Dr.

Ali’s Uworld Notes For Step 2 CK

Respiratory
Nonallergic rhinitis (NAR), also known as vasomotor rhinitis - Features that help
differentiate NAR from allergic rhinitis include predominant nasal congestion or stuffiness,
postnasal drip (dry cough), and no specific identifiable triggers. In contrast, patients with
allergic rhinitis have predominant eye symptoms, itching, and sneezing, along with specific
identifiable triggers in most cases.

Nonallergic rhinitis usually presents with one of the chronic rhinitis symptoms (nasal
congestion, rhinorrhea, sneezing, and postnasal drainage) without a specific etiology.
Routine allergy testing is not necessary prior to initiating empiric treatment. Depending on
the severity of the symptoms, patients should be treated with an intranasal antihistamine,
intranasal glucocorticoids, or combination therapy
Sarcoidosis - Painful shin lesions and bilateral hilar adenopathy on x-ray suggest
Sarcoidosis. Sarcoidosis is a chronic multisystem disorder due to noncaseating
granulomatous inflammation deposited into various organs. It typically affects young
adults, is 3-4 times more common in African Americans, and affects more women than
men. Sarcoidosis is frequently detected incidentally on chest x-ray but can also present with
symptoms such as cough, dyspnea, fever, malaise, and weight loss.

Sarcoidosis primarily involves the lungs. Chest x-ray classically shows bilateral hilar
adenopathy and/or reticular opacities. Up to 30% of sarcoidosis patients present initially
with extrathoracic manifestations commonly involving the skin ( eg, erythema nodosum
with painful shin lesions), eyes (uveitis), and musculoskeletal system ( eg, polyarthralgia).
Elevated calcium and angiotensin-converting enzyme levels are often seen but are not
specific for diagnosis. Definitive diagnosis can be established with m e d ia s ti n o s co p y or
bronchoscopy for tissue biopsy. Symptomatic patients are usually treated with
corticosteroids.
Examination of the respiratory system follows the same general principles of inspection,
palpation, percussion and auscultation. In the case of a normal lung, the lung will be
resonant on percussion. Auscultation will reveal vesicular breath sounds which consist of a
quiet inspiratory phase and an almost inaudible expiratory phase.

When a portion of the lung is consolidated the examiner will detect dullness to percussion.
Sound conduction through the consolidated region will result in bronchial breath sounds
which are louder and have a more prominent expiratory component.

IMPORTANT: This holds true only if the airways are patent! If the airways are blocked the
breath sounds over the consolidated lung tissue would be decreased! Increased sound
transmission over the consolidated lung region can also be assessed by asking the patient to
say the letter E and listening with a stethoscope. If it sounds like "A" with a nasal or bleating
quality, it is called egophony and suggests consolidation. Crackles are often also heard in
patients with a consolidation.

Palpable vibration felt on the chest wall is known as fremitus. Sound travels faster in solids
(consolidation) than in an aerated lung, resulting in increased fremitus in pneumonia. The
presence of egophony, bronchophony, or whispered pectoriloquy also suggests a consolidative
process. Presence of fluid or air outside the lung interrupts the transmission of sound, resulting
in decreased fremitus in pleural effusion and pneumothorax. Percussion shows
Placing a consolidated lung segment in the dependent position can increase the right-to-left
shunt in a patient with pneumonia. Ex – patient with left lower lobe pneumonia

Decreased breath sounds and increased fremitus over the LLL indicate consolidation. and
rhonchi indicate narrowed conducting airways (possibly due to mucous plugging). In
consolidated lung segments the alveoli are filled with exudate and do not participate in
pulmonary gas exchange. so their ventilation is essentially zero. i.e .. blood perfusing
consolidated areas is not oxygenated. Positions that increase the proportion of pulmonary
blood flow passing through such segments decrease the patient's oxygen saturation (right-to-
left shunt). When this patient lies on his right side, the consolidated LLL is at a higher vertical
height (less dependent) and therefore receives a reduced proportion of the pulmonary blood
flow, minimizing the shunt caused by the consolidated LLL. Conversely, when this patient is on
his left side, the consolidated LLL is more dependent, receives an increased proportion of the
pulmonary blood flow. and worsens the shunt.

hyperresonance in patients with pneumothorax and dullness in those with pleural effusions or
pneumonia
Recurrent pneumonias in the same anatomic region of the lung suggest bronchial obstruction
due to an underlying abnormality. While there are numerous potential causes of this
obstruction, bronchogenic carcinoma is the most concerning possibility. Other possible causes
include carcinoid tumor (usually endobronchial), foreign body, and bronchial stenosis Chest
computed tomography (CT) is indicated to visualize underlying parenchymal abnormalities.

Pulmonary Embolism - Over half of the patients with a DVT in a proximal leg vein will
experience a PE manifesting clinically with sudden onset dyspnea, tachypnea, and pleuritic
chest pain. Arterial blood gas analysis in this setting typically shows respiratory alkalosis and
a widened alveolar-arterial oxygen gradient due to ventilation/perfusion mismatch. Chest
x-ray can be normal or show evidence of atelectasis and/or pleural effusion. When pleural
effusions develop, The pleural fluid can be exudative (more common) or transudative, with
varying composition. While pulmonary angiography is the gold standard for diagnosing PE,
helical computed tomography scan is the diagnostic test of choice in practice.

Risk factors for DVT include prolonged immobility, oral contraceptive use, obesity,
smoking, recent abdominal or orthopedic surgery, occult malignancy and other
hypercoagulable conditions, including sickle cell trait. Patients typically present with sudden
onset dyspnea, cough, tachypnea and pain worsened with respiration. An elevated A-a
gradient is commonly seen in patients with pulmonary embolism.

Factor V Leiden is the most common inherited disorder causing hypercoagulability and
predisposition to thromboses, especially DVT of lower extremities.

In patients with pulmonary thromboembolism, you expect to reveal a relatively large area of
perfusion defect without ventilation defect called mismatched defect.

Acute massive pulmonary embolism can present initially with syncope and shock. Right heart
catheterization in patients with massive pulmonary embolism will show elevated right atrial and
pulmonary artery pressures, along with normal pulmonary capillary wedge pressure.
The thrombus increases pulmonary vascular resistance and right ventricular pressure, causing
right ventricular hypokinesis and dilation, decreased preload, and hypotension.

The finding of a thrombus in the right pulmonary artery on CT angiogram is diagnostic of PE.
Though PE may arise from the right heart, pelvic veins, or upper extremity veins, the deep veins
of the lower extremities are the most frequent source. Lower extremity deep vein thrombosis is
divided into two categories: proximal vein thrombosis (above the knee) and calf vein
thrombosis. The proximal deep veins (iliac. femoral and popliteal veins) are the source of >90%
of acute PE's, probably because of their large caliber and proximity to the lungs. Therefore, the
iliofemoral vein is the most likely source of this patient's PE.

The first step in evaluating a patient with suspected PE is supportive care with oxygen for
hypoxia and intravenous fluids for hypotension.

Anticoagulation (eg, low-molecular-weight heparin or unfractionated heparin) should be given

prior to diagnostic testing in patients with likely PE. After giving heparin, then decide if he can
receive thrombolytics or IVC Filter. Anticoagulation prevents further clotting but does not lyse
the existing clot.

The most definitive tests used to diagnose PE include ventilation-perfusion (V/Q) scanning,
pulmonary angiography (gold standard) and spiral CT scanning of the chest. Of these, the
spiral CT scan is the most commonly used

Wedge-shaped pleural-based opacification is likely to occur distal to a completely occluded

pulmonary artery. Pulmonary infarct areas may also occasionally be seen on chest x-ray as a
Hampton's hump. Pulmonary artery filling defects are usually visible on contrast-enhanced CT
scans. In addition, pulmonary embolisms are a common cause of both transudative and
exudative pleural effusions.
Travel associated Legionnaire's disease is a well-documented phenomenon that has been
linked to cruise ship and hotel water supplies. Symptoms that help distinguish Legionella
from other causes of CAP include high-grade fever (>39.o•q, gastrointestinal symptoms.
and neurologic symptoms. Lung exam typically reveals rales and chest radiograph most
often reveals focal lobar consolidation. Legionella pneumophila is a Gram negative rod that
stains poorly because it is primarily intracellular. Therefore, sputum gram stain showing
many neutrophils but no organisms is also characteristic. The definitive diagnosis may be
made by culturing the bacteria on charcoal agar and/or urinary antigen testing.
Legionnaire's disease is treated with either macrolides ( azithromycin) or newer generation
fluoroquinolones (levofloxacin)

Causes of atypical pneumonia - include Mycoplasma pneumoniae, Chlamydia pneumoniae,

Legionella, Coxiella, and influenza. Mycoplasma pneumoniae is the most common cause of
atypical pneumonia in the ambulatory setting. Atypical pneumonia is distinguished from
pyogenic pneumonia by its more indolent course, non-productive cough, and higher
incidence of extrapulmonary symptoms, multiple extrapulmonary symptoms including
headache, sore throat and skin rash (erythema multiforme) is typical of Mycoplasma,
Mycoplasma is an organism that does not have a cell wall, and therefore does not stain with
Gram stain. Hence the finding of only polymorphonuclear cells on sputum Gram stain
analysis. It occurs most frequently in elderly patients and smokers. The urine Legionella
antigen test is helpful in making the diagnosis.

Anaerobic pneumonia as a complication of upper Gl endoscopy (aspiration pneumonia) -

Patients with pneumonia caused by anaerobic organisms typically present with systemic
symptoms such as fever and malaise as well as a characteristic foul-smelling sputum.
Patients with poor dentition. who have a greater quantity of anaerobic organisms in their
mouth, are at greater risk of anaerobic aspiration pneumonia. The location of the infiltrate
depends on the patient's body position when the aspiration occurs as the infectious agents
tend to settle in dependent lung zones, such as the posterior segments of the upper lobes
(recumbent) and the superior and basilar segments of the lower lobes (standing). Adding an
antibiotic with anaerobic coverage, such as clindamycin, is the most reasonable next step.

The important risk factors for aspiration pneumonia are:

1. Altered consciousness- seizures, alcoholism, drug overdose. and CVA, etc.

2. Dysphagia - esophageal reflux, diverticula, obstruction. etc.

3. Neurologic disorder- advanced dementia, Parkinsonism, myasthenia etc.

4. Sedation to procedures, such as bronchoscopy, intubation, endoscopy, etc.

Patients with impaired consciousness, advanced dementia, and other neurologic disorders
are predisposed to aspiration pneumonia due to impaired epiglottic function.

Pleural Effusion - Pleural effusion is present when there is an excess quantity of fluid in the
pleural space. When pleural effusion is suspected or diagnosed, the first step is to determine the
cause of pleural effusion, and management starts with determining whether the fluid is
transudate or exudate.

Diagnostic thoracentesis is the preliminary investigation of choice in the management of

pleural effusion, except in patients with classic signs and symptoms of congestive heart failure,
where a trial of a diuretic is warranted.

The classic Light's criteria classify an exudate as having at least one of the following:
• Pleural fluid protein/serum protein ratio >0 .5

• Pleural fluid lactate dehydrogenase (LDH)/serum LDH ratio >0 .6

• Pleural fluid LDH > 2/3 of the upper limit of normal for serum (LDH greater than 200).

The next step is to determine whether the effusion is complicated, uncomplicated, or an

empyema. For this you need to see Pleural fluid glucose level and PH. Complicated
parapneumonic effusions involve persistent bacterial invasion into the pleural space, which
decreases pleural fluid glucose <60 mg/dl (utilized by bacteria) and increases LDH (from lysis of
neutrophils). The culture is usually negative, and the effusion resolves with antibiotics as
bacteria can be cleared easily from the pleural space. Complicated effusions can progress to
empyema, which is frank pus in the pleural space requiring chesttube drainage. The pH of the
fluid should always be assessed. Low pH ( < 7 .2) is almost always indicative of an empyema
and indicates removal of the fluid by thoracostomy

Exudative Effusion causes – Infection (pneumonia and tuberculosis) ,malignancy, pulmonary

embolism (PE), connective tissue disease like Rheumatoid Pleuricy & Drug Induced Lupus
and iatrogenic causes. The Mechanism of exudative effusion is Increased Capillary
Permeability. An elevated pleural fluid lymphocyte count, is suggestive of tuberculosis,
sarcoidosis, lymphoma, or rheumatoid arthritis.

Transudative Effusion – Liver Failure (Due to Decreased Plasma Oncotic Pressure), CHF
(Due to Increased Hydrostatic Pressure) & PE

Parapneumonic effusions usually occur from pneumonia. It is just effusion due to pneumonia.
The fluid may be aspirated to determine if empyema has set in. The aspirated fluid should
always be analyzed for the protein content (exudates have more than transudates), gram stain,
cell count, cytology (rule out malignancy), and glucose levels (low in rheumatoid arthritis,
tuberculosis, empyema, malignancy, and esophageal rupture).
The pH of the fluid should always be assessed. Low pH (< 7 .2) is almost always indicative of an
empyema and indicates removal of the fluid by thoracostomy. Lactate dehydrogenase is
generally higher in exudates than in transudates.

Empyema most commonly occurs in the setting of untreated pneumonia due to bacterial
seeding of a pleural effusion. Inflammation and collection of pus in the pleural cavity leads to
the formation of a loculated, abnormally contoured effusion with adjacent pulmonary
consolidation.

Glucose concentrations less than 30 mg/dl suggest an empyema or rheumatic effusion. A

glucose concentration between 30-50 mg/dl indicates an effusion due to malignancy, lupus,
esophageal rupture, or tuberculosis. Glucose concentration is thought to be decreased in
exudative pleural effusions due to the high metabolic activity of leukocytes (and/or bacteria)
in the fluid.

Increased permeability of the right hemidiaphragm is thought to contribute to the development

of right-sided pleural effusions in cirrhosis, also known as a hepatic hydrothorax. Effusions due
to cirrhosis are typically transudates.
Glucose of less than 60mg/dL is also an indication for tube thoracostomy. LDH levels are
elevated in a number of conditions including myocardial infarction, cirrhosis and generalized
ischemia.

Empyema is an infection in the pleural space. Empyema can occur from Parapneumonic
effusions. They can also occur as a result of contamination of the pleural space by rupture of a
lung abscess, a bronchopleural fistula, penetrating trauma, a thoracotomy, and infection from
a hepatic or subphrenic abscess, or from a ruptured viscus (esophagus). One common cause of
empyema is after a hemothorax. The residual blood in the chest is an excellent medium for the
growth of bacteria.

Empyema is best diagnosed with a CT scan. When the empyema is localized, complex, and has
a thick rim, only surgery is the answer. In surgery, the thick pleural peel is removed, the pus is
removed, and the chest is drained. All old blood clots are drained and removed. Empyema,
which is recent in onset, can be removed by fibrinolytic therapy. Both streptokinase and
urokinase have been used. However, in a patient with a recent motor vehicle trauma,
fibrinolytic therapy is contraindicated.

When an empyema fails to be drained by a single chest tube, another chest tube may be placed
just in case the first one is blocked. However, for complex empyema, chest tube insertion can be
difficult and is best done under ultrasound or CT scan guidance. When a thick peel is present, a
second chest tube usually does not work. The removal of the thick fibrinous peel in surgery is
called decortications.

Blastomycosis Pneumonia - low-grade fever, night sweats, productive cough, and weight
loss could be explained by chronic infection, malignancy, or rheumatologic disease the skin
involvement, lytic bone lesions, and geographic location make Blastomycosis the most likely
cause of his illness. Blastomycosis is a fungal infection that occurs most often in the vicinity
of the Great Lakes, Mississippi river and Ohio River basins. (Wisconsin has the highest
infection rate.) The pulmonary symptoms and chest x-ray findings of Blastomycosis may
resemble tuberculosis and histoplasmosis. However, s ys te mic Blastomycosis may cause
characteristic ulcerated skin lesions and lytic bone lesions.

Broad-based budding yeast grown from the sputum confirm the diagnosis. ltraconazole or
amphotericin B may be used to treat symptomatic disease.

PCP Pneumonia - Pneumocystis jiroveci is an opportunistic pathogen and an important cause of

pneumonia in immunocompromised hosts – post Chemotherapy or AIDS
Cataplexy - Narcolepsy is a sleep disorder characterized by poorly regulated rapid eye
movement (REM) sleep. It, like OSA, is characterized by excessive daytime sleepiness, but
patients also suffer from cataplexy, sleep attacks, hypnagogic/hypnopompic hallucinations,
and sleep paralysis.

Obstructive Sleep Apnea – it is a phenomenon of nocturnal hypoventilation. There are two

types of abnormal ventilation during sleep: 1) apnea (cessation of breathing for more than 10
seconds) or 2) hypopnea (reduced airflow causing Sa02 to decrease by 4%). The most common
cause for both of these in the United States is obstructive sleep apnea (OSA), a transient upper
airway obstruction due to poor pharyngeal muscle tone. In OSA, the patient continues to
contract the diaphragm in an attempt to breathe, but airflow is impeded by upper airway
obstruction. OSA is the most common medical cause of excessive daytime sleepiness in this
country, affecting over seven million people. Risk factors for OSA include obesity, tonsillar
hypertrophy, and hypothyroidism. Men are more frequently affected than women.

Patients with sleep apnea alone hypoventilate at night, which causes transient hypoxia and
hypercarbia that resolves during wakefulness. The typical presentation of sleep apnea
syndrome includes a moderately obese middle-aged man complaining of daytime somnolence,
morning headaches, increased fatigability, and who is noted to snore loudly. Try weight
reduction, avoidance of sedatives and alcohol, and avoidance of supine posture during sleep
as a first step.

Obesity Hypoventilation Syndrome (OHS) also known as Pickwickian syndrome - Patients with
OHS classically demonstrate extreme obesity (BMI=55. nl 18.5-24 .9) a thick neck and
hypersomnolence. The patient's distant heart sounds, low voltage QRS complexes on EKG and
poor quality chest x-ray are all findings consistent with obesity. This patient also has
polycythemia secondary to alveolar hypoventilation another common finding in OHS. The leg
edema noted on physical exam may be a sign of right heart failure.

This patient's ABG reveals respiratory acidosis (normal pH is 7.35-7 .45), hypercapnia and
hypoxemia (normal P02 is 70-1 DO). In OHS. derangement of the ABG is usually a consequence
of decreased chest wall compliance, which leads to increased work of breathing.
Eventually, The work of breathing becomes so high that the CNS chemoreceptors establish a
higher pC02 set-point causing resultant hypoventilation, hypercapnia and hypoxemia.
Respiratory muscle weakness also occurs in many OHS patients but it is not the major cause of
the clinical findings.

Patients with obesity hypoventilation syndrome do not have respiratory mechanics that
allow them to resume normal ventilation during wakefulness and hence develop chronic
respiratory failure. Consequences of obesity hypoventilation syndrome include pulmonary
hypertension with cor pulmonale. Secondary erythrocytosis, hypoxia, chronic hypercapnia
(due to persistent hypoventilation) and respiratory acidosis. In a compensatory effort to
maintain a normal pH. the kidney increases bicarbonate retention and decreases chloride
reabsorption.

Theophylline Toxicity - Theophylline has a narrow therapeutic index, and toxicity can occur
from accumulation by reduced clearance or decreased metabolism due to saturation of
metabolic pathways. Theophylline is metabolized predominantly by the cytochrome
oxidase system in the liver. Inhibition of these enzymes by concurrent illness (eg, cirrhosis,
cholestasis, respiratory infections with fever) or drugs ( eg. cimetidine. ciprofloxacin.
erythromycin. clarithromycin. verapamil) can raise serum concentration and cause toxicity.

Symptoms of toxicity usually manifest as central nervous system stimulation (eg. headache.
insomnia. seizures), gastrointestinal disturbances ( eg. nausea. vomiting) and cardiac
toxicity (arrhythmia).

Pancoast Tumor - An apical lung tumor can cause compression of the sympathetic trunk
(Horner syndrome), the brachial plexus (Pancoast syndrome), the right recurrent laryngeal
nerve (hoarse voice) and the superior vena cava (SVC syndrome). Compression of the
brachial plexus by such a tumor can cause pain, paresthesias and I or weakness of the right
arm. Specifically, Pancoast syndrome is characterized by shoulder pain radiating into the
arm in an ulnar distribution and is caused by tumor invasion of the eighth cervical and first
thoracic nerves

COPD – In chronic obstructive pulmonary disease (COPD) chest x-ray shows increased
radiolucency of the lung parenchyma, elongated and narrow heart shadow, barrel-shaped
chest, and a flat diaphragm. Later stages of COPD often have "air trapping" (increased
residual volume) and progressive hyperinflation (increased total lung capacity). Lung
hyperinflation preserves maximum expiratory airflow as the higher lung volume increases
elastic recoil pressure. The enlarged airways decrease overall airway resistance.
hyperinflation also flattens the diaphragm. Large lung volumes and diaphragmatic flattening
make it more difficult to decrease intrathoracic pressure during inhalation and thus increase
the work of breathing. Lung volume reduction surgery involves reducing lung volume via
excision of emphysematous tissue. This increases the diaphragm length and returns its
curvature.

Pulmonary compliance is actually increased due to loss of alveolar and elastic tissue seen
in COPD. In contrast, patients with restrictive lung disease have decreased lung compliance.
COPD patients have significant airflow limitation with reduced inspiratory and expiratory
flow rates. Chronic obstructive pulmonary disease patients have increased total lung
capacity, functional residual capacity, and residual volume leading to hyperinflation and
diaphragmatic flattening. Flattening of the diaphragm increases the work of breathing.

Typically due to cigarette smoking, COPD causes gradually decreasing expiratory flow rates,
increased lung compliance, and increased lung volumes. The only therapies proven to
prolong survival in patients with COPD are smoking cessation, supplemental oxygen, and
lung reduction surgery in certain patients.

The criteria for initiating long-term oxygen therapy in COPD patients are as follows:

1. All COPD patients with Pa02 < 55 mmHg or Sa02 < 88% on room air.

2. Patient with cor pulmonale, evidence of pulmonary hypertension or hematocrit > 55%
should be started on home oxygen therapy even when Pa02 is 60 mmHg with Sa02 >
89%.

3. Home oxygen may also be used in patients who has resting awake P02 > 60 with Sa02 >
90% if they become hypoxic during exercise or sleep (nocturnal hypoxia).

The mainstays of treatment are inhaled bronchodilators, especially anticholinergic

medications like ipratropium and tiotropium. Anti-muscarinic agents may be combined with
shortacting beta agonists like albuterol.
In all patients with COPD, the two modalities that have been shown to decrease mortality
are home oxygen therapy and smoking cessation.

Acute Exacerbation of COPD - Upper airway infections (bacterial or viral) are the most
common precipitants of COPD exacerbations. Look for a COPD patient with a recent history of
Fever & Cough. Examination typically shows bilateral wheezes, and ABG findings include
respiratory acidosis and hypoxia. Recommended therapy for an acute bacterial exacerbation
of COPD includes supplemental oxygen, inhaled bronchodilators (B2 agonists and
anticholinergics), broad-spectrum antibiotics, a two-week corticosteroid taper and
smoking cessation.

Even after the above therapy, if the ABG values of patient don’t get better, Non Invasive
Positive Pressure Ventilation can be tried. NIPPV is an excellent option for patients with COPD
exacerbation refractory to standard management. It should be tried before intubation and
mechanical ventilation in COPD patients with C02 retention.

CO2 Narcosis - COPD patients have baseline chronic hypoxia and chronic hypercapnia. This
shifts the respiratory drive from a hypercapnic to a hypoxic drive. Hypoxia causes pulmonary
vasoconstriction, directing blood to better ventilated or perfused areas. Deoxyhemoglobin has
a higher C02 affinity, which increases C02 excretion as it is carried by the hemoglobin back to
the lungs to be exhaled. Thus, correcting hypoxia with excess supplemental oxygen in COPD
patients can exacerbate C02 retention by blunting the hypoxic respiratory drive. The increase
in oxygenated hemoglobin has a lower C02 affinity (Haldane effect). which further worsens
hypercapnia as it causes C02 to be released from the red blood cells into the surrounding areas.
Oxygen also causes pulmonary vasodilation to increase dead space ventilation and further
worsen the ventilation-perfusion mismatch. Intravenous narcotics or benzodiazepines can also

depress the respiratory drive and should be used very carefully in COPD patients. C02 narcosis
causes decreased level of consciousness, seizures and potential cardiac arrhythmias.

COPD Vs CHF Exacerbation - On pulmonary examination, patients with worsening CHF will
commonly have bibasilar crackles. Decreased breath sounds at the bases could be due to
pleural effusions from CHF. Wheezing can occasionally be present in heart failure (cardiac
asthma). It is also a possibility that this patient may have concomitant COPD. The blood gas
findings show hypoxia, hypocapnia, and RESPIRATORY ALKYLOSIS these are highly suggestive
of CHF compared to COPD. More specific testing for CHF would include assessment of the B-
type natriuretic peptide (BNP) and the pulmonary capillary wedge pressure.

In COPD exacerbation, examination typically shows widespread bilateral wheezes and ABG
findings include RESPIRATORY ACIDOSIS and hypoxia.

COPD & Infection Susceptibility - Patients with COPD are at high risk of respiratory infection
due to underlying pathological abnormalities, like histological abnormaflities in the airways
and an impaired local host immune system. The most common bacteria responsible for
acute exacerbation of COPD are S. pneumoniae, H. influenza, and M. catarrhalis.

COPD can also cause Bronchiectasis.

All patients with suspected bacterial pneumonia should have a chest x-ray done as the first
step, and antibiotics should be administered as soon as possible without waiting for sputum
gram stain or cultures.

New clubbing in patients with COPD often indicates the development of lung cancer.

COPD & Spontaneous Pneumothorax - Cigarette smoking markedly increases the risk of a
pneumothorax, and it is thought that smoking leads to chronic airway inflammation and a form
of respiratory bronchiolitis. The chronic destruction of alveolar sacs leads to the formation of
large alveolar blebs (generally in the upper lobes), which can eventually rupture and leak air
into the pleural space. Patients with pneumothorax typically present with acute onset of chest
pain and shortness of breath. On the affected side, breath sounds are markedly reduced and
the chest is hyperresonant to percussion. In a patient with COPD presenting with catastrophic
worsening of their respiratory symptoms, spontaneous secondary pneumothorax should
always be suspected.

Cor Pulmonale - The most common cause of isolated right-sided heart failure is pulmonary
disease, and when it occurs is known as cor pulmonale. Cor pulmonale is most commonly
caused by chronic obstructive pulmonary disease (COPD). The combination of an elevated
JVP, hepatomegaly, ascites and lower extremity edema without evidence of pulmonary
congestion is suggestive of isolated right-sided heart failure. Dyspnea can be a sign of LV
failure, but there are no rales on examination and the CXR does not reveal significant
pulmonary congestion. Chest radiograph shows a normal sized heart with some prominent
pulmonary vessels and flattened diaphragms. Less frequent causes include pneumoconiosis,
pulmonary fibrosis, kyphoscoliosis, primary pulmonary hypertension, and repeated episodes
of pulmonary embolism. The predominant symptoms of compensated cor pulmonale are
related to the pulmonary disorder and include chronic cough, exertional dyspnea, wheezing,
and fatigability. When the pulmonary disease is severe enough to cause RV dysfunction,
signs of right-sided heart failure develop (i.e., jugular venous distension, right sided S3,
right ventricular heave, hepatomegaly, ascites, and dependent edema). A chest radiograph
may reveal a prominent right ventricle and pulmonary artery, in addition to any lung disease
that can be visualized.

Chronic Hypercapnic Respiratory Failure due to COPD –Patients have around normal pH
because kidneys have increased bicarbonate retention to compensate for the increased
pC02 Patients with chronic hypoventilation due to COPD, obesity hypoventilation syndrome,
or neuromuscular causes have gradual increases in the pC02 that results in respiratory
acidosis. To compensate, the kidneys increase bicarbonate retention.

Peak airway pressure is the sum of airway resistance and plateau pressure. The plateau
pressure is the sum of the elastic pressure and positive end-expiratory pressure (PEEP) and
is calculated by performing the end-inspiratory hold maneuver. PEEP is calculated with the
end-expiratory hold maneuver.

Secondary Malignancy Post Chemo/Radiation Therapy - Hodgkin's disease is a curable

lymphoma that tends to affect young patients. Unfortunately, patients can develop
secondary malignancies from chemotherapy and/or radiation, especially those treated
before the age of 30. The risk of secondary malignancy is highest when chemotherapy is
combined with radiation, reaching up to 3.2% within 20 years of treatment. Lung and
breast cancers are among the most common secondary malignancies affecting patients
previously treated for Hodgkin's disease. The patient above has developed a secondary
cancer in his left lung.

Patients who have received lung field radiation are at risk for radiation-induced fibrosis,
whichtypically presents as dyspnea 4-24 months after therapy. Fibrosis typically causes a
more diffuse process on chest x-ray, rather than a discrete lesion as shown above.

Intubation Verification - Right mainstem bronchus intubation is a relatively common

complication of endotracheal intubation. It causes asymmetric chest expansion during
inspiration and markedly decreased or absent breath sounds on the left side on
auscultation. Repositioning the endotracheal tube by pulling back slightly will move the tip
between the carina and vocal cords and solve the problem.

Pneumonia Severity Index (PSI) - The predictor variables used for calculating PSI are based
on medical history, physical examination, and readily available laboratory and radiographic
findings. The first step in the management of CAP is to decide whether the patient needs
hospitalization. The decision to admit the patient is generally made using the Pneumonia
Severity Index (PSI)
The patient who have other comorbidities, such as heart failure, chronic obstructive
pulmonary disease, and coronary artery disease and appears hypoxic, requiring oxygen,
febrile, tachycardic, borderline low blood pressure, and has lobar pneumonia require
admission into the hospital.

Cystic fibrosis can affect a variety of organ systems including the respiratory tract, sinuses,
pancreas, intestines, and reproductive systems secondary to abnormally thickened
secretions. Recurrent pulmonary infections and bronchiectasis are commonly seen in the
lungs. Decreased exocrine function of the pancreas leading to fat malabsorption is also
often present.

GERD In Asthma - Gastroesophageal reflux disease (GERD) occurs in 30%-90% of patients

with asthma risk factors for and symptoms of GERD, including obesity, supine position soon
after a large meal, laryngitis, and change in voice quality. Additional symptoms of GERD
include heartburn, regurgitation, dysphagia, and chest pain.

Nocturnal respiratory symptoms may occur as gastroesophageal reflux can exacerbate

asthma. GERD can exacerbate airflow obstruction in asthmatics through increased vagal
tone, heightened bronchial reactivity, and microaspiration of gastric contents into the
upper airway. Initial treatment of GERD includes lifestyle modifications such as elevating the
head of the bed, dietary changes, and weight loss. Treatment with proton pump inhibitors
has been shown to improve peak expiratory flow in patients with asthma, nocturnal
respiratory symptoms, and GERD.

Exercise Induced Asthma - In exercise-induced asthma, the trigger is high minute ventilation
of dry, cold air, which stimulates mast cell degranulation and airway constriction. Beta
agonists and mast cell stabilizers are both important in the management of exercise-induced
asthma. Short-acting beta-adrenergic agonists used 20 minutes prior to exercise are
typically sufficient to prevent symptoms and are considered first-line therapy. Long-acting
beta-adrenergic agonists may be used in children or athletes who engage in athletic
activities throughout the day

Management Of Asthma Chronically The management of asthma varies depending on

symptom severity. Asthma is classified into four categories:
Intermittent,

Mild persistent,

Moderate persistent and

Severe persistent.

The category is determined by assessing the frequency of a patient's daytime symptoms,

nighttime awakenings, and use of short-term beta agonists, plus pulmonary function testing.

In intermittent asthma, daytime symptoms occur ~2 days/week, nighttime awakenings

~2x/month, use of beta agonists ~ 2x/week, baseline FEV1 and FEV1/FVC are normal, and there
are no limitations on daily activities. The appropriate pharmacologic management for
intermittent asthma is a short acting bronchodilator (e.g. albuterol) for as needed (PRN) use,
with no need for daily controller medication.

In addition to a PRN albuterol inhaler, patients with mild persistent asthma (symptoms >2
days/week but less than daily, nighttime awakenings 3-4x/month, minor limitation of activities,
and normal PFTs) should be prescribed a low-dose inhaled corticosteroid

(SABA + ICS)

In addition to a PRN albuterol inhaler and low-dose inhaled corticosteroid, patients with
moderate persistent asthma (daily symptoms, weekly nighttime awakenings, and FEV1 60-
80% of predicted) should be prescribed a long-acting inhaled beta-2 agonist inhaler.

(SABA + ICS + LABA)

Patients with severe persistent asthma (symptoms throughout the day, frequent nighttime
awakenings, extremely limited activity, and FEV1 <60% predicted) should receive a PRN
albuterol inhaler, long-acting beta- 2 agonist inhaler, and high-dose inhaled corticosteroids.
Oral prednisone can also be used in cases of severe persistent asthma.

(SABA + ICS (Increase dose) + LABA + OCS)

Side effects - The most common adverse effect of inhaled corticosteroid therapy is
oropharyngeal thrush (oral candidiasis). Glucocorticoids cause neutrophilia by increasing the
bone marrow release and mobilizing the marginated neutrophil pool. Eosinophils and
lymphocytes are decreased.
Inhaled albuterol and systemic steroids are appropriate treatments for acute asthma attacks.
Patients on High doses of beta-2 agonists may develop hypokalemia, which may present with
muscle weakness, arrhythmias and EKG abnormalities. Other common side effects of beta-2
agonists include tremor, palpitations and headache.

Management Of Acute Asthma Exacerbation –

Indicators of a severe asthma attack include normal to increased Pco2 values, speech
difficulty, diaphoresis, altered sensorium, cyanosis, and 'silent' lungs. Acute asthma
exacerbation causes increased respiratory drive and hyperventilation, leading to decreased
arterial partial pressure of carbon dioxide (PaC02). An elevated or even normal PaC02 suggests
decreased respiratory drive (likely due to respiratory muscle fatigue) and impending
respiratory failure.

Mild-to-moderate asthma exacerbation usually responds to oxygen and inhaled short-acting

beta agonists (SABAs) to effectively reverse airflow obstruction. Patients who do not respond
require systemic corticosteroids (usually oral).

Moderate-to-severe asthma exacerbation requires SABA, ipratropium nebulizer, and systemic

corticosteroids. Adding ipratropium to SABA causes greater bronchodilation than either agent
alone. The current guidelines recommend the addition of ipratropium for management of
severe exacerbations early in the course of the disease. Systemic glucocorticoids (oral or
intravenous) increase the rate of symptomatic improvement, but their beneficial effects are not
clinically apparent for several hours after administration. A one-time infusion of intravenous
magnesium sulfate is also recommended for severe asthma exacerbation without improvement
after 1 hour of therapy or for life-threatening asthma with impending respiratory failure.

Severe Asthma with Impending Respiratory failure - In patients with acute asthma
exacerbation, an elevated or even normal arterial partial pressure of carbon dioxide suggests
decreased respiratory drive (likely due to respiratory muscle fatigue) and impending respiratory
failure. Look for

• Decreased breath sounds

• Absent wheezing

• Decreased mental status

• Marked hypoxia with cyanosis & Normal or Elevated CO2 levels

In these patients, treatment involves endotracheal intubation and mechanical ventilation,

inhaled short-acting beta-2-agonist, inhaled ipratropium, and systemic corticosteroids.

Both asthma and chronic obstructive pulmonary diseases (COPD) are chronic inflammatory
diseases of the respiratory tract. the clinical presentations of asthma and COPD may overlap
significantly without an easy way to differentiate between them.

A bronchodilator response test is conducted by measuring forced expiratory volume (FEV1)

before and after administration of a bronchodilator, usually beta2-agonist. Significant
improvement in FEV1 after bronchodilator administration ( 15% or greater) indicates
reversibility of obstruction, and this finding is more consistent with asthma.

Low diffusion capacity (DLCO) and characteristic chest CT findings are also supportive of COPD.

Cough Main Causes - Cough is caused by mechanical stimulation of the afferent limb of the
cough reflex in the upper airway in these conditions nasopharyngitis, Sinusitis, vasomotor
rhinitis & Allergic Rhinitis.
The 3 most common causes of chronic cough (lasting >8 weeks) are upper-airway cough
syndrome (postnasal drip), asthma, and gastroesophageal reflux disease (GERD). Upper-
airway cough syndrome is caused

The diagnosis of upper-airway cough syndrome is confirmed by the elimination of nasal

discharge and cough with the use of H1 histamine receptor antagonists.

Laryngeal Edema - dyspnea difficulty swallowing and physical findings suggestive of upper
respiratory obstruction. Laryngeal edema is likely the cause of his respiratory symptoms given
history of food allergies and urticaria & sudden onset of dyspnea & Dysphagia. Patients with
laryngeal edema typically present with acute-onset dyspnea. There is usually an identifiable
precipitating event. e.g. peanut ingestion in a patient with a history of peanut allergies.

Physical examination may reveal stridor and harsh respiratory sounds from the trachea.
Wheezing is generally absent on lung auscultation.

Chronic dry cough is a very common side effect of the therapy with ACE inhibitors like enalapril.
Chronic cough was reported in up to 20% of patients treated with these agents. Taking into
account the growing popularity of ACE inhibitors in the treatment of various conditions, this side
effect is getting more important in the differential diagnosis of the chronic cough syndrome. The
pathogenesis of the cough is related to an accumulation of the inflammatory or roinflammatory
mediators bradykinin, substance P, thromboxanes, and prostaglandins. If the cough is
disturbing, ACE inhibitor therapy should be discontinued.

Pulmonary tuberculosis presents with productive cough, hemoptysis, and recurrent fevers.
Weight loss may also be present. Imaging most commonly reveals upper lobe cavitary
lesions. TB must be suspected in patients from endemic regions with subacute or chronic
pulmonary complaints.

Reactivation of latent tuberculosis typically causes an apical cavitary lesion on chest x-ray.
Clinically, patients complain of chronic low-grade fever, night sweats, weight loss and a
cough productive of blood-tinged sputum. In the United States, most cases of tuberculosis
occur in patients who have immigrated from developing countries with a high incidence of
the disease.

Patients with hemoptysis and high clinical suspicion for pulmonary tuberculosis (coming from
an endemic area, symptoms, and upper-lobe involvement) should be placed in respiratory
isolation to prevent the spread of infection before further diagnostic evaluation and treatment.
Bronchoscopy should be performed to directly visualize and control the site of bleeding in
patients with massive hemoptysis (>600 ml/day or 100 ml/hr).

Aspergillosis is a fungal infection, characterized by coarse fragmented septae. Hyphae are

typically seen. The chest x-ray may demonstrate a crescent radiolucency next to a rounded
mass. Cavitary lesions may form because of destruction of the underlying pulmonary
parenchyma, and debris and hyphae may coalesce and form a fungus ball, which lies free in
the cavity and moves around with position change.

A mobile cavitary mass in the lung, which presents with intermittent hemoptysis, is usually
indicative of aspergilloma.

Histoplasmosis - Histoplasma capsulatum is a common and usually asymptomatic infection in

endemic areas like Mississippi and Ohio River valleys and Central America. It is usually found in
soil with a high concentration of bird or bat guano droppings. Less than 5% of infected people
develop the symptomatic disease. The extent of disease is determined by the amount of
exposure and immunity of the host Symptomatic lung infection is mostly characterized by self-
limiting fever, chills and a non-productive cough. A chest x-ray may show patchy lobar or
multinodular lobar infiltrates. Chronic cavitary pulmonary histoplasmosis is a progressive. fatal
form of histoplasmosis that usually develops in older chronic obstructive pulmonary disease
patients. Disseminated histoplasmosis is seen in immunocompromised adults and young
children. It can also cause a solitary pulmonary nodule.

Friedlander's pneumonia or Klebsiella pneumonia most frequently affect the upper lobe and
produce currant jelly-like sputum with tissue necrosis and early abscess formation and a
fulminant course. Klebsiella is one of the most common organisms responsible for pneumonia
in alcoholics. It is an encapsulated GNB and grows as mucoid colonies.

Lung abscess may occur from an infection behind a blocked bronchus. The infection is
usually due to anaerobes and may be associated with alcohol abuse or aspiration. Patients
usually appear sick with an elevated WBC. The lung abscess typically presents with an air
fluid level on a chest x-ray.
Histoplasmosis is the most common fungal infection in the USA. The yeast infection is
acquired by inhalation and usually resolves without treatment. Calcified nodes in the lung,
mediastinum, spleen, and liver may occur. The chest x-ray may demonstrate central or
target calcification. A solitary nodule may be seen sometimes.

Hypertrophic osteoarthropathy (HOA) is a condition where digital clubbing is accompanied

by sudden-onset arthropathy. Commonly affecting the wrist and hand joints, Hypertrophic
pulmonary osteoarthropathy (HPOA) is a subset of HOA where the clubbing and arthropathy
are attributable to underlying lung disease like lung cancer, tuberculosis, bronchiectasis or
emphysema.

Heparin + Warfarin to Warfarin Only Transformation -Heparin serves several functions in

the acute setting. First. it retards additional thrombus formation by binding to antithrombin
Ill and enhancing its activity. This helps stabilize but does not lyse the clot. Second. It
provides anticoagulation until warfarin achieves therapeutic levels. Warfarin works by
inhibiting activation of the vitamin K-dependent clotting factors (II. VII. IX. and X). However.
the first vitamin K-dependant factors to be affected are proteins C and S. which are actually
anti-thrombogenic. Thus in the absence of a second anticoagulant, warfarin may initially be
thrombogenic. Typically. warfarin takes 5-7 days to achieve therapeutic anticoagulation.
so concomitant heparin is used initially as a "bridge" to a therapeutic INR.

So, Start with Heparin + Warfarin, Give Heparin for 5-7days then stop it and continue
only Warfarin

Anaphylacti Shock - acute onset of hypotension and tachypnea after a bee sting consistent with
anaphylactic shock, a serious allergic reaction that can rapidly progress to respiratory failure and
death. Anaphylaxis is associated with symptoms (e.g .. hives. flushing. pruritus. and swollen lips
or tongue) after an allergic exposure causing either respiratory distress (e.g .. dyspnea.
wheezing. stridor. and hypoxia) or hypotension. Patients with anaphylaxis usually have prior
exposure to the offending agent (most commonly bee stings. food. and medications). Therefore.
they have preformed lgE to cause a type 1 hypersensitivity reaction with widespread histamine-
mediated peripheral vasodilation, hypotension and ultimate circulatory collapse.

Anaphylaxis is a medical emergency. The first step is the intramuscular administration, which
achieves higher plasma and tissue levels more effectively than does the subcutaneous route of
epinephrine into the thigh.
Mediastinal Tumors - The diagnosis of mediastinal tumors is based on chest-x rays and CT scans.
A bronchogenic cyst may be seen on the AP chest x-ray. The diagnosis is best made with a CT
scan.

Anterior - Thymoma is usually found in the anterior mediastinum. The diagnosis is suspected
when an anterior mediastinal mass presents in a young male or female. About 20% of patients
with myasthenia gravis have a thymoma. Other anterior mediastinal masses include:
retrosternal thyroid, teratoma and lymphoma.

Middle - Bronchogenic cysts are located in the middle mediastinum and are benign entities
other middle mediastinal masses include: tracheal tumors, pericardial cysts, lymphoma, lymph
node enlargement, and aortic aneurysms of the arch.

Posterior - All neurogenic tumors are located in the posterior mediastinum. These include:
meningocele, enteric cysts, lymphomas, diaphragmatic hernias, esophageal tumors and aortic
aneurysms. MRI is the best modality to evaluate posterior mediastinal masses

Bronchogenic cysts are usually found in the middle mediastinum. Thymoma is usually found in
the anterior mediastinum. All neurogenic tumors are located in the posterior mediastinum.

Wegener’s Granulomatosis - combination of kidney disease and upper and lower respiratory
tract disease suggests granulomatosis with polyangiitis (Wegener's) (GPA). Upper airway
involvement may cause bloody/purulent nasal discharge, oral ulcers and sinusitis. Vasculitic

cutaneous lesions (tender nodules, palpable purpura, ulcerations) are common external
manifestations. Lower airway symptoms include dyspnea, cough, and hemoptysis. The renal
disease in GPA generally manifests as renal insufficiency, microscopic hematuria, and red blood
cell casts (rapidly progressive glomerulonephritis). Systemic symptoms like fever, weight loss.
and fatigue are also common. Chest x-ray may demonstrate nodular densities and
alveolar/pleural opacities. In all patients with suspected GPA, the serum should be tested for
antineutrophilic cytoplasmic antibody ( c-ANCA) as it is positive in >90% of affected individuals
Biopsy from a site of active disease (preferably nasopharyngeal) makes the definitive
diagnosis.

Idiopathic Pulmonary Fibrosis - Idiopathic pulmonary fibrosis (IPF) is a restrictive lung disease of
unknown etiology. In IPF, chronic inflammation of the alveolar walls causes progressive
widespread fibrosis and destruction of the normal lung architecture. Patients present with
chronic progressive dyspnea, nonproductive cough and digital clubbing. Fever and chest pain
are typically absent. Examination demonstrates dry, end-inspiratory crackles. Pulmonary
function tests (PFTs) in patients with this condition show a restrictive pattern (decreased TLC,
FEV1 and FVC; normal FEV1/FVC). The diffusing capacity is progressively reduced, largely due to
ventilationperfusion mismatch, resulting in an increased A-a gradient. Chest x-rays in IPF
typically demonstrate decreased lung volumes, airway fibrosis giving a "honeycomb" pattern,
and pulmonary vascular congestion most evident in the hilum.

Systemic Sclerosis and any of the occupational diseases can cause Pulmonary Fibrosis.

Asbestosis - Individuals with an occupational history involving mining, shipbuilding, insulation,

or pipe work are at risk for asbestosis. Symptoms tend to develop 20-30 years after the initial
exposure. The most common clinical presentation is dyspnea without cough or sputum
production. Bibasilar end-inspiratory crackles and clubbing are seen in approximately 40-50% of
patients with advanced disease. Asbestos exposure increases the risk of malignancy,
pulmonary fibrosis and pleural plaques. In terms of malignancies, both bronchogenic
carcinoma and mesothelioma are linked to asbestos exposure, with bronchogenic carcinoma
being the more common cancer in these patients.

SVC Syndrome - superior vena cava (SVC) syndrome, a condition where obstruction of the SVC
impedes venous return from the head, neck and arms to the heart. Signs and symptoms include
dyspnea, venous congestion, and swelling of the head, neck and arms. Malignancy is the most
common cause of obstruction (i.e. lung cancer, non-Hodgkin lymphoma), accounting for >60% of
cases. Chest x-ray (Choice C) can identify the cause of SVC syndrome in >80% of cases.
Abnormalities on chest x-ray warrant follow-up with chest CT and histology to determine the
tumor type and to guide therapy. Can also occur due to thrombosis secondary to indwelling
central venous devices

TB Reactivation - Initial infection by M. tuberculosis typically causes a peripheral pulmonary

focus of infection accompanied By mediastinal or hilar lymphadenopathy evident on chest x-ray.
This initial infection is typically asymptomatic, and the primary site of infection, the Ghon focus,
typically remains as a calcified granuloma. Reactivation of an M. tuberculosis infection can
occur, especially during periods of immunosuppression. Patients with HIV in particular have a 1
0% risk per year of reactivation tuberculosis. Patients with reactivation tuberculosis typically
present with complaints of fever, night sweats, fatigue, weight loss, productive cough,
hemoptysis and pleuritic chest pain. Such a symptom complex, especially in a high risk patient
such as the one described, should prompt a chest x-ray. Reactivation tuberculosis most
commonly causes an apical cavitary pulmonary lesion. M. tuberculosis preferentially
reactivates in the apices of the lungs because it is an aerobic organism, and the oxygen tension
is highest in this segment of the lungs.

Aspirin Sensitivity Syndrome - The clues to the correct diagnosis include aspirin ingestion,
persistent nasal blockage, and episodes of bronchoconstriction. The pathogenesis of aspirin
sensitivity syndrome is believed to involve 'pseudo-allergic reaction,' that is an exaggerated
release of vasoactive and inflammatory mediators in susceptible individuals. Aspirin is a
cyclooxygenase (COX-1 and COX-2) inhibitor. As the result of its pharmacologic action,
arachidonate diverges from blocked COXs to a 5-lipoxygenase pathway. Accumulation of
leukotrienes and changed prostaglandin/leukotriene balance triggers characteristic reactions
(bronchoconstriction, polyp formation) in susceptible individuals. includes avoidance of NSAIDs
and the use of leukotriene receptor antagonists (drug of choice).

Pulmonary HTN - Pulmonary hypertension is defined as a mean pulmonary arterial pressure

greater than 25 mmHg at rest or 30 mmHg with exercise. It is seen following the narrowing of
the precapillary vessels. the loss of the pulmonary capillary bed. or passive backpressure from
the post capillary vessels from any cause. It can be classified as follows:

1. Pulmonary hypertension associated with disorders of the respiratory system Hypoxemia or

both

2. Pulmonary hypertension due to pulmonary venous hypertension (left ventricular heart

disease, mitral valve disease or pulmonary vena-occlusive disease).

3. Pulmonary hypertension following chronic thromboembolic disease.

4. Pulmonary arterial hypertension (primary pulmonary hypertension. pulmonary hypertension

associated with vasculopathy).

5. Pulmonary hypertension due to disorders directly affecting the pulmonary vasculature

(pulmonary capillary hemangiomatosis).
Right ventricular failure develops late in the disease and manifests with right ventricular heave.
jugular venous distension, tender Hepatomegaly, ascites, edema etc. Chest x-ray would show
enlargement of the pulmonary arteries with rapid tapering of the distal vessels (pruning) and
enlargement of the right ventricle. An EKG may show right axis deviation. which is secondary to
right ventricular strain and hypertrophy due to pulmonary hypertension. Untreated pulmonary
hypertension would eventually lead to Cor pulmonale.

Gestational Trophoblastic Disease - Choriocarcinoma is a form of gestational trophoblastic

disease (GTD) that may occur after a normal gestation (25% of cases), Molar pregnancy (50%),
or abortion (25%). All forms of GTD tend to present with irregular vaginal bleeding, an
enlarged uterus and pelvic pain. Irregular vaginal bleeding beyond 8 weeks post-partum is
abnormal, and should raise suspicion for GTD. Malignant forms of GTD include invasive
gestational trophoblastic neoplasia (GTN) and choriocarcinoma. While either may arise after a
normal pregnancy, GTN is almost always only locally invasive while choriocarcinoma is highly
metastatic. The most frequent site of metastatic spread in choriocarcinoma is to the lungs.
pulmonary symptoms (chest pain and dyspnea) are consistent with this diagnosis. Hemoptysis
is also common. Obtaining a quantitative beta HCG is the appropriate next step in confirming
the diagnosis.

Pressure Volume Loops

Laryngeal Edema - Fixed upper airway obstruction produces a distinctive flow-volume loop,
demonstrating flow limitation with both inspiration (below the horizontal line) and expiration
(above the horizontal line). A fixed upper airway obstruction will decrease the airflow rate
during inspiration. active expiration and passive expiration.

ARDS - ARDS most often develops in the clinical setting of sepsis, pneumonia, aspiration, toxic
ingestions, trauma and/or burns. A history of alcoholism is a further risk factor for ARDS. The
pathophysiology of ARDS involves release of inflammatory mediators as a result of local or
distant tissue injury. These inflammatory mediators cause alveolar damage, increased alveolar
capillary permeability, and leakage of proteinaceous fluid into the alveoli. Clinically, this leads to
the acute onset of tachypnea, tachycardia, fever, and dyspnea. Arterial blood gas reveals
hypoxemia and chest x-ray reveals bilateral alveolar infiltrates. The differential diagnosis for
hypoxemia and bilateral infiltrates on chest x-ray also includes cardiogenic pulmonary edema.
An important diagnostic tool for differentiating ARDS from cardiogenic pulmonary edema is
measurement of the pulmonary capillary wedge pressure (PCWP). A PCWP < 18 mmHg
suggests ARDS while a value > 18 mmHg suggests cardiogenic pulmonary edema.
Hemoptysis - Hemoptysis is defined as any expectoration of blood, with a wide spectrum from
minimal blood streaking in sputum to the presence of frank blood and/or clots. Despite the
many causes of hemoptysis, pulmonary airway disease ( eg, chronic bronchitis, bronchogenic
carcinoma, bronchiectasis) ranks as the most common cause. Chronic bronchitis is defined as a
chronic productive cough for 3 months in 2 successive years, with cigarette smoking as the
leading cause.

Acute bronchitis is a common cause of blood-tinged sputum and is usually viral in etiology. It
presents with a sore throat and productive cough in a patient with no Hx of smoking. Bilateral
wheezing is present. In an afebrile patient with new-onset blood-tinged sputum without
significant signs of more serious disease, observation and close clinical follow-up is the best
treatment strategy since antibiotics are not needed (Viral origin). It Produces NON PURULENT
Sputum.

Chronic bronchitis is characterized by a chronic productive cough for at least 3 months over 2
consecutive years and not attributed to other causes. It occurs following prolonged exposure of
the tracheobronchial tree to nonspecific irritants and is characterized by hypersecretion of
mucus and structural changes in the tracheobronchial tree. The presence of a chronic
productive cough, prominent bronchovascular marking, mild flattening of the diaphragm, and
normal DLCO is suggestive of chronic bronchitis. If DLCO also decreased, its Chronic Bronchitis +
Emphysema = COPD.

Bronchiectasis - In bronchiectasis, recurrent infection produces episodes of cough (>90%) with

mucopurulent sputum that often responds to antibiotics. Hemoptysis is seen in 25% of the
patients. Bronchiectasis may be either inherited or acquired. Cystic fibrosis is the most common
inherited cause. An infectious insult damages the mucociliary clearance mechanism, which in
turn leads to airway obstruction and dilatation, mucus plugging, and suppuration. Impaired
host defense, such as in patients with hypogammaglobulinemia or immunosuppression, also
contributes to the disease process. Smoking greatly increases the likelihood of bronchiectasis.
This means any smoker who presents with thick PURULENT sputum production who gets well
with antiobiotics has Bronshiectasis. Chest x-ray is frequently abnormal but not sufficient for
diagnosis of bronchiectasis. High-resolution CT scan is the definitive test for diagnosis. The CT
image demonstrates dilated central bronchi which are larger than the adjacent pulmonary
artery branches as well as thickening of the bronchial walls, which is consistent with
bronchiectasis.
Massive Hemoptysis – It is defined as >600 ml of expectorated blood over a 24-hour period or
a bleeding rate >100 ml/hour. The greatest danger in massive hemoptysis is not
exsanguinations but asphyxiation due to the airway flooding with blood. Initial management
involves establishing an adequate patent airway, maintaining adequate ventilation and gas
exchange, and ensuring hemodynamic stability. The patient should be placed with the bleeding
lung in the dependent position (lateral position) to avoid blood collection in the airways of the
opposite lung.
Bronchoscopy is the initial procedure of choice in such patients as it can localize the bleeding
site, provide suctioning ability to improve visualization, and include other therapeutic
interventions ( eg, balloon tamponade, electrocautery).

Solitary Pulmonary Nodule - A solitary pulmonary nodule (SPN) is defined as a lesion (usually
<3 cm) that is within and completely surrounded by pulmonary parenchyma. The first step in
evaluating an SPN is to determine if the nodule has a low, intermediate, or high probability of
malignancy.

HX of any previous cancer also puts the patient in HIGH CANCER RISK.
Lesions with high malignancy risk require surgical excision; lesions with low risk can be
monitored with serial computed tomography scans. Lesions with intermediate risk for
malignancy should undergo further imaging and excision depending on imaging findings.
Hypersensitivity Pneumonitis - HP is caused by repeated inhalation of an inciting antigen, which
leads to alveolar inflammation. Common responsible antigens include aerosolized bird
droppings ("bird fancier's lung") and molds associated with farming ("farmer's lung"). Acute
episodes may present with cough, breathlessness, fever and malaise that occur 4-6 hours after
antigen exposure. With chronic exposure, patients may develop pulmonary fibrosis and a
restrictive pattern on lung spirometry. Classic radiographic findings include ground glass
opacity, or "haziness," of the lower lung fields. Studies have shown that the best treatment for
HP is avoidance of antigen exposure.

Good Pasteur’s Disease - Goodpasture's disease affects the lungs (causing cough, dyspnea, and
hemoptysis) and kidneys (causing nephritic range proteinuria, acute renal failure, and
dysmorphic red cells red cell casts on urinalysis). Systemic symptoms are uncommon. Diagnosis
is made by renal biopsy showing linear lgG antibodies along the glomerular basement
membrane.

Recurrent Pulmonary Infections - Recurrent bacterial infections in an adult patient may indicate
a humoral immunity defect. lgA deficiency and common variable immunodeficiency are also
possible. Quantitative measurement of serum immunoglobulin levels helps to establish the
diagnosis.