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5th Year Revision > Y3 - Resp > Flashcards

Y3 - Resp Flashcards

1
Q

What is the MRC Dyspnoea score?

A

​Grades of breathlessness

  1. not troubled by breathlessness except on Strenous exercise
  2. SOB when hurrying or walking up a slight hill
  3. Walks slower than contemporaries on level ground due to SOB, has to stop for breath
  4. Stops for breath after walking 100m or after a few mins on level ground
  5. too breathless to leave house, breathless dressing
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2
Q

What is the WHO performance status?

A
  1. fully active no restriction
  2. restricted in strenous activity, able to carry out light work
  3. capable of self care but unable to carry out any work (up and about over 50% of waking hours)
  4. capable of limited self care, confined to bed/chair >50% waking hours
  5. completely disabled, cannot self care, totally confined to bed/chair
  6. Dead
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3
Q

What is FVC? What is FEV1? What is Vital Capacity?

A

FVC = vol of air that can be forcibly expelled from lungs from max inspiration

FEV1 = vol of air that can be forcibly expelled from the lungs in the 1st second, from max inspiration

Vital capacity = vol fo air expired from lungs from max inspiration using a slow relaxed breath out

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4
Q

What would obstructive and restrictive spirometry look like

A

Obstructive = copd, asthma, bronchiectasis, CF

  • reduced FEV1 (<80% than normal)
  • Reduced FVC but less reduced than FEV1
  • FEV1/FVC ratio reduced <0.7

Restrictive = intersitital pulmonary fibrosis, pulmonary oedema, pregnancy etc

  • reduced FEV1 (<80% of normal)
  • reduced FVC (<80% of normal)
  • FEV1/FVC ration normal (>0.7)
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5
Q

How would flow volume loops look in restrictive/ obstructive disease?

A

scalloping - think obstructive

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6
Q

what sign on an abg would make you think someone had copd?

A

someone being give o2 that was in co2 retention but it was being metabolically compensated so pH is normal

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7
Q

How would you manage anaphylaxis and angioedema?

A
  • A-E
  • Maintain airway
  • IM Adrenaline 0.5mg of 1:1000
    • repeat in 5 mins if necessary
  • IV hydrocortisone 200mg
  • IV chlorphenamine 10mg

Bronchospasm = NEB salbutamol

Laryngeal oedema = NEB adrenaline

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8
Q

How would you diagnose severity of an asthma exacerbation?

Mild- Life threatening

A

Mild = pefr >75%

Mod = pefr 50-75%

Severe = peft 33-50%, RR>25, HR>110, cannot complete sentences

Life threatening = pefr<33%, sats<92%, pco2 raised on abg, silent chest sounds, cyanosis

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9
Q

How would you manage an acute asthma exacerbation?

A
  • A-E = remember abg with o2
  • O2 to 94-98% or 88-92% depending
  • nebs 5mg salbutamol
    • add nebs ipratropium bromide 500mcg if severe
  • 40mg oral prednisolone or iv hydrocortisone

Life threatening or fatal

  • above steps, call ICU and anaesthetist asap
  • MgSo4
  • IV aminophylline
  • IV Salbutamol
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10
Q

How would you manage a COPD exacerbation?

A
  • A-E
  • o2 to 88-92% (use abg)
  • nebs salbutamol 5mg + ipratropium 0.5mg
  • prednisolone 30mg stat
  • antibiotics if raised crp/wcc/purulent sputum
  • CXR
  • IV aminophylline
  • NIV BiPAP for Type 2 resp failure (if ph7.25-7.35)
    • if ph <7.25 then ITU
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11
Q

How would you do CURB65?

A

C = confusion

Urea >7

RR>30

Bp <90mmhg systolic or <60mmhg diastolic

>65 years old

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12
Q

How would you manage massive haemoptysis?

A
  • A-E
  • lie them on side of suspected lesion
  • oral tranexamic acid
  • stop nsaids, aspirin, anticoags
  • antibiotics if infection
  • Vitamin K
  • CT aortogram to undertake bronchial artery embolisation
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13
Q

How would a tension pneumothorax present?

How would you manage it?

A

Presentation

  • deviated trachea away
  • hypotension
  • tachycardia
  • mediastinal shift away

Management

  • wide bore canula into 2nd ICS mid clavicular line
  • insert chest drain
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14
Q

How would a PE present?

How would you manage it?

A
  • SOB
  • tachycardia
  • hypotension
  • haemoptysis
  • raised JVP
  • pleural rub
  • gallop rhythm
  • pleuritic chest pain
  • ECG = S1Q3R3
  • DVT potentially

Management

  • calculate wells score
  • O2 if hypoxic, fluid resus if hypovolaemic
  • Thrombolysis if massive PE = alteplase 10mg IV
  • or give DOAC like apixaban as you wait for d dimer and just continue it long term
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15
Q

What is asthma? Pathophysiology

A

Chronic inflammatory disease of the airways that is reversible via bronchodilators.

Most common cause of wheeze.

Triggers = pollen, dust, food, cold air, pets, etc

Inflammatory reaction:

  • caused by eosinophils, t lymphocytes, mast cells
  • inflammatory mediators release histamine, leukotrienes, prostaglandins, cytokines
  • causes smooth muscle hyperplasia and hypertrophy
  • mucus plugging occurs in fatal asthma
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16
Q

How does asthma present?

A
  • dry cough or wheeze that is worse at night
  • hx of atopy (hay fever, allergies, asthma)
  • hx of trigger exposure
  • chest tightness, dyspnoea, expiratory wheeze
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17
Q

What is safe criteria for asthma discharge after an exacerbation?

A
  • pefr>75%
  • at least 5 days oral prednisolone
  • gp follow up in 2 days
  • resp clinic follow up in 4 weeks
  • stop regular nebs 24 hours prior to discharge
  • inpatient asthma nurse review for technique and adherence
  • provided pefr meter and written asthma action plan
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18
Q

How would you manage their asthma long term? (NICE 17 and over)

A

Offer a SABA reliever therapy for newly diagnosed

Then if uncontrolled add 1st line maintenance therapy = low dose ICS

  • if asthma related symptoms 3x a week or more
  • or waking at night on just reliever

Then add Leukotriene Receptor Antagonist to low dose ICS

  • review in 4-8 weeks

Then offer Long Acting Beta2 Agonist to add to low dose ICS

  • if LTRA helped, keep. if not, don’t.

Then once they are on LABA+ICS (+/-LTRA) change them to a low ics MART (just combo ics/laba inhaler for maintenance and relief as required)

If they are on a low ics dose MART and it is uncontrolled, put them on a mod ics MART.

If it is still uncontrolled, put them on a high maintenance dose ICS MART.

  • or add an aditional drug = long acting muscarinic receptor antagonist OR theophylline OR consult an expert
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19
Q

What is the pathophysiology of COPD?

A

COPD = emphysema + chronic bronchitis

Causes = smoking, a1antitrypsin deficiency, industrial exposure eg. soot

  • mucous gland hyperplasia + hypersecretion
  • loss of cilial function
  • emphysema = alveolar wall destruction = enlargement of air spaces distal to terminal bronchioles
  • chronic inflammation (macrophages + neutrophils) and fibrosis of airways = reduced elasticity
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20
Q

How would you investigate COPD?

A
  • spirometry shows obstructive picture of fev1:fvc<70%
  • ecg = R Hypertrophy, cor pulmonale
  • ABG
  • a1 antitrypsin
  • CXR
    • hyperinflation
    • cylindrical heart
    • flat hemidiaphragm
    • emphysematous bullae can form
    • large central pulmonary arteries
    • decreased peripheral vascular markings
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21
Q

How would COPD present?

A
  • breathlessness (dyspnoea)
  • productive cough
  • tachypnoea
  • accessory muscle use
  • hyperinflation (resonant chest sounds)
  • decreased chest expansion
  • pursed lip breathing (traps air to keep alveoli open)
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22
Q

How would you manage COPD?

A
  • smoking cessation!!!
  • pulmonary rehabilitation = 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, disease education
  • weight loss
  • Long term oxygen therapy = continuous o2 at least 16 hours/day for survival benefit
    • must be non smokers and not retain high co2 levels
  • Lung vol reduction if appropriate
  • surgery = lung transplant in end stage emphysema

Long term Medications (GOLD criteria for treatment)

  • <1 exacerbation a year = any bronchodilator
    • Severe = long acting bronchodilator (Laba like salmeterol or Lama like tiotropium bromide)
  • >2 exacerbations or >1 requiring hospitalisaiton = Lama
    • Severe = Lama + Laba
    • or ICS + LABA if eosinophil count >300

Other long term meds = mucolytics, steroids, antimuscarinics, bronchodilators

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23
Q

How would a pneumonia present?

A
  • SOB
  • purulent cough
  • sometimes haemoptysis but rare
  • fever (elderly can be apyrexic, just confused)
  • rigors, vomiting, headache, loss of appetite
  • pleuritic chest pain and pleural rub (esp in strep)
  • CXR = consolidation
  • Dyspnoea, tachypnoea, tachycardia

Typical organisms = strep pneumonia, staph arueus, group a strep, klebsiella, h influenza, moraxella catarrhalis

Atypical = mycoplasma pneumonia, chlamydia pneumoniae, Legionella pneumophila

***if high CURB65 then do atypical pneumonia screen!!! urine legionella test

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24
Q

What is the pathophysiology of TB?

A
  • mycobacterium tuberculosis bacteria reach pulmonary alveoli
  • alveolar macrophages engulf them
  • the bacteria replicate in the macrophages and infect them
  • lymphocytes and fibroblasts surround the infected macrophages = granuloma complexes
  • These are typically in the upper lobes of lungs.
  • Sometimes bacteria enters blood stream and forms tubercles throughout the body = extrapulmonary tb.
25
Q

Clinical features of TB

A
  • pyrexia and “drenching” nocturnal sweats
  • weight loss
  • malaise
  • resp TB = cough, purulent sputum, haemoptysis, pleural effusion
  • Non resp TB = erythema nodosum, lymphadenopathy, pericardial effusion if cvs, meningitis if cns, abdo/joint pain if affected
26
Q

What are some risk factors of TB?

A
  • past hx of tb
  • known hx of tb contact
  • born in country of high tb incidence
  • foreign travel to country with high tb incidence
  • immunosuppression eg. IVDU, HIV, organ transplant recipient, renal failure/dialysis, malnutrition, DM, alcholism etc
  • overcrowding
27
Q

How would you investigate TB?

A

Latent TB

  • Interferon Gamma Release Assay
    • does not differentiate latent and active though
  • Tuberculin Skin Testing
    • false +ve in immunised, false -ve in sarcoidosis/hodgekins lymphoma

Active TB

  • Admit to side room and start infection control (-ve pressure, masks etc)
  • CXR = patchy nodal shadows in upper zones, cavitating lesions, Miliary = multiple 1-10mm nodules
  • 3 Sputum samples (incl one early morning) for acid fast bacilli
    • Ziehl Neelsen Stain
    • start treatment first if clinical suspicion, as culture can take 6-8 weeks
  • Bronchoscopy if no productive cough
  • Miliary TB = MRI brain/spine then also LP
28
Q

How would you manage TB? + SE

A

4 antibiotics for 2 months

  • Rifampicin
    • se = hepatitis, rashes, orange/red secretions.
    • interacts with warfarin and ocp
  • Isoniazid (+pyridoxine to prevent peripheral neuropathy)
    • se = hepatitis, rashes, peripheral neuropathy, psychosis
  • Pyrazinamide
    • se = hepatitis, rashes, vomiting, arthralgia
  • Ethambutol
    • se = retrobulbar neuritis

then 2 antibiotics for 4 months

  • Rifampicin
  • Isoniazid
  • antibitoics are weight dependent so do their weight!!
  • check baseline LFTs and monitor
  • check visual acuity before ethambutol
  • compliance is CRUCIAL = directly observed therapy
29
Q

What is bronchiectasis?

A

Chronic dilation of one or more bronchi! Poor mucus clearance which predisposes them to recurrent/chronic bacterial infection.

  • Common Bacteria = haem influenza, pseudomonas aeruginosa, moraxella catarrhalis
  • Fungi = aspergillus, candida
  • CF = staph aureus
30
Q

What are some causes of bronchiectasis?

A
  • post infective = tb, whooping cough
  • immune def = hypogammaglobulinaemia
  • CF, primary ciliary dyskinesia, Youngs syndrome, Kartageners syndrome
  • secondary immune def = HIV, malignancy
  • RA
  • associated with IBD, yellow nail syndrome
31
Q

How would you manage bronchiectasis?

A

Diagnose with High resolution CT = signet right sign

(bronchial dilation greater than adjacent blood vessels, bronchial wall thickening)

Management

  • Physio for airway mucus clearance
  • antibiotics according to sputum cultures
  • flu vaccine, bronchodilators if needed
  • pulmonary rehabilitation if MRC dyspnoea>=3
32
Q

What is cystic fibrosis?

A

autosomal recessive disease resulting in mutation of CFTR gene on the long arm of chromosome 7

affects chloride ion channels = thickened secretions

33
Q

How would you diagnose CF?

A

A characteristic pnehotypic feature:

  • hx of CF in a sibling
  • OR +ve newborn screening test result

AND

  • increased >60mmol/l sweat chloride conc in Sweat Test
  • OR genotyping showing 2 CF mutations
  • OR abnormal nasal epithelial ion transport
34
Q

What are some CF tests?

A
  • Guthrie test
    • increased immunoreactive trypsin in babies with CF
  • decreased faecal elastase indicating pancreatic insufficiency
  • Sweat Test
35
Q

How would CF present first? (4)

A
  • Meconium Ileus
    • signs of intestinal obstruction, bilious vomiting, abdo distension, delay in meconium passing after birth
  • Intestinal malabsorption
    • severe def of pancreatic enzymes
  • Recurrent chest infections
  • Newborn Screening
36
Q

What are some complications of CF? (4)

A
  • resp infections that may need physio, and prophylactic antibiotics
  • low body weight due to pancreatic insufficiency
    • give pancreatic enzyme replacements + PPIs to help enzymes function
    • encourage high calorie intake and give fat soluble vits (ADEK)
  • Distal intestinal obstruction syndrome (DIOS)
    • faecal obstruction in ileocaecum
    • intestinal contents in distal ileum/proximal colon are thick, dehydrated faeces
    • typically due to insufficient pancreatic enzymes, non compliance to prescribed enzymes, salt deficiency, hot weather, etc
    • present with a palpable RIF mass. do AXR to show faecal loading.
  • CF related Diabetes.
37
Q

How would you manage CF?

A
  • prophylactic antibiotics sometimes
  • nebulised saline to reduce exacerbations
  • mucolytics to make mucous less viscous
  • postural drainage + physiotherapy to help clear airways
  • No smoking
  • avoid other CF patients
  • avoid people with colds/infections
  • avoid jacuzzis = pseudomonas
  • avoid stables, compost, rotting vegetation = aspergillus fumigatus
  • annual influenza immunisation
  • sodium chloride tablets in hot weather
38
Q

What are some risk factors for pneumothorax?

A
  • lung disease like asthma, COPD, sarcoidosis
  • height
  • smoking/cannabis
  • trauma/chest procedure eg. subclavian cvp line insertion, pleural aspiration, +ve pressure ventilation
  • diving
  • connective tissue conditions like Marfans, ED
  • Young thin men can help ruptured subpleural bulla (primary)
39
Q

How would pneumothorax (not tension) present?

A
  • sudden dyspnoea
  • pleuritic pain
  • assymetrical expansion
  • hyperresonant
  • decreased breath sounds on affected side
40
Q

How would you manage a pneumothorax? (not tension)

A

If symptomatic and cxr shows rim of air >2cm

  • aspirate and give o2.
  • if unsuccessful put in an intercostal drain (4-6ics mid axillary line).
  • remove drain after full re-expansion/cessation of air leak.

If asymptomatic or <2cm rim of air then just discharge, review in 2 weeks

41
Q

How would pleural effusion present?

A
  • dyspnoea
  • pleuritic pain

O/E

  • decreased tactile vocal fremitus and vocal resonance
    • increased resonance indicates increased tissue density eg consolidation/tumour/lobar collapse
    • decreased resonance indicates fluid/air around the lung eg pleural effusion/pneumothorax
  • stony dull percussion
  • tracheal deviation away in a big one
  • decreased breath sounds and chest expansion
  • somtimes pleural rub
42
Q

How would you investigate pleural effusion?

A
  • CXR
    • blunting of constophrenic angle, homogenous density with meniscus, trachial dev away in a big one
  • Ultrasound Guided Pleural Aspiration
    • biochemistry, cytology, microbiology including alcohol and acid fast bacilli culture
    • make sure you do this before getting a chest drain and draining all the fluid!! (unless there is underlying empyema eg pleural fluid ph<7.2 or there is pus in aspirate)
  • Thoracoscopy or CT pleural biopsy
43
Q

What are some causes of a transudate/exudate effusion?

A

Transudate is pleural protein<30g/L

  • HF, cirrhosis, nephrotic syndrome causing hypoalbuminaemia
  • Rare = hypothyroidism, PE

Exudate is when pleural protein>30g/L

  • Malignancy, infections (TB, hiv, etc)
  • Less common = other inflammatory like RA, pancreatitis, pulmonary infarction in a pe, SLE, etc.
44
Q

What is Lights Criteria?

A

Use it when the pleural fluid protein level is 25-35g/L ie borderline.

It is exudate if it is one or more of the following…

  • pleural fluid/serum protein >0.5
  • pleural fluid/serum LDH>0.6
  • Pleural fluid LDH> 2/3 of upper limit of normal
45
Q

There are 3 interstitial lung diseases you need to know:

  1. Idiopathic Pulmonary Fibrosis
  2. Hypersensitivity Pneumonitis or Extrinsic Allergic Alveolitis
  3. Sarcoidosis.

What are the mechanisims of the first two?

A

IPF

  • overproduction of fibroblasts and deposition of extracellular matrix in intersititum
  • results in loss of elasticity and ability to perform gas exchange
  • so progressive dyspnoea

HSP/ EAA

  • typically due to mouldy vegetation (farmer’s lung), birds/pigeons, humidfying systems/ air conditioners, mouldy cheese or grapes
  • Acute exposure = fever, malaise, dyspnoea, cough
    • symptoms will resolve if you remove the antigen in 24-48 hours!
  • Subacute exposure = acute symptoms + weight loss
    • symptoms will resolve in weeks-months if you remove the exposure
  • Chronic exposure = acute symptoms + weight loss + clubbing
46
Q

How would you investigate/manage Idiopathic Pulmonary Fibrosis?

A
  • CXR = small vol lungs with increased reticular shadowing at bases
  • Spirometry shows restrictive FEV/FVC>70%
  • High Res CT = subpleural reticulation, traction bronchiectasis, honeycombing
  • Lung Biopsy

Manage with pirfenidone (antifibrotic agent that slows fvc decline)

47
Q

How would you investigate/manage Hypersensitivity pneumonitits/ Extrinsic Allergic alveolitis?

A
  • auscultation = inspiratory squeaks and bilateral fine crackles
  • High Res CT = nodules with ground gas opacity, air trapping, increased reticulation and honeycombing in advanced disease (mid/upper zones)
  • Lung biopsy
  • Spirometry shows restrictive change
  • Bronchoalveolar lavage = lymphocytosis
  • Low CD4:CD8 ratio differentiates it from sarcoidosis

Get rid of the irritant! Then give prednisolone if symptoms persist

48
Q

How does sarcoidosis present ?

A
  • Lofgren Syndrome is a favourable prognosis = bilateral hilar lymphadenopathy + erythema nodosum + arthralgia + fever
  • Pulmonary manifestations = cough, exertional breathlessness, chest discomfort
  • Extrathoracic manifestations = fever, weight loss, fatigue, anterior uveitis, lupus pernio, erythema nodosum, hypercalcaemia, lymph nodes, etc
49
Q

How would you investigate sarcoidosis?

A
  • CXR stages
  1. bilateral hilar lymphadenopathy (highest rate of spontaneous remission)
  2. pulmonary infiltrates + BHL
  3. pulmonary infiltrates and no BHL
  4. Fibrosis (irreversible)
  • High res CT = beading along airways, honeycombing, increased reticulation
  • hypercalcaemia and hypercalciuria
  • Bronchoalveolar lavage = raised CD4:CD8 ratio
  • Transbronchial biopsy = pulmonary non-caseating granulomatosis

***other causes of BHL = lymphoma, pulmonary TB, bronchial carcinoma

50
Q

How would you manage sarcoidosis?

A
  • prednisolone!
  • can also use methotrexate/ azathioprine/ hydrochloroquine
  • Lung transplant for stage 4 cxr
51
Q

Lung cancer on cancer notes!!!

A
52
Q

What is obstructive sleep apnoea? (pathophysiology)

A

Upper airway narrowing provoked by sleep.

Results in sufficient sleep resulting in significant daytime symptoms like excessive sleepiness.

Pathophysiology

  • pharyngeal dilator muscles in your upper airway relax in sleep
  • some narrowing is normal. but excessive narrowing causes symptoms.
  • Excessive narrowing is due to either:
    • an already small pharyngeal size that undergoes normal narrowing in sleep thus becoming super narrow
    • or excessive narrowing during sleep.
53
Q

What are some causes of small pharyngeal size?

And excessive narrowing?

A

small pharyngeal size

  • fatty infiltration of pharyngeal tissues and external pressures from increased neck fat/muscle bulk
  • large tonsils
  • craniofacial abnormalities
  • extra submucosal tissue eg. myxoedema

Excessive narrowing

  • obesity
  • neuromuscular disease eg. stroke, mnd, myotonic dystrophy
  • muscle relaxants like alcohol or sedatives
  • old age
54
Q

How does sleep apnoea present?

A
  • Severe = repetitive airway collapse with arousal required to re-activate pharyngeal dilators
    • in airway collapse you get hypoxia and hypercapnoea
    • this is corrected when you wakeup and have a inter-apnoeic hyperventilatory period
  • frequent arousals result in fragmented/unrefreshed sleep
    • typically present as snoring or apnoea attacks that their partner may notice
  • Excessive daytime sleepiness (epworth sleep scale >9)
  • With every arousal they also get a rise in BP over 50mmHg. This eventually results in a rise in daytime BP
  • Nocturia
  • Increased risk of stroke, HTN, ROAD DANGER
    ​
55
Q

How would you investigate OSA?

A
  • Overnight oximetry
  • Limited sleep study
  • Fully polysomnography (essentially limited sleep study + eeg + emg)
56
Q

How would you manage OSA?

A

This is based on severty of symptoms affecting QOL, not how severe their disease is based on sleep study.

Simple

  • weight loss, sleep decubitus, avoid evening alcohol intake, stop smoking
  • tell them to notify the DVLA!! don’t drive when sleepy

Mild OSA

  • mandibular advancement devices or pharyngeal surgery last resort

Significant OSA

  • CPAP via nasal mask
  • gastroplasty/bypass
  • tracheostomy rarely

Severe OSA & CO2 retention

  • Period of NIV prior to CPAP if they are getting acidotic
57
Q

How would you go about treating someone with suspected PE?

A

If haemodynamically unstable/pregnant/gave birth in the past 6 weeks, admit!!!

Otherwise Use the Wells Score

  • if Wells >4 points = PE IS LIKELY
    • admit and do CTPA
    • if can’t do CTPA immediately, give interim therapeutic anticoag like DOAC
  • if Wells of 4 or less = PE UNLIKELY
    • do a DDimer with result available in 4 hours
      • if can’t do test within 4 hours, give ITA like DOAC
    • if DDimer +ve, admit and do CTPA
    • if DDimer -ve, stop ITA and think of another diagnosis

1st line Interim Therapeutic Anticoag = apixaban or rivaroxaban

do fbc, u&es, lfts, prothrombin time, aptt as you start the ITA but don’t delay ITA for these.

Moral of the story, DDimer is only for Wells of 4 or less in a PE.

58
Q

how would you differently treat primary and secondary pneumo??

A

5th Year Revision (14 decks)

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