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Path 11 Vessels
LECOM Path Ch 11 Blood Vessels
| Question | Answer |
|---|---|
| As Arterial vessels get smaller the ratio of wall thickness to lumen diameter | becomes greater |
| These are the principal points of physiologic resistance to blood flow | arterioles |
| Halving the diameter of a vessel increases resistance by how much | 16 fold |
| Vascular leakage preferentially happens where | postcapillary venules |
| Relative to arteries, Veins typically have larger____, Larger_____ and thinner____ | larger diameters, larger lumens, thinner walls |
| Vasculogenesis vs Angiogenesis | denovo in embryogenesis vs in mature organism |
| Arteriogenesis | remodeling of existing arteries in response to chronic changes |
| These are found in vascular endothelial cells walls | Weibel-Palade bodies |
| Weibel-Palade bodies store | von Willebrand’s factor |
| Stereotypical response to vessel wall injury is | intimal thickening Are intimal and neo-intimal cells identical? |
| Cardiac output determined by (3) | heart contractility, heart rate, blood volume |
| mutations in the renal Na+ channel lead to | Liddle Syndrome |
| 2 types of small vessel disease in HTN | hyaline and hyperplastic arteriolosclerosis |
| Hyaline arteriolosclerosis: Cause | plasma protein leakage across damaged endothelial cells |
| Arterioles with homogenous, pink hyaline thickening and luminal narrowing. Dx? | Hyaline arteriosclerosis |
| Hyperplastic arteriolosclerosis: Seen in | malignant/severe HTN |
| Arterioles with concentric laminated thickening of walls and luminal narrowing. Reduplicated BM and smooth muscle cells. Dx? And what else do you see ? | Hyperplastic arteriolosclerosis; fibrinoid deposits and necrotizing arteriolitis esp in the kindney |
| Calcific, even bone, deposits in walls of muscular arteries after the age of 50. Dx? And is it dangerous? | Monckeberg medial sclerosis; no |
| Demographic for AAA | 50+yo male smokers |
| MC location of a AAA | below the renal arteries and above the bifurcation |
| What do AAAs usually contain inside of them | poorly organized, bland, laminated mural thrombus |
| Inflammatory AAA shows | dense periaortic fibrosis with increased lymphs and m acrophages |
| Mycotic AAA shows | infection usually with Salmonella, with suppurative desctruction of the media |
| 3 size classes of AAA and risk of rupture | 4-5cm 1%; 5-6cn 11%; >6cm 25% |
| Dysfunction endothelial cells show (3) | increased permeability, enhanced leukocyte adhesion, altered gene expression |
| 7 steps in atherosclerosis | Endothelial injury; Accumulation of LDL; Monocyte adhesion; platelet adhesion; Factor release; SM cell proliferation and ECM production; lipid accumulation; E.A.M.P.F.SmEc.L |
| 3 places plaques like to form | exiting vessels, branch points, posterior aorta wall |
| Dominant lipids in atheromatic plaques | cholesterol and cholesterol esters |
| Production of this protein on ECs increases plaque formation | VCAM-1 |
| What converts a fatty streak into a mature atheroma | intimal SM cell proliferation and ECM deposition |
| 3 growth factors that cause ECM and SM cell growth in atheromas | PDGF, FGF, and TGF-α |
| 2cm lesion with lipid-filled macrophages in the intima of the aorta of a 10yo. Normal or disease? Dx? | Normal; fatty streak |
| 2 key processes in atherosclerosis | intimal thickening and lipid accumulation |
| Thoracic or abdominal aorta involved in atherosclerosis more often? | Abdominal |
| 3 components of atherosclerotic plaques | cells: SM, T cell, macrophage; ECM: collagen, elastic, and proteoglycans; lipids intra and extracellular |
| Critical stenosis is Dx when what happens? And at what % typically? | when demand exceeds supply and 70% occlusion |
| 3 catagories of plaque change | Rupture/Fissure; Erosion/Ulceration; Hemorrhage into the atheroma |
| Vulnerable plaques have either | large volume of lipid accumulation or thin fibrous cap |
| Inflammation of a plaque can cause rupture how | decreases TIMP production leading to increased fibrous cap reabsorption |
| One stabilizer of plaques and one exacerbator of them, pharmacologically | statin and adrenergic stimulation |
| Most common time for MI | 6am to noon |
| Saccular or fusiform aneurysm are true or false | true aneurysm |
| Arterial dissection is Dx when blood | enters the arterial wall itself |
| Marfan’s: defect and causes what in vessels | fibrilin gene defect, weakening and progressive dilation |
| Loey-Deitz Syndrome: defect and what happens in vessels | mutated TGF-β receptors, vessels rupture easily |
| Ehler-Danlos syndrome: defect and what is seen in vessels | defective Collagen Type III; Weak vessel walls |
| Cystic medial degeneration: caused by and what is seen | ischemia/scurvy/Marfan; degenerative changes, SM cell loss, increasing GAGs |
| MC location of Aneurysms associated with atherosclerosis | abdominal aorta |
| Atherosclerosis causes wasting of what layer of vessel | media |
| Soft yellow lesion in a vessel, lipid core, white fibrous cap, protruding into the lumen. Dx? | atherosclerotic plaque |
| Most significant independent risk factor for atherosclerosis | genetic/ family history |
| Modifiable risk factors for atherosclerosis (5) | hyperlipidemia, HTN, DM, C-reactive protein, Cigarette smoking |
| Atherosclerosis is initiated by what | endothelial damage/dysfunction |
| Aortic dissection occurs in what 2 demographics | men 40-60 with HTN or youth with connective tissue diseases |
| MC preexisting histology present in dissections | cystic medial degeneration |
| MC location for aortic dissection | ascending aorta, within 10 cm of aortic valve |
| Where the dissection usually happens in the layers of the aorta | middle and outter 3rds |
| Type A disections are | between the aortic valve and arch, proximal lesions |
| Type B disections are | not involve the ascending aorta, usually after SC artery |
| What causes injury in Immune complex vasculitis (2) | compliment activation or recruitment of Fc-receptor bearing cells |
| Drug hypersensitivity with vascular involvement is mediated by | antibody complexes |
| Vasculitis secondary to virus is usually mediated by? And example | antibody complex; HBV and 30% w/ polyarteritis nodosa |
| ANCAs are directed against what? (3) | neutrophil primary granules; monocyte lysosome; EC |
| What is p-ANCA or MPO-ANCA directed against | lysosomal enzyme creating ROS |
| What is c-ANCA or PR3-ANCA directed against | neutrophil azurophilic granule |
| 2 diseases characteristic with p-ANCA | microscopic polyangiitis and Churg-Strauss syndrome |
| Disease charachteristic with c-ANCA | Wegener granulomatosis |
| Anti-endothelial cell Ab charachteristic of what disease | Kawasaki disease |
| MC vasculitis is elderly Americans | Giant Cell Arteritis |
| Granulomatous vasculitis, medium and small arteries, an affect aorta | Giant Cell Arteritis |
| Temporal Arteritis, characteristic findings | multinucleated giant cells and elastic tissue fragmentation, intimal scarring |
| 50% of Giant Cell Arteritis Pt’s present with | ophthalmic artery involvement and permanent blindness |
| Demographic of Giant Cell Arteritis | elderly population |
| Granulomatous vasculitis of medium to large arteries, transmural fibrous thickening, of the aortic arch | Takayasu Arteritis |
| Early perivascular monos around vasa vasorum, later with medial fibrosis, granulomas, and acellular intimal thickening | Takayasu Arteritis |
| Weakening of upper extremity perfusion pressures Dx (2 names) | Pulseless disease or Takayasu arteritis |
| Takayasu vs Giant Cell Aortitis Different in Dx | younger than 50 is Takayasu |
| Demographic of Takayasu arteritis | young people, if over 50 it’s giant cell |
| Necrotizing vasculitis of small to medium arteries, pulmonary circulation is spared | PAN |
| 4 tissues affected in PAN, in order | Kidney, heart, liver, GI |
| Linked to PAN in 30% of Pt’s | HBV |
| ANCA’s with PAN | none |
| Lesions in PAN, same age or different | different ages |
| Sharply circumscribed arterial fibrinoid necrosis with neutrophilic infiltrates. Dx and stage | PAN; acute lesion |
| Marked fibrotic thickening of artery with associated elastic lamina fragmentation. Dx and stage | PAN; healed lesion |
| PAN, demographic | young adults with NSC |
| Acute febrile disease in infants and children | Kawasaki Disease |
| T cell hypersensitivity mediated arteritis of medium-large vessels, unknown Ag, in children | Kawasaki Disease |
| MI in a baby without Chagas | Kawasaki Disease |
| Child, LA, fever, skin rash, oral/conjuctival erythema Dx | Kawasaki Disease |
| 2 common causes of infectious vasculitis from local invasion | Aspergillus and Mucor |
| Heavy smoker with extremity vascular involvement | Buerger Syndrome |
| Segmental, thrombosing, acute/chronic inflammation of medium/small vessels in extremities | Buerger |
| Necrotizing or granulomatous vasculitis in small to medium upper airway/lung vessel; necrotizing granulomas of upper/lower respiratory track; glomerulonephritis | Wegener Granulomatosis |
| Mediator and ANCAs in Wegener’s | T-cell vs inhaled antigen or microbe; c-ANCA |
| Demographic and outcome in Wegener | 40yo men; 80% 1 year mortality w/o Tx |
| Granulomas that may coalesce to produce nodules that cavitate in the respiratory track | Wegener |
| Necrotizing arteritis of very small vessels | Microscopic Polyangiitis |
| Microscopic Polyangiitis lesions vs PAN | MPA all same stage |
| ANCAs associated with Microscopic Polyangiitis | p-ANCA |
| Fragmented neutrophilic nuclei, fibrinoid necrosis, necrotizing glomerulonephrosis and pulmonary involvement | Microscopic Polyangiitis |
| Small-vessel necrotizing vasculitis associated with asthma, allergic rhinitis and extravascular necrotizing granulomas | Churg-Strauss Syndrome |
| PAN like lesions with addition of eosinophils and granulomas | Churg-Strauss |
| MCC of mortality of Churg-Strauss | eosinophilic infiltrates of the heart/cardiac involvement |
| Young women, drastic vasoconstriction, benign clinical course Dx? | Primary Raynaud |
| Vascular insufficiency due to arterial narrowing by other condition. Dx? | Secondary Raynaud |
| Superficial lower extremity veins, tortuous and dilated | varicose vein |
| 2 specific varicosities | hemorrhoids and esophageal varicies |
| 4 common predisposing factors for DVT | hypercoaguable state, prolonged immobilization, infection, CHF |
| SVC syndrome: Cause and effects | tumor compression or invasion of SVC; dusky appearance, dilation of head, arm, neck veins |
| IVC Sydrome: Cause and effects | tumor compression or invasion; dilated leg and lower body veins, proteinuria |
| Common bacterial cause of lymphangitis | β-hemolytic Strep |
| Spread of infection into lyphatics Dx? | lymphangitis |
| This is caused by obstructionof the lymphatic system, increases interstitial fluid | lymphedema |
| Cause of primary lymphatic agenesis | Milroy Disease |
| 3 types of hemangioma | capillary hemangioma, Cavernous hemanioma, Pyogenic granuloma |
| MC vascular tumor | capillary hemangioma |
| Un-encapsulated clustering of tiny thin walled vessels, usually on skin | Capillary hemangioma |
| Un-encapsulated lesion with large thin walled vascular spaces, on skin, liver, CNS | cavernous hangioma |
| Proliferating capillaries with interposed edema and inflammation, Ulcerated polypoid variant, often after trauma | Pyogenic Granuloma |
| Small blister like bleb filled with small lymphatic channels, lined with EC | Simple/Capillary lymphangioma |
| Poorly encapsulated, can be large, found in children’s neck and axilla | Cystic hygroma/ Cavernous lymphangioma |
| Tiny spot usually under fingernail with aggregate, nests, and masses of specialized glomus cells, with branching vascular channels | Glomangioma |
| Vascular ectasias are actually just | dilation of pre-existing vessels Nevus flammeus is |
| Minute, subcutaneous arterioles, in a radial fasion | spider telangiectasia |
| Rare autosomal disease with multiple small, aneurysmal telangiectasias, on skin and mucous membranes | Hereditary Hemorrhagic telangiectasia / Osler-Weber-Rendu disease |
| Vascular proliferation from opportunistic infection in the immunocompromised | Bacillary Angiomatosis |
| Bacterial cause of bacillary Angiomatosis | Gram negative Bartonella sp. |
| 4 types of Kaposi Sarcoma | Classic, African/endemic, transplant-associated, AIDS associated |
| Virus associated with Kaposi Sarcoma | HHV-8 or KSHV |
| 3 stages of Kaposi Sarcoma lesions | Patches; Raised Plaques; Nodular lesions |
| A well differentiated angiosarcoma is called | hemangiosarcoma |
| 3 causes of hepatic angiosarcomas | arsenic/pesticides; polyvinyl chloride; Thorotrast |
| Gray-white soft-tissue mass; in arm of woman post-radical mastectomy in lymph | lymphangiosarcoma |
Created by:
csheck
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