30 - Herring Bone Pattern

*We will start from basics :

*Question No.1: What is Herring?
-Answer: It is the name given to a type of fish which looks something like the figure shown below and is usually found in the shallow waters of north pacific and north atlantic.

*Question No.2: What is Herring Bone?
-Answer: The Herring Bone is nothing but the name given to the skeleton of the Herring fish, that looks something like the image shown below.

*Question No.3: What is so unique about the pattern of bones in the Herring fish skeleton, that it got the name Herring bone pattern?
-Answer: As is obvious from the image of the Herring Bone/Skeleton above, the skeleton of the herring fish has a beautiful pattern that is exploited in various industries like Cloth making and Tile making or it could just be a coincidence that the bone pattern matches the design.Have a look at the Herring Bone pattern on a cloth and on a pavement in the images below.

*Question No.4: Ok Ok Ok, But what the hell does this have to do with Medicine?
-Answer: Suppose you are the surgical oncologist/radiologist/General Surgeon/Paediatrician/Physician in a hospital and you came across a patient with a soft tissue tumor in some part of the body. The patient was operated upon and the soft tissue tumor was removed. The next step in the process is usually that the Specimen of tumor tissue is sent to the pathology department for confirmation of the diagnosis. The pathologist does all the preliminary things and finally colours it with dyes and watches the slide made from the specimen under the microscope.

                                                  If the pathologist sees the same HERRING BONE PATTERN, i was talking about previously in the slide, then the resected tumor is probably FIBROSARCOMA(congenital/infantile type or adult type). The slide will look something like the image shown below because of arrangement of cells{fibroblasts} in columns of short parallel lines with all the lines in one column sloping one way and lines in adjacent columns sloping the other way.

*It has to be remembered this same pattern can appear in a case of MONOPHASIC SYNOVIAL SARCOMA, which is another type of soft tissue tumor.

*To keep things simple - Herring Bone pattern on histology is seen in soft tissue tumors like fibrosarcoma(congenital/infantile or adult) or Monophasic synovial sarcoma.

-I would like to thank Wikipedia for the images.

29 - Differential diagnosis of Nephritic syndromes based on Complement levels

*Nephritic syndromes with low complement levels :
   (Immune complex glomerulonephritis)
- Idiopathic proliferative glomerulonephritis
- Crescentric glomerulonephritis
- Membranoproliferative glomerulonephritis
- Lupus nephritis
- Cryoglobulinemia
- Bacterial endocarditis
- Shunt nephritis
- Post infectious glomerulonephritis (post streptococcal)

*Nephritic syndromes with Normal complement levels :
- Anti GBM disease : Good pasture syndrome
- Pauci immune glomerulonephritis : Wegener's granulomatosus and Microscopic PAN.
- Immune complex mediated : Henoch schonlein purpura, IgA nephropathy and Fibrillary glomerulonephritis.

*An important point to be noted is that, in Post streptococcal glomerulonephritis : Serum C3 levels are depressed within 2 weeks, however these usually return to normal levels within 6 to 8 weeks. Persistent depressed levels after this period should suggest another cause such as presence of C3 nephritic factor (Membranoproliferative glomerulonephritis).

------

Given below are two MCQs which appeared in the AIPGME 2004 paper related to the above topic.

1Q: Serum C3 is persistently low in all of the following except :
a. Post streptococcal glomerulonephritis
b. Membranoproliferative glomerulonephritis
c. Lupus nephritis
d. Glomerulonephritis related to bacterial endocarditis

answer a. Post streptococcal glomerulonephritis.

2Q: All of the following are associated with low complement levels except
a. Lupus nephritis
b. Mesangio capillary glomerulonephritis
c. Diarrhea-associated HUS
d. Post-infectious glomerulonephritis

answer c. Diarrhea-associated HUS.

Essential Pediatric McQs
MCQs in Pediatrics 2nd edition
MCQs in Pediatrics ; Over 600 Questions with Explanatory Notes

28 - Types of Bodies in Pathology

ASTEROID BODIES	Sporotrichosis
COUNCILLMAN BODIES	Yellow fever
TORRES BODIES	Yellow fever
LEISHMAN-DONOVAN BODIES	Kala Azar
HALBERSTEADTER-PROWAZEKI BODIES	Trachoma
MIYAGAVA'S BODIES	Lymphogranuloma venerum
LEVINTHAL-COLE-LILLIE BODIES	Psittacosis
NEGRI BODIES (Intracytoplasmic,intraneuron,hippocampus)	Rabies
GUARNERI'S BODIES	Vaccinia (intracytoplasmic)
BOLLINGER'S BODIES	Fowl pox (intracytoplasmic)
HENDERSON-PETERSON'S BODIES	Molluscum contagiosum
COWDRY TYPE-A BODIES	Yellow fever, Herpes virus infection
COWDRY TYPE-B BODIES	Adeno virus, Polio virus (mnem:BAP)
ASCHOFF BODIES	Rheumatic fever
RUSSELL'S BODIES	Multiple Myeloma
SCHAUMAN'S/CONCHOID BODIES (Calcium and iron complexes)	Sarcoidosis and Berylliosis
ASTEROID BODIES (Eosinophilic inclusions)	Sarcoidosis
CALL-EXNER BODIES	Granulosa cell tumor of ovary
VERROCAY BODIES	Neurilemmoma
CIVATTE (COLLOID) BODIES	Lichen planus
MICHAELIS-GUTTMAN BODIES	Malakoplakia
LEWY BODIES	Parkinson's disease
LAFORA BODIES	Familial myoclonus
HIRANO BODIES	Alzheimer's disease
WEIBEL-PALADE BODIES	Storage organelles of VonWillebrand's factor in platelets and endothelium
PAPPENHEIMER BODIES	Non haem iron pigments in siderocytes
HOWELL JOLLY BODIES	Splenectomy
HECTOID BODIES	Sickle cell anemia
HEINZ BODIES	Thalassemia
DOHLE BODIES	Cytoplasmic inclusion bodies in neutrophils seen in bacterial infection
HISTIOCYTOSIS-X(BIRBECK GRANULES)	Histiocytosis-X
GAMMA-GANDY BODIES	Congestive splenomegaly
MALLORY BODIES	Hyaline inclusions in hepatocytes seen in alcoholic and childhood cirrhosis
APOPTOTIC BODIES	Membrane bound spherical structures in apoptosis
PSAMMOMA BODIES	Dystrophic calcification in meningioma, papillary serous cystadenoma of ovary and papillary carcinoma of thyroid
LE Bodies (HEMATOXYLIN BODIES)	SLE
DUMBELL SHAPED ASBESTOS BODIES	Asbestos fibres coated with glycoprotein and hemosiderin, stained with prussian blue stain
LUYS BODY	Subthalamic nucleus
DAVIDSON'S BODY	Sex chromatin in neutrophils (dumbell shaped)
HERRING BODIES	Pars nervosa of pituitary gland
DONOVAN BODY	Granuloma inguinale
NISSELS BODIES	Cytoplasmic inclusions in neurons
MOOSER'S BODIES	Typhus fever
LIPSCHULTZ BODIES	Intranuclear inclusions in herpes simplex infection
ZEBRA BODIES	Cytoplasmic inclusions in schwann cell degeneration
BABES-ERNST METACHROMATIC GRANULES	Diptheria
REILLY'S BODIES	Hurler's syndrome
GAMMA-FAVRE BODIES	LGV
WINKLER'S AND ROSS' BODIES	Syphilis
SANDSTORM BODIES	Parathyroid gland

27 - Chronic Myeloid Leukemia (CML) mcqs

Which of the followings are correct about chronic myeloid leukemia?

A. It is common in young adults and children.
B. It typically takes a biphasic chronic and acute course.
C. Pseudo-Gaucher cells are present in the bone marrow.
D. Immunohistochemistry for terminal deoxynucleotidyl transferase is a helpful way to confirm the diagnosis.
E. Immunohistochemistry for tryptase is a helpful way to confirm the diagnosis.

answer C is the only true statement.

Summary: Chronic myeloid (myelogenous) leukemia (CML) is a clonal (neoplastic) myeloproliferative disorder of hematopoietic stem cells with leukemia as the cardinal clinical and pathologic feature. It is essentially a disease of older people and takes a triphasic (chronic, accelerated, and blast crisis). Demonstration of translocation t(9;22) or Bcr-Abl fusion (Philadelphia chromosome) is the gold standard for diagnosis.

Behavior and Prognosis:

• Untreated cases: CML takes a triphasic course (chronic, accelerated, and blast phase). After a median of 3 to 5 years, untreated patients with chronic phase CML inevitably progress to blast phase, which is rapidly fatal. The risk of transformation to CML-BP is estimated at 3% to 4% per year.
• Treated cases: Therapeutic options before the imatinib era included cytotoxic drugs such as busulfan and hydroxyurea, interferon-α and allogeneic stem cell transplantation. Imatinib is the standard therapy for CML today because of its remarkable activity and mild toxicity profile. However, it has a history of only 5 years, and does not seem to cure this leukemia by itself, since the discontinuation of therapy is followed by recurrence in most cases.

Age:

• The incidence increases with age with the peak incidence at 65 years of age.
• CML is exceedingly rare in children.

Sex: Slight male predominance, M:F of 1.4:1.

Incidence:

• Very common: CML accounts for approximately 15 to 20 percent of cases of leukemia in adults.
• Annual incidence: 1.6 cases per 100,000 adults

Clinical features:

• Onset: The onset is slow. The initial symptoms are very non-specific and patients may be asymptomatic. The diagnosis is made incidentally after a routine CBC in nearly 50% of the patients.
• Symptomatic patients, the symptoms are generally related to the expansion of CML cells and consist typically of malaise, weight loss, and abdominal discomfort caused by splenomegaly. Tenderness over the lower sternum, due to an expanding bone marrow, is sometimes seen.
• Bleeding episodes due to platelet dysfunction can occur.
• Acute gouty arthritis may also present at this time, due to overproduction of uric acid.
• Hyperviscosity: In cases of very high WBC count signs and symptoms are related to of hyperviscosity, and include retinal hemorrhage, priapism, cerebrovascular accidents, tinnitus, confusion, and stupor.
• Spleen, liver, lymph nodes, and bone marrow: The excess of neoplastic and immature  neutrophils will lead to splenomegaly, and occasionally hepatomegaly or lymphadenopathy, and by varying degrees of myelofibrosis and extramedullary hematopoiesis.

Triphasic clinical course:

• Chronic phase: present at the time of diagnosis in approximately 85 to 90 percent of patients.
• Accelerated phase: The neutrophil differentiation becomes progressively impaired and leukocyte counts are more difficult to control with myelosuppressive medications
• Blast phase (crisis): A condition that resembles acute leukemia in which myeloid or lymphoid blasts fail to differentiate. After a median of 3 to 5 years, untreated patients with chronic phase CML inevitably progress to blast phase, which is rapidly fatal. The risk of transformation is estimated at 3% to 4% per year.

Molecular Pathology:

• Translocation t(9;22) (Philadelphia Chromosome): The "gold standard" for the diagnosis of CML is either the demonstration of the Philadelphia chromosome by conventional cytogenetic techniques, or the demonstration of the products of the underlying t(9;22) translocation, namely the BCR-ABL fusion mRNA or the Bcr-Abl protein.
• Alternate breakpoint: The occasional patients with CML who have an alternate breakpoint in chromosome 22, producing a p190 Bcr-Abl fusion protein rather than the classic p210 Bcr-Abl fusion protein, tend to have monocytosis and a low neutrophil/monocyte ratio in the peripheral blood.
• FISH and RT-PCR: In 5 – 10 % of patients with clinical features of CML Ph chromosome can not be detected by cytogenetic analysis. However, in majority of those patients the evidence of BCR-ABL gene fusion can be identified by metaphase or interphase FISH analysis or RT-PCR.
• CML without Philadelphia chromosome: However, about one-third of the group lacked molecular evidence of BCR-ABL fusion. In general, these patients have distinct clinical features, including short survival, poor response to therapy, absence of basophilia, frequent thrombocytopenia, and may progress with increasing leukocytosis, organomegaly, extramedullary infiltrates, and marrow failure, some without a terminal acute leukemia phase.
• Accelerated phase and blast phase: Additional cytogenetic abnormalities develop in patients in the accelerated phase and blast phase: trisomy 8, trisomy 19, duplication of the Ph chromosome, and isochromosome 17q.

Peripheral Blood:

• Chronic phase: CBC shows leukocytosis with a prominent left shift in the differential count, basophilia and often thrombocytosis. Occasionaly platelet count can be low. In rare instances the white blood cell (WBC) count can be as high as 1000 X 10⁹/L.  The leukocyte alkaline phosphatase (LAP) score is abnormally low, with essentially normal phagocytic function.

·         Differential count: Virtually all cells of the neutrophilic series at different stage of maturation, from mature neutrophils to myeloblasts, are present in the blood. Number of blasts in peripheral blood does not exceed 2 percents. Absolute basophilia and eosinophilia are almost universal findings.

·         “Leukemic hiatus”: The presence of a greater percent of myelocytes than the more mature metamyelocytes ("leukemic hiatus") is one of the classic findings in CML.

• Accelerated phase- presence of at least 1 of the followings :

·         10 – 19 % of blasts in the peripheral blood or bone marrow.

·         20% or more peripheral blood basophils.

·         Platelet counts lower than 100 X 10⁹/L unrelated to therapy.

·         Platelet counts higher than 1000 X 10⁹/l, despite of treatment.

• Blast phase (crisis)- presence of 1 or more of the followings:

·         >20 % of peripheral blood or bone marrow blasts.

·         Large foci or clusters of blasts on the bone marrow biopsy.

·         Presence of extramedullary blastic infiltrates (eg, myeloid sarcoma or "chloroma").

• Myeloid markers in blast cells: Blastic cells in myeloid CML blast phase closely resemble acute myeloid leukemia (AML), and blast cells express myeloid markers such as CD13, CD33, and CD117. Myeloperoxidase staining may be strongly or weakly positive or negative.
• Lymphoid markers in blast cells: Blasts may also express lymphoid markers, such as terminal deoxynucleotidyl transferase (TdT), commonly found in poorly differentiated B and T cells tumors. In most cases of lymphoid CML blast phase, blasts exhibit a B-cell immunophenotype, expressing CD10, CD19, and CD22. Frequently, myeloid markers such as CD13 and CD33 may be expressed in patients with lymphoid CML blast phase.

Bone Marrow:   

• Hypercellular and pseudo-Gaucher cells: Bone marrow aspiration and biopsy in patients with CML in chronic phase shows hypercellularity and absence of fat. All stages of myeloid maturation are present, with predominance of myelocytes. The sum of myeloblasts and promyelocytes usually accounts for less than 10% of the marrow cellularity. Megakaryocytes may be increased, and pseudo-Gaucher cells can be observed in 10 to 30 % of cases.

·         Pseudo-Gaucher cells or sea-blue histiocytes, are derived from the neoplastic clone, secondary to increased cell turnover. The electron microscopy distinguishes them from true Gaucher cells. They arise as a result of overloading of 1- glucosidase by excessive cell turnover; hence there is a relative rather than an absolute deficiency of the enzyme.

• Fibrosis: As CML progresses, varying degrees of reticulin fibrosis and vascularity may be seen, which can be related to effect of platelet-derived growth factor, transforming growth factor β, and basic fibroblastic growth factor, whose plasma levels are significantly increased in CML.

Differential Diagnosis:

Juvenile myelomonocytic leukemia, chronic myelomonocytic leukemia, chronic eosinophilic leukemia, and other Ph positive leukemias (acute precursor B-cell lymphoblastic leukemia, adult AML.

26 - Gastrointestinal Stromal Tumor (GIST) mcqs

1.Which of the following(s) is/are true about gastrointestinal stromal tumor (GIST):

1. Most commonly seen in small intestine.
2. The most common histopathologic picture is that of spindle cells and epithelioid cells arranged in storiform pattern.
3. Common in young patients under 30 years of age.
4. Positive for CD117 (c-kit) and CD34.

A. 1, 2, and 3 are correct.
B. 1 and 3 are correct.
C. 2 and 4 are correct.
D. Only 4 is correct.
E. All are correct.

answer C is true. 2 and 4 are correct.

Discussion: Gastrointestinal stromal tumor (GIST) is best defined as cellular spindle cell, epithelioid, or occasionally pleomorphic mesenchymal tumors of the gastrointestinal tract that express the c-kit (CD117) protein as detected by immunohistochemistry.
About 79% of them are also positive for CD34. GISTs may vary in size from small to large and in biological behavior from benign to malignant. They are the most common mesenchymal tumor of the gastrointestinal tract. GISTs are most commonly seen in the stomach (60-70%) and small intestine (20-30%), followed by colon and rectum (less than 5%), and esophagus (less than 5%). Most of them occur in middle aged and eldery patients over 50 years of age.

2. The presence of myxoid stroma in gastrointestinal stromal tumor (GIST) of stomach is a histologic feature associated with benign behavior?

a. true
b. false

answer b. false 

Discussion: For gastric stromal tumors, unfavorable prognostic sign include tumor size greater than or equal to 7 cm, high cellularity, mucosal invasion, high nuclear grade, mitotic counts greater than or equal to 5/50 high power fields, mixed cell type, and the presence of a myxoid background and/or absence of stromal hyalinization.

25 - Antioncogenes ( Tumor suppressor genes )

A tumor suppressor gene, or antioncogene is a gene that protects a cell from one step on the path to cancer. When this gene is mutated to cause a loss or reduction in its function, the cell can progress to cancer, usually in combination with other genetic changes.

TWO-HIT HYPOTHESIS :

Unlike oncogenes, tumor suppressor genes generally follow the 'two-hit hypothesis', which implies that both alleles that code for a particular gene must be affected before an effect is manifested. This is due to the fact that if only one allele for the gene is damaged, the second can still produce the correct protein. In other words, mutant tumor suppressors alleles are usually recessive whereas mutant oncogene alleles are typically dominant. The two hit hypothesis was first proposed by A.G. Knudson for cases of retinoblastoma. Knudson observed that the age of onset of retinoblastoma followed 2nd-order kinetics, implying that two independent genetic events were necessary. He recognized that this was consistent with a recessive mutation involving a single gene, but requiring biallelic mutation. Oncogene mutations, in contrast, generally involve a single allele because they are gain of function mutations. There are notable exceptions to the 'two hit' rule for tumors suppressors, such as certain mutations in the p53 gene product. p53 mutations can function as a 'dominant negative', meaning that a mutated p53 protein can prevent the function of normal protein from the un-mutated allele. Other tumor suppressor genes which are exceptions to the 'two-hit' rule are those which exhibit haploinsufficiency. An example of this is the p27Kip1 cell cycle inhibitor, in which mutation of a single allele causes increased carcinogen susceptibility.

FUNCTIONS :

Tumor suppressor genes, or more precisely, the proteins for which they code, either have a dampening or repressive effect on the regulation of the cell cycle or promote apoptosis, and sometimes do both.

The functions of tumor suppressor proteins fall into several categories including the following:

Repression of genes that are essential for the continuing of the cell cycle. If these genes are not expressed, the cell cycle will not continue, effectively inhibiting cell division.
Coupling the cell cycle to DNA damage. As long as there is damaged DNA in the cell, it should not divide. If the damage can be repaired, the cell cycle can continue.
If the damage cannot be repaired, the cell should initiate apoptosis (programmed cell death) to remove the threat it poses for the greater good of the organism.
Some proteins involved in cell adhesion prevent tumor cells from dispersing, block loss of contact inhibition, and inhibit metastasis. These proteins are known as metastasis suppressors.

EXAMPLES :

The first tumor suppressor protein discovered was the Retinoblastoma protein (pRb) in human retinoblastoma; however, recent evidence has also implicated pRb as a tumor survival factor.

Another important tumor suppressor is the p53 tumor suppressor protein encoded by the TP53 gene. Homozygous loss of p53 is found in 70% of colon cancers, 30–50% of breast cancers and 50% of lung cancers. Mutated p53 is also involved in the pathophysiology of leukemias, lymphomas, sarcomas, and neurogenic tumors. Abnormalities of the p53 gene can be inherited in Li-Fraumeni syndrome (LFS), which increases the risk of developing various types of cancers.

PTEN acts by opposing the action of PI3K, which is essential for anti-apoptotic, pro-tumorogenic Akt activation.

Other examples of tumor suppressors include APC and CD95.

25 - abnormal hemoglobins with altered synthesis and function mcqs

1q: what is the hemoglobin that results when glutamate in the 6th position of beta chain is replaced by valine ?

a. hemoglobin S or sickle cell hemoglobin
b. hemoglobin C
c. hemoglobin E
d. hemoblogin Yakima

answer a . sickle cell hemoglobin also called as hemoglobin S . this is mostly seen in African population and is characterized by anemia and ischemic infarcts .

2q: what is the hemoglobin that results when glutamate in the 6th position of the beta chain is replaced by lysine ?

a. hemoglobin S or sickle cell hemoglobin
b. hemoglobin C
c. hemoglobin E
d. hemoblogin Yakima

answer b . hemoglobin C . this is mostly seen in African population .hemoglobin C is characterized by mild anemia and interacts with HbS ./option>

3q: what is the hemoglobin that results when glutamate in the 26th position of the beta chain is replaced by lysine ?

a. hemoglobin S or sickle cell hemoglobin
b. hemoglobin C
c. hemoglobin E
d. hemoblogin Yakima

answer c . hemoglobin E . HbE is characterized by microcytic anemia, splenomegaly and thalassemic phenotype. This is mostly seen in southeast asian population .

4q: what is the hemoglobin that results when valine in the 98th position of the beta chain is replaced by methionine ?

a. Hb koln
b. Hb Yakima
c. Hb Kansas
d. Hb M. iwata

answer a . Hb koln . this type of hemoglobin is not specific to one kind of population and occurs sporadically. It is characterized by hemolytic anemia, Heinz bodies when splenectomized .

5q: what is the hemoglobin that results when aspartate in the 99th position of the beta chain is replaced by histidine ?

a. Hb koln
b. Hb Yakima
c. Hb Kansas
d. Hb M.iwata

answer. Hb Yakima . it occurs sporadically and is characterized by polycythemia .

6q: what is the hemoglobin that results when asparagine in the 102nd position of the beta chain is replaced by lysine ?

a. Hb koln
b. Hb Kansas
c. Hb M.iwata
d. Hb Yakima

answer b . Hb kansas . this also occurs sporadically and is characterized by mild anemia

7q: what is the hemoglobin that results when histidine in the 87th position of the alpha chain is replaced by tyrosine ?

a. Hb koln
b. Hb Kansas
c. Hb Yakima
d. Hb M.iwata

answerd. Hb M.iwata . this also occurs sporadically and is characterized by methemoglobinemia .

24 - AIIMS november 2008 pathology mcqs

53.MHC IS LOCCATED ON WHICH CHROMOSOME?

A. 10
B. 6
C.X
D. 13

answer is B . 6 th chromosome .

54.BRCA 1 IS LOCATED ON CHROMOSOME?

A. 13
B. 11
C. 17
D. 22

the answer is C . 17 th chromosome .

55. GENE FOR FOLATE CARRIER PROTEIN IS LOCATED ON CHROMOSOME?

A. 5
B. X
C. 21
D. 9

the answer is C. 21 st chromosome .

56.ALL ARE TRUE ABOUT THROMBOTIC THROMBOCYTOPENIC PURPURA EXCEPT?
]
A. MICROANGIOPATHIC HEMOLYTIC ANEMIA
B. THROMBOCYTOPENIA
C. NORMAL COMPLEMENT LEVEL
D. THROMBOSIS

57.ESSENTIAL FOR TUMOUR METASTASIS IS?

A. ANGIOGENESIS
B.TUMOROGENESIS
C. APOPTOSIS
D. INHIBITION OF TYROSINE KINASE ACTIVITY

58. COMMON COMPLEMENT COMPONENT FOR BOTH PATHWAYS IS?

A. C3
B. C5
C. C1q
D. C8

59.ENZME RESPONSIBLE FOR RESPIRATORY BURST IS?

A. OXIDASE
B. DEHYDROGENASE
C. PEROXIDASE
D.CATALASE



60.MOST POTENT STIMULATOR OF NAÏVE T CELL IS?

A. MATURE DENDRITIC CELL
B. FOLLICULAR DENDRITIC CELL
C. MACROPHAGE
D. B CELL

answer is B . dendritic cell. its a repeat from the old AIIMS papers.

61.NITROBLUE TETRAZOLIUM TEST IS USED FOR?

A. PHAGOCYTES
B. COMPLEMENT
C. T CELL
D. B CELL

62.HYPERSENSITIVITY VASCULITIS IS SEEN IN?

A. POST CAPILLARY VENULES
B. ARTERIOLES
C. VEINS
D. CAPILLARIES

to view all the 200 mcqs of AIIMS november 2008 click here

23 - immunoglobulins mcqs and faqs

1. Ig that crosses the placenta ?

Answer: Ig G .

2. Ig present in milk ?

Answer: Ig G and Ig A

3. Ig in seromucinous glands ?

Answer: Ig G and Ig A

4. Ig in primary immune response ?

Answer: Ig M

5. Ig in secondary immune response ?

Answer: Ig G

6. Ig with maximum molecular weight ?

Answer: Ig M

7. Ig with maximum sedimentation rate ?

Answer: Ig M

8. Ig with minimum sedimentation coefficient ?

Answer: Ig G

9. Blood group antibodies belong to which type of immunoglobulins ?

answer: Ig M

10. Rheumatoid factor belongs to which type of immunoglobulins ?

answer: Ig M ( antibody against Fc fragment of Ig G )

11. Immunoglobulin that is heat labile ?

answer: Ig E .

12. Immunoglobulin mediating the prausnitz kustner reaction ?

Answer: Ig E

13. Ig appearing first in life ?

Answer: Ig M

14. homocytotropism is seen in which Ig ?

answer: Ig E .

15. Ig with maximum serum concentration ?

Answer: Ig G

16. Ig with minimum serum concentration ?

Answer: Ig E

17. Ig with longest half life ?

Answer: Ig G

18. Ig with shortest half life ?

Answer: Ig E

19. Ig with maximum synthesis per day ?

Answer: Ig A

20. Ig with minimum synthesis per day ?

Answer: Ig E

21. Ig responsible for hypersensitivity pneumonitis ?

Answer: Ig G

22. binary exposure to an antigen results in sudden increase in ?

answer: Ig G

23. Ig to fix complements via classical pathway ?

Answer: Ig G1 and Ig M

24. Ig to fix complements via alternate pathway ?

Answer: Ig A , Ig D , Ig G4