Glomerulonephritis

Characterized by inflammation of the glomerulus.

Clinical manifestations:
Nephrotic syndrome (nephrosis) → Most often caused by glomerulonephritis.

Laboratory findings:
(i) Proteinuria (albuminuria) and lipiduria—proteins and lipids are present in urine.
(ii) Hypoalbuminemia—decreased serum albumin due to albuminuria.
(iii) Hyperlipidemia—especially an increase in plasma levels of low-density lipoproteins and cholesterol.

Symptoms

severe edema, resulting from a decrease in colloid osmotic pressure due to a decrease in serum albumin.

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

Bronchitis

Bronchitis is an obstructive pulmonary disease characterized by inflammation of the bronchi of the lungs

Signs and symptoms

persistent cough that produces sputum

shortness of breath (dyspnea) on exertion

hypercapnia

insufficient oxygenation of the blood hypoxemia leading to cynosis

Severe chronic bronchitis will commonly lead to cor pulmonale and heart failure.

Pathology

an increase in the number of goblet cells with mucus blocking the airway clusters of pigmented alveolar macrophages

the presence of inflammatory cells (e.g. neutrophils) scarring (fibrosis) of the walls of the bronchioles

Diagnosis

• decreased intensity of breath sounds (rhonchi) and extended expiration.
• a sputum culture has pathogenic microorganisms
• a chest x-ray that reveals hyperinflation and increased bronchovascular markings
• a pulmonary function test that shows an increase in the lung's residual volume and a decreased vital capacity

Pathophysiology

• The initiating event in developing bronchitis appears to be chronic irritation due to inhalation of certain chemicals
• earliest clinical feature of bronchitis is increased secretion of mucus by submucousal glands of the trachea and bronchi
• Damage caused by irritation of the airways leads to inflammation and infiltration of the lung tissue by neutrophils
• The neutrophils release substances that promote mucousal hypersecretion
• As bronchitis persists to become chronic bronchitis, a substantial increase in the number of goblet cells in the small airways is seen
• The role of infection in the pathogenesis of chronic bronchitis appears to be secondary.

Treatment

Quit smoking, Oxygen therapy, bronchodilator drugs

Prognosis

Pulmonary hypertension, cor pulmonale, and chronic respiratory failure are possible complications of chronic bronchitis

In severe chronic bronchitis is poor

CHRONIC INFLAMMATlON

When the inflammatory reaction instead of subsiding after the acute phase (or without entering an acute phase), persists as a smouldering lesion, it is called chronic inflammation. .

Characteristics

• Predominantly mononuclear response.
• Inflamation.and..repair going on simultaneously.
• Usually results in more prominent-scarring.

Causes:

Chronicity may be due to :

- Defective defence mechanisms.

- Persistence of injurious agent.

(a) Certain organisms resist phagocytosis and destruction e.g tubercle bacillus, fungi

(b) insoluble particulate matter e.g., crystals. fibres suture materials.

(c) Constants supply of causative agent as in autoimmune disease where body reacts against its own tissues.

- Defective healing.

Granulomatous inflammation

It is a type of chronic inflammation characterised by localised collections of histiocytes.

These cells are usually accompanied by lymphocytes, fibroblasts and giant cells also.

Granulomas are characteristically seen in diseases like tuberculosis. syphilis, leprosy, sarcoidosis, fungal infections etc. In some of these, the lesion is morphologically distinct  enough to point to the type of underlying disease. These are sometimes called' specific' granulomas. Granulomas can also be elicited by particulate, insoluble foreign material e.g. granuloma, suture granuloma, cholesterol granuloma (organising haemorrhages).

Rocky Mountain Spotted Fever (Spotted Fever; Tick Fever; Tick Typhus)

An acute febrile disease caused by Rickettsia rickettsii and transmitted by ixodid ticks, producing high fever, cough, and rash.

Symptoms and Signs

The incubation period averages 7 days but varies from 3 to 12 days; the shorter the incubation period, the more severe the infection. Onset is abrupt, with severe headache, chills, prostration, and muscular pains. Fever reaches 39.5 or 40° C (103 or 104° F) within several days and remains high (for 15 to 20 days in severe cases),

Between the 1st and 6th day of fever, most patients develop a rash on the wrists, ankles, palms, soles, and forearms that rapidly extends to the neck, face, axilla, buttocks, and trunk. Often, a warm water or alcohol compress brings out the rash. Initially macular and pink, it becomes maculopapular and darker. In about 4 days, the lesions become petechial and may coalesce to form large hemorrhagic areas that later ulcerate

Neurologic symptoms include headache, restlessness, insomnia, delirium, and coma, all indicative of encephalitis. Hypotension develops in severe cases. Hepatomegaly may be present, but jaundice is infrequent. Localized pneumonitis may occur. Untreated patients may develop pneumonia, tissue necrosis, and circulatory failure, with such sequelae as brain and heart damage. Cardiac arrest with sudden death occasionally occurs in fulminant cases.

Pemphigoid
1. Ulcerative lesions on the skin and oral mucosa.
2. An autoimmune disease in which patients have autoantibodies against basal cells (desmosome attachment to the basement membrane).
3. Histologically, the entire epithelium appears to separate from the connective tissue. There is no acantholysis.
4. A positive Nikolsky sign is observed.
5. Complications include blindness, due to ocular lesions present in some patients.
6. Treatment: corticosteroids.