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Term 3: Immunology/Pathology > Inflammation > Flashcards

Inflammation 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

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?

A
  • Lipoxins
  • TGF-beta
  • Nitrous Oxide
25
Q

What types of stimuli can elicit a chronic inflammatory response without an accute inflammation?

A
  • Autoimmune
  • Viral diseases
  • Persistent infections (TB)
26
Q

What immune cells come along with chronic inflammation?

A
  • lymphocytes
  • plasma cells
  • macrophages
27
Q

What is Granulomatous Inflammation?

A
  • type of chronic inflammation
  • focal collection of “epithelioid” histiocytes
  • seen with “poorly digestible” agents
  • *need intact T cell immunity
28
Q

What are epithelioid histiocytes?

A
  • histiocytes (macrophages) that have been activated
  • large with abundant pink cytoplasm
  • resemble epithelial cells
29
Q

What is the differential diagnosis of granulomatous inflammation?

A
  • Tuberculosis
  • bacteria such as syphilis or cat scratch disease
  • fungal disease, parasitic
  • foreign materials**
  • sarcoidosis
30
Q

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. A special type of chronic inflammation

31
Q

What are the two forms of tissue repair?

A
  • regeneration

- fibrosis

32
Q

What is fibrosis?

A
  • scarring

- replacement of lost cells by collagen

33
Q

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

A. Cells that are always dividing

34
Q

What are labile cells?

A
  • cells that are always dividing

- located in skin, bone marrow, and GI mucosa

35
Q

What are stable cells?

A
  • cells that can enter the cell cycle and divide if they so desire
    e. g. hepatocytes, renal tubular cells, endothelial cells
36
Q

What is EGF?

A
  • growth factor for epithelial cells

- produced by keratinocytes, macrophages, and inflammatory cells

37
Q

What is HGF

A
  • hepatocyte growth factor
  • mitogenic for hepatocytes and biliary epithelium, lung kidney, and mammary gland cells
  • produced by fibroblasts and most mesenchymal cells
38
Q

What is PDGF

A
  • 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
Q

What is VEGF?

A
  • vascular endothelial growth factor
  • potent inducer of blood vessel formation
  • promotes angiogenesis
40
Q

What is FGF?

A
  • fibroblast growth factor

- contributes to wound healing, hematopoiesis, angiogenesis, developent and others

41
Q

What is TGF-beta?

A

-Transforming growth factor beta

  • wide variety of actions:
  • growth inhibitor for epithelial cells
  • potent fibrinogenic
  • strong anti-inflammatory effects
42
Q

What are the steps in the wound repair process?

A
  • angiogenesis
  • migration and proliferation of fibroblasts
  • deposition of ECM
  • remodeling
43
Q

What are the three phases of cutaneous wound healing?

A
  • inflammation
  • proliferation
  • maturation (collagen matrix & wound contraction)
44
Q

Which of the following is considered a systemic effect of inflammation:

A. Edema
B. Fever
C. Redness
D. Warmth

A

B. Fever

45
Q

What is the difference between healing and fibrosis?

A
  • fibrosis implies persistent tissue damage & inflammation

- Healing implies a single/self-limited tissue injury

46
Q

What is a granuloma?

A
  • contains epithelioid macrophages/histiocytes
  • peripheral lymphocutes
  • giant cells
  • may or may not be necrotic (caseous?)
47
Q

What is healing by first intention?

A

The edges of the wound can be brought together

48
Q

What is healing by second intention?

A

The edges of the wound cannot be brought together, much wider and usually deeper

49
Q

Is granulation tissue a granuloma?

A

NOOOOOO

50
Q

What IS granulation tissue then?

A

-small vessels with lots of edema and inflammation

51
Q

What is the difference between serous and fibrinous inflammation?

A

Serous = lots of fluid (effusions & blisters)

Fibrinous = more severe vascular leak (larger molecules leak out)

52
Q

What is suppuration

A

Formation of pus

53
Q

What is cellulitis?

A

-diffuse inflammmation of soft tissues

54
Q

What is the difference between fibrinous and fibrous?

A

Fibrinous = deposition of fibers

Fibrous = proliferation of fibroblasts

55
Q

What is Leukocytosis?

A
  • increased WBCs in peripheral blood
  • a systemic effect of inflammation
  • presence of left shift = immature white cells in blood

Term 3: Immunology/Pathology (17 decks)

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