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112 Cards in this Set
- Front
- Back
Large Vessel Vasculitis |
1) Temporal Giant Cell Arteritis
2) Takayasu Arteritis |
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Medium Vessel Vasculitis |
1) Polyarteritis Nodosa
2) Kawasaki Disease
3) Buerger Disease |
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Small Vessel Vasculitis |
1) Wegener Granulomatosis (Granulomas w/ Polyangiitis)
2) Microscopic Polyangiitis
3) Churg-Strauss Syndrome
4)Henoch-Schonlein Purpura |
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MOST COMMON vasculitis in older adults
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Temporal Giant Cell Arteritis |
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Temporal Arteritis clinical symptoms? |
Affects large branches of carotid artery leading to headache (temporal artery), and visual disturbances(ophthalmic artery) and jaw claudication (artery supplyinh jaw muscles)
Some pts. have flu like symptoms w/ joint/muscle pain = polymyalgia rheumatica -> Elevated ESR (>100)
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What is at risk to be damaged if Giant Cell Arteritis is not treated?
How is it Tx? |
Ophthalmic Nerve ischemic damage causing blindness
Tx. w/ corticosteroids |
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Takayasu Arteritis:
type of arteritis? demographic? |
Granulomatous vasculitis
Young Asian females < 50 years old |
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Takayasu Arteritis Pathology? clinical symptoms? Tx.? |
same pathology as Temporal Giant Cell Arteritis just defined as different dz. based on the arteries involved: at more proximal Aortic Arch branch points, rather than more distal brances of Carotid A. (Temp. Giant cell Arteritis)
involves the aortic arch at branch points, leading to upper extremity absent pulses("pulseless disease") -ESR up Presents with visual and neurological symptoms similar to giant cell arteritis Tx. w/ corticosteroids |
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Polyarteritis Nodosa |
Necrotizing vasculitis of MULTIPLE ARTERIES (Poly-arteritis)
Multiple Arteries -> Involvement of MOST Organs (BUT LUNGS Spared)
young adults |
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Polyarteritis Nodosa clinical symptoms? Classic finding? a/w? |
Depends on Arteries Involved
Hypertension if Renal artery involvement,
Abdominal pain with melena (Mesenteric artery involvement)
Neurologic symptoms (blood vessels to CNS) & Skin Lesions (Blood vessels to skin)
HBs (Hep B Surface Ag often found in these pts.) |
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Diseases associated with 'String of pearls'
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Polyarteritis Nodosa
Fibromuscular Dysplasia |
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What drug treats Polyarteritis Nodosa vasculitis? |
1) Corticosteroids (stop Inflammation)
2) Cyclophosphamide (its metabolite phosphoramide mustard is only formed in cells that have low levels of ALDH. Phosphoramide mustard forms irrversible DNA crosslinks between and w/in DNA strands -> cell apoptosis of TH cells. Cyclophosphamide has little chemotherapy toxicity as [ALDH] is HIGH in BM stem cells, liver and intestinal epithelium, therefore phosphoramide mustard is NOT made in those cells
FATAL if NOT Treated
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Kawasaki Disease demographic |
Asian children < 4 years old |
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Kawasaki Disease presentation |
Non-specific symptoms similar to infection in beginning: Fever Conjunctivitis Erythymatous Rash on palms and soles Lymphadenopathy of Cervical Lymph nodes
Coronary Artery involvement common-> infarction (damaged endothelial cells lead to exposure of tissue Factor exposure->COag Cascade activated -> Thrombosis->Infarction->MI in 4 year old)
and/or aneurysm (weakened vessel wall can lead to dilitation and rupture) |
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Kawasaki Disease clinical signs |
Rash on the palms of their hands and soles of their feet. |
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Kawasaki Disease treatment |
1) Aspirin -- prevents platelet aggregation via COX inhibition-> Decreased TXA2 = Therefore decreased chance of MI.
We do not give Aspirin to children w/ Viral Infection b/c can cause Reye Syndrome = encephalopathy & massive liver necrosis b/c viral infection causes a lot of systemic inflammation (some Free Radical damage of Mitochondria in Liver @ CNS neurons) and on top of this Aspirin can cause even more Mitochondrial damage
2) IVIG (IVIG reduces vasculitis in KD by suppressing the marked immune activation associated with this disease b/c it upregulates Suppressor Tcells that block release of IFN-Gamma/IL-1 & TNF that drive the pathophysiology of Kawasaki's)
B/c Disease is self-limited, if we can prevent MI, then chance is that child will recover and be OK
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Buerger Disease HY associations |
SMOKING disease
Tx = STOP Smoking |
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Wegener's Granulomatosis |
Involves nasopharynx, lungs and kidneys. |
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middle aged male with nasopharyngeal ulceration, lung infiltrates and hematuria |
Wegener's Granulomatosis
Renal problem is Rapidly Progressive Glomerulonephritis |
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Wegener's Granulomatosis vs. Microscopic Polyangiitis |
Same 1) Both involve multiple (Poly-angitis) 2) Both involve Lung & Kidney 3) Tx. Cyclophosphamide & Corticosteroids 4) Relapses are common
Different: Unlilke Wegener's Granulomatosis, Microscopic Polyangitis has:
1) No Nasopharangeal involvement i
2) p-ANCA (p-ANCA levels correlate w/ severity of Dz.) NOT c-ANCA
3) No granulomas
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Microscopic Polyangiitis vs. Churg-Strauss Syndrome |
Same 1) Involves multiple organ systems 2) Involve LUNGS -> particularly LUNGS (Churg-Strauss) 3) p-ANCA +
Different: Unlike Microscopic Polyangitis, Churg-Strauss has:
1)Necrotizing Granulomatous Vasculitis w/ 2) Eosinophils (peripheral eosinophilia) leading to... 3) Asthma 4) Involves Heart
Churg-Strauss presents with Asthma, Granulomas and peripheral eosinophilia. |
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Nephropathy following Upper Respiratory infection? |
Vasculitis due to IgA Immune complex deposition
IgA nephropathy associated with Henoch-Schonlein Purpura b/c IgA generated in Upper Resp. Infection. The IgA then forms IgA Immune complexes that deposit in the mesangium (Glomerulus), causing RBC's to leak through |
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Henoch-Schonlein Purpura demographic
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most common vasculitis in children |
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Henoch-Schonlein Purpura clinical signs
Tx.? |
1) palpable purpura on buttocks and legs (papable b/c also inflammation not just bruising)
2) GI pain and bleeding (IgA is in GI)
3) IgA nephropathy -> Hematuria
Tx. w/ Corticosteroids if necessary, but Dz. is self-limited |
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Important cause of stenosis in young females?
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fibromuscular dysplasia(frequently involves renal artery) |
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Atherosclerotic Clefts characterized by cholesterol clefts
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Etiology of aneurysm
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Arteriolosclerosis types...
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Hyaline and hyperplastic type |
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Hyaline Arteriolosclerosis caused by...
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Benign Hypertension and diabetes |
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Hyaline Arteriolosclerosis classically causes...?
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Glomerular Scarring(arteriolonephrosclerosis) This is what causes chronic renal failure in chronic hypertension/diabetes.
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Hyperplastic arteriosclerosis caused by
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malignant hypertension
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Hyperplastic arteriosclerosis leads to...
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end organ ischemia due to reduced vessel caliber. FIBRINOID necrosis with possible hemorrhage. "onion skin" appearance |
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'flea bitten' appearance of kidney
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acute renal failure due to hyperplastic arteriolosclerosis in response to malignant hypertension
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Etiology of Aortic Dissection due to HTN
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Describe clinical syndromes that could predispose to aortic dissection
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Marfan's Syndrome(fibrillin defect) or Ehlers-Danlos Syndrome(collagen defect)
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Complications of aortic dissection
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Most common cause of death due to aortic dissection
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pericardial tamponade
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Classically causes thoracic aneurysm
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tertiary syphilis which causes endartertis of the vaso vasorum resulting in 'tree barkin' of the aorta.
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Major complication of thoracic aneurysm
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dilation of the aortic valve root, resulting in regurgitation
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Abdominal Aortic Aneurysm demographic
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male smokers >60 with history of hypertension
etiology: Atherosclerosis increases the diffusion barrier to the media, resulting in atrophy and weakness of vessel wall |
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Reddish growth that blanches on pressure
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Hemangioma -- will go away with growth of child
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Reddish rash that does not blanch on pressure
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Kaposi's Sarcoma
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Kaposi's Sarcoma demographic
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Older Eastern European males -- tumor remains localized to skin
AIDS and Transplant patients -- tumor spreads early. |
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Associated with exposure to PVC?
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Liver angiosarcoma
also a/w arsenic and Thorotrast |
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Liver angiosarcoma association?
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Poly-vinyl Chloride
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high risk of blindness without treatment in this disorder. What treatment?
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Giant Cell Temporal Arteritis |
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Weak or absent pulse in upper extremities
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Takayasu's Arteritis
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Takayasu involves which branches of vasculature?
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Branch points of Aortic Arch
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Organ spared in PAN
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lungs
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associated with HBsAg
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PAN
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transmural inflammation with fibrinoid necrosis
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PAN
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intimal fibrosis with _______ is what?
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with giant cells is |
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Which vasculitis is fatal if not treated
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PAN - treat with cyclophosphamide and corticosteroids
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myocardial infarction in young asian child
treat with? |
Kawasaki Disease - can also result in aortic aneurysms with rupture |
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Layers of Blood Vessel |
1) Intima = Endothelial cells on BM
2) Media = Smooth Muscle
3) Adventitia - Connective Tissue |
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Vasculitis |
Inflammation of Blood vessel
Cause is usually unknown but NOT likely to be Infectious |
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Clinical Features of Vasculitis |
1) Non-specific Symptoms - B/c pt. has inflammation-> fever, fatigue, weightloss, myalgia Seen in all Vasculitides
2) Symptoms of Organ Ischemia (each type of vasculitis is more/less likely to occlude Blood Vessel to specific organ) Due to:
a) Inflammation-> Damage to Endothelium exposes Subendothelial Collagen/ Tissue Factor -> Activation of Coag. Cascade-> Formation fo a Thrombus-> Organ Ischemia
OR
b) Following inflammation, Fibrosis occurs as part of Healing Process. Repeated Inflammation followed by fibrosis, can narrow lumen -> Organ Ischemia |
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How are Vasculitides Divided? |
Large Vessel - Involve aorta or its major branches
Medium Vessel - supply organs
Small Vessel - Arterioles |
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what is seen on biopsy in pts with Temporal Giant Cell Arteritis? |
1) Inflamed vessel wall w/ Giant Cells (DUE TO GRANULOMATOUS inflammation)
2) Intimal fibrosis in blood vessel due to healing following all the inflammation |
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What should pathologist keep in mind when evaluating biopsy of Temporal Giant Cell Arteritis |
segmental lesions: THEREFORE
1) take very long piece of blood vessel (to increase probability that you find inflamed portion with granuloma)
2) Chop up this long piece into small ones so that you can evaluate all of them under microscope
3) If you don't see any Temporal Giant Cell Arteritis in the biopsied section, it does not exclude the possibility that it exists somewhere else |
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where does fibrosis take place in Temporal Giant Cell Arteritis? |
Intimal fibrosis In between Intima (Endothelial Cells on BM) and the Media (Smooth Muscle)
Normally they are juxtaposed, but in vasculitis there is tons of fibrosis in between->lumen narrowed-> ischemia |
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What else will be seen in vessel wall in Temporal Giant Cell Arteritis? |
Inflamamtion = Neutrophils
Giant Cells (multiple nuclei) = Granuloma |
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Tx. for Temporal Giant cell Arteritis |
Corticosteroids = MUST BE DONE QUICKLY - b/c HIGH risk of Blindness if fibrosis/occlusion of Opthalmic artery takes place |
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Takayasu Arteritis |
Pathophysiologically same disease as Temporal Giant Cell Arteritis - also has GRANULOMAtous Vasculitis,
BUT, it is found in different vessels = AORTIC ARCH at Branch Points(Not Carotid)
AND <50 y.o. = young Asian female |
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Takayasu Arteritis Clinical Presentation |
B/c Aortic Branch Points affected, Expect: Neurological symptoms, Visual disturbances Weak or Absent Pulses in Upper extremity ("Pulseless Dz.")
ESR elevated
Tx w/ Corticosteroids |
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Medium-Vessel Vasculitis |
Involve Muscular Arteries
Muscular Arteries supply Organs
Therefore Organs affected |
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Pathophysiology of Polyarteritis Nodosa |
Lesions take place at different times, that is why, when looking at an entire muscular artery affected by Polyarteritis Nodosa, there will be lesions at varying stages.
Stage 1) Transmural Inflammation of Blood Vessel (Transmural = involves entire wall) ->this damage will cause necrosis w/ deposit of proteins inside that wall = Fibrinoid Necrosis (caused by Malignant HTN & Vasculitis). This section when initially weaked by transmural Inflammation can form an outpouching = Aneurism
Stage 2) When the Early Lesion finally Heals ->Leads to Massive Fibrosis (not just random proteins like in Fibrinoid Necrosis but Fibroblasts make collagen) that is HARD & Nodular -> the name Nodosa
At any given time, looks like "String of Pearls" b/c Some sections will be dilated (Stage 1 lesions that have aneurisms) and others will be hard due to dense fibrosis Nodules =string (Stage 2) |
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Systolic/Diastolic BP |
Normal <120/80
HTN ≥ 140/90 (usually boh Increase)
Systolic BP determined by Stroke Volume
Diastolic BP determined by Arteriolar Resistance
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Causes of HTN |
1° Unknown Etiology (95% of all HTN cases)
2° Renal Artery Stenosis (5% of all HTN cases) |
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Since Etiology rarely known, what are the Risk Factors associated w/ HTN? |
Age Race Obesity Stress Lack of Physical Activity Salt intake = (Incr Systolic BP/Stroke Volume by causing volume retention) & (Incr Diastolic BP/Peripheral Resistance b/c causes Incr Renin (b/c more Na+ reaches JG cells) Renin -> Ang II->potent vasoconstrictor of Arteries & veins>Incr TPR |
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Renal Artery Stenosis |
Renal Artery Stenosis -> Decreased Blood Flow to Kidney->Increased Renin->Incr. Angiotensinogen
Unilateral Atropy of involved Kidney |
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Causes of Renal Stenosis |
Atherosclerosis (elderly males)
Fibromuscular Dysplasia (young females)
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Fibromuscular dysplasia |
Developmental Defect of Blood vessel wall->irregular thickening of large & Medium sized Arteries |
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Benin vs Malignant HTN |
Benign - Clinically silent, vessels & ofgans damaged over time
Malignant HTN is > 200/120. May arise from preexisting benign HTN or de novo |
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How do pts w/ Malignant HTN present |
1) Acute End organ damage->
2) Acute Renal Failure/Headache/Papilledema
MED EMERGENCY!!!!!
3) Develop Fibrinoid Necrosis in Blood vessel walls |
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Arteriosclerosis |
Arterio = Arteries Sclerosis = Hardening
Hardening of the Arterial Wall as it thickens due to deposition of material
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3 pathologic patterns of Arteriosclerosis |
3 ways Arterial Wall can thick/hard
1) Atherosclerosis - Intima thickening in blood vessel wall in Medium/Large sized vessels
2) Arteriolosclerosis - in Arterioles = small vessels. Thickening due to: a) Hyaline Arteriolosclerosis - deposition of protein in the wall b) Hyperplastic Arteriolosclerosis - Hyperplasia of smooth muscle in Arteriole wall
3) Mönckeberg Medial Sclerosis - Calcification of Media of blood vessel, but this calcification replaces Media as opposed to thickening it (harder but not thicker), therefore not clinically significant
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Atherosclerosis |
Intimal Plaque that obstructs blood flow |
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Components of Atherosclerotic plaque |
Necrotic Lipid core of cholesterol (often undergoes dystrophic calcification = saponification of cholesterol/fats by Ca2+)
covered by
Fibromuscular Cap that faces the lumen |
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Most common arteries (Large/medium sized) involved w/ Atherosclerosis |
Abdominal Aorta
Coronary A.
Popliteal A. = supplies knee, thigh, & calf
Internal Carotid A. = supplies Brain |
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Modifiable Risk factors for Atherosclerosis |
1) HTN
2) Hypercholesteremia
3) Smoking
4) Diabetes
All these drive Pathophysiology fo Atherosclerosis |
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Non-Modifieable Risk factors for Atherosclerosis |
1) Age - # of lesions Incr. w/ age
2) Gender - Males >> than pre-menopausal Females (b/c estrogen protective)
3) Genetics - Family History highly predictive od risk |
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Pathogenesis of Atherosclerosis |
Intima is Endothelial cells sitting on BM
1) Lipid Invasion of Intima = Endothelial damage allows lipids to interact w/ BM
2) The lipids are oxidized
3) Oxidized lipids Phagocytosed by Macrophages (Macrophages called in to clear these oxidized lipids)
4) Collection of Macrophages filled with lipids are now in Intima = FATTY STREAK - yellow streaks running along large blood vessels - already seen in teenagers
5) Macrophages activate Inflammation, followed by healing-> Fibromuscular cap
6) Each bout of inflamamtion, brings more lipids into the intima->more lipid laden Macrophages->More inflmmation. Therefore the atherosclerotic plaque continues to grow if there is Increased inflmmation and LDL cholesterol in blood
7) Fibromuscular cap is part of the Healing Process, as deposition of ECM (granulation tissue), proliferation of smooth muscle (both can be done by fribroblasts)
8) As the plaque expands, it increasingly occludes blood flow |
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Epidemiology of Complications of Atherosclerosis |
Account for >50% of Dz.in Western World |
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Large Vessel Vasculitis |
Temporal Giant Cell Arteritis |
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Complications of atherosclerosis |
1) Stenosis of Medial Blood vessels - Lumenal Caliber (flow potential) is DECREASED->Ischemia
2) Plaque rupture w/ Thrombosis
3) Plaque Rupture w/ Embolization
4) Weakening of Blood Vessel Wall |
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Symptoms of Stenosis of Medial Blood vessels seen in Atherosclerosis |
1) Peripheral Vascular Dz. (peripheral = legs/arms)/ e.g. Popliteal A. obstruction that supplies knee/thigh/calf
2) Angina= episodic chest pain - Coronary A. obstruction
3) Ischemic Bowl Dz.- Obstruction of Mesenteric Arteries
No symptoms until >70% Stenosis |
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Plaque rupture w/ Thrombosis in Atherosclerosis |
Rupture of plaque at the NECK = edges, causes release of lipid core and exposure of tissue underneath to lumen of blood vessel->Activation of COAG Cascade->Rapid Development of Thrombus -> Infarction of Medium sized vessel supplying the Organ
MI = usually Plaque Rupture->Thrombosis
Plaque Rupture->Thrombosis in Coronary A. ->MI
Plaque Rupture->Thrombosis in Middle Cerebral A. ->Stroke |
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Plaque Rupture w/ Embolization in Atherosclerosis |
Part of Atherosclerotic Plaque breaks off at Neck & Travels through Blood Vessel until it lodges in Distal site = Called Embolization
Hallmark of Atherosclerotic Embloli = Cholesterol Clefts - Embolus has large clear areas where Cholesterol was found |
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Weakening of Blood Vessel Wall in Atherosclerosis |
Normally layers of Blood vessel (Intima/Media/Adventitia) have O2 directly diffuse from lumen to supply O2 to the tissues making up these layers
If Atherosclerotic Plaque w/ Fibromuscular cap becomes thick, it forms a deffusion barrier for O2, that decreases O2 supply to these tissues in the blood vessel wall ->
Wall becomes atrophic->Wall becomes weak->Aneurism of balooning of wall happens because wall is weak and pressures are high in lumen |
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Types of Arteriolosclerosis |
Involves Arterioles
1) Hyaline Arteriosclerosis - Deposition of pink proteinaceous material Benign HTN - High BP forces protein into the wall
Diabetics - get Non-Enzymatic Glycosilation of BM that weakens vessel wall (Endothelium connection to BM) allowing for Protein to leak in
2) Hyperplastic Arteriosclerosis |
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Consequence of Hyaline Arteriolosclerosis |
Reduced Vessel Caliber ->End-Organ Ischemia (End-organ = ultimate organ supplied by this Blood Vessel)->
Classicaly -> GLOMERULAR SCARRING
As Blood Vessel wall thickened -> Decreased blood flow to Glomerulus-> Glomerulus Scars due to lack of blood flow->low O2->necrosis
Over time, patients w/ Benign HTN/Diabetes get Chronic Renal Failure, as more and more Glomeruli are Scarred/Non-funcitonal
Glomerular Scarring = ArterioloNephroSclerosis (sclerosis of Arterioles & Glomeruli) -> shrinking kindney as scarring replaces functional tissue, and you see bumps = scars on periphery of kidney (cortical glomerular scarred)
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Hyperplastic Arteriolosclerosis |
Thickening of Arterioles (Small Blood Vessels)
due to Hyperplasia of Smooth Muscle in Vessel wall -> "Onion Skin Appearance"-> Reduces Caliber -> Decreased blood flow to end-organ->End Organ Ischemia
Due to MALIGNANT HTN b/c Blood vessel trying to contain that Super High Blood Pressure
Classically See: Acute Renal Failure (due to damage from Super High BP) w/ Flee Bitten Appearance (places in kidney where blood vessels are blown out (hemorrhage) due to high pressure)
The High Pressure in Malignant HTN can also lead to Fibrinoid Necrosis(seen in Malignant HTN & Vasculitis) as layers of the wall Necrose & are replaced by proteinaceous material
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Mönckeberg Medial Sclerosis |
Non-obstructive Calcification of Media of blood vessel, but this calcification replaces Media as opposed to thickening it (harder but not thicker), therefore not clinically significant
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If you see calcification moving in vascular pattern on Mammography |
Incidental finding on Mammography due to Mönckeberg Medial Sclerosis (Non-obstructive (asymptomatic) Calcification of Media of Blood Vessel). FInding Calcification is the goal of Mammography.
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Aortic Dissection |
1) Blood flowing in Aorta Tears Intima
2) Blood access the Media and continues to rip through the Media (Dissection of the wall of the Aorta) |
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What is necessary for Aortic Dissection to take place? |
1) Ton of Stress on Aortic Wall = Typically occurs in first 10 cm of Aorta where Pressure is Greatest
2) Preexisting weakness of the Media |
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MCC of Preexisting Weakness of the Media |
HTN
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Etiology of HTN causing Aortic Dissection |
1) B/c the first 10 cm of Aorta are very thick so that they can withstand high pressures, enough O2 can not diffuse from Aortic lumen to suppy entire wall. Therefore Aorta has its own blood supply (Vasa Vasorum: small blood vessels) to augment O2 supplied via diffusion.
2) Due to Benign HTN, Vasa Vasorum will undergo Hyaline Arteriosclerosis (High BP forces proteinaceous material into wall of Vasa Vasorum)-> Decreased Caliber of Lumen of Vasa Vasorum
3) Decreased Caliber of Lumen of Vasa Vasorum ->ischemia to outer half of Aortic wall-> Atrophy of Media of Aorta-> weakening of Media->
4) Aortic Dissecrtion |
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Disorders that cause Preexisting weakness of the Media |
Inherited defects of Connective Tissue
1) Marphans - Fibrillin defect(Elastic Fibers are normally laid on top of Fibriliin)
2) Ehler-Danlos - velvety skin |
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How does Aortic Dissection present? |
Sharp, Tearing Chest Pain Radiating to back |
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Complications of Aortic Dissection |
1) Pericardial Teponade = MCC of Death This is due to Dissection moving in Reverse toward the Heart, filling the Pericardium->Pericardial Temponade->Death
2) Rupture/Hemorrhage into Mediastinum-> Fatal Hemorrhage
3) Obstruction of Arteries branching off of Aorta (Dissection roceeds along Aortic wall until it reaches a perpendicular branch point. B/c it can't continue forward it compresses that Artery: e.g. Renal Artery->End-Organ Ischemia to kidney) |
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Aneurism
Where do they occur? |
Ballon-like Dilitation fo Blood Vessel wall
Thoracic Aorta
Abdominal Aorta |
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What is necessary for Aneurism to occur? |
Weakness in Aortic Wall |
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Cause of Aortic wall weakeness ->Thoracic Aortic Aneurism |
Classically: Tertiary Syphillis b/c
Tertiary Syphillis ->Endarteritis (inflammation of the Intima of Small Blood vessels)
Endarteritis of Vasa Vasorum (that supply O2 to Aortic Wall)->Fibrosis (healing) follows Inflamamtion->Atrophy of the wall of the blood vessel->Weakening of Blood Vessel->Dilitation of the Aortic wall
"Tree Bark Appearance" of Aorta - due to Scarring/Fibrosis due to Endarteritis from 3ry Syphillis |
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Complications of Thoracic Aneurism |
1) Balloon-like Dilitation of Aorta will pull Aortic Valve Root->Aortic Valve pulled apart->Aortic Insufficiency (Aortic Regurge) b/c Valve can't close properly
2) Compression of Mediastinal Structures as Thoracic Aortic Aneurism pushes OUT
3) Thrombosis & Embolism - No laminar blood flow at site fo Aneurism. Turbulent Blood Flow Increases Activation of Coag Cascade-> Thrombosis at site of Aneurism->Thrombus can Emoblise |
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AAA - Abdominal Aortic Aneurism |
Baloon-like dilitation of Abdominal Aorta
Below Renal Arteries BUT Above Aortic Bifurcation |
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What causes weakening of Abdominal Aortic Wall leading to Aneurism? |
Atherosclerosis b/c
Atherosclerotic plaque causes thickening of Intima->Interference of O2 deffusion from lumen to supply entire thickness of Abdominal Aorta Wall->Atrophy of wall->Weakness of wall->Balloon like dilitation of Abdominal Aorta = AAA |
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Classic Pt. w/ AAA |
Same as for Atheroclerosis b/c it drives the Etiology of AAA
Male Smoker >60 y.o. HTN
The Abdominal Aorta is one of the most common sites of Atherosclerosis
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How do pts present w/ AAA? |
Pulsatile Abdominal Mass - you feel it more b/c turbulent instead of laminar flow that Grows with time->Increasing Chance of RUPTURE |
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Major Complication of AAA? |
Rupture! Especially when Abdominal Aorta >5cm Diameter
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How does Abdominal Aorta Rupture Present? |
1) Hypotension - b/c losing blood from circulation
2) Pulsatile Abdominal Mass - B/c blood flowing through it
3) Flank Pain b/c kidneys getting less blood b/c initially resistance is smaller at site of ruptured Aneurism
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