respiratory 2 Flashcards
1
Q
what are the different classifications of pneumonia?
A
If the pneumonia developed outside of hospital it is labeled labelled “community acquired pneumonia”. If it develops more than 48h after hospital admission it is labelled “hospital acquired pneumonia”. If it develops as a result of aspiration, meaning after inhaling foreign material such as food, then it is labelled “aspiration pneumonia”
2
Q
how does pneumonia present?
A
presentation: Shortness of breath Cough productive of sputum Fever Haemoptysis (coughing up blood) Pleuritic chest pain (sharp chest pain worse on inspiration) Delirium (acute confusion associated with infection) Sepsis
Signs - deranged basic observations - they may indicate sepsis secondary to pneumonia
Tachypnoea, Tachycardia, Hypoxia, Hypotension, Fever, Confusion
3
Q
what are the three characteristic chest signs of pneumonia?
A
- Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by consolidation of the lung tissue around the airway.
- Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.
- Dullness to percussion due to lung tissue collapse and/or consolidation.
4
Q
how is the severity of pneumonia assessed?
A
NICE recommend using the scoring system CRB-65 out of hospital and CURB-65 in hospital. The only difference is that out of hospital you do not count urea.
When you see someone out of hospital with a CRB-65 score of anything other than 0 NICE suggest considering referring to the hospital.
C – Confusion (new disorientation in person, place or time)
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65
The CURB 65 score predicts mortality (score 1 = under 5%, score 3 = 15%, score 4/5 = over 25%). The scoring system is there to help guide whether to admit the patient to hospital:
Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment
5
Q
what are the common causes of CAP?
A
streptococcus pneumoniae - aka pneumococcus
also haemophilus influenza
6
Q
what are the common causes of HAP?
A
gram negative bacilli, staph aureus
7
Q
what is the most common cause of pneumonia in those with COPD?
A
H.influenzae
8
Q
who is moraxella catarrhalis pneumonia common in?
A
Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease
9
Q
what is a common cause of pneumonia in those with cystic fibrosis?
A
pseudomonas aeruginosa
staph aureus
10
Q
what is atypical pneumonia ?
A
The definition of atypical pneumonia is pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain. They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).
11
Q
what are the different types of atypical pneumonia?
A
- Legionella pneumophila
- mycoplasma pneumoniae
- chlamydophila pneumoniae
- coxiella brunettii - aka Q fever
- chlamidya psittaci
12
Q
how does legionella pneumonia present?
A
Legionella pneumophila (Legionnaires’ disease). This is typically caused by infected water supplies or air conditioning units. It can cause hyponatraemia (low sodium) by causing an SIADH. The typical exam patient has recently had a cheap hotel holiday and presents with hyponatraemia.
13
Q
how does mycoplasma pneumoniae present?
A
This causes a milder pneumonia and can cause a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient in the exams.
14
Q
how does chlamydophila pneumoniae present?
A
Chlamydophila pneumoniae. The presentation might be a school aged child with a mild to moderate chronic pneumonia and wheeze. Be cautious though as this presentation is very common without chlamydophilia pneumoniae infection.
15
Q
how does coxiella burnetii present?
A
Coxiella burnetii AKA “Q fever”. This is linked to exposure to animals and their bodily fluids. The MCQ patient is a farmer with a flu like illness.
16
Q
how does chlamydia psittaci present?
A
Chlamydia psittaci. This is typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.
17
Q
what is a common cause of fungal pneumonia?
A
Pneumocystis jiroveci (PCP) pneumonia occurs in patients that are immunocompromised. It is particularly important in patients with poorly controlled or new HIV with a low CD4 count. It usually presents subtly with a dry cough without sputum, shortness of breath on exertion and night sweats. Treatment is with co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”. Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.
18
Q
what is a common cause of pneumonia in alcoholics?
A
klebsiella pneumoniae
this is also seen often in diabetics
and commonly causes lung abscess formation and empyema
19
Q
what investigations would you perform for pneumonia?
A
CXR - will show a new shadowing (consolidation)
FBC - raised WCC
U&E’s - for urea - assess for severity of disease
CRP - for inflammation and infection
ABG
in patients with moderate/severe:
sputum cultures
blood cultures
legionella and pneumococcal urinary antigens
20
Q
how is CAP managed?
A
low severity
1st line - amoxicillin (if allergic to penicillin use either a macrolide (clarithromycin) or tetracycline (doxycycline) - give Abx for 5 days
high severity
dual antibiotic therapy is recommended with amoxicillin and a macrolide
21
Q
what are the complication of pneumonia?
A
sepsis pleural effusion empyema lung abscess death
22
Q
how is HAP managed?
A
within 5 days of admission: co-amoxiclav or cefuroxime
more than 5 days after admission: piperacillin with tazobactam or a broad spectrum caphalosporin e,g, ceftazidime or a quinolone e.g. ciprofloxacin
23
Q
where is the most common place of lung cancer?
A
95% are carcinoma of the bronchus
2% are alveolar tumours
24
Q
what can cause secondary lung cancer?
A
breast kidney uterus ovary testes thyroid
25
what are some causes of lung cancers?
```
smoking - causes 90%
urban living opposed to rural
passive smoking
asbestos (will cause mesothelioma)
arsenic
iron oxide
chromium
petroleum products
oil
radiation
scarring e.g. post TB
```
*tumours associated with occupational factors tend to be adenocarcinomas
26
what are the different types of lung cancer?
small cell lung cancer - around 15-20% of cases - generally carry a worse prognosis. Usually found around the hilum/central. SCLC cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.
non small cell lung cancer
- squamous cell carcinoma - 35%
- adenocarcinoma - 25%
- large cell - 10-15%
- alveolar cell carcinoma - not smoking related, lots of sputum
- bronchial adenoma - mostly carcinoid
27
how does a squamous cell carcinoma of the lung usually present?
- usually presents as obstructive lesions of the bronchus leading to infection
- occasionally they will cavitate - this will occur when the central part of the tumour undergoes necrosis - on x-ray this may look like and abscess, or a TB cavity, but on a CT, you will clearly be able to see the jaggered edge of the cavity.
- local spread is common, but mets are normally late - but frequent
- often will cause hypercalcaemia - by bone destruction or production of PTH analogues
- there may be hyperthyroidism due to ectopic TSH
28
what are the features of a lung adenocarcinoma?
Arises from mucous cells in the bronchial epithelium
Commonly invades the mediastinal lymph nodes and the pleura, and spreads to the brain and bones
Does not usually cavitate
Can cause excessive mucous secretion
Proportionally more common in non-smokers, women and in the Far East
i.e. these are the least likely to be related to smoking
May sometimes be confused with mesothelioma
Most likely to cause pleural effusion (as are mesotheliomas)
there may be gynaecomastia
there may be hypertrophic pulmonary osteoarthropathy
29
what are the features of large cell carcinomas?
These are basically just less well differentiated versions of adenocarcinomas and squamous cell carcinoma – i.e. squamous cell and adenocarcinomas have a longer time to develop before presentation, they will present as large cell carcinomas.
They metastasise early
Associated with poor prognosis
they may secrete B-HCG
30
what are the features of bronchoalveolar carcinoma?
These are very rare
It is a variation of adenocarcinoma
they account for 1-2% of all lung carcinoma
they will present as a single nodule, or many small nodular lesions
occasionally they cause production of huge amounts of mucous (which will be coughed up as sputum)
may appear like consolidation on the CXR
Causes ‘bronchorrhoea’ – diarrhoea of the bronchus – produces huge amounts of white sputum!
31
what are the features of a small cell lung cancer?
they arise from endocrine cells - kulchitsky cells - these are ADPU cells and as a result these tumours will secrete many poly-peptides.
some of these poly-peptides will cause auto-feedack and induce further cell growth.
they are associated with ectopic ADH and ACTH secretion
so they can presentations such as addisons and cushings (ACTH - won't be typical cushing, hypertensions, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than a buffalo hump) and hyponatraemia (ADH), lambert-eaton syndrome
almost always inoperable at presentation - they do respond to chemo but prognosis is generally poor.
32
what are ADPU cells?
Amine - high amine content
Precursor Uptake - high uptake of amine precursors
Decarboxylase - high content of the enzyme decarboxylase
APUD cells – there are two types:
Open – secrete products in response to luminal contents, as well as nervous and hormonal stimuli
Closed – have no luminal receptors, and just respond to nervous and hormonal stimuli.
33
where may lung tumour spread?
pleura
chest wall
sympathetic ganglion
nodal spread - supraclavicular and mediastinal lymph nodes
blood borne spread - mets to the liver, bone, adrenal glands, skin, brain
34
what can happen when a lung cancer spreads to the chest wall?
when it spreads to chest wall there can be damage to intercostal nerves or brachial plexus
the sympathetic ganglion may also be involved
** the primary tumour, or lymph node mets can spread to the mediastinum and invade or compress the heart, oesophagus, SVC, trachea and phrenic (will cause diaphragm weakness and presents with SOB) or left recurrent laryngeal nerves (presents with hoarse voice)
35
what happens when lung tumour damages the brachial plexus?
this is caused by tumours in apex of the lung - superior sulcus tumours, they can affect the lower part of the brachial plexus - C8, T1 and T2 which will cause severe pain in the shoulder and down the inner surface of the arm. There is also weakness of the hand. This is known as Pancoast's tumour - the pain is known as Pancoast's syndrome.
36
what happens if a lung tumour damages the sympathetic ganglion?
if the sympathetic ganglion is damaged it can result in Horner's syndrome.
Horner's syndrome is a result from damage to the sympathetic nervous system.
clinical features of Horner's syndrome include a drooping eyelid - ptosis, resulting from improper innervation of the superior tarsal muscle - ptosis, miosis and dilation lag
there may be anhydrosis (decreased sweating) and enopthalmosis (an impression that the eye has sunk in)
37
what can happen if lung tumour compress the SVC?
early morning headache
oedema of the upper limbs
facial congestion and distension of the jugular vein and veins on the chest
38
what are the endocrine complications of lung cancer?
usually caused by SCLC
Inappropriate ADH secretion – this can cause hyponatreamia – be careful! – this hyponatraemia is not caused by lack of sodium – but by ‘dilation’ of body fluids, due to excess secretion of ADH – not enough water is being secreted.
So by denying the patient fluids, you can bring the sodium back to normal!
Ectopic ACTH secretion – causing Cushing’s syndrome – will produce symptoms similar to those on steroids – and these patients (unlike those just on steroids) will be very heavily pigmented.
Hypercalcemia – due to the secretion of parathyroid hormone related peptides (PTH). This mostly occurs with squamous cell cancer.
39
what is the definition of para-neoplastic syndrome?
The definition of a paraneoplastic syndrome is a non-endocrine, non-metastatic complication.
they are general quite rare
40
what are some para-neoplastic syndromes associated with lung cancer?
Neurological complications
- polyneuropathy - caused by antibodies against the myelin sheath, the damage is irreversible. It can present with virtually any neurological symptom
- Cerebella degeneration - and other encephalopathies
- Lambert-eaton syndrome - essentially MG secondary to lung carcinoma
Vascular and haematological complications
- thrombophlebitis migrans
- anaemia - can be microcytic or normocytic
HPOA - hypertrophic pulmonary osteoarthropathy
- this occurs in 3% of cases (mostly small cell and adenoma). There will be joint stiffness, and severe pain in the wrists and ankles, sometimes also gynaecomastia. On x-ray there will be proliferative periostitis at the ends of the long bones, which have an ‘onion skin’ appearance. This is also associated with finger clubbing where cancer is the cause. It is thought to be caused by a blood borne factor released by the tumour – when patients have the primary tumour removed the pain goes away!
Finger clubbing - caused by NSCLC
Carcinoid syndrome - presents with hepatomegaly, flushing and diarrhoea
41
what is Lambert-Eaton myasthenic syndrome?
Lambert-Eaton myasthenic syndrome is a result of antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones. This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). This weakness gets worse with prolonged used of the muscles.
This syndrome has similar symptoms to myasthenia gravis although the symptoms tend to be more insidious and less pronounced in Lambert-Eaton syndrome. In older smokers with symptoms of Lambert-Eaton syndrome consider small cell lung cancer.
42
what is mesothelioma?
Mesothelioma is a lung malignancy affecting the mesothelial cells of the pleura. It is strongly linked to asbestos inhalation. There is a huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years. The prognosis is very poor. Chemotherapy can improve survival but it is essentially palliative.
43
how does lung cancer present?
```
cough
chest pain
haemoptysis
chest infections - recurrent pneumonia
malaise
weight loss
SOB
hoarseness
weight loss
lymphadenopathy
```
44
what might you find on examination of someone with lung cancer?
there may be absent breath sounds and dullness to percussion at the lung base
involvement of the pleura may cause a pleural rub and signs of pleural effusion
45
what investigations would you perform for lung cancer?
CXR - is the 1st line investigation
staging CT scan of chest, abdomen and pelvis - should be contrast enhanced
PET-CT - useful for staging
Bronchoscopy with endobronchial ultrasound - useful to obtain cytology and biopsy
Histology of a biopsy
46
what on a CXR is suggestive of lung cancer?
Hilar enlargement
peripheral opacity - a visible lesion in the lung field
pleural effusion - usually unilateral in cancer
collapse
47
how is lung cancer staged?
NSCLC - TNM staging
SCLC - limited or extensive
Limited – confined to one lung/hemithorax. May have spread to lymph nodes on the same side
Extensive – distant metastasis, may have spread liver, bones, adrenals, brain, skin
48
what is the life expectancy of lung cancer?
small cell lung cancer
Limited disease – life expectancy average is around 3 months from presentation. With chemotherapy, this may be up to 1 year.
Extensive disease – life expectancy average around 1 month at presentation. With chemotherapy can improve to around 8 months. The 5-year survival is 5%
90% of SCC will respond to chemotherapy. Only 50% of NSC will.
non-small cell cancer
Stage 1 – operable – 70% survival at 5 years after surgery.
Stage 2 – survival drops to 40% after surgery.
Stage 2a – 25% survival – although many surgeons don’t like to operate on these. Adjuvant chemotherapy, given after the operation, improves survival by 5%
Stage 4 – only chemotherapy offered. If you give no treatment – they have a 6% chance of being alive after 1 year. With chemotherapy, about 12% will still be alive after 1 year.
49
what is asbestosis?
| what would examination show in asbestosis?
This is fibrosis of the lung tissue secondary to exposure to asbestos.. Is a progressive condition that will present 5-10 years after exposure. Causes severe reduction in lung function and progressive dyspnoea. Restrictive pattern. There may also be finger clubbing, and bilateral end-inspiratory crackles.
50
what would an X-ray show in asbestosis?
dark streaks, honeycomb appearance (honeycomb lung)
51
how is asbestosis managed?
There is no curative treatment, although steroids are often prescribed
52
what is interstitial lung disease ?
aka - Diffuse parenchymal lung disorders
Interstitial lung diseases (ILDs) affect the lung interstitium, i.e. the space between the alveolar epithelium and the capillary endothelium, causing inflammation and fibrosis.
The two main types of interstitial lung disease are pulmonary fibrosis and sarcoidosis. Other types include occupational lung diseases (pneumoconiosis), and interstitial lung disease secondary to connective tissue diseases.
53
what are the different types of interstitial lung disease?
Idiopathic pulmonary fibrosis - poor prognosis, typically older adults
Sarcoidosis - usually good prognosis - can affect younger adults
Pneumoconiosis - variable prognosis depending on the cause
Drug induced ILD - amioderone, methotrexate
Hypersensitivity ILD - usually a good prognosis if the allergen is avoided
54
how does interstitial lung disease present?
often slowly progressive - occasionally may mimic an acute pneumonia
dry cough
progressive SOB
may have clubbing
diffuse inspiratory crackles
wheeze, haemoptysis and chest pain are rare
55
what are the clinical features of a fibrotic lung?
dry cough
dyspnoea
clubbing
diffuse inspiratory crackle
56
what is pulmonary fibrosis and what is it characterised by?
pulmonary fibrosis is the end result of many diseases
it is characterised y
- scar tissue in the lung
- decreased compliance giving a restrictive pattern in pulmonary function tests
- end stage is honeycomb lung -cystic spaces in fibrotic lungs
57
what is idiopathic pulmonary fibrosis?
it is a chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs.
No underlying cause
IPF is typically seen in patients aged 50-70 years and is twice as common in men
58
what are the features of idiopathic pulmonary fibrosis?
```
progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
weight loss
fatigue/malaise
```
over time the diseases progresses to cause pulmonary hypertension, cor pulmonale and type 1 respiratory failure
signs:
reduced chest expansion
end expiratory crackles
clubbing
59
what investigations would you perform in idiopathic pulmonary fibrosis?
Bloods - Rheumatoid factor + in 10-20%, ANA + in 10-20%
CXR - basilar, peripheral, bilateral, asymmetrical, reticular opacities
CT - high resolution CT, ground glass opacification later progressing to honeycomb
Pulmonary function tests - will classically show a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
60
how is idiopathic pulmonary fibrosis managed?
Two meds can slow progression of disease:
Pirfenidone is an antibiotic and anti-inflammatory
Nintedanib is a monoclonal antibody targeting tyrosine kinase
smoking cessation
pulmonary rehabilitation
oxygen therapy
2nd line - lung transplant
61
what is sarcoidosis?
sarcoidosis is a multi-system granulomatous disorder of unknown aetiology.
it commonly affects the lungs and lymphatic system but can affect any organ.
Black africans are at highest risk
EXAM TIP - the typical patient is a 20-40 year old black female presenting with a dry cough and SOB. They may have nodules on their shins suggesting erythema nodosum.
62
what is a granuloma?
granulomas are nodules of inflammation full of WBC (mononuclear cells and macrophages) surrounded by lymphocytes, plasma cells, mast cells, fibroblasts and collagen.
63
what organs can be affected by sarcoidosis?
it can affect almost any organ in the body
most commonly lungs
Lungs (affecting over 90%) - Mediastinal lymphadenopathy, Pulmonary fibrosis, Pulmonary nodules
Systemic Symptoms - Fever, Fatigue, Weight loss
Liver (affecting around 20%) - Liver nodules, Cirrhosis, Cholestasis
Eyes (affecting around 20%)- Uveitis, Conjunctivitis, Optic neuritis
Skin (affecting around 15%)- Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat), Lupus pernio (raised, purple skin lesions commonly on cheeks and nose), Granulomas develop in scar tissue
Heart (affecting around 5%)- Bundle branch block, Heart block, Myocardial muscle involvement
Kidneys (affecting around 5%) - Kidney stones (due to hypercalcaemia), Nephrocalcinosis, Interstitial nephritis
Central nervous system (affecting around 5%) - Nodules, Pituitary involvement (diabetes insipidus), Encephalopathy,
Peripheral Nervous System (affecting around 5%) - Facial nerve palsy, Mononeuritis multiplex
Bones (affecting around 2%), Arthralgia, Arthritis, Myopathy
64
what is Lofgren's syndrome?
This is a specific acute presentation of sarcoidosis. It is characteristic by a triad of:
- Erythema nodosum
- Bilateral hilar lymphadenopathy
- Polyarthralgia (joint pain in multiple joints)
65
what is Mikulicz syndrome?
where there is enlargement of the parotid and lacrimal glands due to sarcoidosis, TB or lymphoma
however there is overlap with sjogrens syndrome so this syndrome is considered outdated and unhelpful
66
what is Heefordt's syndrome?
aka uveoparotid fever
| there is parotid enlargement, fever and uveitis secondary to sarcoidosis
67
what are some differentials for sarcoidosis?
```
Tuberculosis
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis
```
68
what investigations would you perform for sarcoidosis?
- CXR - hilar and/or paratracheal adenopathy with upper lobe predominant, bilateral infiltrates
- FBC - may have anaemia or leukopenia - usually secondary to splenic and or bone marrow involvement
- Serum urea and creatinine - may be elevated in cases of renal involvement
- serum calcium - hypercalcaemia due to dysregulated production of calcitriol by activated macrophages
- Pulmonary function tests - to monitor disease. May be restrictive, obstructive or mixed pattern
- ECG - to exclude cardiac involvement - there may be conduction defects
- High resolution CT of the thorax will show hilar lymphadenopathy and pulmonary nodules
- MRI scan will show CNS involvement
- PET scan will show active inflammation in affected areas
69
how is sarcoidosis staged from CXR?
Stage 0 – normal CXR
Stage 1 – BHL – bilateral hilar lymphadenopathy
Stage 2 – BHL + Infiltrates
Stage 3 – Peripheral pulmonary infiltrates alone
Stage 4 – Progressive pulmonary fibrosis ± bulla (honeycombing on CXR
70
how is sarcoidosis managed?
sometimes resolves spontaneously
Steroid management - oral prednisolone
second line methotrexate or azathioprine
71
what is pneumoconiosis ?
a term used to describe a range of interstitial lung diseases caused by inhalation of mineral dusts, resulting in interstitial fibrosis
they are usually occupations diseases - but not always
asbestosis
silicosis
coal worker's pneumoconiosis
72
what are the diagnostic features of pneumoconioses?
- presence of risk factors
- dyspnoea on exertion
- cough
73
what investigations should you perform for pneumoconioses?
CXR
| spirometry
74
what can cause drug induced pulmonary fibrosis?
amiodarone
cyclophosphamide
methotrexate
nitrofurantoin
75
what can pulmonary fibrosis occur secondary to?
alpha-1 antitripsim deficiency
RA
SLE
systemic sclerosis
76
what is hypersensitivity pneumonitis?
Hypersensitivity pneumonitis aka extrinsic allergic alveolitis is a type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in people that are sensitive to that allergen.
77
what are some specific causes of hypersensitivity pneumonitis?
Bird-fanciers lung is a reaction to bird droppings
Farmers lung is a reaction to mouldy spores in hay
Mushroom workers’ lung is a reaction to specific mushroom antigens
Malt workers lung is a reaction to mould on barley
78
how does extrinsic allergic alveolitis present?
acutely - 4-8 hours after exposure, SOB, dry cough, fever
| chronic
79
what investigations should you perform for extrinsic allergic allveolititis?
> CXR - infiltrates, nodular or patchy; fibrosis
> CT chest - ground glass shadowing
> bronchoalveolar lavage: lymphocytosis
> pulmonary function tests - restrictive; mixed restrictive/obstructive
> FBC - non specific findings in acute and chronic settings - leukocytosis; normocytic, normochromic anaemia
> ESR - raised
> albumin - low - may be low in chronic disease but is non-specific
80
how is hypersensitivity pneumonitis treated?
avoid antigen
| prednisolone
