T9-L1: Cardiovascular Pathology 1 Flashcards
What is Ischaemic Heart Disease?
General designation for a group of syndrome resulting from myocardial ischaemia. Ischaemia is an imbalance between demand and supply of oxygenated blood to the heart.
It is most commonly due to coronary artery atherosclerosis Sometimes it can be due to hypertrophy where there is an increased demand.
Give the IHD syndromes.
- Myocardial Infarction
- Angina
- Chronic IHD with heart failure
- Sudden Cardiac Death
MI, Unstable Angina and Sudden cardiac death together make up Acute Coronary Syndrome.
Give risks factors for IHD.
- Found greatest in Northern England
- Smoking
- DM
- Lack of exercise
- Dyslipidemia
- HTN
What is the pathogenesis of an MI?
There is fixed vessel narrowing and abnormal vascular tone as a result of atherosclerosis deposition in the wall and endothelial dysfunction.
The fixed coronary obstruction can lead to plaque disruption and platelet aggregation.. The plaque can rupture leading to an occlusive thrombus or emboli flying off.
What is the pathophysiology of IHD?
Myocardial infarction is the death of cardiac muscle from prolonged ischaemia. It usually starts in the sub endocardium - this is the least perfused area of the ventricular wall. This then leads to a transmural infarction.
The plaque material is made of necrotic matter - foam cells, cholesterol, cellular debris, etc. There is then a Fibrous cap that holds it made of smooth muscle cells, macrophages, foam cells. Lymphocytes etc. The endothelial lining is then present on top of the fibrous cap. The endothelial lining is dsyfucntional. Damage to the lining exposes the material from the plaque leading to platelet aggregation, which can cause thrombus formation and so occlusion the lumen.
What are the myocardial changes after an MI?
In the first 24 hours the tissue is normal.
1-2 days later it is pale, oedematous, filled with neutrophils and myocyte necrosis.
3-4 days - Yellow with haemorrahagic edge, myocyte necrosis, macrophages etc.
1-3 weeks later it is pale, thin with granulation tissue and then becomes fibrous
3-6 weeks - a dense fibrous scar remains
What are complications of an MI?
- Arrythmias - either directly or by limited perfusion to the conduction system structures such as the SAN or Bundle of His
- Cardiac Tamponade - rupture of the myocardium can lead to blood filling up in the pericardial cavity
- Congestive Heart Failure - due to contractility dysfunction or by papillary muscle (holding down the leaflets of the valves) infarct leading to severe Mitral regurgitation
- Pericarditis - acuity inflammation occurs in the first 48 hours
- Cardiogenic Shock - due to hypotension, reduced perfusion and therefore increasing organ ischaemia
- Thromboembolusm - due to not contracting causing thrombus formation due to stasis. This can cause a stroke or infracts in other organs. Occurs a few days later.
What biomarkers can we use for IHD?
- Creatinine
- Troponin T&I (most sensitive)
- AST
- LDH Isoenzyme
- Myoglobin
How do we define primary hypertension?
Essential hypertension is one extreme of the variable blood pressure rather than a distinct disease.
A sustained diastolic pressure greater than 90 mmHg and a Sustained systolic pressure greater than 140 mmHg can be used as a guide towards the definition of hypertension.
Give causes of secondary hypertension.
- Endocrine - Cushing’s syndome, Acromgelay. Thyroid Disease, Hyperparathyroid disease
- Adrenal - Conn’s disease, Adrenal hyperplasia, Pheochromocytoma
- Renal - Diabetic nephropathy, Chronic glomerulonephritis, Adult Polycystic Disease
- CVS - Renal artery stenosis, Polyarteritis nodosa
- Drugs - Oral contraceptives, NSAIDs, Steroids etc.
What is the action of Angiotensin II?
- Increase vascular resistance and arterial pressure
- Increase sodium and water uptake
- Causes the release fo aldosterone
- Stimulates thirst
- Stimulates the release of vasopressin (ADH) from the posterior pituitary
- Stimaulates cardiac hypertrophy and vascular hypertrophy increasing cardiac output
- Stimulates norepinephrine release and inhibiting its uptake
What is Malignant Hypertension?
Sustained BP > 180/120 mmHg. Clinical signs and symptoms of organ damage are evident - such acute hypertensive encephalopathy, nephropathy with retinal haemorrhages/papilledema. This requires urgent treatment to preserve organ damage.
What are complications of Hypertension?
- Nephropathy
- Increased risk of cerebrovascular disease
- Hypertensive heart disease - presents as hypertrophy of the heart pumping against increased resistance. Hypertrophy is therefore an adaptive mechanism but can lead to dilation of the left heart, congestive hear failure and sudden death. The criteria is left ventricular concentric hypertrophy and a history or pathological evidence of HTN.
What is Cor Pulmonale?
This is right sided hypertensive heart disease. Right ventricular hypertrophy, dilation and potentially heart failure secondary to pulmonary HTN caused by disorders of the lung to pulmonary vasculature. Right ventricular hypertrophy secondary to disease of the left side and congenital causes are generally excluded in the definition; but pulmonary venous HTN that follows left sided disease is common.
Causes include:
- Disease of the pulmonary parenchyma such as COPD, CF, Bronchiectasis
- Diseases of pulmonary vessels - Pulmonary HTN, Recurrent pulmonary thromboembolism
- Diseases affecting chest movement such as Kyphoscoliosis
- Diseases inducing pulmonary arterial compression such as metabolic acidosis, hypoxia
What is the difference between a dissection and a true and a false anyeursm?
True aneurysms: an abnormal dilation of an artery due to a weakened vessel wall.
False aneurysm: (pseudoaneurysm) of the vessels, occurs when a blood vessel wall is injured and the leaking blood collects in the surrounding tissue.
A dissection is a tear within the wall of a blood vessel, which allows blood to separate the wall layers.
