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.
Lymphopenia:
Causes
-As part of pancytopenia.
-Steroid administration.
Nephrolithiasis, urolithiasis
Formation of calculi (calcium stones) in the kidney (nephrolithiasis) or urinary tract (urolithiasis).
Commonly associated with hyperparathyroidism.
Signs and symptoms
urinary tract obstruction, severe pain, and pyelonephritis.
Note: an enlarged prostate can also cause urinary tract obstruction in males.
Cor pulmonale
a failure of the right side of the heart. It is caused by prolonged high blood pressure in the right ventricle of the heart, which in turn is most often caused by pulmonary hypertension - prolonged high blood pressure in the arteries or veins of the lungs. People with heart disease, or lung diseases such as cystic fibrosis, are at greater risk.
Pathophysiology
There are several mechanisms leading to pulmonary hypertension and cor pulmonale:
Pulmonary vasoconstriction
Anatomic changes in vascularisation
Increased blood viscosity
Primary pulmonary hypertension
Causes
Acute:
• Massive pulmonary embolization
• Exacerbation of chronic cor pulmonale
Chronic:
• COPD
• Loss of lung tissue following trauma or surgery
Autoimmune(acquired) Haemolytic anaemia
Auto antibodies are usually Ig g type (may be Ig M or Ig A). They may or may not bind complement and may be active in warm or cold temperature They may be complete (agggIutinating) or incomplete. Haemolysis s may be intravascular due to destruction of the antibody coated cells by RE system.
Causes:
a. Idiopathic
b. Secondary to
o Drugs - Methyldopa, Mefanamic acid
o Disease like
-> Infections especially viral.
-> Autoimmune disease especially SLE.
-> Lymphomas and chronic lymphatic leukaemia.
-> Tumours.
Diagnosis : is based on
• Evidences of haemolytic anaemia.
• Demonstration of antibodies
- On red cell surface by direct Coomb’s test
- In serum by indirect Coomb’s test.
Multiple sclerosis
a. A demyelinating disease that primarily affects myelin (i.e. white matter). This affects the conduction of electrical impulses along the axons of nerves. Areas of demyelination are known as plaques.
b. The most common demyelinating disease.
c. Onset of disease usually occurs between ages 20 and 50; slightly more common in women.
d. Disease can affect any neuron in the central nervous system, including the brainstem and spinal cord. The optic nerve (vision) is commonly affected.
Immunoglobulins. (Ig)
These are made up of polypeptide chains. Each molecule is constituted by two heavy and two light chains, linked by disulfide (S-S) bonds. The h~ chains are of 5 types, with corresponding, types or immunoglobulin. IgG (gamma), IgM (mu µ ), IgA(alpha α), IgD(delta ), IgE(epsilon)
Each of these can have light chains of either kappa (k) or lambda type.Each chain has a constant portion (constant for the subtype) land a variable portion (antigen specific).
Enzyme digestion can split the Ig molecule into.2 Fab (antibody binding) fragments and one Fc (crystallisable, complement binding ) fragment.