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128 Cards in this Set

  • Front
  • Back
How do hormones function?
feedback inhibition
What are the chemical messengers that interact with target organ cell receptors?
1. polypeptides and amines
2. steroid hormones
Polypeptides and Amines
-interact with receptors on cell surface
-second messenger cAMP
-modify cells function
Steroid Hormones
-penetrate membranes
-interact with cytoplasmic receptors
-translocate into nuc., bind DNA, transcribe and translate new proteins which mediate hormone effects
Feedback Inhibition
hypothalmic releasing hormones go to the pituitary and regulate secretion at the pituitary gland, then pituitary tropic hormones stimulate target organ to release hormones
What are the organs of the endocrine system? (4)
1. pituitary
2. thyroid
3. parathyroids
4. adrenal glands
Anterior Lobe of Pituitary Gland
-secretory epi cells
Posterior Lobe of Pituitary Gland
-unmyelinated nerve fibers containing neurosecretory granules of stored hormones
What is the embryology of the anterior lobe?
-derived from oral canal (Rathke's pouch) and grows up to base of brain and is cut off by sphenoid bone creating the sella turcica
What are the rests of epithelial cells sometimes deposit because of the upward growth of the pituitary gland?
1. pharyngeal pituitary
2. extrasellar craniopharyngioma
What is the embryology of the posterior lobe?
derived form an outpouching of floor of 3rd ventricle and grows downward alongside ant. lobe
Pituitary Stalk
neural connection between the hypothalamus and posterior lobe that persists
The anterior pituitary has __ cells types producing __ hormones.
What are the 5 cells types and 7 hormones produced by the anterior pituitary?
1. somatotrophs- GH
2. mammotrophs- prolactin
3. corticotrophs- ACTH, MSH
4. thryotrophs- TSH
5. gonadotrophs- FSH and LH
How do the anterior pituitary cells stain?
1. acidophilic
2. basophilic
3. chromophobic
What do hypothalamic regulatory horomones do?
controls relase of tropic hormones
What are the hypothalamic regulatory hormones?
1. TRH for TSH and prolactin
2. GnRH for FSH and LH
3. CR for ACTH
4. GHRH for GH
5. somatostatin- inhibits release of GH
6. dopamine- inhibits prolactin
Macroadenoma (pituitary adenoma)
-local mass effect
-enlarement of sella turcica
-inc. intracranial pressure
-half of all hyperfunctioning tumors
Bitemporal Hemianopsia
visual field defect from pressure on adjacent optic chiasm or optic nerves on crossing central fibers of optic chiasm
-spare uncrossed lateral fibers
-deective vision in the upper temporal quadrants
excess hormone production by the ant. pituitary
-almost always implies adenoma
What are the rare causes of hyperpituitarism?
carcinoma, nontumorous hyperplasia, hypothalamic lesions, visceral cancers
Somatotroph Tumors (growth hormone)
-acidophilic, largest adenoma, subtle clinical manifestations, mass effects
-acromegaly- adults
-gigantism- children
-glucose intolerance, osteoporosis, HTN
What is the largest adenoma?
somatotroph tumors
Gonadotroph Adenomas (FSH, LH)
-basophilic, no assoc, syndrome, diagnose by elevated FSH/LH, local mass effect
What adenoma represents 10-20% of macroadenomas in middle aged men and women?
gonadotroph adenomas
-acidophilic or chromophobic
-amenorrhea-galactorrhea syndrome in women
-usually micro in premenapausal women
-can be macro in males and older females
What is the most common hyperfunctioning tumor of the pituitary?
Corticotroph Adenomas (Cushing's Disease)
-basophilic, produce ACTH
-stim. excess secretion fo adrenal cortical steroids
-tend to be microadenoma
-occurs w/ loss of 75% of ant. pituitary parenchyma
-less commonly occurs with isorders that interfere with delivery of pit. hormone-releasing factors from the hypothalamus
"Null Cell" adenomas
Hypopituitarism- non-secretory pit. adenoma
Sheehan's syndrome (post-partum nerosis)
ischemic necrosis of the ant. pit.
Empty sella syndrome
-enlared, empty sella turcica due to chronic herniation or the subarachnoid space caused by defect in the diaphragm sellae
-classic patients are obese, multiparous women
Posterior Pituitary
compsed of modified glial cells (pituicytes) and axonal processes extending from hyposthalmic nuclei
-supraoptic nuc.
-paraventricular nuc.
Paraventricular nucleaus of the Hypothalamus
-secretes oxytocin
-stored in post. pit.
-potentiates uterine contrations, milk ejection
Supraoptic Nucleus of the Hypothalamus
-secretes ADH to maintain serum osmolality
-acts on renal tublules- water resorption
-also causes vasoconstriction
Diabetes insipidus
-deficiency of ADH
What are the symptoms of diabetes insipidus?
poyuria, low urine specific gravity, high serum sodium and osmolality
What are the causes of diabetes insipidus?
head trauma, neoplasms, inflamm. disorders, sergery involving pit. or hypo.
Nephrogenic Diabetes Insipidus
normal ADH but kidneys unresponsive
Thyroid Gland Anatomy
bilobed gland below and anterior to larynx
Thyroid Gland Embryology
-develops from evagination of pharyngeal epi that descends to normal position in neck
-downward migration accounts for developmental anomalies
lingual thyroid
substernal gland
Thyroid Hormones
1. T3 and T4- regulate carb, lipid, and protein metabolism
2. calcitonin- promotes bony absorption of calcium and inhibits resorption of bone
hypermetabloic tate caused by elevated levels of free T3 and T4
What causes hyperthyroidism? (4)
1. diffuse hyperplasia of thryroid (Grave's disease)
2. exogenous thyroid hormone
3. hyperfunctional multinodular goiter (Plummer's syndrome)
4. hyperfunctional adenoma
What are the less common causes of hyperthyroidism? (3)
1. thyroiditis
2. TSH-secreting pit. adenoma
3. Struma ovarii
What are the clinical findings with hyperthyroidism?
weight loss, tachycardia, arrhythmias, diarrhea, weakness, tremor, nervousness, heat intolerance
Thyroid Storm
medical emergency, acute exacerbation of hyperthyroidism precipitated by illness, surgery, trauma
What are the lab findings with hyperthyroidism?
decreased TSH and elevated free T4
What is the most common cause of endogenous hyperthyroidism?
Graves' Disease
Graves' Disease
-IgG autoantibody stimulates TSH receptor
-diffuse enlargement of gland (goiter)
-female 5:1
What is the etiology of hypothyroidism? (5)
1. chronic thyroiditis (autoimmune)
2. surgery or readioactive iodine
3. iodine/enzyme deficiency
4. idiopathic
5. hypopituitarism (secondary)
(symptoms of hypothyroidism)
-apathy/mental sluggishness
-weight gain
-cold intolerance
-coarse hair
-dry skin
-inc. TSH
-dec. T4
-childhood hypothyroidism that presents with mental retardation, short stature, large head and tongue
What are the three causes of cretinism?
1. iodine deficiency
2. enzyme deficiency
3. agenesis of thyroid
-inflammation of the thyroid
-hyperthyroid, euthyroid, or hypothyroid
-females 10:1
-painful and painless goiter
What are the five types of thyroiditis?
1. suppurative (infectious) thyroiditis
2. nonspecific lymphocytic thyroiditis
3. subacute granulomatous thyroiditis
4. Hashimoto's thyroiditis
5. Riedel's thyroiditis (fibrosis)
Hashimoto's Thyroiditis
-chronic autoimmune thryoidits
What is the most common cause of hypothyroidism in the US?
Hashimoto's Thyroiditis
What is the pathogenesis of Hashimoto's thyroiditis?
-formation of CD8+ cytotoxic T cells
-anti-TSH receptor antibodies that block action of TSH, unlike autoantibodies in Graves' disease wich stimulate TSH receptor
What are the clinical findings with Hashimoto's Thyroiditis?
-females 10:1
-painless goiter
-hyperthyroidism followed by hypothyroidism
-increased incidence of other autoimmune disorder and B-cell lymphomas
What is the histology of Hashimoto's Thyroiditis?
-lymphocytes and plasma cell infiltrate
-germinal center formation
-Hurthle cells- eosinophilic epi. cells
enlargement of the thyroid gland that can occur with euthyroid, hypothyroid, hyperthyroid
What are the three stages of goiter?
1. impaired thyrodi hormone synthesis
2. inc. TSH production
3. Hypertrophy/hyperplasia of thyroid follicular cells
When is goiter endemic?
when there is iodine deficiency
When is goiter sporadic?
-hereditary enzyme defects
-ingestion of excesscalcium or cruciferous vegetables
Diffuse non-toxic goiter occurs _____ while multinodular goiter occurs _____.
Follicular Adenoma
benign thyroid tumor
-encapsulated "normal-appearing tissue"
-painless cold nodule (rarely hyperthyroid)
-usually solitary
-difficulty swallowing
Papillary Carcinoma
malignant thyroid tumor
-60-80% of thyroid cancers
-usually <40yo
-radiation exposure
-slow growing -10yr survival >80%
-spread via lymphatics
-solitary or multifocal lesions
What is the pathology of papillary carcinoma?
-papillary folds
-orphan annie ees
-psammoma bodies (calcified)
Follicular Carcinoma
malignant thryoid tumor
-15-25% of thyroid cancer
-50% 10yr survival
-history of nodular goiter
-solitary cold nodule
-spreads to bone, lung, liver via bloodstream
Is papillary carcinoma or follicular carcinoma more agressive?
follicular carcinoma
What is the pathology of follicular carcinoma?
-infitrative or circumscribed
-resembles normal thyroid
-Hurthle cells
Medullary Carcinoma
malignant thryoid tumor
-5% of thyroid cancers
-solitary nodule or multifocal
-neck mass, dysphagia, hoarseness
-40% 10yr survival
-80% sporadic; 20% MEN syndrome
Neuroendocrine tumor
medullary carcinoma
C cell tumor, may produce calcitonin and other hormones
What is the pathology of medullary carcinoma?
-polygonal to spindle-shaped cells
-form nests, trabeculae, and follicles
-C cell hyperplasia prominent in familial cases
-calcitonin demonstrated in cells by immunohistochemistry
Anaplastic Carcinoma
malignant thyroid tumor
-10% thyroid cancers
-rapidly fatal neck mass
-occur in areas of endemic goiter
What is the pathology of anaplastic carcinoma?
-bulky mass invading neck structures
-three morphological patterns
1. pleiomorphic giant cells
2. sarcomatous spindle cells
3. squamoid cells
Parathyroid Glands
-produce parathyroid hormone
-maintains serum calcium
-PTH secretion controlled by circulating free calcium not by trophic hormones secreted by hypothalamus and pituitary
What are the actions of PTH on the bone?
-osteoclast activation
-resorption of calcium and phosphorus
What are the actions of PTH on the kidney?
-activation of vit. D
-reabsorption of calcium
-clearance of phosphorus
What are the actions of PTH on the intestine?
absorption of calcium with vit. D
Primary Hyperparathyroidism
-common endocrine disorder leading to hypercalcemia
-women > men
What is the etiology of primary hyperparathyroidism?
-adenoma (80-90%)
-hyperplasia (10-20%)
-carcinoma (rare)
What are the clinical features of primary hyperparathyroidism?
-"painful bones, renal stones, abdominal groans, and psychic moans"
-skeletal = osteitis fibrosa cystica
-renal = nepholithiasis, nephrocalcinosis
-GI = constipation, nausea, ulcers, pancreatitis
-CNS = depression, lethargy, seizures
-neuromuscular = weak, hypotonia
Secondary Hyperparathyroidism
overactivity of parthyroids induced by conditions leading to chronic hypocalcemia
What is the etiology of secondary hyperparathyroidism?
-renal failure (most common)
-calcium and vit. D deficiency
What are the mechanisms in renal failure causing secondary hyperpaprathyroidism?
-dec. PO4 exretion leads to hyperphophatemia
-serum Ca is depressed, causing secondary hyperplasia of parathyroids and PTH secretion
-also, reduced kidney activation of vit. D causes reduced intertinal absorption of calcium
What are the clinical features of secondary hyperparathyroidism?
-similar to primary, but less severe
-renal osteodystrophy
-calciphylaxis-calcification of blood vessels leading to ischemia of skin and other organs
syndrome involving low serum calcium due to underproduction of PTH
What is the etiology of hypoparathyroidism?
-surgical- thyroidectomy
-congenital abscence- thymic aplasia, DiGeorge syndrome
-autoimmune- hereditary polyglandular deficiency syndrome
What are the clinical findings in hypoparathyroidism?
dec. calcium and inc PO4, tetan, convulsions, laryngospasm, paresthesias, Chvostek and Trousseau's signs
What are physical ailments that results from hypoparathyroidism?
catarcts, dental root hypoplasia, spotty alopecia, nail fragility, basal ganglia calcification
inc. PTH, inc. PO4, dec. calcium
-developmental anomalies, short stature, short metacarpals and metatarsals, mental retardation
What is the etiology for psuedohypoparathyroidism?
-end organ resistance to PTH
-urle out renal failure, malabsorption syndrome and vit. D deficiency
What are the three zones in the adrenal cortex?
1. zona glomerulosa- mineralocorticoids
2. zona fasciculata- glucocorticoids, androgens
3. zona reticularis- glucocorticoids, androgens
How is secretion of cortisol stimulated and what is the function?
-cortisol secretion is stimulated by ACTH and functions to inhibit glucose uptake by cells, promote fat deposition, and inc. hepatic gluconeogenesis
Hyperadrenalism- Cushing's Syndrome
-excess cortisol caused by:
-long term steroid use (most common)
-ACTH-producing neoplasm of pituitary
-excess hypothalamic stim. of ACTH release
-functional adrenal neoplasm or hyperplasia
-ectopic ACTH produced by malignancy
What are the maniferstation of Cushing's Syndrome?
central obesity, buffalo hump, moon faces, hyperglycemia, hirsutism, excess androgens, osteoporosis, psychiatric, HTN, acne
What are the three types of lesions the determine the pathology of Cushing's Syndrome?
1. nodular cortical hyperplasia
2. adrenal tumor
3. atrophy
What test do we use to determine if someone has Cushing's Syndrome?
Dexamethasone Suppresion Test
determines plasma cortisol, plasma ACTH and urine steroids
-controlled by renin-angiotensin axis
-ACTH may also stim. release
-sodium retention and excretion of potassium
*major regulator of fluid volume
What is the course of the renin-angiotenin axis?
1. angiotensinogen to Angiotensin I by renin
2. angiotensin I to angiotensin II by ACE
3. angiotensin II to aldosterone excretion
What are the clinical features of hyperaldosteronism?
HTN, fatigue, inc. Na, dec. K, metabolic acidosis
What is primary hyperaldosteronism and what does the lab reveal?
-adrenal adenoma Conn's Syndrome adrenocortical hyperplasia
-inc. aldosterone, dec. renin
What is secondary hyperaldosteronism and what does the lab reveal?
-CHF-diminished renal perfusion or renal areter stenosis
-inc. aldosterone, inc. renin
steroid hormones converted to testosterone in peripheral tissue to accentuate male characteristics
Congenital Adrenal Hyperplasia
group of autosomal recessive disorder characterized by defect of an enzyme involved in cortisol biosynthesis
What are the clinical manifestations in congenital adrenal hyperplasia?
-androgen excess or deficiency
-defects of sodium metabolism
-glucoccorticoid deficiency
What is the most common form of congenital adrenal hyperplasia?
21-hydroxylase deficiency that has several variants, androgen excess and 1/3 of cases have Na wasting due to aldosterone deficiency
17-hydorxylase deficiency
-another form of congenital adrenal hyperplasia where there is androgen deficiency and accumulation of precursors with mineralocorticoid activity
-leads to sodium retention and HTN
-teated with glucocorticoids
What are the two types of primary hypoadrenalism?
1. acute- Waterhouse-Friedericksen
2. chronic- Addison's disease
What are the four types of secondary hypoadrenalism?
1. pituitary lesion
2. hypothalamic lesion
3. prolonged administration of glucocorticoids
4. no pigmentation or electrolyt abnormalities
What are the clinical features of Addison's Disease?
weakness, fatigue, dec. glucose, N and V, wt. loss, psychosis, hyperpigmentation, hypotension, dec. sodium, inc. potassium, inc. ACTH, inablity to withstand stress
What is the etiolgy of Addison's Disease?
-autoimmune (60-70%)
-viral infection- herpes, CMV, AIDS
-chronic infection- funal, TB
-metastic cancer- lung, brease, melanoma
-systemic disease- amyloidosis, sarcoid, hemochromatosis
What is the pathology of Addison's disease?
-shrunken atrophic glands
-medulla intact
-lymphoid infiltrate
-granulomas (TB, fungus)
Adrenal Neoplasms: Cortical
Adenomas- most are nonsecreting, most common functional adenomas secrete aldosterone

Carcinoma- large, >2cm, 50% functional, highly malignant, most virilizing adrenal neoplasms are carcinomas
Neoplasm of the adrenal medulla: Pheochromocytoma
-tumor of neural crest chromaffin cells in adrenal medulla
-secrete catecholamines
-clinical findings include: HA, sweating, palpitations, paroxysmal attacks, HTN
Pheochromocytoma: "Rule of 10's"
10% familial- MEN, neurofibromatosis, von Hippel-Lindau, Sturge-Weber
10% extra adrenal- Organ of Zuckerkandi, arotic body (paragangliomas)
10% bilateral
10% malignant
What is the pathology of pheochromocytoma?
spindle shaped chromaffin cells in nests (Zellballen)
neoplasm of adrenal medulla
-very malignant childhood tumor that is the most common extracranial solid tumor
-80% <5yo
-arise anywhere in sympathetic nervous system
-most common in abdomen from adrenal medulla or retroperitoneal sypathetic ganglia
-metastatic to bone, live, lung, lymph nodes
MEN Syndromes
-group of familial disease asccociated with neoplasms and/or hyperplasia of various endocrine organs
-autosomal dominant
-three variants
MEN I- "the 3 P's"
1. parathyroid hyperplasia
2. pancreas- Gastinoma (Zolliner-Ellison Syndrome)
3. pituitary adenoma
What is the defect in MEN I?
defect involves tumor suppressor gene on chromosome 11 (11q13)
MEN II (Sipple's Syndrom)
-medullary carcinoma of thryoid
-parathyroid hyperplasia
What is the defect in MEN II?
defect involves mutations in RET protooncogene on chromosome 10
MEN II b (William Syndome)
-medullary cancer of thyroid
-mucocutaneous ganglioneuromas
-marfanoid body habitus
-no parathyroid involvement
What is the defect in MEN II b?
defect of RET protooncogene distinct from that of MEN II