Respiratory Flashcards

(144 cards)

1
Q

what is acute respiratory distress syndrome + pathophysiology? (ARDS)

A

Diffuse inflammation of the lungs due to acute injury leads to increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli and decreased production of surfactant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

diagnostic criteria of ARDS? (4)

A

1) onset within 1 week if a known clinical insult
2) presence of bilateral opacities on CXR not explained by other pathology
3) respiratory failure not explained by other pathology
4) presence of hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

management of ARDS?

A

oxygenation/ventilation to treat the hypoxaemia
vital organ support
treat underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathophysiology of TB?

A

Mycobacterium tuberculosis is acquired via airborne spread. Once in the lungs, it is ingested by alveolar macrophages, where it multiples and forms a granuloma, which eventually spreads to the surrounding lymph nodes and forms the Gohn complex. Often the TB remains dormant within the Gohn complex for months until it becomes reactivated causing active TB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Types of TB?

A

Milliary TB (disseminated)
CNS TB/meningitis
urogenital TB
Potts disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Symptoms of TB?

A
fever
night sweats
weight loss
lymphadenopathy 
purulent cough 
chest pain 
(may be asymptomatic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

investigations of TB?

A

1) CXR- cavitation, consolidation, calcification, fibrosis (CCCFUCK)
2) sputum smear for acid fast bacilli and sputum culture
3) NAAT/zeihl neelsen stain and rapid direct microscopy
4) blood test- interferon gamma release assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what test is used to assess relatives of TB?

A

mantoux test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

management of TB + SE for each?

A

Rifampicin (red secretions)
Isoniazid (peripheral neuropathy- give with pyridoxine)
Pyrazinamide (LFT)
Ethambutol (optic neuritis)

RIPE - 2 months
RI - for further 4 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is bronchiectasis?

A

permanent dilation of the airways secondary to chronic infection or inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pathophysiology of bronchiectasis?

A

chronic infection/irritation of airways leads to ongoing inflammation, which causes thickening and dilation of the airways and inability to clear mucous.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of bronchiectasis?

A
childhood respiratory infections 
immunodeficiency 
connective tissue disorders 
asthma 
EAA
TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the most common organisms isolated from patients with bronchiectasis?

A

pseudomonas aeurginosa
Haemophilus influenza
klebsiella spp.
strep. pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

presentation of bronchiectasis?

A
productive chronic cough 
SOB
dyspnoea
haemoptysis 
chest pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

signs of bronchiectasis?

A

coarse inspiratory crackles
large ariway rhonchi
wheeze
clubbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

investigations of bronchiectasis?

A

CXR: tramlines
HRCT: gold standard shows bronchial wall thickening and dilation
spriometry: normal, restrictive or obstructive
sputum microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

management of bronchiectasis?

A

lifestyle intervention
physiotherapy - airway clearance and postural drainage
antibiotics
DO NOT TREAT WITH - corticosteroids, LTRA or mucolytics as no inflammation to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

genetics of CF?

A

autosomal recessive condition

CFTR gene on chromosome 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pathophysiology of CF?

A

failure of chloride channels to transport ions across the epithelial cells, leading to thickened secretions across multiple organs.
lungs- thickened mucopurulent secretions leading to ineffective clearance of bacteria and multiple infections
pancreas- ducts become blocked with secretions leading to pancreatic enzyme deficiency
GI- thickened meconium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the screening programme for CF?

A

all newborns are screened during the heel prick blood spot test (guthrie)
sweat test is suspected in later life - high conc of sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

name 6 diseases that are screened for in the Guthrie heel prick test of a newborn?

A

CF, sickle cell, hypothyroidism, maple syrup urine disease, phenylketonuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

symptoms of CF in infancy?

A

meconium ileus, prolonged neonatal jaundice, failure to thrive, recurrent chest infections, malabsorption, steatorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

symptoms of CF in young child?

A

bronchiectasis, rectal prolapse (due to bulky stools), nasal polyps, recurrent infections, failure to thrive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

symptoms of CF in adolescents/adults?

A

DM, pneumothorax, intestinal obstruction, infertility (absence of vas deferens), pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
signs of CF on examination?
hyperinflation of chest coarse inspiratory crepitations expiratory wheeze finger clubbing
26
investigations of CF?
sweat test genetic testing for CFTR gene CXR spriometry- FEV1 declines steadily with disease progression
27
management of CF?
``` physiotherapy for airway clearance and postural drainage prophylactic antibiotics pancreatic replacement therapy high calorie diet fat soluble vitamin supplements ```
28
most common organisms grown in CF?
pseudomonas aureginosa - most common Hib strep pneumoniae
29
symptoms of pneumonia?
SOB pyrexia purulent cough- rust coloured bronchial breathing
30
signs of pneumonia on examination?
pleural rub | crepitations
31
most common organisms of CAP?
strep pneumoniae haemophilus influenza staph aureus mycoplasma
32
most common organisms of HAP?
pseudomonas aeruginosa | MRSA
33
score used to assess severity of CAP?
CURB-65 ``` C- confusion U-urea > 7 R- RR > 30 B- BP < systolic below 90 or diastolic < 60 65- age > 65 years ``` score of 2 or higher = hospital admission recommended
34
investigations of pneumonia?
``` CXR- consolidation sputum sample - microscopy and culture FBC - ESR, CRP blood cultures pulse oximetry ```
35
management of CAP?
amoxicillin 5 day course | add flucloxacillin if staph aureus is suspected
36
management of HAP?
IV co-amoxiclav or doxycycline if severe switch to ceftriaxone if septic or MRSA suspected switch to vancomycin + ticoplanin
37
symptoms of pneumothorax?
sudden onset SOB + chest pain
38
types of pneumothorax? (2)
primary - pneumothorax occuring in previously fit and well individuals secondary- occuring in patients with pre-existing lung disease
39
management of tension pneumothorax?
emergency insertion of wide bore needle into 2nd and 3rd intercostal space, midclavicular line
40
signs of pneumothorax on examination?
loss of chest sounds over one side hyperpercussion tracheal deviation unilateral reduced chest expansion
41
investigations of pneumothorax?
CXR | ABG- hypoxia
42
management of pneumothorax?
high flow 100% O2 analgesia if <2cm - discharge and review if > 2cm - chest drain and admit
43
where do you place a chest drain for pneumothorax?
triangle of safety- lattisimus dorsi, pectoralis major, nipple line = form a triangle place chest drain in the 5th intercostal space, mid axillary line within the triangle
44
complication of pneumothorax if not treated?
SVC obstruction due to mediastinal shift, causing cardio-respiratory arrest
45
which conditions are restrictive? (7)
``` sarcoidosis ILD EAA pulmonary fibrosis good pastures ARDS mesothelioma ```
46
which conditions are obstructive? (3)
asthma bronchiectasis COPD
47
what is the pattern of restrictive lung disease?
FEV1- reduced FVC- significantly reduced FEV1:FVC - normal or reduced
48
what is the pattern of obstructive lung disease?
FEV1- significantly reduced FVC- reduced or normal FEV1:FVC- reduced
49
symptoms of pulmonary embolism?
pleuritic chest pain dyspnoea haemoptysis DVT symptoms
50
signs of PE?
``` tachycardia tachypnoea raised JVP (can cause RHF) pleural rub crackles pyrexia ```
51
what are the 4 main causes of raised JVP?
heart failure cardiac tamponade fluid overload constrictive pericarditis
52
what vessel is used to assess JVP?
right internal jugular vein
53
risk factors for PE?
``` recent surgery immbolisation active malignancy pregnancy varicose veins px PE IVDU ```
54
investigations of PE?
CXR! two level Wells score if suspected after Wells score - CTPA + VQ scan
55
what score on a wells score indicates PE is likely?
greater than 4
56
what should be done if a PE is suspected, however there is a delay in getting the CTPA?
administer low molecular weight heparin until the scan is performed
57
what should be done is wells score is <4 when a PE is suspected?
arrange a d-dimer test
58
ECG changes in PE?
large S wave in lead I, a large Q wave in lead III, and inverted T wave in lead III (S1Q3T3) RBBB may also be seen
59
management of non massive PE?
LMWH or fondaparinux for at least 5 days | wafarin for at least 3 months if provoked, and at least 6 months if unprovoked
60
management of a massive PE?
thrombolysis (unfractionated heparin)
61
management pathway of DVT?
if score 0-1 -> D-dimer -> if +ve do a venous duplex scan if score 2 or above> venous duplex scan if available -> if not available then d-dimer and treat until available
62
examples of antiplatelets?
aspirin clopidogrel ticagrolor
63
when are antiplatelets mainly used?
heart attack and stroke
64
examples of anticoagulants?
LMWH warfarin fondaparinux
65
when are anticoagulants mainly used?
DVT AF PE
66
what is mesothelioma?
aggressive tumour of the mesothelial cells that occur in the pleura
67
what is the pathophysiology of mesothelioma?
deposition of asbestos fibres in the parenchyma of the lung results in penetration of the visceral pleura. From here the fibre is carried to the pleura surface, causing the formation of aggressive tumours of mesothelial cells
68
presentation of mesothelioma?
``` weight loss SOB clubbing pleural effusion hx of asbestos exposure ```
69
investigation of mesothelioma?
CXR- pleural thickening | pleural CT
70
management of mesothelioma?
symptomatic relief surgical resection chemotherap - platinum based radiotherapy for pain
71
what three physiological processes cause asthma? (3)
1) increased mucous production 2) bronchiole constriction + spasm 3) bronchiole inflammation
72
what is the pathophysiology of asthma?
(Type 1) IgE mediated hypersensitivity reaction where MAST cells and macrophages react to a benign antigen causing the release of histamine and immune response
73
symptoms of asthma?
``` wheeze cough nocturnal variation - worse at night exacerbated by cold weather, air pollutants, spray chest pain ```
74
investigations of asthma?
PEF reduced | obstructive pattern FEV1:FVC < 0.7 for diagnosis
75
management of asthma (chronic)?
1) SABA 2) SABA+ ICS 3) SABA + ICS + LTRA 4) SABA + LABA + ICS 5) SABA + MART +/- LTRA 6) SABA + MART (increase dose) 7) SABA + MART + LRTA + theophylline 8) specialist review
76
management of asthma (Acute)?
``` O2 (high flow) Salbutamol neb Hydrocortisone IV Ipratropium bromide neb Theophyline IV Magnesium sulphate IV salbutamol ```
77
signs of life-threatening asthma attack?
``` PEFR < 33% O2 < 92% silent chest cyanosis bradycardia hypotension exhaustion confusion coma ```
78
what are the three main subtypes of COPD?
emphysema chronic bronchitis chronic asthma
79
pathophysiology of chronic bronchitis?
chronic inflammation of bronchioles (often due to irritant exposure) leads to obstruction of the airway, leading to V/Q mismatch and chronic hypoxia and hypercapnia
80
what are the systemic effects of chronic bronchitis?
1) polycythemia - to compensate for hypoxia 2) shunting of blood away from dead space- RVHF 3) RVHF-> fluid rentention
81
what is the pathophysiology of emphysema?
irritant causes neutrophil recruitment. Neutrophils secrete elastase which breaks down the elastin in the alveolar wall, causing loss of alveolar recoil. This causes air trapping, leading to an increased end expiratory volume causing barrel chest and hypoxia and hypercapnia
82
causes of COPD?
smoking | alpha 1 anti-trypsin deficiency
83
symptoms of COPD?
productive cough dyspnoea wheeze RVHF-> fluid, breathless
84
investigations of COPD?
post-bronchodilator spirometry- shows FEV1:FVC ratio < 70% CXR- hyperinflation, bullae, flat hemidiaphragm FBC ABG ECG
85
first line management of COPD?
smoking cessation | SABA or SAMA
86
second line management of COPD?
if no asthmatic features- LABA + LAMA | if asthmatic features- LABA + ICS
87
which patients with COPD are given LTOT? `
secondary polycythemia peripheral oedema pulmonary HTN
88
which 3 organisms most commonly cause infective exacerbations of COPD?
HiB strep penumorniae moraxella catarrhalis
89
management of infective exacerbation of COPD?
increase frequency of bronchodilator use prednisolone 30mg for 7-14 days oral antibiotics if signs of acute bacterial infection (purulent sputum) (amoxicillin or clarithromycin)
90
where is SCLC located?
central, near main bronchus
91
what is SCLC associated with?
smoking
92
which paraneoplastic syndromes is SCLC associated with?
SIADH Cushings syndrome Lambert-eaton syndrome
93
what is lambert eaton syndrome?
tumour produces antibodies to voltage calcium channels leading to myasthenia type syndrome
94
management of SCLC?
surgical resection if very early disease chemotherapy radiotherapy if ex
95
what are the three types of non-small cell lung cancer?
large cell squamous cell adenocarcinoma
96
where is large cell NSCLC found?
peripherally located
97
what does large cell NSCLC secrete?
b-HCG
98
where is NSCLC adenocarcinoma found?
typically peripheral
99
which type of NSCLC is most common in non-smokers?
adenocarcinoma
100
where is squamous cell NSCLC most commonly found?
typically central
101
what does squamous cell NSCLC secrete?
PTHrP leading to hypercalcaemia
102
symptoms of hypercalcaemia?
``` brittle bones loss of appetite urination and thirst constipation headaches ```
103
which NSCLC form pancoast tumours?
adenocarcinoma and squamous cell
104
what is a carcinoid tumour?
slow growing cancer that secretes serotonin
105
pathophysiology of Goodpastures syndrome?
antibodies are produced against the alveoli and glomeruli basement membranes, which are found in the kidneys are lungs
106
how does Goodpastures commonly present?
``` AKI haemoptysis - due to pulmonary haemorrhage weight loss chest pain nausea and vomiting chills and fever ```
107
investigations of Goodpastures syndrome?
CXR renal biopsy urinalysis ELISA for antibodies
108
pathophysiology of idiopathic pulmonary fibrosis?
normal lung parenchyma is replaced by fibrosed thickened tissue, leading to reduced lung compliance and stiffness, reducing the lungs gas exchange capacity
109
what are the 3 most common drugs to cause idiopathic pulmonary fibrosis?
amiodarone nitrofurantoin cyclophosphamide
110
how does idiopathic pulmonary fibrosis present?
dyspnoea persistent SOB dry cough clubbing
111
investigations of idiopathic pulmonary fibrosis?
CXR- honeycomb appearance + reduced lung volume CT- ground glass appearance reduced TLCO
112
signs of idiopathic pulmonary fibrosis?
bilateral fine end inspiratory crackles | clubbing
113
management of idiopathic pulmonary fibrosis?
symptomatic relief nintedanib - tyrosine kinase inhibitor O2 therapy pulmonary rehab
114
pathophysiology of extrinsic allergic alveolitis?
presence of allergic antigen leads to an exaggerated immune response causing granulomatous inflammation
115
give some examples of EAA?
``` bird fanciers lung cheese workers lung farmers lung hot tub lung malt workers lung ```
116
symptoms of EAA?
``` flu like symptoms pyrexia tight chest malaise fatigue headache arthalgia symptoms appear a few hours after exposure and resolve in a few days ```
117
investigations of EAA?
``` FEV1:FVC- restrictive pattern FBC, ESR/CRP CXR: fibrosis bronchoalveoar lavage: lymphocytosis CT provocation testing ```
118
management of EAA?
oxygen if hypoxic corticosteroids identify and avoid allergen
119
what is the pathopshyiology of sacroidosis?
inflammation causes the formation of non-caseating granulomas with mutlinucleated giant cells
120
presentation of sarcoidosis (from each system)?
``` fever night sweats malaise fatigue lupus pernio uveitis dry cough erythema nodosum derranged LFT bilateral hilar lympahdenopathy ```
121
how to males with sarcdoiosis commonly present?
with hypercalcaemia due to increased secretion of ACE by granulomas
122
investigations of sarcoidosis?
CXR- used for staging spirometry - restrictive pattern serum ACE- raised (especially in males) transbronchial biopsy - non caseating granulomas
123
management of sarcoidosis?
first line- oral glucocorticoids/inhaled corticosteroids second line - methotrexate. cyclophosphamide etc. anti-TNF, monoclonal antibodies third line- lung transplant
124
what is the staging for sarcoidosis?
stage 1: bilateral hilar lymphadenopathy stage 2: bilateral hilar lymphadenopahty + interstitial infiltrates stage 3: diffuse interstitial infiltrates stage 4: diffuse fibrosis
125
what test can be used to diagnose asthma?
bronchodilator challenge- improvement in FEV1 by 15% after administration of bronchodilator
126
what are the stages of severity of COPD?
FEV1 > 80% - mild 50-79% - moderate 30-49% - severe < 30 % - very severe
127
how are the number of pack years calculated?
1 pack year = 20 cigarettes so calculate no. of pack years i.e. - 30 cigarettes is 1.5 pack years multiple 1.5 x no. of years smoked that amount
128
how to manage patients who have chronic lung disease (i.e. copd) and require oxygen?
oxygen titrated via venturi mask - aiming for sats of 88-92%
129
prevalance of CF?
1 in 2500 births
130
what type of respiratory failure is most commonly seen in PE?
type 1 respiratory failure
131
Why does T1 resp failure occur in PE?
V/Q mismatch due to area of reduced perfusion
132
what is the normal range of INR?
2-3
133
investigations for suspected lung cancer?
``` CT scan PET scan bone scan CXR bronchopscopy - take sample ```
134
what conditions are associated with idiopathic pulmonary fibrosis?
SLE systemic sclerosis sjrogrens inflammatory bowel disease
135
Which lung conditions are associated with clubbing?
idiopathic pulmonary fibrosis mesothelioma bronchiectasis
136
what are the risk factors for obstructive sleep apnoea?
large tonsils/adenoids nasal polyps alcohol obesity
137
how is sleep apnoea diagnosed?
Sleep studies
138
management of sleep apnoea?
``` CPAP weight loss avoid alcohol removal of large tonsils sleep upright ```
139
what are some causes of bilateral hilar lymphadenopathy?
sarcoidosis TB bronchial carcinoma lymphoma
140
what are some S/E of long-term steroids?
``` weight gain buffalo hump + moon face skin thinning and easy bruising peptic ulceration cataracts bone density reduction, avascular necrosis of femoral head muscle wasting psychosis + emotional lability ```
141
what commonly causes transudate effusions?
cardiac failure liver failure/cirrhosis renal failure -> aka. bodies own fluid pulmonary embolism
142
what commonly causes exudate effusions?
infection inflammation malignancy
143
what is the criteria for exudate and transudate?
exudate > 30g of protein (high) transudate < 30g of protein (low) exudate > 0.6 LDH (high) transudate < 0.6 (low)
144
management of recurrent pleural effusions?
pleurodesis + talc or bleomycin installation of an irritant such as talc causes inflammation and adherence of the pleura to the pleural wall, preventing separation and accumulation of fluid