flashcards for exam 3
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| Max lipid lowering effect of bile acid sequestrants | decrease LDL 15-30%, increase HDL 3-5%, no change or increase in TG
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| Max lipid lowering effect of cholesterol absorption inhibitor | decrease LDL 18%, increase HDL 1%, decrease TG 8%
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| Max lipid lowering effect of statins | decrease LDL 18-55%, increase HDL 5-15%, decrease TG 7-30%
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| Max lipid lowering effect of Niacin | decrease LDL 5-25%, increase HDL 15-35%, decrease TG 20-50%
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| Max lipid lowering effect of fibric acid derivatives | decrease LDL 5-20%, increase HDL 10-20%, decrease TG 20-50%
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| Max lipid lowering effect of omega-3 fatty acids | may increase LDL, decrease TG up to 45%
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| Starting age and interval for testing cholesterol | >20 years of age, screen at least every 5 years
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| Goals for TC, HDL, and TG | <200mg/dL, >40mg/dL, <150mg/dL
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| Primary diagnostic for lipids | LDL<100mg/dL
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| Equation for calculating LDL (and when the equation does not work) | LDL = TC - (HDL + TRG/5)
Equation does not work when TG>400mg/dL
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| C-reactive protein | Marker of low-level inflammation, helps in predicting CHD risk beyond LDL and major CHD risk factors
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| 5-risk factors for CHD involved in LDL modification | 1. Age (men≥45, women≥55)
2. Family hx of premature CHD events (men <55, women <65)
3. HTN (≥140/90mmHg) or on any anti-HTN medication
4. HDL <40mg/dL (≥60mg/dL is -1 RF)
5. Cigarette smoking within past month
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| Determine patient's LDL goals | CHD or CHD risk equivalent: <100mg/dL
2+ risk factors: <130mg/dL
0-1 risk factors: <160mg/dL
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| When to calculate Framingham score | Calculate if patient has 2+ risk factors in order to determine CHD risk category
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| What Framingham result tells you | % risk of developing CHD over a 10 year period –serves as basis for deciding how intensively to treat hypercholesterolemia and other risk factors
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| CHD risk equivalents (conditions that put a patient at >20% risk of developing CHD over a 10-year period) | CHD= MI, unstable/chronic angina, coronary bypass, angioplasty, stents
CHD risk equivalent= multiple risk factors with 10-year risk for CHD>20%, diabetes, PAD, AAA, symptomatic CAD (stroke, TIA)
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| Non-HDL | Non-HDL goal = LDL target + 30mg/dL
Estimates cholesterol carried by all Apo-B-containing lipoprotein particles—represents sum of LDL, VLDL, and other TRG-rich particles
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| When to initiate TLC or drug therapy; how much of LDL reduction possible through TLC? | Adequate trial of TLC in all patients (3 months)
Consider drug therapy when LDL >30+ above goal. TLC can reduce LDL by 10%
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| TLC | Saturated fats to <7% of total calories (↓ trans fats)
Dietary cholesterol <200mg/day
Plant stanols/sterols 2g/day
Soluble fiber 10-25 g/day
Weight reduction
Increase physical activity (expend >200calories/day)
Consider: alcohol and smoking
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| Calculating recommended saturated fat intake/day | (Desired daily calorie intake x 0.07) / 9
7% of total calories; 9 kcal=1g fat
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| Definition of liver toxicity | LFTs greater than 3x the upper limit
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| Definition of myopathy | CK greater than 10x the upper limit
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| MOA of statins | HMG-CoA reductase inhibitors
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| Common AE of statins | Constipation, abdominal pain, diarrhea, dyspepsia, nausea
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| Statins not metabolized by cyp3a4, therefore have no interaction with grapefruit juice | Pravastatin, rosuvastatin, fluvastatin (minimal)
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| When to focus on TG lowering over LDL | When TG>500, trumps focus over LDL
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| Interaction with grapefruit juice and statins | GPJ inhibits CYP3A4 metabolism in the gut, allowing more drug to be absorbed and reach higher levels, increasing chance of adverse effects. GPJ>1 quart to have significant impact on inhibiting PGP efflux.
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| Order of statin's potency | Rosuvastatin>atorvastatin>simvasatatin>
lovastatin=pravastatin>fluvastatin
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| Monitoring for statins | Baseline LFT, then 6-12 weeks after starting therapy or increase dose, then annually. Check CK if muscle pain and/or brown urine, discontinue therapy if >10x normal upper limit
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| Contraindications of statins | Active liver disease, elevated serum transaminases, concomitant use of strong CYP3A4 inhibitors, concomitant use of gemfibrozil, pregnancy, breast-feeding
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| Precautions of statins | Hepatic impairment/alcohol use, renal impairment
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| MOA of bile acid-binding resins/sequestrants | Bind to bile acids in gut, forming complex that is excreted in the feces. Loss of bile causes compensatory conversion of hepatic cholesterol to bile, causing an upregulation of LDL receptors
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| Adverse effects of BAS's | Limited to GI tract: nausea, constipation, bloating, flatulence
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| Precautions of BAS's | Renal impairment, separate dose 1 hr before or 4 hrs after other medications
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| MOA of Zetia | Blocks biliary and dietary cholesterol absorption via NPC1L1 transporter in brush border of small intestine-causes decrease delivery of cholesterol to liver, reduction of hepatic cholesterol stores, induce upregulation of LDL receptors
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| Contraindications of Zetia | Active liver disease, unexplained persistent elevations in LFTs, pregnancy, breastfeeding
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| Precautions of Zetia | hepatic impairment, renal impairment
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| Adverse effects of Zetia | diarrhea, fatigue, arthralgia, URTI, sinusitis, influenza, elevated transaminases
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| MOA of Niacin | inhibit fatty acid release from adipose tissue, inhibits fatty acid and TG production in liver cells. Result: increase degradation of Apo B and decrease LDL. Reduces uptake of HDL particles.
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| Ways to minimize flushing with niacin | take with food, avoid hot liquids, take NSAID or aspirin 30 mn prior, start at lowest dose and gradually titrate up
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| Adverse effects of niacin | flushing, pruritis, gastric distress, HA, HA, hepatotoxicity, hyperglycemia, hyperuricemia
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| Precautions of niacin | can raise uric acid levels (caution with gout), can raise blood glucose levels in diabetic patients. Renal impairment, hepatic impairment
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| MOA of fibric acid derivatives | decrease APOs B, C-III, and E; increase Apos A=I and A-II thru activation of PPAR-alpha. Result: decrease TG-rich VLDL and IDL, and increase HDL
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| Adverse effects of fibric acid derivatives | Nausea, diarrhea, abdominal pain, rash, dyspepsia, flatulence, muscle pain, fatigue, increased risk of rhabdomyolysis when taken with a statin. Associated with gallstones, myositis, hepatitis
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| Contraindications of fibric acid derivatives | Gall bladder disease, liver dysfunction, severe kidney dysfunction, breastfeeding
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| Fibric acid derivatives with statins | Increased risk of rhabdomyolysis. Prefer fenofibrate over gemfibrozil due to potential less inhibition of glucuronidation/clearance of statins.
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| Contraindications of niacin | Active liver disease, unexplained persistent elevation in LFTs, active peptic ulcer, arterial hemorrhage
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| MOA of O3FAs | modulation thru PPAR-alpha and decrease Apo B-100 secretion
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| Adverse effects of O3FAs | Diarrhea, excess bleeding, may increase glucose levels
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| Counseling points for O3FAs | Take with meals. Need dose 4g/day for effect on TGs
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| When should a repeat lipid panel be drawn? | TC>200mg/dL or LDL>100mg/dL
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| Which cholesterol medications require LFT monitoring? | Statins,eztimibe, niacin, fibric acid derivatives
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| Which cholesterol medications require creatinine monitoring? | All of them (all have caution or contraindication of renal impairment except O3FAs)
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| Components used in assessment of overweight or obese patient | BMI, waist circumference, comorbidities, readiness to lose weight
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| BMI classification for weight | Underweight <18.5kg/m2
Normal weight 18.5-24.9 kg/m2
Overweight 25-29.9 kg/m2
Obese (1) 30-34.9 kg/m2
Obese (2) 35-39.9 kg/m2
Extreme obesity (3) >40 kg/m2
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| High-risk waist circumference for men and women | Men > 40in (102cm)
Women > 35in (88cm)
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| Comorbidities that heighten need for treatment of overweight or obese patient | HTN (>140/90) or on bp med, LDL >160, LDL >130 + 2 RF, HDL <40, impaired FPG (100-125 mg/dL), CHD, atherosclerosis, T2DM, sleep apnea
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| Risk factors that heighten need for treatment of overweight or obese patient | Cigarette smoking, family history of premature CHD (male <55, female <65), males >45, females >55
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| Recommended initial weight loss goal and time frame | 10% weight loss with 1-2 lbs (0.45-0.9kg) per week, meeting goal in 6 months
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| Who is weight loss indicated for? | Patients with BMI 25-29.9kg/m2 or elevated waist circumference + 2 or more comorbidities. Any patient with BMI >30kg/m2
(After 6 months of lifestyle changes)
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| How many calories reduces equals one pound of weight loss? | 3500kcal (500kcal/day for 1 week)
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| When should pharmacotherapy be initiated in addition to lifestyle modifications? | BMI>30kg/m2 or BMI>27kg/m2 with other obesity-related risk factors
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| Qsymia components | Phentermine/topiramate
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| MOA of Qsymia | P: sympathomimetic, result in CNS stimulation and appetite suppression
T: appetite suppression and satiety enhancement, block VG-Na channels, enhance GABA, antagonize AMPA, weakly inhibit carbonic anhydrase
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| Duration of Qsymia treatment | Titrating up, may take for up to 7 months
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| Dosing of Qsymia | Titrate up dose to maximum of 15mg/92mg ER once daily. Do not D/C abruptly due to risk of seizure
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| Adverse effects of Qsymia | HA, insomnia, xerostomia, constipation, palpitations, chest discomfort, DZ, anxiety, depression, fatigue, irritability, abnormal taste, nausea, blurred vision, kidney stones
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| CI of Qsymia | Hyperthyroidism, glaucoma, concomitant MAOI use, pregnancy, (kidney stones)
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| Monitoring patients on Qsymia | Periodic blood chemistry profile, HR, signs of depression, BP
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| MOA of phentermine | increase NE and dopamine release in CNS--CNS stimulation, appetite suppression
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| Duration of phentermine treatment | Up to 6 months
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| Adverse effects of phentermine | Palpitations, tachycardia, increase BP, stimulation, restlessness, DZ, insomnia, euphoria, dysphoria, tremor, HA, dry mouth, constipation, diarrhea, abuse potential
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| CI of phentermine | Unstable cardiac status, HTN, hyperthyroidism, agitated states, glaucoma, concomitant MAOI, alcohol use, hx of substance abuse, patients <16 y/o
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| MOA of diethylpropion | Sympathomimetic amine-CNS stimulation and appetite suppression
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| Duration of diethylpropion treatment | Up to 12 months
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| AE of diethylpropion | overstimulation, restlenssness, DZ, insomnia, euphoria, tremor, HA, jittery, anxiety, nervousness, depression, DQ, malaise, mydriasis, blurred vision, decrease seizure threshold, tachycardia, increase BP, palpitation, dry mouth, constipation
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| CI of diethylpropion | Pulmonary HTN, advanced arteriosclerosis, severe HTN, hyperthyroidism, agitated states, glaucoma, hx of substance abuse, MAOI use, anorectic agents, pt <16 y/o
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| MOA of lorcaserin (Belviq) | Activate 5-HT2c receptors, stimulating POMC neurons resulting in satiety and decreased food intake
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| Duration of lorcaserin (Belviq) treatment | Evaluate at week 12, maximum 2 years
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| Adverse effects of lorcaserin (Belviq) | Abuse potential (euphoria, hallucinations), HA, hypoglycemia in DM patients, back pain, URTI, HTN, DZ, fatigue, anxiety, insomnia, nausea, diarrhea
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| CI of lorcaserin (Belviq) | Pregnancy
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| MOA of orlistat | act locally in GI tract-inhibit pancreatic and gastric lipases and TG hydrolysis-undigested TGs not absorbed, result in caloric deficit and weight loss
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| Duration of orlistat treatment | Maximum of 4 years
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| Dosing of orlistat | Take during or up to 1 hour after meal. Omit dose if meal missed or contains little fat. May need multivitamin with fat-soluble ADEK
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| Adverse effects of orlistat | Local: fatty/oily stools, oily spotting/evacuation, abdominal pain, flatulence, soft stools, N/V/D, increased defecation, fecal incontinence, bloating
Dypepsia, HA
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| CI of orlistat | Pregnancy, breastfeeding, chronic malabsorption syndrome, cholestasis (kidney stones)
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| Location, severity, duration, and frequency of migraines | Unilateral, moderate to severe, 4-72 hours (w/o aura) 4-60 mns (w/ aura); 5+ attacks (w/o aura), 2+ attacks (w/ aura)
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| Location, severity, duration, and frequency of TTH | bilateral, mild to moderate, 30mn-7 days, 10+ attacks on avg less than 1day
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| Chronic tension headache | Avg headache frequency >15 days/month (180 days/yr) for >6 months
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| Symptoms of migraine | Pulsating/throbbing pain that interrupts or worsens with physical activity, N/V, photophobia, phonophobia, osmophobia, seek quiet and solitude. Possible aura.
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| Examples of aura symptoms | May be positive or negative symptoms. + visual perception of flickering lights, spots, or wavy lines. - partial loss of vision, scotoma. dysphasic speech, change in smell, feeling of euphoria/dysphoria, something out of the norm.
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| Symptoms of TTH | band-like tightness or pressure around head, nonpulsating pain, possible anorexia, either photophobia or phonophobia (not both)
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| Symptoms of cluster headache | Intermittent, explosive, excruciating, short, stabbing pain. conjunctival injecting, lacrimation, nasal congestion, rhinorrhea, sweating, eyelid edema, miosis, ptosis. excited, restless during attacks
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| Location, severity, duration, and frequency of cluster headaches | unilateral (orbital, supraorbital, temporal), severe, lasts 2 seconds-10 minutes (15-180mn). 1 qod to 8/day. 5+ attacks.
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| Theories for pathophysiology for migraine | 1. Tissue pain generated by vascular reactivity (not supported).
2. Pain induced by neuronal imbalances accompanies by trigeminovascular system overactivity (supported)
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| Current accepted theory for pathophysiology for migraine | Depressed neuronal activity spread across brain, activate trigeminal sensory nerves, release vasoactive peptides to produce inflammation around vascular structures
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| "Red Flags" for headaches | New onset sudden and/or severe pain
Onset >40 y/o
Stereotyped pattern worsens
Systemic signs
Focal neurologic symptoms (other than aura)
Papilledema
Cough, exertion, or valsalva-triggered HA
Pregnancy or postpartum
Pt with cancer, HIV, etc
Seizur
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| Information for headache diary | Date, day of week, onset time, duration, intensity/severity, location, nausea, light/sound sensitive, triggers, meds taken
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| Behavioral triggers of HA | fatigue
menstruation
menopause
sleep excess or deficit
stress
vigorous physical activity
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| Environmental triggers of HA | flickering lights
high altitude
loud noises
strong smells
tobacco smoke
weather changes
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| Food triggers of HA | MSG (Asian food, seasoned salts)
Nitrates (processed meats)
Saccharin/aspartame (diet soda, diet food)
sulfites (shrimp)
tyramine (cheese, wine, meats)
yeast
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| Medication triggers of HA | cimetidine
estrogen
OCs
indomethacin
nifedipine
nitrates
reserpine
theophylline
withdrawal due to overuse of analgesics/BZDs/decongestants/ergotamines
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| Why start pharmacologic treatment early for acute headache? | Abort intensification of pain, improve response to therapy
Initial severity of headache correlates with symptomatic response
Delay may lead to decreased analgesia thru dvpt of refractory central pain sensitization
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| Nonpharmacologic management of HA disorders | Limit exposure to triggers
Rest in dark, quiet area
Relaxation, stress management
Limit alcohol use, stop tobacco use
Psychological interventions
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| Triptan with long half-life | Frovatriptan (Frova)
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| Triptan with dosage repetition after 4 hours | Naratriptan (Amerge)
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| Triptan with dosage repetition after 1 hour | Sumatriptan injection (Imitrex)
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| Triptans with ODT dosage form | Rizatriptan (Maxalt)
Zolmitriptan (Zomig)
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| Triptans with nasal dosage form | Sumatriptan (Imitrex)
Zolmitriptan (Zomig)
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| Triptan with injection dosage form | Sumatriptan (Imitrex)
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| Triptans with potential CYP3A4 interaction | Almotriptan (Axert)
Eletriptan (Relpex)
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| Rebound headache | Acute withdrawal as result of overuse of APAP causing tolerance or dependence--result of poor attention to prevention therapies leading to chronic use of daily analgesics
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| Headache recurrence | Return of headache pain, usually within 24 hrs, after an initially good response to medication (triptans, ergots)
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| Drug of choice for mild to moderate headache attacks | APAP (not recommended alone), aspirin, NSAIDs
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| Drugs of choice for moderate headache attacks | APAP, aspirin, NSAIDs, Ergots, Triptans, combination
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| Drug of choice for severe headache attacks | IM or IV DHE; SQ or oral triptan; IM or IV ketorolac; IM, IV, intranasal or oral opioids
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| Dosage forms best for treatment of cluster headache? | Intranasal, SQ, IM, IV (Need rapid onset of action due to rapid onset/short duration of cluster headache)
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| Primary novel therapy for treatment of cluster headaches | High-flow-rate oxygen: 100% at 5-10 L/min for 15 minutes
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| Options available for adjunctive therapy for patient experiencing nausea? | Metoclopramide, chlorpromazine, prochlorperazine
Begin at first sign of HA
Best given 15-30 mn before abortive med
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| When is prophylactic (TTH) headache treatment warranted? | If headache is severe and frequent, or if TTH use of NSAIDs more than 2 days/week
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| Main option for TTH prophylaxis | TCAs (amitriptyline)
Also, propranolol
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| Main option for cluster HA prophylaxis | CCB verapamil
Also, lithium, ergotamine, corticosteroids
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| Common side effects of triptans | Dizziness, sensation of warmth, chest tightness, nausea, fatigue, tingling, weakness, somnolence. May precipitate ischemic vascular events
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| CI of triptans | associated with neurologic focality, hx of previous stroke, uncontrolled HTN, unstable angina, pregnancy, concurrent ergotamine administration (w/in 24h), liver/kidney disease
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| CI for specific triptans | Severe renal impairment (nara)
Severe hepatic impairment (ele, nara, zolmi NS)
MAOI w/in 14 days (suma, riza, zolmi)
Potent CYP3A4 inh w/in 72hr (ele)
Propranolol (riza)
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| Common side effects of ergots | N/V/D, itching, vertigo, muscle pain, weakness, increase BP, numbness or tingling in fingers or toes
DHE nasal: rhinitis, DZ, somnolence, N/V/D, taste disturbances, pharyngitis
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| Extreme side effect of ergots | Ergotism-severe peripheral ischemia and development of gangrene
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| CI of ergots | CAD, uncontrolled HTN, peripheral vascular disease, liver/kidney disease, pregnancy, w/in 24 hrs of taking triptan, breastfeeding
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| Indication for prophylactic tx of migraines | Frequent, prolonged, or severe/disruptive migraine attacks
More than 2-4 times/month, last more than 48 hrs, or cause dysfunction
Symptomatic therapies have failed or serious SE
Pt unable to cope with HA attacks
HA occur in a predictable pattern
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| General guidelines for migraine prophylaxis | Monotherapy preferred
Consider comorbid conditions
Gradual dose increase
Minimum trial of 2 months
Re-evaluate after 6-8 months
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| Difference between cortical bone and trabecular bone | Cortical: dense, compact, responsible for bone strength. 80% of skeleton. on surface of long and flat bone
Trabecular: sponge-like, along inner surfaces of long bones, more susceptible to bone remodeling due in part to larger SA
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| Osteoclasts versus osteoblasts | -clasts: resportion/breakdown of bone, continuously create miscroscopic cavities in bone tissue
-blasts: bone formation, continuously mineralize new bone in cavities created by osteoclasts
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| What age do patients attain peak bone mass? | 25-35 years old
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| Difference between t-score and z-score | T: # of SD from mean bone mineral density in normal young adult, sex adjusted
Z: # of SD from mean bone mineral density of age- and sex- matched controls
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| WHO definitions of normal, osteopenia, or osteoporosis | Normal: >-1
Osteopenia: -2.5 to -1
Osteoporosis: <-2.5
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| Recommended standardized approach to bone mineral density measurement | Measuring bone mineral density at the lumbar spine and femoral neck (hip)
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| Indications for BMD testing | All women 65+ and men 70+
Postmenopausal women, men 50-69 with clinical RFs
Fracture after age 50
Medical conditions or medications
Assessment for osteoporosis treatment initiation/monitoring
D/C of estrogen therapy
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| Calcium intake recommendations (RDA) | 1000mg: men 25-65, women 25-50, women 51-65 on estrogens
1500mg: women 51-65 not on estrogens, people >65
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| Vitamin D recommendations | <50: 200 IU
50+: 800-1000 IU
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| Max amount of calcium that can be taken at one time | 500-600 mg/dose
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| Amount of calcium that can lead to toxicity | 2500 mg/day
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| What patients are recommended for osteoporosis treatment? | >50 with: hx of hip or vertebral fracture; t-score <2.5 at femoral neck/spine; or osteopenia & 3%+ 10-year probability of hip fracture or 20%+ 10-year probability of major osteoporosis related fracture
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| What does FRAX tell you? | Evaluates an individual's 10-year risk for hip and major osteoporotic fracture
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| MOA of bisphosphonates | decrease bone resorption by binding to bone matrix and inhibiting osteoclast activity
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| MOA of raloxifene | SERM, estrogen-like activity on bones and cholesterol metabolism and estrogen antagonist activity in breast and endometrium-reduce bone resorption and decrease overall bone turnover
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| MOA of calcitonin | inhibits bone resorption by binding to osteoclast receptors
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| MOA of teraparatide | recombinant human parathyroid hormone-stimulates osteoblastic activity to form new bone when administered once daily
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| MOA of denusumab | human monoclonal antibody that inhibits receptor activator of nuclear factor-kappa B ligand (RANKL) action (antiresorption)
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| BBW warning of Forteo and maximum duration of use | In animal studies, associated with an increase in osteosarcoma. Do not use for longer than 2 years
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| Osteonecrosis of the jaw case reports--drug, dosage form, patient type? | IV bisphosphonates in cancer patients
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| HRT use in osteoporosis | Prevention only. Puts pts at higher risk for breast cancer and venous thromboembolism
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| Raloxifene (Evista) use in osteoporosis: use, benefits, risks | SERM. Treatment and prevention in postmenopausal women. Reduces the risk of breast cancer. Risks-thromboembolic events, CHD.
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| Boniva (ibandronate) use in osteoporosis | IV is treatment only, given every 3 months
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| Reclast (zoledronic acid) use in osteoporosis: use, risks | Infusion given once a year. Risk-higher rate of afib, increase SCr, infusion-related SE
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| Which osteoporosis agents can be used in men and women? | Alendronate, risedronate, teriparatide
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| Calcitonin salmon use in osteoporosis | Available nasal or parenteral route, good for patients with or at risk for vertebral fractures
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| Forteo (teriparatide) use in osteoporosis | Only agent that actually helps rebuild bones, can improve t-score. SC, needs to be refrigerated.
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| Recommendation for patients starting glucocorticoid treatment longer than 3 months? | Bisphosphonate therapy and adequate calcium and vitamin D intake
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| How many months of amenorrhea should pt have experienced to be diagnosed as in menopause? | 12 months
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| Which hormone is elevated with loss of ovarian follicular activity? | FSH (10-15 fold increase)
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| What is perimenopause/climacteric? | Transitional period prior to menopause when hormonal/biologic changes begin. Can occur 2-8 years prior, lead to irregular menstrual cycles, increase interval, decrease length. Also, may have hot flashes, night sweats
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| Common symptoms of menopause | Vasomotor symptoms (hot flashes, night sweats)
Irregular menses, episodic amenorrhea
Sleep disturbances
Vaginal dryness
Depression, mood swings
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| Less common symptoms of menopause | Fatigue
Irritability
Migraine
Arthralgia
Myalgia
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| Criteria for diagnosis of menopause | Amenorrhea for 1 year
FSH greater than 40 mIU/mL
5-fold increase in LH
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| Why is HRT only recommended for treatment of vasomotor and vaginal symptoms? | HRT is not protective against the development of CHD
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| What contraindications exist for HRT? | Hx of or active thromboembolic disease, breast cancer, or estrogen-dependent neoplasm, pregnancy, liver disease, undiagnosed vaginal bleeding
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| Is HRT approved for prevention and treatment of osteoporosis? | No! HRT is only approved for prevention of osteoporosis, and should only be used short-term
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| Risks of HRT identified in WHI study? | Could increase risk in of CHD in women with underlying risk factors, increase risk of breast cancer after 3 years of therapy
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| When is use of a progestin required for HRT? | Women who have an intact uterus
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| Disadvantage of cyclic HRT administration? | Return of menses in 90% of women 1-2 days following last progestin dose
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| Disadvantage of continuous HRT administration? | Unanticipated breakthrough bleeding or spotting during the month
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| First-line dosage form for vulvovaginal atrophy? | Topical preparations
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| Is a progestin needed with topical HRT? | No, normal doses should have minimal systemic absorption
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| Can estradiol be used in treatment of vulvovaginal atrophy in patient with CI to estrogen therapy? | Yes, topical creams, tablets, or rings
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| Estring vs. Femring | Femring has systemic absorption, releases more estradiol per day
Estring does not have significant systemic absorption and is considered topical
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| What is bio-identical hormone therapy (BHRT) | exogenous hormones identical to those produced in woman's body, commercially manufactured or chemically compounded
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| General approach to HRT | Lowest dose for shortest duration possible (preferably <5 years)
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| Risk of BHRT? | Custom HT formulation comopounded according to prescription: Not tested for efficacy, safety, batch standardization, or purity
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| Estrogen AE | nausea
HA
Bloating
Breast tenderness
Bleeding
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| Progestin AE | Nausea
HA
Weight gain
Bleeding
Irritability
Depression
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| Benefits of HRT? | relieve vasomotor symptoms and vulvovaginal atrophy
osteoporosis prevention
May reduce risk of colon cancer (inconsistent data)
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| Risks of HRT? | cardiovascular disease
breast cancer
venous thromboembolism
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| Options for assisting with discontinuation of HRT | Taper by dose decrease or day decrease
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| Nonpharmacologic interventions available for treatment of vasomotor symptoms | Smoking cessation, limit alcohol/caffeine/hot beverages/spicy foods, keep cool, stress reduction, increase exercise, paced respiration
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| Nonpharmacologic interventions available for treatment of dyspareunia | Water-based lubricants, moisturizers
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|
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| Nonpharmacologic interventions available for treatment of stress incontinence | Kegel exercises to strengthen pelvic floor muscles
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| Alternative treatment options for menopausal symptoms | SSRIs (citalopram, paroxetine, venlafaxine, fluoxetine)
Gabapentin
Clonidine
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|
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| "Natural" treatment options that have no benefit for hot flashes | Red clover
Dong Quia
Vitamin E
Evening Primrose oil
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|
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| "Natural" treatment options that have some benefit for hot flashes | *Black cohosh (remifemin): avoid if breast cancer, hepatotoxic-this is only one she'd recommend if forced
Soy: may contribute to breast cancer
Micronized progesterone creams
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| Normal VitD lab value | >30 ng/mL
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|
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| Calcium citrate vs clacium carbonate | Calcium carbonate requires an acidic gastric environment. Patients on PPI or H2RAs should take calcium titrate.
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| 4 functional phases of female menstrual cycle | Follicular: FSH increase, estrogen increase, endometrium proliferate
Ovulatory: surge of LH day 14 allows ovulation
Luteal: luteal cells need LH and progesterone
Menstrual: less progesterone/estrogen allow menses
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| Function of LH | Promote androgen production, ovulation and oocyte maturation, convert cells to luteal cells that secrete progesterone after ovulation
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| Function of FSH | promote growth of follicle in preparation for ovulation by causing granulosa clels to grow and produce estrogen
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|
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| At what point during menstrual cycle are FSH and LH at peak levels? | Just prior to ovulation
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|
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| How to adjust OC if continued bleeding after menses (1st week) | Higher estrogen content or have lower early progestin component in triphasic pills
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|
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| How to adjust OC if have spotting or bleeding midcycle (2nd week) | Difficult to determine cause, increase both estrogen and progestin component
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|
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| How to adjust OC if have spotting or bleeding before finish active pills (week 3) | Higher progestin content to increase endometrial support
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|
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| Type of OC regimen recommended for patient diagnosed with dyslipidemia? | Replace androgenic progestin with more estrogenic progestin. If TG >350mg/dL, EE 20-25mcg or progestin-only formulation
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|
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| Formulation for patient having headaches during placebo week of OC | Eliminate pill-free interval for 2-3 consecutive cycles
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|
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| Which progestins believed to have less androgenic activity | Synthetic "third generation" progestins: desogestrel and norgestimate
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| What OCs are FDA-approved for treatment of acne? | Ortho Tri-Cyclen (EE/norgestimate)
Estrostep Fe (EE/norethindrone)
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|
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| Primary mechanism by which OCs prevent pregnancy? | suppression of midcycle surge of both FSH and LH (mimics physiologic changes that occur during pregnancy)
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|
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| Additional mechanisms by which OCs prevent pregnancy | Induce changes in cervical mucus and endometrium that make sperm transport and implantation of embryo unlikely
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|
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| Benefits of using combined OCs | Reduction in risk of endometrial and ovarian cancer. Improve regulation of menstruation. Relief of benign breast disease. Prevent ovarian cysts. Reduce risk of symptomatic pelvic inflammatory disease. Improvement in acne control.
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| Risks of using combined OCs | Increased risk of STDs
Increase risk of MI or stroke w/ high dose EE and uncontrolled HTN
Increase risk of venous thromboembolism
Glucose intolerance, gallbladder disease w/ pre-existing gallstones. Hepatic tumors, cervical cancer.
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| Absolute CIs to using combined OCs | Hx of: thromboembolic disease, stroke, CAD, breast carcinoma, estrogen-dependent neoplasm, hepatic tumor
Undiagnosed abnormal uterine bleeding
Pregnancy
Heavy smokers (>15/day) who are >35y/o
Active liver disease
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| Relative CIs to using combined OCs | Smoking >15/day at any age
Hx of migraine headache disorder
HTN
Fibroid tumors of uterus
Breastfeeding
DM
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|
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| Lybrel and Amethyst | Continuous cycle OC (non-cyclic), active pills taken every day of year.
Advantage: no periods
SE: spotting, breakthru bleeding in initial months
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|
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| Seasonale and Seasonique | Monophasic, 91-day cycle (84 active, 7 placebo). Allow 4 menses/yr. Higher rate of D/C due to unacceptable bleeding/spotting
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|
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| Ortho Tri-Cyclen and Estrostep Fe | Approved for moderate acne in females 15+
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|
||||
| Yasmin | anti-androgenic properties, anti-mineralcorticoid activity
Risk for hyperkalemia
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|
||||
| Mircette | 21 active, 2 placebo, 5 low dose EE
Minimize bleeding during menstrual cycle
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|
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| Ovcon 35 | CHEWABLE TABLET! spearmint flavoring
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|
||||
| Ortho-Evra | transdermal patch applied once weekly for 3 weeks, then 1 patch-free week
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|
||||
| NuvaRing | transvaginal delivery system, insert on or before day 5 of cycle, remove 3 weeks later, then 7 ring-free days
If falls out for >3 hrs, use backup for 7 days
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|
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| DepoProvera | injectable depot of progestin-only, administer IM every 3 months. Return of fertility can be delayed 10-12 months
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|
||||
| Depo-SubQ Provera | injectable depot of progestin-only, adminstered SQ every 3 months. Lower dose of medroxyprogesterone compared to DepoProvera
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|
||||
| Mirena or Skyla | levonorgestrel-releasing IUD: up to 5 years
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|
||||
| Paragard T 380A | Copper IUD: up to 10 years
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|
||||
| Implanon or Nexplanon | Etonogestrel-releasing system surgically implanted under skin of upper arm: up to 3 years
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|
||||
| Plan-B | Levonorgestrel 0.75mg: take 1 tablet w/in 72 hrs of unprotected intercourse, second dose 12 hours later
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|
||||
| Progestin-only pills | MicroNor, Camilla, Errin, Heather, Jolivette, NorQD
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|
||||
| How to handle 1 missed dose of combined OCs? | Take ASAP, take next pill at regular time. No back up needed
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| How to handle missing 2 doses of combined OC? | Take 1 extra pill per day for 2 days. Use backup for 7 days.
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| How to handle missing 3+ doses of combined OC? | Discard pack and restart as previously instructed. Use backup for 7 days
Sunday starter: may take 1qd until Sunday, then start new pack.
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|
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| When to begin a progestin-only pill (POP)? | Start on first day of menses and use backup for 7 days. Take pill at same time each day!
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| What to do if miss a dose of progestin-only pill? (POP) | If missed by more than 3 hours, use backup method for 48 hours. Do not take missed doses if past 3 hour time-frame.
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|
||||
| Candidates for POPs? | Breastfeeding
High risk for estrogen adverse effects
Smoker >35 years (?)
lower efficacy rate than COCs
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|
||||
| Candidates for implantable contraceptives? | Women >1 child (except Skyla)
Monogamous relationship
No hx of PID
No hx or risk of ectopic pregnancy
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|
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