Academic Week 2 Flashcards

1
Q

What is the definition of Asthma?

A

Asthma is the presence of symptoms (1+ of wheeze, breathlessness, chest tightness or cough) and of variable airflow obstruction. They may also have airway hyperresponsiveness or airway inflammation as part of the disease.

Alternatively, Asthma is a heterogenous disease characterised by chronic airway inflammation. There will be a history of symptoms such as wheeze, SOB, chest tightness and cough which may vary over time and in intensity. There will be variable expiratory airflow limitation.

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2
Q

What is an endotype?

A

This is the biological process which drives the phenotype

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3
Q

How is asthma diagnosed?

A

History of characteristic symptoms and evidence of variable airflow limitation. This is tested with bronchodilator reversibility testing and a 12% improvement in spirometry confirms asthma. Spirometry is the GOLD standard test.

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4
Q

Define an asthma exacerbation

A

An acute or sub-acute worsening of symptoms and lung function compared with normal status

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5
Q

How should an asthma exacerbation be treated?

A

ABCDE approach. A severe attack will have the patient sitting hunched over, tachypnoeic, tachycardic, SATs lower than 90, using words not sentences and accessory muscles in use. Peak flow less than 50% predicted.

They need short acting beta agonists (salbutamol and ipratropium bromide), oxygen, oral steroids and IV steroids. Consider IV magnesium as a bronchodilator or high dose inhaled corticosteroids.

All patients who have had an exacerbation are at increased risk of having another one as chronic asthma care may not be good enough.

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6
Q

When is an asthma exacerbation life threatening?

A

PEF > 33%, silent chest, cyanosis, poor respiratory effort, arrhythmias, hypotension, exhaustion and altered consciousness.

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7
Q

What is the most common new presentation of HIV?

A

Pneumonia with pneumocystitis jirovecii the causative organism. This has a classic Bat wing presentation on X-ray.

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8
Q

What are the risk factors for pneumonia?

A

People who regularly take inhaled corticosteroids, those who smoke, aged over 65 and travel history.

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9
Q

How can pneumonias be differentiated on X-ray?

A

Bacterial pneumonia has a lobar consolidation in a focal area whereas viral pneumonia has a ground glass presentation.

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10
Q

What is the most common cause of pneumonia?

A

Streptococcus Pneumonia

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11
Q

What is the CURB65 score?

A

This is used to assess management of pneumonia. Greater than 3 means there is significant risk of death within the next 30 days.
C = Confused on admission?
U = Blood Urea Level - greater than 7 is concerning
R = Respiratory rate greater than 30
B = Blood pressure below 90/60
65 = Aged over 65?

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12
Q

How does the CURB65 score relate to treatment?

A

CURB65: 0-1 = Amoxicillin
CURB65: 2 = Amoxicillin and erythromycin
CURB65: 3+ = Co-amoxiclav and clarithromycin

HAPs and VAPs will need broader cover because there is an increased risk of anaerobe infection.

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13
Q

How is pulmonary TB treated?

A

This can either be treated with rifampicin and Isoniazid for 4 months or rifampicin, Isoniazid, pyrazinamide and ethambutanol for 2 months.

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14
Q

How is TB tested for?

A

The Montu test is a skin test where TB proteins are inserted under the skin. If the area of induration becomes very large then it is likely the person has TB.

TB contact tracing can also be done through IGRA blood tests where T cell are exposed TB antigens to see if they react.

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15
Q

How should flu be treated in people at high risk?

A

A PCR test can be done to confirm the diagnosis. Treatment is with supportive care and Oseltamivir if it has been caught early enough.

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16
Q

What are the causes of lung cancer?

A

Smoking (daily but no threshold), passive smoke (1.3x risk), asbestos exposure, radioactive emissions, volatile hydrocarbons, diesel fuel and pulmonary fibrosis.

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17
Q

What are the symptoms of lung cancer?

A

Haemoptysis, cough, wheeze, chest pain and breathlessness. These are non-specific and often presents late. Many cases are found on imaging for other reasons.

Lung cancer should always be confirmed on CT.

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18
Q

Describe metastatic manifestations of lung cancer?

A

Intrathoracic manifestations include Horner’s syndrome, left recurrent laryngeal nerve palsy, SVC obstruction, phrenic nerve palsy, pericardial effusion, pleural effusion and dysphagia.

Extrathoracic metastases include brain, liver, bone and adrenal metastases.

Lung cancer also also present with finger clubbing, Cushing’s syndrome and gynaecomastia.

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19
Q

What cancers metastasise to the lungs?

A

Breast, GI and sarcomas.

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20
Q

How should lung cancer be managed?

A

The first step is to measure lung function with spirometry.

Performance should then be assessed and scored:
0 - Able to carry out normal activities
1 - Able to carry out light work
2 - Unable to carry out light work
3 - Limited self care
4 - Completely disabled

CT biopsies or flexible bronchoscopy biopsies are used to stage the tumour. A PET scan uses a radioisotope to stage the tumour. Lymph nodes are needed to determine if surgery is viable.

EBUS is a bronchoscope with a USS to check lymph nodes and avoid surgery if possible. Pleural effusions which are found will need draining.

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21
Q

What are small cell lung tumours?

A

These are extremely aggressive tumours which have a very poor prognosis.

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22
Q

What types of lung cancers are treatable?

A

Squamous, adenocarcinomas and non-small cell tumours of unknown morphology.

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23
Q

What types of lung cancers can be targeted with tyrosine kinase inhibitors?

A

These target single genomic drivers such as EGFR, ALK, ROS1, BRAF, NTRK, MET, RET and HER2.

These are almost always adenocarcinomas. The FISH test is used to check for ALK mutations.

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24
Q

What types of lung cancers can be treated with immune modulators?

A

These work by attacking PD-L1 and tumour mutational burden (TMB)

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25
Q

What is the definition of general anaesthetic?

A

This is the absence of sensation associated with a reversible loss of consciousness. These drugs work via the CNS.

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26
Q

Generally how do anaesthetic drugs work?

A
  1. Inhibition of the excitatory pathways and neurotransmitters in the CNS, this reduces neural transmission and leads to reduced consciousness (Glutamate is targeted by ketamine via the NMDA receptor)
  2. Potentiation of the inhibitory pathways and neurotransmitters in the CNS, this reduces neuronal transmission leading to unconsciousness. (Glycine and GABA)
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27
Q

Describe how the GABAa receptor works

A

The GABAa receptor is a pentameric (5 sub units) chloride channel. The chloride ions are negatively charged to make the membrane potential more negative and prevent action potential being proposed at the threshold potential is harder to reach with an excitatory impulse.

many anaesthetics cause an increase in GABAa movement making the neurone more negatively charged. This causes unconsciousness.

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28
Q

What is the binding site of most general anaesthetics?

A

The beta subunit of the GABAa receptor.

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29
Q

What is an induction agent and give some examples?

A

This is a drug which is used to get a patient to sleep. IV agents will achieve this within a minute but other options are available.

The two most common IV drugs used are propofol and thiopentone.

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30
Q

What does thiopentone do?

A

Reduces airway reflexes, causes respiratory depression, reduces cardiac output, causes tachycardia and vasodilation and will cause unconsciousness. There is a risk of severe anaphylaxis and reduced renal output.

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31
Q

What does propofol do?

A

This causes reduced airway reflexes, vasodilation, hypotension, unconsciousness, antiemetic, hyperlipidaemia and can turn urine green.

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32
Q

What are inhalation anaesthetics and what are they used for?

A

Once induction has been achieved, anaesthesia is maintained with inhalation anaesthetics. These include isoflurane, desflurane and sevoflurane. These are often administered with oxygen and nitrous oxide.

Sevoflurane can also be used as an induction agent.

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33
Q

What is the significance of nitrous oxide in anaesthetics?

A

Nitrous oxide is not a very potent anaesthetic but is a strong analgesic. Entonox is when nitrous oxide is mixed with oxygen.

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34
Q

When should nitrous oxide not be given?

A

Pneumothorax or severe emphysema, air embolus, skull fractures and intestinal obstruction.

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35
Q

Discuss the physiology of acetylcholine

A

Acetylcholine is an important neurotransmitter which is released at neuromuscular junctions and throughout the CNS.

It is synthesised by choline acetyl transferase which combines acetyl co-enzyme A with choline. It is then broken down in the synaptic cleft after release by acetylcholinesterase.

36
Q

How are muscle relaxants classified?

A

These are either depolarising (Suxamethonium) or non-depolarising.

Non depolarising are further divided into amino steroidal (rocuronium, vecuronium and pancuronium) or benzyliso-quinoliniums (atracurium, mivacurium and tubocurarine)

37
Q

Describe the mechanism of action of suxamethonium?

A

This is a depolarising muscle relaxant used in anaesthesia. The speed of action (30 seconds) means that the patient can be intubated with less risk of aspiration.

Suxamethonium is an acetylcholine receptor agonist. It initially causes muscle twitching but it does not get broken down causing paralysis.

Suxamethonium causes loss of airway reflexes, apnoea, occasional bradycardia, paralysis, muscle pain and hyperkalemia.

38
Q

Describe the mechanism of action of some non-depolarising muscle relaxants such as atracurium and rocuronium

A

These are competitive antagonists of the acetylcholine receptor. These have a slow onset but long length of action.

39
Q

Why should muscle relaxants not be given to patients with myasthenia gravis?

A

Patients with myasthenia gravis are at high risk of respiratory arrest if they are given any medications that interfere with nerve transmission. They should also not be given amino glycoside antibiotics such as gentamicin.

40
Q

What drugs are used to reverse the effects of muscle relaxants?

A

Acetylcholine esterase inhibitors.
Short acting: Edrophonium
Intermediate acting: Neostigmine
Permanent inhibition (until new enzyme is synthesised): Organophosphates

41
Q

Which muscle relaxant can be reversed immediately?

A

Rocuronium can be reversed immediately with sugammadex as this removes it from the acetylcholine receptor. This is only used in emergencies.

42
Q

Define COPD

A

This is a disease characterised by airflow obstruction, usually progressive, not fully reversible which does not change markedly over several months. This is primarily caused by smoking.

43
Q

What are the risk factors for COPD?

A

Tobacco smoke, occupational chemicals and dust, alpha-1-anti-trypsin deficiency, low birth weight, pollution, secondhand smoke, allergy and hyper-responsive airways.

44
Q

How are lung volumes affected in COPD?

A

FEV1/FVC is reduced below 80% with both FEV1 reduced and FVC slightly reduced. This is because of the lack of elastic recoil, 80% is mild whereas 49% or less is severe.

45
Q

What is the definition of an acute exacerbation of COPD?

A

A sustained acute worsening of symptoms from their usual stable state which goes beyond their normal day to day variations.

Exacerbations are almost always caused by viruses, bacteria or pollution. The inflamed airways cause greater inflammation, increased smooth muscle contraction and mucus production. This increases the airflow limitation and dynamic hyperinflation causing the exacerbation.

46
Q

How is an acute exacerbation of COPD diagnosed?

A

Two of the following criteria are needed for the diagnosis:

  1. Increased breathlessness
  2. Increased sputum production
  3. Increased sputum purulence
47
Q

How is an acute exacerbation of COPD managed?

A

Increase the bronchodilators available, provide antibiotics, and culture sputum in case they fail to respond to first line antibiotics. A corse of oral prednisolone should be given to speed up recovery.

Acute management is with oxygen, aminophylline, ventilation, post exacerbation pulmonary rehabilitation and then home care.

48
Q

Why should COPD patients have a SATs between 88-92%?

A

COPD patients are at high risk of hypercapnia, (type 2 respiratory failure) so oxygen levels should be run at 88-92%. Hypercapnia is too much oxygen.

49
Q

Describe the non-pharmacological treatment of COPD?

A

Smoking cessation, influenza and pneumococcal vaccines, pulmonary rehabilitation, self management, lung transplant, chronic ventilation and lung volume reduction surgery.

50
Q

Describe the pharmacological treatment of COPD?

A

SABA, LABA/LAMA (main treatment), inhaled corticosteroids, theophylline, roflumilast, low dose antibiotics and long term oxygen.

51
Q

When should COPD patients be offered long term antibiotics?

A

Azithromycin should be offered to COPD patients who do not smoke and who have had four or more exacerbations in the last year.

52
Q

When is long term oxygen given to COPD patients?

A

This is used to treat chronic hyperaemia. Ambulatory oxygen is given to people who have a SATs lower than 88% when walking. Palliative oxygen can also be givem

53
Q

What is pulmonary rehabilitation?

A

This is supervised exercise and education alongside disease management programmes if the patient is symptomatic with breathlessness.

54
Q

Why is lung volume reduction surgery used for COPD patients?

A

This is where a bronchoscope is used to collapse areas of lung which are redundant because of emphysema. This improves areas of good parenchyma.

55
Q

Define sleep apnoea

A

Sleep apnoeas can either be obstructive (airway is partially or completely blocked) or they are central (patient fails to make any effort to breathe). Obstructive failure is the failure of the upper airway to maintain latency when the upper airway dilator muscles relax with sleep.

56
Q

Define obstructive sleep apnoea?

A

The occurrence of obstructive sleep abnormalities on a sleep study combined with excessive daytime sleepiness.

57
Q

How should obstructive sleep apnoea be investigated?

A
  1. Oximetry
  2. Respiratory polygraph which detect breathing, effort, heart rate and sats
  3. Polysomnography which should only be used for non-respiratory sleep problems such as leg movements and narcolepsy
58
Q

What is management of obstructive sleep apnoea?

A

Treating the underlying cause is the main treatment, especially when the cause is hypothyroidism, obesity, alcohol or acromegaly.

Losing weight will be beneficial for all patients and some should be offered gastroplasty. Postural training may also be helpful to prevent patients sleeping on their backs.

Surgery and dental devices can be provided but the mainstay of treatment is CPAP.

59
Q

What are the signs and symptoms of obstructive sleep apnoea?

A

Excessive daytime sleepiness, headache, waking at night, swollen ankles, signs of cor pulmonale, cardiomegaly, right sided heart failure and raised bicarbonate on ABG

60
Q

How should patients with heart failure and Obstructive Sleep Apnoea be treated differently?

A

NIV reduces hypercapnia, improves hypoxia and is often better tolerated than CPAP.

61
Q

What is narcolepsy?

A

Excessive daytime sleepiness due to a neurological condition caused by failure of neurotransmission in a small subset of neurones. It is usually caused by viral infections which damage the hypocretin/orexin and some patients have a genetic predisposition.

62
Q

What is cataplexy?

A

A sudden loss of muscle tone which is triggered by strong emotional reactions. This occurs in narcolepsy.

63
Q

How should narcolepsy be treated?

A

Scheduled nap times and sodium oxybutate to stop the cataplexy.

64
Q

How are interstitial lung diseases classified?

A
  1. Known cause such as connective tissue disease, occupational causes or drug related
  2. Idiopathic interstitial pneumonias such as IPF, non-specific interstitial pneumonia and cryptogenic.
  3. Granulomatous such as sarcoidosis and hypersensitivity pneumonitis
  4. Miscellaneous such as lymphangioleiomyomatosis and histocytosis X
65
Q

What lung function abnormalities will be found with interstitial lung diseases?

A

Decreased spirometry and decreased DLCO. DLCO is a direct measure of the severity of ILD

66
Q

Describe asbestosis pathology, symptoms and treatment

A

Asbestosis is characterised by slowly progressing pulmonary fibrosis caused by inhalation of asbestos fibres. The lungs cannot break down the fibres but the persistent attempts by the immune system leads to fibrosis 20-40 years after exposure.

Pleural plaques are indicative of exposure and treatment is with supportive care, avoiding further exposure and anti-fibrotic drugs.

67
Q

Describe hypersensitivity pneumonitis

A

This is a disease caused by an abnormal immune response to an inhaled antigen which causes the formation of granulomas. This is often seen in bird fanciers lung.

The disease is IgG and lymphocyte driven and needs repeated exposure to develop. On CT there will be granulomas and a mosaic pattern which may lead to honeycombing. Diagnosis is through lung biopsy or bronchoscopy of non-caseating granulomas.

Management is with antigen avoidance, steroids, immunosuppression, and best supportive care. Occupational causes should always be investigated.

68
Q

Describe the pathophysiology, symptoms and treatment of sarcoidosis

A

This is a multi system disease characterised by tissue infiltration and non-caseating granulomas. Left untreated it will progress to end-stage organ damage. This is more common in women.

It is diagnosed radiologically, clinically, ruling out alternatives and the presence of non-caseating granulomas on biopsy. These granulomas will be tighter and more rounded than in hypersensitivity pneumonitis.

Extra-pulmonary involvement will include skin, eyes, joints and thoracic nodes. Management is with observation if mild.

In severe cases immunosuppressive therapy or corticosteroids may be required.

69
Q

Describe the pathophysiology, diagnosis and management of idiopathic pulmonary fibrosis

A

This is a chronic progressive fibrotic lung disease of unknown cause. It occurs in men between 50-70. It has a five year prognosis.

It can be genetic and the life expectancy is dependent on number and severity of severe exacerbations.

Diagnosis is made on the basis of progressive restrictive pulmonary disease with no causes and radiological findings.

Management is with anti-fibrotic therapy such as nintedanib and pirfenidone. This should be used if FVC is 50-80% of predicted. Otherwise supportive care or lung transplantation. Acute exacerbations require hospital admission as there is a high mortality rate.

70
Q

Describe the pathophysiology, diagnosis and management of non-specific interstitial pneumonia

A

This is a chronic IIP that is characterised by a homogenous appearance of dense interstitial fibrosis with mine to moderate chronic interstitial inflammation.

It is usually idiopathic but can be associated with connective tissue diseases such as scleroderma, sjogren’s and myositis. It may also be seen in HIV.

Management is with observation, immunosuppression or corticosteroids.

71
Q

Describe the types of non-opioid analgesics

A

These are classified by their site of action such as non-selective COX inhibitors, preferential COX inhibitors, selective COX inhibitors and antipyretics with poor inflammatory action.

72
Q

Describe some adjuvant analgesics

A

These are drugs which are primarily used for other indications but also have an effect on pain. These include SSRIs, Gabapentin, Baclofen, diazepam and Lidocaine (local anaesthetic)

73
Q

What are the main steps in the WHO ladder?

A
  1. Non-Opioid analgesic
  2. Weak opioid
  3. Strong opioid
74
Q

How does paracetamol work?

A

This is a COX inhibitor which acts on the serotoninergic pathway. The conversion of arachnoid acid into prostaglandin H is catalysed by prostaglandin H synthase.

Prostaglanding H synthase is composed of COX-1 and COX-2 which is inhibited by paracetamol on the peroxidase site of the enzyme.

Paracetamol also increases the dose dependent concentration of serotonin in the cortex, hypothalamus, hippocampus and brainstem. This is useful as serotonin is involved in inhibiting pain in the CNS.

75
Q

What are the risks of paracetamol?

A

Rash, blood disorders such as neutropenia, thrombocytopenia and agranulocytosis but the major concern is overdose cause hepatotoxicity.

Paracetamol is toxic because 90% undergoes in the liver through C450 enzymes but 5% of these breakdown products are toxic. In overdose there will be structural and metabolic damage to the liver due to a high concentration of these toxic products.

76
Q

What are the side effects of NSAIDs?

A

Peptic ulcers, GI bleeding, sodium and water retention, hypertension, AKI and stoke

77
Q

What is type 1 respiratory failure?

A

This is a low oxygen concentration but normal CO2 concentration. This is a failure of oxygenation and is caused by pneumonia, PE, asthma, interstitial lung disease, pulmonary oedema and acute lung injuries.

78
Q

What is type 2 respiratory failure?

A

This is low oxygen and high CO2 concentration. This is a failure of ventilation. Conditions which cause this include COPD, neuromuscular disease, obesity, benzodiazepines and opiates.

A bounding pulse and a flap are signs of CO2 retention.

79
Q

What does the type of back pain indicate about the cause?

A

Localised pain: Typically indicative of muscular strain, facet joint injury or fracture

Radiating pain: Heightened risk of spinal cord, nerve root or brachial plexus injury

Acute onset: Mechanical injury

Pain which persists despite changes in position: Inflammatory pain such as strain, sprain and contusion.

Pain which depends on position: Nerve root compression

80
Q

What are the red flags for cauda equina?

A

Severe of progressive bilateral neurological deficit of the legs such as motor weakness with knee extension, ankle eversion or foot dorsiflexion.

Recent onset urinary retention or incontinence

Recent onset faecal incontinence

perianal or perineal sensory loss (saddle anaesthesia or parasthesia)

Unexpected anal sphincter laxity

81
Q

What are the red flags for a spinal fracture?

A

Sudden onset of severe central spinal pain which is relieved by lying down

A history of major trauma or minor injury with a background of osteoporosis

Point tenderness on a vertebrae

Structural deformity of the spine

82
Q

What are the red flags for cancer with back pain?

A

Patient aged over 50

Gradual onset of symptoms

Severe unremitting pain that remains when a person is supine, aching night pain which disturbs sleep, pain aggravated by straining and thoracic pain

Localised spinal tenderness

No symptomatic improvement after 4-6 weeks of conservative low back pain therapy

Unexplained weight loss

PMH of cancer such as breast, lung, GI, prostate, renal and thyroid cancers which are more likely to metastasise to the spine.

83
Q

What are the red flags for infection of the spine such as discitis, vertebral osteomyelitis or spinal epidural abscess.

A
Fever
TB
Recent UTI
Diabetes
History of IVDU
HIV or other immunosuppression
84
Q

Provide some non-skeletal causes of back pain?

A

Skin: Shingles and fibromyalgia

Brain: Psychogenic and central pain syndrome

Vascular: Dissecting aortic aneurysm

Referred pain: Oesophageal tumours, PE, mesothelioma, dissecting aortic aneurysm, MI, gastric cancer, perforating peptic ulcer, renal infarction, renal calculi, pancreatitis, pelvic inflammatory disease, ovarian tumours, ovarian cysts and testicular cancer.

85
Q

What are the yellow flags for back pain?

A

obesity, older age, increased severity of pain, disability, neurological involvement, anxiety, depression, emotional distress, somatisation, lack of education, smoking, inactivity, involvement in litigation or lack of employer satisfaction.

86
Q

What cancers metastasise to the spine?

A

Breast, lung, prostate, thyroid and renal

87
Q

What do ABPIS scores indicate (Ankle brachial pressure index)

A
  1. 9-1 = normal
  2. 5-0.9 = Presence of intermittent claudication

<0.5 = critical ischaemia