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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is a vital reaction

A

Only happens in living tissue

Ex: Inflammation

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2
Q

5 cardinal signs of inflammation

A
  1. Calor (heat)
  2. Rubor (redness)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Functio laesa (disturbed function)
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3
Q

4 major categories of changes in inflammation

A

Circulatory
Vascular
Humoral
Cellular

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4
Q

Circulatory changes

A

First response to injury is change in blood flow
Increased blood flow to capillaries = redness, swelling, warmth
Inflammatory edema leaks from capillaries and venules due to increased pressure

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5
Q

Hyperemia definition

A

Increased blood flow

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6
Q

Rouleax

A

More than 4 red blood cells stacked together
Go to the middle of the flow and slow it
Due to proteins covering the negative charges so they can stick together

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7
Q

3 steps in pathogenesis of inflammation

A
  1. Margination of neutrophils
  2. Adhesion of platelets
  3. Pavementing of neutrophils
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8
Q

Vascular changes

A

Increased permeability (caused by 4 things)

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9
Q

4 things that cause increased permeability

A

Increased hydrostatic pressure
Slowed circulation
Leukocyte and platelet adhesion to endothelial cells
Soluble mediators

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10
Q

2 classes of inflammatory mediators and what defines them

A
  1. Plasma derived (need to be activated)

2. Cell-derived (pre-fromed, formed de novo, or may need to be activated)

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11
Q

Histamine

A

Releases from platelets and mast cells
Stimulates contraction of endothelial cells
Inactivated by histaminase, so is an immediate transient reaction

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12
Q

Enzyme that inactivates histamine

A

Histaminase

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13
Q

Bradykinin

A

Works like histamine but slower

Also causes pain

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14
Q

2 complement proteins that are anaphylatoxins

A

C3a

C5a

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15
Q

Arachadonic acid

A

Part of cell membranes

Has to be acted on by enzymes to do anything

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16
Q

2 paths that arachadonic acid can enter

A
  1. Lipoxygenase pathway

2. Cyclooxygenase pathway

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17
Q

Lipoxygenase pathway

A

Makes leukotrienes and lipoxins

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18
Q

Leukotrienes

A

Promote chemotaxis and increase vascular permeability
Cause contraction of smooth muscle (bronchospasm)
Allergy and anaphylaxis

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19
Q

Lipoxins

A

Negative regulators

Counteract the effects of leukotrienes

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20
Q

Cyclooxygenase pathway

A

Makes thromboxanes, prostaglandins, and prostacyclins

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21
Q

Thromboxanes

A

Promote platelet aggregation and vasoconstriction

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22
Q

Prostaglandins

A

Cause vasodilation and increased permeability

Pain and fever

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23
Q

Prostacyclin

A

Negative regulator

Counteracts effects of thromboxanes and prostaglandins

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24
Q

Transudation

A

Leakage of fluid into interstitial space

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25
Q

Transudate

A

Fluid that leaks out of leaky vessels at site of inflammation
Has lots of proteins and few blood cells

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26
Q

Exdate

A

Formed by emigration of cells across vascular walls
More protein that transudate
Contains inflammatory cells

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27
Q

Neutrophils

A 
Also called polymorphonuclear cells
Most abundant WBC
Involved in acute inflammation
Mobile, phagocytic, acute mediator, involved in pain
Short life spane
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28
Q

Monocyte

A

Big phagocytic cell

Turns into macrophage in tissue

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29
Q

Eosinophils

A

Involved in chronic inflammation (last longer in blood)

Allergies and parasitic infections

30
Q

Basophils

A

Contain similar molecules to eosinophils
Store and release histamine
IgE mediated allergies
Works similarly to mast cells but in blood

31
Q

Lymphocytes

A

B, T, NK cells

Involved in cellular immunityy

32
Q

Platelets

A

Fragments of megakaryocytes
No nucleus
Granules with mediators
Form primary plug in clotting

33
Q

4 ways to classify inflammation

A

Duration
Etiology
Location
Morphology/pathological characteristics

34
Q

Acute versus chronic inflammation

A

Acute: sudden onset, duration of hours to days
Chronic: duration of weeks to years

35
Q

Primary versus secondary chronic inflammation

A

Primary: no acute phase
Secondary: follows an acute phase (usually this way)

36
Q

Serous inflammation

A

Mild inflammation
Exudation of serum (liquid part of blood, lots of proteins)
Typical of many viral infections
Can also be found in autoimmune diseases affecting the serosa
Joint swelling can be due to physical trauma
Blisters can be due to thermal injury
Serous fluid is usually reabsorbed and lesions heal without permanent consequences

37
Q

Fibrinous inflammation

A

Exudate is rich in fibrin (large protein)
Causes larger defects - severe inflammation!
Ex: strep throat, bacterial pneumonia, bacterial pericarditis
Resolution, not reabsorption. Requires reorganization (new blood vessels, ingrowth of fibroblasts, obliteration of tissue space)

38
Q

Purulent inflammation

A

Involves formation of pus
Also rich in fibrin (fibropurulent)
Pus can accumulate on or within tissue/organ

39
Q

Pus

A

A viscous yellow fluid

Made of dead/dying neutrophils and necrotic tissue

40
Q

2 genera of pus forming bacteria

A

Streptococci

Staphylococci

41
Q

Sinus definition

A

When an abscess in a solid tissue comes into contact (communicates) with open air

42
Q

Fistula defintion

A

A hollow space comes into contact with another hollow organ or the outside air
Ex: bladder to colon, or colon to air

43
Q

Empyema definition

A

Accumulation of pus in a preformed cavity

Ex: pleural cavity, gallbladder, etc

44
Q

Ulcerative inflammation

A

Ulceration is the loss of epithelial lining of a body surface or mucosa
Ulcers may extend into deeper connective tissue

45
Q

Pseudomembranous inflammation

A

Ulcerative inflammation combined with fibropurulent exudation
Exudate forms a pseudomembrane on the surface of ulcers
If pseudomembrane is scraped away, ulcer can bleed badly
C dificile can cause this, or diptheria

46
Q

Chronic inflammation

A

Defined by duration
Exudate contains lymphocytes, macrophages, plasma cells
Stimulate fibroblast proliferation, recruit new inflammatory cells
Loss of parenchymal cells and scarring occurs
Scarring may affect tissue/organ function

47
Q

Granulomatous inflammation

A

Granulomas are destructive accumulations of cells that form nodules (of lymphocutes, epithelioid cells, and multinucleated giant cells)
T cells accumulate and secrete cytokines, which attract macrophages
Infectious granulomas - caseous necrosis

48
Q

Caseous necrosis

A

In the center of the granuloma the tissue dies

Looks kind of cottage cheese

49
Q

4 branches of the innate immune system

A 
Mechanical (barriers like the skin, pH differences in our body, mucus in linings)
Phagocytosis (monocytes, macrophages, neutrophils – can recognize complement opsonized pathogens)
NK cells (don’t need to see antigen – always ready to kill a cell – if a cell is expressing enough self proteins then they won’t kill)
Protective proteins (have a lot of functions)
50
Q

3 main mechanisms the innate immune system protects us through

A

Inflammation
Combating viral infections
Mounting a general response to damaged cell products

51
Q

Antigen versus immunogen

A

Antigen: any substance that binds specifically to antigen receptors
Immunogen: any substance that elicits an immune response

52
Q

Antigen-antibody complexes bind and activate complement which does… (3 things)

A

Lysis of cells
Agglutination
Recruitment of inflammatory cells

53
Q

Functions of:
IgM
(2)

A

Complement fixation

Neutralization

54
Q

Functions of:
IgG
(3)

A

Opsonization
Can fix complement
Transported across placenta

55
Q

Functions of:
IgA
(2)

A

Found in body secretions and at mucosal sites

Neutralization

56
Q

Functions of:
IgE
IgD
(1 each)

A

E: Allergy
D: Activation of B cells

57
Q

What are the 4 hypersensitivity reactions?

A

Type I: Anaphylactic or atopic reaction
Type II: Cytotoxic antibody-mediated reaction
Type III: Immune complex-mediated reaction
Type IV: Cell-mediated or delayed type reaction

58
Q

Type 1 hypersensitivity

A

Anaphylactic or atopic reaction
Mediated by IgE and mast cells or basophils
Examples: hay fever, atopic dermatitis, bronchial asthma, anaphylactic shock

59
Q

Type 2 hypersensitivity

A

Cytotoxic antibody-mediated reaction

Ex: erythroblastosis fetalis, transfusion reactions, Graves disease, Goodpasture syndrome, Myasthenia gravis

60
Q

Graves’ disease

A

Type 2 hypersensitivity
Hyperthyroidism caused by autoantibodies to the TSH receptor on follicular cells of the thyroid
Antibodies cause overproduction of thyroid hormones

61
Q

Myasthenia Gravis

A

Type 2 hypersensitivity
Antibodies to receptors for acetylcholine on surface of striated muscle cells
Muscle contraction is blocked
Progressive muscle weakness and paralysis

62
Q

Goodpasture’s syndrome

A

Type 2 hypersensitivity
Antibodies to collagen type IV activate complement and attract neutrophils that contribute to the damage and rupture the glomerular basement membrane
In the kidney

63
Q

Type 3 hypersensitivity

A

Immune complex-mediated
Systemic: immune complexes are in circulation
Local: immune complexes are formed in tissue
Examples: serum sickness, systemic lupus erythematosus, post-strep GN, polyarteritis nodosa

64
Q

Serum sickness

A

Type 3 hypersensitivity
Immune complexes form during antigen excess, and are deposited in tissue
Tissue legions caused by activated complement and leukocytes attracted to immune complexes

65
Q

Systemic lupus erythematosus

A

Type 3 hypersensitivity
Immune complexes formed of antibodies and autoantigens
Deposited in tissues, causing kidney disease, arthritis, skin disease, etc

66
Q

Post-streptococcal glomerulonephritis

A

Type 3 hypersensitivity
Acute kidney disease after strep throat
Antibodies react with soluble streptococcal antibodies “planted” onto glomerular basement membranes during filtration
Or, form immune complexes in circulation and deposit in in glomerular basement membrane
Complement-mediated inflammatory response

67
Q

Polyarteritis nodosa

A

Type 3 hypersensitivity
Antigen-antibody complexes precipitate, usually in vessel wall
Complement is activated, which attracts white blood cells
Localized acute inflammatory response occurs, characterized by fibrinoid necrosis of the vessel wall
Damaged vessels tend to thrombose and become occluded, causing tissue ischemia and infarcts

68
Q

Type 4 hypersensitivity

A

Cell-mediated or Delayed type
Involves T cells and macrophages, which typically form granulomas at the site of injury
Antigen is taken up by macrophages and presented to T cells, which become activated and produce IFN-γ
Infections (M. tuberculosis, M. leprae, fungi), tumors, idiopathic (e.g., sarcoidosis)

69
Q

IFN-gamma

A

Recruits more macrophages, turns them into epithelioid macrophages, activates them, makes them fuse into giant multinucleated cells

70
Q

Definitions:
Autograft
Allograft
Xenograft

A

Grafted tissue comes from the recipient
Grafted tissue comes from someone else
Grafted tissue comes from another species

Pathology (19 decks)

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