Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

18 Cards in this Set

  • Front
  • Back
Origins of acute inflammation
1. Infection
2. Mechanical trauma
3. Tissue anoxia
4. Physical agents (e.g. chemical or thermal burns)
Transient vasoconstriction
1. Affects precapillary arterioles and meta-arterioles
2. Earliest response lasting seconds
3. Regulated by neurogenic and chemical mediatiors (Thromboxin A2)
4. Characterized as temporary decrease blood flow to limit hemorraging
5. Minor clinical significance
1. Affect precapillary and metaarterioles
2. Lasts minutes
3. Characterized as increased vascular caliber and opening of inactive capillary beds
4. HYPEREMIA - increased blood flow to affected tissue
5. Actively mediated with bradykinin, histamine, and prostacyclin (thus, ACTIVE HYPEREMIA)
6. TRANSUDATION due to increase hydrosatic forced
7. Clinically seen as erythema (redness) and warmth
Immediate transient response
1. Immediate transient response
- Leakage is rapid and short-lived
- Due to mild injuries
- Mediated by bradykinin, histamine, prostaglandins, C3a, C5a, substance P, leukotrines, TNF, IL-1
- Venules affected
Immiedate sustained response
1. Due to direct damage damage to endothelial cell; not elicited by chemical mediators

2. Immediate cell death with rapid leackage until holes are repaired

3. Occurs in sever injuries like burns

4. All levels of microcirculation affected
Delayed prolonged response
1. Not elicited by chemical mediators

2. Delayed cell death with long-lasting leakage

3. Example is sunburn

4. Venules and capillaries are affected
What happens when microvessels become leaky in acute inflammation?
1. Exudate - fluid with plasa proteins escape into intersitial tissues

2. Abnormal swelling causes pain from tissue turgor and chemical mediators (PGE3, bradykinin) on nerve endings

3. ↑ Hemoconcentration causing ↑ blood viscosity and stasis (slow blood flow which promotes margination andemigration of leukocytes)

4. Edema (abnormal tissue accumulation of fluid outside of cell) is essentially an exudate
1. Promotes immunologic response
2. Dilutes toxins
3. localize infection (e.g. fibrin)
4. Supplies protective Ab
5. Provides nutrients for cellular elements)
Cardinal clinical manifestations of inflammation
1. Redness (rubor)
2. Warmth (calore)
3. Swelling from edema (tumor)
4. Pain (dolore)
5. Loss of function (functio laesa)

- These are NOT characteristic of chronic inflammatory processes

- Manifested locally on body surface but not so apparent if on organs
Leukocyte margination
1. Normally leukocytes limited to central column of laminar blood flow with surrounding sheath of plasma

2. Stasis causes leukocytes to "fall out" of central axis and contact and attach to vascular endothelium
Adhesion molecules of leukocyte margination
1. SELECTINS - prsent on Leukocytes, Platelets, and Endothelium (L,P,E-selectins)

2. Ig SUPERFAMILY MOLECULES present on endothelium (e.g. ICAM-1, VCAM-1)

3. INTEGRINS present on leukocytes (e.g. α4β7, α4β1)
Mechanism of adhesion molecules in leukocyte margination
1. Cell adheion molecules in cytoplasm redistributed to cell surface (e.g. by histamine)

2. Adhesion molecule synthesis induced on endothelium and leukocytes by chemical factors (e.g. by IL-1, TNF)

3. Conformational changes of intgrin molecules cause ↑ avidity of binding (e.g. C5a)
Leukocyte emigration

2. Cytoplasimic pseudopod extends through endothelial cell junction in ameboid fashion

3. Mediated by PECAM-1

4. Leukocyte secretion of collagenase facilitates emigration

5. Venules in systemic circulation AND capillaries in pulmonary circulation preferred sites for margination/emigration
T/F: Macrophages and lymphocytes are considered to be acute inflamatory cells
FALSE: Neutrophils are considered to be acute inflammatory cells because they predominate at the injured site in the early phases of acute inflammation.

Later, macrophages and lymphocytes predominate at the injured site during the healing phase
Leukocyte chemotaxis
1. The process of leukocytes following increasing gradient of CHEMOATTRACTANTS

2. Chemoattractants trigger assemply of contractile elements for cell mobility

3. Examples of chemotactic factors: bacterial products, C5a, leukotriene B4, and chemokines
Leukocyte phagocytosis
1. Recognition: Opsonization of foreign particle with opsisin like Fc fragment of IgG, C3b, collectins

2. Engulfment: Psuedopods extend to engulf and create phagosome ⇒ + lysosome ⇒ phagolysosome ⇒ + degranulation enzymes ⇒ foreign particle degradation

3. Bacterial killing: Superoxide radicals (HOCL) created; requires MYLOPEROXIDASE + O2 ⇒ HYPOCHLORITE
In the absence of myloperoxidase, how else can leukocytes degrade/kill foreign particles?
1. Proteins that ↑ bacterial permeability

2. Lysosomes

3. Lactoferrin - against parasites

4. Major basic protein
5 outcomes of acute inflammation
1. Healing by compete resolution - regeneration of native cells

2. Healing by complete fibrous scarring - involes ORGANIZATION and FIBROPLASIA to replace injured tissue with fibrous CT

3. Healing by repair process - combo of regeneration and fibrous scarring (common outcome)

4. Abcess formation - especially in response to pyogenic organisms

5. Progression in chronic inflammation