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2a - SBCS > Respiratory > Flashcards

Respiratory Flashcards

1
Q

2 common lower respiratory tract infections

A

Pneumonia
Tuberculosis

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2
Q

Define pneumonia

A

Acute inflammation of lung parenchyma (terminal bronchioles and area surrounding the alveoli)
Usually caused by an infection

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3
Q

Describe the 2 categories of acquired pneumonia

A
  • Hospital acquired pneumonia - community or <48h in hospitals
  • Community acquired pneumonia - >48h after hospital admission
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4
Q

RFs of pneumonia (5)

A
  • Infants and elderly
  • COPD, asthma
  • Nursing home residents
  • Immunocompromised - long term steroids
  • Alcoholics or IVDU
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5
Q

Name 3 bacteria that commonly cause CAP

A
  • Strep. pneumoniae
  • Staph. aureus
  • Haem. influenzae (mc in COPD)
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6
Q

Name 4 atypical bacteria that cause CAP

A
  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Coxiella burnetti
  • Legionella pneumophilia - typical returning from holiday
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7
Q

Why are atypical bacteria difficult to detect

A
  • Intracellular
  • Don’t grow on agar easily
  • Need serology
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8
Q

What class of Ab are atypical bacteria resistant to and how are they treated

A
  • Not susceptible to Beta lactams/ penicillin’s
  • Treat with macrolides (clarithromycin), tetracyclines (doxycycline) or fluoroquinolones (ciprofloxacin)
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9
Q

Bacterial causes of HAP

A
  • Strep pneumoniae
  • MRSA
  • Pseudomonas aeruginosa
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10
Q

Viral causes of pneumonia

A
  • Influenza virus A/B
  • respiratory syncytial virus
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11
Q

Fungal cause of pneumonia and how it is treated

A

Pneumocystis jirovecii
Co-trimoxazole

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12
Q

Who is mc affected by P.jirovicii

A

Most people who get Pneumocystis pneumonia have a medical condition that weakens their immune system, like HIV/AIDS

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13
Q

Pathophysiology of pneumonia

A

Invasion of mainly bacteria in lung parenchyma which overwhelms host defences and produces intra-alveolar exudates
* Atypical pneumonia infection outside the alveoli in the interstitium

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14
Q

Give 3 ways pathogens can reach the LRT

A
  • Inhalation
  • Aspiration
  • Haematogenous spread
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15
Q

Symptoms of pneumonia

A
  • Productive cough: mucopurulent sputum = bacterial, scant/watery = atypical
  • Fever, night sweats, rigor
  • Pleuritic chest pain and dyspnoea
  • Confusion
  • Lethargy, malaise
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16
Q

Signs of pneumonia

A
  • Tachycardia and tachypnoea
  • Fever
  • Dullness to percussion
  • Crackles and wheeze
  • Decreased breath sounds
  • Low blood pressure
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17
Q

Describe the findings of the GS Investigation for pneumonia

A

CXR
* Consolidation: air bronchogram i.e. air filled bronchi made visible by adjacent fluid filled alveoli
* Multiple abscesses = S.aureus
* Multi-lobar suggest S.pneumoniae, S.aureus or Legionella
* Upper lobe lesions suggest klebsiella (but must exclude TB)

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18
Q

Other investigations for pneumonia (exc CXR)

A
  • Sputum and blood culture - causative organism
  • U+E - deranged = severe
  • CRP elevated
  • FBC - leukocytosis
  • Pulse oximetry - assess severity and (if done with ABG) defines RF
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19
Q

Describe the assessment of CAP severity

A

CURB65 score - 1pt for each
* Confusion - abbreviated mental score <8
* Urea >(=)7 mmol/L
* Respiratory rate >(=) 30/min
* BP; low systolic < 90mm/Hg or diastolic <(=) 60mm/Hg
* Age >(=) 65

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20
Q

Describe the implication of CURB65 score

A
  • 0-1 = mild, at home Tx
  • 2 = moderate = admit
  • 3-5 = severe, admit and monitor closely (consider ICU)
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21
Q

How is CURB65 adjusted in a community setting

A
  • Urea is not available = CRB65
  • 0= mild, 1-2 = moderate and 3-4 = severe
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22
Q

General treatment for pneumonia

A
  • 02 if needed
  • Analgesia
  • Ab depending on trust and causative pathogen
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23
Q

Management for low risk pneumonia (CRB65 0) in a primary care setting

A
  • Oral amoxicillin
  • Clarithromycin or doxycycline
  • 5 day course
  • treatment at home
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24
Q

Management of intermediate risk (CRB65 1-2) pneumonia in a primary care setting

A
  • Oral amoxicillin + clarithromycin
  • 7-10 day course
  • hospital assessment should be considered
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25
Q

Management of high risk pneumonia (CRB65 3-4) in a primary care setting

A
  • IV co-amoxiclav + clarithromycin
  • Alternative: cefuroxime + clarithromycin
  • 7-10 day course
  • urgent admission to hospital
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26
Q

When should all cases of pneumonia have a repeat chest X-ray and why?

A

6 weeks after clinical resolution to ensure consolidation has resolved and to check for any underlying secondary abnormalities (e.g., lung tumour)

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27
Q

What are the discharge criteria for pneumonia

A

Patients should not be routinely discharged if, in the past 24 hours, they have had 2 or more of the following findings:

  • Temperature > 37.5°C
  • Respiratory rate ≥ 24 breaths per minute
  • Heart rate > 100 beats per minute
  • Systolic blood pressure ≤ 90 mmHg
  • Oxygen saturation < 90% on room air
  • Abnormal mental status
  • Inability to eat without assistance
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28
Q

Tx of pseudomonas aeruginosa

A

IV Ceftazidime or Piperacillin-tazobactam

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29
Q

Tx of suspected or confirmed MRSA

A
  • Vancomycin
  • Linezolid
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30
Q

What are 4 non-infectious causes of pneumonia

A
  • Malignancy
  • Vasculitis
  • Drugs
  • Chronic interstitial pneumonia
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31
Q

What is tuberculosis

A

Infectious granulomatous disease caused by Mycobacterium tuberculosis
* mc involves lungs but can affect almost any organ system

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32
Q

Features of M. TB

A
  • Slow growing
  • Waxy mycolic acid capsule - hard to culture and treat
  • Non-motile and non-spore forming
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33
Q

RFs of TB

A
  • Exposure to infection
  • HIV infection - progresses HIV more rapidly and Tx drugs interact
  • Silicosis
  • Immunosuppressants
  • Endemic country - Asia, Latin America, Africa
  • Homeless/ crowded housing
  • IVDU
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34
Q

Describe the initial exposure to TB

A
  • TB phagocytosed by macrophages but resist killing and form granulomata
  • macrophages and lymphocytes contain and kill majority of infecting bacilli
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35
Q

Describe the pathophysiology of primary TB

A
  • Cell mediated immune response from T cells
  • Central region of granuloma undergoes caseating necrosis = Ghon focus
  • This is a type 4 hypersensitivity reaction
  • Ghon complex is a Ghon focus that spreads to hilar lymph node
  • Often ASx
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36
Q

Describe latent TB

A
  • Occurs after primary infection
  • Patient remains asymptomatic and bacteria is dormant ( = -ve sputum)
  • Infection is contained within granulomas but TB doesn’t die
  • Disease can progress/reactivate in immunocompromised Px
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37
Q

Describe miliary TB

A

This occurs when TB spreads systemically via the lympho-haematogenous spread
Bacteria spread via pulm venous system

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38
Q

Describe secondary infection of TB

A
  • Latent TB reactivates resulting in features of haemoptysis and fever
  • Typically occurs in lung apex where pO2 is highest and mycobacteria are aerobic
  • Bacteria can spread locally (caseating granulomata) or systemically (miliary TB)
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39
Q

Presentation of TB

A
  • Systemic: weight loss, anorexia, malaise, night sweats, low grade fever
  • Dyspnoea, pleuritic chest pain
  • Cough
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40
Q

Presentation of extrapulmonary TB

A
  • CNS TB - meningitis
  • Enlarged lymph nodes
  • Genito-urinary TB - haematuria & dysuria
  • Bone - joint pain and swelling
  • Abdo TB - ascites, ileal malabsorption
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41
Q

Investigation of TB

A
  • Sputum microbiology - Ziehl-Neelsen stain will turn red, +ve acid-fast bacilli
  • Lymph node biopsy
  • CXR - ghon complex (latent), patch/ nodular consolidations, millet seeds uniformly distributed (miliary), hilar lymphadenopathy
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42
Q

Describe investigation of latent TB

A
  • Mantoux screening (tuberculin skin test) - Won’t distinguish active from passive and -ve doesn’t exclude active
  • Interferon-gamma release assay: Measure the response of T cells to TB antigens in order to diagnose prior exposure. More sensitive than Mantoux
  • Less sensitive in immunocompromised or miliary TB (false -ve)
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43
Q

Treatment of active TB

A

ROPE
* Rifampicin - 6m
* Isoniazid - 6m
* Pyrazinamide - first 2m only
* Ethambutol - first 2m

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44
Q

Describe the MOA of rifampicin and SEs

A
  • Inhibition of bacterial RNA polymerase = prevents protein synthesis
  • Red/orange urine, hepatitis, Impaired combined oral contraceptive pill function
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45
Q

Why should Pyridoxine be administered with isoniazid

A

Prevent isoniazid associated peripheral neuropathy

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46
Q

Which vaccine should be taken to prevent TB and when

A

Neonatal BCG

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47
Q

Causes of pharyngitis

A
  • Viral (80%): rhinovirus, adenovirus and EBV
  • Bacterial: Group A beta-haemolytic streptococci
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48
Q

Give 3 other diseases associated with GABHS

A
  • Scarlet fever
  • Post-streptococcal glomerulonephritis
  • Rheumatic fever
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49
Q

Presentation of pharyngitis

A
  • Pyrexia - >38 degrees
  • Red, inflamed and enlarged tonsils
  • pharyngeal exudate = GABHS
  • Fever, headache
  • Viral can be distinguished from GABHS by presence of cough and nasal congestion
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50
Q

Tx of pharyngitis

A

Most are self limiting and Sx last a week
* Phenoxynethylpenicillin 10 days
* Amoxicillin or clarithromycin

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51
Q

Define sinusitis

A

inflammation of the mucosal lining of the nasal cavity and paranasal sinuses

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52
Q

Describe causes of sinusitis

A
  • Mostly viral infection -
  • Bacterial - Strep. pneumo, H.influenzae
  • Duration of Sx for >10 days often indicates bacterial cause
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53
Q

Sx of sinusitis

A
  • Purulent nasal discharge
  • Facial pain/ pressure
  • Fever and cough
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54
Q

Tx of sinusitis

A

Usually self limiting
* Amoxicillin if bacterial and not resolving
* Nasal corticosteroids

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55
Q

What is mesothelioma

A

Aggressive lung malignancy affecting mesothelial cells of the pleura

56
Q

3 RFs of mesothelioma

A
  • Asbestos exposure (80%)
  • Age 60-80
  • Male
57
Q

Describe the relationship between asbestos exposure and mesothelioma

A

There is a latency period where the development of mesothelioma occurs 20-40 years after asbestos exposure

58
Q

Give 5 ways mesothelioma presents

A
  • Dry and non-productive cough
  • Cancer Sx - fatigue, fever, sweats and weight loss
  • Dyspnea and diminished breath sounds
  • Dullness to percussion - pleural effusion
  • Signs of metastases - bone and abdo pain
59
Q

3 investigations done for mesothelioma

A
  • CXR
  • Contrast CT chest
  • Video-assisted thoracoscopic surgery (VATS) - evaluate pleural lining and obtain optimal biopsy
60
Q

Give 3 findings that may be seen on a CXR of suspected mesothelioma

A
  • Unilateral pleural effusion
  • decreased lung volumes
  • Parenchymal changes
61
Q

Give 2 findings that may be seen on a contrast CT of suspected mesothelioma

A
  • Pleural thickening
  • Pleural plaques
62
Q

Why is mesothelioma often inoperable

A

Often metastasised by diagnosis

63
Q

How is inoperable mesothelioma treated

A
  • Chemo with cisplatin and pemetrexed
  • Radiotherapy and palliative care
64
Q

What is a pancoast tumour

A

Tumour in the pulmonary apex

65
Q

What syndrome can a pancoast tumour cause and how

A

Horners syndrome
Pancoast tumour presses on the sympathetic ganglion

66
Q

Triad of symptoms of horners syndrome

A
  • ptosis
  • anhidrosis ( lack of sweat)
  • miosis (constricted pupil)
67
Q

Which category of lung cancer is most common

A

Non small cell lung cancer

68
Q

Give 4 types of non small cell lung cancers

A

Adenocarcinoma - 40%
Squamous cell carcinoma - 25-30%
Large cell - 10%
Carcinoid

69
Q

Describe adenocarcinoma of the lung

A

Peripheral lesion that originates from mucus-secreting glandular cells

70
Q

Which paraneoplastic syndrome is associated with squamous cell lung carcinoma

A

Tumour secreting Parathyroid hormone-related protein (PTHrP) which results in hypercalcaemia

71
Q

Describe typical location of small cell lung cancers

A

Fast growing, Central lesion near main bronchus
Originate from neuroendocrine cells

72
Q

Give 3 paraneoplastic syndromes associated with small cell lung cancer

A
  • SIADH - hypOnatraemia
  • Ectopic ACTH - Cushing’s syndrome
  • lambert Eaton myasthenia syndrome
73
Q

5 symptoms of lung cancer

A
  • persistent cough
  • dyspnoea
  • weight loss
  • hayemotypsis
  • chest/ shoulder pain
74
Q

Describe 3 ways in which lung cancers are investigated

A
  • GS: bronchoscopy + biopsy
  • CCT neck, thorax and upper abdo - TNM stagings, lymphadenopathy, enlarged hilar
  • CXR - pleural effusion, pulm nodules, lung collapse
75
Q

5 RFs of lung cancer

A
  • smoking
  • env tobacco exposure (2nd hand smoking)
  • FHx
  • COPD
  • radon gas
76
Q

5 complications of lung cancer

A
  • super vena cava syndrome - facial swelling, distended neck veins, SOB
  • recurrent laryngeal nerve palsy - hoarse voice
  • metastasis
  • Pancoast tumour
  • paraneoplastic syndromes
77
Q

What sign is likely to be positive in superior vena cava syndrome
Describe the sign

A

Pemberton’s sign
Bilateral arm elevation above head results in facial swelling and cyanosis

78
Q

State the mc type of non-small cell lung cancer

A

Adenocarcinoma

79
Q

What is hypersensitivity pneumonitis

A

The result of non-IgE (mainly T3) mediated immunological inflammation of the lungs

80
Q

Give 4 RFs of hypersensitivity pneumonitis

A
  • Bird keeping
  • Smoking
  • Pre-existing lung condition
  • Occupation, e.g. farming
81
Q

Give 4 different causes of hypersensitivity pneumonitis

A
  • Farmer’s lung - reaction to mouldy spores in hay
  • Bird fanciers lung - reaction to bird droppings
  • Mushroom picker’s lung
  • Malt workers lung - mould on barley
82
Q

Explain the pathophysiology of hypersensitivity pneumonitis

A
  • Mainly T3 hypersensitivity but can be type 4
  • Previous exposure produces IgG Ab that retain immune memory of Antigen
  • 2nd exposure result in Ab-Ag complexes forming and these deposit in the lungs where they are not properly cleared
  • Repeated exposure to Ag = repeated Sx
83
Q

Describe how hypersensitivity pneumonitis may present (6)

A
  • Dyspnea
  • Cough
  • Fever/ chills
  • Malaise, weight loss
  • Clubbing
84
Q

Give 4 ways hypersensitivity pneumonitis is investigated

A
  • CT chest
  • CXR - nodular
  • +ve serum IgG
  • Abnormal pulmonary function tests
85
Q

Would hypersensitivity pneumonitis show a restrictive or obstructive pattern on PFTs?

A

Restrictive
Can be mixed in fibrotic HP

86
Q

Describe the possible CT chest findings of someone with hypersensitivity pneumonitis

A
  • Ground-glass shadowing
  • Poorly defined micronodules
  • Fibrotic HP - mosaic attenuation
87
Q

How is hypersensitivity pneumonitis treated

A
  • Identify and avoid trigger/ allergen
  • Smoking cessation
  • Prednisolone if Sx persist despite avoidance
88
Q

Define cystic fibrosis

A

Inherited autosomal recessive, multi-system disease affecting mucous glands

89
Q

Explain the pathophysiology of cystic fibrosis

A
  • Mutation in the CF transmembrane conductance regulator (CFTR)
  • CFTR is a channel protein that mumps chloride into secretion which makes then thin and watery
  • Defective CFTR gene = thick secretions
90
Q

Explain how cystic fibrosis causes lung issues

A
  • Impaired mucociliary clearance due to thick mucus
  • This increases infection and inflammation which can lead to bronchiectasis
91
Q

Which chromosome is the gene coding for CFTR found on

A

chromosome 7

92
Q

2 RFs of cystic fibrosis

A

FHx
Caucasian

93
Q

Describe how cystic fibrosis may present in neonates

A
  • failure to pass meconium (1st stool)
  • meconium ileus - too thick to pass through bowel and causes obstruction
94
Q

Describe the presentation of cystic fibrosis in the following systems:
GIT, Resp, GU

A
  • Resp: thick and sticky sputum, recurrent airway infection, wet-sounding cough
  • Genital: bilateral absence of vas deferens = infertility
  • GI: steatorrhea, GORD, Failure to thrive despite voracious appetite (untreated pancreatic insufficiency)
95
Q

Describe 3 investigations conducted for cystic fibrosis

A
  • GS: Sweat test - induce sweating and analyse chloride concentration. +ve if Cl- >60mmol/L
  • Genetic testing - 2 disease causing mutations
  • Newborn screening - +ve immunoreactive trypsinogen
96
Q

Give 3 infection commonly affecting cystic fibrosis patients

A
  • Staph. aureus
  • H. influenzae
  • P. aeruginosa
97
Q

How is cystic fibrosis treated

A
  • Resp: chest physio, salbutamol, mucolytics
  • Infection: Ab, e.g. oral amoxicillin/ ciprofloxacin
  • Pancreatic insufficiency: Pancreatin + omeprazole, Fat-soluble Vit supplements
  • Lung transplant in severe cases
98
Q

Define bronchiectasis

A

Permanent dilation of bronchi due to destruction of elastic and muscular parts aof bronchial wall

99
Q

Give 4 RFs of bronchiectasis

A
  • Cystic fibrosis
  • HIV
  • Primary ciliary dyskinesia
  • Infection
100
Q

Explain the pathophysiology of bronchiectasis

A
  • Dilation and thickening of bronchi due to chronic inflammation
  • This leads to increased mucus production and damage to cilia by immune cell cytokines
  • This ultimately increases risk of persistent infection leading to progressive airway damage
101
Q

Describe the presentation of bronchiectasis (6)

A
  • Productive cough with lots of sputum ( +/- flecks of blood)
  • Dyspnoea with exertion
  • Crackles on pulmonary auscultation
  • Recurrent fever
  • Wheezing
  • Pleuritic chest pain during exacerbation
102
Q

Give 4 investigations conducted for bronchiectasis

A
  • GS - High resolution chest CT
  • CXR
  • Sputum culture
  • Spirometry
103
Q

Describe the possible findings on a chest CT of bronchiectasis

A
  • Thickened, dilated airways
  • Cysts
  • Signet ring sign
104
Q

Describe the possible findings on a CXR of bronchiectasis

A
  • Thin-walled ring shadows
  • Volume loss
105
Q

Would bronchiectasis show a restrictive or obstructive pattern on spirometry

A

Obstructive

106
Q

Describe how bronchiectasis is treated (4)

A
  • Chest physio
  • Bronchodilators
  • Ab for infection
  • Anti-inflammatory agents, e.g. long term azithromycin to decrease exacerbation frequency
107
Q

What is a pleural effusion

A

Excess fluid accumulation within the pleural space

108
Q

Describe a transudative pleural effusion

A
  • protein <30g/L
  • transparent effusion
109
Q

Describe the protein level and appearance of an exudative pleural effusion

A
  • Protein >30g/L
  • Cloudy effusion
110
Q

What causes an exudative effusion
Give 3 specific examples

A
  • Caused by inflammation/ infection of the lung leading to capillary leakage of fluid into the pleural space
  • E.g. Malignancy, pneumoniae/ TB, pancreatitis
111
Q

What causes a transudative effusion
Give 3 specific examples

A
  • Caused by increased hydrostatic pressure/ reduced oncotic pressure
  • E.g. Congestive HF, Liver cirrhosis, hypothyroidism
112
Q

Describe how pleural effusions present

A
  • Dyspnoea due to decreased lung volume
  • Dullness to percussion over effusion (stony)
  • Pleuritic chest pain - worse with inspiration and exacerbated by cough and movement
  • Cough (+/- sputum)
  • Quieter breathing sounds over effusion
  • Decreased/ absent tactile fremitus - decreased vibration of chest wall when speaking
113
Q

Describe the 2 main investigations conducted for a pleural effusion

A
  • CXR
  • Aspiration and pleural fluid analysis
114
Q

Give 3 findings that may be seen on CXR of a pleural effusion

A
  • Blunting of costophrenic angle (area where diaphragm meets rib)
  • Excess fluid appears white
  • Tracheal and mediastinal deviation
115
Q

Describe the expected results of a pleural fluid analysis

A
  • Glucose - low
  • Protein - Trans/ Exu
  • pH - low, acidic
  • Microscopy - possible bacterial culture
  • WBC - raised
116
Q

How is a pleural effusion treated

A
  • Congestive HF - furosemide
  • Infection - IV Ab, e,g, amoxicillin
  • Malignant: thoracentesis (severe) - drain excess fluid
    pleurodesis - adhesion of pleural layers together
117
Q

What is empyema

A

Infected pleural effusion

118
Q

What will pleural aspiration show if there is empyema

A
  • Pus
  • Low pH
  • Low glucose
  • Raised LDH
119
Q

How is an empyema treated

A
  • Ab - Co-amoxiclav, clindamycin
  • Thoracostomy - drainage
120
Q

How is an empyema treated

A
  • Ab - Co-amoxiclav, clindamycin
  • Thoracostomy - drainage
121
Q

What criteria is used to differentiate between transudative and exudative effusions

A

Light’s criteria

122
Q

Describe Light’s criteria

A

States that an exudate is defined as the presence of any of the following:
* Pleural protein to serum protein ration >0.5
* Pleural lactate dehydrogenase to serum LDH ratio >0.6
* Pleural LDH greater than 2/3 of upper limit of normal for serum

123
Q

What are the 3 components of virchow’s triad

A
  • Endothelial damage
  • Venous stasis
  • Hypercoagulability
124
Q

State 3 things that can cause venous stasis

A
  • Immobility
  • Varicose veins
  • Recent surgery
125
Q

State 4 things that can cause endothelial damage

A
  • trauma
  • prior deep vein thrombosis
  • venous catheters
  • smoking
126
Q

State 4 things that can cause hypercoagulability

A
  • Pregnancy
  • Contraception
  • Cancer
  • IBD
127
Q

Describe the presentation of pulmonary embolism (6)

A
  • Dyspnoea
  • Unilateral pleuritic chest pain
  • Pain and swelling in one/ both legs
  • HypOtension
  • cough
  • Rapid breathing
128
Q

What is the gold standard investigation of a pulmonary embolism

A

CT pulmonary angiogram

129
Q

When is the GS investigation for a pulmonary embolism avoided

A
  • Renal impairment
  • contrast allergy
  • Avoid in young people
130
Q

What test are conducted alongside the GS to investigate a pulmonary embolism

A
  • D-dimer
  • ECG
  • Ventilation-perfusion scan - area won’t be perfused
  • CXR - usually normal
131
Q

Describe the ECG findings of a pulmonary embolism

A
  • S1Q3T3: Large S wave lead I, large Q wave Lead III, inverted T wave lead III
  • Sinus tachycardia
  • RBBB
132
Q

What scoring system is used to determine the probability of a pulmonary embolism in non-pregnancy people

A

Wells score

133
Q

Give 5 criterion used in the wells score

A
  • Sx of DVT (leg swelling, pain on palpitation) - 3pts
  • PE most likely diagnosis - 3pts
  • Tachycardia - 1.5pts
  • Active cancer - 1pt
  • Haemoptysis - 1pt
134
Q

Describe how wells score is categorised

A
  • Score >(=)4 = PE likely
  • Score <4 = PE unlikely
135
Q

What test should be ordered if a patients wells score is below 4

A

D-dimer

136
Q

Describe the treatment of a confirmed case of PE in a haemodynamically unstable patient

A
  • Start IV unfractionated heparin prior to thrombolysis
  • Thrombolysis (clot dissolver) - alteplase
  • surgical embolectomy if thrombolysis is CI/ ineffective
137
Q

Describe the treatment of a confirmed case of PE in a haemodynamically stable patient

A

Anticoagulants
* Apixaban or rivaroxaban
* Low molecular weight heparin if above is unsuitable

2a - SBCS (9 decks)

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