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Endocrine Flashcards

1
Q

Growth hormone adenomas of the anterior pituitary produce ______ in children, and ________ in adults.

Secondary ________ is also often present, because growth hormone reduces glucose uptake by cells

A

Gigantism; acromegaly

Diabetes

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2
Q

Diagnosis of growth hormone adenoma may be based on elevated GH and _____, as well as lack of GH suppression by oral _______

A

IGF-1; glucose

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3
Q

Treatment options for growth hormone adenomas

A

Octreotide

GH receptor antagonists

Surgery

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4
Q

Pt presents with poor lactation and loss of pubic hair following delivery of baby in which birth was complicated by hemorrhage. Most likely dx?

A

Sheehan syndrome

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5
Q

What hormones are made in the posterior pituitary?

A

NONE

ADH and Oxytocin are made in the hypothalamus and STORED in the posterior pituitary

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6
Q

Clinical features of central diabetes insipidus include polyuria, polydipsia, _____natremia and _____ serum osmolality, with ______ urine osmolality and specific gravity

A

Hypernatremia; high; low

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7
Q

What is the water deprivation test?

A

Used to dx diabetes insipidus

Positive if water deprivation fails to increase urine osmolality

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8
Q

Classic psychiatric drug associated with drug-induced nephrogenic diabetes insipidus

A

Lithium

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9
Q

Clinical features of SIADH include _____natremia and ______ serum osmolality, as well as mental status change and seizures

A

Hyponatremia; low

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10
Q

List potential causes of SIADH

A

Ectopic production (e.g., small cell carcinoma of the lung)

CNS trauma

Pulmonary infection (even in COPD)

Drugs (e.g., cyclophosphamide)

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11
Q

Treatment options for SIADH

A

Free water restriction

Demeclocycline — blocks effect of ADH

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12
Q

Hyperthyroidism involves increased level of circulating thyroid hormone, which increases the basal metabolic rate as well as the sympathetic nervous system activity.

How does thyroid hormone increase the BMR and SNS activity?

A

Increases BMR by increasing synthesis of Na/K-ATPase

Increases SNS activity by activity at beta-1 adrenergic receptors

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13
Q

How do cholesterol and glucose levels tend to change with hyperthyroidism?

A

Hypocholesterolemia

Hyperglycemia

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14
Q

What causes Grave’s disease?

A

Autoantibody (IgG) that stimulates TSH receptor, leading to increased synthesis and release of thyroid hormone

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15
Q

Most common cause of hyperthyroidism

A

Graves disease

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16
Q

Classic finding on histology indicating Graves disease

A

Scalloping of the colloid (along with diffuse hyperplasia)

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17
Q

Treatment options for Graves disease

A

Beta-blockers

Thioamide (blocks thyroid peroxidase)

Radioiodine ablation

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18
Q

One of the feared complications of Graves disease is thyroid storm, characterized by elevated _______ and massive hormone excess (stress) leading to arrhythmia, hyperthermia, and vomiting with hypovolemic shock.

This is treated with _____, ______, and ______

A

Catecholamines

PTU; beta-blockers; steroids

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19
Q

A multinodular goiter is an enlarged thyroid gland with multiple nodules, often due to relative ______ deficiency. It is usually nontoxic (euthyroid), but rarely the regions may become TSH-independent (‘toxic goiter’)

A

Iodine

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20
Q

______ = hypothyroidism in neonates and infants associated with mental retardation, short stature with skeletal abnormalities, coarse facial features, enlarged tongue, and umbilical hernia

A

Cretinism

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21
Q

Potential causes of cretinism

A

Maternal hypothyroidism during early pregnancy

Thyroid agenesis

Dyshormonogenetic goiter (most common enzyme deficiency is thyroid peroxidase)

Iodine deficiency

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22
Q

_______ = term for hypothyroidism in older children or adults characterized by weight gain despite normal appetite, slowing of mental activity, muscle weakness, and cold intolerance with decreased sweating

A

Myxedema

[myxedema refers to the fact that tissue appears edematous with dough-like consistency, but this is not due to fluid — it deposition of glycosaminoglycans. Classic areas of myxedema in hypothyroid are larynx (leads to deepening of voice) and tongue (appears enlarged)]

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23
Q

How do cholesterol levels change in hypothyroid?

A

Hypercholesterolemia

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24
Q

Hashimoto thyroiditis = autoimmune destruction of the thyroid associated with HLA-_____. This initially may present as hyperthyroidism, but progresses to hypothyroidism with decreased T4 and increased TSH.

________ and ________ antibotides are often present, which are markers of thyroid damage

A

DR5

Antithyroglobulin; antimicrosomal

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25
Q

Most common cause of hypothyroidism where iodine levels are sufficient

A

Hashimoto thyroiditis

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26
Q

Histological findings in pts with hashimoto thyroiditis

A

Chronic inflammation with formation of germinal centers

Hurthle cells

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27
Q

What cancer are pts with hashimoto thyroiditis at increased risk for?

A

Marginal zone B cell lymphoma

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28
Q

Granulomatous thyroiditis that follows a viral infection; presents as a tender thyroid with transient hyperthyroidism

A

Subacute (deQuervain) granulomatous thyroiditis

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29
Q

T/F: subacute (dequervain) thyroiditis presents with transient hyperthyroidism, and later progresses to hypothyroidism

A

False — it does present with transient hyperthyroidism, but this is self-limited and does NOT progress to hypothyroidism

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30
Q

Chronic inflammation with extensive fibrosis of the thyroid; presents as hypothyroidism with ‘hard as wood’ nontender thyroid gland. Fibrosis may extend to local structures (e.g., airway)

A

Reidel fibrosing thyroiditis

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31
Q

Both Reidel fibrosing thyroiditis and anaplastic thyroid carcinoma may progress to invade local structures (e.g., airway) — what is the main differentiating factor between these entities on patient presentation?

A

Reidel fibrosing thyroiditis classically occurs in a young female

Anaplastic thyroid carcinoma is a disease of the elderly

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32
Q

On 131-Iodine radioactive uptake studies, Graves disease or nodular goiter will show ______ uptake

A

Increased

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33
Q

On 131-Iodine radioactive uptake studies, adenoma and carcinoma will show ______ uptake, which warrants a _______ biopsy

A

Decreased; FNA

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34
Q

What is the mechanism for biopsy of the thyroid?

A

Fine needle aspiration (FNA)

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35
Q

Follicular adenoma is a thyroid neoplasm that is a benign proliferation of follicles surrounded by a fibrous capsule. Are these usually functional?

A

No, usually nonfunctional

[but rarely may secrete thyroid hormone]

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36
Q

4 types of thyroid carcinoma

A

Papillary carcinoma
Medullary carcinoma
Follicular carcinoma
Anaplastic carcinoma

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37
Q

Most common type of thyroid carcinoma

A

Papillary carcinoma (80% of cases)

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38
Q

Papillary carcinoma is the most common type of thyroid carcinoma. What is the major risk factor for developing it?

A

Exposure to ionizing radiation in childhood

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39
Q

Histologic features of papillary carcinoma of thyroid

A

Orphan Annie Eye Nuclei

Nuclear grooves

Psammoma bodies

40
Q

Papillary carcinoma of the thyroid often spreads to the ______ nodes; it has a _______ prognosis

A

Cervical; excellent

41
Q

Follicular carcinoma of the thyroid is a malignant proliferation of follicles surrounded by a fibrous capsule with INVASION through the capsule.

T/F: the gold-standard for differentiating follicular carcinoma and follicular adenoma is FNA biopsy

A

False — FNA would not allow you to assess for invasion beyond the capsule, result would be the same in either case just showing follicular cells

In order to assess/differentiate, would need to see gross specimen or look for microscopic signs of invasion on histology of the capsule itself

42
Q

Follicular carcinoma of the thyroid is capable of metastasis, which generally occurs via _________ spread

A

Hematogenous

[note difference from papillary, which is lymphatic spread]

43
Q

Medullary carcinoma of the thyroid is a malignant proliferation of ___________ cells, resulting in high levels of _______ produced by the tumor which may lead to lab finding of _________

A

Parafollicular C cells; calcitonin; hypocalcemia

44
Q

With MTC, calcitonin often deposits within the tumor as _____

A

Amyloid

[characteristic histology description is malignant cells in an amyloid stroma]

45
Q

Familial cases of medullary thyroid carcinoma are often due to ______ and _______ syndromes.

These are associated with mutations in the _____ oncogene, detection of which warrants prophylactic thyroidectomy

A

MEN2A; MEN2B

RET

46
Q

Undifferentiated malignant tumor of the thyroid, usually seen in the elderly; often invades local structures leading to dysphagia or respiratory compromise and carries a poor prognosis

A

Anaplastic carcinoma

47
Q

The key cell of the parathyroid gland is the _____ cell which regulates free (ionized) calcium via PTH secretion

A

Chief

48
Q

3 major actions of PTH

A

Increases bone osteoclast activity (via osteoblast activation)

Increases small bowel absorption of calcium and phosphate (via Vitamin D activation)

Increases renal calcium reabsorption phosphate excretion

49
Q

Primary hyperparathyroidism is excess PTH due to disorder of the gland itself. What is the most common cause?

A

Parathyroid adenoma (>80% of cases)

[other causes: sporadic hyperplasia, parathyroid carcinoma]

50
Q

Parathyroid adenoma is a benign neoplasm, usually involving one gland, and most often resulting in asymptomatic hypercalcemia. If symptoms are present, what are they likely to be?

A

Nephrolithiasis (calcium oxalate)

Nephrocalcinosis (deposition in tubules —> renal insufficiency with polyuria)

CNS disturbance

Constipation, PUD, acute pancreatitis (calcium activates enzymes w/i pancreas)

Osteitis fibrosa cystica

[all consequences of increased PTH and hypercalcemia]

51
Q

Lab findings in hyperparathyroidism including serum calcium, serum phosphate, urinary cAMP, and serum alkaline phosphatase

A

Increased serum calcium

Decreased serum phosphate

Increased urinary cAMP (PTH receptor is a Gs GPCR; activation results in increased cAMP)

Increased serum alkaline phosphatase

52
Q

Secondary hyperparathyroidism is an excess production of PTH due to disease process extrinsic to parathyroid gland. What is the most common cause?

A

Chronic renal failure

[Renal insufficiency leads to decreased phosphate excretion. The increased serum phosphate binds free calcium, thus decreasing free serum calcium. This stimulates all four parathyroid glands leading to PTH release.]

53
Q

Lab findings in secondary hyperparathyroidism including serum calcium, serum phosphate, and alkaline phosphatase

A

Decreased serum calcium

Increased serum phosphate

Increased alkaline phosphatase

[calcium is low because remember this process is driven by the fact that phosphate is high, which binds free calcium in the blood]

54
Q

Hypoparathyroidism is defined as low PTH; causes include autoimmune damage, surgical excision, and ______ syndrome

A

DiGeorge

[failure to develop 3rd and 4th pharyngeal pouch]

55
Q

Clinical presentation of hypoparathyroidism including labs (PTH, calcium)

A

Numbness and tingling (typically perioral)

Muscle spasms (tetany) — Trousseau or Chvostek’s sign

Decreased PTH and decreased serum calcium

56
Q

_________ is due to end-organ resistance to PTH, often due to defect in Gs stimulatory protein.

The _______ ________ inherited form is associated with a short stature and short 4th and 5th digits

A

Pseudohypoparathyroidism

Autosomal dominant

57
Q

Pseudohypoparathyroidism is due to end-organ resistance to PTH. Labs will show what changes in calcium and PTH levels?

A

Hypocalcemia

Increased PTH levels

58
Q

The endocrine pancreas is composed of cells termed islets of langerhans. A single islet consists of multiple cell types, each producing one type of hormone. Insulin is secreted by ______ cells, which lie at the ______ of islets.

Glucagon is secreted by ______ cells

A

Beta; center

Alpha

59
Q

T1D is caused by autoimmune destruction of beta cells by T lymphocytes, which is a type ____ HSR. This leads to inflammation of the islets.

T1D is associated with HLA-____ and _____. Autoantibodies against _____ are often present

A

Type IV HSR

DR3; DR4; insulin

60
Q

DKA is a complication of T1D, and manifests due to excessive serum ketoacids. This often arises with stress (e.g., infection) in which _______ increases secretion of _______, exacerbating lipolysis (along with gluconeogenesis and glycogenolysis). The increased lipolysis leads to increased FFAs, which go to the liver where they are converted to ketone bodies.

A

Epinephrine; glucagon

61
Q

DKA may present clinically with Kussmaul respirations, dehydration, nausea, vomiting, mental status change, and fruity smelling breath. What will labs show regarding glucose levels, blood gases, and potassium?

A

Hyperglycemia (>300 mg/dL)

Anion gap metabolic acidosis

Hyperkalemia

[note that while labs show hyperkalemia, this is an effect of cellular K+ loss, which will eventually be peed out, so on correction of DKA watch for signs of hypokalemia and replace K+ as needed]

62
Q

Treatment for DKA

A

Fluids
Insulin
Replacement of electrolytes (e.g., potassium)

63
Q

What is the mechanism of insulin-resistance in obese pts with T2D?

A

Obesity leads to decreased numbers of insulin receptors

64
Q

In T2D, insulin levels are increased early in disease. Insulin deficiency develops later due to beta cell exhaustion. Histology reveals _____ deposition in islets

A

Amyloid

65
Q

Laboratory diagnostic criteria for T2D (random glucose, fasting glucose, glucose tolerance test)

A

Random glucose > 200 mg/dL

Fasting glucose >126 mg/dL

Glucose tolerance test > 200 mg/dL two hours after glucose load

66
Q

While the primary feared complication of T1D is DKA, the feared acute complication in T2D is _____________

[what are the clinical features?]

A

Hyperosmolar non-ketotic coma

Presents with high glucose levels (>500 mg/dL), leading to life-threatening diuresis, hypotension, and coma. Ketones are characteristically absent

67
Q

2 major mechanisms by which complications of T2D arise

A

Non-enyzmatic glycosylation

Osmotic damage

68
Q

One mechanism of complications in T2D is nonenzymatic glycosylation (NEG) of vascular basement membranes.

NEG of large- and medium-sized vessels leads to __________, which is the mechanism of CV disease in diabetes.

NEG of small vessels leads to _______ _________, which is the mechanism of diabetic nephropathy.

NEG of hemoglobin leads to ______.

A

Atherosclerosis

Hyaline arteriosclerosis

HbA1c

69
Q

Another mechanism of complications in T2D is osmotic damage. This occurs when sugar enters certain cells and is converted to sorbitol by aldose reductase. What are the 3 primary tissues affected by osmotic damage in T2D?

A

Schwann cells — leads to peripheral neuropathy

Pericytes of retinal blood vessels — leads to retinopathy, hemorrhage, blindness

Lens — leads to cataracts

70
Q

Pancreatic endocrine tumors are tumors of islet cells and are often a component of MEN1 (along with parathyroid hyperplasia and pituitary adenoma).

List the 5 different types of pancreatic endocrine tumors

A

Insulinoma

Gastrinoma

Somatostatinoma

Glucagonoma

VIPoma

71
Q

Pancreatic endocrine tumor characterized by episodic hypoglycemia with mental status changes relieved by glucose

A

Insulinoma

72
Q

Lab results (glucose, insulin, c-peptide) associated with insulinoma

A

Decreased glucose

Increased insulin

Increased c-peptide

73
Q

Pancreatic endocrine tumor characterized by treatment-resistant peptic ulcers; may be multiple and can extend to jejunum

A

Gastrinoma

[treatment resistant peptic ulcers = zollinger ellison syndrome]

74
Q

Pancreatic endocrine tumor characterized by achlorhydria, cholelithiasis, and steatorrhea

A

Somatostatinoma

[achlorhydria is due to inhibition of gastrin; cholelithiasis and steatorrhea due to inhibition of CCK]

75
Q

Pancreatic endocrine tumor characterized by watery diarrhea, hypokalemia, and achlorhydria

A

VIPoma

76
Q

3 layers of adrenal cortex and their products

A

Glomerulosa — mineralocorticoids (aldosterone)

Fasciculata — glucocorticoids (cortisol)

Reticularis — sex steroids

77
Q

What are 3 ways cortisol causes immune suppression?

A

Inhibition of phospholipase A2 — can’t generate arachidonic acid metabolites

Inhibition of IL-2 — immune cell growth factor

Inhibition of histamine release from mast cells — essential for vasodilation and increased vascular permeability in immune response

78
Q

Diagnostic test for Cushing syndrome

A

Increased 24-hour urine cortisol level

79
Q

4 major causes of Cushing syndrome

A

Exogenous corticosteroids (most common cause)

Primary adrenal adenoma, hyperplasia, or carcinoma

ACTH-secreting pituitary adenoma

Paraneoplastic ACTH secretion (classically small cell carcinoma of the lung)

80
Q

In differentiating the causes of cushing syndrome, you can look at the size of the adrenals. In exogenous corticosteroid use, both adrenals become atrophied. In primary adrenal hyperplasia/adenoma/carcinoma, the contralateral adrenal will be atrophied.

However, in both ACTH-secreting pituitary adenoma AND paraneoplastic ACTH secretion, both adrenals will be hyperplastic — so you can tell them apart based on this. So how do you differentiate between ACTH-secreting pituitary adenoma and paraneoplastic ACTH secretion as the underlying cause of cushing syndrome?

A

High-dose dexamethasone suppression test

This will suppress ACTH production by a pituitary adenoma, but will FAIL to suppress ectopic ACTH production by a small cell lung carcinoma

81
Q

Hyperaldosteronism results in HTN as well as what changes in sodium, potassium, and blood gases?

A

Hypernatremia

Hypokalemia

Metabolic alkalosis

82
Q

Primary hyperaldosteronism is most commonly due to ______ _____. Sporadic hyperplasia and carcinoma are less common causes. This condition is characterized by _____ aldosterone and _____ renin

A

Adrenal adenoma; high; low

83
Q

Secondary hyperaldosteronism involves activation of the RAAS (e.g., renovascular HTN), and is characterized by _____ aldosterone and _____ renin

A

High; high

84
Q

Congenital adrenal hyperplasia is characterized by excess sex steroids with hyperplasia of both adrenal glands. A _______ deficiency is the most common cause, in which steroidogenesis is shunted towards sex steroid production

A

21-hydroxylase

85
Q

In 21-hydroxylase deficiency, there is a deficiency of ______ which leads to increased _____, which results in bilateral adrenal hyperplasia

A

Cortisol; ACTH

86
Q

Clinical features of 21-hydroxylase deficiency

A

Salt wasting with hyponatremia, hyperkalemia, and hypovolemia

Life-threatening hypotension

Clitoral enlargement (females) or precocious puberty (males)

87
Q

Adrenal insufficiency = lack of adrenal hormones. This may arise acutely with ___________ syndrome resulting in bilateral adrenal hemorrhage, classically in the setting of Neisseria infection in which child develops DIC and massive hypotension due to lack of cortisol

A

Waterhouse-Friderichsen syndrome

88
Q

Chronic adrenal insufficiency may arise due to progressive destruction of adrenal glands, autoimmune destruction, TB, or metastatic carcinoma. The classic metastatic carcinoma that goes to the adrenal glands is ______ cancer

A

Lung

89
Q

Clinical features of adrenal insufficiency

A

Hypotension

Hyponatremia, hypovolemia, hyperkalemia

Weakness

Hyperpigmentation

Vomiting and diarrhea

90
Q

The adrenal medulla is composed of _____ _____-derived _______ cells. These are the main source of catecholamines (epinephrine and NE)

A

Neural crest; chromaffin

91
Q

Brown tumor composed of chromaffin cells causing classic clinical manifestations of episodic HTN, headaches, palpitations, tachycardia, and sweating

A

Pheochromocytoma

92
Q

Diagnosis of pheochromocytoma

A

Increased serum metanephrines

Increased 24-hour urine metanephrines and VMA

93
Q

Treatment for pheochromocytoma is surgical excision. _______ must be given prior to surgery to prevent effects of excessive catecholamine release

A

Phenoxybenzamine

94
Q

Rule of 10s for pheochromocytoma

A

10% bilateral

10% familial

10% malignant

10% located outside adrenal medulla

95
Q

10% of pheochromocytomas are located outside the adrenal medulla. What is one classic location?

A

Bladder wall

96
Q

3 syndrome associations with pheochromocytoma

A

MEN2A and 2B

VHL disease

NF type 1

Boards Pathology (19 decks)

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