Respiratory System Flashcards
1
Q
How many resp tract infections per year do children have? adults?
A
children 2-5
adults 1-2
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
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
4
Q
Why are sinuses sterile?
A
outward flow of liquid
5
Q
Where are the commensal organisms in the resp tract?
A
nasal cavity
oral cavity
pharynx
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
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)
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
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%
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
11
Q
when does rhinovirus typically infect (most common, can infect all year)
A
spring and autumn
12
Q
does rhinovirus infect upper or lower resp?
A
both but upper more
13
Q
How long is the incubation period for rhinovirus? how long do symptoms last?
A
12-72 hours incubation
7-22 days symptoms
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
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
16
Q
How does rhinovirus attach?
A
capsid protein to receptors of host cells
17
Q
What syndrome can coronavirus cause that is worrying?
A
severe acute respiratory syndrome
18
Q
What are the severe conditions that parainfluenza virus can cause
A
croup, bronchitis, bronchiolitis, pneumonia
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
20
Q
what symptoms does a child infected with the respiratory syncytial virus show
A
wheezing and respiratory distress
21
Q
How does respiratory syncytial virus cause pathology?
A
bronchiolitis and releases secretions
both narrow the airways
22
Q
What is a normal breathing rate for a baby? child? adult?`
A
baby 40-60
child 30-40
adult <20
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)
24
Q
what causes TB
A
mycobacterium tuberculosis / bovis
25
describe the pathogen that causes TB (8)
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
26
What are the groups of people most at risk of TB infections
```
prisons
industrialisation
over crowded areas
close homes
homeless
ivdu
alcoholics
poverty
born in high prevalence area
race: African, Indian, Pakistani
malnourished
```
27
how is TB transmitted?
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
28
Where do TB mycobacteria prefer to settle in lungs?
apex because less blood and more air so best survival
29
What happens when the mycobacteria first infect the lungs? What happens in the best case scenario vs. the other option?
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
30
In how many people does PTB occur vs no infection?
>95% of people kill all mycobacteria or contain it effectively
2-5% get PTB clinically evident
31
What is latent TB?
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.
32
What happens if after the initial infection of TB the bacilli are not contained?
Pulmonary TB occurs
33
What can happen if after latent TB or pulmonary TB bacilli are still not contained
Miliary TB aka Serious non-pulmonary TB
34
What happens in pulmonary TB?
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.
35
What is in the granuloma during TB
```
fibroblasts
epithelium
macrophages
lymphocytes
bacilli
```
36
what is the aim of the granuloma in TB
wall of the bacilli and stop it from getting nutrition
37
What thing can the patient do and what thing can the primary focus (the TB granuloma) do to increase transmission
patient can cough and expel bacilli which were in the cavity
| cavity can erode into the airways
38
What is miliary TB/ serious non-pulmonary TB
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.
39
Give 5 examples of where TB can occur other than pulmonary?
```
joint and bone TB
pleural TB
genitourinary TB
meningitis TB
Abdominal TB
```
40
What are the systemic symptoms of TB (4)
night sweats - most predictive 2nd
weight loss - most predictive 1st
malaise
low-grade fever
41
what are the symptoms of TB that are pulmonary specific
```
cough >3 months
chest pain
breathlessness
haemoptysis
and possible: consolidation, pleural or pericardial effusion, lobar collapse
```
42
why would lobar collapse happen with TB
if a bronchus is obstructed
43
What are some non-pulmonary organ TB symptoms? give two example for each organ
bone: bone pain, swelling of joint
abdomen: ileum malabsorption, ascites
CNS: meningitis, paralysis
lymph: enlargement, secretions
GU: epididymitis, dysuria
44
What investigations do you want to carry out to diagnose TB:
Microscopy, culture, PCR, mycobacteria growth indicator tube, whole genome sequence
Bloods
XR
45
What are you looking for when analysing bloods for TB?
```
Prolonged inflammatory markers:
thrombocytosis
normocytic anaemia
hypoalbuminaemia
hypercalcaemia
hypergammaglobulinaemia
sterile pyuria
raised ESR, CRP
```
46
What samples can we collect for analysing (other than blood)?
```
sputum
urine
CSF
pleural fluid
biopsy: bone, peritoneum, lymph
```
47
What stains can we use for TB microscopy?
ZN stain
| Auramine phenol stain (needs less number of bacilli to spot them unlike ZN which needs more)
48
How do cultures and mycobacteria growth indicator tube help TB grow
they have low levels of antibiotics to prevent growth of other bacteria which grow quickly
have glycerol to promote the mycobacteria tuberculosis growth
49
What laboratory technique can we use to check TB drug sensitivity
PCR
| whole genome sequences
50
What test can we do to diagnose latent TB?
Mantoux test (protein injected intradermally to get type 4 delayed hypersensitivity reaction)
51
How many drugs are used to treat TB? Name them
```
4 PERI
Pyrazinamide
Ethambutol
Rifampicin
Isoniazid
```
52
How long do we give the drugs for TB?
Pyrazinamide 2 months
Ethambutol 2 months
Rifampicin 6 months
Isoniazid 6 months
53
Do we ever give a longer duration of drugs for TB?
for CNS TB we give 12 months
54
How do the drugs used for TB work?
Pyrazinamide - initially bactericidal
Ethambutol - bacteriostatic by blocking cell wall synthesis
Rifampicin- bactericidal by blocking protein synthesis
Isoniazid- bactericidal by blocking cell wall synthesis
55
What are the side effects for the drugs used for TB?
Pyrazinamide - rash, arthralgia, hepatitis
Ethambutol- optic neuritis
Rifampicin - hepatitis, red urine benign
Isoniazid - hepatitis and neuropathy
56
What can happen if people aren't taking their medication
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
57
How can we prevent TB? (4)
case finding e.g. testing risk groups
find latent TB before it can become active
chemoprophylaxis
vaccines (BCG vaccine)
58
How can we treat Latent TB?
3month rifampicin and isoniazid
or
6 month isoniazid
59
Which group of patients can't have the BCG vaccine for TB and why?
immunocompromised as they get BCG-osis
60
What are occupational lung disorders?
Lung disorders that occur due to exposure at workspace that damages the respiratory system
61
How much does FEV1 decrease for men and women as they age normally?
30ml for men
| 25ml for women
62
What type of things can cause occupational lung disorders?
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
63
What type of things can cause occupational lung disorders?
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
64
How can we divide exposures of OLD into timescale?
historic, current, future
65
Describe historic exposures, what we can do for patients
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
66
Describe current exposures, what we can do for patients
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.
67
Name 7 common occupational lung disorders
```
occupational asthma
extrinsic allergic alveolitis/ hypersensitivity pneumonitis
pleural plaque
diffuse pleural thickening
mesothelioma
asbestosis
chronic inflammation e.g. COPD
```
68
Name 4 common occupational lung diseases which are related to asbestos
asbestosis
mesothelioma
pleural plaques
diffuse pleural thickening
69
What proportion of adult-onset asthma is due to occupational asthma?
9-15%
70
What is occupational asthma due to? Give proportions to how common each of the causes is
occurs due to sensitisation (allergy) to inhaled agent (90%)
| due to massive accidental irritant exposure that causes direct damage to airways (10%)
71
What are 3 common causative agents of occupational asthma?
wood dust
flour
cleaning products
72
Can we cure occupational asthma?
possible if we remove exposure but not always. prognosis will improve though definitely if remove exposure
73
What is EEA/HP and why does it happen
extrinsic allergic alveolitis/ hypersensitivity pneumonitis
| occurs due to sensitisation to environmental or occupational allergen
74
What causes EEA/HP. divide into 4 classes and give examples:
microorganisms - cheese workers, sewer workers
animals - birds, rodents
vegetation - coffee, wood
chemicals - pesticide, plastic
75
what does EEA/HP cause and what is the pathophysiology
interstitial lung disease
| air gets trapped in lungs and fibrosis occurs
76
Classify EEA/HP into 3 subtypes and describe them
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
77
what are the symptoms of EEA/HP
wheezing, shortness of breath, productive cough
| constitutional symptoms: headache, weight loss
78
what does the chest XR of TB show
pleural effusion, pathy or nodular shadow
79
What are the normal causes of occupational COPD
historical exposures typically e.g. grain, coal, silica
80
What is asbestos?
naturally occurring mineral fibre
81
What are pleural plaques made off?
pleural collagen and calcified on top
82
How are pleural plaques linked to asbestos?
asbestos causes pleural plaques but not linear relationship. More asbestos does not equal more plaques
83
Are pleural plaques linked to cancer
no they are not pre-malignant
84
What can diffuse pleural thickening do to the lungs and what are the symptoms
restrict the lungs from expanding so shortness of breath and respiratory failure can occur
85
How do you treat diffuse pleural thickening
no effective treatment
86
Does removing the exposure stop pleural thickening from advancing
no because it can develop slowly even if the exposure stops
87
What lung problem and pleural problem accompanies asbestosis
pulmonary fibrosis
| +/- pleural plaques
88
How much asbestos exposure do you need for asbestosis to occur
lots
89
Does asbestosis kill
yes
90
does removing the exposure stop asbestosis from advancing
no continues even if exposure stops
91
What can we do to prevent OLD
```
1 eliminate
2 substitute
3 workers education
4 engineering changes e.g. exhaust ventilation
5 protective equipment e.g. masks
```
92
Why are health surveillance good
identify problems early
| if residual risk can check workers' health annually.
93
what are the three types of non-neoplastic lung diseases?
restrictive
obstructive
gas exchange
94
Describe restrictive and obstructive lung problems: what? FEV1 to FVC? FEV1/FVC?
restrictive: problems with air getting IN. FEV1>FVC FEV1/FVC>80%
obstructive: problems with air getting OUT. FEV1
95
What could cause acute obstruction?
tumour or foreign body
96
What are the consequences of the acute obstruction
lobar collapse OR over expansion (valve effect)
| secretions can complicate this
97
What does pulmonary function tests look like in acute obstruction
normal
98
where are chronic obstructions mainly focused
bronchus and bronchioles
99
Give 4 examples of chronic obstructive conditions
bronchitis
emphysema
asthma
bronchiectasis
100
Give 3 risk factors for bronchitis
smoking
chronic pollution
recurrent Haemophilus influenza, strep. pneumonia, adenovirus infections
101
Give one feature to how we diagnose bronchitis for COPD
productive cough for 3 months for 2 consecutive years
102
what do the bronchioles look like in bronchitis in chronic cases
chronic inflammation can cause squamous metaplasia
| mucous gland hyperplasia with mucus hypersecretion in respiratory bronchioles
103
what is the progression like for bronchitis
mild start and progress to severe
104
Give a symptom and 2 signs of bronchitis in chronic
cyanosis
hypoxaemia
hypercapnia
105
what is a complication of bronchitis in chronic
right heart failure
106
What is emphysema and how does it occur
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
107
What are three things that can increase the risk of emphysema
smoking
coal dust
alpha-1-antitrypsin deficiency
108
emphysema increases the risk of (2)... but not of (1)...
increased risk of pulmonary hypertension and bad oxygen delivery to tissues
not increased risk of cancer
109
What are two specific types of emphysema
senile emphysema that occurs with age
| compensatory emphysema that occurs when one lung is not working
110
when do symptoms start in emphysema
after 1/3 of lung capacity has been lost
111
what is a complication of emphysema
right heart failure
112
What is bronchiectasis and what is affected
permanent dilation and thickening of the bronchus and bronchioles with inflammation and fibrosis signs
113
what is the pathophysiology of bronchiectasis
inflammation and obstruction. inflammation causes damage to mucociliary escalator so there is further obstruction
114
what causes bronchiectasis
severe infections e.g. Haemophilus influenza
immunodeficiency
excessive and persistence influx of inflammatory cells
115
what are the symptoms of bronchiectasis
shortness of breath, haemoptysis, productive cough, wheeze
116
what is the morphology of the bronchi and bronchioles in bronchiectasis
inflammation, fibrosis, dilation
117
how do you treat bronchiectasis
antibiotics if infection
supportive care
inhaler if obstruction but limited effect
physical therapy
118
what are complications of bronchiectasis
more infections
| respiratory failure
119
What are four conditions that can cause restrictive lung diseases
obesity
neuromuscular
interstitial lung disease
chest wall diseases
120
What is kyphoscoliosis
the deformity of the spine, causes restrictive lung disease
121
what four things does interstitial lung disease do to the lungs
thickening of membrane between alveoles and capillary
alveolar surface area reduction
reduced compliance
increased stiffness
122
what 6 things can cause acute respiratory distress syndrome
```
gas inhalation e.g. smoke
trauma
infection
radiation
narcotic abuse
shock
```
123
What are the two main types of interstitial lung diseases
idiopathic pulmonary fibrosis
| sarcoidosis
124
What are 4 symptoms/signs/complications of acute/adult respiratory distress syndrome
tachypnea
dyspnea
arterial hypoxemia
pulmonary oedema
125
what is idiopathic pulmonary fibrosis and how does it occur
fibrosis of interstitium of lung in patchy pattern.
min. inflammation
proliferation of fibroblasts and deposition of collagen
126
what causes pulmonary fibrosis
idiopathic, unknown
| link to asbestosis, radiation, sarcoidosis
127
what is another name for idiopathic pulmonary fibrosis
alveolitis fibrosis
128
What is the presentation of idiopathic pulmonary fibrosis
shortness of breath
finger clubbing
dry cough
129
what are some complications of pulmonary fibrosis
pulmonary hypertension
cor pulmonale
respiratory failure
130
briefly describe the epidemiology of pulmonary fibrosis
men>female
| >60
131
how do you diagnose pulmonary fibrosis
xr: honeycomb lung
bloods: low oxygen normal co2
132
how do you treat pulmonary fibrosis
high dose prednisolone
lung transplant
NEW drugs to slow progression: pirfenidone and Nintedanib
133
What is sarcoidosis?
multisystem disease affecting skin lungs eyes
non-caseating granulomas form
autoimmune condition
134
What age group are most affected by sarcoidosis
20-40
135
what are the symptoms of sarcoidosis
dry cough, dyspnea
| nodules under skin
136
what are two complications of sarcoidosis
renal damage, respiratory failure
137
How is sarcoidosis diagnosed
chest xr
| high ACE serum
138
What is asthma
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)
139
What are the two types of asthma
eosinophilic and non-eosinophilic
140
Subdivide eosinophilic asthma
non-atopic non-allergic
| atopic allergic
141
describe eosinophilic atopic allergic asthma
indirect activation of mast cells
extrinsic allergens e.g. fungus, occupation, pets
family history often present
142
describe eosinophilic non-atopic non-allergic asthma
Direct activation of mast cells
Intrinsic allergens
late onset usually
143
describe non-eosinophilic asthma
large number of neutrophils compared to eosinophils
| direct activation of mast cells
144
Name three type of non-eosinophilic asthma
non-smoking non-eosinophilic asthma
smoking-associated asthma
obesity-associated asthma
145
How does asthma occur?
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
146
Give 9 differences between COPD and Asthma
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
147
What are the differences in the inflammation process of asthma and COPD
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
148
Symptoms of asthma
```
episodic wheeze
cough
tight chest
shortness of breath
diurnal pattern (3-4am worse)
```
149
Diagnosis of asthma
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
150
What is severe asthma
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
151
What are the treatment options available for asthma
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
152
Why do we not give inhaled steroids for everyone with asthma
side effects bad: osteoporosis, thin skin, adrenal suppression
153
give an example of a short and long-acting beta agonist used for asthma
short-acting: salbutamol
| long-acting: salmeterol (not for acute attack as takes longer to start working)
154
give an example of steroid used to treat asthma
prednisolone
155
give two examples of biological therapies used to treat asthma
omalzumab
| mepolzumab
156
What is the treatment path most used in asthma therapy
short acting beta agonist -> inhaled steroid -> long acting beta agonist -> more steroids -> hospital
157
Do the biological therapies work with all the types of asthma
no, only eosinophilic atopic asthma
158
What are the classifications of an asthma attack
uncontrolled/ moderate
severe
life-threatening
near-fatal
159
describe moderate asthma attack
PEFR >50%
Resp rate <25
Pulse rate <110
normal speach
160
describe severe asthma attack
PEFR 33%-50%
Resp rate >25
Pulse rate >110
Speach deteriorating
161
describe life-threatening asthma attack
PEFR <33%
PaO2<8kPa
PaCO2 NORMAL
unconsious ~
162
describe near-fatal asthma attack
PaCO2 raised
| ventilation
163
what investigations do you use to recognise an asthma attack
PEF
Spirometry
Blood gases
XR (if life-threatening, suspect pneumothorax)
164
Is PaCO2 raised or low in life-threatening asthma attack
normal
165
Treatment of asthma attack
```
oxygen 40-60%
salbutamol
prednisolone
check PEFR, ABG, potassium, glucose and consider rehydration
Discharge plan
```
166
What is the discharge plan after an asthma attack
```
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
```
167
What is COPD
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
168
What are the risk factors for getting
| COPD
```
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
```
169
How does COPD occur?
Airflow resistance: inflammation, fibrosis, increased mucus production
Parenchymal destruction: elastin loss, alveolar attachment loss
170
Explain why the COPD patient breathes as they do?
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.
171
What is dynamic hyperinflation
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
Describe two vascular changes in COPD
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
Symptoms of COPD
```
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
What are the two phenotypes of COPD
```
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
Diagnosis of COPD
FEV1/FVC post dilator <0.7 PEFR and Spriometer
XR (lungs black not grey because fresh air not being removed)
Questionnaires
176
What Questionnaires can help diagnose COPD
COPD assessment tool (CAT)
| Medical research council dyspnea
177
Describe what is assessed in CAT (COPD assessment tool)
8 things including SOB at hills etc, daily activities ability, sleep, energy, sputum, chest tightness, cough
178
Describe the scores for MRC dyspnea test
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
What treatment options are there pharmacologically and machinery for COPD?
```
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
What is the most cost-effective management for COPD
FLU vaccine
181
What management option has the greatest capacity to improve natural history of COPD
Smoking
182
What is the go-to treatment plan for COPD patients
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
What are two risks of COPD and its treatments?
Respiratory failure
| Pneumonia (with steroids)
184
What is a respiratory exacerbation
```
acute event
worsening of patient condition different to normal day to day variations
change in medication
accelerates lung function decline
increases mortality
```
185
Main cause of COPD exacerbation
viral infections
| infections
186
What are common viral causes of pharyngitis
rhinovirus
adenovirus
glandular fever- Epstien Barr virus (suggests HIV)
187
What are bacterial causes of pharyngitis
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
What are we most worried about with pharyngitis
Epstien Barr virus (because of worry of HIV)
| Bacterial causes
189
How do we know if the pathogen causing the sore throat is viral or bacteria without doing laboratory tests?
```
if 3 or 4 of these not met, then 80% chance viral
fever >38C
tonsilar exudate
tender anterior cervical adenopathy
cough
```
190
Sinusitis common causes:
viral most common: rhinovirus, coronavirus
bacterial: haemophilus influenzae
streptococcus pneumonia
191
What makes you suspect bacterial causes of sinusitis
unilateral pain
purulent discharge +/- fever
acutely or with complications of brain abscess etc. presentation
192
Epiglottis symptoms
```
dysphagia
pain on swallowing
high pitched wheeze
loss of weight
feeling unwell for past 6 months
sore throat
fatigue
```
193
What is a worrying complication of Epiglottis
can swell enough to block airways
194
What is the most likely cause of epiglottis
Haemophilus influenza
195
How do you treat epiglottis from H. influenza
co-amoxiclav
196
What are the four main disease categories
infection
inflammation
neoplastic
vascular
197
What are the investigations we usually conduct with respiratory pathologies
```
lung function tests
functional assessments
imaging
bronchoscopy
tracheoscopy
oximetry
```
198
What lung function tests are there available
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
when is transfer factor high vs low
high for pulmonary haemorrhage
| low for emphysema, anaemia
200
Give two examples of functional assessments used in lung problem diagnosis
6 minute walk
| incremental shuttle
201
What are the risks of bronchoscopy
pneumonia
haemorrhage
pneumothorax
202
what can bronchoscopy be used for
collecting samples
| therapy e.g. putting a stent in, brachytherapy, laser
203
WHat direction of XR direction is preferred?
posterior to anterior lying flat
| if patient cannot then we do anterior to posterior but has to be labelled because organs look bigger
204
What order to we first review the XR
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
how do we identify abnormalities in XR
```
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
What are the key silhouette signs to check on XR
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
How do you check behind the heart in an XR
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
What is a sail sign on an XR
behind the heart abnormality
| triangular capacity has two different densities
209
What does a vale like covering over the left lung mean on XR. the left heart border is missing
left upper lobe collapse anteriorly
210
What would you worry about with a movement of the mediastinum
pneumothorax
211
What kind of imaging do PET scans take and why
take functional imaging
| dye taken up more by fast dividing cells so cancers, inflammation and other things.
212
In health what work do our muscles do to breath
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
In pathology states what work do our muscles do to breath
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
What is the ventilation pattern in obstruction lung pathologies
hyperinflation with rib expansion
accessory muscle use
increased diaphragm work
increased abdominal muscle use for expiration
215
Which gas is mostly used to control breathing
co2
216
Do you breath faster at day or night and when do you get most signals for breathing
faster at day because more signals
217
when are you first likely to spot respiratory failure
during sleep at night so sleep studies are used in assessments of respiratory failure
218
What are four causes of ventilation problems that cause hypoxaemia
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
Why are alterations of PaCO2 useful when diagnosing hypoxaemia
changes to co2 are purely to do with air getting in and out so purely alveolar hypoventilation which is a worrying diagnosis
220
What are two patterns of breathing for a dying patient
Cheyne-stokes respiration
| agonal breathing
221
Describe cheyne-stoke respiration
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
describe agonal breathing
4-8 breathes than no breathing (apnea) and then back to the 4-8 breaths
223
What are some reasons for hypoventilation to do with the central control system
hypothyroidism
metabolic alkalosis
post-sedation
224
What are some reasons for hyperventilation to do with central control system
hyperthyroidism
anxiety
metabolic acidosis
225
What are some problems to do with load on resp system that can cause resp failure
increased co2 production e.g. from infection or exercise
obstruction of airways e.g. copd asthma
elasticity damage e.g. copd fibrosis
226
What are some problems to do with capacity of patient that can cause resp failure
decreased central drive e.g. from opioids
decreased strength of muscles e.g. diaphragm paralysis
sleep
227
What oxygen level must someone have to be considered in resp failure
lower than 94%
228
What are the steps to assessing what is causing the resp failure and the type
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
What are likely causes of type 1 resp failure with a chronic presentation
COPD
acute asthma
diffuse interstitial lung disorder
230
What are likely causes of type 1 resp failure with an acute presentation and localised findings
pulmonary embolism
pneumonia
(v/q mistmatch)
231
What are likely causes of type 1 resp failure with an acute presentation and diffuse findings
heart failure with cardiogenic oedema
| adult respiratory distress sydrome
232
What are likely causes of type 2 resp failure with a previously normal lung condition
sedation
neuromuscular problem
upper airway obstruction
233
what are likely causes of type 2 resp failure with a previously abnormal lung condition
copd
| asthma
234
signs and symptoms of type 1 resp failure
```
confusion
low blood pressure
low cardiac output
tachycardia
tachypnea
cyanosis
accessory muscle use
```
235
signs and symptoms of type 2 chronic resp failure
```
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
signs and symptoms of type 2 acute resp failures
```
confusion
warm peripheries
drowsiness
seizures
flapping termor
bounding pulse
```
237
What is the management plan for someone with respiratory failure
```
ABC
complete history and examination
treat underlying condition if possible
oxygen
breathing support
```
238
What concentration of oxygen do you give for someone with resp failure
type 1 resp failure and never on type 2: 94-98%
| type 2 resp failure: 88-92%
239
why do you give a lower concentration of oxygen to someone with type 2 resp failure?
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
What are the breathing support available for resp failure and when do you use them
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
If you saw a drug that ended in -mab what would the first guess be to what type of drug it is
monoclonal antibody
242
If you saw a drug that ended in -lone/-sole what would the first guess be to what type of drug it is
corticosteroid
243
If you saw a drug that ended in -terol what would the first guess be to what type of drug it is
bronchodilator
244
If you saw a drug that ended in -nib what would the first guess be to what type of drug it is
kinase inhibitor
245
Give to ways we can deliver drugs to the lungs directly
inhaler
| nebuliser
246
what are the advantages to administrating drugs to the lungs
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
What are the differences in conductive and respiratory airways that change drug delivery to these areas
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
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
resp airways: 1-5um
conductive airways 5-10um
mouth and throat 10-15um
too small just be exhaled
249
What things other than size of drug must we consider for delivery of drug
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
Name something that can affect retention of the drug in the lungs
solubility higher
251
How does pirfenidone work and what is it used for
slows idiopathic pulmonary fibrosis progression
anti-fibrotic, anti-inflammatory, anti-oxidant
less fibroblast proliferation, less collagen deposition
252
How does nintedanib work and what is it used for
slows idiopathic pulmonary fibrosis progression
| inhibits vascular endothelial growth factor receptors which drive fibrosis
253
Give the 3 forms of beta 2 agonists available
short-acting beta agonists
long-acting beta-agonists
ultra-long-acting beta agonists e.g. indacaterol
254
Why is it good to use beta-agonists and inhaled corticosteroids
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
why do we use anticholinergics to treat obstruction
```
muscarinic receptors (m1-5) activated by Ach cause smooth muscle constriction so we antagonise that and stop constriction
e.g. tiotropium
```
256
what does tiotropium come from originally
nightshade plant
| atropine
257
What cancers are included when we say lung cancer
primary lung cancers
| and metastatic spread of tumours reaching the lungs
258
give a brief overview of the epidemiology of lung cancers
```
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
What are the causes of lung cancers
```
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
What are the two most common types of lung cancers
bronchial
| pleural
261
what are the two types of malignant bronchial cancers
non-small cell carcinoma
| small cell carcinoma
262
What is the proportion of malignant to benign bronchial cancers
95% malignant
| 5% benign
263
What are the two commonest types of non small cell carcinoma
squamous
| adenocarcinoma
264
how do you treat non small cell carcinoma vs small cell carcinoma
NSCC radiotherapy and surgery
| SCC chemotherapy
265
Give a feature of the cells in small cell carcinoma
little cytoplasm
266
which carcinoma of NSCC and SCC has the worst prognosis
SCC
metastatic on presentation (nscc somtimes)
grows faster if not treated than nscc
SCC always high grade but NSCC can be variety
267
what risk factor are SCC and NSCC strongly associated with
smoking
268
What are some benign bronchial tumours
lipoma
leiomyoma
fibroma
269
What are the most common primary tumours of the bronchial
35% adenocarcinoma
25% squamous
20% small cell carcinoma
10% undifferentiated non-small cell carcinoma
270
what is the most common cancer in non-smokers
adenocarcinoma
271
What are symptoms of local lung cancer
```
cough
SOB
wheeze
hoarseness
dysphagia
haemoptysis
chest pain
arm, neck swelling
malaise
```
272
what are metastatic lung cancer symptoms
```
bone pain
hepatic pain
abdominal pain
neurological deficits
Seizures
headaches
```
273
where do lung cancers commonly metastasis to
```
bone
brain
liver
lymph glands
adrenal glands
```
274
What does paraneoplastic changes mean
non-metastatic manifestations of malignant disease
275
in how many people do paraneoplastic changes for lung cancer occur in
2-5%
276
What causes the paraneoplastic changes in lung cancers
production of PTH
| production of ADH
277
what can excessive secretion of ADH lead to
syndrome of inappropriate ADH secretion
278
What are the symptoms of paraneoplastic changes in lung cancer
```
finger clubbing
anorexia
weight loss
hypercalcaemia
hyponatraemia
peripheral neuropathy
```
279
Can people with lung cancer present asymptomatically
yes and/or with constitutional symptoms only
| these people have the best cure rate
280
What staging do we use for lung cancer
TNM
281
What do we need to know when diagnosing lung cancer
Is it lung cancer? what cell type? what stage
282
what do we need to know when assessing the patient before treatment for lung cancer
operability
283
What investigations do we carry out for diagnosis of lung cancer
XR
CT
PET
biopsy
284
What does XR show for lung cancer
round, fluffy, spiking, shadow
285
What type of biopsy can we do for lung cancer
ct guided biopsy
vacuum assisted biopsy
surgical biopsy
286
To stage the lung cancer what do we need to check for
resectability: bloods
| check for mets: CT
287
What do we check for in inoperability of lung cancer
ecg
lung function
exercise capacity
performance status
288
what are the scores you can get for performance status with lung cancer
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
Why do we somtimes delay treatment for lung cancer
if operability of patient is low, we try and treat symptoms first to improve the patient's performance status
290
What treatments do we use for NSCC
limited disease: surgery/ radical radiotherapy +/- chemotherapy
extensive: palliative chemotherapy
291
what treatments do we use for SCC
limited: chemotherapy and radiotherapy
extensive: less chemotherapy
292
are there treatments for lung cancer other than radio/chemo/surgery
5% of patients have genetics that allow them to have monoclonal antibodies that help immune system fight the tumour
293
what do we mean by limited lung cancer
tumour in one hemithorax and can include if it's in ipsilateral lymph nodes
294
What tumours commonly spread to the lung from other sites
```
breast
prostate
thyroid
kidney
colorectal
melanoma
lymphoma
```
295
What are the types of cancers that can cause pleural cancers?
malignant e.g. mesothelioma
| benign e.g. pleural fibroma
296
what is mesothelioma
neoplasm of mesothelial cells (the mesothelium) which lines the pleural cavity, the pericardial cavity)
297
where is the mesothelioma most common and why is it bad
pleural cavity
compresses on the lungs
erodes into the lungs
increase risk of infection
298
what is metastasis like in mesothelioma
highly likely to occur even in early disease
| spreads often to vertebra, liver, brain, chest
299
briefly describe the epidemiology of mesothelioma
men > women
| over 75 more common
300
what are the risks to mesothelioma
asbestos
| genetic small
301
what are the symptoms of mesothelioma
```
SOB
chest pain
lethargy
anorexia
abdominal pain
sweating
```
302
what do we use for diagnosis of mesothelioma
XR - pleural effusion, rib destruction
CT
pleural aspiration- straw-coloured to blood-stained
biopsy- best for diagnosis
303
Treatment of mesothelioma
```
not many options
surgery to debulk
palliative chemotherapy and radiotherapy
psychological support
symptom support esp. pain
```
304
What is the average duration from diagnosis to death
8-12 months
305
what is a condition that you must not cremate the body
mesothelioma death because have to let coroner check for occupational link to asbestos
306
What are the phases of whooping cough
incubation 5-21 days
catarrhal 1-2 weeks
paroxysmal 1-6 weeks
convalescent
307
What are the symptoms of whooping cough in the catarrhal phase
low grade fever
conjunctivitis
lymphocytosis
rhinorrhea
308
what are the symptoms of whooping cough in the paroxysmal phase
spasm cough
post-cough vomiting
whoop sound when inspiring air
309
What causes whooping cough
bordetella pertussis gram negative bacillus
310
How does the bacteria cause whooping cough
bordetella pertussis causes hyperplasia of lymph nodes so inflammation and whooping
311
what treatment do we give for whooping cough
clarithromycin
chemo-prophylaxis
vaccines
312
what are the complications of whooping cough
pneumonia
encephalopathy
sub-conjunctivitis haemorrhage
313
What is croup
laryngo-tracheobronchitis
314
what causes croup
parainfluenza virus mostly
| also RSV, influenza A and other viruses
315
What are the symptoms of croup
```
barking cough
interstitial recessions
high resp rate
febrile
cyanosed
inspiratory stridor
```
316
what age group is affected by croup
3 months to 6 years
317
what is the clinical picture of whooping cough in adults
chronic cough and in 1/2 of patients post-cough vomiting
318
What is pneumonia
inflammation of the lungs and the lung parenchyma with neutrophil infiltration
319
% of pneumonia patients hospitalised and in ITU
20-50% hospitalised
| 5-10% UTI
320
Mortality rate for community, hospital, ITU patients with pneumonia
1% for community
10% for hospital
30% for UTI
321
what are the risk groups for pneumonia
```
infants, elderly
COPD, swallowing dysfunction
IVDU, alcoholics
diabetes, congestive heart disease
nursing home residents, immunocompromised
```
322
what pathogens cause pneumonia in immunocompromised patients
all bacteria but with atypical presentations and also Pseudomonas aeruginosa
viral: adenovirus, RSV, cytomegalovirus
fungus: pneumocystis pneumonia
323
What are the steps of pathophysiology to pneumonia (6)
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
What are the symptoms of pneumonia
```
fever
rigours
sweats
cough
shortness of breath
systemic features: headache, weakness, malaise
+/- sputum
pleuritic chest pain
```
325
what are the signs of pneumonia
```
high resp rate, high pulse rate
low blood pressure dehydration
fever
dull to percussion
hypoxia and sometimes signs of resp failure
crackle
```
326
What is atypical pneumonia
when the systemic symptoms are more than the other symptoms
327
what is rusty coloured sputum in pneumonia suggestive of?
streptococcus pneumonia
328
what non-pulmonary symptoms does legionella cause in pneumonia?
neurological- confusion, encephalitis
| gastrointestinal- diarrohea, abnormal liver function, intestinal nephritis
329
What things should you do for investigations of pneumonia and finding the causative organism
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
What things in the XR are you looking for in pneumonia
consolidation
abscess
diffuse shadowing
pleural effusion
331
What does consolidation in multiple lobes on XR suggest in pneumonia
strep. pneumonia
staph. aureus
legionella
332
What do multiple abscesses suggest in XR in pneumonia
staph aureus
333
what does a cavity in upper lobe XR pneumonia suggest
Klebsiella pneumonia (after ruling out TB)
334
What does diffuse shadowing in XR for pneumonia suggest
pneumocytosis pneumonia
335
What do you do with a pleural collection in XR pneumonia
drain it and manage
336
What microbiology samples do you need for pneumonia investigations
sputum and blood and urine
337
what cultures do you do with the sputum for pneumonia
ZN for TB
chocolate agar
blood agar
PCR for TB
338
What could grow on the chocolate agar plate for sputum fro pneumonia patient
strep. pneumonia
staph aureus
haemophilus influenza
gram negative bacillus
339
What cultures do you expect to grow with blood cultures in pneumonia
aerobic: strep pneumonia, staph aureus, h. influenza
anaerobic: strep pneumonia
340
what are you looking for in the urine sample for microbiology in pneumonia
legionella antigen
| strep pneumonia
341
what part of the history would suggest legionella for pneumonia
hot place travel
| confusion
342
What serology and PCR would you want to do when investigating pneumonia
viruses
atypical pathogens
mycoplasm pneumonia
343
How do you know if you should admit someone with community-acquired pneumonia to hospital
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
What do the scores from the CAP severity assessment mean?
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
Do you treat after diagnosis of pneumonia or after?
before empirically and then when you know what the cause is narrow treatment to be more specific
346
What do you give for mild pneumonia
amoxicillin oral or clarithromycin oral
347
what do you give for moderate pneumonia
amoxicillin + clarithromycin oral
348
what do you give for severe pneumonia
IV co-amoxicav + clarithromycin
OR
IV cefuroxime + clarithromycin
349
what are the most common causative infections for patients hospitalised from pneumonia
```
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
What are the most common causative infections for patients hospitalised in ITU for pneumonia
strep. pneumonia
staph. aureus
legionella pneuomophilia
viruses
351
What drugs do you give for strep. pneumonia causing pneumonia
amoxicillin or cefuroxime
| or clarithromycin
352
what drugs do you give for Haemophilus pneumonia causing pneumonia
co-amoxiclav
| or doxycycline
353
what drugs do you give for staph aureus causing pneumonia
flucloxacillin or cefuroxime
| resistent vancomycin
354
klebsiella pneumonia
co-amoxiclav
355
What are the atypical pathogens that cause pneumonia
legionella pneumophila
mycoplasm pneumonia
chlamydophila pneumonia
356
What do we give to treat atypical pathogens that cause pneumonia
clarithromycin
ciprofloxacin
doxycycline
357
What makes the atypical pathogens that cause pneumonia harder to treat
they grow in cells
| intracellular
358
what drug do you give for necrotising pneumonia
clindomycin, rifampicin
359
what drug do you give for pseudomonas aeruginosa causing pneumonia
ceftazidime +/-gentamycin
360
What is a hospital-acquired pneumonia infection
that acquired at least 48 hours after being admitted
361
How do you diagnose a hospital-acquired pneumonia
new fever
new leukocytosis
higher demand for oxygen
new radiological signs on xr
362
What are the causative pathogens of hospital-acquired pneumonia
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
What are the common and serious multi-drug-resistant pathogens
```
ESKAPE
Enterococci
staph aureus
klebsiella pneumonia
aeruginosa bacumani
pseudomonas pneumonia
enterobacter
```
364
How do you prevent pneumonia infections
vaccines: pneomococcal vaccine, influenza vaccine
| smoking cessation
365
Who is given a pneumococcal vaccine for pneumonia prevention
>65
splenic dysfunction
chronic medical diseases
immunocompromised
366
What is para-pneumonic empyema
pus in pleural space due to pneumonia
367
How often does para-pneumonic empyema and effusion occur
30-60% of community-acquired pneumonia patients
368
what are the signs of an effusion or empyema
fever/inflammation not settling with antibiotics
pain on deep inspiration
dull to percussion
369
How do you investigate para-pneumonic effusion or empyema
pleural aspiration to see if fluid will heal on own or empyema/ complicated effusion so needs treating.
370
after a pleural aspiration, what would you find if the fluid needs drainage due to pneumonia
pH<7.2
glucose<3.3mmol/L
pus or thick fluid
positive bacterial culture
371
How do you treat para-pneumonic effusion and empyema
drainage of fluid via chest tube or cardio-thoracic surgery
| antibiotics long duration: co-amoxiclav, meropenem
372
Name two groups of people more likely to have lung abscess
alcoholics
| poor oral health
373
What are 4 examples of causative organisms of lung abscesses
strep milleri
klebsiella pneumonia
If from metastatic infection from venous system could be: staph aureus, fusobacteria
374
what is a complication of lung abscess
empyema
375
how do you treat lung abscesses
antibiotics long course e.g. 6 weeks
| surgical drainage
376
What is bronchiolitis
inflammation of bronchioles and mucus production occurs causing obstruction
377
What causes bronchiolitis
RSV
378
What is bronchitis
inflammation of epithelium of bronchus, usually self-limiting, due to infection
different presentation with acute and chronic (chronic in COPD)
379
What are the causative agents of acute bronchitis
viral usually
| if bacteria consider immunocompromised e.g. chlamydia pneumonia, mycoplasma pneumonia, bordetella petussis
380
What are the clinical signs of acute bronchitis
cough +/- productive lasts over 5 days (usually 1-3 weeks)
wheeze and SOB
fever and systemic features suggestive of pneumonia or influenza
381
How do we investigate bronchitis in acute
XR to exclude pneumonia, normal in bronchitis usually
throat viral and bacterial swab
serology for mycoplasma pneumonia and chlamydia pneumonia
382
how do we treat acute bronchitis
viral- supportive care, self-limiting
| bacteria- little evidence that anti-microbial's are helpful unless bordetella pertussis
383
name 3 emerging respiratory viral infections
severe acute respiratory syndrome from coronavirus
middle eastern respiratory syndrome from novel coronavirus
avian influenza from new form of influenza A
384
What family does Influenza family belong to
orthomyxoviridia
385
How many influenza genera are there
3 A B C
386
Describe Influenza A
lots of mutation
can infect pigs, birds, horses, humans
causes large outbreaks, severe, pandemics
387
Describe influenza B
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
Describe influenza C
less mutations
mild symptoms
or asymptomatic
389
How many antigenic sites does influenza have, name them
```
4
hemagglutinin
neuraminidase
M2 ion channel
ribonucleoprotein
```
390
Which influenza genera are more common
A B
391
Which two antigenic sites does influenza A and how many subtypes are there
hemagglutinin 15
| neuraminidase 9
392
What is hemagglutinin used for and what does immunity to one subtype do
attachment and entry to cell by virus
| immunity against one subtype gives you protection against that one subtype
393
What is neuraminidase used for and what does immunity against one subtype do
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
What subtypes of influenza A are found in humans vs birds
humans: H1,2,3 (RARE 5) n1, 2
Birds: all
395
what is the genetic material of flu A like
8 RNA single stranded RNA pieces
396
what three ways can mutations occur in flu A
genome segmentation with gene re-assortment
gene swapping
no proof reading mechanism
397
when do genome segmentation occur to flu A RNA
co-infection with two different flu A viruses
398
when does gene swapping occur to flu A RNA
co-infection with human and avian virus
| can occur directly or with intermediate pig
399
What occurs to cause seasonal outbreaks vs pandemic outbreaks of flu A
antigenic drift: seasonal outbreaks
| antigenic shifts: pandemics
400
What are the methods of transmission of flu A
aerosol e.g. cough
| hand to hand contact
401
what is the definition of reproductive number
average number of secondary cases generated from primary case in susceptible population
402
what is the reproductive number of influenza A
1-3 in pandemics
| 1.3-1.5 in seasonal outbreaks
403
Who are the at risk groups of influenza A
chronic heart, pulmonary, renal, metabolic, neurology problems
old
immunocompromised
404
What are the symptoms of influenza A
```
lower and upper resp infection symptoms
fever
malaise
weakness
sore throat
dry cough
```
405
When is seasonal flu occurring in northern and southern hemispheres
north: dec-march
south: may-sept
406
What is a complicattion of flu
bacterial and viral pneumonia
407
How do you treat flu
symptomatic phase: supportive care: oxygen, fluids, nutrition, prevent 2 infections
Tamiflu (oseltamivir) within 48 hours of first symptoms
408
What is tamiflu's role
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
How does oseltamivir treat influenza
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
what is the difference between an outbreak, an epidemic, a pandemic
outbreak: 2 or more linked cases
epidemic: more cases in region/ country
pandemic: epidemics that cross international borders
411
Why do we have annual vaccines for flu
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
What do pandemic flus cause
high mortality and morbidity
social disruption
economic disruption
413
What subtype of influenza A caused the spanish flu
H1N1
414
Which subtype of influenza A is documented to spread from birds to humans but not humans to humans
h5n1
415
which subtype of influenza A caused two historical pandemics
H1N1
1918 and 2009
in 2009 the older population were mostly immune due to 1918 infection giving them immunity
416
How long in advance do we need to make a flu vaccine
6-9 months
417
how many strains of flu A are in the annual vaccine
3
418
in a pandemic of flu what is the incubation period
1-4 days
419
in a pandemic of flu what is the infectious period
start of symptoms until 4-5 days after end of symptoms
| 10% infectious before symptoms
420
how many phases are there to managing a pandemic of flu
containment and treatment phase
| 2
421
what occurs in the containment phase of managing a pandemic of flu
identify cases, treat them, contact tracing
infection control: hand hygiene, stop mass gatherings
flu surgeries
422
when does treatment phase of managing a pandemic flu start
when cases so many no point trying to contain the disease, it's no longer contained
423
what is the plan for treatment phase of pandemic flu management
treat flu patients only
| manage patients so some hospital some antivirals at home etc.
424
why will we get more pandemics likely
more travel
more people
more intensive farming so more chance of antigenic shift
425
why will we not get a pandemic likely
better overall health
anti-virals
vaccines
methods of controlling avian flu
