acute and chronic inflammation, hypersensitivity 08 20 14

Question 1

cellular infiltrate in acute vs chronic inflammation

Answer 1

acute: mostly neutrophils
chronic: monocytes and macrophages, lymphocytes

Question 2

tissue injury in acute vs chronic inflam

Answer 2

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

Question 3

local and systemic signs in acute vs chronic inflam

Answer 3

acute: prominent
chronic: may be subtle

Question 4

stimuli for acute inflam

Answer 4

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

Question 5

How are antigens recognized?

Answer 5

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

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

Question 6

diff btwn toll like receptor and inflammasome

Answer 6

toll like recognizeds extracellular microbes

inflammasome recongizes parts of dead cells and some microbes

Question 7

vasodilatation caused by

Answer 7

histamine and nitric oxide

Question 8

increased vascular permeability caused by

Answer 8

histamine, bradykinin

endothelial cell injury (burns, etc)

Question 9

bradykinin causes

Answer 9

vasodilatation
increasedy vascular permeability
pain

Question 10

diff btwn transudate and exudate

Answer 10

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

Question 11

edema

Answer 11

excess fluid in interstitium or serosal cavities

Question 12

transudate definition

Answer 12

hypocellular and low protein content

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

Question 13

excudate def

Answer 13

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

Question 14

pus definition

Answer 14

purulent exudate rich in leukocytes

Question 15

steps in leukocyte recruitment to injury site

Answer 15

margination
rolling
adhesion
transmigration
chemotaxis

Question 16

role of selectins in inflammation

Answer 16

help with rolling and loose attacment to endothelial cells

present on endothelial cells, platelets, leukocytes

Question 17

role of integrins in inflammation

Answer 17

stable attachment of leukocytes to endothelium

Question 18

what drives transmigration in inflammation

Answer 18

chemokine CD31 (PECAM1) on leukocytes and endothelial cells

Question 19

list chemotactic factors to help leukocytes migrate to injury site

Answer 19

bacterial products
chemokines
complement
leukotrienes

Question 20

whend does leukocyte activation occur

what activates leukocytes

Answer 20

after recruitment of leukocyte to site of injury

what activates leukocyte? microbes, necrotic tissue, mediators

Question 21

how do leukocytes that do phagocytosis recognize microbe?

Answer 21

specific surface receptors on leukocyte or

opsonins (igG, complement proteins, lectins)

Question 22

how do leukocytes deal with injury?

Answer 22

killing-within phagolysosome, ROS

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

Question 23

what are the principal mediators of inflammation

Answer 23

histamine, NO
histamine, bradykinin
IL-1, TNF, bacterial products
IL-1, TNF
bradykinin
ROS, NO

Question 24

how can defects in leukocyte fxn come about?

Answer 24

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

less common:
genetic causes

Question 25

why is chronic inflam not good

Answer 25

can lead to fibrosis/scarring and loss of fxn

Question 26

list morphologic patterns of acute inflam

Answer 26

serous fibrinous suppurative ulcer

Question 27

serous inflam

Answer 27

mildest form of acute inflam | outpouring of thin fluid that is protein-poor from plasma or serosal cavity linings

Question 28

ex of serous inflam

Answer 28

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)

Question 29

fibrinous inflam

Answer 29

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

Question 30

ex of fibrinous inflam

Answer 30

fibrinous pericarditis from uremia, transmural myocardial infarct, acute rheumatic fever fribrnous pleuritis overlying pulmonary infarct fibrinous peritonitis from ascites

Question 31

suppurative (purulent) inflam

Answer 31

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

Question 32

ex of suppurative (purulent) inflam

Answer 32

acute appendicitis, acute brnchopneumonia, acute meningitis

Question 33

ulcer

Answer 33

local defect caused by necrotic cells and sloughing of necrotic and inflammatory tissue surface of organ or tissue

Question 34

ex of ulcers

Answer 34

``` peptic ulcer skin ulceration (in circulatory deficiencies) ```

Question 35

what causes chronic inflammation

Answer 35

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

Question 36

macrophages in acute vs chronic inflam

Answer 36

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

Question 37

morphologic features of chronic inflam

Answer 37

mononuclear cell infiltrate-macrophages, lymphocytes, plasma cells

Question 38

chronic inflam produces

Answer 38

angiogenesis, mononuclear cell infiltrate, fibrosis

Question 39

acute inflam can produce

Answer 39

resolution, pus, or fibrosis

Question 40

granulomatous inflam

Answer 40

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

Question 41

systemic effects of inflam

Answer 41

fever elevated plasma levels of acute-phase proteins leukocytosis

Question 42

how does fever occur?

Answer 42

pyrogens (LPS or IL1, TNF) | prostaglandins (specifically PGE2)-stimulate hypothalamus

Question 43

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

Answer 43

they bind to microbe wall aiding in elimination

Question 44

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

Answer 44

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