A/22-25 INFLAMMATION (Tamer) Flashcards
Sequence of events in acute inflammation
Margination, Rolling, Adhesion –>Transmigration (DIAPEDESIS) –>Chemotaxis --> PMN activation–> Phagocytosis–>Termination
three possible outcomes:
- 100% Resolution
- Scar
- Chronic inflammation
give at least 3 stimuli for acute inflammation
- *-INFECTIOUS**
- *-PHYSICAL**
- *-CHEMICAL**
- Tissue Necrosis
- Foreign Bodies (FBs)
- Immune „responses” or „complexes
what is the purpose of the vascular reactions during acute inflammation ?
The purpose of the inflammatory vascular reaction is to deliver the humoral and cellular factors to the site of defence reaction
mention the vascular events of inflammation
Changes in vascular flow and caliber
Changes in vascular permeability
steps of EXTRAVASATION of PMNs
- MARGINATION- (PMN’s go toward wall)
- ROLLING (tumbling and HEAPING)
- ADHESION
- TRANSMIGRATION (DIAPEDESIS)
mention 2 types of molecules important for adhesion
-Selectins (E,P and L) from endothelial cells
-Integrins from many cells (ICAM, VCAM)
Transmigration is mediated by
CD31
upon activation of leukocytes
1) Produce Eicosanoids (arachidonic acid derivatives)
- Prostaglandin/thromboxanes
- Leukotrienes
- Lipoxins
2) Undergo DEGRANULATION
3) Secrete CYTOKINES
Steps of Phagocytosis
• RECOGNITION
• ENGULFMENT
• KILLING
(oxygen dependent and independent mechanisms)
give at least 3 general features of chemical mediators
1) From plasma or cells
2) Have triggering stimuli
3) Usually have specific targets
4) Can cause a cascade
5) Are short lived
Name at least 3 classic chemical mediators
–Histamine
- Serotonine
- Complement
- Kinins
- Clotting factors
where is histamine released from ? what is its function ?
released from Mast Cells, Basophils
• POWERFUL Vasodilator
- IgE on mast cell
- (Vasoactive „amine”)
where is Serotonin released from ? what is its function?
SEROTONIN • (5HT, 5-Hydroxy- Tryptamine)
- Platelets and EnteroChromaffin Cells release it
- vasodilatation, but more indirect
- Evokes N.O. synthetase (a ligase-from argenine)
give at least 3 general features of the complement system
- >20 components, in circulating plasma
- Multiple sites of action, but LYSIS is the underlying theme
give at least 3 general features of the KININ SYSTEM
• BRADYKININ is KEY component,
• from circulating plasma
• ACTIONS
− Increased permeability
− Smooth muscle contraction, NON vascular
− Pain
give 3 features of CLOTTING FACTORS
- from circulating plasma
- Coagulation, i.e., production of fibrin
- Fibrinolysis
mention 3 EICOSANOIDS
(ARACHIDONIC ACID DERIVATIVES)
• Part of cell membranes •
1) Prostaglandins (incl. Thromboxanes)
2) Leukotrienes
3) Lipoxins (new)
3 functions of PROSTAGLANDINS
(THROMBOXANES INCLUDED)
- Pain
- Fever
- Clotting
give 3 function of LEUKOTRIENES
- Chemotaxis
- Vasoconstriction
• Increased Permeability
give 3 function of LIPOXINS
- INHIBIT chemotaxis
- Vasodilatation
- Counteract actions of leukotrienes
GIVE 3 FEATURES OF PLATELET-ACTIVATING FACTOR (PAF)
- ITS A Phospholipid
- From MANY cells, like eicosanoids
- ACTIVATE PLATELETS, powerfully
WHAT ARE CYTOKINES AND CHEMOKINES?
GIVE 2 EXAMPLES OF CYTOKINES
• CYTOKINES are PROTEINS produced by LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation -
TNFa, IL-1 by macrophages
• CHEMOKINES are small proteins which are attractants for PMNs (>40)
GIVE 2 FEATURES OF NITRIC OXIDE
- Potent vasodilator
- Produced from the action of nitric oxide synthetase from arginine
GIVE AT LEAST 3 EXAMPLES OF PRIMARY LYSOMAL CONSTITUENTS
(A.K.A AZUROPHILIC, or NON-specific )
- Myeloperoxidase
- Lysozyme (Bact.)
- Acid Hydrolases
GIVE AT LEAST 3 EXAMPLES OF SECONDARY LYSOMAL CONSTITUENTS (Also called SPECIFIC)
- Lactoferrin
- Lysozyme
- Alkaline Phosphatase
- Collagenase
NAME 3 FREE RADICALS
HOW DESTRUCTIVE ARE THEY ?
- O2 –(SUPEROXIDE)
- H2O2 –(PEROXIDE)
- OH- –(HYDROXYL RADICAL)
VERY VERY DESTRUCTIVE
SYSTEMIC EFFECTS OF INFLAMMATION
-ACUTE PHASE PROTEINS
bind microbial cell walls and may act as opsonin and fix complement . also bind chromatin aiding in clearing of necrotic cell nuclei
e.g. CRP , fibrinogen , SAA
-LEUKOCYTOSIS - white cells (the leukocyte count) increased above the normal range in the blood .
(15,000-20,000 cells/microliter sometimes >40,000)
especially seen in bacterial infection (neutrophillia) but also in bone tumors as well as leukemia.
- others :
- increased TNF (in sepsis) will cause DIC –> thrombosis
- cytokines injure the liver- Hypoglycemia
- cytokines induce over production of NO by cardiac myocytes and vascular smc’s –> Heart failure ,Loss of Perfusion Pressure (respectively) –> HEMODYNAMIC SHOCK
All together - heart failure , hypoglycemia , hemodynamic disorders –> SEPTIC SHOCK
prolonged production of acute phase proteins may lead to what disorder?
secondary amyloidosis in chronic inflammation (especially SAA)
elevated serum CRP is used as a marker for what ?
A high level of CRP in the blood is a marker of inflammation. for example inflammation of the blood vessels of the heart which can mean increased risk of myocardial infarction .
Classification of acute inflammation is based on what ?
exudate
Name at least 3 types of exudate and give their morphological description home boii
assuming that sarah loves big dicks we can use the following mnemonic
“Sarah Fucks Paul Hard & Good”
Serous
seen in mild inflammation, relatively low protein. consistency resembles that of serum, usually seen in diseases like TB.
Common cold,
pleuritis exs
burns
catarrhal inflammation of mucous membranes
Fibrinous
composed of fibrinogen and fibrin. seen in severe injuries difficult to resolve due to blood vessels growing into the exudate filling space that was occupied by fibrin. large amounts of antibiotics for resolution.
exudate may be degraded by FIBRINOLYSIS
Serous membranes:
Pleuritis/pericarditis sicca,
Peritonitis fibrinosa
Mucous memebranes:
Diphtery -PSEUDOMEMBRANE
typhoid fever
dysentery
Purulent
morphology : consists of plasma with active/dead neutrophils, fibrinogen, and necrotic parenchymal cells. found in more severe infections (s.pyogenes) , and is referred to as pus (whitish-yellow)
folliculitis, furuncule, carbuncule
Abscess: circumscibed pus in parenchymal organs Empyema: circumscribed pus in preformed body cavity(e.g. pleura)
Phlegmone: inflammation spreading in tissue spaces
Haemorrhagic
plague
smallpox
anthrax
flu
Gangraenous - failure of inflammation
what’s an Ulcer ? where is it common ?
local defects on the surface of an organ produced by inflammation.
common sites - stomach , intestines
acute stage - infiltration of pmns+vasodilation
long term - infiltration of lymphocytes ,plasma cells,macrophages +fibroblastic proliferation,scarring
what’s chronic inflammation ?
is a response of prolonged duration(weeks or months) in which inflammation,tissue injury, and repair coexist, in varying combinations.
“proliferative” rather than “exudative”
give at least 3 causes of chronic inflammation
- Persistent infections
- Hypersensitivity diseases - autoimmune diseases
-Prolonged exposure to toxic agents
(exogenous/endogenous)
- in neurodegenerative diseases,metabolic syndrome ,type 2 diabetes, certain cancers
- Foreign bodies
name at least 3 cellular players in chronic inflammation
- macrophages- The dominant cells in most chronic inflammatory reactions , derive from monocytes , once monocyte are in the extravscular tissue they become macrophages which have longer half life and higher phagocytic capacity
- lymphocytes- provides defense against infectious pathogens
- plasma cells- In immune reactions mediated by IgE and in parasitic infections
- eosinophils
- mast cells
give at least 3 Morphological Features of chronic inflammation
- Not exsudative
- Infiltration with mononuclear cells
- Tissue destruction
- Attempts of healing
