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19 Cards in this Set
- Front
- Back
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Components of Cardio Vascular System |
Heart Arteries Arterioles Capillaries Venules Veins |
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Overview of Vardiovascular Disease |
Disease of heart and blood vessles Secondary effects: Brain, limbs and kidney Leading cause of death 80% of CVD is due to modifiable factors |
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Atherosclerotic Vascular Disease Stages |
Due to invasion and accumilation of immune cells 1. Foam cells 2. Fatty streaks made of T cells and smooth muscle with lipids 3. 2+ pools of lipids 4. Atheroma made of cholesterol crystals and Ca 5. Fibrous tissue/Fissue, Haemorrhage or Thrombus |
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Define Foam Cells |
Macrophages that have consumed excess modified lipoproteins becoming foam cells They release growth factors and cytokines that stimulate movement of smooth muscle from the media to intima. |
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Exravation of immune cells |
T cells are free in blood, when certain chemotaxins are released T cells can begin to roll along an artery wall via intergrin and P-selectin proteins this is adhesion Once the site of inflammation is reached the T cells can exit the artery capillary at the site of inflmmation |
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Risk Factors |
Hypertension Hyperlipidemia Diabetes Obesity Smoking |
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Lesion types |
Stenotic- Few, thick cap, fiboritic, less compensatory enlargement Non-Stenotic- Many, Lipid rich, Thin cap, compensatory enlargement |
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Clinical Manifestations of Lesion Types |
Stenotic- Angina Pectoris, Positive Exercise Test, Perfusion Defect Non-Stenotic- Infarction |
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Definitions |
Ischaemia- depletion of oxygen Necrosis - death Angina pectoris: induces myocardial ischaemia Myocardial infarction: results in myocardial necrosis Zone of perfusion: area at risk |
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Type of myocardial infarcions |
Type 1- Plaque rupture with thrombus Type 2- 1) Vasospasm or epithelial dysfunction, 2) Fixed athersclerosis thus supply demand imbalance, 3) Supply and demand imbalance |
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Clinical symptoms |
Angina pectoris at rest Radiation to neck, jaw, back, abdomen and left arm Sweating Nausea Vomiting 30% of patients have silent myocardial infarctions |
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Masquerade of symptoms of Myocardial Infarctions |
Heart failure Angina Localisation of pain Anxiety Confusion Pulmonary embolism |
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ECG |
Always carried out before blood tests Records electrical activity of the heart ECG changes after myocardial infarction Early after: ST elevation Hours: ST depression 1 Day: T wave inversion Note you can have a non ST elevation myocardial infarction (NSTEMI) but this could also mean unstable angina |
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Diagnosis |
Angina percoris for over 30 mins Resistant to nitroglycerine Combined with ST elevation from 2 lead ECG Troponin T positive sufficient for diagnosis |
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Cardiac Markers |
Troponin T and I( Only marker specific for heart tissue) LDH Creatine kinase Myoglobin Natriuretic peptides |
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Creatine Kinase |
Not specific for MI Highest conc in skeletal muscle Make energy needed to move 3 forms CK-MB: heart CK-BB: brain CK-MM: Heart and other muscles Peaks within 24hrs of MI |
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LDH |
Not organ specific Raises 24hrs after MI Peaks at 3 days and stays elevated for 8-9 days |
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Cardiac Troponins |
Specific to MI TC- Ca binding sub-unit, non-cardiac form TI- Actomyosin-ATP-inhibiting subunit, Cardiac specific TT- Tropomyosin binding subunit, Cardiac specific, also raises in renal disease Elevated in patients with unsatable angina and non Q wave MI Released 4-6 hrs after MI Peaks at 12, remains elevated for 2-10 days |
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Treatment |
Thrombolytic drugs Coronary intervention: Bypass surgery Stent or balloon angioplast |
