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USMLE Pathology > Acute Inflammation 2 > Flashcards

Acute Inflammation 2 Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the 3 major phases of acute inflammation?

A
  • Fluid phase
  • Neutrophil phase
  • Macrophage phase
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2
Q

When does the macrophage phase peak approximatly?

A

2-3 days in

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3
Q

What is margination?

A

Heavy particles predominantley sit at the centre of a blood vessel
- During vasodilation these particles can spread to the periphery of the blood vessel

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4
Q

What is step 1 of margination?

A
  • Vasodilation slows blood flow in postcapillary venules

- Cells marginate from center of flow to periphery

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5
Q

What is step 2?

A

Rolling

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6
Q

What does rolling involve?

A

Large molecules hit selcetins (act like speedbumps)

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7
Q

What is P-selectin released from?

A

Weibel-Palade bodies

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8
Q

What is P-selectin mediated by?

A

Histamine

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9
Q

What is E-seletin induced by?

A

TNF and IL-1

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10
Q

What are the 2 key proteins within Weibel-Palade bodies?

A
  • Von Willebrand

- P-selectin

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11
Q

What protein on neutrophils binds to selectin, allowing the leukocytes to roll along the vessel wall?

A

Sialyl Lewis X

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12
Q

What are cellular adhesion molecules upregulated on the endothelium by?

A
  • TNF

- IL-1

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13
Q

What is the 5 steps involved for neutrophils in acute inflammation?

A
  • Margination (migration to periphery)
  • Rolling
  • Adhesion
  • Transmigration and chemotaxis
  • Phagocytosis
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14
Q

What are integrins upregulated on leukocytes by?

A
  • C5a

- LTB4

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15
Q

What does the interaction between integrins (from the leukocyte) and cellular adhesion molecules allow for?

A

Firm adhesion to vessel wall

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16
Q

What do the endothelial cells express to allow for adhesion?

A

Cellular adhesion molecules

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17
Q

What is the defect in leukocyte adhesion deficiency?

A

AR

  • Defect of integrins
  • CD18 subunit
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18
Q

What are the high yield clinical features associated with Leukocyte Adhesion Deficiency? (3)

A
  • Delayed seperation of umbilical cord
  • Increased circulating neutrophils
  • Recurrent bacterial infections lacking pus
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19
Q

What is pus?

A

Dead neutrophils sitting in fluid

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20
Q

What are neutrophils attracted by?

A
  • IL-8
  • C5a
  • LTB4
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21
Q

What is phagocytosis enhanced by?

A

Opsonins (IgG and C3b)

22
Q

At what point in the blood vessel do leukocytes transmigrate across the endothelium?

A

Postcapillary venules

23
Q

Describe how phagocytosis occurs

A

The leukocyte will draw out pseudopods (arm like structures) around the pathogen and consume it

  • This will then create a vesicle inside the leukocyte - known as a phagosome
  • This will then merge witha lysosome to create a phagolysosome
24
Q

What is the mechanism behind Chediak-Higashi Syndrome?

A
  • Protein trafficking (Microtubule) defect

- Impaired phagolysosome formation - infections

25
Q

How is Chediak-Higashi Syndrome inherited?

A

AR

26
Q

What are the clinical features of Chediak-Higashi syndrome?

A
  • Increased risk of pyogenic infections
  • Neutropenia
  • Giant granules in leukocytes
  • Defective primary hemostasis
  • Albinism (melanin transport)
  • Peripheral neuropathy
27
Q

What cells create melanin and what cells express it?

A

Melanin is created by melanocytes but transported to keratinocytes which express it - show pigmentation

28
Q

What does NADPH oxidase convert?

A

O2 into superoxide

29
Q

What does superoxide dismutase convert?

A

Superoxide into Hydrogen peroxide (H2O2)

30
Q

What does myeloperoxide convert?

A

Hydrogen peroxide (H2O2) into HOCl

31
Q

What substance is generated in phagocytes in O2-dependent killing?

  • Known as ‘Oxidative burst’
A

Bleach (HOCl)

32
Q

What enzyme is there a defect in in Chronic Granulomatous Disease (CGD)?

A

NADPH oxidase defect

- Poor O2-dependent killing

33
Q

How is CGD inherited?

A
  • X-linked OR

- Aut Recessive

34
Q

What type of organisms are those with CGD vulnerable to?

A

Catalase +ve organisms

35
Q

What are the catalase +ve organisms?

A
  • S. aureus
  • P cepacia
  • S marcescens
  • Nocardia
  • Aspergillus
36
Q

Via what pathway can the leukocytes create bleach in individuals with CGD?

A

They can take hydrogen peroxide from the bacteria to create bleach

37
Q

Why are those with CGD vulnerable to catalase +ve organisms?

A

Bacteria with catalase can break down hydrogen peroxide therefore, the bacteria cannot use the hydrogen peroxide to make bleach

38
Q

What does the Nitroblue tetrazolium test screen for?

A

CGD

39
Q

What does the Nitroblue tetrazolium test involve?

A

Turns blue if O2- (superoxide) is created from O2

  • Blue if NADPH oxidase is working
  • Colourless if NADPH oxidase is defective
40
Q

What are MPO deficient patients vulnerable to (what organisms)?

A

Usually asymptomatic

- Candida

41
Q

What will a NBT (Nitroblue tetrazolium) test show in MPO deficiency?

A

Normal

- Turns blue

42
Q

What step of the conversion to bleach is defective in MPO deficiency?

A

H2O2 to HOCl-

43
Q

What does O2-independent killing occur via?

A

Enzymes present in leukocyte secondary granules (e.g. lysozyme and major basic protein)

44
Q

What is more effective O2 dependent or independent killing?

A

O2 dependent

45
Q

What is the final step for neutrophils in inflammation?

A

Resolution - Apoptosis

  • Disappear within 24 hrs after resolution of inflammatory stimulus
  • Creates pus
46
Q

What cells predominate after neutrophils in acute inflammation?

A

Macrophages

47
Q

When do macrophages peak after inflammation?

A

2-3 days after inflammation occurs

48
Q

How do macrophages destroy material?

A
  • Ingest via phagocytosis

- Destroy phagocytosed material using enzymes in secondary granules

49
Q

What do the macrophages produce to start resolution and healing?

A

IL-10 and TGF-Beta

50
Q

What can macrophages produce to continue acute inflammation?

A

IL-8

51
Q

What can macrophages create which is known as an area of walled off acute inflammation?

A

Abscess

52
Q

What do macrophages express antigens on to produce chronic inflammation?

A

MHC class II

USMLE Pathology (15 decks)

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