Respiratory system Flashcards
Define asthma?
Common chronic disorder of the airways that is complex and characterized by
variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness and an underlying inflammation
Reversibility (hallmark)
Reversible spontaneously or after treatment
FEV1/FVC ratio increase 12% before and after bronchodilator (SABA) treatment
What is the assessment of severity of exacerbation for asthma?
What are asthma associated syndromes?
What is the classification of asthma?
What are RF for asthma?
Genetics
* Defects of genes that encode for β-adrenoceptors/ IFN-γ
o IgE upregulation
o Decreased bronchodilation
Atopy: Predisposition towards developing certain allergic hypersensitivity
* More than 80% of asthmatics are atopic Gender
* Severe and uncontrolled asthma usually occurs in females
Ethnicity: Caucasian has higher prevalence rate than the Chinese
Environment
* Tobacco smoke
* Air pollution
* Viral respiratory infections
* Diet and drugs
* Obesity
Airway hyper-responsiveness: Inborn
What are the triggering factors of atopy?
Allergens: dusts, pollen grains, animal dander, fecal pallets of household mites
Respiratory irritants: smoking, air pollution, cold air
What is the ddx for obstructive and restrictive lung diseases?
What is the ddx of asthma?
- Acute bronchiolitis
- Pneumonia
- Foreign body aspiration +/- aspiration pneumonia
- Bronchiectasis: recurrent infections
- GERD
- Bronchopulmonary dysplasia (BPD): history of prematurity
- Primary ciliary dyskinesia: recurrent infections
- Cystic fibrosis
What is the functional changes in asthma
Spirometry
What is the pathogenesis of asthma?
- Airway inflammation
Naive helper T cells become Th2 cells: Th2 response generates cytokines that mediate allergic inflammation. Mast cells are sensitized and contains allergen specific IgE. Inhaled allergens attach to specific IgE antibodies on the suface of mast cells. Cross linking of IgE receptors leads to intracellular signaling. Degranulation of mast cells and release of mediators.
Inflammation cells infiltration: increased vascularity permeability due to acute inflammation. Infiltration of eosinophils and lymphocytes. - Airflow obstruction
Bronchoconstriction: IgE mediated allergic response, smooth muscle constriction due to release of histamine, heparin and serotonin
Mucous plug formation: mucous hypertension: hypertrophy of mucous gland, hyperplasia of goblet cells
Airway edema: mucosal congestion and edema. Congestion refers to engorgement of blood within vessels.
Airway remodelling: chronic inflammation, affect reversibility of airway obstruction - Bronchial hyperresponsiveness
Airways narrow excessively in response to a variety of stimuli that provoke little or no bronchoconstriction in normal individuals
Caused by atopy, thickened bronchial wall, enhanced muscle contractility, epithelial damage
What is the assessment of asthma control?
Asthma control test (GINA assessment)
What triggering factors to asses in asthmatic attack?
- Allergens
o Dusts
o Pollen grains
o Animal dander (new pets)
o Fecal pellets of household dust mites (new curtains/ carpets/ mattress/ blanket/ dolls)
Requires frequent washing every week with water > 55oC - Respiratory irritants
o Smoking (first or second-hand)
o Air pollution
o Cold air
o Change of living environment (ongoing construction work) o Change in occupation (work-related exposure) - Medical conditions
o Upper respiratory tract infection (URTI)
o Gastroesophageal reflux disease (GERD) - Drug-induced
o Aspirin/ NSAIDs
o ACEI
o β-blockers - Exercise-induced
- Emotional stress
How to assess effect of asthmatic medication?
How to assess the severity of asthma using GINA 2009?
How to do a PE in asthmatic patient?
Inspection
Use of accessory muscles for breathing
Hyperinflation of chest
Seated position with use of extended arms to support upper chest (tripod position)
Pulsus paradoxus: occurs in acute exacerbation of asthma
Abd paradoxus: occurs in acute exacerbation of asthma, paradoxical movement
Auscultation
* Prolonged expiration phase
* Wheezing: widespread high pitched expiratory wheeze. Different from single pitch (monophasic) wheezing of local bronchial narrowing (e.g. aspiration of foreign body or bronchogenic cancer) which repeatedly begins and ends at the same point in each respiratory cycle.
* Silent chest: severe asthma exacerbation (status asthmaticus) or sever airway obstruction such that patient is unable to generate airflow to wheeze
Percussion: resonant
What dx tests can be done for athma?
Lung function test
Peak expiratory flow (PEF)
<80% personal best is consistent with poor control, <50% personal best is consistent with poor exacerbation
Brochial (metacholine) challenge test
Exclude airway hyperresponsiveness in patients with atypical presentation
Procedures: apply various dosage of metacholine that normally does not cause bronchoconstriction
E+ve early and late asthmatic reactions (bronchoconstriction) with decrease in FV1 >20%
-ve: straight line similar to normal pattern
Skin prick test: if not done before to confirm atopy.
Biochemical tests
CBC with DC: polycythemia (chronic hypoxia), leukocytosis (secondary infection ), eosinophilia (AGPA/Churg Strauss syndrome)
ABG: indicated when sO2 <92% on room air –> evaluate for resp failure
Aspergillus skin test +ve: suspected ABPA
Serum Ig level: suspected ABPA (increased total Ige level (typically >1000IU/ml)
When is step up and down treatment considered for asthma?
What are the 5 steps of treatment of asthma?
What must LABA be used with in asthmatic patients?
What are short acting, long acting B agonist used for asthma?
Muscarinic receptor antagonists?
mechanism
What complications?
What corticosteroids (inhaled, oral) used in asthma?
MoA
EA?
What is the mast cell stabilizer for asthma
MoA and Ae
What is the anti IgE antibodie for asthm
MoA and Ae
What are the leukotriene pathway inhibitors used for asthma?
MOA?
What are the different types of inhalers used for asthma?
What are the different types of delivery devices for asthamtic medication?
What is mx of asthmatic attack in children
mild to moderate
What is mx of asthmatic attack in children
severe asthmatic attack
What is mx of asthmatic attack in children
life threatening asthmatic attack
What is the management of asthmatic attack in adults?
What is asthmatic discharge plan in children?
What are the complications of severe asthmatic attack?
- Pneumothorax or pneumomediastinum
- Pulmonary infections: predisposed to mucous accumulation and stasis airflow e.g. pneumonia
- Resp failure: ventilatory failure (type 2 respiratory failure)
What other treatment modifications should be considered at this stage?
How do you distinguish exercise-induced asthma from exertional dyspnea?
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
What oxygen delivery systems are there and the O2 flow?
What are the indications of mechanical ventilation?
Indications of non invasive positive pressure ventilation (NPPV)?
What are the adv of mechanical ventilation?
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
What are the variables on the ventilator?
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
What are the basic principles of ventilators?
What are the modes of non invasive positive pressure ventilation (NPPV)?
Define acute cough, subacute cough and chronic cough
- 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
What is the cough reflex arch?
What are the different phases of cough and its significance?
What are the disorders resulting in ineffective cough
What is the consequence of ineffective cough
What are the causes of acute cough in children?
What are causes of chronic cough in children?
What are the causes of chronic cough in adults?
What are the warning signs for severe cough in children?
Hypoxemia
Purulent sputum
Hemoptysis
Chest pain
Exertional dyspnea
Failure to thrive
Growth retardation
What is history taking for cough?
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
What is done for PE of coughing?
What Ix for cough?
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
Treatment for cough (requires management of underlying cause)
A patient presents with dull percussion note with decreased breath sound and vocal resonance over the right lower zone. There is fine inspiratory crackles bilaterally over middle and lower zones.
What ddx
what ix done
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
What are the causes of pleural effusion in patients with idiopathic pulmonary fibrosis (IPF)?
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
A patient undergoes physical examination which is normal on inspection, palpation and percussion. On auscultation, there is fine end-inspiratory, lower zone crackles bilaterally. There is a small amount of clear whitish sputum in a cup at bedside.
What is most likely ddx?
What disease commonly give rise to clubbing together with inspiratory crackles?
Idiopathic pulmonary fibrosis
Bronchiectasis
Pulmonary fibrosis
CA lung with obstructive pneumonia
What are types of lung cancer?
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
Compare SCLC and NSCLC in general features
What are the modes of spread of lung cancer?
What are the RF for lung cancer?
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
What is the pathogenesis of lung cancer?
What is the carcinogenesis process of lung cancer
genes involved
What are the paraneoplastic syndromes of lung CA
What are endocrine disturbances in lung CA?
- PTH-rP: Hypercalcemia
- ADH: Hyponatremia (SIADH)
- ACTH: Hypokalemia (Cushing’s syndrome)
- ILP: Hypoglycemia
What are symptoms caused by metastatic disease?
What is done for PE of lung CA?
What Ix for lung CA?
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
What must be tested before treatment of lung cancer?
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
What is the treatment strategy of lung cancer?
- SCLC
- AD
- SCC
- LCC
What are the principles of targeted therapy in lung cancer?
What is medical treatment for lung cancer?
What is the prognosis for lung cancer?
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
CA right lung Pneumonia TB
What ix should be done?
What are the principles of underlying treatment of carcinoma of lung?
What are the causes of hypoNa in CA lung patients?
Syndrome of inappropriate ADH (Most common)
Depletional hyponatremia due to poor oral intake
Cortisol insufficiency due to bilateral adrenal metastasis
How are patients with brain metastasis from CA lung treated?
Whole brain radiotherapy
* Gamma knife for isolated brain metastasis
Systemic corticosteroids (i.e. dexamethasone)
* Relieve cerebral edema
What is the classification of pneumothorax?
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
What are the causes of pneumothorax?
- 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)
What is the pathophysiology of pneumothorax?
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
What is the pathogenesis of tension pneumothorax?
- 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.
What are the SS for pneumthorax/tension pneumothorax?
What PE for pneumothorax?
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
What Ix and results for pneumothorax?
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
What treatment for pneumothorax?
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
What is the mechanism of 3 bottle system in chest drain?
What are the components of a chest drain?
What does swinging and bubbling indicate?
What are the precautions, risks and how to remove the chest drain?
What procedure may be indicated in patients with recurrent pneumothorax or persistent air leaks?
Lifestyle modification of pneumothorax?
What is the classification of atelactasis?
What are the different causes of atelactasis?
What is the physiology of maintaining an open alveoli?
What is the PE and results for atelactasis?
What Ix for atelactasis?
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
What is treatment for atelactasis?
Depends on etiology
What are the causes of pleural effusion?
What is the pathophysiology of pleural effusion?
What is PE and results for pleural effusion?
What are the biochemical tests for pleural effusion and results?
What radiological Ix and specific tests for pleural effusion?
How can one proceed to make dx?
What are the SS of right sided HF?
What is the PE and results for pulmonary hypertension?
What is the general management of patients with pulmonary hypertension?
What is medical and surgical treatment for pulmonary hypertension?
What are the RF for OSA?
What is the physiology of sleep?
What is the effect of sleep on respiratory mechanics?
What are the SS of OSA?
What is the diagnostic criteria for OSA?
What assessment tool used to assess OSA in history taking?
What is gold standard Ix for OSA?
What are the complications of OSA?
Asthma attacks
Pulmonary edema
Obstructive sleep apnea (OSA)
Rhinitis with severe nasal blockage
Panic attacks
What further questions asked regarding the breathing difficulty?
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
What are the causes of acute adult respiratory distress syndrome?
What is the diagnostic guidelines to make the dx of acute ARDS?
What is the diagnostic criteria for acute ARDS?
What is treatment for ARDS?
Complications?
What are the viral etiologies of the common cold?
What are the specific features of adenovirus infection?
Clinical, biochemcial and radiological
What is the mechanism of common cold infection?
What are the SS of common cold?
How to differentiate URTI and LRTI from SS?
What is the ddx for common cold?
What history taking and biochemical tests for influenza patient?
What patient counselling done for influenza patients
What are indications for more targeted treatment
What antiviral medications can be given for influenza?
When are they indicated to be given
What AE?
What are the complications of influenza?
What are the eligible groups for seasonal influenza vaccine?
What is the classification of sinusitis based on symptom duration or etiology/clinical manifestation?
What are the RF for sinusitis?
What are the different nasal sinuses, blood and nerve supply?
What are the SS of sinusitis?
What is the diagnostic criteria for sinusitis?
What is the PE for sinusitis?
What treatment for sinusitis?
What are the complications of acute rhinosinusitis?
What are the patterns of pneumonia?
What are the RF for pneumonia?
What are the pathogens of pneumonia in children vs adults?
Etiological agents of pneumonia in adults?
What are the pathogens causing pneumonia in children?
Define recurrent pneumonia in children
What disorders must you suspect in recurrent pneumonia?
What is the micbio of bacteria causing pneumonia?
What is the micbio of virus and fungi causing pneumonia?
What are the different stages of pneumonia?
What are the SS of pneumonia in adults?
What are the SS of pneumonia in children?
What history taking for pneumonia?
What PE and results for pneumonia?
What is antibiotics duration for pneumonia
Choice of antibiotics in pregnancy and infants
What antibiotics not used alone?
What antibiotics for mycoplasma pneumoniae due to resistance?
What is treatment for community acquired pneumonia?
What is treatment for hospital acquired pneumonia?
What is treatment for pneumonia according to casuative organisms?
How to managem mycoplasma or MRSA pneumonia?
What is used to assess whether patient should be admitted for pneumonia?
What are the complications of pneumonia?
How to make dx of latent TB and active TB?
What are the sites of extrapulmonary TB?
Are they infectious?
What are general features of TB lymphadenitis
How to make dx
Treatment
What are general features of TB pleuritis
How to make dx
Treatment
What are general features of TB skeleton
How to make dx
Treatment
What are general features of TB meningitis?
How to make dx
Treatment
What are the RF for TB?
What is the micbio of TB?
What is the natural history of TB infection?
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
What are SS of TB?
How to interpret the results of tuberculin test?
Causes of FN and FP results?
What are CXR features of TB?
What is the types of drug resistance of TB?
What is treatment regimen for TB and for how long?
What side effects
What are the different types of TB drugs?
What is treatment regimen of TB in immunocompromised hosts?
How is case finding done for TB?
What is effective chemotherapy in TB?
What is done for BCG vaccination and health education in TB?
What is the complications of TB?
What is the pathogenesis of bronchiectasis?
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]
What are the causes of bronchiectasis (infectious insult, airway obstruction)?
Pertussis is not as common, but could still be present in some South-East Asian countries
What are the causes of bronchiectasis (impaired drainage, defective host response, miscallenous)?
CFTR gene mutation leads to cystic fibrosis
What is SS for bronchiectasis
PE and results
Bronchiectasis is a chronic suppurative lung disease + hypoxemia (clubbing may indicate underlying inflammation)
Catabolic state: Thin, cachexia (not absolute, but may be seen)
What features in CXR and HRCT thorax for bronchiectasis?
What is the medical treatment of bronchiectasis?
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)
