Drug Side Effects

Question 1

Red man syndrome

Answer 1

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.

Question 2

Warfarin is increased by waht drugs

Answer 2

Most antibiotics that kill gut microbiome

Question 3

Methotrexate toxicity is induced by

Answer 3

Most antibiotics

Question 4

Alcohol disulfiram reaction

Answer 4

metronidazole. avoid even for 48hr post last dose

Question 5

Reduced efficacy of these antibiotics when drinking alcohol

Answer 5

doxycycline and erythromycin

Question 6

ototoxicity and nephrotoxicity

Answer 6

gentimicin (hardly ever used so you probably wont see this except for intraabdominal sepsis AGM), vancomycin (more commonly used- C diff infections and MRSA)

Question 7

Thrombocytopenia and neutropenia

Answer 7

Vancomycin

Question 8

ondansetron side effect and the reason it is not used in palliative care?

Answer 8

Constipation!

Question 9

tamoxifen side effects

Answer 9

endometrial carcinoma and dvt and hot flushes

Question 10

Budesonide doesnt cause adrenal suppression as it only works topically in the gut. true or false?

Answer 10

true

Question 11

adrenal suppression can be reduced by doubling the dose but then taking alternate day dosing

Answer 11

true

Question 12

adrenal suppression is reduced most by taking it AM at normal time when adrenaline is produced

Answer 12

true

Question 13

antiplatelets can cause gastric ulcers

Answer 13

yes so prescribe PPI

Question 14

Which of the antiepileptics cause SIADH?

Answer 14

Carbamezapine

Question 15

Which antidepressants cause SIADH?

Answer 15

amytriptylline and SSRI

Question 16

strontium side effects

Answer 16

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

Question 17

raloxifene side effects?

Answer 17

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 decrease the risk of breast cancer

Question 18

side effects of LMWH/UFH?

Answer 18

HYPERKALAEMIA
- Causes inhibition of aldosterone secretion

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.

Question 19

Clindamyicin biggest side effect ?

Answer 19

it has the highest risk of C diff so only prescribed in those with SEVERE penicillin allergy as an alternative

Question 20

quinolones biggest side effectS (6)?

Answer 20

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

Question 21

SNRI- SSRI/SNRI side effects?

Answer 21

SNRI- SSRI/SNRI antidepressant medicines: small increased risk of postpartum haemorrhage when used in the month before delivery (January 2021).

Question 22

why is fidaxocin 2nd line for C diff?

Answer 22

Fidaxomicin is EXPENSIVE- £2000 per course. hence why it is 2nd line to vancomycin

Question 23

biggest side effect of beta blockers?

Answer 23

impotenence

Question 24

Side effect of ACE I?

Answer 24

Angioedema esp. in black patients

Question 25

Amlodipine contraindications

Answer 25

unstable angina (reflex tahcycarida)
Cardiogenic shock and
significant aortic stenosis

Question 26

why do NSAIDS increase risk of CVD, stroke and fluid retention?

Answer 26

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.

Question 27

Does vancomycin cause renal impairment ? what are its warnings/side effects ?

Answer 27

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

Question 28

donepezil side effects

Answer 28

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).

Question 29

beta blocker. if someones heart rate is 54 what do you do?

Answer 29

1. anything under 60 u want to bring up (as this is marked bradycardia)
2. so you need to reduce the dose.
3. 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.

Question 30

which drugs cause constipation out of the following:

Amlodipine
Bisoprolol
Amiodarone
Lithium

Answer 30

All except lithium

Question 31

Which of the following drugs cause sun sensitivity?

amiodarone
azathiopurine
lithium
doxycycline
hydroxychloroquine
ciprofloxacin
antifungals

Answer 31

Amiodarone
doxycycline
ciprofloxacin

Question 32

Medications that cause postural hypotension

Answer 32

Nitrates
Diuretics
Anticholinergic medications
Antidepressants
Beta-blockers
L-Dopa
Angiotensin-converting enzyme inhibitors - (ACE) inhibitors

Question 33

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?

Answer 33

1. reaction to black seed oil, contact dermatitis allergic reaction around the eyes too.
2. Addisonian crisis secondary to suboptimal prednisolone levels secondary to black seed oil interaction
3. digoxin toxicity secondary to black seed oil interaction
4. 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!)
5. 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.

Question 34

Peripheral neuropathy, lymphadenopathy, and bleeding gums

Answer 34

Phenytoin is an antiepileptic drug that can cause side effects such as peripheral neuropathy, characterized by numbness and reduced sensation in a glove-and-stocking distribution. Additionally, phenytoin can cause gingival hyperplasia, which may lead to bleeding gums. Lymphadenopathy is another potential side effect of phenytoin.

Question 35

blurred vision, bumping into things and dizziness

Answer 35

Carbamazepine can cause side effects such as dizziness, ataxia, and diplopia.

Question 36

other than being teratogenic, topiramate can also cause… (topiramate is used for migraines)

Answer 36

Topiramate can cause side effects like weight loss (as it inhibits glutamate and enhances GABA which has appetite suppressing effects), cognitive impairment (GABA slows neuronal processing), and kidney stones (it inhibits carbonic anhydrase which means urine becomes more alkanised which precipitates the formation of calcium phosphate stones as these form in alkaline urine).

Question 37

tremors, and hair loss and diarrhoea/constipation.

Answer 37

Sodium valproate can cause gastrointestinal disturbances, tremors, and hair loss.

Question 38

Stevens-Johnson syndrome, headache and dizziness.

Answer 38

Lamotrigine

Question 39

Warfarin why skin necrosis and why we start heparin initially?

Answer 39

it inhibits protein anticoagulant C faster than it inhibits clotting factors

Question 40

heparin side effects

Answer 40

bleeding
thrombocytopenia - see below
osteoporosis and an increased risk of fractures
hyperkalaemia - this is thought to be caused by inhibition of aldosterone secretion

Question 41

sildenafil

Answer 41

nasal congestion

sildenafil inhibits cGMP-specific PDE-5, which enhances the effect of NO. NO causes congestion in the penis, nose, head (headache), skin (flushing), blood vessels (low blood pressure),

cyanopsia- blue vision

Question 42

verapmil or diltiazem ankle swelling and flushing?

Answer 42

verapmil- flushing
diltiazem- ankle swelling

Question 43

Triptans side effects with oral use > nasal use

Answer 43

20 to 50% of patients who initially respond will have a rebound headache within 48 hours. If this is an issue naratriptan may be better as it has a slower onset and offset.

Question 44

safety netting advice for terbinafine

Answer 44

stop terbinafine and seek prompt medical assessment if they develop symptoms of liver injury (e.g. flu-like illness, gastrointestinal symptoms, pruritus, and jaundice), infection (e.g. fever, sore throat), or mouth ulcers (ten, sjs), or skin rash.

Question 45

rare but serious side effects of ACE inhibitors is

Answer 45

rare but serious side effects of ACE inhibitors is angioedema, characterised by marked tongue and facial swelling as described in this scenario. This reaction can occur at any time during treatment, even weeks or months after initiation.

Question 46

Medications which may cause vertigo?

Answer 46

Quinine
Anticonvulsants, e.g. phenytoin, carbamazepine
Diuretics, e.g. furosemide
Antibiotics, e.g. erythromycin, minomycin, aminoglycosides
NSAIDs, e.g. aspirin, ibuprofen, naproxen, indomethacin
Cytotoxics
Alcohol

Question 47

Common causes of SIADH?

Answer 47

Opioids
ACE-i or ARBs
PPI
Anticonvulsants (such as sodium valproate, lamotrigine, and leviteracetam).
Amiodarone.
Theophylline.
Dopamine antagonists (metoclopramide and domperidone).
Antidiabetics (insulin, chlorpropamide, and tolbutamine).
NSAIDS
MDMA (ecstasy).

Question 48

Thiazides side effects and where do they act on the kidney?

Answer 48

Thiazides- cause sodium loss- this decreases circulating volume and triggers ADH release- which causes purely water absorption leading to euvolemic hyponatremia.? So not exactly SIADH as it is appropraite just not desired.

Question 49

Allopurinol risks to make patient aware of?

Answer 49

Rash within first 6 weeks - discontinue and get in touch if it occurs

Question 50

A 28-year-old man presents to his GP with a painless ulcer on his penis which has been present for several weeks.
He otherwise has no symptoms and is generally well in himself. On examination. he also has non-tender inguinal lymphadenopathy.
The GP prescribes penicillin. Several hours later, the patient presented with fever and a new rash to the Emergency Department. On examination. he appears well but has marked flushing of his torso. There is good air entry on
auscultation. with no wheeze. Observations are as follows:
* Heart rate: 98 beats/min
* Respirator rate: 18 breaths/min
* Blood pressure: 132/72 mmHg
* Temperature: 37

what is happening and how to treat?

Answer 50

The Jarisch-Hersheimer reaction unlike an anaphylactic reaction will NOT present with hypotension and wheeze.

It is key to note here that the patient did not then present with an anaphylactic reaction to penicillin - he appeared well on examination with normal auscultation and no hypotension. He instead presented with the Jarisch-Herzheimer reaction. which is sometimes seen following treatment of SYPHILLUS thought to be due to the release of endotoxins It presents as fever, rash and tachycardia but there is crucially no wheeze and no hypotension No treatment is required except for antipyretics if needed

Question 51

Answer 51

Question 52

Answer 52

furosemide doesnt need to be stopped

Question 53

Answer 53

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.

Question 54

as well as monitoring hepatic function for terbutaline what else should you tell the patient to report and stop using terbutaline if this happens?

Answer 54

RUQ pain, consistent N/V, bleeding/bruising, pruritis, jaundice, dark urine and pale stools.

Question 55

lansoprazole side effects long term to make patients aware of/check in a medication review

Answer 55

bone fractures due to reduced Ca, Mg absorption. Check Ca and Mg levels. Mg should be monitored throughut and before treatment starts if going to be on it long term.

Gut infections.

B12 deficiency – symptoms include feeling very tired, a sore and red tongue, mouth ulcers and pins and needles.