Man is what he thinks he is …
Pathology of Tuberculosis
Dr. Venkatesh M. Shashidhar Senior Lecturer in Pathology Fiji School of Medicine
Introduction:
Infects one third of world population..! 3 million deaths due to TB every year Under privileged population over crowding, malnutrition
Since 1985 incidence is increasing in west
AIDS, Diabetes, Immunosuppressed patients. Drug resistance
Microbiology of TB:
M. tuberculosis (air) & M. bovis (milk)
Aerobic, no toxins, no spore, non motile
Mycolic acid in bacterial wall - Acid & Alcohol fast (AFB) M. avium, M.intracellulare in AIDS Atypical tuberculosis.
AFB - Ziehl-Nielson stain
Pathogenesis of TB:
Type IV hypersensitivity - Granuloma
Escape killing by macrophages
Mycolic acid wax coat
Cord Factor - surface glycolipid
Tuberculous Granuloma 1. Rounded outlines.
2. Central Caseous necrosis. 3. Transformed macrophages
called epithelioid cells.
4. Lymphocytes, plasma cells,
and fibroblasts.
5. Langhans giant cells.
Tuberculous Granuloma
Primary Tuberculosis
In Non Immunized individuals (Children) Primary Tuberculosis:
Self Limited disease Ghons complex or Primary complex.
Primary Progressive TB
10% of adults, Immunosuppressed individuals Common in malnourished children Miliary TB and Meningitis.
Secondary Tuberculosis:
Post Primary in immunized individuals.
Reactivation or Reinfection
Apical lobes or upper part of lower lobes
Caseation, cavity - soft granuloma
Pulmonary or extra-pulmonary Local or systemic/Miliary
Primary or Ghon’s Complex
Primary tuberculosis is the pattern seen with initial infection with tuberculosis in children. Reactivation, or secondary tuberculosis, is more typically seen in adults.
Ghon Complex
Cavitary Tuberculosis
When soft, necrotic center drain out leave behind a cavity. Cavitation is typical for large granulomas.
Cavitation is more common in the reactivation tuberculosis seen in upper lobes.
Tuberculous Granulomas
Caseation Necrosis
Epitheloid cells in Granuloma
Systemic Miliary TB
Adrenal TB - Addison Disease
Spinal TB - Potts Disease
Miliary Tuberculosis
Extensive infection Hematogenous spread Low immunity
Pulmonary or Systemic types.
PPD Testing
PPD Testing
“Life’s battles don’t go always to the stronger or faster man,
But sooner or later, The man who wins is the man who thinks he can”.
Lung Tumours
Dr. Venkatesh M. Shashidhar
Senior Lecturer in Pathology Fiji School of Medicine
Lung Cancer:
Most common visceral malignancy. Top public enemy in western world. 3rd of all cancer deaths due to lung cancer. Significant increase in incidence. Dramatic increase among females – 90% of lung cancers are related to smoking..! (passive smoking in 5%)
Lung Cancer & Smoking:
Depends on duration, amount of daily smoking & deep inhaling.
10 fold greater risk than non smokers. 20 fold risk if >40cigarettes per day
Atypical cells in 96.7% of smokers compared to 0.9% in non smokers. Significant proportion of over 1200 substances in smoke are carcinogenic. (not nicotine)
Initiaters – Benzo[o]pyrenes Promoters – Phenol derivatives Radioactive substances – Polonium, C14, K40
Classification (Bronchogenic Carcinoma):
Squamous cell carcinoma Adenocarcinoma
Brochial (acinar/papillary) Bronchioalveolar (1-9%)
35% 30%
Small cell carcinoma
Oat cell carcinoma
22%
Bronchogenic Carcinoma:
Bronchogenic Carcinoma:
Bronchogenic Carcinoma:
AdenoCarcinoma:
Direct Spread of carcinoma
Oat cell Carcinoma:
Lung Metastasis
(Gross)
Squamous Cell Carcinoma:(CT)
Normal Chest Radiograph
Lung Metastasis
(Multiple coin shadows)
Squamous Cell Carcinoma:
Adenocarcinoma:
Oat Cell Carcinoma:
(High power)
Pleural effusion:
(Gross)
Paraneoplastic Syndromes:
Hormone producing neoplasms.
ADH - Hyponatremia
ACTH – Cushings syndrome
Parathyroid hormone – Hypercalcemia
Gonadotrophins – Gynecomastia
“Find the key to yourself..
and every door in the world is open to you”
Thank You...
Dr. Venkatesh M. Shashidhar
Senior Lecturer in Pathology Fiji School of Medicine