NEET MDS Lessons
General Pathology
Cartilage-Forming Tumors
1. Osteochondroma (Exostosis) is a relatively common benign cartilage-capped outgrowth attached by a bony stalk to the underlying skeleton. Solitary osteochondromas are usually first diagnosed in late adolescence and early adulthood (male-to-female ratio of 3:1); multiple osteochondromas become apparent during childhood, occurring as multiple hereditary exostosis, an autosomal dominant disorder. Inactivation of both copies of the EXT gene (a tumor suppressor gne) in chondrocytes is implicated in both sporadic and hereditary osteochondromas. Osteochondromas develop only in bones of endochondral origin arising at the metaphysis near the growth plate of long tubular bones, especially about the knee. They tend to stop growing once the normal growth of the skeleton is completed. Occasionally they develop from flat bones (pelvis, scapula, and ribs). Rarely, exostoses involve the short tubular bones of hands and feet.
Pathological features
• Osteochondromas vary from 1-20cm in size.
• The cap is benign hyaline cartilage.
• Newly formed bone forms the inner portion of the head and stalk, with the stalk cortex merging with cortex of the host bone.
Osteochondromas are slow-growing masses that may be painful. Osteochondromas rarely progress to chondrosarcoma or other sarcoma, although patients with the multiple hereditary exostoses are at increased risk of malignant transformation.
2. Chondroma
It is a benign tumor of hyaline cartilage. When it arises within the medullary cavity, it is termed enchondroma; when on the bone surface it is called juxtacortical chondroma. Enchondromas are usually diagnosed in persons between ages 20 and 50 years; they are typically solitary and located in the metaphyseal region of tubular bones, the favored sites being the short tubular bones of the hands and feet. Ollier disease is characterized by multiple chondromas preferentially involving one side of the body. Chondromas probably develop from slowly proliferating rests of growth plate cartilage.
Pathological features
• Enchondromas are gray-blue, translucent nodules usually smaller than 3 cm.
• Microscopically, there is well-circumscribed hyaline matrix and cytologically benign chondrocytes.
Most enchondromas are detected as incidental findings; occasionally they are painful or cause pathologic fractures. Solitary chondromas rarely undergo malignant transformation, but those associated with enchondromatosis are at increased risk.
3. Chondrosarcomas are malignant tumors of cartilage forming tissues. They are divided into conventional chondrosarcomas and chondrosarcoma variants. Each of these categories comprises several distinct types, some defined on microscopic grounds & others on the basis of location within the affected bone, for e.g. they are divided into central (medullary), peripheral (cortical), and juxtacortical (periosteal). The common denominator of chondrosarcoma is the production of a cartilaginous matrix and the lack of direct bone formation by the tumor cells (cf osteosarcoma). Chondrosarcomas occur roughly half as frequently as osteosarcomas; most patients age 40 years or more, with men affected twice as frequently as women
Pathological features
Conventional chondrosarcomas arise within the medullary cavity of the bone to form an expansile glistening mass that often erodes the cortex. They exhibit malignant hyaline or myxoid stroma. Spotty calcifications are typically present. The tumor grows with broad pushing fronts into marrow spaces and the surrounding soft tissue. Tumor grade is determined by cellularity, cytologic atypia, and mitotic activity. Low-grade tumors resemble normal cartilage. Higher grade lesions contain pleomorphic chondrocytes with frequent mitotic figures with multinucleate cells and lacunae containing two or more chondrocytes. Dedifferentiated chondrosarcomas refers to the presence of a poorly differentiated sarcomatous component at the periphery of an otherwise typical low-grade chondrosarcoma. Other histologic variants include myxoid, clear-cell and mesenchymal chondrosarcomas. Chondrosarcomas commonly arise in the pelvis, shoulder, and ribs. A slowly growing lowgrade tumor causes reactive thickening of the cortex, whereas a more aggressive high-grade neoplasm destroys the cortex and forms a soft tissue mass. There is also a direct correlation between grade and biologic behavior.
Size is another prognostic feature, with tumors larger than 10 cm being significantly more aggressive than smaller tumors. High-grade Chondrosarcomas metastasize hematogenously, preferentially to the lungs and skeleton.
OEDEMA
Excessive accumulation of fluid in the extra vascular compartment (intersttitial tissues). This includes ascites (peritoneal sac), hydrothorax (pleural cavity) hydropericardium (pericardial space) and anasarca (generalised)
Factors which tend to accumulate interstitial fluid are:
- Intravascular hydrostatic pressure
- Interstitial osmotic pressure.
- Defective lymphatic drainage.
- Increased capillary permeability.
Factors that draw fluid into circulation are:
- Tissue hydrostatic-pressure (tissue tension).
- Plasma osmotic pressure,
Oedema fluid can be of 2 types:
A. Exudate.
It is formed due to increased capillary permeability as in inflammation.
B. Transudate
Caused by alterations of hydrostatic and osmotic pressures.
|
|
Exudate |
Transudate |
|
Specific Gravity |
>1.018 |
1.012 |
|
Protein Content |
High |
Low |
|
Nature of Protein |
All Plasma Protein |
Albumin mostly |
|
Spontaneous Clotting |
High(Inflammatory Cells) |
Low |
Local Oedema
1. Inflammatory oedema. Mechanisms are.
- Increased capillary permeability.
- Increased vascular hydrostatic pressure.
- Increased tissue osmotic pressure.
2.Hypersensitivity reactions especially types I and III
3. Venous obstruction :
- Thrombosis.
- Pressure from outside as in pregnancy, tourniquets.
4. Lymphatic obstruction:
- Elephantiasis in fillariasis
- Malignancies (Peau de orange in breast cancer).
Generalized Oedema
1. Cardiac oedema
Factors :Venous pressure increased.
2. Renal oedema
- Acute glomerulonephritis
- Nephrotic syndrome
3. Nutritional (hypoproteinaemic) oedema. it is seen in
- Starvation and Kwashiorkor
- Protein losing enteropathy
4. Hepatic oedema (predominantly ascites)
Factors:
- Fall in plasma protein synthesis
- Raised regional lymphatic and portal venous pressure
5. Oedema due to adrenal corticoids
As in Cushing's Syndrome
Pulmonary oedema
- Left heart failure and mitral stenosis.
- Rapid flv infusion specially in a patient of heart failure.
Hepatitis B virus (“serum hepatitis”)
- Hepatitis B (HBV) may cause acute hepatitis, a carrier state, chronic active disease, chronic persistent disease, fulminant hepatitis, or hepatocellular carcinoma
- It is caused by a DNA virus, the virions are called Dane particles.
b. Incubation period: ranges from 4 to 26 weeks, but averages 6 to 8 weeks.
a. Symptoms last 2 to 4 weeks, but may be asymptomatic.
c. The hepatitis B viral structure has also been named the Dane particle.
Transmission is through contact with infected blood or other body fluids. It can be transmitted by sexual intercourse and is frequently transmitted to newborns of infected mothers by exposure to maternal blood during the birth process
- Associated antigens include core antigen (HBcAg) and surface antigen (HBsAg).
The latter is usually identified in the blood for diagnosis. HbsAg is the earliest marker of acute infection.
HBeAg is also associated with the core. Its presence indicates active acute infection; when anti-HBeAg appears, the patient is no longer infective
- HBV is associated with hepatocellular carcinoma; HBsAg patients have a 200-fold greater risk of hepatocellular carcinoma than subjects who have not been exposed.
Antibodies
- Antibodies to surface antigen (anti-HBs) are considered protective and usually appear after the disappearance of the virus.
-Antibodies to HBcAg are not protective. They are , detected just after the appearance of HBsAg and are used to confirm infection when both HBsAg and anti HBs are absent (window).
- Antibodies to HBeAg are associated with a low risk of infectivity.
d. Infection increases the risk for hepatocellular carcinoma.
e. Laboratory assay of hepatitis B antigens and antibodies:
(1) HBsAg—present only in acute infection or chronic carriers.
(2) HBsAb—detectable only after 6 months post-initial infection. HBsAb is present in chronic infections or vaccinated individuals. Note: HBsAb is also being produced during acute infections and in chronic carriers; however, it is not detectable via current laboratory methods.
(3) HBcAg—present in either acute or chronic infection.
(4) HBeAg—present when there is active viral replication. It signifies that the carrier is highly infectious.
(5) HBeAb—appears after HBeAg. It signifies that the individual is not as contagious.
f. Vaccine: contains HBsAg.
g. Prevention: immunoglobulins (HBsAb) are available.
STREPTOCOCCAL INFECTIONS
Most streptococci are normal flora of oropharynx
Group A streptococci: Str. pyogenes
Group B streptococci: Str. agalactiae
Str. pneumoniae
Strep viridans group
Group D: Enterococcus (lately Strep. Fecalis and E. fecium), causes urinary tract infections,
Seborrheic keratosis
1. A round, brown-colored, flat wart.
2. Most often seen in middle-aged to older adults.
3. A benign lesion.
Acute viral hepatitis
Clinical features. Acute viral hepatitis may be icteric or anicteric. Symptoms include malaise, anorexia, fever, nausea, upper abdominal pain, and hepatomegaly, followed by jaundice, putty-colored stools, and dark urine.
In HBV, patients may have urticaria, arthralgias, arthritis, vasculitis, and glomerulonephritis (because of circulating immune complexes). Blood tests show elevated serum bilirubin (if icteric), elevated transaminases, and alkaline phosphatase.
The acute illness usually lasts 4-6 weeks.
Pathology
(1) Grossly, there is an enlarged liver with a tense capsule.
(2) Microscopically, there is ballooning degeneration of hepatocytes and liver cell necrosis.
Lymphocytosis:
Causes
-Infections in children and the neutropenic infections in adults.
-Lymphocytic leukaemia.
-Infectious mononucleosis.
-Toxdplasmosis.
-Myast'henia gravis.