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HUMAN HEALTH AND DISEASE > Anti-Inflammatory Drugs > Flashcards

Anti-Inflammatory Drugs Flashcards

(42 cards)

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1
Q

What is an inflammatory response?

A

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

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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
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3
Q

What are the common inflammatory mediators in acute inflammation?

A

-Histamine
-Bradykinin
-Nitric oxide
-Eicosanoid
-Neuropeptides

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4
Q

What are the arterioles and venules involved in?

A

Arterioles = blood pressure changes

Venule = Oedema formation and cell accumulation

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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

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6
Q

Is histamine preformed?

A

Yes

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

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7
Q

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

A

Histamine formed from histidine

Major source: mast cells & basophils

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8
Q

When is histamine released?

A

Released in allergic/ hypersensitivity (IgE) responses.

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9
Q

What do H1 receptors mediate?

A

Increased blood flow,

increased microvascular permeability,

itch

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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

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11
Q

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

A

Allergy,

allergic rhinitis,

urticaria,

hay fever

skin irritations

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12
Q

Which sensory nerves are the pain fibres?

A

C and Aδ fibres

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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)

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14
Q

What does the stimulation of the sensory nerves include?

A

Mechanical (pressure)

Temperature (cold & heat)

Chemical (mediators & capsaicin)

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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)

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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

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17
Q

What are good anti-itch agents?

Study These Flashcards
A

Anti-histamines are effective

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

18
Q

What is arachidonic acid?

Study These Flashcards
A

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

19
Q

How can arachidonic acid be metabolised?

Study These Flashcards
A

Either via the cyclo-oxygenase pathway to prostaglandins & thromboxanes

OR

via the lipoxygenase pathway to leukotrienes

20
Q

What are eicosanoids?

Study These Flashcards
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?

Study These Flashcards
A

Prostaglandins = Synthesised by the cyclo-oxygenate enzymes

leukotrienes = synthesised by 5-lipoxygenase

22
Q

What does the cyclo-oxygenase pathway look like?

Study These Flashcards
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?

Study These Flashcards
A

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

24
Q

What are the characteristics of NSAIDs?

Study These Flashcards
A

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

anti-inflammatory, reduce fever but can enhance bleeding

25
What are some examples of NSAIDs?
Salicylates (Aspirin) Acetic acides (Indomethacin, Diclofenac) Proprionic acides (Ibuprofen, naproxen) Oxicoms (Piroxicam, phenylbutazone) Fenamates (Meclofenamate)
26
Summarise what is used to reduce acute injury.
- 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
What are some mediators of arthritis?
Primary mediator: TNFα (Cytokine) Other mediators: IL-1, IL-6, IL-8, IL-10, IL-17, PGE2
28
What is the 'therapeutic pyramid' in rheumatoid arthritis (and a range of other inflammatory diseases)?
slide 17
29
What 2 forms does cyclo-oxygenase (COX) exist in?
COX-1 & COX-2
30
What are the differences between COX-1 & COX-2?
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
From a clinical view, which one is important to inhibit, COX-1 or COX-2?
COX-2 as it releases high levels of prostaglandins at inflammatory sites, PG's contribute to clinical signs of inflammation.
32
What should patients with a cardiovascular risk taking COX inhibitors be taking/doing alongside taking it?
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
What are DMARDs?
Disease modifying anti-rheumatic drugs
34
What types of DMARDs are there?
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
What is rheumatoid arthritis?
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
What are the pros of using anti-inflammatory steroids?
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
What are the cons (side effects) of using anti-inflammatory steroids?
Osteoporosis Increased risk of infection Adrenal atrophy Diabetes Infection
38
What is the most common DMARD?
Methotrexate
39
What is methotrexate and when is it used?
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
Can methotrexate be toxic?
Yes, so you have to get blood tests to monitor it
41
What are the traditional & modern treatments of RA (rheumatoid arthritis)?
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
What are examples of some biologics and when is it used?
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)

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