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General Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Inflammation is the reaction of blood vessels which leads to accumulation of _______ and ___________ in extravascular spaces

A

Fluids; leukocytes

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2
Q

Inflammation is fundamentally a defense mechanism in order to ___________ the initial cause of injury and the ____________ of that injury, and finally initiate _______.

A

Eliminate; consequences; repair

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3
Q

True or False: Inflammation has the potential to be more damaging to tissues than the stimulus that caused the initial damage

A

True

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4
Q

Immediate and early response to tissue injury (physical, chemical, microbiologic, etc.); occurs in seconds to minutes and last from hours to a few days

A

Acute inflammation

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5
Q

What are the outcomes of acute inflammation?

A

Complete resolution, healing by fibrosis, abscess formation, progression to chronic inflammation

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6
Q

Prolonged inflammatory response lasting weeks to years in which continuing inflammation, tissue injury, and healing (often by fibrosis) proceed simultaneously

A

Chronic inflammation

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7
Q

What is the pathologic definition of acute inflammation?

(Name the identifying components involved)

A

Edema, fibrin, and neutrophils

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8
Q

What is the pathologic definition of chronic inflammation?

(Name the identifying components involved)

A

Macrophages, lymphocytes, plasma cells, few neutrophils, fibrosis

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9
Q

What are the positive/beneficial aspects of inflammation?

A
  • Diluting/inactivating biological & chemical toxins
  • Killing/sequestering microbes, foreign material, necrotic tissue, and neoplastic cells
  • Providing wound healing factors
  • Restricting movement for healing/repair
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10
Q

What are the negative/harmful aspects of inflammation?

A
  • Excessive/prolonged release of inflammatory mediators
  • Excessive fibrosis
  • Hypersensitivity and autoimmunity
  • Link between chronic inflammation and neoplastic transformation
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11
Q

What are the two major components of acute inflammation?

A

Vascular changes (fluidic phase) and cellular components (cellular phase)

(Both orchestrated by many different chemical mediators!)

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12
Q

What is acute inflammation clinically characterized by?

(4 things)

A
  • Heat/redness (hyperemia and vasodilation)
  • Swelling (edema and emigration of leukocytes)
  • Pain (chemical mediators)
  • Loss of function (can preserve tissue & allow healing)
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13
Q

What are some causes of acute inflammation?

(Many possible answers)

A

Infectious bacteria/viruses/parasites, trauma, physical agents (heat/cold), toxins, tissue necrosis (any origin), foreign bodies, immunological reactions

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14
Q

What is the purpose of the fluidic phase of acute inflammation?

A

Dilute, isolate, and contain the stimulus + damage

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15
Q

What is the purpose of the cellular phase of acute inflammation?

A

Kill/digest (inactivate) the stimulus

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16
Q

What is the purpose of the reparative phase of acute inflammation?

A

Return the tissue to normal structure and function (involves movement of MQs to remove cellular debris and stimulate tissue repair)

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17
Q

Thin and watery and contain few cells or proteins; mechanisms include increased hydrostatic pressure, decreased osmotic pressure, and lymphatic obstruction

A

Transudate

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18
Q

Transudate that has been modified by the addition of proteins and inflammatory cells; mechanisms include endothelial damage and increased vascular permeability

A

Exudate

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19
Q

Vasoactive amines, C5a, C3a, prostaglandins, leukotrienes, PAF, IL-1, and TNF are all mediators for…

A

Vascular permeability (increase)

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20
Q

Retraction of endothelial cells, direct endothelial cell injury, and leukocyte-mediated vascular injury are all mechanisms for…

A

Increased vascular permeability

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21
Q

True or False: Retraction of endothelial cells is the least common mechanism for endothelial gap formation and very long-lived

A

False; this mechanism is the MOST common and rapid/short-lived

(also is mediated by vasoactive amines, NO, IL-1, and TNF)

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22
Q

Direct endothelial cell injury is caused by…

A

Burns and some microbial toxins (injury is rapid and may be long-lived)

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23
Q

Direct endothelial cell injury activates…

A

Platelets, clotting, and complement cascades

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24
Q

Leukocyte-mediated vascular injury is associated with…

A

Late stages of inflammation (injury is long-lived)

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25
Q

During leukocyte-mediated vascular injury, neutrophils and other leukocytes attach to endothelial cells and release _____ and _________ enzymes (from lysosomes)

A

ROS; proteolytic

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26
Q

What proteins are found in transudate and exudate, respectively?

A

Transudate = albumin
Exudate = fibrinogen and globulins

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27
Q

Presence of _______ in exudate means endothelial damage and increased vascular permeability

A

Fibrin

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28
Q

Fibrin is chemoattractant to neutrophils, which means…

A

Neutrophils will accumulate if inflammation does not resolve or it is exacerbated by chemical mediators (pro-inflammatory cytokines)

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29
Q

What are the 4 steps of the leukocyte adhesion cascade?

A
  1. Margination
  2. Rolling
  3. Activation and stable adhesion
  4. Transendothelial cell migration

(Process mediated by adhesion molecules and cytokines/chemokines)

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30
Q

What occurs during “margination”?

A

With vasodilation, leukocytes exit central region of vascular lumen and move to periphery near endothelial cell surface

31
Q

What occurs during “rolling”?

A

Leukocytes and endothelial cells make initial contact; transient, weak binding interactions occur between selections (adhesion molecules) and their receptors

32
Q

During rolling, endothelium expresses P-selection and E-selection under the influence of ____________. This reduces the velocity of the traveling leukocyte, creating the microenvironment for ________ and ________ adhesion.

A

Cytokines (histamine, TNF, IL-1); activation; stable

33
Q

What needs to happen before stable adhesion can occur?

A

Neutrophils and endothelial cells need to become activated

mediated by cytokines (IL-1, TNF) and chemokines (IL-8)

34
Q

What occurs during “stable adhesion”?

A

Binding of integrins on leukocytes to VCAM and ICAM on endothelial cells

35
Q

What occurs during “transendothelial cell migration (emigration)”?

A

Firmly adhered leukocytes emigrate across the endothelial layer by passing between endothelial cells

36
Q

Transendothelial cell migration (emigration) is mediated by expression and binding of _______ and _______ on leukocytes and endothelial cells

A

PECAM-1 (platelet endothelial cell adhesion molecule 1); JAM (junctional adhesion molecule)

37
Q

What are the major chemokines involved in chemotaxis?

A

Bacterial products, IL-8, complement components (C5a and C3a), arachidonic acid metabolites (LTB4)

38
Q

Upon entering the site of inflammation, neutrophils kill pathogens and degrade foreign materal by two mechanisms…

A
  • Phagocytosis (ROS)
  • Secretion of granule contents into exudate
39
Q

Neutrophils can contribute to tissue injury by secreting granule contents - which enzyme is the most responsible for ROS formation, leading to tissue damage and pus formation?

A

Myeloperoxidase (MPO)

40
Q

In the fluidic stage, vascular tone is controlled by vasodilator substances, namely ___ and ____________, produced by endothelial cells

A

NO; prostacyclin (PGI2)

41
Q

Where are mast cells and basophils located, and what is their role in inflammation?

A

Located around small blood and lymphatic vessels of connective tissue; both play a role in IgE-mediated hypersensitivity reactions

42
Q

IgE, C3a, C5a, heat, cold, and trauma all stimulate the release of __________ from mast cells

A

Histamine

43
Q

True or False: Neutrophils are the first leukocytes to enter exudate, and they are tasked with killing/eliminating microbes, tumor cells, and foreign materials

A

True

44
Q

What happens to neutrophils after acute inflammation resolves and cytokines withdraw?

A

Apoptosis - neutrophils lose capacity to activate and degranulate, preventing release of lysosomal enzymes and allowing for phagocytosis by MQs

45
Q

Cells recruited in response to allergic or parasitic diseases; often appear in transition from acute to chronic inflammation; chemoattractants are histamine, C5a, eotaxin, and cytokines (IL-4, IL-5, IL-13)

A

Eosinophils

46
Q

What are some examples of tissue MQs that reside within specific organs/tissues?

A

Histiocytes, alveolar MQs, Kupffer cells, osteoclasts, microglial cells

47
Q

What are some examples of tissue MQs that are derived from monocytes?

A

Monocyte receptors bound by CKs, antigens, etc mature into MQs

48
Q

Which chemical mediators of inflammation are cell-derived and preformed (in granules)?

A

Histamine, serotonin

49
Q

Which chemical mediators of inflammation are cell-derived and synthesized?

A

Prostaglandins, tromboxanes, leukotrienes, lipoxins, cytokines, and chemokines

50
Q

Which chemical mediators of inflammation are plasma protein derived (produced in liver as a inactive precursor)?

A

Complement products

51
Q

Binds to receptors on target cells and often activates them or causes them to secrete additional inflammatory regulators (either pro- or anti-inflammatory); local or systemic effects possible

A

Chemical mediator

52
Q

True or False: Once activated and secreted, most inflammatory mediators decay rapidly, are destroyed enzymatically, and are scavenged by protective mechanisms (like antioxidants)

A

True

53
Q

Mast cells, basophils, and platelets all produce…

A

Histamine

54
Q

Prostaglandins, thromboxanes, leukotrienes, and lipoxins are ____________ acid metabolites (lipid mediators)

A

Arachidonic

55
Q

The cyclooxygenase pathway produces ____________ and _______________.

A

Prostaglandins and thromboxanes

56
Q

The lipoxygenase pathway produces ___________ and _________.

A

Leukotrienes and lipoxins

57
Q

Which enzyme marks the beginning of the arachidonic acid pathway?

A

Phospholipase A2 (activated when cell injury increases intracytoplasmic Ca2+ concentration)

58
Q

Cytokines which have critical roles in WBC recruitment by promoting adhesion to endothelium and migration through vessels

A

TNF, IL-1, IL-6

59
Q

What happens during endothelial activation?

A

Cytokines increase expression of endothelial adhesion molecules (selectins and ligands for WBC integrins)

60
Q

What happens during cytokine activation of WBCs and other cells?

A

TNF augments response of neutrophils and stimulates microbicidal activity of MQs

61
Q

What happens during the systemic acute-phase response?

A
  • Cytokines induce systemic acute-phase response associated with infection or injury
  • Increased production of C-reactive protein, serum amyloid A, fibrinogen, hepcidin
  • Decreased production of albumin
62
Q

Chemoattractants for leukocytes, recruiting monocytes, neutrophils, and other effector cells from the blood to sites of infection or tissue damage

A

Chemokines

63
Q

What cells do each of these chemokines attract:

IL-8, eotaxin, MCP-1, and RANTES

A
  • IL-8 = neutrophils
  • Eotaxin = eosinophils
  • MCP-1 = MQs
  • RANTES = T lymphocytes and eosinophils
64
Q

The part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen cell membrane

A

Complement system

65
Q

Inactive _______ ________ made in the liver are activated after tissue injury, and they generate pro-inflammatory, chemotactic, opsonizing, microbicidal molecules

A

Plasma proteins

66
Q

Part of the complement system; perforates cell membrane of foreign invaders and naive host cells

A

Membrane attack complex (MAC)

67
Q

What are the three levels of regenerative capacity for cells, and what are some examples of each level?

A
  • Labile = bone marrow stem cells, GI epithelium, keratinocytes
  • Stable = hepatocytes, renal tubular epithelium
  • Permanent = neurons, skeletal and cardiac mm.
68
Q

Leakage or accumulation of fluid with a low concentration of plasma proteins and no/low numbers of leukocytes; seen in cases of burns, acute allergic response, and vesicular stomatitis (foot and mouth disease)

A

Serous/Transudate

69
Q

Thick, gelatinous fluid; seen in tissues with abundant goblet cells or mucous glands (respiratory and GI tracts)

A

Catarrhal (Mucoid) Exudate

70
Q

Fluid with a high concentration of plasma proteins; associated with endothelial cell damage and increased vascular permeability; seen in cases of viral infection, bacterial toxins, bacterial bloodstream dissemination, etc.

A

Fibrinous Exudate

(Fibrin = yellow and friable)

71
Q

Fluid with a high number of neutrophils (both viable and dead)

A

Suppurative (Purulent) Exudate

72
Q

Type of exudate that is mostly composed of blood

A

Hemorrhagic exudate

73
Q

An acute inflammatory reaction in which the predominant change is necrosis

A

Necrotizing

74
Q

When necrotic mucosa is covered by a layer of fibrin and cellular debris

A

Fibronecrotic (pseudomembranous)

General Pathology (10 decks)

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