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Flashcards in Acute Inflammation Deck (22):
1

what are three major components of acute inflammation?

- blood vessels (increased blood flow to affected area)
- cells (leukocytes)
- chemical mediators (structural changes in vasculature--movement of fluid and plasma proteins from circulation into tissue)

2

What stimuli trigger acute inflammation?

- tissue necrosis (ischemia, trauma, physical and chemical agents)
- infections and microbial toxins
- foreign bodies (sutures, splinter)
- immune reactions (autoimmune, hypersensitivity)

3

What are the various types of extracellular fluid collections?

- transudate (clear, low protein density)
- exudate (high protein density; often contains neutrophils and cellular debris)
- edema (excess fluid in interstitial space)
- pus (purulent exudate, contains WBCs, sometimes bacteria, cellular debris -- neutrophils!)

4

What are two major results of vascular response in acute inflammation?

- vasodilation (to increase blood flow to area -- occurs through action of histamine and nitric oxide and affects arterioles)

- increased vascular permeability (in post-capillary venules due to actions of histamine -- allows fluid, proteins to move into tissues)

5

Histamine increases _____ in post-capillary venules

permeability

6

What forces favor fluid movement out of vessels?

- increased blood flow increases hydrostatic pressure, pushing fluid out of vessel
- loss of protein decreases oncotic pressure inside vessel, which helps make net direction of flow out into tissue

7

What chemical mediator is commonly implicated in primary, transient vascular permeability response?

histamine
(increased permeability primarily occurs in post-capillary venules by forming endothelial gaps)

8

What is sequence of events in leukocyte extravasation?

- Margination: leuks acucmulate in specific location due to changes in blood flow

- Rolling: leuks bind to SELECTIN on surface of endothelial cells an droll along the surface of vessel

- Adhesion: leuks bind to endothelial surface via INTEGRINS (more tightly bound); cells come to rest

- Transmigration: leuks squeeze through the endothelium via diapedesis; process is mediated via IMMUNOGLOBINS

Leukocytes travel to area of inflammation via chemotaxis

9

What are the three main steps of phagocytosis?

- RECOGNITION AND ATTACHMENT: macrophages/phagocyte binds to opsonins, bacterial products, or cytokines (luek surface receptors bind microbes)
- ENGULFMENT: phagocyte extends pseudopods of cytoplasm around cell or toxin to engulf (phagosome and lysosome fuse)
- KILLING AND DEGRADATION: phagosome merges with lysosome inside cell forming phagolysosome to digest the particles. This is oxygen dependent.

10

What two oxygen-dependent processes are important in third step of phagocytosis (killing and degradation step)?

- Generation of reaction oxygen species (ROS) that can react with foreign contents
- Myeloperoxidase: enzyme that converts hydrogen peroxide to an antimicrobial agent like hypochlorite that can break down foreign material

11

What are two disease that occur due to defects in leukocyte function?

- CHEDIAK-HIGASHI SYNDROME: defect in phagolysosome fucntion; decreased numbers of neutrophils; defective degranulation; delayed microbial killing

- CHRONIC GRANULOMATOUS DISEASE: defects in microbicidal activity; recurrent bacterial infections

12

What are the two main types of vasoactive amines?

- histamine: released by mast cells; causes blood vessels to dilate and increases permeability of post-cap venules (primary, transient response)

- serotonin: released by platelets; causes dilate of arterioles and increased permeability of past-cap venules

13

What are the two main pathways of the arachadonic acid cascade? Understand role of anti-inflammatory medications in inhibiting the production of prostaglandins and leukotrienes.

- Cyclooxygenase pathway: produces prostaglandins. Responsible for pain. Effects platelet aggregation and vascular tone and permeability. COX-1 and COX-2 enzymes.

- Lipoxygenase pathway: produces leukotrienes (effect chemotaxis, vasoconstriction, vascular permeability, and bronchospasm) and lipoxins (inhibits leukocyte recruitment).

- NSAIDS (aspirin, non-steroidal anti-inflammatory drugs) inhibit COX-1 and COX-2, inhibiting prostaglandins in cyclooxygenase pathway

- Corticosteroids are broad and inhibit both pathways

- Zileuton, Montelukast are asthma medications that block the lipoxygenase pathway and production of leukotrienes/lipoxins

14

Explain how nitric oxide acts as an endogenous regulator of inflammation

- Nitric oxide is produced by endothelial cells and macrophages. It reduces the effects of inflammation. It is a vasodilator, reduces platelet aggregation, inhibits mast cells and regulates leukocyte recruitment.

- has antimicrobial function in macrophages

15

What are the two main cytokines involved in inflammation and describe their major effects

- IL-1: interleukin-1
- TNF: tumor necrosis factor

- They trigger the systemic acute phase response to acute inflammation: fever, loss of appetite, slow wave sleep, and release of neutrophils into circulation.

16

Recognize the complement, kinin and clotting systems as enzyme cascades that can act to modify the inflammatory response.

- Complement system acts in immune defense. Can attack cells or opsonize them. Also causes vascular dilation, increased permeability, leukocyte adhesion, chemotaxis, and more effective phagocytosis

- Kinin system: interacts closely with clotting system. Forms bradykinin, which increases vascular permeability, contraction of smooth muscle, dilation of blood vessels, and causes pain

- Clotting system: cascade that results in formation of fibrin clot. Acute inflammation can trigger clotting cascade, while cascade components can bind to receptors on platelets, endothelial cells and smooth muscle cells to induce inflammation

17

What are the four common morphologic patterns of acute inflammation in tissues?

- serous inflammation
- fibrinous
- suppurative
- ulcer

18

Give examples of serous inflammation (one of common morphologic patterns of acute inflammation in tissues)

- blister
- outpouring of thin fluid (transudate) in body cavities

19

Give examples of fibrinous patter (one of common morphologic patterns of acute inflammation in tissues)

- fluid plus larger proteins such as fibrin (e.g., fibrinous pericarditis where heart has sandpapering tissue all over it)
- more severe injury than serous
- occurs in body cavities

20

Give examples of suppurative patern (one of common morphologic patterns of acute inflammation in tissues)

- Acute appendicitis
- Large amounts of purulent exudate
- Neutrophils, necrotic debris, microbes
- Abscess

21

Give examples of ulcer (one of common morphologic patterns of acute inflammation in tissues)

- Peptic ulcer
- Localized defect in the surface of an organ or tissue
- Sloughing off of injured/necrotic cells
- GI tract, genitourinary tract, skin

22

What are the three main outcomes of acute inflammation. Explain factors favoring each outcome. Explain why some types of ongoing or repeated injury responses may display a mixed (both acute and chronic) inflammatory picture.

- complete RESOLUTION: occurs when injury is limited or short-lived, and tissue destruction is minimal.

- Healing by connective tissue replacement (FIBROSIS): tissue destruction is significant, and tissue is unable to regenerate (or fibrinous exudate cannot be quickly removed). Connective tissue grows into area of injury creating a scar.

- PROGRESSION TO CHRONIC INFLAMMATION: body cannot resolve the acute inflammation due to persistent injury/stimulus or interference with the normal healing process.

* Base of chronic inflammation may be present with superimposed acute inflammation during periods of active injury.