Clinical presentation in respiratory system disease


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Brief description of common clinical features in respiratory system disease.

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Clinical presentation in respiratory system disease

  1. 1. Clinical Presentation in Respiratory System Disease 1) Respiratory Distress. a. Subjective. i. Exertional Dyspnoea. ii. Orthopnoea. b. Objective. i. Tachypnoea ii. Inspirtory Retractions iii. Active accessory muscles of respiration iv. Adventitious sounds 2) Cough. a. Dry. b. Productive. 3) Haemoptysis. 4) Cyanosis. a. Central. b. Peripheral. c. Chemical. Respiratory Distress Exertional Dyspnoea Dyspnoea: subjective feeling of difficulty in breathing due to increased respiratory effort. Exertional: provoked or increased by physical activity Types • Physiologic: with more than usual daily activity • Pathologic - Psychogenic: mainly at rest, with frequent sighing - Organic Grades 1) Provoked by more than usual daily activity 2) Provoked by usual daily activity 3) Provoked by less than usual daily activity 4) Present at rest Progression to Grade 4 may occur over: • Minutes (Acute Dyspnoea): foreign body aspiration, bronchial asthma, pulmonary embolism
  2. 2. • Days: rapidly accumulating pleural effusion • Months: interstitial lung disease • Years: emphysema Orthopnoea It is dyspnoea produced or aggravated on lying down, relieved (partially or completely) in the upright position. It may result from abdominal distension pushing the diaphragm upwards. Objective Signs of Respiratory Distress Tachypnoea • Normal adult rate: 12 – 20/min • Tachypnoea is a common sign of respiratory distress. • Respiration may be rapid and deep as well: acidotic or Kussmaul breathing. Inspiratory Retractions • Suprasternal, supraclavicular • Intercostal • Epigastric Active Accessory Muscles of Respiration • Sternomastoid • Scalene • Trapezius Adventitious Sounds • Wheezes (rhonchi): continuous musical sounds that denote bronchial obstruction • Stridor: It sounds like wheezes but arises from obstruction of upper airway (trachea, above). It is mainly an inspiratory sound. Cough It is forced expiratory effort against a closed glottis which then suddenly opens with a jet of air expelled out, possibly along with secretions. Types • Dry (Irritant): The irritant stimulus may be obvious (smoke, dust, pharyngitis) and may not. Two common "concealed" causes of resistant dry cough are post- nasal discharge and GERD (gastro-oesophageal refflux disease). • Wet (Productive): - Frothy Pink: pulmonary oedema - Mucoid: bronchial asthma, chronic bronchitis
  3. 3. - Mucopurulent, Purulent (yellowish, thick): infections - Rusty: lobar pneumonia - Greenish/Bluish: Gram negative infection - Foul Smelling: anaerobic infection - Blackish: smoker, coal workers Haemoptysis It is coughing of blood or blood tinged sputum due to bleeding from the respiratory tract below the vocal cords. Bleeding originating above vocal cords (nose, mouth, larynx) may produce false haemoptysis. Haemoptysis Haematemesis It is Coughing of blood Vomiting of blood Color Bright red Dark red Odor --- sour Reaction alkaline acidic Mixed with Sputum, air (frothy) food Sputum Blood tinged for 12 – 24 h after the attack normal Stool normal melena Cyanosis It is bluish discoloration of skin, mucous membranes due to presence of: - > 5 gm deoxy Hb /100 mL blood Or - abnormal Hb (met or sulph Hb) in surface capillaries. Normal level of deoxy Hb/100 mL blood: - Arterial: 0.75 gm - Capillary 2.25 gm - Venous 3.75 gm Etiology Central Cyanosis (↓ O2 loading by cardiopulmonary circulation) 1) Hypoventilation - ↓ alveolar PO2: eg, high altitude - Obstructive lung diseases - Restrictive lung diseases 2) Shunt - Cardiac Rt to Lt shunt (congenital cyanotic heart disease): eg, Fallot tetralogy - Pulmonary: pulmonary AV fistula 3) Diffusion Defect (Alveolo-Capillary Block)
  4. 4. - Pulmonary fibrosis - Pulmonary oedema 4) Ventilation Perfusion (V/Q) Mismatch - Pulmonary embolism (ventilation > perfusion = dead space effect) - Atelectasis/collapse (perfusion > ventilation = shunt effect) - Most pulmonary disorders produce hypoxia by more than one mechanism. V/Q mismatch is the most common. Peripheral Cyanosis Stagnant circulation • Generalized Stagnation (low cardiac output) - Heart failure - Shock • Localized Stagnation - Arterial: o Lumen: thrombosis, embolism o Wall:  Spasm: Raynaud`s disease, ergotism  Organic Changes: Buerger`s disease o Outside: compression by space occupying lesion. - Venous: venous obstruction, eg Superior vena cava obstruction → peripheral cyanosis in tongue and lips (exceptional) Chemical Cyanosis Abnormal Hb causes: • Dark color by itself. • Reducing the normal Hb, bec it has much higher affinity for O2 Causes of Methaemoglobinaemia: • Congenital • Nitrite producing intestinal flora (enterogenous cyanosis) • Drugs: nitrates, sulphonamides Central Cyanosis Peripheral Cyanosis Cause ↓ O2 saturation of core arterial blood (↓ O2 loading by cardiopulmonary circulation) Stagnant circulation → - ↓ peripheral arterial flow - ↑ O2 extraction by tissues Distribution Warm areas (tongue, interior of lips), all over Cold areas: tip of nose, lobule of ear, fingers, toes Temperature Warm Cold Clubbing + - Polycythaemia + - Effect of - Exercise May ↑ ↓
  5. 5. - Warming - Oxygen No effect ↓ to variable extent, maximal in low atmospheric PO2 and minimal in shunt ↓ No effect CyanosisHypoxia Type CentralHypoxic Hypoxia PeripheralStagnant Hypoxia ---Anaemic Hypoxia ---Histotoxic Hypoxia
  6. 6. - Warming - Oxygen No effect ↓ to variable extent, maximal in low atmospheric PO2 and minimal in shunt ↓ No effect CyanosisHypoxia Type CentralHypoxic Hypoxia PeripheralStagnant Hypoxia ---Anaemic Hypoxia ---Histotoxic Hypoxia