30 - PGI december 2003 pharmacology mcqs

note : questions can have multiple answers .

1q: side effects of timolol maleate ?

1. asthma
2. depression
3. tachycardia
4. hypotension
5. hypertension

answer: a , b , d .

2q: methotrexate acts by ?

1. inhibition of dihydrofolate reductase
2. aldose dehydrogenase
3. glutathione reductase
4. inhibition of sterol synthesis

answer: a .

3q: true about carvedilol ?

1. alpha 1 blocker
2. beta 1 blocker
3. beta 2 blocker
4. antioxidant
5. used in hypertension

answer: a , b , c , d , e .

4q: prophylaxis of migraine ?

1. flunarizine
2. cinarizine
3. beta blockers
4. sodium valproate
5. carbamazepine

answer: a , c , d .

5q: which of the following are prodrugs ?

1. mercaptopurine
2. dipivefrine
3. enalapril
4. phenytoin
5. linezolid

answer: a , b , c .

6q: first pass metabolism is seen in ?

1. lignocaine
2. propranolol
3. salbutamol
4. dypyridamol
5. erythromycin

answer: a , b , c .

7q: true about quinidine

1. it increases the effective refractory period
2. used in hypertension
3. causes paradoxical tachycardia
4. it decreases absolute refractory period
5. cinchonism is seen

answer: a , c , e .

8q: regarding ritonavir in AIDS patient which of the following are true ?

1. interacts with terfenadine
2. gastrointestinal symptoms are seen
3. contraindicated in renal failure
4. it is NNRTI
5. should not be used in AIDS patient with bleeding disorder

answer: a , b .

9q: anti hypertensive drug beneficial or neutral role in lipid metabolism ?

1. prazocin
2. propranolol
3. furosemide
4. losartan
5. chlorthiazide

answer: a , d . prazocin and losartan .

10q: neurochemical mechanism of analgesia

1. VR-1
2. Nicotinic cholinergic
3. Nocistatin pattern
4. Nociceptin pattern
5. Anandomide

Answer: a, b , d , e .

11q: side effects of phenytoin are ?

1. gum hypertrophy
2. alopecia
3. subungual exostosis
4. onycholysis
5. acne rosacea

answer: a .

12q: ototoxicity of aminoglycosides is increased with concurrent use of which of the following drugs ?

1. cisplatin
2. furosemide
3. vancomycin
4. vincristin
5. erythromycin

answer: a , b , c , e .

13q: treatment of pencillinase producing neisseria gonorrhea is/are ?

1. amoxicillin
2. ciprofloxacin
3. cefotaxime
4. azithromycin
5. doxycycline

answer: b , c .

14q: true about lispro-insulin ?

1. action is faster and short in duration than regular insulin
2. it is given 15 minutes prior to meal
3. source is lamb
4. action is faster and long in duration than regular insulin

answer: a , b .

15q: true about pseudocholine esterase ?

1. present in neuromuscular junction
2. level is increased in pregnancy
3. succinyl choline is metabolized
4. organophosphorous inhibits it

answer: c .

16q: alkylating agents are ?

1. vincristin
2. actinomycin-D
3. chlorambucil
4. 5-FU
5. Cyclophosphamide

Answer: c , e .

29 - ezetimibe

Ezetimibe is an anti-hyperlipidemic medication which is used to lower cholesterol levels. It acts by decreasing cholesterol absorption in the intestine. It may be used alone when other cholesterol-lowering medications are not tolerated, or together with statins (e.g. ezetimibe/simvastatin, marketed as Vytorin and Inegy) when cholesterol levels are unable to be controlled on statins alone. It is marketed by Schering-Plough and Merck under the trade names Ezetrol, Zetia and Ezemibe. Ezetimibe was originally discovered by a team of four Schering-Plough research chemists: Drs. Stuart B. Rosenblum, Duane A. Burnett, John W. Clader and Brian A. McKittrick.

Ezetimibe localises at the brush border of the small intestine, where it inhibits the absorption of cholesterol from the diet. Specifically, it appears to bind to a critical mediator of cholesterol absorption, the Niemann-Pick C1-Like 1 (NPC1L1) protein on the gastrointestinal tract epithelial cells as well as in hepatocytes. In addition to this direct effect, decreased cholesterol absorption leads to an increase in LDL-cholesterol uptake into cells, thus decreasing levels in the blood plasma.

Ezetimibe is indicated as an adjunct to dietary measures in the management of:

• Hypercholesterolaemia
• Homozygous sitosterolemia (phytosterolemia)

On 9 June 2006, U.S. regulators approved the use of ezetimibe in combination with fenofibrate to treat mixed hyperlipidaemia.

Common adverse drug reactions (greater than or equal to 1% of patients) associated with ezetimibe therapy include: headache and/or diarrhea. Infrequent adverse effects (0.1–1% of patients) include: myalgia and/or raised liver function test (ALT/AST) results. Rarely (less than 0.1% of patients), hypersensitivity reactions (rash, angioedema) or myopathy may occur.

Ezetimibe is available as 10 mg tablets in most markets. A combination preparation ezetimibe/simvastatin, which combines ezetimibe with a statin, is also available.

On January 14, 2008, it was reported in the New York Times that a clinical trial (ENHANCE trial) of Zetia that was designed to show that the drug could reduce the growth of fatty plaques in arteries instead resulted in growth of plaques. However, the growth noted was less than it would have been had the patients been on placebo alone. Merck and Schering-Plough completed the clinical trial in April 2006 and had initially planned to release the findings no later than March 2007. The companies missed several self-imposed deadlines, and in December 2007, finally agreed to publish the results "soon" after the delays were publicized in news reports.

It should be recognized that the ENHANCE trial was not a clinical-outcome trial, but merely an imaging study. Formally, the American College of Cardiology (ACC) maintains that Zetia may be a reasonable option for patients who cannot tolerate a statin or cannot be controlled on a high dose statin. Results from the trial have provoked three large clinical-outcome trials. The results from these trials will be presented in the next three to four years. However, a March 30th, 2008 meeting of the ACC resulted in negative press for drugs like Zetia as Yale University Cardiologist Harlan Krumholz and concurring colleagues called into question the efficacy of such drugs. Krumholz' statements maintained that such pharmaceuticals should not be the first or even second option for prescribing doctors. Definitive conclusions of the efficacy and safety of Zetia can be made such a time when the results of more substantial and comprehensive trials are released, such as the upcoming IMPROVE-IT Trial which has an enrollment of 18000 patients and will report results in 2012.

28 - cephalosporins - 1st,2nd,3rd and 4th generations

1^st generation parenteral cephalosporins :

1. cephalothin
2. cefazoline

1^st generation oral cephalosporins

1. cephalexin
2. cephradine
3. cefadroxil

2^nd generation parenteral cephalosporins

1. cefuroxime
2. cefoxitin

2^nd generation oral cephalosporins

1. cefaclor
2. cefuroximeaxetil

3^rd generation parenteral cephalosporins

1. cefotaxime
2. cetizoxime
3. cefoperazone
4. ceftriaxone
5. ceftazidime

3^rd generation oral cephalosporins

1. cefixime
2. cefpodoximeproxetil
3. cefdinir
4. ceftibuten

4^th generation parenteral cephalosporins

1. cefepime
2. cefpirome

27 - Dopamine agonists, antagonists and depleters

Dopamine agonists :

1. dopamine
2. bromocriptine
3. apomorphine

dopamine is an inhibitor of prolactin release , so these drugs cause a decrease in the plasma level of prolactin and hence are used in the treatment of galactorrhea .

Dopamine antagonists :

1. metoclopramide
2. chlorpromazine
3. haloperidol

these drugs cause an increase in the plasma level of prolactin .

Dopamine depleters

1. reserpine
2. methyldopa

26 - pseudotumor cerebri causing drugs

1. hypervitaminosis A

2. oral contraceptive pills

3. tetracyclines

4. glucocorticoids ( withdrawal )

5. amiodarone

6. mineralocorticoids ( withdrawal )

try this stupid mnemonic : HOT Glucose And Minerals – treat pseudotumor cerebri.

25 - gynaecomastia causing drugs with mechanism of action

Various drugs are implicated in gynecomastia and can be classified into the following categories:

• Estrogens or drugs with estrogen like activity such as diethylstilbestrol, digitalis, phytoestrogens, and estrogen-contaminated food and estrogen-containing cosmetics

• Drugs that enhance estrogen synthesis such as gonadotropins, clomiphene, phenytoin, and exogenous testosterone

• Drugs that inhibit testosterone synthesis or action such as ketoconazole, metronidazole, alkylating agents, cisplatin, spironolactone, cimetidine, flutamide, finasteride, and etomidate

• Drugs that act by unknown mechanisms such as isonicotinic acid hydrazide, methyldopa, busulfan, tricyclic antidepressants, diazepam, penicillamine, omeprazole, phenothiazines, calcium channel blockers, ACE inhibitors, alcohol, marijuana, and heroin

• Drugs in the same class do not all cause gynecomastia to the same extent

24 - Hemolysis causing drugs in G6PD deficiency

1. Dapsone

2. Cotrimoxazole

3. Sulfonamides

4. Aspirin

5. Anti-malarials eg: primaquine

6. Nitrofurantoin

7. phenacetin

8. probenecid

9. chloramphenicol

try this stupid mnemonic : Deepa Caught Selling Aspirin At Primetime Night. Phone Probe Closed .

please visit this page for a very detailed list of drugs which carry a definite risk , possible risk and doubtful risk of hemolysis in glucose 6 phosphate dehydrogenase deficient patients .

23 - prodrugs and active forms

MCQ: all of the following are prodrugs except ?

a. lisinopril

b. enalapril

c. levodopa

d. sulindac

answer: a . lisinopril .

PRODRUGS AND ACTIVE FORMS

1. LEVODOPA ------------------- dopamine

2. ENALAPRIL ------------------- enalaprilat

3. SULINDAC --------------------- sulfide metabolite

4. BECAMPICILLIN –---------- ampicillin

5. SULFASALAZINE –---------- 5 – aminosalicyclic acid

6. PREDNISONE ----------------- prednisolone

7. ZIDOVUDINE ----------------- zidovudine triphosphate

8. CYCLOPHOSPHAMIDE --- aldophosphamide