NEET MDS Lessons
General Pathology
Autoimmune(acquired) Haemolytic anaemia
Auto antibodies are usually Ig g type (may be Ig M or Ig A). They may or may not bind complement and may be active in warm or cold temperature They may be complete (agggIutinating) or incomplete. Haemolysis s may be intravascular due to destruction of the antibody coated cells by RE system.
Causes:
a. Idiopathic
b. Secondary to
o Drugs - Methyldopa, Mefanamic acid
o Disease like
-> Infections especially viral.
-> Autoimmune disease especially SLE.
-> Lymphomas and chronic lymphatic leukaemia.
-> Tumours.
Diagnosis : is based on
• Evidences of haemolytic anaemia.
• Demonstration of antibodies
- On red cell surface by direct Coomb’s test
- In serum by indirect Coomb’s test.
Strep viridans
Mixed species, all causing α-hemolysis. All are protective normal flora which block adherence of other pathogens. Low virulence, but can cause some diseases:
Sub-acute endocarditis can damage heart valves.
Abscesses can form which are necrotizing. This is the primary cause of liver abscesses.
Dental caries are caused by Str. mutans. High virulence due to lactic acid production from glucose fermentation. This is why eating sugar rots teeth. Also have surface enzymes which deposit plaque.
Erythema multiforme is a hypersensitivity reaction to an infection (Mycoplasma), drugs or various autoimmune diseases.
- probable immunologic disease
- lesions vary from erythematous macules, papules, or vesicles.
- papular lesions frequently look like a target with a pale central area.
- extensive erythema multiforme in children is called Stevens-Johnson syndrome, where there is extensive skin and mucous membrane involvement with fever and respiratory symptoms.
Bronchiectasis
- Bronchiectasis is abnormal and irreversible dilatation of the bronchi and bronchioles (greater than 2 mm in diameter) secondary to inflammatory weakening of bronchial wall.
- Occur in childhood and early adult life
- Persistent cough with copious amount of foul smelling purulent sputum
Aetiopathogenesis
Bronchial wall destruction is due to:
- Endobronchial obstruction due to foreign body
- Infection due to local obstruction or impaired defence mechanism
Clinical conditions:
- Hereditary and congenital factors
- Obstruction
- Secondary complication
Hereditary and congenital factors:
- Congenital bronchiectasis due to developmental defects
- Cystic fibrosis causing defective secretion resulting in obstruction
- Hereditary immune defiency diseases
- Immotile cilia syndrome- immotile cilia of respiratory tract, sperms causing Kartagener’s syndrome (bronchiectasis, situs inversus and sinusitis) and male infertility
- Allergic bronchial asthma patients
Obstruction:
Localised variety in one part of bronchial system.
Obstruction can be due to
Foreign body
Endobronchial tumors
Hilar lymph nodes
Inflammatory scarring (TB)
Secondary complication:
Necrotizing pneumonia in Staph infection and TB
Morphologic changes
- Affects distal bronchi and bronchioles
- Lower lobes more frequently
- Lungs involved diffusely/segmentally
- Left lower lobe than right
- Pleura fibrotic & thickened adherent to chest wall
C/S lung: Honey-combed appearance
Microscopic examination:
Bronchiole-dilated
Bronchial epithelium-normal, ulcerated, squamous metaplasia
Bronchial wall-infiltration by ac & Ch inflammatory cells,
destruction of muscle, elastic tissue
Lung parenchyma-fibrosis, surrounding tissue pneumonia
Pleura-fibrotic and adherent
Immunohistochemistry
This is a method is used to detect a specific antigen in the tissue in order to identify the type of disease.
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
Cholecystitis
It is inflammation of the gall bladder. It may be acute or chronic.
In 80-90% of cases, it is associated with gall stones (Calcular cholecystis).
Causes and pathogenesis:-
Obstruction of cystic or common bile duct- By stones, strictures, pressure from the outside, tumors etc.
Obstruction , chemical irritation of the gall bladder, Secondary bacterial infection, stone formation, trauma to the wall of gall
bladder
Secondary bacterial infection
Usually by intestinal commensals E.coli, streptococcus fecalis. They reach the gall bladder by lymphatics.
S.typhi reaches the gall bladder after systemic infection
Acute cholecystitis
Gall bladder is enlarged edematous and fiery red in color.
- Wall is edematous, hyperemic, may show abscesses or gangrenous dark brown or green or black foci which may perforate.
Serous covering show fibrinosuppurative inflammation and exudation. Mucosa is edematous, hyperemic and ulcerated.
- If associated with stones, obstruction results in accumulation of pus leading to Empyaema of the gall bladder.
Fate:- Healing by fibrosis and adhesions.
Complications:-
- Pericholecystic abscess.
- Rupture leading to acute peritonitis.
- Ascending suppurative cholangitis and liver abscess
Chronic cholecystitis
May follow Acute cholecystitis or starts chronic. Gall stones are usually present.
Pathology
1. If associated with obstruction: Gall bladder is dilated. Wall may be thickened or thinned out. Contents may be clear, turbid or purulent.
2. If not associated with obstruction: - Gall bladder is contracted, wall is markedly thickened.
3. Serosa is smooth with fibrous adhesions. Draining lymph nodes are enlarged.
4. Wall is thickened, opaque and gray-white with red tinge.
5. Mucosa is gray- red with ulcerations and pouches.
6. Stones are usually present