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Pathology-1 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Acute Inflammation

A

-edema and neutrophils

Coordinated, multistep, rapid (hours to days) response to injury or infection

goal: to deliver immune cells, plasma proteins (Ab’s, immunomodulators), chemical mediators to site

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2
Q

What are the cardinal features of inflammation

A

heat (calor)- vasodilation

redness (rubor)- vasodilation

pain (dolor)- compression on nerve ending from edema

swelling (tumor)

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3
Q

What are the stumuli for acute inflammation?

A
  • infections (baterial/viral/fungal/parasitic)
  • tissue necrosis (ischemia/trauma/physical or chemical injury)
  • foreign bodies (dirt/sutures/medical devices)
  • immune/autoimmune reactions (‘bystandard’ damage to self)
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4
Q

What are the alteration in acute inflammation?

A
  1. Increased blood flow–>vasodilation–>calor, rubor (erythemia)
  2. slowing of circulation (congestion and increased permeability of microvaculature; causing extravasation of fluid (tumor), hemoconcentration, statis, margination of leukocytes)
  3. mechanisms of increased vascular permeability
    a. endothelial contraction (histamine, and other inflam mediators)
    b. endothelia injury (eg. burns)
    c. neutrophil-mediated injury
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5
Q

What does the slides represent?

A

Normal lung–>vascular congestion and stasis–>leukocyte infiltrate.

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6
Q

How do lymphatic vessels respond to inflammation?

A

Increased lymphatic drainage of edema fluid

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7
Q

Lymphangitis

A

inflammation of lymphatic-red streaks below the skin

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8
Q

lymphadenitis

A

inflammation in draining LN

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9
Q

what does lymphagitis physical finding indicate?

A

finding that indicates local wound infection

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10
Q

What are the mediators for vasodilation?

A

prostaglandins

NO

histamine

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11
Q

what are the mediators for increased vascular permeability?

A

histamine, bradykinin, C3a, C5a

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12
Q

what are the mediators in fever?

A

TNF, prostaglandins

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13
Q

What are the mediators in pain?

A

prostaglandins, bradykinin

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14
Q

Mediators of the cardinal signs

A

rubor: histamine
calor: histamine
tumor: histamine

Dolor: PGE2, bradykinin

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15
Q

What are the mediator involved in vasocontriction?

A

TXA2

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16
Q

What are the mediators involved in chemotaxis?

A

C5a, LTB4, IL8

17
Q

Neutrophils play a huge role in what type of immunity?

A
  • major actor in innate immunity
  • normal adult ANC~1500-2000ul

1X 1011produced daily

90+% sitting in bone marrow, circulating amt increase 10fold in setting of infection

circulating half-life of 6-10hrs

18
Q

Neutrophil granules

A
  • specific granules (lactoferrin, lysozyme, alkaline phosphate, type IV collagenase, Leukocyte adhesion molecules, plasminogen activation, phopholipase A2)
  • azurophil granules (*myloperoxisase, etc)
19
Q

What are the steps in leukocyte recruitment to sites of infection and injury?

A
  1. normal: tumbling along in bloodstream
  2. slowed flow (stasis)–> migration, rolling, and adhesion to an **activated **endothelium
  3. migration across the vessel wall (diapedesis)
  4. migration down chemotactic gradiets
20
Q

Endothelial activation

A

(secondary to tissue damage or infection)

  • cytokines secreted from MO attrack leukocytes/neutrophils to endothelial wall.
21
Q

Migration

A

vasodilation slow blood flow in post cap venules. white blood cells get pushed against the wall so opportunity to interact with endothelium, red cels flow in center bc they are smaller.

22
Q

Rolling

A

leuko attach to adhesion molecules and detach to tumble on surface. cytokines, etc stimulate expression of selection on leuko and endo.

  1. p-selectins released form wiebel palade (wilkerbran/pselectin proteins) bodies; mediated by histamine
  2. e-selectin is induced by TNF and IL-1
  3. selectins bind to sialyl lewis X on leukocytes, which results in rolling.
23
Q

Adhesion

A
  1. adhesion molecules (ICAM and VCAM) are upregulated on endothelium by TNF and IL-1
  2. Integrins are upregulated on leukocytes by C5a and LTB4.
  3. interaction btw CAMS and integrins results in firm adhesion of leukocytes to vessel wall
24
Q

Transmigration/Diapedesis

A
  1. leukocytes transmigrate across endothelium of postcap venules move towards chemical attractants (chemotaxis)
  2. attracted by bacterial products IL-8, C5a, LTB4
25
Q

What role do toll like receptors play? Toll like receptors on MO and dentritic cells recognize?

A

mediators of acute inflammation

PAMP

(ex. CD14 recognize LPS on Gram- bacteria—->activates nfKb which is a transcription factor and becgins to make immune mediators)

26
Q

What are the three steps in phagocytosis?

A
  1. receptor mediated binding
  2. engulfment
  3. killing and degradation
27
Q

How do microbes get recognized in receptor mediated binding step of phagocytosis?

A
  • mannose, opsonin (IgG and C3b), scavenger receptor
  • integrins
28
Q

What occurs during the engulfment phase of pahocytosis?

A

phagolysosomal fusion

29
Q

what happens in the killing and degradation phase of phagocytosis?

A
  • “respiratory burst” ROS generation via NADPH oxidase complete
  • azyrophilic granule MPO: OCl-
  • generation of peroxynitrite: NOS-derived
30
Q

Leukocyte Adhesion Deficiency

A

LAD1: beta2 integrin deficiency

-AR defect on CD18 subunit

31
Q

Phagolysome: Chediak-Higashi Syndrome

A
  • defective lysosome fusion
  • AR protein trafficing defect (microtubules), cannot form phagolysosome
32
Q

Respiratory Burst: Chronic Granulomatous Disease

A

Multiple defects in NADPH oxidase subuibts

AR, poor 02 dependent killing

33
Q

Acquired defects in leukocyte recuitment to infection site

A

myelosuppression (chemo, XRT) or bone marrow involvement by leikemia or cancer

34
Q

What are some outcomes of acute inflammation?

A
  1. resolution
  2. healing by fibrosis (*scarring in tissues that don’t regenerate or lots tissue damage fills with CT. very severe CT deposition= fibrosis)
  3. chronic inflammation
35
Q

Morphology of acute inflammation: fibrunous inflammation

A

see on organ surfaces

fibrogen exudes from elaky vessels, polymerizes to fibrin

can serve as nidus for scarring

36
Q

What does this slide show?

A

morphology of acute inflmmation: purulent inflammation

37
Q

What does this slide show?

A

morphology of acute inflammation: ulcer

Pathology-1 (5 decks)

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