Pathology: AIIMS MAY 2012

Q-1. A young female patient came for routine examination. On examination a mid systolic click was found. There is no history of RHD the histopathological examination is most likely to show?
a) Myxomatous degeneration and prolapsed of the mitral valve
b) Fibrinous deposition on the tip of papillary muscle
c) Rupture of chordae tendinae
d) Aschoff nodule on the mitral valve

Answer: Myxomatous degeneration and prolapsed of the mitral valve
Explanation:
Myxomatous degeneration and prolapsed of the mitral valve:
Mitral valve prolapse is defined as abnormal bulging of the mitral valve leaflets into the left atrium during ventricular systole.
Mitral valve prolapse is a common condition that is a risk factor for mitral regurgitation, congestive heart failure, arrhythmia, and endocarditis.
Myxomatous degeneration is the most common cause of mitral prolapse and progression of myxomatous mitral prolapse is the most common cause of mitral regurgitation.
Important points:
Most patients with mitral valve prolapse are asymptomatic and condition is discovered only on routine examination by presence of mid-systolic click.
Mitral valve prolapse is defined and revealed by echocardiography.

Q-2. Which of the following is the characteristic of irreversible injury on electron microscopy?
a) Disruption of ribosomes
b) Amorphous densities in mitochondria
c) Swelling of endoplasmic reticulum
d) Cell swelling

Answer: Amorphous densities in mitochondria
Explanation:
Reversible injury is characterized by:
Generalized swelling of cell ant its organelles
Blebbing of plasma membrane
Detachment of ribosomes from RER
Clumping of nuclear chromatin
Irreversible injury is characterized by:
Swelling and disruption of lysosomes
Presence of large amorphous densities in swollen mitochondria
Disruption of cellular membrane
Profound nuclear changes> nuclear condensation (Pyknosis)> Fragmentation (Karyorrhexis)> Dissolution (Karyolysis)

Q-3. Which of the following statement is true?
a) Chronic myeloid leukemia occurs beyond 50 years of age
b) Hairy cell leukemia in less than 50 years has a good prognosis
c) Acute lymphoid leukemia in less than 1 year has a poor prognosis
d) Chronic lymphocytic leukemia occurs in less than 50 years of age

Answer: Acute lymphoid leukemia in less than 1 year has a poor prognosis
Explanation:
Prognostic factors for children with ALL:
Age at diagnosis and initial white blood cell count are thought to be the most important.
Age at diagnosis:
Children younger than 1 year and children 10 years or older are considered high-risk patients.
Initial white blood cell (WBC) count:
Children with ALL who have very high WBC counts (greater than 50,000 cells per cubic millimeter) when they are diagnosed are classified as high risk.

Q-4. Which of the following regarding Bombay blood group is false?
a) Lack of H, A and B antigen on RBCs
b) Lack of H, A and B substance in saliva
c) Lack of antigens of several blood group systems
d) H, A and B antibody will always be present in serum

Answer: Lack of antigens of several blood group systems
Explanation:
Bombay blood group:
First discovered in Bombay in 1952, termed as the (hh) type of blood
The biosynthesis of the H antigen and the A and B antigens involves a series of enzymes (glycosyl-transferases) that transfer monosaccharides.
H antigen itself is derived from precursor oligosaccharide by a specific fucosyl-transferase enzyme.
Depending upon a person’s ABO blood type, the H antigen is converted into either the A antigen, B antigen, or both. If a person has blood group O, the H antigen remains unmodified. Therefore, the H antigen is present in the highest amounts in blood type O and in the least amounts in blood type AB.
People with Bombay blood group cannot convert precursor oligosaccharide to H antigen, subsequently all the ABO antigens derived from H antigen are absent.
Other blood group antigens like Lewis antigen are directly converted from precursor oligosaccharide, so these antigens are present in Bombay blood group.
People, who carry Bombay blood group, can accept blood only from another Bombay Blood type individual, and not from anyone who is O, A, B or AB type.
Bombay blood group: Important points
H and ABO antigens are not expressed on RBCs.
H and ABO antigens are not found in saliva.
Serum contains anti-H.
Other blood group antigens like Lewis antigen are present in Bombay blood group.

Q-5. In an ablated animal, myeloid series cells are injected. Which of following is seen after incubation period?
a) RBC
b) Fibroblast
c) T lymphocytes
d) Hematopoietic stem cell

Answer: RBC
Explanation:
The hematopoietic stem cells differentiate into two progenitors:
Common lymphoid progenitors:
They can generate B lymphocytes, T lymphocytes and NK cells.
Common myeloid progenitors:
They can generate red cells, platelets, granulocytes, monocytes, dendritic cells and macrophages.
Important point:
The hematopoietic stem cells are not present because animal is ablated. Thus bone marrow cannot be reconstituted i.e., mature blood cells of other lineage cannot be generated.

Q-6. Hematopoietic stem cell differ from progenitor stem cell in that they can
a) Form terminally differentiated cells
b) Long term reconstitution of bone marrow
c) Produce growth factors
d) Have receptors for anchoring proteins

Answer: Long term reconstitution of bone marrow
Explanation:
See above explanation.

Q-7. The role of Bradykinin in process of inflammation is
a) Vasoconstriction
b) Broncho-dilation
c) Pain
d) Increased vascular permeability

Answer: Increased vascular permeability
Explanation:
The role of Bradykinin:
Increased vascular permeability
Vasodilatation
Pain
It also causes contraction of non-vascular smooth muscle in the bronchus and gut.
Important point:
Bradykinin is a nonapeptide synthesized by the proteolytic cleavage of an inactive precursor molecule kininogen.
Kininogen are synthesized by the hepatocytes and released in plasma.
In the plasma, the kininogen is acted upon by proteases to release Bradykinin.

Q-8. A 23 year-old female presented with jaundice and pallor for 2 months. Her peripheral blood smear shows the presence of spherocytes. The most relevant investigation to arrive at a diagnosis is
a) Retics count
b) Osmotic fragility test
c) Coombs test
d) Test for PNH

Answer: Coombs test
Explanation:
Morphological findings in hereditary spherocytosis:
Spherocytes apparent on smears as abnormally small, dark staining (Hyper-chromic) red cells lacking the normal central zone of pallor
Howell Jolly Bodies (Small dark nuclear remnants) are also present in red cells of asplenic patient.
Spherocytosis is also seen in auto-immune hemolytic anemia.
Hereditary spherocytosis usually presents in childhood or infancy.
Auto-immune hemolytic anemia:
A 23 year-old female with anemia, jaundice and peripheral blood demonstrating spherocytes> Auto-immune hemolytic anemia
Diagnosis of auto-immune hemolytic anemia requires the detection of antibodies/ or complement on patient red cells by the direct Coombs anti-globulin test.
The direct anti-globulin (Coombs) test:
The direct anti-globulin (Coombs) test is used to determine whether RBC-binding antibody (IgG) or complement (C3) is present on RBC membranes.
The patient’s RBCs are incubated with antibodies to human IgG and C3. If IgG or C3 is bound to RBC membranes, agglutination occurs–a positive result.
A positive result suggests the presence of auto-antibodies to RBCs.

Q-9. The fixative used in histopathology
a) 10% buffered neutral formalin
b) Bouins fixative
c) Glutaraldehyde
d) Ethyl alcohol

Answer: 10% buffered neutral formalin
Explanation:
The most widely used fixative for routine histopathology is 10% neutral buffered formalin.
This fixative can effectively prevent autolysis and provides excellent preservation of tissue and cellular morphology.

Q-10. A newborn baby presented with profuse bleeding from the umbilical stump after birth. Rest of the examination and PT, APTT are within normal limits. Most of probable diagnosis is
a) Factor X deficiency
b) Glanzmann Thrombasthenia
c) Von Willebrand disease
d) Bernard–Soulier syndrome

Answer: Glanzmann Thrombasthenia
Explanation:
Glanzmann Thrombasthenia is a rare genetic platelet disorder in which the platelets have qualitative or quantitative deficiencies of the fibrinogen receptor alpha-IIb-beta-3.
Neonate may present with umbilical stump bleeding and/or delayed cord separation, intracranial hemorrhage.
Patients with Glanzmann Thrombasthenia who are bleeding require platelet transfusion.