Category: Quiz

Buerger Disease

Buerger Disease

Q. 1

All of the following are the clinical feature of thromboangitis obliterans except :

 A Raynaud’s phenomenon

 B

Claudication of extremeties

 C

Absence of popliteal pulse

 D

Migratory superficial thrombophlabitis

Q. 1

All of the following are the clinical feature of thromboangitis obliterans except :

 A

Raynaud’s phenomenon

 B

Claudication of extremeties

 C

Absence of popliteal pulse

 D

Migratory superficial thrombophlabitis

Ans. C

Explanation:

Ans. is ‘c’ i.e., Absence of popliteal pulse


Q. 2

Commonest site of thromboangitis obliterans is 

 A

Femoral artery

 B

Popiteal artery

 C

iliac artery

 D

None

Q. 2

Commonest site of thromboangitis obliterans is 

 A

Femoral artery

 B

Popiteal artery

 C

iliac artery

 D

None

Ans. D

Explanation:

Ans. is ‘None’ 
Distal circulation is involved in Buerger’s disease, usually distal to popliteal and brachial artery.


Q. 3

Thromboangitis obliterans is associated with

 A

HLA B27

 B

HLA – DR4

 C

HLA – B5

 D

HLA – DR2

Q. 3

Thromboangitis obliterans is associated with

 A

HLA B27

 B

HLA – DR4

 C

HLA – B5

 D

HLA – DR2

Ans. C

Explanation:

Ans. is ‘c’ i.e., HLA – B5 

Thromboangitis obliterans (Berger disease)

  • Thrombangitis obliterans is a distinctive disease that is characterized by segmental, thrombosing acute and chronic inflammation of medium sized and small sized arteries, and sometimes secondarily extending to veins and nerves.
  • Thromboangitis obliterans occurs almost exclusively among heavy-cigarrete-smoking persons.
  • It is more common in men but incidence is increasing in women because of increasing smoking habit in women. o Buerger disease is associated with HLA B-5 and HLA-A9.
  • In thrombongitis obliterans there is acute and chronic segmental inflammation of vessels with accompanied thrombosis in the lumen.
  • Typically, the thrombus contains microabscesses with a central focus of neutrophils surrounded by gran u lomatous inflammation.
  • Later, the inflammatory process extends into contiguous veins and nerves and in time all three structures (arteries, veins and nerves) become encased in fibrous tissue, a characterstic that is very rare with other form of vasculitis.
  • Clinical manifestations
  • Thrombangitis obliterans affects vessels of upper and lower extremities.
  • Symptoms are due to vascular insufficiency, i.e. Ischemia of toes, feet and fingers that can lead to ulcer and frank gangrene.
  • Due to neural involvement, there may be severe pain, even at rest.

Q. 4 True about Buerger disease

 A

Affects larger artery only

 B

Younger males are more commonly affected

 C

Phlebitis migrans is characteristic

 D

Cold intolerance

Q. 4

True about Buerger disease

 A

Affects larger artery only

 B

Younger males are more commonly affected

 C

Phlebitis migrans is characteristic

 D

Cold intolerance

Ans. B:C:E

Explanation:

Answer- B,Younger males are more commonly affected C,Phlebitis migrans is characteristic E,Veins may involved
Also called as Thromboangiitis Obliterans
It is a inflammatory occlusive vascular disorder involving small and medium sized arteries and veins in upper and lower extremities.
It involves tibial and radial arteries and sometimes secondarily extending to veins and nerves of extremities.
The clinical features of thromboangiitis obliterans includes a triad of claudication of the affected extremity, Raynaud’s phenomenon, and migratory superficial vein thrombophlebitis.

Quiz In Between



Ectopic Testis

ECTOPIC TESTIS

Q. 1 Ectopic testis is found in all location except ‑

 A

Lumbar

 B

Perineal

 C

Intra abdominal

 D

Inguinal

Q. 1

Ectopic testis is found in all location except ‑

 A

Lumbar

 B

Perineal

 C

Intra abdominal

 D

Inguinal

Ans. C

Explanation:

Ans. is C

  • Sites of ectopic testis-

a) Superficial inguinal pouch
b) Perineum
c) Root of the penis
d) Femoral triangle (thigh)


Q. 2

Complication of ectopic testis is ‑

 A

Seminoma

 B

Atrophy

 C

Torsion

 D

All

Q. 2

Complication of ectopic testis is ‑

 A

Seminoma

 B

Atrophy

 C

Torsion

 D

All

Ans. C

Explanation:

Ans. is ‘c’ i.e., Torsion 

Quiz In Between



Mucocele Of Gall Bladder

Mucocele of Gall Bladder

Q. 1

The treatment of choice for a mucocele of gall bladder is –

 A Aspiration of mucous

 B

Cholecystectomy

 C

Cholecystostomy

 D

Antibiotics and observation

Q. 1

The treatment of choice for a mucocele of gall bladder is –

 A

Aspiration of mucous

 B

Cholecystectomy

 C

Cholecystostomy

 D

Antibiotics and observation

Ans. B

Explanation:

Ans. is ‘b’ i.e., Cholecystectomy 

  • Mucocele of the Gall bladder ‑

It is one of the complications of Gall stones.

Caused due to obstruction of the stone at the neck of the bladder.

In course of time the bile is absorbed and replaced by the mucus secreted by the Gall bladder epithelium. Due to this the Gall bladder may because distended and palpable.

  • Treatment

The t/t is early cholycystectomy.

–  If early t/t is not done following complications can occur‑

Empyema

Perforation

– Gangrene

Quiz In Between



Hemoglobinopathies

HEMOGLOBINOPATHIES

Q. 1 Sickle cell disease is:
 A Inherited as AR
 B Inherited as AD
 C Inherited as XLR
 D Inherited as XLD
Q. 1 Sickle cell disease is:
 A Inherited as AR
 B Inherited as AD
 C Inherited as XLR
 D Inherited as XLD
Ans. A

Explanation:Inherited as AR


Q. 2

Sickle cell trait patient do not have manifestations as that of Sickle cell disease, because:

 A

50% HbS is required for occurrence of sickling

 B

HbA prevents sickling

 C

50% sickles

 D

HbA prevent polymerization of Hbs

Q. 2

Sickle cell trait patient do not have manifestations as that of Sickle cell disease, because:

 A

50% HbS is required for occurrence of sickling

 B

HbA prevents sickling

 C

50% sickles

 D

HbA prevent polymerization of Hbs

Ans. A

Explanation:

In Sickle cell trait, the patient is heterozygous and only one parent contributes the abnormal S gene.
in each cell of these patients approximately 40% of the hemoglobin is HbS.
The rate of sickling is influenced by the intracellular concentration of hemoglobin S and by the presence of other hemoglobins within the cell. In Sickle cell trait the low level of HbS is insufficient to produce sickling unless there is profound hypoxia.
 
Sickle cell disease is  an autosomal recessive disorder in which an abnormal hemoglobin leads to chronic hemolytic anemia with numerous clinical consequences.
It is caused by a single DNA base change  leading to an amino acid substitution of valine for glutamine in the sixth position on the beta-globin chain.
In Sickle cell disease patients are homozygous and 80% of their hemoglobin is HbS. Hemoglobin S is unstable and polymerizes in the setting of various stressors, including hypoxemia and acidosis, leading to the formation of sickled red blood cells.
 
Ref: Rosen’s Emergency Medicine – Concepts and Clinical Practice  By John Marx page 1597. Core Topics in Paediatric Anaesthesia  edited by Ian James, page 67. Linker C.A., Damon L.E., Damon L.E., Andreadis C. (2013). Chapter 13. Blood Disorders. In M.A. Papadakis, S.J. McPhee, M.W. Rabow, T.G. Berger (Eds), CURRENT Medical Diagnosis & Treatment 2014.

Q. 3

What is the cause of sickling of RBC in sickle cell disease?

 A

Decreased Solubility

 B

Decreased Stability

 C

Altered Function

 D

Altered 02 binding capacity

Q. 3

What is the cause of sickling of RBC in sickle cell disease?

 A

Decreased Solubility

 B

Decreased Stability

 C

Altered Function

 D

Altered 02 binding capacity

Ans. A

Explanation:

In sickle cell disease glutamic acid is replaced by valine.
The charge and location of this substitution cause HbS to be converted from a soluble state into a polymer when it undergoes structural changes that accompany release of oxygen. Hypoxia, acidosis, and hypertonicity facilitate polymer formation.
The polymerization of hemoglobin cause the red cell to transform from a deformable, biconcave disk into a rigid, sickle shaped cell.

Ref: Rudolph’s Fundamentals of Pediatrics By Abraham M. Rudolph, Pages 528-30

Quiz In Between


Q. 4

True about Sickle cell disease are all, Except:

 A

Single nucleotide change results in change of Glutamine to Valine

 B

Deoxygenated Hb 1/t exposure of sticky end d/ t replacement of nonpolar residue by polar residue

 C

HbS confers resistance against malaria in heterozygotes

 D

RFLP results from a single base change

Q. 4

True about Sickle cell disease are all, Except:

 A

Single nucleotide change results in change of Glutamine to Valine

 B

Deoxygenated Hb 1/t exposure of sticky end d/ t replacement of nonpolar residue by polar residue

 C

HbS confers resistance against malaria in heterozygotes

 D

RFLP results from a single base change

Ans. B

Explanation:

B i.e. Deoxygenated Hb Vt exposure of sticky end d/t replacement of nonpolar residue by polar residue


Q. 5

All of the following are true about Sickle cell disease, Except:

 A

Single nucleotide change results in change of Glutamine to Valine

 B

RFLP results from a single base change

 C

‘Sticky patch’ is generated as a result of replacement of a non polar residue with a polar residue

 D

HbS confers resistance against malaria in heterozygotes

Q. 5

All of the following are true about Sickle cell disease, Except:

 A

Single nucleotide change results in change of Glutamine to Valine

 B

RFLP results from a single base change

 C

‘Sticky patch’ is generated as a result of replacement of a non polar residue with a polar residue

 D

HbS confers resistance against malaria in heterozygotes

Ans. C

Explanation:

C i.e. ‘Sticky patch’ is generated as a result of replacement of a non polar residue with a polar residue

In sickle cell anemia- Glutamic acid is replaced by valine at sixth position in /3 – globin chainQ.

Sticky patch is generated as a result of replacement of polar residue (negatively charged glutamate amino acid) with a nonpolar hydrophobic residue (valine)Q. This change makes HbS (sickle cell hemoglobin) less soluble, when deoxygenated and cause sicklingQ.

HbS confers resistance against malaria in heterozygotesQ.


Q. 6

Sickle cell trait patient do not have manifestations as that of Sickle cell disease, because‑

 A

50% HbS is required for occurrence of sickling

 B

HbA prevents sickling

 C

50% sickles

 D

HbA prevents polymerazitation of Hbs

Q. 6

Sickle cell trait patient do not have manifestations as that of Sickle cell disease, because‑

 A

50% HbS is required for occurrence of sickling

 B

HbA prevents sickling

 C

50% sickles

 D

HbA prevents polymerazitation of Hbs

Ans. A

Explanation:

Ans. is ‘a’ i.e., 50% Hbs is required for occurence of sickling

  • Sickle cell disease occurs in following forms

1.  Heterozygous state, i.e., sickle cell trait.
2.  Homozygous state, i.e., sickle cell anemia.

o The most important factor for sickling is the amount of HbS in the cell.

o In sickle cell trait (heterozygous state), only about 40% of the hemoglobin is HbS, this is insufficient to produce sickling manifestations.

o In homozygous state, almost all the hemoglobin in the red cell is HbS, therefore they undergo sickling.

Quiz In Between


Q. 7 In sickle cell disease:     
September 2007

 A

Glutamtic acid, at position No.5 of beta-globin chain of haemoglobin is replaced by valine

 B

Glutamtic acid, at position No.6 of beta-globin chain of haemoglobin is replaced by valine

 C

Valine at position No.6 of beta-globin chain of haemoglobin is replaced by glutamtic acid

 D

Valine at position No.5 of beta-globin chain of haemoglobin is replaced by glutamtic acid

Q. 7

In sickle cell disease:     
September 2007

 A

Glutamtic acid, at position No.5 of beta-globin chain of haemoglobin is replaced by valine

 B

Glutamtic acid, at position No.6 of beta-globin chain of haemoglobin is replaced by valine

 C

Valine at position No.6 of beta-globin chain of haemoglobin is replaced by glutamtic acid

 D

Valine at position No.5 of beta-globin chain of haemoglobin is replaced by glutamtic acid

Ans. B

Explanation:

Ans. B: Glutamtic acid, at position No.6 of beta-globin chain of haemoglobin is replaced by valine

Sickle haemoglobin (HbS) is a structural variant of haemoglobin in which glutamic acid, an amino acid, at position No.6 of beta-globin chain of haemoglobin is replaced by valine.

This happens due to change of a nucleotide, adenine to thymine (GAGgGTG) of codon 6 of beta-globin gene. This substitution of amino acid changes the net charge of haemoglobin, oxygen affinity and three-dimensional structure thus rendering it as unstable haemoglobin.

Sickle haemoglobin gets polymerized at low oxygen tension and deforms the red blood cell from discoid shape to sickle like (crescent) form


Q. 8

Person having heterozygous sickle cell trait is protected from infection of:

 A

P. falciparum

 B

P. vivax

 C

Pneumococcus

 D

Salmonella

Q. 8

Person having heterozygous sickle cell trait is protected from infection of:

 A

P. falciparum

 B

P. vivax

 C

Pneumococcus

 D

Salmonella

Ans. A

Explanation:

Ans. a. P. falciparum

  • Person having heterozygous sickle cell trait is protected from infection of P. falciparum.
  • “People who are heterozygous for the sickle cell trait (HbS) become infected with P. falciparum, but they are less likely to die from infection°. The HbS trait causes the parasites to grow poorly or die because of the low oxygen concentrations°.” – Robbins 8/e p387

Host Resistance to Plasmodium

  • Two general mechanisms of host resistance to Plasmodium:
  • Inherited alterations in red cells make people resistant to Plasmodium°.
  • Repeated or prolonged exposure to Plasmodium species stimulates an immune response that reduces the severity
  • People who are heterozygous for the sickle cell trait (HbS) become infected with P. falciparum, but the yare less likely to die from infection°.
  • The HbS trait causes the parasites to grow poorly or die because of the low oxygen concentrations°.
  • The geographic distribution of the HbS trait is similar to that of P. falciparum°, suggesting evolutionary selection of the HbS trait in people by the parasite
  • HbC, another common hemoglobin mutation, also protects against severe malaria by reducing parasite proliferation°.

Host Resistance to Plasmodium.

  • People can also be resistant to malaria due to the absence of proteins to which the parasites bind°.
  • P. vivax enters red cells by binding to the Duffy blood group antigen°.
  • Many Africans, including most Gambians, are not susceptible to infection by P. vivax because they do not have the Duffy antigen°.
  • Antibodies and T lymphocytes specific for Plasmodium reduce disease manifestations. Cytotoxic lymphocytes may also be important in resistance to P. falciparum

Q. 9 After a point mutation, glutamic acid is replaced by valine, which leads to formation of sickle cell hemoglobin. The mobility of HbS as compared with normal hemoglobin on gel electrophoresis will be:

 A

Decreased

 B

Increased

 C

Dependent on HbS concentration

 D

Unchanged.

Q. 9

After a point mutation, glutamic acid is replaced by valine, which leads to formation of sickle cell hemoglobin. The mobility of HbS as compared with normal hemoglobin on gel electrophoresis will be:

 A

Decreased

 B

Increased

 C

Dependent on HbS concentration

 D

Unchanged.

Ans. A

Explanation:

Ans: A. Decreased
(Ref: Harper 30/e p460, 28/e p49, 357. 3197-398; Lippincott 5/e p|75-177; Lehinger 5/e pl(t8-l69t)
HbS mobility on gel electrophoresis:

  • Decreased mobility – Compared to normal hemoglobin.

Electrophoresis of hemoglobin:

  • Obtained from lysed red blood cells.
  • Used in sickle cell trait & disease diagnosis.

Sequence of Movement: HbA2 < HbC < HhS < HbF < HbA

Quiz In Between



Gene Therapy

GENE THERAPY

Q. 1

Gene therapy is given in ‑

 A

Cystic fibrosis

 B

Thalassemia

 C

Sickle cell anemia

 D Severe combined 
Q. 1

Gene therapy is given in ‑

 A

Cystic fibrosis

 B

Thalassemia

 C

Sickle cell anemia

 D Severe combined 
Ans. D

Explanation:

Severe combined immunodeficiency [Ref KDT 6m/e p. 843, 8441

Gene therapy

  • Gene therapy refers to introduction of functional genetic material usually D.N.A. into target cells to replace or supplement defective genetic material.
  • In contrast to all other therapies or drugs, gene therapy imparts, new functions to a cell.
  • Gene defects result in.fallure to synthesize a functional protein or in the synthesis of a dysfunctional protein.
  • Equipping the cell with a normal copy of the defective gene would overcome the deficieny at the site where it is needed on a long term.

Approaches in gene therapy 😕

  • Gene therapy tries to either modify or transfer the genes.

Gene modification

  • This involves correction of the defective portion of a genomic sequence or removal of the whole defective gene and its replacement by a normal copy.

Gene transfer

  • This involves introduction of genes without removing or altering the existing ones.

Gene transfer is carried out in the following ways?

i)      Injection of naked D.N.A.

ii)     Transfer of generic material using virus as a carrier with D.N.A. incorporated into its genome.

iii)    Transfer of D.N.A. encapsulated within a liposome

Applications of Gene therapy (where genetherapy is being considered) 😕

  • Cystic fibrosis (insertion of CFTR gene into respiratory epithelial cells)
  • Severe combined immunodeficiency disease (introducing genes for adenosine deaminase)
  • Growth hormone deficiency
  • Familial hypercholesterelimia
  • Lysch Nyhan syndrome
  • Parkinsonism
  • Alzhiemer’s disease, Huntington’s chorea. Familial amyotrophic lateral sclerosis, Gaucher’s disease
  • Stroke, head injury, multiple sclerosis
  • Duchenne muscular dystrophy
  • Prevention of restenosis of grafted coronary vessel
  • Anemia
  • Sickle cell anemia
  • Haemophilia
  • HIV infection
  • Cancers

Current status of Gene therapy (www.Fda.gov/Biologic.s bloodvaccines/cellular gene therapy)

  • The food and drug administration has not yet approved any human gene therapy product for sale.

– Current gene therapy is experimental and has not proven very successful in clinical trials.

– Clear cut success in gene therapy has been achieved in Severe combined immunodeficiency (adenosine deaminase deficiency).

– But there were reports that children treated with gene therapy in severe combined immunodeficiency developed leukemia.

– Based on current data, the efficacy of gene transfer, .for severe combined immunodeficiency is convincing there have been no complications in the six children treated on this protocol, but longer term follow up

will be required to determine whether this approach is sufficiency safe to he used in place of pegylated form of the enzyme adenosine deaminase.


Q. 2 Purpose of Gene therapy:

 A

Replacement of abnormal gene by normal gene

 B

Replacement of normal gene by abnormal gene

 C

Knock out of abnormal gene

 D

Introduction of viral gene

Q. 2

Purpose of Gene therapy:

 A

Replacement of abnormal gene by normal gene

 B

Replacement of normal gene by abnormal gene

 C

Knock out of abnormal gene

 D

Introduction of viral gene

Ans. A

Explanation:

A i.e. Replacement of abnormal gene by normal gene.


Q. 3

Gene therapy methods are:

 A

Electroporation

 B

Intranuclear injection

 C

Site directed mutagenesis

 D

All

Q. 3

Gene therapy methods are:

 A

Electroporation

 B

Intranuclear injection

 C

Site directed mutagenesis

 D

All

Ans. D

Explanation:

A i.e. Electroporation, B i.e. Intranuclear infection, C i.e. Site directed mutagenesis


Q. 4

The first gene therapy (somatic enzyme) was successfully done in:

 A

SCID

 B

Phenylketonuria

 C

Thalassemia

 D

Cystic fibrosis

Q. 4

The first gene therapy (somatic enzyme) was successfully done in:

 A

SCID

 B

Phenylketonuria

 C

Thalassemia

 D

Cystic fibrosis

Ans. A

Explanation:

A i.e. SCID

– The goal of gene therapy is replacement of abnormal mutant gene by normal geneQ.

– Technique to transfer genes (foreign material) into cells include – transfection, microinjection, electroporation, site directed recombination, transduction using adenovirus or retrovirus and plastnid liposome complexQ etc.

SCID (Severe combined imuunodeficiency disease) or bubble baby syndrome is the first disease treated successfully by gene therapy.


Q. 5

Which of the following techniques is used in gene therapy-

 A

Electroporation

 B

Electrofocusing

 C

Selectively targeted recombination

 D

a and c

Q. 5

Which of the following techniques is used in gene therapy-

 A

Electroporation

 B

Electrofocusing

 C

Selectively targeted recombination

 D

a and c

Ans. D

Explanation:

Ans. is ‘a’ i.e., Electroporation; ‘c’ i.e., Selectively targeted recombination

Gene therapy

o Gene transfer is a novel area of therapeutics in which the normal gene (DNA sequence) is delivered to target somatic cells.

o Because delivery of naked DNA or RNA to a cell is inefficient process, most gene transfer is carried out using a vector (gene delivary vehile).

Methods of introducing genes into cells for gene therapy

o Intranuclear injection                     o Electropolation                 o Plasmid liposome complexes o Adenovirus

o Transfection                                   o Retroviruses                      o Site directed recombination

Quiz In Between



Venous Ulcers

Venous ulcers

Q. 1 Complications of obesity is/are:

1. Venous ulcer
2. Pulmonary embolism
3. Pickwickian syndrome
4. Hernias
5. Pulmonary hypertension
 A 1,2,3 & 4

 B

2,3,4 & 5

 C

1,2,3 & 5

 D

All are true

Q. 1

Complications of obesity is/are:

1. Venous ulcer
2. Pulmonary embolism
3. Pickwickian syndrome
4. Hernias
5. Pulmonary hypertension
 A 1,2,3 & 4

 B

2,3,4 & 5

 C

1,2,3 & 5

 D

All are true

Ans. D

Explanation:

Clinical presentation of obesity

The morbidly obese patients often presents with chronic weight-related problems such as migraine headaches; back and lower extremity joint pain from degenerative joint disease; venous ulcers; dyspnea on exertion; biliary colic; stress urinary incontinence; dysmenorrhea; infertility; gastroesophageal reflux; and inguinal, umbilical, and incisional hernias.
 
Obesity has a profound effect on overall health and life expectancy. The morbidly obese are predisposed to developing serious weight-related comorbidities, including hypertension, CAD, adult onset DM, sleep apnea and/or obesity hypoventilation syndrome (Pickwickian syndrome), deep venous thrombosis, pulmonary embolism, hypercoagulability, hyperlipidemia, and depression among others.
 
Physiological abnormalities resulting from OSA include hypoxemia, hypercapnia, pulmonary and systemic vasoconstriction, and secondary polycythemia (from recurrent hypoxemia).
These result in an increased risk of ischemic heart disease and cerebrovascular disease.
Right ventricular failure can occur from hypoxic pulmonary vasoconstriction.
 
Obesity is now considered to be the second leading cause of preventable death behind cigarette smoking.
The incidence of comorbidities and mortalities is directly related to the degree of obesity. in a study with 12 year follow up, mortalities rates for those weighing 50% over average weight were doubled. Mortalities and morbidities is largely attributable to the comorbidities of obesity.
 
Ref: Schwartz 9/e, Page 1743.

Q. 2 The following is the commonest site for venous ulcer:
March 2013 (a, e)

 A

Lower third of leg and ankle

 B

Instep of foot

 C

Lower 2/ 3rd of leg

 D

Middle 1/3rd of leg

Q. 2

The following is the commonest site for venous ulcer:
March 2013 (a, e)

 A

Lower third of leg and ankle

 B

Instep of foot

 C

Lower 2/ 3rd of leg

 D

Middle 1/3rd of leg

Ans. A

Explanation:

Ans. A i.e. Lower third of leg and ankle

  • Venous ulcers usually lie just proximal to the medial or lateral malleolus.
    • Venous ulcers are accompanied by lipodermatosclerosis and hemosiderosis (if these are not present then the ulcer is probably not of venous origin).

Quiz In Between



Lymphangiosarcoma

Lymphangiosarcoma

Q. 1

Lymphangiosarcoma occurs in?

 A Lymphangiomas
 B

Lymphomas

 C Lymphedema
 D

Serous cavity tumors

Q. 1

Lymphangiosarcoma occurs in?

 A Lymphangiomas
 B

Lymphomas

 C Lymphedema
 D

Serous cavity tumors

Ans. C

Explanation:

Lymphedema REF: Sabiston 18th ed chapter 69

“Lymphangiosarcoma is a rare tumor that develops as a complication of long-standing (usually more than 10 years) lymphedema”

Clinically, patients present with acute worsening of the edema and appearance of subcutaneous nodules that have a propensity toward hemorrhage and ulceration. The tumor can be treated, as other sarcomas, with preoperative chemotherapy and radiation followed by surgical excision, which usually takes the form of radical amputation. Overall, the tumor has a poor prognosis


Q. 2 The most common site of lymphangiosarcoma is

 A

Liver

 B

Spleen

 C

Post mastectomy edema of arm

 D

Retroperitoenum

Q. 2

The most common site of lymphangiosarcoma is

 A

Liver

 B

Spleen

 C

Post mastectomy edema of arm

 D

Retroperitoenum

Ans. C

Explanation:

Ans. is ‘c’ i.e., Post mastectomy edema of arm 
Lymphangiosarcoma is a rare tumor that develops as a complication of long standing (usually more than 10 years) lymphedema.

Quiz In Between



Grafts

SKIN GRAFTS

Q. 1

Skin grafts stored at 40 C can survive up to?

 A 1 week
 B

2 weeks

 C 3 weeks
 D

4 weeks

Q. 1

Skin grafts stored at 40 C can survive up to?

 A 1 week
 B

2 weeks

 C 3 weeks
 D

4 weeks

Ans. B

Explanation:

2 weeks REF: Facial Plastic and Reconstructive Surgery by Ira D. Papel Page 44, http://sydney.edu.au/medicine/foundation/sydneyburns/research/msg.php

Excess split-skin autografts harvested and meshed during a surgical session are often stored at short-term for later burn surgery or graft failure.

The current procedure in skin graft storage involves wrapping the meshed autograft on a piece of ringer lactate or normal saline-moistened gauze, transferring it into a sterile container and storing it in a 4° C for 2 weeks. The graft should never be totally immersed in saline because it will become macerated. After 14 days of storage the respiratory activity of skin graft reduced by 50%.


Q. 2 The organism causing destruction of skin grafts is ‑

 A

Streptococcus

 B

Staphylococcus

 C

Pseudomonas

 D

Clostridium

Q. 2

The organism causing destruction of skin grafts is ‑

 A

Streptococcus

 B

Staphylococcus

 C

Pseudomonas

 D

Clostridium

Ans. A

Explanation:

Ans. is ‘a’ i.e., Streptococcus 


Q. 3

Which one of the following statements about Mesh Skin Grafts is not correct? –

 A

They permit coverage of large areas

 B

They allow egrees of fluid collections under the graft

 C

They contract to the same degree as a grafted sheet of skin

 D

They “take” satisfactorily on a granulating bed

Q. 3

Which one of the following statements about Mesh Skin Grafts is not correct? –

 A

They permit coverage of large areas

 B

They allow egrees of fluid collections under the graft

 C

They contract to the same degree as a grafted sheet of skin

 D

They “take” satisfactorily on a granulating bed

Ans. C

Explanation:

Ans. is ‘c’ i.e., They contract to the same degree as a grafted sheet of skin
Meshed skin grafts are split-thickness grafts cm 7.5

  • Meshing can be done using a machine which creates regular slits in the graft, allowing it to be expanded. Thus it can cover larger areas. The slits also allow blood from the wound to escape to the surface, reducing the chances of hematoma and therefore improving graft take.
  • Meshed grafts are particularly valuable in burned patients where large areas of skin need to be covered.

Drawbacks of meshed grafts are

suboptimal appearance

– tendency to contract


Q. 4 Split skin grafts in young children should be harvest­ed from:
March 2013

 A

Buttcoks

 B

Thigh

 C

Trunk

 D

Upper limb

Q. 4

Split skin grafts in young children should be harvest­ed from:
March 2013

 A

Buttcoks

 B

Thigh

 C

Trunk

 D

Upper limb

Ans. B

Explanation:

Ans. B i.e. Thigh

Skin grafts

  • Partial thickness skin grafts/ Theirsch graft: Consist of epidermis & variable thickness of dermis
  • Full thickness/ Wolfes graft: Consists of epidermis & all of the dermis
  • Composite grafts: Consist of skin & some underlying tissue (fat, cartilage etc.)

Quiz In Between



Malignant Melanoma

Malignant melanoma

Q. 1 Skin biopsy of a patient shows evidence of malignant melanoma. Which is the common type of malignant melanoma?

 A

Superficial spreading

 B

Lentigo maligna melanoma

 C

Nodular

 D

Acral lentiginous

Q. 1

Skin biopsy of a patient shows evidence of malignant melanoma. Which is the common type of malignant melanoma?

 A

Superficial spreading

 B

Lentigo maligna melanoma

 C

Nodular

 D

Acral lentiginous

Ans. A

Explanation:

Superficial spreading melanoma comprises approximately 60% to 70% of melanomas and represents the most common melanoma subtype.
They often arise in a preexisting nevus and typically develop as a spreading pigmented plaque with irregular borders and variation in color and surface contour.
They often exhibit the classic clinical features of melanoma.
Areas of regression may result in pink to white areas within the black or brown tumor.
They may progress to a vertical growth phase faster than lentigo maligna.

 
Ref: Ludgate M.W., Wang T.S. (2009). Chapter 100. Skin Cancer. In J.B. Halter, J.G. Ouslander, M.E. Tinetti, S. Studenski, K.P. High, S. Asthana (Eds), Hazzard’s Geriatric Medicine and Gerontology, 6e.

 


Q. 2

Marker of malignant melanoma is?

 A

HMB 45               

 B

S-100

 C

Synaptophysin

 D

Both A and B

Q. 2

Marker of malignant melanoma is?

 A

HMB 45               

 B

S-100

 C

Synaptophysin

 D

Both A and B

Ans. D

Explanation:

Ans. is ‘a’ i.e., HMB 45 & ‘b’ i.e., S-100


Q. 3

Marker for malignant melanoma is –

 A

Cytokeratin

 B

MBN- 45

 C

Alpha FP

 D

S 100

Q. 3

Marker for malignant melanoma is –

 A

Cytokeratin

 B

MBN- 45

 C

Alpha FP

 D

S 100

Ans. D

Explanation:

Ans. is ‘d i.e., S-100

Tumor markers for malignant melanoma —4 S – 100, TA – 90.

These two markers can be used to look for the spread of melanoma.

Quiz In Between


Q. 4 Most common malignant melanoma is

 A

Superficial spreading

 B

Lentigo maligna melanoma

 C

Nodular

 D

Acral lentiginous

Q. 4

Most common malignant melanoma is

 A

Superficial spreading

 B

Lentigo maligna melanoma

 C

Nodular

 D

Acral lentiginous

Ans. A

Explanation:

Ans. is ‘a’ i.e. Superficial spreading type 

  • There are 4 common type of melanoma (these are in order of decreasing frequency)

a)      Superficial spreading type (most common)

b)         Nodular

c)         Lentigo maligna

d)         Acral lentiginous (least common)

  • Also remember:
  • MC type in dark skinned people —> Acral lentiginous type

Q. 5 The most malignant form of malignant melanoma is ‑

 A

Nodular

 B

Hutchinson’s melanotic freckle

 C

Acral lentiginous type

 D

Superficial spreading

Q. 5

The most malignant form of malignant melanoma is ‑

 A

Nodular

 B

Hutchinson’s melanotic freckle

 C

Acral lentiginous type

 D

Superficial spreading

Ans. A

Explanation:

Ans. is ‘a’ i.e. Nodular

Schwartz 9/e p415 writes that- “In general, there is no significant difference between different histologic tumor types in terms of prognosis, when matched for tumor thickness, gender, age, or other. Nodular melanomas have the same prognosis as superficial spreading types when lesions are matched for depth of invasion. Lentigo maligna types, however, have a better prognosis even after correcting for thickness, and acral lentiginous lesions have a worse prognosis.”


Q. 6 All of the following statements about malignant melanoma are true except:

 A

prognosis is better in female than in male

 B

Acral lentiginous melanoma carries a good prognosis

 C

Stage II A shows satelite deposits

 D

A and b

Q. 6

All of the following statements about malignant melanoma are true except:

 A

prognosis is better in female than in male

 B

Acral lentiginous melanoma carries a good prognosis

 C

Stage II A shows satelite deposits

 D

A and b

Ans. D

Explanation:

Ans. is ‘b’ i.e. acral lentiginous melanoma carries a good prognosis & ‘c’ i.e. stage II A shows satellite deposits

Acral lentignous melanoma has the worst prognosis

  • Satellite deposits are foci of tumor adajent but separate from the primary melanoma also k/a in-transit metastasis. In the original staging system, satellite deposits or lesions were classified as stage II ds.

Conventional staging of melanoma

  • Stage I Primary tumor
  • Stage II Presence of satellites or regional lymph nodes
  • Stage III –> Spread beyond regional lymph nodes
  • But according to latest AJCC classification (2002) presence of satellite lesions is classified as stage III.

More facts about melanoma

  • Most of the melanomas develop in benign nevus.
  • ABCD of melanoma – Lesions that are suspicions of melanoma can be identified by their clinical characteristic often referred to as ABCD.
  • Some books also have an ‘E’. E stands for ‘evolution of lesion’ or ‘elevation’.
  • The treatment is primary surgical
  • Diagnosis is confirmed by biopsy

Quiz In Between


Q. 7 True about malignant melanoma:

 A

Lymphatic spread

 B

Lymph node biopsy is done always

 C

Block dissection to be done when sentinel node is involved

 D

All

Q. 7

True about malignant melanoma:

 A

Lymphatic spread

 B

Lymph node biopsy is done always

 C

Block dissection to be done when sentinel node is involved

 D

All

Ans. D

Explanation:

Ans. is all 

Management of Malignant Melanoma

  • Wide local excision of the primary tumor is the management of choice. The recommended margin of resection depends on the thickness of the tumor.

Recommended Margins for Surgical Resection of Primary Melanoma

Tumor thickness

Margin Radius

< 1.0 mm

1.0 cm

 

1-4 mm

2.0 cm

 

>4 mm

3.0 cm

(Schwartz)

 Sabiston (18/e p773) and Harrison (I7/e p547) differ somewhat from Schwartz. According to Sabiston‑

Recommended Margins for Surgical Resection of Primary Melanoma

Tumor thickness

Margin Radius

In situ

0.5 cm

 

< 1.0 mm

1.0 cm

 

1-2 mm

1.0 – 2.0 cm

 

> 2.0 mm

> 2.0 cm

(Sabiston)

 According to Harrison —

Recommended Margins for Surgical Resection of Primary Melanom:

Tumor thickness

Margin Radius

 

In situ

0.5 cm

 

< 1.0 mm

1.0 cm

 

> 1.0 mm

2.0 cm

(Harrison)

 

  • Sentinel lymph node biopsy is done for tumors more than 1 mm thick. If biopsy is positive complete lymph node dissection is done.

Also know

Treatment of subungual melanoma — amputation of the distal digit to provide a 1 cm margin from the tumor. For fingers, amputation commonly involves only the distal phalanx; ray amputation is not required. (Sabiston 18/e p775) About option ‘d’ i.e. Microsatellitism

[Ref: http://www.moffitt.org/CCIRoot/v12n4/pdf/223.pdf http://www.pubmedcentranih.gov/articlerenderfcgi?artid=1250595 Ann Surg. 1984 December; 200(6): 759-763. http://archderm.ama-assn.org/cgi/reprint/141/6/739.pdf%5D

  • Microsatellites are discrete tumor nests greater than 0.05 mm in diameter that are separated from the main body of the tumor by normal reticular dermal collagen or subcutaneous fat.
  • Microsatellites constitute a risk factor for local recurrence. Melanomas with microsatellites are associated with a greater frequency of local clinical metastasis than those without.
  • Microsatellites are different from Satellite lesions. Satellite lesions are macroscopic finding whereas microsatellites are histopathological findings. Satellite lesions are foci of tumor adajacent to but separate from the primary melanoma. They are also called in-transit metastases, implying that secondary melanomas have grown in the skin on their way to spreading to local lymph nodes.

Q. 8

All are true statement about malignant melanoma except –

 A Clark’s classification used for prognosis

 B

Women have better prognosis

 C

Acral lentigenous have better prognosis

 D

Limb perfusion is used for local treatment

Q. 8

All are true statement about malignant melanoma except –

 A

Clark’s classification used for prognosis

 B

Women have better prognosis

 C

Acral lentigenous have better prognosis

 D

Limb perfusion is used for local treatment

Ans. C

Explanation:

Ans. is ‘c’ i.e., Acral lentigenous have better prognosis 


Q. 9

Prognosis of malignant melanoma depends on

 A

Grade of tumor

 B

Spread of tumor

 C

Depth of invasion

 D

Metastasis

Q. 9

Prognosis of malignant melanoma depends on

 A

Grade of tumor

 B

Spread of tumor

 C

Depth of invasion

 D

Metastasis

Ans. C

Explanation:

Ans. is ‘c’ i.e., Depth of invasion 

Quiz In Between


Q. 10

Least malignant melanoma is

 A

 Lentigo malignant melanoma

 B

Superifcial spreading

 C

Nodular

 D

Amelanotic

Q. 10

Least malignant melanoma is

 A

 Lentigo malignant melanoma

 B

Superifcial spreading

 C

Nodular

 D

Amelanotic

Ans. A

Explanation:

Ans. is ‘a’ i.e., Lentigo maligna 


Q. 11

Malignant melanoma of the choroid will produce:
September 2012

 A

Retinal dialysis

 B

Exudative retinal detachment

 C

Traction retinal detachment

 D

Rhegmatogenous retinal detachment

Q. 11

Malignant melanoma of the choroid will produce:
September 2012

 A

Retinal dialysis

 B

Exudative retinal detachment

 C

Traction retinal detachment

 D

Rhegmatogenous retinal detachment

Ans. B

Explanation:

Ans. B i.e. Exudative retinal detachment


Q. 12

Prognosis of malignant melanoma depends upon:
March 2011, March 2013

 A

Grade of tumour

 B

Age of the patient

 C

Invasion of nearby nodes

 D

Site of lesion

Q. 12

Prognosis of malignant melanoma depends upon:
March 2011, March 2013

 A

Grade of tumour

 B

Age of the patient

 C

Invasion of nearby nodes

 D

Site of lesion

Ans. C

Explanation:

Ans. C: Invasion of nearby nodes

The presence of lymph node metastases is the single most important prognostic index in melanoma, outweighing both tumour and host factors

Melanoma:

  • May be familial
  • Originate from melanocytes
  • Cutaneous melanoma arises from epidermal melanocytes
  • Spread by the lymphatic channels or the bloodstream
  • Lentigo maligna (least common) involves face commonly
  • Superficial spreading is the MC type
  • Nodular melanoma is the most malignant type

Quiz In Between


Q. 13

Most common site of distant metastasis inintraorbital malignant melanoma is‑

 A Brain

 B

Lung

 C

Liver

 D

Lymph nodes

Q. 13

Most common site of distant metastasis inintraorbital malignant melanoma is‑

 A

Brain

 B

Lung

 C

Liver

 D

Lymph nodes

Ans. C

Explanation:

Ans. is `c i.e., Liver

  • Malignant melanoma mostly arise in uvea and uveal malignant melanoma is the most common primary intraocular tumor.
  • The most common site for distant metastasis of uveal melanoma is liver.
  • The liver is the most common site of metastasis of uveal melanoma”                   — Clinical oncology
  • The liver is the most common site of metastatis from primary ocular melanoma”   — Smith & Nesi’s

Uveal melanoma

  • Uveal melanoma is the most common primary intraocular tumor in adults.
  • Most of the (85%) uveal melanomas arise in the choroid.
  • So, choroidal melanoma is the most common primary intraocular tumor in adults.
  • Tumor arises from dendritic melanocytes (neural crest, neuroectodermal origin).
  • Histologically choroidal melanoma can be divided into: –

Spindle cell melanomas : – These melanomas contain predominantly spindle cells.

  • These melanomas are further subdivided into Spindle A or Spindle B depending upon the type of cells.

Epitheloid cell melanomas : – Contain epitheloid like cells.

Mixed cell melanomas : – Contain both spindle cells and epitheloid cells.

  • Choroidal melanoma presents as a sessile or dome shaped mass located deep to the sensory retina.
  • A secondary non-rheugmatogenous retinal detachment frequently occurs.

Involvement of vortex vein by tumor results in glaucoma.

  • With continued growth, a choroidal melanoma can rupture Bruch’s membane and assume a mushroom shape.
  •  When that occurs, tumor has a tendency to bleed, and vitreal or subretinal hemorrhage may occur.

Q. 14 Risk factor for malignant melanoma all the following are risk factors fore malignant melanoma except

 A

Giant congenital nevi

 B

Family history melanoma

 C

Exposure to UV light

 D

HPV infection

Q. 14

Risk factor for malignant melanoma all the following are risk factors fore malignant melanoma except

 A

Giant congenital nevi

 B

Family history melanoma

 C

Exposure to UV light

 D

HPV infection

Ans. D

Explanation:

Answer- D. HPV infection
risk factor for malignant melanoma is exposure to (UV radiation)

  1. Dysplastic nevus (DN) syndrome; 5-10% risk of forming superficial spreading mil*o^u.
  2. Xeroderma pigmentosum
  3. Historyon nonmelanoma skin cancer (NMSC)
  4. Family history of melanoma (high risk)
  5. Congenital nevi

Quiz In Between



Mondor Disease

Mondor Disease

Q. 1 Mondor’s disease of breast is a variant of:

 A

Mycotic infection

 B

Malignancy

 C

Thrombophlebitis

 D

Lymphadenitis

Q. 1

Mondor’s disease of breast is a variant of:

 A

Mycotic infection

 B

Malignancy

 C

Thrombophlebitis

 D

Lymphadenitis

Ans. C

Explanation:

Mondor’s disease is a variant of thrombophlebitis that involves the superficial veins of the anterior chest wall and breast.

In 1939, Mondor described the condition as “string phlebitis,” a thrombosed vein presenting as a tender, cord-like structure.

Frequently involved veins include the lateral thoracic vein, the thoracoepigastric vein, and, less commonly, the superficial epigastric vein.

Typically, a woman presents with acute pain in the lateral aspect of the breast or the anterior chest wall.


A tender, firm cord is found to follow the distribution of one of the major superficial veins 
 
Ref: Schwartz’s principle of surgery 9th edition, chapter 17.

Q. 2

Mondor’s disease is ‑

 A

Thrombophlebitis of the Superficial veins of Breast

 B

Carcinoma of the breast

 C

Premalignant condition of the breast

 D

Filariasis of the breast

Q. 2

Mondor’s disease is ‑

 A

Thrombophlebitis of the Superficial veins of Breast

 B

Carcinoma of the breast

 C

Premalignant condition of the breast

 D

Filariasis of the breast

Ans. A

Explanation:

Ans is ‘a’ i.e., Thrombophlebitis of Superficial veins of Breast

  • Mondor’s disease
  • is thrombophlebitis of the superficial veins of anterior chest wall and breast although it has also been seen in the arm.
  • frequently involved veins are lateral thoracic vein, thoracoepigastric vein and superficial epigastric veins.
  • aetiology is unknown
  • also known as ‘string phlebitis’, it presents as a tender cord-like structure.
  • The women may present with acute pain in the lateral asepct of breast or the anterior chest wall. A tender cord-like superficial thrombosed vein is formed and when the skin over the breast is stretched by raising the arm, a narrow shallow subcutaneous groove alongside the cord becomes apparent.
  • rarely it may be bilateral.
  • Management

it’s a benign self-limited disorder
The differential diagnosis is lymphatic permeation from an occult carcinoma of breast
When the diagnosis is uncertain or a mass is present near the cord, a biopsy may be done. Treatment

  • antiinflammatory drugs and warm compresses
  • restricted arm movements as well as brassiere support of breast
  • it usually resolves within 4 to 6 weeks. When symptoms persists or are refractory to treatment, the involved vein segment may be excised.

Q. 3 About Mondor’s disease –

 A

Superficial thrombophlebitis

 B

Lymphatic infiltration tumour cell

 C

Cord like apperance of subcutanous veins

 D

a and c

Q. 3

About Mondor’s disease –

 A

Superficial thrombophlebitis

 B

Lymphatic infiltration tumour cell

 C

Cord like apperance of subcutanous veins

 D

a and c

Ans. D

Explanation:

Answer (a) Superficial thrombophlebitis; (c) Cord like apperance of sub. cut. veins 

  • In Mondor’s disease the thrombophlebitis is mostly limited to areas around the breast and there is no evidence of thrombophlebitis in other parts of body.
  • Lymphatic infiltration from tumor cells is a differential diagnosis of Mondor’s disease.

Quiz In Between



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