Vascular Diseases Flashcards
What is the normal thickness of the left ventricular wall
14mm
What is the normal thickness of the right ventricular wall
Less than 4mm
What does white in heart muscle represent
Necrotic tissue
What is arteriosclerosis
Group of disorders that have in common thickening and loss of elasticity of arterial walls
What is atherosclerosis
Progressive disease affecting the intima (affects the lumen) of elastic and muscular arteries characterised by focal atheromas (fibrofatty plaques) consisting of a lipid core covered by a fibrous cap.
What is Monckeberg’s medial scloeriss
Calcification of media (composed of smooth muscle cells) of muscular arteries
What is arteriolosclerosis
Proliferative or hyalien thickening of the walls of small arteries and arterioles
What are RF for atherosclerosis
diet and hyperlipidaemias, hypertension (systolic and diastolic), smoking, DM
What is T1 of atheromatous plaque
Lipid is present in the macrophages in the intima (can go between gaps in adjacent endothleium cells or use lipoprotein receptors - process of transcytosis)
What is T2 of atheromatous plaque
Smooth muscle cell i addition to macrophages. Smooth muscle cells can migrate into intima from underlying media. In the intima, smooth muscle cells start phagocytosing lipid and start synthesising collagen
What is T3 of atheromatous plaque
Lesions in the aorta
What is T4 of atheromatous plaque
Complex plaque (stains with Elastic van Gieson - collagen is red). Plaque causes underlying muscle to atrophy. Arterial wall becomes weaker. Can get abnormal swelling of the wall. The intima and inner 2/3rd of the media is usually oxygen and nutrients by diffusion from blood in the lumen of the artery. Oxygen and nutrients cannot diffuse through plaque.
What is the sequence of atherogenesis
Atheromas are occlusive, compromising blood flow to distal tissues and causing ischaemic injury. Most problems occur in coronary arteries
What happens after the rupture of a fibrous cap of the plaque
Sub endothelium collagen is exposed and lipids to coagulation factors in the blood. Thrombosis can then develop on top of plaque. Can precipitate sudden change in coronary flow -> NSTEMI or STEMI
What is thrombosis
Complication of late stage atherosclerosis. Organisation of thrombi may contribute to plaque formation and luminal encroachment. Fibirin can usually be detected
How does endothelial injury contribute to atherogenesis
Increased expression of vascualr cell adhesion molecules ICAM-1 and VCAM-1 increases monocyte adhesion
What are the effects of atherosclerosis
Slow, insidious narrowing of the vascular lumina, resulting ischaemia of the tissues perfused by the involved vessels - seen as intermittent claudication in the legs
Sudden occulsion of the lumen by superimposed thrombosis or haemorrhage into an atheroma, producing ischaemia
What is the P wave
Atrial depolarisation
What is the QRS complex
Ventricular depolarisation
What is Q
Intraventricular septum depolarisation
What is R
Main mass depolarisation
What is S
Base depolarisation
What is ST
Period of zero potential between ventricular depolarisation and repolarisation
What is the T wave
Ventricular repolarisation
How is MI diagnosed
Troponin T and I - T binds to tropomyosin, interlocking them to form troponin-tropomyosin complex. and I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in palce
What does cardiac I and T indicate
Myocardium damage
How do cardiac muscles contract
Calcium induced calcium release mechanisms. Ca2+ enters L type calcium channels. Ca22+ detected by ryanodine receptors, causing a positive feedback response. Ca2+ binds to troponin C, moving the tropomyosin complex off the acting binding site, allowing the myosin head to bind to the actin filament
Why is chest pain felt
Ischaemia->metabolites accumulate in the interstitium of heart muscle->adenosine accumulation so ATP isn’t recharged->activate nerve endings
What causes angina
Plaque can restrict blood flow to cause stable angina. When stenosis reaches 70%, blood flow can no longer reach demand
What are the sensations of MI
Site and radiation (diffuse, anterior chest, left arm, neck)
Character (tight, pressure, weight, constriction, dull)
Triggers (exercise, cold, meals, psychological stress)
Relief (rest, GTN0
What is the duration of MI sensation
Less than 30 minutes is angina, over 30 minutes is infarction
What causes STEMI
Epicardial coronary artery blockage
What happens when an atherosclerotic plaque ruptures
Platelets initiate clotting cascade. Fibrinogen is polymerising to form fibrin, trapping RBCS
What does statin do
Lower’s cholesterol
Why does SOB occur with MI
Starling’s law of the heart -> left ventricular end-diastolic pressure needs to increase -> left atria pressure increase -> Starling’s law of capillary flow -> increase in hydrostatic pressure pushes fluid out of capillaries into the interstitium of the lungs -> pO2 drops more than pCO2 goes up
What are the advantages of mechanical reperfusion
Faster
Less stroke and bleeds
Lower mortality
High % reperfusion
What is the difference between STEMI and NSTEMI
Reperfusion therapy necessary for STEMI as it indicates a completely blocked artery. In NSTEMI, blood flow is limited by stenosis.
What is a T1 MI
Spontaneous MI (plaque rupture, ulceration, erosion or dissection)
What is a T2 MI
MI secondary to ischaemic imbalance (endothelial dysfunction, spasm, coronary embolism, tach/brady arrhythmia, anemia, hypoxia, hypotension)
What is a T3 MI
MI causing death before biomarkers available
What is the assessment steps for suspected MI
Start therapy before troponin results
Measure cardiac troponin in all px with symptoms of ACS
Measure serial cardiac troponin I or T at 3-6 hours after symptom onset
Use risk scores to assess prognosis
What are anti-anginal drugs
Beta-adrenoreceptor blockers L type calcium channel blockers Nitrates ATP sensitive potassium channel openers If channel blockers
What are thrombolytic drugs contraindicated for
NSTEMI
Unstable angina
What are examples of thrombolytic durgs
Most drugs target fibrin:
Streptokinase
Anistreplase
What is an infarct
Area of ischaemic necrosis within a tissue or organ, produced by occulsion of either its arterial supply or its venous drainage
Why is venous infarction less common
Arrest of flow due to venous obstruction is unusual as most tissues have numerous venous anastamoses
Where are venous infarctions likely to occur
Thrombosis of mesenteric veins -> intestinal infarction
Thrombosis in the superior sagittal sinus -> brain
Thrombosis in testis or ovary following torsion
What happens when bowels infarct
Becomes permeable -> develops into peritonitis resulting in gram negative sepsis
How are infarcts divides
Colour (red/haemorrhagic vs white/anaemic) and presence (septic infarcts) or absence (bland infarcts) or bacterial contamination
What are white infarcts
Arterial occlusion and in solid tissues e.g. heart, spleen, kidneys
What are transmural heart infarcts
Ischaemic necrosis involving full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. Preservation will be thin band of tissue next to endocardium.
What do transmural heart infarcts invovle
Coronary atherosclerosis - left anterior descending, left circumflex (supplies left lateral wall, right coronary), subseqeutnyl plaque rupture and superimposed thrombosis -> STEMI
What are subendocardial infarcts
Constitutes an area of ischaemic necrosis limited to the inner one third of the ventricular wall. There is diffuse stenosing coronary atherosclerosis and global reduction of coronary flow but no plaque rupture and no thrombosis. NSTEMI
What morphological complications follow MI
Pericarditis
Cardiac rupture
Mural thrombosis
Ventricular aneurism
What occurs in pericarditis
2nd or 3rd day after MI - fibrinous or fibrnohaemorrhagic
What occurs in cardiac rupture
Mechanical weakness in necrotic and inflamed myocardium
Ventricular free wall 0> haemopericardium or cardiac tamponade
Rupture of intraventricular septum -> left to right sunt
Rupture of papillary muscles -> severe acute mitral incompetence
What is an embolism
Transfer of abnormal material by the bloodstream and its impaction in a vessel
List the types of emboli
Fragments of thrombus, material from ulcerating atheromatous plaques, septic emboli, fragment of tumour (gives rise to metastases) growing into a vein, fat globules, air emboli (300ml), parenchyma cell
When is a thrombus pale
Fast moving blood
When is a thrombus red
Slow moving blood
Where is fat embolism a problem
Lung fields, can be diagnosed with urine test, fat embolism in capillaries of brain is fatal
Explain DVT and PE
Detachment of a thrombus in a systemic vein, usually in deep vein plexus in the leg. large thrombi may be detached en mass -> right side of the heart. Cause sudden blockage of the pulmonary trunk. Death either immediate or after a short period of resp distress
Where are fatal emobli derived from
Femoral or iliac veins. Commonest around 10th post operative day
What is the definition of IBS
Recurrent abdo pain or discomfort 3 days per month in the last 3 months, associated with two or more of the following:
Improvement with defecation
Onset associated with a change in frequency of stool
Associated with change in form of stool
What is chronic fatigue
Persistent or relapsing, debilitating fatigue for at least 6 months
What is fibromyalgia
Widespread pain index and symptom severity scores. Present for at least 3 months. Does not have a disorder that would otherwise explain the pain
