CONGESTION

Congestion or hyperaemia means an increase in the content of blood in an organ. It may be :

A. Active - due to increased arterial flow to the organ with dilatation of micro vessels as in

• Inflammation.
• Increased metabolic activity.
• Neurogenic blushing.

B. Passive - due to decreased venous drainage resulting in pooling of blood. There is always an associated element of oedema.

DIPHTHERIA

An acute, contagious disease caused by Corynebacterium diphtheriae, characterized by the formation of a fibrinous pseudomembrane, usually on the respiratory mucosa, and by myocardial and neural tissue damage secondary to an exotoxin.

Cutaneous diphtheria (infection of the skin) can occur when any disruption of the integument is colonized by C. diphtheriae. Lacerations, abrasions, ulcers, burns, and other wounds are potential reservoirs of the organism. Skin carriage of C. diphtheriae is also a silent reservoir of infection.

Pathology

C. diphtheriae may produce exotoxins lethal to the adjacent host cells. Occasionally, the primary site is the skin or mucosa elsewhere. The exotoxin, carried by the blood, also damages cells in distant organs, creating pathologic lesions in the respiratory passages, oropharynx, myocardium, nervous system, and kidneys.

The myocardium may show fatty degeneration or fibrosis. Degenerative changes in cranial or peripheral nerves occur chiefly in the motor fibers

In severe cases, anterior horn cells and anterior and posterior nerve roots may show damage proportional to the duration of infection before antitoxin is given. The kidneys may show a reversible interstitial nephritis with extensive cellular infiltration.

The diphtheria bacillus first destroys a layer of superficial epithelium, usually in patches, and the resulting exudate coagulates to form a grayish pseudomembrane containing bacteria, fibrin, leukocytes, and necrotic epithelial cells. However, the areas of bacterial multiplication and toxin absorption are wider and deeper than indicated by the size of the membrane formed in the wake of the spreading infection.

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.

B. 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.

Seborrheic keratosis
1. A round, brown-colored, flat wart.
2. Most often seen in middle-aged to older adults.
3. A benign lesion.

OEDEMA

 Excessive accumulation of fluid in the extra vascular compartment (intersttitial tissues). This includes ascites (peritoneal sac), hydrothorax (pleural cavity) hydropericardium (pericardial space) and anasarca (generalised)

Factors which tend to accumulate interstitial fluid are:

- Intravascular hydrostatic pressure

- Interstitial osmotic pressure.

- Defective lymphatic drainage.

- Increased capillary permeability.

Factors that draw fluid into circulation are:

- Tissue hydrostatic-pressure (tissue tension).

- Plasma osmotic pressure,

Oedema fluid can be of 2 types:

A. Exudate.

It is formed due to increased capillary permeability as in inflammation.

B. Transudate

Caused by alterations of hydrostatic and osmotic pressures.

Local Oedema

1. Inflammatory oedema. Mechanisms are.

- Increased capillary permeability.

- Increased vascular hydrostatic pressure.

- Increased tissue osmotic pressure.

2.Hypersensitivity reactions especially types I and III

3. Venous obstruction :

- Thrombosis.

- Pressure from outside as in pregnancy, tourniquets.

4. Lymphatic obstruction:

- Elephantiasis in fillariasis

- Malignancies (Peau de orange in breast cancer).

Generalized Oedema

1.         Cardiac oedema

Factors :Venous pressure increased.

2. Renal oedema

- Acute glomerulonephritis

- Nephrotic syndrome

3. Nutritional (hypoproteinaemic) oedema. it is seen in

- Starvation and Kwashiorkor

- Protein losing enteropathy

4.  Hepatic oedema (predominantly ascites)

Factors:

- Fall in plasma protein synthesis

- Raised regional lymphatic and portal venous pressure

5. Oedema due to adrenal corticoids

As in Cushing's Syndrome

Pulmonary oedema

- Left heart failure and mitral stenosis.

- Rapid flv infusion specially in a patient of heart failure.

Pulmonary Hypertension 

Sustained elevation of mean pulmonary arterial pressure.

Pathogenesis 
Elevated pressure, through endothelial cell dysfunction, produces structural changes in the pulmonary vasculature. These changes ultimately decrease pulmonary blood flow and stress the heart to the point of failure. Based on etiology, pulmonary hypertension is divided into two categories.

Primary (idiopathic): The cause is unknown.
Secondary: The hypertension is secondary to a variety of conditions which increase pulmonary blood flow or increase resistance to blood flow. Example: Interstitial fibrosis.
Pathology 
The changes involve large and small pulmonary blood vessels and range from mild to severe. The major changes include atherosclerosis, striking medial hypertrophy and intimal fibrosis of small arteries and arterioles, and plexogenic arteriopathy. Refer to Figure 15-7 in your textbook.

Pathophysiology 
Dyspnea and fatigue eventually give way to irreversible respiratory insufficiency, cyanosis and cor pulmonale.