Vascular Pathology Part 2 - Dr. Hillard Flashcards by Radhika Patel

Arteriosclerosis means what and 3 types

hardening of the arterial wall

Arteriolosclerosis
Atherosclerosis
Monckeberg medial sclerosis

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Artheriolosclerosis

hylaine (pink) + hyperplastic (onion ring + punctate hemorrhages) arteriosclerosis
= can cause downstream Ischemia

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MI death prevalence

number 1 cause of death and 1/4 of all US deaths

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atherosclerosis genetic common cause

Familial hypercholesterimia

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atherosclerosis risks and preventions

RISK : male, 40-60yo, FH, genes

PREVENT : female (estrogen) + premenopausal estrogenized women + exercise + alcohol

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diets that can increase cholesterol

animal products, cheese, eggs

transfat foods also

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2 diseases that increase atherosclerosis due to increased oxydation of LDL

DM and Hyperhomocystenimia

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atherosclerosis what happens

migration of SM—-> intinal thickening
fibrous cap bounded by intema (internal elastic lamina)
neovascularization

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LDL oxidized causes

GF released to migrate more SM to intima layer thickning it

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GFs that cause SM migration and proliferation + ECM deposition

PDGF
FGF
TGF-a

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true vs false aneurysm

true : dilation of A wall

false : rupture through the wall into a hematoma blood filling under extravascular Connective Tissue

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dissection A

inside the intima blood fillas

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Cystic Medial Degeneration what happens when is it seen what can it cause

=normal elastin replaced by fragmented elastin
= Marfan, EDS
= Aortic dissection, Aortic Aneurysm

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EDS that effects vasculature mutation and inheritance and sx

COL3A1
AD
thin skin, arterial and uterine rupture, bruising, joint hyperextension

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most important risk factor for AAA

Atherosclerosis (men and age also)

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AAA location common and common thing to see inside

below renal A, and above bifurcation

= bland laminated mural thrombus

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AAA tx

above 5cm in diameter = surgical bypass

- otherwise watch for rupture sxs

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AAA Inflammatory type if from and what do you see

IgG4
= lymphocytes and fibrosis
= plasma cells secrete IgG4

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AAA from inflammatory type TX

steroids

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Thoracic Aortic Aneurysm most important risk factor

HTN

marfans, Vasculitis - giant cell and takayasu, syphillis

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TAA sx

compression of adjacent structures
= SOB
= Dysphagia
= Cough (recurrent laryngeal N)

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pathogen causing TAA, sx, what it does, risk that can happen

Teritary Syphilis
after 5yr infection, genital ulcer non-painful,
Obliterative endarteritis of vasa vasorum (X small vessels for the Aorta and its wall) —-> TCC**
Aortic Valve Regurg

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Aortic Dissection triad

thoracic pain
pulse abnormalities
mediastinal widening CXR

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Aortic Dissection cause

HTN

CT disorder

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classification in Aortic Dissection

DaBakey type : 1 = start at ascending A to at least aortic arch, usually continues more 2. = only in ascending aorta 3 = starts in descending and down

Aortic Dissection most common location

proximal to left common carotid artery = DeBakey type 1

Vasculitides disease effecting Aorta and its primary branches 2`

1. Giant Cell arteritis | 2. Takayasu arteritis

Giant Cell Arteritis which 3 major arteries and sx

``` AORTA 1. Temporal 2. vertebral 3. opthalmic = headache, ocular sx (vision loss), facial pain, fever ```

Giant Cell Arteritis happens why and prevalence

= T cell mediated autoimmune to endotheliial and SM cells | = over 50yo

Giant Cell Artertis vessel looks like

occludes the artery

Giant Cell Artertis vessel looks like

= BIOPSY is must | occludes the artery (giant cells with intimal thickening, fragmented disrupted internal elastic lamina****)

Takayasu arteritis sx and prevalence

female under 50yo or 40yo = weakening upper extr. PULSE* = can have ocular disturbance*

Takayasu arteritis happens why

granulomatous autoimmune vasculitis to AORTA and (its pulm, coronary, renal As)

Takayasu arteritis vessel looks like

Giant cells with intimal thickening looks like Giant cell arteritis

Polyarteritis nodosa

HEPB | young adults

Polyarteritis nodosa locations and sxs

1. renal, heart, GI, skin vessels | 2. rapid increase HTN, abd pain/blood, myaligia, renovascular htn

Polyarteritis nodosa vessel looks like

fibrinoid necrosis , inflammation segmental

Kawasaki Disease also called and prevalence

Mucocutaneous LN Syndrome | = children, infants

Kawasaki Disease location and due to what

``` coronary a (aneurysm rupture of these As) = viral trigger usually, activating T-cell and M ```

Kawasaki Disease sx

``` = fever = strawberry tongue super red = conjunctivitis = red palm and soles, lips = genital rash ```

Churg- Strauss Syndrome what happens and why

= necrotizing granulomatosis allergic reaction | = EOSINOPHILS

Churg- Strauss Syndrome sx and dx

1. asthma, hypereosinophilia, lung infiltrates, purpura palpable on skin, GI bleeding, renal disease 2. ANCA +

Churg- Strauss Syndrome risk

MI*, cardiomyopathy*, myocarditis*,

Wegeners Granulomatosis is what and vessels look like

Granulomatosis necrosis vasculitis RESPIRATORY + polyangitis = can have renal necrosis

Wegeners Granulomatosis happens from what cell and prevalence

T-cell mediated hypersensitivity | = male over 40yo

Wegeners Granulomatosis dx

PR3-ANCA (c-ANCA)

kidneys histology in Wegeners Granulomatosis

epithelial cells grow around compressing it = crescentic glomerulonephritis + focal necrosis

Microscopic Polyangiitis location and disease stages in vessel

1. A, V, caps all (unlike PAN) | 2. uniform stage of disease in all vessels (unlike PAN)

Microscopic Polyangiitis location in body it effects and dx

1. Kindey**, Lung**, peripheral nerves, GI | 2. MPO- ANCA

Microscopic Polyangiitis vessels have NO

immunoglobulin deposits (like in immune complex vasculitis)

Behcets Disease is what TRIAD and association and what happens in vessel + Tx BOARDS ONLY

1. oral ulcer, genital ulcer, uveitis 2. HLA-B51 3. NEUTROPHILIC vasculitis 4. steroids

Thromboangiitis Obliterans

``` BUERGER DISEASE = tibial and radial As vasculitis = smokers (hypersensitive to toxins)** = under 35yo = gangrene of fingers and toes ```

Buergers disease sx stages

1. Raynauds 2. intermittent pain with exertion 3. pain in rest 4. ulcer --> gangrene

Raynauds phenomenon has 3 colors

RED = vasodilation (proximal) WHTIE = vasoconstriction (central) BLUE = O2 insufficiency (all happen)

Raynaud's Phenomenon usually induced by

cold or emotion

Giant cell arteritis associated with

Polymyalgia rheumatica (stiff neck and shoulders)

PCI

percutaneous coronary intervention - for MI prevention , catheter into coronary artery

Balloon angioplasty + endovascular stent work how

1. go into vessel and balloon at site of plaque (compressing it 2. stent is placed to prevent rupture or thrombosis of any part of it + give antithrombotic drugs

how to prevent thrombosis and replaquing in area where you have ballooned and stented

Drug eluting stents (release antiproliferative drugs)

coronary metallic stent

expandible metallic mesh (can injure vessel and cause restenosis so give ANTI-thrombotics)

vascular grafts is used for what

replace or bypass and vascular segment with a lot of atherosclerosis

vascular grafts is for what vessels

large vessels only like in AAA (place in artery and go past it)

CABG is what

coronary artery graft (graft saphenous vein, internal mammary A****) harvest that vein or A and use that to bypass a vessel

- ANCA is seen in what vasculitis usually

1. Polyarteritis nodosa 2. Buerger 3. Giant cell 4. Takayasu 5. Behcets