Case 1- illness Flashcards
Atheroma
Also known as atherosclerosis, is a progressive disease characterised by the accumulation of lipids and fibrous elements in the large arteries. The atherosclerotic plaques may eventually disrupt the flow of blood
Thrombosis
Rupture of an atherosclerotic plaque with partial or complete obstruction of the artery
Embolism
Blockage of a blood vessel due to an atherosclerotic plaque
Plaques and their ability to rupture
‘High risk plaques’ have a thin cap and a large lipid cores with more inflammatory cells and fewer smooth muscle cells. More likely to rupture
What are the clinical consequences of atheroma
Aneurysm, thrombosis, embolism, stenosis, ischaemia
Stenosis
Abnormal narrowing of a blood passage
Ischaemia
Inadequate blood supply to an organ or pat of the body
Mechanism involved in the development of atheroma
- The artery wall or endothelium is damaged. The LDL (low density- lipoprotein) moves into the tunica intima and deposits cholesterol, this oxidises causing an inflammatory response.
- The inflammation attracts monocytes which enter the tunica intima and transform into macrophages, they attempt to digest the cholesterol and become foam cells.
- Foam cells accumulate beneath the endothelium forming fatty streaks.
- Within the artery wall, foam cells degenerate and release their contents
- Calcium salts and fibrous tissue accumulates within the atheroma and a hard plaque forms. The artery wall elasticity is reduced and the artery lumen narrows, causing blood pressure to increase.
- Plaques have a lipid core and a fibrous cap.
Formation of thrombosis
- The endothelium ruptures over the heard plaque, exposing collagen.
- Platelets come into contact with collagen, they stick together forming a platelet plug.
- Thromboplastin is released stimulating the conversion of the blood clotting protein prothrombin to the enzyme thrombin.
- Thrombin converts soluble blood clotting protein fibrinogen to insoluble fibrin.
- The fibrin forms a tangled mesh which traps blood cells and a blood clot (thrombus) is formed. This restricts the flow of blood in the artery or can break off and form a blockade somewhere else. If this happens in a blood vessel that feeds to the heart it can cause a heart attack.
Risk factors for atheroma
High cholesterol and lipoproetin levels, high blood pressure, smoking, diabetes, obesity, lack of physical activity, unhealthy diet (high in fat and salts), older age, family history, inflammation, male, low birth weight, sleep apnoea, stress, alcohol
Atheroma epidemiology
Usually manifests later in life but its early phases are present in teenagers and young adults. Common in western and urban populations but still occurs in low and middle income countries. It is the number one cause of death globally
Difference between cardiac and vascular diseases
Cardiac refers to the heart and vascular refers to blood vessels
Hypertension
High blood pressure in the arteries
The numbers in a blood pressure recording
Should be below 140/80, the first number is the systolic blood pressure and the other number is the diastolic blood pressure. Measured at the brachial artery in the arm
White coat hypertension
Blood pressure recorded in a doctors office is higher then it normally is because the person is stressed
How to get round white coat hypertension
Use an ambulatory blood pressure monitor (ABPM), it does repeated blood pressure checks throughout the day to produce an average result
Why is hypertension bad
Risk factor for lots of cardiac diseases as it damages blood vessels by making them stiff or narrow. The narrowing makes it easier for fatty material to clog them
Stage 3 hypertension
> 180/120
Stage 2 hypertension
> 160/100
ABPM >150/95
Stage 1 hypertension
> 140/90
ABPM >135/80
How does hypertension cause left ventricular hypertrophy (LVH)
There will be an increase in the force required for the heart muscle to push blood through the aortic valve. Initially there will be an increased left ventricular afterload. This will cause increased levels of multiple hormones and increased muscle contractions. As with any muscle, repeated stimulation of a muscle causes it hypertrophy (enlargement).
Afterload
The pressure the heart must work against
To test for LVH
- ECG changes – left axis deviation, use the Sokolov-Lyon criteria (S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm).
- Echocardiogram – direct visualisation of ventricular hypertrophy, evidence of aortic valvular disease (stenosis or regurgitation), evidence of mitral regurgitation, evidence of heart failure.
Causes of arteriosclerosis
Tunica intima starts to fill with cellular waste forming a lesion. This then matures into different forms of atherosclerosis with the loss of elasticity in the arterial wall. Less blood can flow through the arteries reducing the supply to different organs and causing ischaemia. Only in arteries
Main signs and symptoms of arteriosclerosis
Numbness in the face and lower limb muscles, fatigue, shortness of breath, mental confusion, difficulty in speech and problems in vision
Monckeberg’s arteriosclerosis
Also known as medial calcific sclerosis, mostly seen in the elderly. Only occurs in the lower extremities
Hyperplastic arteriosclerosis
Type of arteriosclerosis that affects large and medium sized arteries
Hyaline type arteriosclerosis
Can be divided into two types arterial hyalinosis and arteriolar hyalinosis. Lesions form due to deposition of hyaline in the small arteries and arterioles.
