Vascular Pathology

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chris_hoff334
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Vascular Pathology
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2011-08-20 14:29:50
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From Robbins Ch 10
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  1. Congenital Anomalies

    Aberrations in vascular anatomy particularly
    important in surgical procedures
    Two important congenital abnormalities:

    berry aneurysms – occur in the Circle of Willis

    • arteriovenous fistulas – abnormal communication
    • btwn arteries and viens – looks like a web – normally in the CNS but can be
    • anywhere
  2. Vessels are made up of Endothelial cells and smooth muscle
    Endothelial cells:

    monolayer which lines entire vascular system

    elongated cells which form junctional complexes with neighboring cells contain Weibel-Palade bodies (storage site for von Willerbrand factor which help with clotting factors – deficiencies lead to excess bleeding)

    • Smooth muscle cells:
    • doesn’t regulate BP very well in big arteries but well regulated in small ones

    spindle-shaped with single elongated nuclei

    contractile function (mediated by actin and myosin)

    migratory and proliferative capacity regulated by growth promoters and inhibitors = angiogenesis

    tumors require angiogenesis so they give off hematopoetic factors that will promote BV growth
  3. Vascular Injury
    After superficial loss (not serious) of endothelial cells, neighboring endothelial cells migrate and proliferate to “fill the gap”

    After severe injury, ”neointima” forms:

    smooth muscle cells migrate from media to intima

    intimal cells multiply

    synthesis and deposition of extracellular matrix occurs which holds everything together

    exaggerated healing response results in intimal thickening which can block off the lumen of the BV can produce stenosis of small to medium-sized vessels or vascular grafts
  4. Arteriosclerosis
    • Literally means “hardening of the arteries”Generic term for three patterns of vascular
    • disease:

    atherosclerosis– narrowing of a lumen of a BV by deposition of fatty material

    Monckeberg medial calcific sclerosis – all of us get calcium deposited in our arteries as we get old –doesn’t cause disease really tho

    arteriolosclerosis – almost like atherosclerosis but it’s only in arterioles – especially problematic in diabetics because there are arterioles in kidneys, etc. If you get this, it can lead to renal failure.
  5. Atherosclerosis
    • °
    • Characterized by intimal lesions called
    • atheromas or fibrofatty plaques

    • °
    • Plaques protrude into vessel lumen, weaken
    • media, and can undergo calcification and
    • rupture

    • °
    • May be concentric (around evenly) or eccentric (more
    • on one side, more unstable and can lose it’s cap easier)

    • °
    • Contributes to 1/2 the mortality in the Western
    • world
  6. Atherosclerosis
    primarily affects
    • elastic
    • arteries (aorta, carotids, and iliacs) and large and medium-sized muscular
    • arteries (coronaries and popliteals)
  7. Atherosclerosis
    Begins
    • ° in
    • childhood, but symptoms appear in adulthood
  8. Symptomatic
    atherosclerotic disease often localized to arteries supplying WHAT
    • heart,
    • brain, kidneys, lower extremities, and small bowel
  9. Atherosclerosis Manifestations
    include
    • myocardial infarction, stroke, aortic
    • aneurysms, gangrene of legs, and ischemic encephalopathy
  10. °
    Atheromas
    • ³
    • raised focal plaques within the intima composed
    • of a lipid core and a covering fibrous cap

    • ³
    • appear whitish yellow

    • ³
    • involves the aorta, coronaries, popliteals,
    • internal carotids, and vessels of circle of Willis
  11. °
    Atheromas have three main components:
    • ³
    • cells (smooth muscle, macrophages, and other leukocytes)

    • ³
    • connective tissue extracellular matrix
    • (collagen, elastic fibers, and proteoglycans)

    • ³
    • intracellular and extracellular lipid deposits
  12. °
    Atheromas may become complicated:
    • ³
    • Calcification

    • ³
    • rupture/ulceration (with atheroemboli – fat embolism that broke thru and is
    • floating in blood stream)

    • ³
    • hemorrhage

    • ³
    • thrombosis (stationary blood clot – if it moves it’s called a thromboemboli)

    • ³
    • aneurysmal dilation
  13. °
    Fatty streaks Atherosclerosis
    • ³
    • multiple yellow flat spots made of lipid-filled
    • foam cells, T-lymphocytes, and extracellular lipid

    • ³
    • occur in all children >10 years regardless of race, sex, or
    • environment

    • ³
    • not all fatty streaks progress to
    • atherosclerotic plaques
  14. Four
    major modifiable conditions:
    • diabetes,
    • hyperlipidemia, hypertension, and cigarette smoking
  15. °
    Hyperlipidemia:
    • ³
    • mainly hypercholesterolemia, but also
    • hypertriglyceridemia

    • ³
    • increased risk with high LDL

    • ³
    • decreased risk with high HDL
  16. Aneurysms
    • °
    • Localized dilation of a blood vessel

    • °
    • Occurs most commonly in the aorta (abdominal) and
    • heart
  17. Two
    types of Aneurysms
    • ³
    • true
    • aneurysms – the entire wall of the BV is bulging out – all 3 layers

    • ³
    • false
    • aneurysms - only a part of the BV wall
    • is bulging out – ex. 1 of 3
  18. Causes of Aneurysms
    • 
    • Atherosclerosis
    • – most common

    • ‚ cystic
    • medial degeneration - degenerative disease
    • of the media of the aorta and
    • other arteries with loss of elastic tissue and muscle cells.

    • ‚
    • People with CT diseases like ehlars-danlos
    • syndrome or marfan’s syndrome

    • ƒ
    • congenital defects like Berry aneurysms and
    • atrioveneous fistulas

    • „
    • infection
    • (mycotic aneurysms)

    • …
    • syphilis

    • †
    • trauma

    • ‡
    • systemic
    • disease (immunologic injury)
  19. Abdominal Aortic Aneurysm (aka triple A)
    • ‡
    • Most common site of atherosclerotic aneurysms

    • ‡
    • Usually located below the renal arteries (below
    • belly botton) but above the aortic bifurcation

    • ‡
    • Area very prone because of the slowing down of
    • blood when branching into the common illiacs - get more deposition here

    • ‡
    • May be saccular (round) or fusiform (spindle
    • shaped)

    • ‡
    • Vary in size (SIZE MATTERS)



    • ‡
    • Occurs in areas of severe complicated
    • atherosclerosis (destroys the tunica media, weakening the aortic wall)

    • ‡
    • Mural (wall) thrombus frequently present (embolism common) – because blood slows
    • down around this area, it allow a clot to sorta form there

    • ‡
    • May be accompanied by smaller fusiform or
    • saccular dilations of the iliac arteries

    • ‡
    • If have a BIG AAA, the branches are more likely
    • they have smaller ones
  20. Triple A Occurs
    most commonly in

    and why???
    • ‡
    • males >50
    • Because you are predisposed to Atherosclerosis




    • ‡
    • Causes :

    • ‡
    • atherosclerosis

    • familial/genetic predisposition (Marfan
    • Syndrome)

    • overproduction of certain tissue enzymes causing
    • degradation of extracellular matrix
  21. Abdominal Aortic Aneurysm

    Clinical detection depends on size and location:

    Some detection depends on:
    • 
    • rupture with fatal hemorrhage

    • 
    • occlusion
    • of branch vessel

    • 
    • embolism
    • from atheroma or thrombus

    • 
    • impingement on adjacent structures like the
    • bladder, kidneys, etc

    • 
    • abdominal
    • mass (pulsating) – in thin people u can see their abdomen pulsating
  22. Abdominal Aortic Aneurysm

    Rupture is most serious complication, the risks of rupture depend on
    • 
    • very low for small (<4 cm) aneurysms

    • 
    • 11-25%
    • for aneurysms >5 cm

    • °
    • Large aneurysms treated surgically (prosthetic
    • graft put in place)

    • 
    • 5%
    • mortality if unruptured

    • 
    • >50%
    • mortality for emergent surgery (if it has already ruptured)
  23. Syphilitic
    (Luetic) Aneurysm
    • °
    • Tertiary syphilis classically involves the
    • cardiovascular and nervous systems

    • °
    • Characteristic vascular lesion is obliterative
    • endarteritis (lymphocytes and plasma cells that attack the adventitia of the
    • aorta)

    • 
    • involves
    • small blood vessels and vasa vasorum of aorta (thoracic aortitis)

    • °
    • Usually involves in the thoracic cavity around
    • the arch of the aorta

    • °
    • The aneurysm can get so big and cause backflow
    • into the heart and the heart can actually dialate over time (called Cor bovinum (cow
    • heart) refers to a massive hypertrophy of the left
    • ventricle)

    • 
    • may cause
    • aneurysmal dilation of aorta and aortic
    • annulus
  24. Aortic Dissection
    • °
    • Tear in the outer wall of the BV and blood
    • starts flowing within the length of a BV

    • °
    • Dissection of blood along the laminar planes of
    • the aorta

    • °
    • A blood-filled channel forms (dissecting intramural hematoma)


    • °
    • Often rupture, causing massive hemorrhage – MEDICAL EMERGENCY
  25. AD Occur
    in two patient populations
    • Þ
    • 40 - 60 year old males with hypertension

    • Þ
    • patients
    • with connective tissue abnormalities (such as Marfan syndrome)
  26. Aortic Dissection
    Morphology:
    • Þ
    • usually begins with an intimal tear extending
    • into the tunica media

    • Þ
    • tear is
    • usually within 10 cm of the aortic valve where blood in pounding into the
    • vessel wall and keeps drilling into the aorta, transverse or oblique, and 1 - 5
    • cm in length with jagged edges

    • °
    • If it tears into the aorta, into the BV, then
    • back into the lumen of the arota (as opposed to out of the aorta) then you get
    • a double barreled aorta – best outcome but still need to be fixed

    • Þ
    • can extend proximally toward the heart as well
    • as distally (as far as femorals)

    • Þ
    • spread
    • occurs along the middle and outer thirds of the aortic wall
  27. Aortic Dissection Most common cause of death
    • °
    • is rupture into a body cavity (hemopericardium
    • (Can get cardiac tamoinade where blood gets into the cardiac sac and keeps the
    • heart from beating efficiently), hemothorax, or hemoperitoneum)

    • °
    • Extension of the dissection may occur if problems in

    •  aortic valve > aortic insufficiency
    • 
    • coronary artery > myocardial infarction

    spinal arteries >transverse myelitis
  28. Aortic Dissection causes
    • ° Most frequent cause of AD is cystic medial
    • degeneration (CMD)

    • ° CMD consists of elastic tissue fragmentation and
    • the formation of small cystic spaces in the tunica media filled with amorphous cellular material

    • ° hypertension is the major risk factor, but its
    • contribution to CMD is unknown

    ° inherited connective tissue disorders (Marfan syndrome)
  29. ° Marfan syndrome:
    > autosomal dominant disease

    >mutations noted in the fibrillin gene

    • > characterized by skeletal, ocular and
    • cardiovascular manifestations

    • (aortic dissection, dilation of
    • aortic root, and mitral valve prolapse)
  30. Aortic Dissection
    type A, DeBakey type I and II
    • proximal
    • lesions involving the ascending aorta are most
    • dangerous – b4 subclavian artery
  31. type B, DeBakey type III
    lesions distal to the subclavian artery
  32. Aortic Dissection
    Symptoms:
    • Þ
    • onset of
    • excrutiating RADIATING chest pain, to the shoulder, radiating to back, moving
    • downward as dissection progresses

    • Þ
    • may be
    • mistaken for myocardial infarction – you have to rule out a MI b4 you know that
    • it is an AD – rule out by enzyme test (troponin)
  33. Aortic Dissection
    Diagnosis:
    • °
    • imaging studies – Radiograph won’t help, CT or
    • MRI prob will because they will show the abnormal accumulation of blood
  34. Aortic Dissection
    Prognosis:
    • °
    • once invariably fatal

    • °
    • now
    • treatments available including placation (sewing it up) of aortic wall and
    • antihypertensive therapy so that they won’t get another dissection

    • °
    • survival
    • rate of 65-75%
  35. Vasculitis
    2 types or mechanisms:
    • °
    • inflammation of vessel wall

    • °
    • 2 types or mechanisms:

    • Þ
    • immune-mediated* (immune complexes and
    • autoantibodies attack the vessels)

    • Þ
    • direct
    • invasion of vessel wall by infectious agent
  36. Noninfectious Vasculitis (Immunologic vasculitis) use antineutrophil cytoplasmic antibodies detected by 2 types immunofluorescense patterns
    • °
    • c-ANCA (cytoplasmic antineutrophilic cytoplasmic antibodies),
    • target antigen PR-3, seen in Wegener granulomatosus
    • ° Fluorescense around the nucleus in the cytoplasm

    • °
    • p-ANCA (perinuclear antineutrophilic cytoplasmic antibodies),
    • targets myeloperoxidase, seen in leukocytoclastic vasculitis

    • °
    • either ANCA may occur in small vessel vasculitis
  37. Giant Cell (Temporal) Arteritis
    (Immunologic vasculitis)
    • °
    • acute and chronic, often granulomatous,
    • inflammation of medium-sized and small arteries

    • °
    • affects principally the arteries of the head
    • (particularly the temporal arteries)

    • °
    • may affect aortic arch (giant cell aortitis)

    • °
    • affects patients >50, usually with facial
    • pain in the distribution of the temporal artery
  38. Giant Cell (Temporal) Arteritis (Immunologic vasculitis)
    Treatment
    • involving
    • anti-inflammatory agents is very effective
  39. Giant
    Cell (Temporal) Arteritis diagnosis
    • °
    • depends on biopsy (requires 2 - 3 cm segment of
    • artery)

    • °
    • lesions are segmental and may be missed in
    • biopsy

    • °
    • presumptive diagnosis and prompt treatment may
    • be necessary because it can cause blindness associated
  40. Microscopic
    Polyangitis (Immunologic vasculitis)
    • °
    • Affects arterioles, capillaries, and venules

    • °
    • All lesions tend to be same age

    • °
    • ANCA present in majority of cases

    • °
    • May affect every organ system, but in many cases
    • is limited to the skin (Cutaneous Microscopic Polyangitis )
  41. Microscopic
    Polyangitis (Immunologic vasculitis)
    Clinical features
    • °
    • hemoptysis (couphing up blood), hematuria,
    • proteinuria (affecting the kidney), GI bleeding, muscle pain
  42. Cutaneous vasculitis or (Cutaneous Microscopic
    Polyangitis )
    • °
    • may be related to drugs,microorganisms,
    • proteins, or tumor antigens

    • °
    • Histologically, segmental fibrinoid necrosis (vessel
    • wall gets pink and dead LOOKING) and fragmented neutrophils (leukocytoclasia –
    • break down of leukocytes – so disease can be called leukocytoclastic vasculitis
    • = microscopic polyangitis)

    • °
    • Patients respond well to removal of offending
    • agent
  43. Wegener Granulomatosis
    (Immunologic Vasculitis)


    °
    Necrotizing vasculitis characterized by triad
    of:
    • 
    • acute necrotizing granulomas of the upper
    • respiratory tract

    • 
    • focal
    • necrotizing granulomatous vasculitis

    • ƒ
    • renal
    • disease (crescentic glomerulitis)
  44. Wegener Granulomatosis affects who???
    • ƒ
    • Males affected more often than females


    Average age of 40

    • ƒ
    • Immune
    • complexes in vessel walls and response to immunosuppressive agents suggest
    • immunologic mechanism
    • ƒ
    • 90% of cases have c-ANCA in serum
  45. Thromboangiitis Obliterans
    Also known as Buerger disease
    • ƒ
    • Segmental, thrombosing, acute and chronic
    • inflammation of medium-sized and small arteries

    • ƒ
    • Occurs
    • almost exclusively in cigarette smokers

    • ƒ
    • Leads to vascular insufficiency
  46. Thromboangiitis Obliterans
    Manifestations:
    • ƒ
    • superficial nodular phlebitis – formation of
    • blood clots in veins

    • ƒ
    • cold
    • sensitivity bc of constriction of bv

    • ƒ
    • pain of
    • the instep caused by exercise

    • ƒ
    • Chronic ulceration of extremities may lead to
    • gangrene

    • early stages, cessation of smoking may relieve
    • symptoms
  47. Infectious Arteritis
    Caused by:
    • ƒ
    • direct invasion by bacteria or fungus
    • (aspergillosis and mucormycosis)

    • ƒ
    • lodging
    • of septic embolus – cruse ship for bacteria

    • ƒ
    • seeding
    • from bacteremia

    • ƒ
    • Infection may weaken vascular wall and cause a
    • mycotic (infectious) aneurysm
  48. Raynaud Phenomenon
    • °
    • Paroxysmal pallor and cyanosis of the feet or
    • hands, rarely nose, earlobes, or lips


    • °
    • Caused by vasoconstriction of local small
    • arteries or arterioles
  49. 2 types of

    Raynaud Phenomenon
    • ±
    • Primary (young females, exaggerated response to
    • cold or emotion)

    • ±
    • Secondary (systemic lupus erythematosus,
    • systemic sclerosis aka scleroderma, atherosclerosis, Buerger disease) – rule these
    • out and you have the primary cause
  50. Varicose Veins
    • °
    • Abnormally dilated veins produced by prolonged
    • increased intraluminal pressure and loss of support of vessel wall (caused by
    • chronic standing)

    • °
    • Superficial veins of leg most common site

    • °
    • May thrombose (rarely embolize if superficially,
    • unlike deep vein thrombosis)
  51. Varicose Veins

    Symptoms and who is it normally seen in
    • °
    • Symptoms: pain, persistent edema, stasis
    • dermatitis, and ulceration

    • °
    • Seen frequently in obese females >50 y/o
  52. Other
    Varicose Veins

    Esophageal varices
    • °
    • occur in patients with cirrhosis (from alcoholis
    • or hepatitis B or C) and portal hypertension

    • °
    • rupture may cause massive hemorrhage
  53. Varicose Veins
    Hemorrhoids
    • °
    • dilation of anorectal venous plexus

    • °
    • caused by pelvic congestion
  54. Thrombophlebitis - formation of blood clots within veins

    Predisposing factors:
    • °
    • cardiac
    • failure

    • °
    • neoplasia


    • °
    • pregnancy

    • °
    • obesity

    • °
    • post-operative state

    • °
    • immobilization
    • (prolonged bed rest)
  55. °
    Sources of Thrombophlebitis:
    • 
    • deep leg
    • veins (90% of cases)

    • 
    • periprostatic venous plexus

    • 
    • pelvic
    • veins

    • 
    • large
    • veins of skull and venous sinuses

    • …
    • portal
    • vein
  56. Presentation of Thrombophlebitis :
    • …
    • Early stages à
    • few or no symptoms (edema, cyanosis, dilated superficial veins, heat,
    • tenderness, redness, pain, swelling)
    • …
    • Embolism may be first manifestation
  57. Migratory Thrombophlebitis
    Also known as Trousseau’s sign
    • …
    • Neoplasms such as adenocarcinoma of the
    • pancreas, colon, or lung initiate hypercoagulability

    • … Venous thromboses appear
    • spontaneously, disappear, and are followed by thromboses in other veins can be
    • an early sign of a adenocarcinoma
  58. Superior Vena Caval Syndrome
    • …
    • Obstruction of SVC producing cyanosis (blue
    • color) and marked dilation of veins of head, neck, and arms

    • …
    • Caused by neoplasms that compress or invade the
    • SVC (most commonly primary bronchogenic carcinoma or mediastinal lymphoma)

    • …
    • Rarely caused by aortic aneurysms
  59. Inferior Vena Caval Syndrome
    • …
    • Compression of the IVC with resulting edema of
    • lower extremities, distention of veins of lower abdomen, and massive
    • proteinuria when the renal vein is involved

    • …
    • Caused by neoplasms that compress or penetrate
    • the IVC (particularly hepatocellular carcinoma and renal cell carcinoma) or
    • thrombus from the femoral or iliac veins
  60. …
    Lymphangitis
    • …
    • acute inflammatory involvement of lymphatic
    • channels by bacterial infections (most common agents are the group A b - hemolytic streptococci)

    may lead to acute lymphadenitis
  61. …
    Lymphedema
    • …
    • Primary (congenital or familial) disorders

    • …
    • Secondary (acquired) disorders
    • usually associated with inflammation or cancer
  62. Therapeutic Interventions
    If chronic ischemia or infarction give:
    • …
    • Balloon angioplasty (dilation of atheromatous
    • stenosis by a balloon catheter)

    • …
    • Stent placement (inserting metallic mesh tubes
    • to hold artery open)

    • …
    • Vascular replacement
    • synthetic grafts may be used in large or small vessels, but perform best in large
    • diameters

    • …
    • autologous grafts (saphenous or internal
    • mammary artery) are patients’ native vessels transplanted to a different site –
    • usually the best and last the longest
  63. About Coronary Artery Bypass Graft
    • °
    • Uses autologous saphenous vein or internal
    • mammary artery to bypass stenotic vessels

    • ±
    • 50% of saphenous grafts are patent at 10 years

    • ±
    • 90% of IMA grafts are patent at 10 years (would
    • rather use this for the graft but it’s much shorter and might not be long
    • enough)

    • ±
    • Graft failure is due to thrombosis, intimal
    • thickening, and atherosclerosis

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