Lymphangitis 
is the acute inflammation due to bacterial  infections spread into the lymphatics most common are group A β-hemolytic streptococci. 
lymphatics are dilated and filled with an exudate of neutrophils and monocytes.  
red, painful subcutaneous streaks (the inflamed lymphatics), with painful enlargement of the draining lymph nodes (acute lymphadenitis).  
subsequent passage into the venous circulation can result in bacteremia or sepsis. 

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

Plasma Cell Pathology

A. Multiple myeloma

1. Plasma cell neoplasm that results in the proliferation of monoclonal plasma cells. These tumor cells produce nonfunctional immunoglobulins.

2. Laboratory findings include:

a. Monoclonal IgG spike.

b. Bence-Jones proteins found in urine.

3. Radiographic findings: characteristic “punched-out” radiolucencies in bones.

Pathology gives explanations of a disease by studying the following four aspects of the disease.

1. Etiology,

2. Pathogenesis,

3. Morphologic changes and

4. Functional derangements and clinical significance.

1. Etiology Etiology of a disease means the cause of the disease. If the cause of a disease is known it is called primary etiology. If the cause of the disease is unknown it is called idiopathic. Knowledge or discovery of the primary cause remains the backbone on which a diagnosis can be made, a disease understood, & a treatment developed. There are two major classes of etiologic factors: genetic and acquired (infectious, nutritional, chemical, physical, etc).

2. Pathogenesis Pathogenesis means the mechanism through which the cause operates to produce the pathological and clinical manifestations. The pathogenetic mechanisms could take place in the latent or incubation period. Pathogenesis leads to morphologic changes.

3. Morphologic changes The morphologic changes refer to the structural alterations in cells or tissues that occur following the pathogenetic mechanisms. The structural changes in the organ can be seen with the naked eye or they may only be seen under the microscope. Those changes that can be seen with the naked eye are called gross morphologic changes & those that are seen under the microscope are called microscopic changes. the morphologic changes will lead to functional alteration & to the clinical signs & symptoms of the disease.

4. Functional derangements and clinical significance The morphologic changes in the organ influence the normal function of the organ. By doing so, they determine the clinical features (symptoms and signs), course, and prognosis of the disease.

Thalassaemia. Genetic based defect in synthesis of one of the normal chains.

Beta thalassaemia --->  reduced Hb A and increased HbF (α2, Y2) HBA2(α2)

Alpha thalassaemia  --->   reduced  Hb-A, Hb-A2 and Hb-F-with formation of Hb-H(β4) and Hb Barts (Y4).
Thalassaemia may manifest as trait or disease or with intermediate manifestation.

Features:
•    Microcytic hypochromic RBC is in iron deficjency.
•    Marked anisopoikilocytsis  with prominent target cells.
•    Reticulocytosis and nucleated RBC seen.
•    Mongoloid facies and X-ray findings characteristic of marrow hyperplasia
•    Decreased osmotic. fragility.
•    Increased marrow iron (important difference from iron deficiency anaemia).
•    Haemosiderosis, especially with repeated transfusions.

Diagnosis is by Hb electrophoresis and by Alkali denaturation test (for HbF).

DEGENERATION

Definition:   Reversible cell injury.

(1) Water accumulation in the form   of 

(i)          Cloudy   swelling.

(ii)         Vacuolar   degeneration.

.(ill)        Hydropic   degeneration.

This change  is commonly   seen  in parenchymal   cells  e.g.  kidneys.

Gross appearance: The organ is swollen, soft and pale.

Microscopic appearance: Cells show varying degrees of swelling. Cytoplasm may be granular, vacuolated, homogenously pale and ballooned out.     

(2)  Fatty   change An excessive,   demonstrable accumulation of fat  is common   in  parenchymal cells of liver  and heart

In the liver, it can be due to:   .

(i) Excess  fat  entry  into  the  liver  as occurs  in  starvation  and  in  steroid excess due to mobilization from stores.

(ii) Excess triglyceride formation

(iii) Reduced phosphorlyation  of fat.  

(iv) Decreased release as lipoprotein due to protein deficiency.

Causes

(i) Hypoxia  as  in severe  anaemia  and  venous  stasis

(ii) Protein  malnutrition.

(iii) Hepatotoxins like CCl₄.

(iv) Alcoholism

(v) Metabolic defects like Diabetes mellitus

(vi) Infections.

Gross appearance: The organ is enlarged, soft and greasy, with a pale yellowish colour. It may involve the organ uniformly or patchily ( thrush breast or tabby cat heart)

Microscopic appearance: The cells contain clear vacuoles (stainable by fat-sudan  stains on frozen sections). These may be small and dispersed or large, displacing the nucleus peripherally. Several such cells may fuse to form fat cysts.

(3) Hyaline degeneration

In alcoholic liver damage, the cytoplasmic organelles are damaged and give the cytoplasm a deep eosinophilic staining-Mallory hyaline.