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Pathology and MuscSkel > Acute and Chronic Inflammation and Hypersensitivity > Flashcards

Acute and Chronic Inflammation and Hypersensitivity Flashcards

1
Q

What are the 5 signs of inflammation?

A 
calor (heat)
rubor (redness)
tumor (swelling)
dolor (pain)
functio lasea (loss of function)
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2
Q

What are the features of acute inflammation?

A

fast
mainly neutrophil infiltrates
usually mild and self-limited tissue injury and fibrosis
local and systemic signs are prominent

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3
Q

What are the features of chronic inflammation?

A

onset is slow
cellular infiltrates monocytes/macrophages and lymphocytes
tissue injury and fibrosis are often sever and progressive
local and systemic sign are less prominent; maybe subtle

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4
Q

What are the stimuli for acute inflammation?

A 
infecitons and microbial toxins
physical trauma
physical and chemical agents
tissue necrosis
foreign  bodies
immune reactions
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5
Q

What are the abnormal stimulus recognized by for initation of inflammation?

A 
epithelial cells (skin, linings of GI and resp tract)
dendritic cells (epithelia and most organs)
phagocytes (connective tissue and organ)
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6
Q

Receptor recognize molecular tructure on microbes by what?

A

toll like receptor: located in plasma membrane
inflammasome: cytoplasmic complex recognizing part of dead cells
trigger activation of casapse-1 which activates IL-1

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7
Q

Key difference between TLR and inflammasome is what?

A

TLR recognize extracellular microbes and Patterns associated with external things
Inflammasome recognizes products of dead cells and some microbes.

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8
Q

What mediators cause pain and vasodilation in inflammation?

A

increase permeablility and pain

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9
Q

What are the role of selectins?

A

Seen on endothelial cells, platelets, leukocytes
P-selectin, L-selectin, etc.
aid in rolling and loose attachment to endothelial cells

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10
Q

What are the role of integrins in inflammation?

A

expression of chemokines on endothelial cells activate integrins
TNF adn IL-1 secreted by macrophages at the site of injury increase endothelial cell ligan expression
result in more stable attachment of leukocytes

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11
Q

What endothelial cell marker causes transmigration?

A

PECAM1 (CD31)

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12
Q

What are the chemotactic factors that cause cells to migrate to injury site?

A

bacterial products
chemokines
complement (3a and 5a)
leukotrienes

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13
Q

What are opsonins?

A

include IgG complement protein and lectins

-coat microbes and increase rate of phagocytosis

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14
Q

What are the 2 ways in which phagocytosed things are degraded?

A

ROS (reactive oxygen species) dependent mechanisms

and enzyme destruction either from elastase, or lysozymes

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15
Q

What are the vasodilators involved in inflammation?

A

histamine (mast cell, basophils, platelets) , nitric oxide (endotehlium, macrophages) and prostaglandins (mast cells, leukoctyes)

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16
Q

What are the principle mediators that increase vascular permeability?

A

Histamine, serotonin (mast cells, basophils, platelets)
C3a, C5a
Bradykinin
leukotrienes C4, D4, E4 (mast cells, leukocytes)
platelet activating factor (mast cells, leukocytes)
Substance P (leukocytes, axons)

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17
Q

What are the principles mediators of chemotaxis, leukocytes recruitment and activation?

A

IL-1, TNF (macrophages, endothelial cell, mast cells)
Chemokines (leukocytes, activated macrophages)
C3a, C5a
Leukotriene B4 (Mast cells, leukocytes)
Bacterial products

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18
Q

What are the principle mediators of Fever?

A

IL-1 and TNFalpha (macrophages, endothelial cells, mast cells)

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19
Q

What are the mediators of tissue damage in inflammation?

A

lysosomal enzymes of leukocytes (leukocytes)
ROS (leukocytes)
Nitric oxide (endothelium, macrophages)

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20
Q

What are the outcomes of acute inflammation?

A

1 termination of acute and inflammatory response
-meditors degrade, leukoctyes die, debris cleared by macrophages
2. progression to chronic inflammation
3 scarring or fibrosis

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21
Q

What are the morphologic patterns of acute inflammation (4)?

A
    • serous
    • fibrinous
    • suppurative
    • ulcer
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22
Q

What are the serous inflammation signs?

A

mildest form of acute inflammation
outpuring of thing fluid from plasma or serosal cavity
ie peritoneal, pleural, pericardial, skin blister, viral infection

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23
Q

What are the signs of fibrinous inflammation?

A

occurs secondary to more severe injury
larger vascular leaks, passage of fibrinogen, conversion to fibrin
affects linings
may resolve completely or may organize leading to scarring

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24
Q

What are the signs of suppurative (purulent) inflammation?

A

when large number of neutrophils present along with necrotic cells, eema fluid and bacteria = PUS

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25
Q

What is an abscess?

A

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

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26
Q

What is an ulcer?

A

local defect, surface of organ or tissue

sloughing of surface covering and necrotic inflammatory tissue

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27
Q

What are the signs of chornic inflammation?

A

leukocytes present, inflammation of prolonged duration

active inflammation, injury and healing occuring at teh same itme

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28
Q

What are causes of chronic inflammation?

A

persistent infection that are difficult to eradicate
prolonged exposure to toxic agents
immune-mediated inflammatory diseases( autoimmune)

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29
Q

What do macrophages do in chronic ifnlammation?

A

they persist, secrete products that result in continued tissue injury, IFNgamma one of persistance

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30
Q

What cells are involved in chronic inflammation?

A 
Adaptive immune response is activated
Lymphocytes
Plasma cells
Immunoglobulins
Eosiophils in parasitic inflammation
Mast Cells: found in connective tissue
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31
Q

What are the symptoms of granulomatous inflammation

A

Distinctive pattern of chronic inflammation
prominent activated macrophages with epithelioid appearance
Develop in response to:
-specific infections
inert foreign bodies
immune rxns against self antigen

32
Q

What are the histological signs of granulomatous inflammation?

A 
aggregate of epithelioid histiocytes (macrophages)
mutlinucleated giant cells
-fusion of many macrophages
-IFNgamma induces giant cell formation
-collar of lymphocytes, plasma cells
-- surrounding fibrosis
--with TB, central caseous necrosis
-- also seen with foreign bodies; otehr infections
33
Q

What are the systemic effects of inflamation?

A

fever
– response to LPS or IL-1 and TNF
elevated plasma levels of acute-phase proteins
leukocytosis

34
Q

What are the acute-phase proteins?

A

synthesized in liver; stim by IL-6
C-reactive protein, Fibrinogen, serum amyloid A
binds to microbe wall aiding in elimination
fibrinogen binds to erythocytes causing stacks that sediment more rapidlay than normal

35
Q

What are the systemic leukocytosis?

A

TNF and IL-1 stim

WBC count usually goes to 15,000 and 20,000

36
Q

What does neutrophilia seem to imply?

A

bacterial infection
accelerated release of immature neutrophils
“left shift”

37
Q

What does lymphocytosis imply in pt with inflammation?

A

viral infections usually

38
Q

What does eosinophilia imply in pt with inflammation systemically?

A

allergies, asthma, parasitic infections

39
Q

What does leikopenia imply systemically in infection?

A

typhoid, rickettsia, some prtozans from sequestering in lymph

40
Q

How is type 1 hypersensitivity mediated?

A

IgE

41
Q

How is type 2 hypersensitivity mediated?

A

direct antibody-mediated cytolytic hypersensitivity

42
Q

How is type III hypersensitivity mediated?

A

immune complex-mediated damage usually from depositiona nd complement

43
Q

How is type 4 hypersensitivity mediated?

A

CD8 or CD4 T cells

44
Q

What is the definition of hypersensitivity?

A

excessive or abnoraml secondary immune response to sensitizing agent

45
Q

What are some examples of type 1 hypersensitivity?

A

anaphylaxis, some forms of bronchial asthma, eczema, atopy

46
Q

What are some examples of type 2 hypersensitivity?

A

autoimmune hemolytic anemia, erythroblastosis, myasthenia gravis, goodpasture syndrome, erythroblastosis fetalis, rheumatoid fever

47
Q

What are some examples of type 3 hypersensitivity?

A

arthus reaction, serum sickness, systemic lupus erythematosus, certain forms of acute glomerulonephritis

48
Q

What are some examples of type 4 hypersensitivity?

A

tuberculosis, contact dermatitis, transplant rejection

49
Q

What is the pathophysiology of allergic disease ( type 1 hypersensitivity)?

A

specific allergen, presentation of allergen to TH2 which release IL-4 and IL-6 leading to production of specific IgE, loaded onto Mast cells (around 4 weeks)
allergens cross-link IgE on Mast cells leading to mediator release
4-6 hours later late release de novo

50
Q

What is the difference between allergen and irritant?

A

allergen IgE mediated, require sensitation, not usually dose-dependent

Irritant not mediated through IgE, dose dependent, will affect everyone at high enough dose

51
Q

What cells are type 1 hypersensitivity reactions dependent on?

A

mast cella nd or basophils

52
Q

What are the medaitors of early phase type 1 reaction?

A 
exposure; 15 minutes later
-histamine
-tryptase
-PGD2
-Thromboxane
LTC4
53
Q

What are the late phase mediators in type 1 reactions?

A 
LTB4, LTC4
PGD2, PGE2, PGF2
Kinins
Histamine
GM-CSF, IL5
Eosiniphilic cationic protein
Major Basic protien
-Eosinophil peroxidase

These are suually madde de novo hence the 4 hour delay

54
Q

What enzyme is measured that is the best marker of mast cell degraunlation?

A

tryptase

only mast cells make it last 4 hours after degranulation

55
Q

What does IL-4 and IL-13 drive from mast cells after exposure to allergen?

A

associated with Th2 and Ig class swithcing to IgE

56
Q

What does IL-3, IL-5 and GM-CSF promote when released from mast cell in hypersensitivity 1?

A

promote survival and activation of eosinophils

57
Q

What does TNF do after mast cell exposure to hypersensitivity 1?

A

activates endothelium and leads to ahesion molecule expression
some exist as preformed mediatrs

58
Q

What chemokines are produced by mast cells?

A

delayed MIP1alpha–chemotactic for monocytes, macrophages, etc
RANTES and Eotaxin– chemotactic for T cells and eosinophis

59
Q

What lipid mediators are produced by mast cells?

A

leukotrienes– lead to eosinohpil migration, smooth muscle contraction, vascular permeability, mucus secresion
Platelet activating factor

60
Q

What drug block 5-lipoxygenase and prevents formation of leukotrienes?

A

zileuton

61
Q

What drug blocks LT C/D/E receptors to prevent LTD4 and LTE4 and LTC 4 ability to bind receptor?

A

zafirlukast

62
Q

What decreases threshold of mast cells for histamine release?

A 
cytokines and chemokines
antigen exposure
histamine releasing factor 
autoantibody
psychological factors
63
Q

What increases threshold of mast cells for histamine release?

A

corticosteroids, antihistamines, cromolyn sulfate (in vitro)

64
Q

What causes elevated eosinophil count?

A 
NAACP
Neoplasia
Asthma
Allergy 
Connective tissue disease
Parasitic disease
65
Q

What is the role of CCR3 on eosinophils?

A

only known receptor for eotaxin

66
Q

Where is eotaxin found?

A

at sites of allergic inflammation cause chemotaxis to site for eosinohpils

67
Q

What does corticosteroids do to eosinophils?

A

Steroids induce rapid apoptosis of eosinophils

inhibit production of IL-5, leading to decreased release from marrow as well as increased apoptosis

68
Q

How is hte effect of corticosteroids on eosinophils mediated?

A

by steroid binding to GR-alpha and inhibiting AP-1 and NFkB

69
Q

What si the role of IL-5 on eosinophils?

A 
produced by Th2 and other cells
prolongs eosinophil survival, enhances leukotriene production and cytotoxicity for parasites
infusion causes eosinophiia
conversion to hypodense phenotype
augment B2 integrin adhesion
70
Q

What is the histological structure of eosinophil?

A

nucleas horhsoe with crystalloid granules

crystalloid granules have both a core and a matrix

71
Q

Asthma pathophysiology is composed of what?

A

inflammatory cell infiltrate consists of mainly eosinophils and lymphocytes
Sudden death asthma associated with neutrohpil infiltrate
Denudation of airway epithelium
mucus gland hyperplasia and hypersecretion
smooth muscle cell hyperplasia
submucosal edema and vascular dilatation
fibring deposotion/airway reomodeling

72
Q

What are the mediators of anaphylaxis?

A

histamine
-H1: smooth muscle contractiona dn vascular permeability
H2: vascular permeability
H1+H2 Vasodilation, pruritis

Leukotrienes
smooth muscle contraction
vascular permeability and dilation

NO
smooth muscle relaxation
vascular permeability and dilation

73
Q

In type II hypersensitivity to some drugs what does IgG react wtih?

A

the cell bound drug

74
Q

What disease does type II hypersensitivity cause when drug is hypersensitive?

A

beocme antigenic when bound to erythrocytes or platelets;

may result in destruction of erythrocytes or platelets and damage to spleen

75
Q

Where does type III hypersensitivity damage usually occur?

A

kidneys, vessels, joints and skin

76
Q

What is the pathophysiology of type III hypersensitivity?

A 
circulating complexes fix complement
deposition of complexes
phagocytic cell influx
activation of phagocytes with release of lysosomal enzymes
resultant tissue destruction

Pathology and MuscSkel (15 decks)

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