Respiratory system Flashcards

Question

What are the different types of inhalers used for asthma?

Answer 1

Salmeterol is LABA***

Answer 2

* Pneumothorax or pneumomediastinum * Pulmonary infections: predisposed to mucous accumulation and stasis airflow e.g. pneumonia * Resp failure: ventilatory failure (type 2 respiratory failure)

Answer 3

 Exercise-induced asthma * Onset o 5 – 15 mins after a brief (5 mins) exercise (OR) o 15 mins after going into a prolonged exercise * Offset o Resolve with rest after 30 – 60 mins  Exertional dyspnea * Onset o Shortly after onset of exertion * Offset o 5 mins after stopping exercise

Answer 4

 Advantages of mechanical ventilation * Improves gaseous exchange o ↑ Oxygenation by improving V/Q matching o ↑ Alveolar ventilation o Reverse acute respiratory acidosis * Relieve respiratory distress o ↓ Work of breathing o ↓Respiratory muscle fatigue

Answer 5

 FiO2 = Fraction of inspired air that is O2  VT = Tidal volume = Volume of breath delivered  F = Respiratory rate  PEEP = Positive end-expiratory pressure * Positive pressure applied during exhalation via resistor in exhalation port * Beneficial in terms of preventing alveolar collapse, decrease shunting, increase O2 via alveolar recruitment and improved compliance * Cardiac effects o ↓ Preload by increasing intrathoracic pressure which decrease venous return o ↓ Afterload by decreasing cardiac transmural pressure

Answer 6

* Acute cough: one lasting for <3 weeks * Subacute cough: one latsing for 3-8 weeks * Chronic cough: british thoracic cavity defined as one lasting for >8 week

Answer 7

 Hypoxemia  Purulent sputum  Hemoptysis  Chest pain  Exertional dyspnea  Failure to thrive  Growth retardation

Answer 8

onset of cough: acute or subacute paroxysmal cough --> pertussis, chronic paroxysmal cough --> astham, present during day and disappaer at night --> psychogenic or habitual cough Nature of cough Productive cough --> bronchiectasis/bacterial bronchitis/asthma Barking/brassy cough --> croup (laryngotracheobronchitis)/laryngotracheomalacia/foreign body aspiration Whooping cough --> pertussis Staccato cough --> chlamydai infection Honking cough disappearing at night --> psychogenic or habitual cough Triggering factors Smoking, excercise, cold air, allergens, viral infection --> asthma Swallowing --> laryngeal cleft/tracheoesophageal fistula Exacerbating factors Worse in the morning --> bronchiectasis Worsen before sleep --> asthma (decreased cortisol at night by circadian rhythm which has anti inflammatory effect) Worsen after meal or lying supine --> GERD Associated symtpoms Haemoptysis --> bronchiectasis/bronchitis/CA lung/TB Failure to thrive and weight loss --> immuno deficiency and chronic infection Medical history History of atopy: eczema/ allergic rhinitis/allergic conjunctivitis Previous URTI: post infectious cough Recurrent pneumonia: immunodeficiency, tracheoesophageal fistula Drug history ACEI: increased kinins and substance P which are normally metabolized by ACE --> leads to activation of arachidonic acid pathway. Increased PG which stimulates C fibers in the airway. Increased thromboxane which potentiates bronchoconstriction Antihistamiens Bronchodilators Family history: atopy, primary ciliary dyskinesia, cystic fibrosis Social history: smoking, contact with pets, close contact with TB individuals Birth history Prematurity with low birth weight Presidposes to atopic sensitization and asthma Precursor for bronchopulmonary dysplasia

Answer 9

 CBC with differentials  Nasopharyngeal aspirate  Throat swab  Sputum smear  Sputum culture with sensitivity testing  Blood culture  Lung function test * Spirometry to document obstructive or restrictive lung pattern * FEV1.0/ FVC ratio post-bronchodilator (SABA) increase >12% in asthma  Ambulatory 24-hour esophageal pH monitoring * Indicated in patients with suspected GERD  Tuberculin skin test (Mantoux test) (PPD test) * Presentation of TB in children can be subtle and hence should be considered even in the absence of obvious signs and symptoms

Answer 10

 Pulmonary fibrosis with right pleural effusion  Bronchiectasis with pleural effusion  Heart failure with pleural effusion  CXR  HRCT thorax  Lung function test (restrictive pattern)  Arterial blood gas (ABG)  Lung biopsy  Immunological blood test * ANF * RF

Answer 11

 Respiratory infection * Especially for patients receiving corticosteroids  Associated CA lung * IPF is a risk factor  Associated pleuritis in pulmonary fibrosis complicating connective tissue disease such as rheumatoid arthritis

Answer 12

 Idiopathic pulmonary fibrosis  Bronchiectasis  Pulmonary fibrosis  CA lung with obstructive pneumonia

Answer 13

SCLC: round nucleoli, absent nucleoli, hyperchromatic, scanty cytoplasm. Produces ACTH, ADH. NSCLC (more common) SCC (20-30%): morphology (squamous differentiation, keratinization, keratin pearl formation, intercellular bridges). Location: found near hilum --> usually metastasize through lymphatics. Extensive necrosis: cavities within tumors (cavitations) seen in CXR Adenocarcinoma (45-55%: most common). Morphology. Glandular patterns: papillary, micropapillary. Location: peripheral lung. Distant metastasis common --> lymphatic and blood spread common Large cell carcinoma (5-10%). Remarks: high grade, aggressive tumor, poor prognosis

Answer 14

Smoking associated with SCC and SCLC. Adenocarcinoma is the most common type in non smokers Occupation exposure: asbestos, arsenic compounds, radioactive substances, heavy metals (beryllium, cadmium, chromium, nickel) Genetics Diet: protective effects of antioxidants

Answer 15

* PTH-rP: Hypercalcemia * ADH: Hyponatremia (SIADH) * ACTH: Hypokalemia (Cushing’s syndrome) * ILP: Hypoglycemia

Answer 16

CBC with DC: anemia (haemoptysis, anemia of chronic disease, bone marrow infiltration) LFT: deranged liver function in liver metastasis, increased ALP in bone metastasis (increased bone turnover) RFT: hypoNa due to SIADH, hypoK due to ectopic ACTH production, hyperK due to adrenal metastasis and destruction LFT: preop assessment Sputum cytology: gram smear and culture with sensitivity testing including acid fast bacilli (AFB) Pathological tests Cytological exam: sputum, pleural fluid, bronchial washing and brushing, fine needle aspiration of LN Histological exam: bronchial or transbronchial biopsy, pleural biopsy, LN biopsy Radiological tests CXR CT thorax, upper abdomen, brain PECT Fiberoptic bronchoscopy with endobronchial ultrasound guided biopsy (FOB-EBUS): fibreoptic bronchoscopy: assess airways and sampling of specimen, BAL or lung biopsy. Endobronchial ultrasound: transbronchial needle aspiration (EBUS-TBNA) can be performed: assess subcarinal, upper and lower paratracheal and hilar LN, indicated for staging of cancer (N) Pleuroscopy: assess pleural metastasis

Answer 17

Genetic testing: EGFR mutation, ALK and ROS1 translocation and PD-L1 Guide decision on targeted therapy. EGFR mutation have better survival when treated with targeted therapy. Wild type EGFR have better survival when treated with conventional chemotherapy Indicated in patients with confirmed lung cancer, patients required systemic therapy due to inappropriate candidateas for surgery: stage 3b/4 lung cancer Types of mutations: hotspots for EGFR mutations are exons 18-21 of tyrosine kinase domain Mechanism of acquired EGFR mutation: secondary mutation in T790M, amplification of HER2, activation of Met pathway Sample collection: tissue biopsy at time of progression is now the gold standard. Liquid biopsy gaining popularity. Sample sources: surgically resected cancers, biopsy (bronchoscopy/pleural biopsy/LN biopsy), cytology (FNA/pleural fluid aspiration) Sample limitations: small DNA amount leading to FP result due to random amplifcation, low tumor to normal cell ratio leading to FN result. TKI sensitive: L856R mutation/exon19 mutations Known resistnace T790M mutation

Answer 18

 SCLC * Worst prognosis * Few patients survive more than a year  NSCLC * Better prognosis for patients with early surgical excision * 30 – 40% of patients with completely excised early stage cancer may survive for >5 years

Answer 19

 CA right lung  Pneumonia  TB

Answer 20

 Syndrome of inappropriate ADH (Most common)  Depletional hyponatremia due to poor oral intake  Cortisol insufficiency due to bilateral adrenal metastasis

Answer 21

 Whole brain radiotherapy * Gamma knife for isolated brain metastasis  Systemic corticosteroids (i.e. dexamethasone) * Relieve cerebral edema

Answer 22

Primary pneumothorax * Always spontaneous and thus called primary spontaneous pneumothorax (PSP) * Without underlying respiratory disorder * Presence of emphysematous lung blebs or bulla formed on lung surface usually at apices: blebs are probably formed after puberty but its origin is still idiopathic. Rupture of blebs because they are so thin walled Secondary pneumothorax * TB * Asthma * COPD * Bronchiectasis * Lung abscesses * Marfan syndrome Tension pneumothorax * Pneumothorax state where interpleural pressure becomes more +ve than atmospheric pressure

Answer 23

* Spontaneous: idiopathic emphysematous lung blebs or bulla * COPD: thin walled, diseased lung bulla can spontaneously rupture, most common cause (50-70%) of secondary pneumothorax * TB: infection or inflammation damages lung parenchyma can spontaneously rupture * Pneumonia * Neoplasm: sinus formation and fistulation results from internal necrosis in tumor --> creates a path for air to leak out from the lung * Connective tissues diseased (leads to weakened parenchyma which spontaneously rupture) e.g. Marfan syndrome, RA, dermatomyositis, systemic sclerosis * Trauma: perforation of lung: rib fracture, penetration of chest wall: stabbing or gunshot * Iatrogenic: thoracentesis, bronchoscopy, FNAC of pulmonary nodules, percutaneous/transbronchial lung biopsy, positive pressure ventilation, insertion of central venous catheter (CVC)

Answer 24

Chest pain * Visceral pleura is insensitive to pain since it is innervated by autonomic nerve fibers: visceral pleura contains stretch receptors. Increased relative collapsing or stretching of the partly deflated lung in pneumothorax leads to chest pain * Parietal pleura is sensitive to pain since it is innervated by somatic intercostal nerve and phrenic nerves. Parietal pleura contains pain receptors but chest pain in pneumothorax is not attributable to this since air is not irritant to pleura at all Dyspnea * Air enters pleural space leads to loss of normal -ve pleural pressure * Partial deflation of lung means collapse of small terminal airways and alveoli: less gas exchange surface can be recruited for respiration * Relative compressibility or expansibiloity of air impedes ability to inflate chest wall and deflate: muscles expend more than expected effort with each breath as some work is used to expand and compress the air of pneumothorax instead of ventilating the lung

Answer 25

* Air sucked into pleural space during inspiration Opening of a ruptured bleb on lung surface. Opening of a pleuro-cutaneous fistula or wound * Air cannot escape out of pleural space during expiration Collapse of the defect or bleb or wound on collapsing the chest during exhalation * Results in rapid addition of a volume of air to pleural space with each breath Building up of tension within pleural space. Lethal when pressure in chest rise to higher than RA pressure (central venous pressure) leading to loss or reversal of pressure gradient. Allow caval blood to return to the chest. Consequent loss of cardiac output and patient dies of shock.

Answer 26

 Palpation * Tracheal & mediastinal deviation away from affected side * Displaced apex beat away from affected side * ↓ Chest expansion (Affected side)  Auscultation * ↓ Breath sounds * ↓ Tactile fremitus  Percussion * Hyper-resonance

Answer 27

CXR should be done in erect position: 2cm separation between visceral pleural line to the chest wall at the level of hilum approximate to a radiographic pneumothorax volume of 50% of hemithoraxi volume Small pneumothorax <2cm separation Large pneumothorax: >2cm separation Lung fields Area of blackness: border: present with a lung edge, distribution: unilateral Lung edge Lung markings (bronchi and blood vessels) Decreased vasscular markings since lung is replaced by air Primary or secondary spontaneous pneumothorax * Presence of ipsilateral lung edge * Translucent lung without lung markings * Contralateral mediastinal shift * Deep sulcus sign: air collects anteriorly and basally in costophrenic angle, dark and deep costophrenic angle Tension pneumothorax * Flattening of diaphragm * Widening of intercostal sapce * Deviation of mediastinum to contralateral side * Deviation of trachea to contralateral side * Hearat is shifted to contralateral side ABG: assess degree of hypoxemia, hypercapnia and respiratory acidosis pO2<80mm in 75% of patients

Answer 28

Observation for primary pneumothorax, lung edge <2cm from chest wall, non breathless patient O2 supplementation: speeds resolution of spontaneous pneumothorax --> breathing in high flow O2 leads to increased O2 content and decreased N2 content in serum Not given to treat breathless, not given to treat desaturation Giving excessive O2 can lead to oxygen toxicity in lungs, O2 therefore not given at 100% via a mask or nasal cannula. O2 should be given intermittently rather than continously for 24h daily Surgical Percutaneous needle aspiration at 2nd ICS at MCL for tension pneumothorax. 60-80% chance of avoiding a chest drain Intercostal tube drainage (chest drain) indications: secondary pneumothorax, significant underlying chronic lung disease, patients >50 years old inserted at 5th ICS MAL or safety triangle (anterior: lateral border of pectoralis major, posterior: anterior border of latissimus dorsi, superior: horizontal line drawn from nipple, apex: below axilla) Structures that causes pain during chest drain insertion: skin --> subcutaneous fat --> serratus anterior --> intercostal muscle --> parietal plerua. Skin, periosteum and parietal pleura are most sensitive to pain and should be specifically targeted when giving LA

Answer 29

CBC with DC: absence of changes in CBC help to differentiate atelactasis from pneumonia Sputum smear, culture and cytology. Smear and culture for acid fast bacilli, cytology for malignant cells

Answer 30

Depends on etiology

Answer 31

Treatment of non malignant pleural effusion * Primarily involves treatment of underlying etiology Treatment of malignant pleural effusion * Repeat therapeutic thoracentesis * Indwelling pleural catheter placement: indicates in patients with shorter life expectancy * Chest drain insertion + pleurodesis: indicated in patients with longer life pleurodesis

Answer 32

Thoracentesis * Pleural tapping should not be performed for bilateral pleural effusion in clinical setting strongly suggestive of transudate process unless there is a presence of atypical features or failure to respond * Large volume thoracentesis refers to removal of >1L of pleural effusion confiremd by PE and CXR (not recommended) Indications * Large non purulent pleural effusion >40% of hemithorax * Frank pus or turbid pleural fluid on thoracentesis * Pleural fluid analysis shows: positive gram + positive culture, LDH>1000IU/L, glucose <2.2mmol/L, pH <7.2 * Radiological findings: loculation on CXR, pleural thickening with contrast enhancement on CT thorax Complications: pain at puncture site, bleeding, soft tissue infection, splenic or liver puncture, tumor seedling along needle tract Reexpansion pulmonary edema (non cardiogenic pulmonary edema), related to negative pleural pressure created during pleural fluid removal in the setting of an unexpandable lung (atelactasis/endobronchial obstruction) Pneumothorax: risk of pneumothorax increases with the volume of fluid withdrawn. Related to negative pleural pressure created during pleural fluid removal in the setting of an unexpandable lung Chest drain insertion indications * Haemothorax * Empyema * Complicated parapneumonic effusion * Symptomatic malignant pleural effusion Pleurodesis * Induction of pleural inflammation and fibrosis * Chemical pleurodesis: achieved with sclerosants such as talc instilled via chest tube, indwelling catheter or at time of thoracoscopy. Clamp drain for 1-2 hours post sclerosant application than release clamp. Chest tube kept unclamped thereafter for drainage until daily output <150ml/day and CXR shows reexpansion of lung with most of the effusion drained * Surgical pleurodesis; achieved through mechanical irrigation of the pleura

Answer 33

 Pulmonary fibrosis with right pleural effusion  Bronchiectasis with pleural effusion  Heart failure with pleural effusion

Answer 34

 Respiratory infection * Especially for patients receiving corticosteroids  Associated CA lung * IPF is a risk factor  Associated pleuritis in pulmonary fibrosis complicating connective tissue disease such as rheumatoid arthritis

Answer 35

Elevated mean arterial pressure >25mmHg at rest PA mean = CO x PVR +PA wedge pressure Transpulmonary pressure gradient (TPG) = PA mean -PA wedge pressure

Answer 36

Group 1: pulmonary arterial hypertension Idiopathic PAH, heritable PAH, drug induced, associated conditions (connective tissue diseases: SLE, RA, scleroderma, mixed connective tissue disease), congenital heart disease (ASD/VSD/PDA), portal hypertension) Group 1': pulmonary venoocclusive disease (PVOD) and/or pulmonary capillary haemangiomatosis (PCH): characterized by extensive diffuse occlusion of pulmonary veins resulting in tortuous dilation of pulmonary capillaries Group 1'': persistent pulmonary hypertension of the newborn: occurs when pulmonary vascular resistance remains abnormally elevated after birth Group 2: PT due to left heart disease: left ventricular systolic/diastolic dysfunction. Left sided valvular disease. Mitral valve: MS/MR, aortic valve: AS/AR Group 3: PT due to lung disease an/or chronic hypoxemia (COPD, ILD, OSA, alveolar hypoventilation disorders, chronic exposure to high altitude) Group 4: chronic thromboembolic pulmonary hypertension (CTEPH): pulmonary embolism Group 5: PT due to unclear multifactorial mechanism. Haematological disorders: chronic hemolytic anemia (thalassemia), spherocytosis, sickle cell anemia. Myeloproliferative disorders, splenectomy. Metabolic disorders: thyroid disorders, glycogen storage disease. Systemic disorders: sarcoidosis. langerhans cell histiocytosis (pulmonary), neurofibromatosis (NF), vasculitis Others: tumor obstruction, fibrosing mediastinitis, chronic renal failure

Answer 37

 Dyspnea  Exertional chest pain * Subendocardial hypoperfusion caused by increased RV wall stress and myocardial oxygen demand (RV ischemia) * Dynamic compression of left main coronary artery by an enlarged pulmonary artery  Exertional syncope * Inability to increase CO during activity or reflex bradycardia secondary to mechanoreceptor activation in RV  Fatigue

Answer 38

CCB with DC (group 5): assess for chronic hemolytic anemia LFT (group 1): rule out pulmonary hypertension Serum autoantibodies (group 1): ANA, Anti dsDNA, Anti Scl 70, RF HIV serology: rule out HIV associated PAH Radiological Ix * CXR * ECG: RBBB, RVH, right atrial enlargement (P pulmonale with peaked P wave) * Excercise testing (6 min walk test 6MWT) or cardiopulmonary excercise testing * Echocardiography: estimation of pulmonary artery systolic pressure. Technique takes advantage of TR that usually exists and measures the maximum TR jet velocity (TRV). RA pressure estimated from the size and respiratory variation of flow in IVC. Assess RV size, thickness and function, assess LA size (group 2), assess for valvular heart lesions * Right heart catheterization (gold standard in dx of pulmonary hypertension). Pulmonary HT confirmed when mean pulmonary arterial pressure >25mmHg at rest (normal =8-20mmHg) Spirometry and DLCO (group 3): rule out obstructive or lung restrictive lung diseases with FEV1/FVC. ILD will give a restrictive pattern on spirometry with FEV1/FVC>70% and decreased DLCO Polysomnography (Group 3) Ventilation perfusion VQ scan (group 4): normal VQ scan excludes chronic thromboembolic disease CT pulmonary angiography (group 4): indicated when PE suspicion is high

Answer 39

Obstructive sleep apnea * Recurrent obstructive apnea and hypopneas caused by repetitive collapse of upper airway (functional occlusion) during sleep * Presence of respiratory effort meaning thoracic and abd movement * No resulting inspiratory flow Central sleep apnea * Can be due to central (lack of resp drive), NMJ (myasthenia gravis) or muscular diseases (muscular dystrophy) * Absence of respiratory effort * No resulting inspiratory flow

Answer 40

 Insufficient sleep  Central sleep apnea  Periodic limb movement of sleep  Obesity hypoventilation syndrome  Primary respiratory diseases  Narcolepsy * Excessive daytime sleepiness with cataplexy, hypnagogic hallucination and sleep paralysis  Depression  Fibromyalgia

Answer 41

CPAP indications for ugent CPAP * Pickwanin syndrome with daytime alveolar hypoventilation * Pulmonary hypertension or cor pulmonale * Nocturnal malignant arrhythmia related to OSA * Nocturnal angina related to OSA * Severe excessive daytime sleepiness that may impose risk to patient and others Mechanism: maintenance of positive pharyngeal pressure so that intraluminal pressure exceeds surrounding pressure. Stabilize upper airway through increased end expiratory volume to prevent airway collapse Oral applianaces Protrude the mandible forward or hold the tongue in a more anterior position Surgical treatment Nasal procedures: turbinectomy (turbinate reduction), septoplasty, rhinoplasty, nasal valve surgery Upper pharyngeal prodecures: tonsillectomy and adenoidectomy, uvulopalatopharyngoplasty (UPPP) Lower pharyngeal and laryngeal procedures: genioglossus advancement Global upper airway procedures: upper airway stimulation (upper airway stimulation via an implantable neurostimulator device activates the protrusion muscles of tongue via hypoglossal nerve (CN12) stimulation Lifestyle modication Weight loss Alcohol avoidance: depress CNS, exacerbate OSA, worsen sleepiness and promote weight gain Change sleep position: supine to lateral recumebnt position Drug avoidance: BDZ receptor agonist, antiepileptics, antidepressants, antihistamines and opaites

Answer 42

 Asthma attacks  Pulmonary edema  Obstructive sleep apnea (OSA)  Rhinitis with severe nasal blockage  Panic attacks

Answer 43

 Symptoms of wheezing * Suggest asthma or pulmonary edema  Characteristics of breathing difficulty * OSA: Suffocation/ Gasping/ Choking * OSA: Resolves immediately on waking * Pulmonary edema: Relief by sleeping with several pillows * Asthma: Cough with expiratory wheeze

Answer 44

 Snoring  Witnessed breathing pauses during sleep  Excessive daytime sleepiness despite adequate hours of sleep  Feeling unrefreshed on waking up

Answer 45

Characterized by acute onset of bilateral alveolar infiltrates and hypoxeia ARDS is a consequence of an alveolar injury producing diffuse alveolar damage that leads to * Increased pulmonary vascular permeability * Increased lung weight * Loss of aerated tissue

Answer 46

Diffuse alveolar damage * Alveolar edema and focal hemorrhage * Acute inflammation of alveolar wall * Hyalinzation of membrane

Answer 47

* Alveolar injury produces diffuse alveolar damage --> release inflammatory cytopkines such as TNF, inflammatory cytokines recruit and activate neutrophils --> release of toxic mediators such as ROS and proteases --> damage of capillary endothelium and alveolar epithelium * Allows proteins to escape from the vascular space and the oncotic gradient that favors resopriton of fluid is lost with fluid pouring hte interstitium to overwhelm the lymphatics * Increase in interstitial fluid combined with damage to alveolar epithelium causes air spaces to fill with bloody, proteinaceous edema fluid and debris from degenerating cells Consequences * Impaired gaseous exchange: V/Q mismatch due to physiological shunting and physiological dead space * Pulmonary hypertension: hypoxic pulmonary vasoconstriction, vascular compression by positive airway pressure, parenchymal destruction, airway compliance * Decreased lung compliance: due to stiffness of poorly non aerated lungs

Answer 48

* Cardiogenic pulmonary edema * Acute exacerbation of interstitial lung disease * Idiopathic acute eosinophilic pneumonia * Cryptogenic organizing pneumonia * Acute interstitial pneumonia

Answer 49

PE: auscultation: diffuse crepitations Biochemical tests ABG: hypoxemia, diffusion impairment, respiratory alkalosis (excess ventilatory compensation) CXR: bilateral alveolar infiltrates (opacities) CT thorax Echocardiography

Answer 50

Hand contact: direct contact via an infected person (self inoculation of ones own conjunctiva or nasal mucosa after touching a person being contaminated the cold virus. Indirect contact with a contaminated environmnetal surface Small particle droplet (droplet transmission) Large particle droplet (droplet transmission): requires close contact with an infected person Incubation perdio: time between contact with infectious material until onset of symptoms Most common cold virus = 24-72 hours Period of infectivity: low level of viral shedding may persist for up to 2 weeks

Answer 51

* Rhinovirus infections in september (autumn months) * Parainfluenza virus infecton in october and november (autumn monhts) * Coronavirus, influenza virus and respiratory syncytial virus infection in december to february (winter months)

Answer 52

Analgesics (headache, ear pain, muscle and joint pain): acetaminophen/NSAIDs Antihistamine/decongestant combination: combination is more effective than either component alone * H1 receptor antagonist (antihistamine): diphenhydramine * Decongestant (alpha adrenergic agonist causing vasoconstriction): phenylephrine Cough suppressant: NMDA receptor antagonist (Decreases sensitivity of cough receptors --> interrupts cough impulse transmission by depressing medullary cough center through sigma receptor stimulation): dextromethorphan Expectorants: increases effective hydration of respiratory tract --> improves ciliary clearance and reduces viscosity of respiratory mucus Relief of nasal symptoms: cromolyn sodium (mast cell stabiizer), ipratropium bromide (intranasal): anticholinergic agents --> inhibits serous and seromucous gland secretions to reduce rhinorrhea Vit C: reduction in duration of cold symptoms. Vit C given after symptom onset does not reduce symptoms duration or severity Panadol Acetaminophen: analgesia Phenylephrine hydrochloride: nasal decongestant Nasocapine: cough susppressant Terpin hydrate: expectorant to increase bronchial secretion Caffeine: relieve tiredness Ascorbic acid: facilitate recovery

Answer 53

Influenzae virus A: may lead to pandemics --> divided into 18H (H1-H18) and 11N (N1-11) subtypes Influenza virus B: do not lead to pandemics Influenzae virus C: do not lead to pandemics

Answer 54

Seasonal influenza (H1N1/H3N2): common respiratory tract infection caused by human seasonal influenza viruses Avian influenza (H5N1/H7N9/H9N2): influenza viruses that mainly affect birds and poultry. People may become infected through direct contact with infected birds and poultry, their droppings and contaminated environment Influenza pandemics (H1N1/H2N2/H3N2): caused by emergence and global spread of a new influenza virus originated from an animal influenza virus such as avian influenza virus and is marked different from viruses circulating in the population

Answer 55

Antigenc shift: major change in envelop glycoproteins (hemagglutinin and neuraminidase): only occurs in influenza A Host infected by 2 different strains of influenza viruses --> gene reassortment occurs among influenza viruses whose genomes consist of 9 distinct segmetns of RNA. Changes in antigenic composition resulting in appearance of a new haemagglutunin or neuraminadase Antigenic drigs * Minor changes in envelop glycoproteins (haemagglutinin and neuraminidase) * Occurs in both influenza A and B viruses Physiology: point mutations in RNA gene segments that code for haemagluttunin and neuraminidase. Mutations result in new strains of viral particles which cannot be inhibited effectively by antibodies that were originally targeted against previous strains.

Answer 56

* Enveloped RNA virus * Haemagglutinin: attached to host cells by binding their cell receptors. Binds to sialic acid residues on respiratory epithelial cell surface glycoproteins. Interaction is necessary for initiation of infection * Neuraminidase: promotes viral release after viral infection in cells --> facilicatetes release and spread of virus through mucin of respiratory tract

Answer 57

Season influenza vaccination: requires about 2 weeks after vaccination for antibodies to develop and provide protection against influenza virusr infection. Efficacy in individuals age <65 years = 70-90% protection Indications All people aged >6 months except those with contraindications High priority groups * Persons aged >50 * Children between age 6 months-11 years * Pregnant women: inactivated seasonal vaccine is safe in pregnancy but not for live attenuated virus * Elderly living in residential care homes * Long stay residents of institutions for persons with disability * Healthcare workers * Poultry workers * Pig farmers and pig slaughtering industry personnel * Chronic medical problems: children and adolescents aged 6 months-18 years on long term aspirin therapy. Chronic CVS, lung, liver or kidney diseases. Chronic neurological conditions taht can compromise respiratory functions or handling of respiratory secretions. History of invasive pneumocococcal disease. CSF leakage. Immunocompromised states related to weakened immune system due to conditions such as asplenia, HIV/AIDS or cancer/steroid treatment Contraindications * Allergy to previous dose of inactivated influenza vaccine or other vaccine components * Allergy to egg if severe or history of anaphylaxis

Answer 58

* GBS: paralysis and respiratory distress * Meningitis/encephaliits * Anaphylaxis

Answer 59

* No. The virus in the inactivated vaccine are dead virus * Yes. The circulating seasonal influenza strains change from time to time and the vaccine composition is updated every year to enhance protection. The immunity built up in a vaccinated person in prior season will decrease over time and insufficient to provide protection in next season. * Yes. Injectable inactivated vaccine does not interfere with effectiveness of other vaccines. Different vaccines should be given at different injection sites.

Answer 60

Droplet precautions: particles do not remain suspended in air for extended periods of time. Particles do not travel beyond several feet (usually <1m) Placement of patient: spatial separation of >1m between infected patients and other patients Transport of patient: place a surgical mask, only move if essential Healthcare workers: wear surgical asmk Other diseases requiring droplet precaution: neisseria meningitiditis, bordetella pertussis

Answer 61

 Acute bacterial rhinosinusitis * Streptococcus pneumoniae * Haemophilus influenzae * Moraxella catarrhalis  Acute viral rhinosinusitis * Rhinovirus * Influenza virus * Parainfluenza virus

Answer 62

* X ray sinuses * CT sinuses with/without contrast: common findings include air fluid levels, mucosal edema and thickening, air bubbles within sinuses and opacification. CT with contrast is required to identify complications of sinusitis and evaluate disease location and extent of involvement beyond the sinuses * MRI sinuses

Answer 63

* Community acquired pneumonia * Hospital acquired pneumonia * Healthcare associated pneumonia

Answer 64

Typical organisms: include S. pneumoniae, H.influenzae, S. aureus, S. pyogenes, aerobic gram-ve bacteria and anaerobes Atypical pneumonia: chlamydia pneumoniae, chlamydia psittaci, mycoplasma pneumoniae and legionella pneumophila Afebrile pneumonia of infancy: syndrome seen between 2-4 months of life: classically caused by chlamydia trachomatis but other agents such as mycoplasmsa hominis, ureaplasma urealyticum and CMV are also implicated. Clinical presentation: insidious onset of rhinorrhea, conjunctivitis and tachypnea followed by a staccato cough (individual cough separated by inspiration)

Answer 65

 Use of antibiotics in preceding 90 days  Hospitalization for ≥ 2 days in preceding 90 days  High frequency of antibiotic resistance in community or hospital  Home wound care  Residence in nursing home or extended care facility  Family member with MDR pathogens  Immunosuppressive therapy

Answer 66

* Bronchiolitis * Lemierre syndrome (jugular vein suppurative thrombophlebitis): vessels of the carotid sheath become infected typically by fusobacterium sp leading to bacteremia and metastatic spread of infection to lungs and mediastinum

Answer 67

* CBC with DC: leukocytosis with leftward shift suggestive of pyogenic bacterial disease * Inflammatory markers: increased ESR and CRP * LFT * RFT: hypoNa due to SIADH * Blood culture * Sputum smear and culture * NPA for viral IF/PCR + mycoplasma PCR: Rapid diagnostic testing including enzyme immunoasay (EIA) immunofluorescence or PCR for viruses * Throat swab for PCR: PCR for mcyoplasma pneumoniae * Urine antigen detection: antigen detection for legionalla pneumophila * Bronchoalveolar lavage (BAL): indicated in not responsive to treatment, recurrent pneumonia, suspected unusualy organism or suspected aspiration in children Radiological Ix * CXR Consolidation: homogenous opacification in lobar pattern in lobar pneumonia. Multiple small nodular or reticulonodular opacities in bronchopneumoniae Infiltrations: alveolar infiltrates indicates bacterial pneumonia Air bronchogram: black airways against white background: alveolar space filled with fluid and thus appear white. Airways retain air and thus appear black. Left heart border: not clearly seen --> leson in LLL Right heart border: right heart border not clearly seen --> lesion in RML Bronchoscopy with bronchoalveolar lavage (BAL): ideal specimen for dx of pneumocystic jirovecci pneumonia

Answer 68

* Primary TB: describes new TB infection or active disease in a previously naive host * Latent TB: 90% of individuals with intact immunity can control further replication of bacilli after primary infection * Reactivation TB: chronic TB or post primary TB * Miliary TB: haematogenous dissemination of mycobacterium tuberculosis. Radiological appearance of small firm white nodules resembling millet seeds. Results from both progressive primary infection or via reactivation of latent focus with subsequent haematogenous spread via bloodstream * Endobronchial TB: tuberculous infection of the tracheobronchial tree. Develop via direct extension to bronchi from an adjacent parenchymal focus or via spread of organisms to bronchi via infected sputum. Complications of endbronchial TB include atelactasis, bronchiectasis, obstruction and tracheal stenosis

Answer 69

* Rounded mass lesions that can develop during primary infection or when a focus of reactivation TB becomes encapsulated * Fine needle aspiration or lung biopsy may be necessary for diagnosis

Answer 70

Immunocompromised patients * HIV infection * Malignancy * Chronic renal failure * Uncontrolled DM * Organ transplant recipients * Immunosuppressant * Malnutrition * Alcoholism

Answer 71

 Bronchiectasis  Pneumonia  Lung abscess  Lung cancer  Sarcoidosis  Silicosis

Answer 72

1 of 4 possible outcomes * Immediate clearance of the organism * Primary disease: immediate onset of active disease * Latent infection * Reactivation disease: onset of active disease many years following a period of latent infection Primary disease: tubercle bacilli establish infection in the lungs after they are carried in droplets small enough to reach alveolar spaces. Failure to eliminate the infection by innate defense system leads to proliferation of bacilli inside alveolar macrophages --> macrophages and neutrophils form a nodular granulomatous structure known as tubercle. Progressive destruction of lung with development of caseating necrosis. Tubercle enlarges and bacilli enters local draining LN leading to lymphadenopathy. Continous bacterial growht leads to haematogenous spread to bacilli to produce disseminated TB infection

Answer 73

Host response to infection by tubercle bacilli is primary cellular and specific acquired immune response is largely cell mediated. Local tissue damgae caused by delayed (type 4) hypersensitivity reaction to mycobacterial protein antigens Pathogenesis * Dendritic cells carry the MTB antigen to LN: MTB induces the dendritic cells to produce IL12 * Activated Th1 and B cells migrate to the site of infection * Activated macrophage by MTB is unable to clear the infection: macrophages will continously present MTB antigens to Th1 clels --> MTB inhibits fusion of lysosomes with phagosomes. Granuloma fence off infectious agents and prevents dissemination providing a local environment for multiplication of MTB * Chronic inflammation occurs with mycobacteria in the center: cellular immunity results in control of infection as well as tissue damage

Answer 74

 General examination * Lymphadenopathy  Palpation * ↓ Chest wall expansion  Percussion * Stony dullness in pleural effusion  Auscultation * ↓ Breath sounds * Bronchial breathing * Pain-inspiratory crackles * Wheezing in endobronchial TB

Answer 75

* CBC with DC: leukocytosis, thrombocytopenia/thrombocytosis, pancytopenia occurs in bone marrow infiltration * Inflammatory markers: CRP, ESR * Electrolyte profile: HypoNa in SIADH Microbiological tests * Sputum * Bronchoalveolar lavage and brushings * Tissue biopsy Other specimens * Pleural fluid by tapping or pleural biopsy in TB pleuritis * LN fine needle aspiration or biopsy in TB lymphadenitis * Lumbar puncture for CSF fluid analysis in TB meningitis * Paracentesis for ascitic fluid analysis in TB peritonitis AFP smear microscopy: ZN stain (bacilli stained red with a blue background) Mycobacterial culture: LJ medium. Allow drug sensitivity testing for HREZ. Disadv: time consuming with solid media requiring 3-8 weeks and liquid media requiring 1-3 weeks NAAT (PCR): does not replace the roles of AFB smear and culture in diagnostic algorithm for TB Adv high sensitivity and specificity: rapid dx requiring 1-2 days old. Histopathology: demonstrates caseating granulomatous inflammation. Characteristic caseation necrosis. Contains epithelioid macrophages, langhans giant cells (horseshoe appearance with nuclei locate peripherally) and lymphocytes. Specific tests for TB infection Tuberculin skin test Based on Type 4 hypersensitivity reaction to M.tuberculosis --> for dx of latent TB infection. Procedure: intradetrmal injection of 0.1mL purified protien derivative (PPD). Interpretation: results should be read at 48-72 hours, palpation with finger or use ballpen method. Measure maximal transverse diameter Inferferon gamma release assay: IGRA (designed for latent TB infection): +ve results supports dx of active TB but -ve results does not rule out active TB Other tests: urine lipoarabinomannan (LAM) antigen detectin but not routinely available in HK CXR CT chest Bronchoscopy: BAL or bronchial brushing

Answer 76

1. Hepatotoxicity (drug induced hepatitis): isoniazid/rifampicin/pyrazinamide. Ehionamide/prothionamide Withhold treatment if ALT >3x ULN or bilirubin >2x ULN. Management: stop anti-TB treatment. Reintroduction may be considered when ALT is <2x ULN in case treatment is prompty required Non hepatotoxic interim SLE regimen (S+fluoroquinolone (L)+E) is initiated. Subsequent addition of H,R and Z with the aim of administering HR together if possible. R at maximum dosage at day 1. H at maximum dosage at day 8, Z at maximum dosage at day 15. 2. Ocular toxicity caused by ethambutol Management: stop anti TB treatment --> both isoniazid and ethambutol should be stopped immediately if severe ocular toxicity occurs. Isonidazid should also be stopped 6 weeks after stopping ethambutol if ocular condition does not improve. 3. Nephrotoxicity: rare complication of rifampicin administration. Due to type 2/3 hypersensitivity reaction: forms immune complexes that are deposited in renal vessels, glomerular endothelium and interstitial area 4. GI disturbances Exclude hepatitis with blood tests when ALT <3x ULN, total bilirubin <2x ULN Management: administer drugs with food, adminsiter medication at bedtime, prescribe anti-emetics for symptomatic relief 5. Peripheral neuropathy due to isoniazid Prophylactically given vit B6 at 10-20mg daily, high dose vit B6 at 50-100mg daily given to patients complicated by peripheral neuropathy 6. Cutaneous hypersensitivity Stop all chemotherapy until reaction has subsided. Consider use of antihistamines/topical steroids. Reintroduction of TB drugs one by one. Start with drug least likely to be responsible for reactin (HR) at a small challenge dose (isoniazid at 50mg)

Answer 77

* Case finding * Effective chemotherapy * Treatment of latent TB infection * BCG vaccination * Health education

Answer 78

Targeted groups for LTBI treatment in Hong Kong * Patients age < 35 years old if tuberculin response ≥ 15 mm * Infants close contacts of smear +ve patients * Tuberculin skin test +ve patients with HIV * Tuberculin skin test +ve patients with silicosis

Answer 79

 Rifampicin * Potent inducer of CYP450 system including CYP3A and CYP2C, which account for more than 80% of CYP450 isoenzymes * Results in a decrease in the serum concentrations of many drugs  Oral hypoglycemic agents  Warfarin  Oral contraceptives  Immunosuppressant  Phenytoin  Protease inhibitor and NNRTI in HIV patients

Answer 80

 Oral contraceptives * Recommend female patients of reproductive age to use other contraceptive methods other than pills when prescribing rifampicin  Warfarin * Inform cardiologist that the patient will require an unusually high maintenance dose of warfarin in order to produce a therapeutic INR * Warn cardiologist to decrease dosage of warfarin on withdrawal of rifampicin after TB treatment  Steroids * Increase dosage of steroids for SLE patients so as to achieve the desired therapeutic level

Answer 81

If there is GERD/reflux symptoms, at night, when the patient is asleep and cannot protect their airway/discoordination of upper digestive tract = silent aspiration = worsen control of disease in long run Ask about sinusitis (Kartagener’s syndrome = problems with clearing sinus secretions [chronic rhinosinusitis] = may present with runny nose) = post-nasal drip [cough + aspiration]

Answer 82

Pertussis is not as common, but could still be present in some South-East Asian countries

Answer 83

CFTR gene mutation leads to cystic fibrosis

Answer 84

 Asthma * Presents with dyspnea, coughing, tenacious sputum production and recurrent exacerbation in patient who might not have been a smoker  COPD * Classically presents with virtually identical symptoms in a smoker * High prevalence of bronchiectasis among patients diagnosed to have COPD  TB  Chronic rhinosinusitis * Affects up to 60% of cases with bronchiectasis  Interstitial lung disease * Idiopathic pulmonary fibrosis (Cryptogenic fibrosing alveolitis)  GERD

Answer 85

Bronchiectasis is a chronic suppurative lung disease + hypoxemia (clubbing may indicate underlying inflammation) Catabolic state: Thin, cachexia (not absolute, but may be seen)

Answer 86

* CBC with DC: leukocytosis * Sputum smear and culture * Lung function test (spirometry) * Pulse oximeter * Arterial blood gas * Immunoglobulin measurement * Serum alpha1-antitrypsin levels * Sweat chloride level or mutation analysis of CFTR gene (evaluate for cystic fibrosis --> more in Western countries) CXR: ring shadows, tramline shadows HRCT thorax: airway dilatation and lack of tapering, signet ring sign, thickening of bronchial wall, mucopurulent plugs, cyst off the bronchial wall distribution of bronchiectasis: * Central distribution = allergic bronchopulmonary aspergillosis * Upper lobe predominance = cystic fibrosis/post radiation fibrosis * Middle lobe predominance = primary ciliary dysfunction/non tuberculous mycobacterium infection * Lower lobe predominant Bronchoscopy: BAL when sputum studies are negative and MTB suspected Specific tests 24 hour esophageal pH monitoring to exclude GERD Ciliary study

Answer 87

Pseudomonas aeruginosa MOST common in patients coming in and out of the hospital Klebsiella pneumoniae (esp. associated with diabetes!) [don’t forget endophthalmitis, associated with liver abscess] Streptococcus pneumoniae E. Coli (may be cultured, indicating aspiration) Burkholderia pseudomallei (difficult to grow)

Answer 88

1.  Bronchiectasis and left-sided apical fibrosis 2.  Bronchiectasis  Idiopathic pulmonary fibrosis  CA lung with localized pathology 3.  TB  Post-radiation  Ankylosing spondylitis

Answer 89

 Obstructive pattern on spirometry in 60% of patients (disease itself presents with airflow obstruction = reflects underlying obstructive lung disease [chronic sputum production])  Can have normal lung function, obstructive (common), or mixed pattern  H. influenzae in early disease  P. aeruginosa in late disease NTM Mycobacterium fortuitum causes haemoptysis Mycobacterium leprae Mycobacterium marinuum Mycobacterium kansasii

Answer 90

 Early or mild cases (against H. influenzae) * Amoxicillin with clavulanic acid (Augmentin) * Azithromycin  Late or severe cases (against P. aeruginosa) * Ceftazidime * Levofloxacin Macrolides are use for immunomodulatory function = used if there are many exacerbations in a year (long-term problem with repeated exacerbations) = it is still an antibiotics, so remember that the dosage is different For immunomodulation, we use it 2-3 times a week, longer term with half the dosage [alternate day] = months to a year before we see immunomodulatory effect. For antibiotics function, we use it 7-10 days, then stop. PCP prophylaxis is similarly not given everyday

Answer 91

 Inhaled corticosteroids (e.g. fluticasone) * Anti-inflammatory drugs to prevent further damage and enhance QOL * Reduce exacerbation frequency and sputum production  Antibiotics * Indicated for each exacerbations * Inhaled antibiotics can be used if there are >3 or more exacerbations (inhaled tobramycin) [aminoglycoside] for Pseudomonas colonisation  Chest physiotherapy * Useful as retained infected mucus is harmful * Teach better cough technique * Postural drainage * Physical/nebulisation to clear sputum * Chest percussion (with cupped hand)  Remarks * Disease is greatly irreversible * Treatable causes such as immunodeficiency and GERD should be looked for and treated

Answer 92

 Bed rest  Antibiotics * Until sputum volumes or coughing returns to baseline values or fever settles  Thrombotic agents (e.g. transamine) * Not recommended routinely as they could obstruct airways leading to lung collapse, further infection and respiratory failure * Also pose risk to stroke, MI or peripheral vascular obstruction

Answer 93

Pay attention to Hx of patient - If patient used to have NTM, we are bound to collect samples with NTM (fast-grower) = grow much faster than conventional mycobacterium tuberculosis - Culture result = Look at specimen collection date (if specimen collection is just one week ago, then it turns AFB +, this is likely fast-grower) = MTB takes 6-8 weeks to grow, fast grower NTM can come up in 1-2 weeks - Smear can be positive immediately after collection, so timing is not as important - If clinically indicated, we can order further tests, i.e. IGRA, call patient to treat empirically, i.e. smear + without previous evidence to explain presentation

Answer 94

Aim of inhaled antibiotics: - Symptom relief, reduce sputum and improve FEV1 - Try to achieve bacteriostatic status in patient with chronic colonisation of Pseudomonas - Given by nebulisation, 2 time a day, 28 days (on-off administration), alternate 2-4 weeks - Cannot use Aminoglycoside too frequently = ototoxicity and nephrotoxicity

Answer 95

Prevent exacerbation of Bronchiectasis - Some patients are selected for regular antibiotics - Preemptive IV antibiotics, rather than wait for patient to have an exacerbation and get admitted, or even develop haemoptysis If it is mild, can use oral form of antibiotics, if it is getting bad, IV form or inhaled form (seldomly practiced in HK, more common in patients with cystic fibrosis)