NEET MDS Lessons
General Pathology
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.
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
Str. agalactiae
β-hemolytic, with its capsule being the major virulence factor. Capsule inhibits phagocytosis and complement activation. The CAMP factor (a hemolysin) is another virulence factor.
Group B strep are normally found in GI tracts and vaginas.
Major disease is neonatal sepsis/meningitis after passage through infected birth canal. May lead to meningitis, and CNS damage is high. Mothers colonized with Group B strep should be treated pre-delivery.
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
Nevus
1. Commonly known as moles.
2. A benign, pigmented tumor of melanocytes, found deep within connective tissue.
3. Types of skin nevi:
a. Junctional nevus—found in the epidermis.
It is the only type of nevus that may be considered to be premalignant.
b. Compound nevus—found in both the epidermis and underlying dermis.
c. Intraepidermal nevus—found in the dermis.
Staphylococcal aureus
- cutaneous infections
- furuncles (boils)
- carbuncles (more complicated furuncle with multiple sinuses)
- impetigo (often mixed with Streptococcus and has a more bullous appearance than crusted)
- hidradenitis suppurative (abscess of apocrine glands→e.g., axilla)
- nail bed (paronychial infection)
- postoperative wound or stitch abscess
- postpartum breast abscesses
toxin related skin rashes
- infants and young children develop toxic epidermal necrolysis or Ritter's syndrome (scalded baby syndrome)→large, red areas of denuded skin and generalized bulla formation.
- toxic shock syndrome (TSS) is due to a toxin producing strain of Staphylococcus aureus (bacteriophage induced) usually, but not exclusively in tampon wearing (hyperabsorbent type), menstruating women; 1-4 day prodrome of high fever, myalgias, arthralgias, mental confusion, diarrhea and on erythematous rash that occurs during or soon after menses; rash predominantly on hands and feet with eventual desquamation in 5-12 days.
Acute viral hepatitis
Clinical features. Acute viral hepatitis may be icteric or anicteric. Symptoms include malaise, anorexia, fever, nausea, upper abdominal pain, and hepatomegaly, followed by jaundice, putty-colored stools, and dark urine.
In HBV, patients may have urticaria, arthralgias, arthritis, vasculitis, and glomerulonephritis (because of circulating immune complexes). Blood tests show elevated serum bilirubin (if icteric), elevated transaminases, and alkaline phosphatase.
The acute illness usually lasts 4-6 weeks.
Pathology
(1) Grossly, there is an enlarged liver with a tense capsule.
(2) Microscopically, there is ballooning degeneration of hepatocytes and liver cell necrosis.