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 |
Sunday, October 18, 2009
28 - Types of Bodies in Pathology
Saturday, October 17, 2009
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.
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.
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.
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
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.
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.
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
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.
Friday, May 29, 2009
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.
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.
Thursday, March 12, 2009
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
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
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
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
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
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
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
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