Inflammation Flashcards
Define it?
It is defence mechanism.
It is local change in living tissues when exposed to an injury not so severe to cause death of cell.
The reaction of living tissue to all forms of injury, & involves vascular, neurologic, humoral & cellular responses at the site of injury.
What is the principal features of acute inflammation?
Dilation and leaking of vessels, and involvement of circulating neutrophils.
Types of inflammation
Acute inf… : sudden onset, short duration, characterized by edema and neutrophiles, has severe systemic effect.
Chronic infla…: gradual onset, long duration, characterized by mononuclear cells and tissue destruction repair, has less severe systemic effect.
Name of Inflammation of pleura and lung?
Pleuristy and pneumonia.
Name of inflammation of:
- Togue
- stomach
- Testis
- Liver
- Kidney
- Glossitis
- gastristis
- orchitis
- hepatitis
- nephritis
Clinical significance of inflammation
Protective response:
Contain and isolate injury, destroy invading microorganisms, inactivate toxins, prepair tissue for healing and repair.
Inflammation may be harmful
Hypersensitivity ti a bee sting can cause anaphylactic shock and death.
Progressive organ damage (chronic inflammation and fibrosis) e.g RA
Causes of inflammation:
Same as cell injury: 1.Non living agent: A.physical: burn, trauma, radiation. B.chemical: toxins, caustic subs. 2.Living agent: A.(infective): microorganism 3.Immunological reaction
T or F
Chronic inflammation is the immediate and early response to injury.
F
Acute inflammation not chronic.
Cells that involve in acute inflammation:
Neutrophilis
Macrophages
Cardinal signs of acute inflammation:
Redness, heat, pain, swelling and loss of function.
Components of acute inflammation:
Vascular response
Neurological response: vasoconstriction
Cellular response
Humoral response (Chemical mediators)
Vascular changes in acute infla..:
Initial inconstant vasoconstriction then VASODILATATION that leads to increase blood VOLUME and FLOW
increase PERMEABILITY and VISCOSITY and STASIS
Margination of PMN is a feature of:
Acute inflammation
How to Increase vascular permeability in acute infla..
Endothelial contraction, retraction, direct injury and leukocyte dependent endothelial injury.
T or F
Retraction of endothelial cells occurs mainly in venules and induced by histamine, NO and other mediators.
True
T or F
Retraction of endothelial cells occurs mainly in arterioles and induced by histamine, NO and other mediators.
F
It occures mainly in venules.
Endothelial injury occures in arterioles, capillaries and venules and caused by:
Burns, some microbial toxins
Leukocyte mediated vascular injury occures mainly in:
Pulmonary capillaries
And associated with late stage of inflammation
Increased transcytosis in acute infla… occurs in:
Occurs in venules and induced by vascular endothelial growth factor (VEGF).
Cellular phase in acute inflammation:
Margination, Adhesion Diapedesis and chemotaxis
Main differences b/w Exudate and Transudate:
T:clear, protein poor fluid, and It appears at an early stage of the inflammation and hypoalbumnemia
E:cloudy, protein rich fluid and Neutrophils and It appears at a later stage of the inflammation
T or F
PMNs are predominant cells in acute inflammation.
T
Sequence of leukocyte response in acute inlfammation:
- Margination, rolling and adhesion
- Emigration and chemotaxis
- Phagocytosis, degranulation and killing
How leukocyte kills microoganisms in acute infla…
- Recognition and attachment
- engulfment and phagocytic vacuole formation
- Degranulation and killig
Define the chemical mediators and give some examples
They are chemicals released during acute inflammation and are responsible for all inflammatory processes.
Eg: vasoactive amines like histamine and serotin
Binding of adhesion molecules on WBC and endothelial cell modulated by:
chemical mediators
T or F
In the bacterial infection, PMN first emigrate then replaced by monocytes.
T
T or F
In the tubercle or typhoid infections monocytes emigrate from beginning.
T
In the viral imfection and immune reactions, lymphocytes emigrate from the beginning
T
In hypersensitivity reactions, eosinophils predominante.
T
Endothelial adhesion receptors:
Selectin,(E,P,L), immunoglobulin family molecule (ICAM1, VCAM1), WBC receptors, integrins (CD1 1/18, VLA0R), mucin like glycoproteins
Migration of PMN across endothelium (transmigration) is mediated by :
CD31
What is the chemotaxis?
Unidirectional movement of leukocytes towards the site of injury, mediated by diffusible chemical attractants.
Chemotactic factors for Neutrophils:
C5a, leukotrine B4, Bacterial products
Chemotactic factors for monocyte-Macrophages:
C5a C3a, leukotriene B4, Bacterial products
Chemotactic factors of Eosinophils:
Eosinophil chemotactic factor of anaphylaxis
PG D2
Histamine
Cells undergooing extravasation
Neutrophils : during 6-24h, more abundant, short lived, respond more rapidly
Monocytes: after 24-48h, Survive longer, come to end acute inflammation, (if they persist –》 chronic inflammation)
Definition of phagocytosis
Is a process by which neutrophils and macrophages engulf the offending pathogen.
It is the major benefit of leukocyte accumulation
Mechanism of attachment of pathogen on leukocytes
The pathogen is coated by opsonins.
Fc fragment of Ig to Fc receptor on leukocytes
And complement fragment C3b to C3b receptor
Phagocytosis steps:
Recognition and attachment
Engulfment
Killing and degradation
Engulfement mechanism
By pseudopods which encircle the pathogen creating a phagosome.
Pathogen killing and degradation:
2 mechanisms:
O2 dependent and independent
O2 dependent mechanism:
The most important:
Activation of NADPH oxidase 》conversion of O2 to reactive species with the help of lysosomal myeloperxidase (MPO)》Powerful bactericidal agents (bleach)
O2 independent mechanism:
Act by increasing membrane permeability of thebacteria.
Mediated by substances in leukocyte lysosomal granules:
Lysozyme, Lactoferrin, Bactericidal permeability increasing protein, Defensins
Cell derived mediators( chemical mediators:
Performed mediatora in secretory granules:
Vasoactive amines : H, 5HT
Lysosomal enzymes
Newly synthesized: PGs, leukorienes, platelet-activating factor, cytokines, Leukocyte product, neuropeptide, NO and O2 derived free radicals
Plasma derived mediators:
Complement activation: C3a, C5a, C5b
Hageman factor activation: kinin system (bradykinin) and coagulation-fibrinolysis system
Source of histamine:
Stored in granules of mast cells, basophiles and platelets
Action of histamine:
VD and increase VP
chemotactic to eosinophil
Bronchial S.M contraction
How histamine released?
Mechanical stimuli e.g trauma cold…
Anaphylatoxins of complement system
Type 1 hypersensitivity reaction (Ag binds to IgE on mast cell surface)
Cytokines
Source of serotonin:
Stored in platelets
Action of serotonin:
Potent V.C of venules.
+ VP (immediate phase).
S.M contraction and bronchospasm
How sertonin released?
Contact with collagen
Ag-Ab reaction
PAF (Platelet activation factor)
Action of lysosomal enzymes of neutrophils and macrophages:
+ VP
Microbial killing and degradation during phagocytosis
Chemotaxis
Tissue damage - proteases
Macrophage lysosomal emzymes are important in chronic inflammation
Definition of cytokines:
They are group of soluble mediators generated principally by lymphocytes and macrophages that modulate the function of other cell types.
E.g of cytokines:
Interleukins
Interferons (apha, beta, gamma)
TNF (alpha, bita)
Chemokines (chemotaxis)
Source and action of PAF:
Mast cells and other leukocytes. Platelet aggregation and release VD and + VP Chemotaxis Stimulates the synthesis of PG and leukotrienes
O2 derived free radicals:
Formed in neutrophils and macrophages
Include: superoxide anione, hydorgen peroxide, hydroxyl radical
Action of O2 derived free radicals:
Micorbial killing during phagocytosis may be released extracellularly
Endothelial cell damage - + VP
Tissue damage
Define The complement system:
It is a group of 20 plasma proteins which are activated in cascades by the classic or alternate pathways
C3b function:
Opsonins
Bradykinin functions:
+ VP, VD and causes pain
Factor Xa function:
Increas permeability, WBC exudation)
Summary of chemical mediators:
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Neutrophil defects e.g:
Failure of neutrophils to respond to chemotacic stimuli in diabetes
Failure of neutrophils to phagocytized due to:
Diabetics, complements and Ig deficiencies.
Too few circulating neutrophils “neutropenia”; as in:
Radiation injury and cancer therapy.
Neutrophil adherence molecule defects due to:
Heredity, glucocorticoid administration, diabetes, or ethanol in the bloodstream
Defective microbial killing due to :
Insufficient production of H2O2 in “chronic granulomatous disease” of childhood.
there are too few neutrophils, they do not respond properly to chemotactic stimuli, and their lysosomes fail to fuse with phagosomes
Which diease?
Chediak-higashi syndrome
Types of acute inflammation
Nonsuppurative
Suppurative(septic or pyogenic)
Suppurative or purulent inflammation characterized by:
Production of pus or purulent exudateby pyogenic organism.
E.g of suppurative inflammation:
Appendicitis, pneumonia, folliculitis(infection of hair folicle) and furuncle or boil(suppurative infection of subcutaneous tissue)
Cellulitis or phlegmon
Abscess : localized collection of pus
Sinus
cellulitis(phlegmon)?
Spreads rapidly to large areas of tissue e.g entire arm.
What is the sinus?
An abnormal connection (lined by granulation tissue) b/w a deep seated abscess and the skin or mucosal surface e.g osteomyelitis
Pus forming:
Microorganisms, liquefied necrotic tissue, inflammatory exudate, polymorphs, pus cells, RBC’s Macrophages
Mild non suppurative infla.. characterized by Excessive accumulation of fluid with variable protein content but no fibrin due to modest increase in VP
Serous inflammation
Sites of serous inflammation :
Serous cavities called effusions
Skin e.g mild burn and blisters
Sites of catarrhal inflammation:
Any mucous membrane, nasal passages, bronchi, GIT
Mild non suppurative infla… characterized by excessive mucous secretion
Catarrhal inflammation
Moderate non suppurative infla… characterized by excessive accumulation of fluid exudate rich in fibrin due to marked increase in VP:
Serofibrinous and fibrinous inflammation
Sites of serofibrinous inflammation:
Serous cavities, joints and lung alveoli
Severe non suppurative infla.. characterized by formation of false membrane on mucus suface
Membranous inflammation (pseudomembranous)
Sites and consequences of membranous inflammation:
Larynx》Diphtheria
Colon》bacillary dysentry
Uterus》puerperal sepsis
Pathogenesis of membranous inflammation:
Bacteria remain on the mucosal surface and produce powerful exotoxin 》patchy mucosal necrosis and acute inflammation of underlying tissues
Gross and microscopic pic of memebranous and serofibrinous inflammation:
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Severe non suppurative infla.. characterized by an exudate rich in RBCs usually associated with vascular damage:
Hemorhagic inflammation
Mild to severe inflammation due to hypersensitivity reaction:
MP: Exudate rich eosinophils
Allergic inflammation
Severe acute inflammation complicated with superadded necrosis amd putrefaction of tissues
Gangrenous (necrotizing) inflammation
E.g of gangrenous inflammation
Gangrenous appendicitis, gangrenous pneumonia
Septicemia “sepsis” means:
Bacteria actually multiplying in the bloodstream along with their toxins.
Systemic inflammatory response syndrome
Represents toxicity from excessive production of the cytokines and/or other white-cell products.
Define ulcer?
A discontinuity of the surface epithelium
Is a local defect or excavation of a surface of an organ or tissue that is produced by shedding of inflammatory necrotic tissue
When unlcer is formed?
When necrosis has involved a body surface and portion of it is sloughed.
Diff b/w ulcer and erosion
In ulcer, there must be necrosis of both the epithelium and at least some of the underlying connective tissue.
If there is necrosis only of the epithelium, we call it an EROSION
E.g of ulcer deu to specific micro-organism
Syphilitic, tuberculous (lupus valgaris), soft chancre, Actinomycosis, Tropical ulcer (lishmaniasis) and typhoid ulcer in smooth intestine
Malignant ulcers
Rodent ulcer
Ulcerating adenocarcinoma
Margolin’s ulcer
Edge is the best site for biopsy in:
Malignant ulcer
Other special types of ulcer:
Peptic ulcer
Cushing’s ulcer
Curling’s ulcer
Define fistula and give e.g
An abnormal communication b/w two epithelial surfaces
E.g: recto-vesical fistula, recto-vaginal fistula and vesico-vaginal fistula
Systemic effects of fistual:
Fever, malaise, loss of appetite Leucocytosis WBCs>12,000 Extreme elevation of WBC count is refered to as leukemoid reaction Certain infections are associated with leukopenia e.g typhoid fever Change in plasma protein level \+++ ESR \+++ C-reactive protein
What is the leukemoid reaction?
Non-leukaemic condition giving rise to a peripheral blood picture resembling that of leukaemia
Leukemoid reaction characterized by:
Marked elevation of WBC upto 200,000 mm3 and immature cells..
Diagnosis of Leukemoid reaction:
By doing neutrophil alkaline phosphatase staining
Consequences of acute inflammation:
Complete resolution
Healing by scarring
Abscess formation
Progression to chronic inflammation
Progression of acute inflammation to chronic occurs when:
- Persistence of injurious agent
2. Interference in the normal process of healing
Abscess formation occurs in:
Infection with pyogenic organism
Scarring means:
Laying-down of dense (type 1) collagen
Scar tissue is formed by fibroblasts
What is chronic inflammation?
Is an inflammation of prolonged duration (weeks to months to years) in which active inflammation, tissue injury, damage and healing proceed stimultaneously
