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MDTI > Inflammation > Flashcards

Inflammation Flashcards

1
Q

5 cardinal signs of inflammation

A

dolor (pain), tumor (swelling), rubor (erythema), calor (heat), functio laesa (loss of function)

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2
Q

stages of acute inflammatory response

A

irritation, sensation, activation of vascular/cellular responses, leukocyte migration, invasion, evacuation, systemic rejection

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3
Q

transudate

A

not due to increased vascular permeability, no increase in protein concentration, occurs with osmotic or hydrostatic imbalance (i.e. nephrotic syndromes)

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4
Q

exudate

A

acute inflammatory fluids due to increased vascular permeability, protein & cellular debris present

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5
Q

4 possible types of acute inflammation

A

serous, fibrinous, suppurative, ulcerative inflammation

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6
Q

pus

A

a purulent exudate composed of many neutrophils and necrotic cell debris with/without microbes

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7
Q

abscess

A

part of suppurative inflammatory response

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8
Q

ulcer

A

focal erosion of a superficial tissue plane (usually skin or mucosal surface) with active acute inflammation. margins become more defined with chronicity

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9
Q

morphology of chronic inflammation

A

presence of lymphocytes, macrophages, eosinophils, neutrophils. alteration of tissue architecture

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10
Q

morphology of granuloma

A

aggregates of epithelioid histocytes/activated macrophages with multinucleated giant cells. if necrotizing, caseous necrosis is present.

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11
Q

mechanism of granulomatous inflammation

A

foreign antigen activates CD4 T cell, which produces cytokines (TNF, IL17) that recruit monocytes to activate (INF gamma) tissue macrophages=fusion to giant cells and granuloma.

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12
Q

general causes of inflammation

A

microbial infections, necrotic tissue, physical agents, foreign bodies, immune rxns, trauma, chemical agents

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13
Q

ultimate goal of inflammatory process

A

phagocytosis and restoration of tissue integrity and function

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14
Q

characteristics of acute inflammation

A

rapid onset, short duration, increased tissue fluid, accumulation of neutrophils

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15
Q

characteristics of chronic inflammation

A

longer duration, infiltration of macrophages/monocytes/lymphocytes, alteration of tissue histoarchitecture including fibrosis

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16
Q

pathophysiology of rubor/calor

A

vascular dilation, increased blood flow during acute inflammatory response

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17
Q

pathophysiology of tumor

A

increased vascular permeability leading to tissue edema and accumulation of neutrophils

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18
Q

pathophysiology of dolor

A

chemical mediators such as bradykinin

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19
Q

pathophysiology of function laesa

A

tissue damage, pain, swelling

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20
Q

components of acute inflammation

A

vascular and cellular response

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21
Q

three major processes of acute inflammation

A
  1. alterations in vascular caliber that lead to an increase in blood flow
  2. structural changes in the microvasculature that permit plasma proteins and leukocytes to leave circulation
  3. emigration, accumulation, activation of leukocytes to eliminate offending agent
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22
Q

components of acute inflammatory vascular rxn

A

vasodilation (histamine, NO), increased permeability (endothelial gaps due to histamine, bradykinin, leukotrienes), stasis, leukocyte accumulation

23
Q

components of acute inflammatory cellular rxn

A

leukocyte extravasation (cell surface molecules), leukocyte activation (arachidonic acid metabolites/cytokines), phagocytosis, termination of inflammatory response

24
Q

increased permeability via gaps due to endothelial contraction

A

histamine, bradykinin, leukotrienes

25
Q

mechanisms for increased vascular permeability

A

endothelial gaps, direct injury, leukocyte mediated injury, increased transcytosis pathways, new vessel formation (inherently leaky)

26
Q

edema

A

increased fluid in interstitial tissues or serous cavities

27
Q

effusions

A

pathologic accumulation of fluid in a body cavity

28
Q

ascites

A

specific term for an effusion of the abdominal or peritoneal cavities

29
Q

adhesion molecules in acute inflammation

A

selectins, immunoglobulin family adhesion proteins, integrins

30
Q

selectins

A

(E,P,L-selectins) expressed on leukocytes and endothelial cells that facilitate the rolling of neutrophils. but don’t bind to each other

31
Q

Ig family adhesion proteins

A

(ICAM, PECAM) expressed on endothelial cells and bind to integrins on the surface of leukocytes to facilitate leukocyte adhesion and transmigration

32
Q

integrins

A

expressed on leukocytes and participate in rolling and extravasation

33
Q

chemotactic factors for neutrophils

A

bacterial products, complement components especially C5, arachidonic acid metabolites (leukotrienes), and kallikrein

34
Q

histamine

A

early mediator of vascular rxn including vasodilation and increased permeability. preformed in mast cells, act mainly on endothelial receptors

35
Q

serotonin

A

vasodilation, increased permeability. preformed in platelets (released upon aggregation) and neuroendocrine cells.

36
Q

arachidonic acid

A

fatty acid residing in cell membrane phospholipids. can be converted into prostaglandins, leukotrienes, lipoxins, TxA2, chemotactic molecules, etc.

37
Q

cytokines involved in inflammation

A

TNF alpha & IL1 (from inflammasome) =both local and systemic effects. fever, fatigue, endothelial effects, fibroblast effects, increased cytokine production

38
Q

nitric oxide

A

produced by endothelial cells and macrophages, relaxes vascular smooth muscle resulting in dilation. inhibits platelet aggregation

39
Q

platelet activating factor (PAF)

A

triggers release of histamine, activates platelets, enhance neutrophil adhesion

40
Q

importance of factor 12 in inflammation

A

links kinin (kallikrein=chemotaxis), coagulation (intrinsic pathway), and complement systems.

41
Q

leukocytosis

A

elevated white blood count (left shift, bandemia)

42
Q

erythrocyte sedimentation rate (ESR)

A

nonspecific test for systemic inflammatory response. increased fibrinogen leads to rouleaux formation and increased density=faster sedimentation

43
Q

how does increased fibrinogen cause rouleaux formation?

A

it reduces the surface negative charge on cells so that RBCs don’t repel each other and actually clump together

44
Q

when is ESR increased?

A

inflammation, malignancy, pregnancy

45
Q

when is ESR decreased?

A

polycythemia, sickle cell anemia, congestive heart failure, hypofibrinogemia, microcytosis

46
Q

serous inflammation

A

fluid collection (vascular>cellular). blisters

47
Q

fibrinous inflammation

A

vascular permeability increases sufficiently to allow increasingly large molecules such as fibrinogen to lead to sticky coagulum (common on body linings)

48
Q

suppurative inflammation

A

inflammatory exudate composed of bacteria, sloughed/necrotic cells, and neutrophils

49
Q

4 possible outcomes of acute inflammation

A

complete resolution, abscess formation, chronic inflammation, scar formation

50
Q

complete resolution of acute inflammation

A

most often occurs when injurious agent is eliminated and process is short lived.

51
Q

abscess

A

cavitated lesion of acute inflammation with central accumulation of neutrophils plus cell and tissue debris. over time a fibrous ring separates the cavity from the surrounding tissue

52
Q

chronic infection initiator cells

A

macrophages via INF-gamma

53
Q

causes of granulomatous inflammation

A

TB!!!!, mycobacteria, leprosy, syphilis, foreign bodies, autoimmune mediated, etc

MDTI (42 decks)

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