NEET MDS Lessons
General Pathology
HAEMORRHAGIC DISORDERS
Normal homeostasis depends on
-Capillary integrity and tissue support.
- Platelets; number and function
(a) For integrity of capillary endothelium and platelet plug by adhesion and aggregation
(b) Vasoactive substances for vasoconstriction
(c) Platelet factor for coagulation.
(d) clot retraction.
- Fibrinolytic system(mainly Plasmin) : which keeps the coagulation system in check.
Coagulation disorders
These may be factors :
Deficiency .of factors
- Genetic.
- Vitamin K deficiency.
- Liver disease.
- Secondary to disseminated intravascular coagulation.or defibrinatian
Overactive fibrinolytic system.
Inhibitors of the factors (immune, acquired).
Anticoagulant therapy as in myocardial infarction.
Haemophilia. Genetic disease transmitted as X linked recessive trait. Common in Europe. Defect in fcatorVII Haemophilia A .or in fact .or IX-Haemaphilia B (rarer).
Features:
- May manifest in infancy or later.
- Severity depends on degree of deficiency.
- Persistant wound bleeding.
- Easy Bruising with Hematoma formation
Nose bleed , arthrosis, abdominal pain with fever and leukocytosis
Prognosis is good with prevention of trauma and-transfusion of Fresh blood or fTesh plasma except for danger of developing immune inhibitors.
Von Willebrand's disease. Capillary fragility and decreased factor VIII (due to deficient stimulatory factor). It is transmitted in an autosomal dominant manner both. Sexes affected equally
Vitamin K Deficiency. Vitamin K is needed for synthesis of factor II,VII,IX and X.
Deficiency maybe due to:
Obstructive jaundice.
Steatorrhoea.
Gut sterilisation by antibiotics.
Liver disease results in :
Deficient synthesis of factor I II, V, Vll, IX and X Incseased fibrinolysis (as liver is the site of detoxification of activators ).
Defibrination syndrome. occurs when factors are depleted due to disseminated .intravascular coagulation (DIC). It is initiated by endothelial damage or tissue factor entering the circulation.
Causes
Obstetric accidents, especially amniotic fluid embolism. Septicaemia. .
Hypersensitivity reactions.
Disseminated malignancy.
Snake bite.
Vascular defects : (Non thrombocytopenic purpura).
Acquired :
Simple purpura a seen in women. It is probably endocrinal
Senile parpura in old people due to reduced tissue support to vessels
Allergic or toxic damage to endothelium due to Infections like Typhoid Septicemia
Col!agen diseases.
Scurvy
Uraemia damage to endothelium (platelet defects).
Drugs like aspirin. tranquillisers, Streptomvcin pencillin etc.
Henoc schonlien purpura Widespeard vasculitis due to hypersensitivity to bacteria or foodstuff
It manifests as :
Pulrpurric rashes.
Arthralgia.
Abdominal pain.
Nephritis and haematuria.
Hereditary :
(a) Haemhoragic telangieclasia. Spider like tortous vessels which bleed easily. There are disseminated lesions in skin, mucosa and viscera.
(b) Hereditary capillary fragilily similar to the vascular component of von Willbrand’s disease
.(c) Ehler Danlos Syndrome which is a connective tissue defect with skin, vascular and joint manifestations.
Platelet defects
These may be :
(I) Qualitative thromboasthenia and thrombocytopathy.
(2) Thrombocytopenia :Reduction in number.
(a) Primary or idiopathic thrombocytopenic purpura.
(b) Secondary to :
(i) Drugs especially sedormid
(ii) Leukaemias
(iii) Aplastic-anaemia.
Idiopathic thrombocytopenic purpura (ITP). Commoner in young females.
Manifests as :
Acute self limiting type.
Chronic recurring type.
Features:
(i) Spontaneous bleeding and easy bruisability
(ii)Skin (petechiae), mucus membrane (epistaxis) lesions and sometimes visceral lesions involving any organ.
Thrombocytopenia with abnormal forms of platelets.
Marrow shows increased megakaryocytes with immature forms, vacuolation, and lack of platelet budding.
Pathogenesis:
hypersensitivity to infective agent in acute type.
Plasma thrombocytopenic factor ( Antibody in nature) in chronic type
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.
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
DEGENERATION
Definition: Reversible cell injury.
(1) Water accumulation in the form of
(i) Cloudy swelling.
(ii) Vacuolar degeneration.
.(ill) Hydropic degeneration.
This change is commonly seen in parenchymal cells e.g. kidneys.
Gross appearance: The organ is swollen, soft and pale.
Microscopic appearance: Cells show varying degrees of swelling. Cytoplasm may be granular, vacuolated, homogenously pale and ballooned out.
(2) Fatty change An excessive, demonstrable accumulation of fat is common in parenchymal cells of liver and heart
In the liver, it can be due to: .
(i) Excess fat entry into the liver as occurs in starvation and in steroid excess due to mobilization from stores.
(ii) Excess triglyceride formation
(iii) Reduced phosphorlyation of fat.
(iv) Decreased release as lipoprotein due to protein deficiency.
Causes
(i) Hypoxia as in severe anaemia and venous stasis
(ii) Protein malnutrition.
(iii) Hepatotoxins like CCl4.
(iv) Alcoholism
(v) Metabolic defects like Diabetes mellitus
(vi) Infections.
Gross appearance: The organ is enlarged, soft and greasy, with a pale yellowish colour. It may involve the organ uniformly or patchily ( thrush breast or tabby cat heart)
Microscopic appearance: The cells contain clear vacuoles (stainable by fat-sudan stains on frozen sections). These may be small and dispersed or large, displacing the nucleus peripherally. Several such cells may fuse to form fat cysts.
(3) Hyaline degeneration
In alcoholic liver damage, the cytoplasmic organelles are damaged and give the cytoplasm a deep eosinophilic staining-Mallory hyaline.
Seborrheic dermatitis is a scaly dermatitis on the scalp (dandruff) and face.
- due to Pitysporium species
- can be seen in AIDS as an opportunistic infection
TOXOPLASMOSIS
Infection with Toxoplasma gondii, causing a spectrum of manifestations ranging from asymptomatic benign lymphadenopathy to life-threatening CNS disease, chorioretinitis, and mental retardation.
Symptomatic infections may present in several ways
Acute toxoplasmosis may mimic infectious mononucleosis with lymphadenopathy, fever, malaise, myalgia, hepatosplenomegaly, and pharyngitis. Atypical lymphocytosis, mild anemia, leukopenia, and slightly abnormal liver function tests are common. The syndrome may persist for weeks or months but is almost always self-limited.
A severe disseminated form characterized by pneumonitis, myocarditis, meningoencephalitis, polymyositis, diffuse maculopapular rash, high fevers, chills, and prostration. Acute fulminating disease is uncommon.
Congenital toxoplasmosis usually results from a primary (and often asymptomatic) acute infection acquired by the mother during pregnancy. The risk of transplacental infection increases from 15% to 30 to 60% for maternal infections acquired in the 1st, 2nd, or 3rd trimester of gestation, respectively
Viral meningitis
1. Can be caused by many different viruses, including cytomegalovirus, herpes virus, rabies, and HIV.
2. CSF fluid from a spinal tap differs from that seen in a bacterial infection. It shows mononuclear cells, higher levels of protein, and normal levels of glucose.