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Pathology Flashcards

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1
Q

What are the 5 cell types in anterior pituitary?

A
  • Somatotrophs
  • Lactotrophs
    -Corticotrophs
  • Thyrotrophs
  • Gonadotrophs
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2
Q

Describe somatotrophs

A

Secrete GH, Acidophilic, PAS negative

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3
Q

Describe Lactotrophs

A

Secrete PRL, acridophilic, PAS negative

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4
Q

Describe corticotrophs

A

Secrete Adrenocorticotropic hormone, Basophilic, PAS positive

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5
Q

Describe thyrotrophs

A

Secrete TSH, Basophilic, PAS positive

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6
Q

Describe Gonadotrophs

A

Secrete FSH, LH, basophilic, PAS positive

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7
Q

What hormones are synthesizes in the hypothalamus and stored within the axon terminals residing in the posterior pituitary?

A

Oxytocin, ADH

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8
Q

What is the most common cause of hyperpituitarism?

A

Pituitary adenoma

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9
Q

How are pituitary adenomas classified?

A

On the basis of hormones produced by the neoplastic cells; detected by immunohistochemical stains

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10
Q

What is the tumor type common for corticotroph?

A

ACTH cell adenoma

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11
Q

What is the associated syndrome for corticotrophs?

A

Cushing Syndrome

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12
Q

What is the tumor type for somatotrophs?

A

GH cell adenoma

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13
Q

What is the associated syndrome for somatotrophs (GH)?

A

Gigantism and acromegaly

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14
Q

What is the associated syndrome for lactotrophs?

A

Galactorrhea, amenorrhea, sexual dysfunction, infertility

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15
Q

What is the associated syndrome for Gonadotrophs?

A

Hypogonasism, mass effects, hypopituitarism

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16
Q

What do pituitary adenomas look life?

A

Soft and well circumscribedIn

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17
Q

In pituitary adenomas, if mitotic acitivity is brisk and nuclear p53 immunoreactivity is extensive, they will exhibit

A

aggressive behavior

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18
Q

Describe prolactinomas

A
  • Increased prolactin secretion
  • May cause amenorrhea/galactorrhea/decreased libido/infertility
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19
Q

What is treatment for prolactinomas?

A

Surgery or bromocriptine

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20
Q

Describe somatotropinoma

A
  • Excessive GH (stimulates hepatic secretion of IGF-1)
  • Gigantism in children, acromegaly in adults
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21
Q

What is treatment for somatotropinoma?

A

Surgery or somatostain analogs

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22
Q

Describe ACTH cell adenomas

A
  • Usually small micro adenomas at time of diagnosis
  • Excessive production of ACTH
  • Hypercortisolism (bushings)
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23
Q

MEN1 syndrome is characterized by what type of neoplasms?

A
  • Parathyroid (adenoma)
  • Anterior pituitary (adenoma)
  • Pancreasa
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24
Q

What non-neuroendocrine neoplasms are associated with MEN1 syndrome?

A
  • Facial angiofibroma
  • Meningioma
  • Ependymoma
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25
What are some causes of hypopituitarism?
- Ischemic injury, surgery or radiation - Inflam rxns - Nonfunctional pituitary adenomas
26
In hypopituitarism, at least 75% of _________ is lost, mosly because of a destructive process
parenchyma
27
What is pituitary apoplexy?
Bleeding into or impaired blood supply of pituitary- usually in presence of tumor
28
What are symptoms of pituitary apoplexy?
Sudden onset of headache, visual symptoms, altered mental status and hormonal dysfunction
29
What are clinical manifestations of hypopituitarism assoc with LH and FSH?
Amenorrhea, infertility
30
ADH binds to receptors on cells in collecting ducts of kidney and promotes _______________
reabsorption of water back into circulation
31
In a syndrome of inappropriate ADH secretion, there will be reabsorption of
excessive amounts of free water
32
Hypothalamic suprasellar tumors are significant because they may cause:
- Hypofunction or hyperfunction of anterior pituitary - DIabetes insipidus - Gliomas or craniopharyngiomas
33
What are craniopharyngiomas?
Slow-growing tumor that accoudns for 1-5% of intracranial tumors. COmmonly cystic and multiloculates
34
Craniopharyngiomas arise from
remnants of the cranipharyngeal duct and/or Rathke's pouch
35
What do craniotomypharyngiomas in children look like?
Adamantinomatous: squamous epi, wet keratin and calcification, systs contain machine oil
36
What are craniopharyngiomas of adults like?
Papillary, lack keratin, calcification and cysts
37
What is the WHO grade 1 for gliomas?
Pilocytic astrocytomaW
38
What is WHO Grade II for gliomas?
Diffuse astrocytoma- show only nuclear atypia
39
What is the WHO grade III for gliomas?
Anaplastic astrocytoma- show nuclear atypia, significant increase in proliferation activity
40
What is WHO Grade IV for gliomas?
Glioblastoma multiforme- show nuclear atypia, signifiacnt increase in proliferation activity, microvascular proliferation or necrosis
41
Example of endocrine effect of pineal lesions
Precocious puberty due to melatonin deficiency
42
Examples of neurologic effects of pineal lesions
- Increased intracranial pressure due to mass effect
43
What do chief cells of parathyroid gland synthesize?
PTH in response to low calcium
44
What are oxyphil cells?
Cells that appear at puberty, present as single cells or small clusters. Rich in mitochondria, no secretory granules
45
How is actiivty of parathyroid controlled?
By levels of free (ionized) calcium in blood
46
Tumors of parathyroid usually come to attention from what?
Excessive PTH secretion rather than mass effects
47
Primary Hyperparathyroidism is an important cause of incidental
hypercalcemia
48
What are possible causes of primary hyperparathyroidism?
- Adenoma - Hyperplasia - Carcinoma
49
Adenomas that cause primary hyperparathyroidism are associated with
Cyclin D1 and MEN1 mutations
50
Describe adenomas of primary hyperparathyroidism
- Solitary - Well circumscribed, encapsulated, tan brown nodule - Rim of parathyroid tissue seperated by fibrous capsule - Almost entirely chief cells and few oxyphil cells - Adipose tissue is inconspicuous
51
What is the difference between adenoma and hyperplasia of parathyroid?
Hyperplasia involves more than one gland generally
52
Describe masses of parathyroid carcinomas (hyperparathyroidism)
Gray-white irregular masses that exceed 10 grams. Cytological similarity to adenomas
53
What are morphologic changes in other organs from primary hyperparathyroidism?
- Skeletal Changes (Increased clastic activity, blastic activity, osteitis fibrous cystic, occasionally form brown tumors) - Urinary tract stones - Calcifications in stomach, lungs, myocardium, BVs STONES, BONES, GROANS
54
What is secondary hyperparathyroidism?
Compensatory parathyroid hyperplasia from conditions causing chronic decreased calcium
55
In chronic renal failure, loss of renal substance reduced the availability of alpha-1-hydroxylase necessary for
synthesis of the active form of vit D (thereby reducing intestinal absorption of calcium)
56
Treatments of secondary hyperparathyroidism includes
dietary Vit D supplements and phosphate binders
57
What is tertiary hyperparathyroidism?
When parathyroid activity becomes autonomous and excessive with resultant hypercalcemia
58
What is treatment of teritary hyperparathyroidism?
Parathyroidectomy
59
What are possible causes of hypoparathyroidism?
- Congenital absence - Surgery/radiation - Autoimmune - Familial
60
What are some clinical manifestations of hypoparathyroidism?
- Tetany, neuromuscular irritability - Anxiety, depression, psychosis - Calcifications of basal ganglia, Parkinsonian-like movement - QT prolongation
61
What are oral manifestations of hypoparathyroidism?
Dental hypoplasia, failure of eruption, defective enamel and root formation
62
What does pseudohypoparathyroidism occur due to?
End-organ resistance to the actions of PTH
63
What are serum PTH levels in pseudohypoparathyroidism?
Normal or elevated
64
What are goitrogens in the thyroid?
Chemical agents that inhibit the function of thyroid gland. They suppress T4/T3 synthesis
65
What are examples of goitrogens?
Propylthiouracil, iodides and vegetables (Cabbage, turnips, cassava)
66
What are cardiac manifestations of hyperthyroidism?
Increased cardiac output with tachycardia, palpitations, arrhythmias (Earliest and most consistent sign)
67
What are neuromuscular manifestations of hyperthyroidism?
Tremor, hyperactivity, emotional lability, anxiety, inability to concentrate - Proximal muscle weakness and descred muscle mass
68
What effects does Hyperthyroidism have on BMR?
Increases BMR (heat intolerance, weight loss)
69
What are ocular and GI changes in hyperthyroidism?
- Wide, staring gaze and lid lag - Hypermotility, malabsorption, diarrhea
70
What does a thyroid storm result from?
An acute elevation in catecholamine levels (possibly from infection, surgery, cessation of antithryoir meds, stress)
71
What are laboratory findings in hyperthyroidism?
- Low TSH - Elevated T3/T4 - Radioactive iodine uptake test
72
What ages is the peak incidence of Graves? (Hyperthyroid)
20-40s
73
What is the antibody associated with Graves?
Thyroid-stimulating immunoglobulin (IgG antibody binds to TSH receptor and mimics action of TSH)
74
What are lab findings of Graves?
- Elevated T4/T3 - Depressed TSH levels - Diffuse and increased uptake of radioactive iodine
75
What does histo look like for untreated cases of Graves?
- Tall follicular epi cells forming papillae that enrich on colloid Pale colloid with scalloped margins
76
What are lab findings of primary hypothyroidism?
High TSH, Low T4
77
What are lab findings for secondary hypothyroidism?
Low TSH, low T4
78
What are examples of primary hypothyroidism?
- Congenital - Acquired - Autoimmune (Hashimotos)
79
What are classic clinical manifestations of hypothyroidism?
- Cretinism - Myxedema
80
Describe cretinism
Develops at young age - SHort stature, severe mental retardation and coarse facial features
81
Describe myxedema
Cold intolerance, overweight, constipated, decreased sweating, cold and pale, reduced cardiac output - Increased cholesterol and LDL
82
Describe thyroiditis
- Inflam of thryoid - causes primary hypothyroidism - Many types (Hashimotos, Subacute, infectious)
83
How is Hashimotos characterized?
Gradual thyroid failure from autoimmune dsestruction of thyroid gland
84
What ages is Hashimotos most prevelant?
45-65 years
85
What are lab findings of Hashimotos?
- Elevated serum levels of antibodies to thyroglobulin, thyroid peroxidase and TSH receptors
86
Describe morphology of Hashimotos
- Diffusely enlarged with intact capsule - Pale, yellow-tan, firm, nodular - Mononuclear inflammatory infiltrate with well formed germinal centers, atrophic follicles, Hurthle cell change and fibrosis
87
What triggers subacute thyroditis (De Quervain Thyroiditis)
Viral infections
88
What is Riedel thyroiditis?
Extensive fibrosis involving thyroid and contiguous neck structures. Clinically simulated thyroid carcinoma
89
Riedel Thyroiditis may be associated with
idiopathic fibrosis in other sites in the body, such as the retroperitoneum
90
How does De Quervain thyroiditis appear on histology?
Granulomatous inflam with giant cells and lymphocytes; destruction of follicles COllagen fibers around infiltrate Can result in extensive scarring
91
How does Riedel thyroiditis appear on histology?
Massive scarring Loose lymphocytic and histiocytic infiltrates Stony hard fibrosis; iron collar
92

Systems 1 (50 decks)

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