Key 2- Inflammation, Apoptosis and necrosis Flashcards
The alternative pathway, which can be triggered by…………………
microbial surface molecules (e.g., endotoxin, or LPS), complex polysaccharides, cobra venom, and other substances, in the absence of antibody.
Leukotriene B4 = FUNCTION?
Chemotaxis
Leukotriene C4, D4, E4 …FUNCTIONS? (AGGRAVATED IN ASPIRIN USE)
Broncho Constriction- smooth muscle
(NON-ATOPIC ASTHMA)
THROMBOXANE a2- FUNCTION?
PROMOTE PLATELET AGGREGATION
STOP THIS MEDICATION TO PREVENT CLOT!!
CONTRACTION OF SMOOTH MUSCLE IS CAUSED BY?
PG
MUSCLE WASTING, DEATH IN CANCER PATIENT (MEDIATOR)?
Tumor necrosis factor-alpha
PROSTACYCLIN FUNCTION?
VASODILATATION
(ALSO NITRIC OXIDE)
and
Inhibit platelet Aggregation
Interleukin-1 FUNCTION?
- Acute phase reaction (eg: fever)
- Endothelial effect (Leukocyte adhesion, pro & anticoagulant effect)
- Fibroblast Effect (collagen synthesis – scar)
BAD!!!, IS NOT IT?
MEDIATOR ACTIVATE MACROPHAGE?
Interferon-gamma FROM CD4 CELLS
(ALSO IL-12 CAUSES INCREASED PRODUCTION OF INF)
MEDIATOR, THAT INCREASES SAA, FIBRINOGEN, CRP IS?
IL-6
TEST ESR!
NEUTROPHIL’S Specific (or secondary) granules PRODUCE?
Lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and alkaline phosphatase.
NEUTROPHIL’S Azurophil (or primary) granules PRODUCE?
Myeloperoxidase (THINK P-ANCA), bactericidal factors (lysozyme=THINK ABSCESS FORMATION), defensins).
MACROPHAGE AND LIQUIFRACTIVE NCROSIS IN BRAIN- DISCUSS
– acid proteases (only active within lysosomes).
– neutral proteases such as elastase and collagenase are destructive in ECM.
Typical in Liquefactive necrosis- BRAIN
C3a, C5a: ==?
stimulate histamine release from mast cells and thereby increase vascular permeability and cause vasodilation
C5a:===?
chemotactic agent for neutrophils, monocytes, eosinophils, and basophils
Opsonization and phagocytosis: ?
C3b AND IG
MAC (MEMBRANE ATTACH COMPLEX)- deficiency of the terminal components of complement predisposes to ………………..infections.
Neisseria
MAC•This tube LIKE STRUCTURE forms a channel allowing the passage of ions and small molecules. Water enters the cell by ……………and the cell lysis.
THIS PROCESS SEEN IN WHICH CONDITIONS?
….Osmosis
A-In immune hemolysis (MISMATCHED BLOOD TRANSFUSION)
A-PNH
•C1 inhibitor (C1 INH)
–blocks the activation of C1, the first protein of the classical complement pathway. Inherited deficiency of this inhibitor is the cause of …………………….
hereditary angioedema
•Decay-accelerating factor (DAF) and CD59
–DAF prevents the formation of ……………………..and CD59 inhibits the formation of the ………………………
•An acquired deficiency of the enzyme leads to excessive …………………activation and lysis of red cells in the disease called ………………………..
C3 convertases, membrane attack complex (C5b-9)
complement, paroxysmal nocturnal hemoglobinuria (PNH)
HISTAMINE (Mast CELL-DERIVED/PREFORMED GRANULES)- FUNCTIONS?
EARLY VASODILATION AND PERMEABILITY
OTHER FUNCTIONS=
–physical injury, such as trauma, cold, or heat, BEE STRING,
–binding of antibodies to mast cells, which underlies immediate hypersensitivity (allergic) reactions [(ASTHMA EARLY PHAGE MEDIATOR)] and
–products of complement called anaphylatoxins (C3a and C5a)
–Neuropeptides (e.g., substance P) and cytokines (IL-1, IL-8) may also trigger the release of histamine
PAF FUNCTION-…………?
PLATELET ACITIVATION, VASODILATION AND PERMEABILITY
Kinins FUNCTIONS?
Increased vascular permeability, smooth muscle contraction, vasodilation, pain
Lipoxygenase inhibitors. 5-lipoxygenase is not affected by …………………
NSAIDs
DIAGNOSIS?
COAGULATIVE NECROSIS
FATE- SCAR
MECHANISM?
NEUTROPHIL LYSOZYME INDUCED NECROSIS
HISTOLOGICAL FINDING: COAGULATIVE NECROSIS AND BLOOD=…?
REPERFUSION INJURY
DIAGNOSIS?
NON CASEATING GRANULOMA
The destruction of cells during embryogenesis…?
APOPTOPSIS
Involution of hormone-dependent tissues upon hormone withdrawal…?
APOPTOSIS
Formation of cytoplasmic blebs IN SINGLE CELL..?
APOPTOSIS
Phagocytosis of apoptotic cells or cell bodies, usually by ………………
macrophages
Anti-apoptotic. …..GENES?
BCL2, BCL-XL
Pro-apoptotic………………..
BAX and BAK
APOPTOSIS: The best-known death receptors are the …………….receptor
type 1 TNF
The mitochondrial pathway leads to activation of the initiator caspase-……
9
Executioner caspases, such as ……………………, act on many cellular components
caspase-3 and -6
However, if the DNA damage is too great to be repaired successfully, ……………..triggers apoptosis.
p53
Once released into the cytosol, …………………….binds to a protein called APAF-1 (apoptosis-activating factor-1), forming a multimeric structure called the apoptosome AND START THE PROCESS OF APOPTOSIS
cytochrome c
FasL is expressed on T cells that recognize self-antigens (and functions to eliminate self-reactive lymphocytes). AN EXAMPLE OF THIS PROCESS IS?
cytotoxic T lymphocytes (which kill virus-infected and tumor cells).
(Steps of apoptosis =intrinsic)?
IMPORTANT TO KNOW!!!
DNA DAMAGE- BCL2 INACTIVATION- BAX ACTIVATION- RELEASE OF CYTOC- ACTIVATION OF CASPASE 9- ACTIVATION OF CASPASE 3/6- ENDONUCLEASE ACTIVATION- APOPTOSIS
SAD!!!
VIRUS INFECTION- FAS+TNF1 INTEGRATION- ACTIVATION OF CASPASE 8/10- ACTIVATION OF CASPASE 3/6- ENDONUCLEASE ACTIVATION- APOPTOSIS
RECALL CD8 CELL FUNCTION :)
= THIS PROCESS IS KNOWN AS—?
The Extrinsic (Death Receptor-Initiated) Pathway of Apoptosis!
KNOW THIS!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
SUN EXPOSED SKIN BIOPSY FINDING.
WHATS THE MECHANISM OF THIS FORMATION OF THIS PINK CELL
APOPTOSIS VIA INTRINSIC PATHWAY!!!
PINK CELLS- SEEN IN HEPATITIS B VIRAL INFECTION (IMAGE).
NAME THE CELL?
MECHANISM?
COUNCILMAN BODY
APOPTOSIS EXTRINSIC PATHWAY!!!
Steps of the vascular event of acute inflammation?
- The release of mediators, notably histamine
- Vasodilation
- Increased blood flow
- Increased permeability of the microvasculature
- Slowing of blood flow
- Stasis
- Loss of axial flow
- Margination
Steps of the cellular event of acute inflammation?
- Margination-
- Rolling
- Activation (Neutrophils)
- Adhesion (Including firm adhesion)
- Diapedesis of neutrophils- transmigration (part of migration)
- Chemotaxis (part of migration))
- and Phagocytosis
