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BDS2 PMI > PMI03-2014 > Flashcards

PMI03-2014 Flashcards

1
Q

Describe an acute inflammatory response.

A

Microvascular effects triggered by a variety of cell and plasma in and around these vessels, including local hormones and inflammatory mediators

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2
Q

Give examples of some inflammatory mediators.

A

Histamine

Bradykinin

Nitric oxide

Eicosanoids (prostaglandins, leukotrienes, thromboxanes)

Neuropeptides (substance P, CGRP)

Cytokines

Complement

VEGF

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3
Q

What type of molecule is histamine and what is it derived from?

A

Amine

From histidine

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4
Q

What type of molecule is bradykinin?

A

Peptide

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5
Q

What type of molecule are eicosanoids and what are they derived from?

A

Lipids

From arachidonic acid

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6
Q

What are the major sources of histamine in the body?

A

Mast cells and basophils

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7
Q

When is histamine typically released?

A

Allergic/type I hypersensitivity reactions

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8
Q

What do histamine/H1 receptors mediate?

A

Increased blood flow

Increased microvascular permeability

Itch

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9
Q

Give an example of a sedating H1 antagonist.

A

Chlorpheniramine

Diphenhydramine

Promethazine

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10
Q

Give an example of a non-sedating H1 antagonist.

A

Loratadine

Cetirizine

Terfenadine

Astemizole

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11
Q

Are H1 antagonists preferred to be sedating or non-sedating nowadays?

A

Non-sedating

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12
Q

What are the main pain neurons?

A

C and Aδ fibres

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13
Q

What do the pain neurons do?

A

Transmit sensory info to CNS/initiate reflexes = pain/itch

Release neuropeptides, including substance P and CGRP

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14
Q

What percentage of afferent C fibres in skin mediate itch?

A

5%

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15
Q

Describe the C fibres that mediate itch.

A

Respond to histamine and are unresponsive to mechanical stimuli

Slow conducting velocities of 0.5m/s (half that of normal C fibres)

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16
Q

What type of medication is an effective anti-itch agent?

A

Anti-histamine

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17
Q

What enzyme catalyses the formation of prostaglandins?

A

COX (cyclooxygenase)

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18
Q

What are the two types of COX and when are they present?

A

COX-1 = prevalent all the time

COX-2 = inducible and found at inflammatory sites

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19
Q

What is the chemical name of arachidonic acid?

A

5, 8, 11, 14-eicosatetraenoic acid

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20
Q

Which enzyme catalyses the formation of leukotrienes?

A

5-lipoxygenase

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21
Q

What does COX do?

A

Converts arachidonic acid to prostaglandins

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22
Q

What does 5-lipoxygenase do?

A

Converts arachidonic acid to leukotrienes

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23
Q

What cells release PGE2 and PGI2 and what do these molecules do?

A

Released by endothelial cells and white blood cells

Mediate increased blood flow and hyperalgesia (increased sensitivity to pain)

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24
Q

What cells release PGD2?

A

Mast cells

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25
Q

What common condition are leukotriene (LT) antagonists used for?

A

Asthma

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26
Q

What do LTC4 and LTD4 do?

A

Increase microvascular permeability

Bronchoconstriction

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27
Q

What does LTB4 do?

A

Chemotaxin = recruits neutrophils to inflammatory sites

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28
Q

What is the pathway of prostaglandin formation?

A 
Arachidonic acid
|
PGG2
|
PGH2
|
PGI2 or PGE2 or PGD2 or PGF2α (or TXA2)

Mediated by COX (mainly)

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29
Q

Give an example of a cyclic endoperoxide.

A

PGG2

PGH2

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30
Q

What is an alternative name for COX?

A

Prostaglandin-endoperoxide synthase

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31
Q

What is another name for PGI2?

A

Prostacyclin

32
Q

Where is PGF2α found?

A

Lungs and reproductive tissues

33
Q

What enzyme do NSAIDs inhibit?

A

Cyclooxygenase

34
Q

What are the effects of NSAIDs?

A

Analgesic (pain-relieving)

Anti-inflammatory

Fever-reducing

May enhance bleeding and stop normal vasodilatation and mucus secretion

35
Q

Why may NSAIDs enhance bleeding?

A

Inhibit COX

No TXA2 formed by activated platelets which is essential in haemostasis

36
Q

Give some of the types of NSAIDs.

A

Salicylates (aspirin)

Acetic acids (indomethacin, diclofenac)

Propionic acids (ibuprofen, naproxen)

Oxicoms (piroxicam, phenylbutazone)

Fenamates (meclofenamate)

37
Q

What type of NSAID is aspirin?

A

Salicylate

38
Q

What type of NSAID is ibuprofen?

A

Propionic acid

39
Q

What is the difference with paracetamol and typical NSAIDs effect-wise?

A

Paracetamol is not anti-inflammatory

40
Q

What is another name for paracetamol?

A

Acetaminophen

41
Q

Why do we use ice to treat some injuries?

A

Suppresses vasoactive components to reduce swelling

42
Q

Why do we use noradrenaline to treat some injuries?

A

Reduces blood flow (=> inflammation)

43
Q

What is the approximate ratio of men to women suffering from rheumatoid arthritis?

A

1:3

44
Q

Give some of the inflammatory mediators and their functions in joints in arthritis.

A

TNF-α (primary mediator)

IL-1 = TNF-α and IL-1 upregulate each other’s activity

IL-6, IL-8, IL-17 = pro-inflammatory

IL-10 = anti-inflammatory

PGE2 = hyperalgesic

45
Q

Where do most of the inflammatory mediators in the joints in arthritis come from?

A

Synovial membrane

46
Q

What does DMARD stand for?

A

Disease-modifying anti-inflammatory/rheumatic drug

47
Q

Describe the function of COX-1.

A

Found in most cells

Involved in normal physiology:

  • GI tract = PGs important in maintaining good blood flow and enabling mucus production
  • vasculature = TXA2 stimulates thrombus formation, PGI2 inhibits this
48
Q

Describe the function of COX-2.

A

Induced in inflammatory cells by inflammatory stimuli

Allows release of high levels of PGs at inflammatory sites

49
Q

Which form of COX do we want to inhibit clinically?

A

COX-2

50
Q

What does celecoxib do?

A

Inhibits COX-2

51
Q

What is the use of oral NSAIDs often associated with?

A

Proton pump inhibitors to inhibit GI reflux due to excess acid - NSAIDs inhibit PG formation so inhibit formation of mucus and substances that neutralise stomach acid

(may choose to use PG analogues, like misoprostol, alongside to protect stomach and maintain bloodflow in CV risk patients)

52
Q

When are DMARDs and biologics prescribed?

A

When there is definite disease, and NSAIDs and painkillers are insufficient

53
Q

What is the usual first choice DMARD?

A

Methotrexate

54
Q

Which DMARD is used for SLE and rare diseases?

A

Azathioprine

55
Q

Which DMARD has cardiac side effects?

A

Anti-malarials (chloroquine)

56
Q

Give examples/types of DMARDs.

A

Methotrexate

Azathioprine

Anti-malarials (chloroquine)

Sulphasalasine

Penicillamine

Anti-inflammatory steroids

Immunosuppressives

57
Q

What are biologics?

A

Larger MW DMARDs (antibody therapy)

Injected

58
Q

What are “targeted” DMARDs?

A

Oral

Target specific molecules (eg JAK inhibitor)

59
Q

Give an example of an anti-inflammatory steroid.

A

Hydrocortisone

Dexamethasone

Prednisolone

60
Q

What are the pros of using anti-inflammatory steroids?

A

Anti-inflammatory:

  • inhibit arachidonic acid release
  • inhibit cytokines
  • downregulation of adhesion molecules
  • inhibition of enzyme (COX, NOS) induction

Inhibition of T cell proliferation

(Induces apoptosis)

61
Q

What are the possible cons of using anti-inflammatory steroids?

A

Osteoporosis

Increased risk of infection

Adrenal atrophy

Diabetes

62
Q

How can you decrease the possible cons of anti-inflammatory steroids?

A

Give anti-inflammatory steroid locally:

  • intra-articular
  • aerosol
  • topically
63
Q

What does “steroid sparing” mean?

A

Can take less steroid to give the same effect which reduces side effects

64
Q

Describe the use of methotrexate.

A

Folate antagonist

Most widely used anti-metabolite in cancer chemotherapy but may act via other mechanisms for anti-inflammatory effects which may allow lower doses

Better if used early, used in the young and elderly

Can be toxic so monitored with blood tests

May be best when used with an NSAID (co-therapy)

65
Q

What happens when TNF-α binds its receptor?

A

Inflammation and tissue damage

66
Q

How may biologics be used to target TNF-α activity?

A

Anti-TNF antibodies (monoclonal, synthesised) or soluble TNF receptor constructs can be used if DMARDs fail

Can be given as co-treatments, well-tolerated (compared to other anti-inflammatory drugs

67
Q

What are the cons with using biologics to target TNF-α?

A

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

Expensive

Patient may suffer from opportunistic infection (eg TB)

68
Q

Give an example of anti-TNF biologic treatment.

A

Anti-TNF antibodies = infliximab (remicade), adalimumab (humira)

TNF receptor constructs = etanercept (enbrel)

69
Q

What may IL-17 receptor antagonists be used for in the future?

A

Psoriatic arthritis

70
Q

What may IL-6 blockers be used for in the future?

A

Non-responders to anti-TNF or biologics

Effective in treating cytokine storms

71
Q

What is Tocilizuma/RoActemra examples of?

A

IL-6 blockers (biologic)

72
Q

What is canakinumab?

A

Anti-IL-1 antibody

Treatment for juvenile arthritis and atherosclerosis

73
Q

What is rituximab/MabThera?

A

New drug that removes antibody-producing white blood cells

74
Q

What does abatacept/Orencia do?

A

Inhibits action of T cells

75
Q

What are biosimilars?

A

Biologic medical product that is almost an identical copy of another original product that may be manufactured by a different company

Cheaper as patent runs out

76
Q

Describe what the traditional methods of treating rheumatoid arthritis are like.

A

Treating symptoms of pain and swelling

Less aggressive and less toxin (usually NSAIDs)

77
Q

Describe the modern methods of treating rheumatoid arthritis.

A

Limiting join destruction with early aggressive treatment (eg methotrexate)

Combination therapy

Use of biologics

BDS2 PMI (21 decks)

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