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Seva Visc. Endocrine

Dr. Seva's Visceral Pathology Endocrine

QuestionAnswer
What glands are included in the endocrine system? Pituitary Thyroid Parathyroid Adrenal cortex and medulla Pancreas
What glands are not controlled by the pituitary? Parathyroid Adrenal medulla Pancreas
What are the 2 parts of the pituitary? Adenohypophysis Neurohypophysis
What are the most common tumors of the pituitary? Adenoma Craniopharyngioma (locally aggressive)
What can be involved in pituitary tumors? visual field defects b/c pressing on optic chiasm.
What do functioning tumors of the pituitary do? Produce excess of any one or combination of pituitary hormones (hyperpituitary)
What do non-functioning tumors of the pituitary do? Get enlarged and compress on the rest of the gland (hypopituitary)
What hormones does the adenohypophysis secrete? Somatotropin: GH Prolactin ACTH TSH FSH & LH (both gonadotropin)
What is hypopituitarism? Deficient secretion of one or more pituitary hormones.
What is panhypopituitarism? Total failure of pituitary function
What is Sheehans's Syndrome? Rare; ischemic necrosis of the pituitary gland d/t severe hypotension from postpartum hemorrhage.
What are consequences of Sheehan's Syndrome? Agalactia Amenorrhea Hypothyroidism Adrenocortical insufficency
What is pituitary apoplexy? Hemorrhage or infarction can occur in normal pituitary leading to hypopituitarism.
What is Iatrogenic hypopituitarism and trauma? Radiation damage or neurosurgical procedures can lead to hypopituitarism.
What is Kallmann Syndrome? hypogonadotropic = decreased GnRH
What are clinical features of Kallmann Syndrome? Delay in appearance of secondary sexual characteristics; Anosmina and cleft palate
What is Empty sella syndrome? Enlarged sella w/ a thin, flat pituitary secondary to a congenital defective or absent diaphragma sella. Allows leakage of CSF and pressure causing hypopituitarism.
What does growth hormone deficiency lead to? Dwarfism
What do most pituitary adenomas cause? Hyperpituitarism. Impinge on the optic chiasm, giving severe HA, bitemporal hemianopsia and loss of central vision.
What occurs w/ hyperprolactinemia or prolactinoma? Tumor secretes excess prolactin and with increased prolactin decreased LHRF so LH not released so no ovulation in females and low testosterone in males.
What are clinical features of hyperprolactinemia/prolactinoma in M/F? F: causes amenorrhea, infertility and galactorrhea (milk prod. w/o pregnancy) M: Absence of libido and impotence
What results from excess somatotropin before skeletal maturity? Gigantism: body grows abnormally longer, w/ an excessive uniform growth at the epiphyses of long bones.
What results from excess somatotropin after skeletal maturity? Acromegaly: growth increased in soft tissues, like ear, nose, lips and increased space b/w upper incisor teeth and prognathism.
What are other features present w/ acromegaly? Enlargement of the feet, hand and jaws, Visceraomegaly in the liver, heart and thyroid, supraorbital ridge prominent, joint abnormalities, HTN, DM, HA, paresthesias, arthralgias and m. weakness.
What results from excess ACTH? Cushing's Dz, bilateral adrenal involvement (high aldosterone and cortisol)
What 2 pathologies arise from hyper- or hypo- ADH? Diabetes insipidus Syndrome of inappropriate ADH (SIADH)
Describe diabetes insipidus. Deficient ADH -> deficient water reabsorption in the renal collecting tubules -> increased amount of urine w/ low specific gravity.
What are clinical features of diabetes insipidus? Extreme thirst (polydipsea) and excessive water intake. Serum osmolality is increased (high Na and electrolytes) and hypernatremia results
What is SIADH? Syndrome of inappropriate ADH; often seen w/ oat cell carcinoma, increased level of ADH causes more reabsorption of water from the collecting tubules.
What are clinical features of SIADH? Urine is extremely concentrated, serum osmolality is decreased, hyponatremia.
What is the thyroid important for? Basal metabolic rate.
What happens to T3 and T4 levels w/ hyper- and hypothyroidism? Hyper-: above normal Hypo-: below normal
What happens to TSH level w/ hyper- and hypothyroidism? Hyper-: below normal Hypo-: above normal
What happens to protein synthesis (BMR) w/ hyper- and hypothyroidism? Hyper-: above normal Hypo-: below normal
What happens to body weight w/ hyper- and hypothyroidism? Hyper-: below normal Hypo-: above normal
What happens to activity w/ hyper- and hypothyroidism? Hyper-: above normal Hypo-: below normal
What happens to reflexes w/ hyper- and hypothyroidism? Hyper-: above normal Hypo-: below normal
What happens to heart rate w/ hyper- and hypothyroidism? Hyper-: above normal Hypo-: below normal
What happens to GIT peristalsis w/ hyper- and hypothyroidism? Hyper-: increased peristalsis Hypo-: decreased peristalsis
What happens to the hair w/ hyper- and hypothyroidism? Hyper-: softer, shiny Hypo-: dry, coarse
What happens to the skin w/ hyper- and hypothyroidism? Hyper-: wet Hypo-: dry
What happens to the eyes w/ hyper- and hypothyroidism? Hyper-: exopthalmos (Grave's only) Hypo-: periorbital edema
How do tremors or edemas manifest w/ hyper- and hypothyroidism? Hyper-: fingers and tongue fine tremor Hypo-: pretibial edema (myxedema)
What 2 pathologies are seen w/ hypothyroidism? Cretinism (children) Myxedema/Hashimoto's thyroiditis (adults)
What is cretinism? Failure of thyroid hormone synthesis during pregnancy leads to irreversible mental retardation if not treated (perinatal dx is mandatory)
What are clinical features of cretinism? lethargy, hypothermia, rough and harsh cry, hypotonia of muscles, large protruding tongue, umbilical hernia.
What is myxedema/hashimoto's thyroiditis? Deposition of mucopolysaccharides in the CT. Thyroid is rubbery, firm and nodular.
What is present in myxedema/hashimoto's thyroiditis and what does it cause? Presence of antithyroid AB; destruction of the follicles by infiltration of lymphocytes. All hypothyroidism s/s are present and non-pitting edema.
What is a goiter? Bigger thyroid, only lab tests will tell if hypo- or hyper-.
What 3 conditions are seen w/ hyperthyroidism? 1. Grave's Dz 2. Subacute thyroiditis 3. Riedel's thyroiditis
What is Grave's Dz? Seen in females (15-40 y/o), familial, autoimmune, IgG anitbody. Thyroid is enlarged, extremely vascular, neck bruit, exopthalmos.
What is subacute thyroiditis? De Quervain's thyroiditis; both sexes, all ages, viral etiology, enlarged painful thyroid (anything viral can lead to this for a short period of time).
What are clinical features of subacute thyroiditis? Painful neck Fever Enlarged cervical lymph nodes
What is Riedel's thyroiditis? chronic cond'n affects elderly females. Enlarged, stony hard, painless thyroid.
What are clinical features of Riedel's thyroiditis? Dysphagia, dyspnea, hoarseness of voice; large thyroid compresses on trachea, esophagus and recurrent laryngeal nerve.
What is a benign neoplasm of the thyroid? Follicular adenoma
What are risk factors for thyroid carcinoma? 1. X-ray therapy to neck 2. Familial in medullary carcinoma
What 6 types of thyroid cancer are possible? 1. Papillary carcinoma 2. Medullary carcinoma 3. Follicular carcinoma 4. Anaplastic carcinoma 5. MEN I 6. MEN II
What is seen in medullary carcinoma of the thyroid? Familial, arises from parafollicular cells (secrete calcitonin) of the thyroid -> much calcitonin in serum.
What is MEN I? Multiple Endocrine Neoplasia I; Werner's syndrome; pituitary adenoma, parathyroid adenoma and pancreatic islets neoplasm.
What is MEN II? Multiple Endocrine Neoplasia II; Sipple's syndrome; medullary carcinoma of the thyroid, pheochromocytoma of adrenal and parathyroid adenoma.
What happens w/ hyperparathyroidism? Increased PTH, Increased Calcium, and decreased phosphate.
What are 2 types of hyperparathyroidism? Primary: parathyroid adenoma Secondary: chronic renal failure, i.e. retention of phosphorous drives calcium down and PTH up
What is the etiology of hyperparathyroidism? Parathyroid adenoma, radiotherapy
What are clinical features of hyperparathyroidism? 1. Stone: kidney (from all the filtering) 2. Bone: osteitis fibrosa cystica 3. Moan: depression 4. Abdominal groan: high Calcium -> high gastrin prod'n and peptic ulcer Dz (nausea, vomiting, constipation) 5. Cardiac arrhythmias: asystole
What is the etiology of hypoparathyroidism? Neck surgery for thyroid, mostly idiopathic
What are clinical features of hypoparathyroidism? Decreased serum calcium Hyperphosphatemia 1. Perioral numbness 2. Numbness & tingling of hands and feet 3. Carpopedal spasm 4. tetany
What hormone is Cushing's Syndrome caused by and the etiology? Increased cortisol; adrenal (2nd layer) adenoma, bilateral adrenal hyperplasia from pituitary (Cushing's Dz), secondary to oat cell carcinoma
What are clinical features of Cushing's Syndrome? Moon face, thick web neck, truncal obesity, thin extremity, muscle wasting, depression, abdominal striae
What are s/s of Cushing's syndrome in females? Hirsutism, acne, infertility, menstrual disturbances.
What are s/s of Cushing's Syndrome in both males and females? Infection, HTN, diabetes mellitus
What hormone causes Conn's Syndrome and etiology? Primary hyperaldosteronism; aldosterone secreting neoplasm
What are clinical features of Conn's Syndrome? HA, high BP, hypokalemia, and increased serum aldosterone; retaining Na -> HTN, young individual, increase in mineralocorticoids
What is acute adrenal insufficiency? Addisonian Crisis, both aldosterone and cortisol levels decreased; shock in patients using prednisone in high doses and stop suddenly w/o tapering; very low BP, very low HR and severe abdominal pain
What is chronic adrenal insufficiency? Addison's Dz; autoimmune; CFs: combination of cortisol and aldosterone deficiency; hypoglycemia, hyperpigmentation (high ACTH->high MSH->skin pigmentation), hypotension, hyperkalemia and cardiac arrhythmias d/t potassium retention.
What is Congenital Adrenal Hyperplasia? A congenital anomaly: a defect in one of they enzymes that are necessary for the synthesis of cortisol (21, 17 or 11 hydroxylase); effects testosterone, cortisol decreased, ACTH increased
What are clinical features of male and female persons w/ congenital adrenal hyperplasia? Female infants w/ ambiguous genitalia; Female: amenorrhea and virilization (becoming male-like) Male: Precocious puberty
What does pheochromocytoma cause? Increased catecholamines, increased sympathetic activity; increased HR and BP
What is Diabetes Mellitus? Hyperglycemia, inadequate action of insulin on body tissues; decreased circulating levels of insulin (type I) or resistance of target tissues to actions of insulin (type II)
What are clinical features of Diabetes Mellitus? Increased urine volume w/ glycosuria Increased thirst Weight loss (type I) Infection (fungal/bacterial) of skin, vulva and urinary tract Blurring of vision
What are 3 acute complications of diabetes mellitus? 1. Ketoacidosis 2. Hyperosmolar non-ketotic coma 3. Hypoglycemic coma
What is ketoacidosis? Only in IDDM (type I); glycosuria, hyperglycemia, ketonnemia, ketouria, Kussmaul's respiration (increased breath rate), odor of acetone on breath, marked dehydration (shock)
What is Hyperosmolar non-ketotic coma? Type II IDDM, in elderly patients, precipitated w/ infection, altered consciousness.
What is hypoglycemic coma? Insulin shock, decreased serum glucose d/t either increased insulin dosage or delay in ingestion of a meal or increased physical activity; adrenergic stimulation; very low glucose levels, brain can't function
What are chronic complications of DM? Microvascular disorders: small blood vessels of the eye, kidney, medium and large blood vessels.
What happens to small blood vessels of the eye in chronic complications of DM? Blot hemorrhage, cotton wool spots in retina, blindness d/t bleeding, cataract (retinal changes).
What happens to the kidneys w/ chronic complications of DM? Renal failure, proteinuria, end stage kidney Dz
What happens to medium and large blood vessels w/ chronic complications of DM? Involving the nervous system: poly- or mononeuropathy, autonomic neuropathy (impotence, atonic (can't contract) bladder)
What does Chvostek's sign test for and what makes it present? Hypoparathyroidism; tap by ear where facial n. exits and twitching of facial mm. is a present Chvostek
What layer of the adrenal gland is problematic in Cushing's syndrome, Conn's syndrome and congenital adrenal hyperplasia (CAH)? Cushing's: Fasciculata (cortisol) Conn's: Glomerulosa (aldosterone) CAH: Reticulata (sex hormones)
Who has type I diabetes and a description? Younger persons up to 20-25; decreased circulating levels of insulin; antibodies against pancreas, insulin dependent
Who has type II diabetes and a description? Older individuals above 40 y/o; resistance of target tissues to actions of insulin; not insulin dependent, hypoglycemic prescription
Created by: kabrown