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What is the definition of chronic cough?
- 1) duration greater than 8 weeks
- 2) non-smoker
- 3) Not on ACEi
- 4) Normal lung function
- 5) Normal CXR
- (i.e. no obvious lung disease)
In order of prevalence, what are the top 3 (4) causes of chronic cough?
- 1) Asthma/eosinophilic bronchitis
- 2) Upper airway cough syndrome (formerly, post-nasal drip)
- 3) GERD
In a normal lung, what happens when pulmonary artery or venous pressureincreases? Generally how high is pulm resistance relative to systolic vasc res
as pressure increases, the resistance decreases due to recruitment and distension
normally this resistance is 1/10 of systolic
What are the numerical definitions of pulm HTN and pulm arteriole HTN
PH: mean pulm art. pressure (PAP)>= 25 mmhg
PAH: same as above + post capp. wedge pressure (right sided capp's) or LVEDP <= 15mm Hg
What are the three major mechanisms of pulm HTN?
- 1) hypoxic vasoconstriction
- 2) decreased area of vascular bed
- 3) RV volume and pressure overload
Describe the approach to PH in categorizing PAH, lung disease, thromboembolitic PH, unclear causes, and heart disease.
- Pre-capillary: PAH
- Low PCWP: Lung disease, TE PH, unclear causes
- post-capp (high PCWP): heart disease
What are the 5 classifications of pulmonary HTN?
- PAH (an orphan disease, no other comp's)
- owing to left heart disease (most common)
- due to lung disease (e.g. COPD)
- chronic TE Pulm HTN
- unclear/multifactorial causes
What are the three elements that combine in PAH?
- 1) vasoconstriction
- 2) vascular wall remodeling
- 3) thrombosis in-situ
What are the three pathways involved in PAH?
- Endothelin (most potent vasoconstrictor in the body)
- Nitric oxide (dilator)
- prostacyclin (dilator)
What are the three major classes in PAH specific therapies
- the prostenoids
- endothelin receptor antagonists
- PDE-5 inhibitors
All of these vasodilate
Remember the three things that lead to PE? What are they?
- Venous stasis
- Endothelial cell damage
- Hypercoagulable states
What are six substances that cause PE?
- 1) clot
- 2) fat
- 3) talc
- 4) air
- 5) septic
- 6) amniotic fluid
What is the most common cause of preventable death in hospitalized patients?
venous thrombo embolism
When should you suspect PE?
sudden dyspnea, chest pain, or collapse 1-2 weeks after surgery
What is on the DDx when someone comes in with sign and symptoms for PE (top 5, other than PE)
- basically the DDx for chest pain:
- Aortic dissection
Define and describe what you would do for a low well's score. What about an intermediate/high score?
Low (0-1): use D-dimer to rule out, if it is positive, then do a CT scan to rule in/out
intermediate or high: go straight to CT scan to rule in or out
How long do you need to anticoagulate in PE? When can you not use warfarin to do this?
- reversible cause (surgery, injury, pregnancy, etc): 3-6 mon
- unprovoked:>3 months and then re-evaluate (high bleeding risk: 3 months, low bleeding risk: extend)
- Irreversible risk factor (ongoing cancer, etc): 12 months to indefinite
Cannot use warfarin in cancer, in pregnant/postpartum ladies, or in high bleeding risk (can reverse heparin, not warfarin)
What are the top three indications for thrombolysis in PE
- 1) Hypotension
- 2) free-floating RA/RV clot
- 3) Patent Foramen Ovale
Describe the A-a gradient and how to calculate it
The difference b/n Alveolar and arterial oxygen. Basically determines if an acceptable amount of the oxygen that makes it down to the alveoli is making it into the blood. Normal is 10-12 mm Hg
A-a = [0.21x(P(barometric)-47)-(Pa(CO2)/0.8)] - Pa(O2)
How do you know if you have a good chest X-Ray
- Rotation: T3 should be between clavicles
- Inspiration: should see 6 anterior - 9 posterior ribs
- Contrast: larynx and costophenic angles visible?
- Exposure: should be able to see the vertebrae behind the heart
What is the DDx of increased A-a gradient? (3)
- -diffusion problem
- -V/Q mismatch
Describe the approach to diagnosing hypoxia (3 steps)
- 1) is Pa(CO2) elevated: if yes, then this is hypoventilation. If no, go to 2
- 2) is the A-a gradient increased: if no, this is low inspired Pi(O2). If yes go to three
- 3) is the hypoxia fixed if you give O2: If yes, V/Q mismatch. If no, this is a shunt
What is your approach for analysing a CXR
- Airways, and hilar Adenopathy
- Bones and Breast shadows
- Cardiac sihouette and Costophrenic angles
- Diaphragm and Digestive tract
- Edges of pleura
- Fields (lung fields)
Compare airspace and interstitial infiltrates on a CXR
airspace: hazy, indistinct margins, respect lobar boundaries, air bronchograms (bronchi become visible when they are filled with pus)
Interstitial: does not respect lobar boundaries, no air bronchograms
What are some causes of airspace being visible on CXR (5)?
Describe the 3 interstitial patterns you see
- reticular - lines
- nodular - dots
- reticulonodular - both of these
What is the DDx for cavitating lesions (nodes) on CXR
- CAVITY mnemonic
- Autoimmune (Wegner's, RA)
- Vascular (septic emboli)
- Infectious (TB, abscess)
- Trauma (pneumatocele)
- Young ( bronchogenic cyst, laryngotracheal papillomatosis)
Where are most LC mets found
- in the LABB
classify and describe lung cancer
- 1) small cell: most likely to produce mets, smoking
- 2) non-small cell carcinoma: less likely to produce mets
- -adenocarcinoma: most common LC, not associated with smoking
- -squamous CC: smoking
- -Large CC: poor prognosis, smoking
What are the 4 things that can cause an anterior mediastinal mass?
- remember the 4 T's
- Terrible lymphoma
When thinking about interstital lung disease what are some important questions to ask (3)?
- occupational Hx (for them and spouse)
- medications or chest irradiation
Identify and describe 5 idiopathic interstitial pneumonias. What Sx are common to all
common Sx: progressive dyspnea and dry cough
- -usual interstitial pneumonia (aka IPF): honeycombing on CT, in old men
- -desqumative interstitial pneumonia: mostly in young males
- -lymphoid interstitial pneumonia
- -non-spec interstitial pneumonia: often related to other diseases (Connective tissue disease, HIV, drugs, etc)
- -acute interstitial pneumonia: 50% mortality
What tips you off to Cryptogenic Organizing Pneumonia
presents like a bacterial pneumonia, but does not respond to Abx treatment
Describe sarcoidosis. how would you diagnose
sarcoidosis is a multi-system granulomatous disease, diagnose with Bx
Which interstitial lung disease go with the following time courses: days-weeks, weeks-months, months-years
- d-w: acute interstital pneumonia, hypersens pneum, cryptogenic organizing pneumonia
- w-m: sarcoidosis, CT disease
- m-y: IPF (UIP), sarcoidosis
How would you treat interstitial lung disease?
anti-inflammatories and removal of offending agent
What are some types/causes of hypersens pneumonitis? What are they all characterized by? How would you treat?
- Farmer's lung: mouldy hay
- malt worker's lung: fungi
- bird feeder's lungs: avian protiens
Char. by: lymphocytic alveolitis and granulomatous pneumonitis
treat: REMOVE FROM EXPOSURE
, steroids, oxygen
What are the three types of pneumoconiosis and where would you expect to see the fibrosis on CXR
- Silicosis: upper>lower lobes, rounded opacities (looks like shot)
- Asbestosis: asbestos fibre looks like dumbell under microscope, bilateral diaphragmatic and pleural plaques are specific for this, lower>upper lobes
- Coal worker's lungs: upper> lower lobes
What is the acute pericarditis triad?
ECG changes, friction rub (sounds like crunchy snow), chest pain (pleuritic, worse laying on back)
What are five functions of the pericardium
- -maintains heart position
- -barrier to infection
- -lubrication between layers
- -secretes prostaglandins
- -restraining effect on cardiac volume
What can cause acute pericarditis?
- usually idiopathic
- also infectious, inflammatory, MI etiologies
- ask about neoplasms or radiation
How would you treat acute pericarditis?
- idiopathic is usually self limited
- treat underlying cause, pain, and inflammation
What is the classic quartet of cardiac tamponade
- -increased JVP
- -tachycardia (heart tries to maintain CO)
- -PULSUS PARADOXUS
How can you differentiate cardiac tamponade from restrictive pericarditis?
-Tamponade: always pulsus paradoxus, electrical alternaans
-RP: rarely pulsus paradoxus, square root sign on catheter, pericardial "knock" due to abrupt stop in filling
describe the pathophysiology of pericardial effusions (cardiac tamponade) and constrictive pericaditis
pericardial effusions (can lead to cardiac tamponade): increased pressure in pericardial cavity reduces venous return, which in turn reduces CO and BP
constrictive pericarditis: rapid filling is ABRUPTLY stopped by a fibrosed pericardium, creating a knocking sound. +/- hypotension
Describe pulsus paradoxus
more than 10 mm Hg drop in sBP on inspiration
Who gets TB? (3)
- -1/3 of people infected with HIV (30x more likely to get TB)
- -highest number of cases are foreign born people
- -highest rates (a per capita) measurement are in Canadian-born aboriginals
describe the disease progression of people infected with TB
- 1) primary infection: 5% get progressive primary infection, 95% go to latent infection
- 2) latent infection: 5% reactivate, 90% get no disease ever. 10% reactivation rate in HIV patients
What are the contraindication to tuburculin skin testing?
- -severe reactions in the test
- -if they have a documented Hx of active TB
- -if they have a viral infection (or had one in the past month)
describe when you would say a TST test is positive
What are the 4 drugs used to treat active TB? Side effects for each
- RIPE mnemonic:
- Rifampin: Hepatitis, rash, GI upset
- Isoniazid (INH): hepatitis, neuropathy
- Pyrazinamide: Hepatitis, rash, aches
- Ethambutamol: optic neuritis
He also had SM on there: causes ear and renal toxicity
What is mult drug res TB (MDR) and extensively drug resistant (XDR) TB resistant to?
MDR: resistant to isoniazide and Rifampin
XDR: same as MDR + any fluoroqionolone + 1 of the 3 injectable 2nd line agents (capremycin, kanamycin, amikacin)
What are the phases of lung development and what are the chances of survival for each
- psuedogladular: no alveoli, no survival (mesenchyme is too thick)
- canalicular (16-24 weeks): gas exchange surface, can survive if all goes well
- Saccular phase (24-36 weeks): will likely survive, lots of gas exchange surf
- alveolar (36-40 weeks): alveolar sacs
What are three things you can do to prevent surfactant problems in neonates?
- small amounts of prenatal corticosteroids to promote lung dev
- surfactant therapy
- avoid excess oxygen exposure
what advice can you give pregnant ladies to decrease asthma in the baby (both before and after birth)
fish oil, vitamin E (avocados, nuts) while pregnant
What dietary/lifestyle advice can you give people with asthma?
- -more omega 3,
- -get adequate magnesium,
- -less salt (less than 1500 mg),
- -increase dietary antoxidants (especially vit C)
- -don't become a fatty
- -chill out (mind-body relaxation)
What is the indication for lung transplant
Chronic end-stage lung disease failing on MAXIMAL medical therapy. Refer when survival is less than two years. Want to get as much out of the old lungs as possible.
What are the absolute contraindications in lung transplant (5)?
- -untreatable advanced dysfunction in other organ
- -malignancy < 2years
- -non curable infection
- -non-compliance with previously issued drugs
- -substance addiction in past six months
What BODE index scores for COPD lung transplant referral, listing
When do you refer/list for pulmonary fibrosis (UIP, NSIP)
refer when you get a positive biopsy for either
- list when UIP + any of the following:
- DLCO less than 39%
- PVC decreased by 10% in 6 months
- honeycombing on HRCT
What diseases would you transplant lungs for?
COPD, pulm fibrosis, cystic fibrosis, PAH
What is hypoxemia?
- -insufficient oxygenation
- -low oxygen tension in the blood
- -decrease of partial pressure of oxygen in blood
What is the definition of resp failure? What are the subtypes?
- PaO2 < 60 mm Hg AND/OR PaCO2 > 46 mm Hg
- AND pH<7.35
- Type I: involves lung itself. Acute Hypoxemic RF -> low O2, alkalosis, normal or low CO2
- Type II: failure of alveolar vent: Acute Hyoxemic Hypercapnic RF. All three of the above criteria.
What are the 5 causes of hypoxemia? What is their effect on A-a grad
- 1) V/Q mismatch (increases it)
- 2) alveolar hypoventilation (no change)
- 3) R to L shunt (increases it)
- 4) low ambient oxygen (mountains) (no change)
- 5) diffusion block (like in interstitial lung disease) (increased)
What is the cut off for acidosis and alkalosis
- acidosis < 7.35
- alkalosis > 7.45
What are the 4 causes of hypoxia?
- reduced oxygen delivery to tissues
- decreased tissue oxygen uptake
What is the Lights criteria for differentiating transudative and exudative pleural effusions?
- transudative (need all three):
- -protein (pleural/serum): <0.5
- -LDH (pleural/serum): <0.6
- -Pleural LDH: < 2/3 upper limit of N serum LDH
exudative (only need one): > than all of the above values
Transudative means formation and absorption of pleural fluid is faulty (HTN, low oncotic pressure, etc; only fluid is getting through)
exudative means faulty pleural capillaries (everything is getting through)
What are the risk factors for pneumothorax?
- -iatrogenic (thoracentesis, etc)
- -underlying lung disease
What are the top five things on the DDx for dyspnea?
- heart failure
Top 3 treatments for asthma with names
- beta 2 agonists: Salbutamol
- Anti-cholinergics: Atrovent
- Corticosteroids: bethamethasone, prednisone
What do you see on PE for COPD?
- Signs of hypoemia:
- Signs of hypercapnea
- -altered mental status
What is a normal PaO2?
90-100 mm Hg
What is a normal A-a gradient?
normal is 10-12 mm Hg, but this increases with age.
What shifts the oxygen curve to the right?
- CADET right face
- DPG increase
Think that these are the conditions in an exercising muscle
What does DLCO depend on?
- membrane thickness
- hemoglobin conc
- cardiac output
low low flow oxygen, how much does 1 L of O2 give you for oxygen content? What about for every litre above that?
- 1L - 24%
- an additional 3-4% for every litre after that