Respiratory Pathology Table PDF

Preview

Summary

Condition Signs and symptomsCauses Risk factors Pathophysiology Diagnosis Treatment ComplicationsCoughSymptom – PROTECTIVE MECHANISMAn important protective role for the airways and lungs – keeps the airways clear and unwanted irritants and particles.3 PHASESInspiratory phase – inhalation generates v...

Description

Condition

Cough

Breathlessness SOB

Acute asthma

Signs and symptoms

Symptom – PROTECTIVE MECHANISM

Common symptom with many causes

Wheeze – expiratory and polyphonic Cough SOB

Causes

An important protective role for the airways and lungs – keeps the airways clear and unwanted irritants and particles.

Risk factors

Diagnosis

Atopy, prepuberty, infantile respiratory infections,

Respiratory causes: asthma, COPD, pneumonia, pneumothorax, pleural effusion, lung cancer, interstitial lung disease, occupational lung disease Non-respiratory: Shock, anaemia, pulmonary oedema, tachyarrhythmia, valve disease, MSK, neuro Bronchial smooth muscle contraction triggered by a range of stimuli, mucosal swelling and

Treatment

Complications

Voluntary = originates in cerebral cortex Reflexive cough = caused by direct activation of receptors in airway sensory nerves

3 PHASES Inspiratory phase – inhalation generates volume necessary for effective cough Compression phase – closure of larynx, chest wall muscle contraction, diaphragm and abdominal wall Expiratory phase – glottis opens, high expiratory airflow and airway compression

Hypoxia, hypercapnia, airway obstruction, decreased lung compliance, acute right heart strain, chest wall stiffness, acidosis, anaemia

2 PHASES Immediate phase Allergens (extrinsic asthma) trigger bronchoconstriction.

Pathophysiology

2 afferent pathways from vagus nerve 1) Mechanoreceptors (myelinated) 2) Chemoreceptors (unmyelinated) Efferent fibres – vagus, phrenic and spinal motor nerves to innervate, larynx, diaphragm and abdominal muscles.

Find and treat the cause Bronchodilators and steroids, oxygen, lignocaine, morphine, diazepam, retraining and exercise, cognitive control

Peak expiratory flow readings Spirometry with

1) Salbutamol inhaler 2) Salbutamol inhaler + inhaled beclomethasone 3) Salbutamol +

Chest tightness Episodic, diurnal and triggers are present.

Chronic asthma

Intermittent dyspnoea, wheeze, cough (often nocturnal) and sputum

More susceptible to bronchodilators. Type 1 hypersensitivity: mast cells degranulate releasing histamine and prostaglandins. Late phase Bronchoconstriction, airway inflammation, oedema, hyperresponsiveness. Less susceptible to bronchodilators. Type 4 hypersensitivity: cell-mediated with Th2 lymphocytes which release cytokines.

tobacco exposure, premature/lo w birth weight, obesity, social deprivation, exposure to inhaled particles

inflammation from mast and basophil cell degranulation. Results in the release of inflammatory mediators and increased mucus production.

bronchodilator reversibility

Same as above along with rhinovirus, parainfluenza, respiratory syncytial virus RSV

Same as above. Narrowing of airways, hyperresponsiveness to due a range of stimuli. Increased mucosal inflammation and recruitment of eosinophils, mast cells, neutrophils and T lymphocytes. Hypersecretion of mucus and oedema. CHRONIC –

SAME AS ABOVE

Fractional exhaled FeNO

salmeterol + beclomethasone. Can increase steroid and trial leukotriene antagonist/theophyl line. 4) Above + aminophylline/the ophylline + montelukast 5) Oral steroid, low dose. Maintain high dose inhaled steroid. Inhalers plus refer to specialist.

SAME AS ABOVE

LIFE THREATENING 1) Inability to complete full sentences 2) High resp rate 3) PEFR < 33% 4) Hypoxaemia TREATMENT Immediate nebulised B2 agonist Ipratropium bromide Oxygen IV Steroids Xanthines

Pulmonary oedema

Acute breathlessness Wheezing Anxiety Tachypnoea Pink frothy sputum Tachycardia Basal crackles/wheeze

Anaphylaxis

Rash General itchiness Wheeze/stridor SOB

1) Increased venous hydrostatic pressure 2) Injury to alveolar capillary wall/vessels – increased permeability 3) Blockage of lymphatic drainage

remodelling of airway with increased smooth muscle – irreversibly airway narrowing. Abnormal increase in the interstitial fluid in the lungs. Increased hydrostatic pressure or reduced oncotic pressure = increased interstitial fluid. 1) Fluid accumulates in loose connective tissue around bronchi and large vessels 2) Fluid then distends the thick collagen alveolar wall 3) Accumulatio n of fluid in alveolar spaces Immune mediated systemic reaction to pathogen. Mediated by IgE and mast cells.

Blood – brain natriuretic peptide CXR

Sitting position IV diuretics Morphine to sedate and cause vasodilation Aminophylline GTN infusion can help

Patch test

IV fluids and oxygen IM adrenaline Chlorphenamine (antihistamine)

Tachycardia Hypotension GI symptoms

Obstructive sleep apnoea

Cystic fibrosis

Chronic snoring with pauses in breathing – choking and gasping after Daytime somnolence Morning headaches Difficulty concentrating Mood swings Dry throat

Obesity Adenotonsillar hypertrophy Macroglossia Nasal obstruction Alcohol Smoking Sedative drugs

Neonate Failure to thrive, sweaty skin Cough, wheeze, recurrent infections,

Pseudomonas aeruginosa = can cause infections

2 types Obstructive Central Mostly affects overweight middle- aged men

Release of cytokines and inflammatory mediators e.g. histamine. Causes bronchial smooth muscle contraction and vascular leakage around body. Obstructive Occlusion of upper airway caused by adipose tissue. Furthering narrowing caused by smooth muscle tone. Airway occluded, patient wakes up and airway reopens. Central Airway remains patent but there is no efferent output from respiratory centres in brain. Increased PC02 wakes patient to rebalance gases. Autosomal recessive condition. Mutations in CF transmembrane conductance regulator CFTR. This leads to defective

Hydrocortisone

Epworth Sleepiness scale Normal= 16 Sleep study

CPAP = Continuous positive airway pressure to keep airways patent Theophylline BiPAP = Bilevel positive airway pressure. Surges of oxygen administered during inhalation and is not continuous.

Sweat test Guthrie = heel prick Sweat sodium and chloride Genetics

MDT management Physiotherapy for airway drainage. Antibiotics for acute infective exacerbations and prophylactically.

Hypertension Pulmonary hypertension Cor pulmonale Ischaemic heart disease Stroke

bronchiectasis, pneumothorax, resp failure, pancreatic insuffiency, gall stones, cirrhosis

Tuberculosis

Cough Sputum production Haemoptysis Fevers Night sweats Fatigue Weight loss

chloride secretions and increased sodium absorption across airway epithelium. This changes the composition of airway surfaces.

Close contact with TB Immunocompromised Homeless Drugs/alcohol abuse Mycobacterium tuberculosis

Primary TB Small lesion subpleural in middle/upper zones. Lesion becomes a granulomatous inflammatory tubercle. It then undergoes caseous necrosis. Liquefaction occurs. Lymphatic spread of mycobacterium occurs. Secondary TB Reactivation of primary infection. Posterior/apical upper lobe or

Screening for known common CF mutations Blood Sputum sample CXR – hyperinflation and bronchiectasis Abdominal ultrasound Spirometry CXR – hilar lymphadenopa thy 3 sputum samples Ziehl-Neelsen stain The Mantoux tuberculin skin test – to check if person is infected with M.tuberculosis Interfrongamma release assay IGRAs – measures immune system reaction

Mutation-specific therapies Ivacaftor and lumacaftor. Reduce misfolding in the CLchannels.

Isoniazid Rifampicin Ethambutol Pyrazinamide PREVENTION BCG vaccine

Lung cancer

Adenocarcinoma Coughing Haemoptysis Chest pain Weight loss

Adenocarcinoma – non smoking elderly women and Far East.

superior lower lobe. Tubercle follicles develop, lesions enlarge by new follicles forming. Infection spreads via lymphatics and delayed hypersensitivity occurs. Lesions are bilateral and cavitating. Non small-cell (squamous, adenocarcinoma and large cell) and smallcell. Squamous Squamous epithelium in large bronchi. Paraneoplastic syndromes. Hilar tumours and prone to necrosis and cavitation. Adenocarcinoma Diffuse pulmonary fibrosis and honeycomb lung. Formed from glandular tissue. Small cell

to M.tuberculosis

CXR CT Fibreoptic bronchoscopy Transthoracic fine needle aspiration biopsy

Surgery Radiology Chemotherapy Terminal care Prednisolone Opioid analgesia Laxatives

Ulceration of bronchus Bronchus obstruction Central necrosis Pancoast syndrome

Chronic bronchitis (COPD)

Symptoms Cough Sputum Dyspnoea Wheeze Signs Tachypnoea Use of accessory muscles Hyperinflation Reduces cricosternal distance, chest expansion, hyperinflation

Emphysema (COPD)

Genetic (alpha1antitrypsin deficiency↓) (2-3% of cases) Air pollution

Clinically defined: cough and sputum production for 3 months over 2 consecutive years. Symptoms improve if they stop smoking

Age, smoking, occupation

Histologically defined: enlarged air spaces distal to terminal

Endocrine cells. Most aggressive. Large bronchi. Paraneoplastic syndromes seen. Cigarette smoke and exposure to other triggers activates inflammatory cells. Epithelial cells, macrophages and neutrophils release inflammatory mediators and proteases. Increased mucus production and impaired mucocilliary action.

Same as above. Triggers cause neutrophils to release neutrophil elastase enzyme that

CXR: hyperinflation, flat hemidiaphrag ms, large central pulmonary arteries CT: bronchial wall thickening, scar ring, air space enlargement Spirometry: obstructive + air trapping ABG: low Pa02, hypercapnia ECG: right ventricular have – cor pulmonale CXR: hyperinflation, flat hemidiaphrag ms, large

Start with SAMA/SABA Then LAMA LABA + inhaled corticosteroid LAMA + LABA + inhaled corticosteroid Oral immunomodulators, prophylactic azithromycin 3* week.

Start with SAMA/SABA Then LAMA LABA + inhaled corticosteroid

Acute exacerbations with infection, polycythaemia, respiratory failure, cor pulmonale, pneumothorax and lung carcinoma

Acute exacerbations with infection, polycythaemia, respiratory failure, cor pulmonale,

Smoking (85% of cases) Exposure through occupation (15% of cases) Second-hand smoke exposure

Pulmonary Hypertension

Nonspecific symptoms -dyspnoea on exertion -SOB -palpitations -chest pain -light headedness -syncope Signs Increased JVP RVH Pedal oedema Hepatic

bronchioles, with destruction of alveolar walls but often visualised on CT.

Can be due to -increased pulmonary vascular resistance -hypoxia/embolus -back flow -LSHF -can be secondary to another condition e.g. mitral stenosis/LA conditions

destroys elastin in alveoli. This causes alveolar destruction. Centriacinar Septal destruction and dilation limited to the centre of the acinus around terminal bronchioles and mostly affects upper lobes. Panacinar Whole of the acinus is involved distal to terminal bronchioles and lower lobes are mostly affected. A1 antitrypsin deficiency. Mean pulmonary artery pressure of >25mmHg at rest and 30 mmHg on excretion. Endothelial damage causes release of vasoconstrictive agents as well as procoagulant factors. This results in thrombus formation. Vascular remodelling occurs, leading to

central pulmonary arteries CT: bronchial wall thickening, scar ring, air space enlargement Spirometry: obstructive + air trapping ABG: low Pa02, hypercapnia ECG: right ventricular have – cor pulmonale

LAMA + LABA + inhaled corticosteroid Oral immunomodulators, prophylactic azithromycin 3* week.

Right heart catheterization PA pressure can be measured directly, and LA pressure estimated.

Calcium channel blockers COPD patients O2 therapy Thromboembolism Warfarin Anticoagulation IPAH Anticoagulation

Echocardiogra m– RV systolic pressure and visualise LA, mitral valve, RV, look for

Type 5 phosphodiesterase inhibitors (sildenafil) reduce vascular remodelling. Chronic infusions/nebulisations of

pneumothorax and lung carcinoma

enlargement Increased S2 Right ventricular dysfunction = SEVERE

Community acquired pneumonia

Symptoms: fever, rigor, malaise, anorexia, dyspnoea, cough, purulent sputum, haemoptysis and pleuritic pain. Signs: pyrexia, cyanosis, confusion, tachypnoea, tachycardia, hypotension, consolidation, dull percussion, reduced chest expansion, bronchial breathing and pleural rub.

irreversible fibrosis of the pulmonary system.

Most common: streptococcus pneumoniae. Then haemophilus influenzae, Moraxella catarrhalis.

Very old or young Smoking Chronic lung disease Chronic heart disease Alcohol excess Immunosuppr ession

congenital abnormalities CXR Pulmonary function test ABG V/Q scan – check for chronic thromboemboli sm Assess oxygenation ABG and SaO2 Blood test: FBC, CRP CXR: lobar/multilobe infiltrates, cavitation and pleural effusion. Sputum culture: test microbiology Urine, pleural fluid and bronchoscopy. Severity C – confusion 94%. IV Fluids anorexia, dehydration and shock, prophylaxis.

Pleural effusion, empyema, lung abscess, respiratory failure, septicaemia, brain abscess, pericarditis, myocarditis, cholestatic jaundice.

Hospital acquired pneumonia

SAME AS ABOVE

Pulmonary/venous Dyspnoea embolism Pleuritic chest pain Syncope Tender calves Haemoptysis Tachypnoea Severe = RV failure

Type 1 respiratory failure

Type 2 respiratory

Dyspnoea, restlessness, agitation, confusion, central cyanosis. Long standing: polycythaemia, pulmonary hypertension, cor pulmonale Headache,

>48hrs after hospital admission. Most common: gram negative enterobacteria or staph aureus. Immobilisation Oral contraceptive pill Malignancies Cardiac failure Chronic pulmonary disease Surgery Fractures of pelvis/lower limbs Hypercoagulable states e.g. pregnancy

Very old or young

SAME AS ABOVE

>7mmol/L R – resp rate >30/min B – BP...