Resp Flashcards

asthma, COPD, ILD, lung cancer, TB, sarcoidosis, OSA, cystic fibrosis

1
Q

Asthma = recurrent episodes of dyspnoea, cough and wheeze - Precipitants, differential dx and exam findings

A

Precipitants
o Cold, exercise, emotion, allergens, infection, smoke, NSAIDS, B blockers

Exam findings
General - Tachypnoea, Audible wheeze
Peripheries and Face (nasal polyps?)
Chest
- hyperinflated chest
- hyper-resonant percussion
- diminished air entry
- longer expiration
- widespread polyphonic wheeze

DIFFERENTIAL DIAGNOSIS
- COPD
- Large airway obstruction or SVC obstruction
- Pneumothorax or PE
- Bronchiectasis or obliterative bronchiolitis
- Sinusitis
- Foreign body aspiration

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2
Q

IX and management of asthma (acute + chronic )

A

INVESTIGATIONS
Acute Attack
- Bloods: FBC, U+E, CRP, cultures, ABG
- Peak flow, Sputum culture, CXR

Chronic
- Peak expiratory flow monitoring - Diurnal variation

  • Spirometry
    o Obstructive defect (low FEV1/FVC, low residual volume)
    o > 15% increase in FEV1 following B agonist.
  • CXR ->Hyperinflation
  • RAST testing (radioallergosorbent test to detect specific IgE abs to determine allergy
  • Aspergillus serology (IgE)

MANAGEMENT
Acute:
-Nebulized salbutamol
-Oxygen
-Hydrocortisone or prednisolone
-If persisting – add ipratropium nebs and give
magnesium sulphate

Chronic
Non-Pharmacological
- Smoking cessation
- Avoidance of precipitants
- Twice daily PEF
- Written emergency action plan

SMART therapy:
o Budesonide (ICS)/formoterol (LABA)
o used for maintenance
and relief of sx prn

Can add on for poor control with SMART:
1. Leukotrine receptor antagonist (Oral Monteleukast) or theophylline
2. Oral prednisone
3. Tiotropiumbromide (LAMA)

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3
Q

Bronchiectasis - causes, exam, complications, differentials

A

CAUSES
Primary (congenital)
- Cystic fibrosis
- Primary cilia dyskinesia
- Congenital hypogammaglobulinemia

Secondary (acquired)
- childhood infection (TB, pneumonia, measles, whooping cough)
- Localized disease (bronchial adenoma, TB, foreign body)
- Allergic bronchopulmonary aspergillosis
- Rheumatoid arthritis
- COPD
- Recurrent aspiration
- ILD and pneumoconiosis
- Idiopathic 50%

EXAMINATION
General Observation
- Unpleasant sputum
Hands ttyy- Clubbing
Chest
- Position of apex beat
- Wheeze
- Crackles insp, gurgly noises
- RHF sx
- Pectus carinatum
Associated conditions to looks for: rheumatoid
arthritis, IBD, CF,GORD

Consider the following complications and look for
them:
- Pneumonia
- Pleurisy
- Empyema
- Lung abscess
- Cor pulmonale
- Amyloidosis

DIFFERENTIAL DIAGNOSIS
- Chronic bronchitis
- COPD
- TB
- Asthma

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4
Q

IX and management of bronchiectasis

A

INVESTIGATIONS
- Chest X-Ray
o Cystic lesions
o Streaky infiltration
o Thickened bronchial walls

  • Sputum microscopy and culture
    o Common organisms are
    haemophilus influenzae,
    pseudomonas, Escherichia coli, pneumococcus, mycobacteria, staph
    aureus
  • Testing for cystic fibrosis (sweat test) and
    immotile cilia syndrome in young adults
  • Spirometry
    o For assessing severity not diagnosis
    o FEV1 < 40%  severe
  • High resolution CT
    o Confirms diagnosis
    o Perform when patient stable
    o Airway dilatation diameter greater
    than accompanying pulmonary artery)
  • Bronchoscopy (to locate site of haemoptysis
    and obtain sample for culture)
  • FBC and IgE for Aspergillus

MANAGEMENT
-Twice daily postural drainage
- Physiotherapy
- Influenza and pneumococcal vaccines
- Smoking cessation
- Home oxygen may be offered to nonsmoking patients with severe disease (FEV1 < 40%) and oxygen saturation <93% on RA.

Pharmacological
- Antibiotics
o During exacerbations, use according to sensitivities, if >3/year consider long term abx
- Bronchodilators: Facilitate clearance of sputum
- Treatment of heart failure

Invasive
- Surgery if localized disease or severe haemoptysis
- Transplant is occasionally appropriate for end stage disease

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5
Q

COPD exam and investigations

A

General Observation
- Pursed lip breathing, use of accessory muscles
- Prolonged forced expiratory time
- Sputum pot
- Signs of cachexia
- Tachypnea

Hands
- Cyanosis, polycythemia
- Asterixis if CO2 retention

Face and Neck
- Cyanosis
- Tracheal tug
- Reduced cricosternal distance (<3cm)

Chest
- Inspection: Intercostal recession, Increased AP diameter-barrel chest

  • Palpation/Percussion
    Reduced chest wall
    movement/chest expansion
    , Hyper-resonant percussion
  • Auscultation
    o Reduced breath sounds
    o +/- wheeze
    o Early course inspiratory crackles

INVESTIGATIONS
Spirometry is required to make a diagnosis in this
clinical context (obstructive)
- Post bronchodilator FEV1/FVC < 0.7 confirms persistent airflow limitation
- (mild) – FEV1 > 80% predicted
- (moderate) – 50% FEV1 <80%
-(severe) – 30% FEV1 < 50%
- (very severe) – FEV1 < 30%

  • CXR – hyperinflation (>6 anterior ribs seen, flat hemidiaphragms)
  • ECG – RVH from cor pulmonale
  • ABG – PaO2 decreased, with or without hypercapnia
  • FBC – exclude secondary polycythemia
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6
Q

Assessment of COPD (3 aspects in hx and exam)

A

Symptoms
- Degree of airflow obstruction (using
spirometry)

  • Risk of exacerbations
    o Precious exacerbations, how many per year, hospital admissions, ICU admissions.
  • Treatment
    o Use of prednisone, how long inhalers last for.
  • Comorbidities
    o CVD, osteoporosis, depression and anxiety, skeletal muscle dysfunction,
    metabolic syndrome, lung cancer.
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7
Q

Differential dx for dyspnoea for lung diseases onset, hx, sx worse

A
  • COPD
    o Onset mid life
    o Symptoms slowly progressive
    o History of tobacco smoking or exposure
  • Asthma
    o Onset early in life
    o Symptoms vary widely from day to day
    o Symptoms worse at night/early morning
    o Allergy, rhinitis and/or eczema also present
    o Family history of asthma
  • Congestive Heart Failure
    o Fluid overload
    o CXR shows A – alveolar oedema (bats wings), B – kerley B lines (interstitial oedema), C – cardiomegaly, D – dilated, prominent
    upper lobe vessels, E – pleural effusion.
    o Pulmonary function tests indicate volume restriction not airflow limitation
  • Bronchiectasis
    o Large volumes of purulent sputum
    o Commonly associated with bacterial infection
    o Chest X-ray/CT shows bronchial dilation, bronchial wall thickening
  • Chronic Bronchitis
    o Cough and sputum production for at
    least three months in each of two consecutive years, not necessarily associated with airflow limitation
  • Tuberculosis
    o Onset all ages
    o CXR shows lung infiltrate
    o Microbiological confirmation
    o High local prevalence
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8
Q

Aim of COPD treatment

A

C – Confirm the diagnosis
- O – Optimize function
- P – Prevent deterioration
- D – Develop a plan of care
- X – Manage exacerbations

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9
Q

Chronic treatment of COPD - pharm for less symptoms, more symptoms

A

Non-Pharmacological
- Smoking cessation
- Pulmonary Rehab
- Physical Activity
- housing and nutrition
- Flu Vaccine/ pertussis/pneumococcal

Pharmacological
Less symptoms, low exacerbation risk
LAMA. (eg. incruse ellipta umeclidium)

  • If needed move to LABA/LAMA
    Spiolto respimat - tiotroprium olodaterol

HIgh exac risk start with same but can move to
- ICS/ LABA if eosinophilia eg. seretide, breo
- LABA/LAMA/ICS eg. trelegy ellipta

Asthma COPD overlap
- ICS LABA pluse LAMA

  • (Long term monotherapy with oral and inhaled corticosteroids is not recommended. Increased risk of pneumonia)
  • If cor pulmonale = diuretics
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10
Q

Ix and treatment of acute exacerbation of COPD

A

Investigations
- ABG
o Pa02 < 8.0kpa =Resp Failure
o PaC02 <6.7kpa =Type I Resp Failure
o PaC02 > 6.7kpa = Type II Resp Failure
 (CO2 only increases when
global ventilation affected)

  • CXR
    o Exclude other diagnoses
  • ECG
    o Aid in diagnosis of coexisting cardiac problems
  • Bloods
    o FBC – polycythemia or bleeding
    o U+E – electrolyte disturbance, diabetes, poor nutrition
  • Spirometry not recommended

Treatment
- Oxygen
- Short acting inhaled beta agonists +/-short
acting anticholinergics (i.e. salbutamol nebs + ipratropium nebs)
- Systemic corticosteroids

  • Antibiotics should be given to patients (if evidence of infection)
    o Febrile with elevated WCC and consolidation on CXR
    o Amoxicillin
    o Sputum culture not required unless not responding to tx
  • Aminophylline if not responding
  • Adjunct therapies
    o Fluid balance
    o Physiotherapy to clear sputum
    o Attention to medication particularly diuretics and anticoagulants
    o Treatment of comorbidities
    o Smoking cessation advice
    Consideration of DVT and PE risk, thromboprophylaxis measures.
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11
Q

Interstitial lung disease causes and exam

A

Known cause
- Occupational
o Asbestosis
o Silicosis
o Bird poo
o Coal
radiotherapy , fungal spores

  • Drugs
    o Methotrexate, amiodarone
  • Hypersensitivity
    o Extrinsic allergic alveolitis -> granuloma
  • Infections
    o TB  granuloma
    o Fungal

Associated with systemic disorders
- Sarcoidosis  granuloma
- Rheumatoid arthritis
- Connective tissue diseases e.g. SLE, Sjogren’s syndrome, systemic sclerosis
- Ulcerative colitis, renal tubular acidosis,
autoimmune thyroid disease

Idiopathic
- Idiopathic pulmonary fibrosis (most common cause of ILD)
- Cryptogenic organizing pneumonia
- Lymphocytic interstitial pneumonia

EXAM
General
Peripheries and Face
- Clubbing
- Cyanosis
Chest
- Velcro fine crackles, ↓02, ↑RR
- Signs of pulmonary hypertension
o Elevated JVP with large V wave
o Parasternal impulse (RV heave)
o Tricuspid regurgitation

Other
- Signs of systemic disease

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12
Q

Ix and treatment of Interstitial lung disease

A

INVESTIGATIONS
- Imaging
o CXR - may be normal, decreased lung volume, diffuse opacity

o High Resolution CT
 Localised or Diffuse e.g. honeycomb lung of IPF (sometimes seen on
CXR)
 Essential for diagnosis
 Pleural thickening e.g.
asbestosis

  • Spirometry
    o Usually reveal restrictive patterns (low FEV1, v low FVC, normal/high FEV1/FVC)
  • Bloods
    o FBC – high ESR/CRP, eosinophilia
    o Hypogammaglobulinemia
    o Raised LDH
    o Rheum serology – ANA, RF

o ABG – low Pa02 normal or high PaCO2. Wide Aa gradient

  • Bronchoalveolar lavage
    o Increased lymphocytes –> active inflammation thus more likely to respond to treatment and better prognosis e.g. drug induced, EAA, acute granulomatous disease
    o Polymorphonuclear cells (basophils, eosinophils, neutrophils) – more likely to not respond to treatment, poorer prognosis
  • Biopsy
    o Transbronchial
     Rule out infection
     Sarcoidosis
     Lymphangitic spread of
    carcinoma
    o Thorascopic
     For diagnosis of idiopathic
    ILD if clinical uncertainty
    and result could change management.

TREATMENT
Non-Pharmacological
- smoking cessation
- remove exposure
- pneumococcal and influenza vaccine
- home 02 for symptomatic relief of hypoxic patients
- pulmonary rehab

Pharmacological
- Treatment will not reverse established fibrosis
- If active inflammation, treatment may help.

Steroid (1mg/kg/day, reduced to half after 4-12 weeks) with follow up spirometry to document response. Consider maintenance steroids for patients who improved or stablised. NOT for idiopathic

  • Immunosuppressive agents for sarcoidosis, mesothelioma, secondary to inflammatory/rheumatoid condition
  • Unilateral lung transplantation considered in final stages esp. IPF.
  • Palliative care input
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13
Q

Lung cancer complications (local, metastatic) and exam

A

COMPLICATIONS

Local
- Recurrent laryngeal nerve palsy
- Phrenic nerve palsy
- SVC obstruction
- Horner’s Syndrome (Pancoast’s tumour)
- Rib erosion
- Pericarditis
- AF

Metastatic
- Brain
- Bone - >anaemia, high Ca
- Liver
- Adrenals -> Addison’s

Endocrine
- Ectopic hormone secretion
o SIADH and ACTH by small cell tumours (low Na, high ADH, cushingoid)
o PTH by squamous cell (high Ca)

Neurological
- Eaton-lambert syndrome (proximal myopathy and decreased reflexes),
confusion, fits, cerebellar syndrome, neuropathy, polymyositis

Other
- clubbing
- Hypertrophic Pulmonary OA
- Dermatomyositis
- Acanthosis nigricans
- Thrombophlebitis migrans

EXAMINATION
General
- Cachexia, pallor
- Fever
- Gynecomastia (any kind), cushingoid features (small cell)
- Hoarse voice

Peripheries and Face
- Clubbing (non-small cell)
- HPOA (hypertrophic pulmonary osteoarthropathy) causing wrist pain
- Supraclavicular/axillary nodes (non-small cell)
- Horner’s syndrome, SVC compression

Chest
- May be none
- Inspection - dilated veins (SVC obstruction)
- Palpation - Bony pain
- Auscultation/Percussion – Consolidation, collapse, pleural effusion

Neuro
- Confusion (cortical degeneration)
- Peripheral/autonomic neuropathy
- Eaton Lambert’s syndrome (small cell)

Skin
- DIC, migrating thrombophlebitis
- Acanthosis nigricans
- Purpura
- Scleroderma

Signs of Metastases
- Bone tenderness
- Hepatomegaly
- Focal neuro signs/confusion
- Cerebellar syndrome

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14
Q

Differential dx for lung nodule on CXR

A
  • Malignancy
  • Abscesses
  • Granuloma
  • Carcinoid tumour
  • Pulmonary hamartoma
  • AV malformation
  • Cyst
  • Foreign body
  • Skin tumour
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15
Q

IX for dx, staging, treatment of lung cancer,

A

INVESTIGATIONS for dx
- Cytology
o Sputum if central
o Pleural fluid if effusion (LIGHTs)

o CXR
 Peripheral nodule (adenocarcinoma)
 Hilar enlargement (small
cell)
 Consolidation, collapse,
pleural effusion
 Bony secondaries

  • Bronchoscopy
     Biopsy/fine needle Aspirate
     Assess operability
  • Percutaneous FNA or video-assisted thoracoscopy biopsy

INVESTIGATIONS FOR STAGING - TNM
o FBC, Ca, LFT’s
o ACTH, ADH, Na
o CT
o PET
- Bone scan if suspect metastases

INVESTIGATIONS FOR TREATMENT
- Lung function tests
o If FEV1 > 1.5L indicates that patient could tolerate a pneumonectomy
o Patient that can climb three flights of stairs
o ECOG status

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16
Q

Management of small cell and non-small cell

A

Non-small Cell

  • Excision if localized and no mets (1/3rd patients)
  • Curative radiotherapy if resp reserve poor
  • Chemo + radio for more advanced disease
    (Stage IV)

Small Cell
- Immunotherapy plus…
- Chemotherapy with platinum-based drugs
e.g. cisplatin but invariably relapse
- Prophylactic cranial irradiation in patients
with complete responses
- Palliation
o Radiotherapy for bronchial
obstruction, SVC obstruction, haemoptysis, bone pain and cerebral mets

o Endobronchial therapy e.g. tracheal stenting, cryotherapy, brachytherapy

o Pleural drainage for symptomatic pleural effusions

o Drugs like analgesia, steroids, antiemetics, cough suppressants, bronchodilators, antidepressants

17
Q

Differential dx for daytime sleepiness + risk factors

A

DIFFERENTIAL DIAGNOSIS OF DAYTIME SLEEPINESS
- Not enough sleep/poor sleep hygiene
- Poor adjustment to shift work
- Use of sedative/stimulant drugs
- Depression, with or without early morning
waking
- Idiopathic hypersomnolence (sleepiness despite plenty of sleep without snoring)
- Narcolepsy

MEDICAL CONDITIONS WHICH INCREASE RISK
- pregnancy
- heart failure
- renal disease
- lung disease (asthma, COPD, ILD etc)
- CVA
- acromegaly
- hypothyroidism
- PCOS
- T2DM
- Parkinson’s

18
Q

Exam for OSA - cessation of breathing >10s + complications of untreated OSA

A

General
- BMI
- Acromegaly (big hands feet face-pit tumour)

Peripheries and Face
- Blood pressure
- Fundi for signs of HTN
- Signs of hypothyroidism
- Head/neck/mouth for signs of uvular enlargement/macroglossia/tonsillar hypertrophy.
- Neck circumference

Chest
- Respiratory usually normal
- Look for signs of pulmonary hypertension
- Signs of cor pulmonale
o Cyanosis, tachycardia, raised JVP with prominent a and v waves, RV heave, loud P2, pansystolic murmur
(tricuspid regurgitation),
hepatomegaly, oedema.

Neurological
- Causes of obstructive sleep apnoea
o Myasthenia gravis
o Muscular dystrophy

  • Causes of central sleep apnoea
    o Autonomic neuropathy
    o Brain stem lesions
    o Spinal cord disease

COMPLICATIONS
Pulmonary hypertension -> right ventricular dysfunction –> cor pulmonale –>type two respiratory failure

Risk of MVAs

Neuropsychiatric dysfunction
Cardio morbidity
T2DM and NA-FattyLD
OSA is also an independent risk factor for HTN

19
Q

Ix, dx and treatment of OSA

A

INVESTIGATIONS
- Sleep study/polysomnography (measures oxygen sats, airflow at nose and mouth, ECG, chest wall movements) is diagnostic
- TFT’s (for hypothyroidism
- ECG to Assess RV dysfunction
- Epworth Sleepiness Scale

Dx
- > 5 apnoeic episodes per hour, over several hours, lasting > 10 seconds each
- Apnoea Hypopnoea Index (AHI) = number of episodes/number of hours slept
o Mild 5 – 15
o Moderate 16 – 30
o Severe > 30

TREATMENT
- Weight loss
- Avoid tranquilizers, sedatives
- Alcohol and smoking reduction
- Reverse underlying cause if possible- eg. Thyroid replacement, Surgical correction of upper airways
narrowing (polyps, macroglossia, tonsillectomy)

  • Vigorously treat concomitant diseases
    o Cardiac failure, hypertension, asthma
  • CPAP for moderate to severe OSA
    o Modafinil if residual sleepiness
  • BiPAP for central sleep apnoea (stroke)
20
Q

Sarcoidosis clinical presentation/ features (10)
Usually affects adults 20-40s, Northern
Europe, Blacks > whites. More frequently women.
Associated with HLA-DRB1 and DQD1 alleles

A

50% incidental Bilateral hilar lymphadenopathy on CXR
- acute presentation - E.nodosum, polyarthralgia, fever, & BHL – resolves
spontaneously

  • Pulmonary disease (90% have)
    o Bilateral hilar lymphadenopathy
    o Pulmonary infiltrates or fibrosis
    o Dry cough, progressive dyspnoea, reduced exercise tolerance, chest pain
    o 10-20% sx progress w subsequent deterioration in lung function.
  • Extra-pulmonary manifestations (~30%)
    o lymphadenopathy
    o Abdo: hepatomegaly, splenomegaly
    o Eye: uveitis, conjunctivitis,
    keratoconjunctivitis sicca, glaucoma
    o Enlarged lacrimal and parotid glands
    o Terminal phalangeal bone cysts
    o Skin: erythema nodosum (a), lupus pernio (c), subcutaneous nodules
    o Heart: cardiomyopathy, arrhythmias
    o hyperCa, renal stones
    o Neuro: Bell’s palsy, optic neuritis, meningitis, Brown sequard & spinal syndromes, space-occupying lesion
21
Q

Investigations for sarcoid
- staging on CXR (4)

A

Blood: Raised ESR, lymphopenia, raised LFT, raised serum ACE, raised Ca and Ig.
Urine: Raised Ca - macrophages make more vit D
Tuberculin skin test: Neg (60%)

CXR (stages)
- 1 – BHL
- 2 – BHL + peripheral pulmonary infiltrates
- 3 – peripheral pulmonary infiltrates alone
- 4 – Pulmonary fibrosis, bulla (honeycombing), pleural involvement

USS: may show nephrocalcinosis, or
hepatosplenomegaly

PulFT: N or reduced volumes, impaired gas transfer, restrictive pattern

Biopsy: non-caseating granulomata (diagnostic)

Bronchoalveolar lavage:
- Raised lymphocytes in active disease
- Neutrophils in pulmonary fibrosis
Bone x-rays: punched out lesions in terminal phalanges

CT/MRI: pulmonary disease severity or Dx neurosarcoidosis. Panda sign; enlarged parotids/lacrimal
glands. Lambda sign; R paratracheal + L hilar.

Ophthalmology assessment: if eye involvement

22
Q

Management + monitoring for sarcoidoidosis
PROGNOSIS
60% thoracic sarcoidosis resolve over 2yrs.
20% respond to steroid Tx; in the rest, improvement unlikely despite Tx

A

MANAGEMENT
BHL alone don’t need Tx – most recover

Acute sarcoidosis: bed rest & NSAIDs

Indications for steroids;
- Parenchymal lung disease (Sx, static,progressive)
- Uveitis
- Hypercalcaemia
- Neuro, renal or cardiac involvement

Prednisone 20-40mg OD for 4-6 weeks then decrease dose over 1yr according to clinical status.
(Higher doses may be warranted in very severe
cases.)
Topical steroids: skin manifestations.
Other:
- If severe illness, IV methylpred

23
Q

Differential dx for Bilateral hilar lymphadenopathy
granulomatous disease

A

*DDx for BHL
- sarcoidosis
- infection; TB, mycoplasma
- Malignancy: lymphoma, carcinoma, M/S
- Extrinsic allergic alveolitis
- Histiocytosis X

  • DDx granulomatous disease
  • Infections: TB, leprosy, syphilis, cat scratch fever,
  • Autoimmune: PBC, granulomatous orchitis
  • Vasculitis: GCA, polyarteritis nodosa, Takayasu’s arteritis
  • Organic: silicosis, berylliosis
  • Idiopathic: Crohn’s, Sarcoidosis, de Quervain’s
    thyroiditis
  • Other: EAA, Histiocytosis X
24
Q

Clinical manifestations of TB - what to look for - risk factors is renal disease, malignancy, HIV, T2DM, age extremes

A

Pulmonary:
silent or cough, sputum, malaise, weight loss, night
sweats, pleurisy, haemoptysis, pleural effusion, superimposed pulmonary infection

Milliary:
Haematogenous spread. Non-specific or
overwhelming signs. Nodular opacities on CXR.
Look for retinal TB.

Genitourinary:
Dysuria, freq, loin pain, haematuria, sterile pyruia

Bone:
Vertebral collapse and Pott’s vertebra

Skin (lupus vulgaris):
jelly-like nodules on face/neck

Meningitis:
Prodrome: fever, headache, V, abdo pain, drowsy,
meningism, delirium over 1-3wks. CND+S signs of CN palsies, papilloedmea
Dx by LP, TB PCR, look for immunosuppression elsewhere (i.e. HIV), MRI/CT. 30% mortality.

25
Q

Investigations for diagnosis of TB

A

Latent TB
- Mantoux test (skin test – positive = immunity and strong positive = infection),
then if strong positive do QuantiFERON Gold test

Active TB
- CXR - consolidation, cavitation, fibrosis,
calcification (upper > lower lobe).
- sputum sample – at least 3, send for microscopy, culture and staining for Acid Fast Baciliss. (may do bronchoscopy +lavage if can’t make sample .
- PCR – enables detecting of MultiDR TB

Active Non-respiratory TB
- Try get a sample of sputum, pleura & pleural
fluid, urine, ascites, peritoneum, BM, or even
CSF (culture for up to 12wks!)
- CXR – check for respiratory TB
- PCR – enables detecting of MDR TB
Histology: hallmark is caseating granulomata

26
Q

Treatment of pulmonary TB initial and continuation phase

A
  1. Start therapy without culture results if clinical picture strong - stress importance of compliance
  2. contact public health tracing

Initial phase
- 8wks on 4 drugs, once daily dose of;
o Rifampicin 600mg
o Isoniazid 300mg (+/- pyridoxine (reduce risk of peripheral neuropathy) if thin, DM, CKD, HIV, alcoholic)
o Pyrazinamide 2g (not in pregnancy, gout)
o Ethambutol 15mg/kg
- Directly Observed Therapy to help w compliance

Continuation Phase
16wks on 2 drugs;
o Rifampicin
o Isoniazid + Pyridoxine
- Get advice on resistance

27
Q

Cystic fibrosis - aetiology, presentation as baby and young adults

A

Aetiology
- autosomal recessive in caucasians.
- mutations to the CFTR gene for Cl- ion channels causing defective secretions throughout the body. (viscid intestinal secretions, loss of pancreatic exocrine function, abnormally thick mucus.

Neonates
- = failure to thrive, meconium ileus, rectal prolapse

Young adult
- Bronchiectasis, pneumothorax, haemoptysis, cor pulmonale,
- pancreatic insufficiency - dm/ steatorrhoea, intestinal obstructions, gall stones, cirrhosis
- Male infertility
- osteoporosis, arthritis, vasculitis, nasal polyps sinusitis, HPOA

28
Q

What are the exam findings and diagnostic tests for cystic fibrosis

A

Exam
-look for cyanosis, finger clubbing, bilateral coarse crackles, signs of HF, intestinal obstruction

Diagnostic tests
- -sweat test (sweat sodium and chloride measured)
– high levels of chloride is diagnostic)
-genetic testing – for known CF mutations
-faecal elastase = simple and useful test for exocrine pancreatic dysfunction

29
Q

Management for chest, gastro and other + monitoring tests for CF

A

Chest
-physiotherapy regularly,
antibiotics for acute infections and prophylactically,
- mucolytics, bronchodilators.
If advanced – oxygen at home, ventilation, lung transplantation
- diuretics for cor pulmonale

-ongoing tests:
-FBC, U+E, LFT
-sputum cultures
-CXR for signs of bronchiectasis
-aspergillus serology/skin test (20%
develop ABPA)

Gastro
- pancreatic enzyme replacement,
fat soluble vitamin supplements, liver transplant if severe cirrhosis
- monitor: -clotting (liver function),faecal fat analysis

-other – treat diabetes:
-annual glucose tolerance test
screen and treat for osteoporosis, fertility counselling

30
Q

What are the 4 classifications of pneumonia and likely organanisms

A

LASSIFICATIONS
1) Community-acquired pneumonia (CAP) – may be primary or secondary to lung disease.
- Strep pneumonia most common
cause, then haemophilus influenza. Viruses account for 15% (usually influenza).

2) Hospital-acquired (nosocomial) - >48 hours after admission to a hospital.
- Most commonly gram negative enterobacteria or staph aureus.

3) Aspiration pneumonia – those with stroke, myasthenia, bulbar palsies, reduced consciousness, oesophageal disease or poor dental hygiene
- pneumococcus, haemophilus influenzae, staph aureus and anaerobes

4) Immunocompromised patient – can be any bacteria, fungus or virus.
- Commonly pneumocystis jiroveci in HIV.

31
Q

Signs/ symptoms on exam for pneumonia

A

Obs :
Fever, cyanosis, confusion (very common in elderly), tachypnoea, tachycardia, hypotension,

Chest
consolidation (reduced expansion, dull percussion, increased tactile fremitus and vocal resonance, bronchial breathing) and a pleural rub/crackles

symptoms
-fever, rigors, cough +/- sputum, dyspnoea, haemoptysis, malaise, pleuritic pain

32
Q

What are the investigations and CURB score for pneumonia (what mean?)

A

CXR – look for lobar or multil obar/diffuse consolidation, effusions, cavitations, air bronchograms
Oxygen saturations and consider ABGs if severe
Bloods – FBC, U+Es, CRP, blood culture
Sputum – for microscopy and culture
Urine – for pneumococcal and legionella antigen
PCR sputum – for viruses
Pleural fluid – for culture if needed
Consider bronchoscopy and lavage if in ICU

CURB
SCORING (CURB 65)
1 point for each of:
-Confusion
-Urea (>7mmol/L)
-Respiratory rate (>30)
-BP (<90 systolic)
-Age (>65)
Results:
1.1 = home
2 = hospital treatment
3 or more = severe pneumonia with high mortality, send to ICU

33
Q

Management of pneumonia and difference in mild, moderate and severe CAP, vs HAP

A

-Oxygen – as required
-IV fluids
-Analgesia – if pleurisy (paracetamol)
-Repeat CXR if not improving
-Follow-up at 6 weeks with CXR looking for malignancy
- pneumococcal vaccine should be offered prophylactically
- ABX

Mild CAP - amoxicillin 500mg PO TDS
Moderate CAP - amox 1g IV Q8H + azithromycin 500mg PO daily
Severe CAP - augmentin 1.2g IV Q8H + azithromycin 500mg PO daily / erythromycin 500mg IV q6h

HAP: augmentin 1.2g IV Q8H
COmplex HAP: tazocin 4.5g IV Q8H

For all IV switch to orals in 48 hr

34
Q

What are the complications of pneumonia

A

-pleural effusion
-empyema
-lung abscess
-respiratory failure
-septicaemia
-pericarditis

35
Q

What do before TB treatment and Side effects of TB treatment

A

BEFORE treatment
- - test colour vision & VA before, during Tx
(ethambutol causes ocular toxicity)
- FBC, U&E, LFT
- Renal function – if CrCl 10-50;
o Rifampicin: decrease dose by 50%
o Ethambutol: monitor U&E
o Don’t change to others

SIDE EFFECTS
- renal, hepatic failure or pregnancy - seek help
1. Rifampicin: raised LFT (stop if bili rises), reduced plts, orange discolouration of urine/tears/contact lens, inactivation of COCP, flu Sx.
2. Isoniazid: raised LFT, reduced WCC, stop if
nephropathy.
3. Ethambutol: optic neuritis
4. Pyrazinamide: Hepaitis, arthralgia (CI: gout)