Key 1 of 2- Inflammation and Wound Healing Flashcards by AMITABHA BASU

The function of LPS in gram-negative infections

PAF and NO= Peripheral vasodilatation

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PGE2 functions (4)

Increased vascular permeability
Vasodilation
Fever
Pain

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Where does vasodilation occur specifically

Arteriole

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

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

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classical complement pathway is activated by

IgG or IgM binding C1

‘GM makes Classic cars”

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Alternative pathway activated by

Microbes directly activate complement

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Common product of all 3 complement pathway

C3 convertase, which produces C3a and C3b

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C3a and C5a functions

Anaphylatoxins –> trigger mast celld egranulation

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C3b function

Opsonin

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3 key mediators of Redness and Warmth

Bradykinin
HIstamine
PGs

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2 key mediators of swelling

Histamine

Tissue damage

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2 mediators of pain

Bradykinin

PGE2

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Mechanism of fever in bacterial infection

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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What do selectins bind to on the leukocyte?

Silalyl Lewis X

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3 structures mediating cellular adhesion

ICAM/VCAM on endothelial cell

Integrins on leukocyte

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Leukocyte adhesion deficiency is a defect in

Integrins

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3 hallmark features of LAD

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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Chediak Higashi defect

Defective lysosomal trafficking regulator Gene (LYST)

Results in microtubule defects and poor phagolysosome formation

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Clinical features of Chediak higashi (5)

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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NADPH Oxidase deficiency

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

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CGD inheritance

X linked recessive

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Hallmark of CGD

Recurrent infection with catalase-positive organisms

Pseudomonas, Candida, Ecoli, Staph

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How to differentiate b/w CGD and MPO deficiency

Check free radical is present or not

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2 mechanisms by which neutrophils kill

O2 dependent&raquo_space;> O2 independent (lysosyme)

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Major macrophage killing mechanism

Lysozyme...O2 independent (Stroke)

2 cytokines produced by TH1

IL2 | INFy

TH2 CD4 cells secrete

IL4 | IL5

Hallmark histology of granulomatous inflammation

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

2 cytokines involved in granuloma formation

INFy from TH1 cells --> macrophages become epithelioid histiocytes

XLinked Agammaglobulinemia defect

Phagocytosis defect

C1 inhibitor normal function

Prevents activation of compliment cascade

3 classic symptoms in Sjogren

Keratoconjunctivitis Xerostomia (dry mouth) Bilateral parotid enlargement

Autoantibodies found in Sjogren

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

Limited Scleroderma findings

CREST Syndrome ``` Calcinosis Raynaud Esophageal Dysmotility Sclerodactyly Telangiectasias ``` Skin involvement of face and hands only

Limited scleroderma autoantibody

Anti-centromere

Diffuse scleroderma findings

Widepsread skin involvement with rapid progression

What is anti Scl 70

Anti DNA topo I

General principle to determine which tissues repair and which regenerate

Tissues that are labile will regenerate (occasionally stable) Permanent tissue will repair

3 Granulation tissue components (red and granular in gross)

Fibroblasts Proliferating blood vessels Myofibroblasts

Type 1 collagen is found in which 4 structures

Bone Skin Tendon Fascia

Type 2 collagen is found in 3 structures

Cartilage (hyaline included) Vitreous body Nucleus pulposus

Type III collagen found in 4 structures

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

Type III collagen deficiency is found in which disease

Ehler Danlos (visceral rupture)

Type IV collagen found in 3 structures

Basement Membrane Basal Lamina Lens

Function of fibroblasts in wound healing

Lay down type III collagen

Collagen difference between granulation tissue and scar

``` Granulation = 3 Scar = 1 ```

Cell type that contracts the wound

Myofibroblasts

Importance of Vitamin C in wound healing

Cofactor for hydroxylation of proline and lysine

Vitamin C deficiency results in

Failure of collagen cross linking

Keloid collagen type

Type III

Steps of healing

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

Organ findings in septic shock (or any shock)

Lung- ARDS- what it is composed of (hyaline membrane?) Brain- Laminar cortical necrosis Kidnet- tombstone appearance

Integrin function

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

Fibronectin function

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

DM why delayed healing

glycosylation

Starvation and Vit C deficiency- why delayed healing

deficiency of collagen and Failure of collagen cross-linking

The most important cell in healing

macrophage

Example of resolution

Lobar pneumonia

Compensatory hyperplasia see in...

Liver

Phases of healing

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 1 year depending of the tissue) type III collagen remodeled to type I collagen vessels mature and excess vasculature involutes erythema and raised appearance of wound resolves

Why complete regeneration occur in Hepatitis A infection

Because stromal tissues (ECM) are not damaged 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.

Wound Strength after repair

approximately 70% of the strength of normal skin

Wound strength with stuture is removed (1 week)?

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.

Key 1 of 2- Inflammation and Wound Healing Flashcards

(63 cards)