Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/52

Click to flip

52 Cards in this Set

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