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M3 Path B1 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Endogenous Chemoattractants (3)

A

Leukotrine B4
C5a
IL-8

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2
Q

Hallmark of Acute Inflammation (4)

A

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

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3
Q

Vascular Events (3)

A

Vasodilation of arterioles
Increased permeability of venules
Slowing of blood flow

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4
Q

Cardinal Signs

A

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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5
Q

Cellular Events

A

Leukocyte extravasation

Phagocytosis

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6
Q

Important opsonins

A

C3b

IgG

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7
Q

Bruton’s Agammaglobulinemia (recognition and attachment for

A

Defective IgG receptor, so reduced IgG

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8
Q

Chediak-Higashi Syndrome (engulfment)

A

A defect in membrane fusion prevents phagolysosome formation

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9
Q

Microbial Killing: O2 dependent patway

A

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

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10
Q

Microbial Killing: O2-INDEPENDENT pathway enzymes (4)

A

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

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11
Q

Neutrophil (PMN): Primary (Azurophilic) Granules

A

Myeloperoxidase

Lysozyme

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12
Q

Neutrophil (PMN): Secondary (specific) Granules

A 
Lactoferrin 
Leukocyte Alkaline Phosphatase (LAP) 
  Seen in normal PMNS 
  Benign process: high LAP 
  Malignant: Low LAP
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13
Q

Defects in Neutrophil (PMNs, 4)

A

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

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14
Q

Defects in Neutrophil: CGD of Childhood

A

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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15
Q

Defects in Neutrophil: Myeloperoxidase Deficiency

A

Infections with candida

NBT TEST IS POSTIVE (normal)

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16
Q

Defects in Neutrophil: Chediak-Higashi Syndrome

A

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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17
Q

Defects in Neutrophil: LAD Type 1

A

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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18
Q

Defects in Neutrophil: LAD Type 2

A

Absence of Sialyl-Lews on neutrophils

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19
Q

Plasma Derived Chemical Mediators (3)

A

Kinin System
Clotting System
Complement System

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20
Q

Cell Derived Chemical Mediators (4)

A

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

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21
Q

Cell Derived Chemical Mediators - Vasoactive Amines

A

Histamine
Serotonin
Caricinoid syndrome

22
Q

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

A

Pain (dolor)
Increases vascular permeability
Vasodilation
Bronchoconstrictor

23
Q

Plasma Derived Chemical Mediators - The Kinin System

A

Intiated by ACTIVATED Hageman factor 12

24
Q

Factor 12 initiates

A

Kinin system, coagulation, and the plasminogen complement systems

25
Q

Other Mediators of Acute Inflammation: PAF

A

Derived from basophils, mast cells, and enthothelial cells

Actions: Activates and aggregates platelets, activates arachidonic acid metabolism

26
Q

Other Mediators of Acute Inflammation: Nitric Oxide

A

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

Important in endotoxic shock

27
Q

Other Mediators of Acute Inflammation: Chemokines

A

Activate and attract leukocytes

IL-8
MCP-1
Eotaxin

28
Q

Other Mediators of Acute Inflammation: Lysosomal Constituents

A

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)

29
Q

Other Mediators of Acute Inflammation: O2-derived free radicals

A

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)

30
Q

Exogenous chemotactants

A

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

31
Q

Complete System Pathology Diseases (2)

A

Paroxysmal Nocturnal Hemoglobinuria

Hereditary Angioedema

32
Q

Paroxysmal Nocturnal Hemoglobinuria

A

complement mediated lysis of RBCs

Defect/lack of DAF and CD59

33
Q

Hereditary Angioedema

A

Deficiency of C1 inhibitor

34
Q

Overall Outcome of Acute Inflammation (3) 1

A
  1. Complete resolution
  2. Healing by Fibrosis
  3. Abscess
  4. Progression to chronic inflammation
35
Q

Overall Outcome of Acute Inflammation: Complete Resolution

A

Regeneration of damaged epithelium WITHOUT SCAR TISSUE FORMATION

Restores structure and fxn of tissue

36
Q

Overall Outcome of Acute Inflammation: Healing by Fibrosis

A

Organization and repair WITH SCAR TISSUE FORMATION

Scar tissue laid down by FIBROBLASTS (distorts structure and fxn)

37
Q

Overall Outcome of Acute Inflammation: Abscess

A

Tissue destruction and persistent acute inflammation

Pus from pyogenic bacteria

38
Q

Overall Outcome of Acute Inflammation: Progression to Chronic Inflammation

A

When acute inflammation can’t remove noxious agents

Marked by:
Replacement of PMNS by macrophages, lymphocytes, and plasma cells
Angiogenesis
Healing by fibrosis

39
Q

Serous Inflammation

A

Outpourig of thin protein poor water fluid

Skin blister 
Body cavities (effusions)
40
Q

Fibrinous inflammation

A

Protein rich fluid (fibronogen) that has bread and butter appearance

Fibrinous pericarditis (shaggy, fibrinous exudate)

41
Q

Suppurative (purulent) Inflammation

A

Production of pus
Staphylococcus

Abscess
Suppurative conjunctivitis
Suppurative meningitis
Lung abscess

White and milky on surface it adheres to like eye or brain

42
Q

Catarrahal Inflammation

A

Excessive mucus secretion

Runny nose from rhinoviral infection

43
Q

Cellulitis

A

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

Erysipelas and Impetigo

44
Q

Pseudomembranous Inflammation

A

Toxin induced –> resulting in necrotic membrane formation

E.g. psedomembrane of diphtheria (thick, gray coating on BACK OF THROAT)

Pseudomembranous colitis from C. Difficile

45
Q

Ulcers

A

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

46
Q

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

A

Principal cells: lymphocytes

47
Q

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

A

Eosinophils dominate from start to finish

48
Q

Exceptions to Acute Inflammatory by PMNS: Acute dermatitis

A

Lymphocytes predominate

49
Q

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

A

Lymphocytes prodominate

50
Q

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

A

Little to no PMNS

M3 Path B1 (29 decks)

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