NEET MDS Lessons
General Pathology
Osteomyelitis
This refers to inflammation of the bone and related marrow cavity almost always due to infection. Osteomyelitis can be acute or a chronic. The most common etiologic agents are pyogenic bacteria and Mycobacterium tuberculosis.
Pyogenic Osteomyelitis
The offending organisms reach the bone by one of three routes:
1. Hematogenous dissemination (most common)
2. Extension from a nearby infection (in adjacent joint or soft tissue)
3. Traumatic implantation of bacteria (as after compound fractures or orthopedic procedures). Staphylococcus aureus is the most frequent cause. Mixed bacterial infections, including anaerobes, are responsible for osteomyelitis complicating bone trauma. In as many as 50% of cases, no organisms can be isolated.
Pathologic features
• The offending bacteria proliferate & induce an acute inflammatory reaction.
• Entrapped bone undergoes early necrosis; the dead bone is called sequestrum.
• The inflammation with its bacteria can permeate the Haversian systems to reach the periosteum. In children, the periosteum is loosely attached to the cortex; therefore, sizable subperiosteal abscesses can form and extend for long distances along the bone surface.
• Lifting of the periosteum further impairs the blood supply to the affected region, and both suppurative and ischemic injury can cause segmental bone necrosis.
• Rupture of the periosteum can lead to an abscess in the surrounding soft tissue and eventually the formation of cutaneous draining sinus. Sometimes the sequestrum crumbles and passes through the sinus tract.
• In infants (uncommonly in adults), epiphyseal infection can spread into the adjoining joint to produce suppurative arthritis, sometimes with extensive destruction of the articular cartilage and permanent disability.
• After the first week of infection chronic inflammatory cells become more numerous. Leukocyte cytokine release stimulates osteoclastic bone resorption, fibrous tissue ingrowth, and bone formation in the periphery, this occurs as a shell of living tissue (involucrum) around a segment of dead bone. Viable organisms can persist in the sequestrum for years after the original infection.
Chronicity may develop when there is delay in diagnosis, extensive bone necrosis, and improper management.
Complications of chronic osteomyelitis include
1. A source of acute exacerbations
2. Pathologic fracture
3. Secondary amyloidosis
4. Endocarditis
5. Development of squamous cell carcinoma in the sinus tract (rarely osteosarcoma).
Tuberculous Osteomyelitis
Bone infection complicates up to 3% of those with pulmonary tuberculosis. Young adults or children are usually affected. The organisms usually reach the bone hematogenously. The long bones and vertebrae are favored sites. The lesions are often solitary (multifocal in AIDS patients). The infection often spreads from the initial site of bacterial deposition (the synovium of the vertebrae, hip, knee, ankle, elbow, wrist, etc) into the adjacent epiphysis, where it causes typical granulomatous inflammation with caseous necrosis and extensive
bone destruction. Tuberculosis of the vertebral bodies (Pott disease), is an important form of osteomyelitis.
Infection at this site causes vertebral deformity and collapse, with secondary neurologic deficits. Extension of the infection to the adjacent soft tissues with the development of psoas muscle abscesses is fairly common in Pott disease. Advanced cases are associated with cutaneous sinuses, which cause secondary bacterial infections. Diagnosis is established by synovial fluid direct examination, culture or PCR
Paroxysmal nocturnal haemoglobinuria (PNH).
Feature:
- Acquired RBC rnembrane defect rendering it susceptible to complement lysis.
- Features of intravascular haemolysis.
- Blood picture of haemolysis anemais with pancytopenia.
- Ham’s acid serum test (lysis at 37COin acid pH) + ve
Alzheimer’s disease
a. The most common cause of dementia in older people.
b. Characterized by degeneration of neurons in the cerebral cortex.
c. Histologic findings include amyloid plaques and neurofibrillary tangles.
d. Clinically, the disease takes years to develop and results in the loss of cognition, memory, and the ability to ommunicate. Motor problems, contractures, and paralysis are some of the symptoms at the terminal stage.
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
Parkinson’s disease
a. Characterized by the degeneration of neurons in the basal ganglia, specifically the substantia nigra and striatum.
b. Histologic findings in affected neurons include Lewy bodies.
c. Clinically, the disease affects involuntary and voluntary movements. Tremors are common. Symptoms include pin-rolling tremors, slowness of movements, muscular rigidity, and shuffling gait.
Haemolytic anaemia
Anemia due to increased red cell destruction (shortened life span)
Causes:
A. Corpuscular defects:
1.Membrane defects:
- Spherocytosis.
- Elliptocytosis.
2. Haemoglobinopathies:
- Sickle cell anaemia.
- Thalassaemia
- Hb-C, HBD, HbE.
3. Enzyme defects .deficiency of:
- GIucose -6 phosphate dehydrogenase (G6-PD)
- Pyruvate kinase
4. Paroxysmal nocturnal haemoglobinuria.
B. Extracorpusular mechanisms
1. Immune based:
- Autoimmune haemolytic anaemia.
- Haemolytic disease of new born.
- Incompatible transfusion.
- Drug induced haemolysis
2. Mechanical haemolytic anaemia.
3. Miscellaneous due to :
- Drugs and chemicals.
- Infections.
- Burns.
features of haemolytic anaemia
- Evidence of increased Hb breakdown:
-> Unconjugated hyperbilirubinaemia.
-> Decreased plasma haptoglobin.
-> Increased urobilinogen and stercobilinogen.
-> Haemoglobinaemia, haemoglobinuria and haemosiderinuria if Intravascular haemolysis occurs.
- Evidence or compensatory erythroid hyperplasia:
-> Reticulocytosis and nucleated RBC in peripheral smear.
-> Polychromasia and macrocytes
-> Marrow erythroid hyperplasia
-> Skull and other bone changes.
- Evidences of damage to RBC:
-> Spherocytes and increased osmotic fragility
-> Shortened life span.
-> Fragmented RBC.
-> Heinz bodies.
Infectious Mononucleosis
It is an Epstein Barr virus infection in children and young adults.
Features
-Constitutional symptoms.
-Sore throat.
-Lymphnode enlargement.
-Skin rashes
-Jaundice.
-Rarely pneumonia, meningitis and encephalitis.
Blood Picture
- Total count of I0,000. 20,000 /cu.mm.
- Lymphocytosis (50-90%) with atypical forms. They are larger with more cytoplasm which may be vacuolated or basophilic. Nucleus may be indented. with nucleoli (Downy type I to III).
- Platelets may be reduced.
- Paul Bunell test (for heterophil antibody against sheep RBC) is positive