PATHOPHYSIOLOGY LECTURE

Prepared by Habtamu Bayih (MD)

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Introduction Pathology  is "Scientific study of disease"  Study of structural and functional changes in disease.  deals with knowledge of what causes disease, how disease starts, progresses & it explains the reason for signs and symptoms of patient" Branches of Pathology:  Histopathology / Anatomic Pathology : Pathologists specialising in anatomical changes in disease. Usually using a tissue biopsy.  Cytopathology: Pathologists specialising in study of body fluids & Cells.  Haematology: Study of blood and blood forming organs.  Morbid Anatomy: Autopsy or Post mortem study for legal or educational purpose. Aspects of disease
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 Pathogenesis- Study of disease progression or evolution.  Morphology - Study of structural changes in disease (Gross & microscopic)  Clinical Significance - Study of how clinical features are related to changes.  Factors causing disease  are mainly two types. 1. Environmental or external factors /acquired  Physical  Chemical  Nutritional  Infections  Immunological  Psychological 2. Genetic or Internal factors.  Age  Gene
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 Congenital disease Diseases which present since birth .  Familial diseases Diseases which occur in families  Major groups of diseases 1. Inflammatory disorders  are due to damage to tissues by various injuries (physical, chemical, infections etc.) 2. Degenerative disorders  are due to lack of growth or ageing. 3. Neoplastic disorders  are due to excess cell division forming tumours.  Cell injury, Adaptations, Necrosis & Ageing  Reversible injury  mild injury which causes stress on the cell but not cell death,,  such cells develop structural or functional changes to overcome injury known as adaptation.
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 Irreversible injury  severe enough injury which causes death of cell  Changes occurring in dead cells is known as necrosis.  Gangrene necrosis of large areas of tissue  Ageing: is time related gradual loss of structural and functional capacity of cells.  tissue injury and inflammation  Inflammation is "dynamic response of vascularized tissues to injury".  It is a complex multi step process of tissue response to injury.  The purpose of Inflammation is to defend against injurious agent and start healing & repair of injured tissue.  Inflammation is an important part of body's defence mechanisms.  Inflammation brings together defence forces such as WBC, antibodies and other chemicals apart from bringing more nutrients and healing factors to the site of injury.

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 Mechanism of Inflammation:  Vaso dilatation - Hyperemia  Exudation – Edema  Emigration of cells  Chemotaxis & phagocytosis  Antibodies and other chemical mediators regulate these events  Clinical signs of inflammation.  Rubor(redness),  tumor(swelling),  Calor(Heat),  Dolor (pain) and  Loss of function

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 Techniques in Pathology  Gross Pathology:  Light Microscopy  Histochemistry, Biochemical  Immunohistochemistry  Electron Microscopy  Cell Cultures, Medical Microbiology  Molecular Pathology

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Disease of respiratory system Rhinitis (Common cold )  Inflammation of nasal mucosa .  Inflammations of respiratory system are commonly caused by viral infections.  Coryza is common name for viral Rhinitis, occurs in two phases.  Viral infection phase:  shows all features of inflammation  loss of surface epithelium but without cellular exudates.  this destruction weakens mucosa.  Common viruses are Rhinoviruses  Bacterial secondary infection phase.  Invasion of weak mucosa by many normal throat bacteria to produce cellular exudates or pus. E.g. streptococci & Haemophillus.  As the immunity is only for short duration, and viruses are of many types and ubiquitous in nature, repeated infections are common
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Sinusitis  Inflammation of paranasal air sinuses  Common types of sinusitis are maxillary, mastoid, frontal sinusitis etc.  Sinusitis can be acute or chronic.  Usually sinusitis results from extension of infection from nasal or pharyngeal regions.  Chronic sinusitis results from Repeated acute inflammations causing destruction of mucosa and bacterial or fungal infections Allergic Rhinitis & Bronchitis or Hay fever:  Due to allergens like pollen grains, dust mite etc.  Usually seasonal with repeated attacks.  Initial antigen antibody reaction producing severe inflammation and increased mucous production producing typical secretions.  It may be followed by secondary infection producing mucopurulent exudates (pus).
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Pneumonia  Inflammation of lung of lung parenchyma caused by infectious & noninfectious agents  Result when defense mechanism of RT or resistance of the host is impaired  based their anatomic distribution pneumonias are classified in to: 1. Lobar pneumonia  Involvement of a large portion of or an entire lob of the lung  Appr. 90% are caused by strep.pneumonia  Tissue changes in lobar pneumonia divided in to 4 stages  Congestion: vascular engorgement of the alveolar vessels & transudation of serous fluid into the alveoli.  Lasts about 24 hrs  Red hepatization:extravasation of RBCs and fibrine into the alveoli  lasts from 2nd to 3rd day of the disease

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 Gray hepatization: accummulation of fibrine and disintegration of the inflammatory WBC &red cells.  Lasts from 4th to 8th day of the disease  Resolution: enzymatic digestion & removal of inflammatory exudate from the infected lung area 1. Bronchopneumonia  Patchy consolidation with involvement of several lobules  Usually involve basal areas of both lungs 2. Interstitial pneumonia  Inflammatory process confined within the walls that surrounds the alveoli & bronchioles  Usually seen in immunocmromised patients

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Tuberculosis:  caused by Mycobacterium tuberculosis.  Affect every organ in the body, but Lungs are most commonly involved.  Affects immunosuppressed or malnourished individuals living in crowded condition.  In endemic areas first infection occurs early in life (Primary TB) and usually heals with no complications  Secondary tuberculosis occurs later in age due to breakdown of body resistance.  Secondary TB is a Chronic slowly progressive disease, causing much tissue damage & complications.  Damage & Necrosis are due to cytolytic enzymes of the macrophages and not due to bacteria.  Tubercle is the microscopic lesion of TB.  Central caseous necrosis surrounded by macrophages, giant cells & lymphocytes with fibrosis around.
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Chronic obstructive lung disease 2.Emphysema  Loss of lung elasticity & abnormal dilatation of the air spaces distal to the terminal bronchioles with destruction of the alveolar walls & capillary beds  Suspected causes are alpha1 – antitrypsin deficiency & cigarette smoking  Lungs are grossly hyperinflated with diffuse air filled blebs  Microscopically abnormal fenestration of alveolar wall or other parts of acinus are seen  Clinically dyspnea, cough, barrel chest may be there 3.Chronic bronchitis  Chronic infllammation of bronchi  Characterized cinically by persistence of cough with sputum producion for at least 3 months in at least 2 consecative years.  Chronic irritation from ciggaret smoking & env,l pollutants and microbiologic infection are factors for its genesis
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 Hypertrophy & hyperplasia of mucus glands of bronchi and loss ciliated cells of the air ways from chronic irritation result in  Increase mucus production & accumulation  Obstruction of bronchi  20 bacterial infection  Clinical features are  Productive cough  Cyanosis  Hypoxemia  Hypercapia (↑ Co2 ) 1. Bronchial asthma  Chronic relapsing inflammatory disorder characterized by  Hyper reactive airway & ↑ hyperresponsiveness of TB tree to various stimuli  Episodic & reversible bronchoconstriction  Edema of the mucosal surface of the bronchioles  Increase production of mucus
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 Classified in to two  Extrinsic (allergic)  induced by exposure to extrinsic antigen such as pollen, dust, etc  Seen in persons with a family history of allergy  Onset occurs during childhood or adolescence  Intrinsic  Initiated by nonimmune mechanisms such as infection, ASA use,cold, etc  No familial history  Onset usually after age of 35  Pathologic changes include  Hyperinflated lung  Thickening of BM of bronchial epithelium  Edema & inflammatory infiltrate in to the bronchial wall  Hypertrophy of bronchial smooth muscles  Clinical feature  paroxysms of dyspnea, cough, & wheeze
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Bronchoectasis  Abnormal dilatation of bronchioles associated with chronic necrotizing infection of the bronchi  Causes include  Bronchial obstruction due to tumors, foreign bodies, mucus impaction, etc  Congenital conditions associated with abnormal dep't of bronchi  Cystic fibrosis  Pathogenesis  Obstruction & infection are major & necessary predisposing factors  Bronchial obstruction → atectasis → smooth muscle relaxation &dilatation of the walls of the airways  Infection inflammation, weakening & further dilatation of the walls of bronchioles  Pathologic change  Dilated airways up to 4x  Necrotizing inflammatory change of the affected airway
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