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USMLE > Endocrine - Pathology > Flashcards

Endocrine - Pathology Flashcards

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USMLE® Step 1 flashcards
1
Q

Symptoms of nonfunctional pituitary adenoma (3)

A

Mass effects

  1. headache
  2. bitemporal hemianopsia (compression of optic chiasm)
  3. hypopituitarism
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2
Q

Most common pituitary adenoma

A

prolactinoma

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3
Q

Prolactinoma: Presentation

A

Female: galactorrhea, amenorrhea
Males: decreased libido, headache

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4
Q

Prolactinoma: Treatment

A 
Dopamine agonists (bromocriptine, cabergoline)
Surgery for larger lesions
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5
Q

Growth hormone cell adenoma: Presentation

A

Children: gigantism (increased linear bone growth because epiphyses are not fused)

Adults: acromegaly

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6
Q

Acromegaly: Presentation

A

Enlarged bones of hands, feet, jaw
Coarse facial features
Growth of visceral organs leading to dysfunction (e.g. cardiac failure)
Enlarged tongue

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7
Q

What is often present with GH adenoma?

A

Secondary diabetes mellitus (induces liver gluconeogenesis)

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8
Q

Growth hormone cell adenoma: Diagnosis

A

Elevated GH/IGF-1
Lack of GH suppression by oral glucose
Pituitary mass on brain MRI

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9
Q

Growth hormone cell adenoma: Treatment

A

Octreotide (somatostatin analog)
GH receptor antagonists
surgery

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10
Q

Common cause of death in acromegaly

A

Heart failure from cardiomyopathy

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11
Q

ACTH cell adenoma: Presentation

A

Cushing syndrome

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12
Q

Causes of Hypopituitarism (5)

A
  1. Mass effect or pituitary apoplexy (bleeding): pituitary adenoma in adults and craniopharyngioma in children

2 Sheehan syndrome

  1. Empty sella syndrome
  2. Brain injury, hemorrhage
  3. Radiation
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13
Q

Sheehan syndrome: Presentation

A

Poor lactation, loss of pubic hair, fatigue

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14
Q

Sheehan syndrome: Mechanism

A

Pregnancy-related infarction of pituitary gland

Gland doubles in size during pregnancy but blood supply does not -> blood loss during parturition precipitates infarction

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15
Q

Empty sella syndrome: Presentation

A

absent (empty sella) pituitary gland on imaging

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16
Q

Empty sella syndrome: Mechanism

A

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

Common in obese women

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17
Q

Central diabetes insipidus: Presentation

A

Polyuria, Polydipsia with riks of life-threatening dehydration; intense thirst

ab: urine specific gravity < 1.006; serum osmolality > 290 mOsm/L
hypernatremia and high serum osmolality

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18
Q

Central diabetes insipidus: Mechanism

A

ADH deficiency (pituitary tumor, trauma, infection, inflammation)

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19
Q

Central diabetes insipidus: Diagnosis

A

Water deprivation test

Urine osmol does not increase, but respond to desmopressin

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20
Q

Central diabetes insipidus: Treatmet

A 
Intranasal desmopressin (ADH analog)
Adequate fluid intake
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21
Q

Nephrogenic diabetes insipidus: Treatment

A

HCTZ, indomethacin, amiloride

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22
Q

Nephrogenic diabetes insipidus: Mechanism

A

impaired response to ADH

Mutation or drugs (lithium an demeclocycline)

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23
Q

Nephrogenic diabetes insipidus: Presentation

A

Similar to central diabetes insipidus, but does not respond to desmopressin

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24
Q

SIADH: Presentation

A

Hyponatremia and low serum osmolality

Mental status changes and seizures (neuronal swelling and cerebral edema)

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25
Q

SIADH: Causes

A

Ectopic ADH (small cell lung cancer)
CNS disorder/head trauma
Pulmonary disease
Drugs (cyclophosphamide)

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26
Q

SIADH: Treatment

A

Fluid restriction, IV saline, conivaptan, tolvaptan, demeclocyline

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27
Q

Hyperthyroidism: Presentation (12)

A
  1. weight loss despite increased appetite
  2. heat intolerance/sweating
  3. tachycardia with increased CO
  4. arrhythmia (Afib) in elderly
  5. tremor, anxiety, insomnia, heightened emotions
  6. staring gaze with lid lag
  7. diarrhea with malabsorption
  8. oligomenorrhea
  9. bone resorption with hypercalcemia (osteoporosis)
  10. decreased muscle mass with weakness
  11. hypocholesterolemia
  12. hyperglycemia
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28
Q

Graves’ disease: Mechanism

A

Type II hypersensitivity

Autoantibody (IgG) stimulates TSH receptor -> increase syntehsis and release of thyroid hormone

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29
Q

Most common cause of hyperthyroidism

A

Gaves’ disease

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30
Q

Graves’ disease: Risk group

A

Women of childbearing age (20-40 years)

Often presents during stress (e.g. childbirth)

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31
Q

Graves’ disease: Presentation

A
  1. Hyperthyroidism
  2. Diffuse goiter (constant TSH stimulation leads to thyroid hyperplasia and hypertrophy)
  3. Exophthalmos and pretibial myxedema
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32
Q

Mechanism of exopthalmos and pretibial myxedema in Graves’ disease?

A

Fibroblasts behind orbit and overlying shin express TSH receptors

Glycosamnoglycan (chondroitin sulfate and hyaluronic acid) build up, inflammation, fibrosis, and edema

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33
Q

Graves’ disease: Histology and Lab

A

Irregular follicles with scalloped colloid and chronic inflammation

Lab: high total and free T4, hypocholesterolemia, increased serum glucose

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34
Q

Graves’ disease: treatment

A

Beta-blockers, thioamide, radioiodine ablation

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35
Q

Thyroid storm: Mechanism

A

Elevated catecholamines and massive hormone excess, usually in response to stress (surgery, childbirth)

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36
Q

Thyroid storm: Presentation

A

Arrhythmia, hyperthermia, and vomiting with hypovolemic shock

May also see increased ALP due to increased bone turnover

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37
Q

Thyroid storm: Treatment

A

PTU, beta-blockers, steroids

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38
Q

Multinodular goiter: Presentation and Cause

A

enlarged thyroid gland with multiple nodules, usually nontoxic
Due to relative iodine deficiency

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39
Q

Toxic multinodular goiter: Presentation and Malignancy

A

Focal patches of follicular cells working independently of TSH due to mutation in TSH receptor
Increased T3, T4
Rarely malignant

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40
Q

Jod-Basedow phenomenon

A

Thyrotoxicosis if patient with iodine deficiency goiter is made iodine replete

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41
Q

Cretinism: Mechanism and Causes

A

Hypothyroidism in neonates and infants

Causes: maternal hypothyroidism during early pregnancy, thyroid agenesis, dyshormonogenetic goiter, iodine deficiency

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42
Q

What is dyshormonogenetic goiter?

A

Congenital defect in thyroid hormone production - thyroid peroxidase

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43
Q

Cretinism: Presentation

A

Mental retardation, short stature with skeletal abnormalities, coarse facial features (puffy faced-child), enlarged tongue, umbilical hernia (pot bellied, protruding umbilicus), pale

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44
Q

Myxedema: Presentation (9)

A

Hypothyroidism in older children/adults

  1. Myxedema (accumulation of glycosaminoglycans in skin and soft tissue - deepening of voice and large tongue)
  2. weight gain despite normal appetite
  3. slowing of mental activity
  4. muscle weakness
  5. cold intolerance with decreased sweating
  6. bradycardia with decreased CO; SOB and fatigue
  7. oligomenorrhea
  8. hypercholesterolemia
  9. constipation
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45
Q

Most common causes of hypothyroidism

A

iodine deficiency and hashimoto thyroiditis

Others: drugs (lithium), surgical removal or radioablation of thyroid

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46
Q

Hashimoto thyroiditis: Mechanism

A

Autoimmune destruction of thyroid gland

HLA-DR5

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47
Q

Hashimoto thyroiditis: Presentation

A 
Initial hyperthyroidism (follicle damage)
Progresses to hypothyroidism (low T4 and high TSH)

Antithyroglobulin and antimicrosomal antibodies often present (signs of damage)

Moderately enlarged, non-tender, firm thyroid

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48
Q

Hashimoto thyroiditis: Histology

A

Chronic inflammation (lymphocytic infiltrate) with germinal centers and Hurthle cells (eosinophilic metaplasia of cells that line follicles)

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49
Q

Hashimoto thyroiditis: Complications

A

Increased risk of B-cell (marginal zone) lymphoma (presents as enlarging thyroid gland late in disease course)

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50
Q

Subacute granulomatous (de quervain) thyroiditis: Presentation

A

Granulomatous thyroiditis that follows viral infection
Tender thyroid with transient hyperthyroidism; jaw pain, increased ESR

Self-limited

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51
Q

Subacute granulomatous (de quervain) thyroiditis: Histology

A

multinucleated giant cells, histocytes, and lymphocytes (granulomatous inflammation)

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52
Q

Reidel fibrosing thyroiditis: Mechanism

A

Chronic inflammation with extensive fibrosis of thyroid gland
IgG4-related systemic disease

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53
Q

Reidel fibrosing thyroiditis: Presentation

A

Hypothyroidism with “hard as wood”, non-tender thyroid gland
May extend to involve local structures (airways)

Clinically mimic anaplastic carcinoma, but patients are younger (40s) and malignant cells are absent

54
Q

What are cold and hot nodules? Examples of each.

A

Hot nodule (increased uptake): Graves’ disease or nodular goiter

Cold nodules (decreased uptake): adenoma and carcinoma - warrant biopsy

131I radioactive uptake

55
Q

Follicular adenoma: Histology

A

Benign proliferation of follicles surrounded by fibrous capsule
Usually non-functional

56
Q

Most common type to thyroid carcinoma

A

Papillary carcinoma

57
Q

Papillary carcinoma: Risk factors

A

exposure to ionizing radiation in childhood (severe acne)

58
Q

Papillary carcinoma: Histology

A

Papillae lined by cells with clear ‘Orphan Annie eye’ nuclei (empty appearing nuclei) and nuclear grooves
Assocated with psammoma bodies

59
Q

Papillary carcinoma: Metastasis and Prognosis

A

Spread to cervical (neck) lymph nodes, but prognosis is excellent

60
Q

Follicular carcinoma: Histology

A

Malignant proliferation of follicles surrounded by fibrous capsule with invasion through capsule (FNA cannot make distinction between adenoma and carcinoma)

61
Q

Follicular carcinoma: Metastasis

A

Hematogenously

62
Q

Medullary carcinoma: Mechanism and Presentation

A

Malignant proliferation of parafollicular C cells (5% of thyroid carcinoma)
Can lead to hypocalcemia

63
Q

Medullary carcinoma: Histology

A

Sheets of malignant cells in amyloid stroma (calcitonin deposits within tumor as amyloid)

64
Q

Which hereditary diseases are associated with medullary carcinoma? And what mutation?

A

MEN2A and 2B
RET oncogene

Detection of RET mutation warrants prophylactic thyroidectomy

65
Q

Anaplastic carcinoma: Histology

A

undifferentiated malignant tumor of thyroid

66
Q

Anaplastic carcinoma: Presentation

A

Usually in elderly
Invades local structures, leading to dysphagia or respiratory compromise
Poor prognosis

67
Q

Most common cause of primary hyperparathyroidism

A 
Parathyroid adenoma (80%)
Sporadic parathyroid hyperplasia and carcinoma are less common causes
68
Q

Parathyroid adenoma: Presentation and Mechanism

A

Benign neoplasm, usually involving 1 gland

Results in asymptomatic hypercalcemia or symptomatic

69
Q

What are symptoms of hypercalcemia? (5)

A
  1. Nephrolithiasis (calcium oxalate stones)
  2. nephrocalcinosis: metastatic calcification of renal tubules leading to renal insufficiency and polyuria
  3. CNS disturbances (depression seizures)
  4. Constipation, peptic ulcer, acute pancreatitis
  5. Osteitis fibrosa cystica: resoprtion of bone leading to fibrosis and cystic spaces
70
Q

Parathyroid adenoma: Laboratory findings

A

High PTH, High calcium, Low phosphate

High urinary cAMP, High serum alkaline phosphatase

71
Q

Parathyroid adenoma: Treatment

A

Surgical removal

72
Q

Most common secondary hyperparathyroidism

A

Chronic renal failure
Decreased phosphate excretion -> increase phosphate binding to calcium -> decrease free calcium stimulates all 4 parathyroid glands

73
Q

Secondary hyperparathyroidism: Laboratory findings

A

High PTH, Low calcium, High phosphate, High alkaline phosphatase

74
Q

Hypoparathyroidism: Mechanism and Causes

A

Low PTH

Autoimmune damage, surgical excision, DiGeorge syndrome

75
Q

Hypoparathyroidism: Presentation and Lab

A

Presentation related to low serum calcium

Lab: Low PTH levels and low calcium

76
Q

Low serum calcium: Presentation

A
  1. Numbness and tingling (circumoral)

2. Muscle spasms (tetany) - Troussea sign (blood pressure cuff) and Chvostek sign (tapping on facial nerve)

77
Q

Pseudohypoparathyroidism: Presentation and Association

A

Autosomal dominant form: short stature and short 4/5th digits
End-organ resistance to PTH
Hypocalcemia with High PTH level

78
Q

Type 1 Diabetes mellitus: Mechanism

A

Insulin deficiency leading to hyperglycemia

Autoimmune destruction of beta ells by T lymphocytes (Type IV hypersensitivity) characterized by inflammation of islets

79
Q

Type 1 Diabetes mellitus: Genetics

A

HLA-DR3 and DR-4

Autoantibodies against insulin often present and may be seen years before clinical disease develops

80
Q

Type 1 Diabetes mellitus: Presentation

A

Age group: children <30
High serum glocuse
Weight loss, muscle loss, polyphagia
Polyuria, polydipsia, lipolysis, glucosuria

81
Q

Type 1 Diabetes mellitus: Treatment

A

lifelong insulin

82
Q

Diabetic ketoacidosis: Mechanism

A

Excessive serum ketones
Stress/Infection -> epinephrine stimulates glucagon secretion increasing lipolysis -> increase FFA -> converted to ketones

83
Q

Diabetic ketoacidosis: Presentation

A

Hyperglycemia (>300), anion gap metabolic acidosis, hyperkalemia
Kussmaul respirations, dehydration, nausea, vomiting, mental status changes, fruity smelling breath (acetone)

Depleted intracellular K+ due to transcellular shift from decreased insulin

84
Q

Diabetic ketoacidosis: Treatment

A

Fluids (correct dehydration), insulin and potassium

85
Q

Diabetic ketoacidosis: Complications

A

mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure

86
Q

Type 2 Diabetes mellitus: Mechanism and Prevalence

A

End-organ insulin resistance

Most common type of diabetes (90%); 5-10% of US population

87
Q

Type 2 Diabetes mellitus: Risk group

A 
Middle aged, obese adults
Family history (strong genetic predisposition)
88
Q

Progression of Diabetes Mellitus Type 2

A

Initial rise in insulin early, but later, insulin deficiency due to beta cell exhaustion (amyloid deposits in islets - AIAAP)

89
Q

Type 2 Diabetes mellitus: Presentation and Lab

A

Polyuria, polydipsia, hyperglycemia

Lab:
random glucose >200
fasting glucose >126
glucose tolerance test >200 2 hours after glucose loading

90
Q

Type 2 Diabetes mellitus: Treatment

A 
Weight loss (diet and exercise)
Drug therapy or exogenous insulin after exhaustion of beta cells
91
Q

Hyperosmolar non-ketotic coma

A 
High glucose (>500) leads to life-threatening diuresis with hypotension and coma
Ketones absent due to circulating insulin
92
Q

Type 2 Diabetes mellitus: Complications (Nonenzymati glycosylation)

A

Nonenzymatic glycosylation of vascular basement membrane

  • atherosclerosis (cardiovascular and peripheral vascular disease)
  • hyaline arteriolosclerosis of renal (preferentially efferent) progressing to nephrotic syndrome (Kimmelstiel-Wilson nodules)
  • glycated hemoglobin (HbA1C) marker of glycemic control
93
Q

Type 2 Diabetes mellitus: Complications (Osmotic damage)

A

Glucose enter Schwann cells, pericytes of retinal blood vessels and lens

Aldose reductase converts glucose to sorbitol, leading to osmotic damage

Peripheral neuropathy, impotence, blindness and cataracts

94
Q

What is the leading cause of death among diabetics?

A

Cardiovascular disease

95
Q

What is the leading cause of blindness in the developed world?

A

Diabetes

96
Q

Cushing syndrome: Mechanism

A

Excess cortisol

97
Q

Cushing syndrome: Presentation (6)

A
  1. muscle weakness with thin extremities (break down muscle for gluconeogenesis)
  2. Moon facies, buffalo hump, truncal obesity
  3. Abdominal striae (impaired synthesis of collagen)
  4. Hypertension
  5. Osteoporosis
  6. Immune suppression
98
Q

Cushing syndrome: Diagnosis

A

Diagnosis by 24-hour urine coritsol levels

99
Q

Cushing syndrome: Causes (4)

A
  1. exogenous corticosteroids (bilateral adrenal atrophy)
  2. Primary adrenal adenoma, hyperplasia or carcinoma - 15% (unilateral atrophy)
  3. ACTH-secreting pituitary adenoma -70% (bilateral hyperplasia)
  4. Paraneoplastic ACTH - 15% (e.g. small cell carcinoma) - bilateral hyperplasia
100
Q

What is the high-dose dexamethasone test?

A

Dexamethasone is a cortisol analog that suppresses ACTH production in pituitary adenoma but not in ectopic ACTH (cortisol remains high)

101
Q

Conn syndrome: Mechanism

A

Excess aldosterone, most commonly due to adrenal adenoma

102
Q

Conn syndrome: Presentation

A

Hypertension with hypernatremia, hypokalemia, metabolic alkalosis

103
Q

How to distinguish between primary and secondary hyperaldosteronism?

A

Both have high aldosterone, but primary hyperaldosteronism has low renin (high blood pressure downregulates renin)

104
Q

Examples of Secondary Hyperaldosteronism

A

Activation of renin-angiotensin

Renovascular hypertension, CHF, renal artery stenosis, nephrotic syndrome

105
Q

Primary Hyperaldosteronism: Treatment

A

Surgery to remove tumor

Spironolactone as aldosterone antagonist

106
Q

Secondary Hyperaldosteronism: Treatment

A

Spironolactone

107
Q

Adrenal insufficiency: Acute and Chronic Causes

A

Acute: Waterhouse-Friderichsen syndrome

Chronic: autoimmune, TB, metastitic carcinoma (lung)

108
Q

Addison’s disease: Presentation

A

Hypotension, hyponatremia, hypovolemia, hyperkalemia, weakness, hyperpigmentation (increased ACTH by-products stimulate melanocytic production of pigment), vomiting, diarrhea

109
Q

Waterhouse-Friderichsen syndrome: Mechanism

A

Hemorrhagic necrosis of adrenal glands, classically due to DIC in young children with N. meningitidis

Lack of cortisol exacerbates hypotension, often leading to death

110
Q

Addison’s disease: Mechanism

A

Primary adrenal insufficiency

Adrenal atrophy and absence of hormone production (all 3 cortical divisions)

111
Q

How is primary and secondary adrenal insufficiency differentiated?

A

Secondary adrenal insufficiency: low pituitary ACTH - no skin hyperpigmentation and no hyperkalemia

112
Q

Pheochromocytoma: Mechanism

A

Tumor of chromaffin cells

Increased serum catecholamines

113
Q

Pheochromocytoma: Presentation

A

Episodic hypertension, headache, palpitations, tachycardia, sweating

114
Q

Pheochromocytoma: Diagnosis

A

Increased serum metanephrines and increased 24-hour urine metanephrines and vanillymandelic acid

115
Q

Pheochromocytoma: Treatment

A

Surgical excision

Phenoxybenzamine (irreversible alpha-blocker) administered perioperatively to prevent hypertensive crisis

116
Q

What is Pheochromocytoma’s rule of 10?

A

10% bilateral
10% familial
10% malignant
10% outside of adrenal medulla (bladder wall or organ of Zuckerkandl at inferior mesenteric artery root)

117
Q

What hereditary conditions are associated with pheochromocytoma?

A

MEN 2A, 2B
Von hippel-lindau
Neurofibromatosis 1

118
Q

Neuroblastoma: Presentation

A

Occur anywhere along sympathetic chain

Elevated homovanillic acid in urine (breakdown product of dopamine)

119
Q

What gene is associated with neuroblastoma and tumor progression?

A

N-myc

120
Q

Carcinoid tumor: Mechanism

A

Carcinoid tumors (neuroendocrine cells), especially in small bowel which secretes high levels of serotonin.

No carcinoid syndrome if within GI tract (first-pass metabolism in liver)

121
Q

Carcinoid syndrome: Presentation

A

Recurrent diarrhea, cutaneous flushing, asthmatic wheezing, R sided valvular disease

Increased 5-HIAA in urine, niacin deficiency

122
Q

Carcinoid syndrome: Treatment

A

Somatostatin analog (Octreotide)

123
Q

What is the most common tumor fo the appendix?

A

Carcinoid tumor

124
Q

What is carcinoid tumor/s rule of 1/3

A

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

125
Q

Zollinger-Ellison syndrome: Mechanism

A

Gastrin-secreting tumor of pancreas or duodenum

126
Q

Zollinger-Ellison syndrome: Histology

A

Stomach shows rugal thickening with acid hypersecretion

Can cause recurrent ulcers

127
Q

What hereditary disorder is associated with Zollinger-Ellison syndrome?

A

MEN 1

128
Q

MEN 1 (Wermer’s syndrome): Presentations

A 
Pituitary tumor (prolactin/GH)
Parathyroid tumor
Pancreatic tumor (ZE, insulinoma, VIPoma, glucagonoma)

Kidney stones and stomach ulcers

129
Q

MEN 2A (Sipple’s syndrome: Presentations

A

Medullary thyroid carcinoma
Pheochromocytoma
Parathyroid tumors

130
Q

MEN 2B: Presentations

A

Medullary thyroid carcinoma
Pheochromocytoma
Oral/intestinal ganglioneuromatosis
(associated with marfanoid habitus)

USMLE (13 decks)

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