Cardiovascular Pathology 1:
Blood Vessels
Jonalyn Mendez, M.D.
Cardiac Pathology Outline
Blood Vessels Blood
Heart
Normal blood vessel
Normal Blood Vessels
Large (elastic) arteries aorta, common carotid, iliac lots of elastic fibers pulsatile
Medium (muscular) arteries coronary, renal arteries mostly smooth muscle cells Small arteries/arterioles all smooth muscle cells blood pressure controlled here
Normal Blood Vessels
Capillaries diameter of RBC tons of them, with thin walls, slow flow great for exchanging oxygen, nutrients Venules/veins large diameter, thin walls compressible, penetrable by tumor valves Lymphatics drain excess interstitial fluid pass through nodes, checking for
infection
Atherosclerosis
> Disease of large and medium-sized arteries that results in the progressive accumulation within the intima of smooth muscle cells, lipids and connective tissue
Characterized by atheromas
Half of deaths in US!
Coronary artery disease (MI) Carotid atherosclerotic disease (stroke)
Atherosclerosis: Major Risk Factors
Non-modifiable Increasing age Gender Family history Genetic abnormalities Potentially modifiable
Hyperlipidemia Hypertension Cigarette smoking Diabetes
Atherosclerosis: Lesser Risk Factors
Obesity Physical inactivity Stress
Postmenopausal estrogen deficiency
High carbohydrate intake Lipoprotein (a)
Trans-fat intake
Chlamydia pneumoniae infection
How to Make an Atheroma
Chronic endothelial injury
How to Make an Atheroma
Endothelial dysfunction Monocyte adhesion and emigration
How to Make an Atheroma
Macrophage activation Smooth muscle recruitment
How to Make an Atheroma
Macrophages and smooth muscle cells engulf lipid
How to Make an Atheroma
Smooth muscle proliferation Collagen and extracellular lipid deposition
Contents of a plaque
Natural history of atherosclerosis
Prevention of Atherosclerosis
Primary prevention Lessen risk factors Secondary prevention
Aspirin, statins, beta blockers
Surgery
Hypertension
Common problem (25% of population) Assymptomatic until late Contributes to coronary artery disease,
stroke, cardiac hypertrophy, heart failure
Mechanisms largely unknown - called
essential hypertension
>140/90
Hypertension: Types
Benign hypertension
Essential (idiopathic) hypertension Secondary hypertension
Malignant hypertension
Essential Hypertension
Idiopathic! But probably related to
- Reduced renal sodium excretion - Vascular changes - Genetic factors - Environmental factors
Essential Hypertension
Accelerates atherogenesis Potentiates aortic dissection and stroke Causes small blood vessel disease:
Cardiac Pathology Outline
Blood Vessels
Atherosclerosis Hypertension Aneurysms
Aneurysms
Aneurysm: localized abnormal vessel dilation True aneurysm: involves all three layers
False aneurysm: hole covered with hematoma
True and false aneurysms
Aneurysms: Causes
Atherosclerosis Cystic medial degeneration of wall Trauma Congenital defects (berry aneurysm) Infection (mycotic aneurysms)
Abdominal Aortic Aneurysm
Males >50 Atherosclerosis Below renal arteries, above bifurcation May present as pulsating abdominal mass May rupture, obstruct branches or embolize
Aortic Dissection
Blood tracks up through media, creating a
channel Hypertensive men, 40-60 (most cases) Sudden onset excruciating pain Can rupture massive hemorrhage or cardiac tamponade Rapid diagnosis, surgery = 65-75% of patients survive
Cardiac Pathology Outline
Blood Vessels
Atherosclerosis Hypertension Aneurysms Vasculitis
Vasculitis
Inflammation of vessel walls Many possible symptoms Constitutional signs/symptoms common Immune-mediated or infectious
Summary of Vasculitides
Vessel Large Disease Giant-cell arteritis Takayasu arteritis Polyarteritis nodosa Kawasaki disease Wegener granulomatosis Small Churg-Strauss syndrome Microscopic polyangiitis >50. Arteries of head. F <40. Pulseless disease Young adults. Widespread. Coronary disease. Lymph nodes. Lung, kidney Lung. Eosinophils. Asthma. Lung, kidney.
Medium
Giant-Cell (Temporal) Arteritis
Most common type of vasculitis Patients >50 Chronic, granulomatous inflammation of
large to small arteries, especially in head Symptoms vague (fever) or localized (headache, vision loss) Treatment: corticosteroids
Takayasu Arteritis
Women <40 Granulomatous vasculitis of aortic arch Severe narrowing of major branches Weakening of pulses in upper
extremities (pulseless disease) Ocular disturbances
Polyarteritis Nodosa
Young adults Necrotizing vasculitis in many different organs Different stages coexist even in same artery Puzzling, varied symptoms Fatal if untreated, but steroids and
cyclophosphamide are curative
Kawasaki Disease
Children <4 Acute, febrile, usually self-limiting Danger: involvement of coronary arteries)
Mucocutaneous lymph node syndrome
Delayed-type hypersensitivity reaction? Treatment: intravenous Ig
Wegener Granulomatosis
Most common age = 40s Triad: respiratory tract granulomas, vasculitis, renal
disease T-cell mediated hypersensitivity response Untreated: fatal in 1 year Churg-Strauss: similar, but associated with allergies and asthma, and no renal disease
Microscopic (Leukocytoclastic) Polyangiitis
Widespread, necrotizing vasculitis of smaller
vessels Lung and kidney especially Antibody response to drugs or bugs Neutrophils in vessels Type III hypersensitivity reaction? Removing offending agent usually works
Cardiac Pathology Outline
Blood Vessels
Atherosclerosis Hypertension Aneurysms Vasculitis Tumors
Hemangioma
Very common benign tumor of blood vessels Capillary hemangioma Skin, oral mucosa, sometimes organs Strawberry type present at birth, regresses Cavernous hemangioma Organs, sometimes skin Cosmetic problem (unless in brain) Pyogenic granuloma Rapidly growing red nodule on skin, in mouth Microscopically resembles granulation tissue
Glomus tumor
Benign but very painful Arise from glomus body cells Distal digits, especially under fingernails Excision is curative
Kaposi Sarcoma
Low-grade malignancy of endothelial cells Four forms: Chronic (older Ashkenazi
Jewish males), African, transplantassociated, AIDS-associated Clinical course varies (chronic = best) Excision can be curative
Angiosarcoma
Malignancy of endothelial cells
Prefers skin, soft tissue, breast, liver Arsenic and PVC increase risk Well-differentiated to anaplastic Metastasize rapidly. 5ys 30%.
Vascular Occlusion (arterial/venous)
Vascular Occlusions depends on: Type of tissue involved How quickly the occlusions develops Availability of collateral circulation
Results: Thrombosis Embolism Artherosclerosis External compression Spasm
THROMBOSIS Arterial
Middle aged and elderly Common: with artherosclerosis Common risks: smoking and DM
Venous
Any age Immobile or forced to be immobilized(post operative) Complains of pain on calf muscle &swelling of the foot and ankle
Thrombus Formation (Rudolf Ludwig Karl Virchow) Formation depends on: Alteration of the constituent of the blood Damage to the endothelial layer of the Blood vessel Changes in the normal flow of the blood Virchow triad 3 main components platelets soluble blood proteins of the coagulation pathway Vessel Wall
CRUCIAL POINT Normal Hemostatic mechanism must be stopping blood form leaking but they must also be finely controlled so that thrombus does not form under normal circumstances. Sequences of the events in Thrombus formation Injury Vasoconstriction (slow the blood flows) Primary haemostatic plug(platelet Adhesion) Fibrin formation
Acts to stabilize the platelet plug Secondary heamostasis
Preventing Blood loss Platelet Plug Platelets do not stick to each other or to Blood vessel Upon damage to blood vessels and endothelium plts.
With the help of vWF adhere to collagen Stimulated by & then release more thromboxane and ADP which attract still more plts. Stck to exposed collagen fibers and form plt. Plug
Blood Clotting/coagulation Formation of a clot (network of protein fibers called fibrin) Blood clotting begins with the extrinsic or intrinsic pathway
Both pathway end with the production of activated factor X Extrinsic pathway begins with the release of Thromboplastin from damaged tissue Intrinsic pathway begins with the activation of factor XII
