroid regulates Ca ATPase leades to SOB and less exercise capacity
Decreased blood flow: cool and pale skin
Decreased sympathetic activity: constipation and decreased sweating
Increase cholesterol and LDL
Accumulation of GAGs, hyaluronic acid in skin, SC nd viscera resulting in non pitting edema , broade and coarse facial features, large tongue and deep voice

23
Q

Symmetrical , diffuse painless enlargement in neck
Decreased TSH, Radioactive iodine uptake is low, initially raised T3 and T4.
Then levels fall with increase in TSH.

A

mononuclear inflammatory infiltrate, germinal centres

Hashitoxicosid: initially a hyper state due to disruption of thyroid follicles with release of thyroid hormones

#hurthle cells: abundant eosinophilic granular cytoplasm (metaplasia), many mitochondrion
#may be atrophic dur to fibrosis

24
Q

Neck pain wd swallowing
Fever,malaise, enlargement
ESR raised also leukocyte cpunt
History of respiratory infection

A

Subacute granulomatous thyroiditis , de quervain

25
Q

Pathogenesis of graves disease

A

Thyroid stimulating immunoglobulin mimics TSH : stimulates adenylyl cyclase.
Same by thyroid growth stimulating immunoglobulins.
TSH binding inhibitor immunoglobulins.

Infiltrative opthalmopathy: T cell mediated
Volume of retro orbit CT and extraocular muscles increase (fats, mononuclear cells, edema,matrix)

26
Q

Morphology of Graves’ disease

A

Diffuse hypertrophy and hyperplasia
Capsule intact
Small papillae but LACK FIBROVASCULAR CORE
Lymphoid hyperplasia

27
Q

Large neck mass, dysphagia, breathing problem, SVCsyndrome,
No dermopathy or eye changes

A

Graves disease

Thyrotoxicosis may develop due to autonomous nodules (TOXIC MULTINODULAR GOITRE)