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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
Q

pus

A

thick white/yellow fluid, rich in exudate and leukocytes

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26
Q

edema

A

accumulation of fluid in the tissue as a response to vessel permeability

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27
Q

effusion

A

escape of fluid into a body cavity

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28
Q

list the changes of vascular flow in acute inflammation in order.

A
  1. initial transient vasoconstriction
  2. vasodilation (heat and redness)
  3. increase in vascular permeability
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29
Q

how does mean capillary pressure affect vascular permeability?

A

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

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30
Q

what causes in increase mean capillary pressure during acute inflammation?

A

increased vascular flow

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31
Q

what causes edema in acute inflammation?

A

increase vascular permeability allows protein rich fluid (exudate) to escape into interstitium

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32
Q

what are the 3 main steps to leukocyte emigration during acute inflammation?

A
  1. leukocyte extravasation
  2. chemotaxis
  3. leukocyte activation
  4. phagocytosis
33
Q

what are the 4 steps to leukocyte extravasation and migration?

A
  1. margination
  2. rolling adhesion
  3. transmigration
  4. migration through interstitial tissues
34
Q

chemotaxis

A

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
Q

what are the three steps to phagocytosis?

A
  1. recognition and attachment through opsonization
  2. engulfment
  3. killing or degradation of ingested material
36
Q

describe 3 main acute phase reactions

A
  1. fever (mostly associated w/ bacterial infections)
  2. changes in peripheral WBC count
  3. changes in plasma protein levels
37
Q

list possible outcomes of acute inflammation

A
  1. complete resolution
  2. suppuration/abcess formation
  3. progression to chronic inflammation
  4. repair
38
Q

discuss suppuration/abcess formation as an outcome of acute inflammation

A

collection of walled-off area containing pus, occurs with pyogenic organisms.

39
Q

discuss progression to chronic inflammation as an outcome of acute inflammation

A

happens when acute inflammation cannot be resolved. acute and chronic inflammation can coexist.

40
Q

discuss repair as an outcome of acute inflammation

A

healing by connective tissue replacement (fibrosis) and scarring. occurs after substantial tissue destruction or when inflammation occurs in tissue that can not regenerate.

41
Q

Staphlococcus aureus morphology

A

GP, cocci, clusters

42
Q

Staphlococcus aureus S/S

A

Main: TSS (fever, rash, diarrhea, hypotension)

Other: skin infections (faruncles, boils), osteomyelitis, arthritis, endocarditis, pneumonia, sepsis, food poisoning, UTI, scalded skin syndrome

43
Q

Staphlococcus aureus pathogenesis

A

cell wall, exotoxins

44
Q

Staphlococcus aureus diagnostic work up

A

catalase +

coagulase +

45
Q

catalase test

A

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
Q

coagulase test

A

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
Q

MSSA

A

methicillin susceptible staph. aureus

48
Q

MRSA

A

methicillin resistant staph. aureus

49
Q

Staphlococcus aureus management

A

source control, antibiotic treatment (test for sensitivities)

MRSA: vancomycin

50
Q

Streptococcus pneumonia morphology

A

GP, cocci, strips

51
Q

Streptococcus pneumonia S/S

A

Main: pneumonia

Other: meningitis, sinusitis, otitis media

52
Q

Streptococcus pneumonia pathogenesis

A

capsule, pneumolysin and autolysin

53
Q

most common cause of pneumonia

A

Streptococcus pneumonia

54
Q

Streptococcus pneumonia diagnostic work up

A

alpha hemolytic (important test for determining type of strep)

55
Q

Streptococcus pneumonia management

A

vancomycin and penicillin-G (some strep resistant to penicillin-G)

56
Q

Listeria monocytogenes morphologies

A

GP, rod, diplococcic or short chain, aerobic

57
Q

Listeria monocytogenes S/S

A

Main: food poisoning

Other: meningitis, sepsis

58
Q

Listeria monocytogenes pathogenesis

A

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
Q

Listeria monocytogenes diagnostic work up

A

blood and CSF cultures (if meningitis), catalase +, beta hemolytic, + motility

60
Q

Listeria monocytogenes

A

ampicillin and Bactrim (trimethoprim/sulfamethoxilizone)

61
Q

granulomatous inflammation

A

distinctive pattern of chronic inflammation (focal accumulation of activated macrophages)

62
Q

granulomas

A

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
Q

what types of cells are present in granulomas?

A

activated macrophages, Langhan’s giant cells, lympthocytes

64
Q

in what type of tissue damage are granulomas present?

A

persistent infection, foreign body, chronic stimuli

65
Q

what are 4 ways to diagnose acute inflammation?

A
  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
Q

what are 5 ways to diagnose chronic inflammation?

A
  1. Bx
  2. micro cultures
  3. immunologic studies
  4. serologic studies for Abs
  5. skin tests (Tb, fungi)
67
Q

what are some ways to treat pathological inflammation?

A
  1. drugs (NSAIDs, steroids)

2. physical (debridement, excision)

68
Q

abrasion

A

epidermis or dermis removed by friction

69
Q

laceration

A

tearing of shredding of skin that results from a cut

70
Q

incisions

A

therapeutic cut

71
Q

crush

A

devitalization of tissue and underlying vessels and nerves from crushing injury

72
Q

degloving

A

circumferential removal of tissue

73
Q

puncture

A

small opening that can create a pathway for microorganisms to enter the body

74
Q

avulsion

A

section of tissue that has been removed down to the bone

75
Q

bite

A

puncture of dermis caused by teeth

76
Q

primary intention

A

healing of a wound w/o granulation

77
Q

secondary intention

A

wound closure in which edges are separated, granulation tissue fills in gap, epithelium grows over granulations (producing a scar)

78
Q

tertiary intention

A

AKA delayed primary closure, granulation tissue fills in gap, epithelium grows over granulations at slower rate, scar is larger than secondary intention

79
Q

what are the 4 phases of wound healing?

A
  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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