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BDS2; CHHD > Anti-inflammatory and immunosuppressive drugs > Flashcards

Anti-inflammatory and immunosuppressive drugs Flashcards

1. Knowledge of common anti-inflammatory and immunosuppressive drugs and their indications 2. Knowledge of their mechanisms of action and common side effects 3. Knowledge of likely drug interactions when used with medications prescribed by dentist 4. Knowledge of pre and post treatment screening/monitoring investigations

1
Q

What are the different types of anti-inflammatory drugs and give examples of them

A
  1. Steroidal anti-inflammatory drugs e.g. Corticosteroids like Prednisolone
  2. NSAIDs e.g. Acetyl salicylic acid (Aspirin)
  3. Traditional/ non-selective NSAIDs e.g. Ibuprofen, Naproxen
  4. COX-2 inhibitors e.g. Celecoxib
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2
Q

How is the immune inflammatory response normally initiated

A

Phospholipids in the bilayer are broken down by phospholipase A2 enzyme to arachidonic acid which breaks down into 5-LOX and COX

  • COX-1 is always expressed (as it stimulates normal body functions) and binding causes thromboxane and prostaglandin release which causes vasoconstriction
  • COX-2 is induced at the inflammation site and causes prostaglandin release resulting in active inflammatory response
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3
Q

How do corticosteroids work

A

They inhibit phospholipase A2 which prevents the production of arachidonic acid and so the production of prostaglandins

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4
Q

How do NSAISs work

A

They inhibit COX 1/2

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5
Q

What does COX-1 and COX-2 collectively stimulate

A
  1. Endothelium (PGO2) causing vasodilation and decreasing platelet aggregation
  2. Kidney (TXA2) causing vasoconstriction and increasing platelet aggregation
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6
Q

What does COX-1 stimulate

A
  1. Platelets (TXA2) causing vasoconstriction and increasing platelet aggregation
  2. Gastric mucosa (PGE2 + PGI2) inhibiting gastric acid and protecting the mucosa
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7
Q

What does COX-2 stimulate

A
  1. Joints (PGE2 + PGI2) causing pain and inflammation
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8
Q

What is aspirin

A

An analgesic, anti-inflammatory and anti-thrombotic NSAID

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9
Q

Where is aspirin metabolised and excreted

A 
Metabolised = liver
Excreted = kidney
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10
Q

Which patients should avoid aspirin usage

A

Those with severe liver damage and those on dialysis

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11
Q

What negative effects does aspirin cause

A

It permanently affects platelet cohesiveness for their life span (10-14 days) and causes a prolonged bleeding time (primary haemostasis)

  • has no effect on platelet count, PT/INR and APPT
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12
Q

Give examples of traditional/non-selective NSAIDs and how they work

A

Ibuprofen, Naproxen, Diclofenac, Mefenamic acid, Indometacin = analgesics, anti-inflammatory and antipyretic actions

These inhibit COX-1 and COX-2

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13
Q

What are the side effects of traditional/non-selective NSAIDs

A
  1. Gastric irritability (increased risk of peptic ulcers which can bleed and cause haemorrhage)
  2. Platelet dysfunction (affecting cohesiveness)
  3. Acute renal failure (not with short term low dosage)
  4. Leukotriene overproduction causing bromchoconstriction (should be avoided in asthmatics)
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14
Q

Give examples of selective NSAIDs/COX-2 inhibitors

A

These are specific analgesic, anti-inflammatory and antipyretic drugs such as Celecoxib or Etoricoxib

These do not affect the gastric mucosa so decrease the risk of peptic ulcers

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15
Q

When should Selective NSAIDs/COX-2 inhibitors be avoided

A

They are metabolised in the liver and excreted through the kidneys so should be avoided in patients with problems here; High doses can cause acute renal failure

These drugs promote platelet aggregation and so should be avoided in patients with history of atherosclerosis as this increases risk of thrombotic events (MI/Stroke)

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16
Q

What are anti mitotic agents and give exmples

A

These are drugs inhibiting cell division

  1. Azathioprine = cytotoxic in early phase of lymphoid cell proliferation
  2. Cyclophosphamide = cytotoxic to lymphoid cells, B/T cells therefore inhibits establishment of immune response
  3. Chlorambucil
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17
Q

What are calcineurin inhibitors and give examples

A

These inhibit macrophage + T-cell iteractions and T-cell responsiveness

  1. Ciclosporin (Cyclosporine) = protein phosphatase III activating T-cells to stimulate an immune response
  2. Tacrolimus
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18
Q

What is Dapsone and how does it work

A

Anti-inflammatory and immunomodulatory drug

  • blocks granulocyte adherence
  • blocks release of prostaglandin E2
  • blocks release of lysosomal enzyme
19
Q

What is Mycophenolate mofetil and how does it work

A

Anti-inflammatory and immunomodulatory drug derived from Penicillium stoloniferum

Inhibits enzyme needed for purine synthesis in T-cells therefore impairs cytotoxic T cells, lymphocytes and the formation of antibodies from B cells

20
Q

What are biological response modifiers and give examples

A

These are more specific immunosuppressive and anti-inflammatory drugs which are less immunosuppressive and more expensive

  • Adalimumab
  • Infliximab
  • Etanercept
21
Q

How do corticosteroids reduce the inflammatory reaction

A

By limiting capillary dilatation and permeability of vascular structures through inhibiting the complement system

It restricts the accumulation of polymorphonuclear leukocytes and macrophages and reduces the release of vasoactive kinins (which locally induce SM contraction and vasodilation)

22
Q

When are corticosteroids prescribed

A
  1. Primary/Secondary adrenocortical insufficiency
  2. Psoriatic arthritis, Rheumatoid arthritis, Acute gouty arthritis, Ankylosing spondylitis, Bursitis
  3. Systemic lupus erythematousus (SLE), Pemphigus, Acute rheumatic fever
  4. Leukaemia’s, Lymphomas, Thrombocytopenia purpura, Autoimmune haemolytic anaemia
  5. Coeliac disease, Ulcerative colitis, Liver disorders
23
Q

What pre-treatment screenings are done for corticosteroid administration

A
  1. Blood pressure
  2. Body weight
  3. Height (esp. in children and adolescents)
  4. HBA1c, triglycerides and potassium
  5. Eye assessment (glaucoma and cataract)
24
Q

What are the side-effects of long-term oral corticosteroids (>3weeks)

Endocrine
GI
Psychiatric
Musculoskeletal
Ophthalmic
CVS
Skin 
Other
A
  1. Endocrine: adrenal insufficiency, weight gain, DM
  2. Gastrointestinal: peptic ulceration with proliferation + haemorrhage, dyspepsia, abdominal distension, oesophageal ulceration
  3. Psychiatric: confusion, irritability, delusions, suicidal thoughts
  4. Musculoskeletal: osteoporosis and proximal myopathy
  5. Ophthalmic: glaucoma, cataract, blurred vision
  6. Cardiovascular: hypertension
  7. Skin: thinning, easy bruising, delayed wound healing
  8. Immunosuppression, Cushing’s syndrome (reversible with treatment withdrawal), irreversible growth suppression

Corticosteroids may also mask the clinical signs of other serious systemic disorders/infections

25
Q

How can the side-effects of corticosteroids be minimised

A
  • Low dose for minimum time
  • Take med in morning on alternate days
  • Provide steroid treatment card
  • Prescribe proton pump inhibitor for GI protection for patients with high risk GI bleed (ameprozol/lansoprazol)
  • Withdrawal needs to be gradual as if done rapidly it will trigger adrenal insufficiency
26
Q

Outline the presenting signs of adrenal insufficiency

A
  1. Tiredness
  2. Poor appetite, weight loss, affected growth
  3. Abdominal pain
  4. Nausea, vomiting
  5. Joint pain
  6. Dizziness
  7. Fever
27
Q

What is Azathioprine and how does it work

A

It is am immunosuppressive and antimetabolite drug which is converted into 6-mercaptopurine in the body

It inhibits purine and DNA synthesis necessary for cell proliferation (esp.. leukocytes and lymphocytes)

28
Q

What is Azathioprine used for

A
  • Rheumatoid arthritis
  • Preventing renal transplant rejection
  • Crohn’s disease
  • Recurrent oral ulceration
  • Behcet’s disease
  • Colitis
29
Q

Why is pre-treatment screening before prescription of Azathioprine important

A

Because need to check serum levels of TPMT (thiopurine methyltransferase) as if it is high, there will be much of the inactive metabolite formed from azathioprine so it will not be as effective, meaning a higher dose is needed so that the active metabolite (6-TGN) can be incorporated into DNA causing immune suppression by decreasing WBC replication and increasing WBC apoptosis

30
Q

What are the side effects of Azathioprine

A
  • Myelosupression, hetapotoxicity, leucopenia, thrombocytopenia, infections, lymphoproliferative disorders, teratogenicity (birth defects)
31
Q

What are the clinical signs of toxicity to Azathioprine

A
  • rash
  • oral ulceration
  • abnormal bruising
  • severe sore throat
32
Q

What does low TMPT increase the risk of when taking Azathioprine

A

Myelosupression and other side effects so the dosage should be reduced

33
Q

How does cyclosporin (cilosporin) work

A

It is an immunosuppressant with specific action of T-lymphocytes which binds to immunophilins, inhibiting calcinurine (responsible for activating IL-2 transcription)

It inhibits lymphokine production and interleukin release and preferentially inhibits T-helper and littler T-cells

34
Q

Where is cyclosporin metabolised

A

Liver

35
Q

When is cyclosporin administrated

A
  • organ transplant
  • rheumatoid arthritis
  • severe psoriasis
36
Q

What are the side effects of ciclosporin

A

Hypertension, nephrotoxicity, neurotoxicity, gingival hypertrophy/hyperplasia, lymphoproliferative disorders, malignancies, teratogenicity

37
Q

Which common drugs used in dentistry interact with cyclosporin

A
  1. Antibiotics = Macrolides (Erythomycin and Clarithromycin) increase toxicity
  2. Antifungals = Fluconazole, Miconazole increases toxicity
  3. Analgesics = NSAIDs with cyclosporin promotes nephrotoxicity which leads to acute renal failure
38
Q

When is Mycophenolate mofetil used

A

It is a prophylaxis of organ rejection (immunosuppressive agent) used in combination with cyclosporin and prednisolone

It prevents the proliferation of T-cells, lymphocytes and formation of antibodies from B-cells by blocking biosynthesis of purine nucleotides by inhibiting inosine monophosphate dehydrogenase

39
Q

What are the side effects of Mycophenolate mofetil

A

Fever, chills, hyperglycaemia, hypertension, easy bruising/ bleeding, skin reactions, abdominal pain: nausea, vomiting, dyspepsia, diarrhoea, oesophagi’s, gastritis, GI bleed, increased infection risk due to low WBCs, leucopenia, thrombocytopenia, depression

40
Q

When are biological response modifiers used

A
  • Rheumatoid arthritis, Ankylosing spondylitis, Psoriasis
  • Crohn’s disease, Ulcerative colitis
  • Malignancies
  • Vesiculo-bullous disease
  • Lichen planus
  • Behcet’s disease
41
Q

Post treatment monitoring for corticosteroids

A
  1. Blood pressure
  2. Body weight
  3. Triglycerides and potassium
  4. HbA1c
  5. Osteoporosis risk and fall risk assessment
  6. Growth suppression
  7. Adrenal suppression
  8. Adverse effects
42
Q

Why might biological response modifiers be used

A

For diseases which haven’t responded to conventional therapy and for patients that are intolerant of or have contraindications to this

43
Q

How are biological response modifiers administered

A

Via injection or infusion and they are commonly TNF-alpha inhibitors (TNF-a usually mediates immunity and inflammation)

BDS2; CHHD (32 decks)

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