Clinical Enquiry Comment/Case Management

1 Simvastatin + -patient has been just diagnosed with Withdraw Simvastatin and re-introduce
Amiodarone/ rhabdomyolysis due to enhanced effect of at capped dose of max 20mg, once
Amlodipine/Verapamil/ simvastatin. CK levels raised. Urine is darkly myopathy subsides.
Diltiazem (simvastatin coloured.
should be max 20mg) OR

Q. Reason for dark urine? You can suggest changing simvastatin to

Dark urine and muscle weakness and muscle pain pravastatin because it’s not significantly
Told that are symptoms of rhabdomyolysis. When muscle is metabolised by CYP 450 so it will not be
hypercholesterolaemia damaged, a protein called myoglobin is released affected by the diltiazem and hence
has been stabilised for into the bloodstream. Myoglobin effects kidney. reduce the risk of myopathy. (lectures:
Where there is a potential for drug interactions,
past 3 months. (not pravastatin can be recommended over simvastatin, as it
relevant?) is not significantly metabolised by the CYP450 enzymes
in the liver).

Pravastatin and fluvastatin have lower

Verapamil and diltizem act as enzyme inhibitor!
number of reported cases of myopathy
Simvastatin + fibrate =
and rhabdomyolysis.
max simvastatin 10mg
OR
change simvastatin to atorvastatin

also
If transaminases (ALT, AST) are raised to
three times the upper limit of normal
consider stopping statin.

2 Lithium and NSAIDs =
TOXICITY
Patient is on regular Lithium tablets he started Stop ibuprofen and monitor lithium.
suffering nervousness, tremor, vomiting.
Lithium levels should be taken 12 hours
He also says he was prescribed two antibiotics after the last dose and if the level is toxic
(Penicillin, Flucloxacillin) and Ibuprofen 400mg TDS then management is essentially to try
two days ago in walk in clinic. and increase urine flow (without
diuretics as they can also affect renal
NSAIDs can deteriorate renal function; and lithium function).
is renally excreted so less is eliminated from body
therefore… toxicity occurs as it’s a narrow Li+ above 1.5mmol/l can be fatal and
therapeutic drug. toxic-this patient is exhibiting signs of Li+
toxicity!
Lithium levels should be 0.4-1mmol/L.
– Early signs of toxicity (Li+ ~ 1.5mmol/L): tremor,
agitation, twitching
– Intermediate: lethagy
– Late (Li+ ~ >2mmol/L) spasms, coma, fits, renal
failure

3 ACEI + NSAIDs = both Paracetamol, Diclofenac, Aspirin, Simvastatin,
cause renal Ramipril and Atenolol.
deterioration
Patient has had previous cardiovascular event and
osteoarthritis. Renal function is dropping. What
should you do?
-Interaction between diclofenac and ramipril =
increased risk of renal impairment
Change NSAID to weak opioid e.g.
codeine.
Withhold ACEI until renal function
improves.
Recheck U&Es and reintroduce at lower
dose perhaps and re-titrate up or if renal
function adequate can reintroduce same
dose!
 -Diclofenac reduces blood flow to kidneys so
replace to weak opioid.
4 Iron-deficiency Low MCV, Low haematocrit, low Hb, Low RBC.
anaemia
What are the signs and symptoms, how would you
Must mention treat it? Signs = pallor
Microcytic Anaemia symptoms=fatigue, dyspnoea (SOB), palpitations,
headaches
Causes of the iron-deficiency anaemia are blood
loss, particularly menorrhagia or GI bleeding e.g.
from oesophagitis, peptic ulcer, carcinoma, colitis,
diverticulitis or haemorrhoids.
Patient on diclofenac, paracetamol and codeine
for pain relief = potentially NSAID-induced GI bleed
so remove Diclofenac.
5 Iron-deficiency Pt on Codeine, warfarin, digoxin, paracetamol.
anaemia
6 Vit b12 deficiency High MCV, but Low Hb/Hct/RBCs Further tests =
(macrocytic anaemia) low B12
A raised MCV indicates vitamin B12 or folate
deficiency, these should therefore be tested.
Low B12 then further Schillings test to determine
whether there is malabsorption or whether there
is a lack of intrinsic factor.
A reduced vitamin B12 and Hb and raised MCV
suggests pernicious anaemia. This disease affects
all the cells of the body and is due to
malabsorption of B12 resulting from atrophic
gastritis and lack of intrinsic factor secretion.
(oxford handbook)
Symptoms - tiredness and weakness, dyspnoea,
sore red tongue, diarrhoea and mild jaundice
7 Morphine to fentanyl Currently = MST 30mg BD and Oramorph
patch 10mg/5mL, 15mL daily. So currently taking 30mg
for breakthrough pain.
What would she take and how much for
breakthrough pain?
Total daily dose of morphine = 90mg
So fentanyl ‘25’ patch (25mcg/hour for 72 hours)
• The cause will need to be investigated
and treated = STOP NSAID change
painkiller to weak opioid, or stronger as
this patient is already getting a weak
opioid.
PPI for treatment and prevention for
NSAID –associated GI bleed/ulceration.
If Hb<8g/dl patient should be considered
for blood transfusion.
• She would be offered oral iron eg
ferrous sulphate 200mg TDS (side
effects include constipation and black
stools) • Hb should rise 1g/dL/week –
continue until Hb is normal and for
atleast 3 months to replenish stores
Withhold warfarin, as patient may be
suffering from haemorrhage. (Check
INR) If bleed confirmed and Vit K for
reversal! (BNF)
Treatment of anaemia ferrous sulphate
200mg TDS – and 3 months after!
Treated by replenishing stores with
hydroxocobalamin (B12) 1mg IM
alternate days for 2 weeks. Maintenance
1mg IM every 2 months FOR LIFE
-any counselling related to condition and
treatment?
Should we gradually reduce morphine?
No.
Counselling on patient: How the fentanyl
patch can be administered?
Apply the patch to dry, non-irritated,
non-irradiated, and non-hairy skin on
upper arm or torso. Remover after 72
hours and apply a new patch to a
 can be given.
New dose for breakthrough pain = 90/6 = 15mg (so
7.5mL of Oramorph 10mg/5mL)
1/6 total daily dose every four hours when
required
What should be done when switching patient from
oral morphine to fentanyl patches?
Make sure patients’ chronic pain is generally
controlled. Patch is not suitable for acute pain.
8 Switch MAOI to SSRI A patient was on MAOI (Phenelzine). He asks his
GP to switch him to Fluoxetine because he heard
Phenelzine to there’s more evidence for it.
fluoxetine
9 Switch SSRI to MAOI Fluoxetine to MAOI
10 Reduced renal function eGFR = 30ml/min. Patient on simvastatin, aspirin,
and Metformin metformin high doses for all -- patient had
declined renal function. A list of blood results and
had a high creatinine level and patient on
metformin and the red flag was to mention lactic
acidosis.
different area. (BNF under Fentanyl,
p.272)
How to initiate fentanyl? Fentanyl patch
should be applied at the same time as
last m/r morphine tablet so allow time
for fentanyl to reach steady state.
Patch will take 12-24hrs to reach steady
state – can advise to apply first patch at
the same time as taking their last
morphine tablet – this gives 12 hrs pain
relieve while plasma levels of fentanyl
rise
Phenelzine is an MAOI, fluoxetine is an
SSRI
If an antidepressant is taken for longer
than 8 weeks must gradually decrease
over a period of 4 weeks.
So gradual withdrawal of MAOI (slowly
reduce the dose) due to risk of
withdrawal syndrome. Symptoms on
withdrawal can be agitation, irritability,
movement disorders, insomnia, etc.
Then allow a 2 week washout period
(MAOI stopped completely) before
starting SSRI, to prevent risk of
serotonin syndrome.
Continue to avoid tyramine rich foods
(e.g mature cheese) for 2 weeks after
stopping MAOI.
SSRI withdrawal symptoms = GI
disturbances, headaches, anxiety
sweating. Tapper the dose off over a few
weeks; gradual withdrawal.
Then stop SSRI. Washout period is
generally 1 week before starting MAOI
(or RIMA). BUT … wait 2 weeks after
stopping sertraline.
Fluoxetine have longer half-life so
washout period is 5 weeks.
Withhold metformin until renal function
improves. (eGFR must be above
45ml/min)
Simvastatin max dose =10mg when
eGFR is <30ml/min
 blood lactate >5mmol/L
Signs of Lactic Acidosis = N+V, hyperventilation.
Specialist referral
11 Choosing antibiotic for Pregnant lady with UTI, the infection was sensitive
UTI to trimethoprim or nitrofurantoin.
eGFR low
12 NSAID associated renal A 50 yr old man with osteoarthritis suddenly
impairment experienced renal failure. There was a list of drugs.
He was prescribed Diclofenac two weeks ago and
he had been taking the other drugs for at least 2
months.
Most likely cause would be the NSAID.
-The mechanism of action of NSAIDS and how they
affected renal function?
NSAIDs M/A = inhibit COX-1 and COX-2 which
inhibit inflammatory PGs.
Renal perfusion is reduced by NSAIDs and can
cause renal function to deteriorate as they are
vasoconstrictors of the afferent artertioles
13 Cholestatic jaundice Raised ALP and total bilirubin. Also has nausea
caused by co-amoxiclav and abdominal discomfort. Started taking co-
amoxiclav 10 days.
Cholestatic jaundice is a complication of drugs
including co-amoxiclav, Flucloxacillin,
erythromycin and chlorpromazine.
Jaundice and it said it is self-limiting (BNF)
provided that co-amoxiclav isn’t taken for more
than 14 days. It is very rarely fatal.
If patient is also on ACEI = carefully
monitored to ensure it’s ongoing
suitability
Reduced Renal function means
nitrofurantoin is not very effective
therefore trimethoprim should be
selected. BUT trimethoprim is
teratogenic and should be avoided in
pregnancy.
Can suggest trimethoprim if patient isn’t
in 1st trimester of pregnant = 7 days
supply 200mg bd (3days may enough for
women!)
In pregnancy. Can choose amoxicillin or
Cefalexin= not known to be harmful
however broad spectrum so can have a
higher chance of resistance concerns!
e.g Cefalexin (2 tablets a day for 3 days
but can give upto 7 days tx)
stop NSAID immediately and manage his
pain using alternatives weak opioid such
as codeine, continue Paracetamol.
Monitor renal function closely.
Stop co-amoxiclav and monitor hepatic
function!
It is self-limiting once the drug is
stopped it will correct itself so yes with
drugs that cause a chile static reaction
stop treatment and give an alternative
antibiotic if necessary.
Other drugs can cause hepatitis
characterised by prominent elevation of
ALT (which is not elevated in this case)

14 Hyperkalaemia (ACEI +
Spironolactone)
15 Hyperglycaemia
related to Steroid and
acute infection
Hyperglycaemia in type 1 DM
16 Angioedema induced
by ACEI
17 Compliance issues with
alendronic acid
– The CSM has advised that cholestatic jaundice
can occur either during or shortly after the use of
co-amoxiclav. An epidemiological study has shown
that the risk of acute liver toxicity was about 6
times greater than with amoxicillin. Cholestatic
jaundice is more common in patients above the
age of 65 years and in men.
Hyperkalaemia with mild renal impairment.
Taking Digoxin, Furosemide, Lisinopril and
Spironolactone and a few more. Digoxin excreted
through kidneys, risk of toxicity.
Patient on COPD and diabetes (humulin,
metformin) meds. Given amoxicillin and
prednisolone short-term [for exacerbation of
COPD].
Hyperglycaemia, confusion experienced.
Infection (most likely upper respiratory tract) and
the steroids (prednisolone) contribute to
hyperglycaemia.
Why is the patient confused?
Excessively high blood glucose. Need to increase
diabetic control. Insulin should help but keep
monitoring blood glucose.
Diabetic ketoacidosis (DKA) may be cause due to excessively
high glucose levels. Symptom of DKA includes confusion.
DKA occurs because the body has insufficient insulin to process
glucose into fuel, so the body breaks down fats to use for
energy. When the body breaks down fat, ketones are produced
as by-products. It this occurs, it’s a medical emergency.
65 years old afro carribean male on
Bendoflumethiazide, Lisinopril Simvastatin. He had
angioedema. The causative drug is Lisinopril.
Heartburn and mouth ulcers caused by alendronic
acid of daily supply and patient chew tablets
because couldn't swallow.
Incorrect usage of the drug. Alendronic acid should
not be chewed as it can cause mouth ulcers. And
the patient may not have been taking it correctly
hence the oesophageal irritation (heartburn).
Swallowing difficulty – oesophageal irritation
Also not sutiable to give oral bisphosphonates in
bed ridden patients – who cant sit/stand upright.
for example isoniazid, hydralazine,
rifampicin and paracetamol (in
overdose).
Stop spironolactone and also withhold
ACEI. Recheck K+ levels and can
reintroduce while monitoring U&Es and
renal function.
Patient is only given prednisolone for 5
to 7 days so there’s no need to stop it.
Continue course or infection might not
be fully cleared and could reoccur and
cause another exacerbation of asthma/
COPD.
Monitor more closely blood glucose
levels and amend diabetic meds
according to response (i.e. increase dose
to improve glycaemic control)
Also hyperglycaemia in short term is not
usually a problem. Chronic
hyperglycaemia is associated with
complications.
Need insulin
So stop ACEI monitor renal function, add
amplodipine (CCB first line anyways) for
hypertension control and reduce the
dose of simvastatin to max 20mg
(because of the addition of amlodipine).
Investigate further to ensure patient is
not suffering from oesophageal
ulceration. Refer to specialist? STOP
alendronic acid!
Mouth ulcers management?
Options
Oral solution: Patient cant swallow
tablets so should be offered oral
 solution instead (which is available as
70mg/100mL). Still counsel that the oral
solution should be taken with plenty of
water on an empty stomach at least
30minutes before food, and the patient
should sit or stand to remain upright for
30 minutes post dose.

IV infusion annually given as day patient

IV Ibandronic acid for tx of post-

menopausal women give iv inj over 15
to 30 seconds – 3mg every 3 months
(BNF)

Denosumab – inj every 6 months

Also can suggest for the alternative for

alendronic is strontium ranelate (but cant find
why)

18 Long term risks of Long term risks of prednisolone for a COPD patient -Bisphosphonates for prophylaxis of
prednisolone osteoporosis.
-Advice on balanced diet as it can
increase appetite and it also increases
risk of induce diabetes in long-term use.
(monitoring of blood glucose may be
needed)
-Avoid abrupt withdrawal.
-Avoid infectious people! (increased risk
of susceptibility to infections)
-Carry your steroid card with you.

GI protection..

 Take prednisolone tablets with

food. The enteric-coated tablets
may be taken before or after food.
But there is still GI risk!

 If you have been given enteric-

coated prednisolone, swallow
these tablets whole. Do not chew
or crush them. You should avoid
taking indigestion remedies at the
same time as enteric-coated
prednisolone as these can
interfere with the special coating
on your tablets.

19 Amiodarone skin Amiodarone was stopped a month ago but Stay out of the sun
reaction patients been in sun and experienced very red Use high factor sunscreen
 skin. Photosensitivity known ADR of amiodarone. Has a long half –life so cause for weeks
Despite having discontinued, likely to be causing after discontinuation
the ADR as it has a long half-life (extending to
several weeks)

20 SSRI+ tramadol Increased risk of serotonin syndrome- Avoid both together, change tramadol
Increased risk of seizures. to different analgesic – see if patient has
tried codeine first
Other signs mental status, autonomic hyperactivity
(tachycardia, diarrhoea) and neuromuscular
abnormalities (hyperreflexia)

21 SSRI + NSAIDS Increased risk of GI bleeds Change NSAID

22 Paracetamol overdose Patient also on enzyme inducing – carbamazepine Use methionine if within 10-12 hours of
but hypersensitive to so high risk overdose and make sure patient isn’t
acetylcysteine vomiting!

23 Epileptic patient Ciprofloxacin = quinolone = lower the threshold of Change antibiotic

needing ciprofloxacin seizures
Also avoid NSAIDs with quinolones = can
also cause convulsions

24 NSTEMI 2 antiplatelet for 1 year (clopidogrel +

aspirin)

Also beta-blocker/ statin/ ACEI

GTN spray – 999

-spray under tongue wait 5 mins
- can do that up to 3 times and if pain
doesn’t go away = call 999 = suggests
further MI

Good luck in sha Allah it will be cool  Hira 