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Pathophys Block I > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

list the two arachidonic acid metabolites in our objectives and discuss how they contribute to the immune response

A
  1. leukotrienes: chemotactic agent involved in intense vasoconstriction, bronchospasm, and vascular permeability
  2. prostaglandins: involved in generation of pain and fever
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2
Q

name two examples of vasoactive amines and discuss their role in inflammation

A

histamine and seratonin: increase vasodilation and vascular permeability, secreted in response to physical injury, heat/cold/allergic rxns.

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3
Q

discuss the role of the compliment system in immunity

A

20 circulating proteins that are involved in both adaptive and innate immunity. complement cascade causes: vascular permeability, vasodilation, leukocyte adhesion, chemotaxis, activation and phagocytosis (C3 and C5 are most important inflammatory mediators)

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4
Q

name the 6 features that are activated by the compliment system during acute inflammatory response

A
  1. vascular permeability
  2. vasodilation
  3. leukocyte adhesion
  4. chemotaxis
  5. activation
  6. phagocytosis
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5
Q

what are the 4 actions of the kinin system

A
  1. increase vascular permeability
  2. contraction of smooth muscle
  3. dilation of blood vessels
  4. pain
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6
Q

what are 2 important examples of cytokines in acute immunity

A

IL-1 and TNF

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7
Q

what are the main roles of TNF and IL-1 in acute inflammation

A

systemic acute phase reactions: fever, loss of appetite, release of neutrophils into bloodstream, release of corticosteroids and hemodynamic effects of septic shock

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8
Q

what is the role of nitric oxide in immunity

A

increase vasodilation in response to acute injury

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9
Q

what are oxygen-derived free radicals and what do they contribute to the immune response?

A

product of oxidative metabolism by neutrophils (called respiratory burst) that occurs during phagocytosis. these oxygen-derived free radicals act to further immune response by helping to destroy harmful bacteria.

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10
Q

what are the 5 cardinal signs of acute inflammation

A
  1. rubor (redness)
  2. calor (increase heat)
  3. tumor (swelling)
  4. dolor (pain)
  5. functio laesa (loss of function)
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11
Q

what is the onset of chronic inflammation? acute?

A

chronic: insidious
acute: acute

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12
Q

what is the specificity of chronic inflammation? acute?

A

chronic: specific (where immune response is activated)
acute: nonspecific

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13
Q

what types of inflammatory cells are active in chronic inflammation? acute?

A

chronic: lymphocytes, plasma cells, macrophages, fibroblasts
acute: neutrophils, macrophages

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14
Q

what types of vascular changes are associated with chronic inflammation? acute?

A

chronic: new vessel formation (granulation tissue)
acute: active vasodilation, increase permeability

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15
Q

are fluid exudation and edema present in chronic inflammation? acute inflammation?

A

chronic: no
acute: yes

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16
Q

is tissue necrosis present in chronic inflammation? acute?

A

chronic: yes, ongoing
acute: not usually, sometimes suppurative and necrotizing inflammation can occur

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17
Q

is fibrosis present in chronic inflammation? acute?

A

chronic: yes
acute: no

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18
Q

what types of host response are present in acute inflammation?

A
  1. plasma factors: complement, immunoglobulins
  2. neutrophils
  3. non-immune phagocytosis
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19
Q

what systemic manifestations are present with chronic inflammation? acute?

A

chronic: low-grade fever, anemia, weight loss
acute: often high fever

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20
Q

what types of peripheral blood changes are present in chronic inflammation? acute?

A

chronic: frequently not present, variable leukocyte changes, increase plasma immunoglobulin
acute: neutrophils, lymphocytosis (in viral infections)

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21
Q

exudate

A

thick fluid that consists mainly of protein, cells, neutrophils with a higher SG than whater.

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22
Q

exudation

A

accumulation of exudate in fibrinous and purulent inflammation

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23
Q

transudate

A

substance involved in serous inflammation that has few cells and is mostly fluid

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24
Q

transudation

A

accumulation of transudate as a response to inflammation

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25
pus
thick white/yellow fluid, rich in exudate and leukocytes
26
edema
accumulation of fluid in the tissue as a response to vessel permeability
27
effusion
escape of fluid into a body cavity
28
list the changes of vascular flow in acute inflammation in order.
1. initial transient vasoconstriction 2. vasodilation (heat and redness) 3. increase in vascular permeability
29
how does mean capillary pressure affect vascular permeability?
hydrostatic pressure (pushing out of vessel) increases, colloid osmotic pressure (pressure pushing into vessel) stays the same, resulting in a net flow out of vessels
30
what causes in increase mean capillary pressure during acute inflammation?
increased vascular flow
31
what causes edema in acute inflammation?
increase vascular permeability allows protein rich fluid (exudate) to escape into interstitium
32
what are the 3 main steps to leukocyte emigration during acute inflammation?
1. leukocyte extravasation 2. chemotaxis 3. leukocyte activation 4. phagocytosis
33
what are the 4 steps to leukocyte extravasation and migration?
1. margination 2. rolling adhesion 3. transmigration 4. migration through interstitial tissues
34
chemotaxis
process by which WBCs are drawn to the site of inflammation by a chemical gradient/chemoattractant. these chemoattractants can be either exogenous (example bacteria) or endogenous (complement, leukotrienes, cytokines)
35
what are the three steps to phagocytosis?
1. recognition and attachment through opsonization 2. engulfment 3. killing or degradation of ingested material
36
describe 3 main acute phase reactions
1. fever (mostly associated w/ bacterial infections) 2. changes in peripheral WBC count 3. changes in plasma protein levels
37
list possible outcomes of acute inflammation
1. complete resolution 2. suppuration/abcess formation 3. progression to chronic inflammation 4. repair
38
discuss suppuration/abcess formation as an outcome of acute inflammation
collection of walled-off area containing pus, occurs with pyogenic organisms.
39
discuss progression to chronic inflammation as an outcome of acute inflammation
happens when acute inflammation cannot be resolved. acute and chronic inflammation can coexist.
40
discuss repair as an outcome of acute inflammation
healing by connective tissue replacement (fibrosis) and scarring. occurs after substantial tissue destruction or when inflammation occurs in tissue that can not regenerate.
41
Staphlococcus aureus morphology
GP, cocci, clusters
42
Staphlococcus aureus S/S
Main: TSS (fever, rash, diarrhea, hypotension) Other: skin infections (faruncles, boils), osteomyelitis, arthritis, endocarditis, pneumonia, sepsis, food poisoning, UTI, scalded skin syndrome
43
Staphlococcus aureus pathogenesis
cell wall, exotoxins
44
Staphlococcus aureus diagnostic work up
catalase + | coagulase +
45
catalase test
catalase converts hydrogen peroxide to water and oxygen, important test for determining type of GP organism (e.g distinguishing different types of staph species)
46
coagulase test
coagulase is an enzyme that causes clot to form, is expressed when some bacteria is exposed to plasma, important for determining staph aureus (coagulase +) from other staph bacteria that are (coagulase -)
47
MSSA
methicillin susceptible staph. aureus
48
MRSA
methicillin resistant staph. aureus
49
Staphlococcus aureus management
source control, antibiotic treatment (test for sensitivities) MRSA: vancomycin
50
Streptococcus pneumonia morphology
GP, cocci, strips
51
Streptococcus pneumonia S/S
Main: pneumonia Other: meningitis, sinusitis, otitis media
52
Streptococcus pneumonia pathogenesis
capsule, pneumolysin and autolysin
53
most common cause of pneumonia
Streptococcus pneumonia
54
Streptococcus pneumonia diagnostic work up
alpha hemolytic (important test for determining type of strep)
55
Streptococcus pneumonia management
vancomycin and penicillin-G (some strep resistant to penicillin-G)
56
Listeria monocytogenes morphologies
GP, rod, diplococcic or short chain, aerobic
57
Listeria monocytogenes S/S
Main: food poisoning Other: meningitis, sepsis
58
Listeria monocytogenes pathogenesis
obligate intracellular parasite (enters cell by phagocytosis), pili, membrane degrading phospholipase, produces listeriolysin which facilitates spreading from cell to cell, immunocompromised individuals are more susceptible
59
Listeria monocytogenes diagnostic work up
blood and CSF cultures (if meningitis), catalase +, beta hemolytic, + motility
60
Listeria monocytogenes
ampicillin and Bactrim (trimethoprim/sulfamethoxilizone)
61
granulomatous inflammation
distinctive pattern of chronic inflammation (focal accumulation of activated macrophages)
62
granulomas
focal masses/collections of immune/inflammatory cells that form at sites of persistent tissue inflammation/infection. form in order to wall off threats due to inability to eliminate disease due to a failure of neutrophils and monocytes to generate O2.
63
what types of cells are present in granulomas?
activated macrophages, Langhan's giant cells, lympthocytes
64
in what type of tissue damage are granulomas present?
persistent infection, foreign body, chronic stimuli
65
what are 4 ways to diagnose acute inflammation?
1. examination of eduxate (SG and protein levels) 2. ID presence of inflammatory cells (neutrophils: bacterial, lymphocytes: viral, eosinophils: parasitic) 3. Bx and examination of tissue 4. diagnostic tests: gram stain, Ab levels, complement protein levels
66
what are 5 ways to diagnose chronic inflammation?
1. Bx 2. micro cultures 3. immunologic studies 4. serologic studies for Abs 5. skin tests (Tb, fungi)
67
what are some ways to treat pathological inflammation?
1. drugs (NSAIDs, steroids) | 2. physical (debridement, excision)
68
abrasion
epidermis or dermis removed by friction
69
laceration
tearing of shredding of skin that results from a cut
70
incisions
therapeutic cut
71
crush
devitalization of tissue and underlying vessels and nerves from crushing injury
72
degloving
circumferential removal of tissue
73
puncture
small opening that can create a pathway for microorganisms to enter the body
74
avulsion
section of tissue that has been removed down to the bone
75
bite
puncture of dermis caused by teeth
76
primary intention
healing of a wound w/o granulation
77
secondary intention
wound closure in which edges are separated, granulation tissue fills in gap, epithelium grows over granulations (producing a scar)
78
tertiary intention
AKA delayed primary closure, granulation tissue fills in gap, epithelium grows over granulations at slower rate, scar is larger than secondary intention
79
what are the 4 phases of wound healing?
1. inflammation 2. epithelialization (at 12 hours starts to form a seal, formation of granulation tissue) 3. collagen synthesis (4 days-6 weeks) 4. scar maturation (6 weeks=50% strength)

Pathophys Block I (8 decks)

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