Inflammation Flashcards

(70 cards)

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
Transudate
Fluid that leaks out of leaky vessels at site of inflammation Has lots of proteins and few blood cells
26
Exdate
Formed by emigration of cells across vascular walls More protein that transudate Contains inflammatory cells
27
Neutrophils
``` Also called polymorphonuclear cells Most abundant WBC Involved in acute inflammation Mobile, phagocytic, acute mediator, involved in pain Short life spane ```
28
Monocyte
Big phagocytic cell | Turns into macrophage in tissue
29
Eosinophils
Involved in chronic inflammation (last longer in blood) | Allergies and parasitic infections
30
Basophils
Contain similar molecules to eosinophils Store and release histamine IgE mediated allergies Works similarly to mast cells but in blood
31
Lymphocytes
B, T, NK cells | Involved in cellular immunityy
32
Platelets
Fragments of megakaryocytes No nucleus Granules with mediators Form primary plug in clotting
33
4 ways to classify inflammation
Duration Etiology Location Morphology/pathological characteristics
34
Acute versus chronic inflammation
Acute: sudden onset, duration of hours to days Chronic: duration of weeks to years
35
Primary versus secondary chronic inflammation
Primary: no acute phase Secondary: follows an acute phase (usually this way)
36
Serous inflammation
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
Fibrinous inflammation
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
Purulent inflammation
Involves formation of pus Also rich in fibrin (fibropurulent) Pus can accumulate on or within tissue/organ
39
Pus
A viscous yellow fluid | Made of dead/dying neutrophils and necrotic tissue
40
2 genera of pus forming bacteria
Streptococci | Staphylococci
41
Sinus definition
When an abscess in a solid tissue comes into contact (communicates) with open air
42
Fistula defintion
A hollow space comes into contact with another hollow organ or the outside air Ex: bladder to colon, or colon to air
43
Empyema definition
Accumulation of pus in a preformed cavity | Ex: pleural cavity, gallbladder, etc
44
Ulcerative inflammation
Ulceration is the loss of epithelial lining of a body surface or mucosa Ulcers may extend into deeper connective tissue
45
Pseudomembranous inflammation
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
Chronic inflammation
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
Granulomatous inflammation
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
Caseous necrosis
In the center of the granuloma the tissue dies | Looks kind of cottage cheese
49
4 branches of the innate immune system
``` 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
3 main mechanisms the innate immune system protects us through
Inflammation Combating viral infections Mounting a general response to damaged cell products
51
Antigen versus immunogen
Antigen: any substance that binds specifically to antigen receptors Immunogen: any substance that elicits an immune response
52
Antigen-antibody complexes bind and activate complement which does... (3 things)
Lysis of cells Agglutination Recruitment of inflammatory cells
53
Functions of: IgM (2)
Complement fixation | Neutralization
54
Functions of: IgG (3)
Opsonization Can fix complement Transported across placenta
55
Functions of: IgA (2)
Found in body secretions and at mucosal sites | Neutralization
56
Functions of: IgE IgD (1 each)
E: Allergy D: Activation of B cells
57
What are the 4 hypersensitivity reactions?
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
Type 1 hypersensitivity
Anaphylactic or atopic reaction Mediated by IgE and mast cells or basophils Examples: hay fever, atopic dermatitis, bronchial asthma, anaphylactic shock
59
Type 2 hypersensitivity
Cytotoxic antibody-mediated reaction | Ex: erythroblastosis fetalis, transfusion reactions, Graves disease, Goodpasture syndrome, Myasthenia gravis
60
Graves' disease
Type 2 hypersensitivity Hyperthyroidism caused by autoantibodies to the TSH receptor on follicular cells of the thyroid Antibodies cause overproduction of thyroid hormones
61
Myasthenia Gravis
Type 2 hypersensitivity Antibodies to receptors for acetylcholine on surface of striated muscle cells Muscle contraction is blocked Progressive muscle weakness and paralysis
62
Goodpasture's syndrome
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
Type 3 hypersensitivity
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
Serum sickness
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
Systemic lupus erythematosus
Type 3 hypersensitivity Immune complexes formed of antibodies and autoantigens Deposited in tissues, causing kidney disease, arthritis, skin disease, etc
66
Post-streptococcal glomerulonephritis
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
Polyarteritis nodosa
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
Type 4 hypersensitivity
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
IFN-gamma
Recruits more macrophages, turns them into epithelioid macrophages, activates them, makes them fuse into giant multinucleated cells
70
Definitions: Autograft Allograft Xenograft
Grafted tissue comes from the recipient Grafted tissue comes from someone else Grafted tissue comes from another species