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Pathology 3240A > Inflammation > Flashcards

Inflammation Flashcards

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
Q

Felon

A
  • deep infection at the end of the finger joint

- may cause osteomyelitis

26
Q

Empyema

A
  • localized pus in the pleural cavity
27
Q

Ulcer

A
  • 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
Q

Pseudomembranous Inflammation

A
  • inflammation produced by a powerful necrotizing toxin
  • forms a pseudomembrane over the area = precipitated fibrin, necrotic epithelium, WBCs
  • on mucosal surfaces
29
Q

Fistula

A
  • abnormal passage between 2 hollow organs both lined by epithelium or an epithelium
  • usually due to inflammation
30
Q

Sinus

A
  • abnormal tract between a solid organ/tissue to an epithelium covered surface (skin)
  • usually caused by inflammation
31
Q

Furuncle

A

boil

32
Q

Bacteriemia

A
  • bacteria circulate in blood

- doesn’t appear sick

33
Q

Septicemia

A
  • bacteraemia with clinical manifestation of illness

- fever, chills, abscesses

34
Q

Toxemia

A
  • clinical illness due to bacterial toxins in blood instead of the actual bacteria
35
Q

Journey of Lymphatic Flow

A

–> lymph node –> circulation –> RES

36
Q

Why don’t lymph nodes collapse by edema fluid?

A

System of Fibrils attached at right angles on the walls which extend to adjacent tissues, makes lymph vessels open up

37
Q

Pathogenesis of Rubor (redness)

A

= vasodilatation (microcirculation) by chemical mediators (esp. prostaglandins)

38
Q

Pathogenesis of tumour (swelling)

A
  • exudation of fluid (edema)
  • breakdown of tissues
  • mediated by vasoactive amines, C3a and C5a, Bradykinin, Leukotriene C D E
39
Q

Pathogenesis of Calor (heat)

A
  • more blood flow

increased local metabolic rate

40
Q

Pathogenesis of Impaired Function

A
  • swelling

- inhibition of muscular contraction by pain

41
Q

pathogenesis of pain

A
  • direct stimulus of nerve endings

- signalling of neural system by chemical mediators (bradykinin, histamine, G-OH-tryptamine)

42
Q

Systemic Effects of Inflammation

A
  1. Fever
  2. Leukocytosis
  3. Antibody production
  4. Other (anorexia, discomfort)
43
Q

What are the vascular events leading to swelling?

A

Increased permeability
increased hydrostatic pressure
vasodilatation

44
Q

What facilitates development of Exudate?

A
  • CAMs

- chemotaxis

Pathology 3240A (5 decks)

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