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Endocrine > Pathology Highlights > Flashcards

Pathology Highlights Flashcards

1
Q

What are 3 other causes of Hyperthyroidism besides Grave’s?

A
  1. Multinodular Goiter
  2. Adenoma
  3. Iodine Induced Hypothryoidism
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2
Q

What HLA type is associated with Grave’s?

A

HLA-DR3

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3
Q

What is Plummer Syndrome?

• 2 causes?

A

Multinodular Goiter that is Toxic

Causes:
• Focal Patches
• Jod-Basedow Phenomenon (from iodine deficiency - opposite of Wolff-Chiakoff)

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4
Q

Who is most likely to get toxic mulinodular goiter?

A

Women with long standing sporadic endemic goiter

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5
Q

What histological feature differentiates toxic multinodular goiter from a follicular neoplasm?

A

TMG has a thin capsule while follicular neoplasms have a thick capsule

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6
Q

What is most commonly the cause of death in thyroid storm?

A

Tachyarrhythmia

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7
Q

T or F: carpal tunnel syndrome and delayed tendon relaxation are features of Grave’s disease?

A

False, this are features of hypothyroidism

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8
Q

Who is most commonly affected by Hashimoto’s Thyroiditis?

A

Women 45-65

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9
Q

What cells are responsible for mediating the autoimmune attack in Hashimoto’s?
• what are some key markers to look for in the serum?

A

T cells (CD4+) mediate Hashimoto’s

Key Markers:
• Anti-thyroglobulin Antibodies
• Anti-thyroid peroxidase Antibodies

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10
Q

What HLA type(s) is/are associated with Hashimoto’s?

A

HLA-DR5**, and HLA-DR3

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11
Q

What is a feared complication of Hashimoto’s Thyroiditis?

A

• Large Diffuse B-cell Lymphoma

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12
Q

What histological changes would you see in Hashimoto’s?

A

Germinal Centers + Hurthle Cell Changes

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13
Q

What are the chances of subacute lymphocytic thyroiditis progressing to Hashimoto’s?

A

1/3 progress to Hashimoto’s

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14
Q

What would you expect to see in Histologically in Reidel’s Thyroiditis that is associated with IgG4 autoimmune disease?

A

Fibrosis and Lymphocytes

Note: this is typically a woman in her 40s

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15
Q

Who most commonly presents with Granulomatosis Thyroiditis? (De Quervain’s)

A

40-60 year old woman with hx of Flu-like symptoms and a painful thyroid (often present in the summer due to association with summertime viruses like coxsackie and adenovirus)

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16
Q

What do you expect to see histologically in someone who has Granulomatosis Thyroiditis?

A

Giant Cells and Granulomas

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17
Q

T or F: most neoplasms of the thyroid are benign

A

True

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18
Q

What features make a thyroid nodule more likely to be neoplastic?

A
  • Solitary
  • Young Person
  • Male
  • Hx of radiation to the head
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19
Q

Are hot or cold nodules more likely to be associated with mutations in the the TSH receptor and GNAS1?

A

Hot (BENIGN) nodules are most commonly associated with these mutations

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20
Q

What mutations are most commonly seen in cold nodules?

• where else are these mutations seen?

A

RAS and PIK3A mutations are most commonly seen in COLD nodules and in FOLLICULAR carcinomas of the thyroid

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21
Q

What are the key histological features of a thyroid Adenoma?

A
  • Hurthle Cells (not that these are parafollicular C cells)
  • ENCAPSULATION is the most important feature to look for
  • this tissue will be impinging on NL thyroid tissue
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22
Q

What is the typical age of presentation of papillary thyroid CA?

A

20-50

Remember mets have little prognostic significance

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23
Q

What mutations are associated with Papillary thyroid CA?

A

RET and BRAF (worse px)

Remember tall cell variants are also associated with a bad PX

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24
Q

What mutations are associated with Follicular thyroid CA?

A

RAS and PI3K, PTEN is also associated with this

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25
Q

T or F: Like papillary CA, the px Follicular CA does not change much even with the presence of mets?

A

FALSE, extensive METs puts people with follicular CA at a much greater risk of dying
Remember most mets from follicular are hematogenous

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26
Q

What age groups commonly get medullary thyroid CA?

A

Young - MEN2 pts.

40’s and 50’s - sporadic and FMTC

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27
Q

What cell type is medullary thyroid CA composed of?

A

C-cells - these deposit CALCITONIN AMYLOID as they proliferate

•Spindle cell changes may also be seen on histo

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28
Q

What mutation is associated with Medullary thyroid CA?

A

RET => remember the association with MEN2

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29
Q

T or F: Medullary CA of the thyroid is a neuroendocrine tumor.

A

True

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30
Q

Who most commonly presents with anaplastic thyroid carcinoma?
• what do you expect to see histologically?

A

65 or older with a history of well differentiated thyroid cancer

Histo:
• Multinucleated Osteoclast-like cells and spindle shaped cells

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31
Q

What do you need to do for a women on thyroid hormone therapy that gets pregnant?

A

GIVE MORE T3 and T4 because she will have more TGB

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32
Q

T or F: hot nodules decrease activity elsewhere in the thyroid

A

True

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33
Q

What is derived from the 3rd branchial pouch?

A

Inferior Thyroids and the Thymus

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34
Q

What is derived from the 4th branchial pouch?

A

Superior Parathyroid Glands

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35
Q

What is the most common cause of primary hyperparathyroidism?
• who typically present with it?
• how?

A

Pituitary Adenomas are the Most Common Cause
• Patient typically in 50s with Stones, Moans, and Bones

Note: this is the most common cause of asymptomatic hypercalcemia

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36
Q

What mutations are often associated with Primary Hyperparathyroidism?
• what do you expect to see histologically?

A

Cyclin D1 and MEN1

HISTO:
• Rim or normal parathyroid surrounds tissue that almost look like NL parathyroid but it LACKS FAT

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37
Q

What is the most common cause of hypoparathyroidism?

• hallmark symptoms?

A

Surgical Removal is the most common cause (followed by autoimmune disease and diGeorge Syndrome)

TETANY is the hallmark symptom (Chvostek, Trousseau)

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38
Q

What is the most common pathologic lesion of the pituitary?

• what should you look for histologically?

A

NON-FUNCTIONAL adenomas are the most common lesion of the pituitary

HISTO:
• Monomorphism and a Reticulin Network

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39
Q

What is a common gene mutated in FUNCTIONAL pituitary adenomas?

A

GNAS1 (most common mutation in GH adenomas and some ACTH adenomas)

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40
Q

If a family has a strong history of pituitary adenomas what genes might you expect are mutated?

A

MEN1 (Menin gene) could be mutated

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41
Q

If someone had an atypical, aggressive, and recurrent pituitary adenoma, what gene might be mutated?

A

P53

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42
Q

What other hormone is often secreted concurrently with GH in somatotroph adenomas?

A

Prolactin

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43
Q

What pituitary adenoma is PAS positive?

A

Corticotroph adenomas because glycosylated ACTH accumulates

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44
Q

What is NELSON SYNDROME?

A

Microadenoma that starts hypersecreting ACTH after adrenals are inappropriately removed because of Cushing syndrome

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45
Q

Someone has a recurring pituitary tumor that has been determined to be carcinoma because of chronic recurrence. Is it most likely functional or non-functional?

A

FUNCTIONAL

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46
Q

What are 3 causes of HypOpituitism?

A
  1. Non-funcitoning Adenoma
  2. Sheehan Syndrome
  3. Empty Sella Syndrome
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47
Q

Why is the anterior pituitary more likely to infarct in Sheehan Syndrome?
• what is a key sign that a woman has Sheehan?

A

Anterior pituitary is supplied by a portal system, so it only has venous supply

Sheehan => POST PARDUM INABILITY TO LACTATE

48
Q

Who do we most often see PRIMARY empty sella syndrome in?

• Secondary?

A

Primary:
• Obese person with multiple pregnancies

Secondary:
• Surgery on pituitary

49
Q

What is the most common cause of hypothalamic suprasellar tumors?

A

Craniopharyngiomas

50
Q

What is the age distribution of craniopharyngiomas?
• what are they derived from?
•What signaling pathway is often messed up?

A
  • Bimodal
  • Derived from Rathke’s Pouch
  • WNT/ß-catenin is often thrown off
51
Q

Craniopharyngiomas histo?

A
  • Wet Keratin
  • Basaloid Cells
  • Cholesterol Clefts

Note: surgeons will comment on motor-oil like substance coming from the tumor

52
Q

What are the major factors contributing to the pathogenesis of T2DM?

A
  • Circulating FAs (inflammasome activation => IL-1ß)
  • Adipokines
  • Inflammatory Mediators
53
Q

What is the root cause of most of the chronic complications seen in DM?

A

Persistent Hyperglycemia

54
Q

What manifestations of Diabetes are due to small vessel disease?

A
  • HTN
  • Hyaline Arteriolosclerosis
  • Retinopathy
  • Nodular Glomerular Sclerosis
55
Q

What manifestations of Diabetes are due to osmotic damage?

A
  • Neuropathy

* Cataracts

56
Q

What is the leading cause of death in patients with DM?

A

Myocardial Infarction due to Large Vessel Disease and Athlerosclerosis

Note: large vessel disease is also responsible for limb loss too*

57
Q

What complication of Diabetes is associated with activation of PKC?

A

Retinopathy - PKC causes activation of VEGF that leads to neovascularization

58
Q

What tissues are most affected by disturbances in the polyol pathway?

A
  • Cornea
  • Schwann Cells

This is a problem in insulin independent tissues like Brain, RBCs, Intestine, Cornea, Kidney, Liver (BRICK L)

59
Q

Differentiate the vascular disease caused by DM in large vessels and small vessels.

A

Small - Hyaline Arteriolosclerosis

Large - Athlerosclerosis

60
Q

What is the major cause of vision loss in DM?

• what happens in this type of eye disease?

A

• Retinopathy => PROLIFERATIVE

Pathogenesis:
• Neovascularization (PKC/VEGF mediated)
• Vitreous Hemorrhage
• Retinal Detachment

61
Q

What do you do if you see evidence of retinopathy in a diabetic patient?

A

• Treat it fast and aggressively

62
Q

T or F: diabetic neuropathy is most often bilateral and symmetric.

A

TRUE - can cause GASTROPARESIS and BLADDER DYSFUNCTION

63
Q

What are the 3 glomerular lesions seen in diabetic nephropathy?

A
  1. Basement membrane thickening
  2. Diffuse Mesangial Sclerosis
  3. Nodular Glomerulosclerosis
64
Q

Other than indicating kidney involvement of DM, what is the significance of microalbuminuria in patients with DM?

A

Increased risk of CV death

65
Q

What is nephrosclerosis?

A

Nodular Gross appearance of kidney in long standing DM

66
Q

What changes are seen in end-stage renal disease?

A
  1. Arteriolosclerosis
  2. Fibrotic Cortex
  3. Sclerotic Glomeruli
  4. Thickened Arteries
  5. Thyroidization of Tubules
67
Q

What histology would you expect to see in Necrotizing Papillitis?

A

Lack of Cellularity with Pink Cellular Exudates

68
Q

What rash associated with diabets has RED/BROWN margins?

A

Necrobiosis Lipodica

69
Q

What should you start looking for in a patient with Acanthosis Nigricans?

A

DM is common, but this is also associated with paraneoplastic syndromes

70
Q

What is the earliest histopathologic change in neurons in DM?

A

Segemental Demyelination (less blue staining with luxol fast blue stain)

71
Q

What causes decreased immune function in patients with DM?

A

Impaired Neutrophil Mobilization
• increased expression of CD11b on neutrophils and ICAM, VCAM, and E-selectin on endothelial cells

Impaired Oxidative Burst (aldose reducase steals all of the NADPH

72
Q

What causes decreased immune function in patients with DM?

A

Impaired Neutrophil Mobilization
• increased expression of CD11b on neutrophils and ICAM, VCAM, and E-selectin on endothelial cells

Impaired Oxidative Burst (aldose reducase steals all of the NADPH

73
Q

What is the most common cause of ACTH dependent Cushing’s syndrome?

A

Cushing DISEASE

• ACTH secreting pituitary adenoma

74
Q

Why do hypertrophic adrenals in Cushing’s look so yellow?

A

Because there is a ton of lip in the ER

75
Q

What are 3 important causes of endogenous ACTH independent Cushing’s Sydrome?
• which is most common?

A
  1. 10% are adenomas (MOST COMMON)
  2. 5% adrenal Carcinomas
  3. McCune Albright Syndrome
76
Q

In what type of Cushing’s would you expect to see contralateral adrenal atrophy?

A

Endogenous ACTH independent Cushing’s syndrome caused by some type of CORTISOL secreting tumor

77
Q

What causes Conn syndrome?

• who presents with it?

A

Conn Syndrome = Primary Hyperaldosteronism (low renin, high aldosterone HTN)

Typical presentation is a 30-40 year old women who is hypertensive and hypokalemic

78
Q

IF Primary Hyperaldosteronism is caused by an adenoma, what side is that adenoma most likely to reside on?

A

Most Common on the LEFT side

79
Q

What would you expect to see in the histology of someone who is being treated for Conn Syndrome?

A

Spironolactone Bodies

80
Q

What are 3 general causes of Secondary Hyperaldosteronism?

A
  1. Low Renal Perfusion - nephrosclerosis or renal artery stenosis
  2. Arterial Hypovolemia and Edema - CHF, liver failure, liver cirrhosis, and nephrotic syndrome
  3. Pregnancy - ESTROGEN INDUCED INCREASE IN RENIN ACTIVITY
81
Q

What is the inheritance of 21ß-hydroxylase deficiency?

• what labs abnormal in these people?

A

Autosomal Recessive

• Elevated 17-hydroxyprogesterone

82
Q

What labs will be abnormal in 11ß-hydroxylase Deficiency?

A

Elevated:
• DHEA, and Adrostrendione, DOC = causes of the HTN

Depressed:
• Renin

83
Q

What labs will be abnormal in 17 alpha hydroxylase deficiency?

A

Elevated:
• DOC, FSH and LH

Depressed:
• DHEA, Estrogen, testosterone, Androstiendione

84
Q

What labs will be abnormal in someone with a 3ß-hydroxysteriod dehydrogenase deficiency?
• how do males with this disease present?

A

Labs: increased (delta5 pregnenolone) / (progesterone) ratio

Males: may have pseudohermaphroditism

85
Q

What is the triad of McCune Albright syndrome?

• mutation?

A

Cafe-au-lait
Fibrous Dysplasia
Autonomous Endocrine Hyperfunction

86
Q

What are 3 causes of acute adrenal insufficiency?

A
  1. Withdrawl of glucocorticoids
  2. Stress to great for adrenals (consider ppl. with Addison’s etc.)
  3. Massive Hemorrhage (anticoagulation, traumatic delivery, Waterhouse FS)
87
Q

What are 4 causes of secondary adrenal insufficiency?

A
  1. Hypopituitism
  2. Trauma
  3. Removal of ACTH secretory tumors
  4. Granulomatous Disease
88
Q

What two stains can you use on adrenal medullary tumors?

A

Chromogranin

Synaptophysin

89
Q

What Syndromes/mutations are often associated with Pheochromocytomas?

A

MEN2A/B => RET
Neurofibromatosis => NF1
VHL
Sturge Weber

90
Q

What do you expect to see histologically in a pheochromocytoma?

A
  • Basophilic Cytoplasm

* ZELLBALLEN (cells in clusters)

91
Q

What are 4 possible triggers for pheochromocytoma?

A
  1. Postural Changes
  2. Emotional Stress
  3. Excercise
  4. Urination
92
Q

What cells do neuroblastomas arise from?

• WHERE do they most commonly arise?

A
  • Post Ganglionic Sympathetic Neurons

* Common in the Adrenal Medulla

93
Q

What are some clinical indicators of Neuroblastoma?

A
  1. Palpable Abdominal Mass
  2. Diastolic HTN
  3. VMA and HMA
94
Q

Who do we most commonly see Adrenal Cortical Adenomas in?

• Histological Appearance?

A

Mostly in women 30-50 years old = THESE ARE TYPICALLY NON-FUNCTIONAL

Histo:
• Neoplastic Cells are Vacuolated from Intracytoplasmic Lipid

95
Q

Where is adrenal cortical carcinoma most likely to metastasize to?

A
  • Adrenal Vein
  • Vena Cava
  • Lymph
96
Q

Are adrenal cortical carcinomas typically functional or non-functional?

A

• Typically these are functional

**Median survival is only 2 yrs

97
Q

Who most commonly gets pancreatic neuroendocrine tumors (NETs)?
• are these typically functioning or non-functioning?

A

Middle aged people get these and most (75%) are NON-FUNCTIONING

98
Q

What do you stain pancreatic NETs with?

A

Chromogranin A (carcinoid tumor stain) will stain these cells whether or not they are functional

99
Q

What hereditary disorders are associated with Pancreatic NETs?

A

MEN1
VHL syndrome
Neurofibromatosis
Tubular Sclerosis

100
Q

How are pancreatic NETs graded?

A
  1. Ki-67 stain

2. Number of Mitosis

101
Q

Glucagonoma

3 key findings

A

Anemia
Diabetes
Necrotic Migratory Erythema

102
Q

Somatostatinoma

3 key findings

A

Achlorhydria
Diabetes
Steatorrhea

103
Q

Cell type that gives rise to Gastrinomas?

A

G-cells (gastrin stimulates parietal cells)

104
Q

What is the most common functional Pancreatic NET?

A

Insulinoma

105
Q

What is the only pancreatic net that is NOT automatically considered malignant?

A

Insulinomas are the only ones considered not malignant

106
Q

VIPoma

3 key findings

A

Diarrhea
Hypokalemia and Acidosis
Hypovolemia

107
Q

How do people with Insulinomas often present?

A

EPISODIC sever hypoglycemia (often precipitated by Fasting or Excercise)

Labs will show a high insulin to glucagon ratio

108
Q

What Histological features are seen in Insulinomas?

A

• Abundant Amyloid in the Islets with a cord/nest configuration that is often separated by other tissue with a capsule

109
Q

Why might a child be born and immediately have a severe hypoglycemic episode?

A

Maternal Diabetes is often the cause because hyperglycemia in the mother leads to the need for the child to secrete more insulin

110
Q

Who gets Hyperinsulinism besides children born of mothers who have maternal DM?

A

People with Beckwith Wiedelmann Syndrome

People with mutations in the Beta cell Potassium Channel

111
Q

T or F: most people with Gastrinomas have Mets at the time of dx/

A

True

112
Q

What is the association of Gastrinomas and MEN?

A

MEN 1 is associated with gastinomas in 25% of gastrinoma cases

SO LOOK FOR CONCURRENT HYPERPARATHYROIDISM

113
Q

Who most often presents with a glucagonoma?

A

Peri/Post menopausal women with extremely high glucagon levels

114
Q

Why would people with somatostatinomas tend to get Cholelithiasis?

A

Inhibition of CCK prevents gallbladder contraction

115
Q

VIPomas are also known as WDHAs (watery diarrhea hypokalemia achlorhydria) syndrome is associated with what Neural Crest Tumors?

A

Neuroblastomas
Ganglioneuroblastomas
Ganglioneuromas
Pheochromocytomas

116
Q

What is the most common manifestation of MEN1?

• what is the most common cause of death?

A

Hyperparathryoidism

Most common cause of death:
•Pancreatic Tumors (remember gastrinomas (ZOLLIGER ELLISON SYNDROME), insulinomas)

117
Q

How do MEN2 A and B differ clinically?

A

MEN2A:
• Parathyroid Hyperplasia

MEN2B:
• Neuromas and ganglioneuromas
• Marfan’s-like-appearance

Endocrine (4 decks)

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