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CRRAB I Final > Cardiac Pathology - Vascular Disease > Flashcards

Cardiac Pathology - Vascular Disease Flashcards

1
Q

What are the 5 main mechanisms of vascular disease?

A
  1. Gradual lumen obstruction (atherosclerosis (arteries/aorta) or arteriolosclerosis (arterioles))
  2. Sudden lumen obstruction (thrombosis, emoblism, or aortic/arterial dissection)
  3. Aneurysm/dissection (prefers larger caliber arteries (esp. aorta) with principle risk of rupture
  4. Vasculitis (spectrum of inflammatory diseases affecting aorta down to arterioles/capillaries/venules)
  5. Extrinsic vascular compression
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2
Q

What are examples of extrinsic vascular compression?

A
  • Compartment syndromes: vascular collapse from surrounding hemorrhage/edema/inflammation. in a limited anatomic compartment (extremities, abdomen)
  • -Vena cava syndromes (SUPERIOR & inferior): obstruction to caval flow usually caused by surrounding neoplastic adenopathy or occasionally from intra-caval tumor thrombus
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3
Q

What is MECHANISM #1 for vasculitis?

A
  • VAST MAJORITY of most clinically morbid disease is ARTERIAL and dominated by ATHEROSCLEROSIS
  • atherosclerosis prefers larger vessels (aorta, medium to large arteries): causing gradual lumen obstruction +/- aneurysmal dilation.
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4
Q

What are the main risk factors for atherosclerosis?

A

-Older age, male gender, post-menopausal women, FAMILIAL tendency (typically polygenic/multifactorial), hypercholesterolemia, hypertension, diabetes mellitus, and smoking

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5
Q

What is the pathogenesis associated with atherosclerosis?

A
  • Only crudely understood
  • “endothelial injury” leading to:
  • -intimal collection of lipid-laden macrophages
  • -Smooth muscle migration from media into intima
  • -Intimal accumulation of extra-cellular matrix
  • -WBCs as co-factors in above
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6
Q

What is an unstable plaque?

A

Inc. risk of surface rupture and platelet aggregation/fibrin clot formation = thrombosis - with risk of complete/sudden lumen occlusion

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7
Q

What is HTN or diabetes mellitus is present with atherosclerosis?

A
  • Large vessel atherosclerosis is accelerated

- Arterioles become gradually obstructed (arteriolosclerosis)

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8
Q

What does arteriolosclerosis cause in HTN and diabetes?

A

Typically non-bypassable disease in the microcirculation: kidneys, retina, CNS/peripheral nervous system, heart and skin (e.g. diabetic foot ulceration)
-Untreatable small vessel vasculitis

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9
Q

What are the two types of hypertension?

A

95% - “essential” with multifactorial/polygenic/familial factors
5% - “secondary” (usually from reveal artery or adrenal disease) = potentially curable cases (DONT MISS)

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10
Q

What is malignant/accelerated HTN?

A

Medical emergency!!

Inc. risk of acute end-organ injury: heart, CNS, kidneys

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11
Q

What causes chronic end organ effects in HTN?

A

-Arteriolosclerosis, accelerated atherosclerosis and Inc. left ventricular and aortic strain: CAD/ischemic heart disease, thoracic aortic aneurysm, LVH/CHF, stroke (ischemic or hemorrhagic), retinopathy, nephropathy

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12
Q

What is the #2 mechanism of atherosclerosis?

A

-Sudden lumen occlusion
–> most common cause of life-threatening vascular events
Arterial: acute myocardial infarction, stroke, mesenteric ischemia/bowel infarction and acute leg ischemia/gangrene

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13
Q

What is an embolism?

A

Cardiac source until proven otherwise (e.g. left atrial or left ventricular thrombus)

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14
Q

Sudden lumen occlusion: Arterial:

A
  • Acute myocardial infarction, stroke, mesenteric ischemia/bowel infarction and acute leg ischemia/gangrene
  • Vast majority: unstable atheromatous plaque with rupture causing overlying occlusive thrombosis
  • Embolism
  • Aortic dissection can suddenly occlude orifices of exiting arteries
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15
Q

What happens in Veins with occlusive thrombosis?

A
  • DVT: (usually iliofemoral veins) with risk of PE and sudden death: serum D-dimer testing and CT angiography
  • Splanchnic venous thrombosis (mesenteric, portal/splenic, hepatic veins) = risk of bowel infarction or Budd-Chiari syndrome: Inc. likelihood of associated congenital hyper coagulable state or chronic myeloproliferative syndrome
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16
Q

What do you see and what is first treatment in PE?

A

Shortness of breath, chest pain

-Tx: first heparin, then may need vena cava filter/”strainer” if more traveling thrombi

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17
Q

With any DVT, what is it usually caused by?

A

Surgery/trauma/sepsis OR due to serious underlying congenital or acquired hyper coagulable state (e.g. malignancy)?

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18
Q

What is the #3 mechanism of atherosclerosis?

A

Aorta/large artery aneurysm or dissection due to arterial wall weakening

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19
Q

What is aneurysmal dilation?

A
  • Especially affects aorta (Laplace’s law) but also can involve medium to large arteries
  • Mechanism of weakening:
  • -Ordinary atherosclerosis (esp. infra-renal abdominal aorta in smokers)
  • Hypertension (esp. ascending throacic aorta)
  • Misc. causes: inherited connective tissue disease (e.g. Marfan’s), vasculitis (Takayasu’s and giant cell - big vessel vasculitis), connective tissue/autoimmune diseases, and infection or aortic/arterial wall
  • –> most feared complication: rupture and exsanguination
20
Q

What is Aortic Dissection?

A

Dissecting hemorrhage/hematoma within aortic wall

  • Type A (most lethal) = ascending +/- more distal aorta –> may lead to tamponade & coronary artery occlusion
  • Type B = descending aorta and/or aortic arch
21
Q

What are the pre-disposing factors for dissection?

A
  • HTN if patient > 40 yrs

- Inherited connective tissue disorder (e.g. Marfan’s) if patient

22
Q

What is the #4 mechanism of atherosclerosis, Vasculitis?

A

=inflammation of vascular wall ranging from neutrophilic to granulomatous

  • lumen compromise secondary to inflammatory reaction +/- overlying thrombosis
  • can be associated with secondary aneurysms
  • Clinically a spectrum from benign skin limited disease (luekocytoclastic vasculitis) commonly to aggressive visceral vasculitis disease with high mortality (e.g. ANCA-associated vasculitides)
23
Q

What age groups are vasculitic diseases/symptoms common?

A
  • Largely adult diseases:
  • -Except Henoch-Schonlein Purpura (HSP = IgA-related vasculitis) and Kawasaki disease (risk of coronary vasculitis)
  • Vasculitis in middle-aged/elderly adults:
  • if affecting distribution of external carotid artery = GIANT CELL (TEMPORAL) arteritis with risk of vision loss: diagnose with temporal artery biopsy and Rx with corticosteroids
24
Q

What vasculitis might you see commonly in practice?

A

Giant cell arteritis: external carotid system is inflamed –> risk of vision loss

25
Q

What are 5 life-threatening/aggressive vasculitis in adults?

A
  1. Anti-neutrophil cytoplasmic antibody (ANCA) - associated diseases (small vessel vasculitis)
    - -Wegener’s: anti-PR3 antibodies (c-ANCA)
    - -Microscopic polyangiitis: anti-myeloperoxidase Ab (MPO = pANCA)
  2. Goodpasture’s syndrome = anti-glomerular basement membrane antibodies (anti-GBM)
  3. Occasionally connective tissue diseases (e.g. SLE)
  4. Polyarteritis nodosa (PAN)
  5. Churg-Strauss syndrome (asthma with partial association with anti-MPO)
26
Q

What is on your differential if you see a vasculitis with pulmonary-renal syndrome?

A
  • Diffuse pulmonary hemorrhage plus rapidly progressive glomerulonephritis
  • -> Ddx: ANCA-associated vasculitis vs. Goodpasture’s vs. SLE
27
Q

How to diagnose vasculitis using clinical suspicion?

A

Often challenging differential diagnosis exercise (variable/non-specific symptoms)

28
Q

How to diagnose vasculitis using serological testing?

A
  • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) = systemic inflammation markers
  • Antibody detection: ANCA (PR3/MPO), ANA/anti-ds DNA, anti-GMB, IgA detection in tissues with immunofluorescence
  • Misc: cryoglobulins, complement (C3/C4), and Hepatitis B and C serology
29
Q

What are routine things you order for vasculitis diagnosis?

A

ANCA panel + autoimmune panel!

30
Q

What imaging studies do you use for vasculitis diagnosis?

A 
Especially aorta (Takayasu's disease) and organ-directed angiography (small aneurysm formation in PAN: kidneys, mesentery)
-Chest X-ray/CT scan (Wegener's/pulmonary-renal syndrome)
31
Q

What tissue biopsies are used for vasculitis diagnosis?

A

Skin or deeper
-Especially ANCA-associated disease/pulmonary-renal syndromes (lung or kidney Bx), giant cell arteritis (temporal artery), HSP (kidney/skin), connective tissue disease with a dominant vasculitic component (varied site biopsies) and leukocytoclastic vasculitis (skin)

32
Q

What are the rarest vasculitis categories?

A

-Polyarteritis nodosa
-Churg-Strauss syndrome
-Thromboangiitis obliterans
(Buerger’s disease) = distal extremity arteritis in heavy cigarette smokers

33
Q

What are the benign types of vascular neoplasms?

A
  1. Hemangiomas
  2. Lymphangiomas
  3. Glomus tumor
  4. Bacillary angiomatosis
34
Q

What is a Hemangioma?

A

Most common type of benign vascular neoplasm.

  • Dominantly prefer the skin (cherry/purple papules)
  • May involve any visceral organ: but favors liver, spleen and soft tissue
  • Pyogenic granuloma - rapidly growing/friable capillary hemangioma in response to trauma - unpredictable response to trauma - not concerning
35
Q

What are lymphangiomas?

A

Uncommon

-Largest examples most frequently in neck/axilla of young children (cystic hygroma)

36
Q

What is a glomus tumor?

A

Glomus cell proliferation associated with vascular channels: PAINFUL small tumors of distal digits.

37
Q

What is Bacillary angiomatosis?

A

Vascular proliferation associated with Bartonella infection (e.g. cat scratch species) in immunosuppressed patients

38
Q

What are vascular ecstasies?

A
  • Usually discrete lesions with dilated pre-existing vessels resembling hemangiomas but appearing flat/non-papular
  • Very common in skin/mucous membranes
  • Common cause of birth marks (e.g. port wine stain): extreme form = Sturge-Weber syndrome
  • Systemic vascular ectasia syndrome with risk of serious bleeding (epistaxis, GI, GU) = Osler-Weber-Rendu (Hereditary Hemorrhagic Telangiectasia)
39
Q

What are arteriovenous malformations?

A
  • Tangled mass of arteries and veins without intervening capillary bed
  • If large enough: can cause high output heart failure
  • In brain: risk of rupture with fatal cerebral hemorrhage
40
Q

What is an arteriovenous fistula?

A

Short circuiting of vascular system.

  • From penetrating vascular injury
  • Arterial aneurysm rupturing into adjacent vein
  • Surgically created for hemodialysis
41
Q

What are two malignant, LOW GRADE vascular proliferations?

A
  1. Kaposi’s sarcoma

2. Epithelioid hemangioendothelioma

42
Q

What is Kaposi’s sarcoma?

A

SKIN +/- visceral involvement:

  • Associated with HHV-8
  • HIV and non-HIV associated types
  • Immunosuppressed vs. non-immunosuppressed patients
  • Very common in Africa
  • Some older males have slow growing kaposi sarcoma on their lower legs
43
Q

What is Epithelioid hemangioendothelioma?

A

Esp. liver and soft tissue

44
Q

What is the most common HIGH GRADE malignant vascular neoplasia?

A

Angiosarcoma

45
Q

What is Angiosarcoma?

A
  • Tendency to occur in skin of head and neck in elderly but any visceral soft tissue site can be affected (e.g. liver, breast)
  • Typically aggressive reddish/purple lesions in skin: often recurrent disease with hematogenous metastases.
  • Patients with chronic lymphedema: Inc. risk of angiosarcoma (e.g. post mastectomy, radiation, ancillary dissection patients = Stewart-Treves Syndrome)

CRRAB I Final (21 decks)

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