Interstitial accumulation of lymph due to impaired drainage
Lymphedema: Primary v Secondary
•Classification of lymphedema based on etiology, age of onset, and
–Congenital (onset less than 1 year of age)
•Familial (Milroy’s disease)
–Lymphedema praecox (onset from 1-35 years of age)
•Familial (Meige’s disease)
–Lymphedema tarda (onset after 35 years of age)
–Lymph node excision/radiation
Lymphedema Signs, Complications, Treatment
•Ulcerations rare (unlike venous stasis)
–Sequential mechanical compression
most important risk factor for coronary artery disease
HTN prevalence was highest among
Coronary Artery Disease risk factor:
High sensitivity C-reactive protein
•HsCRP adds prognostic information at all levels of LDL cholesterol and at all levels of risk, as determined by the Framingham Risk Score
•In clinical terms, absolute vascular risk is higher in individuals with elevated hsCRP levels and low levels of LDL cholesterol than in those with elevated LDL cholesterol but low levels of hsCRP
Coronary artery disease risk factor - Homocystein
marker of inflammation
Hiperhomocysteinemia patients present with endothelial dysfunction, accelerated oxidation of LDL cholesterol, impairment of flow-mediated endothelium-derived relaxing factor with subsequent reduction in arterial vasodilation, platelet activation and oxidative stress
Coronary artery disease risk factor:
•Markers of fibrinolytic function - t-PA
Impaired fibrinolysis can result from an imbalance between the clot dissolving enzymes t-PA or urokinase-type plasminogen activator and their endogenous inhibitors, primarily PAI-1
A consistent series of prospective studies has linked abnormalities of fibrinolysis to increased risk of arterial thrombosis
The close homology between Lp(a) and plasminogen has raised the possibility that this lipoprotein may inhibit endogenous fibrinolysis by competing with plasminogen binding on the endothelium
Acute MI presentation
Same as angina: Retrosternal chest pressure, burning or heaviness; radiating occasionally to neck, jaw, epigastrium, shoulders, or left arm.
Sudden onset, usually lasting 30 minutes or longer. Often associated with shortness of breath, weakness, nausea and vomiting.
Sharp, pleuritic pain aggravated by changes in position; highly variable duration
Pericardial friction rub
Pulmonary embolism presentation
Sudden onset of dyspnea and pain, usually pleuritic with pulmonary infarction
Dyspnea, tachypnea, tachycardia, and signs of right heart failure
Pulmonary HTN presentation
Substernal chest pressure, exacerbated by exertion.
Pain associated with dyspnea and signs of pulmonary hypertension.
Burning discomfort in midline with dyspnea.
Abrupt onset of dyspnea and pain.
Pleuritic pain, usually brief, over involved area.
Pain pleuritic and lateral to midline, associated with dyspnea.
Creatine Kinase (CK): Serum CK often increases within ____ hours after the onset of STEMI, declines to normal within day ____
4 to 8 hours after the onset of STEMI
declines to normal within day 2 or 3
Myoglobin and MI
•Released from injured myocardial cells
•Peak levels are reached 1 to 4 hours after the onset of MI
•Should be supplemented by troponins (cTnI or cTnT)
•cTnT and cTnI:
Start to rise by 3 hours after the onset of chest pain
Elevations of cTnI may persist for 7 to 10 days after MI
Elevations of cTnT may persist for up to 10 to 14 days
Very useful for late diagnosis of MI
ACUTE CORONARY SYNDROME
The definition of acute coronary syndrome (ACS) includes unstable angina (UA), non-ST segment elevation myocardial infarction (non-STEMI), and ST segment myocardial infarction (STEMI). However, in practice, ACS is used to indicate UA and non-STEMI
Accute Coronary Syndrome Cause
ACS is result of a mismatch between myocardial oxygen supply and demand
Occasionally, this is due to anemia, hyperthyroidism, infection, tachyarrhythmias, or valvular heart disease
MOST COMMON CAUSE of change from stable CAD to ACS is disruption or fissuring of a vulnerable atherosclerotic plaque; this is followed by platelet-mediated thrombosis and vasoconstriction with or without elevation of cardiac markers
Almost all MIs result from
coronary atherosclerosis, with thrombosis
Plaque fissuring and disruption
Plaques prone to disruption overexpress metalloproteinase enzymes
Plaque disruption can be produced by stresses induced by intraluminal pressure, coronary vasomotor tone, tachycardia and disruption of nutrient vessels
BP, HR, blood viscosity, t-PA, PAI-1, cortisol and epinephrine in high levels may cause plaque disruption
NONATHEROSCLEROTIC CAUSES OF MYOCARDIAL INFARCTION