Respiratory System PDF

The Respiratory System 1 Upper RT – Nose, sinuses, larynx, trachea, main bronchi Effected areas Nose Sinuses Larynx trachea Symptoms Mild/transient Cause...

The Respiratory System 1 Upper RT – Nose, sinuses, larynx, trachea, main bronchi Effected areas Nose Sinuses Larynx trachea Symptoms Mild/transient Cause Viral Lower RT – bronchi, lungs, terminal bronchi Effected areas Bronchi Terminal bronchi Lung parenchyma Symptoms Serious - mortality Cause 2nd to irritants Bacteria Viruses Atypical fungi Defence mechanism of respiratory organs: Cough reflex (aspiration) Nasal hairs Ciliary apparatus Secretion of IgA antibodies Phagocytic activity by alveolar macrophages Accumulation of secretions Alveolar fluid Cell mediated immunity (chronic diseases) Virulent infections Primary infections: Viral, bacterial, mycoplasma, fungal Secondary bacterial: following a viral infection. Secondary to irritants. Viral infections: Common cold: ○ Acute inflammation of eyes and throat with congestion and watery exudate ○ Secondary bacterial infection Viral sore throat: ○ Adenovirus (pharyngitis) ○ Secondary infection (purulent- pus) Influenza: ○ Involves mainly upper respiratory tract. Bacterial: ○ Streptococcus Pyogenes Acute laryngitis/ epiglottis: ○ Haemophilus influenza type B/ Streptococcus Pyogenes Pneumonia: ○ infection of alveolar spaces which generates a host reaction (alveolar exudates) ○ Complications: pleurisy Bronchopneumonia: Inflammation starts in the bronchus and spreads to adjacent alveolar spaces Streptococcus pneumoniae/ Staphylococcus Aureus White yellowish foci of condensation, separated by normal lung parenchyma. Lobar Pneumonia Streptococcus pneumoniae Inflammation starts in the alveoli and moves to the entire lobe. Congestion, red and grey hepatization. Viral pneumonia Interstitial pneumonia, initially atypical pneumonia. Influenza A + B, Adenovirus, SARS Pulmonary Tuberculosis- Mycobacterium tuberculosis Primary tuberculosis in childhood (rare)  Primary lesion (ghon focus- below pleura in mid lung, heal with fibrosis/ calcification) ○ TB survives in Foci and becomes the source of later infection. ○ Patient develops cell mediated immunity. Secondary tuberculosis: new infection or by reactivation of microbe ○ Coughing up caseous material provides a source of infection. __________________________________________________________________________________________ The Respiratory System 2 ‘Define chronic bronchitis and emphysema.’ ‘Discuss the pathogenesis of emphysema’ COPD Chronic bronchitis ○ Persistent cough with sputum production Emphysema ○ big weak air spaces which causes air to enter in chest cavity which can cause pneumothorax (enlargement of air spaces distal to the terminal bronchiole) ○ destruction of alveolar walls ○ pathogenesis: proteases/ antiproteases produce elastase. ○ Prognosis: with severe emphysema (cor pulmonale) death can occur. Both chronic bronchitis + emphysema are accompanied by obstruction to air flow. ‘Discuss the pathogenesis of asthma.’ Asthma Paroxysmal constriction of the bronchial airways. Bronchi are occluded by thick mucous plugs. Eosinophils in bronchial walls. Allergic asthma (type 1)- IgE  Occupational chemicals (type 1 and cell mediated)- after repeated exposure Type 1: activates mast cells and basophils hence it releases histamine (vasodilation) ‘Describe the classification of malignant lung tumours.’ Lung Tumours Epithelial (90-95%) ○ Non-small cell carcinoma (70-80%) Squamous cell: (25-40%) from smokers Arises in a main bronchus from squamous epithelium Large friable mass which extends into surrounding lung, main airways Adenocarcinoma: (25-40%) Peripheral tumours Originate from glandular epithelium Large cell (10-15%) Small cell carcinoma (20-25%) Oat cell Carcinoid Lymphoma ‘Discuss the incidence, cause and prognosis of primary lung carcinoma’ ‘Describe the spread of primary bronchial carcinoma.’ Bronchial carcinoma Incidence 40-70 yrs Cause Cigarettes Prognosis Poor surgical resection when practical possible in only 20 - 30% of patients 30-40% 5yr survival after surgery Spread and metastases Spread and ○ Local; lung, hilar tissues, large blood vessels. metastases: ○ Lymphatics: hilar first, cervical ○ Blood: liver, adrenal glands Non-metastatic systemic effects finger clubbing, cachexia, neurological syndromes Paraneoplastic Syndromes Paraneoplastic: hormone production ACTH / ADH / PTH Small cell or squamous cell Secondary- multiple nodules, any tumour, breast kidney and testicular tumours. Distinguish secondary lung tumours from primary lung tumours. Feature Primary Lung Tumors Secondary Lung Tumors Origin Arise from lung tissue or bronchi. Metastases from other primary cancers. Morphology Solitary mass; squamous, Multiple nodules scattered in adenocarcinoma, etc. the lungs. Common Primary Lung tissue itself. Breast, kidney, testis, etc. Sites Histology Differentiated lung-specific cell Histology matches primary types. tumor (non-lung). Prognosis Depends on type and stage. Reflects prognosis of primary tumor. Neoplasia: Definitions/nomenclature Neoplasia New growth - benign or malignant Tumor Benign or malignant Cancer Malignant Oncology Study of cancer Pathologist Studies disease Oncologist Treats cancer patients Benign (-OMA) Cannot metastasize but can still be lethal ex: CNS Malignant (-CARCINOMA) Tumour acquired ability to invade and spread Differentiation How closely cancer resembles original site of origin DESCRIPTIVE TERMS FOR MALIGNANCY Pleomorphism Varies in size and shape Mitotically active proliferates  Hyperchromasia Darker nuclei Anaplasia Wild appearance Cell types Epithelium Lining tissue Mesenchymal Bone, cartilage, muscle Germ cell Reproductive systems – testes, ovaries May be benign (cannot metastasis but can still be lethal) or malignant (can spread). Benign: suffix – oma - (Lipoma, chondroma, adenoma (gland) Benign vs malignant Benign Malignant/metastasis Cannot metastasize but can still be lethal Cancer spreads from original site of origin ex: CNS Ex: Lymphatic – carcinomas Blood – sarcomas Epidemiology - study of how often diseases occur in different groups of people and why 1. Environmental 2. Ageing population 3. Iatrogenic – chemotherapy related cancers Genetics – influences: 1. Balance between cell replication and cell death 2. Oncogenes vs tumour suppressor genes 3. Mutations a. Hereditary – family history b. Acquired – somatic i. Environment ex: sun ii. Occupation iii. Diet Mutations answer Point Change at point Deletions Deletion of part of gene Rearrangements Rearrangement of genetic material Amplification Increasing copy numbers Gain or loss of Gain of func – promote cell growth function Loss of function – promote cell death 4. Oncogenesis = mutations leading to cancer development