NEET MDS Lessons
General Pathology
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.
Leukaemias
Uncontrolled proliferation of leukocyte precursors (may be with associated red cell and platelet series proliferation).
Factors which may playa causal role are.
- Viral
- Radiation.
- Genetic.
Classification
1. Acule leukaemia:
a. Lymphocytic (lymphoblastic).
b. Myelocytic and promyelocytic (myeloblastic).
c. Monocytic.
d. Myelomonocytic.
e. Undifferentiated (Stem cell).
2. Chronic leukaemia:
a. Lymphocytic
b. Myelocytic
3. Miscellaneous:
a. Erythroleukaemia (De Guglielmo's disease).
b. Eosinophilic leukaemia.
c. Megakaryocytic leukaemia.
Myocardial infarction (MI)—heart attack
A. Ischemia versus MI: Ischemia is a reversible mismatch between the supply and demand of oxygen. Infarction
is an irreversible mismatch that results in cell death caused by the lack of blood flow (oxygenation). For instance, chest pain caused by ischemia can be relieved by administering nitroglycerin (a vasodilator) to the patient. If the patient has an MI, the pain will not be relieved with nitroglycerin.
1. MIs most commonly occur when a coronary artery is occluded by a thrombus generated in an atherosclerotic artery.
2. Symptoms include:
a. Chest pain, shortness of breath.
b. Diaphoresis (sweating), clammy hands.
c. Nausea, vomiting.
3. Consequences:
a. Death (one third of patients).
b. Arrhythmias (most common immediate cause of death).
c. Congestive heart failure.
d. Myocardial rupture, which may result in death from cardiac tamponade.
e. Thrombus formation on infarcted tissue; may result in systemic embolism.
LUNG ABSCESS Lung abscess is a localised area of necrosis of lung tissue with suppuration.
It is of 2 types:
- Primary lung abscess that develops in an otherwise normal lung. The commonest cause is aspiration of infected material.
- Secondary lung abscess that develops as a complication of some other disease of the lung or from another site
ETIOPATHOGENESIS.
The microorganisms commonly isolated from the lungs in lung abscess are streptococci, staphylococci and various gram-negative organisms. These are introduced into the lungs from one of the following mechanisms:
1. Aspiration of infected foreign material.
2. Preceding bacterial infection.
3. Bronchial obstruction.
4. Septic embolism.
5. Miscellaneous (i) Infection in pulmonary infarcts, (ii) Amoebic abscesses, (iii) Trauma to the lungs. (iv) Direct extension from a suppurative focus.
Abscesses may be of variable size from a few millimeters to large cavities, 5 to 6 cm in diameter. The cavity often contains exudate. An acute lung abscess is initially surrounded by acute pneumonia and has poorly-defined ragged wall. With passage of time, the abscess becomes chronic and develops fibrous wall.
Microscopic Examination
The characteristic feature is the destruction of lung parenchyma with suppurative exudate in the lung cavity. The cavity is initially surrounded by acute inflammation in the wall but later there is replacement by exudate of lymphocytes, plasma cells and macrophages. In more chronic cases, there is considerable fibroblastic proliferation forming a fibrocollagenic wall.
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.
FUNGAL INFECTION
Histoplasmosis
A disease caused by Histoplasma capsulatum, causing primary pulmonary lesions and hematogenous dissemination.
Symptoms and Signs
The disease has three main forms. Acute primary histoplasmosis is usually asymptomatic
Progressive disseminated histoplasmosis follows hematogenous spread from the lungs that is not controlled by normal cell-mediated host defense mechanisms. Characteristically, generalized involvement of the reticuloendothelial system, with hepatosplenomegaly, lymphadenopathy, bone marrow involvement, and sometimes oral or GI ulcerations occurs, particularly in chronic cases
Progressive disseminated histoplasmosis is one of the defining opportunistic infections for AIDS.
Chronic cavitary histoplasmosis is characterized by pulmonary lesions that are often apical and resemble cavitary TB. The manifestations are worsening cough and dyspnea, progressing eventually to disabling respiratory dysfunction. Dissemination does not occur
Diagnosis
Culture of H. capsulatum from sputum, lymph nodes, bone marrow, liver biopsy, blood, urine, or oral ulcerations confirms the diagnosis
Coccidioidomycosis (Valley Fever; San Joaquin Fever)
A disease caused by the fungus Coccidioides immitis, usually occurring in a primary form as an acute benign asymptomatic or self-limited respiratory infection, occasionally disseminating to cause focal lesions in skin, subcutaneous tissues, lymph nodes, bones, liver, kidneys, meninges, brain, or other tissues.
Primary coccidioidomycosis is usually asymptomatic, but nonspecific respiratory symptoms resembling influenza or acute bronchitis sometimes occur or, less often, acute pneumonia or pleural effusion. Symptoms, in decreasing order of frequency, include fever, cough, chest pain, chills, sputum production, sore throat, and hemoptysis.
Progressive disseminated coccidioidomycosis may develop a few weeks, months, or occasionally years after primary infections,, is more common in men than women and is more likely to occur in association with HIV infection, immunosuppressive therapy
Symptoms often are nonspecific, including low-grade fever, anorexia, weight loss, and weakness. Extensive pulmonary involvement may cause progressive cyanosis, dyspnea, and discharge of mucopurulent or bloody sputum. Extrapulmonary lesions are usually focal, involving one or more tissue sites in bones, joints, skin, subcutaneous tissues, viscera, brain, or meninges. Draining sinus tracts sometimes connect deeper lesions to the skin. Localized extrapulmonary lesions often become chronic and recur frequently, sometimes long after completion of seemingly successful antifungal therapy.