Brainscape's Knowledge GenomeTM

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


See full index

PACES > Respiratory > Flashcards

Respiratory Flashcards

1
Q

VATS indications?

A

Wedge resection, segmentectomy, lobectomy, decortication, pleurectomy, bullectomy, treatment of recurrent pneumothoraces, biopsy

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

Advantage of VATS over open thoracotomy?

A

Less invasive so reduced pain, wound complications, healing time, length of stay

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

Indications for lobectomy? (Ox)

Indications for pneumonectomy? (Ox)

A

Malignancy (NSCLC), bronchiectasis with uncontrolled symptoms, TB, CF, lung abscess

Malignancy, bronchiectasis, TB

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

Investigate lung Ca?*

A

History, examination, bloods (raised platelets, Ca, anaemia)

Diagnose mass:
-Chest x-ray (collapse, mass, pleural effusion, hilar lymphadenopathy, bone erosion)
-CT thorax with contrast

Pleural fluid
Exudative, low pH, low glucose, raised amylase, cytology

Determine cell type:
-Tissue diagnosis (biopsy by bronchoscopy +/- EBUS if central lesion or CT guided percutaneous needle biopsy if peripheral)
-Induced sputum cytology (good yield for endobronchial tumours e.g. SCLC and squamous, not for peripheral e.g. adenocarcinoma)

-Staging CT (including lower neck, liver, adrenals)/PET (for potentially curative disease, better at assessing mediastinal nodal mets)
-NSCLC: TNM staging to assess operability
-SCLC: has TNM staging now

-Brain imaging depending on symptoms and stage
-Bone scan if bone mets suspected

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

How to work up patient for surgery for lung Ca?

A

FEV1 (FEV1 >1.5 for lobectomy, FEV1 >2 for pneumonectomy = operable)

If uncertainty around operability, full PFTs and transfer factor

If risk still uncertain, exercise testing (VO2max >15ml/kg/min

Sometimes an echo
Smoking cessation

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

Lung Ca histological subtypes?*

A

SCLC (24%) NSCLC (adenocarcinoma, squamous, alveolar, large cell)

N.B. SCLC and squamous have strongest correlation with smoking

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

Treatment options for lung Ca?*

A

MDT and smoking cessation

SCLC (rapidly progressive so often diagnosed late so surgery not often an option unless very early)

Most with limited disease receive chemoradiotherapy, benefit with 6 courses chemotherapy

Patients with more extensive disease are offered palliative chemotherapy

NSCLC curative surgery in 20%, curative or palliative radiotherapy (single fractionation versus hyper-fractionation), chemotherapy benefit unknown but if eGFR positive for erlotinib

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

What is the TNM classification?*

Versus staging system?*

A

Classification system which takes into account:
Degree of spread of primary tumour T
LN involvement N
Presence of metastases M

Stage I confined to lung
Stage II and III confined to chest
Stage IV spread beyond the chest

Highlights candidates suitable for resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors for lung Ca? (Ox)

A

Smoking
ILD
Radon
Asbestos
Arsenic
Chronium
Iron oxide
Coal tar
Radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Prognosis of lung Ca?*

A

SEER predicts 5-year survival SCLC 6%, NSCLC 24%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Complications of lung Ca?*

A

SVC obstruction

Recurrent laryngeal nerve palsy

Horner’s signs and wasted small muscles hand (if Pancoast’s)

Endocrine: SIADH (SCLC), Cushing’s (SCLC, ACTH), hypercalcaemia (NSCLC, PTHRP), gynaecomastia (ectopic beta-HCG)

Neurological: LEMS, subacute cerebellar degeneration, sensory neuropathy

Dermatological: dermatomyositis, clubbing, acanthosis nigricans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Palliative care in lung Ca?*

A

Brain metastasis: dexathametasone and radiotherapy

SVCO: dexamethasone and radiotherapy/stent

Haemoptysis, bone pain, cough: radiotherapy

Effusion: talc pleurodesis

Cough and pain: opiates

Analgesia, antidepressants, anxiolytics

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

Signs of lung Ca on examination?

A

Cachexia

Clubbing
Tar staining
Wasting small muscles hand
Hypertrophic pulmonary osteoarthropathy

Hoarse voice
Horner’s syndrome if apical/Pancoast signs
SVCO signs

Palpable LNs

Radiotherapy tattoo
VATS scar
IC drain scar
Thoracotomy scar
Signs of collapse/pleural effusion
Localised wheeze with tumour causing obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Difference in clinical findings for lobectomy versus pneumonectomy? (N.B. Thoracotomy scar looks same)

A

Both:
Reduced expansion
Thoracotomy scar

Lobectomy:
-Central trachea
-Reduced breath sounds
-Lower dull percussion note over LZ with absent breath sounds
-Upper may be normal examination, may be hyper-resonant over UZ, may be dull percussion at base where hemi-diaphragm elevated

Pneumonectomy:
-Grossly deviated
-Absent breath sounds
-Dull percussion throughout
-Bronchial breathing in UZ, reduced breath sounds throughout remainder of hemithorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Respiratory causes clubbing?

A

ILD

Chronic suppurative lung disease (CF, bronchiectasis)

Lung Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Indications for double lung transplant?*

A

Wet lung conditions:
CF
Bronchiectasis
Pulmonary hypertension

N.B. Better survival than single transplant

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

Indications for single lung transplant?*

A

Dry lung conditions:
COPD
Pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Indications for lung transplant? (JHLT)

A

Lung transplantation should be considered for adults with chronic,
end-stage lung disease who meet all the following general
criteria:
1. High (>50%) risk of death from lung disease within 2 years if
lung transplantation is not performed
2. High (>80%) likelihood of 5-year post-transplant survival
from a general medical perspective provided that there is
adequate graft function

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

Complications of lung transplant?

A

Primary graft dysfunction

Chronic rejection (due to BOS)

Infection (bacterial, mycobacterial, fungal, viral)

Malignancy (post-transplant lymphoproliferative disease, skin cancer)

Steroid side effects: Cushing’s, skin thinning, diabetes
Tacrolimus: tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CI to lung transplant? (JHLT)

A

-Lack of patient willingness
-Malignancy with high risk of recurrence or death
-eGFR <40
-Recent ACS/stroke
-Liver cirrhosis with portal hypertension or synthetic dysfunction
-Acute liver failure, renal failure or active extra-pulmonary infection
-Limited functional status or progressive cognitive impairment
-Active substance use including smoking

Relative contraindications:
-Chronic infection e.g. with M. abscessus
-Obesity BMI >35
-Age >65

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

How would you investigate a patient with possible pulmonary fibrosis?*

A

History (occupational, environmental, drug, systems review for CTD)

Bloods (including ESR, RF, ANA, rheumatoid factor, consider ACE and ANCA) and urine dip

ECG ?PH

CXR (reticulonodular changes, loss of definition of either heart border, small lungs)

ABG (T1RF)

PFTs (FEV1/FBC >0.8, low TLC and reduced TLCO and KCO) and 6 minute walk test

HRCT (bi-basal subpleural honeycombing typical of UIP, widespread ground-glass shadowing more likely NSIP which is often associated with AI disease, if apical think sarcoidosis, ABPA, old TB, hypersensitivity pneumonitis)

Consider bronchoalveolar lavage (exclude infection prior to any immunosuppressants, if lymphocytes > neutrophils indicates better response to steroids ad better prognosis)

Echo (pulmonary hypertension)

Occasionally lung biopsy if diagnostic uncertainty (though morbidity 7%)

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

Treatment of ILD? (BTS)

A

-Smoking cessation
-Discontinue toxic medications
-Treatment of infections

-Immunosuppression if likely to be inflammatory e.g. steroids
-Referral to ILD service for consideration of an antifibrotic agent if FEV1 50-80%

-Pulmonary rehabilitation
-Consider LTOT

-Single lung transplant

-Symptom control e.g. opiates
-Occupational theapy
-Palliative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Prognosis of ILD?*

A

Variable as depends of aetiology

Highly cellular with ground-glass infiltrate responds to immunosuppression 80% 5-year survival

Honeycombing on CT no response to immunosuppression 80% 5 year mortality

Increased risk of bronchogenic carcinoma

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

Causes of basal fibrosis?*

A

CAID:

Connective tissue diseases (e.g. scleroderma which tends to cause more NSIP) and autoimmune disease (RA which tends to cause more UIP)

Asbestosis/Aspiration (right main bronchus is shorter, wider and straighter so foreign bodies more likely to enter)

IPF causing UIP

Not in textbook but:
Drugs (methotrexate, bleomycin, nitrofurantoin, amiodarone)

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

Causes of apical fibrosis?*

A

TRASH:

TB
Radiation
Ankylosing spondylitis/ABPA
Sarcoidosis/Silicosis/Berrylliosis
Hypersensitivity pneumonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of ILD?*

A

-Respiratory failure
-Pneumonia
-Pulmonary hypertension and cor pulmonale
-Lung Ca

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

Rheumatoid lung manifestations?

A

PPPPBBCCI

-Pulmonary fibrosis (UIP more common, trials using anti-fibrotics used in IPF)
-Pulmonary nodules
-Pleural effusion (exudate)
-Pleurisy

-Bronchiolitis obliterans (obstructive pattern on spirometry
centrilobular nodules, bronchial wall thickening)
-Bronchiectasis

-Complications of drug therapy e.g. methotrexate pneumonitis
-Caplan’s syndrome (massive fibrotic nodules with occupational coal dust exposure)

-Infection (possibly atypical) secondary to immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is COPD?

A

Progressive and irreversible airflow obstruction due to chronic bronchitis (clinical diagnosis) or emphysema (pathological diagnosis, enlargement of distal air spaces air spaces and destruction of their walls)

Results from imbalance between protease and anti-protease activity, triggered by smoking

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

Causes of COPD?*

A

Environmental: smoking and industrial dust exposure

Genetic: alpha-1 antitrypsin deficiency (deficiency in enzyme which inhibits neutrophil elastases, different phenotypes with ZZ most severe)

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

Investigations for ?COPD?*

A

Bloods (WCC, Hb for secondary polycythaemia, alpha-1 antitrypsin, albumin)

ABG (type II respiratory failure)

Sputum culture

CXR (hyper-expanded with flattened hemidiaphragms, bullae, prominent pulmonary vasculature, pneumothorax)

ECG RVH +/- strain and MAT

Spirometry (obstructive) and gas transfer (low TLCO)

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

How to manage COPD? (BMJ)

A

According to GOLD classification of severity:
-Mild GOLD A: short or long-acting bronchodilator
-Moderate GOLD B: LABA/LAMA
-Severe GOLD E: LABA/LAMA (plus ICS if eosinophils over 300)

Consider mucolytic, theophylline, roflumilast or azithromycin under specialist guidance

Also:
-Smoking cessation single most beneficial management strategy
(cessation clinics and NRT)
-Pulmonary rehabilitation
-Consider LTOT or LTNIV
-Vaccinations
-Exercise, education, psychological support, nutrition
-Palliative care involvement

Surgical treatment:
-Bullectomy if occupying at least 30% of the hemithorax
-Lung reduction surgery
-Endobronchial valve insertion
-Single lung transplant

32
Q

How to manage AECOPD?

A

To treat acute exacerbation:
-Controlled oxygen
-Bronchodilators
-Antibiotics
-Steroids
-NIV/IMV

33
Q

Prognosis in COPD?*

A

Acute exacerbation have 15% mortality

34
Q

Differential of wheezy chest?*

A

COPD
Asthma
Pulmonary oedema
Bronchiectasis
—

GPA (OB)
RA (OB)
Post-lung transplant (OB)

35
Q

Criteria for LTOT?*

A

-Non-smoker (carboxyhaemoglobin <3%)
-PaO2 <7.3 RA
-PaCO2 which doesn’t rise excessively on oxygen

-If evidence of cor pulmonale PaO2 <8.0

-2-4L/min via NC for at least 15 hours/day

-Improves average survival by 9 months

36
Q

COPD severity?

A

GOLD criteria, based on FEV1:
>80% mild
50-80% moderate
30-50% severe
<30% very severe

37
Q

What is cor pulmonale? Treatment?

A

1) Chronic hypoxia
2) Hypoxic vasocontriction
3) Pulmonary hypertension
4) Right-heart failure

Treatment:
LTOT
Diuretics

38
Q

How would you investigate a possible bronchiectasis patient?*

A

-Bloods
-Sputum culture and cytology
-CXR (tramlines and ring shadows)
-HRCT (‘signet ring sign’ which is thickened dilated bronchi larger than adjacent vascular bundle)

-Immunoglobulins IgG and IgA (hypogammaglobulinaemia)
-Aspergillus RAST or skin prick testing (ABPA if bronchiectasis affects upper lobe)
-Rheumatoid serology
-Nasal nitric oxide (PCD)
-Sweat chloride test or genetic screening (CF)
-History of IBD?
-Alpha-1 antitrypsin

N.B. PFTs may be normal or may be obstructive (if airway obstruction due to secretions or co-existent obstructive airways disease)

39
Q

Causes of bronchiectasis?*

A

-Congenital (Kartagener’s and CF)
-Childhood infection (measles, pertussis and TB)
-Immune overactivity (ABPA, IBD-associated, rheumatoid lung)
-Immune underactivity (hypogammaglobulinaemia, CVID)
-Aspiration if localised to RLL (alcoholics, post-stroke)

40
Q

Treatment of bronchiectasis?*

A

MDT management:
-Chest physiotherapy
-Smoking cessation
-Nutrition and exercise
-Immunisations (and confirm immunity)

-Prompt antibiotic therapy for exacerbations
-Long-term treatment with low-dose azithromcyin three x/week
-Pseudomonas eradication if isolated

-Bronchodilators/ICS if any airflow obstruction
-Mucoactive agents e.g. nebulised saline

Consider LTOT

-Surgical resection if localised disease
-Bronchial artery embolisation if massive haemoptysis

41
Q

Complications of bronchiectasis?*

A

-Respiratory failure
-Pneumonia and empyema
-Collapse
-Pulmonary hypertension and cor pulmonale
-Secondary amyloidosis
-Massive haemoptysis (mycotic aneurysm)

42
Q

Pathophysiology of bronchiectasis?*

A

Bronchial wall dilatation, destruction and transmural inflammation

Caused by destruction of muscular and elastic components of bronchial walls

Causes impaired clearance of secretions causes colonisation and infections

43
Q

Most common respiratory pathogens in bronchiectasis?*

A

Staphylococcus aureus
H. influenza
Pseudomonas

44
Q

What historical techniques were use to treat TB?*

A

Plombage (polystyrene balls into thoracic cavity)
Phrenic nerve crush
Thoracoplasty (rib removal, lung not resected)
Apical lobectomy
Streptomycin introduced in 1950s

45
Q

Side effects of TB treatments?*

A

Rifampicin: hepatitis and increased metabolism of COCP
Isoniazid: peripheral neuopathy (Rx pyridoxine) and hepatitis
Pyrazinamide: hepatitis
E: retrobulbar neuritis and hepatitis

46
Q

Causes of pleural effusion?*

A

Transudate (<30):
-CCF
-Chronic renal failure
-Chronic liver failure
-Hypothyroidism
-Hypoalbuminaemia (and nephrotic syndrome)
-Peritoneal dialysis

Exudate (>30 protein):
-Neoplasm (primary or secondary)
-Infection (pneumonia and TB)
-Infarction
-Inflammation (RA and SLE)
-Pancreatitis
-Yellow nail syndrome

47
Q

How would you investigate a possible pleural effusion?*

A

Bloods (FBC, U+Es, LFTs, protein and albumin, LDH, BNP, amylase, TFTs, RF, autoimmune profile)
ABG if hypoxic
CXR
Pleural tap (protein, LDH, glucose, pH, amylase, cholesterol, cytology, microscopy and culture, ZN staining, RF)

In addition:
CT chest, biopsy, bronchoscopy (lung malignancy)
CT-PA (if PE suspected)
Echo (CCF)
CT-AP (malignancy)

Light’s criteria (exudate if one or more present):
-Pleural fluid protein divided by serum protein >0.5
-Pleural fluid LDH divided by serum LDH >0.6
-Pleural fluid LDH more than two-thirds the upper limits of
normal serum LDH

Empyema if pH <7.2, exudate and low glucose

48
Q

Differential diagnosis of dullness to percussion?*

A

Pleural effusion
Pleural thickening
Collapse
Consolidation
Raised hemidiaphragm
Lower lobe lobectomy

49
Q

How to treat a pleural effusion?*

A

Pleural drainage
If recurrent consider pleurodesis, pleuro-peritoneal ‘window’, VATS pleurectomy/decortication

Empyema: IV antibiotics and intrapleural DNase plus tPA
Mesothelioma: surgery and chemotherapy, although treatment response is often poor

50
Q

Complications of pleural fluid drainage?*

A

Infection
Bleeding
Pneumothorax
Re-expansion pulmonary oedema
Tube blocks or falls out

51
Q

What is an empyema?*

A

Collection of pus within the pleural space
Most frequent organisms anaerobes, staphylococci and gram negative organisms
Associated with bronchial obstruction e.g. carcinoma, recurrent aspiration, poor dentition and alcohol dependence

52
Q

What is a mesothelioma?*

A

Tumour affecting the pleura
Associated with asbestos exposure in 80% of cases, pleural plaques on CXR and effusions

53
Q

What is CF?*

A

Autosomal recessive condition affecting 1/2500 live births
It involves chromosome 7q, and affects he gene which encodes the CFTR Cl- channel

Secretions are thickened and block the lumens of various structures:

Bronchioles (bronchiectasis)
Pancreatic ducts (loss of exocrine and endocrine function)
Gut (distal intestinal obstruction syndrome)
Seminal vesicles and fallopian tubes (infertility)

54
Q

How would you investigate a ?CF patient?*

A

Screen at heel prick test at birth (low immunoreactive trypsin)
Sweat test (Na >60 with false positive in hypothyroidism and Addison’s)
Genetic screening

55
Q

Treatment for a patient with CF?*

A

Chest physiotherapy (postural drainage and active cycle breathing techniques)
Mucolytics e.g. DNase
Prompt antibiotics for infections
Pancreatic enzymes and fat-soluble vitamin supplements
Immunisations

CFTR modulators if suitable CFTR mutations:
Improve production and function of the receptor
Improves intracellular trafficking of receptor to cell membrane

Double lung transplant (50% survival at 5 years)

Gene therapy is under development

56
Q

Prognosis of CF?*

A

Medial survival is 40 years but rising

Poor prognosis if becomes infected with Cepacia

57
Q

How would you investigate a ?pneumonia?*

A

Bloods (WCC, CRP, urea)

Blood culture
Sputum culture
Urine for atypical screen (and haemoglobinuria as mycoplasma causes haemolysis)
Respiratory viral swabs

CXR consolidation, abscess and effusion

58
Q

Common organisms in CAP?*

A

Streptococcus pneumoniae 50%
Mycoplasma pneumoniae 6%
Haemophilus influenzae (especially in COPD)

59
Q

How to treat CAP?*

A

CURB-65

Antibiotics
(Note cover for Staph. aureus if post-influenza, anaerobes if aspiration, fungal/PCP/CMV if immunocompromised)

Vaccinations to at-risk groups
Smoking cessation

60
Q

Complications of CAP?*

A

Lung abscess
Para-pneumonic effusion or empyema
Haemoptysis
Septic shock and multi-organ failure

61
Q

How to investigate someone with possible PH?*

A

Echo (RV size and function, TR velocity to estimate PASP)

Bloods (autoimmune screen for scleroderma and SLE, TFTs for hyperthyroidism, LFTs for porto-pulmonary PH)

CT-PA for proximal chronic thrombi but also parenchymal lung disease

PFTs for underlying lung disease (ILD versus COPD)

Right heart catheter to confirm raised pulmonary pressures plus estimation of LA pressures (wedge pressure)

62
Q

WHO classification of group 5?*

A

Group 1: PAH (idiopathic, heritable, drugs (amphetamines), connective tissue)
Group 2: left heart disease
Group 3: lung disease
Group 4: chronic thromboembolic disease
Group 5: miscellaneous (thyrotoxicosis, long-term HD)

63
Q

How do we treat PH?*

A

Group 1: phosphodiesterase 5 inhibitors (sildenafil), endothelin receptor antagonists (ambrisentan), prostacyclin analogues (iloprost), double lung transplant

Group 4: lifelong anticoagulation, pulmonary endarterectomy (if proximal), balloon pulmonary angioplasty (if distal)

Groups 2, 3 and most of 5: treat the underlying cause

64
Q

Complications of PH?*

A

Death from right heart failure

Atrial arrhythmias

Dilation of proximal pulmonary artery (stretching of recurrent laryngeal nerve, external compression of LAD causing angina-like CP, external compression of right middle lobe bronchus causing localised bronchiectasis)

65
Q

TB?

A
66
Q

Pneumothorax?

A
67
Q

Consolidation? In addition to pneumonia bits above.

A
68
Q

Collapse?

A
69
Q

SVC obstruction?

A
70
Q

Stridor?

A
71
Q

Signs of pulmonary hypertension?

A
72
Q

Yellow nail syndrome signs?

A

Thickened, dystrophic or discoloured nails

Bronchiectasis and/or pleural effusion

Lymphoedema

73
Q

Investigations for asthma?

A

-History
-Bloods (FBC U+Es CRP IgE eosinophils)
-CXR
-Peak expiratory flow diary (reduced in early mornings, >20% variability)
-Spirometry (obstructive, BDR improvement in FEV₁ of 12% or more in response to beta agonists and increase in volume of 200 mL)

-Allergy testing
-FeNO (increased)
-Consider referral for bronchial challenge

-ABG if hypoxic in acute setting

74
Q

Treatment for asthma?

A

Education and environmental control
Smoking cessation

Stepwise approach:
1) SABA
2) Add-on ICS
3) Add-on ICS plus LABA +/- montelukast

Then referral to specialist (consideration of add-on LAMA, theophylline, oral steroids or biologics)

75
Q
A

PACES (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions