Inflammation Flashcards
1
Q
- Septa of lung regeneration? Liver? Heart? Kidney?
- Non neoplastic injury? (4)
- Collateral damage: Cells responsible? Substances responsible? Which leads to?
- Acute phase response: Goals? (3)
1. ) Liver Role: Acute phase proteins? (4) Stimulated by? (3); Albumin? Transferrin?
2. ) Brain Role: Hypothalamus does what?
3. ) Bone Marrow Role?
A
- Can not regenerate; great regeneration; none; epithelia high but glomeruli low
- trauma, infection, inflammation, ischemia
- Neutrophils die releasing contents and mac; inflammatory mediators = reactive O2 species
- limit injury, increase inflammation, activate systems
- antiproteases, scavengers, C reactive protein, fibrinogen; IL1, TNF, IFN’s; Both decrease
- Fever anorexia
- Pt’s and WBC’s
2
Q
Inflammatory Cells:
- ) Neutrophils: Chronic or Acute? Role? (3) Cytoplasmic contents? (3)
- ) Monocyte/Mac: Phase? Function? (2) Cyto contents? (3)
- ) Lymphocytes: Phase? Function?
- ) Eosinophil: Phase? Role? (3) Cytoplasmic contents?
- ) Mast Cell/Baso: Role? (2) Cyto contents? (2)
- ) Platelets: Role? (3) Cytoplasmic contents? (2)
A
- Acute; inflamm response, damage bugs, phago; enzymes, reactive O2, plasminogen
- Chronic; phago, initiate repair; ecasanoids, cytokines, lysozymes
- Chronic, Adaptive response
- Chronic, parasites, T1 hyper., phago, granule enzymes
- Bind IgE, T1 Hyper; Histamine, serotonin
- Thrombosis, mesenchymal repair, regulate pereability; TXA2, seratonin
3
Q
Acute/Chronic Response:
- Vascular response?
- Inflammatory cells involved?
- Source of cells?
Transudate/Exudate:
- Transudate: Etiology? Transport through? Spec. gravity? protein [ ], glucose [ ], cells?
- Exudate: Etiology? Spec. gravity? protein [ ], glucose [ ], cells?
A
- Dilation, increased perm. vs. endolthelia activated
- PMN’s vs. macs/lymphs
- peripheral blood vs. sentinal (local)/peripheral blood
- Increased hydro pressure and decreased oncotic pressure; tight junctions; none for the rest
- Inflammation, increased, increased, decreased, yes (leukocytes)
4
Q
- Types of Inflammation:
1.) Fibrinopurulent/supporative: Cells? Histological features? (3) Differential diagnosis? (2) This is called?
2.) Granulomatous: Cells? Histological features (3)? Differential? (3) Walled off?
3.) Eosinophillic: Cells? Histological features? Differential? (2)
Inflamation appearance:
1.) Fibrinopurulent/supporative: Location? Cells?
2.) Abscess: Location? Cells?
3.) Empyema: Location? Cells? (2)
4.) Cellulitis: Location? (2)
5.) Granuloma: Location? Cells? (3)
A
- ) PMN’s; PMN’s fibrin, +/- hemmorhage; any insult, infectious; pus
- ) Macs, mixed chronic cells, +/- necrosis, +/- foreign material; infectious, inflamm, foreign body; yes
- ) Eisonophils, eisinophils, parasites, allergic rxn
- ) Anywhere non confined; N’s
- ) Within parachema confined space, N’s
- ) Within a cavity; N’s early then macs/lymphos
- ) Skin/fascia
- ) within paranchyma; Macs, lymphs, plasma cells
5
Q
- Granulation tissue: What is it? Components? (3)
- Regeneration: What is it? 3 options and definitions?
- Acute injury can lead to?
- Persisitant injury can lead to?
- Scar:
1. ) Normal: Initial? Remodel?
2. ) 2 types of pathologic scars? - Factors influencing repair: Systemic? (3) Local? (5)
- Components of repair: GF secretion? Neovascularization? Collagen deposition? Scar stuff? Re-epithelialization?
A
- Infrastructure (scar); fibroblasts, endothelial cells, inflammatory cells
- Suprastructure: 1.) Reepi = New epi from stem cells 2.) Regeneration: Such as liver 3.) No fix
- Regeneration, repair (scar), fibrosis
- Fibrosis
- Collagen 3; collagen 1
- Hypertrophic: Outside boundary and regresses; keloid: outside boundary and does not
- S: Nutrition, metabolic, vascular
- L: Infection, persistant insult, new trauma, foreign material, size/location
- Macs, Endothelial cells, Fibroblast, fibroblast, hepatocytes or epithelial
6
Q
- ) Angiogenesis: Def? Cells? (3)
- ) Granulation tissue: Def? Cells? (3)
- ) Re-epitheliazation: Def? Cells? (2)
- ) Regeneration: Def? Where does this occur? (2) Cells? (2)
A
- Form new blood vessels; Macs (GF’s), pericytes, bone marrow stem cells
- Infastrcuture; fibroblasts, inflammatory cells, endothelial cells
- Suprastructure; adjacent cells, stem cells
- Fully repaired with no scar; epi, liver; macrophages and stem cells
7
Q
Action of mediators:
- ) Vasodilation? (5)
- ) Increased permeability? (5)
- ) Chemotaxis? (5)
- ) Tissue damage/antimicrobial? (4)
- ) Fever? (2)
- ) Pain? (3)
A
- Histamine, eicosonoids, NO, Complement, Bradykinin
- Histamine, eicosonoids, Substance P, Complement, Bradykinin
- eicosonoids, NO, cytokines, complement, cytoplasmic granules
- Reactive oxygen, NO, Complement, Cyto gran
- eicosonoids, cytokines
- eicosonoids, Substance P, Bradykinin
8
Q
- ) Vasoactive amines (His/Ser): Key actions? (4) Cells that release it? (2) Preformed?
- ) PG’s: Key action? (4) Cells? Pre?
- ) LT’s: Effect? (2) Cells? Pre?
- ) TxA2: Effect? (2) Cells? Pre?
- ) PAF: Effect? (4) Cells? Pre?
- ) Reactive Oxygen: Effect? Cells? (3) Pre?
- ) NO: Effect? (2) Cells? (2) Pre?
- ) TNF: Effect? (2) Cells? (3) Pre?
- ) IL: Effect? (2) Cells? (2) Pre?
- ) IFN: Pre?
- ) Chemokines: Effect? (1) Cells? (4) Pre?
- ) Cyto granule: Effect? (2) Cells? (2) Pre?
- ) Substance p: Effect? (2) Cells? (1) Pre?
A
- ) Ana, smooth contr., inc. perm, chemo; mast, ppt.; P
- ) VD, +/- pt. ag, fever/pain; all (mast most); S
- ) Incr. perm, bronch con; all but ptts; S
- ) ptt. agg, vaso con; ptts; s
- ) vaso con, ptt ag, chemo, bron con; all but lympho; s
- ) Tissue damage; Macs, Lymphs, PMN; S
- ) vaso/broncho dilate, macs, endo, s
- ) Chemo, fever; mast, mac, lymph, s
- ) Chemo, fever; macs, endo, s
- ) S
- ) Chemotaxis; macs, mast, lymphs, endo, s
- ) Chemo, damage; Macs, PMN; P
- ) Pain, incr. vasc; nerve fibers, P
9
Q
- Liver Derived Mediators:
1.) C3A, C5A: Effect? (4) Cells?
2.) Bradykinin: Effect? (4) Cells?
3.) Thrombin: Effect? Cells?
4.) Plasmin: Effect? Cells?
Factor 12: Activated by? (3) Goes to? This acts on what 2 cascades? These create? (3) Fibronogen + Thrombin? Pasminogen –> Plasmin? Plasmin then makes what cascade? To create what? What else acts on this?
-Thrombin activated in what cascade? - Fibrinolysis from what cascade?
- Kallikenein from what cascade?
A
- vasodil, stim. mast, chemo, tissue damage; liver
- incr. perm, vaso dil, pain, constrict bron; liver
- ptt agg; liver
- vaso dil; liver
- ptt’s, basement membrane, collagen; F12a; Clotting and kallekrien kinin cascade; Bradykinin, plasminogen; thrombin; Fibrin; to fibrin; Fibrinolytic cascade; C3/C5; Kinin cascade on C5
- Thrombin
- Plasmin
- Kallikrein