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Seva Visc. Endocrine
Dr. Seva's Visceral Pathology Endocrine
| Question | Answer |
|---|---|
| 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
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