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viva Flashcards

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1
Q

what is pneumonia?

A

inflammation of the lung parenchyma associated with the alveoli filling with exudate.
caused by bacterial/viral/fungal infection which triggers an immune system response leading to the alveoli being filled with fluid and pus

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2
Q

what are the main symptoms of pnuemonia?

A

hypoxaemia / SOB due to V/Q mismatch
consolidation
cough
pleuritic chest pain
infection - fever, weightloss
inflammation - leaky capillaries, haemoptysis

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3
Q

pneumonia auscultation

A

bronchial breath sounds (loud, harsh, inspiration = expiration, pause between inspiration and expiration)
Early or dry stage → may hear fine crackles as alveoli collapse and reopen.
Later/resolving stage (with sputum) → may hear coarse crackles due to mucus in airways.

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4
Q

pneumonia x ray

A

consolidation - white patchy areas

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5
Q

complications of pneumonia

A

respiratory failure
pleural effusion / empyema

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6
Q

treatments for pneumonia

A

Oxygen therapy
antibiotics if bacterial
analgesics for pain
ACBT for sputum

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7
Q

what is asthma?

A

Asthma is an allergic inflammatory disease of the airways that causes reversible airway narrowing. atopic and non atopic.
airway obstruction / reduced airflow due to mucosal oedema, bronchoconstriction and secretions in airway lumen

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8
Q

what is atopic asthma?

A

atopic - a genetic susceptibility to produce IgE directed towards common environmental allergens (house dust mites, animal proteins, funghi). IgE sensitises and activates mast cells causing a powerful inflammatory reaction

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9
Q

what is non atopic asthma?

A

imbalance of PNS and SNS responses in the airways. later in adult life. release of acetocholine by PNS causes bronchoconstriction and SNS stimulates mast cells producing inflammatory response

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10
Q

symptoms of asthma

A

chest tightness
cough
air trapping -> reduced compliance -> increased WOB and SOB + V/Q mismatch

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11
Q

auscultation - asthma

A

widespread expiratory polyphonic wheeze as air pushed through narrowed airways

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12
Q

treatment - asthma

A

inhalers - SABAs and LABAs (bronchodilators)
steroids - decreases inflammatory response
combined
PEFM diary
positioning
ACBT
education
exercise
oxygen if hypoxic

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13
Q

what is COPD?

A

a disease state characterised by airflow obstruction resulting from chronic bronchitis and/or emphysema. irreversible damage to airways

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14
Q

what is chronic bronchitis?

A

persistent cough with sputum production for at least 3 months of the year for 2 consecutive years
repeated inhalation of pollutants (usually cigarette smoke) causes irritation of the airway mucosa, hypertrophy and hyperplasia of the mucus glands leading to excessing mucus in the airways
airway narrowing due to mucosal oedema, smooth muscle hypertrophy and peribronchial fibrosis
reduced ciliary function, retained secretions, chest infections

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15
Q

what is emphysema?

A

the permanent enlargement of the air spaces distal to the terminal bronchiole
protein breakdown of elastic -> erosion of alveolar septa -> dilation of distal air spaces (bullae) -> destruction of elastic fibres
less radial tracation in the lung parenchyma -> floppy airways that close on expiration -> gas trapping and hyperinflation
smoking is the main cause but can be genetic - alpha 1 antitrypsin deficiency

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16
Q

symptoms of COPD

A

cough
breathlessness
retained secretions -> chest inflections
air trapping -> hyperinflation -> reduced compliance -> increased WOB, SOB, VQ mismatch

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17
Q

auscultation - emphysema

A

decreased breath sounds (reduced airflow due to air trapping)
wheezing (airway narrowing)

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18
Q

auscultation - chronic bronchitis

A

coarse crackles

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19
Q

spirometry - COPD

A

fev1/fvc < 0.7
fev1 60-80% mild, 40-60% moderate, <40% severe

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20
Q

emphysema x ray

A

bullae
hyperinflation

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21
Q

complications of COPD

A

cor pulmanole
respiratory failure
hypercapnic + high O2 -> reversal of HPVC, the haldane effect, loss of hypoxic drive

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22
Q

management of COPD

A

bronchodilators (SAMAs and LAMAs)
steroids
oxygen in hypoxic
education (inhalers, smoking cessation)
breathlessness management
ACBT if sputum
pulmonary rehab

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23
Q

what is cystic fibrosis?

A

inherited disease of the exocrine glands caused by a genetic defect on chromosome 7 and a mutation in the cystic fibrosis transmembrane regulator gene.
CTFR acts as a chloride channel in airway epithelial cells. decreased secretions of chloride and water by the airway epithelial cells resulting in thick, sticky, dehydrated intraluminal mucus
predominantly upper lobes
mucus is difficult to clear -> bronchiectatic changes and frequent chest infections can lead to fibrosis

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24
Q

clinical features CF

A

chest infections
cough
bronchiectasis (inflammation and infection)
fibrosis (chronic inflammation)
airway resistance -> air trapping and hyperinflation -> reduced compliance -> increased WOB and SOB and V/Q mismatch

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25
complications of CF
cor pulmanole pneumothorax pneumonia (infection) atelectasis (plugging)
26
auscultation - CF
coarse crackles if fibrosis, fine inspiratory crackles
27
management CF
antibiotics DNASE - breaks down sputum to make it less sticky hypertonic saline - draws water into airway to facilitate sputum clearance inhaled mannitol - draws water into airway (if DNASE and saline dont work) oxygen dietician (pancreatic malabsorption) ACBT awareness of normal sputum exercise but not group (cross infection)
28
what is DMD?
inherited NMD in males gradual loss of muscle fibres and those fibres are replaced with fat and connectiev tissue wheelchair bound by 12 affect respiratory muscles so cant take a deep breath in - restrictive
29
what is GBS?
mistargetted immune response. attacks the peripheral nerves leading to rapid onset muscle weakness and paralysis. starts distal, progresses proximal often following a viral / bacterial infection potential for complete recovery. treated with immunoglobulin therapy
30
what is MND?
progressive NMD that attacks the upper and lower motor neurones leads to muscle weakness and wasting, functional loss of mobility, difficulties with speech, swallowing and breathing starts in hands and feet. unknown cause. mean age 58. more men mean duration of survival 3-4 years
31
clinical features of NMD?
weak insp muscles -> poor chest expansion -> hypoventilation -> increased CO2 reduced ability to cough and clear mucus (weak exp muscles) weak bulbar muscles -> difficulty swallowing -> aspiration risk
32
complicaitions of NMD
pneumonia (retained secretions, infection) atelectasis (blocked airways, lung collapse) respiratory failure
33
auscultation NMD
reduced breath sounds - weak insp effort crackles if sputum
34
management of NMD
ACBT, focus on LTEEs, manual techniques + assisted cough IPPB non invasive ventilation for acute exacerbations long term nocturnal ventilation to improve survival and QoL intubation and ventilation if reversible (GBS) - rests respiratory musles and allows for spontaneous recovery
35
what is interstitial pulmonary fibrosis?
progressive fibrotic disorder of the lungs. unknown aetiology but risk factors include cigarette smoke, infections, environmental pollutants scarring of the lung interstitum -> stiff and non compliant lungs non specific insults to the epithelia barrier and lung parenchyma -> growth factors secreted, firboblasts recruited and differentiate into myofibroblasts, secrete collagen, thickening of alveolar walls adults > 40, males > females, mean survival time 2.5-3.5 yrs
36
clinical features of IPF
breathlessness increased WOB non productive cough hypoxaemic - finger clubbing
37
auscultation - IPF
fine inspiratory crackles
38
chest xray - IPF
honeycomb
39
management - IPF
no consensus for medical management pulmonary rehab - breathlessness and QoL breathlessness management long term oxygen therapy lung transplant
40
what is bronchiectasis?
chronic disease of one or more airways leading to the destruction of bronchial wall, cartilage, blood vessels, elastic tissue and smooth muscle components destruction of bronchial wall -> widening of airways -> impaired mucociliary clearance -> accumulation of mucus -> chest infections -> further inflammation and damage caused by TB, measles, whooping cough, CF, primary ciliary dyskinesia, immune deficiencies, obstruction (tumour), allergic bronchopulmonary aspergillosis
41
clinical features - bronchiectasis
persistent, often productive cough haemoptysis breathlessness finger clubbing chest pain (infection causing pleuritic or MSK from coughing)
42
diagnosis of bronchiectasis
CT scan
43
auscultation of bronchiectasis
crackles
44
management of bronchiectasis
breathlessness monitoring sputum pulmonary rehab antibiotics for infection bronchodilators + steroids lobectomy / lung transplant
45
what is tuberculosis?
bacterial infection (mycobacterium tuberculosis) that mainly involves the lungs but may spread to other organs (lymph nodes, kidney, liver, bones) transferred by breathing in air droplets may stay dormant in the lungs for years can be parenchymal, pleural or miliary risk factors - weakened immune system e.g. HIV, chemotherapy, homelessness (poor environment and nutrition)
46
clinical features TB
finger clubbing (advanced disease) enlarged/tender lymph nodes pleural effusion productive / non productive cough (normally non productive) haemoptysis sweats, fatigue, fever, unintentional weight loss chest pain
47
auscultation - TB
crackles
48
treatment TB
antibiotics (normally combo of 4 drugs) ACBT breathlessness management pulmonary rehab
49
what do you need for intercostal drain?
unobstructed tube one way mechanism (such as water seal) a collecting container below chest level
50
what does bubbling mean?
drainage of air
51
fluid level swinging with respiration mean
air leak
52
what does a sudden change in volume suggest?
haemmorhage (excessive bleeding)
53
what do you do if the ICD falls out
cover with glove and sterile gauze ASAP to prevent lung collapse
54
when do you remove ICD
no bubbling of air no swinging of fluid level lung inflated on xray no change in lung volume with ICD clamped 24 hrs
55
whats the additional management you would do for a patient that has had an ICD?
shoulder ROM
56
whats a thoracotomy and where?
lung incision, usually at the back between ribs
57
what is a sternoctomy and where?
heart surgery incision, down the middle of the sternum
58
what is a laprotomy and where?
abdomen surgery
59
why are positions of ease used for breathlessness?
moves abdominal contents so the anterior portion of the diaphragm is raised. optimises the lenght tension status of the diaphragm
60
what is the purpose of breathing control
promotes relaxation and prevents hyperventilation
61
wheres optimally ventilated and why?
dependent lung - highest are too expanded, top of compliance curve, lowest are squished so have more potential to expand
62
wheres optimally perfused and why?
zone 3 zone 1 and 2 large alveolar pressure, compressed capillaries zone 4 weight of lung on diaphragm compresses and reduces perfusion
63
why do we want to get patients mobilised after surgery?
encourage deeper breaths and increase tidal volume movement improves V/Q matching
64
why do we get patients upright after surgery?
abdominal contents move down allowing diaphragm to descend more on inspiration increasing tidal volume
65
how do we choose patients position
maximise V/Q relieve breathlessness assist drainage of secretions
66
what is CPAP
medical therapy if oxygen therapy is ineffective used for type 1 respiratory failure provides positive end expiratory pressure throughout inspiration and expiration. increases FRC, recruits alveoli. splints them open, stops them collapsing down increases lung compliance, reduces WOB increased surface area for gas exchange
67
why not CPAP for type 2 respiratory failure
need to increase tidal volume to remove CO2
68
what do TEEs do?
increase lung volume above tidal volume, recruits collateral channels, enhances interdependence to help move secretions
69
what does the FET do?
dynamic compression of airways to facilitate movement of bronchial secretions towards the mouth
70
what do vibrations/shaking do?
performed through the expiration phase of LTEEs increases expiratory flow rate and sheer mucus off airway walls
71
what does OPEP do?
increases end expiratory lung volumes, reducing airway resistance and small airway closure recruits collateral channels and allows air to flow behind sputum plugs facilitating secretion movement hgih frequency oscillations create airway vibrations that mobilise excess secretions reduces sputum viscoelasticity
72
how does the acapella work?
uses counterweighted rocker and magnet
73
how to you use an acapella?
breathe in through nose, out thorugh acapella. 4-8 quite deep inspirations with hold, one maximal inspiration with hold followed by forced expiration through acapella. follow with huff/cough if necessary
74
what is IPPB
provides a positive inspiratory pressure, triggered by a small breath from the patient increases tidal volume, decreases WOB (offloads respiratory muscles) aids sputum clearance - gets under sputum plugs via collateral channels and interdependence
75
what are the settings on IPPB?
sensitivity - how easily a patient can trigger a breath flow rate - how fast the air is delivered pressure - max pressure the machine delivers during inspiration
76
what is an assisted cough
application of compressive force replaces the work of the expiratory muscles. timing is crucial
77
dysfucntional breathing management
diaphragmatic breathing control compensatory breath holds after sighing / yawning to allow CO2 to rise rescue techniques - hand over mouth breathing to rebreathe CO2, rest positions, fan on face to reduce RR, speech management, exercise
78
what is pulmonary rehab
Six to eight weeks of group-based twice weekly supervised exercise and education sessions and one additional unsupervised exercise session
79
why would you use a venturi mask?
fixed performance device - you know exactly how much oxygen you are giving and it gives a high flow rate which is good for breathless patients

Respiratory (14 decks)

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