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Clinical sciences > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What defines ‘restrictive’ lung disease?

A

FEV1/FVC >80 %

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2
Q

What is transfer coefficient?

A

Ability of oxygen to diffuse across alveolar membrane

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3
Q

How is transfer coefficient measured?

A

Low does CO inhaled and breath held at TLC for 10 seconds. Gas transferred is measured

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4
Q

In what conditions is transfer coefficient high and low?

A

High in pulmonary haemorrhage

Low in anaemia, severe emphysema and fibrosing alveolitis

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5
Q

If patient presents with wheezing, FEV1/FVC of <80%, what in the history would distinguish between asthma, COPD and lung cancer?

A

Asthma = Young/ non-smoker, variable in response to fumes, exertion, cold air. Worse at night

COPD = smoker, insidious onset

Lung cancer = smoker, rapid onset and progressive. Likely >40

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6
Q

Give at least 5 causes of diffuse parenchymal lung disorders (interstitial lung disease)

A
  1. Idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis)
  2. Asbestosis
  3. Sarcoidosis
  4. EAA
  5. Post infective (TB)
  6. Radiotherapy
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7
Q

What conditions is clubbing seen in?

A

Lung cancer, diffuse parenchymal lung disorder (DPLD)(fibrosis)

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8
Q

Give 3 potential complications of bronchoscopy

A

Pneumonia, pneumothorax, haemorrhage

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9
Q

Give the indications for bronchoscopy

A
  1. Radiological - lobar collapse, mass, persistent consolidation
  2. Haemoptysis
  3. Cough, wheeze, stridor, dyspnoea
  4. Undiagnosed infection (esp. in immunocompromised)
  5. Suspected aspiration of foreign body
  6. Therapeutic -stent, laser, brachytherapy
  7. Transbronchial biopsy for interstitial disease
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10
Q

Give 3 early symptoms of lung cancer and 2 later symptoms

A

Early- wheeze, change in cough, haemoptysis (sinister if not with purulent sputum)

Late - weight loss, lethargy

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11
Q

Define pneumonia

A

Inflammation of lung parenchyma

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12
Q

Describe the pathogenesis of pneumonia

A
  1. Bacteria translocate normally sterile distal airway
  2. Overwhelm resident host defence (macrophages use chemokines and cytokines to recruit neutrophils- exudate follows and fills alveolar space)
  3. Macrophages fail to phagocytose neutrophils –> severe inflammation and lung damage
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13
Q

Symptoms of pneumonia (5 main)

A
  1. Sputum (rusty = S.pneumoniae) but can be any colour
  2. Fever/sweats/rigors
  3. Cough
  4. SOB
  5. Pleuritic chest pain
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14
Q

4 main signs of lung consolidation on percussion/auscultation

A
  1. Dull on percussion
  2. Bronchial breathing
  3. Crackles
  4. Increased vocal resonance
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15
Q

Give 5 abnormal vital signs in pneumonia

A
  1. Increased HR
  2. Increased RR
  3. Low BP
  4. Fever
  5. Dehydration
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16
Q

If on a chest X ray, pneumonia is multilobar, what types of bacteria are more likely to have caused it?

A

S.pneumoniae, S.aureus and Legionella

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17
Q

What bacteria causes multiple abscesses in pneumonia?

A

S.aureus

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18
Q

If there is an upper lobe cavity in a pneumonia, what bacteria is likely to have caused the pneumonia?

A

K. pneumoniae

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19
Q

If a patient’s pneumonia shows interstitial and diffuse shadowing on chest x ray, what is likely to have caused it??

A

PCP (pneumocystis pneumonia) in HIV or immunocompromised

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20
Q

What 4 things would you look for to assess severity of pneumonia? (Systemic response)

A
  1. Delerium
  2. Urea rise (impaired organ perfusion and tissue hypoxemia = renal impairment)
  3. Increased oxygen demand (tissue hypoxia)
  4. Systolic and diastolic BP drop
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21
Q

What scoring system is used to assess community acquired pneumonia?

A

CURB65

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22
Q

What does CURB65 stand for?

A 
Confusion
Urea >= 7mmol/L
Respiratory rate >=30/min
Blood pressure - Low sytolic <90mm/Hg or diastolic <=60mm/Hg
65 - Age >=65
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23
Q

What score on a CURB65 would be high enough to want to admit the patient?

A

2

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24
Q

What are the general pathogens considered when looking at pneumonia?

A
  1. S.pneumoniae
  2. S.aureus
  3. H.influenzae
  4. K.pneumoniae
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25
Q

What bacteria are termed atypical causes of pnuemonia but nevertheless are found typically?

A
  1. Mycoplasma pneumoniae
  2. Chlamydophila pneumoniae
  3. Legionella pneumophila
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26
Q

Patient suspected pneumonia. On gram film has shown purple cocci. On blood agar has gone green and on optochin disc will not grow near it. What is likely to be the cause of this pneumonia?

A

S. pnuemoniae

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27
Q

Which antibiotics do not work against H.influenzae pneumonia?

A

Macrolides (clarithromycin, erythromycin)

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28
Q

Why are atypical pneumonia bacteria difficult to detect?

A

Grow intracellular, so cannot be grown on agar

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29
Q

What kind of antibiotics work efficiently against atypical pneumonia bacteria? and what antibiotics don’t work against them?

A

Work efficiently = macrolides (clarithromycin/erythromycin) fluroquinolones (ciprofloxacin) or tetracyclines (doxycycline)

Don’t work = B-lactam/penicillins

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30
Q

What extrapulmonary features are common in mycoplasma pneumoniae infections?

A

Haemolytic anaemia, raynauds (cold agglutinins) erythema multiforme, bullous myringitis and encephalitis

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31
Q

What organisms do Legionella live inside?

A

Amoeba

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32
Q

What extrapulmonary symptoms occur in legionella infection?

A

Diarrhoea, myalgia (raised CK levels), hyponatraemia, encephalitis, abnormal liver function

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33
Q

In what individuals are C.burnetti and C.psittaci infections found?

A

C.burnetti- exposure to animals eg. sheep

C.psittaci - contact with sick birds

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34
Q

What investigations would be done in suspected pneumonia?

A
  1. Chest X ray
  2. Sputum, for gram stain, culture and sensitivity tests
  3. Serology (antibody testing)
  4. Arterial Blood Gases (to indicate severity
  5. Urine- legionella and pneumococcal testing
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35
Q

What antibiotic/s would be used in mild CAP?

A

Amoxicillin, or if allergic, clarithromycin or doxycyline

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36
Q

What antibiotic/s would be used in moderate CAP?

A

Amoxicillin + clarithromycin

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37
Q

What antibiotic/s would be used in severe CAP?

A

IV co-amoxyclav and clarithromycin (substitute cefuroxime for co-amoxyclav if allergic)

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38
Q

How long would you administer treatment for mild-moderate pneumonia?

A

5 days

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39
Q

In what cases would you adminster treatment for pneumonia for 14-21 days?

A
  • S.aureus
  • Gram -ve bacteria
  • Legionella
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40
Q

What antibiotic must be administered in a pneumonia caused by legionella?

A

Ciprofloxacin

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41
Q

Give 4 methods of prevention of pneumonia

A
  1. PPV - doesn’t actually protect against pneumonia but does against invasive pneumococcal disease
  2. Flu vaccine
  3. Stop smoking
  4. PCV (pneumococcal conjugate vaccine)
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42
Q

How do parapneumonic effusions turn into empyema?

A

Bacteria invade fluid in pleural space

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43
Q

What signs suggest parapneumonic effusion?

A
  • Pain on deep inspiration
  • Failure of markers (WBC/CRP) to settle on antibiotics
  • Signs of pleural collection (stony dull on percussion, reduced air entry)
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44
Q

What markers on thoracocentesis of a parapneumonic effusion suggest drainage is necessary?

A

a) Pus or thick fluid
b) Gram stain or culture positive
c) pH <7.2
d) LDH >1000
e) Glucose <3.3

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45
Q

For pneumonia to be classed as hospital acquired, how long after admission must it have been to be recognised as this?

A

48 hours

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46
Q

What is the most common cause of bronchiolitis in paeds?

A

Respiratory Syncytial Virus (RSV)

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47
Q

What organisms most commonly cause bronchitis?

A

Viruses

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48
Q

Symptoms of bronchitis?

A

Cough (productive or non-productive) lasting more than 5 days, wheeze, SOB

No signs of focal consolidation

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49
Q

What are the two main types of asthma?

A

Eosinophilic and non-eosinophilic

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50
Q

Define atopy

A

The tendency to develop IgE mediated reactions to common aeroallergens

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51
Q

What does non-eosinophilic asthma show to have a relationship with?

A

Obesity and smoking

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52
Q

Give a classic presentation of asthma

A
  1. Cough/SOB
  2. Wheeze
  3. Diurnal variation
  4. Provoking factors: cold air, infections, menstrual cycle, exercise, allergens, laughter/emotion
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53
Q

What is brittle asthma?

A

Form of disease associated with recurrent severe attacks. Split into type 1 (chronic, severe) or type 2 (sudden dips)

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54
Q

What 3 factors make up Samter’s triad (Aspirin Exacerbated Respiratory Disease)?

A
  1. Sensitivity to aspirin and other NSAID’s
  2. Recurrent sinus disease (with nasal polyps)
  3. Asthma
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55
Q

Key questions in taking asthma history?

A
  1. Age of onset
  2. Family history (inc. home environment - pets?)
  3. Other atopic illnesses/allergies
  4. Triggers
  5. Occupation (what they ado and is it relieved at any point)
  6. Samter’s triad
  7. What drugs do they take (B-blockers, sensitive to aspirin, theophylline taking (interactions))
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56
Q

What are the RCP’s 3 questions for assessing asthma severity?

A
  1. Recent nocturnal waking?
  2. Usual asthma symptoms in the day?
  3. Affecting ADL’s
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57
Q

Other than the RCP’s 3 questions to assess asthma severity, what other measures or questions can be asked?

A
  1. How many inhalers are used
  2. Recent admissions to A&E
  3. Attendance at GP for courses of antibiotics/steroids?
  4. DO ASTHMA CONTROL TEST (out of 25)
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58
Q

What two factors allow you to distinguish between COPD and asthma?

A

COPD is often a disease of smokers, and will have much less diurnal variation that an asthmatic.

Although is worth noting that there can be overlap

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59
Q

What do you expect to see in a physical examination of an asthmatic?

A

Can be normal

Often will have wheeze, polyphonic

Absence of crackles, sputum

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60
Q

What are the characteristics of intrinsic, eosinophilic asthma?

A

Often presents in middle age, no definite external cause but many patients will show a degree of atopy and on questioning describe childhood asthma.

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61
Q

Which chromosome has a genetic affect on asthma and atopy?

A

Chromosome 5 - IL-4 gene cluster lies here and this controls the production of cytokines IL-3,4,5 and 13- which affect mast cell and eosinophil development and longevity + IgE production

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62
Q

What are the 3 primary abnormalities in asthma?

A

Narrowing of the airway due to:

  1. Smooth muscle contraction
  2. Thickening of airway wall by cellular infiltration and inflammation
  3. Presence of secretions within the airway
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63
Q

What are the typical findings on the lung function tests of an asthmatic?

A
  1. Airflow obstruction (reduced FEV1 and reduced FEV1/FVC ratio)
  2. Diurnal PEFR
  3. Increased responsiveness to challenge agents (metacholine/histamine)
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64
Q

On examination, during an asthma attack what symptoms present?

A

Reduced chest expansion
Prolonged expiratory time
Bilateral expiratory polyphonic wheeze

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65
Q

Give an example of a short acting and a long acting B2- Adrenoreceptor agonist

A
  1. Short acting - Salbutamol

2. Long acting - Salmeterol

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66
Q

Briefly outline the stepwise management of asthma in adults

A

STEP 1 PEFR 100% predicted
Inhaled SABA

STEP 2 PEFR >=80% predicted
Inhaled SABA and low dose corticosteroid (<800 μg daily)

STEP 3 PEFR 50-80% predicted
Inhaled SABA, corticosteroid and LABA - if still not controlled add theophylline

STEP 4 PEFR 50-80% predicted
Same but increase corticosteroid to <2000 μg daily

STEP 5 <=50% predicted
Add 40mg prednisolone

STEP 6 <=30% predicted Hospitalisation

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67
Q

How is severe asthma defined?

A

Using ATS consensus definition (1 major 2 minor)

Majors being continuous or near continuous oral steroids or requirement for high dose inhaled steroids

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68
Q

What increases an individual’s chance of asthma death?

A
  1. 3 or more types of treatment
  2. Recent admission/ frequent attender
  3. Previous near-fatal disease
  4. Brittle disease
  5. Psychosocial factors
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69
Q

How do corticosteroids reduce inflammation in asthma?

A

Induce the synthesis of inhibitory factor Kappa B- which traps and inactivates nuclear factor Kappa B.

This protein activates cytokine genes - so by using steroids this is stopped, preventing airway inflammation, oedema and secretion of mucus into airway

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70
Q

Why aren’t oral steroids used in all asthmatics over inhaled steroid?

A

Many more side effects - diabetes, cataracts, osteoporosis, hypertension, skin thinning, osteonecrosis of femoral head, hoarse voice, oral candida, growth retardation

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71
Q

What drug is used mainly in atopic eosinophilic asthma to dull the atopic response?

A

Omalizumab (monoclonal antibody that binds to IgE)

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72
Q

What therapy is mainly used in non-eosinophilic asthmatics?

A

Steroid therapy and bronchodilators

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73
Q

What distinguishes between life threatening and near fatal acute asthma?

A

Near fatal requires ventilation with raised airway pressure and will have PaCO2 that is raised

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74
Q

In life threatening asthma, SaO2 will be….(under what percentage) and PaO2 will be under what number?

A

<92%

<8kPa

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75
Q

How would you manage an acute asthma attack (life-threatening)?

A

a) Oxygen 40-60%
b) Salbutamol 5mg neb + ipratropium 0.5mg neb
c) Prednisolone 30-60mg

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76
Q

What tests woud you do on an acute asthmatic on presentation?

A

1) PEFR (check within 15-20 mins/regularly)
2) ABG - want to obtain SaO2>92% - repeat 2 hrs
3) Chest X ray if suspect pneumothorax, consolidation, or failing to respond

ITU transfer if not responding or hypercapnia, or increasing hypoxia or coma

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77
Q

What PEFR would you want to achieve in an asthmatic, post acute attack before they can be discharged + what follow up would they receive?

A

PEFR >75% predicted
<25% variability

Prednisolone for minimum 7-14 days

Increase treatment

Nurse led follow up and early clinical review 48 hours @ GP

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78
Q

What is bronchiectasis?

A

Abnormal, permanently damaged, dilated central and medium sized airways.

This leads to impaired clearance of bronchial secretions with secondary bacterial infection and bronchial inflammation

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79
Q

What are the 3 possible macroscopic appearances of bronchioles in bronchiecstasis?

A
  1. Cylindrical
  2. Varicose (fusiform)
  3. Cystic (secular)
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80
Q

What are the common causes of bronchiecstasis?

A
  1. CF
  2. End point of disease processes (pneumonia, tb, whooping cough)
  3. Immunodeficiency
  4. Ciliary defect
  5. Airway obstruction
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81
Q

Symptoms of bronchiecstasis?

A
  1. Cough >90% *usually productive
  2. Recurrent chest infections and long recovery time
  3. Haemoptysis
  4. Breathlessness/wheeze

Note/ foul smelling green sputum in copious amounts in severe disease

Rarely pyrexial

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82
Q

On examination of patient with bronchiecstasis, what is often found?

A
  1. Crepitations

2. Clubbing

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83
Q

What do the ‘tram track’ and ‘signet ring’ signs indicate on high resolution CT?

A

Bronchiecstasis

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84
Q

What investigation is termed the ‘gold standard’ for diagnosis of bronchiecstasis?

A

High resolution CT

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85
Q

When should sputum samples be done in a patient with bronchiecstasis?

A

At least yearly and on any infective exacerbation

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86
Q

What kind of disease is bronchiecstasis?

A

Obstructive

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87
Q

In a patient with bronchiecstasis what are the 4 main goals of management?

A
  1. Improved mucus clearance (physio and hypertonic saline nebs)
  2. Bronchodilation (B2 agonist)
  3. Decreased inflammation of bronchi - (inhaled steroids)
  4. Decrease exacerbations (antimicrobial therapy)
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88
Q

When is antimicrobial therapy delivered to a patient with bronchiecstasis?

A

When patient has increased cough, sputum production or purulence.

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89
Q

How long is a course of antibiotics for a patient with bronchiecstasis?

A

10-14 days unless P.aeruginosa in which case long term therapy of nebulised aminoglycosides e.g. gentamycin

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90
Q

In bronchiecstasis there is a progression of microbiology from common pathogens such as S.aureus to rarer ones such as

A

P. aeruginosa

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91
Q

Cystic fibrosis is much less common in what populations?

A

Afro-caribbean and Asian

92
Q

The most common mutation for cystic fibrosis is what, and found on what chromosome?

A

ΔF508 (deletion) CFTR

Chromosome 7

93
Q

How does the mutation in the gene coding for CFTR affect the individual suffering with CF?

A

i) Alters viscosity of mucus produced at epithelial surfaces in lungs, pancreas, GI and reproductive tract
ii) Increases salt content of sweat gland secretions

94
Q

Why are 98% of males with CF infertile?

A

Atrophy of vas deferens

95
Q

At birth, how may a child with CF present?

A

Normally, but with meconium ileus (blocked bowel due to sticky contents)

96
Q

How is diagnosis of CF made?

A

Must have 1 or more clinical or genetic factor:

a) Chronic sinopulmonary disease
b) Gastrointestinal and nutrional disorder
c) Salt loss syndrome
d) Male obstructive aspermia
e) History in sibling or positive screening test

And

Evidence of CFTR malfunction:

a) Sweat test (Cl>= 60mmol/L)/ nasal PD/ small bowel study
b) Presence of CF producing abnormalities on both chromosomes

97
Q

Name 3 bacteria that are unusual but cause very serious infections in an individual with CF

A 
P. aeruginosa
Burkholderia cepecia (fulminating skin lesions)
Mycobacteria Abscessus (multiresistant problem)
98
Q

What condition is assosciated with CF and a decline in lung function and early death?

A

Diabetes

99
Q

Every clinic that a CF patient visits they will get…

A

Cough swab
Nasal swab
Sputum

100
Q

How is prevention of CF promoted?

A
  1. Segregation
  2. Hygiene
  3. Vaccination (pneumococcal, pseudomonas, influenza)
101
Q

What diet is recommended for individual with CF?

A

High fat, calorie an protein, as well as pancreatic enzyme supplementation

102
Q

What are the main risk factors for TB?

A

Born in high prevalence area, IVDU, homeless, alcoholic, prisoner or HIV+

103
Q

How is TB spread?

A

Aerosol from one persons lung to another

Or drinking unpasteurised cow’s milk if cow has TB (m.bovis)

104
Q

How does being smear positive for TB affect the chances of transferring the disease to another individual?

A

27-50% chance passing to household member if smear positive whereas only <5% chance transferring is not smear positive

105
Q

What is the generation time for TB?

A

15-20hrs

106
Q

How does TB establish itself in an individual’s lung? Can the human body defend against it?

A

95% of people have immune response that will wall off and encapsulate bacteria. (Pulmonary infection only)

However, in 5% this is not the case, and the macrophages will coalesce to form a granuloma. (Primary ‘ghon’ focus)- This is primary disease

As this granuloma grows it will turn into a cavity and burst, spreading the mycobacteria

107
Q

What does a primary ‘ghon’ complex consist of?

A

Mediastinal lymph nodes + primary focus (granuloma)

108
Q

Where is a primary ‘ghon’ focus most likely to be found in a lung?

A

Apex - increased o2 supply and decreased blood supply (so fewer circulating immune cells)

109
Q

What are the systemic features of TB? (Two main ones and others)

A
  1. Weight loss
  2. Night sweats
  3. Fever
  4. Anorexia
  5. Malaise
110
Q

What are the pulmonary symptoms of TB?

A

Cough >3/52, chest pain, breathlessness, haemoptysis, potential collapse of lobes or pleural effusion

111
Q

What is miliary TB?

A

Widespread dissemination of mycobacterium tuberculosis ‘seeding of bacilli’ throughout the lung by the bloodstream

112
Q

If TB becomes reactivated after being latent, what is this disease called?

A

Post primary disease

113
Q

Where can TB reactivate?

A

Anywhere in the body, usually the lung

114
Q

Looking at blood tests of an individual with TB, what will be seen?

A 
Raised ESR &amp; CRP
Thrombocytosis
Hypoalbuminaemia
Hypercalcaemia
Hypergammaglobulinaemia (normally IgM)
Sterile pyuria
115
Q

What investigations would you do to confirm suspected TB?

A 
Blood tests
Sputum (Ziehl-Neelson)
Urine (sterile pyuria)
CSF (miliary TB)
Pleural tap
Biopsy
116
Q

What test would you use to diagnose latent TB?

A

Mantoux or IGRA - interferon gamma release assay (QuantiFERON)

QuantiFERON uses antigens specific to M.Tuberculosis so can tell between this and BCG. Note does not confirm active disease, only exposure to TB

117
Q

What is the standard treatment for TB and latent TB?

A

4 drugs for 6 months

Rifampicin} First 6 months
Isoniazid}
Pyrazinamide*
Ethambutol * First two months

Latent TB: 6 months isoniazid and 3 months rifampicin

118
Q

Why is treatment given for latent TB?

A

Decreases chance of turning active by 2/3

119
Q

Why is treatment for TB delivered for at least 6 months?

A

Because reactivation of dormant bacilli is the opportunity for killing so if on drugs for longer, more likely to catch a reactivation

120
Q

Who is given the BCG?

A

Neonates from high risk groups

121
Q

What type of hypersensitivity is atopic asthma?

A

Type 1

122
Q

What type of hypersensitivity is occupational asthma?

A

Type 3

123
Q

How is a diagnosis for chronic bronchitis made?

A

Persistent cough for more than 3 months in 2 consecutive years

124
Q

In chronic bronchitis, how are the VC, FEV1/FVC ratio and PEFR affected?

A

VC reduced
FEV1/FVC = <80%
PEFR reduced

125
Q

What is the difference in pathology between chronic bronchitis and asthma?

A

Chronic bronchitis has more accentuated fibrosis and destruction of local tissue.

Will get mucus oversecretion, goblet cell hyperplasia and respiratory bronchiolitis (macrophages in resp bronchioles and alveoli –> fibrosis)

126
Q

In chronic bronchitis, metaplasia is often seen. The cells change from what to what?

A

Pseudostratified columnar ciliated epithelium to squamous

127
Q

What are the causes of COPD?

A

Smoking, exposure to pollutants at work, inhalation of smoke (e.g. in developing countries biomass fuels burnt for cooking and eating) or Alpha-1 antitrypsin deficiency (early onset)

128
Q

What are the 3 types of emphysema, where are they found in the lung and what causes them?

A

Centri-acinar begins in respiratory bronchioles and spreads peripherally. Involves upper half of lung and caused by smoking

Pan-acinar Destroys alveolus uniformly and predominant in lower half of lung. Patients normally have alpha-1 antitrypsin deficiency

Distal acinar - Affects alveolar ducts and sacs. Can lead to pneumothorax

129
Q

What is bullous emphysema?

A

Damaged alveoli that distend to form exceptionally large air spaces and gas trapping. Often will present as pneumothorax when one of these air spaces ruptures.

Normally seen in upper part of the lung

130
Q

How is the damage in emphysema caused?

A

By inflammatory mediators that release matrix destructive enzymes

131
Q

In patients with COPD they will often use the accessory muscles of breathing. What are they?

A

Scalene and sternocleidomastoid

132
Q

Which conditions are associated with the terms ‘pink puffer’ and ‘blue bloater’?

A

Pink puffer = emphysema. Mainly breathless and are not cyanosed

Blue bloater = chronic bronchitis.
Hypoventilate are cyanosed, oedematous, with features of CO2 retention

133
Q

What are the key features of CO2 retention?

A

Flapping tremor of outstretched hand

Bounding pulse

Warm peripheries

Confusion in severe cases

134
Q

In interstitial lung diseases how is the FEV1/FVC ratio affected?

A

It is increased >80%

135
Q

What are interstitial lung diseases?

A

Diseases of the alveolar - capillary interface. Cellular infiltrates and extracellular matrix (scar tissue) deposition distal to the terminal bronchioles

136
Q

How do patients with interstitial lung disease often present?

A

Seem fine until have to walk

137
Q

What are the 5 major types of interstitial lung disease?

A
  1. Associated with systemic disease (rheumatology)
  2. Caused by environmental triggers (EAA)
  3. Granulomatous disease (Sarcoidosis, granulomatosis with polyangiitis)
  4. Idiopathic - IPF, NSIP, DIP, COP
  5. Other LAM
138
Q

In IPF what is the most prominent feature on chest xray/CT?

A

Reticular shadowing especially at periphery and base

Histological pattern of UIP (honeycomb)

139
Q

In IPF what are the most common symptoms and clinical features on examination?

A

CF: Cough (non productive), SOB
Clinical exam: Clubbing, crepitations

Often will develop respiratory failure, pulmonary hypertension and cor pulmonale (right sided HF) - due to pulmonary hypertension

140
Q

What are the main respiratory conditions that lymphadenopathy is often seen in?

A

Lymphoma/ sarcoid

141
Q

When looking to diagnose interstitial lung disease what 3 finding would you look for on pulmonary function tests?

A

Restrictive disease (>80% FEV1/FVC)

Reduced gas transfer (tlco)

Low/normal PaO2

142
Q

In what two types of interstitial lung disease will neutrophil levels be increased?

A

IPF, DIP

143
Q

What is the treatment for IPF?

A

There is no treatment to prolong life other than transplant.

Large doses of prednisolone are used (steroid, so decreases inflammation) or pirfenidone if FEV (50-80% expected), may slow deterioration in lung function

Will all be given best supportive care (oxygen, treat reflux, treat cough)

144
Q

If examining at individual with hypersensitivity pneumonitis (EAA) what clinical features would you expect to see?

A

Fever, malaise, cough, SOB after exposure to antigen

Physical exam would see tachypnoea, coarse-end inspiratory crackles and wheeze

Weight loss if chronic disease

145
Q

A chest x ray of 64 y.o man with fever, malaise and cough has come back showing fluffy nodular shadowing with development of streaky shadows in upper zones. What is most likely diagnosis?

A

Hypersensitivity pneumonitis

146
Q

What drugs are often used if an individual has pleural disease and it’s shown to be rheumatological?

A

Steroids (prednisolone)

+ cyclophosphamide / rituximab

147
Q

Who is age range is normally affected by sarcoidosis?

A

Young and middle aged adults

148
Q

How does sarcoidosis normally present?

A

Bilateral hilar lymphadenopathy

Pulmonary infiltrations

Skin and eye lesions

Dyspnoea

149
Q

What is sarcoidosis?

A

Multisystem granulomatous disorder of unknown cause

150
Q

What histology does sarcoidosis show?

A

Granulomatous (accumulations of epitheliod cells/macrophages/lymphocytes)

151
Q

What are the 4 stages in sarcoidosis?

A
  1. BHL
  2. BHL and inflitrates
  3. Infiltrates only
  4. Advanced parenchymal disease
152
Q

What is Lofgren’s syndrome

A

An acute form of sarcoidosis, triad of erythema nodosum, arthralgia, bilateral hilar lymphadenopathy

153
Q

What two blood tests will be abnormal in sarcoidosis?

A

Serum ACE- raised

Hypercalcaemia

154
Q

How would you treat sarcoidosis?

A

Prednisolone but only if stage IV or stage II/III symptomatic

155
Q

What is the most common cause of pneumothorax in pregnancy?

A

Lymphangiolyomyomatosis

156
Q

What is Langerhans cell histiocytosis?

A

Rare condition in which dendritic cells found elsewhere other than just skin and major airways

Histiocytes are either macrophages or dendritic cells

157
Q

What is alveolar proteinosis?

A

Rare condition whereby body has autoantibodies against GM-CSF, so alveolar macrophages don’t mature and there is abnormal surfactant accumulation - causes increased predisposition to infections

158
Q

What does ANCA stand for?

A

Anti neutrophil cytoplasmic antibody

159
Q

What are the two main mechanisms of ANCA’s?

A
  1. Molecular mimicry (double bound antibody)

2. Defective apoptosis

160
Q

What are the main diseases causing ANCA assosciated vasculitis?

A
  1. Microscopic polyangiitis (p-ANCA MPO)
  2. Granulomatosis with polyangiitis (c-ANCA PR3)
  3. Eosinophilic granulomatosis with polyangiitis (p-ANCA)
161
Q

How would you treat immune mediated lung diseases?

A
  1. Immunosupress - steroids and cyclophosphamide
  2. Plasma exchange
  3. Maintenance with rituximab
162
Q

How does rituximab work?

A

Is an anti-B cell drug. I probably reduces B cells producing ANCA as well as other mechanisms

163
Q

Name 5 conditions in the lung that can be associated with rheumatoid arthritis

A
  1. Vasculitis
  2. Pleural effusion
  3. Fibrosing alveolitis
  4. Bronchitis / bronchiecstasis
  5. Pulmonary hypertension
  6. Drug toxicity with MTX
164
Q

A patient presents with PMH of flu 6 weeks ago which got better. They then began to get weaker, lost tendon reflexes and can no longer look over their shoulder. Respiratory failure and ended up ventilated on ITU. What condition has caused this?

A

Guillain- Barre syndrome

165
Q

What triggers Guillain-Barre syndrome?

A

Usually infection such as campylobacter jejuni, EBV, CMV

166
Q

Why can infections such as campylobacter jejuni, EBV and CMV cause Guillain-Barre syndrome?

A

Infectious organism shares epitopes (antigen binding point to antibody) with antigen in peripheral nerve tissue leading to autoantibody mediated nerve cell damage.

167
Q

What are the symptoms of Guillain-Barre syndrome?

A

Progressive onset of limb weakness
Reflexes lost early in illness
Sensory symptoms such as paraesthesia
Involvement of respiratory and facial muscles, potentially leading to respiratory failure

168
Q

How do you treat Guillain-Barre syndrome?

A

Plasma exchange or IV immunoglobulin

169
Q

Give the 5 mechanisms of immune mediated damage?

A
  1. Bystander damage (chronic neutrophil recruitment if infection won’t clear eg. CF)
  2. Excessive immune response e.g asthma EAA
  3. Failure to control natural immune activation eg. alpha-1 antitrypsin deficiency
  4. On target immune response -bronchiolitis obliterans(GvHD)/ destruction of lung transplant
  5. Off target immune response (AAV/goodpasteur’s)
170
Q

Give a brief description of the pathology of Goodpasteur’s syndrome

A

Antibodies directed at basement membrane of both the kidney and lung after viral infection. (They attack alpha 3 subunit of type 4 collagen)

171
Q

What are the key symptoms of goodpasteur’s syndrome?

A

Cough, haemoptysis, tiredness, followed by acute glomerulonephritis

172
Q

How would you treat goodpasteur’s syndrome?

A

Corticosteroids

173
Q

85% of malignant bronchial tumours are of what kind?

A

Non small cell

174
Q

What are the 3 forms of non small cell tumour and which is the most prevalent?

A

Squamous
Adenocarcinoma (most common)
Large

175
Q

What does EGFR stand for and what is its significance?

A

Epidermal growth factor receptor - Mutation on this gene makes cells grow faster.

But/ EGFR inhibitors are taken orally and stop these cells from growing as fast. Are active in about 8% all cancers

Will eventually mutate again and continue to grow quickly

176
Q

Give 5 causes of lung cancer

A
  1. Smoking
  2. Asbestos
  3. Radon
  4. Coal tar
  5. Chromium

or/ iron oxide, arsenic, petroleum

177
Q

How do PET scans work?

A

Positron emission tomography, FDG taken up by rapidly diving cells and lights up on scan

178
Q

What are the 5 main sites of metastatic disease?

A
  1. Bone
  2. Brain
  3. Lymph
  4. Liver
  5. Adrenal gland
179
Q

What are the main symptoms of local disease (cancer) of the lung?

A

Cough, breathlessness, haemoptysis, dysphagia, chest pain, head neck and arm swelling (SVCO) hoarseness (recurrent laryngeal)

180
Q

What are the main symptoms of metastatic disease of the lung?

A

Bone pain, headache, seizures, neurological defecit, hepatic pain, abdominal pain.

181
Q

What is a paraneoplastic syndrome?

A

Altered immune response to neoplasm - non-metastatic systemic effect eg. finger clubbing, peripheral neuropathy, anorexia

182
Q

What is the staging used for NSCLC?

A

TNM

183
Q

What is the staging used for SCLC?

A

Limited or extensive disease (1/3 to 2/3)

184
Q

What ECOG performance status is associated with 100% death rate if individual given chemotherapy?

A

4

185
Q

If an individual could self care but could not do any work, but is out of bed >50% of the time, what WHO(ECOG) performance status score would you give them?

A

2

186
Q

What scoring system is used in palliative care to describe a patients functional status? And what score would advise avoiding surgery?

A

ECOG

2

187
Q

How would you define limited small cell disease?

A

Disease limited to one hemithorax including ipsilateral supraclavicular, mediastinal or hilar lymph nodes

188
Q

Which cancers can spread to the lung?

A

Breast, colorectal, prostate, kidney, melanoma, thyroid, lymphoma

189
Q

Surgery is not possible within how many weeks of an MI?

A

6

190
Q

What is the definition of neo-adjuvant?

A

Treatment that is the first step before main treatment

191
Q

What is the difference between radical and palliative chemo?

A

Radical attempts to have a big impact. Protracted course of treatment to minimise late toxicity

Palliative is the fewest visits possible to allow symptom control. Minimise acute toxicity

192
Q

What is the conventional radiotherapy regime?

A

Radiotherapy every day MON-FRI for 4-6 wks

OR

CHART = Treatment 3 times a day for 12 days inc weekends

193
Q

What is conformal radiotherapy and what is the name of the ‘improved version’?

A

Radiotherapy that targets the tumour specifically. Decreases local toxicity to surrounding cells but increased chance of missing the tumour.

Improved version - stereotactic ablative radiotherapy (SABR) allows room for breathing

194
Q

Palliative radiotherapy will help what symptoms?

A

Haemoptysis, chest pain, cough, anorexia, depression and anxiety

195
Q

What are the potential side effects of radiotherapy?

A

Oesophagitis, fatigue, anorexia, cough, systemic symptoms and skin irritation

196
Q

What are the side effects of chemo?

A

Alopecia, nausea and vomiting, peripheral neuropathy, constipation, diarrhoea, mucositis, rash, fatigue, anaphylaxis and bone marrow suppression

197
Q

How do SCLC’s often present?

A

Perihilar mass or peripheral coin lesion

198
Q

What prophylactic therapy can increase survival in SCLC patients that are initally responding well to treatment?

A

Prophylactic cranial irradiation

199
Q

Where is the neurovascular bundle found in relation to a rib?

A

Just below, although posteriorly is found more in midline

200
Q

What are the 3 main purposes of the pleura?

A
  1. Allows movement of lung against chest wall
  2. Clears fluid from pulmonary interstitium
  3. Couples lung and chest wall
201
Q

What is the normal amount of pleural fluid and what is normally found in the pleural fluid?

A

15ml

Proteins (albumin, fibrinogen, globulin) and cells such as mesothelial, lymphocytes and monocytes

202
Q

What is the maximum volume of fluid that the pleura can drain a day?

A

500ml

203
Q

What is a pleural effusion?

A

Fluid in the pleural space

204
Q

What are the five key symptoms of a patient that has a pleural effusion?

A
  1. Breathless
  2. Hypoxic
  3. Hypotensive
  4. Tachycardic
  5. Dull on percussion

Occasionally mediastinal and trachea shift is seen

205
Q

What is the gold standard technique for obtaining a pleural biopsy?

A

VATS (video-assisted thoracoscopic surgery)

206
Q

The fluid in a pleural effusion can either be transudate or exudate. What is the difference?

A

Transudate = fluid pushed through the capillary due to increased hydrostatic pressure eg. heart or renal failure, hypoalbuminaemia

Exudate= fluid leaks around cells of capillaries due to inflammation eg. PE, malignancy, infection, trauma

207
Q

Thoracentesis is another word for what?

A

Pleural tap

208
Q

What criteria is used to determine whether a pleural effusion is likely to be exudative or transudative?

A

Light’s criteria

209
Q

According to Light’s criteria a pleural effusion is likely to be exudative if … (2 things)

A
  1. Ratio of LDH in pleural fluid/ that in serum is greater than 0.6
  2. Ratio of pleural fluid protein/serum protein is greater than 0.5
210
Q

Patient presents with confirmed pleural effusion that is exudative, what tests would you request to rule out malignancy or parapneumonic effusion as a cause?

A

To rule out malignancy: cytology

To rule out parapneumonic: MC&S (microbiology culture and senstitivy)

211
Q

What is the management for a patient with pleural effusion caused by LBBB?

A

Diuretics

212
Q

What are the pros and cons of VATS vs. image guided cutting needle pleural biopsy?

A

VATS 95% sensitive for malignancy is comparison to 87% for image guided

VATS has potential complication eg. infection/trapped lung whereas image guided doesn’t

213
Q

What is a parapneumonic effusion?

A

Pneumonia with pleural effusion

214
Q

What signs distinguish a pleural effusion from parapnemonic effusion?

A

Productive cough, pleuritic chest pain, feverish and sweaty

215
Q

A parapneumonic effusion is complicated if… (5 factors)

A
  1. Looks like pus (empyema)
  2. Microorganisms in fluid (empyema)
  3. pH<7.2
  4. Glucose<2.2mmol/L
  5. LDH>1000
216
Q

How would you manage a complicated parapneumonic effusion?

A

Drain and intrapleural fibrinolytics

Potentially surgery (decortication to remove layer) if empyema

217
Q

What is a pneumothorax?

A

Air in the pleural space

Also known as a collapsed lung

218
Q

What are the main causes of pneumothorax?

A
  1. Trauma
  2. Spontaneous (primary eg. Marfans, secondary eg. COPD)
  3. Infections (PCP, TB)
  4. Catamenial
  5. Iatrogenic (central line, pacemaker)
219
Q

What are the signs of a tension pneumothorax?

A
  1. Deviated trachea

2. Haemodynamic instability (unstable bp)

220
Q

How would you manage a pneumothorax?

A

Drain

Apart from if tension pneumothorax, this is a medical emergency and so must receive immediate needle aspiration followed by drained

221
Q

What are the symptoms of a pneumothorax?

A

SOB, dry cough, pleuritic chest pain

222
Q

What kind of pain is pleuritic chest pain?

A

Sharp, worse on deep inhalation

223
Q

What is pleurodesis and when would it be used?

A

Talc through chest drain and causes inflammation between two pleural layers meaning that they adhere and prevents further pneumothorax/pleural effusion

224
Q

In what situations are chest drains required?

A

Pneumothorax, pleural effusion (if malignant and symptomatic, empyema or complicated parapneumonic effusion or if traumatic haemothorax or if post op or ventilated)

225
Q

Pleuritic chest pain can be referred to where?

A

Shoulder

Clinical sciences (10 decks)

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