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All the things continued > 2.1 acute inflammation, part 2 > Flashcards

2.1 acute inflammation, part 2 Flashcards

1
Q

What are the three major, general phases of inflammation?

A
  1. Fluid phase
  2. PMN phase
  3. Macrophage phase
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2
Q

What is the peak time of the PMN phase of inflammation?

A

24 hours

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3
Q

What is the peak time of the macrophage phase of inflammation?

A

2-3 days

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4
Q

Where in the blood stream to heavy particles sit? What happens to them with vasodilation?

A
  • Center

- Move toward the periphery with vasodilation

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5
Q

What is the first step of PMN arrival? What is involved in this step?

A

Margination

  • Vasodilation slows blood flow
  • Cells marginate from center of flow to the periphery
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6
Q

Where do PMNs marginate at?

A

Post capillary venule

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7
Q

What is the second step in PMN migration, and what occurs with this?

A

Rolling

-Selectins (speed bumps) slow down the rolling marginated PMNs

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8
Q

What are the “speed bumps” that cause the rolling phase of PMN migration? What cells do these come from?

A

P-selectin
-Weibel-Palade bodies

E-selectin induced by TNF and IL-1

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9
Q

What are the chemokines that induce E-selectin upregulation?

A

TNF and IL-1

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10
Q

What are the two proteins contained within Weibel-Palade bodies?

A

P-selectin

vWF

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11
Q

What chemokine induces WP bodies to release P-selectin?

A

Histamine

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12
Q

What is the molecule on leukocytes that bind selectins? What does this interaction cause?

A
  • Sialyl Lewis X

- Interaction results in rolling of leukocytes along the vessel wall

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13
Q

What is Sialyl Lewis X, and what does it do?

A

Molecule on leukocyte that binds to selectins on endothelium that results in rolling

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14
Q

What is the third step of PMN migration? What occurs with this?

A

Adhesion:

-Cellular adhesion molecules upregulated on endothelium

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15
Q

What are the cytokine that upregulate adhesion molecules on the endothelium?

A

TNF and IL-1

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16
Q

What are the cytokines that upregulate integrins on leukocytes, to facilitate bind to ICAMs and VCAMs on the endothelium?

A

C5a and LTB4

17
Q

What is the pathophysiology of leukocyte adhesion deficiency? Inheritance pattern?

A

AR defect of integrins (CD18 subunit)

18
Q

What are the clinical findings of leukocyte adhesion deficiency? (3)

A
  • Delayed separation of the umbilical cord
  • Increased circulating PMNs
  • Recurrent bacterial infections that lack pus formation
19
Q

Delayed separation of the umbilical cord = ? Why?

A
  • Leukocyte adhesion deficiency

- No PMNs to cause inflammation to necrotic umbilical cord

20
Q

Recurrent bacterial infections that lack pus = ?

A

Leukocyte adhesion deficiency

21
Q

Why is there an increase in the circulating PMNs with leukocyte adhesion deficiency?

A

Marginated pool shrinks d/t lack of ability to adhere

22
Q

What, generally, is pus? Why, then, is there no pus with leukocyte adhesion deficiency?

A
  • Dead PMNs sitting in fluid

- No PMNs d/t lack of adhesion

23
Q

What is the 4th and final step of PMN migration?

A

Transmigration and chemotaxis

-Leukocytes transmigrate across the endothelium of postcapillary venule

24
Q

What guides PMNs once they cross the postcapillary venules? (4)

A

chemoattractants:

  • IL-8
  • C5a
  • LTB4
  • Bacterial products
25
Q

What are the two major opsonins that enhance phagocytosis by PMNs?

A

IgG

C3b

26
Q

How does the general process of phagocytosis occur?

A

Pseudopods from leukocytes extend to form phagosomes, which then internalize and merge with lysosomes to form phagolysosomes

27
Q

What is Chediak-Higashi syndrome? Inheritance pattern?

A

AR Protein trafficking defect, characterized by impaired phagolysosome formation

28
Q

What are the components of the BAILIN mnemonic for Chediak-Higashi syndrome?

A
  • Bleeding disorders
  • Albinism
  • Infections
  • Leukopenia
  • Infiltrative lymphohistiocytosis
  • Neuropathy
29
Q

Why is there neutropenia in Chediak-Higashi syndrome?

A

No way to separate cells d/t defective microtubules

30
Q

Why are there giant granules in leukocytes in Chediak-Higashi syndrome?

A

Inability to distribute granules produced by the golgi

31
Q

Why is there defective primary hemostasis with Chediak-Higashi syndrome?

A

Loss of platelets d/t loss of movement out of megakaryocytes

32
Q

Why is there peripheral neuropathy with Chediak-Higashi syndrome?

A

Inability to traffic nutrients to the periphery

33
Q

Why is there albinism with Chediak-Higashi syndrome?

A

Melanocyte cannot transfer melanin to the keratinocytes d/t crappy microtubules

All the things continued (28 decks)

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