Lymphomas

A. Hodgkin’s disease

1. Characterized by enlarged lymph nodes and the presence of Reed-Sternberg cells (multinucleated giant cells) in lymphoid tissues.

2. Disease spreads from lymph node to lymph node in a contiguous manner.

3. Enlarged cervical lymph nodes are most commonly the first lymphadenopathy observed.

4. The cause is unknown.

5. Occurs before age 30.

6. Prognosis of disease depends largely on the extent of lymph node spread and systemic involvement.

B. Non-Hodgkin’s lymphoma

1. Characterized by tumor formation in the lymph nodes.

2. Tumors do not spread in a contiguous manner.

3. Most often caused by the proliferation of abnormal B cells.

4. Occurs after age 40.

5. Example: Burkitt’s lymphoma

a. Commonly associated with an EpsteinBarr virus (EBV) infection and a genetic mutation resulting from the translocation of the C-myc gene from chromosome 8 to 14.

b. The African type occurs in African children and commonly affects the mandible or maxilla.

c. In the United States, it most commonly affects the abdomen.

d. Histologically, the tumor displays a  characteristic “starry-sky” appearance.

Cholecystitis 
 
It is inflammation of the gall bladder. It may be acute or chronic.
In 80-90% of cases, it is associated with gall stones (Calcular cholecystis). 

Causes and pathogenesis:-
Obstruction of cystic or common bile duct- By stones, strictures, pressure from the outside, tumors etc.
Obstruction , chemical irritation of the gall bladder, Secondary bacterial infection, stone formation, trauma to the wall of gall
bladder 

Secondary bacterial infection

Usually by intestinal commensals E.coli, streptococcus fecalis. They reach the gall bladder by lymphatics. 
S.typhi reaches the gall bladder after systemic infection

Acute cholecystitis

Gall bladder is enlarged edematous and fiery red in color. 
- Wall is edematous, hyperemic, may show abscesses or gangrenous dark brown or green or black foci which may perforate.
Serous covering show fibrinosuppurative inflammation and exudation. Mucosa is edematous, hyperemic and ulcerated.
- If associated with stones, obstruction results in accumulation of pus leading to Empyaema of the gall bladder.

Fate:-  Healing by fibrosis and adhesions.

Complications:-  
- Pericholecystic abscess.
- Rupture leading to acute peritonitis.
- Ascending suppurative cholangitis and liver abscess 

Chronic cholecystitis
May follow Acute cholecystitis or starts chronic. Gall stones are usually present. 

Pathology

1. If associated with obstruction: Gall bladder is dilated. Wall may be thickened or thinned out. Contents may be clear, turbid or purulent. 
2. If not associated with obstruction: - Gall bladder is contracted, wall is markedly thickened.
3. Serosa is smooth with fibrous adhesions. Draining lymph nodes are enlarged.  
4. Wall is thickened, opaque and gray-white with red tinge.
5. Mucosa is gray- red with ulcerations and pouches.
6. Stones are usually present

Clinical genetics (cytogenetics),

This is a method in which inherited chromosomal abnormalities in the germ cells or acquired chromosomal abnormalities in somatic cells are investigated using the techniques of molecular biology.

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.

Malnutrition

 A. Marasmus - calorie malnutrition 
 A child with marasmus suffers growth retardation and loss of muscle. The loss of muscle mass results from catabolism and depletion of the somatic protein compartment.
 With such losses of muscle and subcutaneous fat, the extremities are emaciated; by comparison, the head appears too large for the body. Anemia and manifestations of multivitamin deficiencies are present, and there is evidence of immune deficiency, particularly of T cell-mediated immunity. 
 B. Kwashiorkor - protein malnutrition - importance of protein quality as well as quantity
Marked protein deprivation is associated with severe loss of the visceral protein compartment, and the resultant hypoalbuminemia gives rise to generalized, or dependent, edema.

The weight of children with severe kwashiorkor is typically 60% to 80% of normal. 
However, the true loss of weight is masked by the increased fluid retention (edema).

Children with kwashiorkor have characteristic skin lesions, with alternating zones of hyperpigmentation, areas of desquamation, and hypopigmentation, giving a "flaky paint" appearance.

Hair changes include overall loss of color or alternating bands of pale and darker hair, straightening, line texture, and loss of firm attachment to the scalp.

An enlarged, fatty liver (resulting from reduced synthesis of carrier proteins) and a tendency to develop early apathy, listlessness, and loss of appetite. 

 The bone marrow in both kwashiorkor and marasmus may be hypoplastic, mainly because of decreased numbers of red cell precursors. How much of this derangement is due to a deficiency of protein and folates or to reduced synthesis of transferrin and ceruloplasmin is uncertain. Thus, anemia is usually present, most often hypochromic microcytic anemia, but a concurrent deficiency of folates may lead to a mixed microcytic-macrocytic anemia.
 
 
 C. Most cases of severe malnutrition are a combination of A and B usually characterized by:
 
• Failure of growth
• Behavioral changes
• Edema (kwashiorkor)
• Dermatosis
• Changes in hair
• Loss of appetite
• Liver enlargement
• Anemia
• Osteoporosis 
 

HYPERTROPHY
Increase in the size of an organ or tissue due to increase in the size of its Constituent cells.

1. Skeletal muscle due to -exercise.

2. Cardiac muscle of:
- Left ventricle in:
    o    Hypertension.
    o    Aortic valvular lesion.
    o    Severe anaemia.
- Right ventricle in :
    o    Mitral stenosis
    o    Cor pulmonale
    
3. Smooth muscle of:

- GIT proximal to strictures.
- Uterus in pregnancy.