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3rd BDS IHD > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what are the resections of the respiratory tract

A

sinuses
pharynx
larynx
trachea
bronchiole
alveolus

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2
Q

what are the main defences of the respiratory tract

A

saliva, mucous, cilia that beat and clear particles from the respiratory tract

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3
Q

what are the two types of respiratory infection

A

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

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4
Q

explain surface respiratory infections (2) with 2 examples

A

local spread, doesn’t move around body
short incubation
common cold, oral Candida

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5
Q

explain systemic respiratory infections (2) with examples

A

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

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6
Q

what are the two types of respiratory pathogen invaders

A

Professional invaders:- infect healthy respiratory tract
Secondary invaders: - infect compromised tract

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7
Q

what is rhinitis and sinusitis also called

A

the common cold

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8
Q

what are the main infections of the nasopharynx

A

rhinitis and sinusitis = common cold

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9
Q

explain how cold viruses work and get removed

A

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.

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10
Q

what viruses can cause common cold

A

Rhinoviruses
Coxsackie virus A
Influenza virus
Parainfluenza virus
Coronaviruses
Adenovirus (41 types)
Echovirus (34 types)

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11
Q

what can coxsackie virus cause after common cold

A

herpangina and hand foot and mouth

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12
Q

what can adenoviruses cause

A

common cold
mainly pharyngitis; also conjunctivitis, bronchitis

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13
Q

if we have a sore throat, what is the likely cause of our cold

A

adenovirus

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14
Q

what is the most differential symptom for an adenovirus

A

sore throat

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15
Q

how do adenoviruses attach to epithelia

A

Attach via the adhesins on end of penton fibres

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16
Q

what percent are pharyngitis and tonsillitis caused by viruses

A

70%

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17
Q

what is found in 70-90% of glandular fever patients

A

Epstein Barr Virus

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18
Q

what is Epstein bar virus associated with

A

Glandular fever

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19
Q

what type of disease is caused by Paramyxovirus

A

Mumps

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20
Q

what type of virus causes mumps

A

Paramyxovirus

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21
Q

what complication can come from an adult male getting mumps

A

Orchitis
Swelling of the testis, very painful
doesnt affect fertiility

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22
Q

what is and what causes Orchitis

A

Mumps (caused by Paramyxovirus)
Swelling of the testis, very painful
doesnt affect fertility

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23
Q

what is the main symptom of mumps

A

Swollen lymph nodes, cervical lymph nodes, thick neck alongside cold symptoms

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24
Q

what 3 virus groups often causes Laryngitis and tracheitis

A

parainfluenza viruses
adenovirus
influenza

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25
Q

what is the main symptom of laryngitis/Tracheitis

A

Burning pain in the larynx and trachea, ‘loose voice’

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26
Q

what is croup cough and what is it associated with

A

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

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27
Q

how might we tell a patient has laryngitis from a radiograph

A

Inverted V on x-ray- steeple sign in the tracheal area showing a constriction in the airway

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28
Q

give several viral causes for bronchitis and 1 atypical cause

A

Rhinoviruses, coronaviruses (SARs, COVID-19), adenoviruses and influenza
Atypical pathogens: Mycoplasma pneumoniae

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29
Q

what does ‘atypical’ mean in terms of respiratory infections

A

caused by bacteria not by virus

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30
Q

what is 75% of bronchiolitis caused by and how does it act

A

Respiratory Syncytial Virus RSV
causes large fused cells Syncytia

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31
Q

what does RSV cause

A

Respiratory Syncytial Virus causes 75% of bronchiolitis

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32
Q

what virus have most infants been infected with and how might coronavirus altered this

A

Respiratory Syncytial Virus
covid = isolation less exposure = less kids immune

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33
Q

what are differential diagnosis of infants with Cough, cyanosis, shallow rapid respiratory rate

A

pneumonia and bronchiolitis
bronchiolitis caused by RSV

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34
Q

how do you treat severe bronchiolitis

A

bronchodilators and hydrators

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35
Q

why do more respiratory infections occur during the colder months of the year

A

people are inside more and this gives way to more passage by particle droplets

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36
Q

what is asthma (3)

A

temporary reversible narrowing of the airways due to an inflammatory process occurring
within those airways

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37
Q

what is Atopic Asthma (3)

A

triggered by environmental agents e.g. dust
family history of asthma, hay fever etc.
type I hypersensitivity reaction

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38
Q

explain why atopic asthma occurs briefly (3)

A

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.

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39
Q

give 4 ways to treat asthma

A

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)

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40
Q

what is in the brown and blue inhalers for asthma

A

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

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41
Q

how does the brown inhaler work and what are its limitations

A

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.

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42
Q

what is disodium cromoglicate used for and how does it work

A

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

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43
Q

in chronic obstructive disorders, is the problem mainly on exhalation or inhalation

A

mainly on exhalation

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44
Q

what is COPD a mixture of

A

chronic bronchitis and emphysema

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45
Q

what defines chronic bronchitis

A

cough and sputum for 3 months over 2 consecutive years

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46
Q

what is the aetiology of chronic bronchitis

A

cigarette smoking
air pollution (nitrous oxide important from cars)

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47
Q

who is likely to get chronic bonrchitis

A

people in heavy pollution areas e.g. china
men smokers

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48
Q

explain where the symptoms of chronic bronchitis come from

A

mucus hypersecretion
chronic inflammation
squamous metaplasia = recurrent infections
dysplasia (but a feature of the causative agent)

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49
Q

how might Haemophilus influenzae affect someone

A

once a patient has had influenza, this bacteria may cause an atypical recurrance of the disease

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50
Q

define emphysema

A

anatomical
enlargement of airspaces distal to the terminal bronchioles with destruction of elastin in walls (holes in alveolous)

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51
Q

what percent of lung degration by emphysema do we start seeing significant problems

A

20-30% left

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52
Q

what would emphysema look like radiographically and anatomically

A

look black on an xray due to reduced tissue so more xrays get through
anatomically we would see small holes

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53
Q

what would cause focal emphysema

A

coal dust gets focal emphysema around it where around the carbon particles, the lung degrades

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54
Q

what causes lung cancer

A

cigarette smoking 85-90% all cases
asbestos exposure
radon exposure
nickel, chromate etc

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55
Q

what cells line the airwyas

A

simple ciliated columnar epithelia

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56
Q

what happens to respiratory epithelium under cigarette smoke (cancer)

A

metaplasia
columnar ciliated epithelium turns to stratified squamous cells with no cilia
cells become dysplastic and can become cancerous and invade local tissues

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57
Q

what types of lung cancer are there

A

small cell
non small cell = adeno or squamous

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58
Q

what type of lung cancer is associated with smoking

A

squamous non-small cell lung cancer

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59
Q

which type of non-small cell lung cancer has higher prognosis

A

adeno = non smoking cause = more prognosis
sqamous = smoking = lower prognosis

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60
Q

what is the treatment and prognosis of small cell lung cancer

A

low and chemotherapy - will not cure

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61
Q

if a lung cancer is large and near the periphery of the lung on xray what type is it likely to be

A

non-small cell adenocarcinoma of the lung

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62
Q

why might we not see some lung cancer on xray and what do we do instead

A

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

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63
Q

what is the best diagnostic tool for lung cancer

A

CT scan due to no superimposition on mediastinum or heart

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64
Q

what is the best diagnostic tool for lung cancer

A

CT scan due to no superimposition on mediastinum or heart

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65
Q

what percent of lung cancers are good prognosis

A

<10% 5 year survival rate as only 15-20% are removable

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66
Q

What is atopic asthma

A

Allergic asthma that is, in 80% of people, related to ezma, hayfeveer and food allergies

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67
Q

what should be included in a patient history (8)

A

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

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68
Q

what causes bronchiolitis and what else can it cause

A

Respiratory Syncytial Virus
most infants get this by 2 years old
can also cause pneumonia

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69
Q

what is the main distinguishing factor of influenza

A

very fast onset of fever and sickness, symptoms for 3 days and very tired, cant move around and very tired

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70
Q

how does influenza virus work

A

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

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71
Q

what can occur after an influenza infection

A

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

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72
Q

explain the structure of the influenza virus

A

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

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73
Q

if a virus has 8 parts of ssRNA in it, what is it likely to be and what is the significance of this

A

influenza virus
8 segments favours antigenic shift causing pandemics

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74
Q

what are the two surface glycoproteins of influenza virus

A

HA- Haemagglutinin first point of contact
NA- Neuraminadase released from cell afterwards

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75
Q

what is the importance of HA Haemagglutinin

A

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

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76
Q

what is the major source of antigenic variation of influenza

A

Haemagglutinin HA - surface glycoprotein on surface membrane

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77
Q

what are the three types of Influenza and explain their significance

A

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

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78
Q

what do the parts of this classification man: A/ Hong Kong / 1234/ 2009 (H1N1)

A

Influenza type A
location of isolation = hong kong
strain type = 1234
date of isolation = 2009
Antigens H1N1

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79
Q

how many NA and HA types are human adapted

A

16 H antigens but 3 human
9 N antigens but 2 human

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80
Q

how do new influenza viral strains occur (3) and give this name (1)

A

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

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81
Q

why are flu vaccines not suitable for vegans or egg allergy

A

Vaccine strains chosen in February for northern hemisphere
Strains grown in embryonated hen eggs: not applicable to individuals with Egg allergy

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82
Q

when would a flu pandemic occur

A

where the predicted viral adaptation from the opposite hemisphere doesnt correlate with a new mutation of the influenzas virus

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83
Q

compare antigenic drift and antigenic shift for influenza

A

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

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84
Q

explain antigenic shift (4) and the reason influenzas is favoured for this

A

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

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85
Q

how can we combat influenzas pandemics

A

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

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86
Q

what is the most common influenza anti-viral

A

NA inhibitors block release via NA inhibition

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87
Q

what types of organisms can cause pneumonia (3)

A

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

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88
Q

what size must a microbe be to fit into an alveolus

A

5micro meters

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89
Q

if a neonate has pneumonia, what could be a cause of this

A

Chlamydia acquired from the mother

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90
Q

describe the difference between child and adult pneumonia

A

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

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91
Q

what is pneumonia

A

swelling and inflammation of the lung tissue in one or both lungs

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92
Q

list 5 viruses that can cause pneumonia

A

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

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93
Q

how many coronaviruses affect humans

A

7 types

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94
Q

what type of genetic information is held in a covid virus

A

RNA genome

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95
Q

what protein does coronavirus attack and how did this affect symptoms

A

ACE2 - angiotensin converting enzyme 2
found in eyes, nose, lungs, nose, heart, kidney, liver
causes inflammation in these areas in compromised patients

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96
Q

compare the age : death graphs for coronavirus and influenza

A

COVID = gradua slope only peaking at old age
influenza = W shaped graph

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97
Q

give a brief (2) explanation of the structure of COVID

A

Trimeric Spike protein binds to ACE2
RNA genome inside

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98
Q

what is atypical pneumonia

A

bacterial pneumonia that is NOT caused by S. pneumoniae
NOT treatable by Penicillins
symptoms generally less severe- WALKING PNEUMONIA

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99
Q

what causes atypical pneumonia

A

Mycoplasma pneumoniae
Chlamydophila (formerly Chlamydia)
Legionella pneumophila

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100
Q

what is significant about Mycoplasma pneumoniae

A

very small 0.5Mbp
no peptidoglycan in cell wall, just cholesterol therefor penicillin resistant

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101
Q

how would we normally treat pneumonia and why might we not be able to with atypical

A

penicillin
Atypical can be caused by Mycoplasma pneumoniae which has no peptidoglycan in its cell wall meaning beta lactams are useless against them

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102
Q

what is Chlamydophila pneumoniae

A

related to sexually transmitted chalmydia
bacteria that cause atypical pneumonia
No peptidoglycan (Pen insensitive)
Flu-like illness
Detection by ELISA or MicroImmunofluorescence

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103
Q

how and why do we detect chlamydophila pneumoniae

A

ELISA testing
as the bacteria live inside other cells so cannot be grown on agar

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104
Q

how does Legionella pneumophila cause disease (3)

A

Acquired from environmentally derived aerosols
Ubiquitous in environment (symbiosis with amoeba)
Intracellular invader of phagosomes and lung cells

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105
Q

what is significant about legionella penumophilia

A

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

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106
Q

explain shape and gram of legionella pneumophilia and how we test for it

A

Motile aeerobic Gram-negative rod
Isolation on BCYE medium (Buffered Charcoal Yeast Extract)
Urinary antigen test (antigens secreted in urine)

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107
Q

what would we use BCYE medium (Buffered Charcoal Yeast Extract) to detect

A

Legionella Pneumophilia

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108
Q

if a patient has recently been to a conference in Spain and is showing signs of general illness, what is likely the cause

A

Legionella Pneumonia causing
Atypical Pneumonia (bacterial pneumonia that is NOT caused by S. pneumoniae, not treatable by penicillin, mildeer symptoms)

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109
Q

what is the prevalence of COPD

A

3M
5year survival <30%

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110
Q

what is FEV1

A

forced expiratory volume in 1 second

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111
Q

how do we diagnose COPD

A

FEV1 < 70% with emphysema or chronic bronchitis

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112
Q

what is COPD

A

chronic obstructive pulmonary disease
combination of obstructive airway diseases such as emphysema and chronic bronchitis
FEV1 < 70%

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113
Q

what is FVC

A

forced vital capacity - how much exhaled after a big breath

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114
Q

what is a genetic form of COPD

A

Alpha-1 Antitrypsin Deficiency-related COPD

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115
Q

what is SOBOE

A

shortness of breath on exertion

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116
Q

what are some symptoms of chronic and acute COPD

A

chronic: SOBOE, Wheeze, Cough, Weight loss - late term
Acute: Acute sob/wheeze, worsening sputum production, Fever, Drowsiness/CO2 narcosis

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117
Q

what are signs of COPD

A

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

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118
Q

what is cachexia

A

muscle degradation

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119
Q

what happens to oxygen and co2 levels with COPD

A

patient fails to exhale enough CO2 and keeps it in the blood
not enough oxygen in the blood

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120
Q

what is JVP and when is it elevated

A

jugular venous pressure and elevated in COPD

121
Q

what chest signs would a person with COPD have (3)

A

Hyper-expanded chest barrel shape
Hyperresonant - sounds resonant with tapping
Reduced breath sounds

122
Q

what is the diagnosis pathway for COPD

A

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%

123
Q

what is significant pack years

A

anything over 10

124
Q

why might muscle dysfuction be a sig of lug disease

A

less use of lungs, less exercise, less use of muscles

125
Q

how do we measure breathlessness with scores

A

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

126
Q

what is MRC stage 1 and 2

A

1 = breathless on strenuous exercise
2 = okay on flat, breathless on hills

127
Q

what is MRS 3 and 4

A

3 - slower than most, breathless after 15 mins/1 mile
4 - breathless every 100 yards

128
Q

what is MRS stage 5

A

too breathless to leave the house

129
Q

what is a cat score

A

severity score for breathlessness
used to monitor respiratory disease

130
Q

what are the NICE fundamental COPD treatments before inhaled therapy

A

we first must advise:
-stop smoking
- pneumococcal vaccine (strep. Penumonia)
- flu vaccine
- muscle rehab

131
Q

what is LABA and LAMA and SABA and ICS

A

long acting beta agonist
long acting muscarinic agonist
short acting beta agonist
inhaled corticosteroid

132
Q

what medication do we give COPD patients initally

A

SABA/SAMA

133
Q

what would we provide if the patient is still breathless after SABA/SAMA

A

if NOT asthmatic/ high eosinophil count:
LABA and LAMA

if asthmatic / high eosinophil count:
LABA and ICS

134
Q

when would we put a patient onto triple COPD medication

A

if patient is asthmatic and is still breathless after LABA and ICS, we would provide triple treatment being:
LABA, ICS and LAMA

135
Q

what s there an increased risk with ICS

A

inhaled corticosteroids increase risk of penumonia infection

136
Q

what does pneumonia look like on an xray

A

focal part of consolidation on the lung = infection

137
Q

what is roflumilast and what does it do

A

PDE4 inhibitor
reduces exacerbation frequency

138
Q

why is roflumilast only used in severe cases

A

lots of side effects like GI upsets and insomnia
highest rate of efficacy in severe exaccerbation pts

139
Q

what might a high sputum producer be on

A

Mucolytics

140
Q

if a patient is on mucolytic, what is their problem

A

high sputum producers
COPD

141
Q

what is the treatment process for COPD

A

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

142
Q

what is LTOT

A

pt is on oxygen minimum 14 hours a day
due to hypoxia due to COPD and possibly polycythaemia

143
Q

what types of oxygen therapy are there

A

LTOT on oxygen 14 hours or more per day
Ambulatory 2L tank if they can prove their saturation reduces in 6 mins of walking

144
Q

why do COPD patients have pursed lips

A

keeps mouth closed
creates more pressure down in the lungs
keeps alveoli open for more gas diffusion

145
Q

when do we give COPD patients antibiotics

A

2 or more:
-worsening dysopnea (SOB)
-change in colour of sputum
-increase sputum volume

146
Q

how do we ask a respiratory patient about exacerbations

A

how many rounds of antibiotics have you had in the past 12 months

147
Q

why is high steroid use throughout the year a risk for dental procedures

A

adrenal suppression
don’t produce enough steroids (cortisol)
cant deal with stress, need steroids before treatment

148
Q

what would a patient with COPD get, in terms of drugs, if exacerbating

A

antibiotics
oral prednisolone

149
Q

what are the advantages and disadvantages of oral prednisolone for COPD exacerbations

A

more rapid improvement in physiology
shortens hospital time
risk adrenal supression

150
Q

compare type 1 and 2 respiratory failure

A

<8kPa ppO2 in both
type 1 - low or normal CO2
type 2 - high >6kPa CO2

151
Q

what cause chronic and acute type I respiratory failure

A

chronic: fibrosling lung disease
acute: infection, pneumonia asthma

152
Q

what causes acute and chronic type II respiratory failure

A

acute: overdose opiates, trauma
chronic: COPD, neuromuscular

153
Q

why does blood CO2 rise in COPD

A

pt less able to force CO2 out of their lungs

154
Q

how many people have asthma

A

10%

155
Q

if we suspect asthma in a patient, what can we ask (3)

A

onset and timing of breathlessness
any triggers
on any medications

156
Q

if we suspect asthma, what sings might we see (5)

A

elevated respiratory rate
inability to complete sentence’s
audible wheeze
tachycardia
cyanosis - hypoxia

157
Q

what are some symptoms of asthma 4

A

breathlessness
triggers
wheeze
tight chest
nocturnal duration

158
Q

what are triggers of asthma 4

A

dust
pollen
stress
temperature
exertion

159
Q

what two groups of ‘asthmatics’ do we place patients in

A

asthma suspected
asthma diagnosed

160
Q

how can we diagnose asthma

A

spirometry, history
trial of ICS inhaler
if symptoms reduce = asthma

161
Q

if a patient has an acute asthma attack and cannot wield their own inhaler, what do we do

A

use a spacer inhaler
give 4 pumps initially and then 2 pumps every 2 minutes for max 10

162
Q

what is omalizumab and what conditions are to its use

A

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

163
Q

how do IL-5 blockers work and why are they advantageous

A

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

164
Q

what types of monoclonal antibody treatment is there for asthma (3)

A

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

165
Q

what condition do 1% of asthmatics have

A

ABPA - allergic bronchopulmonary aspergillosis

166
Q

what is ABPA and what does it lead to

A

allergic bronchopulmanory aspergillosis
allergic reaction to mould spores in the air
IgG response –> lung consolidations
leads to bronchiectasis

167
Q

what is bronchiectasis and what are its major symptoms

A

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

168
Q

how do we diagnose ABPA (4)

A

high eosinophil, IgE and IgG levels
CT scan showing bronchiectasis
skin reaction to aspergilllus
previous asthma

169
Q

what conditions can asthma pre-dispose

A

EGPA and ABPA

170
Q

describe asthma severity (4)

A

mild: PEF% >75
moderate: PEF% 50-75
severe: PEF% 33-49, RR > 25, HR >110min, not talking
Life Threatening: PEF% <33, bradycardia, silent chest

171
Q

what would a severe asthma case entail (4)

A

33 < PEF% < 49
not talking
HR > 110min
RR > 25

172
Q

what is the prelevence of lung cancer

A

69 in 100,000
2nd most common in men and women
89% preventable
5% survival after 10 years

173
Q

how much lung cancer is SC and NSC

A

85% NSC
15% SC

174
Q

what percent of lung cancer is operable at diagnosis

A

10%

175
Q

what are symptoms of lung cancer

A

lobular collapse, breathlessness
lymphangitis
effusion
chest pain - rib envolvement, envasion
cough (blood in cough)
NORMAL SYMPTOMS
weight loss
loss of appetite
tiredness

176
Q

a patient smokes and is very tired and loosing weight, differential diagnosis?

A

lung cancer
emphysema

177
Q

what is a paraneoplastic syndrome

A

where a hormone secretion is liked to a cancer e.g hyperthyroidism due to thyroid cancer

178
Q

give examples of lung paraneoplastic syndromes (3)

A

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

179
Q

what is lambert eaton syndrome

A

paraneoplastic syndrome related to lung cancer
neuromuscular weakness

180
Q

what is SIADH

A

syndrome of inappropriate anti-diuretic hormone
lung cancer paraneoplastic syndrome
fits, confusion, little salt in blood

181
Q

what are signs of lung cancer

A

finger clubbing
neck nodes
palpable liver in late stage
chest signs
cachexia
horner syndrome = drooping eyelid and wasting between thumb and first finger

182
Q

what are signs of horner syndrome and what is this a sign of

A

wasting between thumb and first finger + eye drooping
sign of lung cancer

183
Q

how do we diagnose lung cancer

A

signs and symptoms
XRAY < CT < PET
pet expensive and false positives uses radioactive glucose
biospy = bronchoscopy, transthoracic incision, surgical

184
Q

what is treatment for NSCLC (85%)

A

based on performance levels, chemo , immuno

185
Q

what is the WHO performance grading

A

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

186
Q

what dictates how NSCLC patients are treated

A

WHO performance status WPs
0-2 treated

187
Q

what is ILD

A

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

188
Q

what are the symptoms of ILD

A

interstitial lung disease
cough, breathlessness, fever

189
Q

what is a classic cause of ILD

A

birds

190
Q

what are signs of ILD

A

connective tissue disorder
nail clubbing
steroid use
immunosuppression
sclerodactyl (tight skin on hands)
crackling chest

191
Q

what is scerodactly and what respiratory disease might this be a sign of

A

tight skin across the hands
ILD interstitial lung disease

192
Q

who is likely to get IPF

A

idiopathic pulmanory fibrosis
old men

193
Q

how do we diagnose IPF

A

CT scan scarring on the lungs
ratio of FEV1 and FVC is above 70 (unlike COPD)
both have decreased

194
Q

what is IPF

A

idiopathic pulmonary fibrosis

195
Q

how do we treat IPF

A

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%)

196
Q

what is EAA

A

extrinsic allergic alveolitis
within ILD
Classical triggers
Occupation – Baker
Farmer
Moulds, carpenters

197
Q

what are common triggers for EAA

A

extrinic allergic alveolitis
Classical triggers
Occupation – Baker
Farmer - BIRDS
Moulds, carpenters

198
Q

a patient has fibrosis on the lungs and owns lots of pets, what are they likely to have

A

ILD caused by EAA - extrinisic allergic alveolitis

199
Q

how do we treat EAA

A

remove allergen, avoidance
steroid use
possible bisphosphonates

200
Q

what is sleep apnea

A

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

201
Q

what is sleep hypopnea

A

reduction of flow for 10 seconds by 30% <

202
Q

compare sleep apnea and hypopnea

A

apnea = cessation of flow for 10 seconds
hypopnea = reduction in flow for 10 seconds of 30%

203
Q

what are the three types of sleep apnea

A

OSA - obstructive sleep apnea = over weight
central sleep apnea = miscommunication from brain
mixed sleep apnea

204
Q

what is OSA

A

obstructive sleep apnea

205
Q

what are risk factors for OSA

A

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

206
Q

what is the cause of OSA and how does this effect the body

A

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

207
Q

how can we measure tiredness and how can this alter life

A

Epworth Sleepiness Score
can diagnose OSA
high score = loss of driving liscence

208
Q

how might we diagnose sleep apnea (3)

A

pulse oximetry drop between 10-15% during night
(4% = brain awakens)
Epworth sleepiness score
polysomnography (gold standard)

209
Q

wha

A
210
Q

how can we differentiate OSA and central sleep apnea

A

if overweight or not
polysomnography : if nose moves, OSA, if nose doesnt move, central as brain isnt telling body to ventilate

211
Q

compare pulse oximetry and polysomnography

A

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,

212
Q

how do we treat sleep apnea (4)

A

weight loss/ lifestyle change
Continuous Positive Airway Pressure (CPAP)
Mandibular Advancement Device (MAD)
Pharmocotherapy & surgery?

213
Q

what is CPAP

A

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

214
Q

if CPAP doesn’t effectively work against OSA, what else can we do

A

MAD - mandibular advancement device
keeps back of airway open
adherence is key

215
Q

how do SABAs work

A

short acting beta agonist
Increase in cAMP with reduction in cell Ca2+ leading to relaxation of smooth muscle
Immediate bronchodilation
4-6hour duration

216
Q

what do we use SABA for

A

asthma and COPD
immediate releif

217
Q

what are the side effects of SABA (4)

A

Increased HR & palpitations
Tremor
Hypokalaemia
Headache
Nervousness

218
Q

what should not be used asa monotherapy for asthma

A

LABAs long acting beta agonists
can cause cardiac death

219
Q

why might SAMA be better than SABA

A

less side effects
only used for COPD, not really used for asthma

220
Q

what is the mainstay drug for asthmatics

A

inhaled corticosteroids
no immediate effect
protection over time

221
Q

what are some side effects of ICS

A

Oral candida
Voice change
Risk of skin bruising, bone mineral density change and cataracts with high dose

222
Q

what is a common ICS medication

A

beclomethasone

223
Q

when is prednisolone used for respiratory treatment

A

oral steroid
used in acute exaccerbations of asthma
or chronically in eosinophilic asthma

224
Q

side effects of oral steroids

A

body weight increase
BP increase
infection risk increase
catarax increase
blood glucose increase

225
Q

what is CO2 drive

A

in healthy individuals,
chemoreceptors detect high CO2 and increase breathing rate to expel CO2

226
Q

what happens to CO2 drive in COPD patients

A

body looses ability to detect CO2 = breathing increase
more CO2 remains the the body
hypoxic drive takes over = oxygen –> breathing

227
Q

why would oxygen be dangerous to give to an exacerbating COPD patient

A

they may have a hypoxic drive
this means that oxygen chemoreceptors control breathing
high oxygen may = reducing RR = death

228
Q

what is normal RR and when would we detect an acute asthma attack

A

normal = 18 (30-40 at exertion)
asthma attack = >25

229
Q

compare a peak flow monitor and spirometer

A

PFM = detects PEF = speed of expiration
Spirometer = detects PEF, FEV1 and FVC much more diagnostic

230
Q

what is normal FEV1, FVC and FEV1/FVC

A

normal FEV1 and FVC = >80
normal FEV1/FVC = >70

231
Q

what is the relevance of an asthma patient having history on ITU

A

ITU is intensive treatment unit where there is multiple organ failure and ventilation
sign of severe life threatening asthma

232
Q

compare HDU and ITU

A

ITU = multiple organ failure = more severe
HDU = higher dependency unit = single organ failure

233
Q

how might anxiety link to asthma

A

anxiety leads to stress
stress supresses the immune system
stress acts as a agrevator for asthma attacks

234
Q

why might anaesthetic cause an episode of asthma attack

A

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

235
Q

why might stress cause worsened asthma (4)

A

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

236
Q

how do we manage any acute attack

A

ABC - airway, breathing, circulation

237
Q

if a pt has an asthma attack, what do we do in the dental surgery

A

ABC
use a spacer and blue salbutamol SABA inhaler and give 2 puffs every 2 minutes
high flow oxygen at 15L/min

238
Q

what 2 relivers could be given in an asthma attack

A

salbutamol = SABA
Ipratropium bromide = Anticholinergic (acetylcholine is a neurotransmitter used to constrict bronchial smooth muscle)

239
Q

give 4 indications of asthma attack

A

wheeze
PEF peak flow less than 50% (predicted) (life threatening if PEF < 33%)
Cannot complete sentences
RR > 25
HR > 110

240
Q

what HR and RR is indicative of asthma attack

A

RR > 25
HR > 110

241
Q

what PEF measure indicats asthma attack and what rate is life threatening

A

PEF peak flow less than 50% (predicted) (life threatening if PEF < 33%)

242
Q

why do we only give 2 puffs of salbutamol in acute asthma

A

pt is primarily low on oxygen
if we give too much salbutamol, they wont get enough oxygen and become hypoxic

243
Q

what rate of oxygen can we give for ventilation

A

15L/min

244
Q

what is a nebuliser

A

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

245
Q

what would be hospital treatment of asthma attack

A

Nebuliser with high flow oxygen
salbutamol 5mg and Ipratropium bromide 0.5mg (releiver)
Prednisolone 40mg (prevent late T cell response)

246
Q

if nebulisers don’t work in a hospital environment, what can be given as a last resort to asthma attack pt (2)

A

Aminophylline can cause arrhythmias
Magnesium in form magnesium sulphate

247
Q

how much stronger is the salbutamol given in hospital vs 2 puffs of inhaler

A

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

248
Q

what is prednisolone given for in asthma attacks

A

preventative oral steroid
after asthma attacks, we get a delayed T cell response causing another acute attack 24 hours later
prednisolone prevent this occuring

249
Q

is it safe to give a severe COPD patient high flow oxygen

A

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

250
Q

list 5 things that can cause asthma attack

A

Stress
Allergens/Triggers e.g. pollen
Exercise
Aspirin/Ibuprofen
Cigarette smnoke

251
Q

how many deaths of TB have occured in the past 200 years

A

1 billion

251
Q

what are the three groups of mycobacterium

A

MTB - Mycobacterium Tuberculosis Bacteria
non-tuberculosis mycobacterium
Non - cultivable (not able to grow on agar) - only M.Leprae

252
Q

what makes M.Leprae different to other mycobacteria

A

non-cultivable, cannot be grown on agar. must be grown in a living organism

253
Q

describe the staining, oxygen dependency and morphology of M. Tuberculosis (4)

A

Gram positive bacillus rod with a kink in the middle
Ziehl-Neelsen acid fast positive
Aerobic and non-motile

254
Q

describe how the structure of M.Tb affects its staining (2)

A

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

255
Q

why can M. Tuberculosis survive in harsh environments

A

very high lipid mycolic acid content
waxy cell wall
resistant to low pH and can survive in macrophages

256
Q

what is the replication time of M. Tuberculosis

A

15-20 hours

257
Q

what 3 consequences come of the replication rate of M. Tuberculosis being slow

A

Slow growth in humans = gradual onset
Slow growth in culture = slow diagnosis
Slow response to treatment = 6-9 months

258
Q

how many people are expected to be carrying TB

A

1 in 4

259
Q

explain primary tuberculosis (2)

A

Initial contact made by alveolar macrophages in the lungs
Bacilli taken in lymphatics to hilar lymph nodes (central lung)

260
Q

what is latent tuberculosis and how is it detectable

A

no clinical signs
there is detectable CMI to TB on tuberculin skin test

261
Q

explain how latent tuberculosis occurs (3)

A

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

262
Q

which part of the lung is likely to get a pulmonary TB

A

In apex of lung there is more air and less blood supply (fewer defending white cells to fight)

263
Q

what is a primary TB complex composed of (3)

A

granuloma
Lymphatics
Lymph nodes

264
Q

what is the major cell type invovled in killing M. Tb and what is the active protein

A

CD4 T cells
generate INF-gamma to induce macrophage intracellular killing

265
Q

why is TB the leading cause of death in HIV patients (3)

A

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

266
Q

what inflammatory marker do CD4 cells produce to kill TB and how does it work (2)

A

IFN-gamma
induces intracellular killing within macrophages

267
Q

what is the major histological marker of TB

A

granuloma formation

268
Q

what would we find inside a TB granuloma (6)

A

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’

269
Q

how is a TB granuloma walled off from the tissues surrounding

A

fibroblasts produce collagen around the granuloma

270
Q

what three changes to macrophages might we see in a granuloma

A

Large Foamy macrophages
Highly stimulated macrophages become epithelioid cells
Some macrophages fuse with each other to form giant multinucleated cells - ‘langerhans giant cells’

271
Q

what three changes to macrophages might we see in a granuloma

A

Large Foamy macrophages
Highly stimulated macrophages become epithelioid cells
Some macrophages fuse with each other to form giant multinucleated cells - ‘Langerhans giant cells’

272
Q

what are the two fates of a TB granuloma

A

stay stable = dormant TB
burst and collapse = depletion = TB infection

273
Q

what two inflammatory mediators stabalise TB granulomas

A

IFN-gamma
TNF-alpha

274
Q

what can lead to granuloma depletion in latent TB (2)

A

CD4 disease e.g. HIV = reduced IFN-gamma
TNF-alpha reduction e.g. in arthritis treatment

275
Q

what is the result from TB granuloma depletion (2)

A

in the lungs this can result in formation of a cavity full of live mycobacteria and eventual disseminated disease (consumption)

276
Q

what is the average risk of granuloma depletion in TB cases

A

first 2 years = 10%
increased by 0.1% each year

277
Q

what are risks of developing infection from latent TB

A

age = young or elderly
immunocompromised
intensity of exposure
malnutrition (CD4 depletion)
on arthritis TNF-alpha medication
HIV = reduced CD4 = reduced INF-gamma

278
Q

what are the three ways of diagnosing TB

A

PCR - best way
solid or liquid cultures + ziehl-neelsen acid fast positive
Tuberculin skin test

279
Q

what are some disadvantages = of culture diagnosis of TB

A

very slow growth
must sterilise off other bacteria
doesn’t determine strain e.g. resistance

280
Q

what is the best way to diagnose TB and why

A

PCR
fast, doesn’t rely on replication
identifies strain and resistance to antibiotics

281
Q

explain the tuberculin skin test (4)

A

even if a patient is latent TB
will have increased hypersensitivity to tuberculin protein
purified protein injected intra-dermally
hypersensitivity reaction = swell and red

282
Q

what are the four first line antibiotics for TB

A

Standard therapy isoniazid (INH)
Rifampicin
Pyrazinamide
Ethambutol x 2 months followed by rifampicin for 4 month

283
Q

what injected broad spectrum drugs are used as second line treatment for TB

A

Fluoroquinolones
Injectable agents e.g. streptomycin
Prothionamide may be used if resistance

284
Q

what is DOTs and how does it work

A

directly observed treatment. Combine drugs and management. This is where we watch TB patients take medications to ensure complience.

285
Q

what side effects are there from first line antibiotics for TB (3)

A

Hepatotoxicity (INH, RIF, PZA) - cannot drink at all
Peripheral neuropathy with INH (give vit B6 to protect)
Optic neuritis (ETH)

286
Q

what supplement is given with standard therapy isoniazid

A

first line treatment for TB
vitamin B6 to protect peripheral neuropathy

287
Q

why are there usually high side effects to TB treatment

A

very long treatment
multiple drugs used at the same time

288
Q

how long is TB treatment generally

A

6-9 months

289
Q

what four ways of antibiotic resistant are found in TB

A

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

290
Q

how does a mutation in the 22aa region of rpoB cause problems with treatment of TB (2)

A

disrupts mechanism of Rifampicin = resistant
induces mutation-prone, non-regulated replication = more likely to get mutations and more resistance

291
Q

mutations in KatG affect which TB treatment

A

Isoniazid
needed to activate the anti-biotic to be able to inhibit metabolism

292
Q

what anti-TB drug would amutaiton in pncA

A

Pyrazinamide
needed for activation

293
Q

what is XDR-TB (2)

A

extremely drug resistance tuberculosis
where a strain is resistant to the 4 first line treatments of TB
6% of strains

294
Q

how many TB strains are XDR-Tb

A

6%

295
Q

how do we treat XDR-Tb

A

BPal Regimen
Bedaquiline: inhibits ATP synthase
Pretomanid
Linezolid
all oral pill 6 months

296
Q

what is TDR-Tb

A

totally drug resistant tuberculosis
no solution as of yet

297
Q

If a pt is on the BPal Regimen, what are they being treated for

A

XDR-Tb
extremely drug resistant tuberculosis

3rd BDS IHD (14 decks)

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