Clinical Problem 1:
Mr.X suffering from schizophrenia was given [Link] 100mg. After 10 days he
developed muscle rigidity and tremor. The patient was assured and advised to take T.
Levodopa 250 mg twice daily.
In this scenario:
1. what are his reason symptoms suggestive of?
2. Mention the drugs which can induce parkinsonism.
3. Is Levodopa indicated to this patient?
4. Outline the management and the rationale for the drug chosen?
Answer:
1. Symptoms are suggestive of drug induced parkinsonism as Mr X has developed
extrapyramidal motor Side Effects due to D2 receptor blocking property of
chlorpromazine.
2. Metoclopramide, fluphenazine, prochlorperazine, haloperidol, chlorpromazine
can induce parkinsonism.
3. Levodopa is not indicated to this patient (schizophrenia) as it is not effective
since D2 receptors are blocked.
4. An atypical antipsychotic should be used in this case as parkinsonian symptoms
are less. Centrally acting anticholinergics are the only drugs effective in drug
induced parkinsonism. They act by reducing the unbalanced cholinergic activity
in the striatum of parkinsonian patients.
Clinical Problem 2:
[Link], 44 year old male was on tablet warfarin 5mg for DVT prophylaxis. One day
he developed severe chest pain. He was diagnosed with acute MI, underwent
appropriate treatment, and was discharged. He was advised to take following
medicines as combination therapy.
• T Aspirin 75 mg OD
• [Link] 25 mg OD
• [Link] 150 mg BD
• [Link] mononitrate 5mg OD
• [Link] E 400mg OD
In addition to these drugs, he had to continue warfarin. After few days he developed
haematuria.
[Link] is the reason for haematuria?
[Link] 2 drugs which produce similar effects.
[Link] is the mechanism of action of warfarin?
[Link] are the uses of anticoagulants?
Answer:
1. Aspirin produces hypoprothrombinemia & displaces warfarin from plasma
protein binding. Excess warfarin leads to extension of pharmacological actions
causing bleeding hematuria.
2. Cefaperazone, cefomandole, erythromycin, celecoxib, cimetidine,
metronidazole.
3. Warfarin inhibits synthesis of vitamin K dependent clotting factors. (II,VII,IX,X)
4. DVT, pulmonary embolism, MI, unstable angina, rheumatic heart disease,
prosthetic heart valves, atrial fibrillation.
Clinical Problem 3:
A 30 year old sales manager was on treatment for intestinal amoebiasis with
[Link]. He attended a party and consumed alcohol. Suddenly he developed
Nausea, vomiting, giddiness, sweating, chest pain, headache and flushing. ECG was
normal; BP-100/70 mm Hg.
In this scenario:
1. what is the reaction called?
2. what could have been the cause?
3. Name Other Drugs producing similar effects?
4. Name drugs used in aversion technique of chronic alcoholism.
Answer:
1. Disulfiram-like reaction.
2. Metronidazole inhibits aldehyde [Link] is metabolized to
[Link] to enzyme inhibition, acetaldehyde (toxic metabolite)
[Link] acetaldehyde causes Nausea, vomiting, Flushing,
Sweating, Giddiness, Headache, Chest pain, [Link], alcohol intake
during metronidazole therapy leads to disulfiram-like reaction.
3. Disulfiram, Tinidazole, Ornidazole, Secnidazole, Cefoperazone, Cefotetan,
Chlorpropamide, Procarbazine, Griseofulvin.
4. Disulfiram, Naltrexone, Acamprosate.
Clinical Problem 4:
Mr. Rajesh, 45 year old male, a known peptic ulcer patient developed severe headache.
He went to a medical shop and asked for medicine to relieve his headache. The
pharmacist gave him a tablet and his headache resolved, but he developed severe
epigastric pain and vomiting which was blood stained.
In this scenario:
1. [Link] could be the reason for hematemesis?
2. what is the role of prostaglandins in peptic ulcer?
3. [Link] the PG analogues used in peptic ulcer.
4. Write 2 other uses of prostaglandins.
Answer:
1. The pharmacist most likely gave an NSAID (e.g., aspirin, ibuprofen, diclofenac) for
headache.
In a known peptic ulcer patient, NSAIDs:
Inhibit COX-1 → ↓ prostaglandin synthesis
Reduce gastric mucus and bicarbonate secretion
Increase gastric acid–mediated mucosal injury
This leads to erosion of gastric/duodenal mucosa → bleeding →
hematemesis.
2. Prostaglandins (mainly PGE2 and PGI2) have a protective role in the gastric
mucosa:
• ↑ Secretion of mucus and bicarbonate
• ↓ Gastric acid secretion
• ↑ Mucosal blood flow
• Promote epithelial regeneration
Thus, prostaglandins maintain gastric mucosal integrity and prevent ulcers.
3. Misoprostol (PGE1 analogue) – especially useful in NSAID-induced ulcers
4. uses of prostaglandins:
Induction of labor / cervical ripening (Dinoprostone, Misoprostol)
Medical termination of pregnancy
Prevention of postpartum hemorrhage (Misoprostol)
Glaucoma (Latanoprost, Travoprost)
Maintenance of patent ductus arteriosus (Alprostadil – PGE1)
Clinical Problem 5:
[Link] a known diabetic was on treatment for diabetes mellitus with Tab.
Glibenclamide 5mg OD. He developed UTI and a nearby physician prescribed Tab.
cotrimoxazole. He took the drug and suddenly developed giddiness, behavioral
changes, confusion, fatigue, palpitation.
In this scenario:
1. what were the symptoms due to?
2. what are the advantages of metformin?
3. Name 2 DPP4 inhibitor?
4. what is Acarbose? How it should be taken?
Answer:
1. The symptoms are due to hypoglycemia.
Reason:
Glibenclamide (sulfonylurea) causes insulin release → risk of hypoglycemia
Cotrimoxazole inhibits hepatic metabolism of sulfonylureas. This potentiates
glibenclamide action, leading to severe hypoglycemia.
Symptoms of hypoglycemia:
Giddiness, confusion, behavioral changes, Fatigue, palpitations
Sweating, tremors (may also occur)
2. Advantages of metformin:
Does not cause hypoglycemia
Causes weight loss / weight neutral
Improves insulin sensitivity
Decreases hepatic gluconeogenesis
Reduces cardiovascular risk
Useful in obese type 2 diabetic patients
3. Sitagliptin, Vildagliptin
4. Acarbose is an α-glucosidase inhibitor, 50 -100mg is taken at the beginning of the
three major meals because it inhibits intestinal α-glucosidase enzymes & delays
carbohydrate digestion, thereby reducing post-prandial hyperglycemia.
Clinical Problem 6:
A 25 years old unmarried female presented to the clinic with excessive tiredness, loss
of appetite and excessive hair fall. On examination: pallor, spooning of nails and
geographic tongue were noted. Lab test revealed the following: Hb – 8.8 g/dL; RBC –
hypochromic & microcytic; Serum iron & ferritin levels – low; Total iron binding
capacity – elevated. She was diagnosed as iron deficiency anemia and was prescribed
syrup FERRIC HYDROXY POLYMALTOSE (50 mg/5 ml) 5 ml early morning on empty
stomach. After 1 month, she returned with the complaints of non-improvement in her
old symptoms and in addition she developed blackening of teeth and upper abdominal
pain. She was now prescribed Tab. FERROUS SULPHATE 200 mg TDS & Cap.
OMEPRAZOLE 20 mg b.d.
In this scenario:
1. What is the reason(s) for non-improvement in her symptoms?
2. What is the alternative step that can be taken to improve her old symptoms?
3. Why did she develop blackening of tongue and how could it have been avoided?
4. Is parenteral iron indicated in this patient? Explain with reason(s).
5. Comment about the role of Cap. OMEPRAZOLE in this scenario.
Answer:
1. Though ferric hydroxy polymaltose has high iron content with no metallic taste,
the bioavailability of iron in this preparation is low in humans as the complex
releases little free iron. Ferrous salts are better absorbed than ferric salts (as
divalent transport in mucosa transports divalent ion – ferrous). The
recommended dose of oral iron therapy is 150 – 200 mg of elemental iron daily.
Hence the iron delivered by the syrup is 50 mg which too low to correct the
anemia.
2. Different oral iron preparations having ferrous salt like ferrous sulfate or ferrous
succinate with correct required dose can be prescribed.
3. Iron in the syrup formulation can cause staining of tongue and teeth leading to
the blackening of tongue. The iron syrup taken with straw can avoid the above
side effects.
4. Parenteral iron is required if patients has oral iron intolerance, severe anemia
(Hb < 6 g/dL) and in hemodialysis. In this setting, the oral iron intolerance is due
to incorrect advice (taking iron syrup on empty stomach). Moreover, the anemia
is mild. Hence parenteral iron is not indicated for this patient.
5. Omeprazole was prescribed as the patient developed gastritis due to intake of
iron syrup in the empty stomach. Simple advice like taking iron preparation along
with food will prevent the development of gastritis. Also omeprazole may reduce
the bioavailability of iron and hence it can be avoided.
Clinical Problem 7:
A 26 year old married female, weighing 65 kg, on the second month of continuation
phase of anti-tuberculosis treatment was brought to the hospital by her husband. She
was now on T. RIFAMPICIN 600 mg and T. ISONIAZID 600 mg thrice weekly. Since the
couple wishes to have a child in near future, they asked the village health nurse about
the risks and benefits. The village health nurse advised to follow contraception for next
6 months and she advised her low dose combined oral contraceptive pills (Ethinyl
estradiol 20 mcg + Desogestrel 0.15 mg). One month later she presented to the clinic
with complaints of missed periods. Despite taking OCP daily on regular time period, she
has become pregnant.
In this scenario:
1. What is/are the reason(s) for the failure of contraception? How could it have
been avoided?
2. Why did the village health nurse advise contraception?
3. What are the contra indications for combined oral contraceptive pills?
4. What is the ideal/preferable method of contraception in this scenario?
Answer:
1. The failure of contraception in this scenario is due to pharmacokinetic interaction
between rifampicin and OCP. Ethinyl estradiol is mainly inactivated by CYP3A4
into 2-hydroxycatechol by hydroxylation. Rifampicin is a potent inducer of
CYP3A4 enzyme and hence ethinyl estradiol is metabolized/inactivated in higher
rate leading to the failure of contraception. This interaction should have been
foreseen and an alternative choice of contraception should have been provided.
2. ATT induced teratogenicity is a known complication of ATT therapy in pregnant
women. Hence patient taking ATT should use suitable contraceptive measures.
3. OCPS are contraindicated in the following conditions:
a. Absolute contra-indication:
i. Porphyria
ii. Active liver disease
iii. Malignancy of breast/genitals
iv. Severe hypertension
b. Relative contra-indication:
i. Migraine
ii. Gall bladder disease
iii. Obesity and diabetes
iv. Smoker
4. The preferable contraception in this setting would be barrier method
(male/female or both to decrease the failure of contraception)
Clinical Problem 8:
Mr. Rangan, 40 years of age presented to the emergency after having sustained a snake
bite at his left calf at 3 AM. He presented to the casualty at 5 AM after getting treated
by a local unqualified person who made 8 cm X 0.25 cm incision over the calf and tied
his left thigh tightly with a nylon rope. His left leg was swollen, bluish in color and he
was in severe pain. The patient has a clotting time of 23 minutes. He also brought the
body of the snake as its head was crushed by the patient during the incident. He was
then administered anti-snake venom and he developed itching, swelling of lips and
difficulty in breathing.
In this Scenario:
1. Is the emergency treatment made by the local person correct? Justify
2. Is the identification of the type of snake essential for treatment? Justify.
3. What are the indications of ASV in snake bite?
4. Why did he develop the above symptoms after ASV administration and how will
you manage further?
Answer:
1. The emergency measures taken by the local person were INCORRECT. Making
incision over the bitten area and bloodletting are proven as ineffective measures
in delaying the absorption of snake venom and it can increase the risk of
[Link] the limb tightly will reduce the arterial supply and hence may
increase the chances of gangrene of limb.
2. Yes. In India, the drug used for all snake bite is anti-snake venom which is a
mixture of antibodies against venom of four snakes (Common cobra, common
krait, Russell’s viper and saw scaled viper). Though the drug administered is same
for all snake bite, complications in snake bite differs with the type of
venom/snake. Cobra and krait venom is predominantly neurotoxic while viper
venom is predominantly hemo-toxic. Hence to foresee the complication and
monitoring, identification of snake is essential for the management of snake bite.
3. The following are the indications of ASV:
a. Evidence of coagulopathy (Clotting time > 20 minutes, visible spontaneous
bleeding)
b. Evidence of neurotoxicity (ptosis, neck muscle paralysis)
c. Severe local swelling (involvement of more than half of the bitten limb)
d. Rapid extensions of swelling
e. Presence of cardiac abnormalities
4. ASV is biochemically a foreign serum (antibodies against the venom) and hence
can cause anaphylaxis. If patient develop anaphylaxis, he must be treated with
0.5 mg adrenaline i.m + 100 mg hydrocortisone i.v + pheniramine 22.5 mg i.v.
ASV should be continued after stabilization of the patient at the earliest.
Clinical Problem 9:
A junior resident of general surgery got needle stick injury while suturing a laceration in
a 35 year old male who was brought to casualty due to minor road traffic accident. The
needle stick injury was over his left thumb about 2 – 3 mm depth. As the patient had
generalized lymphadenopathy, the patient was tested for HIV. The investigation
showed that he is positive for HIV – RNA (low titre) and his CD4 count is high. The
patient was not under any medication. The junior resident was started with the post
exposure prophylactic (PEP) regimen for HIV. After 3 weeks, the junior resident
developed frequent fever and fatigue. His neutrophil count was 820 cells /mm 3&
hemoglobin was 8 g/dL.
In this scenario:
1. What are the criteria to start post exposure prophylaxis in a health care worker?
2. What are the different types of regimen available in PEP for HIV? Explain.
3. What is the recommended duration of PEP therapy for this junior resident?
Justify.
4. Why did the junior resident develop frequent fever and fatigue? Explain with
reason(s).
Answer:
1. The criteria to start PEP in a health care worker are as following:
a. Accidental needle stick injury or by other sharp instruments from a HIV
positive patient
b. Direct contact with biological fluids or blood transfusion from a HIV
positive patient
2. The different regimen available for PEP are:
a. Basic two drug regimen for low risk exposure
(Zidovudine 300 mg + Lamivudine 150 mg) twice daily for 4 weeks
b. Extended three drug regimen for high risk exposure
(Zidovudine 300 mg + Lamivudine 150 mg) twice daily for 4 weeks
and Indinavir 800 mg thrice daily for 4 weeks.
3. Junior resident requires treatment for basic two drug regimen of PEP for 4
weeks. It should be ideally initiated within 2 hours but certainly within 72 hours.
As the injury sustained by the junior resident is minor and patient’s viral load is
low, the risk of exposure is low. Basic two drug regimen is recommended for low
risk exposure.
4. Bone marrow suppression is the most serious adverse effect caused by
zidovudine. Frequent fever and decreased neutrophil count suggests neutropenia
by zidovudine. Neutropenia with anemia suggests bone marrow depression by
zidovudine. Stavudine 30 mg twice daily can be given instead of zidovudine.
Clinical problem 10:
Mr. Ramu, 56 year obese old male, a known case of ischemic heart disease (IHD) came
to the clinic with complaints of frequent urination and loss of weight and excessive
tiredness. On investigation, his fasting blood glucose was 190 mg/dL and post prandial
was 280 mg/dL. His HbA1C was 8 %. He was prescribed T. GLIMEPIRIDE 2 mg BD for one
month. He was already on [Link] 20 mg BD, T. ATORVASTATIN 10 mg HS and
T. ASPIRIN 150 mg OD for IHD. After 2 weeks he was brought to the casualty in
unconscious state and RBS was 40 mg/dL. He was treated with intravenous dextrose.
In this scenario:
1. What is the probable reason for the sudden development of hypoglycemic
shock?
2. What is/are the symptoms of hypoglycemia?
3. Why did this patient not perceive the symptoms of hypoglycemia? Explain with
reason(s).
4. What are the steps need to be taken to prevent the hypoglycemic shock in this
patient in future? What is the modification to be done in the drugs prescribed for
him?
Answer:
1. The most common adverse effect of glimepiride is hypoglycemia. Being insulin
secretagogues, glimepiride often causes hypoglycemia due to excessive insulin
release or when patient takes inadequate meals. Here the starting dose of
glimepiride is high and hence it could be the probable reason for hypoglycemia.
2. Sweating, tremors, palpitations, irritability, dizziness, headache and muscular
incoordination (neuroglucopenic symptoms) are the symptoms of hypoglycemia.
3. Reflex sympathetic stimulation occurs usually in hypoglycemia leading to release
of adrenaline and noradrenaline. In liver, this will increase glycogenolysis and
prevents glycolysis to maintain blood glucose level from decreasing. Propranolol
is a non specific beta blocker and can block the tachycardia, sweating and
tremors produced by adrenaline in hypoglycemia. Hence the patient did not
perceive the symptoms.
4. Patient should be instructed to have a candy always and take as soon he
perceives the symptoms of hypoglycemia. The dose of glimepiride should be
adjusted to 1 mg OD. Propranolol should be replaced with selective cardiac beta
blockers like atenolol 25 mg OD or beta blockers with intrinsic agonist activity
like acebutalol 200 mg BD. Acebutalol had no negative impact on serum glucose
and lipids.
Clinical problem 11:
Rekha, a 6 years old female child weighing 20 kg, was brought to the clinic by her
mother with complaints of 8 episodes of vomiting since morning. She was given
injection METOCLOPRAMIDE 10 mg i.v for vomiting. After 15 minutes, the child was
rushed to the clinic as she developed tongue thrusting with deviation of neck to her left
side and not responding to vocal stimuli properly. Her mother was very anxious. The
child was again given INJECTION X and the symptoms subsided.
In this scenario:
1. Why did the child develop these symptoms after the injection and what is it
called as?
2. What is the mechanism behind the development of these symptoms?
3. What is INJECTION X?
4. Comment about the role of INJECTION X in this scenario.
Answer:
1. The child developed the above mentioned symptoms due to metoclopramide
injection. These symptoms are called as acute muscular dystonia.
2. Metoclopramide is a dopamine receptor antagonist and can cross blood brain
barrier. Hence blockade of D2 receptors in extra pyramidal tract can cause acute
muscular dystonia often especially when metoclopramide is administered
intravenously.
3. Injection X could be an anti-histaminic drug with predominant central anti-
cholinergic action. Injection promethazine 30 mg is commonly used in this
scenario.
4. Promethazine has both anti-histaminic and anti-cholinergic property. The central
anti-cholinergic action reverses the acute muscular dystonia effectively.