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Pnematocoeles Are?

Often form secondarily to an uri caus by streptococcus pneumonia. S aureus can result in blood streaked sputum and multiple midfield lung cavity in CXR suggesting an acute necrotizing pnemonia

Which patients are the most sensitive to asthma-like symptoms? (cough, wheeze, SOB, CHEST tightness) in RX?

ASA (aspirin) sensitive asthema - if patient has asthma or a polyp - the use of ASA could force an exacerbation that resembles asthma like symptoms

BERYLLIOSIS can have similar clinical findings to sarcoid. What is the diagnostic test associated with its diagnosis?

Beryllium lymphocyte proliferation test

O2 delivery systems

1. Low flow v. HIGH flow:

Low: nasal cannula (<0.40 FiO2); Simple face mask (0.4-0.6 FiO2)

High: venturi mask (<0.5 FiO2); nonbreathing mask (0.70-0.80 FiO2)

primary pneumothorax versus secondary pneumothorax?

1. Primary: heathy, tall, young, lean male
-spontaneous subpleural bleds at apex, escape of air yeilds collapsed lung
-recurrence rate 50%/2 years
-sufficient pulmonary reserve therefore not life threatening

2. Secondary: complicated
-underlying disease like COPD, asthema, ILD, CF< TB, life threateneing bc lack of pulmonary reserve

IN COPD = FEV1 is _____ and the FEV1/FEV ratio is?

Pulmonary symptoms?

FEV1< 70% if mild or <50% if severe.

Decreased FEV1/FEV (<0.75-0.80)
Increased TLC, RV, FRC due to air trapping
Decreased vital capacity

Dyspnea, cough ,sputum production; wheezing

Pathophysiology of ARF

1. V/Q mismatch - hypoxia without hypercapnia is the MOST COMMONY MECHANISM THAT DOES REPOND TO O2 SUPPORT AND SUPPLEMENTAL
2. Shunting - little or no ventilation in perfused areas due to collapsed or fluid filled alveoli - the venous shunts to the arterial circulation without O@ ocygenation
3. Hypoventilation leads to hypercapnia
4. Increased CO2 production - hypercarbic
5. Diffusion impairment

How is cor pulmonadle diagnosed?

3 tests:


1. CXR - enlargement of the RA, RV, pulm arteries. Right heart enlargment
2. ECG - right axis deviation, P pulmonale (peaked P waves), right venticular hypertrophy
3. Echo - RV dilitation; normal LV size and function; rule our LV dysfunction

Treatment: underlying pulmonary disorder, diuretic therapy cautiously (if preload dep) O2 therapy

CNS: bilateral bells palse CNVII/ CNI optic
Lungs: dry cough, SOB
Skin: eryethma nodosum; plaques; subq nodules
Eyes: anterior uveitis (75%) > posterior
Heart: arrhythmia, HB, sudden death
MUS: bone lesions




Whiat treatments are used in acute COPD exacerbations?


Both are inhaled steroids that are anti-inflammatory in nature.

symptoms of acute Respiratory FAILURE

SIGNS: Diagnosis:

Signs: elevated HR, elevated RR, cannot speak in full sentences

-SOB is the first symptom
-COUGH (+/-)

Signs: 1. talk in complete sentences depends upon underlying cause; use of accessaory muscle (SCM/trap). 2. Tachypnic (elevated RR). 3. Tachycardic (inc HR). 4. Cyanosis. 4. Impaired mentation

What triggers asthma?

4 classic features of asthmatics (clinically)

1. exercise
2. pollens
3. house dust
5. cockroaches
7. cold air
8. viral infection
9. tobacco smoke
10. BB and ASA

Four major presented findings: SOB, COUGH, WHEEZE, CHEST TIGHTNESS

Which pneumoconiosis increases the risk of bronchogenic carcinoma and malignant mesothelioma?



No specific traetment abailable
-bilateral hazy infiltrates with linear, opacities

What is PEEP?

positive pressure applied during mechanical ventilation at the end of passive exhale that keeps alveoli open. differs from CPAP which is used in pts who spontanously breathe. Pts with PEEP are under mechanical ventilation

-2.5-10cm H2o appropriately set
-used in ARDS patients
-good = increases lung compliance/O2 and presvents alveolar collapse

If patient presents with COPD exacerbation - what are the following steps appropriate for its diagnosis?

1. CXR
2. B2 agonist (albuterol)/anticholinergic (ipra)
3. Systemic corticosteroids
4. AB (r/o infection)
5. Supplemental O2 therapy
6. Non-invasive PPV if needed like a CPAP or BIPAP

Parapneumonic effusion treatment:

P effusion + pneumonia
1. uncmplicated = AB alone
2. complicated = EMPYEMA - pus in the effusion
-chest tube draininage
-intrapleural injection of thrombolytic agents (streptokinase, urokinase)
-surgical lysis of adhesions may be required

Acute respiratory failure = either ______ oxygenation or blood or ________ ventilation of _________.

Decrease the O2 of PaO2 (inadequate perfusion)
Decreased the CO2 ventilation of PaCO2

Thus hypoxia is PaO2< 60mmHg and PaCOD > 50 mmHg

Thus hypercapnia PaCO2 > 50 mm Hg

What is the number one diagnosis of a mediastinal mass?

CHEST CT - discovered by CXR incidentally

SIMv = synchronous intermittent mandatory ventilation

TV is NOT determined or preset by ventilation but the RATE is.
-breathe on their own above mandatory rate without help from ventilator (TV of extra breaths is not determined by the ventilator)
-delivers mandatory breath in syncrhony with pts intitiated spontaneous breathe so the two dont overlap
-if the patient breathes spontanously - no preset volume (gets it at rate) if doesnt breathe, gets predetermined breath rate

ALL patients, including those who are pregnant with HCV chronically should receive vaccinations against both ____ and _____ if not already immune.


Hepatitis c perinatal transmission is less frequent (2-5%). Increased risk if pt is HIV positive with high HCV viral load. Both interferon and ribairon for the treatment of pts with chronic HCV must be held during pregnancy. Some evidence that sexual transmission of HCV occurs, but the incidence is extremely low. Thus no barrier precaustion between stable monogamous sexual partners is required.

Increased risk of ILD (SOB, later on exertion, COUGH, FIBROSIS) in dividuals with mining, stone cutting

Increased risk of TB


signs of ILD that differs from OLD (COPD/CB)

-rales at lung base
-pulmonary HTN/cyanosis
-CXR with honeycombing = scarred shrunken lung ciliated air spaces, fibro scars in interstitium.
-CT scan show groundglassing
-FEV1/FVC normal - high in restrictive lun disease, has low TLC and low RV unlike that of obstructive. Also has decreased ERC and decreased TV
-decreased diffusion capacity

Key parameteres of mechanical ventilation

minute ventilation (RR x TV)
I:E ratio

EGOPHONY ON Lung auscultation:

Say EEE sounds like AA indicates lung consodidation

When might DIGOXIN be used in patients to treat COR PULMONALE?

only is 2/2 LV failure. Otherwise stick to diuretic therapy cautiously

Treatment of ARDS:

Keep O2 sat > 90%
-mechanical ventilation with PEEP
-increased lung olue by opening collapsed alveoli and decreasing the shunt
-fluid management (PCWP 12-15) maintain vasopressors used to mantain BP
-treat underlying cause
-tube feeding > than parenteral

How is sarcoidosis staged?

Stage I = bilateral hilar LAD without infiltrates
Stage II = hilar LAD+ infiltrate
Stage III = diffuse infiltrate without HILAR --> WORST PROG
Stage IV = fibrosis and honeycoming - this is an ILD and thus has restrictive lung pattern....

Diff diagnosis of hemoptysis

1. Bronchitis (50% of cases viral)
2. Lung CA - bronchogenic carcinoma
3. TB
4. Bronchiectass - seen in CF
5. Pneumonia
6. CVD - good pastures, PE with pulmonary infarct, aspergilloma, mitrial stensosis

Inhalation of coal dust (both carbon and silica) by coal workers can either be assymptomatic or result in respiratory disability by fibrosis (ILD)

coal workers pneumoconiosis

How does CF present:

Most common infections;
Most likely treatment?

#1 AR disease in caucasians that includes a defect in the CL- channel @ F508 chromosome 7. This leads to the dec ablity to secrete Cl- in the mucous glands and dec ability to absorb Cl- in the sweat glands leading to think, nonwatery mucus plugging - bronchiectatsis (obstructive), pancreativ insufficiency, GI complicatiosn and increased Cl- sweat > 65

Infection = Pseudomonas aeruginosa (gram -) and treatment is FLUOROQUINOLONEs

Rx: Pancreatic enzyme replacements; FAT soluble vitamin replacement chest percussions and antibiotics

MORGAGI Hernia v. BOCHDALAK's Hernia

Congenitdal diaphragmatic hernia (CDH)
1. Morgagi - herniation through foramen (2%) moragni located adjacent to xiphoid process of sternum/anterior defect of the diaphragm

2. BOCHdalaks - posteriolateral diaphragmatic hernia (95%)/allows passage of adbominal viscera into chest cavity on L side

What is a pneumoconiosis?

example of "dust" particles?

accumulation of dust in the lungs and the tissue reaction 2.2 to its presense:

1. SIlica
2. Beryllium
3. Asbestos
4. Coal dust
5. Graphite
6. Carbon black
7. Aluminum
8. Talc

FiO2 parameter on ventilator

100% set
-quickly titrate and use lowest possible to maintain paO2 50-60mmHg (or sat 90%) to avoid O2 intox
-FiO2 < 60% safe
-FiO2 of 0.5 doesnt result in adequat PaO2 thus add PEEP or CPAP to reduce FiO2 to suppor PaO2 and lower FiO2

Which environmental causes exposures?

Restrictive interstitial lung disease?

Coal workers pneumoconiosis


1. Status asthmaticus
2. Acute respiratory failure (2/2) respiratory muscle failure
3. Pneumonthorax, atelectasis, penumomediastinum

Incidental discovery of a solitary pulmonary nodule on a radiograph imaging is common. The first step in the workup of such nodules is to:

obtain any previous radiographic lung images.

Absense of growth over time rules out malignancy. If previous radigrpah films are not available thn the nodule is assigned either alow, intermediate or HIGH probability of malignancy based on clinical and radiogrpahic data.

Low: followed by high resolution chest CT
intermediate: further investigated with PET scan and/or biopsy
HIGH probability nodules are removed surgically

Primary lower extremity sites responsible for PE?

Lower extremity DVT
#1 - iliofemoral DVT (area above the knee)
#2 = deep veins of the pelvis
## - calf vein emboli => proximal veins, increase incidence

What is the treatment for NSCLC: SQUAA LC, adenocarcinoma, large cell

1. Surgical removal: if mets out of chest - then not a candidate for removal
2. Radiation therapy prior to surgery - patients with
3. Chemotherapy is of uncertain benefit

NSCLC is staged by TNM, whereas SCLC is staged by?

1. Limited to chest plus supravlacicular node but not cervical/axillary
2. Extensive- outside of chest and SC nodes.

Normal ranges of ABGs? (doesnt req mechanical ventilation)

PaO2 of (50-60)
PaCo2 (40-50)
pH = 7.35-7.50

What causes a pleural effusion?

1. Increased fluid into the plerual space/drainage
2. Increased production of fluid by cells into the pleural space
3. Decreased drainage of fluid from the pleural space

In patients with COPD, which vaccinations are required?

Influenza vaccination annually
Pneumococcus polysaccaride vaccination of 5-6 years

postoperative cholestasis can develop after a prolonged surgery characterized by hypotension, extensive blood loss in tissues, and massive blood replacement.

T or F


Alveolar filling diseases causing restrictive lung disease?

-idiopathy hemosiderosis
-alveolar proteinosis

How might one diagnose air in stomach by auscultation?

ET tube may not have been placed correcly by ventialtion - check bilateral breath sounds and CXR. 3-5 cm above carina

Clinical features of COR PULMONALE

decreased exercise tolerance
cyanosis/digital clubbing
signs of RVHF; hepatomegaly, edema, JVD
parasternal life at P2 (seen in p HTN)
polycythemia vera present if COPD cause of COR pulmonale

Underlying cause of clubbing in patients?

#1 cause is chronic hypoxia
Diff diagnosis: LUNG cancer, CF,ILD, empyema, sarcoid, mesothelioma, heart dz, bacterial endocarditis, cirrhosis, IBD, primary biliary cirrhosis


Causes of COR pulmonale:

1. Right sided counterpart to LV heart dz due to systemic HTN - RVH with eventual RVF from pulm HTN 2/2 pulm disease

2. Doesnt include pulm HTN du to left sided HD like MS of LVF

Causes: 2dary to COPD; recurrent PE, ILD, asthma, CF, sleep apnea, penumoconiosis

Noncaseating granulomas involving the lungs at hilar (LAD). Eyes, skin, heart, MS, CNS also involved.

#1 cause of death = H.D.
#1 population affected:

1. AA females <40YO
-85% change of acute (noncronic) infection

Classic criteria of ARDS:

1. hypoxemia that is refractory to oxygen therapy ==> ratio of PaO2/FiO2 </= 200
2. bilateral diffuse pulmonary infiltrates on CXR
3. No evidence of CHF: PCWP </= 18 mm Hg

Fever night sweats wt loss hemoptysis

B SYMPTOMS - associated with TB and HIV

Centrilobar emphysema v. panlobar emphysema

-centrilobar is the most common
-destruction at respiratory bronchioles (proximal) with little distal change.
-upper lungs

-alpha1antitrypsin deficiency
-proximal and distal acini
-goes for bases of lungs

What is the I:E ratio?

amount of time alloted to I in comparison to Expire in 1 breath.

duration of each breath preset by RR. This increases the time spenin in INHALATION and decreases the time spend in EXPIRATION.

Want 1:2 for (I:E)

Mixed capillary (at site of A-->V) and prevapillary causes of PULMONARY HTN:

Lung dz of the parenchyma or of the pulmonary vessels
-includes obstructive - COPD, asthma, CB
-includes restrictive lung disease ILD

Malignant mesothelioma

2/2 abesteos exposure
-dyspnea, weight loss, cough, bloody effusoin on thoracentesis

MODALITIES for Asthma:

1. Rescue inhalants for ACUTE ATTACKS
2. Longer acting with nighttime asthma and exercise induced asthma
3. Decreased airway hyperresponsivity, decreased annual number of exacerbations

Albuterol - ST B2 agonist
Salmeterol LT B2 agonist
Inhaled corticosteroids
-inc risk core throat/candidiasis (thrush)
-increased risk of hoarseness

Diagnosis of lung CANCER
1. CXR =
2. CT scan =
3. Cytoloic sputum exam =
4. Fiberoptic bronchoscope =
5. Transsthoracic needle biopsy =
6. Mediastinoscopy =

1. Most important study for diagnosis but NOT for screening. If greater than 2 years without change in the lesion; then BENIGN
2. Staging lung CA; LOCAL v. DISTAL met
3. CYTO = centra tumor diagnosis (80 %) not peripheral more likely to be detected early.
4. Fiberopti goes 2/2 branches of the tree - good dz of the central CA IF VISIBLE, diagnostic jumps to 95% of causes.
5. TNB = highly accurate, good for peripheral lesions as well - invasice, selected pts only.
6. MED = direct visualization of medistinum

What are the subtypes of the 75% of Lung CA that are 2/2 NSCLC?


How does this compare to that of SCLC?

1. SQCC (30% of all LUNG CA) -- Central location -- Cavitation on CXR
2. Adeno (25% of all LUNG CA) -- Peripheral location -- Pleural involvement (20%) without smoking, may have pulmonary fibrosis
3. Large cell (5-10% of all LUNG CA) -- peripheral

SCLC -- (20-25% all LUNG CA) -- narrow bronchi (associated with LE syndrome) 50-75% mets

Clinical features of mediastinal masses

1. Due to compression or invasion of neighboring structures
2. Cough
3. Chest pain
4. Post obstructive pneumonia
5. Dysphagia
6. SVC
7. Compressed nerves (recurrent laryngeal CN X)
-horners SCG
-diaphragmatic paralysis (C3-c5)

AC Ventilation

assisted controlled ventilation
-guarantees a backup minute ventilation that has been present
-delivers breath when patient intitiates breath
-if the patient doesnt initiate breath, ventillation takes control and delierates a predetermined breathe.
-delivers the same predetermined TV

Primary PULMONARY Htn (PPH?)

1. Pulmonary HTN in absense of heart dz or LUNG dz
2. Diagnosis of exclusion
3. INcreased PA pressure leads to thickening of pulmonary arteriolar walls thus worsense pulm HTN, increases wall thickening
4. #1 in middle aged women
5. Poor prognosis (2-3 years)

Evaluation of hemoptysis

1. CXR
-look if TB, penumonia, granuloma, opacities
-if normal, then increased risk of PE

-perform CXR, if normal, then do this to r/o MALIG
-look for small tumor

3. CT of chest

For lung CA, what lab tests should be ordered/imaging to confirm diagnosis of NSCLC v. SCLC?

CXR, CT scan, TISSUE biopsy

Tissue biopsy is what determines that between NSCLC and SCLC

DI-restrictive lung diseases

AMIODARONE (K+ channel blocker)

When should a pateint be taken off the ventilator

1. Check if the patient has an adequate respiratory drive
2. Intact cough
3. PaO2 > 79 mmHg PaCo2 < 45
4. O2 saturdation > 90% with PEEP of < 0.5cm H2O; FiO2 < 40-50%
5. TV > 5mL/kg
6. RR < 30 breaths/minute
7. VC = 10-15
8. NegI pressure <-20cm

Recuurent pneumonia in the same lobe location should be a red flag for?

LUNG CA - get CT of the chest

How does elastase result in a change in alveolar wall destruction in emphysema?

excessive elastase will be produced in cases with alpha1antitrypsin or a deficiency of antiprotease activity in lung.
-macrophages and pmns digest human lung

how might pulmonary HTN be characterized?

PAPressure > 25 mm Hg at rest
PAPressure > 30 mm Hg exercise


1. To determine the underlying mechanism of hypoxeima
-PaCO2 level
-A-a gradiant
-Response to supplemental O2

2 A-a gradiant is normal if HYPOVENTILATION or low inspired O2 is the only mechanism

3. If V/Q mismatch/shunting presenting then both PaCO2 and A-a gradient elevated

4. Supplemental O2 differs between two mechanisms

What is the number 1 parameter used to decipher ARDS from CHF?

PCWP - if low (< 18mmHg) then ARDS
PCWP - if hi (> 18) cardiogenic PEdema

How to diagnosis primary pulmonary htn

1. Cardiac cathederization
2. CX shows enlarged central pulmonary arteries, increased RV with CLEAR LUNG FIELDS!
3. PFT shows restrictive pattern

Treatment of aspirations and aspirations pneumonia

CAB - airway breathing circulation = SUPPLEMENTAL o2

Penicillin G - to cover gram +
CLindamycin - to cover the anaerobes

If foul smelling sputum think ANAEROBIC COVERAGE NEEDED! go for the good antibiotics for anaerobes (that includes bacteroidies, clostridium, pepto)

How is airway obstruction diagnosed?


Normal --> elevated TLC, elevated RV, elevated FRC
Decreased FEV1
Decreased vital capacity

Clinical features of aspirations pneumonia

~40% develop symptoms 2-3 days post organisms areobic --> anaerobic (primary klebsiella)

-acute repiratory distress
-SOB, cough fever, tachypnia, hypoxemia, frothy sputum

causes = decreased level of consciousness, aspirations by alcohol, vomiting, ileus

HOW is the diagnosis of ASTHMA made?

1. PFT required = obstructive pattern with elevated TLC and RV and elevated FRV however will have lower TV low FEV1 and low FEV1/FVC ratio

2. SPIROMETRY = get before and after albuterol (B2 agonist) if increased FEV1 or FVC by 12%, then confirms the diagnosis.

3. PFR = peak flow rate: (450-650 in males; 250-500 in females); mild >300; moderate = 100-300; severe = <100

4. Bronchovocation test if no PFT

Goodpastures syndrome

Autoimmune (HLA DR2) antigbm type II hs to the alpha3-chain of collagen type 4 (IgG-AB)

1. Hemoptysis *cough up blood
2. SOB
3. Hematuria
4. Burning urination - renal failure and protein in urine

Diagnosis by: TISSUE BIOPSY

What is minute ventilation?

(RR x Vt) = measures ventilation. To decrease PaCO2 in patient, decrease the RR or TV.

Want patients baseline < 45 mmHg (PaCO2)
-initial TV of 8-10 mL/kg is appropriate in most cases (lwoer TV recommneded in patients with ARDS and COPD)
-10-12 breaths /minappropriate

What is ILD - classifications?

Intersitital lung disease (RESTRICTIVE LUNG PATTERN)
-inflammatory lung disease involving the alveolar wall (resulting in widespread fibroelastic proliferations, collagen deposition leading to irreversible firbosis/imparied O2 exchange/change in lung struccture

-environmental lung dz
-ILD with granulomas (sarcoid)
-Alveolar filling disease (ARDS)
-HS lung disease

Treatment of an acute exacerbation on hospital admission (asthma)?

PEV < 60% of predicted - req systemic steroids

1st - inhaled B2 agonists
-via nebulizer/MDI (metered dose inhalter)
-occurs in min

2nd - corticosteroids
-administer IV intiailly then orally when clinical improvement seen
-then inhaled

3rd - theophylline and IV magnesium
-keep O2 saturation >90%

Workup of PE:

Tests providing basis for treatment of PE with anticoag
1. Intraluminal filling defects in pulm atery on helical CT
2. DVT diagnosed on US and clinical suspician
3. Positive pulmonary angiogram (proves PE)

Rule OUT PE:
1. Low probability V/Q scan or normal helical scan and low clinical suspician
2. Negative pulmonary angiogram
3. Negative D-dimer

Increased intrathoracic pressure causing pulmonary HTN?

Increased blood viscosity causing pulmonary arterial pressure of > 25?

1. Mechanical ventilation with PEEP, COPD, causes pulmonary HTN (>25 mmHg at rest)


<50 YO, non smoker, <2.0cm nodule, no growth in > 2 years, circular, regular, central laminated with Ca2+

>50YO, prior smoker, >3.0 steady growth, nodule grossly irregular, stippled or eccentric pattern of calcification


ILD with restirctive pattern and honeycoming or ground glass on CXR. Cause is unknown and definitive diasnosis requires a lung biopsy

-presents with gradual SOB, nonproductive cough, dry cough and as survivial of 3-7 years

Treatment: no effective treatment available - majority of patients >70% do not improve with O2, corticosteroids, lung transplant

When does a patient require mechanical ventialtion?

significant respiratory distress (increases RR)
-impaireddec level of consciousness; cannot protect airway
-metabolic acidosis (doesnt adequately compensate with hyperventilation thus hypoV) and decreased pH
-respiratory muscle fatigue
-PaO2 < 70 mmHg or hypercapnia PaCo2 > 50; respiratory acidosis (pH<7.2) with hypercapnia

Diagnosis of PULMONARY HTN

ECG: RVH, RA-deviation, right atrial abnormality (myxoma)

ECHO: dilated pulmonary artery; dilitation/hypertrophy of RA/RV; abnormal movement of IV septum; right heart catheterization shows increased PA pressure

WHen should O2 therapy in patient with COPD be considered?

If PaO2 is 55mmHg or O2 saturaation is < 88%
If PaO2 55-59 mmHg + Polycythemia vera or COR Pulmonale (RCHF)

"All causes of wheezes"?

#1 is asthma but not ALL wheezes are asthma, but all that have asthma do wheeze.

1. CHF - edema in airways and mucosa
2. COPD - inflammation causes narrowing
3. Cardiomyopathyies - pericardial dz, edema near bronchi
4. Lung CA due to obstruction of AIRWAYS

Treatment of PE:

1. Supplemetnal O2 for hypoxia
2. Acute anticoag therapy of UFMH or LMWH
-start immediately if suspect
-give one bolus with IV infusion 5-10 days to maintain apTT 1.5-2.5x
3. Oral warfarin LT - start hep on day 1 and continue 3-6 months
4. Streptokinase/tPA

local invasion symptoms of lung CA v. metastatic disease sites?

Local invasion:
1. SVC syndrome -obstructed SVC by mesdiastinal tumor = seen in SCLC facrial features = seen in SCLC facial fullness, JVD, ARM edema.
2. Phrenic nerve palsy
3. Recurrent laryneal nerve palse
4. Horner's syndrome (PTOSIS, MIOSIS, ANHIDROS)
5. Pancoast tumor - SUPERIOR SULCUS TUMOR
6. MALIGNANT pleural effusion


ILD associated with granulomas

1. Sarcoidosis -along with other organs
2. Histocytosis x - langerhands cells CD1 esterase
3. Wegeners granulomas (sinus infection/hemoptosis plus hematuria)
4. Churg-strauss syndrome (IgE)

CPAP - continuous posistive airways pressure

positive pressure (0-20 cm H20) delivered continuously by ventilator but doesnt change volume of breaths delivered
-the patient breaths on own.
-set PEEP and pressure support

What is the diagnosis of a pleural effusion?

1. CXR - PA and LA view - blunted costophrenic angle - ~250 mL of fluid must accumulate to detect effusion on CXR. Determine if free flowing or loculated.
2. CT scan more reliable than CXR
3. THORACENTESIS - useful if unknown etiology
-75% diagnosis of patients; >10mm think of LLdecub
-therapeutic - drainage for relief
-pneumothorax - complication in 10-15% patients
-send fluid for: CHEMISTRY (protein, glucose); CYTOLOGY; CBC and CULTURE

Necrotizing granulomatous vasculitis that affects:
1. lungs/hemoptysis
2. kidneys (+/- hematuria - RPGN)
3. Upper airway/lower resp
4. cANCA
5. perforated nasal septum


How is COPD monitored?

1. Serial FEV1
2. Pulse Ox
3. Exercise intolerance


TLC = IRV + TV + ERV + RV = VC + RV

If a 36 yo patients comes to office with cc of progressive fatigue with a PMH of infiltrative TB and a blood culture indicating two populations of RBC (hypochromic and normochromic) - what is the next best step in this patients management if already on the "RIPE" regimen and a lab value status indicating (CBC) microcytic anemia with elevated serum iron levels and decreased TIBC?

Addition of pyridoxine - why?

Because the patient has a probably SIDEROBLASTIC ANEMIA. his condition results from defective heme synthesis that is most commonly 2/2 imparitment in the early steps of heme synethesis. Because the patient is on the TB regimented treatments, and ISONIZED comparitively can act as a antagnosit to pyridoxine, pateints should be expected to have an acquired sideroblastic anemia.

This will result in two groups of RBc on microscopy (one group in which manifests as microcytic hypochromic anemia that simulates iron deficiency anemia, and another group that are normochromic - hence the dimorphic population of cells). The decreased TIBC and elevated iron helps to differenciate sideroblstic anemia from that of iron-def anemia

What complications, then, are associated with mechanical ventilation?

1. Anxiety/agigtation/discomfort
-must sedate, use benzos or morphine, use propofol
2. Difficulty with tracheal secretions
3. Nosocominal pneumonia (if intub > 72 hr)
3. Extubation
5. barotrauma (high PEEP/O2 toxicitiy if FiO2 > 0.6) for greater than 2-3 days.
6. Hypotension 2/2 increased thoracic pressure by PEEP (increased intrathoracic pressure that decreases venous return and increased SVR - and ultimately cor pulmonale



Treatment with steroids

HOw might PPH be treated for?

1. Pulmonary vasodilators like (PROSTCYCLINS - EPOPROSTENOL)
2. CCB decreased PVR
3. Vasodilator trial = O, IV adenosine, ORAL CCB
4. Anticoag with warfarin 2/2 venous statis and prevention of PE
5. Lung transplantation


Cardio: CHF, JVD, EDEMA, Hepatomegaly, P. Edema, Tachypnea, Tachycardia, volume overload.

ARDS: sepsis, increase RR, increased HR, doesnt respond to supplemental O2; cannot ventilate bc high peak airway pressures 2/2 stiff lungs.



Although the effects of both CARDIOGENIC PULMONARY (FLASH) EDEMA and ARDS are the same, how does the causality differ?

Increaed alveolar capillary permeability causes ARDS; thus the interstitial edema, SOB, increased HR and RR, hypoxemia with shunting that doesnt respond to O2.

In cardiogenic pulmonary edema - congestive hydrostatic forces cause the increased interstitial fluid.


-SOB (most often NOT releived by albuterol)
-Increased sputum production and cough that is (NOT relieved by theophylline)
-Increased respiratory failure +/- ventilation (O2 therapy for HYPOXIA)

What is INR?

What increases the value?

"therapeutic range"?

International ratio that reports the PROTHROMBIN TIME (PT) by that of the extrinsic pathway affected by warfarin (wafarin thus increases the INR at clotting factors 2, 7, 9, 10 and protein C and S)

Therapeutic = 2-3

What are some causes of hypersenitivity pneumonitis and differentiates it from other causes?

Acute: flu-like with fever, chills, cough, SOB - CXR infiltrate
Chronic: Restictive lung disease

Extrinsic allergic alveolitis:
1. Farmers lung, modly hay
2. Birds breeders lung
3. Air conditionals lung
4. Bagassosis (sugar cane)
5. Msuchroom workers lung
6. Spores of thermophilic actinomycetes

Diagnosis of IgG and IgA in serum with ILD symptoms

Post capillary causes of pulmonary HTN (> 25 mm Hg)

primary due to L side of heart that will increase pressures on the PULMONARY VEINS like that of MITRIAL stensis (will be a diastolic murmur with OS).

ex: Mitrial stneosis (backs up blood into lungs and icnreases pressure of pulmonary capillary); LV dysfunction (LVH can cause); ATRIAL MYXOMA primary lipoma located in the R atriaum that is most liekly to cause a mid diastolic murmur in patients with no other underlying etiology and CAN result in a thrombus formation that can undergo embolic stroke.; CONSTRICTIVE PERICARDITIS

Mediastinal masses

1. Metastatic cancer (#1 lung) most common cause of mediastinal mass in older patients
2. Anterior = thyroid, thymoma, lymphoma
3. Middle = lung, lymphoma, aneurysms, cysts
4. Posterior = neurogenic tumor, esophageal tumor

Chronic treatment of ASTHMA
1. Mild intermittent
2 . Moder persistent
3. Sev persistent

1. Mild intermittent - 2x/week == NONE (chronically)
2. Moderate persistent - daily ---DAILY INHALED corticosteroid
3. SEVERE continuous ---daily inhaled corticosteroids, LT B2 agonist

Ventilation versus oxygenation?

Both are unrelated to one another - o2 saturdation can be 100% with increased PaCO2 and be in ventilary failure

ventilation monitored by PACO2
-to decreased paCO2, must INCREASE or INCREASE TV
-minute ventilation = RR x VT
-to decrease paCO2, want to increase ventilation and thus increase RR and VT

oxygenation monitored by O2 saturation
PaO2 - to decrease PaO2 in the ventilated patient one must either decreased FIo2 or decreased PEEP

CLINCIAL features of a tension pneumothorax?

1. Hypotension - cardiac filling decreased due to compression of great veins
2. JVD
3. Mediastinal deviation away from side of lesion
4. Decreased breath sounds over collapsed lung
5. Hyperresonance


-chronic ILD with ABNORMAL PERFORATION OF the langerhan cells of bone marrow that can migrate
-90% smokers
-localized to bone or lung (eosinophilic granuloma or 2dary types - HAND-SULLER CHRISTIAN OR LETTERER-SIWE disease)

Treatment of tension pneumothorax


2-3rd intercostal space in the midclavicular line - then chest tube it

What is the FEF50% for normal , obstructed, restricted lung?

Forced expiratory flow (FEF50%)
-normal = 3.2
-obstructed = 0.5
-restricted = 1.9

Prognosis of patients with PE diagnosis?

1. recurrence common (clinically silent)
-can lead to chroni PULM HTN and CHRONIC COR PULMONALE

2. PULM HTN (2/3) pts
-30% death d/t recurrent PE left undiagnosed

Paraneoplastic syndromes associated with

- PTHrP-hormone with elevated Ca2 decreased phos and elevated parathyroid hormone)
-hypertrophic pulmonary osteoarthropathy

2. SCLC -
-Lambert eaton syndrome at NMJ;
-SIADH from ectopic tissue;
-ACTH secretion from ectopic tissue (carcinoid?) increased cortisol and increased cushings

3 Adenocarcinoma - hypertrophic pulmonary osteoarthropahty


75% NSCLC 25% SCLC
-SQUAA (30)
-Adenocarcinoma (35%)
-Large cell LC (5-10%)

Increased P2 on auscultation on/at 2nd parasternal border L side with a subtle lift of sternum


Rare condition due to excess accumulation of surfactant-like protein and phospholipids in alveoli


Dry cough, SOB, rales, HYPOXIA

Diagnositc: LUNG BIOPSY
CXR: ground glass appearance with bilateral alveolar infiltrations that resumble a bat shape

Exudative effusion treatment

Treat underlying disease
-bacterial inf/tb
-viral infectoin

What are the requirements to use NPPV?

1. Neurologically intact - aware, cooperative, protect airway

If doesnt improve, BIPAP should be d/c and conventional therapy for endotrachial intubation and mechanical ventilation.

Gold standard to diagnose PE:

Decision to rule criteria (DUKES!)

Pulmonary angiography - definitive diagnosis of exclude PE but is invasive

Symptoms and signs of DVT = 3 pts
ALT dx less likely thank PE = 3 pts
HR > 100 bpm = 1.5 pts
Immobilization > 3days/surgery past 4 weeks = 1.5 pts
Previous DVT = 1.5 pts
Hemoptysis = 1.0
Malignancy = 1.0

APICAL tumor of the lung involving C8 and T1-T2 nerve roots (radiating) pain down arm: Most common in SQUA CC with CENTRAL cavitation

(+) Association with HORNERS 60% of the time


Pleural effusion

1. In increased pleural fluid amylase, think:
2. If milky, opalescent fluid, think:
3. If purulent fluid/pH < 7.2 think:
4. If bloody effusion think:
5. If exudative + lymphocyte think:
6. If pH < 7.2 think:

1. Esophageal rupture, pancreatitis, malignancy
2. Chylothorax
3. Empyema - pus in the pleura
4. Malignant if bloody

What is the first treatment for spontanous pneumothorax? Why?

Supplemental O2
-hastens the resorption of air in the pleural space

Hypercapnia --> ___ ____
can lead to SOB, VASODILATION OF CEREBRAL VESSELS with increased intracranial pressure and papilledema and coma

respiratory acidosis
PCO2 > 35 mmHg

Granulomatous vasculitis in patients with asthema, increased pulmonary infiltrates and RLD; increased RASH and increased eosinophilia


Churg strauss syndrome


When a pateint is ventilator dependent for 2 or more weeks, a tracheostomy is usually performed to prevent softening of tracheal cartilage

Interstitial pulmonary inflammation that occurs in patients with prio treatment to breast, lung, lymphoma, thymoma, CANCER

1. Acutely forms 1-6 mo post treatment or chronically 1-2 years later with alveolar thickening and pulmonary fibrosis leding t a dever, couh, chest fullness, pleruitis chest pain and hemoptysis

2. CT SCAN - DIFUSE INFILTRATES WITH GROUND GLASS densities with pleural/pericardial effusion

SOB on exertion + syncope + fatigue + chest pain on exertion


What causes bronchiectasis? How can this be treated

Cause: permanent dilitation of the bronchioles and destruction of the bronchial walls with damaged cilia.

#1 - CYSTIC FIBROSIS most common AR in causcasions (~50%) for delta-F508 CFTR gene mutation

#2 - infection, humoral immunodeficiency or airway obstruction

Hypoxemic respiratory failure and oxygenation

Hypercarbic respiratory failure and oxygenation

1. Lowest concentration of oxygen that provides sufficient O2 to avoid O2 toxicity (free radical)

2. High concentrations of O2 causes CO2 retention especially in patients with COPD because pt doesnt ventilate off of CO2 - thus hyPOventilation.

What are the classic types of COPD?

List the four risk factors:

1. Chronic Bronchitis - productive and chronic cough of sputum for at least 3months/year
2. Emphysema - permanent enlargement of air spaces due to surfactant destruction of alveolar walls at terminal bronchi

Risk factors:
1. Tobacco use (90%) COPD
2. alpha-antitrypsin
3. second hand smoke
4. chronic athsma

Which lung is most common to develop aspirations penumonia 2/2 anatomy?

Lower segment of right upper lobe
upper segment of right lower lobe

Because the RM bronchus follows straight path

Which paraneoplastic syndromes are associated with SCLC (20-25%) of ALL lung CA?

1. SIADH - 10% - ectopic tissue which increased ADH; this causes increased H2O retention that will bind and increase AQP2R while likewise increases that of sodium out. Thus, will have hypoatremia bc body trying to unload with hypervolemia and decrease RAAS

2. ECTOPIC ACTH: SCLC, increased cortisol, increased cushings
3. Lambert-eaton syndrome

Peripheral pulmonary infiltrates with a fever and elevated eosinophils without changes in IgG and IgA


What is the treatment of SPONTANEOUS pneumothorax?

1. PRIMARY --> If small and patients is asymptomatic then
-OBSERVE - resolves in 10 days
-small CHEST TUBE (one way valve)

2. PRIMARY --> if LARGE/symptomatic (cough, SOB, sudden and UNILATERAL CP
-chest tube placement/insertion


Causes of acute repiratory failure 2/2 shunts? (ittle or no ventilation in perfused areas due to collapsed or fluid filled alveoli - pneumonia - the venous shunts to the arterial circumation without getting oxygenatued and thus results in that of ARF 2/2 decreased oxygenation)

1. Atelectasis (collapsed)
2. Fluid build up in alveoli
-pneumonia/pulmonary edema
3. Drect RIGHT to LEFT shunt d/t congenital abnormality

doesnt respond to supplemental O2



What are the clinical features of pulmonary embolism

increased HR, RR, SOB

1. DYSPNEA (72%)
3. COUGH (27%)
4. Hemoptysis (13%)

1. Tachypnea (RR) *70%) - hypercarbic ventilatory failure
2. Rales (51%)
3. Tachycardia (30%) increased HR
4. S4 (24%)


1. Passive = resistance to pumonary venous drainage. Not actively in pulmonary best - further down. Mitrial stensosis, LVF, ATRIAL myomxa (most common cause of a mid diastolic heart murmur)
2. Hyperkinetic = L--> R cardiac shunts that include VSD, ASD, PDA
3. Obstructive = resistance to flow through P. arteries = PE, PA setnosis
4. Obliterative = resistance due to fibrosis PPH (primary pulmonary HTN, CVD, crest)
5. Vasoconstrictive - hypoxia induced (COPD)

What are the risk factors for LUNG CA?

1. Cigarette smoking > 85% of cases
-adenocarcinoma lower associated lung CA to smoking.
2. Passive smoking (2nd hnd)
3. Asbestos: ship building, construction, cars, smoking and asbestos increase risk
4. RADON - found in basements
5. COPD - independent risk factor once smoking considered

What are the clinical features of pulmonary HTN?

Symptoms: SOB on exertion, fatigue, chest pain (exertional), syncope (exertional) with severe disease)

Signs: loud pulmonic component of P2 and lift of the sternum (RV dilitation); when RVfailure occurs = JVD, peripheral edema, ascites


-lung lavage or GSCMF - increase the granulocytes by stimulatied neulasta or filgrastin.

Hypocarbia is common is asthmatics under respiratory distress, why?

Have increased respiratory rate thus should cause PaCO2 to decrease (breathing off the CO2)

Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction thus INTUBATION may be required

CXR: egg shell calcifications
-localized and nodular peribronchial firbosis of the UPPER LOBES that can be acute (rapid onset + death) or chronic (symptoms yrs post exp)
-#1 symptom = exertional dyspnea


Diagnosis of acute respiratory failure:

1. ABG
2. CXR or CT scan
3. CBC and metabolic panel
4. If cardiogenic P. edema, get enzymes

When are DDIMERs elevated?

DIC (SEPSIS - 2dary)

What are the constitutional symptoms of LUNG CA - both SCLC and NSCLC?

1. Anorexia, weight loss, weakness
2. Indicates advanced stage is cachexia
3. SOB, hemoptysis, cough, wheeze
4. Recurrent pneumonia

Decreased tactile frematis; decreased breath sounds over effusion, dullness to percussion:

pleural effusion

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