Problem solving

Question-1
[Link]. Ravi who was a chronic alcoholic voluntarily
opted for de-addiction. He was hospitalized and was
put on antabuse 500mg/day. 10days later when he was
allowed to go home for a brief visit in the evening, he
could not control himself and consumed alcohol.

[Link] signs and symptoms do you expect in this

patient?
[Link] is the underlying mechanism? Give
treatment.
[Link] 2 other drugs which cause antabuse
like reaction.
[Link] signs and symptoms do you expect in this
patient?

signs & symptoms of Disulfiram –alcohol

reactions(Aldehyde syndrome)
Flushing of the skin, Increase in heart rate,
shortness of breath, nausea, vomiting , severe
headache, Visual disturbances, mental confusion,
postural fainting & circulatory collapse, cardiac
arrest, coma and death.
[Link] is the underlying mechanism? Give treatment.

⚫ Disulfiram blocks the conversion of acetaldehyde to acetic

acid by blocking the enzyme acetaldehyde
dehydrogenase.
⚫ Resulting in aldehyde syndrome (accumulation of
acetaldehyde) which produces harmful effects
⚫ ALCOHOL---------alcoholdehydrogenase----
ACETALDEHYDE --- aldehyde dehydrogenase----
ACETATE + CO2
Treatment
Management Antabuse- alcohol reactions
⚫ Symptomatic and suppressive care is the mainstay in the
treatment of antabuse-alcohol reactions
⚫ Maintain airway.., and vitals
⚫ Treat hypotension with vasopressors like NE, Dopamine
(I.V)
[Link] 2 other drugs which cause Antabuse like
reactions or disulfiram like reaction

⚫ Metronidazole
⚫ 1st generation sulphonylureas- Tolbutamide
⚫ Cephalosporins- cefoperazone & cefotetan
⚫ Griseofulvin –antifungal drug
⚫ Chlorpropramide
Question.2
b. Mr. Joseph a known hypertensive for the past 5 years
was on Propranolol and hydrochlorothiazide. He was
put on digoxin 0.25 mg/day for the treatment of mild
CCF.

[Link] he developed severe bradycardia, which drug

interaction do you Suspect?
[Link] he developed ectopic beats and tachyarrhythmia,
which drug interaction do you suspect? Explain.
[Link] antihypertensive agent received by him might
reduce inotropic efficacy of digoxin? Explain.
[Link] he developed severe bradycardia, which drug
interaction do you Suspect?

• Digoxin belongs to the class of cardiac glycosides

Having positive inotropic and negative chrono tropic
effect .
• Propranolol belongs to class of beta blockers which are
competitive antagonist of catecholamine's and block the
β1 receptors in the heart
• Probable mechanism: combined use of β blockers like
Propranolol and digoxin may result in additive cardiac
effects like bradycardia both decrease the heart rate
2. If he developed ectopic beats and
tachyarrhythmia, which drug interaction do you
suspect? Explain.

Hydrochlorothiazide a thiazide diuretic can lower

blood potassium, sodium & magnesium levels. Low
potassium(Hypokalemia) and magnesium
levels(Hypomagnesemia) leads to ectopic beats and
abnormalities in heart rhythm, in patients taking
digoxin
[Link] antihypertensive agent received by him
might reduce inotropic efficacy of digoxin?
Explain.

⚫ β blockers reduced the inotropic effect of digoxin

because β blockers depress the cardiac properties
and are having negative inotropic effect
⚫ These drug have additive depressant effect on S-A
& A-V node.
Question-3
⚫ [Link] 30mg 4th hourly was given to a
patient suffering from myasthenia gravis. His
muscle strength was improved but he was having
excessive salivation, nasal stuffiness and
diarrhoea.

1. Give your comment.

2. Discuss further management.
1. Give your comment.

⚫ All the above symptoms are the muscarinic side effect of

Neostigmine.
⚫ Neostigmine belongs to the group of
anticholinesterases.
2. Discuss further management.

⚫ If muscarinic side effect become prominent

(during therapy with Neostigmine )
⚫ treatment can done with Atropine – 0.5 mg S.C
 Question-4

⚫ d. A patient suffering from Angina Pectoris was

prescribed warfarin 5mg daily and subsequently
tablet aspirin was also prescribed to control the
symptoms of Rheumatic joint pain. One week
later the patient was brought to casualty with
severe hematemesis
Questions:
⚫ 1. What is your explanation?
⚫ 2. Could it have been prevented?
⚫ 3. How will you treat the present emergency?
Answer:-
⚫ 1,Warfarin is an oral anticoagulant.
⚫ Aspirin is a NSAID & has anti-aggregatory action and Ulcer
producing action. Also aspirin displaces warfarin from the
plasmaprotein binding site,raises the level of warfarin.
⚫ Hence this combination precipitates hematemesis

⚫ 2,Other antiplatelet, Anti aggregatory drugs like clopidogel can

be suggested.
⚫ 3,Emergency Management
⚫ Stop oral ASPIRIN
⚫ Blood - for grouping and cross matching
⚫ Bleeding and clotting time
⚫ Relative blood donor is kept ready.
⚫ Infusion of FFP- two units
⚫ [Link] K 10mg IM for 3 days
⚫ Tab. clopidogel 75mg/day for 15 days
⚫ H2-Antagonist or
⚫ Cap. omeprazole 40mg BD for 6 months
 Question-5

⚫ e. A patient suffering from Depressive psychosis

was put on Tranylcypromine. After few days of
treatment, the patient took pickled meat and fish.
Next day his B.P. was 240/160 mmHg and when he
consulted his doctor, the doctor advised him not
to take pickled meat and fish.
⚫ Questions:
⚫ 1. What is the cause for sudden rise in B.P?
⚫ 2. How will you manage this condition?
⚫ [Link] of sudden rise in BP :
⚫ Sudden rise in BP is due to development of cheese
reaction (hypertensive crisis). It is an example of food
– drug interaction.
⚫ Tranylcypromine is a nonhydrazine MAO Inhibitor
which interact with Tyramine containing foods such as
Pickled meat & cheese & produces hypertensive crisis.
Tyramine is not degraded in liver, intestine which
causes release of neurotransmitters like adrenaline,
NA. This causes increase in BP.
⚫ [Link] :
⚫ First line of drug is Inj. Phentolamine 5 mg slow IV
bolus, repeated after 15 mins until BP is stabilized
⚫ Second line of drug is Inj. Sod. Nitroprusside 50mg
IV Infusion along with 500ml of 5% dextrose, dose
started with 0.5 – 10 mcg/kg/min
⚫ Third line of drug is Inj. Diazoxide 50 – 100 mg slow
IV bolus, repeated after 10 mins till BP is brought to
normal
⚫ Also Cap. Nifedipine (CCB) given sublingually
Problem solving
6.A patient suffering from Difficulty in walking, Excessive
salivation, fine tremor of fingers put on L-Dopa and
Benzhexol and subsequently by he was fairly relieved of his
symptoms. He took B-complex tonic to improve his general
health. Instead of improvement the symptoms were started
manifesting slowly.

Questions:
[Link] could be the initial diagnosis?
[Link] for recurrence of symptoms.
Vitamine tonic-[Pyridoxine (Vit.B6)]
⚫ Effects of levodopa is reduced or abolished by the concurrent use
of pyridoxine,

Mechanism: -Enhances peripheral decarboxylation of [Link]

DA decarboxylase ( periphery)→ (-) carbidopa

pyridoxi
ne

Levodopa DA
pyridoxal-5-phosphate(co
factor)

⚫ an increase in theL-Dopa
signseffects-reduced
and symptoms of parkinsonism
or abolished
1. What could be the initial diagnosis?
It could be Parkinsonisons disease

2. Reason for recurrence of symptoms?

a). The effects of levodopa are reduced or abolished
due to concurrent use of pyridoxine

The conversion of levodopa to dopamine within

the body requires the presence of
pyridoxal-5-phosphate (derived from
pyridoxine) as a co-factor. When he took
B-complex tonic containing pyridoxine, the
peripheral metabolism of levodopa is increased
so that less is available for entry into the CNS
and hence its effects are reduced accordingly. So
he will have recurrence of signs and symptoms
of parkinsonism
⚫ b). Small intestine is the major site of absorption for levodopa.
Anticholinergic drugs will produce delayed gastric
emptying due to GIT smooth muscle relaxation, so
peripheral conversion of levodopa to dopamine will be
more. This results in decreased absorption of [Link],
bioavailability & therapeutic failure.
⚫ 7. A patient suffering from Pernicious Anemia was
prescribed a tablet which contains Folic acid and
ferrous fumarate. When he was revived he
complained of weakness in the lower limbs
though he feels better on the whole.
⚫ Questions:
⚫ 1. What is the cause for his complaint?
⚫ 2. Discuss further treatment
⚫ 1. Cause :
⚫ The causes are due to deficiency of vitamin B12 and
intrinsic factor of castle
⚫ 2. Management :
⚫ [Link] / Vit. B12
⚫ - 1 mg IM daily for 7 days
⚫ - 1 mg IM weekly until normalization
of anemia
⚫ - Maintenance of 1 mg IM monthly for
life time
⚫ 8. After injecting succinylcholine IV to have
muscle relaxation, during a surgical procedure
the patient developed prolonged apnoea.

⚫ Questions:
⚫ What could be the probable cause?
⚫ Whether Edrophonium is suitable antidote?
⚫ What is the line of treatment you would suggest?
Answer:-
⚫ Probable cause of succinylcholine apnoea is due
to the absense of pseudocholineestrase or
presense of atypical pseudocholineestrase as
succinyl choline is metabolised by
pseudocholineestrase ,here in this case succinyl
choline is not metabolised patient not recovered
from anaesthesia or sufferering from apnoea.

⚫ Edrophonium does not inhibit plasma

cholinesterase.

⚫ Fresh blood transfusion.

9. A Schizophrenic patient put on long term therapy with
chlorpromazine developed pulmonary Tuberculosis for
which the patient was given short course therapy of
SM + INH, + RIFAMPICIN and PYRAZINAMIDE.
This patient subsequently complained of Nausea,
vomiting, loss of appetite and passing yellow coloured
urine.
Question:
[Link] could be the possible cause for these complaints?
[Link] is the future course of treatment?
 1. What could be the possible cause for these
complaints?
⚫ It could be drug-induced hepatitis

2. What is the future course of treatment?

✔For INH induced hepatitis:

RMP + PZA + ETB for 12 months.

✔For RMP induced hepatitis : INH + PZA+ETB for 12 months.

✔For both INH + RMP induced hepatitis :

PZA + ETB+ SM (or Ethionamide) + Ciprofloxacin (or ofloxacin
or levofloxacin), for 12-18 months.

✔For PZA : INH + RMP + ETB/ SM for 12 months.

⚫ 10. Inj. Triflupromazine was given to a patient
suffering from vomiting due to Acute Gastritis.
Next day the patient was brought with neck
Rigidity, Difficulty in speaking & Torticollis.
There was no other neurological deficit. (Page
no.109)
⚫ Question:
⚫ 1. What is the probable cause?
⚫ 2. How will you manage?
⚫
⚫ 1. Cause :
⚫ The neck rigidity is due to the extrapyramidal side
effects caused by the drug. It also causes muscle
dystonias, dyskinesias and parkinsonism
⚫ 2. Management :
⚫ Stop the anti emetic drug immediately
⚫ [Link] HCl 25 -50 mg by Oral
⚫ Inj. Benztropine (anticholinergics) 1 – 2 mg IV
PROBLEM SOLVING
 Question.1
11. Whenever the physician prescribes clonidine for
the patient of essential hypertension. He must
advise the patient not to stop treatment abruptly.

1. Why the doctor must advise so. Explain?

[Link] further management
• 1. Why the doctor must advise so. Explain?

• Sudden stoppage of clonidine causes

withdrawal syndrome, which is symptomised by
headache, nervousness, tachycardia, sweating ,
tremors, palpitation and rebound
hypertension.
❖ All these associated with increase level of
catecholamine's and is due to
▪ super sensitivity of α1 receptors
▪ Release of large amount of stored catecholamines in
synaptic cleft.
▪ Sudden stoppage clonidine produces rebound
hypertension due to supersensitivity of the newly
formed α1 receptors
[Link] further management

• Should not stop clonidine suddenly with out

consulting doctor
• Oral clonidine
• Sodium nitroprusside 20-300 µg/min
or
• Labetalol 50mg/5min till B.P is controlled
• Arteriolar + veno dilators
• Sod. Nitroprusside-nitrovaso dilator as it
release NO . Nitrosmoiety is active residue .
• Sod. Nitroprusside releases GC directly or
through NO .
• GC - -------- GTP -------cGMP ----- relaxation
• Dialates both A+V
12. A male executive aged 42 years is suffering from
angina pectoris. He is already on nitrates. A beta
adrenergic blocking drug is added to the treatment.
He is an asthmatic.

• Questions:

1. What is the justification for using beta blockers?

2. Which beta blocker should be selected? Why?

1
 Question:
1. What is the justification for using beta blockers?
• By↓ H.R, ↓ B.P and ↓ contractility of heart,(β1 R
action) thereby ↓ myocardial oxygen requirement
at rest and during exercise.
• Prevent exercise & stress precipitated arrhythmia
in angina pt.
• β-blockers reduces myocardial O2 demand and
afford additional benefit by reducing risk of
impending MI/sudden cardiac death.

2
2. Which beta blocker should be selected? Why?
Cardioselective β-Blockers(β1) like metoprolol ,
atenolol acebutolol, bisoprolol & nebivolol are more
preferable one.
These drugs are more potent in blocking cardiac (β1)
than bronchial (β2) receptors.
Nonselective beta-blockers.
• Non selective β-Blockers are Contraindicated in Variant
angina by Blocking β2-receptors which is present in
coronary blood vessels, produce unopposed
alpha-mediated coronary vasoconstriction → coronary
vasospasm & broncho constriction in patients with
COPD or asthma. due to Blocking β2-receptors at
bronchial smooth muscle. So cardio selective group of
β-Blockers are safer in asthmatic patient with angina
3
13. A field worker with a history of handling insecticides is
brought to the hospital with convulsions sweating and
laboured breathing. On examination pupils were pin
point, salivation++, and pulse rate 50/min and there
were rales and rhonchi all over the lungs.
Questions:
1. What is the probable diagnosis?
• Diagnosis
• Organo phosphorus Poisoning
2. What is the specific treatment for this
condition?
Specific Treatment
• Atropine 2 mg I.V every 10 minutes till
(Muscarinic symptoms lost)-dryness of mouth
dilatation of pupil achieved
• Pralidoxime-2gm I.V initially then 1 gm
repeated every 8hrs.
• In severe poisoning infusion of 500mg per
hour.
14. An obese diabetic women was on tolbutamide (SU)
therapy. On periodic estimation of her blood sugar to
assess the prognosis of the disease, it was also found
that her blood cholesterol was high. She was prescribed
clofibrate. Then she was complained of giddiness on
and off.

9
 Questions:
[Link] you reason out the likely cause for
her giddiness?
The cause for her giddiness is due to
hypoglycemia, induced by Tolbutamide.
Fibrates potentiate the effects of sulfonylureas
in diabetic patients by displacing the tolbutamide
from their protein bound site. So plasma level of
tolbutamide was increased and to cause
excessive lowering of plasma glucose levels in
this patient.
10
[Link] further management.
Being a obese, Type 2 DM with high blood cholesterol pt
Biguanide group of drug Metformin is a ideal choice of
drug.
Unlike SU, Biguanides cause little or no hypoglycaemia in
non diabetic subjects and even in diabetics episodes of
hypoglycaemia due to metformin are rare. Metformin is
reported to improve lipid profile as well in type 2
diabetics. Clofibrate can be given safely along with
metformin, no drug interaction have been seen in these 2
drugs.

11
15. MRS. Padmavathy aged 45 years was on
Phenytion 100mg tid for the past 2 years. Her
plasma Phenytion level was 15mcg/ml. She had
developed rheumatiod arthritis for which she
was given Phenylbutazone 100mg. tid after 5
days she developed ataxia, nystagmus and
macular rash on the skin her plasma Phenytoin
level was 30mcg/ml.
• Question:
• 1. Explain this and suggest further treatment.
• 1. Explanation
• This is a pharmacokinetic type of drug interactions
between Phenytoin and Phenylbutazone
• Phenytoin is an antiepileptic drug having high
affinity to bind with plasma proteins
• Phenylbutazone is a NSAID given for treatment of
Rheumatoid arthritis also having high plasma
protein binding capacity. It displaces Phenytoin
from plasma binding site and increases the
Phenytoin concentration in plasma / body
• Ataxia, nystagmus and macular rash on the skin
are all due to increased level of free Phenytoin in
plasma
• Treatment
• Stop Phenylbutazone immediately
• Start with other analgesic drugs like Etoricoxib
60 mg 1 OD (or) Diclofenac 50 mg BD
16. A male patient aged 35 years was suffering from
polyuria due to diabetes insipidus. For that he
consulted the doctor, the doctor prescribed
chlorothiazide diuretic to him.
Questions:
• 1. Is the treatment justified?
• 2. If so, why? If not, explain?
Answer
• Treatment is justified
• In Nephrogenic diabetic insipidus ,low sodium
diet and thiazide diuretics can be given.