Category: Quiz

Tetracycline

TETRACYCLINE

Q. 1

All of the following statements about adverse effects of tetracyclines are true, except:

 A

May lead to discolouration of teeth

 B

Are a common cause of superinfections

 C

May precipitate Liver damage

 D

Are not known to be teratogenic

Q. 1

All of the following statements about adverse effects of tetracyclines are true, except:

 A

May lead to discolouration of teeth

 B

Are a common cause of superinfections

 C

May precipitate Liver damage

 D

Are not known to be teratogenic

Ans. D

Explanation:

Tetracyclines are known to have teratogenic effects. Consumption of Tetracycline during pregnancy may cause dental enamel dysplasia and bony deformities in the child.

Ref: KDT, 6th Edition, Page 714; Basic and Clinical Pharmacology By Katzung, 10th Edition, Page 748


Q. 2

Which of the following represent the mechanism of action of tetracycline?

 A

Inhibits peptidyl transferase

 B

Causes misreading of mRNA

 C

Causes termination of peptide chain elongation

 D

Binds to A site and inhibits attachment of tRNA

Q. 2

Which of the following represent the mechanism of action of tetracycline?

 A

Inhibits peptidyl transferase

 B

Causes misreading of mRNA

 C

Causes termination of peptide chain elongation

 D

Binds to A site and inhibits attachment of tRNA

Ans. D

Explanation:

Tetracyclines are bacteriostatic antibiotics.

It inhibits protein synthesis by binding to 30S ribosomal subunit, and prevents the attachment of aminoacyl tRNA to the mRNA – ribosome complex. As a result peptide chain fails to grow.

Ref: Essentials of Medical Pharmacology, 5th Edition, Page 668-73


Q. 3

Tetracycline is used in prophylaxis of which of the following diseases?

 A

Cholera

 B

Brucellosis

 C

Leptospirosis

 D

Meningitis

Q. 3

Tetracycline is used in prophylaxis of which of the following diseases?

 A

Cholera

 B

Brucellosis

 C

Leptospirosis

 D

Meningitis

Ans. A

Explanation:

Tetracycline is the drug of choice for chemoprophylaxis of cholera.

Ref: Preventive and Social Medicine, by K.Park, 19th edition, Page 106, 193, 194, 141, 142; Harrison’s Internal Medicine, 16th edition, Page 917, 991.

Quiz In Between


Q. 4

Drug of choice in rhinoscleromatosis is:

 A

Tetracycline

 B

Fluoroquinolone

 C

Aminoglycosides

 D

None of the above

Q. 4

Drug of choice in rhinoscleromatosis is:

 A

Tetracycline

 B

Fluoroquinolone

 C

Aminoglycosides

 D

None of the above

Ans. A

Explanation:

In rhinoscleromatosis, organism may be difficult to eradicate, despite aggressive therapy.

A combination of conservative surgical debridement and long-term antibiotic coverage is the mainstay of therapy for rhinoscleroma.

Tetracycline has been shown to be effective and inexpensive for patients unless contraindicated.

Fluoroquinolones may be used as an alternative, given their excellent gram-negative activity and convenient dosing regimen


Q. 5

Which of the following is the drug of choice for chemoprophylaxis of cholera –

 A

Tetracycline

 B

Doxycycline

 C

Furazolidone

 D

Cotrimoxazole

Q. 5

Which of the following is the drug of choice for chemoprophylaxis of cholera –

 A

Tetracycline

 B

Doxycycline

 C

Furazolidone

 D

Cotrimoxazole

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tetracycline 


Q. 6

Fatty change in liver is seen with use of –

 A

Tetracycline

 B

Erythromycin

 C

Chlorpromazine

 D

Acetoaminohen

Q. 6

Fatty change in liver is seen with use of –

 A

Tetracycline

 B

Erythromycin

 C

Chlorpromazine

 D

Acetoaminohen

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tetracycline

Quiz In Between


Q. 7

Rate of newly synthesized osteoid mineralization can be best estimated by

 A

Tetracycline labeling

 B

Alizarin red stain

 C

Calcein stain

 D

Van kossa stain

Q. 7

Rate of newly synthesized osteoid mineralization can be best estimated by

 A

Tetracycline labeling

 B

Alizarin red stain

 C

Calcein stain

 D

Van kossa stain

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tetracycline labeling

Tetracycline labeling for osteoid mineralization

o Tetracycline labeling is the method of choice fir estimating newly systhesized osteoid mineralization in human. o Tetracycline is incorporated into new areas of osteoid that are being laid down but not yet mineralized (osteoid seams) o To estimate the rate of newly synthesized osteoid mineralization tetracycline is administered to the subject at two

defined time points.

o If the time interval between the two course is known , both the rate and extent of mineralization can be measured. o Tetracycline labelling allows a distinction to be made between defective mineralization (osteomalacia) and increased osteoid synthesis (bone remodeling states) by revealing the calcification front.

Other stain used for osteoid mineralization

o Other stain can also be used for this purpose, but they are inferior to tetracycline:

it) Alizarin red

ii) Calcein

Von-Kossa


Q. 8

Which of the following acts by inhibition of 30 S ribosome

 A

Tetracycline

 B

Chloramphenical

 C

Erythromycin

 D

Penicillin

Q. 8

Which of the following acts by inhibition of 30 S ribosome

 A

Tetracycline

 B

Chloramphenical

 C

Erythromycin

 D

Penicillin

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tetracycline


Q. 9

Tetracycline inhibits protein synthesis by

 A

Inhibiting initiation and causing misreading of mRNA

 B

Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

 C

Inhibiting peptidyl transferase activity

 D

Inhibiting translocation

Q. 9

Tetracycline inhibits protein synthesis by

 A

Inhibiting initiation and causing misreading of mRNA

 B

Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

 C

Inhibiting peptidyl transferase activity

 D

Inhibiting translocation

Ans. B

Explanation:

Ans. is ‘b’ i.e., Binding to 30S Subunit and inhibits binding of aminoacyl tRNA

o Tetracycline interact with small ribosomal subunits, blocking access of aminoacyl- tRNA to the mRNA-ribosome complex.

o Tetracyclines bind to 30 S subunit of ribosome.

Quiz In Between


Q. 10

Mechanism of action of tetracycline is –

 A

Binds to A site and inhibit attachment of t-RNA.

 B

Inhibits peptidyl transferase

 C

Causes misreading of mRNA

 D

Causes termination of peptide chain elongation

Q. 10

Mechanism of action of tetracycline is –

 A

Binds to A site and inhibit attachment of t-RNA.

 B

Inhibits peptidyl transferase

 C

Causes misreading of mRNA

 D

Causes termination of peptide chain elongation

Ans. A

Explanation:

Ans. is ‘a’ i.e., Bind to A site and inhibit attachment of t-RNA


Q. 11

Which of the following is not true regarding tetracycline –

 A

It is not teratogenic

 B

It can cause tooth discoloration

 C

It can result in superinfection

 D

It can lead to pseudomembranous colitis.

Q. 11

Which of the following is not true regarding tetracycline –

 A

It is not teratogenic

 B

It can cause tooth discoloration

 C

It can result in superinfection

 D

It can lead to pseudomembranous colitis.

Ans. A

Explanation:

Ans. is ‘a’ i.e., It is not teratogenic

o Tetracycline is teratogenic – causes discoloration and defects of teeth and altered bone growth of the fetus.

o Tetracycline can cause superinfection (including pseudomembranous colitis).


Q. 12

Tetracycline injection causes palsy of which nerve‑

 A

Ulnar

 B

Median

 C

Radial

 D

Superficial Radial Nerve injury

Q. 12

Tetracycline injection causes palsy of which nerve‑

 A

Ulnar

 B

Median

 C

Radial

 D

Superficial Radial Nerve injury

Ans. C

Explanation:

Ans. is ‘c’ i.e., Radial

o As with all intramuscular preparations, terramycin (oxytetracycline) intramuscular solution should be injected well within the body of a relatively large muscle.

o In infants and small children the periphery of the upper outer quadrant of the gluteal region should be used only when necessary, such as in burn patients, in order to minimize the possibility of damage to the sciatic nerve.

o The deltoid area should be used only if well developed such as in certain adults and older children, and then only with caution to avoid radial nerve injury.

Quiz In Between


Q. 13

Which of the following drug causes Pseudotumour cerebri –

 A

Sparfloxacin

 B

Tetracycline

 C

Gentamicin

 D

Clofazimine

Q. 13

Which of the following drug causes Pseudotumour cerebri –

 A

Sparfloxacin

 B

Tetracycline

 C

Gentamicin

 D

Clofazimine

Ans. B

Explanation:

Ans. is ‘b’ i.e., Tetracycline

Drugs causing Pseudotumour cerebri

o A miodarone                                           o Mineralocorticoids (withdrawl)                o Oral contraceptives

o Glucocorticoids (withdrawl)                  o Hypervitaminosis A                                  o Tetracyclines

o Quinolones


Q. 14

Rate of mineralization of newly formed osteoid can be estimated by the following:

 A

Von Kossa staining for calcium

 B

Alzarin red stain

 C

Labeled tetracycline

 D

Immunofluorescence Calcein Stain

Q. 14

Rate of mineralization of newly formed osteoid can be estimated by the following:

 A

Von Kossa staining for calcium

 B

Alzarin red stain

 C

Labeled tetracycline

 D

Immunofluorescence Calcein Stain

Ans. C

Explanation:

C i.e. Labelled tetracycline

• Tetracycline administered in vivo becomes fixed in new forming mineralizing boneQ and exhibit a characteristic fluorescence when viewed by ultraviolet light.
• The tetracycline labelled bone fluoresces a bringt yellow (dimethyl chlortetracycline) to yellowish green (oxytetracyline) on faint magenta background and mature bone fluoresces a faint blue. Under fluorescent microscopy, narrow bands of fluorescence are observed where bone was actively formed while exposed to the recently administered tetracycline. When two doses of tetracycline are given a number of days apart, two bands of fluorescence will be separated by an interval of unlabeled new bone that has formed during the period between dosesQ. By using two types of tetracyclines, each type produces its distinctive fluorescent colors; which are easily identified, thus simplifying measurement of new formed bone.
• Rate of newly synthesized osteoid material mineralization (bone formation or remodeling) can be estimated by tetracycline labeling (method of choice)Q. Tetracycline HC1, dimethylchlor tetracycline and oxytetracycline are most commonly used for fluorochrome (fluorescent) tetracycline labeling.
• Alizarin red stain, calcein stain and Von kassa (black) stain can also be used to measure rate of bone mineralization but these are inferior (and too toxic for humans) in comparison to tetracycline labeling. So these are only used in animal research.


Q. 15

Treatment of granuloma inguinale is-

 A

Tetracycline

 B

Sulphanomide

 C

Streptomycin

 D

Pencillin

Q. 15

Treatment of granuloma inguinale is-

 A

Tetracycline

 B

Sulphanomide

 C

Streptomycin

 D

Pencillin

Ans. A

Explanation:

A i.e. Tetracycline

Quiz In Between


Q. 16

The drug of choice for chemoprophylaxis in contacts of a patient of penumonic plague is – 

 A

Penicillin

 B

Rifampicin

 C

Erythromycin

 D

Tetracycline

Q. 16

The drug of choice for chemoprophylaxis in contacts of a patient of penumonic plague is – 

 A

Penicillin

 B

Rifampicin

 C

Erythromycin

 D

Tetracycline

Ans. D

Explanation:

Ans. is ‘d’ i.e., Tetracycline 

Chemoprophylaxis

o Chemoprophylaxis refers to the administration of a drug for the purpose of preventing disease or infection.
Indications for chemoprophylaxis

Disease                                                 Chemoprophylaxis

Cholera                                                 Tetracycline or furazolidone for house-hold contacts

Conjuncitivitis                                         Erythromycin ophthalmic ointment

Diphtheria                                              Erythromycin (and first dose of vaccine)

Influenza                                               Amantadine (effective only for type A) for contacts suffering from chronic diaeases

Malaria                                                 Chloroquine

Meningitis                                              Sulphadiazine for 4 days only

meningococcal                                       if the strain is shwon to be non-resistant, for household and close community contacts; immunization should be initiate in all cases (against serogrops A,

                                                          and C). However, now rifampicin is the DOC for chemoprophylaxis.

Plague                                                  Tetracycline for contacts of

pneumonic plague


Q. 17

Chemoprophy laxis with tetracycline is useful in which of the following ?

 A

Cholera

 B

Brucellosis

 C

Meningitis

 D

Leptospirosis

Q. 17

Chemoprophy laxis with tetracycline is useful in which of the following ?

 A

Cholera

 B

Brucellosis

 C

Meningitis

 D

Leptospirosis

Ans. A

Explanation:

Ans. is ‘a’ i.e., Cholera 

o Tetracycline is the drug of choice for chemoprophylaxis in cholera and plague.


Q. 18

Which of the following is the drug of choice for chemoprophylaxis of cholera – 

 A

Tetracycline 

 B

Doxycycline

 C

Furazolidone 

 D

Cotrimoxazole

Q. 18

Which of the following is the drug of choice for chemoprophylaxis of cholera – 

 A

Tetracycline 

 B

Doxycycline

 C

Furazolidone 

 D

Cotrimoxazole

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tetracycline 

  • Tetracycline is the drug of choice for chemoprophylaxis.

o Indication

 Chemoprophylaxis is indicated only for household contacts or of a closed community in which cholera has occured.

Remember

Mass chemoprophylaxis is not advised in the total community as it can not stop the spread of cholera. So mass K chemoprophylaxis has no role in controlling the epidemic.

Quiz In Between


Q. 19

Chemoprophylaxis in cholera – 

 A

Tetracycline 

 B

Ciprofloxacin

 C

Erytromycin

 D

None

Q. 19

Chemoprophylaxis in cholera – 

 A

Tetracycline 

 B

Ciprofloxacin

 C

Erytromycin

 D

None

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tetracycline 


Q. 20

Prophylaxis for health personnel working in a plague ward is –

 A

Vaccine

 B

Tetracycline throughout the duty

 C

A cource of tetracycline

 D

a and b

Q. 20

Prophylaxis for health personnel working in a plague ward is –

 A

Vaccine

 B

Tetracycline throughout the duty

 C

A cource of tetracycline

 D

a and b

Ans. D

Explanation:

Ans. is ‘a’ i.e., Vaccine; ‘b’ i.e., Tetracycline throughout the duty 


Q. 21

Coloured halos are seen in all, EXCEPT 

 A

Mucopurulent conjunctivitis

 B

Acute anterior uveitis

 C

Tetracycline

 D

Glaucoma

Q. 21

Coloured halos are seen in all, EXCEPT 

 A

Mucopurulent conjunctivitis

 B

Acute anterior uveitis

 C

Tetracycline

 D

Glaucoma

Ans. C

Explanation:

C i.e. Tetracycline

  • Glucomas Q

-Primary angle closure glucoma (due to corneal edema & stretching Q)

– Open angle glucomaQ

  • Acute mucopurulent conjunctivitis Q (due to mucus)
  • Corneal scar
  • Krukenberg spindle (Pigmentary glucoma)Q
  • Cataract Q (lens opacity)
  • Vitreous opacities – e.g. haemorrhage, asteroid bodies, synchysis scintillans etc.
  • Any haze of ocular media Q
  • Contact lens overwear (due to corneal abrasion)
  • Too intense exposure to light as in snow blindness
  • Asymmetrical placement of intraocular lens in relation to pupillary aperture
  • Drugs – acetophenazine, acetyldigitoxin, amiodarone, amodiaquine, amyl nitrite, butaperazine, carphenazine, chloroquine, chlorine dioxide, chlorpromazine, cortisone, deslanoside, dexamethasone, diethazine, digitalis, digitoxin, digoxin, ethopropazine, ethylene diamine, fluorometholone, fluphenazine, gitalin, hydrocortisone, hydroxychloroquine, lanatoside C, medrysone, mesoridazine, methidilazine, methotrimeprazine, methylprednisolone, nitroglycerin, nitronaphalene, oral contraceptives, ouabain, paramethadione, perazine, pericyazine, promazine, promethazine, propiamazine, quinacrine, thiethylperazine, thiopropazine, thioproperazine, thioridazine, trifluoperazine, triflupromazine, trimeprazine, trimethadione and sterile water.

* Tetracycline is not included in this long drug list & haze in ocular media can occur in acute anterior uveitis due to aqueous flare & K.P’s.

Quiz In Between


Q. 22

Drug of choice of trachoma is

 A

Penicillin

 B

Sulfonamide

 C

Tetracycline

 D

Chloramphenicol

Q. 22

Drug of choice of trachoma is

 A

Penicillin

 B

Sulfonamide

 C

Tetracycline

 D

Chloramphenicol

Ans. C

Explanation:

C i.e. Tetracycline

Treatment of Trachoma

  • Oral tetracycline, doxycycline, azithromycin, clarithromycin, erythromycin, rifampicin & sulfonamides
  • Oral tetracycline cannot be given to children < 8 years, pregnant women or nursing mothers.
  • Sulfonamides have high risk of stevens Johnson syndrome and erythema multiforme.
  • Topical treatment with tetracycline or erythromycin or sulfacetamide (less preffered) is cheaper more effective and has no risk of systemic side effects.

Q. 23

Tetracycline ointment for mass prophylaxis:

 A

0.1%

 B

0.5%

 C

1%

 D

5%

Q. 23

Tetracycline ointment for mass prophylaxis:

 A

0.1%

 B

0.5%

 C

1%

 D

5%

Ans. A

Explanation:

Ans. 0.1%


Q. 24

Drug of choice for lymphogranuloma venerum:

March 2005

 A

Tetracycline

 B

Chloramphenicol

 C

Erythromycin

 D

Ampicillin

Q. 24

Drug of choice for lymphogranuloma venerum:

March 2005

 A

Tetracycline

 B

Chloramphenicol

 C

Erythromycin

 D

Ampicillin

Ans. A

Explanation:

Ans. A: Tetracycline

Lymphogranuloma venereum (LGV) is a sexually transmitted infection caused by unique serovars of Chlamydia trachomatis (L1, L2, L3) that are unlike those that typically cause urethritis, cervicitis, and proctitis (A-K).

The hallmark of LGV is unilateral or bilateral tender lymphadenopathy that dramatically evolves 2 to 6 weeks after the primary lesion.

The involved lymph nodes increase rapidly in size, and pain and erythema are common. If adjacent to one another, several involved lymph nodes may coalesce. The central areas of such lymph nodes can then undergo necrosis. Fluctuant and suppurative lymph nodes then develop, causing the classic ‘bubo’ of LGV.

The bubo may then rupture and drain purulent material, which is associated with relief from symptoms. The ‘groove sign’ characteristic of LGV is seen if both the inguinal and the femoral nodes are involved.

Tetracycline is the first choice drugs for LGV.

Apart from LGV, tetracyclines are drug of choice for:

  • STDs-Chlamydial non-specific urethritis/endocervicitis, granuloma inguinale
  • Atypical pneumonia
  • Cholera
  • Brucellosis
  • Plague
  • Relapsing fever
  • Rickettsial infections-typhus, rocky mountain spotted fever, Q fever etc.

Quiz In Between


Q. 25

Which of the following drug can be used topically in eye:

September 2007

 A

Erythromycin

 B

Ganciclovir

 C

Clindamycin

 D

Tetracyclines

Q. 25

Which of the following drug can be used topically in eye:

September 2007

 A

Erythromycin

 B

Ganciclovir

 C

Clindamycin

 D

Tetracyclines

Ans. D

Explanation:

Ans. D: Tetracyclines

Tetracyclines are broad spectrum antibiotics with considerable bacteriostatic action against both gram-positive and gram-negative organisms as well as some fungi, rickettsiae and the chlamydiae.

They are essentially used in the form of drops or ointment for superficial ocular infections such as trachoma. They get deposited in bones and teeth and hence not to be used in children and pregnant/lactating women.


Q. 26

Tetracycline is the drug of choice for all except‑

 A

LGV

 B

Cholerra

 C

Plague prophylaxis

 D

Pneumocystis carinii

Q. 26

Tetracycline is the drug of choice for all except‑

 A

LGV

 B

Cholerra

 C

Plague prophylaxis

 D

Pneumocystis carinii

Ans. D

Explanation:

Ans. is ‘d’ i.e., Pneumocystis carinii


Q. 27

Tetracycline inhibits protein synthesis by‑

 A

Inhibiting initiation and causing misreading of mRNA

 B

Binding to 30 S subunit and inhibits binding of aminoacyltRNA

 C

Inhibiting peptidyltransferase activity

 D

Inhibiting translocation

Q. 27

Tetracycline inhibits protein synthesis by‑

 A

Inhibiting initiation and causing misreading of mRNA

 B

Binding to 30 S subunit and inhibits binding of aminoacyltRNA

 C

Inhibiting peptidyltransferase activity

 D

Inhibiting translocation

Ans. B

Explanation:

Ans. is ‘b’ i.e., Binding to 30 S subunit and inhibits binding of aminoacyl tRNA

Tetracyclines

Tetracyclines are classified into three groups –

  • Group I – Tetracycline, oxytetracycline, chlortetracycline.
  • Group II – Lymecycline, Demeclocycline.
  • Group III – Minocycline, Doxycycline.
  • Tetracyclines are bacteriostatic and broad spectrum antibiotics.
  • Tetracycline interact with small ribosomal subunits, blocking access of aminoacyl- tRNA to the mRNA-ribos­ome complex.
  • Oral absorption of tetracyclines is impaired by food except doxycycline and minocycline which are absorbed completely irrespective of food.
  • Most tetracyclines are primarily excreted in urine by glomerular filtration; dose has to be reduced in renal failure; doxycycline is an exception – doxycycline can be used in renal failure.
  • Tetracyclines can cross placenta and secreted in milk → contraindicated during pregnancy and lactation.

Quiz In Between



Classification Of Anti-Microbials

CLASSIFICATION OF ANTIMICROBIALS

Q. 1 All drug inhibit bacterial cell wall synthesis EXCEPT
 A Spectinomycin    
 B Vancomycin
 C Aztreonam
 D Cephalexin
 
Q. 1 All drug inhibit bacterial cell wall synthesis EXCEPT
 A Spectinomycin    
 B Vancomycin
 C Aztreonam
 D Cephalexin
 
Ans. A

Explanation:

Spectinomycin is an aminocyclitol antibiotic that inhibits bacterial protein synthesis. The other drugs all inhibit bacterial cell wall synthesis. Vancomycin and bacitracin inhibit early steps in the biosynthesis of the peptidoglycan component of the cell wall, whereas 3– lactams such as aztreonam (a monobactam), penicillins, cephalosporins, and carbapenems inhibit the cross-linking (transpeptidation) of the cell wall peptidoglycan polymers.


Q. 2 All of the following are true regarding cephalosporins, except:
 A Bacteriocidal agents
 B Active against only gram negative
 C Resistant to beta lactamases by Bird generation cephalosporins
 D None of the above
Q. 2 All of the following are true regarding cephalosporins, except:
 A Bacteriocidal agents
 B Active against only gram negative
 C Resistant to beta lactamases by Bird generation cephalosporins
 D None of the above
Ans. B

Explanation:

Bacteriocidal agents


Q. 3

Cell wall synthesis is inhibited by all of the following, EXCEPT:

 A

Amoxycillin

 B

Penicillin G

 C

Tetracycline

 D

Cefotetan

Q. 3

Cell wall synthesis is inhibited by all of the following, EXCEPT:

 A

Amoxycillin

 B

Penicillin G

 C

Tetracycline

 D

Cefotetan

Ans. C

Explanation:

Tetracyclines act by inhibiting the protein synthesis and they do not inhibit the cell wall synthesis. 

 
Antibiotics that act by inhibiting cell wall synthesis are Penicillins Cephalosporins, Cycloserine, Vancomycin and Bacitracin.
 
Ref: KDT, 6th Edition, Page 668; Essentials of Medical Pharmacology By K D Tripathi, 6th Edition, Page 738; An Evaluation of Current Cholera Treatment By Bhattacharya SK, National Institute of Cholera and Enteric Diseases (2003). 4 (2): 141

Quiz In Between


Q. 4

Antipseudomonal action is a characteristic of which of the following  antimicrobials?

 A

Cefopodoxime

 B

Cefoperazone

 C

Cefotetan

 D

Ceforanide

Q. 4

Antipseudomonal action is a characteristic of which of the following  antimicrobials?

 A

Cefopodoxime

 B

Cefoperazone

 C

Cefotetan

 D

Ceforanide

Ans. B

Explanation:

Cefoperazone is 3rd generation cephalosporin, which is active against gram positive as well as gram negative bacterias. It is one of the few antibiotics that have anti-pseudomonal action. It exerts its action by inhibiting bacterial cell wall growth. Main adverse effect of this drug is Hypothrombinemia and Disulfiram reaction.

Ref: Sherwood L. Gorbach, John G. Bartlett, Neil R. Blacklo (2004), Chapter 19, “Cephalosporins”, In the book, “Infectious Diesases”, 3rd Edition, Lippincott Publications, USA, Page 196


Q. 5

Drug that inhibits cell wall synthesis is?

 A

Tetracyc I ins

 B

Penicillins

 C

Aminoglycosides

 D

Chloramphenicol

Q. 5

Drug that inhibits cell wall synthesis is?

 A

Tetracyc I ins

 B

Penicillins

 C

Aminoglycosides

 D

Chloramphenicol

Ans. B

Explanation:

Ans. is ‘b’ i.e., Penicillins


Q. 6

Which of the following Antimicrobials has antipseudomonal action –

 A

Cefopodoxime proxetil

 B

Ceforanide

 C

Cefotetan

 D

Cefoperazone

Q. 6

Which of the following Antimicrobials has antipseudomonal action –

 A

Cefopodoxime proxetil

 B

Ceforanide

 C

Cefotetan

 D

Cefoperazone

Ans. D

Explanation:

Ans. is ‘d’ i.e., Cefoperazone

Quiz In Between


Q. 7

Which of the following statements is not true about Tacrolimus –

 A

It is macrolide antibiotic

 B

It is indicated for the prophylaxis of organ transplant rejection

 C

Glucose intolerance is a well recognized side effect

 D

It can be safely administered with any nephrotoxic drug

Q. 7

Which of the following statements is not true about Tacrolimus –

 A

It is macrolide antibiotic

 B

It is indicated for the prophylaxis of organ transplant rejection

 C

Glucose intolerance is a well recognized side effect

 D

It can be safely administered with any nephrotoxic drug

Ans. D

Explanation:

Ans. is ‘d’ i.e., It can be safely administered with any nephrotoxic drug


Q. 8

Fk-506 is a –

 A

It is a macrolide antibiotic

 B

Immunoglobulin antibody

 C

Non depolarising muscle relaxant

 D

Opioid analgesic

Q. 8

Fk-506 is a –

 A

It is a macrolide antibiotic

 B

Immunoglobulin antibody

 C

Non depolarising muscle relaxant

 D

Opioid analgesic

Ans. A

Explanation:

Ans. is ‘a’ i.e., It is a macrolide antibiotic

o Fk-506 is commonly known as Tacrolimus.

o Tacrolimus is a macrolide antibiotic produced by streptomyces tsukubaensis.


Q. 9

Drug which inhibit protein synthesis are all of the following except:   

March 2007

 A

Tetracycline

 B

Chloramphenicol

 C

Erythromycin

 D

None

Q. 9

Drug which inhibit protein synthesis are all of the following except:   

March 2007

 A

Tetracycline

 B

Chloramphenicol

 C

Erythromycin

 D

None

Ans. D

Explanation:

Ans.  d none

Drugs which act by inhibiting protein synthesis:

  • Aminoglycosides (streptomycin, amikacin, tobramycin, neomycin, etc.),
  • Spectinomycin
  • Chloramphenicol
  • Clindamycin
  • Tetracycline (and minocycline, doxycycline, etc.)
  • Erythromycin (and azithromycin)
  • Fusidic acid
  • Linezolid

Penicillin/beta-lactamase antibiotics act by interfering with the synthesis of bacterial cell wall.

Quiz In Between


Q. 10

Bacteriostatic anti TB drug ‑

 A

INH

 B

Rifampicin

 C

Ethambutol

 D

Pyrazinamide

Q. 10

Bacteriostatic anti TB drug ‑

 A

INH

 B

Rifampicin

 C

Ethambutol

 D

Pyrazinamide

Ans. C

Explanation:

Ans. is ‘c’ i.e., Ethambutol

Remember the following facts

  • All cell wall synthesis inhibitors are bactericidal.
  • All antibacterial drugs that act on cell membrane are bactericidal.
  • All first line antitubercular drugs are bactericidal except ethambutol that is bacteriostatic.
  • All protein synthesis inhibitors are bacteriostatic except aminoglycosides & streptogramins which are bactericidal.
  • All drugs affect intermediary metabolism are bacteriostatic.
  • Now, it will be very easy to remember the following table

Q. 11

Following drugs are cell wall synthesis inhibitors except‑

 A

Colistin

 B

Fosfomycin

 C

Bacitracin

 D

Cycloserine

Q. 11

Following drugs are cell wall synthesis inhibitors except‑

 A

Colistin

 B

Fosfomycin

 C

Bacitracin

 D

Cycloserine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Colistin

Quiz In Between



Acetylcholinesterase (Ache) Inhibitors

AChE inhibitors

Q. 1

Which of the following is the most sensitive test for the diagnosis of myasthenia gravis?

 A

Repetitive nerve stimulation test

 B

Positive edrophonium test

 C

Measurement of jitter by single fibre electromyography

 D

Measurement of serum ACh-receptor binding antibodies

Q. 1

Which of the following is the most sensitive test for the diagnosis of myasthenia gravis?

 A

Repetitive nerve stimulation test

 B

Positive edrophonium test

 C

Measurement of jitter by single fibre electromyography

 D

Measurement of serum ACh-receptor binding antibodies

Ans. B

Explanation:

 

Myasthenia gravis is a neuromuscular disorder, due to decrease in the number of acetylcholine receptors at the neuromuscular junction secondary to an antibody mediated autoimmune attack. It is characterized by weakness and fatigability of skeletal muscles. It can be diagnosed by the increase in muscle strength following administration of anticholinesterase drug. Most sensitive test in diagnosing myasthenia is edrophonium test. In this test, after administration of edrophonium, muscle strength improves and lasts for 5 minutes.
 
Ref: Harrison’s Internal Medicine, 18th Edition, Chapter 386; Clinical Neurology By Roger P. Simon, 7th Edition, Chapter 5

Q. 2

Neostigmine –

 A

It is a quartarnary amounium compound

 B

Metabolised in liver

 C

It can cross the blood brain harrier

 D

Prominent effect on smooth muscles

Q. 2

Neostigmine –

 A

It is a quartarnary amounium compound

 B

Metabolised in liver

 C

It can cross the blood brain harrier

 D

Prominent effect on smooth muscles

Ans. A

Explanation:

Ans. is `a’ i.e., It is a quartarnary amounium compound

Tertiary amine Vs quartenary ammonium compound

o Neostigmine is a quartenary ammonium compound.

o Quartenary ammonium compounds are lipid insoluble and diffuse poorly across the membrane : – Li Oral absorption —> Poor

         CNS penetration –> poor No CNS action

         Applied to eye         No penetration of cornea.

         More marked effect on skeletal muscles, ganglia, but muscarinic effects are less prominant.

o In contrast, physostigmine is a tertiary amine derivated.

o Tertiary amine compounds are lipid soluble and diffuse easily across the membrane :-

 Oral absorption       Good

         CNS penetration —> Good      Produce CNS actions.

         Applied to eye –> Penetrate cornea.

         More marked muscarinic and CNS effect.


Q. 3

Neostigmine antagonizes nondepolarizing blockade by all of the following mechanisms, except

 A

Decreasing the breakdown of Acetylcholine at the motor end plate

 B

Preventing K+ efflux from the cell

 C

Increasing the release of Acetylcholine at the motor end plate

 D

Depolarization of the motor end plate

Q. 3

Neostigmine antagonizes nondepolarizing blockade by all of the following mechanisms, except

 A

Decreasing the breakdown of Acetylcholine at the motor end plate

 B

Preventing K+ efflux from the cell

 C

Increasing the release of Acetylcholine at the motor end plate

 D

Depolarization of the motor end plate

Ans. C

Explanation:

Ans. is ‘c’ i.e., Increasing the release of Acetylcholine at the motor end palate

o Anticholinestrases act by inhibiting the action of acetylcholinesterase (an enzyme that degrades acetylcholine by causing its hydrolysis).

o Anticholinesterases thus increase the level of acetylcholine at the neuromuscular junction.

o Neostigmine also has some additional direct action on cholinergic receptors i.e., it depolarizes motor end plate.

o It does not increase the release of ACH. Accumulated ACH acts on prejunctional muscarinic autoreceptors and inhibits the release of ACH.

Quiz In Between


Q. 4

All are true about neostigmine except –

 A

Tertiary ammonium compound

 B

Given to reduce effect of depolarising muscle relaxation

 C

Given to reduce post operative paralytic ileus

 D

Help in urinary retention

Q. 4

All are true about neostigmine except –

 A

Tertiary ammonium compound

 B

Given to reduce effect of depolarising muscle relaxation

 C

Given to reduce post operative paralytic ileus

 D

Help in urinary retention

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tertiary ammonium compound

o Neostigmine is a synthetic compound (a carbamic acid ester) and is a quarternary ammonium compound.

o It causes reversal of the paralysis of competitive neuromuscular blocking drugs.

o Neostigmine enhances gastric contractions and increases the secretion of gastric acid so it is used in the treatment of paralytic ileus.

o Neostigmine is used for the treatment of atony of the detrusor muscle of the urinary bladder, thus postoperative dysuria is relieved, and the time interval between operation and spontaneous urination is shortened.


Q. 5

Diagnosis of Myasthenia Gravis is by using –

 A

Edrophonium

 B

Neostigmine

 C

Succinylcholine (SCh)

 D

Atropine

Q. 5

Diagnosis of Myasthenia Gravis is by using –

 A

Edrophonium

 B

Neostigmine

 C

Succinylcholine (SCh)

 D

Atropine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Edrophonium

  • Edrophonium (anticholinesterase) injected slowly i.v improves muscle strength only in myaesthenia gravis and not in other muscular dystrophies.

Q. 6

Edrophonium test is used in the diagnosis of

 A

Marcus gunn jaw winking ptosis

 B

Homer’s syndrome

 C

Blepharophimosis syndrome

 D

Myasthenic ptosis

Q. 6

Edrophonium test is used in the diagnosis of

 A

Marcus gunn jaw winking ptosis

 B

Homer’s syndrome

 C

Blepharophimosis syndrome

 D

Myasthenic ptosis

Ans. D

Explanation:

Ans. is ‘d’ i.e., Myasthenic ptosis

Quiz In Between


Q. 7

Donepezil is used in the treatment of which of the following conditions –

 A

Schizophrenia

 B

Depression

 C

Anxiety

 D

Alzheimer dementia

Q. 7

Donepezil is used in the treatment of which of the following conditions –

 A

Schizophrenia

 B

Depression

 C

Anxiety

 D

Alzheimer dementia

Ans. D

Explanation:

Ans. is ‘d’ i.e., Alzheimer disease

o Donepezil is a cerebroactive drug. It is used in Alzheimer’s disease (AD).


Q. 8

A patient of Alzheimer’s disease is on rivastigmine therapy and develops symptoms of depression. Use of which of the following drug would decrease efficacy of rivostigmine –

 A

TCAs

 B

SSRI

 C

MAO inhibitor

 D

RIMA

Q. 8

A patient of Alzheimer’s disease is on rivastigmine therapy and develops symptoms of depression. Use of which of the following drug would decrease efficacy of rivostigmine –

 A

TCAs

 B

SSRI

 C

MAO inhibitor

 D

RIMA

Ans. A

Explanation:

Ans. is ‘a’ i.e., TCAs

o Cholinergic transmission is diminished in Alzheimer’s disease.

o All agents that benefit the conduction act to enhance acetyhcholine activity by inhibition of the acetylcholinesterase which metabolises and inactivates acetylcholine.

o Consequently acetylcholine remains usable for longer.

o Rivastigmine acts in similar way.

o Tricyclic antidepressants (TCAs) have anticholinergic property, therefore they counteract that cholinergic effect of rivastigmine.


Q. 9

Which of the following drugs should not be used with rivastigmine in patients with alzheimer’s disease –

 A

SSRI

 B

Tricyclic antidepressant

 C

RIMA

 D

Atypical antidepressants

Q. 9

Which of the following drugs should not be used with rivastigmine in patients with alzheimer’s disease –

 A

SSRI

 B

Tricyclic antidepressant

 C

RIMA

 D

Atypical antidepressants

Ans. B

Explanation:

Ans. is ‘b’ i.e., Tricyclic antidepressant

Rivastigmine (cholinesterase inhibitor) should not be used with drugs that have cholinergic antagonistic activity like tricyclic antidepressants (TCA) as the combination is counter productive.

Quiz In Between


Q. 10

Neostigmine is used for reversing the adverse effect of:

 A

dTC + pancuronium

 B

d TC only

 C

Alcuronium only

 D

Ketamine complication

Q. 10

Neostigmine is used for reversing the adverse effect of:

 A

dTC + pancuronium

 B

d TC only

 C

Alcuronium only

 D

Ketamine complication

Ans. A

Explanation:

A i.e. dTC + Pancuronium

As d-TC & Panduronium, both are non-depolarizing muscle relaxant, so neostigmine is used to reverse the drugs.


Q. 11

A thirty five year old female has proximal weakness of muscles, ptosis and easy fatigability.

The most sensitive test to suggest the diagnosis is:

 A

Muscle Biopsy

 B

CPK levels

 C

Edrophonium test

 D

EMG

Q. 11

A thirty five year old female has proximal weakness of muscles, ptosis and easy fatigability.

The most sensitive test to suggest the diagnosis is:

 A

Muscle Biopsy

 B

CPK levels

 C

Edrophonium test

 D

EMG

Ans. C

Explanation:

Answer is C (Edrophonium test):

Edrophonium test is the most sensitive test to suggest the diagnosis of myasthenia gravis amongst the options provided.

Proximal weakness of muscles, ptosis and easy fatigability suggests a diagnosis of Myasthenia Gravis.

Edrophonium (Tensilon) test is a highly sensitive test with 85% sensitivity in ocular and 95% sensitivity in systemic myasthenia.

The diagnosis of MG is highly probable if Edrophonium test is unequivocally positive.

Note

Conventional (EMG) is not a sensitive diagnostic test for MG.

The conventional needle EMG is usually normal in patients with MG although certain findings may indicate probability of MG.

Conventional EMG evaluation in MG serves mostly in excluding other causes of weakness like motor neuron disease, neuropathy or myopathy


Q. 12

21 yearold female presents with history of mild bilateral ptosis, proximal muscle weakness and easy fatiguability. Which amongst the following, is best in diagnosing this condition:       

March 2013 (b)

 A

Muscle biopsy

 B

Edrophonium test

 C

Repetitive nerve stimulation test

 D

Electromyography

Q. 12

21 yearold female presents with history of mild bilateral ptosis, proximal muscle weakness and easy fatiguability. Which amongst the following, is best in diagnosing this condition:       

March 2013 (b)

 A

Muscle biopsy

 B

Edrophonium test

 C

Repetitive nerve stimulation test

 D

Electromyography

Ans. B

Explanation:

Ans. B i.e. Edrophonium test

Myasthenia gravis

Decreased myoneural junction transmission

Features:

Dysarthria,

Dysphagia,

Proximal muscle weakness,

Sensory modalities and deep tendon reflexes are NORMAL

  • MC used cholinergic drugs: Pyridostigmine/neostigmine
  • Surgical procedure (should be done in all cases): Thymectomy

Quiz In Between


Q. 13

A 35 year old female patient presents with proximal weakness of muscles, ptosis and easily fatiguability.

September 2011

 A

Muscle biopsy

 B

CPK levels

 C

EMG

 D

Edrophonium test

Q. 13

A 35 year old female patient presents with proximal weakness of muscles, ptosis and easily fatiguability.

September 2011

 A

Muscle biopsy

 B

CPK levels

 C

EMG

 D

Edrophonium test

Ans. D

Explanation:

Ans. D: Edrophonium test

The intravenous injection of the short acting anticholinesterase, edrophonium bromide, is a valuable diagnostic aid (the tensilon test) for myasthenia gravis

Myasthenia gravis/ MG:

  • A disease characterized by episodic muscle weakness, chiefly in muscle innervated by cranial nerves and characteristically improved by anti-cholinesterase inhibiting drug

There is decreased myoneural junction transmission due to auto-immune attack on the acetylcholine receptor of the post-synaptic neuromuscular junction, which results in loss of dysfunction of Ach receptors and jeopardizing normal neuromuscular transmission

  • Dysarthria, dysphagia and proximal limb weakness is common
  • Sensory modalities and deep tendon reflexes are normal
  • Pyridostigmine/ Neostigmine are the MC used cholinergic drugs
  • Thymectomy is indicated in all patients with generalized MG
  • Plasmapheresis may be useful for preparing refractory cases fro thymectomy and during respiratory crisis

Q. 14

Neostigmine is used in the following except ‑

 A

Myasthenia gravis

 B

Cobra bite

 C

Atony of bladder

 D

Glaucoma

Q. 14

Neostigmine is used in the following except ‑

 A

Myasthenia gravis

 B

Cobra bite

 C

Atony of bladder

 D

Glaucoma

Ans. D

Explanation:

Ans. is ‘d’ i.e., Glaucoma


Q. 15

Shortest acting anticholinesterase is ‑

 A

Edrophonium

 B

Pyridostigmine

 C

Glycopyrrolate

 D

Neostigmine

Q. 15

Shortest acting anticholinesterase is ‑

 A

Edrophonium

 B

Pyridostigmine

 C

Glycopyrrolate

 D

Neostigmine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Edrophonium

Edrophonium is the shortest acting anti-ChE.

Why is it so, lets see :

When carbamates (other than edrophonium) and organophophates react with cholinesterase, they form covalent bond at esteratic site, which is considerably resistant to hydrolysis.

In contrast, edrophonium binds electrostatically and by hydrogen bonds at anionic site (not at esteratic site) of cholinesterase. The enzyme inhibitor complex does not involve a covalent bond and is correspondingly short lived (2-10 minutes).

So edrophonium is also called as noncovalent inhibitor.

Quiz In Between


Q. 16

Which of the following is the most sensitive test for the diagnosis of a patient having a clinical presentation of an eye as shown in the picture below? 

 A

Repetitive nerve stimulation test.

 B

Positive edrophonium test.

 C

Measurement of jitter by single fibre electromyography.

 D

Measurement of serum ACh-receptor binding antibodies.

Q. 16

Which of the following is the most sensitive test for the diagnosis of a patient having a clinical presentation of an eye as shown in the picture below? 

 A

Repetitive nerve stimulation test.

 B

Positive edrophonium test.

 C

Measurement of jitter by single fibre electromyography.

 D

Measurement of serum ACh-receptor binding antibodies.

Ans. C

Explanation:

The patient represented in the picture above is most probably suffering from myasthenia gravis as drooping eyelid is the most frequently early sign in these cases.

The diagnostic sensitivity of three laboratory tests [serum antiacetylcholine receptor antibody (AChR-ab) assay, the repetitive nerve stimulation (RNS) test, and, the single fiber EMG (SFEMG)] for myasthenia gravis (MG) was compared in 120 patients. In all cases, at least one of the tests was abnormal. SFEMG was the most sensitive test, being abnormal in 92% of cases, followed by the RNS test (77%) and the AChR-ab assay (73%). SFEMG was abnormal in all cases with negative AChR-ab and RNS tests, in 97% of cases with negative AChR-ab assay, in 89% of cases with negative RNS test, and in 89% of cases with mild MG. We conclude that one of these three tests is abnormal in all cases of MG, and that the SFEMG is most sensitive in the diagnosis of MG.


Q. 17

Rivastigmine & donepezil are drugs used predominantly in the management of ‑

 A

Depression

 B

Dissociation

 C

Delusions

 D

Dementia

Q. 17

Rivastigmine & donepezil are drugs used predominantly in the management of ‑

 A

Depression

 B

Dissociation

 C

Delusions

 D

Dementia

Ans. D

Explanation:

Ans. is ‘d’ i.e., Dementia

  • Rivastigmine, Donepezil, Galantamine and tacrine all are central cholinesterase inhibitors and are used in senile dementia of Alzheimer’s desease.

Quiz In Between



Organophosphates Poisoning (Opp)

OP Poisoning

Q. 1

Signs of organophosphorous poisoning are all EXCEPT:

 A Bradycardia
 B

Salivation

 C Miosis
 D

Bronchodilatation

Q. 1

Signs of organophosphorous poisoning are all EXCEPT:

 A Bradycardia
 B

Salivation

 C Miosis
 D

Bronchodilatation

Ans. D

Explanation:

Bronchodilatation REF: Textbook of Forensic Medicine and Toxicology: Principles and Practice, 5/e By Krishan Vij page 533

“Bronchoconstristition (bronchospasm) not bronchodilatation is seen in OPC poisoning”

Muscarinic signs of OPC poisoning can be remembered as SLUDGE- BBB: Salivation, Lacrimation, Urination, Defecation, Gastric upset, Emesis, Bronchospasm, Blurred vision (Miosis), Bradycardia.


Q. 2 Not a sign of Organophosphorus poisoning is:
 A Bradycardia
 B Salivation
 C Miosis
 D Bronchodilatation
Q. 2 Not a sign of Organophosphorus poisoning is:
 A Bradycardia
 B Salivation
 C Miosis
 D Bronchodilatation
Ans. D

Explanation:

Bronchodilatation


Q. 3

Which of the following is not a feature of organophosphorous poisoning?

 A

Miosis

 B

Increased salivation

 C

Asthma

 D

Tachycardia

Q. 3

Which of the following is not a feature of organophosphorous poisoning?

 A

Miosis

 B

Increased salivation

 C

Asthma

 D

Tachycardia

Ans. D

Explanation:

Organophosphorous poisoning causes bradycardia and not tachycardia.

Manifestations of organophosphorous poisoning includes muscarinic and nicotinic.

Muscarinic manifestations includes bradycardia, vomiting, diarrhea, abdominal cramps, miosis, bradycardia, sweating and excess salivation.

Nicotnic effects includes muscle fasciculations, tremors and weakness. 

Quiz In Between


Q. 4

Delayed onset polyneuropathy after organophosphorous poisoning is seen after a period of:
 A

1-2 weeks

 B

2-4 weeks

 C

4-6 weeks

 D

6-8 weeks

Q. 4

Delayed onset polyneuropathy after organophosphorous poisoning is seen after a period of:
 A

1-2 weeks

 B

2-4 weeks

 C

4-6 weeks

 D

6-8 weeks

Ans. B

Explanation:

Organophosphate-induced delayed polyneuropathy (OPIDP) occurs 2-3 weeks after exposure to large doses of certain organophosphates (OPs) and is due to inhibition of neuropathy target esterase.

Distal muscle weakness with relative sparing of the neck muscles, cranial nerves, and proximal muscle groups characterizes OPIDP. Recovery can take up to 12 months.


Q. 5

What is the case fatality rate of organophosphorous poisoning in India?

 A

15-30%

 B

5-10%

 C

40-50%

 D

2-4%

Q. 5

What is the case fatality rate of organophosphorous poisoning in India?

 A

15-30%

 B

5-10%

 C

40-50%

 D

2-4%

Ans. A

Explanation:

poor intensive care management. Treatment for acute poisoning is essentially supportive, with atropine, oximes, and diazepam.

Atropine is the mainstay of treatment but there are no clear guidelines on dose and duration.

Early resuscitation with atropine, oxygen, respiratory support, and fluids improves oxygen delivery to tissues.

A 2009 double blind randomised placebo controlled trial showed that pralidoxime, commonly given in acute poisoning, does not improve survival. New agents such as magnesium sulphate are in use, but clinical efficacy has not been shown.

Ref: 
1. Srinivas Rao CH, Venkateswarlu V, Surender T, Eddleston M, Buckley NA. Insecticide poisoning in south India—opportunities for prevention and improved medical management. Trop Med Int Health 2005;10:581-8.

2. Eddleston M, Buckley NA, Checketts H, Senarathna L, Mohamed F, Sheriff MH, et al. Speed of initial atropinisation in significant organophosphorus pesticide poisoning—a systematic comparison of recommended regimens. J Toxicol Clin Toxicol2004;42:865-75; 

3. M, Eyer P, Worek F, Juszczak E, Alder N, Mohamed F et al. Pralidoxime in acute organophosphorus insecticide poisoning— a randomised controlled trial. PLoS Med 2009;6:e1000104; Death by insecticide; BMJ 2013;346:f2029.


Q. 6

In organophosphorous compound poisoning, organophosphorous compound actions are:

 A

Phosphorylated enzyme

 B

Irreversibly inhibit cholinesterase

 C

Oximes effective when given beyond 24 hours

 D

a and b

Q. 6

In organophosphorous compound poisoning, organophosphorous compound actions are:

 A

Phosphorylated enzyme

 B

Irreversibly inhibit cholinesterase

 C

Oximes effective when given beyond 24 hours

 D

a and b

Ans. D

Explanation:

A i.e. Phosphorylate enzyme; B i.e. Irreversibly inhibit cholinsterase

Quiz In Between


Q. 7

Most specific test for organophosphorous poisoning is:

 A

RBC cholinesterase level

 B

Plasma cholinestrase level

 C

RBC uroporphyrin level

 D

Measurment of serum level of organophosphorous

Q. 7

Most specific test for organophosphorous poisoning is:

 A

RBC cholinesterase level

 B

Plasma cholinestrase level

 C

RBC uroporphyrin level

 D

Measurment of serum level of organophosphorous

Ans. B

Explanation:

B i.e. Plasma cholinesterase level


Q. 8

Asthma like symptoms is seen in … poisoning :

 A

Arsenic

 B

Organophosphorous

 C

Lead

 D

Gold

Q. 8

Asthma like symptoms is seen in … poisoning :

 A

Arsenic

 B

Organophosphorous

 C

Lead

 D

Gold

Ans. B

Explanation:

B i.e. Organophosphorous


Q. 9

In acute organophosphorus poisoning which of the following is seen :

 A

Dry lungs

 B

Edematous lungs

 C

Pneumonia

 D

All

Q. 9

In acute organophosphorus poisoning which of the following is seen :

 A

Dry lungs

 B

Edematous lungs

 C

Pneumonia

 D

All

Ans. B

Explanation:

B i.e. Edematous lung

Quiz In Between


Q. 10

All are features of organophosphorus poisoning except

 A

Dilated pupil

 B

Brady cardia

 C

Lacrimation

 D

Sweating

Q. 10

All are features of organophosphorus poisoning except

 A

Dilated pupil

 B

Brady cardia

 C

Lacrimation

 D

Sweating

Ans. A

Explanation:

A i.e. Dilated pupil


Q. 11

Which is not a feature of organophosphorus poisoning:

 A

Sweating

 B

Miosis

 C

Tachycardia

 D

Resp. depression

Q. 11

Which is not a feature of organophosphorus poisoning:

 A

Sweating

 B

Miosis

 C

Tachycardia

 D

Resp. depression

Ans. C

Explanation:

C i.e. Tachycardia


Q. 12

In organophosphorous poisoning, following are seen except:

 A

Pupillary dilatation

 B

Salivation

 C

Bronchospasm

 D

Sweating

Q. 12

In organophosphorous poisoning, following are seen except:

 A

Pupillary dilatation

 B

Salivation

 C

Bronchospasm

 D

Sweating

Ans. A

Explanation:

A i.e. Pupillary dilation

Quiz In Between


Q. 13

A patient comes with Pinpoint pupil, salivation, tremors and red tears. Cholinesterase activity was 30% of Normal. Probable Diagnosis is:

 A

Opium

 B

Organophosphate poisoning

 C

Dhatura

 D

Organochloride pesticide poisoning

Q. 13

A patient comes with Pinpoint pupil, salivation, tremors and red tears. Cholinesterase activity was 30% of Normal. Probable Diagnosis is:

 A

Opium

 B

Organophosphate poisoning

 C

Dhatura

 D

Organochloride pesticide poisoning

Ans. B

Explanation:

B i.e. Organophosphorus

– Most common way of suicide is by use of insectisidesQ.

Malathion is alkyl phosphateQ, whereas parathion, paraoxon, diazinon (TIK-20) and folidol are aryl phosphatase. – Patient with organophosphorus poisoning presents with chromolacryorroea (sheding of pink tears d/t accumulation of porphyrin), increased bronchial secretion (edematous lung) & broncho-constriction simulating asthma, miosis/ pin point pupil (not mydriasis) , bradycardia (not tachycardia), hypertension, fasciculation, excessive lacrymation/ sweating/ salivation, confusion, unconsciousness, coma with depression of respiratory & circulatory centersQ.

Patients with organophosphorus poisoning have BradycardiaQ (not tachycardia). In Organophosphorus poisoning there is miosisQ due to cholinergic effect (not mydriasis).

Features of Organophosphorus ps. are ‘B3 with increased/ water loss’ i.e. Bronchospasm, Bradycardia, Blurring of vision & Sweating/ Lacrimation/ Salivation/ Micturation/ DiarrheaQ

– Organophosphorus irreversibly inhibit cholinesterases by phosphorylationQ. Plasma cholinesterase is more sensitive and falls more rapidly & prior to RBC cholinesterasesQ. Monitoring of levels are done as plasma ChE levels reach normal in 7-10 days in treated and 4 weeks in untreated cases. Oximes should be started as early as possible preferably within 24 hours before phosphorylated enzyme becomes resistant to hydrolysis.

The drug of choice for organophosphorous poisoning is AtropineQ. The cholinesterase reactivators, the oxime compounds (Pralidoxime, Obidoxime, Diacetyl monoxime) are used to supplement atropine. Atropine (antidote) is highly effective in counteracting peripheral muscarinic effects, and higher doses are required to antagonize central (CNS) effects. However it is not effective against nicotinic actionsQ. It is ineffective on respiratory centre in presence of severe asphyxia and also if BP fallsQ. When cyanosis is present maximum oxygenation should be achieved, before giving atropine to avoid increased risk of ventricular tacky cardiaQ associated with hypoxia.


Q. 14

A 20 yrs aged patient, presents in coma with pin point pupils and fasciculations but no fever. Most probable diagnosis is:

 A

Head injury

 B

Dhatura

 C

Pontine haemorrhage

 D

Organophosphorus poisoning

Q. 14

A 20 yrs aged patient, presents in coma with pin point pupils and fasciculations but no fever. Most probable diagnosis is:

 A

Head injury

 B

Dhatura

 C

Pontine haemorrhage

 D

Organophosphorus poisoning

Ans. D

Explanation:

D i.e. Organophosphorus poisoning

Pinpoint pupils (miosis) is seen in ‘Bar Car OR Mor – Chlor’ i.e. Barbiturates, Carbolic acid (Phenol), Organophosphorus, Morphine (Opioid), Choral hydrate.Q & Pontine haemorrhageQ

So we are left with two options – Pontine haemorrhage & Organophosphorus.

Not useful in Carbamate

poisoning

Useful in Organophosphorus

poisoning

Physo / Pyrido / Riva/Neo –

ParathionQ & MalathionQ

stigmineQ

– Dyflos (DEP – D-iso fluro

– Ambenonium &

phosphateQ)

EdrophoniumQ

Diazinon (TIK – 20)

– Carabaryl (sevin)

EchothiophateQ

– PropoxurQ (Baygon)

– Tabun, Sarin, Soman

– Demecarium

 

– Donepezil

 


Q. 15

Pinpoint pupil is seen in which of the following conditions :

 A

Organophosphorus poisoning

 B

Opium poisoning

 C

Celephos poisoning

 D

a and b

Q. 15

Pinpoint pupil is seen in which of the following conditions :

 A

Organophosphorus poisoning

 B

Opium poisoning

 C

Celephos poisoning

 D

a and b

Ans. D

Explanation:

A i.e. Organophosphorus; B i.e. Opium

Quiz In Between


Q. 16

Organophosphate inhibits –

 A

Anionic site ofAchEs

 B

Esteratic site ofAchEs

 C

Ach

 D

None

Q. 16

Organophosphate inhibits –

 A

Anionic site ofAchEs

 B

Esteratic site ofAchEs

 C

Ach

 D

None

Ans. B

Explanation:

Ans. is ‘b’ i.e., Esteratic site of AchEs

  1. Acetylcholinesterase has two sites:

i)         Catalytic or esteratic site –9 Active site

ii)       Anionic site

  • It is quite obvious that to inhibit the action of acetylcholinesterase the active site has to be inhibited and it is esteratic site:

i)        Organophosphates phosphorylate esteratic site.

Carbamates carbomylate esteratic site.


Q. 17

Antidote for organophosphorous poisoning is

 A

Atropine

 B

Neostigmine

 C

Succinylcholine

 D

D-Tubocurarine

Q. 17

Antidote for organophosphorous poisoning is

 A

Atropine

 B

Neostigmine

 C

Succinylcholine

 D

D-Tubocurarine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Atropine

Pharmacological treatment of organonhosphatepoisoning

Atropine

o Atropine is the mainstay of treatment (antidote of choice).

o Atropine antagonizes the muscarinic parasympathetic effects of organophosphate (excessive secretion and vasodilation), but does not antagonize nicotinic effects, i.e., neuramuscular blockers (Atropine blocks muscarinic receptors, i.e., it is an antimuscarinic)

o Atropine antagonizes both peripheral as well as central nervous system effects of organophosphates. Cholinesterase regenerator compounds (oximes)

o Pralidoxime is most commonly used oxime.

o Unlike atropine, they antagonize both muscarinic and nicotinic effects.

o They antagonize only peripheral effects, but not central effects except for diacetylmonoxime (DAM) which crosses BBB and antagonizes central effects also.


Q. 18

Atropine is useful in organophosphate poisoning because it –

 A

Reactivates acetylcholinesterase

 B

Competes with acetylcholine release

 C

Binds with both nicotinic and muscarinic acetylcholine receptors

 D

Is a competitive antagonist of acetylcholine

Q. 18

Atropine is useful in organophosphate poisoning because it –

 A

Reactivates acetylcholinesterase

 B

Competes with acetylcholine release

 C

Binds with both nicotinic and muscarinic acetylcholine receptors

 D

Is a competitive antagonist of acetylcholine

Ans. D

Explanation:

Ans. is ‘d’ i.e., Is a competitive antagonist of acetylcholine

o Atropine acts as competitive antagonist at muscarinic receptors. It has no activity on nicotinic receptors and has nothing to do with Ach release.

Quiz In Between


Q. 19

Atropine-mechanism of action in organophosphate poisoning-

 A

Reactivation of choline-esterase

 B

Acts on central and peripheral post.ganglionic receptors

 C

Acts on central and peripheral cholinergic receptors

 D

Acts on peripheral cholinergic receptors only

Q. 19

Atropine-mechanism of action in organophosphate poisoning-

 A

Reactivation of choline-esterase

 B

Acts on central and peripheral post.ganglionic receptors

 C

Acts on central and peripheral cholinergic receptors

 D

Acts on peripheral cholinergic receptors only

Ans. C

Explanation:

Ans. is ‘c’ i.e., Acts on central and peripheral cholinergic receptors

o In organophosphate poisoning, atropine counteracts the peripheral muscarinic symptoms and at higher doses central effects as well.

o Atropine does not reverse nicotinic action i.e., peripheral muscular paralysis.


Q. 20

All are organophosphorus poison, except

 A

Abate

 B

Dibenanone

 C

Propoxur

 D

Malathione

Q. 20

All are organophosphorus poison, except

 A

Abate

 B

Dibenanone

 C

Propoxur

 D

Malathione

Ans. C

Explanation:

Ans. is ‘c’ i.e., Propoxur 


Q. 21

Organophosphate insecticides are all except 

 A

Dieldrin

 B

Fenthion 

 C

Diazinon

 D

All

Q. 21

Organophosphate insecticides are all except 

 A

Dieldrin

 B

Fenthion 

 C

Diazinon

 D

All

Ans. A

Explanation:

Ans. is `a’ i.e., Dieldrin

Quiz In Between


Q. 22

Drug NOT given in organophosphorous poisoning:

September 2012

 A

Atropine

 B

Pralidoxime

 C

Activated charcoal

 D

Physostigmine

Q. 22

Drug NOT given in organophosphorous poisoning:

September 2012

 A

Atropine

 B

Pralidoxime

 C

Activated charcoal

 D

Physostigmine

Ans. D

Explanation:

Ans. D i.e. Physostigmine

Organophosphate poisoning

  • It results from exposure to organophosphates (OPs), which cause the inhibition of acetylcholinesterase (AChE), leading to the accumulation of acetylcholine (ACh) in the body.
  • The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM: (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal motility, Emesis, miosis)
  • An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.

Pyridostigmine is a parasympathomimetic and a reversible cholinesterase inhibitor.


Q. 23

NOT a feature of organophosphate poisoning:

March 2013 (a, c, d, e, g)

 A

Diarrhea

 B

Dilated pupil

 C

Salivation

 D

Bradycardia

Q. 23

NOT a feature of organophosphate poisoning:

March 2013 (a, c, d, e, g)

 A

Diarrhea

 B

Dilated pupil

 C

Salivation

 D

Bradycardia

Ans. B

Explanation:

Ans. B i.e. Dilated pupil


Q. 24

Drug of choice for organophosphorous poisoning:

March 2013 (e)

 A

EDTA

 B

BAL

 C

PAM

 D

All of the above

Q. 24

Drug of choice for organophosphorous poisoning:

March 2013 (e)

 A

EDTA

 B

BAL

 C

PAM

 D

All of the above

Ans. C

Explanation:

Ans. C i.e. PAM

Treatment of organophosphate poisoning

  • Current antidotes for OP poisoning consist of a pretreatment with carbamates to protect AChE from inhibition by OP compounds and post-exposure treatments with anti-cholinergic drugs.
  • Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE.
  • Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime)

Quiz In Between


Q. 25

Antidote for organophosphates poisoning are all except:          

September 2009 March 2013 (b, d)

 A

Physostigmine

 B

Activated charcoal

 C

Pralidoxime

 D

Atropine

Q. 25

Antidote for organophosphates poisoning are all except:          

September 2009 March 2013 (b, d)

 A

Physostigmine

 B

Activated charcoal

 C

Pralidoxime

 D

Atropine

Ans. A

Explanation:

Ans. A: Physostigmine

The mainstays of medical therapy in organophosphate (OP) poisoning include ‑

  • Atropine-arrests muscarinic effects,
  • Pralidoxime (2-PAM)-acts by competing for the phosphate moiety of the organophosphorus compound and release it from the cholinesterase enzyme
  • Benzodiazepines (e.g., diazepam)-For convulsions

Intravenous glycopyrrolate or diphenhydramine may provide an alternative centrally acting anticholinergic agent used to treat muscarinic toxicity if atropine is unavailable or in limited supply


Q. 26

Best indicator for beneficial effect of atropine in a patient with organophosphorous poisoning is:

March 2012

 A

Heart rate

 B

Pupil

 C

Blood pressure

 D

Ventilation

Q. 26

Best indicator for beneficial effect of atropine in a patient with organophosphorous poisoning is:

March 2012

 A

Heart rate

 B

Pupil

 C

Blood pressure

 D

Ventilation

Ans. A

Explanation:

Ans: A i.e. Heart rate

In organophosphate poisoning, atropine should be administered in doses of 0.6-2 mg i.v., repeated every 10-25 minutes until secretions are controlled, the skin is dr./ and there is sinus tachycardia.


Q. 27

Organophosphorus insecticides are all, except:

MP 11

 A

Chlorpyriphos

 B

Gardona (tetrachlorvinphos)

 C

Dimethoate

 D

Diethyltoluamide (DEET)

Q. 27

Organophosphorus insecticides are all, except:

MP 11

 A

Chlorpyriphos

 B

Gardona (tetrachlorvinphos)

 C

Dimethoate

 D

Diethyltoluamide (DEET)

Ans. D

Explanation:

Ans. Diethyltoluamide (DEET)

Quiz In Between


Q. 28

which is an organophosphate: 

AFMC 12

 A

Diazinon

 B

Endrin

 C

Malathion

 D

Parathion

Q. 28

which is an organophosphate: 

AFMC 12

 A

Diazinon

 B

Endrin

 C

Malathion

 D

Parathion

Ans. B

Explanation:

Ans. Endrin


Q. 29

All are features of organophosphorus poisoning, except:           

UPSC 07; DNB 10; SGPGI 11; FMGE 13

 A

Mydriasis

 B

Bradycardia

 C

Lacrimation

 D

Sweating

Q. 29

All are features of organophosphorus poisoning, except:           

UPSC 07; DNB 10; SGPGI 11; FMGE 13

 A

Mydriasis

 B

Bradycardia

 C

Lacrimation

 D

Sweating

Ans. A

Explanation:

Ans. Mydriasis


Q. 30

A patient was found in a locked room having labored breathing, kerosene-like smell, pin-point pupils, frothing from mouth, cyanosed and pulse rate of 40/min. Likely diagnosis is:  

KCET 13

 A

Cocaine poisoning

 B

Opium poisoning

 C

Organophosphorus poisoning

 D

Alcohol poisoning

Q. 30

A patient was found in a locked room having labored breathing, kerosene-like smell, pin-point pupils, frothing from mouth, cyanosed and pulse rate of 40/min. Likely diagnosis is:  

KCET 13

 A

Cocaine poisoning

 B

Opium poisoning

 C

Organophosphorus poisoning

 D

Alcohol poisoning

Ans. C

Explanation:

Ans. Organophosphorus poisoning

Quiz In Between


Q. 31

Which of the following is not a phase of organophosphorus poisoning:           

Odisha 11

 A

Acute cholinergic phase

 B

Intermediate syndrome

 C

OPC induced delayed polyneuropathy

 D

Late onset proximal myopathy

Q. 31

Which of the following is not a phase of organophosphorus poisoning:           

Odisha 11

 A

Acute cholinergic phase

 B

Intermediate syndrome

 C

OPC induced delayed polyneuropathy

 D

Late onset proximal myopathy

Ans. D

Explanation:

Ans. Late onset proximal myopathy


Q. 32

A patient comes with pinpoint pupil, salivation, tremors and red tears. cholinesterase activity was 30% of Normal. Probable diagnosis is:

 A

Opium

 B

Organophosphate poisoning

 C

Dhatura

 D

Organochlorine pesticide poisoning

Q. 32

A patient comes with pinpoint pupil, salivation, tremors and red tears. cholinesterase activity was 30% of Normal. Probable diagnosis is:

 A

Opium

 B

Organophosphate poisoning

 C

Dhatura

 D

Organochlorine pesticide poisoning

Ans. B

Explanation:

Ans. b. Organophosphate poisoning

  • Pinpoint pupil, excessive salivation, tremors and red tears in a patient with 30% cholinesterase activity of normal are almost diagnostic of organophosphate poisoning.

Organophosphorus Poisoning

  • The effect of acute intoxication by one anti-choninesterase agents are manifested by muscarinic and nicotinic signs and symptoms.
  • Systemic effects appear within minutes after inhalation of vapors or aerosols.
  • In contrast, the onset of symptoms is delayed after GI and percutaneous absorption.
  • Typical smell of organophosphorus compounds, which is a pungent garlic-like odouQ

Organophosphorus irreversibly inhibits acetyl cholinesterase decreasing its activity

Severity of poisoning Acetyl cholinesterase activity
Mild poisoning 20-50% of normal
Moderate poisoning 10-20% of normal
Severe poisoning <10% of normal

Manifestation:

  • Nicotinic action at NMJ of skeletal muscle consists of fatigability and generalized weakness, involuntary twitchings, scattered fasciculations and eventually severe weakness and paralysisQ
  • The most serious consequence is paralysis of the respiratory muscleQ
  • Ocular Manifestations: Miosis, pain, conjunctival congestion, diminished vision, ciliary spasm
  • Respiratory effects: Tightness in the chest, wheezing respiration
  • GI effects: Anorexia, nausea, vomiting, cramps
  • Others: Extreme salivation, involuntary defecation, lacrimation, bradycardia, hypotension, penile erection

Red Tears or Chromolacryorrhea

  • Shedding of red tears due to accumulation of porphyrin pigments in lacrimal glands
  • Very rare phenomenon, seen in organophosphorus poisoning°

Treatment:

  • Termination of further exposure to the poison
  • Maintain patent airway, positive pressure ventilation if it is failing
  • Supportive measures: Maintain BP, hydration, control of convulsions with judicious use of diazepam
  • Specific antidote:
  • – Atropine: It is highly effective in counteracting the muscarinic symptoms but higher doses are required to antagonize the central effects. It doesn’t reverse peripheral muscular paralysisQ.

Q. 33

Fat mesentry is sent for investigation in which poisoning-

 A

Carbon monoxide

 B

Organophosphorous

 C

Arsenic

 D

Lead

Q. 33

Fat mesentry is sent for investigation in which poisoning-

 A

Carbon monoxide

 B

Organophosphorous

 C

Arsenic

 D

Lead

Ans. B

Explanation:

Ans. is ‘b’ i.e., Organophosphorous

  • For organophosphorous (pesticides/insecticides) poisoning fatty tissue from abdominal wall, perinephric fat and brain are preserved.
  • The viscera should be preserved in cases of suspected poisoning and must be send for toxicological examination. The viscera are preserved according to suspected poison :
  1. Brain (100 gm of cerebrum or cerebellun) : Carbon monoxide, cyanide, organophosphates, organic volatile poisons, opiates, barbiturates, alkaloids, strychnine (nux vomica).
  2. Spinal cord (entire length) : Strychnine.
  3. Heart : Strychnine, digitalis.
  4. Lung (one) : Gaseous poison (e.g. CO), alcohol, chloroform, cyanide.
  5. Bone (10 cm shaft femur) : Subacute and chronic poisoning by heavy metals, e.g. arsenic, antimony, radium, thallium.
  6. Hair (20-30 in number or 5 gm) and nails (all finger and toe) : Subacute and chronic poisoing by heavy metals, e.g. arsenic, antimony, radium, thallium.
  7. Uterus, its appendages and upper part of vagina : Criminal abortion.
  8. Fat (10 gm from abdomen or perinephric region) : Pesticides and insectisides.
  9. Vitreous humor : Alcohol, chloroform.
  10. Bile : Glutathione, cocaine, barbiturates, methadone, narcotics.
  11. Skin : Injection of insulin, morphin, heroin, cocain etc.
  12. Urine : Alcohol, barbiturate and opium.

Q. 34

Type II paralysis in organophosphorous poisoning treatment is ‑

 A

Atropine

 B

Oximes

 C

Symptomatic treatment 

 D

No treatment

Q. 34

Type II paralysis in organophosphorous poisoning treatment is ‑

 A

Atropine

 B

Oximes

 C

Symptomatic treatment 

 D

No treatment

Ans. C

Explanation:

Ans. is ‘c’ i.e., Symptomatic treatment 

  • Paralysis due to organophosphate (OP) poisoning can be three types ‑

1. Type I (cholinergic phase)

  • It involves acute paralysis secondary to persistent depolarization at the neuromuscular junction caused by persistent stimulation by excessive Ach.
  • Treatment of choice is atropine with or without oximes.

2. Type II

  • It is also called as intermediate syndrome.
  • It develops 1-4 days after resolution of acute cholinergic symptoms.
  • It is manifested as paralysis and respiratory distress.
  • It involves proximal muscles with relative sparing of distal muscle groups.
  • The pathogenesis presumed to be dysfunction of neuromuscular junction caused by downregulation of presynaptic and postsynaptic nicotinic receptors due to release of excessive Ach and Ca’ respectively.
  • Atropine is ineffective, symptomatic treatment is given.

3. Type III

  • It involves OP-induced delayed polyneuropathy (OPIDN).
  • It occurs 1-3 weeks after exposure and is associated with demyelination of axons.
  • It is not caused by cholinesterase inhibition but rather by neuropathy target esterase (NTE) inhibition.
  • It involves distal muscles with relative sparing of neck muscles, cranial nerves, and proximal muscles.

Quiz In Between



Glaucoma Pharmacological Management

Glaucoma Pharmacological Management

Q. 1

In a hypertensive patient with glaucoma which of the following is not used:

 A

Dipivefrine

 B

Alpha blocker

 C

Alpha agonist

 D

Laser trabeculoplasty

Q. 1

In a hypertensive patient with glaucoma which of the following is not used:

 A

Dipivefrine

 B

Alpha blocker

 C

Alpha agonist

 D

Laser trabeculoplasty

Ans. A

Explanation:

Ans. Dipivefrine


Q. 2

In primary open-angle glaucoma pilocarpine eye drops lowers the intraocular pressure by its direct action on the:

 A

Trabecular meshwork

 B

Ciliary epithelium

 C

Longitudinal fibres of the ciliary muscle

 D

All of the above

Q. 2

In primary open-angle glaucoma pilocarpine eye drops lowers the intraocular pressure by its direct action on the:

 A

Trabecular meshwork

 B

Ciliary epithelium

 C

Longitudinal fibres of the ciliary muscle

 D

All of the above

Ans. C

Explanation:

Ans. Longitudinal fibres of the ciliary muscle


Q. 3

In primary angle-closure glaucoma pilocarpine lowers the intraocular pressure by its direct action on the:

 A

Sphincter pupillae muscle

 B

Ciliary epithelium

 C

Trabecular meshwork

 D

All of the above

Q. 3

In primary angle-closure glaucoma pilocarpine lowers the intraocular pressure by its direct action on the:

 A

Sphincter pupillae muscle

 B

Ciliary epithelium

 C

Trabecular meshwork

 D

All of the above

Ans. A

Explanation:

Ans. Sphincter pupillae muscle

Quiz In Between


Q. 4

Combination of pilocarpine and epinephrine use in glaucoma treatment may inhibit:

 A

Pigmented pupillary cyst

 B

Retinal detachment

 C

Vitreous haemorrhage

 D

Iridocyclitis

Q. 4

Combination of pilocarpine and epinephrine use in glaucoma treatment may inhibit:

 A

Pigmented pupillary cyst

 B

Retinal detachment

 C

Vitreous haemorrhage

 D

Iridocyclitis

Ans. A

Explanation:

Ans. Pigmented pupillary cyst


Q. 5

Drug CONTRAINDICATED in glaucoma patients suffering from bronchial asthma is:

September 2012, March 2013 (g)

 A

Betaxolol

 B

Brimonidine

 C

Timolol maleate

 D

Latanoprost

Q. 5

Drug CONTRAINDICATED in glaucoma patients suffering from bronchial asthma is:

September 2012, March 2013 (g)

 A

Betaxolol

 B

Brimonidine

 C

Timolol maleate

 D

Latanoprost

Ans. C

Explanation:

Ans. C i.e. Timolol maleate

Contraindications of Timolol maleate

  • Bronchial asthma;
  • A history of bronchial asthma;
  • Severe chronic obstructive pulmonary disease
  • Sinus bradycardia;
  • Second or third degree atrioventricular block;
  • Overt cardiac failure
  • Cardiogenic shock;
  • Hypersensitivity to any component of this product.

Q. 6

Pain in absolute glaucoma is best relieved by:

March 2004

 A

Retrobulbar injection of alcohol

 B

Analgesics

 C

Trabeculectomy

 D

Miotics

Q. 6

Pain in absolute glaucoma is best relieved by:

March 2004

 A

Retrobulbar injection of alcohol

 B

Analgesics

 C

Trabeculectomy

 D

Miotics

Ans. A

Explanation:

Ans. A i.e. Retrobulbar injection of steroid

Quiz In Between


Q. 7

Drug which should be avoided in angle closure glaucoma is:      

 A

Acetazolamide

 B

Atropine

 C

Timolol

 D

Mannitol

Q. 7

Drug which should be avoided in angle closure glaucoma is:      

 A

Acetazolamide

 B

Atropine

 C

Timolol

 D

Mannitol

Ans. B

Explanation:

Ans. B: Atropine

Anticholinergic drugs (atropine 1%, homatropine2%) dilates the pupil

In a patient above 60 years of age having hypermetropia and a shallow anterior chamber, mydriasis may precipitate acute angle closure glaucoma


Q. 8

Which antiglaucoma drug decreases aqueous formation

 A

Prostaglandins

 B

Beta – blockers

 C

Mannitol

 D

Pilocarpine

Q. 8

Which antiglaucoma drug decreases aqueous formation

 A

Prostaglandins

 B

Beta – blockers

 C

Mannitol

 D

Pilocarpine

Ans. B

Explanation:

Ans. is ‘b’ i.e., Beta – blockers


Q. 9

Selective alpha 2 agoinst used in glaucoma

 A

Tirriolol

 B

Epinephrine

 C

Dipivefrine

 D

Brimonidine

Q. 9

Selective alpha 2 agoinst used in glaucoma

 A

Tirriolol

 B

Epinephrine

 C

Dipivefrine

 D

Brimonidine

Ans. D

Explanation:

Ans. is ‘d’ i.e., Brimonidine

Quiz In Between


Q. 10

Drug kept as a last resort in the management of primary open angle glaucoma is ‑

 A

Latanoprost

 B

Topical beta blocker

 C

Brimonidine

 D

Oral acetazolamide

Q. 10

Drug kept as a last resort in the management of primary open angle glaucoma is ‑

 A

Latanoprost

 B

Topical beta blocker

 C

Brimonidine

 D

Oral acetazolamide

Ans. D

Explanation:

Ans. is ‘d’ i.e., Oral acetazolamide

Treatment of POAG (Primary open angle glaucoma) 

Following treatment options are available for POAG :

Medical therapy :- Total medical therapy is the treatment of choice for POAG. Topical 13-blockers (Timolol, Betoxalol, Levobunolol, carteolol) are the drugs of choice. Topical prostaglandin analogues (Latanoprost, bimatoprost, travoprost) are the second choice drugs. Other topical drugs for POAG are:- LI Alpha agonists (non – selective : epinephrine, dipivefrine; and Selective – a2: apraclonidine, brimonidine)

Carbonic anhydrase inhibitors (Dorzalamide, brinzolamide)

Cholinomimetic drugs (Pilocarpine, physostigmine, echothiophate, carbachol) Pilocarpire has several drawbacks, therefore, is being considered as an adjunctive therapy only as a last resort.

Approach to treatment of POAG

  • Start monotherapy with topical P-blocker or latanoprost.
  • If target IOT is not attained either change over to the alternative drug or use both the above concurrently.
  • Brimonidine/dorazolamide/dipivefrine are used only when there are contraindications to PG analogues or 13-blockers.
  • Topical miotics and oral acetazolamide are added only as the last resort.
  • Systemic therapy is considered only as a last resort. Drugs used for systemic therapy are :- (i) Carbonic anhydrase inhibitors (Acetazolamide, Dichlorphenamide, methazolamide), (ii) Hyperosmotic agents (mannitol, glycerol).

Q. 11

Main MOA brimonidine in glaucoma ‑

 A

Decreased aqueous secretion

 B

Increased trabecular outflow

 C

Increased uveoscleral outflow

 D

Reduce vitreous volume

Q. 11

Main MOA brimonidine in glaucoma ‑

 A

Decreased aqueous secretion

 B

Increased trabecular outflow

 C

Increased uveoscleral outflow

 D

Reduce vitreous volume

Ans. A

Explanation:

Ans. is ‘a’ i.e., Decreased aqueous secretion


Q. 12

Latanoprost used topically in glaucoma primarily acts by‑

 A

Decreasing aqueous humor formation

 B

Increasing uveoscleral outflow

 C

Releasing pupillary block

 D

Increasing trabecular outflow

Q. 12

Latanoprost used topically in glaucoma primarily acts by‑

 A

Decreasing aqueous humor formation

 B

Increasing uveoscleral outflow

 C

Releasing pupillary block

 D

Increasing trabecular outflow

Ans. B

Explanation:

Ans. is ‘b’ i.e., Increasing uveoscleral outflow

Quiz In Between


Q. 13

Drug used in refractory glaucoma ‑

 A

Systemic glucocorticoid

 B

ACE inhibitor

 C

Alpha agonist

 D

Beta blocker

Q. 13

Drug used in refractory glaucoma ‑

 A

Systemic glucocorticoid

 B

ACE inhibitor

 C

Alpha agonist

 D

Beta blocker

Ans. C

Explanation:

Ans. is ‘c’ i.e., Alpha agonist

Drug of choice for initial treatment of open angle glaucoma is either an topical β-blocker or topical PG analogue (latanoprost)

It target IOT is not attained either change over to alternative drug or use both concurrently.

In refractory cases (who are not responding to (3-blockers and PG analogues), topical α-agonist (Brimozidine) or topical carbonic anhydrase inhibitor (dorazolamide) is added.

It target IOT is still not attained, laser trabeculoplasty is considered.


Q. 14

Acute angle closure glaucoma first line treatment‑

 A

Iv mannitol

 B

Acetazolamide

 C

Pilocarpine

 D

Beta blocker eyedrops

Q. 14

Acute angle closure glaucoma first line treatment‑

 A

Iv mannitol

 B

Acetazolamide

 C

Pilocarpine

 D

Beta blocker eyedrops

Ans. A

Explanation:

Ans. is ‘a’ i.e., I.V. Mannitol

Treatment of angle closure glaucoma

  • Definitive treatment (treatment of choice) is surgery. However, intially drugs are used to decrease KW during an acute attack. Approach of treatment is as follows:-
  • Start i.v. mannitol or i.v. acetazolamide
  • When IOT starts falling, start topical pilocarpine or β-blocker (timolol).
  • Apraclonidine/latanoprost may be added.
  • Once IOT is reduced, surgery is done.
  • Topical pilocarpine 2% is the preferred antiglaucomatous drug.
  • After control of IOP, Laser (Nd : YAG) peripheral irodotomy is the definitive management of choice. If laser is not available surgical peripheral iridectomy is the procedure of choice. Other surgical procedures used are filteration surgeries (like trabeculectomy, deep sclerotomy, Viscoanulostomy).
  • Symptomatic treatment during an attack also includes analgesics, antiemetic and topical corticosteroids to reduce inflammation. Mydriatics (e.g. atropine) are contraindicated as they precipitate glaucoma.
  • PACG is a bilateral disease, the fellow eye is at risk of developing an acute attack in 50% cases in future. Therefore a prophylactic peripheral laser iridotomy should be performed in the fellow eye.

Q. 15

A patient with glaucoma is being treated with systemic beta blocker. All of the following can be given to the patient except

 A

Brimonidine

 B

Dorzolamide

 C

Levobunolol

 D

Prostaglandin

Q. 15

A patient with glaucoma is being treated with systemic beta blocker. All of the following can be given to the patient except

 A

Brimonidine

 B

Dorzolamide

 C

Levobunolol

 D

Prostaglandin

Ans. C

Explanation:

Ans. c. Levobunolol

  • Brimonidine, dorzolamide and prostaglandin are topical anti-glaucoma drugs. These drugs do not have systemic side effects, while levobunolol (beta-blocker) is systemic anti-glaucoma drug given orally, having systemic side effects. That is why in patients with glaucoma treated with systemic beta blockers, levobunolol may add on the side effects of beta-blockers, hence avoided in the above mentioned patient.

Topical Anti-glaucoma Drugs

Adrenergic agonist

  • Non-selective: Epinephrine, Dipivefrine
  • Alpha2-selective: Apraclonidine, Brimonidine

Adrenergic antagonist

  • Beta—blocker (Non-selective): Timolol, Levobunolol, Carteolol, Metipranolol, Adapralol
  • Betal-blocker: Betaxolol

Miotics (direct parasympatomimetics)

  • Pilocarpine, Physostigmine
  • Ecothiophate, Carbachol, Demacarium

Prostaglandin analogues

  • Latanoprost

Carbonic anhydrase inhibitors

Dorzolamide

Systemic Antiglaucoma Drugs

Carbonic anhydrase inhibitors

  • Acetazolamide
  • Dichlorphenamide
  • Methazolamide

Hyperosmotic agents

  • Mannitol
  • Glycerol

Quiz In Between


Q. 16

Which of the following antiglaucoma medications can cause drowsiness

 A

Latanoprost

 B

Timolol

 C

Brimonidine

 D

Dorzolamide

Q. 16

Which of the following antiglaucoma medications can cause drowsiness

 A

Latanoprost

 B

Timolol

 C

Brimonidine

 D

Dorzolamide

Ans. C

Explanation:

Ans. is ‘c’ i.e., Brimonidine 

Important systemic side effects of topical agents

  • n-blockers : Bronchospasm, bradycardia, .cardiac output, hypotension, depression, impotence, altered lipid profile (hypercholesterolemia).
  • Sympathomimetics
  • Non selective (Dipivefrine, epinephrine) :- Hypertension, arrhythmias
  • Selective a-2 (Brimonidine):- Drowsiness, fatigue, BP changes
  • Selective a-1 & a2 (Apraclonidine) :- Drowsiness, Headache, fatigue
  • Chlinomimetics (Pilocarpine) :- Sweating, salivation, urinary frequency, diarrhea, bronchospasm.
  • Carbonic anhydrase inhibitors (Dorzolamide, brinzolamide) :- Bitter taste, headache, asthenia, renal calculi.
  • Prostaglandin analogues (Latanoprost) :- Headache, symptoms of URTI.

Q. 17

. Which of the antiglaucoma drug is contra­indicated in sulfonamide hypersensitivity ‑

 A

3-blockers

 B

Pilocarpine

 C

Acetazolamid

 D

Prostaglandin analogues

Q. 17

. Which of the antiglaucoma drug is contra­indicated in sulfonamide hypersensitivity ‑

 A

3-blockers

 B

Pilocarpine

 C

Acetazolamid

 D

Prostaglandin analogues

Ans. C

Explanation:

. Ans. is ‘c’ i.e., Acetazolamide 

Carbonic anhydrase inhibitors (acetazolamide) are contraindicated in sulfonamide hypersensitivity.

Important contraindications of topical agents of POAG

13-blockers (non-selective) :- Asthma, COPD, CHF, sinus bradycardia, AV block

Cholinomimetic (Pilocarpine) :- Uveitis

 Sympathomimetic agentsq                  

Dipiveferine :-Angle closure glaucoma, cardiovascular disease.

 Brimonidine, Apraclonidine :- Use of MAO inhibitors, hypertensive crisis, Parkinsonism.

 Carbonic anhydrase inhibitors :- Hypersensitivity to sulfonamide, eye injury   

Prostaglandin analogues :- Ocular inflammation or infection

 


Q. 18

Drug of choice for open angle glaucoma –

 A

Acetazolamide

 B

Latanoprost

 C

Timolol

 D

Brimonidine

Q. 18

Drug of choice for open angle glaucoma –

 A

Acetazolamide

 B

Latanoprost

 C

Timolol

 D

Brimonidine

Ans. C

Explanation:

Ans. is ‘c’ i.e., Timolol 

Important acts

Angle closure glaucoma

Treatment of choice for acute congestive glaucoma Laser iridotomy (1″ choice), Peripheral iridectency (2″ choice)

Drug of choice for acute congestive glaucoma Pilocarpine

Initially IOP is controlled (first drug used)→ Systemic mannitol or acetazolamide

Open angle glaucoma

Treatment of choice                                   Topical antiglaucoma drugs

Drug of choice                                           /3 – blocker (Timolol, betaxolol, levobunalol)

Surgery of choice                                      Argon or diode laser trabeculoplasty


Q. 19

Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it 

 A

Produces no miosis

 B

Possess membrane stabilizing activity

 C

Increases outflow of aqueous humor

 D

Is a selective beta-adrenoceptor blocker

Q. 19

Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it 

 A

Produces no miosis

 B

Possess membrane stabilizing activity

 C

Increases outflow of aqueous humor

 D

Is a selective beta-adrenoceptor blocker

Ans. A

Explanation:

Ans. is ‘a’ i.e., Produces no miosis 

Advantages of topical n-blockers (timolol) over miotics (pilocarpinel

No change in pupil size (no miosis)              →       No fluctuation in I.O.T.

No induced myopia                                     →       Convenient once/twice daily applications

No ciliary spasm (no spasm of accomodation)  →    Few systemic side effects.

Quiz In Between



Beta Adrenergic Receptor Antagonist / Beta-Blockers

Beta adrenergic receptor antagonists or beta-blockers

Q. 1 Beta blockers are contraindicated in?
 A Decompensated CCF
 B

Asthma

 C Atherosclerosis
 D

All of the above

Q. 1 Beta blockers are contraindicated in?
 A Decompensated CCF
 B

Asthma

 C Atherosclerosis
 D

All of the above

Ans. D

Explanation:

All of the above REF: KDT 6th ed p.139

CONTRAINDICATIONS OF BETA BLOCKERS:

  • Decompensated CCF
  • Bradycardia , HR< 60/min
  • COPD , Asthma
  • Variant angina
  • Carbohydrate intolerance
  • Hyperlipidemia
  • Atherosclerosis
  • Partial and complete heart block
  • Raynaud’s disease (95) 

Q. 2

Beta blockers are antiarrhythmic agents of type:

 A I
 B II
 C III
 D IV
Q. 2

Beta blockers are antiarrhythmic agents of type:

 A I
 B II
 C III
 D IV
Ans. B

Explanation:

II


Q. 3 Which of the following is not a cardioselective beta blocker:
 A Acebutol
 B Atenolol
 C Pindolol
 D Metoprolol
Q. 3 Which of the following is not a cardioselective beta blocker:
 A Acebutol
 B Atenolol
 C Pindolol
 D Metoprolol
Ans. C

Explanation:

Pindolol

Quiz In Between


Q. 4 Beta blockers are contraindicated in:
 A Angina
 B Hypertension
 C Asthma
 D Hyperthyroidism
Q. 4 Beta blockers are contraindicated in:
 A Angina
 B Hypertension
 C Asthma
 D Hyperthyroidism
Ans. C

Explanation:

Asthma


Q. 5

All of the following statements regarding pharmacokinetics of Beta blockers are TRUE, EXCEPT:

 A

Atenolol is longer acting than metoprolol

 B

Labetalol has both alpha and & beta blocking action

 C

Carvedilol has alpha1 agonist and selective b1 blocking action

 D

Nadolol has longest half life

Q. 5

All of the following statements regarding pharmacokinetics of Beta blockers are TRUE, EXCEPT:

 A

Atenolol is longer acting than metoprolol

 B

Labetalol has both alpha and & beta blocking action

 C

Carvedilol has alpha1 agonist and selective b1 blocking action

 D

Nadolol has longest half life

Ans. C

Explanation:

Carvedilol has approximately equal alpha blocking and and non selective beta blocking action. It reduces mortality in patients with heart failure and is therefore particularly useful in patients with both heart failure and hypertension.

Metoprolol and atenolol are are cardioselective beta blockers. Metoprolol has a short half life of 4-6 hrs whereas atenolol is not extensively metabolized and is excreted primarily in the urine with a half-life of 6 hours. 
Labetolol has both alpha and beta blocking properties so it is used in treating the hypertension of pheochromocytoma and hypertensive emergencies. 
Ref: Benowitz N.L. (2012). Chapter 11. Antihypertensive Agents. In B.G. Katzung, S.B. Masters, A.J. Trevor (Eds), Basic & Clinical Pharmacology, 12e.

Q. 6

Which of the following Beta blocker is contraindicated in renal failure?

 A

Sotalol

 B

Pindolol

 C

Propranolol

 D

Oxyprenolol

Q. 6

Which of the following Beta blocker is contraindicated in renal failure?

 A

Sotalol

 B

Pindolol

 C

Propranolol

 D

Oxyprenolol

Ans. A

Explanation:

Sotalol is a non specific beta adrenergic receptor blocker.

It shortens the sinus cycle period, lengthens the atrial and ventricular refractory period and QT interval.

It has negative ionotropic effect and can reduce left ventricular contractile force and increase filling pressure.

It is excreted by the kidneys with an elimination half life of 10-15 hours, so it should be avoided in renal failure.

Ref: SCAI Interventional Cardiology Board Review Book By Morton J. Ker, Page 41; The Modern Role of Beta-Blockers in Cardiovascular Medicine By John Malcolm Cruickshank, Page 32; Medical Toxicology By Richard C. Dart, Page 685.

Quiz In Between


Q. 7

Which of the following is not a cardioselective beta blocker­

 A

Nebivolol

 B

Atenolol

 C

Betaxolol

 D

Oxprenolol

Q. 7

Which of the following is not a cardioselective beta blocker­

 A

Nebivolol

 B

Atenolol

 C

Betaxolol

 D

Oxprenolol

Ans. D

Explanation:

Ans. is ‘d’ i.e., Oxprenolol

Selective 131 blockers are (cardioselective) :

  1. Atenolol                  3. Bisoprolol                         5. Celiprolol          7. Metoprolol
  2. Acebutalol              4. Betoxolol                          6. Esmolol             8. Nebivolol

o These agents are preferred in DM, hyperlipidemia, PVD, asthma.


Q. 8

All of following are selective beta blockers, except

 A

Atenolol

 B

Esmolol

 C

Bisprolol

 D

Celiprolol

Q. 8

All of following are selective beta blockers, except

 A

Atenolol

 B

Esmolol

 C

Bisprolol

 D

Celiprolol

Ans. D

Explanation:

Ans. is ‘d’ i.e., Celiprolol


Q. 9

Beta blocker without local anaesthetic effect is

 A

Metoprolol

 B

Pindolol

 C

Atenolol

 D

All

Q. 9

Beta blocker without local anaesthetic effect is

 A

Metoprolol

 B

Pindolol

 C

Atenolol

 D

All

Ans. C

Explanation:

Ans. is ‘c’ i.e., Atenolol

β-blockers with membrane stabilizing (Local anaesthetic action

o Pindolol             o Acebutolol        o Carvedilol          o Betaxolol

o Propranolol        o Metoprolol         o Labetalol

Quiz In Between


Q. 10

All of the following are nonselective beta blockers with additional actions except –

 A

Carvedilol

 B

Betoxalol

 C

Carteolol

 D

Labetolol

Q. 10

All of the following are nonselective beta blockers with additional actions except –

 A

Carvedilol

 B

Betoxalol

 C

Carteolol

 D

Labetolol

Ans. B

Explanation:

Ans. is ‘b’ i.e., Betoxalol


Q. 11

Beta blocker that can be used in renal failure is all except-

 A

Propranolol

 B

Pindolol

 C

Sotalol

 D

Oxyprenolol

Q. 11

Beta blocker that can be used in renal failure is all except-

 A

Propranolol

 B

Pindolol

 C

Sotalol

 D

Oxyprenolol

Ans. C

Explanation:

Ans. is ‘c’ i.e., Sotalol

  • “Sotalol is not metabolized in liver, excretion is predominantly by the kidney in the unchanged form”. – Katzung 101Ve p. 229
  • Since it is primarly excreted in urine, it should not be used in renal failure.
  • 0-blockers which are primarily excreted by kidney and should not be given in renal failure –> Atenolol, Sotalol, nodolol

About other options

Approximately 50% of pindolol is metabolized in liver, the remainder of the drug is excreted unchanged in urine –  – Goodman Gillman

o Propranolol and oxprenolol are mainly metabolized in liver.


Q. 12

Beta blockers are contraindicated in ?

 A

Sick sinus syndrome

 B

Angina pectoris

 C

Acute aortic dissection

 D

Post MI

Q. 12

Beta blockers are contraindicated in ?

 A

Sick sinus syndrome

 B

Angina pectoris

 C

Acute aortic dissection

 D

Post MI

Ans. A

Explanation:

Ans. is ‘a’ i.e., Sick sinus syndrome

Quiz In Between


Q. 13

Beta blockers are contraindicated in?

 A

Decompensated CCF

 B

Asthma

 C

Atherosclerosis

 D

All of the above

Q. 13

Beta blockers are contraindicated in?

 A

Decompensated CCF

 B

Asthma

 C

Atherosclerosis

 D

All of the above

Ans. D

Explanation:

All of the above

o Asthma and decompensated heart failure are contraindications for the use of β -blockers.

o Atherosclerosis in peripheral vessels (Peripheral vascular disease) is not a contraindication for use of β -blockers. However, β -blockers can cause worsening of PVD, therefore, they should be avoided in PVD.


Q. 14

Beta blockers are not indicated in ‑

 A

Acute CHF

 B

Hypertension

 C

Chronic CHF

 D

Arrhythmia

Q. 14

Beta blockers are not indicated in ‑

 A

Acute CHF

 B

Hypertension

 C

Chronic CHF

 D

Arrhythmia

Ans. A

Explanation:

Ans. is ‘a’ i.e., Actue CHF

β -blckers are contraindicated in acute decompensated heart failure.


Q. 15

Combination use of beta blockers and calcium channel blockers cause –

 A

Heart block

 B

Hypertension

 C

Hypotension

 D

All

Q. 15

Combination use of beta blockers and calcium channel blockers cause –

 A

Heart block

 B

Hypertension

 C

Hypotension

 D

All

Ans. A

Explanation:

Ans. is ‘a’ i.e., Heart block

o CCBs (verapamil, diltiazem) have negative chronotropic effect (↓ SA node automaticity →↓ heart rate) and negative dromotropic effect (1AV node conduction).

o β-blockers have similar effect by blocking β1 sympathetic receptors on heart (normally stimulation of β1 receptors increases heart rate and conduction).

o Simultaneous use of these drugs can cause marked bradycardia and AV block.

Amongst CCBs, DHPs (nefidipine) can be used with β-blockers because DHPs have no direct negative chronotropic and dromotropic effect, rather they cause tachycardia by reflex sympathetic stimulation.

Quiz In Between


Q. 16

Drugs which interfere with anesthesia are :

 A

Calcium channel blocker nifedipine

 B

Beta blockers

 C

Aminoglycosides

 D

All

Q. 16

Drugs which interfere with anesthesia are :

 A

Calcium channel blocker nifedipine

 B

Beta blockers

 C

Aminoglycosides

 D

All

Ans. D

Explanation:

A i.e. Calcium channel blockers; B i.e. Beta Blockers; C i.e. Aminoglycoside

Aminoglycoside, Tetracycline & Polypeptide antibioticsQ (Mnemonic ATP) potentiate neuromuscular block

– B Blockers & Calcium channel blockerQ may cause Bradycardia & AV block with anesthesia


Q. 17

Contraindication of topical beta blockers

 A

Hypertension

 B

Asthma

 C

Tachycardia

 D

Hypotension

Q. 17

Contraindication of topical beta blockers

 A

Hypertension

 B

Asthma

 C

Tachycardia

 D

Hypotension

Ans. B

Explanation:

B i.e. Asthma


Q. 18

First line drug choice for management of hypertension in patients with angina:

 A

Beta Blockers

 B

ACE Inhibitors

 C

Calcium Channel Blockers

 D

Hydralazine

Q. 18

First line drug choice for management of hypertension in patients with angina:

 A

Beta Blockers

 B

ACE Inhibitors

 C

Calcium Channel Blockers

 D

Hydralazine

Ans. A

Explanation:

Answer is A (Beta Blockers)

‘Hypertension: A companion to Braunwald’s Heart Disease (Elsevier) 2007/335

Beta-blockers are the first line drugs of choice for treatment of hypertension in patients with coronary artery disease & stable angina

`Beta blockers are the first line choice when treating hypertension in a patient with coronary artery disease’ — Evidence Based Medicine Guidelines (John Wiley & Sons)

‘Beta blockers reduce angina symptoms, improve mortality and lower BP, and they should be the drugs offirst choice in hypertensive patients with CAD and stable angina’ — ‘Hypertension: A companion to Braunwald’s Heart Disease’

Quiz In Between


Q. 19

Beta blocker drug CONTRAINDICATED in asthma patients:           

September 2012

 A

Metoprolol

 B

Atenolol

 C

Propranolol

 D

Acebutolol

Q. 19

Beta blocker drug CONTRAINDICATED in asthma patients:           

September 2012

 A

Metoprolol

 B

Atenolol

 C

Propranolol

 D

Acebutolol

Ans. C

Explanation:

Ans. C i.e. Propranolol

Propranolol should be used with caution in people with:

  • DM or hyperthyroidism, since signs and symptoms of hypoglycemia may be masked.
  • PVD and Raynaud’s syndrome, which may be exacerbated
  • Phaeochromocytoma, as hypertension may be aggravated without prior alpha blocker therapy
  • Myasthenia gravis, may be worsened
  • Other drugs with bradycardic effects

Propranolol is contraindicated in patients with:

  • Reversible airways disease, particularly asthma or COPD
  • Bradycardia (
  • Sick sinus syndrome
  • AV block (second or third degree)
  • Shock
  • Severe hypotension
  • Cocaine toxicity
  • PVD/ Peripheral Vascular Disease

Q. 20

Effect of beta blocker’s on heart are all of the following except: 

 A

Decrease in heart rate

 B

Decreases duration of systole

 C

Decreases cardiac output

 D

Precipitates heart failure

Q. 20

Effect of beta blocker’s on heart are all of the following except: 

 A

Decrease in heart rate

 B

Decreases duration of systole

 C

Decreases cardiac output

 D

Precipitates heart failure

Ans. B

Explanation:

Ans. B: Decreases duration of systole

In the presence of increased sympathetic tone, beta blocker reduces the automaticity and prevents rise in heart rate; reduces myocardial contractility, cardiac output and stroke work; slows AV conduction, reduces myocardial oxygen demand and improves exercise tolerance

  • Beta blockers/Beta-adrenergic blocking agents/Beta-adrenergic antagonists/Beta-adrenoreceptor antagonists/Beta antagonists
  • They are particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction, and hypertension.
  • As beta adrenergic receptor antagonists, they diminish the effects of epinephrine (adrenaline) and other stress hormones.
  • Beta blockers block the action of endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular, on beta-adrenergic receptors, part of the sympathetic nervous system which mediates the “fight or flight” response.
  • There are three known types of beta receptor, designated beta-1, beta-2 and beta-3 receptors.
  • Beta-1-adrenergic receptors are located mainly in the heart and in the kidneys.
  • Beta-2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.
  • Beta-3-adrenergic receptors are located in fat cellsStimulation of beta-1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity.Stimulation of beta-1 receptors on the kidney causes renin release.Stimulation of beta-2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle.
  • Stimulation of beta-3 receptors induces lipolysis.
  • Beta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects.That is, they reduce excitement/physical exertion on heart rate and force of contraction, and also tremor and breakdown of glycogen, but increase dilation of blood vessels and constriction of bronchi.It is therefore expected that non-selective beta blockers have an antihypertensive effect.Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand.
  • Negative chronotropic properties of beta blockers allow the lifesaving property of heart rate control.
  • The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods.
  • Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin angiotensin aldosterone system with a resultant decrease in blood pressure due to decreased sodium and water retention
  • Referred to as intrinsic sympathomimetic effect, this term is used particularly with beta blockers that can show both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker) and the concentration of the antagonized agent (usually an endogenous compound such as norepinephrine).
  • Some beta blockers (e.g. oxprenolol, pindolol, penbutolol and acebutolol) exhibit intrinsic sympathomimetic activity (ISA).
  • These agents are capable of exerting low level agonist activity at the beta-adrenergic receptor while simultaneously acting as a receptor site antagonist.
  • These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.Agents with ISA (intrinsic sympathomimetic acitivity) are not used in post-myocardial infarction as they have not been demonstrated to be beneficial.
  • They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia
  • Some beta blockers (e.g. labetalol and carvedilol) exhibit mixed antagonism of both beta- and alpha-1-adrenergic receptors, which provides additional arteriolar vasodilating actionThey can also be used to treat glaucoma because they decrease intraocular pressure by lowering aqueous humor secretion.

Non-selective agents

  • Alprenolol
  • Bucindolol
  • Carteolol
  • Carvedilol (has additional a-blocking activity)
  • Labetalol (has additional a-blocking activity)
  • Nadolol
  • Oxprenolol
  • Penbutolol (has intrinsic sympathomimetic activity)
  • Pindolol (has intrinsic sympathomimetic activity)
  • Propranolol              
  • Timolol
  • Beta-I-Selective agents

Acebutolol (has intrinsic sympathomimetic activity)

  • Atenolol
  • Betaxolol
  • Bisoprolol
  • Celiprolol

Esmolol

  • Metoprolol
  • Nebivolol
  • Beta-2-Selective agents
  • Butaxamine (weak alpha-adrenergic agonist activity) – No common clinical applications.
  • Pharmacological differences

Agents with intrinsic sympathomimetic action (ISA)

  • Acebutolol, carteolol, celiprolol, mepindolol, oxprenolol, pindolol, labetalol.

Agents with greater aqueous solubility (hydrophilic beta blockers)

  • Atenolol, celiprolol, nadolol, sotalol

Agents with membrane stabilizing effect

  • Acebutolol, betaxolol, pindolol, propranolol

Agents with antioxidant effect

  • Carvedilol, nebivolol
  • Indication differences

Agents specifically indicated for cardiac arrhythmia

  • Esmolol, sotalol, landiolol

Agents specifically indicated for congestive heart failure

  • Bisoprolol, carvedilol, sustained-release metoprolol, nebivolol

Agents specifically indicated for glaucoma

  • Betaxolol, carteolol, levobunolol, metipranolol, timolol

Agents specifically indicated for myocardial infarction

  • Atenolol, metoprolol, propranolol

Agents specifically indicated for migraine prophylaxis

  • Timolol, propranolol
  • Propranolol is the only agent indicated for control of tremor, portal hypertension, and esophageal variceal bleeding, and used in conjunction with alpha-blocker therapy in phaeochromocytoma
  • Indications for beta blockers include:

Angina pectoris

  • Atrial fibrillation
  • Cardiac arrhythmia
  • Congestive heart failure
  • Essential tremor
  • Glaucoma
  • Hypertension
  • Migraine prophylaxis
  • Mitral valve prolapse

Myocardial infarction

Phaeochromocytoma, in conjunction with alpha-blocker

  • Postural orthostatic tachycardia syndrome
  • Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
  • Acute aortic dissection
  • Hypertrophic obstructive cardiomyopathy
  • Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications)
  • Prevention of variceal bleeding in portal hypertension
  • Social anxiety disorder and other anxiety disorders

Q. 21

First line drug for primary open angle glaucoma is:

March 2012

 A

Pilocarpine

 B

Dorzolamide

 C

Dipivefrine

 D

Beta blockers

Q. 21

First line drug for primary open angle glaucoma is:

March 2012

 A

Pilocarpine

 B

Dorzolamide

 C

Dipivefrine

 D

Beta blockers

Ans. D

Explanation:

Ans: D i.e. Beta blockers

Drugs for primary open angle glaucoma

  • Adjunctive drugs for primary open angle glaucoma are dipivefrine, dorzolamide & pilocarpine
  • First line drugs for primary open angle glaucoma includes beta blockers, brimonidine & prostaglandin analogues

Quiz In Between


Q. 22

Beta blocker with membrane stabilizing property are all except ‑

 A

Acebutolol

 B

Betaxolol

 C

Carvedilol

 D

Bevantolol

Q. 22

Beta blocker with membrane stabilizing property are all except ‑

 A

Acebutolol

 B

Betaxolol

 C

Carvedilol

 D

Bevantolol

Ans. D

Explanation:

Ans. is ‘d’ i.e., Bevantolol


Q. 23

Shorest acting beta blocker ‑

 A

Esmolol

 B

Nodalol

 C

Acebutolol

 D

Sotalol

Q. 23

Shorest acting beta blocker ‑

 A

Esmolol

 B

Nodalol

 C

Acebutolol

 D

Sotalol

Ans. A

Explanation:

Ans. is ‘a’ i.e., Esmolol

Nodalol is longest acting β-blocker.

Esmolol is shortest acting β-blocker.

Acebutolol possesses all activities i.e., cardioselectivity, partial agonist activity, membrane stablizing activity and lipid insolubility.


Q. 24

Patient on verapamil should not be given beta blocker as ‑

 A

Conduction block

 B

Bronchospasm

 C

Neurogenic shock

 D

Anaphylaxis

Q. 24

Patient on verapamil should not be given beta blocker as ‑

 A

Conduction block

 B

Bronchospasm

 C

Neurogenic shock

 D

Anaphylaxis

Ans. A

Explanation:

Ans. is ‘a’ i.e., Conduction block

Adverse effects of CCBs

  • Nausea, constipation and bradycardia are more common with verapamil.
  • Verapamil can accentuate conduction defect-should be avoided in 2nd & 3rd degree block, in sick sinus syndrome and along with 13-blocker.
  • Most common side effects of DHPs are palpitation, flushing, hypotension, headache, ankle edema, drowsiness and nausea.
  • Nifedipine can paradoxically increase the frequency of angina in some patients.
  • Nifedine can cause voiding difficulty in elderly (relaxant effect on bladder) and glucose intolerance (decreases insulin release).

Quiz In Between


Q. 25

Mechanism of action of timolol is ‑

 A

Nonselective beta blocker

 B

Nonselective alpha blocker

 C

Selective beta 1 blocker

 D

Selective beta 2 blocker

Q. 25

Mechanism of action of timolol is ‑

 A

Nonselective beta blocker

 B

Nonselective alpha blocker

 C

Selective beta 1 blocker

 D

Selective beta 2 blocker

Ans. A

Explanation:

Ans. is ‘a i.e., Nonselective beta blocker

Timolol is a non selective beta blocker (betal + beta 2).

Thus when it is used in the treatment of glaucoma it can precipitate an attack of asthma by blocking beta 2 receptors.


Q. 26

Beta blockers mask all effects of hypoglycemia except ‑

 A

Sweating

 B

Palpitations

 C

Dizziness

 D

Tremors

Q. 26

Beta blockers mask all effects of hypoglycemia except ‑

 A

Sweating

 B

Palpitations

 C

Dizziness

 D

Tremors

Ans. C

Explanation:

Ans. is ‘c’ i.e., Dizziness

Symptoms of hypoglycemia are attributable to :-

i) Sympathetic stimulation : Sweating, tremor, tachycardia palpitations and anxiety. These are the warning signs.

ii) Cerebral glucose deficiency : Decreased cognitive functions, dizziness and decreased concentration.

  • Use of beta-blockers, especially in diabetics who are taking treatment, may mask typical sympathetic system mediated symptoms of hypoglycemia such as sweating, tremor, tachycardia, and palpitations.
  • Thus, dangerous severe hypoglycemia can occur without any warning signs.

Q. 27

Tachycardia due to nitrates in a patient with angina pectoris is blocked by‑

 A

Digoxin

 B

Dobutamine

 C

Beta blocker

 D

Calcium channel blocker

Q. 27

Tachycardia due to nitrates in a patient with angina pectoris is blocked by‑

 A

Digoxin

 B

Dobutamine

 C

Beta blocker

 D

Calcium channel blocker

Ans. C

Explanation:

Ans. is ‘c’ i.e., Beta blocker

Use of beta blocker and long acting nitrate combination is rational in classical angina because :

  1. Tachycardia due to nitrate is blocked by beta blocker
  2. The tendency of beta blocker to cause ventricular dilatation is countered by nitrate
  3. The tendency of beta blocker to reduce the total coronary flow is opposed by nitrate

Quiz In Between


Q. 28

Which of the following is not a cardioselective beta blocker?

 A

Esmolol

 B

Nebivolol

 C

Acebutolol

 D

Oxprenolol

Q. 28

Which of the following is not a cardioselective beta blocker?

 A

Esmolol

 B

Nebivolol

 C

Acebutolol

 D

Oxprenolol

Ans. D

Explanation:

Ans. is d i.e., Oxprenolol


Q. 29

Following features are true about lipid insoluble beta blockers except‑

 A

Do not cross blood brain barrier

 B

Have good membrane stabilizing effect

 C

Incompletely absorbed orally

 D

Are long acting

Q. 29

Following features are true about lipid insoluble beta blockers except‑

 A

Do not cross blood brain barrier

 B

Have good membrane stabilizing effect

 C

Incompletely absorbed orally

 D

Are long acting

Ans. B

Explanation:

Ans. is `b i.e., Have good membrane stabilizing effect

Lipid insolubile drugs have following features

  • Do not cross Blood Brain Barrier and therefore produce no CNS effects.
  • Have good renal excretion
  • Have no membrane stabilizing activity
  • Are incompletely absorbed orally
  • Are long acting
  • Are effective in narrow dose range

Lipid insoluble β-blockers

  1. Acebutolol
  2. Betoxalol
  3. Atenolol
  4. Carteolol
  5. Bisoprolol
  6. Celiprolol
  7. Esmolol
  8. Nodalol
  9. Sotalo
  10. Labealol
  11. Pindolol

Q. 30

Which of the following is not a cardioselective beta blocker ‑

 A

Nebivolol

 B

Atenolol

 C

Betaxolol

 D

Oxprenolol

Q. 30

Which of the following is not a cardioselective beta blocker ‑

 A

Nebivolol

 B

Atenolol

 C

Betaxolol

 D

Oxprenolol

Ans. D

Explanation:

Ans. is ‘d’ i.e., Oxprenolol 

Quiz In Between



Cholinergic Receptors

Cholinergic receptor

Q. 1 All of the following statements regarding activity at the neuromuscular junction are true except:

 A Action potentials on the alpha motor neuron release acetylcholine (Ach) from the axon terminal
 B Ach stimulates nicotinic cholinergic receptors on the muscle endplate
 C Cholinergic receptors on the muscle endplate are cation channels
 D Alpha motor neurons excite, and Renshaw cells inhibit, the muscle endplate
 
Q. 1 All of the following statements regarding activity at the neuromuscular junction are true except:

 A Action potentials on the alpha motor neuron release acetylcholine (Ach) from the axon terminal
 B Ach stimulates nicotinic cholinergic receptors on the muscle endplate
 C Cholinergic receptors on the muscle endplate are cation channels
 D Alpha motor neurons excite, and Renshaw cells inhibit, the muscle endplate
 
Ans. B

Explanation:

There are no Renshaw cells at the neuromuscular junction. Renshaw cells inhibit motor neurons in the anterior gray horn of the spinal cord. Action potentials on the alpha motor neuron release acetylcholine (ACh) from the axon terminal. The ACh diffuses across the synaptic cleft and stimulates nicotinic receptors on the muscle endplate, generating an action potential that causes contraction of the muscle fiber. Cholinergic receptors on the muscle endplate are cation channels.


Q. 2

In Myasthenia gravis, antibodies are present against –

 A

Muscarinic receptor proteins

 B

Nicotinic receptor proteins

 C

Protein actin

 D

Protein myosin

Q. 2

In Myasthenia gravis, antibodies are present against –

 A

Muscarinic receptor proteins

 B

Nicotinic receptor proteins

 C

Protein actin

 D

Protein myosin

Ans. B

Explanation:

Ans. is ‘b’ i.e., Nicotinic receptor proteins

o Myasthenia gravis is an autoimmune disorder due to development of antibodies against Nm type of nicotinic receptors.


Q. 3

Nicotine receptor sites include all of the following except-

 A

Bronchial smooth muscle

 B

Adrenal medulla

 C

Skeletal muscle

 D

Sympathetic ganglia

Q. 3

Nicotine receptor sites include all of the following except-

 A

Bronchial smooth muscle

 B

Adrenal medulla

 C

Skeletal muscle

 D

Sympathetic ganglia

Ans. A

Explanation:

Ans. is ‘a’ i.e., Bronchial smooth muscle

  • Smooth muscles have muscarinic receptors (M3 type).

Quiz In Between


Q. 4

Which has maximum nicotinic effect-

 A

Bethanechol

 B

Carbachol

 C

Pilocarpine

 D

Methacholine

Q. 4

Which has maximum nicotinic effect-

 A

Bethanechol

 B

Carbachol

 C

Pilocarpine

 D

Methacholine

Ans. B

Explanation:

Ans. is ‘b’ i.e., Carbachol

o Amongst the given options carbachol has maximum nicotinic actions. It has nicotinic as well as muscarinic action.


Q. 5

All of the following are actions of muscarinic antogonists, except :

 A

Decrease gastric secretions

 B

Decrease respiratory secretions

 C

Contract radial muscles of iris

 D

Fascilitates AV conduction

Q. 5

All of the following are actions of muscarinic antogonists, except :

 A

Decrease gastric secretions

 B

Decrease respiratory secretions

 C

Contract radial muscles of iris

 D

Fascilitates AV conduction

Ans. C

Explanation:

Ans is ‘c’ i.e. Contract radial muscles of iris

  • Radial muscles are innervated by sympathetic systems not by parasympathetic (muscarinic) system

Iris muscles that control the size of pupil

 There are two types of muscles in iris that control the size of pupil:

  1. The iris sphincter or constrictor pupillae (circular muscles): These muscles are innervated by the parasym­pathetic system and cause constriction of pupil (miosis).
  2. The iris dilator or dilator pupillae (radial muscles): These muscles are innervated by sympathetic (a, adren­ergic) system and cause dilatation of pupil (mydriasis)
  • So, pupil size may be altered by following mechanisms by different ANS drugs:

A. Mydriasis (dilatation of pupil)

  • Sympathomimetic drugs (a, agonists): By contraction of radial muscles (dilator).
  • Antimuscarinic drugs: By blocking the action of circular muscles (pupillary sphincter).

B. Miosis (constriction of pupil)

  1. Parasympathomimetic (muscarinic) drgus: By stimulating the contraction of circular muscles (pupillary sphincter).
  2. Sympatholytic drugs (a, antagonists): By blocking the action of radial muscles (iris dilator) About other options
  • Muscarinic antagonists (antimuscarinic drugs) decrease both gastric and respiratory (bronchial) secretions o Antimuscarinic drugs facilitate AV conduction (see previous explanations).

Q. 6

Oxybutynin acts by –

 A

Nicotinic receptor stimulation

 B

Muscarinic receptor stimulation

 C

Muscarinic receptor inhibition

 D

a-receptor inhibition

Q. 6

Oxybutynin acts by –

 A

Nicotinic receptor stimulation

 B

Muscarinic receptor stimulation

 C

Muscarinic receptor inhibition

 D

a-receptor inhibition

Ans. C

Explanation:

Ans. is ‘c’ i.e., Muscarinic receptor inhibition

Oxybutnin

o Oxybutynin is an anticholinergic drug.

o It is relatively selective for M3 receptors, so it has selective action on urinary bladder.

  • Because of its vesicoselective action it is used for detrusor instability and urinary incontinence.

Quiz In Between


Q. 7

D-tubocurarine acts by –

 A

Inhibiting nicotinic receptors at myoneural junction

 B

Inhibiting nicotinic receptors at autonomic ganglion

 C

Producing depolarizing block

 D

By inhibiting reuptake of acetylcholine

Q. 7

D-tubocurarine acts by –

 A

Inhibiting nicotinic receptors at myoneural junction

 B

Inhibiting nicotinic receptors at autonomic ganglion

 C

Producing depolarizing block

 D

By inhibiting reuptake of acetylcholine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Inhibiting nicotinic receptors at myoneural junction

o D-tubocurarine is a skeletal muscle relaxant that acts by competitive inhibition of NM receptors at neuron-muscular junction.


Q. 8

Dry mouth during antidepressant therapy is caused by blockade of –

 A

Muscarinic acetylcholine receptors

 B

Serotonergic receptors

 C

Dopaminergic receptors

 D

GABA receptors

Q. 8

Dry mouth during antidepressant therapy is caused by blockade of –

 A

Muscarinic acetylcholine receptors

 B

Serotonergic receptors

 C

Dopaminergic receptors

 D

GABA receptors

Ans. A

Explanation:

Ans. is ‘a’ i.e., Muscarinic acetylcholine receptors

“Blurred vision, dry mouth, urinary hesitancy or retention, and constipation represent the most common antimuscarinic complaints”.


Q. 9

Nicotinic receptors are seen in all except:

September 2007

 A

Neuromuscular junction

 B

Autonomic ganglia of autonomic nervous system

 C

Bronchial smooth muscle

 D

Brain

Q. 9

Nicotinic receptors are seen in all except:

September 2007

 A

Neuromuscular junction

 B

Autonomic ganglia of autonomic nervous system

 C

Bronchial smooth muscle

 D

Brain

Ans. C

Explanation:

Ans. C: Bronchial Smooth Muscle

The nicotinic cholinergic receptors are found in the neuromuscular junctions of somatic muscles; stimulation of these receptors causes muscular contraction. They are also found in the autonomic ganglia of autonomic nervous system and

central nervous system

Muscarinic receptors are found in:

M 1-brain M 2-heart

M 3-smooth muscle

M 4-smooth muscle, pancreatic acinar and islet tissue

Quiz In Between


Q. 10

In myasthenia gravis, antibodies are present against:

September 2012

 A

Muscarinic receptor proteins

 B

Nicotinic receptor proteins

 C

Protein actin

 D

Protein myosin

Q. 10

In myasthenia gravis, antibodies are present against:

September 2012

 A

Muscarinic receptor proteins

 B

Nicotinic receptor proteins

 C

Protein actin

 D

Protein myosin

Ans. B

Explanation:

Ans. B i.e. Nicotinic receptor proteins

Myasthenia gravis

  • It is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigability.
  • It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors throughout neuromuscular junctions.
  • Myasthenia is treated medically with acetylcholinesterase inhibitors or immunosuppressants, and, in selected cases,thymectomy.



Q. 11

True regarding bupropion is:     

September 2009

 A

Dopamine reuptake stimulator

 B

It is an antianxiety drug

 C

No precipitation of seizures

 D

Nicotinic receptor antagonist

Q. 11

True regarding bupropion is:     

September 2009

 A

Dopamine reuptake stimulator

 B

It is an antianxiety drug

 C

No precipitation of seizures

 D

Nicotinic receptor antagonist

Ans. D

Explanation:

Ans. D: Nicotinic receptor antagonist

Bupropion/amfebutamone is an atypical antidepressant and smoking cessation aid.

It acts as a norepinephrine and dopamine reuptake inhibitor (NDRI), as well as alpha3 beta4-nicotinic receptor antagonist.

Bupropion belongs to the chemical class of aminoketones and is similar in structure to stimulants cathinone and diethylpropion, and to phenethylamines in general.

Bupropion is an effective antidepressant on its own but it is particularly popular as an add-on medication in the cases of incomplete response to the first-line selective serotonin reuptake inhibitor (SSRI) antidepressant.

Since it does not inhibit serotonin reuptake at all (or very insignificantly), bupropion does not cause weight gain or sexual dysfunction like the SSRI group of antidepressants.

It precipitates seizures


Q. 12

Drug used for muscarinic symptoms seen in cobra envenomation:     

CMC (Vellore) 13

 A

Neostigmine

 B

Pralidoxime

 C

Prazocin

 D

Naloxone

Q. 12

Drug used for muscarinic symptoms seen in cobra envenomation:     

CMC (Vellore) 13

 A

Neostigmine

 B

Pralidoxime

 C

Prazocin

 D

Naloxone

Ans. A

Explanation:

Ans. Neostigmine

Quiz In Between


Q. 13

Acetylcholine acting on nicotinic receptors produces:

KCET 12

 A

Contraction of skeletal muscle

 B

Secretion of saliva

 C

Bradycardia

 D

Pupillary constriction

Q. 13

Acetylcholine acting on nicotinic receptors produces:

KCET 12

 A

Contraction of skeletal muscle

 B

Secretion of saliva

 C

Bradycardia

 D

Pupillary constriction

Ans. A

Explanation:

Ans. Contraction of skeletal muscle


Q. 14

Which of the following is an ionic channel ‑

 A

α -1 receptors

 B

β – 1 receptors

 C

Nicotinic cholinergic receptors

 D

Muscarinic cholinergic receptors

Q. 14

Which of the following is an ionic channel ‑

 A

α -1 receptors

 B

β – 1 receptors

 C

Nicotinic cholinergic receptors

 D

Muscarinic cholinergic receptors

Ans. C

Explanation:

Ans. is ‘c’ i.e., Nicotinic cholinergic receptors


Q. 15

Varenicline acts by ‑

 A

Partial nicotine receptor agonist

 B

Nicotine receptor antagonist

 C

Both agonist and antagonist at nicotine receptor

 D

None of the above

Q. 15

Varenicline acts by ‑

 A

Partial nicotine receptor agonist

 B

Nicotine receptor antagonist

 C

Both agonist and antagonist at nicotine receptor

 D

None of the above

Ans. A

Explanation:

Ans. is ‘a’ i.e., Partial nicotine receptor agonist

Varenicline

  • It is partial agonist at the nicotine receptor.
  • It is used in nicotine addicts.

Quiz In Between


Q. 16

Cardiac conduction defect seen with Tricyclic an­tidepressants are due to ‑

 A

 NE & serotonin uptake inhibitor

 B

 Antimuscarinic action on heart

 C

 Only NE uptake inhibition

 D

 Both NE uptake inhibition and antimuscarinic action on heart

Q. 16

Cardiac conduction defect seen with Tricyclic an­tidepressants are due to ‑

 A

 NE & serotonin uptake inhibitor

 B

 Antimuscarinic action on heart

 C

 Only NE uptake inhibition

 D

 Both NE uptake inhibition and antimuscarinic action on heart

Ans. D

Explanation:

Ans. is ‘d’ i.e., Both NE uptake inhibition and antimuscarinic action on heart 

  • The commonest cardiovascular effect of tricyclic antidepressant overdose is sinus tachycardia, which is attributable
  • to the inhibition of norepincphrine reuptake and the anticholinergic action.
  • However, the most important toxic effect of tricyclics is the slowing of depolarisation of the cardiac action potential by inhibition of the sodium current and this delays propagation of depolarisation through both myocardium and conducting tissue.
  • This results in prolongation of the QRS complex and the PR/QT intervals with a predisposition to cardiac arrhythmias.
  • This inhibition of sodium flux into myocardial cells can occur to such an extent that depressed contractility can result and this, coupled with the reduction in peripheral resistance, contributes to hypotension.

Q. 17

Muscarinic cholinergic receptors are seen at allsites, except ‑

 A

Stomach

 B

CNS

 C

Neuromuscular junctio

 D

Glands

Q. 17

Muscarinic cholinergic receptors are seen at allsites, except ‑

 A

Stomach

 B

CNS

 C

Neuromuscular junctio

 D

Glands

Ans. C

Explanation:

Ans. is ‘c’ i.e., Neuromuscular junction 

Cholinergic receptors

  • There are two types of cholinergic receptors :
  • Muscarinic → Found at – All postaganglionic parasympathetic sites, Few postaganglionic sympathetic sites (sweat gland & blood vessels), CNS.
  • Nicotinic —4 Found at – Ganglia (both sympathetic and parasympathetic), Skeletal muscles, Adrenal medulla, CNS

 

Muscarinic receptors

 

Nicotinic receptors

Type

Organ

Type

Organ

M1

Gastric gland

NM

Neuromuscualr junction

M2

Heart

 

(Skeletal muscle)

M3

Smooth muscles, glands and

endothelium

NN

Ganglia, adrenal medulla

M4

CNS

 

 

M5

CNS

 

 

Quiz In Between



Alpha adrenergic receptor

Alpha adrenergic receptor

Q. 1 Alpha 1 blocker used for BHP is:
 A Tamsolusin
 B Prazosin
 C Oxazosin
 D Dolazoline
Q. 1 Alpha 1 blocker used for BHP is:
 A Tamsolusin
 B Prazosin
 C Oxazosin
 D Dolazoline
Ans. A

Explanation:

Tamsolusin


Q. 2 Alpha 1 blocker used for BHP without any effect on blood pressure is:
 A Tamsolusin
 B Terazosin
 C Oxazosin
 D Dolazoline
Q. 2 Alpha 1 blocker used for BHP without any effect on blood pressure is:
 A Tamsolusin
 B Terazosin
 C Oxazosin
 D Dolazoline
Ans. A

Explanation:

Tamsolusin


Q. 3

Which of the following is an Alpha la adrenergic blocker which give symptomatic relief in BPH?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Dolazoline

Q. 3

Which of the following is an Alpha la adrenergic blocker which give symptomatic relief in BPH?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Dolazoline

Ans. A

Explanation:

Alpha 1A receptor is predominantly found in bladder base and prostate. Tamsulosin is a uroselective alpha1 blocker effective for symptomatic relief in BPH.

Prazosin is a highly selective alpha 1 blocker having alpha1: alpha 2 selectivity ratio 1000:1. It blocks alpha 1 receptors in bladder trigone and prostate and improves urine flow and reduces residual urine in bladder in a case of BPH.

Quiz In Between


Q. 4

Which of the following is an Alpha 1 blocker without any effect on blood pressure?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Terazocin

Q. 4

Which of the following is an Alpha 1 blocker without any effect on blood pressure?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Terazocin

Ans. A

Explanation:

Tamsulosin a nonquinazoline, is a long acting selective alpha 1A adrenergic receptor antagonist.

Tamsulosin and its metabolites are most specific for prostatic alpha 1A adrenergic receptor and less specific for vascular alpha 1A adrenergic receptor thereby having less effect on blood pressure.

It is very effective for treating bladder outlet obstruction associated with BPH.


Q. 5

Which of the following alpha blocker is useful in BPH?

 A

Phentolamine

 B

Prazosin

 C

Tolazoline

 D

Phenoxybenzamine

Q. 5

Which of the following alpha blocker is useful in BPH?

 A

Phentolamine

 B

Prazosin

 C

Tolazoline

 D

Phenoxybenzamine

Ans. B

Explanation:

BPH is treated with the alpha-blocker terazosin, prazosin, or doxazosin to relax the prostate, and finasteride or dutasteride to decrease the mass of the prostate.

Must know:
  • Prazosin is a peripheral acting alpha-adrenergic blocker used primarily to treat hypertension.
  • Phentolamine is an α-adrenergic blocker used for controlled hypotension, treatment of perioperative hypertensive crisis that may accompany pheochromocytoma removal, prevention or treatment of dermal necrosis or sloughing after intravenous administration or extravasation of barbiturate or sympathomimetic.
  • Tolazoline is a competitive α1 and α2 adrenergic blocking agent. It also relaxes vascular smooth muscles, producing a peripheral vasodilatation.
  • Phenoxybenzamine is an irreversible, non-competitive α1 and α2 adrenergic receptor antagonist which decreases vascular resistance and lowers both the supine and the standing blood pressure.

Ref: Essentials of Pharmacology for Health Occupations By Ruth Woodrow, Bruce J. Colbert, David M. Smith, 2010, Page 474; Advanced Therapy of Prostate Disease By Martin I. Resnick, Ian Murchie Thompson, 2000, Page 533; Goodman and Gillman’s, 11th edition, Page 172,173,183.


Q. 6

Dale’s vasomotor reversal is due to –

 A

Alpha blocker

 B

Beta blocker

 C

ACH inhibitor

 D

All of the above

Q. 6

Dale’s vasomotor reversal is due to –

 A

Alpha blocker

 B

Beta blocker

 C

ACH inhibitor

 D

All of the above

Ans. A

Explanation:

Ans. is ‘a’ i.e., Alpha blocker

o In Dale’s vasomotor reversal

Neurotransmitter —> Adr

Blockade —> a – receptors

Stimulation —> [32-receptors

o Re-reversal of vosomotor reversal is due to propranolol ((3-blockers).

Quiz In Between


Q. 7

All are alpha blocker except –

 A

Atenolol

 B

Prazosin

 C

Indoramine

 D

Idazoxan

Q. 7

All are alpha blocker except –

 A

Atenolol

 B

Prazosin

 C

Indoramine

 D

Idazoxan

Ans. A

Explanation:

Ans. is ‘a’ i.e., Atenolol


Q. 8

Alpha 1 blocker without any effect on blood pressure is?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Terazocin

Q. 8

Alpha 1 blocker without any effect on blood pressure is?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Terazocin

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tamsulosin

o Tamsulosin is selective for aiA receptors which are found predominantly on prostate and bladder.

It does not act on ai B receptors which are found predominanly on blood vessels. Therefore, it has littel effect on BP.


Q. 9

Alpha la adrenergic blocker giving symptomatic relief in BPH?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Dolazoline

Q. 9

Alpha la adrenergic blocker giving symptomatic relief in BPH?

 A

Tamsulosin

 B

Prazosin

 C

Oxazocin

 D

Dolazoline

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tamsulosin

Tamsulosine is a uroselective blocker (α1A blocker)

  • It decreases the tone of smooth muscle in bladder trigone, sphincter and prostate → urine flow in patient with BHP is improved.

Quiz In Between


Q. 10

Wrong about clonidine is –

 A

Alpha 2 receptor agonist

 B

First line for AMID

 C

Sudden withdrawal causes rebound hypertension

 D

Controls loose motions due to diabetic neuropathy

Q. 10

Wrong about clonidine is –

 A

Alpha 2 receptor agonist

 B

First line for AMID

 C

Sudden withdrawal causes rebound hypertension

 D

Controls loose motions due to diabetic neuropathy

Ans. B

Explanation:

Ans. is ‘b’ i.e., First line for ADHD

o Behavioural therapy is the first line therapy for the treatment of ADHD. The first line drug for ADHD is Methylpheni date.

o Clonidine is a partial agonist with high affinity and high intrinsic activity at α2 receptors.

  • Sudden withdrawal of clonidine may cause life threatening hypertensive crisis.

o Clonidine is used to control loose motions due to diabetic neuropathy. It may be acting by α2 receptor mediated enhancement of salt absorption in gut mucosa.


Q. 11

In a hypertensive patient with glaucoma which of the following is not used:

 A

Dipivefrine

 B

Alpha blocker

 C

Alpha agonist

 D

Laser trabeculoplasty

Q. 11

In a hypertensive patient with glaucoma which of the following is not used:

 A

Dipivefrine

 B

Alpha blocker

 C

Alpha agonist

 D

Laser trabeculoplasty

Ans. A

Explanation:

Ans. Dipivefrine


Q. 12

Alpha agonist has all of the following actions except:

September 2009

 A

Hypotension

 B

Hypertension

 C

General anesthesia

 D

Nasal decongestant

Q. 12

Alpha agonist has all of the following actions except:

September 2009

 A

Hypotension

 B

Hypertension

 C

General anesthesia

 D

Nasal decongestant

Ans. C

Explanation:

Ans. C: General Anesthesia

Alpha-adrenoceptor agonists bind to alpha-receptors on vascular smooth muscle and induce smooth contraction and vasoconstriction, thus mimicking the effects of sympathetic adrenergic nerve activation to the blood vessels. Vascular smooth muscle has two types of alpha-adrenoceptors: alphal and alpha2.

The alphal-adrenoceptors are the predominant alpha-receptor located on vascular smooth muscle.

Depending on the tissue and type of vessel, there are also alpha2-adrenoceptors found on the smooth muscle.

There are also alpha2-adrenoceptors located on the sympathetic nerve terminals that inhibit the release of norepinephrine and therefore act as a feedback mechanism for modulating the release of norepinephrine.

Alpha-agonists constrict both arteries and veins; however, the vasoconstrictor effect is more pronounced in the arterial resistance vessels (small arteries and arterioles).

Alphal-adrenoceptor agonists (systemic vasoconstrictors)

  • Methoxamine
  • Phenylephrine
  • Oxymetazoline
  • Tetrahydralazine
  • Xylometazoline

Methoxamine and phenylephrine are used as pressor agents in treating hypotension and shock.

Oxymetazoline, tetrahydralazine, xylometazoline and some preparations of phenylephrine are used as nasal decongestants.

Alpha2-adrenoceptor agonists (centrally-acting vasodilators)

  • Clonidine
  • Guanabenz
  • Guanfacine
  • Alpha-methyldopa

The alpha2-adrenoceptor agonists are used very occasionally as centrally-acting sympatholytic vasodilators for the treatment of hypertension.

Quiz In Between


Q. 13

Alpha 2 agonist used in glaucoma is ‑

 A

Brimonidine

 B

Timolol

 C

Phenylephrine

 D

Reserpine

Q. 13

Alpha 2 agonist used in glaucoma is ‑

 A

Brimonidine

 B

Timolol

 C

Phenylephrine

 D

Reserpine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Brimonidine


Q. 14

Selective alpha 2 agoinst used in glaucoma

 A

Tirriolol

 B

Epinephrine

 C

Dipivefrine

 D

Brimonidine

Q. 14

Selective alpha 2 agoinst used in glaucoma

 A

Tirriolol

 B

Epinephrine

 C

Dipivefrine

 D

Brimonidine

Ans. D

Explanation:

Ans. is ‘d’ i.e., Brimonidine


Q. 15

Drug with beta adrenergic blocking, with antioxidant, with calcium channel blocking, with alpha 1 antagonist activity is ‑

 A

Esmolol

 B

Carvedilol

 C

Nebivolol

 D

Levobunolol

Q. 15

Drug with beta adrenergic blocking, with antioxidant, with calcium channel blocking, with alpha 1 antagonist activity is ‑

 A

Esmolol

 B

Carvedilol

 C

Nebivolol

 D

Levobunolol

Ans. B

Explanation:

Ans. is ‘b’ i.e., Carvedilol

Carvedilol

  • Carvedilol is a β1 + β2 + α1 adrenoceptor blocker with α : β blocking property of 1 : 9.
  • It has antioxidant and antimitotic property.
  • It produces peripheral vasodilation due to α-1 blockade as well as calcium channel blockade (direct effect).
  • It is used in hypertension and angina.
  • It is used as cardioprotective in CHF.
  • t1/2 is 2-8 hrs.
  • It is eliminated through liver and kidney.
  • It causes orthostatic hypotension.

Quiz In Between


Q. 16

Drug used in refractory glaucoma ‑

 A

Systemic glucocorticoid

 B

ACE inhibitor

 C

Alpha agonist

 D

Beta blocker

Q. 16

Drug used in refractory glaucoma ‑

 A

Systemic glucocorticoid

 B

ACE inhibitor

 C

Alpha agonist

 D

Beta blocker

Ans. C

Explanation:

Ans. is ‘c’ i.e., Alpha agonist

Drug of choice for initial treatment of open angle glaucoma is either an topical β-blocker or topical PG analogue (latanoprost)

It target IOT is not attained either change over to alternative drug or use both concurrently.

In refractory cases (who are not responding to (3-blockers and PG analogues), topical α-agonist (Brimozidine) or topical carbonic anhydrase inhibitor (dorazolamide) is added.

It target IOT is still not attained, laser trabeculoplasty is considered.


Q. 17

The drug shown in the picture below is a ? 

 A

Alpha blocker.

 B

Beta blocker.

 C

Gamma blocker.

 D

None of the above.

Q. 17

The drug shown in the picture below is a ? 

 A

Alpha blocker.

 B

Beta blocker.

 C

Gamma blocker.

 D

None of the above.

Ans. A

Explanation:

Ans:A.)Alpha Blocker.

Prazosin

  • Prazosin is a selective α-1-adrenergic receptor antagonist
  • Indications:
    • For treatment of hypertension, symptomatic benign prostatic hyperplasia, and severe congestive heart failure.
    • May also be used alone or in combination with β-blockers in the preoperative management of signs and symptoms of pheochromocytoma.



Q. 18

Wrong about clonidine is

 A

Alpha 2 receptor agonist

 B

First line for ADHD

 C

Sudden withdrawal causes rebound hypertension

 D

Controls loose motions due to diabetic neuropathy

Q. 18

Wrong about clonidine is

 A

Alpha 2 receptor agonist

 B

First line for ADHD

 C

Sudden withdrawal causes rebound hypertension

 D

Controls loose motions due to diabetic neuropathy

Ans. B

Explanation:

Ans. is ‘b’ i.e., First line for ADHD

o Behavioural therapy is the first line therapy for the treatment ofADHD. The first line drug forADHD is Methylphenidate.

Clonidine

  • It acts (partial agonist) on a2 receptors, especially a24 in brainstem → Stimulation of a2A receptors in medulla (vasomotor centre) → decrease sympathetic outflow → fall in BP and bradycardia (also due to enhanced vagal tone). 
  • a.2, receptor stimulation is responsible for sedation produced by clonidine.
  • Clonidine also binds to a nonadrenergic receptor, imidazoline receptor, which may also mediate antihypertensive effect. 
  • Rilmenidine and moxonidine are selective cerebral imidazoline receptor agonists with little a, action→equivalent antihypertensive action with low sedative property.
  • Rapid i.v. injection of clonidine raises BP transiently due to activation of peripheralpostsynaptic vasoconstrictor a2B receptors at high concentrations so attained. Oral doses producing lower plasma levels cause only fall in BP, because clonidine has lower intrinsic activity on a2t,receptors which predominate in vascular smooth muscle.
  • Uses of clonidine

Hypertension                       Opioid withdrawl            Menopausal syndrome

Alcohal withdrawal               Smoking cessation         Loose motions in diabetic neuropathy

Test for pheochromocytoma

  • Abrupt discontinuation of clonidine therapy can lead to rebound hypertension (treated with phentolamine); therefore this drug is not suitable for people having travelling job like business executives who are likely to miss the doses.

Quiz In Between



K+ Sparing Diuretics

K+sparing diuretic

Q. 1

In patients with decompensated cirrhosis on diuretic therapy with tender gynaecomastia the best diuretic to substitute is:

 A

Amiloride for spironolactone

 B

Furosemide for spironolactone

 C

Spironolactone for amiloride

 D

Torsemide for spironolactone

Q. 1

In patients with decompensated cirrhosis on diuretic therapy with tender gynaecomastia the best diuretic to substitute is:

 A

Amiloride for spironolactone

 B

Furosemide for spironolactone

 C

Spironolactone for amiloride

 D

Torsemide for spironolactone

Ans. A

Explanation:

Amiloride (10-40 mg/day) can be substituted for spironolactone in patients with tender gynecomastia. Amiloride is more expensive and less effective

Ref: HEPATOLOGY, June 2009

Q. 2

The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension is:

 A

Furosemide 160 mg and spironolactone 400 mg

 B

Furosemide 80 mg and spironolactone 400 mg

 C

Furosemide 160 mg and spironolactone 200 mg

 D

Furosemide 80 mg and spironolactone 200 mg

Q. 2

The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension is:

 A

Furosemide 160 mg and spironolactone 400 mg

 B

Furosemide 80 mg and spironolactone 400 mg

 C

Furosemide 160 mg and spironolactone 200 mg

 D

Furosemide 80 mg and spironolactone 200 mg

Ans. A

Explanation:

Usual maximum doses of diuretic for the treatment of ascites in decompensated cirrhosis are 400 mg/day of spironolactone and 160 mg/day of furosemide.

Furosemide can be temporarily withheld in patients presenting with hypokalemia, which is very common in the setting of alcoholic hepatitis.
 
Ref: HEPATOLOGY, June 2009.

Q. 3

Spironolactone is used in the treatment of patients with Conn’s syndrome. Which of the following is the MOST important adverse reaction of spironolactone therapy?

 A

Antiandrogen

 B

Cardiac arrhythmia

 C

Dehydration

 D

Hyperkalemia

Q. 3

Spironolactone is used in the treatment of patients with Conn’s syndrome. Which of the following is the MOST important adverse reaction of spironolactone therapy?

 A

Antiandrogen

 B

Cardiac arrhythmia

 C

Dehydration

 D

Hyperkalemia

Ans. A

Explanation:

Spironolactone is a competitive antagonist of the aldosterone receptor. Hypokalemia and hypertension in patients with primary aldosteronism can be controlled by spironolactone, 50-100 mg/d. Although spironolactone is an effective aldosterone receptor antagonist, it is not without side effects that can limit its use in the chronic treatment of this disease. The most important are anti-androgenic reactions.

Spironolactone acts as an antiandrogen by decreasing the production of testosterone by the adrenal gland and by preventing DHT (dihydrotestosterone) from binding to its androgen receptor. As a result of this, in the long run, gynecomastia occurs in more than 10% of the treated men. Impotence, loss of libido, and menstrual irregularities are also common side effects of spironolactone therapy. On the other side, these spironolactone features are the basis for its usage in the treatment of hirsutism, acne, and alopecia.

Spironolactone is also used by transsexuals in the feminizing regimen because of its anti-androgenic actions. 

Cardiac arrhythmia is not a frequent adverse reaction to spironolactone treatment, and it is seen only in the presence of significant hyperkalemia.

Dehydration is usually very mild, and can be prevented with adequate water intake.

Hyperkalemia develops in 5-10% of treated patients, especially if renal function is compromised, or the patient is diabetic, or elderly.

Also Know:

Spironolactone (Aldactone) is a direct aldosterone receptor antagonist in collecting tubules. It acts to inhibit aldosterone-mediated Na+ reabsorption and K+ secretion.
 
Ref: Morgan, Jr. G.E., Mikhail M.S., Murray M.J. (2006). Chapter 31. Renal Physiology & Anesthesia. In G.E. Morgan, Jr., M.S. Mikhail, M.J. Murray (Eds), Clinical Anesthesiology, 4e

Quiz In Between


Q. 4

All of the following drugs acts as potassium sparing diuretics, EXCEPT:

 A

Spironolactone

 B

Eplerenone

 C

Triamterene

 D

Thiazide

Q. 4

All of the following drugs acts as potassium sparing diuretics, EXCEPT:

 A

Spironolactone

 B

Eplerenone

 C

Triamterene

 D

Thiazide

Ans. D

Explanation:

Potassium-sparing diuretics prevent K+ secretion by antagonizing the effects of aldosterone at the late distal and cortical collecting tubules. Inhibition may occur by direct pharmacologic antagonism of mineralocorticoid receptors (spironolactone, eplerenone) or by inhibition of Na+ influx through ion channels in the luminal membrane (amiloride, triamterene).
 
Ref: Katzung, 11th edition, Chapter 15.

Q. 5

Which of the following potassium sparing diuretics cause renal stones?

 A

Spironolactone

 B

Eplerenone

 C

Triamterene

 D

Amiloride

Q. 5

Which of the following potassium sparing diuretics cause renal stones?

 A

Spironolactone

 B

Eplerenone

 C

Triamterene

 D

Amiloride

Ans. C

Explanation:

Triamterene is only slightly soluble and may precipitate in the urine, causing kidney stones.
 
Ref: Katzung, 11th edition, Chapter 15.

Q. 6

Spironolactone should NOT be given with the following pharmacological agent:

 A

Chlorothiazide

 B

b-blocker

 C

ACE inhibitors

 D

Amlodipine

Q. 6

Spironolactone should NOT be given with the following pharmacological agent:

 A

Chlorothiazide

 B

b-blocker

 C

ACE inhibitors

 D

Amlodipine

Ans. C

Explanation:

Unlike most other diuretics, K+-sparing diuretics reduce urinary excretion of K+ and can cause mild, moderate, or even life-threatening hyperkalemia.
The risk of this complication is greatly increased by renal disease (in which maximal K+ excretion may be reduced) or by the use of other drugs that reduce or inhibit renin (beta blockers, NSAIDs, aliskiren) or angiotensin II activity (angiotensin- converting enzyme inhibitors, angiotensin receptor inhibitors).
Since most other diuretic agents lead to K+ losses, hyperkalemia is more common when K+-sparing diuretics are used as the sole diuretic agent, especially in patients with renal insufficiency.
 
Ref: Ives H.E. (2012). Chapter 15. Diuretic Agents. In B.G. Katzung, S.B. Masters, A.J. Trevor (Eds), Basic & Clinical Pharmacology, 12e.

Quiz In Between


Q. 7

Which of the following potassium sparing diuretic alters cardiac mortality-

 A

Spironolactone

 B

Amiloride

 C

Triamterene

 D

Epleronone

Q. 7

Which of the following potassium sparing diuretic alters cardiac mortality-

 A

Spironolactone

 B

Amiloride

 C

Triamterene

 D

Epleronone

Ans. A

Explanation:

Ans. is ‘a’ i.e., Spironolactone

o Among potassium sparing diuretics, aldosterone antagonists (Spironolactone, eplerenone) reduce mortality in CHF.


Q. 8

The primary site of action of triameterene and spironolactone is the –

 A

Proximal tubule

 B

Distal tubule

 C

Ascending Loop of Henle

 D

Descending Loop of Henle

Q. 8

The primary site of action of triameterene and spironolactone is the –

 A

Proximal tubule

 B

Distal tubule

 C

Ascending Loop of Henle

 D

Descending Loop of Henle

Ans. B

Explanation:

Ans. is ‘b’ i.e., Distal tubule

 o Potassium sparing diuretics (Sprionolactone and triameterene) act on late distal tubule and collecting duct.


Q. 9

Potassium sparing diuretics include –

 A

Spironolactone

 B

Triamtrene

 C

Amiloride

 D

All

Q. 9

Potassium sparing diuretics include –

 A

Spironolactone

 B

Triamtrene

 C

Amiloride

 D

All

Ans. D

Explanation:

Ans. is ‘a’ i.e., Spironolactone; ‘b’ i.e., Triamterene; ‘c’ i.e., Amiloride

Potassium sparing diuretics

Aldosterone antagonists          Renal epithelial Na+ channel inhibitors

o Spironolactone                         o Amiloride

o Epleronone                              o Triamterene

o Canrenone

o Potassium canrenone

o Prorenone

o Mexrenone

Quiz In Between


Q. 10

Aldosterone antagonist are –

 A

Eplerenone

 B

Sprionolactone

 C

Amiloride

 D

a and b

Q. 10

Aldosterone antagonist are –

 A

Eplerenone

 B

Sprionolactone

 C

Amiloride

 D

a and b

Ans. D

Explanation:

Ans is ‘a’i.e., Eplerenone & b’i.e. Sprionolactone

o Aldosterone antagonists are spironolactone, eplerenone, canrenone, prorenone, mexrenone.


Q. 11

Spironolactone is the first drug to be given for?

 A

Cirrhotic edema

 B

Cardiac edema

 C

Idiopathic edema

 D

Nutritional edema

Q. 11

Spironolactone is the first drug to be given for?

 A

Cirrhotic edema

 B

Cardiac edema

 C

Idiopathic edema

 D

Nutritional edema

Ans. A

Explanation:

Ans. is ‘a’ i.e., Cirrhotic edema

“Although can be used in all kinds of edema, spironolactone is the drug of choice for initial management of edema of liver cirrhosis”.


Q. 12

Spironolactone should not be given with

 A

Chlorothiazide

 B

β – blocker

 C

ACE inhibitors

 D

Amlodipine

Q. 12

Spironolactone should not be given with

 A

Chlorothiazide

 B

β – blocker

 C

ACE inhibitors

 D

Amlodipine

Ans. C

Explanation:

Ans. is ‘c’ i.e., ACE inhibitors

o  Spironolactone is a potassium sparing diuretic, therefore, it can cause hyperkalemia decreasing the potassium diuresis.

o ACE inhibitors can also cause hyperkalemia by inhibiting the production of angiotensin I, an inmmediate precursor of angiotensin II. Angiotensin causes excretion of Kt by increasing the secretion of aldosterone (Normally aldosterone enhances absortion of Na’ in distal tubules in exhange of active secretion of Kt).

o ACE inhibitors decrease potassium excretion by inhibiting the generation of Angiotensin.

o Therefore, More pronoundced hyperkalemia can occur in patients receiving ACE inhibitors with sprironolactone.

Quiz In Between


Q. 13

Spironolactone is contraidicated with of the following-

 A

Enalapril

 B

Atenelol

 C

Verapami I

 D

None of the above

Q. 13

Spironolactone is contraidicated with of the following-

 A

Enalapril

 B

Atenelol

 C

Verapami I

 D

None of the above

Ans. A

Explanation:

Ans. is ‘a’ i.e., Enalapril

o More pronounced hyperkalemia can occur in patients receiving ACE inhibitors/ungiotensin receptor blockers with spironolactone.


Q. 14

Mainstay of treatment of Nephrogenic Diabetes Insipidus is:

 A

Desmopressin

 B

Thiazide / Amiloride diuretics and salt restriction

 C

Desmopressin and salt restriction

 D

Vasopressin and salt restriction

Q. 14

Mainstay of treatment of Nephrogenic Diabetes Insipidus is:

 A

Desmopressin

 B

Thiazide / Amiloride diuretics and salt restriction

 C

Desmopressin and salt restriction

 D

Vasopressin and salt restriction

Ans. B

Explanation:

Answer is B (Thiazide / Amiloride diuretics and salt restriction):

The treatment of Nephrogenic Diabetes Insipidus is usually achieved through a combination of thiazide / amiloride diureties and dietary salt restriction. A prostaglandin synthesis inhibitor (indomethacin) may be added.

  • Thiazide diuretics and salt restriction can reduce urinary output by inducing a state of mild volume contraction thereby promoting increased proximal reabsorption of isotonic fluid and inhibiting the delivery of free water to the collecting duct. A combination of thiazide – amiloride formulation will avoid thiazide induced hypokalemia.

Addition of Indomethacin may further reduce urinary output by inhibiting prostaglanding synthesis-Harrison

  • Thiazide diuretics in combination with amiloride and indomethacin are the most useful pharmacological agents in the treatment of Nephrogenic diabetes insipidus’- Pediatric Endocrinology (CDC Press) 2007/668

Desmopressin is usually ineffective in Congenital Nephrogenic Diabetes Insipidus. If renal resistance is partial, it may be overcome by ten fold higher doses of desmopressin but this treatment is too expensive and inconvenient to be useful chronically.


Q. 15

Which of the following is a potassium sparing drug:

September 2005, March 2013

 A

Indapamide

 B

Frusemide

 C

Spironolactone

 D

Mannitol

Q. 15

Which of the following is a potassium sparing drug:

September 2005, March 2013

 A

Indapamide

 B

Frusemide

 C

Spironolactone

 D

Mannitol

Ans. C

Explanation:

Ans. C: Spironolactone

Potassium-sparing diuretics do not promote the secretion of potassium into the urine; thus, potassium is spared and not lost as much as in other diuretics. The term “potassium-sparing” refers to an effect rather than a mechanism or location; nonetheless, the term almost always refers to two specific classes that have their effect at similar locations:

  • Aldosterone antagonists: Spironolactone, which is a competitive antagonist of aldosterone. Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late distal tubule of the nephron. Spironolactone prevents aldosterone from entering the principal cells, preventing sodium reabsorption. A similar agent is potassium canreonate.
  • Epithelial sodium channel blockers: amiloride and triamterene.

Quiz In Between


Q. 16

All of the following are true regarding diuretics except:         

March 2008

 A

Spironolactone is a potassium sparing drug

 B

Mannitol is an osmotic diuretic

 C

Thiazides act by inhibiting Sodium-potassium­chloride cotransport

 D

Acetazolamide inhibits carbonic anhydrase enzyme

Q. 16

All of the following are true regarding diuretics except:         

March 2008

 A

Spironolactone is a potassium sparing drug

 B

Mannitol is an osmotic diuretic

 C

Thiazides act by inhibiting Sodium-potassium­chloride cotransport

 D

Acetazolamide inhibits carbonic anhydrase enzyme

Ans. C

Explanation:

Ans. C: Thiazides act by inhibiting Sodium-potassium-chloride cotransport

High Efficacy diuretics:

–  High ceiling diuretics/Loop diuretics, such as furosemide, inhibit the body’s ability to reabsorb sodium (by inhibiting sodium-potassium-chloride cotransport) at the ascending loop in the kidney which leads to a retention of water in the urine as water normally follows sodium back into the extracellular fluid (ECF). Other examples of high ceiling loop diuretics include ethacrynic acid, torasemide and bumetanide.

Medium efficacy diuretics:

– Thiazide-type diuretics such as hydrochlorothiazide, Clopamide, act on the distal convoluted tubule and inhibit the sodium-chloride symporter leading to retention of water in the urine, as water normally follows penetrating solutes. The short-term anti-hypertensive action is based on the fact that thiazides decrease preload, decreasing blood pressure. On the other hand the long-term effect is due to an unknown vasodilator effect that decreases blood pressure by decreasing resistance.

– Thiazide like diuretics includes chlorthalidone, metolazone, xipamide, indapamide

Weak/adjunctive drugs:

– Carbonic Anhydrase Inhibitors inhibit the enzyme carbonic anhydrase which is found in the proximal convoluted tubule. This results in several effects including bicarbonate retention in the urine, potassium retention in urine and decreased sodium absorption. Drugs in this class include acetazolamide and methazolamide.

– Potassium-sparing diuretics do not promote the secretion of potassium into the urine; thus, potassium is spared and not lost as much as in other diuretics. The term “potassium-sparing” refers to an effect rather than a mechanism or location; nonetheless, the term almost always refers to two specific classes that have their effect at similar locations:

  • Aldosterone antagonists: spironolactone, which is a competitive antagonist of aldosterone. Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late distal tubule of the nephron. Spironolactone prevents aldosterone from entering the principal cells, preventing sodium reabsorption. A similar agent is potassium canreonate.
  • Epithelial sodium channel blockers: amiloride and triamterene.

Osmotic diuretics as mannitol are filtered in the glomerulus, but cannot be reabsorbed. Their presence leads to an increase in the osmolarity of the filtrate. To maintain osmotic balance, water is retained in the urine.


Q. 17

Spironolactone is least commonly used in which of the following:       

September 2011

 A

Congestive heart failure

 B

Cirrhotic edema

 C

Hypertension

 D

Primary hyperaldosteronism

Q. 17

Spironolactone is least commonly used in which of the following:       

September 2011

 A

Congestive heart failure

 B

Cirrhotic edema

 C

Hypertension

 D

Primary hyperaldosteronism

Ans. C

Explanation:

Ans. C: Hypertension

As an add-on drug, spironolcatone may be useful in hypertensive patients with significant hyperuricemia, hypokalemia, or glucose intolerance

Spironolactone

  • It is a synthetic 17-lactone drug that is a renal competitive aldosterone antagonist in a class of potassium-sparing diuretics

It used primarily to treat heart failure, ascites in patients with liver disease, low-renin hypertension, hypokalemia, secondary hyperaldosteronism (such as occurs with hepatic cirrhosis), and Conn’s syndrome (primary hyperaldosteronism).

On its own, spironolactone is only a weak diuretic because its effects target the distal nephron (collecting tubule), where urine volume can only be slightly modified; but it can be combined with other diuretics to increase efficacy.

  • Due to its antiandrogen effect, it can also be used to treat hirsutism.
  • It is also used for treating hair loss and acne in women, and can be used as a topical medication for treatment of male baldness.
  • It is commonly used to treat symptoms of polycystic ovary syndrome (PCOS) such as excess facial hair and acne.
  • Spironolactone can cause gynecomastia in males and, unless regularly monitored, should not be given with potassium supplementation for fear of development of hyperkalemia.

Spironolactone inhibits the effect of aldosterone by competing for intracellular aldosterone receptors in the cortical collecting duct.

  • This decreases the reabsorption of sodium and water, while decreasing the secretion of potassium.
  • Spironolactone has a fairly slow onset of action, taking several days to develop, and, so, the effect diminishes slowly.
  • Spironolactone has anti-androgen activity by directly binding to and blocking androgens from interacting with the androgen receptor, by blocking androgen production, and by increasing estrogen levels.
  • Production of androgens is decreased by inhibiting 17alpha-hydroxylase and 17, 20-desmolase, which are enzymes in the testosterone biosynthesis pathway.
  • Estrogen levels are increased by enhancing the peripheral conversion of testosterone to estradiol and by displacing estradiol from sex hormone-binding globulin (SHBG)
  • Spironolactone is a synthetic steroid that acts as a competitive antagonist to aldosterone.
  • Its onset and duration of action are determined by the kinetics of the aldosterone response in the target tissue.
  • Substantial inactivation of spironolactone occurs in the liver and hepatitis or cirrhosis can lead to secondary aldosteronism, which is one indication for treatment.
  • Spironolactone is associated with an increased risk of bleeding from the stomach and duodenum
  • Because it also affects androgen receptors and other steroid receptors, it can cause gynecomastia, menstrual irregularities and testicular atrophy.
  • Spironolactone often increases serum potassium levels and can cause hyperkalemia, therefore, it is recommended that people using this drug avoid potassium supplements and salt substitutes containing potassium.
  • Long-term administration of spironolactone gives the histologic characteristic of spironolactone bodies in the adrenal cortex.
  • Spironolactone bodies are eosinophilic, round, concentrically laminated cytoplasmic inclusions surrounded by clear halos in preparations stained with hematoxylin and eosin.

Q. 18

Potassium sparing diuretics ‑

 A

Spironoloctone

 B

Triameterene

 C

Amiloride

 D

All of the above

Q. 18

Potassium sparing diuretics ‑

 A

Spironoloctone

 B

Triameterene

 C

Amiloride

 D

All of the above

Ans. D

Explanation:

Ans. is ‘d’ i.e., All of the above

Quiz In Between



Staphylococcus aureus: Virulence and Toxin

Staphylococcus aureus: Virulence and Toxin

Q. 1

All of the following statements about staphylococcus aureus are true, EXCEPT:

 A

Most common source of infection is cross infection from infected people

 B

About 30% of general population are healthy nasal carriers

 C

Epidermolysin and TSS toxin are superantigens

 D

Methicillin Resistance is chromosome mediated.

Q. 1

All of the following statements about staphylococcus aureus are true, EXCEPT:

 A

Most common source of infection is cross infection from infected people

 B

About 30% of general population are healthy nasal carriers

 C

Epidermolysin and TSS toxin are superantigens

 D

Methicillin Resistance is chromosome mediated.

Ans. A

Explanation:

Carriers of staphylococcus aureus are the primary source for cross infection to individuals who do not normally have this bacterium in their commensal microflora.

Individuals normally free from s.aureus may have less immunity against the lethal consequence of S.aureus infection compared with those who are persistent carrier of the species and suffer from endogenous infection.
 
Most individuals who develop staphylococcus aureus infections are infected with their own colonizing strains.

However, S. aureus may also be acquired from other people or from environmental exposures.
Ref: Jawetz, Melnick and Adelberg’s Medical Microbiology, 23rd Edition, Pages 224 – 228; Staphylococci in Human Disease By Kent B. Crossley, Page 265; Microbiology and Immunology By Monica Gandhi, Page 4; Harrison’s Principles of Internal Medicine, 17th edition, Pages 873 – 879.

Q. 2

An enzyme produced by Staphylococcus aureus that dissolves fibrin clots is:

 A

Hyaluronidase

 B

Catalase

 C

Staphylokinase

 D

Lipase

Q. 2

An enzyme produced by Staphylococcus aureus that dissolves fibrin clots is:

 A

Hyaluronidase

 B

Catalase

 C

Staphylokinase

 D

Lipase

Ans. C

Explanation:

Pathogenic bacteria release exoenzymes that increase their ability to invade body tissue. These include coagulase, kinases, lipase, hyaluronidase, and collagenase.
All Staphylococci produce catalase, an enzyme responsible for conversion of toxic hydrogen peroxide to water and oxygen which accumulates during bacterial metabolism or is released following phagocytosis.
 
Kinases dissolve fibrin clots thus enabling the organism to invade and spread throughout the body. Staphylococcus aureus produces staphylokinase which is fibrinolytic.
 
Coagulase is the exoenzyme produced by Staphylococcus aureus and it clots the plasma.
Lipase hydrolyzes lipids, and aids in the survival of staphylococci in the sebaceous glands.
Hyaluronidase enables pathogen to spread through connective tissue by breaking down hyaluronic acid, the “cement” that holds tissue cells together.
 
Ref: Francis C.W., Crowther M. (2010). Chapter 23. Principles of Antithrombotic Therapy. In J.T. Prchal, K. Kaushansky, M.A. Lichtman, T.J. Kipps, U. Seligsohn (Eds), Williams Hematology, 8e.

Q. 3

Toxin of staphylococcus –

 A

Hemolysin

 B

Leucocidin

 C

Enterotoxin

 D

All

Q. 3

Toxin of staphylococcus –

 A

Hemolysin

 B

Leucocidin

 C

Enterotoxin

 D

All

Ans. D

Explanation:

Ans. is ‘d’ i.e., All 

Quiz In Between


Q. 4

Staphylococcus aureus remains in the skin for longer period because of –

 A

Catalase

 B

Coagulase

 C

Hyaluronidase 

 D

None

Q. 4

Staphylococcus aureus remains in the skin for longer period because of –

 A

Catalase

 B

Coagulase

 C

Hyaluronidase 

 D

None

Ans. C

Explanation:

Ans. is ‘c’ i.e., Hyaluronidase 

Hyaluronidase breaks down the connective tissue and helps in the spread of infection.


Q. 5

Toxic shock syndrome is Staphylococcus infection is due to –

 A

Superantigen

 B

Alpha-hemolysis

 C

Coagulase

 D

Penton Valentine factor

Q. 5

Toxic shock syndrome is Staphylococcus infection is due to –

 A

Superantigen

 B

Alpha-hemolysis

 C

Coagulase

 D

Penton Valentine factor

Ans. A

Explanation:

Ans. is ‘a’ i.e., Superantigen 

Quiz In Between



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