week 8 Flashcards
what is the medical imaging definition for cardiomegaly
when the heart takes up greater than 50% of the thoracic cavity
what is evidence of pleural effusion on a CXR
blunted costophrenic angles
when you lose the right heart border due to pleural effusion on an CXR whcih lobe is affected
middle
when you lose the hemi-diaphragm due to pleural effusion on an CXR which right lobe is affected
lower lobe
what are air bronchograms indicative of
pulmonary oedema
how many phases of covid 19 and brief description of each
3
stage 1 = asymptomatic, innate immune response
stage 2 = severe symptoms uncontrolled immune response due to cytokine storm
stage 3 = post covid symptoms (long covid)
what are the primary targets of covid 19
epithelial cells of the resp tract, specifically binding to ACE2 receptors
two receptors taht covid 19 uses
ACE 2 receptor to attach to host cell
TMPRSS2 receptor to fuse into host cell
role of ACE 2 receptors
convert angiotensin 2 into its anti-inflammatory form ANG1-7
functions of ANG 1-7 5
decrease inflammation
decrease autophagy
decrease vasodilation
decrease insulin resistance
decrease oxidative stress
what cytokine activates the cytokine storm
PANoptosis
what does the cytokine storm mean?
Panoptosis triggers the formation of panaptosome complexes which trigger excessive cytokine release resulting in the cytokine storm which leads to end organ damage
symptoms of covid 7
fever
cough
fatigue
anosmia
dyspnoea
headache
what is anosmia
abrupt loss in someones ability to taste
what causes ARDS in covid
cytokine storm leading the destruction of type 2 pnuemocytes causing lack of surfactant causing alveolar collapse
build up of fluid in the lungs
how does ARDS lead to multi organ collapse 3
the two changes (cytokine storm=type 2 pneumoycte destruction=lack of surfactant + build up of fluid)
can causes respiratory failure, penuomothroax and barotrauma which leads to a lack of ventilation and perfusion
treatments for covid 3
analgesics
oxygen therapy
antivirals
pneumonia definition
acute infection of the lung parenchyma
aetiological classification of pneumonia 5
bacterial
viral
aspiration
atypical
opportunistic
what is the most common cause of pneumonia
streptococcus penumoniae
acquisition based classification of pneumonia
community acquired
healthcare acquired
ventilator acquired
presentation of pneumonia (symptoms) 5
productive cough
pleuritic chest pain
dyspnoea
fatigue
fever
phsyical examination symptoms of pneumonia 4
dullness on percussion
decreased breath sounds
bronchial breathing
coarse crackles
what is required for diagnosis of pneumonia? 1 +1 of 4
consolidation on CXR with one of the following symptoms:
fever >38
dyspnoea
pleuritic pain
productive cough
curb 65 score def
score to assess the severity of community acquired pneumonia
curb 65 definition
c = confusion
u = urea
r = resp rate
b = blood pressure
65 = greater than 65
how do clinical symptoms in TB vary to taht of pneumonia aka what are the clinical symptoms of TB 6
chronic cough
night sweats
weight loss
persistent low grade fever
persistent fatigue and malaise
general differentiation in symptoms of pneumonia to TB
pneumonia presentation and symtpoms more acute - TB commonly low grade persisting
diagnostic investigations in TB 2
lesions on CXR
positive TB skin test
pathogenesis of pneumonia
- aspiration
- colonisation in nasopharynx
- micro aspiration transmission to lung parenchyma
- replication in lung parenchyma
- cytokine release causing inflammation
- systemic inflammation
end organ damage
complictations of pneumonia 5
sepsis
lung absces
respiratory failure
kidney failure
neurological effects
key investigation in pneumonia
CXR
other investigations in pneumonia 6
CBE
EUC
viral swab
Sputum MCS
Pleural fluid aspirate+culture
bronchoscopy
when would you do a bronchoscopy in pneumonia 4
- immunosupressed
- severe pneumonia unresponsive to normal treatment
- conern of endo-bronchial obstruction
- concern of hyper sensitivity pneumonitis
pneumonia treatment (viral, bacterial, mild, severe)
viral = wait and watch
bacterial = antibiotics
mild = oral
severe = intravenous
additional management therapies in pneumonia 4
oxygen if <92
IV fluids
analgesia
pulmonary rehabilitation
oral antibiotics in pneumonia 2
amoxicillin and doxycyclin
intravenous antibiotics in pneumonia
axzythromyosin
three things whcih need to be assessed prior to antibiotic treatment in pneumonia 3
CXR and tests to diagnose pneumonia and pathogen
kidney tests to determine funciton and which antibiotic to use
whether pneumonia is mild or severe to determine whether intravenous or oral antibiotics are used
what is the main cause of pulmonary tb
mycobacterium tuberculosis
what are two characteristics of TB which increase its virulence
slow growth which makes it hard to treat and prolongs infection
waxy cell wall which is lipid rich protecting it from environmental stresses and host immune responses
pathogenesis of TB 4
myocbacterium TB enters upper airways
attempted phagocytosis by alveolar macrophages
migrates to lung parenchyma or to lymph nodes
further cuases
what happens when TB enters the lung parenchyma 4
active infection
inflammation
granuloma development
causes lung damage and dysfunction
what happens when TB enters the lymph nodes
activates B and T cells
they will differentiate into epithelioid cells to form granulomas
advanced symptoms of TB 4
haemoptysis
chest pain
loss of appetite
dyspnoea
clinical findings in TB 3
pallor
wasted appearance
clubbing
systemic manifestations of TB 5
haematuria
headache
backpain
hoarseness
abdominal discomfort
investigations in TB 5
CXR
sputum microscopy and culture
TB skin test
TB blood test
Sputum microscopy use in TB 2
used to observe for acid fast bacilli of which mycobacterium TB is one
its not specific, only confirms diagnosis
sputum culture in TB diagnosis
key diagnostic tool used to identify mycobacterium TB
what is used to detect latent TB 3 points
TB skin test
TB blood test
they cannot distinguish between active and latent
what can be present on CXR for TB
fibro-nodular changes and lesions
not diagnostic though
complications of TB
pleural effusion
haematogenous
cardiac TB
ocular TB
hepatic TB
GIT TB
what are the rules for good treatment in TB 3
combination drug therapy
standardised
good treatment adherance
what is the standard treatment for TB (overall duration, phase duration)
6 months divided into 2 phases
2 months: intensive phase w 4 drugs to kill multiplying baccili
4 months: continuation phase w 2 drugs killing semi-dormant
what is DOT in TB treatment
Directly observing therapy used to ensure strict adherence and assess any side effects from high drug load
what is the key drug used in the first phase of TB
isoniazid
what is the key drug used in the second phase of TB
Rifampicin
example of drug resistant TB strain
MDR-TB = multi drug resistant TB resistant to both isoniazid and rifampicin
definition of an acute chest infection
infection that lasts <3 weeks
definition of a chronic chest infection
infection that lasts >3 weeks often characterised by periods of stability and then exacerbations
physiological risk factors for chest infection development
impaired mucous removal
reduced respiratory effort
decreased cough reflex
immunocomprimised patients
bronchiectasis definition
chronic inflammation of upper airways leading to:
- mucous build up
- scarring
- abnormal widening of bronchi
Pathogenesis of bronchiectasis 6
impaired drainage
obstruction due to structural abnormalities and mucuous accumulation
inflammatory response
transmural inflammation
loss of elasticity in bronchial walls
airway remodelling and dilatation
symptoms features of bronchiectasis 4
productive cough
dyspnoea
wheeze
recurrent infections
clinical findings in bronchiectasis 2
clubbing
coarse crackles
clincal investigations in bronchiectasis 5
sputum culture
CXR
lung function tests
CBE
blood test
treatments for bronchiectasis 4
mucolytics
antibiotics
physiotherapist
pulmonary rehabilitation
genetic characteristics of CF 2
autosomal recessive
most common genetic disease
6 classes of cystic fibrosis
these are based off of severity of gene mutation
1 = no protein produced
2 = no trafficking, cell degrades protein prior to docking
3 = no function
4 = reduced function
5 = less protein
6 = less stable
pathogenesis of CFTR protein
mutation in CFTR gene
CFTR protein not produced properly
Causes defective chlorine channel
affects ion transportation
More sodium retained in cells
Liquid depletion in fluids
leaves thickened mucous
decreased mucociliary clearance
inflammation and infection
what and why does CFTR impact so many organs 5
CFTR protein found on epithelial cells across the body, therefore affects multiple systems including:
- lungs
- pancreas
- liver
-glandular
- reproductive organs
why is genotyping useful in CF management
determine the specific mutation and therefore direct management
groups of treatment pathways in CF 3
symptomatic therapy
CFTR modulator drugs
genetic therapies
symptomatic therapy treatments in CF 4
mucolytics
pancreatic enzymes
chest physio
antibiotics
CFTR modulator drugs characteristics 4
only for certain mutations
increase CFTR activity
slow disease progression
example is Trikafka
where is ground glass opacity common
interstitial lung disease
what are miliaries
multiple well defined nodules spread diffusely through the lungs
what includes correct procedure for inhaler usage 5
- shaking puffer before use
- if using spacer coating inside w one puff prior to use
- exhale fully first
- large inhale
- rinse mouth after
