LOCO2 Drugs Flashcards
Which drug can be used to determine how mineralised bone is? [1]
Tetracycline can be used to see how mineralised bone is. Tetracycline gets taken up on the calcium ions, and becomes deposited here and auto-fluoresces
A 36-year-old woman presents to her GP with pain in both hands. It is worse in the morning and occurs for more than 30 minutes.
A diagnosis of rheumatoid arthritis is suspected and blood tests are organised before the patient is referred to secondary care for a rheumatology opinion. The rheumatologist confirms the diagnosis and prescribes a first-line disease-modifying anti-rheumatic drug: methotrexate.
What medication should be co-prescribed for this patient?
Fluorouracil
Folic acid
Furosemide
Nicotinic acid
Vitamin B12
Folic acid
A 76-year-old woman presents to her physician with non-healing mucosal ulcers and loose teeth. She has a past medical history of recurrent falls, bilateral hip replacement, diabetes and asthma.
Examination findings show periodontal disease.
Radiology reports show sclerotic lesions in the mandible and maxilla consistent with osteonecrosis.
Which one of the following drugs may be the cause of her presentation?
Insulin
Denosumab
Vitamin D supplements
Calcium supplements
Alendronate
Alendronate
Bisphosphonates can cause osteonecrosis of the jaw
You are a junior doctor working in orthopaedic surgery and have been asked to see a 44-year-old woman who is booked in for surgery tomorrow for repair of an open radial fracture sustained after falling from her bike. She has a past medical history of severe psoriasis, gastro-oesophageal reflux disease, polycystic ovary syndrome and depression. You order some routine bloods prior to surgery, and are surprised by the following results:
Bilirubin 17 µmol/L (3 - 17)
ALP 89 u/L (30 - 100)
ALT 354 u/L (3 - 40)
γGT 61 u/L (8 - 60)
Albumin 34 g/L (35 - 50)
Which of her medications is most likely to be responsible for this derangement?
Combined oral contraceptive pill
Fluoxetine
Methotrexate
Morphine
Omeprazole
Methotrexate: cause hepatotoxicity
A 77-year-old woman is reviewed on the orthogeriatrics ward round 5 days following a hemiarthroplasty for a fractured neck of femur. The consultant decides to start her on a RANK ligand inhibitor for secondary prevention of osteoporosis.
Which of the following medications will you commence?
Alendronic acid
Denosumab
Letrozole
Raloxifene
Teriparatide
Denosumab
A 42-year-old woman complains to her General Practitioner of general fatigue during the last two months. She says the joints in both her hands and wrists are increasingly painful and stiff, especially in the morning and she finds it difficult to write. Her X-ray is diagnostic of rheumatoid arthritis and she is started on methotrexate and sulfasalazine. Which enzyme does methotrexate inhibit?
Dihydroorotate dehydrogenase
Cyclooxygenase 2
Dihydrofolate reductase
Matrix metalloproteinase 1
Serine hydroxymethyltransferase
Dihydrofolate reductase
A 27-year-old woman is referred to a rheumatology clinic as she has developed pain and stiffness in the small joints of her hands. She is diagnosed with rheumatoid arthritis and is started on methotrexate.
Given her diagnosis and management, the risk of which side effect is reduced by giving a folate supplement?
Infection
Hepatitis
Myelosuppression
Pneumonitis
Teratogenesis
Myelosuppression
A 65-year-old retired firefighter presents to the general practice surgery with recurrent burning central chest pain. He finds the pain is worse after eating a take-away and drinking alcohol and he feels that he is belching more than usual.
Past medical history is significant for high cholesterol, type two diabetes and osteoarthritis. His medications are atorvastatin, metformin, gliclazide, naproxen and omeprazole which he often forgets to take.
Which of his medication is the most likely cause of his symptoms?
Atorvastatin
Gliclazide
Metformin
Naproxen
Omeprazole
Naproxen: Peptic ulcers are a side effect of NSAIDs
A 59-year-old female presents to the rheumatology clinic, she has a diagnosis of rheumatoid arthritis and has been started on a new medication to help prevent disease progression and joint destruction. However, with this she needs to take daily folic acid and have frequent blood tests. Which medication is she likely to be on?
Sulfasalazine
Prednisolone
Methotrexate
Rituximab
Etanercept
Methotrexate
A 46-year-old female with poorly controlled rheumatoid arthritis and a history of significant large bowel resection. She has just had sulfasalazine, a prodrug, added to her medications, however the consultant is worried that she will be unable to convert the prodrug into its active form with her shortened colon.
Which therapeutically active compound is her medication converted to in the colon?
TNF-alpha
6-mercaptopurine
Methotrexate
Sulfamethoxazole
5-ASA (5-aminosalicylates)
5-ASA (5-aminosalicylates)
A 74-year-old woman attends her GP following a diagnosis of osteoporosis after sustaining a radial fracture during a fall. The doctor explains that they would like to prescribe alendronic acid, a bisphosphonate, to help prevent further fractures.
What is the mechanism of action of this drug?
Increased cholecalciferol synthesis
Increased serum calcium levels
Osteoblast inhibition
Osteoclast inhibition
Osteoclast stimulation
Osteoclast inhibition
A 48-year-old male discusses his secondary prophylaxis medications after suffering from a myocardial infarction last week. Aspirin is included in the several drugs but he is hesitant due to suffering from multiple bouts of acid reflux despite gastric protection. Celecoxib another COX (cyclooxygenase) inhibitor is prescribed instead.
What best describes the mechanism of action of this drug?
Reversible COX-1 inhibitor
Reversible COX-2 inhibitor
Non-reversible COX-1 inhibitor
Non-reversible COX-2 inhibitor
Non-reversible COX-1 and 2 inhibitor
Reversible COX-2 inhibitor
A 63-year-old woman has been referred by her GP to the osteoporosis clinic for alternate bone-sparing treatment. She has recently had a bone density scan following a low impact distal radial fracture. Her T-score in her hip and spine has returned as -2.6 and -2.2 respectively. She was subsequently commenced on bone-sparing treatments but she developed significant gastrointestinal side effects despite the trial of different preparations of bisphosphate including alendronate and risedronate. A decision has been made at the clinic to commence patient on a receptor activator of nuclear factor kappa-Β ligand (RANKL) inhibitor.
Which of the following is this treatment referring to?
Denosumab
Strontium ranelate
Teriparatide
Zoledronic acid
Raloxifene
Denosumab
An 81-year-old woman is admitted following a fall. Upon subsequent examination and imaging, she is diagnosed with a wrist fracture. This is deemed to be a fragility fracture given the low impact mechanism of injury.
Two weeks later, she is discharged on a new medication to increase bone density as per the National Institute for Health and Care Excellence (NICE) guidance.
What is the mechanism of the drug she has been prescribed?
Increases calcium availability to bone
Inhibits osteoblasts
Inhibits osteoclasts
Promotes osteoblasts
Promotes osteoclasts
Inhibits osteoclasts
A 68-year-old woman with breast cancer is started on a chemotherapy regimen including methotrexate.
Which enzyme is inhibited by this drug?
Thymidylate synthase
Methionine synthase
Dihydrofolate reductase
Methylenetetrahydrofolate reductase
Folylpolyglutamate synthase
Dihydrofolate reductase
RA
Methotrexate and Rituximab would be
First line treatment
Second line treatment
Third line treatment
Fourth line treatment
Third line treatment
RA
Methotrexate and a 2nd line DMARD would be
First line treatment
Second line treatment
Third line treatment
Fourth line treatment
First line treatment
RA
Methotrexate & a TNF-inhibitor would be
First line treatment
Second line treatment
Third line treatment
Fourth line treatment
Second line treatment
Methotrexate inhibits which enzyme? [1]
dihydrofolate reductase
RA
Sulfasalazine is a prodrug for [1]
5-ASA
Hydroxychloroquine blocks:
TLR7
TLR8
TLR9
TLR10
TLR11
TLR9
RA
Leflunomide inhibits which enzyme? [1]
What is the effect of this? [2]
Dihydroorotate dehydrogenase (DHODH): stops pyrimidine synthesis & therefore reduces pro-inflammatory cytokines: IL-1, TNF-A and IL-6; Blocks T cell proliferation
Which is the staple treatment for RA?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which is the staple treatment for RA?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA inhibits dihydrofolate reductase?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA inhibits dihydrofolate reductase?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA reduces purine synthesis?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Methotrexate
Which treatment for RA reduces pyrimidine synthesis?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Leflunomide
Which treatment for RA is safe for pregnant people?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Sulfasalazine
Which treatment for RA is prodrug that operates in large intestine?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA is prodrug that operates in large intestine?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA that targets TLR-9?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Hydroxychloroquine
Which treatment for RA that reduces dendritic cell activation?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Hydroxychloroquine
Which is a treatment for RA that inhibits dihydro-orotate dehydrogenase?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Hydroxychloroquine
Which treatment for RA requires folate to be given alongside?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Methotrexate
Which treatment for RA is a tumor necrosis factor-alpha (TNF-alpha) inhibitor?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Infliximab
Which treatment for RA is a monoclonal antibody?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Infliximab
Which treatment for RA is an anti-CD20 monoclonal antibody?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Rituximab
Which treatment for RA causes B cell depletion?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Rituximab
Which treatment for RA leads to decreased T-cell proliferation and cytokine production?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Abatacept
Which treatment for RA is an IL-1 antagonist?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Anakinra
Which treatment for RA targets IL-6?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Tolizumab
Which treatment for RA targets upregulates CTLA-4, which switches T cell off?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Tolizumab
OA - fill in about colexcicb
State the treatment pyramid for RA:
Pain management: [2]
First line disease treament (Mild RA): [2]
Second line disease treatment (moderate RA) [2]
Second line disease management: (severe RA) [2]
Pain management: NSAID & Opioids
First line: Methotrexate & 2nd line DMARD
Second line disease treatment (moderate RA) Methotrexate & TNF-inhibitor
Second line disease management: (severe RA) Methotrexate & Rituximab
If have a flair of RA which drug might be used as adjunct therapy? [1]
Oral corticosteroid pulse (e.g. prednisilone)
How may you start DMARD treatment if have severe RA? [2]
Start with high dose and taper down once under control
OR
Add prednisilone
State 3 reasons why may not prescribe methotrexate [3]
Liver damage (methotrexate metabolised in liver)
Pregnant
Co-morbidities
State two factors that DMARDs improve [2]
What does DMARD not improve? [1]
Improves:
* early improves number of swollen
* improves radiographic progression
No effect:
* the patients fatigue severity
Explain MoA of methotrexate [4]
How is it administered? [1]
Oral dose (can change to subcut. or IM)
MoA:
* Folic acid antagonist which will limits DNA and RNA synthesis by inhibiting dihydrofolate reductase and thymidylate synthetase
* Causes a reduction in purine synthesis
* Induce ROS
* Causes activation of apoptosis
* Inhibits pro-inflam cytokines IL-1 & NF-kB
State three side effects of methotrexate [2]
Can cause liver problems
Can affect blood count
Hair
Describe MoA of Sulfasalazine [5]
Mode of action in RA not well understood:
* Metabolised in the colon by gut bacteria to 5-ASA
* 5-ASA stays in large intestine lamina propria and has local anti-inflammatory actions
* Supresses generation of superoxide radicals and cytokine production by inflammatory cells
* IL8 decreased in synovial fluid and decreased production of IgM and IgG, and decreased angiogenesis
* Inhibits IL-1 and TNF-a
Describe the MoA of Hydroxychloroquine [2]
- Accumulates in lysosomes increasing the pH decreasing protein modifications
- Blocks Toll-like receptor 9 which recognises DNA containing immune complexes decreases activation of dendritic cells: less autoantobodies produced
Describe MoA of Leflunomide [3]
Pro-drug: gets metabolised in liver
Inhibits dihydroorotate dehydrogenase (DHODH) and therefore stops pyrimidine biosynthesis
Reduces pro-inflammatory cytokines: IL-1, TNF-A and IL-6
Blocks T cell proliferation
Name two TNF-a blockers for RA [2]
Etanercept
Infliximab
Explain MoA of Etanercept:
What is etanercept a fusion protein for? [1]
What is etanercept Fc for? [1]
When TNF-a is released: finds receptors on cells, activates and causes signal transduction
Etanercept is a fusion protein human TNF receptor 2 and Fc human IgG.
Etanercept binds to TNF-a before TNF-a can get to cell and cause inflammatory, signalling
Describe MoA of Infliximab [1]
Monoclonal antibody against TNFα
Infliximab often prescribed alongside which drug? [1]
Infliximab and methotrexate
Name another TNF-inhibitor used in RA [1]
Adalimumab
Name a Human recombinant IL-1 receptor antagonist to treat RA
Anakinra
Despite good efficacy, why is Anakina not as commonly prescribed for RA? [1]
Requires subcut daily injections
Describe MoA of Anakinra [1]
Monoclonal antibody that is a IL-1 antagonist
Describe MoA of Rituximab
Monoclonal antibody that targets CD20 on B cells
Means B cell can’t become activated
Destroys normal and malignant B cells
AEs of Rituximab?
Risk of infection as B cells destroyed
How long does Rituximab take before positive effect? [1]
3 months after infusions
Describe MoA of Abatacept
Blocks T cell activation which thus means macrophages and B cells cannot be activated.
Competes with CD28 binding to CD80/86 by upregulating CTLA-4, which switches T cell off
Reduces production of TH17 cells
Thus reducing inflammation
Tocilizumab targets which IL? [1]
Describe MoA [2]
Interleukin 6
Monoclonal antibody that binds to IL-6 cytokine before it reaches target receptor
What drug class is the first oral biological? [1]
JAK inhibitors
State three JAK inhibitors used to treat RA [3]
Tofacitinib, baricitinib and upadacitinib
Describe the MoA of JAK inhibitors
Targets Janus kinase (JAK) pathways: means that multipe cytokines are blocked
Describe the MoA of JAK inhibitors
Targets Janus kinase (JAK) pathways: means that multipe cytokines are blocked
Explain the mechanism of neutralising ADAs [2] & non-neutralising ADAs [2]
Because they are chimeric / humanised antigens you get anti-drug antibodies:
Neutralising ADA
* Directly interferes with the biological drugs ability to work
* Bind to the antibody/biological directly and stop it being able to bind to TNF-alpha, IL-1, etc
Non-neutralising ADA
* May form immune complexes around injection site reducing drug concentration and pharmacokinetics
Increased clearance
leflunomide has a similar mechanism of action to
Etanercept
Infliximab
Methotrexate
Sulfasalazine
Hydroxychloroquine
Methotrexate
Both block block on RNA and DNA synthesis via different, synergestic pathways
State which of the following blocks pyrimidine or purine synthesis:
Methotrexate
Leflunomide
Methotrexate: stops purine synthesis
Leflunomide: stops pyrimidine synthesis
Which of the following acts quicker:
Infliximab
Etanercept
Infliximab
Etanercept
Describe efficacy of IL-1 antagonists c.f TNF-alpha blockers
IL-1 receptors antagonists are not as effective in RA as TNF-alpha blockers
State why biologicals, despire their efficacy are not used straight away for RA treatment? [2]
Due to the develop of anti-drug antibodies that will develop no matter what - decrease efficacy
RA
Methotrexate and Rituximab would be
First line treatment
Second line treatment
Third line treatment
Fourth line treatment
Third line treatment
RA
Methotrexate and a 2nd line DMARD would be
First line treatment
Second line treatment
Third line treatment
Fourth line treatment
First line treatment
RA
Methotrexate & a TNF-inhibitor would be
First line treatment
Second line treatment
Third line treatment
Fourth line treatment
Second line treatment
Methotrexate inhibits which enzyme? [1]
dihydrofolate reductase
RA
Sulfasalazine is a prodrug for [1]
5-ASA
Hydroxychloroquine blocks:
TLR7
TLR8
TLR9
TLR10
TLR11
TLR9
RA
Leflunomide inhibits which enzyme? [1]
What is the effect of this? [2]
Dihydroorotate dehydrogenase (DHODH): stops pyrimidine synthesis & therefore reduces pro-inflammatory cytokines: IL-1, TNF-A and IL-6; Blocks T cell proliferation
Which is the staple treatment for RA?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which is the staple treatment for RA?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA inhibits dihydrofolate reductase?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA inhibits dihydrofolate reductase?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA reduces purine synthesis?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Methotrexate
Which treatment for RA reduces pyrimidine synthesis?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Leflunomide
Which treatment for RA is safe for pregnant people?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Sulfasalazine
Which treatment for RA is prodrug that operates in large intestine?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA is prodrug that operates in large intestine?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Which treatment for RA that targets TLR-9?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Hydroxychloroquine
Which treatment for RA that reduces dendritic cell activation?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Hydroxychloroquine
Which is a treatment for RA that inhibits dihydro-orotate dehydrogenase?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Hydroxychloroquine
Which treatment for RA requires folate to be given alongside?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Methotrexate
Which treatment for RA is a tumor necrosis factor-alpha (TNF-alpha) inhibitor?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Infliximab
Which treatment for RA is a monoclonal antibody?
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab
Infliximab
Which treatment for RA is an anti-CD20 monoclonal antibody?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Rituximab
Which treatment for RA causes B cell depletion?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Rituximab
Which treatment for RA leads to decreased T-cell proliferation and cytokine production?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Abatacept
Which treatment for RA is an IL-1 antagonist?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Anakinra
Which treatment for RA targets IL-6?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Tolizumab
Which treatment for RA targets upregulates CTLA-4, which switches T cell off?
Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab
Tolizumab
State a non-pharmological adjunct for OA pain relief [1]
Transcutaneous electrical nerve stimulation (TENS)
State 6 surgical interventions for OA [6]
Arthroscopic lavage
Arthroscopic lavage plus debridement
Microfracture
Mosiacplasty (osteochondral transplant)
Chondrocyte grafts
Joint replacement
Treatment for OA
Which IL can you target / block to treat OA? [1]
IL-1 blockage
OA treatment
Adalimumab targets which cytokine? [1]
TNF inhibition
How would you treat acute gout / gout attack? [4]
NSAIDs:
* Start with highest dose for 2-3 days & taper down over 2 weeks
Colchicine:
* 2nd line (narrow therapeutic window and risk of toxicity)
Corticosteroids
* For those that can’t use NSAID or colchicine
IL1 biologicals
* Rilonacept, canakinumab, anakinra
* Reduces length of attack and reoccurrences
* Used for patients who have severe and frequent flares
How long should gout symptoms be absent for before stopping NSAID treatment for gout? [1]
2 days
Which IL1 biologicals can be used to treat acute gout? [3]
Rilonacept, canakinumab, anakinra
Why are IL-1 biologicals not as useful for treating gout than RA? [1]
have to be used daily, yet with gout flares they are only used acutely for short periods of time. Only used if a patient has severe and frequent flare due to their extreme cost.
Describe how you treat chronic gout [5]
Allopurinol:
* Blocks xanthine oxidase, which is responsible from converting xanthine (which comes from purines in the diet) to urate
Febuxostat:
* non-purine selective inhibitor of xanthine oxidase
uricosuric:
* increases uric acid excretion
Probenecid:
* increases the secretion of uric acid
* fewer side effects than allopurinol.
Rasburicase:
* Catalyses conversion of uric acid to allantoin
Which ARB can be used to treat chronic gout? [1]
Losartan
Name drug A used to treat osteoporosis [1]
Denosumab
Name drug A used to treat osteoporosis [1]
Teriparatide
What is first line treatment for osteoporosis? [1]
Describe MoA [3]
Bisphosphonates:
- inhibits osteoclast activity
- promotes osteoclast apoptosis
- Decreases RANKL expression (so osteoblasts don’t turn into osteoclasts [?])
Describe complications of bisphosphonates
Kills off osteoclasts: don’t remove old bone: thickened bone
Get giant osteoclasts: poisoned osteoclasts
Osteonecrosis occurs
Osteoporosis treatment
Describe the MoA of Teriparatide [2]
Teriparatide is a recombinant PTH:
- PTH upregulates RANKL - signals osteoblast to differentiate when have low Ca2+: work indirectly on osteoclasts to boost bone making potential
- Intermittent exposure to PTH activates osteoblasts more than osteoclasts
Osteoporosis treatment
Describe the MoA of Denosumab [2]
PTH normally inhibits OPG.
Denosumab is a an osteoprotegrin artificial antibody & acts as a monoclonal antibody to RANK:
Denosumab: human monoclonal antibody that inhibits RANKL and helps regulate turnover in healthy bone. Denosumab binds with high specificity and affinity to the cytokine RANKL, inhibiting its action; as a result, osteoclast recruitment, maturation and action are inhibited, and bone resorption slows
Colchicine - inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity
Describe treatment regime of dermatomyositis [4]
Prednisilone (type of corticosteroid):
* 1 mg / kg per day until creatine kinase normal
Azthioprine
Methotrexate
Rituximab
Describe treatment regime of dermatomyositis [4]
Prednisilone (type of corticosteroid):
* 1 mg / kg per day until creatine kinase normal
Azthioprine
Methotrexate
Rituximab
Treatment for DMD? [2]
Prednisilone
Gene alterations
Name and describe how two therapeutic drugs cause myopathy [2]
Corticosteroids; cause dose dependent type 2 atrophy
Hydroxychloroquine: not dose dependent atrophy; lysosomes damaged
Hydroxychloroquine causing lysosome damage
Treatment options for fibromyalgia? [4]
Amitriptyline (TCA)
Fluxetine (SSRI)
Exercise
Complementary therapy
How do you treat chronic osteomyelitis? [5]
Puncture drainage if abscessed
Surgical debridement
Reconstruct bone (allograft/ autograft)
Antibiotics (4-6wks, at least 2 IV):
* Vancomyocin cement beads
* Flucoxallin (gram +ve)
* Clindamycin
* Piperacillin
* Ciprofloxacilin
Describe treatment of chronic osteomyeltis [5]
Puncture drainage if abscess identified
Reconstruct bone (allograft or autograft)
Surgical debridement to remove dead bone
Antibiotics for 4-6 weeks (at least 2wks IV):
* vancomycin cement beads: dissolve and give steady supply of vancomycin
Bone graft (& muscle graft)
Which antibiotics would you give for chronic osteomyelitis [1]
Vancomycin cement beads
Management of infections that have occurred from joint replacement infections? [2]
Removal of prosthesis, antibiotics for 6wks, re-implantation of new prosthesis 4 weeks after removal - 90%+ success
Long term suppressive antibiotics
Treatment for folliculitis? [3]
Oral antibiotic
Retinoic acid & Vit. A: reduces amount of sebum
Tx of impetigo?:
Simple cases [1]
Severe cases? [1]
Most people? [1]
Oral or topical antibiotic for severe cases that have spread to other body areas
NICE recommends 1% hydrogen peroxide cream for simple cases
But most people will get better without treatment within 3 weeks
Treatment of scalded skin syndrome? [2]
Treatment:
* Conservative: rehydration antipyretics
* Parenteral antibiotics
Therapy for Necrotising fascitis? [3]
Treatment:
* Surgical debridement
* Empiric antibiotics
* Hyperbaric oxygen (Add on therapy)
Treatment for HPV: viral warts and veruccas? [5]
Topical salicylic acid
Fluorouracil cream
Cryosurgery
Surgical curettage
Laser treatment (CO2 laser 582nm)
Treatment of Molluscum contagiosum? [1]
Usually resolves without treatment
If severe or in genital area then OTC wart treatments, cryo-surgery
Treatment of Pityriasis versicolour (tinea versicolour)? [3]
- Antifungal shampoo (ketoconazole)
- Selenium sulphide (off-label)
- For small areas antifungal creams
Treatment of scabies? [3]
Treatment:
* permethrin
* ivermectin
* crotamiton
Treatment for leprosy? [3]
Rifampicin, dapsone and clofazimine
How do you treat enthesitis:
- If mechanical? [2]
- If Inflammatory [5]
Mechanical:
* RICE
* NDSAIDs
Inflammatory:
* Sulfasalazine
* Methotrexate
* Anti-TNF therapy (restricted use for severe autoimmune enthetitis)
* Local radiotherapy
* Corticosteroid injection
* Hyperosmolar dextrose (initiates proliferation of intrinsic fibroblasts - race to repair damage c.f. osteoblasts)
Which drug class is used for ankylosing spondylitis enthesitis? [1]
Anti-TNF treatment
Treatment for tenosynovitis?
Treatments [4]
Surgery - for trigger finger [1] and De Quervains [1]
Treatment:
* RICE
* Splinting
* Anti-inflam
* Corticosteroids
Surgery:
* TF: cut annular ligament
* DQ: shave styloid processs or cut sheath
DMARD treatments for SLE? [4]
Cylcophosphamide
Mycophenolate mofetil
Methotrexate
Tacrolimus
Describe two biological DMARDs for SLE? [2]
Belimubab: inhibits BAFF (B cell activating factor)
Rituximab: CD20 blocker
How can you treat resistant urticaria and asthma?
Omalizumab: binds free IgE in the serum, forming trimers and hexamers
Treatment of Pemphigus Vulgaris? [3]
Oral steroids
Immunosuppresion: mycophenolate mofetil or azathioprine
Rituximab (targeting CD20 on B cells)
New drug class treatments for AA and Vitiligo? [1]
Name an example drug [1]
JAK Inhibitors
E.g Ruxolitinib
Two potential AEs of JAK inhibitors? [2]
Thromboembolic events
Cancer related events
