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Intro to path > acute and chronic inflammation, hypersensitivity 08 20 14 > Flashcards

acute and chronic inflammation, hypersensitivity 08 20 14 Flashcards

1
Q

cellular infiltrate in acute vs chronic inflammation

A

acute: mostly neutrophils
chronic: monocytes and macrophages, lymphocytes

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2
Q

tissue injury in acute vs chronic inflam

A

acute: mild, self-limited
chronic: usually severe and progressive

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3
Q

local and systemic signs in acute vs chronic inflam

A

acute: prominent
chronic: may be subtle

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4
Q

stimuli for acute inflam

A

infections
physical trauma
physical and chemical agents (burns, frostbite, irradiation, chemicals)
tissue necrosis
foreign bodies
hypersensitivity rxns (environmental substances and self antigens)

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5
Q

How are antigens recognized?

A

Toll-like receptors (once activated, stimulate TNF release)

Inflammasome (activates caspase-1, activating IL-1, which causes leukocyte recruitment)

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6
Q

diff btwn toll like receptor and inflammasome

A

toll like recognizeds extracellular microbes

inflammasome recongizes parts of dead cells and some microbes

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7
Q

vasodilatation caused by

A

histamine and nitric oxide

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8
Q

increased vascular permeability caused by

A

histamine, bradykinin

endothelial cell injury (burns, etc)

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9
Q

bradykinin causes

A

vasodilatation
increasedy vascular permeability
pain

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10
Q

diff btwn transudate and exudate

A

transudate is when there’s fluid movement across the capillary wall

exudate is protein and fluid that leak out across capillary wall due to inflammation

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11
Q

edema

A

excess fluid in interstitium or serosal cavities

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12
Q

transudate definition

A

hypocellular and low protein content

non-inflammatory extravascular fluid, ultrafiltrate of plasma, low SPECIFIC GRAVITY <1.012

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13
Q

excudate def

A

cellular and protein rich
inflammatory extravascular fluid
high specific gravity >1.020
caused by change in normal blood vessel permeability

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14
Q

pus definition

A

purulent exudate rich in leukocytes

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15
Q

steps in leukocyte recruitment to injury site

A 
margination
rolling
adhesion
transmigration
chemotaxis
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16
Q

role of selectins in inflammation

A

help with rolling and loose attacment to endothelial cells

present on endothelial cells, platelets, leukocytes

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17
Q

role of integrins in inflammation

A

stable attachment of leukocytes to endothelium

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18
Q

what drives transmigration in inflammation

A

chemokine CD31 (PECAM1) on leukocytes and endothelial cells

19
Q

list chemotactic factors to help leukocytes migrate to injury site

A

bacterial products
chemokines
complement
leukotrienes

20
Q

whend does leukocyte activation occur

what activates leukocytes

A

after recruitment of leukocyte to site of injury

what activates leukocyte? microbes, necrotic tissue, mediators

21
Q

how do leukocytes that do phagocytosis recognize microbe?

A

specific surface receptors on leukocyte or

opsonins (igG, complement proteins, lectins)

22
Q

how do leukocytes deal with injury?

A

killing-within phagolysosome, ROS

secreting enzymes into extracellular space (releasing enzymes like elastase that degrade microbes and dead tissue)

23
Q

what are the principal mediators of inflammation

A 
histamine, NO
histamine, bradykinin
IL-1, TNF, bacterial products
IL-1, TNF
bradykinin
ROS, NO
24
Q

how can defects in leukocyte fxn come about?

A

acquired:
defect in leukocyte production
defect in adhesion to endothelium and chemotaxis
defect in pahgocytososis and microbicidal activity

less common:
genetic causes

25
Q

why is chronic inflam not good

A

can lead to fibrosis/scarring and loss of fxn

26
Q

list morphologic patterns of acute inflam

A

serous
fibrinous
suppurative
ulcer

27
Q

serous inflam

A

mildest form of acute inflam

outpouring of thin fluid that is protein-poor from plasma or serosal cavity linings

28
Q

ex of serous inflam

A

peritoneal, pleural, pericardial EFFUSIONS (congestive heart failure, fluid overload)-effusions are defined as fluid in a serous cavity

skin blister from burn, viral infection , or trauma (fluid from traumatized epithelium or leaky endothelium)

29
Q

fibrinous inflam

A

more severe injury
larger vascular leaks, passage of fibrinogen through leak, fibrinogen converted to FIBRIN

affects linings like pericardium, pleura, peritoneum, meninges

could resolve or become scarring

30
Q

ex of fibrinous inflam

A

fibrinous pericarditis from uremia, transmural myocardial infarct, acute rheumatic fever

fribrnous pleuritis overlying pulmonary infarct

fibrinous peritonitis from ascites

31
Q

suppurative (purulent) inflam

A

large numbers of neutrophils present along with necrotic cells, edema fluid, and bacteria…usually becomes liquefied into PUS

occurs with infections; some bacteria more likely to produce this rxn (called pyogenic bacteria-like Staph)

ABSCESS: central area of necrotic tissue surrounded by preserved neutrophils, dilated vessels, and fibroblastic proliferation

32
Q

ex of suppurative (purulent) inflam

A

acute appendicitis, acute brnchopneumonia, acute meningitis

33
Q

ulcer

A

local defect caused by necrotic cells and sloughing of necrotic and inflammatory tissue

surface of organ or tissue

34
Q

ex of ulcers

A 
peptic ulcer
skin ulceration (in circulatory deficiencies)
35
Q

what causes chronic inflammation

A

persistent infections
prolonged exposure to toxic agents
immune-mediated inflammatory diseases (autoimmune diseases)

36
Q

macrophages in acute vs chronic inflam

A

in acute: monocytes becomes the tissue macrophages and participate in acute inflam

in chronic: macrophages persist because of continuous release of dead cells and microbes and stimulation by cytokines from activated T cells

37
Q

morphologic features of chronic inflam

A

mononuclear cell infiltrate-macrophages, lymphocytes, plasma cells

38
Q

chronic inflam produces

A

angiogenesis, mononuclear cell infiltrate, fibrosis

39
Q

acute inflam can produce

A

resolution, pus, or fibrosis

40
Q

granulomatous inflam

A

distinctive pattern of chronic inflam (prominent macrophages/histiocytes w/ epithelioid apperance)

multinucleated giant cells-giant cell formation induced by INF-gamma

develop as a result of specific infec, foreign bodies, immune rxn against self antigen

collar of lymphocytes, plasma cells

surrounding fibrosis

41
Q

systemic effects of inflam

A

fever
elevated plasma levels of acute-phase proteins
leukocytosis

42
Q

how does fever occur?

A

pyrogens (LPS or IL1, TNF)

prostaglandins (specifically PGE2)-stimulate hypothalamus

43
Q

what is the action of acute-phase proteins made by liver?

A

they bind to microbe wall aiding in elimination

44
Q

types of leukocytosis and what they say about underlying cause of inflam

A

neutrophilia-bacterial infec–left shift
lymphocytosis-viral infec
eosinophilia-allergies, asthma, parasites
leukopenia-typhoid, rickettsiae, some protozoans

Intro to path (15 decks)

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