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Midterm #1
therapeutics fall 2011
| Question | Answer |
|---|---|
| What cardiac imaging technique is the only portable one? | echocardiograph |
| What imaging modalities can visualize the hemodynamics of the heart? | ECHO and CMR |
| What imaging modalities can visualize the intracardiac flow | ECHO and CMR |
| What cardiac imaging modalities can visualize cardiac structure and function | ECHO., CMR and CT |
| WHat cardiac imaging modalities can assess myocardial perfusion | nuclear imaging, CMR with gadolinium, ECHO with microbubbles and CT with contrast |
| What cardiac imaging modalities can assess coronary anatomy | CT |
| What is CARPA and what is it a problem with in terms of cardiac imaging? | Complement activation related pseudo-allery. Results from microbubble contrast imaging with ECHO. sx are similar to anaphylaxis but it is anaphylactoid since the reaction is not IgE mediated type I allergic reaction. It can occur upon first exposure. |
| What does an ECG show? | shows QT elongation, detects ischemia and MI, tachy/bradycardia, evaluate pacemaker function, detect drug effects |
| disadvantages of MRI | limited resolution, procedures are prolonged, contrast material (gadolinium) is contraindicated in end stage renal failure and decreased GFR, patients with devices or claustrophobia have problems. |
| Disadvantages of cardiac CT | large doses of irradiation, risk of iodinated contrast agents causing anaphylactoid reactions, need to decrease HR for CTA, limited resolution if significant calcium or for in stent restenosis, limited assessment of myocardial viability |
| adverse events with exercise testing | MI and death 1/2500 |
| adverse events with dobutamine stress testing | MI, VF 1/2000 |
| adverse events with iodinated contrast agents | potentially or immediately life threatening reactions more common with low osmolarity media |
| adverse events with diagnostic cardiac catheterization | death, MI, arrhythmia, neuro event, vascular complication contrast reaction 1/500 |
| adverse events with ultrasound contrast agents | anaphylactoid reaction, severe fatal allergic reaction |
| what is TEE | transesophageal ECG where the pt swallows the probe in order to view the heart through the esophagus rather than the lungs. results in clearer images. |
| What is Bayesian Theory? | stress testing is the most useful when the person has intermediate likelihood of angina and the pts with low and high likelihood will have less change and the test is less effective. |
| What are the modifiable risk factors for developing atherosclerosis | LDL >100, HDL <40, BMI >30, smoking, physical inactivity, diabetes |
| What are the non-modifiable risk factors for developing atherosclerosis | Age men>45 women>55, family history of a first degree relative with CHD <55man or <65woman, being male or postmenopausal female |
| What are the layers of the arterial wall and the major components of each | endothelium, intima contains mostly ECM with some smooth muscle cells, media contains mostly smooth muscle cells, adventitia contains mostly connective tissue |
| What is the role of the endothelium | barrier, produces NO for modulating vascular tone, maintains the nonthrombogenic blood tissue interface, promotes modification of lipoproteins in arterial wall(proretention), regulation of cell growth, regulate immune and inflammatory reactions |
| What is the key factor in the initiation of atherosclerosis | migration and retention of apo-B containing lipoproteins in the arterial wall |
| What characteristics do plaques have when they are about to rupture? | a large necrotic lipid core with lots of inflammatory cells and a this fibrous cap. when one ruptures they cause acute coronary event |
| What are the steps of clot formation | once the plaque ruptures, platelets adhere to the exposed tissue, become activated, aggregate and activate the clotting cascade forming a clot of platelets held together by fibrin |
| What is efferocytosis and what happens when this process goes wrong | apoptotic cells in the intima are removed by phagocytotic cells. when this goes awry, you get leaking of these phagocytes into the ECM and the necrotic core develops. This mainly happens in unstable plaques, thinning of the cap and rupture |
| How often should adults be screened for a fasting lipid panel | if over 20 years old then every 5 years |
| What is the NCEP ATP III optimal level for LDL-c | <100 mg/dL |
| Who should get drug therapy and who should just do TLC | all patients should implement TLC. only intermediate to high risk patients should use drug therapy. Unless a 30-40% change is needed TLC should be used only |
| What lipid parameter should be calculated in patients with metabolic syndrome and how do you calculate it? | non-HDLc is calculated by subtracting HDL from total cholesterol |
| What lipid levels are indicative of atherogenic dyslipidemia and what are the parameters | patients with serum TGs of 200-499mg/dL should be assessed for dyslipidemia and metabolic syndrome. this is indicated by low HDL and high small dense LDL |
| When should combination drug therapy be implemented | when greater reductions in LDL are needed or if HDL and TGs and not at optimal levels |
| What cholesterol particles have apoB100 | LDL, VLDL, IDL, small dense LDL (Lpa) |
| What is the Friedwald formula | calculates LDL LDL=TC-(HDL+TG/5) |
| What are the characteristics of hypercholesterolemia | high LDL normal TG and normal HDL |
| what are the characteristics of mixed dyslipidemia | high LDL high TG and low to normal HDL |
| what are the characteristics of hypertriglyceridemia | high TG normal LDL and low to normal HDL |
| What total cholesterol should a parent have to warrant getting their child;s lipids checked? | total cholesterol of greater than 240 mg/dL |
| How do you calculate VLDL | TG/5 |
| When is it appropriate to use the Friedewald equation | when TGs and <400 if greater then that you need to measure LDL directly |
| What condition are you worried about when TGs are >500 | pancreatitis |
| What are some common drugs that tend to increase cholesterol and TG | estrogen/progestins, protease inhibitors, steroids, isotrentinoin, cyclosporine, atypical antipsychotics |
| What are the CHD risk factors | age, smoking, hypertension >140/90, HDL<40, family history of premature CAD ***a negative risk factor is HDL of greater than 60 so if you have two of the above you can say you only have one |
| When do you need to use the Framingham algorhythm when calculating a patients future CHD risk | if they have 2 or more risk factors , if they have CAD or a CAD risk equivalent (like PAD or DM) you can assume their risk is >20% and if they only have one risk factor you can assume its <10% |
| according to NCEP ATP III guidelines, if a patient has 2+ risk factors and a framingham of 10-20% then what is their LDL goal and at what point do you begin drug therapy? | LDL<130 (optional <100) and all patients should get TLC, and they shoudl consider drug therapy at greater than or equal to 130 |
| according to NCEP ATP III guidelines, if a patient has 2+ risk factors and a framingham of <10% then what is their LDL goal and at what point do you begin drug therapy? | their LDL goal is <130 and you begin drugs at >or equal to 160. TLC if greater than 130 |
| according to NCEP ATP III guidelines, if a patient has 0-1 risk factors then what is their LDL goal and at what point do you begin drug therapy? | <160 with TLC at >160 and drug therapy could begin if they get to >190 |
| If a patients goal LDL is 70 and you can't get them that low what would be a good decrease to shoot for while implementing more aggressive treatment | a decrease of 50% should be attainable |
| What is the cumulative potential LDL decrease possible with TLC alone | ~20-30% if all aspects are followed |
| What constitutes a diagnosis of metabolic syndrome | at least 3 of the following: waist circumference of >40"in men and >35" om women (this is 5"less in asians), BP >130/85, FPG >100, HDL <40 men <50 women, TGs >150 or on drug treatment for any of the above |
| What is the non-HDL goal for people with metabolic syndrome and what triglyceride range do these people tend to have. | TGs 200-500 may have metabolic syndrome and you calculate that by subtracting HDL from TC, this goal is 30 greater than the LDL goal |
| What are the top 3 drugs for treating high triglycerides and how much can they lower them | fibrates and niacin can lower TGs by 20-50% and omega 3 fatty acids (Lovaza only) can lower by 10-45% |
| What are the lipid lowering capabilities of statins | decrease LDL by 18-63% decrease TGs by 7-30% and inc HDL by 5-15% |
| What are the lipid lowering capabilities of niacin | decrease LDLby 5-25% inc HDL by 15-35% and inc TGs by 20-50% |
| What are the lipid lowering capabilities of fibrates | variant effects on LDLs so not given alone, usually with a statin but ~5-20%,inc HDL by 10-20% and decrease TGs by 20-50% |
| What are the most common side effects of statins | myopathies and increased liver enzymes |
| What are the most common statin drug interactions | CYP 3A4 is an issue with simvastatin, lovastatin, fluvastatin and atorvastatin. antifungals like ketoconazole, amiodarone, clarithromycin, diltiazem/verapamil, some SSRIs, cimetidine, omeprazole, quinine, cyclosporine etc |
| What statins are metabolized by cyp 2C9 | fluvastatin, pitavastatin, rosuvastatin |
| Which statins are metabolized by cyp 2C8 | flucastatin, pitabastatin |
| Which statin is metabolized by 2C19 | rosuvastatin |
| What are the ACC/AHA/NHLBI risk factors for myopathy associated with statins | age >80, severe chronic kidney disease, impaired liver function, alcohol, perioperative periods, grapefruit juice with certain statins, interacting medications, hypothyroidism |
| What is the problem with using fibrates with statins | gemfibrozil competes with statins for glucuronidation and increases serum levels of statins. not all fibrates are contraindicated. increase in statin levels leads to myalgia. |
| Why is coenzyme Q10 considered an option for people who have myalgia with a statin | statins lower Q10 levels so in theory if you inc Q10 by supplementation you will decrease the myalgia. This doesn't appear to be strictly true. |
| What monitoring parameters are associated with statins | get a baseline LFT and TC. retest at 4-6 weeks if goal is reached continue therapy and if not reevaluate. get a baseline CK and reassess if needed |
| common side effects of niacin | flushing, itching, gi distress, hepatotoxicity, hyperglycemia, hyperuricemia |
| Contraindications for niacin | gout, diabetes or uncontrolled glucose, liver disease, peptic ulcer |
| describe the three dosage forms of niacin | immediate release available as RX and OTC has most flushing. sustained release is not FDA approved and is OTC has more risk of hepatic tox but less flushing. Extended release niaspan has less flushing and low liver tox FDA approved and RX only. |
| less common niacin side effects | blurred vision, GI bleeding, nausea and vomiting, palpitations, gout, decreased platelet count (11%) |
| monitoring parameters for niacin | medical history to rule out contraindications, baseline and periodic checks of FPG, A1C, LFTs, uric acid, |
| patient education for niacin | take in evening with low fat snack, avoid spicy foods and EtOH, 325mg ASA 30 min before to avoid flushing, report signs of liver dysfunction |
| lipid lowering potential of Zetia | dec LDL by 15-18%, inc HDL 1-3%, dec TG 1-5% |
| Side effects of Zetia | some inc in serum transaminases >3x ULN) not significant or frequent |
| What is the only time you would use Zetia alone | homozygous sitosterolemia-cant eliminate plant sterols on you own |
| lipid lowering potential of BAS | dec LDL 15-30%, dec HDL 3-5%, may possibly increase TGs |
| common side effects of BAS | GI distress and constipation (can be decreased by mixing with enough fluid so it is saturated before entering the intestine), decreased absorption of other drugs |
| What is the benefit of colesevelam over cholestyramine | can hold more bile acids per molecule so you can use a lower dose and get less side effects |
| If there are drugs that interact with BAS when should they be taken | 1 hour before or 4 hours after |
| maximum TGs a patient should have before contraindication with BAS | >400 mg/dL should only be initiated in patients with TGs <200mg/dL |
| Patient information for BAS | take 1-2 times daily with a meal, titrate slowly, mix in 6-8 oz of non-carbonated drink before taking, inc fluids and fiber to enhance GI tolerance, take other drugs 1 hour before or 4 hours after |
| lipid lowering potential of fibrates | dec TG 20-50%, inc HDL 10-20% but may actually increase LDL (sometimes given with a statin), dec small dense LDL |
| side effects of fibrates | GI distress, gall stones, myopathy (inc with statins) |
| What is the fibrate of choice for patients with renal impairment | gemfibrozil unless on a statin. fenofibrates are non dialyzable and will be filtered out must also adjust dose depending on GFR |
| monitoring parameters for fibrates | basline serum creatinine, monitor for myopathy, monitor patients on warfarin, avoid in gall stone patients |
| patient education for fibrates | taken in the evening, do not take with EtOH, report signs of liver problems or myopathy, full disclosure of all medications and supplements, avoid if preggers of breast feeding |
| how much omega 3 should a patient with documented CHD get per day | ~1g (preferably from diet) |
| how much omega 3 should a patient get if they need triglyceride lowering | 2-4 grams of supplements prescribed by physician |
| lipid lowering potential of Lovaza | dec non-HDL 14%, inc HDL 9%, dec TG 45% |
| Whats the big deal with the HATS trial | looked at effects of simvastatin plus niacin and its long term (5yr) impact on stenosis and clinical outcomes. overall showed that by adding the niacin you got definite improvement |
| Whats the big deal with ARBITER 2 trial | looked at CIMT change when niacin was added to statin therapy. by adding Ex niacin you got less progression of CIMT. |
| What was the big deal with AIM HIGH trial | niacin+statin vs statin to prevent vascular events. NIH pulled plug though cuz showed no benefit but may inc stroke risk. does improve lipid panel though. |
| Whats the big deal with the ACCORD trial | will statin+fibrate decrease CVD in DMII pts at high risk for CVD. didn't show much improvement overall but men tended to benefit while harmful in women so results may be skewed. use in pts with high TG and low hDL cuz all studies support this |
| Whats the big deal with the ENHANCE trial | looking at FH heterozygous pts. looking at CIMT and FIMT. compare statin plus zetia vs stain alone. baseline CIMT was high but low for this subgroup so there was a positive change when used together. decreased LDLs and c reactive protein levels |
| What outcome is associated with Zetia and how should this affect its use | linked to cancer but not conclusively. zetia and statin work together to improve lipid panel but SEAS trial showed some cancer risk but other trials are not seeing that. should be used if pt on high dose statin and still not reaching their goals. |
| risk factors for PAD | family history of vascular disease, smoker past or present, high BP, high cholesterol, diabetes, age ***smoking is the highest risk |
| What are the clinical presentations of PAD | intermittent claudication, cold skin, shiny skin, thickened toenails, hairlessness, poorly palpable pulses, atrophy of calf muscles. most common is claudication and pain at rest in lower extremeties or critical limb ischemia |
| Who is most at risk for PAD | people <50 with diabetes or another atherosclerosis risk factor. people btn 50 and 69 who are smokers or have diabetes. anyone over 70. or people with sx of PAD |
| How do you diagnose PAD | must rule out the following: peripheral neuropathy, arthritis, DVT and myopathy. Then you must check pulses by doing an ABI |
| What is an ABI and what are normal/abnormal readings | ankle/brachial index. the difference between the BP in the arm vs the ankle. above 0.9 is normal. 0.71-0.9 is mild obstruction, 0.7-0.41 is moderate and below 0.4 is severe obstruction some diabetics have high ABI. >1.3 is abnormal |
| What imaging tests are used to diagnose PAD | color duplex ultrasound, peripheral CTA, contrast angiography (reserved for patients who may need surgical intervention) |
| according to ACC/AHA guidelines what are the best ways to manage PAD | stop smoking, decrease BP to 140/90 or 130/80 for diabetics, beta blocker, poss ACEi, dec LDL to <100 or for high risk <70, A1C<7%, proper foot care, structured exercise, antiplatelet therapy such as ASA or clopidogrel, cilostazol in bad claudication |
| WHat is the black box warning for cilostazol | torsades des pointes, only use in pts without heart failure who have lifestyle limiting claudication |
| side effects of cilostazol | Headache, palpitations, diarrhea |
| what drug interactions should be considered with cilostazol | 3A4 and 2C19 |
| when is it appropriate to do revascularization | when there;s pain at rest due to ischemia, non healing ischemic ulcerations, lifestyle limiting claudication despite maximum treatment |
| Ischemic Heart Disease encompasses two conditions what are they | chronic stable angina or vasospastic angina and acute coronary syndrome(MI and unstable angina) |
| What are the clinical features of chronic stable angina | reproducibility, repetitiveness of attacks (predictability), stable for long periods of time |
| What drug class is contraindicated in vasospastic/printzmental angina and why | beta blockers - will leave alpha stimulation unopposed Calcium channel blockers and nitrates are preferred |
| What are the differences in drug treatment of silent ischemia when compared to CSA | silent ischemia is better treated with a beta blocker. CCBs and Nitrates are less effective |
| What are the four main epicardial vessels | right coronary artery, left main coronary artery, circumflex artery and left anterior descending branch. |
| What is the cause of vasospasm in the artery | probably endothelial dysfunction. |
| What are the criteria for typical angina./ ***must meet all three | 1)substernal chest pressure or heaviness and may have discomfort in the neck, jaw shoulder, nausea etc. 2) provoked by exertion or emotional stress 3) relieved by rest or sublingual nitroglycerine |
| what are the criteria for atypical angina. ***must meet two of the sx for typical angina then one or more of the following | indigestion/heartburn/radiating back pain/SOBetc, random onset, lasts longer than typical angina, (women, elderly, diabetics more likely to have this), variable response to SL NTG |
| What are the canadian cardiovascular society functional angina classifications | Class I: ordinary physical activity does not cause angina but strenuous activity does. Class II: slight limitation of ordinary activity. Class III: Marked limitation of ordicary physical activity. Class IV: all activity causes pain. must go to ER |
| What drug should all patients with a history of angina get | sublingual NTG |
| Patient education for sublingual nitroglycerine | take one tablet at onset of angina. wait 5 min if no relief call EMS and take a second tab. may repeat one more time for a total of 3 tablets |
| What is the ACC/AHA recommended first line therapy for chronic stable angina | beta blockers in pts with HTN you can add ACEi and another agent to reach target |
| If you have to use a beta blocker in vasospastic angina which ones are acceptable and why | metoprolol, atenolol and bisoprolol cus they are more cardioselective |
| What did the ASIST study look at and what were the results | atenolol silent ischemia study had angina and silent ischemia with the addition of 100 mg atenolol decreased CV events outcomes |
| What are the key points in dosing beta blockers in pts with angina | start low and slow and titrate to a resting HR or 50-60 bpm, avoid abrupt withdrawal, side effects can limit the ability to titrate the dose, |
| What is the second line drug for treatment of angina according to ACC/AHA guidelines | calcium channel blockers second line for CSA but first line for vasospastic angina |
| What are the two types of CCBs and which ones are safe to use with beta blockers | dihydropyridines such as nifedipine, amlodipine and felodipine are safe to use with beta blockers but avoid IR nifedipine. Nondihydropyridines such as verapamil and diltiazem are not safe to use with beta blockers cuz you get bradycardia. |
| What can you add to a beta blocker or calcium channel blocker to patients who have inadequate symptom control of their CSA | long acting nitrates are second or third line for chronic maintenance for stable angina. |
| How is the effect of diminished response dealt with in long acting nitrate therapy | tends to lead to tolerance so you need ~8-12h of nitrate free time each day. long term nitrate monotherapy is not appropriate. |
| What drug class is an important contraindication in long acting nitrate therapy | PDE-5 inhibitors like Cialis |
| What is the role of ACEi in CSA | vasculoprotection. use them if the patient's BP can tolerate it. |
| WHat's the big deal with the COURAGE trial | looks at optimal medical therapy with or without PCI for stable coronary disease. showed no statistically significant benefit to PIC when on OMT especially in patients who are an less risk. Overall it may help in severe cases and will probably dec sx |
| What is considered OMT optimal medical therapy | antiplatelet, angina meds, ACE or ARB, lipid lowering agents |
| What are some secondary causes of hypertension | renal disease, coarctation of the aorta, primary aldosteronism, thyroid/parathyroid disease, cushings, peochromocytoma, sleep apnea, increased intracranial pressure, drugs |
| What drugs can inc BP | steroids, alcohol, anorectics, cocaine, Buproprion plus NRT, cyclosporine, decongestants, EPO, licorice, bitter orange, MAOi, NSAIDS, OC, hyperthyroid, SNRI, |
| How do you classify HTN according to JNC-7 | normal is <120/80, prehypertension 120-139/80-89, hypertension stage 1 140-159/90-99, stage 2 <160/100 |
| WHat is required to diagnose HTN | at least 2 readings on at least 3 separate occasions (6 total readings minimum). unless >180/100 the category is established based on the higher of systolic or diastolic |
| WHat method of BP monitoring is recommended by both CHEP and NICE. How does the cutoff for HTN differ with this technique | ambulatory BP monitoring (24 hour monitoring)the cutoff is 135/85 here cuz you eliminate white coat syndrome. some ppl have masked HTN where they are more relaxed in the office and less so at home. |
| What is the standard baseline workup for a person with HTN | take a history and physical exam. get baseline labs of CBC, UA, blood chemistry (incl FBG, electrolytes), lipid panel and creatinine, do a baseline ECG. |
| What are you looking for when you do organ system screenings | Cardiac: LVH, dysfunction, cardiac failure, CAD etc. Cerebrovascular: TIA, stroke, vascular dementia. Peripheral vascular: absence of pulses, aneurism, bruits etc. Renal: GFR <60ml/min, proteinuria, microalbuminuria. retinopathy: hemorrhages, papilledema |
| Therapeutic goal for HTN | <140/90 in non diabetics and 130/80 in diabetics |
| What is the recommended EtOH limit for ppl wanting to improve TLC | Men less than 2 drinks per day and 14 per week. Women 9 drinks per week |
| How does smoking cessation affect BP | it doesn't directly but it improves CVD risk by 50% after 1 year |
| What qualities must an idea antihypertensive drug have | prevent complications, efficacy as monotherapy, inc or neutral quality of life, does not worsen condition, once daily, inexpensive |
| What are the common side effects of thiazide diuretics | inc in lipids and glucose at high dose but not at low dose. with Beta blockers they can inc risk of new cases of DMII. decrease in K, Mg and Na so cautionwith arrhythmias. inc uric acid and calcium so careful with gout |
| Major drug interactions with thiazide diuretics | NSAIDS, Corticosteroids, lithium |
| How long does it take to see therapeutic effects with beta blockers | 1 full month which is unusual as it usually takes 2 weeks with most medications |
| What changes occur with diuretic effectiveness when creatinine clearance is less than 30 ml/min | metazolone and indapamide retain diuresis effectiveness and HCTZ retains its hypotensive effects |
| What was the big deal with the ALLHAT study | found no advantage of amlodipine or lisinopril over chlorthalidone in preventing HTN complications in DMII and was better at preventing CHF despite increased risk of new cases of DM. Also found to be better than doxazosin which had a higher rate of CVD |
| Whats the best way to deal with diuretic induced hypokalemia | discontinue diuretic, use potassium supplement if you decide to continue diuretic, add potassium sparing diuretic, add spironolactone as long as you don't mind man boobs. |
| What hypertensive drugs are not as effective in the elderly | beta blockers |
| What groups of young people is it appropriate to use beta blockers | young women of child bearing potential, migraine prophylaxis, intolerance to ACEi or ARB |
| Beta blockers can cause problems in people with the following conditions | asthma, COPD, heart block, diabetes (by aggravating glycemic controle and by masking hypotension symptoms except sweating), PVD, may worsen lipid profile |
| What are the side effects of beta blockers | excercise intolerance, fatigue, insomnia, cold extremities, postural hypotension, |
| why should beta blockers be tapered off of | tachycardia, angina MI |
| drug interactions with beta blockers | NSAIDS, clonidine withdrawal, sympathomimetics like cocaine, rifampin, nonDHPs |
| What characteristic of alpha blockers make it wise to pair with a thiazide diuretic | tolerance may develop leading to fluid retention and tachyphylaxis |
| When should the first dose of an alpha blocker be taken and why | at bedtime cuz there is a risk of falls especially in the elderly. if tolerated this should wear off over time. |
| side effects of alpha blockers | first dose orthostasis, aggravation of stress incontinence |
| What drugs are in the class of central alpha agonists | clonidine, guanabenz, guanfacine, methyldopa |
| what are the side effects of the central alpha agonists | sedation and dry mouth, severe rebound HTN that is dose related with abrupt cessation, methyldopa can cause fluid retention and associated with severe hepatic reactions, |
| What is the primary agent used during pregnancy for preggers induced HTN | methyldopa |
| what drugs are the direct vasodilators | hydralazine and minoxidyl |
| when would you use a direct vasodilator | only in severly refractive pts with chroniv renal insufficiency. can be used in preggers and with a diuretic or beta blocker or other centrally acting agent to control fluid retention and reflex tachycardia |
| main side effects of direct vasodilators | fluid retention and reflex tachycardia at high doses hydralazine is associated with a lupus-like syndrome and minoxidil cause hair growth |
| ACE inhibitors are considered first line therapy for most guidelines. What subpopulation is this not true for | african americans seem to benefit less when given ACE.m less BP decrease and more CVD events. |
| What conditions provide a compelling indication for use of an ACEi | reduce complications of CHF, prevent progression of diabetic nephropathy and chronic renal disease, therapy of high risk CVD patients, post MI patients |
| what are the adverse effects of an ACEi | severe hypotension with first dose especially in pts with severe volume depletion, CHF, hyponatremia, renovascular hypertention. angioedema, cough, hyperkalemia esp with k+ sparing diuretic, |
| What are the common drug interactions with ACEi | lithium, NSAIDS, potassium or potassium sparing diuretics |
| How do ARBs compare in efficacy to ACEi | they are comparable but there is less outcome data for them, |
| What was wrong with the LIFE study and what drugs were being compared | losartan was shown to be better than Atenolol but the study group was the elderly in which atenolol is not a good option so not a good control |
| What drug is the direct renin inhibitor and why isn't it used more | Tekturna is metabolized by Cyp 3A4 so has lots of potential side effects. also very expensive, not better efficacy when compared to beta blockers or ARBs, low bioavailability, and on top of all that it causes diarrhea |
| If a patient has systolic dysfunction CHF, what drug class is not recommended and what drug from this class is ok if one must be used | calcium channel blockers and nonDHP amlodipine is the best option., |
| What are the side effects of non DHPs | constipation (verapamil only), dizziness, fatigue, peripheral edema, heart failure, depressed AV conduction. |
| what is the process for treatment of HTN | make sure of diagnosis, rule out secondary causes, manage total cardiovascular risk by modifying risk factors, patient education and monitoring |
| what is the appropriate treatment for prehypertension | life style modification and no drugs without compelling indication |
| what is the appropriate treatment for stage 1 HTN | thiazide diuretic for most. |
| what is the appropriate treatment for stage 2 HTN | 2 drug combination for most such as thiazide and ACE or ARB or CCB |
| what are the compelling indications for initiating drug therapy for HTN | ischemic heart disease, systolic heart failure, diabetes mellitus 130/80, chronic renal disease 130/80, cerebrovascular disease 160/100 |
| what are the first line therapies for african american htn pts | CCBs and thiazides |
| How should you follow up with a hypertension patient | follow up every month until they meet their goal. more frequent with stage 2. once at goal and stable they can be seen every 3-6 months |
| what are the two types of hypertensive crisis and what is the difference between the two. what is the definition of hypertensive crisis | hypertensive emergency (severe HTN with acute end organ damage)and hypertensive urgency (without organ injury). hypertensive crisis is defined as diastolic BP above 120 mmHG |
| what is the first thing you do in hypertensive urgency | put pt in a dark room to calm them down. recheck BP after 30 min. |
| What drugs are commonly used during hypertensive emergency | nitroprusside, labetolol and NTG BP needs to be reduced by 20-25% or 100 mmHG whichever is higher |
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mollyjuhlin
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