Lecture 9 2/8/24 Flashcards by Danika Boltz

What is inflammation?

reaction within a living vascularized tissue to local injury

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What types of injury can occur that cause inflammation?

-infectious microbes
-mechanical trauma
-heat
-cold
-radiation
-cancerous cells

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What is the purpose of inflammation?

-to dilute, isolate, and eliminate cause of injury
-to repair tissue damage resulting from the injury

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What are the basics of inflammation?

-requires a stimulus
-major players are in circulation/blood
-only in living tissue
-allied with healing and repair
-can be harmful

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What are the benefits of inflammation?

-dilutes/inactivates biological and chemical toxins
-kills/sequesters microbes and neoplastic cells
-degrades foreign material
-provides growth factors to help with healing phase

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What are the harms of inflammation?

-can destroy normal tissue
-cardinal signs of inflammation

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What are the cardinal signs of inflammation?

-heat
-redness
-swelling
-pain
-loss of function

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What descriptors should be included in a morphologic diagnosis?

-severity
-duration
-distribution
-modifiers
-process
-organ

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Which terms can be used to describe the severity of a diagnosis?

-minimal
-mild
-moderate
-marked
-severe

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Which terms can be used to describe the chronicity of a diagnosis?

-peracute: hours
-acute: hours to days
-subacute: many days
-chronic: weeks to years
-chronic-active: ongoing acute stimulus

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How can a process be determined to be acute vs. chronic?

based on the type(s) of inflammatory cells and other gross changes

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Which terms can be used to describe distribution of a diagnosis?

-focal
-multifocal
-locally/regionally extensive
-diffuse
-multifocal to coalescing
-segmental
-unilateral/bilateral
-cranioventral (lungs)

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Which terms can be used when having to provide a modifier for an inflammatory process?

-suppurative
-necrotizing
-ulcerative
-hemorrhagic
-lymphoplasmacytic
-granulomatous
-eosinophilic

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What are some examples of terms that can be used when providing a modifier for a specific location?

-bronchopneumonia
-interstitial pneumonia
-glomerulonephritis
-portal hepatitis

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Which leukocytes are involved with inflammation?

-neutrophils
-monocytes/macrophages
-lymphocytes
-plasma cells
-eosinophils
-basophils
-mast cells

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Which non-leukocytes are involved with inflammation?

-endothelial cells
-platelets
-fibroblasts

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What are the characteristics of inflammatory mediators?

-derived from cells or plasma
-can be produced as needed or pre-formed and stored
-short-lived

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What are the master cytokines?

-IL-1
-TNF

What part of the arachidonic acid pathway is inhibited by steroids?

phospholipase function

What part of the arachidonic acid pathway is inhibited by leukotriene receptor antagonists?

leukotrienes

What part of the arachidonic acid pathway is inhibited by COX-1/2 inhibitors?

cyclooxygenase

How is it possible for some membrane lipids to not form arachidonic acid (omega 6 fatty acid)?

-dietary omega 3 fatty acids insert into cell membrane
-insertion of dietary omega 3 fatty acids decreases arachidonic acid

What are the impacts of increased omega 3s in the cell membrane?

-less inflammation
-less pain
-less-free radical-mediated damage

What are the characteristics of histamine?

-pre-formed
-released in response to trauma, cytokines, etc.

What are the effects of histamine?

-vasodilation -increased vascular permeability -pain and itching -eosinophil attraction

What are the steps of inflammation?

-initiation -vasodilation -increased vascular permeability -activation of leukocytes -diapedesis -chemotaxis -phagocytosis

What are examples of potential stimuli for inflammation?

-infectious agents -trauma -abnormal cells -necrotic cells -foreign material

Why do stimuli trigger inflammation?

PRRs on epithelial cells and leukocytes recognize PAMPs and DAMPs

How do resident macrophages initiate inflammation?

-recognize non-self or DAMPs -release IL-1

How do lymphocytes initiate inflammation?

-recognize non-self -release IL-1

How does direct damage to cells initiate inflammation?

-damage to mast cells leads to mast cell degranulation/histamine release -release of IL-1

How does indirect damage initiate inflammation?

-sunburn irritates keratinocytes -keratinocytes release IL-1

How does amplification of signaling initiate inflammation?

-IL-1 can trigger mast cell degranulation -histamine triggers more IL-1 release

What occurs during vasodilation?

-increased blood flow to area causes heat and redness -slowing of blood leads to margination of neutrophils

What effect does histamine, IL-1, and TNF have on the blood vessels?

makes endothelial cells contract, causing leaky vessels

How does increased vascular permeability result in edema and an increase in marginated neutrophils?

-fluid leaks out of vessels, resulting in hemoconcentration -increased viscosity of blood leads to blood "sludging" -sludging of blood results in more marginated neutrophils

What is lost due to increased vascular permeability?

-fluid -proteins/fibrinogen

What happens when fibrinogen is exposed to collagen outside of the vessels?

triggers the clotting cascade, leading to fibrin formation

How do IL-1 and TNF play a role in increased vascular permeability?

increase expression of adhesion molecules, increasing the number of marginated neutrophils

Which adhesion molecules are present on vessel endothelial cells?

-E-selectin -P-selectin -ICAM-1

How do IL-1 and TNF increase leukocyte binding, in terms of the leukocyte?

increase the expression and avidity/stickiness of integrins on leukocyte surface

How are histamine, TNF, and IL-1 involved in leukocyte activation?

-upregulation of adhesion molecules -increase in cytokine and prostaglandin production

What are the characteristics of diapedesis?

-movement of leukocytes out of vessels -primarily neutrophils -depends on upregulation of adhesion molecules -mediated by PECAM-1