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.

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

CLASSIFICATION

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.

INFLAMMATION

Response of living tissue to injury, involving neural, vascular and cellular response.

ACUTE INFLAMMATION

It involves the formation of a protein .rich and cellullar exudate and the cardinal signs are calor, dolor, tumour, rubor and function loss

The basic components of the response are

Haemodynamic changes.

Permeability changes

Leucocyte events.

1. Haemodynamic Changes :

• Transient vasoconstriction followed by dilatation.
• Increased blood flow in arterioles.
• More open capillary bed.
• Venous engorgement and congestion.
• Packing of microvasculature by RBC (due to fluid out-pouring)
• Vascular stasis.
• Change in axial flow (resulting in margination of leucocytes)

.2. Permeability Changes:

Causes.

• Increased intravascular hydrostatic pressure.
• Breakdown of tissue proteins into small molecules resulting in
• increased tissue osmotic pressure.
• Increased permeability due to chemical mediators, causing an
• immediate transient response. .
• Sustained response due to direct damage to microcirculation.

3. White Cell Events:

.Margination - due to vascular stasis and change in axial flow.

Pavementing - due to endothelial cells swollen and more sticky.

Leucocytes more adhesive.

Binding by a plasma component

Emigration - of leucocytes by amoeboid movement between endhothe1ial cells and beyond the basement membrane. The passive movement of RBCs through the gaps created during emigration is called diapedesis

Chemotaxis - This is a directional movement, especially of polymorphs and monocytes towards a concentration gradient resulting in aggregation of these cells at the site of inflammation. .Chemotactic agents may be:

• Complement components. (C₃and C₅  fragments and C₅₆₇)
• Bacterial products.
• Immune complexes, especially for monocyte.
• Lymphocytic factor, especially for monocyte.

 Phagocytosis - This includes recognition, engulfment and intracellular degradation. It is aided by .Opsonins., Specific antibodies., Surface provided by fibrin meshwork.

Functions of the fluid and cellular exudate

1. Dilution of toxic agent.

2. Delivers serum factors like antibodies and complement components to site of inflammation.

3. Fibrin formed aids In :

• Limiting inflammation
• Surface phagocytosis
• Framework for repair.

4. Cells of the exudate:

Phagocytose and destroy the foreign agent.

Release lytic enzymes when destroyed, resulting in extracellular killing of organisms- and digestion of debris to enable healing to occur

Chickenpox (varicella)
 - primarily a childhood disease (70%)
 - incubation period 14-16 days; highly contagious; infectious 2 days before the vesicles until the last one dries.
 - present with generalized, intensely pruritic skin lesions starting as macules vesicles pustules (MVP-most valuable player) usually traveling centrifugally to the face and out to the extremities; unlike smallpox vesicles, chickenpox vesicles appear in varying stages of development as successive crops of lesions appear; intranuclear inclusions similar to HSV.
 - pneumonia develops in 1/3 of adults; MCC death in chickenpox.
 - association with Reye's syndrome if child takes aspirin. 

Chemical Mediators In Inflammation

Can be classified as :

A. Neurogenic

Also called the Triple Response of Lewis. It involves neurogenic vasodilatation of arterioles due to antidromic axon reflex arc. The constituents of the response are:

1. arteriolar vasoconstriction followed by

2. arteriolar vasodilatation

3. swelling

B. Chemical

1. Amines: Histamine and 5 hydroxytryptamine. Released  from platelets and mast cells.

Actions: Immediate and short lived.

Dilatation of arterioles.

Increased capillary premeability.

Kinins: Bradykinin and kallidin These are present in inactive from and are  activated by kinin forming proteases

Actions:

Arteriolar dilatation.

Increased vascular permeability

Pain

Kinin forming proteases Plasmin and Kallikrein. Present as inactive precursors.

Cleavage products of complement C₃a und C₅a are called anaphylatoxins

Actions:

Histamine release from mast cells

Chemotaxis (also C₅₆₇ )

Enhance phagocytosis.

 Polymorph components

Cationic: proteins which cause

Increased permeability

Histamine release.

Chemotaxis of monocytes

Neutral proteases which:

Cleave C3 and C5 to active form

Convert Kininogen to Kinin

Increase permeability.

Acid proteases which liberate leucokinins

Slow reacting. substance of anaphylaxis: (SRS-A) is a lipid released from mast cell.

Action --Increases vascular permeability

Prostaglandins: E1 + E2 _.

Platelets are rich source

Action:

Platelets are a rich source.

Vasodilatation.

Increased permeability.

Pain.

VIII. Miscellaneous: like

Tissue lactic acid.

 Bacterial toxins.

POLYCYTHEMIA

 It is an increase in number of RC per unit volume of blood (Hb more than 1.9.5 gms% and 18 gms% for women)
 
Causes :

True polycythemia.
- Idiopathic Polythemia vera.

- Secondary to :

    o    Hypoxia of high altitude , heart disease, chronic lung disease etc.
    o    Erythopoietin  oversecretion as in renal diseases , tumours of liver, kidney and adrenal etc.
    o    Compensatory in haemogIobinopathies
    
- Relative polycythemia due to reduction in plasma volume as in dehydration or in redistribution off fluids

Polycythemia vera: It is a myeloprolifeative disorder, usually terminating in myelosclerosis.

Features: are due to hypervolaemic circulation and tendency to tbrombosis and haemorrhage 

    -Headaches, dizziness and cardiovascular accidents.
    -Hypertension.
    -Peripheral vascular thrombosis.
    -GIT bleeding. retinal haemorrhage.
    -Gout.
    -Pruritus.

Blood Finding

-Increased Hb. PCV and RBC count.
-Leucocytosis with high alkaline  phosphatase.
-Platelets increased.

Marrow picture Hypercellular with  increase in precursors of all series 
Course Chronic course ending in myelosclerosis or acute  leukaemia.
 

Nephrosclerosis
 Disease of the renal arteries.

 Clinical manifestations:
 (1) Benign (arterial) nephrosclerosis →  Caused by the formation of atherosclerotic plaques in the renal artery. Results in narrowing of the arterioles.

(2) Malignant nephrosclerosis → Caused by malignant hypertension. Common signs of malignant hypertension include severe hypertension, retinal hemorrhages, and hypertrophy of the left ventricle. Results in inflammatory changes in the vascular walls, which may lead to rupture of the glomerular capillaries.