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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Inflammatory Cells:

  1. ) Neutrophils: Chronic or Acute? Role? (3) Cytoplasmic contents? (3)
  2. ) Monocyte/Mac: Phase? Function? (2) Cyto contents? (3)
  3. ) Lymphocytes: Phase? Function?
  4. ) Eosinophil: Phase? Role? (3) Cytoplasmic contents?
  5. ) Mast Cell/Baso: Role? (2) Cyto contents? (2)
  6. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
  1. ) PMN’s; PMN’s fibrin, +/- hemmorhage; any insult, infectious; pus
  2. ) Macs, mixed chronic cells, +/- necrosis, +/- foreign material; infectious, inflamm, foreign body; yes
  3. ) Eisonophils, eisinophils, parasites, allergic rxn
  4. ) Anywhere non confined; N’s
  5. ) Within parachema confined space, N’s
  6. ) Within a cavity; N’s early then macs/lymphos
  7. ) Skin/fascia
  8. ) within paranchyma; Macs, lymphs, plasma cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. ) Angiogenesis: Def? Cells? (3)
  2. ) Granulation tissue: Def? Cells? (3)
  3. ) Re-epitheliazation: Def? Cells? (2)
  4. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Action of mediators:

  1. ) Vasodilation? (5)
  2. ) Increased permeability? (5)
  3. ) Chemotaxis? (5)
  4. ) Tissue damage/antimicrobial? (4)
  5. ) Fever? (2)
  6. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. ) Vasoactive amines (His/Ser): Key actions? (4) Cells that release it? (2) Preformed?
  2. ) PG’s: Key action? (4) Cells? Pre?
  3. ) LT’s: Effect? (2) Cells? Pre?
  4. ) TxA2: Effect? (2) Cells? Pre?
  5. ) PAF: Effect? (4) Cells? Pre?
  6. ) Reactive Oxygen: Effect? Cells? (3) Pre?
  7. ) NO: Effect? (2) Cells? (2) Pre?
  8. ) TNF: Effect? (2) Cells? (3) Pre?
  9. ) IL: Effect? (2) Cells? (2) Pre?
  10. ) IFN: Pre?
  11. ) Chemokines: Effect? (1) Cells? (4) Pre?
  12. ) Cyto granule: Effect? (2) Cells? (2) Pre?
  13. ) Substance p: Effect? (2) Cells? (1) Pre?
A
  1. ) Ana, smooth contr., inc. perm, chemo; mast, ppt.; P
  2. ) VD, +/- pt. ag, fever/pain; all (mast most); S
  3. ) Incr. perm, bronch con; all but ptts; S
  4. ) ptt. agg, vaso con; ptts; s
  5. ) vaso con, ptt ag, chemo, bron con; all but lympho; s
  6. ) Tissue damage; Macs, Lymphs, PMN; S
  7. ) vaso/broncho dilate, macs, endo, s
  8. ) Chemo, fever; mast, mac, lymph, s
  9. ) Chemo, fever; macs, endo, s
  10. ) S
  11. ) Chemotaxis; macs, mast, lymphs, endo, s
  12. ) Chemo, damage; Macs, PMN; P
  13. ) Pain, incr. vasc; nerve fibers, P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly