1
Q
How do you grade dyspnoea
A
- MRC Dyspnoea Scale
- Grade 1 – Breathless on strenuous exercise
- Grade 2 – Breathless on walking up hill
- Grade 3 – Breathless that slows walking on the flat
- Grade 4 – Stop to catch their breath after walking 100 meters on the flat
- Grade 5 – Unable to leave the house due to breathlessness
2
Q
spirometry findings in COPD
A
- FEV1 /FVC ratio is <0.7
3
Q
how is severity of airflow obstruction graded
A
- Stage 1: FEV1 >80% of predicted
- Stage 2: FEV1 50-79% of predicted
- Stage 3: FEV1 30-49% of predicted
- Stage 4: <30% of predicted
4
Q
COPD investigations
A
- CXR
- To exclude other pathology like lung cancer
- FBC
- For polycythaemia which is a response to chronic hypoxia
- BMI
- As a baseline to assess weight loss (cancer or severe COPD) or weight gain (due to steroid therapy)
- Sputum culture
- To assess for chronic infections like pseudomonas
- Serum alpha-1 antitrypsin
- Alpha-1 antitrypsin deficiency leads to early onset and more severe COPD
- Transfer factor for carbon monoxide
- TLCO is decreased in COPD and can give an indication of severity of disease
5
Q
Long term COPD management
A
- Smoking cessation
- Annual pneumococcal and flu vaccines
- Pulmonary rehab
- Stage 1
- SABA (e.g. salbutamol) or SAMA (e.g. ipratropium) to use as needed
- Stage 2
- LABA (e.g. formoterol, salmeterol) plus LAMA (e.g. tiotropium)
- Stage 3
- LABA plus LAMA plus ICS
- If no improvement in 3 months then switch back to LABA plus LAMA
6
Q
management of acute exacerbation of COPD
A
- Nebulised bronchodilators (salbutamol and ipratropium)
- Steroids (hydrocortisone or oral prednisolone)
- Antibiotics if evidence of infection
- Physiotherapy
- If not responding to first line treatment
- IV aminophylline
- Non-invasive ventilation
- Intubation and ventilation with admission to intensive care
- Doxapram
7
Q
investigation of asthma in the community
A
fractional exhaled nitric oxide
spirometry with bronchodilator reversibility
8
Q
how would you define good asthma control
A
No daytime symptoms.
No night-time waking due to asthma.
No need for rescue medication.
No asthma attacks.
No limitations on activity including exercise.
Normal lung function (FEV1 and/or PEF > 80% predicted or best).
Minimal side-effects from medication.
9
Q
additional management of asthma in the community
A
yearly asthma review
emergency plan
yearly flu jab
10
Q
describe asthma treatment ladder in adults
A
- everyone gets a SABA
- SABA + low dose ICS (beclametasone)
- SABA + low dose ICS + LTRA (montelukast)
- SABA + low dose ICS + LABA (salmeterol) +/- LTRA (depending on response to LTRA)
- MART (maintenance and reliever therapy) +/- LTRA
- MART includes fast acting LABA and low dose ICS
- used as daily maintenance and as a reliever
- Switch to a MART with moderate dose ICS +/- LTRA
- consider additional drug such as theophylline or switching to high dose ICS
11
Q
asthma treatment ladder in children
A
- SABA
- SABA + low dose ICS (beclametasone)
- SABA + low dose ICS + LTRA (montelukast)
- SABA + low dose ICS + LABA (salmetarol)
- SABA + MART (low dose ICS in the MART)
- SABA + moderate dose ICS + LABA (either as MART or fixed dose regimen)
- here you can either increase to high dose ICS or trial new drug such as theophylline
12
Q
how can you establish whether someone’s asthma is well controlled
A
- answering no to all three of the RCP Three Questions is consistent with well controlled asthma
- are you having trouble sleeping because of your asthma symptoms?
- have you recently had your asthma symptoms during the day?
- has your asthma interfered with your normal activities?
13
Q
how do you grade asthma attacks
A
- Mild: PEFR >75%
- Moderate: PEFR <75%
- Severe:
- PEFR <50%
- can’t complete sentences
- RR >25
- PR >110
- Life threatening (33 92 CHEST)
- 33: PEFR <33%
- 92: Sats <92%
- Cyanosis
- Hypotension
- Exhaustion
- Silent chest
- Tachycardia
14
Q
management for moderate asthma attack
A
Nebulised beta-2 agonists (i.e. salbutamol 5mg repeated as often as required)
Nebulised ipratropium bromide
Steroids. Oral prednisolone or IV hydrocortisone. These are continued for 5 days
Antibiotics if there is convincing evidence of bacterial infection
15
Q
management of severe asthma attack
A
16
Q
management of life threatening asthma attack
A
IV magnesium sulphate infusion
admission to HDU/ICU
Intubation - however this should happen early as it’s very difficult to intubate in bronchospasm
17
Q
ABGs in an asthma attack
A
Initially patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2.
A normal pCO2 or hypoxia is a concerning sign as it means they are tiring and indicates life threatening asthma.
A respiratory acidosis due to high CO2 is a very bad sign in asthma.
18
Q
what are the different types of lung cancer and how common are they
list sub-types in order of prevalence
A
- Non small cell lung cancer (80%)
- adenocarcenoma
- squamous cell carcinoma
- large cell carcinoma
- other
- small cell lung cancer (20%)
*
19
Q
signs and symptoms of lung cancer
A
finger clubbing
coughing
haemoptysis
lymphadenopathy
recurrent pneumonia
weightloss
cough
20
Q
investigations of lung cancer
A
- chest x ray
- contrast enhanced CT
- bronchoscopy
- biopsy (by bronchoscopy or percutaneously) and histological diagnosis
21
Q
is prognosis generally better for small cell lung cancer or non-small cell lung cancer
A
non-small cell lung cancer generally has a better prognosis
22
Q
treatment options for lung cancer
A
- surgery
- lobectomy
- segmentectomy
- wedge resection
- radiotherapy
- chemotherapy
- curative
- palliative
- treatment for small cell lung cancer
- outcomes usually worse so normally just radiotherapy and chemo
- palliative
- endobronchial treatment with stents and debulking works for palliative treatment of obstruction caused by cancer
23
Q
list 9 extra pulmonary manifestations of lung cancer
A
24
Q
what is recurrent laryngeal nerve palsy
A
presents as hoarse voice and is caused by lung cancer pressing on the recurrent laryngeal nerve
25
what is phrenic nerve palsy
due to compression of the phrenic nerve and results in diaphragm weakness - presents as shortness of breath
26
what happens with superior vena cava obstruction
* it is a complication of lung cancer and is caused by direct compression of the tumour on the superior vena cava
* it presents with
* facial swelling
* difficulty breathing
* distended veins in the neck and upper chest
* pemberton's sign is where raising the hands over the head causes facial congestion and cyanosis - this is a medical emergency
27
what is horner's syndrome
triad of partial ptosis, anhidrosis and miosis
28
why might a lung cancer cause a horner's syndrome
it is caused by a pancoast tumour (tumout of the pulmonary apex) pressing on the sympathetic ganglion
29
why might lung cancer cause SIADH and how does it present
ectopic ADH secretion by a small cell lung cancer and presents with hyponatraemia
30
why might lung cancer cause cushing's syndrome
ectopic ACTH secretion by a small cell lung cancer
31
why might lung cancer cause hypercalcaemia
ectopic parathyroid hormone secretion from a squamous cell carcinoma
32
what is limbic encephalitis and how is it caused
* small cell lung cancer causes immune system to make antibodies to tissue in the brain - specifically the limbic system
* this causes
* hallucinations
* confusion
* seizures
* memory impairment
* associated with anti-Hu antibodies
33
what is lambert-eaton myasthenic syndrome and why do you get the specific symptoms
* immune system produces antibodies against the small cell lung cancer
* these cross-react with voltage gated calcium channels sited on presynaptic terminals in motor neurons
* it mainly affects
* proximal muscles
* intraocular muscles
* diplopia
* levator muscles
* ptosis
* pharyngeal muscles
* slurred speach and dysphagia
* also causes autonomic dysfunction
* dry mouth
* blurred vision
* impotence
* dizziness
34
cxr findings in lung cancer
hilar enlargement
consolidation
lung collapse
pleural effusion
bony secondaries
35
rare causes of PE (i.e. not clot in legs)
* right ventricular thrombosis (post MI)
* septic emboli (right sided endocarditis)
* fat embolus
* air embolus
* amniotic fluid embolus
* neoplastic cells
* parasites
36
what is the risk score for PE
wells criteria for PE
37
what are the wells criteria for PE
* clinical signs and symptoms of DVT
* PE is #1 diagnosis or equally likely
* heart rate \>100
* immobilisation in the last 3 dats or surgery in the previous 4 weeks
* previous, objectively diagnosed PE or DVT
* hemoptysis
* malignancy with treatment in the last 6 months or palliative
38
risk factors for PE
immobility
recent surgery
long haul flights
pregnancy
hormone therapy with oestrogen
malignancy
polycythaemia
systemic lupus erythematosus
thrombophilia
39
signs of PE
pyrexia
cyanosis
tachypnoea
tachycardia
hypotension
raised JVP
pleural rub
pleural effusion
40
thromboprophylaxis of patients admitted to hospital
low molecular weight heparin such as enoxaparin
41
investigations of PE based on wells score
likely: perform a CTPA
unlikely: d-dimer and if positive perform a CTPA
42
diagnosis of PE
* CTPA
* this is first choice
* IV contrast highlights pulmonaty arteries to demonstrate blood clots
* VQ scan
* used in patients with
* renal impairment
* contrast allergy
* risk from radiation
* area of embolism will be ventilated but not perfused
* CXR may be normal
43
cxr findings in PE
* may be normal
* oligaemia of affected segment
* dilated pulmonary artery
* linear atelectasis
* small pleural effusion
* wedge-shaped opacities
44
ecg findings in PE
* may be normal
* tachycardia
* RBBB
* right ventricular strain
45
initial management of PE
* apixaban or rivaroxaban started immediately before confirming diagnosis
* where there is massive PE and they are haemodynamically unstable
* thrombolysis
* inject fibrinolytic medication such as
* alteplase
* streptokinase
* tenecteplase
* either IV or catheter directed thrombolysis directly into pulmonary arteries
* this is risky
46
long term anticoagulation following PE
* options are
* warfarin
* target INR 2-3
* a noac
* apixaban
* rivaroxaban
* dabigatran
* LMWH
* first line treatment in pregnancy or cancer
* continue anticoagulation for
* 3 months if obvious reversible cause
* beyond 3 months if cause unclear, if recurrent VTE or an irreversible underlying cause such as thrombophilia
* 6 months in active cancer
* then review
47
describe the bacteria that causes TB
mycobacterium tuberculosis
acid fast bacilli
48
what staining technique is used for TB
zeihl neelsen stain
this turns TB bright red against a blue background
49
disease course of TB
* active TB is where there is active infection in various areas within the body
* small granulomas (tubercles) form around the infection when host macrophages engulf the organism
* in 80% of cases these tubercles heal spontaneously
* in 20% of cases you get latent TB
* this is where the infection is encapsulated but not eliminated
* individual is otherwise healthy
* if latent TB reactivates it is known as secondary TB
* this is usually precipitated by impaired immune function
* miliary TB occurs when primary infection is not adequately contained and invades the bloodstream
* results in severe disseminated disease
50
TB presentation
* 70% is pulmonary TB
* lethargy
* fever
* night sweats
* cough with or without haemoptysis
* lymphadenopathy
* erythema nodosum
* spinal pain in spinal TB
* this is AKA pott's disease of the spine
51
investigating TB
* difficult because bacteria grow slowly
* two tests for immune response to TB
* mantoux
* interferon-gamma release assay
* if active disease is suspected
* X ray
* sputum cultures
52
CXR findings in TB
* pulmonary TB is unlikely with a normal CXR
* primary TB
* central apical portion with lower lobe infiltrate or pleural effusion
* cavitation
* reactivated TB
* no pleural effusion and lesions are apical in position
* cavitation
* severe disease with poor immune response can produce a picture like millet seeds over the CXR
* uniform 1-10mm shadows
53
obtaining samples for suspected pulmonary TB
* need at least three sputum samples for culture and microscopy
* including one early morning sample
* if spontaneous not possible consider bronchoscopy and lavage
* or in children gastric washing
* start treatment without culture results if clinical signs and symptoms of TB
* complete treatment even if culture results are negative
54
obtaining samples for suspected non-respiratory TB
* needle aspiration
* lymph node biopsies
* early morning urine
* start treatment if histology and clinical picture are consistent with TB before culture results are available
* continue treatment even if results are negative
* CXR should be done for co-existing respiratory TB in all patients with non-resp TB
55
how are TB samples analysed
staining with Ziehl-Neelsen stain
rapid direct microscopy for acid fast bacilli
they appear red on a blue background
culture on a lowenstein-jensen slope which takes 4-8 weeks due to slow bacterial growth
sensitivity cultures then take a further 3-4 weeks
56
contact screening in TB
mantoux testing to diagnose LTBI in people who are household contacts or close contaccts of all patients with TB
mantoux may well be positive in those with the BCG so offer interferon gamma as first line in these people
if positive refer to TB specialist
57
public health stuff following diagnosis of TB
* all cases must be notified under the public health regulations 1988
* admit to negative pressure single side-room vented to the outside until they are proven to be non-infectious
58
drug treatment of active TB without CNS involvement
* start all at the same time
* isoniazid for 6 months
* rifampicin for 6 months
* pyrazinamide for two months
* ethambutol for two months
59
drug treatment of active TB of the CNS
60
side effects of rifampicin
* red orange discolouration of urine and tears
* cytochrome P450 inducer --\> OCP
* during first two months of rifampicin transient derangement of LFTs is common and generally doesn't require change of treatment
61
side effects of isoniazid
peripheral neuropathy
prescribe pyridoxine (B6)
62
side effects of pyrazinamide
hyperuricaemia which may result in gout
63
side effects of ethambutol
can reduce visual acuity and cause colour blindness
64
which people should be treated for latent TB (LTBI)
* people mantoux positive without prior BCG
* people mantoux positive and interferon-gamma positive is prior BCG
* people with TB scars on CXR without history of prior treatment
* people with HIV who are close contacts of those with sputum-smear-positive respiratory TB
65
drug treatment of LTBI
* either if no HIV
* 6 months of isoniazid or
* 3 months of isoniazid and rifampicin
* any LTBI with HIV
* 6 months of isoniazid
66
what are bronchial breath sounds
harsh breath sounds equally loud on inspiration and expiration
caused by consolidation of the lung tissue around the airway
67
how do you assess severity of pneumonia
* in hospital
* CURB65
* Confusion
* Urea \>7
* Resp rate \>30
* Blood pressure \<90 systolic or \<60 diastolic
* 65 Age \>65
* in comunty
* CRB65
* no urea testing
* if CRB score of anything other than 0 consider referring to hospital
68
CAP treatment in adults
* CRB65 of 0 (low severity)
* amoxicillin 500mg 3 times per day for 5 days
* if penicillin allergy then
* doxycycline 200mg on first day then 100mg once a day for 4 days
* CRB65 of 1/2 (moderate severity)
* amoxicillin 500mg 3 times a day for 5 days AND
* clarithromycin 500mg twice a day for 5 days
69
CURB 65 interpretation
score 0/1: consider treatment at home
score 2 or more: consider admission
score 3 or more: consider intensive care assessment
70
most common atypical pneumonias
M. pneumoniae
C. pneumoniae
Legionella pneumophila
71
what is the definition of hap
hospital acquired pneumonia
new infection of lung parenchyma appearing more than 48hrs after admission to hospital
72
HAP occuring less than 5 days after hospital admission is normally caused by
S.pneumoniae
73
HAPs occuring more than 5 days after hospital admission are normally caused by
H.influenzae
MRSA
pseudomonas aeruginosa
74
legionella pneumophila presentation
typically caused by infected water supplies or air conditioning units. It can cause hyponatraemia (low sodium) by causing an SIADH.
75
treatment for atypical pneumonias
Macrolides such as clarithromycin
Quinolones such as levofloxacin
Tetracyclines such as doxycycline
76
mycoplasma pneumoniae presentation
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.
77
coxiella burnetii presentation
aka Q fever
linked to exposure to animals and their bodily fluids. The MCQ patient is a farmer with a flu like illness.
78
chlamydia psittaci presentation
typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.
79
Pneumocystis jiroveci (PCP) management
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.
80
should you prescribe abx in tonsillitis
* centor criteria
* history of fever
* tonsillar exudates
* no cough
* tender anterior cervical lymphadenopathy
* abx should be limited to patients with three or four criteria
81
bacterial tonsilitis is most commonly caused by
Group A Streptococcus (GAS) mainly streptococcus pyogenes
82
when should you give abx for tonsillitis and what should you give
if centor criteria is 3 or more
Penicillin V aka phenoxymethylpenicillin for a 10 day course
NICE guidelines are supportive of considering a delayed prescription in the community where patients can collect antibiotics if the symptoms don’t improve or get worse after 3 days.
83
criteria for tonsillectomy
Sore throats are due to acute tonsillitis.
The episodes of sore throat are disabling and prevent normal functioning.
Seven or more well-documented, clinically significant, adequately treated sore throats in the preceding year; or
Five or more such episodes in each of the preceding two years; or
Three or more such episodes in each of the preceding three years.
84
presentation of otitis media
management
difficult to distinguish between bacterial and viral otitis media. It presents with ear pain. Examination will reveal a bulging red tympanic membrane. If the ear drum perforates there can be discharge from the ear.
Otitis media usually resolves within 3-7 days without antibiotics. If systemically unwell consider admission.
amoxicillin if necessary in community
85
subtypes of otitis media
acute otitis media
otitis media with effusion
chronic supperative otitis media
mastoiditis
cholesteatoma
86
what is acute otitis media
acute inflammation of the middle ear
caused by bacteria or viruses
87
what is otitis media with effusion
chronic otitis media without acute inflammation
often follows slowly resolving acute otitis media
effusion of glue like liquid behind the intact tympanic membrane
no signs of acute inflammation
88
what is mastoiditis
acute inflammation of the mastoid periosteum and air cells occuring when acute otitis media spreads from middle ear
89
what are the most common causative bacteria in otitis media
haemophilus influenzae
streptococcus pneumoniae
moraxella catarrhalis
streptococcus pyogenes
90
what are the most common viral pathogens causing otitis media
RSV
rhinovirus
91
abx in otitis media
usually resolves in 3-7 days
give amoxicillin on delayed prescription if it doesn't resolve in 4 days
92
different types of sinusitis
Acute: an infection lasting 7-30 days.
Subacute: the inflammation lasts 4-12 weeks.
Recurring: there are \>3 significant acute episodes in a year lasting ≥10 days with no intervening symptoms.
Chronic: symptoms persist for \>90 days (these may be caused by irreversible changes in the mucosal lining of the sinuses), with or without acute exacerbations
93
risk factors for sinusitis
Upper respiratory tract infection.
Allergy.
Asthma.
Smoking.
Hormonal status (eg, pregnancy).
Nasal dryness.
Diabetes mellitus.
Presence of a foreign body.
Inhalation of irritants (eg, cocaine).
Iatrogenic (eg, nasogastric tubes, mechanical ventilation).
Dental problems (eg, trauma, infection).
Some sporting activities (eg, swimming, diving, high-altitude climbing).
Mechanical obstruction (eg, normal anatomical variations, nasal polyps).
Previous history of trauma (nose, cheeks).
Immunocompromise.
94
diagnosis of acute sinusitis
acute sinusitis is diagnosed if there is:
* Facial discomfort (often worse when bending forwards) or pain.
* Nasal obstruction or (purulent) nasal discharge or postnasal drip.
* Decreased or absent sense of smell.
95
management of sinusitis
Symptoms for less than 10 days: No antibiotics.
No improvement after 10 days: 2 weeks of high-dose steroid nasal spray
No improvement after 10 days and likely bacterial cause: consider delayed or immediate prescription of antibiotics
96
what is the most common interstitial lung disease
IPF
97
most common causative organisms in infective exacerbation of COPD
streptococcus pneumoniae
moraxella catarrhalis
haemophilus influenzae
98
antibiotic for infective exacerbation of COPD
co-amoxiclav
99
medical management of COPD
100
mnemonic for respiratory causes of clubbing
Asbestosis
Bronchiectasis
Cancer (lung)
Do not say COPD
Empyema
(There are some more respiratory causes such as interstitial lung disease)
101
what is granulomatosis with polyangiitis
GPA is a systemic vasculitis that involves small and medium-sized vessels. It classically presents with upper and lower respiratory tract involvement and pauci-immune glomerulonephritis
102
serology in GPA
granulomatosis with polyangiitis is usually cANCA-associated (c. 80%) but 10-15% is pANCA-associated.
103
what is the best abx for penicillin allergic severe pneumonia
levofloxacin
104
what is IPF
Idiopathic pulmonary fibrosis (IPF, also called cryptogenic fibrosing alveolitis) is specific form of
chronic,
progressive,
fibrosing
interstitial pneumonia of unknown cause,
occurring in adults and limited to the lungs.
It is associated with the histopathologic and/or radiologic pattern of usual interstitial pneumonia (UIP).
105
what drugs are sometimes used to treat IPF
Idiopathic pulmonary fibrosis
Pirfenidone
106
how is interstitial lung disease diagnosed
ground glass appearance on high resolution ct
107
management of interstitial lung disease
Remove or treat the underlying cause
Home oxygen where they are hypoxic at rest
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine
Advanced care planning and palliative care where appropriate
Lung transplant is an option but the risks and benefits need careful consideration
pirfenidone if recommended by nice
108
life expectancy of idiopathic pulmonary fibrosis
median survival is 2.5 years from the time of diagnosis
109
three types of fibrosis seen in the lungs and their causes
* replacement fibrosis secondary to damage: e.g. infarction, tuberculosis and pneumonia
* focal fibrosis in response to irritants: e.g. coal dust and silica
* diffuse parenchymal lung disease: IPF and hypersensitivity pneumonitis
110
median age of presentation of IPF
70
111
presentation of IPF
* age over 45
* persistent breathlessness on exertion
* persistent dry cough
* bilareral inspiratory crackles on auscultation of chest
* clubbing of fingers
* spirometry may be normal, restrictive or obstructive
112
diseases associated with IPF
thyroid disease
systemic sclerosis
rheumatoid arthritis
autoimmune liver disease
SLE
113
who is pirfenidone suitable for
pirfenidone is recommended for the treatment of IPF if:
* FVC is between 50% and 80% of expected
* there is evidence of disease progression if the treatment is stopped
114
who is nintedanib suitable for
* nintedanib is recommended for the treatment of IPF if:
* FVC is between 50% and 80% predicted
* there is evidence of disease progression if the treatment is stopped
115
which drugs can cause pulmonary fibrosis
amiodarone
cyclophosphamide
methotrexate
nitrofurantoin
116
what is pirfenadone
antifibrotic and anti-inflammatory drug used to treat IPF
117
what is nintendanib
monoclonal antibody that targets tyrosine kinase
118
what diseases can pulmonary fibrosis be secondary to
Alpha-1 antitripsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis
119
what type of hypersensitivity reaction is hypersensitivity pneumonitis
type III
120
hypersensitivity reactions associated with hobbies and their causes
* farmer's lung: mouldy hay
* bird fanciers lung: avian proteins
* cheese workers lung: cheese mould penicillium casei
* malt worker's lung: mouldy malt
* hot tub lung: mycobacterium avium in poorly maintained hot tubs
* chemical worker's lung: manufacture of dyes, plastics, polyurethane foam and rubber
* mushroom worker's lung
121
three forms of hypersensitivity pneumonitis
acute
subacute or intermittent
chronic
122
difference between different forms of hypersensitivity pneumonitis
* acute
* 4-8hrs after exposure
* flu like with fever, chest tightness and dry cough
* symptoms directly related to level of exposure
* subacute or intermittent
* may be history of acute attacks
* less severe symptoms with more gradual onset
* after exposure removed it can take weeks or months for symptoms to resolve
* chronic
* often no systemic symptoms except weight loss
* gradual loss of exercise tolerance
* clubbing may develop
* after antigen removed there may only be partial improvement
123
management of hypersensitivity pneumonitis
remove exposure to antigen
corticosteroids but these don't alter long term outcomes
azathioprine and mycophenolate can be used as steroid sparing agents
lung transplantation in specific cases
124
complications of hypersensitivity pneumonitis
pneumothorax
pulmonary fibrosis
emphysema
respiratory insufficiency or failure
cor pulmonale
125
what is sarcoidosis
a granulomatous inflammatory condition. Granulomas are nodules of inflammation full of macrophages. The cause of these granulomas developing is unknown.
126
what is the typical exam patient with sarcoidosis
a 20-40 year old black woman presenting with a dry cough and shortness of breath, erythema nodosum and lymphadenopathy
127
which organs does sarcoidosis affect
mainly lungs (90%)
but can affect almost any organ in the body
128
effects of sarcoidosis by system
* systemic
* fever
* weightloss
* fatigue
* liver
* nodules
* cirrhosis
* cholestasis
* lungs
* mediastinal lymphadenopathy
* pulmonary fibrosis
* pulmonary nodules
* eyes
* uveitis
* conjunctivitis
* optic neuritis
* skin
* erythema nodosum
* lupus pernio
* granulomas in scar tissue
* heart
* arrhythmias
129
what is lofgren's syndrome
* specific presentation of sarcoidosis characterised by the following triad
* erythema nodosum
* bilateral hilar lymphadenopathy
* polyarthralgia
130
investigations of sarcoidosis
* bloods
* raised serum ACE
* hypercalcaemia
* raised serum soluble IL-2 receptor
* raised CRP
* raised Ig
* imaging
* CXR - hilar lymphadenopathy
* high res CT - hilar lymphadenopathy and pulmonary nodules
* MRI may show cns involvement
* PET can show active areas of inflammation
* Biopsy and histology
* this is gold standard
* shows non-caseating granulomas with epithelioid cells
131
treatment for sarcoid
* mild or no symptoms
* no treatment as 60% will resolve spontaneously within 6 months
* first line
* oral steroids with bisphosphinates to protect against osteoporosis from steroids
* second line
* azathioprine and methotrexate
* lung transplant
* rare
132
what is the inheritance pattern of CF
autosomal recessive
133
what is the mutation in CF
cystic fibrosis transmembrane conductance regulatory gene on chromosome 7.
There are many variants of this mutation, the most common is the delta-F508
134
how common is it to be a carrier of CF mutation
1 in 25 are carriers of the mutation
135
how common is CF
1 in 2500 children have CF
136
what are 3 key consequences of CF mutation
* thick pancreatic and biliary secretions
* block the ducts resulting in lack of digestive enzymes such as pancreatic lipase
* low volume thick airway secretions
* reduced clearance
* susceptibility to infections
* bacterial colonisation
* congenital bilateral absence of the vas deferens
137
what is commonly the first sign of CF
meconium ileus almost always means CF
happens in about 20% of babies with CF
it means not passing meconium within 24hrs of birth
138
presentation of CF
* screened for with newborn blood spot test
* meconium ileus
* if not picked up ad birth may present later in childhood
* recurrent lower resp tract infections
* failure to thrive
* pancreatitis
139
symptoms of CF
* chronic cough
* thick sputum
* steatorrhoea
* recurrent resp tract infections
* abdo pain and bloating
* failure to thrive
140
signs of CF
lower weight or height on growth charts
nasal polyps
finger clibbing
crackles and wheezes on auscultation
abdo distention
141
causes of clubbing in children
Hereditary clubbing
Cyanotic heart disease
Infective endocarditis
Cystic fibrosis
Tuberculosis
Inflammatory bowel disease
Liver cirrhosis
142
diagnosis of CF
* Newborn blood spot testing is performed on all children shortly after birth and picks up most cases
* The sweat test is the gold standard
* Genetic testing for CFTR gene by amniocentesis or chorionic villous sampling
143
what happens during sweat test for CF
pilocarpine applied to skin patch
electrodes placed either side of patch with small current running through
this causes skin to sweat
sweat absorbed by gauze
chloride concentration \>60mmol/L is diagnostic
144
what are the two key colonisers to remember with CF
staph aureus: patients with CF take long term prophylactic flucloxacilling to prevent staph aureus infection
pseudomonas aeruginosa: remember because it's particularly hard to treat and worsens prognosis
145
How is pseudomonas aeruginosa infection managed in patients with CF
dangerous ass leads to increased mortality and morbidity and v difficult to eliminate
CF patients with pseudomonas treated in seperate clinic rooms
long term nebulised abx such as tobramycin and ciprofloxacin for infected pts
146
what vaccines should CF pts get
influenza
pneumococcal
varicella
147
8 aspects of CF management
* chest physio
* high calorie diet
* CREON to replase missing lipase in pancreatic insufficiency
* prophylactic flucloxacillin to reduce risk of bacterial infections such as staph aureus
* bronchodilators such as salbutamol
* nebulised DNAse (dornase alpha) breaks down DNA material making secretions less viscous and easier to clear
* nebulised hypertonic saline
* vaccination for pneumococcus, varicella and influenza
148
difference between exudate and transudate
exudate is \>3g/dL
transudate is \<3g/dL
149
exudative causes of pleural effusion
lung cancer
pneumonia
rheumatoid arthritis
tuberculosis
150
Transudative causes of pleural effusion
congestive cardiac failure
hypoalbuminaemia
hypothyroidism
meig's syndrome
151
what is meig's syndrome
triad of benign ovarian tumor with ascites and pleural effusion
152
how does pleural effusion appear on x ray
blunting of costophrenic angle
fluid in lung fissures
larger effusions will have a meniscus
tracheal and mediastinal deviation if it is a massive effusion
153
Investigations of pleural effusion
* CXR
* sample of pleural fluid by aspiration or chest drain to analyse for:
* protein count
* pH
* glucose
* LDH
* microbiology
154
what is an empyema
this is an infected pleural effusion
155
how do you know if someone's pleural effusion is empyema
Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever.
Pleural aspiration shows pus, acidic pH (pH \< 7.2), low glucose and high LDH.
156
how is empyema treated
antibiotics
chest drain to remove the pus
157
what is the treatment for pleural effusion
conservative if small as they will resolve on their own
pleural aspiration although you may need to do this more than once
chest drain to drain effusion and it also prevents it recurring
158
how do you measure a pneumothorax
measure horizontally from the lung edge to the inside of the chest wall at the level of the hilum on x ray
159
managment of pneumothorax
* if no SOB AND \<2cm rim of air on CXR then no treatment
* follow up in 2-4 weeks
* if SOB or \>2cm rim of air then aspiration
* if aspiration fails twice then chest drain
* chest drain straight away for
* unstable patients
* bilateral pneumothorax
* secondary pneumothorax
160
signs of a tension pneumothorax
* tracheal deviation away from side of pneumothorax
* reduced air entry to affected side
* increased resonance to percussion on affected side
* tachycardia
* hypotension
161
what is the management of a tension pneumothorax
* “Insert a large bore cannula into the second intercostal space in the midclavicular line.”
* do not wait for investigations
* once pressure relieved with cannula then insert chest drain for definitive treatment
162
where are chest drains inserted
* into triangle of safety between:
* 5th intercostal space
* mix axillary line
* anterior axillary line
* insert needle just above the rib to avoid neurovascular bundle that runs below the rib
* once inserted get a chest x ray to check positioning
163
when is BiPAP used
* for TYPE 2 respiratory failure
* the criteria for initiating are:
* pH \<7.35
* PaCO2 \>6
* despite adequate medical treatment
164
what is NIV
non invasive ventilation can be either BiPAP or CPAP
165
contraindictations for BiPAP
* untreated pneumothorax
* if it doesn't delay they should have a CXR to exclude pneumothorax before the BiPAP is initiated
166
IPAP and EPAP for BiPAP
* IPAP (inspiratory positive airway pressure)
* sensible starting point for average male pt: 16-20cmH2O
* EPAP (expiratory positive airway pressure)
* sensible starting point for average male pt: 4-6cmH2O
167
monitoring BiPAP
repeat ABG 1hr after every change and every 4hrs after that until stable
IPAP is increased by 2-5cm increments until the acidosis resolves
168
causes of pulmonary hypertension
can be split into 5 groups
1. primary pulmonary hypertension or connective tissue disease like SLE
2. left heart failure usually due to myocardial infarction or systemic hypertension
3. chronic lung disease like COPD
4. pulmonary vascular disease such as pulmonary embolism
5. misc causes
1. sarcoid
2. glycogen storage disease
3. haematological disorders
169
signs and symptoms of pulmonary hypertension
* SOB main symptom
* others
* syncope
* tachycardia
* raised JVP
* hepatomegaly
* peripheral oedema
170
ECG changes in pulmonary hypertension
* right sided heart strain produces:
* right axis deviation
* right bundle branch block
* right ventricular hypertrophy
* larger R waves on the right sided chest leads (V1-3)
* S waves on the left sided chest leads (V4-6)
171
how do you treat primary pulmonary hypertension
* IV prostanoids (e.g. epoprostenol)
* endothelin receptor agonists (e.g. macitentan)
* phosphodiesterase-5 inhibitors (e.g. sildenafil)
172
what is the way of assessing someone for sleep apnoea
epworth sleepiness scale
173
what is GPA
granulomatosis with polyangiitis - rare form of vasculitis
174
how is GPA classified
ELK classification:
* E indicates ear nose and throat as it most commonly affects URT
* L indicates lung involvement (most patients)
* K indicates kidney involvement (\>75% patients)
can also affect many other areas of the body - i.e. joints
175
symptoms of GPA
can be literally anything :
Fatigue, malaise
Fever, night sweats
Weakness
Loss of appetite
Weight loss
Rhinorrhoea
Sinusitis
Facial pain
Hoarseness
Cough
Dyspnoea
Wheezing
Chest pain
Joint pains
Hearing loss
176
distinctive signs in GPA
subglottic stenosis causing hoarseness, stridor, dyspnoea or cough
rashes - petychial or purpuric
177
investigations for GPA
ESR
U&E for renal involvement
c-ANCA and p-ANCA detectible in nearly all patients with active severe GPA
biopsy of affected tissue looking for presence of vasculitis and granulomas
178
treatment for GPA
* asymptomatic patients with no organ damage
* methotrexate to induce remission
* patients with life-threatening organ damage
* cyclophosphamide
* with prednisolone
* rituximab if they can't have cyclophosphamide
* with prednisolone
* once in remission switch to methotrexate with prednisolone
* titrate this down or up if relapses
* if relapse they may need plasma exchange
179
what is GPA AKA
wegeners granulomatosis
180
what is goodpastures
co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage
it is a specific autoimmune disease caused by type II antigen-antibody reaction
181
what antibodies circulate in goodpastures
anti-glomerular basement membrane antibodies
anti-GBM
this is diagnostic
182
which HLA type is goodpastures linked to
HLA-DRB1
183
typical presentation of goodpastures
Typically presents as acute kidney injury caused by a rapidly progressive glomerulonephritis, accompanied by pulmonary haemorrhage that may be life-threatening
184
management principles of goodpastures
1. remove circulating antibodies with plasmapheresis
2. stop further production of antibodies with immunosuppression
1. IV methylprednisolone with cyclophosphamide or azathioprine
3. remove identifiable causes of antibody production
185
186
187
188
189
formative 3b
flashcards
Decks in class (18)
# Cards
-
Respiratory189
-
Cardiology Peer Teaching176
-
Haematology Peer Teaching155
-
GI Peer Teaching146
-
Liver and Friends209
-
MSK Peer Teaching160
-
Renal/GU191
-
Neuro283
-
Endocrinology Peer Teaching147
-
Public Health319
-
COTE peer teaching83
-
Obs & Gynae Cards393
-
paeds brief266
-
Paediatrics247
-
Psychiatry and Neurology182
-
ENT118
-
Opthalmology121
-
quick orthopaedics from ZTF168
