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52 Cards in this Set
- Front
- Back
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obesity-related-diseases
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hypertension
type II DM stroke CHD hypercholesterolemia |
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concerning LDL and HDL what increases the risk of CHD
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high LDL levels
low HDL levels |
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How should you treat diabetics
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Treat all diabetics as if they have CHD bcz they have equal risk for MI as those who have had one
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What is metabolic syndrome X
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metabolic disorders that result from the primary disorder of insulin resistance
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To have syndrome X you must have 3 of these conditions and DM II
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Central obesity
hypertension abnormalities of blood clotting low HDL and high LDL cholesterol levels high triglyceride levels |
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this may be a stronger predictor of recurrent MI after CABG than LDL
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Hypertriglyceridemia
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4 main categories of cholesterol medications
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Bile acid binding resins
Niacin Fibric acid derivatives Statins |
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Un-conventional Risk Factors for CAD
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Dense LDL
Lp (a) Homocysteine Inflammatory markers Infectious agents Insulin resistance Apolipoprotein B Stress |
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what is Lp (a) APOLIPOPROTEIN
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Form of LDL
Prevents clots from dissolving Stimulates overgrowth of smooth muscle cells in arterial wall Target < 15umoles/L |
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Two Inflammatory markers
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CRP, fibrinogen
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Infectious agents that increase the risk of CAD
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Chlamydia pneumoniae, mouth bacteria, Helicobacter, CMV
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clotting pathway
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Prothrombin
thrombin fibrinogen fibrin clot |
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Presentation of an MI
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Chest pain
Shortness of breath Diaphoresis “feeling of doom” Epigastric discomfort |
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unstable angina means
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new onset, changing pattern, more difficult to relieve, occurring at rest
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Acute MI treatment
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Mona sees all patients”
Morphine Oxygen Nitrates Aspirin |
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Additional MI treatments
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Thrombolytics
Beta-blockers ACE inhibitors Other platelet inhibitors (Glycoprotein IIB/IIIA inhibitors, thienopyridines) IV nitroglycerine |
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Procedures to treat AMI
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PTCA/Stent
“Angiojet” CABG Surgery |
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Treatment after an acute event
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Aspirin
platelet inhibition Beta-blockers ACE inhibitors Nitrates if ischemia remains |
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the number one killer of both men and women in this country
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CAD
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EKG results that indicate high probability of AMI are
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ST-segment elevation greater than 1 mm in 2 contiguous leads and new Q waves
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There 3 components to diagnosing an MI:
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1. H/P
2. Cardiac Enzymes 3. EKG |
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The Cardiac Enzymes
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1. Troponin I & T.-falls 14 days
2. CK-MB. 3. LDH (1 & 2). 4. SGOT (AST). 5. Myoglobin. |
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Troponin is important bcz?
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Most sensitive & specific
If negative p 12hrs = no MI |
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rise and fall of this enzyme is characteristic of MI
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CK-MB peaks at 24hrs
falls 48-72 hrs |
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The most common physical finding in an MI
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an S4 sound
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what are PT and PTT
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clotting factors
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An MI diagnosis cannot be made with an EKG having these
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LBBB or WPW
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What is Brugada?
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ST elevation with RBBB in leads V1-V3; resp for 1/2 SCD in young people
Pt presents with syncope and fam hist of SCD |
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age indeterminate MI
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return of ST to baseline, c T wave inversion
Loss of R wave c QS pattern |
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Non Q wave MI =
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without a Q wave, non-transmural (subendocardial).
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Normal Q waves may be seen in which leads?
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Small q’s may be normal in V5, V6, I, aVL, III, aVR or V1 as long as they're not in 2 contiguous leads
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Reciprocal Changes will show
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ST Depression
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Anterior ST elevations may show reciprocal changes where?
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Inferior and true posterior
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Inferior ST elevations may show reciprocal changes where?
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Anterior or lateral I,aVL
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causes of SCD include
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Brugada syndrome, long-QT syndrome, preexcitation syndrome, and commotio cordis.
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EKG signs of pericarditis,
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ST segment elevation throughout almost all leads and usually flat or concave, may not be in aVR, V1 and V3, look for PR depression
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An outward ballooning of the wall of a ventricle; can cause persistent ST elevation in most of the chest leads
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ventricular aneurysm
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Additional ED interventions
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Morphine sulphate
Anxiolytic Heparin Thrombolysis Platelet aggregation (IIb/IIIa receptor) inhibitor ACE inhibitor Antiarrhythmic agent |
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A cardiologist should be consulted for the following:
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Patients who may benefit from angiography, PTCA, or intra-aortic balloon pump
Patients in cardiogenic shock Patients with hemodynamically significant new or worsening murmur Patients who are not candidates for thrombolytic intervention because of a contraindication |
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Drugs assoc with increased mortality rates and increased adverse outcomes after an AMI
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Lidocaine and Calcium channel blockers
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IN/OUT Pt Meds:
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Salicylates
Thrombolytics Beta-blockers Nitroglycerin Heparin Analgesics |
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Nonischemic causes of ST-segment elevation include
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LVH, pericarditis, ventricular paced rhythms, hypothermia, hyperkalemia, and LV aneurysm
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levels of syndrome X
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Insulin Resistance (when the body can’t absorb blood sugar or insulin properly)
Abdominal fat – in men this means a 40 inch waist or larger, in women 35 inches or larger High blood sugar levels – at least 110 milligrams per deciliter (mg/dL) after fasting High triglycerides – at least 150 mg/dL in the blood stream Low HDL (the “good” cholesterol) – less than 40 mg/dL Pro-thrombotic state (e.g. high fibrinogen or plasminogen activator inhibitor in the blood) Blood pressure of 130/85 mmHg or higher |
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Obesity BMI and waist circumference ranges
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BMI >25 kg/m2 overweight, >30 obese
Waist circumference >40in. men problem, >35in. women |
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Risk levels of HDL and LDL
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(< 35 mg/dl) (HDL)
(> 160 mg/ dl) LDL |
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You should seek this level of triglycerides to be low risk of CAD
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Seek levels < 130 mg/dL
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how do you test for occluded arteries in a patient with unstable angina?
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labeled nucleotide that travels to perfused myocardium thereby identifying non-perfused segment (technicium, thallium) in a patient at rest
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asa, ticlopidine, clopidogrel, glycoprotein
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block the clotting cascade
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what causes MIs
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90% resulting from atherosclerosis (10% from vasospasm; Prinzmetal’s
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First EKG sign on an acute Q wave MI
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hyperacute T waves
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what valve could be responsible for systemic edema
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mitral valve regurgitation
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What do you suspect with people 55 and older with SOB and nausea?
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suspect MI and do EKG
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