Term 3: Immunology/Pathology > Inflammation > Flashcards

Inflammation Flashcards

(55 cards)

Study These Flashcards
1
Q

What are the two broad classes of Inflammation?

A

Acute

Chronic

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2
Q

What are the events of Acute inflammation?

A
  • Increase of vascular flow and permeability
  • cells migrate to affected area
  • Chemical mediators attract cells, kill microorganisms, and give rise to inflammation
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3
Q

What are the three cardinal signs of inflammation? What is responsible for them?

A
  1. Rubor (redness)
  2. Calor (warmth)
  3. Tumor (swelling)

-caused by vascular changes

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4
Q

What is transudate?

A
  • Fluid only!
  • A clinical term for low protein fluid, with low specific gravity, and few inflammatory cells collected outside the blood vessels
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5
Q

What is Exudate?

A

-a clinical term for high protein fluid, with high specific gravity, and many inflammatory cells collected outside the blood vessels

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6
Q

How do we turn off inflammation?

A
  • inflammatory mediators have a very short half life
  • Production of Lipoxins
  • Production of TGF-beta
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7
Q

What pathway leads to Lipoxin synthesis?

A

Arachidonic acid metabolism

**not the COX pathway

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8
Q

What are the four possible outcomes of Acute inflammation?

A
  • resolves completely = regeneration
  • becomes localized, forming an abscess
  • heals with scarring
  • Progresses to chronic inflammation
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9
Q

What is the difference in immune cells that mediate acute and chronic inlfammation?

A

Acute = neutrophils

Chronic = lymphocytes and macrophages

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10
Q

Is angiogenesis associated with acute or chronic inflammation?

A

Chronic

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11
Q

Which of the following clinical features is suggestive of acute inflammation?

A. Alopecia
B. Blanching
C. Redness
D. Sweating

A

C. Redness

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12
Q

What are the stimuli of acute inlfammation?

A
  • infections
  • necrosis
  • foreign bodies
  • immune reactions
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13
Q

(T/F) Viral infections don’t recruit neutrophils.

A

T

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14
Q

What ends up killing bacteria in phagolysosomes?

A

Reactive oxygen species (ROS)

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15
Q

What is Chediak-Higashi syndrome?

A
  • defective fusion of phagosomes and lysosomes

- leads to susceptibility to infections, albinism, nerve defects, platelet defects, and bleeding disorders

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16
Q

WHat is Chronic Granulomatous Disease (CGD)?

A
  • defects in bacterial killing and recurrent infections

- cannot generate superoxide

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17
Q

What are the Types of Inflammatory Mediators?

A
  • Vasoactive amines
  • Plasma proteases
  • Arachidonic acid metabolites
  • platelet activating factor
  • cytokines, NO, lysosomal contents, free radicals, neuropeptides
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18
Q

What are the vasoactive amines?

A

-histamine & serotonin

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19
Q

What are the Arachadonic acid metabolites?

A
  • Prostaglandins
  • Leukotrienes
  • Lipoxins
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20
Q

What cytokines cause fever?

A
  • TNF

- IL-1

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21
Q

What are the three types of Nitrous Oxide?

A
  • Endothelial
  • Neuronal
  • Inducible
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22
Q

What does NO do in inflammation?

A
  • promotes vasodilation

- inhibits the inflammatory response

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23
Q

The classic morphologic appearance of acute inflammation in tissue sections is:

A. Eosinophils
B. Lymphocytes
C. Neutrophils
D. Plasma cells

Study These Flashcards
A

C. Neutrophils

**remember! viruses don’t recruit Neutrophils!

  • Lymphocytes in chronic infection
  • Plasma cells in later stage of infection
24
Q

What are the factors involved in turning off inflammation?

Study These Flashcards
A
  • Lipoxins
  • TGF-beta
  • Nitrous Oxide
25
What types of stimuli can elicit a chronic inflammatory response without an accute inflammation?
- Autoimmune - Viral diseases - Persistent infections (TB)
26
What immune cells come along with chronic inflammation?
- lymphocytes - plasma cells - macrophages
27
What is Granulomatous Inflammation?
- type of chronic inflammation - focal collection of "epithelioid" histiocytes - seen with "poorly digestible" agents * *need intact T cell immunity
28
What are epithelioid histiocytes?
- histiocytes (macrophages) that have been activated - large with abundant pink cytoplasm - resemble epithelial cells
29
What is the differential diagnosis of granulomatous inflammation?
- Tuberculosis - bacteria such as syphilis or cat scratch disease - fungal disease, parasitic - foreign materials** - sarcoidosis
30
A granuloma is: A. A special type of chronic inflammation B. Pathognomonic for tuberculosis C. Seen only in the lung D. Characterized by giant cells and necrosis
A. A special type of chronic inflammation
31
What are the two forms of tissue repair?
- regeneration | - fibrosis
32
What is fibrosis?
- scarring | - replacement of lost cells by collagen
33
Labile cells are: A. Cells that are always dividing B. Cells that are in G0 but can enter the cell cycle C. Cells that are undergoing apoptosis D. Cells that cannot divide
A. Cells that are always dividing
34
What are labile cells?
- cells that are always dividing | - located in skin, bone marrow, and GI mucosa
35
What are stable cells?
- cells that can enter the cell cycle and divide if they so desire e. g. hepatocytes, renal tubular cells, endothelial cells
36
What is EGF?
- growth factor for epithelial cells | - produced by keratinocytes, macrophages, and inflammatory cells
37
What is HGF
- hepatocyte growth factor - mitogenic for hepatocytes and biliary epithelium, lung kidney, and mammary gland cells - produced by fibroblasts and most mesenchymal cells
38
What is PDGF
- platelet-derived growth factor - stored in platelets, released when platelets are activated - causes migration and proliferation of fibroblasts, smooth muscle cells, and many tumor cells
39
What is VEGF?
- vascular endothelial growth factor - potent inducer of blood vessel formation - promotes angiogenesis
40
What is FGF?
- fibroblast growth factor | - contributes to wound healing, hematopoiesis, angiogenesis, developent and others
41
What is TGF-beta?
-Transforming growth factor beta - wide variety of actions: - growth inhibitor for epithelial cells - potent fibrinogenic - strong anti-inflammatory effects
42
What are the steps in the wound repair process?
- angiogenesis - migration and proliferation of fibroblasts - deposition of ECM - remodeling
43
What are the three phases of cutaneous wound healing?
- inflammation - proliferation - maturation (collagen matrix & wound contraction)
44
Which of the following is considered a systemic effect of inflammation: A. Edema B. Fever C. Redness D. Warmth
B. Fever
45
What is the difference between healing and fibrosis?
- fibrosis implies persistent tissue damage & inflammation | - Healing implies a single/self-limited tissue injury
46
What is a granuloma?
- contains epithelioid macrophages/histiocytes - peripheral lymphocutes - giant cells - may or may not be necrotic (caseous?)
47
What is healing by first intention?
The edges of the wound can be brought together
48
What is healing by second intention?
The edges of the wound cannot be brought together, much wider and usually deeper
49
Is granulation tissue a granuloma?
NOOOOOO
50
What IS granulation tissue then?
-small vessels with lots of edema and inflammation
51
What is the difference between serous and fibrinous inflammation?
Serous = lots of fluid (effusions & blisters) Fibrinous = more severe vascular leak (larger molecules leak out)
52
What is suppuration
Formation of pus
53
What is cellulitis?
-diffuse inflammmation of soft tissues
54
What is the difference between fibrinous and fibrous?
Fibrinous = deposition of fibers Fibrous = proliferation of fibroblasts
55
What is Leukocytosis?
- increased WBCs in peripheral blood - a systemic effect of inflammation - presence of left shift = immature white cells in blood
Term 3: Immunology/Pathology
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