![Atherosclerosis Scoring
The traditional Framingham Risk Score
[QRISK score (http://www.qrisk.org)
Reynolds Risk Score
(http://www.reynoldsriskscore.org)]
The Society for Heart Attack and Eradication (SHAPE)
guidelines ; they advocate assessment of biomarkers in
all intermediate risk patients, a position not yet
endorsed by NLA. ACC/AHA
Guideline for Assessment of Cardiovascular Risk in
Asymptomatic Adults (2010) lists a few diagnostic tests
as Class IIa recommendations.](https://image.slidesharecdn.com/atherosclerosis-180504175041/85/Atherosclerosis-74-320.jpg)
More Related Content
Atherosclerosis
- 1. ATHEROSCLEROSIS Dr.Jyoti Priyadarshini Shrivastava AssociateProfessor Department of Pathology Gajra Raja Medical College
- 3. PATHOLOGY Bridging Discipline General Pathology and Systemic /Special Pathology CORE OF PATHOLOGY 1.Etiology 2.Pathogenesis 3.Morphology 4.Clinical Significance
- 4. BLOOD VESSELS Closed circuitsfor the transport of blood from the heart to the tissues for exchange of gases and nutrients and vice versa. Arteries Veins Capillaries
- 5. The Vascular System The arterial system - high-pressure system, so arteries have thick walls that appear round in cross section. The venous system - lower-pressure system, containing veins that have larger lumens and thinner walls. They often appear flattened. Arteries, arterioles, venules, and veins are composed of three tunics known as the tunica intima, tunica media, and tunica externa. Capillaries have only a tunica intima layer (An adult's blood vs. be closer to 100,000 miles long) (300 million capillaries in the human body. ) Capillary bed: network of 10–100 capillaries connecting arterioles to venules
- 7. Distribution of Blood •Systemiccirculation 84% •Systemic veins 64% •Systemic arteries 13% •Arterioles 2% •Muscular arteries 5% •Elastic arteries 4% •Aorta 2% •Systemic capillaries 7%
- 10.
- 11. INTRODUCTION Atherosclerosis is acondition where the arteries become narrowed and hardened due to a build up of plaque in the artery wall.
- 12. Sclerosis= Hardening Arteriosclerosis=Hardening of Arteries Three Patterns: 1.Atherosclerosis 2.Monkeberg’s Medial calcific sclerosis 3.Arteriolosclerosis Hypertension Diabetes Mellitus 4.Senile Arteriosclerosis
- 13. DEFINITION Atherosclerosis is aspecific form of arteriosclerosis affecting intima of large(elastic) and medium sized muscular arteries characterised by fibrofatty plaques or atheromas. Athero- porridge,gruel Sclerosis-Scarring/Connective tissue Atherosclerosis: Hardening and loss of elasticity
- 14. Points to remember 1.Progressivedisease 2.Intima 3.Fatty streaks(Precursor) 4.Eccenteric lesions at branching points
- 17. PLAQUE Plaque is asticky substance made up of fat, cholesterol, calcium, and other substances found in the blood. The presence of the plaque induces the muscle cells of the blood vessel to stretch, compensating for the additional bulk, and the endothelial lining thickens, increasing the separation between the plaque and lumen. Plaque hardens and narrows your arteries. That limits the flow of oxygen-rich blood to your body.
- 20. Masson trichrome stainingis used to discriminate collagen fibers from muscular tissues on histological slides.
- 21. SITE OF LESION SITE: Large(Elastic) ,Medium sized(muscular) arteries Arteries: AORTA(Post.wall) Abdominal aorta (Aneurysm) Coronary Cerebral Renal Peripheral vessels Mesenteric vessels
- 23.
- 24. ETIOLOGY Major riskFactors: Modifiable-Dyslipidaemia, HTN, D.M., Smoking Non- Modifiable-Age, Sex, Genetic Factors, Family/race (Constitutional) Emerging Risk Factors: Environmental factors Obesity Hormones Physical inactivity Stress Homocystinuria Alcohol Prothrombotic factors Infections(Herpes,CMV) High CRP
- 25. Two risk factors–Increased risk by 4 Folds Three risk factors- Increased risk by 7 Folds
- 26. Age A dominantinfluence Atherosclerosis begins in the young, but does not precipitate organ injury until later in life. Gender Men more prone than women, but by age 60--7070 about equal frequency. Oestrgen and HDL are protective . Family History Familial/racial cluster of risk factors- Blacks Genetic differences
- 27. Emerging Risk Factors 1.Environmental influences: > in developed nations, Western world 2.Obesity: >20% overweight 3.Physical inactivity/lack ofexercise 4.Stress:Type A personality 5.Homocystinuria(inborn error of metabolism) 6.Infections:CMV,HSV, C.pneumoniae 7.CRP:
- 28. Major risk Factors Modified by Life Style /Pharmacotherapy LIPID DISORDERS: Virchow-Cholesterol crystals in Atheromatous lesions Hyperlipidemia : (Increased Cholesterol,Triglycerides,Liporoteins) Major factor Directly proportional EVIDENCES: 1. Bad cholesterol(LDL,IDL)-Connstituent of plaque 2. HDL: Removes cholesterol Ratio of LDL:HDL::4:1 3. Experimental animals 4. Diseases inducing hypercholesterolemia- Dm, Nephrotic Syndrome, Myxoedema,Xanthomaosis 5. IHD more in H+chol.
- 29. HYPERLIPIDEMIA Higher-than-normal levelsof cholesterol, triglycerides, and other lipids and Lipoproteins in the blood. 1.Familial 2.Acquired
- 30. FAMILIAL HYPERLIPIDEMIA Familial:Inherited Autosomal Recessive/Dominant trait. LDL receptor via apolipoprotein E Gene mutation of apolipoprotein, Hepatic Lipoprotein receptors, Lipoprotein lipase enzyme. LDL accumulation- Atheromas Xanthoma
- 31. ACQUIRED HYPERLIPIDEMIA I.Dietary Factors: Cholesteroland Saturated Fats> 40% Saturated fat intake > 10% of total calories. (single bonds,stable,deposited under skin) II.Diseases: Diabetes Myxoedema Nephrotic syndrome Hypothyroidism III. Obesity and Smoking IV. Progesterone V.Hypertension : (lipid lowering drugs reduces the chances of IHD)
- 32.
- 33. Insudation Hypothesis/Lipid theory/Response toInjury Hypothesis(Virchow) (Rudolf Ludwig Carl Virchow "the father of modern pathology") Imbibed lipids from blood Cellular proliferation of Intimal cells
- 34. Encrustation Hypothesis/Thrombogenic theory:(Rockitansky) Atheroma encrustedon arterial wall Thrombus –platelets,fibrin and leucocytes Thrombosis not a sole factor Merged with Response -to-injury Hypothesis
- 35. Reaction to InjuryHypothesis(Ross) Widely accepted Encorporates Lipid theory + Thrombogenic theory
- 36. Components of Reaction-to-injury Hypothesis 1.EndothelialInjury 2.Intimal SMC proliferation 3.Role of Blood Monocytes 4.Role of Dyslipidemia 5.Thrombosis
- 37. Endothelial injury 1.Mechanicaltrauma 2.Haemodynamic forces(Branching/openings) 3.Immunological/chemical mechanisms Metabolic agent: Chronic Dyslipidemia Homocystinuria Infections Hypoxia Radiation Carbon monoxide Tobacco products
- 38. Intimal SMC proliferation Enothelial damage Subendothelium exposed Adherence,Aggregation and platelet release reactions Inflammatory cells enter Proliferation Of SMC’s (IL-1,TNF)Production of extracellular matrix PDGF,FGF----SMC proliferation in Intima TGF-B andIFN- Gamma activate T lymphocytes.Collagen synthesis NO and Endothelin-SMC,Collagen,Elastic fibres
- 39. Role of BloodMonocytes LDL in monocyte---Oxidised LDL----foam cells. For endothelium—Oxidised LDL----- Cytotoxic. Death of Foam cells by Apoptosis releases Lipids to form Lipid Core of Plaque.
- 41. Role of Dyslipidemia 1.Endothelial Injury and Dysfunction 2.Increased permeability 3.Foam cell formation by Oxidised LDL, (HDL—Anti atherogenic)
- 42. THROMBOSIS 1.Endothelial damage 2.Platelet aggregation 3.Inflammatory reaction 4.Thrombus formation+Foam cells 5.Atheromatous Plaque 6.Fibrin and WBC’s
- 44. Monoclonal Hypothesis SMCproliferation is initial event Monoclonal proliferation(Neoplasms) SMC show only one form of G6PD isoenzymes. Monoclonality is due to mutation by Chemicals Metabolites Viruses
- 49.
- 50. STAGES Intimal Thickening Fatty Streaksand Dots Fibrous Plaque Atheroma Atherosclerosis
- 51. Fatty Streaks At Birth Asymptomatic Dotsor streaks 1 mm in size Disappear with age Aorta(Post.wall),major arteries
- 52.
- 54. Gelatinous Lesions AtBirth Oval ,Round Gross: Grey elevations 1 cm. in diameter Microscopy: Increased Ground substance and Thinned endothelium. Intermediate, transitional stage in the complex histogenesis of the atherosclerotic plaque.
- 55. Atheromatous/fibrofatty plaque Site:Abdominalaorta Descending thoracic aorta Aortic arch Ostia: Iliac Femoral Carotid Coronary Cerebral
- 56. Atheromatous Plaque Gross: White toyellowish 1-2 cm Raised Cut Section: 1.Fibrous Cap 2.Necrotic centre
- 57. Fibrous cap Superficialluminal part Covered by enothelium SMC,Dense connective tissue, ECM(Proteoglycans, collagen) Cellular Area Macrophages Foam cells Lymphocytes SMC +/- Lipids Deeper central soft core Lipid,Cholesterol cleft, Fibrin,NecroticDebris, Lipid laden Foam cells Advanced Lesion: Thick fibrous cap
- 58.
- 59. Typical Atheroma/Type IVlesion
- 60.
- 61. Calcification Intima and necroticarea Different from Monckebergs degeneration-Medial calcification
- 63.
- 64.
- 66. HAEMORRHAGE Intimal haemorrhage fromulceration Common in coronary arteries Hematoma contains hemosiderin laden macrophages
- 67. ANEURYSM FORMATION BasicallyIntimal disease Advanced----Media and adventiia show secondary changes Media---Atrophy Thinning Fragmentation of IEL Adventitia: Fibrosis Inflammation
- 70. Rupture of AorticAneurysm
- 72. Clinical effects ofAtherosclerosis
- 73. Atherosclerosis Score Index(ASI) Whole-body magnetic resonance angiography (WB-MRA) has shown its potential for the non-invasive assessment of nearly the entire arterial vasculature within one examination. Association between the GES(Gene Expression Score ) based on age, sex and peripheral blood cell expression levels of 23 genes measured by quantitative real-time PCR (qRT-PCR)and coronary arterial Plaque Burden and Stenosis by CT-angiography
- 74. Atherosclerosis Scoring Thetraditional Framingham Risk Score [QRISK score (http://www.qrisk.org) Reynolds Risk Score (http://www.reynoldsriskscore.org)] The Society for Heart Attack and Eradication (SHAPE) guidelines ; they advocate assessment of biomarkers in all intermediate risk patients, a position not yet endorsed by NLA. ACC/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults (2010) lists a few diagnostic tests as Class IIa recommendations.
- 75.