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FOP/TAS > resp > Flashcards

resp Flashcards

1
Q

describe embryology of resp tract

A

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

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2
Q

factors shifting oxygen dissociation curve to the left

A

= 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

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3
Q

factors shifting oxygen dissociation curve to the right

A

= reduced affinity of oxygen for haemoglobin so more oxygen release to tissues

increased CO2
increased H+ ions
increased 2,3 DPG
increased temp

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4
Q

cause of tonsillitis

A

viral ! - ebv
group A beta haemolytic strep

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5
Q

criteria for assessing if need abx in tonsillitis

A

CENTOR CRITERIA
1. presence of tonsillar exudate
2. fever
3. absence of cough
4. cervical lymphadenopathy

> 3/4 criteria -> abx

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6
Q

management of bacterial tonsillitis

A

penicillin for 10 days

consideration of tonsillectomy if recurrent tonsillitis, peritonsillar abscess, OSA

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7
Q

Symptoms of allergic rhinitis

A

sneezing, itching , rhinorrhoea, snoring, post nasal drip, mouth breathing

post exposure to allergens

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8
Q

cause of cleft palate

A

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

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9
Q

complication of sinusitis

A

subdural empyema
- MRI head
- caused by strep aginosis (Group H)

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10
Q

risk factors for OSA

A

obesity
prader willi syndrome
downs sydnrome
adenotonsillar hypertrophy (reduces airway size and increases upper airway resistance)

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11
Q

complication of OSA

A

COR PULMONALE

chronic hypoxia -> increased pulmonary resistance -> right ventricular failure

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12
Q

gold standard test for OSA

A

sleep studies !!!!

IL-8, IL-6, CRP, TNF alpha increased (IL-10 reduced)

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13
Q

management of OSA

A

adenotonsillectomy

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14
Q

define conductive deafness

A

diminished air conductance but normal bone conduction
obstruction of sound wave transmission

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15
Q

define sensorineural deafness

A

cochlear or neuronal damage and equal impairment of bone and air conductance

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16
Q

risk factors for hearing loss

A
  1. TORCH infections - CMV *
  2. FH of permanent hearing loss
  3. anatomical deformities e.g. cleft palate (incorrect insertion of tensor veli palatini), ear pits
  4. ototoxic medications e.g. alcohol, cocaine, streptomycin
  5. prematurity
  6. genetic syndromes e.g. turners, klinefelters, mutation in GJP2 gene, waardenburg syndrome (mutation in PAX3 gene, bright blue eyes + hair between eyebrows)
  7. meningitis
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17
Q

hearing loss in decibels and severity

A

25-39 = mild
40-69 = moderate
70-94 - severe
>95 = profound

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18
Q

hearing tests at newborn

A
  1. automated otoacoustic emissions

dependent on vibrations of basilar membrane
if fails, referred for auditory brainsteam response

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19
Q

embryology of ear

A

external ear develops at week 6 and complete by week 20

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20
Q

hearing test in different age groups

A
  1. distraction test - 6- 12 months old
  2. visual reinforcement audiometry * - 6-30 months
  3. play audiometry - 2-5 y/o
  4. pure tone audiometry > 5/o
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21
Q

cause of otitis media

A

RSV
rhinovirus
pneumococcus
h.influenza

increased exudate full of neutrophils in middle ear

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22
Q

complications of otitis media

A
  1. mastoiditis - infection spread to mastoid cells and cause protruding pinna and red tender mastoid area
  2. meningitis
  3. chronic otitis media - recurrent discharge for >2 weeks which travels from middle ear through perforated ear drum. refer to ENT
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23
Q

signs of otitis media

A

fever
tympanic membrane red and bulging
loss of light reflection in TM
+/- acute perforation

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24
Q

management of acute otitis media

A

supportive - analgesia, most resolve spontaneously
delayed abx script if symptoms >3 days

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25
Q

describe otitis media with effusion = glue ear

A

= collection of fluid in the middle ear
macrophages and lymphocytes predominant
caused by recurrent ear infections

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26
Q

signs of glue ear

A

asymptomatic
decreased hearing
ear drum dull and retracted with fluid level visible

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27
Q

management of glue ear

A

usually resolves spontaneously
grommet insertion for 12 months - most common cause of conductive hearing loss

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28
Q

describe the travel of sound in ear

A
  1. sound enters external auditory canal and eardrum vibrates
  2. ossicles (malleus, incus and stapes) amplify sound to cochlea
  3. causes movement of fluid in cochlea
  4. stimulates hair cells at top of basilar membrane
  5. auditory nerve (CN VIII) connects cochlea to brain
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29
Q

cause of croup

A

parainfluenza ****
rhinovirus, RSV
in 6 months - 6 y/o children in the autumn

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30
Q

presentation of croup

A

barking cough ( due to tracheal oedema and collapse)
inspiratory stridor (harsh)
fever, coryza
symptoms worse at night
chest recessions

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31
Q

management of croup

A
  1. oral dexamethasone (half life 36-72 hours, works within 90 minutes) or nebulised budesonide
  2. nebulised adrenaline in oxygen
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32
Q

x ray of croup

A

frontal neck x ray shows steeple sign

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33
Q

cause of epiglottitis

A

h. influenza type b - vaccination led to 99% reduction

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34
Q

presentation of epiglottitis

A

sudden onset
high fever + unwell looking child
soft stridor
intensely painful throat - cant speak or swallow, drooling
resp distress - worsening over hours
no cough

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35
Q

management of epiglottitis

A
  1. intubation and ventilation
  2. IV antibiotics (cefurozime)and blood culture
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36
Q

prophylaxis of epiglottitis

A

rifampicin for household members

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37
Q

presentation of bacterial tracheitis

A

caused. by staph auresu
high fever
ill looking child
thick airway secretions
loud harsh stridor

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38
Q

presentation of inhaled foreign body

A
  1. sudden onset
  2. cough, wheeze, SOB
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39
Q

management for inhaled foreign body

A
  1. chest x ray - usually R main bronchus as wider and more vertical, hyperexpansion on one side +/- mediastinal shift
  2. rigid bronchoscopy to remove
  3. antibiotics and steroids for inflammataion
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40
Q

describe pathophysiology of bronchiolitis

A
  1. neutrophilic inflammation produces IL-8 from epithelial cells and macrophages
  2. increased mucus secretion and airway oedema to cause distal airway narrowing
  3. air trapping
  4. causes mucus plugging and impaired ventilation
  5. reduced CO2 clearance
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41
Q

cause of bronchiolitis

A

RSV (80%)
rhinovirus, adenovirus, influenza

2-3 % infants admitted a year

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42
Q

risk factors for severe disease of bronchiolitis

A

chronic lung disease
prematurity
congenital heart disease
neuromuscular disease
< 3 months old
immunodeficiency

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43
Q

monoclonal antibody for prevention of bronchiolitis in high risk babies

A

PAVALIZUMAB - monoclonal antibody (IgG) against RSV antigen to prevent fusion and replication

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44
Q

management of bronchiolitis

A
  1. cap gas - resp acidosis with high PCO2
  2. extended NPA
  3. humidified air/ oxygen via optiflow/ airvo
  4. support with feeding via NG feeds or IV fluids
  5. assisted ventilation via CPAP or mechanical ventilation
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45
Q

bronchiolar lavage results of VIW

A

neutrophil activation
vs asthma whih is eosinophilic

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46
Q

risk factors for asthma

A

family history / parental history
personal history of atopy - eczema, hayfever, rhinitis, food allergy
male sex
cigarette exposure
obesity
low birth weight

47
Q

pathophysiology and stages of asthma

A
  1. exposure to antigen
  2. stimulates B cells to produce IgE antibodies + airway oedema
    3.attack antigens and attach to surface of mast cells
  3. mast cells degranulate and releases inflammatory mediators e.g. histamine, cytokines, prostaglandins and leukotrienes
  4. causes bronchoconstriction, oedema and excessive mucus production
  5. eosinophils in late stages of asthma
48
Q

3 main pathologies in asthma

A
  1. bronchial inflammation
  2. bronchial hyper responsiveness
  3. airway narrowing (reversible)
49
Q

symptoms of asthma

A

nocturnal cough
SOB on exposure to allergens, exercise, cold
interval symptoms
wheeze
chest tightness

50
Q

diagnosis of asthma

A
  1. clinical history and examination
  2. peak expiratory flow rate - monitor with diary to see response with steroids
  3. spirometry
  4. FeNo - shows eosinophilic inflammation
51
Q

spirometry results in asthma

A

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

52
Q

spirometry in restrictive disease

A

reduced FEV1 and reduced FVC
normal FEV1:FVC ratio

53
Q

stepwise management of asthma

A
  1. conservative - avoid triggers, avoid smoking, allergen testing
    • SABA PRN e.g. salbutamol
    • ICS e.g. budesonide, beclometasone, fluticasone
  4. < 5 y/o -> + leukotriene receptor antagonist e.g. monteluklast and review response in 4-8 weeks
  5. > 5 y/o -> + LABA e.g. salmeterol
    • slow release theophyllline
54
Q

monoclonal antibody that can be used in asthma

A

omalizumab = monoclonal antibody that binds to IgE so stops activating inflammattory cells

SE= SLE, hypersensitivity, skin rashes, headaches

55
Q

mechanism of SABA

A

binds to beta 2 adrenoreceptors on bronchial smooth muscle to cause bronchodilation and inhibit mast cell degranulation
hydrophilic

56
Q

mechanism of ICS

A

reverses airway hypersensitivity + decreases airway inflammation

SE = reduces growth velocity

57
Q

mechanism of montelukast

A

leukotriene receptor antagonist- blcoks action of leukotriene D4 in the lungs and bronchial airways

SE = sleep disturbance, increasingly thirsty

58
Q

mechanism of theophylline

A

phosphodiesterase inhibitor - increases cAMP and causes bronchodilatation
short half life
metabolised in liver

58
Q

severe asthma features

A

sats < 92%
PEFR 33-50%
too breathless to talk
use of accessory muscles
audible wheeze

59
Q

life threatening asthma features

A

sats < 92%
PEFR < 33% predicted
silent chest
poor resp effort
altered consciousness, agitation, confusion
exhaustion
cyanosis

60
Q

management of acute asthma

A
  1. oxygen therapy if required
  2. bronchodilators - via spacer or nebuliser
    • ipratropium nebuliser
  4. corticosteroids - dex for 3/7
61
Q

mechanism of ipratropium

A

muscarnic antagonist

side effects = unequal pupils (M3 muscarinic receptors in sphincter pupilla of eye -> give pilocarpine eye drops )

62
Q

management of acute severe asthma

A
  1. IV salbutamol
  2. IV magnesium
  3. IV aminophylline - loading dose over 20 minutes and tyhen continuous infusion
63
Q

causes of bacterial pneumonia

A

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

64
Q

role of pneumocytes

A
  1. type 1 pneumocytes - responsible for gas exchange
  2. type 2 pneumocytes - produce surfactant to reduce surface tension of pulmonary fluids and increase surface area for gas exchange
65
Q

stages of lobar pneumonia

A
  1. initial = vascular congestion and alveolar oedema with high number of infective organism
  2. 2nd stage = significant infiltration of RBCs, fibrin, neutrophils (RED HEPATISATION)
  3. 3rd stage = breakdown of fibrin and BCs to create fibrinopurulent exudate (= GREY HEPATISATION)
  4. resolution caused by macrophage clearing of the exudate

increased thickness of resp membrane causes reduced gas exchange
low transfer factor

66
Q

complications of pneumonia

A
  1. ABSCESS
  2. 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
67
Q

management of pneumonia

A
  1. 1st line = amoxicillin
    + macrolide (clarithromycin/ azithromycin) if atypical or suspecting mycoplasma (lacks cell wall so amoxicillin wont treat)
68
Q

symptoms of TB

A

fever
cough + haemoptysis + persistent
night sweats
weight loss
dyspnoea
erythema nodosum
lympahdenopathy

69
Q

diagnosis of TB

A
  1. chest x ray - isolated focus, hilar lymphadenopathy, lobar collapse
  2. sputum sample x 3 - test for acid fast bacilli
  3. interferon testing (quantiferon) - doe snot diffentiate between latent and active tB
70
Q

how does mantoux test work

A

tuberculin skin test - administer intradermal tuberculin protein
leads to T cell mediated reaction in sensitised individuals
measure size in 48-72 hours
>15mm = positive

71
Q

management of tB

A
  1. rifampicin - 6 months
  2. isoniazid - 6 months
  3. Pyrazinamide - 2 months
  4. ethambutol - 2 months
72
Q

signs of tension pneumothorax

A

hyper resonant on affected side
tracheal deviation
reduced air entry
severe dyspnoea
distended neck veins

73
Q

epidemiology of CF

A

autosomal recessive
1 in 25 caucasians are carriers

74
Q

pathophysiology of CF

A

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

75
Q

how do newborns with CF present

A

meconium ileus - thick mec causes obstruction
vomiting, abdo distension, failure to pass mec

managed with gastrogaffin enema

76
Q

CF presentation in children

A
  1. faltering growth
  2. recurrent resp infections: staph aureus -> pseudomonas aeruginosa (causes fast decline in lung function) -> burkholderia (abscess, bronchiectasis)
  3. wet purulent cough
  4. steattorhoea and malabsorption
  5. nasal polyps
  6. sinusitis
  7. lack of pancreatic digestive enzymes - ineffective bicarbonate secretion + inappropriate zymogen secretion
77
Q

CF presentation in older children

A
  1. diabetes
  2. cirrhosis and portal HTN
  3. distal intestinal obstruction
  4. infertile males
78
Q

how is CF detected on newborn screening

A

guthrie heel prick test - detects rtaised immunoreactive trypsinogen

79
Q

diagnosis of CF

A
  1. sweat test ** - chloride in sweat elevated >60
  2. CF gene mutation testing
80
Q

how does ivacaftor work

A

CFTR potentiator
5% have missense mutations G551D (class 3) and causes defective Cl channel opening
ivacaftor increases stimulated cL and cilia motility

81
Q

management of CF

A
  1. Ivacaftor and lumicaftor
  2. physiotherapy and chest clearance twice a day
  3. prophylactic abx
  4. nebulised hypertonic saline or DNAse (dornase alpha)
  5. fat soluble vitamins
  6. creon - enzyme replacement
82
Q

inheritance of primary ciliary dyskinesia

A

autosomal recessive

83
Q

pathophysiology of PCD

A

defect in structure or function of ciliary proteins causing reduced efficacy or inaction of cilia (cilia beat frequency affected)

84
Q

presentation of PCD

A

recurrent infections
productive cough
purulent nasal discharge
chronic ear infections + conductive hearing loss
rhinorrhoea
male and female infertility
hydrocephalus

85
Q

what is kartagener syndrome

A
  1. PCD
  2. sinus vertus
  3. dextrocardia
86
Q

gold standard test for PCD

A

bronchial brush biopsy (records ciliary beat frequency) + transmission electron microscopy

87
Q

screening test for PCD

A

nasal exhaled nitric oxide - low in PCD

88
Q

presentation of e-cigarette associated lung injury

A

cough, SOB, chest pian, weight loss
CXR - bilateral lung infiltrates
caused by tetrahydrocannabinol - chemical compound isolated in broncholavage

89
Q

definition of pulmonary hypertension

A

mean artery pressure > 25mmHg
REDUCED LEVELS OF PROSTACYCLIN SYNTHASE

90
Q

causes of pulmonary hypertension

A
  1. L -> R shunts e.g. ASD, VSD, AVSD, PDA
  2. chronic alveolar hypoxia e.g. OSA, CF, asthma
  3. pulmonary venous hypertension e.g. aortic stenosis, l sided heart failure
  4. primary vascular disease e.g. persistent pulmonary hypertension of newborn
  5. conditions e.g. HIV, sarcoidosis, portal hypertension
91
Q

presentation of pulmonary hypertension

A

dyspnoea
fatigue
recurrent resp infections
syncope
chest pain

92
Q

investigations for pulmonary hypertension

A
  1. ECG - RV hypertrophy (enlarged QRS V1-3), r atrial hypertrophy ( large p waves)
  2. CXR
  3. ECHO
  4. diagnostic cardiac catheter
93
Q

management of pulmonary hypertension

A
  1. sildenafil - phosphodiesterase inhibitor which increases nitric oxide (fromL-arginine) production
  2. nifedipine
  3. corrective surgery
94
Q

high risk determinants for pulmoanry hypertension

A

venous saturations < 60%
R aretry and right ventricle enlargement
pericardial effusion
reduced LV size
mean R atrial pressure >10
sysetmic cardiac index < 2.5

95
Q

describe respiratory system during sleep

A

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

96
Q

how to improve oxygenatation on ventilator

A

O2 determined by mean airway pressure
MEAN AIRWAY PRESSURE = INSPIRATORY TIME (PIP) + EXPIRATORY TIME (PEEP)

  1. increase PEEP - increases basic volume of the lungs at all times during ventilation cycle. keeps alveoli open so greater surface area for gas exchange
  2. increase FiO2
  3. decease PIP
  4. Increasing inspiration time
97
Q

how to improve cO2 clearance on ventilator

A

CO2 clearance determined by minute ventilation
MINUTE VENTILATION = TIDAL VOLUME X RESP RATE

  1. increase resp rate - increases minute volume ventilation
    2.increase PIP - increase tidal volume
  2. increase tidal volume
  3. decrease PEEP
98
Q

describe pierre robin sequence

A
  1. micrognathia
  2. glossoptosis
  3. airway obstruction

+ inverted U shaped cleft palate

99
Q

how to interpret rinnes and webers

A

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

100
Q

causes of type 1 resp failure

A

hypoxia + normal CO2

prolonged high altitude
pneumonia
PE
pulmonary oedema

101
Q

causes of type 2 resp failure

A

hypoxia + hypercarbia (due to hypoventilation)

kyphoscoliosis
asthma exacerbation
raised ICP
neuromuscular disease
opiates
airway obstruction e.g. foreign body
cardiac arrest

102
Q

what is grunting

A

increases the functional residual capacity

sound produced when glottis closed during expiration and increases end expiratory pressure in the lungs

103
Q

what is surfactant made up of

A

lipids (90%) - mostly palmitoylphosphatidyl choline
protein - hydrophobic surfactant proteins SP-B and SP-C AND Hydrophilic SP-A and SP-D
cholesterol

104
Q

action of surfactant

A

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

105
Q

describe alveolar capillary dysplasia

A

= 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

106
Q

what is laryngomalacia

A

shortened aryepiglottic folds

107
Q

define vital capacity

A

maximal volume of air that can be expired following maximum inspiration

= tidal volume + inspiratory reserve volume + expiratory reserve volume

108
Q

define forced vital capacity

A

total volume of air that is forcibly exhaled following maximum inspiration in 1 second

109
Q

define functional residual capacity

A

volume of air remaining in the lungs after quiet expiration

110
Q

treatment of pseudomonas aeruginosa in CF

A

oral ciprofloxacin and nebulised colistimethate sodium

111
Q

how to test for carbon monoxide poisoning

A

exhaled breath test

112
Q

exudative pleural effusions

A

high protein and LDH

caused by:
- pneumonia
- malignancy
- pericarditis
- SLE

FOP/TAS (12 decks)

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