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110 Cards in this Set
- Front
- Back
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Put the exogenous corticosteroids in order of glucocorticoid effect (least to highest).
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aldosterone, hydrocortisone, prednisolone, fludrocortisone, dexamethasone
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Put the exogenous corticosteroids in order of mineralocorticoid effect (least to highest).
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prednisolone, hydrocortisone, dexamethasone aldosterone/fludrocortisone
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What are the blood level side effects with acarbose?
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no hypoglycemia, small reductions in serum calcium and B6
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What does calcitonin do?
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promotes absorption of calcium by bone, inhibits reabsorption by osteoclasts
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What lifestyle factors can cause osteoporosis?
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cigarette smoking, heavy alcohol use, physical inactivity, low calcium, thin build, low sunlight exposure
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What do you lab test in osteoporosis?
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renal, hepatic, hyperparathyroidism, paraprotein conditions
CBC and platelets TSH free calcium testosterone in males 25-OH vitamin D level |
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Why do you need vitamin D?
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maximizes absorption of calcium from GI tract
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What happens when you have both calcium and vit D deficiency?
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excess PTH, bone resportion is increased, bone mass is lost, osteomalacia
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Which patients need urinary calcium monitoring?
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current/previous history of hypercalcemia, no renal calculi
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What's the deal with calcium carbonate?
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usual, needs acid to dissociate
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What's the deal with calcium citrate?
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better GI tolerance, more expensive, absorbed well even without gastric acid
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What puts you at risk for vitamin D deficiency?
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elderly, decreased intake, decreased sun exposure, decreased activation of vit D in the kidney
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What happens when you get Vitamin D intoxication?
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hypercalcemia, renal failure
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Where do you get Vitamin D2?
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diet
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Where do you get Vitamin D3?
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skin
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Where is the first hydroxylation of Vitamin D?
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position 25, liver
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What upregulates the second hydroxylation of vitamin D?
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PTH
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What are the causes of vitamin D deficiency?
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dietary lack, poor sunlight exposure, malabsorption, anticonvulsant therapy, chronic liver disease, chronic renal disease, vitamin D-dependent osteomalacia
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What is cholecalciferol?
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vitamin D3
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What is ergocalciferol?
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vitamin D2
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What is alendronate?
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weekly vitamin D drug
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How do you maintain bone mass?
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estrogen replacement therapy or selective estrogen receptor modulators
low dose bisphosphonates, adequate dietary Ca, don't smoke, avoid excessive alcohol, weight-bearing physical exercise, adequate vitamin D intake |
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What are the non-PTH mediated causes of hypercaclemia?
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malignancy, vitamin D, vitamin A, adrenal insufficiency, hyperthyroidism, immobilization, thiazides, milk-alkali syndrome
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What are the non-parathyroid causes of hypocalcemia?
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pseudohypoparathyroidism, hypomagnesemia, vitamin D deficiency, 1alpha-hydroxylase deficiency, osteoblastic metastasis, tumor-lysis syndrome, acute pancreatitis, toxic shock syndrome
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What can lead to the disease process of osteomalacia?
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vitamin D deficiency or impaired metabolism, lack of Ca or phosphorus
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What kind of drug is Alendronate?
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bisphosphate
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Why do you give Alendronate?
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prevention and treatment of post-menopausal osteoporosis, prevention of steroid-induced osteoporosis
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What is Alendronate's MOA?
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anti-resorptive, slowed recruitment of osteoclast precursors to bone, inhibition of osteoclast activation
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What are the negative effects of Alendronate?
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poorly absorbed, acute phase reaction, hypocalcemia can occur, osteonecrosis of hte jaw, esophageal ulceration
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What are the risk factors for osteonecrosis of hte jaw with Alendronate?
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cancer, poor oral hygiene, smoking, pre-existing dental disease, anemia, coagulopathy, infection
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How do you prevent esophageal ulceration with Alendronate?
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wet esophagus first, drink fluid after, avoid lying down after taking the drug
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To whom should you not give Alendronate?
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patients with esophageal stricture or severe motility disorders, inability to remain upright, aspiration risk, hypocalcemia, poor renal function
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Why would you give Raloxifene?
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decreased bone resorption, increased bone density
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What kind of drug is Raloxifene?
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selective estrogen receptor modulator
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What is Raloxifene's MOA?
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estrogen agonist in bone and lipid profile, estrogen antagonist in breast and uterus
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What are the negatives of Raloxifene?
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no data for hip fracture reduction
icnreased risk of thromboembolic events, hot flashes |
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Who should get Raloxifene?
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post-menopausal women, decreased risk of breast cancer, can't take bisphosphonate
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What kind of drug is teriparatide?
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recombinant PTH
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What does teriparatide do?
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increase in BMD, reduces spine fracture
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In whom do you use teriparatide?
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patients at high risk of fracture, failed other agents
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In which patients should you avoid giving teriparatide?
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Paget's disease, irradiated bone, open epiphyses, unexplained elevation in alkaline phosphates
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How does estrogen change teh TBG?
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decreased clearance of the protein from plasma, increased circulating pool of TBG, increases circulating bound fraction of total T4, but doesn't change free fraction
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How do you treat hypopituitarism?
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replacement corticosteroids, thyroid hormone, testotsterone, estrogen, growth hormone
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What are the drug interactions with oral thyroid hormones?
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estrogenic steroids,
androgens, salicylates, glucocorticoids, phenytoin, carbamazepine cause decreased protein binding, accelerate clearance diminished GI absorption with carafate, cholesterol binding resins, aluminum hydroxide |
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What causes plasma insulin to rise fastest, oral or IV glucose?
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oral
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How are MODY and Type 1 diabetes different?
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MODY doesn't start during childhood, has a stronger family inheritance, no antibodies, and partial insulin deficiency
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What is insulin's effect on the liver?
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decreases gluconeogenesis and glycogenolysis
decreases hepatic gluconeogenic substrate increased glucose uptake in the liver |
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What does insulin do to muscle?
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suppresses proteolysis, increase glucose uptake, inhibits muscle protein degradation
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What does insulin do to fat?
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increases uptake of glucose in fat, suppresses lipolysis in adipose tissue, suppresses
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How long does Lispro act?
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3-4h
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How long does Regular act?
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5-8 h
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How long does Glargine act?
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24+ h
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How do you give Lispro?
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at the beginning of a meal
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How do you give REgular?
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every 6 hours with tube feeding
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What drugs increase insulin requirements?
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glucococorticoidsteroids, sympathomimetic therapy
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What disease processes increase insulin needs?
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obesity, inactivity, Type II diabetes, infection, inflammation, acromegaly, hyperthyroidism, ketoacidosis, genetics, pregnancy, TPN
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What physical changes decrease insulin needs?
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physical activity, lean body, kidney disease, liver disease, early pregnancy, Addison's, ACTH deficiency
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What are the negative effects of insulin?
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hypoglycemia, varied absorption, edema, allergy, cutaneous reactions, lipodystrophy/lipoatrophy
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What happens with insulin allergy?
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insulin resistance, hypoglycemia
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What is octeotide?
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long-acting somatostatin analogue
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What are the side effects of Octreotide?
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suppresses intestinal secretions, insulin release, worsen diabetes, cause nausea, vomiting, and flatulence
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Where do T4 and T3 live?
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circulate in the bloodstream, bound to plasma hormones
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How do you estimate fraction of hormone bound to TBG?
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T3 resin uptake test
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What converts T4 to T3?
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5' monodeiodinase
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Which thyroid hormone is active?
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T3
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How does the pituitary 5' deiodinase different from peripheral tissue 5' deiodinase?
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pituitary enzyme is selenocystein-dependent, low Km, selective for T4 over reverse T3
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How do reverse T3 levels affect T3 synthesis?
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inverse relationship
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Which enzyme deactivates T4?
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Type III deiodinase, generates reverse T3
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Which thyroid hormone has the shorter half life?
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T3
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Why wouldn't you give exogenous T3?
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body can convert T4 into T3 as needed, no advantage to using synthetic T3
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Why would you use exogenous T3?
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managing patients with radioiodine therapy for metastatic thryoid carcinoma
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Why would you use beta blockers?
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to block thyroid-induced effects of beta adrenergic receptors in the heart
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What does lithium do to the thyroid?
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can cause goiter and hypothyroidism, esp with unrecognized Hashimotos
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What do steroids do to the thyroid?
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treatment of thyrotoxicosis, can't inhibit peripheral T3 to T4
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What does Amiodarone do to the thyroid?
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can change thyroid function tests to hypo or hyperthyroid
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What is the mechanism of sulfonylureas?
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bind receptor-like proteins associated with ATP-dependent K channels, closes channels, depolarizes beta cell
depolarization opens voltage-gated Ca channels, influx of EC Ca in response to glucose that stimulates insulin secretion |
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When do you see extrapancreatic effects of sulfonylureas?
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when beta cell reserve exists
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What are the extrapancreatic effects of sulfonylureas?
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imrpoved peripheral and hepatic insulin sensitivity, enhanced insulin receptor binding, increased glucose transport in muscles and adipocytes, increased skeletal muscle glycogen synthase activity, reduced hepatic glucose production
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What kind of drug is Chlorpropamide?
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sulfonylurea
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What kind of drug is Glipizide?
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sulfonylurea
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What kind of drug is Glyburide?
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sulfonylurea
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Which drugs are sulfonylureas?
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Chloirpropamide, Glipizide, Glyburide
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What are the side effects of glipizide?
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weight gain, skin rash, leukopenia, thrombocytopenia, hemolytic anemia
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What are the side effects of glyburide?
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hypoglycemia, skin rash, leukopenia, thrombocytopenia, hemolytic anemia
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What are the drug interactions of glyburide?
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salicylates, warfarin, allopurinol
enhance hypoglycemic potency |
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What are the drug interactions of glipizide?
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salicylates, warfarin, allopurinol
enhance hypoglycemic potency |
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Which sulfonylurea is shorter acting?
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glipizide
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Which sulfonylureas are longer acting?
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glyburide, chlorpropamide
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Who should not get glipizide?
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type I, sulfonylurea allergies, pregnancy, lactation
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Who should not get chloropropamide?
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type I, sulfonylurea allergy, pregnancy, lactation, renal insufficiency
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Who should not get glyburide?
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type I, sulfonylurea allergy, lactation
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Who should get glipizide?
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elderly patients, erratic meal schedule, hepatic/renal/cardiac dysfunction
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What is the MOA of meglitinides?
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K channel blocker, acts as insulin secretagogues
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What are the pharmacokinetics of meglitinides?
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rapid onset, short duration of action
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What kind of drug is metformin?
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biguanide
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What is metformin's MOA?
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suppresses hepatic glucose production, enhanced insulin action in muslce and fat, inhibition of fatty-acid oxidation, no stimulation of insulin secretion, activates AMP-activated protein kinase in skeletal muscle and liver
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How is metformin secreted?
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renally
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What are the side effects of metformin?
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lactic acidosis, GI effects, hypoglycemia, metallic taste, fall in B12 levels
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What are the risk factors for lactic acidosis with metformin?
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renal insufficiency, hepatic insufficiency, heart failure, hypoxia, alcohol abuse, severe illness/surgery, IV radio contrast
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What are the drug interactions of metformin?
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furosemide, nifedipine, cimetidine, digoxin, amiloride, triamterene, procainamide, trimethoprim increase metformin levels
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What are the contraindications for metformin use?
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renal insufficiency, hepatic insufficiency, cardiac or respiratory insufficiency, hypoxia, alcohol abuse, metabolic acidosis, acute illness or surgery, volume depletion, IV contrast, preganancy, lcatation, age > 80 years
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What are the clinical indications for metformin use?
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monotherapy, combination with other hypoglycemic agents/insulin in patients failing monotherapy, not sub for failure of sulfonylurea
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What drug is an alpha-glucosidase inhibitor?
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acarbose
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What is acarbose's MOA?
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locally in digestive tract, delays digestion and absorption of ingested carbs with delayed and reduced postprandial rise in b/g and insulin levels
competitive and reversible inhibition of alpha-glucosidase enzymes (alpha-amylase, sucrase, maltase, isomaltase, glucoamylase) |
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Where is acarbose metabolized?
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in gut, mostly by bacteria
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How potent is acarbose?
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less potent than SU or metformin
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What are the GI side effects of acarbose?
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flatulence, diarrhea, ab pain
related to delivery of undigested carbs to colon with subsequent digestion by colonic bacteria, gas formation |
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What are the hepatic side effects of acarbose?
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acarbose-induced hepatitis with elevated transaminases at high doses
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How do you treat hypoglycemia in a patient taking acarbose?
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pure glucose or milk, sucrose, etc will not be absorbed
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What are the contraindications for acarbose therapy?
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liver dysfunction, cirrhosis, chronic intestinal disorders iwth gut inflammation, malabsorption, dysmotility, pregnancy, lcatation
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