Respiratory COMPLETE Flashcards
Respiratory failure, COPD, Asthma, Pneumonia, DVT/PE inc prevention and anticoag, Pneumothorax, Lung cancer, Pleural effusion, OSAS
Give 5 broad causes of Type I Respiratory Failure.
VQ mismatch e.g. PE, atelectasis
Shunt e.g. patent foramen ovale, atrial septal defects
Low inspired oxygen concentration e.g. high altitude
Alveolar hypoventilation e.g. neuromuscular disorders, chest wall deformities, interstitial lung disease
Altered gas diffusion e.g. pneumonia, ARDS, pulmonary fibrosis
Give 4 broad causes of Type II Respiratory Failure.
Reduced breathing effort; sedation, brainstem disorders, obesity, drugs
Neuromuscular diseases; GBS, MND, spinal cord lesions, MG
Thoracic wall abnormalities e.g. kyphoscoliosis
Increased airway resistance e.g. asthma, COPD, pneumonia, lung fibrosis
Explain the differences between CPAP and NIV (BiPAP).
NIV / BiPAP; creates inspiratory and expiratory positive airway pressure, leading to air moving via a pressure gradient. Facilitates CO2 clearance, airway opening and reduces work of breathing. CO2 retention and COPD very useful. High expiratory positive airway pressure also reduces preload and decreases stroke volume
CPAP; continuous positive airway pressure through all phases of ventilation, facilitating oxygenation by stenting open airways. Congestive HF and OSA very useful. Increases intrathoracic pressure and therefore reduces preload. Care should be taken in patients with low BP.
Give the 3 principles of treating respiratory failure.
- Ensuring adequate oxygenation
- Treating the underlying cause of respiratory failure
- Providing supportive care e.g. hydration, nutrition, electrolyte imbalances
** Be aware in type 2 failure that oxygen must be very carefully controlled, as some patients are at risk of CO2 retention.
Give 3 modes of assisted ventilation, and also give 5 mechanisms of damage that assisted ventilation can cause.
HFNO; heated and humidified, through a NC, up 60L/min. Generates PEEP, reducing work of breathing. Cannot be used if reduced respiratory drive.
NIV / BiPAP
CPAP
Oxygen toxicity
Volutrauma / overstretching
Barotrauma / pressure overload
Biotrauma / shear forces
Cardiac overstimulation
Describe the oxygen / co2 concentrations in I and II respiratory failure.
Type I - low oxygen, low / normal CO2. Primary cause is VQ mismatch
Type II - hypoxia + raised CO2.
Give some differential diagnoses for asthma.
COPD
Upper airway obstruction e.g. tumour, laryngeal oedema
Foreign body aspiration
LV failure
Recurrent pulmonary emboli
Eosinophilic pneumonia
Give 5 different types of investigation commonly used when asthma is suspected, and outline the results that would point towards a diagnosis of asthma.
First line: FeNO (or eosinophil count). FeNO ADULTS >50ppb is diagnostic, >35ppb 5-16yrs diagnostic.
Bronchodilator reversibility testing with spirometry:
>12% increase and 200ml or more from pre-bronchodilator measurement OR >10% of predicted normal FEV1.
PEF variability; diagnose asthma if PEF variability >20%, measuring BD for 2 weeks.
If asthma is not confirmed by eosinophil count, FeNO, BDR or PEF variability, refer for:
Bronchial challenge testing (histamine / methacholine)
Give 4 classic symptoms of asthma and 2 clinical signs.
Wheeze
Dry cough worse at night
SOB
Chest tightness
Widespread polyphonic expiratory wheeze
Reduced PEFR
Outline some risk factors for asthma, not including personal / FHx of atopy.
Antenatal; maternal smoking, RSV infection
Low birth weight
Not breastfed
High exposure to allergens e.g. dust mites
Air pollution
What chemical is the culprit for the most common cause of occupational asthma?
Isocyanates - spray painting and foam moulding using adhesives.
Investigation of asthma in children is fairly similar to adults, but some steps are slightly different. Outline these differences.
In adults, eosinophil count is taken first line alongside FeNO, but this is NOT done in children.
Bronchial challenge testing is not considered as soon as in adults (after FeNO, BDR, PEF), but the next line is skin prick testing to house dust mite or measuring total IgE and blood eosinophil count.
Diagnosis of asthma can be made from these two if there is evidence of sensitisation OR a raised total IgE and eosinophil count is >0.5 x 10^9/L
When asthma is uncontrolled, it’s important to consider reasons for this. What could some reasons be?
Environmental e.g. air pollution, dust exposure
Poor adherence to medication
Smoking
Inhaler technique is poor
Alternative Dx or comorbidities
Measure FeNO if uncontrolled, and if high could indicate poor compliance with medication or need for higher ICS dose.
After starting medications for asthma, when should the patient be reviewed?
8-12 weeks later
What type of drug is formoterol?
Fast-acting long acting beta2 agonist.
Acts on airway to relax airway smooth muscle.
What is the discharge criteria following an acute asthma attack (3).
On discharge medications and stable for 12-24 hours.
Checked and recorded inhaler technique.
PEFR >75%.
Discuss management of an acute asthma attack in an adult, including timescale of escalation of treatment.
- Oxygenation if hypoxic.
- High dose inhaled SABA; normally a pMDI. Oxygen driven nebulised is preferred in life threatening.
- Oral prednisolone 40mg / 5 days. Continue normal ICS during this period.
- Ipratropium Bromide
- IV mag sulf
?Aminophylline
?Intubation and ventilation
What is usually seen on an ABG in a patient intially presenting with an acute exacerbation of asthma?
Respiratory alkalosis, as tachypnoea initially causes a drop in CO2.
Normal CO2 is a bad sign, of exhaustion.
Respiratory acidosis due to high CO2 is very bad.
When should follow up of a mild acute exacerbation of asthma occur, and how should it be managed?
Within 48 hours.
SABA via spacer.
Quadrupled dose of ICS for up to 2 weeks.
Consider oral steroids.
?Abx if convincing infection
What are the potential side effects of salbutamol therapy?
Hypokalaemia (K+ is absorbed from blood into cells, must be monitored)
Tachycardia
Lactic acidosis
What is the most common type of lung cancer overall, and the most common type among non-smokers?
Squamous Cell (nsclc)
Adenocarcinoma more common in non-smokers.
Which type of lung cancer arises from central airways, grows quickly and spreads early?
Small cell lung cancer
Describe the paraneoplastic features seen in squamous cell lung cancer.
PTHrP secretion causing hypercalcaemia.
Clubbing
HPOA - hypertrophic pulmonary osteoarthropathy
Ectopic TSH causing hyperthyroidism
What is Lambert-Eaton myasthenic syndrome, and which 3 types of cancer can it be associated with?
Mainly SCLC, but breast and ovarian too.
Antibody directed against calcium channel in PNS; causes limb girdle weakness, repeated muscle contractions, hyporeflexia, autonomic sx including dry mouth, impotence and micturation difficulty.
Apart from Lambert-Eaton syndrome, what other 2 paraneoplastic features are associated with sclc?
ADH, causing hyponatraemia (SIADH)
ACTH; hypertension, hyperglycaemic, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc.
ACTH secretion can cause bilateral adrenal hyperplasia, and high levels of cortisol can lead to hypokalaemic alkalosis.
What 2 paraneoplastic features can be seen in adenocarcinomas?
Gynaecomastia
HPOA
A CXR is often done first line in suspected lung cancer, but what is the investigation of choice?
CT
What type of scan is done to establish curative eligibility in lung cancer?
PET scan - mostly in NSCLC
18-flurodeoygenase is taken up by neoplastic tissue
Improves diagnostic sensitivity in local ad distant mets in NSCLC
Not many lung cancers are suitable for surgery (20% of NSCLC). State some contraindications to surgery.
IIIB / IV (mets present)
FEV1 <1.5L
Malignant pleural effusion
Tumour near hilum
Vocal cord paralysis
SCVO
When should you refer a person with suspected lung cancer?
Refer via USOC:
CXR findings suggestive of lung cancer
>40 with unexplained haemoptysis
Offer urgent within 2 weeks CXR:
>40 if 2 or more, or smoker/ever smoked with 1 or more UNEXPLAINED:
cough
fatigue
SOB
Chest pain
weight loss
appetite loss
Consider 2 weeks CXR in >40s if:
Persistent or recurrent chest infection
Clubbing
Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
Chest signs consistent with lung cancer
Thrombocytosis (raised platelets)
What does Pemberton’s sign refer to and what is this a sign of?
Raising arms above the head causes facial congestion and cyanosis.
Caused by direct compression of a tumour on the SVC; SVCO.
Presents with facial swelling, difficulty breathing and distended veins in neck and upper chest.
What is Horner’s syndrome?
Ptosis, anhidrosis and miosis.
Can be caused by a Pancoast tumour in the pulmonary apex pressing on the sympathetic ganglion.
What is limbic encephalitis?
Paraneoplastic syndrome in SCLC where anti-Hu antibodies are made against the limbic system in the brain.
Causes inflammation in these areas; causes short term memory impairment, hallucinations, confusion and seizures.
What method is used to biopsy a lung cancer?
Bronchoscopy with EBUS
What is the criteria for a diagnosis of ARDS?
Acute onset <1 week of known RF
Bilateral infiltrates on CXR showing pulmonary oedema
Non-cardiogenic (pulmonary artery wedge pressures can be done if unsure)
pO2 / FiO2 <40kPa / 330mmHg
Briefly describe the physiological changes in ARDS and the clinical signs it may present with.
Caused by increased permeability of alveolar capillaries, leading to fluid accumulation in the alveoli (i.e. non-cardiogenic pulmonary oedema).
Due to marked lung inflammatory response, includes surfactant dysfunction.
Acute onset and severe symptoms:
SOB
RR increased
Crackles heard bilaterally
Reduced oxygen saturations
(Severe respiratory failure on the background of non-cardiogenic pulmonary oedema due to alveolar failure)
Give some known causes of ARDS.
Sepsis
Pneumonia
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
Severe burns
DIC
Near-drowning
Cardio-pulmonary bypass
Write down asthma prescribing guidelines (2024) for patients aged over 12.
https://www.nice.org.uk/guidance/ng245/resources/algorithm-c-pharmacological-management-of-asthma-in-people-aged-12-years-and-over-bts-nice-pdf-13556516367
Write down asthma prescribing guidelines (2024) for patients aged 5-11.
https://www.nice.org.uk/guidance/ng245/resources/algorithm-d-pharmacological-management-of-asthma-in-children-aged-5-to-11-years-bts-nice-sign-pdf-13556516368
Write down asthma prescribing guidelines (2024) for patients aged under 5.
https://www.nice.org.uk/guidance/ng245/resources/algorithm-e-pharmacological-management-of-asthma-in-children-under-5-bts-nice-sign-pdf-13556516369
What is OSAHS, including pathophysiology.
Sleep-disordered breathing characterised by pharyngeal / upper airway collapse, causing obstructive apnoeas and hypopnoeas with desaturation.
Respiratory muscle activity is reduced during sleep, only the diaphragm is the active muscle. Apnoeas occur when airway at the back of the throat is sucked closed when breathing (usually upper airway muscles e.g. genioglossus and palatal keep this open during the day).
Partial narrowing = snoring
Complete = apnoeic episode
Apnoea causes hypoxia, and strenuous respiratory effort ensues to try and combat this. Central hypoxic stimulation + the strenuous effort awakens the patient from sleep, but these awakenings are often so brief that the patient does not remember them at all, but they wake up in the morning having had a very unrefreshing sleep.
Correctable features of OSA occur in 1/3 of cases. State some of these correctable factors.
Nasal obstruction; deformities, polyps, adenoids
Respiratory depression: sedatives, strong analgesics / opioids, alcohol
Encroachment on pharynx; acromegaly, obesity, enlarged tonsils
Give a description of a classic patient presenting with OSA.
Middle aged, overweight man who snores very loudly and is complaining of daytime sleepiness, causing him to nod off at work. Wife reports snore-silence-snore cycle every night. He sometimes wakes up with a headache.
Some environmental factors can be risk factors for OSA. Give some of these, and then also some other medical conditions that can presdispose to OSA.
Obesity
Alcohol use at night
Hypothyroidism, acromegaly and amyloidosis can cause macroglossia
Marfan’s is also a risk factor
Give 9 symptoms of OSA, from most to least common.
Loud snoring
Daytime somnolence
Unrefreshed sleep
Restless sleep
Morning headache
Nocturnal choking
Reduced libido
Morning ‘drunk’
Ankle swelling
Give 2 complications of severe OSA, and 2 conditions it increases the risk of.
Hypertension
Heart failure
Increased risk of stroke and MI
What is the scale that OSA severity is graded on?
Apnoea Hypopnoea Index (AHI): number of apnoeic episodes per hour (<5 normal)
Mild 5-15
Moderate 15-30
Severe >30
Describe the different levels of investigation into suspected OSA.
Collateral histories
Overnight pulse oximetry
Polysomnography inc EEG, EMG, RR, snoring etc.
Give some initial lifestyle advice for treating OSA, and then further interventions that may be required.
Lose weight
Alcohol reduction esp close to bed time
CPAP is first line for moderate or severe
Intra-oral device e.g. mandibular advancement
State some important features that should be present when making a diagnosis of OSA.
Collateral history if available
Poor concentration
Not feeling refreshed from sleep
Classic sx overnight
Epworth sleepiness scale worth doing; excessive = >9. OSA is one of the major causes of this, others include narcolepsy and restless leg.
How many mls must be present in a pleural effusion in order to detect it on a) CXR and b) clinically?
> 300ml CXR
> 500ml clinically
What two categories can pleural effusions be put into, and what is the broad cut off?
Exudative; protein >30g/L. LDH tends to be >200.
Transudative; protein <30g/L. LDH tends to be <200.
Describe Light’s criteria and what it indicates.
Identifies an exudative effusion
Fluid protein : serum protein >0.5
Fluid LDH : serum LDH > 0.6
Fluid LDH >2/3 upper limit of normal of serum LDH
Describe the cause of an exudative pleural effusion, and give some examples.
Exudative is due to inflammation, protein leaks out of tissues into pleural space.
Malignancy e.g. lung, mesothelioma
Infection e.g. pneumonia, TB
RA/SLE
+ pancreatitis, Dressler’s, PE
Describe the cause of a transudative pleural effusion and give some examples.
Fluid only, more pressure related.
Congestive HF
Hypoalbuminaemia e.g. nephrotic syndrome
Hypothyroidism
Meig’s syndrome
Constrictive pericarditis
When should Light’s criteria be used to assess a pleural aspirate?
When protein is borderline; 25-35g/L
Pleural fluid can also have other features apart from protein and LDH levels that can point to a cause. Give 3 of these features and discuss what they might indicate.
Low glucose; RA, TB
Raised amylase; pancreatitis, oesophageal perforation
Heavy blood staining; mesothelioma, PE, TB
When should a chest tube be placed to manage a pleural effusion (2 indications)?
Purulent / turbid / cloudy fluid
Clear fluid BUT pH <7.2 in patients with suspected pleural infection
What is a chylothorax, and what can cause it?
Lymph fluid in the pleural space due to leakage from the thoracic duct following trauma or infiltration from carcinoma.
Give 4 options for managing patients with recurrent pleural effusions.
- Repeated drainage
- Pleurodesis using talc or tetracyclines
- Indwelling pleural catheter
- Drugs for symptoms e.g. opioids to relieve dyspnoea
Give 4 CXR features of a pleural effusion.
Blunting of costophrenic angles.
Meniscus sign.
Fluid in lobar fissures.
Tracheal and mediastinal deviation (if very large).
Describe the management of a spontaneous pneumothorax.
https://handbook.ggcmedicines.org.uk/static/uploads/pneumothorax_-_1508.pdf
Discuss 3 lifestyle factors that a patient who has had a pneumothorax needs to be aware of.
Flying - can only fly after radiologically confirmed to be gone, and 1 week post this confirmation. 2 weeks after drainage if no residual air.
Diving - permanently avoided unless bilateral surgical pleurectomy and normal lung function and CT chest post-op.
Should be encouraged to stop smoking.
Discuss the classification of pneumothoraces.
Primary spontaneous e.g. tall, thin man. No underlying lung conditions. Due to bleb rupture.
Secondary spontaneous; pre-existing lung disease e.g. COPD, asthma, CF, lung cancer, pneumocystic pneumonia. Marfan’s is also a risk factor.
Iatrogenic e.g. CVC insertion, ventilation, lung biopsy.
Traumatic e.g. blunt trauma, penetrating trauma leading to lung injury and air accumulation.
What is a catamenial pneumothorax, and what percentage of spontaneous pneumothoraces does it account for?
3-6% of spontaneous pneumothoraces that occur in menstruating women.
Thought to be due to endometriosis within the thorax.
Give 2 symptoms and 5 signs of a pneumothorax.
Dyspnoea
Pleuritic chest pain
Reduced chest expansion
Hyperresonance on percussion
Reduced breath sounds
Tachypnoea
Tachycardia
A tension pneumothorax can present with similar symptoms to a normal one, but will have some extra adverse features. What could these be?
Sudden onset of symptoms
Hypotension
Respiratory distress
Tracheal deviation
Presence of high risk characteristics in a pneumothorax can potentially interfere with management. What are these 6 characteristics set out by the BTS?
Haemodynamic compromise
Significant hypoxia
Bilateral pneumothoraces
Underlying lung disease
> 50 with significant smoking Hx
Haemothorax
A patient has no symptoms but has a pneumothorax of >3cm. How should this be managed?
No symptoms = conservative
How do you manage a tension pneumothorax?
Insert wide bore cannula into triangle of safety; 4th/5th intercostal space, anterior to mid-axillary line.
What are some causes of a tension pneumothorax, split into traumatic, iatrogenic and spontaneous?
Traumatic; penetrating or blunt chest trauma
Iatrogenic; Thoracocentesis, CVC insertion, positive pressure mechanical ventilation
Spontaneous; underlying disease e.g. COPD, CF. Lung blebs rupture spontaneously.
Describe the pathophysiology of a tension pneumothorax, including 4 mechanical consequences and their physiological outcomes.
Air enters the pleural space but cannot escape, creating a one-way valve effect. Continuous filling increases intrapleural pressure, constant positive pressure that exceeds atmospheric pressure throughout the respiratory cycle.
Lung Collapse - affected lung is compressed, leading to reduction in efficient gas exchange and functional residual capacity.
Mediastinal Shift - pressure pushes mediastinum to contralateral side. Can compress opposite lung. Tracheal deviation is a late sign.
Impaired Venous Return - mediastinal shift and raised intrathoracic pressure compresses the great veins and reduces venous return to the heart - obstructive shock can occur (hypotension and tachycardia).
Reduced Cardiac Filling - pressure on heart and reduced venous return causes impairment of RV and LV filling, lowering CO and systemic BP.
Describe the MRC Dyspnoea scale.
1 Breathless on strenuous exercise
2 Breathless walking uphill
3 Breathless causes them to slow down walking on the flat
4 Cannot walk <100m on the flat
5 Housebound due to breathlessness
How is the severity of COPD graded?
When post-bronchodilator FEV1/FVC is <0.7, FEV1 is used to grade severity.
Stage 1 = >80% predicted
Stage 2 = 50-79% predicted
Stage 3 = 30-49% predicted
Stage 4 = <30% predicted
Who does NICE recommend considering a diagnosis of COPD for?
Anyone >35 who is a smoker / ex-smoker with exertional SOB, chronic cough or regular sputum production.
State 4 recommended investigations for COPD and explain why each is important.
Spirometry with post-bronchodilator tests; to see lack of reversibility and FEV1/FVC ratio.
CXR; hyperextended lungs. Also to look for other differentials e.g. cancer, fibrosis.
FBC; check for secondary polycythaemia
BMI; weight loss occurs in late disease
Smoking is the most common cause of COPD (over 90% in the developed world). What are some other, much rarer causes?
Alpha-1 antitrypsin deficiency
Cadmium, coal, cotton, cement and grain??
What is Meig’s syndrome?
Triad of pleural effusion, benign ovarian tumour e.g. fibroma, and ascites.
CXR, spirometry, FBC and BMI are the standard recommended tests for COPD. Give some other investigations that might be relevant.
Alpa-1 antitrypsin (to check for deficiency, especially in younger, non-smoking patients)
Sputum culture for chronic infection e.g. pseudomonas
ECG and echo to assess for HF and cor pulmonale
CT thorax for alternative diagnoses
TLCO (transfer factor for carbon monoxide) tests diffusion of inhaled gas into the blood (reduced in COPD)
What does cor pulmonale refer to, and give 5 potential causes of it.
Right-sided heart failure caused by respiratory disease.
Pulmonary hypertension limits RV, causing back pressure into the RA, vena cava and systemic venous system.
Causes include:
COPD
Cystic fibrosis
PE
Interstitial lung disease
Primary Pulmonary Hypertension
There are several factors that put people at an increased risk of a PE. State 9.
Surgery
Malignancy
Polycythaemia
SLE
Thrombophilia
Immobilisation
Recent flights / long haul
Hormone with oestrogen use e.g. COCP, HRT
Discuss VTE prophylaxis in hospital, including contraindications.
LMWH given to most patients, either halved dose or given UFH in renal disease
UNLESS already on a DOAC or warfarin
+ antiembolism stockings unless PVD.
PE can be asymptomatic or can cause symptoms so severe they can be fatal. Give 9 possible signs or symptoms of a pulmonary embolus.
SOB
Cough
Haemoptysis
Pleuritic chest pain
Hypoxia
Tachycardia
RR up
Low grade fever
Haemodynamic instability
?clinical signs of a DVT
What criteria make up the PERC score, and when do you use it?
PERC = PE rule-out criteria
Score 0 = <2% chance of PE, consider alternate Dx
Age >50
HR >100
O2 sats <95%
Unilateral leg swelling
Haemoptysis
Recent surgery or trauma <4 weeks
Prior PE / DVT
Hormone use e.g. oestrogen based OCP or HRT
What makes up the 2-level PE Wells score, when do you use it, and what do the results mean?
3 points; clinical DVT
3 points; PE number 1 diagnosis
1.5 points; HR >100
1.5 points; Immobilisation for 3 days OR surgery in previous 4 weeks
1.5 points; previous PE or DVT
1 point; haemoptysis
1 points; malignancy with active treatment in last 6 months or palliative
If a PE is ‘likely’ according to a 2-level Wells score what further investigations should be done? Discuss suspected PE diagnosis and initial management.
https://www.nice.org.uk/guidance/ng158/resources/visual-summary-pdf-11193380893
What is the investigation of choice for suspected PE if there is severe renal impairment and why? And when is it appropriate.
V/Q scan, as no contrast is used.
Can only be used if there is a normal CXR, no cardiopulmonary compromise / symptomatic problems and is indicated due to severe renal impairment.
Other causes of an abnormal VQ scan can include an old PE, AVM, vasculitis or previous radiotherapy.
Discuss some changes that may be seen on an ECG in a patient with a PE.
S1Q3T3;
Large S wave in Lead I
Large Q wave in Lead III
Inverted T wave in Lead III
(Only in 20% of patients however)
Also sinus tachycardia, RBBB and right axis deviation may be seen.
What might you see on a CXR in a patient with a PE?
Usually no change on a CXR
Where should patients with a confirmed diagnosis of a PE be managed?
Depends on clinical status; low risk PEs can be managed in the community.
High risk includes things like haemodynamic compromise, comorbidities, HR, BP, O2 sats etc.
When should immediate admission be arranged in a suspected PE?
Haemodynamic instability
Pregnant or up to 6 weeks post partum
What length of time should anticoagulation be continued for post PE diagnosis?
Provoked; 3 months, unless uncorrectable cause e.g. thrombophilia
Unprovoked; 3-6 months. Use ORBIT score to assess bleeding
What is the preferred anticoagulation method for a) pregnancy b) antiphospholipid syndrome c) severe renal impairment
Pregnancy; use LMWH
Antiphospholipid syndrome; use LMWH as a bridge and then warfarin
Severe renal impairment e.g. <15/min ; LMWH bridge then warfarin
Discuss the management of a massive PE with haemodynamic compromise.
UFH infusion
Consider thrombolysis (alteplase, streptokinase)
High risk of bleeding, so must be carefully considered.
Who should be considered for IVC filters, and how do they work?
Repeat PEs, despite adequate anticoagulation.
They stop clots formed in deep veins of the legs from moving to pulmonary arteries.
Which score should be used to decide whether a patient with a PE should be treated in hospital or in the community?
PESI score
Discuss the DVT 2-level Wells score, including criteria and what results would indicate.
DVT Wells score: perform if DVT suspected.
DVT likely = 2 points or more.
Unlikely = 1 point or less.
Previous DVT/PE
Active cancer
Paralysis / recent plaster immobilisation of lower extremities
Recently bedridden for 3 days or more or major surgery within 12 weeks requiring GA or regional anaesthesia
Localised tenderness along deep vein distribution
Entire leg swollen
Calf swelling >3cm
Pitting oedema on sx leg
Collateral superficial veins
Previously documented DVT
[Alternative Dx is at least as likely as a DVT = MINUS 2]
Discuss the further investigations / management of a suspected DVT.
https://www.nice.org.uk/guidance/ng158/resources/visual-summary-pdf-11193380893
There are a number of risk factors for developing VTE and this should be assessed in all hospital patients. What specific surgical / trauma risk factors are there?
Hip / knee replacement
Hip #
GA and surgical duration >90 mins
GA and surgical duration >60 mins if pelvis or lower limb surgery
Acute surgical admission with inflammatory / intra-abdominal condition
Surgery with significant reduction in mobility
Some surgical procedures require post-procedure prophylaxis. State 3 and the options that should be considered for anticoagulation.
Elective hip; rivaroxaban 28 days, or LMWH then aspirin 28 days, or LMWH 28 days
Elective knee; Rivaroxaban, LMWH 14 days or Aspirin 14 days
Fragility # of pelvis, hip or proximal fever; VTE proph for 1 month but use ORBIT score to assess bleeding, LMWH 6-12 hours post surg or fondaparinux 6 hours post surg.
Discuss symptoms and signs of a typical pneumonia.
Cough
Fever
Sputum production
SOB
Pleuritic chest pain
?haemoptysis
Crackles in chest
Dullness to percuss
Reduced O2 saturations
Discuss blood results that may have been tested in pneumonia.
FBC; wcc raised
CRP
U+Es; urea, AKI
*CRP and WCC rises generally correlate with disease severity. CRP rises 6 hours post onset of inflammation and peaks at 24-48 hours.
Discuss the CURB65 score and what it indicates.
It predicts mortality at 30 days.
0/1 = low risk <3%
2 = medium risk 3-15%
3-5 = high risk >15%
State 8 risk factors for contracting a pneumonia.
COPD/CF
Immunosupression
<5 / >65
Smoking
Aspiration risk
IVDU
Recent viral URTI
Underlying comorbidities e.g. T2DM
Which lobes are most likely to be affected in aspiration pneumonia and why?
Right lower and middle lobes, due to larger and straighter right main bronchus.
Streptococcus pneumoniae (pneumococcus) is the most common cause of CAP. Give 4 characteristic features of pneumococcal pneumonia.
Rapid onset
High fever
Pleuritic chest pain
Herpes labialis (cold sores)
State 5 atypical organisms that can cause pneumonia and give a few defining features of each one, and state the mnemonic to remember them.
Legions of Psittaci MCQs
Legionella; water e.g. air con / hot tubs. Causes SIADH / hyponatraemia, test with urine antigen.
Chlamydia psittaci; birds
Mycoplasma; erythema multiforme
Chlamydophila pneumoniae
Q fever; coxiella burnetii; from exposure to animal’s bodily fluids.
Why do atypical pneumonias often not respond to penicillins or cephalosporins?
Lack of peptidoglycan cell wall.
Mycoplasma pneumoniae is a cause of atypical pneumonia. It often affects younger patients, typically with a prolonged and gradual onset, with flu like symptoms preceding a dry cough. State some complications that it can cause.
Haemolytic anaemia
Erythema multiforme
ITP / thrombocytopenia
Myocarditis / pericarditis
Encephalitis / GBS
Acute glomerulonephritis
Pneumocystis jirovecii / PCP is the most common opportunistic infection in AIDS. Who gets PCP prophylaxis, and what are the typical features?
CD4 count <200/mm3
SOB exercise induced
Dry cough
Few chest signs
Fever
Complication: pneumothorax. Also 1% have hepatosplenomegaly / lymphadenopathy.
What are the investigation and management options for PCP?
CXR; bilateral pulmonary infiltrates
BAL is often indicated with silver staining to see characteristic cysts as doesn’t show up on sputum.
Investigate for exercise induced desaturations.
Co-trimoxazole
IV pentamidine if required
If O2 sats <9.3 give steroids
If a patient with a typical, low severity CAP pneumonia is allergic to penicillin, which classes of antibiotic should be considered?
Amoxicillin 5 days is first line BUT:
Tetracycline
Macrolide
Moderate and high-severity CAP recommended treatment:
Amoxicillin + macrolide, 7-10 day course
High severity; use a beta-lactamase stable penicillin e.g. co-amoxiclav, ceftriazone or PipTaz + macrolide
What information should be given to patients regarding recovery from their symptoms of pneumonia?
1 week - fever should be gone
4 weeks - chest pain and sputum production subsided
6 weeks - SOB and cough subsided
3 months - all sx resolved but fatigue present
6 months - should feel normal
A patient should NOT be discharged with a pneumonia if in the past 24 hours they have had 2 or more of the following:
Temp >37.5 (solo factor)
HR >100
RR >=24
SBP <90
Abnormal mental status
Inability to eat without assistance
Who should get a CXR post pneumonia , and when should this be done?
6 weeks, if:
Symptoms and signs that persist despite treatment
Higher risk of underlying malignancy e.g. smokers, >50 years
Which infective agent is the most common type of pneumonia to occur following an influenza infection?
Staphylococcus aureus
What is the most common organism found in pneumonia in alcoholics?
Klebsiella pneumoniae
What does triple positive refer to in antiphospholipid syndrome?
Anti-cardiolipin ab +ve
Lupus anticoagulant +ve
Anti-B2-GP1 +ve
When should you consider emergency admission for a person with an acute exacerbation of COPD?
Severe breathlessness
Acute confusion / impaired consciousness
Cyanosis
O2 sats <90%
Social reasons e.g. inability to cope at home or living alone
Significant comorbidity e.g. cardiac disease / insulin dependent diabetes
Explain the mechanism of how excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients.
V/Q Mismatch:
In COPD, patients optimise their gas exchange by hypoxic vasoconstriction, leading to altered alveolar VQ ratios. In over-oxygenation, this is overcome and there is increased blood flow to poorly ventilated alveoli, increasing the V/Q mismatch and increasing physiological deadspace. This occurs in both CO2 retainers and non-retainers but is more profound in certain patients.
Haldane effect:
Deoxygenated Hb binds CO2 with greater affinity than oxygenated haemoglobin. Oxygen therefore induces a right shift of the C02 dissociation curve. In patients with severe COPD who cannot increase minute ventilation, the Haldane effect accounts for 25% of total PaCO2 increase due to oxygen administration.
How should you safely manage oxygen delivery in a COPD patient who you think may be at risk of being a CO2 retainer?
Initial 88-92% scale, but VBG done ASAP and venous CO2 and bicarbonate assessed; adjust to normal 94-98% in absence of hypercapnia.
Venturi mask 28L at 4L/min
What management options are available to a patient who requires hospital admission for an exacerbation of COPD?
Oxygen therapy
Nebulised bronchodilator e.g. SABA salbutamol or SAMA ipratropium
Steroids, oral pred or IV hydrocortisone
?IV theophylline if patients not responding to nebulised bronchodilators
NIV / BiPAP if T2RF occurs
Give 4 general management strategies for stable COPD.
One off pneumococcal vaccine
Annual influenza vaccine
Smoking cessation help e.g. nicotine replacement therapy, varenicline or buproprion
Pulmonary rehab if people view themselves as functionally disabled by COPD, MRC 3 or above
What is the first line treatment for stable COPD?
SABA or SAMA
If first line treatment with SABA or SAMA is not optimal, patients must be assessed for asthmatic / steroid-responsiveness features. State 4 criteria that NICE recommend for this.
Previous, secure Dx of asthma / atopy
High blood eosinophil count
Variation in FEV1 over time at least 400ml
Diurnal variation in PEF >20%
If a patient with COPD is confirmed to have asthmatic / steroid responsive features. the next line of management is …
LABA + ICS
If they remain breathless or have exacerbations, then offer triple therapy with LAMA + LABA + ICS
*If already taking a SAMA, switch to SABA in triple therapy.
If a patient with COPD is confirmed to NOT have asthmatic / steroid responsive features. the next line of management is …
LABA + LAMA (switch from SAMA to SABA)
Discuss use of prophylactic antibiotic therapy in COPD.
Thorough assessment inc imaging is needed to exclude other possible causes of symptoms e.g. TB, antibiotic resistant organisms and bronchiectasis.
People with 3 exacerbations requiring steroid therapy and at least one requiring hospital admission in the previous year should be considered for a referral to a specialist in respiratory medicine to start azithromycin; 500mg 3 times per week.
Important points / investigations to consider before and after commencing oral macrolides.
BEFORE:
ECG to assess QTc interval
Baseline LFTs
Counsel about SEs inc gi upset, hearing and balance disturbance, cardiac effects
Sputum culture / microscopy for non-tuberculous myobacterium (CI)
AFTER
Consider dose reduction if GI SEs at 500mg doses
LFTs 1 months after starting treatment and then every 6 months
ECG 1 month after to chec QT
When does NICE recommend PDE-4 inhibitor use in COPD, and give an example of this type of drug.
Rofumilast
FEV1 post bronchodilator <50% predicted normal (severe disease)
AND
2 or more exacerbations in previous 12 months despite triple inhaled therapy (LAMA, LABA and ICS)
Oxygen is a treatment for hypoxia, not breathlessness. LTOT can improve survival in people with stable COPD and chronic hypoxia. When should a patient be referred for specialist assessment for LTOT?
O2 sats 92% or less
Very severe FEV1 <30%, or severe 30-49%
Cyanosis
Polycythaemia
Peripheral oedema
Raised JVP
