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(SG) Phase 2A lectures > resp > Flashcards

resp Flashcards

1
Q 
21 y/o male
normally fit n well
dry cough
breathless
no chest pain
looks blue

possible diagnoses?
any other info needed?

A 
asthma
pneumonia
pulmonary embolism
pneumothorax
heart failure
  • full Hx
  • explore in depth (onset, timing, variation, severity, exacerbating/relieving, associated symptoms)
  • PMH, FH, DH
  • SH (occupation, travel)
  • exam findings
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2
Q

list some lung function tests

A

spirometry
lung volumes
transfer factor (lol tf is this?)
mouth pressures ?

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3
Q

list some radiological tests for resp

A

plain XR

CT

US

CMR/MRPA

ventilation/perfusion scan

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4
Q

what are some other resp tests?

A

objective assessment of function

bronchoscopy

thoracoscopy

oximetry

transcutaneous CO2 monitor

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5
Q

what is spirometry?

A

common office test used to assess how well your lungs work by measuring how much air you inhale/exhale and how quickly you exhale

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6
Q

what is the transfer factor test?

A

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

1 of the most clinically valuable tests of lung function …

measures the ability of the lungs to transfer gas from inhaled air to the RBC in pulmonary capillaries !

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7
Q

what is a CMR?

A

cardiovascular magnetic resonance (CMR) scan

gives us info on the structure of your heart and BV & how well they’re working

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8
Q

what is MRPA?

A

magnetic reasoning pulmonary angiography

2nd line to CTPA

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9
Q

what is CTPA?

A

CT pulmonary angiography

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10
Q

what is thoracoscopy?

A

medical procedure involving internal exam, biopsy, and/or resection of disease or masses within the pleural/thoracic cavity

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11
Q

define T1 resp failure ! LOL :)

A

low PaO2

normal/low PaCO2

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12
Q

define T2 resp failure

A

low PaO2

high PaCO2

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13
Q

what is common btwn t1 and t2 resp failure

A

both have low PaO2

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14
Q

what is the diff btwn t1/t2 resp failure

A

t1 is normal/low co2

t2 is high co2

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15
Q

what is PAO2?

A

ALVEOLAR O2

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16
Q

what is PaO2?

A

arterial O2

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17
Q

is PAO2 higher usually or PaO2?

A

PAO2

bc PaO2 is closer to mixed venous air than it is to inspired

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18
Q

what is the alveolar-arterial gradient normally?

A

less than 2 kPa

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19
Q

list some causes of a raised A-a gradient (alveolar-arterial) gradient

A

hypoventilation

v/q mismatch

anaemia

diffusion limitation

shunt (R-L or L-R)

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20
Q

how do u calculate PAO2?

A

≈ FiO2(PATM – pH2O) – (PaCO2/RER)

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21
Q

if there’s a normal gradient but low PaO2 what does this mean?

A

PAO2 must be low

hypoventilation

reduced FiO2 (or PATM)

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22
Q

what is ambient hypoxia

A

eg at altitude

NB: ambient = relating to the immediate surroundings of something

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23
Q

what can ambient hypoxia lead to?

A

widespread HPV

increasing pulmonary artery pressure

can (rarely) lead to pulmonary oedema

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24
Q

when does high altitude pulmonary oedema happen?

A

2-3d after ascent

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25
Q

how do u treat high altitude pulmonary oedema

A

descent

oxygen

pulmonary vasodilaotors

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26
Q

where does gas exchange begin?

bronchi, terminal bronchioles, respiratory bronchioles, alveolar ducts OR alveoli?

A

respiratory bronchioles

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27
Q

what is the path of air from trachea to alveoli?

A

trachea

main bronchus

segmental bronchus

bronchioles

terminal bronchioles

respiratory bronchioles

?alveolar ducts

?alveoli

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28
Q

list 5 functions of the lungs

A

gas exchange

acid-base balance

defence

hormones

heat exchange

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29
Q

what are diff aspects of the defence mechanisms in the lung?

A 
mucosal barrier
mast cells
macrophages
mucociliary clearance
cough reflex
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30
Q

what kind of a disease is CF

A

single gene

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31
Q

what is the commonest monogenic recessive disorder

A

cystic fibrosis

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32
Q

what happens in CF? (6)

A

abnormal ion transport (Cl-)

impaired mucociliary clearance

recurrent and chronicinfections

impaired digestion

fertility problems

liver disease, diabetes

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33
Q

if FEV1/FVC ratio is < 0.7 (70%)

what is it? obstructive or restrictive?

A

obstructive

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34
Q

if FEV1/FVC ratio is <0.8

what is it? obstructive or restrictive?

A

restrictive

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35
Q

if there is an airways problem, is it obstructive or restrictive?

what is the FEV1/FVC ratio?

A

obstructive

FEV1/FVC ratio <0.7

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36
Q

what is lung parenchyma?

A

portion of the lung involved in gas transfer

  1. the alveoli
  2. alveolar ducts
  3. respiratory bronchioles
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37
Q

if there’s a problem w the lung parenchyma (alveoli/ducts/resp bronchioles) is it restrictive or obstructive?

what is the FEV1/FVC ratio?

A

restrictive

FEV1/FVC ratio normal

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38
Q

if there’s a problem with the chest wall/pleura is it restrictive or obstructive?

A

restrictive

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39
Q

what is transfer factor aka

A

diffusing capacity

test that looks at eg if u breathe CO, how well it is perfused and so acts as a surrogate for oxygen

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40
Q

what happens with low (transfer factor) TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

thickening of the alveolar-capillary membrane

reduced lung volumes

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41
Q

what happens with high (transfer factor) TLCO

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

increased capillary blood volume

pulmonary haemorrhage

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42
Q

which, nearly always, reduces (transfer factor) TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

COPD

pulmonary fibrosis

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43
Q

does COPD reduce TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

yes

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44
Q

does polcythaemia reduce TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

no

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45
Q

does pulmonary fibrosis reduce TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

yes

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46
Q

does asthma reduce TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

no

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47
Q

does L-R inracardiac shunt reduce TLCO?

a test of the diffusing capacity of the lungs for CO (DLCO, also known as transfer factor for carbon monoxide or TLCO)

A

no

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48
Q

what is interstitial lung disease?

A

an umbrella term for a large group of disorders that cause scarring (fibrosis) of the lungs

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49
Q

what is sarcoidosis a part of?

A

interstitial lung disease (which is an umbrella term)

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50
Q

what are some causes of breathlessness?

A

mechanical interference

weakness of resp pump

increased resp drive

increased wasted ventilation

psychological dysfunction

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51
Q

what is dyspnea

A

SOB

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52
Q

list some examples of mechanical interference with ventilation (which can lead to SOB)?

A

obstruction to airflow

resistance to expansion of lungs (stiff lungs)

resistance to expansion of chest wall/diaphragm

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53
Q

asthma, emphysema, bronchitis

what can they lead to?

A

obstruction to airflow

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54
Q

fibrosis, LVF …

what can they lead to?

A

stiff lungs / resistance to expansion of lungs

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55
Q

pleural sickening, obesity, abdo mass …

what can they lead to?

A

resistance to expansion of chest wall/diaphragm

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56
Q

hypoxemia can lead to what?

metabolic acidosis can lead to what?

decreased cardiac output can lead to what?

A

increased respiratory drive

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57
Q

list some examples of things that may cause increased resp drive which can lead to SOB?

A

hypoxaemia

metabolic acidosis (renal disease, anaemia etC)

decreased CO

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58
Q

what can contribute to increased wasted ventilation

what might this result in?

A

capillary destruction eg emphysema/interstitial lung disease

large-vessel obstruction eg pulmonary emboli

SOB

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59
Q

what can contribute to increased wasted ventilation

what might this result in?

A

capillary destruction eg emphysema/interstitial lung disease

large-vessel obstruction eg pulmonary emboli

SOB

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60
Q

what can cause capillary destruction? what can this lead to?

A

emphysema, interstitial lung disease etc

causes increased wasted ventilation

which then can cause SOB

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61
Q

what is somatisation?

A

the manifestation of psychological distress by the presentation of physical symptoms

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62
Q

what are the 3 ways in which u can categorise lung disease?

A
  1. infection
  2. inflammation
  3. cancer
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63
Q

what does mouth pressure look at?

A

resp muscle weakness

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64
Q

if ur looking for a blood clot, what type of scan do u do?

A

CTPA

(CT pulmonary angiogram)

looks at pulmonary arteries

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65
Q

if ur looking for pleural fluid in the chest, what type of scan might u do?

A

ultrasound

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66
Q

if ppl have chronic pul hypertension, what are some tests used?

A

CMR

MRPA

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67
Q

what is an objective measure of SOB?

A

objective assessment of function

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68
Q

what are some practical non-radioactive procedureS?

A

bronchoscopy

thoracoscopy

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69
Q

if ur hypoventilating, what is co2 like?

A

normal or high

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70
Q

does anaemia affect oxygen tension?

A

no

but it does matter how much oxygen ur blood can take in total (capacity)

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71
Q

what is V/Q mismatch?

A

effectively R-L shunting

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72
Q

will a L-R shunt cause raised A-a gradient?

A

no, bc ur shunting oxygen in ur blood through ur lungs

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73
Q

what happens in asthma? (5)

A

increased irritability of bronchi causing spasm

paroxysmal attacks

overdistended lungs

mucus plugs in bronchi

enlarged bronchial mucous glands with excess secretions

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74
Q

what are the 2 broad clinical categories of asthma?

A

extrinsic and intrinsic

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75
Q

what are the 2+ types of extrinsic asthma

A

atopic = IgE/t1 hypersensitivity

occupational = t2 hypersensitivity

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76
Q

what is the barometric pressure like at high altitude?

A

lower

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77
Q

what is the PO2 like at high altitude (4000m) compared to sea-level?

A

≈60%

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78
Q

which of these is a well-recognised response to hypoxia?

a) bradycardia
b) atrial fibrillation
c) systemic vasoconstriction
d) pulmonary vasoconstriction
e) syncope

A

d) pulmonary vasoconstriction

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79
Q

if ur hypoxic, what happens systemically?

A

vasodilation

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80
Q

if ur hypoxic, what happens with pulmonary vessels?

A

vasoconstrict

so oxygen delivery is matched w/ oxygenation of alveoli

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81
Q

at high altitude, what do pulmonary vessels do?

A

vasoconstrict

has implications eg high altitude pulmonary oedema

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82
Q

WILL HIGH ALTITUDE PULMONARY OEDEMA COME UP ON THE EXAM

A

APPARENTLY NOT

“this will not come up in ur exam”

according to the lecturer

so I really wasted my time writing this huh

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83
Q

where does gas exchange begin?

A

respiratory bronchioles

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84
Q

what is the diff btwn small and large airways

A

small <2mm

large >2mm

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85
Q

what constitutes large airways?

>2mm

A

trachea
bronchi
bronchioles

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86
Q

what constitutes small airways?

<2mm

A

terminal bronchioles
resp bronchioles
alveolar ducts
alveolar sacs

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87
Q

what is the conducting zone of the resp pathway

A

trachea-bronchi-bronchioles-terminal bronchioles

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88
Q

what is the transitional and resp zone of the resp pathway

A

resp bronchioles-alveolar ducts-alveolar sacs

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89
Q

what breaks a breath hold?

A

raised CO2 in CSF!

central chemoreceptors sensing CO2 which diffuses readily across BBB and lowers CSF pH

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90
Q

which chemoreceptors respond to raised CO2 in CSF? central or peripheral?

A

central

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91
Q

what are central chemoreceptors sensitive to?

A

the pH of their environment

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92
Q

where are chemoreceptors OF THE CV system located?

A

carotid bodies

aortic bodies

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93
Q

where are carotid bodies located?

A

in carotid arteries than run through neck to brain

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94
Q

where are aortic bodies found?

A

aortic arch

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95
Q

what is an aortic body?

A

1 of several small clusters of peripheral chemoreceptors located along aortic arch

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96
Q

what are peripheral chemoreceptors?

A

extensions of PNS

repsond to changes in blood molecule conc (oxygen/CO2)

help maintain cardio-rest homeostasis

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97
Q

what is the diff btwn central and peripheral chemoreceptors

A

central - medullary chemoreceptors

peripheral - systemic arterial chemoreceptors in carotid/aortic bodies

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98
Q

why are central (medullary) chemoreceptors important?

A

mediate response to a rise in PaCO2

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99
Q

why are peripheral (arterial) chemoreceptors important?

A

essential for response to hypoxia/drop in blood pH (acidosis)

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100
Q

why are the lungs defence organs?

A

bc we inhale a lot of shit

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101
Q

what is the key genetic resp disorder?

A

CF

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102
Q

“CF IS IMPORTANT, MAY GET QUESTIONS ON IT IN THE EXAM”

A

…..hmmmmmmmm

remember to read over it!!!

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103
Q

what does the Bradford hill criteria look at?

A

causation

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104
Q

what does reduced FEV mean

A

reduction in amount of gas breathed out in a second

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105
Q

what is 1 of the key measures for obstructive lung disease

A

FEV

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106
Q

what does obstruction mean?

A

difficult to get air out

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107
Q

what does restriction mean?

A

difficult to get air in and out

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108
Q

wait…. what is TLCO again?

A

transfer factor bro

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109
Q

“bronchiectasis will probs come up in the context of infection”

A

LOOOOOL

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110
Q

what is the commonest site of infection

A

resp tract

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111
Q

approx how many resp tract infections do children/adults have ?

A

children: 2-5
adults: 1-2

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112
Q

define tonsilitis

A

infection of the tonsils

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113
Q

what is a sore throat aka

A

pharyngitis

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114
Q

what is inflammation of the trachea (spell it right too smh)

A

tracheitis

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115
Q

what is laryngitis

A

infection of the larynx

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116
Q

what is bronchiolitis

A

infection of small airways - bronchioles

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117
Q

what is inflammation of the pleura termed?

its often caused by an infection

A

pleurisy

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118
Q

what is bronchitis?

A

infection of large airways - bronchi

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119
Q

what is pneumonia?

A

infection of the alveoli and surroundinglung

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120
Q

the skin keeps everything in apart from what?

A

sweat

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121
Q

what is the urine systems defences against infection?

A

its sterile

urine flow is outwards

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122
Q

why are lungs prone to infection?

A

bc we need a v thin membrane for gas transfer

so there’s not much space for barriers or immune system or commensals

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123
Q

what are the sinuses like ?

A

sterile

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124
Q

what do u have in the upper resp tract?

A

commensal flora

help to some extent

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125
Q

20% of us can be colonised by what? in the resp tract

A

S aureus

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126
Q

u can be colonised in a way that’s not harmful to u, but can be harmful to others

A

:/ upper RT to 1 person can be meningitis in the next person

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127
Q

how are pathogens cleared via swallowing?

A

normal swallowing reflex, epiglottis

neuro (timing) and anatomical factors

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128
Q

what is vital abt lung anatomy?

A

ciliated epithelium (mucociliary escalator)

mucus

goblet cells btwn ciliated cells - prod mucus

cilia helps waft everything upwards into trachea, throat, cough/swallow etc

constantly clearing out gunk

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129
Q

deep down into final terminal acinus/alveoli .. what are the humeral n cellular factors?

A

soluble factors: Ig’s, defensives, collectins

alveolar macrophages (1st responders, security guards) keeping a look out

B & T cells

neutrophils if required

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130
Q

what makes u more susceptible to resp infection?

A

swallowing can be affected by stroke/MND, surgery etc

altered lung physiology may be caused by CF, emphysema, bronchiectasis etc

OR extrinsic stuff like near problems, obesity, surgery

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131
Q

what is pneumonia?

A

infection that inflames the air sacs in one or both lungs.

air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing.

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132
Q

if a pt has suspected pneumonia, what else do u look at?

A

How sick is the patient?

Should they be managed in hospital?

Does the patient need antimicrobials?

Is there an alternative diagnosis;
Heart failure
Pulmonary embolus
Cancer
TB
Interstitial lung disease
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133
Q

what are DD for pneumonia?

A 
HF
pulmonar embolus
cancer
TB
interstitial lung disease
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134
Q

what is hop avg for pneumonia

A

6-8 days

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135
Q

who’s at risk of pneumonia?

A

infants/elderly

COPD, other chronic lung

immunocompromised

nursing home residents

diabetes

congestive heart disease

alcohol/IVDU

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136
Q

what are symptoms of pneumonia?

A

fevers
sweats
rigors

(basically generic infection response)

cough, sputum

SOB

may get pleuritic chest pain (worse on deep breathing)

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137
Q

any sensation from inside lungs .. not pain .. feels like irritation - cough

lining of lung has nerve endings so can localise pain

hence pleuritic pain!

A

:)

hurts patient to take a big breath

don’t wanna cough, can’t aerate lungs

PAIN CONTROL IS V IMPORTANT IN PNEUMONIA TO HELP PPL GET BETTER!

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138
Q

what are some signs of pneumonia?

A

abnormal vital signs:

raised HR, raised RR
low BP
fever
dehydration

signs of lung consolidation:

  • dull to percussion
  • decreased air entry
  • bronchial breath sounds
  • ± hypoxia
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139
Q

what are some investigations for pneumonia?

A

CXR

FBC (WBC - marker of severity, diagnosis)

biochem (U&E, LFTs)

CRP (for diagnosis)

pulse oximetry (severity, if required, ABG for failure)

microbio tests

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140
Q

always check for what with pneumonia patients?

A

HIV

pneumonia is common in HIV patients

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141
Q

what are some indicators of pneumonia severitY?

A

Delerium = Confusion

Renal impairment = Urea rise

Increased oxygen demand -
Respiratory rate high

BP drop

????SEPSIS!

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142
Q

who is sepsis more likely in

A

those who’s physiology already impaired by age or comorbidity

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143
Q

what is CURB65?

A

mnemonic for pneumonia that predicts mortality!!!!! (higher score is higher mortality)

C - confusion
U - urea ≥7mmol/L is bad
R - resp rate ≥30/min
B - BP; low
A - age ≥65
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144
Q

generally, if someones sick?

A

broad spectrum

IV

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145
Q

what are disadvantages of using a multiple-AB (nuclear missile approach)

A

promotes AB resistance

side effects

AB associated diarrhoea etc

expensive

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146
Q

what are disadvantages/adv of using a “sniper” single, small AB approach?

A

Might miss

More tolerable

Saves other choices

Cheaper

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147
Q

what is the most common cause of pneumonia?

A

Streptococcus pneumoniae (40%)

also mycoplasma pneumonia (≈10% that peaks in epidemic seasons)

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148
Q

how do u treat S. pneumoniae

A

beta-lactam ABs; amoxicillin

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149
Q

if TB is suggestive, consider what?

A

acid fast bacilli stain

culture for TB

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150
Q

what is TB?

A

bacterial infection

spread through inhaling tiny droplets from the coughs/sneezes of an infected person.

mainly affects the lungs. but can affect any part of the body, including the glands/bones/NS

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151
Q

what is TB caused by

A

mycobacterium tuberculosis (MTB)

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152
Q

when are lung abscesses seen?

A

in aspiration

alcoholics often :(

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153
Q

how do u treat lung abscesses

A

prolonged ABs - for up to 6 weeks

may need surgical drainage

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154
Q

what is the diff btwn HAP and CAP

A

hospital acquired pneumonia

community acquired CAP

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155
Q

what is HAP

A

hosp acquired pneumonia

acquired min 48h after hosp admission
(elderly, post op etc)

diagnosis: new fever, new radiological findings, CRP incr, increasing oxygen requirements)

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156
Q

what is the gen principle for treatment for HAP?

A

‘start broad’

then ‘focus’ treatment

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157
Q

what happens in bronchiolitis?

A

inflammation of bronchioles/mucus production

causes airway obstruction

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158
Q

what are examples of sore throats

A

pharyngitis

tonsilitis

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159
Q

what are examples of a common cold

A

rhinitis

sinusitis

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160
Q

in healthy adults, w/ bronchitis, is bacteria often a cause?

A

nah, its rarely a cause in healthy adults

majority are viral, as those causing other infections of upper airways

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161
Q

what are some clinical features of bronchitis?

A

cough
SOB, wheeze
fever

systemic features of infection unusual - suggest flu/pneumonia

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162
Q

what are some investigations for bronchitis?

A

CVR to exclude pneumonia, usually normal

viral/bac throat swabs

serology 4 mycoplasma, chlamydia

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163
Q

what is the treatment for bronchitis?

A

none usually, bc its viral

little evidence for antimicrobials being helpful

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164
Q

what happens in asthma, pathology wise

A

bronchial obstruction

mucus plugging of bronchi

bronchial inflammation

bronchial wall smooth muscle hypertrophy

thickening of bronchial BM

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165
Q

what is intrinsic asthma associated with

A

recurrent chest infections

chronic bronchitis

not immune-mediated

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166
Q

what is the mechanism for aspirin induced asthma?

A

unknown

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167
Q

what is occupational asthma caused by?

A

work-associated inhaled agent

acts as either a non-specific stimulus

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168
Q

what can acute chronic localised obstruction progress to

A

bronchiectasis

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169
Q

what is classical for chronic obstruction?

A

centred on bronchi/bronchioles

‘obstructive’ pulmonary function tests

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170
Q

what happens in chronic bronchitis

A

productive cough for 3m in 2 consecutive years

mucus hyper secretion - bronchial mucous gland hypertrophy

tobacco smoking-induced mainly

some asthma effects

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171
Q

who does chronic bronchitis tend to affect

A

middle aged heavy smokers

some following chronic pollution

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172
Q

how does chronic bronchitis progress

A

often starts mild

severe;:

hypercapnia
hypoxaemia
cyanosis (blue bloaters)
coexisting emphysema (pink puffers)

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173
Q

what does blue bloater refer to?

A

generalised term referring to a person who is blue and overweight.

usually SOB and chronic cough.

old term - now recognised as severe chronic BRONCHITIS

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174
Q

what does pink puffer refer to?

A

generalized term for a person who is thin, breathing fast and is pink.

usually SOB and pursed lip breathing

old term - now recognised as as severe EMPHYSEMA

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175
Q

what happens in emphysema

A

alveolar airspaces enlarge

destruction of elastin in walls

frequent association with chronic bronchitis

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176
Q

what is emphysema?

A

permanent enlargement of airspaces distal to terminal bronchioles due to destruction of walls

(linked w cig smoking)

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177
Q

what is a major cause of cig smoking?

A

emphysema

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178
Q

what is emphysema a type of?

A

COPD

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179
Q

what happens in emphysema over time?

A

air sacs weaken and rupture - creating larger air spaces instead of many small ones.

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180
Q

what proportion of lung capacity is destroyed before symptoms of emphysema

A

1/3

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181
Q

what are clinical features of ‘pure’ emphysema

A

reduced PaCO2
normal PaO2
at rest
(due to overventilation - pink puffers)

also:

  • weight loss bc metabolic demands
  • RHF
  • overinflated chest
  • poor O2 delivery to tissues
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182
Q

define bronchiectasis

A

permanent dilatation of bronchi/bronchioles

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183
Q

what is permanent dilatation of bronchi/bronchioles termed?

A

bronchiectasis

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184
Q

which lung lobes are usually affected by bronchiectasis?

A

lower

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185
Q

what are symptoms of bronchiectasis

A

chronic cough

large quantities of foul-smelling sputum

flecked with blood sometimes

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186
Q

what are some complications of bronchiectasis?

A

pneumonia

fungal colonisation

emphysema

septicaemia

metastatic abscesses eg brain/heart

further necrosis/destruction of lung tissue leading to pulmonary fibrosis

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187
Q

summarise bronchiectasis (3)

A

results from bronchial obstruction w/ distal infection n scarring

destruction of bronchial and alveolar walls

dilatation of the airways

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188
Q

what happens in interstitial lung disease?

A

increased amount of lung tissue

increased stiffness n decreased compliance

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189
Q

is chronic interstitial disease fibrosis + or - ?

A

+

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190
Q

what is fibrosing alveolitis aka

A

idiopathic pulmonary fibrosis

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191
Q

what happens in fibrosing alveolitis/idiopathic pulmonary fibrosis ?

A

finger n toe clubbing

results in end-stage fibrosis (honeycomb lung)

unknown aetiology

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192
Q

what is pneumoconiosis?

A

lung disease caused by inhaled dust

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193
Q

what is sarcoidosis?

A

granulomatous disease affecting mainly lungs, but also LN in a greater freq

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194
Q

do more men or women get lung cancer

A

men

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195
Q

what proportion of all cancer deaths come from lung cancer

A

1/3

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196
Q

list some causes of lung cancer

A

cigarettes (majority)
- passive smoking = 2x normal

occupational eg asbestos

lung fibrosis

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197
Q

what are some symptoms of lung cancer?

A

cough

recurrent chest infections

haemoptysis (coughing up blood)

increasing SOB

general malaise

weight loss

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198
Q

what is haemoptysis?

A

coughing of blood

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199
Q

what is the most common lung cancer?

A

metastatic carcinoma

more common than primary lung carcinoma

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200
Q

what are lung cancers broadly divided into?

A

small cell lung carcinoma

non-small cell lung carcinoma

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201
Q

what is the spread of small cell lung carcinoma like at presentation?

A

usually has spread

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202
Q

what is the primary/standard treatment for small cell lung carcinoma?

A

chemotherapy

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203
Q

what is the primary/standard treatment for non-small cell lung carcinoma (large cell)?

A

surgery/radiotherapy

chemo may be offered

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204
Q

what are investigations for lung cancer?

A

cytology

histology

via sputum/biopsy etc

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205
Q

resp drug nomenclature: if it ends in “….mab” ????

A

Monoclonal AntiBody

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206
Q

resp drug nomenclature: if it ends in …sone/lone ?????

A

corticosteroid

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207
Q

resp drug nomenclature: if it ends in ….terol ????

A

bronchodilators

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208
Q

resp drug nomenclature: if it ends in ….nib ???

A

kinase INhiBitor

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209
Q

what is an example of a monoclonal antibody resp drug

A

reslizuMAB

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210
Q

what are 2 examples for corticosteroids resp drugs

A

dexamethaSONE

prednisoLONE

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211
Q

what is an example of a bronchodilator (resp) drug

A

salmeTEROL

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212
Q

what is an example of a kinase inhibitor resp drug

A

nintedaNIB

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213
Q

how are inhaled medicines delivered?

A

directly to the lung

via oral or nasal route

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214
Q

what do inhalers deliver

A

dry powder formulation

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215
Q

what do nebulisers deliver

A

medication in the form of aerosols

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216
Q

what are conducting airways like in terms of drugs?

A

smaller SA

lower regional blood flow

high filtering capacity (mucociliaryescpalator)

removes up to 90% of delivered drugs

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217
Q

what is the resp circulation like in terms of drugs?

A

accounts for 95%+ of lungs SA

directly connected to systemic circulation

bettter than conducting airways

218
Q

other than IV - what’s the 2nd best way of getting drugs in?

A

inhaled

219
Q

why is inhalation technique important?

A

if patients inhale too forceful - particle deposition in upper aiways/mouth/throat is dominant n lung deposition falls

220
Q

intranasal or oral which is better?

A

oral bc allowed to administer v small particles .. nose has anatomical limitation bc narrow airway lumen

221
Q

list some delivery systems for inhaled drugs

A

pressurised metered-dose inhalers (PMDIS) [like Ammi]

spacer devices

dry powder inhalers (DPIS)

nebulisers

222
Q

what are some adv to inhaled meds?

A

lungs - naturally permeable to peptides

large SA

rapid absorption

fewer drug metabolising enzymes than blood/liver

223
Q

how do PMDIS work

A

device is activated by the user pressing down on the top of the container

resulting in the release of a fine spray containing propellant and drug

224
Q

how do spacer devices work

A

slow down the particles of the drug and allow more time for evaporation of the propellant so that more of the drug can be inhaled

225
Q

how does DPIS (dry powder inhalers) work

A

dpis do not have a propellant — instead, on activation, the device releases a small amount of drug in powder form, which is then inhaled

(this requires the person to have sufficient inspiratory effort to breathe in the powder).

226
Q

how do nebulisers work

A

nebulizers work by dispersing a liquid into a fine mist which can be inhaled through a mask or mouthpiece.

main adv is that no coordination is required by the user, and high doses of drug can be delivered to the airways.

227
Q

what are 2 reasons why airways may be obstructed

A

tightening of airway smooth muscle

lumen occlusion by mucus and plasma airway wall thickening

228
Q

what can bronchoconstriction lead to

A

airflow obstruction

229
Q

when is bronchoconstriction most commonly seen?

A

asthma and COPD

230
Q

how is ASM (airway smooth muscle) primed in asthma?

A

to contract

and is resistant to relaxation

231
Q

what are the most frequently used inhaled meds

A

bronchodilators

232
Q

what are bronchodilators split into?

A

adrenergic - SYMPATHETIC

(causes bronchodilation)

anti-cholinergic - PARASYMPATHETIC

(block bronchoconstriction)

233
Q

what do adrenergic bronchodilators do?

A

cause bronchodilation

234
Q

what do anticholinergics do?

A

block bronchoconstriction

235
Q

how do b2 agonists act on b2 adrenoceptors?

A

cause smooth muscle relaxation

bronchodilator

inhibits histamine release from lung mast cells

236
Q

what are SABAs

A

short acting b2-adrenoceptor agonists

237
Q

what is an example of SABA

A

salbutamol

238
Q

what is an example of a LABA

A

formoterol

or salmeterol

239
Q

what do ultra-LABAs allow

whats an example

A

once-daily dosing

indacaterol

240
Q

what are LABAs often combined with?

and why?

A

corticosteroids

for the treatment of asthma and with an inhaled long-acting antimuscarinic agent (LAMA) for treating COPD patients

241
Q

what does LAMA stand for

A

long-acting antimuscarinic agent

242
Q

what is the role of ACh in the resp system?

A

contracts ASM (airway smooth muscle)

by activating muscarinic receptors

on smooth muscle cells

243
Q

what do anticholinergics do?

A

block ACh binding to muscarinic receptors (M1-5)

244
Q

when anticholinergics block muscarinic receptors on ASM, what does it prevent?

A

muscle contraction

gland secretion

also enhances neurotransmitter release

245
Q

what is atropine?

A

naturally occurring anticholinergic

reverses bronchoconstriction caused by PS nerve stimulation

246
Q

anticholinergics are often used in combo with anti-inflammatory steroids in the treatment of what?

A

asthma

COPD

247
Q

inflammatory cells such as neutrophils and eosinophils inappropriately persist in the airway and lead to …. (2)

A

direct tissue damage

perpetuation of inflammation

248
Q

what are corticoseroids aka

A

glucocorticoids

249
Q

what is the most effective anti-inflammatory for asthma

A

corticosteroids/glucocorticoids

250
Q

are glucocorticoids effective in COPD/CF ?

A

nope :/

251
Q

severe asthmatics can become resistant to what?

A

glucocorticoids

252
Q

what is an ICS inhaler?

A

inhaled corticosteroid

253
Q

name an example of a ICS inhaler

A

beclomethasone dipropionate

254
Q

how do inhaled corticosteroids (ICS) reduce inflammation? (3)

A

suppress prod of mediators

reduce adhesion molecule expression

inhibit inflammatory cell survival in the airway

255
Q

what do ICS inhalers do?

A

reduce number of inflammatory cells in the airways

256
Q

what are some side effects of ICS inhalers such as beclomethasone dipropionate

A

loss of bone density

adrenal suppression

cataracts, glaucoma

257
Q

when is corticosteroid resistance common?

A

in COPD

less common in asthma

258
Q

COPD patients who are responsive to corticosteroids are thought to have what?

A

concomitant asthma

which may explain the element of sensitivity to ICS

259
Q

inhaled b2-agonsits are frequently used together with what (for asthma)

A

glucocorticoids as a fixed combo inhaler

260
Q

what is bronchiectasis

A

abnormal dilation of the bronchi

261
Q

what are 2 signs of bronchiectasis

A

excessive sputum production

chest pain

262
Q

what is bronchiectasis associated with

A

cystic fibrosis

263
Q

what does bronchiectasis have an overlap with

A

COPD

asthma

264
Q

what is pathophysiology of bronchiectasis thought to be de to?

A

excessive and persistent inflammation in the lung

265
Q

how do u treat bronchiectasis? (3)

A

ABs to treat infective elements

physical therapy clears airways

surgery n transplantation for severe disease

BUT strategies aim to reduce symptoms rather than underlying cause

266
Q

excessive fibrous connective tissue leads to what? (3)

A

permanent scarring

airway wall thickening

breathing difficulties

267
Q

what is a hallmark of interstitial lung diseases?

A

fibrosis

268
Q

what is a lace-like network of tissue that extends throughout lungs and provides support to alveoli?

A

the interstitium of the lung

269
Q

what is the tissue btwn alveoli and bloodstream called

A

interstitium

270
Q

how do interstitial diseases present typically?

A

present with :

cough and/or breathlessness
on exertion

271
Q

what are treatment options like for fibrosis?

A

limited

272
Q

what is the best option for fibrosis?

A

transplantation

273
Q

some forms of fibrosis respond to what?

A

corticosteroids

274
Q

what is pirfenidone?

A

a new/commoly used AB in fibrosis

has an AF, AI & AO properties

(oral)

275
Q

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A

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276
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286
Q

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–

287
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288
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289
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290
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291
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294
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295
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296
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297
Q

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298
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299
Q

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300
Q

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301
Q

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302
Q

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303
Q

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304
Q

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305
Q

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306
Q

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307
Q

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A

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308
Q

-

A

-

309
Q

define resp failure

A

inability of lungs to adequately oxygenate arterial blood supply and/or eliminate CO2 from venous supply

310
Q

does hypoxia break breath hold?

A

no, hypercapnia does

311
Q

remember, shunt in resp med = diff to shunt in CVS

A

…

312
Q

what is v/q mismatch

A

imbalance btwn ventilation and perfusion

313
Q

what is normal V/Q?

A

0.8

314
Q

when there’s dead space, what is V/Q ratio?

A

infinity (bc dividing by 0)

eg pulmonary embolus

no blood flowing through capillary

fully ventilated alveolus w no blood flow through it

315
Q

normal alveolus
red blood supply

what is the V/Q ratio like?

A

increased V/Q

316
Q

shunt - normal blood supply
can’t pick up oxygen
problem at alveolar level

what is the V/Q ratio like?

A

V/Q = 0

317
Q

what are some signs of t1 resp failure

A

cyanosis

incr RR (tachypnoea)

accessory muscle use

tachycardia

318
Q

-

A

-

319
Q

-

A

-

320
Q

-

A

–

321
Q

-

A

-

322
Q

–

A

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323
Q

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A

–

324
Q

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A

–

325
Q

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A

-

326
Q

-

A

–

327
Q

-

A

-

328
Q

–

A

-

329
Q

-

A

–

330
Q

what kind of person is obstructive sleep apnoea more common in?

A

obese ppl

fat around neck occludes ___________

331
Q

-

A

-

332
Q

what are some clinical signs of hypercapnia

A 
bounding pulse
?
?
?
?
333
Q

treatment of resp failure?

A

depends on cause !

334
Q

treatment of t1 resp failure?

A

oxygen

treat underlying cause

if unable to maintain adequate oxygenation –> CPAP

335
Q

treatment of t1 resp failure? (3)

A

oxygen (94-98%)

treat underlying cause

if unable to maintain adequate oxygenation –> CPAP (continuous positive airways pressure)

336
Q

how is oxygen delivered

A

nasal cannula (up to 4L/min)

simple face mask (can’t measure inspired amt)

venturi mask (v important)

non-rebreathe mask

337
Q

treatment of t2 resp failure? (3)

A

oxygen, but be careful (88-92%)

treat underlying cause within 1hr of med treatment

if unable to maintain adequate oxygenation/removal of CO2 –> NIV (non-invasive ventilation)

338
Q

what is target sats for t1 resp failure

A

94-98%

339
Q

what is target sats for t2 resp failure

A

88-92%

340
Q

go over case studies from this lecture

A

-

341
Q

with a flare of asthma, expect to see what co2?

A

low

when it goes high - sig warning sign!!!!!!!!!!!

sign that pt is becoming tired

need to take it seriously

342
Q

what is the most common cause of hyperaemia?

A

V/Q mismatch

343
Q

alveolar hypoventilation can cause what?

A

t2, hypercapnia resp failure

344
Q

usually give what in resp failure?

A

oxygen

345
Q

what is crucial in guiding management of resp failure patients?

A

ABG

346
Q

what are interventions for COPD (cheapest/PH –> to most expensive)

A

flu vaccination

stop smoking support

pulmonary rehab

tiotropium

LABA

347
Q

what does COPD lump together

A

bit vague
inc lots

emphysema (pathological - destruction of lung tissue)
bronchitis (clinical - cough/phlegm)
bronchiolitis (clinical)

348
Q

what is the NICE definition of COPD (4/5)

A

characterised by airflow obstruction

usually progressive

not fully reversible

doesn’t change markedly over several months

predominantly caused by smoking

[not NICE] s/t to do with inflammation, env, noxious particles/gases. its an inflammatory response to that

349
Q

what is the predominant cause of resp deaths

A

COPD

350
Q

can’t have COPD unless u fill which spirometric criteria?

A

FEV1/FVC < 0.7

351
Q

what is the diff btwn COPD and asthma?

A

asthma is reversible

352
Q

what are the 2 mechanisms underlying airflow limitation in COPD?

A

small airways disease

parenchymal destruction

353
Q

what happens in small airways disease

A

airway inflammation

airway fibrosis, luminal plugs

increased airway resistance

THUS airflow limitation

354
Q

what happens parenchymal destruction?

A

loss of alveolar attachments

decrease of elastic recoil

THUS airflow limitation

355
Q

what are physiological changes in COPD?

A

poor v/Q match

low PaO2

poor ventilation may give high pCO2

obliteration/vasoconstriction –> pulmonary hypertension

356
Q

list 9 clinical features of COPD

A 
old old patients
smoker
male predominance
SOB
cough
phlegm
wheeze
raised respiratory weight
hyperexpansion/barrell shaped chest
cyanosis
weight loss
'cor pulmonale' - heart failure
357
Q

WHAT IS COR PULMONALE

A

abnormal enlargement of the RHS of heart as a result of disease of the lungs or the pulmonary BV

358
Q

what is a phenotype for pink puffers?

A

weight loss
breathless
emphysematous
maintained PO2

359
Q

whats a phenotype for blue bloaters?

A

cough
phlegm
cor pulmonale (enlarged RHS of heart)
resp failure

360
Q

what is a typical COPD patient

A

older

smokers

male traditionally

361
Q

apart from smoking, what are some COPD risk factors?

A

occupational dust/chemicals

env tobacco smoke

indoor/outdoor air pollution

socioeconomics - of parent ! in-utero development

362
Q

what is the effect of mixing cannabis and marijuana for COPD?

A

synergestic effect !

worse effect than either on their own .. nobody knows why

363
Q

what is the MRC dyspnoea scale for COPD pts?

A

1 - SOB on marked exertion
2 - SOB on hill
3 - has to stop for breath when at own pace
4 - stops for a few mins after walking on flat level
5 - too breathless to leave house or on dressing/undressing

364
Q

what are DD for COPD

A 
other causes of SOB
HF
pulmonary emmbolus
pneumonia
lung cancer
asthma
bronchiectasis
365
Q

what is bronchiectasis

A

LT cond - airways become abnormally widened

–> leading to a build-up of excess mucus that can make the lungs more vulnerable to infection.

most common symptom is phlegmmy cough

366
Q

allergic inflammation (asthma) is characterised by the recruitment of what?

A

eosinophils

367
Q

what is atopy?

A

the tendency to develop IgE mediated reactions to common aeroallergens

368
Q

what subgroups can asthma be divided into?

A

eosinophilic

non-eosinophilic

369
Q

what can eosinophilic asthma be divided into?

A

atopic asthma (developing immune response to common aeroallergens)

and non-atopic

370
Q

name 3 causes of atopic asthma

A

fungal allergy

common aeroallergens

occupation, pets, exposures

371
Q

what are 3 types of non-eosinophilic asthma?

A

non-smoking, non-eosinophilic

smoking associated

obesity related

372
Q

what is often the presenting complaint w asthma?

A

episodic wheeze

cough, breathlessness

diurnal variation

373
Q

list some provoking factors for asthma

A

allergens

infections

menstrual cycle

exercise

cold air

laughter/emotion (LOOOL)

374
Q

how do u check the severity of asthma?

A

level of treatment required (no. of inhalers)

A&E attendances, admissions, HDU/ITU care, ventilation

attendance at GP for courses of ABs/steroids

375
Q

how do u assess day to day severity of asthma

A

recent nocturnal waking?

usual asthma symptoms in a day?

interference with ADLs?

376
Q

what does ADL stand for

A

activities of daily living

377
Q

what do u look at in an asthma history (4)

A

age of onset (did it get better at any point?)

childhood resp disease

any unusual features at start eg sudden onset, weight loss

obvious causes such as chlorine exposure

378
Q

what are some associated problems w asthma?

A

eczema, hayfever

nasal disease

other food/drug allergies

reflux disease

379
Q

what PMH do u look at w asthma?

A

always vital part of history

previous pneumonias (bronchiectasis?)

neuro/renal problems (vasculitis?)

380
Q

what do u look at in terms of drugs w asthma patients?

A

what should they be taking?

what do they ACTUALLY take?

are they taking beta blockers orally or topically?

are they sensitive to NSAIDs or aspirin?

any drugs w potential interactions? eg theophyllines

381
Q

what do u look at in family history of asthmatics!

A

DO THEY SMOKE?

atopy is an inherited tendency

FHx of asthma, eczema and hayfever

are there pets?

psych history

382
Q

is atopy environmental?

A

inherited

383
Q

what do u look at in an occupational history?

A

exposure to dusts/fumes/allergens

lab workers, vet staff, animal breeders

paint sprayers

bakers

is asthma worse at work/better on holiday?

384
Q

how is COPD diff to asthma?

A

COPD - later disease of mainly smokers

COPD is mores progressive SOB

COPD has less diurnal variation/diurnal variation

385
Q

what do u expect to see in a physical exam of an asthmatic

A

may be normal

wheeze, polyphonic, expiratory, widespread

absence of crackles, sputum, other signs

386
Q

what tests do u do for asthma

A

blood count: eosinophils

tests for atopy/allergy: IgE, SPTs

chest XR often useful

oxygen sats

387
Q

what do u find in lung function testing (asthmatics)

A

airways obstruction may be present

(reduced FEV1 and FEV1/FVC ratio)

PEFR reductions from % predicted

388
Q

what is a marker of eosinophilic inflammation?

what is a problem w this?

A

exhaled nitric oxide (FeNO)

not specific
suppressed in smokers
elevated with viral infections and rhinitis

389
Q

who is at risk of asthma death? (5)

A

≥3 classes of treatment

recent admission/frequent attender

previous near-fatal disease

brittle disease

psychosocial factors

390
Q

what are some DD for asthma? (8)

A 
bronchiolitis
bronchiectasis
CF
PE
hyperventilation
bronchial obstruction (foreign body, tumour)
COPD
391
Q

what is bronchiolitis

A

inflammation of bronchioles

caused by a virus known as the respiratory syncytial virus (RSV), which is spread through tiny droplets of liquid from the coughs or sneezes of someone who’s infected.

the infection causes the bronchioles to become infected & inflamed

392
Q

what are the 4 goals for asthma treatment?

A

to improve control

to address important issues for the patient eg exercise

393
Q

what is important in asthma care?

A

avoidance of triggers !!!! (allergens, occupational)

394
Q

list some examples of bronchodilators for asthma

A

beta agonists

LABAs

anticholinergics

395
Q

are steroids inflammatory or anti-inflammatory?

A

steroids = short for corticosteroids

decrease inflammation so anti-inflammatory !

396
Q

what do bronchodilators treat ?

A

symptoms not the disease

397
Q

why are bronchodilators and steroids used for asthma?

A

bronchodilators for symptoms

steroids to reduce airway inflammation nd decrease mortality risks

398
Q

why isn’t everyone given oral steroids? (3)

A

systemic (diabetes, cataracts, osteoporosis, skin thinning, easy bruising etc)

topical (hoarse voice, oral candida, etc)

adrenal suppression

399
Q

why may a spacer be used? (2)

A

to improve delivery

minimise side effects

400
Q

which 2 tests are always done at TB units?

A

acid-fast bacilli (AFB) smear and culture

401
Q

what is the top infectious killer in the world?

A

TB

402
Q

list some risk factors for TB

A

born in high prevalence area

IVDU

homeless

alcoholic

prisons

HIV+

403
Q

how do you catch TB?

A

aerosol/spitting/sneezing

from infected individual’s lung to another

404
Q

what is omalizumab anti?

A

anti-IgE

for atopic allergic disease

405
Q

what is TB caused by?

A

mycobacterium tuberculosis (so a mycobacteria)

406
Q

what is pneumonia?

A

lung inflammation caused by bacterial/viral infection

407
Q

how you recognise a severe asthma attack?

A

do PEFR, full clinical assessment

oximetry

CXR if suspect pneumothorax, life threatening asthma, failure to respond

408
Q

what values do u get for a severe asthma attack?

A

any 1 of:

PEFR 33-50% predicted

RR ≥ 25

HR ≥ 110

inability to complete sentences

409
Q

what values do u get for a life threatening asthma attack?

A

any 1 of:

PEFR < 33%

SaO 2 < 92%
PaO2 < 8kPa

normal PaCO2 4.6-6kPa

altered conscious level, exhaustion, arrhythmia, hypotension, silent chest, cyanosis

410
Q

what is immediate management for asthma attack?

A

oxygen 40-60%

salbutamol neb 5mg (± ipratropium if life threatening)

prednisolone 30-60mg (± hydrocortisone 200mg IV)

ABGs

watch for key complications: tension pneumothorax, arrhythmias, hypokalaemia

CXR if suspected as above or failure to respond to treatment

411
Q

what is pneumothorax?

A

when air leaks into the space between your lung and chest wall.

this air pushes on the outside of your lung and makes it collapse.

412
Q

how do u monitor response to asthma treatment?

A

PEFR check within 15-30 mins

oximetry to maintain sats > 92%

repeat ABG within 2hrs if severe attack

if deteriorating despite maximal treatment with worsening hypoxia/hypercapnia etc –> ITU transfer

watch K+, glucose

consider rehydration

413
Q

whens should an asthma patient be transferred to ITU

A

if deteriorating despite maximal treatment

worsening hypoxia/hypercapnia

coma/exhaustion

414
Q

when do u discharge an asthma patient? (6)

A

opportunity to educate and prevent readmissions

achieve PEFT >75% and <25% variability

prednisolone 7-14d

asthma action plan

nurse-led follow up

early clinical review (48hrs at GP surgery)

415
Q

what does enteral admission refer to?

A

food/drug administration via the human GI tract

416
Q

what is TB caused by?

A

mycobacterium tuberculosis (so a mycobacteria)

417
Q

how do u treat a latent TB infection

A

single drug for a long time

418
Q

what is tuberculosis caused by?

A

mycobacterium tuberculosis

419
Q

what % of ppl infected w TB are aware they’re infected?

A

abt 5%

420
Q

when may TB present?

A

if immune system becomes debilitated eg AIDS/immune issues

421
Q

what happens in extra pulmonary TB?

A

lymph node TB

bone

abdo TB

GU TB

CNS TB

422
Q

what kinda symptoms do u get with primary TB?

A

asymptomatic

mild flu like illness

423
Q

what can systemic TB affect?

A

kidneys - sterile pyuria

meningitis

hepatitis etc

424
Q

what do u get if u have a positive result for TB?

A

CXR to see active disease

425
Q

which kind of TB sufferers are most infectious?

A

adults w reactivated TB

426
Q

what do visitors of TB patients do?

A

wear masks that filter 95% of aerosols

427
Q

how do u treat an active TB infectin

A

AB combo

428
Q

how do u treat a latent TB infection

A

single drug for a long time

429
Q

what % of ppl don’t have any disease?

A

≈95%

430
Q

who is the BCG vaccine given to?

A

neonates from high risk groups

if 1 parent is born in a highTB risk country

431
Q

what happens in pulmonary TB?

A

cough over 3/52w
chest pain
breathlessness
haemoptysis (coughing up blood)

432
Q

how do u diagnose active TB definitively

A

microbio

sputum
urine
CSF
biopsy specimen: any LN

433
Q

for any chronic illness with fever and weightloss, think what?

A

TB

434
Q

what is Mantoux?

A

tuberculin skin test

uses an ID injection of tuberculin.

435
Q

Is TB curable

A

yes

436
Q

what are the 3 separate “genera” of the orthomyxoviridae family

A

influenza A, B & C

437
Q

what is crucial to reduce relapse/resistance of TB?

A

compliance

438
Q

who gets increased risk of drug resistance to TB? (4)

A

previous treatment

high risk area

contact of resistant TB

poor response to therapy

439
Q

which vaccine is given for TB?

A

BCG

440
Q

who is the BCG vaccine given to?

A

neonates from high risk groups

if 1 parent is born in a highTB risk country

441
Q

where can TB affect?

A

any site

442
Q

what is the commonest site of TB infection?

A

lung

443
Q

for any chronic illness with fever and weightloss, think what?

A

TB

444
Q

what is influenza?

A

acute resp illness caused by infection w/ influenza virus

445
Q

what is influenza a member of?

A

the orthomyxoviridae family

446
Q

what are the 3 separate “genera” of the orthomyxoviridae family

A

influenza A, B & C

447
Q

what are the main human pathogens

A

influenza A and B

448
Q

what causes seasonal epidemics of flu?

A

antigenic drift

449
Q

what causes pandemics of flu?

A

antigenic shift

450
Q

what is antigenic shift?

A

gene re-assortment and major antigenic variation

451
Q

what is antigenic drift?

A

minor antigenic variation

452
Q

what is the diff btwn epidemic n pandemic?

A

epidemic - within a community

pandemic - world-wide

453
Q

which out of influenza A, B & C is a relatively minor disease?

A

C (mild symptoms/asymptomatic)

454
Q

which influenza is most often seen in children?

A

influenza B

455
Q

what kinda outbreaks can influenza B cause?

A

sporadic eg schools, care homes, garrisons

most often seen in children

456
Q

which type of ppl is flu mortality risk higher?

A

those w underlying medical conditions

chronic cardiac and pul. diseases, old age, chronic met diseases, immunosuppressed

457
Q

what kinda influenza causes severe outbreaks/pandemics?

A

Influenza A

458
Q

what makes something an outbreak?

A

2+ linked cases

459
Q

out of smallpox, HIV, pandemic flu, seasonal flu and measles what generates the highest number of secondary cases?

A

measles

460
Q

how is measles transmitted

A

airborne

461
Q

how is smallpox transmitted

A

social contact

462
Q

how is HIV transmitted

A

sexual contact

463
Q

how do govts work prior to pandemics?

A

int. surveillance

virus/vaccine research

stock piling of drugs

464
Q

how can flu be characterised? (symptom wise?

A

upper and lower resp tract symptoms

465
Q

what are some complications of flu?

A

bacterial pneumonia

can be life threatening

466
Q

what type of treatment is good for flu?

A

supportive care

eg oxygenation, hydration, maintain homeostasis

467
Q

what makes something an outbreak?

A

2+ linked cases

468
Q

what is infection control for flu? (4)

A

hand hygiene

universal precautions

surgical masks

patient segregation

469
Q

what is the incubation period for pandemic flu, and when is it infectious?

A

IP - 1-4days

infectious from onset to 4-5 days after

470
Q

what are 3 factors that might mean we will get more pandemics?

A

more travel

more people

intensive farming (more animal contacts w ppl, factory farming breeding grounds for viruses)

471
Q

how do u control avian flu (mild disease in birds)

A

reduce population of (cull) affected birds

disinfect farms

vaccinate workers

472
Q

how do govts work prior to pandemics?

A

int. surveillance

virus/vaccine research

stock piling of drugs

473
Q

what are some staff issues bc of a flu?

A

anxiety/unwilling to work

childcare

adequate protection

474
Q

what are possible population-wide interventions for flu?

A

travel restrictions

restrictions of mass public gatherings

schools closure

screening of ppl entering UK

voluntary home isolation of cases

475
Q

what is swine flu a reassortment of?

A

swine, avian and human flu virus

476
Q

what are the 2 phases of managing flu?

A

containment phase (identifying cases, treatment, contact tracing, large scale prophylaxis)

treatment phase (treat cases only, national flu pandemic service)

477
Q

how do u manage cases of flu?

A

call centres

non medical staff manage cases according to an algorithm

home delivery of anti virals

478
Q

how is the UK prepared for a flu outbreak? what drug?

A

stockpiling of antiviral drugs

mostly tamiflu

479
Q

how does tamiflu work?

A

UK stockpiles 30mill courses

given within 24-48h of contact

reduces hose by 50%

480
Q

when are face masks useful?

A

worn correctly

changed frequently

removed properly

disposed safely

used in combo w good universal hygiene practice

481
Q

what are some staff issues bc of a flu?

A

anxiety/unwilling to work

childcare

adequate protection

482
Q

what are possible population-wide interventions for flu?

A

travel restrictions

restrictions of mass public gatherines

schools closure

screening of ppl entering UK

voluntary home isolation of cases

483
Q

how does the PEF vary in COPD vs asthma?

A

COPD - minimal variation

asthma - day-to-day and diurnal variation

484
Q

all COPD patients benefit from regular what?

A

physical activity

485
Q

what is spirometry in asthma like

A

may be normal

486
Q

how does COPD respond to steroids?

A

not v well

487
Q

how do asthmatics respond to steroids?

A

well

488
Q

COPD is often found with what?

A

other diseases

489
Q

what can COPD be comorbid with (long list)

A 
cardiac disease
cancer
renal failure
diabetes
weight loss
depression
anxiety
osteoporosis
490
Q

what happens w reduced COPD risk? (3)

A
  1. prevented disease progression
  2. prevented/treated exacerbations
  3. reduced mortality
491
Q

which 2 things reliably increase LT smoking abstinence rates?

A

pharmacotherapy

nicotine replacement

492
Q

all COPD patients benefit from regular what?

A

physical activity

493
Q

LABD reduce what in COPD?

A

exacerbations, related hospitalisations

494
Q

inhaled corticosteroid therapy is associated with what?

A

increased risk of pneumonia

495
Q

list some therapeutic COPD meds

A

SABAs, LABAs

SAACs, LAACs

496
Q

what are the 2 goals of COPD therapy?

A

to reduce symptoms

to reduce risk

497
Q

what happens w reduced COPD symptoms? (2)

A
  1. improved exercise tolerance

2. improved health status

498
Q

what happens w reduced COPD risk? (3)

A
  1. prevented disease progression
  2. prevented/treated exacerbations
  3. reduced mortality
499
Q

which medications are central to symptomatic management of COPD?

A

bronchodilators (b2 agonists, anticholinergics, combo)

500
Q

the effects of work on health can be what? (4)

A

acute

cumulative

progressive (disease progression after exposure ceases)

diseases with latencies

501
Q

LABD reduce what in COPD?

A

exacerbations, related hositalisations

502
Q

inhaled corticosteroid therapy is associated with what?

A

increased risk of pneumonia

503
Q

what is occupational medicine?

A

branch of medicine concerned w/ interaction btwn work n health

504
Q

what 4 aspects does occupational med look at?

A
  1. individual workers
  2. groups of workers
  3. workplace effects on surrounding population
  4. health of employers’ customers/clients
505
Q

what is the most common work-related ill health in GB?

A

stress, depression, anxiety :(

506
Q

long-time worklessness is a great risk to health, why?

A

social exclusion n poverty

loss of fitness/wellbeing

trapped on benefits to retirement

2-3x risk of MH/poor health

507
Q

how will action to reduce health inequalities ave economic benefits?

A

in reducing losses from illness associated with health inequalities

508
Q

the effects of work on health can be what? (4)

A

acute

cumulative

progressive (disease progression after exposure ceases)

diseases with latencies

509
Q

what is the diff btwn hazard and risk

A

hazard = potentially harmful

risk = probability of harm

510
Q

what are the 10 key components of good work?

A
  1. precariousness (Stable, risk of loss)
  2. individual control
  3. work demands
  4. fair employment
  5. opportunities
  6. prevents social isolation/discrim/violence
  7. share info, participate in decision making
  8. work/life balance
  9. reintegrates sick/disabled
  10. promotes health n wellbeing
511
Q

what 3 factors should raise suspicion of an occupational aetiology?

A

an illness that fails to respond to standard treatment

does not fit the typical demographic profile

or is of unkwnown cause

512
Q

what are 5 occupational screening questions?

A
  1. what type of work do u do?
  2. do u think ur health problems might be related to ur work?
  3. are ur symptoms different at work and at home?
  4. are u current exposed to chemicals, dusts, metal, radiation, noise or repetitive work or have been in the past?
  5. are any of ur co-workers exp similar symptoms?
513
Q

what does occupational lung disease represent?

A

a wide-range of resp conditions

caused by inhaling a harmful substance in the workplace

514
Q

long-time worklessness is a great risk to health, why?

A

social exclusion n poverty

loss of fitness/wellbein

trapped on benefits to retirement

2-3x risk of MH/poor health

515
Q

how will action to reduce health inequalities ave economic benefits?

A

in reducing losses from illness associated with health inequalities

516
Q

define disability

A

physical/mental impairment

which has a substantial LT adverse effect on a person’s ability to carry out normal activities

517
Q

how can employers reasonably adjust work for disabled ppl?

A

altered working hours

allow absences for medical treatment

give additional training

special equipment

provide additional support

518
Q

what are 3 primary preventions for occupational health?

A

monitor risk

controlling hazards

promotion

519
Q

what are 3 secondary preventions for occupational health?

A

screening

early detection

task modification

520
Q

what are 2 tertiary preventions for occupational health?

A

rehab

support

521
Q

what does occupational lung disease represent?

A

a wide-range of resp conditiosn

caused by inhaling a harmful substance in the workplace

522
Q

what is the diff btwn inhalable vs respirable dusts?

A

inhalable - can enter resp tract

respirable - can penetrate to an alveolar level

523
Q

dusts are solid particles usually how many microns in size?

A

1-1000

524
Q

inhalable dust is how big?

A

less than 100 microns

525
Q

respirable dust is how big?

A

less than 10 microns

526
Q

what is occupational asthma like ?

A

latent period

deteriorating symptoms

gradual improvement

depression

527
Q

what are fumes?

A

small (less than 1 micron) solid particles suspended in the air

528
Q

dust and fumes are both solid particles suspended in the air. what’s the diff?

A

size

dust = 1-1000 microns
fumes = less than 1 micron
529
Q

what is mist?

A

liquid particles suspended in the air

530
Q

list 4/5 causes of occupational lung disease

A 
dust
mist
fumes
inhaled vapours
n gases
531
Q

a workers response to a workplace exposure is variable and dependant on a range of factors including? (3)

A
  1. physical/chemical nature of the agent
  2. duration/dose of exposure
  3. individual susceptibility
532
Q

what % of all adult onset asthma is occupational?

A

15%

533
Q

what is the majority of occupational asthma induced by?

A

allergy to inhaled agent at work

534
Q

what is pneumoconiosis?

A

lung disease caused by inhalation of a mineral dust eg asbestosis

535
Q

name 3 asbestos-related lung diseases

A

pleural disease

pulmonary fibrosis

cancer

536
Q

what is a harmless marker of exposure ?

A

pleural plaques

537
Q

what do pleural plaques consist of

A

layers of collagen

often calcified

538
Q

what happens w asbestosis?

A

progressive breathlessness

decades long latency
no effective treatment
may progress slowly

539
Q

what is asbestosis?

A

interstitial lung fibrosis associated with asbestos inhalation

540
Q

what is a mesothelioma?

A

rapidly progressive and incurable pleural cancer

541
Q

what often presents as an unexplained pleural effusion?

A

mesothelioma

(SG) Phase 2A lectures (14 decks)

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