Granulomatous Inflammation: - Cells involved? - Histologic findings? - Differential Diagnosis?

- Macrophages - Mixed chronic inflammatory cells; +/- central necrosis; +/- foreign material - Infectious (AFB/Fungus); Inflammatory (Arthritis); Foreign Body (Suture)

Eosinophilic Inflammation: - Cells involved? - Histologic findings? - Differential Diagnosis?

- Eosinophils - Abundant Eosinophils - Infectious (parasites); Inflammatory (Allergic process- eg asthma)

Inflammation Flashcards by Jim Resczenski

Fibrinopurulent/Purulent/Suppurative Inflammation:

Cells involved?
Histologic findings?
Differential Diagnosis?

Fibrinopurulent/Purulent/Suppurative Inflammation:
-PMNs
-PMNs; Fibrin/blood products; +/- hemorrhage
-Infectious (Bacteria/Some Fungi)
Notes: Pus

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Granulomatous Inflammation:

Cells involved?
Histologic findings?
Differential Diagnosis?

Macrophages
Mixed chronic inflammatory cells; +/- central necrosis; +/- foreign material
Infectious (AFB/Fungus); Inflammatory (Arthritis); Foreign Body (Suture)

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Eosinophilic Inflammation:

Cells involved?
Histologic findings?
Differential Diagnosis?

Eosinophils
Abundant Eosinophils
Infectious (parasites); Inflammatory (Allergic process- eg asthma)

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Fibrinopurulent exudate:
Location?
Inflammatory cells?
Diagnosis?

Anywhere, though typically non-confined
PMNs
Bacterial/Fungal infection

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Abscess:
Location?
Inflammatory cells?
Diagnosis?

Within parenchyma/confined space (eg brain, liver, lung)
PMNs
Bacterial/Fungal infection

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Empyema:
Location?
Inflammatory cells?
Diagnosis?

Within a confined anatomic space/cavity (eg pleural; subdural; appendix/gallbladder/uterus/joint)
PMNs predominate early; can later be macrophages/lymphocytes
Bacterial/Fungal infection

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Cellulitis:
Location?
Inflammatory cells?
Diagnosis?

Skin; Fascia
none listed
Bacterial infection; Inflammatory

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Granuloma:
Location?
Inflammatory cells?
Diagnosis?

Within parenchyma (eg lung, lymph node, liver, spleen) w/ a rounded/nodular appearance
Macrophages (epithiliod; giant cells); lymphocytes, plasma cells
Bacterial (AFB)/Fungal infection; Inflammatory (collagen vascular disorder; foreign body)

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LOCAL clinical signs of inflammation?

Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)
Functio Laesa (loss of fxn)

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Systemic clinical signs of inflammation?

Fever
Blood Pressure (Hypotension/shock)
Sleepiness
Anorexia

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Key actions of Histamine (cell derived)

Vasodialate
Incr vascular permeability
Constricts Bronchial SMC

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Key actions of Serotonin (cell derived)

-Incr vascular permeability

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Key actions of Prostaglandins (cell derived)

Incr vascular permeability
Constricts Bronchial SMC
Fever
Pain {prosta-te exam}

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Key actions of Leukotrienes (LT-C4, D4, E4) (cell derived)

Incr vascular permeability

- Constricts Bronchial SMC

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Key actions of Leukotrienes (LT-B4) (cell derived)

WBC/Chemotaxis

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Key actions of Thromboxanes (cell derived)

Vasoconstrictor

- Platelet aggregation

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Key actions of Platelet Activating Factor (PAF) (cell derived)

Vasodialates at low [ ]s
Vasoconstricts
Incr vascular permeability at low [ ]s
WBC/Chemotaxis
Platelet aggregation
Constricts Bronchial SMC

Key actions of ROS (cell derived)

Tissue/Microbe damage

Key actions of NO (cell derived)

Vasodialation
WBC/chemotaxis (iNOS only)
Relaxes Bronchial SMC
Tissue/Microbe damage (iNOS only)

Key actions of Tumor Necrosis Factor (TNF) (cell derived)

WBC/chemotaxis

- Fever

Key actions of Interleukin (IL-1, IL-6) (cell derived)

WBC/chemotaxis

- Fever

Key actions of Chemokine/cytokine (cell derived)

WBC/chemotaxis

Key actions of Cytoplasmic Granule content (cell derived)

WBC/chemotaxis

- Tissue/Microbe damage

Key actions of Substance P (cell derived)

Incr vascular permeability

- Pain

Key actions of C3a/C5a (Plasma Derived)

- Vasodialate (mast cell stim) - Incr vascular permeability (mast cell stim) - WBC/chemotaxis - Tissue/microbe damage (MAC effect on microbe)

Key actions of Bradykinin (Plasma Derived)

- Vasodialate - Incr vascular permeability - Constricts Bronchial SMC - Pain

Key actions of Thrombin (Plasma Derived)

- WBC/Chemotaxis

Key actions of Plasmin (Plasma Derived)

- Vasodialate

Key mediators of Vasodialation

- Prostaglandins - NO - Histamine

Key mediators of Increasing Vascular Permeability

- Histamine/Serotonin - C3a/C5a - Bradykinin - Leukotrienes C4, D4, E4 - PAF - Substance P

Key mediators of WBC/Chemotaxis

- TNF/IL1 - Chemokines - C3a/C5a - Leukotriene B4 - Bacterial Products

Key mediators of Fever

- IL-1/TNF | - Prostaglandins

Key mediators of Pain

- Prostaglandins {prosta-te exam} - Bradykinin {kin-da hurts} - Substance P {Substance Pain}

Key mediators of Tissue/Microbial Damage

- Lysosomal enzymes of Leukocytes - ROS - NO

What 3 cascades are activated by Factor XII?

- Kinin cascade (=>bradykinin, C5a and C3a (via the fibrinolytic system)) - Clotting Cascade (=> Thrombin=>Fibrin) - Complement Cascade (from C3a/C5a) (see figure 2-15)

Define hypertrophic scar

raised scar that grows beyond the boundries of injury but REGRESSES

Define Keloid scar

raised scar that grows beyond the boundries of injury but DOES NOT REGRESS

What systemic effects may impede the repair/regeneration process?

- Nutritional deficiency (protein/VitC) - Metabolic (diabetes; glucocorticoids) - Vascular (ischemia/venous drainage)

What local effects may impede the repair/regeneration process?

- Infection - Persistence of Insult - Trauma (early movement or foreign material) - Size/Location

Does Exudate of Transudate have increased protein content? Which has increased leukocytes? Which has decreased glucose levels? Why?

Exudate has incr protein/leukocytes and decreased glucose as the glucose is eaten by the inflammatory cells.

What are the 3 elements that can contribute to Thrombosis?

Virchow's Triad: - Endothilial injury - Abnormal Blood flow - Hypercoagulability