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Cardiovascular System > Peripheral Vascular Disease > Flashcards

Peripheral Vascular Disease Flashcards

1
Q

What is an aneurysm?

What is an arterial dissection?

A

Aneurysm:

  • Localized dilatation of a blood vessel (aorta) or heart
  • Types:
    • True: involves all three layers of wall
    • False (pseudoaneurysms): Wall defect leading to extravascular hematoma

Arterial dissection:

  • blood enters the wall of the artery
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2
Q

What are the two pathologic processes that can cause an aneurysm?

A
  • Inadequate or abnormal syntheses of collagen

or

  • Excessive connective tissue degradation
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3
Q

What syndromes are caused by inadequate or abnormal syntheses of collagen?

What is the pathogenesis for each?

A
  1. Marfan syndrome
    • 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
  2. Ehlers-Danlos syndrome
    • One variant has defective synthesis of Type III collagen
    • Leads to aneurysm formation
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4
Q

How can excessive connective tissue degradation lead to anuerysm formation?

A
  • Occurs with increased matrix metalloproteinase (MMP) or decreased tissue inhibitors of metalloproteinase (TIMP)
  • In the setting of inflammation (atherosclerosis) polymorphisms of MMP &/or TIMP genes may predispose to aneurysm formation
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5
Q

What can loss of smooth muscle cells lead to in the vascular wall?

A
  • Loss of smooth muscle cells
    • Thickening of intima (due to atherosclerosis)
  • Leads to ischemia of inner media
    • Systemic hypertension
  • **Narrows vasa vasorum **⇒ ischemia of outer media
    • Morphologic results is cystic medial degeneration
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6
Q

What are the most common causes of aneurysms?

A
  1. Atherosclerosis – abdominal aorta
  2. Hypertension – ascending aorta
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7
Q

What are some uncommon causes of aneurysms?

A
  • Congenital defects
  • Infections (bacteria, fungi)
  • Trauma – AV (fistula) aneurysm
  • Vasculitis
  • Genetic defects in collagen (Marfan’s & Ehlers-Danlos)
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8
Q
  1. What congenital defects lead to aneurysm formation?
  2. What infections lead to aneurysm formation?
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)
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9
Q
  • What is the most common location of arotic aneuryms?
  • What are some less common locations?
  • What is the most common etiology of aortic anuerysms?
  • What is the most common association of aortic aneurysms?
A
  • Abdominal aortic aneurysm (AAA): MOST COMMON LOCATION
    • Below renal arteries and above bifurcation
  • Less common: Arch of aorta, thoracic aorta and iliac arteries
  • Most common cause – atherosclerosis
  • More common in men & smokers
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10
Q

Describe the **morphology **of aortic aneurysms:

A
  • Up to 15 cm diameter
  • Thinning & destruction of media
  • Mural thrombus
  • Saccular or fusiform
  • Variants:
    • inflammatory – unknown etiology
    • mycotic – secondary infection (salmonella gastroenteritis) of an atherosclerotic wall
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11
Q

What is the classic clinical presentation of AAA?

What complications can arise from AAA?

A
  • More common in men over 50
  • Present as pulsatile abdominal mass

​Complications:

  1. Rupture into peritoneum or retroperitoneum
  2. Vascular obstruction – renal, mesenteric, spinal arteries
  3. Embolism of atheroma or mural thrombus to kidneys or lower extremities
  4. Impingement of ureter(s)
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12
Q

Risk of rupture is directly proportional to ____.

A

size

  • Aggressive management for large aneurysms (> 5 cm)
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13
Q

What are causes of thoracic arotic aneurysms?

A
  1. Hypertension
  2. Marfan’s syndrome
  3. Syphilis (tertiary)
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14
Q

What are clinical features associated with thoracic aortic aneurysms?

A
  1. Mediastinum encroachment
    • Tracheal compression
    • Esophageal compression
    • Bone erosion
    • Cough due to irritation of recurrent laryngeal nerve
  2. Cardiac Symptoms
    • Heart failure due to aortic valve insufficiency
  3. Aortic rupture
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15
Q

What causes an aortic dissection?

What is the pathogenesis of aortic dissections?

A
  • Blood between and along laminar planes of media
    • Causes a blood-filled channel that easily ruptures
  • Pathogenesis/etiology
    • Hypertension (40-60 years of age):
      • > 90% of cases
    • Connective tissue abnormality (younger ages): in association with Marfan’s syndrome or Ehlers-Danlos syndrome
    • Ascending aorta most commonly involved
    • Rare causes:
      • post-procedural – arterial cannulation
      • pregnancy
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16
Q

What is the morphology of aortic dissection?

What patients have a pre-existing condition to aortic dissection?

A
  • Intimal tear within 10 cm of aortic valve
  • Dissection plane between middle and outer thirds of wall, in media
    • Usually extends anterograde
    • Usually ruptures “out”
    • May reenter and form a double-barreled lumen
  • In hypertensive patients
    • Vasa vasorum: hyaline arteriolosclerosis
    • Media: loss of smooth muscle cells
  • Pre-existing pathology of cystic medial degeneration in patients with connective tissue disorder (Marfan syndrome)
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17
Q

What is responsible for aortic dissection in Marfan’s Syndrome?

A
  • Cystic medial necrosis causes connective tissue weakness
  • Pools of blue mucinous ground substance disrupt elastic fibers
18
Q

What is the clinical course of an aortic dissection?

A
  • Dependent on level of aorta involved
  • Sharp pain of anterior chest, uneven pulses and widened mediastinum
  • Types A and B
  • Classic clinical symptoms:
    • Sudden onset of tearing
    • Stabbing pain in anterior chest radiating to back
19
Q

What are complications associated with aortic dissection?

A
  • Hemopericardium occurs when blood dissects through media, proximally
    • causes tamponade
  • May also rupture into pleural or peritoneal cavities
20
Q

What is vasculitis?

What general pathologic processes can cause it?

A
  • Inflammation of vessel walls; may affect any size vessel
  • Pathogenesis
    1. Immune-mediated processes
    2. Infectious origin
    3. Unknown
21
Q

Pathogenesis of Immune-mediated Vasculitis:

Immune-compex mediated

A
  1. SLE (Systemic Lupus Erythematosis): DNA – anti-DNA complexes
  2. Hypersensitivity to drugs
  3. Viral infections
    • HBsAg – anti-HBSsAg
22
Q

Pathogenesis of Immune-mediated Vasculitis:

Anti Neutrophil Cytoplasmic Antibodies (ANCA) associated

A
  • Autoantibodies against enzymes in granules of neutrophils
    • Ab titers mirror clinical severity
  • Two main patterns:
    1. Antiproteinase-3 (PR3-ANCA) – Wegener Granulomatosis
      1. Target antigen: PR3 (neutrophil granule constituent)
      2. FYI PR3-ANCA = c-ANCA
    2. Anti-myeloperoxidase (MPO-ANCA) – Microscopic polyangiitis and Churg-Strauss syndrome
      • Target antigen: myeloperoxidase
      • FYI MPO-ANCA = p-ANCA
23
Q

What disease is associated with antibodies to endothelial cells?

A

Kawasaki disease

24
Q

Vasculitis of infectious origin & unknown origin:

A
  1. Infectious
    1. Direct invasion
      • Syphilis
      • Aspergillus & mucormycosis
    2. Indirect
      • Immune mechanisms triggering cross-reactivity
  2. Unknown
    • Giant cell arteritis
    • Takayasu arteritis
    • Polyarteritis nodosa
25
1. **Large vessel vasculitis: ** 2. **Medium vessel vasculitis: ** 3. **Small vessel vasculitis: **
1. **Large vessel vasculitis:** Granulomatous disease * _Giant cell arteritis_ * _Takayasu arteritis_ 2. **Medium vessel vasculitis:** * _Polyarteritis nodosa_ - immune complex mediated * _Kawasaki disease_ - anti-endothelial antibodies 3. **Small vessel vasculitis:** * _Microscopic polyangitis_ * _Wegener granulomatosis_ * _Churg-Strauss syndrome_
26
**Giant Cell (Temporal) Arteritis:** * What does it affect? * What is the etiology? * What is the clinical presentation, diagnosis and treatment?
* **Most common form of systemic vasculitis in adults** * **Affects aorta and its major branches** * temporal artery, ophthalmic, and vertebral arteries * Pathogenesis: uncertain * **Clinical:** * _\> 50 y_, often with painful superficial temporal artery, diplopia, visual loss, headache * _Increased ESR_ * Diagnosis: biopsy * Treatment: steroids
27
What is the **morphology **of temporal (giant cell) arteritis?
* _Nodular thickenings of artery with narrowed lumen_ * Patchy (discontinuous) segments affected * Biopsy requires 2-3 cm * Multiple levels examined
28
What is the **histology** of temporal arteritis?
* _Granulomatous inflammation of inner half of media_ _around internal elastic lamina_ * Destruction of internal elastic lamina * Multinucleated giant cells (but not always!)
29
Describe what is seen in Takayasu Arteritis:
* **Pulseless disease** (upper extremities), ocular disturbances * **Japanese women younger than 40 yrs** * _Granulomatous inflammation of aortic arch and its branches_ * **Pulmonary arterties are involved 50%** * **​**coronary and renal arteries may be involved * **Pathogenesis:** _autoimmune_ etiology * **Histology:** lymphocytes, giant cells, collagenous fibrosis
30
What is **polyarteritis nodosa**? What is the pathogensis? How is it treated?
* **Systemic segmental transmural necrotizing inflammation** of _small or medium-sized muscular arteries_ * **Renal and visceral arteries affected, spares lung** * Focal, random, episodic * _All stages of inflammation and fibrosis co-exist_ * **Aneurysms** * _Necrosis with karyorrhexis_ * **Young adults (30% Hep B antigen), no ANCA** * Acute, chronic, subacute, or remittent course * _90% remission or cure_ - **corticosteroids, cyclophosphamide**
31
What is the **classic presentation** of polyarteritis nodosa?
1. **Rapidly accelerating hypertension** (renal artery involvement) 2. **Abdominal pain & bloody stools** 3. **Peripheral neuritis**
32
**Kawasaki Syndrome:** * Where is endemic? * What vessels are affected? * What is the most common demographic?
* _Endemic in Japan_ * Rare, but increasing in the US * Large, **medium** and small arteries * often coronaries with aneurysm formation * _With mucocutaneous lymph node syndrome_ * Mucous membrane inflammation * Enlarged lymph nodes * 80% are \< 4 yrs * **Leading cause of acquired heart disease in children** (in Japan)
33
What does Kawasaki syndrome resemble on histology? What is the etiology of Kawasaki syndrome?
* **Histology:** Necrosis and inflammation, aneurysms, _resembles polyarteritis nodosa_ * Etiology: * ? _autoantibodies to endothelial cells_ and smooth muscle cells * ? _Infectious agent_ (virus) trigger
34
**Microscopic Polyangitis** * What vessels are affected? * What type of ANCA? (if any) * How will it appear on histology?
* **Arterioles, capillaries, venules** * Skin, mucous membranes, lungs, brain, heart, GIT, kidneys, muscles * **Necrotizing glomerulonephritis (90%)** and _pulmonary capillaritis_ * **MPO-ANCA + in 70%** * Immunologic reaction to antigens- drug, Strep, tumor proteins * **Histology:** fibrinoid necrosis, neutrophils, nuclear dust (karyorrhexis)
35
What determines the major clinical features in microscopic polyangitis?
* Major clinical features are _dependent on vascular bed involved_: 1. hemoptysis 2. hematuria 3. proteinuria 4. abdominal pain or bleeding 5. muscle pain or bleeding 6. cutaneous purpura
36
**Wegener Granulomatosis** * What areas are affected? * What type of ANCA? (if any)
* **Necrotizing vasculitis** * Granulomas of lung &/or upper respiratory tract (ear, nose, sinuses, throat) * Vasculitis of _small to medium sized vessels_ in lungs & upper respiratory tract * Glomerulonephritis * **PR3-ANCAs present in \>95%** * Likely cell-mediated hypersensitivity response against inhaled infections or environmental antigen
37
What is the most common demographic affected by Wegener granulomatosis? What is the prognosis and associated symptoms?
* **M \> F, ~40 years of age** * Prognosis: * Without treatment: 1 yr – 80% mortality * Symptoms: * Pneumonitis (95%) * Sinusitis (90%) * Nasopharyngeal ulcerations (75%) * Renal disease (80%)
38
What type of vasculitis is Churg-Strauss syndrome?
**allergic granulomatosis and angiitis**
39
**Churg-Strauss Syndrome:** * What is it associated with? * What are the clinical symptoms? * Is there ANCA association?
* **Small vessel vasculitis associated with** * **Asthma** * Allergic rhinitis * Lung infiltrates * **Peripheral eosinophilia & infiltration of vessels by eosinophils** * _Extravascular necrotizing granulomas_ * **Clinical symptoms** * Palpable purpura * GI bleeding * Renal impairment * Cardiomyopathy * _Possible hyper-responsiveness to allergic stimulus_ * MPO-ANCAs – present in minority
40
**Thromboangiitis Obliterans (Buerger disease): ** * What areas are affected? * What are the clinical features?
* Inflammation and thrombosis of medium to **small sized muscular arteries** and _secondarily the veins and nerves_ * **Tibial and radial arteries** * **Smokers\*** * \< 35 yrs, Israeli, Indian subcontinent, & Japanese * Painful ischemic disease * _Gangrene_ of limbs, requiring amputation * Etiology unknown * Direct endothelial cell toxicity by a component of tobacco
41
What is **Raynaud's phenomena**? What is the difference between primary and secondary?
**Paroxysmal pallor or cyanosis of fingers, toes, nose or ears** * **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_ * Can be due to SLE, SS (Systemic sclerosis – Scleroderma), atherosclerosis, Buerger disease

Cardiovascular System (35 decks)

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