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Respiratory Patho
BMS263
| Term | Definition |
|---|---|
| Pulmonary Disease Classification | Acute or Chronic. Infectious or Non-Infectious. Obstructive or Restrictive (fundamentally different, however many similar manifestations) |
| Obstructive Lung Disease | Characterised by airway obstruction. Bronchial asthma, Bronchiectasis, COPD (Chronic bronchitis, Emphysema). FVC is normal, but FEV1 is impacted |
| Restrictive Lung Disease | Characterised by decreased compliance of lungs. Acute respiratory distress syndrom, Inhalation disorders. FVC is impacted, but FEV1 is normal. |
| Asthma | Chronic Inflam disorder of lungs. Mast cells, eosinophils, T lymphocytes, macrophages, neutrophils & epithelial cells. Causes wheezing, breathlessness, chest tightening, coughing. Widespread, reversible airflow obstruction. 2 phases: bronchospasm & inflam |
| Asthma Risk Factors | Family history, allergen exposure, city living/ air pollution, smoking, recurrent respiratory viral infections. |
| Pathophysiology Of Asthma | Allergen/irratant exposure = Cascade mast cell degranulation & release of inflammatory mediators = bronchospasm, mucus secretion, impaired mucociliary function, contraction bronchial SM = Bronchial hyperresponsiveness and airway obstruction |
| Acute Asthmatic Response | Allergen/irritant exposure. Allergen binds to preformed IgE on the surface of mast cells, release of mediators (histamine) = Bronchospasm, mucosal oedema, mucus secretion = Bronchial hyperresponsiveness & airway obstruction. Can last for up to 2 hrs |
| Late Asthmatic Response | 4-8 hrs after allergen/irritant exposure. Inflam cell recruitment (neutro, baso & eosinophils). 2nd rnd of pathophysiology = Bronchial hyperresponsiveness & airway obstruction. Lasts up to 24 hrs. Can cause Resp. Alkalosis > Resp. Acidosis in later stages |
| Bronchodilators | B2 Adrenergic Agonists, Xanthines, Cys-leukotriene receptor antagonists, Muscarinic Antagonists |
| β2 adrenergic agonists | Relax smooth muscle by physiological antagonism. Will be effective no matter what the stimulus. Short acting = salbutamol (ventolin). Long acting = salmeterol (seretide) |
| Xanthines | 3 types: Theophylline (coffee, tea), Caffeine (coffee, tea) & Theobromine (cocoa). Only theophylline used clinically. Bronchodilatation. Side effects: nervousness, tremor stimulate heart, CNS, respiration diuretic, anorexia, nausea, vomiting |
| Cysteinyl-Leukotriene Receptor Antagonists | Mild bronchodilators. 33% as effective as salbutamol. Act by different mechanism to β² agonists, therefore effect is additive. Montelukast and zafirlukast. Oral tablets rather than inhalants |
| Glucocorticoids | Affect late phase only. No bronchodilatation. Decrease inflam only (preventative). Decrease formation of cytokines. Inhibit formation of vasodilators, spasmogens & chemotaxins. Up-regulate β adrenergic receptors, to cause bronchodilation |
| Glucocorticoid Effects | Thrush. Dysphonia (impaired vocal sounds). Adrenal suppression. Increased BGL, muscle wastage, osteoporosis, etc. Fluticasone propionate (type of glucocorticoid) is poorly absorbed from the GI tract and first pass nears 100%, thus drug is inhaled |
| Cromoglicate | Not bronchodilator. Prevents early and late phase if given regularly. Prevents histamine release from mast cells. Suppresses irritant receptors. May inhibit release of cytokines. Not all asthmatics respond |
| Muscarinic Antagonists | Example: Ipratropium. Relaxes parasympathetic induced bronchconstriction. Most effective in irritant induced asthma. May assist in allergic asthma. Inhibits mucous secretion. May increase mucociliary clearance. No effect on late phase inflammation |
| Chronic Obstructive Pulmonary Disease (COPD) | Syndrome. Includes pathological lung changes consistent with emphysema &/or chronic bronchitis. Generally in the elderly. Caused by smoking. Causes emphysema, Chronic obstructive bronchitis & bronchiectasis |
| Mechanisms of COPD | Inflam & fibrosis of bronchial wall. Hypertrophied mucus glands = excess mucus & obstructed airflow. Loss of alveolar tissue = decreased surface area for gas exchange. Loss of elastic lung fibres = Airway collapse, obstructed exhalation, air trapping |
| Emphysema | Pink Puffers. Loss lung elasticity. Abnormal enlargement air spaces distal to terminal bronchioles. Destruct of alveolar walls & capillary beds = hyperinflated lungs & increase in TLC. Cause smoking, α1 antitrypsin deficiency (neutrophils damage alveoli) |
| Chronic Bronchitis | Blue Bloaters. Caused by smoking. Chronic irritation of airways = Increased number of mucus cells, Mucus hypersecretion, Hypertrophy of the submucosal glands in the trachea and bronchi. Productive cough: usually in the morning associated with dyspnoea |
| Consequences of COPD | COPD --> Decrease ability to exhale --> air in lungs becomes stale. Central chemoreceptors triggered = increase resp = High CO2 --> hypercapnia. Peripheral chemoreceptors increase respiration = Low O2 --> Hypoxia |
| COPD Treatment | Stop smoking. Immunisation against flu & pneumococcus. No current treatments reduce progression of COPD or inhibit inflam. Medication: Bronchodilators (Short/Long acting), Oxygen therapy, Glucocorticoids, Broad spectrum antibiotics |
| Bronchiectasis | Caused by an infection and inflammation destroying smooth muscle in airways, causing permanent dilation of the bronchi and bronchioles. Causes productive cough. Irreversible. Occurs in variety of ages |
| Mechanims of Acute Respiratory Distress Syndrome (ARDS) | Clinical lung injury --> massive pulmonary inflammation --> severe pulmonary oedema & hypoxaemia --> injury to pulmonary capillary endothelium, platelet aggregation and thrombus formation |
| Consequences of ARDS | Develops within 24 hrs of initial lung injury. Can result in death due to respiratory acidosis and reduced CO due to hypotension |
| ARDS Treatment | Supportive, to maintain tissue oxygenation and minimise lung injury. Often require mechanical ventilation |
| Pneumonia | Infection lower respiratory tract causes inflam of alveoli & bronchioles. Productive cough. At Risk: Age, immunocompromised, underlying lung disease, alcholism, smoking, immobilisation. Causative microorganism influence clinical presentation & treatment |
| Tuberculosis | World’s foremost cause of death from a single infectious agent. Causative organism: M tuberculosis. Transmission is communicable.Manifest in lungs & then bones, GIT, lymph nodes, meninges, skin. Primary and secondary infections |
| Primary TB Infection | Infection --> Acute exudate-lesion develop --> Rapid spread to lymphatics & LN --> LN undergo caseation & calcification (Ghon foci) |
| Ghon Complex | Ghon focus with lymph node. Nodules in lung tissue and lymph nodes. Caseous necrosis inside nodules. Calcium may deposit in the fatty area of necrosis. Visible on X-rays. Related to TB |
| Secondary TB Infection | Reinfection (can be many yrs later). Gradual progress of primary infection. Reactivation of previously healed primary lesion. Cause can be from drug interaction or immunodeficiency – e.g. HIV infection, or immunosuppressive drug |
| Clinical Features of TB | Lung symptoms include productive cough and coughing blood, chest pain, fatigue, night sweats, weight loss. If systemic can cause symptoms in bones, GIT, urogenital and meninges. Also Anaemia + leucocytosis; hyponatraemia (non-specific) |
| Treatment of TB | BCG vaccine. 1st phase of treatment (2 months). Combination of antibiotics (Isoniazide, Rifampicin, and pyrazinamide). 2nd phase of treatment (4 - 20 months). Combination of antibiotics (Isoniazide and Rifampicin) |
| Isoniazide | Absorbed by GIT. Penetrates TB lesion. Pass freely into cells. Halts growth of resting & kills dividing mycobacteria. Pro drug activated by bacterial enzymes. Inhibit synthesis of mycolic acids. Resistance likely. HL 1-3 hrs. Excreted urine unchanged drug |
| Rifampicin | Binds and inhibits DNA dependent RNA polymerase in prokaryotic cells. Resistance can develop instantly due to mutation in microbe. Absorbed by GIT, widely distributed to tissues. Half life of 1-5 hours – excreted in urine and bile |
| Pyrazinamide | Absorbed by GIT, widely distributed to tissues. Inactive at neutral pH. Activated (tuberculostatic) when in contact with the low pH phagolysosomes of macrophages and can effectively destroy the intracellular organisms within the macrophage |
| Influenza | Transmission is by aerosol or direct contact. Incubation up to 3-7 days. Onset is abrupt & lasts 3-5 days. Upper respiratory infection, cough & fever. Can cause viral pneumonia. Management: bed rest, analgesic, decongestant, etc |
| Cystic Fibrosis | Genetic condit. Fluid secretion in exocrine glands in epithelial lining of resp, GIT, reproduct tracts. Disorder in chloride transport proteins. High NaCl in sweat. Less Na & H2O in respiratory mucus (thicker). Obstructs airways, pancreatic, biliary ducts |
| Cystic Fibrosis Treatment | Promote lung mucus clearance – chest physio, bronchodilators, aerosolised DNase, Inhaled antibiotics, Lung Transplantation. Newborns in Australia screened for CF. Sweat test determines level of Cl- |
| Lung Cancer | Bronchogenic carcinoma. Arises from epithelial cells lining the lungs. Causes: Smoking (genetic mutations in bronchial cells, damaged bronchial mucosa), toxins, radiation, air polut, TB. Manifest from organ funct changes or above listed smoking changes |
| Management of Lung Cancer | 1- Diagnosis: Radiology, Bronchoscopy or CT guided biopsy, sputum cytological examination. 2- Treatment: Depends on type & grade of cancer. Surgery, radiotherapy, chemotherapy or combination |
| Cough | Protective reflex that cleanses lower airways by explosive expiration. Reflex stim by irritant receptors in airways. Acute less than 3 weeks (URTI, acute bronchitis). Chronic more than 3 weeks (asthma, reflux OR smokers: chronic bronchitis, lung cancer) |
| Cough Suppressants | Cause thickening and retention of sputum (should not be used for chronic pulmonary infections). Antitussives act on brainstem to depress “cough centre". Codeine weak opioid. Side effects: inhibits ciliary activity, constipation |
Created by:
Mandyrox300
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