Inflammation Flashcards

(44 cards)

1
Q

What is Exudate

A
  • fluids rich in proteins and cells flow from vessels into interstitium/body cavities
  • implies big changes in normal permeability of small blood vessels in that area
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2
Q

What is Transudate

A
  • fluids with little protein (albumin) flows = “ultra filtrate of plasma”
  • due to hydrostatic imbalance
  • permeability is normal
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3
Q

What is Edema

A
  • excess interstitial fluid
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4
Q

What is Pus

A
  • purulent exudate
  • cell rich with mainly PMNs and cell debris
  • powerful lysosomal enzymes
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5
Q

5 Characteristics of Inflammation

A
  • redness
  • swelling
  • heat
  • pain
  • impaired function
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6
Q

Oxygen-Dependent Bactericidal Mechanisms

A
  1. H2O2 myeloperoxidase halide system (most efficient)
    - Cl- = physiological halide
    - HOCl = final reactive radical
    - powerful oxidant and antimicrobial (chlorination)
  2. MPO independent killing
    - OH- = the free radical

**mocoytes lose MPO when transforming into macrophages

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7
Q

Reasons for a burst in oxygen use during phagocytosis

A
  • increase of glycogenolysis
  • increased glucose oxydance (hexose-monophosphate shunt)
  • production of active oxygen metabolites via 2 oxygen-dependent mechanisms
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8
Q

Oxygen-Independent Bactericidal Mechanisms

A
  • increased lactate + action carbonic anhydrase –> increased H+ –> reduced intravacuolar pH
  • action of substances from leukocyte granules
  • degradation via acid hydrolase within phagolysosomes
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9
Q

During phagocytosis, leukocytes release..

A
  • lysosomal enzymes
  • oxygen derived metabolites
  • products of arachidonic acid metabolism (prostaglandins, leukotrienes)
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10
Q

Leukocyte products are released during which three process during phagocytosis:

A
  1. regurgitation during feeding
  2. reverse endocytosis (frustrated phagocytosis)
  3. cytotoxic released (following cell death)
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11
Q

What are the mediators of increased vascular permeability?

A
  • cell derived vasoactive mediators
    • arachidonic acid metabolites
    • platelet activating factors (PAFs)
    • amines: histamine, serotonin
    • endothelins
  • plasma derived vasoactive mediators
    • kinins and coagulation cascade
    • complement system
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12
Q

What are the mediators involved in cell recruitment?

A
  • C5a
  • bacterial products
  • arachidonic acid metabolites
  • chemokine (IL-8) and other cytokines
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13
Q

Characteristics of Acute Inflammation

A
  • dominant changes = vascular (vasodilation, inc permeab.) and exudative (fluids and cells)
  • mainly PMN’s (because faster)
  • short lived (due to treatment or self-limiting)
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14
Q

Characteristics of Chronic Inflammation

A
  • when inflammation has lasted more than 2-4 weeks
  • lots of proliferation of cells and connective tissue
  • exudation is less conspicuous (lymphs, plasma cells)
  • follows acute or chronic from onset, or chronic with persisting acute
  • mainly mononuclear cells; macrophages, lymphocytes, plasma cells, eosinophils
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15
Q

Cells involved in acute

A
  • PMNs

- other cells too though

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16
Q

Cells involved in chronic

A
  • macrophages
  • lymphocytes (NK, T, B cells)
  • plasma cells (humeral immunity - mediated by Abs)
  • eosinophils (for parasitic infections and allergic rxns)
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17
Q

Two types (and characteristics of) Chronic Inflammation

A
  1. non-specific
    - no pattern of tissue ran
    - cells = mononuclear cells (monocytes, lymphocytes, plasma cells) and connective tissue (fibroblasts)
  2. granulomatous
    - special tissue rxn
    - cells = reticuloendothelial cells and their derivatives (macrophages)
    - due to: certain infections (TB, syphillis), presistant foreign body infections, rheumatic fever, rheumatoid arthritis
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18
Q

Describe a granuloma

A
  • central focus = nectrotic tissue (usually)
  • surrounded by macrophages (modified to epithelioid cells)
  • outer rim of lymphocytes and/or plasma cells

** giant cells (multinucleate because made up of macrophages combined together) are present among the inner cells

19
Q

Serous Exudate

When? What? Examples? Identified how?

A
  • mild injuries
  • only albumin
  • derived from secretions of serial mesothelial cells

Examples: burn blisters, pulmonary TB

Identified: difficult (abnormally dilated spaces, fine precipitate of protein)

20
Q

Fibrinous Exudate (When? What? Examples? Identified how?)

A
  • more severe
  • contains fibrin (clot)
  • in acute but also in active zones of chronic
  • fibrin can be removed
    Examples: rheumatic fever (bread and butter pericarditis), pneumococcal pneumonias

Identified: easily because precipitated fibrin is in strands and bands, in part fibrillar and is acidophilic (stained with acid stains)

21
Q

Suppurative/Purulent Exudate

When? What? Examples? Identified how?

A
  • liquefactive necrosis cause by pyrogens (pus-producing bacteria)
  • exudate has lots of pus

Examples: characteristically in pyogenic infections by staphylococcus and pneumococcus etc., acute appendicitis, tooth abscess, zit

Identified: pools of numerous PMNs (viable and dead)

22
Q

Sanguinous Exudate

When? What? Examples? Identified how?

A
  • lots of RBCs
  • indicates serious damage to endothelial
  • almost never pure but in a mixed form with other type of exudate

Examples: TB, inflammations due to tumour invasion, frostbite, SARS

Identified: by RBCs in exudate

23
Q

Abscess

A
  • LOCALIZED collection of pus caused by suppuration

- caused by an irritant of great intensity (staph, turpentine) that stays localized leadings to lots PMNs coming

24
Q

Paronychia

A
  • infection around the fingernail
25
Felon
- deep infection at the end of the finger joint | - may cause osteomyelitis
26
Empyema
- localized pus in the pleural cavity
27
Ulcer
- loss of epithelium due to inflammation - local defect of the surface of the epithelium on an organ - produced by sloughing of inflammatory necrotic tissue on/near the surface
28
Pseudomembranous Inflammation
- inflammation produced by a powerful necrotizing toxin - forms a pseudomembrane over the area = precipitated fibrin, necrotic epithelium, WBCs - on mucosal surfaces
29
Fistula
- abnormal passage between 2 hollow organs both lined by epithelium or an epithelium - usually due to inflammation
30
Sinus
- abnormal tract between a solid organ/tissue to an epithelium covered surface (skin) - usually caused by inflammation
31
Furuncle
boil
32
Bacteriemia
- bacteria circulate in blood | - doesn't appear sick
33
Septicemia
- bacteraemia with clinical manifestation of illness | - fever, chills, abscesses
34
Toxemia
- clinical illness due to bacterial toxins in blood instead of the actual bacteria
35
Journey of Lymphatic Flow
--> lymph node --> circulation --> RES
36
Why don't lymph nodes collapse by edema fluid?
System of Fibrils attached at right angles on the walls which extend to adjacent tissues, makes lymph vessels open up
37
Pathogenesis of Rubor (redness)
= vasodilatation (microcirculation) by chemical mediators (esp. prostaglandins)
38
Pathogenesis of tumour (swelling)
- exudation of fluid (edema) - breakdown of tissues - mediated by vasoactive amines, C3a and C5a, Bradykinin, Leukotriene C D E
39
Pathogenesis of Calor (heat)
- more blood flow | increased local metabolic rate
40
Pathogenesis of Impaired Function
- swelling | - inhibition of muscular contraction by pain
41
pathogenesis of pain
- direct stimulus of nerve endings | - signalling of neural system by chemical mediators (bradykinin, histamine, G-OH-tryptamine)
42
Systemic Effects of Inflammation
1. Fever 2. Leukocytosis 3. Antibody production 4. Other (anorexia, discomfort)
43
What are the vascular events leading to swelling?
Increased permeability increased hydrostatic pressure vasodilatation
44
What facilitates development of Exudate?
- CAMs | - chemotaxis