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145 Cards in this Set
- Front
- Back
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High waist circuference (visceral fat) highly correlates with
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CHD and Type II diabetes
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Total fat in the diet is to be limited to
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25%-35% of total daily calories
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What are types of fat
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Saturated
Unsaturated fats Trans fat Sat and trans are the BAD fats |
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Saturated fat is "bad fat" is usually SOLID at room temp sources
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meat, high fat dailry, fried food, butter
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Recommended daily intake of Saturated fat
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<10% of calories from sat fat
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Does Saturated fat have some benefits besdies increasing LDL
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yes does increase HDL and lower TG's
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What is ultimate bad fat (increases LDL decreases HDL )
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trans fats
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How is trans fat produced
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through process of hydrogenation
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Examples of Trans fats
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stick margine, crackers, baked good
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What are types of unsaturated fats
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mono
poly |
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Examples of Monounsatruated fats (liquids at room temp)
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olive oil, canola oil
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Examples of polyunstaurated fats
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sunflower, soybean, asafflower
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AHA recommends 25-35% of caloreis from unsatruated fats
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YES
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Omega-3 fatty acids are mainly from
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fatty fish--slamon, mackeral, turn, flax seed oil (wild is better)
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Omega 3 ahve antiinflammatory action, AHA recommendes how many servings a week
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2-3 servings of fish a week
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Are antioxdiant supplements helpful
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NO
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Hypertesnsion and Hyperlipemia both require weight loss, physical activity and icnrease fruit and veggies, differnnces
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HTN--decrease Soidum intake
Hyperlidpemia requires decrease saturaraed fat and trans fat intake, and increases mono fat and omega 3 |
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High animal protein intake is associated with
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increase blood lipids
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Higher protein from plant sources is assoicated with
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LOWER lipids
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Should hormone therapy (combined estrogens) be initiated or continued to prevent CVD in postmenopausal women)
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NO--small increase in risk for CVD even though increases HDL
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What is primary strategy of antiplatelet therapy
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inhibiting platelt aggreation and minimize the risk of thrombosis
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What is the final step of thombosis development in AVD
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platelet activation
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Should anticoagulant drugs be used for AVD
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NO
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What is most commonly used anti-thrombotic therapy
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Low dose aspirin
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What is role of Thrombaoxane A2 and Prostacyclin
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Thromboxane A2 induces platlet aggreation and vasoconstriction
Prostacylin INHIBITS platelt agreeation and produces vasodialtion |
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What does Low does ASA irrversibely inhibits COX in platelets leading to
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inhibits TXA2 (doesnt really inbhiti protacyclin
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What patients is low Dose ASA used in
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ALL secondary prevention pts
Primary prevetion pts with framignham risk > or equal to 10% |
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What are major bleeding complications of ASA
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GI bleeding from gastric ulcers, hemorrhagic storke decrease in hemoglocin
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What are minor bleedings of ASA
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bursing, prolonged bleeding epistaxis
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What are Risk factors for MAJOR GI bleeding from low dose ASA
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Advanced Age >75
History of PUD Concurrent use of NSAIDS, coricosteriod, antigocagulants |
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What is the benefit of Enteric coating
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ONLY minimiez dyspepsia--DOES not reduce risk of ULCER
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For pts with high risk of serious GI bleeding, co-administration of what can minimize risk of gastric ulcers
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PPI or misoprostol
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Does a H2RA help reduce risk for serious GI bleeds
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NO---DOES NOT WORK
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What is bad about combining ASA and Ibuprofen
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together blocks the antipletlet effect of ASA, speparte dosing or use diclofenac
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What is use of CLopidogel (Plavix)
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alternative for pts with ASA allergy
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Colpdioegrel is dosed
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75mg once daily
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MOA of Clopidogrel
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inhibits platelt aggregation by ihbiting adenosine diphosphate
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Why isnt ticlopidine NOT used
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b/c of higher risk fo TTP
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Using ASA with clopidogrel is not recommenede in
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primary prevention pts b/c of increased risk of bleeding
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May ASA with clopidogrel be used in secondary prevention pts
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YES--ok
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What are antioxidant vitamins
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Beta-carotene, Vit C, Vitamin E, and Vita A
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Are antioxidants benfitical
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NO--
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Are antioxidants harmful at high doses
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YES---small increased risk of death
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Homocysteine conc are elevated in ptatient with CV what can reduces serum homocystein conc
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Folic acid, vitam B6, and vit B12
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Does Folic acid supplmentation + vita B6, and vit B12 reduce CV events or mortailtiy
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NO
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What invidiausl is INACTIVATED influenze vaccination recommeneded in
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seoncdary prevention patietns
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Is live attenuated influenza vaccine contraindication for persons with CV conditions
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YES
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How does PAD initally present
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asymptomatic initially, followed by pain and discomfort later
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Two common characteristic of PAD
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intermittnet claudication (primary indicator)
pain at rest in lower extremities |
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Intermittent claudication is the primary indicator, symptoms include
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fatiuge, discomfort, cramping, pain, numbness, tingling,
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Where is intermittent claudication usually located
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buttock, thigh, or calf
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When does intermittent claudication occur
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occurs with exercise, relevied within minutes after rest
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What happens when you have pain at rest in lower extemeites
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later manifestation of disease, sign of progession,
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When does pain at rest in lower extremites occur
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often at nightime at rest in the toes or heel of foot
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What is ctirical limb ischemia considered
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severe actue manifestation (limb theratengin) where lwoer extremity blood flow is compromised
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How is PAD dianosed
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ankle-brachial index
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What is a normal ankle-brachial index
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1
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What ankle-brachial index indicates PAD
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<.9
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What are goals of therapy in PAD
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increase maximal walking distanaces
Control co-morbidites improve QOL |
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What is non-pharm of PAD
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exerise--increases pain free walking, and decreases onset of intermittent cluadication
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What co0morbidites increase PAD
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HTN, dyslipidemia, diabetes
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What is goal for treating HTN with PAD
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goal BP <130/80
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Are beta-blockers contraindicated in PAD
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no---should choose mixed alpha/beta blocker
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What is goal for treating Dylipidemia in PAD
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LDL <70,
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What is goal in Diabetes
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glycemic control goal of A1c <7%
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What are 2 treatments of PAD
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antiplatlet therapy reduces risk fo CV event
or therapy for SYMPTOMS of intermittent claudication |
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Does Antipletelt therapy for PAD reduce risk of CV events
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YES---does not prevent or delay PAD
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What are antipletelt thaerpy for PAD
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ASA
CLopidogrel |
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What is pharamcotherapy for SYMPTOMS of intermittent claudication
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Cilostazol
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Cliostazol should always be used with
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antiplaetlet--ASA or clopidogrel
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Cliostazol only treat symtpoms of intermittent cluadication--it is CONTRATINDACTED IN
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heart failure pts
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Should Pentoxifylline be used
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NO
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Angina is a SYMPTOM, not a disease, angina is
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chest pain cuased by myocaridal ischemia
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What is the disease that cuases chest pain (angina)
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CAD or ischemic heart diseas
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What is silent ishcemia
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asymtpomatic myocardial ischemai (use ECG to recognzie)
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What is stable angina
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classic angina
variant angina |
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What is unstable angine
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newly-diagnosised agninga or change in anginal pattent
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Angina is pain caused when coranary blood flow
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is inadequate to O2 supply leading to ischemia
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What causes the pain from angina
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subtances released during hypoxia, and by normal metabolites not removed b/c of decrease cornary blood flow
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What is Classic angina associated with
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atherosclertoic diease of cornary arteries,
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When does classic angina occur
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when metabolic needs of the myocardium exceeds abilify of occluded cornary to deliver adequate blood flow
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What causes classic angina
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factors taht icnrease work demands--exericse, expousre to cold, emotional stress
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In Classic angina pain is relieved by
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rest or NTH
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What is variant angina associated with
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Vasospasm of cornary arteries
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What causes variant anigina
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hyperactive Sympatheic NS, and defective Ca+ by corarny vascular smooth msucle,
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What is altered in Variant Agina
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altered endothetlium, increase endothetlin or AII, and decrease PGI or NO, promotes vasoconstriction
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When does varinat agina occur
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during rest or minimal exercise--noctular or cyclic (occurs on regular basis
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What is unstable angina associated with
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OBSTRUCTIVE CAD
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What causes obstructive CAD in unstable angina
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thrombotic occulation of conrary artery caused by platelt aggregation
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When does Unstable angina occur
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during rest, apprears more frequently and last long
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What are the targets for therapy since mycardium can't extract from O2 from blood or blood cant carry more O2--
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Increased O2 demands are met by increase coronary blood flow
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What increases mycardial O2 demand
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Wall stress
HR Contractility |
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How does Wall stress increase O2 demand
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increase radius of ventcile, increase filling, and icrease filing and increase O2
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What increases Coronary Blood flow
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Increased aortic dialstolic pressure
Increase duration of distole Decreased cornary vascular bed resistance |
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Why does increase aortic diastolic pressure increase cornary blood flow
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this is when blood presfuses heart
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How do you increase duration of diastole to increase cronary blood flow
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decrease HR---more blood perfuses to heart
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HOW do you decrease cornary vascular bed resistance
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vasodialate
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How do you decrease wall stress
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decrease filling, decrease O2 demand
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What is the therapeutic objective of drug
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balance O2 supply and demand
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How do Nitrates relax blood vessels by
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by relase of Nitric Oxidie, which activates guanylate cyclase--which results in smooth muscle relaxation
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NO relaxes which smooth muscle more
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Veins>arteries
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Two main effects of NO
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dilation of veins and ateriolar dialation
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What happens as result of dialtion of veins
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decrease verouns return, which decrease ventricular volume, decreases cardaic work and decrease myocardial oxygen consumption
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Decreased myocardial oxygen consumption is good target for
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classic angina
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What is benift of ateriolar dialtion
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conaray vessel dialtion, and decrease afterload, decreases cardiac work, decreases myocaridal oxtygen consumption
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What is benefit of decrease ventricular filling
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Decreases compression of endocardial vessels, and icnrease endocarial blood flow
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What is benefit of relaxation of epicaridal cornary vessels
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decreased cornary artery spasm good for variant
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Nitrates do NOT cause a gernalized vasodialtion, rather
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collarteroal dialtion which bypasses obstruction and conrary flow is redistruted
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What is negative of dilation of all vessels
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coranary steal--blood only being perfused to good areas
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Nitrates redistribute cornary flow from noramal to iscehmic areas via
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collateral vessels
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SEs of Nitrates
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orthostatic hypotnsion, dizzines,
Throbbing HA flushing tolerance |
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Orthostatic hypotension results from decreases venous return which decreases CO, which leads to
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decreases arotic pressure, and decreases coranary perfusion
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Too large of doses of Ntirates result in Decreased ventricular filling also leads to decreases CO, which results in
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increase sympathetic discahrge, and icnrease HR and contractilitya dn icnreases O2 consumption
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Nitrates can also lead to tolerance and dependence, what must have to prevent tolerance
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pt must have 8hr abstinece to prevent tolerance
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Dependeces results from continual exposure to nitrates, removal of nitrate for 1-2 days results in
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conrary vasospasm and MI
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In chronic usesrs must you tirtrate down gradually
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YES
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Indications of Nitrates
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acutely or prophylactically
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Adminstiration of Ntirate with viagra results in large drop of BP why
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viagra is a phophodiaterae which inhibits cGMP breakdown, lead to increase vasodialtion
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MOA of Calcium channel antagoinsts
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inhibt voltage depend calcium channels, and decrease Ca+ influx which results in smooth muscle relaxation
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What is benefit of Calcium Channel blockers vasodialtion in angina
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decreases PVR, decrease afterload, decrease wall strech, and decrease O2 use
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What is benifit of decrease conary artery tone
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increases conray perfusion, increase blood flow and O2 supply
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Verapamil>diltizem affect heart--how
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decrease Ca+ influx in myocardial cells which decreases cardiac contractility and decreases O2 demand
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Verapamil and dilitziem slow SA node which also decrease HR which
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decreases O2
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SEs of Calcium channel antagoinsts
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hypotension, dizziness, fatiuge, cardiac depression
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Verpamil or diltizem + B blocker can lead to
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AV block and decrease venticular function
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Can CCB drugs be contradicated in heart failure
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YES
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Beta Blockers decrease HR and contracility what is benifit in angina
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decrease myocardial O2 demand, and decreased HR increases duration of diastolic, which increases myocardial perfusion
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Over the long term B-blockers decrease BP by
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decreases PVR--which decreases afterload, and decreases O2 demand
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Problems with beta blockers decrease HR
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increases End-diastolic volume and increases wall stress, and increase O2 demand give with nitrate
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Examples of Partial fatty oxidation inhibitiors (pFOX)
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ranolazine
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In iscehmic myocardium what is the preferred energy source
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fatty acids
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When ischemia occurs your smpatethic activation lead to
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increased FFAs in blood, and decreased glucose oxidation
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Fatty acids increase more ATP than glucose but
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use more O2--less efficent than glucose
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Decreaes glucose oxidation results in
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increased lactic acid formation and tissue acidosis
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MOA of Partial fatty acid oxidation inhibtiors
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activation of pyruvate dehydrogenase and inhibtior of fatty acid oxidation, allowing for consumption of glucose
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If using glucose as an energy supply you decrease O2 compution and that also decreases
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lactic acid formation (no longer using fatty acids)
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SEs of pFOX inhibitors bseids dissinezz, constiaption, nausea
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interacts with inhibtors of CYP3A (grapefruit juce, diltizem, ketoconazole,
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Can pFOX inhibitors also prolong QT interaval
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yes which can lead to dyrrhtmias
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General benifical effecs of nitrates
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decreases arterial pressure
End diastolic volume |
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General negative reflex effect of nitrates
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increased HR and contractility
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General benefits of B-blockers or Ca+ channel blockers
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Decrease HR, contractilty and arterial pressure
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General negative effects of B-blockers or Ca channel blockers
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increases End diastolic volume
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Are combinations of nirates + b-blockes or Ca+ channel blockers good
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YES
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What are good drugs for unstable angina
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anticoagulangts
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What are examples of anticoagulants
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ASA, clopidogrel, heparin, enoxaprain, and dalteparin--prevent thrombus formation
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