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MBBS VI Medicine > Respiratory notes > Flashcards

Respiratory notes Flashcards

1
Q

What are discharge medications for COPD?
What is the GOLD guidelines for usage of ICS?

A

Inhaled bronchodilator: b2 agonists (LABA), anticholinergics

Escalate treatment from use of LABA + LAMA to use of LABA +ICS (in severe exacerbation)
Gold guidelines for usage of ICS
* Hospitalizations for COPD exacerbation
* >2 moderate COPD exacerbation/year
* Eosinophil level >300
* History/concomitant asthma

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2
Q

Blood gases : pH : 7.37
PaO2 : 7 kPa (on 2L O2)
PaCO2 : 5.5 kPa
BE : + 2 mmol/L
Total bicarbonate: 26 mmol/L

Acute exacerbation of COPD

What is the dx and management?

A

Type 1 respiratory failure

Increase supplemental oxygen to 3L and monitor closely (to avoid further further spO2 drop due to oxygen dissociation curve)

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3
Q

How do you assess history of exertional dyspnoea in suspected COPD?

A

mMRC: modified medical research council

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4
Q

How to assess severity of respiratory distress in general examination?

A

General inspection: tripod sign, use of accessory respiratory muscles
Central cyanosis
GCS: drowsiness due to retained CO2 in the brain resulting in low respiratory rate (in T2 resp failure)

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5
Q

What is the mode of SABA admin for medium severity and severe asthmatic attack?

A

Metered dose inhaler for medium severity
Nebulization for severe condition (requires no respiratory effort)

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6
Q

If pleural effusion and do thoracocentesis reveals blood what should be done?

A

Let sample sit: if clots it means thae there is active clotting factors = active bleeding (requires embolization, resuscitation)
If no clotting after a while –> there is underlying pathology

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7
Q

How to classify pleural infection?

A

Simple, complicated, empyema

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8
Q

What is the management of loculated pleural effusion?

A

Chest drain/pig tail catheter 14Fr (preferred as studies show the efficacy is same as chest drain) may require 2nd or 3rd USG guided insertion if multiple locules. Or catheter thoracostomy.

Patients who fail antibiotic therapy and initial drainage should undergo fibrinolysis of septums
* Fibrinolytics: urokinase, streptokinase, tPA (most used)
* Intrapleural tPA with DNase

If these treatments have minimal/no response –> then VATS is typically indicated (video assisted thoracoscopic surgery)

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9
Q

If there is salmonella entericus empyema what must you test for?

A

Pleural empyema is a result of bacteremia from salmonella enteridis which is associated with underlying immunodeficiency, sickle cell anemiae and lung cancer. If there is any abnormal encapsulated bacterial infection think immunodeficiency (can be splenectomy).

Must do HIV PCR test

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10
Q

If there is salmonella entericus in septicemia, what other manifestations can there be?

A
  • Meningitis
  • Endocarditis
  • Mycotic aneurysm (non typhoidal salmonellae): abd aorta is the most common (S. typhimurium is most common)
  • Septic arthritis
  • Pneumonia (due to bacteremia)
  • Abscessation: spleen, ovary, heart, lungs

Complications during pregnancy
* Chorioamnionitis, transplacental infection, preterm labor and abortion

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11
Q

Compare NSIP vs UIP in respond to steroids and prognosis
In dermatomyositis/polymyositis what is affected?

A

NSIP (non specific interstitial pneumonia): good response to steroids and good prognosis
Deratomyositis/polymyositis causes NSIP

UIP (usual interstitial pneumonia): poor response to steroids

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12
Q

What is measured in a lung function test?

A

Spirometry
* FEV1/FVC
* Lung volumes

Diffusing capacity: DLCO

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13
Q

What is included in a basic PSG for sleep disorder?

A
  • EEG: testing for sleeping and arousal (wakefulness)
  • Oximetry: periods of desaturation
  • Submental EMG: detect hypotonia in REM
  • Leg EMG: periodic leg syndrome
  • Abd and thoracic belt:
    Obstructive OSA there is paradoxical movement (There is diaphragm contraction for inspiration which moves the abd up. However, due to obstruction there is no inflation of the lungs so the thorax does not move up. Normally both the thorax and abd will move upon inspiration.)
    Central OSA: there is a lack of ventilatory drive so diaphragm not moving (no paradoxical movement as both thorax and abd dont move)
    Both will have desaturation after event
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14
Q

Can asthma can present with spirometry results that are not reversible by bronchodilator?

A
  • Yes, in chronic asthma there is airway remodelling which results in fibrotic airways. These fibrotic airways are not reversible to bronchodilator
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15
Q

What are the indications for usage of antifibrotic agent?

A

Slow progression of disease
* Idiopathic pulmonary fibrosis
* Progressive pulmonary fibrosis

Nintedanib

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16
Q

Any drug for asthma that is taken in tablet form?
What drugs can cause dizziness?

A

Leukotriene receptor antagonist (useful for excercise induced asthma and aspirin/NSAID exacerbated respiratory disease)
Salmeterol, leukotriene receptora ntagonist

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17
Q

How would you assess the severity of asthma?

A

GINA assessment
* Daytime symptoms (>2 a week)
* Nocturnal symptoms (night awakening, nocturnal cough, sleep disturbance)
* Activity limitation
* Reliever use (>2 a week)

Hospitalization, away from work

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18
Q

If patient is admitted with acute exacerbation of asthma, how to assess patients severity?

A

GINA
* breathlessness, talkng, alertness
* RR, pulse, sO2, pO2, pCO2
* PE: wheezing, use of accessory muscles, pulsus paradoxus. Tripod position and use peak flow meter.

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19
Q

Use of peak flow meter in asthma?

A
  • Check patients severity and obstructive pattern
  • Can be used to demonstrate diurnal variation in obstruction
  • Baseline for checking efficacy of treatment
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20
Q

What would you expect in PE of severe asthma?
What is wheeze?
At which phase?
More than that if really severe attack? What is it called?

A
  • Use of accessory muscles, bilaterally reduced chest expansion, prolonged expiratory phase and wheeze on auscultation
  • Wheeze: continous oscillation of opposing walls of an airway that is narrowed almost to the point of closure. High pitched and during expiration
  • Expiratory phase
  • Absence of breath sound
  • Silent chest
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21
Q

Acute SOB ddx?

A
  • Acute exacerberation of asthma
  • pneumothorax
  • COPD
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22
Q

If COPD in very young agent, what deficiency does this patient have?

A

Alpha 1 antitrypsin deficiency

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23
Q

In severe asthma cases, what treatment can be given other than bronchodilators and corticosteroids?

A
  • Antimuscarinics: tiotropium
  • LTRA: montelukast
  • Biologics. Anti IgE antibody (omalizumab) for atopic asthma (IgE>30). anti IL5: mepolizumab. Anti IL5a: benralizumab
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24
Q

ddx of bronchiectiasis?

A
  • Idiopathic: majority
  • Congenital/primary: primary ciliary dyskinesia (kartagenners syndrome), cystic fibrosis (CFTR gene mutation), alpha 1 antitrypsin deficiency, hypogammaglobulinemia
  • Acquired: infection (TB, severe pneumonia, EGPA), traction bronchiectasis (connective tissue disease)
  • GERD
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25
Q

Workup for the dx of bronchiectasis?

A
  • CBC (leukocytosis), sputum for smear and C/S
  • Lung function test (obstructive pattern: FEV1/FVC <70%)
  • Pulse oximetery (sO2), ABG
  • CXR (bunch of grapes appearance, tramline shadows, irregular peripheral opacities representing mucopurulent plugs)
  • HRCT (tramline shadows, signet ring sign, thickened bronchial wall, mucopurulent plugs
  • Spirometry
  • Sputum R/M, C/ST, gram stain, AFB smear
  • Additional: Ig measurement, serum alpha 1 antitrypsin level, mutation analysis for cystic fibrosis
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26
Q

How to manage patient with massive haemoptysis?

A

100-200ml

ABCDE and resuscitation
Immediately placed into positon in which the presumed bleeding lung is in the dependent position (right bleeing lung –> right side down decubitus position
Establish a patent airway and give O2 (e.g. unilateral lung ventilation in the non bleeding lung)

Control the bleeding
* Bronchoscopy (balloon tamponade, topical adrenaline)
* Arteriographic embolization (urgent contrast CT and bronchial artery embolization by IR)
* Surgery (pneumectomy)

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27
Q

Organisms associated with bronchiectasis?
Tx?

A
  • early or mild cases: H.influenzae (augmentin, macrolides: azithromycin)
  • late or severe cases: P. aeruginosa

1st line is tazocin (piperacillin-tazobactam)
ceftazidine, meropenem

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28
Q

Causes of haemoptysis?
How will DLCO be affected?

A
  • Pneumonia, bronchiectasis, CA lung, TB
  • Small vessel vasculitis: wegeners (GPA), EGPA
  • Rheumatic: Goodpasture syndrome (anti GBM antibody directed against an intrisic antigen to the GBM (NC1 domains of the alpha 3 chain of the type 4 collagen, which is found in GBM and alveoli), lupus pneumonitis, GPA, Behcet syndrome
  • DLCO is increased
  • Other causes of increased DLCO: polycythemia, left to right shunt, asthma due to increased pulmonary capillary blood volume
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29
Q

Typical findings of allergic bronchopulmonary aspergillosis (ABPA) on CT thorax and mechanism?

A
  • ABPA is a cause of bronchiectasis
  • Hypersensitivity reaction to aspergillus fumigatus that colonized airway, almost exclusively occurs in patients with asthma or cystic fibrosis
  • Clinical picture = recurrent exacerbations of asthma
  • Bronchial wall thickening, bronchiectasis, centrilobular nodules, mucoid impaction, mosaic perfusion, atelectasis and consolidation, tram lining
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30
Q

dx criteria for ABPA?

A

Predisposing conditions: asthma, cystic fibrosis
Obligatory criteria
* Aspergillus skin test +ve or detectable IgE levels against aspergillus fumigatus
* Elevated total serum IgE concentration
Other criteria:
* Precipitating serum antibodies to A. fumigatus (IgG, IgA)
* Radiographic pulmonary opacities consistent with APBA
* Eosinophilia

31
Q

Standard TB regimen and AE?

A

2HREZ/4HR3 = 2 months of HREZ daily, than 4 months of HR, taken 3 rtimes per week

H (isoniazid). AE: peripheral neuroopathy, hepatotoxicity
R (rifampicin). AE: orange urine, GI upset, BM suppression and haemolytic anemia
Z (pyrazinamide). AE: gout and arthralgia, hepatotoxicity
E (ethambutol). AE: optic neuropathy, arthralgia, cytopenias

32
Q

Ix for PE?

A
  • CBC
  • Clotting profile, LRFT
  • D-dimer
  • ABG (type 1 respiratory failure)
  • Thrombophilaia screen
  • ECG (sinus tachycardia, S1Q3T3, right heart strain)
  • CXR (hamptons hump, westermark sign, pleural effusion, atelactasis): hamptons hump (wedge shaped opacity in the periphery of hte lung with its base against the pleural surface), westermark sign (dilatation of pulmonary vessels proximal to the embolism along with collapse of distal vessels often with a shart cut off)
  • Venous duplex USG (for DVT)
  • CT pulmonary angiogram (filling defects in pulmonary trunk –> diagnostic
  • V/Q scan (high sensitivity, low specificity)
33
Q

Treat PE?

A
  • ABC: monitor vitals (BP, pulse, spO2, RR)
  • Analgesics
  • Haemodynamically unstable: IV rTPA followed bgy heparin infusion, catheter directed treatment (thrombectomy), surgery (embolectomy)
  • Anticoagulation: SC LMWH heparin for 5+ days and warfarin initiated simultaneously –> heparin stopped at D5/6 when INR reached target of 2.5
  • Use NOACs better (does not require regular monitoring): direct thrombin inhibitor (dabigatran), F10a inhibitors (rivaroxaban, apixiban)
34
Q

Duration of NOAC post PE?

A

Provoked PE: 3 months
Unprovoked PE or persistent risk factors: 6m or indefinite

35
Q

Causes of persistent pneumothorax (reason for chest drain)?

Why would chemical pleurodesis not work?

A
  • Secondary to bullae in emphysema COPD due to chornic smoking (parasternal heave, hepatomegaly, raised JVP, ankle edema)
  • Marfans syndrome (AR and MVP murmur)
  • Bronchopulmonary fistula

Chemical pleurodesis requires good opposition of the visceral and parietal pleural membranes, so if you get persistent pneumothorax with a bronchopleural fistula theyre not gonna oppose and they cant inflame and stick together

36
Q

ddx for cavitating lung lesion?

A
  • Cancer – most frequently SCC
  • Autoimmune granulomas – Wegener, RA nodules
  • Vascular – emboli
  • Infection – abscess, TB
  • Trauma – pneumatoceles
  • Youth – airway malformation, cyst, pulmonary sequestration
37
Q

Bronchiectasis CXR and HRCT features?

A

CXR: ring shadows (dilated bronchi), tramline shadows (2 white parallel lines separated by black), tubular shadows
HRCT features: dilated airways, mucus plugging, atelactasis and consolidation

38
Q

ddx of cavitatory lung mass

A
  • Malignancy +/- superimposed infection
  • TB
  • Empyema with air fluid interface
  • Chronic cavitatory aspergillosis
  • Nodular silicosis
  • Wegeners granulomatosis
  • RA
  • Sarcoidosis (deposition disease)
  • Hydatid cyst (echinococcus)
  • Infected pulmonary sequestration
39
Q

Life threatening features of acute asthma

A
  • Silent chest (no air entry)
  • Hypotension
  • 1/3 of best/predicted PEF
  • Cyanosis
  • Confusion
40
Q

Features of asthmatic exacerabtion that warrant ICU care?

A
  • life threatening features: silent chest, hypotension, 1/3 of best/predicted PEF (peak flow meter), cyanosis, confusion
  • Deterioration in PEF/FEV1
  • Worsening or persistent hypoxia or hypercapnia
  • Respiratory failure requiring IPPV
  • Respiratory or cardiorespiratory arrest
41
Q

How to manage acute exacerbation of COPD?
What Ix should you do?

A

Ix: CXR (rule out pneumothorax, pneumonia), pulse oximetry (SaO2) and ABG (possible T2RF)

Tx
* Supplemental oxygen (start with 1-2L/min by nasal prongs to maitain SpO2 88-92% (but not higher –> over aggressive O2 therapy will lead to suppression of hypoxic respiratory drive. Patients from chronic hypercapnia have increased HCO3- compensation in blood and CSF w/o increase in pH. there chemorecetpor response to increased pCO2 will be blunted and will depend on hypoxic drive to maintain their respiratory drive. A high po2 will lead to decreased RR and therefore Co2 retention and narcosis.
* SABA (ventolin) +/- ipratropium bromide (atrovent) with sapcer
* Corticosteroids (IV hydrocortisone or oral prednisolone). Discontinued after the acute episode (e.g. 5-10 days)
* Antibiotics in patients requriing invasive or non invasive ventilation (NIV) and/or at least 2 cardinal symptoms (increased sputum purulence): increased dyspena, sputum volume, purulence
* NIV to relieve dyspnea by decreased work of breahting. Respiratory acidosis (pCO2 >6kPa and pH<7.35)
* Immediate intubation and mechanical ventilation if no improvement
i.e. diminished consiosuness, massive aspiration or persistent vomiting, severe haemodynamic instability without response to fluid and vasoactive drugs, severe arrhythmia

42
Q

Distribution of interstitial lung disease to upper and lower zone depending on causes?

A
43
Q

Causes for bronchiectasis?

A
44
Q

Signs of bronchiectasis

A
  • General: cachexia, clubbing, halitosis
  • Increased secretions: coarse crackles that disappear/change in quality after coughing
  • Obstructive pattern: decreased breath sounds, decreased chest wall movement
  • Chronic localized fibrorsis: bronchial breath sounds
  • Severe: cor pulmonale
  • Severe –> cor pulmonale (increased JVP, peripheral edema, hepatic congestion, parasternal heave, loud P2)
  • Severe –> resp failure (central cyanosis)
45
Q

CXR and HRCT features of bronchiectasis?

A

CXR (abnormal in 50%): ring shadows (dilated bronchi end on), tramline shadows (dilated bronchi seen side on: normally lower lobes), tubular shadows
HRCT: bronchial airway dilatation (signet ring sign), bronchial wall thickening (ring shadows on CXR), mucus plugging (darker than airway wall): tree in bud appearance, mosaic appearance on expiratory film indicating air trapping

46
Q

Ix done for bronchiectasis?

A
  • CXR, HRCT
  • Lung function test: obstructive or obstructive/restrictive pattern
  • Sputum: C/ST (guides Mx), AFB
  • Screening tests for underlying cause if <50y or deteriorating clinical course
  • Ig pattern for immunodeficiency (esp hypogamma globulinemia)
  • CBZC, serum IgE, sIgE vs aspergillus fumigatus for ABPA
  • RF, anti CCP, ANA, ANCA for RA and CTD
  • Bronchoscopy to r/o endobronchial lesion (if localzied disease) and look for NTM
47
Q

Mx of acute exacerbation of bronchiectasis

A
  • Antibiotic therapy: tazocin is 1st line. Potential organisms are h.influenzae, m.catarrhalis, s. aureus

Acute haemoptysis
* Transamin for moderate to severe haemoptysis –> risks of tenacious clots obstructing airway, risk of thromboembolism
* Bronchial arterial angiogram and embolization (BAE) if prolonged severe or massive life threatening
* Surgical resection if emobolization unsuccessful

48
Q

Effect of intrathoracic spread of lung cancer?

A
  • Lympangitis carcinmoatosis: diffuse pulmonary lymphatic spread of malignancy –> reticulonodular shadows raditing out from hilum due to thickening of interlobular septae
  • Pleural fluid and effuson
  • Pericardial effusion and cardiac tamponade
  • Chest wall and ribs –> chest pain and swelling
  • Phrenic nerve: diaphragmatic paralysis –> elevated hemidiaphragm on CXR
  • SVC obstruction by malignant nodes or tumors: dyspnea and stridor, facial plethora, dilated veins on chest wall and neck. Pembertons sign: lift both arms.
  • Left recurrent laryngeal nerve: hoarsenss
  • Brachial plexus –> Pancoast syndrome (classically a/w NSCLC)
  • Inferior cervical sympathetic chain: horner syndrome (ipsilateral partial ptosis, miosis, enopthalmos, anhidrosis)
  • Esophagus –> dysphagia
49
Q

What are systemic non metastatic effects of lung cancer?

A
  • Haemat: anemia of chronic disease, leukocytosis, thrombocytosis
  • Connective tissues: clubbing, hypertrophic pulmonary osteoarthropathy: clubbing and painful periosteitis of distal long bones
  • Ectopic hormones
    SIADH (SCLC): hypoNa –> confusion, weakness
    ACTH (SCLC): cushing syndrome (ectopic ACTH)
    PTHrP (SCC): hyperCa –> polyuria, thirst, confusion
  • Neuromuscular
    LAMS: weakness
    Paraneoplastic encephalitis
    Peripheral neuropathy: paresthesia
    Dermatomyositis and polymyositis
50
Q

mx principle of lung cancer

A
  • SCLC: metastasis tends to be early. All patients consider chemo and RT
  • NSCLC: treatment depends on staging and molecular markers
    Surgery as defintiive tx
    Adjuvant chemo for pathologic stage 2-3 or high risk 1B
    Adjuvant RT for +ve surgical margin or mediastinal LN involvement detected intraop
    Criteria for resectability in NSCLC
  • Appropriate stage: stage 1, stage 2, T3N1, selected T1N0-1
  • No mediastinal involvement (N2 precludes resection)
  • Adequate cardiac and lung reserve)
51
Q

What is Tx for advanced NSCLC?

A

genetic testing to identify driver mutations
* EGFR: use TKI: gefitnib, erlotonib. If T790M than use 3rd gen TKI: osimertinib
* ALK translocation/ROS1 rearrangement. 1st gen ALK TKIs: crizotinib. Resistance –> start 2nd gen ALK TKIs e.g. ceritinib

No actionable driver mutations
PDL1 high –> pembrolizumab monotherapy
PDL1 low –> pembrolizumab and platinum based doublet chemo (carboplatin/pemetrexed)

52
Q

Tx of SCLC

A

Staging workup
* Locoregional staging: CXR, CT thorax and abd
* Systemic staging: MRI brain, whole body PET (bone metastasis)

cT1-2N0M0 limited stage disease
* Primary surgery: lobectomy +mediastinal LN sampling/ dissection
* Adjuvant chemotherapy: 4 cycles of cisplatin based chemotherapy
* +/-adjuvant chemo/RT if LN involvement

Unresectable limited stage disease
* Chemoirradiation
* Prophylactic cranial irradiation: if respond well to initial chemo/RT w/o brain mets. Often brain mets occurs in SCLC wo neurological symptoms –> brain mets often as sole site of relapse. Prophylactic cranial irradiation –> increases overall survival and decreased incidence of brain metastasis

Extensive stage
Induction chemo: 4-6 cycles (atezolizumab, PD-L1 mAb)
Further thoracic EBRT +PCI if good response to initial chemo

53
Q

Causes of primary, secondary spontaneous pneumothorax and other secondary pneumothorax

A
  • PSP: smoking, thin/tall stature (marfans), subplerual blebs, previous pneumothorax
  • SSP: COPD (60% majority of cases), TB, PCP. CF, asthma, CA lung, pleural mets, bullae
  • Other secondary pneumothorax. Iatrogenic: PPV, thoracic procedures (e.g. transthoracic biopsy, pleural tap, chest drain)
54
Q

What are the types of pneumothorax?

A
  • Closed: airway pleural space communication sealed as lung deflates and does not reopen. Pleural pressure = negative. Spontaneous reabsorption of air –> lung reexpansion occurs over days/weeks
  • Open: airway pleural space communication not sealed and continously patent. pleural pressure =atmospheric. Mechanism = rupture of emphysematus bullae (COPD), TB cavity, lung abscess into pleural space –> bronchopulmonary fistula with continuous air leak
  • Tneison: one way valve –> progressive accumulation of air within pleural space. Pleural pressure = positive. Mediastinal shift –> press on contralateral lung + impair systemic venous return –> obstructive shock with cardiopulmonary collapse
55
Q

What lung cancer most common in lung cancer, what paraneoplastic syndromes?
If there is wrist pain, what ddx do you have and mechanism?

A
  • SCC
  • PTHrP (only SCLC (15% of total lung cancer cases) has ectopic SIADH, SIADH, LAMS)

Wrist pain caused by hypetrophic osteoparthropathy: symmetric polyarthritis and proliferative periostosis of the long bones: clubbing, tenderness over long bones, large joint synovial effusions
* Platelet derived and other growth factors –> circulatory bypass of the lung by megakaryocyts that could release factors into the distal extremities –> tumor derived VEGF that promote vascular proiferation, edema formation, and new born formation.

Wrist pain by pancoast syndrome –> involves brachial plexus if there is small hand muscle wasting

56
Q

Most common chemo regimen for lung cancer?

A

Carbotaxel (carboplatin + paclitaxel)

Bevacizumab: anti VEGF Ab (prevents increased angiogenesis as it binds to VEGF). AE: bleeding tendency, hypertension

Check point inhibitor=immunotherapy (can be used for all lung cancer patients regardless of mutations)
Atezolimab: anti PDL1 ab. AE: dermatitis, pneumonitis

57
Q

Autonomic dysfunction SS

A
  • Orthostatic syncope
  • Abnormal sweating
  • Constipation
  • Urinary retention
  • Erectile dysfunction
58
Q

Where does ALP come from and why elevated in bone met?
Is there any condition which ALP wont be raised despite osteolysis?

A
  • Osteoblast: in bone met the bone turnover is increased, indeed it is overall osteolytic process but the osteoblastic activity is also increased but just that the net result is increase in osteolytic activity. So ALP is reflecting osteoblastic activity.
  • Multiple myeloma
59
Q

Causes of monocytosis in CBC?

A
  • Infxn – usu TB, SBE, listeria, brucella, rickettsia, fungi, parasites
  • inflm – IBD, sarcoidosis, CVD
  • malig – HL, leukemia, MPD, carcinomas
60
Q

CNS effect from paraneoplastic synromes?

A
  • Rapidly progressive cerebellar syndrome (bilateral effected –> in comparison to normal unilateral cerebellar lesions)
  • Opsoclonic myoclonus syndrome
  • Encephalitis/encephalomyelitis
  • Stiff person syndrome spectrum disorders
61
Q

In late stage bronchiectasis what pathogens?
How long is antibiotics given?

A
  • Pseudomonas aeruginosa
  • Non tuberculous mycobacteria: M. marinum, M. leprae, M. bovis, M. abscessus)
  • Given IV tazocin (piperacillin-tazobactam (gram+ve and -ve coverage) 10-14 days
  • Nebulized colomycin or gentamicin
62
Q

What is antibiotics for typical pneumonia?
If not responding to antibiotics what pathogens can be the cause?

A

Augmentin (gram+ve) and doxycycline (gram-ve –> used over macrolide as there is increasing macrolide resistance in mycoplasma)

Atypical pneumoniae: legionella (urinary antigen), pneumophila, chlamydophila

63
Q

PCR TB will take long time, what other ix for faster result?

A

Bronchoscopy, pleurosscopy for biopsy showing granulomatous inflammation

64
Q

What is ADA in pleural fluid?

A

Found in lymphocyte (as they are rapidly dividing) –> elevated in various inflammatory conditions including TB, pyogenic pneumonia, CA lung and thus not specific to TB

65
Q

Causes for massive one sided pleural effusion but not centrally located trachea?

A
  • Concomitant lung collapse
  • Loculated pleural effusion
66
Q

CA lung what EGFR inhibitor has high CNS penetration?

A

Osimertinib

67
Q

Patient has recurrent malignant pleural effusion, tx?

A
  • Pleurodesis
  • Pleurodectomy
68
Q

What tests for TB and MoA?

A

IGRA (interferon gamma release assay): measure T cell release of IFN gamma following stimulation by antigens specific to MTB complex –> diagnose latent infection
Tuberculin skin test (mantoux test): uses tuberculin puriified protien derivative and relies on type 4 HS peak induration at 24 hours.

69
Q

Which 5 classes of antibiotics used for bronchiectasis?

A

Must cover pseudomonas

Anti pseudomonal penicillins (1st line): piperacillin-tazobactam (tazocin)
3rd and 4th gen cephalosproin e.g. ceftazidime
Carbapenems e.g. meropenem, imipenem
Aminoglycosides e.g. amikacin (not as monotherapy due to increased resistance rate)
Fluoroquinolones

70
Q

Long term treatment for bronchiectasis?

A
  • Treat underlying etiology (GERD, NTM) and comorbidities (asthma, COPD)
  • General: annual flu vaccination, pneumococcal vaccination (13 valent conjugated pneumococcal vaccine better than 23 valent)
  • Airway clearance: postural change, active cycle of breathing technique –> may ofer resp PT coaching
  • Mucoactive drugs
  • Long term antibiotics for immunomodulatory effect to decrease exacerbations. Indications if >3 exacerbations per year. Oral macrolides (should exclude NTM infection before initiation as macrolide is important component of treatment of many NTMs)
  • Inhaled/nebulizer colistin (gentamicin)
  • Intermittent IV antibiotpics for repeated >5 infections/yr despite other tx
71
Q

When cant a lung function test be done?

A
  • Unstable (acute setting)
  • Functional state poor (old age, bed bound, intubated)
  • Extremes of age: young age (only at 6 years old does it become reliable)
72
Q

What 3 factors are considered when treating infection in airway diseases?

A
  • Radiological changes
  • Symptoms
  • Isolation of organism that requires specific treatment (colonisiation or pathogen)
73
Q

What are the surgical interventions for severe COPD?

A
  • Endobronchial one way valve (reduce lung hyperinflation by allowing the trapped air to escape. Lung function may improve when the healthier areas of the lungs provide the necessary oxygen exchange. (sephyr valve/spiration valve) via bronchoscopy
  • Lung volume reduction surgery

MBBS VI Medicine (92 decks)

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