Gastrointestinal pathology MCQs – Useful for Pathology residents preparing for, NEET-SS/ DM- Oncopathology/ DM Histopathology, Fellowships, FRCPath- Histopathology and American Board of anatomic and clinical pathology (AP/CP) boards.
Nephrogenic rests are abnormally per sistent foci of embryonal cells (still pre sent after 36 weeks of gestation) that are potentially capable of developing into nephroblastoma (also called Wilms tumour). The presence of diffuse or multifocal nephrogenic rests is called nephroblastomatosis.
Nephrogenic rests are found in 25-40% of patients with nephroblastoma, and in approximately 1% of term infant autopsies.
Nephrogenic rests can be found adjacent to nephroblastoma or in the surrounding renal parenchyma. They are classified into perilobar and intralobar types.
Here are 5 differences between perilobar and intralobar nephrogenic rests.
Perilobar nephrogenic rests are peripherally located, wheras intralobar nephrogenic rests are randomly intermingled between the renal parenchyma, typically located in the central areas of the lobe.
2. DEMARCATION FROM ADJACENT PARENCHYMA
Perilobar nephrogenic rests are sharply demarcated from the surrounding tissue, whereas intralobar nephrogenic rests are poorly demarcated, usually infiltrate among native nephrons.
Perilobar nephrogenic rests have scanty stroma, whereas intralobar nephrogenic rests are and are composed mainly of stromal and epithelial elements.
Perilobar nephrogenic rests are usually multifocal whereas, intralobar nephrogenic rests are mostly unifocal (often single).
5. ASSOCIATED CONDITIONS
Perilobar nephrogenic rests are associated with hemihypertrophy and overgrowth syndromes such as Beckwith-Wiedemann syndrome. lntralobar nephrogenic rests are associated with Denys-Drash syndrome (which is associated with nephroblastoma, pseudohermaphrodit ism, glomerulopathy, and renal failure) and WAGR syndrome (Wilms tumour / nephroblastoma, aniridia, genitourinary anomalies, and mental retardation syndrome).
PERILOBAR AND INTRALOBAR NEPHROGENIC RESTSHISTOPATHOLOGICPICTURES.
DICER-1 SYNDROME IS A Rare Autosomal Dominant cancer syndrome Caused by inactivating germline mutations in genes encoding DICER-1. It is an RNase involved in the generation of mature miRNA.
CONDITIONS ASSOCIATED WITH DICER-1 SYNDROME.
1. PLEUROPULMONARY BLASTOMA:
Type I tumors are cyst -like tumors in the lung. They are most common in children aged 2 years and younger and have a good chance of recovery. …
Type II tumors are cyst-like with some solid parts. These tumors sometimes spread to the brain or other parts of the body.
Type III tumors are solid tumors
2. OVARIAN SERTOLI- LEYDIG CELL TUMOR:
Sertoli-Leydig cell tumor (SLCT) is a rare cancer of the ovaries. The cancer cells produce and release a male sex hormone called testosterone. The exact cause of this tumor is not known
3. CYSTIC NEPHROMA OF KIDNEY:
Cystic nephroma is a rare kidney neoplasm belonging to the entity of cystic tumours. It is a slow-growing tumour, which develops insidiously, sometimes reaching a considerable size. The diagnosis is more often accidental (except for mass syndrome in children). It is a benign tumour that may be treated by partial sparing nephrectomy
Multinodular Goiter (MNG) is defined as the special condition of thyroid glands, where there are multiple lumps (nodules) formed.
5. PITUTARY TUMOR:
Pituitary tumors are abnormal growths that develop in your pituitary gland. Some pituitary tumors result in too much of the hormones that regulate important functions of your body. Some pituitary tumors can cause your pituitary gland to produce lower levels of hormones.
6. OCULAR MEDULLOBLASTOMA:
Medulloblastoma is the commonest childhood malignant central nervous system tumour. It occurs in the midline of the cerebellum
7. EMBRYONAL RHABDOMYOSARCMA:
Embryonalrhabdomyosarcoma (ERMS) ERMS usually affects children in their first 5 years of life, but it can occur at older ages as well. ERMS tends to occur in the head and neck area, bladder, vagina, or in or around the prostate and testicles.
Pineoblastoma is more aggressive than other types of pineal gland tumors. Its fast growth usually causes cerebrospinal fluid (CSF) to build up in the brain. This condition is called hydrocephalus. While pineoblastoma may spread through the CSF in 10% to 20% of cases, most of the time the tumors do not spread to other parts of the body.
Vital, supravital and intravital staining are three different types of staining techniques. However, vital and supravital terms are often used interchangeably.
Let’s look at some of the major differences in staining between the three and why these terms shouldn’t be used interchangeably.
1. VITAL STAINING
1.Contrary to the name, vital stains are taken up by dead cells and not by living cells.
2. Demonstration of nuclear staining using a vital stain signifies cells death, because living cells are impermeable to the stain.
3. Example: Tryptan blue and propiodine iodine
VITAL STAINS ATE TOO BULKY OR TOO CHARGED THEY CANNOT ENTER LIVE CELLS- Hence only stain dead cells.
2. SUPRAVITAL STAINS
1. Supravital staining is a method of staining used in microscopy to examine living cells that have been removed from an organism.
2. Those that enter and stain living cells are called supravital stains
3. Examples New Methylene Blue and Brilliant Cresyl Blue for reticulocyte staining.
3. INTRAVITAL STAIN
1. Intravital staining of living cells is done by injecting the dye into any part of the animal body (either intravenous, intraperitoneal or subcutaneous), producing specific coloration of certain cells, particularly those of the reticulo-endothelial system.
2. Common dyes used are lithium, carmine and India ink.
Molecular progression of serous ovarian tumor. Borderline low and high grade
1.Molecular progression of low grade ovarian serous tumors. There is data to suggest progression from serous cystadenoma / cystadenofibroma with BRAF / KRAS mutations → SBT (serous borderline tumor) → LGSC (Low grade serous carcinoma) ; however, this is still controversial
2. Molecular progression of high grade serous ovarian tumors.
TP53 alterations in nearly all cases of high grade serous carcinoma
Germline, somatic or promoter hypermethylation (inactivation) of BRCA1 and BRCA2 in ~50% of cases
Gastrointestinal pathogens are very common in routine practice. It takes experience and keen observation to differentiate gastrointestinal pathogens from one another. In case of confusion, go with your ‘GUT’ feeling.
Lets look at a few differentiating features of Giardia lamblia, Cryptosporidium parvum and Isospora belli.
Pear shaped trophozoites with 2 ovoid nuclei, present in the luminal surface. They are 10-15 microns in length and 5-9 microns in width.
GIARDIA IS SEEN IN THE LUMINAL SURFACE
CRYPTOSPORIDIUM IS SEEN ATTACHED TO ENTEROCYTES LIKE SMALL BEADS.
2. CRYPTOSOPORIDIUM PARVUM
In tissue biopsies, 2 – 5 μm basophilic round bodies are seen protruding from the apex of enterocytes (“blue beads”) within the cell membrane. Parasites bulge out of apex of epithelial cells
ISOSPORA IS LARGEST AMONG THE THREE. IN CONTRAST TO GIARDIA AND CRYPTOSPORIDIUM – ISOSPORA DOES NOT HAVE AN APICAL LOCATION, INSTEAD LOCATED IN THE TIP OF VILLI.
3. ISOSPORA BELLI
Oocysts are generally ovoid to ellipsoid in shape, range from 10-40µm in length by 10-30µm in width. Cysts are present in PARASITO- PHOROUS VACUOLE. Does not have an apical location.