DYSPLASIA
 It is disturbed growth or  cells in regard to their size, shape arrangement. In its mild degrees it represents a reversible reaction to chronic inflammation whereas the most severe degrees warrant a labelling of intraepithelial neoplasia. Hence it includes a wide spectrum of changes ranging from a reversible disorientation to 'carcinoma-in-situ'.

Histologically it is characterized by:

o    Basal cell hyperplasia.
o    Variation in size and shape of cells.
o    Disorderly maturation.
o    Increased mitotic activity.
o    Disorientation of arrangement of cells (loss of polarity)

Dysplasia is commonly seen in:

o    Squamous epithelium of cervix.
o    Bronchial epithelium in habitual smokers.
o    Gastric and colonic mucosa in long standing inflammation
o    Oral and vulval leucoplakia
 

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.

Hereditary spherocytosis.

Functionally normal cells which are destroyed .in spleen because of the structural abnormality. It is transmitted as an autosomal dominant trait 

Congenital hemolytic anemia due to genetically determined abnormal spectrin and ankyrin molecules, leading to defects in red blood cell membrane, causing spherical shape and lack of plasticity
Red blood cells become trapped within spleen and have less than usual 120 day lifespan
Splenic function is normal
Osmotic fragility: increased; basis for diagnostic testing 

Description

Firm, deep red tissue, thin capsule, no grossly identifiable malpighian follicles, 100-1000g
Peripheral blood images
Marked congestion in cords
Sinuses appear empty but actually contain ghost red blood cells
May have prominent endothelial lined sinuses, hemosiderin deposition, erythrophagocytosis

Primary vs. secondary disorders - Most nutritional disorders in developed countries are not due to simple dietary deficiencies but are rather a secondary manifestation of an underlying primary condition or disorder.

• Chronic alcoholism
• Pregnancy and lactation
• Renal dialysis
• Eating disorders
• Prolonged use of diuretics
• Malabsorption syndromes
• Neoplasms
• Food fads
• Vegans
• AIDS 

Nephrosclerosis
 Disease of the renal arteries.

 Clinical manifestations:
 (1) Benign (arterial) nephrosclerosis →  Caused by the formation of atherosclerotic plaques in the renal artery. Results in narrowing of the arterioles.

(2) Malignant nephrosclerosis → Caused by malignant hypertension. Common signs of malignant hypertension include severe hypertension, retinal hemorrhages, and hypertrophy of the left ventricle. Results in inflammatory changes in the vascular walls, which may lead to rupture of the glomerular capillaries.

Cholelithiasis (Biliary calculi)
- These are insoluble material found within the biliary tract and are formed of bile constituents (cholesterol, bile pigments and calcium salts). 

Sites: - -Gall bladder, extra hepatic biliary tract.  Rarely, intrahepatic biliary tract. 

Predisposing factors:- 
- Change in the composition of bile. - It is the disturbance of the ratio between cholesterol and lecithin or bile salts which may be due to Hypercholesterolaemia which may be hereditary or the 4 F (Female, Forty, Fatty, Fertile). Drugs as clofibrate and exogenous estrogen. High intake of calories (obesity).
Increased concentration of bilirubin in bile- pigment stones
Hypercalcaemia:- Calcium carbonate stones.

2- Staisis.
3- Infection. 

Pathogenesis   i- Nucleation or initiation of stone formation:- The nidus may be cholesterol “due to supersaturation” Bacteria, parasite
RBCs or mucous.  
ii- Acceleration:- When the stone remains in the gall bladder, other constituents are added to the
nidus to form the stone. 

Complications of gall stones:- 
- Predispose to infection.- Chronic irritation leading to 
a. Ulceration       b. Squamous metaplasia & carcinoma.