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PATH MAGIC > Key 1 of 2- Inflammation and Wound Healing > Flashcards

Key 1 of 2- Inflammation and Wound Healing Flashcards

1
Q

The function of LPS in gram-negative infections

A

PAF and NO= Peripheral vasodilatation

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2
Q

PGE2 functions (4)

A

Increased vascular permeability
Vasodilation
Fever
Pain

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3
Q

Leukotriene (C,D,E) functions (3)

A 
Bronchoconstriction-Think Asthma after aspirin use
Vasoconstriction
Increased Permeability (via pericyte contraction)
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4
Q

Classical complement pathway is activated by

A

IgG or IgM binding C1, so C2 and C4 will be low.

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5
Q

Alternative pathway activated by

A

Microbes directly activate complement, so C2 and C4 will remain normal.

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6
Q

Common product of all 3 complement pathway

A

C3 convertase, which produces C3a and C3b

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7
Q

C3a and C5a functions

A

Anaphylatoxins –> trigger mast cell degranulation (Type III hypersensitivity)

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8
Q

C3b function

A

Opsonin

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9
Q

3 key mediators of Redness and Warmth

A

Bradykinin
HIstamine
PGs

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10
Q

2 key mediators of swelling

A

Histamine

Tissue damage

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11
Q

2 mediators of pain

A

Bradykinin

PGE2

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12
Q

Mechanism of fever in bacterial infection/sepsis

A

Pyrogens from bacteria cause macrophages to release IL1 and TNF

IL1 and TNF increase COX in perivascular cells of hyopthal –> increase set point

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13
Q

What do selectins bind to on the leukocyte?

A

Silalyl Lewis X

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14
Q

3 structures mediating cellular adhesion

A

ICAM/VCAM on endothelial cell

Integrins on leukocyte

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15
Q

Leukocyte adhesion deficiency is a defect in

A

Integrins

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16
Q

3 hallmark features of LAD

A

1- Delayed separation of umbilical cord
2- Increased neutrophil count (detachment of marginated pool)
3- recurrent bacterial infection w/o pus formation

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17
Q

Chediak Higashi defect

A

Defective lysosomal trafficking regulator Gene (LYST)

Results in microtubule defects and poor phagolysosome formation

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18
Q

Clinical features of Chediak higashi (5)

A
  • Recurrent pyogenic infections
  • albinism (unable to move melanin to keratinocytes
  • peripheral neuropathy
  • Pancytopenia (no microtubules = no cell division)
  • Giant granules in granulocytes
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19
Q

NADPH Oxidase deficiency

A

Chronic granulomatous disease (unable to produce reactive oxygen species)- get granuloma in bacterial infection!

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20
Q

CGD inheritance

A

X linked recessive

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21
Q

Hallmark of CGD

A

Recurrent infection with catalase-positive organisms

Pseudomonas, Candida, Ecoli, Staph

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22
Q

How to differentiate b/w CGD and MPO deficiency

A

Check free radical is present or not

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23
Q

2 mechanisms by which neutrophils kill

A

O2 dependent&raquo_space;> O2 independent (lysosyme)

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24
Q

Major macrophage killing mechanism

A

Lysozyme…O2 independent (Stroke)

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25
Q

2 cytokines produced by TH1

A

IL2

INFy

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26
Q

TH2 CD4 cells secrete

A

IL4

IL5

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27
Q

Hallmark histology of granulomatous inflammation

A 
Epithelioid Histiocytes (macrophages with lots of pink cytoplasm)
Giant cells + a Rim of lymphocytes+ a rim of fibrosis
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28
Q

2 cytokines involved in granuloma formation

A

INFy from TH1 cells –> macrophages become epithelioid histiocytes

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29
Q

XLinked Agammaglobulinemia defect

A

Phagocytosis defect (Due to decreased Immunoglobulin)

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30
Q

C1 inhibitor normal function

A

Prevents activation of compliment cascade

31
Q

3 classic symptoms in Sjogren

A

Keratoconjunctivitis
Xerostomia (dry mouth)
Bilateral parotid enlargement

32
Q

Autoantibodies found in Sjogren

A

antiribonucloprotein: SSA (anti Ro) and SSB (antiLa)

ANA

33
Q

Limited Scleroderma findings

A

CREST Syndrome

Calcinosis 
Raynaud
Esophageal Dysmotility
Sclerodactyly
Telangiectasias

Skin involvement of face and hands only

34
Q

Limited scleroderma autoantibody

A

Anti-centromere

35
Q

Diffuse scleroderma findings

A

Widepsread skin involvement with rapid progression

36
Q

What is anti Scl 70

A

Anti DNA topo I

37
Q

General principle to determine which tissues repair and which regenerate

A

Tissues that are labile will regenerate (occasionally stable)

Permanent tissue will repair

38
Q

3 Granulation tissue components (red and granular in gross)

A

Fibroblasts
Proliferating blood vessels
Myofibroblasts

39
Q

Type 1 collagen is found in which 4 structures

A

Bone
Skin (delayed wound healing)
Tendon
Fascia

40
Q

Type 2 collagen is found in 3 structures

A

Cartilage (hyaline included)- in Osteoarthritis
Vitreous body
Nucleus pulposus

41
Q

Type III collagen found in 4 structures

A

Reticulin (skin, blood vessels, uterus, granulation tissue)

42
Q

Type III collagen deficiency is found in which disease

A

Ehler Danlos (visceral rupture)

43
Q

Type IV collagen found in 3 structures

A

Basement Membrane
Basal Lamina
Lens

44
Q

Function of fibroblasts in wound healing

A

Lay down type III collagen

45
Q

Collagen difference between granulation tissue and scar

A 
Granulation = 3
Scar = 1
46
Q

Cell type that contracts the wound

A

Myofibroblasts

47
Q

Importance of Vitamin C in wound healing

A

Cofactor for hydroxylation of proline and lysine

48
Q

Vitamin C deficiency results in

A

Failure of collagen cross linking

49
Q

Keloid collagen type

A

Type I, III

50
Q

Steps of healing

A

Hemostasis Phase. Hemostasis is the process of the wound being closed by clotting. …
Inflammatory Phase. …
Proliferative Phase. …
Maturation Phase

51
Q

Organ findings in septic shock (or any shock)

A

Lung- ARDS- what it is the composition of the hyaline membrane?
Brain- Laminar cortical necrosis
Kidnet- tombstone appearance

52
Q

Integrin function

A

Integrins interact with the extracellular matrix proteins (e.g., fibronectin) and the epithelium

53
Q

Fibronectin function

A

Adhesive glycoproteins such as fibronectin help to maintain a cellular scaffolding for growth and repair, but they do not contract, early to develop.

54
Q

DM why delayed healing (similat with abundant farry food intake)

A

glycosylation of ECM, reduced cross linking

55
Q

Starvation (shipwreck) and Vit C deficiency- why delayed healing

A

deficiency of collagen and Failure of collagen cross-linking

56
Q

The most important cell in healing

A

macrophage

57
Q

Example of resolution

A

Lobar pneumonia

58
Q

Compensatory hyperplasia see in…

59
Q

Phases of healing

A

hemostasis (1 - 24h)

inflammation (1 - 5d)

proliferation (4 - 21d)

granulation tissue (newly laid collagen with neovascularization) forms
epithelialization occurs from surrounding basal keratinocytes and hair follicle basal cells
maturation (21d to up to 7/8 weeks depending on the tissue)
type III collagen remodeled to type I collagen
vessels mature and excess vasculature involutes
erythema and raised appearance of wound resolves

60
Q

Why complete regeneration occur in Hepatitis A infection

A

Because 1) stromal tissues (ECM) are not damaged and 2) because of hepatocyte beling Stable cell in HAV infection! only cells die…they regenerate without fibrosis!

The type and extent of tissue injury affects the subsequent repair. Complete restoration can occur only in tissues composed of stable and labile cells; even then, extensive injury will probably result in incomplete tissue regeneration and at least partial loss of function. Injury to tissues composed of permanent cells must inevitably result in scarring with, at most, attempts at functional compensation by the remaining viable elements. Such is the case with healing of a myocardial infarct.

61
Q

Wound Strength after repair

A

approximately 70-80% of the strength of normal skin

62
Q

Wound strength with stuture is removed (1 week)?

A

When sutures are removed, usually at 1 week, wound strength is approximately 10% of that of unwounded skin, but this increases rapidly over the next 4 weeks.

63
Q

Growth factors for angiogenesis

A

VGEF (the Notch signaling pathway ), PDGF, Basic FGF

64
Q

……………….. stimulates fibroblast migration and proliferation, increased synthesis of collagen and fibronectin

65
Q

The degradation of collagens and other ECM components is accomplished by a family of………………….

A

matrix metalloproteinases (MMPs)>A family of enzymes related to MMPs is called ADAM (a disintegrin and metalloproteinase seen in TTP).

66
Q

The skin blister resulting from a burn represents the accumulation of ………………………

A

serous fluid (due to direct endothelial injury)

67
Q

Morphology: fibrinous exudate ?

A

Histologically, fibrin appears as an eosinophilic meshwork of threads or sometimes as an amorphous coagulum

68
Q

Examples: fibrinous exudate

A

Peritonitis, Acute pericarditis, Uremia carditis

69
Q

Purulent inflammation is characterized by……………….

A

the production of pus, an exudate consisting of neutrophils, the liquefied debris of necrotic cells, and edema fluid

70
Q

Abscesses are …………………………

A

localized collections of purulent inflammatory tissue caused by suppuration buried in a tissue, an organ, or a confined space (liquefactive necrosis) surrounded by granulation tissue.

71
Q

Suppurative inflammation

A

A type of purulent inflammation. Pus leaks out. Usually by an infection with bacteria that cause liquefactive tissue necrosis, such as staphylococci; these pathogens are referred to as pyogenic (pus-producing) bacteria. A common example of an acute suppurative inflammation is acute appendicitis

72
Q

Empyema

A

The collection of pus in a cavity in the body, especially in the pleural cavity.

73
Q

Marphan defect?

A

Fibrillin gene, elastic tissue

PATH MAGIC (21 decks)

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