Sunday, May 10, 2015

AIPGMEE 2016 Pharmacology MCQ

The neurotransmitter agent that is normally released in the sinoatrial node of the heart in response to a blood pressure increase is
(a) Acetylcholine
(b) Dopamine
(c) Epinephrine
(d) Glutamate
(e) Norepinephrine

Saturday, May 9, 2015

AIPGMEE 2016 MCQ Pediatric Ophthalmology

All of the following would be considered in the differential diagnosis of vitreous hemorrhage
in an 8-year-old child except:
A) trauma
B) juvenile X-linked retinoschisis
C) pars planitis
D) melanocytoma
Answer -
D) Melanocytoma
Causes of vitreous hemorrhage in children include conditions such as pars planitis, juvenile Xlinked
retinoschisis, and trauma. Melanocytomas are elevated, deeply pigmented lesions most
often found at the optic nerve head. Histologically, they appear as a benign proliferation of
melanocytic cells. They are not known to cause vitreous hemorrhage

Toxicology General Notes AIPGMEE 2016 Forensic Medicine

A poison is a substance (solid, liquid or gaseous), which introduced into the living body or brought into contact with any part there of, will produce illhealth
or death, by its
constitutional or local effects or both.
The intent with which any act is committed is an important element in law, Administration of any substance with the intention of causing injury of death and which causes
injury or death as a result, is legally sufficient for awarding punishment, whether the substance is one which can be called poison or not. Administering poison to a person
with criminal intent is by itself a criminal offence, whether actual hurt is caused or not.
Criminal Offences: The administration of poison is a criminal offence whenever:
1. It is with intent to kill.
2. With intent to cause serious injury.
3. Used recklessly even though there is no intent to kill.
4. For stupefying to facilitate a crime, e.g., robbery or rape.
5. To procure an abortion.
6. To annoy the victim.
7. To throw poison at another person with intention to injure him.
Causes of Poisoning:
1. The administration of poison for criminal purposes.
2. The swallowing of poison in mistake for innocuous substance.
3. The inhalation through ignorance or accident, of the vapours of a poison.
4. The incorrect compounding of medicines containing a poison.
5. The accidental taking of a large dose of medicine containing a poison.
6. Excessive selfmedication.
7. Addiction to drugs.
8. Bite by a poisonous animal.
9. Food infected with bacteria or their toxins.
Poisoning and the Pathologist
The pathologist is concerned with evaluating poisons as a cause or contribution to death.His main task is to confirm or exclude other nontoxic factors in the death.He has to
collect suitable samples for analysis and, when the laboratory results are available to interpret them in the light of his knowledge of the history,clinincal features and autopsy
appearances.
Signs and symptoms of poisoning:
1. The symptoms appear suddenly in a healthy person.
2. The symptoms appear immediately or within a short period after food or drink.
3. The symptoms are uniform in character and rapidly increase in severity.
4. When several persons partake at the same time in the same source of poison, all suffer from similar symptoms at or about the same time.
5. The discovery of poison in food taken, in the vomit or in the excreta is strong proof of poisoning.
Collect (1) Stomach wash. (2) 10 ml. of blood. (3) Urine. (4) Faeces.
10 mg. of Sodium fluoride for 10 ml. of blood acts both as a preservative and as an anticoagulant.
DIAGNOSIS IN THE DEAD: Investigation of drug deaths involves team work.
1. Investigator should observe for (a) drugs available, (b) circumstances, (c) appearance and position of body.
2. Pathologist must do a complete autopsy to: (a) recognize drug cases, (b) collect proper specimens, (c) lend direction to toxicologist.
3. Toxicologist should (a) review case with Pathologist, (b) analyse in orderly manner, (c) discuss interpretation of findings with Pathologist.
1. PRELIMINARY STEPS: Scene of death:
2. History of suicidal tendencies or previous attempts at suicide.
3. Check for glasses, bottles, tablets, capsules, etc.
4. Look for suicide notes.
5. Note the appearance and position of the body.
6. Ascertain when deceased was last seen alive.
1. Deaths occurring after hospitalization:
2. Check clinical course for compatibility with drug overdose.
3. Find out if stomach wash was done.
4. Find out if any blood sample has been taken.
5. Check the record for reports of drug levels.
1. Suspected death from Drugs:
2. In cases where the history suggests involvement of drugs.
3. Deaths in teenagers and young adults without a history of preexisting
serious disease.
In most poisonings the major function of the autopsy is to evaluate any other conditions present, both from trauma and natural diseasebut
also to collect suitable material
for laboratory analyis.The proper retention of optimal samples, their correct preservation and dispatch to the Toxicologist is of fundamental importance.
II. AUTOPSY: (A) EXTERNAL:
1. The surface of the body and clothes may show stains or marks of vomit, faeces or the poison itself. Dark brown stains about the lips, chin, cheeks etc. are
suggestive of burning by corrosives.
2. Color of postmortem
staining: The skin may be yellow in phosphorus and acute copper poisoning. Cherry red staining suggests poisoning by carbon monoxide. Bright
red staining is seen in hydro cyanic acid poisoning. In poisoning by nitrates, potassium chlorate and aniline the color is brown or deep blue.
3. Smell about the mouth and nose. Compress chest and inhale near nose. Substances which may be recognized by their odor are alcohol, ether, chloroform, cyanides,
phenol, opium, organ phosphorus compounds, endrin, camphor, paraldehyde, etc.
4. The natural orifices may show the presence of poisonous material or the signs of its having been used.
5. Injection marks should be looked for with care.
6. Look for old scars from previous suicide attempts.
7. Look for blisters on extremities from barbiturates, sedatives, carbon monoxide, etc.
(B). INTERNAL:
1. Smell: On opening the body notes any peculiar smell. It will be strongest in the stomach.
2. Mouth and throat: Examine for any evidence of inflammation, erosion or staining.
3. Oesophagus: Corrosives produce marked softening and desquamation of the mucous membrane.
4. Upper respiratory tract: Examine for evidence of volatile irritants or inhaled poisonous matter. Laryngeal oedema is usually found in alcohol and barbiturate poisoning.
5. Lungs: Congested and oedematous in most cases. Laryngeal oedema is usually seen in deaths from alcohol and barbiturates.
6. STOMACH: (a) Hyperaemia is caused by an irritant poison, is usually marked at the cardiac end and greater curvature of stomach. It is usually patchy and of a deep
crimson colour. The ridges are more involved. The ridges are more involved. The mucous membrane is often covered with a viscid secretion and shows small
haemorrhagic foci. (b) Softening: Corrosives and irritants damage the epithelium. Excess of mucus is secreted. Softening of mucous membrane especially at its
cardiac end and greater curvature of the stomach. It appears as an erosion with thin friable margins. The surrounding mucosa is softened due to inflammation and
there is diffuse hyperaemia. (d) Perforation: It may occur in sulphuric acid poisoning. The stomach is blackened and extensively destroyed. The aperture is irregular,
the edges sloughing and the adjacent tissues easily torn.
7. Liver: Arsenic, phosphorus and rarely ferrous sulphate produce a fatty yellow liver. Arsephenamine, chloroform, carbonatetetrachloride,
etc., may produce liver
necrosis.
8. Kidneys: Degenerative changes are usually found in irritant metal poisoning and in cantharidine poisoning. Extensive necrosis of proximal convoluted tubules may be
found in poisoning by mercury, phenol and carbontetrachloride.
9. Heart: Subendocardial
haemorrhages in the left ventricle occur in most cases of acute arsenic poisoning.
10. Brain: May show swelling or pressure cone. There may be symmetrical necrosis of basal ganglia.
11. Bladder: It is usually distended, and often the only clue to death from drugs.
12. Vagina and Uterus: Should be examined for the effect of poison in criminal abortion.
13. Intravascular: Sickling may be triggered by drug ingestion.
Collection of Autopsy samples for Toxicological analysis.
The investigation of a death from suspected poisoning may stand or fall upon the correctness or otherwise of the sampling of fluids and tissues from the body.Unsuitable
samples,inadequate amounts,incorrect sampling sites,and delayed or unsatisfactory storage and transport to the Laboratory may frustrate or distort proper analysis.the final
outsome may be wrong,either failing to detect poison actually present,in measuring only part of that originally present or in some caseseven
producing falsely high results
that then lead to an incorrect cause of death.Not only most samples be in the optimal condition,but the accompanying information from the pathologist in analyst needs to
be as accurate and comprehensive as possible,so that the most appropriate techniques are used,and allowance made for any interfering substances which may be present.
Time of sampling
When an autopsy cannot be performed quickly after death,interms of few hours,then mortuary refregiration is the first line of defence to slow up putrefactive and autolytic
processes.If delay is forseen,usually because of administrative problems in obtaining consent or authority for autopsy,it may be possible to obtain a sample of blood through
the body surface,such as puncturing the femoral vein by needle and syringe.The blood can be kept in optimal condition,with preservatives where needed,and perhaps with
the serum or plasma separated from the cells to avoid hemolysis.Similarly,urine could be drawn off by catheter or even suprapubic puncture,unless strict regulations,forbid
this as anticipating autopsy permission.
Collection of Specimens:
1. Stomach and its contents. Open along lesser curvature. Examine wall for fragments of adherent poison. (a) Measure contents. (b) Look for tablets or capsules. (c)
Preserve whole contents if small amount is present; if there is a large amount, take an aliquot.
2. Upper part of small intestine and its contents.
3. Liver 100200gm,.
4. Kidney: 50gm from each Kidney.
5. Blood: 30 ml. from the heart. Do not mix with pericardial fluid and do not collect from the chest cavity.
6. Urine 30 ml.
Special Procedures:
1. Narcotic poisoning: Collect bile and onehalf
of one lung
2. Inhalation poisons: (a) Tie trachea, (b) collect bronchial air. (c) Collect entire lung and keep in airtight container.e.g.Nylon with out preservatives.
3. Pesticides: Fatty tissue from abdominal wall or perinephric region and brain.
4. Heavy metals: Hair, nails and bone.
5. Pneumoconioses: lung.
6. In deaths from extensive trauma: Vitreous fluid for alcohol.
Containers
1. Clean containers void of any ingrediadents.
2. Blood 30ml
Screwcapped containers or 5ml plasticcapped
containers.
3. Bile/UrineUniversal
Containers
4. Stomach(wall and contents)250ml
plastic or glass jars lid tight screw thread.
5. Intestine(contents)/LiverFew
hundred gramsLarger
plastic or glass container.
6. Vitreous Humour/CSF small bijou bottles5ml
capacity used.
7. Lungsnylon
bag used (solvent abuse or volatile poison).
Suitable Preservatives added with samples and anticoagulants added
Homicidal Poisoning:
1. Take extra care to avoid crosscontamination
during collection of specimens.
2. Prove route of administration. (a) Collect sample of air and lungs. (b) Excise injection site including skin, fat, muscle (take control from the opposite side).
3. Verify the drug by as many analytical methods as possible.
4. Rule out all possible unrelated causes of death.
5. Take sample of hair, nails, bone, etc.
6. Maintain chain of possession.
III. Chemical Analysis: Prevent contamination of the solid viscera with the contents of the gastrointestinal
tract, because an idea of the length of time since ingestion may
be had from the relative amounts of poison in the stomach, intestines and the solid organs. If the poison is only found in the contents of stomach and none in the solid
organs and is not an irritant, doubts may be thrown on the actual cause of death. Poison found in a viscus (other than stomach or intestine) is proof of absorption.
(IV) Animal Experiments.
(V) Circumstantial Evidence: Consists of motive, the evidence of witnesses about the recent purchase of the poison, his behavior before and after the commission of the
offence, and the recovery from the possession of the accused or the premises of a poison.
Cause of Death: The blood level of the drug or chemical is useful to determine the cause of death, in correlation with other findings. The blood level of a drug need not
always be in the lethal range for it to reflect the cause of death, especially in a treated case. Low levels may be due to passage of time after ingestion with resulting
metabolism of drug. Less than lethal levels of drug may trigger other mechanisms of death, e.g., (a) Positional asphyxia, (b) intravascular sickling in certain
haemoglobinopathies, (c) postictal
respiratory failure. When the presence of a highly toxic material is established, even in trace amounts, the inference that the poisoning is
the cause of death is justified.
Death may occur 1 to 2 weeks after ingestion of drugs from apparent unrelated causes, e.g., (a) Bronchopneumonia. (b) The rapeutic from tracheostomy. (c) Hepatitis. (d)
Fungal or bacterial endocarditis. (e) Encephalomalacia. (f) Haemotologica problems.
No Poison Found: Cases are observed in which no trace of poison is found on analysis, although from other circumstances it is almost or quite certain that the poison was
the cause of illness or death. The possible explanations of negative findings are (1) The poison may have been eliminated by vomiting and diarrhoea, e.g., in irritant poisons.
(2) The whole of the poison has disappeared from the lungs by evaporation or oxidation, (3) The poison after absorption may be detoxified, conjugated and eliminated from
the system. (4) Some vegetable alkaloidal poisons cannot be definitely recognized by analytical methods. (5) Some substances, e.g., toxins of tetanus or salmonella cannot
be detected chemically. (6) Some organic poisons especially alkaloids and glucosides may be oxidation during life or due to faulty preservation, or a long lapse of time, or
from decomposition of the body may deteriorate and cannot be detected chemically. (7) Many drugs present in very small amounts may require considerable amounts of
viscera for identification. (8) The wrong or insufficient material may have been sent for analysis.
Precautions:
1. Do a complete autopsy in every case, including microscopic examination.
2. If viscera are sent for chemical examination, keep the cause of death pending till the report is received.
3. Give the cause of death as due to drugs, after considering investigator’s report, autopsy protocol, laboratory and microscopic reports.
4. If low levels are found in viscera, consider: (a) Polypharmacy.
(b) Time lapse after ingestion with resulting metabolism of drug. (c) Positional asphyxia. (d)
Intravascular sickling in certain haemoglobinopathies. (e) Postictal respiratory failure.
5. If the victim survives for a week or two, do not give cause of death as bronchopneumonia, but give as bronchopneumonia following drug ingestion.
6. Consider all factors, to determine manner of death.
7. Maintain chain of custody.
HOUSEHOLD POISONS
DOMESTIC POISONS:
Preparation Toxic substance
Cosmetics
Cuticle remover: Potassium hydroxide,
trisodium phosphate
Depilatories Barium sulphide; thallium
Hair wave lotion Thioglycollate salts; perborates;
bromates
Nail polish removers Acetone
Suntan
lotions Denatured alcohol;
methyl
Salysilate.
Baby powder: Boric acid.
Kitchen
Baking powder Tartaric acid 50%
Baking soda Sodium bicarbonate
Dish washing compounds Sodium polyphosphates; sodium
carbonate, sodium silicates.
Fire extinguishing fluids Carbon tetrachloride; sodium
carbonate; methyl bromide.
Matches Antimony; Phosphorus; sesquisulphide,
potassium chlorate
Rat Poisons
Rat paste Aluminum phosphide; zinc phosphide; Arsenious
oxide; red
squill; thallium sulphate
Rodine Yellow phosphorus
Cockroach Powder Yellow phosphorus
Sanitary
Deodorant tablets Formaldehyde; naphthalene
Drain cleaners Sodium hydroxide
Disinfectants: Phenol; bleaching powder.
Miscellaneous
Insecticide spray D.D.T., Gammexane, etc
Moth Balls: Naphthalene
Marking ink: Aniline
Ink remover Sodium hyphochlorite 5%
Antirust
products: Ammonium sulphide, hydrofluoric acid,naphtha,
oxalic acid
Cleaning solvents Petroleum hydrocarbons; carbon
tetrachloride; trichloroethylene
Flourescent lamps Beryllium
Furniture Polish Turpentine; petroleum hydrocarbons
Paint remover Sodium hydroxide; lead acetate
Shoe polish Aniline; nitrobenzene
Hair bleach Potassium permanganate; hydrogen Peroxide.
Toys (paints): Lead
Fire works Arsenic; mercury; antimony; lead, phosphorus;
thiocyanate
Crayons (chalk): Salts of arsenic, copper, lead
Crayons (wax): Paranitroaniline
GARDEN POISONS
Insecticides Organophophorus compounds;
chlorinated hydrocarbons; nicotine;
Tar oils.
Fungicides Lead arsenate; copper
Compounds; organic mercurial;
Lime sulphur
Weed killers: Sodium chlorate; arsenious oxide,
and arsenites; dinitrocresol; paraquat
A.THERAPEUTIC POISONS:
1) Antiseptics: Iodine, benzoin.
(2) Tonic tablets: Iron.
(3) Tonic syrup: Strychnine
(4)Sleeping tablets: Barbiturates
(5)Head ache tablets: Aspirin.
(6)Cough remedies: Codeine
(7) Throat tablets: Potassium chl
(8) Pep tablets: Benzedrine.
(9) Others: Antidepressants; tranquillizers.

Friday, May 8, 2015

AIPGMEE 2016 MCQ Ophthalmology

1 On a T2-weighted MRI, which would appear hyperintense?
A) Fat
B) Blood in the carotid
C) Bone
D) Vitreous
2 A 30-year-old man was hit in his left eye at work and complains of sudden visual loss. You
measure his best acuity to be light perception in this eye. Ophthalmic examination is normal.
Which test does not rely on the patient’s interpretation of visual information?
A) Red/green spectacles
B) Optokinetic nystagmus (OKN) drum
C) Stereo acuity
D) Color vision
Answers-
1-D) Vitreous
MRIs allow excellent soft tissue definition by varying radiofrequency pulse sequences and
measuring the resulting signal produced by the tissue. T1- and T2-weighted MRIs are able to
highlight structures by the intensity of the signal generated after the magnetic pulse. Table 4-1
lists some of the differences between T1- and T2-weighted images. Air, fast-moving blood, and
bone generally produce no signal and are thus hypointense on the MRI. Fat and vitreous are
opposite to one another in both the T1- and T2-weightings.
2-B) Optokinetic nystagmus (OKN) drum
A number of tests can be used to determine whether a patient has functional visual loss. Direct
tests do not require the patient to verbally respond or interpret the visual information. Tests
such as the swinging light test, OKN response, and mirror test make it very difficult for a patient
to feign disease. Indirect tests rely on the patient’s cooperation and allow more definite
measurement of visual acuity in the “injured” eye.

Thursday, May 7, 2015

AIPGMEE 2016 Pathology MCQ Genetics

The Cellular and Molecular Basis of Inheritance

1. Base substitutions:
a. May result in nonsense mutations
b. Can affect splicing
c. Are always pathogenic
d. Can affect gene expression
e. Result in frameshift mutations
2. Transcription:
a. Describes the production of polypeptides from the
mRNA template
b. Occurs in the nucleus
c. Produces single-stranded mRNA using the antisense
DNA strand as a template
d. Is regulated by transcription factors that bind to the
3′ UTR
e. Precedes 5′ capping and polyadenylation
3. The following are directly involved in
DNA repair:
a. Glycosylases
b. DNA polymerases
c. Ligases
d. Splicing
e. Ribosomes
4. During DNA replication:
a. DNA helicase separates the double-stranded DNA
b. DNA is synthesized in one direction
c. Okazaki fragments are synthesized
d. DNA is synthesized in a conservative manner
e. Uracil is inserted to pair with adenine
ANSWERS
1. Base substitutions:
a. True. When a stop codon replaces an amino acid
b. True. For example, by mutation of conserved splice
donor and acceptor sites
c. False. Silent mutations or substitutions in noncoding
regions may not be pathogenic
d. True. For example promoter mutations may affect
binding of transcription factors
e. False. Frameshifts are caused by the insertion or
deletion of nucleotides
2. Transcription:
a. False. During transcription mRNA is produced from
the DNA template
b. True. The mRNA product is then translocated to
the cytoplasm
c. True. The mRNA is complementary to the
antisense strand
d. False. Transcription factors bind to regulatory
sequences within the promoter
e. True. The addition of the 5′ cap and 3′ poly(A) tail
facilitates transport to the cytoplasm
3. The following are directly involved in
DNA repair:
a. True. The DNA glycosylase MYH is involved in
base excision repair (BER)
b. True. They incorporate the correct bases
c. True. They seal gaps after abnormal base excision
and correct base insertion
d. False. Splicing removes introns during mRNA
production
e. False. Ribosomes are involved in translation
4. During DNA replication:
a. True. It unwinds the DNA helix
b. False. Replication occurs in both directions
c. True. These fragments are joined by DNA ligase to
form the lagging strand
d. False. DNA replication is semiconservative as only
one strand is newly synthesized
e. False. Uracil is incorporated in mRNA, thymine
in DNA

Wednesday, May 6, 2015

AIPGMEE 2016 MCQ Surgery

A 60-year-old woman complains of air and stool coming from
her vagina. Digital rectal examination reveals an area of induration
on the rectovaginal septum, although contrast barium
enema does not demonstrate any abnormality. Which of the
following statements regarding her probable condition is true?
A. Eighty-five percent of fistulas caused by obstetric trauma
heal spontaneously.
B. Low rectovaginal fistulas may be treated effectively by
fistulotomy.
C. Rectovaginal fistulas associated with Crohn’s disease
usually necessitate proctectomy.
D. Radiation-induced fistulas generally necessitate a colostomy.
E. High rectovaginal fistulas respond well to fibrin glue.


COMMENTS: Rectovaginal fistulas are classified according to
location and cause, which influence the type of corrective surgery
required. High fistulas require an abdominal approach, whereas
low or midline fistulas can be repaired through a transanal, transperineal,
or transvaginal approach. The causes of these fistulas
include obstetric injuries, irradiation for pelvic cancers, recurrent
cancer, inflammatory bowel disease, violent trauma, or infection
(e.g., tuberculosis or lymphogranuloma venereum). Five percent of
all vaginal deliveries are accompanied by third- or fourth-degree
perineal lacerations. Approximately 10% of the repairs become
disrupted and result in incontinence and, potentially, a rectovaginal
fistula. Approximately 50% of these obstetric fistulas heal spontaneously
(not 85%); therefore, if the patient’s symptoms are not
disabling, a 3- to 6-month waiting period is recommended. This
waiting period also allows the tissue inflammation and edema to
subside before surgical intervention. Repair of a fistula secondary
to an obstetric injury can be performed transvaginally or transrectally.
With the former, the tract is excised and the rectovaginal
septum is inverted with serial purse-string sutures. With the latter,
a flap consisting of mucosa, submucosa, and muscularis is advanced
to cover the rectal side of the fistula. A diverting colostomy is not
required unless multiple previous surgical attempts have failed. An
anovaginal fistula may be treated by fistulotomy, but rectovaginal
fistulas (even distal ones) should not be treated by this method.
Partial or total incontinence may result if the fistula tract is divided.High rectovaginal fistulas are best treated through a transabdominal
approach so that coexisting pathologic conditions such
as diverticulitis, cancer, or inflammatory bowel disease can be
addressed. The rectovaginal septum is mobilized, the fistula is
divided, the vagina is closed, and normal tissue (such as omentum
or a muscle flap) is used to buttress the repair. Because the colon
is not usually normal (inflammation or radiation injury), bowel
resection is generally necessary.
Fistulas secondary to Crohn’s disease do not necessitate proctectomy
if the symptoms are minimal, the rectum is relatively
healthy, and continence is normal. In such cases, an advancement
flap can lead to healing. Refractory rectal Crohn’s disease (especially
the stricturing form) or incontinence usually necessitates
proctectomy. Radiation-induced fistulas may necessitate a colostomy
as sole therapy (e.g., poor-risk patient with recurrent, unresectable
cancer) or to divert stool from an anastomosis after
resection of diseased bowel.
A N S W E R : D

Tuesday, May 5, 2015

Common Causes of Pleural Effusion

Common Causes of Pleural Effusion

  • Heart failure
  • Low blood protein levels
  • Cirrhosis
  • Pneumonia
  • Blastomycosis
  • Coccidioidomycosis
  • Tuberculosis
  • Histoplasmosis
  • Cryptococcosis
  • Abscess under the diaphragm
  • Rheumatoid arthritis
  • Pancreatitis
  • Pulmonary embolus
  • Tumors
  • Systemic lupus erythematosus
  • Heart surgery
  • Injury to the chest
  • Drugs such as hydralazine, procainamide, isoniazid, phenytoin, chlorpromazine, and rarely, nitrofurantoin, bromocriptine, dantrolene, procarbazine
  • Improper placement of feeding tubes or intravenous catheters