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96 Cards in this Set
- Front
- Back
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B cells do what
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make antibodies
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what is monoclonal gamoopathy
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excess immunoglobulins made are usually functional, benign, can become multiple myeloma
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multiple myeloma produces
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IgG and IgA and excess light chains
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what factor plays a big role in multiple myeloma
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IL-6 it is osteoclast activating factor make osteolytic lesions
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what other factor is associated with multiple myeloma
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IL-1 also an osteoclast activator
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What is bence jones protein
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k and gamma chains portion of antibody by cells is malignant lose genetic material to make intact ones
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what else do you see deposited
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amyloids
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What about calcium?
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hypercalcemia
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Bone marow?
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anemia and leukocytopenia, more infections
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what test would you do to find this?
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not a UA that will be (-) need to do more`
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what is M-spike
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monophasic, high amount of monoclonal proteins use a SPEP or UPEP
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Waldenstrom's is
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solid tumor of antibody-producing B cells
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whats the antibody over produced in waldenstrom's?
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igM
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what does excess igM cause
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hyperviscosity syndrome (thick blood)
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what are flame cells
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eosinophilic neoplastic plasma cells
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who is at risk for phlebothrombosis
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anyone with any of the virchow's triad
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what is virchow's triad
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blood stasis, hypercoaguability, and endothelial cell damage
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why is blood stasis bad
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flow slowly through portal system, more likely to form clots if sittin around
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how does hypercoaguability increase risk
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anything like OCP or factor V laden--> no C and S would so cause more clots, can actiavte cascade whenevr
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factor V and VIII are inhibited by
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C and S
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why does cirrhosis of the liver increase risK?
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having bands of liver prevents good blood flow
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why does endothelilal cell damage incr risk?
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exposes VWF get platelets and VIII activated use clot factors and platelet aggregation
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what is the problem in artherosclerosis
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very high LDL
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if LDL is low what happenes
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get damaged cell membrane especially in MYELIN, and hormones
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myelin is purely made of
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layers and layers of cholesterol
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if LDL is too high what happens
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deposits in cell walls causing artherosclerosis
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foam cells are what
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a macrophage eating all these cholesterol droplets from the wall but it cant destroy it!
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if macrophage is trying to phacotyize it what is released
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IL-1 and TNF alpha
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artherosclerosis is a disease of
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inflammation by these macrophages!!!
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this big mound of macrophages causes what
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poor BV and eventually bulge out= anyeursm
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in any artherosclerotic plaque you have a cap made of
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Ca
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what happens if this cap bursts
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platelets adhere- making a huge clot, occluding... ischemia and infarction to tissues distal
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what can you get from arthersclerosis
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stroke, PVD (artherscloertic lesions in pelvic and LE, decr blood flow so much you have pain w walking) low blood flow everywhere
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calf claudication is a sign of
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PVD, so much artherosclerosis in pelvic and LE- prevented by plaques
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how does ichemic heart disease work
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low blood flow bc impeding can cause MI, UA, SA
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if theres a stable artherosclerosis sitting on coronary vessel you get
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stable angina
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if the plaque bursts and get platelet aggregation you get
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unstable angina/MI
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what is mesenteric ischemia
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celiac artery, SMA, IMA w artherosclerotic plaque- problems w bowel oxygen deliver
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People w chronic mesenteric ischemia get pain after they
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eat, need to digest need more O2...bc of these plaques there they cant deliver blood
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acute mesenteric ischemia
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plaque in vessel and the plaque is disrupted- crack it, platelets adhere and occlude it, that segment bowel- deprived of blood--> severe profound generalized abdominal pain
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aortic aneurysm works by
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if have arthersclerotic plaque- weakened underlying muscle- get a bulging, lesion is a plaque- synonms: intima (endothelial) plaque
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who is at high risk w/o high cholesterol
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smokers- they already at risk & homocysteine made naturally but in excess= inflammation
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how to reduce homocysteine levels
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give them B12- natural way
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3 main effects of plaques
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decrease luminal dimensions, atrophy mdia, attract platelets to clot- occludes or breaks off to go down stream and obstruct blood flow
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what cell layer is artheosclerosis associated with
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intima
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what layer is monckebergs associated with
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media
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big different btwn artherosclerosis and monckebergs
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malignant vs benign
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what is a hypertensive emegrnecy
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systolic > 210, diastolic > 150
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what is malignant hypertension
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any with end-organ damage, destruct bV
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how do we tell if someone is at risk
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evaluate the retina, kidney w UA...need to do a neurologic exam, fundoscopic, and UA...to see any end-organ damage
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what are the compensatory mechanisms?
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hyperplastic arteriosclerosis- onion skin hyperplasia
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the media becomes hyperplastic creating
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layers of sm muscle "onion skin" but also extra strength
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what gives the most strength?
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media/muscle layer
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to prevent further damage the
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sm muscle proliferates
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as we age we all get
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hyaline arteriosclerosis
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what are the main mechanisms of arteriosclerosis
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inflammation and use
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where is this lesion located
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inner-lining, the order is
BM, then theres the media! |
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BM pathology is
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hyaline arteriosclerosis
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thickens BM does what
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narrows the lumen, nephrosclerosis in the kidney etc. mostly the ones to glomerulus end up seeing not only hyaline arteriosclerosis- or nephrosclerosis
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what are elastic laminae
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give RBC elastic recoil ability
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what happens after they lose elasticity- get media atrophy
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muscle is going awya, making BV very weak allowing for ectasia (bulge) get anyeursms
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as we age we all incr risk for
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anyerusms!
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higher the BP higher the prognosis to have
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hyalin arteriosclerosis causing further weaking of the walls
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pneumonic for multiple myeloma = CRAB
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hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions/Back pain, multiple myeloma: Monoclonal M protein
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palpable purpura is key to
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hypersensitivity arteritis
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why is this highly seen in buttock
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because you push on it when sit etc. on capillaries- sit down and rupture- painful and pruritis- C3a C5a...complement--> mast cells basophils--> histamine make it itchy
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what type of hypersensitivity is hypersensitivity arteritis
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type III bc immune complex form and float then deposit MAc comes to destroy and lands on walls
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skin gets an immune complex deposit then what happens
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get complements--> MAC--> destroy capillaries more prone to burst, get bleeding in the skin and can palpate it
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whats the difference btwn hypersensitivity arteritis and henoch-schonlein purpura?
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H-S has igA in the blood, this is usually protecting mucous membranes but now its active in blood therefore activating MAC
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what's the population for H-S?
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children
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why do you see diarrhea with H&S?
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bc the capillaries burst commonly in the butt
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viral upper respiratory infection will develop what response?
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H-S
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vaccinations are a common cause to stimulate
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H-S
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whenever someone has polyarteritis nodosa you do a
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hepatitis screening
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features of polyarteritis nodosa
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necrotizing inflammation of arterial walls, WBC invade blood vessel walls and cause inflammatory damage
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What does PAN occur secondary to
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HBV, HCV, or hairy cell luekemia
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WHat are some symptoms seen with this?
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fever, abdominal pain throughout, renal disease w/o glomerulonephritis (b/c those capillaries are too small) HTN, diffuse myalgia
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what size BV does this affect
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medium-size
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what is the small BV version of this
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microscopic polyangitis- does same but on small blood vessels!
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what does it become thats pretty bad
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the most severe acute nephritis
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who is at highest risk for Buerger's disease
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jewish male < 35 that smokes
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what BV size does it effect
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medium and small
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what does a high ESR mean
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lots of inflammation bc tons of fibinogen on RBC
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why would giant cell arterities cause blindness
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messes with temporal artery-->external carotid-->common carotid-->internal carotid-->opthalmic branch
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what do you do when you see this
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start them on steroids right away then do the lab testing
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what age population are you most likely to see this in
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females > 50
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what is thomboangitis obliterans
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a hypersensitivity reaction to tobacco
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where are the primary effects of this
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tibial and radial arteries
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what do you see in the vessel walls
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collections of neutrophils in the vessel walls
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what can this possible cause
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pain in the distal limb that progresses to gangrene
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what is giant cell arteritis
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granulomatous inflammation of vessel walls
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What is likely seen with giant cell arteritis
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hi ESR< temporal arteritis, fever, fatigue, blindness eventually
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what is polymyalgia rheumatica
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systemic manifestation of giant cell arteritis
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what do you see w polymyalgia
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systemic manifestation of giant cell arteritis
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What kind of symptoms w polymylagia rheumatica
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flu-like symptoms, very hi ESR, limb claudication, CVA, MI, aortic anyeursm, and visceral organ infarction
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What is Wegener's Granulomatosis
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granulomas in vessel walls + c-ANCA, symptoms like sinusitis and sinus polyp formations
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