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General Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Inflammation

Definition + Design

A

reaction of vascularized living tissue to local injury

inflammatory reactions are designed to:
- eliminate injurious stimulus
- repair associated tissue damage

evoked, defensive response
- doens’t happen spontaneously or proactively

stereotypical phenomenon
- limited # + type of inflammatory responses
- different stimuli can elicit same response

can also cause harm by doing more damage than original stimuli

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2
Q

5 cardinal signs of inflammation

A

heat
redness
swelling
pain
loss of function

not all 5 have to be present at once

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3
Q

Inflammation + Death

A

cannot or begin after death

identifying inflammatory changes can differentiate anthemortem necrosis from postmortem autolysis

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4
Q

Not all inflammatory responses are created equal

A

altho responses are stereotyped, they can vary significantly in:
- intensity
- magnitude
- duration

depends on multiple factors:
- innate immune response
- immunological status of host
- type of agent involved

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5
Q

Inflammation is a key component of host defense

A
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6
Q

5 Phases of Inflammation

A

1) recognition of inflammatory stimulus
2) acute vascular response
3) acute cellular response
4) chronic cellular response
5) resolution

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7
Q

Exogenous Substances v Endogenous Substances Inducing Tissue Injury

A

Exogenous:
- microbes = viruses, bacteria, protozoa, etc.
- foreign bodies = suture, plant material, etc.
- mechanical action = injury
- physical actions = thermal/freezing injury
- chemical substances caustic agents, venoms, etc.

Endogenous:
- autoimmune reactions = antibodies directed at self-antigens
- IC signals released from injured/dying cells

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8
Q

PAMPs

Pathogen-Associated Molecular Patterns

A

highly conserved microbial ligands

recognized as “non-self” by host cells = macrophages, leukocytes, mucosal epithelium

recognized by PRRs on/within host cells

binding results in downstream induction of inflammatory mediators

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9
Q

DAMPS

Damage-Associated Molecular Patterns

A

endogenous mol. released from damage/dying cells

their presence extracellularly alters nearby cells to presence of injury

binds PRRs for downstream induction of inflammatory mediators

Mechanims:
- EC presence of some mol. signals for damaged cell membranes
- release of IC enzymes causes breakdown of EC components which can also be recognized as DAMPs
- circulating antibodies may recognize IC antigens to activate complement system

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10
Q

PAMPs v DAMPs

A
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11
Q

Mast Cells

1st responders

A

1st responders = already present in tissues

often close to site of injury = situated around vessels + close to peripheral nerves

contained preformed vasoactice mediators within granules:
- histamine
- serotonin

Receptors:
- FcE = Binds IgE
- PRRs
- complement receptors
- other

degranulate in response to receptor binding, physical trauma, temp extremes, etc. = release histamine + serotonin
- vasodilation
- increased vascular permeability

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12
Q

Resident Tissue Macrophages

1st responders

A

recognize inflamatory stimuli + initiate inflammatory response via binding of PRRs

already present in tissue = no need to recruit from distant sites

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13
Q

Epithelial Cells

1st responders

A

may secrete cytokines when injured or recognize inflammatory stimuli via PRRs

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14
Q

Platelets

as initiators of inflammation

A

active role in inflammation + coagulation

aggregate + accumulate at sites of endothelial injury

activated by collagen to release inflammatory mediators
- vasoactive amines (serotonin + histamine)
- complement activators
- platelet activating factor
- coagulation factors

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15
Q

other vasoactive mediators

A

Bradykinin
- released from damaged vascular endothelium
- causes vasodilation

Prostaglandins + Leukotrienes
- produced by many cell types in response to PRR activation
- cause vasodilation + increased vascular permeability

Platelet-Activating Factor (PAF)
- produced by many cell types in response to PRR activation
- causes increased vascular permeability + smooth muscle contraction

these become active later in the inflammatory response

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16
Q

Vascular Permeability Response is Biphasic

A

initial arteriolar dilation + increased vascular permeability occur almost immediately
- histamines, kinins, etc.

second wave of vascular permeability changes occurs following de novo synthesis synthesis of inflammatory mediators
- IL-1, TNFα, kinins, etc.

17
Q

Histamine Effects on Capillary Beds

A

arteriolar dilation drives increased blood flow
venule dilation causes blood stasis

net effect = increased capillary hydrostatic pressure
- leakage of fluid + plasma proteins
- compounded by increased vascular permeability

18
Q

Vascular permeability mechanisms

A
19
Q

Effects of Acute Vascular Response

A

“active hyperemia” = aka redness
- vasolidation
- blood stasis

tissue swelling
1) leakage of plasma proteins
- increased hydrostatic pressure
- increased vascular permeability
2) +/- leakage of macromolecules + leukocytes
- endothelial gaps
- endothelial injury

20
Q

Fluid leaks from vasculature during inflammatory responses

A

usually rich in both cells + protein

cell types may reflect cause + duration of inflammation

characteristics change with time = reflect duration

analyzing cell makeup of inflammatory lesion is an important tool in diagnosis of many infectious diseases + other pathologic processes

21
Q

Neutrophils

Inflammation Respose

A

often predominant if response is acute +/or bacterial

key effector cell in acute inflammatory response

1st cell to enter area of injury from bloodstream
- move rapidly by amoeboid motion (crawl on substrate)

segmented nucleus (2-5 nuclear segments)

intensely phagocytic

granules are lyzosomes which contain powerful degradative enztmes

unstable + short-lived in circulation
- more persistent in tissue

22
Q

Neutrophils + Macrophages

Inflammation Respose

A

lesions which are subacute to chronic

relative # of macropjages tends to increase with chronicity

23
Q

Eosinophils

Inflammation Respose

A

parasitic disease + acute hypersensitivity reactions

24
Q

Lymphocytes + Plasma Cells

Inflammation Response

A

antigenic stimulation or delayed-type hypersensitivity

appearance signifies chronic

25
Q

Movement of cells into inflammatory lesion

A
26
Q

PMNCs

Polymorphonuclear cells

aka granulocytes

A

contian distinctively lobulated/segmented nuclei

granules contain enzymes + mediators of inflammation
- neutrophils = nonstaining/pink granules
- eosinophils = bright red/orange granules
- basophils = dark blue/purple granules

terminally differentiated = do not divide + short half-life

found circulating in blood + tissues
- normal conc. in blood varies by species

27
Q

H

Heterophils

Birds + Reptiles

A

elongate red granules

not as antibacterial as mammalian neutrophils
- lack myeoloperoxidase
- both morphologic + functional difference

28
Q

Heterophils

Rabbits, Guinea Pigs, Elephants, etc.

A

bright red granules

no difference in function compared to neutrophils
- only diff is morphology on blood smear
- heterophils based on appearance, neutrophils based on function
- terminology is pathologist or clinician dependent

29
Q

How do neutrophils move from vasculature to tissue?

A

3 step process:
- adherence
- migration
- chemotaxis

30
Q

Adherence

Stasis + Margination

A

Stasis = blood flow through affected tissues is slowed

Margination = neutrophils move toward endothelial surface as blood stasis occurs

Endothelium expresses selectins = P-selectin + E-selectin
- in response to histamine, thrombin, PAF, etc
- preformed in endothelial granules (Weibel-Palade bodies)

31
Q

Adherence

Rolling

A

neutrophil ligands specifically interact with endothelial selectins
- Slialyl Lewis X-modified glycoproteins
- L-selectin (variable by species)

Rolling = continued binding + unbinding slows neutrophils to an eventual stop along endothelial surface

memory tip for selectins = L for lekocytes

still reversible

32
Q

Adherence

Pavementing

aka stable adhesion

A

irreversible process

flattening of neutrophil on endothelial surface

induced by IL-1 + TNFα

Mediated by:
- β2-integrins (CD11/Cd18) on neutrophils
- ICAM-1 + VCAM-1 on endothelial cells

33
Q

Migration

A

neutrophils exit vessel by diapedesis
- PECAM-1 in endothelial cell junctions + on leukocytes bind to itself
- leukocytes squeeze through endothelial cell junctions = occurs at post-cap venules + capillaries

34
Q

Leukocyte Adhesion Cascade

A

General Pathology (15 decks)

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