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Physiology: Alessio > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the features of Acute inflammation?

A

Rapid
Short duration
Associated with leukocytes (neutrophils)
Fluids and plasma proteins (edema)

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2
Q

What are features of Chronic inflammation?

A

Longer duration
Presence of lymphocytes and macrophages
Proliferation of blood vessels, fibrosis and tissue disruption

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3
Q

What are the clinical features of inflammation?

A

Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)

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4
Q

What are the 5 steps of acute inflammation?

A

1) Vasodilation
2) Increased blood flow
3) Increased permeability of the microvasculature
4) Increased viscosity og the blood (^ vessel diameter)
5) Stasis (slowly moving red cells)
6) Neutrophils accumulation

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5
Q

What are the stimuli for acute inflammation?

A 
Infections (bacteria)
Tissue necrosis (uric acid)
Foreign bodies (dirt)
Immune reactions (autoimmune)
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6
Q

What is inflammation?

A

A complex reaction in tissue that consists mainly of WBCs

A protective response designed to remove the cause of cell injury.

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7
Q

What are the three steps of leukocyte recruitment to sites of injury?

A

1) Margination
2) Rolling
3) Adhesion

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8
Q

What is margination?

A

Leukocytes redistribute themselves among the endothelium

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9
Q

What is Rolling?

A

Rows of leukocytes adheere, detach and adhere again firmly

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10
Q

Which protein is Rolling mediated by?

A

Selectins

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11
Q

What is Adhesion?

A

Leukocytes are firmly adhered to the endothelium

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12
Q

Which protein is Adhesion mediated by?

A

Integrins

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13
Q

What happens after the leukocytes are firmly attached to the endothelium?

A

They migrate through the endothelium (transmigration/diapedesis)

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14
Q

Give the name of an adhesion molecule that helps diapedesis?

A

PECAM-1/CD31

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15
Q

What do the leukocytes do to the membrane?

A

Pierce the basement membrane by secreting collagenases and enter the extravascular site

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16
Q

What is the Chemotaxis of Leukocytes?

A

The leukocytes emigrate towards the site of injury by following chemoattractants

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17
Q

What are the three steps that take place during Phagocytosis?

A

1) Recognition and attachment
2) Engulfment
3) Killing and degradation

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18
Q

What are the three types of receptors?

A

Mannose receptors
Scavenger receptors
Opsonin receptors

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19
Q

What are mannose receptors?

A

Bind terminal sugars, residues part of molecules found on microbial cell walls.

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20
Q

What are scavenger receptors?

A

Bind a variety of microbes

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21
Q

What are the two types of mediators of inflammation?

A

Cell-derived inflammations

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22
Q

Which two cell mediators play a central roll in acute inflammation?

A

Prostaglandins

Leukotrienes

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23
Q

Where are cell-derived mediators produced?

A

Produced locally

24
Q

Where are plasma-protein derived mediators produced?

A

In the liver

25
Q

Which enzyme releases Arachidonic acid from membrane phospholipids?

A

Phospholipase A2

26
Q

Which enzyme converts AA in prostaglandins?

A

COX-1

27
Q

What are the two ‘things’ that are generated by PGH2?

A

Prostacyclin (PGI2)

Thromboxane A2

28
Q

Which enzyme directly synthesises TXA2?

A

Thromboxane-A-synthase

29
Q

What does Thromboxane A2 (TXA2) cause?

A

Vasoconstriction

Promotes platelet aggregation

30
Q

What does Prostacyclin (PGI2) cause?

A

Vasodilation

Inhibits platelet aggregation

31
Q

Which is the other enzyme that the AA activates?

A

5-lipoxyegenase

32
Q

What does 5-lipoxygenase do?

A

Converts AA to 5-HPETE, precursor of leukotrienes.

33
Q

What are some examples of COX1/2 inhibitors?

A

Aspirin, Ibuprofen, Idomethacin, Paracetamol (NSAIDs)

34
Q

What effects do COX1/2 inhibitors have?

A

Anti-inflammatory effect
Analgesic effect
Anti-pyretic effect

35
Q

How is an anti-flammatory effect achieved?

A

Blocking of prostaglandin production (reduce vasodilation and edema)

36
Q

How is an analgesic effect achieved?

A

Reduce pain by inhibition of PGs that sensitize nociceptors to inflammatory mediators

37
Q

How is an anti-pyretic effect achieved?

A

Lower body temperature

38
Q

What are the main systemic effects of acute inflammation?

A

Fever- body temp elevation of 1-4
LPS (lipopolysaccharide)
induces an immune response and IL-1 and TNF

39
Q

What is the name of transcription factor that effects inflammation?

A

NF-KB transcription

40
Q

Give examples of stimuli that activated the NF-KB transcription factor?

A

Cytokines
Virus
Bacteria
Cell stress

41
Q

Which cytokines does NF-KB regulate?

A

IL-1, IL-6, TNF

42
Q

Name 4 anti-inflammatory drugs that target NF-kB transcription?

A

1) IKK Inhibitors
2) Proteasome inhibitors
3) Inhibitors that bock nuclear translocation
4) Inhibitors of NF-kB DNA-binding activity

43
Q

Give an example of a drug that is an IKK inhibitor

A

Bortezomib

44
Q

Give an example of a drug that inhibits nuclear translocation blocker

A

Tacrolimus

45
Q

Give an example of a drug which inhibits NF-kB binding activity

A

Glucocorticoids

46
Q

What are some causes of chronic inflammation? (3)

A

1) Persistent infections
2) Immune-mediated inflammatory diease
3) Prolonged exposure to toxic agents

47
Q

How does a persistent infection cause chronic inflammation?

A

It can lead to granulomous reaction (aggregation of macrophages that are transformed into epithelial-like cells)

48
Q

How does immune-mediated inflammatory diseases cause chronic inflammation?

A

XS and inappropriate activation of the immune system.

49
Q

How does prolonged exposure to toxic agents cause chronic inflammation?

A

Long exposure to exogenous or endogenous

50
Q

What are 3 features of chronic inflammation?

A

1) Infiltration with mononuclear cells
2) Tissue destruction
3) Attempt at healing

51
Q

What are the 3 cells in chronic inflammation?

A

1) Macrophages
2) Lymphocytes
3) Plasma cells

52
Q

What role do macrophages play in chronic inflammation?

A

Eliminate injury agents and to initiate the process of repair.

53
Q

Which cell is responsible for much of the tissue injury in chronic inflammation?

A

Macrophage

54
Q

What role do lymphocytes play in chronic inflammation?

A

They communicate with macrophages through release of cytokines.

55
Q

What role do plasma cells play in chronic inflammation?

A

Develop from activated B cells and produce antibodies against the persistent foreign antigen at the inflammatory site.

Physiology: Alessio (5 decks)

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