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Pathophysiology > Unit 1: Inflammation & Repair > Flashcards

Unit 1: Inflammation & Repair Flashcards

1
Q

What is acute inflammation?

A
  • Stereotyped response to recent injury or infection
  • Always the same no matter the cause of inflammation
  • Characterized by vasodilation, increased capillary permeability
  • Neutrophils are main players
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2
Q

What is vasodilation?

A

increased blood flow-redness and heat

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3
Q

What happens when capillary permeability increases?

A

Fluid and proteins leak out into tissues, causing swelling. Fibrinogen also leaks.

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4
Q

Role of fibrinogen in cell repair

A

major clotting protein, when it comes in contact with stuff outside of a blood vessel, it leads to a series of rxns that causes a clot that forms a scaffold for healing cells to regenerate tissue

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5
Q

Define margination

A

when fluid content of blood cells decrease, contents of RBC roll alongside of blood vessel via adhesion. Depends on neutrophil & endothelial adhesion molecules.

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6
Q

Define emigration or diapedesis

A

Neutrophils pass through capillary walls to tissue. Driven by C5a and leukotrienes.

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7
Q

Define chemotaxis

A

Neutrophils follow chemical signals to damage/infection. Driven by C5a and leukotrines

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8
Q

Define phagocytosis

A

Neutrophils engulfs pathogens and debris. Driven by opsonins IgG & C3b.

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9
Q

Define degranulation

A

Neutrophils release cytoplasmic granules. These granules contain substances that cause pain and pressure on nerve endings.

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10
Q

Histamine response

A

mast cells release histamine when tissue injury or infection occurs, making vasodilation & capillary permeability occurs

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11
Q

Products released by degranulation (4)

A
  1. Prostaglandins
  2. Leukotrienes
  3. Free Radicals
  4. Lysosomal enzymes: leak out into cytoplasm
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12
Q

What interferes with neutrophil function?

A

Steroids: specifically interferes with margination
Diabetes: bad inflammatory responses thus bad at healing

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13
Q

What are the 4 outcomes of acute inflammation?

A
  1. Complete resolution with no tissue damage
  2. Healing by scarring
  3. Abscess formation
  4. Progression to chronic inflammation (neutrophils & mediators unable to remove the noxious agent)
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14
Q

What is pus comprised of?

A

WBC and liquefactive necrosis

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15
Q

Triple Response of Lewis

A
  1. Red scratch (histamine)
  2. Flare around scratch (autonomics)
  3. Swollen area around flare (histamine)
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16
Q

What are inflammatory mediators?

A

Chemicals responsible for aspects of inflammation that are derived from various sources.

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17
Q

Bradykinin

A

Vasodilation & capillary permeability. Causes pain

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18
Q

Complement system

A

Collection of plasma proteins. React together in cascades.

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19
Q

C3a/C5a

A

Histamine release, responsible for type 1 allergy response, anaphylotoxins as it can cause anaphylaxis

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20
Q

C5a

A

chemotaxis

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21
Q

C5-C9 “membrane attack complex”

A
  1. Inserts itself into biological membranes, cylindrical shape that allows to perforate membrane
  2. Punches holes in membranes
  3. Effect pathogenic membranes but host cells too
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22
Q

C3b

A

opsonin for phagocytosis

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23
Q

Arachidonic acid pathway

A

inflammatory response released by phospholipase A2 from cell membranes.

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24
Q

What converts AA to prostaglandins?

A

Cyclooxygenase

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25
Q

What converts AA to leukotrienes?

A

5-lipoxygenase

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26
Q

What inhibits prostaglandin production?

A

aspirin & NSAIDs

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27
Q

What inhibits AA production?

A

glucocorticoids

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28
Q

Thromboxane A2

A

produced by platelets, vasoconstriction, platelet aggregation

29
Q

Prostacyclin (PGl2)

A

produced by endothelial cells, vasodilation, prevents platelet aggregation

30
Q

Prostaglandin E2

A

vasodilation, potentiates bradykinin (pain), fever

31
Q

Leukotriene C4

A

increased capillary permeability, breaks down LTD4 & LTE4, each causes smooth muscle constriction

32
Q

Leukotriene B4

A

neutrophil & monocyte chemotaxis

33
Q

Monokines

A

released from monocytes (circulation)/ macrophages (tissues)

34
Q

Acute Phase RXN

A

Produced by monokines. Responsible for malaise because CRP is being created by the liver which requires more energy.

35
Q

What does an acute phase reaction produce?

A

Increased erythrocyte sedimentation rate due to CRP changing viscosity of plasma.

36
Q

What is a persistent elevation of CRP a marker of?

A

CAD and nonspecific inflammation

37
Q

Systemic Inflammatory Response Syndrome

A

Exuberant production of inflammatory mediators. Multisystem organ failure due to normal tissue damage.

38
Q

SIRS Criteria

A
  • Temp > 38 C or < 36 C
  • HR > 90 BPM
  • RR > 20 mm or PCO2 < 33 mmHg
  • WBC > 12000 or <4000 or more than 10% immature neutrophils
39
Q

Define chronic inflammation

A
  • more variable response to ongoing injury or infection, depending on etiology of inflammation
  • occurs when acute inflammation fails
  • orchestrated by t helper cells
  • infiltration by mononuclear cells (monocytes, lymphocytes, plasma cells)
40
Q

Granulomas

A
  • when macrophages adhere to each other and wall off stuff

- also produced from large FB

41
Q

Granulomatous diseases (4)

A
  1. Foreign bodies
  2. TB
  3. Deep fungal infections
  4. Sarcoidosis
42
Q

What type of cell is the best at handling intracellular threats?

A

T-lymphocytes

43
Q

Predominant cell to fight common bacterial infections

A

neutrophil

44
Q

Predominant cell to fight viral infections

A

lymphocyte

- T lymphocytes are the best at handling intracellular threats

45
Q

Predominant cell to fight spirochete diseases (syphilis and lyme disease)

A

plasma cell (b cell)

46
Q

Predominant cell to fight TB and fungal infections

A

Monocyte/macrophages that produces granulomas

47
Q

Predominant cell to fight worms

A

Eosinophil

48
Q

2 courses following inflammation

A
  1. regeneration of functional cells

2. repair by fibrous tissue (scar)

49
Q

Labile cells

A

Continuous replicators. Most epithelium, no free edges.

50
Q

Stable cells

A

Discontinuous replicators. Glandular cells, fibroblasts, endothelium, osteoblasts.
Ex: liver regeneration

51
Q

Permanent cells

A

Non-replicators.

Ex: Glia, neurons, heart.

52
Q

Repair via connective tissues replacing permanent cells

A
  1. Fibroblasts proliferate: produces ground substances & collagen fibers
  2. Endothelial cells proliferate: form new, leaky vessels
  3. Both then invades the clot
53
Q

Granulation Tissue

A

Immature scar, proud flesh, evidence of endothelial and fibroblast generation

54
Q

Maturing scar

A
  • enough collagen to fill the void
  • re-epitheliazation completed
  • Type III collage replaced by type I
  • fibroblasts contract & return to rest
  • most new vessels reabsorb, scar tissue relatively avascular in comparison to its original granulomatous state
  • never attains strength of original tissue
55
Q

Primary Intention

A

Ideal situation for wound healing.

Ex: well approximate surgical wounds

56
Q

What happens to a wound after minutes?

A

Clotting cascade activated, stops the bleeding

57
Q

What happens to a wound after 24 hours?

A

Neutrophils enter epithelial cells are regenerating from the edges

58
Q

What happens to a wound after 3 days?

A

Macrophages enter, granulation tissue appears, epithelial cells now cover the wound surface. (why surgeons say you can shower after 3 days)

59
Q

What happens to a wound after 5 days?

A

Granulation tissue fills the entire wound

60
Q

What happens to a wound after 2 weeks?

A

Fibroblasts multply, collage accumulates

61
Q

What happens to a wound after 4 weeks?

A

Overlying epidermis complete sans adnexal structures, capillary involution and scar contraction occurring, red scar turns white

62
Q

Secondary Intention

A

No approximation, larger fibrin meshwork, causes more inflammation, infection and granulation tissue. Complete re-epithelialization pushes scab off. Much longer to complete healing. Always produces deformity.

63
Q

Tertiary Intention

A

When a wound is initially closed, got infected, opened again and subsequently heals via secondary intention after infection clears.

64
Q

Contracture

A

fibroblasts contract too much, can be crippling

65
Q

Hypertrophic scar

A

exuberant scar tissue formation

  • stays within wound margins
  • usually regress
66
Q

Keloids

A

Exuberant scar tissue formation

  • goes beyond wound margins
  • darkly pigmented individuals
  • usually enlarge
67
Q

Is old age a hindrance to healing?

A

No, older people just tend to have comorbidities

68
Q

What are hindrances to healing?

A
  1. Inadequate nutrition (protein, vitamin c, zinc)
  2. Poor blood supply
  3. Foreign bodies
  4. Infection
  5. Glucocorticoid (steroid) therapy

Pathophysiology (5 decks)

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