IC5 Flashcards
Example of PGxdrugs causing allergies/ hypersensitivity
- Allopurinol/ Phenytoin: SJS/ TEN
- Carbamazepine: SJS/TEN/ DRESS
- Abacavir: Hypersensitivity reactions
Immediate treatment for anaphylaxis and how?
Epinephrine (adrenaline) -> To counteract bronchoconstriction and vasodilation
Treatment of anaphylaxis if managed to reach hospital/ ambulance
- IV fluids to restore volume/ BP
- Intubation if needed to save airway
- Norepinephrine (Noradrenaline) if shock
- Other agents: steroids, glucagon, ranitidine (H2) + diphenhydramine (H1)
Treatment for SCAR (serious cutaneous adverse reaction)
Treatment less defined;
Supportive care: wound care, fluids, nutritional support, pain management, temp regulation, prevention of infection;
Steroids use is controversial
Definition of autoimmune diseases and possible causes
- when the body is attacked by its own immune system
- caused by genetic / environment stimuli e.g. smoking and infection
Why are autoimmune diseases difficult to treat?
- a large proportion do not respond to treatment, do not tolerate or have adverse effects
- poorly indicated, mostly off-label use; great variability of tx
- drugs are usually costly
- stigma > viewed as a weakness > ppl less likely to seek tx
Why are autoimmune diseases difficult to treat?
- a large proportion do not respond to treatment, do not tolerate or have adverse effects
- poorly indicated, mostly off-label use; great variability of tx
- drugs are usually costly
- stigma > viewed as a weakness > ppl less likely to seek tx
Definition and possible causes of systemic lupus erythematosus (SLE)
- autoimmune disease a/w auto-antibody production
- strong genetic disposition + environmental triggers e.g. smoking, infection & certain drugs
Pathophysiology of SLE
- characterised by disorder of innate & adaptive immune system
- T & B cell activation & signalling is altered -> abnormal clearance of apoptotic debris containing nuclear material which can stimulate immune responses
- num of plasma cells increased in active SLE and these cells produce autoantibodies which cause tissue damage
Clinical presentation of SLE
- Lupus nephritis
- Neuropsychiatric lupus: psychosis, seizure, anxiety, cerebrovascular disease (stroke), cognitive dysfunction, peripheral neuropathy, confusion, etc
- Cardiovascular: pericarditis, myocarditis, accelerated atherosclerosis
Labs presentation for SLE
Full blood count: Reduced RBC, WBC & PLT
Immunologic: Anti-nuclear antibodies, Anti- ds DNA, Anti-smith antibodies, anti-nuclear ribonucleoprotein, low complement (C3, C4, CH50)
Treatment goal for SLE
- Remission/ achieve low disease activity (more realistic)
- Prevent flares & other organs, slow disease activity, reduce use of steroids, improve QoL while minimising adverse effects
- Evaluate and treat other comorbidities alongside Lupus
- Lifestyle (quit smoking) & support group
Drug treatment for SLE
- FDA-Approved drugs: hydroxychloroquine, aspirin, prednisone & belimumab
- Usually start on hydroxychloroquine (including pregnant women) > takes about 4-8w to have effect; minimal adverse effects
General pharmacologics for SLE + examples
- NSAIDs: first line for acute symptoms
- Steroids: Monotherapy or adjunctive to control flares/ maintain low disease activity; Concern over high dose/ LT use
- Biologics: targets and disrupts functioning of B cells -> Belimumab & Rituximab
- Immunosuppressant: IV/ PO Cyclophosphamide (severe organ involvement; induction); Mycophenolate (induction & maintenance); Azathioprine (alternative for maintenance)
What syndrome may also be found in SLE patients? What are the consequences and general treatment?
- Antiphospholipid syndrome; Positive for antiphospholipid antibodies
- High risk of clotting and pregnancy morbidity
Treatment: - Primary thromboprophylaxis: hydroxychloroquine + aspirin
- Secondary thromboprophylaxis: warfarin
