Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BVSc2 AD1 > Anti-inflammatories > Flashcards

Anti-inflammatories Flashcards

1
Q

What is the precursor to histamine?

A

Histadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the roles of histamine?

A

Tissue repair
inflammation
vasodilation
allergic/anaphylactic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is histamine found?

A

In mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where are mast cells produced?

A

Bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the IgE receptor on mast cells?

A

FcER1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does mast cell degranulation occur?

A

Exposure to allergen creates IgE antibodies which bind to mast cells
second exposure to mast cells bind to IgE on mast cell surface and activates mast ecll

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can inhibit histamine release?

A

cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the main histamine receptor called?

A

H1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the H1 receptor cause?

A

Systemic vasodilation
increased vascular permeability
itching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are used to treat allergies?

A

H1 receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the two types of H1 receptor antagonists?

A

1st gen - shorter generation, cross blood brain barrier

2nd gen - longer, dont cross

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do H2 receptors do?

A

Inhibit gastric acid secretion

treat gastric ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is used to treat anaphylaxis?

A

Adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are eicosanoids generated from and when?

A

Phospholipids, on demand rather than stored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the intermediate form of eicosanoids?

A

Arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the enzyme which changes phospholipids into arachidonic acid/eicosanoids?

A

Phospholipase A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 eicosanoids?

A

Prostaglandins
Thromboxanes
Leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What can stimulate phospholipase A2?

A 
Bradykinin
Mast cells
thrombin
complement
cell damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which prostaglandins are involved in inflammation?

A

PGE2 and PGI2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What converts arachidonic acid to prostaglandins?

A

Cyclooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the two isoforms of cyclooxygenase?

A

COX1 and COX2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the difference between COX1 and COX2?

A

1 is normally expressed in most cells

2 is not normally present, induced by inflammation

23
Q

What is significant about cyclooxygenase?

A

It is the target of corticosteroids and NSAIDS

24
Q

What effect does PGE2 and PGI2 have on vascular smooth muscle?

A

Relaxation

25
Q

What effect does PGE2 have on bronchial muscle?

A

Dilation

26
Q

What other effects do prostaglandins have on the body?

A

Hyperalgesia - increased pain sensitivity

PGE2 also causes fever

27
Q

What actions do thromboxanes cause?

A

Vasoconstriction and bronchoconstriction

Induce platelet aggregation

28
Q

How is thromboxane synthesised?

A

From PGH2

TXA2 synthase activates it

29
Q

Where is TXA2 synthase found?

A

in platelets

30
Q

What enzyme converts arachidonic acid to leukotrienes?

A

Lipoxygenase

31
Q

Where are leukotrienes produced?

A

Leukocytes, mast cells

32
Q

What do leukotrienes do?

A

activates leukocytes and cytokines

cause bronchoconstriction and vasodilation - asthma

33
Q

What are the main sources of prostaglandins?

A

Mast cells, leukocytes

34
Q

Where are glucocorticoids synthesised?

A

Zona fasciculata in the adrenal gland

35
Q

What is the main glucocorticoid in animals?

A

Corticosterone (cortisol)

36
Q

What causes glucocorticoid release?

A

Hypothalamus releases CRF - corticotrophin releasing factor

Anterior pituitary releases ACTH

37
Q

What is the pattern of glucocorticoid release?

A

Pulsetile

38
Q

What do glucocorticoids cause?

A

Increased or decreased gene transcription
Hyperglycaemia
increased protein catabolism - muscle wasting
redistribution of fat
increased Ca2+ excretion - hypocalcaemia

39
Q

What is the condition called from reduced glucocorticoids?

A

Addisons disease

40
Q

What is the condition for excess corticosteroids called?

A

Cushing’s syndrome

41
Q

What are the symptoms of cushing’s disease?

A

Hyperglycaemia
Muscle wasting
Osteoporosis

42
Q

What effects do glucocorticoids have on inflammation?

A

Glucocorticoids decrease the expression of COX2 so cant produce prostaglandins
Inhibits the early inflammatory response - good
inhibits late response - bad

43
Q

What are glucocorticoids used to treat?

A

Asthma, hypersensitivity, inflammatory skin conditions

44
Q

What is bad about glucocorticoids?

A

Inhibits late inflammatory response

Supresses immune response by preventing Th cell proliferation

45
Q

What are chondroprotective drugs?

A

Provide the building blocks to make the cartilage matrix

46
Q

What is cartilage made up of?

A

Collagen
Hyaluronic acid
Glycosaminoglycan
Proteoglycan

47
Q

What do NSAIDs do?

A

Inhibit cyclooxygenase

reduce prostaglandin and thromboxane synthesis

48
Q

What symptoms do NSAIDs treat?

A

Inflammation
fever
pain

49
Q

What is the binding pocket like on COX2?

A

Wider than COX1

50
Q

What are the side effects of NSIADs?

A

Gastric ulceration

51
Q

What do NSAIDs cause gastric ulceration

A

Inhibit PGE2 and PGI2 which usually protect mucosa

also inhibit platelet aggregation

52
Q

Why are NSAIDs particularly dangerous for dogs?

A

Have enterohepatic recycling
from liver out in bile
increases time drug is in GI tract

53
Q

What is a problem with COX2?

A

Increases sodium retention in the kidney

reduce kidney function

54
Q

How are NSAIDs metabolised?

A

Hepatic metabolism

glucouronidation - cats cant

BVSc2 AD1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions