Respiratory Flashcards

1
Q

Helpful videos

A

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

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2
Q

Lateral CXR

A

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

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3
Q

Prosthetic cardiac valves

A

Pulmonic valve most superior
Tricuspid valve most anterior
Aortic in front of mitral on lateral

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4
Q

Azygos lobe fissure

A

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

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5
Q

Segmental lung

A

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

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6
Q

Variant airway anatomy

A

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

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7
Q

Mediastinal anatomy

A

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

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8
Q

Mediastinal variant anatomy

A

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

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9
Q

Atelectasis (incomplete lung expansion)

A

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

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10
Q

Atelectasis primary and secondary signs

A

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

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11
Q

Lobar patterns collapse

A

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.

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12
Q

Lobar patterns collapse continued

A

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

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13
Q

CXR localization

A

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

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14
Q

Bacterial infection

A

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.

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15
Q

Post bone marrow transplant

A

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

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16
Q

AIDS related pulmonary infection

A

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

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17
Q

AIDS infection by CD4

A

> 200 bacterial infections, TB
<200 PCP, atypical mycobacterial
<100 CMV, disseminated fungal, mycobacterial

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18
Q

TB

A

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

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19
Q

TB facts

A

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

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20
Q

Non TB mycobacteria

A

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.

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21
Q

Aspergillus

A
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

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22
Q

Mucormycosis

A

Aggressive fungal infection usually in impared patients (AIDS, steroids, diabetics). Invasion of mediasitnum, pleura and chest wall

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23
Q

CMV

A

Two scenarios:

  1. Reactivation of latent virus after prolonged suppression (post bone marrow transplant)
  2. 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.

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24
Q

Viral trivia

A

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.

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25
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
26
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 ```
27
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
28
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
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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
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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.
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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.
32
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
33
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
34
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.
35
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
36
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
37
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
38
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
39
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.
40
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
41
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
42
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.
43
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
44
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
45
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
46
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.
47
Emphysema
Permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of the alveolar wall without clear fibrosis. CXR Flattening of hemidiaphragms. AP diameter increases. Retrosternal clear spaces enlarges.Paucity or pruning of vessels. COPD trivia Diffuse coronal narrowing of trachea, sparing extrathoracic portion. Can have surgery to remove bad lung (volume reduction). CENTRILOBULAR By far most common. Asymptomatic elderly. Apical to basal gradient favouring upper zones of each lobe. Focl lucencies within secondary pulmonary lobule often with central dot representing central bronchovascular bundle. Central dot sign is buzzword. Dominant in smokers PANLOBULAR Favours lower lobes. More uniform distribution accross parts of secondary pulmonary lobule. Associatin with alpa 1 antitrypsin deficiency. Ritalin lung can have this pattern. Lower lobe predominance. Smoking accelerates process. PARASEPTAL Adjacent to pleura and septal lines with peripheral distribution within secondary pulmonary lobule. Affected lung is almost always subpleural and demonstrates small focal lucencies up to 10mm. Looks like honeycombing but less than 3 bubbles thick. Smoking vs idiopathic
48
Pneumoconiosis
Inhaled and upper lobe predominant. Centrilobular or perilymphatic nodules
49
Asbestos
ASBESTOS EXPOSURE Similar to UIP. Parietal pleural thickening. Asbestosis is fibrosis associated with exposure not the the actual exposure. 20 year latency between initial exposure and develoment of lung cancer or mesothelioma. Association with extrapulmonary cancer including peritoneal mesothelioma, GI/renal/laryngeal cancer and leukemia. benign pleural effusions earliest phenomenon at 5 years past exposure. BENIGN ASBESTOS RELATED CHANGES Pleural effusion earliest and most common. Pleural plaques can develop 20-30 years after with calcs at 40 years. Plaques spare apices and costophrenic angles. Round atelectasis sometimes called asbestos pseudotumour
50
Malignant mesothelioma
Most common cancer of pleura. 80% have had asbestos exposure. Development not dose dependent. Lag time 30-40 years. Circumferential pleural thickening extending to medial pleura near heart. Pleural thickness >1cm. Extension into fissure suggestive.
51
Silicosis
Miners and quarry workers. SIMPLE Multiple nodular opacities favouring upper lobes with egg shell calcification in LNs. Also get perilymphatic nodules COMPLEX Progressive massive fibrosis. Large masses in upper lobes with radiating strands. Can sometimes cavitate - raises suspicion of TB. SILICOTUBERCULOSIS Silicosis raises suspicion of TB 3 fold. If see cavitation, consider TB
52
Coal workers pneumoconiosis
Result of exposure to washed coal. Simplae and complicated form. Increased risk of TB. SIMPLE Multiple nodular opacities with calcifications showing a central dot. Perilymphatic distribution. COMPLEX Progressive massive fibrosis similar to silicosis.
53
Secondary pulmonary lobule
Basic unit of pulmonary structure and function. Smallest part of lung that is surrounded by connective tissue. In the middle runs a terminal bronhchiole with an accompanying artery. Around the periphery runs veins and lymphatics.
54
Nodules
PERILYMPHATIC Subpleural and peribronchovascular. Sarcoid, lymphangitic spread, silicosis RANDOM Pleural nodules, no predominance Miliary TB, mets, fungal CENTRILOBULAR No pleural nodules Infection, RB-ILD, Hypersensitivity pneumonitis
55
Interlobular septal thickening
Reticular abnormality that outlines the characteristic shape and size. Kerley B lines on CXR SMOOTH/SYMMETRIC Pulmonary oedema NODULAR/ASYMMETRIC Lymphangitis carcinomatosis
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Honeycombing
Cystic areas of lung destruction in a subpleural location. Hallmark of UIP. Paraseptal emphysema is a mimic but distinction made by how many rows of bubbles One row = paraseptal emphysema 2-3 rows = honeycombing
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Idiopathic interstitial pneumonias
``` CAUSE Idiopathic Collagen vascular disease Medications Inhalation ``` ANSWER UIP - bad prognosis Not UIP - does ok
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Usual interstitial pneumonia UIP
Most common ILD. If idiopathic, IPF. Reticular pattern with reduced lung volumes. ``` Traction bronchiectasis Honeycombing Heterogenous Reticular abnormalities Subpleural and basal predominant ```
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Fibrosis and cancer
Pulmonary fibrosis is RF for cancer. Cancer favours lower lobes in fibrosis Favours interface between fibrotic syts and normal lung, Progressive wall thickening or developing nodule within a cyst is suspicous for cancer.
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Non specific interstitial pneumonia NSIP
Less common than UIP. Homogenous inflammation or fibrosis (UIP heterogenous). Common in collagen vascular disease (esp scleroderma) and drug reactions. Cellular or fibrotic ``` Ground glass Gradient less obvious but still lower lobes Homogenous histology Micronodules Subpleural sparing ``` Lower lobe posterior peripheral predominance with subpleural sparing in 50%. Immediate subpleural sparing is highly suggestive. Ground glass is NSIP equivalent of honeycombing.
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RB-ILD and DIP
Smoking related diseases. RB-ILD Apical centrilobular ground glass nodules. Upper lobe predominant. Respiratory bronchiolitis and symptoms = RB-ILD. DIP (desquamative interstitial pneumonia) More diffuse GGO with patchy or subpleural distribution. 50yo heavy smokers. Peripheral lower lobe predominant GGO with small cystic spaces
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Sarcoid
Multi system disease that creates non-caseating granulomas. 20-40yo. lungs most commonly affected 90%. Acute sarcoid is Lofgren syndrome. Bilateral hilar LN enlargement, arthritis (ankles) and erythema nodosum. Mediastinal LNs seen 60-90% in 1-2-3 pattern (bilateral hilar and right paratracheal. Perilymphatic nodules with upper lobe predominance. Late changes include upper lobe fibrosis and traction bronchiectasis. Late stage can get aspergillomas. ``` CXR staging 0 = normal 1 = Hilar/mediastinal LNs only 2 = Nodes and parenchymal disease 3 = parenchymal disease 4 = end stage fibrosis ```
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CHF
Can mimic ILD on CXR. CCF can occur due t cardiac failure, fluid overload, high resistance in circulation. STAGE 1 Redistribution. Cephalization of vessels, big heart, big vascular pedicle. STAGE 2 Interstitial edema. Kerley lines, peribronchial cuffing, less distinct contour of central vessels. STAGE 3 Alveolar oedema. Airspace fluffy opacity Pleural effusion
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Right heart failure
Less common than LHF. LHF is most common cause of RHF. LHF causes pulmonary venous HTN which causes pulmonary arterial HTN which causes RHF. Also can be caused by chronic PE, right isded valve issues (tricuspid regurg). Imaging sees dilated azygous vein, RA enlargement, SVC dilatation, ascites, big liver and contrast reflux into hepatic veins.
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Swan Ganz catheter
Used to measure pressure in LA, evaluate cardiac output and help cardiogenic vs non cardiogenic ARDS forms of pulmonary oedema, Catheter normally positioned between MPA and interlobar arteries (can be prox right or left MPA). Tip too far out can cause pulmonary infarcts. Too far in can cause arrythmias
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Lung transplant
For end stage pulmonary disease. IMMEDIATE <24 hours Donor recipient size mismatch Hyperacute rejection EARLY 24 hours - one week Reperfusion injury Air leak/persistent pneumothorax INTERMEDIATE 8 days - 2 months Acute rejection Bronchial anastomotic complications LATE 2 - 4 months CMV infection ``` LATER >4 months Chronic rejection Cryptogenic organizing pneumonia PTLD Upper lobe fibrosis ```
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Transplant continued
CHRONIC REJECTION/BRINCHIOLITS OBLITERANS Major late complication, affects at least half of the transplants at 5 years. Bronchiectasis, bronchial wall thickening, air trapping, and interlobular septal thickening. Air trapping on expiration after 6 months is chronic rejection RECURRENCE OF PRIMARY Sarcoid most common recurrent primary around 35% LUNG CANCER AFTER TRANSPLANT Native lung still diseased. Highest rate with pulmonary fibrosis. Most common RF heavy tobacco
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Pulmonary alveolar proteinosis PAP
Aunt minnie. Crazy paving (interlobular septal thickening with ground glass. Primary 90% or secondary 10%. Secondary causes are cancer or inhalation (silico-proteinosis). Increased risk of nocardia infections. Smoking is strongly associated. Can progress to pulmonary fibrosis. Treatment is bronchoalveolar lavage. CRAZY PAVING Interlobular septal thickening and GGO. Isnt always PAP. Differential includes common things like oedema, haemorrhage, BAC, acute interstitial pneumonia and COVID.
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Lipoid pneumonia
Endogenous vs exogenous EXOGENOUS Seen in older people who drink/aspirate mineral oil. Can also be seen with aspiration of vegetable oil or other animal oils. Low attenuation/fat density in consolidation. ENDOGENOUS More common results from post obstructive processes. Build up of lipid lade macrophages.
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Organizing pneumonia
Used to be called BOOP. Granulation tissue deposition within the alveolar spaces secondary to fibroblast proliferation. Responds to steroids and has good prognosis. Reverse halo sign is classic, consolidation around GGO centre. Idiopathic, prior infection, drugs (amiodarone), collagen vascular disease, fumes etc. Persistent symptoms following treatment for pneumonia. Patchy air space opacification or GGO in a peripheral or peribronchial distribution. Opacities irregular in shape. Both OP and Chronic eosinophilic pneumonia can present as peripheral consolidation.
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Chronic eosinophilic pneumonia
Idiopathic or with known antigen. Peripheral eosinophilia usually present. Asthma in 50%. Peripheral consolidation. Peripheral GGO or consolidation. Upper lobes favoured.
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Halo signs
``` HALO Nodule with ground glass in it. Represents haemorrhage /invasion into surrounding tissues. Invasive aspergillosis is classic. Haemorrhagic mets. BAC Wegeners ``` ``` REVERSE (ATOLL) Central ground glass with rim of consolidation COP is classic TB Pulmonary infarct Invasive funga and Wegeners COVID ```
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Hypersensitivity pneumonitis
Common. Inhaled organic antigens. Acute, subacute and chronic stages. SUBACUTE Patchy GGO. Ill defined centrilobular ground glass nodules. Mosaic perfusion and air trapping. CHRONIC UIP with air trapping.
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Tracheal diseases
Does it involve posterior membrane? Is it focal or diffuse? Are there calcs? SABER SHEATH Coronal diameter less than 2/3 sagittal diameter. COPD. Normal wall thickness and bronchi size. RELAPSING POLYCHONDRITIS Spares posterior membrane. Diffuse anterior and lateral thickening. No calcs. Recurrent cartilage inflammation and pneumonia POST INTUBATION STENOSIS Focal subglottic circumferential stenosis WEGENERS Circumferential thickening focal or long segment. No calcs ``` TRACHEOBRONCHOPATHIA OSTEOCHONDROPLASTICA (TBO) Spares posterior membrane. Cartilagenous and osseous nodules within submucosa of tracheal and bronchial walls. ``` AMYLOIDOSIS Irregular focal or short segment thickening which can involve posterior membrane. Calcs common
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Tracheal diseases continued
SPARES POSTERIOR MEMBRANE Relapsing polychondritis Tracheobronchopathia Osteochondroplastica TBO DOES NOT SPARE POSTERIOR MEMBRANE Amyloid Post intubation Wegeners
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Tracheal tumours
CARCINOID Rare. Central endobronchial location. Slow growing and locally invasive. Cause obstructive symptoms, can cause haemoptysis. No association with smoking. Octreotide scan useful. Can be cold on PET. Can cause carcinoid syndrome ADENOID CYSTIC Favours upper trachea. Variable look. Not associated with smoking. 2nd most common tracheal malignancy. SQUAMOUS CELL Most common tracheal malignancy. Associated with smoking. Favours lower trachea. METS Usually direct extension SQUAMOUS CELL PAPILLOMA Most common benign tumour of trachea. Single papilloma think smoking. Multiple think HPV.
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Cystic fibrosis
Sodium pump doesnt work and end up with thick secretions and poor pulmonary clearance. Damage by recurrent infections. ``` Bronchiectasis - begins as cylindrical and progresses to varicoid. Apical predominance Hyperinflation Pulmonary artery HTN Mucus plugging (finger in glove) ``` Abnormal mucus, cilia cant move Normal sperm, absent vas deferens
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Primary ciliary dyskinesia
Cilia dont work so cant clear secretions. Bilateral lower lobe bronchiectasis. Chronic sinusitis and impaired fertility (sperm cant swim, girls get ectopics). Chronic mastoid effusions and conductive hearing loss. 50% have Kartageners
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CF vs PCD
CF Abnormal mucus, cilia cannot move it Normal sperm, absent vas deferens. Upper lobe bronchiectasis PCD Normal mucus, cilia dont work Abnormal sperm (cant swim), normal vas deferens Lower lobe bronchiectasis
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Rare cases
WILLIAMS CAMPBELL SYNDROME Congenital cystic bronchiectasis from deficiency of cartilage in 4-6th order bronchi MOUNIER KUHN Tracheobronchomegaly Massive dilatation of trachea.
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Small airways disease
INFECTIOUS BRONCHIOLITIS Tree in bud with air trapping. RB-ILD Smokers, centrilobular GG nodules, upper lobe preodminant SUBACUTE HYPERSENSITIVITY PNEUMONITIS Inhaling dust, cetrilobular GG nodules FOLLICULAR BRONCHIOLITIS RA and Sjogrens, centrilobular GG nodules CONSTRICTIVE BRONCHIOLITIS Viral, drugs, transplant, inhalation, air trapping.
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Aspiration pneumonia
Stroke patients and alcoholics. Posterior segment of upper lobes and superior segment of lower lobes if supine. Bilateral basal lower lobes if upright. May favour right side. Can get empyema with subsequent bronchopleural fistula
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Aspiration patterns
GASTRIC ACID Mendelsons syndrome. Airspace opacity. WATER/NEUTRALIZED GASTRIC ACID Fleeting opacity which resolves in hours GERMS/MOUTH BUGS Real pneumonia, parapneumonic effusion, empyema, bronchopleural fistula OIL Lipoid pneumonia
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Collagen vascular disease
LUPUS Pleural and pericardial effusions. Can get shrinking lung but fibrosis uncommon RHEUMATOID Looks like UIP and COP. Lower lobes favoured. Reticulation with or without honeycombing. Consolidative opacities. SCLERODERMA NSIP pattern. Lower lobe predominant. Look for dilated fluid filled esophagous SJOGRENS LIP pattern. GGO with thin walled cysts ANKYLOSING SPONDYLITIS Upper lobe fibrobullous disease. Unilateral progressing to bilateral
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Caplan syndrome
Rheumatoid arthritis and upper lobe predominant lung nodules. Nodules can cavitate. and may get pleural effusion
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Shrinking lung
Progressive loss of lung volume in patients with Lupus. Either diaphragm dysfunction of pleuritic chest pain
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Hepatopulmonary syndrome
Liver patients, SOB when sitting (opposite of CCF). Develop distal vascular dilatation in lung bases which dont taper normally. When sitting up these engorge and shunt blood making them SOB.
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Wegeners granulomatosis (granulomatosis with polyangitis)
Triad of upper tract (nasal septal perforation)(cavitatory nodules), lung and kidneys. Nodules with cavitation. Random distribution. GGO which may represent haemorrhage.
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Goodpasture syndrome
Autoimmune pulmonary renal syndrome which favours young men. Non specific look with bilateral coalescent airspace opacity representing haemorrhage. Resolves quickly. If recurrent haemorrhage they can get fibrosis. Pumonary haemosiderosis can occur from recurrent episodes of bleeding making sall ill defined nodules
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Pleural cacifications
``` Asbestos - 20-30 year lag, spares costophrenic angles Old haemothorax Old infection TB Extraskeletal osteosarcoma ```
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Mesothelioma
Most common cancer of pleura. 80% have asbestos exposure. Lag time 30-40 years from exposure. Pleural rind all way around lung. Extension into fisure is suggestive
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Solitaryfibrous tumour of pleura
Solitary tumour arising from visceral pleura. Not associated with asbestos, smoking or other pollutants. Can get very large and be a source of chest pain although mostly incidentally seen. Usually benign even when large.Hypertrophic osteoarthropathy occures 30%.
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Pleural mets
Adenocarcinoma most likely to met to pleura. Lung is most common with breast 2nd and lymphoma 3rd. Pleural effusion most common manifestation.
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Pleural lipoma
Most common benign tumour of pleura. Feel urge to cough. Will not erode rib. Differential is extrapleural fat but this will be bilateral and symmetric.
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Pleural effusion
Needs to be 175cc on frontal to see them and t5cc on lateral. Transudative or exudative based on protein concentration. SUBPULMONIC EFFUSION Pleural effusion between lung base and diaphragm. Mor common on right with lateralization of the diaphragmatic peak. ENCYSTED PLEURAL EFFUSION Pleural fluid collect between layers of pleura creating oval appearance.
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Empyema vs pulmonary abscess
EMPYEMA Lentiform shape. Split pleura sign. Treated with chest tube. Infection pleural effusion. Enhancement of pleura, septations or gas. EMPYEMA NECESSITANS eats through chest wall into soft tissues. TB or actinomyces. PULMONARY ABSCESS Round. Claw sign. Not treated with chest tube due to risk of bronchopleural fistula.
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Diaphragmatic hernia
Acquired or congenital. Congenital are Bochdaek (back left) or Morgagni (front right). Traumatic more common on left as liver is protective.
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Diaphragmatic paralysis
Idiopathic 70% time but can be from phrenic nerve cmpression from lung cancer. Normally right diaphragm higher. Fluoroscopic sniff test see paradoxical movement.
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Anterior mediastinal masses
``` 4 Ts Thyroid Teratoma Thymus Terrible lymphoma ```
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Thymus
REBOUND Can rebound from chemotherapy. Hot on PET THYMIC CYST Congenital or acquired. Acquired after thoracotomy, chemotherapy or HIV. THYMOMA Spectrum from non invasive to invasive to thymomic carcinoma. Calcs makes more aggressive. Carcinomas invade adjacent fat/structures. Can drop met to pleural and retroperitoneum. THYMOLIPOMA Fatty mass with interspersed soft tissue
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Germ cell tumour
75% teratoma. Most common extragonadal germ cell tumour. Ocure in kids and adults 20-30. Benign but small risk of malignant transformation. Immature subtypes almost exclusively in men. Association of mature teratoma with Klinefelter. Usually 90% cystic with some fat. Can have calcs or teeth.
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Pericardial cyst
Uncommon and benign. Usually right anterior cardiophrenic angle.
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Fibrosing/sclerosing mediastinitis
Proliferation of fibrous tissue in mediastinum. Bot subtypes can cause SVC syndrome GRANULOMATOUS Classically by histoplasmosis. Others are TB and sarcoifd. Soft tissue mass with calcs infiltrating mediastinal fat. NON GRANULOMATOUS More rare. Idiopathic or as response to an autoimmune disease. Associated with retroperitoneal fibrosis. Lacks calcs and can enhance.
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Bronchogenic cyst
Congenital and usually within mediastinum., usually subcarinal or less commonly intraparenchymal.
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Lymphadenopathy
Mets, infection, reactive.
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Mediastinal lipomatosis
Excess unencapsulated fat in patients with iatrogenic steroid use, cushings and obesity
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Posterior mediastinal masses
NEUROGENIC Most common posterior mediastinal masses are neurogenic. Includes schwannoma, neurofirboma and malignant peripheral nerve sheath tumours. Extramedullary haematopoeisis is a response to failure of bone marrow to respond to EPO. Seen in CML, polycythemia vera, myelofibrosis, sickle cell ad thalasemia.
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PE on CXR
Westermark sign: regional oligemia (translucency due to no vessels seen - central clot) Fleischner sign: enlarged pulmonary artery Hamptons hump: peripheral wedge shaped opacity Pleural effusion: 30% of PEs
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Acute vs chronic PE
ACUTE Clot is central. Venous dilatation. Perivenous soft tissue oedema. Pleural effusion common. Sudden death from arrhythmia or acute RHF. CTPA exam of choice CHRONIC Clot if seen is more peripheral. Shrunken veins with collateral vessels. Calcs within thrmobi and venous walls. Mosaic attenuation. Pulmonary HTN. VQ superior to CT Massive PE needs hypotension <90 SBP. Right heart strain: Dilated RV with septal flattening or left bowing. Contrast felux hepatic veins
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Pulmonary infarct mimic
Pulmonary infarct is wedge shaped opacity that resolves slowly but can cavitate. Differentials include cancer and TB.
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Pulmonary veno-occlusive disease
Uncommon variant of pulmonary HTN that affects post capillary pulmonary vasculature. PAH and normal wedge pressure.
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Pulmonary artery aneurysm
Iatrogenic from Swan Ganz. Behcets lymphoma Chronic PE Hughes Stovin syndrome: Cause of pulm art aneurysms. Recurrent thrombophlebitis and Pulm art aneurysm and rupture Rasmussen aneurysm: pseudoaneurysm secondary to pulmonary TB. Upper lobes in reactivation TB. TOF repair: patch aneurysm from RVOT repair.
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Pulmonary HTN
PRIMARY Idiopathic, women in 20s. Uncommon SECONDARY Chronic PE. RHF/strain. Lung parenchymal problems (emphysema, fibrosis). COPD IMAGING Compare aorta and MPA. Calcs of central pulmonary arteries is Eisenmenger phenomenon. RV dilatation. Centrilobular GG nodules
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Trauma
DIAPHRAGMATIC INJURY Left side more common (liver protective). Most ruptures are radial and in posterolateral corner. Collar sign is waist like appearance of herniated organs. TRACHEOBRONCHIAL INJURY Uncommon. Within 2cm of carina. Close to carina causes pneumomediastinum rather than pneumothorax. Tracheal lacs are at juntion of cartilagenous and membranous portions of trachea. MACKLIN EFFECT Most common cause of pneumomediastinum in truama. Alveolar rupture from blunt trauma, air dissects along bronchovascular sheaths into mediastinum BOERHAAVE Rupture esophageal wall from vomiting resulting in pneumomediastinum/mediastinitis FLAIL CHEST 3 or more segmental rib fractures or more than 5 adjacent. Paradoxical motion with breathing
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Trauma continued
PTX Dont miss tension. Inversion of flattening of ipsilateral diaphragm MALPOSITIONED CHEST TUBE Can be in parenchyma, most commonly if background lung disease or pleural adhesions. Bronchopleural fistula can occur. HTX Pleural fluid in trauma is probably blood. 35-70HU EXTRAPLEURAL HAEMATOMA Injury to chest wall without damage to parietal pleura. Persistent fluid collection after pleural drain/tube placement. Displaced extrapleural fat. PULMONRY CONTUSION Most common lung injury from blunt trauma. Alveolar haemorrhage without alveolar disruption. Non segmental ill defined areas of consolidation with subpleural sparing. Should disappear within 72 hours. PULMONARY LACERATION Tear in lung will look like pneumatocoele. Gas fluid level. Masked by surrounding haemorrhage early on. Laceration resolves more slowly than contusion. AORTA Injured most commonly at isthmus. Next is aortic root and diaphragm. Main mimic is ductus bump which is normal variant. BLUNT CARDIAC INJURY Haemopericardium in setting of trauma. FAT EMBOLIZATION SYNDROME Long bone fracture or rod placement. Fat embolized to lungs, brain and skin. 1-2 days after femur fracture. GG appearance without PE. BAROTRAUMA Positive pressure ventilation causing alveolar injury with air dissecting into mediastinum. Acute lung injury or COPD higher risk. Fibrosis protected as dont stretch.
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Lines and devices
CENTRAL LINES Abrupt bend near tip of cather at cavoatrial junction makes you think its in azygos. If on left of heart think either arterial or in duplicated SVC. Central lines are risk for SVC occlusion ETT Tip should be 5cm from carina. Tip will go down when chin tucked. Tube in right main bronchus most common problem which can lead to left lung collapse. Can purposefully intubate one lung if massive pulmonary hamorrhage in the other. INTRA-AORTIC BALLOON PUMP IABP Cardiogenic shock to help with diastolic augmentation. Provides back pressure to vessels of arch get back perfused. Used to decrease LV afterload and increase myocardial perfusion. Balloon should be prox descending aorta. below origin of LSA. Complications are dissection and obstruction of LSA
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Cardiac conduction devices
Pacemakers, implantable cardiac defibrillator or mixed RV lead: cross midline on frontal RA and RV leads: anterior on lateral LV lead: posterior on lateral RA lead: courses down then back up to go into RA appendage Most commonly fractured in region of clavicle and first rib. Twiddler syndrome when geenrator gets flipped/rotated in pocket.