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Pathology for Health Professionals > W9.Ch.17. The Endocrine System > Flashcards

W9.Ch.17. The Endocrine System Flashcards

1
Q

Glands which comprise the endocrine system

A

adrenal, pituitary, thyroid, parathyroid

-scattered cells in the gonads, pancreas, intestine

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2
Q

Primary Function of the Endocrine system

A
  • to produce hormones
  • ductless glands - hormones secreted into blood or extracellular space
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3
Q

Endocine Glands Image

A
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4
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A
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5
Q

Pituitary hormones and target tissues image

A
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6
Q

Secretion of hormones in anterior pituitary

A

-regulated by positive stimulation exerted by the cells in the hypothalamus centers and by negative feedback inhibition created by hormones produced by the targen endocrine cells of the thyroid, adrenals, and gonads

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7
Q

The adrenal medula secretes

A

-epi and norepi

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8
Q

The posterior pituitary secretes

A

-oxytocine and ADH

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9
Q

Describe the cells of the thyroid

A
  • Follicular cells: secrete thyroid hormones (t4, t3)
  • C-cells: secrete calcitonin (level is influenced by calciumin serum)
  • t3 and t4 are regularted by TSH
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10
Q

The parathyroid gland secretes

A

-parathormone- stimulates the release of calcium from bones, and resorption of calcium in the kidneys

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11
Q

Facts to know about Endocrine Pathology: stimuli

A

1.) Function of endocrine glands are tightly controled by positive and negative stimuli

The function of the thyroid, adrenals, and gonads is regulated by the anterior pituitary, which secretes the trophic hormones, such as TSH, ACTH, LH, or FSH.

The function of the pituitary is in turn regulated by the hypothalamic releasing factors (e.g., gonadotropin-releasing hormone [GnRH]).

The hormones of the peripheral target glands released into the blood have a negative inhibi-tory influence on the hypothalamus and the pituitary

Lack of trophic stimuli leads to incom-plete development or atrophy of peripheral endocrine glands.

For example, congenital developmental disor-ders involving the hypothalamus result in hypogonadism(i.e., small testes or ovaries). A lack of response from the target peripheral endocrine organ and decreased feedback inhibition leads to hypersecretion of pitu-itary trophic hormones. For example, destruction of”

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12
Q

Facts to know about the endocrine systm: prolonged release

A
  • prolonged hyperstimulation of tropic hormones or metabolic signals leads to both hyperfunction and physical enlargement of the peripheral endocrine glands
  • thyroid, when overstimulated by TSH, enlarges and becomes nodular
  • hyperfunctioning endocrine glands may be hyperplastic or neoplastic.
  • -usually englarged, may be due to hyperplasia or benign malignant tumors. Distinction between the two not always apparent

-

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13
Q

Facts to know about the endocrine sysyem: hypo

A

-hypofunction of the endocrine gland is usually due to incomplete development, atrophy, or destruction of secretory cells

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14
Q

Facts to know about the endocrine system:

A

-Neoplastic or hyperplastic enlargement of endocrine glands, results in mass lesions that compress adjascent structures

  • -pituitary and optic nerve,
  • thyroid tumors bulge on side of neck or compress larynx, trachea, or blood vessels.
  • Adrena enlargement rarely compresses unless it invavdes
  • parathyroid adenomas are so small, they dont compress

Adenomas of pituitary, parathyroid, and adrenals can not be distinguished from carcinomas based on histology. Usually, presence of metasteses.

Tumors of endocrine glands may be associated withneoplasia/hyperplasia of other glands. ex. Multiple Endocrine Neoplasia

Endocrine symptoms may be paraneoplastic, caused by hormones released y tumors in non endocrine glands

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15
Q

endocrine insufficiency of pituitary causes

A
  • hypofunction
  • rare, but can occur in any age group
  • may be all cells (panhypopituitary) or select ex. hypogonadism
  • causes include: congenital defects, tumors (compress pituitaary, or destroy of hypothalamus), circulatory disturbances (ishcemia), or trauma

-

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16
Q

panhypopituitary in adults

A
  • marked by weakness, cold intolerance, poor appetite, weight loss, hypotension
  • women-do not menstruate, men-low libido
  • childhood- results in dwarfism
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17
Q

Diabetes insipidus

A
  • lack of ADH secondary to destructive lesions in the hypothalamus or pituitary stalk, or tumors in posterior pituitary
  • may be caused by tumors, infection of meneges, intracranial hemmorhage, trauma involving bones in the base of the skull
  • ADH prevents the resorption of water from fluid filtered in the renal glomeruli, therefore, patients with diabetes insipidus secrete large amounts of hypotonic urine. 5-6L/day
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18
Q

Non-functioning pituitary tumors

A
  • 25% do not produce hormone symptoms, and are hormonally silent
  • tumor mass may compress pituitary gland causing hypopitutaryism or diabetes insipidus
  • may compress optic chaism and cause blindness, or icreaced ICP
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19
Q

What is hyperthyroidism:

most nb causes

A

-is a hypermetabolic state that results from the excess of free thyroid hormones (T3, T4).

Most NB causes:

  • Autoimmunity, as in Graves disease, accounts for 85%
  • idiopathic nodular hyperplasia (toxic goiter)
  • tumors, such as hyperfunctioning thyroid adenoma
  • other causes: temp. thyroid hyperfunction in hashimotos, or unregulated intake of thyroid pills in weight loss
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20
Q

Graves Disease

A
  • autoimmune disorder resulting from the breakdown of self-tolerance to one or more thyroid components, which become autoantigenic
  • caused by antibodies to the TSH receptor on the surface of thyroid follicular cells that stimulate the production of thyroid hormones
  • in addition to these, some patients have thyroid growth stimulating antibodies, which cause the proliferation of thyroid follicular cells
  • some have TSH binding inhibitor immunoglobulins, which may stimulate or inhibit thyroid function
  • occurs 10x more often in women, and associated with other immune diseases
  • the thyroid is diffusely enlarged-also contains lymph follicles which points to autoimmunity
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21
Q

Nodular Goiter: hyperthyroid

A
  • less common cause of hyperthyroid
  • thyroid is enlarged and nodular
  • surgical removal may cause hypothyroid
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22
Q

Thyroid Adenoma

A
  • may occasionally be hyperactive and cause hyperthyroid
  • appears as solitary nodules that concentrate radioactive iodine, and diagnosed as “hot nodules” on radioactive scanning
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23
Q

symptoms of hyperthyroid

A
  • result from excess thyroid horomes, include restlessness, nervousness, emotional lability, sweating, and tachycardia.
  • cardiac palpitations, muscular tremmor, diarrhea are common
  • low output heart failure may occur in some
  • weight loss in the setting of increased appetite
  • in Graves disease, exophthalamus is commong (bulging of eyes)
  • minority of patients - scaling and induration over shins
  • goiter and adenoma: do not have exophthalamus or tibirla myexedma
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24
Q

Treatment for hyperthyroid

A
  • depends on the underlying process
  • best results if nodules can be removed surgically
  • graves - tx. with antithyroid drugs, or removal of thyroid
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25
Q

What is hypothyroid

A

-results from functional failure of the thyroid gland, and inability to meet body demands for T3 and T4

26
Q

Causes of hypothyroid

A
  • developmental
  • iodine defficiency
  • Hashimotos: more common in women over 60
  • thyroidectomy
27
Q

pathology of hypothyroid

A
  • depends on cause
  • children with genetic defects may show dyshormonogenic goiter
  • hashimotos leads to thyroid enlargement which is symetric. Is infiltrated with lymphocytes that destroy throid folicles. Healing and firbrosis reduces size.
  • deficiency in iodine is associated with nodular enlargement of thyroid (goiter). b/c thyroid can not produce enough T3 or T4, its folicles undergo compensatory hyperplasia in an attempt to increase levels. In many cases, this is not sufficient and the levels remain low. These low concentrations do not provide feedback inhibition in the pituitary, which responds to low levels by overproducing TSH. TSH production without iodine further promotes enlargement of the thyroid, but does not correct the hormone deficiency.
28
Q

Symptoms of hypothyroid: in children

A

children: affects growth, but specifically the CNS. stunts growth (dwarfism), or mental retardation (cretinism)

numerous metabolic disturbances

29
Q

Symptoms of hypothyroid in adults

A
  • myxedema: skin puffy and swollen
  • affects all organs- slow function. Sleepy, lacks energy
  • bradycardia, constipation, skeletal muscles are weak, stiff, and achy
30
Q

Diagnosis of Hypothyroid

A

-low T3, low T4, high TSH

31
Q

Nodular Thyroid Goiter

A
  • enlargement of the thyroid
  • can be from iodine deficiency, but mostly cause is not known
  • most goiters are euthyroid, so they do not cause hyper or hypo
  • symptoms r/t compression of adjascent structures. ex. coughing and hoarseness due to compression of larynx
  • some cases may present with hyperthyroid
    tx. is resection
32
Q

Thyroid tumors: fact

A
  • Can be benign or malignant
  • Benign more common - found in 3-4% of adults. Little clinical significance
  • Malignant: Rare, ounumbered by benign 10:1. More common in women, mortality is low.
33
Q

Follicular Adenoma

A
  • most common benign tumor of the thyroid
  • presents as a nodule - small, well encapsulated, and formed of thyroid follicles
  • on scan, can not be distinguised from other tissue, dx. is made by biopsy
  • not pre-malignant, so no tx., larger removed for cosmetic reasons
34
Q

Carcinoma of the Thyroid

A
  • Papillar, follicular, medullary, anaplastic
  • all except medullary, originate from the follicular cells. Medullar from C cells.
  • biggest risk factor is radiation (Japan and atomic bomb)
35
Q

Papillary Carcinoma

A
  • Accounts for 80% of malignant thyroid tumors
  • low grade, hormonally inactive, usually presents as a cold nodule on radioscan
  • metastasizes to local lymph nodes - distant metastases is in late stages.
  • Found more commonly in woman 4x than in men
  • occurs early in life with peak incidence in 3rd to 5th decade
  • Favorable prognosis - 80% are alive 10 years after dx.
36
Q

Follicular Carcinoma

A
  • accounts for 15% of thyroid cancer
  • most people are older than 40, and 75% are female
  • grows aggressively, but has good prognosis
  • 65% survive after 10 years
  • tumor cells resemble follicular cells of the thyroid and form coloid
  • form slowly growing nodule. Tumors that do not concentrate iodine can be treated with radioactive iodine
37
Q

Medullary Carcinoma

A
  • From C cells
  • produces calcitonin
  • can be inherited - familiary usually diagnosed early and have a good prognosis if removed
  • sporatic tumors, which occur after 60, have less favorable, only 50% of patients survive after 5 years
38
Q

Anaplastic thyroid carcinoma

A
  • rare, accounting for 1-2% of all thyroid neoplasms
  • most die within a year
39
Q

Diseases of parathyroid glands cause distrubances in

A

-homeostasis of calcium and phosphate

40
Q

Hyperparathyroidism

A
  • hyperfunction that results in increased levels of PTH
  • can be primary: caused by hyperplasia or neoplasia. 80% primary caused by parathyroid adenoma. Remaining 10% have hyperplasia.
  • secondary: r/t chronic renal failure
  • less than 5% is hereditary

less than 1% of hyperparathyroidism is carcinoma

41
Q

Hyperplasia of parathyroid gland

A
  • primary: cause not known
  • secondary: occurs in pts with end stage kidney disease
  • enlargement and hyperfunction of parathyroid glands represents a compensatory mechanism triggered by hypocalcemia and hyperphosphatemia seen in chronic renal disease.
42
Q

Pathology of hyperplastic and neoplastic parathyroid gland

A
  • histologically very similar, must be evaluatated with clinical and microscopic. Most likely one of these 3:
    1. ) Parathyroid Adenoma (benign, 1 in 4 parathyroid glands)
    2. )Parathyroid Gland Hyperplasia (found in all)
    3. ) Parathyroid carcinoma (rare)
43
Q

Clinical Features of Hyperparathyroidism

A

-increased ADH in circulation. This acts on the bones and the kidneys. The bones release calcium into circulation, and the kidneys increase calcium resporption. Also acts in kidneys to form vtitamin D, which facilitates uptake of calcium from the intestines.

This results in hypercalcemia, and compensatory hypophosphatemia

  • bones show loss of calcium and are painful, prone to fractures
  • increased calcium in the kidneys can cause stones
  • lethargy (with moaning), muscle weakness, conduction defects in the heart, abdominal pain , polyuria
44
Q

treatment of hyperparathyroid

A

-surgical resection or kidney transplant

45
Q

hypoparathyroidism

A
  • decreased or loss of function. Very rare, usually during inadventant removal of all 4 parathyroid glands during surgury.
  • deficiency of PTH, results in hypocalcemia, results in neuromuscular excitability and muscle contraction.
  • skeletal muscle spastic, heart action irregular
  • activity can be fluctuatin of excitability and despression
  • symptoms can be ameliorated with hormone therapy with substitutuionall PTH
46
Q

Adrenal Hyperfunction Image

causes

A
47
Q

Adrenal Cortical Hyperfunction

A
  • Most common is cushings, caused by adrenal hyperplasia or neoplasia
  • in 70%, cushings results from ACTH released from pituitary adenomas
  • Adrenal cortical tumors account for 20% of hypercortisolism
  • 10% caused by extrapituitary tumors such as small cell cancer in the lung - releases ACTH
  • use of steriods for autoimmune diseases
48
Q

Hypercortisolism and cushings image

A
49
Q

Adrenal tumors appear

A
  • nodules, or irregular enlargement
  • benign or malignant
  • usually yellow b/c of high lipid content
50
Q

Symptoms of hypercortisolism

A
  • central obseity that is promenent in the trunk, and face. Moon face and buffalo hump.
  • red face, HTN, thin skin
  • glucose intolerance
  • weakness, emotionally unstable
51
Q

In practice, most common cause of cushings

A
  • exogenous corticosteriod therapy
  • responds well to tapering off therapy
52
Q

Addisons vs. Cushings image

A
53
Q

Hyperaldosteronism

A
  • rare, typically caused by adenoma of zona glomerulosa
  • 70% adenoma, 30% hyperplasia
  • presents with retention of sodium and loss of potassium
54
Q

Adrenocortical Hypofunction

A
  • usually as a result of adrenal destruction
  • can be acute (Waterhouse-Friedrickson) or chronic -autoimmune
  • Infection -such as TB, or tumor can cause adrenal destruction (carcinoma of breast of lungs - most common metastase to the adrenals)
  • Adrenal insuficiency results in Addisons. 70% caused by autoimmune, and 25% from infection (most common in immunocompromised or AIDS)
55
Q

Pathogenesis of Addisons Disease

A
  • varies
  • in early autoimmune, the cortex is infiltrated with lymphocytes and plasma cells
  • in later stages, entire cortex is destroyed and may be replaced with fibrous or fat
  • granulomas, pathogen-induced necrosis
  • tumoral destruction: overgrowth of malignant cells and loss of adrenal cortical tissue
56
Q

Clinical Features of Addisons

A
  • incidiously with fatigue, weight loss, and nausea
  • hypotensive, frequent syncope
  • susceptible to infections
  • can not tolerate stress, do not work or maintain routines
  • numerous metabolic disturbances
  • low levels: sodium, chloride, glucose, steriod levels
  • high levels of k
  • final dx. made by ACTH test- normally secretes corticosteriod
57
Q

Diseases of Adrenal Medulla

A
  • neuroblastoma
  • pheochromocytoma
58
Q

What is neuroblastoma?

A
  • tumor composed of neuroblasts (undifferentiated precursors of neural cells and adrenal mudullary cells)
  • if the neuroblast cells do not differentiate, then they undergo malignant transformation
  • adrenal gland is the most common site of neuroblastomas
  • they are developmental malignant lesions that tend to occur in neonates and young children
  • they grow fast, and form large abdominal masses
  • highly malignant, most habe metastesized by time of dx.
  • The few cells that do differentiate evolve into neurons, they release neurogenic amines which can be detected in the urine as catacholamines, or degradation products such as vanillylmandelic acid (VMA)
  • with chemo, medical, and radiation - 90% can be cured
59
Q

Pheochromocytoma

A

Most common tumor involving adrenal medula in adults

  • occurs rarely, 1:10 000 per year
  • causes surgically treatable hypertension
  • If tumor is dx. and removed, HTN will resolve
  • most occur sporatically, but can be inherited
  • in most cases it is benign, solitary tumor, orginating from the adrenal medula
  • 10% arise from extra-renal (paragangliomas)
  • 10% are multiple, and 10% are malignant
60
Q

Clinical Features of Pheochromocytoma

A
  • Functionally active tumors that secrete epinephrine and nor-epinephrine.
  • The release of these catacholamines causes HTN
  • Pts have episodes of paroxysmal HTN correstponding to a release of catacholamines from the tumor
  • prolonged exposure to epi and norepi can cause heart lesions (catacholamine cardiomyopathy)
  • dx. made clinically, but confirmed biochemically with increased circulating catacholamines, levels of VMA (degradation product of biologic amines) are elevated in urine
  • Treated surgically, prognosis is excellent, because 90% are benign, well encapsulated, and easily removed

Pathology for Health Professionals (14 decks)

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