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BRS 1b > cardioresp > Flashcards

cardioresp Flashcards

1
Q

what is a vegetation and which heart condition is it found in

A

bacterial infection surrounded by a layer of fibrin and platelets found in infective endocarditis

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2
Q

which bacterial infection is the most common cause of infective endocarditis

A

streptococci

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3
Q

how do you diagnose infective endocarditis

A

Duke’s criteria
- SYMPTOMS: fever, malaise, sweating, unexplained weight loss
- BLOOD TEST: anaemia, raised inflammatory markers
- BLOOD CULTURE: micro-organism found
- EXAMINATION: new heart murmur
- ECHOCARDIOGRAM: shows vegetation, abscess, valve perforation, dihescnce of valve prosthesis, regurgitation of the affected valve - transoesophageal echo is more sensitive than transthoracic

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4
Q

what are the features of cardiac decompensation in infective endocarditis

A

frequent coughing
swelling of abdomen and legs
shortness of breath
fatigue
raised JVP (jugular venous pressure)
lung crackles
oedema

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5
Q

name the vascular, embolic and immunological phenomena of infective endocarditis

A

vascular/embolic:
- stroke
- janeway lesions (irregular non tender hemorrhagic macules on hands and feet)
- splinter/conjunctival haemorrhages

immunological:
- osler’s nodes (painful red lesions of hands and feet)
- Roths spots (white centred retinal hemorrhagic)

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6
Q

what part of the heart does infective endocarditis affect

A

endocardium
- mostly the valves as the bacteria rush towards sight of damage and the most turbulent blood flow is around the valves
- mostly the aortic valve
aortic>mitral>right sided valves

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7
Q

what increases risk of infective endocarditis

A

IV drug user: more likely for bacteria to get into the blood, which is the first step
Routine surgeries eg dental surgery - also more likely for bacteria to get into blood
Immunosuppression
Cardiac myopathies: more likely to have damage - bacteria more likely to stick to damaged endocardium

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8
Q

what is dilated cardiomyopathy

A

dilated and thin walled cardiac chambers with reduced contractility

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9
Q

what does echo show for dilated cardiomyopathy

A

dilated left ventricle with reduced systolic function (ie reduced ejection fraction) and global hypokinesia

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10
Q

commonest causes of dilated cardiomyopathy

A

alcoholism
thyroid disease
drugs
familial
autoimmunity

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11
Q

management of dilated cardiomyopathy

A
  • fluid with Na+ restriction
  • heart failure meds: ACE inhibitors, beta blockers, diuretics
  • anticoagulants
  • cardiac devices
  • transplant
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12
Q

what is the gold standard treatment for early stage lung cancer

A

lung resection

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13
Q

what is the first line treatment for metastatic non small cell lung cancer with no mutation and PDL1 > 50% (ie PDL1 positive)

A

immunotherapy - Anti PD-1 and Anti PD-L1
eg pembrolizumab

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14
Q

what is the first line treatment for metastatic non small lung cancer with no mutation and PDL1 < 50% (ie PDL1 negative)

A

chemotherapy + immunotherapy

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15
Q

frequent side effects of chemotherapy

A

fatigue, nausea, bone marrow suppression, nephrotoxicity

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16
Q

first line treatment for metastatic non small cell lung cancer with targetable mutation

A

oncogene directed treatment (against EGFR, ALK, ROS1) –> tyrosine kinase inhibitor
eg
crizotinib
erlotinib

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17
Q

side effects of oncogene directed lung cancer treatment

A

rash, diarrhoea, pneumonitis

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18
Q

what is the efficacy of oncogene directed treatment for lung cancer in contrast to standard chemotherapy

A

improvement in progression free survival but not necessarily overall survival vs standard chemotherapy

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19
Q

treatment for locally advanced lung cancer involving thoracic lymph nodes

A

surgery + chemotherapy
or
chemotherapy + radiotherapy + immunotherapy

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20
Q

what is the efficacy of immunotherapy treatment for lung cancer in contrast to standard chemotherapy

A

improvement in progression free survival and overall survival vs standard chemotherapy

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21
Q

what is the role of PDL1 on lung tumour cells

A

binds to PD1 on T cells, this renders the T cell inactive and stops it killing the tumour cell
-allows tumour cell to survive and proliferate

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22
Q

what is the radical radiotherapy for lung cancer called

A

SABR
stereotactic ablative body radiotherapy

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23
Q

signs of advanced lung cancer

A

bone pain
neurological symptoms eg seizures, focal weakness, spinal cord compression
paraneoplastic symptoms eg hypercalcaemia, hyponatramia, clubbing, cushings
cachexia
horners syndrome
pembertons sign (SVC obstruction)

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24
Q

definitive imaging used for staging lung cancer

A

PET - CT

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25
Q

list the 3 types of biopsies used for lung cancer

A

bronchoscopy
EBUS/TBNA (endobronchial ultrasound, transbronchial needle aspiration)
CT guided lung biopsies

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26
Q

which biopsy method is used for central airway tumours

A

bronchoscopy

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27
Q

which biopsy method is used for peripheral lung tumours

A

CT guided lung biopsy

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28
Q

which biopsy method is used for mediastinum/mediastinal lymph nodes in lung cancer

A

EBUS/TBNA

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29
Q

which biopsy method is used for staging and tissue diagnosis in lung cancer

A

EBUS/TBNA

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30
Q

which lung cancer oncogene is linked especially with smokers

A

BRAF (downstream cell cycle signalling mediator

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31
Q

which lung cancer oncogene is sometimes seen in adenocarcinomas

A

epidermal growth factor receptor (EGFR) tyrosine kinase

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32
Q

describe the pathogensis of lung cancer and how inhaled carcinogens interact with the lungs

A

inhaled carcinogens interact with the airway epithelium to form DNA adducts (DNA bound to cancer causing chemicals)
if these DNA adducts persist they lead to the formation of mutations which can cause lung cancer especially if they occur in tumour suppressor genes or oncogenes

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33
Q

what are the levels 0 to 5 of the WHO performance status for lung cancer

A

0 - asymptomatic
1 - symptomatic but completely ambulatory
2 - symptomatic, in bed <50% of daytime
3 - symptomatic, in bed >50% of day, not bed bound
4 - bed bound
5 - death

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34
Q

which cells do squamous cell carcinomas of lung cancer originate from

A

bronchial epithelium

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35
Q

which cells do adenocarcinomas of lung cancer originate from

A

mucus producing glandular tissue

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36
Q

3 cardinal features of asthma

A

atopy/allergic sensitisation
reversible airway obstruction
airway inflammation - eosinophilic or type 2

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37
Q

what does reversible airflow obstruction in asthma manifest as

A

expiratory wheeze

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38
Q

which 2 chromosomes have been found to be associated with asthma

A

IL33
GSDMB

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39
Q

describe type 2 inflammation in asthma

A

APCs present antigens to naive CD4 T cells causing them to become Th2 cells
this causes formation of
IL13 –> production of mucus and narrowing of airways
IL5 –> eosinophil production
IL4 –> IgE production

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40
Q

what is that test for allergen sensitisation (in asthma)

A

blood tests for specific IgE antibodies against allergens of interest

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41
Q

what are the 3 tests for eosinophilia and their cut offs for asthma

A

1) blood test –> above/equal to 300 cells/mcl
2) sputum sample –> above/equal to 3%
3) exhaled nitric oxide –> above/equal to 35 ppb in children, above/equal to 40 ppb in adults

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42
Q

what are the asthma cut offs for spirometry

A

FEV1/FVC less than/equal to 0.7 in adults, less than/equal to 0.8 in children

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43
Q

what is the test for reversible airway obstruction and what is the asthma cut off

A

bronchodilator reversibility
greater/equal to 12 %

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44
Q

what are the 3 aims of asthma management and list drugs used for each aim

A

1) reduce airway inflammation
- leukotriene receptor antagonist
- inhaled corticosteroids

2) acute symptomatic relief (smooth muscle relaxation)
- anticholinergics
- beta 2 agonists

3) steroid sparing therapies for severe asthma
- biologics against IgE –> anti IgE antibodies
- biologics against eosinophil –> anti IL5 antibody, anti IL5 receptor antibody

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45
Q

what is mepolizumab

A

biologic for severe eosinophilic asthma
anti IL5 antibody
IL5 regulates recruitment, activation, production of eosinophils

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46
Q

mepolizumab prescribing criteria

A

over/equal to 6 years of age
blood eosinophils over/equal to 300 cells/mcl in the last 12 months
over 4 exacerbations requiring oral steroids in past 12 months

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47
Q

how do corticosteroids reduce eosinophilic inflammation

A

reduce recruitment of eosinophils from blood to airways
induce apoptosis of eosinophils if they enter airways

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48
Q

what is omalizumab

A

anti IgE monoclonal antibody
binds to and captures IgE, preventing it from interacting with mast cells and basophils

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49
Q

prescription criteria for omalizumab

A

severe and persistent allergic (IgE mediated) asthma
over/equal to 6 years of age
4 or more courses of oral corticosteroids in the past year
total serum IgE count is 30 - 1500 IU/ml

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50
Q

describe the pathogenesis of an acute lung attack in a school child

A

reduced IFN alpha, beta, gamma
- reduced antiviral response, increased viral proliferation –> prolonged illness

eosinophilic inflammation –> responsive to corticosteroids

reduced peak expiratory flow rate
- increased airway obstruction causing acute wheeze –> responsive to bronchodilators

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51
Q

describe the amount of ventilation across the lung

A

top of lung:
pleural pressure is more negative
greater transmural pressure gradient
larger and less compliant alveoli
less ventilation

bottom of lung:
pleural pressure is less negative
smaller transmural pressure gradient
smaller and more compliant alveoli
more ventilation

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52
Q

describe the amount of perfusion across the lung

A

top of lung:
lower intravascular pressure
less recruitment
greater resistance to flow
lower flow rate

bottom of lung:
greater intravascular pressure (gravity effect)
more recruitment
less resistance to flow
higher flow rate

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53
Q

what is the pressure of oxygen in the alveoli

A

13.5 kPa (101 mmHg)

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54
Q

what is the oxygen pressure in the blood before and after oxygen transport at the alveoli

A

before - 5.3 kPa (40mmHg)
after - 13.5 kPa (101 mmHg)

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55
Q

what is the oxygen saturation of the blood before and after oxygen transport at the alveoli

A

before - 75%
after - 100%

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56
Q

what is normal value for gas exchange time and for pulmonary transit time

A

gas exchange time - 0.25 s
pulmonary transit time - 0.75 s

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57
Q

what is compliance and how do you calculate it

A

the tendency of a material to distort under pressure

change in volume / change in pressure

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58
Q

what is elastance and how do you calculate it

A

the tendency of a material to recoil to its original volume

change in pressure / change in volume

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59
Q

give causes of acute respiratory failure

A

pulmonary - aspiration, infection, primary graft dysfunction
extra pulmonary - trauma, pancreatitis, sepsis
neuromuscular - mysasthenia gravis, GBS (guillain barre syndrome)

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60
Q

give causes of chronic respiratory failure

A

pulmonary - COPD, CF, lung fibrosis, lobectomy
musculoskeletal - muscular dystrophy

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61
Q

give causes of acute on chronic respiratory failure

A

infective exacerbation of CF, COPD
myasthenia crisis
post operative

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62
Q

what is normal minute ventilation value and how is it calculated

A

tidal volume x breathing rate = 0.5 L x 12 breaths/min= 6 L/min

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63
Q

what is normal alveolar ventilation and how is it calculated

A

(tidal volume - dead space) x breathing rate = 0.35 x 12 = 4.2 L/min

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64
Q

what are respiratory failures 1 - 4

A

1) hypoxamic (oxygen <60)
increased shunt fraction (fraction of cardiac output that is deoxygenated)
2) hypercapnic (co2 >45)
decreased alveolar minute ventilation
3) perioperative resp failure
hyperaemic or hypercapnic
4) shock associated

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65
Q

list the pulmonary and extra pulmonary causes/triggers of ARDS

A

pulmonary
- infection
- aspiration
- burns (inhalation)
- surgery
- drug toxicity
- trauma

extra pulmonary
- infection
- pancreatitis
- trauma
- surgery
- drug toxicity
- burns
- transfusion
- bone marrow transplant

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66
Q

list the in vivo evidence for ARDS

A

leucocyte activation and migration
release of DAMPs: HMGB-1 and RAGE
release of cytokines: IL6, IL8, IL 1B, TNF gamma
TNF signalling
cell death

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67
Q

which therapies have been trailed for ARDS

A

salbutamol
statins
steroids
surfactant
neutrophil esterase
N acetyl cysteine
GM- CSF

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68
Q

which therapies are currently being trialed for ARDS

A

microvesicles
mesenchymal stem cells
keratinocyte growth factor
ECCO2R
high dose vitamin C, thiamine, steroids

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69
Q

list 4 drugs used to treat ARDS

A

pyridostigmine
plasma exchange
IViG
Rituximab

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70
Q

list the order of respiratory support from mild ARDS to severe progressed ARDS

A

conservative fluid management
low volume ventilation
Increasing PEEP (positive end expiratory pressure)
prone positioning
neuromuscular blockade
inhaled pulmonary vasodilators
extracorporeal membrane oxygenation (ECMO)

71
Q

what are the two pressure points that the lungs should be kept between

A

lower inflection point: minimal pressure needed to keep airways open/needed for optimal alveolar recruitment

upper inflection point: above this point, will need to apply disproportionally more pressure to achieve same increase in gas exchange/alveolar recruitment

72
Q

what is gas trapping in ventilation

A

for some people on ventilation it takes a longer time for them to expire
so they may not be able to expire all the air out of their lungs
so with each breath, more air gets stuck in the lungs, increasing the pressure inside
this impacts on alveolar recruitment and lung perfusion

73
Q

2 key requirements for using ECMO

A

reversible disease process
and
unlikely to lead to prolonged disability

74
Q

describe the events in the inflammatory response of ARDS

A

apoptosis/necrotic of type 1 alveolar cells
denunded basement membrane
resident macrophages release IL6, IL8, TNF alpha
activation of alveolar neutrophils - release PAF (platelet actuating factor), leukotrienes, oxidants, proteases
damaged endothelial cells of capillaries and holes in epithelium of capillaries
neutrophils leak out of capillaries into inetrstitium (space between capillaries and alveoli)
results in oedema and secondary inflammation
get a widened oedematous interstitium

75
Q

describe the symptoms of an upper respiratory tract infection

A

cough
sneezing
runny/stuffy nose
headache
sore throat

76
Q

describe the symptoms of a lower resp tract infection

A

fever
fatigue
muscle aches
productive cough
wheezing
breathlessness

77
Q

pneumonia symptoms

A

chest pain
high fever
cyanosis - blue tinting of lips
severe fatigue

78
Q

what is a DALY

A

disability adjusted life years
= YLL (years of life lost) + YLD (years lost to disability)

79
Q

common causative agents of bacterial respiratory infections

A

streptococcus pneumoniae
myxoplasma pneumoniae
haemophilus influenzae
mycobacterium tuberculosis

80
Q

common causative agents of viral respiratory infections

A

influenza A / B
human rhinovirus
human metapneumovirus
respiratory syncytial virus
coronavirus

81
Q

is streptococcus pneumoniae gram positive or negative

A

gram positive

82
Q

list 3 properties of streptococcus pneumonia as a pathogen

A

gram positive
extracellular
opportunistic pathogen

83
Q

causative agents of community acquired pneumonia

A

streptococcus pneumoniae
myxoplasma pneumoniae
chlamydia pneumoniae
haemophilus influenzae
staphylococcus aureus

84
Q

causative agents of hospital acquired pneumonia

A

E coli
psuedomonas aeruginosa
Klebsiella species
Enterobacter spp
acinetobacter spp
staphylococcus aureus

85
Q

causative agents of ventilator associated pneumonia

A

psuedomonas aeruginosa
staphylococcus aureus
enterobacter

86
Q

how does pneumonia lead to ARDS

A

pneumonia –> lung injury –> arterial hypoxaemia –> ARDS

87
Q

how does pneumonia lead to sepsis

A

lung injury, bacteraemia, systemic inflammation –> organ dysfunction and injury –> sepsis

88
Q

what is the scoring method used for bacterial pneumonia

A

CURB 65
confusion
urea > 7 mmHg
resp rate >= 30 breaths/min
bp systolic <90 mmHg, diastolic <= 60 mmHg
age >= 65 years

89
Q

medication for severe and non severe Hospital acquired pneumonia

A

not severe = doxycycline
severe = tazocin + gentamicin

(for 5-7 days)

90
Q

medication for Community acquired pneumonia with a CURB65 score of 0

A

amoxicillin

91
Q

medication for Community acquired pneumonia with a CURB65 score of 1 -2

A

amoxicillin + clarithromycin

92
Q

medication for Community acquired pneumonia with a CURB65 score of 3 - 5

A

benzylpenicillin + clarithromycin

93
Q

supportive therapy for bacterial pneumonia

A

oxygen
fluids
analgesia
nebulised saline (helps with expectoration)
chest physiotherapy

94
Q

what do penicillin antibiotics target

A

proteins in bacterial cell wall
this prevents transpeptidation

95
Q

what do macrolide antibiotics target

A

bacterial ribosomes
this prevents protein synthesis

96
Q

what is an opportunistic pathogen

A

takes advantage of changes in conditions to become pathogenic (eg immunosuppression)

97
Q

what is a pathobiont

A

normally commensal but becomes pathogenic when it enters the wrong environment eg a different anatomical site

98
Q

describe the pathophysiology of viral infections and how they cause disease

A

viral infections cause
- local immune memory
- mediator release
- cellular inflammation
- damage to epithelium
–> loss of chemoreceptors
–> loss of cilia
–> bacterial growth
–> poor barrier to antigens

99
Q

3 factors which cause severe disease

A

highly pathogenic strains
no prior immunity
predisposing conditions/diseases eg diabetes, pregnancy, copd, asthma,

100
Q

what does H1N1 influenza A target and in which part of resp tract

A

hameogluttinin of H1N1 targets alpha 2,6 sialic acid in upper airway

101
Q

what does H5N1 avian flu target and in which part of resp tract

A

haeogluttinnin of H5N1 targets alpha 2,3 sialic acid in lower airway

102
Q

what does SARS CoV 2 target and in which part of resp tract

A

spike protein of SARS CoV2 targets ACE 2 in nasal epithelium and pneumocyets

103
Q

describe the features of the respiratory epithelium that prevent infection spread

A

tight junctions - prevent systemic infection

antimicrobials - recognise and degrade pathogens and their products

interferon pathways - stimulated by viral infection - up regulate antiviral proteins and apoptosis

mucosal/ciliary epithelium - prevents attachment and clears airways

pathogen recognition receptors -recognise pathogens inside and outside of cell

104
Q

which part of resp tract is IgA found

A

nasal cavity
- many IgA receptors
- IgA homodimer is stable in this protease rich environment

105
Q

which part of resp tract is IgG found

A

alveoli
- thin alveolar walls allow passing of plasma IgG into alveolar space

106
Q

why are smokers more susceptible to SARS CoV 2 infection

A

they have more ACE 2 –> this is targeted by the spike protein on the virus

107
Q

why is the vaccination for influenza poor

A

vaccine induced immunity quickly disappears/decreases
immunity is homotypic
need yearly vaccine

108
Q

why is there no vaccine for RSV

A

poor immunogenicity

109
Q

which has a longer incubation period, RSV or influenza

A

RSV

110
Q

RSV symptoms in infants

A

croupy cough
hypoxameia and cyanosis
chest wall retractions
tachypnoea and apneic episodes
expiratory wheeze
prolonged expiration
rales and rhonchi
nasal flaring

111
Q

risk factors for RSV in infants

A

premature birth
congenital heart and lung disease

112
Q

anti inflammatories for SARS CoV 2

A

dexamethasone
tocilizumab (anti IL6R)
sarilumab (anti IL6)

113
Q

anti virals for SARS CoV2

A

remdesivir - blocks RNA-dependant RNA polymerase activity
paxlovid - antiviral protease inhibitor
casirivimab + imdevimab - monoclonal neutralising antibodies

114
Q

interplay between viral infections and chronic lung disease

A

viral bronchiolitis causes asthma
rhinovirus causes copd and asthma exacerbations
viral infections cause secondary bacterial pneumonia

115
Q

interplay between viral infections and bacterial infections

A

pattern of cerebrospinal meningitis after pneumonia/influenza

116
Q

what are the advantages and disadvantages of the cardiopulmonary exercise test

A

advantages
- continuous monitoring for safety
- quantifies result in relation to metabolism
- precise and reproducible result

disadvantages
- needs skilled supervision
- expensive
- needs dedicated space

117
Q

what is measured in a cardiopulmonary exercise test and what is the primary output

A

ECG
ventilation
O2
Co2

whilst on cycle ergometer or treadmill with incremental inverse in intensity

(primary output is peak VO2)

118
Q

what type of test is the 6 minute walk test

A

sub maximal

119
Q

what type of test is the 6 minute walk test

A

sub maximal

120
Q

what is measured in the six minute walk test

A

how far can walk in six minutes - distance
heart rate
pulse oximetry
perceived exertion

121
Q

advantages and disadvantages of 6 minute walk test

A

+
cheap
participant controlled pace
applicable to many clinical populations

  • need long unobstructed course
    doesn’t take pace into account
122
Q

what is measured in incremental shuttle walk test and what is primary outcome

A

total distance walked - 10m circuit, beeps 1 minute apart, with each beep the laps you have to do increases, until you voluntarily stop
heart rate
pulse oximetry
perceived exertion

primary outcome = distance walked

123
Q

advantages and disadvantages of incremental shuttle walk test

A

+
cheap
participant controlled pace
applicable to many clinical populations

  • need long unobstructed course
    incremental nature may be difficult for some
    ceiling effect at 1020 m
    participants with poor pace management may be penalised
124
Q

which two cells mostly make up the interstitium of the lungs

A

fibroblasts
macrophages

125
Q

contrast type 1 and 2 alveolar cells/pneumocytes

A

1: flatter shape, squamous cell, involved in gas exchange
2: cuboidal shape, have microvilli, secrete surfactant, divide into type 1 and 2 cells

126
Q

contrast prognosis of UIP and DIP/NSIP patterns of ILD

A

UIP - much worse prognosis over time than DIP/NSIP

127
Q

what test is done for checking the diffusing capacity of the lungs

A

DLCO is reduced - test measuring lungs diffusing capacity for carbon monoxide

128
Q

histopathology pattern seen in IPF (idiopathic pulmonary fibrosis)

A

UIP (usual interstitial pneumonia) pattern: spacial and temporal heterogeneity with microscopic honeycomb cysts and fibroblastic foci

129
Q

what is seen on IPF CT scan

A

traction bronchiectasis
sub pleural honeycombing
basal predominance

130
Q

which medication makes IPF worse

A

corticosteroids –> they are immunosuppressants so increase risk of death

131
Q

effect of anti fibrotic on IPF

A

slow down progression but do not cure

132
Q

IPF treatment

A

O2 therapy and anti fibrotic
but only definitive treatment is lung transplant

133
Q

predisposing factors for IPF

A

genetic - MUC5B, DSP
environmental triggers - smoke, dust, pollutants, viruses
cellular ageing - telomere attrition, senescence

134
Q

proposed mechanism for IPF

A

damage to epithelium - type 1 pneumocytes release TGF beta 1
causes type 2 pneumoncytes to stimulate fibroblasts to become myofibroblasts
myofibroblasts produce collagen and elastic fibres then apoptose

get too much proliferation of type 2 pneumocytes, resulting in too many myofibroblasts which also don’t apoptosis properly
get lots of collagen and interstitial thickens
this remodelling and scar tissue affects gas exchanged ventilation (lung becomes thick)

134
Q

proposed mechanism for IPF

A

damage to epithelium - type 1 pneumocytes release TGF beta 1
causes type 2 pneumoncytes to stimulate fibroblasts to become myofibroblasts
myofibroblasts produce collagen and elastic fibres then apoptose

get too much proliferation of type 2 pneumocytes, resulting in too many myofibroblasts which also don’t apoptosis properly
get lots of collagen and interstitial thickens
this remodelling and scar tissue affects gas exchanged ventilation (lung becomes thick)

135
Q

Is hypersensitivity pneumonitis reversible if the cause is removed

A

yes, if not left for so long that chronic inflammation and irreversible changes occur

136
Q

symptoms/cause of acute vs chronic hypersensitivity pneumonitis

A

acute: SOB, fever, chest tightness, headache –> due to intermittent and high level exposure
chronic: sustained SOB, due to long term low level exposure

137
Q

what is heard on auscultation in hypersensitivity pneumonitis

A

inspiratory squeaks

138
Q

what is seen on BAL for hypersensitivity pneumonitis

A

lymphocytes > 30%

139
Q

what patterns are seen on CT for hypersensitivity pneumonitis

A

centrilobular ground glass nodules
ground glass
air trapping
mosaic attenuation pattern
three density patterns

140
Q

investigations for hypersensitivity pneumonitis

A

lung biopsy - granulomas and lymphocytes
auscultation - inspiratory squeaks
check for specific IgG
BAL
HRCT
pulmonary function tests

141
Q

treatment for hypersensitivity pneumonitis

A

immunosuppression
corticosteroids
anti fibrotic
remove the cause

142
Q

mechanism of hypersensitivity pneumonitis

A

inhaled antigen in alveolus is picked up by macrophage and taken to lymph node
presented on MHC 2 to naive T cells causing maturation
T cell stimulates B cells to produce IgG
TYPE 3 HYPERSENSITIVITY: IgG with antigen forms immune complexes which settle in capillary wall and trigger inflammation and necrosis
(complement cascade –> neutrophil degranulation –> vessel inflammation and necrosis)

and

TYPE 4 HYPERSENSITIVITY: T cells and macrophages surround antigen, forming granulomas

143
Q

2 types of systemic sclerosis and effects on lungs

A

limited cutaneous SSc - pulmonary hypertension
diffuse cutaneous SSc - ILD

144
Q

skin manifestations of SSc

A

digital ulcers
sclerodatyly
abnormal nail bed on capillaroscopy
telangiectasia
reynauds

145
Q

treatments for SSc ILD

A

immunosuppressants
anti fibrotics

146
Q

which treatment to avoid for SSc

A

corticosteroids - high dose causes renal failure

147
Q

which treatment to avoid for SSc

A

corticosteroids - high dose causes renal failure

148
Q

HRCT pattern for SSc ILD

A

NSIP (non specific interstitial pneumonia) pattern

149
Q

what does microvascular heterogeneity mean

A

the vascular endothelial structure is different depending on the tissue function - organotypic expression profiles

150
Q

how do you calculate (estimate) rate of diffusion

A

(surface area x concentration gradient) / membrane thickness

151
Q

roles of nitric oxide as an anti inflammatory

A

reduces
VSMC proliferation
platelet activation
LDL activation
release of super-oxide radicals
monocyte adhesion

induces
vasodilation

152
Q

list some triggers for endothelial activation

A

smoking
mechanical stress
oxidised LDL deposition
High glucose

153
Q

list the 3 layers of artery walls

A

tunica adventitia
tunica media
tunica intima

154
Q

which vessels have pericytes in their walls and name a role of them

A

capillaries
they’re also called pericapillary cells
can help construct the vessel

155
Q

what are VEGF-A and FSF-1, what are they secreted by and what is their role

A

angiocrine factors
secreted by the capillary endothelium
maintain tissue homeostasis and repair

156
Q

3 most common sites for atherosclerosis and why

A

carotid bifurcation
coronary artery
aortic bifurcation

157
Q

what are the 2 intracellular oxidative enzymes that macrophages use to further oxidise oxLDLs they have engulfed, and turn into foam cells

A

NAPDH oxidase
myeloperoxidase

158
Q

what are the 3 roles of IL1 in atherosclerosis

A

positive feedback to Nuclear Kappa Factor beta (up-regulates it)
triggers intracellular cholesterol crystals
up regulates VCAM1 expression –> increases monocyte migration through endothelium into proteoglycan matrix

159
Q

role of PDGF (platelet derived growth factor) in atherosclerosis

A

stimulates SMC proliferation

160
Q

role of TGF B (transforming growth factor beta) in atherosclerosis

A

changes SMCs from contractile into synthetic - synthetic SMCs produce collagen - this ECM they lay down will form the fibrous capsule for the atherosclerotic plaque

161
Q

what are PCSK9 inhibitors used for and how do they work

A

used for severe / statin resistant hyperlipidaemia
PCSK9 degrades the LDL receptor (LDLR)
the LDLR removes cholesterol from the blood and stops cholesterol biosynthesis

162
Q

is MCP1 a cytokine or chemokine

A

chemokine

163
Q

which receptor does MCP1 bind to

A

a monocyte G protein coupled receptor CCR2

164
Q

what are the proteins on the surface of lipoproteins called

A

apoproteins

165
Q

surgical interventions for atherosclerosis

A

percutaneous coronary intervention
carotid endarterectomy
percutaneous transluminal balloon angioplasty
bypass surgery

166
Q

investigations for familial hypercholestrolaemia

A

lipid profile
genetic testing

167
Q

how does familial hypercholestrolaemia accelerate the process of atherosclerosis

A

mutation means the the LDLR on hepatocytes is absent
so hepatocytes can’t take up LDL
so LDL levels in plasma increase
so more LDL is taken up by macrophages
this accelerates the process of atherosclerosis

168
Q

how does coves infection cause procoagluation

A

infection –> cytokine storm –> endothelial activation –> procoagulant switch

169
Q

effect on thromboinflammation on the lungs

A

causes ARDS
- microthrombi form in the lungs
- increased capillary permeability in lungs
- causes pulmonary oedema
- reduced gas exchange
- type 1 resp failure

170
Q

how is tumour vasculature different from normal vasculature

A

vessels are irregularly shaped, dilated, more leaky and haemorrhagic

171
Q

describe the process of sprouting angiogenesis

A

1) selection of sprouting endothelial cells
- changes in polarity
- modulation of EC-EC contacts
- ECM degradation

2) start of sprouting
- new ECM is deposited
- EC proliferation
- invasive behaviour

3) lumen formation
- proliferation of stalk cell

4) maturation and perfusion
- stabilisation of EC-EC adhesions and PC contacts
- full blood flow through the lumen
- reduction in EC proliferation
- increase in quiescent signals

172
Q

describe the process of sprouting angiogenesis

A

1) selection of sprouting endothelial cells
- changes in polarity
- modulation of EC-EC contacts
- ECM degradation

2) start of sprouting
- new ECM is deposited
- EC proliferation
- invasive behaviour

3) lumen formation
- proliferation of stalk cell

4) maturation and perfusion
- stabilisation of EC-EC adhesions and PC contacts
- full blood flow through the lumen
- reduction in EC proliferation
- increase in quiescent signals

BRS 1b (10 decks)

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