Mastering the INI-CET demands a strategic approach to preparation, with an emphasis on high-yield topics proving to be a successful tactic. This blog zeroes in on exactly that – a curated list of high-yield questions in pharmacology that are highly likely to appear on the INI-CET. By acquainting yourself with these questions and their detailed explanations, you'll deepen your understanding of Pharmacology concepts, enhancing your confidence and readiness for exam day.
1. A 16-year-old girl with breathing issues was given IV corticosteroids. Looking at the plasma concentration-time graph of the drug, what's true about its kinetics?
A. Half-life is less at low concentrations and more at high concentrations
B. Most drugs follow zero-order kinetics
C. Clearance is less at low concentrations
D. The rate of elimination is proportional to plasma concentration
Correct Option D - The rate of elimination is proportional to plasma concentration:
The corticosteroids follow first-order kinetics. In this kinetics, the rate of elimination is proportional to the plasma concentration.
In zero-order kinetics, the rate of metabolism remains constant and is independent of the plasma concentration of a drug at a steady state.
In first-order kinetics, the rate of metabolism is directly proportional to the plasma concentration of the drug.
Incorrect Options:
Option A - Half-life is less at low concentrations and more at high concentrations:
The corticosteroids follow first-order kinetics
In first-order kinetics, half-life remains constant.
Option B - Most drugs follow zero-order kinetics:
Most of the drugs follow first-order kinetics.
There are very few drugs that follow zero-order kinetics, such as aspirin, warfarin, theophylline, phenytoin and tolbutamide.
Option C -Clearance is less at low concentrations:
In first-order kinetics, clearance remains constant.
In zero-order kinetics, clearance is more at low and less at high concentrations.
2. Which of the following statements about the given plasma concentration curve is correct?
A. Tmax of the drug is 3 hours
B. The Cmax of the drug in this graph is 100 mg/dl
C. The area under the curve is the extent of absorption
D. The graph can be used to calculate ED50
Correct Option C - The area under the curve tells the extent of absorption:
The graph shown in the image above is a graded dose-response curve.
The area under the curve (AUC) is bioavailability. It tells us about the extent of absorption.
Incorrect Options:
Option A - Tmax of the drug is 3 hours:
Tmax is the time required to attain Cmax (Maximum Concentration).
It is 2 hours in the graph involved in this case.
It describes about the rate of absorption.
Option B - The Cmax of the drug in this graph is 100 mg/dl:
Cmax is the maximum concentration obtained with a particular dose.
It is 120 mg/dL in the given graph
Option D - The graph can be used to calculate ED50:
The graph involved in this case is a graded dose-response curve.
ED50 and LD50 are calculated from the quantal dose-response curve.
3. A young 22-year-old male presents in an outpatient clinic with the complaint of cough and difficulty breathing while lying down; He was stung by a scorpion while camping. He is diagnosed with hypertension and pulmonaryedema due to a scorpion sting. This patient can be best managed by?
A. Carvedilol
B. Prazosin
C. Spironolactone
D. Phentolamine
Option B: Prazosin
Scorpion stings cause excessive stimulation of alpha-1 receptors.
Of the above-mentioned drugs, Prazosin acts by blocking alpha-1 receptors.
Therefore the drug of choice for a Scorpionsting is Prazosin.
It is a sympatholytic drug.
Option A: Carvedilol
Carvedilol is a non-selective β-antagonist that also blocks alpha adrenoreceptors, but it is not a drug of choice in case of a scorpion sting.
Option C: Spironolactone
Spironolactone is a direct antagonist of aldosterone, thereby preventing salt retention, myocardial hypertrophy and Hypokalemia.
Option D: Phentolamine
Phentolamine produces a competitive block of alpha-1 and alpha-2 receptors but is not an appropriate choice in the case of scorpionsting since it only needs an alpha1 receptorblocking agent.
4. A 55-year-old male presents to the clinic for a follow-up visit. On examination, his blood pressure is 170/110 mmHg and bilateralpittingedema is noted. Medication history includes digoxin. The physician prescribes a drug to control blood pressure and prevent digoxin toxicity. Identify the drug?
Hydrochlorothiazide
Amiloride
Spironolactone
Furosemide
Option B: Amiloride
The drug is amiloride.
Amiloride and triamterene are K+-sparing diuretics that act by inhibiting epithelial Na+ channels.
In the distal tubules and collecting ducts, three separate channels are present (one for Na+, K+ and H+ each). Aldosterone acts on the distalconvolutedtubule (DCT) and collecting duct (CD) to cause reabsorption of Na+.
This generates a lumen negative potential difference across the membrane of this part of the nephron. To maintain electrical neutrality, K+ and H+ are secreted in the lumen.
When amiloride and triamtereneinhibit epithelial Na+ channels, the transepithelial potential difference is not generated, and therefore, K+ and H+ are not secreted in the lumen.
Thus due to more retention of K+, amiloride may avoid hypokalemia which can precipitatedigoxin toxicity.
Option A: Hydrochlorothiazide
Inhibit NaCl reabsorption in early distalconvoluted tubules.
Thiazide diuretics deliver a high luminal sodium load with a resulting physiologicalsecretion of potassium, thus causing hypokalemia which can precipitatedigoxin toxicity.
Option C: Spironolactone
The main function of aldosterone is to secretepotassium into the urine.
Spironolactone is an aldosterone antagonist.
It decreases the secretion of potassium by antagonizing aldosterone, thus increasing serum potassium.
Though it increases serumpotassium levels, it does not act on electrogenicluminal sodium channels.
Option D: Furosemide
Furosemide inhibits the cotransport system (Na+/K+/2Cl-) of the thick ascending loop of Henle.
Therefore, it enhances the secretion of sodium, potassium and chloride and causes hypokalemia.
5. A 23-year-old female presents to the clinic requesting for effective oral contraceptives. The patient is vitally stable, but lab analysis show decreased haemoglobin concentration. She is sexually active with multiple partners. The tablets that were prescribed are shown below:
Which of the following is most likely associated with the pills mentioned above?
Monophasic pill
Diphasic pill
Triphasic pill
Progestogen-only pills
Correct Option C - Triphasic pill:
Triphasic oral contraceptive pills contain three different doses of hormones (estrogen and progestin) over the course of a 28-day pill pack.
These pills mimic the natural hormonal fluctuations of a woman's menstrual cycle more closely than monophasic or biphasic pills.
The three phases typically consist of seven days of low-dose estrogen, followed by seven days of increasing estrogen and progestin, and finally, seven days of the highest doses of both hormones.
This variation in hormone levels aims to reduce side effects and provide better cycle control.
Incorrect Options:
Option A - Monophasic pill:
Monophasic pills contain a constant dose of hormones throughout the entire pill pack.
They do not mimic the natural hormonal fluctuations of the menstrual cycle as closely as triphasic pills.
Option B - Diphasic pill:
Biphasic pills contain two different doses of hormones over the course of a 28-day pill pack.
These pills have a lower hormone dose in the first half of the cycle and a higher dose in the second half.
Option D - Progestogen-only pills:
Progestogen-only pills, also known as mini-pills, contain only progestin and no estrogen.
They are often prescribed to women who cannot tolerate estrogen-containing contraceptives due to medical reasons.
Progestogen-only pills are taken continuously without a pill-free interval.
6. A 66-year-old female has been diagnosed with osteoporosis. The drug X has been prescribed for it. Its mechanism of action is shown in the figure below?
Which of the following is most likely drug" X"?
Teriparatide
Alendronate
Denosumab
Estrogen
Correct Option C - Denosumab:
The most likely drug is denosumab
Denosumab is a drug primarily targeting RANKL, a protein crucial for bone resorption.
Overexpression of RANKL can lead to bone loss by overwhelming the body's natural bone density maintenance mechanisms.
Denosumab prevents RANKL from activating its receptor, RANK, on osteoclasts and their precursors.
By inhibiting the RANKL/RANK interaction, Denosumab reduces osteoclast formation, function, and survival, thus decreasing bone resorption and increasing bone mass and strength.
Indications for Denosumab include:
Treatment of postmenopausal women with osteoporosis at high risk for fractures.
Reduction of vertebral, nonvertebral, and hip fracture incidences.
Increasing bone mass in women receiving adjuvantaromataseinhibitor therapy for breast cancer.
Treatment for men with osteoporosis at high fracture risk or those receiving androgendeprivation therapy for nonmetastatic prostate cancer to increase bone mass.
Incorrect Options:
Option A - Teriparatide:
Teriparatide is a PTH analogue.
It does not work through the RANK receptor.
It increases bone mineral density by increasing osteoblastic activity.
Option B - Alendronate
Alendronate is a bisphosphonate.
It resembles hydroxyapatite and works by inhibiting osteoclastic activity.
Option D - Estrogen
Estrogen helps maintain bone density mainly by reducing bone resorption. It decreases osteoclastogenesis and increases the apoptosis of osteoclasts. Estrogen promotes osteoprotegerin synthesis.
Promoting osteoprotegerinsynthesis suppresses the RANK-L to receptor interaction and thus stops osteoclast activation.
7. The figure shows the mechanism of action of which of the following drugs?
Nilotinib
Methotrexate
Pertuzumab
Cisplatin
Option A: Nilotinib
The image shows the mechanism of a drug that inhibits tyrosine kinase.
Targeted tyrosine kinase inhibitors are first-line therapy for CML.
Tyrosine kinase activated by ABL-BCR fusion results in CML.
This enzyme can be inhibited by
Bosutinib
Imatinib
Nilotinib
Dasatinib
Ponatinib
Option B: Methotrexate
A drug that competitively inhibits dihydrofolate reductase and AICAR transformylase.
Primarily used as an antineoplastic agent, immunosuppressant, and DMARD.
Option C: Pertuzumab
It is an antineoplastic agent and humanized anti-human epidermal growth factorreceptor (HER/neu) type 2.
It is a monoclonal antibody.
It is used for the treatment of breast cancer.
Option D: Cisplatin
It is a platinum-based alkylating agent that prevents the replication of tumour cells by causing intrastrand links between DNA.
It is used for the treatment of many cancers including ovarian, bladder and testicular tumours.
It can cause nephrotoxicity and ototoxicity.
8. A 45-year-old man came to the OPD with knee and shoulder joint pain. After diagnosis and starting methotrexate, his arthritis persisted. The physician considers adding another DMARDtargetingdihydroorotate dehydrogenase. Which drug is being considered?
Sulfasalazine
Infliximab
Leflunomide
Abatacept
Option C: Leflunomide
Leflunomide is an immunomodulator
It rapidly converts into an active metabolite that inhibits Dihydro-orotate dehydrogenase and pyrimidinesynthesisin actively dividing cells.
It is one of the disease-modifying agents used in rheumatoid arthritis
It inhibits the proliferation of stimulated lymphocytes and helps suppress the arthritic symptoms and radiological progression of the disease. Also, the antibody production by the B-cells may be depressed
Adverse effects include diarrhoea, headache, nausea, rashes, loss of hair, thrombocytopenia, leucopenia, increased chances of chest infection and raised hepatic transaminases
Not to be used in children and pregnant/lactating women.
Leflunomide can serve as an alternative to or be combined with Methotrexate, although the combined use is associated with increased hepatotoxicity. The addition of sulfasalazine enhances the overall therapeutic benefits.
Option A: Sulfasalazine
It has a therapeutic effect on rheumatoid arthritis
It consists of 5-aminosalicylic acid (5-ASA) with sulfapyridinelinked through an azo bond split by colonic bacteria to release 5-ASA and sulfapyridine.
5-ASA exerts a local anti-inflammatory effect by inhibiting COX and LOX, decreased prostaglandin and leukotriene production plays some role in therapeutic effects; the major contribution is inhibiting cytokine, platelet-activating factor, TNF-alpha and NFκB.
Option B: Infliximab
Can be used if non-biological DMARDs are not reducing symptoms of rheumatoid arthritis.
Infliximab is an anti-TNF antibodyindicated in rheumatoid arthritis
It is a costly drug
Option D: Abatacept
It is used in severe active rheumatoidarthritis that does not respond to methotrexate.
Abatacept is a Selective T-cell costimulation Blocker. It is a recombinant fusion protein that combines part of the Fc domain of human IgG with the extracellular domain of the T-cell inhibitoryreceptor CTLA4.
Binding to CD80 and CD86 molecules prevents the second signal for the costimulation of T-cells.
9. A 38-year-old woman with rheumatoidarthritis presents for a follow-up, complaining of hand pain and 2-hour morning stiffness. She's on methotrexate, sulfasalazine, and leflunomide. Her vital signs are normal.
Upadacitinib
Fedratinib
Entrectinib
Talazoparib
Option A: Upadacitinib
It is an oral Janus-associated kinase inhibitor.
Upadacitinib exhibits a more selective and pronounced inhibitory effect on JAK 1 than on JAK 2 and 3.
It is one of the disease-modifying anti-rheumatoid drugs (DMARDs).
It is used for rheumatoid arthritis to slow down the disease progression.
Contraindicated in people with active tuberculosis and other severe infections, severe liver impairment (Child–Pugh score C), and during pregnancy.
Ketoconazole, itraconazole, or clarithromycin, increase upadacitinib concentrations in the body by inhibiting the liver enzyme CYP3A4.
Option B: Fedratinib
It is an oral JAK-2 inhibitor used to treat myelofibrosis.
It is not approved for treating rheumatoid arthritis.
Option C: Entrectinib
It is an oral tyrosine kinaseinhibitor for ROS-1-positive non-small cell lung cancer and Neurotrophic Tyrosine ReceptorKinase(NTRK)-positive solid tumours.
It is not approved for treating rheumatoid arthritis.
Option D: Talazoparib
It is a poly-ADP ribosepolymerase (PARP) inhibitor.
It is used for treating breast cancer.
10. A 24-year-old woman has a throbbing headache, nausea, vomiting, and subsequent tingling, numbness, and blue discoloration of a finger tip. Which drug is most likely responsible for these symptoms?
A.Dihydroergotamine
B. Sumatriptan
C. Aspirin
D. Butorphanol
Option A: Dihydroergotamine
Dihydroergotamine is a potent vasoconstrictor and causes ischemia as an adverse effect.
Mechanism of action:
Dihydroergotamine is formed through the hydrogenation of ergotamine.
Serotonergic and alpha-adrenergic agonist actions are reduced, while alphareceptorblocking property is enhanced.
Uses:
Used for acutemigraine attacks.
Adverse effects:
Common side effects include nausea, vomiting, abdominal pain, muscle cramps, weakness, paresthesias.
Vascular spasms of coronary and other vessels can cause chest pain, myocardial ischemic disease, and worsen peripheralvascular disease.
Sumatriptan is a vasoconstrictor which can result in limb paresthesia, weakness and coronary vasospasm.
However, these are infrequent side effects and are short lasting.
Ergot derivates are more likely to cause these symptoms. due to their broader spectrum of vasoconstrictive effects
Option C: Aspirin
Aspirin inhibits the enzymes COX-1 and COX-2 leading to inhibition of prostaglandin synthesis.
Inhibition of the thromboxane A2 synthesis leads to increased bleeding time from impaired platelet aggregation.
However, it does not cause vasoconstriction of peripheral vessels and does not cause ischemic vascular disease.
Option D: Butorphanol
It is an opioid κ receptoragonist that works as an analgesic and causes nausea, sedation, respiratory depression and cardiac stimulation.
It should be avoided in patients with cardiac ischemia.
It has no effects on the peripheral vessels leading to ischemic disease
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