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BCPS study guide
Endochrine and metabolic disorders
| Question | Answer |
|---|---|
| most common hyperthyroid disorder | toxic diffuse goiter (Graves' Disease) |
| mechanism of Graves' Disease | Thyroid stimulating antibodies directed at thyrotropin receptors mimic TSH and stimulate production of t3 and t4 |
| mechanism of pituitary adenomas in hyperthyroid | production of TSH that doesn't respond to normal T3 feedback |
| Diagnosis of hyperthyroid | elevated free T4. suppressed TSH. radioactive iodine test shows uptake increased [if depressed likely due to thyroiditis or hormone ingestion] |
| what condition is described below: weight loss, increased appetite, lid lag, heat intolerance, goiter, fine hair, heart palpitations, anxiety, insomnia, mentrual disturbances, sweating or warm moist skin, exopthalmos. | hyperthyroid condition |
| when do you typically implement antithyroid pharmacotherapy | when a pt is awaiting surgical resection or ablative therapy. when pt not a candidate for either. when pt fails ablative or surgery. mild disease/small goiter/low or neg antibody titers. limited life expectance. mod-severe Graves ophthalmopathy. |
| mechanism of thioureas - and drug names | methimazole and PTU inhibit iodination and synthesis of thyroid hormones. PTU may also block T4/T3 in periphery. |
| preferred agent for Graves' disease according to AACE. when would PTU be the better choice? | methimazole. woudl use PTU in first trimester of preggers. |
| black box warning with PTU | hepatotoxicity - get baseline LFTs |
| ADEs for the thioureas | rash, arthralgias, lupus-like sx, fever, agranulocytosis within first 3 mo of theray - get baseline CBC but no routine monitoring indicated. |
| mg to mg what is the relative potency of the two thioureas | methimazole is 10 times more potent than PTU |
| typical thiouria duration of therapy for Graves'. | 12-18 months. |
| beta blockers to use for hyperthyroid | non-selective - typically propranolol. occasionally nadolol. |
| mechanism of propranolol in hyperthyroid | blocks hyperthyroidism manifestations mediated by beta adrenergic receptors. may also block T4 conversion to T3. |
| dosing of propranolol in hyperthyroid | start with 20-40 mg TID-QID up to 240-480 mg QD |
| when to use propranolol in hyperthyroid | typically for sx relief. rec use in elderly, or others with HR >90bpm but can use in all symptomatic pts. |
| alternatives to beta blockers for sx relief of thyroid storm | clonidine, non-DHP CCBs |
| mechanism of iodine in hyperthyroid | inhibits release of stored thyroid hormone. helps decrease cascularity and size of thyroid prior to surgery. |
| dosage forms of iodine for hyperthyroid | Lugol's solution (6.3-8 mg iodide per drop), saturated solution of potassium iodide (38-50 mg iodide per drop), potassium iodide tablets (130 mg tablet has 100 mg iodide). |
| typical dose of iodide for hyperthyroid | 120-400 mg divided TID |
| ADEs for iodine | hypersensitivity, metallic taste, soreness ro burning in mouth or tongue. |
| typical uses for iodine in hyperthyroid | used 7-10 days temporarily prior to surgery. also used post ablative therapy for 3-7 days to inhibit thyroiditis mediated release of stored hormone. also used acutely in thyroid storm. |
| causes of thyroid storm | trauma, infection, antithyroid agent withdrawal, severe thyroiditis, postablative therapy. |
| presentation of thyroid storm | fever, tachycardia, vomiting, dehydration, coma, tachypnea, delerium. |
| most common hypothyroid disorder in areas of iodine sufficiency | Hashimoto's |
| what is iatrogenic hypothyroid | usually due to thyroid resection or radioiodine ablative therpay |
| common drugs that cause hypothyroid | lithium and amiodarone |
| diagnosis of hypothyroid | decreased free T4, elevated TSH (>10), thyroid antibodies such as antithyroid peroxidase and antithyroglobulin autoantibodies, |
| what condition is described below: cold intolerance, dry skin, fatigue, lethargy, weakness, weight gain, bradycardia, slow reflexes, coarse skin adn hair, periorbital swelling, menstrual disturbances, goiter. | hypothyroid condition |
| initial dose of levothyroxine | 1.6 mcg/kg/day using ideal body weight. pts 50-60 yrs old consider 50 mcg/day. if CVD consider 12.5-25 mcg/day. |
| what patient population tends to require higher doses of levothyroxine | preggers |
| how long should you give between dose changes or to assess efficacy in new starts for levothyroxine. | 4-8 weeks. (7 day half life for T4) |
| ADEs for levothyroxine | hyperthyroidism, cardiac abnormalities, risk of fractures with high doses or oversupplementation |
| severe and life threatening decompensated hypothyroidism with a mortality rate of 30-60% | myxedema coma |
| causes fo myxedema coma | trauma, infections, heart failure, medications such as sedatives, narcotics, anesthesia, lithium, amiodarone. |
| treatment for myxedema coma | IV thyroid hormone replacement. 100-500 mcg LD followed by 75-100 mcg/day until pt can tolerate PO. can do T3 as it is more biologically active and T3/T4 conversion may be suppressed in myxedema coma but levothyroxine is cheaper and more available. |
| conditions resulting from growth hormone secreting pituitary adenomas | acromegaly, gigantism |
| most common cause of hyperprolactinemia | prolactinomas. also, drugs such as SSRIs and antipsychotics or CNS lesions |
| diagnosis of acromegaly | failure of an oral glucose tolerance test to suppress growth hormone serum concentrations but with elevated insulin like growth factor I (IGF-1) |
| clinical presentation of acromegaly | excessive sweating, osteoarthritis, joint pain, paresthesias, neuropathies, coarsening of facial features, increased hand volume/risg size, inc shoe size, HTN, heart disease cardiomyopathy, sleep apnea, DMII |
| cause of acromegaly or gigantism | growth hormone secreting pituitary adenoma |
| treatment options for acromegaly | dopamine agonists, somatostatin analog such as octreotide, growth hormone receptor antagonist such as pegvisomant |
| circumstances where use of pharmacotherapy is preferred over surgical resection of tumor in acromegaly | for control before surgery or irradiation. when pt not a surgical candidate, when surgery has failed or if pt relapses post surgery. |
| mechanism of action of dopamine agonists and examples | bromocriptine, cabergoline. dopamine agonist that in acromegaly causes paradoxical decrease in GH production |
| ADEs of dopamine agonists | fatigue, dizziness, nervousness, diarrhea, abdominal pain |
| mechanism of action of octreotide | a somatostatin analog that blocks GH secretion. 40 times more potent than endogenous somatostatin |
| ADEs for octreotide | diarrhea, nausea, cramps, farts, fat malabsorption, arrhythmias, hypothyroid, biliary tract disorders, changes in glucose - typiclaly decrease. |
| mechanism fo GH receptor antagonist | pegvisomant. GH derivative that binds to liver GH receptors and inhibits IGF-1 |
| ADEs fo pegvisomant | nausea, vomiting, flu-like sx, reversible elevations in hepatic transaminase |
| clinical presentation of hyperprolactinemia | amenorrhea, anovulation, infertility, hirsutism, acne -in women ED, decreased libido, moooobs, reduced muscle mass -in men headache, visual disturbances. |
| treatments for hyperprolactinemia | surgical resection of tumor, dopamine agonists such as bromocriptine or cabergoline |
| what serve as provocative pharmacologic challenge for GH concentrations | insulin, clonidine or GH releasing hormone |
| clinical presentation of GH deficiency | delayed growth velocity/short stature. central obesity, immaturity of the face or prominence of the forhead |
| treatment of GH deficiency | somatropin (recombinant GH) |
| ADEs of somatropin | arthralgias, injection site pain, idiopathic intracranial hypertension (rare but serious) |
| Mechanism of Cushing's syndrome | excessive ACTH secretion via pituitary corticotroph adenoma |
| treatment of choice for Cushing's syndrome | resection of tumor. |
| Pasireotide MOA | somatostatin analog blocks ACTH secretion from pituitary, leading to decreased circulating cortisol levels |
| ADEs for pasireotide and pretests to consider | hyperglycemia, hypocorticalism, diarrhea, nausea, gallstones, headache, bradycardia. Get ECG, FPG, A1C, LFTS and gallbladder US before use. |
| ketoconazole ADE | moobs, abdominal discomfort, reversible hepatic transaminase elevations |
| metyrapone use in cushings | compassionate use only |
| metyrapone MOA | hinders secretion of cortisol by blocking the final step in cortisol synthesis through inhibiting 11 hydroxylase activity |
| metyrapone ADEs | hypoadrenalism, hypertension, worsening of hirsutism and acne if present before treatment, headache, abdominal discomfort |
| place in therapy of mifepristone for cushings | used to treat hyperglycemia via limiting binding of cortisol. may reduce insulin requirements and improve clinical symptoms associated with hyperglycemia |
| typical causes of hyperaldosteronism | bilateral adrenal hyperplasia and aldosterone-producing adenoma. |
| typical presentation of hyperaldosteronism | hypernatremia, hypokalemia, hypomagnesemia, glucose intolerance, elevated plasma aldosterone:renin ratio, HTN, muscle weakness/fatigue, headache, polydipsia, nocturnal polyuria. |
| MOA spironolactone for hyperaldosteronism | competitively inhibits aldosterone biosynthesis |
| dosing of spironolactone for hyperaldosteronism | 25-50 mg up to 400 mg QD |
| ADEs of spironolactone | hyperkalemia, moobs, abdominal discomfort |
| diagnostic test for Addison's disease | abnormal rapid cosyntropin (synthetic ACTH) stimulation test (blunted increase in cortisol concentrations) suggests adrenal insufficiency |
| Clinical presentation for Addison's disease | hyperpigmentation caused by elevated ACTH concentrations, weight loss, dehydration, hyponatremia, hyperkalemia, elevated BUN |
| treatment for Addison's disease | steroid replacements, hydrocortisone/cortisone/prednisone/dexamethasone, fludrocortisone (to replace losses of mineralcorticoid), DHEA (for women with decreased libido or energy) |
| what is the advantage of using hydrocortisone over prednisone, cortisone acetate or dexamethasone in pts with Addisons? | you can sometimes avoid the need for mineralocorticoid replacement with fludrocortisone |
| ADEs associated with orlistat | greasy poops, farts, fecal urgency/incontinence esp with high fat meal, reduced absorption of ADEK, hepatotoxicity, kidney stones |
| MOA of orlistat | inhibits fat absorption by inhibition of gastric and pancreatic lipases |
| MOA of lorcaserin | reduces hunger by stimulating serotonin 2C receptors in the brain. |
| ADEs of lorcaserin | HA, dizziness, nausea, dry mouth, constipation, memory or attention disturbances, hypoglycemia in pts with DMII, Serotonin syndrome with multiple serotonin modulating drugs |
| MOA phentermine/topiramate. | phentermine promotes appetite suppression and decreased food intake secondary to its sympathomimetic activity. topiramate is unknown but possibly increased gaba aminobutyrate activity. |
| ADEs of phentermine/topiramate | dry mouth, parasthesia, constipation, dysgeusia, insomnia, attention memory disturbances, increased heart rate. |
| cause of PCOS | insulin resistance with subsequent compensatory insulin hypersecretion or increased insulin action. this stimulates androgen secretion by the ovaries and or adrenal cells, leading to increased luteinizing hormone secretion but normal or low FSH levels. |
| clinical signs of hyperadnrogenism | hirsutism, acne, pattern alopecia, elevated free or total serum testosterone, increased LH/FSH ratio greater than 3, irregular menses, infertility. |
| non pharm therapy for PCOS/hyperandrogenism | weight loss if overweight/obese |
| drugs of choice to improve fertility in PCOS pts | clomiphene citrate, gonadotropin, metformin |
| drugs of choice that do not affect fertility in PCOS pts | estrogen/progesterone contraceptive, spironolactone, pioglitazone |
| MOA of clomiphene | induces ovulation as a selective estrogen receptor modulator that improves LH-FSH secretion |
| ADEs of clomiphene | flushing, GI discomfort, vision disturbances, vaginal dryness, multiple pregnancies |
| When do you screen for gestational diabetes | at first prenatal visit to check for undiagnosed DMII in all pts with DMII RFs. and again at 24-48 weeks of gestation using a 75 g OGTT |
| microvascular complications of DM | retinopathy, nephropathy, neuropathy |
| macrovascular complications of DM | cardiovascular, cerebrovascular and peripheral vascular diseases |
| other than glycemic control, benefits of TZDs | increases HDL, Pioglitazone better LDL and TG profile |
| ADEs of metformin | GI effects, decrease B12 levels, lactic acidosis typically with renal impairment - limit to Scr 1.5 in men or 1.4 in women. d/c if CrCl <30 |
| S/Sx of lactic acidosis | acidosis, nausea, vomiting, increased respiratory rate, abdominal pain, shock and tachycardia |
| age cutoff for metformin | ~80 yrs old, if absolutely need to use, watch renal function carefully. |
| fasting plasma glucose indicating DM | 126+ mg/dL |
| random plasma glucose indicating DM | 200 mg/dL or greater with sx of hyperglycemia |
| a1c indicating DM | 6.5% or greater |
| diagnosis of gestational diabetes | get OGTT at weeks 24-28. fasting will be 92 or greater, 1 hour post OGTT 180 or greater, 2 hours post OGTT 153 or greater. |
| A1C GOAL in DM | <7.0% |
| fasting/preprandial glucose goal in DM | 70-130 |
| post prandial goal in DM | 180 |
| BP goal for diabetics per ADA guidelines | 140/80 |
| LDL/TG goals for diabetics | LDL goal = <100 or <70 if CVD. TG goal = 150 or less |
| treatments for gastroparesis | metoclopramide (10 mg AC) or erythromycin (40-250 mg AC) |
| most common cause of morbidity/mortality with DM | CVD |
| when is a statin indicated in DM | if lipid levels indicate based upon cholesterol guidelines, if pt has established CVD, or if pt is >40 yrs with at least one cardiovascular risk factor other than DM |
| it a pt cannot reach their lipid goal what is an alternative option | a 30-40% reduction in LDL-c |
| HDL goal in DM | >40 mg/dL for men, >50 for the ladies. |
| TG goal for DM | <150 |
| when should a pt with DM be put on antiplatelet therapy | ASA indicated in all DM pts with CVD, OR for primary prevention if 10 year risk >10% - typically once men>50 and women >60 with at least one CV risk factor. Plavix can be used in place of ASA if pt is intolerant. |
| immunizations needed for DM pts | flu annually, pneumococcal, hep B |
Created by:
mjuhlin
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