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phase 4 > respiratory > Flashcards

respiratory Flashcards

1
Q

questions to ask about shortness of breath

A

onset, progression, duration, wheeze, chest tightness, diurnal variation, cough, haemoptysis, sputum, chest pain, night sweats, weight loss, oedema, exacerbating factors, distance they can walk, severity, change in QoL

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2
Q

potential exacerbating factors of breathlessness

A

cold, air, flour, dust, URTI, occupation, allergies, medications (ask how they avoid these)

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3
Q

questions to ask about sputum

A

colour, consistency, amount, onset, timing, diurnal variation, odour

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4
Q

what would these sputum results suggest: rust, frothy pink, blood, odours

A

rust = pneumococcal pneumonia
frothy pink = pulmonary oedema
blood = malignancy
odours = bronchiectasis, lung abscess

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5
Q

questions to ask about haemoptysis

A

origin, colour, quantity, consistency, sputum, weight loss, fever, night sweats, trauma, other bleeding

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6
Q

drugs to ask about in respiratory history

A

nsaids, aspirin, inhalers, steroids, antibiotics, ace-i, amiodarone, BBs, O2

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7
Q

specific family history questions in respiratory

A

allergic rhinitis, hay fever, eczema, asthma, lung cancer, family infections, CF, alpha-1-antitrypsin deficiency

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8
Q

social history in respiratory

A

occupation, smoking, pets, travel, living conditions, alcohol, exercise, ADLs, indepedence

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9
Q

if not a respiratory illness, what are the DDx

A

cardiac, gastro, msk, neuro

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10
Q

Ddx of respiratory illness

A

PE, asthma, pulmonary fibrosis, CF, bronchiectasis, COPD, TB, lung cancer, sarcoidosis, pneumonia

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11
Q

hand findings in resp exam

A

clubbing, tar stain, wasting of intrinsic muscles, flapping astrexis, fine tremor, pulses paradoxes, bounding pulse

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12
Q

eye findings in resp exam

A

Horner’s, chemosis

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13
Q

face findings in resp exam

A

facial swelling, central cyanosis, dental caries

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14
Q

what is chemosis

A

conjunctival oedema in hypercapnia due to copd

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15
Q

cause of raised JVP in resp

A

raised = cor pulmonate

raised and non pulsatile = SVCI

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16
Q

chest inspect findings in resp exams

A

barrel chest, severe kyphoscoliosis, severe pectus excavatum, pectus carinatum, hamson’s sulci , recession, symmetry, scares, muscle wasting, accessory muscle

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17
Q

what does tracheal and apex deviation mean

A

towards pulmonary fibrosis and collapse, away from tension pneumothorax or massive effusion

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18
Q

4 things to do in palpate for resp

A

tracheal dev, apex dev, chest expansion, tactile vocal resonance

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19
Q

results of vocal resonance

A

increased in consolidation

reduced in effusion or pneumothorax, is suspect consolidation - do whispering pectoriloquy

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20
Q

what you could hear on auscultation

A

bronchial breathing, wheeze, crackles, crepitations, fine inspiratory crackles, coarse crackles, pleural rub

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21
Q

what to do to complete resp exam

A 
SPOT X
sputum
peak flow
O2 sats
temperature
xray

lymph nodes and oedema

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22
Q

CXR findings in pneumonia

A

opacification in a zone (if atypical = reticulonodular opacities)

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23
Q

acute management of pneumonia

A

ABCDE
if SIRS = sepsis 6
CURB-65 score to see if admission needed
antibiotics

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24
Q

causative organisms of CAP

A

streptococcus pneumonia, mycoplasma, haemophillus, staphlococcus aureus

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25
Q

atypical pneumonia organisms

A

mycoplasma, legionella, chlamydia

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26
Q

causative organisms of HAP

A

e.coli, klebsiella, pseudomonas, MRSA

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27
Q

type of pneumonia in: COPD, IVDU, alcoholics, hotels, bird fancier

A

h.influenza
s.aureus
klebsiella
legionella
chlamydia

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28
Q

CURB 65

A 
confusion
urea >7
rr >30
BP <90/60
age >65
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29
Q

results of curb 65

A 
0-1 = home
2 = hospital 
3+ = ITU
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30
Q

auscultation of pneumonia

A

areas of consolidation, increased vocal resonance/whispering pectoriloquy, reduced air entry, crackles

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31
Q

investigations for pneumonia

A 
SPOT X
sputum - culture
peak flow
o2 sats 
temperature 
xray chest - opacification (consolidation)

urine antigens for atypical
BAL and immuno-flourence for PCP, bloods

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32
Q

antibiotics for pneumonia

A

CAP - amoxicillin or co-amoxiclav with clarithromycin

HAP - co-amoxiclav, tazocin, vancomycin, gentamycin

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33
Q

complications of pneumonia

A

sepsis, res failure, hypotension, AF, lung abscess

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34
Q

symptoms of bronchiectasis

A

persistent cough and sputum for > 1 year, recurrent chest infections, wheeze

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35
Q

pathophysiology of bronchiectasis

A

chronic infection of bronchi leads to permanent dilation and thickened vessel wall and retained mucus as failed clearance - causing airway damage

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36
Q

common organisms in brochiectasis

A

h.influenzae, pseudomonas, strep pneumonia, staph aureus

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37
Q

symptoms of acute exacerbation of bronchiectasis

A

increased sputum, change in sputum colour/appearence, haemoptysis, SOB

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38
Q

investigations

A 
SPOTX
sputum, peak flow (obstructive), O2 sats, temp, X-ray chest (tramlines and signet ring)
CT CT CT dilated and thickened airways 
CF sweat test 
aspergillum skin test
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39
Q

management of bronchiectasis

A

chest physio, Abx, bronchodilators nebs

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40
Q

causes of bronchiectasis

A

CF, post infection, hypogammaglobulinaemia, tumour, ABPA, autoimmune

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41
Q

CXR in CF

A

bronchiectasis

thick dilated airways, tramlines, mucus plugs/fluid lines, signet ring, patchy shadowing

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42
Q

neonate presentation of CF

A

FTT, meconium ileus, rectal prolapse, chronic cough, increased appetite

FIBROSIS
FTT, ileus meconium, buttocks wasting, recurrent infection, polyps nasal, steatorrhoea

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43
Q

symptoms of CF

A 
nose - polyps, sinusitis 
resp - cough, wheeze, bronchiectasis (recurrent infections)
pancreas - steatorrhoea, DM
GI - gallstones, intestinal obstruction
fertility - infertility in men
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44
Q

pathophysiology of CF

A

AR - CFTR gene mutation, delta 508, leading to abnormal chloride channels so thick airway secretions, malabsorption, poor growth, pancreatic enzyme deficiency

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45
Q

screening for CF

A

carrier testing
antenatal test = amniocentesis and chronic villi samping
5 day heel prick test

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46
Q

counselling patients with CF

A

osteoporosis, infertility, clubbing, vasculitis, cor pulmonale, Segregation of patients with CF, reduced lifespan (40 years)

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47
Q

managing a child with CF

A

FAUVISM

  • fat soluble vitamins (ADEK)
  • antibiotics
  • urodeoxycholic acid for impaired hepatic function
  • vaccines (pneumococcal and flu)
  • insulin
  • salbutamol bronchodilators
  • MDT
  • pancreatic enzyme supplements (exocrine), mucolytics (neb DNAse), chest physiology, high calorie diet
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48
Q

diagnosing CF

A

sweat test, genetics, faecal elastase, immunotrypsinogen reactive test heel prick

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49
Q

investigations for CF

A 
CXR, CT
spirometry - obstructive 
aspergillum skin prick test
sputum MC+S
bloods 
abdo US - fatty liver, cirrhosis, pancreatitis
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50
Q

what the child can do to help in CF

A

regular exercise to shift the mucus, increased calories needed, avoid smoking and pollution, make sure everyone in the house washes hands, leaflets, support groups, websites

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51
Q

what is an autosomal recessive disease in CF

A

25% of having a disease if both parents are carriers, could be a carrier

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52
Q

respiratory complications of CF

A

increased chest infections, wheeze, bronchiectasis, cough

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53
Q

gastro complications of CF

A

fatty liver, cirrhosis, gallstones, intestinal obstruction

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54
Q

CXR on pleural effusion

A

blunted costophrenic angles, opacification, tracheal and mediastinal deviation away meniscal level, dense shadow, at the bottom

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55
Q

difference between transudate and exudate pleural effusion

A

transudate has protein <25g/l due to increased hydrostatic and reduced oncotic forces

exudate has protein >35g/L due to increased capillary permeability

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56
Q

causes of transudate pleural effusion

A

stuff not in the lungs

CCF, renal failure, liver failure, reduced albumin, hypothyroidism, meigs

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57
Q

causes of exudate pleural effusion

A

stuff happening in the lung

infection, neoplasm, inflammation (CTD, RA, SLE), infarction, TB, pneumonia, abscess, pancreatitis

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58
Q

what is light’s criteria

A

used when protein 25-35, takes into account protein and LDH

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59
Q

what would you find on examination of pleural effusion

A

reduced air entry, stony dull percussion, reduced vocal resonance, reduced chest expansion, bronchial breathing

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60
Q

investigations of pleural effusion

A 
CXR
find the cause
bloods 
US guided tap for diagnosis
send for protein, LDH, pH, glucose, amylase, bacteria, cytology, immunology
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61
Q

treatment of pleural effusion

A

treat the cause, avoid drainage if transudate

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62
Q

complication of pleural effusion

A

parapneumonic effusion and bronchopleural fistula

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63
Q

CXR in pneumothorax

A

absent lung markings to the periphery of one side, mediastinal shift away, evidence of cause, flat diaphragm

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64
Q

management of pneumothorax

A

depends on size and severity

  • observe (asymptomatic, <2cm, no underlying lung disease)
  • needle aspiration (primary but >2cm or symptomatic OR secondary 1-2cm)
  • chest drain (failure to resolve after aspiration, unstable, secondary >2cm)
  • needle decompression with large bore cannula and chest drain (tension)
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65
Q

examination findings of pneumothorax

A

reduced air entry, resonant percussion, reduced chest expansion, reduced breath sounds

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66
Q

risk factors of pneumothorax

A

primary = young thin male smokers = spontaneous
secondary = COPD, CTD, pulmonary fibrosis, sarcoidosis
trauma
iatrogenic = CVP line insertion, post aspiration

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67
Q

symptoms in tension pneumothorax

A

respiratory distress, cardiac arrest, mediastinal shift away, increased JVP, increased HR, low BP

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68
Q

investigations of pneumothorax

A

CXR, ABG, US (shouldn’t CXR tension as emergency)

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69
Q

borders of chest drain

A

2nd ICS mid axillary line

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70
Q

causes of coin shaped lesion on CXR

A

foreign body, abscess, malignancy, granuloma (TB), structural

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71
Q

risk factors of lung cancer

A

occupation , FHx, smoking, abscess, COPD, male

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72
Q

red flags for lung cancer

A

weight loss, haemoptysis, hoarseness, Horner’s, enlarged virchows node, paraneoplastic syndromes (hypercalcaemia, bone pain, gynaecomastia, flushing, hyponatraemia, bushings)

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73
Q

types of lung cancer

A 
non small cell
small cell
squamous 
adenocarcinoma
carcinoid
mesothelioma
pancoast (apex of lung)
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74
Q

lung symptoms to ask in lung cancer history

A

cough, haemoptysis, chest pain, dyspnoea, orthoptera, exertion dyspnoea, hoarseness, pleuritic chest pain

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75
Q

systemic symptoms to ask in lung cancer history

A

weight loss, anorexia, fever, anaemia, clubbing, lymphadenopathy

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76
Q

CXR in lung cancer

A

coin shaped lesions, pleural effusion, collapse, consolidation

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77
Q

symptoms of mets in lung cancer

A 
bone = bone pain and pathological fractures
liver = hepatomegaly
brain = confusion
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78
Q

paraneoplastic syndrome of each lung cancer

A

squamous = hyperparathryodism, hypercalcaemia, bone pain
adenocarcinoma = gynaecomastia
carcinoid = flushing, wheeze, diarrhoea
small cell = SIADH (hyponatraemia) and Cushing’s and Lambert Eaton syndrome
pancoats = corners and shoulder tip pain and hand wasting due to branchial plexus and T1 nerve involvement, SVCO

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79
Q

investigations in lung cancer

A 
bloods
CXR
CT/MRI
luft
sputum 
radio nucleotide bone scan 
biopsy
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80
Q

treatment of lung cancer

A

chemo, surgery, radio, analgesia, drains, dexamethasone, stents, smoking cessation

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81
Q

local symptoms to ask in lung cancer history

A

recurrent laryngeal nerve palsy, phrenic nerve palsy, SVCO, horners, AF

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82
Q

which lung cancer is caused by smoking

A

squamous

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83
Q

which asbestos fibre causes mesothelioma

A

blue (crocidolite)

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84
Q

what will investigations show in mesothelioma

A

pleural thickening, pleural plaques, pleural mass, mediastinal enlargement, diaphragmatic plaques

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85
Q

treatment of mesothelioma

A

chemo, palliative, surgery, compensation

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86
Q

causes of haemoptysis

A

trauma, coagulation defect, malignancy, lung abscess, PE, bronchiectasis, bronchitis, TB, pneumonia, aspergillioma

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87
Q

occupational lung diseases

A

coal workers lung
silicosis (quarrying and sandblasting)
asbestosis (demolition, ship building)
pneumoconiosis

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88
Q

lung diseases caused by animal exposure

A

Extrinsic allergic alveolitis - bird fanciers lung, farm workers, malt workers lung

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89
Q

causes of lower lobe pulmonary fibrosis

A 
STAIR
sarcoidosis
toxins - BANS ME = bleomycin, amiodarone, nitrofurotoin, sulfasalazine, methotrexate 
asbestosis
interstitial pulmonary fibrosis
rheumatological
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90
Q

causes of upper lobe pulmonary fibrosis

A 
A TEA SHOP
ABPA
TB
EAA
sarcoidosis
histiocytosis
occupational 
pneumonitis
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91
Q

investigations in pulmonar fibrosis

A

HRCT = honeycombing, septal thinking
CXR - ground glass
lung biopsy = fibroblastic foci and interstitial fibrosis
LuFT - restrictive (reduced FEV, normal FEV1/FVC, reduced FVC, reduced total lung capacity)
reduced transfer factor

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92
Q

examination in pulmonary fibrosis

A

fine inspiratory crackles

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93
Q

treatment of pulmonary fibrosis

A

stop smoking, pulmonary rehab, O2 therapy, palliation,

in exacerbation, steroids and immunosuppression

monitor symptoms and lung function

lung transplant

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94
Q

describe FVC and FEV1

A 
FVC = forced vital capacity
FEV1 = forced expiratory volume in 1 second
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95
Q

causes of restrictive lung disease

A

pulmonary fibrosis, asbestosis, sarcoidosis, ARDS, RDS, anky spon, obese, neuromuscular disorders

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96
Q

what is sarcoidosis

A

a multisystem non caseating granuloma disorder

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97
Q

symptoms of sarcoidosis

A

lungs - dyspnoea, cough
skin - erythema nodosum, lupus pernio
eyes - uveitis, photophobia, keratoconjunctivitis, sick/sjogrens
systemic - non tender lymph nodes, fatigue, weight loss, joint pain, hepatosplenomegaly, pituitary dysfunction, polyneuropathy, parotitis

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98
Q

CXR in sarcoidosis

A

bilateral hilar lymphadenopathy

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99
Q

tissue biopsy histopathological finding in sarcoidosis

A

non caseating granulomas

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100
Q

what to monitor in sarcoidosis

A

ophthalmology
bloods - ESR, serum ACE, Ig, LFTS, calcium
luft
CT/MRI

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101
Q

treatment of sarcoidosis

A

acute - NSAIDs, rest

chronic - steroids (with PPI and bisphosphonates), immunosuppression

102
Q

differentials of bilateral hilariously lymphadenopathy

A 
TIMES
TB
idiopathic pulmonary fibrosis
malignancy
EAA
sarcoidosis
103
Q

granuloma DDx

A

TB, leprosy, syphilis, PBC, GCA, PAN, wegeners, takaysus, chrons, sarcoidosis, EAA, silicosis

104
Q

CXR pulmonary oedema

A

bat wing opacification

105
Q

what is pulmonary oedema

A

accumulation of fluid in alveolar and parenchyma

106
Q

cariogenic causes of pulmonary oedema

A

MI, arrhythmia, fluid overload (renal causes, fluid challenge)

107
Q

non cardiogenic causes of pulmonary oedema

A

ARDS (sepsis, post op, trauma, pancreatitis), upper airway obstruction, head injury

108
Q

symptoms of pulmonary oedema

A

orthopnoea, dyspnoea, pink frothy sputum

109
Q

management of pulmonary oedema

A 
ABCDE - o2, IV, ecg, bloods
diamorphine
metaclopramide 
furosemide 
GTN
investigate
dobutamine (inotrope) if shock 
cpap
110
Q

investigations in pulmonary oedema

A

bloods = FBC, U+E, troponin, BNP, ABG
CXR
ECG
ECHO

111
Q

treatment of collapsed lung

A

ABCDE

find and treat the cause (malignancy, mucus plugging)

112
Q

life threatening chest injuries

A 
ATOM FC
aortic/airway disruption
tension pneumothorax
open pneumothorax
massive haemothorax 
flail chest 
cardiac tamponade
113
Q

extra pulmonary features associated with mycoplasma pneumonia

A

haemolytic anaemia, dry cough and erythema multiforme

114
Q

symptoms of TB

A

cough >2 weeks, night sweats, fever, weight loss, haemoptysis, recent travel, enlarged lymph node, sputum, pleuritic chest pain

115
Q

would MG be type 1 or 2 res failure

A

type 2

116
Q

CXR of TB

A

upper lobe round caveating lesion

may also have consolidation, aviation, fibrosis, calcification

117
Q

extrapulmonary symptoms of TB

A

LUTS, ascites, vertebral collapse, Potts vertebra, lupus vulgaris, peritoneal, Addison’s, meningitis

118
Q

extrapulmonary symptoms of TB

A

LUTS, ascites, vertebral collapse, Potts vertebra, lupus vulgaris, peritoneal, Addison’s, meningitis, constrictive pericarditis

119
Q

investigations of active TB

A

sputum sample x3 with one in the morning to look for acid fast bacilli with ziehl nelson stain on low stein jensen media

if sputum sample in suggestive, do CXR

120
Q

investigations in latent TB

A

mantoux tuberculin test and IFN gamma release assay

121
Q

what can give false positive on mantoux tuberculin test

A

previous immunisation, sarcoidosis, hodgkins lymphoma

122
Q

treatment of TB

A 
rifampicin
isonzaid
pyrazidamide
ethambutol
treat w/o culture if clinical picture looks like it
NOTIFY PUBLIC HEALTH
123
Q

side effects of rifampicin

A

orange secretions and hepatotoxicity

124
Q

side effects of isonzaid

A

peripheral neuropathy and hepatotoxicity

125
Q

side effects of pyrazidamie

A

muscle weakness and arthralgia and hepatotoxicity

126
Q

side effects of ethambutol

A

optic neuritis and hepatotoxicity

127
Q

what should be monitored during TB treatment

A

FBC, LFTs, visual acuity, urate

128
Q

prophylaxis of TB

A

rifampicin and isoniazid

129
Q

how does rifampicin work

A

inhibits RNA polymerase abd DNA transcriptase

130
Q

how does isonzid work

A

inhibits cell wall synths

131
Q

how does pyrazmdamide work

A

disrupts fatty acid synthesis

132
Q

organism in TB

A

mycobacterium tuberculosis

133
Q

pathophysiology of TB

A

organism multiplys at pleural surface to create ghon focus macrophages take TB infection to lymph nodes to form Ghon complex, fibrosis of the complex leads to calcified nodule

134
Q

explain asthma

A

airflow limitation due to a hyperresposiveness to stimuli which causing airway narrowing and hyper secretion in the airway lumen and inflammation of the bronchi, smooth muscle hypertrophy and thickened walls

135
Q

difference of acute and chronic asthma

A

acute - igE antibodies cause mast cells to release histamine and cause bronchoconstriction, muscus plugs and mucosal swelling

chronic - Th2 cells release IL3/4/5 to cause inflammatory cell recruitment and airway remodelling

136
Q

symptoms of asthma

A

wheeze, SOB, chest tightness, cough, diurnal (worse at night and early morning), exacerbates, atopy, reduced air entry, hyper inflated chest

137
Q

precipitators of asthma

A

cold, exercise, stress, emotion, smoking, pollution, factories, URTI, dust mites, pollen, food, animals, fungus, occupation

138
Q

investigations in asthma

A

SPOTX
sputum, peak flow, O2 sats, temp, X-ray chest (hyperinflation)

Bloods - eosinophilia, increased IgE, aspergillosis serology
LuFT - obstructive
peak flow - diurnal variation >20%, morning dip
atopy skin prick
histology

139
Q

what does histology show in asthma

A

smooth muscle hypertrophy
increased mucosal goblet cells
airway remodelling

140
Q

general day to day management of asthma

A 
TAME
technique for inhaler - spacer
avoid precipitants
monitor with peak flow
educate
141
Q

risk factor of childhood asthma

A

maternal smoking, viral infections during pregnancy, low birth weight, not breast fed, air pollution

142
Q

how to use salbutamol depending on age in children

A

<3yrs - close fit mask

>3yrs - inhaler and spacer

143
Q

side effects of salbutamol

A

fine tremor, hypokalaemia, VF/VT

144
Q

example of a low dose inhaled corticosteroid

A

beclomethosone

145
Q

side effect of beclamethasone

A

oral candidiasis

146
Q

example of a LTRA

A

montelukast

147
Q

example of LABA

A

salmetrol

148
Q

side effect of montelukast

A

headache and Gi disturbance, churg strauss

149
Q

when to increase asthma treatment

A

having to use inhaler >3 times a week, symptomatic, worsening QoL, needing >6 puffs in one go

150
Q

what should you always check in asthma management

A

are they being compliant with treatment

151
Q

what medications should be avoided in asthma

A

Nsaids and BBs because they decrease prostaglandin and cause overproduction of pro-inflammatories

152
Q

how does salbutamol work

A

leads to bronchial smooth muscle relaxation and bronchodilator

153
Q

what should be monitored in salbutamol

A

potassium

154
Q

when is montelukast used

A

a LRTA, for asthma (preventer), allergic rhinitis and aspirin induced asthma

155
Q

montelukast interactions

A

increases anticoagulant effect of warfarin

156
Q

questions in acute severe asthma attack

A

precipitants, usual treatment, compliance, previous attacks, ICU, best PEFR

157
Q

when should you admit in asthma attack

A

life threatening symptoms, features of severe despite treatment

158
Q

symptoms of moderate asthma attack

A

worsening symptoms, PEFR 50-75%

159
Q

symptoms of severe asthma

A

PEFR <50%
RR >25
HR >110
can’t complete sentences in single breath

160
Q

symptoms of life threatening asthma

A 
PEFR <33%, spo2 <92%, pao2 <8, pco2 >4.6
CHEST
cyanosis
hypotension
exhaustion 
silent chest/poor respiratory effort
tachy/brady/arrythmias
161
Q

treatment of asthma attack

A 
sit up, 100% o2, 15L non rebreathe 
salbutamol nebuliser every 15 minutes and monitor potassium with ECG 
hydrocortisone
ipratropium bromide neb
theophylline IV
MgSo4 IV 
salbuatmol IV
ITU for invasive ventilation
162
Q

when can you discharge asthma attack

A

PEFR >75% within 1hr of Tx

been stable on discharge meds for 24hrs

163
Q

discharge plan for asthma attack

A

TAME - technique of inhaler, avoid precipitants, monitor PEFR, educate
steroids (5 days of prednisone)
GP appointment
resp clinic in 1 month

164
Q

causes of wheeze in child

A

anaphylaxis, viral induced wheeze, broncholitis, asthma, inhaled foreign body, heart failure, GORD

165
Q

additional diseases associated with asthma

A

cows milk protein intolerance, eczema, hay fever, allergies

166
Q

what age can you use a peak flow meter

A

4-5years

167
Q

what is a peak flow test

A

how quickly you can blow air out your lungs

168
Q

how should you record peak flow

A

do it 3 times and record the highest and do morning and evening

169
Q

how does the hygiene hypothesis relate to asthma

A

early exposure to micro organisms protects against allergic diseases by contributing to the immune system

170
Q

how long can a spacer be used for

A

replace every 6-12 months

171
Q

how to wash a spacer

A

wash once a week with warm water and leave to dry naturally without a cloth

172
Q

advantages of using a spacer

A

helps get the inhaler medication to reach deep into the lungs without the complexity of getting the technique right

173
Q

pathophysiology of copd

A

a combination of chronic bronchitis (productive cough on most days for 3 months a year over 2 successive years) and emphysema (enlargment of air spaces in the terminal bronchioles leading to inefficient gas exchange ratios and poor air outflow)

174
Q

symptoms of COPD

A

cough, sputum, weight loss, early inspiratory crackles, cor pulmonate, oedema, barrel chest, hyper-resonant, co2 flap, dyspnoea

175
Q

risk factors of COPD

A

smoking, age, family history, pollution, A1ATD

176
Q

spirometry in copd

A

obstructive
FEV1/FVC <70%
FEV1 <80%
increased TLC

177
Q

what is the bode classification

A

the copd survival prediction

stands for BMI, airflow obstruction, dyspnoea and exercise capacity

178
Q

investigations in copd

A 
SPOTX
sputum
peak flow/spirometry
o2 sats
temperature
xray
bloods
ECG
ECHO
mMRC dyspnoea score
bode classification
179
Q

what will bloods show in copd

A

polycythaemia
abg
A1ATD

180
Q

what will CXR show in COPD

A

he fucking breathes
hyperinflation
flat diaphragm
bullae

exclude lung cancer

181
Q

what will ECHO show in copd

A

primary hypertension

182
Q

lifestyle treatment in copd

A

smoking cessation, vaccines, copd nurse, depression screen, control BMI, educate, pulmonary rehab, treat comorbidities , mucolytics

183
Q

how do you define an acute exacerbation of copd

A

worsening symptoms usually caused by an infection

184
Q

treatment of acute exacerbation of copd

A

COAL BINS

chest physio
o2 (aim 88-92%)
Abx
LMWH

bronchodilators (SABA and SAMA)
invasive ventilation
NIV (BiPAP)
steroids (hydrocortisone IV and prednisone PO)

185
Q

treatment of copd FEV >50%

A 
SABA/SAMA
then LABA/LAMA
then LABA+LAMA+ICS
then LTOT
then surgery
186
Q

treatment of copd FEV<50%

A 
SABA/SAMA
then LABA/LAMA +ICS
then LABA+LAMA+ICS
then LTOT
then surgery
187
Q

pros of LTOT

A

increases survival

188
Q

indications of LTOT in copd

A

if clinically stable, non smoker, paO2 <7.3 or have pulmonary HTN, cor pulmonale, polycythaemia, nocturnal hypoxaemia, terminally ill

189
Q

discharge for COPD

A

SHEDS vaccines

spirometry 
home assessment
establish maintenance therapy
doctors appointment 
steroids for prevention
190
Q

abg in acute exacerbation of copd

A

respiratory acidosis due to inappropriate high flow o2 or respiratory depression

191
Q

why does smoking cause copd

A

leads to increased neutrophils and oxidative stress causing elastin breakdown and inactivation of A!AT

192
Q

most common organism in copd

A

h.influenza

193
Q

complications of copd

A 
cor pulmonale
pulmonary HTN
polycythaemia
respiratory failure
pneumothorax (ruptured bullae)
lung cancer
infections/exacerbations
194
Q

causes of type 1 resp failure

A

PE, pulmonary HTN, pulmonary shunt (R to L), asthma, pneumothorax, pulmonary oedema, pneumonia, infarction, fibrosis

195
Q

causes of type 2 resp failure

A

any cause of type 1 if severe enough

copd, asthma, lung fibrosis, sedatives, CNS tumours, trauma, neuromuscular disease (MG, GBS), flail chest

196
Q

symptoms of acute hypoxia

A

dyspnoea, agitation, confusion, cyanosis

197
Q

symptoms of chronic hypoxia

A

polycythaemia, pulmonary HTN, cor pulmonale

198
Q

symptoms of hypercapnia

A

headache, flushing, bounding pulse, flap, coma

199
Q

explain co2 retention in copd

A

in copd they optimise gas exchange with hypoxic vasoconstriction so when there is an increased o2, respiratory drive is lowered and hypercapnia respiratory failure occurs due to altered V/Q ratio

200
Q

o2 sat aims in resp failure

A

hypoxic = 94-98
hypercapnia 88-92

try and do abg first

201
Q

how does bipap work

A

adds pressure during inspiration and expiration to increase tidal volume and co2 clearance

202
Q

how does cpap work

A

maintains minimum airway pressure to keep alveoli inflated

203
Q

risks of bipap

A

non tolerance, gastric distension, aspiration, failure

204
Q

types of invasive ventilation

A

tracheostomy

ET tube

205
Q

indications of invasive ventilation

A

emergency surgery, history of sev reflux, protect airway, GCS <8 or rapidly decreasing

206
Q

risks of invasive ventilation

A

trauma, pneumothorax, lung injury, alveolar rupture, abdominal distension, water retention, emphysema, muscle relaxant

207
Q

methods to give O2

A

nasal cannula, simple face mask, resovoir/non rebreathe, venturi mask, non invasive ventilation, invasive ventilation

208
Q

what is ARDS

A

pulmonary oedema

209
Q

criteria of ARDS

A

<1 week, CXR change, PaO2:FiO2 <200, no evidence of congestive HF

210
Q

causes of ARDS

A

sepsis, trauma and pancreatitis or direct pulmonary injury lead to increased inflammatory mediators, increased capillary permeability, and non cariogenic pulmonary oedema

211
Q

CXR in ARDS

A

bilateral opacity and perihilar infiltrates

212
Q

treatment of ARDS

A 
ABCDE - o2, IV, ecg, bloods
diamorphine
metaclopramide 
furosemide 
GTN
ITU, ventilation, supportive, Abx, nutritional support, invasive BP monitors
213
Q

what is obstructive sleep apnoea

A

intermittent closure/collapse of airway leading to apnoea episodes during sleep

214
Q

risk factors of obstructive sleep apnoea

A

obese, male, smoker, alcohol, IPF, structural pathology, MND

215
Q

investigations in OSA

A

polysomonography for diagnosis
SpO2
epworth sleepiness scale

216
Q

symptoms of OSA

A

snoring, choking, gasping, morning headache, reduced memory and attention, irritable

217
Q

treatment of OSA

A

weight loss, avoid alcohol and smoking, CPAP mask at night, surgery

218
Q

complications of OSA

A

pulmonary HTN, type 2 res failure, cor pulmonate, depression, DM, HTN

219
Q

definition of pulmonary HTN

A

pulmonary artery pressure >25mmHG and capillary wedge pressure <15mmHg

220
Q

symptoms of pulmonary HTN

A

leads to RVH and RHF so cor pulmonale, increased JVP, pulsatile HSM, murmurs, left parasternal heave, ascites, peripheral oedema

221
Q

investigations in pulmonary HTN

A

ECG = p pulmonale, RVH, RAD
ECHO = R side hypertrophy and dysfunction and tricuspid regurgitation
right heart catheterisation for MPAP. PVR, CO, vasoreactivity test

222
Q

treatment of pulmonary HTN

A

treat the cause and reduce pulmonary vascular resistance

anticoag, transplant

223
Q

how to reduce pulmonary vascular resistance

A

LTOT, CCB, sildenafil, prostaglandins

224
Q

what is virchows triad

A

venous stasis, vessel damage and hypercoaguloable state

225
Q

risk factors of PE

A 
SPASMODIC
sex = female
pregnancy
age increase
surgery
malignancy
oestrogen (COCP/HRT)
DVT/PE
immobility
colossal size
antiphospholipid antibodies 
lupus anticoagulant

chemo, trauma, thrombophillia

226
Q

symptoms of PE

A

dyspnoea, pleuritic chest pain, haemoptysis, syncope, fever, cyanosis, tachypnoea, RHF

227
Q

symptoms of DVT

A 
limb tenderness/pain
unilateral swelling of calf
increased skin temperature
skin discolouration 
distended superficial veins 
pitting oedema
228
Q

PE wells score

A 
clinical signs of DVT = 3
PE most likely = 3
HR >100bpm = 1.5
recent PE/DVT = 1.5
recent surgery/immbolisation = 1.5
haemoptysis = 1
malignancy = 1

4 or more = PE

229
Q

DVT wells score

A 
active cancer = 1
bedridden >3days or major surgery in past 4 weeks = 1
calf swelling >3cm = 1
collateral superficial veins present = 1
entire leg swollen = 1
localised tenderness = 1
pitting oedema = 1
paralysis/recent immobile leg = 1
previous DVT = 1

2 or more is DVT

230
Q

what is PESI

A

pulmonary emboli severity index = prognosis of PE in 30 days

231
Q

PERC rule

A

risk of PE if no risk factors present <50 years (HADCLOTS)

232
Q

DVT management

A

if suspected do wells, if 2 or more do PVUSS in 4 hrs, >4hrs, anticoagulate then PVUSS

if wells <2 - do d-dimer

233
Q

PE management

A

do wells, if 4 or more do CTPA, if delayed do anticoagulant then CTPA

234
Q

Pe management in renal disease

A

do V/Q scan instead of CTPA

235
Q

investigations in PE

A

bloods = FBC, U+E, clotting, dimer, troponin
ABG = low O2, increased lactate
CXR = exclude pneumothorax, wedge shaped infarct, pleural effusion, vascular dilation
ECG = exclude MI, tachycardia, S1Q3T3, RBBB, RVs strain and deviation, AF
d dimer
VQ scan
thrombophilia/cancer screen

236
Q

prophylaxis of PE/DVT

A

graduated compression stockings for 2 years, early mobility, hydration, LMWH, avoid RF, TED stockings in hospital

237
Q

DD of PE

A

MI, pneumothorax, pericarditis, MSK, pneumonia, malignancy

238
Q

ECG in PE

A 
rule out MI
tachycardia/AF
S1Q3T3 = s wave in lead one, q wave in lead 3 and t wave invasion lead 3
RBBB
RV strain
RV deviation
239
Q

issue with d dimer

A

high sensitivity, low specificity

240
Q

acute management of PE

A

ABCDE
metaclopramide and morphine
anticoagulant
if BP <90 give fluids and dobutamine (an inotrope)

241
Q

methods of anticoagulation in PE

A

LMWH (dalteparin) or fondaparinux (Xa inhibitor) until INR 2-3 or 5 days then give warfarin for 6 months if unprovoked or 3 month if first

242
Q

what would an unprovoked PE suggest

A

cancer

243
Q

what to do in VTE while on anticoagulants

A

could be a thrombophilia (Factor V Leiden, Protein c and S deficiency, antiphopsholipd syndrome, antithrombin deficiency), so increase INR to 3-4 and do clotting screen

244
Q

anticoagulant of PE in anticoagulant CI or recurrent

A

IVC filter to prevent clots from moving to lung

245
Q

when should you use unfractioned heparin in PE

A

if unstable, severe renal impairment or increased bleed risk

246
Q

NOAC mechanism

A

apixaban = xa inhibitor

247
Q

pros and cons of NOAC

A 
pro = don't need measuring, faster onset and offset
cons = bleed and bruise, heparin induced thrombocytopenia
248
Q

precautions in NOAC use

A

pregnancy, alert card, monitoring, side effects, lifestyle impact

249
Q

what to monitor during LMWH use

A

FBC (platelets), APTT, U+Em LFTs, weight

250
Q

4 types of hypersensitivity

A

ACID
1 = allergy IgE = due to mast cells releasing histamine e.g. anaphylaxis, hay fever, asthma

2= cytotoxic antibody dependent e.g autoimmune and transfusions

3 = immune activation of complement e.g. SLE, post strep GN

4 = delayed T cell mediated e.g. TB, contact dermatitis

251
Q

methods to assess respiratory pre op

A

METS, ECG, ECHO, CXR, functional capacity assessment, BMI, Bloods

252
Q

vasculitis and resp

A

wegener cANCA

charge strauss pANCA

phase 4 (19 decks)

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