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Flashcards in Resp Deck (104)
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1
Q

in an anapylaxis allergic reaction what is immedietly doen?

A

remove trigger, maintain airway, 100% o2

IM adrenaline 1/1000 0.5mg (500 micrograms), repeat every 5 mins

2
Q

what are the featuers of a mild asthma attack?

A

no features of severe asthma and PEFR>75%

3
Q

what are teh features of a mdoerate asthma attack?

A

no features of severe asthma
PEFR >50-75%

4
Q

what are the features os a severe asthma attack?

A

PEFR 33-50% of ebst or predicted
cannot complete sentences in one breath
resp rate >25/min
HR >110/min

5
Q

what are teh features of a lfie threatening asthma attack?

A

PEFR <33% of best or predicted
sats <92% or ABG pO2 <8kPa
cyanosis, poor resp effort, near or fully silent chest
exhaustion, confusion ,hypotension, or arrythmias
normal pCO2

6
Q

what is the main distinguishing feature fo a near fatal asthma attack?

A

raised pCO2!!!

7
Q

what is doen for the management of an acute asthma attack?

A
  • ABCDE
  • aim fro SpO2 94-98% with O2, ABG is sats <92%
  • 5mg neb salbutamol (can repeat after 15 mins)
  • 40mg oral prednis STAT (IV hydrocort if PO not poss)
8
Q

managment for a severe asthm aattack>

A

ABCDE
aim for SpO2 94-94% with O2, ABG if sats < 92%
neb ipatropium bromide 500 micrograms
consider back to back neb salbutamol

9
Q

what is the managemnt of life threatening or near fatal asthma attack

A

urgent ITU or anaesthetist assessment
urgent portable CXR
IV aminophylline
consider IV salbutamol if neb route ineffective

10
Q

what features point you towards an infective COPD exacerbation over non infective?

A

change in sputum colour/volume
- raised WBS +/- CRP
- fever

11
Q

what is management of COPD exacerbation?

A

ABCDE
aim for SpO2 94-98% , if evidence of type II resp failure then aim SpO2 88-92%

NEBs - salbutamol and ipratropium
steroids - prednisolone 30mg STAT and OD for 7 days
ABX if raised CRP / WCC or purulent sputum
CXR
consider NIV if type II resp failure and pH 7.23-7.35
if pH <7.25 consider ITU

12
Q

what are the main features of pneumonia?

A

consolidation on CXR
fever
prurulent sputum
raised WCC/CRP

13
Q

wha t is the managemtn of a patient with pneumonia?

A
  • ABCDE
  • if any features of sepsis - NO DELAY in administering IV ABX and fluids
  • otherwsie treat with ABX as per CURB-65 score, local pneumonia guidlines

Confusion
Urea >7
RR > or = 30/min
BP <90mmHg systolic or <60mmHg diastolic
> 65 yrs

14
Q

what is the initial managament fo heamopytsis?

A
  • ABCDE
  • lie pt on side of suspected lesion
  • oral transexamic acid ofr 5 days (IV)
  • stop NSAIDs/aspirin/anticoags
  • ABx is suspcted infection
  • consider vit k
  • CT aortogram
15
Q

what are teh major signs of a tension pneumothorax?

A

hypotension
tachy
deviation of trachea away from side of pneumothorax
medistinal shift away from pneumothorax
hyper resonant on percussion
reduce sound on auscultation

16
Q

what is the initial managment in a tension pneumothorax?

A

large bore IV cannula into 2nd ICS MCL
chestdrain into affected side

17
Q

what are main synptoms in pt with a PE

A

heamoptysis
SOB
chest pain (pleuritic)
low CO followed by collapse (massive PE)

18
Q

what is the initial managment for PE?

A
  • A-E
  • O2 if hypoxic
  • analgesia if pain
  • subcut LMWH whilst awaiting CTPA
  • fully anticoagulated once confirmed diagnosied on CTPA
19
Q

features of a massive PE?

A

hypotension/cardiac arrest
signs of R heart strain on CT/echo

20
Q

pathophysiology of asthma?

A

asthma is a chronic inflammatory airway disease that is reversible
there is an increased airway responsiveness (narrowing due to increased muscel contraction, increase mucus production) to a variety of stimuli

  • airway epithelial damage - shedding and subepithelial fibrosis, basement membrane thickening
  • inflammatory reaction characterised by T lymphocytes and mast cells. inflmmatory mediators released include histamine, leukotrienes and prostaglandins
  • cytokines amplify inflammatory repsonse
  • increased number of mucus secreting goblet cells and smooth msucle hyperplasia and hypertrophy
  • mucus plugging in fatal and severe asthma
21
Q

what are teh main differentials fro a wheeze heard in a pt?

A
  • acute asthma exacerbation
  • bronchitis - viral or bacterial
22
Q

criteria for safe asthma discharge?

A

PEFR>75%
- stop regular nebs fro 24 hrs prior to discharge
- inpatient asthma nurse review to assess inhaler technique and adherence
- at least 5 days oral prednis
- provide PEFR mete and written astham action plan
- GP follow up within 2 working days
- resp clinic follow up within 2 wks

23
Q

name some asthma triggers

A

smoking
exercise
cold weather
allergens - pollens, dust mites, pets
URTI - mainly viral
drugs - aspirin, beta blockers
- pollution
occupation irritanst
food and drink
stress

24
Q

what is the overview of management for severe asthma?

A
  • use BTS stepwise managemnt guidelines
  • assess and teach inhaler technique
  • use self managment plans
  • avoid trigger factors
25
Q

waht si teh definition of COPD?

A

airflow obstruction that is usually progessive and not fully reversible - predominantly caused by smoking
umbrella term that encompasses emphysema and chronic bronchitis

26
Q

what is the pathophysiology of COPD?

A
  • mucous gland hyperplasia
  • loss of cilial function
  • emphysema - alveolar wall destruction causing irreversible enlargment for air spaces distal to terminal bronchiole (elastases)
  • chronic inflammation (macrophages and neutrophils) and fibrosis of small airwasy
27
Q

what are teh main causes of COPD?

A
  • smoking
  • inherited alpha-1 antitrypsin deifciency
  • industrial exposure e.g. soot
28
Q

what are teh main outpatient COPD managemnt tasks?

A
  • COPD care bundle
  • smoking cessation
  • pulmonary rehab
  • bronchodilators
  • antimuscurinics
  • steroids
  • mucolytics
  • diet
  • LTOT is approapriate
  • lung volume reduction !! if approproate
29
Q

what is LTOT and when should it be offered?

A

long term oxygne therapy is a treatment to help prevent organ hypoxia (NOT SOB) e.g. cardiac or renal damage
needed to be used at least 16 hrs a day for benefits to be seen
LTOT offered if pO2 bewlo 7.3kPa or below 8kPa with cor pulmonale (pts must be non smokers and not retain high levels of co2)

30
Q

what is pulmonary rehab in COPD pts and why is it so important?

A

COPD pts may avoid exercise because of breathlessness whic can lead to a vicious cycle of increasing social isolation and inactivity leading to worsening symptoms

pulmonary rehab breask the vicious cycle -> MDT 6-12 wks programme of supervised exercise, unsupervised hoem exercise, nutrittional advice and disease education

31
Q

what are the common organisms responsible fro community acquired pneumonia?

A
  • strep pneumonias
  • heamophilus influenza
  • morexella catarrhalis
32
Q

what are the common organisms responsible fro atypical pneumonia?

A
  • legionella pneumophila
  • chlamydia pneumoniae
  • mycoplasma pneumoniae
33
Q

what are the common organisms responsible fro hopsital acquired pneumonia?

A
  • E coli
  • MRSA
  • pseudomonas
34
Q

name some common differentials for consolidation on CXR?

A

pneumonia
malignancy
TB
lobar collapse
heamorrhage

35
Q

waht is teh intial managemnt if CAP is suspected?

A
  • ABCDE approach
  • CXR ordered
  • Check CURB-65 score
  • DONT DELAY in initiating ABX (or IV fluids) +/- paracetamol
  • ITU referral if high CURB-65 score
  • FBC, U&E’s, CRP and sputum cultures
  • blood cultures if febrile
  • ABG if low sats
  • need atypical pneumonia screen if CURB-65 high
36
Q

what is the CURB-65 score?

A

it is used to assess to severity of community acquired pneumonia

confusion
urea >7
RR >30/min
BP <90 systolic or <60diastolic
>65 yo

37
Q

what is legionnaires disease?where is it most usually contracted from ?

A

it is a form of (atypical) pneumonia cause by legionella pneumophila
association with infected water inshowers or hot tubs (ask in Hx if recent travel or hotel stay)
associated with higher CURB65 score as is atypical

38
Q

what is tehe pneumonia follow up protocal after it is resolved?

A

follow up in clinic 6 weeks post infection with repeat CXR to ensure resolution

also !! following tests:
- HIV test
- immunoglobulins
- pneumococcal IgG serotypes
- heamophilus influenzae b IgG

39
Q

what are teh cuases of a non resolving pneumonia

A

chaos !

Complication - empyema, lung abscess
Host - immunocomprimised
ABx - inadequate dose, poor oral absorption
Organism - resistant or unexpected organism not covered by empirical ABx
Second diagnosis - PE, cancer, organising pneumonia

40
Q

what is difference between SARS-CoV-2 and COVID-19?

A

SARS-CoV-2 is the name of the virus and COVID-19 is the infectious disease caused by it

41
Q

what are the three common symptoms of patients presenting to hsopital with COVID-19?

A
  • hypoxia
  • lymphopaenia
  • bialateral, lower zone changes on CXR
42
Q

with patients that require hosp admission with COVID-19 what is the managment?

A

O2 supplementation, some going on to CPAP or invasive ventilation
evidence base e.g. dexamethasone (and consider tocilizumab +/- remdesivir)
ABx may needed is suspected superadded bacterial infection

43
Q

what are teh clinical features of lung cancer?

A
  • asymptomatic: icidental finding
  • any resp symptom/systemic deterioration
  • superior vena caval obstruction
  • horners syndrome
  • metastatic disease - liver, adrenals (addisons), bone, pleural, CNS
  • paraneoplastic - clubbing, hypercalcaemia, aneamia, SIADH, cushings syndrome, lambert-eaton myasthenic syndrome
  • increased risk of thrombo-embolic disease
44
Q

risk factors of lung cancer?

A
  • SMOKING
  • increasign age
  • airflow obstruction
  • FHx
  • exposure to other carcinogens e.g. asbestos
45
Q

what are the tests done when lung cancer is suspected?

A
  1. Bloods - FBC, U&Es, calcium, LFTs, INR
  2. CXR
  3. staging CT - spiral CT thorax and upper abdo
  4. histology - US guided neck node FNS if lymphadenopathy, bronchoscopy, CT biopsy, thorascopy if pleural effusion present
  5. PET scan - detect small mets not detected on staging CT
46
Q

name the types of lung cancer

A
  1. small cell lung cancer (SCLC)
  2. non small cell lung cancer (NSCLC) - squamous cell, adenocarcinoma, large cell lung carcinoma, bronchoalveolar
47
Q

describe the WHO performance status of pts with lung cnacer? (0-5)

A

0 - fully active without restriction

1 - restricted in physically strenuous activity but can carry out light work

2 - capable of all self-care but unable to carry out work activities (up and about more than 50% of waking hours)

3 - capable of only limited self -care, confined to bed/chair more than 50% of waking hours

4 - completely disabled, totalyl confined to bed/chair

5 - dead

48
Q

what are the treatment options for lung cancer?

A
  • curative surgery for stage 1 and 2 - assuming fit for surgery
  • surgery and adjuvant chemo clinical trial for stage IIIa - asusming fit for surgery and chemo
  • chemo - cosnider in pts with stage III/IV and PS 0-2
  • radiotherapy - curative for people not fit for surgery or palliative
  • palliative care
  • do nothing ? watch and wait
49
Q

what is the NSCLC 5 yrs survival rate for each stage?

A

all NSCLC - 15-23%
stage I following surgical resection - 65-80%
stage II following resection - 50-60%
stage III - 20%
stage IV - 1-5%

50
Q

what is the prognosis for SCLC?

A

rapid growth rate and almost always too extensive for surgery at time of diagnosis
mianstay treatment is chemo and palliative radiotherapy
untreated - medial survival is 8-16 wks
combo chemo - medical survival 7-15 months

51
Q

what is the pleural cavity?

A

potential space created by the pleural surfaces that contains pleural fluid

outer - parietal
inner - visceral

52
Q

name teh pleural disease

A

pleural effusion - fluid
pneumothorax - air
empyema - infected fluid
pleural tumours - benign of malignant
pleural plaques - dicrete fibroud area
pleural thickening - scarring/calcification causign thickening (benign vs malignant)

53
Q

name the types of pneumothorax

A
  1. spontaneous - primary or secondary
  2. traumatic
  3. tension - emergency
  4. iatrogenic (post central line or pacemaker insertion)
54
Q

what are the risk factors fro a pneumothorax?

A
  • pre existing lung disease
  • height
  • smoking/cannabis
  • diving
  • trauma/chest procedure
  • association with other conditions e.g. marfans
55
Q

what ist eh management for the different types of pneumothorax? (primary, secondary and tension)

A

primary - if symptomatic and rim of air >2cm on CXR give O2 and aspirate. if unsuccessful consider re-aspiration or intercostal drain - remove drain after full re-expansion /cessation of air leak

secondary - as above but lower threshold for ICD

tension - immediate needle decomporession by large bore into 2nd intercostal space mid clavicular line

If persistant air leak >5 days refer to thoracic surgeons
discharge advice - no flying or diving until resolved

56
Q

what investigations are done when a pleural effusion is suspected?

A

Hx and Examination
CXR
ECG
Bloods - FBC, U&Es, LFTs, CRP, bone profile, LDH, clotting
ECHO (if suspected heart failure)
Staging CT is suspect exudate (lung cancer?)

57
Q

what is effective investigations to diagnosis a pleural effusion?

A

US guided pleural aspiration:
- biochem (proteins, pH, LDH)
- cytology
- microbiology

NEVER INSERT A DRAIN unless diagnosis is well established as draining all fluid may hinder oppotunities to obtain pleural biopsies (only indication would be empyema - pH of pleural fluid <7.2 or pus visible)

also consider thoracoscopy or CT pleural biopsy

58
Q

what is difference between exudate and transudate?

A

exudate - higher protein (>30g/L), higher LDH (infective cause)
transudate - <30g/L protein

59
Q

what are the causes of a transudate effusion?

A
  • heart fialure
  • cirrhosis
  • hypoalbumaenia (nephrotic syndrome, peritoneal dialysis)
  • PE, mitral stenosis, hypothyroidism
  • constrictive pericarditis, superior vena cava obstruction
60
Q

what are teh cuases of exudate effusions?

A
  • malignancy
  • infections - TB, HIV, parapneumonic
  • inflammatory (RA, pancreatitis, PE), lymphatic disorders, connective tissue disorders
  • drugs, fungal infections
61
Q

what is lights criteria fro pleural effusions? and when is it used?

A

used when fluid protein level is between 25 g/L and 30g/L

it is exudate if one of the following:
- pleural fluid/serum protein >0.5
- pleural fluid/serum LDH >0.6
- pleural fluid LDH >2/3 of teh upper limit or normal

62
Q

what conditions does the ILD cover?

A
  • usual intersitial pnuemonia (UIP)
  • non specific interstitial pneumonia (NSIP)
  • extrinsic allergic alveolitis
  • sarcoidosis
  • several other conditions
63
Q

are IDLs restrictive or obstructive on PFTs?

A

restrictive!!

64
Q

what are the important/environmental causes of ILD that should always be asked in a Hx?

A
  • silicosis (dust)
  • asbestosis (asbestos)
  • pneumoconiosis (coal workers)
65
Q

what conditions can be associated with ILD? which investgiations should be doen for new ILD diagnosis

A
  • connective tissue disease or SLE - ANA
  • connetive tissue disease - ENA
  • rhematoid arthritis - Rh F
  • vasculitis - ANCA
  • pulmonary renal disease - Anti-GBM
  • sarcoidosis - ACE
  • extrinsic allergic alveolitis - IgG to serum precipitins
  • HIV
66
Q

what are teh classical findings for usual interstitial pneumonia?

A
  • clubbing, reduced chest expansion
  • ausculation - fine inspiratory crepitations (velcro), usually best heard basal/axillary areas
  • CVS - may be features of pulmonary HTN
67
Q

what is teh clinical presentation of extrinsic allergic alveolitis? and what drugs commonly cause it?

A
68
Q

what is sarcoidosis?

A

sarcoidsis is a multisystem inflmmatory conditions of unknown cause

= non caseating granulomas
= immunological response
= commonly is resp system but can affect all organs
= 50% get spontaneous remission, others get progessive disease

69
Q

what are the investigations doen for suspected sarcoidosis?

A
  • 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
70
Q

what are the treatment principles of ILD?

A

dependent on underlying pathology

  • occupational exposure - remove
  • environmental exposure - remove
  • drug associated - avoid
  • stop smoking
  • MDT approach
  • treatment of infective exacerbations
  • O2 if resp failure
  • palliative care
  • transplantation
71
Q

what are the clinical features of TB?

A
  • fever and nocturnal sweats
  • weight loss (gradual)
  • malaise
  • resp TB: cough and purulent sputum/haemopytsis, (+ pleural effusion)
  • non-resp TB: skin (eythema nodosum), lymphadenopathy, bone/joint, abdo, CNS (meningitis), genitourinary, miliary (disseminated), cardiac (pericardial effusion)
72
Q

name the differentials of heamopytsis?

A

infection: TB, pneumonia, bronchiectasis/CF, cavitating lung lesions

malignanyc: lung cancer, mets

haemorrhage: vaculitis, coagulopathy, bronchial artery erosion

other: PE

73
Q

what are the risk factors of TB?

A
  • past history of TB
  • known history of TB contact
  • born in a country with a high TB incidence
  • foreign travel to country with high incidence of TB
  • evidence of immunosupression e.g. HIV, chemo, organ transplants, renal fialure/dialysis, malnutrition, DM, alcoholism, IVDU
74
Q

what are the management principles for TB?

A
  • ABCDE approach and aim to culture whenever possible
  • admit to side room and start infection control (masks and -ve pressure room)
  • if productive cough: x3 sputum samples for AAFB (acid alcohol fast baccili) and TB culture
  • if no productuve cough and pulmonary TB suspected cosnider bronchoscopy
  • routine bloods and include HIV test and and vit D levels
  • consider chest CT if CXR not showing results
  • whilst investigating for TB and pnuemonia suspected then start ABX as per CURB-65
  • if patient critically unwell and increased chance of TB then start anti-TB therapu AFTER sputum samples sent
  • notify cases to TB specialist nurse
  • TB culture can take 6-8 weeks so treatment started before cultures come back
75
Q

what are the basics of anti-TB therapy?

A
  • standard treatment is with 4 ABX for first two months (ripfampicin, isoniazid, pyrazinamide, ethambutol) followed by 4 months on 2 ABX (rifampicin, isoniazid)
  • dose of anti-TB ABX is weight dependent !!
  • check LFTs and monitor closely
  • check visual acuity before administer ethambutol
  • compliance is crucial !!!
  • pyridoxine also given as prophylaxis for peripheral neuropathy
76
Q

what are the major side effects of TB treatment?

A

RIFAMPICIN - hepatitis, rashes, febrile reaction, orange/red secretions, warfarin and OCP drug interactions

ISONIAZID - hepatitis, rashes, peripheral, neuropathy, psychosis

PYRAZINAMIDE - hepatitis, rashes, vomiting, arthralgia

ETHAMBUTOL - retrobulbar neuritis

77
Q

what is bronchiectasis?

A

chronic dilatation of one or mroe bronchi - poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

78
Q

what is teh gold standard test for bronchiectasis?

A

high resolution CT scan

79
Q

what are the causes of bronchiectasis?

A

post infective - whooping cough, TB
immune deficiency - hypogammaglobuinaemia
genetic / mucociliary clearance defect - CF, primary ciliary dyskinesia, Youngs syndrome, Kartagener syndrome
obstruction - foreign body, tumour, extrinsic lymph node
toxic insult - gastric aspiration, inhalation of toxic chemicals
allergic bronchopulmonary aspergillosis
secondary immune deficiency - HIV, malignany
RA
associations - IBD, yellow nial syndrome

80
Q

what are teh common organisms that cuases bronchiectasis?

A
  • heamophilus influenzae
  • pseudomonas aeruginosa
  • moraxellla catarrhalis
  • stenotrophomonas maltophilia
  • fungi - aspergillus, candida
  • non TB mycobacteria
    (-staph aureus)
81
Q

what blood test are doen to try and identify causes fo newly diagnosed bronchiectasis?

A
  • immunoglobulin levels
  • CF genotypes
  • HIV
  • Rhuematoid factor
  • autoantibodies
  • alpha 1 antitrypsin level s
  • aspergillus IgE/IgG and total IgE
82
Q

what is the managment of bronchiectasis?

A
  • TREAT UNDERLYING CAUSE
  • physiotherapy for mucus clearance
  • sputum culture for routine culture as well as NonTB mycobacteria
  • ABX for 10-14 days according to sputum cultures
  • long term ABX fro pts with recurrent infective exacerbations
  • supportive flu/covid vaccines + bronchodilators
  • pulmonary rehab
83
Q

in haemophilus influenzae infected bronchiectasis which ABx would be given?

A

amoxicillin
in pencillin allergy then doxycycline

84
Q

in pseudomonas aeurignose infected bronchiectasis which ABx would be given?

A

ciprofloxacin

85
Q

what is the definition (signs to look out for) for a person with an infective exacerbation of bronchiectasis?

A

a person with bronchiectasis with a deterioration in 3 or more key symptoms for at least 48 hrs:

  • cough
  • sputum volume and or ocnsistency
  • sputum purulence
  • breathlessness and or exercise toelranc e
  • fatigue
  • hemaoptysis
86
Q

what is aspergillus bronchopulmonary aspergillosis (ABPA)?

A

cuased by apergillus fumigatus expsosure( acommon fungus)
ABPA is a combo of type I and type II hypersensitivity reactions following inhalations of fungal spores
repeated damage from tehse immunological reactions leads to bronchectasis
ABPA is seen commonly in asthma and CF patients

87
Q

hwo is the diagnosis of ABPA made?

A

combo of sympotms (often dry cough and wheeze) along with +ve blood tests (raised aspergillus IgE level as well as high total IgE and high eosinophil)
treatment (steroids) may be required if ongoing symptoms and high total IgE level

88
Q

what is teh definition of cystic fibrosis

A

CF is an autosomal recessive disease leading to mutation sin the CTFG gene = multisystem disease characterised by thickening secretions

89
Q

what features are needed to diagnose CF?

A

one ore more of the characteristic phenotypic features:

  1. Hx of CF in siblin g
  2. +ve newborn screenign test result

and
- an increased sweat chloride conc (>60mmol/L) SWEAT TEST
- indentification of two CF mutations by genotyping
- demonsration of abnormal nasal epitheliumm ion transport (nasal ptoential difference)

90
Q

what are the 4 mian CF presentations?

A
  1. meconium ileus - 15-20% of CF newborns the bowel is blocked by sticky secretions therefore signs of intestinal obstruction after birht with bilious vomiting, abdo distention and delya in passing meconium
  2. intenstinal malabsorption - over 90% of CF individuals have intestinal malabsorption - main cause is a sevre deiciency in pancreatic enzymes
  3. newborn screening
  4. recurrent chest infections
91
Q

what are the 4 most common CF complications and describe them

A
  1. resp infections - needs physio and ABX, patient can recieve prophylactix ABX
  2. low body weight - due to pancreatic enzyme insufficiency so need enzyme replacemnt therapy, high calorie intake, extra supplements and osmetimes NG or PEG feeding
  3. distal intenstinal obstruction syndrome (DIOS) - deu to intenstinal contents in distal ileum and proximal colon (thick, dehydrated faeces), presents with palpable RIF mass. PO gastrografin needed to draw water into bowel lumen
  4. CF related diabetes
92
Q

what lifestyle advice is given to CF pts?

A
  • no smoking
  • avoid other CF patients
  • avoid friends /relative with colds/infections
  • avoid jacuzzis
  • clean and dry nebs thoroughly
  • avoid stables, compost or rotting vegetation (aspergillus fumigatus inhalation)
  • annual flu vaccine
  • NaCl tablets in hot weather / vigorous exercise
93
Q

what si teh managemnt for pts with CF?

A
  • physio for mucus clearance
  • exercise
  • mucolytics
  • pancreatic enzyme replacemnt therapy
  • nutritional supplement
  • fat soluble vitamin replacement
  • long term ABX
  • optimiaation of CF related patients (may need insulin therapy)
  • novel CFTR modulators/ potentiators
  • long term monitoring for CF related diabetes, liver disease and osteoporosis
94
Q

what is obstructive sleep apnoea?

A

upper airway narrowing, provoked by sleeping, causinf sufficient sleep fragmentation to result in signifciant daytime symptoms, usually XS sleepiness

*most pts are male and have combo of upper body obesity and relatviely undersized or set back mandible

95
Q

what is the pathphysiology of sleep apnoea?

A

upper airway patency depends on dilator muscle activity
all muscles relax durign sleep and some narrowinf of the upper airway is normal
XS narrowing can be due to either an already small pharyngeal size during awake state OR XS narrowing occuring during relaxation during sleep

96
Q

what are teh cuases of small pharyngeal airway size?

A
  • fatty infiltration of pharygneal tissues and external rpessure from increased neck fat/muscle
  • large tonsils
  • craniofacial abnormalities
  • extra submucosal tissue e.g. myxoedema
97
Q

what are the causes of XS narrowing of airway occuring during sleep

A
  • obesity can enhance residual muscle dialtor action
  • neuromuscular disease with pharyngeal invovlemnt may lead to greater loss of dilator muscle tone .e.g stroke. MND, myotonic dystrophy
  • muscle relaxants - sedatives, alchohol
    increasing age
98
Q

what are the lcinical effects/outcomes of sleep apnoea?

A

leads to repeitive upper airway collapse with arousal required to re-activate the pharyngeal dilators asociated with hypercapnia and hypoxia
recurrent arousals lead to highly fragmented and unfreshing sleep
XS daytime sleepiness
nocturia
with every arousal there is an increase in BP + daytime rise in BP

99
Q

what is the epworth sleepiness scale?

A

points for following:
0= would never dose
1= slight chance
2= moderate chance
3= high chance

  • sitting and reading
  • watching tv
  • sitting in public place
  • passenger in a car for an hour
  • lying down in afternoon to rest
  • sitting and talking
  • sitting quietly after lunch withouth alcohol
  • in a car, while stopped in traffic
100
Q

what sleep studies can be done on a pt with suspected sleep apnoea?

A

overnigth oximetry
oximetry, snoring, body movement, HR, oronasal flow, chest/abdo movements, leg movements (study of choice)
full polysomnography - limited study plus EEG, EMG

101
Q

managemnt fro sleep apnoea?

A

simple: weight loss sleep decubitis, reduce alcoho intake

snores and mild OSA: mandibular advancement devices, consider pharyngeal surgery as last resort

signficant OSA: nasal CPAP, consider gastroplasty/bypass and rarely trachy

severe OSA and co2 retention: may required period NIV prior to CPAP if acidotic but compensated co2 may reverse with CPAP alone

102
Q

drivign advice for pts with OSA?

A
  • not allowed to drive while sleepy
  • pt should notify DVLA on diagnosis
  • Dr’s can advice drivers to stop altogehter
103
Q

what is CPAP?

A
  • usually given via nasal mask but can use mouth/nose mask
  • upper airway splint open with approx 10cm H20 pressure preventing airway collapse, sleep fragmentation and daytime somnelence
  • also open collapsed alveoli and imporve V/Q mismatching
104
Q

CPAP vs BIPAP (NIV) for OSA

A

CPAP supplies constant +ve pressure during inspiration and expiration and is not venilatory support - its used to treat OSA and helps oxygenation in some patients with acute resp failure

NIV does provide ventilatory support with two levels of positive pressure - pressure support provided between selected inspiratory and expiratory positive pressures