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inflammation Flashcards

1
Q

sequence of events

A

-NORMAL HISTOLOGY ->
-VASODILATATION ->
-INCREASED VASCULAR PERMEABILITY ->
-LEAKAGE OF EXUDATE ->
-MARGINATION, ROLLING, ADHESION ->
-TRANSMIGRATION (DIAPEDESIS) ->
-CHEMOTAXIS ->
-PMN ACTIVATION ->
-PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) ->
-TERMINATION ->
-100% RESOLUTION, SCAR, or CHRONIC INFLAMMATION are the three possible outcomes

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2
Q

acute inflammation

A

-1. VASCULAR EVENTS
-2. CELLULAR EVENTS (PMN or PolyMorphonuclear Neutrophil)

-“MEDIATORS”

-Neutrophil
-Polymorphonuclear Leukocyte, PMN
-“Leukocyte”
-Granulocyte, Neutrophilic granulocyte
-Polymorph

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3
Q

stimuli for acute inflammation

A

-infection
-physical
-chemical
-tissue necrosis
-foreign bodies (FBs)
-immune “responses”, or “complexes”

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4
Q

vascular changes

A

-1. Increased Vascular Permeability
-Occurs BEFORE inflammatory cells arrive
-dilation causes slowing down of blood -> margination, stasis, edema
-2. LEAKAGE of proteinaceous fluid (exudate NOT transudate)
-cells leave the vessel lumen to go to the site of injury

….cellular response happens next

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5
Q

cellular response in inflammation overview

A

-immune cells move out of the vessel lumen to site of cellular injury
-Mediated and controlled by adhesion molecules and cytokines
-Step 1: MARGINATION- neutrophils go toward inner wall of vessel
-Step 2: ROLLING- slow down, tumbling and HEAPING
-Step 3: ADHESION- go to area to leave inside the vessel
-Step 4: TRANSMITIGATION- leave, diapedesis
-Step 5: CHEMOTAXIS- neutrophils go to site of injury down chemical gradient

-step 1-3- in vessel lumen
-step 4-5- through the lumen and to the site of injury

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6
Q

adhesion molecules (glycoproteins) affecting adhesion and transmigration!!!!

A

-secretins- rolling -> slow down WBC to go where they need to go
-integrins- adhesion -> help cells go to area to leave the vessel

-KNOW THIS

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7
Q

leukocyte activation

A

-“triggered” by offending stimuli for PMNs to:
-1) Produce arachidonic acid derivatives:
-Prostaglandin (and thromboxanes)
-Leukotrienes

-2) Undergo DEGRANULATION
-3) Secrete CYTOKINES- proteins that send messages

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8
Q

phagocytosis!

A

-eat up bacteria
-RECOGNITION (opsonization)
-opsons coat bacteria -> neutrophil eat it

-ENGULFMENT-
-Ingestion – engulfed microbes form phagosomes which fuse with lysosomes: phagolysosomes -> Dependent on polymerization of actin

-KILLING- (DEGRADATION/DIGESTION)

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9
Q

PMN granules: primary and secondary

A

-dont need to memorize everything

-PRIMARY
-Also called AZUROPHILIC, or NON-specific
-Myeloperoxidase (MPO)!!!!!- A KILLER
-Lysozyme (Bact.)
-MPO produces Hypochlorous acid and tyrosyl radicals, arecytotoxic, used by the neutrophil to killbacteriaand otherpathogens
-makes pus look greenish yellow.

-SECONDARY
-Also called SPECIFIC
-Lactoferrin
-Lysozyme
-Alkaline Phosphatase
-Collagenase

-Lysozymes, are a family ofenzymeswhich damage bacterial cell walls by causinghydrolysis.

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10
Q

phagocytosis- killing

A

-dont memorize details of mechanisms

-ROS (reactive oxygen species):
-NADPH oxidase
-Superoxide dismutase
-Myeloperoxidase

-ROS made within lysosome -> phagolysosome -> ingest particles without damage to host cells
-ROS damage cells via membrane damage, altering protein, and DNA breakage

-Nitric oxide synthetase: also damage cells
-Lysosomal enzymes: also cause damage but controlled by anti-proteases like alpha-antitrypsin

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11
Q

free radicals

A

-O2 – (SUPEROXIDE)
-H2O2 (PEROXIDE)
-OH- (HYDROXYL RADICAL)

-VERY DESTRUCTIVE
-bad for you

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12
Q

Chronic granulomatous disease: absent NADPH oxidase

A

-Genetic
-dont have NADPH oxidase
-Catalase positive organisms ingested but not killed (S. aureus,eg)
-Catalase negative organisms are killed (MPO converts peroxide made by the organism)

-Increased susceptibility to infections, especially from catalase-positive organisms.
-Formation of granulomas -> clusters of immune cells that form in response to chronic infection or inflammation

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13
Q

chemical mediators

A

-from plasma or cells
-have triggering stimuli
-usually have specific targets
-can cause a cascade
-are short lived

-histamine- vasodilation
-serotonin
-complement
-bradykinin- pain
-coagulation cascade
-prostaglandins
-leukotrienes
-lipoxins
-platelet activating factor
-cytokines

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14
Q

histamine

A

-mast cells, basophils
-POWERFUL vasodilator
-vasoactive “amine”

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15
Q

complement system

A

-20+ soluble proteins, host defense against microbes
-WANTS TO LYSE THE MICROBE
-3 PATHWAYS COME TO C3 -> C3A AND C3B -> AT THE END YOU GET C5B-9 -> THIS CAUSES CELL LYSIS
!!!!!!!!

-vascular permeability, chemotaxis, and opsonization
-Complement fixation is end stage -> lysis of cell membranes

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16
Q

complement cleavage products

A

-C3a, C5a, (and C4a) : stimulate histamine and cause increased vascular permeability and vasodilation - known as anaphylatoxins
-C3b : opsonization and phagocytosis
-C5b-9: formation of MAC (membrane attack complex), lysis of microbe

17
Q

infection and inflammation

A

-infections always cause inflammation
-inflammation doesnt only happen from infection

18
Q

bradykinin

A

-Kinins - vasoactive peptides from kininogens (plasma proteins) via kallikreins (enzyme proteases)
-Factor XIIa (from clotting cascade) converts prekallikrein to enzyme kallikrein which cleaves HMW kininogen into bradykinin

-Bradykinin:
-Implicated in anaphylaxis
-Inactivated by kininase
-!Increases vascular permeability
-Potent endothelium-dependent vasodilator, causes contraction of !non-vascular smooth muscle
-!pain

19
Q

clotting factors

A

-Also from circulating plasma
-Coagulation, i.e., production of fibrin
-Fibrinolysis
-coagulation is also a cascade like complement fixation

20
Q

arachidonic acid metabolites: prostaglandin

A

-PROTAGLANDINS COME FROM FATTY ACIDS

21
Q

mediators of inflammation chart

A

-just recognize there is a lot of overlap here

22
Q

cytokines/chemokines

A

-CYTOKINES
-little proteins
-PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES
-many roles in acute and chronic inflammation
-mediators
-tumor necrosis factor, IL-1

-Examples include TNF-alpha and Interleukin-1
-TNF or cachectin- destroys tissues
-key player in “cachexia”

-Interleukin-1- propagates inflammatory response at many levels
-has a significant effect on T-cells

-CHEMOKINES are small proteins which are attractants for PMNs

23
Q

cytokines chart: TNK and IL-1

A

-TNK and IL-1 know them

24
Q

outcomes of acute inflammation

A

1) 100% complete RESOLUTION

2) SCAR
-ex. heart can cell replicate cardiac cells -> scar

3) CHRONIC inflammation

25
Q

morphologic patterns of acute inflammation (exudate)!!

A

-Serous (watery)- blister
-Fibrinous (hemorrhagic, rich in FIBRIN)- pericarditis (bread and butter)
-Suppurative (PUS)- abscess, pus (exudate)
-Ulcerative

26
Q

acute vs chronic inflammation

A

-acute- neutrophils

-CHRONIC
-monocytic cells- 1 nucleus
-lymphocytes!!!!!!
-monocytes (blood)!!!!!!!!
-macrophage (tissue
-histiocyte- tissue cell
-plasma cells
-eosinophils- least frequent

27
Q

causes of chronic inflammation

A

1) PERSISTENCE of Infection
2) PROLONGED EXPOSURE to insult
3) AUTO-IMMUNITY

28
Q

granulomas

A

-Aggregation of macrophages
-forms in response to chronic inflammation.
-immune system attempts to isolate foreign substances that its otherwise unable to eliminate like -> infectious organisms (bacteria (TB) and fungi), foreign objects, keratin, and suture fragments

-4 COMPONENTS
-Histiocytes (macrophages)
-FIBROBLASTS
-LYMPHS
-“GIANT” CELLS

29
Q

granulomatous inflammation

A

CASEATING (TB) - necrotizing
NON-CASEATING – non-necrotizing

30
Q

systemic manifestations (non-specific) of chronic inflammation

A

-FEVER, CHILLS
-C-Reactive Protein (CRP)- acute phase reactant; levels rise dramatically during inflammatory processes in body
-assist in complement binding to foreign and damaged cells and affect the humoral response to disease.
-plays important role in innate immunity, as early defense against infections

-“Acute Phase” Reactants
-Erythrocyte Sedimentation Rate (ESR) increases
-Leukocytosis
-Pulse, Blood Pressure
-Cytokine Effects, e.g., TNF(α), IL-1

31
Q

acute and chronic inflammation chart

A

-monocytosis- cells with 1 nucleus (lymphocytes as well)

patho (11 decks)

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