Chapter 2: I - Acute Inflamantion(Ai)

Front 1

Acute inflammation is:

Back 1

Transient and early response to injury

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Acute inflammation involves release of:

Back 2

chemical mediators

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Acute inflammation leads to:

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stereotypic vessel and leukocyte responses

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Acute inflammation is not:

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synonym for infection

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Cardinal signs of inflammation are:

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Functio laesa (loss of function), Dolor (pain), Tumor (swelling), Rubor (redness) and calor (heat)

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Rubor (redness) and calor (heat) are:

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Histamine-mediated vasodilation of arterioles

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Tumor (swelling) is:

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Histamine-mediated increase in permeability of venules

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Tumor (swelling) is Synonymous with:

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Edema

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Tumor (swelling) or edema is characterized by:

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Increased fluid in the interstitial space

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Cardinal signs of inflammation that are histamine-mediated:

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Rubor, calor, tumor

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Dolor (pain) is characterized by:

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Prostaglandin (PG) E2 sensitizes specialized nerve endings to the effects of bradykinin and other pain mediators

Front 12

Stimuli for acute inflammation and examples:

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Infections (e.g., bacterial or viral infection), Immune reactions (e.g., reaction to a bee sting), tissue necrosis (e.g., acute myocardial infarction), trauma, radiation, burns, foreign body (e.g., glass, splinter)

Front 13

Sequential vascular events are:

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Vasoconstriction of arterioles, Vasodilation of arterioles, Increased permeability of venules, Swelling of tissue (tumor, edema) and Reduced blood flow

Front 14

Vasoconstriction of arterioles is:

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Neurogenic reflex that lasts only seconds

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Vasodilation of arterioles due:

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Histamine and other vasodilators (e.g., nitric oxide) relax vascular smooth muscle, causing increased blood flow.

Front 16

Vasodilation of arterioles causes Increased blood flow that cause a increase in:

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hydrostatic pressure

Front 17

Increased permeability of venules due:

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Release of preformed histamine(Mast cells) and other mediators contract endothelial cells producing endothelial gaps

Front 18

Tight junctions are simpler in:

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venules than arterioles

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Increased permeability of venules causes a ______ to move into the interstitial tissue.

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A transudate (protein and cell-poor fluid)

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Swelling of tissue (tumor, edema) due:

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Net outflow of fluid surpasses lymphatic ability to remove fluid

Front 21

Reduced blood flow due:

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Decrease in hydrostatic pressure caused by outflow of fluid into the interstitial tissue

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Neutrophils are the:

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primary leukocytes in acute inflammation

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Margination is:

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Neutrophils are pushed from the central axial column to the periphery

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Margination is due:

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RBCs aggregate into rouleaux ("stacks of coins") in venules

Front 25

Rolling causes neutrophils to:

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Loosely bind to selectins and "roll" along the endothelium.

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Rolling is due to :

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Activation of selectin adhesion molecules on the surface of neutrophils and endothelial cells

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Adhesion molecules firmly bind neutrophils to:

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endothelial cells

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Neutrophils in the peripheral blood are subdivided into a:

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Circulating pool and a marginating pool (already attached to endothelial cells).

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Normally, ___% of peripheral blood neutrophils are in the circulating pool and ___% in the marginating pool:

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~50%,~50%

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Neutrophil distribution can be altered by:

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Activating or inactivating neutrophil adhesion molecules

Front 31

Neutrophil adhesion molecules are:

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β2-Integrins (CD11a:CD18)

Front 32

Adhesion molecule activation is mediated by:

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C5a and leukotriene B4 (LTB4)

Front 33

Inhibit activation of adhesion molecules:

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Catecholamines, corticosteroids, and lithium

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inhibit activation of adhesion molecules causes:

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Peripheral blood neutrophil count (neutrophilic leukocytosis) to increase because normal marginating pool is now part of the circulating pool

Front 35

Endotoxins enhance activation of:

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adhesion molecules

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enhance activation of adhesion molecules causes:

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Peripheral blood neutrophil count (neutropenia) is decreased because normal circulating pool is now part of the marginating pool

Front 37

Endothelial cell adhesion molecules are:

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Intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM)

Front 38

Intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) bind to:

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integrins on the surface of neutrophils

Front 39

ICAM and VCAM activation is mediated by:

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interleukin 1 (IL-1) and tumor necrosis factor (TNF)

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Leukocyte adhesion deficiency (LAD) inheritance:

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Autosomal recessive disorders

Front 41

Leukocyte adhesion deficiency (LAD) type I is a deficiency of:

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CD11a:CD18.

Front 42

Leukocyte adhesion deficiency (LAD) type II is a deficiency of:

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selectin that binds neutrophils

Front 43

Leukocyte adhesion deficiency (LAD) clinical findings include:

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Delayed separation of the umbilical cord (∼1 month), severe gingivitis, poor wound healing, peripheral blood neutrophilic leukocytosis (loss of marginating pool)

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Delayed separation of the umbilical cord (∼1 month) in Leukocyte adhesion deficiency (LAD) is due to:

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Neutrophil enzymes are important in cord separation

Front 45

Severe gingivitis, poor wound healing, peripheral blood neutrophilic leukocytosis in Leukocyte adhesion deficiency (LAD) are due to:

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Loss of marginating pool

Front 46

Transmigration (diapedesis) are:

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Neutrophils dissolve the basement membrane and enter interstitial tissue

Front 47

In Transmigration (diapedesis) due to dissolving of basement membrane there is, in the interstitial tissue, accumulation of:

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Fluid rich in proteins and cells (i.e., exudate)

Front 48

Functions of exudate:

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(1) Dilutes bacterial toxins, (2) Provides opsonins (IgG, C3b) to assist in phagocytosis

Front 49

Chemotaxis:

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directed migration of neutrophils

Front 50

Neutrophils follow:

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chemical gradients that lead to the infection site

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Chemotactic mediators bind to:

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neutrophil receptors

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Chemotactic mediators include:

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C5a, LTB4, bacterial products, and interleukin (IL) 8

Front 53

Binding causes the release of:

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calcium, which increases neutrophil motility.

Front 54

Phagocytosis is multistep process, consisting of three steps:

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(1) Opsonization (2) Ingestion (3) Killing

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Opsonins attach to:

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bacteria (or foreign bodies)

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Opsonins include:

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IgG, C3b fragment of complement, and other proteins (e.g., C-reactive protein).

Front 57

Neutrophils have membrane receptors for:

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IgG and C3b

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Opsonization enhances neutrophil:

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recognition and attachment to bacteria

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Bruton's agammaglobulinemia is an:

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opsonization defect

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Neutrophils engulf (phagocytose) and then trap bacteria in:

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phagocytic vacuoles

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Primary lysosomes empty hydrolytic enzymes into:

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phagocytic vacuoles producing phagolysosomes

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In Chédiak-Higashi syndrome phagolysosome formation is prevented by:

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a defect in microtubule function

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O2-dependent myeloperoxidase (MPO) system is only present in:

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neutrophils and monocytes (not macrophages)

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O2-dependent myeloperoxidase (MPO) system lead to production of:

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superoxide free radicals, peroxide (H2O2) , bleach (HOCl•)

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__________ converts molecular O2 to superoxide free radicals

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Reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase

Front 66

Superoxide free radicals release energy called:

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Respiratory, or oxidative, burst

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Converts superoxide free radicals to H2O2:

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Superoxide dismutase

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H2O2 is neutralized by:

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glutathione peroxidase

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Some peroxide is converted to:

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hydroxyl free radicals by iron

Front 70

MPO combines H2O2 with chloride (Cl-) to form:

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hypochlorous free radicals (HOCl•), which kill bacteria

Front 71

examples of diseases that have a defect in the O2-dependent MPO system:

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Chronic granulomatous disease and MPO deficiency

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Chronic granulomatous disease has absent:

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NADPH oxidase and respiratory burst

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MPO deficiency normal:

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Respiratory burst

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O2-independent system refers to:

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bacterial killing from substances located in leukocyte granules

Front 75

O2-independent system examples:

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Lactoferrin (binds iron necessary for bacterial reproduction) and major basic protein (eosinophil product that is cytotoxic to helminths)

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Chemical mediators derive from:

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plasma, leukocytes, local tissue, bacterial products

Front 77

Arachidonic acid mediators are released from:

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membrane phospholipids in macrophages, endothelial cells, and platelets

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Chemical mediator have:

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Short half-lives

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most important chemical mediator of acute inflammation:

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Histamine

Front 80

Chemical mediators can act:

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Locally or systemically

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histamine may produce:

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local signs of itching or systemic signs of anaphylaxis

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Cause Vasodilation:

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histamine, nitric oxide, PGI2

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Cause Vasoconstriction:

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thromboxane A2 (TXA2)

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Cause Increase vessel permeability:

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histamine, bradykinin, LTC4-D4-E4, C3a and C5a (anaphylatoxins)

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Produce pain:

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PGE2, bradykinin

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Produce fever:

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PGE2, IL-1, TNF

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Chemotactic are:

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C5a, LTB4, IL-8

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Location, cause, and duration of inflammation determine the:

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morphology of an inflammatory reaction

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Purulent (suppurative) inflammation is a:

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Localized proliferation of pus-forming organisms, such as Staphylococcus aureus (e.g., skin abscess)

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S. aureus contains coagulase, which:

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cleaves fibrinogen into fibrin and traps bacteria and neutrophils

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most common cause of a skin abscess:

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S. aureus

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Fibrinous inflammation is due to:

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increased vessel permeability, with deposition of a fibrin-rich exudate

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Fibrinous inflammation often occurs on:

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serosal lining of the pericardium, peritoneum, or pleura(Danger of adhesions)

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Serous inflammation is due to:

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Thin, watery exudate with Insufficient amount of fibrinogen to produce fibrin

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Serous inflammtion examples:

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Blister in second-degree burns, viral pleuritis

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Pseudomembranous inflammation is due to:

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Bacterial toxin-induced damage of the mucosal lining, producing a shaggy membrane composed of necrotic tissue

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Pseudomembranous inflammation example:

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Pseudomembranes associated with Clostridium difficile in pseudomembranous colitis

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Corynebacterium diphtheriae produces a toxin causing:

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Pseudomembrane formation in the pharynx and trachea

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Fever right-shift the:

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oxygen-binding curve

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Right-shift of the oxygen-binding curve due to fever cause:

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More O2 is available for the O2-dependent MPO system

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Fever provides a:

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hostile environment for bacterial and viral reproduction

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Factors involved in the termination of acute inflammation include:

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Short half-life of inflammatory mediators, Lipoxins, Resolvins, Clearance of neutrophils by apoptosis

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Lipoxins are:

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Anti-inflammatory mediators

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Lipoxins derive from:

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arachidonic acid metabolites (e.g., LXA4, LXB4)

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Lipoxins inhibit:

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transmigration and chemotaxis

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Lipoxins signal:

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macrophages to phagocytose apoptotic bodies

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Resolvins are synthesized from:

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omega-3 fatty acids

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Resolvins inhibit:

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production and recruitment of inflammatory cells to the site of inflammation

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Complete resolution occurs with:

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Mild injury to cells that have the capacity to enter the cell cycle (e.g., labile and stable cells)

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Complete resolution examples:

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first-degree burn, bee sting

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Tissue destruction and scar formation occurs with:

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extensive injury or damage to permanent cells

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Tissue destruction and scar formation example:

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third-degree burns

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Formation of abscesses example:

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Lung abscess in bronchopneumonia

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Consequences of acute inflammation can be:

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Complete resolution, Tissue destruction and scar formation, Formation of abscesses or Progression to chronic inflammation