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Pathoma > Chapter 15 - Endocrine > Flashcards

Chapter 15 - Endocrine Flashcards

1
Q

How do you treat a prolactinoma?

A

Dopamine agonists! Specifically bromocriptine or cabergoline.

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2
Q

Common endocrine abnormality that develops with a growth hormone cell adenoma?

A

Secondary diabetes mellitus. Due to GH induced liver gluconeogenesis.

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3
Q

How to treat a Growth Hormone cell adenoma?

A

Octreotide, which is a somatostatin analog (somatostatin normally inhibits GH release).

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4
Q

What is Sheehan syndrome and how does it present?

A

Hypopituitarism following pregnancy, due to increased size of the gland and same amount of vasculature. Blood loss during parturition leads to infarction.

Presents as poor lactation and loss of pubic hair!

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5
Q

Common drugs that cause nephrogenic diabetes insipidus?

A

Lithium and demeclocycline (antibiotic)

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6
Q

Common cause of SIADH?

A

Small cell carcinoma of the lung

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7
Q

How to treat SIADH?

A

Water restriction or demeclocyline (induces Diabetes insipidus).

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8
Q

What type of embryologic remnant can present as an anterior neck mass?

A

A thyroglossal duct cyst (cystic dilation of thyroglossal duct remnant).

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9
Q

What type of embryologic remnant can present as a base of tongue mass?

A

Lingual thyroid!

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10
Q

What are the two main results of hyperthyroidism and how do they happen?

A
  1. Increased basal metabolic rate - increased synthesis of Na-K ATPase
  2. Increased sympathetic activity - increased expression of B1-adrenergic receptors
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11
Q

What changes in cholesterol and blood sugars are seen in hyperthyroidism?

A

Hypocholesterolemia and hyperglycemia (due to gluconeogenesis and glycogenolysis).

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12
Q

What is Graves disease?

A

Autoantibody that stimulates the TSH receptor (type II hypersensitivity).

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13
Q

What are the non-thyroid symptoms of Graves and what causes them?

A

Exophthalmos and pretibial myxedema.

Due to TSH receptors present on fibroblasts behind the eye and overlying the shin. Leads to glycosaminoglycan buildup, inflammation, fibrosis, and edema.

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14
Q

Irregular follicles with scalloped colloid and chronic inflammation on histo = ?

A

Graves disease

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15
Q

Treatment of Graves disease?

A

b-blockers, thioamide (blocks peroxidase necessary for synthesis of T3/T4), and radioiodine ablation.

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16
Q

How do you treat thyroid storm complication of Graves disease?

A

Give propythiouracil (PTU), which inhibits peroxidase (necessary for oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral conversion of T4 to T3). Also b-blockers and steroids.

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17
Q

What is Cretinism?

A

Hypothyroidism in neonates (presents as mental retardation, short stature, coarse facial features, enlarged tongue, umbilical hernia).

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18
Q

What is the most common cause of dyshormonogenetic goiter leading to cretinism?

A

Congenital defect involving thyroid peroxidase –> cannot make T4/T3!

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19
Q

What is Myxedema?

A

Hypothyroidism in older children/adults. See deepening of voice and large tongue due to accumulation of glycosaminoglycans in the skin and soft tissue.

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20
Q

What is Hashimoto Thyroiditis and what is it associated with?

A

Autoimmune destruction of the thyroid gland, associated with HLA-DR5

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21
Q

Chronic inflammation with germinal centers and Hurthle cells (eosiniphilic metaplasia of cells that line follicles) of the thryoid = ???

A

Hashimoto Thyroiditis

22
Q

What neoplasm is Hashimoto thyroiditis associated with?

A

Increased risk for B-cell (marginal zone) lymphoma.

23
Q

What often presents as a tender thyroid?

A

Subacute Granulomatous (De Quervain) thyroiditis. Follows a viral infection, presents as hyperthyroidism that is self-limited.

24
Q

What often presents with a “hard as wood”, nontender thyroid?

A

Reidel Fibrosing Thyroiditis.

Mimics anaplastic carcinoma, as fibrosis often spreads, but patients are younger and malignant cells are absent.

25
Q

How to biopsy the thyroid???

A

Fine Needle Aspiration!!!

26
Q

What distinguishes follicular adenoma from follicular carcinoma?

A

On surgical resection (NOT FNA), the proliferation does not invade through the capsule!

27
Q

Major risk factor for papillary carcinoma?

A

Exposure to ionizing radiation in childhood.

28
Q

How does follicular carcinoma often metastasize?

A

HEMATOGENOUSLY. Not lymphatics.

29
Q

Malignant cells in an amyloid stroma from thyroid = ???

A

Medullary Carcinoma!

30
Q

What does MEN2 present as?

A

Medullary Carcinoma
Pheochromocytoma
Parathyroid Adenomas (2A) or Ganglioneuromas of the oral mucosa (2B).

31
Q

What is mutated in MEN2? How is this used in clinical practice?

A

RET oncogene. If mutations present, prophylactic thyroidectomy warranted!

32
Q

How does hypercortisolism cause hypertension?

A

By increasing expression of alpha1 receptors on arteriolar walls.

33
Q

How can you distinguish an ACTH secreting pituitary adenoma from an ectopic ACTH producing small cell cancer of the lung?

A

Dexamethasone (cortisol analog) test. Cortisol should be suppressed if pituitary adenoma, but not if SCLC…

34
Q

What levels of aldo and renin are seen in primary hyperaldosteronism?

A

High Aldo and LOW renin…

35
Q

What is Conn syndrome?

A

Hyperaldosteronism

36
Q

What is Waterhouse-Friderichsen syndrome?

A

Hemorrhagic necrosis of the adrenal glands classically due to DIC following N meningitidis infection.

Lack of cortisol exacerbates hypotension, often leading to death.

37
Q

Three common causes of Addison’s disease?

A
  1. Autoimmune destruction
  2. Tb
  3. Metastatic carcinoma (from LUNG)
38
Q

What type of cells make up the adrenal medulla?

A

Neural crest-derived chromaffin cells.

39
Q

How to detect a pheochromocytoma?

A

Increased serum metanephrines and increased 24-hour urine metanephrines and vanillylmandelic acid (both breakdown products of catecholamines)

40
Q

How to treat pheochromocytoma?

A

Surgical removal (pre-treat with PHENOXYBENZAMINE).

41
Q

What syndromes is a pheochromocytoma associated with?

A
  • MEN 2A or 2B
  • von Hippel-Lindau disease
  • NF type 1
42
Q

Uncommon presentations of primary hyperparathyroidism include (5)

A
  1. Nephrolithiasis (calcium oxalate stones)
  2. Nephrocalcinosis (metastatic calcification of renal tubules)
  3. CNS (depression/seizures)
  4. Constipation, Peptic ulcers, and ACUTE PANCREATITIS
  5. Osteitis fibrosa cystica
43
Q

Lab findins with primary hyperparathyroidism?

A

Increased serum PTH, calcium, and alkaline phosphatase (from osteoblastic activity).

Decreased serum phosphate

Increased urinary cAMP! (as PTH coupled to Gs)

44
Q

What is Pseudohypoparathyroidism?

A

End-organ resistance to PTH, resulting in hypocalcemia with INCREASED PTH.

45
Q

Short stature, short 4/5th digits, hypocalcemia, and increased PTH?

A

AD congenital pseudohypoparathyroidism. Usually mutations in Gs that is attached to PTH.

46
Q

Insulin secreted from which cells found where in pancreas?

A

Beta-cells found in the center of islets of Langerhans.

47
Q

How does obesity lead to type II DM?

A

Obesity leads to a decreased number of insulin receptors.

48
Q

Amyloid deposition in the beta cells of pancreas = ???

A

Late finding with Type II DM. Beta cells exhausted.

49
Q

How are neurons damaged in type II DM?

A
  1. Glucose freely enters Schwann cells
  2. Aldose reductase converts glucose to sorbitol, leading to osmotic damage… decreased myelination. Aldose reductase also found in lens and pericytes of retinal blood vessels.
50
Q

What makes up MEN1?

A

Parathyroid hyperplasia, pituitary adenomas, and pancreatic neoplasms (often gastrin producing).

Pathoma (15 decks)

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