Acute Inflammation Flashcards by G V

Endogenous Chemoattractants (3)

Leukotrine B4
C5a
IL-8

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Hallmark of Acute Inflammation (4)

Vasodilation
Increased vascular permeabilty
Exudate formation
Entry of neutrophils to the site of injury

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Vascular Events (3)

Vasodilation of arterioles
Increased permeability of venules
Slowing of blood flow

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Cardinal Signs

Rubor (histamine mediated vasodilation )
Calor (histamine mediated vasodilation)
Tumor (histamine dependent)
Dolor (PGE2 and Bradykinin, PGE2 has stronger)
Loss of function

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Cellular Events

Leukocyte extravasation

Phagocytosis

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Important opsonins

C3b

IgG

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Bruton’s Agammaglobulinemia (recognition and attachment for

Defective IgG receptor, so reduced IgG

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Chediak-Higashi Syndrome (engulfment)

A defect in membrane fusion prevents phagolysosome formation

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Microbial Killing: O2 dependent patway

H2O2-MPO-halide system
Killing of bacteria by ROS and
NAPDH Oxidase, etc. (refer to nt

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Microbial Killing: O2-INDEPENDENT pathway enzymes (4)

Lactoferrin
Major Basic Protein (eosinophil cytotoxic to helminths)
Lysozyme
Bacterial Permeability Increasing Protein (BPI)

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Neutrophil (PMN): Primary (Azurophilic) Granules

Myeloperoxidase

Lysozyme

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Neutrophil (PMN): Secondary (specific) Granules

Lactoferrin 
Leukocyte Alkaline Phosphatase (LAP) 
  Seen in normal PMNS 
  Benign process: high LAP 
  Malignant: Low LAP

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Defects in Neutrophil (PMNs, 4)

CGD of Childhood
Myeloperoxidase Deficiency
Chediak-Higashi Syndrome
LAD 1 and 2

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Defects in Neutrophil: CGD of Childhood

Phagocytic cells INGEST BUT DON’T KILL

Catalase + organisms (staph aureus): they produce catalase that destroys the bacterial H202 (because PMN doesn’t produce H202)

NBT Test –> NEGATIVE

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Defects in Neutrophil: Myeloperoxidase Deficiency

Infections with candida

NBT TEST IS POSTIVE (normal)

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Defects in Neutrophil: Chediak-Higashi Syndrome

A defect in membrane fusion prevents phagolysosome formation (engulfment)
NeutroPENIA
Albinism
Cranial & Peripheral Neuropathy

Abnormal microtubule formation (functional mark)
Large cytoplasmic granules representing abnormal lysosomes (morphological mark)

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Defects in Neutrophil: LAD Type 1

Defect in CD 11/18/ (beta 2 integrain), LFA-1, Mac-1

Example: delayed separation of umbilical cord, increased neutrophils, recurrent bacterial infections that lack pus formation

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Defects in Neutrophil: LAD Type 2

Absence of Sialyl-Lews on neutrophils

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Plasma Derived Chemical Mediators (3)

Kinin System
Clotting System
Complement System

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Cell Derived Chemical Mediators (4)

Vasoactive amines - (Histamine and Serotonin)
AA metabolites
Cytokines
Other

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Cell Derived Chemical Mediators - Vasoactive Amines

Histamine
Serotonin
Caricinoid syndrome

Plasma Derived Chemical Mediators - Bradykinin effects (under Kinin system, 4)

Pain (dolor)
Increases vascular permeability
Vasodilation
Bronchoconstrictor

Plasma Derived Chemical Mediators - The Kinin System

Intiated by ACTIVATED Hageman factor 12

Factor 12 initiates

Kinin system, coagulation, and the plasminogen complement systems

Other Mediators of Acute Inflammation: PAF

Derived from basophils, mast cells, and enthothelial cells Actions: Activates and aggregates platelets, activates arachidonic acid metabolism

Other Mediators of Acute Inflammation: Nitric Oxide

Produced by endothelial cells Stimulates relaxation of smooth muscles (vasodilation), this inhibiting platelet aggreggation Important in endotoxic shock

Other Mediators of Acute Inflammation: Chemokines

Activate and attract leukocytes IL-8 MCP-1 Eotaxin

Other Mediators of Acute Inflammation: Lysosomal Constituents

In granules of neutrophils and monocytes 2 types: Acid proteases (in phagolysosomes) and neutral proteases (active in extracellular matrix, for tissue injury) Proteases controlled by: alpha 2 macroglobulin and alpha 1 anti-trypsin (panlobar emphysema)

Other Mediators of Acute Inflammation: O2-derived free radicals

From NADPH oxidase pathway Include: superoxide, hydroxyl, H2O2 Small dose amplification of inflammatory response Tissue injury: large doses (neutralize alpha-2 macroglobulin and A1-AT (from lysosomal protease constituents)) Protection: antioxidant mechanisms (catalase, superoxide dismutase, and glutathione)

Exogenous chemotactants

Bacterial products (e.g. N-formyl methionine)

Complete System Pathology Diseases (2)

Paroxysmal Nocturnal Hemoglobinuria | Hereditary Angioedema

Paroxysmal Nocturnal Hemoglobinuria

complement mediated lysis of RBCs Defect/lack of DAF and CD59

Hereditary Angioedema

Deficiency of C1 inhibitor

Overall Outcome of Acute Inflammation (3) 1

1. Complete resolution 2. Healing by Fibrosis 3. Abscess 4. Progression to chronic inflammation

Overall Outcome of Acute Inflammation: Complete Resolution

Regeneration of damaged epithelium WITHOUT SCAR TISSUE FORMATION Restores structure and fxn of tissue

Overall Outcome of Acute Inflammation: Healing by Fibrosis

Organization and repair WITH SCAR TISSUE FORMATION Scar tissue laid down by FIBROBLASTS (distorts structure and fxn)

Overall Outcome of Acute Inflammation: Abscess

Tissue destruction and persistent acute inflammation | Pus from pyogenic bacteria

Overall Outcome of Acute Inflammation: Progression to Chronic Inflammation

When acute inflammation can't remove noxious agents Marked by: Replacement of PMNS by macrophages, lymphocytes, and plasma cells Angiogenesis Healing by fibrosis

Serous Inflammation

Outpourig of thin protein poor water fluid ``` Skin blister Body cavities (effusions) ```

Fibrinous inflammation

Protein rich fluid (fibronogen) that has bread and butter appearance Fibrinous pericarditis (shaggy, fibrinous exudate)

Suppurative (purulent) Inflammation

Production of pus Staphylococcus Abscess Suppurative conjunctivitis Suppurative meningitis Lung abscess White and milky on surface it adheres to like eye or brain

Catarrahal Inflammation

Excessive mucus secretion Runny nose from rhinoviral infection

Cellulitis

Thin, watery exudate that spreads throughout subcutaneous tissues (usually from STREPTOCOCCUS which has hyaluronidase) Erysipelas and Impetigo

Pseudomembranous Inflammation

Toxin induced --> resulting in necrotic membrane formation E.g. psedomembrane of diphtheria (thick, gray coating on BACK OF THROAT) Pseudomembranous colitis from C. Difficile

Ulcers

Agend prudicing defect in the epithelial lining of skin or mucosa Ulcer is a loss of continuity of skin or mucosa due to sloughing of inflammatory necrotic tissue Peptic ulcer from H. Pylori induced cytokine damage

Exceptions to Acute Inflammatory by PMNS: Acute Inflammation from Viruses (viral hepatitis)

Principal cells: lymphocytes

Exceptions to Acute Inflammatory by PMNS: Allergic rxns and parasitic infections

Eosinophils dominate from start to finish

Exceptions to Acute Inflammatory by PMNS: Acute dermatitis

Lymphocytes predominate

Exceptions to Acute Inflammatory by PMNS: Whooping Cough (Bordetella pertussis)

Lymphocytes prodominate

Exceptions to Acute Inflammatory by PMNS: Gas gangrene (Clostridium)

Little to no PMNS