NEET MDS Lessons
General Pathology
POLYCYTHEMIA
It is an increase in number of RC per unit volume of blood (Hb more than 1.9.5 gms% and 18 gms% for women)
Causes :
True polycythemia.
- Idiopathic Polythemia vera.
- Secondary to :
o Hypoxia of high altitude , heart disease, chronic lung disease etc.
o Erythopoietin oversecretion as in renal diseases , tumours of liver, kidney and adrenal etc.
o Compensatory in haemogIobinopathies
- Relative polycythemia due to reduction in plasma volume as in dehydration or in redistribution off fluids
Polycythemia vera: It is a myeloprolifeative disorder, usually terminating in myelosclerosis.
Features: are due to hypervolaemic circulation and tendency to tbrombosis and haemorrhage
-Headaches, dizziness and cardiovascular accidents.
-Hypertension.
-Peripheral vascular thrombosis.
-GIT bleeding. retinal haemorrhage.
-Gout.
-Pruritus.
Blood Finding
-Increased Hb. PCV and RBC count.
-Leucocytosis with high alkaline phosphatase.
-Platelets increased.
Marrow picture Hypercellular with increase in precursors of all series
Course Chronic course ending in myelosclerosis or acute leukaemia.
Agranulocytosis. Severe neutropenia with symptoms of infective lesions.
Drugs. are an important cause and the effect may be due to .
-Direct toxic effect.
-Hypersensitivity.
Some of the 'high risk drugs are.
-Amidopyrine.
-Antithyroid drugs.
-Chlorpromazine, mapazine.
-Antimetabolites and other drugs causing pancytopenia.
Bloodpicture: Neutropenia with toxic granules in neutrophils. Marrow shows decrease in granulocyte precursors with toxic granules in them.
Clinical genetics (cytogenetics),
This is a method in which inherited chromosomal abnormalities in the germ cells or acquired chromosomal abnormalities in somatic cells are investigated using the techniques of molecular biology.
Nevus
1. Commonly known as moles.
2. A benign, pigmented tumor of melanocytes, found deep within connective tissue.
3. Types of skin nevi:
a. Junctional nevus—found in the epidermis.
It is the only type of nevus that may be considered to be premalignant.
b. Compound nevus—found in both the epidermis and underlying dermis.
c. Intraepidermal nevus—found in the dermis.
Pemphigus
1. Ulcerative lesions on the skin and oral mucosa.
2. An autoimmune disease in which patients have autoantibodies against hemidemosomal attachment of epidermis cells.
3. Histologically characterized by acantholysis, in which epidermal cells appear to detach and separate from each other, as seen by Tzanck smears.
4. Can be life-threatening if untreated.
5. A positive Nikolsky sign is observed.
Because of sloughing of the epidermis, a red blister forms after pressure is applied to affected skin.
6. Treatment: corticosteroids.
Cholelithiasis (Biliary calculi)
- These are insoluble material found within the biliary tract and are formed of bile constituents (cholesterol, bile pigments and calcium salts).
Sites: - -Gall bladder, extra hepatic biliary tract. Rarely, intrahepatic biliary tract.
Predisposing factors:-
- Change in the composition of bile. - It is the disturbance of the ratio between cholesterol and lecithin or bile salts which may be due to Hypercholesterolaemia which may be hereditary or the 4 F (Female, Forty, Fatty, Fertile). Drugs as clofibrate and exogenous estrogen. High intake of calories (obesity).
Increased concentration of bilirubin in bile- pigment stones
Hypercalcaemia:- Calcium carbonate stones.
2- Staisis.
3- Infection.
Pathogenesis i- Nucleation or initiation of stone formation:- The nidus may be cholesterol “due to supersaturation” Bacteria, parasite
RBCs or mucous.
ii- Acceleration:- When the stone remains in the gall bladder, other constituents are added to the
nidus to form the stone.
Complications of gall stones:-
- Predispose to infection.- Chronic irritation leading to
a. Ulceration b. Squamous metaplasia & carcinoma.
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.