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.
Pneumoconioses—are environmentally related lung diseases that result from chronic inhalation of various substances.
1. Silicosis (stone mason’s disease)
a. Inhalant: silica dust.
b. Associated with extensive fibrosis of the lungs.
c. Patients have a higher susceptibility to tuberculosis infections.
2. Asbestosis
a. Inhalant: asbestos fibers.
b. Associated with the presence of pleural plaques.
c. Consequences include:
(1) Mesothelioma (malignant mesothelial tumor).
(2) Bronchogenic carcinoma.
3. Anthracosis
a. Inhalant: carbon dust.
b. Usually not as harmful as silicosis or asbestosis.
c. Associated with the presence of macrophages containing carbon.
Bacterial meningitis (pyogenic, suppurative infections)
1. Common causes include:
a. Escherichia coli in newborns.
b. Haemophilus influenzae in infants and children.
c. Neisseria meningitides in young adults.
d. Streptococcus pneumoniae and Listeria monocytogenes in older adults.
Clinical findings include severe headache, irritability, fever, and a stiff neck.
a. A spinal tap shows CSF fluid that is cloudy or purulent and is under increased pressure. There is also an increase in protein and a decrease in glucose levels.
3. Can be fatal if left untreated.
Megaloblastic anaemia
Metabolism: B12(cyanocobalamin) is a coenzyme in DNA synthesis and for maintenance of nervous system. Daily requirement 2 micro grams. Absorption in terminal ileum in the presence gastric intrinsic factor. It is stored in liver mainly-
Folic acid (Pteroylglutamic acid) is needed for DNA synthesis.. Daily requirement 100 micro grams. Absorption in duodenum and jejunum
Causes of deficiency .-
- Nutritional deficiency-
- Malabsorption syndrome.
- Pernicious anaemia (B12).
- Gastrectomy (B12).
- Fish tapeworm infestation (B12).
- Pregnancy and puerperium (Folic acid mainly).
- Myeloproliferative disorders (Folic acid).
- Malignancies (Folic acid).
- Drug induced (Folic-acid)
Features:
(i) Megaloblastic anaemia.
(ii) Glossitis.
(iii) Subacute combined degeneration (in B12deficiency).
Blood picture :
- Macrocytic normochromic anaemia.
- Anisocytosis and poikilocytosis with Howell-Jolly bodies and basophilic stippling.
- Occasional megalo blasts may be-seen.
- Neutropenia with hypersegmented neutrophills and macropolycytes.
- Thrombocytopenia.
- Increased MVC and MCH with normal or decreased MCHC.
Bone marrow:
- Megaloblasts are seen. They are larger with a more open stippled chromatin. The nuclear maturation lags behind. the cytoplasmic maturation. Maturation arrest is seen (more of early forms).
- Immature cells of granulocyte series are also larger.
-Giant stab forms (giant metamyelocytes).
Hepatitis D virus—can only infect cells previously infected with hepatitis B.
Delta hepatitis (HDV) is associated with a 35-nm RNA virus composed of a delta antigen-bearing core surrounded by HBV's Ag coat;
HDV requires HBV for replication.
Delta hepatitis can cause quiescent HBV states to suddenly worsened . Its transmission is the same as that of HBV.
Hepatitis E virus—a high mortality rate in infected pregnant women.
Hepatitis E (HEV) is caused by a single-stranded RNA virus. The disease is typically self-limited and does not evolve into chronic hepatitis; it may, however, be cholestatic.
Pregnant women may develop fulminant disease.
Transmission is by the fecal oral route.
HEV occurs mainly in India, Nepal, Pakistan, and Southeast Asia.
THE THYROID GLAND
The thyroid gland develops embryologically from the developing pharyngeal epithelium that descends from the foramen cecum at the base of the tongue to its normal position in the anterior neck. This pattern of descent explains the occasional presence of ectopic thyroid tissue, most commonly located at the base of the tongue (lingual thyroid) or at other sites abnormally high in the neck.
Pemphigoid
1. Ulcerative lesions on the skin and oral mucosa.
2. An autoimmune disease in which patients have autoantibodies against basal cells (desmosome attachment to the basement membrane).
3. Histologically, the entire epithelium appears to separate from the connective tissue. There is no acantholysis.
4. A positive Nikolsky sign is observed.
5. Complications include blindness, due to ocular lesions present in some patients.
6. Treatment: corticosteroids.