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23 General Pathology > 11 - Endocrine System > Flashcards

11 - Endocrine System Flashcards

1
Q

what are the major endocrine glands

A
  1. hypothalamus
  2. pituitary glands
  3. Thyroid gland
  4. Parathyroid gland
  5. Islet cells of the pancreas
  6. Adrenal glands
  7. Testes in men, and the ovaries in women
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2
Q

Source, major target organ(s) and major physiologic effects:

growth hormone

A

source: anterior pit
target: liver, adipose tissue
effects: promotes growth; control of proteins, lipids and metabolism

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3
Q

Source, major target organ(s) and major physiologic effects:

TSH

A

source: anterior pit
target: thyroid gland
effects: stimulates secretion of thyroid hormones

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4
Q

Source, major target organ(s) and major physiologic effects:

adrenocorticotropic hormone ACTH

A

source: anterior pit
target: adrenal gland (cortex)
effects: stimulates secretion of glucocorticosteroids

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5
Q

Source, major target organ(s) and major physiologic effects:

prolactin

A

source: anterior pit
target: mammary gland
effects: milk production

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6
Q

Source, major target organ(s) and major physiologic effects:

LH

A

source: anterior pit
target: ovaries and testis
effects: control of reproducive function

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7
Q

Source, major target organ(s) and major physiologic effects:

FSH

A

source: anterior pit
target: ovaries and testis
effects: control of reproductive function

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8
Q

Source, major target organ(s) and major physiologic effects:

ADH

A

source: posterior pit
target: kidney
effects: conservation of body water

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9
Q

Source, major target organ(s) and major physiologic effects:

oxytocin

A

source: posterior pit
target: ovaries and testis
effects: stimulates milk, ejaculation and uterine contractions

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10
Q

both anterior and posterior lobes of pituitary are under control of ___ which is connected by ___

A

hypothalamus; pituitary stalk

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11
Q

what is the master gland

A

pituitary gland

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12
Q

what are the most common cause of hyperpituitarism

A

pituitary adenomas

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13
Q

what are the types of pituitary adenomas

A

functioning (majority) and nonfunctioning

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14
Q

what size is microadenoma? macroadenoma?

A

<1 cm = microadenoma (means benign tumor)
>1 cm = macroadenoma

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15
Q

The signs and symptoms of pituitary adenoma are related to the ___ and ___

A

endocrine abnormalities and mass effects

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16
Q

can the biologic behavior of the adenoma be reliably predicted from its histologic appearance

A

no

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17
Q

what is the most common hyperfunctioning pituitary adenoma that is prolactin secreting?

A

lactotrophic adenoma

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18
Q

symptoms of lactotrophic adenoma

A

Galactorrhea
Amenorrhea
Infertility
Loss of libido

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19
Q

who gets lactotrophic adenoma? how is it treated

A

> women; between 20-40 years of age
In older women and men, the hormonal
manifestations may be subtle
Treated with dopamine receptor agonists
(bromocroptone) if small; surgery if large

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20
Q

what is a growth hormone secreting adenoma that is the second most type of functioning pituitary adenomas

A

somatotrophic adenoma

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21
Q

what causes giagantism in children and acromegaly in adults?

A

somatotrophic adenoma

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22
Q

what are elevated levels of GH before closure of epiphyseal plates (13-15 years for girls and 15-17 years for boys)

A

gigantism

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23
Q

does growth occur symmetrically in gigantism

A

yes

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24
Q

if increased GH levels persis beyond ephiphyseal closure in gigantism, what happens

A

acromegally is superimposed

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25
Q

Elevated levels of GH after closure of epiphyses; Growth noted in soft tissues, skin, viscera, and bones of face, hands & feet

A

acromegaly

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26
Q

oral manifestation of acromegaly

A

prognathia (protrusion of mandible), teeth separation, and macroglossia

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27
Q

treatment of acrimegaly

A

surgery; dopamine agonits

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28
Q

what disease:
Failure to suppress GH production in
response to an oral load of glucose is one of
the most sensitive tests for acromegaly

A

somatotrophic adenoma

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29
Q

how can somatrotrophic adenoma be removed

A

surgically or treated pharmacologically with GH receptor antagonists

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30
Q

what adenoma:
Excess production of the ACTH leads
to adrenal hypersecretion of cortisol
and the development of
hypercortisolism (Cushing disease)

A

corticotroph adenoma

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31
Q

difference between cushing SYNDROME vs DISEASE

A

syndrome: increase steroid medication, adrenal gland adenoma, increased ACTH production by lung canger, or treat the cause of increased level of cortisol

disease: pituitary gland tumor results in increased ACTH causing hyperplasia of adrenal gland which further results in increased cortisol levels, tx is surgery of pituitary or adrenal gland

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32
Q

what is this:

Moon facies
Buffalo hump
Truncal obesity
Violaceous striae
Hirsutism
Hypertension
Glucose intolerance or diabetes mellitus
Visual symptoms if adenoma large

A

cushing disease (selena gomez)

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33
Q

Refers to decreased secretion of pituitary
hormones, which can result from diseases of
the hypothalamus or the pituitary

A

hypopituitarism

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34
Q

T/F: Hypofunction of the anterior pituitary occurs when approx. 75% of the parenchyma is lost

A

TRUE

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35
Q

When accompanied by posterior pituitary dysfunction (diabetes insipidus), hypopituitarism is almost always of ___

A

hypothalamic origin

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36
Q

most cases of hypopituitarism arise from processes involving what? examples?

A

anterior pituitary

  1. Tumors and other mass lesions
  2. Traumatic brain injury
  3. Pituitary surgery or radiation
  4. Pituitary apoplexy (sudden hemorrhage in pituitary gland, often occurring in a pituitary adenoma)
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37
Q

what is ischemic necrosis of anterior pituitary also called

A

Sheehan syndrome aka postpartum pituitary necrosis

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38
Q

what is the most common form of ischemic necrosis of anterior pituitary

A

sheehan syndrome

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39
Q

with sheehan syndrome during pregnancy, what happens to anterior pit

A

enarlges 2x size

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40
Q

in sheehan syndrome, is the expansion of gland accompanied by increased in blood supply?

A

no

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41
Q

in sheehan syndrome, since posterior pituitary is supplised directly by arterial branches, is it more or less susceptible to ischemic injury

A

less susceptible

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42
Q

what is the absence of lactation called

A

agalactorrhea

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43
Q

symptoms and tx of sheehan syndrome

A

symptoms:
- agalactorrhea
- amenorrhea or oligomenorrhea
- hot flashes
- decreased sex drive

tx: lifelong replacement of deficient hormones

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44
Q

clinical relevant posterior pituitary syndromes involve what

A

ADH

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45
Q

what are posterior pituitary syndromes

A
  1. diabetes insipidus
  2. syndrome of inappropriate secretion of ADH
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46
Q

what is caused by ADH deficiency and characterized by excessive urination (polyurea) due to inability of kidneys to resorb water properly from urine

A

diabeted insipidus

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47
Q

DI can occur from what conditions

A

Head trauma
Tumors
Inflammatory disorders of hypothalamus and pituitary
Surgical complications
Genetic basis (rare)

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48
Q

symptoms of DI and tx

A

Extreme thirst
Dry mouth
Dizziness, fatigue, and nausea
Frequent urination

tx: desmopressin (synthetic aDH)

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49
Q

what is this:
ADH excess causes over resorption of free water, resulting in hyponatremia

A

secretion of inappropriate ADH secretion (SIADH)

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50
Q

most frequent causes of SIADH

A

Secretion of ectopic ADH by malignant neoplasm
(small cell ca of the lungs)
Drugs that increase ADH secretion
A variety of CNS disorders including infections and
trauma

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51
Q

in SIADH, if the total body water is increased, does blood volume remain normal with no peripheral edema

A

YES

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52
Q

what this:

Consists of two lateral lobes connected with a thin isthmus
Located below and anterior to the larynx
It develops from an evagination of the
pharyngeal epithelium that descends from the foramen caecum at the base of the tongue to its position in the anterior neck

A

thyroid gland

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53
Q

the thyroid is divided by thin fibrous septae into lobules composed of what?

A

20-40 follicles

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54
Q

what are thyroid follicles lined by

A

cuboidal or low columnar epi and filled with PAS positive thyroglobulin

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55
Q

In response to ___, TSH is
released from the anterior pituitary gland into the circulation

A

hypothalamic factors

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56
Q

where does TSH bind

A

receptors on thyroid follicular epi cells

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57
Q

thyroid follicular epi cells convert thyroglobulin to what?

A

thyroxine - T4
triiodinethyronine - T3

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58
Q

T3 binds to what in target cells

A

thyroid hormone nuclear receptors

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59
Q

affects of T3 and T4 on cellss

A
  1. Stimulation of carbohydrate and lipid catabolism
  2. Protein synthesis
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60
Q

what is #1 function of thyroid gland

A

increase in basal metabolic rate

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61
Q

what is #2 function of thyroid gland/ohrmone

A

brain development in fetus and neonates

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62
Q

what are chemical agents that inhibit function of thyroid gland

A

goitrogens

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63
Q

why do goitrogens cause hyperplastic enlargement of gland (goiter)

A

they suppress T3 and T4 synthesis and TSH level increases

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64
Q

what is this:

Part of the follicle
Synthesize and secrete the hormone calcitonin
This hormone promotes the absorption of calcium by the skeletal system and inhibits resorption of bones by osteoclasts

A

parafollicular cells (c cells)

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65
Q

what are hyperthyroidism diseaes

A
  1. graves disease (immune mediated)
  2. thyrotoxicosis
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66
Q

what is the hypermetabolic state caused by elevated circulating levels of free T3 and T4

A

thyrotoxicosis (hyperthyroidism)

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67
Q

most common causes of thyrotoxicosis

A
  1. Diffuse hyperplasia of the thyroid associate with Graves disease (85% cases)
  2. Hyperfunction multinodular goiter
  3. Hyperfunction thyroid adenoma
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68
Q

thyrotoxicosis clinical features

A
  1. increase basal metabolic rate
  2. cardiac manifestations
  3. overactivity of sympathetic nervous system
  4. occular changes
  5. skeletal system affected
  6. thyroid storm
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69
Q

what is the most useful single screening test for hyperthyroidism?

A

low TSH values!!! measurement of serum TSH concentration

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70
Q

In occasional patients, can hyper thyroidism result predominantly from increased circulatory levels of T3 (T3 toxicosis); where in these cases, free t4 levels may be decreased?

A

YES

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71
Q

tx for hyperthyroidism

A
  1. beta blockers
  2. thioamide
  3. iodine solution
  4. radioactive iodine
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72
Q

what are hypothyroid diseases

A
  1. cretinism
  2. myxedema
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73
Q

Condition caused by a structural or functional derangement that interferes with the production of thyroid hormone
Prevalence increases with age
women (10W;1M)

A

hypothyroidism

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74
Q

Refers to hypothyroidism that develops in
infancy and early childhood

A

cretinism

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75
Q

clinical features of cretinism

A

Severe intellectual disability
Short stature
Coarse facial features
Protruding tongue
Umbilical hernia

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76
Q

what is hypothyroidism development in older child or adult

A

myxedema

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77
Q

clinical findings of myxedema

A

Early symptoms include generalized fatigue, apathy, and mental sluggishness which mimics depression
Speech and intellectual functions are slowed, and patients are listless, cold intolerance, and frequently overweight
Skin is cold
Reduced cardiac output

78
Q

measurement of what is the most sensitive screening test for hypothyroidism

A

serum TSH levels

79
Q

Diverse group of disorders characterized by
some form of thyroid inflammation

A

thyroiditis

80
Q

what is clinically significant form of thyroiditis

A

hashimoto thyroiditis

81
Q

what is an autoimmune disease, results in destruction of thyroid gland and gradual and progressive thyroid failure, between 45 to 65 years of age, more in women

A

hashimoto thyroiditis

82
Q

Caused by a breakdown in self-tolerance to
thyroid autoantigens
Predisposition has a strong genetic
component

A

hashitomo thyroiditis

83
Q

Painless enlargement of the thyroid gland
associated with some degree of hypothyroidism
> in middle-aged women
Enlargement symmetric and diffuse
Incidences are at an increased risk for
developing other autoimmune disease
They are also at an increased risk of B-cell
lymphoma

A

hashimoto thyroiditis

84
Q

lab values of hashimoto thyroidities

A

Fall in serum levels to T3 and T4
Compensatory increased serum TSH

85
Q

Autoimmune disorder
Peak incidence between 20 and 40 years of age
> women (10:1)
Characterized by the production of autoantibodies against multiple thyroid proteins most importantly the TSH receptors
Most common cause of endogenous hyperthyroidism

A

graves disease

86
Q

clinical findings of graves disease

A
  1. hyperthyroidism
  2. infiltrative opathalmopathy
  3. localized, infiltrative dermoopathy, sometimes called pretibial myxedema
87
Q

graves disease lab values

A

Elevations in serum levels to T3 and T4
Decreased serum TSH

88
Q

graves disease tx

A

Treated by beta blockers (dampened symptoms related to increased sympathetic nervous system activity)
Radioiodine ablation
Thyroidectomy

89
Q

Enlargement of thyroid caused by impaired
synthesis of thyroid hormone, which is most
often the result of dietary iodine deficiency

A

goiter

90
Q

is goiter autoimmune deficiency?

A

no

91
Q

Reduced thyroid hormone production leads to compensatory rise in serum TSH level, which, in turn, causes hypertrophy and hyperplasia of thyroid follicle cells and ultimately enlargement of thyroid gland

A

goiter

92
Q

This increase in the functional mass of the gland in goiter usually overcomes the hormone deficiency, enduring a ___ in most individuals

A

euthyroid metabolic state (normal function)!!!!!

93
Q

two types of goiter

A
  1. diffuse nontoxic goiter
  2. multinodular goiter
94
Q

Causes enlargement of the entire gland
without producing nodularity

A

diffuse nontoxic simple goiter

95
Q

clinical features of diffuse nontoxic goiter

A

Most patients with simple goiter are clinically euthyroid
Therefore, clinical manifestations are
primarily related to mass effect from the
enlarged thyroid gland

96
Q

lab values of diffuse nontoxic goiter

A

Serum T3 and T4 levels are normal
Serum TSH is usually elevated

97
Q

Produce the most extreme thyroid
enlargement; frequently mistaken for
neoplasms

A

multinodular goiter

98
Q

Arise because of variations among follicular
cells in their response to external stimuli,
such as trophic hormones

A

multinodular goiter

99
Q

clinical features of multinodular goiter

A

Dominant feature is causation of mass effect
Cosmetic effects
May cause airway obstruction
Dysphagia
Most patients are euthyroid (normal funcitoning thyroid gland)

100
Q

diffuse nontoxic goiter lab values

A

Serum T3 and T4 levels are normal
Serum TSH is usually elevated

101
Q

what are neoplasms of thyroid

A

thyroid adenoma and thyroid carcinoma

102
Q

do benign thyroid neoplasms or malignant thyroid neoplasms outnumber?

A

benign

103
Q

A history of radiation therapy to the head and neck region is associated with an [ increased OR decreased] incidence of thyroid malignancy

A

increased

104
Q

Typically discrete, solitary masses, derived
from follicle epithelium, and hence they are
known as follicular adenomas
Most are nonfunctional nodules
Solitary painless masses that are discovered
on routine physical examinations
Larger masses may produce difficulty in
swallowing

A

thyroid adenoma

105
Q

thyroid adenoma tx

A

surgical excision of any suspicion nodules

106
Q

5-year SR > 95%
> women
> after the age of 30
Frequently presents without any symptom
Sign: neck mass
Symptoms: hoarseness or change in voice

A

thyroid carcinoma

107
Q

thyroid carcinoma subtypes

A

papillary thyroid carcinoma (follic) (most common)
medullary carcinoma (c cell)

108
Q

lymphoma of thyroid occurs in setting of what? is it curable?

A

setting of autoimune hashimoto thyroiditis
highly curable

109
Q

what are parathyroid gland diseases

A
  1. hyperparathyroidism
  2. hypoparathyroidism
110
Q

how many glands in parathyroid galnd? what cell types?

A

4 glands, composed of 2 cell types:
Chief cells
Oxyphil cells (have secretory granules containing
parathyroid hormones)

111
Q

function of parathyroid gland

A
  1. To regulate calcium homeostasis
  2. The activity of the parathyroid gland is controlled by the levels of free (ionized) calcium in the blood
  3. Decreased levels of free calcium stimulates the synthesis and release of the PTHhormone
112
Q

classifications of hyperparathyroidism

A
  1. primary - adenoma or hyperplasia
  2. secondary - chronic renal failure
  3. tertiary - after renal transplant
113
Q

One of the most common endocrine disorders,
and it is an important cause of hypercalcemia

A

primary hyperparathyroidism

114
Q

1 cause of hyperPTH

A

adenoma

115
Q

Disease of adults
> women
Most common cause is a solitary sporadic
adenoma
May be asymptomatic and identified on
routine blood chemistry profile or associated with the classic clinical manifestations of bones, stones, abdominal groans, and moans

A

primary hyperPTH

116
Q

lab valuses of primary PTH

A

high serum calcium
high serum alkaline phosphatase

117
Q

treatment of primary hyperPTH

A

surgical excision of enlarged gland

118
Q

why is brown tumor brown

A

bc old blood hemorrhage

119
Q

Cystic bone lesions may appear
in severely affected patients
Hemorrhage and old blood give
the brown appearance
May affect jaw bones
Identical to the much more common
central giant cell granuloma
Excessive osteoclast activity

A

brown tumor

120
Q

Most severe skeletal manifestation
Develops from central degeneration
and fibrosis of long-standing brown
tumor

A

Osteitis fibrosa cystica

121
Q

what contains the islents of Langerhans

A

endocrine pancrease

122
Q

major and minor cells types of endocrine pancreas

A

The major cell types are :
a, B, d, and PP (pancreatic polypeptide) cells

Minor cell types:
D1 cells
Enterochromaffin cells

123
Q

___ produce ___, which regulates glucose utilization in tissues, and reduces blood glucose levels

A

beta cells; insulin

124
Q

___ secrete ___, which stimulates glycogenolysis in the liver and thus increases
blood sugar

A

alpha cells; glucacon

125
Q

___ secrete ___, which suppresses
both insulin and glucagon release

A

delta cells; somatostatin

126
Q

___ secrete ___,
which exert several GI effects, such as
stimulation of secretion of gastric and intestinal
enzymes and inhibition of intestinal mobility

A

PP cells; pancreatic polypeptides

127
Q

___ secretes vasoactive intestinal
polypeptides, a hormone that induces
glycogenolysis and hyperglycemia

___ synthesize serotonin

A

D1 cells; Enterochromaffin cells

128
Q

Group of metabolic disorders sharing the
common feature of hyperglycemia, caused
by defects in insulin secretion, insulin
action, or most commonly, both

A

diabetes mellitus

129
Q

what should blood sugar normally be

A

Blood sugar is normally maintained at a very
narrow range of 70-120mg/dL

130
Q

DM fasting plasma glucose

A

> or = to 126mg/dL

131
Q

DM random plasma glucose

A

> or = to 200mg/dL

132
Q

DM 2 hour plasma glucose during oral glucose tolerance test (OGTT) w/ 75 g loadnig dose

A

> or = to 200mg/dL

133
Q

DM glycated hemoglobin HbA1c level

A

< or = to 6.5%

134
Q

Autoimmune disease characterized by pancreatic ß cells destruction and an absolute deficiency of insulin (5%-10% of cases)

Diagnosed in patients younger than 20
years of age

A

Type 1 DM

135
Q

Peripheral resistance to insulin action
A secretory response by pancreatic ß cells
that is inadequate to overcome insulin
resistance (90%-95% cases)
Vast majority of patients are overweight

A

Type 2 DM

136
Q

onset, weight, insulin levels, and ketotic?

type 1 DM

A

onset: childhood
weight: normal or weight los
insulin: progressive decrease in insulin
keto: diabetic keto acidosis in absence of insulin therapy

137
Q

onset, weight, insulin levels, and ketotic?

type 2 DM

A

onset: adults
weight: obese
insulin: early increased blood insulin, later has normal or moderate decrease in insulin
keto: nonketotic hyperosmolar coma more common

138
Q

pathogenesis of type 1 dm

A

dysfunction in T cells selection and regulation leading to breakdown of self toelrance to islet autoantigens

139
Q

pathogenesis of type 2 DM

A

insulin resistance in peripheral tissues, failure of compensation by beta cells

140
Q

pathology of type.1 dm

A

insulitis (inflammatory infiltrate of T cells and macrophages), beta cell depletion, islet atrophy

141
Q

pathology of type 2 dm

A

no insulitis; amyloid deposition in islets, mild beta-cell depletion

142
Q

May arise at any age
Initial 1-2 years after onset, exogenous
requirements may be minimal because of
endogenous insulin secretion
Eventually, however, ß-cell function declines and
insulin requirement increases dramatically

A

t1 dm

143
Q

Typically seen in obese patients older than 40
Medical attention is sought because of unexpected
fatigue, dizziness, or blurred vision
More frequently, diagnosis is made after routine
blood testing in asymptomatic patients

A

type 2 dm

144
Q

Onset of ___ is usually marked by the triad of
polyuria, polydipsia, polyphagia, and when
severe, diabetic ketoacidosis, all resulting
from metabolic derangements

A

type 1 dm

145
Q

Diabetic ketoacidosis is a severe acute
metabolic complication of ___; may occur
less commonly in ___; clinical manifestations of

A

T1D, T2D

146
Q

clinical manifestations of ketoacidosis

A

Fatigue, nausea, and vomiting
Severe abdominal pain
A characteristic fruity odor
Deep labored breathing

147
Q

Patients with ___ may develop hyperosmolar
hyperglycemic state due to severe
dehydration resulting from sustained osmotic
diuresis; occurs in older patients who do not
maintain adequate hydration

A

T2D

148
Q

most common acute metabolic complication ___ is hypoglycemia. what does this cause?

A

in either type of DM

Causes include missing a meal, excessive
physical exertion, or excessive insulin
administration
Signs and symptoms include dizziness, confusion,
sweating, palpation, and tachycardia

149
Q

morbidity associated with long term T1D and T2D is due to what

A

damage induced large and medium sized muscular arteries - diabetic macrovascular disease

small vessels - diabetic microvascular disease by chronic hyperglycemia

150
Q

___ causes accelerated atherosclerosis, resulting in increased risk of myocardial infarction, stroke, and lower extremity ischemia

___ are more profound in
the retina, kidneys, and peripheral nerves

A

Macrovascular disease; Microvascular disease

151
Q

what are consequences of DM

A
  1. hyaline arteriolosclerosis
  2. atherosclerosis
  3. nephropathy
  4. retinopathy
  5. neuropathy
152
Q

where is hyaline arteriolosclerosis most evident

A

skin, muscle, retina, and renal glomeruli

153
Q

what is the most common cause of deaht in diabetics

A

myocardial infarction

154
Q

what is the most severely damaged organ in diabetics

A

kidney

155
Q

how an you tell if kidney is severely damaged on histology slide?

A

Kimmelstiel-Wilson lesion

156
Q

what are oral manifestations of diabetes

A
  1. dental caries
  2. periodontitis
157
Q

what are the zones of adrenal cortex

A
  1. Zona glomerulosa (synthesizes mineralocorticoids)
  2. Zona reticularis (synthesizes estrogen and androgens)
  3. Zona fasciculata (synthesizes glucocorticoids)
158
Q

what is composed of chromaffin cells (synthesize catecholamines, mainly epinephrine)

A

adrenal medulla

159
Q

what causes hyperfunction of adrenal cortex

A

1.Hypercortisolism -Cushing
Syndrome-excess cortisol
2. Hyperaldosteronism- excess
aldosterone
3. Virilizing syndromes

160
Q

what causes hypofunction of adrenal cortex

A

1.Primary adrenocortical
insufficiency-Addison Disease)

161
Q

if pituitary adenoma is responsible for hypercortisolism, it is called what

A

cushing DISEASE

162
Q

what is a disorder caused by conditions that produced elevated glucocorticoid levels (due to cortico steroid therapy, or production of adrenocorticotropic hormone by adrenal adenoma and carcinoma)

A

cushing SYNDROME

163
Q

can an ectopic ACTH be secreted by a small-cell lung carcinoma/cancer

A

yes

164
Q

Unfortunately, therapeutic corticosteroids suppress the production of ACTH by the pituitary gland to the extent that it cannot produce ACTH in response to stress. what is this episode call

A

An acute episode of hypoadrenocorticosteroid
(Addison crisis) may be precipitated

165
Q

For stressful dental and surgical procedures especially, it is often necessary to increase the corticosteroid dose because of the greater need of cortisol

Consultation with the physician who is managing the corticosteroid therapy is advised

why

A

potential of addisonian crisis

166
Q

difference between primary, secondary, and tertiary adrenal insuficciency

A

primary: adrenal problem
secondary: pituitary problem
tertiary: hypothalamus problem

167
Q

Insufficient production of adrenal
corticosteroid hormone caused by the
destruction of adrenal cortex

A

hypoadrenocorticism/addison disease

168
Q

what causes addison disease? #1 cause?

A

1 cause: Autoimmune destruction (most common cause in Western countries)

  1. Infections (TB, deep fungal infections, particularly in AIDS patients)
  2. Rarely, metastatic tumors, sarcoidosis, amyloidosis, or hemochromatosis
169
Q

when do clinical features appear in addison disease

A

until 90% of glandular tissue has been destroyed

170
Q

Caused by elevated levels of pro-
opiomelanocortin (POMC), derived from anterior pituitary and is a precursor of both ACTH and melanocyte stimulating hormone (MSH)

A

hypoadrenocorticism (addison disease)

171
Q

oral manifestations of hypoadrenocorticism (addison disease)

A

Diffuse or patchy, brown, macular
pigmentation of the oral mucosa
Often the oral mucosal changes are the first manifestation of the disease, with the skin pigmentation occurring afterwards

172
Q

difference between primary and secondary hypoadrenocorticism

A

In primary hypoadrenocorticism, plasma
levels of ACTH are high (>100 ng/L)
In secondary hypoadrenocorticism the levels
are normal (9 to 52 ng/L) or low (due to
decreased production of ACTH by the
pituitary gland)

173
Q

treatment for addison DISEASE? must you do for dental procedures

A

hormone replacement therapy

not required for dental procedures using LA and lasting less than 1 hour

174
Q

wat is major source of catecholomines in body

A

adrenal medulla

175
Q

neoplasms of adrenal medulla

A
  1. Neoplasms of chromaffin cells (pheochromocytomas)
  2. Neuronal neoplasms (neuroblastic tumors)
176
Q

adrenal medulla cancers

A
  1. pheochromocytoma
  2. neuroblastoma
177
Q

Rare, chromaffin cell tumor of the adrenal medulla; synthesize and release catecholamines and in some cases peptide
hormones

Important to recognize them because they are a rare cause of surgically correctable hypertension

A

pheochromocytoma

178
Q

pheochromocytoma rule of 10s

A

10% of pheochromocytomas are extra-adrenal

10% of sporadic adrenal pheochromocytomas are bilateral

10% of adrenal pheochromocytomas
are biologically malignant

10% of adrenal pheochromocytomas are not associated with hypertension

179
Q

Cancer composed of immature neuroblasts
(immature nerve cells)

Most commonly arises in and around the
adrenal glands which have similar origin to nerve cells

Common malignant tumor in childhood
Medianage at presentation 23 months, peak 0-4 years

Slightly more common in boys (1.2:1)

A

neuroblastoma

180
Q

what are the multiple endocrine neoplasia syndromes

A

MEN Type 1, 2A, 2B, and 4

THERE IS NO 3

181
Q

is MEN AD or AR? what does this result in

A

AD

hyperplasia, adenoma, and carincoma

182
Q

AD inheritance

Syndrome characterized by mutations in MEN1 gene

Development of multiple endocrine tumors (and other tumor types)

Classic constellation of pituitary, parathyroid and pancreatic tumors (the 3 P’s)

Variety of nonendocrine tumors are also part of this (meningioma, ependymoma,
angiofibroma)

A

MEN 1 Syndrome (Wermer)

183
Q

is men 2a or 2b more common

A

2a

184
Q

what cause men 2 syndrome

A

Both conditions are due to one of the several RET
proto-oncogene mutations

185
Q

how does men 2 affect thyroid and adrenal glands?

A

thyroid - medullary thyroid cancer when yound adults

adrenal glands - pheochromocytomas

186
Q

what is characterized by
Pheochromocytoma
Medullary carcinoma of the thyroid
Parathyroid hyperplasia

A

men 2s - sipple syndrome

187
Q

which men syndrome features ORAL FEATURE

A

men 2b

Ganglioneuromas of mucosa of GI tract, lips & tongue

188
Q

These patients have clinical features that
photocopy MEN-1 patients
In contrast to MEN-1, they harbor germline
CDKN1B mutations leading to reduced levels of
the cell-cycle checkpoints protein p27

A

men 4 syndrome

189
Q

gene mutation for men 4

A

CDKN1B mutations

190
Q

gene mutation for men 2

A

RET proto-oncogene mutations

191
Q

gene mutation for men 1

A

men1 gene

23 General Pathology (24 decks)

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