Pathology Review Flashcards

1
Q

Benign tumor of the anterior pituitary cells

A

Pituitary adenoma

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2
Q

What is the difference between a functional and non functional tumor?

A

Functional = hormone producing

Non functional = silent

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3
Q

How do non functional tumors often present?

A

With a mass effect

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4
Q

Why do pituitary adenomas present with tunnel vision?

A

Pituitary sits adjacent to optic chiasm - mass effect

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5
Q

How will a prolactinoma present in women?

A

Galactorrhea (increased prolactin)

Amenorrhea (due to inhibition of GnRH –> loss of FSH and LH)

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6
Q

How will a prolactinoma present in men?

A

Decreased libido, headache

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7
Q

What is the most common type of pituitary adenoma?

A

Prolactinoma

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8
Q

How are prolactinomas treated?

A

Dopamine agonists such as Bromocriptine or cabergoline (DA inhibits production of Prolactin)

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9
Q

Difference between gigantism and acromegaly

A

Gigantism can occur in children (growth plates not closed)

Acromegaly in adults (big hands, digits, jaw, organs)

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10
Q

Most common cause of death in adults with growth hormone cell adenoma?

A

Cardiac failure (organs grow too much)

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11
Q

Why is diabetes secondary to a growth hormone adenoma?

A

GH decreases glucose uptake into the cell. Too much GH around = too much glucose in blood

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12
Q

How might one diagnose GH adenoma?

A

Oral glucose test (GH not suppressed)
Elevated GH
Elevated IGF-1 (GH leads to increase in IGF-1)

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13
Q

Treatment for GH adenoma

A

Octreotide

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14
Q

Why is octreotide an effective treatment for GH adenoma?

A

Somatostatin inhibits GH release - therefore use a somatostatin analog

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15
Q

At what point does hypopituitarism present?

A

when 75% is lost

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16
Q

2 main causes of hypopituitarism? (adult and child)

A
  1. Adult - pituitary ademona
  2. Child - craniopharyngioma

Both of these are due to mass effect or apoplexy

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17
Q

Who does Sheehan syndrome occur in?

A

Pregnant women - Gland doubles in size during pregnancy but not the blood supply - susceptible to infarction

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18
Q

How does Sheehan syndrome present?

A

Poor lactation
LOSS OF PUBIC HAIR
Fatigue

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19
Q

Two causes of empty sella syndrome?

A

Trauma or Congenital

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20
Q

Pathophysiology of empty sella syndrome?

A

Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland

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21
Q

What two hormones are stored in the posterior pituitary

A

ADH and oxytocin

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22
Q

Are hormones made in the posterior pituitary?

A

No, ADH and Oxy and made in the hypothalamus and transferred via neurons. Stored.

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23
Q

ADH function?

A

Acts on the distal tubule and collecting duct of kidneys to promote free water retention

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24
Q

Oxytocin function?

A

mediates uterine contraction during labor and release of breast milk (let down) in lactating mothers

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25
Pathophysiology of Central DI
ADH deficiency - problem with hypothalamus or posterior pituitary
26
Pathophysiology of Nephrogenic DI
Impaired renal response to ADH - Mutation of drug induced
27
Clinical features of DI
Polyuria and polydipsia (life threatening dehydration) Hypernatremia and high serum osmolality Low urine osmolality and SG (peeing everything)
28
How to treat central DI?
ADH analog (desmopressin)
29
Does desmopressin work in nephrogenic DI?
No, problem with receptor
30
What drugs may cause nephrogenic DI?
Lithium | Demeclocycline
31
What is the most common cause of excessive ADH?
Ectopic production via a small cell carcinoma, CNS trauma, pulmonary infection, drugs
32
Clinical/lab findings of SIADH
Hyponatremia Low serum Osmolality Mental changes and seizures - neuronal swelling and cerebral edema
33
Treatment of SIADH
Free water restriction | Demeclocycline
34
Cystic dilation of the thyroglossal duct remnant results in this condition
Thyroglossal duct cyst | Typically, the thyroglossal duct normally involutes but a persistent duct may undergo dilation
35
How does a thyroglossal ductal cyst present upon exam?
an anterior neck mass
36
Persistent basal tongue mass
Lingual thyroid (doesn't migrate fully from base of the tongue -- site of origin)
37
What are the physiologic consequences on increased levels of circulating thyroid hormone
``` Increased BMR (more Na/K ATP-ase) Increased SNS activity (more B1 expression) ```
38
Name some clinical features of hyperthyroidism
Weight loss (even w/ increased appetite), heat intolerance, tachy and increased CO, arrhytmia, tremor, anxiety, insomnia, staring gaze, diarrhea, oligomenorrhea, bone resorption, decreased muscle mass, hypochlesterolemia, hyperglycemia
39
why hyperglycemia with hyperthyroidism?
Excess thyroid hormone in the blood causes gluconeogenesis and glycogenolysis
40
Pathophysiology of Graves Disease
Autoantibody (IgG) stimulates TSH receptor (type II HS) leads to an increase in synthesis and release of thyroid hormone
41
Most common cause of hyperthyroidism
Graves Disease
42
Typical patient profile for Graves Disease
Woman between the ages of 20 - 40 (childbearing) | Fits other autoimmune disease profile
43
Clinical features of Graves Disease
Hyperthyroidism Diffuse goiter Exophthalmos and pretibial edema
44
MOA of goiter
Constant TSH stimulation leads to thyroid hyperplasia and hypertrophy
45
MOA behind exophthalmos and pretibial edema?
- Fibroblasts behind the orbit and overlying shin express TSH receptor - TSH activation results in glycosaminoglycan buildup, inflammation, fibrosis and edema
46
Microscopic appearance of Graves?
hyperplasia of the thyroid follicle and scalloping of the colloid
47
Lab findings in Graves
Increased T4 ((total and free) Decreased TSH (free T3 downregulates TSH receptors)) Hypocholesterolemia Increased serum glucose
48
Treatment for Graves
B blocker Thioamide (blocks peroxidase) Radioiodine ablation
49
What happens with a thyroid storm?
Stress leads to an elevated level of catacholamines and hormones - arrhythmia, hyperthermia, vomiting - hypovolemic shock
50
Treatment for Thyroid storm
B blocker steroid Propylthiouracil (PTU)
51
MOA of PTU
inhibits peroxidase mediated oxidation, organification and coupling of thyroid hormone synthesis inhibits peripheral conversion of T4 to T3
52
MOA of thioamide?
blocks peroxidase (which catalyzes T3 and T4 synthesis)
53
Enlarged thyroid gland with multiple nodules
Multinodular goiter
54
What is the usual cause of multinodular goiter?
Relative iodine deficiency
55
Hypothyroidism in a neonate or child is often referred to as _______
Cretinism
56
Classical findings of cretinism?
Mental retardation (thyroid hormone needed for brain development) Short stature with skeletal abnormalities course facial features enlarged tongue umbilical hernia
57
What enzyme is most often deficient in dyshormonogenetic goiter?
thyroid peroxidase
58
Hypothyroidism in older children and adults is often called _______
myxedema
59
Some clinical features of myxedema include:
myxedema, weight gain, slowing of mental activity, muscle weakness, cold intolerance, bradycardia and decreased CO, SOB, fatigue, oligomenorrhea, hypercholesterolemia, constipation
60
Two most common causes of myxedema:
1. iodine deficiency | 2. Hashimoto thyroiditis
61
HLA DR5
Hashimoto thyroiditis
62
Autoimmune destruction of the thyroid gland
Hashimoto thyroiditis
63
Most common cause of hypothyroidism in regions with adequate iodine
Hashimoto thyroiditis
64
Why might Hashimoto initially present with hyperthyroidism?
Initial destruction of the follicles results in the hormones leaking to the blood. As more follicles are destroys return to baseline and then drops.
65
What type of abs might you see with Hashimoto
antithyroglobulin | antithyroid peroxidase
66
What does a sample of thyroid with Hashimoto disease look like?
Chronically inflamed with germinal centers and Hurthle cells
67
Patient presents with known Hashimoto and an enlarged thyroid -- this should be high on your differential --
B cell (marginal) lymphoma
68
Tender thyroid -- this should be the top of your differential
Granulomatous throiditis | De Quervain
69
Hypothyroidism with a 'hard as wood' nontender thyroid gland (may involve local structures)
Riedel Fibrosing Thyroiditis (chronic inflammation with fibrosis)
70
``` Thyroid lesion (hard) Local structure involvement young female patient ```
Riedel Fibrosing Thyroiditis
71
Are thyroid nodules more likely to be benign or malignant?
Benign
72
What type of study is used to characterize thyroid nodules?
Radioactive Iodine uptake study
73
Increased radioactive (hot nodule) uptake seen in....
Graves disease | Nodular goiter
74
Decreased radioactive uptake (cold nodule) seen in..
adenoma and carcinoma
75
Mechanism for sampling the thyroid?
FNA (fine needle aspiration) biopsy
76
Most common type of thyroid carcinoma
Papillary carcinoma
77
What is the major risk factor for papillary thyroid carcinoma?
Exposure to ionizing radiation in childhood (face -- acne)
78
What distinguishing features will you see in the cells for Papillary carcinoma
Orphan Annie eye nuclei Nuclear grooves Psammoma bodies
79
How do you distinguish follicular adenoma from follicular carcinoma
Invasion through the capsule Entire capsule must be examined microscopically Therefore cannot distinguish by FNA
80
Malignant proliferation of follicles surrounded by fibrous capsule with invasion through the capsule
Follicular carcinoma
81
Orphan annie eye nuclei | nuclear grooves
Papillary carcinoma
82
Benign proliferation of follicles surrounded by a fibrous capsule
Follicular adenoma
83
Metastasis of papillary carcinoma
Cervical lymph nodes
84
Metastasis of follicular carcinoma
hematogenous
85
Malignant proliferation of the parafollicular C cells
medullary carcinoma
86
Name the four types of thyroid carcinomas
Papillary Follicular Medullary Anaplastic
87
Neuroendocrine cells that secrete calcitonin
C cells
88
What do c cells secrete
calcitonin
89
Calcitonin MOA
lower serum calcium by increasing renal calcium excretion
90
why might a medullary carcinoma present with hypocalcemia?
C cells -- more calcitonin -- more renal calcium excretion
91
Calcitonin often deposits within medullary tumors in this form
amyloid
92
Typical, high yield description of medullary carcinoma biopsy
malignant cells in an amyloid stroma | this is an example of localized amyloidosis
93
Familial cases of medullary carcinoma are due to this disorder
MEN 2
94
Men 2A vs Men 2B
2A: medullary carcinoma, pheochromocytoma, parathyroid adenoma 2B: medullary carcinoma, pheochromocytoma, ganglioneuromas of oral mucosa
95
What mutation is predictive of familial medullary carcinoma (MEN2)
RET mutation | May want prophylactic thyroidectomy
96
Undifferentiated malignancy of thyroid gland
Anaplastic carcinoma
97
Anaplastic carcinoma
undifferentiated malignant tumor of the thyroid
98
What happens when anaplastic carcinoma invades local structures?
May lead to dysphagia or respiratory compromise (by esophagus and trachea)