Inflammation

Question 1

5 cardinal signs of inflammation

Answer 1

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

Question 2

stages of acute inflammatory response

Answer 2

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

Question 3

transudate

Answer 3

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

Question 4

exudate

Answer 4

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

Question 5

4 possible types of acute inflammation

Answer 5

serous, fibrinous, suppurative, ulcerative inflammation

Question 6

pus

Answer 6

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

Question 7

abscess

Answer 7

part of suppurative inflammatory response

Question 8

ulcer

Answer 8

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

Question 9

morphology of chronic inflammation

Answer 9

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

Question 10

morphology of granuloma

Answer 10

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

Question 11

mechanism of granulomatous inflammation

Answer 11

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.

Question 12

general causes of inflammation

Answer 12

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

Question 13

ultimate goal of inflammatory process

Answer 13

phagocytosis and restoration of tissue integrity and function

Question 14

characteristics of acute inflammation

Answer 14

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

Question 15

characteristics of chronic inflammation

Answer 15

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

Question 16

pathophysiology of rubor/calor

Answer 16

vascular dilation, increased blood flow during acute inflammatory response

Question 17

pathophysiology of tumor

Answer 17

increased vascular permeability leading to tissue edema and accumulation of neutrophils

Question 18

pathophysiology of dolor

Answer 18

chemical mediators such as bradykinin

Question 19

pathophysiology of function laesa

Answer 19

tissue damage, pain, swelling

Question 20

components of acute inflammation

Answer 20

vascular and cellular response

Question 21

three major processes of acute inflammation

Answer 21

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

Question 22

components of acute inflammatory vascular rxn

Answer 22

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

Question 23

components of acute inflammatory cellular rxn

Answer 23

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

Question 24

increased permeability via gaps due to endothelial contraction

Answer 24

histamine, bradykinin, leukotrienes

Question 25

mechanisms for increased vascular permeability

Answer 25

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

Question 26

edema

Answer 26

increased fluid in interstitial tissues or serous cavities

Question 27

effusions

Answer 27

pathologic accumulation of fluid in a body cavity

Question 28

ascites

Answer 28

specific term for an effusion of the abdominal or peritoneal cavities

Question 29

adhesion molecules in acute inflammation

Answer 29

selectins, immunoglobulin family adhesion proteins, integrins

Question 30

selectins

Answer 30

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

Question 31

Ig family adhesion proteins

Answer 31

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

Question 32

integrins

Answer 32

expressed on leukocytes and participate in rolling and extravasation

Question 33

chemotactic factors for neutrophils

Answer 33

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

Question 34

histamine

Answer 34

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

Question 35

serotonin

Answer 35

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

Question 36

arachidonic acid

Answer 36

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

Question 37

cytokines involved in inflammation

Answer 37

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

Question 38

nitric oxide

Answer 38

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

Question 39

platelet activating factor (PAF)

Answer 39

triggers release of histamine, activates platelets, enhance neutrophil adhesion

Question 40

importance of factor 12 in inflammation

Answer 40

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

Question 41

leukocytosis

Answer 41

elevated white blood count (left shift, bandemia)

Question 42

erythrocyte sedimentation rate (ESR)

Answer 42

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

Question 43

how does increased fibrinogen cause rouleaux formation?

Answer 43

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

Question 44

when is ESR increased?

Answer 44

inflammation, malignancy, pregnancy

Question 45

when is ESR decreased?

Answer 45

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

Question 46

serous inflammation

Answer 46

fluid collection (vascular>cellular). blisters

Question 47

fibrinous inflammation

Answer 47

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

Question 48

suppurative inflammation

Answer 48

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

Question 49

4 possible outcomes of acute inflammation

Answer 49

complete resolution, abscess formation, chronic inflammation, scar formation

Question 50

complete resolution of acute inflammation

Answer 50

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

Question 51

abscess

Answer 51

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

Question 52

chronic infection initiator cells

Answer 52

macrophages via INF-gamma

Question 53

causes of granulomatous inflammation

Answer 53

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