Respiratory Flashcards
AAFB
Acid and Alcohol Fast Bacili
ABPA
Allergic Bronchopulmonary Aspergilosis
BIPAP
Bilevel Positive Airway Pressure
CPAP
Continuous Positive Airways Pressure
EAA
Extrinsic Allergic Alveolitis
ICD
Intercostal Chest Drain
ILD
Interstitial Lung Disease
INH
Inhaled
LTOT
Long Term Oxygen Therapy
MCL
Mid-Clavicular Line
NIV
Non-Invasive Ventilation
PEFR
Peak Expiratory Flow Rate
PFT’s
Pulmonary Function Tests
PND
Paroxysmal Nocturnal Dyspnoea
SVCO
Superior Vena Cava Obstruction
UIP
Usual Interstitial Pneumonia
Define vital capacity
Volume of air expired from the lungs from a maximal inspiration using a slow/relaxed manoeuvre
Define forced vital capacity
Volume of air than can be forcibly expelled from the lungs from a position of maximal inspiration
Define forced expiratory volume
Volume of air forcibly expelled from the lungs in the first second - following maximal inspiration
Define FEV1/FVC
Volume of air forcibly expired in the first second as a percentage of the total volume exhaled
Obstructive vs Restrictive spirometry
Obstructive - smooth curve reaching close to normal volume over a longer period of time
Restrictive - plateaus at a lower than normal volume
Early small airways obstruction on volume flow chart
Slight depression
Chronic obstructive diseases on volume flow chart
Large depression
Fixed large airway obstruction of volume flow chart
Circular
Restrictive disease on volume flow chart
Normal height but very narrow
Causes of low paO2
Hypoventilation
Diffusion impairment
Shunt
V/Q mismatch
Causes of respiratory acidosis
Hypoventilation
- neuromuscular diseases
Alveolar hypoventilation
- COPD
Define A-a gradient
A=alveolar
a= arterial
Difference between oxygen concentration in the alveoli and arterial system
How to calculate A-a gradient
PAO2 = PIO2 - PaCO2/0.8
PIO2 = room air (20kPa)
Normal A-a gradient
Young healthy people - less than 2kPa
Older people - less than 4kPa
> 4 = lung pathology
Define anaphylaxis/angioedema
Serious allergic reaction Occurs when sensitised individual exposed to specific antigen - insects bites/stings - food - medications
Pathophysiology of anaphylaxis
Immunological response
IgE -> Antigen -> mast cell and basophils -> histamine increases -> body response
Clinical features of anaphylaxis
Occurs in minutes
- pruritus, urticaria, angioedema, hoarseness
Progresses to
- stridor and bronchial obstruction, wheeze and chest tightness from bronchospasm
Treatment for anaphylaxis
Remove trigger, maintain airway - 100% O2
IM adrenaline 0.5 mg
IV hydrocortisone 200 mg
IV chlorpheniramine 10mg
If hypotensive - lie flat and fluid resuscitate
Bronchospasm - NEB salbutamol
Laryngeal oedema - NEB adrenaline
Features of mild asthma attack
No features of severe asthma
PEFR > 75%
Features of moderate asthma attack
No features of severe asthma
PEFR 50-75%
Features of severe asthma attack
PEFR 33-50% of best or predicted
Cannot complete sentences in 1 breath
RR > 25/min
HR > 110/min
Features of life-threatening asthma attack
PEFR < 33% of best or predicted
Sats < 92% or ABG pCO2 < 8kPa
Cyanosis, poor respiratory effort, near or fully silent chest
Exhaustion, confusion, hypotension or arrhythmias
Normal pCO2
Features of near fatal asthma attack
Raised pCO2
Acute asthma management
ABCDE
Aim for SpO2 94-98% with oxygen as needed - ABG if sats < 92%
5mg nebulised salbutamol - repeat after 15 mins
40mg oral Prednisolone STAT - IV hydrocortisone if PO not possible
If severe
- nebulised Ipratropium Bromide 500mg
- back to back salbutamol
If life threatening or near fatal
- urgent ITU or anaesthetist assessment
- urgent portable CXR
- IV aminophyline
- IV salbutamol if nebulised route ineffective
Features of COPD exacerbations
Infective - change in sputum volume / colour - fever - raised WCC +/- CRP Non-infective
Management of COPD exacerbations
ABCDE approach
Oxygen
- via fixed performance face mask due to risk of CO2 retention
- aim for SaO2 88-92% - guided by ABGs
NEBs - salbutamol and Ipratropium
Steroids - Prednisolone 30mg STAT and OD for 7 days
Antibiotics if raised CRP / WCC or purulent sputum
CXR
IV aminophylline
NIV if type 2 respiratory failure and pH 7.25-7.35
If pHh <7.25 consider ITU referral
Features of pneumonia
Consolidation on CXR with fever +/- purulent sputum +/- raised WCC and/or CRP
Management of pneumonia
ABCDE
If features of sepsis - immediately treat using sepsis pathway
Treat with antibiotics as per CURB-65 score
How to calculate CURB-65 score
1 point for Confusion Urea - > 7.0mmol/L RR > 30 BP < 90 mmHg Aged over 65
Definition of massive haemoptysis
> 240mls in 24 hrs
> 100mls/day over consecutive days
Management of massive haemoptysis
ABCDE
Lie patient on side of suspected lesion
Oral tranexamic acid for 5 days - or IV
Stop NSAIDs / aspirin / anticoagulants
Antibiotics if evidence of respiratory tract infection
Consider vitamin K
CT aortogram - bronchial artery embolisation
Features of tension pneumothorax
Hypotension
Tachycardia
Deviation of trachea away from side of pneumothorax - x-ray
Mediastinal shift away from pneumothorax
Management of tension pneumothorax
Large bore IV cannula into 2nd ICS MCL
Chest drain into affected side
Symptoms of PE
Chest pain - pleuritic
SOB
Haemoptysis
Low cardiac output followed by collapse
Risk factors for PE
Surgery - abdo/pelvic - knee/hip replacement - post-op ITU Lower limb - fracture - varicose veins Malignancy - abdo/pelvis/advanced/metastatic Reduced mobility Previous proven VTE
Management of PE
ABCDE Oxygen if hypoxia Fluid resuscitation - if hypotensive Thrombolysis considered if massive PE confirmed on echo or CT - check for contraindications Fully anticoagulated
Features of a massive PE
Hypotension/imminent cardiac arrest
Signs of right heart strain on CT/echo
Consider thrombolysis with IV alteplase
Thrombolysis contraindications
Absolute - haemorrhagic stroke or ischaemic stroke < 6 months - CNS neoplasia - recent trauma or surgery - GI bleed < 1 month - bleeding disorder - aortic dissection Relative - warfarin - pregnancy - advanced liver disease - infective endocarditis
Thrombolysis complications
Bleeding Hypotension Intracranial haemorrhage/stroke Reperfusion arrhythmias Systemic embolisation of thrombus Allergic reaction
Characteristics of asthma
Chronic inflammatory disease of the airways
Airway obstruction that is reversible - spontaneously or with treatment
Increased airway responsiveness to a variety of stimuli
Wheeze differentials
Acute asthma exacerbation
Bronchitis - viral or bacterial
Pulmonary oedema
PE
Asthma pathophysiology
Airway epithelial damage - shedding and sub epithelial fibrosis, basement membrane thickening
Cytokines amplify inflammatory response
Increased numbers of mucus secreting goblet cells and smooth muscle hyperplasia and hyper trophy
Mucus plugging - fatal and severe asthma
Inflammatory cells involved in asthma reactions
Eosinophils
Th2 lymphocytes
Mast cells
Inflammatory mediators released in asthma
Histamine
Leukotrienes
Prostaglandins
Criteria for safe asthma discharge after exacerbation
PEFR > 75%
Stop regular nebulisers for 24 prior to discharge
Inpatient asthma nurse review to reassess inhaler technique and adherence
Provide PEFR meter and written asthma action plan
At least 5 days oral Prednisolone
GP follow up within 2 working days
Respiratory clinic follow up within 4 weeks
Consider psychosocial factors for severe or worse
Differentials for eosinophilia
Airway inflammation - asthma or COPD Hay fever / allergies Allergic Bronchopulmonary Aspergilosis Drugs Vasculitis Eosinophilia pneumonia Parasites Lymphoma SLE Hypereosinophilic syndrome
Triggering factors for asthma
Smoking Upper respiratory tract infections - mainly viral Allergens - pollen - house dust mite - pets Exercise Occupational irritants Pollution Drugs - aspirin - beta blockers Food and drinks - dairy produce - alcohol - orange juice Stress For severe asthma consider - inhaled heroin - pre-menstrual - psychosocial aspects
Steps for a chronic asthma appointment
Use BTS stepwise management guidelines
Assess and teach the inhaler technique
Use self management plans
Avoid trigger factors
COPD definition
Characterised by airflow obstruction
- progressive
- not fully reversible
- does not change markedly over several months
Pathophysiology of COPD
Umbrella term which encompasses emphysema and chronic bronchitis
Mucous gland hyperplasia
Loss of cilial function
Emphysema - alveolar wall destruction causing irreversible enlargement of air spaces distal to the terminal bronchioles
Chronic inflammation - macrophages and neutrophils
Fibrosis of small airways
Causes of COPD
Smoking
Inherited α-1-antitrypsin deficiency
Industrial exposure
Outpatient COPD management
COPD care bundle Smoking cessation Pulmonary rehabilitation Bronchodilators Antimuscarinics Steroids Mucolytics Diet LTOT and lung volume reduction if appropriate
Criteria for long term oxygen therapy
pO2 consistently below 7.3 kPa or below 8 kPa with cor pulmonale
Non-smokers
Not rents in high levels of CO2
Features of LTOT
Continuous oxygen therapy for most of the day - at least 16hrs for survival benefit
Extended periods of hypoxia cause renal and cardiac damage - prevented by LTOT
O2 needs balanced with loss of independence and reduced activity which may occur
Features of pulmonary rehabilitation
Many COPD patients avoid exercise and physical activity because of breathlessness
Leads to a vicious cycle of increasing social isolation and inactivity leading to worsening of symptoms
Pulmonary rehabilitation aims to break this cycle - MDT 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice and disease education
CXR consolidation differentials
Pneumonia TB - usually upper lobe Lung cancer Lobar collapse - blockage of bronchi Haemorrhage
Management of community acquired pneumonia
Prompt assessment and CXR on admission - consolidation
FBC, U&Es, CRP and sputum culture
CURB-65 score to guide management
No delay in initiating antibiotics +/- paracetamol
ITU referral if high CURB-65 score
Pneumonia follow up involves
HIV test Immunoglobulins Pneumococcal IgG serotypes Haemophilia us influenzae b IgG Follow up clinic in 6 weeks with repeat CXR to ensure resolution
Causes of non-resolving pneumonia
C - complication - empyema, lung abscess
H - host - immune compromised
A - antibiotic - inadequate dose, poor oral absorption
O - organism - resistant or unexpected organism not covered by empirical antibiotic
S - second diagnosis - PE, cancer, organising pneumonia
Clinical features of TB
Fever and nocturnal sweats - drenching
Weight loss - weeks-months
Malaise
Respiratory TB - cough, purulent sputum/haemoptysis, pleural effusion
Non-respiratory TB - Erythema nodosum, lymphadenopathy, bone/joint, abdo, meningitis, genitourinary, military, pericardial effusion
TB risk factors
Past history of TB Known history of TB contact Born in country with high TB incidence Evidence of immunosuppression - IVDU - HIV - solid organ transplant recipients - renal failure/dialysis - malnutrition/low BMI - DM - alcoholism
Management of respiratory TB
ABCDE approach and aim to culture
Admit to side room and start infection control
Routine bloods and HIV test and vitamin D levels
CT chest if clinical features/CXR not typical
MRI brain/spine if miliary
If pt critically unwell and high likelihood of TB starts anti-TB therapy after sputum samples sent
Notify TB nurse specialists - support, public health issues and initiate contact tracing
TB culture can take 6-8 weeks - treatment depends on clinical suspicion
Basics of anti-TB therapy
Rifampicin - 6 months
Isoniazid - 6 months
Pyrazinamide - 4 months
Ethambutol - 4 months
Check LFTs
Dose is weight dependent
Directly observed therapy (DOT) sometimes used as compliance is crucial
Pt awareness of common and serious side effects
Pyridoxine given as prophylaxis against peripheral neuropathy
Major side effects of TB treatment
Rifampicin
- hepatitis, rashes, febrile reaction, orange/red secretions, many drug interactions including warfarin and OCP
Isoniazid
- hepatitis, rashes, peripheral neuropathy, psychosis
Pyrazinamide
- hepatitis, rashes, vomiting, arthralgia
Ethambutol
- retrobulbar neuritis
Features of bronchiectasis
Chronic dilation of one or more bronchi
- bronchi exhibit poor mucus clearance
- predisposition to recurrent or chronic bacterial infection
Gold standard diagnostic test = high resolution CT
Causes of bronchiectasis
Post-infective - whooping cough, TB
Immune deficiency - hypogammaglobulinaemia
Genetic/much ciliary clearance defects - cystic fibrosis, Young’s syndrome, Kartagener syndrome
Obstruction - foreign body, tumour, extrinsic lymph node
Toxic insult - gastric aspiration, inhalation of toxic chemicals
Allergic Bronchopulmonary Aspergilosis
Secondary immune deficiency - HIV, malignancy
Rheumatoid arthritis
Associations - IBD, yellow nail syndrome
Bronchiectasis common organisms
Haemophilus influenzae Pseudomonas aeruginosa Moraxella catarrhalis Stenotrophomonas maltophilia Fungi - aspergillus, candidia Non-tuberculous mycobacteria
Bronchiectasis management
Treat underlying cause
Physiotherapy - mucus clearance
Antibiotics according to sputum culture/sensitivities for acute exacerbations and chronic suppressive therapy
Supportive - flu vaccine, bronchodilators
Pulmonary rehab
Cystic fibrosis definition
Autosomal recessive disease leading to mutations in cystic fibrosis transmembrane conductance regulator (CFTR)
Multi system disease characterised by thickened secretions
Criteria for CF diagnosis
One or more characteristic phenotypic features
- or history of CF in sibling
- or positive newborn screening test result
And
- increased sweat chloride concentration - > 60 mol/L Sweat Test
- or identification of two CF mutations - genotyping
- or demonstration of abnormal nasal epithelial ion transport
CF presentations
Meconium ileus
- newborn bowel blocked by sticky secretions
- signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distention and delay in passing meconium
Intestinal malsorption
- mostly evident in infancy
- severe deficiency of pancreatic enzymes
Recurrent chest infections
Newborn screening
Common complications of CF
Respiratory infections
- needs aggressive therapy with physio and antibiotics
- often receive prophylactic antibiotics
Low body weight
- careful monitoring
- pancreatic enzyme replacement therapy
- high calorie intake and extra supplements
- NG or PEG feeding
Distal intestinal obstruction syndrome (DIOS)
- faecal obstruction in ileocaecum
- often due to insufficient prescription of pancreatic enzymes or non-compliance, salt deficiency or hot weather
- presents with palpable right iliac fossa mass
CF related diabetes
CF lifestyle advice
No smoking
Avoid other CF patients
Avoid friends/relatives with colds/infections
Avoid jacuzzis (pseudomonas)
Clean and dry nebulisers thoroughly
Avoid stables, compost or rotting vegetation - risk of aspergillus fumigatus inhalation
Annual influenza immunisation
Sodium chloride tablets in hot weather/vigorous exercise
Define pneumothorax
Air in pleural cavity
Define pleural effusion
Fluid in pleural cavity
Define empyema
Infected fluid in pleural cavity
Define pleural plaques
Discrete fibrous areas
Define pleural thickening
Scarring/calcification causing thickening
Types of pneumothorax
Spontaneous Primary - no lung disease Secondary - lung disease Traumatic Tension Iatrogenic
Pneumothorax risk factors
Pre-existing lung disease Height Smoking/cannabis Diving Trauma/chest procedure Association with other conditions - Marfan's syndrome
Pneumothorax management
Primary
- if symptomatic of >2cm of air on CXR - give O2 and aspirate
Secondary
- lower threshold for ICD
If persistent air leak > 5 days refer to thoracic surgeons
Discharge advice - no flying or diving until resolved
Pleural effusion approach
Hx + Ex
CXR
ECG
Bloods - FBC, U+Es, LFTs, CRP, bone profile, LDH, clotting
Echo - suspected heart failure
Staging CT with contrast - if suspected exudate with cause
Pleural effusion diagnosis
USS guided pleural aspiration - biochemistry - protein, pH, LDH - cytology - microbiology - AAFB Consider thoracoscopy or CT pleural biopsy for new effusion
Causes of transudate effusions
Heart failure Cirrhosis Hypoalbuminaemia - nephrotic syndrome or peritoneal dialysis Hypothyroidism Mitral stenosis PE SVCO
Management of transudate effusions
Often no diagnostic tap required
Treat underlying cause
- stop or reduce treatment if effusion resolves
- if effusion persisted then therapeutic aspiration/drainage required
Criteria for exudate effusion
Pleural protein > 30 g/L
Causes of exudate effusions
Malignancy Infection - parapneumonic, TB, HIV Inflammatory - RA, pancreatitis, benign asbestos effusion, PE
Define Light’s criteria
If pleural fluid protein level between 25 and 35 g/L exudate if one or more of the following
- pleural fluid protein/serum protein > 0.5
- pleural fluid LDH/serum LDH > 0.6
- pleural fluid LDH > 2/3 upper limit of normal
Define interstitial lung disease (ILD)
Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner
- usual interstitial pneumonia (UIP)
- non-specific interstitial pneumonia (NSIP)
- extrinsic allergic alveolitis
- sarcoidosis
Clinical features of UIP
Clubbing
Reduced chest expansion
Fine inspiratory crepitations - best heard basal/axillary areas
Features of pulmonary hypertension
Cause of UIP
Idiopathic
Pathophysiology of extrinsic allergic alveolitis
Inhalation of organic antigen to which the individual has been sensitised
Clinical presentation of extrinsic allergic alveolitis
Acute - short period from exposure - 4-8hrs - reversible - spontaneously settles 1-3 days - can recur Chronic - chronic exposure - less reversible
Define sarcoidosis
Multi system inflammatory condition of unknown cause
Non-caseating granulomas
Immunological response
50% get spontaneous remission, others get progressive disease
Investigations for sarcoidsos
PFTs - fibrosis CXR - 4 stages Bloods - renal function, ACE, calcium Urinary calcium Cardiac involvement - ECG, 24 tape, ECHO, cardiac MRI CT/MRI head - headaches - neuro sarcoid
ILD treatment principles
Depends on underlying pathology Occupational exposure - remove Drug associated - avoid Stop smoking Transplantation Treatment of infections Oxygen MDT Palliative care
Clinical features of lung cancer
Asymptomatic - incidental finding
Any respiratory symptom/systemic deterioration
SVCO
Horner’s syndrome
Metastatic disease - liver, adrenals (Addison’s), bone, pleural, CNS
Paraneoplastic - clubbing, hypercalcaemia, anaemia, SIADH, Cushing’s syndrome, thrombo-embolic disease
Risk factors for lung cancer
Large number of smoking pack years Airflow obstruction Increasing age Family history Exposure to other carcinogens - asbestos
Diagnostic tests for lung cancer
Bloods - FBC, U&Es, calcium, LFT’s, INR
CXR
Staging CT - spiral CT thorax and upper abdo
Histology
- US guided neck node FNA for cytology
- bronchoscopy
- CT biopsy
- thoracoscopy
PET scan - helps detect small metastasis not seen on staging CT
Histological classification of lung cancer
Small cell lung cancer Non-small cell lung cancer - squamous cells - adenocarcinoma - large cell carcinoma - bronchoalveolar cancer
Principles of lung cancer treatment
Curative surgery for stages I and II
Surgery and adjuvant chemotherapy clinical trial for stage IIIa
Chemotherapy - stage III/IV and PS 0-2
Radiotherapy - curative for those not fit for surgery
Palliative care
Watch and wait
SCLC treatment
Rapid growth rate and extensive spread at time of diagnosis for surgery
Chemotherapy mainstay
Palliative radiotherapy
Define obstructive sleep apnoea (OSA)
Upper airway narrowing provoked by slept causing sufficient slept fragmentation to result in significant daytime symptoms - excessive sleepiness
Due to small pharyngeal size or excessive narrowing occurring with relaxation
Causes of small pharyngeal size
Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
Large tonsils
Craniofacial abnormalities
Extra sub mucosal tissue - myxoedema
Causes of excessive narrowing of airway during sleep
Obesity enhance residual muscle dilator action
Neuromuscular disease with pharyngeal involvement may lead to greater loss of dilator muscle tone - stroke, MND, myotonic dystrophy
Muscle relaxants - sedatives, alcohol
Increasing age
Clinical effects of OSA
Excessive daytime sleepiness
Rise in daytime BP
Nocturia
Snoring and apnoea attacks witnessed by partner
Features of epworth sleepiness scale
Points for following - 0=never would dose, 1=slight chance, 2=moderate chance, 3=high chance
- sitting and reading
- watching TV
- sitting in public place
- passenger in car for an hour
- lying down to rest in the afternoon
- sitting and talking
- sitting quietly after lunch without alcohol
- in car whilst stopped in traffic
Diagnosis of OSA
Overnight oximetry alone
Management of OSA
Treatment given based on symptoms/QoL
Weight loss, sleep decubitus rather than supine, avoid/reduce evening alcohol intake
Snores and mild OSA - Mandible advancement devices, consider pharyngeal surgery
Significant OSA - nasal CPAP, gastroplasty/bypass
Severe OSA and CO2 retention - NIV prior to CPAP if acidotic
Features of CPAP
Usually given via nasal mask
Upper airways splinted open with 10cm H2O pressure - prevents airway collapse, sleep fragmentation and daytime somnolence
Opens collapsed alveoli and improves V/Q matching
Examples of sympathomimetics
Short acting - Salbutamol - Terbutaline Long acting - Formeterol - Salmeterol
Indications of sympathomimetics
Bronchospasm
Action of sympathomimetics
β2-selective adrenergic agonists
- increase cAMP in SMCs resulting in relaxation thus bronchodilation
Metabolism of sympathomimetics
Metabolised - liver
Excreted - urine
Side effects of sympathomimetics
Tremor Headache GI upset Palpitations Tachycardia Hypokalaemia
Examples of antimuscarinics
Short acting
- Iptropium
Long acting
- Tiotropium
Indications for antimuscarinics
Bronchospasm - typically COPD
Action of antimuscarinics
Muscarinic antagonist
- decreases cGMP which affects the intra cellular calcium -> decreased SMC contractility
Metabolism for antimuscarinics
Metabolised - partially in the liver
Excreted - urine
Common side effects of antimuscarinics
Dry mouth
Constipation
Cough
Headache
Examples of xanthines
Aminophylline
Theophylline
Main indications for xanthines
Asthma
COPD
Action of xanthines
Block phosophodiesterases -> decreased cAMP breakdown -> bronchodilation
Metabolism of xanthines
Metabolised - liver
Excreted - urine
Common side effects of xanthines
Headache GI upset Reflux Palpitations Dizziness
Other effects of xanthines
Positive chronotropic and inotropic effects
Diuretic action
Therapeutic window of xanthines
Plasma level 10-20 mg/L Toxic effects are serious - arrhythmias - seizures - N+V - hypotension
Examples of inhaled glucocorticoids
Beclomethasone
Budesonide
Fluticasone
Indications for inhaled steroids
Asthma
COPD
Actions of inhaled steriods
Increases airway calibrate by decreasing bronchial inflammation +/- modifying allergic reactions
Weak mineralcorticoid activity
Metabolism of glucocorticoids
Metabolised - liver
Excreted - urine
Side effects of inhaled glucocorticoids
Cough
Oral thrush
Unpleasant taste
Hoarseness
Examples of glucocorticoids
Prednisolone - PO
Hydrocortisone - IV/IM
Dexamthasone - PO/IV
Triamcinolone - IM
Actions of glucocorticoids
Alters gene transcription
Anti-inflammatory, immunosuppressive, increased gluconeogenesis, decreased glucose utilisation, increased protein catabolism
Common side effects of non-inhaled glucocorticoids
Adrenal suppression - courses > 3 weeks Hyperglycaemia Psychosis Insomnia Indigestion Mood swings Diabetes Cataracts Glaucoma Peptic ulceration Susceptibility to infections Osteoporosis Muscle wasting Skin thinning Cushingoid appearance
Considerations for long term steroid use
PPI - reduce GORD
Bisphosphonates - bone protection
Steroid card
Should not be withdrawn abruptly
