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Path Part Deaux > MT Notes Endocrine > Flashcards

MT Notes Endocrine Flashcards

1
Q

Pituitary disease clinical manifestations

A

-Hyperpituitarism
•Excess secretion of trophic hormones
•Caused by tumors, hypothalamic disorders
-Hypopituitarism
•Deficiency of trophic hormones
•Caused by ischemia, surgery, radiation, inflammation, tumor
-Local mass effects
•Sella turcica deformation
•Optic chiasm compression- bitemporal hemianopsia
•Increased intracranial pressure

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2
Q

Pituitary adenomas

A 
-Functional adenomas
  •Associated with hormone excess
  •Classified based on hormone produced, ie lactotroph adenoma
-Nonfunctional adenomas
  •Without hormone excess
-Peak incidence 35-65 years
-Nonfunctional tend to be larger when diagnosed
  •Microadenomas < 1 cm
  •Macroadenomas > 1cm
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3
Q

Lactotroph adenoma

A 
-Prolactin-secreting adenoma
  •Increased serum prolactin- hyperprolactinemia
-MC functional pituitary adenoma
  •30% of cases
-Manifestations:    
  •Amenorrhea (responsible for ¼ of cases)
  •Galactorrhea (milky nipple discharge)
  •Loss of libido
  •Infertility
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4
Q

Somatotroph adenoma

A

-Growth hormone-secreting adenoma
•2nd MC functioning pituitary adenoma
-Primary manifestations:
•Gigantism in children
•Acromegaly in adults (after epiphyseal closure- soft tissue affected)
•Effects may be subtle
•Leads to late diagnosis and relatively large tumor
-Also associated with:
•Gonadal dysfunction, diabetes mellitus, hypertension, arthritis, muscle weakness, congestive heart failure, GI cancers

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5
Q

Corticotroph adenomas

A

-Adrenocorticotrophic hormone (ACTH) secreting adenomas
•Leads to adrenal hypersecretion of cortisol
•Development of hypercortisolism (Cushing’s)
-Treated with removal of adrenal glands
•Can lead to large destructive pituitary adenomas
•Known as Nelson syndrome

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6
Q

Other anterior pituitary adenomas

A 
-Gonadotroph adenomas
  •Produce LH and FSH
  •Inefficient production; effectively nonfunctioning
       •Diagnosed by mass effect symptoms
-Thyrotroph adenomas
  •Very rare
  •Lead to hyperthyroidism
-Nonfunctioning adenomas
   •25-30% of pituitary tumors
-Pituitary carcinoma
  •Very rare
  •Craniospinal or systemic metastases
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7
Q

Hypopituitarism

A

-Decreased secretion of pituitary hormones
-Results from hypothalamic or pituitary disease:
•Tumors and other mass lesions
•Traumatic brain injury / subarachnoid hematoma
•Pituitary surgery or radiation
•Pituitary apoplexy
•Sudden hemorrhage into pituitary causing rapid expansion
•Ischemic necrosis of pituitary
•Sheehan’s syndrome
•AKA postpartum necrosis of anterior pituitary
•Obstetric hemorrhage causes vasoconstriction to enlarged pituitary

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8
Q 
Hypopituitarism
Causes (continued):
A

-Rathke cleft cyst
-Empty sella syndrome
•Any destruction of part or all of pituitary
•Primary: diaphragma sella defect allows CSF herniation into sella
•Secondary: Mass enlarges sella then is removed or undergoes infarction
•Hypothalamic lesions
•Interfere with hormone-releasing hormones
•Generally tumors, benign or malignant
•Inflammation / infection
•Genetic defects

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9
Q

Hypopituitarism

Manifestations:

A
  • Growth failure in children (pituitary dwarfism)
  • Gonadotropin deficiency -> amenorrhea, infertility, decreased libido
  • Hypothyroidism, hypoadrenalism
  • Failure of postpartum lactation
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10
Q

Posterior pituitary syndromes Manifestations involve ADH:

A
  • Central diabetes insipidus
    • Inadequate ADH production
  • Syndrome of inappropriate ADH (SIADH)
    • Excess secretion of ADH
    • Increased blood volume
    • Hyponatremia
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11
Q

Thyroid gland

A
  • -Hyperthyroidism- hypermetabolic state caused by elevated circulating levels of free T3 and/ or T4
    • Primary: Intrinsic thyroid abnormality
    • Secondary: Due to external process such as TSH-secreting pituitary tumor
  • MC causes:
    • Diffuse hyperplasia of thyroid associated with Graves (85% of cases)
    • Hyperfunctional multinodal goiter
    • Hyperfunctional thyroid adenoma
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12
Q

Hyperthyroidism Clinical manifestations:

A
  • Increase in BMR
  • Warm and flushed skin
  • Heat intolerance
  • Sweating
  • Weight loss despite increased appetite
  • tachycardia
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13
Q

Hyperthyroidism Cardiac manifestations:

A
  • Tachycardia, palpitations, cardiomegaly
  • Congestive heart failure
  • Fibrous changes
  • Thyrotoxic / hyperthyroid cardiomyopathy- left ventricular dysfunction and “low output” heart failure
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14
Q

hyperthyroid sympathetic overactivity presentations

A
  • Sympathetic overactivity
  • Tremor, hyperactivity, emotional lability, anxiety, insomnia
  • GI- hypermotility, diarrhea, decreased absorption
  • Thyroid myopathy- proximal muscle weakness and atrophy
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15
Q

hyperthyroid ocular changes

A
  • Wide, staring gaze and lid lag
    • Due to sympathetic overstimulation of superior tarsal m.
  • Thyroid ophthalmopathy occurs only in Graves
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16
Q

skeletal changes

A

osteoporosis and increased fracture risk

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17
Q

thyroid storm

A
  • Abrupt onset of severe hyperthyroidism
  • Medical emergency
  • Untreated patients may die of cardiac arrhythmia
  • MC in Graves
    • Due to elevated catecholamine due to surgery, infection, other stress
  • Fever, tachycardia common
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18
Q

apathetic hyperthyroidism

A
  • Thyrotoxicosis symptoms may be blunted in older patients due to reduced response to thyroid hormones
  • Often diagnosed incidentally during lab work-up for weight loss
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19
Q

hyperthyroidism diagnosis

A
  • Serum TSH concentration is most diagnostic
  • Free T4 usually elevated
  • Radioactive iodine uptake determines etiology (graves, toxic adenoma, thyroiditis)
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20
Q

Hyperthyroidism: Graves Disease

A

Clinical triad:
-Hyperthyroidism associated with diffuse enlargement of thyroid gland
-Infiltrative ophthalmopathy with resultant exophthalmos
Protrusion of eyeball
-Localized dermopathy (pretibial myxedema)

-MC in women 20-40 years old

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21
Q

Hyperthyroidism:

Graves disease pathogenesis

A

Production of antibodies against thyroid proteins, especially TSH receptor

  • MC thyroid-stimulating immunoglobulin (TSI)
  • Mimics TSH and causes release of thyroid hormone
  • Minority of patients may also have blocking antibodies leading to hypothyroidism
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22
Q

Goiter

A
  • enlargement of thyroid gland
  • Caused by impaired synthesis of thyroid hormone (MC iodine def.)
  • TSH production increases to compensate
  • Increased TSH causes hypertrophy of thyroid
  • Hypertrophy is usually able to compensate and TH levels are normal
    • Euthyroid metabolic state
23
Q

Diffuse nontoxic (simple) goiter

A
  • Enlargement of entire gland without nodularity
  • AKA colloid goiter due to follicles filling with colloid
  • Can be endemic (in areas of low iodine) or sporadic
24
Q

Multinodular goiter

A
  • Most longstanding simple goiter progresses to multinodular
  • Due to recurrent episodes of enlargement and involution
  • Produces most extreme thyroid enlargements
  • Frequently mistaken for neoplasm
25
Q

Hypothyroidism-

A
  • condition caused by structural or functional derangement that
  • interferes with TH production
  • May affect up to 4% subclinically
  • 10:1 Female:male ratio
  • Results from defect anywhere in hypothalamic-pituitary-thyroid axis
26
Q

Congenital hypothyroidism

A
  • MC result of endemic iodine deficiency
  • Other rare forms:
    • Dyshormonogenetic goiter- inborn errors of thyroid metabolism
    • Thyroid agenesis- complete absence of thyroid parenchyme
    • Thyroid hypoplasia- genetic mutations causing reduced size
27
Q

Autoimmune hypothyroidism

A
  • MC cause in iodine-sufficient areas
  • Majority of cases due to Hashimoto’s thyroiditis
    • Autoantibodies produced against thyroid (anti-microsomal, antithyroid peroxidase, antithyroglobulin)
  • May be associated with autoimmune polyendocrine syndrome
28
Q

Iatrogenic hypothyroidism

A
  • Caused by surgical or radiation-induced ablation
    • Resection for treatment of hyperthyroidism, neoplasm can lead to hypothyroidism
  • IV drugs can reduce thyroid function intentionally or as side effect
29
Q

Cretinism

A
  • hypothyroidism that develops in infancy or early childhood
    -Manifestations:
    -Mental retardation
    Severity depends on maternal thyroid hormone levels
    -Impaired skeletal, CNS development
    -Short stature
    -Coarse facial features
    -Protruding tongue
    -Umbilical hernia
30
Q

Myxedema

A
  • hypothyroidism developing in older children or adults
    -Slowing of physical and mental activity
    -May initially mimic depression
    -Speech and intellectual functions slowed
    -Cold intolerance
    Overweight
    -Decreased sympathetic activity
    -Constipation, decreased sweating, cool pale skin
    -Reduced cardiac output
    -Shortness of breath, decreased exercise capacity
31
Q

Cushing syndrome

A

-Elevated glucocorticoids
2 types:
1) Exogenous Cushing
2) Endogenous Cushing

32
Q

Exogenous Cushing

A

Caused by administration of glucocorticoids (iatrogenic)

Accounts for vast majority of cases

33
Q

2) Endogenous Cushing

A

2 forms:

  • ACTH-dependent
  • ACTH-independent
34
Q

ACTH-dependent cushings

A
  • adrenocorticotrophic hormones- released by anterior pituitary
  • 70% ACTH-secreting pituitary microadenomas (“Cushing disease”). May also be pituitary macroadenoma or corticotroph cell hyperplasia
  • 10% Ectopic ACTH secretion by non-pituitary tumors, MC small cell lung carcinoma
35
Q

-ACTH-independent

A
  • Primary adrenal neoplasms secrete glucocorticoids
  • MC adrenal adenoma (10%) and carcinoma (5%)
  • Elevated cortisol, low ACTH
36
Q

cushings Hypercortisolism clinical mainfestations

A
  • slow onset
  • moon face
  • buffalo hump
  • fast twitch muscle atrophy
  • 2ndary diabetes
  • thin skin
  • osteoporosis
37
Q

primary hyperaldosteronism

A
  • chronic
  • suppression of renin-angiotensin pathway
  • blood pressure elevation is MC manifestation
38
Q

Primary hyperaldosteronism is caused by?

A

3 mechanisms:

1) bilateral idiopathic hyperaldosteronism (IHA)
2) adrenocortical neoplasm
3) glucocorticoid remediable hyperaldosteronism

39
Q

bilateral idiopathic hyperaldosteronism

A
  • Nodular hyperplasia of adrenal glands
  • 60% of cases
  • MC in older patients
  • Characterized by relatively less severe hypertension
40
Q

Adrenocortical neoplasm

A
  • Either aldosterone-producing adenoma (MC) or carcinoma (rare)
  • 35% of cases involve single adenoma (Conn syndrome)
    • MC in middle-aged women
41
Q

Glucocorticoid-remediable hyperaldosteronism

A

Uncommon genetic condition, suppressible by dexamethasone

42
Q

secondary hyperaldosteronism

A
  • Aldosterone released in response to high levels of angiotensin
    • increased serum renin
43
Q

Secondary Hyperaldosteronism Clinical manifestations

A

Hypertension (MC cause of secondary hypertension)
Left ventricular hypertrophy
Increased risk of stroke, MI
Hypokalemia

44
Q

Congenital adrenal hyperplasia

A

-Lack of various enzymes involved in cortical steroid synthesis (cortisol)

45
Q

Congenital adrenal hyperplasia 3 types:

A

1) salt wasting syndrome
2) Simple virilizing adrenogenital syndrome
3) non classic or late onset adrenal virilism

46
Q

Salt-wasting syndrome

A
  • Inability to convert progesterone to deoxycorticosterone due to lack of 21-hydroxylase
  • Virtually no synthesis of mineralcorticoids
  • Salt wasting, hyponatremia, hypokalemia
  • Virilization
    • Females diagnosed in womb
    • Males not diagnosed until salt wasting crisis
47
Q

Simple virilizing adrenogenital syndrome without salt wasting

A
  • 21-Hydroxylase deficiency but with sufficient mineralcorticoid to spare salt
  • Virilization
48
Q

Nonclassic or late-onset adrenal virilism

A
  • MC form
  • Only partial 21-hydroxylase deficiency
  • May be virtually asymptomatic
49
Q

Adrenocortical insufficiency

A
  • May be primary or secondary due to decreased ACTH
  • 3 patterns:
    1) Primary acute adrenocortical insufficiency (adrenal crisis)
    2) Primary chronic adrenocortical insufficiency (Addison disease)
    3) Secondary adrenocortical insuffiency
50
Q

Primary chronic adrenocortical insufficiency (addisons disease)

A
  • progressive destruction of adrenal cortex

- asymptomatic in 9-0%

51
Q

addison’s disease (Primary chronic adrenocortical insufficiency) causes?

A
  • autoimmune adrenalitis
  • infection
    • MC = TB
  • metastatic neoplasm
  • genetic causes
52
Q

addison’s disease (Primary chronic adrenocortical insufficiency) Clinical manifestations:

A
  • Early: progressive weakness and fatigability
  • Gastrointestinal disturbances
  • Hyperpigmentation of skin (only in primary form)
53
Q

Pheochromocytoma

A
  • Neoplasm composed of chromaffin cells
    • Usually located in adrenal medulla
    • Synthesize and release catecholamines, peptide hormones
    • Rare cause of surgically correctable hypertension
    • Clinical features- (“rule of tens”)

Path Part Deaux (14 decks)

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