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Phase 2a Introductory Clinical Science > Respiratory System > Flashcards

Respiratory System Flashcards

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1
Q

How many resp tract infections per year do children have? adults?

A

children 2-5

adults 1-2

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2
Q

give 4 reasons why we get lots of resp infections?

A

pathogens can ascend via the oesophagus from the stomach
large surface area and thin barrier so easy access to blood stream
commensal organisms in upper resp tract don’t stop growth of pathogens
no commensal organisms in lower resp and thin barrier so not lots of room for immune cells and response

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3
Q

give 4 reasons why we don’t get resp infections all the time? i.e. protective factors

A

commensal organisms help resist growth of pathogens
swallowing and epiglottis resist things entering from GI
coughing and sneezing removes pathogens
mucociliary escalator where pathogens get stuck and pushed up to be swallowed or spat out

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4
Q

Why are sinuses sterile?

A

outward flow of liquid

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5
Q

Where are the commensal organisms in the resp tract?

A

nasal cavity
oral cavity
pharynx

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6
Q

name 2 of the commensal organisms per site of where commensals are in the resp tract. (4 for pharynx)

A

nasal: staph. epidermis (+ aureus 20%) & corynebacteria
oral: streptococci & lactobacilli
pharynx: haemaphilus influenza & s. pneumonia & neisseria spp. & streptococci

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7
Q

name 4 soluble and cellular factors that are involved in resp immunity

A

soluble: collectins, lysozyme, defensins, IgA
cellular: macrophages (silent and quick killers), T and B cells (small numbers, aid macrophages), Neutrophils (last resort because collaterol damage)

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8
Q

give 2 conditions that negatively affect the following so that there are more infections:
swallowing
lung physiology (intrinsic and extrinsic to resp system conditions)
immune function

A

swallowing: stroke, surgery
lung physiology intrinsic: emphysema, bronchiectasis
extrinsic: muscle weakness, obesity
immune function: HIV, primary immunodeficiency

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9
Q

name 5 common resp viruses and how likely they are to be the cause of a viral infection?

A 
rhinovirus 45%
influenza A virus 30%
coronavirus 15%
adenovirus 10%
parainfluenza virus 5%
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10
Q

What virus is the most common cause of the common cold? what other two viruses can also cause this?

A

rhinovirus most common, then coronavirus

adenovirus also can cause

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11
Q

when does rhinovirus typically infect (most common, can infect all year)

A

spring and autumn

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12
Q

does rhinovirus infect upper or lower resp?

A

both but upper more

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13
Q

How long is the incubation period for rhinovirus? how long do symptoms last?

A

12-72 hours incubation

7-22 days symptoms

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14
Q

what are the symptoms of rhinovirus? (9)

A 
dry nose
irritative nose
sore throat
headache
pressure on ears and face
lose sense of smell and taste
runny nose
sneezing
cough
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15
Q

how do you treat rhinovirus, adenovirus, coronavirus, parainfluenza virus infections?

A

self-limiting so supportive care e.g. NSAIDs, hydration, rest, anti-histamine

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16
Q

How does rhinovirus attach?

A

capsid protein to receptors of host cells

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17
Q

What syndrome can coronavirus cause that is worrying?

A

severe acute respiratory syndrome

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18
Q

What are the severe conditions that parainfluenza virus can cause

A

croup, bronchitis, bronchiolitis, pneumonia

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19
Q

what is a virus that causes bronchiolitis in young children that is not as common as any of the previous 5 viruses?

A

respiratory syncytial virus

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20
Q

what symptoms does a child infected with the respiratory syncytial virus show

A

wheezing and respiratory distress

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21
Q

How does respiratory syncytial virus cause pathology?

A

bronchiolitis and releases secretions

both narrow the airways

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22
Q

What is a normal breathing rate for a baby? child? adult?`

A

baby 40-60
child 30-40
adult <20

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23
Q

what are some worrying complications from viral resp infections

A

super-bacterial infection
systemic symptoms (usually with influenza A)
sinusitis, pharyngitis, bronchiolitis, pneumonia (rarer)

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24
Q

what causes TB

A

mycobacterium tuberculosis / bovis

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25
Q

describe the pathogen that causes TB (8)

A

non-motile
non-sporing
aerobic
waxy thick outer layer
resistant to phagocytosis by macrophage so granuloma occur
can remain dormant for long time
slow growth of generation time 15-20 hours

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26
Q

What are the groups of people most at risk of TB infections

A 
prisons
industrialisation
over crowded areas
close homes
homeless
ivdu
alcoholics
poverty
born in high prevalence area
race: African, Indian, Pakistani 
malnourished
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27
Q

how is TB transmitted?

A

aerosol (5 microns perfect size of aerosol drop for a few mycobacterium to fit)
spitting or sneezing on hands or surfaces that are later touched
bovine TB via aerosol and oral route e.g. in milk. can cause ileum TB

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28
Q

Where do TB mycobacteria prefer to settle in lungs?

A

apex because less blood and more air so best survival

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29
Q

What happens when the mycobacteria first infect the lungs? What happens in the best case scenario vs. the other option?

A

macrophages and lymphocytes attack and kill mycobacteria.
Best case: all mycobacteria are killed OR the remaining few that couldn’t be killed are contained in granuloma caseating. Remain this way forever or until person immunocompromised.
Other option: Mycobacteria not effectively contained and pulmonary TB occurs

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30
Q

In how many people does PTB occur vs no infection?

A

> 95% of people kill all mycobacteria or contain it effectively
2-5% get PTB clinically evident

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31
Q

What is latent TB?

A

After the patient has contained the mycobacteria, they may lose some immune function e.g. elderly so it can become semi-dormant instead or active and cause TB.

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32
Q

What happens if after the initial infection of TB the bacilli are not contained?

A

Pulmonary TB occurs

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33
Q

What can happen if after latent TB or pulmonary TB bacilli are still not contained

A

Miliary TB aka Serious non-pulmonary TB

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34
Q

What happens in pulmonary TB?

A

The bacilli in the granuloma are not dormant so they grow and the centre of the granuloma gets liquidified and a cavity can form. This is called caseating granuloma. aka as the primary focus or the ghon focus.
Some bacilli survive in macrophage and travel to hilar nodes to cause infection with enlargement. Together, the inflammed nodes and primary focus form a ghon complex.

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35
Q

What is in the granuloma during TB

A 
fibroblasts
epithelium
macrophages
lymphocytes
bacilli
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36
Q

what is the aim of the granuloma in TB

A

wall of the bacilli and stop it from getting nutrition

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37
Q

What thing can the patient do and what thing can the primary focus (the TB granuloma) do to increase transmission

A

patient can cough and expel bacilli which were in the cavity

cavity can erode into the airways

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38
Q

What is miliary TB/ serious non-pulmonary TB

A

this is when the bacilli are not contained and spread via haematogenous manner to other locations to set up infection. This can happen after primary infection or after latent infection.

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39
Q

Give 5 examples of where TB can occur other than pulmonary?

A 
joint and bone TB
pleural TB
genitourinary TB
meningitis TB
Abdominal TB
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40
Q

What are the systemic symptoms of TB (4)

A

night sweats - most predictive 2nd
weight loss - most predictive 1st
malaise
low-grade fever

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41
Q

what are the symptoms of TB that are pulmonary specific

A 
cough >3 months
chest pain
breathlessness
haemoptysis
and possible: consolidation, pleural or pericardial effusion, lobar collapse
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42
Q

why would lobar collapse happen with TB

A

if a bronchus is obstructed

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43
Q

What are some non-pulmonary organ TB symptoms? give two example for each organ

A

bone: bone pain, swelling of joint
abdomen: ileum malabsorption, ascites
CNS: meningitis, paralysis
lymph: enlargement, secretions
GU: epididymitis, dysuria

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44
Q

What investigations do you want to carry out to diagnose TB:

A

Microscopy, culture, PCR, mycobacteria growth indicator tube, whole genome sequence
Bloods
XR

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45
Q

What are you looking for when analysing bloods for TB?

A 
Prolonged inflammatory markers:
thrombocytosis
normocytic anaemia
hypoalbuminaemia
hypercalcaemia
hypergammaglobulinaemia
sterile pyuria
raised ESR, CRP
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46
Q

What samples can we collect for analysing (other than blood)?

A 
sputum
urine
CSF
pleural fluid
biopsy: bone, peritoneum, lymph
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47
Q

What stains can we use for TB microscopy?

A

ZN stain

Auramine phenol stain (needs less number of bacilli to spot them unlike ZN which needs more)

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48
Q

How do cultures and mycobacteria growth indicator tube help TB grow

A

they have low levels of antibiotics to prevent growth of other bacteria which grow quickly
have glycerol to promote the mycobacteria tuberculosis growth

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49
Q

What laboratory technique can we use to check TB drug sensitivity

A

PCR

whole genome sequences

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50
Q

What test can we do to diagnose latent TB?

A

Mantoux test (protein injected intradermally to get type 4 delayed hypersensitivity reaction)

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51
Q

How many drugs are used to treat TB? Name them

A 
4 PERI
Pyrazinamide
Ethambutol
Rifampicin
Isoniazid
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52
Q

How long do we give the drugs for TB?

A

Pyrazinamide 2 months
Ethambutol 2 months
Rifampicin 6 months
Isoniazid 6 months

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53
Q

Do we ever give a longer duration of drugs for TB?

A

for CNS TB we give 12 months

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54
Q

How do the drugs used for TB work?

A

Pyrazinamide - initially bactericidal
Ethambutol - bacteriostatic by blocking cell wall synthesis
Rifampicin- bactericidal by blocking protein synthesis
Isoniazid- bactericidal by blocking cell wall synthesis

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55
Q

What are the side effects for the drugs used for TB?

A

Pyrazinamide - rash, arthralgia, hepatitis
Ethambutol- optic neuritis
Rifampicin - hepatitis, red urine benign
Isoniazid - hepatitis and neuropathy

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56
Q

What can happen if people aren’t taking their medication

A

resistance can occur to the drugs which usually occurs at start of course of treatment and longer duration of drugs needed (>20Months) and more drugs needed

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57
Q

How can we prevent TB? (4)

A

case finding e.g. testing risk groups
find latent TB before it can become active
chemoprophylaxis
vaccines (BCG vaccine)

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58
Q

How can we treat Latent TB?

A

3month rifampicin and isoniazid
or
6 month isoniazid

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59
Q

Which group of patients can’t have the BCG vaccine for TB and why?

A

immunocompromised as they get BCG-osis

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60
Q

What are occupational lung disorders?

A

Lung disorders that occur due to exposure at workspace that damages the respiratory system

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61
Q

How much does FEV1 decrease for men and women as they age normally?

A

30ml for men

25ml for women

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62
Q

What type of things can cause occupational lung disorders?

A

DGVF
dust - solids aerosolised
gases - things that fill the space that they are in
vapour - solids or liquids suspended in air
fumes - vapours or gases that have strong odours

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63
Q

What type of things can cause occupational lung disorders?

A

DGVF
dust - solids aerosolised
gases - things that fill the space that they are in
vapour - solids or liquids suspended in air
fumes - vapours or gases that have specific odours

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64
Q

How can we divide exposures of OLD into timescale?

A

historic, current, future

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65
Q

Describe historic exposures, what we can do for patients

A

exposure occurred in the patient’s past and symptoms are still present or have occurred later. Its difficult to identify the exposure and we cannot remove it so we can only give supportive treatment and benefit advice

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66
Q

Describe current exposures, what we can do for patients

A

agents the patient is exposed to now. We need to recognise occupational aspect early and identify and remove the exposure. Patient may not be able to remove exposure due to job loss. If we remove the exposure FEV1 will improve but not necessarily back to normal.

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67
Q

Name 7 common occupational lung disorders

A 
occupational asthma
extrinsic allergic alveolitis/ hypersensitivity pneumonitis
pleural plaque
diffuse pleural thickening
mesothelioma
asbestosis
chronic inflammation e.g. COPD
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68
Q

Name 4 common occupational lung diseases which are related to asbestos

A

asbestosis
mesothelioma
pleural plaques
diffuse pleural thickening

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69
Q

What proportion of adult-onset asthma is due to occupational asthma?

A

9-15%

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70
Q

What is occupational asthma due to? Give proportions to how common each of the causes is

A

occurs due to sensitisation (allergy) to inhaled agent (90%)

due to massive accidental irritant exposure that causes direct damage to airways (10%)

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71
Q

What are 3 common causative agents of occupational asthma?

A

wood dust
flour
cleaning products

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72
Q

Can we cure occupational asthma?

A

possible if we remove exposure but not always. prognosis will improve though definitely if remove exposure

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73
Q

What is EEA/HP and why does it happen

A

extrinsic allergic alveolitis/ hypersensitivity pneumonitis

occurs due to sensitisation to environmental or occupational allergen

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74
Q

What causes EEA/HP. divide into 4 classes and give examples:

A

microorganisms - cheese workers, sewer workers
animals - birds, rodents
vegetation - coffee, wood
chemicals - pesticide, plastic

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75
Q

what does EEA/HP cause and what is the pathophysiology

A

interstitial lung disease

air gets trapped in lungs and fibrosis occurs

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76
Q

Classify EEA/HP into 3 subtypes and describe them

A

acute- can be self-limiting or quickly progress
sub-acute - constitutional symptoms present but less prominent than acute
chronic - fibrosis has occurred, no constitutional symptoms, irreversible

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77
Q

what are the symptoms of EEA/HP

A

wheezing, shortness of breath, productive cough

constitutional symptoms: headache, weight loss

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78
Q

what does the chest XR of TB show

A

pleural effusion, pathy or nodular shadow

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79
Q

What are the normal causes of occupational COPD

A

historical exposures typically e.g. grain, coal, silica

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80
Q

What is asbestos?

A

naturally occurring mineral fibre

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81
Q

What are pleural plaques made off?

A

pleural collagen and calcified on top

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82
Q

How are pleural plaques linked to asbestos?

A

asbestos causes pleural plaques but not linear relationship. More asbestos does not equal more plaques

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83
Q

Are pleural plaques linked to cancer

A

no they are not pre-malignant

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84
Q

What can diffuse pleural thickening do to the lungs and what are the symptoms

A

restrict the lungs from expanding so shortness of breath and respiratory failure can occur

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85
Q

How do you treat diffuse pleural thickening

A

no effective treatment

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86
Q

Does removing the exposure stop pleural thickening from advancing

A

no because it can develop slowly even if the exposure stops

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87
Q

What lung problem and pleural problem accompanies asbestosis

A

pulmonary fibrosis

+/- pleural plaques

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88
Q

How much asbestos exposure do you need for asbestosis to occur

A

lots

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89
Q

Does asbestosis kill

A

yes

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90
Q

does removing the exposure stop asbestosis from advancing

A

no continues even if exposure stops

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91
Q

What can we do to prevent OLD

A 
1 eliminate
2 substitute 
3 workers education
4 engineering changes e.g. exhaust ventilation
5 protective equipment e.g. masks
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92
Q

Why are health surveillance good

A

identify problems early

if residual risk can check workers’ health annually.

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93
Q

what are the three types of non-neoplastic lung diseases?

A

restrictive
obstructive
gas exchange

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94
Q

Describe restrictive and obstructive lung problems: what? FEV1 to FVC? FEV1/FVC?

A

restrictive: problems with air getting IN. FEV1>FVC FEV1/FVC>80%
obstructive: problems with air getting OUT. FEV1

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95
Q

What could cause acute obstruction?

A

tumour or foreign body

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96
Q

What are the consequences of the acute obstruction

A

lobar collapse OR over expansion (valve effect)

secretions can complicate this

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97
Q

What does pulmonary function tests look like in acute obstruction

A

normal

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98
Q

where are chronic obstructions mainly focused

A

bronchus and bronchioles

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99
Q

Give 4 examples of chronic obstructive conditions

A

bronchitis
emphysema
asthma
bronchiectasis

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100
Q

Give 3 risk factors for bronchitis

A

smoking
chronic pollution
recurrent Haemophilus influenza, strep. pneumonia, adenovirus infections

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101
Q

Give one feature to how we diagnose bronchitis for COPD

A

productive cough for 3 months for 2 consecutive years

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102
Q

what do the bronchioles look like in bronchitis in chronic cases

A

chronic inflammation can cause squamous metaplasia

mucous gland hyperplasia with mucus hypersecretion in respiratory bronchioles

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103
Q

what is the progression like for bronchitis

A

mild start and progress to severe

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104
Q

Give a symptom and 2 signs of bronchitis in chronic

A

cyanosis
hypoxaemia
hypercapnia

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105
Q

what is a complication of bronchitis in chronic

A

right heart failure

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106
Q

What is emphysema and how does it occur

A

permanent enlargement of alveolar and damage to elastin in alveolar
gas gets trapped in alveolar
neutrophils collect because of gas and free radicals so release neutrophil elastase and further damage elastin

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107
Q

What are three things that can increase the risk of emphysema

A

smoking
coal dust
alpha-1-antitrypsin deficiency

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108
Q

emphysema increases the risk of (2)… but not of (1)…

A

increased risk of pulmonary hypertension and bad oxygen delivery to tissues
not increased risk of cancer

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109
Q

What are two specific types of emphysema

A

senile emphysema that occurs with age

compensatory emphysema that occurs when one lung is not working

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110
Q

when do symptoms start in emphysema

A

after 1/3 of lung capacity has been lost

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111
Q

what is a complication of emphysema

A

right heart failure

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112
Q

What is bronchiectasis and what is affected

A

permanent dilation and thickening of the bronchus and bronchioles with inflammation and fibrosis signs

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113
Q

what is the pathophysiology of bronchiectasis

A

inflammation and obstruction. inflammation causes damage to mucociliary escalator so there is further obstruction

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114
Q

what causes bronchiectasis

A

severe infections e.g. Haemophilus influenza
immunodeficiency
excessive and persistence influx of inflammatory cells

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115
Q

what are the symptoms of bronchiectasis

A

shortness of breath, haemoptysis, productive cough, wheeze

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116
Q

what is the morphology of the bronchi and bronchioles in bronchiectasis

A

inflammation, fibrosis, dilation

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117
Q

how do you treat bronchiectasis

A

antibiotics if infection
supportive care
inhaler if obstruction but limited effect
physical therapy

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118
Q

what are complications of bronchiectasis

A

more infections

respiratory failure

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119
Q

What are four conditions that can cause restrictive lung diseases

A

obesity
neuromuscular
interstitial lung disease
chest wall diseases

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120
Q

What is kyphoscoliosis

A

the deformity of the spine, causes restrictive lung disease

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121
Q

what four things does interstitial lung disease do to the lungs

A

thickening of membrane between alveoles and capillary
alveolar surface area reduction
reduced compliance
increased stiffness

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122
Q

what 6 things can cause acute respiratory distress syndrome

A 
gas inhalation e.g. smoke
trauma
infection
radiation
narcotic abuse
shock
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123
Q

What are the two main types of interstitial lung diseases

A

idiopathic pulmonary fibrosis

sarcoidosis

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124
Q

What are 4 symptoms/signs/complications of acute/adult respiratory distress syndrome

A

tachypnea
dyspnea
arterial hypoxemia
pulmonary oedema

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125
Q

what is idiopathic pulmonary fibrosis and how does it occur

A

fibrosis of interstitium of lung in patchy pattern.
min. inflammation
proliferation of fibroblasts and deposition of collagen

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126
Q

what causes pulmonary fibrosis

A

idiopathic, unknown

link to asbestosis, radiation, sarcoidosis

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127
Q

what is another name for idiopathic pulmonary fibrosis

A

alveolitis fibrosis

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128
Q

What is the presentation of idiopathic pulmonary fibrosis

A

shortness of breath
finger clubbing
dry cough

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129
Q

what are some complications of pulmonary fibrosis

A

pulmonary hypertension
cor pulmonale
respiratory failure

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130
Q

briefly describe the epidemiology of pulmonary fibrosis

A

men>female

>60

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131
Q

how do you diagnose pulmonary fibrosis

A

xr: honeycomb lung
bloods: low oxygen normal co2

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132
Q

how do you treat pulmonary fibrosis

A

high dose prednisolone
lung transplant
NEW drugs to slow progression: pirfenidone and Nintedanib

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133
Q

What is sarcoidosis?

A

multisystem disease affecting skin lungs eyes
non-caseating granulomas form
autoimmune condition

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134
Q

What age group are most affected by sarcoidosis

A

20-40

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135
Q

what are the symptoms of sarcoidosis

A

dry cough, dyspnea

nodules under skin

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136
Q

what are two complications of sarcoidosis

A

renal damage, respiratory failure

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137
Q

How is sarcoidosis diagnosed

A

chest xr

high ACE serum

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138
Q

What is asthma

A

reversible obstruction caused by narrowing of lumen of airways by:
bronchiole hypersensitivity
mucus overproduction
hypertrophy and contraction of bronchiole smooth muscle
inflammation (partly from epithelium damage)

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139
Q

What are the two types of asthma

A

eosinophilic and non-eosinophilic

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140
Q

Subdivide eosinophilic asthma

A

non-atopic non-allergic

atopic allergic

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141
Q

describe eosinophilic atopic allergic asthma

A

indirect activation of mast cells
extrinsic allergens e.g. fungus, occupation, pets
family history often present

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142
Q

describe eosinophilic non-atopic non-allergic asthma

A

Direct activation of mast cells
Intrinsic allergens
late onset usually

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143
Q

describe non-eosinophilic asthma

A

large number of neutrophils compared to eosinophils

direct activation of mast cells

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144
Q

Name three type of non-eosinophilic asthma

A

non-smoking non-eosinophilic asthma
smoking-associated asthma
obesity-associated asthma

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145
Q

How does asthma occur?

A

inflammation:
mast cell degranulation occurs (direct activation via non-eosinophilic and for eosinophilic non-atopic and indirect for eosinophilic atopic). degranulation causes:
T cell recruitment which causes:
Mast cell more activation
B cell isotype switching to IgE (only in eosinophilic asthma)
Cytokine release to Epithelium to damage
eosinophils survive and migrate

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146
Q

Give 9 differences between COPD and Asthma

A
  1. COPD less diurnal variation and day to day variation (so spirometry always bad unlike asthma where sometimes good)
  2. COPD doesn’t respond to steroids, asthma does
  3. COPD later onset in age (but asthma can have late onset)
  4. Asthma has epithelium involvement, not COPD
  5. asthma less fibrosis than COPD
  6. reversibility in COPD is <15% but in asthma is >15%
  7. muscle hypertrophy is present in both but asthma has way more
  8. disruption of alveolar only in COPD
  9. Inflammation is present in both but different types of morphology
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147
Q

What are the differences in the inflammation process of asthma and COPD

A

asthma: eosinophils, CD4 T cells, mast cells IL4 histamine, little fibrosis, epithelium shedding
COPD: neutrophils, CD8 T cells, macrophages, IL8, destruction of lungs, fibrosis, squamous metaplasia

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148
Q

Symptoms of asthma

A 
episodic wheeze
cough
tight chest
shortness of breath
diurnal pattern (3-4am worse)
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149
Q

Diagnosis of asthma

A

history: family (atopies and smoking), occupation, any atopic conditions, age of onset, provoking factors
blood tests (check out eosinophil count)
chest XR
atopy/allergic testing
lung function tests: Peak expiratory flow and spirometry
reversibility: increase12% in FEV1 after treatment or increase 200ml in PEF after treatment
20% variability in PEF also suggests asthma

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150
Q

What is severe asthma

A

one of the major and 2 of the minor

major: continuous or near continuous oral steroids, high dose inhaled steroids
minor: daily or near-daily reliever treatment needed, near-fatal past event, 3 or more courses of steroids in year, one or more emergency hospital visits per year, prompt deterioration if less than 25% reduction in steroid dose, persistent obstruction

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151
Q

What are the treatment options available for asthma

A

bronchodilators that change symptoms not disease (i.e. don’t affect inflammation but will treat bronchoconstriction): Short and long-acting beta agonists, theophylline, anticholinergics
Anti-inflammatory drugs (disease modifying): inhaled steroids, biological therapies

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152
Q

Why do we not give inhaled steroids for everyone with asthma

A

side effects bad: osteoporosis, thin skin, adrenal suppression

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153
Q

give an example of a short and long-acting beta agonist used for asthma

A

short-acting: salbutamol

long-acting: salmeterol (not for acute attack as takes longer to start working)

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154
Q

give an example of steroid used to treat asthma

A

prednisolone

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155
Q

give two examples of biological therapies used to treat asthma

A

omalzumab

mepolzumab

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156
Q

What is the treatment path most used in asthma therapy

A

short acting beta agonist -> inhaled steroid -> long acting beta agonist -> more steroids -> hospital

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157
Q

Do the biological therapies work with all the types of asthma

A

no, only eosinophilic atopic asthma

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158
Q

What are the classifications of an asthma attack

A

uncontrolled/ moderate
severe
life-threatening
near-fatal

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159
Q

describe moderate asthma attack

A

PEFR >50%
Resp rate <25
Pulse rate <110
normal speach

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160
Q

describe severe asthma attack

A

PEFR 33%-50%
Resp rate >25
Pulse rate >110
Speach deteriorating

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161
Q

describe life-threatening asthma attack

A

PEFR <33%
PaO2<8kPa
PaCO2 NORMAL
unconsious ~

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162
Q

describe near-fatal asthma attack

A

PaCO2 raised

ventilation

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163
Q

what investigations do you use to recognise an asthma attack

A

PEF
Spirometry
Blood gases
XR (if life-threatening, suspect pneumothorax)

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164
Q

Is PaCO2 raised or low in life-threatening asthma attack

A

normal

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165
Q

Treatment of asthma attack

A 
oxygen 40-60%
salbutamol
prednisolone
check PEFR, ABG, potassium, glucose and consider rehydration
Discharge plan
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166
Q

What is the discharge plan after an asthma attack

A 
educate patient
reach 75% PEFR and <25% variability
Give prednisolone for 7-14 days and dont stop till improvements seen
GP visit within 48 hours
increase previous treatment
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167
Q

What is COPD

A

Chronic obstructive pulmonary disease
progressive airway obstruction
not a lot of variation over months
FEV1/FVC post dilator is <0.7 (i.e. poorly reversible)
Includes other conditions: emphysema, bronchitis

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168
Q

What are the risk factors for getting

COPD

A 
older age (rare in under 35)
men>women
smoking (largest risk)
co-morbidities
pollution
occupation
socio-economic status (lower more at risk)
childhood infection that means lungs didn't develop well
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169
Q

How does COPD occur?

A

Airflow resistance: inflammation, fibrosis, increased mucus production
Parenchymal destruction: elastin loss, alveolar attachment loss

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170
Q

Explain why the COPD patient breathes as they do?

A

They can breathe in normally
Breathing out has a scooped pattern. At first breathing out is fine but then quickly the airways collapse because the elastin can’t keep them open
Residual volume is lower in COPD even for tidal breathing so patient must have a higher end-expiratory volume so that they breathe tidal volume on top of that.

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171
Q

What is dynamic hyperinflation

A

end-expiratory volume must be higher than relaxation volume because the residual volume is low. So patient breathes have a higher initial volume and the tidal volume is breathed on top of that. occurs in COPD.

172
Q

Describe two vascular changes in COPD

A

fibrosis can cause pulmonary hypertension
V/Q mismatch (poor ventilation and maintained cardiac output) (in bronchitis COPD esp. poor ventilation lead to high CO2)

173
Q

Symptoms of COPD

A 
shortness of breath
cough productive
high respiratory rate
cyanosis
heart failure (but cardiac output is maintained so not really HF)
Wheeze
Peripheral effusion
Barrel-shaped chest
weight change
174
Q

What are the two phenotypes of COPD

A 
pink puffer (more emphysema in COPD, maintain O2 because high respiration rate, weight loss)
blue bloater (more bronchitis in COPD, high CO2 cyanosis, swollen ankles, "heart failure")
Can be overlaps and not tightly linked to underlying pathology
175
Q

Diagnosis of COPD

A

FEV1/FVC post dilator <0.7 PEFR and Spriometer
XR (lungs black not grey because fresh air not being removed)
Questionnaires

176
Q

What Questionnaires can help diagnose COPD

A

COPD assessment tool (CAT)

Medical research council dyspnea

177
Q

Describe what is assessed in CAT (COPD assessment tool)

A

8 things including SOB at hills etc, daily activities ability, sleep, energy, sputum, chest tightness, cough

178
Q

Describe the scores for MRC dyspnea test

A
  1. SOB during marked exertion
  2. SOB during hills, fast walk
  3. SOB during slow, flat terrain
  4. Excercise limit 100-200 yards
  5. Housebound
179
Q

What treatment options are there pharmacologically and machinery for COPD?

A 
Bronchodilators: anticholinergics, anti-muscarinic, beta agonist, theophylline (long-acting can reduce exacerbations not short)
Steroids inhaled improve symptoms and lung function and reduce exacerbations
Oxygen therapy (long term >15 hours per day)
Non-invasive ventilator (hold airway open but you breathe on own)
180
Q

What is the most cost-effective management for COPD

A

FLU vaccine

181
Q

What management option has the greatest capacity to improve natural history of COPD

A

Smoking

182
Q

What is the go-to treatment plan for COPD patients

A

Flu vaccines and smoking cessation
pulmonary rehabilitation (improve exercise strong link to lung function)
SABA/ short-acting anti-muscarinic (SAAM)/ short-acting anticholinergic
LABA/LAAM/LAAC
ICS
Combinations
Long-term oxygen therapy

183
Q

What are two risks of COPD and its treatments?

A

Respiratory failure

Pneumonia (with steroids)

184
Q

What is a respiratory exacerbation

A 
acute event
worsening of patient condition different to normal day to day variations
change in medication
accelerates lung function decline
increases mortality
185
Q

Main cause of COPD exacerbation

A

viral infections

infections

186
Q

What are common viral causes of pharyngitis

A

rhinovirus
adenovirus
glandular fever- Epstien Barr virus (suggests HIV)

187
Q

What are bacterial causes of pharyngitis

A

Group A Beta Haemolytic Streptococcus (strep. pyogene) (scarlet fever, rheumatic fever causes)
other streptococci (treat with amoxicillin)
Neisseria gonorrhoea (STI)
Corynebacterium diphtheria (grey membrane attached to tonsils, pharynx, treat with erythromycin)
Mycoplasm pneumonia

188
Q

What are we most worried about with pharyngitis

A

Epstien Barr virus (because of worry of HIV)

Bacterial causes

189
Q

How do we know if the pathogen causing the sore throat is viral or bacteria without doing laboratory tests?

A 
if 3 or 4 of these not met, then 80% chance viral
fever >38C
tonsilar exudate
tender anterior cervical adenopathy
cough
190
Q

Sinusitis common causes:

A

viral most common: rhinovirus, coronavirus
bacterial: haemophilus influenzae
streptococcus pneumonia

191
Q

What makes you suspect bacterial causes of sinusitis

A

unilateral pain
purulent discharge +/- fever
acutely or with complications of brain abscess etc. presentation

192
Q

Epiglottis symptoms

A 
dysphagia
pain on swallowing
high pitched wheeze
loss of weight
feeling unwell for past 6 months
sore throat
fatigue
193
Q

What is a worrying complication of Epiglottis

A

can swell enough to block airways

194
Q

What is the most likely cause of epiglottis

A

Haemophilus influenza

195
Q

How do you treat epiglottis from H. influenza

A

co-amoxiclav

196
Q

What are the four main disease categories

A

infection
inflammation
neoplastic
vascular

197
Q

What are the investigations we usually conduct with respiratory pathologies

A 
lung function tests
functional assessments
imaging
bronchoscopy
tracheoscopy
oximetry
198
Q

What lung function tests are there available

A

PEFR measures peak expiratory flow
Spirometry measures FEV1 and FEV and other lung volumes
Transfer factor measures the ability of oxygen to move past the alveolar membrane

199
Q

when is transfer factor high vs low

A

high for pulmonary haemorrhage

low for emphysema, anaemia

200
Q

Give two examples of functional assessments used in lung problem diagnosis

A

6 minute walk

incremental shuttle

201
Q

What are the risks of bronchoscopy

A

pneumonia
haemorrhage
pneumothorax

202
Q

what can bronchoscopy be used for

A

collecting samples

therapy e.g. putting a stent in, brachytherapy, laser

203
Q

WHat direction of XR direction is preferred?

A

posterior to anterior lying flat

if patient cannot then we do anterior to posterior but has to be labelled because organs look bigger

204
Q

What order to we first review the XR

A

hemidiaphragm- can see both sides fully, smooth, no gas
heart- not dilated, check behind (by checking density around)
aortic knuckle- not dilated
hilar points (between pulmonary upper and lower vessels) - not ascending or pushed down
pleura- can identify fully
ribs- can see spaces between. check similarities
missed points- apex of lung, bones, below diaphragm

205
Q

how do we identify abnormalities in XR

A 
dense or translucent (i.e. mass or gas)
mass effect or volume loss (mass effect push structures away from mass, volume loss pull structures towards loss)
consolidation- doesn't move structures because filling up space already there, white squiggly lines
silhouette signs (if missing then density either side same so air and air or tissue and tissue)
206
Q

What are the key silhouette signs to check on XR

A

RUL and upper heart
RML and lower heart anterior aspect and diaphragm
RLL and lower heart posterior aspect and diaphragm
LLL and lower heart and diaphragm
LUL and upper heart and diaphragm

207
Q

How do you check behind the heart in an XR

A

look for the triangular capacity which is behind the heart. It should be continuously dense which you can tell by the heart being one colour. If there are two colours then there is a change of density and we can this a sail sign.

208
Q

What is a sail sign on an XR

A

behind the heart abnormality

triangular capacity has two different densities

209
Q

What does a vale like covering over the left lung mean on XR. the left heart border is missing

A

left upper lobe collapse anteriorly

210
Q

What would you worry about with a movement of the mediastinum

A

pneumothorax

211
Q

What kind of imaging do PET scans take and why

A

take functional imaging

dye taken up more by fast dividing cells so cancers, inflammation and other things.

212
Q

In health what work do our muscles do to breath

A

low energy
inspiration via contraction of diaphragm to overcome flow resistance and elasticity (exercise use intercostals)
expiration passive relaxation of diaphragm to overcome flow resistance

213
Q

In pathology states what work do our muscles do to breath

A

higher energy use
inspiration: diaphragm contraction and accessory muscles, overcome hyperinflation and elastic recoil
expiration: accessory muscles used to overcome bronchoconstriction
muscle weakness can affect and increase energy use

214
Q

What is the ventilation pattern in obstruction lung pathologies

A

hyperinflation with rib expansion
accessory muscle use
increased diaphragm work
increased abdominal muscle use for expiration

215
Q

Which gas is mostly used to control breathing

A

co2

216
Q

Do you breath faster at day or night and when do you get most signals for breathing

A

faster at day because more signals

217
Q

when are you first likely to spot respiratory failure

A

during sleep at night so sleep studies are used in assessments of respiratory failure

218
Q

What are four causes of ventilation problems that cause hypoxaemia

A

low FiO2 (high altitude)
diffusion problems e.g. COPD, fibrosis
V/Q mismatch e.g. pulmonary embolism, pneumonia
hypoventilation e.g. muscle weakness, strokes, obesity

219
Q

Why are alterations of PaCO2 useful when diagnosing hypoxaemia

A

changes to co2 are purely to do with air getting in and out so purely alveolar hypoventilation which is a worrying diagnosis

220
Q

What are two patterns of breathing for a dying patient

A

Cheyne-stokes respiration

agonal breathing

221
Q

Describe cheyne-stoke respiration

A

switching between 60 second cycles of hyper and hypoventilation
during hyperventilation CO2 decreases so signals stop so slow down breathing and as co2 increases again signals start so hyperventilation occurs again

222
Q

describe agonal breathing

A

4-8 breathes than no breathing (apnea) and then back to the 4-8 breaths

223
Q

What are some reasons for hypoventilation to do with the central control system

A

hypothyroidism
metabolic alkalosis
post-sedation

224
Q

What are some reasons for hyperventilation to do with central control system

A

hyperthyroidism
anxiety
metabolic acidosis

225
Q

What are some problems to do with load on resp system that can cause resp failure

A

increased co2 production e.g. from infection or exercise
obstruction of airways e.g. copd asthma
elasticity damage e.g. copd fibrosis

226
Q

What are some problems to do with capacity of patient that can cause resp failure

A

decreased central drive e.g. from opioids
decreased strength of muscles e.g. diaphragm paralysis
sleep

227
Q

What oxygen level must someone have to be considered in resp failure

A

lower than 94%

228
Q

What are the steps to assessing what is causing the resp failure and the type

A

1 is their oxygen below 94%= resp failure
2 is their CO2 high= type 2 resp failure OR is it normal/low= type 1 resp failure
3 is their history suggestive of previously normal lungs/acute condition OR abnormal lungs/chronic condition
4 is the abnormality seen/findings suggestive of a localised problem or diffuse problem

229
Q

What are likely causes of type 1 resp failure with a chronic presentation

A

COPD
acute asthma
diffuse interstitial lung disorder

230
Q

What are likely causes of type 1 resp failure with an acute presentation and localised findings

A

pulmonary embolism
pneumonia
(v/q mistmatch)

231
Q

What are likely causes of type 1 resp failure with an acute presentation and diffuse findings

A

heart failure with cardiogenic oedema

adult respiratory distress sydrome

232
Q

What are likely causes of type 2 resp failure with a previously normal lung condition

A

sedation
neuromuscular problem
upper airway obstruction

233
Q

what are likely causes of type 2 resp failure with a previously abnormal lung condition

A

copd

asthma

234
Q

signs and symptoms of type 1 resp failure

A 
confusion
low blood pressure
low cardiac output
tachycardia
tachypnea
cyanosis
accessory muscle use
235
Q

signs and symptoms of type 2 chronic resp failure

A 
confusion
drowsiness
increased daytime sleeping
nightmares
witnessed apnea
disturbed sleep
dyspnea
orthopnea
headaches morning
seizures
frequent chest infections due to impairment of cough reflex
236
Q

signs and symptoms of type 2 acute resp failures

A 
confusion
warm peripheries
drowsiness
seizures
flapping termor
bounding pulse
237
Q

What is the management plan for someone with respiratory failure

A 
ABC
complete history and examination
treat underlying condition if possible
oxygen
breathing support
238
Q

What concentration of oxygen do you give for someone with resp failure

A

type 1 resp failure and never on type 2: 94-98%

type 2 resp failure: 88-92%

239
Q

why do you give a lower concentration of oxygen to someone with type 2 resp failure?

A

type 2 resp failure patient has become dependent on O2 for control of breathing because CO2 always high so stopped responding to co2. So if you give high oxygen, breathing stops because thinks you have enough and co2 dramatically increases leading to end-stage resp failure

240
Q

What are the breathing support available for resp failure and when do you use them

A

continuous positive airway pressure (CPAP) for type 1 resp failure usually- keeps airways open and lungs open
non-invasive ventilation (NIV) for type 2 resp failure often- keeps airways open
respiratory stimulants: caffiene, theophylline

241
Q

If you saw a drug that ended in -mab what would the first guess be to what type of drug it is

A

monoclonal antibody

242
Q

If you saw a drug that ended in -lone/-sole what would the first guess be to what type of drug it is

A

corticosteroid

243
Q

If you saw a drug that ended in -terol what would the first guess be to what type of drug it is

A

bronchodilator

244
Q

If you saw a drug that ended in -nib what would the first guess be to what type of drug it is

A

kinase inhibitor

245
Q

Give to ways we can deliver drugs to the lungs directly

A

inhaler

nebuliser

246
Q

what are the advantages to administrating drugs to the lungs

A

robust- can handle repeated exposure to the medication
less enzymes to change or break down the drug
drug can stay in lungs or go systemically so better control and less side effects systemically.

247
Q

What are the differences in conductive and respiratory airways that change drug delivery to these areas

A

conductive: small surface area, small blood flow so less absorption but high filtration so bigger drugs stop here
respiratory: large surface area and lots of blood flow and fast absorption rate

248
Q

what size do you want a drug to be to reach the respiratory airways, the conductive airways, or to stay in the mouth and throat

A

resp airways: 1-5um
conductive airways 5-10um
mouth and throat 10-15um
too small just be exhaled

249
Q

What things other than size of drug must we consider for delivery of drug

A

fast delivery and absorption needs small hydrophobic drug
intranasal route is worse than oral because smaller passage
forceful inhalation of drug means most drug lodged in upper airways

250
Q

Name something that can affect retention of the drug in the lungs

A

solubility higher

251
Q

How does pirfenidone work and what is it used for

A

slows idiopathic pulmonary fibrosis progression
anti-fibrotic, anti-inflammatory, anti-oxidant
less fibroblast proliferation, less collagen deposition

252
Q

How does nintedanib work and what is it used for

A

slows idiopathic pulmonary fibrosis progression

inhibits vascular endothelial growth factor receptors which drive fibrosis

253
Q

Give the 3 forms of beta 2 agonists available

A

short-acting beta agonists
long-acting beta-agonists
ultra-long-acting beta agonists e.g. indacaterol

254
Q

Why is it good to use beta-agonists and inhaled corticosteroids

A

work well together:

  1. the steroid increase transcription of beta 2 receptor gene so more beta 2 receptors on cell
  2. LABA increase translocation of growth factors to nucleus after steroid activates the cell
255
Q

why do we use anticholinergics to treat obstruction

A 
muscarinic receptors (m1-5) activated by Ach cause smooth muscle constriction so we antagonise that and stop constriction
e.g. tiotropium
256
Q

what does tiotropium come from originally

A

nightshade plant

atropine

257
Q

What cancers are included when we say lung cancer

A

primary lung cancers

and metastatic spread of tumours reaching the lungs

258
Q

give a brief overview of the epidemiology of lung cancers

A 
males: females 2:1
1/3 cause of all cancer deaths
3rd most common cancer for women
2nd most common cancer for men
lowest 5 year survival compared to prostate, colon, breast cancers
259
Q

What are the causes of lung cancers

A 
smoking
asbestos
radon
chromium
nickel refining
coal tar
petroleum products
aluminium
beryllium
genetics: loss of P53 more cell proliferation and apoptosis, loss of MYC more cell proliferation
iron oxide
arsenic
Lung fibrosis
260
Q

What are the two most common types of lung cancers

A

bronchial

pleural

261
Q

what are the two types of malignant bronchial cancers

A

non-small cell carcinoma

small cell carcinoma

262
Q

What is the proportion of malignant to benign bronchial cancers

A

95% malignant

5% benign

263
Q

What are the two commonest types of non small cell carcinoma

A

squamous

adenocarcinoma

264
Q

how do you treat non small cell carcinoma vs small cell carcinoma

A

NSCC radiotherapy and surgery

SCC chemotherapy

265
Q

Give a feature of the cells in small cell carcinoma

A

little cytoplasm

266
Q

which carcinoma of NSCC and SCC has the worst prognosis

A

SCC
metastatic on presentation (nscc somtimes)
grows faster if not treated than nscc
SCC always high grade but NSCC can be variety

267
Q

what risk factor are SCC and NSCC strongly associated with

A

smoking

268
Q

What are some benign bronchial tumours

A

lipoma
leiomyoma
fibroma

269
Q

What are the most common primary tumours of the bronchial

A

35% adenocarcinoma
25% squamous
20% small cell carcinoma
10% undifferentiated non-small cell carcinoma

270
Q

what is the most common cancer in non-smokers

A

adenocarcinoma

271
Q

What are symptoms of local lung cancer

A 
cough
SOB
wheeze
hoarseness
dysphagia
haemoptysis
chest pain
arm, neck swelling
malaise
272
Q

what are metastatic lung cancer symptoms

A 
bone pain
hepatic pain
abdominal pain
neurological deficits
Seizures
headaches
273
Q

where do lung cancers commonly metastasis to

A 
bone
brain
liver
lymph glands
adrenal glands
274
Q

What does paraneoplastic changes mean

A

non-metastatic manifestations of malignant disease

275
Q

in how many people do paraneoplastic changes for lung cancer occur in

A

2-5%

276
Q

What causes the paraneoplastic changes in lung cancers

A

production of PTH

production of ADH

277
Q

what can excessive secretion of ADH lead to

A

syndrome of inappropriate ADH secretion

278
Q

What are the symptoms of paraneoplastic changes in lung cancer

A 
finger clubbing
anorexia
weight loss
hypercalcaemia
hyponatraemia
peripheral neuropathy
279
Q

Can people with lung cancer present asymptomatically

A

yes and/or with constitutional symptoms only

these people have the best cure rate

280
Q

What staging do we use for lung cancer

A

TNM

281
Q

What do we need to know when diagnosing lung cancer

A

Is it lung cancer? what cell type? what stage

282
Q

what do we need to know when assessing the patient before treatment for lung cancer

A

operability

283
Q

What investigations do we carry out for diagnosis of lung cancer

A

XR
CT
PET
biopsy

284
Q

What does XR show for lung cancer

A

round, fluffy, spiking, shadow

285
Q

What type of biopsy can we do for lung cancer

A

ct guided biopsy
vacuum assisted biopsy
surgical biopsy

286
Q

To stage the lung cancer what do we need to check for

A

resectability: bloods

check for mets: CT

287
Q

What do we check for in inoperability of lung cancer

A

ecg
lung function
exercise capacity
performance status

288
Q

what are the scores you can get for performance status with lung cancer

A

0- normal
1- limited strenuous work, can do light work
2- can do self-care, cant do work for >50% of day
3- limited self-care, bed/chair bound for >50% of day
4- no self care, bed/chair bound all day

289
Q

Why do we somtimes delay treatment for lung cancer

A

if operability of patient is low, we try and treat symptoms first to improve the patient’s performance status

290
Q

What treatments do we use for NSCC

A

limited disease: surgery/ radical radiotherapy +/- chemotherapy
extensive: palliative chemotherapy

291
Q

what treatments do we use for SCC

A

limited: chemotherapy and radiotherapy
extensive: less chemotherapy

292
Q

are there treatments for lung cancer other than radio/chemo/surgery

A

5% of patients have genetics that allow them to have monoclonal antibodies that help immune system fight the tumour

293
Q

what do we mean by limited lung cancer

A

tumour in one hemithorax and can include if it’s in ipsilateral lymph nodes

294
Q

What tumours commonly spread to the lung from other sites

A 
breast
prostate
thyroid
kidney
colorectal
melanoma
lymphoma
295
Q

What are the types of cancers that can cause pleural cancers?

A

malignant e.g. mesothelioma

benign e.g. pleural fibroma

296
Q

what is mesothelioma

A

neoplasm of mesothelial cells (the mesothelium) which lines the pleural cavity, the pericardial cavity)

297
Q

where is the mesothelioma most common and why is it bad

A

pleural cavity
compresses on the lungs
erodes into the lungs
increase risk of infection

298
Q

what is metastasis like in mesothelioma

A

highly likely to occur even in early disease

spreads often to vertebra, liver, brain, chest

299
Q

briefly describe the epidemiology of mesothelioma

A

men > women

over 75 more common

300
Q

what are the risks to mesothelioma

A

asbestos

genetic small

301
Q

what are the symptoms of mesothelioma

A 
SOB
chest pain
lethargy
anorexia
abdominal pain
sweating
302
Q

what do we use for diagnosis of mesothelioma

A

XR - pleural effusion, rib destruction
CT
pleural aspiration- straw-coloured to blood-stained
biopsy- best for diagnosis

303
Q

Treatment of mesothelioma

A 
not many options
surgery to debulk
palliative chemotherapy and radiotherapy
psychological support
symptom support esp. pain
304
Q

What is the average duration from diagnosis to death

A

8-12 months

305
Q

what is a condition that you must not cremate the body

A

mesothelioma death because have to let coroner check for occupational link to asbestos

306
Q

What are the phases of whooping cough

A

incubation 5-21 days
catarrhal 1-2 weeks
paroxysmal 1-6 weeks
convalescent

307
Q

What are the symptoms of whooping cough in the catarrhal phase

A

low grade fever
conjunctivitis
lymphocytosis
rhinorrhea

308
Q

what are the symptoms of whooping cough in the paroxysmal phase

A

spasm cough
post-cough vomiting
whoop sound when inspiring air

309
Q

What causes whooping cough

A

bordetella pertussis gram negative bacillus

310
Q

How does the bacteria cause whooping cough

A

bordetella pertussis causes hyperplasia of lymph nodes so inflammation and whooping

311
Q

what treatment do we give for whooping cough

A

clarithromycin
chemo-prophylaxis
vaccines

312
Q

what are the complications of whooping cough

A

pneumonia
encephalopathy
sub-conjunctivitis haemorrhage

313
Q

What is croup

A

laryngo-tracheobronchitis

314
Q

what causes croup

A

parainfluenza virus mostly

also RSV, influenza A and other viruses

315
Q

What are the symptoms of croup

A 
barking cough
interstitial recessions
high resp rate
febrile
cyanosed
inspiratory stridor
316
Q

what age group is affected by croup

A

3 months to 6 years

317
Q

what is the clinical picture of whooping cough in adults

A

chronic cough and in 1/2 of patients post-cough vomiting

318
Q

What is pneumonia

A

inflammation of the lungs and the lung parenchyma with neutrophil infiltration

319
Q

% of pneumonia patients hospitalised and in ITU

A

20-50% hospitalised

5-10% UTI

320
Q

Mortality rate for community, hospital, ITU patients with pneumonia

A

1% for community
10% for hospital
30% for UTI

321
Q

what are the risk groups for pneumonia

A 
infants, elderly
COPD, swallowing dysfunction
IVDU, alcoholics
diabetes, congestive heart disease
nursing home residents, immunocompromised
322
Q

what pathogens cause pneumonia in immunocompromised patients

A

all bacteria but with atypical presentations and also Pseudomonas aeruginosa

viral: adenovirus, RSV, cytomegalovirus
fungus: pneumocystis pneumonia

323
Q

What are the steps of pathophysiology to pneumonia (6)

A
  1. translocation of pathogen to previously sterile lower airways
  2. phagocytosis by macrophages
  3. if too much pathogen or resistant to phagocytosis macrophage recruits other immune cells e.g. neutrophils
  4. neutrophils kill pathogen but cause inflammation which forms exudate of dead pathogens, dead immune cells, inflammatory proteins which causes consolidation on XR
  5. resolution phase remove the exudate via apoptosis. if all removed then full recovery
  6. but if not, e.g. severe pneumonia, communication with blood cells and systemic disease occurs
324
Q

What are the symptoms of pneumonia

A 
fever
rigours
sweats
cough
shortness of breath
systemic features: headache, weakness, malaise
\+/- sputum
pleuritic chest pain
325
Q

what are the signs of pneumonia

A 
high resp rate, high pulse rate
low blood pressure dehydration
fever
dull to percussion
hypoxia and sometimes signs of resp failure
crackle
326
Q

What is atypical pneumonia

A

when the systemic symptoms are more than the other symptoms

327
Q

what is rusty coloured sputum in pneumonia suggestive of?

A

streptococcus pneumonia

328
Q

what non-pulmonary symptoms does legionella cause in pneumonia?

A

neurological- confusion, encephalitis

gastrointestinal- diarrohea, abnormal liver function, intestinal nephritis

329
Q

What things should you do for investigations of pneumonia and finding the causative organism

A

XR
Bloods- U&E, FBC, WBC, C-reactive protein, LFT (check response to treatment and check liver and kidneys)
Microbiology- culture, serology, sensitivity
ABG- check o2 good and not resp failure

330
Q

What things in the XR are you looking for in pneumonia

A

consolidation
abscess
diffuse shadowing
pleural effusion

331
Q

What does consolidation in multiple lobes on XR suggest in pneumonia

A

strep. pneumonia
staph. aureus
legionella

332
Q

What do multiple abscesses suggest in XR in pneumonia

A

staph aureus

333
Q

what does a cavity in upper lobe XR pneumonia suggest

A

Klebsiella pneumonia (after ruling out TB)

334
Q

What does diffuse shadowing in XR for pneumonia suggest

A

pneumocytosis pneumonia

335
Q

What do you do with a pleural collection in XR pneumonia

A

drain it and manage

336
Q

What microbiology samples do you need for pneumonia investigations

A

sputum and blood and urine

337
Q

what cultures do you do with the sputum for pneumonia

A

ZN for TB
chocolate agar
blood agar
PCR for TB

338
Q

What could grow on the chocolate agar plate for sputum fro pneumonia patient

A

strep. pneumonia
staph aureus
haemophilus influenza
gram negative bacillus

339
Q

What cultures do you expect to grow with blood cultures in pneumonia

A

aerobic: strep pneumonia, staph aureus, h. influenza
anaerobic: strep pneumonia

340
Q

what are you looking for in the urine sample for microbiology in pneumonia

A

legionella antigen

strep pneumonia

341
Q

what part of the history would suggest legionella for pneumonia

A

hot place travel

confusion

342
Q

What serology and PCR would you want to do when investigating pneumonia

A

viruses
atypical pathogens
mycoplasm pneumonia

343
Q

How do you know if you should admit someone with community-acquired pneumonia to hospital

A

CAP severity assessment. give a point for each:
confusion
urea > or equal to 7mmol/L
Resp rate > or equal to 30/min
>65 age
blood pressure low (dyastole<60, systole<90)

344
Q

What do the scores from the CAP severity assessment mean?

A

0-1: mild, only admit if single worrying factor
2: moderate admit
3-4: severe, admit and monitor
4-5: admission consider to ITU

345
Q

Do you treat after diagnosis of pneumonia or after?

A

before empirically and then when you know what the cause is narrow treatment to be more specific

346
Q

What do you give for mild pneumonia

A

amoxicillin oral or clarithromycin oral

347
Q

what do you give for moderate pneumonia

A

amoxicillin + clarithromycin oral

348
Q

what do you give for severe pneumonia

A

IV co-amoxicav + clarithromycin
OR
IV cefuroxime + clarithromycin

349
Q

what are the most common causative infections for patients hospitalised from pneumonia

A 
strep. pneumonia (40%)
chlamydophilia pneumonia (13%)
mycoplasma pneumonia (11%)
haemaphilus influenza (5%)
legionella pneumophilia (4%)
klebseilla pneumonia (low% but in IVDU, homeless)
staphylococcus auresu (low%)
viruses (13%)
350
Q

What are the most common causative infections for patients hospitalised in ITU for pneumonia

A

strep. pneumonia
staph. aureus
legionella pneuomophilia
viruses

351
Q

What drugs do you give for strep. pneumonia causing pneumonia

A

amoxicillin or cefuroxime

or clarithromycin

352
Q

what drugs do you give for Haemophilus pneumonia causing pneumonia

A

co-amoxiclav

or doxycycline

353
Q

what drugs do you give for staph aureus causing pneumonia

A

flucloxacillin or cefuroxime

resistent vancomycin

354
Q

klebsiella pneumonia

A

co-amoxiclav

355
Q

What are the atypical pathogens that cause pneumonia

A

legionella pneumophila
mycoplasm pneumonia
chlamydophila pneumonia

356
Q

What do we give to treat atypical pathogens that cause pneumonia

A

clarithromycin
ciprofloxacin
doxycycline

357
Q

What makes the atypical pathogens that cause pneumonia harder to treat

A

they grow in cells

intracellular

358
Q

what drug do you give for necrotising pneumonia

A

clindomycin, rifampicin

359
Q

what drug do you give for pseudomonas aeruginosa causing pneumonia

A

ceftazidime +/-gentamycin

360
Q

What is a hospital-acquired pneumonia infection

A

that acquired at least 48 hours after being admitted

361
Q

How do you diagnose a hospital-acquired pneumonia

A

new fever
new leukocytosis
higher demand for oxygen
new radiological signs on xr

362
Q

What are the causative pathogens of hospital-acquired pneumonia

A

early onset <5 days same organisms as community-acquired pneumonia
late onset >5 days: staph aureus, Pseudomonas aeruginosa, Acinetobacter bacumani, Klebsiella pneumonia usually multi-drug resistant

363
Q

What are the common and serious multi-drug-resistant pathogens

A 
ESKAPE
Enterococci
staph aureus
klebsiella pneumonia
aeruginosa bacumani
pseudomonas pneumonia
enterobacter
364
Q

How do you prevent pneumonia infections

A

vaccines: pneomococcal vaccine, influenza vaccine

smoking cessation

365
Q

Who is given a pneumococcal vaccine for pneumonia prevention

A

> 65
splenic dysfunction
chronic medical diseases
immunocompromised

366
Q

What is para-pneumonic empyema

A

pus in pleural space due to pneumonia

367
Q

How often does para-pneumonic empyema and effusion occur

A

30-60% of community-acquired pneumonia patients

368
Q

what are the signs of an effusion or empyema

A

fever/inflammation not settling with antibiotics
pain on deep inspiration
dull to percussion

369
Q

How do you investigate para-pneumonic effusion or empyema

A

pleural aspiration to see if fluid will heal on own or empyema/ complicated effusion so needs treating.

370
Q

after a pleural aspiration, what would you find if the fluid needs drainage due to pneumonia

A

pH<7.2
glucose<3.3mmol/L
pus or thick fluid
positive bacterial culture

371
Q

How do you treat para-pneumonic effusion and empyema

A

drainage of fluid via chest tube or cardio-thoracic surgery

antibiotics long duration: co-amoxiclav, meropenem

372
Q

Name two groups of people more likely to have lung abscess

A

alcoholics

poor oral health

373
Q

What are 4 examples of causative organisms of lung abscesses

A

strep milleri
klebsiella pneumonia
If from metastatic infection from venous system could be: staph aureus, fusobacteria

374
Q

what is a complication of lung abscess

A

empyema

375
Q

how do you treat lung abscesses

A

antibiotics long course e.g. 6 weeks

surgical drainage

376
Q

What is bronchiolitis

A

inflammation of bronchioles and mucus production occurs causing obstruction

377
Q

What causes bronchiolitis

A

RSV

378
Q

What is bronchitis

A

inflammation of epithelium of bronchus, usually self-limiting, due to infection
different presentation with acute and chronic (chronic in COPD)

379
Q

What are the causative agents of acute bronchitis

A

viral usually

if bacteria consider immunocompromised e.g. chlamydia pneumonia, mycoplasma pneumonia, bordetella petussis

380
Q

What are the clinical signs of acute bronchitis

A

cough +/- productive lasts over 5 days (usually 1-3 weeks)
wheeze and SOB
fever and systemic features suggestive of pneumonia or influenza

381
Q

How do we investigate bronchitis in acute

A

XR to exclude pneumonia, normal in bronchitis usually
throat viral and bacterial swab
serology for mycoplasma pneumonia and chlamydia pneumonia

382
Q

how do we treat acute bronchitis

A

viral- supportive care, self-limiting

bacteria- little evidence that anti-microbial’s are helpful unless bordetella pertussis

383
Q

name 3 emerging respiratory viral infections

A

severe acute respiratory syndrome from coronavirus
middle eastern respiratory syndrome from novel coronavirus
avian influenza from new form of influenza A

384
Q

What family does Influenza family belong to

A

orthomyxoviridia

385
Q

How many influenza genera are there

A

3 A B C

386
Q

Describe Influenza A

A

lots of mutation
can infect pigs, birds, horses, humans
causes large outbreaks, severe, pandemics

387
Q

Describe influenza B

A

lots of mutations but less than A
less severe than A but still bad
sporadic outbreaks e.g. in schools, care homes
more in children

388
Q

Describe influenza C

A

less mutations
mild symptoms
or asymptomatic

389
Q

How many antigenic sites does influenza have, name them

A 
4
hemagglutinin
neuraminidase
M2 ion channel
ribonucleoprotein
390
Q

Which influenza genera are more common

A

A B

391
Q

Which two antigenic sites does influenza A and how many subtypes are there

A

hemagglutinin 15

neuraminidase 9

392
Q

What is hemagglutinin used for and what does immunity to one subtype do

A

attachment and entry to cell by virus

immunity against one subtype gives you protection against that one subtype

393
Q

What is neuraminidase used for and what does immunity against one subtype do

A

gets new viruses out of cell and stops them from clumping together
immunity against one subtype means less of that subtype viruses but not full immunity

394
Q

What subtypes of influenza A are found in humans vs birds

A

humans: H1,2,3 (RARE 5) n1, 2
Birds: all

395
Q

what is the genetic material of flu A like

A

8 RNA single stranded RNA pieces

396
Q

what three ways can mutations occur in flu A

A

genome segmentation with gene re-assortment
gene swapping
no proof reading mechanism

397
Q

when do genome segmentation occur to flu A RNA

A

co-infection with two different flu A viruses

398
Q

when does gene swapping occur to flu A RNA

A

co-infection with human and avian virus

can occur directly or with intermediate pig

399
Q

What occurs to cause seasonal outbreaks vs pandemic outbreaks of flu A

A

antigenic drift: seasonal outbreaks

antigenic shifts: pandemics

400
Q

What are the methods of transmission of flu A

A

aerosol e.g. cough

hand to hand contact

401
Q

what is the definition of reproductive number

A

average number of secondary cases generated from primary case in susceptible population

402
Q

what is the reproductive number of influenza A

A

1-3 in pandemics

1.3-1.5 in seasonal outbreaks

403
Q

Who are the at risk groups of influenza A

A

chronic heart, pulmonary, renal, metabolic, neurology problems
old
immunocompromised

404
Q

What are the symptoms of influenza A

A 
lower and upper resp infection symptoms 
fever
malaise
weakness
sore throat
dry cough
405
Q

When is seasonal flu occurring in northern and southern hemispheres

A

north: dec-march
south: may-sept

406
Q

What is a complicattion of flu

A

bacterial and viral pneumonia

407
Q

How do you treat flu

A

symptomatic phase: supportive care: oxygen, fluids, nutrition, prevent 2 infections
Tamiflu (oseltamivir) within 48 hours of first symptoms

408
Q

What is tamiflu’s role

A

oseltamivir
48 hours or before of first symptoms
reduces transmission as it:
reduces infective period of patient and symptoms of patients by 1-1.5 days
can be used as prophylaxis to at risk groups

409
Q

How does oseltamivir treat influenza

A

stops virus attaching to respiratory epithelium and entering so replication reduces as does inflammation
inflammation usually causes cough and spread of aerosols so less of cough and less transmissions

410
Q

what is the difference between an outbreak, an epidemic, a pandemic

A

outbreak: 2 or more linked cases
epidemic: more cases in region/ country
pandemic: epidemics that cross international borders

411
Q

Why do we have annual vaccines for flu

A

seasonal outbreaks occur every year dec-march
usually due to antigenic drift with change in virus so previous immune from last year vaccine or infection not immune to changed virus

412
Q

What do pandemic flus cause

A

high mortality and morbidity
social disruption
economic disruption

413
Q

What subtype of influenza A caused the spanish flu

A

H1N1

414
Q

Which subtype of influenza A is documented to spread from birds to humans but not humans to humans

A

h5n1

415
Q

which subtype of influenza A caused two historical pandemics

A

H1N1
1918 and 2009
in 2009 the older population were mostly immune due to 1918 infection giving them immunity

416
Q

How long in advance do we need to make a flu vaccine

A

6-9 months

417
Q

how many strains of flu A are in the annual vaccine

A

3

418
Q

in a pandemic of flu what is the incubation period

A

1-4 days

419
Q

in a pandemic of flu what is the infectious period

A

start of symptoms until 4-5 days after end of symptoms

10% infectious before symptoms

420
Q

how many phases are there to managing a pandemic of flu

A

containment and treatment phase

2

421
Q

what occurs in the containment phase of managing a pandemic of flu

A

identify cases, treat them, contact tracing
infection control: hand hygiene, stop mass gatherings
flu surgeries

422
Q

when does treatment phase of managing a pandemic flu start

A

when cases so many no point trying to contain the disease, it’s no longer contained

423
Q

what is the plan for treatment phase of pandemic flu management

A

treat flu patients only

manage patients so some hospital some antivirals at home etc.

424
Q

why will we get more pandemics likely

A

more travel
more people
more intensive farming so more chance of antigenic shift

425
Q

why will we not get a pandemic likely

A

better overall health
anti-virals
vaccines
methods of controlling avian flu

Phase 2a Introductory Clinical Science (7 decks)

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