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General Pathology - NEETMDS- courses
NEET MDS Lessons
General Pathology

Immunodeficiency

This may be :- 
- Congenital (Primary)
- Acquired (Secondary)

Features : Complete or near complete lack of T & B lymphoid tissue. Fatal early in life Even with marrow grafting, chances of graft versus host reaction is high.


T Cell Defects :

- Thymic dysplasia
- Digeorge’s syndrome
- Nazelof’s syndrome
- Ataxia teltngiectaisa
- Wiscott Aldrich’s syndrome

These  lessons show predominantly defective cell mediated immunity. But they may also show partial immunoglobulin defects cell mediated immunity. But they may also show partial immunoglobulin defects due to absence og T-B co-operation.

C. Humoral immunity defects.
Bruron type- aggammaglobulinaemia.
- Dysgammaglobulinaemias-variable immunodeficiency’s of one or more classes.

Acquired deficiency

A. Immuno suppression by :
- Irradiation.
- Corticoids.
- Anti metabolites.
- Anti lymphocyte serum.

B. Neaplasia  of lymphoid system :

- Hodgkin's and Non Hodgkin's lymphomas.
- Chronic lymphocytic leukaemia..
- Multime myeloma and other paraproteinaemias (normal immunoglobulins reduced in spite of hyperglobulinaemia).

c. excessive protein loss.
- Nephrotic Syndrome.
- Protein losing enteropathy.

 

Acute tubular necrosis

Characterized by impaired kidney functions due to the destruction of the renal tubule epithelium.

Caused by a variety of conditions that lead to ischemia of the renal tubules, usually resulting from renal tubular injury or problems with vascular flow. It can also be induced by ingesting toxins or drug-related toxicity (e.g., gentamicin). 
The most common cause of acute renal failure.
Is a reversible condition, although it can be fatal.

NEOPLASIA

 

 An abnormal. growth, in excess of and uncoordinated with normal tissues Which persists in the same excessive manner after cessation of the stimuli which evoked the change.

Tumours are broadly divided by their behaviors into 2 main groups, benign and malignant.

 

Features

Benign

Malignant

General

Rate of growth

Mode of growth

 

Slow

Expansile

 

Rapid

Infiltrative

Gross

Margins

 

Haemoeehage

 

Circumscribed often Encapsulated

Rare

 

III defined

 

Common

Microscopic

Arrangement

Cells

 

Nucleus

Mitosis

 

Resemble Parent Tissues

Regular and uniform in shape and size

Resembles parent Cells

Absent or scanty

 

Varying degrees of structural differentiation

Cellular pleomorphism

 

Hyper chromatic large and varying in shape and size

Numerous and abnormal

 

 

Through most tumours can be classified in the benign or malignant category . Some exhibits an intermediate behaviours.

 

CLASSIFICATION

 

Origin

Benign

Malignant

Epithelial

Surface epithelium

Glandular epithelium

Melanocytes

 

Papilloma

Adenoma

Naevus

 

Carcinoma

Adenoca cinoma

Melanocarcinoma(Melanoma)

Mesenchymal

 

Adipose tissue

Fibrous tissue

Smooth tissue

Striated muscle

Cartilage

Bone

Blood vessels

Lymphoid tissue

 

 

Lipoma

Fibroma

Leiomyoma

Rhabdomyoma

Chondroma

Osteoma

Angioma

 

 

 

Liposarcoma

Fibrosarcoma

Leimyosarcoma

Chondrosarcoma

Osteosarcoma

Angiosarcoma

Lymphoma

Some tumours can not be clearly categorized in the above table e.g.

  • Mixed tumours like fibroadenoma of the breast which is a neoplastic proliferation of both epithelial and mesenchmal tissues.
  • Teratomas which are tumours from germ cells (in the glands) and totipotent cells

(in extra gonodal sites like mediastinun, retroperitoneum and presacral region). These are composed of multiple tissues indicative of differentiation into the derivatives of the three germinal layers.

  • Hamartomas which are malformations consisting of a haphazard mass of  tissue normally present at that site.

Biliary cirrhosis(16%)

It is due diffuse chronic cholestaisis (obstruction of the biliary flow) leading to damage and scarring all over the liver. Two types are known  
1. Primary biliary cirrhosis and
2. Secondary biliary cirrhosis. 

Primary biliary cirrhosis
It is destructive chronic inflammation of intrahepatic bile ductules and small ducts leading to micronodular cirrhosis. 
-Typically affects middle aged women. 
- Patients present with fatigue, pruritis and eventually, jaundice. 

Cause:-  Autoimmune. Patients have autoantibodies directed against mitochondrial enzymes (AMA). 

Pathology:- 

 Liver is enlarged, dark green in color (cholestaisis). Cirrhosis is micronodular. 

M/E :-
- Early, portal tracts show lymphocytes and plasma cell infiltrate the bile ducts and destroy them.
- Granulomatous inflammation surrounding the damaged and inflamed bile ducts is the hallmark of (PBC).
- Cholestatic changes such as bile ductular proliferation, periportal Mallory’s hyaline and increased copper in periportal hepatocytes.
- In the end stage disease, micro nodular cirrhosis occurs and the inflammatory changes subside 

Secondary biliary cirrhosis:-
 It is extra hepatic (surgical) cholestaisis due to prolonged extra hepatic major bile duct obstruction. 

Causes - Obstruction of hepatic or common bile duct by: 
   - Congenital biliary atresia.       
   - Pressure by enlarged LN or tumor   * Biliary stones. 
   - Carcinoma of the bile duct, ampulla of Vater or pancreatic head

Effects of obstruction:- 
Complete obstruction leads to back pressure all over the biliary tract           
 - damage by inspessated bile          
 - inflammation and scarring.
Incomplete obstruction  leads to acute suppurative cholangitis and cholangiolitis. 

THROMBOPHLEBITIS AND  PHLEBOTHROMBOSIS 
- The deep leg veins account for more than 90% of cases (DVT) 
- the most important clinical predispositions are: congestive heart failure, neoplasia, pregnancy, obesity, the postoperative state, and prolonged bed rest or immobilization 
- local manifestations: distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, and pain 
- migratory thrombophlebitis (Trousseau sign): hypercoagulability occurs as a paraneoplastic syndrome related to tumor elaboration of procoagulant factors 

Neutrophilia
Causes
    
-Pyogenic infections.
-Haemorrhage and trauma.
-Malignancies.
-Infarction.
-Myelo proliferative disorders.

Hereditary spherocytosis.

Functionally normal cells which are destroyed .in spleen because of the structural abnormality. It is transmitted as an autosomal dominant trait 

Congenital hemolytic anemia due to genetically determined abnormal spectrin and ankyrin molecules, leading to defects in red blood cell membrane, causing spherical shape and lack of plasticity
Red blood cells become trapped within spleen and have less than usual 120 day lifespan
Splenic function is normal
Osmotic fragility: increased; basis for diagnostic testing 

Description

Firm, deep red tissue, thin capsule, no grossly identifiable malpighian follicles, 100-1000g
Peripheral blood images
Marked congestion in cords
Sinuses appear empty but actually contain ghost red blood cells
May have prominent endothelial lined sinuses, hemosiderin deposition, erythrophagocytosis

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