Respiratory Flashcards
what are the resections of the respiratory tract
sinuses
pharynx
larynx
trachea
bronchiole
alveolus
what are the main defences of the respiratory tract
saliva, mucous, cilia that beat and clear particles from the respiratory tract
what are the two types of respiratory infection
Epithelium surface: that infect and stay localised to the epithelial layer, such as the viruses that cause the common cold or candida infections which live on the oral and vaginal epithelium
Then there are the more systemic ones that start at the epithelium and then can migrate to other organs but then return to the respiratory tract for replication and shedding.- MUMPS
explain surface respiratory infections (2) with 2 examples
local spread, doesn’t move around body
short incubation
common cold, oral Candida
explain systemic respiratory infections (2) with examples
spreads from mucosal site of entry to other site in the body
returns to surface for final shedding stage
Longer incubation- days-weeks
e.g. measles, mumps, rubella, covid19
what are the two types of respiratory pathogen invaders
Professional invaders:- infect healthy respiratory tract
Secondary invaders: - infect compromised tract
what is rhinitis and sinusitis also called
the common cold
what are the main infections of the nasopharynx
rhinitis and sinusitis = common cold
explain how cold viruses work and get removed
virus particles bind to ciliated epithelium and avoid being flushed away
enter cell and replicate and damages the cell leading to loss of cell and inflammatory response
And leads to activation of host defences release of cell debris and transient damage to ciliated epithelium.
Then there is an immune response that might be accompanied by overgrowth of normal flora and finally recovery and regeneration of ciliated epithelium.
what viruses can cause common cold
Rhinoviruses
Coxsackie virus A
Influenza virus
Parainfluenza virus
Coronaviruses
Adenovirus (41 types)
Echovirus (34 types)
what can coxsackie virus cause after common cold
herpangina and hand foot and mouth
what can adenoviruses cause
common cold
mainly pharyngitis; also conjunctivitis, bronchitis
if we have a sore throat, what is the likely cause of our cold
adenovirus
what is the most differential symptom for an adenovirus
sore throat
how do adenoviruses attach to epithelia
Attach via the adhesins on end of penton fibres
what percent are pharyngitis and tonsillitis caused by viruses
70%
what is found in 70-90% of glandular fever patients
Epstein Barr Virus
what is Epstein bar virus associated with
Glandular fever
what type of disease is caused by Paramyxovirus
Mumps
what type of virus causes mumps
Paramyxovirus
what complication can come from an adult male getting mumps
Orchitis
Swelling of the testis, very painful
doesnt affect fertiility
what is and what causes Orchitis
Mumps (caused by Paramyxovirus)
Swelling of the testis, very painful
doesnt affect fertility
what is the main symptom of mumps
Swollen lymph nodes, cervical lymph nodes, thick neck alongside cold symptoms
what 3 virus groups often causes Laryngitis and tracheitis
parainfluenza viruses
adenovirus
influenza
what is the main symptom of laryngitis/Tracheitis
Burning pain in the larynx and trachea, ‘loose voice’
what is croup cough and what is it associated with
Specific type of cough with Stridor inhalation caused by a constriction of the airway leading to a small airway opening and if child has smaller airways very little oxygen can get through this can cause problems
Laryngitis and Tracheitis
how might we tell a patient has laryngitis from a radiograph
Inverted V on x-ray- steeple sign in the tracheal area showing a constriction in the airway
give several viral causes for bronchitis and 1 atypical cause
Rhinoviruses, coronaviruses (SARs, COVID-19), adenoviruses and influenza
Atypical pathogens: Mycoplasma pneumoniae
what does ‘atypical’ mean in terms of respiratory infections
caused by bacteria not by virus
what is 75% of bronchiolitis caused by and how does it act
Respiratory Syncytial Virus RSV
causes large fused cells Syncytia
what does RSV cause
Respiratory Syncytial Virus causes 75% of bronchiolitis
what virus have most infants been infected with and how might coronavirus altered this
Respiratory Syncytial Virus
covid = isolation less exposure = less kids immune
what are differential diagnosis of infants with Cough, cyanosis, shallow rapid respiratory rate
pneumonia and bronchiolitis
bronchiolitis caused by RSV
how do you treat severe bronchiolitis
bronchodilators and hydrators
why do more respiratory infections occur during the colder months of the year
people are inside more and this gives way to more passage by particle droplets
what is asthma (3)
temporary reversible narrowing of the airways due to an inflammatory process occurring
within those airways
what is Atopic Asthma (3)
triggered by environmental agents e.g. dust
family history of asthma, hay fever etc.
type I hypersensitivity reaction
explain why atopic asthma occurs briefly (3)
mast cells on the bronchi have IgE on their surface that have been made by the body against a specific allergen
when allergen binds to IgE, this causes the IgE antibodies to cross link
leading to degranulation of the mast cell where a large number of inflammatory mediators are released from the mast cell into the surrounding cells in the
bronchus causing an acute inflammatory reaction.
give 4 ways to treat asthma
avoid the allergen
remove mast cells from lungs by inhaled steroid (brown inhaler) beclomethasone
disodium cromoglycate in spin inhalers bind and stabilise membranes stopping degranulation
militate the efects of the inflammatory mediators. salbutamol which is a beta-adrenergic stimulant that raises cyclic AMP levels within cells and reduces inflammatory efects such as oedema of the bronchi which causes bronchial narrowing (blue inhaler)
what is in the brown and blue inhalers for asthma
brown = beclomethasone steroid = decreases mast cell number
blue = salbutamol = a beta-adrenergic stimulant that raises cyclic AMP levels within cells and reduces inflammatory effects such as oedema of the bronchi which causes bronchial narrowing
how does the brown inhaler work and what are its limitations
beclomethasone is a steroid inhaler that reduces the number of mast cells in the lungs. This needs time to kick in so has to be taken once a day for a while before it acts.
what is disodium cromoglicate used for and how does it work
treatment for asthma
comes in capsule and put in a spinning inhaler
when taken it binds to and stabilises the mast cell walls preventing/reducing degranulation
therefore less inflammatory reaction
in chronic obstructive disorders, is the problem mainly on exhalation or inhalation
mainly on exhalation
what is COPD a mixture of
chronic bronchitis and emphysema
what defines chronic bronchitis
cough and sputum for 3 months over 2 consecutive years
what is the aetiology of chronic bronchitis
cigarette smoking
air pollution (nitrous oxide important from cars)
who is likely to get chronic bonrchitis
people in heavy pollution areas e.g. china
men smokers
explain where the symptoms of chronic bronchitis come from
mucus hypersecretion
chronic inflammation
squamous metaplasia = recurrent infections
dysplasia (but a feature of the causative agent)
how might Haemophilus influenzae affect someone
once a patient has had influenza, this bacteria may cause an atypical recurrance of the disease
define emphysema
anatomical
enlargement of airspaces distal to the terminal bronchioles with destruction of elastin in walls (holes in alveolous)
what percent of lung degration by emphysema do we start seeing significant problems
20-30% left
what would emphysema look like radiographically and anatomically
look black on an xray due to reduced tissue so more xrays get through
anatomically we would see small holes
what would cause focal emphysema
coal dust gets focal emphysema around it where around the carbon particles, the lung degrades
what causes lung cancer
cigarette smoking 85-90% all cases
asbestos exposure
radon exposure
nickel, chromate etc
what cells line the airwyas
simple ciliated columnar epithelia
what happens to respiratory epithelium under cigarette smoke (cancer)
metaplasia
columnar ciliated epithelium turns to stratified squamous cells with no cilia
cells become dysplastic and can become cancerous and invade local tissues
what types of lung cancer are there
small cell
non small cell = adeno or squamous
what type of lung cancer is associated with smoking
squamous non-small cell lung cancer
which type of non-small cell lung cancer has higher prognosis
adeno = non smoking cause = more prognosis
sqamous = smoking = lower prognosis
what is the treatment and prognosis of small cell lung cancer
low and chemotherapy - will not cure
if a lung cancer is large and near the periphery of the lung on xray what type is it likely to be
non-small cell adenocarcinoma of the lung
why might we not see some lung cancer on xray and what do we do instead
may be very small
may lie centrally on the bronchi, behind the heart and large vessels and mediastinum
CT scan seperates lung tissue from heart
what is the best diagnostic tool for lung cancer
CT scan due to no superimposition on mediastinum or heart
what is the best diagnostic tool for lung cancer
CT scan due to no superimposition on mediastinum or heart
what percent of lung cancers are good prognosis
<10% 5 year survival rate as only 15-20% are removable
What is atopic asthma
Allergic asthma that is, in 80% of people, related to ezma, hayfeveer and food allergies
what should be included in a patient history (8)
introduce self and check full name and DOB
patient complaint and Socrates
history of complaint
past medical history
drug history and allergies
family history
social history
close session
what causes bronchiolitis and what else can it cause
Respiratory Syncytial Virus
most infants get this by 2 years old
can also cause pneumonia
what is the main distinguishing factor of influenza
very fast onset of fever and sickness, symptoms for 3 days and very tired, cant move around and very tired
how does influenza virus work
virus attaches to sialic acid receptors on epithelial cells via viral HA protein
1-3 days: liberated cytokines result in systemic chills, malaise, fever and muscle aches, runny nose and cough
what can occur after an influenza infection
Usually recover after 1 week, but some develop pneumonia and bronchitis and have lingering symptoms - very bad reaction and will be in bed for a few days
Secondary invaders can cause lethal infections: pneumococci, staphylococci
explain the structure of the influenza virus
a host derived viral evnelope
with Two surface glycoproteins:
HA- Haemagglutinin first point of contact
NA- Neuraminadase released from cell afterwards
Inside we find
ssRNA genome: 8 segments
Nucleoprotein and polymerases
if a virus has 8 parts of ssRNA in it, what is it likely to be and what is the significance of this
influenza virus
8 segments favours antigenic shift causing pandemics
what are the two surface glycoproteins of influenza virus
HA- Haemagglutinin first point of contact
NA- Neuraminadase released from cell afterwards
what is the importance of HA Haemagglutinin
one of the 2 surface glycoproteins of the influenzas virus (other being NA)
major antigenic determinant
- HA binds sialic acid receptors on epithelial cell surface
- Major source of antigenic variation
what is the major source of antigenic variation of influenza
Haemagglutinin HA - surface glycoprotein on surface membrane
what are the three types of Influenza and explain their significance
Type A: most common, animal reservoir meaning genetic variation is high, Yearly epidemics and occasional serious worldwide epidemics- important animal reservoirs in birds and pigs, vaccine against this
Type B: yearly epidemics, no animal reservoir
Type C: minor respiratory illness- no epidemics, no animal reservoir
what do the parts of this classification man: A/ Hong Kong / 1234/ 2009 (H1N1)
Influenza type A
location of isolation = hong kong
strain type = 1234
date of isolation = 2009
Antigens H1N1
how many NA and HA types are human adapted
16 H antigens but 3 human
9 N antigens but 2 human
how do new influenza viral strains occur (3) and give this name (1)
Small point mutations in HA and NA that accumulate in population over time
Result in new variant viruses that can re-infect individuals
Mutations typically occur in antigenic parts of molecule- prevent antibody binding
antigenic drift
why are flu vaccines not suitable for vegans or egg allergy
Vaccine strains chosen in February for northern hemisphere
Strains grown in embryonated hen eggs: not applicable to individuals with Egg allergy
when would a flu pandemic occur
where the predicted viral adaptation from the opposite hemisphere doesnt correlate with a new mutation of the influenzas virus
compare antigenic drift and antigenic shift for influenza
antigenic drift is small point mutations over time , resulting in small antigenic changes and usually predicted in the flu vaccine, more common, less likely to cause pandemic
Antigenic shift is Less common, Results in major shift in viral composition, Major gene reassortment resulting in new HA and NA types, only type A
explain antigenic shift (4) and the reason influenzas is favoured for this
Simultaneous infection of human/animal with Human and ‘other’ influenza virus
Reassortment of genes due to homologous recombination with existing human virus
Dissemination through immunologically naïve population
very different combinations of N and H antigens that there are no antibodies for
WORLDWIDE PANDEMIC
influenza has 8 segments of RNA in genome favouring this process
how can we combat influenzas pandemics
vaccine but these take 3-6 months
antivirals:
Amantadine blocks M” uncoating function
siRNA might block transcription replication
NA inhibitors block release via NA inhibition - most common
what is the most common influenza anti-viral
NA inhibitors block release via NA inhibition
what types of organisms can cause pneumonia (3)
Many organisms cause identical symptoms
Only organisms less than 5mm can enter the alveoli
Often secondary to preceding damage- Cystic Fibrosis or influenza
Influenced by Immunocompromisation
what size must a microbe be to fit into an alveolus
5micro meters
if a neonate has pneumonia, what could be a cause of this
Chlamydia acquired from the mother
describe the difference between child and adult pneumonia
Children: = much more suseptible usually by viral
- mainly viral causes – RSV, parainfluenza (chlamydia from mother)
- secondary bacterial infections
Adults
Bacterial causes more common-: e.g. Strep. pneumoniae formerly most common
what is pneumonia
swelling and inflammation of the lung tissue in one or both lungs
list 5 viruses that can cause pneumonia
Influenzas A and B = pre-dispose for secondary bacterial infection e.g. Strep. Pneumonia
Parainfluenza = children under 5
Adenovirus = pharyngitis
RSV respiratory syncytial virus = bronchiolitis
MEasles = common bacterial secondary infection with immunocompromised patients
how many coronaviruses affect humans
7 types
what type of genetic information is held in a covid virus
RNA genome
what protein does coronavirus attack and how did this affect symptoms
ACE2 - angiotensin converting enzyme 2
found in eyes, nose, lungs, nose, heart, kidney, liver
causes inflammation in these areas in compromised patients
compare the age : death graphs for coronavirus and influenza
COVID = gradua slope only peaking at old age
influenza = W shaped graph
give a brief (2) explanation of the structure of COVID
Trimeric Spike protein binds to ACE2
RNA genome inside
what is atypical pneumonia
bacterial pneumonia that is NOT caused by S. pneumoniae
NOT treatable by Penicillins
symptoms generally less severe- WALKING PNEUMONIA
what causes atypical pneumonia
Mycoplasma pneumoniae
Chlamydophila (formerly Chlamydia)
Legionella pneumophila
what is significant about Mycoplasma pneumoniae
very small 0.5Mbp
no peptidoglycan in cell wall, just cholesterol therefor penicillin resistant
how would we normally treat pneumonia and why might we not be able to with atypical
penicillin
Atypical can be caused by Mycoplasma pneumoniae which has no peptidoglycan in its cell wall meaning beta lactams are useless against them
what is Chlamydophila pneumoniae
related to sexually transmitted chalmydia
bacteria that cause atypical pneumonia
No peptidoglycan (Pen insensitive)
Flu-like illness
Detection by ELISA or MicroImmunofluorescence
how and why do we detect chlamydophila pneumoniae
ELISA testing
as the bacteria live inside other cells so cannot be grown on agar
how does Legionella pneumophila cause disease (3)
Acquired from environmentally derived aerosols
Ubiquitous in environment (symbiosis with amoeba)
Intracellular invader of phagosomes and lung cells
what is significant about legionella penumophilia
Pneumonia symptoms often accompanied by neurological presentations such as confusion
No human-human transmission
Acquired from environmentally derived aerosols
Air-conditioning, Spa-baths, Hot-air heating, shower systems, cooling tower reservoirs
Commonly in hospitals, high rise blocks, hotels, student residences, factory air-con sources
explain shape and gram of legionella pneumophilia and how we test for it
Motile aeerobic Gram-negative rod
Isolation on BCYE medium (Buffered Charcoal Yeast Extract)
Urinary antigen test (antigens secreted in urine)
what would we use BCYE medium (Buffered Charcoal Yeast Extract) to detect
Legionella Pneumophilia
if a patient has recently been to a conference in Spain and is showing signs of general illness, what is likely the cause
Legionella Pneumonia causing
Atypical Pneumonia (bacterial pneumonia that is NOT caused by S. pneumoniae, not treatable by penicillin, mildeer symptoms)
what is the prevalence of COPD
3M
5year survival <30%
what is FEV1
forced expiratory volume in 1 second
how do we diagnose COPD
FEV1 < 70% with emphysema or chronic bronchitis
what is COPD
chronic obstructive pulmonary disease
combination of obstructive airway diseases such as emphysema and chronic bronchitis
FEV1 < 70%
what is FVC
forced vital capacity - how much exhaled after a big breath
what is a genetic form of COPD
Alpha-1 Antitrypsin Deficiency-related COPD
what is SOBOE
shortness of breath on exertion
what are some symptoms of chronic and acute COPD
chronic: SOBOE, Wheeze, Cough, Weight loss - late term
Acute: Acute sob/wheeze, worsening sputum production, Fever, Drowsiness/CO2 narcosis
what are signs of COPD
Cachexia - muscle loss
Use of accessory muscles
Pursed lips - tight lips
Cyanosis - bluish discolouration
Drowsiness in CO2 narcosis
Hyper-expanded chest barrel shape
Hype resonant - sounds resonant with tapping
Reduced breath sounds
Wheeze
Elevated JVP jugular venous pressure & peripheral oedema in late disease
what is cachexia
muscle degradation
what happens to oxygen and co2 levels with COPD
patient fails to exhale enough CO2 and keeps it in the blood
not enough oxygen in the blood
what is JVP and when is it elevated
jugular venous pressure and elevated in COPD
what chest signs would a person with COPD have (3)
Hyper-expanded chest barrel shape
Hyperresonant - sounds resonant with tapping
Reduced breath sounds
what is the diagnosis pathway for COPD
Need correct history >35 years hx of smoking and at least 1 of following: exertional breathlessness, chronic cough, regular sputum production, frequent winter bronchitis or wheeze. Weight loss, waking at night breathless, ankle swelling, fatigue, occupational hazards, chest pain and haemoptysis are all common respiratory symptoms.
Spirometry to conclude FEV1<70%
what is significant pack years
anything over 10
why might muscle dysfuction be a sig of lug disease
less use of lungs, less exercise, less use of muscles
how do we measure breathlessness with scores
MRC scale
1- not troubled until strenous exercise
2- okay on flat but breathless on hill
3- slow, has to stop every 15 miuntes
4- stops for breath every 100 yards
5- too breathless to leave the house or dressing
what is MRC stage 1 and 2
1 = breathless on strenuous exercise
2 = okay on flat, breathless on hills
what is MRS 3 and 4
3 - slower than most, breathless after 15 mins/1 mile
4 - breathless every 100 yards
what is MRS stage 5
too breathless to leave the house
what is a cat score
severity score for breathlessness
used to monitor respiratory disease
what are the NICE fundamental COPD treatments before inhaled therapy
we first must advise:
-stop smoking
- pneumococcal vaccine (strep. Penumonia)
- flu vaccine
- muscle rehab
what is LABA and LAMA and SABA and ICS
long acting beta agonist
long acting muscarinic agonist
short acting beta agonist
inhaled corticosteroid
what medication do we give COPD patients initally
SABA/SAMA
what would we provide if the patient is still breathless after SABA/SAMA
if NOT asthmatic/ high eosinophil count:
LABA and LAMA
if asthmatic / high eosinophil count:
LABA and ICS
when would we put a patient onto triple COPD medication
if patient is asthmatic and is still breathless after LABA and ICS, we would provide triple treatment being:
LABA, ICS and LAMA
what s there an increased risk with ICS
inhaled corticosteroids increase risk of penumonia infection
what does pneumonia look like on an xray
focal part of consolidation on the lung = infection
what is roflumilast and what does it do
PDE4 inhibitor
reduces exacerbation frequency
why is roflumilast only used in severe cases
lots of side effects like GI upsets and insomnia
highest rate of efficacy in severe exaccerbation pts
what might a high sputum producer be on
Mucolytics
if a patient is on mucolytic, what is their problem
high sputum producers
COPD
what is the treatment process for COPD
primary:
-stop smoking
-muscle training
-loose weight to decrease BMI
-Strep. Pneumoniae vaccine
Inhalers:
SABA or SAMA
if not working LAMA, LABA or ICS (if asthmatic) or triple therapy if non-resposive
Mucolytics for high sputum or roflumalist for severe exaccerbation
oxygen treatment LTOT 14 hours min or ambulatory
Antibiotics if 2 or more:
-increasing volume of sputum
-change in colour of sputum
-worsening dyspnea (SOB)
surgery/transplant if extremely severe
what is LTOT
pt is on oxygen minimum 14 hours a day
due to hypoxia due to COPD and possibly polycythaemia
what types of oxygen therapy are there
LTOT on oxygen 14 hours or more per day
Ambulatory 2L tank if they can prove their saturation reduces in 6 mins of walking
why do COPD patients have pursed lips
keeps mouth closed
creates more pressure down in the lungs
keeps alveoli open for more gas diffusion
when do we give COPD patients antibiotics
2 or more:
-worsening dysopnea (SOB)
-change in colour of sputum
-increase sputum volume
how do we ask a respiratory patient about exacerbations
how many rounds of antibiotics have you had in the past 12 months
why is high steroid use throughout the year a risk for dental procedures
adrenal suppression
don’t produce enough steroids (cortisol)
cant deal with stress, need steroids before treatment
what would a patient with COPD get, in terms of drugs, if exacerbating
antibiotics
oral prednisolone
what are the advantages and disadvantages of oral prednisolone for COPD exacerbations
more rapid improvement in physiology
shortens hospital time
risk adrenal supression
compare type 1 and 2 respiratory failure
<8kPa ppO2 in both
type 1 - low or normal CO2
type 2 - high >6kPa CO2
what cause chronic and acute type I respiratory failure
chronic: fibrosling lung disease
acute: infection, pneumonia asthma
what causes acute and chronic type II respiratory failure
acute: overdose opiates, trauma
chronic: COPD, neuromuscular
why does blood CO2 rise in COPD
pt less able to force CO2 out of their lungs
how many people have asthma
10%
if we suspect asthma in a patient, what can we ask (3)
onset and timing of breathlessness
any triggers
on any medications
if we suspect asthma, what sings might we see (5)
elevated respiratory rate
inability to complete sentence’s
audible wheeze
tachycardia
cyanosis - hypoxia
what are some symptoms of asthma 4
breathlessness
triggers
wheeze
tight chest
nocturnal duration
what are triggers of asthma 4
dust
pollen
stress
temperature
exertion
what two groups of ‘asthmatics’ do we place patients in
asthma suspected
asthma diagnosed
how can we diagnose asthma
spirometry, history
trial of ICS inhaler
if symptoms reduce = asthma
if a patient has an acute asthma attack and cannot wield their own inhaler, what do we do
use a spacer inhaler
give 4 pumps initially and then 2 pumps every 2 minutes for max 10
what is omalizumab and what conditions are to its use
IgE monoclonal antibody to help treat severe asthma with an allergy component
when pt has 4 exaccerbations a year or on continuous oral steroids
they have maximised LABA
very frequent daytime/nightime sympmtoms
how do IL-5 blockers work and why are they advantageous
bone marrow makes eosinophils –> blood –> lungs
IL-5 antibodies reduce eosinophils
expensive and has to be approved and be adherent
monoclonal antibodies for IL-5
reduce steroid intake and better quaity of life
what types of monoclonal antibody treatment is there for asthma (3)
Omalizumab - IgE monoclonal antibody to help treat severe asthma with an allergy component
IL-5 monoclonal antibodies to reduce eosinophil number - other ones
IL-13 and IL-4 mabs work in similar way - Dupilumab
what condition do 1% of asthmatics have
ABPA - allergic bronchopulmonary aspergillosis
what is ABPA and what does it lead to
allergic bronchopulmanory aspergillosis
allergic reaction to mould spores in the air
IgG response –> lung consolidations
leads to bronchiectasis
what is bronchiectasis and what are its major symptoms
damage to lungs leads to widening of tubes and formation of pouches
Symptoms typically include a chronic cough with mucus production. Other symptoms include shortness of breath, coughing up blood, and chest pain. Wheezing and nail clubbing may also occur
how do we diagnose ABPA (4)
high eosinophil, IgE and IgG levels
CT scan showing bronchiectasis
skin reaction to aspergilllus
previous asthma
what conditions can asthma pre-dispose
EGPA and ABPA
describe asthma severity (4)
mild: PEF% >75
moderate: PEF% 50-75
severe: PEF% 33-49, RR > 25, HR >110min, not talking
Life Threatening: PEF% <33, bradycardia, silent chest
what would a severe asthma case entail (4)
33 < PEF% < 49
not talking
HR > 110min
RR > 25
what is the prelevence of lung cancer
69 in 100,000
2nd most common in men and women
89% preventable
5% survival after 10 years
how much lung cancer is SC and NSC
85% NSC
15% SC
what percent of lung cancer is operable at diagnosis
10%
what are symptoms of lung cancer
lobular collapse, breathlessness
lymphangitis
effusion
chest pain - rib envolvement, envasion
cough (blood in cough)
NORMAL SYMPTOMS
weight loss
loss of appetite
tiredness
a patient smokes and is very tired and loosing weight, differential diagnosis?
lung cancer
emphysema
what is a paraneoplastic syndrome
where a hormone secretion is liked to a cancer e.g hyperthyroidism due to thyroid cancer
give examples of lung paraneoplastic syndromes (3)
from lung cancer:
PTH secretion = high calcium = abdominal pain, confusion, constipation
Lambert Eaton Syndrome = neuromuscular weakness from lung cancer
SIADH syndrome of inapropriate diuretic hormone = too little salt, confusion, fits
what is lambert eaton syndrome
paraneoplastic syndrome related to lung cancer
neuromuscular weakness
what is SIADH
syndrome of inappropriate anti-diuretic hormone
lung cancer paraneoplastic syndrome
fits, confusion, little salt in blood
what are signs of lung cancer
finger clubbing
neck nodes
palpable liver in late stage
chest signs
cachexia
horner syndrome = drooping eyelid and wasting between thumb and first finger
what are signs of horner syndrome and what is this a sign of
wasting between thumb and first finger + eye drooping
sign of lung cancer
how do we diagnose lung cancer
signs and symptoms
XRAY < CT < PET
pet expensive and false positives uses radioactive glucose
biospy = bronchoscopy, transthoracic incision, surgical
what is treatment for NSCLC (85%)
based on performance levels, chemo , immuno
what is the WHO performance grading
way of grading every day life for patients
0 = no restriction to activity
1 = slight restriction on exertion
2 = able to walk around but not work, up and about ore than 50% of the time
3 = unable to work and n bed 50% of time
4 = completely bed ridden
what dictates how NSCLC patients are treated
WHO performance status WPs
0-2 treated
what is ILD
interstitial lung disease
group of lung diseases, most of which lead to scarring of lung tissue
sometimes has trigger e.g. birds
lead to idiopathic pulmonary fibrosis, EAA
what are the symptoms of ILD
interstitial lung disease
cough, breathlessness, fever
what is a classic cause of ILD
birds
what are signs of ILD
connective tissue disorder
nail clubbing
steroid use
immunosuppression
sclerodactyl (tight skin on hands)
crackling chest
what is scerodactly and what respiratory disease might this be a sign of
tight skin across the hands
ILD interstitial lung disease
who is likely to get IPF
idiopathic pulmanory fibrosis
old men
how do we diagnose IPF
CT scan scarring on the lungs
ratio of FEV1 and FVC is above 70 (unlike COPD)
both have decreased
what is IPF
idiopathic pulmonary fibrosis
how do we treat IPF
pulmanory rehab
anti-fibrotics e.g. Pirfenidone (anti-fibroblast activity with effect on survival & lung function) when FVC<80%
Nintenadib (anti-fibroblast FVC 50-80%)
what is EAA
extrinsic allergic alveolitis
within ILD
Classical triggers
Occupation – Baker
Farmer
Moulds, carpenters
what are common triggers for EAA
extrinic allergic alveolitis
Classical triggers
Occupation – Baker
Farmer - BIRDS
Moulds, carpenters
a patient has fibrosis on the lungs and owns lots of pets, what are they likely to have
ILD caused by EAA - extrinisic allergic alveolitis
how do we treat EAA
remove allergen, avoidance
steroid use
possible bisphosphonates
what is sleep apnea
daytime sleepiness due to flucuating oxygen levels through the night, making patient not sleep well and be tired through the day
cessation of flow for 10 seconds
what is sleep hypopnea
reduction of flow for 10 seconds by 30% <
compare sleep apnea and hypopnea
apnea = cessation of flow for 10 seconds
hypopnea = reduction in flow for 10 seconds of 30%
what are the three types of sleep apnea
OSA - obstructive sleep apnea = over weight
central sleep apnea = miscommunication from brain
mixed sleep apnea
what is OSA
obstructive sleep apnea
what are risk factors for OSA
obstructive sleep apnea
neck > 17inch
men 2/3x more risk
age
Cranio-facial & upper airway abnormalities e.g short mandible, tonsillar/adenoid hypertrophy, wide craniofacial base
what is the cause of OSA and how does this effect the body
soft tissues in the back of the throat e.g. soft palate too big or flappy
causing local airway blockage
disrupted oxygen levels through the night, drop by 4% the brain stays more awake and doesnt rest proerallyt
how can we measure tiredness and how can this alter life
Epworth Sleepiness Score
can diagnose OSA
high score = loss of driving liscence
how might we diagnose sleep apnea (3)
pulse oximetry drop between 10-15% during night
(4% = brain awakens)
Epworth sleepiness score
polysomnography (gold standard)
wha
how can we differentiate OSA and central sleep apnea
if overweight or not
polysomnography : if nose moves, OSA, if nose doesnt move, central as brain isnt telling body to ventilate
compare pulse oximetry and polysomnography
PO: cheap, easy, measures oxygen drops 4% is supicios, 10-15% drop = sleep apnea, use at home
Polysomnography: differentiate OSA and CSA, nose, leg and eye movement detected, expensive and requires hospital admission,
how do we treat sleep apnea (4)
weight loss/ lifestyle change
Continuous Positive Airway Pressure (CPAP)
Mandibular Advancement Device (MAD)
Pharmocotherapy & surgery?
what is CPAP
continuous positive airway pressure
Delivery of constant pressure by face/nasal mask
Abolition of apneas/hypopneas with improvement in oxygen saturation
Very effective
Adherence variable
Essential for 4 hours a day to maintain licence validity
if CPAP doesn’t effectively work against OSA, what else can we do
MAD - mandibular advancement device
keeps back of airway open
adherence is key
how do SABAs work
short acting beta agonist
Increase in cAMP with reduction in cell Ca2+ leading to relaxation of smooth muscle
Immediate bronchodilation
4-6hour duration
what do we use SABA for
asthma and COPD
immediate releif
what are the side effects of SABA (4)
Increased HR & palpitations
Tremor
Hypokalaemia
Headache
Nervousness
what should not be used asa monotherapy for asthma
LABAs long acting beta agonists
can cause cardiac death
why might SAMA be better than SABA
less side effects
only used for COPD, not really used for asthma
what is the mainstay drug for asthmatics
inhaled corticosteroids
no immediate effect
protection over time
what are some side effects of ICS
Oral candida
Voice change
Risk of skin bruising, bone mineral density change and cataracts with high dose
what is a common ICS medication
beclomethasone
when is prednisolone used for respiratory treatment
oral steroid
used in acute exaccerbations of asthma
or chronically in eosinophilic asthma
side effects of oral steroids
body weight increase
BP increase
infection risk increase
catarax increase
blood glucose increase
what is CO2 drive
in healthy individuals,
chemoreceptors detect high CO2 and increase breathing rate to expel CO2
what happens to CO2 drive in COPD patients
body looses ability to detect CO2 = breathing increase
more CO2 remains the the body
hypoxic drive takes over = oxygen –> breathing
why would oxygen be dangerous to give to an exacerbating COPD patient
they may have a hypoxic drive
this means that oxygen chemoreceptors control breathing
high oxygen may = reducing RR = death
what is normal RR and when would we detect an acute asthma attack
normal = 18 (30-40 at exertion)
asthma attack = >25
compare a peak flow monitor and spirometer
PFM = detects PEF = speed of expiration
Spirometer = detects PEF, FEV1 and FVC much more diagnostic
what is normal FEV1, FVC and FEV1/FVC
normal FEV1 and FVC = >80
normal FEV1/FVC = >70
what is the relevance of an asthma patient having history on ITU
ITU is intensive treatment unit where there is multiple organ failure and ventilation
sign of severe life threatening asthma
compare HDU and ITU
ITU = multiple organ failure = more severe
HDU = higher dependency unit = single organ failure
how might anxiety link to asthma
anxiety leads to stress
stress supresses the immune system
stress acts as a agrevator for asthma attacks
why might anaesthetic cause an episode of asthma attack
asthma is often atopic = caused by allergens
if pt is allergic to anaesthetic agent e.g. lidocaine/adrenaline
causes immune response and mast cell degranulation
leading to bronchospasm and restricted airways and wheeze
adrenaline can also cause palpitations and SOB which may cause asthma attack
why might stress cause worsened asthma (4)
you’re more likely to react to your usual asthma triggers, including colds and respiratory infections, have worse symptoms, or your asthma may feel harder to manage
you get angry more easily and anger is an emotional asthma trigger
you may drink or smoke more, which can put you at more risk of asthma symptoms
it’s harder to stick to your medicine routine.
stress might cause panic attacks = SOB
how do we manage any acute attack
ABC - airway, breathing, circulation
if a pt has an asthma attack, what do we do in the dental surgery
ABC
use a spacer and blue salbutamol SABA inhaler and give 2 puffs every 2 minutes
high flow oxygen at 15L/min
what 2 relivers could be given in an asthma attack
salbutamol = SABA
Ipratropium bromide = Anticholinergic (acetylcholine is a neurotransmitter used to constrict bronchial smooth muscle)
give 4 indications of asthma attack
wheeze
PEF peak flow less than 50% (predicted) (life threatening if PEF < 33%)
Cannot complete sentences
RR > 25
HR > 110
what HR and RR is indicative of asthma attack
RR > 25
HR > 110
what PEF measure indicats asthma attack and what rate is life threatening
PEF peak flow less than 50% (predicted) (life threatening if PEF < 33%)
why do we only give 2 puffs of salbutamol in acute asthma
pt is primarily low on oxygen
if we give too much salbutamol, they wont get enough oxygen and become hypoxic
what rate of oxygen can we give for ventilation
15L/min
what is a nebuliser
looks like oxygen mask but with a well before the mouthpiece where liquid medication is atomised and enters with high flow oxygen e.g. salbuatmol or Ipratropium bromide
what would be hospital treatment of asthma attack
Nebuliser with high flow oxygen
salbutamol 5mg and Ipratropium bromide 0.5mg (releiver)
Prednisolone 40mg (prevent late T cell response)
if nebulisers don’t work in a hospital environment, what can be given as a last resort to asthma attack pt (2)
Aminophylline can cause arrhythmias
Magnesium in form magnesium sulphate
how much stronger is the salbutamol given in hospital vs 2 puffs of inhaler
5mg given in hospital is 50x more than given in 2 puffs
2.5x more absorption due to being in a sealed circuit
125 x
what is prednisolone given for in asthma attacks
preventative oral steroid
after asthma attacks, we get a delayed T cell response causing another acute attack 24 hours later
prednisolone prevent this occuring
is it safe to give a severe COPD patient high flow oxygen
yes
may be acting on hypoxic drive
this means that CO2 drives ventilation, so oxygen reduces ventilation
however this takes 4 hours to set in, so safe to give for 4 hours
also 0.5% of chronic bronchitis patients have hypoxic drive
list 5 things that can cause asthma attack
Stress
Allergens/Triggers e.g. pollen
Exercise
Aspirin/Ibuprofen
Cigarette smnoke
how many deaths of TB have occured in the past 200 years
1 billion
what are the three groups of mycobacterium
MTB - Mycobacterium Tuberculosis Bacteria
non-tuberculosis mycobacterium
Non - cultivable (not able to grow on agar) - only M.Leprae
what makes M.Leprae different to other mycobacteria
non-cultivable, cannot be grown on agar. must be grown in a living organism
describe the staining, oxygen dependency and morphology of M. Tuberculosis (4)
Gram positive bacillus rod with a kink in the middle
Ziehl-Neelsen acid fast positive
Aerobic and non-motile
describe how the structure of M.Tb affects its staining (2)
cell wall contains large single peptidoglycan wall = gram positive
very high lipid content with mycolic acids in the cell wall make mycobacteria resistant to gram stain
= Ziehl-Neelsen acid fast positive
why can M. Tuberculosis survive in harsh environments
very high lipid mycolic acid content
waxy cell wall
resistant to low pH and can survive in macrophages
what is the replication time of M. Tuberculosis
15-20 hours
what 3 consequences come of the replication rate of M. Tuberculosis being slow
Slow growth in humans = gradual onset
Slow growth in culture = slow diagnosis
Slow response to treatment = 6-9 months
how many people are expected to be carrying TB
1 in 4
explain primary tuberculosis (2)
Initial contact made by alveolar macrophages in the lungs
Bacilli taken in lymphatics to hilar lymph nodes (central lung)
what is latent tuberculosis and how is it detectable
no clinical signs
there is detectable CMI to TB on tuberculin skin test
explain how latent tuberculosis occurs (3)
macrophages cause granulomas to form
if CD4 cells are present and good INF-gamma levels good
granulomas stay formed and bacteria is kept separate preventing infection into tissue
which part of the lung is likely to get a pulmonary TB
In apex of lung there is more air and less blood supply (fewer defending white cells to fight)
what is a primary TB complex composed of (3)
granuloma
Lymphatics
Lymph nodes
what is the major cell type invovled in killing M. Tb and what is the active protein
CD4 T cells
generate INF-gamma to induce macrophage intracellular killing
why is TB the leading cause of death in HIV patients (3)
TB is mainly combated by the immune system through CD4 cells producing INF-gamma to induce macrophage intercellular killing
HIV hides in and destroys CD4 cells
what inflammatory marker do CD4 cells produce to kill TB and how does it work (2)
IFN-gamma
induces intracellular killing within macrophages
what is the major histological marker of TB
granuloma formation
what would we find inside a TB granuloma (6)
Large Foamy macrophages form
Highly stimulated macrophages become epithelioid cells
Some macrophages fuse with each other to form giant multinucleated cells - ‘langerhans giant cells’
T cells infiltrate mycobacterial lesion
Angiogenesis occurs to get a blood supply
Fibroblasts laid down around granuloma to ‘wall off’
how is a TB granuloma walled off from the tissues surrounding
fibroblasts produce collagen around the granuloma
what three changes to macrophages might we see in a granuloma
Large Foamy macrophages
Highly stimulated macrophages become epithelioid cells
Some macrophages fuse with each other to form giant multinucleated cells - ‘langerhans giant cells’
what three changes to macrophages might we see in a granuloma
Large Foamy macrophages
Highly stimulated macrophages become epithelioid cells
Some macrophages fuse with each other to form giant multinucleated cells - ‘Langerhans giant cells’
what are the two fates of a TB granuloma
stay stable = dormant TB
burst and collapse = depletion = TB infection
what two inflammatory mediators stabalise TB granulomas
IFN-gamma
TNF-alpha
what can lead to granuloma depletion in latent TB (2)
CD4 disease e.g. HIV = reduced IFN-gamma
TNF-alpha reduction e.g. in arthritis treatment
what is the result from TB granuloma depletion (2)
in the lungs this can result in formation of a cavity full of live mycobacteria and eventual disseminated disease (consumption)
what is the average risk of granuloma depletion in TB cases
first 2 years = 10%
increased by 0.1% each year
what are risks of developing infection from latent TB
age = young or elderly
immunocompromised
intensity of exposure
malnutrition (CD4 depletion)
on arthritis TNF-alpha medication
HIV = reduced CD4 = reduced INF-gamma
what are the three ways of diagnosing TB
PCR - best way
solid or liquid cultures + ziehl-neelsen acid fast positive
Tuberculin skin test
what are some disadvantages = of culture diagnosis of TB
very slow growth
must sterilise off other bacteria
doesn’t determine strain e.g. resistance
what is the best way to diagnose TB and why
PCR
fast, doesn’t rely on replication
identifies strain and resistance to antibiotics
explain the tuberculin skin test (4)
even if a patient is latent TB
will have increased hypersensitivity to tuberculin protein
purified protein injected intra-dermally
hypersensitivity reaction = swell and red
what are the four first line antibiotics for TB
Standard therapy isoniazid (INH)
Rifampicin
Pyrazinamide
Ethambutol x 2 months followed by rifampicin for 4 month
what injected broad spectrum drugs are used as second line treatment for TB
Fluoroquinolones
Injectable agents e.g. streptomycin
Prothionamide may be used if resistance
what is DOTs and how does it work
directly observed treatment. Combine drugs and management. This is where we watch TB patients take medications to ensure complience.
what side effects are there from first line antibiotics for TB (3)
Hepatotoxicity (INH, RIF, PZA) - cannot drink at all
Peripheral neuropathy with INH (give vit B6 to protect)
Optic neuritis (ETH)
what supplement is given with standard therapy isoniazid
first line treatment for TB
vitamin B6 to protect peripheral neuropathy
why are there usually high side effects to TB treatment
very long treatment
multiple drugs used at the same time
how long is TB treatment generally
6-9 months
what four ways of antibiotic resistant are found in TB
Drug inactivation by MTB producing beta-lactamase breaking down any beta lactam antibiotic
Drug titration = bacteria overproduce the target receptor to dilute
Alteration of drug target by mutation
Altered Cell envelope = increased permeability and drug efflux = pumping the drug out
how does a mutation in the 22aa region of rpoB cause problems with treatment of TB (2)
disrupts mechanism of Rifampicin = resistant
induces mutation-prone, non-regulated replication = more likely to get mutations and more resistance
mutations in KatG affect which TB treatment
Isoniazid
needed to activate the anti-biotic to be able to inhibit metabolism
what anti-TB drug would amutaiton in pncA
Pyrazinamide
needed for activation
what is XDR-TB (2)
extremely drug resistance tuberculosis
where a strain is resistant to the 4 first line treatments of TB
6% of strains
how many TB strains are XDR-Tb
6%
how do we treat XDR-Tb
BPal Regimen
Bedaquiline: inhibits ATP synthase
Pretomanid
Linezolid
all oral pill 6 months
what is TDR-Tb
totally drug resistant tuberculosis
no solution as of yet
If a pt is on the BPal Regimen, what are they being treated for
XDR-Tb
extremely drug resistant tuberculosis
