NEET MDS Lessons
General Pathology
INFARCTION
Definition : a localized area of ischaemic necrosis in an organ infarcts may be:
Pale :as in
→ Arterial obstruction.
→ solid organs.
Red as in
→ Venous occlusion
→ Loose tissue.
Morphology
Gross: infarcts are usually wedge shaped the apex towards the occluded vessel They are
separated from the surrounding tissue by an hyperemic inflammatory zone
Microscopic:
- An area of coagulative necrosis with a rim of congested vessels and acute inflammatory infiltration of the tissue .
- The polymorphs ale later replaced by mononuclear cells and granulation tissue.
- With time, scar tissue replaces necrosed tissue.
Alcoholic (nutritional, Laennec’s) cirrhosis
Pathology
Liver is at first enlarged (fatty change), then return to normal size and lastly, it becomes slightly reduced in size (1.2 kg or more).
- Cirrhosis is micronodular then macronodular then mixed.
M/E
Hepatocytes:- show fatty change that decreases progressively. Few hepatocytes show increased intracytoplasmic haemochromatosis.
b. Fibrous septa:- Regular margins between it and regenerating nodules.
-Moderate lymphocytic infiltrate.
– Slight bile ductular proliferation.
Prognosis:- It Progresses slowly over few years.
Respiratory Viral Diseases
Respiratory viral infections cause acute local and systemic illnesses. The common cold, influenza, pharyngitis, laryngitis (including croup), and tracheobronchitis are common.
An acute, usually afebrile, viral infection of the respiratory tract, with inflammation in any or all airways, including the nose, paranasal sinuses, throat, larynx, and sometimes the trachea and bronchi.
Etiology and Epidemiology
Picornaviruses, especially rhinoviruses and certain echoviruses and coxsackieviruses, cause the common cold. About 30 to 50% of all colds are caused by one of the > 100 serotypes of rhinoviruses.
Symptoms and Signs
Clinical symptoms and signs are nonspecific.
After an incubation period of 24 to 72 h, onset is abrupt, with a burning sensation in the nose or throat, followed by sneezing, rhinorrhea, and malaise.
Characteristically, fever is not present, particularly with a rhinovirus or coronavirus. Pharyngitis usually develops early; laryngitis and tracheobronchitis vary by person and causative agent. Nasal secretions are watery and profuse during the first days, but become more mucoid and purulent.
Cough is usually mild but often lasts into the 2nd wk.
Asthma
Asthma is
(1) An obstructive lung disease characterized by narrowing of the airways.
Inflammation of the airways is a major component of asthma.
(2) Common symptoms are dyspnea, wheezing on expiration, and coughing.
(3) Two types:
(a) Extrinsic (allergic, atopic) asthma
(i) An atopic allergy caused by a type I immediate hypersensitivity immune reaction to an allergen.
(ii) Seen in children, adults.
(b) Intrinsic (nonallergic) asthma
(i) Not caused by an allergic reaction.
(ii) Mostly seen in adults.
The disorder is a chronic inflammatory condition in which the airways develop increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, inflammation, increased mucus production, and intermittent airway obstruction.
Signs and symptoms
- The clinical hallmarks of an attack are shortness of breath (dyspnea) and wheezing
- A cough—sometimes producing clear sputum—may also be present
- The onset is often sudden; there is a "sense of constriction" in the chest, breathing becomes difficult, and wheezing occurs
- Signs of an asthmatic episode are wheezing, rapid breathing (tachypnea), prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), and over-inflation of the chest.
- During very severe attacks asthma sufferer can turn blue due to lack of oxygen , can experience chest pain or even loss of consciousness, may lead to respiratory arrest and death
Pathophysiology
Bronchoconstriction : asthma is the result of an abnormal immune response in the bronchial airways. The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli, these stimuli include allergens, medications , air pollution, early child hood infection, exercise, emotional stress
Bronchial inflammation asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen presenting cells These activate an humoral immune response. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack
Symptomatic Treatment
Episodes of wheeze and shortness of breath generally respond to inhaled bronchodilators which work by relaxing the smooth muscle in the walls of the bronchi., More severe episodes may need short courses of inhaled, oral, or intravenous steroids which suppress inflammation and reduce the swelling of the lining of the airway.
Bronchodilators (usually inhaled)
Short-acting selective beta2-adrenoceptor agonists(salbutamol, terbutaline)
less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets
Antimuscarinics
Systemic steroids
Oxygen to alleviate the hypoxia that is the result of extreme asthma attacks.
If chronic acid indigestion ( GERD) is part of the attack, it is necessary to treat it as well or it will restart the inflammatory process
Preventive Treatment
most effective preventive medication are
Inhaled corticosteroids
Long-acting beta2-adrenoceptor agonists
Leukotriene modifiers
Mast cell stabilizers
Methylxanthines (theophylline and aminophylline),
Antihistamines, often used to treat allergic symptoms
Microbiological examination
This is a method by which body fluids, excised tissue, etc. are examined by microscopical, cultural and serological techniques to identify micro-organisms Microbiological examination responsible for many diseases.
INFLAMMATION
Response of living tissue to injury, involving neural, vascular and cellular response.
ACUTE INFLAMMATION
It involves the formation of a protein .rich and cellullar exudate and the cardinal signs are calor, dolor, tumour, rubor and function loss
The basic components of the response are
Haemodynamic changes.
Permeability changes
Leucocyte events.
1. Haemodynamic Changes :
- Transient vasoconstriction followed by dilatation.
- Increased blood flow in arterioles.
- More open capillary bed.
- Venous engorgement and congestion.
- Packing of microvasculature by RBC (due to fluid out-pouring)
- Vascular stasis.
- Change in axial flow (resulting in margination of leucocytes)
.2. Permeability Changes:
Causes.
- Increased intravascular hydrostatic pressure.
- Breakdown of tissue proteins into small molecules resulting in
- increased tissue osmotic pressure.
- Increased permeability due to chemical mediators, causing an
- immediate transient response. .
- Sustained response due to direct damage to microcirculation.
3. White Cell Events:
.Margination - due to vascular stasis and change in axial flow.
Pavementing - due to endothelial cells swollen and more sticky.
Leucocytes more adhesive.
Binding by a plasma component
Emigration - of leucocytes by amoeboid movement between endhothe1ial cells and beyond the basement membrane. The passive movement of RBCs through the gaps created during emigration is called diapedesis
Chemotaxis - This is a directional movement, especially of polymorphs and monocytes towards a concentration gradient resulting in aggregation of these cells at the site of inflammation. .Chemotactic agents may be:
- Complement components. (C3and C5 fragments and C567)
- Bacterial products.
- Immune complexes, especially for monocyte.
- Lymphocytic factor, especially for monocyte.
Phagocytosis - This includes recognition, engulfment and intracellular degradation. It is aided by .Opsonins., Specific antibodies., Surface provided by fibrin meshwork.
Functions of the fluid and cellular exudate
1. Dilution of toxic agent.
2. Delivers serum factors like antibodies and complement components to site of inflammation.
3. Fibrin formed aids In :
- Limiting inflammation
- Surface phagocytosis
- Framework for repair.
4. Cells of the exudate:
Phagocytose and destroy the foreign agent.
Release lytic enzymes when destroyed, resulting in extracellular killing of organisms- and digestion of debris to enable healing to occur
Pernicious anaemia
The special features are:
- Due to intrinsic factor deficiency
- Gastric atrophy with histamine fast achlorhydria
- Genetic basis (racial distribution and blood group A).
- Seen with auto immune disorders.
- Antibodies to parietal cells and to intrinsic factors are seen