3

Question 1

where do you get URTIs and where do you get LRTIs

give examples of each type of infection

Answer 1

URTIs are infections above the epiglottis in the nose or pharynx. For example nasopharynogitis (cold) and pharyngitis (sore throat) and laryngitis (croaky voice).

LRTIs are infections in the airways such as the trachea, bronchi and alveoli
For example influenza, bronchitis, tuberculosis and pneumonia.

Question 2

how does spiking in influenza, RSV and colds change through the year

why are there more cases of colds in the present day

Answer 2

there is a spike of influenza every winter but the severity changes each year
there is a spike of RSV each winter but the severity is constant
rhinovirus is present all year round but more so in winter

our ability to detect viruses has improved so there seems to be more cases. This has come with the discovery of PCR which can help to detect viruses but it needs the primer to do this.

Question 3

what are two other ways, which are not PCR, to detect viruses and evaluate their success

Answer 3

high throughput screening if effective but expensive

virocaptive sequencing for vertebrate viruses allows screening for a huge amount of viruses and there is no need for primers.

Question 4

who catches RSV and how common is it

what is it a major cause of in infancy and why can you catch it twice

Answer 4

60% of children will catch RSV in their first winter and nearly all children will have by 2-3 years.
it is a major cause of low RTIs in infancy and childhood
you can be infected by it multiple times and it mutates.

Question 5

what are the first symptoms of RSV and who is most likely to show the more severe symptoms

who else can RSV infect

Answer 5

severe cold, but in 2-3% of babies they will develop severe bronchiolitis, this will most likely happen to premature babies due to their underdeveloped lungs.

RSV protective immunity decreases over time so can infect older people with cardiovascular morbidity, COPD or immunocompromised patients where their reaction may be more severe

Question 6

what is our immune system like when we are born and how does this affect our ability to handle RSV

how does this change as we grow up
what happens to those that developed severe RSV

Answer 6

when we are born we have a less mature immune system (Th2) so we are less able to handle the virus and development of RSV bronchiolitis is more likely.

As we grow the immune system develops to Th1 and we only get colds.
children that got RSV bronchiolitis are more likely to develop post bronchiolitic wheeze and go onto develop asthma
as we become older it is a cause of exacerbations in people with asthma and COPD and as our immune system declines with age we get more severe illness.

Question 7

what do enveloped viruses do
what is the g protein on the envelope and what can it attach to

how do viruses gain entry into the cell

Answer 7

takes components of our cell membrane to make its own envelope
the G protein is a highly glycosylated attachment protein and the potential receptors are found on our cells (annexin II on airway epithelial cells and L selectin and CX3CRI on immune cells).

to gain entry into the cell the virus will use F (fusion) protein.

Question 8

what family and category is RSV

what receptors can RSV be detected by

Answer 8

negative sense ssRNA virus of the paramyovridae family

it can be detected by many PRRs- TLR2, 4, 6 which will bind to the F protein .
TLR7 binds to the ssRNA and so does NOD2.

Question 9

what detects RSV and what processes happen following this in the body
how does the body try and limit the infection

what happens when dendritic cells are infected

Answer 9

TLRs and RIGI recognise the cell is under attack.
this will result in release of inflammatory mediators, and interferons will feed back onto the cell and neighbouring cells to cause apoptosis of infected cells.
CXCL8 causes neutrophil recruitment
CXCL10 causes natural killer cell recruitment

dendritic cells migrate to the lymph nodes when infected with RSV and present the antigens to T cells which cause RSV specific antibodies and cytotoxic T cells to get rid of the virus and create immune memory

Question 10

how can RSV prevent an effective host immune response

6 things and think about the diagram

Answer 10

Non structural proteins/n proteins on the RSV can bind to RIGI and prevent its signalling.

They can also bind to IRF3 and 7 which stops them from binding to targets in the nucleus (NFKB) and this will prevent type 1 interferon production.

The non structural proteins can bind to STAT2 which causes its degradation so it cannot go onto activate interferon stimulated genes

F protein binding can be prevented

Many G proteins are released from infected cells and binds to CX3CRI on dendritic cells and T cells to prevent their activation. They can also bind to antibodies and stop their interaction.

N protein can inhibit synapse formation between T cells and dendritic cells or it can inhibit dendritic cell maturation

Question 11

which cells are affected by the RSV and what happens to them

Answer 11

airway epithelial cells are highly permissive to RSV.
the replication of RSV causes epithelial damage and necrosis.
there is also the recruitment of neutrophils and lymphocytes
submucosal oedema
mucus secretion
bronchoconstriction
these cause severe obstruction of the airway lumen.

Question 12

what happens to a monolayer of epithelial cells in a dish when RSV is added

why is this reaction more severe

Answer 12

huge gaps will appear in the monolayer and syncitia will form (cells infected with the virus will fuse together and form big elongated cells)
There are no immune cells in the lab so the effects will be more severe

Question 13

what was used in the first vaccine for RSV and what results did it have

how is RSV normally detected

why did the first RSV vaccine fail

Answer 13

they used an inactivated version of the virus and the results showed no protection against the infection and it even caused a higher viral load than before.

normally RSV is detected by TLR4 on the cell surface and it enters the cell and its replication is detected by RIGI and MDA5. TLR7 will also recognise the single stranded RSV RNA.
This will lead to TF activation and antibody production,

But because the vaccine was inactivated it was still able to activate the TLR4, but it could not enter the cell and replicate so there was no TF activation or antibody production and so the people didn’t have an immune response.

Question 14

what is a known treatment for RSV

Answer 14

monthly injection of anti RSV F protein monoclonal antibody called palivizumab which can be successfully given to infants at risk but it is very expensive

Question 15

how does severe bronchiolitis affect the immune response polarisation

Answer 15

it will alter the Th1/Th2 response and cause Th2 polarisation and enhances sensitisation to allergens and induces development of a chronic asthma phenotype

Question 16

how can genetics affect your risk of RSV severity

Answer 16

20% of the variation in risk for RSV is determined by genes but there are no confirmed genes so far.
TLR4 mutations 299 and 399 are over expressed in infants hospitalised for RSV bronchiolitis
the mutations cause a failure of TLR4 to translocate to the cell surface and this will mean there’s reduced NFKB signalling

Question 17

comparing RSV and rhinovirus…
inducer or trigger?
when do people get infected?

Answer 17

RSV is an inducer of wheezing and asthma
rhinovirus is a trigger
rhinovirus is all year round and RSV is winter.

Question 18

what is the most common cause of UTRIs
but what else can this cause

what is croup

Answer 18

rhinovirus
exacerbations, asthma development, severe bronchiolitis in infants, fatal pneumonia in the elderly and immunocompromised

barking cough

Question 19

what type of virus is HRV

what receptors allow it into the cell and how many of each use each type of receptor

Answer 19

non enveloped single stranded virus, it is small and positive ssRNA

there are three receptors that allow the virus into cells and the virus can be categorised based on the receptors it uses or genetically.
96 major viruses use ICAM1 (intracellular adhesion molecule 1)
12 minor viruses use LDL receptor
50 C viruses use CDHR3 to enter and cause severe illness.

Question 20

what are the different genes for HRV and how many serotypes do they have
what receptors do these use

Answer 20

HRV-A have 77 serotypes (ICAM and LDL)
HRV-B have 30 serotypes (ICAM)
HRV-C around 50 serotypes (CDHR3)

Question 21

which causes more damage to airways RSV or HRV

Answer 21

RSV causes more damage

Question 22

how does HRV replicate

Answer 22

it enters and replicates within the airway epithelium cells.
the cells are sloughed due to HRV but the airway lining remains structurally intact.
HRV will interact with TLR3 which up regulates RIGI and cause the release of chemokine and cytokines.

Question 23

what do macrophages release

What are neutrophils attracted by and what can the levels of them tell you, what do they release

Answer 23

TNFA, IL1, CXCL8, MIP1A/CCL3, INFA,B,Y.

IL8/CXCL8.
levels of neutrophils in the nasal lavage fluid can correlate with the severity of the symptoms.
neutrophils release TNFA and make elastase.

Question 24

what are eosinophils recruited in response to

what are T cells recruited in response to and what do they trigger

Answer 24

RANTES/CCL5

RANTES/CCL5 and IPI0/CXCL10. they trigger the antibody mediated response.

Question 25

what causes 50-85% of exacerbations in people with underlying airway conditions are these people more likely to get a cold and what happens when they do get one

Answer 25

HRV they are not more likely to get a cold but when they do get one it is more likely to progress into a LRTI.

Question 26

what is released in response to HRV entry and what does it do

Answer 26

the growth factor VEGF which will impact fibroblasts and smooth muscle causing airway remodelling

Question 27

why does HRV make exacerbations more likely how do interferons work and how is it related to this

Answer 27

they could have increased access to epithelial cells due to previous damage, or there could be deficiency in innate anti viral immunity. It has been found that people with asthma and COPD have higher viral loads than normal people when infected. interferons block viral entry to control viral transcription and translation, cleave RNA and cause apoptosis. Failure to induce interferon response causes uncontrolled viral replication and increased inflammation. so if patients are deficient in type 1 interferon production this could explain why they have more exacerbations.

Question 28

what is the susceptibility phenotype for people who have frequent exacerbations

Answer 28

deficient interferon production decreased production of Th1 antiviral cytokines increased suppressor of cytokine signalling protein (SOCSI) which will suppress viral induced interferon B activity. or increased ICAM1 expression which is how the majority of HRV enters the cell.

Question 29

what two things cause an increased HRV infection in people with asthma

Answer 29

the inflammation in asthma causes IL4 and 13 production which will cause increased ICAM1 expression on bronchial epithelial cells and this leads to more HRV infection. Deficient production of IL2 and interferons causes impaired apoptosis and the killing of infected cells and more viral replication.

Question 30

How does HRV increase the bacterial infection susceptibility three things what is activated in response to HRV and what do they do

Answer 30

HRV affects tight junctions so it could allow bacteria to enter the airway cell wall 25-50% of COPD patients tend to have bacterial infections in their airways. HRV causes increased release of cytokines and more ICAM1 expression and some bacteria can also use ICAM1 to enter the cells. HRV can cause increased activation of TFs and more expression of PAFR which allows increased adherance of bacteria macrophages will be activated by HRV to reduce cytokine production in response to bacteria

Question 31

what are some novel treatments of viral induced exacerbations

Answer 31

inhaled interferons to cancel out the lack of interferons but this did not show success which is thought to be because the interferons are needed at the very start of the infection. target IL4+5 and IgE to mediate inflammatory mediators maybe try and block ICAM1

Question 32

what is the illness causing sore throat, tender glands, fever, large tonsils and pus, throat swab showing gram positive cocci what type of bacteria is this and what microbe usually causes this disease with examples

Answer 32

gram positive cocci are usually good bacteria. this is pharyngitis which is usually viral by rhinovirus or adenovirus (70-80%)

Question 33

what are three examples of other viruses that can cause pharyngitis how severe will it be if the pharyngitis is bacterial and what are most cases caused by what can happen to a small amount of people that contract pharyngitis what else can cause pharyngitis

Answer 33

glandular fever, epstein barr virus, HIV. if it is bacterial most of the time you can clear it yourself and 10-30% are caused by streptococcus pyogenes. a small amount of people can get a serious associated condition such as Scarlett fever, PSGN, rheumatic fever. STIs such as gonorrhoea

Question 34

what disease can cause severe sore throat, fever, malaise for two days, large glands and rapid breathing, thick grey membrane on tonsils swab is taken and it grows gram positive rods they have recently been to Russia what is the membrane called on the tonsils what bacteria causes this and how can it be treated

Answer 34

pseudomembrane is the grey membrane covering the tonsils corynebacterium diphtheria it is treated with an anti toxin to stop the toxin made by the bacteria killing airway cells and creates a pseudomembrane. it is also treated with the antibiotic erythromycin. there is also a diphtheria vaccine

Question 35

what disease is likely to be seen in a housewife with a fever, pain in the left ear and into teeth and purulent nasal discharge and they had a cold 10 days ago. what microbe usually causes this and explain what the part of the body affected is

Answer 35

this is sinusitis and is usually viral. sinuses are in the frontal bone of the head and around the nose and they are spaces in the bone that have only air in them and are lined with mucosa, they exist so our skull can be a sound box for resonating voices.

Question 36

what happens to the mucosa in sinuses during an infection and what can this cause how can viral infections lead to further bacterial infections because of this disease how can you tell if it is bacterial or viral what can this progress to in some people

Answer 36

the mucosa gets inflamed during a cold and can swell and block the entrance and exit so fluid can get stuck and it can become a culture medium for bacteria. sinusitis can also be viral but these infections are self limiting because of the viral cold, the sinuses can get blocked and are prone to further bacterial infection you can tell if its bacterial or viral by the symptoms. some people with bacterial infections can have spreading to surrounding structures causing brain abscess, vein thrombosis and orbital cellulitis

Question 37

what disease is likely to be causing sore throat, fever and pain on swallowing in an old African lady. what is it called when a high pitch wheezing noise is made on breathing in what microbe causes this what is the epiglottis and how is it affected here what kinds of people normally are infected with this and why

Answer 37

epiglottis inspiratory stridor the epiglottis is the tissue that covers the oesophagus when you breathe. epiglottitis is inflammation and swelling of the epiglottis which causes blocking of the airway. the main cause of this is haemophilia influenza type B but now it is rare due to the vaccine. so people who get this have not been vaccinated or they are immunocompromised

Question 38

what is an old term for COPD what does acute bronchitis cause what is bronchitis

Answer 38

chronic bronchitis cough, phlegm, breathlessness and is almost always caused by a virus self limited infection of bronchi epithelia due to UTRIs

Question 39

what causes these symptoms - 4 week long cough, it comes in bouts and causes vomitting and she has no fever. can this be treated what part of the body is inflamed here and what does it normally do

Answer 39

this is a sub conjunctival haemorrhage which causes whooping cough there is a vaccine for this the conjunctive is what joins the eyelid to the front of the eyeing it becomes inflamed and bleeds.

Question 40

what is whooping cough caused by what does it make in the body to allow its survival and what side effects does this cause what is the whooping part of the cough what could be some complications of the whooping cough

Answer 40

bacteria- bordatella pertusis which makes gram negative bacillus rods. the bacteria makes many virulence factors to let it outcompete many flora and get a niche, they also can inhibit many immune cells and damage the epithelium. the build up of dead cells blocks airways and this will contribute to the chronic cough. the whooping is deep breaths in after coughing episodes pneumonia, encephalopathy and subconjunctival haemorrhage

Question 41

what other two vaccines are in the one for whooping cough and what kind of immunity does this cause

Answer 41

tetanus and diphtheria | it may not give lifelong immunity

Question 42

what does black and white mean on a chest x ray what is consolidation and what does it cause what disease can present this

Answer 42

black- airated lung white- dense material alveoli are full of a dense material containing pus, fluid and dead cells and bacteria this will cause inflammation and the lining of the lung is irritated causing pain when you breathe and difficulty breathing. this will cause and cough and bring up sputum which is pneumonia

Question 43

what does the word pneumonia actually mean how many of those with pneumonia get hospitalised who is at risk

Answer 43

it is a general term which is attached to inflammation of the lung parenchyma 20-50% and 5-10% require intensive care infants, elderly, immunocompromised, someone who has neuromuscular problems and cannot cough, strokes stop the swallowing reflex, someone with COPD or another lung disease, nursing home residents, diabetes, congestive heart disease and alcoholics

Question 44

when bacteria enters the lung what is the first cell it interacts with and what does this cell do what is released by neutrophils and what does it do what can fluid in the airways cause what is the resolution phase

Answer 44

alveolar macrophages respond to the first problems and if they become overwhelmed they recruit neutrophils and produce pro inflammatory cytokines IL8 is released and it causes bone marrow to make more neutrophils, and the capillaries develop holes to allow neutrophils and tissue fluid to leak out into the alveolar space. this fluid in the airways can affect gas exchange this is where the bacteria are cleared and the inflammatory cells are removed by apoptosis and it leads to complete recovery

Question 45

what can happen if inflammation is too excessive

Answer 45

the pathogen may have caused a lot of lung damage and so it could enter the bloodstream and cause serious disease

Question 46

what are some signs of pneumonia how is it diagnosed 4 ways

Answer 46

fever, rigor, weakness, malaise, fast HR, rapid breathing, low oxygen, cough and sputum, pleuritic chest pain and lung consolidation sputum is taken and grown in the lab and it will make gram positive cocci or you could check the blood for bacteria or you could check the urine for antigen excretion you could look at genetic material using PCR which is good for viruses that don't grow easily in culture

Question 47

what cocci does s pneumonia make and how many serotypes are there what does this mean for how easy it is to treat

Answer 47

gram positive and there are 90 serotypes (different antigens) it is hard to be protected against all the antigens and we only have vaccines for 13 and 23.

Question 48

what is there if there is a chest x ray showing a lung abscess with black bits

Answer 48

it contains tar and needs surgical drainage

Question 49

what atypical pathogens may cause pneumonia

Answer 49

legionella and mycoplasma are hard to culture and they grow in lukewarm water so they can grow in the shower or in air conditioning

Question 50

who is at risk from hospital acquired pneumonia and what is it defined as being

Answer 50

elderly and post operative patients as they can't take deep breaths defines as being in hospital for more than five days

Question 51

what are classic symptoms of tuberculosis

Answer 51

cough for 2 weeks, given antibiotics, and there were no improvements, fever, losing weight, chest pains and blood in sputum lots of small white tubercles which contain bacilli

Question 52

where was the earliest that tb was found what are some other names for tb who developed the germ theory and what is it

Answer 52

early Egyptian mummies consumption, white death, phthisis Robert Coch said that germs cause human disease

Question 53

what is the microbiology of tb like and what is special about the cell wall and how does it help the bacteria what is the growth of tb like

Answer 53

aerobic, non spore forming, non motile bacillus the cell wall has many high weight lipids which act as a tough armour casing and this is important because they are environmental the casing helps them to survive phagocytosis in organisms the cell wall contains mycolic acids and lipoarbinomannam they are very slow growing because they take time to make the cell wall, normal bacteria take one hour and tb takes 15-20 hours. this means that it will also have a slow response to treatment

Question 54

how is tb spread and what is contained within the microdroplets what has to occur for a smartest to be positive

Answer 54

spread in aerosol from infected individuals lung to another lung or it is spread via spitting coughing or sneezing the droplets in the cough contain bacilli of five microns which can lodge in the alveoli or small airways smear test is positive if you can see bacteria under a microscope and if you are smear positive 27-50% of household contacts become infected.

Question 55

what happens when tb is detected by macrophages and why may this go wrong how can the body keep the tb inactive

Answer 55

the bacteria is engulfed and trafficked to the phagolysosme where it will be killed by acidification and microbicidal molecules digestion by proteases causes antigen presentation to the T cells. tb can withstand phagocytosis and escape into the cytosol the immune response is unsuccessful in some and the tb is kept trapped within a granuloma

Question 56

what happens if you have a pulmonary infection only and not disease how often does this occur and what is the container called

Answer 56

the bacilli settle in the lung and are surrounded by macrophages and T cells which starves the bacilli of nutrients. this will happen to 95% of tb infections granuloma are lesions that try and contain the bacilli

Question 57

what happens to highly stimulated macrophages during tb infection and what do they look like what will this go onto form and what other cells are involved what will the centre of this look like how is a tubercle formed what helps to keep this all together what does tb do in response to this

Answer 57

the become epitheloid cells and look more like a polygon, they will fuse together to form giant multinucleate cells langerhans giant cells T cells infiltrate the lesion and around the edge of this fibroblasts are laid down around the granuloma to stop anything getting in or out the central tissue may necrose and form a cheese like caesating granuloma large granulomas become tubercles proinflammatory factors keep the granuloma together and working tb shuts down metabolically in order to survive and goes into latency, but if this fails an abcess will form full of live mycobacteria

Question 58

what happens if the tb infection develops into pulmonary disease and what does this do to the lung how is this spread where in the lung is tb usually found

Answer 58

the granuloma develops into a cavity which is like a fluid filled space containing puss or live and dead bacteria, this will erode the lung and become a large airway and when you cough puss containing the live bacteria is released in the upper half

Question 59

how many sputum samples do you need for tb diagnosis and what can you see in them can we use and gram stain what else could be used and how does it work

Answer 59

three, can see pink lesions in the sputum it is resistant to gram stain because of the high lipid content and so we use zeihl neelsen stain for acid fast bacilli it uses methylene blue and carbon fuschin and you cannot wash out the stain. you need 10,00 bacteria per ml of sputum before you can see them so doing 3 tests is useful

Question 60

what medium did we used to grow tb on what do we use now what is another way to detect tb

Answer 60

used to grow tb on egg based Lowenstein Jensen medium which contained the right nutrients and antibiotics to stop other bacteria taking over now we use liquid culture MGIT, which increases the likelihood of seeing tb in 3 weeks nucleic acid detection using PCR

Question 61

why can tb infect other parts of the body and what can this cause

Answer 61

tb can infect other parts of the body due to haematogenous dissemination and cause extra pulmonary tb in 30% of people the macrophages containing tb travel to the lymph nodes and could go to other parts of the body and cause infection there straight away or after a time of latency. For example tb meningitis (brain), miliary tb (everywhere) or pleural tb (lung lining).

Question 62

what would a scan of pleural tb look like

Answer 62

wide mediastinum due to swollen lymph nodes and fluid in the bottom of the lung

Question 63

what things can cause the tb to reactivate after being dormant

Answer 63

granuloma failure can cause this, could be due to old age or malnutrition, immunosuppression or intensity of exposure, or if you take medication that suppresses the immune system (crohns)

Question 64

what is the infection process of tb what is the primary infection and what is this likely to cause could there be a second infection and what may this do what proportion of people die before the tb reactivates

Answer 64

primary infection of tb causes no disease mostly, but 1 in 20 get primary progressive disease. but most people will get latent tb and 5% will reactivate it later in life and cause post primary disease. there could also be a second infection, which started the process again. 18 in 20 die before the tb can reactivate

Question 65

how much of the population have latent tb and what does this mean which people have a higher incidence of tb

Answer 65

1 in 4 so it is very difficult to eradicate non UK borns

Question 66

what are some bacteria that can cause other chronic pneumonias

Answer 66

nocardia, burkholderia pseudomallei, non tuberculous mycobacteria

Question 67

what can nocardosis cause where is it found what does an infection cause who will catch this and how

Answer 67

it can cause chronic pneumonia it is found in the environment, typically in standing water and decaying plants and soil. there is a slow onset and prolonged fever, weightloss, cough, chest pain. can form granuloma in the lung and can spread to other parts of the body. most people who catch it are immunocompromised, you can catch it by inhaling dust that contains the bacteria or a patient can be infected with contaminated medical equipment.

Question 68

what is another name for burkholderia pseudomallei and where does it come from where is it found and how is it spread what are the symptoms who is most likely to catch it

Answer 68

meliondosis and it comes from the tropical climates. the bacteria is found in water and soil and can be spread by direct contact the symptoms are slow development, cough, chest pain, fever headache, weightloss, lung abscess and can spread to other organs. you have an increased risk if immunocompromised or have renal disease, thalassemia or cancer.

Question 69

where is non tuberculous mycobacteria found and what smear is done how fast does it grow and what are symptoms who is most at risk

Answer 69

found in soil and water acid fast bacilli on ZN smear slow growth granulomas, cough, fatigue, fever, weightless, short of breath immunocompromised and COPD

Question 70

what does it mean if a fungus is dimorphic, what is an example of one and what can it cause symptoms

Answer 70

can have 2 types of structure histoplasma capsulatum and can cause pneumonia visible lymph nodes on the x ray

Question 71

what is an example of a parasite that can cause pneumonia | how can we get infected and what are the symptoms

Answer 71

echinococcus granulosis (dog tapeworm) we eat it to get infected many lesions and sacks of fluid in the lungs which contain worm offspring

Question 72

what is different about a chest x ray of someone with emphysema what does IPF stand for and what does the chest x ray look like

Answer 72

bigger lungs due to hyperinflation idiopathic pulmonary fibrosis and the x ray will have lots of white scarring

Question 73

what are the four types of interstitial lung disease

Answer 73

IPF (idiopathic pulmonary fibrosis) sarcoidosis CTD-ILD chronic hypersensitivity pneumonitis

Question 74

what is FVC and FEV1 and how are they changed in obstructive and restrictive lung diseases what can be used to measure them

Answer 74

spirometry is used to measure them FVC is the forced vital capacity which is how much you can breath out in one go. FEV1 is the volume you can release in one second. obstructive lung diseases can reach the full FVC but the FEV1 is reduced and so is the ratio. restrictive lung diseases reduce both the FVC and the FEV1 so the ratio stays the same.

Question 75

what does ILD do to gas exchange how can we test for ILD

Answer 75

ILD has inflammation and fibrosis which thickens the layer between the airway and bloodstream gas exchange is harder for O2 but not for CO2. carbon monoxide is used in a lung function test and they breathe in a very small amount and the amount exhaled is measured, they find that there is a reduced uptake of CO in ILD. or exercise testing called incremental shuttle walk test where you walk around two cones and you have to reach the end before the bleep and the bleeps speed up.

Question 76

what is the pathogenesis of ILD

Answer 76

a heterogenous mix of lung diseases which combines fibrosis and and inflammation.

Question 77

IPF: cause, what is the main problem is causes, who usually gets it, what isa. risk factor what is the characteristic radiology

Answer 77

not a clear cause. scarring that prevents O2 entering the blood stream fibrosis of the lung parenchyma usually males over 60 smoking is a risk factor the radiology is usual interstitial pneumonia UIP, the UIP shows that IPF mainly affects the base of the lung, you get honeycombing (small holes) usually in the periphery of the lungs and there is also traction bronchiectasis (irreversible dilation of bronchi)

Question 78

scan terminology: honeycombing traction brocnhiectosis

Answer 78

small holes irreversible dilation of bronchi

Question 79

why might some people be more likely to have IPF how does the scarring develop and what will this do to gas exchange

Answer 79

IPF is thought to occur in people with a genetic predisposition or an environmental trigger. fibroblasts come to repair the damaged tissue, and become myofibroblasts which deposit collagen in the ECM and this will cause scarring. myofiboblasts proliferate and form fibroblastic foci and this thickened tissue causes a reduction in gas exchange

Question 80

what genes are thought to be involved with IPF

Answer 80

mutations in genes involved in the maintenance of telomere length (TERT) also genes responsible for cell adhesion and integrity. a single nucleotide polymorphism of MUC5B increases the risk of IPF

Question 81

what are five key features of IPF

Answer 81

collections of fibroblasts (fibroblastic foci) thickening of alveolar interstitum destruction and honeycombing of alveoli affects periphery and base of lung spatial heterogeneity (normal tissue next to abnormal tissue

Question 82

what can cause HP and what binds to the allergen what is the main problem occurring from this how can HP be detected

Answer 82

BASICALLY HYPERSENSITIVITY TO INHALED THINGS CAUSING IMMUNE RESPONSE repeated exposure to environmental agents, the most common one being pigeons, IgG antibodies will bind to the pigeon allergen and cause an immune response causing inflammation and alveolitis and granulomatous inflammation which progresses to fibrosis. inflammation and air trapping which is from a type 3 hypersensitivity reaction which involves the immune complex. the immune response causes there to be many lymphocytes and this can be detected by counting cells in a bronchoscopy and if 20% of all cells are lymphocytes then it means HP.

Question 83

what has to have occurred for a type 3 hypersensitivity reaction what happens when the allergen is detected because of this

Answer 83

there has to be prior sensitisation the IgG antibodies made by the lymphocytes retain immune memory of the antigen. so on the second exposure the antibody antigen complexes are formed and are deposited in the lungs and cannot be cleared repeated exposure leads to more inflammation and eventually fibrosis and a decline in lung function

Question 84

what cells is HP associated with what other factors and jobs can cause HP

Answer 84

increases of CD4 T cells and the CD4/CD8 ratio and Th2 activity mould, hay, pigeons, feather pillows, bacteria, hot tubs. metal workers with oil or mist or coolant, farming, air conditioning, cleaning agents