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Pathology > Pathology of the endocrine system > Flashcards

Pathology of the endocrine system Flashcards

1
Q

Hypopituitarism: etiology

A
  • Nonfunctioning pituitary adenomas
  • Ischemic injury (i.e. Sheehan syndrome)
  • Surgery
  • Radiation
  • Inflammation
  • Hypothalamic disorders
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2
Q

Sheehan syndrome

A

Postpartum necrosis of the anterior pituitary, and the most common cause of ischemic necrosis of it. The anterior pituitary enlarges during pregnancy, without an increase in blood supply. This enlarged gland is thus susceptive to ischemic injury.

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3
Q

Hypopituitarism: clinical course

A

Depending on the lacking hormone:

  • GH -> growth failure
  • GnRH -> amenorrhea and infertility (women); decreased libido and impotence (men)
  • TSH -> hypothyroidism
  • ACTH -> hypoadrenalism
  • Prolactin -> failure of lactation
  • MSH -> pallor
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4
Q

Hyperfunctioning pituitary adenomas

A
  • Prolactinoma
  • GH-producing adenomas
  • Corticotroph cell adenoma
  • TSH-producing adenoams
  • FSH/LH-producing adenomas
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5
Q

Prolactinoma

A
  • Can be anything from small microadenomas to large masses

- Hyperprolactinemia cause amenorrhea, galactorrhea, loss of libido and infertility

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6
Q

GH-producing adenomas

A
  • Proliferation of somatotroph cells
  • Gigantism: in children; increased body size with disproportionally long limbs
  • Acromegaly: mostly seen in soft tissues, skin and viscera; jaw enlargement; hands and feet enlarge
  • Other disturbances: abnormal glucose tolerance (GH stimulates hepatic secretion of insulin-like GF I)
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7
Q

Corticotroph cell adenomas

A
  • Usually microadenomas
  • Can cause hypercortisolism (Cushing syndrome), as ACTH stimulates the adrenal cortex
  • Hyperpigmentation may occur (MSH)
  • Surgical removal (i.e. after Cushings) can cause Nelson syndrome, characteristic of a loss of inhibitory effect of the adrenal corticosteroids
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8
Q

Pituitary adenomas: pathogenesis

A
  • Usually due to G-protein mutations (Gs encoded by the GNAS1 gene), causing an unchecked cell proliferation
  • 5% are associated with MEN-1 syndrome (familial)
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9
Q

Pituitary adenomas: morphology

A
  • Well circumscribed, soft lesions
  • Can compress the optic chiasm, causing bitemporal hemianopsia, hemorrhages and/or necrosis
  • Histo: uniform, polygonal cells arranged in sheets, cords or papillae; pleiomorphic nuclei
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10
Q

Posterior pituitary syndromes

A

Usually affect ADH production. Excess ADH causes excessive amounts of water.

  • Clinically presented as hyponatremia, cerebral edema and neurological symptoms
  • Etiology: ectopic ADH-production (i.e. small cell lung cc)

Diabetes insidipus is caused by ADH deficiency

  • Etiology: brain trauma, neoplasm, idiopathic
  • Clinical: large volume of diluted urine, hypernatremia, increased osmolarity, thirst and polydipsia
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11
Q

Clinical manifestations of thyrotoxicosis

A
  • Soft and warm skin
  • Heat intolerance and excess sweating
  • Weight loss due to hypermetabolism
  • Gut: hypermotility, diarrhea and malabsorption
  • Ocular manifestations: wide, staring gaze
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12
Q

The three main manifestations of Grave’s disease

A
  1. Thyrotoxicosis
  2. Opthalmopathy - exopthalmus
  3. Dermopathy - pertibial myxedema
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13
Q

Grave’s disease: epidemiology and pathogenesis

A
  • HLA-DR3 association
  • Polymorphism in CTLA-4 and PTPN22 (tyrosine phosphatase)

An autoimmun disorder with a variety of antibodies found in the serum:

  • Thyroid-stimulating immunoglobulin: IgG antibody binds the TSH receptor and increases TH synthesis; most specific for the disease
  • Thyroid growth-stimulating immunoglobulin: proliferation of thyroid follicular epithelium
  • TSH-binding inhibitor immunoglobulin: prevents TSH from binding its receptor
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14
Q

Grave’s disease: morphology

A
  • Diffuse enlargement; smooth and symmetric
  • Follicular epithelium is tall, columnar and more crowded; may form papillae
  • Lymphocytic infiltration (mainly T cells)
  • Lymphoid hyperplasia
  • Opthalmopathy: increased volume of retro-orbital CT and ocular muscles; fatty infiltration
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15
Q

Hypothyroidism: etiology

A

Primary:

  • Hashimito thyroiditis
  • Iodine deficiency
  • Drugs
  • Thyroid dysgenesis

Secondary:
- Pituitary or hypothalamic failure

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16
Q

Hypothyroidisim: clinical manifestations

A

Cretinism:

  • Untreated congenital deficiency of thyroid hormones
  • Maternal deficiency of iodine
  • Causes impaired development of the skeletal system and CNS

Myxedema:

  • Appears as apathy and mental sluggishness
  • Mucopolysaccharide-rich edema accumulates in the skin, subcutaneous tissue and other visceral sites -> decreased bowel motility (-> constipation) and pericardial effusion (-> heart failure)
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17
Q

Hashimoto thyroiditis: main features

A

An autoimmune disease causing painless enlargement and hypothyroidism.

There’s an immunologic destruction of the gland by three mechanisms:

  • CD8+ T cell-mediated direct thyrocyte death
  • CD4+ Th1 cells IFNγ -> activation of macrophages -> cell killing
  • Binding of antithyroid antibodies -> antibody-dependent cell-mediated cytotoxicity (NK cells)

Usually preceded by thyrotoxicosis, so there’ll be a transient hyperthyroidism before hypothyroidism develops.

18
Q

De Quervain thyroiditis: main features

A
  • Usually caused by viral infections or a postviral inflammatory process
  • Disruption of follicles and colloid extravasation causes polymorphonuclear infiltration which eventually triggers formation of a granulomatous reaction
  • A transient hyperthyroidism may occur, followed by
    transient hypothyroidism if the disease progresses
  • Clinical: pain in the neck, fever and malaise
  • Usually self-limiting
19
Q

Subacute lymphocytic thyroiditis: main features

A
  • Often following pregnancy (postpartum thyroiditis)
  • Possibly autoimmune, as circulating antithyroid antibodies are found in most patients
  • Initially presents as thyrotoxicosis
20
Q

Riedel thyroiditis: main features

A

(Rare)

  • Extensive fibrosis involving the thyroid and other neck structures (possibly also fibrosis of the retroperitoneum)
  • The thyroid appears as a hard and fixed mass (wood-hard)
  • Antithyroid antibodies are present in most cases
21
Q

Goiter: morphology, etiology and consequences

A
  • Can be either diffuse or multinodular
  • Usually presents in areas where the diet lacks iodine
  • Iodine deficiency triggers hyperplasia and hypertrophy of the gland, hence gross enlargement of the gland
  • May cause airway obstruction, dysphagia and compression of large neck vessels
22
Q

Benign neoplasm(s) of the thyroid gland and their main features

A

Follicular adenoma is the only one:

  • Usually non-functional, but some may secrete thyroid hormones (toxic adenomas) and cause thyrotoxicosis
  • They are solitary and encapsulated
  • Present as painless nodules that take up iodine less avidly, thus appear as “cold” nodules (non-toxic adenomas)
  • Toxic adenomas however, appear as “hot” nodules
  • Toxic adenomas involve GOF somatic mutations in the TSH receptor, causing increased cAMP and clonal expansion of thyroid epithelial cells
  • 20% of follicular adenomas are related to point mutations on the RAS oncogene family
23
Q

Subtypes of thyroid carcinomas (4)

A
  1. Papillary cc (85%)
  2. Follicular cc
  3. Medullary (the only one derived from parafollicular (C) cells, the others arise from follicular epithelium)
  4. Anaplastic
24
Q

Papillary cc of the thyroid gland: pathogenesis

A

Related to exposure to ionixing radiation.

Two major genetic alterations are seen, both leading to activation of the MAP kinase signalling pathway:

  1. Chromosomal rearrangements of RET and NTRK1 genes forming a fusion gene
  2. Activating (GOF) point mutations in BRAF
25
Q

Papillary cc of the thyroid gland: morphology

A
  • Solitary or multifocal
  • Encapsulated or infiltrative
  • Often cystic, fibrotic and calcified
  • Diagnosis is made by nuclear features: optically clear nuclei (“Orphan Annie eye”) and invaginations of the cytoplasm looking like intranuclear inclusions
  • Psammoma bodies are often seen inside the papillae
26
Q

Papillary cc of the thyroid gland: clinical features

A
  • Nonfunctional
  • Painless neck mass
  • Good prognosis
  • 50% metastasize to cervical lymph nodes
27
Q

Follicular cc of the thyroid gland: etiology and pathogenesis

A
  • Presents at an older age and is more common in women
  • Increased incidence in areas of dietary iodine deficiency (thus there’s also a predisposition to nodular Goiter)
  • 50% have mutations in the PI-3/AKT oncogenic signalling pathway
28
Q

Follicular cc of the thyroid gland: clinical features

A
  • Present as solitary “cold” thyroid nodules

- Hematogenous metastasis to lungs, bone and the liver

29
Q

Medullary cc of the thyroid: main features

A
  • Neuroendocrine neoplasm derived from parafollicular (C) cells (C cells secrete calcitonin)
  • Usually arise sporadically, but 30% are related to MEN-2 syndrome
  • Morphology: solitary nodule or lesions of both lobes; larger lesions show hemorrhage and necrosis
  • Histo.: amyloid deposits (from changed calcitonin molecules) and calcitonin demonstrated in the cytoplasm
30
Q

Anaplastic cc of the thyroid: main features

A
  • VERY aggressive, appearing in older people
  • Arise de novo or by dedifferentiation of a well-differentiated papillary or follicular epithelium
  • Grows into adjacent neck structures
  • These highly anaplastic cells appear as large, pleomorphic giant cells, spindle cells or mixed spindle and giant cell lesions
31
Q

Parathyroid tumors: pathogenesis

A
  • Cyclin D1 gene inversions

- MEN1-gene mutations

32
Q

Parathyroid adenomas: morphology

A
  • Soft, tan nodule with a capsule
  • Confined to a single gland
  • Histo.: mostly composed of chief cells
  • The edge of the adenoma consists of compressed, non-neoplastic parathyroid tissue
33
Q

Parathyroid hyperplasia: morphology

A
  • Usually multi-glandular
  • Chief cell hyperplasia
  • Clear cytoplasm due to glycogen accumulation
34
Q

Parathyroid cc: morphology

A
  • Can look like adenomas or be invasive
  • Nodular pattern
  • Enclosed by a dense fibrous capsule
35
Q

Organ changes in primary hyperparathyroidism

A
  • Skeleton: increased osteoclastic and osteoblastic activity
  • Osteitis fibrosa cystica: thin cortex with a marrow containing fibrous tissue with hemorrhage and cysts
  • Kidney: PTH-induced hypercalcemia -> kidney stones and calcification
36
Q

Primary hyperparathyroidism: clinical features

A
  • Increased serum calcium
  • Increased serum PTH (decreased in case of non-parathyroid disease)
  • Main symptoms: painful bones, renal stones, abdominal groans and psychic moans
  • GI disturbances: constipation, ulcers, pancreatitis, gallstones
  • CNS alterations: depression, lethargy
  • Neuromuscular abnormalities
  • Polyuria and secondary polydipsia
37
Q

Secondary hyperparathyroidism

A

Usually caused by renal failure. (Chronic) renal insufficiency decreases phosphate excretion, which consequently depresses serum calcium levels and stimulates PT activity.

Also, loss of renal substances downgrades vitamin D synthesis and reduces the intestinal absorption of calcium.

38
Q

Secondary hyperparathyroidism: clinical features

A
  • Bone abnormalities: renal osteodystrophy
  • Normal serum calcium
  • Metastatic calcification of blood vessels -> ischemic damage of other organs
  • Can progress to tertiary hyperparathyroidism
39
Q

Hypoparathyroidism: etiology

A
  • Surgical: thyroidectomy where the PT glands are removed as well
  • Congenital absence (Di George syndrome)
  • Autoimmune
40
Q

Hypoparathyroidism: clinical features

A
  • Neuromuscular irritability: tingling, muscle spasms etc.
  • Cardiac arrhytmias
  • Increased intracranial pressure
41
Q

Hypercortisolism: etiology

A
  • Exogenous GC administration

Endogenous causes:

  • Primary hypothalamic-pituitary disease with hypersecretion of ACTH: adenoma or hyperplasia
  • Primary adrenal neoplasm and primary cortical hyperplasia (ACTH-independent Cushing)
  • Ectopic ACTH-secretion by non-endocrine neoplasm

Pathology (14 decks)

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