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CV II Exam 2 > Blood Vessels Day 2 > Flashcards

Blood Vessels Day 2 Flashcards

1
Q

Describe the six step pathogenesis of atherosclerosis

A
  1. Chronic endothelial injury (dysfunction)
  2. Accumulation of lipoproteins (mainly LDL) with subsequent oxidation
  3. Adhesion of monocytes with migration into the intima (now macrophages)
  4. Adhesion and activation of platelets
  5. Migration of smooth muscle cells becoming neointimal smooth muscle cells (proliferate and deposit extracellular matrix/collagen)
  6. Accumulation of lipids in macrophages (foam cells), smooth muscle cells and extracellular spaces
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2
Q

What is an aneurysm?

A

•Localized abnormal dilation of a blood vessel or the wall of the heart

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3
Q

The most important causes of aortic aneurysms are:

A

Atherosclerosis with associated inflammation (abdominal aorta)
- macrophage metalloproteinases and inflammation induced smooth muscle apoptosis weaken vessel wall

Hypertension via ischemic medial cystic degeneration (thoracic aorta)

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4
Q

How can mycoses cause aneurysms?

A

•Mycotic aneurysms (infections)

  • from embolization of a septic embolus (infective endocarditis)
  • from extension of an adjacent suppurative process
  • from circulating organisms infecting the arterial wall
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5
Q

In addition to atherosclerosis, HTN, and mycoses, what are some other causes of aneursysms?

A

•Marfan syndrome (fibrillin),

Loeys-Dietz syndrome (TGF-β receptors),

Ehlers-Danlos syndrome (type III collagen),

scurvy (collagen x-linking),

trauma (traumatic aneurysms or arteriovenous aneurysms),

congenital defects (berry aneurysms),

syphilis and

vasculitides

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6
Q

What is the difference between a true aneurysm and a false aneurysm?

A

true - bounded by arterial wall component or myocardium

false/pseudoaneurysm - transmural rupture creating hematoma, bound by extravascular CT

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7
Q

What are the 2 appearances of true aneurysms?

A
  • Saccular aneurysm – appears rounded
  • Fusiform aneurysm – involves long segment of artery and is not rounded
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8
Q

Where in the body do abdominal aortic aneurysms typically appear? How does this afect the sequelae? Who gets them?

A

Usually below the renal arteries
Renal complications with involvement of renal arteries

•M>F, smokers and age >50 years

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9
Q

What are the causes of AAA?

A
  • Inflammatory AAA (5-10%) - lymphocytes, plasma cells and macrophages +/- giant cells (uncertain cause and occur at younger age)
  • IgG4 related disease with aortis and periaortitis - infiltrating IgG4+ plasma cells (may affect pancreas, biliary system, and salivary gland with fibrosis)
  • Mycotic abdominal aortic aneurysms - atherosclerotic AAAs that have become infected (Salmonella gastroenteritis)
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10
Q

How are thoracic aortic aneurysms similar to AAA?

A

Thoracic aortic aneurysms also occur with similar complications plus involvement of coronary ostia

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11
Q

What are the clinical consequences of aortic aneurysm?

A
  • Rupture into the peritoneum or retroperitoneal tissues (fatal in > 50%)
  • Risk of rupture per year: size <4.0 cm (0%), 4.0-4.9 (1%); 5.0-5.9 (11%); >6.0 (25%) [usually repair >5 cm]
  • Obstruction of a vessel leading to ischemic tissue injury
  • Embolism from atheroma or mural thrombus
  • Impingement on an adjacent structure, such as compression of a ureter or erosion of vertebrae
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12
Q

How do AAAs typicall present?

A

•Presentation as an abdominal mass (often palpably pulsating) that simulates a tumor

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13
Q

What do aneurysms and tertiary syphilis have in common?

A

•Obliterative endarteritis

in tertiary stage of syphilis (lues) involves vasa vasorum (arterioles) of the thoracic aorta

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14
Q

What is syphilitic aortitis?

A

•Syphilitic aortitis

  • obliterative endarteritis of vasa → ischemic injury of the media → loss of the medial elastic fibers and muscle cells
  • Can lead to aneurysmal dilation that can include the aortic annulus leading to aortic valve incompetence
  • Can involve coronary ostia
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15
Q

What is “tree-barking” in regards to the aorta?

A

histological finding

contraction of fibrous scars with intervening segments of intima

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16
Q

What is an aortic dissection?

A

Something typically repaired frantically by surgeons while anesthesiologists compare arm tans

Dissection of blood between planes of the media

Blood has entered (dissected) the wall of the vessel and separated the layers. Although this is shown as occurring through a tear in the lumen, dissections can also occur by rupture of the vessels of the vasa vasorum within the media.

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17
Q

What patients is aortic dissection more common in? Does it always occur with aneurysm? What conditions predispose you towards it?

A

•May or may not occur with an aneurysm

•> 90% occur in men 40-60 with hypertension
•Arteriolosclerosis → smooth muscle cell loss

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18
Q

What are some other conditions - other than arteriosclerosis - that predispose people towards aortic dissection?

A
  • In younger people may be connective tissue disorder (Marfan, Ehlers-Danlos, Vit. C deficiency)
  • Can be iatrogenic (arterial cannulation)
  • Rarely occurs during or following pregnancy
  • Occasionally 2ry to vasa vasorum rupture
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19
Q

How is aortic dissection treated?

A

Antihypertensive therapy and aortic plication (65-75% survival)

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20
Q

Can aortic dissection be a consequence of small vessel disease?

A

yes - vasa vasorum abruption into media tunica

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21
Q

What is the clinical presentation of an aortic dissection?

A

•Sudden onset of excruciating pain, usually involves anterior chest, radiating to the back, and moving downward

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22
Q

What is the most common COD with aortic dissection?

A

•Most common cause of death is rupture into the body cavities

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23
Q

How many ways can an aorta dissect?

A
  • Retrograde dissection into the aortic root → aortic valvular apparatus dysfunction with aortic insufficiency
  • Can dissect into neck, coronary, renal, mesenteric, or iliac arteries, and compression of spinal arteries may cause transverse myelitis
  • Occasionally the dissection can rupture back into vessel lumen causing a dual lumen vessel
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24
Q

What can you do to potentially halt aortic dissection?

A

•Aggressive treatment of HTN may halt dissection

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25
Q

What is the classification scheme for aortic dissections? What is the worst classification?

A

Type A (proximal) involves the ascending aorta, either as part of a more extensive dissection (DeBakey I) or in isolation (DeBakey II).

Type B (distal or DeBakey III) dissections arise after the take-off of the great vessels.

Type A dissections typically have the most serious complications and greatest associated mortality.

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26
Q

Where along the aorta do aortic dissections arise?

A

Usually arise within 10 cm of aortic valve

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27
Q

What conditions is aortic dissection rarely comorbid with?

A

Dissection is unusual in substantial atherosclerosis or other cause of medial scarring such as syphilis

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28
Q

What are the genetics behind Marfan Syndrome?

A

Loss of function mutation of fibrillin (1 per 5,000)

  • 75% of cases are familial (autosomal dominant pattern); rest are sporadic
  • Once incorrectly thought to be a dominant negative mutation!!!
  • Heterozygotes have clinical symptoms
  • > 500 mutations of FBN1 gene (15q21) for fibrillin 1
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29
Q

What is the pathology behind Marfan Syndrome?

A

Loss of function mutation of fibrillin (1 per 5,000)
Mutant fibrillin 1 prevents the assembly of normal microfibrils

With ↓fibrillin-1 there is ↑TGF-β activity and serum levels

  • Fibrillin 1 is involved in forming a complex that binds and inactivates TBF-β
  • TGF-β involved in embryonic development, cell growth and apoptosis
  • TGF-β ↑ collagen production and extracellular matrix (ECM) remodeling
  • leads to overgrowth of bones and myxomatous changes in mitral valves
  • Losartan (angiotensin II, type 1 receptor antagonist) for Rx?
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30
Q

How is Losartan helpful for Marfan’s syndrome?

A

Losartan lowers BP, which will help control adverse outcome of aortic dissection

  • will also reduce TGF-beta problem, whose activity is too high and causes too much growth
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31
Q

What is Loeys-Dietz syndrome, and why is it related to Marfan’s?

A

Mutations in the TGF-β receptors give rise to a similar syndrome called Loeys-Dietz syndrome (Marfan syndrome, type II)

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32
Q

What are the principal clinical manifestations of Marfan Syndrome?

A
  • Skeleton: Slender with abnormally long legs, arms, and fingers (arachnodactyly); high-arched palate; hyperextensibility of joints; spinal deformities (kyphoscoliosis); pectus excavatum or pigeon-breast
  • Eyes: Bilateral dislocation (subluxation/ectopia lentis) of lens from weakness suspensory ligaments (ciliary zonules holding lens are made up exclusively of fibrillin)
  • Cardiovascular system: Aneurysmal dilation and aortic dissection; dilation of the aortic valve ring (aortic incompetence); mitral and tricuspid valve floppy valve syndrome giving rise to congestive cardiac failure
  • Death from aortic rupture is the most common cause of death
  • Can occur at any age
  • Cardiac failure also causes deaths
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33
Q

What is cystic medial degeneration?

A

Cross-section of aortic media from a patient with Marfan syndrome shows elastin fragmentation and areas devoid of elastin that resemble cystic spaces but are actually filled with proteoglycans (asterisks)

Normal media will have regular layered pattern of elastic tissue - when stained black, resembles wood grain

34
Q

How is vasculitis typically separated, clinically and pathologically?

A

Large vessel vasculitis

  • granulomatous disease
  • giant cell arteritis, Takayasu arteritis

Medium Vessel Vasculitis

  • imm complex mediated - polyarteritis nodosa
  • antiendothelial cell Ab - Kowasaki disease

Small Vessel Vasculitis

  • paucity of imm complexes - often with ANCA
  • imm complex mediated
35
Q

What are some important immune complex mediated pathogenesis of vasculitis?

A

Polyarteritis nodosa (HBsAg/HBsAg-Ab)

Drug-induced hypersensitivity reactions

Antineutrophil cytoplasmic antibody (ANCA)-mediated (pauci-immune)

Wegener granulomatosis - PR3-ANCA (c-ANCA)

Microscopic polyangiitis/polyarteritis

Churg-Strauss syndrome

Direct antibody mediated

Goodpasture syndrome (anti-glomerular basement membrane Ab)

Kawasaki disease (anti-endothelial Ab and also anti smooth muscle cell Ab)

36
Q

What are some ANCA-mediated pathologies/causes for vasculitis? Which ANCA is each associated with?

A

PR3-ANCA (c-ANCA)

Wegener granulomatosis

MPO-ANCA (p-ANCA)

Microscopic polyangiitis/polyarteritis

Churg-Strauss syndrome

37
Q

What can cause infectious vasculitis?

A

•Sometimes from direct invasion of bacteria (pseudomonas) or fungi (Aspergillus and mucormycosis)

  • Can frequently accompany bacterial pneumonia
  • Can occur adjacent to caseous tuberculous abscesses
  • Can occur in superficial cerebral vessels in meningitis
  • Can be secondary to septic emboli
  • Pseudomonas and Aspergillus both thrive in vessel walls
38
Q

What can result from an infectious vasculitis?

A

•May result in a mycotic aneurysm or induce thrombosis and infarction

39
Q

How helpful are the associated symptoms of vasculitis in making a diagnosis? Why?

A

Vasculitis = Non-specific Constitutional Symptoms
•Fever
•Weight loss
•Myalgia
•Arthralgia
•Malaise
•Fatigue

Not specific enough to make a good Dx

40
Q

What is Giant Cell/Temporal Arteritis?

A

Granulomatous arteritis of aorta, major branches and often the temporal arteries (can be tender on palpation)

41
Q

What is the typical presentation of Giant Cell Arteritis?

A

Usually >50 and often associated with polymyalgia rheumatica

Most common vasculitis of elderly in US

People will present with headache, visual disturbance

  • lumpy bumpy that hurt when palpated, d/t d/c vasculitis, lumpy areas are inflamed

The temporal artery of a patient with classic giant cell arteritis shows a thickened, nodular, and tender segment of a vessel on the surface of head (arrow).

42
Q

What is the pathology behind Giant Cell/Temporal Arteritis?

A

Unknown mechanism, giant cells frequently involved

2/3 have anti-endothelial and/or anti-smooth muscle antibodies

43
Q

What are some important associations with Temporal arteritis and other diseases/problems?

A

Ophthalmic arterial involvement →diplopia and permanent blindness

May cause giant cell aortitis and thoracic aortic aneurysm

Can involve coronary arteries

44
Q

How should a clinician approach suspected Temporal Arteritis? How thoroughly should pathology examine an arterial specimen for this?

A

will cause blindness if untreated, medical emergency

Call surgeon who will take patient to surgery immediately

  • get 3 cm of temporal aa, send to lab/pathology, get confirmation. Have to look for inflammation, then use elastic stain, if steroids used for too long then inflammation won’t be present. Examine until inflammation is found, inflammation pattern is intermittent.
  • start high dose steroids to get inflammation down
45
Q

What cellular changes will a pathologist appreciate with Temporal Arteritis?

A

Hematoxylin and eosin stain of section of temporal artery shows giant cells at the degenerated internal elastic lamina in active arteritis

Elastic tissue stain demonstrating focal destruction of internal elastic lamina and intimal thickening characteristic of long-standing or healed arteritis

46
Q

What is Takayasu Arteritis?

A

Granulomatous inflammation of the aorta and its major branches.

47
Q

You’re on your third year rotations and got stuck with a first year resident on a night shift. The resident is assessing an older women who appears to not have a pulse. The resident then concludes the patient is a zombie and pulls out a gun to double-tap the pending epidemic. You are thinking more quickly, and give the resident an explanation of Takayasu Arteritis to save the patients life. What do you say?

A

Patients usually <50 (females < 40)

Thickening and narrowing of aortic arch and branches

Marked weakening of pulses (Pulseless Disease) and reduced blood pressures of upper extremities

48
Q

Your resident is intrigued and asks you to explain associated problems of Takayasu arteritis. You say:

A

Ocular (retinal hemorrhages, blindness)

Neurologic

+/- Pulmonary (50%) (pulmonary HTN)

+/- Coronary arteries (myocardial infarcts)

+/- Renal (50%) arteries (renal HTN)

+/- Aortic valve insufficiency

49
Q

What would you expect to see on angiogram, cross sections of carotid arteries, and histological appearance for Takayasu arteritis?

A

Aortic arch angiogram showing narrowing of brachiocephalic, carotid, and subclavian arteries

Gross photograph of two cross-sections of the right carotid artery taken at autopsy of the patient shown in A, demonstrating marked intimal thickening and adventitial fibrosis with minimal residual lumen.

Histologic appearance in active Takayasu aortitis, illustrating destruction and fibrosis of the arterial media associated with mononuclear infiltrates and inflammatory giant cells (arrows).

50
Q

How are temporal and takayasu arteritis similar?

A

Similar presentation in both

  • <50 yo it’s oft Takayasu, >50 yo it’s often Temporal

Treatment for both is high dose steroids

51
Q

What is Kawasaki disease?

A

Arteritis involving large, medium-sized or small arteries

Usually self limited in children (80% < 4 years)

52
Q

What is the pathology behind Kawasaki disease?

A

Anti-endothelial cell and smooth muscle autoantibodies

53
Q

What is the presentation of Kawasaki disease?

A

Main cause of acquired pediatric heart disease in North America and Japan (epidemic)

1% fatality rate

Coronary arteries often involved +/- aneurysms

Aorta and veins may be involved

+/- vascular aneurysms and thrombi

Associated with mucocutaneous lymph node syndrome

  • acute usually self-limited disease with fever, conjunctival and oral erythema (strawberry tongue) and erosion, edema of the hands and feet, erythema of the palms and soles, a desquamative skin rash and enlargement of cervical lymph nodes
54
Q

What is the treatment for Kawasaki disease?

A

Rx Immunomodulation (IV immunoglobulins) + anti- platelet agent (aspirin)

  • high dose steroids
55
Q

Is Kawasaki disease an infection?

A

Happens in young kids, present with what looks like an infection

  • not an infection, despite constitutional symptoms
  • hints include a skin rash on palms and soles, strawberry tongue
  • order anti-endothelial cell Ab
  • medical emergency, treat with high dose steroids right away
56
Q

What is Buerger Disease?

A

Thromboangiitis Obliterans (Buerger Disease)

Segmental, thrombosing, acute and chronic inflammation of medium-sized and small arteries (tibial and radial), and extending to veins and nerves of the extremities

57
Q

What is the clinical presentation for Buerger disease?

A

Previously occurred almost exclusively among heavy cigarette-smoking men, increasing in women

Begins before age 35 in most cases

Chronic ulcerations of the toes, feet, or fingers and gangrene

Secondary Raynaud phenomenon

Exercise induced instep claudication

Nodular phlebitis

Severe pain, even at rest (nerve involvement)

58
Q

What is the pathology behind Buerger disease?

A

Massive reaction to tobacco antigens

Clinical presentation is often good enough to make a DX

Often involves entire neurovascular bundle

  • often have claudification

Vessels are often thrombosed, end up with ulcers to skin

59
Q

What is the treatment for Buerger disease?

A

Rx- stop smoking (during early disease)

60
Q

What changes would you expect, histologically, for Buerger disease?

A

The lumen is occluded by a thrombus containing abscesses, and the vessel wall is infiltrated with leukocytes.

61
Q

What is polyarteritis nodosa?

A

Polyarteritis nodosa (classic)

Necrotizing inflammation in small to medium arteries, arterioles, capillaries or venules

62
Q

What is the clinical presentation of polyarteritis nodosa?

A

Usually of young adults

Malaise, fever, weight loss, HTN, abdominal pain and melena, muscular aches/pains, ulcers, infarcts, peripheral neuritis (mostly motor)

63
Q

What is the pathology behind polyarteritis nodosa?

A

30% have hepatitis B surface Ag/Ab complexes

segmental fibrinoid necrosis and thrombotic occlusion of the lumen of this small artery. Note that part of the vessel wall at the upper right (arrow) is uninvolved.

Recurrent bouts possible, lesions can be of variable age

64
Q

What should you associate with polyarteritis nodosa?

A

hepatitis B

65
Q

What is Behcet’s disease?

A

Neutrophilic vasculitis of small to medium arteries

66
Q

What triad is the clinical presentation of Behcet’s disease? What other systems can be involved?

A

Triad

  • *1.recurrent oral aphthous ulcers
    2. genital ulcers
    3. uveitis**

Can also have GI, pulmonary and neurologic symptoms.

Can rupture aneurysms

67
Q

What is useful for dx’ing Behcet’s disease?

A

Can have positive pathergy test – minor trauma (sterile pinprick) causes exaggerated reaction

Also, Associated with HLA-B51

68
Q

What is Wegener granulomatosis?

A

Granulomatosis with polyangiitis (Wegener granulomatosis)

  • a small to medium vessel vasculitis
69
Q

What is the triad for the disease for Wegener granulomatosis? Why is the triad important?

A

Triad –

  1. Acute necrotizing granulomas of the upper and/or lower respiratory tract
  2. Necrotizing or granulomatous vasculitis in the lungs and upper airways +/-other sites (eyes, skin, heart)
  3. Renal disease with focal necrotizing glomerulonephritis (crescentic) with hematuria/proteinuria +/- renal failure

Triad is important for test questions, otherwise it’s hard to distinguish it from Goodpasture’s.

70
Q

What is the pathological association you should make with Wegener granulomatosis?

A

c-ANCA (PR3-ANCA) - antineutrophil cytoplasmic autoantibodies targeting proteinase 3 (PR3) in azurophilic granules are highly specific

present in 95%

71
Q

What does limited disease for Wegener’s granulomatosis mean?

A

Limited disease means triad not entirely present

72
Q

What is the clinical presentation of Wegener granulomatosis?

A

Clinical presentation

M > F; ~40 years

Persistent pneumonitis; bilateral nodular and cavitary infiltrates in 95%

Chronic sinusitis in 90%

Mucosal ulcerations of the nasopharynx in 75%

Renal disease in 80%

Skin rashes

Muscle pains

Articular involvement

Mononeuritis or polyneuritis

Fever

73
Q

How should Wegeners granulomatosis be treated? Can you leave it untreated?

A

Responds to immunosupression (steroids, chemo, and anti-TNF)

Always treat:

Untreated disease is malignant; 80% of patients die within 1 year

74
Q

What is Churg-Strauss syndrome?

A

allergic granulomatosis and angiitis

75
Q

What pathological associations should you make with Churg=Strauss syndrome?

A

Eosinophil-rich and granulomatous necrotizing vasculitis

Possible hyper-responsiveness to allergen

Strong association with allergic rhinitis, bronchial asthma, lung infiltrates

Blood eosinophilia

p-ANCA (MPO-ANCA) perinuclear antimyeloperoxidase in 50%

76
Q

What are some clinical associations you can make with Churg-Strauss? Clinical presentation?

A

Palpable purpura

Involves respiratory tract

Coronary arteritis and eosinophilic myocarditis are the principal causes of morbidity and mortality

Severe renal disease is infrequent

77
Q

What is microscopic polyangiitis?

A

leukocytoclastic vasculitis

Small Vessel Vasculitis

78
Q

What is the pathology behind microscopic polyangiitis?

A

Necrotizing vasculitis with few or no immune deposits (pauci-immune) involving capillaries and small vessels. Can see fragmentation of neutrophils in and around blood vessel walls, with all lesions of same age in histological examination.

Possible reaction to drugs, organisms, or exogenous or tumor proteins

p-ANCA (MPO-ANCA) targeting perinuclear antimyeloperoxidase in lysosomes + in >70%

79
Q

What are some of the clinical presentation of microscopic polyangitis?

A

“Palpable purpura” of skin

Necrotizing glomerulonephritis (90% of patients)

Pulmonary capillaritis is common

Hemoptysis, arthralgia, abdominal pain or bleeding, hematuria, proteinuria, hemorrhage, and muscle pain or weakness

80
Q

What are some other disorders associated with vasculitis?

A

Seen with rheumatoid arthritis, SLE, malignancy, mixed cryoglobulinemia and Henoch-Schönlein purpura

Vasculitis resembling hypersensitivity angiitis or classic polyarteritis nodosa

Rheumatoid vasculitis after long-standing, severe rheumatoid arthritis

visceral infarction

may cause a clinically significant aortitis

Lupus vasculitis

vs antiphospholipid antibody syndrome

aggressive anti-inflammatory therapy

vs aggressive anticoagulant therapy

81
Q
A

CV II Exam 2 (8 decks)

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