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128 Cards in this Set
- Front
- Back
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How do hormones function?
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feedback inhibition
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What are the chemical messengers that interact with target organ cell receptors?
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1. polypeptides and amines
2. steroid hormones |
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Polypeptides and Amines
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-interact with receptors on cell surface
-second messenger cAMP -modify cells function |
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Steroid Hormones
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-penetrate membranes
-interact with cytoplasmic receptors -translocate into nuc., bind DNA, transcribe and translate new proteins which mediate hormone effects |
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Feedback Inhibition
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hypothalmic releasing hormones go to the pituitary and regulate secretion at the pituitary gland, then pituitary tropic hormones stimulate target organ to release hormones
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What are the organs of the endocrine system? (4)
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1. pituitary
2. thyroid 3. parathyroids 4. adrenal glands |
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Anterior Lobe of Pituitary Gland
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-adenohypophysis
-secretory epi cells |
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Posterior Lobe of Pituitary Gland
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-neurohypophysis
-unmyelinated nerve fibers containing neurosecretory granules of stored hormones |
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What is the embryology of the anterior lobe?
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-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
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What are the rests of epithelial cells sometimes deposit because of the upward growth of the pituitary gland?
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1. pharyngeal pituitary
2. extrasellar craniopharyngioma |
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What is the embryology of the posterior lobe?
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derived form an outpouching of floor of 3rd ventricle and grows downward alongside ant. lobe
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Pituitary Stalk
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neural connection between the hypothalamus and posterior lobe that persists
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The anterior pituitary has __ cells types producing __ hormones.
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5
7 |
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What are the 5 cells types and 7 hormones produced by the anterior pituitary?
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1. somatotrophs- GH
2. mammotrophs- prolactin 3. corticotrophs- ACTH, MSH 4. thryotrophs- TSH 5. gonadotrophs- FSH and LH |
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How do the anterior pituitary cells stain?
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1. acidophilic
2. basophilic 3. chromophobic |
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What do hypothalamic regulatory horomones do?
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controls relase of tropic hormones
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What are the hypothalamic regulatory hormones?
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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 |
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Macroadenoma (pituitary adenoma)
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->10mm
-local mass effect -enlarement of sella turcica -inc. intracranial pressure |
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Microadenoma
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-<10mm
-half of all hyperfunctioning tumors |
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Bitemporal Hemianopsia
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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 |
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Hyperpituitarism
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excess hormone production by the ant. pituitary
-almost always implies adenoma |
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What are the rare causes of hyperpituitarism?
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carcinoma, nontumorous hyperplasia, hypothalamic lesions, visceral cancers
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Somatotroph Tumors (growth hormone)
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-acidophilic, largest adenoma, subtle clinical manifestations, mass effects
-acromegaly- adults -gigantism- children -glucose intolerance, osteoporosis, HTN |
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What is the largest adenoma?
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somatotroph tumors
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Gonadotroph Adenomas (FSH, LH)
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-basophilic, no assoc, syndrome, diagnose by elevated FSH/LH, local mass effect
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What adenoma represents 10-20% of macroadenomas in middle aged men and women?
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gonadotroph adenomas
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Prolactinomas
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-acidophilic or chromophobic
-amenorrhea-galactorrhea syndrome in women -usually micro in premenapausal women -can be macro in males and older females |
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What is the most common hyperfunctioning tumor of the pituitary?
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prolactinomas
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Corticotroph Adenomas (Cushing's Disease)
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-basophilic, produce ACTH
-stim. excess secretion fo adrenal cortical steroids -tend to be microadenoma |
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Hypopituitarism
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-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 |
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"Null Cell" adenomas
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Hypopituitarism- non-secretory pit. adenoma
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Sheehan's syndrome (post-partum nerosis)
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ischemic necrosis of the ant. pit.
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Empty sella syndrome
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-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 |
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Posterior Pituitary
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compsed of modified glial cells (pituicytes) and axonal processes extending from hyposthalmic nuclei
-supraoptic nuc. -paraventricular nuc. |
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Paraventricular nucleaus of the Hypothalamus
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-secretes oxytocin
-stored in post. pit. -potentiates uterine contrations, milk ejection |
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Supraoptic Nucleus of the Hypothalamus
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-secretes ADH to maintain serum osmolality
-acts on renal tublules- water resorption -also causes vasoconstriction |
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Diabetes insipidus
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-deficiency of ADH
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What are the symptoms of diabetes insipidus?
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poyuria, low urine specific gravity, high serum sodium and osmolality
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What are the causes of diabetes insipidus?
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head trauma, neoplasms, inflamm. disorders, sergery involving pit. or hypo.
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Nephrogenic Diabetes Insipidus
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normal ADH but kidneys unresponsive
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Thyroid Gland Anatomy
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bilobed gland below and anterior to larynx
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Thyroid Gland Embryology
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-develops from evagination of pharyngeal epi that descends to normal position in neck
-downward migration accounts for developmental anomalies lingual thyroid substernal gland |
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Thyroid Hormones
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1. T3 and T4- regulate carb, lipid, and protein metabolism
2. calcitonin- promotes bony absorption of calcium and inhibits resorption of bone |
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Hyperthyroidism
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hypermetabloic tate caused by elevated levels of free T3 and T4
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What causes hyperthyroidism? (4)
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1. diffuse hyperplasia of thryroid (Grave's disease)
2. exogenous thyroid hormone 3. hyperfunctional multinodular goiter (Plummer's syndrome) 4. hyperfunctional adenoma |
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What are the less common causes of hyperthyroidism? (3)
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1. thyroiditis
2. TSH-secreting pit. adenoma 3. Struma ovarii |
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What are the clinical findings with hyperthyroidism?
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weight loss, tachycardia, arrhythmias, diarrhea, weakness, tremor, nervousness, heat intolerance
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Thyroid Storm
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medical emergency, acute exacerbation of hyperthyroidism precipitated by illness, surgery, trauma
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What are the lab findings with hyperthyroidism?
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decreased TSH and elevated free T4
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What is the most common cause of endogenous hyperthyroidism?
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Graves' Disease
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Graves' Disease
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-IgG autoantibody stimulates TSH receptor
-diffuse enlargement of gland (goiter) -female 5:1 -autoimmune |
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What is the etiology of hypothyroidism? (5)
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1. chronic thyroiditis (autoimmune)
2. surgery or readioactive iodine 3. iodine/enzyme deficiency 4. idiopathic 5. hypopituitarism (secondary) |
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Myxedema
(symptoms of hypothyroidism) |
-apathy/mental sluggishness
-weight gain -cold intolerance -lethargy -coarse hair -dry skin -inc. TSH -dec. T4 |
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Cretinism
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-childhood hypothyroidism that presents with mental retardation, short stature, large head and tongue
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What are the three causes of cretinism?
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1. iodine deficiency
2. enzyme deficiency 3. agenesis of thyroid |
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Thyroidistis
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-inflammation of the thyroid
-hyperthyroid, euthyroid, or hypothyroid -females 10:1 -painful and painless goiter |
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What are the five types of thyroiditis?
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1. suppurative (infectious) thyroiditis
2. nonspecific lymphocytic thyroiditis 3. subacute granulomatous thyroiditis 4. Hashimoto's thyroiditis 5. Riedel's thyroiditis (fibrosis) |
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Hashimoto's Thyroiditis
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-chronic autoimmune thryoidits
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What is the most common cause of hypothyroidism in the US?
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Hashimoto's Thyroiditis
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What is the pathogenesis of Hashimoto's thyroiditis?
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-formation of CD8+ cytotoxic T cells
-anti-TSH receptor antibodies that block action of TSH, unlike autoantibodies in Graves' disease wich stimulate TSH receptor |
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What are the clinical findings with Hashimoto's Thyroiditis?
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-females 10:1
-painless goiter -hyperthyroidism followed by hypothyroidism -increased incidence of other autoimmune disorder and B-cell lymphomas |
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What is the histology of Hashimoto's Thyroiditis?
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-lymphocytes and plasma cell infiltrate
-germinal center formation -Hurthle cells- eosinophilic epi. cells -fibrosis |
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Goiter
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enlargement of the thyroid gland that can occur with euthyroid, hypothyroid, hyperthyroid
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What are the three stages of goiter?
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1. impaired thyrodi hormone synthesis
2. inc. TSH production 3. Hypertrophy/hyperplasia of thyroid follicular cells |
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When is goiter endemic?
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when there is iodine deficiency
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When is goiter sporadic?
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-hereditary enzyme defects
-ingestion of excesscalcium or cruciferous vegetables -idiopathic |
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Diffuse non-toxic goiter occurs _____ while multinodular goiter occurs _____.
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initially
late |
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Follicular Adenoma
benign thyroid tumor |
-encapsulated "normal-appearing tissue"
-painless cold nodule (rarely hyperthyroid) -usually solitary -difficulty swallowing |
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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 |
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What is the pathology of papillary carcinoma?
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-papillary folds
-orphan annie ees -psammoma bodies (calcified) |
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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 |
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Is papillary carcinoma or follicular carcinoma more agressive?
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follicular carcinoma
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What is the pathology of follicular carcinoma?
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-infitrative or circumscribed
-resembles normal thyroid -Hurthle cells |
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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 |
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Neuroendocrine tumor
medullary carcinoma |
C cell tumor, may produce calcitonin and other hormones
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What is the pathology of medullary carcinoma?
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-polygonal to spindle-shaped cells
-form nests, trabeculae, and follicles -amylid -C cell hyperplasia prominent in familial cases -calcitonin demonstrated in cells by immunohistochemistry |
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Anaplastic Carcinoma
malignant thyroid tumor |
-10% thyroid cancers
-60-80yo -rapidly fatal neck mass -metastic -occur in areas of endemic goiter |
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What is the pathology of anaplastic carcinoma?
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-bulky mass invading neck structures
-three morphological patterns 1. pleiomorphic giant cells 2. sarcomatous spindle cells 3. squamoid cells |
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Parathyroid Glands
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-produce parathyroid hormone
-maintains serum calcium -PTH secretion controlled by circulating free calcium not by trophic hormones secreted by hypothalamus and pituitary |
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What are the actions of PTH on the bone?
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-osteoclast activation
-resorption of calcium and phosphorus |
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What are the actions of PTH on the kidney?
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-activation of vit. D
-reabsorption of calcium -clearance of phosphorus |
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What are the actions of PTH on the intestine?
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absorption of calcium with vit. D
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Primary Hyperparathyroidism
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-common endocrine disorder leading to hypercalcemia
-women > men |
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What is the etiology of primary hyperparathyroidism?
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-adenoma (80-90%)
-hyperplasia (10-20%) -carcinoma (rare) |
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What are the clinical features of primary hyperparathyroidism?
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-"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 |
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Secondary Hyperparathyroidism
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overactivity of parthyroids induced by conditions leading to chronic hypocalcemia
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What is the etiology of secondary hyperparathyroidism?
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-renal failure (most common)
-calcium and vit. D deficiency |
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What are the mechanisms in renal failure causing secondary hyperpaprathyroidism?
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-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 |
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What are the clinical features of secondary hyperparathyroidism?
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-similar to primary, but less severe
-renal osteodystrophy -calciphylaxis-calcification of blood vessels leading to ischemia of skin and other organs |
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Hypoparathyroidism
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syndrome involving low serum calcium due to underproduction of PTH
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What is the etiology of hypoparathyroidism?
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-surgical- thyroidectomy
-congenital abscence- thymic aplasia, DiGeorge syndrome -autoimmune- hereditary polyglandular deficiency syndrome |
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What are the clinical findings in hypoparathyroidism?
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dec. calcium and inc PO4, tetan, convulsions, laryngospasm, paresthesias, Chvostek and Trousseau's signs
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What are physical ailments that results from hypoparathyroidism?
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catarcts, dental root hypoplasia, spotty alopecia, nail fragility, basal ganglia calcification
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Pseudohypoparathyroidism
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inc. PTH, inc. PO4, dec. calcium
-developmental anomalies, short stature, short metacarpals and metatarsals, mental retardation |
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What is the etiology for psuedohypoparathyroidism?
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-end organ resistance to PTH
-urle out renal failure, malabsorption syndrome and vit. D deficiency |
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What are the three zones in the adrenal cortex?
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1. zona glomerulosa- mineralocorticoids
2. zona fasciculata- glucocorticoids, androgens 3. zona reticularis- glucocorticoids, androgens |
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How is secretion of cortisol stimulated and what is the function?
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-cortisol secretion is stimulated by ACTH and functions to inhibit glucose uptake by cells, promote fat deposition, and inc. hepatic gluconeogenesis
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Hyperadrenalism- Cushing's Syndrome
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-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 |
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What are the maniferstation of Cushing's Syndrome?
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central obesity, buffalo hump, moon faces, hyperglycemia, hirsutism, excess androgens, osteoporosis, psychiatric, HTN, acne
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What are the three types of lesions the determine the pathology of Cushing's Syndrome?
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1. nodular cortical hyperplasia
2. adrenal tumor 3. atrophy |
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What test do we use to determine if someone has Cushing's Syndrome?
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Dexamethasone Suppresion Test
determines plasma cortisol, plasma ACTH and urine steroids |
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Aldosterone
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-controlled by renin-angiotensin axis
-ACTH may also stim. release -sodium retention and excretion of potassium *major regulator of fluid volume |
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What is the course of the renin-angiotenin axis?
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1. angiotensinogen to Angiotensin I by renin
2. angiotensin I to angiotensin II by ACE 3. angiotensin II to aldosterone excretion |
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What are the clinical features of hyperaldosteronism?
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HTN, fatigue, inc. Na, dec. K, metabolic acidosis
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What is primary hyperaldosteronism and what does the lab reveal?
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-adrenal adenoma Conn's Syndrome adrenocortical hyperplasia
-inc. aldosterone, dec. renin |
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What is secondary hyperaldosteronism and what does the lab reveal?
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-CHF-diminished renal perfusion or renal areter stenosis
-inc. aldosterone, inc. renin |
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Androgens
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steroid hormones converted to testosterone in peripheral tissue to accentuate male characteristics
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Congenital Adrenal Hyperplasia
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group of autosomal recessive disorder characterized by defect of an enzyme involved in cortisol biosynthesis
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What are the clinical manifestations in congenital adrenal hyperplasia?
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-androgen excess or deficiency
-defects of sodium metabolism -glucoccorticoid deficiency |
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What is the most common form of congenital adrenal hyperplasia?
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21-hydroxylase deficiency that has several variants, androgen excess and 1/3 of cases have Na wasting due to aldosterone deficiency
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17-hydorxylase deficiency
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-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 |
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What are the two types of primary hypoadrenalism?
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1. acute- Waterhouse-Friedericksen
2. chronic- Addison's disease |
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What are the four types of secondary hypoadrenalism?
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1. pituitary lesion
2. hypothalamic lesion 3. prolonged administration of glucocorticoids 4. no pigmentation or electrolyt abnormalities |
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What are the clinical features of Addison's Disease?
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weakness, fatigue, dec. glucose, N and V, wt. loss, psychosis, hyperpigmentation, hypotension, dec. sodium, inc. potassium, inc. ACTH, inablity to withstand stress
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What is the etiolgy of Addison's Disease?
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-autoimmune (60-70%)
-viral infection- herpes, CMV, AIDS -chronic infection- funal, TB -metastic cancer- lung, brease, melanoma -systemic disease- amyloidosis, sarcoid, hemochromatosis |
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What is the pathology of Addison's disease?
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-shrunken atrophic glands
-medulla intact -lymphoid infiltrate -granulomas (TB, fungus) -neoplasm |
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Adrenal Neoplasms: Cortical
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Adenomas- most are nonsecreting, most common functional adenomas secrete aldosterone
Carcinoma- large, >2cm, 50% functional, highly malignant, most virilizing adrenal neoplasms are carcinomas |
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Neoplasm of the adrenal medulla: Pheochromocytoma
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-tumor of neural crest chromaffin cells in adrenal medulla
-secrete catecholamines -clinical findings include: HA, sweating, palpitations, paroxysmal attacks, HTN |
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Pheochromocytoma: "Rule of 10's"
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10% familial- MEN, neurofibromatosis, von Hippel-Lindau, Sturge-Weber
10% extra adrenal- Organ of Zuckerkandi, arotic body (paragangliomas) 10% bilateral 10% malignant |
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What is the pathology of pheochromocytoma?
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spindle shaped chromaffin cells in nests (Zellballen)
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Neuroblastoma
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 |
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MEN Syndromes
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-group of familial disease asccociated with neoplasms and/or hyperplasia of various endocrine organs
-autosomal dominant -three variants |
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MEN I- "the 3 P's"
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1. parathyroid hyperplasia
2. pancreas- Gastinoma (Zolliner-Ellison Syndrome) 3. pituitary adenoma |
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What is the defect in MEN I?
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defect involves tumor suppressor gene on chromosome 11 (11q13)
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MEN II (Sipple's Syndrom)
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-medullary carcinoma of thryoid
-pheochromocytoma -parathyroid hyperplasia |
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What is the defect in MEN II?
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defect involves mutations in RET protooncogene on chromosome 10
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MEN II b (William Syndome)
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-medullary cancer of thyroid
-pheochromocytoma -mucocutaneous ganglioneuromas -marfanoid body habitus -no parathyroid involvement |
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What is the defect in MEN II b?
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defect of RET protooncogene distinct from that of MEN II
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