Endo-PATOHMA Flashcards

1
Q

Sheehan syndrome

  • etiology
  • presentations (4)
A
  • ischemic infarct of pituitary due to postpartum heavy bleeding => hypopituitarism
  • presentations
    1. lack of lactation (PRL)
    2. loss of pubic hair (LH)
    3. absent mensturation (FSH/LH)
    4. cold intolerance (TSH)
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2
Q

Physical exam finding in thyroglossal duct cyst?

A

anterior neck mass

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3
Q

How does T3/T4 increases basal metabolic rate? what about increasing heart rate/contractility?

A
  • BMR: increased activity of Na+/K+ ATPase
  • > increased O2 consumption
  • HR: increased level of beta 1 adrenergic receptors
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4
Q

Describe histologic finding of Graves disease

A

scalloped colloid
: white dots on the periphery of colloid

  • PATHOMA p. 161
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5
Q

Multinodular goiter: nontoxic vs. toxic

  • compare each
  • which one is more common?
A
  • nontoxic: cold nodule (euthyroid)
  • toxic: hot nodule (hyperthyroidism)
  • nontoxic is more common
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6
Q

HLA in Hashimotto?

A

HLA-DR 3 and 5

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7
Q

Hashimotto is associated with increased risk for development of what cancer?

A

non-hodgkin B cell lymphoma

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8
Q

Reidel fibrosing thyroiditis vs. Anaplastic thyroid carcinoma: similarity and difference?

A
  • they both show fibrosis that may involve other structures ( airway for example)
  • Riedel thyroiditis presents in young patients, IgG4 related systemic diseases (acute pancreatitis for example)
  • Anaplastic thyroid carcinoma presents in old patients, no association with IgG4
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9
Q

Follicular adenoma vs. Follicular carcinoma

  • key histologic finding for both?
  • Difference between two? can FNA do it?
A
  • follicles within fibrous capsule
  • follicles not invading fibrous capsule in adenoma, while invasion is seen in carcinoma.
  • FNA is taking small malignant cells, so FNA alone will not be sufficient to visualize invasion. Gross examination is required.
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10
Q

ionizing radiation in childhood: what thyroid cancer may develop?

A

papillary thyroid carcinoma

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11
Q

RET mutation detection warrants what procedure for prevention of familial MEN2A/MEN2B cancer?

A

Detection of RET mutation pretty much guarantees development of medullary thyroid carcinoma (which makes sense as it presents in BOTH MEN2A and MEN2B)
=> prophylactic thyroidectomy is indicated

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12
Q

hyperparathyroidism: How does it change the level of
- urinary cAMP
- serum ALP
Explain physiology

A
  • increased urinary cAMP
    : PTH binds to its receptor -> Gs -> cAMP pathway
  • increased ALP
    : PTH promotes osteoblast (which subsequently releases RANK-L, which activates osteoclast)
    => bone destruction and bone synthesis occurs
    => increased ALP (marker for bone synthesis)
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13
Q

What is the most common cause of secondary hyperparathyroidism

A

chronic renal failure

=> hyperphosphatemia and hypocalcemia (excess phosphate binds to Ca2+, reducing free Ca2+)

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14
Q

pseudohypoparathyroidism

  • inheritance pattern
  • PTH level? serum Ca2+ level?
  • molecular mechanism
  • physical exam finding
A
  • autosomal dominant
  • high PTH (why it is pseudo), low Ca2+
  • Gs mutation (remember PTH utilizes Gs pathway)
  • > peripheral tissues are PTH resistance
  • short statue, short 4th/5th digits
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15
Q

Where beta cells are located in pancreatic islets?

A

center

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16
Q

Type 1 DM vs. Type 2 DM: genetic predisposition?

A

Type 2 DM has higher genetic predisposition than type 1

17
Q

Type 1 DM vs. Type 1 DM: islet histology?

A

Type 1 DM: inflammatory infiltrates (autoimmune destruction)

Type 2 DM: amyloid (amylin) deposition

18
Q

Three tissue types that are vulnerable to osmotic damage in diabetes? why?

A
  • kidney
  • retina-> cataracts
  • schawann cells-> peripheral neurophathy
  • These three cell types lack sorbitol dehydrogenase, leading to accumulation of sorbitol -> osmotic damage

glucose -> sorbitol -> fructose

  • first rxn: aldose reductase (NADPH dependent)
  • second rxn: sortibol dehydrogenase
19
Q

Waterhouse-Friderichsen syndrome: gross appearance of adrenal glands?

A

hemorrhagic necrosis

20
Q

What primary cancer can goes to adrenal gland as metastasis? what is consequence of this metastasis?

A

lung cancer

can cause adrenal insufficiency (it is just chunk of tumor cells with no adrenal gland function)

21
Q

Embryological origin of chromaffin cells of adrenal medulla?

A

neural crest

MOTEL PASS, E- Enterochormaffin, which is not exactly same as chormaffin cells, but whatever. chromaffin,

22
Q

Patient develops tachycardia, diaphoresis, headache during urination? what is going on?

A

pheochromocytoma located in bladder wall (10% of pheo indeed is located outside of adrenal medulla, bladder wall is the most common site)