resp Flashcards
describe embryology of resp tract
respiratory bud arises from ventral surface of foregut (derived from endoderm) at 3-5 weeks
ciliated cells from 12 weeks
surfactant production from 23 weeks
1/5 alveoli of adult present at birth and continues growing until 8 y/o
factors shifting oxygen dissociation curve to the left
= increased affinity of oxygen to haemoglobin (less oxygen release to tissues)
fetal Hb - due to low 2,3 DPG levels
hypothermia
decreased H+ ions
carbon monoxide
factors shifting oxygen dissociation curve to the right
= reduced affinity of oxygen for haemoglobin so more oxygen release to tissues
increased CO2
increased H+ ions
increased 2,3 DPG
increased temp
cause of tonsillitis
viral ! - ebv
group A beta haemolytic strep
criteria for assessing if need abx in tonsillitis
CENTOR CRITERIA
1. presence of tonsillar exudate
2. fever
3. absence of cough
4. cervical lymphadenopathy
> 3/4 criteria -> abx
management of bacterial tonsillitis
penicillin for 10 days
consideration of tonsillectomy if recurrent tonsillitis, peritonsillar abscess, OSA
Symptoms of allergic rhinitis
sneezing, itching , rhinorrhoea, snoring, post nasal drip, mouth breathing
post exposure to allergens
cause of cleft palate
failure of fusion of medial nasal and maxillary processes in week 5 of gestation -> cleft lip
failure to fuse and form primary palate in week 5-12
complication of sinusitis
subdural empyema
- MRI head
- caused by strep aginosis (Group H)
risk factors for OSA
obesity
prader willi syndrome
downs sydnrome
adenotonsillar hypertrophy (reduces airway size and increases upper airway resistance)
complication of OSA
COR PULMONALE
chronic hypoxia -> increased pulmonary resistance -> right ventricular failure
gold standard test for OSA
sleep studies !!!!
IL-8, IL-6, CRP, TNF alpha increased (IL-10 reduced)
management of OSA
adenotonsillectomy
define conductive deafness
diminished air conductance but normal bone conduction
obstruction of sound wave transmission
define sensorineural deafness
cochlear or neuronal damage and equal impairment of bone and air conductance
risk factors for hearing loss
- TORCH infections - CMV *
- FH of permanent hearing loss
- anatomical deformities e.g. cleft palate (incorrect insertion of tensor veli palatini), ear pits
- ototoxic medications e.g. alcohol, cocaine, streptomycin
- prematurity
- genetic syndromes e.g. turners, klinefelters, mutation in GJP2 gene, waardenburg syndrome (mutation in PAX3 gene, bright blue eyes + hair between eyebrows)
- meningitis
hearing loss in decibels and severity
25-39 = mild
40-69 = moderate
70-94 - severe
>95 = profound
hearing tests at newborn
- automated otoacoustic emissions
dependent on vibrations of basilar membrane
if fails, referred for auditory brainsteam response
embryology of ear
external ear develops at week 6 and complete by week 20
hearing test in different age groups
- distraction test - 6- 12 months old
- visual reinforcement audiometry * - 6-30 months
- play audiometry - 2-5 y/o
- pure tone audiometry > 5/o
cause of otitis media
RSV
rhinovirus
pneumococcus
h.influenza
increased exudate full of neutrophils in middle ear
complications of otitis media
- mastoiditis - infection spread to mastoid cells and cause protruding pinna and red tender mastoid area
- meningitis
- chronic otitis media - recurrent discharge for >2 weeks which travels from middle ear through perforated ear drum. refer to ENT
signs of otitis media
fever
tympanic membrane red and bulging
loss of light reflection in TM
+/- acute perforation
management of acute otitis media
supportive - analgesia, most resolve spontaneously
delayed abx script if symptoms >3 days
describe otitis media with effusion = glue ear
= collection of fluid in the middle ear
macrophages and lymphocytes predominant
caused by recurrent ear infections
signs of glue ear
asymptomatic
decreased hearing
ear drum dull and retracted with fluid level visible
management of glue ear
usually resolves spontaneously
grommet insertion for 12 months - most common cause of conductive hearing loss
describe the travel of sound in ear
- sound enters external auditory canal and eardrum vibrates
- ossicles (malleus, incus and stapes) amplify sound to cochlea
- causes movement of fluid in cochlea
- stimulates hair cells at top of basilar membrane
- auditory nerve (CN VIII) connects cochlea to brain
cause of croup
parainfluenza ****
rhinovirus, RSV
in 6 months - 6 y/o children in the autumn
presentation of croup
barking cough ( due to tracheal oedema and collapse)
inspiratory stridor (harsh)
fever, coryza
symptoms worse at night
chest recessions
management of croup
- oral dexamethasone (half life 36-72 hours, works within 90 minutes) or nebulised budesonide
- nebulised adrenaline in oxygen
x ray of croup
frontal neck x ray shows steeple sign
cause of epiglottitis
h. influenza type b - vaccination led to 99% reduction
presentation of epiglottitis
sudden onset
high fever + unwell looking child
soft stridor
intensely painful throat - cant speak or swallow, drooling
resp distress - worsening over hours
no cough
management of epiglottitis
- intubation and ventilation
- IV antibiotics (cefurozime)and blood culture
prophylaxis of epiglottitis
rifampicin for household members
presentation of bacterial tracheitis
caused. by staph auresu
high fever
ill looking child
thick airway secretions
loud harsh stridor
presentation of inhaled foreign body
- sudden onset
- cough, wheeze, SOB
management for inhaled foreign body
- chest x ray - usually R main bronchus as wider and more vertical, hyperexpansion on one side +/- mediastinal shift
- rigid bronchoscopy to remove
- antibiotics and steroids for inflammataion
describe pathophysiology of bronchiolitis
- neutrophilic inflammation produces IL-8 from epithelial cells and macrophages
- increased mucus secretion and airway oedema to cause distal airway narrowing
- air trapping
- causes mucus plugging and impaired ventilation
- reduced CO2 clearance
cause of bronchiolitis
RSV (80%)
rhinovirus, adenovirus, influenza
2-3 % infants admitted a year
risk factors for severe disease of bronchiolitis
chronic lung disease
prematurity
congenital heart disease
neuromuscular disease
< 3 months old
immunodeficiency
monoclonal antibody for prevention of bronchiolitis in high risk babies
PAVALIZUMAB - monoclonal antibody (IgG) against RSV antigen to prevent fusion and replication
management of bronchiolitis
- cap gas - resp acidosis with high PCO2
- extended NPA
- humidified air/ oxygen via optiflow/ airvo
- support with feeding via NG feeds or IV fluids
- assisted ventilation via CPAP or mechanical ventilation
bronchiolar lavage results of VIW
neutrophil activation
vs asthma whih is eosinophilic
risk factors for asthma
family history / parental history
personal history of atopy - eczema, hayfever, rhinitis, food allergy
male sex
cigarette exposure
obesity
low birth weight
pathophysiology and stages of asthma
- exposure to antigen
- stimulates B cells to produce IgE antibodies + airway oedema
3.attack antigens and attach to surface of mast cells - mast cells degranulate and releases inflammatory mediators e.g. histamine, cytokines, prostaglandins and leukotrienes
- causes bronchoconstriction, oedema and excessive mucus production
- eosinophils in late stages of asthma
3 main pathologies in asthma
- bronchial inflammation
- bronchial hyper responsiveness
- airway narrowing (reversible)
symptoms of asthma
nocturnal cough
SOB on exposure to allergens, exercise, cold
interval symptoms
wheeze
chest tightness
diagnosis of asthma
- clinical history and examination
- peak expiratory flow rate - monitor with diary to see response with steroids
- spirometry
- FeNo - shows eosinophilic inflammation
spirometry results in asthma
obstructive pattern
1. FEV1 reduced <80%- improvement of >12% with bronchodilator . most sensitive test of small to moderate airway obstruction **
2. FEV1: FVC < 70%
3. normal FVC
4. residual volume increased
spirometry in restrictive disease
reduced FEV1 and reduced FVC
normal FEV1:FVC ratio
stepwise management of asthma
- conservative - avoid triggers, avoid smoking, allergen testing
- SABA PRN e.g. salbutamol
- ICS e.g. budesonide, beclometasone, fluticasone
- < 5 y/o -> + leukotriene receptor antagonist e.g. monteluklast and review response in 4-8 weeks
- > 5 y/o -> + LABA e.g. salmeterol
- slow release theophyllline
monoclonal antibody that can be used in asthma
omalizumab = monoclonal antibody that binds to IgE so stops activating inflammattory cells
SE= SLE, hypersensitivity, skin rashes, headaches
mechanism of SABA
binds to beta 2 adrenoreceptors on bronchial smooth muscle to cause bronchodilation and inhibit mast cell degranulation
hydrophilic
mechanism of ICS
reverses airway hypersensitivity + decreases airway inflammation
SE = reduces growth velocity
mechanism of montelukast
leukotriene receptor antagonist- blcoks action of leukotriene D4 in the lungs and bronchial airways
SE = sleep disturbance, increasingly thirsty
mechanism of theophylline
phosphodiesterase inhibitor - increases cAMP and causes bronchodilatation
short half life
metabolised in liver
severe asthma features
sats < 92%
PEFR 33-50%
too breathless to talk
use of accessory muscles
audible wheeze
life threatening asthma features
sats < 92%
PEFR < 33% predicted
silent chest
poor resp effort
altered consciousness, agitation, confusion
exhaustion
cyanosis
management of acute asthma
- oxygen therapy if required
- bronchodilators - via spacer or nebuliser
- ipratropium nebuliser
- corticosteroids - dex for 3/7
mechanism of ipratropium
muscarnic antagonist
side effects = unequal pupils (M3 muscarinic receptors in sphincter pupilla of eye -> give pilocarpine eye drops )
management of acute severe asthma
- IV salbutamol
- IV magnesium
- IV aminophylline - loading dose over 20 minutes and tyhen continuous infusion
causes of bacterial pneumonia
streptococcus pneumoniae **
mycoplasma pneumoniae - atypical, adolescents, wheeze, persistent
H.influenza - rare due to vaccine
staph aureus - rust coloured sputum, empyema
group B strep - newborns
most common type of pneumonia < 2 y/o = VIRAL
role of pneumocytes
- type 1 pneumocytes - responsible for gas exchange
- type 2 pneumocytes - produce surfactant to reduce surface tension of pulmonary fluids and increase surface area for gas exchange
stages of lobar pneumonia
- initial = vascular congestion and alveolar oedema with high number of infective organism
- 2nd stage = significant infiltration of RBCs, fibrin, neutrophils (RED HEPATISATION)
- 3rd stage = breakdown of fibrin and BCs to create fibrinopurulent exudate (= GREY HEPATISATION)
- resolution caused by macrophage clearing of the exudate
increased thickness of resp membrane causes reduced gas exchange
low transfer factor
complications of pneumonia
- ABSCESS
- EMPYEMA - if fever > 7 days and persistent
use small bore chest drain with connection to collection chamber and underwater seal with fibrinolytic agent / video assisted thoracoscopy surgery
management of pneumonia
- 1st line = amoxicillin
+ macrolide (clarithromycin/ azithromycin) if atypical or suspecting mycoplasma (lacks cell wall so amoxicillin wont treat)
symptoms of TB
fever
cough + haemoptysis + persistent
night sweats
weight loss
dyspnoea
erythema nodosum
lympahdenopathy
diagnosis of TB
- chest x ray - isolated focus, hilar lymphadenopathy, lobar collapse
- sputum sample x 3 - test for acid fast bacilli
- interferon testing (quantiferon) - doe snot diffentiate between latent and active tB
how does mantoux test work
tuberculin skin test - administer intradermal tuberculin protein
leads to T cell mediated reaction in sensitised individuals
measure size in 48-72 hours
>15mm = positive
management of tB
- rifampicin - 6 months
- isoniazid - 6 months
- Pyrazinamide - 2 months
- ethambutol - 2 months
signs of tension pneumothorax
hyper resonant on affected side
tracheal deviation
reduced air entry
severe dyspnoea
distended neck veins
epidemiology of CF
autosomal recessive
1 in 25 caucasians are carriers
pathophysiology of CF
defective CFTR (cystic fibrosis transmembrance conductase regulator) gene on chromome 7
most commonly mutation in F508 delta (class 2 mutation = defective protein folding so cant reach apical membrane)
CFTR is a cAMP dependent Cl channel so Cl not moved across membrane to mucus -> causes viscid thick mucus and inflammation from neutrophils and IL-8
how do newborns with CF present
meconium ileus - thick mec causes obstruction
vomiting, abdo distension, failure to pass mec
managed with gastrogaffin enema
CF presentation in children
- faltering growth
- recurrent resp infections: staph aureus -> pseudomonas aeruginosa (causes fast decline in lung function) -> burkholderia (abscess, bronchiectasis)
- wet purulent cough
- steattorhoea and malabsorption
- nasal polyps
- sinusitis
- lack of pancreatic digestive enzymes - ineffective bicarbonate secretion + inappropriate zymogen secretion
CF presentation in older children
- diabetes
- cirrhosis and portal HTN
- distal intestinal obstruction
- infertile males
how is CF detected on newborn screening
guthrie heel prick test - detects rtaised immunoreactive trypsinogen
diagnosis of CF
- sweat test ** - chloride in sweat elevated >60
- CF gene mutation testing
how does ivacaftor work
CFTR potentiator
5% have missense mutations G551D (class 3) and causes defective Cl channel opening
ivacaftor increases stimulated cL and cilia motility
management of CF
- Ivacaftor and lumicaftor
- physiotherapy and chest clearance twice a day
- prophylactic abx
- nebulised hypertonic saline or DNAse (dornase alpha)
- fat soluble vitamins
- creon - enzyme replacement
inheritance of primary ciliary dyskinesia
autosomal recessive
pathophysiology of PCD
defect in structure or function of ciliary proteins causing reduced efficacy or inaction of cilia (cilia beat frequency affected)
presentation of PCD
recurrent infections
productive cough
purulent nasal discharge
chronic ear infections + conductive hearing loss
rhinorrhoea
male and female infertility
hydrocephalus
what is kartagener syndrome
- PCD
- sinus vertus
- dextrocardia
gold standard test for PCD
bronchial brush biopsy (records ciliary beat frequency) + transmission electron microscopy
screening test for PCD
nasal exhaled nitric oxide - low in PCD
presentation of e-cigarette associated lung injury
cough, SOB, chest pian, weight loss
CXR - bilateral lung infiltrates
caused by tetrahydrocannabinol - chemical compound isolated in broncholavage
definition of pulmonary hypertension
mean artery pressure > 25mmHg
REDUCED LEVELS OF PROSTACYCLIN SYNTHASE
causes of pulmonary hypertension
- L -> R shunts e.g. ASD, VSD, AVSD, PDA
- chronic alveolar hypoxia e.g. OSA, CF, asthma
- pulmonary venous hypertension e.g. aortic stenosis, l sided heart failure
- primary vascular disease e.g. persistent pulmonary hypertension of newborn
- conditions e.g. HIV, sarcoidosis, portal hypertension
presentation of pulmonary hypertension
dyspnoea
fatigue
recurrent resp infections
syncope
chest pain
investigations for pulmonary hypertension
- ECG - RV hypertrophy (enlarged QRS V1-3), r atrial hypertrophy ( large p waves)
- CXR
- ECHO
- diagnostic cardiac catheter
management of pulmonary hypertension
- sildenafil - phosphodiesterase inhibitor which increases nitric oxide (fromL-arginine) production
- nifedipine
- corrective surgery
high risk determinants for pulmoanry hypertension
venous saturations < 60%
R aretry and right ventricle enlargement
pericardial effusion
reduced LV size
mean R atrial pressure >10
sysetmic cardiac index < 2.5
describe respiratory system during sleep
decrease in minute volume due to decreased chemosensitivity of cO2 and O2
DEPRESSION OF GABA neurones causing resp depression
minute volume at it lowest during REM sleep
how to improve oxygenatation on ventilator
O2 determined by mean airway pressure
MEAN AIRWAY PRESSURE = INSPIRATORY TIME (PIP) + EXPIRATORY TIME (PEEP)
- increase PEEP - increases basic volume of the lungs at all times during ventilation cycle. keeps alveoli open so greater surface area for gas exchange
- increase FiO2
- decease PIP
- Increasing inspiration time
how to improve cO2 clearance on ventilator
CO2 clearance determined by minute ventilation
MINUTE VENTILATION = TIDAL VOLUME X RESP RATE
- increase resp rate - increases minute volume ventilation
2.increase PIP - increase tidal volume - increase tidal volume
- decrease PEEP
describe pierre robin sequence
- micrognathia
- glossoptosis
- airway obstruction
+ inverted U shaped cleft palate
how to interpret rinnes and webers
conductive hearing loss:
Rinnes: bone conduction > air conduction (negative)
webers: localises to affected ear
sensorineural hearing loss
rinnes: air conduction >bone (positive)
webers: localises to opposite ear
causes of type 1 resp failure
hypoxia + normal CO2
prolonged high altitude
pneumonia
PE
pulmonary oedema
causes of type 2 resp failure
hypoxia + hypercarbia (due to hypoventilation)
kyphoscoliosis
asthma exacerbation
raised ICP
neuromuscular disease
opiates
airway obstruction e.g. foreign body
cardiac arrest
what is grunting
increases the functional residual capacity
sound produced when glottis closed during expiration and increases end expiratory pressure in the lungs
what is surfactant made up of
lipids (90%) - mostly palmitoylphosphatidyl choline
protein - hydrophobic surfactant proteins SP-B and SP-C AND Hydrophilic SP-A and SP-D
cholesterol
action of surfactant
1.reduces surface tension of the fluid -prevents air spaces from collapsing on exhalation
2.improves oxygenation and ventiltation.
3, improves lung compliance
4. maintains residual lung volume
5. reduces critical closing volume
describe alveolar capillary dysplasia
= deficiency alveolar capillaries within the alveolar walls
usually caused by FOXF1 gene mutation
neonates present with resp distress, pulmonary hypertension which is resistant to treatment, poor prognosis
what is laryngomalacia
shortened aryepiglottic folds
define vital capacity
maximal volume of air that can be expired following maximum inspiration
= tidal volume + inspiratory reserve volume + expiratory reserve volume
define forced vital capacity
total volume of air that is forcibly exhaled following maximum inspiration in 1 second
define functional residual capacity
volume of air remaining in the lungs after quiet expiration
treatment of pseudomonas aeruginosa in CF
oral ciprofloxacin and nebulised colistimethate sodium
how to test for carbon monoxide poisoning
exhaled breath test
exudative pleural effusions
high protein and LDH
caused by:
- pneumonia
- malignancy
- pericarditis
- SLE
