Pulmonology 🫁 Flashcards
Which two parts of mechanical ventilation determine O2?
PEEP and FiO2
When do we not do a thoracentesis 1st for effusion
If we suspect CHF, we do a diuretics trial first
Name some CIs for non invasive ventilation
Agitated patient, high risk of aspiration, non resp organ failure, ARDS, severe acidosis, cardio respiratory arrest, upper airway obs, facial trauma, esophgeal anastomosis
Think airway protection, need for invasive over non invasive, and mechanical issues
Myasthenia crisis Mx
Intubate, and IVig and CSs
4 interventions to decrease mortality in COPD
O2, rehab, Vx, stop smoking
Criteria for long term O2 therapy in COPD patients
- Resting arterial oxygen tension (PaO2) ≤55 mm Hg or pulse oxygen
saturation (SaO2) ≤88% on room air - PaO2 ≤ 59 mm Hg or SaO2 ≤ 89% in patients with cor pulmonale,
evidence of right heart failure, or hematocrit >55%
Lung abcess 1st and 2nd line Abx
Ampi and sulbactam
Then clindamycin 2nd line
Patient on ventilation, what criteria is there for spontaneous breathing trial?
pH > 7.25, adequate O2 on minimal support, intact insp effort and no AMS
Treatment for invasive aspergillosis
Voriconazole and echinocandin.. then voriconazole alone.
Best confirmation Invx for aspergillosis
Bronchoscopy with bronchoalveolar lavage
Signs of transient tachypnoea of the newborn
Risk factors (premature etc.). Signs of resp distress. Increase lung volume and clear breath sounds. Interlobular fissure seen on X-RAY
Contrast aspiration pneumonia and chemical pneumonitis. Main differences in presentation
Chemical (acid) = rapid onset, bilateral,
Pneumonia = unilateral, over days, fever, sputum
What is post surgical atelectasis . How to prevent from occurring
Atelectasis after surgery. Usually after 2 days, due to pain restricting TV and thus causing lobar collapse. Causes low O2, increase RR and elevated pH. Prevent by doing post operative deep breathing excersizes
What is respiratory failure due to asthma. What are the signs. Three steps in Mx
Asthma attack signs, with accessory muscle use, silent chest, wheezing actually decreases. K+ may decrease (alkalosis), lactate may increase, and O2 will go down. Do albuterol, LAMA, CS, Mg first. Can quickly trial NIPPV (not as effective as for COPD). Very low threshold for intubation
Lung issue in CREST syndrome
PAH (literally the pulmonary artery endothelial hyperplasia type) not a Pulm HTN secondary to some fibrosis.
Laryngomalacia
Where the supraglottic structures are flabby and collapse. Causes stridor, worse in supine. Presents in infants
Unilateral choanal atresia presentation
Assume usually until adulthood, causing chronic nasal discharge
What are vascular rings, and how do they usually present
Where the great vessels wrap around the trachea and esooahgus. Presents with biphasic stridor, improved with neck extension.
Can you get pulmonary edema in altitude sickness? Treatment aims?
Yes, from the hypoxia vasoconstriction in the lungs causing very high pressure and thus a transudate. Do things to increase oxygen to reduce the vasoConstriction, and to therefor reduce the edema. Take of backpack to reduce o2 consumé, give o2, decent
Why does someone with bronchopulomary dysplasia have HTN
There is increase circulating catecholamines….. causing HTN
And 5 ways to decrease the risk of VAP
Subglottic secretion suction
Avoid PPI use unless 100% needed
Decrease movement of patient
Avoid excess sedation
Elevate head to a 45° angle
Discuss the concepts of ventilation in ARDS
Aim to limits alveolar distension. So Vt (TV) can be low (6-8). This can cause hypoventilation, but we allow this persmissive hypercapnia. The collapsed airways don’t all open up, so giving high pressure or Vt just damages open alveoli. Prone positioning is good. Still use PEEP to recruit some alveoli. Keep FiO2 at its lowest to avoid oxygen toxicity
Aspiration pneumonia Tx
Same as CAP. ceftriaxone and azithromycin… not as heavily anaerobic as once thought
Presentation of high alititude pulmonary edema, and how to differentiate from pneumonia
Our vasoconstriction is very high in some areas of the lung, causing transudate formation. Presents like patchy pneumonia . But will have not too high Leuk, patient will have recently been at high altitudes, procalcitonin normal. Rapid improvement with supplemental O2
What does increase peak pressure and increase plateau pressure mean for lungs
Increase airflow resistance and decrease compliance respectively
When to give O2 Tx, ABx, nocturnal ventilation in COPD
If o2 less than 88
If AECOPD Hx
If hypercapnia
How to Dx carboxyhemoglobin? How to Tx
Do ABG (tells you the HbCO), since pulse ox doesn’t. And Tx with 100% O2
When is inhaled Nitrates given to a neonate
In neonatal pulmonary hypertension
Recall ARDS mx flowchart
Apnoea and gasping, do bag valve mask ventilation. Improves do CPAP, remains to mechanical vent and consider surfactant. If apnoea or gasping at first , do CPAP.
General Tx ideas for otitis media
Oral Abx (if less than 6mo, or more than 6mo patient with serious signs). Amox is first line, then amox plus clavulanic acid 2nd, clinda if allergic. Tympanostomy if 3 or more episode in 6month, or if continuously for 3months .
Most common non hereditary sensory loss in kids
Cong3tninal CMV infx
Dx criteria for obesity hypoventilation syndrome
BMI above 30. Daytime CO2 elevation. No other cause
bronchiectasis secondary to CF is mostly found where in lung
Upper lobes (characteristic of CF Bronchiec)
What are mandibular tori, and what are the general features of benign oral masses. How to Tx
Bong exostosis of the bone…. Into the floor of the mouth. Symmetrical, painless, smooth mucosal cover, slow growth. Reassure patient
Sialolithiasis and sialdenitis Tx?
Lith, give moist heat, water and milk gland, can give NSAID. If infected, give Abx and consider referral to ENT to remove stone,
Screening for lung cancer (what’s done and indications)
More than 20 pack year history (unless haven’t smoked for more than 15 yrs). Above 50 yo. Yearly low dose CT
BPD Dx
A clinical diagnosis. If a premat still requires O2 after 1 month.
If have nasal foreign body…. How do we manage (if seen or non seen)
Remove… if cannot see refer to ENT
Signs and symptoms of laryngomalacia. General Mx
Floppy larynx on around 6 mos. When Inspire the larynx collapses. Causes nosing breathing and insp stridor, worse when supine, and feeding issues. Often GERD concomitantly. Resolved around 18mo, can do Sx if severe
Out the following in order or lines of Tx for massive hemoptysis
Bronchoscopy
Artery embolisation
Thoracotomy
That order is correct
Links between asthma and atelectasis
Asthma causes mucous plugging and thus atelectasis
Compare and contrast Acute and chronic hypersensitivity pneumonitis (and the Tx)
Acute is early on, high dose exposure, tIII hypersensitivity. Forms nodular interstitial opacities. Just remove exposure.
Whereas chronic is due to long term fibrosis and tIV reaction. These patients have reticular interstitial opacities. Likely need GCs or even lung transplant.
Need to drainage of effusion in adults is based on fluid analysis. But in kids, is this the case?
It’s based more on volume. So large, moderate effusion should be drained
Most common lung CA in young non smokers
Bronchial carcinoid
Chronic aspergillosis clinical diagnosis
More than 3 months of signs and symptoms. IgG to aspergillos, and a caviars leasion
Significance of high bnp and troponin in PE case
Signifies high mortality
Causes of recurrent same lobe pneumonias
Consider obstruction first (do CT). Then consider aspiration causes
If different lobes, may be immunodeficiency issues
Blunt thoracic aortic injury invx (consider if stable or not)
Stable, do CTA. Unstable do Transesoph US
Which bacteria are prevalent in CF patients. Consider ages
At first STAPH STAPH STAPH, then around 20 years old it becomes more pseudomonas.
Review the intubation protocol/ criteria for burns patients.
Always five 100% O2 via a non rebreather mask. Then the criteria for intubation is any of the following: face burn, inflam of oropharynx, stridor, HbCO > 10, confined to a burning building, eyebrow singe,
TACO Tx
O2 therapy, and diuretics (furosemide)
X-ray sign of transient tachypnoea of the newborn
Perihilar streaking. (In the interlobular fissure)
Way to differentiate CHD hypoxia and respiratory hypoxia
If O2 therapy helps, then it’s more likely pulmonology based
Main three causes of neonatal respiratory distress
Pulmonary nodules with surrounding ground glass. In a patient with fever, neutropenia
Halo sign, in invasive aspergillosis.
Diagnostic marker for invasive aspergillosis… issue with the test? What to do if -ve
Galactomannan assay. Not sensitive, so if negative, should do BAL or biopsy
Tx of invasive aspergillosis
2 weeks voriconazole
PCP vs invasive aspergillosis
PCP: non productive, diffuse bilateral infiltrates
Invasive aspergillosis: productive, hemoptysis, more localised halo sign
Main differential for acute SoB when CVC inserted
Tension pneumothorax and air emboli
Out of the two protective/reducing mortality inputs to COPD Mx…. Which is most Important and why
To reduce smoking…. In all patients! O2 therapy only if O2 is less than 88**
How to tell if a hemoptysis is from alveolar or non alveolar causes,
Do Bronchoscopy and serial lavage. Many bloody vials will indicate alveoli and point towards diffuse alveolar haemorrhage
Empyema over 2 weeks and has foul smelling drainage . Cause?
Anaerobe . Others like strep cause over 1 week, and don’t smell foul
Why do we love azithromycin so much for COPD
Because it also decreases neutrophil degradation and remodelling of airway (like an extra effect it has)
What do we see in post nasal drip (on oropharynx)
Cobblestoning
Do we give a bit of oral steroid for acute asthma exac? Why?
We do, to decrease the late stage of inflam. So give once a day ~50 mg. This prevents the reexacerbation
What do we see in PCP on CT
Ground glass, patchy infiltrates
Why is mystethnic crisis often hidden from signs and symptoms
Often due to the inability to look like they are in respiratory distress (no use of accessory muscles)
Myasthenia crisis Mx
Low threshold for intubation (any sign of resp failure, met ac, low TV), and either plasmapheresis/IVIg and CSs
Abx that can worsen or even cause mysasthenic crisis. Name one other famous drug
Quinolones or aminoglycosides. Beta blockers
Main cause of sleep apnoea in peads
Adenotonsillar hypertrophy
What is delayed emergence from anaesthesia? What causes it (3). Mx?
Low RR and more, beyond what is expected (often 30 mins or more). Can be a seizure, stroke, high ICP, drug effect or interaction, metabolic disturbance. Either reintubate or put mask on, and consider reversal agents
Signs and risk factors for severe life threatening asthma
Poor control, previous ICU or intubation visit, use of systemic GCs, emergency visit.
RR more than 30, HR more than 120, sat less than 90, PaCO2 high, peak flow less 50% predicated.
Accessory muscle use, AMS, no wheeze and silent chest, marked accessory muscles, severe SoB
Following trauma, what is likely happening if there is excessive extra pulmonary air (in the pleura). For example, the tube was put in to Tx pneumothorax, yet more air comes out still
Tarcheobronchial injury. Do Bronchoscopy
Patient with ARDS, who then has fluids…. At risk of what? Discuss?
Risk of pulmonary edema. So although we need initial fluids, be very conservative after (dry lung is a happy lung). Have a neutral or negative fluid balance. Limit boluses, give diuretics etc.
Over pride of ARDS Mx
Recap on relationship between FiO2 in ARDS
Do initially fairly high, to then take the ABG to see how bad it is. Lower it, to where PaO2 is roughly 92-96, to avoid O2 tox. Cannot really decrease PEEP, since at least 10 PEEP is needed to recruit
Patient with AECOPD who still has issues with medical therapy? Indications to intubate?
For NIPPV (recall how it helps). If AMS, unstable, pH <7.1, then can intubate. Also if done 2 hour trial with NIPPV, and no improvement, do intubation
Indications and CI for NIPPV
Noninvasive positive pressure ventilation
Indications
(strongest evidence)
• COPD (severe exacerbation, prevent extubation failure)
• Cardiogenic pulmonary edema
• Acute respiratory failure
• Postoperative hypoxemic respiratory failure
• Immunosuppressed patients
Facilitate early extubation
Contraindications
Medical instability
• Cardiac or respiratory arrest (or impending arrest)
• Severe acidosis (pH <7.1)
Acute respiratory distress syndrome
• Nonrespiratory organ failure
• Unstable cardiac arrhythmia/hemodynamic instability
• Encephalopathy (Glasgow Coma Score <10)
• Gastrointestinal bleed
Inability to protect airway
• Uncooperative or agitated
• Inability to clear secretions/high aspiration risk
Mechanical issues
• Recent esophageal anastomosis
• Facial or neurologic surgery, deformity, or trauma
Upper airway obstruction
Two types of shock that aortic dissection can cause
Tamponade (obs) and Hemorrhage (hypovolemia)
RFs for pneumonia
HIV, DM, immuno surp, above 65, COPD, CF, URI, smoker, alcoholic, esoph dysmotlity, PPI, sedatives, quietapine
Risk factors for spontaneous pneumomediastinum
Cough violent, tall and thin male, bad asthma exac.
Mx of spontaneous mediastinum
Rest, analgesia, avoid valsalva
Talk a bit about flail chest
Breakage of 3 or more ribs in at least 2 locations. Causing isolated rib cage that doesn’t move with rest of thorax. Causing increase work of breathing. On X-ray, suspect when there is blunt trauma, desat, and many rib fractures
ID a the associated neonatal pathology with the X-ray findings
Interstitial infiltrates and interlobular fissure prominent
Course margins and cystic changes
Bilateral infiltrates and hyperinflation
Diffuse reticular ground glass and air bronchogram
Transient tachypnoea of the newborn
BPD
Meconium aspiration
NRDSO
Rough pHs of empyema, exudate, transudate and normal
Less than 7.3
7.3-7.45
7.4-7.55
7.6
Resp
Two occasions we might see high amylase in pleural fluid
From pancreatitis extension or boerhave (from saliva)
Diaphragmatic rupture invx and Tx
X-ray first, then CT to Dx. Surgery needed to repair
First line therapy for IPF
Pirefenidone. Antifibrotic
Broad ways to tell between aspiration abcess and Tb
Tb will have our usual risk factors. Air fluid levels seem more in abcess. Putrid foul smelling sputum is an aspiration abcess thing. Tb occurs over weeks, abcess over a week
Which is the only shock with elevated SVO2?
Distributive. Also the only one with elevated cardiac index
LV vs RV apical hypokinesis in shocks?
Cardiogenic and obstructive (PE) respectively
Hall mark signs for meconium aspiration syndrome s
Meconium stained amniotic fluid
What is hepatic hydrothroax
Patients with cirrhosis and the diaphragm has high permeability…. Causing hydrothorax on the right
Two main disease causing very low glucose pleural effusion
RA pleurisy and empyema. Both due to lots of WBCs in the pleural fluid
Main mx for amniotic fluid emboli sydmrome
Supportive. Intubate if needed, give vasopressors. Consider transfusion
Difference between pulmonary nodule and mass
Nodule is 3 cm or less
Factors increasing the likelihood that a pulmonary nodule is malignant
Large size*
• Advanced patient age
• Female sex
• Active or previous smoking
• Family or personal history of lung cancel
• Upper lobe location
• Spiculated radiographic appearance
Size correlates to malignant risk. <0.6cm you can even just reassure. >0.8cm and other risks you should biopsy or excise
Cystic fibrosis is famous for having changes in what portions of the lung
Upper lobes
Patient on steroids. Has pneumonia signs, CXR negative, what to do? And why?
CT, since it can reveal a pneumonia. Steroids can lower the consolidation quantity and make it invisible on CXRAY
When to do lung screening
Above 50, and 20 yr pack Hx (unless quite for more than 15 yrs). Do low dose CT every year
Patient with DVT and severe renal issues. How to anticoag
UFH
Naloxone for opioid withdrawal main aim
Give in small doses and titrate. Otherwise can cause withdrawal. And only need to fix Resp rate, not AMS issues
Child with multiple episodes of croup or upper resp tract infections, what should we expect this patient have
Asthma
Hypersensitivity pneumonitis acute and chronic symptoms
History/PE
Acute: Dyspnea, fever, malaise, shivering, and cough starting 4 to 6 hours after exposure;
the physician should gather a job/travel history to determine exposure
Chronic: Presents with progressive dyspnea; physical examination reveals fine bilateral
rales
Loefflor syndrome vs lofgren syndrome
Loffler syndrome is a form of eosinophilic pulmonary disease characterized by absent or
mild respiratory symptoms (most often dry cough), fleeting migratory pulmonary opacities,
and peripheral blood eosinophilia. Lofgren is a sarcoid type, with bilateral hilar LN, arthritis and erythema nodosum
Pulmonary infiltrates less than 24 hrs after injury… contusion or ARDS
more likely contusion. Infiltrates take longer in ARDS
In left heart failure, PEEP is beneficial, why?
as + intrathoracic pressure causes + preload and low afterload. On the other hand, + PEEP worsens right heart failure (increased intrathoracic and pulmonary vascular pressures).
How does PEEP thoracic pressure and venous return
Increases thoracic pressure and decreases venous return and thus BP
Patient on ventilation, with drop in BP…. Three things that could do this
Tension pneumothorax (chest pain, sudden and peak inspiratory pressure would increase), opioid use, high peep
Symptoms of massive PE
Acute massive pulmonary embolism: Presents with hypotension, JVD, and new-onset right
bundle branch block.
Lung cancer mets LABBS
Liver adrenal brain bone
Who is at higher risk of disseminated Cocciodes infx
Filipino, African, HIV, preg
Adenoid hypertrophy signs and symptoms
History of mouth breathing, hyponasal voice, adenoid facies, rhinorrhea, and postnasal drip is commonly described.
Signs and symptoms of tonsillar hypertrophy
History of recurrent infections (most commonly viral and then bacterial) and airway and feeding difficulties, such as dysphagia and SDB with OSA. Voice changes and dental malocclusion may be seen.
Briefly explain the following rhinitis’s.
Irritants, vasomotor, gustatory, drug induced, hormonal, Senile.
Irritants: Cigarette smoke (tobacco), pollutants, occupational (chemicals such as cleaning
products)
Vasomotor: Caused by increased blood flow to the nasal mucosa; it is instigated by
temperature changes or dry air and irritant odors
Gustatory: Clear rhinorrhea after ingestion of food (most often spicy)
Drug induced: Due to antihypertensives, NSAIDs, PDE-5 inhibitors, or cocaine
Hormonal rhinitis: Onset during pregnancy; it resolves with end of pregnancy
Senile rhinitis (also called atrophic rhinitis): occurs in older adults when the nasal glands
that produce moisture fail to function adequately
Compare and contrast intermittent and persistent allergic rhinitis
Intermittent/seasonal: Allergic reactions to grass/trees or pollen (hay fever); occurs in
late spring/summer
Persistent/perennial: Allergic reactions to house dust, dust mites, molds, dogs, cats
Pain difference between uncomplicated, complicated parapneumonic effusions and Empyema
Uncomplicated: just same as exudate. Abx only
Empyema: same as above but culture and gram positive. Abx and chest tube
Classify mild, iterate, severe and massive hemoptysis
Hemoptysis is often classified as mild
(<30 mL), moderate (31-100 mL), severe (100-600 mL), or massive. Massive hemoptysis is
defined by a number of criteria, often ranging from 100 mL to more than 600 mL over 24
hours with respiratory or hemodynamic compromise.
Sudden chest pain, SOB, and with hypotension, JVD, and new-onset right
bundle branch block.
Acute massive pulmonary embolism:
Loffler syndrome…. What is it
a form of eosinophilic pulmonary disease characterized by absent or
mild respiratory symptoms (most often dry cough), fleeting migratory pulmonary opacities,
and peripheral blood eosinophilia.
Why is mechanical ventilation needed for flail chest
By increasing positive intrathoracic pressure, positive-pressure ventilation improves oxygenation and causes the flail segment to move normally. Whereas normally, flail chest is disconnected to the rest of the ribs, and will move paradoxically when there is negative IP pressure.
Tx for bronchiolitis
Supportive usually
Presentation of bronchiolitis
Nasal cong , cough… then resp distress and wheeze and crackles.
Main risky outcome for patients with apnoea of prematurity
Ischemia to the watershed which can cause cerebral palsy
General step approach to manage croup
Oral dexameth, inhaled racemic epinephrine, intubate
If stridor at rest give inhaled epinephrine
Malignancy on imaging of lungs… what are the high risk factors
Large size* above 2cm is 50% chance
• Advanced patient age
• Female sex
• Active or previous smoking
malignant probability
• Family or personal history of lung cancer
• Upper lobe location
• Spiculated radiographic appearance
Risk factors for a solitary pulmonary nodule to be malignant
Large size* above 2cm is 50% chance
• Advanced patient age
• Female sex
• Active or previous smoking
malignant probability
• Family or personal history of lung cancer
• Upper lobe location
• Spiculated radiographic appearance
Why don’t pancoast tumours present with usual lung cancer signs. Like cough, hemoptysis, SoB
Because they are away from the main bronchus
Paint cliché Picture for case of post op atelectasis
Surgery 2-5 days ago (sub diaphragmatic Sx), now has SoB, no chest pain. Maybe lil cough. Temp normal. Smoker. Sats high 80s. Dull and decreased breath sounds. Opaque on CXR, with mediastinal shift toward issue
Why are asthmatics at risk of atelectasis
Due to mucous plugging
Distant heart sounds in COPD?
Due to hyperinflation
Why patients in OHS, “can’t breath” and “won’t breath”
patients with OHS “can’t breathe” (due to excess weight and altered lung mechanics) and “won’t breathe”
(due to decreased chemosensitivity to hypercapnia from persistent nocturnal hypoventilation).
Presentation of fat embolus syndrome. Consider CTPA finding. Consider main causes
Resp distress, Neuro issues, petechia rash, TCP. High in any bone marrow manipulation (femoral head fracture for example). CTPA would show ARDS like findings, due to big inflam induction, but no filling defects (too small).
Why might intubation worsen anaphylaxis BP
PEEP can decrease VR, thus worsen BP
General treatment for immediate analphylaxis
Epinephrine (most important):
• IM preferred, may be repeated (eg, 3 doses)
• IV in severe/refractory cases
IV crystalloid & Trendelenburg positioning for hypotension
Albuterol for bronchospasm
Early intubation for upper airway obstruction
Semi recumbent positioning used when
Semirecumbent positioning may lower the risk of ventilator-acquired pneumonia in intubated patients
on mechanical ventilation.
Mx of venous air fluid emboli
High flow O2 to resorb air, and left lateral decubitus position (allows air to trap in right ventricle and prevents entry to pulmonary artery)
Some signs of cor pulmonary on X-ray
Large central pulmonary artery
How does wegners looks on the CXR
Pulmonary nodules and alveolar consolidation are typical findings
Loss of elastin in the lung matrix occurs in what disease
alpha-1-antitrypsin (AAT) deficiency
Compare PFTs between ILD and chest wall restriction
Both are restrictive, but ILD will have low FRC, TLC, RV…. chest wall issues are usually normal in those
Compare high altitude pulmonary edema and multi focal pneumonia
Both cause high leuk, both causes patchy infiltrates on X-ray. HAPE reposnds to O2 right away, occurs days after high altitude, has normal procalcitonin, leukocytes below 15. Vice versa for pneumonia
How are SqCLC and SmCLC seen in CXR
Small cell and squamous cell lung cancers can also present as contrast-enhancing primary
masses involving the central airways, frequently causing hemoptysis due to endobronchial invasion. Small cell carcinoma most often presents radiographically as a bulky hilar and mediastinal mass; squamous cell carcinoma often presents with central cavitation (ie, heterogeneous density) due to tumor necrosis.
Compare and contrast CXR of chronic bronchitis and emphysema
The chest ×-ray findings in chronic bronchitis reflect airway inflammation, including prominent thickened bronchovascular markings. In contrast, chest -ray findings in emphysema reflect obliteration of the alveolar septa and include decreased lung tissue density (hyperlucency) and bullae.
How to differentiate sarcoid and histoplasmosis
Sarcoidosis and histoplasmosis may present with similar symptoms and chest x-ray findings, but histoplasmosis infection is rare in an immunocompetent patient and leukocytosis would be expected.
Clinical findings of patella dislocation
Examination shows a flexed knee with reduced range of motion and lateral displacement of the
patella (seen as a large, immobile deformity in this patient) out of the trochlea, which may be palpable as a depression at the anterior knee.
What ligament torn in Patela dislocation
patellar dislocation, lateral displacement with associated tear of the medial patellofemoral ligament
Quick recap on Patellar tendonitis
Patellar tendonitis (“jumper’s knee”) is a chronic overuse injury characterized by anterior knee
pain that worsens with activity. Examination may show tenderness at the inferior pole of the patella, but range of motion and patellar position are normal.
Medial collateral ligament tears recap
Medial collateral ligament tears are caused by severe valgus stress (eg, blow to the lateral
tee) or twisting injury. Ligamentous laxity may be masked in the acute phase by swelling and muscle
spasm, but range of motion is preserved, and the patella would not be displaced.
PMR, polymositis… which has high muscle enzymes
Polymositis
Does polymyositis cause pain?
Usually not
Pathophys of pes anserin bursitis
Strength discrepancy between quads and hamstrings. Causes stress in the bursa (and bone, tendons too)
Main ortho complication of downs. How to Dx and Tx
Atlanto axial subluxation. Do lateral X-ray of the c spine in flex and extend. do surgical fusion
What is the provocation manuvre for pronation teres syndrome
Pronation
against
resistance
How can drowning cause ARDS
Washes surfactant out, ruins the osmotic gradient, toxic stuff in the water…..
Aside from being able to culture or stain bacteria from pleural fluid, how else can we determine uncomplicated and complicated parapneumonic effusion
LDH, glucose, pH, leukocytes
Someone with sepsis or low IV vol…. Given NE to boost the MAP. What’s the issue?
Can worsen tissue perfusion causing ischemia to digits
How might blunt thoracic trauma cause cardiogenic pulmonary edema
Myocardial stunning, causing LV function issues, causing pulmonary edema
Some pulmonary outcomes for SCD
Can cause Pulmonary fibrosis. Can also cause pulmonary artery hypertension (the chronic inflam can cause hyperplasia of vessel lining). DLCO and X-ray can tell between the two
Hypersensitivity pneumonitis vs occupational asthma (clinically)
Hypersensitivity pneumonitis chases ground glass on CXR. Consituational symptoms often.
Occupational asthma, does not have above…. More asthma of course. Can Dx with peak flow worsening after exposure
When to do thoracotomy in hemothorax
If initial drain of blood >1.5 L, more than 200ml per hour for 2 or more hours, or unstable
Who gets prevention for RSV. An what do we give
Less than 29 weeks gest
CHD (hemodynamiccally bad)
Underlying lung of prematurity
Give pavalizumab
Main complications for bronchiolitis
Apnea (especially if <2 mo old), and respiratory failure if severe, long term wheezing/asthma
Overview of pulmonary contusion
Manifestations of pulmonary contusion include tachypnea, hypoxemia, and (often) decreased breath sounds (due to alveolar infiltrates). Because clinically significant alveolar edema may take hours to accumulate, the initial chest x-ray is often negative. CT scan (more sensitive) or repeat chest x-ray (as in this patient) may be necessary to reveal the patchy, irregular alveolar infiltrates characteristic of pulmonary contusion. they are typically nonlobular (not restricted by anatomic landmarks). Management is supportive and involves pain control, pulmonary hygiene, and respiratory support.
What is the danger space in the pharyngeal area
If contiguous infx from the pharynx behind the alar fascia, then it can easily extend into the mediastinum. This area behind the alar is the danger space
How does atelectasis cause a transudate
Causes low intraalveolar pressure, which draws transduatuve fluid out of the capillary
Aspiration pneumonitis Mx
Supportive only
What increase in FEV1 is required when giving An SABA to diagnose asthma
12% or more increased
Recall the PA CO2 and PA02 limits in MMHG to incubate in an asthma exacerbation
Less than 50 O2, more than 50 CO2
 Patient has asthma symptoms more than two times a month but less than five times a week. What step are they in
Step two
Patient has asthma symptoms most days, but not every day a week. And wakes up around once for the symptoms
Step three
A patient has asthma symptoms almost every day. And wakes up more than once a week for symptoms. What steps are there in
Step four and five
Patient has mild asthma. Less than two times a month
Step one
Bronchiectasis, the antibiotic we tend to give empirically
Respiratory quinolone
In a queue COPD exacerbation what is the O2 we aim for
88 to 92%
When do we give O2 in chronic management for COPD
If 02 88% or less. Or 89% or less if cor pulmonale/elevated Htc
Compare and contrast IPS and cryptogenic organising pneumonia
COP is patchy on x-ray, has good prognosis, sometimes has fever, and is more acute. Give corticosteroids
IPF is diffuse on chest x-ray, has no fever, is insidious, and as a poorer prognosis. Give pirfenidone
The rough tidal volume settings for ventilation for COPD or are ARDS
6 to 8 for COPD. 6 for ARDS
The rough inspiration: exploration ventilator setting for COPD or ARDS
1:3 for COPD.
1:1.5 for ARDS
The rough respiratory rate ranges for COPD and ARDS for ventilators
10 to 14 for COPD
14 to 18 for ARDS
These really depend on ABG
PF ratio less than 200 on ventilator. What modality do you Usually increase
Increase PEEP
PF ratio less than 150 in ARDS and the Fi O2 is above 60%. And the peep is Max as you wanna do it. What would you consider
Prone patient
What is Berlin criteria
It’s the definition of ARDS. Has to be a cute, proven on an x-ray, with a PF ratio of less than 300. Heart failure ruled out
By what age do patients have functional asplenia and sickle cell disease
2 to 4 years
Most common cause for sepsis and meningitis in sickle cell disease
Strep pneumonia
If have really severe lead poisoning, which is causing enceph.
What treatment combo is good
I’ve EDTA and dimercaprol
First line treatment for lead poisoning
Succimer . Penilliamine the second line
Which size pneumothorax do we just give O2 for
<2cm
Investigations once established exudate with Lights
Amylase, glucose, cytology, culture, gram, tb, RF, CCP, ana. Depends on symptoms
STOP BANG survey
Survey to determine if sleepy and likely to have OSA. If positive then consider polysomn
AHI DX criteria for OSA
AHI is the apnoea + hypoapnoea / total hrs of sleep
5 or more and symptoms
15 or more generally
Hyperventilation syndrome Mx
My diaphragm breathing. Reassure. Lil lorazepam if above doesn’t work
List three complications of drowning. And mention when each can occur
 respiratory distress (often occurs insidiously after hours), cerebral edema (in patients who get hypoxia, and have delayed resus). Arrhythmia (usually due to the hypoxia)
Metronidazole is good for obligate or facultative anaerobes?
 it is good for obligate anaerobes, not facultative anaerobes. For example, for lung abscess, we don’t use metronidazole.
Why can the oxygen saturation decrease when a patient lies on the side that their pneumonia is?
Because we have increased blood flow, going to the lungs which are poorly aerated. Thus, causing an intrapulmonary shunt.
Diagnosis and treatment of alpha one antitrypsin deficiency
Measure the AAT level. And do pulmonary function test and LFT. Treatment consists of giving the AAT supplement, and doing steroid/bronchodilator as needed. 
Two types of high lactate we can get in acute asthma, exacerbation
 Type a (diaphragm work of breathing), type B (SA B,A use) 
Compare and contrast the use of NIPPV for asthma and COPD
For COPD,NIPPV is great, as it can stent open the collapsed airway. However, it is hit and miss with asthma (hard to stent, smooth, muscle hypertrophy), therefore can consider a small trial in a select patient group, but have a low threshold to intubate straight away. 
Can DLCO be effected in PE
Yes, due to mismatch
Diagnosed this: one-year-old child, had a recent upper respiratory tract infection. Now has harsh cough, inspiratory, strider, and low-grade fever.
Croup 
Respiratory related lung/breathing changes
Progesterone induced increase respiratory rate. Title volume also increases a bit. Thus minute ventilation increases. Functional residual capacity decreases (due to basilar atelectasis).
What is the criteria for candidacy for spontaneous breathing trial off ventilator?
Patient has good mental status, no potential diaphragm issue. Good oxygenation on minimal support (PA02 of at least 60, PEEP of at least five or less, FIO2 less than 40%. PH must be above 7.25
Contrast, acute and chronic lung transplant rejection
Acute happens within six months. Usually fairly insidious, but can present with fever. And cough/sort of breath. Give a glucocorticoids. Chronic can happen even years after the transplant, and presents usually with slow onset shortness of breath. Presentation is in keeping with bronchiolitis obliterans may have to do a retransplantation.
If patient has bleeding in the lung, how do we position the patient?
 they should be lying lateral with the bleeding lung below. This is to prevent the blood from getting and collapsing the good lung.
If bronchoscopy fails to treat a lung bleed, what usually usually comes next arteriography or thoracotomy
Usually arteriography and embolisation. Thoracotomy is basically the last line.
How does carbon dioxide elevation towards a decreased level of consciousness?
It increases gabba and glutamine, and decreases aspartate and glutamate 
Samter triad
A triad of characteristics to remember aspirin, exacerbated respiratory disease
Asthma, chronic rhinitis associated with polyps, worsened with aspirin
Three. Main areas/cavities that have high space for blood to fill.
Thorax, abdomen/pelvis/retroperitoneum, thigh
Management of haemothorax
Tube thoracostomy, if around more than 1.5 L drained, proceeded to surgical thoracotomy
Right main stem bronchi intubation will increase the resistance or elastic pressure on ventilation
Elastic
Which ventilator manoeuvre can calculate auto peep
And expiration hold
Micro nodular opacities vs diffuse reticular opacities. Relate to hypersensitivity pneumonitis
Micro nodular is acute. Reticular is chronic
Talk to me about methotrexate induced lung injury
Usually occurs a few months after starting the drug. Causes a mixed CT picture (opacities, consolidations, reticular, infiltrates, et cetera). It is granulomatous. Includes excluding infection, and discontinuing methotrexate to see if it improves. Note, that this reaction is idiosyncratic.
Contrast the first line treatment for postnasal drip and rhinitis
Rhinitis (unless infectious) is required to have intranasal glucocorticoids. Postnasal drip benefits from first generation antihistamines.
When to give Abx in AECOPD
If 2 or more cardinal symptoms. I’ve been lied to
Name some risk factors for VP, and ways that we can combat this and decrease the risk of this
Recumbent position. Excess sedation. Cuff movement. Acid suppression.
Reduce acid suppression, head to 30 to 45°. Avoid sedation. Avoid excess movement of the patient and the cuff.
Hepatic hydrothroax is trans or ex
Transudate
Incentive spirometry, other than preventing atecatsis , can prevent post-operative complications
Post-operative pneumonia. It is the best intervention to prevent this
Dyspnoea of pregnancy versus asthma in pregnancy
Both are exacerbated. Just look for symptoms. Dyspnoea of pregnancy is not going to be intermittent, won’t have cough, won’t have chest tightness
Halo sign on x-ray
Our nodule with ground glass around it. Seen in aspergillosis
Patient with asthma exacerbation given Saba and corticosteroid. Hours later gets tremor comedy tendon reflex low and muscle weakness in all groups
Maybe hypokalaemia from albuterol
If in septic shock fluid resource isn’t working, what can we give second
Norepinephrine
Carbon monoxide patient on pulse oximetry what do we see
A normal O2. Need a BG to See HBCO levels
 Post-operative eight electrolysis courses which acid base disturbance
Usually a respiratory alkalosis
Patient with HIT, but also has an elevated aPTT, what could this be
That’s just the heparin causing that elevation in aPTT
Why do premature have low haemoglobin
The longer they are in utero, the longer they are in a hypoxic environment, the more they can build up their red blood cell supply.
 Patient with hemoptysis, fever/weight loss, chronic rhinosinusitis,
Wegener
What is the x-ray finding for Wagner
Bilateral lung nodules and some cavitation
The two main medications we give for AECOPD
IV corticosteroid and inhaled SABA. Antibiotics usually given, some form of ventilation usually given
If you have an ARDS patient put on ventilation. 10 minutes after the ABG shows and mild respiratory acidosis, and a PaO2 of 105. What sort of intervention should you
Decrease the FiO2. We allow a bit of permissive hypercapnia. But this patient doesn’t need a Patho to that hi, Anthos we need to prevent oxygen toxicity and bring down the FiO2
Does pyridostigmine have any place in acute myasthenic crisis
No. Even discontinue it. Go straight to your IVIg and corticosteroid and intubate
Generally speaking if you have a systemic disorder, and keep saying either erythema and ulcers in the ear canal, sinuses, bronchi, what is this a sign of
Wegner
Recurrent pneumonia in a patient above 50 with a smoking history. What kind of things can we do
We can either do a CT. Oh wait six weeks and do a chest x-ray. I sent she was screaming for malignancy
He’s coughing very hard, you can obviously get pneumothorax, but you can also get just what kind of leakage of air
Spontaneous Pneumomediastinum
Other than that of course long findings et cetera. What is another vital sign that will be changed in bronchopulmonary dysplasia
Hypertension
For massive haemoptysis, give me the first, second, third line
Bronchoscopy, arteriography, thoracotomy
Why is a flat diaphragm (and COPD) bad for breathing
Because it decreases the amount of diaphragm force generated
Main management for foreign body aspiration
Rigid bronchoscopic removal
Patient with potential TB signs, has the risk factors. Has orthostatic hypotension, high potassium, Hight eosinophil
Miliary TB causing infectious adrenalitis
Management of amniotic fluid embolism syndrome
Ventilate, vasopressor, transfuse
A Horners syndrome can cause which radiculopathy
The C8 to T1
Which nationality is at risk for ace inhibitor cough
Chinese
How does oxygen therapy help altitude sickness (lung wise)
Since HAPE is due to vasoconstriction causing a Translate. Oxygen will cause less vasoconstriction
Which lung cancer has the central necrosis
Squamous cell
Patient 1h after operation, respiratory rate really low, patient quite drowsy, slight respiratory acidosis
Could be delayed emergence from Anastasia
What to do if tracheobronchial tree injury (I was scenario of chest drain keeps draining air for a long time)
Do bronchoscopy
Why do we allowed permissive hypercapnia in incubation (especially in ARDS)
To keep the tidal volume low. High tidal volume can cause over extension and damage to the lung
Talk to me about non-invasive positive pressure ventilation and intrinsic peep
The NIPPV Can essentially stent open the airway, allowing for more emptying and release of intrinsic peep. this allows more emptying, less trapping, diaphragm can relax more, decreasing the work of the muscle
After an acute exacerbation, why do we have to give oral prednisone for a bit
Decrease the delayed immune response
When somebody has a plural effusion we always do a thoracocentesis. When do we not do you want
100% sure it’s from congestive heart failure
Myasthenic patient with a little pneumonia, and has shallow breathing, respiratory acidosis. What’s going on what do we do
Myasthenic crisis, intubate, Ivy immunoglobulin, corticosteroid
Can I give you doacs in cancer patient
No, risk of bleeding
In terms of pulmonology, what is the risk factor of quetiapine
Pneumonia
Take me through the pH values for Empyema, exudate, translate and normal plural fluid
Leston 7.3, 7.3 to 7.4, 7.4 to 7.5, around 7.6
Does rheumatoid plural effusion have low glucose
Yes, because white blood cells are there
Diaphragmatic hernia. Is CT needed
Yes
Suspect hairy leukoplakia do what
HIV test
How long are the episodes in Merniere
Like recurrent 30 minute episodes
DVT impatient with severe renal insufficiency which is the anticoagulant we give
Unfractioned heparin
To echo findings that can be seen with large PE
Bowing of the septum, akinetic right ventricle
Patient has pneumonia, but cannot see it because they’re on steroids. What investigation can help me
CT
Bronchial nodule, lung cancer, Localised wheeze ,recurrent same place pneumonias, in a young patient. Could all be a sign of what
Carcinoid
Main side effect/complication of apnoea of prematurity
Watershed ischaemia in the brain
We know that the stepped approach for croup management is corticosteroids, then epinephrine and intubate. But what do we skip to if the patient has stridor at rest
Go straight to epinephrine
If a patient gets post operative atelectasis, what management can be done
Do CPAP, physiotherapy, pain control. Incentive spirometry kind of his preventative only
If you see low oxygen, shortness of breath, increase respiratory rate, dullness in areas and no breath sounds in places. Following surgery. Just consider atelectasis unless prove otherwise
A lot of UW Qs
Discipline is for inpatient or outpatient pneumonia
For outpatient only
In terms of CURB. Can you remember the numbers
BUN above 20, respiratory rate above 30, blood pressure less than 90
