Acute and Chronic Inflammation Flashcards

1
Q

A tissue must be _______ and ________ to become inflamed.

A

living and vascularized

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2
Q

What are the five cardinal signs of inflammation?

A

Tumor, calor, rubor, dolor, functio laesa

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3
Q

What are the three components of inflammation?

A
  1. Vascular
  2. Cellular
  3. Chemical
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4
Q

What is the function of inflammation?

A

To localize and eliminate the cause of injury and initiate the repair process to attempt to restore normal structure and function.

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5
Q

What are the three possible inflammatory outcomes?

A

Resolution (best)
Scar
Chronic inflammation

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6
Q

Does scar tissue function as well as the original tissue?

A

Nope

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7
Q

The severity of injury determines the ________ phase of the inflammatory process.

A

amplification

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8
Q

An inability to eliminate the offending agent often results in _______ ________.

A

chronic inflammation

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9
Q

What cells infiltrate tissues during acute inflammation?

A

Neutrophils (type of polymorph)

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10
Q

What cells infiltrate tissues during chronic inflammation?

A

macrophages, lymphocytes (NK cells, B cells, T cells)

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11
Q

Compare tissue injury and fibrosis in acute inflammation with chronic inflammation.

A

In acute, tissue injury and fibrosis are mild and localized whereas in chronic inflammation it is severe and progressive.

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12
Q
Define the following:
Transudate
Exudate
Fibrinous exudate
Purulent exudate
A

Transudate is edema fluid with low protein content. (<1.015)
Exudate is edema fluid with high protein content.
Fibrinous exudate has a large amount of fibrin.
Purulent exudate has lots of cellular components.

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13
Q

Describe the changes blood vessels undergo during acute inflammation.

A
  1. Immediate vasoconstriction - short lasting.
  2. Vasodilation (hyperemia) and increased vascular permeability.
  3. Stasis (blood flow slows).
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14
Q

What is the “immediate transient response” of blood vessels during acute inflammation?

A

The vasodilatory effects caused by mediators such as histamine.

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15
Q

What is leukocyte margination?

A

Same thing as extravasation - leukocytes migrate out of vessels into tissues.

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16
Q

Which molecule is responsible for initiation of leukocyte “rolling” along the endothelium? Which molecule helps anchor the leukocyte to the endothelium?

A

P-selectin helps roll. Integrin helps anchor.

17
Q

What do chemokines do to leukocytes?

A

They are chemoattractants and also activate the leukocyte to express high avidity integrin surface molecules.

18
Q

What are Weibel-Palade bodies?

A

Storage bodies of P-selectin and von Willebrand Factor in endothelial cells.

19
Q

How long do polymorphs live after they have extravasated into tissues?

A

7-8 hours

20
Q

What cell types are capable of the respiratory burst?

A

Immune cells such as neutrophils.

21
Q

What are the two general types of leukocyte deficits?

A

Congenital (Chediak-Higashi, etc.) and acquired (chemo, radiation, leukemia, etc).

22
Q

What is Chediak-Higashi Syndrome?

A

Defective phagocytosis due to poor chemotaxis and defective lysosomal granules.

23
Q

What is chronic granulomatous disease?

A

Deficient NADPH oxidase - no respiratory burst capability

24
Q

What is serous inflammation? Name an example.

A

Outpouring of a watery, protein-poor fluid that derives from either plasma or mesothelial cells. Example is a skin blister - called an effusion.

25
Q

What is fibrinous inflammation? What causes it? Name one example.

A

Caused by more severe injury that allows large molecules such as fibrinogen to pass the endothelial barrier. Fibrinogen polymerizes –> fibrin –> scarring. Ex. fibrinous pericarditis.

26
Q

What is supperative (purulent) inflammation?

A

Collection of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid. Often caused by pyogenic organisms.

27
Q

What is an ulcer?

A

A local defect or excavation of the surface of an organ that is produced by sloughing of inflamed necrotic tissue.

28
Q

What does Sialyl-Lewis-X on leukocytes do?

A

Promotes leukocyte rolling along the endothelium

29
Q

What do LFA-1 and MAC-1 (on leukocytes) and ICAM-1 and VCAM-1 (on endothelial cells) do?

A

They promote stable adhesion between leukocytes and endothelial cells.

30
Q

What does CD31 (PECAM-1) on endothelial cells do?

A

Promotes transmigration of leukocytes

31
Q

Coagulation, fibrinolytic molecules, Kinins, and complement molecules are _______-derived.

A

plasma

32
Q

Arachidonic acid-derived, histamine, serotonin, and NO are ____-derived.

A

cell

33
Q

Infiltration of mononuclear cells such as macrophages, lymphocytes, and plasma cells is often due to _______ inflammation.

A

chronic

34
Q

What is a granuloma?

A

A collection of immune cells called granulocytes and epithelioid cells (activated macrophages) that forms when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate.

35
Q

Name six causes of granulomatous inflammation.

A
  1. Fungal infections
  2. TB
  3. Leprosy
  4. Syphillis
  5. Persistent foreign material
  6. Some autoimmune diseases
36
Q

Name six systemic effects of inflammation.

A
  1. Fever from IL-1, TNF
  2. Increased acute phase proteins
  3. Increased leukocytes (leukocytosis)
  4. Increased HR and BP
  5. Chills
  6. Septic shock
37
Q

What are C5a, LTB4, and IL-8 involved in?

A

Chemotaxis

38
Q

What does the presence immature neutrophils (neutrophilia) indicate?

A

Systemic inflammation - body is pulling all the WBCs out of the bone marrow even though they aren’t ready.