The wall of this intramyocardial coronary artery is thickened and the lumen is narrowed due to abundant deranged muscle and fibrous tissue.
<ul><li>MOST IMPORTANT DISEASES OF BLOOD VESSELS </li></ul><ul><li>Arteriosclerosis & atherosclerosis. </li></ul><ul><li>Vasculitis. </li></ul><ul><li>Varicose veins,thrombophlebitis </li></ul><ul><li>Vascular tumors </li></ul><ul><li>Arteriosclerosis: is thickening and hardening of arterial wall. it affect small arteries and arterioles. </li></ul><ul><li>Morphological types of arteriosclerosis. </li></ul><ul><li>Senile </li></ul><ul><li>Hypetensive. </li></ul>
<ul><li>Monckeberg’s(medial calcific sclerosis) </li></ul><ul><li>Atherosclerosis. </li></ul><ul><li>Hypertensive arteriosclerosis. </li></ul><ul><li>Two morphological disease affecting arterioles and small muscular arteries. </li></ul><ul><li>Hyaline Arteriosclerosis. Occur physiologically in aging pathologically in benign hypertension and DM. </li></ul><ul><li>PATHOGENESIS . Increased protein is deposit in vessel wall leakage of plasma across the vascular endothelium. </li></ul><ul><li>Pathological changes: visceral arteries are particularly involve. The vascular wall thickened and Lumina narrowed or even obliterated. </li></ul><ul><li>Micro : thickened vessel show homogenous pink hyaline material </li></ul>
Hyaline arteriolosclerosis, which can be seen in patients with diabetes mellitus and with hypertension. This glomerulus stained with PAS shows nodular deposits of amorphous material (nodular glomerulosclerosis) along with a thickened arteriole at the lower right.
<ul><li>Hyperplastic arteriosclerosis: is a feature of malignant hypertension, hemolytic uremic syndrome ‘scleroderma & toxemia of pregnancy. </li></ul><ul><li>Pathology: the morphological changes affect mainly the intima esp the interlobular arteries in kidneys. Three types of intimae thickening occurs . </li></ul><ul><li>Onion skin lesion : consist loosely placed concentric layer of hyperplasic intimal smooth muscle cells. The basement membrane also thickened and reduplicated. They are accompanied by fibrinoid deposits and vessel </li></ul>
This is hyperplastic arteriolosclerosis, which most often appears in the kidney in patients with malignant hypertension. The arteriolar wall is markedly thickened and the lumen is narrowed.
Sometimes the small arteries and arterioles can be damaged so severely in malignant hypertension that they demonstrate necrosis with a pink fibrin-like quality that gives this process its name--fibrinoid necrosis.
<ul><li>Wall necrosis necrotizing arteriolitis esp in kidney </li></ul><ul><li>Mucinous intimal thickening: deposition of amorphous ground substance, proteoglycans, with scanty cell. </li></ul><ul><li>Fibrous intimal thickening is less common consist bundle of collagen fiber and hyalin deposit in intima </li></ul><ul><li>Monckeberg medial sclerosis ; charec by calcific deposits in muscular arteries in person typically older than 50yrs. The deposit may under go metaplastic </li></ul><ul><li>change in bone. Deposition of calcium salt in media with out associated inflammation </li></ul>
Monckeberg's medial calcific sclerosis, which is the most insignificant form of arteriosclerosis (both atherosclerosis and arteriolosclerosis are definitely significant). Note the purplish blue calcifications in the media;
Atherosclerosis is a disease of the arteries in which fatty material is deposited in the vessel wall, resulting in narrowing and eventual impairment of blood flow. Severely restricted blood flow in the arteries to the heart muscle leads to symptoms such as chest pain. Atherosclerosis shows no symptoms until a complication occurs. atherosclerosis
ATHEROSCLEROSIS <ul><li>Atherosclerosis is a slow, complex disease in which fatty substances, cholesterol, cellular waste products, calcium, and other substances build up – called plaque - in the inner lining of an artery. . </li></ul><ul><li>Atherosclerosis is the pathological process in the coronary arteries, cerebral arteries, iliac and femoral arteries, and aorta that is responsible for coronary heart disease (CHD), stroke, and peripheral arterial disease (PAD). </li></ul>
<ul><li>Lipoprteins are spherical particles composed of apoprotein,phospholipid, cholestrole , cholestrole ,easters and triglycerides </li></ul><ul><li>Chylomicrons transport dietary triglycerides and cholesterol from the intestine to the liver, and carry triglycerides to adipose tissue and muscle. (Triglycerides are an important source of energy for muscle and many other tissues.) </li></ul><ul><li>Require apolipoproteinB-48 for assembly and secretion </li></ul><ul><li>VLDL transports cholesterol and triglycerides that have been synthesized in the liver to muscle and adipose tissues. After triglycerides are removed from VLDL, the molecule is converted into cholesterol rich LDL. </li></ul><ul><li>Require apolipoprotein B-100 for assembly and secretion </li></ul><ul><li>LDL binds to LDL receptors found on many cells in the body (including endothelium) and delivers cholesterol to various tissues. </li></ul><ul><li>HDL is a cholesterol scavenger. It removes excess cholesterol from tissues, gets re-converted to LDL, and returns cholesterol to the liver where it is excreted in bile. </li></ul>Lipoprotein metabolism
The risk factors for atherosclerosis are diagrammed here in relation to the mechanisms that favor development of arterial atheroma formation.
<ul><li>PATHOGENESIS: </li></ul><ul><li>Endothelial cell damage of muscular and elastic arteries. </li></ul><ul><li>Lesion progress through interaction of modified lipoproteins, monocytes derived macrophages and T lymphocytes. </li></ul><ul><li>Following are pathogenic events: </li></ul><ul><li>Endothelial injury: </li></ul><ul><li>Accumulation of lipoproteins (LDL & its oxidized form) </li></ul>
<ul><li>Monocytes adhesion to endothelium tranform into foam cells </li></ul><ul><li>Platelet adhesion </li></ul><ul><li>Smooth muscle cell recruitment. </li></ul><ul><li>Lipid accumulation both intra & extra cellular </li></ul>
Sequence of cellular interaction in atherosclerosis
MORPHOLOGY OF ATHEROSCLEROSIS <ul><li>The key process is intimal thickening and lipid accumulation </li></ul><ul><li>Early AS : Fatty Streaks are earliest lesion occur at sites of altered arterial shear, and associated with abnormal endothelial function. They developed when inflm cell spec. Monocytes bind to recepter express by endothelial cell, migrate into intima take up oxidized LDL from plasma and become lipid laden foam cell or macrophages. Extra cellular lipid appear in intimal spaces when foam cells die and release their contents. </li></ul>
<ul><li>In response to cytokines and growth factor activated macrophages, smooth muscle cell migrate from media of arterial wall into intima. Fatty streak either disappear or may lead to atheromatous plaques. </li></ul><ul><li>Grossly: lesion may appear as flat or slightly elevated & yellow . </li></ul><ul><li>Microscopically. Lying under the endothelium and composed closely – packed foam cells lipid containing smooth muscle cells few lymphocytes and ECM. </li></ul>
The pale yellow lipid streaks in the aorta are the earliest lesion of atherosclerosis.
Three aortas are shown to demonstrate mild, moderate, and severe atherosclerosis from bottom to top.
This is mild coronary atherosclerosis. A few scattered yellow lipid plaques are seen on the intimal surface of the opened coronary artery traversing the epicardial surface of a heart. The degree of atherosclerosis here is not significant enough to cause disease, but could be the harbinger of worse atherosclerosis to come.
The plaques are formed of 1- Central core of cholesterol and cholesterol esters, lipid laden macrophages (foam cells), necrotic debris and calcification. 2- Subendothelial fibrous cap formed of proliferated smooth muscle cells, foam cells and extra cellular matrix
<ul><li>Advance AS : in an established plaque macrophage mediate inflm and smooth muscle cell promote repair. Cytokine such as TNF α IFN γ PDGF and MMP release by activated macrophages, and may cause the intimal smooth muscle cell over lying the plaque to become weak resulting in thinning of protective fibrous cap they may also digest collagen with in the plaque. These changes make the lesion vulnerable to the effect of mechanical stress and may lead to erosion, fissuring or rupture the plaque surface. </li></ul><ul><li>Most often and most sever affected is abdominal aorta. </li></ul>
<ul><li>There are two types of plaque: </li></ul><ul><li>Vulnerable plaque; are charect. by lipid rich core, a thin fibrocellular cap, an increase in inflam. Cells </li></ul><ul><li>and release specific enzyme that degrade matrix protein. </li></ul><ul><li>Stable plaque; have small lipid pool, thick fibrous cap, calcification and plentiful collagenous fibers </li></ul><ul><li>Grossly : atheromatous plaque are white to yellowish- white lesions, varying in diameter from 1-2cm and raised on surface from few mm to cm in thickness </li></ul><ul><li>Cut section show firm white fibrous cap and central core contain soft porridge like material. </li></ul>
Grossly - Multiple irregular patches more around ostea of branches. - Color ranges from yellow to white according to relative amount of fat and fibrous tissue. - Covered by glistening intima (if not complicated)
<ul><li>Microscopically: </li></ul><ul><li>the superficial part of fibrous cap cover by endothelium composed of smooth muscle cells (SMC) </li></ul><ul><li>dense connective tissue & ECM . </li></ul><ul><li>the cellular area under the fib cap comp macrophages, foam cells, lymphocytes few SM which contain lipid. </li></ul><ul><li>The dipper central soft core contain EC lipid material,cholestrol cleft, fibrin, necrotic debris and lipid-laden macrophages. </li></ul>
Normal coronary artery with no atherosclerosis thrmbus
At higher magnification, many foam cells (macrophages full of lipid material) and a cholesterol cleft are seen in this atheromatous plaque. The plaque contains amorphous pink material with slit-like "cholesterol clefts" of lipid material. There is overlying recent hemorrhage at the left. Thrombus may form on top of such a plaque.
This is the gross appearance of severe coronary atherosclerosis, which involves virtually 100% of the surface of this coronary artery. There is extensive calcification, especially at the right where the lumen is narrowed. Calcification
The degree of atherosclerosis is much greater in this coronary artery, and the lumen is narrowed by half. A small area of calcification is seen in the plaque at the right.
Here is a coronary artery with atherosclerotic plaques. There is recent hemorrhage into the plaque. This is one of the complications of atherosclerosis. Such hemorrhage could acutely narrow the lumen and produce an acute coronary syndrome with ischemia and/or infarction of the myocardium. Hemorrhage
Thrombosis of the coronary artery Thrombosis on top of atheroma of the coronary artery
<ul><li>Complications of atherosclerosis </li></ul><ul><li>1- Narrowing of vascular lumen…chronic ischemia. </li></ul><ul><li>2- Superimposed thrombosis…acute ischemia. </li></ul><ul><li>3- Ulceration with liberation of fatty core … acute ischemia, fat emboli, DIC. </li></ul><ul><li>4- Pressure atrophy of the media with fibrosis….weakening of the wall …. Aneurysmal dilatation. </li></ul><ul><li>5- Dystrophic calcification. </li></ul>
DIAGNOSIS <ul><li>A weak or absent pulse below the narrowed area of the artery * Decreased blood pressure in an affected limb * Whooshing sounds (bruits) over the arteries, heard with a stethoscope * Signs of a pulsating bulge (aneurysm) in the abdomen or behind the knee * Evidence of poor wound healing in the area where the blood flow is restricted </li></ul>
<ul><li>* ANGIOGRAPHY –a tube-like instrument is inserted into an artery through which dye is injected to help determine the degree of blood flow. When done in the heart, this test is called Cardiac Catheterization. * ULTRASOUND –a test that uses sound waves to examine the inside of the body, in this case the size and shape </li></ul>
<ul><li>Treatment may include: MEDICATIONS * Drugs to interfere with the formation of blood clots, such as Aspirin or Clopidegril (Plavix) </li></ul><ul><li>Statins is class of drug inhibit HMG-CoA reductase * Drugs to control blood pressure , if elevated * Drugs to lower cholesterol , if elevated * Drugs that improve the flow of blood through narrowed arteries, such as Cilostazol (Pletal) or Pentoxifylline (Trental) </li></ul>
<ul><li>CATHETER-BASED PROCEDURES * BALLOON ANGIOPLASTY – * STENTING – usually done after angioplasty; a wire mesh tube is placed in a damaged artery to support the arterial walls and keep them open. * ATHERECTOMY – </li></ul><ul><li>SURGERY ENDARTERECTOMY </li></ul><ul><li>ARTERIOPLASTY – </li></ul><ul><li>BYPASS </li></ul>
Aneurysm. <ul><li>Aneurysm. </li></ul><ul><li>a localised abnormal dilatation of blood vessels or the heart .When it invove intact attenuated atrial wall or thinned ve ntricle wall of heart called true aneurysm. </li></ul><ul><li>Pseudo aneurysm are </li></ul><ul><li>activated hematomas or abscessf ormed due to rupture in the wall of artery the lumen of Pseudo aneurysmare communicate with the lumen of artery through vessel wall defect. Afibrous capsule may formed. </li></ul><ul><li>Aneurysm. May classieied as </li></ul><ul><li>Fusiform </li></ul><ul><li>Cylendroidor tubular </li></ul><ul><li>saccular </li></ul><ul><li>Berry. </li></ul>
AORTIC DISSECTION <ul><li>AD result from forceful separation of layer of aortic wall due to entry of blood b/w the layers. It result from tear in intima the allow the blood to penetrate into vessel wall and produce hematoma dissecting b/w intima and media or media and adventitia or through the layer of media. </li></ul><ul><li>CAUSES: Atherosclerosis. </li></ul><ul><li>Hypertension </li></ul><ul><li>Marfan syndrome </li></ul><ul><li>Ehlers-danlos syndrome or osteogenic imperfecta </li></ul>
Vasculitis <ul><li>Vasculitis means inflammation of blood vessels. The effects of vasculitis depend on the sizes of the blood vessels that are affected and on the parts of the body involved. </li></ul><ul><li>Vasculitis may have any cause but most often immunological mediated </li></ul>
Giant cell arteritis <ul><li>Granulomatous lage vessel vasculitis invoving </li></ul><ul><li>Age adult greater than 50yrs </li></ul><ul><li>Pahtogenesis: Tcell mediat immune response against vessel wall antigen </li></ul><ul><li>Morphology. Involve arterial seg ment develop nogular intimal thickening that reduce lumenal diameter </li></ul><ul><li>Medial granulomatous inflam lead to elastic lamina fragmentation. </li></ul><ul><li>Infiltration of T-cell. Multinucleated giant cell present </li></ul>
Temporal Arteritis This figure is a high power view of a biopsy of a temporal artery in a subject with temporal arteritis. The black arrow demonstrates the endothelium with red blood cells in the intravascular space. The endothelium shows pathologic changes with edema and a proliferative subintimal response. The yellow arrow points out the disrupted elastic lamina and the blue arrow a granuloma typical of this form of large vessel vasculitis.
Takayasu’s disease <ul><li>Granulomatous large and medium vessel vasculitis involve aortic arch vessels. and </li></ul><ul><li>Occular disturbance & marked weakining of pulse in upper extremities </li></ul><ul><li>Occur in young Asian women and children. </li></ul><ul><li>Histological changes show advetitia mononuclear infiltarion with perivascular cuffing of vasavasorum. </li></ul><ul><li>Granulomatous inflam,giant cell formation and patchy media necrosis </li></ul>
Takayasu’s arteritis showing fibrosis in all the layers of the vessel wall and markedly thickened intima (arrow)
Kawasaki Disease <ul><li>Kawasaki disease is a generalized vasculitis of unknown etiology that has also been called mucocutaneous lymph node syndrome and infantile periarteritis nodosa. </li></ul><ul><li>Pathophysiology: The vasculitis is most severe in medium-sized vessels, including the renal, paraovarian, paratesticular, mesenteric, pancreatic, iliac, hepatic, splenic, and axillary arteries, resulting in systemic aneurysms. </li></ul><ul><li>In severely affected vessels, the media develops inflammation with necrosis of smooth muscle cells. can split </li></ul>
<ul><li>The internal and external elastic laminae , can split leading to aneurysms. </li></ul><ul><li>The intima proliferates and thickens. The vessel wall eventually becomes narrowed or occluded owing to stenosis or a thrombus. Cardiovascular death usually occurs from a myocardial infarction secondary to thrombosis of a coronary aneurysm or from rupture of a large coronary aneurysm. </li></ul>
Oral manifestations of Kawasaki disease: red lips and strawberry tongue.
Small coronary artery with segmental necrosis and inflammation in a patient with Kawasaki disease. Small coronary artery with segmental necrosis and inflammation in a patient with Kawasaki disease.
Polyarteritis Nodosa <ul><li>Polyarteritis nodosa is a serious blood vessel disease in which small and medium-sized arteries become swollen and damaged. </li></ul><ul><li>Causes </li></ul><ul><li>Polyarteritis nodosa is a disease of unknown cause that affects arteries, the blood vessels that carry oxygenated blood to organs and tissues. It occurs when certain immune cells attack the affected arteries. </li></ul><ul><li>More adults than children get this disease. It damages the tissues supplied </li></ul>
Thrombosed pseudoaneurysm in the pancreas of a patient with polyarteritis nodosa Renal involvement by polyarteritis nodosa. Note dark thrombosed pseudoaneurysms and pale peripheral infarc
Thromboangitis obliterans (Buerger's disease ) <ul><li>Thromboangiitis obliterans is a rare disease in which blood vessels of the hands and feet become obstructed. </li></ul><ul><li>Occur in young 20-30 yrs male smokers. </li></ul><ul><li>Charect affect the peripheral arteries and giving rise to claudication in feet and rest pain in finger and toes </li></ul>
Necrotizing granulomatous inflammation in the lung of a patient with Wegener's granulomatosis
Churg-Strauss Vasculitis <ul><li>Churg- strauss syndrome is relatively rare small-vessel necrotising vasculitis. </li></ul><ul><li>Effect children and adult </li></ul><ul><li>classically associated with asthma, allergic rhinitis, lungs infiltrate , peripheral hypereosinophlia and extra vascular grnulomas. </li></ul><ul><li>Most often myeloperoxidase ANCA is present. </li></ul>
Churg-Strauss Vasculitis The figure is a high power view of hematoxylin and eosin stained skin biopsy in a subject with Churg-Strauss vasculitis. The small blood vessel demonstrates findings of perivascular eosinophil infiltration (black arrows) of a small blood vessel wall, indicated by the white arrow head. These findings are similar to hypersensitivity vasculitis except for the predominance of eosinophils and involvement of both arterioles and venules.
Necrotizing and granulomatous arteritis in the lung of a patient with Churg-Strauss syndrome
Necrotizing glomerulonephritis with a cellular crescent, which may occur as a component of microscopic polyangiitis and other forms of small-vessel vasculitis.
Hypersensitivity Vasculitis This figure shows a low power view of hemotoxylin and eosin stained skin biopsy in a subject with hypersensitivity vasculitis. The biopsy demonstrates leukocytoclastic vasculitis. The black arrows point to small blood vessels in the subcutaneous tissue with perivascular leukocytes. A high power view would show blood cell extravasation and nuclear debris from lysed white blood cells (nuclear dust).
Raynaud's Disease <ul><li>Raynaud's disease and Raynaud's phenomenon are rare disorders that affect blood vessels. These disorders are marked by brief episodes of vasospasm (narrowing of the blood vessels). Vasospasm causes decreased blood flow to the fingers and toes, and rarely to the nose, ears, nipples, and lips. The fingers are the most commonly affected area, but the toes also are affected in 40 percent of people with Raynaud's. </li></ul>
<ul><li>When this disorder occurs without any known cause, it is called Raynaud's disease, or primary Raynaud's. When the condition occurs along with a likely cause, it is known as Raynaud's phenomenon, or secondary Raynaud's. Primary Raynaud's is more common and tends to be less severe than secondary Raynaud's. </li></ul><ul><li>When you have primary or secondary Raynaud's, cold temperatures or stressful emotions can trigger attacks. </li></ul>
<ul><li>During these attacks, there is a brief lack of blood flow to the affected body part(s), and the skin can temporarily become white then bluish. As blood flow returns to the area, the skin turns red. The affected areas can throb or feel numb and tingly. With severe Raynaud's, prolonged or repeated episodes can cause sores or tissue death (gangrene). </li></ul>
Massive pulmonary hemorrhage in a patient with Goodpasture's syndrome.
Esophageal varices with prominent red wale spots.
VARICOSE VEINS <ul><li>Vricose veins are abnormally dilated tortous veins produced by prolong, increase intraluminal pressure and loss of vessel wall spport. </li></ul><ul><li>The superficial veins of upper and lower legs are typically involved. </li></ul><ul><li>Risk Factors: Age Family history Female gender Pregnancy, especially multiple pregnancies, is one of the most common factors accelerating the worsening of varicose veins. </li></ul>
Sinusoidal hemangioma. The vascular spaces are widely dilated.
HEMANGIOMA <ul><li>Hemangiomas are benign vascular tumor-like growths that usually present themselves at birth or soon thereafter. The abnormal dense collections of blood vessels may occur in the muscles, internal organs, and mucous membranes, but are most familiar along the surface of the skin. Hemangiomas of the skin are usually classified into three basic groups: capillary hemangiomas, immature hemangiomas, and cavernous hemangiomas. </li></ul>
Syphilitic Lymphadenitis Lymph Node in Secondary Syphilis : Newly formed blood vessels in the capsular and pericapsular regions show endothelial swelling and perivascular cuffs of plasma cells and lymphocytes. Prominent vasculitis is an important diagnostic clue in secondary syphilis