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Patho - endocrine
| Question | Answer |
|---|---|
| positive feedback loop | when cells respond to a hormone & need more of it, it'll stimulate it to get more |
| negative feedback loop | when cell is full, signals the end organ to shut down signals & releasing the hormones |
| thyrotropin - releasing hormone (TRH) | stimulates release of TSH |
| corticotropin- releasing hormone (CRH) | stimulates the secretion of adrenocorticotropic hormone |
| gonadotropin- releasing hormone (GnRH) | stimulates secretion of LH and FSH |
| growth hormone- releasing hormone (GHRH) | stimulates the secretion of growth hormone |
| growth hormone (GH) | stimulates growth and metabolism in bones and muscles |
| adrenocorticotropic hormone (ACTH) | stimulates synthesis & secretion of adrenal cortisol hormones |
| thyroid - stimulating hormone (TSH) | stimulates synthesis & secretion of thyroid hormone |
| follicle stimulating hormone (FSH) | female stimulates growth of ovarian follicle; male sperm production |
| luteinizing hormone (LH) | female - estrogen & progesterone male - testosterone |
| prolactin | prepares female breast for breast feeding |
| antidiuretic hormone (ADH) | regulates water balance in the body by increasing water reabsorption in the kidneys |
| oxytocin | stimulates contraction of pregnant uterus, milk ejection from breasts after childbirth |
| primary endocrine disorders | dysfunction of endocrine gland |
| secondary endocrine disorders | dysfunction of pituitary gland |
| tertiary endocrine disorders | dysfunction of hypothalamus |
| hyper GH | acromegaly |
| hypo GH | dwarfish |
| Addison's disease | hypo secretion of cortisol |
| cushing syndrome | hyper secretion of cortisol |
| signs and symptoms of addison's disease | dark pigmentation in skin, bronzing, increasing risk of death |
| signs and symptoms of cushing syndrome | obesity, buffalo hump in neck, moon face, hyperglycemia |
| hyper ADH hormone | syndrome of inappropriate ADH |
| hypo ADH hormone | diabetes insipidus |
| t3, t4, calcitonin | controls cellular metabolic activity |
| hyper thyroidism | too much t3 & t4 |
| hypo thyroidism | too little t3 & t4 |
| grave's disease | auto immune disease of thyroid gland |
| hyper parathyroidism | too much parathormone |
| hypo parathyroidism | too little parathormone |
| cortisol (sugar) | glucose metabolism, inhibit inflammatory response, suppress allergic response, severe stress response |
| aldosterone (salt) | electrolyte metabolism, maintain long term Na balance & fluid balance through RAAS |
| androgens (sex) | male sex hormones, small amounts of estrogen or female sex hormones |
| pheochromocytoma | tumor in the adrenal gland |
| most important issue with pheochromocytoma | if not treated, it may cause severe damage |
| alpha cells | produce glucagon, which has the opposite effect of insulin, helps increase blood glucose levels by promoting the breakdown of glycogenin the liver and the release of glucose into the bloodstream |
| beta cells | produce insulin -> transport the blood glucose into body cell -> decrease blood glucose level |
| delta cells | produce somatostatin -> reduce food absorption from the GI tract -> decrease blood glucose level |
| type 1 DM | destruction of pancreatic beta cells -> no insulin production |
| type 2 DM | insulin resistance and impaired insulin secretion from beta cells |
| gestational DM | secretion of placental hormone, increases insulin resistance and glucose intolerance |
| describe risk factors for type 1 DM and type 2 DM | family history/ genetic, obesity, ethnicity, age > 45 |
| glucose | main sugar found in blood |
| gluconeogenesis | the formation of glucose form non-carbohydrates, such as protein or fat |
| glycogenolysis | hepatic glycogen is breakdown into glucose -1- phosophate |
| hypoglycemia normal labs | BG less than 70 mg / dL |
| hyperglycemia normal labs | BG greater than 200 mg/ dL |
| how does insulin work in the body ? | increase the transport of glucose into liver & muscle into adipose tissue increase protein syntehsis by inhibiting glucose |
| acute complications of diabetes: ketoacidosis | more likely in 1 DM lack of insulin leads to increase fatty acids -> increase ketone production in the liver |
| acute complications of diabetes: hyperosmolar hyperglycemic state | more likely in 2 DM physiologic stress causes osmotic diuresis *no ketones present |
| acute complications of diabetes: hypoglycemia | excessive exogenous insulin -> CNS changes: brain relies almost entirely on glucose for energy *medical emergency |
| classic signs of type 1 DM | abrupt; symptomatic (polyuria, polydipsia, dehydration) often with severe ketoacidosis |
| classic symptoms of type 2 DM | gradual; usually subtle; often asymptomatic |
| long term complications from diabetes: arteriosclersois | vascular disease where blood vessels are damaged |
| long term complications from diabetes: peripheral arterial disease | narrowing or blockage of the vessels that carry blood from the heart to the legs |
| long term complications from diabetes: peripheral neuropathy | when the nerves that are located outside of the brain & spinal cord are damaged |
| long term complications from diabetes: retinopathy | damage to the blood vessels of the light- sensitive tissue at the back of the eye |
| long term complications from diabetes: nephropathy | the deterioration of kidney function |
| long term complications from diabetes: poor wound healing/ diabetic foot ulcers | an open sore or wound located on the bottom of the foot |
| long term complications from diabetes: immunosuppression | body's inability to fight infections & other diseases |
| long term complications from diabetes: autonomic neuropathy | when there is damage to the nerves that control automatic body functions |
Created by:
sammy.e7
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