بسم الله الرحمن الرحيم
Cardiovascular System
Vascular Diseases
Dr. Samar Al Hakeem
Department of Pathology
Faculty of Medicine
University of Mosul
Mechanisms Of Diseases Due To Vascular Pathology narrowing or complete obstruction of the lumen weakening of the wall leading to dilation or rupture
Types Of Vessels Based On Their Size And Structure
large or elastic arteries medium-sized or muscular arteries small arteries (less than 2mm in diameter) arteriolesArteriosclerosis
Hardening of blood vessels (Thickening & loss of elasticity of arterial wall)Three patterns depend on blood vessels size:1-Atherosclerosis (atheroma): large blood vessels affected2-Monkeberg’s arteriosclerosis (medial calcific sclerosis): medium-sized blood vessels affected3-Arteriolosclerosis: small-sized blood vessels affectedHyaline arteriolosclerosisHyperplastic arteriolosclerosisMonkeberg’s arteriosclerosis Characterized by focal calcification in the media of small to medium-sized muscular arteries, typically arteries of neck, upper & lower limbs & genitalia It characterized by affect old age group of little clinical significance with radiological curiosity
Hyaline arteriolosclerosis
Characterized by diffuse, pink, hyaline thickening of arteriolar wall Occurs typically in Elderly patients Diabetics Mild chronic hypertensionEffect Associated with lumonal narrowing causing ischemia afferent & efferent arterioles in kidneys causing benign nephrosclerosis
Hyperplastic arteriolosclerosis
Concentric laminated (onion skin) arteriolar thickening with reduplicated basement membrane & smooth muscle cells proliferation Characteristic of malignant hypertension Leads to luminal narrowing Frequently associated with fibrinoid necrosis (necrotizing arteriolitis)Atherosclerosis
A disease of large & medium-sized muscular & elastic arteries. Characterized by intimal thickening due to the presence of patches or plaques of fibrous tissue, smooth muscle fibers & lipid A disease of elderly people Leads to narrowing of vessels or complete occlusionNatural history and main consequences the lesion is divided into 6 stages -fat dots -fatty streak -intermediate -atheroma -fibroatheroma -complicated atheroma
Morphology of atherosclerosis Gross: Raised, irregular, yellowish-white plaques up to several cm. Lesion coalesce to form map-like confluent lesions. Consists of 2 parts: a white superficial thick cap & a soft yellow center (atheromatous or fibrofatty plaque) Either lipid rich, fibrofatty or fibrous plaque
Fat Streak
Aorta, mild atherosclerosisAorta, severe atherosclerosis
Complicated Atherosclerosis
Histology: Cells: SM cells, foamy macrophages & few lymphocytes Connective tissue fibers & matrix Lipid core & cholesterol clefts New blood vesselsAorta, fatty streak
Components of atheromaDistribution of plaques Lower abdominal aorta (esp. posterior surface) Coronary artery Descending thoracic aorta, Popliteal artery Internal carotid artery Circle of Wills Vessels of upper extremities are spared
Risk Factors associated with AS
1// Constitutional (non modifiable) factors 1- Age: 40-60 year there is 5 times increase in myocardial infarction 2-Sex: less in pre-menopause (due to effect of estrogen). Whereas female at 70 year M=F 3-Familial predisposition: derangement in lipoproteins result in high blood lipid level2// Acquired (modifiable) factors 1- Hyperlipidemia: most important factor before 45 years Low density lipoprotein +++ association Very low density lipoprotein + association 2- Hypertension: More important than hyperlipidemia after the age of 45 years In male between 42-60 with bl pr 160/95 has 5 times myocardial infarction than person with 140/90 bl pr
3-Smoking: 1 packet/day for years increase myocardial infarction by 2-3 times 4-Diabetes: 2 times increase in myocardial infraction 100-150 times increase in gangrene Stroke increase by ++
3// Soft risk factors Decrease physical activity Type A personality Obesity Oral contraceptive Hyperuricaemia High carbohydrate intake Alcohol Unsaturated fatty acid (hardened fat) Chlamydial pneumonia AS may develop in absence of known RFs
Pathogenesis of atherosclerosis
Reaction to injury hypothesisReaction to injury hypothesis
Smoking HypercholestEndothelial injury Diabetes Hypertension
1- Increase permeability to lipoprotein lipid in intima 2- Adherence of platelets & monocytes macrophage & foamy cells 3- Release of chemotacting & growth F migration & prol of SM
Complication of atheromatous plaques
1- Ulceration or fissuring: result in Thrombosis Thromboemboli Microemboli of atheromatous materials 2- Hemorrhage: result in Narrowing Occlusion 3- Medial atrophy: result in aneurysm 4- Dystrophic calcification: cause loss of elasticityEffects of atherosclerosis
1- Aorta Thrombosis Emboli formation Aneurysm Narrowing of ostia of aortic branches 2- Smaller arteries (coronary, cerebral, popliteal) Narrowing: result in ischemia Narrowing & thrombosis: result in ischemic necrosis Hemorrhage in plaque: result in ischemic necrosisAneurysm localized abnormal dilation (saccular or fusiform) of blood vessels or the wall Classified into -True -False Causes -atherosclerosis -congenital -trauma -infection -inflammation
Aneurysms
Abdominal Aortic Aneurysm (AAA) most frequently due to atherosclerosis rare before the age of 50 years, more common in males positioned between renal arteries origin and bifurcation of aorta either saccular or fusiform up to 15cm in diameter and 25cm in lengthAbdominal aortic aneurysm
Clinical Course rupture (related to size) obstruction of blood vessels embolism pressure on adjacent structures abdominal massAortic Dissection catastrophic illness characterized by -dissection of blood between the laminar planes of the media -formation of a blood filled channel within the aortic wall which often ruptures either outward or into the lumen with second distal tear affects 2 groups of patients -hypertensive men of 40-60y of age -young people with systemic or localized abnormality of connective tissue
morphology transverse or oblique intimal tear within 10cm of aortic valve 1-5cm in length dissection extends proximally and distally the hematoma is between the middle and outer thirds of the wall histology, cystic medial degeneration
Aortic dissection
pathogenesistrigger for intimal tear once the tear has occurred, increased systemic blood pressure maintains progression of the medial hematoma This condition occurs in 2 settings iatrogenic as a complication of arterial cannulation rarely during pregnancy
Vasculitis
Inflammation of the wall of the blood vessels either Localized systemic It result in fever, myalgias, malaise, arthralagia +/- skin rash Two common mechanisms of vasculitis 1- Immune mediated inflammation 2-Direct invasion of vascular wall by infectious agents 3-Others: Physical (radiation) & chemical injuries1- immune mediated inflammation immune complex cell mediate ANCA mediate direct antibodies mediate injury 2- direct invasion by infectious agents bacteria (Neisseria) fungal (Aspergillous) viral (CMV, HSV) Rickettsia
Classification of vasculitis
classification depends on -size and anatomic site of involved vessel -histology of involved vessel -clinical manifestation1- large vessels vasculitis
1- Giant cell (temporal) arteritis 2-Takaysu arteritis (pulseless disease)1-granulomatous arthritis of aorta 2-most common arteries involved are (temporal, ophthalmic, aorta) 3-pt > 50 years 4-female > male 5-high ESR 6-ass with polymyalsia rheumatica 1- granulomatous inflammation of aortic arch and its branches 2- pt < 50 years 3- female > male 4- orifice of subclavian artery mostly affected 5-lower blood pressure and weaker pulses of upper extremities compared to lower extremities
Takayasu arteritis, aortic arch, carotid artery
2- Medium-sized vasculitis1- Polyarteritis nodosa
1-segmental, focal & transmural necrotizing infl of medium-sized blood vessels 2-affecting all organs except lungs 3- not causing glomerulonephritis 4-male > female affected 5-all stages from acute necrotizing inflammation to chronic healing sclerotic stage can be seen at the same time, even within the same vessels 6-60% associated with ANCA
2- Medium-Sized vasculitis
2-Kawasaki disease
3/ Small-Sized Vasculitis
1-Wegener granulomatosis1-necrotizing infl affecting small to medium-sized blood vessels 2-granulomatous infl of upper & lower respiratory tract 3-necrotizing glomerulonephritis 4-male > female affecting 5-peak 5th decade 6-90 % associated with ANCA
Wegener granulomatosis, granulomatous vasculitis, lung with cavitating lesions
3/ Small -Sized Vasculitis2-Microscopic polyarteritis 3-Churg-strauss Syndrome
3/ Small -Sized Vasculitis
necrotizing eosinophilic vasculitis accompanied by granulomas has strong association with -allergic rhinitis -bronchial asthma -eosinophiliaThrombo Angiitis Obliterans (Buerger Disease) segmental thrombosing acute and chronic inflammation of medium-sized and small arteries (tibial and radial) with secondarily involvement of the adjacent veins and nerves starts in patients younger than 35y relationship to cigarette smoking -direct toxicity -hypersensitivity
Thromboangitis obliterans
Primary Raynaud Phenomenon paroxysmal pallor or cyanosis of the digits (hands, feet), the tips of the nose or ears, owing to cold-induced vaso- constriction of arteries, precapillary arterioles and cutaneous artero-venous shunts median age is 14 years the course is benign
Raynaud’s phenomenon Raynaud’s phenomenon
Secondary Raynaud Phenomenon arterial insufficiency of the extremities caused by various conditions -SLE -systemic sclerosis -atherosclerosis -Buerger diseasePathology of Veins
Varicose veins abnormally dilated, tortuous veins due to increase intraluminal pressure & loss of tissue support to their walls A common condition the majority are without symptoms Risk factors: Age, female sex, obesity, posture, hereditary, pregnancy, increase venous pressure veins show variation in wall thickness edema, pain, stasis dermatitis, ulcers, emboliPathology of lymphatics
Pathology of lymphatics Lymphangitis: infection of lymphatics draining a focus of infection usually by group A beta hemolytic strept Lymphedema Secondary; postinflammatory tumors surgery radiation Primary (congenital)Tumors of blood vessels
Benign tumorsHemangiomacapillary, cavernous & pyogenic granulomaGlomus tumor (glomangioma)Intermediate gradeHemangioendotheliomaMalignant tumorsAngiosarcoma, Hemangiopericytomakaposi’s sarcoma
Capillary Hemangioma: Usually in skin & mucus membrane Size few mm to several cm in diameter Grossly may be muscular, papular or pedinculated Histology: unencapsulated, lobulated closely packed capillaries separated by connective tissue stroma
Cavernous Hemangioma Often occurs in skin & mucosal surfaces, also in viscera e.g., liver, spleen & pancreas May be large in infants (birth mark or port wine nevus) Red-blue compressible spongy lesions 2-3 cm Histology: large, irregular endothelium lined spaces some filled with blood
Hemangioma
Kaposi SarcomaIt is intermediate-Grade (Borderline) Tumors Kaposi sarcoma (KS) is a vascular neoplasm caused by Kaposi sarcoma herpesvirus (KSHV, also known as human herpesvirus-8, or HHV-8). Although it occurs in a number of contexts, it is by far most common in patients with AIDS;
kaposi sarcoma
AngiosarcomaIt is malignant tumor of blood vessels Seen in skin (sun exposed areas), soft tissue, breast, liver & spleen Liver angiosarcoma is associated with polyvinyl chloride & thorotrast Histology: anastomosing blood vessels Metastasize widely & usually fetal