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.

Paget Disease (Osteitis Deformans) 

This unique bone disease is characterized by repetitive episodes of exaggerated, regional osteoclastic activity (osteolytic stage), followed by exuberant bone formation (mixed osteoclastic-osteoblastic stage), and finally by exhaustion of cellular activity (osteosclerotic stage). The net effect of this process is a gain in bone mass; however, the newly formed bone is disordered and lacks strength. Paget disease usually does not occur until mid-adulthood but becomes progressively more common thereafter. The pathognomonic histologic feature is a mosaic pattern of lamellar bone (likened to a jigsaw puzzle) due to prominent cement lines that haphazardly fuse units of lamellar bone. (Fig. 12-5) The axial skeleton and proximal femur are involved in the majority of cases. In patients with extensive disease, hypervascularity of the marrow spaces can result in high-output congestive heart failure. Cranial nerves impingement also occurs and can lead to head ache and auditory disturbances. Rarely Paget disease is complicated by bone sarcoma (usually osteogenic). 

Urinary tract infection
Most often caused by gram-negative, rod-shaped bacteria that are normal residents of the enteric tract, especially Escherichia coli.

Clinical manifestations: 

frequent urination, dysuria, pyuria (increased PMNs), hematuria, and bacteriuria.

May lead to infection of the urinary bladder (cystitis) or kidney (pyelonephritis).

Eczematous Dermatitis
Eczematous dermatitis includes a large category of skin lesions characterized by severe pruritus and distinctive gross and microscopic features.
 - type I hypersensitivity is involved with atopic dermatitis in patients who have an allergic history.
 - type IV hypersensitivity is involved in contact dermatitis (poison ivy).
 - acute eczematous dermatitis is characterized by a weeping, pruritic rash, while a chronic eczematous dermatitis presents with dry, scaly, plaque-like thickening of the skin, a process called lichenification.  

Thyroid goitres

A goitre is any enlargement of part or whole of the thyroid gland. There are two types:
1. Toxic goitre, i.e. goitre associated with thyrotoxicosis.
2. Non-toxic goitre, i.e. goitre associated with  normal or reduced levels of thyroid hormones.

Toxic goitre
Graves disease
This is the most common cause of toxic goitre 

Toxic multinodular goitre
This results from the development of hyperthyroidism in a multinodular goitre 

Non-toxic goitres
Diffuse non-toxic goitre (simple goitre)

This diffuse enlargement of the thyroid gland is classified into:

Endemic goitre—due to iodine deficiency. Endemic goiter occurs in geographic areas (typically mountainous)) where the soil, water, and food supply contain little iodine. The term endemic is used when goiters are present in more than 10% of the population in a given region. With increasing availability of dietary iodine supplementation, the frequency and severity of endemic goiter have declined significantly. Sporadic goiter is less common than endemic goiter. The condition is more common in females than in males, with a peak incidence in puberty or young adult life, when there is an
increased physiologic demand for T4.

Sporadic goitre—caused by goitrogenic agents (substances that induce goitre formation) or familial in origin. Examples of goitrogenic agents include certain cabbage species, because of their thiourea content, and specific drugs or chemicals, such as iodide, paraminosalicylic acid and drugs used in the treatment of thyrotoxicosis. Familial cases show inherited autosomal recessive traits, which interfere with hormone synthesis via various enzyme pathways (these are dyshormonogenic goitres). 
Hereditary enzymatic defects interfering with thyroid hormone synthesis (dyshormonogenetic goiter).

Physiological goitre—enlargement of the thyroid gland in females during puberty or pregnancy; the reason is unclear.

Multinodular goitre

This is the most common cause of thyroid enlargement and is seen particularly in the elderly (nearly all simple goitres eventually become multinodular). The exact aetiology is uncertain but it may represent an uneven responsiveness of various parts of the thyroid to fluctuating TSH levels over a period of many years.

Morphological features are:

• Irregular hyperplastic enlargement of the entire thyroid gland due to the development of wellcircumscribed nodules of varying size.
• Larger nodules filled with brown, gelatinous colloid; consequently, it is often termed multinodular colloid goitres.

Clinical features 

- A large neck mass, goiters may also cause airway obstruction, dysphagia, and compression of large vessels in the neck and upper thorax.
 - A hyperfunctioning ("toxic") nodule may develop within a long-standing goiter, resulting in hyperthyroidism. This condition is not accompanied by the infiltrative ophthalmopathy and dermopathy. 
 - Less commonly, there may be hypothyroidism.

Str. Pneumoniae

Probably the most important streptococci.  Primary cause of pneumonia.  Usually are diplococci.  Ste. pneumoniae are α-hemolytic and nutritionally fastidious.  Often are normal flora.

Key virulence factor is the capsule polysaccharide which prevents phagocytosis.  Other virulence factors include pneumococcal surface protein and α-hemolysin.

Major disease is pneumonia, usually following a viral respiratory infection.  Characterized by fever, cough, purulent sputum.  Bacteria infiltrates alveoli.  PMN’s fill alveoli, but don’t  cause necrosis. Also can cause meningitis, otitis, sinusitis.

There are vaccines against the capsule polysaccharide.  Resistance to penicillin, cephalosporins, erythromycins, and fluoroquinalones is increasing.