Quiz
P2-Inflammation
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Questions in this quiz (43)
1Simplistically, acute inflammation occurs when primary cells leaving vessels are [blank_start]neutrophils[blank_end]
- Aneutrophils
2Chronic inflammation occurs when primary cells leaving blood vessels are [blank_start]lymphocytes[blank_end]
- Alymphocytes
3TLRs are present on innate immune cells (e.g. macrophages and dendritic cells) and adaptive immune cells (e.g. lymphocytes). They are activated by [blank_start]PAMPs[blank_end] (molecular patterns commonly shared by microbes). Activation results in upregulation of [blank_start]NF-kB[blank_end], a [blank_start]nuclear transcription factor[blank_end] that activates genes producing multiple immune mediators. They are a major mediator of the inflammatory response.
- APAMPs
- BNF-kB
- Cnuclear transcription factor
4Arachidonic acid metabolites and are another major set of mediators of inflammation that are innate to the cell, released in response to tissue damage or inflammation. They are released from the cell membrane by [blank_start]phospholipase A2[blank_end] then metabolized by [blank_start]cyclooxygenase[blank_end] (making [blank_start]prostaglandins[blank_end]) or 5-[blank_start]lipoxygenase[blank_end] (making [blank_start]leukotrienes[blank_end]).
- Aphospholipase A2
- Bcyclooxygenase
- Cprostaglandins
- Dlipoxygenase
- Eleukotrienes
5PG[blank_start]D2[blank_end], PG[blank_start]E2[blank_end], and PG[blank_start]I2[blank_end] mediate vasodilation and increased vascular permeability. PG[blank_start]E2[blank_end] also mediates pain and [blank_start]fever[blank_end].
- AD2
- BE2
- CI2
- DE2
- Efever
6Among key leukotrienes, LT[blank_start]B4[blank_end] attracts and activates neutrophils. LT[blank_start]C4[blank_end], LT[blank_start]D4[blank_end], and LT[blank_start]E4[blank_end] mediate vasoconstriction, [blank_start]bronchospasm[blank_end], and increased vascular permeability, and are important in the physiology of [blank_start]anaphylaxis[blank_end].
- AB4
- BC4
- CD4
- DE4
- Ebronchospasm
- Fanaphylaxis
7Mannose binding lectin pathway is activated when [blank_start]MBL[blank_end] binds to [blank_start]mannose[blank_end] on bacteria, activating [blank_start]complement[blank_end]
- AMBL
- Bmannose
- Ccomplement
8Complement is comprised of proinflammatory serum proteins. Activation can occur through (1) classical pathway ([blank_start]C1[blank_end] binds [blank_start]IgG[blank_end] or [blank_start]IgM[blank_end] bound to antigen), (2) alternative pathway (microbial products directly activate), or (3) [blank_start]mannose binding lectin[blank_end] pathway ([blank_start]MBL[blank_end] binds [blank_start]mannose[blank_end] on microbes and activates complement). All pathways result in production of [blank_start]C3 convertase[blank_end], (cleaves [blank_start]C3[blank_end] to [blank_start]C3a[blank_end] and [blank_start]C3b[blank_end]), leading to production of [blank_start]C5 convertase[blank_end] (cleaves [blank_start]C5[blank_end] to [blank_start]C5a[blank_end] and [blank_start]C5b[blank_end]). [blank_start]C5b[blank_end] complexes with [blank_start]C6[blank_end]-[blank_start]C9[blank_end] to form the [blank_start]membrane attack[blank_end] complex. [blank_start]C3a[blank_end] and [blank_start]C5a[blank_end] are "[blank_start]anaphylotoxins[blank_end]," causing mast cell degranulation. [blank_start]MAC[blank_end] lyses microbes by putting hole in cell membrane.
- AC1
- BIgG
- CIgM
- Dmannose binding lectin
- EMBL
- Fmannose
- GC3 convertase
- HC3
- IC3a
- JC3b
- KC5 convertase
- LC5
- MC5a
- NC5b
- OC5b
- PC6
- QC9
- Rmembrane attack
- SC3a
- TC5a
- Uanaphylotoxins
- VMAC
9In addition to TLRs and AA metabolites, mast cells are important mediators of acute inflammation. They are widely distributed throughout [blank_start]connective[blank_end] tissue, and are activated by (1) tissue trauma, (2) complement proteins [blank_start]C3a[blank_end] and [blank_start]C5a[blank_end], or (3) cross-linking of [blank_start]IgE[blank_end] by antigen. Immediate response is due to release of histamine granules, causing arteriolar vasodilation and increased vascular permeability. Delayed response involves production of [blank_start]arachidonic acid[blank_end] metabolites.
- Aconnective
- BC3a
- CC5a
- DIgE
- Earachidonic acid
10A final mediator of inflammation is Hagemon factor (Factor [blank_start]XII[blank_end]), an inactive proinflmmatory protein produced in the [blank_start]liver[blank_end]. It is activated on exposure to subendothelial or tissue [blank_start]collagen[blank_end], and activates (1) coagulation and [blank_start]fibrinolysis[blank_end], (2) [blank_start]complement[blank_end] system, and (3) [blank_start]kinin[blank_end] system ([blank_start]kinin[blank_end] cleaves [blank_start]high molecular weight kininogen[blank_end], i.e. [blank_start]HMWK[blank_end], to make [blank_start]bradykinin[blank_end], which causes vasodilation, increased vascular permeability, and sensation of [blank_start]pain[blank_end].
- AXII
- Bliver
- Ccollagen
- Dfibrinolysis
- Ecomplement
- Fkinin
- Gkinin
- Hhigh molecular weight kininogen
- IHMWK
- Jbradykinin
- Kpain
11What causes fever? Pyrogens like [blank_start]LPS[blank_end] from bacteria cause [blank_start]macrophages[blank_end] to release IL-[blank_start]1[blank_end], IL-[blank_start]6[blank_end], and [blank_start]TNF[blank_end]. These increase [blank_start]COX[blank_end] activity in the [blank_start]perivascular[blank_end] cells of the [blank_start]hypothalamus[blank_end], which releases [blank_start]PGE2[blank_end] and causes fever.
- ALPS
- Bmacrophages
- C1
- D6
- ETNF
- FCOX
- Gperivascular
- Hhypothalamus
- IPGE2
12Pain is mediated by sensitization of nerve endings by [blank_start]bradykinin[blank_end] and PGE2.
- Abradykinin
13O2-dependent killing:
In the oxidative burst, [blank_start]O2[blank_end] is converted to [blank_start]superoxide[blank_end] ([blank_start]O2-[blank_end]) by [blank_start]NADPH oxidase[blank_end]. [blank_start]Superoxide[blank_end] is converted to [blank_start]hydrogen peroxide[blank_end] ([blank_start]H2O2[blank_end]) by [blank_start]superoxide dismutase[blank_end] ([blank_start]SOD[blank_end]). [blank_start]H202[blank_end] (acronym) is converted to [blank_start]bleach[blank_end] ([blank_start]HOCl[blank_end]) by [blank_start]myeloperoxidase[blank_end] ([blank_start]MPO[blank_end]).- AO2
- Bsuperoxide
- CO2-
- DNADPH oxidase
- ESuperoxide
- Fhydrogen peroxide
- GH2O2
- Hsuperoxide dismutase
- ISOD
- JH202
- Kbleach
- LHOCl
- Mmyeloperoxidase
- NMPO
14A disease of impaired O2-dependent killing is [blank_start]chronic granulomatous disease[blank_end] ([blank_start]CGD[blank_end]), which is due to a defect in [blank_start]NADPH oxidase[blank_end]. Genetics are [blank_start]x-linked[blank_end] or [blank_start]autosomal[blank_end] [blank_start]recessive[blank_end]. It leads to chronic [blank_start]granulomatous[blank_end] infections with [blank_start]catalase positive[blank_end] organisms, particularly: Staph aureus, [blank_start]pseudomonas cepacia[blank_end], serratia marascens, [blank_start]nocardia[blank_end], and aspergillus. Screening is done with [blank_start]nitroblue tetrazolium[blank_end] ([blank_start]NBT[blank_end]) test in which dye is incubated with leukocytes, and turns blue if [blank_start]superoxide[blank_end] is formed.
- Achronic granulomatous disease
- BCGD
- CNADPH oxidase
- Dx-linked
- Eautosomal
- Frecessive
- Ggranulomatous
- Hcatalase positive
- Ipseudomonas cepacia
- Jnocardia
- Knitroblue tetrazolium
- LNBT
- Msuperoxide
15[blank_start]MPO deficiency[blank_end] leads to defective conversion of H2O2 to HOCl. Leads to increased risk of [blank_start]candida[blank_end] infections. Most patients are [blank_start]asymptomatic[blank_end].
- AMPO deficiency
- Bcandida
- Casymptomatic
16O2-independent killing is less effective. Occurs in leukocyte [blank_start]secondary granules[blank_end]. Enzymes include [blank_start]lysozyme[blank_end] in macrophages and [blank_start]major basic protein[blank_end] in eosinophils.
- Asecondary granules
- Blysozyme
- Cmajor basic protein
17Neutrophils undergo apoptosis within [blank_start]24 hours[blank_end] of end of inflammatory stimulus.
- A24 hours
18[blank_start]Macrophages[blank_end] predominate after neutrophils, peak 2-3 days after inflammation begins.
- AMacrophages
19Macrophages principally kill via [blank_start]O2-independent[blank_end] killing in [blank_start]secondary granules[blank_end] (e.g. with lysozyme). They can release IL-[blank_start]10[blank_end] and [blank_start]TGF-beta[blank_end] to promote resolution, or IL-[blank_start]8[blank_end] to promote ongoing acute inflammation. Can also release fibrogenic growth factors and cytokines to promote [blank_start]abscess[blank_end], or present antigen to activate [blank_start]CD4+[blank_end] helper cells leading to chronic inflammation.
- AO2-independent
- Bsecondary granules
- C10
- DTGF-beta
- E8
- Fabscess
- GCD4+
20Chronic inflammation is triggered by (1) persistent infection (most common), (2) infection with virus, [blank_start]micobacteria[blank_end], parasite, fungi, (3) autoimmunity, (4) foreign bodies, (5) cancers.
- Amicobacteria
21T lymphocytes are produced in [blank_start]bone marrow[blank_end] and mature in the [blank_start]thymus[blank_end] where they develop into subtypes (e.g. CD4+, CD8+). They use TCR complex (TCR and [blank_start]CD3[blank_end]) for surveillance, and recognize antigen presented on MHC. CD4+ recognize MHC [blank_start]II[blank_end], and CD8+ recognize MHC [blank_start]I[blank_end]. Activation requires binding to antigen on MHC plus second signal.
- Abone marrow
- Bthymus
- CCD3
- DII
- EI
22CD4+ helper cells ultimately activate killer T cells or B cells, and recognize [blank_start]extracellular[blank_end] antigen on MHC [blank_start]II[blank_end]. Second signal occurs when [blank_start]B7[blank_end] on APC binds [blank_start]CD28[blank_end] on T cell. Activated CD4+ cells are divided into 2 subtypes. Th[blank_start]1[blank_end] cells activate killer T cells by [blank_start]macrophages[blank_end]. Th[blank_start]2[blank_end] cells activate B cells and [blank_start]eosinophils[blank_end]. Th1 cytokines include IL-[blank_start]2[blank_end] (CD8+ activation) and IFN-gamma ([blank_start]macrophage[blank_end] activator). Th2 cytokines include IL-[blank_start]4[blank_end] (B-cell class switching to IgG and Ig[blank_start]E[blank_end]), IL-5 (eosinophils, B cell maturation to plasma cells), and IL-[blank_start]10[blank_end] (inhibits Th1).
- AII
- BB7
- CCD28
- D1
- E2
- F2
- Gmacrophage
- H4
- IE
- J10
- Kextracellular
- Lmacrophages
- Meosinophils
23CD8+ T cells recognize [blank_start]intracellular[blank_end] antigen on MHC [blank_start]I[blank_end], expressed on all nucleated cells and platelets. Second signal is IL-[blank_start]2[blank_end] from [blank_start]Th1[blank_end]. Killing occurs when [blank_start]perforin[blank_end] makes holes, allowing [blank_start]granzyme[blank_end] to enter and cause apoptosis. Also expresses [blank_start]Fas ligand[blank_end], which binds [blank_start]Fas[blank_end] on target cells to cause apoptosis.
- AI
- Bintracellular
- C2
- DTh1
- Eperforin
- Fgranzyme
- GFas ligand
- HFas
24Granulomatous inflammation is characterized by [blank_start]epithelioid histiocytes[blank_end] ([blank_start]macrophages[blank_end] with abundant pink cytoplasm) surrounded by [blank_start]giant cells[blank_end] and a rim of lymphocytes. Caseating granulomas are marked by central [blank_start]necrosis[blank_end], and are characteristic of TB and [blank_start]fungal[blank_end] infections. Noncaseating granulomas lack [blank_start]necrosis[blank_end] and can occur due to foreign bodies, [blank_start]sarcoidosis[blank_end], beryllium exposure, Crohn disease, and [blank_start]cat scratch[blank_end] disease.
- Aepithelioid histiocytes
- Bmacrophages
- Cgiant cells
- Dnecrosis
- Efungal
- Fnecrosis
- Gsarcoidosis
- Hcat scratch
25[blank_start]DiGeorge syndrome[blank_end] is a primary immunodeficiency caused [blank_start]22q11[blank_end] microdeletion causing failure of development of [blank_start]3rd[blank_end] and [blank_start]4th[blank_end] [blank_start]pharyngeal pouches[blank_end] which include the [blank_start]thymus[blank_end]. Presents with [blank_start]T cell[blank_end] deficiency, [blank_start]hypocalcemia[blank_end] (no parathyroid), and abnormalities of heart, great vessels, and face.
- ADiGeorge syndrome
- B22q11
- C3rd
- D4th
- Epharyngeal pouches
- Fthymus
- GT cell
- Hhypocalcemia
26[blank_start]Severe combined immunodeficiency[blank_end] ([blank_start]SCID[blank_end]) is defective cell-mediated AND humoral immunity. Common causes are: 1) [blank_start]cytokine[blank_end] receptor defects, 2) [blank_start]adenosine deaminase[blank_end] deficiency ([blank_start]adenosine[blank_end] buildup is toxic to lymphocytes), 3) MHC [blank_start]II[blank_end] deficiency (no CD4+ helper cells). Susceptible to all forms of infection and live vaccines. Treatment is "[blank_start]bubble baby[blank_end]" approach and [blank_start]stem cell[blank_end] transplantation.
- ASCID
- BSevere combined immunodeficiency
- Ccytokine
- Dadenosine deaminase
- Eadenosine
- FII
- Gbubble baby
- Hstem cell
27[blank_start]X-linked agammaglobulinemia[blank_end] is the complete lack of [blank_start]Ig[blank_end] due to abnormal [blank_start]B cell[blank_end] maturation (naive cannot mature to plasma). Due to [blank_start]x-linked[blank_end] mutation in [blank_start]Bruton tyrosine kinase[blank_end]. Presents after [blank_start]6[blank_end] months when mom's Ig clears out with recurrent bacterial, [blank_start]enterovirus[blank_end] (e.g. polio, cocksackie virus), and [blank_start]giardia[blank_end] infections. Must avoid [blank_start]live vaccines[blank_end].
- AIg
- BX-linked agammaglobulinemia
- CB cell
- Dx-linked
- EBruton tyrosine kinase
- F6
- Genterovirus
- Hgiardia
- Ilive vaccines
28[blank_start]Common variable immunodeficiency[blank_end] ([blank_start]CVID[blank_end]) is a primary immunodeficiency characterized by [blank_start]low[blank_end] Ig due to B cell or Th defects, like a less severe form of [blank_start]x-linked agammaglobulinemia[blank_end]. Presents with recurrent bacterial, enterovirus (e.g. [blank_start]cocksackie[blank_end] virus), and [blank_start]giardia[blank_end] infections in late childhood. Increased risk [blank_start]autoimmune[blank_end] disease and [blank_start]lymphoma[blank_end].
- ACommon variable immunodeficiency
- BCVID
- Clow
- Dx-linked agammaglobulinemia
- Ecocksackie
- Fgiardia
- Gautoimmune
- Hlymphoma
29[blank_start]IgA[blank_end] deficiency is the most common Ig deficiency with low [blank_start]serum[blank_end] and [blank_start]mucosal[blank_end] Ig[blank_start]A[blank_end]. Most patients are asymptomatic, but with increased risk of [blank_start]mucosal[blank_end] and [blank_start]viral[blank_end] infection.
- AIgA
- Bserum
- Cmucosal
- DA
- Emucosal
- Fviral
30Hyper-Ig[blank_start]M[blank_end] syndrome is marked by elevated Ig[blank_start]M[blank_end] due to mutated [blank_start]CD40L[blank_end] on Th cells or [blank_start]CD40 receptor[blank_end] on B cells. Second signal can't be delivered during [blank_start]B cell[blank_end] maturation, so only Ig[blank_start]M[blank_end] is made. Low levels of other Ig (IgA, IgG, IgE) lead to recurrent pyogenic infections.
- AM
- BM
- CCD40L
- DCD40 receptor
- EB cell
- FM
31[blank_start]Wiskott-Aldrich[blank_end] syndrome is due to [blank_start]x-linked[blank_end] mutation in WASP gene. Marked by [blank_start]eczema[blank_end] (skin), [blank_start]thrombocytopenia[blank_end] (blood), [blank_start]bloody diarrhea[blank_end] (secondary to the [blank_start]thrombocytopenia[blank_end]), and recurrent infection.
- AWiskott-Aldrich
- Bx-linked
- Ceczema
- Dthrombocytopenia
- Ebloody diarrhea
- Fthrombocytopenia
32Complement deficiencies (C[blank_start]5[blank_end]-C[blank_start]9[blank_end]) increase risk of [blank_start]neisseria[blank_end] infection ([blank_start]gonococcal[blank_end] and [blank_start]meningococcal[blank_end])
- A5
- B9
- Cneisseria
- Dgonococcal
- Emeningococcal
33Systemic lupus erythematosus (SLE) is a common autoimmune condition causing damage via type [blank_start]II[blank_end] ([blank_start]cytotoxic[blank_end]) and type [blank_start]III[blank_end] ([blank_start]antigen-antibody[blank_end] complex) hypersensitivity. Common in women, African Americans. Clinical features include:
- Inflamed joints
- Fever, weight loss
- Hair loss, mouth ulcers
- Lymphadenopathy
- Malar rash
- Cardiac inflammation (pleuritis, pericarditis, endocarditis, myocarditis) - classic finding is [blank_start]Libman-Sacks[blank_end] endocarditis marked by small, [blank_start]sterile[blank_end] deposits on either side of [blank_start]mitral valve[blank_end]
- CNS [blank_start]psychosis[blank_end]
- Renal damage ([blank_start]diffuse proliferative glomerulonephritis[blank_end])
[blank_start]ANA[blank_end] is sensitive, anti-[blank_start]dsDNA[blank_end] is specific.
[blank_start]Antihistone[blank_end] antibody suggests [blank_start]drug-induced[blank_end] SLE.
[blank_start]Anticardiolipin[blank_end] and lupus anticoagulant antibodies are characteristic of [blank_start]antiphospholipid antibody[blank_end] syndrome, seen in 30% of SLE cases. Leads to falsely elevated [blank_start]PTT[blank_end] (patient is actually in [blank_start]hypercoagulable[blank_end] state, and prone to arterial and venous thrombosis) and false positive on [blank_start]RPR[blank_end] or [blank_start]VRDL[blank_end] tests for [blank_start]syphilis[blank_end]. Common sites of thrombi include hepatic vein, DVT, [blank_start]placental[blank_end] (recurrent pregnancy loss), and stroke. Requires lifelong anticoagulation.- AII
- Bcytotoxic
- CIII
- Dantigen-antibody
- ELibman-Sacks
- Fmitral valve
- Gsterile
- Hpsychosis
- Idiffuse proliferative glomerulonephritis
- JANA
- KdsDNA
- LAntihistone
- Mdrug-induced
- NAnticardiolipin
- Oantiphospholipid antibody
- PPTT
- Qhypercoagulable
- RRPR
- SVRDL
- Tsyphilis
- Uplacental
34Sjogren syndrome is autoimmune destruction of lacrimal and [blank_start]salivary[blank_end] glands caused by type [blank_start]IV[blank_end] ([blank_start]lymphocyte[blank_end]-mediated) hypersensitivity with [blank_start]fibrosis[blank_end]. Presents with [blank_start]keratoconjunctivitis[blank_end] (dry eyes), [blank_start]xerostomia[blank_end] (dry mouth), and recurrent [blank_start]dental carries[blank_end] in older women (50-60 years).
Characterized by [blank_start]ANA[blank_end], and anti-[blank_start]RNP[blank_end] antibodies including anti-[blank_start]SSA[blank_end] ([blank_start]Ro[blank_end]) and anti-[blank_start]SSB[blank_end] ([blank_start]La[blank_end]).
Many patients have other autoimmune disease as well, especially [blank_start]rheumatoid arthritis[blank_end].
Increased risk of [blank_start]marginal zone[blank_end] [blank_start]B[blank_end] cell lymphoma, presenting late as [blank_start]unilateral[blank_end] enlargement of [blank_start]parotid[blank_end] gland.- Asalivary
- BIV
- Clymphocyte
- Dfibrosis
- Ekeratoconjunctivitis
- Fxerostomia
- Gdental carries
- HANA
- IRNP
- JSSA
- KRo
- LSSB
- MLa
- Nrheumatoid arthritis
- Omarginal zone
- PB
- Qparotid
- Runilateral
35Scleroderma is an autoimmune disease involving activation of [blank_start]fibroblasts[blank_end] and [blank_start]collagen[blank_end] deposition ([blank_start]fibrosis[blank_end]). Can be diffuse or localized.
Diffuse type has skin and early visceral involvement, with worse prognosis. Almost any organ can be involved. Common sites are [blank_start]esophagus[blank_end] (dysmotility causing dysphagia for liquids and solids), lungs. Characterized by [blank_start]ANA[blank_end] and anti-[blank_start]DNA topoisomerase[blank_end] I ([blank_start]Scl-70[blank_end]) antibodies.
Localized type prototypically involves [blank_start]CREST[blank_end] syndrome.
[blank_start]Calcinosis[blank_end] (and anti-[blank_start]Centromere[blank_end] antibodies)
[blank_start]Raynaud[blank_end] phenomenon
[blank_start]Esophageal[blank_end] dys[blank_start]motility[blank_end]
[blank_start]Sclerodactyly[blank_end]
[blank_start]Telangiectasias[blank_end] on skin- Afibroblasts
- Bcollagen
- Cfibrosis
- Desophagus
- EANA
- FDNA topoisomerase
- GScl-70
- HCREST
- ICalcinosis
- JCentromere
- KRaynaud
- LEsophageal
- Mmotility
- NSclerodactyly
- OTelangiectasias
36Mixed connective tissue disease can take on mixed characteristics of SLE, systemic sclerosis, [blank_start]polymyositis[blank_end]. Characterized by antibodies against [blank_start]U1[blank_end] [blank_start]RNP[blank_end].
- ARNP
- BU1
- Cpolymyositis
37In wound healing, type [blank_start]III[blank_end] [blank_start]collagen[blank_end] ([blank_start]granulation[blank_end] tissue) is replaced by type [blank_start]I[blank_end] [blank_start]collagen[blank_end] to form scar. This is performed by [blank_start]collagenase[blank_end] requiring [blank_start]zinc[blank_end] as a cofactor.
- AIII
- Bgranulation
- CI
- Dcollagen
- Ecollagen
- Fcollagenase
- Gzinc
38Delayed wound healing can be caused by:
- [blank_start]Infection[blank_end] (particularly with [blank_start]Staph aureus[blank_end])
- [blank_start]Vitamin C[blank_end] deficiency: Co-factor for hydroxylation of [blank_start]procollagen[blank_end] residues
- [blank_start]Copper[blank_end] deficiency: Co-factor for lysyl oxidase enzyme performing collagen [blank_start]cross-linking[blank_end]
- [blank_start]Zinc[blank_end] deficiency: Co-factor for [blank_start]collagenase[blank_end] responsible for type [blank_start]III[blank_end] collagen removal
- Foreign body
- Ischemia
- Diabetes
- Malnutrition
[blank_start]Keloid[blank_end] is excess production of type [blank_start]III[blank_end] collagen leading to scar tissue outside bounds of original wound.- AInfection
- BStaph aureus
- CVitamin C
- Dprocollagen
- ECopper
- Fcross-linking
- GZinc
- Hcollagenase
- IIII
- JKeloid
- KIII
39Neutrophil functioning involves steps of margination, rolling, adhesion, transmigration ([blank_start]chemotaxis[blank_end]), phagocytosis, and destruction of phagocytosed material. Margination occurs in the [blank_start]postcapillary[blank_end] [blank_start]venule[blank_end]s (slower flow). Rolling occurs when [blank_start]selectin[blank_end] "speed bumps" are put on vessel walls -- specifically, release of [blank_start]P[blank_end] [blank_start]selectin[blank_end] from [blank_start]Weibel[blank_end]-[blank_start]Palade[blank_end] [blank_start]bodies[blank_end] is mediated by [blank_start]histamine[blank_end], while [blank_start]E[blank_end] [blank_start]selectin[blank_end] is induced by TNF and IL-1. TNF and IL-1 also upregulate cellular adhesion molecules [blank_start]ICAM[blank_end] and [blank_start]VCAM[blank_end] on endothelium. [blank_start]Integrins[blank_end] are upregulated on leukocytes. Interaction of [blank_start]CAM[blank_end]s and [blank_start]integrins[blank_end] results in adhesion.
- Achemotaxis
- Bpostcapillary
- Cvenule
- Dselectin
- EP
- Fselectin
- GWeibel
- HPalade
- Ibodies
- Jhistamine
- KE
- Lselectin
- MICAM
- NVCAM
- OCAM
- PIntegrins
- Qintegrins
40[blank_start]Leukocyte adhesion deficiency[blank_end] is due usually to autosomal recessive defect in [blank_start]integrins[blank_end]. Clinical features are delayed [blank_start]separation of umbilical cord[blank_end], increased circulating [blank_start]neutrophils[blank_end], and bacterial infections [blank_start]without pus[blank_end] (no neutrophils!).
- ALeukocyte adhesion deficiency
- Bintegrins
- Cseparation of umbilical cord
- Dneutrophils
- Ewithout pus
41Neutrophils are attracted by bacterial products IL-[blank_start]8[blank_end], C[blank_start]5a[blank_end], and LT[blank_start]B4[blank_end]
- A8
- B5a
- CB4
42Phagocytosis is enhanced by opsonins Ig[blank_start]G[blank_end] and C[blank_start]3a[blank_end]
- AG
- B3a
43[blank_start]Chediak[blank_end] [blank_start]Higashi[blank_end] syndrome is an [blank_start]autosomal recessive[blank_end] (genetics) disorder where protein trafficking problem impairs phagolysosome formation, leading to increased pyogenic infections, [blank_start]neutropenia[blank_end] (from intramedullary death of neutrophils), and [blank_start]giant[blank_end] granules in leukocytes. Other features are [blank_start]albinism[blank_end] (skin), [blank_start]peripheral[blank_end] [blank_start]neuropathy[blank_end] (nerves), and defective primary [blank_start]hemostasis[blank_end] (from abnormal [blank_start]dense[blank_end] granules in platelets). Finally, destruction of phagocytosed material occurs via oxygen dependent and independent killing. In O2-dependent killing, HOCl free radicals are generated by the oxidative burst in phagolysosomes.
- Aautosomal recessive
- BChediak
- CHigashi
- Dneutropenia
- Egiant
- Falbinism
- Gperipheral
- Hneuropathy
- Ihemostasis
- Jdense
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- Description
- Medicine Quiz on P2-Inflammation, created by Annie Berens on 10/04/2017.
- Author
- Annie Berens
- Language
- English
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