Endocrine - Pathology (Part 2) Flashcards Preview

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Flashcards in Endocrine - Pathology (Part 2) Deck (136)
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1
Q

What is the risk of the nodules in a toxic multinodular goiter becoming malignant?

A

None; the nodules in a toxic multinodular goiter are not malignant

2
Q

What mutation is responsible for the activity of the follicles in a toxic multinodular goiter?

A

A mutation in the thyroid-stimulating hormone receptor makes these cells function independently of thyroid-stimulating hormone

3
Q

What is the Jod-Basedow phenomenon?

A

Thyrotoxicosis when a patient with endemic goiter moves to an iodine-replete area

4
Q

Which thyroid cancer is the most common?

A

Papillary carcinoma

5
Q

Which thyroid cancer has the best prognosis?

A

Papillary carcinoma

6
Q

What are the histological findings of papillary carcinoma of the thyroid?

A

Psammoma bodies, "ground-glass" nuclei (Orphan Annie), nuclear grooves

7
Q

Place the following thyroid cancers in order from best to worst prognosis: follicular, undifferentiated/anaplastic, and papillary.

A

Papillary, follicular, and undifferentiated/anaplastic

8
Q

Medullary carcinoma of the thyroid originates from which cells?

A

Parafollicular C cells

9
Q

Medullary carcinoma of the thyroid produces what substance?

A

Calcitonin

10
Q

What are the histological findings of medullary carcinoma of the thyroid?

A

Sheets of cells in amyloid stroma

11
Q

Medullary carcinoma of the thyroid is associated with what two genetic syndromes?

A

Multiple endocrine neoplasia types 2A and 2B

12
Q

Undifferentiated/anaplastic carcinoma of the thyroid is most commonly found in what population?

A

Older patients

13
Q

What type of cancer is associated with Hashimotos thyroiditis?

A

Lymphoma of the thyroid

14
Q

What risk factor is associated with papillary carcinoma of the thyroid?

A

Childhood irradiation

15
Q

What mnemonic illustrates the causes of hypercalcemia?

A

Calcium ingestion, Hyperparathyroidism, Hyperthyroidism, Iatrogenic (thiazides), Multiple myeloma, Pagets disease, Addisons disease, Neoplasms, Zollinger-Ellison syndrome, Excess vitamin D, Excess vitamin A, Sarcoidosis (remember: CHIMPANZEES)

16
Q

What is the most common cause of primary hyperparathyroidism?

A

A parathyroid adenoma

17
Q

What are the relative levels of parathyroid hormone, calcium, phosphate, and alkaline phosphatase in primary hyperparathyroidism?

A

Increased parathyroid hormone, calcium, and alkaline phosphatase and decreased phosphate

18
Q

What is the classic triad of symptoms in primary hyperparathyroidism?

A

When present, symptoms include weakness, constipation, and renal stones (remember: stones, bones, and groans)

19
Q

What is the mechanism by which a patient develops secondary hyperparathyroidism?

A

Decreased calcium absorption from the gut and increased levels of phosphate lead to secondary hyperplasia of the parathyroid gland

20
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic renal disease

21
Q

What are the relative levels of parathyroid hormone, calcium, phosphate, and alkaline phosphatase in secondary hyperparathyroidism?

A

Increased parathyroid hormone, phosphate, and alkaline phosphatase, and decreased serum calcium

22
Q

How does chronic renal disease contribute to secondary hyperparathyroidism?

A

Renal failure leads to decreased activation of vitamin D which, in turn, leads to decreased absorption of calcium from the gut

23
Q

What is the bone pathology associated with osteitis fibrosa cystica?

A

Cystic bone spaces filled with brown fibrous tissue causing pain; due to elevated levels of parathyroid hormone

24
Q

What bone pathology might you see in a dialysis patient?

A

Renal osteodystrophy, caused by secondarily elevated parathyroid hormone levels

25
Q

What neuromuscular finding is common among patients with hypoparathyroidism?

A

Tetany, secondary to hypocalcemia

26
Q

Following thyroid surgery, a patient presents with muscle spasms; what electrolyte abnormality is likely present?

A

Hypoparathyroidism and resultant hypocalcemia

27
Q

List three causes of hypoparathyroidism.

A

Accidental surgical excision (thyroid surgery), autoimmune destruction and DiGeorges syndrome

28
Q

Upon tapping the facial nerve, a patient has twitching in the ipisilateral facial muscles; what is the sign?

A

Chvosteks sign, indicating hypocalcemia

29
Q

After occluding the brachial artery with a blood pressure cuff, your patient has spasms in the wrist; what is the name of the sign?

A

Trousseaus sign, indicating hypocalcemia

30
Q

What is the name of the condition in which the kidneys are unresponsive to parathyroid hormone?

A

Pseudohypoparathyroidism, a genetic condition

31
Q

In what manner is pseudohypoparathyroidism inherited?

A

Autosomal dominant

32
Q

A patient with hypocalcemia is of short stature and has shortened fourth/fifth digits. What genetic condition should be considered?

A

Pseudohypoparathyroidism, also known as Albright hereditary osteodystrophy

33
Q

Would parathyroid hormone be increased or decreased in pseudohypoparathyroidism?

A

Increased; since the end-organ targets are resistant to the hormone, serum calcium levels will remain low, causing increased secretion of parathyroid hormone.

34
Q

What is the most common type of pituitary adenoma?

A

Prolactinoma

35
Q

A patient complains of amenorrhea, galactorrhea, and low libido. She has been trying to get pregnant for 3 years. What tumor should be considered?

A

Prolactinoma

36
Q

What is the medical treatment for a prolactinoma?

A

Bromocriptine or cabergoline (dopamine agonists)

37
Q

A 40-year-old patient presents with a headache and cannot see on the temporal sides of his visual fields; what should you look for?

A

Brain imaging may reveal a pituitary adenoma, which can impinge on the optic chiasm and cause bitemporal hemianopsia

38
Q

Acromegaly is the result of an excess of what hormone?

A

Growth hormone

39
Q

Excess growth hormone in children causes what disease?

A

Gigantism (increased linear bone growth)

40
Q

A 50-year-old patient has a large tongue with deep furrows, a deep voice, large hands and feet, and coarse facial features; what is the likely diagnosis?

A

Acromegaly

41
Q

What is the treatment of acromegaly?

A

Pituitary adenoma resection followed by octreotide administration

42
Q

A patient has an elevated growth hormone level; what are three situations in which this increase in growth hormone production is normal?

A

Stress, exercise, and hypoglycemia

43
Q

How is acromegaly diagnosed with lab tests?

A

Increased insulin-like growth factor-1 or failure to suppress serum growth hormone following oral glucose tolerance test

44
Q

What causes Sheehans syndrome?

A

Postpartum infarction of the anterior pituitary gland following severe bleeding during delivery

45
Q

Why are pregnant women more susceptible to pituitary infarction?

A

An increased number of lactotrophs without an increase in the blood supply to the anterior pituitary

46
Q

A postpartum patient has fatigue, anorexia, difficulty lactating, and thin sparse pubic and axillary hair; what is the likely diagnosis?

A

Postpartum hypopituitarism, or Sheehans syndrome

47
Q

A patients comes to the emergency room with intense thirst, polyuria, and very dilute urine; what endocrine disorder should be on your differential?

A

Diabetes insipidus

48
Q

What is the primary defect in central diabetes insipidus?

A

Lack of antidiuretic hormone production

49
Q

What is the primary defect in nephrogenic diabetes?

A

Lack of renal response to antidiuretic hormone

50
Q

What are some causes of central diabetes insipidus?

A

Pituitary tumor, trauma, surgery, histocytosis X

51
Q

What are some causes of nephrogenic diabetes insipidus?

A

Hereditary or secondary to hypercalcemia, lithium, demeclocycline

52
Q

What test is used to diagnose diabetes insipidus?

A

Water deprivation test (urine osmolality does not increase even with low fluid intake)

53
Q

How does the urine-specific gravity help diagnose patients with diabetes insipidus?

A

It is low, often below 1.006 g/mL

54
Q

How does the serum osmolality help diagnose patients with diabetes insipidus?

A

It is high, often above 290 mOsm/L

55
Q

What lifestyle change can be used to manage both central and nephrogenic diabetes insipidus?

A

Adequate fluid intake

56
Q

What treatment is specifically used for central diabetes insipidus?

A

Intranasal desmopressin, an antidiuretic hormone analog

57
Q

Name three drugs used in the treatment of nephrogenic diabetes insipidus.

A

Hydrochlorothiazide, indomethacin, and amiloride

58
Q

How can one distinguish between central and nephrogenic DI?

A

Administration of desmopressin. In central diabetes insipidus symptoms will improve with exogenous antidiuretic hormone; in nephrogenic diabetes insipidus the kidneys are resistant to antidiuretic hormone and addition of antidiuretic hormone will have no effect

59
Q

A patient with pneumonia is found to be hyponatremic with high urine osmolarity and low serum osmolarity; what is the likely diagnosis?

A

Syndrome of inappropriate antidiuretic hormone secretion

60
Q

In patients with syndrome of inappropriate antidiuretic hormone secretion, there is excessive retention of what substance in the kidneys?

A

Water

61
Q

What serum electrolyte abnormality is characteristic of syndrome of inappropriate antidiuretic hormone secretion?

A

Hyponatremia

62
Q

What neurologic condition is associated with severe hyponatremia?

A

Seizures; hyponatremia must be corrected slowly to avoid central pontine myelinolysis

63
Q

How do you treat a patient with syndrome of inappropriate antidiuretic hormone secretion?

A

Water restriction or demeclocycline are the treatments for syndrome of inappropriate antidiuretic hormone secretion

64
Q

Give an example of an ectopic source of antidiuretic hormone.

A

Small cell lung cancer (paraneoplastic syndrome)

65
Q

Name four causes of syndrome of inappropriate antidiuretic hormone secretion.

A

Ectopic antidiuretic hormone (small cell lung cancer), central nervous system disorders/head trauma, pulmonary diseases, drugs (eg, cyclophosphamide)

66
Q

List four acute manifestations that can be seen in both type 1 and 2 diabetes mellitus.

A

Polydipsia, polyuria, polyphagia, and weight loss

67
Q

________ ________ is an acute manifestation of type 1 diabetes; it is not generally seen in type 2 diabetes.

A

Diabetic ketoacidosis

68
Q

_____ _____ is an acute manifestation of type 2 diabetes; it is not generally seen in type 1 diabetes.

A

Hyperosmolar coma

69
Q

What three direct effects on cellular metabolism can a diabetic insulin deficiency create?

A

Decreased glucose uptake, increased protein catabolism, and increased lipolysis

70
Q

What are the effects of decreased cellular glucose uptake?

A

Hyperglycemia, glycosuria, osmotic diuresis, and electrolyte depletion

71
Q

List two direct effects of increased protein catabolism in diabetes.

A

Increased plasma amino acids and nitrogen loss in urine

72
Q

In diabetes, what process directly causes ketogenesis and increased plasma free fatty acids?

A

Increased lipolysis

73
Q

In diabetic patients, what is the underlying mechanism of dehydration?

A

Hyperglycemia overwhelms the ability of the renal tubules to reabsorb glucose leading to increased glucose in the urine; this, in turn, leads to osmotic diuresis and dehydration

74
Q

Why are patients with uncontrolled diabetes often acidemic?

A

Ketone bodies are acids, and osmotic diuresis causes lactic acidosis by decreased intravascular volume and decreased perfusion of the vital organs

75
Q

Failure to treat a diabetic patient who is severely volume depleted and has a low serum pH may result in what?

A

Coma and death

76
Q

The chronic manifestations of diabetes can be broken down into what two categories on the basis of pathogenesis?

A

Nonenzymatic glycosylation and osmotic damage

77
Q

In patients with diabetes, the chronic manifestations of nonenzymatic glycosylation can be broken down into what two categories?

A

Small-vessel disease and large-vessel disease

78
Q

You are looking at histological samples from a patient with longstanding diabetes mellitus; what do you expect to see in the small vessels?

A

A diffuse thickening of basement membrane

79
Q

List three pathologic processes caused by small-vessel disease in patients with diabetes.

A

Retinopathy, glaucoma, and nephropathy

80
Q

What might you see on fundoscopic exam of a patient with longstanding diabetes mellitus?

A

Hemorrhages, exudates, microaneurysms, and vessel proliferation

81
Q

List four forms of renal disease that can occur as a result of diabetic nephropathy.

A

Nodular sclerosis, progressive proteinuria, chronic renal failure, and arteriosclerosis leading to hypertension

82
Q

Name three specific vascular diseases that can result from large vessel atherosclerosis as a result of diabetes.

A

Coronary artery disease, peripheral vascular occlusive disease and gangrene, and cerebrovascular disease

83
Q

In patients with chronic diabetes, osmotic damage can cause what two disease states?

A

Neuropathy and cataracts

84
Q

Does diabetic neuropathy affect the motor, sensory, or autonomic nervous systems?

A

Diabetic neuropathy can affect motor, sensory, and autonomic nerves

85
Q

What accumulates in the lens to cause cataracts in patients with diabetes mellitus?

A

Sorbitol, due to high circulating glucose levels

86
Q

What three glucose-related tests are diagnostically useful for diabetes?

A

Fasting serum glucose, glucose tolerance, and glycosylated hemoglobin (HbA1c)

87
Q

Which blood test is used to monitor long-term diabetic control?

A

Glycosylated hemoglobin (HbA1c)

88
Q

What is the underlying etiology of type 1 diabetes mellitus?

A

The viral or immune destruction of -cells

89
Q

What is the underlying etiology of type 2 diabetes mellitus?

A

Increased resistance to insulin

90
Q

Insulin is always necessary for the treatment of which type of diabetes mellitus?

A

Type 1 diabetes mellitus; it is sometimes necessary to treat type 2 diabetes mellitus

91
Q

What age group is most commonly affected by type 1 diabetes mellitus?

A

Individuals who are less than 30 years old

92
Q

What age group is most commonly affected by type 2 diabetes mellitus?

A

Individuals who are greater than 40 years old

93
Q

Which form of diabetes mellitus has an association with obesity?

A

Type 2 diabetes is associated with obesity

94
Q

Whereas diabetes mellitus always has a polygenic inheritance, familial history is a strong predictor in type _____ and weak in type _____ diabetes.

A

Type 2; type 1

95
Q

Which human leukocyte antigen types are associated with diabetes mellitus?

A

Human leukocyte antigens DR3 and DR4 are associated with type 1 diabetes mellitus; there is no association between human leukocyte antigen and type 2 diabetes mellitus

96
Q

Glucose intolerance is severe in patients with type _____ diabetes mellitus but is mild to moderate in patients with type _____ diabetes mellitus

A

Type 1; type 2

97
Q

Ketoacidosis is common in patients with what form of diabetes mellitus?

A

Type 1; ketoacidosis is rare in type 2 diabetes mellitus

98
Q

What happens to the number of beta cells in the islets of patients with type 1 diabetes mellitus?

A

They are decreased

99
Q

What happens to the number of β-cells in the islets of patients with type 2 diabetes mellitus?

A

Their numbers are variable; amyloidosis is seen

100
Q

What happens to the serum insulin level in patients with type 1 diabetes mellitus?

A

The serum insulin level is decreased

101
Q

What happens to the serum insulin level in patients with type 2 diabetes mellitus?

A

The serum insulin level is elevated initially and is variable during disease progression, often low late in the course

102
Q

The classic symptoms of polyuria, polydipsia, thirst, and weight loss are common with what form of diabetes mellitus?

A

Type 1

103
Q

What is the pathogenesis of diabetic ketoacidosis?

A

Diabetic ketoacidosis is usually caused by an increase in insulin requirements as a result of an increase in stress (eg, infection)

104
Q

A diabetic patient has high circulating levels of ketone bodies and is determined to be in diabetic ketoacidosis; how were the ketone bodies formed?

A

Increased fat breakdown and free fatty acids increase the ketogenesis pathway, converting free fatty acids into ketone bodies

105
Q

A diabetic patient presents with Kussmauls respirations, nausea and vomiting, abdominal pain, and delirium; what is the diagnosis and volume status?

A

This patient is likely in diabetic ketoacidosis and is dehydrated

106
Q

Describe Kussmauls respirations.

A

Deep respirations and air-hunger characteristic of diabetic ketoacidosis

107
Q

The fruity breath sometimes encountered in patients with diabetic ketoacidosis is the result of what?

A

Exhaled acetone

108
Q

You suspect diabetic ketoacidosis in an emergency room patient; what would the glucose, pH, and bicarbonate levels be?

A

Increased glucose, low pH (increased H+ levels), and decreased bicarbonate

109
Q

What acid-base disturbance is found in patients with diabetic ketoacidosis?

A

Anion gap metabolic acidosis

110
Q

The chemistry panel on a patient with diabetic ketoacidosis shows a high potassium level. Why?

A

Although the extracellular potassium is elevated, the intracellular and total potassium levels are depleted because of the bodys excess of hydrogen ions

111
Q

What causes intracellular potassium depletion in diabetic ketoacidosis?

A

Increased hydrogen ions and decreased insulin cause a shift of potassium out of the cells

112
Q

Name an infectious complication of diabetic ketoacidosis that can prove fatal if not treated

A

Mucormycosis, or Rhizopus, infection

113
Q

Give an example of a common neurologic complication of diabetic ketoacidosis.

A

Cerebral edema

114
Q

Give two examples of common cardiovascular complications of diabetic ketoacidosis.

A

Arrhythmias and heart failure

115
Q

List the three core components of the treatment of diabetic ketoacidosis.

A

Fluids, insulin, and potassium

116
Q

When would it make sense to give glucose to patients with diabetic ketoacidosis?

A

When they are becoming hypoglycemic from continuing insulin treatment (so that they can continue to be given insulin)

117
Q

What are the two types of ketone bodies made during diabetic ketoacidosis?

A

-hydroxybutyrate, acetoacetate

118
Q

What causes carcinoid syndrome?

A

Neuroendocrine tumors that secrete high levels of serotonin

119
Q

A patient with a known carcinoid tumor in the small intestine presents with wheezing and flushing; do you expect liver metastases on imaging? Why or why not?

A

Carcinoid syndrome occurs only with metastasis; this patient likely has liver metastases because serotonin secreted by tumors that have not metastasized undergo first-pass metabolism in the liver

120
Q

A patient has diarrhea, flushing, and asthmatic wheezing, and you suspect carcinoid syndrome; what might the cardiac exam reveal?

A

Tricuspid regurgitation due to right-sided valvular disease

121
Q

What is the most common tumor of the appendix?

A

Carcinoid tumor

122
Q

What urinary finding might assist in the diagnosis of carcinoid syndrome?

A

An elevated urine 5-hydroxyindoleacetic acid

123
Q

Carcinoid syndrome can be treated with what drug?

A

Octreotide, a somatostatin analogue

124
Q

Zollinger-Ellison syndrome is the result of a tumor that secretes what substance?

A

Gastrin

125
Q

Gastrinomas causing Zollinger-Ellison syndrome are usually found in which two sites?

A

The pancreas and the duodenum

126
Q

A patient has failed several proton pump inhibitors and is noted to have many ulcers on endoscopy, including several in the jejunum; what malignancy should you consider?

A

Zollinger-Ellison syndrome caused by a gastrin-secreting tumor

127
Q

Zollinger-Ellison syndrome may be associated with what genetic syndrome?

A

Multiple endocrine neoplasia type I

128
Q

What three tumors are associated with multiple endocrine neoplasia 1, or Wermers syndrome?

A

Multiple endocrine neoplasia 1 = 3 Ps: Pancreas, Pituitary, and Parathyroid

129
Q

Name four pancreatic endocrine tumors seen in multiple endocrine neoplasia 1.

A

Zollinger-Ellison syndrome (gastrinomas), insulinomas, vasoactive intestinal peptide tumors, and rarely glucagonomas

130
Q

Which of the multiple endocrine neoplasia syndromes commonly presents as nephrolithiasis and ulcer disease?

A

Multiple endocrine neoplasia 1, or Wermers syndrome; elevated parathyroid hormone can cause renal stones, and ulcers may be associated with a gastrinoma

131
Q

What three tumors are associated with multiple endocrine neoplasia 2A, or Sipples syndrome?

A

Medullary thyroid carcinoma, Pheochromocytoma, Parathyroid tumors (remember: multiple endocrine neoplasia 2A = 2 Ps)

132
Q

An elevation in which serum marker may indicate medullary thyroid cancer?

A

Calcitonin

133
Q

What three tumors are associated with multiple endocrine neoplasia 2B?

A

Medullary thyroid carcinoma, Pheochromocytoma, oral or intestinal ganglioneuromas (remember: multiple endocrine neoplasia 2B = 1 P)

134
Q

Which multiple endocrine neoplasia syndrome is associated with a marfanoid body habitus?

A

Multiple endocrine neoplasia 2B

135
Q

What is the likelihood that a child of a parent who has any of the multiple endocrine neoplasia syndromes will also have the disease?

A

50%; all multiple endocrine neoplasia syndromes have autosomal-dominant inheritance

136
Q

What gene mutation is seen in multiple endocrine neoplasia 2A and multiple endocrine neoplasia 2B?

A

A mutation in the ret gene