NEET MDS Lessons
General Pathology
Biliary cirrhosis(16%)
It is due diffuse chronic cholestaisis (obstruction of the biliary flow) leading to damage and scarring all over the liver. Two types are known
1. Primary biliary cirrhosis and
2. Secondary biliary cirrhosis.
Primary biliary cirrhosis
It is destructive chronic inflammation of intrahepatic bile ductules and small ducts leading to micronodular cirrhosis.
-Typically affects middle aged women.
- Patients present with fatigue, pruritis and eventually, jaundice.
Cause:- Autoimmune. Patients have autoantibodies directed against mitochondrial enzymes (AMA).
Pathology:-
Liver is enlarged, dark green in color (cholestaisis). Cirrhosis is micronodular.
M/E :-
- Early, portal tracts show lymphocytes and plasma cell infiltrate the bile ducts and destroy them.
- Granulomatous inflammation surrounding the damaged and inflamed bile ducts is the hallmark of (PBC).
- Cholestatic changes such as bile ductular proliferation, periportal Mallory’s hyaline and increased copper in periportal hepatocytes.
- In the end stage disease, micro nodular cirrhosis occurs and the inflammatory changes subside
Secondary biliary cirrhosis:-
It is extra hepatic (surgical) cholestaisis due to prolonged extra hepatic major bile duct obstruction.
Causes - Obstruction of hepatic or common bile duct by:
- Congenital biliary atresia.
- Pressure by enlarged LN or tumor * Biliary stones.
- Carcinoma of the bile duct, ampulla of Vater or pancreatic head
Effects of obstruction:-
Complete obstruction leads to back pressure all over the biliary tract
- damage by inspessated bile
- inflammation and scarring.
Incomplete obstruction leads to acute suppurative cholangitis and cholangiolitis.
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
HERPES ZOSTER (Shingles)
An infection with varicella-zoster virus primarily involving the dorsal root ganglia and characterized by vesicular eruption and neuralgic pain in the dermatome of the affected root ganglia.
caused by varicella-zoster virus
Symptoms and Signs
Pain along the site of the future eruption usually precedes the rash by 2 to 3 days. Characteristic crops of vesicles on an erythematous base then appear, following the cutaneous distribution of one or more adjacent dermatomes
Eruptions occur most often in the thoracic or lumbar region and are unilateral. Lesions usually continue to form for about 3 to 5 days
Geniculate zoster (Ramsay Hunt's syndrome) results from involvement of the geniculate ganglion. Pain in the ear and facial paralysis occur on the involved side. A vesicular eruption occurs in the external auditory canal, and taste may be lost in the anterior two thirds of the tongue
Ichthyosis vulgaris is a genetic disease characterized by increased cohesiveness of the cells in the stratum corneum, resulting up in a piling up stratum corneum (scales like a fish).
DIPHTHERIA
An acute, contagious disease caused by Corynebacterium diphtheriae, characterized by the formation of a fibrinous pseudomembrane, usually on the respiratory mucosa, and by myocardial and neural tissue damage secondary to an exotoxin.
Cutaneous diphtheria (infection of the skin) can occur when any disruption of the integument is colonized by C. diphtheriae. Lacerations, abrasions, ulcers, burns, and other wounds are potential reservoirs of the organism. Skin carriage of C. diphtheriae is also a silent reservoir of infection.
Pathology
C. diphtheriae may produce exotoxins lethal to the adjacent host cells. Occasionally, the primary site is the skin or mucosa elsewhere. The exotoxin, carried by the blood, also damages cells in distant organs, creating pathologic lesions in the respiratory passages, oropharynx, myocardium, nervous system, and kidneys.
The myocardium may show fatty degeneration or fibrosis. Degenerative changes in cranial or peripheral nerves occur chiefly in the motor fibers
In severe cases, anterior horn cells and anterior and posterior nerve roots may show damage proportional to the duration of infection before antitoxin is given. The kidneys may show a reversible interstitial nephritis with extensive cellular infiltration.
The diphtheria bacillus first destroys a layer of superficial epithelium, usually in patches, and the resulting exudate coagulates to form a grayish pseudomembrane containing bacteria, fibrin, leukocytes, and necrotic epithelial cells. However, the areas of bacterial multiplication and toxin absorption are wider and deeper than indicated by the size of the membrane formed in the wake of the spreading infection.
THE ADRENAL GLANDS
ADRENAL CORTEX
The adrenal cortex synthesizes three different types of steroids:
1. Glucocorticoids (principally cortisol), which are synthesized primarily in the zona fasciculata
2. Mineralocorticoids, the most important being aldosterone, which is generated in the zona glomerulosa; and
3. Sex steroids (estrogens and androgens), which are produced largely in the zona reticularis.
ADRENAL MEDULLA
The adrenal medulla is populated by cells derived from the neural crest (chromaffin cells) and their supporting (sustentacular) cells.
They secrete catecholamines in response to signals from preganglionic nerve fibers inthe sympathetic nervous system.
Plasma Cell Pathology
A. Multiple myeloma
1. Plasma cell neoplasm that results in the proliferation of monoclonal plasma cells. These tumor cells produce nonfunctional immunoglobulins.
2. Laboratory findings include:
a. Monoclonal IgG spike.
b. Bence-Jones proteins found in urine.
3. Radiographic findings: characteristic “punched-out” radiolucencies in bones.