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Pathology > Chapter 24- The Endocrine System > Flashcards

Chapter 24- The Endocrine System Flashcards

1
Q

What are the two classes of hormones and how do they differ?

A
  1. Peptide/amino acid derived- bind cell surface receptors

2. Steroid- bind intracellular receptors

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2
Q

What gland primarily controls the pituitary?

A

The hypothalamus

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3
Q

What are the two lobes of the pituitary and how do they differ?

A
  1. Anterior/adenohypophysis- secretes hormones

2. Posterior/neurohypophysis- extension of the hypothalamus, stores oxytocin and ADH

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4
Q

What are the five basic cell types in the anterior pituitary and what do they secrete?

A
  1. Somatotrophs- GH
  2. Lactotrophs- Prl
  3. Corticotrophs- ACTH, MSH, endorphins, lipotropin, proopiomelanocortin
  4. Thyrotrophs- TSH
  5. Gonadotrophs- FSH, LH
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5
Q

What can cause hyperpituitarism?

A

Anterior adenomas

Hyperplasia

Malignancy

Hormone secretion by non-pituitary tumours

Hypothalamic disorders

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6
Q

What can cause hypopituitarism?

A

Ischemic injury

Surgery

Radiation

Inflammation

Nonfunctional compressive tumours

Hypothalamic disorders

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7
Q

What is pituitary apoplexy?

A

Acute hemorrhage into an adenoma

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8
Q

What is the most common cause of hyperpituitarism?

A

Adenomas

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9
Q

Nonfunctional pituitary adenomas affect the pituitary in what way?

A

Hypopituitarism (loss of normal tissue)

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10
Q

What is the most common form of pituitary adenoma?

A

Lactotroph

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11
Q

What is Sheehan syndrome?

A

The pituitary doubles in size during pregnancy but blood supply does not change

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12
Q

What disorders affect the secretion of ADH and how do they exert their effects?

A

Posterior pituitary syndrome- ADH deficiency (kidney can’t resorb water), DI

SIADH- excess ADH secretion causes hyponatremia

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13
Q

What are the most common causes of hypothalamic suprasellar tumours?

A

Gliomas and craniopharyngiomas

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14
Q

What are the morphologies of craniopharyngiomas?

A

Mix of squamous cells and stroma

Adamantinomatous- often calcify, kids

Papillary- often calcify, adults

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15
Q

What hormones does the thyroid produce and what are their functions?

A

T3/T4- regulate metabolic rate, influence growth and maturation

Calcitonin- lowers blood calcium (inhibits osteoclasts)

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16
Q

T3/T4 is regulated by what pituitary hormone?

A

TSH

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17
Q

What epithelium lines the thyroid follicles?

A

Cuboidal/low columnar

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18
Q

How is T3/T4 secreted?

A

TRH is released from the hypothalamus when levels are low

Stimulates TSH release from the pituitary

Stimulates thyroid growth and hormone synthesis

Thyroglobulin is concerted to T3/T4

T3/T4 binds receptors forming TRE and upregulating the transcription of certain genes

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19
Q

What is the feedback mechanism for T3/T4?

A

Reduced levels stimulate TRH release

Increased levels suppress TRH secretion

Negative feedback

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20
Q

What is thyrotoxicosis?

A

Increased circulating T3/T4

Hypermetabolic state

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21
Q

What is thyroid storm?

A

Abrupt onset of severe hyperthyroidism

Acute elevation of circulating catecholamines

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22
Q

What are the most common causes of primary hypothyroidism worldwide and in iodine sufficient areas?

A

Worldwide- iodine deficiency

Sufficient areas- Hashimoto’s

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23
Q

What are the forms of hypothyroidism in children and adults?

A

Children- cretinism, impaired development (skeletal system, CNS)

Adults- myxedema, fatigue, reduced mental activity and sympathetic activity, CHF

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24
Q

What are the two forms of cretinism?

A

Endemic (iodine deficiency, goiter)

Sporadic (hormone synthesis defects)

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25
Q

What are the different causes of thyroiditis and what are their characteristics?

A
  1. Hashimoto’s/autoimmune- diffusely enlarged, intact capsule, Hurthle cells (eosinophilic cytoplasm)
  2. Granulomatous/De Quervain- viral infection causes self limited immune response, symmetric or irregular enlargement, firm, yellow-white involved areas
  3. Subacute lymphocytic/painless- autoimmune in middle aged women, goiterous enlargement, mild hyperthyroidism (overtime can become hypo)
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26
Q

What is the most common cause of thyroid pain?

A

Granulomatous thyroiditis

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27
Q

What is the most common cause of endogenous hyperthyroidism?

A

Graves’ disease

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28
Q

What triad of findings is associated with Graves’ disease?

A
  1. Hyperthyroidism with diffuse gland enlargement
  2. Exophthalmos
  3. Pretibial myxedema
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29
Q

What causes Graves’ disease?

A

Auto antibodies against thyroid proteins

Binding and stimulation of the TSH receptor

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30
Q

What is the morphology of Graves’ disease?

A

Symmetrically enlarged

Red/meaty

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31
Q

What causes goiter formation?

A

Impaired synthesis of thyroid hormone leads to increased TSH and thyroid enlargement

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32
Q

What are the different types of goiters and their characteristics?

A
  1. Diffuse nontoxic/simple- no nodularity
  2. Multinodular- recurrent episodes of hyperplasia and involution produce irregular enlargement, fibrosis with colloid-like areas, follicles can rupture
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33
Q

What are the malignant risk factors associated with thyroid neoplasms?

A

Single nodule

Younger patient

Male

Head and neck radiation

Nodules that take up radioactive iodine

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34
Q

What are the two types of thyroid neoplasms?

A
  1. Adenomas

2. Carcinomas

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35
Q

What are the characteristics of thyroid adenomas?

A

Discrete solitary masses from follicular epithelium, well, demarcated solitary, encapsulated lesions

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36
Q

Are toxic adenomas functional or nonfunctional?

A

Functional (TSH receptor GOF mutation)

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37
Q

What are the four types of thyroid carcinomas and their characteristics?

A
  1. Papillary- many variations, branching papillae with fibrovascular stalk, psammoma bodies, RET/PTC and BRAF mutations
  2. Follicular- disorganized, tiny follicles histologically, can mimic adenomas, RAS, PI3K/AKT, PTEN mutations
  3. Anaplastic- aggressive elderly variant, can arise from a better differentiated tumour, TP53, bets catenin mutations
  4. Medullary- neuroendocrine (from C-cells), firm, pale and infiltrative, RET, MEN mutations
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38
Q

What are the occurrences of each type of thyroid carcinomas?

A

Papillary >85%

Follicular 5-15%

Anaplastic <5%

Medullary 5%

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39
Q

What are the two forms of medullary thyroid tumours and what are their characteristics?

A

Sporadic- solitary

MEN associated- multiple lesions

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40
Q

What is a useful biomaterial for medullary thyroid carcinoma?

A

Carcinoembryonic Ag

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41
Q

What areas show higher incidences of follicular thyroid carcinoma?

A

Iodine deficient areas

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42
Q

What causes thyroglossal duct cysts?

A

Developmental remnants of thyroid migrating from the tongue foramen cecum

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43
Q

How are thyroglossal ducts cysts differential from branchial cleft cysts?

A

Thyroglossal- midline masses anterior to trachea

Branchial- lateral masses

44
Q

How does the location affect thyroglossal duct cysts?

A

High in neck- lined by stratifies squamous

Inferior- lined by thyroid acinar epithelium

45
Q

What cell types makes up the parathyroid glands?

A

Chief and oxyphil

46
Q

What is the function of the parathyroid glands?

A

Secretes PTH

Regulates calcium homeostasis (increases blood calcium)

47
Q

What are the clinical symptoms of hyperparathyroidism?

A

Painful bones

Renal stones

Abdominal groans

Psychic moans

48
Q

What are the types of hyperparathyroidism and how are they different?

A

Primary- autonomous increase (adenoma or hyperplasia)

Secondary- compensatory hypersecretion due to hypocalcemia (renal failure)

Tertiary- persistent hypersecretion even after the cause of hypocalcemia is corrected

49
Q

What is a brown tumour and what type of hyperparathyroidism are they associated with?

A

Osteolytic lesions

Secondary

50
Q

What is normally the cause of hypoparathyroidism?

A

Surgery

51
Q

What are the less common causes of hypoparathyroidism?

A

Autoimmune (APSI)

Autosomal dominant (CASR gene)

Familial isolated

Congenital absence

52
Q

Why are the clinical symptoms of hypoparathyroidism?

A

Tetany

Mental status change

Intracranial manifestations

Ocular disease (calcification)

Cardiovascular manifestations

Dental abnormalities

53
Q

What are the different types of cells found in the islets of Langerhans and what do they produce?

A

Beta- insulin

Alpha- glucagon

Delta- somatostatin

PP- pancreatic polypeptide

DI- elaborated VIP glycogenolysis

Enterochromaffin- serotonin

54
Q

DM is a group of metabolic disorders sharing what common feature?

A

Hyperglycemia

55
Q

A random glucose score of what amount indicates DM?

A

> 200mg/dL

56
Q

What are the differences between type I and II DM?

A

I- autoimmune beta cell destruction, younger onset

II- peripheral resistance to insulin and inadequate secretory response by beta cells (hypersecretion then cell failure), associated with obesity

57
Q

How can viral infections lead to DMI?

A

Bystander damage- beta cell injury releases Ags (targeted by immune system)

Molecular mimicry- virus produces protein that mimics beta cell Ags

Virus lies dormant in beta cells, later infection with related virus leads to immune response

58
Q

What are the characteristics of monogenetic forms of DM?

A

Due to primary defect in beats cell function or insulin receptor signalling

Early onset

59
Q

What is the largest subgroup of monogenetic DM?

A

Maturity onset diabetes (MODY)

60
Q

What is the most important stimulation for insulin synthesis and release?

A

Glucose

61
Q

What is the action of insulin?

A

Increases glucose transport into cells (promotes storage)

62
Q

What glucose transporters are present in the pancreas?

A

GLUT2

63
Q

What are the complications associated with DM?

A

Macrovascular disease

Microvascular disease

Diabetic nephropathy

64
Q

Diabetic ketoacidosis is associated with what type of DM?

A

I

65
Q

What is the most common pancreatic neoplasm?

A

Insulinomas

66
Q

What percentage of insulinomas are benign?

A

90%

67
Q

What are the morphological characteristics of insulinomas?

A

Solitary, <2cm, well encapsulated

68
Q

What percentage of “other” pancreatic endocrine neoplasms are malignant?

A

60-90%

69
Q

What is the triad associated with Zollinger-Ellison syndrome?

A
  1. PUD
  2. Gastric hypersecretion
  3. Pancreatic islet lesions
70
Q

What are the two areas of the adrenal glands?

A

Cortex (external)

Medulla (internal)

71
Q

What are the zones in the adrenal cortex and what hormones do they secretes?

A
  1. Glomerulosa- mineralcorticoids (aldosterone)
  2. Fasiculata- glucocorticoids (cortisol)
  3. Reticularis- sex steroids (estrogen, androgens)
72
Q

What is the difference between Cushing syndrome and disease?

A

Syndrome- hypercortisolism (exogenous or endogenous)

Disease- ACTH secreting pituitary adenoma causes hypercortisolism

73
Q

What is the most common cause of endogenous hypercortisolism?

A

ACTH secreting pituitary adenomas

74
Q

What are the most common causes of ACTH independent Cushing syndrome?

A

Adrenal adenoma and carcinoma

75
Q

What is the morphology of Cushing disease?

A

Nodular cortical hyperplasia

76
Q

What is crooke hyaline change?

A

The granular basophilic cytoplasm is ACTH producing cells becomes homogenous and pale due to increases in glucocorticoids

77
Q

What are the four abnormalities seen with hypercortisolism and what are their most likely causes?

A
  1. Cortical atrophy- exogenous glucocorticoids or adenoma
  2. Diffuse hyperplasia- ACTH dependent Cushing syndrome or Cushing disease
  3. Macro/micronodular hyperplasia
  4. Adenoma or carcinoma
78
Q

What pigment is seen in micronodular hyperplasia of the adrenals?

A

Lipofuschin

79
Q

What are the clinical symptoms of Cushing disease?

A

Central obesity, moon face, buffalo hump fat

Muscle atrophy

Secondary diabetes

Poor wound healing

Osteoporosis

Mental disturbances

Hirsuitism

Menstrual abnormalities

80
Q

What are the differences in primary (Conn syndrome) and secondary hyperaldosteronism?

A

Primary- autonomous overproduction of aldosterone (RAS and renin activity suppressed)

Secondary- aldosterone released through RAS activation

81
Q

What are the clinical symptoms of hyperaldosteronism?

A

Hypertension

Hypokalemia

Hypernatremia

82
Q

What are the different forms of Conn syndrome and their characteristics?

A

Bilateral idiopathic- bilateral nodular hyperplasia

Adrenocortical neoplasm- solitary adenoma

Rare hereditable form- remediable with glucocorticoids

83
Q

What can cause secondary hyperaldosteronism?

A

CHF

Reduced renal perfusion

Pregnancy

84
Q

What characterizes androgenital syndromes?

A

Disorders of sexual differentiation

85
Q

What adrenal causes result in androgenital syndromes?

A

Androgen excess- andrenocortical neoplasms and congenital adrenal hyperplasia

86
Q

What is the pathology of congenital adrenal hyperplasia?

A

Inherited metabolic disorders

Precursors to cortical steroids build up and are used in other pathways (androgen production)

Adrenal hyperplasia, increases ACTH, reduced cortisol

87
Q

What is salt wasting syndrome?

A

Cortisol and mineralcorticoid production is blocked

88
Q

What are the different forms of adrenocortical insufficiency and their causes?

A

Primary acute- sudden increase in glucocorticoid requirements in patients with chronic insufficiency

Primary chronic/Addison disease- destruction of ~90% of the cortex

Secondary- hypothalamic or pituitary disorder leads to reduced ACTH

89
Q

How are primary chronic and secondary adrenocortical insufficiency distinguished?

A

Hyponatremia and hyperkalemia are not features of secondary

90
Q

What is a common cause of primary acute adrenocortical insufficiency (what causes a rapid increase in glucocorticoid requirements)?

A

Massive adrenal hemorrhage

91
Q

What familial cancer syndromes increase the risk of adrenocortical carcinoma?

A

Li Fraumeni syndrome (TP53 mutations)

Beckwith-Weidemann syndrome

92
Q

What are the different types of adrenal cortical neoplasms and their characteristics?

A
  1. Adenomas- well circumscribed yellow-brown lesions
  2. Carcinomas- variegated tumours with hemorrhage and central necrosis
  3. Myelolipomas- benign lesions (fat and hematopoietic elements)
93
Q

What is a feature of function adrenocortical adenomas?

A

Cortex is atrophic

94
Q

What cells make up the adrenal medulla?

A

Neuroendocrine chromaffin cells

Sustenacular cells (supporting)

95
Q

What hormones are produced by the adrenal medulla?

A

Epinephrine and norepinephrine

96
Q

The primary pathological finding associated with pheochromocytoma is what?

A

Hypertension

97
Q

What is the “rule of 10s” associated with pheochromocytomas?

A

10% extra adrenal

10% of sporadic cases are bilateral

10% are malignant

10% don’t cause hypertension

98
Q

What is the morphology of pheochromocytomas?

A

Tan hemorrhagic cut surface

Can be necrotic with cystic changes

99
Q

What are the characteristics of multiple endocrine neoplasia (MEN) syndromes?

A

Group of inherited diseases resulting in proliferative lesions of multiple endocrine organs (synchronously)

Young onset

100
Q

MEN onset is preceded by what?

A

Asymptomatic stage of hyperplasia

101
Q

What are the characteristics of MEN type I/Wermer syndrome?

A

Primary hyperparathyroidism

Aggressive and functional tumours of the pancreas

Prolactinomas (most common in pituitary)

Duodenum is the most common site of gastrinomas

102
Q

What are the different forms of MEN type II and their characteristics?

A

2A/Sipple syndrome- medullary thyroid cancer, pheochromocytomas and parathyroid hyperplasia, RET protooncogene mutation

2B- medullary thyroid cancer and pheochromocytomas without parathyroid hyperplasia

Familial medullary thyroid cancer- variant with no other manifestations

103
Q

What are the functions of pineocytes?

A

Photosensory and neuroendocrine

104
Q

What hormone does the pineal gland secrete?

A

Melatonin

105
Q

Tumours of the pineal gland resemble what form of malignancy?

A

Germinomas

106
Q

What are the two forms of pinealomas?

A

Pineoblastomas

Pineocytomas

Pathology (25 decks)

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