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What sets the scene for leukocyte recruitment?

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Pathology

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7 years ago

Date created

Mar 1, 2020

Cards (31)

Section 1

(31 cards)

What sets the scene for leukocyte recruitment?

Front

Stasis: As edema happens due to fluid leaving the blood, the inner-vasculature becomes more concentrated with red blood cells which increases its viscosity making it a little more static.

Back

Which mediators cause increased permeability

Front

Histamine, leukotrienes, Plately Act. factor, kinins

Back

What are the signs of acute inflammation?

Front

1. Rumor (Redness) 2. Tumor (Swelling) 3. Calor (heat) 4 Dolor (pain)

Back

What are the two vasoactive amines, where do they come from and what is their function

Front

Histamine and serotonin Come from, mast cells, platelets, and basophils (histamine) and neuroendocrine cells (serotonin) Actions: vasodilation, increase permeability and activation of selection on endothelial cells.

Back

What happens when the leukocyte reaches the infected cells

Front

Binds to the cell (G-protein coupled receptor, Opsonization, Toll-like receptors, Mannose receptors, scavenger receptors) Leukocyte is "triggered" Phagocytosis: pulling the bad cell in as a phagosome, then fusing it with a lysosome to form a phagolysosome where it kills/degrades the bad cell (ROS etc)

Back

Describe chemotaxis (the 5th step of leukocyte recruitment)

Front

Leukocyte pulls itself to site of injury by using filopodia and following chemoattractants (chemicals that attract it to the site of inflammation—> bacterial products, chemokines, complement, AA metabolites) plexus

Back

Mediators that produce collateral tissue damage

Front

Reactive oxygen species (ROS), leukocyte lysosomal enzymes.

Back

What are the mechanisms of increasing permeability of micro vasculature?

Front

1. Contraction of endothelial cells (histamine, bradykinin, leukotrienes, substance P) 2. endothelial injury (burns, radiation, microbes) 3. Transcytosis

Back

Describe migration (4th step of leukocyte recruitment)

Front

Leukocytes chew through basement membrane by releasing collagen ashes to get to exit the blood vessel (Transmigration/diapedesis)

Back

Function of histamine

Front

Inflammatory mediator that increases vasodilation and increase permeability

Back

Function of prostaglandins

Front

Inflammatory mediator. Causes vasodilation, pain (dolor), fever

Back

What are cytokines and what is their function?

Front

Proteins released from activated macrophages, lymphocytes and endothelial cells in response to inflammatory stimulus. The activate and regulate leukocytes and endothelial cells.

Back

What are the three things cyclooxygenase (COX) produces and what are their functions?

Front

1. Prostaglandins-> Vasodilation, increased permeability, pain and fever 2. Thromboxane (Vasoconstriction, platelet aggregation 3. Prostacyclin (vasodilation, decreased platelet aggregation)

Back

Mediators for vasodilation

Front

Histamine and prostaglandins

Back

What are eicosanoids? (Aracidonic acid metabolites)

Front

Active metabolites synthesized from AA via phospholipases

Back

Mediators that produce chemotaxis, leukocyte recruitment and activation

Front

TNF, IL-1, Chemokines, C3A, C5a, Leukotriene B4

Back

What is the first step in an immune response

Front

Injury (infection, tissue necrosis, foreign material, autoimmune)

Back

What are some of the costs of acute inflammation?

Front

Not completely efficient. Parts of the process are dangerous for host as well (reactive oxygen species-ROS, etc.) Can cause atherosclerosis, tuberculoses, allergic reactions and autoimmunity)

Back

What are the causes of fluid leaving vessels (3)

Front

1. Increased intravascular hydrostatic pressure (eg congestive heart failure) 2. Decrease intravascular colloid osmotic pressure 3. Increased vascular endothelial permeability (Eg inflammation) causing leakage of fluid, cels and debris into extra vascular tissue.

Back

Function of leukotrienes

Front

inflammatory mediator: causes chemotaxis, leukocyte adhesion and activation, increases vascular permeability.

Back

What are some examples of COX inhibitors and what do they do?

Front

Aspirin, NSAIDS They reduce prostaglandin mediated pain and fever.

Back

What are the phases of leukocyte recruitment? (5)

Front

1. Margination 2. Rolling 3. Adhesion 4. Migration 5. Chemotaxis

Back

Describe margination and rolling

Front

Margination: decreased shear forces cause leukocytes to have a peripheral location in the blood vessel Rolling: Transient binding and unwinding to the vessel wall via selections (selection expression is induced by cytokines released by the injured tissue-TNF and IL-1)

Back

Describe adhesion (3rd phase of leukocyte recruitment)

Front

The weak transient binding of the rolling phase allows for strong "adhesion" binding by integrity proteins. Once the leukocyte stops rolling, stable adhesion is achieved.

Back

Mediators that produce pain

Front

Prostaglandins, Bradykinin

Back

Mediators that produce a fever

Front

IL-1, TNF, Prostaglandins

Back

What are the two classifications of edema?

Front

Transudate and exudate

Back

What are the three main components of leukocyte recruitment following tissue injury (part of the inflammatory response)

Front

Basically get more blood into the area: 1. Alteration in vascular caliber (increased blood flow) 2. Structural changes in vasculature (increase permeability) 3. Migration of leukocytes from circulation into the tissues with subsequent leukocyte accumulation and activation.

Back

Mediators for increased vascular permeability

Front

Histamine & serotonin, C3a and C3b, leukotrienes (C4, D4, E4)

Back

How does inflammation stop

Front

First off, neutrophils die within 2-3 hours. Then, once the initiating signal (injury) is eliminated, anti-inflammatory mediators (TGF-beta and IL-10) begin to outnumber pro-inflammatory mediators (TNF-Alpha)

Back

What is the next step in the inflammatory response once injury is detected?

Front

Local and recruited cells release mediators (histamine, prostaglandins, leukotrienes etc)

Back