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					Pulmonary /Critical Care
  Board Review 2010


                 Edited by
                 Jad Skaf
    A 36 year-old woman presents to your office after coughing up 5 to
     10 ml of bright red blood the previous day. Three days earlier she
     noted the onset of coryza and frequent nonproductive cough. She
     denies fever, chest pain, and dyspnea.The rest of ROS is negative
     Denies previous history of hemoptysis. She smoked 1.5 pack /day
     for 16 years.
    Physical exam was normal
    Labs were Nl
    UA : No erythrocytes, 40 WBC, 4+ bacteria, No proteins, No casts
    CXRay : Nl
The most appropriate diagnostic plan at this time is:
1.   Fiberoptic Bronchoscopy
2.   HRCT of chest
3.   Serum ANCA and antiGBM antibody
4.   Repeat CXRay at 3 and 6 month
 5-10cc = small amount, so repeat CXR in 3-
  6 months
 HRCT = bronchiectasis
What is causing hemoptysis in this 60 year old man with severe emphysema?
 Aspergilloma developing on a pre-existing
  cavity. Crescent of air
 Treatment is resection / embolisation
 Systemic ampho doesn’t help, local
  itraconazole can
 3 manifestations of Aspergillosis:
2. Aspergilloma
3. Invasive Aspergillosis
What is causing hemoptysis in this 40 year old with h/o
          chronic cough and bronchorrhea?
 Dilated airway & thick wall – signet ring
 Common causes of hemoptysis:
1. Bronchitis (most common)
2. Tumor
3. TB (massive)
4. Bronchiectasis (with bronchorrhea)

    W/U of Hemoptysis: CXR, if negative
    bronchoscopy (if contra-indicated HRCT)
                   Key Points
 Most common causes of hemoptysis in smoker and non
  smoker is acute viral bronchitis
 Bacterial infection in HIV
 Even small amounts should be investigated
 History and examination are important in diagnosis
 Initial test : CXRay , lead the rest
 Bronchoscopy if >40 pack-year, >40 years age, >30 cc of
  blood daily or recurrent
 HRCT scan if bronchoscopy CI
 Massive hemoptysis(>600 ml / 24 hrs):
     The cause of death is asphyxiation, not exsanguination
     protect airway, adequate O2
     bronchial artery embolisation : bronchiectasis
     For each patient select the most
          likely flow volume loop
1.   A 34 year old woman with dyspnea at rest and
     hoarseness after being intubated for 20 days for
     aspiration pneumonia
2.   A 70 year old woman who smoked 2 packs of
     cigarettes daily for 50 years and who had severe
     exertional dyspnea and diminished intensity of
     breath sounds on auscultation
3.   A 30 year old female with goiter
   1 is vocal cord paralysis, it’s extrathoracic so D
   2 is COPD, Flow loop would be scooped (you can sit on
    it) so B
   3 is goiter, extrathoracic as well so D

   C loop is restrictive, everything is decreased but the flow

   Extra-thoracic is pb during Inspiration: E=I, loop D
   Intra-thoracic is pb during Expiration: I=E, loop E

   Extrathoracic: goiter, vocal cord paralysis
   Intrathoracic: tracheomalacia

   Loop F is “Burger sign” is a fixed obstruction (extra or
    intra): cancer, tracheal stenosis, TB
Extra-thoracic   Intra thoracic
A=IPF   B = COPD   C = Pneumonectomy + smoker
   A: This loop is C – Pneumonectomy. Explanation: FEV
    decr, FVC decr, ratio is decr but this is not
    COPD/obstructive cause lung volumes are decreased
    (TLC is normal or decr)

   Obstr: FEV is decr, FVC is decr, ratio is decr (<70%),
    TLC is normal or high (hyperinflation)
   Restr: all volumes are decreased, flow is normal – ratio
    remains normal or high, FEV is decr, FVC is decr

    A: the next 2 loops are by order:
COPD/obstr (you can sit on the loop), TLC is increased
IPF/restr (all volumes are decreased, ratio is normal)
A=IPF   B = COPD   C = Pneumonectomy + smoker
A=IPF   B = COPD   C = Pneumonectomy + smoker
    What is the most frequent
    cause of chronic cough ?

 Postnasal drip
 Asthma
 Esophageal reflux
 Cigarette smoking
   A: cigarette smoking
   In non smokers it’s post-nasal drip
   If they don’t get better after PNDrip treatment
    (decongestants, antihistamines 1st generation), then we
    do PFTs with metacholine challenge to r/o asthma
    Differential of cavitating/air-fluid opacity on cxr:
TB, squamous cell ca, abscess, infected bullae

Here answer is treat anaerobes with clindamycin

RF for aspiration / abscess:
Seizures, ETOH, bad dentition
   A 66 year old man presents with acute onset
    dyspnea, fever and pleuritic chest pain.
    The initial diagnostic procedure should be
    –   Thoracentesis
    –   Chest computed tomography
    –   Thoracoscopy
    –   Bronchoscopy
    –   Pleural biopsy
   For board purposes, if there is a pleural effusion on
    CXR, you do a lateral decub x-ray, if it’s >1 cmthen do

   If bilateral effusions equal in size: diurese then repeat

   Rapidly progressive empyema that develops in a few
    hours: empyema caused by beta hemolytic strep
    Parapneumonic effusion
 Most common exudative effusion
 40 to 57 % of patient with bacterial
 10-15% complicated
 5% empyema
    Indications for pleural space
     drainage in parapneumonic

 Purulent effusion-absolute indication
 pH < 7.20 or 7.30
 Glucose < 40 or PF/serum<0.5
 LDH > 1,000
 Positive gram stain
 Positive bacterial culture
   A is cirrhosis> ur obstr
   B is esoph perf > Cancer
   C is cancer (decr pH, decr gluc)
   D is ur obstr (incr creat)
   E is RA (decr pH, decr gluc) or esoph perf
   F
      Light Criteria              Analysis of Pleural
                                     Effusion without
An Exudate Possesses
Any One of theFollowing
Characteristics                 An Exudate
Pleural fluid protein–to–        Possesses Any One
serum protein ratio  0.5,       of the Following
or                               Characteristics
Pleural fluid LDH–to–            Pleural fluid LDH > 45%
serum LDH ratio 0.6, or         of serum upper limit of
Total pleural fluid LDH          normal, or
level greater than two-          Pleural fluid cholesterol
thirds the upper limit of        > 45 mg/dL, or
normal for serum LDH             Pleural fluid protein >
                                 2.9 g/dL
 LDH = lactate
    When to do SAAG for pleural effusion (>1.2):

After diuresing a transudate it might look like an exudate, it’s
     called pseudo-exudate (or you can do CT)
    Transudate differential: CHF, cirrhosis, nephrotic – but
     also urinary obstruction (elev creat, called urinothorax),
     hypothyr, may sd (benign ovarian mass), yellow nail sd,
     atelectasis, migrated central catheter (eroded through
     vein), VP shunt, Peritoneal Dialysis
                                                        Causes of Exudative Pleural Effusion

Historical Feature                                                                        Possible Cause
Rheumatologic disorder                                                                    Rheumatoid effusion, lupus pleuritis

Recent myocardial infarction or cardiac surgery                                           Postcardiac injury syndrome

Medications                                                                               Procainamide-induced pleuritis, for example

Weight loss                                                                               Malignant disease, tuberculosis

Asbestos exposure                                                                         Asbestos effusion, mesothelioma

Retching, chest pain                                                                      Esophageal perforation

Fever, cough, parenchymal lung disease                                                    Empyema, tuberculosis

Acute pleuritic chest pain and dyspnea with a thrombophilic situation                     Pulmonary embolism

Hemoptysis                                                                                Bronchogenic carcinoma, tuberculosis
A 41-year-old man with a long history
of asthma has increased wheezing over
the past 2 months. He was treated for
pneumonia while on vacation a month
ago and still requires prednisone, 7.5
mg/d. His FEV l despite prednisone
therapy, has fallen 9% over the past 2
months. He notices that his cough is
more productive, and at times, forms
"casts" of his airways. He has
increased sinus complaints. His
peripheral blood eosinophil percentage
is 11%.
His CT scan is shown
What is your diagnosis?
   CT: Prox bronchiectasis like pic, eosinophilia – ABPA

   Differential: eosinophilia + asthma + peripheral
    neuropathy = Churg-Strauss
    The Major Diagnostic Features of
            ABPA include
 History of asthma
 Immediate skin test reactivity to aspergillus antigens
 Precipitating serum antibodies to A. Fumigatus
 Serum total IgE concentration greater than 1000 ng/ml
 Peripheral blood eosinophilia > 500/mm3
 Lung infiltrates
 Proximal bronchiectasis
 Elevated serum specific IgG and IgA to A. Fumigatus
 A 56-year-old man presenffi with a 3- to 4-
month history of dyspnea and an
intermittently productive cough. He works as
a house painter and has smoked one to one
and a half packs of cigarettes a day for more
than 30 years.
 Physical examination revealsbibasilar
crackles. There is no clubbing.
 Pulmonary function test reveal FVC 96 % of
predicted, TLC 92 % of predicted; DLco 75
%of predicted; and Pao2 56 mm Hg on room
 Laboratory studies show an elevated serum
LDH; a test for the human immunodeficiency
virus (HlV) is negative.
   Xray shows a butterfly like pulm edema: Pulm alveolar
    Proteinosis – negative HIV r/o PCP – trt is lavage –
    diagnosis is by PAS stain – predisposes to infection with
    nocardia > PCP
 A 28 yo HIV +         A
  women with SOB,
  Pao2 of 62 and LDH
  of 1000
 Most common
  Bacteria involved in
  superinfection after
  influenza infection     B
 Most common
  organism that infects
  the lungs of patient
  with PAP              C
   PCP is the 2nd pic in silver (decr PaO2, incr LD)
   Pic A is weak acid fast, nocardia (more red), while
    actinomyces is more blue
   Pic C is staph aureus
   A 28 year-old male
    smoker has had dyspnea
    on exertion for 6 months.
    Physical examination is
    unremarkable. PFT’s
    demonstrate a mixed
    obstructive and restrictive
    ventilatory defect. BAL
    demonstrates Langerhans’
   This is eosinophilic granuloma (histiocytosis only
    isolated to the lung) – trt is steroids, quit smoking –
    langerhans histiocytes on BAL

   Next slide is a CT that shows interst changes,
    micronodules, irregular cysts
A 34-year-old woman
has progressive dysp-
nea and severe airflow
obstruction (FEV1=
34 % of predicted).
One year ago, she had
an episode of
   Woman, hemoptysis, can develop secondary PTX, also
 Women of childbearing age
 Recurrent pneumothorax
 Chylous effusion
 Hemoptysis
 PFTs = obstruction
A 70-year-old male
former smoker has
had progressive
dyspnea and a
nonproductive cough
for 18 to 24 months.
Physical examina-
tion reveals bibasilar
crackles and
   This CXR shows honeycombing, interst changes,
    peripheral cysts: UIP, IPF
   A 68 year old retired
    automative mechanic
    who sandblasted
    radiators for 20 years.
    He has dyspnea on
    exertion and a chronic
    cough. He has
    restrictive lung
    volumes and abnormal
    gaz exchange
   CXR shows ADPs, calcified eggshells, interst changes

   Calcified eggshells: silicosis – sarcoidosis - berylliosis
 Inhilation of silica
 Mining, Tunneling, Quarrying, Foundry,
  Sandblasting, Ceramics, Stone work
 Complications:
       Progressive Massive Fibrosis
       Tuberculosis superinfection
       ? Increase lung cancer risk
 RA may increase the risk
   A 48 year-old bird
    fancier with 3 weeks
    of dyspnea, cough,
    and fever.
   CT shows small ill-defined nodules, bronchiolar
    distribution, also called a farmer’s lung, trt is steroids,
    BAL shows neutrophils, lymphocytes > eosinophils
    Hypersensitivity pneumonitis
 Symptoms start 4-6 hours after exposure
 Fever, chills, sweats, dry cough and
 No wheezing
 Resolves in 18-24 hours and recur on
   A 48 year-old metal
    machinist who has night
    sweats, chronic cough,
    and shortness of breath.
    Transbronchial lung
    biopsy specimen shows
    noncaseating granulomas
    and patchy interstitial
   Histology would show non caseating granulomas, patchy
    interst infiltrates – also could give you in the history
    ceramic work, aerospace = Berylliosis
   Very similar to sarcoidosis except for the exposure

   Stage III sarcoidosis looks like UIP
 Ceramic worker, beryllium processors, and
  some aerospace worker
 Beryllium lymphocyte transformation test
 Mimic sarcoidosis clinical, radiographic,
  and pathology
   A 70 year-old retired
    construction worker, a
    current smoker with
    dyspnea on exertion.
    He has bibasilar
    crackles on respiratory
   Showing pleural plaques, effusion – if no symptoms
    diagnosis is asbestos related plaques, unless + crackles
    and dyspnea = asbestosis
 Interval between exposure and
  bronchogenic carcinoma 15 to 35 years,
  malignant mesothelioma 30 to 40 years
 Pleural plaque is the most common related
 Asbestos exposure alone increase the risk of
  lung cancer minimally
 Asbestos and smoking acts synergistically
   A 30 year-old women
    presents with a 6-weeks
    history of cough, dyspnea,
    and wheezing. PE reveals
    only scattered ronchi. The
    leucocyte count is 15,600
    with 32% eosinophils. The
    ESR is 65 mm/h and
    serum IgE is 350 mg/L.
       Chronic eosinophilic
 Chronoc illnrss of middle-aged patients
 Male:female=2:1
 Fever, dyspnea, cough, wheezing
 High ESR, high IgE, peripheral eosinophilia
 CXR: “ negative “ image of pulmonary
 Respond to steroids
   A 62 year-old woman
    presents to the ER with
    cough, dyspnea, and low-
    grade fever. She is
    nonsmoker and had been
    healthy until 5 weeks ago,
    when she developed a
    viral syndrome associated
    with a paroxysmal cough.
   PE reveals crackles in the
    left lower lobe.
    WBC=13,000 differential
    is nl, c7 is nl. Sputum
    gram stain and AFB are
                               Distinguishing Obliterative Bronchiolitis from Bronchiolitis Obliterans
                                     with Organizing Pneumonia (BOOP)
              Manifeslationc                                BOOP                  Obliterative Branchiolitis.

 Focal alveolar infiltrates                                   Typical                                    No
Airways obstruction (on pulmonary                              No (except
function testing)                                           in smokers)                                  Yes
Intraluminal polypoid masses within                           Typical                                    No
Organizing pneumonia Typical-
Response to corticosteroids                                    Excellent                                  Rare
Prognosis                                                      Excellent                                  Poor
   BOOP, clue is viral illness a few weeks ago

   BOOP: restr, cryptogenic, idiopathic, associated to
    connective tissue disease (SLE, RA, chemotherapy…)
   OB: obstructive, transplant patients
   A 30 year-old man
    presents with hemoptysis,
    dyspnea, and generalised
    weakness. He has no sinus
    or upper airway
    symptoms. PE reveals
    pallor and bibasilar
   Hemoglobin 7.8 ,
    creatinine 3, microscopic
    hematuria and hypoxemia.
A 35 year old atopic man is seeing you for asthma.
His allergic rhinitis has been controlled with
  intranasal corticosteroid use.
He is using his short-acting beta agonist (SABA) 3
  or 4 times a week for intermittent symtoms of
  wheeze and chest tightness after exercise.
His FEV1 is 88 % of predicted.
His IgE level is 400 IU/ml
Skin test is positive for house dust mite
    Which therapeutic approach
        would you advise
 Continue use of PRN SABA
 Add inhaled corticosteroid (ICS)
 Add ICS plus LABA
 Allergen avoidance with the use of allergen
  impermeable bed coverings
 Begin Anti-IgE therapy
    Which therapeutic approach
        would you advise

 Continue use of PRN SABA
 Add inhaled corticosteroid (ICS)
 Add ICS plus LABA
 Allergen avoidance with the use of allergen
  impermeable bed coverings
 Begin Anti-IgE therapy
     Mild Persistent Asthma
 Symptoms > 2x a week and < 1x a day
 Nocturnal symptoms > 2x a month
 FEV1 and PEFR > 80% of predicted
 PEFR variability between 20% and 30%
      Mild Persistent Asthma
      Therapeutic approach
 ICS recommended by NIH and GINA
 ICS reduce severe exacerbations day and
  nightime symptoms (OPTIMA and START)
 No additional benefit from LABA
   Mild persist asthma = ICS, no benefit from LABA – of
    fails then try Ige blockers (zolaire), also in mod/severe
   Mild interm (<2x/week) = PRN SABA
A 45 year old man is referred by his primary
 care physician for poorly controlled asthma.
 He is using his SABA daily for intermittent
 symptoms despite the use of 440 mcg of
His FEV1 is 70 % of predicted .
What is the best add-on strategy
  to contorl his symptoms?

 A leukotriene pathway modifier
 Anhydrous theophylline
 A long-acting beta agonist
 Double the dose of ICS
What is the best add-on strategy
  to contorl his symptoms?

 A leukotriene pathway modifier
 Anhydrous theophylline
 A long-acting beta agonist
 Double the dose of ICS
   Failure of high dose (440) ICS = mod persist = LABA
   Severe: FEV<60, constant sptms
    Moderate Persistent Asthma
 Daily symptoms and use of beta agonist
 > 1 nighttime exacerbation per week
 FEV1 and PEFR between 60% & 80 %
 PEFR variability > 30%
A 34-year-old female medical technician is referred
to you with a diagnosis of asthma. Despite initial
Therapy with inhaled corticosteroids and beta-agonists.
she remains symptomatic with cough and wheeze.
The FEV1 is 78 % of predicted and improves 13 %
after albuterol.
The most important next step in the management of
lis patient is:
A) Increase the corticosteroid dosage
B) Perform a methacholine challenge
C) Perform an inspiratory limb of a flow-volume loop
D) Add theophylline
E) Add a leukotriene receptor antagonist
   Vocal cord dysfunction, vc close on inspiration, can be
    seen and diagnosed by laryngoscopy – described in
    paramedical pop., FEV1 is normal. Extrathoracic
    process= insp dysfunction (saw teeth on insp limb on
    pFTs, which can also be seen in parkinson and OSA)
 All that wheezes is not asthma
 Not all asthmatic wheeze
    Drug-induced bronchospasm
    Vocal cord dysfunction
 Provocation inhalation challenge is used to
  detect latent asthma
 A 59-year-old man is evaluated for snoring,
  abnormal motor behavior during sleep,
  daytime somnolence, systemic hypetension,
  and morning headaches.
 His polysomnography study is shown :
   Morning headaches: OSA, tumor, nocturnal
   95% of OSA is upper airway obstr, sleep study : chest
    muscles keep going on (central 5% all stops)
   Risk factors OSA: age, male gender, obesity, anatomy
    (micrognathism, acromegaly, neck size>16 ½), genetic,
    polycystic ovarian sd,
   50% of CHF have central OSA (cheyne stokesn
    breathing: cresc-decresc-pause)

   Restless leg sd: 75% familial, associated to iron def
    anemia, can be presenting sptm of colon cancer
 A 36-year-old women is referred with gradually
  progressive exertional dyspnea over the last 12
  months, exertinal dizziness and occasional
  syncope, anterior cheat tightness, and fatigue. She
  also has noted Raynaud phenomenon during the
  last 6 months. Examination demonstrates a loud
  P2 and right ventricular heave. The lungs are clear
  to auscultation.
 Pao2 52mm Hg and Sao2 85%
 Which of the following treatment is inappropriate?
A. anticoagulation
B. Vasodilator
C. Systemic high dose steroids
D. Supplemental o2
E. Prostacycline
   CXR shows dilated pulm vasculature = 1ary pulm HTN in a young
    patient. Sptms: hypoxemia, DOE, Chest pain (ischemic in nature),
    decr DLCO, syncope
   In situ thrombosis of pulm vasculature, treat with anticoagulation,
    vasodilators, O2, prostacycline (worng answer is steroids) – last
    option heart-lung transplant
   Class I: no adv therapy
   Class II: endothelin rec inhibitors-sildenafil
   Class IV: IV prostacycline

   GpI: conn tissue dz (RA, scl…)HIV, familial, idiop, R to L shunt,
    meds, : therapy applies to those
   GpII: L heart failure (pulm venous congestion)
   GpIII: thromboembolic
   GpIV: chronic hypoxemic lung disease (COPD, IPF)
   Gp V: misc (sarcoidosis, fibrosing mediastinitis)
Clinical factor,       More likely     More likely
radiographic result     benign         malignant

        Age                 <35 yr        >35 yr
        Sex                 Female         Male
       Smoking               No            Yes
       Symptoms               No           Yes
Exposure to tubercu-
losis, cocci, etc.            Yes            No
Previous malignancy           No             Yes
Nodule size                  <2.0 cm       >2.0 cm
Nodule age                   >2 yr         <2 yr
Doubling time              <30 days      >30 days
Nodule margins              Smooth        Irregular
Calcification                Yes             No
Satellite lesions             Yes             No
   Benign calcifications: lamellar, pop-corn (hamartomas),
    homogeneous concentric
   Highly malignant calcif: spiculated, eccentric, corona

   High risk = lobectomy

   > 1 cm = PET Scan
" For each numbered hemodynamic profile, select the most likely etiology of shock.
    SBP          RAP             PAP             PAOP               C1
 (mm Hg)      (mm Hg)        (mm Hg)          (mm Hg)         (L/min/m2)
1 90/68          18              36/24            22                 1.8
2 90/46           5              22/8              6                 4.7
3 88/40          20              22/16             7                 2.2
4 84/60           3              18/6              5                 1.8
5 90/68          18              32/18            17                 1.8

a. Severe hemorrhage
b. Pneumococcal sepsis
c. Anterolateral myocardial infarction
d. Cardiac tamponade
e. Right ventricular myocardial infarction
    A 24 -year-old woman develops sepsis and ARDS postpartum. She
     has been stable with mechanical ventilation . The ventilator setting
     are : Fio2=0.6; TV=800ml; RR=24/min; PEEP=10 cm H2O
    You are consulted by the nurse because the patient is suddenly
     anxious and agitated.
    Measurements during controlled breaths:
      Peak airway pressure 55 cm H2O (baseline:35)
      Plateau airway pressure 50 cm H2O (baseline :30)
      Tidal Volume 720 ml (baseline 768 ml)
What is the most important next step in the management of this patient:

A.   Sedation with midazolam and observation of patient
B.   Stat portable chest radiography
C.   Endotracheal suctioning and reassessment of patient
D.   Stat electrocardiogram
E.   Increase the ventilatory rate to 28/min and rassessment in 30
Ppeak      ~ Resistance x Elastance
Pplateau   ~   Elastance
Ppeak - Pplateau   ~   Airflow Resistance
 A 68-year-old man, a 56-pack-year smoker,
  undergoes bronchoscopy under topical anesthesia
  for evaluation of streak hemoptysis. One hour
  after he notices bluish discoloration of his finger
  and lips. He has minimal dyspnea and his vitals
  are normal.
 ABG’s Pao2 86 Paco2 46 PH 7.38 Sao2 56%

 A. Polycythemia from copd
 B. Methemoglobinemia
 C.Right to left anatomical shunt
 D.shock
   The ACCP Evidence-based Guidelines for the diagnosis
    and management of lung cancer recommends Low-dose
    CT screening in which of the following situations
    –   All current cigarette smokers
    –   All current and former smokers for more then 10 pk years
    –   Males over 50 and females over 60 with more then 10 pk years
    –   Does not recommend screening
    –   Current and former smokers with FEV1<80% of predicted
   Cxray screening trial 1970’sno mortality benefit
   I-ELCAP study NEJM 2006
     – 31,567 were screened
     – 484 cancer were found (85% stage I)
     – Excellent results
     – BUT numbers misleading!!!
   2007 JAMA article using statistically validated model
     – More diagnosis of lung cancer(144 vs 44 predicted)
     – More surgery (109 vs 11 predited)
     – BUT no mortality benefit at 4.7 years(38vs39 predicted)
 Extremely controversial issue
 Not recommended by any national
  organisation at this time
 Under very active investigation
 We all have high hopes that will be
 We just do not know
Superior vena cava syndrome
 More common with SCLC
 Sensation of fullness in the head and
  dyspnea, less commonly cough, pain, and
 Dilated neck veins, a prominent venous
  pattern on the chest, facial edema, and a
  plethoric appearance
      Pancoast's syndrome
   Cancers arising in the superior sulcus
   More common with NSCLC(squamous)
   Pain (usually in the shoulder, and less
    commonly in the forearm,scapula, and
   Horner's
   Bony destruction
   Atrophy of hand muscles
   Which of the following paraneoplastic
    syndromes is more common with NSCLC
    –   SIADH
    –   Eaton-Lambert syndrome
    –   Cushing’s syndrome
    –   Ectopic production of PTH-like hormone
    –   Alberts-Levine syndrome
    Paraneoplastic phenomena
   Hypercalcemia
    – Bony metastasis or less commonly tumor
      secretion of a parathyroid hormone-related
      protein (PTHrP), calcitriol or other
      cytokines, including osteoclast activating
    – 6 % in one study
    – Squamous>adeno>sclc
    – Advanced disease and few months survival
    Paraneoplastic phenomena
   SIADH secretion
    – 10% of SCLC
    – SCLC responsible of 75% of malignancy
      related SIADH
    – Hyponatremia resolves within weeks of starting
      chemo in majority of patients
   A 64-year-old man, a 38-pack-year smoker,
    presents with recent onset of pain in both
    knees and shins. Examination reveals
    clubbing, gynecomastia, tenderness of both
    shins, and mild expiratory slowing of lung
    Paraneoplastic phenomena
   Hypertrophic Osteoarthropathy(HPO)
    – Clubbing with periosteal proliferation of
      the tubular bones
    – Symmetrical, painful arthropathy of
      ankles, knees, wrists, and elbows
    – Symptoms may resolve after tumor
    – NSAIDS and bisphosphonate if
    Paraneoplastic phenomena
   Dermatomyositis and polymyositis
    – Inflammatory myopathy
    – Manifests by muscle weakness
    – Presenting symptom or develop later
      in the course of disease
    – Other frequent primary:ovary, cervix,
      pancreas, bladder, and stomach
          Cushing's syndrome
   Ectopic secretion of ACTH
   1 % of patients with small-cell lung cancer
   SCLC causes half of all cases. Seen with carcinoid
   Muscle weakness, weight loss, hypertension,
    hirsutism, osteoporosis,hypokalemic alkalosis and
   Worse prognosis
       Paraneoplastic neurologic
   SCLC most common cancer associated
   Thought to be immune-mediated
   Lambert-Eaton Myasthenic syndrome (LEMS)
    – most common
    – 3% of SCLC
    – precedes diagnosis in 80 %
 Cerebellar ataxia, sensory neuropathy, limbic
  encephalitis, encephalomyelitis, autonomic
  neuropathy, retinopathy, and opsomyoclonus
 70 % have limited disease
     Paraneoplastic syndrome
 Caused mostly by primary tumor
 Does not indicate metastatic spread
 Small cell carcinoma:
    1. SIADH
    2. ACTH production
    3. Myasthenic syndrome
   Squamous cell:
    1. Hypercalcemia
    2. Cerebellar ataxia
    3. HPO
   SCLC: SVC Sd (not an emergency anymore), SIADH,
    cushing, eaton-lambert
   NSCLC: PTH, HPO, pancoast tumor with horner sd

   Hypercalcemia: squamous>adenoca>SCLC

   Bluish extremities after bronchoscopy:
   Gave lidocaine which can be absorbed which can give
   Clue is a cyanotic guy who has a normal pulsox (pulsox
    picks up oxyhb as well as methemoglobin)
   ABG shows decr SpO2

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