Drug Side Effects Flashcards
Red man syndrome
Rate related transfusion reaction with vancomycin
going red when you give the vanc or teic TOO FAST- it should be given as an infusion NOT bolus.
Warfarin is increased by waht drugs
Most antibiotics that kill gut microbiome
Methotrexate toxicity is induced by
Most antibiotics
Alcohol disulfiram reaction
metronidazole. avoid even for 48hr post last dose
Reduced efficacy of these antibiotics when drinking alcohol
doxycycline and erythromycin
ototoxicity and nephrotoxicity
gentimicin (hardly ever used so you probably wont see this except for intraabdominal sepsis AGM), vancomycin (more commonly used- C diff infections and MRSA)
What blood abnormalities may you need to watch out for with vancomycin?
thrombocytopenia and neutropenia (opposite of steroids)
ondansetron side effect and the reason it is not used in palliative care?
Constipation!
tamoxifen side effects
endometrial carcinoma and dvt and hot flushes
Budesonide doesnt cause adrenal suppression as it only works topically in the gut. true or false?
true
adrenal suppression can be reduced by doubling the dose but then taking alternate day dosing
true
adrenal suppression is reduced most by taking it AM at normal time when adrenaline is produced
true
antiplatelets can cause gastric ulcers
yes so prescribe PPI
Which of the antiepileptics cause SIADH?
Carbamezapine
Which antidepressants cause SIADH?
amytriptylline and SSRI
strontium side effects
Strontium ranelate
‘dual action bone agent’ - increases deposition of new bone by osteoblasts (promotes differentiation of pre-osteoblast to osteoblast) and reduces the resorption of bone by inhibiting osteoclasts
concerns regarding the safety profile of strontium have been raised recently. It should only be prescribed by a specialist in secondary care
due to these concerns the European Medicines Agency in 2014 said it should only be used by people for whom there are no other treatments for osteoporosis
increased risk of cardiovascular events: any history of cardiovascular disease or significant risk of cardiovascular disease is a contraindication
increased risk of thromboembolic events: a Drug Safety Update in 2012 recommended it is not used in patients with a history of venous thromboembolism
may cause serious skin reactions such as Stevens Johnson syndrome
raloxifene side effects?
firstly its a selective oestrogen receptor modulator (SERM)
has been shown to prevent bone loss and to reduce the risk of vertebral fractures but has NOT shown to reduce the risk of non-vertebral fractures
HAS been shown to increase bone density in the SPINE and proximal femur
THEN SIDE EFFECT WISE
1. may worsen menopausal symptoms
2. increased risk of thromboembolic events
3. may increase the risk of endometrial cancer but decrease the risk of breast cancer
side effects of LMWH/UFH?
HYPERKALAEMIA
- Causes inhibition of aldosterone secretion- only when the dose is theurapeutic
OSTEOPOROSIS
HIT - UFH (Days 5-10 or day 1 if exposed to it in the last month: 4Ts risk tool
30% reduction of platelet count or > 50% from the patient’s baseline platelet count, with thrombosis, or skin allergy.
Clindamyicin biggest side effect ?
it has the highest risk of C diff so only prescribed in those with SEVERE penicillin allergy as an alternative
quinolones biggest side effectS (6)?
MHRA warning-
1. ^ risk of aortic aneurysms,
2. aortic dissection,
3. aortic regurg,
4. suicide and
5. seizure
6. tendinopathy
HUGE WARNING USING THIS EVER
SNRI- SSRI/SNRI side effects?
SNRI- SSRI/SNRI antidepressant medicines: small increased risk of postpartum haemorrhage when used in the month before delivery (January 2021).
why is fidaxocin 2nd line for C diff?
Fidaxomicin is EXPENSIVE- £2000 per course. hence why it is 2nd line to vancomycin
biggest side effect of beta blockers?
impotenence
followed by nightmares
followed by cold peripheries (and vasospasm - that is why it is not used in cardiac arrest caused by cocaine)
Side effect of ACE I?
Angioedema esp. in black patients
Amlodipine contraindications
unstable angina (reflex tahcycarida)
Cardiogenic shock and
significant aortic stenosis
why do NSAIDS increase risk of CVD, stroke and fluid retention?
nsaids
- why diclofenic is bad for heart failure and all NSAIDS in general is because of their action on COX2 - usually COX2 increases the GFR - increasing water and sodium loss. But when you inhibit this more renin is released and more water and sodium are reasborbed. But Diclofenic is the strongest for this, and also therefore has more vasoconstrictive effects hence why its association with stroke and thrombosis (as the lumen narrows are atheromas are more likely to break off)
- Naproxen is generally considered safer than diclofenac becauseit has a lower risk of cardiovascular events and gastrointestinal (GI) issues as it has less effect on COX2.
Does vancomycin cause renal impairment ? what are its warnings/side effects ?
Vancomycin is associated with a higher incidence of nephrotoxicity than teicoplanin.
but not as much as gent- hence why you can give before levels come back
donepezil side effects
bradycardia
potentially inappropriate in patients with a known history of persistent bradycardia (heart rate less than 60 beats per minute), heart block, recurrent unexplained syncope, or concurrent treatment with drugs that reduce heart rate (risk of cardiac conduction failure, syncope, and injury).
beta blocker. if someones heart rate is 54 what do you do?
- anything under 60 u want to bring up (as this is marked bradycardia)
- so you need to reduce the dose.
- But caution - you do NOT do this quickly in any patient with heart disorders because sudden cessation of a beta-blocker can cause a rebound worsening of myocardial ischaemia and therefore gradual reduction of dose is preferable when beta-blockers are to be stopped.
which drugs cause constipation out of the following:
Amlodipine
Bisoprolol
Amiodarone
Lithium
All except lithium
Which drugs cause sun sensitivity?
Tetracyclines (e.g., Doxycycline)
Sulfonamides (e.g., Sulfamethoxazole-Trimethoprim)
Chlorpromazine (Antipsychotic)
Thiazide Diuretics (e.g., Hydrochlorothiazide)
Retinoids (e.g., Isotretinoin, Tretinoin)
Fluoroquinolones (e.g., Ciprofloxacin, Levofloxacin)
Methotrexate (Chemotherapy/Immunosuppressant)
Medications that cause postural hypotension
Alpha blockers- most likely
Nitrates- 2nd most likely
Diuretics- Moderate to High chance
Beta blockers- not on their own
ACE inhibitors- first dose hypotension
Dopaminergic drugs- potentially in elderly
A lady in AMAU in Prince Phillip presents with N/V, blurred vision, tachycardia, palpitations and dehydration. She was taking digoxin, prednisolone for addisons and black seed oil. She had irritated eyes. What else do you want to know and what are your top 3 differentials?
- reaction to black seed oil, contact dermatitis allergic reaction around the eyes too.
- Addisonian crisis secondary to suboptimal prednisolone levels secondary to black seed oil interaction
- digoxin toxicity secondary to black seed oil interaction
- Addisonian crisis- low BP (dizziness, collapse, weakness, headache, blurry vision, feeling faint), electrolyte imbalance (low Na, high K- less urine output, and confusion, Irritability, fatigue), low glucose (similar symptoms to the above), characteristically there is a pain in the abdomen, lower back and legs! (large muscle groups feel the low BP and electrolyte abnormalities the most), hypercalcaemia (irritability, abdominal pains, psychosis, constipation- can go into ileus!)
- digoxin toxicity signs- 1. brady, 2. N/V, 3. Diarrhoea and late stage changes are 1. vision changes and 2. tachyarrhythmias. The adverse pharmacodynamic effects of digoxin are potentiated in the presence of hypokalaemia. A suspicion of digoxin toxicity can be confirmed by measuring the plasma digoxin concentration at least 6 hours after a dose, which should be between 0.8 and 2 micrograms/L.
SO IF THEY ARE POTENTIATED BY HYPOKALAEMIA THEY ARE LESS LIKELY IN ADDISONIAN CRISIS TO CO-OCCUR.
furosemide doesnt need to be stopped
The patient has developed neuroleptic malignant syndrome (NMS). This is a rare, idiosyncratic, potentially life-threatening reaction to a neuroleptic drug. The presentation of NMS varies considerably between patients. There is a gradual onset of symptoms over 1-3 days. Typical features include hyperthermia (temperature >38°C), diaphoresis, rigidity, confusion and fluctuating consciousness. Fluctuating blood pressure and tachycardia are also common, along with raised WCC and serum creatine kinase concentrations and altered liver function tests. Risk factors for MS include the use of high-potency first-generation neuroleptics such as haloperidol and fluphenazine but every class of neuroleptic drug has been implicated.
NMS occurs less commonly with other agents including prochlorperazine, promethazine, atypical antipsychotics (e.g clozapine, risperidone), anticholinergic drugs, metoclopramide and lithium. Other risk factors include a recent or rapid dose increase, rapid dose reduction and the abrupt withdrawal of antipsychotics. In this patient a rapid switch from quetiapine to haloperidol may have increased the risk of NMS.
The patient has a temperature of 38.2°C, tachycardia and labile blood pressure. He is agitated and confused, sweating, hypersalivating and has severe muscle rigidity.
If lead-pipe muscle rigidity alone were present, this could indicate Parkinsonian-like extrapyramidal adverse effects of haloperidol which could be treated with procyclidine or trihexyphenidyl hydrochloride.
However, the patient’s other signs and symptoms are strongly suggestive of NMS.
Treatment of MS includes stopping the neuroleptic drugs) responsible immediately, in this case haloperidol and quetiapine.
Treatment should be withheld for at least 5 days but ideally longer, allowing signs and symptoms to resolve completely.
NMS may persist for 2-14 days after an oral neuroleptic drug is stopped or for up to 21 days if caused by a depot injection. Most episodes resolve within 2 weeks.
Agitation can be treated with benzodiazepines IV if required.
Physical restraint may worsen hyperthermia and should be avoided.
IV fluids are given to reduce the risk of dehydration and acute kidney injury.
The airway and breathing must be protected if compromised.
Pyrexia is treated with cooling devices and antipyretics such as paracetamol.
Drug treatment of MS usually includes dantrolene sodium IV and bromocriptine PO.
Dantrolene is a direct-acting skeletal muscle relaxant and is effective in treating malignant hyperthermia. —> A rapid reduction of heat production as well as rigidity usually occur within minutes of administration. As it is given IV, it is the most appropriate initial treatment.
The dose of dantrolene is 2-3 mg/kg by rapid IV injection, then 1 mg/kg repeated if necessary up to 10 mg/kg/course.
There is a risk of hepatotoxicity and liver function tests should be checked regularly.
Dantrolene may be continued for up to 10 days and possibly tapered slowly to minimise the risk of relapse.
There is approximately a 30% chance of recurrence of NMS when antipsychotic treatment is restarted.
The drug chosen should be structurally unrelated to that which caused the NMS or a drug with low dopamine affinity such as clozapine or aripiprazole.
Quetiapine would normally be included here but was possibly implicated in causing MS in this patient.
Depot preparations must not be used.
Treatment should start at a very low dose and then be titrated very slowly with close monitoring of temperature, pulse and blood pressure.
as well as monitoring hepatic function for terbenafine what else should you tell the patient to report and stop using terbenafine if this happens?
RUQ pain, consistent N/V, bleeding/bruising, pruritis, jaundice, dark urine and pale stools.
hyperthyroidism on amiodarone?
STOP immediately and refer in if symptoms/signs of thyrotoxicosis
how likely are ED drugs to cause psotural hypotension?
<2% !
drugs likely to cause gout or hyperuricemia?
- low dose aspirin (<325mg).
- diuretics (loop)
- ciclosporin or tacrolimus
- chemotherapy
- allopurinol (to begin with)
- some ARBs
why is fentynl so much more dangerous than morphine esp. in street use?
because it has a MUCH MUCH MUCH longer half-life and its like 100x more potent. If you administer naloxone - you need to do it on an infusion so people in the streets need to come in quick.
Why is it more important to warn patients to mention any hearing changes > urinary changes with ototoxic and nephrotoxic drugs?
renal function can the monitored via routine laboratory testing and reduced urine output would be a late sign of damage anyway- kidney injury should be detected with bloods way before this point.
