Author: Renu Maurya

Benzodiazepine

Benzodiazipines

Q. 1

Diazepam poisoning is treated by:

 A Flumazenil
 B

Hemofiltration

 C Charcoal
 D

Resins

Q. 1

Diazepam poisoning is treated by:

 A Flumazenil
 B

Hemofiltration

 C Charcoal
 D

Resins

Ans. A

Explanation:

Flumazenil REF: Harrison’s 17th ed Table e 35-4

See APPENDIX-42 for list of “Antidotes”

“Specific antidote for benzodiazepine poisoning is flumazenil”


Q. 2

Benzodiazepine antagonist ?

 A

Flumazenil

 B

Naloxone

 C Furazolidone
 D

Naltrexone

Q. 2

Benzodiazepine antagonist ?

 A

Flumazenil

 B

Naloxone

 C Furazolidone
 D

Naltrexone

Ans. A

Explanation:

Flumazenil [Ref. K.D.T. 6thIe p399-400 5th/e p 362]

  • Benzodiazepine acts by enhancing presynaptic/postsynaptic inhibition through a specific BZD receptor which is an integral part of the GABA receptor-CI channel complex.
  • Flumazenil is a BZD analogue which has little intrinsic activity, but it competes with BZD agonists as well as inverse agonists for the BZD receptor and reverses their depressant or stimulant effects respectively.
  • Flumazenil is the drug of choice for benzodiazepene overdose. About other options:
  • Naltrexone                        –> Opioid antagonist
  • Butorphanol                      –> Agonist/antagonist at opioid receptors
  • Pralidoxime                      –> Cholinesterase reactivator

Q. 3

The following are the benzodiazepines of choice in elderly and those with liver disease, EXCEPT:

 A

Lorazepam

 B

Orazepam

 C

Temazepam

 D

Diazepam

Q. 3

The following are the benzodiazepines of choice in elderly and those with liver disease, EXCEPT:

 A

Lorazepam

 B

Orazepam

 C

Temazepam

 D

Diazepam

Ans. D

Explanation:

Diazepam generates active metabolites, has slow elimination and tends to accumulate with regular use.

Lorazepam, Oxazepam and Temazepam do not produce active metabolites and are relatively safer in elderly patients and in those with liver disease.

These agents should be used in preference to diazepam.

Ref: Essentials of Pharmacology By K D Tripathi, 5th Edtion, Page 364.

Quiz In Between


Q. 4

Shortest acting benzodiazepine is‑

 A

Flurazepam

 B

Alprazolam

 C

Triazolam

 D

Diazepam

Q. 4

Shortest acting benzodiazepine is‑

 A

Flurazepam

 B

Alprazolam

 C

Triazolam

 D

Diazepam

Ans. C

Explanation:

Ans. is ‘c’ i.e., Triazolam

o Midazolam (slightly shorter acting than triazolam) and triazolam are shortest acting BZDs.


Q. 5

Benzodiazepine without anticonvulsant property is‑

 A

Nitrazepam

 B

Diazepam

 C

Clonazepam

 D

Temazepam

Q. 5

Benzodiazepine without anticonvulsant property is‑

 A

Nitrazepam

 B

Diazepam

 C

Clonazepam

 D

Temazepam

Ans. D

Explanation:

Ans. is ‘d’ i.e., Temazepam

BZDs with significant anticonvulsant property are diazepam, clonazepam, nitrazepam, lorazepam and flurazepam.


Q. 6

Antagonist of Benzodiazepine is ‑

 A

Nalorphine

 B

Carbamazepine

 C

Naloxone

 D

Flumazenil

Q. 6

Antagonist of Benzodiazepine is ‑

 A

Nalorphine

 B

Carbamazepine

 C

Naloxone

 D

Flumazenil

Ans. D

Explanation:

Ans. is ‘d’ i.e., Flumazenil

o Flumazenil is a benzodiazepene analogue which competes with BZD agonists as well as inverse agonists for the BZD receptor and reverses their depressant or stimulant effects respectively.

o It also antagonizes the action of Zolpidem, Zopiclone and Zopeplon as these drugs also act on BZD site.

Quiz In Between


Q. 7

Flumazenil is –

 A

Diazepam inverse agonist

 B

Diazepam antagonist

 C

Opioid antagonist

 D

Opioid inverse agonist

Q. 7

Flumazenil is –

 A

Diazepam inverse agonist

 B

Diazepam antagonist

 C

Opioid antagonist

 D

Opioid inverse agonist

Ans. B

Explanation:

Ans. is ‘b’ i.e., Diazepam antagonist


Q. 8

A 6 yr. old child with acute onset of fever of 104° F developed febrile seizures and was treated. To avoid future recurrence of seizure attacks what should be given –

 A

Paracetamol 400 mg + Phenobarbitone daily

 B

Oral Diazepan 6 hourly

 C

Paracetamol 400 mg 6 hourly

 D

I.V. diazepam infusion over 12 hrs

Q. 8

A 6 yr. old child with acute onset of fever of 104° F developed febrile seizures and was treated. To avoid future recurrence of seizure attacks what should be given –

 A

Paracetamol 400 mg + Phenobarbitone daily

 B

Oral Diazepan 6 hourly

 C

Paracetamol 400 mg 6 hourly

 D

I.V. diazepam infusion over 12 hrs

Ans. B

Explanation:

Ans. is ‘b’ i.e., Oral Diazepan 6 hrly


Q. 9

An anxiolytic benzodiazepine which is also antidepressant :                               

September 2007

 A

Lorazepam

 B

Oxazepam

 C

Alprazolam

 D

Chlordiazepoxid

Q. 9

An anxiolytic benzodiazepine which is also antidepressant :                               

September 2007

 A

Lorazepam

 B

Oxazepam

 C

Alprazolam

 D

Chlordiazepoxid

Ans. C

Explanation:

Ans. C: Alprazolam

Alprazolam is approved for the short-term treatment of panic disorder, with or without agoraphobia. Alprazolam is very effective in the short-term symptomatic relief of moderate to severe anxiety, essential tremor, and panic attacks.

Alprazolam is indicated for the management of anxiety disorders or the short-term relief of symptoms of anxiety. Alprazolam is recommended for the short-term treatment of severe acute anxiety.

Alprazolam is sometimes prescribed for anxiety with associated depression.

The antidepressant effects of alprazolam may be due to its effects on beta-adrenergic receptors. Other benzodiazepines are not known to have antidepressant activity.

Quiz In Between


Q. 10

Benzodiazepine overdose in a patient presenting with coma, is treated by:       

March 2010

 A

Protamine

 B

Flumazenil

 C

Coumarin

 D

Midazolam

Q. 10

Benzodiazepine overdose in a patient presenting with coma, is treated by:       

March 2010

 A

Protamine

 B

Flumazenil

 C

Coumarin

 D

Midazolam

Ans. B

Explanation:

Ans. B: Flumazenil

Decontamination

– Gastric lavage is not recommended but may be considered if the presence of a lethal co-ingestant is suspected and the patient presents within 1 hour of ingestion.

–  Single-dose activated charcoal is recommended for GI decontamination in patients with protected airway who present within 4 hours of ingestion.

  • Respiratory depression may be treated with assisted ventilation.
  • Flumazenil

– Flumazenil is a competitive BZD receptor antagonist and should be used cautiously because it has potential to precipitate BZD withdrawal in chronic users, resulting in seizures.

–  Flumazenil administration is contraindicated in mixed overdoses (e.g., TCAs) because BZD reversal can precipitate seizures and cardiac arrhythmias.

– Ideal indication for flumazenil use is isolated BZD overdose, particularly if overdose is iatrogenic in nature.


Q. 11

Antidote for benzodiazepine poisoning:

FMGE 10, 13; NEET 14

 A

Naloxone

 B

Atropine

 C

Flumazenil

 D

N-acetyl-cysteine

Q. 11

Antidote for benzodiazepine poisoning:

FMGE 10, 13; NEET 14

 A

Naloxone

 B

Atropine

 C

Flumazenil

 D

N-acetyl-cysteine

Ans. C

Explanation:

Ans. Flumazenil


Q. 12

IV diazepam has which of the following effect which is not seen by other routes ‑

 A

Analgesia

 B

Sedation

 C

Hypotension

 D

Coronary dilatation

Q. 12

IV diazepam has which of the following effect which is not seen by other routes ‑

 A

Analgesia

 B

Sedation

 C

Hypotension

 D

Coronary dilatation

Ans. D

Explanation:

Ans. is ‘d’ i.e., Coronary dilatation

Mechanism of action of benzodiazepines (BZDs)

  • Benzodiazepines act preferentially on midbrain ascending reticular formation (which maintains wakefulness) and on limbic system (thought and mental function).
  • Muscle relaxation is produced by action on medulla.
  • Ataxia is due to action on cerebellum.
  • BZDs acts on GABAA receptors.
  • GABA,,, receptor has 5 subunits a / p, p, a / y.
  • GABA binding site is on p. subunit, while BZDs binding site is on a / y subunit.
  • BZDs receptor increase the conductance of Cl- channel.
  • BZDs do not themselves increase Cl- conductance, i.e. they have only GABA facilitatory but no GABA mimetic action. (Barbiturates have both GABA facilitatory and GABA mimetic actions).

Effect on CNS

  • In contrast to barbiturates, BZDs are not general depressant, but exert relatively selective anxiolytic, hypnotic, muscle relaxant and anticonvulsant effects.
  • The antianxiety action of BZDs is not dependent on their sedative property —› with chronic administration relief of anxiety is maintained, but drowsiness wanes off due to development of tolerance.
  • Stage 2 sleep is increased, while REM, Stage 3 & 4 sleep are decreased.
  • Nitrazepam is the only benzodiazepine, which increases REM sleep.
  • Clonazepan and diazepam have more marked muscle relaxant property.
  • Clonazepam, diazepam, nitrazepam and flurazepam have more prominent anticonvulsant activity than other BZDs.
  • Diazepam (but not other BZDs) has analgesic action.
  • Diazepam produces short lasting coronary dilatation on i.v. injection.
  • Diazepam decreases nocturnal gastric secretion and prevents stress ulcers.

Quiz In Between


Q. 13

Inverse agonist of benzodiazepine receptor is –

 A

Phenobarbitone

 B

Flumazenil

 C

Beta carboline

 D

Gabapentin

Q. 13

Inverse agonist of benzodiazepine receptor is –

 A

Phenobarbitone

 B

Flumazenil

 C

Beta carboline

 D

Gabapentin

Ans. C

Explanation:

Ans. is `c’ i.e., Beta carboline


Q. 14

Antidote true is all except‑

 A

Deferoxamine – Iron

 B

Flumazenil – BZDs

 C

Dimercaprol – Arsenic

 D

Naloxone – Dhatura

Q. 14

Antidote true is all except‑

 A

Deferoxamine – Iron

 B

Flumazenil – BZDs

 C

Dimercaprol – Arsenic

 D

Naloxone – Dhatura

Ans. D

Explanation:

Ans. is ‘d’ i.e., Naloxone-Dhatura


Q. 15

Midazolam causes all except:

 A

Anterograde amnesia

 B

Retrograde amnesia

 C

Causes tachyphylaxis during high dose infusions

 D

Decreased cardiovascular effects as compared to propofol

Q. 15

Midazolam causes all except:

 A

Anterograde amnesia

 B

Retrograde amnesia

 C

Causes tachyphylaxis during high dose infusions

 D

Decreased cardiovascular effects as compared to propofol

Ans. B

Explanation:

Ans. b. Retrograde amnesia

At the time of peak concentration in plasma, hypnotic doses of benzodiazepines (midazolam) can be expected to cause varying degrees of lightheadedness, lassitude, increased reaction time, motor incoordination, impairment of mental and motor functions, confusion, and anterograde amnesia.”

Midazolam:

  • It causes anterograde amnesiaQ
  • Tolerance and tachyphylaxis may occur, particularly with longer-term infusionsQ(Shafer A. Complications of sedation with midazolam in the intensive care unit and a comparison with other sedative regimens. Crit Care Med. 1998;26(5): 947-56)
  • Benzodiazepine withdrawal syndrome has also been associated with high dose/ long-term midazolam infusionsQ
  • Compared with propofol infusions, midazolam infusions have been associated with a decreased occurrence of hypotension° but a more variable time course for recovery of function after the cessation of the infusion.

Quiz In Between


Q. 16

Shortest acting Benzodiazepine ‑

 A

Diazepam

 B

Midazolam

 C

Alprazolam

 D

Chlordiazepoxide

Q. 16

Shortest acting Benzodiazepine ‑

 A

Diazepam

 B

Midazolam

 C

Alprazolam

 D

Chlordiazepoxide

Ans. B

Explanation:

Ans. is ‘b’ i.e., Midazolam

  • Ajay Yadav 4th/e p. 85] o Midazolam is the shortest acting benzodiazipine.
  • It is 3 times more potent than diazepam.
  • Midazolam is now very commonly used BZD in intraoperative period.
  • Advantages of midazolam over diazepam are :
  • Water based preparation, so injection is painless.
  • Elimination half life is 2-3 hours, so can be safely used for day care procedures.
  • Reversal with flumezanil is complete (no resedation).
  • Disadvantages are that decrease in BP and peripheral vascularresistance, respiratory depression and incidence of apnea are higher and more profound than diazepam

Q. 17

The antidote for benzodiazepine toxicity is-

 A

Flumazenil

 B

Naloxone

 C

Naltrexone

 D

Dimercaprol

Q. 17

The antidote for benzodiazepine toxicity is-

 A

Flumazenil

 B

Naloxone

 C

Naltrexone

 D

Dimercaprol

Ans. A

Explanation:

Ans. is ‘a’ i.e., Flumazenil


Q. 18

Benzodiazepine without anticonvulsant property is ‑

 A

Nitrazepam

 B

Diazepam

 C

Clonazepam

 D

Temazepam

Q. 18

Benzodiazepine without anticonvulsant property is ‑

 A

Nitrazepam

 B

Diazepam

 C

Clonazepam

 D

Temazepam

Ans. D

Explanation:

Ans. is ‘d’  i.e., Temazepam 

  • BZDs with significant anticonvulsant property are diazepam, clonazepam, nitrazepam, lorazepam and flurazepam. 

Effects of benzodiazepines

  • In contrast to barbiturates, BZDs are not general depressant, but exert relatively selective anxiolytic, hypnotic, muscle relaxant and anticonvulsant effects.
  • The antianxiety action of BZDs is not dependent on their sedative property with chronic administration relief of anxiety is maintained, but drowsiness wanes off due to development of tolerance.
  • Stage 2 sleep is increased, while REM, Stage 3 & 4 sleep are decreased.
  • Nitrazepam is the only benzodiazepine, which increases REM sleep.
  • Clonazepan and diazepam have more marked muscle relaxant property.
  • Clonazepam, diazepam, nitrazepam and flurazepam have more prominent anticonvulsant activity than other BZDs.
  • Diazepam (but not other BZDs) has analgesic action.
  • Diazepam produces short lasting coronary dilatation on     injection.
  • Diazepam decreases nocturnal gastric secretion and prevents stress ulcers.

Q. 19

Shortest acting benzodiazepine is 

 A

Flurazepam

 B

Alprazolam

 C

Triazolam

 D

Diazepam

Q. 19

Shortest acting benzodiazepine is 

 A

Flurazepam

 B

Alprazolam

 C

Triazolam

 D

Diazepam

Ans. C

Explanation:

Ans. is ‘c’ i.e., Triazolam

Quiz In Between



Benzodiazepine

BENZODIAZEPINE


CLASSIFICATION:

  • Long Acting
    • Flurazepam 50-100 t1/2(hrs)
    • Diazepam 30-60 t1/2(hrs)
    • Nitrazepam 30 t1/2(hrs)
    • Flunitrazepam 15-25 t1/2(hrs)
  •  Short-Acting 
    • Temazepam with t1/2 8-12 hrs
      • Benzodiazepine without anticonvulsant property.
    •  Triazolam with t1/2 2-3 hrs
    •  Midazolam 2 t1/2(hrs)
    • Alprazolam 

MOA:

PHARMACOKINETICS:

  • Short-acting BZDs:
  • Eg: Midazolam – IV or IM as an induction agent.
    • Rapid onset of action.
    • Quick drug clearance.
    • Causes anterograde amnesia, tachyphylaxis during high dose infusions.
    • Decreased cardiovascular effects as compared to propofol 
  • Temazepam or oxazepam – Revives insomnia. 
    • At lower doses, relieves acute symptoms of anxiety, such as panic attacks & phobias.
  • Long-acting BZDs: 
    • Slower onset of action following oral administration → Hence prolonged pharmacological action.
    • Sedation.
    • Prevents increased muscle tone of tetanus infection. 
  • Metabolized in liver by dealkylation and hydroxylation.
  • Excreted in urine as glucuronide conjugates.

ACTIONS:

  • Antianxiety
  • Sedation: 
    • Increasing dosage produce sleep & hence considerable as hypnotic
    • I.V administration used extensively to produce conscious sedation during unpleasant procedures. 
    • Eg: Diazepam & midazolam.
    • Cardiovascular stability – IV diazepam 
    • Midazolam potentiates propofol in co-induction technique.
  • Anticonvulsants: 
    • Clonazepam & diazepam – Effective in status epilepticus.
  • Muscle relaxation: 
    • Reduce muscle tone.
  •  Amnesia: 
    • IV benzodiazepines produces antegrade amnesia. 
    • Midazolam – Very intense for 20-30 minutes
    • Lorazepam – Longer amnesia – 6 hr.

DRUGS:

  • Inverse agonist of benzodiazepine receptor – Beta carboline.
  • Benzodiazepine antagonist – Flumazenil

USES:

  • As hypnotic –
    • Daytime sedation (Alprazolam)
  • As anxiolytic.
  • Antidepressant  (Alprazolam)
  • As anticonvulsants, especially emergency control of status epilepticus  
    • To avoid future recurrence of seizure attacks Oral Diazepam 6 hourly is given.
  • As centrally acting muscle relaxant.
  • For anesthetic medication and IV anesthesia 
  • Alcohol withdrawal in dependent subjects 
  • Mostly given along with analgesics (NSAIDs|). 
  • DOC in elderly & with liver disease.
    • Lorazepam, OxazepamTemazepam
  • Spasmolytics.
  • Anti-ulcer.

ADVERSE EFFECT:

  • Dizziness, lassitude, vertigo, disorientation, amnesia, increased reaction time with motor incoordination, impairment of mental coordination occur. 
  • Weakness, blurring of vision, dry mouth and urinary incontinence.
  • BZD poisoning:
    • Benzodiazepine antagonist -Flumazenil
    • Eg: Diazepam poisoning.
  • Paradoxical stimulation, irritability, and sweating may occur with flurazepam.
  • Increase in nightmares and behavioral alterations 
  • Increased psychological effects with usage of short-acting benzodiazepines in insomnia. 
  • Disturbed REM sleep patterns.

Exam Important

  • Diazepam poisoning is treated by Flumazenil
  • Benzodiazepine antagonist  Flumazenil
  • Benzodiazepines of choice in elderly and those with liver disease Lorazepam, Orazepam & Temazepam
  • Shortest acting benzodiazepine is Triazolam
  • Benzodiazepine without anticonvulsant property is Temazepam
  • To avoid future recurrence of seizure attacks Oral Diazepam 6 hourly is given
  • Alprazolam is an anxiolytic benzodiazepine with  antidepressant  action
  • IV diazepam  shows Coronary dilatation
  • Inverse agonist of benzodiazepine receptor is Beta carboline
  • Midazolam causes  Anterograde amnesia, tachyphylaxis during high dose infusions & Decreased cardiovascular effects as compared to propofol
Don’t Forget to Solve all the previous Year Question asked on BENZODIAZEPINE

Module Below Start Quiz

Codons & Genetic code

Codons and genetic codes

Q. 1

A codon in the genetic code consists of:

 A

One molecule of charged-tRNA

 B

A Shine-Dalgarno sequence

 C

Three consecutive nucleotides

 D

Two complementary base pairs

Q. 1

A codon in the genetic code consists of:

 A

One molecule of charged-tRNA

 B

A Shine-Dalgarno sequence

 C

Three consecutive nucleotides

 D

Two complementary base pairs

Ans. C

Explanation:

A codon is a triplet sequence of bases. The tRNA molecule contains an anticodon.

The Shine-Dalgarno sequence is found in the 23S prokaryotic ribosomal RNA. A codon is on the same strand of DNA or mRNA.


Q. 2

Which of the following is the CORRECT explanation for ‘degeneracy of codon’?

 A

More than one codon for a single amino acid

 B

More than one amino acid for a single codon

 C

No punctuation in codons

 D

Termination of protein synthesis

Q. 2

Which of the following is the CORRECT explanation for ‘degeneracy of codon’?

 A

More than one codon for a single amino acid

 B

More than one amino acid for a single codon

 C

No punctuation in codons

 D

Termination of protein synthesis

Ans. A

Explanation:

Three of the 64 possible codons do not code for specific amino acids; these have been termed nonsense codons. These nonsense codons are utilized in the cell as termination signals; they specify where the polymerization of amino acids into a protein molecule is to stop. The remaining 61 codons code for the 20 naturally occurring amino acids. Thus, there is “degeneracy” in the genetic code—that is, multiple codons decode the same amino acid.

 
Ref: Weil P. (2011). Chapter 37. Protein Synthesis & the Genetic Code. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.

Q. 3

Amino acids not coded by triplet codon:

 A

Lysine

 B

Hydroxyproline

 C

Selenocysteine

 D

Pyrrolysine

Q. 3

Amino acids not coded by triplet codon:

 A

Lysine

 B

Hydroxyproline

 C

Selenocysteine

 D

Pyrrolysine

Ans. B

Explanation:

B i.e. Hydroxyproline

Quiz In Between


Q. 4

Stop codons are:

 A

UAA

 B

UAG

 C

UGA

 D

All

Q. 4

Stop codons are:

 A

UAA

 B

UAG

 C

UGA

 D

All

Ans. D

Explanation:

A, B, C i.e. UAA, UAG, UGA


Q. 5

If there are 4 nucleotides instead of 3 in codon, how many amino acids may be formed?

 A

16

 B

21

 C

256

 D

64

Q. 5

If there are 4 nucleotides instead of 3 in codon, how many amino acids may be formed?

 A

16

 B

21

 C

256

 D

64

Ans. C

Explanation:

C i.e. 256


Q. 6

Stop codon:

 A

UAG

 B

UCA

 C

UAC

 D

AUG

Q. 6

Stop codon:

 A

UAG

 B

UCA

 C

UAC

 D

AUG

Ans. A

Explanation:

A i.e. UAG

Quiz In Between


Q. 7

A codon consists of –

 A

One molecule of amono acyl-t RNA

 B

Two complementary base pairs

 C

3 consecutive nucleotide units

 D

4 individual nucleotides

Q. 7

A codon consists of –

 A

One molecule of amono acyl-t RNA

 B

Two complementary base pairs

 C

3 consecutive nucleotide units

 D

4 individual nucleotides

Ans. C

Explanation:

C i.e. 3 consecutive nucleotide units


Q. 8

Nonsense codons bring about-

 A

Elongation of polypeptide chain

 B

Pre-translational modificastion of protein

 C

Initiation of protein synthesis

 D

Termination of protein synthesis

Q. 8

Nonsense codons bring about-

 A

Elongation of polypeptide chain

 B

Pre-translational modificastion of protein

 C

Initiation of protein synthesis

 D

Termination of protein synthesis

Ans. D

Explanation:

D i.e. Termination of protein synthesis


Q. 9

Same aminoacid is coded by multiple codons d/t following :

 A

Degeneracy

 B

Frame-shift mutation

 C

Transcription

 D

Mutation

Q. 9

Same aminoacid is coded by multiple codons d/t following :

 A

Degeneracy

 B

Frame-shift mutation

 C

Transcription

 D

Mutation

Ans. A

Explanation:

A i.e. Degeneracy

Quiz In Between


Q. 10

The anticodon region is an important part of the

 A

r-RNA

 B

m-RNa

 C

t-RNa

 D

hn-RNa

Q. 10

The anticodon region is an important part of the

 A

r-RNA

 B

m-RNa

 C

t-RNa

 D

hn-RNa

Ans. C

Explanation:

C i.e. t – RNA


Q. 11

In transcription anticodon is seen in ‑

 A

t-RNA

 B

m-RNA

 C

r-RNA

 D

None

Q. 11

In transcription anticodon is seen in ‑

 A

t-RNA

 B

m-RNA

 C

r-RNA

 D

None

Ans. A

Explanation:

 A i.e. t – RNA


Q. 12

Amber codon refers to

 A

Mutant codon

 B

Stop codon

 C

Initiating codon

 D

Codon for more than one amino acids

Q. 12

Amber codon refers to

 A

Mutant codon

 B

Stop codon

 C

Initiating codon

 D

Codon for more than one amino acids

Ans. B

Explanation:

B i.e Stop Codon

Quiz In Between


Q. 13

A mutation in the codon which causes a change in the coded amino acid, is known as:

 A

Mitogenesis

 B

Somatic mutation

 C

Missense mutation

 D

Recombination

Q. 13

A mutation in the codon which causes a change in the coded amino acid, is known as:

 A

Mitogenesis

 B

Somatic mutation

 C

Missense mutation

 D

Recombination

Ans. C

Explanation:

C i.e. Missense mutation


Q. 14

A codon codes for a single amino acid. This characteristic is called ‑

 A

Non-overlapping

 B

Unambiguous

 C

Non-punctate

 D

Degeneracy

Q. 14

A codon codes for a single amino acid. This characteristic is called ‑

 A

Non-overlapping

 B

Unambiguous

 C

Non-punctate

 D

Degeneracy

Ans. B

Explanation:

Ans. is ‘b’ i.e., Unambiguous

Characteristics of genetic codes

Genetic codes have following characteristics ‑

1) Universal :- Each codon specifically codes for same amino acid in all species, e.g. UCA codes for serine and CCA codes for proline in all organisms. That means specificity of codon has been conserved from very early stages of evolution. Exception to the universality of genetic coder are found in human mitochondria, where the code :-

α UGA codes for tryptophan instead of serving as a stop codon.

AUA codes for methionine instead of isoleucine.

CUA codes for threonine instead of leucine.

LI AGA and AGG serve as stop codon instead of coding for arginine.

2) Unambiguous/Specific :- A particular codon always codes for the same amino acid. For example CCU always codes for proline and UGG always codes for tryptophan.

3)  Degeneracy/Redundancy :- A given amino acid may have more than one codon. For example, CCU, CCC, CCA and CCG all four codons code for proline. Therefore, there are 61 codons for 20 amino acids.

4) Stop or termination or nonsense codons:- Three of the 64 possible nucleotide triplets UAA (amber), UAG (Ochre) and UGA (opal) do not code for any amino acid. They are called nonsense codons that normally signal termination of polypeptide chains. Thus, though there are 64 possible triplet codons, only 61 codes for 20 amino acids (as remaining three are non-sense codons).

5) Non overlapping and nonpuntate (Comma less) :- During translation, the code is read sequentially, without spacer bases, from a fixed starting point, as a continuous sequence of bases, taken 3 at a time, e.g. AUGCUA GACUUU is read as AUG/CUA/GAC/UUU without “ponctation” (coma) between codons.


Q. 15

Multiple codons code for same amino acid ‑

 A

Ambiguity

 B

Wobble phenomenon

 C

Degeneracy

 D

Mutation

Q. 15

Multiple codons code for same amino acid ‑

 A

Ambiguity

 B

Wobble phenomenon

 C

Degeneracy

 D

Mutation

Ans. C

Explanation:

Quiz In Between


Q. 16

RNA which contains codon for speicific amino acid ‑

 A

tRNA

 B

rRNA

 C

mRNA

 D

None

Q. 16

RNA which contains codon for speicific amino acid ‑

 A

tRNA

 B

rRNA

 C

mRNA

 D

None

Ans. C

Explanation:

Ans. is ‘c’ i.e., m RNA

The m RNA carries genetic information in the form of codons.

  • Codons are a group of three adjacent nucleotides that code for the amino acids of protein.
  • Each mRNA molecule is a transcript of antisense or template strand of a particular gene.
  • Its nucleotide sequence is complementary to that of antisense or template strand of the gene, i.e. adenine for thyamine, guanine for cytosine, uracil for adenine (as RNA does not contain thymine) and cytosine for guanine.
  • For example, if antisense strand of DNA has a gene with sequence 5′-TTACGTAC-3′, its complementary RNA transcript will be 5 ‘-GUACGUAA-3’.

Q. 17

Total mubers of codons are ‑

 A

60

 B

61

 C

62

 D

64

Q. 17

Total mubers of codons are ‑

 A

60

 B

61

 C

62

 D

64

Ans. D

Explanation:

Ans. is ‘d’ i.e., 64 

  • The information needed to direct the synthesis of protein is contained in the mRNA in the form of a genetic code, which inturn is transcribed from template strand of DNA and is therefore complementary to it.
  • The genetic code is the system of nucleotide sequences of mRNA that determines the sequence of amino acids in protein.
  • Codon is a sequence of three adjacent bases that corresponds to one amino acid.
  • There are 64 possible codom sequences.
  • Because four nucleotide bases A,G, C and U are used to produce the three base codons, there are therefore 64(43) possible codon sequences.

Q. 18

Which is non-sense codon –

 A

UGG

 B

AUG

 C

UGA

 D

CCA

Q. 18

Which is non-sense codon –

 A

UGG

 B

AUG

 C

UGA

 D

CCA

Ans. C

Explanation:

Ans. is ‘c’ i.e., UGA 

Stop codons or nonsense codons or termination codons

  • Three of the 64 possible nucleotide triplets UAA (amber), UAG (Ochre) and UGA (opal) do not code for any amino acid.
  • They are called nonsense codons that normally signal termination of polypeptide chains.
  • Thus, though there are 64 possible triplet codons, only 61 codes for 20 amino acids (as remaining three are non­sense codons).

Quiz In Between



Codons & Genetic code

Codons & Genetic code


CODON &GENETIC CODE

  • Codon- is a sequence of three adjacent bases that corresponds to one of the amino acid.
  • There are 64 possible codon of sequence.
  • Four nucleotide bases A, G, C and U.
  • If 4 bases 44 = 256 amino acids.
  • Methionine has only 1 codon.
  • Genetic code is the system of nucleotide sequences of mRNA that determines the sequence of amino acids in protein.
  • Characteristics of genetic codes-

1.  Triplet codon– each amino acid has triplet sequence.

2. Degenerate (Redundant)

  • A given amino acid may have more than one codon.
  • Degeneracy of the codon lies in the 3rd base.

3. Universal– a specific codon represent a specific amino acid in all the  species.

  • Genetic coder are found in human mitochondria, code is-
  1. AUA codes for methionine instead of isoleucine.
  2. AGA and AGG serve as as stop codon.
  3. UGA also codes for Selenocysteine, a mechanism called translational recording.

4.Unambiguous/ Specific– a particular codon always codes for the same amino acid

5. Non overlapping and nonpuntate (comma less)– reading of genetic code does not involve overlapping sequence.

  • E.g.- AUGCUA GACUUU reads as AUG/CUA/GAC/UUU without punctuation (comma) between codons.

6. Stop or termination or nonsense codons

  • The three nucleotide triplets do not code for any amino acid are- UAA (amber), UAG (ochre), UGA (opal) called as nonsense codons that normally signal termination of polypeptide chains.
  • Wobble Hypothesis- states that a single tRNA can recognise more than one codon.
  • Base pairing of 3rd base of codon (at 31 end) often fails to recognize the specific complementary base codon (at 51 end at tRNA)
  • Wobble explains the degeneracy of genetic code.
  • A minimum of 31 tRNAs are required to translate all 61 different codons for the amino acids.
  • Gene- is the smallest functional unit of genome. 2 types
  1. Inducible gene
  2. Constitutive gene (housekeeping genes)- genes whose expression is not regulated
  • Cistron- is the smallest unit of genetic expression.
  • The codons that designate the same amino acid are called synonyms.

 Exam Important

  • Information for synthesis of protein is contained in the mRNA.
  • Thymine is not involved in codons.
  • 64 (43) possible codon sequences.
  • tRNA acts as the adapter molecule between the codon and specific amino acid.
  • UUU is the codon for phenylalanine.
  • Degeneracy of the codon lies in the 3rd base.
  • Amino acid with maximum number codons are Serine, Arginine, Leucine.
  • Monocistronic- e.g. eukaryotic mRNA
  • Polycistronic- e.g. Prokaryotic mRNA
Don’t Forget to Solve all the previous Year Question asked on Codons & Genetic code

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Severe Combined Immunodeficiency (Scid)

Severe combined immunodeficiency

Q. 1

SCID which is true –

 A

Adenosine deaminase deficiency

 B

Decreased circulating lymphocytes

 C

NADPH oxidase deficiency

 D

CI esterase dificiency

Q. 1

SCID which is true –

 A

Adenosine deaminase deficiency

 B

Decreased circulating lymphocytes

 C

NADPH oxidase deficiency

 D

CI esterase dificiency

Ans. A

Explanation:

Ans. is ‘a’ i.e., Adenosine deaminase deficiency


Q. 2

Which of the following about SCID is false ‑

 A

Failure of descent of thymus

 B

Peyer’s patches are present and normal

 C

X-linked type is the most common

 D

Gene therapy can be used

Q. 2

Which of the following about SCID is false ‑

 A

Failure of descent of thymus

 B

Peyer’s patches are present and normal

 C

X-linked type is the most common

 D

Gene therapy can be used

Ans. B

Explanation:

Ans. is ‘b’ i.e., Peyer’s patches are present and normal

Quiz In Between



Severe Combined Immunodeficiency (Scid)

SEVERE COMBINED IMMUNODEFICIENCY (SCID)


SEVERE COMBINED IMMUNODEFICIENCY (SCID)

It is caused due to –

  • Deficiency of Adenosine Deaminase (ADA)
  • Adenosine accumulates and converted to ribonucleotides and deoxyribonucleotides (dATP).
  • dATP inhibits ribonucleotidereductase which decreases production of deoxyribose nucleotides.
  • There is decrease in T and B cells leading to immunodeficiency.
  • X Linked Type is the Most Common Pattern of Inheritance

Clinical features-

  •  Chronic diarrhea
  •   failure to thrive.

Treatment-

  • Gene therapy is the first order to be treated.
  • Enzyme Replacement Therapy with Polyethyleneglycol modified bovine adenosine deaminase (PEGADA).

Exam Important

  • There is a decrease in T and B cells.
  • Adenosine accumulation is seen in SCID.
  • DNA synthesis decreases.
  • X Linked Pattren of Inheritance is most common
Don’t Forget to Solve all the previous Year Question asked on SEVERE COMBINED IMMUNODEFICIENCY (SCID)

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Lesch- Nyhan Syndrome

LESCH-NYHAN SYNDROME

Q. 1

Lesch Nyhan syndrome is associated with deficiency of?

 A

HPRT(partial)

 B

HPRT(total)

 C

PRPP(partial)

 D

PRPP(total)

Q. 1

Lesch Nyhan syndrome is associated with deficiency of?

 A

HPRT(partial)

 B

HPRT(total)

 C

PRPP(partial)

 D

PRPP(total)

Ans. B

Explanation:

A complete deficiency of HPRT, the Lesch-Nyhan syndrome, is characterized by hyperuricemia, self-mutilative behavior, choreoathetosis, spasticity, and mental retardation. A partial deficiency of HPRT, the Kelley-Seegmiller syndrome, is associated with hyperuricemia but no central nervous system manifestations. In both disorders, the hyperuricemia results from urate overproduction and can cause uric acid crystalluria, nephrolithiasis, obstructive uropathy, and gouty arthritis. Early diagnosis and appropriate therapy with allopurinol can prevent or eliminate all the problems attributable to hyperuricemia but have no effect on the behavioral or neurologic abnormalities.

Ref: Burns C.M., Wortmann R.L. (2012). Chapter 359. Disorders of Purine and Pyrimidine Metabolism. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison’s Principles of Internal Medicine, 18e.

 


Q. 2

Lesch Nyhan syndrome is due to deficiency of:

 A

Hypoxanthine phosphoribosyl transferase

 B

Xanthine oxidase

 C

Purine phosphorylase

 D

Adenosine deaminase

Q. 2

Lesch Nyhan syndrome is due to deficiency of:

 A

Hypoxanthine phosphoribosyl transferase

 B

Xanthine oxidase

 C

Purine phosphorylase

 D

Adenosine deaminase

Ans. A

Explanation:

A i.e. Hypoxanthine phosphoribosyl transferase

Quiz In Between



Lesch- Nyhan Syndrome

LESCH- NYHAN SYNDROME


LESCH- NYHAN SYNDROME

Main Features

  • It is X-linked Recessive disorder.
  • It is caused due to complete deficiency of Hypoxanthine guanine phosphoribosyl transferase (HGPRT deficiency).
  • It affects only males.
  • Increased production of purine nucleotide from PRPP via De Novo pathway.
  • Purine degraded into uric acid and its level increases.

Clinical features

  • Hyperuricemia
  • Gouty arithritis
  • Urinary stones
  • Intellectual disability
  • Dystonic movement
  • Dysarthric speech
  • Self mutilation (irresistible urge to bite the fingers and lips)
  • Megaloblastic anaemia

Diagnosis

  • Hyperuricemia
  • HGPRTase enzyme acitivity in RBCs is deficient

Treatment

  • Allopurinol
  • Alkalanization of urine
  • High fluid intake

Exam Important

  • It is a sex linked disorder. (X Linked Recessive Disorder)
  • The structural gene of HGPRT is located on X-chromosome.
  • There is a complete deficiancy of HGPRT 
  • Self mutilation is one of the characteristic feature of the syndrome.
  • Allopurinol is used in the treatment.
Don’t Forget to Solve all the previous Year Question asked on LESCH- NYHAN SYNDROME

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Rapoport- Leubering Cycle

Rapoport Leubering cycle

Q. 1

The phenomenon of cancer cells switching to glycolysis even in the presence of adequate oxygen for oxidative phosphorylation is known as:

 A

Tyndall effect

 B

Warburg effect

 C

Hawthorne effect

 D

None of the above

Q. 1

The phenomenon of cancer cells switching to glycolysis even in the presence of adequate oxygen for oxidative phosphorylation is known as:

 A

Tyndall effect

 B

Warburg effect

 C

Hawthorne effect

 D

None of the above

Ans. B

Explanation:

Even in the presence of ample oxygen, cancer cells shift their glucose metabolism away from the oxygen hungry, but efficient, mitochondria to glycolysis.
This phenomenon, called the Warburg effect and also known as aerobic glycolysis, has been recognized for many years (indeed, Otto Warburg received the Nobel Prize for discovery of the effect that bears his name in 1931), but was largely neglected until recently.

This metabolic alteration is so common to tumors that some would call it the eighth hallmark of cancer.
             
Ref:
Robbins 8th edition Chapter 2.

Q. 2

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all glycolytic enzymes from band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Q. 2

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all glycolytic enzymes from band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Ans. C

Explanation:

During Hypoxia, the glycolytic enzymes that bind in the same region of band 3 of Hb are released from the membrane resulting in an increased rate of glycolysis. Increased glycolysis increases ATP production and the hypoxic release of ATP.
 
Ref: Oxygen Transport to Tissue, Xxxiii, edited by Martin Wolf, David K Harrison, 2012, Page 188.

Q. 3

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia Stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all Glycolytic enzymes from Band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Q. 3

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia Stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all Glycolytic enzymes from Band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Ans. C

Explanation:

C i.e. Hypoxia stimulates release of all glycolytic enzymes from Band 3 on RBC membrane

RBC membrane cytoskeletal protein spectrin is anchored to transmembrane anion exchanger protein Band 3 by protein ankyrin & protein 4.2. Another cytoskeletal protein actin is attached to transmembrane glycophorin C by protein 4.1. Tropomyosin, tropomodulin, adducin and 4.9 are other proteins.

  • Band 3, is a multifunction RBC transmembrane protein, which is important for its cytoskeletal structure, cell shape, anion exchange activity and glycolysisQ. Band 3 is responsible for chloride shift in RBCQ. Hypoxic deoxygenation of hemoglobin causes Band 3 tyrosine phosphorylation and thereby stimulates glycolysis by releasing glycolytic enzymes from band 3 on RBC membraneQ.
  • In kidney, I cells contain Band 3, an anion exchange protein in their basolateral cell membrane, which may function as a

Cl- – HCO3 exchanger for the transport of HCO3 to interstitial fluid.

  • In animal cells, principal regulators of intracellular pH are HCO3 transporters such as Band 3 CI – Hog; exchanger, 3Na+ – Hcq cotransporters and a le – HCO3 cotransporter.

Q. 4

Number of ATP produced by RBC when Glycolysis occurs through Rapoport Leubering pathway

 A

1

 B

2

 C

3

 D

4

Q. 4

Number of ATP produced by RBC when Glycolysis occurs through Rapoport Leubering pathway

 A

1

 B

2

 C

3

 D

4

Ans. A

Explanation:

 

Usually 2 ATP molecules are formed in glycolysis by substrate level phosphorylation.

Quiz In Between



Rapoport- Leubering Cycle

Rapoport- Leubering Cycle


  • Rapoport- Leubering Cycle occurs in RBCs (erythrocytes).

  • In this cycle, 1,3 – BPG is converted into 2, 3 –BPG by an enzyme biphosphoglycerate  mutase.
  • 2,3- BPG is then converted into 3- phosphoglycerate by enzyme 2,3- biphosphoglycerate phosphatase. 

Significance of Rapaport- Leubering Cycle-

  • The 2, 3 – BPG combines with haemoglobin and reduces the affinity towards oxygen. So, its presence has oxyhemoglobin unloads more oxygen to the tissues.
  • 2,3BPG shifts the oxygen Dissociation curve to right.
  • If the glycolysis of RBCs is impaired there will be impaired synthesis of 2, 3 – BPG  which causes left shift of O2  dissociation curve and increase oxygen affinity of haemoglobin.
  • Under hypoxic, high altitude, fetal tissues, anaemic condition the 2, 3- BPG concentration in the RBC increases.

Exam Important

  • Rapoport Leubering cycle occurs in erythrocytes
  • 2, 3 –bisphosphoglycerate combines with hemoglobin & reduces affinity towards oxygen.
  • 2,3 BPG shifts the oxygen Dissociation curve to right due to reduced affinity towards oxygen
  • No ATP is generated (only one molecule generated through glycolysis in RBC utilized)
  • Under hypoxic conditions, 2, 3- BPG increases in RBCs
  • Cancer cells switching to glycolysis even in the presence of adequate O2 for oxidative phosphorylation c/d Warburg effect
Don’t Forget to Solve all the previous Year Question asked on Rapoport- Leubering Cycle

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