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CPR 2 Exam 1 > Hillard Vascular Pathology Part #2 > Flashcards

Hillard Vascular Pathology Part #2 Flashcards

1
Q

Differentiate the three types of arteriosclerosis?

A
  • Arteriolosclerosis:
    • effects small arteries and arterioles has hyaline and hyperplastic changes on histo
  • Atherosclerosis:
    • Gruel and hardening, atheromatous plaque formation
    • Stenosis/occlusion of artery, plaque rupture, aneurysm
  • Monckeberg medial sclerosis
    • age related degeneration
    • Calcification of muscular arteries and IEM
    • No narrowing of lumen
    • NOT clinically significant
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2
Q

What causes Atherosclerosis?

A
  • Coronary, cerebral, and peripheral vascular disease
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3
Q

What are the non modifiable risk factors for atherosclerosis?

A
  • Genetic abnormalities
  • Family history
  • Increasing age
    • 40-60 5x higher risk
  • Males
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4
Q

How does estrogen play a role in atherosclerosis?

A

It is protective in premenopausal estrogenized women, however estrogen therapy post menopause is not protective

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5
Q

Modifiable risk factors for atherosclerosis?

A
  • Hyperlipidemia
  • Htn
  • Smoking
  • Metabolic syndrome
  • Lack exercise
  • Competitive/stressful lifestyle

Synergistic effect

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6
Q

What can help lower LDL?

A
  • Diet higher in soluble fiber
  • Statins
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7
Q

How do you increase HDL?

A
  • Exercise
  • Moderate alcohol
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8
Q

How does hyperhomocysteinemia impact cardiovascular system?

A
  • Increase levels correlate to increased coronary atherosclerosis
  • Increased peripheral vascular disease risk
  • Increased stroke risk
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9
Q

How does increased CRP impact cardiovascular system?

A
  • Measures inflammation
  • Increased by IL 6
  • Correlates with increased CV disease risk
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10
Q

Describe the activated state of endothelium

A
  • Chronic endothelial injury/dysfunction increases expression of procoagulants, adhesion molecules, and proinflammatory factors
  • Alters expression of chemokines, cytokines and growth factors
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11
Q

Pathogenesis of atherosclerosis>

A
  • LDL deposits in the intima of arteries
  • Macrophages take in the lipid and foam cells are created
  • GF’s are signaled such as TGF-a, PDGF, FGF resulting in proilferation of sm muscles and extracellular matrix
  • These foam cells build up in the intima
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12
Q

What re the three “outcomes” of progressive atherosclerotic disease?

A
  • Aneurysm and rupture
  • Occlusion by thrombus
  • Critical stenosis
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13
Q

How does atherosclerotic disease impact brain?

A
  • Can lead to intracerebral hemorrhage
  • Multiple silent strokes appearing as dementia
  • Strokes
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14
Q

How does atherosclerosis impact kidneys?

A
  • Renal artery stenosis leading to developed HTN
  • Chronic renal insufficiency leading to renal failure
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15
Q

How does atherosclerosis impact GI system?

A
  • Can lead to ischemic bowel and potentially rupture leading to sepsis
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16
Q

Describe an aneurysm

A
  • excessive localized abnormal dilation of blood vessel or ventricular wall
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17
Q

True aneurysm vs false?

A
  • True is an intact but thinned muscular wall at site of dilation
  • False is a defect through the wall of vessel communicating with extravascular hematoma that communicates with the intravascular space
    • “pulsating hematoma”
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18
Q

What cardiac risks are associated with Marfan’s

A

Aortic aneurysm and aortic dissection

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19
Q

What are the cardiovascular implications of Ehler’s Danlos syndrome?

A
  • Vascular type (IV)
    • rupture of large arteries
    • MVP
  • Mutation in COL3A1
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20
Q

What is the most important risk factor for AAA?

A

atherosclerosis

21
Q

Describe a symptomatic AAA.

A
  • Non ruptured:
    • pain in abdomen and back
  • Ruptured:
    • severe acute pain
    • pulsatile abdominal mass
    • hypotension
22
Q

When is surgical bypass considered for an AAA?

A

>5cm

23
Q

Describe how the majority of AAA cases are presented?

A
  • Majority are asx
  • have pulsatile abdominal mass
  • Incidental or during workup of PVD find on radiology
24
Q

What type of AAA responds well to steroids?

A
  • IgG4 inflammatory type
25
Q

What is the most important risk factor for thoracic aortic aneurysm?

A
  • Hypertension #1
  • Syphilitic aortitis
  • CTD
  • Vasculitis
26
Q

What are the clinical symptoms of thoracic aortic aneurysm?

A
  • Asymptomatic until rupture
  • Breathing difficulties
  • Respiratory treeBreathing difficulties Esophagus  dysphagiaRecurrent laryngeal nerve  cough
27
Q

Tertiary syphilis impact on CV system?

A
  • Obliterative endarteritis of vasa vasorum leading to thoracic aneurysm
  • Aortic valve regurgitation can also occur
28
Q

How does aortic dissection present? (Triad)

A
  • Sharp ripping tearing thoracic pain
  • Mediastinal widening on CXR
  • Pulse abnormalities
29
Q

Causes of aortic dissection?

A
  • Htn
  • CTD
30
Q

What is the most common type of aortic dissection?

A
  • ascending aorta next to left common carotid artery DeBakey Type I
31
Q

Gian cell (temoral) arteritis what is it how does it present?

A
  • Most common vasculitis in older adults
  • Affects large arteries in the head
    • headache, facial pain, ocular symptoms
32
Q

How does Takayasu arteritis present and what is it?

A
  • Granulomatous autoimmune vasculitis of large to medium arteries
  • Thickening of the aorta and major branch vessels
  • Age <50 and females
  • Weakening of UE pulses & ocular disturbances
33
Q

What type of immune mediated response is giant cell arteritis?

A

T cell mediated

34
Q

Polyarteritis nodosa (PAN) is associated with what disease?

A

HBV

35
Q

How will PAN present?

A
  • Fibrinoid necrosis with vasculitis on biopsy
    *
36
Q

Kawasaki Disease?

A
  • Illness of infancy or early childhood
  • Arteitis of large to medium vessels
  • Infectious viral trigger
  • Febrile illness, strawberry tongue, conjunctivitis, erythema of palms soles, cervical LAD and genital rash
37
Q

Granulomatosis with polyangiitis?

A
  • +/- necrotizing renal pathology
  • Associated with PR3 ANCA (c-ANCA)
  • Males 40 yo
  • Vasculitis of respiratory tract
38
Q

Churg Strauss Syndrome (allergic granulomatosis and angiitis) presentation?

A
  • small vessel vasculitis associated with asthma hypereosinophilia lung infiltrates
  • Palpable purpura, GI tract bleeding & renal disease
  • Cardiomyopathy/myocarditis and infarction
    • Heart involved in 60% patients and accounts for half of deaths
39
Q

Look for key to granulomatosis with polyangiitis key hallmark on histo

A

40 min in

40
Q

Bechet’s Disease presentation

A
  • Classic triad of oral apthous ulcers, genital ulcers, and uveitis
  • Presents with arthritis, skin involvement, lung, GI and CNS
  • Neutrophilic vasculitis
  • Assoc. with HLA-B51
41
Q

Thromboangiitis obliterans (Buerger Disease), who does it affect, what causes it, what arteries does it impact?

A
  • Heavy smokers <35
  • Delayed hsn rxn or toxic reation to cigarette process
  • Thrombosis →Vascular insufficiency → Tissue death
  • Acute and chronic vasculitis of small and med vessels particularly tibial and radial arteries
42
Q

Primary Raynaud’s phenomenon?

A
  • Symmetric involvement of digits
    • young women
    • episodic and spontaneous remission
43
Q

What is meant by red white and blue in Reynold’s phenomenon?

A
  • Proximal vasodilation (Red)
  • Central vasoconstriction (white)
  • Distal cyanosis (blue)
44
Q

Secondary Raynaud’s phenomenon?

A
  • Asymmetric involvement of digits
  • Component of another arterial disease
  • Worsens with time
45
Q

What is microscopic poolyangiitis?

A
  • Necrotizing vasculitis of small vessels particularly capillaries and venules
  • Uniform stage of disease in all vessels
  • Affects any organ system especially kidney lung
  • Associated MPO-ANCA
  • No significant immunoglobulin deposition
46
Q

What happens to the organ systems in Microscopic polyangiitis?

A
  • Hematuria & Proteinuria (nephritis)
  • Hemoptysis
  • Cutaneous purpura
  • muslce weakness
  • Bowel pain/bleeding
47
Q

What are the risks associated with balloon angioplasty with endovascular stenting? How do we overcome this?

A
  • Compression can rupture the occluding plaque
  • Abrupt reclosure can result from thrombosis and spasm
  • Use drug eluting stent which releases anti proliferative drugs to block smooth muscle activation
48
Q

What is CABG?

A
  • Coronary artery bypass grafting
  • Internal mammary artery or great sapenous vein are used to bypass atherosclerotic heart vessels

CPR 2 Exam 1 (21 decks)

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