Brainscape's Knowledge GenomeTM

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


See full index

AAI: Pharmacology + Biology > Arthritis > Flashcards

Arthritis Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

Is Rheumatoid arthritis organ specific?

A

It’s Non-organ specific

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

What is osteoarthritis?

A

Caused by wear and tear of joints causing inflammation

Non-inflammatory disorder (use of synovial joints)

Characterised by cartilage loss

Affects knees, hips + small hand joints

Link to obesity

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

Describe the pain in osteoarthritis

A

Worsened by movement

Eased by rest

Worse at the end of the day

Commonly affects:

  • hands
  • knees
  • spine
  • hips

Unilateral (affect only one joint e.g. left hand only)

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

What are the treatment options for OA?

A

Steroid injections

NSAIDs / Cox-2 inhibitors

Surgery - knee replacement

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

Mechanism of NSAIDs

A

NSAIDs inhibit COX enzyme

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

NSAID use in Osteoarthritis treatment

A

In Arthritis, NSAIDs block cyclooxygenase enzymes (particularly COX-2) which reduces inflammation, pain + stiffness

COX enzymes convert arachidonic acid to prostaglandins

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

How + when do we take corticosteroids injections + what drugs are used

A

Intra-articular (into joints)

When pain is moderate to severe

Drugs:

  • triamcinolone
  • methylprednisolone

Can cause cartilage injury + loss

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

What is Rheumatoid Arthritis?

A

Autoimmune disease in which the body’s immune system attacks the joints causing chronic inflammation.

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

Signs of RA

A

Joint damage

Muscle wastage

Deformity

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

Symptoms of RA

A

Pain

Stiffness

Joint swelling

Joint deformity

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

Blood lab tests for RA

A

WBCs = INCREASED

Erythrocyte sedimentation rate (speed at which your red blood cells clump and fall together to the bottom of a glass tube within an hour) = INCREASED

Anaemia

Rheumatoid factor (group of proteins your body creates when your immune system attacks healthy tissue - Antibodies to IgG) = INCREASED

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

Risk factors of RA

A

Age

Gender - women developing premenopausal

Post-partum

Stress

Genetics - if one twin has, the other is 20% likely

Smoking

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

Describe the pain in Rhematoid Arthritis

A

Improves movement

Worse on waking

Affects small joints

Affects bilateral joints

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

What is Rheumatoid disease?

A

Systemic disease (affects many organs or body as a whole) that affects:

  • Especially at the joints
  • Eyes inflammed (50%)
  • Skin
  • Vasculitis - destroy group of blood vessels
  • Lungs
  • Salivary glands (reduced)
  • Pericarditis (inflammation of pericardium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the type of treatment options for RA?

A

Symptomatic relief

  • Analgesia to reduce need for NSAIDs
  • NSAIDs (+ PPI)

Slow progression

  • DMARDs
  • Steroids
  • Biologicals

Monitor effectiveness

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

Function of DMARDs

(Disease modifying anti-rheumatic drugs)

A

Directly inhibits cell proliferation

(inhibit wide variety of cytokines including interleukins, interferons + TNFalpha)

Slow-acting (may take months for benefits to become apparent)

No analgesic activity

Used for rheumatic disorders + where inflammation does not respond to COX enzyme inhibitors

Slows course of disease

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

Treatment lines of DMARDs

A

1st LINE - Start w/ combination therapy (MTX + 1 other DMARD)

2nd LINE - Mono therapy w/ rapid dose titration

Slow onset of action - take up to 3 months

Used with glucocorticoids until effective (shouldn’t be used long term)

18
Q

Counselling points when using DMARDS

A

Dose increased gradually

Improvement takes a few months

Monitoring is necessary

Nausea

Signs of:

  • Blood dyscrasias (formed elements in blood) = sore throat, tiredness
  • liver toxicity = jaundice
  • lung toxicity

Bone toxicity

Perform LFTS, FBC + U+E before + during treatment

19
Q

What are the drugs in DMARDs?

A

Methotrexate = 1st choice

Sulfasalazine

Leflunomide

IM gold

20
Q

Function of Methotrexate

A

Dihydrofolate reductase inhibitor

(pyrimidine synthesis = inhibits DNA/RNA synthesis)

Immunosuppressant

Commonly used

Dose - 7.5-25 micrograms

Weekly dosing

21
Q

What causes autoimmune diseases

A

Autoimmune diseases is when your immune system attacks its own cells

Leads to tissue damage

Genetic factors can influence it

Can be influenced by pregnancy, infection, diet + environment

22
Q

When do you start on DMARDs?

A

Within 3 months

23
Q

When do we reduce dose of DMARDs?

A

Reduce to a dose when symptom control has been achieved

24
Q

What do patients need to take with Methotrexate

A

Folic acid

To prevent side effects

Folic acid does not prevent inflammatory effects of methotrexate

25
Q

Name other mechanisms of methotrexate in rheumatoid arthritis

A

Folic acid antagonism

Cytokine alteration

Adenosine signalling

Generation of reactive oxygen species

Effects of eiocosanoids + matrix metalloproteases

Effects of methyl donors

26
Q

Counselling points of MTX

A

WEEKLY DOSE

Take folic acid as directed = ONCE WEEKLY but not on the same day as MTX

Regular blood tests

Recognise + report signs of serious side effects

Contraception = avoid pregnancy due to birth defects

Patients given patient information book about MTX

Injectable methotrexate - cytotoxic, sharps bin, disposal etc

27
Q

ADME of Methotrexate

A

Absorption unaffected w/ age

Decreased metabolism + excretion w/ age

Increased risk of toxic effects

NSAIDs interaction - avoid OTC - renal toxicity - reduced excretion of MTX

28
Q

What is Sulfasalazine (SFZ)?

A

Immunosuppressant

500mg OD

Increased weekly - max. 2-3 grams per day in divided doses

Onset of action is 6 weeks

29
Q

What are the side effects of Sulfasalazine?

A

GI intolerance - nausea + vomiting

Blood disorders - bruising + unexplained bleeding

Discolouration of urine + contact lenses (happen in the first 3-6 months)

30
Q

Function of Leflunomide

A

Immunosuppressant

Metabolised to teriflunomide

Inhibits dihydroorotate dehydrogenase (involved in pyrimidine synthesis, inhibiting DNA synthesis)

31
Q

What are the adverse effects of Leflunomide?

A

Diarrhoea

Nausea, rash, alopecia

Abnormal LFT

Teratogen

  • contraception including male treatment
  • additional 2 years post stopping treatment
  • present in breast milk
32
Q

Function of Hydroxychloroquine

A

Used in mild/moderate cases

Alternative 1st line drug

Inhibit lymphocyte function

Long half life

33
Q

Function of Gold

A

Immunosuppressant

e. g. sodium aurothiomalate (deep intramuscular)
e. g. auranofin (oral)

2nd/3rd line treatment

Weekly until response

Rashes, blood disorders

34
Q

Other types of DMARDs

A

Pencillamine - penicillin metabolite

Cyclosporine - T-cell function (severe RA)

Azathioprine - inhibit purine synthesis

Only relieve symptoms - do not modify disease progression so less used

35
Q

Describe the use of Steroids in RA

A

Used orally for flare/exacerbations of RA

Bridging therapy = between starting/switching to reduce symptoms (rapid symptom control)

IM, IA, IV (IV can be toxic)

36
Q

What are the oral steroids used in RA?

A

Prednisolone

Can’t be used long term

Side effects:

  • osteoporosis = bone protection
  • PPI`(for long-term therapy)
37
Q

Anti-TNFalpha therapy in RA

A

Block TNFα which reduce inflammation and joint damage

Licensed for moderate-severe RA where response to other DMARDs is inadequate

Alone/w/MTX

MONOCLONAL ANTIBODIES

Adalimumab - 40mg SC alternate weeks

Infliximab - 3/mg/kg IV @2,6 then 8 weeks

Etanercepts - 25mg SC TWICE WEEKLY

38
Q

Name a interleukin-1 inhibitor used for RA

A

Anakinra = IL-1RI antagonist

IL-1 = pro-inflammatory cytokine which mediates many cellular responses including synovial inflammation (joints)

Injection site reactions

NICE rejected due to weak efficacy

39
Q

Name a new drug for use in RA

A

Tofacitinib

Janus Kinase inhibitor

Janus kinase involved in cytokine signalling + gene transcription

NICE accepts if price reduces

40
Q

What is Abatacept?

A

Drug used to treat autoimmune diseases e.g. rheumatoid arthritis

This is by blocking B7 binding to CD28

NICE not recommended due to cost

AAI: Pharmacology + Biology (11 decks)

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