CV Pathology Flashcards
(27 cards)
What is atherosclerosis ?
-Progressive chronic inflammation of arteries characterised by :
- Inflammation(macrophages engulf LDL = Foam cells)
- Fibrosis = connective tissue matrix formation
- Lipid deposits (cholesterol in cells)
What are the atherosclerosis risk factor (who are at risk) (Aetiology) ?
Non modifiable
-Age 40-60, male, indigenous
Modifiable
- Increase cholesterol
- HTN
- Smoking
- Diabetes
- Obesity
- Metabolic syndrome
What is the Atherosclerosis pathogenesis (Mechanisms of disease) as a whole ?
- Endothelial injury and activation (e.g. HTN or toxins)
- Endothelial inflammation
- Accumulation LDL due to endothelial damage = fatty streaks
- LDL becomes oxidised, immune cells activated, macrophage engulfs and produces foam cells
- Fibrosis occurs (Smooth muscle and calcium) = mature atheroma formation
- Complicated plaque formation (rupture, thrombus then ACS)
Clinical complications of atherosclerosis?
Heart - Angina and MI Brain - Stroke Kidneys - Renal failure GIT - GI ischaemia or infarction Lower extremities - Peripheral vascular disease
Investigations for atherosclerosis ?
Coronary angiogram
How do you manage the risk factors for atherosclerosis ?
- Statins - Control cholesterol
- ACE-I / B-Blockers
- Diet and activity (obesity)
- Decrease smoking and alcohol
- Aspirin (control thrombosis)
- Surgical interventions (Ballon angioplasty/stent bypass surgery)
What clinical manifestations of complicated plaques can occur in atherosclerosis ?
Hint: Think classic CHD
- Plaque rupture (thrombosis) unstable
- Narrowing/calcification - vessel fragility
- Haemorrhage into plaque - narrowing of lumen
- Fragmentation of plaque - distal emboli
- Weakening of vessel wall - aneurysms
(Embolus, Thrombosis, Aneurysm, Haemorrhage)
Describe the Endothelium activation process in atherosclerosis ?
Hint: This causes the initial inflammation process
- Increased cell permeability
- Platelets adhere
- Monocytes adhere and transform to macrophages
- Blood LDLS enter and bind their apolipoprotein receptor which then causes oxidation
- Oxidation of LDL causes inflammation
Describe the local inflammation process in atherosclerosis and fatty plaque formation?
Hint: Cycle feedback loop
- Oxidised LDLS attract immune cells (cytokines, platelets, monocytes, smooth muscle etc.)
- Macrophages engulf oxidised LDL which forms foam cells (lipid laden)
- The building of plaque begins
- Fatty streak gets more profound as foam cells unable to digest lipid content and then die
- This causes cell debris and extracellular lipids
- Oxidised LDL then starts positive feedback loop by attracting immune cells
Differences between atherosclerosis and arteriosclerosis ?
Arteriosclerosis is hardening of any medium or large arteries
Atherosclerosis is hardening of an artery due to an atheromatous plaque
What is a dilated cardiomyopathy ?
It is a progressive dilation & hypertrophy of the heart which causes systolic dysfunction
What are the proposed aetiologies of dilated cardiomyopathy ?
- Commonly idiopathic
- Chronic alcoholism
- Post viral (myocarditis)
- Genetic
- Chemotherapy
- Chronic anemia
What is the Pathogenesis / causes of dilated cardiomyopathy ?
- Heart dilation and systolic dysfunction
- Enlarged non elastic heart
- AV Valve regurgitation (ejected blood re enters through valve)
- Mural thrombi (can embolise)
What are the Clinical features of dilated cardiomyopathy ?
Nothing hugely standout
- Any age
- Presents congestive heart failure
- Dyspnoea
- Fatigue
- Cough
What are Dilated cardiomyopathy complications ?
- Mitral regurgitations
- Arrhythmias
- Possible thrombotic embolism
How would you investigate dilated cardiomyopathy ?
- ECG
- CXR
- Echo (can see heart chambers and decreased ejection fraction)
How does Hypertrophic Cardiomyopathy occur ?
A genetic variation in the muscle cell proteins that causes myofibril disarray an then subsequent muscle cell hypertrophy of ventricular walls / septum.
Why is Hypertrophic Cardiomyopathy a diastolic dysfunction ?
- Hypertrophied septum and ventricular walls causes smaller chamber sites
- This decreases the filling capacity available
- Which is diastolic potion of heart cycle
Clinical features / complications of Hypertrophic Cardiomyopathy ?
- Dyspnoea, orthopnoea
- Syncope caused by ventricular outflow obstruction
- Angina
- Arrhythmias
- Mural thrombus (Stroke)
- Sudden death
Investigations of Hypertrophic Cardiomyopathy ?
ECG
Echo (main one to see diastolic filling)
CXR
Why would Beta-B help in Hypertrophic Cardiomyopathy treatment ?
- Decreases contractility and HR
- High HR + contractility reduces diastolic filling and therefore the ventricular chambers are smaller
- There is now an increased intermittent ventricular outflow obstruction
What are the aetiologies of Restrictive Cardiomyopathy ?
- Amyloidosis (build of / deposit of amyloid protein in the myocardium
- Sarcoidosis (development of granulomas inherit tissue)
- Scleroderma (An AI condition that can result in changes to the skin, blood vessels, muscles, and internal organs)
- Haemochromatosis (Increased iron deposits within the heart)
What is the pathogenesis (follow on from initial cause) of Restrictive Cardiomyopathy and what may you seen upon an echocardiogram ?
- Stiffness of the myocardium reduces the ventricular filling (diastolic dysfunction)
- Consistent ejection fraction due to normal sized and volume ventricles
- However, there is a reduced volume of blood being ejected as a whole
Clinical features (S&S) of Restrictive Cardiomyopathy ?
Symptoms:
- Cough, Dyspnoea
- Fatigue (greatly with exercise)
- Chest pain, palpitations
Signs:
- Elevated Jugular venous pressure
- Peripheral oedema due to blood being backed up
- Arrhythmias
- Lung crepitations
