Pathology - Inflammation Flashcards

1
Q

inflammation - overview

A

*response to eliminate initial cause of cell injury, to remove necrotic cells resulting from the original insult, and to initiate tissue repair
*divided into acute and chronic
*the inflammatory response itself can be harmful to the host if the reaction is excessive (eg. shock), prolonged (eg. persistent infections like TB), or inappropriate (eg. autoimmune diseases like SLE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cardinal signs of inflammation

A
  1. rubor and calor
  2. tumor
  3. dolor
  4. functio lasea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cardinal sign of inflammation: rubor & calor

A

*redness & warmth
*vasodilation (relaxation of arteriolar smooth muscle) → increased blood flow
*mediated by histamine, prostaglandins, bradykinin, NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cardinal sign of inflammation: tumor

A

*swelling
*endothelial contraction/disruption → increased vascular permeability → leakage of protein-rich fluid from postcapillary venules into interstitial space (exudate) → increased interstitial oncotic pressure
*endothelial cell contraction mediated by leukotrienes (C4, C4, E4), histamine, serotonin, bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cardinal sign of inflammation: dolor

A

*pain
*sensitization of sensory nerve endings
*mediated by bradykinin, PGE2, histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cardinal sign of inflammation: functio laesa

A

*loss of function
*inflammation impairs function (eg. inability to make fist due to hand cellulitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

systemic signs of inflammation

A
  1. fever
  2. leukocytosis
  3. increased plasma acute phase reactants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

systemic sign of inflammation: fever

A

*pyrogens (eg. LPS) induce macrophages to release IL-1 and TNF → increased COX activity in perivascular cells of anterior hypothalamus → increased PGE2 → increased temperature set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

systemic sign of inflammation: leukocytosis

A

*increased WBC count; type of predominant cell depends on inciting agent or injury (eg. bacteria = increased neutrophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

systemic sign of inflammation: increased plasma acute-phase reactants

A

*serum concentrations significantly change in response to acute and chronic inflammation
*produced by the liver
*notably induced by IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

acute phase reactant: C-reactive protein (CRP)

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*opsonin; fixes complement and facilitates phagocytosis
*measured clinically as a nonspecific sign of ongoing inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

acute phase reactant: ferritin

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*binds and sequesters iron to inhibit microbial iron scavenging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

acute phase reactant: fibrinogen

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*coagulation factor; promotes endothelial repair; correlates with ESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

acute phase reactant: haptoglobin

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*binds extracellular hemoglobin, protects against oxidative stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

acute phase reactant: hepcidin

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*decreased iron absorption (by degrading ferroportin) and decreased iron release from macrophages → anemia of chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

acute phase reactant: procalcitonin

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*increases in BACTERIAL infections; normal in viral infections

17
Q

acute phase reactant: serum amyloid A

A

*positive acute-phase reactant (upregulated in the presence of inflammation)
*prolonged elevation can lead to secondary amyloidosis (AA)

18
Q

acute phase reactant: albumin

A

*negative acute-phase reactant (downregulated in the presence of inflammation)
*reduction conserves amino acids for positive reactants

19
Q

acute phase reactant: transferrin

A

*negative acute-phase reactant (downregulated in the presence of inflammation)
*internalized by macrophages to sequester iron

20
Q

acute phase reactant: transthyretin

A

*negative acute-phase reactant (downregulated in the presence of inflammation)
*aka prealbumin
*reduction conserves amino acids for positive reactants

21
Q

erythrocyte sedimentation rate (ESR) - overview

A

*RBCs normally remain separated via negative charges
*products of inflammation (eg. fibrinogen) coat RBCs → decreased negative charge → increased RBC aggregation
*denser RBC aggregates fall at a faster rate within the pipette tube → elevated ESR
*often co-tested with CRP

22
Q

causes of elevated ESR

A

*most anemias
*infections
*inflammation
*cancer
*renal disease
*pregnancy

23
Q

causes of decreased (lower-than-expected) ESR

A

*sickle cell anemia
*polycythemia
*heart failure
*microcytosis
*hypofibrinogenemia

24
Q

acute inflammation - overview

A

*transient and early response to injury or infection
*characterized by neutrophils in tissue, often with associated edema
*rapid onset (seconds to minutes) and short duration (minutes to days)
*represents a reaction of the innate immune system

25
Q

acute inflammation - stimuli

A

*infections
*trauma
*necrosis
*foreign bodies

26
Q

acute inflammation - mediators

A

*toll-like receptors (TLRs)
*arachidonic acid metabolites
*neutrophils
*eosinophils
*antibodies (pre-existing)
*mast cells
*basophils
*complement
*Hageman factor (factor XII)

27
Q

acute inflammation - vascular component

A

*vasodilation (→ increased blood flow and stasis) and increased endothelial permeability (contraction of endothelial cells opens interendothelial junctions)

28
Q

acute inflammation: cellular component

A

*extravasation of leukocytes (mainly neutrophils) from postcapillary venules → accumulation of leukocytes in focus of injury → leukocyte activation

29
Q

acute inflammation - potential outcomes

A
  1. resolution and healing (IL-10, TGF-beta)
  2. persistent acute inflammation (IL-8)
  3. abscess (acute inflammation walled off by fibrosis)
  4. chronic inflammation (antigen presentation by macrophages & other APCs → activation of CD4+ Th cells)
  5. scarring