Author: Rajesh Kumar

Image Based Question – 74212

Question

The given image is the pictorial representation of spaces of neck enclosed by cervical fascia. The spaces are labeled as A, B, C and D. Which of these is the danger space of the neck?

A. A

B. B

C. C

D. D

Show Answer

Tumor Protein 53

TUMOR PROTEIN 53 (TP53)

Q. 1

About p53 all are true except 

 A

Encodes 53k Da protein

 B

Located on Chr. 17

 C

Arrests cell cycle at GI phase

 D

Wild type p53 is associated with childhood tumors.

Q. 1

About p53 all are true except 

 A

Encodes 53k Da protein

 B

Located on Chr. 17

 C

Arrests cell cycle at GI phase

 D

Wild type p53 is associated with childhood tumors.

Ans. D

Explanation:

Wild type p53 is associated with childhood tumours [Ref: Bobbin’s 8th/e p. 290, 291, 292]

Wild type 53 is the normal (non mutated form of p53).

  • The normal p53 gene is a tumour suppressor gene that prevents the development of tumours.
  • When wild/normal p53 gene undergoes some mutation, it is called the mutant p53 gene.
  • Mutant p53 gene is associated with various human cancers.

– A little over 50% human tumours contain mutation in this gene.

– Homozygous loss of p53 occurs in virtually every type of cancer including carcinomas of the lung, colon and breast.

p53 Guardian of genome

  • p53 gene is located on chromosome 17Q.
  • It is a tumour suppressor gene.
  • “p53 acts as a molecular policemean that prevents the propagation of genetically damaged cell”.

p53 gene product i.e., p53 protein is a DNA binding protein in the nucleus, when called into action, it controls the transcription of several other genes.

  • The major functional activities of the p53 protein are: ?

Activation of temporary cell cycle arrest (quiescence)

p53 induces transcription of p21°, a CDK inhibitor.

– p21 inhibit cyclin D-CDK-4 e complex leading to arrest of cell cycle late in G1 phase. – This allows time for DNA repair (1.

DNA repair

p53 helps in DNA repair not only by allowing time for DNA repair but also by directly inducing the transcription of GADD 45Q (growth arrest and DNA damage).

GADD 45 encodes a protein that is involved in DNA repair.

– If DNA damage is repaired successfully, p53 activates MDM 2 which in turn causes degradation of p53. This MDM-2 induced degradation of p53 causes relieve in cell cycle block.

Triggering of programmed cell death

p53 directs the transcription of several pro-apoptotic genes such as BAX and PUMA (approved name BBC3) and induces apoptosis.

Induction of pennanent cell cycle arrest (quiescent)

p53 can also cause permanent cell cycle arrest.

It is characterized by specific changes in morphology and the exact mechanism is not known.


Q. 2

In a Teritary level Lab it is observed that chronic, increased exposure to ionizing radiation results in damage to cellular DNA. As a consequence, a protein is now absent that would arrest the cell in the G1 phase of the cell cycle. Subsequent to this, the cell is transformed to acquire the property of unregulated growth. The absent protein is most likely the product of which of the following genes?

 A RAS
 B VHL
 C p53
 D MYC
Q. 2

In a Teritary level Lab it is observed that chronic, increased exposure to ionizing radiation results in damage to cellular DNA. As a consequence, a protein is now absent that would arrest the cell in the G1 phase of the cell cycle. Subsequent to this, the cell is transformed to acquire the property of unregulated growth. The absent protein is most likely the product of which of the following genes?

 A RAS
 B VHL
 C p53
 D MYC
Ans. C

Explanation:

p53


Q. 3 False about p53 is:
 A It is present on chromosomes 17
 B It causes cell cycle arrest in G 1
 C 53 KDa
 D Non mutated wild p53 is asssociated with neoplasm in childhood
Q. 3 False about p53 is:
 A It is present on chromosomes 17
 B It causes cell cycle arrest in G 1
 C 53 KDa
 D Non mutated wild p53 is asssociated with neoplasm in childhood
Ans. D

Explanation:

Non mutated wild p53 is asssociated with neoplasm in childhood

Quiz In Between


Q. 4

What is the half-life of p53 protein in normal cells?

 A

20 minutes

 B

60 minutes

 C

12 hours

 D

1 day

Q. 4

What is the half-life of p53 protein in normal cells?

 A

20 minutes

 B

60 minutes

 C

12 hours

 D

1 day

Ans. A

Explanation:

In non stressed, healthy cells, p53 has a short half-life (20 minutes), because of its association with MDM2, a protein that targets it for destruction.
When the cell is stressed, for example by an assault on its DNA, p53 undergoes post-transcriptional modifications that release it from MDM2 and increase its half-life. Unshackled from MDM2, p53 also becomes activated as a transcription factor.
Ref: Robbins 8th edition Chapter 7.

 


Q. 5

Which of the following statements is not correct regarding p53 gene?

 A

Located on chromosome 17

 B

Arrests cell cycle at Gl phase

 C

Is a 53 kDa protein

 D

Wild type is associated with tumors

Q. 5

Which of the following statements is not correct regarding p53 gene?

 A

Located on chromosome 17

 B

Arrests cell cycle at Gl phase

 C

Is a 53 kDa protein

 D

Wild type is associated with tumors

Ans. D

Explanation:

Wild type of p53 gene refers to the Normal (Non-mutated) form of p53 gene.
The wild type of p53 gene (Normal/Non-mutated) is a tumor suppressor gene that maintains the genetic integrity of cells and prevents the development of tumors.
It is the mutated form of p53 gene (and not the wild type) that is associated with tumors.
 
Ref: Harrison’s Principles of Internal Medicine, 17th Edition, Pages 499, 500; Cancer: Principles and Practice of Oncology By De vita, 6th Edition, Page 19; Robbin’s Illustrated Pathology, 7th Edition, Page 302; Textbook of Pathology By Harsh Mohan, 5th Edition, Pages 2216-17

Q. 6

‘Policemen gene’ or ‘Guardian gene’ is the name given to?

 A

Myc

 B

Meu

 C

P53

 D

Abl

Q. 6

‘Policemen gene’ or ‘Guardian gene’ is the name given to?

 A

Myc

 B

Meu

 C

P53

 D

Abl

Ans. C

Explanation:

p53 acts as a ‘molecular policemen’ that prevents the propagation of genetically damaged cells. p53 is crucial in multicellular organisms, where it regulates the cell cycle and, thus, functions as a tumor suppressor that is involved in preventing cancer.

As such, p53 has been described as “the guardian of the genome” because of its role in conserving stability by preventing genome mutation.

Ref: Robbins Pathology, 7th Ed, page 302

Quiz In Between


Q. 7

Which of the following statement is NOT true about p53 protein?

 A

It is present on chromosomes 17

 B

It causes cell cycle arrest in G1

 C

53 KDa

 D

Non mutated wild p53 is associated with neoplasm in childhood

Q. 7

Which of the following statement is NOT true about p53 protein?

 A

It is present on chromosomes 17

 B

It causes cell cycle arrest in G1

 C

53 KDa

 D

Non mutated wild p53 is associated with neoplasm in childhood

Ans. D

Explanation:

The tumor suppressor p53, a protein of apparent MW 53 kDa.

The gene for human p53 cellular tumor antigen is located on chromosome 17 short arm (17p13).

When DNA Is damaged, the p53 protein accumulates in cells.

It first arrests the cell cycle (at the G1 phase) to allow the DNA to be repaired before it is replicated.

A cell with damaged DNA that cannot be repaired is directed by p53 to either enter senescence or undergo apoptosis.

In view of these activities, p53 has been called the ‘guardian of the genome’. 

With homozygous loss of the TP53 gene, DNA damage goes unrepaired, mutations become fixed in dividing cells, and the cell turns to malignant transformation.
 
Ref: Robbins Basic Pathology By Vinay Kumar, Abul K. Abbas, Nelson Fausto, Richard Mitchell, 2012, Page 20, 185-187

Q. 8

Which of the following is known as the guardian of the genome?

 A

VEGFR-2

 B

p53

 C

Mdm2

 D

4ATM

Q. 8

Which of the following is known as the guardian of the genome?

 A

VEGFR-2

 B

p53

 C

Mdm2

 D

4ATM

Ans. B

Explanation:

Due to its critical importance in maintaining genetic stability p53 is called the “gatekeeper” or “guardian” of the genome.
 
The tumor suppressor protein p53 is a key regulator, of the cellular response to geno-toxic damage, and thus plays a pivotal role in preventing cancer formation. Once DNA damage has been incurred, p53 can elicit several different responses to either correct the errors or destroy the damaged cell. 
 
3 Important actions: 
 
1. p53 can induce G1 cell cycle arrest, which stops the cell from dividing and allows time to repair the damage before the DNA is replicated. 
 
2. p53 can activate DNA repair proteins to drive the repair of damaged DNA. 
 
3. As a last resort, p53 can induce damaged cells to undergo programmed cell death (apoptosis), thereby eliminating damaged and potentially dangerous cells at risk for neoplastic transformation. 
 
Ref: Cancer Genome and Tumor Microenvironment, By Andrei Thomas-Tikhonenko, 2010, Page, 190

Q. 9

Regarding oncogenesis –

 A

Topoisomerase causes breaks in strands

 B

P53 is the most common oncogene mutation causing malignancy in humans

 C

At G2-M-phase there is loss of inhibitors controlling cell cycle

 D

All options are correct

Q. 9

Regarding oncogenesis –

 A

Topoisomerase causes breaks in strands

 B

P53 is the most common oncogene mutation causing malignancy in humans

 C

At G2-M-phase there is loss of inhibitors controlling cell cycle

 D

All options are correct

Ans. D

Explanation:

 

o p53 gene is located on chromosome 17p13 and it is the most common target for genetic alteration in human tumors. A little over 50% human tumors contain mutation in this gene.

o DNA topoisomerase bind tightly to DNA double helix and make transient breaks in both strands.

o Telomerase activity and maintenance of Telomer length are essential for maintenance of relicative potential in tumor cells —> Decrease of telomerase activity cause antitumor effects

o GIS and G2M are cell cycle check point and defect in cell cycle check point component is a major cause of genetic instability in cancer cells.

Quiz In Between


Q. 10

Increased susceptibility to breast cancer is likely to be associated with a mutation in the following gene-      

 A

p53

 B

BRCA-1

 C

Retinoblastoma

 D

a and b

Q. 10

Increased susceptibility to breast cancer is likely to be associated with a mutation in the following gene-      

 A

p53

 B

BRCA-1

 C

Retinoblastoma

 D

a and b

Ans. D

Explanation:

 

o Genetic mutations associated with breast cancer are of two types‑

(i)      Germline mutations (inherited mutations)

o Involved in familial cases of breast cancer

(ii)    Somatic mutations (acquired mutation)

o Involved in sporadic cases of breast cancer

o Tumour suppressor genes involved in Breast cancer

(i) Genes involved in germline mutations (cause familial Breast Ca)

(a)  BRCA-1 and BRCA-2 –> Causes familial breast and ovary Ca

(b)  p53 —> (Li Fraumeni syndrome) — There is increased susceptibility to Ca breast, colon, leukemia, Sarcomas, brain tumours.

(ii) Genes involved in Somatic mutation (cause spordic breast cancer or primary breast cancer) —-> p53

o So p53 gene is involved in both germline mutation and somatic mutation causing breast cancer. Where as BRCA-1 is involved only in germline mutation


Q. 11

Which of the following mutations in a tumour suppressor agent causes breast carcinoma?

 A

p43

 B

p53

 C

p73

 D

p83

Q. 11

Which of the following mutations in a tumour suppressor agent causes breast carcinoma?

 A

p43

 B

p53

 C

p73

 D

p83

Ans. B

Explanation:

Q. 12

Which of the following is known as the “guardian of the genome”?

 A

p53

 B

Mdm2

 C

p14

 D

ATM

Q. 12

Which of the following is known as the “guardian of the genome”?

 A

p53

 B

Mdm2

 C

p14

 D

ATM

Ans. A

Explanation:

 

p53; Guardian of genome

o p53 is a tumor suppressor gene.

o p53 gene is located on chromosome 17.

o p53 acts as molecular policeman that prevents the propagation of genetically damage cell.

o p53 gene product, i.e. p53 protein is a DNA binding protein in the nucleus, when called into action, it controls the transcription of several other genes.

o The major functional activities of the p53 protein are cell cycle arrest and initiation of apoptosis in response to DNA damage.

o When there is DNA damage due to irradiation, UV light or mutagenic chemicals, there is rapid increase in p53

levels.

Quiz In Between


Q. 13

The following statements are true about Tumour Suppressor Gene p53 except –

 A

It regulates cetain genes involved in cell cycle regulation

 B

Its increased levels can induce apoptosis

 C

Its activity in the cells decreases following UV irradiation and stimulates cell cycle

 D

Mutations of the p53 gene are the most common genetic alteration seen in human cancer

Q. 13

The following statements are true about Tumour Suppressor Gene p53 except –

 A

It regulates cetain genes involved in cell cycle regulation

 B

Its increased levels can induce apoptosis

 C

Its activity in the cells decreases following UV irradiation and stimulates cell cycle

 D

Mutations of the p53 gene are the most common genetic alteration seen in human cancer

Ans. C

Explanation:

Q. 14

True statements about P53 gene are all except

 A

Arrest cell cycle at GI Phase

 B

Product is 53 KD protein

 C

Located on chromose 17

 D

Wild/non-mutated form is associated with in­creased risk of childhood tumors.

Q. 14

True statements about P53 gene are all except

 A

Arrest cell cycle at GI Phase

 B

Product is 53 KD protein

 C

Located on chromose 17

 D

Wild/non-mutated form is associated with in­creased risk of childhood tumors.

Ans. D

Explanation:

 

It is mutated form (not non mutated form) of p53 which is associated with increased risk of tumors.

o p53 gene is a tumor suppressor gene and non-mutated form of this gene prevent development of malignancy by :

(i)   Causing cell cycle arrest in late GI phase

(ii)   Inducing apoptosis

(iii)  Helping in DNA repair

o Mutation in p53 gene causes inactivation of p53 gene and abolishen of above function that results in uncontrolled proliferation of cells and malignant transformation.

o Mutation in p53 gene is the most common genetic alteration found in human Cancer.

o The name p53 is in reference to its apparent molecular mass; it runs as a 53 kilodalton (Kda) protein on SDS-page. But based on calculations from its amino acid residues, p53 ‘s mass is actually only 43.7 K Da.

 

o p53 prevents neoplastic transformation by three interlocking mechanisms :

1.  Activation of temporary cell cycle arrest (quiescence)

o It is considered as the primordial response to DNA damage.

o p53 causes arrest in late GI through p2 I .

o This is temporary arrest that gives the cell “breathing time” to repair DNA damage.

o After DNA repair, cell cycle block is relieved by MDM-3 which degrades p53.

2.  Induction of permanent cell cycle arrest (senescence)

o p53 induced sencence is a permanent cell cycle arrest characterized by specific changes in morphology and gene expression that differentiate it from quiescence (temporary or reversible cycle arrest).

o The mechanisms of senscence is unknown, but involve epigenetic changes that result in the formation of heterochromatin at different loci throughout the genome.

3.  Triggering of programmed cell death

o p53 directs the transcription of several pro-apoptotic genes such as BAX and PUMA (approved name BBC3) and induces apoptosis.

o It has been shown that p53 activates transcription of the mir 34 family of micro RNAs (miRNAs),mir 34a.

o mir34 inhibits translation of anti-apoptotic genes such as BCL2 (there by induce apoptosis) and pro-proliferative genes such as cyclins (there by prevent proliferation) p53 induce apoptosis and prevent proliferation through mir34.


Q. 15

True about p53 –

 A

Tumor suppressor gene

 B

Protooncogene

 C

Proapoptotic

 D

a and c

Q. 15

True about p53 –

 A

Tumor suppressor gene

 B

Protooncogene

 C

Proapoptotic

 D

a and c

Ans. D

Explanation:

 

o p 53 is a tumor suppressor gene and it is a proapoptotic factor, i.e. it promotes apoptosis if repair of DNA damage is unsuccessful at G1 arrest.

o The name p53 is in reference to its apparent molecular mass; it runs as a 53 kilodalton (Kda) protein on SDS-page. But based on calculations from its amino acid residues, p53 ‘s mass is actually only 43.7 K Da.

Quiz In Between


Q. 16

False about p53 is –

 A

It is present on chromosomes 17

 B

It cvauses cell cylce arrest in G1

 C

53 KDa

 D

Non mutated wild p53 is associated with neoplasm in childhood

Q. 16

False about p53 is –

 A

It is present on chromosomes 17

 B

It cvauses cell cylce arrest in G1

 C

53 KDa

 D

Non mutated wild p53 is associated with neoplasm in childhood

Ans. D

Explanation:

Ans. is ‘d’ i.e., Non mutated wild p53 is associated with neoplasm in childhood

It is mutated form (not non mutated form) of p53 which is associated with increased risk of tumors.

o p53 gene is a tumor suppressor gene and non-mutated form of this gene prevent development of malignancy by :

(i)       Causing cell cycle arrest in late GI phase

(ii)     Inducing apoptosis

(iii)      Helping in DNA repair

o Mutation in p53 gene causes inactivation of p53 gene and abolishen of above function that results in uncontrolled proliferation of cells and malignant transformation.

o Mutation in p53 gene is the most common genetic alteration found in human Cancer.

o The name p53 is in reference to its apparent molecular mass; it runs as a 53 kilodalton (Kda) protein on SDS-page. But based on calculations from its amino acid residues, p53’s mass is actually only 43.7 K Da.


Q. 17

The tumor suppressor gene P53 induces cell arrest at-

 A

M phase

 B

S – G2 phase

 C

G1 – S phase

 D

Go – phase

Q. 17

The tumor suppressor gene P53 induces cell arrest at-

 A

M phase

 B

S – G2 phase

 C

G1 – S phase

 D

Go – phase

Ans. C

Explanation:

Ans. is ‘c’ i.e., G1 – S phase


Q. 18

In Breast cancer following are expressed: 

 A

HER2/neu

 B

P53

 C

B RCA1

 D

All

Q. 18

In Breast cancer following are expressed: 

 A

HER2/neu

 B

P53

 C

B RCA1

 D

All

Ans. D

Explanation:

Ans. is ‘a’, ‘b’ & ‘c’ i.e. HER2/neu, P53 & BRCA1

Quiz In Between



Tumor Protein 53

TUMOR PROTEIN 53 (TP53)


TUMOR PROTEIN 53/TP53

INTRODUCTION:

  • One among “Tumor suppressor gene”.
  • A Phosphoprotein, barely detectable in nucleus of normal cells.
  • Also referred to as “Molecular policeman”/“Guardian angel of genome” 
    • Due to its protective role in cell cycle.
  • Hallmarks of cancer.
  • In non-stressed, healthy cells has short half-life~20 mins
    • Due to its association with MDM2.
    • MDM2 – Negative regulator of p53 tumor suppressor gene.

STRUCTURE:

  • Located on chromosome 17
  • Encodes d on gene TP53 coding 53k Da protein
  • Has seven domains.

FUNCTIONS:

1. Acts as “Tumor suppressor gene”.

  • Anti-cancer effects due to,
    • Enhances DNA repair, thus preventing mutations.
    • Activates quiescence (temporary cell cycle arrest).
    • Induces senescence (permanent cell cycle arrest).
    • Promotes apoptosis of genetically defective cells.

2. Effects of p53 on cell cycle:

  • Arrests cell cycle in G1phase by inhibiting Cyclin-Dependent Kinase (CDK).
    • Damaged DNA repairs during this time.
    • Normally when DNA damage is repaired by GADD45, p53 destructs itself & relieves cell cycle block.
  • If DNA is unrepaired, p53 along with activated BAX & BAK gene induces apoptosis.
    • Also induces senescence through LINC RNA.

3. Effects of p53 on cell repair:

  • On cell stress/injury,

DNA assaulted due to anoxia/inappropriate oncoprotein activity

DNA damage sensed by (ATM & ATR) protein kinases

Kinases phosphorylate p53 & liberate it from MDM2.

p53 accumulates & suppresses neoplastic transformation.

EFFECTS OF p53 MUTATION:

  • No cell cycle arrest.
  • No DNA repair.
  • Limitless replication leads to cancer.
  • Increases susceptibility to cancers 
    • Li-Fraumeni syndrome.
  • HPV encodes protein E6 binding to p53 thus, inhibiting its action.

Exam Important

  • p53 encodes 53k Da protein
  • p53 is located on Chr. 17
  • p53 arrests cell cycle at GI phase
  • Half-life of p53 protein in normal cells is 20 minutes
  • “Policemen gene’ or ‘Guardian gene’ is the name given to P53
  • P53 is the most common oncogene mutation causing malignancy in humans
Don’t Forget to Solve all the previous Year Question asked on TUMOR PROTEIN 53 (TP53)

Module Below Start Quiz

DELIRIANT POISONS: Dhatura,Strychnine

DELIRIANT POISONS: Dhatura,Strychnine

Q. 1

Signs and symptoms usually develop within 15–30 minutes of strychnine ingestion. What is the fatal dose of strychnine?

 A

10-15 mg

 B

20-40 mg

 C

60-100 mg

 D

100-120 mg

Q. 1

Signs and symptoms usually develop within 15–30 minutes of strychnine ingestion. What is the fatal dose of strychnine?

 A

10-15 mg

 B

20-40 mg

 C

60-100 mg

 D

100-120 mg

Ans. C

Explanation:

Strychnine poisoning:

  • It is an alkaloid derived from the seeds of the tree Strychnos nux-vomica.
  • The potentially fatal dose of strychnine is approximately 50–100 mg (1 mg/kg) and fatal period is 1-2 hours.
  • Strychnine competitively antagonizes glycine, an inhibitory neurotransmitter released by postsynaptic inhibitory neurons in the spinal cord.
  • Muscular stiffness and painful cramps precede generalized muscle contractions, extensor muscle spasms, and opisthotonus. 
  • Death usually is caused by respiratory arrest that results from intense contraction of the respiratory muscles.
 
Ref: Nordt S.P. (2012). Chapter 145. Strychnine. In K.R. Olson (Ed), Poisoning & Drug Overdose, 6e.

Q. 2

Which of the following is the site of action of strychnine poison for its toxicity?

 A

Heart

 B

Anterior horn cells

 C

Posterior horn cells

 D

All of the above

Q. 2

Which of the following is the site of action of strychnine poison for its toxicity?

 A

Heart

 B

Anterior horn cells

 C

Posterior horn cells

 D

All of the above

Ans. B

Explanation:

Strychnine competitively blocks ventral horn motor neuron postganglionic receptor sites in the spinal cord and prevents the effects of glycine, an inhibitory neurotransmitter released by postsynaptic inhibitory neurons in the spinal cord.
Strychnine binds to the chloride ion channel, causing increased neuronal excitability and exaggerated reflex arcs.
This results in generalized seizure-like contraction of skeletal muscles.
Simultaneous contraction of opposing flexor and extensor muscles causes severe muscle injury, with rhabdomyolysis, myoglobinuria, and, in some cases, acute renal failure.
 
Ref: Nordt S.P. (2012). Chapter 145. Strychnine. In K.R. Olson (Ed), Poisoning & Drug Overdose, 6e.

Q. 3

True about strychnine poisoning is :

 A

All muscles affected at the same time

 B

Shoulder girdle affected first

 C

Pelvic girdle affected first

 D

None of the above

Q. 3

True about strychnine poisoning is :

 A

All muscles affected at the same time

 B

Shoulder girdle affected first

 C

Pelvic girdle affected first

 D

None of the above

Ans. A

Explanation:

A i.e. All muscles affected at same time

Quiz In Between


Q. 4

Nux vomica seeds contain 2 alkaloids, strychnine and :

 A

Hyoscine

 B

Hyoscyamine

 C

Brucine

 D

Atropine

Q. 4

Nux vomica seeds contain 2 alkaloids, strychnine and :

 A

Hyoscine

 B

Hyoscyamine

 C

Brucine

 D

Atropine

Ans. C

Explanation:

C i.e. Brucine


Q. 5

The active principles of Dhatura are all of the following except :

 A

Pyricatachol

 B

Hyoscyamine

 C

Atropine

 D

Hyoscine

Q. 5

The active principles of Dhatura are all of the following except :

 A

Pyricatachol

 B

Hyoscyamine

 C

Atropine

 D

Hyoscine

Ans. A

Explanation:

A i.e. Pyricatachol


Q. 6

All the following are characteristic of Dhatura poisoning except:

 A

Delirium

 B

Diplopia

 C

Pin-point pupils

 D

Dysphagia

Q. 6

All the following are characteristic of Dhatura poisoning except:

 A

Delirium

 B

Diplopia

 C

Pin-point pupils

 D

Dysphagia

Ans. C

Explanation:

C i.e. Pinpoint pupil

Quiz In Between


Q. 7

Following is not present in dhatura:           

JIPMER 11

 A

Hyoscine

 B

Hyoscyamine

 C

Muscarine

 D

Atropine

Q. 7

Following is not present in dhatura:           

JIPMER 11

 A

Hyoscine

 B

Hyoscyamine

 C

Muscarine

 D

Atropine

Ans. C

Explanation:

Ans. Muscarine


Q. 8

Treatment of dhatura poisoning is done with:

NEET 15

 A

Pilocarpine

 B

Naloxone

 C

Physostigmine

 D

Neostigmine

Q. 8

Treatment of dhatura poisoning is done with:

NEET 15

 A

Pilocarpine

 B

Naloxone

 C

Physostigmine

 D

Neostigmine

Ans. C

Explanation:

Ans. Physostigmine


Q. 9

Strychnine acts by inhibiting:       

COMEDK 15

 A

GABA

 B

Glycine

 C

Acetylcholine

 D

Dopamine

Q. 9

Strychnine acts by inhibiting:       

COMEDK 15

 A

GABA

 B

Glycine

 C

Acetylcholine

 D

Dopamine

Ans. B

Explanation:

Ans. Glycine

Quiz In Between


Q. 10

Antidote for strychnine poisoning is:          

NEET 13

 A

Fomepizole

 B

Physotigmine

 C

Barbiturates

 D

Naloxone

Q. 10

Antidote for strychnine poisoning is:          

NEET 13

 A

Fomepizole

 B

Physotigmine

 C

Barbiturates

 D

Naloxone

Ans. C

Explanation:

Ans. Barbiturates


Q. 11

In dhatura poisoning 9 ‘Ds’ include all except ‑

 A

Diarrhea

 B

Dysphagia

 C

Dilated pupil

 D

Drowsiners

Q. 11

In dhatura poisoning 9 ‘Ds’ include all except ‑

 A

Diarrhea

 B

Dysphagia

 C

Dilated pupil

 D

Drowsiners

Ans. A

Explanation:

Ans. is ‘a’ i.e., Diarrhea

9-D’ manifestations of Dhatura (anticholinergic) poisoning

  1. Dry hot skin i.e. ‘Hot as a hare’.
  2. Dialation of cutaneous blood vessels 1/t facial i.e. ‘Red as a beet’.
  3. Dialation of pupils with loss of accomodation and unresponsiveness to light i.e. ‘Blind as a bat’.
  4. Dryness of mouth and throat i.e. ‘Dry as a bone’.
  5. Difficulty in talking.
  6. Dysphagia (difficulty in swallowing)
  7. Drunken gait
  8. Drowsiness
  9. Delirium i.e. ‘Mad as wet hen’
  • So symptoms are described as ‘Dry as a bone, Red as a beet, Hot as hare, Blind as a bat and Mad as a wet hen’.

Quiz In Between



DELIRIANT POISONS: Dhatura,Strychnine

DELIRIANT POISONS: Dhatura,Strychnine


DELIRIANT  POISONS

Dhatura  {thorn  apple}

  • Dhatura  (thorn  apple)  grows  on  waste  land  all over  india  and  is  of two  types

(i)  Dhatura alba  and  (ii) Dhatura  niger

 All parts  of plant  is  poisonous, especially  seeds and fruits.

Active  principles  of  dhatura:

  1. levohyoscyamine,
  2. Hyoscine (scopolamine) 
  3. Atropine

Clinical features:poisoning is due to Anticholinergic;  These  features  are described  as ‘9D’

  1. Dry  hot skin: Hot  as a hare.
  2. Dilatation  of cutaneous  blood  vessels  causing  facial  Flush; Red as a beet.
  3. Dialtion  of pupil with loss accommodation and unresponsive to light (dilated and fixed Pupil); Blind  as a hat.
  4. Dryness of throat  and mouth: Dry as a bone.
  5. Delirium (muttering  delirium): Mad as a wet hen.
  6. Drowsiness
  7. Drunken  gait
  8. Dysphagia (difficulty  in  swallowings)
  9. Difficulty  in talking.
  • Earliest  symptom is  bitter taste  in the  mouth
  • After delirium  passes  of patient  may  progress  to  stupor  or coma  and rarely  death  may occur  from  respiratory  paralysis.
  • Cornpicker’s pupil :  It  is  unilateral  mydriasis  caused  by pollen.

Treatment:  physostigmine  is  the  drug  of choice.

  • The  seeds of  dhatura closely  resemble  those  of the  capsicum

STRYCHNINE (NUX  VOMICA /  KUCHILA)

  • spinal  poison.
  • powerful  alkaloid  obtained  from  the  seeds  of strychnos nux  vomica.
  • seeds  are poisonous which contain  active principles  strychnine, brucine and loganin.
  • The main poisonous  alkaloid  is  strychnine.
  • Strychine  is  used  as  a respiratory  stimulant, rodenticide, cattle  poison, and  for  killing  stray  dogs.
  • Strychine stimulates  all parts  of CNS  and particularly  the  anterior  horn cells causing  greatly increased  reflex
  • Cerebral  cortex (brain)  and respiratory  center are stimulated.
  • It causes great incresed reflex activity by antagonizing the action of glycine.

Clinical features :

  • Prodromal  symptoms,  e.g.  incresed  activity  of  perception,  rigidity  of muscles and twitching’
  • Convulsions  afiecting  all  muscles at s time,  they  are  initially  clonic  and  eventually  become  tonic.
  • Between  convulsions,  muscles  are completely relaxed
  • Due  to  spasm  of  jaw  and  facial  muscles, corners  of mouth  are  drawn back   → Risus sardonicus.
  •  Hyperextention  of  whole  body  → Opisthotonus.
  • Spasm  of  abdominal  muscles  my  bend  the  body  forward  (emprosthotonus)  or to  the  side (pleurosthotonus)
  • Mind  (consciousness)  remains  clear throughout  till  death
  • Fatal dose  is  one  crushed  seed  ( 50–100 mg (1 mg/kg))  and  fatal  period  is  1-2  hours’
  • Antidote 
  • short acting  barbiturate,  e.g.  phenobarbital.
  • Brain and spinal  cord  should  be  preserved  for  analysis (in addition  to  usual viscera)  in  deaths  from  suspected strychnine  poisoning.
  • Strychnine  resist putrefaction.
  • Rigor mortis  sets in  almost  immediately  and  passes off  early.

Exam Important

Active  principles  of  dhatura:

  1. levohyoscyamine,
  2. Hyoscine (scopolamine) 
  3. Atropine

Clinical features: poisoning is due to Anticholinergic;  These  features  are described  as ‘9D’

  1. Dry  hot skin: Hot  as a hare.
  2. Dilatation  of cutaneous  blood  vessels  causing  facial  Flush; Red as a beet.
  3. Dialtion  of pupil with loss accommodation and unresponsive to light (dilated and fixed Pupil); Blind  as a hat.
  4. Dryness of throat  and mouth: Dry as a bone.
  5. Delirium (muttering  delirium): Mad as a wet hen.
  6. Drowsiness
  7. Drunken  gait
  8. Dysphagia (difficulty  in  swallowings)
  9. Difficulty  in talking.

Treatment:  physostigmine  is  the  drug  of choice.

STRYCHNINE (NUX  VOMICA /  KUCHILA)

  • Fatal dose  is  one  crushed  seed  ( 50–100 mg (1 mg/kg))  and  fatal  period  is  1-2  hours’
  • Antidote
  • short acting  barbiturate,  e.g.  phenobarbital.
Don’t Forget to Solve all the previous Year Question asked on DELIRIANT POISONS: Dhatura,Strychnine

Module Below Start Quiz

CNS DEPRESSANTS: Barbiturate poisoning & Chloral hydrate

CNS DEPRESSANTS: Barbiturate poisoning & Chloral hydrate

Q. 1

Barbiturate ingestion is associated with hypertrophy of which cellular organelle?

 A

Mitochondria

 B

Endoplasmic reticulum

 C

Golgi apparatus

 D

Nucleolus

Q. 1

Barbiturate ingestion is associated with hypertrophy of which cellular organelle?

 A

Mitochondria

 B

Endoplasmic reticulum

 C

Golgi apparatus

 D

Nucleolus

Ans. B

Explanation:

Hypertrophy usually refers to increase in size of cells or tissues, but sometimes a subcellular organelle may undergo selective hypertrophy. Individuals treated with drugs such as barbiturates show hypertrophy of the smooth endoplamic reticulum (ER) in hepatocytes, which is an adaptive response that increases the amount of enzymes (cytochrome P-450 mixed function oxidases) available to detoxify the drugs.

Ref: Robbins, 8th edition, Chapter 1.


Q. 2

The following are true about chloral hydrate except

 A

Peculiar pungent odour

 B

Crystalline

 C

Used as hypnotic

 D

Sweetish taste

Q. 2

The following are true about chloral hydrate except

 A

Peculiar pungent odour

 B

Crystalline

 C

Used as hypnotic

 D

Sweetish taste

Ans. D

Explanation:

D i.e. Sweetish taste

Chloral hydrate (a hypnotic drug) sometimes known as dry wineQ is used in alcohol to produce sleep. Its action is so rapid that it has been given the name “knock out drops”Q. Chloral hydrate rapidly deteriorates after death. Chemical of the viscera should therefore be done as a matter of urgency.


Q. 3

True about severe barbiturate poisoning EXCEPT:

 A

Hypothermia

 B

Hypertension

 C

Coma

 D

Non-reactive pupil

Q. 3

True about severe barbiturate poisoning EXCEPT:

 A

Hypothermia

 B

Hypertension

 C

Coma

 D

Non-reactive pupil

Ans. B

Explanation:

B i.e. Hypertension

Barbiturates cause hypotension not hypertension.Q


Q. 4

Breathing seen in barbiturate poisoning:

CMC (Vellore) 14

 A

Rapid and deep

 B

Slow and shallow

 C

Normal breathing

 D

Rapid and shallow

Q. 4

Breathing seen in barbiturate poisoning:

CMC (Vellore) 14

 A

Rapid and deep

 B

Slow and shallow

 C

Normal breathing

 D

Rapid and shallow

Ans. D

Explanation:

Ans. Rapid and shallow

Quiz In Between



CNS DEPRESSANTS: Barbiturate poisoning & Chloral hydrate

CNS DEPRESSANTS: Barbiturate poisoning & Chloral hydrate


Barbiturate  poisoning

  • It  is  mostly  suicidal, sometimes  accidental.
  • Manifestations  are due  to  excessive  CNS  depression.
  • patient  is  flabby  and  comatose  with shallow  and failing  respiration  cyanosis.
  • fall  in  BP and  cardiovascular  collapse.
  • Renal shut  down,  pulmonary complications,  bullous eruption  (barbiturate  blisters).
  • Hypothermia ,  Finally  there  is  coma.
  • Individuals treated with drugs such as barbiturates show hypertrophy of the smooth endoplamic reticulum (ER) in hepatocytes

Important  specific  features  are

  • constricted  pupil (there  may  be  alternate  constriction and dilatation,  i.e. happus reaction).
  • liquid  gold  urine.

 Treatment  includes  :

  • Gastric  lavage
  • Haemodialsis
  • Supportive  measures (O2, assissed  respiration,  maintenance  of BP).
  • Forced  alkaline  diuresis.

Chloral Hydrate

  • Chloral  hydrate  is  a colourless,  crystalline  substance  having  peculiar  pungent  odor  and pungent bitter test.
  • It  is  a powerful  hypnotic in doses  produces  natural  sleep,  but in  larger  doses  depresses  CNS  and paralyses  vital centers.
  • It  is  given  in  food  or drink  to  make person  helpless,  called  knock out drops.
  • Mickey finn is  a  combination  of alcohol and chloral  hydrate.
  • Chloral  hydrate  is  also  called  dry  wine.

Exam Important

Barbiturate  poisoning:

  • patient  is  flabby  and  comatose  with shallow  and failing  respiration  cyanosis.
  • fall  in  BP and  cardiovascular  collapse
  • Hypothermia ,  Finally  there  is  coma.
  • Individuals treated with drugs such as barbiturates show hypertrophy of the smooth endoplamic reticulum (ER) in hepatocytes.

Chloral Hydrate:

  • crystalline  substance  having  peculiar  pungent  odor  and pungent bitter test.
  • It  is  given  in  food  or drink  to  make person  helpless,  called  knock out drops.
  • Mickey finn is  a  combination  of alcohol and chloral  hydrate.
  • Chloral  hydrate  is  also  called  dry  wine
Don’t Forget to Solve all the previous Year Question asked on CNS DEPRESSANTS: Barbiturate poisoning & Chloral hydrate

Module Below Start Quiz

Phosphorus Poisioning

phosphorous poisoning

Q. 1

CuSO4 was used as an antidote for:

Maharashtra 11

 A

Dhatura poisoning

 B

Cocaine poisoning

 C

Phosphorus poisoning

 D

Opium poisoning

Q. 1

CuSO4 was used as an antidote for:

Maharashtra 11

 A

Dhatura poisoning

 B

Cocaine poisoning

 C

Phosphorus poisoning

 D

Opium poisoning

Ans. C

Explanation:

Ans. Phosphorus poisoning


Q. 2

Yellow/fatty liver is characteristically seen in:

Jharkhand 11

 A

Datura poisoning

 B

Cocaine poisoning

 C

Phosphorus poisoning

 D

Opium poisoning

Q. 2

Yellow/fatty liver is characteristically seen in:

Jharkhand 11

 A

Datura poisoning

 B

Cocaine poisoning

 C

Phosphorus poisoning

 D

Opium poisoning

Ans. C

Explanation:

Ans. Phosphorus poisoning

Quiz In Between



Phosphorus Poisioning

Phosphorus Poisioning


PHOSPHORUS  POISONING:

  • Phosphorus is  a protoplasmic  poison  affecting  cellular  oxidation  and causing  anoxic  necorbiosis,  classically  affecting liver.  
  • It increases  fat  deposition  and  inhibits  glycogen  deposition  in  liver.  It is  used  in  fire  works  (Diwali  poisoning)  and as  rat  poison. Lethal dose  is  60-120  mg.
  • Earliar CuSO4 was used as an antidote for phosphorous poisoning.

Phosphorus  occurs  in  two  forms:

White/yellow phosphorus:

  • It  is  white,  and  becomes  yellow  on  exposure  to  air.  
  • It  is  translucent, luminous and  crystalline cylinders.
  • It has garlic like  odor. It is  insoluble  in  water  and  luminous  in  dark. 
  • Its  fumes  show  phosphorescence.

Red phosphorus:

  • It is  reddish  brown,  inert,  odourless  and  tasteless. 
  • It  is  nontoxic  (thus  poisoning  occurs  only  due to white phosphorus.
  • It is  put  on  the  sides  (striking  surface)  of match box  (along  with  powdered  glass).

Acute  poisoning

First stage: (GI  irritation): There  is  nausea,  vomiting,  diarrhea and  garlic odor.  This stage lasts  for  8 hours to  3 days.

Second Stage (Asymptomatic) : This  stage lasts  for  3 days.

Third  Stage:

  • There is liver  and  kidney  damage due  to  absorbed  phosphorus.
  • Initially  liver  is  enlarged  due  to  acute  fatty infiItration.
  • Later  liver  shrinks  due to  necrosis,  i.e.  Acute yellow atrophy.

Chronic  poisoning

  • Toothache  is  the  first  symptom  which  is  associated  with  loosening  of  teeth,  necrosis  of  gums  and osteomyelitis  of  jaw.
  • Therefore  chronic  phosphorus poisoning  is  also  known  as  Phossy  jaw or  glass  jaw.

Postmortem appearance

  • There is  garlic odor.  viscera  and  stool  glow in  dark  (due  to  luminosity).
  • To preserve  luminosity,  viscera  are  preserved  in  saturated  saline solution  Rectified  spirit  is  not  used  as it  causes loss  of Iuminosity.

Exam Important

  • Acute yellow atrophy.
  • liver  and  kidney  damage
  • Phossy  jaw or  glass  jaw.
  • There is  garlic odor.  viscera  and  stool  glow in  dark  (due  to  luminosity)
Don’t Forget to Solve all the previous Year Question asked on Phosphorus Poisioning

Module Below Start Quiz

Vegetables, Cantharides and Scorpion Poisons

Vegetable And Cantharides Poisons

Q. 1

Sin needle used to kill animals made of :

 A

Dhatura seeds

 B

Rati seeds

 C

Lead peroxide

 D

Arsenic

Q. 1

Sin needle used to kill animals made of :

 A

Dhatura seeds

 B

Rati seeds

 C

Lead peroxide

 D

Arsenic

Ans. B

Explanation:

B i.e. Rati seeds


Q. 2

Vegetable viper snake poison is

 A

Croton

 B

Madar

 C

Abrus

 D

Semicarpus

Q. 2

Vegetable viper snake poison is

 A

Croton

 B

Madar

 C

Abrus

 D

Semicarpus

Ans. C

Explanation:

C i.e. Abrus


Q. 3

One of the following substance produce injuries which stimulate confusion :

 A

Semicarpus anacardium

 B

Ricinus communis

 C

Abrus percatorius

 D

Capsium annum

Q. 3

One of the following substance produce injuries which stimulate confusion :

 A

Semicarpus anacardium

 B

Ricinus communis

 C

Abrus percatorius

 D

Capsium annum

Ans. A

Explanation:

A i.e. Semicarpus anacardium

Quiz In Between


Q. 4

Average fatal dose of croton oil seed is :

 A

500 drops

 B

Hand ful of seeds

 C

About 4 to 5 drops

 D

20 drops

Q. 4

Average fatal dose of croton oil seed is :

 A

500 drops

 B

Hand ful of seeds

 C

About 4 to 5 drops

 D

20 drops

Ans. D

Explanation:

D i.e. 20 drops


Q. 5

Which of the following protein synthesis inhibitor are non‑plant toxin:

 A

Streptomycin

 B

Abrin

 C

Ricin

 D

Emetine

Q. 5

Which of the following protein synthesis inhibitor are non‑plant toxin:

 A

Streptomycin

 B

Abrin

 C

Ricin

 D

Emetine

Ans. A

Explanation:

A i.e. Streptomycin



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