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USMLE 1 > Endocrinology- Pathology (2) > Flashcards

Endocrinology- Pathology (2) Flashcards

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USMLE® Step 1 flashcards
1
Q

Diagnosing parathyroid disease

A

Pag. 339

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2
Q

Hypoparathyroidism

  • Etiology
  • Findings
A

Due to accidental surgical excision of parathyroid glands, autoimmune destruction, or DiGeorge syndrome.

Findings: tetany, hypocalcemia, hyperphosphatemia

Chvostek sign—tapping of facial nerve (tap the Cheek) contraction of facial muscles.
Trousseau sign—occlusion of brachial artery with BP cuff (cuff the Triceps) Ž carpal spasm.

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3
Q

Pseudohypoparathyroidism type 1A

A

unresponsiveness of kidney to PTH Ž hypocalcemia
despite high PTH levels.

Constellation of physical findings known as Albright hereditary osteodystrophy: shortened 4th/5th digits, short stature, obesity, developmental delay. Autosomal
dominant.

Due to defective Gs protein α-subunit causing end-organ resistance to PTH. Defect must be inherited from mother due to imprinting

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4
Q

Pseudopseudohypoparathyroidism

A

physical exam features of Albright hereditary osteodystrophy but without end-organ PTH resistance (PTH level normal). Occurs when defective Gs protein α-subunit is inherited from father.

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5
Q

Primary hyperparathyroidism

  • Etiology
  • Findings
A

Usually due to parathyroid adenoma or hyperplasia.

Hypercalcemia, hypercalciuria (renal stones), polyuria (thrones), hypophosphatemia, high PTH, high ALP, high cAMP in urine.

May present with weakness and constipation (groans), abdominal/flank pain, neuropsychiatric disturbances (“psychiatric overtones”).

“Stones, thrones, bones, groans, and psychiatric overtones.”

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6
Q

Secondary hyperparathyroidism

A

2° hyperplasia due to low Ca2+ absorption and/or high PO4, most often in chronic renal disease.

Hypocalcemia, hyperphosphatemia in chronic renal failure (vs hypophosphatemia with most other causes), high ALP, high PTH.

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7
Q

Tertiary hyperparathyroidism

A

Refractory (autonomous) hyperparathyroidism
resulting from chronic renal disease. High PTH,
HighCa2+.

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8
Q

Osteitis fibrosa cystica

A

cystic bone spaces filled with brown fibrous tissue (“brown tumor” consisting of osteoclasts and deposited
hemosiderin from hemorrhages; causes bone pain).

Due to High PTH, classically associated with 1° (but also seen with 2°) hyperparathyroidism.

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9
Q

Renal osteodystrophy

A

renal disease Ž 2° andb3° hyperparathyroidism Ž bone lesions.

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10
Q

Familial hypocalciuric hypercalcemia

A

Defective G-coupled Ca2+-sensing receptors in multiple tissues (eg, parathyroids, kidneys).

Higher than normal Ca2+ levels required to suppress PTH. Excessive renal Ca2+ reuptake Ž mild hypercalcemia and hypocalciuria with normal to high PTH levels.

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11
Q

Nelson syndrome

A

Enlargement of existing ACTH-secreting pituitary adenoma after bilateral adrenalectomy for refractory Cushing disease.

Presents with hyperpigmentation, headaches and bitemporal hemianopia.

Treatment: pituitary irradiation or surgical resection.

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12
Q

Acromegaly

  • Etiology
  • Findings
A

Excess GH in adults. Typically caused by pituitary adenoma.

Large tongue with deep furrows, deep voice, large hands and feet, coarsening of facial features with aging, frontal bossing, diaphoresis (excessive sweating), impaired glucose tolerance (insulin resistance), hypertension. Risk of colorectal polyps and cancer.

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13
Q

Acromegaly

- Diagnosis

A

High serum IGF-1; failure to suppress serum GH following oral glucose tolerance test; pituitary mass seen on brain MRI.

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14
Q

Acromegaly

- Treatment

A

Pituitary adenoma resection. If not cured, treat with octreotide (somatostatin analog) or pegvisomant (growth hormone receptor antagonist), dopamine agonists (eg, cabergoline)

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15
Q

Laron syndrome

dwarfism

A

Defective growth hormone receptors Ž decrease linear growth. High GH, Low IGF-1.

Clinical features: short height, small head circumference, characteristic facies with saddle nose and prominent forehead, delayed skeletal maturation, small genitalia.

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16
Q

Diabetes insipidus

  • Clinical features
  • Etiology
  • General findings
A

Characterized by intense thirst and polyuria with inability to concentrate urine due to lack of ADH (central) or failure of response to circulating ADH (nephrogenic).

Urine specific gravity < 1.006
Serum osmolality > 290 mOsm/kg
Hyperosmotic volume contraction

17
Q

Central DI

  • Etiology
  • Findings
  • Water deprivation test
  • Treatment
A

Pituitary tumor, autoimmune, trauma, surgery, ischemic encephalopathy, idiopathic

Low ADH

> 50% increase in urine osmolality only after administration of ADH analog.

Desmopressin + Hydration

18
Q

Nephrogenic DI

  • Etiology
  • Findings
A

Hereditary (ADH receptor mutation), 2° to hypercalcemia, hypokalemia, lithium, demeclocycline (ADH antagonist).

Normal or High ADH levels

19
Q

Nephrogenic DI

  • Water deprivation test
  • Treatment
A

Minimal change in urine osmolality, even after administration of ADH analog.

HCTZ, indomethacin, amiloride + Hydration, dietary salt restriction, avoidance of offending agent

20
Q

Water deprivation test

A

No water intake for 2–3 hr followed by hourly measurements of urine volume and osmolality and plasma Na+ concentration and osmolality.

ADH analog (desmopressin) is administered if serum osmolality > 295–300 mOsm/kg, plasma Na+ ≥ 145
mEq/L, or urine osmolality does not rise despite a rising plasma osmolality
21
Q

Syndrome of inappropriate antidiuretic hormone secretion

- Characterized by

A

ƒƒ Excessive free water retention
ƒƒ Euvolemic hyponatremia with continued urinary Na+ excretion.
ƒƒ Urine osmolality > serum osmolality

22
Q

Why SIADH an eouvolemic hyponatremia?

A

Body responds to water retention with decrease aldosterone and high ANP and BNP Ž increase urinary Na+ secretion Ž normalization of extracellular fluid volume Ž euvolemic hyponatremia.

23
Q

SIADH causes include:

A

ƒƒ Ectopic ADH (eg, small cell lung cancer)
ƒƒ CNS disorders/head trauma
ƒƒ Pulmonary disease
ƒƒDrugs (eg, cyclophosphamide

24
Q

SIADH treatment

A

Treatment: fluid restriction (first line), salt tablets, IV hypertonic saline, diuretics, conivaptan, tolvaptan, demeclocycline.

*Increased urine osmolality during water deprivation test indicates psychogenic polydipsia.

25
Q

Hypopituitarism

- etiology

A

Nonsecreting pituitary adenoma, craniopharyngioma

Sheehan syndrome

Empty Sella syndrome

Pituitary apoplexy

Brain injury

Radiation

26
Q

Empty sella syndrome

Pituitary apoplexy

A

atrophy or compression of pituitary (which lies in the sella turcica), often idiopathic, common in obese women; associated with idiopathic intracranial hypertension.

sudden hemorrhage of pituitary gland, often in the presence of an existing pituitary adenoma. Usually presents with sudden onset severe headache, visual impairment, and features of hypopituitarism.

27
Q

Hyperosmolar hyperglycemic state

- Diagnosis

A

Labs: hyperglycemia (often > 600 mg/dL), high serum osmolality (> 320 mOsm/kg), no acidosis (pH > 7.35, ketone production inhibited by presence of insulin).

28
Q

Glucagonoma

  • clinical features
  • Treatment
A

Presents with dermatitis (necrolytic migratory erythema), diabetes (hyperglycemia), DVT, declining weight, depression.

Treatment: octreotide, surgery

29
Q

Insulinoma

  • Clinical Features
  • Labs
  • Treatment
A

May see Whipple triad: low blood glucose, symptoms of hypoglycemia (eg, lethargy, syncope, diplopia), and resolution of symptoms after normalization of glucose levels.

Symptomatic patients have low blood glucose and
high C-peptide levels (vs exogenous insulin use).

∼ 10% of cases associated with MEN 1 syndrome.

Treatment: surgical resection.

30
Q

Somatostatinoma

  • Clinical features
  • Treatent
A

Decrease secretion of secretin, cholecystokinin, glucagon, insulin, gastrin, gastric inhibitory peptide (GIP).

May present with diabetes/glucose intolerance, steatorrhea, gallstones, achlorhydria.

Treatment: surgical resection; somatostatin analogs (eg, octreotide) for symptom control.

31
Q

Carcinoid syndrome

- Etiology

A

Rare syndrome caused by carcinoid tumors (neuroendocrine cells; note prominent rosettes), especially metastatic small bowel tumors, which secrete high levels of serotonin (5-HT). Not seen if tumor is
limited to GI tract (5-HT undergoes first-pass metabolism in liver).

32
Q

Carcinoid syndrome

  • Clinical features
  • Labs
  • Treatment
A

Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right-sided valvular heart disease (tricuspid regurgitation, pulmonic stenosis).

5-hydroxyindoleacetic acid (5‑HIAA) in urine, niacin deficiency (pellagra). Associated with neuroendocrine tumor markers chromogranin A and synaptophysin.

Treatment: surgical resection, somatostatin analog (eg, octreotide).

33
Q

Carcinoid syndrome

- Rule of 1/3s:

A

1/3 metastasize
1/3 present with 2nd malignancy
1/3 are multiple

Most common malignancy in the small intestine

34
Q

Zollinger-Ellison syndrome

  • Clinical features
  • Diagnosis
A

Acid hypersecretion causes recurrent ulcers in duodenum and jejunum. Presents with abdominal pain, diarrhea (malabsorption).

Positive secretin stimulation test: gastrin levels remain
elevated after administration of secretin, which normally inhibits gastrin release.

May be associated with MEN 1.

35
Q

Multiple endocrine neoplasias

A

“All MEN are dominant” (autosomal dominant)

36
Q

MEN 1

A

3 Ps:
Pituitary tumors (prolactin or GH)
Pancreatic endocrine tumors
Parathyroid adenomas

Associated with mutation of MEN1 (menin, a tumor suppressor, chromosome 11), angiofibromas, collagenomas, meningiomas

37
Q

MEN 2A

A

2 Ps:
Parathyroid hyperplasia
Medullary thyroid carcinoma
Pheochromocytoma (secretes catecholamines)

Associated with mutation in RET (codes for receptor tyrosine kinase) in cells of neural crest origin.

38
Q

MEN 2B

A

1 P:
Medullary thyroid carcinoma
Pheochromocytoma
Mucosal neuromas (oral/intestinal ganglioneuromatosis)

Associated with marfanoid habitus; mutation in RET gene

USMLE 1 (73 decks)

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