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HMS Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Five Cardinal Symptoms of Inflammation

A

Calor (heat)

Rubor (redness)

Tumor (swelling)

Dolor (pain)

Functio laesis (loss of function)

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2
Q

Waves of acute inflammation

A
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3
Q

amplification cascades

A

one mediator activates the next one

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4
Q

Change in vascular flow during acute inflammation

A
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5
Q

Major mediators of vasodilation in acute inflammation

A
  1. Histamine
  2. Nitric oxide
  3. Eicosanoids
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6
Q

Effects on endothelium during inflammation

A

histamine, bradykinin, and leukotrienes -> endothelial contraction

IL-1, TNF-a -> endothelial retraction

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7
Q

endothelial injury

A

As acute inflammation progresses, endothelial cells may die either by necrosis or by apoptosis, resulting in further increases in vascular permeability.

In addition, leukocytes may injure endothelium through the reactive oxygen species, enzymes, and prostaglandins that they release.

Endothelial injury is a major element in the pathology of vascular disease, and in particular atherosclerosis.

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8
Q

Transudation vs Exudation

A

Transudate: filtrate of blood plasma that contains little protein.

Exudate: protein-rich fluid and even cells. Increases the osmotic pressure of the interstitial fluid and creates edema.

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9
Q

Leukocyte rolling

A
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10
Q

Major selectins involved in leukocyte adhesion/rolling

A
  • E-selectin (also called CD62E), confined to endothelium
  • P-selectin (CD62P), present on endothelium and platelets
  • L-selectin (CD62L), on the surface of most leukocytes

Selectins bind oligosaccharides (e.g., sialyl-Lewis X on leukocytes) that decorate mucin-like glycoproteins on their target cells.

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11
Q

E-selectin is expressed in response to . . .

A

IL-1 and TNF-a

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12
Q

Principal integrin interactions that mediate endothelial arrest

A

Endothelium: ICAM-1 (binds to neutrophils, MO, Lymphocytes), VCAM-1 (binds to MO and Lymphocytes, but not neutrophils)

ICAM-1 ligands: LFA-1, Mac-1

VCAM-1 ligands: VLA-4

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13
Q

Phagocytic Engulfment

A
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14
Q

Diapedesis

A

PECAM-1 and CD99-mediated

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15
Q

Chemokine Receptors

A

seven-transmembrane spanning, G protein-coupled receptors to generate diacylglycerol (DAG) and inositol triphosphate (IP3 ), downstream triggering Ca2+ release.

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16
Q

Histamine

A

Preformed histamine is stored in mast cell granules and is released in response to a variety of stimuli:

  • physical injury such as trauma or heat
  • Immune reactions involving IgE
  • anaphylatoxins (C3a and C5a)
  • leukocyte-derived histamine-releasing proteins
  • neuropeptides (Substance P)
  • Certain ​cytokines
17
Q

Nitric oxide in smooth muscle

A

Activates guanylyl cyclase in vascular smooth muscle, resulting in increased cyclic guanosine monophosphate (cGMP) and ultimately smooth muscle relaxation (vasodilation).

18
Q

Roles of nitric oxide in inflammation

A

(1) vascular smooth muscle relaxation (vasodilation)
(2) antagonism of all stages of platelet activation (adhesion, aggregation, and degranulation)
(3) reduction of leukocyte recruitment at inflammatory sites
(4) acting as a microbicidal agent (with or without superoxide radicals) in activated macrophages.

19
Q

Arachadonic acid metabolism overview

A
20
Q

Leukotriene antagonists

A

montelukast and zafirlukast

Block leukotriene receptors, inhibiting the lipoxygenase arm of the eicosanoid pathway, and are used to treat asthma. Antagonizes LTC4-mediated vasoconstriction.

21
Q

Corticosteroids and AA metabolsim

A

Inhibit phospholipase A2 and prevent release of arachidonic acid, blocking both the cyclooxygenase and lipoxygenase pathways.

22
Q

Complement

A
23
Q

Kinin and Clotting Cascades

A
24
Q

Kinins

A

Factor XIIa cleaves prekallikrein to kallikrein, resulting in kinin production.

Most notable among the kinins is bradykinin.

Kinins are responsible for the pain associated with acute inflammation.

25
Q

fibrinolytic system

A

Also activated by kallikrein following Factor XIIa cleavage.

Kallikrein cleaves plasminogen to plasmin, which lyses fibrin clots, and also activates the complement cascade.

26
Q

Thrombin

A

Final target of the coagulation cascade.

In addition to making fibrin (which forms the clot), thrombin is also a direct activator of neutrophils, and thus contributes to acute inflammation.

27
Q

Platelet activating factor (PAF)

A

Like the eicosanoids, is generated from membrane phospholipids by phospholipase A2. PAF acts directly on target cells via a specific G protein-coupled receptor.

PAF can elicit most of the features of inflammation, including enhanced leukocyte adhesion (via integrin conformational changes), chemotaxis, leukocyte degranulation, and the oxidative burst

28
Q

Lysosomal constituents

A

The lysosomal granules of neutrophils and monocytes contain multiple mediators of acute inflammation

While acid proteases have acidic pH optima, and are generally active only within phagolysosomes, neutral proteases, including enzymes such as elastase, collagenase, and cathepsin, are active in the extracellular matrix and cause destructive tissue injury by degrading elastin, collagen, basement membrane, and other matrix proteins.

Neutral proteases can also cleave C3 and C5 to generate the C3a and C5a anaphylatoxins, and can promote the generation of bradykinin-like peptides from kininogen.

29
Q

Acute inflammation mediator summary

A
30
Q

Acute-phase reactions

A

The systemic effects of acute inflammation.

Fever as well as somnolence, malaise, and anorexia. Degradation of skeletal muscle proteins, hypotension, hepatic synthesis of complement and clotting factors, and alterations in the circulating white blood cell pool.

Important mediators include IL-1, IL-6, and TNFα.

31
Q

How inflammation induces fever

A

TNF and IL-1 act on the thermoregulatory center of the hypothalamus (via local PGE2 production) to induce fever.

Hence the efficacy of aspirin and NSAIDs in reducing fever by inhibiting PGE2 production at the hypothalamus.

32
Q

Leukocytosis

A

Increased white blood cell count

Extreme leukocytosis is referred to as leukemoid reaction, since it mimics leukemia.

Most bacterial infections induce a relatively selective increase in neutrophils (neutrophilia), while parasitic infections and allergies induce eosinophilia, and certain viruses cause selective increases in lymphocytes (lymphocytosis).

33
Q
A

Edema

34
Q

Abcess formation

A
35
Q

Fibrinous exudate

A

Fibrin is visible on H&E-stained sections as amorphous, pink, proteinaceous material. It can be distinguished from fibrous connective tissue because it lacks the inherent structure of collagen or reticulin.

36
Q

Ulceration

A
37
Q

Active neutrophils

A

Active neutrophils look less like the “classic” neutrophil, their nucleus is less segmented. You will typically see many cells without nuclei indicating neutrophils that have undergone NETosis.

38
Q

Major neutrophil/macrophage growth factors

A

GM-CSF

G-CSF

IL-17

HMS Pathology (7 decks)

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