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83 Cards in this Set
- Front
- Back
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whats an aneurysm?
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localized dilation of a vessel that is ABNORMAL
**common in heart and aorta False: its like a hemotoma on the vessel, just the extravascular CT pushes out True: bound by complete arterial wall, blood stays in circulatory system |
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what a true and false aneurysm?
what are some common locations for each |
True: bound by artery wall, blood stays in circulatory system
ex: artherolesclerotic, syphilitic, Left vent after MI, congenital False: hematoma on the BV, its not bound by the arterial wall, communicates with intravascular space |
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what are some CT diseases? what does this do to BV
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Marfan
Ehlers Danlos Vit C defici Loeys Dietz Inflammation remodeling can also weaken loss of SM can weaken the wall **all are defect in CT and can make BV weak, increased risk of aneruysm/dissection |
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what is cyctic medial degeneration
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its degenerative changes seen in ischemia, it can lead to scars, bad ECM, and can increase likelyhood of anerursm
**non specific finding of no ECM and weird amorphous ground substance **often the first leision seen in aortic dissection |
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what is it caleld when we dont make ECM and have lots of weird amorphous ground substance
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cyctic medial degeneration
**increased aneurysm risk **also the first leision seen in aortic dissection |
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what are 2 major disorders that predispose aortic aneruysm (what part of aorta more common)
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1. Artherosclerosis (AAA)
2. HTN (ascending aorta) |
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what is a mycotic aneurysm
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infection that weakens the BV wall
**can come from septic embolus, nearby infection, bug in blood |
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artherosclerosis and HTN lead to what kind of aneurysm
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aortic
Artherosclerosis: AAA HTN: ascending AORTIC aneurysm |
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what is it called if an infection weakens the artery wall
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mycotic aneurysm
**caused by septic embolis, nearby infection, bug in blood |
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aneurysms associated with artherosclerosis typically occur...
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in abdominal aortc aneruysm (AAA)
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who gets AAA
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men
over 50 smoker |
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what is a major cuase of AAA
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artherosclerosis
**men, over 50, smoke |
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where are AAA located
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below the renal, above bifurcation
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what does an AAA look like (gross)
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below renal A, above bifurcation
**filled with mural thrombus **usually inflammatory or mycotic (infection) **this is a test picture |
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5 clinical consequences of AAA
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1. Rupture
2. Impingement 3. Occlusion of Branch vessel-ischemia 4. Embolism from artheroma or mural thrombus 5. Creates abdominal mass- palpable, pulsates |
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what size AAA is a rupture risk
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>cm, surgery
**if it ruptures mortality goes WAY up |
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a 65 yp man who smokes and has HTN is at risk for what aneurysm
What if its a 40 yo man with HTN |
AAA
Aortic dissection |
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what disease is TAA (thoracic aortic aneruysm) associated with
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syphalis, affects arch- inflammatory damage
**ascending aorta is associated with HTN |
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what are the clinical sx of thoracic aortic aneurysm
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Gets in the way of throacic structures
1. rupture 2. cardiac disease 3. pain from bone errosion 4. pressure on recurrent laryngeal- cough 5. difficult to swallow- compress esophagous 6. hard to breathe |
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what are the clinical sx of AAA, what about TAA
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AAA
Rupture, impingement on things next door, occlusion of a branch, embolism, palpable mass TAA also rupture and compression of adjacent structures: more structures, recurrent laryngeal, esophagous, lungs, errosion of bone. |
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syphalis predisposes to what aneurysm
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TAA
**can push on thoracic structures |
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what is a dissection
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when blood gets into the intima and tears the layers of the BV wall apart
**often ruptures **may or maynot have dilation **doesnt stretch the BV like an aneurysm does **seen in underlying CT disease (marfan, eherls dalnos) |
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what 2 groups of pts get dissections
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1. Men 40-60, HTN (also see TAA)
2. Pts with CT defect (marfan/ehlers dalnos) |
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what is a predisposing factor for dissection
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HTN
CT disorder |
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what is the most frequent detectable microscopic leision
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cystic medial degeneration
**its the initial intimal tear |
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what is a debakey classification used for
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aortic dissectinos
I whole aorta, creates a tube around aorta II ball before great vessels III after great vessels, affects one side of aorta Type A: proximal leision Type B: distal leision |
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what are the classical clinical sx for dissection? what is this presentaiton similar to?
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sudden onset of super bad pain in the front and radiates to the back and moves down. confused with MI
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what is the most common cause of death with dissections
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rupture
**will cause bloody effusion into the pericardial, pleural or peritoneal area **can be fixed sometimes with folding surgery |
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what is a trpe A/B debakey dissection
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1. Proximal: can affect ascending and or descending
2. Distal to sibclavial |
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fatigue, fever, aches, and pains can be indicative of what
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vaculitis
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what are the common clinical findings in vasculitis
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pain
fever aches pain tissue ischemia |
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what are the 2 most common mechs of vasculitis? why distinguish
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Infectious-
Autoimmune: give steroids/immunosuppressive therapy |
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what 3 mechs initiate non infectious vasculitis
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vasculitis- vessel wall inflammation
1. Immune complex deposition (type 3 hypersensitivity) 2. Antineutrophile AB in cytoplasm 3. AB against endothelium **recall vasculitis can be beither immune mediated or infectious |
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what is ANCA
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lab test to determine non infectious vasculitis
MPO-ANCA, pANCA- necrotizing and granulomatous |
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tell me a little about immune complex mediated vasculitis? when is it seen
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usually mediated by AB and compliment- seen in SLE, drug hypersensitivity, secondary to viral infection
**AB responsible for deposition is unknown |
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what are the 2 types of ANCA's and what is an assiciated disease
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measure for vasculitis, helps dx and monitor disease
1. MPO- ANCA, p-ANCA (microscopic polyangitis, Churg-Strauss Syndrome, necrotizing and granulomatous) 2. PR3-ANCA, c-ANCA (Wegener granulomatous) |
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tell me about Anti-PMN vasculitis
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this is immune mediated, tehre are AB that react with PMN
**we get our ANCA's ehre MPO- ANCA, p-ANCA PR3-ANCA, c-ANCA |
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tell me about vasculitis mediated by antiendothelial AB
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kawasaki predisposes you to it
**recall our immune mediated vasculitis is : immune complex mediated, anti-PMN, anti-Endo |
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1. Giant cell arteritis affects what size vessel
2. what is the major morphology of giant cell vasculitis 3. who is it seen in 4. what is it associated with |
1. large to small- affects the vessels in the temple
2. focal granulomatous infection 3. seen in elderly, most common 4. associated with aorta, giant cell aortitis. also with polymyalgia rheumatica (neck, shoulder pain) |
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1 what are the sx of giant cell arteritis
2 how is dx of giant cell srteritis made 3. what tx is used |
1. insidious- fever, pain, weight loss, headache, ocular if opthalamia a is involved
2. biopsy (good biopsy bc disease is segmented), SUPER HIGH ESR 3. steroids, decrease inflammation |
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so what is it called when an old patient has those temporal arteries that are bulging out
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its a kind of infectious vasculitis, Giant Cell Arteritis
**there is granulomatous inflammation in the large vessel, can also involve aorta, seen in old folks **will have SUPER high ESR |
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A 67-year-old man has a 1-month history of fever, malaise, myalgias, 2-
kg weight loss, and headaches. On examination, there is temporal tenderness on palpation and a bruit, and he has an erythrocyte sedimentation rate of 86 mm/hr (nl 20 mm/hr). whats the dx whats his ANCA going to be what serious complication can occur |
1. Giant cell Arteritis
2. ANCA, negative, no titers 3. Blindness with opthalimc artery involvement **involves old peoples temporal a with granulomatous inflammation |
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Takayasu affects what vessel size?
what is another name for it? what are the 3 main sx what age group does it affect? |
1. LARGE- aorta (arch mostly, or pulm a)
2. Great Pulseless disease, no UE pulse 3. less than 50 (giant cell is older than 50) 3. |
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what type of vasculitis causes granulomatous vasculitis followed by fibrous thickening that can narrow the lumen of the great vessels
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Takayasu, great pulseless disease. the UR pulses decrease
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1. whats the major morphological finding of takauasu vasculitis
2. what is the course of the disease |
1. granulomatous inflammation in aortic arch
2. this then turns to fibrosis and can decrease the lumen of great vessles, and lead to diminished pulse- PULSELESSNESS disease **no specific presentation, ppl less than 50, fever, fatigue, weight loss, cold fingers, ocular disturbance, can be rapid progression or slow. tx with steroids |
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1. PAN (polyarteritis Nodosa) affects what vessel size?
2. What vessels are sparred, what are affected 3. whats the morphology 4. whats the age group |
1. small/medium-systemic, not specific to a great vessel(pulselessness), aorta, or temporal (giant cell) as seen before
2. affects renal and visceral, spares pulmonary, NO glomerulonephritis 3. NECROTZING: seen in acute, healing and fibriod stage. can lead to aneurysm- paplable nodule 4. young adults |
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1. whats the association of PAN and glomerulonephritis
2. manifestations of PAN 3. Course with/with out tx. 4. whats tx |
1. PAN is not associated with glomerulonephritis. can be associated with aneruysm
2. long remissions, sx are those general ones of fever nad HTN, ABDOMINAL PAIN, melena 3. tx with steroids, can die if not treated |
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what vasculitis is characterized by necrotizing inflammation in small/med vessels of young adults
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PAN, Polyarteritis Nodosa
renal and visceral arteries are affected, pulm is spared. No glomerulonephritis |
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1. 3 features of churg strauss syndrome
2. what other vasculitis has the same leision 3. ANCA |
1. asthma, allergic rhinitis, peripheral eosinophilia
2 like PAN (necrotizing inflammatino) 3 P-ANCA (MPO), its only associated in 50% of cases |
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whats another name for mucocutaneous lymph node syndrome
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Kawasaki
**vasculitis that involves the coronaries *transmural necrosis (not as severe as PAN) *affects kids, acute, self limited |
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what is the self limited vasculitis that affects the coronaries in kids with necrotizing inflammation
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kawasaki, mucocutaneous lymph node syndrome
**coronaries can thrombose or aneurysm |
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can you make a good dx for kawasaki clinically
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yep
fever red eyes/throat edema in hands/feet red palms/soles that desquamate cervical lymphadenopathy **this is the one where we get necrotizing inflammation on the coronaries of kids- thrombosis or aneurysm |
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most vasculitis is tx with steroids, what is one that is not
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kawasaki,
tx with IV Ig and asprin **if untreated kids get cardio sequelea (pathology from the disease), usually self limited |
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1. what vessel size is affected with mucroscopic polyangitis
2. how does it present 3. Clinical features 4. whats another name |
1. small, pulm are affected (not in PAN)
2 palpable purpura 3 glomerulonephritis 4 hypersensitivity vasculitis, leukocytoclastic vasculitis |
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what does microscopic polyangitis look like
2. how is it dx 3, how is it distinguished from PAN |
1 segmental fibriniod necrosis
2 P ANCA in 70%, skin biopsy 3. -smaller vessels that are ALL IN SAME STAGE (PAN affects renal and visceral not pulm and has leisions of various ages) -glomerulonephritis (not in PAN) -pulm capillary affected (not in PAN) |
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what vasculitis has leisions of various ages?
what has leisions all the same age |
PAN
Microscopic polyangitis **PAN has no glomerulonephritis, and pulm are spared **Microscopic affects kidney and pulm |
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P ANCA is seen in what 2 vasculitis
C ANCA |
1. Churg Crauss
2. Microscopic polyangitis C ANCA seen in Wegeners (40 yo male) |
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what vasculitis is associated with bowel pain?
HTN, abdominal pain edema/erythema/desquamation of hands/feet |
microscopic polyangitis
PAN Kawasaki **most others are "fever, malaise, aches" |
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what is the triad of wegners
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1. acute necrotizing granuloma of respiratory tract
2. necrotizing or granulomatous vasculitis of small/medium vessels in lung 3. renal disease, glomerulonephritis (also seen in microscopic polyangitis) |
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1. what are the morphological and clinical features of Wegeners vasculitis
2. natural course of disease 3. who is affected 4, Dx? |
1. leisions in respiratory tract- granuloma, ulcers. Renal leision also
2 die w/o tx. relapse/remitt. tx with steroids, TNF antagonists 3 40 yo male 4 C ANCA in 95% |
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what vasculitis is associated with ulcers in tha nasopharynx and granulomas in the respiratory tract
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wegners
*more common in 40 yo males |
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A 41‐year‐old man presents with a chronic
cough. On exam he has mucosal ulcerations of the nasopharynx. Chest x‐ray shows bilateral nodular infiltrates. Labs are significant for an elevated BUN and creatinine (indication of renal disease) and an elevated C‐ANCA titer. Nasal biopsy shows necrotizing granulomatous inflammation. Lung biopsy shows necrotizing vasculitis. Which of the following is the most likely diagnosis? |
wergners
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name the vasculitis
1. C ANCA, ulcers in nasopharynx and granulomas in respiratory tract 2. necrotizing inflammation in the renal but not pulm, HTN and abdominal pain 3. asthma, eosionophillia, P ANCA, necrotizing and granulomatous 4. coronaries thrombose or aneurysm in kids, mucocutaneous lymph node 5. Pulseless disease, people under 50 6. granulomatous, ppl over 50, temporal a 7. necrotizing glomerulonephritis, pulm capillaries, P ANCA |
1 wegners
2 Polyarteris Nodosa (PAN) 3 Churg Strauss 4 kawasaki 5 takayasu 6 giant cell arteritis 7 Microscopic polyangitis |
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what is another name for thromboangitis obliterans
who gets is |
1. Buerger disease
2. males, who smoke and are under 35 **its when your fingers/toes get gangrenous/cold and painful (rayunad) |
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what does thromboanginitis obliterans look like
how can you prevent another attack |
segmental thrombosing/inflammation small arteries in tibia and radius, causes raynaud (cold fingers/toes and pain with exercise. may also be gangrenous)
*stop smoking! this causes the disease |
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what is it called if a young adult man who smokes has segmantal inflammation/thrombosis of small arteries in his tibia and radius? what will his presentation be
why smoke? |
thromboanginitis obliterans, aka buerger disease
**fingers/toes are cold or gangrenous and painful (ryaunad) Smoke causes damage to the endo of BV |
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does raynaud have necrosis?
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not usually, more color changes
**vasoconstrictin of digital arteries *seen in berguer disease (thrombangitis obliterans) |
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infectious vasculitis can be cuased by what? what can be a secondary complication
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direct invasion of bugs, can weaken walls to lead to mycotic aneryrsm or thrombosis/infarct
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what are the clinical feartures of Raynaud?
who gets primary? what ppt the attack? |
exaggerated vasoconstriction of arteries in toes/fingers
fingers turn red, white, blue primary is seen in young females (normal reaponse to cold that is exaggerated) ppt by cold? |
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what is the natural course of raynauds?
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digital arteries constrict so fingers/toes change color, and are painful
**usually a normal response to cold, but this is exaggerated **or there can be an underlying cause like beugers ro SLE |
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what is secondary Raynauds
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primary is common in young women and is just an exaggerated response of normal
*secondary is due to an underlying disease (SLE, scleroderma, artherosclerosis, Buerger) |
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what are varicose veins and what veins are involved? what are the clinical sx
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when superficial veins of LE are dilated and tortuous- due to increased intralumenal pressure, loss of vessel wall support
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what are some predisposing factors for varicose veins, what are sequelae
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when you stand lots- simple orthostatic edema
long plane rides or car rides obese/pregnant SEQUELA ulcers, edema, vulnerable to injury. no serious complicatinos, thromobosis are common |
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what happens to the valves in varicose veins? complication
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they are dilated and tortous so the valves are incompetent
LE ulcers are common **can lead to thrombus (local, not DVT), stasis, congestion pain, edema |
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what predisposes ppl to DVT?
what does a DVT lead to what veins are involved |
DVT: obese, CHF, preg, immobilization (NOT varicose vein)
DVT --> PE deep legs involved in VDT, also thrombophlebitis and phleobothrombitis |
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what veins are affected in thrombophlebitis and phlebothrombosis
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deep leg veins
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why do you make ppl walk after surgery? what are some clinical predispositions to thrombophlebitis/phlebothrombosis
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1. Post op walk to prevent DVT, thrombophlebitis and phlebothrombosis
2. not moving for a long time 3. CHF/preg/obese 4. systemic hypercoaguability |
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what are the local things with thrombophlebitis and phlebothrombosis?
are there serious complications |
Local: edema distal to occlusion, dusky cyanosis, heat, tender, red, swoll, pain. hurts to dorsiflex
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what is migratory phrombophlitis? whats another name for it
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trousseau sign
**venous thrombosis that moves around, seen in cancer pts, hypercoaguable state |
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what is trousseau sign
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migratory thrombophlebitis
**seen in cancer pts, venous thrombis that moves around |
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An 85 year old woman fell and broke her hip. She was
not a good candidate to surgery, so she was confined to bed in a nursing home. Several weeks later, she was being moved to another room and afterwards became short of breath breath. She died soon after. At autopsy, a large pulmonary embolus was found. The vein seen is from the pelvis. The vein is completely occluded by thrombus. Part of the thrombus is old and shows evidence of organization. What are the risk factors for venous thrombosis? –Where do most pulmonary emboli originate? |
obese, preg, hypercoaguable- post op, CHF, immobilization
Deep veins of leg |
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what is superior vena caval system caused by?
what are the clinical features |
1. Obstruction due to neoplasm (bronciogenic, medisteinal lymphoma)
2. dusky cyanosis, dilation of venis in the head |
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what is inferior vena caval syndrome caused by?
what are the clinical features |
1. neoplasm or thrombus
2. Leg edema, proteniuria (renal veins involved), distension of superficial veins in LE nad abdomen |
