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Term 3: Immunology/Pathology > Inflammation > Flashcards

Flashcards in Inflammation Deck (55):
1

What are the two broad classes of Inflammation?

Acute

Chronic

2

What are the events of Acute inflammation?

-Increase of vascular flow and permeability

-cells migrate to affected area

-Chemical mediators attract cells, kill microorganisms, and give rise to inflammation

3

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

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

-caused by vascular changes

4

What is transudate?

-Fluid only!

-A clinical term for low protein fluid, with low specific gravity, and few inflammatory cells collected outside the blood vessels

5

What is Exudate?

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

6

How do we turn off inflammation?

-inflammatory mediators have a very short half life

-Production of Lipoxins

-Production of TGF-beta

7

What pathway leads to Lipoxin synthesis?

Arachidonic acid metabolism

**not the COX pathway

8

What are the four possible outcomes of Acute inflammation?

-resolves completely = regeneration

-becomes localized, forming an abscess

-heals with scarring

-Progresses to chronic inflammation

9

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

Acute = neutrophils

Chronic = lymphocytes and macrophages

10

Is angiogenesis associated with acute or chronic inflammation?

Chronic

11

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

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

C. Redness

12

What are the stimuli of acute inlfammation?

-infections

-necrosis

-foreign bodies

-immune reactions

13

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

T

14

What ends up killing bacteria in phagolysosomes?

Reactive oxygen species (ROS)

15

What is Chediak-Higashi syndrome?

-defective fusion of phagosomes and lysosomes

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

16

WHat is Chronic Granulomatous Disease (CGD)?

-defects in bacterial killing and recurrent infections

-cannot generate superoxide

17

What are the Types of Inflammatory Mediators?

-Vasoactive amines

-Plasma proteases

-Arachidonic acid metabolites

-platelet activating factor

-cytokines, NO, lysosomal contents, free radicals, neuropeptides

18

What are the vasoactive amines?

-histamine & serotonin

19

What are the Arachadonic acid metabolites?

-Prostaglandins

-Leukotrienes

-Lipoxins

20

What cytokines cause fever?

-TNF

-IL-1

21

What are the three types of Nitrous Oxide?

-Endothelial

-Neuronal

-Inducible

22

What does NO do in inflammation?

-promotes vasodilation

-inhibits the inflammatory response

23

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

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

C. Neutrophils

**remember! viruses don't recruit Neutrophils!

-Lymphocytes in chronic infection

-Plasma cells in later stage of infection

24

What are the factors involved in turning off inflammation?

-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