• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/112

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

112 Cards in this Set

  • Front
  • Back

Large Vessel Vasculitis

1) Temporal Giant Cell Arteritis



2) Takayasu Arteritis

Medium Vessel Vasculitis

1) Polyarteritis Nodosa



2) Kawasaki Disease



3) Buerger Disease

Small Vessel Vasculitis

1) Wegener Granulomatosis (Granulomas w/ Polyangiitis)



2) Microscopic Polyangiitis



3) Churg-Strauss Syndrome



4)Henoch-Schonlein Purpura

MOST COMMON vasculitis in older adults

Temporal Giant Cell Arteritis

vasculitis in older adults (>50) usually affects Females

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)



Vascular lesions are SEGMENTAL so a negative biopsy does NOT exclude disease

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

Takayasu Arteritis:



type of arteritis?


demographic?

Granulomatous vasculitis



Young Asian females < 50 years old

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

Polyarteritis Nodosa

Necrotizing vasculitis of MULTIPLE ARTERIES (Poly-arteritis)



Multiple Arteries -> Involvement of MOST Organs (BUT LUNGS Spared)



young adults

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.)

'String of Pearls' appearance on imaging

a/w HBsAg

Diseases associated with 'String of pearls'
Polyarteritis Nodosa
Fibromuscular Dysplasia

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


Kawasaki Disease demographic

Asian children < 4 years old

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)

Kawasaki Disease clinical signs

Rash on the palms of their hands and soles of their feet.
(think of a kid on a motorcycle)
Coronary artery involvement is common! YOUNG CHILD with a thrombosis and MI or ruptured aneurysm

Kawasaki Disease treatment

1) Aspirin -- prevents platelet aggregation via COX inhibition-> Decreased TXA2 = Therefore decreased chance of MI.

Use Aspirin here b/c this is NOT a viral Infection, even though it might present as one due to Non-Specific Symptoms



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


Buerger Disease HY associations

SMOKING disease



Tx = STOP Smoking

presents with Necrotizing vasculitis involving Digits (Fingers & Toes). Associated with Raynauds (vaso-spasm of blood vessels going to digits) (Turn White (b/c blood supply cut off)->Blue (b/c tissue becomes cyanotic)->Red (when blood flow returns after smasm ends)) ->autoamputation of digits w/out Tx.

Wegener's Granulomatosis

Involves nasopharynx, lungs and kidneys.
c-ANCA positive
Treatment is Cyclophosphamide

Rapidly Progressive Glomerulonephritis

middle aged male with nasopharyngeal ulceration, lung infiltrates and hematuria

What likely renal problem arises?

Wegener's Granulomatosis
Renal problem is Rapidly Progressive Glomerulonephritis

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


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.

They BOTH have lung involvement, both express p-ANCA.

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

Henoch-Schonlein Purpura demographic

most common vasculitis in children

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

Important cause of stenosis in young females?

fibromuscular dysplasia(frequently involves renal artery)

Atherosclerotic Clefts characterized by cholesterol clefts
Etiology of aneurysm
Arteriolosclerosis types...

Hyaline and hyperplastic type

Hyaline arteriolosclerosis caused by proteins leaking into vessel wall causing vascular thickening

Hyperplastic arteriosclerosis caused by malignant hypertension

Hyaline Arteriolosclerosis caused by...

Benign Hypertension and diabetes
Hypertension forces protein into membrane

Diabetes -- non-enzymatic glycosylation of basement mebrane making them more leaky to proteins.

Hyaline Arteriolosclerosis classically causes...?
Glomerular Scarring(arteriolonephrosclerosis) This is what causes chronic renal failure in chronic hypertension/diabetes.
Hyperplastic arteriosclerosis caused by
malignant hypertension
Hyperplastic arteriosclerosis leads to...

end organ ischemia due to reduced vessel caliber. FIBRINOID necrosis with possible hemorrhage. "onion skin" appearance

Classically causes acute renal failure with 'flea bitten' appearance

'flea bitten' appearance of kidney
acute renal failure due to hyperplastic arteriolosclerosis in response to malignant hypertension
Etiology of Aortic Dissection due to HTN
Describe clinical syndromes that could predispose to aortic dissection
Marfan's Syndrome(fibrillin defect) or Ehlers-Danlos Syndrome(collagen defect)
Complications of aortic dissection
Most common cause of death due to aortic dissection
pericardial tamponade
Classically causes thoracic aneurysm
tertiary syphilis which causes endartertis of the vaso vasorum resulting in 'tree barkin' of the aorta.
Major complication of thoracic aneurysm
dilation of the aortic valve root, resulting in regurgitation
Abdominal Aortic Aneurysm demographic
male smokers >60 with history of hypertension

etiology: Atherosclerosis increases the diffusion barrier to the media, resulting in atrophy and weakness of vessel wall
Reddish growth that blanches on pressure
Hemangioma -- will go away with growth of child
Reddish rash that does not blanch on pressure
Kaposi's Sarcoma
Kaposi's Sarcoma demographic
Older Eastern European males -- tumor remains localized to skin

AIDS and Transplant patients -- tumor spreads early.
Associated with exposure to PVC?
Liver angiosarcoma

also a/w arsenic and Thorotrast
Liver angiosarcoma association?
Poly-vinyl Chloride
high risk of blindness without treatment in this disorder. What treatment?

Giant Cell Temporal Arteritis

Prednisone, or other corticosteroid

Weak or absent pulse in upper extremities
Takayasu's Arteritis
Takayasu involves which branches of vasculature?
Branch points of Aortic Arch
Organ spared in PAN
lungs
associated with HBsAg
PAN
transmural inflammation with fibrinoid necrosis
PAN
intimal fibrosis with _______ is what?

with giant cells is

Giant Cell Temporal Arteritis

Which vasculitis is fatal if not treated
PAN - treat with cyclophosphamide and corticosteroids
myocardial infarction in young asian child
treat with?

Kawasaki Disease - can also result in aortic aneurysms with rupture

aspirin and IVIG

Layers of Blood Vessel

1) Intima = Endothelial cells on BM



2) Media = Smooth Muscle



3) Adventitia - Connective Tissue

Vasculitis

Inflammation of Blood vessel



Cause is usually unknown but NOT likely to be Infectious

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

How are Vasculitides Divided?

Large Vessel - Involve aorta or its major branches



Medium Vessel - supply organs



Small Vessel - Arterioles

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

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

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

What else will be seen in vessel wall in Temporal Giant Cell Arteritis?

Inflamamtion = Neutrophils



Giant Cells (multiple nuclei) = Granuloma

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

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

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

Medium-Vessel Vasculitis

Involve Muscular Arteries



Muscular Arteries supply Organs



Therefore Organs affected

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)

Systolic/Diastolic BP

Normal <120/80



HTN ≥ 140/90 (usually boh Increase)



Systolic BP determined by Stroke Volume



Diastolic BP determined by Arteriolar Resistance



Causes of HTN

1° Unknown Etiology (95% of all HTN cases)



2° Renal Artery Stenosis (5% of all HTN cases)

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

Renal Artery Stenosis

Renal Artery Stenosis -> Decreased Blood Flow to Kidney->Increased Renin->Incr. Angiotensinogen



Unilateral Atropy of involved Kidney

Causes of Renal Stenosis

Atherosclerosis (elderly males)



Fibromuscular Dysplasia (young females)



Fibromuscular dysplasia

Developmental Defect of Blood vessel wall->irregular thickening of large & Medium sized Arteries

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

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

Arteriosclerosis

Arterio = Arteries


Sclerosis = Hardening



Hardening of the Arterial Wall as it thickens due to deposition of material


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


Atherosclerosis

Intimal Plaque that obstructs blood flow

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

Most common arteries (Large/medium sized) involved w/ Atherosclerosis

Abdominal Aorta



Coronary A.



Popliteal A. = supplies knee, thigh, & calf



Internal Carotid A. = supplies Brain

Modifiable Risk factors for Atherosclerosis

1) HTN



2) Hypercholesteremia



3) Smoking



4) Diabetes



All these drive Pathophysiology fo Atherosclerosis

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

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

Epidemiology of Complications of Atherosclerosis

Account for >50% of Dz.in Western World

Large Vessel Vasculitis

Temporal Giant Cell Arteritis
Takayasu Arteritis

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

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

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

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

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

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

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)



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


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


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.


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)

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

MCC of Preexisting Weakness of the Media

HTN



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

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

How does Aortic Dissection present?

Sharp, Tearing Chest Pain


Radiating to back

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)

Aneurism



Where do they occur?

Ballon-like Dilitation fo Blood Vessel wall



Thoracic Aorta



Abdominal Aorta

What is necessary for Aneurism to occur?

Weakness in Aortic Wall

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

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

AAA - Abdominal Aortic Aneurism

Baloon-like dilitation of Abdominal Aorta



Below Renal Arteries


BUT


Above Aortic Bifurcation

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

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



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

Major Complication of AAA?

Rupture! Especially when Abdominal Aorta


>5cm Diameter



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