NEET MDS Lessons
General Pathology
Post viral (post hepatitic) cirrhosis (15-20%)
Cause:- Viral hepatitis (mostly HBV or HCV)
Acute hepatitis → chronic hepatitis → cirrhosis.
Pathology
Liver is shrunken. Fatty change is absent (except with HCV). Cirrhosis is mixed.
M/E :-
Hepatocytes-show degeneration, necrosis as other types of cirrhosis.
Fibrous septa -They are thick and immature (more cellular and vascular).
- Irregular margins (piece meal necrosis).
- Heavy lymphocytic infiltrate.
Prognosis:- - More rapid course than alcoholic cirrhosis.Hepatocellular carcinoma is more liable to occur
Psoriasis
1. Characterized by skin lesions that appear as scaly, white plaques.
2. Caused by rapid proliferation of the epidermis.
3. Autoimmune pathogenesis; exact mechanism is unclear.
Agranulocytosis. Severe neutropenia with symptoms of infective lesions.
Drugs. are an important cause and the effect may be due to .
-Direct toxic effect.
-Hypersensitivity.
Some of the 'high risk drugs are.
-Amidopyrine.
-Antithyroid drugs.
-Chlorpromazine, mapazine.
-Antimetabolites and other drugs causing pancytopenia.
Bloodpicture: Neutropenia with toxic granules in neutrophils. Marrow shows decrease in granulocyte precursors with toxic granules in them.
Rheumatic fever
Before antibiotic therapy, this was the most common cause of valvular disease.
1. Usually preceded by a group A streptococci respiratory infection; for example, strep throat.
2. All three layers of the heart may be affected. The pathologic findings include Aschoff bodies, which are areas of focal necrosis surrounded by a dense inflammatory infiltration.
3. Most commonly affects the mitral valve, resulting in mitral valve stenosis, regurgitation, or both.
Chronic lymphocytic leukaemia
Commoner in middle age. It starts insidiously and often runs a long chronic course
Features:
- Lymphnode enlargement.
- Anaemia (with haemolytic element).
- Moderate splenomegaly.
- Haemorrhagic tendency in late stages.
- Infection.
Blood picture:
- Anaemia with features of haemolytic anaemia
- Total leucocytic count of 50-100,OOO/cu.mm.
- Upto 90-95% cells are lymphocytes and prolymphocytes.
- Thrombocytopenia may be seen.
Bone marrow. Lymphocytic series cells-are seen. Cells of other series are reduced,
Osteogenesis Imperfecta (OI) (Brittle bone diseases)
It is a group of hereditary disorders caused by gene mutations that eventuate in defective synthesis of and thus premature degradation of type I collagen. The fundamental abnormality in all forms of OI is too little bone, resulting in extreme susceptibility to fractures. The bones show marked cortical thinning and attenuation of trabeculae.
Extraskeletal manifestations also occur because type I collagen is a major component of extracellular matrix in other parts of the body. The classic finding of blue sclerae is attributable to decreased scleral collagen content; this causes a relative transparency that allows the underlying choroid to be seen. Hearing loss can be related to conduction defects in the middle and inner ear bones, and small misshapen teeth are a result of dentin deficiency
Congenital heart defect
Congenital heart defects can be broadly categorised into two groups,
o acyanotic heart defects ('pink' babies) :
An acyanotic heart defect is any heart defect of a group of structural congenital heart defects, approximately 75% of all congenital heart defects.
It can be subdivided into two groups depending on whether there is shunting of the blood from the left vasculature to the right (left to right shunt) or no shunting at all.
Left to right shunting heart defects include
- ventricular septal defect or VSD (30% of all congenital heart defects),
- persistent ductus arteriosus or PDA,
- atrial septal defect or ASD,
- atrioventricular septal defect or AVSD.
Acyanotic heart defects without shunting include
- pulmonary stenosis, a narrowing of the pulmonary valve,
- aortic stenosis
- coarctation of the aorta.
cyanotic heart defects ('blue' babies).
obstructive heart defects
cyanotic heart defect is a group-type of congenital heart defect. These defects account for about 25% of all congenital heart defects. The patient appears blue, or cyanotic, due to deoxygenated blood in the systemic circulation. This occurs due to either a right to left or a bidirectional shunt, allowing significant proportions of the blood to bypass the pulmonary vascular bed; or lack of normal shunting, preventing oxygenated blood from exiting the cardiac-pulmonary system (as with transposition of the great arteries).
Defects in this group include
hypoplastic left heart syndrome,
tetralogy of Fallot,
transposition of the great arteries,
tricuspid atresia,
pulmonary atresia,
persistent truncus arteriosus.