Respiratory Flashcards
(112 cards)
1
Q
What is asthma?
What are the 3 factors that contribute to airway narrowing?
A
A chronic inflammatory disorder of lung airways, characterised by airway hyperresponsiveness leading to bronchospasm and reversible airway obstruction.
-Reversible airway narrowing
- Bronchial muscle contraction (spasm) –> hypersensitive airways react to variety of stimuli e.g exercise, cold air
- Inflammation of mucous membranes
- Increased mucous production and secretions
2
Q
What are the main two types of asthma?
A
- Eosionophilic –> atopy/allergic asthma. Type 1 hypersensitivity. Associated w genetic tendency of immune system to produce IgE in response to common environmental allergens e.g pets, pollens
- Non-eosinophilic —> Not associated w allergy. Thought to involve more local immune response, involves neutrophil recruitment in airways.
3
Q
What are the RF for asthma?
A
- FH or PMH of hayfever, eczema, food allergies, drug allergies. Exposure to dust, fumes, allergens such as occupational dust (type 3 hypersensitivity) or pets.
- Provoking features –> allergens, infections, menstrual cycle, cold air, emotion
- Onset in childhood common,
- 20s-70s onset w no allergies –> late onset non atopic
4
Q
What is the typical presentation of asthma?
A
- Intermittent SOB
- Dry cough –> worse at night and in morning –> Diurnal
- Episodic wheeze
- Morning chest tightness
- Diurnal variation of symptoms, worse 3-5 morning
- Precipitant e.g exercise
-In children –> cough wheezing, may describe tight chest as tummy ache. Ask about premature birth, low birth weight, previous bronchiolitis or croup
5
Q
What are the 1st line and gold standard investigations for asthma?
A
GOLD STANDARD –> exhaled nitric oxide. Fraction of exhaled nitric oxide >40ppb +ve for asthma. Leverl in breath, produced to fight inflamm –> muscle relaxant. Normal <25 adults, <20 children.
1st line –> Spirometry w reversibility. FEV1/FVC ratio <70% adults <85% children. Reversibility testing –> asthma suggested by larger >400ml response to bronchodilators or prednisolone. FEV1 increase 12% and increase 200ml volume.
Alternative when spirometry not available –> peak flow –> PEFR reduced in asthma. Peak flow meter and diary 2-4 weeks aid diagnosis. 20% diurnal variation >3 days a week for two weeks –> typical asthma. Compare to expected values e.g age, gender, height.
-Children <5 can’t perform spirometry –> clinical diagnosis, trial treatment e.g low dose ICS,
6
Q
What is the management for asthma in adults?
What are the features that mean asthma is not being controlled?
A
Aim –> No daytime symptoms, no night time waking, no need for resuce medicaiton, no limitations ADL, no attacks.
Step wise –> Move up and down as needed
1 –> SABA as required for symptom relief. More than OD or night time symptoms –> step 2. Most patients start step 2.
2 –> Add low dose ICS. Beclomethasone, budesomide.
3 –> Add LTRA. Montelukast. Check patients adherence and inhaler technique.
4 –> Add LABA. Salmeterol. W or w/o LTRA depends whether effective.
5 –> Low dose ICS w LABA in MART regimen. Symbicort.
6 –> Increase ICS to moderate.
7 –> Increase ICS to high. Refer to specialist.
MART –> Maintenance and reliever therapy. Combined ICS and LABA in one inhaler.
-Severe eosinophilic –> biologic therapies. Anti IgE –> omalizumab –> removes IgE allergy Ab. £30,000 per year.
7
Q
What is the management for asthma in over 5’s - 16s?
A
1 --> SABA 2 --> Low dose ICS and LTRA 3 --> Stop LTRA, add LABA 4 --> MART 5 --> Moderate dose ICS 6 --> High dose ICS specialist
8
Q
What is the management for asthma in under 5’s?
A
1 --> SABA 2 --> Low dose ICS 3 --> Moderate dose ICS 4 --> Add LTRA 5 --> Stop LTRA, specialist
9
Q
What is a severe asthma attack and how should it be managed?
A
Severe Any one of
- PEFR 33-50% predicted
- RR >25
- Hr >110
- Inability to complete sentences
10
Q
What are the differences in presentation COPD v asthma?
A
- COPD rarely <35s, asthma commonly children
- COPD 85% history smoking. Asthma varies.
- Both w cough, COPD productive and sputum. Asthma nocturnal.
- Both SOB, COPD persistent, asthma intermittent.
- Night time waking in asthma not COPD.
- Asthma diurnal and day to day variation. COPD continual and progressive symptoms.
- Spirometry w reversibility –> asthma yes, COPD no.
11
Q
What is COPD?
A
- Progressive airway obstruction w little or no reversibility. Characterised by infiltration of neutrophils.
- Encompasses chronic bronchitis and emphysema.
Bronchitis
- Hypertrophy and hyperplasia of mucous secreting glands, inflamm of bronchial tubules, airway narrowing and subsequent obstruction.
- Chronic bronchitis –> productive couhg >3 months in two consecutive years, can produce large amounts sputum.
Emphysema
-Destruction of lung parenchyma w dilation f alveolar airspaces w loss of elastic recoil and air trapping.
-Patients w COPD divide into those w predominant breathlessness (emphysema) or predominant exacerbations (chronic bronchitis).
12
Q
What are the risk factors for COPD?
A
- Age >35, middle age
- Smoking of history of smoking 85%
- Occupation exposure e.g dust
- FH alpha 1 antitrypsin deficiency –> younger patients
- Provoking factors infections and cold air
13
Q
What is the typical presentation of COPD?
What is the presentation of an acute excerbation?
-Acute exacerbation –> worsening previously stable COPD, beyond day to day variation. Mya be due to viral or bacterial infection. Increase SOB, sputum volume and purulence.
A
- History of several months of progressive worsening of symptoms –> exertional SOB, chronic cough and sputum
- SOB, chronic cough, regular sputum production, frequent winter bronchitis, wheeze.
- Tachypnoea, use accessory muscles, may be cyanosis.
- May be weightloss –> hard to breath when eat
14
Q
What are the 1st line and gold standard investigations for COPD?
A
1st line and GOLD standard –> spirometry w reversibility testing.
- Airway obstruction defined as <80% predicted and a reduced FEV1/FVC ratio <0.7/70%.
- Reversibility –> spirometry before and after dose of inhaled bronchodilator.
- Clinically significant not present when FEV1 and FEV1/FVC ratio return to normal.
- CXR –> may show hyperinflation
- ECG –> r/o features cardiac disease e.g HF
15
Q
What is ACCOS?
A
- Think when patients also have features of asthma, treat those w ACCOS as those w recurrent exacebations.
- Common variable airflow obstruction but not completely reversible
16
Q
What is the staging for COPD?
A
Stage by FEV1
- Stage 1 –> mild >80%
- Stage 2 –> moderate –> 50-79%
- Stage 3 –> Severe –> 30-49%
- Stage 4 –> <30%
17
Q
What is the MRC dyspnoea scale?
A
Measures impact of SOB on patient
1 –> SOB on exertion
2 –> SOB up hills or walking quickly
3 –> Walks slower or stop on flat as SOB
4 –> Exercise tolerance 100-200 yards on flat
5 –> Housebound, SOB on minor tasks
18
Q
What is the medical management for COPD?
A
Step 1 –> breathless and exercise limitation –> SABA PRN. Continue at all steps.
Step 2 –> Still symptomatic, combination inhaler
- Predominant breathlessness (emphysema) –> LABA (salmeterol) AND LAMA (tiotropium)
- Two or more exacerbations in last 12 months of previous history of confirmed asthma –> ICS and LABA
Step 3 –> Ongoing excaberations (2 or more in 6 months) or admission to hospital.
-Triple therapy –> ICS and LABA and LAMA.
Step 4
-Still symptomatic –> consider theophylline
19
Q
What are the other interventions in COPD?
A
- Smoking cessation advice –> only disease modifying treatment that slows FEV/FVC decline.
- Pulmonary rehabilitation
- Exercise –> exercise training programme –> increases tolerance and improves SOB
- Vaccinations –> flu and pneumococcal
- Mucolytics in those w heavy mucous production
- Long term oxygen therapy in severe COPD causing hypoxia and cyanosis.
- Antidepressants when needed
20
Q
How should exacerbations of COPD be treated?
What should be done when there is no improvement in symptoms?
A
- Increase dose of SABA
- Exacerbation and sputum purulence –> Ab 1st line doxycycline. Alternative amoxicillin. PA clarithromycin.
- Oral corticosteroid –> prednisolone 30mg OD 1-2 weeks.
No improvement in symptoms on first choice for 2-3 days
- Send a sputum sample for culture and susceptibility testing.
- Offer an alternative first choice antibiotic from different class (guided by susceptibilities when available).
If the person is at higher risk of treatment failure e.g frequent antibiotic use, previous or current sputum culture with resistant bacteria or high risk of developing complications)
-Consider prescribing co-amoxiclav 500/125 mg TDS 5 days
21
Q
What is sleep apnoea?
What are the RF?
A
- Intermittent closure/collapse of the pharyngeal air way causing apnoeic episodes during sleep. These are terminated by partial arousal.
- Upper airway obstruction –> episodes apnoea >10 seconds without breathing, usually hundreds in night. –Causes frequent waking, giving sawtooth pattern sleep.
- 90% due to pharyngeal obstruction from large neck particularly >40cm circumference.
- Common in obesity.
- Others due to retrognathia (setback mandible) or enlarged tonsils in children.
- 1 in 4 when BMI >30
- RF –> obesity, age, male, alcohol, smoking, hypothyroidism
22
Q
What is the typical history and presentation of sleep apneoa?
A
- Loud snoring. Snoring gasping and choking during sleep.
- Daytime somnolence.
- Poor sleep quality.
- Morning headache.
- Decreased libido.
- Nocturia.
- Decrease cognitive performance.
- Increase risk HTN
23
Q
What are the investigations for sleep apnoea?
What is the diagnostic test?
A
- Simple studies –> pulse oximetry and video recordings can be all that’s needed to diagnose
- Epworth sleepiness scale –> initial screen >10 –> referral sleep service
- Neck circumference and BMI. Check nasal patency, tongue size, oropharynx for large tonsils or other obstructions.
- BP and glucose
- DIAGNOSTIC TEST –> Polysomonography –> which monitors oxygen saturation, airflow at the nose and mouth, ECG, EMG chest, and abdominal wall movement during sleep. Can be attended or non attended. Apnoea-hypopnea index and scores, >5 mild, >15 moderate, >30 severe. The occurrence of 15 or more episodes of apnoea or hypopnoea during 1h of sleep, on average, indicates significant sleep apnoea.
24
Q
What is the management for sleep apnoea?
A
- Lifestyle –> lose weight, avoidance of tobacco and alcohol.
- Sleep hygiene –> avoid sedatives in evening including alcohol and advise sleeping on side.
- Inform DVLA when OSA and symptomatic w day time sleepiness. Can drive as long as treatment effective.
- 1st line for symptomatic OSA effective QOL –> Nocturnal continuous positive airway pressure CPAP –> CPAP via a nasal mask during sleep is effective and recommended by NICE for those with moderate to severe disease. Often lifelong.
- Surgery to relieve pharyngeal or nasal obstruction, eg tonsillectomy or polypectomy, is occasionally needed.
25
What is acute bronchitis?
What are the RF?
- Short term inflamm of bronchi
- >90% cause is viral --> RSV, rhinovirus, influenza. After cough, sore throat or flu.
- Small % --> mycoplasma pneumonia and Bordetella pertussis
- Irritation of airways --> damage --> inflamm, neutrophils infiltrating lung tissue. Mucosal hypersecretion promoted by substance released by neutrophil.
-RF --> smoking, dust, air pollution
26
What is the typical presentation of acute bronchitis?
What is the differential diagnosis?
Expectorating cough, SOB, wheeze, chest discomfort, fever, fatigue, malaise.
-Symptoms peak after 2-3 days then clear. Commonly takes 2-3 weeks for cough to go completely.
DD --> pneumonia, bronchiolitis, bronchiectasis, COPD, asthma
27
What are the investigations for acute bronchitis?
-Often clinical diagnosis
- Bloods --> FBC, CRP
- Sputum sample showing neutrophil granulocytes (inflammatory WBCs) and culture showing pathogenic microorganisms.
- CXR when possible pneumonia
28
What is the management for acute bronchitis?
When should antibiotics be given?
- Most cases self-limited and resolve in few weeks
- Fluid intake and analgesia --> Paracetamol and NSAIDS to reduce fever
- Stop smoking
- Self-care --> honey, OTC cough medicine
- AB not generally used as don't make large difference to duration symptoms, shorten couhg by ½ day on average. Adverse effects e.g diarrhoea.
- Offer Ab when systemically unwell. And offer back up Ab when higher risk complications e.g pre-existing comorbid condition, >65 w 2 or >80 w 1 --> diabetes/CHF/hospital admission <1 year, using oral corticosteroids.
- Ab --> 1st line --> amoxicillin 500mg TDS 5 days. Alternative --> clarithromycin.
-Refer hospital when acute cough and S+S of more serious e.g PE
29
What is pneumonia and the types e.g CAP?
- Inflamm of the lung parenchyma usually due to bacterial infection.
- CAP --> community acquired pneumonia. Strep. pneumonia, g+ve cocci ---> 31% cases,
- HAP --> hospital acquired pneumonia --> develop at least >48 hours after hospital admission. Most commonly g-ve rods --> kleibsella, e coli, pseudomonas. Also staph aureus --> g+ve cocci --> more likely cause severe.
- Aspiration --> mixed aerobic and anaerobic bacteria.
- Immunosuppression pneumonia --> e.g HIV --> broad range organisms. Important to spot. Not normal CURB65.
- Legionelle pneumonia --> associated w foreign trabel to less economically developed countries and use of air conditioning units.
- Chronic pneumonia --> Not only infectious, also cancer.
30
What are HIV pneumonias?
-Opportunistic pneumonias that occur as a result of immunodeficiency
-Vary across a broad spectrum from bacterial/mycobacterial and viral to fungal and parasitic.
Major cause mortality.
-CD4 count can potentially evaluate which organism is most likely causative agent
-Strep p, haemophilus influenza, pseudomonas, mycobacterium tuberculosis, pneumocystis jirovecii (p carini)
-Pneumocysitis pneumonia --> AIDS defining condition.
31
What are fungal pneumonias?
What are the RF?
How should they be treated?
- Fungal infections commonly affect lungs either directly be affecting lung tissue or throuhg their ability to elicit immunological reaction when fungal material is inhaled.
- In immunocompromised --> funal penumoia can disseminate haematogenously resulting in systemic mycoses
- Usually due to opportunisitic infections
- Common --> mucos spp/aspergillus (mold), candida spp/cryptococcus (yeast), histoplasma spp/blastomyces spp/coccidioides.
RF
- Immunocompromised
- Exposure bat/bird droppings
- Travel to endemic countries --> South America
- Fungus categorised into --> mold, yeast, dimorphic fungus
- -Specific fungal serology tests
- If immunocompromised address cause
- Azole based anti fungals e.g voriconazole.
32
What is the pathophysiology of bacterial pneumonia?
Bacteria over come bodies defences to infect alveoli, Bacteria from URT translocate --> sterile distal airway --> macrophage eat bacteria phagolysosome inside get overwhelmed --> overwhelm host defence --> inflamm response --> cytokines --> neutrophils and some bacteria die --> pus in alveoli.
33
What is the pathophysiology of viral pneumonia?
Virus invades pneumocytes (cells of lung), virus reproduces. Some cells can directly causes pneumocyte death. Bodys inflammatory response further damages tissues w onflux of inflamm cells causing fluid to infiltrate alveroli, impairng oxygenation fo blood.
RF --> Most common in extreme of age.
34
What is the presentation of pneumonia?
What do you find on examination?
GENERAL
- Productive cough --> inflamm in lower lung feels like irritation in back of throat.
- Purulent sputum --> May be none. S pnemoniae is rusty. Kleibsella is red jelly.
- SOB
- Pleuritic chest pain --> particularly in s pnemoniae. Lining of lung --> somatic nerve endings, localise pain.
- Signs infection --> fever, sweats, malaise, weakness.
- Confusion --> can be only sign in elderly
-Increase HR, RR, low BP, fever, dehydration.
Viral v bacterial
- Chest pain more common in bacterial
- Viral --> non productive cough, fever and chills, systemic e.g runny nose, myalgia, fatigue, headaches.
EXAMINATION
- Signs lung consolidation --> eprcussion and auscultation --> dull, decrwase air entry, bronchial breath sounds, crackles and wheeze.
- Non resonant percussion --> fluid and pus not air.
- Hypoxia and signs RF in severe or underlying lung disease
35
What is management pneumonia?
Who gets the vaccine?
CURB 65 0-1 mild --> Amoxicillin 1st line. PA then doxy/clarithro/erthro.
CURB 65 2 moderate --> amxoi and clarith (erythro when pregnant)
CURB 3-5 severe --> Coamoxiclav and clarith/erythro. Can be IV coamoxiclav and clarithromycin.
Complications --> type 1 resp failure, empyema
-Vaccine --> >65s, chronic lung disease, immunosuppression, chronic heart, kidney
Viral
- Most cases self limiting, resolve 1-3 weeks.
- More serious --> respiratory failure.
- Following viral infection --> lung tissue more susceptible to bacterial infection as damage because of virus. (Can get bacterial pneumonia after primary viral infection).
36
What are the investigations for pneumonia?
DIAGNOSTIC --> CXR --> consolidation (lung infiltrates in viral more likely to be bilateral)
- Sputum --> microscopy and culture
- Nasopharyngeal swabs --> viral culture
- Bloods --> CRP. LFT more likely to be deranged when atypical e.g legionella. Check virus w viral PCR.
- Pulse oximetry.
- ABG, respiratory failure.
- Pleural fluid may be aspirated for culture
37
How do you assess the severity of CAP?
CURB 65/CRB65
- Confusion, urea >7mmol, RR >30, BP <90/60, >65
- 0-1 or 0 CRB --> mild, only admit to hospital when social circumstances or single worrying feature.
- 2 OR 1,2 CRB--> moderate --> hospital
- 3-5 or 3,4 CRB --> severe --> admit
38
What is the flu?
- Acute viral infection of lungs and airways
- Spread through droplets
- Influenza --> member orhtomyxoviridae family.
- Three serotypes --> A (severe illness, pandemics), B (mild, only humans), C (minor symptoms, asymptomatic, children)
- Categorised by combination surface antigens.
- Haemogluttinin --> entrance to cells
- Neuramindase (gets virus loose from infected cells)
- Antigenic shirt --> major change
- Antigenic drift ---> minor mutations, seasonal
39
What is the presentation of flu?
- Incubation 1-4 days. Infective from 1 day before to 7 days after symptoms.
- Upper and lower respiratory tract symptoms
- Symptoms 3-5 days. Cough and fatigue 1-2 weeks
- Quick onset
- Cough non productive, coryza
- Fever, rigors, fatigue, anorexia
- Headache, myalgia
- Nausea and vomiting, conjuncitivitis, photophobia
40
What are the investigations for flu?
- Often clinical diagnosis, ENT and chest examination
- Acute onset, fever and cough --> positive predictive value
- Nasal/throat swabs for PCR confirmation in severe
41
What is the management for flu?
- Uncomplicated illness --> conservative --> symptomatic treatment --> rest, increase fluid intake, analgiesia e.g paracetamol.
- Complication --> includes LTRI, excerbation of underlying medical condition needing hospital admission.
- Medical --> selective use antiviral inhibitors --> block viral enzyme --> neuraminidase inhibitiors --> oseltamivir. >1 year old and within 48 hours symptoms.
Pneumonia can result from flu directly or more commonly due to secondary bacterial infection.
42
What is a pulmonary embolism?
What are the RF?
- Occlusion of a pulmonary artery by an embolic thrombus
- Common
- Venous thrombi usually from fragment of detached thrombus from DVT that passes in IVC and embolises through R side of heart through RA and RV, passes into pulmonary arterial circulation and lodges in pulmonary artery --> block blood flow to lungs.
- RF for DVT --> recent surgery or immobility, inherited thrombophilia, long haul flight or car, cancer, pregnancy and OCP, HRT, obesity, other DVT
- Cancer --> activates thrombin
- Oestrogen --> increase fibrinogen and thrombin.
43
What is the presentation of a PE?
- Depends on size of embolus
- Blockage major pulmonary artery --> death as suddent big increase in pulmonary arterial pressure, acute RV failure, cardiac arrest
- Medium --> v/q mismatch
History any RF for DVT
- SOB
- Pleuritic chest pain
- Haemoptysis
- Syncope
- Cyanosis
-Check calves --> pain, warmth, swelling, erythema, tenderness
44
What are the investigations for a PE?
- Wells score DVT and PE. DVT score >2 +ve. PE score >4 +ve.
- Wells PE >4 --> CTPA and LMWH.
- DVT >2 or Wells PE <4 --> d dimer --> +ve then CTPA and LMWH. -ve reassess.
- CXR --> r/o other conditions
- Bloods --> d dimer but low specificity
- Imaging when wells or d dimer +ve
GOLD STANDARD --> CTPA --> CT pulmonary angiogram --> visualise major segmental thrombi. Insert dye where holes emboli.
-V/Q perfusion
Others
- ABG --> decrease O2 and CO2, increase pH
- ECG --> 50% sinuse tachycardia
- Unprovoked --> consider thrombophilia screen
- Look for underlying cancer --> bilateral. Suggest by history, exam, bloods.
45
What is the management for a PE?
-Start treatment before definitive diagnosis, most PE deaths occur within 1 hour.
Acute
-ABCDE --> oxygen when hypoxic, fluids for low BP, morphine, antiemetic
- LMWH or fondaparinux SC 5 days or until INR >2 for >24 hours.
- Consider thrombolysis w alteplase when haemodynamically unstable. Massive PE.
Long term anticoagulation
- Apixaban, rivaroxaban, warfarin.
- Start during admission, overlap w LMWH for 72 hours
- Continue 3 months provoked, 6 months unprovoked. Permanently when second.
- 6 months LMWH active cancer
Below knee compression stockings --> wear on affected leg, 1 week after diagnosis. Change every 6 months for 2 years.
46
What is a pleural effusion?
What is the different categories?
- Accumulation of excess fluid in the pleural space.
- Small amount of fluid normal in pleural space for lubrication.
- Pleural effusion often results from excess production of this fluid. Less commonly due to reduced clearance e.g in lymphatic obstruction in TB or cancer
Effusions divided by their protein concentration
- <25g transudates
- >35 exudates
```
Causes
Transudate
-Increase venous pressure
-Often bilateral and due to organ failure.
-LVF, cirrhosis, nephrotic syndrome.
```
Exudate
- Unilateral. 4 I's.
- Inflammation (RA, SLE)
- Infarction (PE, MI)
- Infection (pneumonia, TB)
- Infiltration (cancer lung breast, lymphoma, malignant mesothelioma
47
What is the presentation of a pleural effusion?
What would you find on examination?
- Small <500ml often asymptomatic, seen on imaging
- Large --> SOB, pleuritic chest pain, cough
- Large --> may be tracheal deviation
- Signs of cause and underlying condition --> e.g JVP in HF, clubbing in lung cancer
- Decreased expansion, decreased or absent breath sounds, stony dull percussion.
- Reduced chest wall movements on the affected side
- Decreased tactile vocal fremitus/vocal resonance and bronchial breathing just above the effusion.
48
What are the investigations for pleural effusion?
- 1st line --> CXR --> diagnosis --> blunting costophrenic angle
- Pleural fluid aspiration indications --> unilateral effusions not thought to be transudative. Not routinely recommended for bilateral transudative.
Lights criteria when between 25g-35g
- Compare pleural fluid to serum protein and LDH
- Fluid:serum protein t<0.5 FBC, CRP infection. LFT, UandE liver or kidney failure. Consider BNP, ECHO HF.
49
What is the management for a pleural effusion?
-In general --> treat underlying cause. Aspiration and chest drain effusion.
Unilateral
- Tx underlying cause
- Can need further investigations e.g bronchoscopy, CT, pleural biopsy
- Therapeutic aspiration or chest drain when symptomatic
- Chest drain when pleural infection --> cloudy fluid, ph <7.2
- w/o treating cause likely to reoccur when aspirated/drain --> possible indwelling pleural catheter or pleurodesis (seal up space between pleura when malignant effusion after previous drainage).
Bilateral
- Tx underlying cause
- Diagnostic aspiration only when diagnostic uncertainty or poor response to treatment
50
What is pulmonary HTN?
What are the causes of pulmonary HTN?
- An increased resistance and pressure of blood in the pulmonary arteries.
- Increasing the pressure and resistance in the pulmonary arteries causes strain on the right side of the heart trying to pump blood through the lungs.
- This also causes a back pressure of blood into the systemic venous system.
Causes
Group 1 --> Primary pulmonary hypertension (no known cause) or connective tissue disease e.g SLE
Group 2 – Left heart failure usually due to myocardial infarction or systemic hypertension
Group 3 – Chronic lung disease e.g COPD
Group 4 – Pulmonary vascular disease e.g PE
Group 5 – Miscellaneous e.g sarcoidosis, glycogen storage disease and haematological disorders
51
What is the typical presentation of pulmonary HTN?
- SOB major
- Syncope
- Tachycardia
- Raised JVP
- Hepatomegaly
- Peripheral oedema
52
What are the investigations for pulmonary HTN?
ECG --> Right sided heart strain --> RVH --> larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6). Right axis deviation. Right bundle branch block
CXR --> Dilated pulmonary arteries, RVH
- A raised NT-proBNF blood test result indicates right ventricular failure
- Echo can be used to estimate pulmonary artery pressure
53
What is the management for pulmonary HTN?
- Prognosis poor 30-40% 5 year survival from diagnosis.
- Can increase to 60-70% where specific treatment is possible.
Primary pulmonary hypertension can be treated with:
- IV prostanoids (e.g. epoprostenol)
- Endothelin receptor antagonists (e.g. macitentan)
- Phosphodiesterase-5 inhibitors (e.g. sildenafil)
- Secondary pulmonary hypertension is managed by treating the underlying cause e.g PE, SLE
- Supportive treatment for complications such as respiratory failure, arrhythmias and heart failure.
54
What is pleurisy and the main causes?
- Visceral pleura inner layer which lines lungs, parietal pleura is outer layer which lines chest wall, rib cage and mediastinum.
- Parietal pleura supplied by phrenic nerve and causes sharp localised pain, visceral pleura autonomic nerve w dull achy pain.
- Between layers --> fluid which acts as lubricant. When pleura inflamed, pleural lining rubs together causing pain.
- Most common causes --> viral infection
- Causes --> pneumonia, trauma, cancers e.g lung, RA, PE, viral respiratory illness, allergic reaction to drugs, HIV, resp conditions e.g asbestos
55
What is the common presentation of pleurisy?
- Chest pain
- Sharp stabbing pain/burning sensation, usually exacerbated by deep inspiration/movement/coughing
- Referred pain to shoulder and neck
- Cough based on cause
- SOB possible but can indicate more serious
- Systemic e.g fever based on cause
56
What are the investigations in pleurisy and the DD they can help to rule out?
DD --> PE, pericarditis, MI, pneumothorax
Investigations
- Done to r/o other causes chest pain
- Distinctive dry/crunching sound on auscultation
- Routine bloods w trop and ABG (maybe D dimer when appropriate)
- ECG r/o cardiac cause
- CXR --> r/o DD e.g pneumothorax, pleural effusions
- Diagnosis --> when exclusions of others.
57
What is the management for pleurisy?
- 1st line --> NSAIDS
- Second line --> Indomethacin
- Treat underlying causes when appropriate e.g Ab
- Usually gets better on own few days
58
What is Cor Pulmonale and it's causes?
- Right ventricle failure due to pulmonary artery HTN due to a lung disorder.
- Right sided heart failure caused by respiratory disease. The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) --> right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries --> back pressure of blood in the right atrium, the vena cava and the systemic venous system.
Causes
- COPD is the most common cause
- Pulmonary Embolism --> acute cor pulmonale
- Interstitial Lung Disease
- Cystic Fibrosis
- Primary Pulmonary Hypertension
RF --> secondary to lung disease. Acute PE, ARDs. Chronic COPD.
59
What is the main presentation of cor pulmonale?
- Often patients with early cor pulmonale are asymptomatic.
- Main --> SOB --> SOB is also caused by the chronic lung diseases that lead to cor pulmonale.
- Peripheral oedema, increased breathlessness of exertion, syncope (dizziness and fainting) or chest pain.
- Hypoxia, cyanosis, tachy, raised JVP (back log in jugular veins), RV heave, pansystolic murmur, hepatomegaly as back pressure in hepatic vein.
60
What are the investigations for cor pulmonale and what would you expect to show?
- Bloods --> FBC
- ABG --> hypoxia
- CXR --> enlarged right atrium and ventricle, prominent pulmonary arteries
- ECG --> P pulmonale; right axis deviation; right ventricular hyper trophy/strain.
61
What is the management for cor pulmonale?
- Treat underlying cause --> COPD and pulmonary infections.
- Treat respiratory failure—in the acute situation give 24% oxygen if PaO2 <8kPa. Monitor ABG and gradually increase oxygen concentration if PaCO2 is stable.
- In COPD patients --> LTOT.
- Treat cardiac failure with diuretics such as furosemide, alternative spironolactone.
- Consider heart–lung transplantation in young patients.
Prognosis Poor. 50% die within 5yrs
62
What is the presentation of an acute exacerbation of COPD?
How should you clinically assess someone?
-Acute exacerbation --> worsening previously stable COPD, beyond day to day variation. Mya be due to viral or bacterial infection. Increase SOB, sputum volume and purulence.
AE - assess severity
- SOB worsening
- Cough
- Increased sputum volume and purulence
- Wheeze
- Fever w no obvious source
- Increase RR or HR >20% above baseline
- URTI in last 5 days
Severe AE
- Marked breathlessness and tachypnoea.
- Pursed-lip breathing and/or use of accessory muscles at rest.
- New-onset cyanosis or peripheral oedema.
- Acute confusion or drowsiness.
- Marked reduction in activities of daily living.
- Check vital signs (including temperature, oxygen saturations [using pulse oximetry], blood pressure and heart rate).
- Assess for confusion or impaired consciousness.
- Examine the chest.
- Check ability to cope at home.
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What is a pneumothorax?
What are the various types?
- The presence of air in the pleural space
- More common in M>F
- Air leaks out of the lung (damaged lung) into pleural space until the pressures equalise --> lung collapses to variable degree depending on size pneumothorax.
RF --> male, age, smoking, previous pneumothorax, marfans
- Primary spontaneous pneumothorax --> no cause thin tall young men
- Secondary pneumothorax --> underlying lung disease --> COPD asthma, pneumonia
- Trauma --> penetrating chest wound, commonly knife
- Iatrogenic --> subclavian artery cannulation
- Tension pneumothorax --> in some cases tissues near the lung defect act as a one way valve --> pressures don't equalise, air builds up during inspiration and can't escape on expiration --> increase pressure pushes mediastinal structures, the trachea moves away form the affected side --> respiratory distress --> cardiorespiratory arrest
-Haemothorax --> Blood in pleural cavity, may cause hypovolaemic shock. Blood can reabsorb when small amount, can need thoracentesis.
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What is the presentation of a pneumothorax?
- Can be asymptomatic --> fit, young w small pneumothorax
- Sudden onset dyspnoea and/r unilateral pleuritic chest pain
- Patients w underlying lung disease --> present w sudden worsening symptoms
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What would you find on examination in pneumothorax?
- Reduced chest expansion --> asymmetrical.
- Hyperresonance to percussion
- Decrease breath sounds on affected side.
- Tension pneumothorax --> trachea pushed away from effected side. Respiratory distress.
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What investigations in pneumothorax?
- CXR --> skip in tension pneumothorax
- CT when diagnostic uncertainty
- ABG --> hypoxic patients and those w chronic lung disease
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What is the management for a pneumothorax?
Primary
- Conservative when small (can self resolve), <2cm and SOB between lung margin and chest wall on x ray at level of hilum and no SOB.
- Otherwise --> needle aspiration --> chest drain when doesn't work.
Secondary
- Conservative when <1cm and no SOB.
- 1-2cm w no SOB --> needle aspiration.
- >2cm or SOB --> chest drain
Tension
- 100% O2
- Needle aspiration to relieve symptoms
- Then chest drain
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What is respiratory failure in general?
- Occurs when gas exchange is inadequate, leading to hypoxia.
- PaO2 <8kPa. PaO2 --> measurement of oxygen pressure in arterial bloods, shows how well oxygen moving lungs to blood
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What is type 1 respiratory failure and it's causes?
- Associated w PaO2 <8kPa but w normal or low PCO2.
- Primarily result of ventilation/perfusion mismatch.
- Increased ventilation removes any excess CO2 but can't compensate for low O2.
- Causes of V/Q mismatch --> PE, severe pneumonia, acute asthma, pulmonary fibrosis, R-L cardiac shunts.
More detail
- Decreased V/Q --> Decreased alveolar ventilation --> e.g due to collapse or congestion --> pulmonary oedema, atelectasis, ARDS, airway obstruction e.g COPD, asthma.
- Increase V/Q --> Decreased alveolar perfusion --> PE
- Decrease O2 intake --? hypoventilation or low FiO2 e.g high altitude
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What is type 2 respiratory failure and its causes?
- Associated w PaO2 <8kPa but w high PCO2.
- Result of generalised alveolar hypoventilation w or w/o V/Q mismatch.
- Transfer of both O2 and CO2 impaired so pCO2 is also raised and low PO2.
- Causes --> pulmonary disease e.g COPD, asthma (attack when respiratory effort starts to fail), opiate OD, pneumonia.
-Chronic retainer --> long term respiratory acidosis e.g in COPD which has been metabolically compensated leading to normal pH.
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What is the presentation of respiratory failure?
- Those of underlying cause w symptoms of hypoxia and possible hypercapnia
- Hypoxia --> SOB, restlessness, agitation, confusion, central cyanosis
- Hypercapnia --> headache, bounding pulse, tremor/flapping, tachycardia
- Acute --> typically develops suddenly in patient w otherwise healthy lungs, obvious respiratory distress w hyperventilation
- Chronic --> more persistent problem n patients w chronic lung diseases. Clinical picture may be undramatic despite low PO2 as compensatory mechanisms.
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What are the investigations in respiratory failure?
- Aimed at determining underlying causes
- ABG
- CXR
- Spirometry
- Microbiology e.g sputum
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What is the management in respiratory failure?
- Depends on the cause
- Type 1 --> treat underlying cause. Oxygen. Possible assisted ventilation.
- Type 2 --> treat underlying cause. Respiratory centre may be relatively insensitive to CO2, respiration could be driven by hypoxia --> controlled O2 therapy.
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What is acute respiratory distress syndrome?
ARDS
-A non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness. The diagnosis of ARDS is based on fulfilling three criteria
- Acute onset (within 1 week)
- Bilateral opacities on chest x-ray
- PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or
continuous positive airway pressure (CPAP) ≥5 cm H₂O
-Most common symptoms and signs are dyspnoea, hypoxaemia, frothy sputum, which progress to acute
respiratory failure.
-Common causes are pneumonia, sepsis, aspiration, pancreatitis, burns and smoke inhalation and severe trauma. Sepsis w pulmonary cause e.g pneumonia is most common.
-CXR, ABG, urine culture, sputum culture, blood culture
-Mortality is between 30% and 50%.
-Tx --> oxygen and ventilation -->Low tidal volume, plateau-pressure-limited mechanical ventilation is the primary treatment that has been shown to reduce mortality.
-In severe acute respiratory distress syndrome (ARDS),
neuromuscular blockade and prone positioning may improve clinical outcomes.
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What is bronchiectasis and its causes?
- Persistent dilation of bronchi due to damage from infection and inflammation.
- Chronic inflamm of bronchi and bronchioles --> weakening of bronchial walls --> permanent dilation and thinning of these airways
- 1/100 >70
- Main organisms --> H influenzae, strep pneumoniae, S aureus
- Not common developed countries?
Causes
- Infection --> frequent and/or severe childhood lung infections
- Asthma
- Immunodeficiency e.g HIV
- Congenital --> CF, a-1 antitrypsin deficiency
- Gastric aspiration
- Obstruction --> foreign body, tumour
- Autoimmune -- > RA, SS
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What is the presentation of bronchiectasis?
- Can be episodic or chronic
- Persistent cough w large amounts of purulent yellow/green sputum – can have blood
- Haemoptysis --> in dry bronchiectasis e.g TB occurs in absence of sputum
- SOB
- Chest pain between exacerbations, commonly non pleuritic
- Systemic --> fever and weight loss
- Coarse early inspiratory crackles
- Inspiratory squeaks (high pitch), ronchi (low pitch, snoring)
- Wheeze
- Clubbing
THINK ADULTS
- Persistent production of mucopurulent or purulent sputum, esp when RF.
- Cough >8 weeks esp w sputum production or history trigger
- RA or IBD --> when have symptoms of chronic productive cough or recurrent chest infections.
- COPD when don't smoke or those w COPD and frequent exacerbations w +ve culture psuedomona.
THINK CHILDREN
- Chronic productive or moist cough not responding to >4 weeks Ab
- Recurrent or persistent wet cough >6 weeks.
- Asthma not responding to Tx
- Unexplained haemoptysis
- Episode severe pneumonia especiailly when doesn't completely resolve.
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What are the investigations for bronchiectasis?
- Bloods --> FBC increase WBC and CRP in infection
- CXR --> abnormal but non specific
- DIAGNOSIS --> high resolution CT --> bronchia dilatation and wall thickening, mucuous plugged small airways, fluid filled cysts
- Spirometry --> obstructive --> decrease FEV1 and FEV1/FVC ration
- Sputum culture --> MC and S
- Bronchoscopy when suspected foreign body
- Investigate cause --> e.g serum a-1, RF, HIV test, CF sweat test
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What is the management for bronchiectasis?
- All people with suspected bronchiectasis should be referred to a respiratory specialists to confirm diagnosis and determine the underlying cause.
- Exacerbations --> most can be managed in primary care --> use past microbiology cultures to guide choice --> Therapeutic --> Ab, long courses >14 days are needed --> Ab according to bacterial sensitivity --> empirical amoxi 1st line or quinolone when colonised w pseudomonas
- General --> stop smoking, flu vaccine, pulmonary rehab
- Prophylatic --> offer when frequent exacerbations --> azithromycin.
- Chest physio --> sputum clearance. Postural drainage.
- Inhaled bronchodilators when some reversibility
- Surgery --> resection of affected lobe. Lung transplant FEV1 <30% predicted.
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What is cystic fibrosis?
- Autosomal recessive mutation in CTFR gene on chromosome 7.
- 1/25 UK are carriers
- CTF --> apical chloride channel --> chloride movement across cell membranes often followed by Na and H2O.
- Upper airways --> CTFR dysfunction --> reduced fluid flow into airways and therefore failure of mucous to be cleared --> recurrent pneumonia w strep pneumo, staph aureus, haemoinfluenza B and eventually pseudomonas.
- Pancreas --> pancreatic interlobular ducts also become clogged w mucous --> impaired secretion digestive enzymes and pancreatic destruction
- Sweat glands --> impaired chloride removal from duct --> salty sweat.
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What is the typical presentation of CF?
What are the differences in presentation between neonates and children/young adults?
-Neonates --> failure to thrive, rectal prolapse, neonatal meconium ileus --> failure to pass tar like first stools of neonates. PC in 10%.
Children and young adults
- Recurrent pneumonia is most common presentation. Cough, wheeze, bronchiectasis.
- Pancreatic insuffiency --> diabetes, steatorrhea.
- Other GI --> rectal prolapse, small bowel obstruction, GORD
- Slow growth
- Clubbing
- Nasal polyps, sinusitis
- Male infertility --> congenital bilateral absence of VD --> obstruction azospermia
- 10% diagnosed >16 --> presenting w pulmonary, sinus, fertility issues
- Cyanosis, finger clubbing, bilateral coarse crackles
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What are the investigations for CF?
-Newborn screening --> picks up most cases
Diagnosis confirmed by combination of two cases
- Sweat test --> >60mmol/L chloride.
- Genetic testing --> showing two disease causing mutations (both alleles).
- Other --> CXR, sputum culture, FEV1 key prognostic factor.
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What is the management for CF?
-MDT
Respiratory
- Mucous clearance --> chest physio (postural drainage etc), nebulised mucolytics
- Antimicrobials --> high dose long course Ab when Tx infections
- Anti inflamms >6 --> long term azithromycin or ibuprofen
- Bilateral lung transplant when medical therapy doesn't work
- Non respiratory --> Pancreatic insufficiency (>80%) --> give enteric coated pancreatic enzymes
- Targeted --> ivacraftor and lumacaftor --> novel CTFR modulators w modest effects on lung function
-Median survival 40-50 years
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What is empyema?
When does it tend to occur?
- Pus in the pleural space.
- Most often due to infections post pneumonia.
- Anaerobic staph and g-ve infections most common causes
- Begins as free flowing pleural fluid that becomes infected.
- RF --> pneumonia, lung abscess, alcoholism, diabetes, COPD.
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What is the presentation of empyema?
What is a DD?
- It should be suspected if a patient with a resolving pneumonia develops a recurrent fever.
- PMH --> pneumonia or lung abscess
- SOB, fever, dry cough, chest pain on inspiration, weight loss
- Tachypnoea, fever, reduced breath sounds, rales, ronchi (low pitched rattling sound, snoring), dullness percussion
DD --> PE
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What are the investigations for an empyema?
- Bloods --> FBC, U and E, CRP
- CXR --> indicates pleural effusion
- Thoracentesis --> aspirated pleural fluid --> yellow and turbid w pH <7.2, low glucose and high LDH.
- Chest drain --> to drain
- Blood cultures
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What is the management for an empyema?
- Thoracentesis
| - Antibiotics
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What is near drowning?
- Respiratory impairment due to submersion in liquid.
- Submerged underwater grasping or holding ones breath for too long --> stimulate apnoea --> cause hyperventilation and subsequent fluid aspiration into lungs and laryngospasm. --> hypoxia, respiratory acidosis and cardiac arrest
- Freshwater drowning more rapid. Salt water hypertonic therefore fluid leaves cells shrinking. Fresh water hypotonic cause water into RBC --> burst --> release potassium --> hyperkalaemia --> heart.
- RF --> children, alcohol use, water sport
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What is the presentation of near drowning?
- Hypothermia
- Unconsciousness
- Intoxication
- Coughing out water
- Tachycardiac and tachypnoea
- Pulmonary odema --> dullness to percussion and wheeze
- Hypothermia
- Reduced GCS
- Check for head and neck injuries
- Abdo distension
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What are the investigations in near drowning?
- Bloods --> ABG, alcohol, plasma osmolarity, UandE
- CXR --> pulmonary oedema
- ECG --> J waves hypothermia
- Neck x-ray --> check fractures
- CT head --> bleeding
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What is the management of near drowning?
- ABCDE
- Treat abnormal findings as find, e.g fluid in airways turn to side
- Resuscitation
- Unconscious then intubate
- Awake and alert then observe for 6 hours (pulmonary oedema can develop late, tends to be within 4 hours)
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Who does viral pneumonia more commonly effect?
-Extremes of age
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In pneumonia what should be used instead of clarithromycin in those who are pregnant?
-Erythromycin
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What finding on examination should make you think of and LRTI as opposed to an LRTI?
-Rales --> should think pneumonia of CHF
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What features on an FBC would be consistent with an influenza infection?
-Lymphocytosis --> during immune response the body produces Ab (lymphocytes) to fight against viral infections.
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When would you expect to see neutrophil/leucocytosis?
-High neutrophils commonly associated w bacterial infections and certain medications.
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When would you expect to see neutropaenia?
-Low neutrophils commonly associated w bacterial infection in immunosuppressed patients.
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What is the most common causative organisms of COPD exacerbations?
-Haemophilus influenza
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When providing patients with a home supply of corticosteroids and Ab for COPD exacerbations what should you inform them?
- Only take the Ab coughing up purulent sputum.
| - Contact you when they are required to use them to ensure no further action is required.
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What does PHE recommend to help guide the use of Ab?
-CRP
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What are the RF for influenza?
-DM, >65, BMI >40, complement disorder
NOT recent URTI
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What is alpha 1 antitrypsin deficiency?
- A common inherited condition caused by a lack of a protease inhibitor (Pi) normally produced by the liver.
- The role of A1AT (made in liver) is to protect cells from enzymes such as neutrophil elastase.
- It classically causes emphysema (i.e. chronic obstructive pulmonary disease) in patients who are young and non-smokers.
- Can also cause severe liver disease
- Commonly found in those 20-50
- Can be diagnosed in the prenatal period (think about when having a family)
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What is the management for alpha 1 antitrypsin deficiency?
- No smoking
- Supportive --> bronchodilators, physiotherapy
- IV alpha1-antitrypsin protein concentrates
- Surgery --> lung volume reduction surgery, lung transplantation
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What is a paraneoplastic syndrome of SCLC?
| What are its features?
- Lambert eaton syndrome --> weakness in proximal muscles of arms and legs.
- Weakness that is worse in the legs.
- Gets slightly better w muscle use
- Muscle tenderness
- Difficulty waling
MG --> affects face and arms earlier, worse w muscle use.
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What are the indications for an individual w COPD exacerbation to go to hospital and how should it be treated?
- Severe SOB
- Sats <90%
- LTOT
- Worsening oedema
- Cyanosis
- Struggling to cope
- Not well
In hospital
- Venturi mask 24-28%, aim sats 88-92%
- Sputum culture, FBC, CXR, ABG, ECG
- Nebulisers SABA and SAMA (stop LAMA)
- Prednisolone 1-2 weeks
- Consider theophylline IV
- Ab?
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What is a catamenial pneumothorax?
A pneumothorax at menustration. Up to 24 hours before or 72 hours after onset.
- 90% in right lung
- Thoracic endometriosis, necrotic holes in diaphragm, air from genital tract into space.
- Women with endometriosis, ask about pleuritic, shoulder or upper abdo pain at time of menustration as increase risk.
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What are the differentials in pneumothorax?
- Pleural effusion --> slower onset and dullness on percussion
- PE --> haemoptysis
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Where do thoracocentisis and chest drains occur?
Thoracocentesis --> large bore cannula, 2nd intercostal space, mid clavicular line
Chest drain --> Inserted into triangle of safety, 4th/5th intercostal space, mid axillary line
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What are the risk factors for foreign body aspiration?
- Inhalation of a foreign body into larynx and respiratory tract
- RF -> decrease level of consciousness (alcohol), ages <4 >70, male, cerebrovascular diseases (dysphagia and impaired cough reflexes in parkinsons), bulbar dysfunction, dementia, seizures
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What is the presentation of foreign body aspiration?
-Depends on size and shape of object AND degree and location of obstruction
- KEY symptoms --> Choking crisis w sudden onset choking and coughing. Unilateral breath sounds and unilateral wheeze.
- Persistent cough following choking episode.
- Initial choking missed in 20% therefore symptoms can last for weeks before diagnosis
- Other symps --> intractable cough, fever, SOB, bilateral wheeze
- Large --> occlude trachea completely --> asphyxia
- Small --> lower lobe airways --> wheeze and cough
-Keep high suspicion when non specific S+S and underlying COPD, CHF.
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How can difference in severity of foreign body inhalation present?
Mild --> Able to breathe, cough effectively and speak. Children are fully responsive, crying or verbally respond to questions; may have a loud cough.
-Severe --> can't breath or speak, wheezy breath sounds, trying to cough is quiet, cyanosis, unconscious
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What are the investigations for an individual who is stable with suspected foreign body inhalation?
- CXR 1st line --> Can only detect radioopaque objects
- CT
- In adults flexible bronchoscopy to confirm or diagnosis other cause of airway obstruction.
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What is the management for foreign body inhalation?
When do you do flexible or rigid bronchoscopy?
Management – when conscious
- 1st line --> encourage cough
- 2nd line --> black blow, chest thrusts (infants), abdominal thrusts
- 3rd line --> removal of foreign body --> either flexible bronchoscopy or rigid bronchoscopy. Alternatively when needed --> thoractomy or surgery.
Management – unconscious
- Secure the airway --> external manoeuvres not effective and patient unconscious because of asphyxiation --> immediate intubation unless object easily removed but don't finger sweep as could push further.
- When can’t immediately intubate --> CPR
- Removal of foreign body --> flexible bronchoscopy or rigid bronchosopy.
- Flexible when cervicofacial trauma or to initially confirm diagnosis and attempt removal.
- Rigid when asphyxiating, stridor, wheezing, unilateral decrease breath sounds, radiopaque object seen on x ray.
