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respiratory_diseases_20190518182909 Flashcards

1
Q

what is coryza

A

acute viral infection of nasal passage spread by direct (droplets) or indirect (door handle)

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2
Q

what is cause of coryza

A

200+ viruses mainly rhinovirus and coronaviruses

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3
Q

what is diagnosis of coryza

A

symptoms based

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4
Q

how is coryza treated

A

self care

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5
Q

what is the symptoms of coryza

A

blocked nosenasal pain and irritation runny nosecough hoarse voice sore throat (pharyngitis)mild fever?

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6
Q

what is complications of coryza

A

sinusitis (frontal or maxillary)acute bronchitis

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7
Q

what is it preceded by

A

coryza

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8
Q

what are symptoms

A

purulent nasal discharge and tender sinuses

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9
Q

how is it diagnosed

A

symptoms based

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10
Q

how is it treated

A

paracetamol decongestant no antibiotics

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11
Q

what are different kinds of decongestant

A

a adrenic agent eg phenylephrine

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12
Q

what is it

A

irritated and inflamed bronchi preceded by coryza

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13
Q

what are the causes

A

influenzacommon cold virus

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14
Q

what are the symptoms

A

hacking productive cough with thick yellow-grey sputum tightness in chest transient wheeze slight fever

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15
Q

how is it treated

A

home care - fluids etc

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16
Q

when are antibiotics given and which ones

A

if vulnerable 1st line - amoxicillin 2nd line - doxycycline

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17
Q

what are complications

A

pneumonia bacterial infection with strep pneumoniae or H.influenzae is common sequel esp in smokers/COPDmay cause respiratory acidosis

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18
Q

what is normally found on examination in an acute exacebation

A

crackles, cyanosed, oedema, wheeze, dyspnoea

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19
Q

what is treatments of acute exacerbation

A

said antibiotics, bronchodilator inhalers, short course of steroids

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20
Q

what is it

A

inflammation and swelling of epiglottis normally in children medical emergency

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21
Q

what are the symptoms

A

temp 38+severe sore throatdifficulty breathing abnormal and high pitched breathing dysphagia

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22
Q

what is cause

A

H. influenza bacteria

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23
Q

how do diagnose it

A

laryngoscopy blood test - WBC and bacteria

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24
Q

how is it treated

A

urgent endotrachael intubation IV broad spectrum antibiotics (ceftazidime, ceftriaxone)

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25
Q

how to prevent it

A

vaccination during childhood

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26
Q

what is the incubation time

A

1-4 days then abrupt onset of symptoms

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27
Q

what is causes

A

influenza A - worldwide pandemicsinfluenza B - localised, milder outbreaks

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28
Q

what is symptoms

A

temp >38dry, chesty cough headache malaise chills and aching limbs myalgia upset stomachclear nasal discharge

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29
Q

how is it diagnosed

A

symptoms based lab not necessary but fourfold increase in haemagglutinin

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30
Q

how is it treated

A

bed rest and paracetomal for risk >65 use neumanidase inhalers

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31
Q

what are the names of these inhalers

A

oscitamivar oral zanamiviar inhaler

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32
Q

what are the complications

A

death primary viral pneumonia (haemoptysis, resp failure in 24 hours)secondary bacterial pneumonia (H. influenza - new fever on day 7)

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33
Q

what is it

A

infiltration of small airways and alveolar walls with neutrophils followed by T lymphocytes and macrophages - leads to non-caseating granulomas

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34
Q

what type hypersensitivity is it

A

type IV (or III)

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35
Q

what are the different causes

A

farmers lung - mouldy hay malt workers lung - whiskey bird fanciers lung - pigeons mushroom farm workers - turning mushroom compost drugs eg gold, bleomycin, sulphasalazine

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36
Q

what are acute symptoms

A

fever (pyrexia)rigors myalgia dry cough dyspnoea crackles (no wheeze)malaise

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37
Q

what are chronic symptoms

A

increasing dyspnoea weight lossexertional dyspnoea type 1 resp failure cor pulmonale

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38
Q

how is acute EAA diagnosed

A

blood - FBC (neutrophilia), ESR (up), ABGCXR - upper zone consolidationLFT - reversible restrictive, reduced gas transfer during attack

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39
Q

how is chronic EAA diagnosed

A

blood - positive serum precipitantsCXR - upper zone fibrosis, honeycomb lung LFT - persistent changes BAL - increased lymphocytes and mast cells

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40
Q

how is acute EAA treated

A

remove allergen give O2oral prednisolone

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41
Q

how is chronic EAA treated

A

allergen avoidance long term steroids

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42
Q

what is it

A

infectious disease of resp tract type 4 hypersensitivity - caseating granulomas and caseous necrosis

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43
Q

what happens during primary exposure (1st time)

A

affects hilar lymph nodes granulomatous due to immune activation

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44
Q

what happens during secondary exposure (2nd time)

A

fibrosing and cavitating apical lesions due to overactive T cell response this is the reactivation of latent TB

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45
Q

what are causes

A

mycobacterium tuberculin m. bovis

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46
Q

what are resp symptoms

A

cough haemoptysisupper lobe crackles dyspnoea

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47
Q

what are GI symptoms

A

peritonitis perforationbowel obstruction pain

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48
Q

what are spinal symptoms

A

pain deformity paraplegia

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49
Q

what are meningeal symptoms

A

drowsy headache fits

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50
Q

what are other symptoms

A

renal failure weight lossnight sweats lymphodenopathy and cold abscess pericardial temponade septic athritis and hypoadrenalism

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51
Q

how is it diagnosed

A

CXR and ZN stain of sputum for acid and alcohol fast bacilli

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52
Q

what does CXR look like

A

upper lobe prominance, cavity formation, tissue destruction, scarring and shrinkage, heals with calcification

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53
Q

when does the CXR contain bilateral infiltrates and reticulonodular shadowing

A

presence of ARDS/miliary TB - result of tubercle bacilli in blood stream

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54
Q

what is treatment

A

2 months RIPE (rifampicin, isoniazid, pyradizamide and ethambutol)4 months RI

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55
Q

what is side effect of rifampicin

A

stains fluids pink/orange break opiate and steroids (the pill)rarely hepatitis

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56
Q

what is side effect of isoniazid

A

polyneuropathy

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57
Q

what is side effect of pyradizamide

A

hepatic toxicity, reduces renal excretion of urate and may precipitate gout

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58
Q

what is side effect of ethambutol

A

optic neuritis, red/green colour blindness

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59
Q

how can it be prevented

A

BCG vaccine - reduces risk by 70% contact tracing

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60
Q

what is latent TB

A

symptom free, granulomas, -ve cultures, leave alone

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61
Q

what reactivates latent TB

A

steroids, immunosuppression and anti-TNF

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62
Q

what is anti-TNF

A

used to treat rheumatoid athritis, crohns, psoriasis, alkylasing spondylitis if have latent TB - give 6 months of I or 3 months of RI before starting anti-TNF

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63
Q

what is it

A

inflammation of one of both of lungs normally due to infection

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64
Q

what causes strep pneumoniae (community)

A

found worldwide - most common cause

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65
Q

what causes staph aureus (community)

A

recent flu, IV drug user

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66
Q

what causes mycoplasma pneumonia (community)

A

older kid, young adult

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67
Q

what causes legionella (community)

A

traveller - bad water

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68
Q

what causes gram negative enterobacteria (community)

A

alcoholic

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69
Q

what causes bordatella pertussis (community)

A

whooping cough / broncho pneumonia

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70
Q

what causes haemophilus influenzae (hospital)

A

atypical, nursery workers, COPD

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71
Q

what causes coxiella burnetti (hospital)

A

Q fever - sheep, goats, cattle, farm

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72
Q

what causes chlamydophilia pstaci (hospital)

A

pet birds

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73
Q

what causes klebsiella pneumoniae (hospital)

A

common in alcoholism, diabetes and chronic lung disease

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74
Q

what are other causes

A

viral (RSV, measles)aspiration fungal (aspergillus - chest infection become pneumonia)chlamydia pneumoniae (person to person)PCP (immunosuppressed patients)

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75
Q

what are the symptoms

A

cough dyspnoea tachypnoea fever rigors sweats pleuritic pain myalgia malaise arthralgia preceding UTIdiarhhoea headache haemoptysis AFconfusion sputum after 24 hours

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76
Q

what are the signs

A

fever rigors pleural rub cyanosis hypotension tachypnoeapleural effusion

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77
Q

what would be found upon examination

A

crepitations dull percussion consolidation tactile vocal fremitus

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78
Q

what other tests are taken to diagnose it

A

serologyblood culture CXR, ABC, FBC, U&Es, LFTssputum culture

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79
Q

what are severity markers

A

temp <35 or >40cyanosis - PaCO2 <9WBC - <4 or >30multi lobar involvement

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80
Q

treatment is dependent on CURB65 score - what is this?

A

confusion - 1 point Urea >7 - 1 point BP<90 or <60 - 1 point RR <30 - 1 point Age >65

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81
Q

community acquired treatment with CURB65 score of 0-2 (mild)

A

amoxicillin 5 days or doxycycline or IV clarithromycin if NBM

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82
Q

community acquired treatment with CURB65 score of 3-5 (severe)

A

co-amoxicillin IV and doxycycline allergic - IV levofloxacin

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83
Q

community acquired treatment if in ICU/HDU or NBM

A

co amoxiclav and clarithromycin allergic - IV levofloxacin

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84
Q

hospital acquired treatment if severe

A

amoxicillin IV and metrondiazole and gentamicinstep down to co-trimoxazole and metrondiazole allergic - IV co-trimoxazole and metrondiazole +/- gentamixin

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85
Q

hospital acquired treatment if non severe

A

PO amoxicillin and metrondiazole

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86
Q

what are complications

A

empyema lung abscess septicaemia

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87
Q

how do you prevent it

A

pneumonia and flu vaccine smoking cessation treat alcohol misuse

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88
Q

what is it

A

childhood condition (<3 most affected), commonInflammatory oedema extends to vocal cords and epiglottis causing narrowing

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89
Q

what are symptoms

A

initial cold symptomsstridorbark like cough hoars croaky voice

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90
Q

what causes it

A

parainfluenza virus

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91
Q

how is it diagnosed

A

symptoms based

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92
Q

how is it treated

A

oral/IM steroid (dexamethasone)nebulised adrenaline - short term relief

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93
Q

what are complications

A

airway obstruction secondary infectionother complications

94
Q

what is it

A

restrictive, occupational diseasegranulomatous and fibrotic changes Increases risk of infection

95
Q

what are causes

A

15-20 years quartz exposure eg granite, stone, mine, boiler, glass, foundry workersinhalation of silica (silicon dioxide)

96
Q

what are symptoms

A

cough and dyspnoea

97
Q

what are signs

A

finger clubbingpleural effusion?

98
Q

how is it diagnosed

A

CXR- egg shell calcification of hilar nodes, pulmonary fibrosis, upper lobe shadowing more than lowerPFT - restrictive - FEV1 and FVC reduced, ratio normal/raised

99
Q

how is it treated

A

palliative

100
Q

complication

A

TBpulmonary hypertension heart failurearthritis kidney disease COPDlung cancer

101
Q

what is it

A

granulomatous disease of unknown cause

102
Q

what is a granuloma

A

mass or nodule composed of chronically inflamed tissue formed by response of mononuclear phagocyte system to insoluble or slowly soluble antigen

103
Q

what type of hypersensitivity

A

type 4

104
Q

what systems commonly involved

A

lungs, lymph nodes, joints, liver, skin, eyes

105
Q

what are symptoms of acute sarcoidosis

A

sweats erythema nodosum (skin lesion)

106
Q

what are symptoms of chronic sarcoidosis

A

lung infiltrates/alveolitis (scarring)skin infiltrates peripheral lymphadenopathyhypercalcaemia SOB persistent dry cough rashes on body

107
Q

how is it diagnosed

A

CXR - bilateral hilum lymphadenopathy CT - check for peripheral nodular infiltrates Bloods - raised calcium and inflammatory markers Restrictive PFT

108
Q

what is treatment of acute sarcoidosis

A

usually do not need specific treatment paracetamol anti-inflammatory

109
Q

what is treatment of chronic sarcoidosis

A

oral steroid (prednisolone) immunosuppression (azathioprine, methotrexate)

110
Q

what is it

A

imbalance in fibrotic repair system of lungs = lay down unrequired scar tissue chronic inflammatory infiltrate (neutrophils) causes fibrosis in alveolar walls and macrophages

111
Q

what does it cause increased risk of

A

infection

112
Q

prevalence

A

more common in males

113
Q

causes

A

idiopathic

114
Q

secondary causes

A

rheumatoid, SLE, system scleorisis, asbestosis, drugs

115
Q

symptoms

A

progressive exertional dyspnoea dry cough

116
Q

signs

A

clubbing bibasal crackles on auscultation dry cough

117
Q

diagnosis

A

CXR - bilateral infiltrates, fine inspiratory crackles HRCT - bilateral lower zone fibrosis/shadowing - ground glassrestrictive PFT and low TLCO

118
Q

treatment

A

oral steroids immunosuppressants (azathioprine)O2 if hypoxic pulmonary rehab lung transplant in young patients

119
Q

complications

A

respiratory failure most patients dead in 5 years

120
Q

what is it

A

restrictive, occupational disease causing granulomatous and fibrotic and restrictive changes major scarring acts like tumour and destroys lung

121
Q

prevalence

A

now quite rare, often associated with COPD

122
Q

what does it increase risk of

A

infection

123
Q

causes

A

inhalation and retention of coal dust in lungs

124
Q

symptoms

A

often asymptomatic when gets to massive fibrosis - cough, tight chest, SOB

125
Q

signs

A

clubbing

126
Q

diagnosis

A

CXR - upper lobe recticular shadowing / fibrosis Lung function not impaired

127
Q

what is treatment

A

palliative - O2 and pulmonary rehab

128
Q

complications

A

caplan’s syndrome (rheumatoid athritis + coal + nodules which cavitate)chronic bronchitis (coal + smoking)

129
Q

what is it

A

pleural disease (fibrosis) affecting lung lining and lung base progressive - latent period after exposure

130
Q

what causes it

A

heavy prolonged asbestos exposure (5 years of daily exposure)

131
Q

what are affects of asbestos exposure

A

benign pleural plaques benign asbestos pleural effusions diffuse pleural thickening acute asbestos pleuritis malignant mesothelioma

132
Q

what is malignant mesothelioma

A

incurable pleural cancer which can invade chest wall - fatal in 2 years and almost always from asbestos exposure

133
Q

what are symptoms of malignant mesothelioma

A

chest pain, PE, sweating, dyspnoea

134
Q

what are signs of asbestosis

A

breathlessnessfinger clubbing

135
Q

how is it diagnosed

A

pleural fluid aspiration - low cytological yieldCXR and CT - effusion, nodularity, local invasion, lung entrapment, upper love fibrosis biopsy - asbestos fibres sputum culture - asbestos bodies

136
Q

what is treatment

A

no treatment known to alter course of disease pulmonary rehab and O2 therapy corticosteroids often prescribed

137
Q

what is it

A

intermittent upper airway collapse in sleeprecurrent sleep arousal

138
Q

what are symptoms

A

excessive daytime sleepiness personality change cognitive impairment major impact on daytime function

139
Q

what are causes

A

obesity enlarged tonsils stroke MSopiates alcohol

140
Q

how is it diagnosed

A

overnight sleep study (oximetry, airflow, thoracic movement monitored, full polysomnography) epworth sleepiness score (normal <10/24)

141
Q

how is it treated

A

correction of treatable factors CPAP - delivered by nasal mark during sleep mandibular advancement device (gum shield - improves snoring) surgery - scar up back of throat to make tougher and resist collapse

142
Q

what are complications

A

raised CRPimpaired endothelial and glucose function independent risk factor for hypertension

143
Q

what are types of non-small cell lung cancer (majority)

A

squamous cell carcinoma adenocarcinoma large cell carcinoma

144
Q

what is characteristics of squamous cell carcinoma

A

hypertrophic pulmonary osteoarthropathymost commonly cavitates

145
Q

what is characteristics of adenocarcinomas

A

most common type usually peripheral in bronchi

146
Q

what is the characteristics of large cell carcinoma

A

typically peripheral, poorly differentiated tumours with poor prognosis, may secrete beta HCG

147
Q

what is characteristics of small cell lung cancer

A

arises from endocrine cells hormones secreted: ADH and ACTHspreads early and almost always inoperable

148
Q

what kind of state does malignant cancer (especially adenocarcinoma) cause

A

hypercoaguable state

149
Q

what is symptoms

A

cough that lasts >2-3 weekslong standing cough that gets worse haemoptysis unexplained dyspnoea malaise weight loss persistent chest pain/shoulder pain

150
Q

what are less common symptoms

A

clubbing, hoarse voice, difficulty or pain swallowing, increased risk of infection

151
Q

what causes it

A

smoking passive smoking occupational exposure

152
Q

how is it diagnosed

A

CXR CT for small tumours and mediastinum (then biopsy)FBC for anaemia Urinanalysis

153
Q

how to treat non small cell lung cancer

A

surgerychemotherapy radiotherapy targeted agents

154
Q

how to treat small cell lung cancer

A

chemotherapy, palliative care

155
Q

what is common sites of metastases

A

kidneyprostatebreastboneGI tractcervix or ovary

156
Q

what is it

A

hyperplasia of smooth muscleoedema accumulation increased mucus secretion bronchoconstriction chronic airway inflammation (eosinophilic)airway remodelling

157
Q

what type hypersensitivity

A

type 1

158
Q

when does it come on

A

it is an episodic reversible bronchoconstriction early or late onset

159
Q

what are intrinsic causes

A

exercise, cold

160
Q

what are extrinsic causes

A

drugs, chemical, smoke, pollen, dust, animal dander, fungi, viral infection

161
Q

what are symptoms

A

dyspnoea tight chest wheezing non-productive cough diurnal variationnon-progressiveepisodic/intermittent

162
Q

how is it diagnosed

A

salbutamol reversibility >15%diurnal variation in peak flow rate normal gas exchange reduced FEV1 to under 75%preserved FVC and TLCOprovocation testing - exercise or allergen may find crackles if infection

163
Q

1st line treatment

A

SABA (salbutamol)

164
Q

2nd line treatment

A

low dose ICS (beclomethasone, budesonide, prednisolone)

165
Q

3rd line treatment

A

add LABA (salmeterol) to low dose ICS

166
Q

4th line treatment

A

leukotriene receptor antagonist (monteleukast)Xanthines (theophylline)LAMA (tiotropium)

167
Q

5th line treatment

A

consider increasing ICS up to high dose or addition of fourth drug eg LTRA, xanthine or LAMA - refer to specialist

168
Q

6th line treatment

A

use daily steroid tablet in lowest dose providing adequate controlmaintain high dose ICS and consider other treatments to minimise use of steroid tabletsrefer to specialist

169
Q

what is COPD split into

A

chronic bronchitis and emphysema

170
Q

what is chronic bronchitis

A

chronic irritation, defensive increase in mucus production and epithelial cell numbers (especially mucus glands) non-reversible obstruction (some may have reversible asthmatic component)

171
Q

what is emphysema

A

tissue destruction in the alveoli leading to loss in alveolar walls and increase in size of airspaces distal to terminal bronchiole (without fibrosis)

172
Q

what causes it

A

smoking passive smoking fumes dust

173
Q

what are symptoms

A

develop over number of yearsincreasing breathlessnesspersistent cough with sputum frequent exacerbationswheezing weight lossmalaise swollen anklesincreased infection risk

174
Q

how is it diagnosed

A

spirometry - decrease in PERF, FEV1, FVC and TLCOFEV1/FVC <75%FEV1 response to B2 <15%CXR - lung infiltrates if infectionBlood test - rule out other causeSputum culture - grow organism causing exacerbation

175
Q

1st line treatment

A

SABA (salbutamol)or SAMA (ipratropium)

176
Q

2nd line treatment (if FEV1>50%)

A

LABA (salmeterol)or LAMA (tiotropium) and discontinue SAMA

177
Q

3rd line treatment (if FEV1<50%)

A

LABA (salmeterol) plus ICS (becomethasone, budesonide, prednisolone)or LAMA (tiotropium) and discontinue SAMA

178
Q

4th line treatment

A

LAMA (tiotropium) plus LABA (salmeterol) plus ICS

179
Q

5th line treatment

A

if patient has 2 or more exacerbations in 12 months despite triple therapy, PD4 receptor antagonist (roflumilast) used

180
Q

what is used in acute exacerbation

A

oral corticosteroids (prednisolone) and antibiotics

181
Q

1st line antibiotics?

A

doxycycline / amoxicillin

182
Q

2nd line antibiotics?

A

clarithromycin, moxifloxacin, (AND IV aminophylline (methylxanthine))

183
Q

what is it

A

excess fluid between layers of pleura

184
Q

what are symptoms

A

worsening dyspnoea coughpleuritic pain

185
Q

what are signs

A

wall movement - reduced unilaterally percussion note - stony dullbreath sounds - absent but bronchial superior to effusionvocal fremitus - absent

186
Q

what is causes of exudative pleural effusion (protein more than 30g/l)

A

neoplasma PEinfections

187
Q

what is cause of transudative pleural effusion (protein less than 30g/l)

A

LVFcirrhosis

188
Q

what are other causes

A

congestive heart failure pneumonia renal failure cancer autoimmune (SLE)

189
Q

how is it diagnosed

A

symptoms and signs CXR - >300 fluid, changes range from obliteration of costophrenic angle to dense homogenous shadowsCTpleural biopsy

190
Q

what is treatment

A

thoracentesis symptomatic reliefpleurodesis (adhesion of pleural membranes)

191
Q

what are complications

A

empyema subcutaneous emphysems haemorrhage vagus nerve irritation

192
Q

what is it

A

abnormal and permanently dilated airways the mucocilary transport mechanism is impaired and frequent bacterial infections ensure

193
Q

what causes it

A

severe childhood infection cystic fibrosis immunodeficiency

194
Q

what are signs

A

cough production of large amount of sputum and dilated and thickened bronchi clubbing breathlessnesshaemoptysis can occur

195
Q

how is it diagnosed

A

exam - coarse crackles at base on inspiration CXR - mid zone tram lines, dilated bronchi CT - bronchial dilation

196
Q

how is it treated

A

damage cant be repaired so basis of management is to prevent or slow down further deterioration antibiotics may be needed bronchodilators useful in those with airflow limitation

197
Q

what antibiotics

A

amoxicillin, clarithromycin, erythromycin, doxycyline if allergic erythromycin in pregnancy and breast feeding

198
Q

what is it

A

collection of air in pleural space resulting in collapsed lung

199
Q

what are primary cause

A

normal lungs then apical bullae rupture

200
Q

what is secondary cause

A

pre-existing lung diseases eg smoking, severe asthma, COPD, marfans

201
Q

who is it common in

A

those with existing respiratory conditions, cannabis users, smokers and tall, thin men

202
Q

what are symptoms

A

sudden onset of pleuritic pain SOBtachycardia

203
Q

what are signs

A

hyper-resonant percussion note reduced expansion quiet breath sounds on auscultation hamman’s sign (click on auscultation at left side)

204
Q

how is it diagnosed

A

CXR - small <2cm rim of air, large >2cmABG - hypoxia

205
Q

treatment if <20%

A

observe, air will usually reabsorb

206
Q

treatment if 20-50%

A

needle aspiration using 16-18G cannula sited in 2nd IC space, mid clavicular line

207
Q

treatment if >50%

A

chest drainage - intercostal small bore drain in 5th IC space, mid auxillary line

208
Q

treatment if recurrence

A

pleurodesis/pleurectomy

209
Q

what is the follow up

A

CXRdiscuss flying and diving (not for 6 weeks)general recurrance risk smoking cessation

210
Q

what is tension pneumothorax

A

medical emergencycan lead to cardiac arrest due to one way valve mechanism (between pleural layers) resulting in increased pressure in pleural space

211
Q

what is signs of tension pneumothorax

A

tracheal deviation mediastinal shift to opposite side hypotension raised JVPreduced air entry

212
Q

what is treatment of TP

A

O2 and needle compression usually with large bore venflon in 2nd intercostal space

213
Q

what is seasonal rhinitis

A

hayfever

214
Q

what is perennial rhinitis

A

symptoms throughout full year, sinusitis occurs in about 50% of cases due to mucosal swelling

215
Q

what is perennial allergic rhinitis

A

allergy to faecal particles of dust mite - more sensitive to cigarette smoke, washing powders, perfumes etc

216
Q

what is vasomotor rhinitis

A

perennial rhinitis with no allergy or nasal eosinophilia

217
Q

what are nasal polyps

A

round smooth soft pale or yellow structures attached to sinus mucosa - occurs in patients with allergic and vasomotor rhinitis

218
Q

what causes it

A

mucus - parasympathetic stimulation allergic rhinitis results due to interaction between inhaled allergen and IgE present on their mast cells (found in increased numbers in nasal secretion)

219
Q

how is it diagnosed

A

history of allergic factors skin prick test indicates mechanism leading to allergic rhinitis

220
Q

how is it treated

A

H1 receptor antagonists (eg loratadine, cetirizine, fexofenadine, cyclizine, cinnarizine)Decongestants (a adrenergic agents) Corticosteroids (beclomethasone or fluticasone propionate - polyps) Leukotriene antagonists (montelukast, zarfirlukast - esp history of NSAID or asthma)Anti-allergic (sodium cromoglicate)

221
Q

what is it

A

alteration of viscosity and tenacity of mucus

222
Q

what is genetics of it

A

autosomal recessive, 1 in 25 people carry CFTR gene

223
Q

what are respiratory effects

A

commonest cause of recurrent bronchopulmonary infection in childhood

224
Q

what is GI effects

A

85% of patients have steatorrhoea (excretion of fat with faeces) due to pancreatic dysfunction or insufficiency

225
Q

what are other symptoms

A

biliary diseasehigh sodium sweatmalnutrition puberty and skeletal maturity delay males almost always infertile

226
Q

how is it diagnosed

A

sweat test confirms in 98%molecular test for CFTR genesinux XR/CT - show opacification of sinuses CXR or CT thorax

227
Q

how is it treated

A

symptomatic G551D - Ivecaftor F508Del - lumacaftor

228
Q

what are complications

A

most of morbidity due to respiratory disease eg bronchiectasis, progressive airflow destruction, cor pulmonale, death

229
Q

what is it

A

rare autoimmune disease in which antibodies attack basement membrane in lungs and kidneys lead to bleeding from lungs and kidney failure

230
Q

what are symptoms

A

symptoms of URTIfollowed by cough intermitten haemoptysis tirednessanaemia

231
Q

how is it diagnosed

A

CXR - transient blotchy shadows due to intapulmonary haemorrhage

232
Q

how is it treated

A

some patients spontaneously improve whilst others proceed to renal failure treat with corticosteroids

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