MOD L6 Atherosclerosis Flashcards
(16 cards)
1) Atherosclerosis. What is it?
Normal arterial wall layers
Macroscopic apperance of atherosclerosis
1) Affects large and medium sized arteries. Large: Aorta, carotid Medium: Coronart, renal
2) Intima - inner most. Lined by endothelium
Media: Smooth muscle
Adevntita: Outer connectivoe tissue
Fatty Streak, simple plaquue, complicated plaque
Fatty Streak:
Seen in children
Lipid deposits in intima
Yellow, slightly raised
No disturbance to bloodflow
Simple Plaque
-Rasied yellow/white
-Often occur around ostia
-Causes turbulent blood flow
Complicated Plaque
-Calcification
-Ulceration
-Thrombosis
-Haemrrohage into plaque
OSTIA: openings/branch points where smaller arteries branch off from larger arteries
🔬 Microscopic Appearance of Atherosclerosis
early changes
Later changes
Early changes:
-smooth muscle proliferation
-formation of FOAM CELLS (macrophages with lipids)
-Extracellular lipid deposits
-Scatted Tlymphocytes
Later changes
-FIOBROSIS, NECROSIS
-CHOLESTROL CLEFTS, CALCIFICASTION
-DAMAGE TO INTERNAL ELASTIC LAMINA
-Neovascularization (new blood vessels)
-Plaque fissuring and rupture –> can lead to thrombosIS
Common sites for atherosclerosis:
Where do symptoms appear?
4 major patterns of atherosclerosis disease
Affects large + medium size arteries, where blood flow is turbulent (like branch pointys/ostia)
-AORTA (especially abdominal aorta)
-Coronary arteries
-Cerebral arteries
-Leg arteries (femoral, popliteal)
Symptoms appear in:
Heart: MI
Brain: Sttroke
Kidneys: Hypertension + kidney failure
Legs: Claudication + gangrene
The four major patterns:
SLIDES.
Ischaemic Heart Disease (IHD)
1) What is it?
2) Symptoms
3) Mechanism
4) Coronary Artery Thrombosis - IMAGE
1) Atherosclerosis in coronary arteries. Reduced blood flwo to heart muscle (myocardium).
2) Leads to:
- Angina pectoris: chest pain due to partial blockage
-Myocardial Infarction: Complete blockage = heart attack
-Chronic heart failure
-Sudden cardiac death from arrythmia
3) Mechanisms
A) B) IMAGE FROM SLIDE
ACS - Acute Coronary Syndrome
1) Stable Angina
-Cause
-ECG
-Troponins
-Ischemia
-Symptoms
2) Unstable Angina
3) NSTEMI
4) STEMI
1) Fixed atherosclerotic plaque. Reduced blood supply during exertion
ECG: NORMAL
TROPNINS: NORMAL
ICHEMIA: DEMAND RELATED, NO INFARCTION
Symptoms: Chest pain on exertion, relieved by rest
2) Plaque rupture + partial thrombus, causing reduced blood flow
ECG: T wave inversion. ST depression
Tropnins - norma
Ischemia- supply related. No infarction
Symptoms: Chest pain at rest with minimal exertion.
3) IMAGE
🧠 Summary Mnemonic:
Angina = Ischemia, no death NSTEMI = Partial blockage → Injury STEMI = Total blockage → Infarction
4 Major Patterns of Atherosclerosis Disease: Cerebral Ischemia
1) Mechanism of Stroke
2) Clinical Outcomes of Cerebral Ischaemia (don’t worry about the details)
1) Atherosclerosis of carotid arteries. Leads to plaque formation.
Thrombus forms over this plaque
Thromboembolism can break off and travel to cerebral arteries
Leads to blockage of blood supply to parts of brain, causing ischaemia or infarction (stroke)
2) IMAGE / LECTURE SLIDE
Abdominal Aortic Aneurysm (AAA)
1) What is it?
2) Cause
3) Features, Risks
1) Dilation of aorta due to wall weakening
2) Due to atherosclerosis in large arteries
3) 10-15 cm in diameter. Supture - fatal. Embolism.
Peripheral Vascular Disease
Cause
Symptoms
Atherosclerosis in leg arteries. (espcially in smokers + diabetics)
- Intermittent claducation (leg paun on exertion, relieved by rest)
- Ischameic rest pain: Pain at night or when legs elevated
-Gangrene - tissue death from lack of blood flow
-Leriche Syndrome: blockage of aorta where it splits nto ilaic arteries
Another effect of Atherosclerosis is Mesenteric Ischaemic + Bowel Infarction
1) What is it?
2) Symptoms/consequences/what doews it lead to/complications
1) Reduced blood flow to intestines due to blockage of meseneteric arteries (espcially SMA)
2) Ischamic collities- damage to colon due to low blood flow
Malapsotption
Inetstinal infarction
How does atherosclerosis happen at a cellular level?
DONT MEMORISE - just for understanding
1) Chronic endothelial injury: damage to endothelium by LDL CHJOLESTROL, HIGH BP, SMOKING TOXINS
2) Endothelial dysfunction - damaged lining becomes stisky, platelets stock to it and release PDGF growth factor. Monocytes enter, turn into macrophages and release inflammatory signals. T cells come in, addting to immune response
3) Smooth muscle migration: smooth muscle cells from media move into intima
4) Foam cell formation: macrophages + smooth muscle cells eat up oxidised LDL. Turn into foam cells
5) Smooth muscle proliferation. These muscle cells multiply and produce: Colagen, fibrous cap, matrix
6) Neo-vascularisation: Small blood vessels form inside plaque.
Atherogenesis
- Cells involved
- DO NOT MEMORISE, just have an idea
1) What happens when an atherosclerotic plaque ruptures?
2) RISK FACTORS for Atherosclerosis (non-modifiable vs modifiable)
1) Exposes inner content to blood
- Triggers intrinsic and extrinsic clotting cascades
- Thrombus (bloos clot) forms, blocks artery, leads to MI
2) Progression:
Starts young and builds slowly over decades.
Gender:
Women are protected (likely due to estrogen) until menopause.
After menopause, risk rises and matches men by old age.
Familial hyperlipidaemia:
Genetic form of high cholesterol.
Can cause MI before age 20.
Often due to defective LDL receptors → high circulating LDL.
Lipid Metabolism
1) What are the transport vehicles for fat in the blood?
2) Main types of Lipoproteins
3) MAIN FUNCTION OF LDL - HIGH YIELD, MENTIONED MANY TIMES IN SLIDES.
4) What allows LDL to stay longer in the blood?
5) Why is oxidised LDL dangerous?
6) HDL Metabolism (function of HDL + mechanism)
7) How does HDL reduce risk of atherosclerosis?Which 2 proteins does it use to help with this?
8) What is used as a marker to see cholestrol levels and risk of atherosclerosis?
1) Lipoproteins
2) VLDL, LDL, HDL, Chylomicrons - REFER TO SLIDE ON FUNCTIONS OF EACH
3) Transport cheolstrol from liver to peripheral tissues. LDL receptor mediated endocytosis
4) No apoC or apoE, not cleared efficiently by liver, so stays longer inj blood
5) LDL half life longer than VLDL or IDL, so LDL more suceptible to oxidative damage. Oxidised LDL taken up my macrophages, that can transform into foam cells, contributing to atherosclerotic plaques.
6) Reverse cholestrol transport: HDL removes cholestrol from tissues + returns it to liver.
7) Clearing foam cells, preventing atherosclerotic plaque formation. ABCA1 and LCAT. (LCAT is an enzyme). ABCA1: facilitates transfer of cholestrol to HDL. LCAT: cholestrol cobverted to to cholestrol ester.
8) APO E
More risk factors of atherosclerosis
- Familial Hyperlipidaemia
- What is it?
- Why it matters?
- Visible signs - Physical signs of lipid disorders (HIGH YIELD!!!!!)
- Smoking
Why is this a risk factor? - Hypertension
- Diabetes
- Alcohol
- Genetic. Abnormal levels of lipoproteins. (fat carrying proteins in blood)
Causes early atherosclerosis.
CORNEAL ARCUS, TENDON XANTHOMAS, XANTHELASMA - Corenal Arcus, Tendon Xanthomas
- Procuagulant. Reduces prostacyclin (prostacyclin prevents platelets from sticking together)
- Damages blood vessels directly (endothelium)
- AGEs - Advanced Glycation End Products: Form when sugar react with protein. AGEs damage proteins (e.g. collagen), stiffen vessels. Makes LDL easier to trap in vessel walls. So, more atherosclerosis.
AGE - bind to vessel wall receptors. Acticats clotting. Protein Kinase C activation. Reduces fibronylisis, more clot formation.
- Heavy drinking (≥5 units/day): ↑ risk of heart disease.
Moderate alcohol might help by raising HDL (“good” cholesterol).
Alcohol risk depends on dose and individual context.
Lack of exercise: Contributes to obesity & poor metabolism.
Obesity: Promotes hypertension, high LDL, and low HDL.
Other contributors:
Soft water: Possible minor association. Oral contraceptives: Small increased risk in certain populations. Type A personality: Possibly linked to stress-related cardiac risk.
📌 Key Point: Multiple risk factors add up — e.g., a smoker with diabetes and high BP has far higher risk than someone with just on
Prvention + Interventions of Atheroslcerosis
