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BCPS study guide

Endochrine and metabolic disorders

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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