Cardiovascular Flashcards
Define atherosclerosis
Inflammatory process characterised by hardened atherosclerotic plaques in the intima of a vessel wall.
name 4 main constituents of an atheromatous plaque
- Lipids
- Cholesterol
- Lymphocytes
- Fibrous tissue
What is the primary cause of atherosclerosis?
Endothelial cell damage.
Outline the progression of athersclorosis.
- High levels of cholesterol damages endothelium.
- LDLs and inflammatory cells like monocytes and macrophages and T-cells begin to accumulate in arterial wall
- Macrophages try to break down, LDLs, turning into foam cells, which produce a LIPID CORE/FATTY STREAK
- This inflammatory reaction leads to tissue repair, so the smooth muscle proliferates forming a fibrous cap that encloses the lipid core.
does Tom have stinky feet?
yes
What are some risk factors for atherosclerosis?
age, gender, genetics, smoking, high blood pressure, high cholesterol, diabetes, and obesity.
Atherosclerosis - when the endothelium is damaged, what happens that leads to inflammation?
the accumulation of LDL-cholesterol in the artery wall, which leads to the activation of inflammatory cells
Atherosclerosis - Once the endothelium wall is inflamed, what will begin to accumulate? What does this lead to?
As the endothelial cells become damaged, they begin to accumulate fats, such as cholesterol, triglycerides, and phospholipids. These fats oxidize and cause the formation of fatty plaques in the artery wall.
What medications can help treat Atherosclerosis?
statins - Lower Cholesterol
blood pressure-lowering medications
Aspirin
Anticoagulants
How does Aspirin help reduce cardiovascular disease? What type of drug is it?
It is a NSAID, can be over the counter, in cardiology, can act As an antiplatelet
It irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.
What type of Drugs are
a) Clopidogrel and
b) GPIIba antagonists? What is their effect on the CV system?
a) P2Y12 receptor blockers - Drugs like Clopidogrel block the P2Y12 receptor to Reduce platelet activation
b) These block glycoprotein IIb/IIIa receptors on their platelet’s plasma membrane and inhibiting fibrinogen binding - also reduce platelet activation.
*BOTH ANTIPLATELET
What do anticoagulants do? Give some examples
Anticoagulants work by preventing the formation of blood clots. They do this by *Inhibiting thrombin in the body that are involved in the clotting process
Eg Warfarin, Heparin
What is acute coronary syndrome (ACS)?
An umbrella term for a spectrum of disease caused by ischaemia
What are the 3 different diseases that fall under the term ACS?
STEMI- ST elevated myocardial infarction
NSTEMI- A non-ST elevated myocardial infarction can be shown by biochemical markers
Unstable angina- all the symptoms of ACS without biochemical or ECG markers
Describe the epidemiology of ACS
- Coronary heart disease is the leading cause of death in the UK
- 50% of deaths occur within the first 2 hours of symptom onset
- 15% of MI’s are fatal
- 300,000 cases per year
What are some risk factors for developing ACS?
Modifiable
- Age (strongest)
- Gender (male)
- Family history ]
Lifestyle
- Hypertension
- Diabetes
- Hyperlipidaemia
- Obesity
- Lack of exercise
- Smoking (damages endothelium)
- Alcohol
Describe how an atherosclerotic plaque forms
- Starts with damage to the endothelial cells of vessels, this can be by lipids, high BP. Changes in flow can cause. Aortic arch susceptible turbulent flow
- This results in accumulation of macrophages at tissue which when combined with lipids form foam cells
- This forms foam cells which secrete cytokines and result in immune activation and platelet aggregation
- This forms a fatty streak
- Over time this fatty streak will become a fibrous plaque as tissue and smooth muscle grows over it. This will narrow the lumen of the blood vessels
What two things usually occur that result in the symptoms of ACS?
- The fibrous cap of the plaque itself gets a superficial injury, and a thrombus forms on it
-In more advanced, unstable plaques, the fibrous cap completely ruptures, and not only can some of the contents escape, but blood can also enter the plaques, forming a thrombus within the remaining cap of the plaque.
This can result in lack of blood flow (ischaemia) which will in turn lead to infarction of the cardiac muscle if it occurs in the coronary arteries
What do platelets secrete which can further worsen an MI?
Serotonin and thromboxane A2 and this causes vasoconstriction in the area resulting in reduced blood flow to the myocardium, and ischaemic injury.
What are the key presentations of ACS?
- Chest pain (lasting longer than 20 mins) that can radiate to back, shoulder and arms
- Dyspnoea (shortness of breath)
- Pallor
- Diaphoresis (sweating)
What percentage of patients have silent MI’s (without chest pain)
30%
In which groups of people are silent MI’s most common?
- Women
- Elderly
- Diabetic patients
What are some signs of ACS?
Increase pulse rate, S4 heart sound - due to impaired left ventricle, hypotension, signs of heart failure e.g., oedema
What other symptoms can be experienced during ACS?
Nausea/vomiting, palpitations, dizziness