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Phase 2 > Resp > Flashcards

Resp Flashcards

1
Q

Causes of COPD

A

CIGARETTE SMOKING!
Chronic exposure to pollutants
Alpha-1-antitrypsin deficiency

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2
Q

Types of COPD

A

Chronic bronchitis and Emphysema

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3
Q

How do you define chronic bronchitis?

A

Cough with sputum for 3 or more months for 2 or more years

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4
Q

State a characteristic of parapneumonic effusion

A

Exudative (> 35 g/L protein)

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5
Q

RF COPD

A

SMOKING
Recurrent lung infections
Environmental tobacco smoke
Genetics
Age
Socio-economic status
Occupational dust and chemical inhalation

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6
Q

Describe the MRC Dyspnoea Scale

A

1 - Not troubled by dyspnoea unless vigorous exertion
2 - Dyspnoea when walking up incline
3 - Walks slower than other people bc of dyspnoea or stops for breath at own pace
4 - Stops for breath after 100m after few mins
5 - Too breathless to leave the house, or on dressing

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7
Q

Pink puffer signs/symptoms

A

Weight loss
Barrel-chested
Thin (low BMI)
Emphysematous
Pursed lips
Normal PaO2

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8
Q

Blue bloater sign/symptoms

A

Cough w/ phlegm
Cyanosis
Overweight
Low PaO2

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9
Q

Ix COPD

A
  1. FeNO (Fraction expired nitrous oxide)
    is raised non-specific in lung damage
  2. Spirometry
    FEV1:FVC < 0.7 = obstruction
  3. Bronchodilator reversibility test
    LESS than 12% increase in FEV1 = irreversible ∴ COPD, not asthma
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10
Q

Key presentation of COPD

A

Productive cough with white or clear sputum, wheeze and breathlessness
Following years of smoker’s cough!!

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11
Q

Tx COPD

A

STOP SMOKING!!!!

SABA - short-acting beta-2-agonist e.g. salbutamol, terbutaline
LABA - long-acting beta-2-agonist e.g. salmeterol, formoterol

SAMA - short-acting musarinic-antagonist e.g. ipratropium
LAMA - long-acting muscarinic-antagonist e.g. tiotropium bromide

ICS e.g. beclomethasone

  1. SABA
  2. SABA + LABA + LAMA
  3. SABA + LABA + LAMA + ICS
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12
Q

When should LTOT be given?

A

NON-SMOKERS!

Chronic readings of < 88% O2 sats
PaO2 < 7.3 kPa

OR PaO2 between 7.3 - 8kPA AND have at least one of following:
- 2° polycythaemia
- Peripheral oedema
- Pulmonary oedema

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13
Q

Describe how LTOT should be given

A

> 15 hrs/day

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14
Q

What surgery can be done for Px with COPD?
When is this most effective?

A

Lung volume reduction surgery
In Px with upper lobe emphysema and low exercise capacity

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15
Q

What treatment should you avoid in COPD Px?

A

Chronic treatment with systemic corticosteroids
bc the benefit to risk ratio is too low

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16
Q

What prophylaxis treatments are offered for COPD Px? Why?

A

Influenza and pneumococcal vaccines
Bc exacerbations caused by recurrent resp diseases

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17
Q

Stages of COPD

A

FEV1 % - compared to predicted value
STAGE 1 - ≥ 80% (mild)
STAGE 2 - 50 - 79% (moderate)
STAGE 3 - 30 - 49% (severe)
STAGE 4 - < 30% (v severe)

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18
Q

What might an XR show for a COPD patient?

A

*Low, flattened diaphragm
Long narrow heart shadow
↓ Peripheral lung markings
Bullae
*HYPER-INFLATED LUNGS

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19
Q

DDx COPD

A

Asthma
Congestive heart failure
Bronchiectasis
Pneumoconiosis
Asbestosis

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20
Q

What are the most common causes of COPD exacerbations?

A

Viral upper respiratory tract infections
Infections of tracheobronchial tree

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21
Q

Ix COPD exacerbations

A

ABG
Chest radiographs
ECG
Bloods - WBC count

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22
Q

Tx COPD exacerbations

A

O2 - target = 88 - 92% !!
Bronchodilators - SABA and/or SAMA
Antibiotics
potentially Non-Invasive ventilation

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23
Q

When should antibiotics be given for COPD exacerbations?

A

3 cardinal signs :
1. ↑ Dyspnoea
2. ↑ Sputum vol
3. ↑ Sputum purulence

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24
Q

Why is the O2 target sat lower for COPD patients?

A

Bc of low respiratory drive
∴ can cause hypercapnia is O2 target sat is normal (94-98%)

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25
Q

What are some indication for hospital admissions in COPD patients?

A

Significant increase in symptom intensity
Severe COPD
Onset of new physical signs
No response to treatment
Serious comorbidities
Freq exacerbations
Elderly patients
Not sufficient home support

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26
Q

COPD is characterised by ?

A

Neutrophilic inflammation

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27
Q

Asthma is characterised by?

A

Eosinophilic inflammation

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28
Q

State some microscopic and macroscopic differences between asthma and COPD

A

Asthma -
Smooth muscle hypertrophy
Basement membrane thickening
Little fibrosis and alveolar disruption

COPD -
Little smooth muscle hypertrophy and basement membrane thickening
Lots of fibrosis and alveolar disruption

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29
Q

Types of asthma

A

Allergic / Eosinophilic (70%)
Allergens & atophy

Non-allergic / Non-Eosinophilic (30%)
Exercise, cold air, stress, obesity

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30
Q

What age does asthma usually present itself?

A

Starts in childhood, 3-5 years
Peak prevalence is 5-15 years

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31
Q

Which countries have a higher prevalence of Asthma?

A

New Zealand, UK, Australia
(HICs)

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32
Q

Name some precipitating factors of Asthma

A

Occupational
Cold air/water
Exercise
Pollution/irritant dust
Emotion
Drugs - NSAIDs, aspirin

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33
Q

Which hypersensitivity reaction is Asthma?

A

TYPE 1

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34
Q

Pathophysiology of Asthma

A

Overexpression of TH2 cells in airway stimulates ↑ IgE production (∴ T1 hypersensitivity)
AND eosinophilia (∴ release of toxic proteins e.g. maltose binding protein)

∴ Leads to chronic remodelling and mucus hypersecretion

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35
Q

Key presentation of Asthma

A

Cough, Dyspnoea, tight chest
DIURNAL VARIATION
Bilateral wheeze on auscultation

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36
Q

Describe the differences between brittle disease type 1 and 2

A

TYPE 1 : severe, bad all the time
TYPE 2 : sudden dips - sometimes ok, sometimes not

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37
Q

Associated symptoms of Asthma!

A

Atopic triad : Asthma, Hayfever, Eczema

Samter’s tried : Asthma, Aspirin allergy, Nasal Polyps

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38
Q

Ix Asthma

A

Same as COPD
Multiple peak flow measurement required!!

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39
Q

How are mast cells involved in asthma?

A

When IgE binds to mast cell receptor, mast cell responds to allergen binding to IgE
∴ releases chemicals

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40
Q

What chemicals do mast cells release when allergens bind to IgE (which in turn is bound to mast cells?)

A

Histamine
Tryptase
Prostaglandin 2
Cysteine leukotrienes
Cytokines - TNF-a, IL3, IL4, IL5

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41
Q

Describe the microscopy of the mucus of an Asthma patient

A

Curshmann spirals
Charcot-Leydig crystals

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42
Q

Describe the stages of an Asthma attack

A

Mild / moderate -
*PEFR > 50%
RR < 25
Pulse < 110
Normal speech

Severe
*PEFR 33-50%
RR >/= 25
Pulse >/= 110
Inability to complete sentences

Life-threatening
*PEFR < 33%
SaO2 < 92% or PaO2 < 8kPa
Normal PaCO2 (4.6-6 kPa)
Altered conscious levels, exhaustion, arrhythmias, hypotension, silent chest!!, cyanosis, poor effort

Near fatal
↑ PaCO2 and/or req ventilation with raised airway pressures

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43
Q

Tx Asthma

A
  1. SABA
  2. SABA + ICS
    ————————— check their technique!!
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA +/- LTRA
  5. ↑ ICS dose
  6. Maybe another drug e.g. omalizumab anti-IgE antibody
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44
Q

Tx for acute asthma attack

A

O SHIT ME

Oxygen

SABA
Hydrocortisone (ICS)
Ipratropium bromide
Theophylline

MgSO4
Escalate care

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45
Q

Draw the graph of different types of lung cancer

A

do it

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46
Q

What questions do you ask to take the history of a Px you suspect has asthma?

A

*RCP 3 Qs -
1. Recent nocturnal waking?
2. Asthma symptoms in day?
3. Interference w/ day to day activities?

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47
Q

Where are the majority of TB cases?

A

Africa and Asia (India, China)

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48
Q

What’s the cause of death for most people with HIV?

A

Tuberculosis

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49
Q

Name the 4 main causes of TB

A

*Mycobacterium tuberculosis
Mycobacterium bovis
Mycobacterium africanum
Mycobacterium microti

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50
Q

Describe the mycobacteral species that cause TB

A

Aerobic, non-motile, non-sporing slightly curved rods/bacilli
Thick waxy capsule
Acid fast bacilli go red/pink with Ziehl-Neelsen

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51
Q

How is cystic fibrosis inherited?

A

Autosomal recessive

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52
Q

Cause of Cystic fibrosis

A

Mutation of chromosome 7 - codes for CFTR protein

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53
Q

RF Cystic fibrosis

A

Caucasian !
FHx

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54
Q

Presentation of Cystic fibrosis

A

Resp - recurrent infections, bronchiectasis
Neonates - jaundice, failure to thrive, meconium ileus
GI - Bowel obstruction, steatorrhoea
Other - male infertility, DM

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55
Q

Other than respiratory problems, what other systemic problem do Px with cystic fibrosis have?

A

Pancreatic insufficiency

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56
Q

What is a common ECG finding for pulmonary embolism?

A

Sinus tachycardia

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57
Q

Why does PE cause tachycardia?

A

Body attempts to increase cardiac output to compensate for hypoxia

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58
Q

Key presentation of cystic fibrosis

A

Cough
Thick mucus production
Pancreatic insufficiency - poor weight gain, steatorrhoea
SALTY SWEAT

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59
Q

Other signs/symptoms of cystic fibrosis

A

Fever
Neonates - meconium ileus
Recurrent infections
Clubbing
Male infertility - absent vas deferens and epidiymis
Nasal polyps
Wheeze
Haemoptysis
Increased freq of gallstones

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60
Q

Ix Cystic fibrosis

A

Lung function test
Faecal elastase test
GS : Sweat test - Na+ and Cl- > 60 mmol/L

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61
Q

Screening test of Cystic fibrosis

A

Genetic newborn screen - used in countries w ↑ prevalence or CF family history
Measures immunoreactive trypsinogen (IRT), neonatal heel prick

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62
Q

Why does pancreatic insufficiency cause steatorrhoea?

A

Enzymes are not released to digest fat
∴ Fatty stools

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63
Q

Tx Cystic fibrosis

A

MDT approach!!

*Nutrition & healthy weight gain (fat soluble vitamins - DAKE, diet = high calorie, high fat)
*Regular chest physio, postural drainage
Inhalers (ICS, SABA)
Prophylactic Abx
*Pancreatic supplementation

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64
Q

What Abx is commonly used against S. Aureus?

A

Flucoxacillin

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65
Q

What Abx is commonly used against H. Influenzae?

A

Amoxicillin

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66
Q

What Abx is commonly used against Psuedomonas aeruginosa?

A

Ciprofloxacin

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67
Q

What are good prognostic markers for CF?

A

Lung function (FEV1) and BMI

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68
Q

What Abx is commonly used against MRSA?

A

Rifampicin and Fucidin

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69
Q

When would a lung transplant for CF be used?

A

Px sick but not too sick i.e. FEV1 close to 30%
Px on max therapy and compliant
HLA compatibility

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70
Q

Complications of CF

A

Bronchiectasis, infections

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71
Q

Brief pathophysiology of CF

A

Normally, CFTR protein allows Cl- to be transported across epithelial into secretions.
However, if damaged this doesn’t happen.
∴ water potential ↑
∴ water doesn’t move into secretions -> becomes thicker
∴ mucus isn’t wafted up ∴ bacteria colonises lungs

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72
Q

What is Sarcoidosis?

A

Interstitial lung disease, disease of alveolar/capillary interface
Immune response occurs repeatedly without a pathogen triggering it, cause not entirely known

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73
Q

Epidemiology of Sarcoidosis

A

20 - 40 years
F > M
African-Caribbeans more affected

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74
Q

RF Sarcoidosis

A

African American
FHx
Prior infection with M. tuberculosis

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75
Q

Key presentation of Sarcoidosis

A

Fever, weight loss, dry cough
Lupus pernio - purple rash on cheeks and shins, seen in chronic
Bilateral hilar lymphadenopathy
Can be asymptomatic & found incidentally on CXR

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76
Q

What organs do sarcoidosis affect?

A

Can affect any organs but mostly lungs

77
Q

State some common extrapulmonary manifestations of Sarcoidosis

A

Ant. uveitis, erythema nodosa, skin papule, peripheral lymphadenopathy, hepatosplenomegaly

78
Q

State some less common extrapulmonary manifestations of Sarcoidosis

A

Bone, heart (arrhythmias), CNS (Bell’s palsy), kidneys

79
Q

Ix Sarcoidosis

A

Bloods - ↑ ACE, ↑ Ca2+
CXR - bilateral hilar lymphadenopathy (used for staging) + pulmonary infiltrates

GS : Biopsy - shows NON caseating granulomas

Other :
ECG - might show arrhythmias or BBB
Bronchoalveolar lavage - ↑ lymphocytes in active disease, ↑ neutrophils if pulmonary fibrosis

80
Q

DDx Sarcoidosis

A

RA
Lymphoma
Metastatic malignancy
TB
Lung cancer
SLE
Idiopathic pulmonary fibrosis
Multiple myeloma

81
Q

Tx Sarcoidosis

A

In early stages, can resolve spontaneously
If persistent - steroids (prednisolone)

Transplant if extreme

82
Q

CXR Staging of Sarcoidosis

A

STAGE 0 - no changes
STAGE I - bilateral hilar lymphadenopathy
STAGE II - ^BHL and diffuse interstitial disease
STAGE III - interstitial disease ONLY (reticulonodular pattern)
STAGE IV - pulmonary fibrosis (honeycombing)

83
Q

Which Sarcoidosis patients do NOT require Tx?

A

Symptomatic patients, Stage 1
Asymptomatic patients, Stage 2 or 3

84
Q

When is the mean onset of Idiopathic pulmonary fibrosis?

A

60s
Presentation is very uncommon < 50 years

85
Q

RF Idiopathic pulmonary fibrosis

A

Male
60+
Cigarette smoking
Infectious agents (Hep C, EBV, CMV)
Drugs - methotrexate, imipramine
GORD
Genetic predisposition
Occupational exposure to metal and wood

86
Q

Pathophysiology of Idiopathic pulmonary fibrosis

A

Tissue becomes damaged by environment
Wound healing mechanism becomes uncontrolled
∴ overproduction of fibroblasts & deposition of extracellular matrix in interstitium w/ little inflammation

∴ loss of elasticity
∴ ↓ Effective gas exchange
∴ Leads to TYPE 1 RESP FAILURE

87
Q

Key presentation of Idiopathic pulmonary fibrosis

A

Exertional dyspnoea, dry cough, bibasal crackles

88
Q

Other signs/symptoms of Idiopathic pulmonary fibrosis

A

Weight loss
Arthralgia
Cyanosis
Clubbing

89
Q

DDx Idiopathic pulmonary fibrosis

A

COPD
Asthma
Bronchiectasis
CHD
Lung cancer
Hypersensitivity pneumonitis
Asbestosis

90
Q

Ix Idiopathic pulmonary fibrosis

A

Bloods :
ABG - ↓ PaO, if severe ↑ CaO2
↑ CRP, ↑ Ig
(Can exclude autoimmune rheumatic diseases by checking for ANA and RhF)

Spirometry function test - shows restrictive pattern! (FEV1:FVC ratio > 0.7 but FVC low! < 75%)

CXR small vol lungs w. ↑ reticular shadowing at base but can be normal in early stages

GS : HIGH RES CT
GROUND GLASS appearance of lungs

91
Q

What other CT findings are there for Idiopathic pulmonary fibrosis? (Other than ground glass appearance)

A

Basal distribution
Sub-pleural reticulation
Traction bronchiectasis
Honey combing - small, cystic airspaces w. irregularly thickened walls, made of fibrous tissue

92
Q

What other Ix can you do for Idiopathic pulmonary fibrosis?

A

Lung biopsy

93
Q

Tx Idiopathic pulmonary fibrosis

A

Supportive care - O2, palliative care i.e. opiates
Non-pharm - stop smoking, physio, up to date vaccines

Pharm - Antifibrotic agent e.g. Pirfenidone
Nintedanib
Treat GORD and cough

Lung transplant as last resort!
Do NOT give high dose steroids

94
Q

Prognosis Idiopathic pulmonary fibrosis

A

Median survival= 2-5years

95
Q

What is Idiopathic pulmonary fibrosis also known as?

A

Cryptogenic organising pneumonia

96
Q

Causes of Bronchiectasis

A

Bronchial obstruction
e.g. foreign body, tumour, thick mucus (CF)

Infection
e.g. Pseudomonas aeruginosa, TB, measles, pneumonia

Congenital
e.g. Ciliary dyskinesia (Kartagener’s syndrome, immotile cilia)

97
Q

Key presentation of Bronchiectasis

A

Chronic cough with large amounts of green foul-smelling sputum

98
Q

Other signs/symptoms of Bronchiectasis

A

Wheeze
Intermittent haemoptysis
Clubbing
Crackles over affected areas (esp base of lungs)
Recurrent chest infections
Dyspnoea
Chest pain

99
Q

Ix Bronchiectasis

A

Lung function test - shows obstructive pattern (FEV1 : FVC < 0.7)
CXR - kerley B lines, SIGNET RING SIGN
Sputum culture
–
GS : HIGH RES CT - thickened, dilated bronchi w/ cysts
airways larger than associated blood vessel

100
Q

GS Ix Bronchiectasis

A

HIGH RES CT - thickened, dilated bronchi w/ cysts
airways larger than associated blood vessel

101
Q

Epidemiology Bronchiectasis

A

F > M
May develop after lung infections
Pathological end point of many diseases
Presents at any age but incidence ↑ with age

102
Q

What are some major pathogens in Bronchiectasis?

A

Haemophilus influenza
Strep. pneumoniae
Staph. aureus
P. aeruginosa

103
Q

Tx Bronchiectasis

A

Improve mucus clearance - chest physio, postural drainage

Bronchodilators - nebulised SABA

Prophylactic Abx

Anti-inflammatory agents e.g. azithromycin (reduces exacerbation freq)

104
Q

Describe the postural drainage that can be done to treat Bronchiectasis

A

Physio tips patient so affected lobes can drain mucus
Done 3x a day for 10-20 mins

105
Q

Abx for Pseudomonas aeruginosa (exacerbation of Bronchiectasis)

A

Oral ciprofloxacin

106
Q

What causes Bronchiectasis exacerbations?

A

H. influenzae
S. aureus

107
Q

Abx for H. influenzae (exacerbation of Bronchiectasis)

A

Oral amoxicillin, co-amoxiclav, doxycycline
If multi-resistant, needs IV cephalosporin

108
Q

Abx for S. aureus (exacerbation of Bronchiectasis)

A

Flucloxacillin

109
Q

How much fluid in pleural space in Pleural effusion to be detected clinically?

A

500 ml

110
Q

How much fluid in pleural space in Pleural effusion to be detected via CXR?

A

300 ml

111
Q

Pleural effusion transudate causes

A

When balance of hydrostatic forces results in ↑ fluid in pleural space -

↑ Hydrostatic pressure
e.g. CHF, Constrictive pericarditis

↓ Plasma oncotic pressure
e.g. Nephrotic syndrome, cirrhosis/hepatic failure

112
Q

Pleural effusion exudate causes

A

Damage/altered pleura (∴ loss of tissue fluid and protein) -

Trauma
Neoplastic e.g. lung carcinoma, lymphoma, metastases, mesothelioma
Inflammatory e.g. vascular diseases (RA, SLE), PE, infarction, pneumonia, empyema

113
Q

Pleural effusion lymphatic causes

A

Damage during surgery
Malignancy

114
Q

What is the function of the pleura?

A

Allows movement of lung against chest wall
Clears fluid from pulmonary interstitium

115
Q

What does pleural fluid contain ?

A

Proteins - albumin, globulin, fibrinogen
Many mesothelial cells, monocytes, lymphocytes

116
Q

When are recurrent pleural effusions seen?

A

In malignant mesothelioma

117
Q

RF Pleural effusion

A

Prev lung damage
Asbestos exposure

118
Q

Describe transudative fluid

A

LESS PROTEIN
< 30 g/L
∴ Appears clear in thoracentesis

119
Q

Describe exudative fluid

A

MORE PROTEIN
< 30 g/L
∴ Appears cloudy in thoracentesis

120
Q

Key presentation of pleural effusion

A

Can be asymptomatic
Dyspnoea on exertion, pleuritic chest pain, cough

121
Q

Other signs/symptoms of Pleural effusion

A

Tracheal deviation AWAY from effusion IF LARGE
↓ Breathing sounds
↓ Tactile fremitus
Stony dull percussion on affected side
Ipsilateral decrease in expansion
Pleural friction rub
Orthopnea

122
Q

Ix Pleural effusion

A

CXR :
Transudate - bilateral
Exudate - unilateral
Costophrenic angle blunt

Thoracentesis or pleural tap

123
Q

Tx Pleural effusion

A

Depends on cause

CHF - loop diuretics
Infective - Abx
Malignant - therapeutic thoracentesis

For large effusions - CHEST DRAIN ! 5TH intercostal space

124
Q

How can you prevent reaccumulation of pleural effusion?

A

Pleurodesis e.g. tetracycline
causes adhesion of visceral and parietal pleura

125
Q

Where is thoracentesis done in reference to the rib? Why?

A

Done just OVER the rib
To avoid the neuromuscular bundle which lies just below the rib

126
Q

What is a huge contraindication of thrombolysis in the history of a patient?

A

A haemorrhagic stroke at ANY TIME IN THEIR LIFE

127
Q

Clinical presentation examples: - Example 1:
* Mrs P. 72 year old
* Previous MI, Type 2 diabetes, CKD, shortness of breath progressively over 2
weeks
* Bilateral reduced air entry
* Bilateral pedal oedema (swelling of foot and ankles)
* ECG - Left Bundle Branch Block (LBBB) - activation of left ventricle delayed
causing it to contract later than the right ventricle
* CXR - Bilateral pleural effusion

A
  • Most likely heart failure! – maybe renal disease thus transudate
  • No need to perform thoracentesis – treat with diuretics
128
Q

Example 2:
* Mr T. 74 year old retired joiner
* 2/12 (2 months) of “nagging back pain”, breathlessness, fatigue and weight
loss (sign of malignancy)
53
KP
All information is taken from lectures and textbooks, there may be mistakes!!
* CXR shows large left sided pleural effusion with mediastinal shift
* Thoracentesis (diagnostic aspiration) - protein 48g/L means an exudate!

A
  • Looks like a malignancy – so do a biopsy now!
  • Do this by visually assisted thoracoscopic surgery – medical thoracoscopy
    means shorter stay in hospital and just as good
129
Q

Pneumonia with associated pleural effusion is called what?

A

Parapneumonic effusion

130
Q

Describe the 3 forms of parapneumonic effusion

A
  1. Simple (non-infected) - resolves spontaneously, not Tx req
  2. Complicated (infected) - reqs drainage/intra pleural fibrolytics/surgery
  3. Empyema - reqs drainage/intra pleural fibrolytics/surgery
131
Q

Types of pneumothorax

A

Spontaneous
Traumatic
Iatrogenic
Lung pathology
Tension

132
Q

Tx Pneumonia

A

CURB score dependent

0-1 = oral amoxicillin, 5 days
(OR macrolide if penicillin allergy)

2 = dual therapy - amoxicillin + macrolide (IV or oral), 7 days

3+ = IV co-amoxiclav + macrolide

133
Q

Ix Pneumonia

A

FBC - ↑ WBC
Sputum culture

GS : CXR - localised/widespread consolidation, effusion, abscesses, empyema
Air bronchogram

134
Q

What does rusty sputum indicate?

A

S. pneumoniae

135
Q

When might pneumonia present with a rash?

A

If mycoplasma

136
Q

In a pneumonia patient with HIV or immunocomp, what bacteria would we assume is the cause?

A

Pneumocystic jiroveci

137
Q

Pneumonia : water cooler/air conditioner/SPAIN
What bacteria?

A

Legionella pneumophilia

138
Q

If a patient has CAP, most likely causal bacteria?

A

**Step. Pneumoniae
H. influenzae

139
Q

If a patient has HAP, most likely causal bacteria?

A

Gram neg bacteria -
Pseudomonas
E.coli
Klebsiella
Staph. aureus (incl MRSA)

140
Q

Describe pathophysiology of Pneumothorax

A

Usually pleural space has negative intrapleural pressure
Breach in pleura causes flow of air into pleural space

141
Q

Key presentation of Pneumothorax

A

Dyspnoea, one sided sharp pleuritic pain
Hyperresonant percussion note ipsilaterally
Reduced breathing sounds

142
Q

Ix Pneumothorax

A

GS and first line CXR
Absent lung markings
Affected area much darker than normal
Tracheal deviation to opp side

IF SUSPECT TENSION PNEUMOTHORAX, STRAIGHT TO Tx WITHOUT CXR !!!!!!!!!!!!!!

143
Q

Key presentation of tension pneumothorax

A

Cardiopulmonary deterioration : Hypotension, Resp disease, Low O2 sats, Tachycardia, Shock

144
Q

Tx Tension pneumothorax

A

Large bore cannula into pleural space through 2nd intercostal space in midclav line

145
Q

Define pulmonary hypertension

A

Resting mean pulmonary arterial pressure (mPAP) > 25 mmHg

Mild : 25-40
Moderate : 40 - 55
Severe : 55+

146
Q

Causes of pulmonary HTN

A

Precapillary - 1º pul HTN, pul amboli
Capillary - COPD, asthma
Post capillary - LV failure

Chronic hypoxaemia - COPD, high altitude

147
Q

Key presentation of Pul HTN

A

Exertional dyspnoea + Fatigue FIRST
then RV failure (JVP distention, periph oedema, cannon A waves)

148
Q

What is a cannon A wave?

A

Large amplitude waves seen in jugular vein

149
Q

Ix Pul HTN

A

GS : RH catheter
measures pressure directly

CXR - RVH
ECG - RA dilation (p = pulmonale, peaked p waves)

150
Q

Tx Pul HTN

A

Sildenafil - viagra!
-> Phosphodiesterase 5 inhibitor

151
Q

HAEMOPTYSIS + HAEMATURIA =

A

GOODPASTURE’S

152
Q

Ix Goodpasture’s

A

Serology - Anti-GBM antibody POS

153
Q

What’s a side effect of ICS inhalers?

A

oral thrush

154
Q

What type of hypersensitivity reaction of Hypersensitivity pneumonitis?

A

Type III

155
Q

Ix Hypersensitivity Pneumonitis

A

Usually diagnosed through Hx and examination

CXR - patchy, nodular infiltrates, fibrosis

156
Q

Tx Hypersensitivity Pneumonitis

A

Remove allergen!!
Steroids

157
Q

How is A1AT-def inherited?

A

Autosomal recessive

158
Q

How is CF inherited?

A

Autosomal recessive

159
Q

What would you see in a Patient’s CT with COPD with A1AT-deficiency as the cause?

A

Panacinar emphysema

160
Q

What would you see on a CT of a patient with Emphysema?

A

Centriacinar (resp bronchioles inv. ONLY - smokers!!)
Panacinar (A1AT def!)

161
Q

Where is EMPYEMA seen?

A

CXR on Pneumonia patient

162
Q

What is EMPHYSEMA?

A

Type of COPD

163
Q

RF Bronchiectasis

A

Infection
CF
Lung cancer

164
Q

Males, 40-70 with asbestos exposure decades ago, dyspnoea
What do you immediately suspect?

A

MESOTHELIOMA

165
Q

Key Presentation Lung cancer

A

Constitutional symptoms - TATT, weight loss etc
Lung Sx - dyspnoea, recurrent chest pain, constant cough w haempotysis

also : recurrent laryngeal compression = hoarse voice, bone pain

166
Q

Ix Lung cancer

A

1st line - CXR, then CT
pleural thickening +/- effusion

GS : BRONCHOSCOPY and BIOPSY

167
Q

What might be raised non-specifically in mesothelioma?
Usually associated with ovarian cancer

A

CA-125

168
Q

Tx Mesothelioma
Why?

A

Purely palliative :(
v severe aggressive cancer! v low survival rates

169
Q

What type of people get SCLC?

A

ONLY SMOKERS!

170
Q

Name 3 paraneoplastic syndromes of SCLC

A

Cushing’s - ACTH
SIADH - ADH
Lambert-Eaton syndrome - dysfunction of ACh at nmj

171
Q

What % of bronchial carcinomas are SCLC?

A

15%

172
Q

Where does SCLC affect?

A

Central resp system (bronchi)

173
Q

How does SCLC appear on biopsy?

A

Small cells w/ minimal cytoplasm

174
Q

Tx SCLC

A

If caught early, chemo/radiotherapy
Usually palliative

175
Q

What % does Squamous cell carcinoma account for bronchial carcinoma?

A

30-35%

176
Q

Where does squamous cell carcinoma arise from?

A

Lung epithelium

177
Q

Squamous cell cancer is the most common type (40% of all lung cancers). Smokers!

Small cell lung cancer = 20-30%. Arises from endocrine cells and in rare cases secretes
ACTH.

Large cell lung cancer = 25% of cases- poorly differentiated.

Adenocarcinoma = most common lung cancer IN NON-SMOKERS.

Bronchial cancer is very rare, starts in the mucous glands and ducts of bronchi or trachea.

A

peak

178
Q

What does squamous cell carcinoma appear as on biopsy?

A

Histologically resembles squamous epithelium

179
Q

Who does Squamous cell carcinoma mainly affect?

A

Smokers

180
Q

Paraneoplastic syndrome of Squamous cell carcinoma

A

PTHrP = hypercalcaemia

181
Q

Why is Squamous cell carcinoma more treatable than SCLC?

A

Metastasises late, usually spreads locally

182
Q

What % of bronchial carcinomas is adenocarcinoma?

A

40-45%

183
Q

Where does adenocarcinoma arise from?

A

Mucus secreting glandular epithelium

184
Q

Main RF for Adenocarcinoma

A

Asbestos exposure

185
Q

What is Adenocarcinoma NSCLC closely linked to?

A

Hypertrophic pulmonary osteoarthropathy

-> triad of :
1. clubbing
2. arthritis
3. long bone swelling

186
Q

Compression of what causes what in Lung cancer

A

Compression of sympathetic chain (T1-L2) from resp tumour (PANCOAST TUMOUR) - causes ipsilateral Horner’s syndrome

187
Q

Describe horner’s syndrome

A

Miosis
Ptosis
Anhidrosis
Right arm weakness

188
Q

Describe Pemberton’s sign
What does it show?

A

Raising arms and facial flushing
Shows SVC obstruction due to compression

Phase 2 (24 decks)

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