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Cardio Path 2009

Dr Any Johnston - basic notes

QuestionAnswer
What is a normal PaO2 reading? 80 - 100%
What is a normal PaCO2 reading? 35 - 45%
What is a normal pH for blood? 7.35-7.45
What is a normal sodium level for an adult? 135 - 145mmol/L
What is a normal potassium level for an adult? 3.5 - 5 mmol/L
What are some of the body's compensatory mechanisms for anaemia? Increased pulmonary and cardiac function; Increased O2 extraction & selective tissue perfusion
What is relative anaemia? A disruption of tissue O2 perfusion such as is caused in pregnancy with a diluting of RBC
What is absolute anaemia? A disruption in haemoglobin
What are the signs and symptoms of anaemia? Vasoconstriction, tachypnoea, pallor, dyspepsia (indigestion), tachycardia, transient murmurs, angina pectoralis, heart failure, muscle cramps, headache, lightheadedness, tinnitus
What is aplastic anaemia? Decreased RBC due to bone marrow dysfunction
How does kidney dysfunction cause anaemia? Decreased erythropoitin production
How does Vitamin B12 (cobalamin) cause anaemia? Disruption of the DNA synthesis of RBC -> macrocytic cells
What is iron deficiency anaemia and what are some of the possible aetiologies? RBC are hypochromic and microcytic. Causes include pregnancy, haemorrhage, chronic renal failure & haemodialysis
What is Thalassemia? Increased cell lysis due to malformed RBC
What is sickle cell anaemia? Abnormal beta-globulin chain (inherited disorder) leading to malformation of cells when deoxygenated
What is G6PD deficiency anaemia? Lack of the G6PD enzyme which RBC need to function
What is haemolytic anaemia? Any of the anaemias where RBC are destroyed, usually in the spleen and usually because of malformation
What is polycythaemia? An excess of RBC's
What is polycythaemia vera? Excessive activation of the red marrow stem cells causing increases in RBC, WBC & platelets
What is secondary polycythaemia? Increased RBC due to low O2 perfusion or a renal tumour. The kidneys produce more erythropoietin.
What is relative polycythaemia? No difference in the production of RBC, but the haematocrit is high because of fluid loss, eg dehydration, stress & smoking
What are petechiae? Capillary haemorrhage into the skin or mucous membrane
What is purpura? Groups / patches of petechiae - usually itchy
What is an ecchymosis? A bruise (blood loss into tissue)
What is a haematoma? A raised ecchymosis
What is haemarthrosis? Bleeding into a joint
What is thrombocytopenia? A lack of platelets, causing disruption of the clotting cascade
What is vonWillebrand's disease? A lack of factor 7 in the clotting cascade
What is haemophilia? Haemophilia A is a lack of Factor 8, and Haemophilia B (Christmas disease) is a lack of Factor 9
What can be a problem with a lack of Vitamin K? Problems with the clotting cascade at Factors 2, 7, 9 & 10
What is a thrombus? A stationary blood clot. In a vein there will be oadema and phlebitis. In an artery there will be iscaemia distal to the clot.
What is an embolus? A freely moving material (clot, air, fat, gas) and lodging in a vessel. Pulmonary, cerebral, coronary most common.
What are varicose veins? Vascular alteration in the superficial (usually leg) veins
What is chronic venous insufficiency? Deep vein alteration causing blood pooling
What is an aneurysm? Arterial dilation, changing the flow and weakening the wall. They include true, false and dissecting aneurysms.
What is an arteriovenous fistula? Where an arteriole connects directly with a vein, shortcutting the capillary and reducing tissue perfusion.
What is CVD? Cardiovascular disease = heart, stroke & vascular diseases often with underlying atheroschlerosis
What is the biggest cause of CVD? Coronary Heart Disease (CHD) = inadequate blood supply -> inadequate O2 and nutrients to myocardium -> angina and tissue death (MI)
What is a transmural MI? A myocardial infarct which occurs through the entire thickness of the (usually left)ventricle wall. Responsive to thrombolytic therapy.
What is a non-Q-wave MI? It occurs in the subendocardial inner 1/3 to 1/2 of the ventricle wall. Better outcomes usually.
What happens 1 - 2 minutes after cell death in MI? Depletion of ATP -> imparied ability to contract
What happens from 0 - 30 minutes after cell death in MI? Hydropic swelling
What happens 40+ minutes after cell death in MI? Irreversible cell damage
What happens from 4+ hours after cell death in MI? Early coagulation and necrosis begins in subendocardial zone and spreading out before cardiac enzymes peak
What happens from 6+ weeks after cell death in MI? Necrotic tissue is replaced with scar tissue
What is the usual ratio of necrosis to apoptosis in cells after an MI? 20& necrotic:80% apoptotic
What is the 4 step treatment for management of blocked coronary arteries? 1. Thrombolysis (eg streptokinase) 2. PTCA with anticoagulation or stent placement 3. Stent to prevent reocclusion 4. coronary artery bypass graft
What is a PTCA? Percutaneous Transluminal Coronary Angioplasty
What is valve stenosis? Incomplete valve opening, created different pressures in the heart chambers -> myocardial hypertrophy & calcification
What are two possible causes for incomplete mitral and aortic valve closure? Rheumatic heart disease & endocarditis
What is rheumatic heart disease? A complication of rheumatic fever following haemolytic streptococci infection
What is dilated cardiomyopathy? Dilation of all 4 heart chambers. Caused by alcohol, genetic abnormality, pregnancy, postviral myocarditis. Transplant is the treatment.
What is hypertrophic cardiomyopathy? Often seen in left ventricle, it is a non-uniform thickened muscle mass & septum -> negative inotropic action. Often has genetic component.
What is restrictive cardiomyopathy? Stiff fibrotic ventricle -> reduced cardiac output -> left side congestive failure
What are the 2 basic classes of congenital heart disease? Obstructive (stenosis or atresia of valves) & shunts (left -> right or right -> left)
Created by: Kbel
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