Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine Finals - Imperial & Quick Medical Revision > Respiratory AS > Flashcards

Respiratory AS Flashcards

1
Q

What are the stages of clubbing?

A

Important nail sign of systemic disease linked with underlying pulmonary, cardiovascular, neoplastic etc.

Described as bulbous uniform swelling of soft tissue of the terminal phalanx of digit between nail and nail bed.

  1. Periungual erythema and softening of the nail bed (Bogginess + fluctuance of nail bed).
  2. increase in angle between proximal nail fold and nail plate. (loss of concave nail fold angle
  3. increased longitudinal and transverse curvature
  4. soft tissue expansion at distal phalanx (drumstick)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of Clubbing?

A 
Respiratory 
- Carcinoma (Bronchial + Mesothelioma) 
- Chronic lung suppuration Empyema, abscess
Bronchiectasis, CF
- Fibrosis 
Idiopathic pulmonary fibrosis
TB

Cardiac

  • Infective endocarditis
  • Congenital cyanotic heart disease
  • Atrial myxoma

GIT

  • Cirrhosis
  • Crohns’ UC
  • Coeliac
  • Cancer: GI lymphoma
Other
- Familial 
- Thyroid acropachy 
- Upper limb AVMs or aneurysm
Unilateral clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is cyanosis?

A

Blue discolouration of mucosal membranes or skin

Deoxygenated Hb >5g/dl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Classification of cyanosis?

A

Peripheral: cold, blue nails
Central: blue tongue, lips

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of cyanosis? Pathophysiology

A

Think of O2 cascade - The OC is the process of diminishing or declining O2 tension from the atmospheric environment down to the cellular level, specifically the mitochondria.

As it moves down through the body to the cell, O2 will be diluted down, extracted or lost, so that at cellular level the PO2 may be 3 or 4 mm/Hg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of Cyanosis

A

Respiratory

  • Hypoventilation: COPD, MSK
  • Decreased diffusion: Pulmonary oedema, fibrosing alveolitis
  • V/Q mismatch: PE, AVM (HHT) - Some areas of the lungs receive perfusion but no oxygen, or some receive oxygen but no perfusion.
  • inadequate transport of oxygen by haemoglobin

Cardiac

  • Congenital: Transposition of great arteries, Tetralogy of Fallot
  • Decreased Cardiac Output: Mitral stenosis, Systolic LVF
  • Vascular: Raynaud’s, DVT

RBC
- Low affinity Hb, may be hereditary or acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is pneumonia?

A

Inflammation of the lungs with consolidation or interstitial lung infiltrates, categorised by causative organism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anatomical classification of pneumonia?

A

Bronchopneumonia
- Patchy consolidation of different lobes

Lobar Pneumonia

  • Fibrosuppurative consolidation of a single lobe
  • Congestion (vasculuar congestion + alveolar oedema) –> red (erythrocytes, neutrophils, desquamated epithelial cells)–> grey (fibrinopurulent exudate) –> resolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Aetiological classification - community acquired pneumonia? Organisms?

A
  • Pneumonia acquired outside hospital.
  • Group of signs + symptoms related to LRTI with fever >38, cough, expectoration, chest pain, dyspnoea, and signs of invasion of alveolar space.

Typical Bacteria

  • Streptococcus Pneumoniae (most common CAP).
  • Haemophilus influenza
  • Staphylococcus aureus
  • Moraxella Catarrhalis

Atypical bacteria

  • Mycoplasma pneumoniae
  • Chlamydophilia pneumoniae
  • Legionella pneumophilia
  • Chlamydia psittaci

Virus

  • Influenza A/B
  • RSV
  • Adeno/Rhin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aetiological classification - Hospital Acquired Pneumonia? Organisms?

A

HAP is an acute LRTI this is by definition acquired after at least 48hr of admission to hospital and is not incubated at time of admission.

Bacteria cause most HAP (mostly aerobic gram-negative bacilli)

  • Pseudomonas Aeruginosa
  • Escherichia coli
  • Klebsiella Pneumoniae
  • Acinetobacter
  • MRSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Aetiological classification - Aspiration Pneumonia?

A

= Results from inhalation of oropharyngeal content into lower airways that leads to bacterial infection. Commonly due to recent intubation on ITU.

  • Commonly due to altered swallow/gag. increased risk from patients with stroke, bulbar palsy, decreased GCS, GORD, Achalasia.
  • Aspiration causes an inflammatory reaction called pneumonitis, results in damage to lung parenchyma. Leads to inflammatory reaction and ultimately aspiration pneumonia.
  • Often Strep Pneumoniae, Staphylococcus aureus, Haemophilus influenza, Pseudomonas aeruginosa.
  • Used to be anaerobes (Bacteroides, Porphyromonas).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Immunocompromised Pneumonia?

A

Pneumocystis Jirovecii Pneumonia (PCP), Aspergillosis, TB, CMV/HSV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Symptoms of Pneumonia?

A
  • Fever, Rigors
  • Malaise, anorexia
  • Dyspnoea
  • Cough, purulent sputum, haemoptysis
  • Pleuritic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Signs of Pneumonia?

A
  • Increased RR
  • Increased HR
  • Cyanosis
  • Confusion
  • Consolidation (filled with liquid not air)
    Decreased expansion
    Dull Percussion
    Bronchial breathing
    Decreased air entry
    Crackles
    Pleural rub
    Increased vocal fremitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk factors of pneumonia?

A 
Age >65
COPD
Exposure to ciggy smoke
Alcohol abuse
HIV
use of steroids, antipsychotics, PPIs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigations for Pneumonia?

A

Bloods: FBC (WBC) , U+E (severity scoring),
LFT (risk factor for patients with cirrhosis, CLD),
CRP (raised) - normally lags in comparison to WCC in treatment of bacterial infection.
Culture (pre-treatment),
ABG (if SpO2 to indicate severity) low, glucose can be elevated.

Urine: Ag test (pneumococcal, legionella)
Sputum: MC+S
Imaging: CXR (infiltrates, cavities, effusion, consolidation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Special Tests of Pneumonia?

A 
Special test 
- Paired sera Abs for atypicals 
Mycoplasma, Chlamydia, 
Legionella 
- Serum Procalcitonin
- Immunofluorescence (PCP) 
- BAL 
- Pleural tap - pleural effusion
- Rapid antigen testing for virus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Assess severity of pneumonia?

A

Severity: CURB-65 (only if x-ray changes)

  • Confusion (AMT <8)
  • Urea >7
  • resp Rate >30/ mins
  • BP <90/60
  • > 65 yr old

Score of 0-1 –> home management
2 –>Hospitalisation
3-5 –> ICU admission 30 day mortality 15-30%.

CRP < 20 mg/L - do not routinely offer antibiotic therapy
CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
CRP > 100 mg/L - offer antibiotic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

General Management of pneumonia - Outpatient?

A
  • Consider limitations of severity score
    Ability to maintain oral intake, history of substance abuse, severe comorbid illness, cognitive impairment, impaired functional status, availability of outpatient support resources
  • Advise not to smoke, to rest, stay hydrated.
  • Advise them to report any chest pain, SOB or lethargy.
  • Reassess at 48hrs.
  • Repeat examination after 10-14 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

General Management of pneumonia - Inpatient?

A 
- If hospital admission needed
Abx 
O2: Pa02 >8, SpO2 94-98% 
Monitor Sats
Fluids
Analgesia
Chest Physio
Consider ITU if shock, hypercapnea, hypoxia

F/up @ 6 weeks with CXR to allow for radiological changes.

Do not routinely discharge if in the past 24hr they have 2 more more

  • Temp 37.5
  • RR 24
  • HR >100
  • SBP 90
  • O2 <90
  • Abnormal mental status

1 week - Fever should be gone
4 weeks - chest pain + sputum production should have substantially reduced
6 weeks - cough + breathlessness reduced
3 months - most symptoms resolved maybe some fatigue
6 months - most feeling normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Antibiotic management for outpatient pneumonia?

A

If CURB-65 = 0
Amoxicillin - 1g PO TDS OR doxycycline 100mg PO BDS OR clarithromycin 500mg PO BDS (where resistance)

If CURB-65 1 or 2 = Amoxicillin + clarithromycin OR doxycyclin 200mg on first day.

  • Consider influenza antiviral cover (Tamiflu)

If comorbidies (DM, chronic heart, liver, renal disease give co-amoxiclav + clarithyromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antibiotic management for inpatient pneumonia?

A
  • IV cefuroxime/ceftriaxone (1-2g IV every 8hr, every 24hr for ceftriaxone) + clarithromycin 500mg orally BDS.
  • Add fluclox if staph suspected.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Antibiotics for MRSA cover?

A

Vancomycin (15mg/kg IV every 12hrs) - consider teicoplanin.
Linezolid (600mg IV every 12hrs) (second line.

MRSA swabbing - nasal and skin lesion or wounds.

Suppression of MRSA once carrier found - mupirocin in white soft paraffin.
Chlorhexidine gluconate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Antibiotics for pseudomonas cover?

A

Tazocin 4.5mg IV every 6hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Atypical bacterial pneumonia management?

A

Generally speaking - Clarithromycin

Azithromycin 500mg orally, then 250mg OD for 4 days

  • For Psittacosis and Q fever (Coxiella burnetii) use doxycyline 100mg orally
  • Legionella/Chlamydia pneumonia - Azithromycin 500mg, levofloxacin 750mg OD, IV
  • PCP - Co-trimoxazole 80/400mg (trimethoprim + sulfamethoxazole)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hospital-acquired pneumonia management?

A

If within 5 days of admission. First line - Non severe = Co-amoxiclav 500/125mg 3x a day then review.
Then consider Doxycyline/Cefalexin.

If more than 5 days after admission. 
If septic/high risk of resistance 
- PipTaz
- Ceftriaxone 
- Meropenem

If patient has no risk factor for resistance pathogen - likely to be Strep Pneumonia, Haemophilis influenza, Staph A, E.coli, Klebsiella, Enterobacter, Proteus.
- Pseudomonas management = tazocin/ceftazidime.

Severe HAP - Likely to be Pseudomonas aeruginosa, K pneuonaemia (ESBL), Acinetobacter, MRSA, Legionella.
Need Ceftazidime, imipenem/meropenem, piptaz.
OR
Tazocin ± vanc ± gent for 7 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Antibiotic for gram negative HAPS (Pseudomonas, Klebsiella)

A 
Cephalosporin - ceftazidime
Carbapenam - meropenem/ imipenem/colastatin
Beta-lactamase inhibitor (pip-taz) 
Fluoroquinolone (cipro/levofloxacin) 
Gentamicin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Antibiotics with gram positive pathogen HAPS?

A

MRSA = Vancomycin or linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ESBL HAP?

A

Carbapenem

Then Fluoroquinolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pneumovax?

A

Vaccine for pneumococcus for hi-risk adults.

> 65 yrs old
Chronic renal, heart, kidney failure or conditions
DM
Immunosuppression: hyposplenism, chemo, HIV
CI: P, B, Fever

Revaccinate every 5yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Complications of Pneumonia - respiratory failure?

A

Respiratory Failure

  • Type 1: PaO2 <8kPa + PaCO2 <6kPa (acute hypoxic respiratory failure)
  • Type 2: PaO2 <8kPa + PaCO2 >6kPa (hypercapnic resp failure + hypoxia).

Type 1
- Severe hypoxaemia (fluid in alveoli, collapse of alveoli etc)

Type 2
- Hypercapnic (poor ventilatory muscle, obstruction of airways (COPD), secretion in small airways (Cystic fibrosis)

Management: oxygen, ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Other complications of pneumonia - Hypotension?

A

Hypotension - septic vasodilation + Dehydration
- Management
= if SBP <90 –> Fluid challenge 250ml over 15mins
If no improvement: central line + IV fluids
If refractory: ITU for inotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Other complications of pneumonia - AF?

A

Usually resolves with Rx

Management: digoxin or B-B for rate control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Other complications of pneumonia - pleural effusion?

A

Indicator of pneumonia severity.

  • Exudate
  • Mx: tap and send for MC+S, cytology and chemistry

Complicated pleural effusion - Should be treated, on its way to becoming an empyema. f

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Other complications of pneumonia - Empyema?

A
  • Pus in the pleural space
  • Associated with pneumonia.
  • Patients have signs of infection and a significant pleural effusion.
  • Anaerobes, Staph, Gm-ve
  • Assoc with recurrent aspiration
  • Pt with resolving pneumonia develops recurrent fever
  • Tap : turbid, pH <7.2, decreased glucose, increased LDH

Management: US guided chest drain must be inserted+ Abx.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Lung Abscess causes?

A

A circumscribed collection of pus in lung leading to cavity formation usually with an air-fluid level visible on chest x-ray.

  • Aspiration (altered consciousness + NG tubes)
  • Bronchial obstruction: tumour, foreign body
  • Septic emboli: sepsis, IVDU, RH endocarditis
  • Pulmonary infarction and secondary infection
  • Subphrenic/hepatic abscess
  • Complication of pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Features of a lung abscess?

A
  • Swinging fever (high grade)
  • Cough, foul purulent sputum (indicative of anaerobes)
  • haemoptysis
  • Murmur due to cardiac murmur (bacterial endocarditis)
  • Cavernous breath sounds
  • Malaise, weight loss
  • Pleuritic pain
  • Clubbing
  • Empyema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Tests for a lung abscess?

A
  • Blood: FBC (WBC), ESR, CRP, cultures
  • Sputum: micro, culture, cytology
  • CXR: cavity with fluid level, consolidation with central cavitation and air-fluid level.
  • Consider CT and bronchoscopy - usually a round cavity with irregular margins - no signs of compression of surrounding lung.
  • Bronchoscopy (proximal airway obstruction by tumour).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Management of lung abscess?

A
  • Abx according to sensitivies
    (ceftriaxone + clindamycin)
  • Aspiration + postural drainage.
  • Surgical excision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Other complications of pneumonia?

A
  • Sepsis
  • Pericarditis/myocarditis
  • Jaundice (usually cholestatic)
    due to sepsis, drugs (fluclox, augmentin), mycoplasma, legionella.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Sepsis criteria?

A

Updated version:
Low risk
- Normal RR (<21), BP (SBP >100), HR (<90), Urine output, temp, no non-blanching rash.

Moderate risk / (high risk)

  • Altered behaviour
  • Impaired immunity, trauma or surgery
  • RR 21-24 (high = >25)
  • SBP 91-100 (high = <90)
  • HR 91-130 (high = >130)
  • No urine passed in previous 12-18 hrs.
  • Signs of infection
  • Mottled appearance/ non-blanching rash

Outdated version >2 =

  • Temperature >38 or <36,
  • HR >90
  • RR >20, or PaCo2 <4.6
  • WCC: >12x10^9, <4 x10^9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Sepsis definition?

A

SIRS caused by infection (Systemic inflammatory response syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Severe sepsis definition

A

Sepsis with at least 1 organ dysfunction or hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Septic shock

A

Severe sepsis with refractory hypotension

  • (persistent hypotension requiring vasopressors to maintain MAP >65
  • Serum lactate level >2mmol despite adequate volume resuscitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Specific pneumonia - pneumococcus - gram positive diplococcus

A

RF: Elderly, EToH, immunosuppresed, CHF, pulmonary disease.

Rapid onset, high fever, pleuritic chest pain, herpes labialis.

Pulmonary features: Lobar consolidation.

Extrapulmonary: Herpes labialis. Causes reactivation of herpes simplex virus resulting in cold sores.

Management - Amoxicillin, BenPen, cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Specific pneumonia

- S.aureus?

A

RF: Influenza infection, IVDU, Co-morbidities.

Commonly occurs after patients have had an influenza virus.

Pulmonary features - Bilateral cavitating bronchopneumonia

Management: Fluclox or Vanc alongside amoxicillin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Specific pneumonia

- Klebsiella?

A

RF: Rare, elderly, ETOH, DM

Pulmonary features: cavitating pneumonia, especially upper lobes. Red-currant jelly sputum. May also cause an empyema

Management: Cefotaxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Specific pneumonia

- Pseudomonas?

A

RF: Bronchiectasis, CF

Management: Taz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Specific pneumonia

- Mycoplasma

A

RF: epidemics

Prolonged onset.

Pulmonary features: Dry cough, reticulo-nodular shadowing or patchy consolidation

Extra-pulmonary

  • Flu-like prodrome: headache/myalgia/arthralgia
  • Known to cause immune-mediated neurological disease. May also cause paraesthesia or neuropathic pain.
  • Haemolysis

Presents with erythema multiforme.

Cold agglutinins --> AIHA (Autoimmune haemolytic anaemia) 
Cryoglobulin
Erythema multiforme
SJS
GBS
Hepatitis

Diagnosis: Serology. X-ray shows bilateral consolidation on x-ray.

Typically does not respomd to penicillin or cephalosporin.

Treatment: Doxy/Clarithro/Cipro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Specific pneumonia

- Legionella?

A

RF: Travel, Air conditioning

Pulmonary Features: Dry Cough/Dyspnoea, bi-basal consolidation

Extra-pulmonary: flu-like prodrome, anorexia, D+V, hepatitis, renal failure, confusion, SIADH –> Decreased Na.

Management: lymphopenia, decreased Na, deranged LFTs.

Dx: urinary ag or serology

Clarithro ± rifampacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Specific pneumonia

- Chlamydia pneumoniae?

A

Pulmonary Features: Pharyngitis, otitis –> pneumonia

Extrapulmonary: Sinus pain

Management: diagnosis with serology, then clarithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Specific pneumonia

- Chlamydia psittica?

A

RF: Parrots

Pulmonary features: Dry cough, patchy consolidation

Extra-pulmonary: Horder’s spots ~ rose spots. Splenomegaly, epistaxis, hepatitis, nephritis, meningo-encephalitis.

Dx: serology then clarithro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Specific pneumonia

- PCP?

A
  • Immunocompromised/HIV
  • Pulmonary Features
    Dry Cough, exertional dyspnoea, bilateral creps
  • CXR: normal or bilateral perihilar interstitial shadowing

Dx: Diagnosed from induced sputum - Visualisation from BAL, Sputus, biopsy

High dose co-trimoxazole or pentamidine

Prophylaxis if CD4 <200 or after 1st attack.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is bronchiectasis?

A
  • Permanent dilation of Bronchi due to destruction of the elastic and muscular components of the bronchial wall. Often causes as a consequence of recurrent and/or severe infections secondary to underlying disorder.
  • Majority of patients will present with a chronic cough and sputum production.
  • Retained inflammatory secretions and microbes –> airway damage + recurrent infection
  • Because of H.influenza, pneumococcus, s.aureus, pseudomonas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Cause of bronchietasis

A
  • Idiopathic in 50%
  • Congenital
    CF (mainly upper lobe infiltration)

Kartagener’s/PCD
Young’s syndrome (azoospermia + bronchiectasis). May also have dextrocardia. May also have recurrent sinusitis.

  • Post-infectious
    Measles, pertussis, pneumonia, TB, bronchiolitis
- Immunodeficiency
Hypogammaglobulinaemia 
X-linked agammaglobulinaemia: Bruton's 
CVID
IgG subclass deficiency
IgA 
HIV
  • Allergic bronchopulmonary aspergillosis
  • Bronchial obstruction:
    LNs, tumour, foreign body
  • Connective Tissue Disorders
    RA
    Sjogren’s
  • IBD
    UC, Crohns
- Yellow nail syndrome 
Yellow nail discoloration and dystrophy
Lymphoedema
Pleural effusion
Bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Symptoms of bronchiectasis?

A

Presence of RF: cystic fibrosis, immunodeficiency, previous infection, PCD, alpha-1 antitrypsin, IBD.

  • Persistent cough with purulent sputum
  • Haemoptysis
  • Fever
  • Weight loss
  • Dyspnoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Signs of bronchiectasis?

A
  • Clubbing
  • Coarse inspiratory crepitation/crackles - squeaks and pops
  • Crackles
  • Wheeze
  • Purulent sputum
  • Cause
    Situs Inversus (+PCD = Kartagener’s syndrome)
    Splenomegaly: immune deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Complications of bronchiectasis?

A
  • Pneumonia
  • Pleural effusion
  • Pneumothorax
  • Pulmonary HTN
  • Massive haemoptysis
  • Cerebral abscess
  • Amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Investigations for bronchiectasis?

A
  • Sputum MCS (gram-positive/gram-negative)
  • Bloods:
    FBC: WBC (eosinophil high = bronchopulmonary aspergillosis, neutrophilia may be infection)
    NNO level in primary ciliary dyskinesia
    Aspergillus precipitins,
    RF,
    a1-AT level
    Test Ig response to pneumococcal vaccine
  • Sweat chloride test (abnormal test >60mmol/L CF is likely) ± CFTR protein gene mutation.
  • CXR: thickened bronchial walls (tramlines and rings)
  • Spirometry:

obstructive pattern (reduced FEV1, elevated RV/TLC) (obstructive = COPD, Asthma, Emphysema, bronchiectasis)

= Restrictive (FEV1 reduced, FVC reduced (FEV1/FVC ratio normal (>0.7). due to pulmonary fibrosis, pulmonary oedema, lobectomy, parenchymal lung tumours, guillian barre, myasthenia gravis, motor neuron disease, ARDS, Sarcoidosis)

  • HRCT chest CT (High resolution) - thickened, dilated airways with/without air fluid levels. Cysts and/or tree-in-bud pattern.
  • Bronchoscopy + mucosal biopsy:
    Focal obstruction
    PCD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Management of bronchiectasis?

A
  • Chest physio: Expectoration, draining, pulmonary rehab (postural drainage, percussion, vibration).
  • ABx for exacerbations: e.g cipro for 7-10days - Consider azithromycin for pseudomonas
  • Bronchodilators: nebulised salbutamol/ipratroprium/tiotropium
  • Inhaled hypertonic saline
  • Treat underlying cause
    CF: DNAase
    ABPA: Steroids ±azole antifungal
    Immune deficiency; IVIg
    or Inhaled tobramycin/gentamicin - infected with pseudomonas.
  • Consider surgery for those with recurrent infections, severe haemoptysis or focal disease.
    This can be resection of bronchiectatic area. or lung transplant in patients with FEV <30% or a rapid decline in FEV.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the pathogenesis of cystic fibrosis?

A
  • Autosomal recessive
  • Mutation of CFTR gene on Chr 7 (delta F508) (anion channel found in the apical membrane of epithelial cells)
  • decrease luminal CL secretion and increase Na reabsorption –> Viscous secretions
  • In sweat glands, decreased Cl and Na reabsorption –> salty sweat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Clinical features of cystic fibrosis in neonates?

A
  • FTT (failure to thrive)
  • Meconium ileus
  • Rectal prolapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Clinical features of cystic fibrosis in children/young adults - NOSE?

A
  • Nose: nasal polyps, sinusitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Clinical features of cystic fibrosis in children/young adults - Resp?

A
  • Resp: cough (prolonged colds, coughing) , wheeze, recurrent infection, bronchiectasis, haemoptysis, pneumothorax, cor pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Clinical features of cystic fibrosis in children/young adults - GI + other?

A

GI

  • Pancreatic insufficiency: DM, steatorrhoea, voracious appetite
  • Distal intestinal obstruction syndrome
  • Gallstones
  • Cirrhosis (secondary to biliary obstruction)/ Splenomegaly

Other

  • Male infertility, osteoporosis, vasculitis
  • CLUBBING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Signs of Cystic fibrosis?

A
  • Clubbing ± HPOA (hypertropic osteoarthropathy)
  • Cyanosis
  • Bilateral coarse crackles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Common respiratory organism in Cystic Fibrosis?

A
  • Early
    S.aureus
    H.influenza

Late

  • P.aeruginosa: 85%
  • B.cepacia: 4%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Diagnosis of cystic fibrosis?

A
  • Sweat test: Na and Cl >60mM
  • Genetic screening for common mutations
  • Faecal elastase (tests pancreatic exocrine function)
  • Immunoreactive trypsinogen (neonatal screening)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Investigations of cystic fibrosis.

A
  • Bloods: FBC, LFTs, Clotting, ADEK levels, glucose TT
  • Sputum MCS
  • CXR: bronchiectasis
  • Abdo US: fatty liver, cirrhosis, pancreatitis
  • Spirometry: obstructive defect
  • Aspergillus serology/skin-test (20% develop ABPA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Management of Cystic Fibrosis - General?

A
  • MDT: Physician, GP, Physio, dietician, specialist nurse
  • Neonate management?
    lactulose to avoid obstruction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Chest management for cystic fibrosis?

A
  • Physio: postural drainage, forced expiratory techniques
  • Abx: acute infections and prophylaxis (inhaled tobramycin or IV tobramycin/piptaz/ceftazatidime).
  • Mucolytics: DNAse (dornase alfa + hypertonic saline inhaled.
  • Bronchodilators (salbutamol in inhaler)
  • Vaccinate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

GI management for cystic fibrosis?

A
  • Pancreatic enzyme replacement: pancreatin (Creon)
  • ADEK supplements
    Insulin
  • Urosdeoxycholic acid for impaired hepatic function (stimulates bile secretion) Oral bile acids.
  • PPI or Antacid to produce more alkaline environent for pancreatic enzyme supplement.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Management of advanced lung disease in cystic fibrosis?

A
  • O2
  • Diuretics for cor pulmonale
  • NIV
  • Heart/lung transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Other management requirements for cystic fibrosis?

A
  • Management of complications: e.g DM
  • Fertility and genetic counselling
  • DEXA osteoporosis screen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the pulmonary aspergillus diseases?

A
  1. Asthma: T1HS reaction to spores
  2. ABPA
    Hypersenstivity reaction to aspergillus antigens. Typically seen in patients with longstanding asthma
  3. Aspergilloma (mycetoma
    Intracavity mass in the lung consistent of massos of aspergillus mycelia.
  4. Invasive aspergillosis
    Local and systemic infiltration (in immunocompromised patients)
  5. Extrinsic Allergic Alveolitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is Allergic Bronchopulmonary aspergillosis?

A

T1 and T3 HS reaction to Aspergillus fumigatus

  • Bronchoconstricton –> Bronchiectasis
  • Patients usually have a prior diagnosis of atopy, asthma or cystic fibrosis.
  • Presents with broncial obstruction, airway inflammation leading to bronchiectasis, fibrosis and respiratory compromise.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Symptoms of ABPA?

A
  • Wheeze (underlying asthma and bronchial hyperreactivity)
  • Productive cough
  • Dyspnoea
  • Mucus plugs

RF: History of Asthma/CF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Investigations for ABPA?

A
  • CXR: bronchiectasis (upper and middle lobe infiltrates)
  • Aspergillus in sputum (black on silver stain)
  • Aspergillus skin test of IgE RAST (positive wheal and flare reaction)
  • Increased IgE and increased eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Management of ABPA?

A
  • Pred 40mg/d + itraconazole for acute attacks (200mg)
  • Environmental control
  • Pred maintenance 5-10 mg/d
  • Bronchodilators for asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is an aspergilloma (mycetoma)

A
  • Fungus ball within a pre-existing cavity (TB or sarcoid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Features of aspergilloma?

A

Usually asymptomatic
Can –> Haemoptysis (may be severe)
Lethargy, decreased weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Investigations for aspergilloma?

A
  • CXR: round opacity within a cavity, usually apical
  • Sputum culture
  • Aspergillus skin test/RAST
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Management of aspergilloma?

A

Consider exicision for solitary lesions/severe haemoptysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is invasive aspergillosis?

A

Causes by filamentous fungi of the Aspergillus species.

Aflatoxins –> Liver cirrhosis and HCC (especially A.flavus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the risk factors for Invasive Aspergillosis?

A

Immunocompromise: HIV, leukaemia, Wegener’s

post-broad spectrum abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Investigations of invasive aspergillosis?

A
  • CXR: consolidation, abscess, cavities
  • Sputum MCS - Aspergillus species
  • BAL - show hypal elements or aspergillus
  • Serial galactomannan (two positive results)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Management of Aspergillosis?

A

Voriconazole for confirmed or amphotericin B for suspected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is Extrinsic Allergic Alveolitis?

A

= Inflammation of alveoli and sital bronchiales caused by immune response to inhaled allergens.

  • Occupational exposure to organic dust.
  • Sensitivity to aspergillus clavatus –> Malt worker’s lung
  • Bird fancier’s lung
  • Famer’s lung: Saccharopolyspora rectivirgula
  • Mushroom workers: thermophilic actinomycetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Key points in a history for EAA? (as part of a hypersensitivty pneumonitis)

A
  • Exposure to avian protein antigen
  • Mould in work environment
  • Occupational exposure to chemicals
  • Productive/non-productive cough.
  • Fevers, malaise, weight loss, diffuse rales, clubbing.
  • Restrictive picture
  • Chest x-ray: upper/mid-zone fibrosis
  • Bronchoalveolar lavage: lymphocytosos
  • NO eosinophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

EAA management?

A

Corticosteroid taper + avoidance of antigen.

First line is avoidance, then corticosteroid avoidance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Types of Lung Cancer?

A 
Non-small cell 
- Squamous Cell Carcinoma (PTH - hypercalcaemia ,clubbing HPOA, hyperthyroidism. 
- Adenocarcinoma 
Gynaecomastia, HPOA. 
- Large cell carcinoma

Small cell Carcinoma (rapid presentation)
- ADH, ACTH, Lambert Eaton Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Epidemiology and behaviour of sqaumous cell carcinoma

A

35% of all LC.
M>F
Smoking + Radon Gas

Pathology
- Centrally located with evidence of squamous differentiation (keratinisatioN).

Behaviour

  • Locally invasive + metastasis late (via LN)
  • Release PTHrP –> increased Ca2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Epidemiology and behaviour of adenocarcinoma?

A

25% of all LC
Females, non-smokers, far east.

Peripherally located
- Histo shows glandular differentiation (gland formation + mucin production).

  • common extrathoracic mets and early.
  • 80% presents with mets.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Epidemiology and behaviour of large cell carcinoma

A

10% - Peripheral or central

Large, poorly differentiated cells with a poor prognosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Epidemiology and behaviour of small cell carcinoma?

A

Central location near the bronchi

  • Histo: poorly differentiated cells.
  • 80% present with advanced disease. Very chemosensitive but v.poor prognosis. Ectopic hormone secretion.
  • Rapid presentation + have paraneoplastic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What other lung tumours do you know?

A
  • Adenoma: 90% are carcinoid tumours
  • Hamartoma
  • Mesothelioma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the epidemiology of all lung cancers?

A

19% of all cancers

27% of all cancer deaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What are the symptoms of lung cancer?

A
  • cough and haemoptysis. New or persistent cough in a current or former smoker.
  • dyspnoea - Dyspnoea because of underlying COPD, pneumonia, or airway obstruction.
  • Chest pain - Most patients with chest pain have tumours invading the pleura or chest wall.
  • Recurrent or slow resolving pneumonia
  • Anorexia and weight loss
  • hoarseness due to recurrent laryngeal nerve palsy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Signs in the chest of lung malignancy?

A
  • Consolidation
  • Collapse
  • Pleural effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

General signs of lung malignancy?

A
  • Cachexia
  • Anaemia
  • Clubbing and HPOA (painful wrist swelling) more common in adenocarcinoma
  • Supraclavicular and/or axillary LNs (Horner’s syndrome presenting with ptosis, miosis, ipsilateral anhydrosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Signs of metastasis

A
  • Bone tenderness
  • Hepatomegaly
  • Confusion, fits, focal neuro
  • Addison’s
  • Cannon-ball mets = most commonly caused by renal cell cancer - CT abdomen is most appropriate to investigate this.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Complications of lung cancer - local?

A
  • Recurrent laryngeal nerve palsy
  • Phrenic nerve palsy
  • SVC obstruction
  • Horner’s (Pancoast tumour) common in NSCLC
  • AF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Paraneoplastic complications of lung cancer endo?

A

Endocrinology - Mostly found on SCLC

  • ADH –> SIADH (euvolaemic decreased in Na) due to small cell lung cancer.
  • ACTH - Cushing’s syndrome
  • Serotonin –> Carcinoid (flushing, diarrhoea)
  • PTHrP –> primary HPT (increased Ca, bone pain) Mainly in squamous cell carcinoma.

Lambert-Eaton syndrome in SCLC - autoimmune attack on VGCC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Paraneoplastic complications of lung cancer rheum?

A

Dermatomyositis/polymyositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Paraneoplastic complications of lung cancer Neuro?

A
  • Cerebellar degenerations (due to Purkinje cells

- Peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Paraneoplastic complications of lung cancer dermatology?

A
  • Acanthosis nigricans (hyperpigmented body folds)
  • Trousseau syndrome: thrombophlebitis migrans (pancreas and lung). vessel inflammation due to blood clots in different part of the body. May present with visually swollen vessels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Metastatic complications of lung cancer?

A
  • Pathological features
  • Hepatic failure
  • Confusion, fits, focal neurology
  • Addison’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Investigations for Lung cancer - blood and sputum?

A

Bloods: FBC (anaemia) , U+E (SIADH + hyponatraemia) , Ca2+ (squamous cell carcinoma), LFTs (metastases)

Cytology: Sputum (malignant cells in sputum), pleural fluid (patients that present a pleural effusion so would want to sample to look for malignant cells)

Lung function tests
- Assess treatment fitness?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Imaging for lung cancer?

A

Offer urgent X-ray (2 weeks) to assess for lung cancer in people 40 or over with 2 or more unexplained symptoms (cough, fatigue, SOB, chest pain, weight loss, appetite loss).

CXR

  • coin lesions
  • Hilar enlargement
  • Consolidation, collapse
  • effusion
  • bony secondaries
  • Contrast-enhanced volumetric CT (neck, thorax + upper abdo)
    Useful for staging, shows location + extent of primary tumour and evaluates hilar/mediastinal lymphadenopathy + distant mets.

Consider

  • PET-CT: Exclude distant mets
  • Radionucleotide bone scan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Types of biopsy for lung cancer?

A
  • Percutaneous FNA: peripheral lesions and LN
  • Bronchoscopy: biopsy and assess operability
  • Endoscopic bronchial US biopsy: mediastinal LNs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are the differentials for a CXR coin lesion?

A

FANGS

  • Foreign body
  • Abscess: Staph, TB, Klebsiella, Mycetoma
  • Neoplasia (primary or secondary)
  • Granuloma: RA, Wegener’s, TB, Sarcoid
  • Structural, AVM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the staging for a non-small cell lung carcinoma?

A

TNM staging

  • Tx = Malignancy cells in bronchial secretions
  • Tis = CIS (carcinoma in situa)
  • T0 = None evidence
  • T1 = <3cm in lobar or more distal airways
  • T2 = >=3cm and >2cm from carina or pleural involvement
  • T3 = <2cm from carina or involves chest wall, diaphragm or >1 tumour in same lobe of lung
  • T4 = Involves mediastinum or malignant effusion in present, or more than 1 lobe.
N0 = none involved
N1 = Peribronchial or ipsilateral hilum 
N2 = Ipsilateral mediastinum
N3 = contralateral hilum or mediastinum or supraclavicular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

General management of lung cancer?

A

Refer using suspected 2ww

  • If they have chest x-ray finding suggesting lung cancer
  • Age 40 and over with unexplained haemoptysis.

MDT: Respiratory physician, oncologist, radiology, histopathologist, specialist nurse, palliative care, GP.

Assess risk of operative mortality: Thoracoscore + cardioresp function + comorbidities

Advise smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

NSCLC management?

A

Contra-indications to surgery

  • Stage IIIb or IV (mets)
  • FEV1 <1.5 litres considered general cut-off
  • Malignant pleural effusion
  • Tumour near hilum
  • Vocal cord paralysis
  • SVC obstruction

Surgical resection
- Management of choice for peripheral lesions with no metastatic spread = Stage I/II (~25%)
- Requires good cardiorespiratory function
- Wedge resection, lobectomy or pneumonectomy
± adjuvant chemo (cisplatin-based) preoperatively for stage II) and post-operatively for Stage 1B and 11.

If not suitable use radiotherapy - if cardioresp reserve is poor.

Chemo±radi for more advanced disease

  • Platinum-based regimes
  • If N2 or less consider surgery.

For palliative: Consider MAbs targeting EGFR (cetuximab) or nintedanib (TKI), bevacizumab, ramucirumab (VEGFR) , pembrolizumab (programmed death-1 receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Management of SCLC?

A
  • Typically disseminated @ presentation

- May respond to chemo but invariably relapses therefore use cisplatin + radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Management of palliation in SCLC?

A
  • Radiotherapy: bronchial obstruction, haemoptysis, bone or CNS mets
  • SVC obstruction: stenting + Radio + dexamethasone
  • Endobronchial therapy: -Stenting, brachytherapy (radioactive material inside body)
  • Pleural drainage
  • Analgesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Prognosis of Lung malignancy?

A

SCLC 5 yr = 12% to 24%

NSCLC 5 yr = Stage 1 = 67%, Stage 3 = 23/25%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the pathogenesis of ARDS?

A
  • May result from direct pulmonary insult or be secondary to sever systemic illness.
  • Non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness
  • Inflammatory mediators –> increased capillary permeability and non-cardiogenic pulmonary oedema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Clinical features of ARDS?

A 
Tachypnoea
Cyanosis
Bilateral fine creps
SIRS/Sepsis
Fever/cough/pleuritic chest pain

Rx: sepsis, aspiration, severe trauma etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Investigations for ARDS?

A

Bloods: ABG (low partial oxygen pressure PaO2/FiO2 inspired oxygen ratio of <300 on PEEP), sputum culture (sepsis), blood culture for sepsis, amylase/lipase for pancreatitis

CXR: Bilateral opacities not explained by effusion or collapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Diagnosis of ARDS?

A
  • Acute onset
  • CXR shows bilateral opacities/infiltrates
  • No evidence of CCF
  • PaO2:FiO2 200 -300 = Mild
    100-200 = Moderate
    <100 = Severe

CLinical indicated of hypoxaemia as it is comparing inspired oxygen to arterial oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Management of ARDS?

A
  • Admit to ITU for organ support and manage underlying cause

Ventilation
- Indications
PaO2 <8kPa (normal is >10.6) despite 60% FiO2
- PaCO2 >6KPa

Method

  • 4-8ml/kg + PEEP (e.g 10cm H20)
  • SE = VILI (ventilator induced lung injury), VAP (pneumonia), Weaning difficulty

Circulation

  • Invasive BP monitoring
  • Maintain CO and DO2 with inotropes. Keep CVP <4cm H20.
  • Dobutamine

Sepsis = Abs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Causes of ARDS?

A

Pulmonary (alveolar damage + diffuse oedema)

  • Pneumonia
  • Aspiration
  • Inhalation injury
  • Contusion

Systemic

  • Shock
  • Sepsis
  • trauma
  • Haemorrhage
  • Pancreatitis
  • Acute liver failure
  • DIC
  • Obs: Eclampsia, amniotic embolism
  • Drugs: aspirin or heroin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is a differential diagnosis of pulmonary effusion?

A
  • Transudate = Forced through by hydrostatic pressure therefore low protein. Therefore ratio is high (SAAG = >1.2)
  • Exudate = Through inflammation therefore high protein. Therefore ratio is low as normal to blood (SAAG <1.2).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Causes of Transudates?

A

Increased capillary hydrostatic pressure

  • CCF
  • Iatrogenic fluid overload
  • Renal failure
  • Relative high in negative pressure pulmonary oedema

Decreased capillary oncotic pressure (opposite effect to hydrostatic, due to low protein levels)

  • Liver failure
  • Nephrotic syndrome
  • Malnutrition, malabsorption, protein-losing enteropathy

Increased interstitial pressure
- Decreased lymphatic drainage: e.d Ca

Exudates
- ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Define Type 1 Respiratory failure?

A
  • PaO2 <8kPa and PaCo2 <6KPa (due to hypoxaemia)

V/Q mismatch and diffusion failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Define Type 2 Respiratory Failure?

A
  • PaO2 <8kPa and PaCO2 >6KPa

- Alveolar hypoventilation ± V/Q mismatch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Causes of a V/Q mismatch and diffusion failure?

A

Either no oxygen or no blood to carry oxygen. Increased Alveolar-arterial gradient.

- Vascular due to 
PE (ventilation good but perfusion bad) 
PHT
Pulmonary Shunt (R--> L)  (perfusion problem) 
- Early Asthma
- Pneumothorax
- Atelectasis
Diffusion failure 
- Fluid 
Pulmomnary oedema
Pneumonia
Infarction
Blood

Fibrosis (both fluid and fibrosis can also cause alveolar hypoventilation and V/Q mismatch due to decreased compliance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Causes of alveolar hypoventilation therefore limit exchange of CO2 with atmosphere.

A

Obstructive

  • COPD
  • Asthma
  • Bronchiectasis
  • Bronchiolitis
  • Intra and Extra-thoracic (Ca, LN, epiglottitis)

Restrictive

  • Decreased drive: CNS sedation, trauma, tumour
  • NM disease: cervical cord lesion, polio, GBS, MG
  • Chest: kyphoscoliosis, obesity
  • Fluid and fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Clinical features of hypoxia?

A

Acute

  • Dyspnoea
  • Tachypnoea
  • Stridor
  • Cyanosis
  • Confusion
  • Agitation

Chronic

  • Polycythaemia
  • PHT
  • cor pulmonale (increase in HR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Clinical features of hypercapnoea?

A
  • Headache
  • Flushing and peripheral vasodilatation
  • Bounding pulse
  • Flap
  • Confusion –> Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Management of Type 1?

A

Give O2 and maintain SpO2 94-98%

Assisted ventilation if PaO2 <8Kpa despite 60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Management of Type 2?

A

Controlled O2 therapy @24% oxygen aiming for SpO2 88-92%.
Check ABG after 20 mins
- If PaCO2 steady or lower can increased FiO2 if necessary
- If PaCO2 increased >1.5KPa and patient still hypoxic, consider NIV or respiratory stimulant.
- BiPAP can be helpful in hypercapnic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Principles of oxygen therapy?

A
  • Critically ill patients should receive high conc O2 immediately.
  • O2 should be prescribed to achieve target SpO2.
    94-98% for most patients
    88-92% for those at risk of hypercapnic resp failure
  • In patients at risk of hypercapnic resp failure
  • Start O2 therapy at 25% and do an ABG
  • Blue Venturi @2-4L
    Clinically: decreased RR with O2 may be useful sign
    If PCO2 <6: increased target SpO2 to 94-98%
    If PCO2 >6kPa: maintain target SpO2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Mechanisms of Oxygen Therapy?

A
  • Nasal Prongs: 1-4L/min = 24-40%
  • Simple Face mask
  • Non-rebreathing mask: reservoir bag allows delivery of high conc of O2.
    60-90% at 10-15L.
  • Venturi Mask
  • Provides precise O2 concentration at high flow rates:
    Yellow: 5%
    White: 8%
    Blue: 24%
    Red: 40%
    Green: 60%
136
Q

Definition of chronic asthma?

A

Episodic, reversible airway obstruction due to bronchial hyper-reactivity to a variety of stimuli.

137
Q

Pathophysiology of asthma?

A

Acute

  • Mast cell-Ag interaction –> histamine release
  • Bronchoconstriction, mucus plugs, mucosal swelling

Chroni

  • Th2 cells release IL3,4,5 –> mast cell ,eosinophil and B cell recruitment
  • Airway remodelling.
138
Q

Triggers of chronic asthma?

A
  • T1 hypersenstivity to variety of antigens
  • Dust mites, pollen, food, animals, fungus.

Stress

  • Cold air
  • Viral URTI
  • Exercise
  • Emotions

Toxins

  • Smoking, pollution
  • Drugs; NSAIDs, B-B.
139
Q

Symptoms of asthma?

A
  • Cough (often at night - Dry night-time cough.
  • Tachypnoea
  • Wheeze (polyphonic wheeze) - Localised wheeze suggests inhaled foreign body.
  • Dyspnoea
  • Diurnal variation with morning - dipping

Features considers for asthma

  • recurrent episodes of symptoms: may be triggered by viral infection, allergen exposure, NSAIDs/beta-blockers and/or exacerbated by exercise, cold air and emotion/laughter in children
  • recorded observation of
    wheeze: due to varying use of language this usually means wheeze documented by a clinician
  • symptom variability: asthma is generally worse at night or early in the morning
    personal history of atopy: e.g. eczema/allergic rhinitis
  • absence of symptoms of alternative diagnosis: e.g. COPD, dysfunctional breathing or obesity*
  • historical record of variable peak flows or FEV1
140
Q

History of asthma?

A
  • Precipitants
  • Diurnal variation
  • Exercise tolerance
  • Life effects: sleep, work
  • Other atopy: hay fever, eczema
  • Home + job environment
141
Q

Signs of asthma?

A
  • Tachypnoea, tachycardia
  • Widespread polyphonic wheeze
  • Hyperinflated chest
  • Decreased air entry
  • Signs of steroid use
142
Q

Associated disease with asthma?

A
  • GORD
  • Churg-Strauss
  • ABPA
143
Q

Differentials for Asthma?

A
  • Pulmonary oedema (cardiac asthma)

- COPD

144
Q

Investigations for asthma?

A

Bloods: Fbc (eosinophilia), increased IgE, aspergillus serology

CXR: hyperinflation

A negative result on spirometry does not exclude asthma as a diagnosis.

  • FeNO: >40
    Spirometry. Levels of NO correlate with inflammation.
    In children FeNO >35
  • Obstructive pattern with FEV1:FVC <0.75 (this is because FEV is decreased whereas in restrictive, both FEV and FVC are reduced).

Reversibility:
- >12% improvement in FEV1 with B-agonist. Response to bronchodilator reversibility. or an increased in volume of 200ml in adults.

Peak Expiratory Flow Rate

  • May be low with diurnal variation of >20%
  • Morning dipping

Atopy: skin-prick, RAST

All patients >=17
- patients should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma

  • All patients should have spirometry with a bronchodilator reversibility (BDR) test
  • All patients should have a FeNO test

Patients 5-16
- all patients should have spirometry with a bronchodilator reversibility (BDR) test

  • a FeNO test should be requested if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility (BDR) test

<5 = Clinical judgement

145
Q

Management of asthma - General measures?

A

General Measure? TAME

- Technique for inhaler use - 
Remove cap, shake before delivery. Breath should be held for 10 s, then gap of 30 seconds. 
- Avoidance: allergens, smoking, dust
- Monitor: Peak flow diary (2-4x/d) 
- Educate 
Liaise with specialist nurse
NEed for Rx compliance 
Emergency action plan
146
Q

Management of asthma - drug ladder?

A

Step 1
- SABA PRN (100 micrograms) up to 4 times daily when required. If use >1/d or nocte symptoms –> Step 2

Step 2
- SABA + LD inhaled steroid: beclometasone 100-400microgram bd. (if symptoms >2x a week but 1 a day). If night-time symptoms ?2 a month.

Step 3
SABA + Low-dose ICS + LTRA. montelukast 10mg)

Step 4.
SABA + low-dose ICS + LABA: salmeterol 50micrograms bd
- If good response: contine
- Benefit but control still poor: increase steroid to 400micrograms bd
- Continue LTRA depending on patient’s response to LTRA

Moderate persistent is: daily symptoms, use of SABA daily, exacerbation >2x a week and may last for days.

  1. Trials of
    - Increased inhaled steroid to up to 1000 micrograms bd
    - Leukotriene receptor antagonist (montelukast 10mg) + medium dose steroids.
    - SR Theophylline
    - MR B agonist PO
    • Oral steroids e.g prednisolone 5-10mg
    • Use lowest dose necessary
    • Maintain high-dose inhaled steroid
    • Refer to asthma clinic

Omalizumab
- Severe, persistent, allergic asthma
- Confirmed IgE -mediated allergy to perennial allergen.
>2 exacerbations required hospital admission in the preceding year.

Doses of inhaled corticosteroid dose

  • <=400 budesonide = low dose
  • 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
  • > 800 micrograms budesonide or equivalent= high dose.

Step down of asthma
- reduce the dose of any steroid to 50% at a time.

147
Q

Presentation of an acute severe asthma attack?

A

Acute breathlessness and wheeze

  • Hx of precipitant: infection, travel, exercise
  • Decrease from baseline in objective measures of pulmonary function, such as PEFV and FEV1.
  • Usual and recent rx
  • Previous attack and severity: ICU?
  • best PEFR

Patients with moderate acute severe asthma should be admitted to hospital in the presence of a previous near-fatal attack.

148
Q

Investigations for acute asthma attack?

A

PEV or FEV1
- Extent of asthma exacerbation can be determined by measuring peak flow as percentage of normal >80 = mild, moderade = 80-60%, severe = <60%.

ABG 
- PaO2 usually normal or slightly low 
- PaCO2 low 
- If PaCo2 high (>6): send to ITU for ventilation 
FBC, U+E, CRP, Blood cultures.
149
Q

Assessment of asthma attack? Severe?

A

If any of

  • PEFR <50%
  • RR >25
  • HR >110
  • Can’t complete sentences in one breath (dyspnoea at rest)

Life threatening: any one of

  • PEFR <33%
  • SpO2 <92%, PCO2 >6 kPa, PaO2 <8kPa
  • Cyanosis
  • Hypotension
  • Exhaustion, confusion
  • Silent chest, poor respiratory effort
  • Tachy/brady/arrhythmias
150
Q

Differentials for Acute Asthma Attack?

A
  • Pneumothorax
  • Acute Exacerbation of COPD
  • Pulmonary Oedema
151
Q

Admission criteria for acute asthma attack?

A
  • Life-threatening attack
  • Feature of severe attack persisting despite initial Rx
  • May discharge if PEFR >75% 1h after initial Rx.
152
Q

When to discharge a patient with an acute asthma attack?

A
  • Been stable on discharge meds for 24hr

- PEFR >75% with diurnal variability <20%

153
Q

What is the discharge plan for a patient with an acute asthma attack?

A
  • TAME patient
    Technique, avoidance, monitor and educate.
  • PO steroids for 5d
  • GP appointment w/i 1 week
  • Resp clinic appointment within 1 month.
154
Q

Initial management of acute exacerbation of asthma?

A

Mild

  • Inhaled SABA (4-8 puffs every 20 mins for up to 4 hrs, then every 1-4 hrs when required).
  • Prednisolone 40-80mg orally.

Moderate to severe

O2, Nebs and Steroids

  • Sit up
  • 100% O2 via non-rebreathe mask (aim for 94-98%)
  • Nebulised salbutamol (5mg) every 20 mins for 3 doses, followed by 2.5 to 10mg every 1-4 hrs when required
  • ipratropium (0.5mg) (anticholingeric)
  • Prednisolone 50mg PO (or both)
  • Write no sedation on drug chart

Then consider

  • Magnesium sulphate
  • Aminophylline/ IV salbutamol
155
Q

Management of acute severe asthma if life threatening?

A
  • Inform ITU
  • MgSO4 2g IVI over 20 mins
  • IV hydrocortisone 100mg every 8hrs
  • Nebulised salbutamol every 15 mins (monitor ECG).
156
Q

Management of Acute Asthma exacerbation If improving on management?

A
  • Monitor SpO2 @ 92-94%, PEFR
  • Continue pred 40mg OD for 5 days which could settle her exacerbation.
  • Nebulised salbutamol every 4hr
157
Q

Management of acute asthma if no improvement in 15-30mins?

A
  • Nebulised salbutamol every 15 mins (monitor ECG)
  • Continue ipratropium 0.5mg 406hr
  • MgSO4 2mg IV over 20 mins
  • Salbutamol IV 3-20 micrograms /min
  • ITU transfer for invasive ventilation
  • Consider aminophylline (Little evidence)
    Load: 5mg/kg IVI over 20mins
    Continue: 0.5mg/kg/hr
    Monitor levels
158
Q

MOnitoring for patient with acute severe asthma?

A
  • PEFR every 15-30 mins
    Pre and post-B agonist
  • SpO2: keep >92%
  • ABG if initial PaCO2 normal or increased.
159
Q

Definition of COPD?

A
  • Airway obstruction:FEV1:FVC <0.7, FEV1 can be >80.
  • Mild can be considered with a FEV1 >80% as mild.
  • Chronic bronchitis: cough and sputum production on most days for 3 months of 2 successive years
  • Emphysema: histological diagnosis of enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls
160
Q

Epidemiology of COPD?

A

Prevalence: 10-20% of >40yr

161
Q

Causes of COPD?

A

Smoking
Pollution
a1ATD - consider this in young person with emphysema-like illness.

162
Q

Symptoms of COPD?

A
  • Cough + Sputum (chronic 3 months)
  • Exertional Dyspnoea
  • Wheeze
  • Weight loss
  • Regular sputum production
  • Regular winter bronchitis
163
Q

Signs of COPD?

A
  • Tachypnoea
  • Prolonged expiratory phase (obstructive picture). Breath in and then out otu out, hear a squeeze. Silent chest has hyperinflation and obstructive disease.
  • Hyperinflation
    decreased cricosternal distance (normal = 3 fingers)
    Loss of cardiac dullness - hyperexpansion.
    Displaced liver edge
  • Wheeze
  • May have early-inspiratory crackles
  • Cyanosis
  • Cor pulmonale: increased JVP, oedema, loud P2.
    -Sign of steroid use
164
Q

What is a Pink Puffer?

A

In EmPhysema

  • Increased alveolar ventilation –> breathless but not cyanosed
  • Normal or near normal PaO2
  • Normal or low PaCO2
  • Progress –> T1 respiratory failure
165
Q

What is a blue bloater?

A

chronic Bronchitis

  • Decreased alveolar ventilation –> cyanosed byt not breathless
  • Decreased PaO2 and Increased PaCO2: rely on hypoxic drive
  • Progress –> T2 respiratory failure and cor pulmonale
166
Q

What criteria can you use for COPD?

A

All have obstructive picture FEV1/FVC <0.7

GOLD criteria?

  • Gold 1 - mild: FEV1 >80% predicted
  • Gold 2 - moderate: 50% - 80% predicted
  • Gold 3- severe: 30-50% predicted
  • Gold 4 - very severe: FEV1 <30% predicted
167
Q

Complications of COPD?

A
  • Acute exacerbations ± infections
  • Polycythaemia
  • Pneumothorax (ruptured bullae) - When placing a chest drain - could mimic a pneumothorax.
  • Cor Pulmonale
  • Lung Carcinoma
168
Q

Investigations for COPD?

A
  • BMI
  • Bloods: FBC (polycythaemia), a1-AT level, ABG (low oxygen sats - 88-90% acceptable, PaO2 <60mmHg suggests respiratory insufficiency).
  • CXR
    Hyperinflation (>6 ribs anteriorly)
    Flattened diaphragm
    Prominent pulmonary arteries
    Peripheral oligaemia
    Bullae
  • ECG
    R atrial hypertrophy: P pulmonale
    RVH, RAD
  • COPD is classified based on patient’s FEV1. Result of FEV1/FVC ratio <7.0. or FEV <80%
  • Assess for reversibility
  • Gas transfer
  • Echo: PHT
169
Q

Chronic General Management of COPD?

A
  • Assess severity
- General measures 
Stop Smoking 
Specialist nurse
nicotine replacement therapy 
Bupropion, vareniciline
Support programme
  • Pulmonary rehab/exercise. At the earlier stages of COPD, recommended to start as soon as they feel short of breath. Improves exercise capacity.
  • Rx poor nutrition and obesity
  • Screen and manage comorbidities
    E.g cardiovascular, lung Ca, osteoporosis
  • influenza + pneumococcal vaccine
  • Review 1-2x/yr
  • Air travel risky if FEV1 <50%
170
Q

Specific management of COPD?

A

1) Breathlessness and/or exercise limitations
- SABA (salbutamol) and/or SAMA (iptratropium) PRN
- SABA PRN may continue at all stages

2) Exacerbations or persistent breathlessness (consider FEV, any previous atopy, higher eosinophil count, substantial diurnal variation in peak expiratory flow)
- Consider asthmatic features suggesting steroid responsiveness: previous diagnosis of asthma, higher blood eosinophil count, substantial variation in FEV1 over time (at least 400ml), diurnal variation in peak expiratory flow (at least 20%).

If no asthmatic features: consider LABA + LAMA.
Stop SAMA, switch to SABA.

If asthma features :
LABA (salmeterol) + ICS combo or (LAMA (tiotropium)

3) THEN OFFER TRIPLE:

Persistent exacerbations or breathlessness

  • LABA + LAMA + ICS
  • Roflumilast/theophylline may be considered
  • Consider home nebs

4) Oral Theophylline
- After trials of long and short acting bronchodilators.

+/- 5) Prophylactic antibiotics
- 250mg azithromycin or 500mg 3x a week.

Must do LFTs and ECG to exclude QT prolongation

Recommended in COPD if they DO NOT SMOKE
- optimised non-pharm management + inhaled therapies + referred for pulmonary rehab + continue to have 1 or more of the following + significant daily sputum production.
: frequency 4 or more a year with sputum production
Prolonged exacerbation with sputum production
exacerbation resulting in hospitalisation

+/- 5) Mucolytics

  • Consider if chronic productive cough
  • Not used to prevent exacerbation in people with stable COP
  • E.g Carbocisteine (CI in PUD)

6) LTOT
- For chronic hypoxia, polycythaemia, pulmonary hypertension, peripheral oedema (cor pulmonale), FEV <30% predicted. Raised JVP.
- Aim: PaO2 >8 for 15h/day (increased survival by 50%)

  • Clinically stable non-smokers with PaO2 <7.3 (stable on two occasions >3 weeks apart)
  • PaO2 7.3-9 + PHT/cor pulmonale (also use loop diuretics)/ polycythaemia/nocturnal hypoxaemia
  • Terminally ill pts

7) Surgery
- Recurrent pneumothoraces
- Isolated bullous disease
- Lung volume reduction

171
Q

Acute Exacerbation of COPD causes?

A
  • Viral URTI (30%)
  • Also bacterial infections
  • Haemophilus Influenza is the most common
  • Streptococcus pneumonia
  • Moraxella catarrhalis
    Staph aureus more likely in patients with post-viral pneumonia
172
Q

Acute Exacerbation COPD Presentations + history?

A
  • Cough + sputum
  • Breathlessness
  • Wheeze
  • Smoking Status
  • Exercise capacity
  • Current treatment
  • Previous exacerbations
173
Q

Investigations for acute exacerbation of COPD?

A
  • PEFR
  • oxygen sats (check patient baseline)
  • Bloods: FBC (may show elevated haematocrit + elevated WBC) , U+E, ABG (respiratory acidosis + compensatory metabolic alkalosis), CROP, cultures
  • CXR: Infections, pneumothorax, will show hyper-expansion, flattened diaphragm, increased retro-sternal air space, bullae.
  • ECG
174
Q

What are the differentials for Acute exacerbation of COPD?

A
  • Pneumothorax
  • Pulmonary Oedema
  • PE
  • Asthma
175
Q

Plans for discharge for acute exacerbation of COPD?

A
  • Spirometry
  • Establish optimal maintenance therapy
  • GP and specialist f/up
  • Prevention using home oral steroids and Abx - Rescue medication.
  • Pneumococcal Flu vaccine
  • Home assessment
176
Q

Management of Acute Exacerbation of COPD?

A

Controlled O2 Therapy
- Sit up
Any critically ill patient should initially be treated with high flow oxygen which is then titrated to achieve target sats.

Do ABG, CXR, ECG, FBC, U+E, MCS, BC.

  • Then - 28% O2 via Venturi mask: SpO2 88-92% at 4L.
  • Vary FiO2 and SpO2 target according to ABG
  • Aim for PaO2 >8 and increase in PCO2 of <1.5kPa
Then 
Nebulised Bronchodilators 
- Air driven with nasal specs
- Salbutamol 5mg/4h
- Ipratropium 0.5mg/6hr

Then
- Steroids (IV or PO)
Hydrocortisone 200mg IV
- Prednisolone 40mg PO for 7-14 days

Abx

  • If evidence of infection, purulent sputum or signs of pneumonia.
  • Doxy 200mg PO STAT then 100mg OD PO for 5 days Or Amoxicllin etc

Then consider NIV if no response (worsening baseline examination, ABG, lung function).
- PaCO2 >6kPA, pH <7.35.
Persistent respiratory acidosis

Use of accessory respiratory muscles, cyanosis.

If they have respiratory acidosis, severe dyspnoea, increased work of breathing.
- Repeat nebs and consider aminophylline IV

  • Consider NIV (BiPAP) if pH <7.35 and/or RR >30. Useful for T2RF. IPAP and EPAP
  • Consider invasive ventilation if pH <7.26
177
Q

What is a pulmonary embolism

A

Consequence of the thrombus formation within a deep vein of the body mostly lower extremities. Occurs due to Virchow’s triad.

178
Q

What causes a pulmonary embolism?

A
  • Usually arises from DVT in proximal legs or iliac veins
  • Rarely (right ventricle post MI)
  • Septic emboli in right sided endocarditis
179
Q

What are the risk factors for a PE?

A

SPASMODICAL

  • Sex
  • Pregnancy
  • Age increased
  • Surgery (10d postop straining at stool)
  • Malignancy
  • Oestrogen: OCP/HRT
  • DVT/PE previous Hx
  • Immobility
  • Colossal size
  • Antiphospholipid Abx
  • Lupus Anti-Coagulant
180
Q

How does a PE present?

A

Symptoms and signs depend on size, number and distribution of emboli?

Symptoms

  • Dyspnoea/Tachypnoea
  • Tachycardia
  • Pleuritic pain
  • Haemoptysis
  • Syncope

Signs

  • Crackles
  • Fever
  • Cyanosis
  • Tachycardia, tachypnoea
  • RHF: hypotension, increased JVP, loud P2
  • Evidence of cause: DVT
181
Q

Investigations of Pulmonary Embolism?

A

CXR - Must happen prior to CTPA or V/Q.

Bloods: FBC, U+E (renal impairment before LMWH) , Clotting (baseline before treating), D-dimers (used to exclude PE in low risk patients - based on Well’s)

ABG: normal or decreased PaO2 and decreased PaCo2, increased pH.

ECG: (used to assess Right ventricular function) Sinus tachycardia, RBBB, right ventricular strain
(inverted T in V1-V4)
S1,Q3,T3 is rare (deep 3 waves in 1, pathological Q waves in III, inverted T waves in III indicating right heart strain).

Doppler US: thigh and pelvis (+ve in 60%)

CTPA + venous phase of legs and pelvis

V/Q is used to patients with renal impairment - scans use a contrast media that is nephrotoxic

182
Q

Diagnosis of PE?

A

Assess using Well’s Score

Criteria for Well’s score

  • Clinical signs of DVT
  • Alternative diagnosis less likely than PE
  • Previous PE or DVT
  • HR >100bpm
  • Surgery or immobilisation within 4 weeks
  • Haemoptysis
  • Active cancer
  • Low probability –> (less than or equal to 4) perform D-dimers
    Negative = exclude PE
    Positive = CTPA
High probability (>4) = CTPA
unless CKD then don't use contrast.
183
Q

Prevention of a PE?

A
  • Risk assessment for all patients
  • TEDS
  • Prophylactic LMWH
  • Avoid OCP/HRT if @ risk
184
Q

Management of PE?

A
  • Sit up
  • 100% oxygen via non-rebreather mask
  • Analgesia
    Morphine ± metoclopramide

If critically ill with massive PE consider thrombolysis (SBP <90)

  • High flow oxygen/fluids (500ml saline) ± adrenaline if SBP <90
  • Alteplase 100mg bolus over 2hrs
  • Surgical or interventional embolectomy

Then

Acutely Anticoagulate with LMWH or Unfractionated (preferred) (heparin and adjust does to APTT) + Warfarin 5mg orally adjust according to INR.
Can be reversed with protamine (UFH) and stopped at an INR 2-3.
Can also give fondaparinux

Those at low risk can have rivaroxaban 15mg orally twice daily.

185
Q

Management of PE if BP refractory to treatment?

A

Dobumatine inotropes: aim for SBP >90

  • Consider addition of norepinephrine.
  • Consider thrombolysis (medical or surgical)
186
Q

On-going management of PE

A
  • TED stocking in hosptial
  • Graduated compression stocking for 2yrs if DVT prevents post-phlebetic syndrome
  • Continue LMWH until INR >2 (at least 5day)

Then continue with warfarin for 3 months.

  • Target INR = 2-3
  • Duration
    Remedial cause: 3months
    No identifiable cause: 6 months
    On-going cause:
  • VC filter if repeat DVT/PE despite anticoagulation (or with an absolute contraindication to anticoagulant therapy, or with patients experiencing major bleeding or with recurrent PE).
187
Q

What is a Pneumothorax

A
  • Accumulation of air in the pleural space with 2ndry lung collapse
188
Q

What is the classification of pneumothorax?

A

Closed: intact chest wall and air leaks from lung into pleural cavity
Open: Defect in chest wall allows communication between PTX and exterior: may be sucking
Tension: air enters pleural cavity through one way valve and cannot escape leading to mediastinal compression

189
Q

What is a primary spontaneous pneumothorax?

A

Occurs without preceding trauma or precipitating event, and develops in a person without clinically apparent pulmonary disease.

Most at risk are those who smoke, Marfan’s. homocystinuria or FHx.
- Young thin men

190
Q

What is a secondary spontaneous pneumothorax?

A

Complication of underlying pulmonary disease. COPD is most common from cigarette smoke.
May also be PCP, Cystic fibrosis, TB.
Pulmonary fibrosis, sarcoidosis

191
Q

Causes of pneumothorax?

A
  • Spontaneous primary and secondary
  • Trauma (penetrating or blunt ± rib fracture) due to flail chest syndrome
  • Iatrogenic (subclavian CVP line insertion, positive pressure ventilation, transbronchial biopsy, liver biopsy).
192
Q

Presentation of pneumothorax?

A

Symptoms

  • Sudden onset
  • Dyspnoea
  • Pleuritic chest pain

Signs

  • Decreased expansion of side affected
  • Resonant percussion (hyperresonant) ipsilateral
  • Decreased breath sounds ipsilateral
  • Decreased vocal resonance
  • Trachea shift in tension to the unaffected side)
  • Crepitus: surgical emphysema
193
Q

Presentation of tension pneumothorax?

A
  • Respiratory distress
  • increased JVP, mediastinal shift, increased HR, decreased JVP
  • Hyper-resonant chest
  • Absent breath sounds
  • Trachea is deviated to the left away from pneumothorax.
  • Insert wide-bore cannula into second intercostal space - mid-clavicular line.
194
Q

Investigations for pneumothorax?

A
  • ABG
  • US
  • CXR (expiratory film may be helpful)
    Translucency + collapse (2cm rim = 50% loss)
    Visualise line of pleura
    Mediastinal shift (away from PTX)
    Surgical emphysema
    Causes: rib fractures, pulmonary distress
195
Q

Management of a tension pneumothorax?

A
  • Resuscitate patient
  • Oxygen therapy >10L/min via a non-rebreather face mask.
  • No CXR
  • Large bore 14G Venflon into 2nd ICS, mid-clavicular line
  • Insert intercostal chest drain

Remember that 22G is paediatric and 14G is the largest.

196
Q

Management of traumatic pneumothorax?

A
  • Resuscitate patient
  • Analgesia e.g morphine
  • 3-sides wet dressing if sucking
  • Insert ICD (intercostal chest drain)
197
Q

Management of a primary pneumothorax?

A

SOB and/or rim >2cm? If yes then aspirate + then if successful discharge. If unsuccessful chest drain.

If no SOB or rim <2cm, then discharge. even following aspiration.

Give oxygen to all 10L/min

For those above 50 or have a significant smoking history, treat as you would 2ndry.

198
Q

Management of secondary pneumothorax?

A
  • Admit
  • 10L oxygen/min
  • SOB and >50 yrs and rim >2cm? Yes then insert chest drain.
  • If not, then aspirate, and then decide to insert ICD.
  • If pneumothorax is less than 1cm then BTS guidelines suggest giving oxygen + admitting for 24hrs.
199
Q

What is a pleural effusion?

A

Fluid collects between the parietal and visceral pleural surfaces of the thorax. A thin layer of fluid is always present in this space for lubrication.

200
Q

How would you classify a pleural effusion?

A

Effusion protein <30g/L = transudate (through a strainer)
Effusion protein >30g/L = exudate (through holes)

If between 25-35 = Light’s Criteria

201
Q

What is Light’s Criteria?

A

Used to differentiate transudate from exudate.

  • an exudate has one of:

Effusion: pleural protein to serum protein ratio >0.5

Effusion: serum LDH ratio >0.6

Effusion LDH is >2/3 upper limit of normal for serum.

Other findings include:

  • Rheumatoid arthritis, tuberculosis
  • Raised amylase: pancreatitis, oesophageal perforation
202
Q

Causes of an exudate?

A

> 30g/L

Increased capillary permeability

  • Infection: pneumonia, TB
  • Neoplasm: bronchial, lymphoma, mesothelioma
  • Inflammation: RA, SLE
  • Pulmonary Embolism
  • Dressler’s Syndrome
  • Yellow Nail syndrome
203
Q

Causes of an transudate?

A 
Increased capillary hydrostatic or decreased oncotic pressure? 
- CCF
- Renal failure 
- Decreased albumin: nephrosis, liver failure, enteropathy
- Hypothyroidism 
- Meig Syndrome 
Right pleural effusion
Ascites 
Ovarian fibroma
204
Q

Presentation of pleural effusion?

A
  • Normally asymptomatic
  • Or presented with dyspnoea (difficult breathing)
  • Pleuritic chest pain

Signs

  • Tracheal deviation away from effusion (towards deviation is in lung collapse or lobe fibrosis)
  • Decreased expansion
  • Stony dull percussion
  • Decreased air entry
  • Bronchial breathing just above effusion
  • Decreased vocal fremitus (air to water). Decreased breath sounds).

Signs of associated disease

  • Cancer: cachexia, clubbing, HPOA, LNs, radiation
  • Chronic liver disease
  • Cardiac failure
  • RA, SLE
  • Hypothyroidism
205
Q

Investigations for Pleural effusion?

A

Diagnostic Tap
- Percuss upper border and go 1-2 spaces below
- Infiltrate down to pleura with lignocaine
- Aspirate with 21G needle
- Send for
Chemistry: protein, LDH (exudate if ratio is >0.5, LDH to serum LDH is >0.6), pH, glucose, amylase
Bacteriology: MCS, auramine stain, TB culture
Cytology (malignant effusion)
Immunology: SF, ANA, complement

Bloods: FBC (WBC), U+E, LFTs, TFTs, Ca, ESR
PA CXR
- Blunt costophrenic angles (key point) 
- Dense shadow with meniscus
- Mediastinal shift away 
- Cause: coin lesion, cardiomegaly

US: Facilitates tapping and recommended.

Volumetric/Contrast CT

Consider Pleural biopsy if fluid inconclusive.

206
Q

What would Emypema, Ca, TB, RA and SLE show on pleural tap?

A
  • Increased protein
  • Decreased glucose <3.3
  • Decreased pH <7.2
  • Increased LDH >0.6 x serum /ULN
207
Q

What would oesophageal rupture show?

A

Oesophageal rupture

  • decreased pH <7.2
  • Increased amylase
208
Q

Management of pleural effusion?

A
  • Manage underlying cause
  • May use drainage if symptomatic (<2L/24hr)
    Repeated aspiration of ICD - using pleural aspiration.
  • Chemical pleurodesis if recurrent malignant effusion
  • Persistent effusion may require surgery
  • Consider therapeutic thoracentesis
  • VATS? –> Video-assisted

If pleural effusion is drained too quickly, a rare but important complication is a re-expansion pulmonary oedema.

Once patient consent has been obtained and patient imaging assessed, the patient should be positioned in a supine position or at a 45º angle. The patient’s forearm may be positioned behind the patient’s head to allow easy access to the axilla. Identify the 5th intercostal space in the midaxillary line.

The area should be anaesthetised using local anaesthetic injection (lidocaine, up to 3mg/kg). The drainage tube should then be inserted using a Seldinger technique. The drain tubing should then be secured using either a straight stitch or with an adhesive dressing.

o avoid re-expansion pulmonary oedema, it is recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours).

209
Q

What is sarcoidosis?

A

Multisystem granulomatous disorder of unknown cause?

210
Q

What is the epidemiology of sarcoidosis?

A

Age: 20-40
Sex: F>M
Geo: Afro Caribbean
HLA-DRB1 and DQB1 alleles

211
Q

Clinical features of sarcoidosis - General?

A

GRAULOMAS

  • 20-40% the disease presents incidentally on CXR
  • Acute sarcoidosis: EN, fever, polyarthralgia, BHL

General

  • Fever
  • Anorexia and weight loss
  • Fatigue
  • Lymphadenopathy and hepatosplenomegaly

Lofgren’s sydnrome: fever, hilar lymphadenopathy, polyarthritis.
Acute form of the disease

Heerfordt’s syndrome - Parotid enlargement, fever and uveitis secondary to sarcoidosis.

212
Q

Respiratory features of sarcoidosis?

A 
Upper: Otitis, sinusitis
Lower (seen in 90%) 
- Dry cough, 
- SOB of gradual onset, 
- chest pain, 
- decreased lung function 
Stage 1: BHL 
Stage 2: BHL + peripheral infiltrates
Stage 3: Peripheral infiltrates alone 
Stage 4: Progressive mid-zone fibrosis with bullae
213
Q

Arthralgic features of sarcoidosis?

A
  • Polyarthralgia

- Dactylitis

214
Q

Neurological features of sarcoidosis?

A
  • Peripheral and cranial polyneuropathy (esp. Bell’s palsy)

- Meningitis, transverse myelitis, SOL

215
Q

Urine features of sarcoidosis?

A

Increased calcium –> renal stones, nephrocalcinosis, DI

216
Q

Low hormones of sarcoidosis?

A

Pituitary dysfunction: e.g amenorrhoea

217
Q

Ophthalmological features of sarcoidosis?

A
  • Uveitis
  • Keratoconjunctivitis
  • Sicca/Mikulicz/Sjogren’s Syndrome
218
Q

Myocardial features of sarcoidosis?

A
  • restrictive cardiomyopathy sndry to granulomas and fibrosis
  • Pericardial effusions
219
Q

Abdominal features of sarcoidosis?

A
  • Hepatomegaly + cholestatic LFTs

- Splenomegaly

220
Q

Skin features of sarcoidosis?

A

Erythema Nodosum: painful erythematous nodules on shins (paniculitis)
Lupus pernio: Raised, dusky purple plaques on nose, cheeks, fingers. Non-itchy, frequently affecting the nose, cheeks, lips and ears.

221
Q

Investigations for sarcoidosis?

A

Bloods

  • Increased ESR
  • Increased Ca (dysregulated calcitriol by macrophages and granulomas)
  • Lymphopenia
  • Increased serum ACE
  • Increase Ig
  • Increased LFTs (elevated AST and ALT)

CXR, CT, MRI for pulmonary involvement.

Tuberculin skin test
- Negative in 2/3

Lung functions test

  • Restrictive pattern with decreased FVC
  • Decreased transfer factor

Tissue Biopsy

  • Lung, LNs, Skin nodules, liver
  • Diagnostic: non-caseating granulomas

Ophthalmology assessment

222
Q

Management of sarcoidosis?

A

Pts with asymptomatic BHL do not require Rx

Acute sarcoidosis

  • usually resolves spontaneously
  • Bed rest, prednisolone (if unable to breath/respiratory failure), NSAIDS

Chronic Sarcoidosis
- Steroids: Prednisolone 40mg/d for 4-6 weeks

NICE recommends = indications for corticosteroid treatment are: parenchymal lung disease, uveitis, hypercalcaemia, neurological or cardiac involvement.

  • Consider second line - methotrexate, ciclosporin, cyclophosphamide

Cutaneous disease
- Topical corticosteroids (triamcinolone) or oral prednisolone 40mg

223
Q

Bilateral Hilar lymphadenopathy differential

A
  • Sarcoidosis
  • Infection: TB, mycoplasma
  • Malignancy: lymphoma, carcinoma
  • Interstitial disease: EAA, Silicosis
224
Q

Interstitial lung disease

A

Large group of disorders for fibrosis of the lungs

  • Exposure related
  • Idiopathic
  • Sarcoidosis
  • Connective tissue disease
225
Q

Principle features of interstitial lung disease?

A
  • Dyspnoea
  • Dry cough
  • Abnormal CXR/CT
  • Restrictive Spirometry
226
Q

Causes of interstitial lung disease?

A 
Known Causes 
- Environmental: asbestosis, silicosis 
- Drug: BANS ME
Bleomycin, Busulfan
Amiodarone
Nitrofurantoin* 
Sulfasalaine
Methotrexate* , Methysergide 
- Hypersensitivity: EAA
- Infection: TB, viral, fungi

Associated with systemic disease

  • Sarcoidosis
  • RA
  • SLE, systemic sclerosis, Sjorgren’s, MCTD
  • UC, ankylosing spondylitis

Idiopathic
- Idiopathic pulmonary fibrosis

227
Q

Causes by Location for interstitial lung disease?

A

Upper Zone - A PENT

  • Aspergillosis: ABPA
  • Pneumoconiosis: coal, Silica
  • Extrinsic allergic alveolitis
  • Ank Spond
  • TB

Lower Zone: STAIR (More common affect the bottom)
- Sarcoidosis (mid zone)
- Toxins: BANS ME
Amiodarone, methotrexate, bleomycin
- Asbestosis
- Idiopathic pulmonary fibrosis
- Rheum: RA, SLE, Scleroderma, Sjogren’s, PM, DM

228
Q

Extrinsic allergic alveolitis?

A

Acute allergen exposure in sensitised pts –> T3HS

Chronic exposure –> granuloma formation and obliterative bronchiolitis (T4Hs)

229
Q

Causes of extrinsic allergic alveolitis?

A
  • Bird fancier’s lung: proteins in bird droppings
  • Farmer’s/mushroom workers
  • Malt worker’s lung: Aspergillus clavatus
230
Q

Clinical features of EAA?

A

4-6hr post exposure

  • Fever, rigors, malaise
  • Dry cough, dyspnoea
  • Crackles (no wheeze)

Chronic

  • Increasing dyspnoea
  • Weight loss
  • T1 respiratory failure
  • Cor pulmonale
231
Q

Investigations for EAA?

A

Ix
- Bloods
Acute: neutrophilia, elevated ESR

+ve se precipitins

  • CXR
    Upper zone reticulonodular opacifications or fibrosis –> honeycomb lung
    BHL
  • Spirometry
    Restrictive defect
    Decreased transfer factor during acute attacks

BAL
- increased lymphocytes and mast cells

232
Q

Management for EAA?

A
  • Avoid exposure
  • Steroids: acute/long-term
  • Compensation may be payable
233
Q

Industrial Lung Diseases?

A

Part of the Pneumoconioses - due to mineral dust exposure or metal. Activate macrophages on alveolus leading to fibrosis.

Coal-workers Pneumoconiosis
Silicosis
Asbestosis

234
Q

Coal-Workers Pneumoconiosis?

A

Black lung disease = occupational lung disease caused by long term exposure to coal dust particles.
-Most are male = due to coal mining.

Coal dust enters lung - reaches terminal bronchioles and engulfed by interstitial macrophages. Macrophages get overwhelmed and accumulate in alveoli - causing damage to lung.

Simple pneumoconiosis

  • Commonest type
  • Patients often asymptomatic
  • May lead to progessive massive fibrosis (Massive fibrotic masses several centimers - in the upper lobe).

Category 1: some opacities but normal lung markings visible.
Category 2: large number of opacities but normal lung markings visible.
Category 3: large number of opacities with normal lung not visible.

  • Progressive massive fibrosis
  • Presents as progressive dyspnoea and chronic bronchitis
  • CXR: Upper zone fibrotic masses
235
Q

Silicosis?

A

From Quarrying, sand-blasting

Upper zone reticular shadowing and egg shell calcification of hilar nodes –> PMF

236
Q

Asbestosis

A

Demolition and ship building

  • Basal fibrosis,
  • pleural plaques - Benign + are calcified.

PLeural thickening

Asbestosis - lower lobe fibrosis

Increased risk of mesothelioma

  • Chest pain, weight loss, clubbing, recurrent effusions, dyspnoea
  • CXR: Pleural effusions, thickening
  • Dx by histology of pleural biopsy

Often palliative chemotherapy + there is also a limited role for surgery and radiotherapy.

237
Q

Management of pneumoconioses?

A

Oxygen therapy
Pulmonary rehab
Bronchodilator therapy

238
Q

Idiopathic Pulmonary Fibrosis (CFA)

A

Rare, life threatening disease that manifests over several years and characterised by formation of scar tissue within lungs and progressive dyspnoea.

239
Q

Epidemiology of Idiopathic pulmonary fibrosis?

A
  • Commonest cause of interstitial lung disease
  • MIddle age
  • M>F = 2:1
  • Associated with AI disease in 30%
240
Q

Presentation for IPF?

A 
Presentation 
- Symptoms 
Dry cough - non-responsive to antitussives
Dyspnoea - progressive over 6 months
Malaise, weight loss
Arthralgia
OSA
Signs 
- Cyanosis
- Clubbing
- Crackles: fine, end-inspiratory 
(coarse crackles typically louder, lowe pitch and early inspiratory. Indicate excess fluid due to pulmonary oedema, bronchitis)
241
Q

Complications for idiopathic pulmonary fibrosis?

A

Increase risk of Ca lung

- Type 2 respiratory failur and cor pulmonale

242
Q

Investigations for IPF?

A

Bloods

  • Increased CRP
  • Increased Ig
  • ANA+ (30%)
  • RF+ (10%)
  • ABG: decreased PaO2, increased PaCO2

CXR

  • Lung volume decreased
  • Bilateral lower zone reticulonodular shadowing
  • Honeycomb lung
  • Ground-glass
  • traction bronchiectasis

HRCT

  • Shows similar changes to CXR
  • More sensitive

Spiro

  • Restrictive defect
  • Decreased transfer factor
Other: 
Lung biopsy: usual interstitial pneumonia 
BAL: may indicate disease activity 
- Increased lymphocytes: good prognosis 
- PMN or eosinophils: bad prognosis

DTPA scan: may reflect disease activity

243
Q

Management of IPF?

A

Supportive care

  • Stop smoking
  • Pulmonary rehab
  • O2 therapy
  • Palliation
  • Rx symptoms of heart failure
  • New management
    Lung Tx offer only cure
244
Q

Pulmonary Hypertension

A

PA pressure >25mmHg

245
Q

Causes of pulmonary HTN?

A

Left heart disease

  • Mitral stenosis
  • Mitral regurg
  • Left ventricular failure
  • L–> R shunt
Lung parenchymal disease 
- Mechanism
Chronic hypoxia --> hypoxic vasoconstriction 
Perivascular parenchymal changes
COPD 
- Asthma: severe, chronic
- Interstitial lung disease
- CF, bronchiectasis

Pulmonary vascular disease

  • Idiopathic pulmonary hypertension
  • Pulmonary vasculitis: scleroderma, SLE, Wegener’s
  • Sickle Cell
  • Pulmonary embolism: acute or chronic
  • Portal HTN: portopulmonary HTN

Hypoventilation

  • OSA
  • Obesity
  • Thoracic cage abnormalitiy: Kyphosis, scoliosis
  • Neuromuscular: MND, MG, Polio
246
Q

Investigations for P HTN?

A

ECG

  • P pulmonale
  • PVH
  • RAD

CXR
- Attentuated peripheral vascular markings

Echo

  • Velocity of tricuspid regurgitation jet
  • Right atrial or ventricular enlargement
  • Ventricular dysfunction
  • Valve Disease
Gold standard 
- Right heart catheterisation: gold standard 
Mean pulmonary artery pressure
Pulmonary vascular resistance 
CO
Vasoreactivity testing to guide Rx
247
Q

What is Cor Pulmonale?

A

RHF due to chronic PHT

248
Q

Symptoms of Cor Pulmonale?

A
  • Dyspnoea
  • Fatigue
  • Syncope
249
Q

Signs of Cor Pulmonale?

A
  1. Increased JVP with prominent a wave
  2. Left parasternal heave
  3. Loud P2 +S3 (due to P HTN)
  4. Murmurs
    PR: Graham Steell EDM
    TR: PSM
  5. Pulsatile hepatomegaly
  6. Fluid: Ascites + Peripheral oedema
250
Q

Investigations of cor pulmonale?

A
  • Bloods: FBC, U+E, LFTs, ESR, ANA,RF
  • ABG: hypoxia ± hypercapnoea
  • CXR
    Enlarged R atrium and ventricle
    Prominent pulmonary arteries
    Peripheral oligaemia
    ECG: P pulmonale (Peaked P wave) + RVH
    Echo: RVH, TR, increased Pa pressure
    Spirometry
    Right HEart catheterisation
251
Q

Management of Cor Pulmonale + PHTN?

A

Manage underlying condition

  • Decreased pulmonary vascular resistance
  • Long Term Oxygen therapy
  • CCB ( nifidipine)
  • Sildenafil (PDE-5 inhibitor_
  • Prostacycline analogues
  • Bosentan (endothelin receptor antagonist)

Cardiac failure

  • ACEi + b-B (cautio if asthma)
  • Diuretics

Heart/Lung transplant

252
Q

OSA?

A

Intermittent closure/collapse of pharyngeal airway –> Apnoeic episodes during sleep.

OSA - pharyngeal collapse
- Central sleep apnoea - Often related to cerebrovascular, cardiac or neuro disease.

253
Q

Risk factors of OSA?

A 
Obesity 
Male
Smoker 
ETOH 
Idiopathic pulmonary fibrosis
Structural airway pathology
NM disease
Hypothyroid
Macroglossia
254
Q

Investigations OSA?

A

SpO2
Polysomnography is diagnostic

Other investigations
= ABG = respiratory metabolic therefore rebound metabolic alkalosis.

MSLT = daytime hypersomnolence. How quickly patients fall asleep.

255
Q

Management of OSA?

A

Weight loss
Avoid smoking + ETOH
CPAP during sleep

Epworth Sleepiness - ESS
- Total score >10 or sleepiness in dangerous situation, even with normal ESS.

256
Q

Clinical features OSA?

A

Nocturnal

  • Snoring
  • Choking, gasping, apnoeic episodes

Daytime

  • Morning headache
  • Drowsiness
  • Decreased memory and attention
  • Irritability, depression
  • Do you get refreshing sleep.
  • Unrefreshing sleep
  • Morning headache.

Pickwickian

  • Obesity hypoventilation syndrome
  • Characterised by obesity, chronic hypercapnia, and sleep disorder breathing.
  • Approx 90% of patients also have OSA

Management: nocutrual CPAP

257
Q

Complications of OSA?

A 
Pulmonary HTN
T2RF 
Cor pulmonale
HTN
Stroke 
Diabetes mellitus
258
Q

Management of OSA?

A 
Decrease weight 
Stop smoking 
CPAP at night via nasal mask
Surgery to releive pharyngeal obstruction. 
- Tonsillectomy 
Uvulopalatpharyngoplasty
259
Q

Smoking Cessation Advice?

A

Very Brief Advise

  • Ask: Enquire as to smoking status
  • Advise: best way to stop is with support and medication
  • Act: provide details of where to get help - NHS stop smoking helpline

Facilitating Quitting
- Refer to specialist stop smoking service
- Nicotine replacement (for pregnancy)
Gum, patches
- Varenicline: selective partial nicotine receptor agonist. Not for pregnancy.
Start whilst smoking
- Bupropion (not for pregnancy and can reduce the epilepsy threshold.

260
Q

Gold standard for staging of COPD?

A

mMRC Dyspnoea Score

  1. Dyspnoea only on vigorous exertion
  2. SOB on hurrying or walking up stairs
  3. Walks slowly or has to stop for breath
  4. Stops for breath after <100m / few min
  5. Too breathless to leave house or SOB on dressing
261
Q

Transfer factor?

A

The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO).

Reduced ability of the lungs to perform gas exchange. Concentration of CO inhaled and exhaled.

Reduction in Gas transfer occurs in both obstructive + restrictive. Restrictive becasue reduce lung volume. Therefore when transfer factor vs alveolar volume the ratio of transfer factor: alveolar volume is not reduced.

In obstructive - loss of alveolar structure suggests that alveolar volume is not lost. Therefore transfer factor: alveolar volume is reduced.

262
Q

Causes of traised TLCO?

A 
asthma
pulmonary haemorrhage (Wegener's, Goodpasture's)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise
263
Q

Causes of lower TLCO

A 
Causes of a lower TLCO
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
264
Q

KCO also tends to increase with age. Some conditions may cause an increased KCO with a normal or reduced TLCO

A

pneumonectomy/lobectomy
- Big scar, mediastinum shift towards pneumonectomy, decreased chest wall expansion, dull percussion, decreased breath sounds, decreased vocal fremitus.
scoliosis/kyphosis
neuromuscular weakness
ankylosis of costovertebral joints e.g. ankylosing spondylitis

265
Q

Lobectomy

A 
TB
Bronchiectasis
Malignancy
Cystic fibrosis 
Lung Abscess
Single Pulmonary Nodule - RA
266
Q

Lung Ca

A

Small cell

  • SIADH
  • ACTH
  • Lambert-Easton

Squamous

  • Hypercalcaemia - PTHrP
  • Hpoerthyroidims - TSH

Adeno - clubbing, HPOA, gynaeocomastia (produced HCG)

267
Q

NSCLC

A

Mostly operated on - adeno, squamous, large cell.

268
Q

Pancoast syndrome

A
  • apical lung tumour involvement of the brachial plexus and cervical sympathetic nerves.
  • Pain in the shoulder/anterior chest wall and arm weakness.
  • Wasting of intrinsic muscles of the hand.
  • Ipsilateral Horner’s syndrome
    (ptosis, miosis, anhydrosis and enopthalmos).

May present with a history of hoarseness of voice. This can compress the recurrent laryngeal nerve causing hoarseness of voice.

Normally in the apices of chest-x ray.

CT scan of chest is diagnostic.

269
Q

Lung transplant

A 
Emphysema 
Idiopathic pulmonary fibrosis 
idiopathic pulmonary hypertension
Bronchiectasis
Cystic fibrosis
270
Q

Complication of lung cancer - SVCO?

A

SVCO

  • Oedema of the face, neck and upper body.
  • Prominent neck and chest wall vessels
  • Facial plethora
  • Stridor
  • Headache
  • Dizziness

Management - Oncologist and emergency radiotherapy.

271
Q

Aspergillus

A

Aspergilloma - risk with repv TB, sarcoid, COPD. fungal ball in cavity.

ABPA - asthma lie ,raised IgE< proximal bronchiectasis.
RAST, positive IGG precipitins.

Invasive - immunodeficiency.

272
Q

Afro-carribean lady presents with breathlessness. She has vague symptoms, fevers, malaise, has a rash on her face. Her bloodworks show increased ACE activity.

A

Sarcoidosis

  • bilateral HLA
  • Afro-caribbean women
  • ACE, Ca, ESR
  • Non-caseating granuloma
  • Kveim test (Kveim - intradermal injection of splenic extraction followed by skin biopsy.
  • biopsy gold standard.
273
Q

Hoarse Voice

A
  • Laryngeal issues - polyp, carcinoma, inflammation (sining, GORD, steroid inhalers - Candida.
  • Vocal cord paralysis: thyroid mass, lung cancer, ortner’s
  • Laryngoscopy - ENT referral.
274
Q

What is tracheal tugging

A

Diaphragm is working hard, feel the trachea stretching. Indicative of respiratory distress

275
Q

Vesicular breathing

A

all that is left through transmission from bronchial breathing

276
Q

In Bronchial breathing

A

This is conducted because of consolidation.

Ask patient to breath through their mouth.

277
Q

Barrell Chest

A

Feel front and back and left and side and compare their diameter to see if barrel chest.

278
Q

Inhaled foreign body

A

End up passing through the right main bronchus as the most direct pathway. Mostly into the inferior or middle lobe bronchi.

279
Q

Indications for NIV?

A
  • COPD with respiratory acidosis pH 7.25-7.35
  • T2RF secondary to chest well deformity, neuromuscular disease, OSA.
  • cardiogenic pulmonary oedema unresponsive to CPAP
  • weaning from tracheal intubation
280
Q

Recommended initial settings for bi-level pressure support in COPD?

A

Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O
back up rate: 15 breaths/min
back up inspiration:expiration ratio: 1:3

281
Q

Lobar collapse causes?

A

Lung cancer
Asthma (due to mucous plugging)
Foreign body

Signs of lobar collapse

  • tracheal deviation towards the side of the collapse
  • mediastinal shift towards the side of the collapse
  • elevation of the hemidiaphragm
282
Q

Causes of respiratory alkalosis

A
  • Hyperventilation
  • Pulmonary Embolism
  • Salicylate poisoning
  • CNS disorder: stroke, Sub Arachnoid (hyperventilation reduces ICP via hypocapnoeic vasoconstriction)
  • Altitude
  • Pregnancy
283
Q

Management of atelectasis

A

Presents with early postoperative shortness of breath, with a raised temperature.

Due to basal alveolar collapse.

Due to obstruction by bronchial secretions obstructing airways.

Management = Chest physiotherapy.

284
Q

Differential for postoperative shortness of breath

A

Atelectasis
Pneumonia
PE

285
Q

Causes of respiratory acidosis?

A
  • COPD
  • Decompensation in other respiratory conditions - life-threatening asthma
  • Neuromuscular disease
  • Obesity hypoventilation syndrome
  • Sedative: benzodiazepines, opiate overdose
286
Q

What is the transfer factor?

A

Describes the rate at which gas will diffuse from alveoli into blood.

CO is used to test the rate of diffusion. Results are given as total gas transfer or that correct for lung volume (transfer coefficient, KCO).

TLCO is an overall measure of gas transfer for the lungs from alveoli into capillaries and reflects how much O2 is being taken up.

KCO is TLCO divided by the alveolar volume - measure of how efficient gas exchange is in relation to the alveolar-capillary surface to volume ratio. Therefore in a small alveolus, there is increased pulmonary blood flow which increases the relative surface area to volume ratio.

287
Q

What are the causes of a raised TLCO? (total lung gas transfer)

A
  • Asthma
  • Pulmonary haemorrhage
  • Left-to-right cardiac shunts
  • Polycythaemia
  • Hyperkinetic state
  • Male gender

This is because the problem is not affecting the alveoli directly or gas exchange, so the lungs try to compensate by improving gas exchange.

KCO is TLCO divided by alveolar volume - this is increased because increased pulmonary blod flow which increases the number of cell which come in contact with gas.

288
Q

What are causes of lower TLCO

A 
Pulmonary fibrosis 
Pulmonary emboli
Pulmonary oedema
Emphysema
Anaemia 
Low cardiac output
289
Q

KCO?

A

Increases with age.

These conditions increased KCO with a normal or reduced TLCO

  • Pneumonectomy/lobectomy
  • Scoliosis
  • Neuromuscular weakness
  • Ankylosis of costovertebral joints.
290
Q

Occupational asthma?

A

Serial measurements of peak expiratory flow are recommended at work and away from work.

Consider referral to specialist

291
Q

Oxygen therapy

A

Acutely ill patient: 94-98%

COPD (hypercapnia patients): 88-92

292
Q

Alpha-1 antitrypsin deficiency

A

Inherited condition caused by lack of protease inhibitor normally produced by liver.

  • May present with emphysema, in the lower lobes. COPD presents with emphysema in the upper lobes.
  • Liver: cirrhosis and HCC in adults, cholestasis in children.
293
Q

Cavitating lung lesions differentials

A 
Abscess (Staph A, Klebsiella, Pseudomonas) 
Squamous Cell lung cancer
TB 
Wegener's Granulomatosis
Pulmonary Embolism
RA
Aspergillosis
294
Q

Granulomatosis with polyangiitis

A

Autoimmune condition associated with a necrotizing granulomatous vasculitis.

  • URT: epistaxis, sinusitis, nasal crusting
  • LRT: dyspnoea
  • Glomerulonephritis
  • Saddle-shaped nose deformity
  • Vasculitis rash, eye, cranial nerve.

WAGs CANCA

Remember Churg-Strauss causes asthma, eosinophilia too. Therefore there are polyps in the nose - positive ANCA.

295
Q

Presence of consolidation below the horizontal fissure

A

Suggests right middle lobe consolidation.

296
Q

Nasogastric tube aspirate placement?

A

If aspirate obtained has a pH <5.5, the NG tube is safe to use.

If aspirate >5.5, request a chest x-ray to confirm the position of the NG tube.

If no aspirate can be obtained -
Turn the patient on their left side

Inject 10-20ml air
offer a drink or mouth care and recheck aspirate in 15-20 mins

Advance or withdraw the NG tube by 10-20cm.

297
Q

Chest X-ray lobar collapse causes?

A

Lung cancer
Asthma (Mucus plugging)
Foreign boy.

General signs of lobar collapse

  • Tracheal deviation towards the side of the collapse
  • Mediastinal shift towards the side of the collapse
  • Elevation of the hemidiaphragm
298
Q

Pneumonectomy

A

Opacified left hemithorax with mediastinal and tracheal shift towards the affected side. Crowding of the ribs over the affected side with compensatory overinflation of normal lung is also seen.

299
Q

Causes of trachea pulled towards with white out?

A

Pneumonectomy
Complete lung collapse
Pulmonary hypoplasia

300
Q

Trachea pushed away from the white-out?

A

Pleural effusion
Diaphragmatic hernia
Large thoracic mass

301
Q

Trachea central with whiteout

A

Consolidation
Pulmonary oedema
Mesothelioma

302
Q

Predominant cough without lung function abnormalities?

303
Q

prominent dizziness, light-headedness, peripheral tingling

A

Dysfunctional breathing

304
Q

Recurrent severe asthma attacks without objective confirmatory evidence

A

Vocal cord dysfunction

305
Q

Predominant nasal symptoms without lung function abnormalities?

306
Q

Postural and food-related symptoms, predominant cough

307
Q

Orthopnoea, paroxysmal nocturnal dyspnoea, peripheral oedema, preexisting cardiac disease

A

Cardiac failure

308
Q

Chronic productive cough in the absence of wheeze or breathlessness

A

Bronchiectasis; inhaled foreign body; obliterative bronchiolitis; large airway stenosis

309
Q

New onset in smoker, systemic symptoms, weight loss, haemoptysis

A

Lung cancer; sarcoidosis

310
Q

Altitude disorders?

A

Acute mountain sickness
High altitude pulmonary oedema
High altitude cerebral oedema

All due to chronic hypobaric hypoxia which develops at high altitudes.

311
Q

What is Acute mountain sickness

A

Start over 2500-3000. Over 6-12hr.

  • Headache
  • Nausea
  • Fatigue

Prevention and treatment of AMS

  • the risk of AMS may actually be positively correlated to physical fitness
  • gain altitude at no more than 500 m per day
  • acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
  • treatment: descent
312
Q

HACE and HAPE

A

A minority of people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions

HAPE presents with classical pulmonary oedema features

HACE presents with headache, ataxia, papilloedema

Management of HACE

  • descent
  • dexamethasone
Management of HAPE
descent
- nifedipine, 
- dexamethasone, 
- acetazolamide, 
- phosphodiesterase type V inhibitors*
- oxygen if available
313
Q

Mesothelioma?

A

Malignancy of mesothelial cells of pleura
Metastases to contralateral lung and peritoneum
Right lung affected more often than left

  • Features include occupational asbestos exposure
  • Family history
  • Latent period

Typically present with

  • Dyspnoea
  • Clubbing
  • 30% secondary to pleural effusion (stony dull percussion note).
  • History of asbestos exposure

Although a chest x-ray is usually the first modality performed - normally see unilateral pleural effusion/thickening.

  • the next step is normally a pleural CT
  • if a pleural effusion is present fluid should be sent for MC&S, biochemistry and cytology (but cytology is only helpful in 20-30% of cases)
  • local anaesthetic thoracoscopy is increasingly used to investigate cytology negative exudative effusions as it has a high diagnostic yield (around 95%)
  • if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used
Management 
- Symptomatic
Industrial compensation
- Chemotherapy, Surgery if operable
- Prognosis poor, median survival 12 months
314
Q

Causes of haemoptysis

A

Lung cancer - smoking, weight loss, anorexia

Pulmonary oedema - dyspnoea, bibasal crackles + S3

TB - fever, night sweats, anorexia, weight loss

PE - Pleuritic chest pain, tachycardia.

LRTI - purulent cough

Bronchiectasis - usually long history of cough daily + purulent sputum production

MS - dyspnoea, AF, malar flush, mid-diastolic murmur

Aspergilloma - past history of TB, haemoptysis, rounded opacity

Granulomatosis with polyangiitis - URT (epistaxis, sinusitus) LRT (dyspnoea, haemoptysis, glomerulonephritis, saddle-shaped nose deformity

Goodpastures - haemoptysis, glomerulonephritis, systemically unwell: fever, nausea

315
Q

Causes of lung metastases?

A 
Breast cancer 
Colorectal cancer
Renal cell cancer
Bladder cancer 
prostate cancer
316
Q

Loss of the left heart border?

A

Left lingula consolidation

317
Q

Bilateral hilar lymphadenopathy?

A 
Lymphoma 
Pneumoconiosis 
Fungi 
TB 
Sarcoid
318
Q

No antibiotic prescribing or delayed antibiotic prescribing for which resp conditions?

A 
Acute otitis media
Acute sore throat
Acute pharyngitis
Acute tonsillitis 
Common cold
Acute rhinosinusitis 
Acute cough/acute bronchitis
319
Q

Consider immediate antibiotic prescribing in which patients?

A

children younger than 2 years with bilateral acute otitis media
children with otorrhoea who have acute otitis media
patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or more Centor criteria are present

320
Q

What is the Centor criteria?

A

The Centor criteria* are as follows: Bacterial cause of sore throat.

  • presence of tonsillar exudate
  • tender anterior cervical lymphadenopathy or lymphadenitis
  • history of fever
  • absence of cough
321
Q

Length of time for each Resp infection?

A

The guidelines also suggest that patients should be advised how long respiratory tract infections may last:
acute otitis media: 4 days
acute sore throat/acute pharyngitis/acute tonsillitis: 1 week
common cold: 1 1/2 weeks
acute rhinosinusitis: 2 1/2 weeks
acute cough/acute bronchitis: 3 weeks

322
Q

Respiratory causes of clubbing

A 
Lung cancer 
Cystic fibrosis, bronchiectasis,  abscess, empyema
TB
Asbestosis, mesothelioma
Fibrosing alveolitis
323
Q

Chest drain swinging?

A

Rises in inspiration
Falls in expiration

Insertion
- Safe triangle

Mid axillary line 5th intercostal space.
Anterior edge of latissimus dorsi, lateral border of pectoralis major, line superior to the horizontal level of the nipple.

324
Q

Thymoma causes what?

A

Myasthenia gravis.

325
Q

Nicotine replacement?

A
  • Patient should be offered NRT, varenicline, bupropion.
    NRT, varenicline, bupropion normally as part of commitment to stop smoking.
  • NRT, varenicline, bupropion should be sufficient to last only 2 weeks after target stop date.
  • If unsuccessful, do not offer repeat prescriptions within 6 months unless special circumstances have intervened. Do not offer NRT, varenicline, bupropion.
326
Q

Adverse effects of NRT?

A

adverse effects include nausea & vomiting, headaches and flu-like symptoms
NICE recommend offering a combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge or nasal spray) to people who show a high level of dependence on nicotine or who have found single forms of NRT inadequate in the past

327
Q

What is varenicline?

A
  • a nicotinic receptor partial agonist
  • should be started 1 week before the patients target date to stop
  • the recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)
    has been shown in studies to be more effective than bupropion
  • nausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreams
  • varenicline should be used with caution in patients with a history of depression or self-harm. There are ongoing studies looking at the risk of suicidal behaviour in patients taking varenicline
  • contraindicated in pregnancy and breast feeding
328
Q

What is bupropion?

A

Bupropion
a norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist
should be started 1 to 2 weeks before the patients target date to stop
small risk of seizures (1 in 1,000)

  • contraindicated in epilepsy, pregnancy and breast feeding.
  • Having an eating disorder is a relative contraindication
329
Q

Respiratory syncytial virus

A

Bronchiolitis

330
Q

Parainfluenza?

331
Q

Rhinovirus

A

Common cold

332
Q

Influenza

333
Q

Strep Pneumonia

A

Most common cause of CAP

334
Q

Haem Influenzae

A

CAP
Most common cause of bronchiectasis exacerbation
Acute epiglottitis

335
Q

Staph Aureus

A

Pneumonia, particular following influenza

Medicine Finals - Imperial & Quick Medical Revision (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions