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Pathology -- Gen Path > Types of Inflammation > Flashcards

Types of Inflammation Flashcards

1
Q

Important roles of inflammation

A

Delivery of phagocytes and proteins from blood to tissue, set up responses for healing and regeneration, enhanced macrophage activation for antigen presentation

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2
Q

Role of Mast cells in inflammation

A

Release histamine on tissue injury

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3
Q

Role of Tissue macrophages in inflammation

A

Release cytokines, particularly in response to infectious agents

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4
Q

Role of endothelial cells in inflammation

A

Mediate responses between tissue and blood supply

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5
Q

Role of parenchymal cells in inflammation

A

signal inflammation on death or injury

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6
Q

Role of platelets in inflammation

A

Initiate inflammatory signals on activation

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7
Q

Review the timeline

A

Page 3

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8
Q

Steps in local vascular events

A
  1. Activation of platelets
  2. Vasodilation and increased blood flow
  3. Stasis
  4. Increased vascular permeability
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9
Q

Causes of increase vascular permeability

A

Inc. hydrostatic pressure, Increased colloid osmotic forces, Activation of endothelial cells, Increased pinocytosis

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10
Q

How to distinguish a transudate from an exudate

A

T – SG under 1.012, under 3% protein, minimal particulate matter
E – SG over 1.020, over 3 percent protein, lots of particulate.

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11
Q

Source of immediate transient state of permeability of vessels? How to stop it?

A

Histamine, Bradykinin, Leukotrienes, Sub P

Block w/ anti-histamines

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12
Q

Causes of delayed prolonged leakage?

A

Prostaglandins and Cytokine production

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13
Q

In a clear way, mediators of increased vascular permeability, early, amplification, and maintenence

A

Early – Histamine, Serotonin
Amplification – Kinin, C3a, C5a (anaphylatoxins)
Maintenance – PGs and Interleukins

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14
Q

Timeline for neutrophil and macrophage migration?

A

Neutrophils days 0-1

Macrophages afterward

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15
Q

Steps in the emigration of leukocytes

A

Margination
Pavement/Adhesion
Transmigration
Chemotaxis

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16
Q

What happens in margination

A

As blood slows, cells move to periphery of the vessel

17
Q

Weak adhesion is caused by interactions between…

A

Selectins and surface carbohydrates

18
Q

Firm adherance is facilitated by binding of…

A

endotheliam CAMS with integrins of invading cells

19
Q

Examples of selectins

A

P-selectin, E selectin

20
Q

Examples of Integrins used in binding

A

ICAM-LFA1 Integrin (PMN)

VCAM - VLA4 integrin (monocyte)

21
Q

Which adhesion molecules facilitate adhesion

A

PECAM-1 or CD31

22
Q

____ and ____ are major chemotactic factors for neutrophils

A

Leukotriene B4 and IL-8

23
Q

In inflamm response – what time should you see PMNs

A

12-72 hours

24
Q

In inflamm response – what time should you see Mphages.

A

48+ hours

25
Q

In inflamm response – what time should you see lymphocytes?

A

72+ hours

26
Q

Chronic inflammation occurs when..

A

Persistence of infection
Inability to neutralize a toxin
Continuos physical injury
Persistence of an immune response

27
Q

E selectin expression is stimulated by ____ for what time frame?

A

IL-1

Peaks at 4 hours, reversed by 24

28
Q

VCAM expression is enhanced by…

A

IL-1, TNF, GM-CSF

29
Q

What is serous inflammation?

A

Extracellular fluid from blood serum associated with mild injury
Example – Blister

30
Q

Difference between fibrinous and fibrosis

A

Fibrinous – Fibrin

Fibrosis – Collagen

31
Q

In a granuloma, macrophages activate T cells with…

A

IL1, IL12, antigen presentation

32
Q

In a granuloma, what do activated TH1 cells do?

A

Secrete IFNg, activate macrophages, epithelioid macrophages, multinucleated giant cells

33
Q

What are epithelioid macrophages?

A

large activated mps, increased phagocytosis, metabolism, and lysosomal enzymes.

34
Q

Two types of giant cells and how to distinguish

A

Langerhans – nuc at periphery, immune type granulomas

Foreign body – nuc at center of cell, response to foreign.

35
Q

What are ulcers?

A

Local excavation/defect in mucosal surface produced by sloughing of necrotic epithelium

36
Q

Differences seen in acute and chronic ulcers?

A

Acute – PMNs, congested BV at margins

Chronic – Lymphocytes, mps, fibrous connective tissue at base

37
Q

Difference between erosions and ulcers

A

Erosions – Superficial only, usually only acute/subacu.

Ulcers – Loss of mucosal layers to muscularis, ALWAYS assocaited with surrounding chronic inflamm. fibrosis

38
Q

Which types of inflammation are primarily acute? chronic? both?

A

Acute – Serous, Suppurative
Chronic – Lymphocytic, Granulomatous
Both – Fibrinous

Pathology -- Gen Path (17 decks)

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