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CV Final Material > Peripheral Vascular Disease Pathology > Flashcards

Peripheral Vascular Disease Pathology Flashcards

1
Q

What type of aneurysm involves all three layers of wall?

A

True aneurysm

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2
Q

Wall defect leading to extravascular hematoma

A

◦ False (pseudoaneurysms):

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3
Q

Arterial dissection is when

A

blood enters the wall of the artery

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4
Q

Understand the difference between true and false aneurysms

A

◦ True: involves all three layers of wall
◦ False (pseudoaneurysms): Wall defect leading to extravascular
hematoma

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5
Q
  • Defective synthesis of fibrillin
  • Fibrillin is “scaffolding” for deposition of elastic tissue
  • Results in cystic medial necrosis of aorta
  • Leads to aneurysm formation & aortic dissection
A

Marfan syndrome

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6
Q

Factors affecting ______ function or structure can lead to aneurysms

A

collagen

*inadequate or abnormal syntheses of collagen

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7
Q
  • One variant has defective synthesis of Type III collagen
  • Leads to aneurysm formation
A

Ehlers-Danlos syndrome

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8
Q

Excessive connective tissue degradation can lead to aneurysm formation:
– Occurs with increased ________or decreased ___________

A

matrix metalloproteinase (MMP)

tissue inhibitors of metalloproteinase (TIMP)

(if inflammation (atherosclerosis) polymorphisms of MMP &/or TIMP genes may predispose to aneurysm formation)

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9
Q

Patho of aneurysms:

Loss of smooth muscle cells leads to what three things?

A
  1. Thickening of intima (due to atherosclerosis) –> ischemia of inner media
  2. Systemic hypertension–> Narrows vasa vasorum, leading to ischemia of outer media
  3. Morphologic results is cystic medial degeneration
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10
Q

Two common underlying causes of aneurysms

A

– Atherosclerosis – abdominal aorta
– Hypertension – ascending aorta

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11
Q

Uncommon causes of aneurysms:

A
  1. Congenital defects
    • Berry aneurysm: bifurcation of cerebral arteries, subarachnoid hemorrhage
  2. Infections (bacteria, fungi)
    • Mycotic aneurysm: septic emboli, direct extension, direct infection by circulating organisms
    • Syphilis (Treponema pallidum)
  3. Trauma – AV (fistula) aneurysm
  4. Vasculitis
  5. Genetic defects in collagen (Marfan’s & Ehlers-Danlos)
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12
Q

Most common location of aortic aneurysm?

A

Abdominal aortic aneyrsm located BELOW renal arteries and ABOVE bifurcation

(arch of aorta/thoracic arota and iliac arteries less common)

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13
Q

What population is most commonly associated with aneurysms?

what is most common cause?

A

Men and smokers

cauase = atherosclerosis

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14
Q

Morphology of aneurysm
– Up to _____ diameter
– Thinning & destruction of______
– Mural thrombus
– Saccular or fusiform

A

15 cm

media

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15
Q

Two variants of aneurysms include inflammatory and mycotic. What are their causes?

A

inflammation = unknown

mycotic = secondary infection of an atherosclerotic wall

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16
Q

AAA is more common in:

how do they present on exam?

how do we manage them?

A

men over 50

present at pulsatile abdominal mass

if aneurysms is >5cm we do aggressive management (risk of rupture is proportional to the size)

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17
Q

Complications of AAA

A

– Rupture into peritoneum or retroperitoneum
– Vascular obstruction – renal, mesenteric, spinal arteries
– Embolism of atheroma or mural thrombus to kidneys or
lower extremities
– Impingement of ureter(s)

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18
Q

What are our two options for repair of an aneurysm?

A

open repair with graft sewn into place

stent-graft insterted through right and left common femoral arteries

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19
Q

Three common causes of thoracic aortic aneurysms

A

▫ Hypertension
▫ Marfan’s syndrome
▫ Syphilis (tertiary)

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20
Q

What clinical features do we see in pts with thoracic aortic aneurysms?

A

In regards to mediastinum encroachment:
▫ Tracheal compression ▫ Esophageal compression ▫ Bone erosion ▫ Cough due to irritation of recurrent laryngeal nerve

Cardiac symptoms: Heart failure due to aortic valve insufficiency

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21
Q

Blood between and along laminar planes of media
– Causes a blood-filled channel that easily ruptures

A

aortic dissection

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22
Q

Two main causes of aortic dissection

A

– Hypertension (40-60 years of age): > 90% of cases
– Connective tissue abnormality (younger ages): in association with Marfan’s syndrome or Ehlers-Danlos syndrome

– Rare causes: post-procedural – arterial cannulation; pregnancy

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23
Q

Most commonly involved vasculature in aortic dissection

A

Ascending aorta

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24
Q

Morphology of Aortic dissection
• Intimal tear within ______of aortic valve
• Dissection plane between middle and outer thirds of wall, in the _____
– Dissection usually extends _____
–Usually ruptures_____

A

10 cm

media

anterograde

“out”

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25
Q

If aortic dissection reenters it can form:

A

double-barreled lumen

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26
Q

In hypertensive patients with aortic dissection we see
– Vasa vasorum with :
–In the media:

A

hyaline arteriolosclerosis

: loss of smooth muscle cells

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27
Q

What’s the reasoning for people with Marfans to get aortic dissection?

A

pre-exsisting pathology of cystic medial degernation in pts with CT disorder such as marfans

the cycsitc medial necrosis cause CT tissue weakness and get pools of blue mucinous ground substance disrupting the elastic fibers

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28
Q
A
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29
Q

Clincal presentation of aortic dissection is dependent on :

What are the classic symptoms

A

level of aorta involved

–Sharp pain of anterior chest, uneven pulses and widened mediastinum

–Sudden onset of tearing or stabbing pain in anterior chest radiating to back

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30
Q

This is a complication of an aortic dissection and occurs when blood dissects through media, proximally
• May also rupture into pleural or peritoneal cavities

A

Hemopericardium

31
Q

Inflammation of vessel walls; may affect any size vessel
Caused by:– Immune-mediated processes– Infectious origin– Unknown

A

Vasculitis

32
Q

Vasculitis can be immune complex mediated, how so?

A

– SLE (Systemic Lupus Erythematosis): DNA – anti-DNA complexes
– Hypersensitivity to drugs
– Viral infections: HBsAg – anti-HBSsAg

33
Q

ANCA: anti Neutrophil Cytoplasmic Antibodies assoicated

What is this?

A

cause of vasculitis.

autoantiBs against enZ in granules of neutrophils and we see as Ab titers get higher; the vasculitis get worse

34
Q

What is the disease associated with and target of Antiproteinase-3 or ANCA3

A

Wegener Granulomatosis

target antigen is PR3 (neutrophil granule consituent)

35
Q

What is the vasculitis associated with Anti-myeloperoxidase (MPO-ANCA)

A

Microsocpic polyangiitis and Churger Strauss syndrome

target antiG is myeloperoxidase

36
Q

Vasculitis of infectious origin & unknown origin
Infectious can be direct or indirect.
– Direct invasion:

– Indirect via :

A

Direct is: syphilis, aspergillus, mucormycosis

Indirect: immune mechanisms triggering cross-reactivity

37
Q

Origin of the following vasculitities

-Giant cell arteritis
– Takayasu arteritis
– Polyarteritis nodosa

A

Unknown origin

38
Q

Most common form of systemic vasculitis in adults
• Affects aorta and its major branches, especially temporal artery, ophthalmic, and vertebral arteries

A

Giant Cell (temporal) arteritis–> affects LARVE VESSELS

39
Q

> 50 y, often with painful superficial temporal artery, diplopia, visual loss, headache
– Increased ESR (Erythrocyte Sedimentation Rate)
What do you suspect and how do you diagnosis it?

A

Suspect Giant Cell Arteritis (above is the classic presentation)

Diagnosis done via biopsy

40
Q

Pt comes in complaning of headachesm vision loss and diploplia. You note this little nug on his head… You order a biopsy of 2-3 cm (bc its required for this disease!!!) and what do you expect to see?

A

Pt has Temporal giant cell arteries:

Nodular thickenings of artery with narrowed lumen
 Patchy (discontinuous) segments affected

41
Q

You dx your pt with temporal arteritis… what do you see on histology?

How do you tx this?

A
  • Granulomatous inflammation of inner half of media around internal elastic lamina
  • Destruction of internal elastic lamina
  • Multinucleated giant cells (but not always!)
42
Q 
Pulseless disease (upper extremities), ocular disturbances
•See in Japanese women younger than 40 yrs
A

Takayasu Arteritis

43
Q

In Takayasu Arteritis we see granulomatous inflammation of :
• Pulmonary arterties are involved _____% of the time

A

aortic arch and its branches

50%

44
Q

What causes Takayasu Arteritis?

What do we see on histology?

A

autoimmune etiology
• Histology: lymphocytes, giant cells, collagenous fibrosis

45
Q

Systemic segmental transmural necrotizing inflammation of small or medium-sized muscular
arteries

A

Polyarteritis Nodosa (classic)

*Medium vessel vasculitities*

46
Q

What arteries are affected and spared in polyarteritis nodosa?

A

Renal and visceral arteries affected, spares lung

47
Q

Describe the inflamation and fibrosis we see in polyarteritis nodosa…

is this a episodic or chronic disease?

A

Focal, random, episodic
• All stages of inflammation and fibrosis co-exist

The episodes are focal, random, episodic

but the disease itself can be acute, chronic, subacute, or remittent course

48
Q
A
49
Q

Polyarteritis nodosa is seen in Young adults specfically with this:

A

(30% Hep B antigen), no ANCA

50
Q

Young patient comes to clinic, she has rapidly accelerating hypertension (renal artery involvement), acute Abdominal pain & bloody stools

Your attending says she also has peripheral neuritis

These is a classical clinical picture of which medium vessel vasculitity?

A

Polyarteritis Nodosa

51
Q

What do we see histologically in pts with polyarteritis nodosa?

A

Necrosis with karyorrhexis (broken down fragments of nuclei)

there is transmural or full thickness involvement with lots of neutrophils and inflammation

52
Q

• Endemic in Japan/ Rare, but increasing in the US
Affects: Large, medium and small arteries, often coronaries with aneurysm formation

A

Kawasaki Syndrome

53
Q

Kawasaki can present with which other sysdrome?

A

With mucocutaneous lymph node syndrome
– Mucous membrane inflammation and Enlarged lymph nodes

54
Q

Age distribution of Kawasakis and histology

A
  • 80% are < 4 yrs; leading cause of acquired heart disease in children (in Japan)
  • Histology: Necrosis and inflammation, aneurysms

****resembles polyarteritis nodosa

55
Q

Vasculitis that affects arterioles, capillaries, venules as well as kkin, mucous membranes, lungs, brain, heart, GIT, kidneys, muscles

A

Microscopic Polyangiitis (Leukocytoclastic Vasculitis)

56
Q

In Microscopic Polyangiitis (Leukocytoclastic Vasculitis) we see

  • _________ + in 70%
  • Immunologic reaction to_____, _______ and _____
A

MPO-ANCA+

antigens- drug, Strep, tumor proteins

57
Q
A
58
Q

If kidney and lung are involved in Microscopic Polyangitis, what do we worry about?

A

Necrotizing glomerulonephritis (90%) and pulmonary capillaritis

59
Q

Histology of a arteriole shows fibrinoid necrosis, neutrophils and nuclear dust. Dx?

A

microscopic polyangiitis (leukocytoclastic vasculitis)… this is in arterioles/capillaries/ venules

simular histology to polyartieritis nodosa and kawasaki but po,yarteritis affects meduim musclar vesses and Kawasaki affects large/medium/small arteries (often coronies)

60
Q

Major clinical features of pts with Microscopic polyangiitis

A

Major clinical features are dependent on vascular bed involved:
• Hemoptysis, hematuria, proteinuria, abdominal pain or bleeding, muscle pain or bleeding, & cutaneous purpura

61
Q

Wegener Granulomatosis is a Necrotizing vasculitis, it causes
– Granulomas of:

– Vasculitis :
– Glomerulonephritis

A

Granulomas of lung &/or upper respiratory tract (ear, nose, sinuses, throat)

Vasculitis of small to medium sized vassels in lungs & upper respiratory tract

62
Q
A
63
Q

In Wegener Granulomatosis______ present in >95%
– Likely cell-mediated hypersensitivity response against inhaled
infections or environmental antigen

A

PR3-ANCAs

64
Q

Who more commonly gets Wegener Granulomatosis?

What is their outcome?

A

M > F, ~40 years of age
– Without treatment: 1 yr – 80% mortality

65
Q

– Symptom profile for
• Pneumonitis (95%)
• Sinusitis (90%)
• Nasopharyngeal ulcerations (75%)
• Renal disease (80%)

A

Wegener granulomatosis

66
Q

Small vessel vasculitis associated with

– Peripheral EOSINOPHILIA & infiltration of vessels by eosinophils
– Asthma
– Allergic rhinitis
– Lung infiltrates
– Extravascular necrotizing granulomas

A

Churg-Strauss Syndrome: allergic granulomatis and angiitis

67
Q

Whats a key difference in Wegeners granulomatosis vs Churg-Strauss?

A

Wegener: Granulomas of lung &/or upper respiratory tract (ear, nose,
sinuses, throat) so focused around vessels

Churg-Strass has Extravascular necrotizing granulomas

68
Q

Clincal symptoms of Churg-Strauss syndrome

A

– Palpable purpura
– GI bleeding
– Renal impairment
– Cardiomyopathy

69
Q

Are ANCAs present in both Wegener and Churg-Stauss?

A

PR3-ANCA present in 95% of Wegener, but ANCA present in minority in Churg-Strauss; its more of a hypersensitivity or allergic stimulus

70
Q

Inflammation and thrombosis of medium to small sized muscular arteries and secondarily the veins
and nerves

A

Thromboangiitis Obliterans

(Buerger disease)

71
Q

What arteries are usually involved in Thromboangiitis Obliterans(Buerger disease)?

What population is it more common in?

A

Tibial and radial arteries (limb involvement)

SMOKERS, <35, Israeli, Indian and Japanese

72
Q

Clincal presentation of Thromboangiitis Obliterans(Buerger disease) and etiology

A

Painful ischemic disease
– Gangrene of limbs, requiring amputation
– Etiology unknown
• Direct endothelial cell toxicity by a component of tobacco

73
Q

Raynaud Phenomenon =
• Paroxysmal pallor or cyanosis of fingers, toes, nose or ears

Primary causes:

Secondary causes:

A

• Primary
– Recurrent vasospasm of unknown cause (exaggerated response to cold)
– Young, healthy women
– No structural changes in the arterial walls (until late in disease)
• Secondary
– Arterial insufficiency due to narrowing and can be due to SLE, SS (Systemic sclerosis – Scleroderma), atherosclerosis, Buerger disease

CV Final Material (16 decks)

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