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NURS 1650 - Here We Go Again > Pathophysiology of Inflammation > Flashcards

Pathophysiology of Inflammation Flashcards

1
Q

What is the purpose of inflammation?

A
  • Mobilize and attract immune components to the site
  • Neutralize invasion of microbes and limit their spread
  • Remove debris and prepare for repair
  • Finally, RESOLVE when the job is done
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2
Q

What are the two types of inflammation?

A

Acute and Chronic

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3
Q

Describe acute inflammation

A
  • Short in duration (<2 weeks)
  • Involves discrete set of events
  • Localized to the area of injury or infection
  • Critical for human health
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4
Q

Describe chronic inflammation

A
  • More diffuse area
  • Extends over longer period
  • Usually maladaptive/harmful
  • May result in scar tissue formation, tissue destruction, deformity
  • May be the cause of illness and disability
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5
Q

Inflammation Path Summary (Based on the diagram)

A

Injury

Neutrophils + macrophages // Vasoactive chemicals // Chemokines

Vasodilation + Vascular permeability

Emigration of neutrophils and macrophages into tissue

Phagocytosis

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6
Q

Acute Inflammation - Sequence of Events

A
  1. Precipitating Event: tissue damage or microbial invasion
  2. Activation of local inflammatory cells (macrophages, dendritic and mast cells, neutrophils)
  3. Generation of local mediators: leukotrienes, prostaglandins, bradykinin, histamine, complement cascade, neutrophil proteases, ROS. Causes VASODILATION, VASCULAR PERMEABILITY
  4. Recruitment and emigration of more neutrophils, macrophages, plasma proteins, including clotting proteins (if needed)
  5. Bacteria, debris, dead cells phagocytosed
  6. If wound present, platelets seal the area –> clotting
  7. Resolution of inflammation: healing, fibrosis, scar
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7
Q

How does inflammation lead to edema?

A

Increased vascular permeability of blood vessels

The gaps between endothelial cells are widened, allowing plasma proteins and leukocytes to enter the site of tissue damage

Fluid leakage through those vessels results in EDEMA

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8
Q

What are the cardinal signs of inflammation?

A
  • Pain
  • Heat
  • Redness
  • Swelling

(loss of function could be a fifth!)

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9
Q

Signs and Symptoms of Inflammation

A
  • Fever
  • Neutrophilia (release of neutrophils)
  • Lethargy, feeling tired
  • Muscle catabolism (increase AA pool for antibody production)
  • Liver releases acute phase proteins in response to IL-1, IL-6, TNF-alpha (pro-inflammatory cytokines released primarily by macrophages, can be measured in patient’s blood)
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10
Q

What are acute-phase proteins?

A

A protein whose plasma concentrations increase during inflammation

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11
Q

Innate Immunity

A

Does not require previous exposure to antigen

Rapid action, quick resolution

Kill invading organisms via phagocytic cells, NK, protein cascade

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12
Q

Acquired Immunity

A

Adaptive Immunity

Previous exposure required

Slower initial activation, can last a lifetime (but response can be rapid on second exposure)

Immune cells (T cells, B cells)

Cell-mediated immunity (cytotoxic killer T cells)

Humoral immunity (B cells, antibodies)

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13
Q

What are the two pathways for leukocyte (WBC) development?

A

Lymphoid

Myeloid

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14
Q

What does the lymphoid pathway give rise to?

A

Lymphocytes

NK cells

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15
Q

What does the myeloid pathway give rise to?

A

Granulocytes, monocytes, macrophages, dendritic cells, megakaryocytes, erythrocytes

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16
Q

What do Helper T cells do?

A
  • Activate other T cells and macrophages
  • Stimulate B cell proliferation and antibody production
  • Secrete pro-inflammatory cytokines
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17
Q

What do cytotoxic, or “killer” T cells do?

A

Kill infected cells (NOT the pathogen, the pathogen-infected cells)

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18
Q

What do B lymphocytes do?

A

Created and developed in bone marrow

Produce antibodies

Long-lived

Have memory cells that produce daughter cells programmed to produced the same antibodies

Differentiate into plasma cells, “antibody factories” that can synthesize large quantities of antibodies when they are needed

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19
Q

What is the relationship between T helper cells and B cells?

A

T helper cells help activate b cells

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20
Q

Antibodies are produced by _____

A

B lymphocytes

Are soluble form of BCRs, circulate in blood, ly,ph, found in mucus

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21
Q

Describe an antibody’s structure

A

Four polypeptide chains

two long heavy chains

two short light chains held together by disulfide bonds

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22
Q

What are some antibody functions?

A
  • Function as antitoxins, bind and neutralize bacterial toxins
  • Are OPSONINS: Coat antigens and make it more recognizable to phagocytes
  • Can activate complement cascade (when bound to antigens on cell membranes)
  • Form antibody-antigen complexes that precipitate out of body fluids, problematic in certain autoimmune disorders
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23
Q

Neutrophils, eosinophils, mast cells, and basophils are examples of _____

A

Granulocytes - Myeloid lineage

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24
Q

Where are mast cells found?

A

Found in tissues, especially tissues that interface the external environment

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25
Q

Where are basophils found?

A

Found in the circulation

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26
Q

Which cells are a part of the myeloid lineage?

A

Granulocytes (neutrophils, eosinophils, mast cells, basophils)

Antigen-presenting cells (monocytes, macrophages, dendritic cells)

RBCs, megakaryocytes

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27
Q

What are granulocytes?

A

White blood cells that have cytoplasmic granules containing enzymes needed to kill bacteria and other invaders

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28
Q

How do granulocytes work (intracellularly and extracellularly)?

A

Intracellularly - break down pathogens that are engulfed and endocytosed

Extracellularly - they release into the nearby environment by the granulocyte, can cause tissue damage

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29
Q

Which cell is the primary cell type of acute inflammation?

A

Neutrophils

They arrive quickly to the site

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30
Q

Function of neutrophils

A

Move from blood into tissue

Phagocytose and kill invading organisms, then undergo apoptosis

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31
Q

How do neutrophils arrive to the area of injury?

A

Chemotaxis // chemotactic factors

includes complement fragments and cytokines

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32
Q

When phagocytosis occurs, what neutrophil killing mechanisms are activated?

A

Generation of ROS –> “oxidative burst”

Breakdown of bacterial proteins by lysosomal proteases

ROS and lysosomal proteases released onto nearby tissues can cause secondary tissue damage including reperfusion injury)

33
Q

How do endothelial cells that line the blood vessels help move WBCs from the blood to tissues?

A

Upregulate protein adhesion molecules that capture WBCs, including neutrophils, monocytes

Physically alter position to aid movement of WBC into tissue (diapedesis)

Have anti-clotting and anti-inflammatory activity

Promoting leukocyte/WBC recruitment and platelet adhesion

Chemokines –> promote movement into the tissue

34
Q

What do selectins promote?

A

Neutrophil rolling

35
Q

What do integrins promote?

A

Neutrophil adhesion

36
Q

What does “shift to the left” refer to?

A

An increase in the percentage of immature neutrophils released from bone marrow (usually during bacterial infection)

AKA, more immature neutrophils pushed out by bone marrow to fight invaders –> push to the left causing a band neutrophil to form

37
Q

During what phase of allergic responses are eosinophils important in?

A

The late phase of allergic responses

38
Q

What do eosinophils do?

A

Contain potent killing agents (mainly proteases) that are meant to be exocytosed onto larger targets (such as parasites) too big for phagocytosis

Can injure healthy tissue –> its usual targets are large, so they can cause damage to healthy human tissue

39
Q

What do basophils contain/do?

A

Contain histamine and other mediators

Circulate in blood in healthy people, but can be recruited to inflamed tissue

40
Q

What do basophils do?

A

They are the major cell of allergic responses

“cousins” of basophils

Contain histamine, other mediators –> vascular permeability, vasodilation

Bind IgE with Fc receptors –> allows antibodies to then bind with antigen

41
Q

Describe how antibodies allow mast cells to bind with antigens

A

The antibody (IgE) binds with mast cells first

This then allows it to bind to an antigen (via mast cell’s Fc receptors)

In other words, mast cells must be “primed” with IgE before they will respond to a particular antigen

42
Q

How does inflammation increase the lifespan of monocytes?

A

Inhibits their apoptosis

Usual lifespan: 1-3 days

43
Q

When a monocyte’s lifespan increases due to inflammation, what can it then do?

A

Differentiate into macrophages

Becomes phagocytic, ingests bacteria and cell debris/cleaning up after tissue injury

Inflammatory, cytokine secretion

Immunological, present antigen to helper T cells

Chronic inflammation, “bad actors”

44
Q

How are macrophages the “bad actors” in chronic inflammation?

A

Remain in the inflammatory focus/state

Secrete stimulatory cytokines

Provide ongoing stimulation of inflammatory processes

Can live for months to years, inhibit their own apoptosis

45
Q

What do dendritic cells do?

A

Capture and present antigens to T cells

Produce chemical messengers (ex. type 1 interferon for viruses suppresses viral replication machinery in nearby cells

46
Q

What are examples of arachidonic acid metabolites?

A

Prostaglandins

Leukotrienes

Thromboxane A2

47
Q

What are the two pathways that result in inflammation (from arachidonic acids)?

A

Cyclooxygenase (COX)

5-Lipoxygenase

48
Q

Describe the COX pathway that results in inflammation

A

Arachidonic acid

COX (1 and 2)

Prostaglandins

Prostacyclin // // Thromboxane A2

Vasodilation, inhibit platelet aggregation // // vasoconstirction, platelet aggregation

PGD2 or PGE2

Vasodilation & increased vascular permeability (just like histamine)

49
Q

What are cytokines?

A

Signaling molecules

Alter the activity of WBCs

Associate with macrophages and lymphocytes (T cells)

examples: TNF-alpha, IL-1, IL-6

50
Q

What 3 pathways activate complement?

A

Classical, lectin, and alternative

51
Q

What are the functions of complement?

A

Enhances inflammation

Induces production of TNF-alpha, IL-1, etc.

Induce mast cell degranulation

Opsonization, greatly enhances phagocytosis

Increase vascular permeability

Direct cytotoxic effect on target cells (Membrane Attack Complex / MAC) –> eventually the cell will lyse

52
Q

What are kinins and what do they cause?

A

Small polypeptides

Vasodilation, inflammation, increased vascular permeability, smooth muscle contractions, pain, helps intimate clotting

53
Q

How does acute inflammation resolve?

A

Neutrophil apoptosis

Macrophage phagocytosis of debris

Stimulation of new tissue growth and angiogenesis

Monocytes and macrophages return to normal lifespan

Fluid and proteins removed via lymphatic drainage

Fibroblasts repair the wound, and create a scar

54
Q

What is fibroblasts’ role in wound healing?

A

They proliferate (due to growth factors released by macrophages)

Synthesized connective tissue (including collagen)

Able to migrate to site

Scar formation

55
Q

What is fibrosis?

A

Thickening of previously-healthy tissues

Can lead to loss of function due to non-elastic tissue (scar tissue)

Happens due to chronic inflammation

56
Q

What are some results of chronic inflammation?

A

Angiogenesis (result in an increase of WBC entering)

Mononuclear cell infiltrate (remain activated)

Fibrosis (scar) –> loss of function due to non-elastic tissue

57
Q

What marks chronic inflammation?

A

Presence of long-lived cell types (macrophages, lymphocytes, plasma cells, and fibroblasts)

Macrophages remain in an activated state –> continue to release cytokines that perpetuate the pro-inflammatory state, their lifespan also increases

Continued cytokine release

58
Q

How do macrophages maintain chronic inflammation?

A

By causing tissue injury and fibrosis

Continue to release pro-inflammatory cytokines (IL-1, TNF-alpha)

59
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome

massive, uncontrolled, systemic inflammatory response

Extremely serious, can be due to infectious or non-infectious causes (burns, pancreatitis, others)

Widespread tissue injury

Can be fatal

60
Q

General S/Sx of SIRS

A

Increased body temp or low body temp

High heart rate

High RR, low arterial PaCO2

High WBC count, presence of band neutrophil (shift to the left)

61
Q

T cells and B cells require a ______ to be activated

A

T cells and B cells require a COSTIMULATORY to be activated; not sufficient to simply recognize and bind to an antigen

62
Q

What is miRNA’s role in the regulation of immune function?

A

Tamps down immune response by preventing translation of genes involved in inflammation

63
Q

How does the immune system recognize “self” from “non-self”?

A

Major Histocompatibility Complex (MHC)

Key role in the activation of helper and cytotoxic T cells

Guide cytotoxic T lymphocytes toward target cells

64
Q

Which class of MHC molecules are found on all nucleated cells?

A

Class I MHC molecules

65
Q

Which class of MHC molecules are found on APCs: B cells, macrophages, and dendritic cells?

A

Class II MHC molecules

66
Q

How do Class I MHC molecules help initiate an immune response?

A

Present self and non-self antigen to cytotoxic T cells

Cytotoxic T cells only react to abnormal antigens

Self antigens are ignored

67
Q

How do Class II MHC molecules help initiate an immune response?

A

Present antigen to helper T cells

68
Q

What is Rheumatoid Arthritis (RA)?

A

An autoimmune disease that is very painful and results in joint destruction

69
Q

Explain how RA causes joint destruction

A

B cells form autoantibodies to multiple molecules/proteins

Rheumatoid factor (RF) is an autoantibody to a person’s own IgG

Anti-cyclic citrullinated peptide antibodies (ACPAs) more specific for RA –> cause inflammation

Often leads to immune complex deposition in the joints

Other autoantibodies can be found as well in the synovial fluid of patients with RA

70
Q

What is the primary target of the autoimmune response in RA?

A

The synovial membrane (synovium)

71
Q

What are the results of RA?

A

Synoviocytes undergo hyperplasia and hypertrophy

Angiogenesis –> provides more SA for leukocyte recruitment

Increased lymphocytes, macrophages, neutrophils, and inflammatory mediators

Synovial membrane transformed into thick, inflammatory tissue –> the pannus (which destroys cartilage)

Cartilage destroyed –> bones deteriorate, joint becomes stiff, immobile, and ankylosing

72
Q

Which hypersensitivity types are mediated by antibodies?

A

Types I, II, III

73
Q

Which hypersensitivity types are mediated by T cells?

A

Type IV

74
Q

Type I Hypersensitivity

A

AKA immediate hypersensitivity

ALLERGY and ALLERGIC REACTION

IgE principle mediating antibody

Mast cells, basophils, histamine

Can become anaphylaxis and potential death if not treated immediately

75
Q

First vs. second exposure: antigen binding to IgE

A

First exposure: T helper cells induce B cell class-switching to IgE antibodies, IgE binds to mast cells (now primed)

Second exposure: immediate release of mast cell granules

76
Q

Anaphylaxis S/Sx

A

SOB, coughing, wheezing 2/2 bronchoconstriction

Hives, itching, flushing

Oropharyngeal or ocular swelling, feeling of tightness in throat

Increased HR, hypotension

Nausea, vomiting

MEDICAL EMERGENCY

77
Q

Describe Type II Hypersensitivity

A

Tissue-specific, cytotoxic, or cytolytic hypersensitivity

Often immediate, but can be delayed

Antibodies attack antigens bound to the surface of specific target cells or tissues

Causes lysis or phagocytosis of target cells

Examples: blood transfusion reactions, thyroiditis, Myasthenia Gravis

78
Q

Describe Type III Hypersensitivity

A

Immune complex reaction

Not tissue-specific

Response to an Ag-Ab complex (antigen-antibody complex)

The immune and phagocytic systems fail to remove these Ag-Ab complexes, they then move into tissues

Activate complement, neutrophils arrive, ROS released –> tissue damage

Examples: systemic lupus, erythematosus, immune complex glomerulonephritis

79
Q

Describe Type IV Hypersensitivity

A

AKA delayed hypersensitivity

No primary antibody involvement

Sensitized T cells react with altered or foreign cells and initiate inflammation and cell destruction

Examples: poison ivy, contact dermatitis, Tuberculin-type hypersensitivity

NURS 1650 - Here We Go Again (20 decks)

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