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AD1 > SF - Anti-inflammatories > Flashcards

SF - Anti-inflammatories Flashcards

1
Q

What is the pathway that forms histamine and how is it deactivated? Which enzymes are involved?

A

Histadine -> histamine (histamine carboxylase)

It is deactivated by diamine oxidase and histamine-N-methyltransferase to form inactive histamine.

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2
Q

Why is histamine deactivated rapidly?

A

To produce a local response.

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3
Q

Where is histamine found in the body?

A

Where the external environment comes into contact with the internal environment. There is high concentrations in the skin, lungs, brain and GI tract.

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4
Q

Where are mast cells produced?

A

Bone marrow

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5
Q

What 2 steps are involved in degranulation of mast cells? Describe both of these steps.

A

Priming of the mast cell. Initial exposure of the allergen causes IgE antibodies to bind to Fc receptors on the surface of mast cells.
Second exposure to the allergen. The allergen binds to IgE antibodies on mast cells. This activates the mast cell and leads to degranulation.

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6
Q

What 3 factors during inflammation causes an increase in intracellular calcium within mast cells? What are the consequences of this?

A

C3a, C5b and IgE. This causes vesicles in the mast cells to fuse to the membrane and release it’s contents.

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7
Q

What is the effect of stimulating H1?

A
  • increased systemic vasodilation
  • Increased vascular permeability
  • itching
  • Also causes an increase in IP3, DAG and calcium release.
  • This receptor is important in the inflammatory response.
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8
Q

What is the effect of stimulating H2?

A
  • stimulates gastric acid secretion.
  • relaxes smooth muscles.
  • increases HR.
  • Also increase cAMP. (This feeds back to inhibit histamine release)
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9
Q

What is the effect of stimulating H3?

A

Inhibits neurotransmitter release from neurones.

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10
Q

What is the effect of stimulating H4?

A

Regulates neutrophil release from bone marrow.

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11
Q

What is type 1 hypersensitivity? What can this cause?

A

Whole body reaction to an allergen. This can cause anaphylaxis.

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12
Q

What are the treatments for type-1 hypersensitivity?

A

Epinephrine. This is required to maintain vascular volume.

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13
Q

What are the broad roles of cytokines during inflammation?

A
  • Up-regulated during inflammation.
  • Interact with each other to stimulate receptor up-regulation.
  • Act at kinase linked receptors of GPCRs.
  • Coordinates an inflammatory response.
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14
Q

What is the relationship between morphine and histamine?

A

Morphine is able to displace histamine from the protein it is bound to. Therefore, acting as an anti-inflammatory.

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15
Q

What reaction does phospholipase-A catalyse?

A

Phospholipids in the cell membrane -> arachidonic acid / platelet activating factor

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16
Q

Describe the nomenclature of prostaglandins.

A

PG - prostaglandins
Letter - describes the structure.
Number - number of double bonds.

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17
Q

How do omega-3 fatty acid precursors differ from arachidonic precursors?

A

Causes 3 double bonds in the prostaglandins, rather than 2. Has more of an anti-inflammatory response.

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18
Q

What is arachidonic acid converted to? Which enzyme catalyses this?

A

Arachidonic acid -> PGG2 -> PGH2 (COX)

Arachidonic acid -> LTA4 (5-lipooxygenase)

19
Q

Which COX is induced by inflammation?

A

COX-2

20
Q

What is the function of PGD2 on vascular smooth muscle, bronchial muscle and it’s other main effects?

A

Vascular smooth muscle - relaxation
Bronchial muscle - constriction.
Other effects - relaxation of GI and uterine muscle.

21
Q

What is the function of PGE2 on vascular smooth muscle, bronchial muscle and it’s other main effects?

A

Vascular smooth muscle - relaxation
Bronchial muscle - dilation
Other effects - Hyperalgesic, fever, increased platelet aggregation, decreased gastric acid secretion.

22
Q

What is the function of PGF2a on vascular smooth muscle, bronchial muscle and it’s other main effects?

A

Vascular smooth muscle - constriction.
Bronchial muscle - constriction.
Other effects - can cause luteolysis in some species. Uterine contractions.

23
Q

What is the function of PGI2 on vascular smooth muscle, bronchial muscle and it’s other main effects?

A

Vascular smooth muscle - relaxation.
Bronchial muscle - no effect.
Other effects - hyperalgesia. Decreased platelet aggregation. Modulates kidney function.

24
Q

What is the pathway fro thromboxane production? Which enzymes?

A

PGH2 -> TXA2 -> TXB2
1 - TXA2 synthase
2 - spontaneous hydrolysis

25
Q

What are the 2 classes of leukotrienes? How do these 2 classes differ?

A

LTB4 - Activation and targeting of leukocytes and cytokine production.
Cysteinyl leukotrienes - causes bronchoconstriction and vasodilation. Involved with asthma.

26
Q

What are the cysteinyl leukotriene receptor anatgonists? What are these used to treat?

A

Zafairlukast and montelukast.

These are targeted to treat asthma.

27
Q

How do glucocorticoids work?

A
  • Binds to receptors in the cytoplasm.
  • Glucocorticoid receptor complex moves to the nucleus.
  • Increases of decreases gene transcription
28
Q

Why does excessive glucocorticoid action lead to hyperglycemia, muscle wasting and osteoporosis?

A

Hyperglycemia - increased gluconeogenesis. Decreased glucose uptake.
Muscle wasting - increase protein catabolism. Decreased protein synthesis.
Osteoporosis - decreased calcium absorption from the GI tract. Increased calcium excretion from the kidney.

29
Q

What are the causes of Addison’s disease?

A

Hypoadrenocorticism.

Caused by destruction of the adrenal glands by chronic inflammation or disease.

30
Q

What are the causes of Cushing’s disease?

A

Hyperadrenocorticism.

Caused by excessive glucocorticoid administration or excessive activity.

31
Q

What are the 4 mechanisms of glucocorticoids that lead to anti-inflammatory actions?

A
  • Increased transcription of anti-inflammatory cytokines, - Increased osteoclast activity
  • Decreased COX-2 expression
  • Increase in lipocortin production.
32
Q

What is the function of lipocortin?

A

It inhibits phospholipase A. This is the first step in the production of thromboaxanes and leukotrienes. So therefore, this has an anti-inflammatory response.

33
Q

Within a T-cell, what do glucocorticoids suppress?

A
  • IL2 production. This prevents T helper cell proliferation.
34
Q

What is the overall function of glucocorticoids?

A

To suppress the early and late inflammatory response.

35
Q

How are some drugs chondroprotective?

A

Provides the building blocks to build the cartilage matrix

36
Q

What are NSAIDs most commonly used for?

A

Non-infectious / non-allergic inflammation to control inflammation and pain.

37
Q

What do NSAIDs inhibit?

A

They inhibit the endoperoxide synthase COX enzyme. This is the enzyme that catalyses:
Arachidonic acid -> PGG2

38
Q

What are the main properties of COX-1?

A

Involved in gastric protection, blood clotting and renal blood regulation.
Has a narrow binding pocket, so NSAIDs cannot bind.

39
Q

What are the main properties of COX-2?

A

Induced by inflammation.

Produces prostaglandins and thromboxanes.

40
Q

What are the effects of inhibiting COX-1? Why is this?

A

Increased gastric acid secretion, decreased gastric mucous secretion and decreased platelet aggregation.
This is because PGE2 and PGI2 synthesis is impaired.

41
Q

What is the effect of enterohepatic recycling on the half life of a drug in the GI tract?

A

It increases the half life of the drug.

42
Q

What are the effects of inhibiting COX-2? Why is this dangerous?

A

Increased sodium retention.
Hypertension.
Reduces the effectiveness of diuretics
It is dangerous because it increases the risk of strokes and heart attacks.

43
Q

Why is the cats ability to metabolise NSAIDs different to other animals?

A

Has a low capacity to glucuronidate NSAIDs. This increases the drugs half life and toxicity.

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