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.

PRIMARY LYMPHEDEMA  
can occur as:
1- A congenital defect, resulting from lymphatic agenesis or hypoplasia.  

2- Secondary or obstructive lymphedema  
- blockage of a previously normal lymphatic; e.g. Malignant tumors 
- Surgical procedures that remove lymph nodes 
- Postirradiation  
- Fibrosis 
- Filariasis 
- Postinflammatory thrombosis and scarring 

Fanconi’s syndrome

Characterized by the failure of the proximal renal tubules to resorb amino acids, glucose, and phosphates.
May be inherited or acquired.

Clinical manifestations include 

glycosuria, hyperphosphaturia, hypophosphatemia, aminoaciduria, and systemic acidosis.

G-6 PD Deficiency

Occurs in Negroes, Mediterranean races, India and far East. It confers a protection Against falciparum malaria.

It is transmitted as X-linked trait of intermediate dominance (variable effect in homozygous females). 

Haemolysis may be induced by :
•    Primaquin and other anti malarials.
•    Other drugs like chloramphenicol , analgesics, antitubercular drugs etc.
•    Infections.
•    Ingestion of Vicia faba bean (favism).
•    Diabetic acidosis
 

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

Growth and spread of tumours

Growth in excess of normal is a feature of all tumours but extension to tissue away from the site of origin is a feature of malignant tumours.

Modes of spread of malignant tumours

- local, invasion. This is a feature of all malignant tumors and  takes place along tissue spaces and facial planes
    o    Lymphatic spread. Most often seen in carcinomas. This can be in the form of 
    o    Lymphatic permeation:  Where the cells extend along the lymphatics as a  solid core 
    o    Lymphatic embolisation: Where a group of tumour cells break off and get carried to the draining mode

-Vascular spread :  This is a common and early mode of spread for sarcomas but certain carcinomas like renal cell carcinoma and chorio carcinoma have a predilection to early vascular spread.

Vascular spread is most often due .to invasion of venous channels and can be by permeation or embolisation.

Lungs, liver, bones and brain are the common sites for vascular metastasis but
different tumours have different organ preference for metastasis, e.g. : Bronchogenic carcinoma often spreads to liver and adrenals.

-Body cavities and natural passages
    o    Gastrointestinal carcinomas spread to ovaries (Krukenberg’s tomour)