Respiratory Flashcards
Helpful videos
https://www.youtube.com/watch?v=ikwN7CLTBlY
COPD https://www.youtube.com/watch?v=qn0KHo8Y6B4
ASTHMA
https://www.youtube.com/watch?v=NbfevYRM2vQ
RSV AND BRONCHIOLITIS
https://www.youtube.com/watch?v=Y62TCz3reZc
COR PULMONALE
https://www.youtube.com/watch?v=UQGRcg35Dmk
PLEURAL EFFUSION
https://www.youtube.com/watch?v=gASiQ2I_4KY
LUNG CANCERS
https://www.youtube.com/watch?v=5DmUfK5gz5g
TB
https://www.youtube.com/watch?v=6P6zBHpWiGA
PNEUMONIA
https://www.youtube.com/watch?v=IAQp2Zuqevc
CF
https://www.youtube.com/watch?v=CqFsAwCFvCM
EMPHYSEMA
https://www.youtube.com/watch?v=TEuSV_7gWA8
CHRONIC BRONCHITIS
https://www.youtube.com/watch?v=Y29bTzKK_P8
COVID 19
https://www.youtube.com/watch?v=DqnrqV6ogGw
Lateral CXR
Taken in left lateral position.
Right ribs magnified and posterior.
Black hole on lateral is LUL bronchus, in front of this is RPA and on top is LPA.
On frontal, left hilum always 1cm higher than right.
Retrotracheal triangle (Raiders triangle) on lateral. Opacity in here is aberrant right subclavian artery
Prosthetic cardiac valves
Pulmonic valve most superior
Tricuspid valve most anterior
Aortic in front of mitral on lateral
Azygos lobe fissure
Variant anatomy. Happens when azygos vein is displaced laterally during development. Resuts in deep fissure is RUL. Not an accessory lobe but variant of RUL. 4 layers of pleura
Segmental lung
RUL
apical, anterior, posterior
RML
Medial, lateral
RLL
Superior, posterior, lateral, anterobasal, medial basal
LUL
anterio, apical posterior
LUL-L
superior, inferior
LLL
Superior, posterior, lateral, antero-medial basal
Variant airway anatomy
PIG/TRACHEAL BRONCHUS
Comes off right trchea prior to bifurctaion. Means nothing clinically but can get air trapping or recurrent infections from impaired ventilation. Recurrent RUL penumonia in kid.
CARDIAC BRONCHUS
Bronchus off bronchus intermedius, opposite to origin of RUL bronchus. Usually blind ending and is supernumary. Means nothing clinically but can get recurrent infection
Mediastinal anatomy
SUPERIOR
Inf border is oblique plane from sternomanubrial junction
ANTERIOR
Posterior border is pericardium
MIDDLE
Heart, pericardium and bifurcation of trachea are all included. Posterior to trachea and anterior to vertebral bodies
POSTERIOR
Back of heart to spine. Contains esophagus, thoracic duct and descending aorta
Mediastinal variant anatomy
PULMONARY VEINS
Pulmonary vein anatomy is variable. Typically 2 upper and 2 lower on each side. Main variant is separate vein draining RML
PROX INTERRUPTION OF PULMONARY ARTERY
Congenital absence of right of left PA with more distal pulmonary vasculature present. Could be shown as volume loss in one hemithorax then contrast CT with only one PA. Seen on opposite side to aortic arch. Associated with PDA. Interrupted left PA is seen with TOF and truncus. Recurrent infections due to lack of blood supply
Atelectasis (incomplete lung expansion)
OBSTRUCTIVE/ABSORPTIVE
Complete obstruction of an airway. No air entering, current air eventually absorbed. Obstructing neoplasm, mucous plugging, foreign body
COMPRESSIVE
Direct mass effect on lung. Usually from pleural effusion or next to mass/hiatal hernia/bleb/tortuous aorta etc
FIBROTIC
Fromscarring/fibrosis which fails to allow lung to collapse completely. Usually TB, radiation or other infections. Anything with fibrosis.
ADHESIVE
Loss of surface tension/inadequate pleural adherence of alveolar walls - surfactant deficiency. Alveoli become unstable and collapse. Causes RDS (premmies), ARDS, PE
Atelectasis primary and secondary signs
SHADOW
Shadow made by opacified collapsed lung. Direct sign, most obvious.
SILHOUETTE
Loss of interface between opacity and adjacent normal structures. Usefull in localization
SHIFT
Movement of structrues as they are pulled toward site of volume loss. Space occupying things push away, atelectasis pulls toward
Lobar patterns collapse
RML
Increased density right heart border with loss of that border. Lateral shows anterior density over heart
- RML/Lady Windermere syndrome is chronic collapse with MAI syndrome in elderly women too proper to cough. Additional nodules and bronchiectasis. Lungula often involved.
RLL
Increased density right heart border similar to RML but you still have right heart border visible. Mediastinal vessels can be pulled to right creating triangle of opacity rightward of trachea (superior triangle sign).
RLL and RML
Sneaky. Loss of visualization of right hemidiaphragm and right heart border. Reverse S sign of Golden is RUL collapse with obstructing mass
RUL
Horizontal fissure bows upward. Hilum may elevate.
Lobar patterns collapse continued
LUL
More subtle with increased density medially. No wel defined borders. Non visualization of aortic knob. May get peaking of diaphragm from upward traction.
Air Sickle sign of hyperinflated apical segment of LLL pinned between medial edge of collapsed segment and aortic arch
LLL
Opacity hidden behind heart. Lateral more obvious with triangle opacity. Flat waist sign is flattened appearance of the contours of hilum and heart border
CXR localization
CERVICOTHORACIC SIGN
Takes advantage of posterior junction line. Things above the clavicles are in posterior mediastinum
HILUM OVERLAY SIGN
Mass at level of hilum arising from hilum with obliterate silhouette of pulmonary vessels. If you can see vessels through mass then it is either anterior or posterior.
PULMONARY vs MEDIASTINAL ORIGIN
Pulmonary will have air bronchograms and make an acute angle with lung. Mediastinal will make an obtuse angle with lung
Bacterial infection
STREP PNEUMONIAE
Lobar consolidation.Favours lower lobes. Most common in AIDS
STAPH AUREUS
Bronchopneumonia, patchy opacity. Bilateral, can make abscess, endocarditis.
KLEBSIELLA
Bulging fissure, exuberant inflammation. Pleural effusions, empyema, cavitates. Currant jelly sputum. Alcoholics, nursing home patients.
HAEMOPHILUS INFLUENZA
Bronchitis, bilat lower lobes. COPD, asplenic patients.
PSEUDOMONAS
Patchy opacities with abscess. ICUers on ventilators. Cavitates in immunosuppressed.
ASPIRATION
Anaerobes, can cavitate. Posterior lower lobes when supine. Favours right side. Empyema, can get bronchopleural fistula.
ACTINOMYSES
Peripheral lower lobes. Can be aggressiveand invade chest wall. Dental procedure gone bad, mandible osteo, aspiration.
MYCOPLASMA
Fine reticular pattern on CXR, patchy airspace opacity. Tree in bud.
Post bone marrow transplant
Pulmonary infections in nearly 50% people after bone marrow transplant. Most common cause of death in this group.
EARLY NEUTROPENIC
0-30 days. Pulmonary oedema, haemorrhage, drug induced lung injury. Fungal pneumonia (invasive aspergillosis)
EARLY
30-90 days. PCP, CMV.
LATE
>90 days. Bronchiolotis obliterans, cryptogenic organizing pneumonia
AIDS related pulmonary infection
PCP
Most classic AIDS infection. Ground glass opacities bilaterally in perihilar regions with sparing of periphery. Thin walled cysts can occur.
Most common airspace opacity - Strep Pneumonia
Ground glass - PCP
Flame shaped perihilar opacity - Kaposi Sarcoma
Persistent opacity - Lymphoma
Lung cysts - LIP
Lung cysts and ground glass and PTX - PCP
Hypervascular LNs - Castleman or Kaposi
AIDS infection by CD4
> 200 bacterial infections, TB
<200 PCP, atypical mycobacterial
<100 CMV, disseminated fungal, mycobacterial
TB
PRIMARY
Inhaled bug, causes necrosis. Body attacks and causes granuloma (Ghon focus). End up with bulky nodal expansion which can calcify and form Ranke complex. Bulky nodes cause compression leading to atelectasis. If node ruptures get endobronchial or haematogenous spread. Haematogenous spread manifests asmiliary patten. Cavitation not common in primary.
PRIMARY PROGRESSIVE
Local progression with development of cavitation (at initial site of infection and/or haematogenous spread. Primary progression uncommon. HIV a risk factor along with anything that akes you immunosuppressed such as transplant patients, steroids. Similar to post primary disease.
LATENT
Positive PPD with a negative CXR and no symptoms. If ou have TB vaccine, considered latent.
POST PRIMARY/REACTIVATION
5% of time this happens. Endogenous reactivation of latent infection. Classic location apical and posterior upper lobe and superior lower lobe (more oxygen, less lymphatics). Post primary infection tend to have progression. Development of cavities. Rasmussed aneurysm is in close by vessel in setting of TB cavitation
TB facts
Pleural invovlement can happen at any time after intitial infection. Pleural fluid usually negative need to biopsy pleura.
Primary = no cavity
Post primary/primary progressive = cavity
Ghon lesion = calcified TB granuloma and sequale of primary TB
Ranke complex = calcified TB granuloma and calcified hilar LNs, healed primary TB
Bulky hilar and paratracheal LNs = in kids
Reactivation TB = posterior/apical upper lobes, superior lower lobes
Miliary spread = haematogenous dissemination
Reactive TB pattern = cavitation seen in HIV patient CD4<200
Primary progressive pattern = adenopathy, consolidation, miliary spread
Non TB mycobacteria
CAVITATORY(CLASSIC)
Usually MAC. Favours old white man with COPD. Looks like reactivatin TB. Upper lobe cavitatory lesion with adjacent nodules
BRONCHIECTATIC (NON CLASSIC)
Lady Windermere. Favours old white lady. Asymptomatic, dont cough. Tree in bud with cylindrical bronchiectasis in RML and lingula
HIV PATIENTS
CD4<100. GI infection disseminated in blood. Big spleen and liver. Can look like anything. Mediastinal LNs common.
HYPERSENSITIVITY PNEUMONITIS
Hot tub lung. Aerosolized bugs. Ill defined ground glass centrilobular nodules.
Aspergillus
NORMAL IMMUNE Fungus ball (aspergilloma) in pre-existing cavity. Didnt make the cavity, found it. Cavity can be from any cause.
SUPPRESSED IMMUNE
Invasive aspergillus. AIDS or transplant patients.
‘halo’ sign is cosolidation with ground glass halo - halo is invasive component.
‘air crescent sign’ is thin cresecent of air within consolidative mass, represents healing as necrotic lung separates from parenchyma.
HYPERIMMUNE
ABPA allergic bronchopulmonary aspergillosis. Long standing asthma or CF. Central sacuular bronchiectasis with mucoid impaction ‘finger in glove’. Need elevated serum immunoglobulin E or positive skin hypersensitive test against fungus. Total IgE >1000
Mucormycosis
Aggressive fungal infection usually in impared patients (AIDS, steroids, diabetics). Invasion of mediasitnum, pleura and chest wall
CMV
Two scenarios:
- Reactivation of latent virus after prolonged suppression (post bone marrow transplant)
- Infusing of CMV positive marrow or in other blood products.
Timing for bone marrow patients is 30-90 days. Get multiple nodules, ground glass or consolidative.
Viral trivia
MEASLES
Multifocal GGO with small nodular opacities. Pneumonia befor or after skin lesions. Complications higher in preg and immunocompromised.
INFLUENZA
Coalescent lower lobe opacity. Pleural effusion rare.
SARS-CoV1
Lower lobe predominant GGO
VARICELLA
Multiple peripheral nodular opacities. Small round calcific lung nodules in healed version. Chickenpox in kids. Pneumonia in immunicompromised adults.
EBSTEIN BARR
LN enlargement. Uncommonly affects lung. Big spleen.
Covid 19/SARS CoV 2
SARS CoV 2 is the virus,COVID 19 refers to 2019 pandemic. Increased risk of DVT, PE, stroke, MI or arterial or venous clots. Increased risk of barotrauma from mechanical ventilation.
CXR
Bilateral peripheral lower zone multifocal opacities. Pleural effusion uncommon.
CT ACUTE
Bilateral peripheral GGO, bronchovascular thickening. Crazy paving and reverse halo.
CT LATE >14 DAYS
Fibrous stripes in regions of previous disease
Septic emboli
Multiple causes. Infected tricuspid valves, infection in body, infected catheters, teeth etc.
Lower lobe predominant, peripheral nodular densities and wedge shaped densities (can infarct). Can cavitate. Feeding vessel sign is nodule with big vessel going into it. Empyema and PTX complications.
LEMIERRE SYNDROME
Jugular vein thrombosis with septic emboli usually after oropharyngeal infection or ENT surgery.
Most common bacteria is fusobacterium necrophorum
CAVITY is acronym Cancer Auto immune (Wegeners/Rheumatoid/Caplan) Vascular septic or bland emboli Infection TB Trauma pneumatocoele Y young or congenital CCAM sequestration
Lung cancer risk factors
RISK FACTORS
>30yo, exposure to harmful chemicals, lung fibrosis, COPD and family history. Fibrosis increases risk 10x. Smoking remains main risk factor
Solitary pulmonary nodule SPN
Round/oval lesion <3cm. Surrounded by lung parenchyma with no adenopathy or effusion. Can have numerous “solitary’ nodules on lungs.
4 benign calc patterns
Solid/diffuse, laminated, central, popcorn.
Eccentric calc is most suspicious calc. Part solid lesion with GG component is most suspicious morphology
BENIGN
Presence of fat, rapid doubling time <1 month, slow doubling time stable at 2 years
MALIGNANT
SPiculate margins, air bronchogram through nodule (think adenocarcinoma in situ), partially solid with GG component
PET for >1cm
Solid nodule HOT cancer, COLD benign
GG nodules HOT infection, COLD cancer
SPN/cancer trivia
Lung cancer more common right lung.
70% cancers in upper lobe, except in pulmonary fibrosis where lower is more common.
SPN in setting of H&N cancer is more likely to be primary bronchogenic carcinoma than metastasis (similar risk factors)
Lung cancer rare <40 (unless AIDS)
Air bronchograms 5x more common in malignant SPN
Air bronchograms 50% BACs
Lung cancer subtypes
SMALL CELL
Central. Most common lung ca to cause SVC obstruction and paraneoplastic syndromes. Bad prognosis. Paraneoplastic syndromes associated with SIADH and ACTH. Lamberteon Eaton syndrome is paraneoplastic syndrome with proximal muscle weakness.
NON SMALL CELL - SQUAMOUS
Central. Strong association with smoking. Cavitation classic. No TTF1 expression. Paraneoplastic syndromes can be associated with ectopic parthyroid hormone.
NON SMALL CELL - LARGE CELL
Peripheral. Least common. Usually large >4cm.. ad prognosis
NON SMALL CELL - ADENOCARCINOMA
Peripheral. Most common 35%. Favours upper lobe. ost likely to present as SPN. Most common in non smoker. Association with pulmonary fibrosis and smoking. May only present with lymphadenopathy.
Central tumours haemoptysis, peripheral tumours pleuritic chest pain.
Bronchoalveolar carcinoma (adenocarcinoma in situ spectrum)
PREINVASIVE LESION SPECTRUM Atyical adenomatous hyperplasia of lung (AAH) Adenocarcinoma in situ Minimally invasive adenocarcinoma (MIA) Invasive mucinous adenocarcinoma
The larger the solid component within a part solid nodule is the more likely it is to be malignant.
Superior sulcus/Pancoast tumour
Typically non small cell cancer. SHould be apical tumour with at least shoulder pain, sometimes C8-T2 radiculopathy and Horner syndrome.
MRI is tool of choice for staging.
Contraindication to surgical resection is invasion of vertebral body, invasion of spinal canal, involvement in upper brachial plexus, diaphragm paralysis or distal mets
Lung cancer staging
Use TNM staging
TUMOUR
T1 = <3cm
T2 = 3-5cm, invading pleura, invading main bronchus, obstruction extending to hilum
T3 = 5-7cm, invades chest wall, invades pericardium, invades phrenic nerve, satellite nodule in same lung lobe
T4 = >7cm, invades mediastinal fat or great vessels, invades diaphragm, involves carina, satellite nodules in another lobe
NODES
N1 = ipsilateral within lung up to hilar nodes
N2 - ipsilateral mediastinal or subcarinal nodes
N3 = contralateral mediastinal or contralateral hilum or scalene/supraclavicular nodes
Lung cancer staging continued
CT unreliable for staging. PETCT far superior regardless of size and threshold. Important boundary to identify is distinction between level 1 and 2 nodes as this may change resectability
Level 1 nodes are above line from lower clavicles to upper manubrium (thoracic inlet).
CONTRAINDICATIONS TO RESECTION Growth through a fissure Invasion of pulmonary vasculature Invasion of main bronchus Invasion of both upper and lower lobe bronchi N2 if tumour is >5cm and N3 disease. Multilobar disease Malignant pleural effusion
Distinction between 3a and 3b is critical as 3b is unresectable.
Lung cancer treatment
WEDGE RESECTION VS LOBECTOMY
If 1a or 1b is peripheral and <2cm can consider wedge resection. Advantage over lobectomy is preserving pulmonary reserve. If >3cm, lobectomy normally done.
BRONCHOPLEURAL FISTULA
Uncommon complication of pneumonectomy. Normally space fills with fluid, if this preogressively fills with air thats a fistula.
COMPENSATORY EMPHYSEMA
Post pneumonectomy syndrome. Vocab used to describe hyperexpansion of one lung to compensate for other.
RADIATION CHANGE
Appearance of radiation pneumonitis is variable and based on volume of lung involved/how much radiation given and if chemo also used. Ribs within field are susceptible to degradation and fracture. In RFA and MWA normal to see bubbles in lesion immediately after.
RECURRENT DISEASE
Recurrence rates relatively high. Look at periphery of radiation bed, regional nodes and bronchial stump. Radiaiton morphology is not round so if you see something round consider recurrence. Other suspicious findings are enhancing solid tissue along resection line which is enlarging. New enlarged mediastinal LNs, new pleural effusion
Mimics/other cancers
PULMONARY HAMARTOMA
Macroscopic fat and popcorn calcification. Most common benign lung mass. Usually incidental. Can be hot on PET but still benign.
KAPOSI SARCOMA
Most common lung tumour in AIDS CD4 <200 (lymphome is 2nd). Tracheobronchial mucosa and perihilar lung are favoured. Buzzword is flame shaped. Most common lung tumour in AIDS, most common hepatic neoplasm in AIDS. Slow growth, asymptomatic patient despite bad look. Blood pleural effusion common 50%. Thallium positive, gallium negative
Metastases
DIRECT INVASION
Most common is esophageal carcinoma, lymphoma or germ cell tumour. Seen in cancer of mediastinum, pleura or chest wall.
HAEMATOGENOUS
Most common manifestation is pulmonary nodules in random distribution favouring lower lobes. Canonball mets classic from RCC or chorio. Nodules smoother than primary. Main culprits breast, kidney, thyroid, colon, H&N squam. Feeding vessel sign is prominent pulmonary vessel heading into nodule but can be seen in septic emboli too.
LYMPHANGITIC CARCINOMATOSIS
Most common casue of unilateral LC is actually BAC invading lymphatics. Most common extrathoracic is breast, stomach, panc and prostate. Nodular thickening of interlobular septa and subpleural intersititium. Does not distort pulmonary lobule
Pulmonary lymphoma
PRIMARY
Rare, usually NHL. 80% low grade MALT
SECONDARY
Pulmonary involvement of systemic lymphoma. Much more common than primary. NHL more common overall but HL more common to involve lungs. HL get nodes and parenchyma, NHL parenchyma only.
PTLD
After solid organ or stem cell transplant. Usually within a year. B Cell lymphoma with a relationship with EB virus. Nodal and extra nodal disease. Typical look is well defined pulmonary nodules/mass, patchy air space consolidation, halo sign, interlobular septal thickening.
AIDS RELATED PULMONARY LYMPHOMA
Second most common lung tumour in AIDS (Kaposi first). High grade NHL. Relationship with EBV. CD4 <100. Presentatin variable, nodules 1-5cm. AIDS patient with lung nodules, pleural effusion and lymphadenopathy = lymphoma
Pulmonary NHL vs HL
SECONDARY NHL
80-90% cases. 45% have intrathoracic disease at presentation. 25% have pulmonary parenchymal disease. Pulmonary involvement in absence of mediastinal disease frequently occurs.
SECONDARY HL
10-20% cases. 85% have intrathoracic disease at presentation. 40% have pulmonary parenchymal disease. Pulmonary involvement almost always associated with intrathoracic LN enlargement.
Nukes
THALLIUM
Potassium analog, anything with functioning Na/K/ATPase are alive and will be thallium positive.
GALLIUM
Iron analong. Iron is inflammatory marker acute phase reactant. Things that are inflamed - infection, active sarcoid, most cancers are Gallium HOT.
Lymphoma is Gall and Thall HOT
kaposi is Thall HOT Gall COLD
Congenital
POLAND SYNDROME
Unilateral absence of pec muscle. Causes hyperluscent lung. Can have other arm/hand abnormalities.
BRONCHIAL ATRESIA
Congenital obliteration of short segment of lobar, segmental or subsegmental bronchus near origin (usually apical posterior LUL). Vascular insult in utero. Nodule near hilum which is mucoid impaction in blind ending brochus. Hyperluscent segment. Asymptomatic unless receurrent pneumonia. Primary differential is endobronchial tumour
AVM
Can occur sporadically. For purpose of MCQ, think HHT (Osler Weber Rendu). Usually in lower lobe and can be a source of right to left shunt. (stroke and brain abscess). Treat once afferent vessel is 3mm.
PERSISTENT LEFT SVC
Most common congenital venous anomaly of chest. Confusing PICC/Pacemaker line location. Drains into coronary sinus or rarely into LA.
SWYER JAMES
Unilateral lucent lung. Typically after viral lung infection in childhood resulting in post infectious obliterative bronhiolitis. Size of effected lobe is smaller than than the other.
HORSESHOE LUNG
Connects at posterior basilar segments of lower lobes behind heart. Associated with scimitar
Cystic lung disease
PULMONARY LCH
Smoker, young 20-30. Centrilobular nodules upper lobe predominance. Nodules eventually cavitate into cysts which begin thin walled then get thicker. Bizarre shaped cysts when they merge. Upper/mid zone predominant. 50% case spontaneously resolve, especially if stop smoking. Spares costophrenic angles.
LYMPHANGIOMYOMATOSIS LAM Tuberous sclerosis (AMLs, tubers) and childbearing age women. Estrogen dependent. Thin walled round cysts. Uniform or diffuse distribution. Usually progressive despite attempts at hormonal therapy (tamoxifen). Association with chylothorax
BIRT HOGG DUBE (BHD)
Bilateral oncocytomas, chromophobe RCC. Bunch of gross skin stuff. Thin walled oval floppy cysts. Lower zone predominant.
Lymphocytic Interstitial Pneumonitis LIP
Benign lymphoproliferative disorder with infiltration into lungs. Association with autoimmune (SLE, RA, SJOGRENS) Sjogrens is in 25% cases. Other one is HIV which is LIP in young patient. Also association with Castlemans. Cystic lung disease is usually thin walled deep within lung parenchyma and predominantly with Sjogrens.
LIP = Sjogrens and HIV (kids)
Cysts and GG nodules
Pneumocystis pneumonia PCP
Most common opportunistic infection in AIDS. GG, predominantly in hilar and mid lung zones. Pneumatocoeles in 30% cases. May have bilateral thin walled upper lung predominant cysts. Gallium shows diffuse uptake.
AIDS and GG lungs = PCP
Cystic form of PCP (after aerosolized prophylaxis) has apical predominant thin walled cysts. High risk for PTX
Vanishing lung syndrome
Idiopathic cause of giant bullous emphysema resulting from avascular necrosis of lung parenchyma and hyperinflation. Favours bilateral upper lobes and is defined as bullous disease occupying at least one third of a hemithorax. Usually young man. 20% have alpha 1 antitrypsin deficiency. Tension PTX is complication.
RF are smoking, alpha 1 antitrypsin deficiency, male
Honeycomb lung
Should think of UIP straight away. However, honeycombing is seen with a variety of causes of end stage fibrotic lung processes. Tightly clustered subpleural cysts. Walls often thick.
