Brainscape's Knowledge GenomeTM

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


See full index

HUMAN HEALTH AND DISEASE > Anti-Inflammatory Drugs > Flashcards

Anti-Inflammatory Drugs Flashcards

1
Q

What is an inflammatory response?

A

A short term, acute response that is defensive and quickly resolved.

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

What does the inflammatory response involve?

A
  1. Acute microvascular changes
  2. Release of inflammatory mediators
  3. Accumulation of inflammatory cells
  4. Repair and healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the common inflammatory mediators in acute inflammation?

A

-Histamine
-Bradykinin
-Nitric oxide
-Eicosanoid
-Neuropeptides

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

What are the arterioles and venules involved in?

A

Arterioles = blood pressure changes

Venule = Oedema formation and cell accumulation

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

What happens in the acute inflammatory response?

A

Microvascular effects are triggered from a variety of cells and plasma in and around these vessels

Inflammatory mediators (also known as local hormones) released

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

Is histamine preformed?

A

Yes

Preformed = already stored in cells of the body (mast cells) ready to be released

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

What is histamine formed from and what is its major source?

A

Histamine formed from histidine

Major source: mast cells & basophils

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

When is histamine released?

A

Released in allergic/ hypersensitivity (IgE) responses.

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

What do H1 receptors mediate?

A

Increased blood flow,

increased microvascular permeability,

itch

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

What 2 categories do H1 antagonists fall into?

A

Sedating: chlorpheniramine, diphenhydramine, promethazine

Non-sedating ones preferred today: loratadine, cetirizine, terfenadine, astemizole

Sedating = causes drowsiness

Non-sedating = less drowsiness

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

Give some examples of conditions where anti-histamines are used.

A

Allergy,

allergic rhinitis,

urticaria,

hay fever

skin irritations

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

Which sensory nerves are the pain fibres?

A

C and Aδ fibres

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

What are the roles of the C and Aδ fibres?

A

They have a dual role:

They transmit sensory information to CNS/initiate reflexes nociception- pain and itch

They release neuropeptides - many including substance P, CGRP and VIP (alleviate migraine)

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

What does the stimulation of the sensory nerves include?

A

Mechanical (pressure)

Temperature (cold & heat)

Chemical (mediators & capsaicin)

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

What is the conducting velocity of this subset of sensory nerves?

A

0.5 m/s (so it’s slow as it’s half the speed of normal C fibres)

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

What distinct subset of sensory nerves mediate itch?

A

~5% of afferent C fibres in skin

They respond to histamine but are insensitive to mechanical stimuli

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

What are good anti-itch agents?

A

Anti-histamines are effective

Local anaesthetics can also be used to reduce pain/itch of course

18
Q

What is arachidonic acid?

A

the key to making proinflammatory cytokines & a 20 carbon polyunsaturated fatty acid

19
Q

How can arachidonic acid be metabolised?

A

Either via the cyclo-oxygenase pathway to prostaglandins & thromboxanes

OR

via the lipoxygenase pathway to leukotrienes

20
Q

What are eicosanoids?

A

The name given to the arachadonic acid metabolites i.e.

prostaglandins, thromboxanes, leukotrienes

21
Q

How are the different eicosanoids synthesised and what are their roles?

A

Prostaglandins = Synthesised by the cyclo-oxygenate enzymes

leukotrienes = synthesised by 5-lipoxygenase

22
Q

What does the cyclo-oxygenase pathway look like?

A
  1. Arachidonic acid = 4 double bonds, poly unsaturated fatty acid
  2. Oxygen is inserted to mediate the cyclic endoperoxides (PGG2 and PGH2)

3.Both unstable with the oxygen inserted, to break up the double bonds.

4.They are metabolised via the enzyme relevant to that tissue

23
Q

What inhibits arachidonic acid metabolism via cyclo-oxygenase?

A

NSAIDs (which leaves the lipoxygenase enzyme unhindered to carry on as normal)

24
Q

What are the characteristics of NSAIDs?

A

They inhibit prostaglandin generation & they’re analgesic (alleviate pain)

anti-inflammatory, reduce fever but can enhance bleeding

25
Q

What are some examples of NSAIDs?

A

Salicylates (Aspirin)

Acetic acides (Indomethacin, Diclofenac)

Proprionic acides (Ibuprofen, naproxen)

Oxicoms (Piroxicam, phenylbutazone)

Fenamates (Meclofenamate)

26
Q

Summarise what is used to reduce acute injury.

A
  • Histamine plays major role in inflammation and itch.

-Non-sedating anti-histamines are the drug of choice.

-NSAIDs that inhibit PG production = used for analgesic/anti-inflammatory/antipyretic properties

-Paracetamol = reduces pain + fever

-Ice, local anaesthetic creams and noradrenaline = important roles if routinely used

-NSAIDS used by dentists to reduce pain but can increase bleeding

27
Q

What are some mediators of arthritis?

A

Primary mediator: TNFα (Cytokine)

Other mediators: IL-1, IL-6, IL-8, IL-10, IL-17, PGE2

28
Q

What is the ‘therapeutic pyramid’ in rheumatoid arthritis (and a range of other inflammatory diseases)?

A

slide 17

29
Q

What 2 forms does cyclo-oxygenase (COX) exist in?

A

COX-1 & COX-2

30
Q

What are the differences between COX-1 & COX-2?

A

COX-1:

-Found in most cells
-Constitutive
-Involved in normal physiology, to maintain homeostasis
E.g. in GI tract, PGs important in maintaining good blood flow
E.g. in vasculature, TxA2 stimulates platelets to aggregate (thrombus) and PGI2 inhibits this

COX-2:

-Induced in inflammatory cells by inflammatory stimuli
-Releases high levels of prostaglandins at inflammatory sites

31
Q

From a clinical view, which one is important to inhibit, COX-1 or COX-2?

A

COX-2 as it releases high levels of prostaglandins at inflammatory sites, PG’s contribute to clinical signs of inflammation.

32
Q

What should patients with a cardiovascular risk taking COX inhibitors be taking/doing alongside taking it?

A

If taking oral NSAIDs:

Associated use of proton pump inhibitors, to inhibit GI reflux due to excess acid (e.g esomeprazole)

Alternatively use prostaglandin analogues (e.g. misoprostol)

Also, gradually increase NSAID use via topical application instead e.g. diclofenac

33
Q

What are DMARDs?

A

Disease modifying anti-rheumatic drugs

34
Q

What types of DMARDs are there?

A

Slow acting anti-rheumatic drugs/second line therapies (all have side effects):
-Methotrexate (1st choice)
-Gold Salts (sodium aurothiomalate & auranofin)
-Anti-malarials (chloroquine)
-Sulphasalasine (used, may prevent oxygen radical damage)
-Penicillamine (can work well decreases cytokines)

Following classed as immune suppressives
(Steroids)
Immunosuppressives (cyclosporine- toxic)

35
Q

What is rheumatoid arthritis?

A

an autoimmune disease.

The immune system mistakenly attacks the body’s own tissues, particularly the synovium (the lining of the membranes that surround joints),

leading to inflammation, pain, and joint damage.

36
Q

What are the pros of using anti-inflammatory steroids?

A

Several anti-inflammatory activities:
Hydrocortisone, dexamethasone, prednisolone

-Inhibit arachidonic acid release (AA)
-Cytokine inhibition
-Down regulation of adhesion molecules
-Inhibition of enzyme induction (COX, NOS)

Several effects on immune response:
-Inhibition of lymphocyte t-cell proliferation
-Induces apoptosis

37
Q

What are the cons (side effects) of using anti-inflammatory steroids?

A

Osteoporosis

Increased risk of infection

Adrenal atrophy

Diabetes

Infection

38
Q

What is the most common DMARD?

A

Methotrexate

39
Q

What is methotrexate and when is it used?

A

Folate antagonist & it’s the most widely used anti-metabolite in cancer chemotherapy (but may act via other mechanisms for anti-inflammatory effects)

It’s also the most widely used disease modifying agent for RA treatment– better if used early & is used in young & old

May be best mixed with NSAID

40
Q

Can methotrexate be toxic?

A

Yes, so you have to get blood tests to monitor it

41
Q

What are the traditional & modern treatments of RA (rheumatoid arthritis)?

A

Traditional:

-Treat symptoms (pain, swelling), thought to be less aggressive
-Less toxic (NSAIDs) used, unlike methotrexate/steroids

Modern:

-Limit joint destruction
-Early aggressive treatment
-Methotrexate used early (including elderly and young)
-Combination therapy
-increasing use of biologics & biosimilars

42
Q

What are examples of some biologics and when is it used?

A

High molecular weight = injected

  1. Anti-TNF antibodies
  2. Soluble TNF receptor construct

-Used when other DMARDs have failed

-Effective for 30% of cases ; can be less successful in follow up treatments

-Expensive

-Well tolerated compared to other anti-inflammatory drugs

-Patients may suffer from opportunistic infections

HUMAN HEALTH AND DISEASE (58 decks)

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