UW 1 Flashcards
Acute bronchitis - etiology
preceding resp ilness (90% viral)
acute bronchitis - clinical presentation
cough for more than 5 days to 3 wks ( +/- purulent sputum, +/- blood)
2. absent systemic findings
3. Wheezing or ronchi, chet wall tenderness
NO FEVER (if present think pneumonia or flu)
acute bronchitis - diagnosis + treatment
- clinical diagnosis, CXR only when pneumonia suspected
2. symptomatic treatment (eg. NSAID, bronchodilators)
Bronchiectasis - sign and symptoms
- cough with daily mucupurulent sputum production
- rhinosinusitis, dyspnea, hemoptysis
- crackles, wheezing
bronchiectasis - etiology
- airway obstraction (eg. ca)
- rheumatic disease (eg. RA, Sjogren), toxic inhalation)
- immunodef (eg. hypogammaglobulinemia)
- Congenital (eg. CF, α-1-antitrypsin def)
bronchiectasis - evaluation
- high resolution CR (needed for initial diagnosis)
- immunoglobulin quantification
- CF testing, sputum culture (bacteria, fungi, mycobacteria
- PFT
the main cause of hypercapnia in COPD
increased dead space ventilaiton
pneumonia mediated hypoventilation - mechanism
R to L intralpulmonary shunting and extreme ventilation /perfusion mismatched
- High O2 inspiration does not correct it
causes of hypoxemia (and example)
- hypoventilation: CNS depression, neuromuscular weakness
- dead-space ventilation (V/Q=infinity): PE
- diffusion limitation: emphysema, interstitial lung disease
- intrapulmonary shunt (V/Q=0): pneumonia, pulm edema, atelectasis
- intracradiac shunt (R-L): Fallot, Eisenmenger
- Reduced PiO2: high altitude
causes of hypoxemia - A-a gradient, corects with O2
- hypoventilation: normal, yes
- dead-space ventilation (V/Q=infinity), increased , yes
- diffusion limitation: increased, yes
- intrapulmonary shunt (V/Q=0): increased, no
- intracradiac shunt (R-L): increased, no
- Reduced PiO2: normal, yes
PFT in asthma
normal to increased TLC
normal FEV1/FVC
normal to increased DLCO
PFT in COPD
increased TLC
low FEV1/FVC
low DLCO (normal in the beginning)
PFT in interstitial lung disease
Low TLC
NORMAL FEV/FVC (or increased)
low DLCO
PFT in pulm arterial hypertension
normal TLC
normal FEV1/FVC
low DLCO
Restrictive chest wall disease
low TLC
normal FEV1/FVC
normal DLCO
DLCO in pulm arterial hypertention
low
hypersensittivity pneomonitis - - definition / manifestation
inflammation of the lung parenchyma caused by antigen exposure
- acute episodes present with cough, breathlessness, fever, malaise that occure within 4-6 h of antigen exposure
chronic: weight loss, clubbing, honycombing of the lung
hypersensitivity pneumonitis - management
avoidance of responsible antigen
sputum and blood culutres in outpatient pneumonia
not required
lung compliance of ARDS
low
ARDS - pulm arterial pressure
increased due to hypoxic vasconstriction, destruction of lung parechyma, and compression of vascular structures from positive airway pressure in mechanicall ventilated patinets
severe asthma exacerbation - management
inhaled short acting β2 agonists, inhaled ipratropium , systemic corticosteroids –> elevated or even normal partial pressure of CO2 suggest failure of medical therapy and resp collapse –> entrotracheal intubation
systemic epinephrine in severe astham exacerbation
only in severe when inhaled therapy cannot be given
mild to moderate asthma asthma exacerbation - management
inhaled β2 agonists –> if no improvement –> systemic steroids
Wegerer - giagnosis
ANCA: PR3, MPO
biopsy: skin (leukocytoclastic vasculitis), kidney (pauci-immune GN) lung (granulomatous vsculitis)
Wegener - management
corticosteroids + immunomodulators (MTX, cyclophosphamide)
it can increased the chance of FP ANCA
HIV
ACEi cause chronic non-productive cough - mechanism
increaesd circulating levels of kinins, substance P, PGE, TXE
(MORE COMMON IN CHINESE)
diagnosis from PFT
- low FEV1/FVC ratio –> obstructive –> DLCO?
- decreased: COPD
- normal/increased: Asthma - normal or high FEV1/FVC –> restrictive –> DLCO?
- normal: chest wall weakness
- decreased: interstitial lung disease
ARDS - how to improve oxygenation
by increaeing either FIO2 or positive end-expiratory prssure (PEEP
- if high levels of FIO2 (more than 60% are required to mainttain oxygenation, PEEP level should be increased to allow for reduction in the FIO2 as oxygenation improves (prolonged high FIO2 causes O2 toxicity)
ALWAYS KEEP LOW TV
increasing of PEEP in ARDS - purpose
reopen of alveoli –> reduce shunting
MC SE of inhaled corticosteroid therapy
oropharyngeal thrush (oral candidiasis)
bornchodilator respone in asthma
improvement of FEV1 more than 12%
asthma severity for patients not on controller medication (step 1)
step 1 (intermittent): max 2 days a week symptoms, max 2 nighttime awakening per month step 2 (mild persistent): more than 2 days / wk, 3-4 awaakenings per month step 3 (moderate): daily symptoms, more than 1 awakening /wk step 4 or 5) (severe): throughout day, 4-7 awakening / wk
asthma treatment
step 1 –> SABA
step 2 –> Low dose inhaled cortic
step 3 –> low dose inhaled cosrticost + LABA or medium inhaled costic
step 4: medium dose inh cortic + LABA
step 5: High dose inh cosrtic + LABA + omalizumab if allegy
step 6: High dose inh cortic + LABA + Oral cortic + Omalizumab if allergy
position dependent hypoxemia - mechanism
positional changes that make the consolidation more gravity dependen worsen ventilation/perfusion mismatch –> increase iintrapulmonary shunting –> worsened hpoxemia
Aspirin exacerbated resp disease - mechanism
non-IgE mediated raction that results from aspirin induced prostagl/leukotriene misbalance
Aspirin exacerbated resp disease - manifestation
mc in history of asthma or chronic rhinsinusitisis with nasal polyposis
- bronchospasm + nasal congestion following aspirin ingestion
aspirin-exacerbated resp disease - treatment
avoidance of NSAID, desensitisation if NSAID are required, use of leukotriene receptor antagonists (eg. montelukast)
illegal that can cause hemoptysis
inhaler cocaine
radiation fibrosis
MC in patients who received lung field radiation –> dyspnea, nonproductive cough, chest pain within 4-24months after therapy
x-ray: volume loss with coarse opacities
ARDS - always low TV - why
decrease the likelihood of overdistending alveoli
(improves mortality) –> causes barotrauma
ARDS under ventilator - hypercapnia
setting the ventilator parameters to provide low TV and low RR decreases minute ventilation –> hypercapnia and acidosis
ARDS - saturation target
greater than 88%
allergic rhinitis - clinical features
- watery rhinorrhea, sneezing, eye symptoms
- early age of onset
- identifiable allergen or seasonal pattern
- pale/bluish nasal mucosa
- associated with other allergic disorders (eczema, asthma etc)
nonallergic rhinitis - clinical manifestation
- nasal congestion, rhinorrhea, sneezing, postnasal drainage (dry cough)
- onset after 20 years old
- parennial symptoms (may worsen with seasonal changes)
- erythematous nasal mucosa
allergic rhinitis - treatment
intranasal glucocorticoids
antihistamines
nonallergic rhinitis - treatment
mild: intranasal antihistamine or glucocorticoids
moderate to severe: combination therapy
nasal cytology in nonallergic rhinitits
eosinophils
not required
clinical signs of pulm hypertension
- Left parasternal lift, RV heave
- Loud P2, right dsided S3
- pansystolic mmurmur of TR
- JVD, periperal edema, hepatsplenomegaly
systemic sclerosis on the lung
- hyperplasia of the intimal SMCs layer –> incr pulm resistance –> pulm hypertension
- interstitial fibrosis
strongest RF for obstructive sleep apnea
obesity
there are 2 types of abnormal ventilation during sleeping
- apnea: cessation of breathing for 10 or more sec)
- hypopnea: reduced airflow causing SaO2 to decrease by 4%
in symptomatic paitnes, experiencing 5 or more obstructive resp events (apneas or hypopneas) per hour is diagnostic of obstructive sleep apnea)
Obesity hypoventilatin syndrome - diagnostic criteria
- BMI more than 30
- awake daytime hypercapnia (more than 45)
- no alternate cause of hypoventilation
obesity hypoventilation syndrome - workup
ABG on room air (normal Aa gradient, hypercapia))
- no intrinsic pulm disease on chest x-ray
- restrictive PFT
- Normal TSH
- polysomonography
obesity hypobentilation synrome - treatment
- nocturnal positive pressure ventilation as 1st line
- wight loss
- avoidance of sedative medication
- resp stimulants (acetazolamide) as last choice
test to confirm bronchiectasias
high resolution CT
Beta 2 agonists - SE
- hypokalemia –> muscle weakness, arrhythnia, EKG abnormalities
- tremor
- palpitations
- headache
asthma related with GERD - management
omeprazole
sarcoidosis effect on the musculoskeletal system
acute polyarthritis
chronic arthritis
Lofgren syndrome
- erythema nodosum
- hilar adenopathy
- migratory polyarthralgia
- fever
ankylosing spondylitis effect in lungs
limited chest expansion + spinal mobility–> restrictive lung disease
sleep apnea syndrome - best initial steps
weight reduction, avoidance of sedatives, avoid alcohol, acoid supine posture during sleep
peak airway pressure
the maximum pressure measured as the TV is being delivered = the sum of the resistive pressure (flow x resistance) and the platue pressure
COPD - seizures after 02 supplementation
increased CO2 retention due to
- loss of compensatory vasoconstriction in areas of ineffective gas exhange worsens V/Q mismatch
- increase on HbO2 reduces the uptake of CO2 from tissues
- Decreased resp drive and slowing of the resp rate causes reduced minute ventilation
- -> reflex cerebral vasodilation –> seizures
pulm contusion - symptoms can be worsen by
fluid overvolume
resp arkalosis in incubated patient - next step
if appropriate TV –> decrease RR
intemediate vs low risk solitary pulm nodule
interm is 8 mm or bigger
pneumothorax - hypertension and tachycardia due to
compression of structures in the mediastinum –> impaired RV filling
ideal location of endotracheal tube / if displaced to bronchus, which bronchus MC
2-6 cm above carina
- right (so left atelectasis)
intubated patients - atelectasis due to misplacement vs pneumothorax
pneumothorax causes hemodynamically instability
parapneumonic effusions - uncomplicated vs complicated regarding etiology
uncompl: sterile exudate in pleural space
complicaetd: bacterial invasion of pleural space –> continue to have symptoms despite antibiotics
parapneumonic effusions - uncomplicated vs complicated regarding pleural fluid analysis
uncompl: ph 7.2 or more, glucose 60 or more, WBC 50.000 or less
complic: ph less than 7.2, glucose less than 60, WBC more than 50.000
parapneumonic effusions - complc vs uncomplicated regarding gram stain + culture
uncompl: negative
complic: FN due tto low bacter count
parapneumonic effusions - uncomplc vs complic regarding treatment
uncomplicated: antibiotics
complic: antibiotics + drainage
increased risk of pneumonia complicated with pleural effusion
immunodeficiency
acute exacerbation of COPD is characterized by a change in at least 1 of the following
- cough severity or frequency
- volume or character of sputum production
- levels of dyspena
Light criteria
at least 1
- Pleural protein/serum protein more than 0.5
- pleural LDH/ serume LDH more than 0.6
- Pleural LDH more than 2/3 of the upper limit of normal for serum LDH
exercise induced bronchoconstriction - management
short acting beta-adrenergic agnostis administered 10-20 mins before exercise are the 1st line treatment if only few times a week
- if daily: inhaled corticosteroids or antileukotriene
normal pleural fluid ph / trandudate fluid ph / edudate
- 7.6
- 7.4-7.55
- exudate: 7.3-7.45 (may be lower)
CHF - where is the fluid
61% bilateral
27% only R
12% only left
