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Gen Path Final > Endocrine disease > Flashcards

Endocrine disease Flashcards

1
Q

I. Normal Pituitary:

• Function

A
  • the “master gland”
  • regulates most other endocrine glands
  • connected to hypothalamus via stalk which releases factors controlling release of trophic hormones
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2
Q

I. Normal Pituitary:

• Embryology

A
  • anterior lobe derived from the primitive oral cavity (Rathke’s Pouch)
  • posterior lobe derived from neuroectoderm
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3
Q

I. Normal Pituitary:

• Anatomy

A
  • contained within the sella turcica of the sphenoid bone
  • connected to hypothalamus via stalk → regulation of pituitary hormones
  • anterior lobe is composed of round cells arranged in cords and nests
  • posterior lobe: composed of modified glial cells and axonal processes extending from hypothalamic neurons
  • Hypothalamic neurons produce oxytocin, antidiuretic hormone (ADH)
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4
Q

somatotroph

A

growth hormone (GH)

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5
Q

lactotroph

A

prolactin (PRL)

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6
Q

corticotroph

A

corticotropin (ACTH)

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7
Q

gonadotroph

A 
Luteinizing hormone (LH) 
Follicle stimulating hormone (FSH)
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8
Q

thyrotroph

A

thyrotropin (TSH)

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9
Q

Anterior Lobe Pathology

A. Hyperfunction (hyperpituitarism)

A

o almost always associated with a pituitary adenoma
o may produce symptoms by hormone production or by local mass effect
• compression of optic nerve leading to visual disturbances
• increased intracranial pressure (headache, nausea, vomiting)

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10
Q

ACTH and other POMC-derived peptides

associated syndrome

A

Cushing syndrome

Nelson syndrome

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11
Q

GH

associated syndrome

A

Gigantism (children)

Acromegaly (adults)

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12
Q

Prolactin

associated syndrome

A

Galactorrhea and amenorrhea (females)

Sexual dysfunction, infertility

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13
Q

Prolactin & GH

associated syndrome

A

Combined features of prolactin and GH

excess

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14
Q

TSH

associated syndrome

A

Hyperthyroidism

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15
Q

FSH, LH

associated syndrome

A

Hypogonadism, mass effects and

hypopituitarism

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16
Q

POMC:

A

Pro-opiomelanocortin

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17
Q

B. Prolactinomas more noticeable in

A

women than in men; can grow to be very large in men before they are noticed.

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18
Q

C. With Growth Hormone adenomas, depends on when the

A

epiphyses closes. Patients with acromegaly will have a prognathic mandible, spacing of dentition, large sausage-like fingers, hypertension, and congestive heart failure.

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19
Q

B. Hypofunction (hypopituitarism)

A

• may manifest as a deficiency of one hormone or multiple hormones

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20
Q

Hypopituitarism: • causes:

A

o nonfunctional pituitary adenoma
o Ischemic necrosis, most commonly from Sheehan’s syndrome (postpartum infarct). Need over 75% of anterior lobe to be destroyed for clinically significant effects.
o Ablation of pituitary by surgery or radiation
o destruction by adjacent tumor

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21
Q

Hypopituitarism: • manifestations

A 
o	Pituitary dwarfism (GH)
o	Amenorrhea and infertility in women and decreased libido, impotence, and lack of pubic/axillary hair in men (gonadotropin)
o	No post-partum lactation (prolactin)
o	Hypothyroidism (TSH)
o	Hypoadrenalism (ACTH)
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22
Q

Posterior lobe pathology

A

• Oxytocin- no significant clinical abnormalities
• Antidiuretic hormone (ADH)
o Functions in kidneys to promote resorption of free water
o diabetes insipidus

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23
Q

Gigantism:

• Caused by an

A

adenoma in the anterior lobe that secretes growth hormone

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24
Q

Gigantism: • Occurs before

A

closure of the epiphyseal plates (growth plates) in the long bones

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25
Q

Gigantism: • Clinical features:

A
  • Generalized increase in the size of the body

* Arms and legs are disproportionately long

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26
Q

Gigantism: • Treatment:

A

surgical removal of the adenoma

• Prognosis: fair to good

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27
Q

Acromegaly:

• Increased

A

growth hormone secretion (also due to an adenoma)

• After closure of the epiphyseal plates (skeletal maturity)

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28
Q

Acromegaly: • Clinical features:

A
  • Enlarged bones of the hands, feet, and face
  • Prognathism, development of a diastema
  • Hypertension and congestive heart failure may be seen
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29
Q

Acromegaly: • Treatment:

A

same as gigantism (remove adenoma)

•

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30
Q

Acromegaly: Prognosis:

A

Guarded—due to complications of hypertension and congestive heart failure

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31
Q

c. Pituitary Dwarfism:

• Potential causes:

A
  • Failure of pituitary gland to produce growth hormone
  • Lack of response to growth hormone by the patient’s tissues

works

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32
Q

c. Pituitary Dwarfism: • Clinical features:

A
  • Short stature

* Small jaws and teeth

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33
Q

c. Pituitary Dwarfism:

• Treatment:

A

if lack of production of growth hormone is the problem, then hormone replacement therapy

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34
Q

c. Pituitary Dwarfism: • Prognosis:

A

Good (if replacement therapy works)

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35
Q

I. Normal Thyroid: Function

A

o Produces hormones that regulate the rate at which the body carries out its necessary functions

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36
Q

I. Normal Thyroid

• Anatomy

A

o Located in the middle of the lower neck, below the larynx and above the clavicles
o “Bow tie” shape

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37
Q

I. Normal Thyroid

• embryology

A

o develops from an invagination of endoderm which arises at the base of the tongue, in the region of the foramen cecum
o migrates caudually to its location anterior and inferior to the thyroid cartilage

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38
Q

I. Normal Thyroid

• histology

A

o follicles filled with colloid and lined by cuboidal follicular cell
o small nests of C-cells scattered between the follicles; not visible without special stains

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39
Q

II. Hyperthyroidism

• Most common causes are

A

o Graves disease (Diffuse toxic hyperplasia) (#1 cause)
o ingestion of excessive exogenous thyroid hormone (TH)
o hyperfunctional multinodular goiter
o hyperfunctional thyroid adenoma
o TSH-secreting pituitary adenoma (Rare)

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40
Q

II. Hyperthyroidism

• Clinical manifestations-

A

Hypermetabolic state, Overactivity of the sympathetic nervous system
o Hypermobility (increased activity—can’t sit still)
o G-I hypermobility, malabsorption and diarrhea
o Tachycardia, palpitations, irritability
o Nervousness, tremor, irritability, proximal myopathy
o Wide, staring gaze with eyelid lag
o Exophthalmos (bulging of the eyes) with Graves’ disease
o Heat intolerance and excessive sweating
o Soft, warm, flushed skin
o Weight loss despite increased appetite

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41
Q

II. Hyperthyroidism:

o Thyroid Storm

A
  • Abrupt onset of hyperthyroidism usually triggered by stress
  • Patients can die of cardiac arrhythmia if untreated – A medical emergency
  • Treatment: Depends on the cause. Reactive iodine can be used to destroy overactive thyroid tissue
  • Prognosis: Good (If identified and treated properly)
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42
Q

II. Hyperthyroidism:

• Diagnosed by

A

elevated TH and decreased TSH (primary hyperthyroidism)

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43
Q

Graves’ Disease

A

• female predominance, F:M 7:1
o Common, 1.5-2% of US women
• hyperthyroidism; exophthalmos (40%); skin lesions
o pretibial myxedema, scaly thickening of skin overlying shins
• autoimmune, significant genetic component
o Autoantibodies to TSH receptor; constantly stimulated

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44
Q

Graves’ disease

• pathology

A

o diffuse enlargement of the thyroid on gross examination
o hyperplasia of follicles with lymphoid infiltrates
o Increase in serum free TH, decreased serum TSH

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45
Q

III. Hypothyroidism:

A

o Primary or secondary

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46
Q

III. Hypothyroidism:

o Common causes

A

o Ablation by surgery or radiation therapy
o Hashimoto thyroiditis (Autoimmune destruction)
o Iodine deficiency

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47
Q

III. Hypothyroidism:

o Clinical manifestations

A

Cretinism

o Myxedema

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48
Q

III. Hypothyroidism:

o Measure serum TSH

A

o Increased in primary due to loss of feedback inhibition

o Not increased in cases caused by primary hypothalamic or pituitary disease

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49
Q

III. Hypothyroidism: o Treatment:

A

Thyroid hormone replacement therapy (Synthroid)

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50
Q

Hypothyroidism: o Prognosis:

A

Good unless treatment is delayed. The damage to skeletal and nervous systems could be permanent

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51
Q

o Cretinism

A
  • Develops in childhood
  • Rare now due to iodine supplementation in diet
  • Impaired development of skeleton and CNS
  • Coarse facial features
  • Short stature
  • Severe mental retardation
  • Protruding tongue
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52
Q

o Myxedema

A
  • Develops in older children and adults
  • Generalized apathy and mental sluggishness (mimics depression)
  • Cold-intolerance, obese
  • Coarse facial features, enlargement of tongue, deepening of voice, constipation, late cardiac effects
  • Accumulation of mucopolysaccharide-rich edema
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53
Q

Hashimoto Thyroiditis

A

o female predominance, 10:1 to 20:1
o usually older women
o significant genetic component
o Most common cause of hypothyroidism where dietary iodine is sufficient
o Autoimmune; progressive destruction of parenchyma with inflammatory infiltrates
o Involves CD4+, CD8+, and NK cells

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54
Q

Hashimoto thyroiditis: o initially

A

euthyroid, with progression of disease most patients will become hypothyroid
o Painless thyroid enlargement with hypothyroidism

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55
Q

Hashimoto thyroiditis: o Some cases are preceded by

A

transient hyperthyroidism

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56
Q

Hashimoto thyroiditis: o Patients usually at risk for

A

other autoimmune diseases and B-cell Non-Hodgkin lymphomas

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57
Q

Hashimoto thyroiditis: o No established risk of

A

development of thyroid neoplasm

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58
Q

Goiters

• Most common manifestation of

A

thyroid disease

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59
Q

Goiters: • Diffuse and multinodular goiters reflect

A

impaired synthesis of thyroid hormone

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60
Q

Goiters: o Most often due to

A

dietary deficiency, though some cases are idiopathic

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61
Q

Goiters: o Impairment of

A

TH synthesis → increase in serum TSH → hypertrophy and hyperplasia of thyroid follicular cells → gross enlargement of gland

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62
Q

Goiters: • Most common clinical features are due to

A 
mass effects
o	Cosmetic problem
o	Airway obstruction
o	Dysphagia
o	Compression of vessels
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63
Q

Goiters: • Hyperfuctional,

A

“toxic’ goiter
o In a minority of patients, the a “toxic” nodule may develop in a long-standing, non-toxic goiter
o Hyperthyroidism

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64
Q

Thyroid Neoplasms

o solitary thyroid nodules may be detected in

A

2-4% of the general population

65
Q

Thyroid Neoplasms: o most nodules are

A

non-neoplastic disease (1% are carcinomas)

66
Q

Thyroid Neoplasms: o Nodules in young patients are

A

more likely to be neoplastic

67
Q

Thyroid Neoplasms: o Nodules in males are more likely to be

A

neoplastic

68
Q

Thyroid Neoplasms: o genetic and environmental factors

A

o exposure to radiation in first 2 decades

69
Q

Follicular Adenoma

A

o solitary nodules, 3-5 cm in diameter
o grossly separated from the normal thyroid by a thin, discrete capsule
o microscopically composed of follicles with varying amounts of colloid

70
Q

0

Papillary Thyroid Carcinoma

A

o accounts for >85% of thyroid cancers
o 3rd-5th decade, F»M
o 60-70% are multifocal
o some cases related to radiation exposure
o Many have mutations in the RET proto-oncogene

71
Q

Papillary thyroid carcinoma: o Pathology

A

o microscopically characterized by papillary projections
o distinctive nuclear changes
o nuclear clearing, aka “orphan annie nuclei”
o nuclear grooves
o nuclear inclusions
o nuclear enlargement

72
Q

Papillary thyroid carcinoma: o Indolent lesions,

A

10-year survival rates >95%

o poor prognostic features include extrathyroidal extension and elderly

73
Q

Follicular Carcinoma

A

o accounts for 5-15% of thyroid cancers
o Older age than papillary; areas with dietary iodine deficiency
o grossly may resemble an adenoma with a discrete capsule
o Must see invasion through the capsule or into the blood vessels

74
Q

Anaplastic Thyroid Carcinoma

A

o Rare <5%; typically presents as rapid enlargement in a long standing goiter
o extremely poor prognosis

75
Q

Medullary Thyroid Carcinoma

A

o uncommon, accounts for 5% of thyroid cancer
o derived from the parafollicular (C) cells
o may be sporadic or familial (component of MEN syndromes)
o All have mutation in the RET proto-oncogene
o Increased serum calcitonin

76
Q

Parathyroid Glands

I. Normal
o embryology

A

o Derived from the third and fourth pharyngeal pouches

77
Q

Parathyroid Glands

I. Normal
o anatomy

A

o typically 4 parathyroid glands, 1 at each corner of the posterior surface of the thyroid

78
Q

Parathyroid Glands

I. Normal
o histology

A

o composed mostly of chief cells (principal cells, clear cells), secrete PTH
o oxyphil cells; unknown function

79
Q

Parathyroid Glands

I. Normal
o PTH

A

o Decreased levels of free calcium in the bloodstream stimulate the synthesis and secretion of PTH, with the following effects
• Increase in renal tubular reabsorption of calcium
• Increase in urinary phosphate excretion
• Increase in the renal conversion of vitamin D into its active form, which in turn increases gastrointestinal calcium absorption
• Increase in osteoclastic activity which releases calcium from the bones
o Net effect: increase in the level of free calcium, which inhibits further PTH secretion

80
Q

II. Hyperparathyroidism

• An important cause of

A

hypercalcemia

81
Q

Hyperparathyroidism: • Excessive secretion of

A

parathyroid hormone (PTH)

82
Q

Hyperparathyroidism:

• Two types

A

o Primary: an autonomous spontaneous overproduction of PTH

o Secondary: a secondary phenomenon in patients with chronic renal failure

83
Q

Hyperparathyroidism: • Treatment:

A

Surgical removal of hyperplastic parathyroid glands. Kidney transplant may be beneficial in patients with hyperparathyroidism secondary to renal failure.

84
Q

Hyperparathyroidism: • Prognosis:

A

Usually good

85
Q

Primary hyperthyroidism:

o Common

A

endocrine disorder generally affecting adults

hyperparathyroidism

86
Q

Primary hyperthyroidism:o Caused by

A

parathyroid adenomas or hyperplasia → hypercalcemia

o Clinical features

87
Q

Primary hyperthyroidism:: o More common in

A

women (4:1); often clinically silent

88
Q

Primary hyperthyroidism:: o Classic constellation of symptoms

o Currently, routine blood tests taken for other reasons often detect clinically silent

A

• Painful bones: Fractures associated with osteoporosis
• Renal stones
• Abdominal groans: Constipation, peptic ulcers, and gallstones
• Psychic moans: Refers to depression, lethargy and seizures
o Weakness and fatigue
o Brown tumor of hyperparathyroidism can develop in the jaws
o Ground glass appearance
o Metastatic calcifications
• Deposition of calcium in throughout body, including blood vessels

89
Q

Secondary hyperthyroidism:

A

• Renal failure is most common cause

90
Q

Secondary hyperthyroidism: o Decreased phosphate excretion

A

→ hyperphosphatemia → depresses serum calcium levels → stimulates parathyroid glands (which become hyperplastic)

91
Q

Secondary hyperthyroidism: • Normally kidneys would increase

A

Vit D synthesis to increase Ca absorption in gut to compensate
• But because they aren’t working, there is decreased renal synthesis of Vitamin D and reduced intestinal absorption of calcium

92
Q

Secondary hyperthyroidism:: • Symptoms are dominated by renal PTH sustains serum calcium

A

failure

93
Q

Secondary hyperthyroidism: • Same manifestations as

A

primary HPT, but usually less severe

• Bone changes- renal osteodystrophy

94
Q

Secondary hyperthyroidism: • Serum calcium remains

A

near normal because the compensatory increase in

95
Q

III. Hypoparathyroidism

A

• Uncommon
• Etiology
o surgical removal of parathyroids (inadvertently during thyroidectomy or other neck dissection)
o congenital absence (DiGeorge’s syndrome)
o auto-immune disease

96
Q

Hypoparathyroidism: • Clinical manifestations

A

o Hypocalcemia
o Increased neuromuscular excitability
o Cardiac arrhythmias
o Increased intracranial pressure and seizures

97
Q

Normal Pancreas

• Embryology

A

o arises from endoderm of the foregut

98
Q

Pancreas: • Histology

A

• Islets of Langerhans –clusters of endocrine cells interspersed among the acinar groups that make up the exocrine pancreas

99
Q

Pancreas: • The pancreas has both

A

exocrine and endocrine functions. The exocrine pancreas makes gastric enzymes.

100
Q

Pancreas: • Cell types:

A 
cell type	hormonal product
beta 	insulin
alpha 	glucagon
delta 	somatostatin
PP	pancreatic polypeptide (VIP)
101
Q

beta

A

insulin

102
Q

alpha

A

glucagon

103
Q

delta

A

somatostatin

104
Q

PP

A

pancreatic polypeptide (VIP)

105
Q

o Glucagon:

A

mobilizes carbohydrates (stored in the liver) into circulation when the body needs them. Promotes glycogenolysis and gluconeogenesis in fasting states.

106
Q

o Insulin:

A

Major anabolic hormone, many synthetic and growth-promoting effects - allows glucose to be transported and stored in cells within the body after meals

107
Q

o Somatostatin:

A

suppresses both insulin and glucagon release

108
Q

o VIP: exerts

A

several G-I effects

109
Q

• Normal Insulin Physiology & Glucose Homeostasis

Homeostasis depends on 3 processes:

A

o Gluconeogenesis
o Glucose uptake by tissues
o Actions of insulin & glucagon
=

110
Q

Insulin increases the rate of

A

glucose transport into certain cells of the body

111
Q

Diabetes Mellitus

• Group of metabolic disorders resulting in

A

hyperglycemia (excessive amounts of glucose in the blood) due to defects in insulin secretion, insulation action, or both
• In 2015, over 30 million Americans affected (7 % of population) with ¼ undiagnosed, with 84 million pre-diabetics
• Vasculopathy with long-term complications involving kidneys, eyes, nerves
• Leading cause of end-stage renal disease (ESRD), blindness, and amputation

112
Q

Classification

• Type 1

A

(aka juvenile onset or insulin dependent diabetes mellitus)
o 5% of cases
o Severe insulin deficiency

113
Q

• Type 2 (aka adult onset or non-insulin dependent)

A

o Caused by a combination of peripheral resistance to insulin action and an inadequate response to insulin secretion by the beta cells.

114
Q

Presenting symptoms of DM

• Type 1

A

o Symptoms appear once 90% of beta cells have been destroyed, usually by age 20
o Polyuria
o Polydipsia
o Polyphagia with weight loss
o Ketoacidosis
• With fat as primary energy source: excess ketones in blood, low blood pH
• Can lead to diabetic coma

115
Q

Presenting symptoms of DM

• Type 2

A

o Usually present after age 40, but not always
o Polyuria and polydipsia may occur
o Diagnosis usually made by routine blood or urine tests
o Enhanced susceptibility of infections, periodontal disease

116
Q

Laboratory DM diagnosis

• Normal glucose is

A

70-120mg/dL

• Random blood glucose concentration of 200mg/dL or higher

117
Q

DM diagnosis: • Fasting glucose greater than

A

126mg/dL on more than one occasion

• Blood glucose greater than 200mg/dL within 2 hours of ingesting 75g of glucose (oral glucose tolerance test)

118
Q

Type 1 DM

A
  • Absolute lack of insulin secondary to autoimmune destruction of beta cells
  • Abrupt onset
  • Patients require insulin from outside sources to survive or kidney/pancreas transplantation
  • Prognosis is guarded due to many complications
119
Q

Type 2 DM

• Results from a

A

collection of multiple genetic defects, each contributing its own predisposing risk and modified by environment.
• Peripheral tissues cannot respond properly to insulin (insulin resistance)

120
Q

Type 2 DM: • Beta cell dysfunction results in

A

inadequate insulin secretion in the face of insulin resistance and hyperglycemia.

121
Q

Type 2 DM: • Disposing factors

A

o Obesity
• 80% of Type 2 DM patients are obese
• 60% of the obese exhibit glucose intolerance
• Obesity in children is implicated in development of DM as adults
• Exercise and weight loss can reverse insulin resistance and clinical evidence of disease
o Pregnancy
o Stress

122
Q

Type 2 DM: • Treatment:

A

Weight loss, improve diet, oral hypoglycemic drugs, insulin

123
Q

Type 2 DM: • Prognosis is

A

fair. Patients have complications similar to those seen in Type I. However, the disease is usually not as severe. Type I patients are more likely to die of the disease than type II patients.

124
Q

Manifestations of DM

• In pancreas

A

o Reduction of the number and size of islets
o Heavy inflammatory infiltrate
o Amyloid deposition

125
Q

Manifestations of DM:

• Vasculopathy

A

o Responsible for 80% of DM-related deaths
o Atherosclerosis is severe and accelerated
o Myocardial infarction and stroke
o Gangrene of lower extremities is 100-fold increased over normal population
o Thickened basement membrane, especially around small blood vessels (microangiopathy)

126
Q

Manifestations of DM: • Kidneys (diabetic nephropathy)

A

o 2nd leading cause behind vascular diseases, leads to HTN and ESRD
o Glomerular lesions
• Diffuse glomerulosclerosis
• 90% of diabetics within 10 years; not specific to diabetics
• Microangiopathy around glomerular capillaries and deposition of matrix
• Proteinuria, total renal failure
o Nodular glomerulosclerosis
• 15-30% of long-term diabetics; specific to diabetics
• Ball-like deposition of matrix at the periphery of the glomerulus
• Total renal failure
• Renal atherosclerosis
• Pyelonephritis

127
Q

Manifestations of DM: • Eye (retinopathy)

A

o 4th leading cause of blindness
o Microangiopathy and microaneurysms
o Retinal detachment and vision loss

128
Q

Manifestations of DM• Diabetic neuropathy

A

o Can affect the peripheral sensorimotor nerves

o Autonomic neuropathy causing disturbances in bowel and bladder function, impotence

129
Q

Manifestations of DM: • Enhanced susceptibility to

A

infections of the skin, TB, pneumonia, deep fungal infections, pyelonephritis

130
Q

Manifestations of DM: • Causes of death

A

o Type 1 > Type 2

o MI, renal failure, cerebrovascular disease, atherosclerosis, infection

131
Q

III. Islet Cell Tumors

•

A

Uncommon (<2% of all pancreatic neoplasms)
• Most are from the exocrine pancreas
• may be functional or nonfunctional
• Insulinoma (Insulin Secreting Islet Cell Tumor)
• Beta cell tumor, hyperinsulinism, most are adenomas
• Hypoglycemia quickly occurs from fasting or exercise
• Many are asymptomatic, 5-10% malignant
• Nervousness, confusion, stupor
• Surgical excision
• Gastrinoma

132
Q

Islet Cell tumors: • Arise in

A

duodenum, peripancreatic tissues, or pancreas

133
Q

With Islet cell tumors, you see:

A
  • gastric acid hypersecretion

* 90-95% of recalcitrant peptic ulcers

134
Q

• Zollinger-Ellison Syndrome

A
  • Pancreatic islet cell tumor, hypersecretion of gastric acid, severe peptic ulcers
  • Most are malignant (60%), surgical resection
135
Q

I. Normal adrenal glands:

A

• Two triangular-shaped glands located on top of the kidneys
• Adrenal Cortex (outer portion of the gland); weight: 4-5 grams; 3 zones
o zona glomerulosa – mineralcorticoids (aldosterone)
o zone fasciculata – glucocorticoids (cortisol)
o zona reticularis – sex hormones (estrogen/androgen)
• Adrenal Medulla (inner portion of the gland);: neural origin, chromaffin, source of catecholamines (epinephrine, norepinephrine and dopamine)

136
Q

Hypercortisolism (Cushing Syndrome):

• Causes

A

o Most commonly by excess administration of exogenous glucocorticoids
o Primary adrenal hyperplasia or neoplasm (e.g. adrenal adenoma)
o Primary pituitary source
• ACTH oversecretion by pituitary microadenoma
• Known as Cushing disease
o Ectopic ACTH secretion by neoplasm, e.g. lung

137
Q

Hypercortisolism (Cushing Syndrome):

• Signs and symptoms
o Short Term

A
  • weight gain and hypertension
  • “Moon facies” (accumulation of fat in the face)
  • “Buffalo hump” (accumulation of fat in the posterior neck and back)
138
Q

Hypercortisolism (Cushing Syndrome):
Signs and symptoms:
o Long Term

A
  • Decreased muscle mass, weakness
  • Diabetes
  • Osteoporosis
  • Cutaneous striae, hirsutism
  • Mental disturbances: mood swings, depression, psychosis
  • Menstrual irregularities
139
Q

Hypercortisolism (Cushing Syndrome):

• Treatment:

A

depends on the cause

• Prognosis: good

140
Q

Hyperaldosteronism

• Characterized by

A

chronic excess aldosterone secretion – causes:
o Sodium retention, Potassium excretion
o Hypertension and hypokalemia

141
Q

Hyperaldosteronism: • Primary

A

o Very rare
o Hyperplasia, neoplasm, idiopathic
o Decreased levels of plasma renin

142
Q

Hyperaldosteronism: • Secondary

A

o Aldosterone release in response to activation of renin-angiotensin system
o Increased levels of plasma renin

143
Q

III. Hypoadrenalism

A
  • Primary or
  • Secondary
  • Decreased stimulation of adrenals from deficiency of ACTH
144
Q

Hypoadrenalism: • Don’t appear until at least

A

90% of adrenal gland has been destroyed

145
Q

Hypoadrenalism:

• Manifestations

A

• Fatigue
• GI disturbances (anorexia, nausea, vomiting, weight loss, diarrhea)
- weakness

146
Q

Acute Adrenocortical Insufficiency

•

A

In patients maintained on exogenous corticosteroids, rapid withdrawal of steroids or failure to increase steroids in response to an acute stress can precipitate an adrenal crisis
• Vomiting, abdominal pain, hypotension, coma, death

147
Q

Acute Adrenocortical Insufficiency

A

• Can also be caused by adrenal hemorrhage or stress in a patient with existing Addison’s

148
Q

Primary Chronic Adrenocortical Insufficiency (Addison’s Disease)

A
  • Progressive destruction of adrenal cortex
  • Serum ACTH may be elevated → skin and mucosal pigmentation
  • Destruction of cortex prevents response to ACTH
  • Potassium retention, sodium loss, hyperkalemia, hyponatremia, volume depletion, and hypotension
149
Q

Primary Chronic Adrenocortical Insufficiency (Addison’s Disease)
• Causes

A

o Autoimmune destruction of steroid-producing cells
• Most common, 60-70% of cases
o TB
o AIDS
o Metastatic disease
• Clinical features
• Progressive weakness—easily fatigued
• GI disturbances: nausea, vomiting, anorexia, weight loss, diarrhea
• Hyperpigmentation—often involves the oral mucosa
• A craving for salt

150
Q

Primary Chronic Adrenocortical Insufficiency (Addison’s Disease)
• Treatment:

A

Corticosteroid replacement therapy

151
Q

Primary Chronic Adrenocortical Insufficiency (Addison’s Disease)
• Prognosis:

A

Guarded. Can result in death if not recognized and treated properly

152
Q

Secondary Adrenocortical Insufficiency

A

• Any disorder of hypothalamus of pituitary that reduces output of ACTH
• Symptoms similar to Addison’s disease
o But no skin/mucosa pigmentation

153
Q

Adrenal Neoplasms

A
  • Pheochromocytoma

* Multiple Endocrine Neoplasia (MEN) Syndromes

154
Q

• Pheochromocytoma

o neoplasm of

A

chromaffin cells, F > M, 30-60 yrs.

155
Q

Chromaffin cells produce

A

epinephrine.

156
Q

Pheochromoctyoma:

A

o Hypertension, tachycardia, tremor, headache
o Surgically correctible
o rule of 10’s: 10 % bilateral, extra-adrenal, malignant, familial syndromes
o large polygonal cells with variable pleomorphism

157
Q

• Multiple Endocrine Neoplasia (MEN) Syndromes

A 
•	Types I, 2A, and 2B
•	Tumors of multiple endocrine organs
      o	Medullary Thyroid Carcinoma
     o	Pheochromocytoma
     o	Parathyroid 
     o	Pituitary
     o	Pancreas
•	RET proto-oncogene
158
Q

• MEN 2B notable for early orofacial manifestations

A

o Mucosal neuromas (tongue, labial commisure)
o Large, blubbery lips
o Marfanoid body habitus
o Early onset medullary carcinoma of thyroid

Gen Path Final (18 decks)

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