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CSIM > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Obstructive Spirometry

A

FEV1:FVC <70% indicates and obstructive airway defect. Reduced FEV1 vital capacity is preserved to an extent. Often pt have prolonged expiration

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2
Q

Causes of obstructive spirometry

A

COPD, Asthma (reversible), Bronchiestasis

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3
Q

Severity of Obstructive lung disease

A 
Assessed by FEv1 usually applies to COPD
Mild >80%
Moderate 50-79%
Severe 30-49%
Very Severe <30%
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4
Q

Bronchodilator challenge

A

Reversibility >15% or increase in peak flow 200ml = asthma. Alternative = diurnal variation in serial peak flows

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5
Q

Restrictive Spirometry

A

FEV1:FVC maintained. FVC approx 50%, FEV1 usually maintained

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6
Q

Causes of restrictive spirometry

A

Obesity, neuromuscular, thoracic cage abnormality, pul fibrosis

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7
Q

Flow volume loops

A

Airflow (L/s) against volume (L) in contrast to spirometry which is airflow over time. Appropriate to lung volume. i.e. slower airflow due to reduced elastic recoil

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8
Q

Diffuse small airway disease

A

Highest flow rate achieved via forced expiration, due to loos of elastic recoil air fails to be expelled. Leading to ski slope shaped curve. Inspiratory curve normal/increases

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9
Q

FEV1:FIV1 is always <1 unless

A

Extra thoracic obstruction increasing tracheal resistance which makes inspiration harder than inspiration. At inspiration the trachea is compressed leading to proportionally greater reduction

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10
Q

Large airway obstruction

A

Leads to squashing of the flow volume loop

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11
Q

Lung volumes

A

Measured in an oxygen tank.

i) Obstructive = Increased RV and TVC
ii) Restrictive = reduced TVC due to restriction of lung expansion

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12
Q

V/Q

A

Better perfusion @ bases better ventilation @ apices

V/Q < 1 normal perfusion with reduced ventilation due to COPD, fibrosis, emphysema, consolidation = shunt

V/Q > 1 normal ventilation poor perfusion due to PE, pulmonary arteritis = physiological dead space leads to increased work of breathing

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13
Q

Transfer factor

A

Functionality of the alveolar capillary membrane. Breathe in fixed vol carbon monoxide and calculating how much diffuses into the blood

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14
Q

KCO

A

Assess functionality per unit volume of lung

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15
Q

COPD transfer factor

A

Reduced TCLO and KCO widespread destruction

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16
Q

Factors affecting TCLO

A

V/Q mismatch, pulmonary HTN, haemoglobin conc, increased alveolar membrane thickness, reduced alveolar area

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17
Q

Extrapulmoary restrictive defect

A

reduced TLCO, increased KCO - compensation of healthy tissue

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18
Q

Spiral CT

A

Done in continuum won’t miss any lesions good if suscpet cancer but unable to find source

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19
Q

HRCT

A

High resolution used for diffuse conditions such as IPF, EAA, bronchiestasis

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20
Q

CXR

A

minimal radiation, 1st line, can pick up large abnormalities

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21
Q

Pneumoconiosis

A

Restrictive lung disease caused by inhalation of fine particles of mineral dust

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22
Q

Caplans

A

Pneumoconiosis + RA nodules

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23
Q

Silicosis PC

A

slowly progressive from exposure usually 10-30 yrs ago
exposure - sand blasting, mining, stone mason
SOB, exertional cough
fatigue, wt loss can progress to cor pulmonate

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24
Q

Diagnosis of silicosis

A

Biopsy = gold standard onion skinned arrangement of collagen fibres, central hyalinisation, birefringent particles under polarised light

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25
Q

Pathogenesis pneumoconiosis

A

1-5 micrometre particles - silica and asbestos very reactive. Some impact @ alveolar bifurcations where they are engulfed by macrophages. IL-1 induces and inflammatory response, fibroblast proliferation and collagen deposition

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26
Q

Invx and Mx Silicos

A

CXR - small nodules in upper lobes, increased hilar size. can lead to progressive egg shell calcification and large patches @ apices

Mx - prevention at workplace -water spray, breathing masks, chest physic, O2 if needed. Transplant - cure

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27
Q

Coal workers

A

Long term exposure due to coal dust incidence falling due to closure of the mines.

Simple - 1-2mm nodular upper zone shadowing
Massive - large conglomerate masses of dense fibrosis . Lung grossly blackened on inspection post mortem, black sputum mixed obstructive and restrictive lung defect

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28
Q

Light asbestos exposure

A

pleural plaques, mesothelioma, pleural fibrosis

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29
Q

Heavy asbestos exposure

A

lung cancer, asbestosis

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30
Q

Asbestos

A

Used in insulation, roofing sheet and shipbuilding commonly. Increased risk of adenocarcinoma

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31
Q

Clubbing in resp disease

A

Lung cancer - squamous, bronchiectasis, CF, IPF, mesothelioma

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32
Q

Haemoptysis differntials

A

Infection, lung cancer, Vasculitis, COPD, TB

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33
Q

Fibrosis O/E and CXR

A

Increased vocal resonance, fine late inspiratory crackles, streaky shadowing, honeycomb appearance

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34
Q

Pleural effusion O/E and CXR

A

Dull to percussion, reduced vocal resonance, absent breathe sounds, blunting of costophrenic angle (500ml)

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35
Q

Spirometry needs

A

Height, age, sex

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36
Q

Risks of smoking

A

COPD, lung cancer, bladder cancer, HTN, IHD, infertility in males, increased neonatal mortality and IUGR

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37
Q

Pleural plaques

A

Seen in 58% of people with asbestos exposure. They are discrete areas of hyaline fibrosis in the parietal pleura often at the diaphragm. Usually asymptomatic.
CXR - holly leaf

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38
Q

Bilateral diffuse pleural thickening

A

Fibrous thickening of the visceral pleura with adherence to parietal and obliteration of the pleural space. Extends over 25% of chest wall. Restrictive lung defect and recurrent pleural effusions

CXR - continuous irregular pleural shadowing, loss of costophrenic angle

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39
Q

Asbestosis

A

Heavy exposure often 5-10 yrs after. Progressive SOB, diffuse basal interstitial fibrosis , severe restrictive defect

CXR - basal honeycomb lung/reticular shadowing

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40
Q

Smoking and asbestosis

A

Synergistic 5x

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41
Q

Mesothelioma

A

Cancer derived from the mesothelium. light asbestos exposure

PC long latency, SOB, pleural effusions, bloody sputum and chest pain. wt loss and night sweats. Mets to liver, adrenals and kidney

Imvx - pleural thickening on CT, calrectin stain on biopsy
Mx - 2yrs then death

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42
Q

Asthma

A

Reversible airway limitation, airway hyper responsiveness to many stimuli and bronchial inflammation - T lymphocytes, mast cells, oedema, SM hypertrophy, mucus plugging

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43
Q

PC Asthma

A

PC - diurnal variation in symptoms worse @ night and morning, triggers by cold weather, emotion and exercise. Wheeze cough and shortness of breathe

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44
Q

Occupational asthma vs work aggravated

A

Occupational - caused by an agent at work either new or substantial deterioration

Aggravated - increased symptoms but can be managed

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45
Q

Hallmarks of Occupational asthma

A

Better after holidays / 3 days off, onset within 1 year at work, associated with nasal and eye symptoms preceding the asthma.

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46
Q

Investigating work place asthma

A

Peak flow diary or OASYS. Plots and interprets serial peak flow readings
Allergen provocation testing - direct inhalation or work place challenge
Skin prick testing and serum IgE levels
Sputum eosinophils are collected using hypertonic saline with a deep cough often linked to HMW allrgens

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47
Q

Methacholine challenge

A

Pt inhales a bronchoconstrictor acts via M3 receptor to narrow the airways, those with pre-existing hyperresponsiveness will react to extremely low doses

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48
Q

High weight allergens

A

Proteins with specific IgE i.e. detergents, animals and pollen, antibiotic and latex, flour and organic dusts

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49
Q

Low weight allergens

A

Reactive chemicals isocyanates, wood dust, complex metal salts, dyes and metal salts

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50
Q

Fractional NO

A

Diagnostic test. NO produced by inflamed bronchial epithelial cells. Often done before and after treatment to assess response. Useful to assess who will be responsive for steroid treatment

51
Q

Risk factors for occupational asthma

A

atopy - esp for MHW ie flour, fish extract - animal allergens
smoking - increased risk for flour, coffee

52
Q

Mx occupational asthma

A

reduced exposure, protective equipement
health surveillance - IgE/skin prick monitoring
BTS guidlines

anti IgE specialist use for severe asthma - omalizumab

53
Q

Pulmonary function test values

A 
FEV1 = forced expiatory volume over 1 second
FVC = volume of air that can be forcibly exhaled 
RV = residual volume of air left in lungs after expiration (increased with age and COPD due to gas trapping)
VC = vital capacity is volume of air breathed out after deepest inhalation
TLC = VC + RV
TV = tidal volume is the volume of air moving in and out of the lung during quiet breathing
54
Q

Mosaic CT pattern

A

Patches of radio dense lung parenchyma show areas of alveolar inflammation. Areas of radiolucent lung tissue (darker) show small airway narrowing bronchiolitis

Inflammatory reaction aims to prevent allergen reaching the alveolus causing gas trapping

55
Q

EAA and health protection

A

Employee has no duty to inform anyone
Dr cant inform employer without employees permission
Employer has a duty to inform health protection england if they know about the problem

Pt needs to be disabled to receive compensation

56
Q

Lung biopsy

A

SE = haemorrhage, infections pneumothorax, seeding of cancer through tumor wall

Crucially allows a histological diagnosis

57
Q

Causes of tracheal deviation

A

Mediastinal lymphadenopathy, goitre, malignancy
lobe collapse - pull towards
tension pneumothorax, large pleural effusion - push away

58
Q

Pleural effusion

A

Collection of fluid within the pleural space. Limits lung expansion and may become infected

59
Q

Exudative causes

A 
Infection - pneumonia, TB
Malignancy - lung cancer, mesothelioma 
Asbestosis
Inflammation - SLE, RA, 
PE

Protein >30g/l,

60
Q

Transudative causes

A

Liver failure or nephrotic syndrome (low albumin), Heart failure or renal failure (increased hydrostatic pressure)
Meigs and hypothyroidism

Protein <30g/l, LDH<200 and fluid:serum LDH <0.6

61
Q

Lights criteria

A

pleural fluid protein: serum protein > 0.5
pleural fluid LDH: serum LDH > 0.6
cloudy, protein > 2.9g/l

62
Q

Interstitial Lung disease

A

Range of diseases which affect the lung parenchyma with cellular infiltrate of the alveoli, interstitium and distal airways

63
Q

Function of interstitium

A

Provides structure between collagen and elastin. In disease it is thickened increasing diffusion distance and reducing efficacy

64
Q

Causes of ILD

A

IPF, sarcoidosis,
drug induced - bleomycin, methotrexate,nitrofurantoin, amiodarone
Hypersensitivity pneumonitis, pneumoconiosis, TB, vasculitis
AI - SLE, RA, systemic sclerosis

65
Q

CXR ILD

A

bilateral interstilial shadowing, reticular nodular pattern, shrunken lungs

66
Q

Idiopathic pulmonary fibrosis PC

A

Chronic progressive and ultimately fatal ILD
Present in 50-60 2x more common in males
dry cough and progressive SOB

67
Q

O/E pulmonary fibrosis

A

clubbing, central cyanosis, reduced chest expansion

fine late-end bibasal inspiratory crackles

68
Q

Drug induced ILD

A

bleomycin, nitrofurantonin, amiodarone, methotrexate, sulfasalazine

69
Q

Mx IPF

A

Prognosis approx 3 years from diagnosis. Supportive care 02 to prevent pulmonary HTN. Transplant = cure

70
Q

Inv IPF

A

Crucial to exclude potentially reversible causes!!

Restrictive pattern of spirometry FEv1:FVC >70%, reduced TLCO and KCO
CXR - small lung volume, reticular shadowing at bases
HRCT = basal distribution, reticulation @ peripherys, honeycombing, bronchiestasis

71
Q

Sarcoidosis

A

Multisystem granulomatous disease characterised by formation of multiple non caesating granulomas. Granuloma = mass/nodule of chronically inflamed tissue formed by response of macrophages to confine a pathogen and prevent surrounding tissue inflammation and destruction

72
Q

Sarcoidosis epidemiology

A

20-40, 4x more common in black population, females

73
Q

PC sarcoidosis

A

fatigue, weakness, wt loss, fever, poor appetite

lungs - dry cough, SOB, bilateral hilar lymphadenopathy, bilateral dry crackles

ENT - uveitis, Sjogrens
Neuro - (rare 2%)mononeuritis multiplex, CN palsys, seziures, peripheral neuropathy, cognitive dysfunction
Cardiac (Rare 3%) - arrhythmias, HB, cardiomyopathy
Hepatomegaly, deranged LFT’s splenomegaly
Erythema nodosum, lupus pernio

74
Q

Lofgrens syndrome

A

bilateral hilar lymphadenopathy, arthralgia and erythema nodosum

75
Q

Staging of sarcoid

A

I - bilateral hilar lymphadenopathy
II - bilateral lymphadenopathy and infiltrates
III - pulmonary infiltrates only
IV - fibrosis

76
Q

Differential of bilateral hilar lymphadenopathy

A

sarcoidosis, TB, lymphoma, metastatic spread of bronchogenic cancer

77
Q

Inv sarcoidosis

A

HRCT - nodules and beading along fissures, enlarged hilar lymph nodes

normocytic anaemia high ESR
hypercalcemia due to activated macrophages hydroxylating vit D independent of PTH
high ACE

Biopsy rules out cancer shows non caesating granulomas

78
Q

Hypersensitivity pneumonitis

A

Allergic reaction affecting the small airways in response to an inhaled allergen

79
Q

PC EEA

A

Acute - 4-6hrs post exposure fever, chills, malaise, SOB, rash

Chronic insidious onset progressive SOB and cough, wt loss and fatigue, finger clubbing, inspiratory crackles

80
Q

Causes of EEA

A

Farmers lung - mouldy hay/vege
Bird fanciers - handling pigeons, cleaning lofts
Malt workers - germinating barley
Mushrooms workers, cheese washers, winemakers

81
Q

Inv and Mx EEA

A

HRCT - ground glass opacity, air trapping, reticular shadowing

Mx - avoid exposure, steroids for acute exacerbations

82
Q

Upper Zone fibrosis

A

Ank spon, TB, EEA, aspergillosis, coal workers pneumoconiosis

83
Q

Lower zone fibrosis

A

Asbestosis, sarcoidosis, IPF, RA, SLE, systemic sclerosis

84
Q

COPD define

A

Combination of emphysema and chronic bronchitis leading to irreversible obstructive airway disease characterised by FEV1:FVC <70%

85
Q

Emphysema

A

Enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of their walls without obvious fibrosis. Can lead to small airway collapse. This leads to expiratory airway limitation and gas trapping due to the loss of elastic recoil

86
Q

Chronic bronchitis

A

Chronic inflammation of the bronchioles leading to increased mucus secretion. Can be improved by stopping smoking.

87
Q

Mx of COPD

A

Crucial to stop smoking, doesnt reverse the damage but slows the rate of decline in lung function. LAMA, LABA and ICS has been shown to improve FEV1, reduce hospital admissions in those who frequently present and prevent severe exacerbations.

Pulmonary rehab has huge benefits, increasing psychological health, endurance and QoL.

CBT may be of benefit in those struggling to come to terms with diagnosis or coexisting depression/anxiety

88
Q

COPD PC

A

Smoking Hx - passive? pubs etc
Urban pollution

PC - productive cough white clear sputum, progressive SOB and wheeze. Frequent exacerbations aggravated by winter

Chronic effects = cor pulmonate, wt loss, cachexia, osteoporosis

89
Q

Alpha-1-antitrypsin

A

Inhibits proteolytic enzymes such as neutrophil elastase, in its absence destruction of alveolar capillary walls in the lung. 2% of emphysema never rule out esp if <40y/o or no smoking Hx

90
Q

O/E COPD

A

tachypnoeic, prolonged expiratory phase, global wheeze, cyanosis centrally or peripherally, accessory muscle use and pursed lip breathing,

Hyperinflation of chest, reduced chest expansion, wheeze on expiration globally

91
Q

Causes of pulmonary hypertension

A
  • Left ventricular failure (MS,AS), MI, cardiomyopathy
  • Lung disease - ILD, COPD, IPF, CF, bronchiectasis
  • Hypoventilation - obesity, OSA, neuromuscular - MND/MG
  • Pulmonary vascular disease - vasculitis, SLE, SS, idiopathic pulmonary hypertension
92
Q

Causes of pulmonary hypertension

A

1 - arterial HTN - idiopathic pul HTN, vasculitis, CTD, drug induced, portal HTN, HIV, congenital heart
2 Left ventricular failure (MS,AS), MI, cardiomyopathy, congenital
3 Lung disease - ILD, COPD, IPF, CF, bronchiectasis, OSA, hypoventilation

93
Q

Pathophysiology of pul HTN

A

2 - LV failure is due to inability of the LV to pump blood effectively to the body this leads to pooling of blood in the pulmonary vasculature causing increased resistance, pleural effusion and oedema

3 - Due to hypoxia or lung disease, hypoxia causes vasoconstriction of the pulmonary arteries. This shunting response is physiological to increase blood flow to areas of the lungs with improved ventilation. In global lung disease this leads to vasoconstriction globally,

94
Q

PC pul HTN

A

fatigue, syncope, dyspnea, angina, abdo distention.

O/E - left parasternal heave, loud p2, tricuspid regurug
RHF = oedema, hepatomegaly, ascites and JVP distention

95
Q

Mx cor pulmonale

A

In pt with RHF, pa02 <7.3 long term oxygen therapy (LTOT) is crucial to prevent hypoxia, this prevents the vasoconstriction of the capillaries and stop RV hypertrophy which will eventually degenerate in to RVF and congestive cardiac failure. Over 15hrs

96
Q

Gold standard measure of pulmonary HTN

A

RA catherisation

97
Q

Invx COPD

A

secondary polycythemia due to chronic hypoxia
ABG - resting hypoxemia,
ECG - P pulmonale evidence of RV hypertrophy
reduced TLCO, KCO and FEV1:FVC <70%

CXR - hyperinflation 6+ ant ribs, flattened diaphragm, huge bullae, signs of infective exacerbation

98
Q

ABG - pH

A

If pH is abnormal = acute problem
<7.35 = acidosis
>7.45 = alkalosis

99
Q

ABG - C02

A

If the pH is acidotic and co2 is low then the pt is hyperventilation to compensate and blow off co2. Therefore metabolic

If pH is alkotic is the CO2 indicating compensatory hypoventilation

100
Q

ABG - HCO3

A

If huge bicarb loss think acute problem i.e. burns, D/V this would causes a metabolic acidosis

101
Q

CPAP

A

Continous positive airway pressure. Helps with hypoexmia increases o2 delivery and intrathoracic pressure to reduced cardiac workload. Prevents alveolar collapse allowing co2 levels to fall.
Uses = OSA, RHF

102
Q

T1RF

A

O2 < 8. Inadequate oxygenation due lung tissue damage either V/Q mismatch or right to left shunts

  • poor o2 delivery PE, pneumonia, pul oedema,
103
Q

T2RF

A

O2 < 8 and co2 > 6

Failure of ventilation co2 begins to accumulate in the blood. Very bad sign. Causes = fatigue life threatening asthma, COPD, reduced GCS, muscle weakness - myathesina

104
Q

Respiratory acidosis

A

Due to abnormal hypoventilation leading to co2 retention

COPD, fatigued asthmatic, drug overdose = reduced GCS, neuromuscular disorders

Slow metabolic compensation by retention of bicarb

105
Q

Respiratory alkalosis

A

Excessive loss of H+ ions due to hyperventilation

aspiring overdose, anxiety attack, PE. Often tachypnoeic and stressed
Slow metabolic compensation to retain H+ and excrete Hco3

106
Q

Metabolic acidosis

A

Reduced HCO3 due to diarrhoea, DKA and strenuous activity, uremic acidosis

PC Kussmauls breathing - deep slow breathiest increase tidal volume or tachypnoea = resp compensation

Mx - IV sodium bicarbonate

107
Q

Metabolic alklosis

A

Loss of H+ due to vomiting,

PC hypoventilation to compensate, weakness, polyuria, hypocalcaemia

Mx - IV KCL

108
Q

Nocturnal hypoventilation detection

A

low 02 and high pco2 at night with transcutaneous co2 monitoring

109
Q

PC of nocturnal hypoventilation

A

somnolence - excessive daytime sleepiness, fatigue
morning headache due to co2 retention
SOB on exertion, orthopnea, anxiety, poor appetite

110
Q

Causes of hypoventilation

A

COPD, OSA, chest wall deformity, muscle disease

111
Q

Inv hypoventilation

A

overnight transcutaneous co2 and o2 monitoring
venous bicarbonate
sleep studies

112
Q

OSA

A

Recurrent nocturnal upper airway obstruction causing repetitive incidence of aponea during sleep. Due to reduced tone in pharyngeal muscles leading to collapse of airway. Reduction in REM sleep due to multiple awakenings

113
Q

Risk factors for OSA

A

Obesity, DM/HTN, COPD, increasing age, tonsilar hypertrophy nasal polyps, acromegaly
respiratory depressive drugs - alcohol, opioids

114
Q

PC OSA

A

loud snoring, daytime sleepiness, restless/unfreshed sleep, morning headache due to co2 retention over night

115
Q

O/E OSA

A

large collar size, enlarged adenoids, nasal polyps, acromegaly

116
Q

Inv OSA

A

Epworth sleepiness score

diagnostic - polysomnogram showing cyclical patterns of obstruction and breathing

117
Q

Mx OSA

A

reduce wt and alcohol, stop medications, tonsillectomy
CPAP
Inform DVLA!

118
Q

DMD and hypoventilation

A

Most common hereditary disorder causing resp failure.. X-linked needs NIV

119
Q

Bronchiestasis

A

Abnormal and permanent dilation of the airways. Characterised by recurrent infection and damage leading to impaired mucocilary clearance and persistent inflammation

120
Q

PC and O/E bronchiestasis

A

Persistant wet cough, large amounts of purulent sputum, SOB and haemoptysis . O/E = clubbing and coarse crackles

121
Q

Causes of bronchiestasis

A

TB, sarcoidosis, CF, post infective brochial damage - bacterial/viral pneumonia, measles etc, immune deficiency

122
Q

NIV

A 
Positive pressure (non-cyclical)
continusous positive airway pressure (CPAP)
used for acute pulmonary edema, asthma, obstructive sleep apnoea (OSA)

Positive pressure (cyclical)
Bilevel positive airway pressure (BIPAP), inspiratory positive airway pressure (IPAP), pressure support ventilation (PSV) and positive pressure ventilation (PPV)
used for COPD, weaning, asthma, neuromuscular disease

123
Q

CI NIV

A

Cardiac / respiratory arrest
Inability to protect airway – poor cough, excessive/ inability to clear secretions, decreased conscious state/ coma
upper airway obstruction
untreated pneumothorax
marked haemodynamic instability (e.g. shock, ventricular dysrhythmias, severe acute myocardial ischaemia GI bleeding)
Following upper GI surgery (some debate about this)
Maxillofacial surgery
base of skull fracture (risk of pneumocephalus)
patient refusal
staff inexperience
Intractable vomiting

CSIM (12 decks)

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