NEET MDS Lessons
General Pathology
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.
Pyelonephritis
- A bacterial infection that affects the renal tubules, interstitium, and renal pelvis.
- One of the most common renal diseases.
- Usually caused by gram-negative, rod-shaped bacteria that are part of the normal flora of the enteric tract. Most commonly caused by Escherichia coli, followed by Proteus, Klebsiella, and Enterobacter.
- The infecting bacteria are usually from the patient’s own enteric flora an example of an endogenous infection.
- Usually associated with a urinary tract infection (acute pyelonephritis) or involved with another precipitating condition, such as obstruction (chronic pyelonephritis).
Infections caused by N. meningiditis
1. Bacteremia without sepsis. Organism spreads to blood but no major reaction.
2. Meningococcemia without meningitis. Fever, headache, petechia, hypotension, disseminated intravascular coagulation. The Waterhouse-Friderichsen Syndrome is a rapid, progressive meningococcemia with shock, organ failure, adrenal necrosis, and death.
3. Meningitis with meningococcemia. Sudden onset fever, chills, headache, confusion, nuchal rigidity. This occurs rapidly.
4. Meningoencephalitis. Patients are deeply comatose.
Diagnosis made by examining CSF.
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
Erythema nodosum is the MCC of inflammation of subcutaneous fat (panniculitis).
- it may be associated with tuberculosis, leprosy, certain drugs (sulfonamides), and is commonly a harbinger of coccidioidomycosis and sarcoidosis.
- commonly presents on the lower extremities with exquisitely tender, raised erythematous plaques and nodules.
- self-limited disease.
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.
Str. Pneumoniae
Probably the most important streptococci. Primary cause of pneumonia. Usually are diplococci. Ste. pneumoniae are α-hemolytic and nutritionally fastidious. Often are normal flora.
Key virulence factor is the capsule polysaccharide which prevents phagocytosis. Other virulence factors include pneumococcal surface protein and α-hemolysin.
Major disease is pneumonia, usually following a viral respiratory infection. Characterized by fever, cough, purulent sputum. Bacteria infiltrates alveoli. PMN’s fill alveoli, but don’t cause necrosis. Also can cause meningitis, otitis, sinusitis.
There are vaccines against the capsule polysaccharide. Resistance to penicillin, cephalosporins, erythromycins, and fluoroquinalones is increasing.