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FPP-MSS > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

What does the inflammasome do?

A

Recognizes dead cells, activates caspase-1 which activates IL-1 which triggers leukocyte recruitment

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2
Q

What is the key difference between TLR and Inflammasome??

A

TLR recognizes extracellular microbes (located in plasma mem) and the inflammasome recognizes products of dead cells and some microbes (located in cytoplasm)

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3
Q

What are the main chemical mediators that induce vasodilation?

A

Histamine and NO

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4
Q

What action causes increased vascular permeability?? What are two mediators of this?

A

Endothelial cell contraction

Histamine and Bradykinin

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5
Q

What is the cytokine that can stimulate histamine release?

A

IL-1

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6
Q

What are the functions of Bradykinin?

A

Causes vasodilation, increased permeability and pain

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7
Q

What causes transudate? How is it different from exudate?

A

Transudate is caused by osmotic/hydrostatic pressure imbalances. It results in fluid leakage due to hypocellular and low protein content. Low s.g.
Exudate is caused by an alteration in normal vessel permeability. Cellular and protein rich. High s.g. Fluid and protein leakage. Happens with inflammation.

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8
Q

Name the steps in leukocyte recruitment to an injury site.

A

Margination– leukocyte accumulation at periphery of vessels
Rolling– week and transient adhesions to endothelium
Adhesion– firm adhesion to endothelium
Transmigration– movement through endothelium to interstitium
Chemotaxis– movement towards injury site

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9
Q

What are the two types of adhesion molecules and the strength of their attachment?

A

Selectins– loose attachment to endothelial cells

Integrins– stable attachment to endothelium

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10
Q

What two cytokines increase endothelial cell ligand expression for integrin binding?

A

IL-1 and TNF (secreted by macrophages)

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11
Q

Definition of diapedesis. Chemokine that drives this action.

A

Movement of leukocytes through vessel wall

CD31 (PECAM1) on leukocytes and endothelial cells

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12
Q

Some examples of chemotactic factors.

A

Bacterial products, chemokines, complement, leukotrienes

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13
Q

What happens after leukocyte recruitment? Results of this.

A

Leukocyte activation

  1. phagocytosis
  2. intracellular destruction
  3. release of substances that destroy dead tissue and microbes
  4. more mediator production
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14
Q

Molecules that mediate recognition of microbe by leukocyte for phagocytosis

A

Opsonins

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15
Q

Principle mediators of vasodilation

A

Histamine and NO

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16
Q

Principle mediators of increased vascular permeability

A

Histamine and Bradykinin

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17
Q

Principle mediators of chemotaxis

A

IL-1 and TNF, bacterial products

18
Q

Principle mediators of fever

A

IL-1, TNF

19
Q

Principle mediator of pain

A

Bradykinin

20
Q

Principle mediator of tissue damage

A

ROS

Nitric oxide

21
Q

What are 3 possible outcomes of acute inflammation?

A

Resolution
Progression to chronic inflammation
Scarring or fibrosis

22
Q

What are the 4 morphological patters of acute inflammation?

A

Serous
Fibrinous
Suppurative
Ulcer

23
Q

Mildest form of acute inflammation; outpouring of thin fluid (protein-poor) from plasma or serial cavity linings

A

Serous inflammation

24
Q

Caused by more severe injury; larger vascular leaks, passage of fibrinogen and conversion to fibrin; May resolve or scar

A

Fibrinous inflammation

25
Q

Large numbers of neutrophils are present along with necrotic cells, edema fluid, and bacteria – PUS; occurs with infections;

A

Suppurative (purulent) inflammation

26
Q

What is an abscess?

A

Central area of necrotic tissue surrounded by preserved neutrophils, dilated vessels and fibroblastic proliferation

27
Q

Local defect to surface of organ or tissue – leads to sloughing of surface covering and necrotic inflammatory tissue

A

Ulcer

28
Q

What is happening with chronic inflammation?

A

Active inflammation, tissue injury and healing all at the same time!

29
Q

Some common causes of chronic inflammation.

A

Persistent infections that are difficult to eradicate
Prolonged exposure to toxic agents
Immune-mediated inflammatory disease (autoimmune)

30
Q

What cell is mainly responsible for chronic inflammation?

A

Macrophages – b/c of steady release of dead cells, microbes etc.

31
Q

Other cells involved in chronic inflammation.

A

Lymphocytes– T & B
Plasma cells– from activated B-lymphocytes
Eosinophils– in parasitic infections and IgE mediated inflammation (allergies)
Mast cells– found in connective tissue

32
Q

A distinctive pattern of chronic inflammation with prominent activated macrophages with epithelioid appearance

A

Granulomatous inflammation

33
Q

What are giant cells and what induces their formation?

A

Multinucleated cells made by fusion of many macrophages

IFN-gamma

34
Q

What are some systemic effects of inflammation?

A
  1. Fever
  2. Elevated plasma levels of acute-phase proteins
  3. Leukocytosis
35
Q

What are some pyrogens that cause systemic effect of fever?

A

IL-1, TNF, PGE2

36
Q

What stimulates acute-phase proteins, where are they synthesized and give some examples?

A

IL-6 stimulates
Synthesis in Liver
C-reactive protein, Fibrinogen, Serum amyloid A protein

37
Q

Will a Sed rate be increased or decreased in infections? Why?

A

Increased because excess fibrinogen binds to erythrocytes causing stacks (rouleaux) that sediment more rapidly than normal

38
Q

What type of leukocytosis indicates a bacterial infection?

A

Neutrophilia

39
Q

What type of leukocytosis indicates a viral infection?

A

Lymphocytosis

40
Q

What type of leukocytosis indicates allergies, asthma, or parasitic infections?

A

Eosinophilia

41
Q

What type of leukocytosis indicates typhoid, rickettsiae or protozoan infection?

A

Leukopenia – from cytokine-induced sequestration in lymph nodes

FPP-MSS (17 decks)

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