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Endo Repro Exam > Endocrine Pathology 1 > Flashcards

Endocrine Pathology 1 Flashcards

1
Q

pituitary adenomas - overview

A

*benign epithelial neoplasm arising from anterior pituitary gland
*most common cause of HYPERpituitarism

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2
Q

pituitary adenomas - classifications

A

*pituitary adenomas are classified based on:
1. size: micro-adenomas (small, < 1 cm) vs. macro-adenomas (large, > 1 cm)
2. hormone production:
-functional = cause clinical syndromes related to overproduction of hormone(s)
-nonfunctional = cause mass effect due to growing to larger size before detection

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3
Q

pituitary adenomas - clinical features

A

*systemic: dependent on excess or deficiency of pituitary hormones
*local: dependent on mass effects:
-visual field abnormalities (bitemporal hemianopsia) due to compression of optic chiasm
-headache, N/V are signs of elevated intracranial pressure

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4
Q

pituitary adenomas - pathogenesis

A
  1. sporadic/acquired somatic mutations:
    -growth hormone releasing hormone receptor (GHRHR)
    -ubiquitin-specific protease 8 (USP8)
  2. familial/inherited: MEN1 germline mutations
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5
Q

pituitary adenomas - pathologic features

A

*solitary, well-circumscribed lesions
*monotonous cells with decreased or no supporting reticulin stroma
*immunohistochemical stains identify the hormones

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6
Q

subtypes of pituitary adenomas: lactotroph adenoma

A

*hormone = prolactin
*associated syndrome = galactorrhea & amenorrhea (in females); sexual dysfunction, infertility

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7
Q

subtypes of pituitary adenomas: somatotroph adenoma

A

*hormone = growth hormone (GH)
*associated syndrome = gigantism (children), acromegaly (adults)

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8
Q

subtypes of pituitary adenomas: mammosomatotroph adenoma

A

*hormone = prolactin, GH
*associated syndrome = combined features of growth hormone and prolactin excess

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9
Q

subtypes of pituitary adenomas: corticotroph adenoma

A

*hormone = ACTH and other POMC-derived peptides
*associated syndrome = Cushing syndrome, mass effect

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10
Q

subtypes of pituitary adenomas: thyrotroph adenoma

A

*hormone = TSH
*associated syndrome = hyperthyroidism

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11
Q

subtypes of pituitary adenomas: gonadotroph adenoma

A

*hormone = FSH, LH
*associated syndrome = hypogonadism (most are silent with mass effect)

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12
Q

craniopharyngioma - overview

A

*epithelial neoplasm arising from Rathke pouch remnants
*proliferation of squamous cells

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13
Q

craniopharyngioma - clinical features

A

*bimodal distribution: children 5-15 years; elderly > 65
*headaches and visual disturbances
*suprasellar (may induce hypo- or hyper-function of pituitary, diabetes insipidus; children may have growth retardation)

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14
Q

craniopharyngioma - pathologic features

A

*keratinizing squamous cells, calcifications, cholesterol crystals, fibrosis
*associated mutations:
1. BRAF mutations → papillary architecture
2. beta-catenin mutations → compact, lamellar (“wet”) squamous epithelium with peripheral palisading

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15
Q

thyroid gland - overview

A

*2 lobes united by an isthmus
*only endocrine organ which stores secretory product
*synthesizes hormones:
-thyroxine (T4) and tri-iodothyronine (T3) = controls basal metabolic rate in cells
-calcitonin = inhibits osteoclast activity

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16
Q

thyroid gland - cell types

A
  1. follicular cells:
    -simple cuboidal epithelium, under the control of TSH
    -exocrine function = thyroglobulin (colloid) production; sufficient stored hormone to supply body ~3 months
    -endocrine function = iodination of thyroglobulin with subsequent secretion of T4 and T3
  2. parafollicular (C) cells:
    -neuroendocrine cells which secrete calcitonin
    -triggered by elevated blood Ca2+
    -inhibits osteoclast activity
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17
Q

goiter - overview

A

*enlargement of the thyroid
*most common clinical manifestation of thyroid disease

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18
Q

goiter - pathogenesis

A

*defective synthesis of T3 and T4 from relative iodine deficiency
*endemic = dietary iodine deficiency
*sporadic goiter = most common in adolescent/young adult women; dietary goitrogens

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19
Q

goiter - pathology

A

*diffuse goiter evolves into multinodular goiter
1. initial diffuse goiter (TSH-induced proliferation of follicular cells → cells involute as demand for thyroid hormones goes down)
2. cycles of proliferation/involution → irregular enlargement

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20
Q

goiter - clinical features

A

*usually functionally silent (euthryoid)
*neck mass may become so large it compresses other structures → airway obstruction, dysphagia, and vascular compromise

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21
Q

pathogenesis of thyroid enlargement in Graves’ Disease

A
  1. IgG antibodies to TSH receptor →
  2. bind to follicular cells →
  3. thyroid hypertrophy/hyperplasia →
  4. increased secretion of T3 and T4
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22
Q

Graves Disease - overview

A

*most common cause of hyperthyroidism
*most prevalent in women of childbearing age
*associated with HLA-DR3
*caused by autoantibodies against TSH receptor, which bind to and stimulate thyroid follicular cells

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23
Q

Graves Disease - clinical features

A
  1. diffuse goiter - due to constant TSH stimulation
  2. hyperthyroidism (note - thyroid storm is a potentially fatal complication)
  3. exophthalmos and/or pretibial myxedema
    -fibroblasts behind the orbit express the TSH receptor
    -TSH activation → glycosaminoglycan build-up, inflammation, and edema in soft tissues
24
Q

Graves Disease - pathology & labs

A

*diffuse hyperplastic thyroid follicles
*labs: hyperthyroidism = increased total and free T4, decreased TSH

25
Q

Hashimoto’s Thyroiditis - overview

A

*most common cause of hypothyroidism
*most prevalent in women of childbearing age
*associated with HLA-DR5
*caused by thyroid destruction by T-cell immune response against thyroid antigens

26
Q

Hashimoto’s Thyroiditis - clinical features

A
  1. hypothyroidism (follicle damage)
    -fatigue, weight gain, feeling cold
    -joint and muscle pain
    -dry and thinning hair
  2. lobular goiter: thyroid enlargement from lymphocytic infiltration and fibrosis
27
Q

pathogenesis of thyroid enlargement in Hashimoto’s Thyroiditis

A

*inflammatory process: thyroid enlargement from lymphocytic infiltration and fibrosis

28
Q

Hashimoto’s Thyroiditis - pathology & labs

A

*lymphocytic infiltration → nodular thyroid fibrosis → progressive thyroid failure
*labs: decreased T4, increased TSH

29
Q

thyroid neoplasms - overview

A

*usually present as distinct, solitary nodule/mass; vast majority are benign
*radioactive iodine scan is useful:
-HOT nodules = toxic adenomas, rarely malignant
-COLD nodules = ~10% are malignant

30
Q

clinical characteristics of MALIGNANT thyroid neoplasms

A
  1. solitary nodule
  2. nodule in male
  3. age: < 20 or > 70
  4. radiation exposure history
  5. cold nodule: failure to take up radioactive iodine in imaging studies
  6. evidence of extrathyroidal extension or enlargement of cervical lymph nodes
31
Q

thyroid neoplasm: follicular adenoma - overview

A

*benign, solitary neoplasm derived from follicular epithelium
*somatic mutations that lead to constitutive activation of the TSH receptor signaling pathway (e.g. gain-of-function mutations of TSH receptor)

32
Q

thyroid neoplasm: follicular adenoma - clinical features

A

*typically painless, incidental thyroid nodule
*vast majority are nonfunctional (euthyroid)
*function “toxic” adenomas cause hyperthyroidism

33
Q

thyroid neoplasm: follicular adenoma - pathology

A

*solitary lesion composed of colloid-filled follicles lined with uniform-appearing epithelial cells
*thin fibrous capsule:
-evaluation of capsule integrity critical
-diagnosis of malignancy would require demonstration of capsular invasion

34
Q

thyroid neoplasm: papillary carcinoma - overview

A

*malignant neoplasm derived from follicular epithelium
*most common malignant thyroid neoplasm
*risk factors: ionizing radiation, particularly during the first 2 decades

35
Q

thyroid neoplasm: papillary carcinoma - clinical features

A

*neck masses: within thyroid and/or metastatic deposits in draining cervical lymph nodes
*nonfunctional (euthyroid)
*indolent

36
Q

thyroid neoplasm: papillary carcinoma - pathogenesis

A

*activating MAP kinase pathway:
1. RET gene rearrangements
2. BRAF activating mutations

37
Q

thyroid neoplasm: papillary carcinoma - pathology

A

*solitary or multiple
*infiltrative
*papillary growth
*cells with empty chromatin (Orphan Annie eyes)
*Psammoma bodies

38
Q

thyroid neoplasm: follicular carcinoma - overview

A

*malignant neoplasm derived from follicular epithelium
*RAS or PI3K/AKT activating mutations

39
Q

thyroid neoplasm: follicular carcinoma - clinical features

A

*solitary, cold nodules
*distant hematogenous metastases

40
Q

thyroid neoplasm: follicular carcinoma - pathology

A

*resemble follicular adenomas, but with capsular invasion
*vascular invasion and/or metastases present

41
Q

thyroid neoplasm: medullary carcinoma - overview

A

*malignant calcitonin-producing neuroendocrine C-cells

42
Q

thyroid neoplasm: medullary carcinoma - pathogenesis

A

*majority are sporadic
*familial = RET activating mutations

43
Q

thyroid neoplasm: medullary carcinoma - clinical features

A
  1. neck mass (sporadic = adults; MEN2A/B = children)
  2. hypocalcemia
  3. increased serum calcitonin
44
Q

thyroid neoplasm: medullary carcinoma - pathology

A

*small round blue cells
*deposits of pink amyloid

45
Q

endocrine pancreas - overview

A

*composed of “Islets of Langerhans:” round endocrine cell group in acinar exocrine tissue
*concentrated in narrow tail region of pancreas

46
Q

endocrine pancreas - cell types

A
  1. alpha cells: produce glucagon - acts on several tissues to make energy stored in glycogen and fat available through glycogenolysis and lipolysis; increases blood glucose content
  2. beta cells: produce insulin - acts on several tissue to cause entry of glucose into cells and promotes decrease of blood glucose content
  3. delta cells: produce somatostatin: inhibits release of other islet cell hormones through local paracrine action; inhibits release of GH and TSH in anterior pituitary and HCl secretion by gastric parietal cells
  4. PP cells: produce pancreatic polypeptide - stimulates activity of gastric chief cells; inhibits bile secretion, pancreatic enzyme and bicarbonate secretion, and intestinal motility
47
Q

type 1 diabetes mellitus - pathogenesis

A

*autoimmune disease
*CD4 and CD8 T cells attack and destroy beta cells, resulting in insulin deficiency
*susceptibility: HLA-DR3 or DR4 haplotypes; environmental influences / “molecular mimicry”
*insulitis: islets “invaded” by T-lymphocytes; beta-cell destruction

48
Q

type 1 diabetes mellitus - pathology

A

*insulitis - infiltration by T lymphocytes
*decreased number/size of the islets of Langerhans (due to autoimmune destruction)

49
Q

type 1 diabetes mellitus - clinical features

A

*commonly presents in childhood
*triad: polyuria, polydipsia, polyphagia
*can present in diabetic ketoacidosis

50
Q

type 2 diabetes mellitus - pathogenesis

A

*complex genetic, environmental, inflammatory disease
1. insulin resistance → decreased response of peripheral tissues
2. beta cell dysfunction → inadequate insulin secretion
*susceptibility: inheritable risk present; environmental factors (obesity, lifestyle, sleep disorders)

51
Q

type 2 diabetes mellitus - pathology

A

*islet AMYLOID DEPOSITION

52
Q

type 2 diabetes mellitus - clinical features

A

*older patients (generally)
*obesity
*typically asymptomatic, following routine bloodwork

53
Q

diabetes complications: vascular lesions

A

*pathogenesis: atherosclerosis/hyalinization of small/medium arteries; deposition of AGEs
*examples:
1. myocardial infarctions
2. ischemic necrosis of the legs (gangrene)
3. small-vessel disease (microangiopathy)
-diffuse thickening of the capillary basement membranes underlies lesions; kidneys, eyes, nerves

54
Q

diabetes complications: diabetic nephropathy

A

*nephrotic syndrome
*glomerulosclerosis: nodular glomerular scarring (Kimmelstiel-Wilson lesions) & capillary basement membrane thickening
*renal hyaline arteriosclerosis (markedly thickened, tortuous afferent arterioles)

55
Q

diabetes complications: diabetic retinopathy

A
  1. nonproliferative: thickened capillaries, aneurysms, hemorrhages; edema/exudates of leaked plasma proteins & lipids
  2. proliferative: local production of VEGF induces neoangiogenesis
    -extensive retinal/vitreous hemorrhages; fibrosis place traction on retina leading to detachment
  3. cataracts, glaucoma
56
Q

diabetes complications: diabetic neuropathy

A

*microangiopathy affecting vessels supplying nerves; may also have component of direct axonal damage
1. symmetric peripheral neuropathy:
-affects mainly SENSORY nerves of legs but may also impair motor function
-upper extremities may be involved, thus “stocking-and-glove” pattern
2. autonomic neuropathy:
-bowel & urinary disturbances; erectile dysfunction
3. diabetic mononeuropathy:
-manifests as sudden foot drop, wrist drop, or isolated cranial nerve palsies

Endo Repro Exam (31 decks)

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