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General Pathology > Exam #1: Acute Inflammation I > Flashcards

Exam #1: Acute Inflammation I Flashcards

1
Q

What is the definition of inflammation?

A

Inflammation is the LOCAL reaction of VASCULARIZED tissue to injury

*No vasculature & no injury= no inflammation

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2
Q

List the timescale for acute, subacute, & chronic inflammation?

A 
Acute= 0-2 days 
Subacute= 2-14 days 
Chronic= >14 days i.e. greater than 2 weeks

*Less than 2 days= acute & greater than 2 weeks= chronic; the middle is subacute

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3
Q

What inflammatory cells mediate acute inflammation?

A

Neutrophils

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4
Q

What inflammatory cells mediate subacute inflammation?

A
  • Neutrophils
  • Monocytes
  • Lymphocytes (B, T & NK Cells)
  • Plasma cells
  • Fibroblasic elements
  • Angioblastic elements
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5
Q

What inflammatory cells mediate chronic inflammation?

A

Mononuclear cells:

  • Monocytes that become macrophages once they’re out of the vascular system
  • Lymphocytes
  • Granuloma cells= macrophage changed cells
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6
Q

Describe the time course of inflammatory cell infiltration.

A

The hallmark of acute inflammation is increased vascular permeability leading to the escape of protein-rich exudate into the extravascular tissue, causing edema

  • Neutrophils are the primary cells present on Day 1
  • By ~Day 2 Monocyte/ Macrophages are more abundant
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7
Q

What are the characteristics of eosinophils?

A
  • Eosinophils contain pink granules
  • Present normally as 5-10 %
  • Predominant inflammatory cells in allergic reactions & parasitic infestations
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8
Q

If you see eosinophilia i.e. an eosinophil concentration greater than 5-8%, what should you consider?

A
  • Allergic reaction

- Parasite infections

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9
Q

List the plasma derived molecules that take part in the inflammatory response.

A
  • Immune system cells (Ab, C3, C5fragments)
  • Kinin system (bradykinin)
  • Clotting (thrombin)
  • Fibrinolytic (plasmin)
  • Acute phase proteins (CRP, ceruloplasmin, haptoglobin)
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10
Q

List the tissue derived molecules that take part in the inflammatory response.

A
  • Vaosactive amines (histamine & 5-HT)
  • Acidic lipids (prostaglandins, leukotrienes, lipoxins)
  • Cytokines (IL-1, TNF) & chemokines (IL-8)
  • Others (PAF, NO, ROS, lysosomal enzymes)
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11
Q

Why is inflammation a “double-edged” sword?

A

Inflammation is fundamentally protective

  • Rids the organism of initial cause of injury
  • Rids the organism of consequences of injury

However, inflammation & repair may be potentially harmful

  • Underlies chronic inflammatory disease
  • Hypersensitivity
  • Scarring
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12
Q

What are the six cardinal signs of inflammation? What causes these six cardinal signs?

A

1) Heat= increased blood flow
2) Redness= increased blood flow
3) Swelling= accumulation of water & cells
4) Pain= pressure of fluid & effect of mediators
5) Loss of function secondary to above
6) Systemic changes= release of humoral factors

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13
Q

List the various causes of acute inflammation?

A
  • Infection
  • Trauma
  • Physical injury from thermal extremes of from ionizing radiation
  • Chemical injury i.e. poisons
  • Immunologic injury
  • Tissue death i.e. inflammatory changes that occur in viable tissue adjacent to necrotic areas
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14
Q

Describe the serous pattern seen in acute inflammation.

A

Serous= outpouring of watery, protein-poor fluid

E.g. pleural effusion & skin blisters

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15
Q

Describe the fibrinous pattern seen in acute inflammation.

A
  • Seen in more severe injury
  • Increased vascular permeability leads to leakage of larger fibrinogen molecules

E.g. fibrinous pericarditis

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16
Q

What happens with fibrinous patterns of inflammation?

A

1) May resolve over time by fibrinolysis & normal tissue structure restored
2) If not resolved, will lead to ingrowth of fibroblasts & blood vessels (organization)–>scarring

17
Q

Describe the suppurative pattern seen in acute inflammation.

A

Suppurative (purulent) inflammation= large amounts of pus (neutrophils, necrotic cells, & edema)
- Pyogenic organisms e.g. streptococci are notorious for causing this type of infection

E.g. acute appendicitis

18
Q

What is an abscess? What happens when an abscess is NOT resolved?

A

An abscess is a focal collection of pus with central necrotic region surrounded by a “preserved” layer of neutrophils

*This may become walled off by fibroblastic proliferation

19
Q

Describe the pattern of ulceration seen in acute inflammation.

A

Ulceration= local defect, excavation produced by sloughing of inflammatory necrotic tissue

  • Acute= neutrophils & vascular dilation
  • Chronic= fibroblastic proliferation

*Can only occur on or near a surface i.e. skin & mucosa
E.g. inflammatory necrosis of the mucosa of the mouth, stomach, intestines, GU tract, or subcutaneous tissue of lower extremities…“Peptic ulcers are a good example”

20
Q

What are the four possible outcomes of acute inflammation?

A

1) Resolution
2) Healing by scarring
3) Abscess
4) Progression to chronic inflammation

21
Q

What are the key events of acute inflammation?

A

1) Changes in vascular caliber that lead to increased blood flow
2) Structural changes that enable plasma proteins & leukocytes to leave the circulation
3) Emigration of leukocytes from microcirculation & their accumulation in the focus of the injury

22
Q

What hemodynamic changes occur in the vasculature during acute inflammation?

A
  • Initial & transient vasoconstriction followed by vasodilation–>increased flow
  • Increased vascular permeability at the level of the postcapillary venules
23
Q

What is transudation?

A

Fluid leakage seen in conditions of:

  • Increased hydrostatic pressure
  • Decreased colloid osmotic pressure

Transudate is a fluid with low protein content, little or no cellular material, and a low specific gravity; essentially, this is an ultrafiltrate of blood plasma

*The connection between endothelial cells are still “tight” enough that proteins are NOT leaking out

24
Q

What is exudation?

A

Fluid AND protein leakage in conditions of (inflammation):

  • Widening of endothelial junctions
  • Monocytes, lymphocytes, and neutrophils leak

Thus, the difference between transudate & exudate= protein

25
Q

What are the consequences of “leakage” in the vasculature?

A
  • Edema
  • Stasis of circulation resulting in increased viscosity
  • Decreased absorption from interstitial space
26
Q

Describe the process of leukocyte extravasation.

A

1) Migration
2) Adhesion
3) Emigration
4) Chemotaxis

27
Q

What is the function of a fliopodium?

A

Movement in the direction of chemotaxis

28
Q

Describe the mechanism of leukocyte exudation.

A

1) Rolling
2) Adhesion due to selectins & integrins
3) Transmigration in the direction of chemotaxis

29
Q

What are cell adhesion molecules?

A

Membrane proteins that promote leukocyte attachment & participation in the inflammatory response

  • Selectins (rolling)
  • Ig family
  • Integrins (adhesion)
30
Q

What are selectins? What is their function?

A
  • Ca++ dependent lectins expressed non-specifically
  • Serve as the homing receptors that mediate ROLLING of leukocytes along the endothelium at sites of inflammation
  • NOT involved in firm adhesion
  • Slow down circulating leukocytes

*****Selectins= rolling

31
Q

What are the different classes of selectins?

A 
P-selectin= platelets
E-selectin= endothelium 
L-selectin= leukocytes
32
Q

What is ICAM-1?

A

This is the LIGAND for LFA-1 & MAC-1 INTEGRINS

  • “Intercellular adhesion molecule-1”
  • Assists in localization of leukocytes to tissue injury
  • Expressed on ENDOTHELIUM
  • Binds integrins, LFA-1 & Mac-1 present on neutrophils & macrophages
33
Q

What is VCAM-1?

A

This is the LIGAND for VLA-4 INTEGRIN

  • “Vascular cell adhesion molecule”
  • Binds integrin VLA-4 on lymphocytes, monocytes, eosinophils, and basophils
34
Q

What is PECAM-1?

A

This is an adhesion molecule present in the intercellular junction between endothelial cells that is involved in the migration of leukocytes
- “Platelet endothelial cell adhesion molecule” or CD31

*Plays and important role in the diapedesis step of leukocyte emigration

35
Q

What are integrins?

A
  • Group of adhesion molecules that are expressed on leukocytes & composed of heterodimers of alpha & beta subunits, which act in regulation of cell-matrix & cell-cell adhesion
  • Transmembrane proteins that link the exterior of the cell to the cytoskeleton
36
Q

What are B1 integrins?

A

VLA-4 is an B1 integrin expressed on leukocytes that binds VCAM-1 on endothelial cells

37
Q

What are B2 integrins?

A

“Leukocyte function associated antigens”

- LFA-1 & Mac-1 ICAM-1 to assist in localization of phagocytes to injury sites and subsequent extravasation

General Pathology (33 decks)

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