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Lung Disorders. COMMON MANIFESTATIONS OF LUNG DISEASE. DYSPNEA. Brought about by several physiologic processes: Increased respiratory effort due to: 1) AIRWAY OBSTRUCTION: COPD, asthma. 2) DECREASED PULMONARY COMPLIANCE: interstitial fibrosis, CHF.

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Dyspnea
DYSPNEA

  • Brought about by several physiologic processes:

  • Increased respiratory effort due to:

  • 1) AIRWAY OBSTRUCTION: COPD, asthma.

  • 2) DECREASED PULMONARY COMPLIANCE: interstitial fibrosis, CHF.

  • 3) DECREASED CHEST WALL COMPLIANCE: obesity, pleural disease.

  • 4) WEAKNESS OF RESPIRATORY MUSCLES: neuromuscular weakness, inanition,, chronic respiratory failure.


Dyspnea1
DYSPNEA

ACUTE DYSPNEA

  • Short list:

  • Asthma, infection.

  • Pulmonary edema.

  • Pneumothorax.

  • Pulmonary embolus.

  • ARDS, panic attack.


Dyspnea2
DYSPNEA

EVALUATION

  • CBC, renal function, CXR, spirometry, oximetry.

  • If > 40 or family Hx → EKG.

  • ABG’s, V/Q Scan, stress testing, echocardiography where appropriate based on Signs / Sxs.


Dyspnea3
DYSPNEA

TREATMENT

  • O2 if hypoxemic.

  • Treat dyspnea-related anxiety w/ “judicious” use of benzodiazepines, Ativan 0.5-1.0 mg q6-8.

  • Pulmonary “rehab,” more appropriate breathing techniques, energy-conserving techniques, etc.

  • Um, smoking cessation.


Cough
COUGH

CHRONIC COUGH

  • Most commonly from COPD.

  • In the non-smoker:

  • GERD, post-nasal drip, asthma.

  • Side-effect of ACE Inhibitors.

    THE EVAL

  • Postnasal drip: sinus series, Rx as sinusitis.

  • PFT’s: asthma, COPD.

  • GERD: barium swallow vs empiric Rx.

  • CXR: for patients w/ other Sxs, hemoptysis, fever, weight loss, etc


Cough1
COUGH

TREATMENT

  • Dependent upon the cause.

  • Elimination of irritant: tobacco, allergen, environmental, occupational.

  • D/C beta blockers, ACE inhibitors.

  • Post-nasal drip: antihistamines, decongestants, intranasal steroids.

  • Chronic sinusitis: prolonged antibiotic Rx, 2-4 weeks.

  • Asthma: inhaled steroids and bronchodilators. If not better another cause needs to be considered.

  • GERD- proton pump inhibitors, H2 blockers may not cut it.


Hemoptysis
HEMOPTYSIS

  • Coughing up of blood “that originates below the vocal cords.”

  • Dual circulation:

  • 1) PULMONARY ARTERIES- from the right ventricle under low pressure to the pulmonary parenchyma.

  • 2) BRONCHIAL ARTERIES- from the aorta under systemic pressure to the airways, blood vessels, hilum, and visceral pleura.

  • The bronchial circulation is only 1-2% of total pulmonary flow, but is common source of hemoptysis.


Hemoptysis1
HEMOPTYSIS

  • CHASING DOWN THE CAUSE ANATOMICALLY

  • 1) FROM THE AIRWAYS: chronic bronchitis, bronchiectasis, bronchogenic carcinoma.

  • 2) FROM THE PULMONARY VASCULATURE: left v. failure, mitral stenosis, PE, AVM.

  • 3) FROM THE PULMONARY PARENCHYMA: pneumonia, inhalation of crack, autoimmune disease such as Goodpasture’s Syndrome and Wegener’s Granulomatosis.


Hemoptysis2
HEMOPTYSIS

CLINICAL FINDINGS

  • In acute bronchitis in an otherwise healthy person, no big work up needed as long as it resolves w/ the illness.

  • Hemoptysis is frequently a sign of serious disease.

  • Identify the patient at risk for pathology.

  • CXR, CBC w/ platelets, renal function, UA.

  • Flexible bronchoscopy.

  • Chest CT.


Hemoptysis3
HEMOPTYSIS

TREATMENT

  • Mild hemoptysis- identify the cause.

  • Massive hemoptysis- secure the airway, intubation, suction, ventilation.

  • Bronchoscopic control sometimes possible.

  • Selective arterial embolization.


Upper airway obstruction
UPPER AIRWAY OBSTRUCTION

ACUTE

  • Can be life-threatening.

  • CAUSES: Foreign body, laryngospasm, laryngeal edema from burns, angioedema, trauma to the pharynx/larynx, infections (retropharyngeal abscess, etc), acute allergic laryngitis.


Asthma
ASTHMA

  • Chronic, inflammatory disorder of the airways.

  • Reversible airway hyper-responsiveness, airway edema, bronchoconstriction, mucous production.

  • 5% of the population, 5000 deaths annually.

  • Prevalence, # hospitalizations, and deaths all increased over the last 20 years.

  • See text for histopathology, underlying inflammatory changes, mast cells, etc.


Asthma1
ASTHMA

  • Genetic predisposition, atopy.

  • Most common trigger is inhaled allergens.

  • Other triggers: exercise, URI’s, rhinitis, sinusitis, postnasal drip, GERD, changes in weather, stress.

  • Also: tobacco smoke, ozone, SO2, NO2.

  • Some cases due to use of aspirin, NSAID’s, tartrazine dyes.

  • Catamenial.

  • “Cardiac asthma.”


Asthma2

Allergens

O “Seasonal pollens

O Year round allergens – dust mites, moulds, pets, and insect parts

O Foods – fish, egg, peanuts, nuts, cow’s milk, and soy

O Additives – sulphites

O Work related agents – latex, flour

Irritants

O Respiratory infections – viral colds, bronchitis, and sinusitis

O Drugs – aspirin, NSAIDs, betablockers

O Tobacco smoke

O Outdoor factors – haze and smog, weather changes, exhaust fumes

from vehicles

O Indoor factors — paint, detergents, deodorants, chemicals and perfumes

O GERD

O Temperature change – night-time

O Exercise in cold dry conditions

O Work-related factors – chemicals, dusts, gases, and metals

O Emotional factors – laughing, crying, yelling and distress

O Hormonal factors – premenstrual syndrome

Asthma



Asthma3
ASTHMA

SIGNS / SYMPTOMS

  • Wheezing, difficulty breathing, chest tightness, cough.

  • Extreme variability in symptoms from one patient to the next.

  • Worse at night, bronchoconstriction max between 3-4 AM.

  • COEXISTING CONDITIONDS: nasal polyps, eczema, atopic dermatitis, other allergic skin disorders.


Asthma4
ASTHMA

SIGNS / SYMPTOMS

  • Wheezing may be absent when bronchoconstriction is extreme, as not enough air is flowing to produce wheezing. This portends respiratory failure.

  • Here we find globally diminished breath sounds and prolonged expiration.

    PFT’s

  • FEV1, FVC, (FEV1 / FVC).

  • Peak expiratory flow meters for home monitoring.


Asthma5
ASTHMA

COMPLICATIONS

  • Exhaustion.

  • Dehydration, airway infection.

  • Cor pulmonale.

  • Pneumothorax.


Asthma6
ASTHMA

LONG-TERM TREATMENT

  • GOALS:

  • 1) Minimize chronic Sxs that impair normal activity.

  • 2) Prevent recurrences.

  • 3) Minimize need for ER / hospitalizations.

  • 4) Maintain near-normal pulmonary function.

  • Daily anti-inflammatory therapy w/ inhaled corticosteroids.


Asthma7
ASTHMA

LONG-TERM TREATMENT

  • Therapy dictated by algorithms set forth by the Expert Panel Report 2 from the NAEPP, step-wise fashion (“stair-step”).

  • Amount of medication and dosing based on severity of Sxs.

  • Begin therapy at a higher level of intensity then back down.


Asthma8
ASTHMA

PHARMACOLOGIC AGENTS

  • 2 CATEGORIES:

  • 1) Those that promote long-term control- address airway inflammation.

  • 2) Those that offer quick relief- bronchodilators


Asthma9
ASTHMA

PHARMACOLOGIC AGENTS

  • LONG-TERM CONTROL MEDICATIONS.

  • QUICK RELIEF MEDICATIONS.


Asthma10
ASTHMA

PHARMACOLOGIC AGENTS

  • LONG-TERM CONTROL MEDICATIONS.

    ANTI-INFLAMMATORY AGENTS

    LONG-ACTING BRONCHODILATORS

    LEUKOTRIENE MODIFIERS

    DESENSITIZATION

    MISCELLANEOUS


Asthma11
ASTHMA

PHARMACOLOGIC AGENTS – LONG-TERM

  • LONG-ACTING BRONCHODILATORS

  • 1) MEDIATOR INHIBITORS- cromolyn sodium, nedocromil. Modulate mast cell and eosinophil function.

  • 2) BETA ADRENERGIC AGENTS- inhaled,long-acting. Onset of action is delayed, not for acute bronchoconstriction, exacerbations. Combined w/ inhaled corticosteroids.


Asthma12
ASTHMA

PHARMACOLOGIC AGENTS – LONG-TERM

  • LONG-ACTING BRONCHODILATORS

  • 3) PHOSPHODIESTERASE INHIBITORS- Theophylline.

  • Mild bronchodilator.

  • Control of nocturnal symptoms.

  • Used in patients w/ moderate to severe persistent asthma along w/ inhaled steroids and beta blockers.

  • See text re serum concentrations, effects of other meds.


Asthma13
ASTHMA

PHARMACOLOGIC AGENTS – LONG-TERM

  • LEUKOTRIENE MODIFIERS

  • Singulair (montelukast), Zileuton.

  • Leukotrienes- think of them as a delayed-onset histamine → vasodilatation, increased capillary permeability, mucous production, and bronchoconstriction.

  • Can minimize need for “rescue” treatment in acute exacerbations; alternatives to inhaled steroids.


Asthma14
ASTHMA

PHARMACOLOGIC AGENTS – LONG-TERM

  • DESENSITIZATION

  • Immunotherapy, “allergy shots.”

  • When response to meds for long-term control is not optimal, ie you’ve tried everything else without adequate control. This is the top rung of the outpatient “stair step.”

  • MISCELLANEOUS

  • Oral sustained-release beta2 agonists.

  • Omalizumab- a recombinant antibody that binds IgE.


Asthma15
ASTHMA

QUICK-RELIEF MEDICATIONS

  • 1) BETA-ADRENERGIC AGENTS

  • 2) SYSTEMIC CORTICOSTEROIDS.


Asthma16
ASTHMA

QUICK-RELIEF MEDICATIONS

  • 1) BETA-ADRENERGIC AGENTS

  • Short-acting, inhaled bronchodilators.

  • For exacerbations only. (“rescue”)

  • β-1 vs β-2.

  • Albuterol, terbutaline, bitolterol, pirbuerol.

  • If need is often for these, long-term control efforts need to be ramped up.


Asthma17
ASTHMA

QUICK-RELIEF MEDICATIONS

  • 2) SYSTEMIC CORTICOSTEROIDS

  • For moderate to severe exacerbations, lack of response to inhaled short-acting β2 therapy.

  • Sometimes necessary for the long-term control of patients w/ severe asthma.

  • PO vs. IV.

  • Adrenal suppression.


Asthma18
ASTHMA

  • ASSESSMENT, MONITORING, PREVENTION.

  • Periodic clinical assessments and self-assessments (peak flow meters) are the primary methods of monitoring asthma

  • Written action plan for self-monitoring, changes to therapy, and treatment of exacerbations.

  • Asthmatics should receive vaccinations for influenza and pneumococcal pneumonia.


COPD

  • Airflow obstruction due to emphysema and chronic bronchitis. Most have features of both.

  • Usually progressive, has variable amounts of airway inflammation, some of which may be reversible.

  • COPD and asthma combined = the 4th leading cause of death in the U.S.

  • Death rate is increasing, esp in elderly men.

  • Almost all due to smoking.

  • Other causes:


COPD

SIGNS & SYMPTOMS

  • Present in the 5th and 6th decades of life.

  • Excessive cough, shortness of breath, and sputum production.

  • Symptoms often present 10 years or more.

  • Progressively worsening dyspnea: w/ exertion → w/ mild exertion → at rest.

  • Late stages → complicated by pneumonia, pulmonary hypertension, cor pulmonale, chronic respiratory failure.


COPD

SIGNS & SYMPTOMS

  • See text for comparison of “pink puffer” (emphysema) vs “blue bloater” (chronic bronchitis).

  • Thin, uncomfortable, quiet chest- emphysema.

  • Obese, noisy chest, rhonchi, wheezes- chronic bronchitis.

  • In reality, most patients have features of both.


COPD

IMAGING

  • Plain X-rays not sensitive enough for a Dx, but show:

  • Hyperinflation, flattening of the diaphragm.

  • Bullae- when present in the right clinical setting → diagnostic of emphysema.


COPD

COMPLICATIONS

  • Spontaneous pneumothorax.

  • Pulmonary hypertension, cor pulmonale.

  • Acute bronchitis, pneumonia, pulmonary thromboembolism, LV failure can worsen otherwise stable COPD.

  • Hemoptysis- can be from chronic bronchitis but bronchogenic carcinoma needs to be considered.


COPD

TREATMENT

  • AMBULATORY PATIENTS

  • 1) Smoking cessation.

  • 2) Oxygen therapy.

  • 3) Bronchodilators.

  • 4) Corticosteroids.

  • 5) Antibiotics.

  • 6) Other measures.


COPD

TREATMENT

1) SMOKING CESSATION

  • Requires an active, multidimensional program, not simply telling patients to quit (5%).

  • Nicotine gum + behavior modification = 22% sustained abstinence at 5 years.


COPD

TREATMENT

2) OXYGEN THERAPY

  • For patients w/ resting hypoxemia.

  • The only therapy (“drug”) that has been shown to improve the natural history of COPD in patients w/ resting hypoxemia.

  • Correlated w/ prolonged survival, reduced hospitalizations, better quality of life.

  • Esp likely to benefit- the hypoxemic patient w/ pulmonary hypertension, cor pulmonale, erythrocytosis, impaired cognitive function, exercise intolerance, nocturnal restlessness, morning headache.


COPD

TREATMENT

3) BRONCHODILATORS

  • The most important pharmacologic agents in the management of COPD.

  • Symptomatic improvement only. Do not alter the progressive deterioration in lung function.

  • Ipratropium bromide- an anticholinergic.

  • Albuterol, metaproterelol- short-acting β2 agonists.

  • Salmetrol, Formoterol- long-acting β2 agonists.

  • Oral theophylline- 3rd line agent.


COPD

TREATMENT

4) CORTICOSTEROIDS

  • Only useful in acute exacerbations.

  • More useful when the predominant component is chronic bronchitis rather than emphysema.

  • See text for details.

  • Inhaled steroids have no effect on the characteristic decline in lung function in COPD.


COPD

TREATMENT

5) ANTIBIOTICS

  • For:

  • 1) To treat an acute exacerbation.

  • 2) To treat acute bronchitis.

  • 3) To prevent acute exacerbations (prophylaxis).

  • Evidence supports use in only the 1st two.

  • Trimethoprim-sulfamethoxazole (Septra).

  • Amoxicillin-clavulanate (Biaxin).


COPD

TREATMENT

6) OTHER MEASURES

  • See text.

  • Graded exercise, hydration to promote clearing of secretions.

  • Expectorants, mucolytics, not helpful.

  • Cough suppressants to be avoided.


Pneumonia
PNEUMONIA

  • Lower respiratory tract infection.

  • We will look at community-acquired pneumonia.

  • See text for Hospital-acquired pneumonia, anaerobic pneumonia, and pneumonia in the immunocompromised.


Community acquired pneumonia
COMMUNITY-ACQUIRED PNEUMONIA

  • Common.

  • Most deadly infectious disease in the U.S.

  • 4th leading cause of death.

  • 14% mortality if hospitalization is required, < 1% if not.


Community acquired pneumonia1
COMMUNITY-ACQUIRED PNEUMONIA

PATHOGENESIS

  • Begins outside the hospital or within 48 hours after admission in a patient who has not been in a long-term care facility for 14 or more days before the onset of symptoms.

  • Occurs when there is a defect in one or more of the defense mechanisms: cough reflex, mucociliary clearance of secretions, immune response.

  • Or when there is a large inoculum or a particularly virulent organism.


Community acquired pneumonia2
COMMUNITY-ACQUIRED PNEUMONIA

PATHOGENESIS

  • THE BACTERIAL BUGS:

  • Strep pneumoniae- 2/3 of cases.

  • H. flu, Mycoplasma, Klebsiella, Chlamydia pneumoniae, Staph aureus, Legionella.

  • THE VIRAL BUGS:

  • Influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus.


Community acquired pneumonia3
COMMUNITY-ACQUIRED PNEUMONIA

PATHOGENESIS

  • THE SCREWY BUGS:

  • Chlamydia psittaci (psittacosis), Coxiella burnetti (Q fever), Francisella tularensis (tularemia aka rabbitt fever), fungi such as Blastomyces, Coccidioides, Histoplasmosis


Community acquired pneumonia4
COMMUNITY-ACQUIRED PNEUMONIA

LAB

  • Sputum culture, possibly gram stain.

  • HIV if hospitalization required. See text for other tests on hospitalized patients.

    IMAGING

  • CXR- to confirm Dx, look for other associated pathology- cavitation, pleural effusion, degree of involvement, etc.

  • Can take up to 6 weeks for CXR findings to clear.


Community acquired pneumonia5
COMMUNITY-ACQUIRED PNEUMONIA

TREATMENT

  • Empiric antibiotic therapy as the organism obtained at culture does not always correlate w/ the actual pathogen.

  • CHOICES:

  • 1) Macrolides; clarithromycin, azithromycin (Zithromax, “Z-Pak”).

  • 2) Doxycycline.

  • 3) Fluoroquinolones- levofloxacin (Levoquin), others.


Community acquired pneumonia6
COMMUNITY-ACQUIRED PNEUMONIA

TREATMENT

  • ALTERNATIVES:

  • Erythromycin, amoxacillin-clavulanate (Biaxin), 3rd generation cephalosporin such as cefuroxime, cefprozil.

  • Duration varies acc to severity, etiologic gent, response to therapy.

  • Treatment until afebrile at least 72 hours is one guideline.

  • 2 weeks for some bugs- see text.


Community acquired pneumonia7
COMMUNITY-ACQUIRED PNEUMONIA

PREVENTION

  • Polyvalent pneumococcal vaccine- prevents or attenuates the severity of the illness in most immunocompetent patients.

  • For patients:

  • 1) 65 years of age.

  • 2) Any chronic illness that increases the risk of community acquired pneumonia

  • Also vaccinate for influenza (flu shot) to prevent the flu and secondary bacterial pneumonia.


TB

  • Infection w/ Mycobacterium tuberculosis.

  • 15 million people infected in the US.

  • REVIEW

  • Inhalation of droplet nuclei w/ M tuberculosis.

  • The immune response, the lymphocyte, the macrophage, the granuloma.

  • Primary / latent TB.

  • Active TB (Reactivation).

  • Extra-pulmonary TB.


TB

SIGNS / SYMPTOMS – OF LATENT TB

  • Pg 261- “Primary TB is “USUALLY” clinically and radiographically silent.”

  • That is, they are asymptomatic, and their CXR is normal.

  • See Pg 262 for findings in those patients whose CXR is not normal. Notice that these findings are different than those patients w/ active TB.


TB

SIGNS / SYMPTOMS – OF ACTIVE TB

  • Slowly progressive symptoms: malaise, anorexia, fever, weight loss, night sweats.

  • Chronic cough.

  • Dry → productive → blood-tinged sputum.

  • Patient looks chronically ill and malnourished.

  • No physical findings on chest eval specific for TB.

  • Occasionally apical rales.


TB

TREATMENT

TREATMENT OF HIV NEGATIVE PATIENTS

  • See pg 265, and table 9-14.

  • Combinations of:

  • INH (isoniazid).

  • Rifampin.

  • Ethambutal.

  • Streptomycin, and

  • Pyrazinamide.

  • Depending on susceptibility test results.

  • 6 vs 9 months, daily vs 2-3x per week.


TB

TREATMENT

TREATMENT OF HIV POSITIVE PATIENTS

  • Requires expertise in the treatment of both TB and HIV.

  • Guidelines per the CDC.

  • Treatment similar to HIV negative, but:

  • Longer duration of therapy.

  • Drug interactions w/ protease inhibitors and reverse transcriptase inhibitors for HIV.

  • DOT for all who are HIV+.


Tuberculosis
Tuberculosis

Pathogenesis: caused by Mycobacterium tuberculosis infection of the lung

• pathogen is distributed systemically within macrophages and survives intracellularly

• respiratory insufficiency

• estimated 2 billion infected worldwide (WHO)

• yearly mortality = 2 million

• incidence in NA is rising

Multi Drug Therapy

  • Isoniazid

    - most effective agent against Mycobacterium tuberculosis

    - able to penetrate macrophages (active intra- and extracellularly)

    - inhibits mycolic acid synthesis (component of mycobacterial cell wall)

  • Rifampin

    - often given in combination with isoniazid (transcription inhibitor)

    - combination cures 95-98% of TB caused by susceptible strains within 9 mo.

    • Others

  • pyrazinamide, ethambutol, streptomycin

    - given in combination with isoniazid plus rifampicin


Tubrculosis
Tubrculosis

  • Drug toxicity:-

  • Isoniazid- Dermatitis/ Polyneuritis/ Hepatitis

  • Rifampin- Red coloration of sweat, urine/ Hepatitis/ Flu like syndrome

  • Ethambutol- Optic neuritis- Color blindness

  • Pyrizinamide- Arthralgias/ Hepatitis


Pleural effusion
PLEURAL EFFUSION

  • An abnormal accumulation of fluid in the pleural space.

  • Systemic disease: CHF, cirrhosis, nephrotic syndrome, sarcoidosis, connective tissue disease, etc.

  • Infection: TB, fungi, rickettsiae.

  • Neoplasia: lung cancer, lymphoma, breast cancer.


Pleural effusion1
PLEURAL EFFUSION

  • BOTTOM LINE: all new accumulations of fluid in the pleural space should be evaluated by thoracentesis to determine composition of fluid, presence of malignant cells, infection.

    SIGNS / SYMPTOMS

  • Dyspnea, cough, pleuritic chest pain.

  • Large effusions more symptomatic than smaller ones, symptoms more common in patients w/ existing cardiopulmonary disease.

  • Dullness to percussion, shifting dullness.

  • Diminished breath sounds.


Pleural effusion2
PLEURAL EFFUSION

  • See text re evaluation of the fluid, transudate vs exudate, etc., cytologic exam, culture.

  • See text re imaging.

  • See text re treatment: the bottom line is that treatment is aimed at the underlying etiology of the effusion.

  • See text re local measures (thoracentesis, pleurodesis) that can be used for relief of effusions causing significant symptoms.


Pneumothorax
PNEUMOTHORAX

  • CLASSIFICATION:

  • SPONTANEOUS VS TRAUMATIC.

  • IF IT’S NOT TRAUMATIC, IT’S SPONTANEOUS

  • PRIMARY- in the absence of pulmonary disease.

  • SECONDARY- due to / is a complication of preexisting pulmonary disease (COPD, asthma).

  • ALSO IATROGENIC (an acupuncture needle).


Pneumothorax1
PNEUMOTHORAX

PRIMARY:

  • Most commonly in tall, thin men between ages 10-30.

  • Rupture of a bleb.

  • Family Hx, smokers.

    SECONDARY:

  • COPD, asthma, cystic fibrosis, TB, menstruation (catamenial pneumothorax), interstitial lung disease (sarcoid), Pneumocystis infection.


Pneumothorax2
PNEUMOTHORAX

TENSION PNEUMOTHORAX

  • A one-way valve effect from chest wall trauma, allowing air into the pleural space with each breath, but it is not self-limiting as in rupture of a bleb.

  • Is a medical/surgical emergency requiring placement of a chest tube.


Pneumothorax3
PNEUMOTHORAX

SIGNS / SYMPTOMS

  • CHEST PAIN- mild to severe, on the affected side.

  • DYSPNEA- 100%.

  • Sxs begin at rest.

  • Respiratory compromise from the pneumo can be life-threatening in patients w/ underlying COPD or asthma.

  • For small pneumo’s (<15%) → only mild tachycardia.


Pneumothorax4
PNEUMOTHORAX

SIGNS / SYMPTOMS

  • For larger pneumo’s → decreased/absent breath sounds over the area of the pneumo, decreased tactile fremitus, decreased movement of the chest.

  • W/ a tension pneumo → marked tachycardia, hypotension, and possibly shift of the mediastinum/trachea away from the affected side.


Pneumothorax5
PNEUMOTHORAX

IMAGING

  • CXR- Detection of a visceral pleural line.

  • Best taken on expiration when the lung is least expanded, allowing better visualization in a smaller pneumo.

  • Pleural effeusion may be present.

  • Tension pneumo- contralateral shift of the trachea and mediastinum.


Pneumothorax6
PNEUMOTHORAX

DIFFERENTIAL Dx

  • Can mimic PE, MI, pneumonia.

    TREATMENT

  • Depends on severity.

  • <15%- observation, resolution.

  • >15%- evacuation by a chest tube, or a 16 gauge intravenous catheter (angiocath) in a pinch like Mark Wahlburg in that Movie w/ George Clooney.

  • Risk of recurrence in smokers is 50%.


Pneumothorax7
PNEUMOTHORAX

TREATMENT

  • Surgery occasionally needed- thoracotomy, thoracoscopy- for recurrences, for bilateral pneumothoraces, and for failure of resolution w/ a chest tube.

  • Surgery- resection of blebs; pleurodesis- installation of a substance (usually talc or doxycycline) that in effect is an irritant and results in fusion of the visceral and parietal pleurae thereby obliterating the pleural space.


Pneumothorax8
PNEUMOTHORAX

PROGNOSIS.

  • After successful treatment, no long-term complications.

  • 30% of patients w/ a spontaneous pneumothorax will experience a recurrence.

  • Surgery/pleurodesis reduces recurrence.


Lung cancer
LUNG CANCER

THE SKINNY

  • AKA BRONCHOGENIC CARCINOMA.

  • The most common cause of cancer death in men and women. Prostate is the most common in men, but mortality is higher for lung. Breast is more common in women, but mortality is higher for lung.

  • 13% of new cancer diagnoses.

  • 28% of all cancer deaths.


Lung cancer1
LUNG CANCER

THE SKINNY

  • More people die of lung cancer than from colon, breast and prostate combined.

  • 80% of lung cancers are related causally to smoking.

  • Other factors: environmental (asbestos, radon gas), industrial (bis-chloromethyl ether), metals (nickel, chromium, arsenic, iron oxide), second-hand cigarette smoke.


Lung cancer2
LUNG CANCER

SURVIVAL

  • Mean age at Dx is 60.

  • 40% survive 1 year.

  • Combined 5 year survival for all stages is 15%, up from 12% from 1974-1976.


Lung cancer3
LUNG CANCER

HISTOLOGIC TYPES

  • Squamous cell carcinoma- 25-35%- arise from the bronchial epithelium, are endobronchial.

  • Adenocarcinoma- 35-40%- arise from mucous glands, appear as a peripheral nodule/mass.

  • Large cell carcinoma- 5-10%.

  • Small cell carcinoma- 15-20%.

  • For staging, separated into small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).

  • SCLC spreads earlier, more aggressive and if untreated median survival is 6-18 weeks.


Lung cancer4
LUNG CANCER

CLINICAL FINDINGS

  • Symptomatic in 75-90% at time of Dx.

  • Presentation depends on the type and location of the primary tumor, the extent of local spread, and presence of distant metastases and any paraneoplastic syndromes.


Lung cancer5
LUNG CANCER

SIGNS / SYMPTOMS

  • Anorexia, weight loss, asthenia- 55-90%.

  • New cough or change in a chronic cough- 60%.

  • Hemoptysis- 6-31%.

  • Pain- non-specific vs pain from bony metastases- ribs, vertebrae, pelvis- 25-40%.

  • Brain mets- 10%- headache, N/V, new-onset seizure, altered mental status.

  • Pleural effusion- 12-33%.


Lung cancer6
LUNG CANCER

SIGNS / SYMPTOMS

  • Bronchial obstruction- “post-obstructive” pneumonia.

  • Change in voice- involvement of the recurrent laryngeal nerve.

  • Superior vena cava syndrome.

  • Horner’s Syndrome- ptosis, miosis, anhydrosis- from involvement of the paravertebral sympathetic chain or inferior cervical ganglia.

  • Liver mets- asthenia, weight loss.


Lung cancer7
LUNG CANCER

PARANEOPLASTIC SYNDROMES

  • SIADH, ACTH, PTH, COUPLE OTHERS

  • 10-20% of lung cancer patients.

  • May be the presenting feature leading to the Dx, and may be a bigger source of morbidity than the malignancy itself.

  • Symptoms of these syndromes can be addressed and improved w/ treatment even in cancers “not curable.”


Lung cancer8
LUNG CANCER

LAB

  • Dx made on the basis of cytology or histology.

  • Cytology is sensitive but low-yield.

  • Thoracentesis of a malignant effusion.

  • Fine-needle aspiration of an abnormal node- supraclavicular, cervical.

  • Bronchoscopy- see text. Can visualize the bronchi and aspirate, biopsy, wash and do all kinds of cool sampling of all kinds of stuff not limited to the bronchi. Also mediastinoscopy, thoracotomy.


Lung cancer9
LUNG CANCER

IMAGING

  • CXR, CT.

  • Identify abnormalities in nearly all cases.

  • Dx still requires cells (cytology) or tissue (histology).


Lung cancer10
LUNG CANCER

STAGING

  • See text, Table 9-15.

    TREATMENT (THE SHORT VERSION)

  • Curable only w/ surgical resection- Stages I & II.

  • Other stages (III, IV) - chemo & radiation- but even this only gives an increase in median survival of from 5 months to 7 months.


Sarcoidosis
SARCOIDOSIS

  • “A systemic disease of unknown etiology characterized in about 90% of patients by granulomatous inflammation of the lung.”

  • Can also involve peripheral nerves, heart, liver, kidney, other tissues.

  • North American blacks (women more than men) and northern European whites.

  • Onset in 3rd or 4th decade.


Sarcoidosis1
SARCOIDOSIS

SIGNS / SYMPTOMS

  • Malaise, fever, dyspnea of insidious onset.

  • Other Sxs based on other organ system involvement.

  • Some are asymptomatic and diagnosed only after an abnormal CXR.

  • Physical findings in the lung often absent- no crackles as you might expect.

  • Other organ system involvement can lead to: lymphadenopathy, hepatosplenomegaly, erythema nodosum, parotid gland enlargement.


Sarcoidosis2
SARCOIDOSIS

LAB

  • Dx requires biopsy, finding of granuloma formation.

  • Lab may show:

  • Leukopenia, elevated sed rate (ESR).

  • Hypercalcemia, hypercalciuria.

  • Elevated levels of angiotensin converting enzyme.

  • PFT’s can show an obstructive defect but more commonly a restrictive defect.


Sarcoidosis3
SARCOIDOSIS

IMAGING

  • Variable.

  • Bilateral hilar adenopathy.

  • Parenchymal involvement.

  • Alone or combined.


Sarcoidosis4
SARCOIDOSIS

TREATMENT

  • Oral corticosteroids for patients with:

  • Disabling constitutional symptoms.

  • Hypercalcemia, CNS or cardiac involvement.

  • Granulomatous hepatitis.

  • Progressive pulmonary lesions.

  • Months to years.


Sarcoidosis5
SARCOIDOSIS

PROGNOSIS

  • Prognosis worse for patients w/ pulmonary parenchymal involvement. Best for patients with hilar adenopathy only.

  • Can progress to pulmonary fibrosis, cavitation, bronchiectasis.

  • Death from pulmonary insufficiency in 5%.

  • See text re cardiac involvement.


Pulmonary embolism
PULMONARY EMBOLISM

  • AKA pulmonary venous thromboembolism

  • 200, 000 deaths per year in the U.S, although later in the chapter it says 50,000.

  • 3rd leading cause of death in hospitalized patients.


Pulmonary embolism1
PULMONARY EMBOLISM

  • REVIEW: risk factors, Virchow’s Triad (venous stasis, hypercoagulability, endothelial damage)

  • REVIEW: things that embolize: air, fat, amniotic fluid, foreign bodies, tumor cells, septic emboli.

  • The most common thing that embolizes is a thrombus, usually formed in the deep venous circulation (popliteal v, ileofemoral v), but can arise from anywhere in the venous circulation or the heart.


Pulmonary embolism2
PULMONARY EMBOLISM

SIGNS / SYMPTOMS

  • Dx is difficult, for 2 reasons:

  • 1) Sxs depend on the size of the embolus and the patients preexisting cardiopulmonary status.

  • 2) Common signs and symptoms of a PE are not specific to this disorder.

  • No Sx or combination of Sxs is specific to PE.

  • Must maintain a high index of suspicion.


Pulmonary embolism3
PULMONARY EMBOLISM

SIGNS / SYMPTOMS

  • Dyspnea-75-85%.

  • Pain on inspiration- 65-75%.

  • Tachypnea- >50%.

  • In one study, 97% of patients had one or more of 3 findings: dyspnea, chest pain, tachypnea.

  • Physical findings- none are diagnostic, and Sxs alone should be enough to consider the Dx of PE regardless of physical findings.


Pulmonary embolism4
PULMONARY EMBOLISM

LAB

  • EKG- abnormal in 70%. Right ventricular strain, right bundle branch block. Done also to R/O MI, pericarditis. See text.

  • ABG- acute respiratory alkalosis; arterial pO2 low; BUT ABG’s alone are not diagnostic.

  • See text for “d-Dimers” etc.

  • “Profound hypoxia w/ a normal CXR in the absence of preexisting lung disease is highly suspicious for PE.”


Pulmonary embolism5
PULMONARY EMBOLISM

IMAGING

  • 1) CXR.

  • 2) LUNG SCANS.

  • 3) CT.

  • 4) VENOUS THROMBOSIS STUDIES.

  • 5) PULMONARY ANGIOGRAPHY.


Pulmonary embolism6
PULMONARY EMBOLISM

IMAGING

  • 1) CXR.

  • Done to R/O other common lung disorders that may explain the patients symptoms.

  • Does not establish the Dx of PE.

  • In a PE the CXR will show: atelectasis, parenchymal infiltrates, pleural effusion.

  • Most helpful when normal.

  • After the CXR, if another Dx is not found, we move to the V/Q scan.


Pulmonary embolism7
PULMONARY EMBOLISM

IMAGING

  • 2) LUNG SCANS

  • The ventilation-perfusion or V/Q scan.

  • Actually it’s 2 scans:

  • 1) The ventilation scan- inhalation of radioactive gas and the distribution of that material is determined via the scan.

  • 2) The perfusion scan- microaggregated albumin tagged w/ a radioisotope is given IV, they lodge in the pulmonary circulation, and their distribution is measured via the scan.


Pulmonary embolism8
PULMONARY EMBOLISM

IMAGING

  • 2) LUNG SCANS

  • A negative scan is one in which ventilation (as measured by the radionuclide scan) is uniform, and perfusion is uniform as well. They “match.”

  • In a PE, there is normal ventilation, but the embolus impairs perfusion in the segment affected by the PE, so there is a “mis-match.”

  • The result ain’t that simple, though; what we get is a low, intermediate, or high probability of a PE.


Pulmonary embolism9
PULMONARY EMBOLISM

IMAGING

  • 2) LUNG SCANS

  • A negative scan is good, a high-probability scan is good.

  • For the low and intermediate probability scan, the next step may be pulmonary angiography.

  • See text for whom we may and may not subject to angiography. Algorithms pg 289. Look at this. Really.


Pulmonary embolism10
PULMONARY EMBOLISM

IMAGING

  • 3) CT

  • See your text.

  • The “Helical” or “Spiral” CT may be on its way to replacing the V/Q scan as the imaging modality of 1st choice, but we’re not there yet.

  • Detects the actual thrombus.


Pulmonary embolism11
PULMONARY EMBOLISM

IMAGING

  • 4) TEST FOR VENOUS THROMBOSIS

  • Since 70% of patients with PE will have DVT, it would follow that if we could document DVT in a patient w/ suspected PE but a non-diagnostic V/Q scan, we could proceed w/ anticoagulation therapy and avoid angiography.

  • Various studies: venous ultrasonography (the procedure of choice), doppler studies, venography.

  • Sensitivity not nearly as good as pulmonary angiography.

  • The d-Dimer test may become the test of choice to make this Dx due ti it’s high sensitivity.


Pulmonary embolism12
PULMONARY EMBOLISM

IMAGING

  • 5) ANGIOGRAPHY

  • Catheterization of the pulmonary arteries w/ injection of dye.

  • The gold standard for diagnosis. ie, has the highest sensitivity and specificity of any current test.

  • Is “safe,” but invasive, and not without risk of complications, death.

  • See text for a few other thoughts re angiography.

  • See text for use of MRI. Right now it’s a research tool.


Pulmonary embolism13
PULMONARY EMBOLISM

IMAGING

  • 5) ANGIOGRAPHY

  • When to use: consider: 1) degree of clinical suspicion for PE, 2) results of V/Q scan, and 3) results of venous ultrasound.

  • See Figure 9-3 for algorithms re how to proceed in establishing the diagnosis. These algorithms speak to how difficult it can be to establish the Dx while trying to do so in a non-invasive manner and without subjecting everyone to angiography.


Pulmonary embolism14
PULMONARY EMBOLISM

PREVENTION

  • Since we know the risk factors and the clinical scenarios in which PE happens, it gives us the opportunity to target prevention.

  • It is still underutilized- your text says about 50% of fatal PE’s receive any preventive therapy.

  • Anticoagulation- “mini-dose” heparin, various types.

  • IPC devices, elastic / compression stockings.

  • Early ambulation post-op.


Pulmonary embolism15
PULMONARY EMBOLISM

TREATMENT

  • 1) ANTICOAGULATION.

  • 2) THROMBOLYTIC THERAPY.

  • 3) OTHER.


Pulmonary embolism16
PULMONARY EMBOLISM

TREATMENT

  • 1) ANTICOAGULATION.

  • “Secondary therapy” in the sense that it stops further clot formation and allows for fibrinolysis to lyse the existing clot.

  • IV heparin acutely followed by 3-6 months of anticoagulation with coumadin / warfarin.

  • Reduces the risk of both recurrent venous thrombosis and death from PE by 80-90%.


Pulmonary embolism17
PULMONARY EMBOLISM

TREATMENT

  • 1) ANTICOAGULATION.

  • HEPARIN- binds to and accelerates the activity of anti-thrombin III, which inactivates thrombin, factor Xa, and factor IXa.

  • WARFARIN- effects synthesis of the Vitamin K dependent clotting factors. Many many drug interactions effecting serum levels resulting in under or over anticoagulation, resulting in hemorrhage which can be fatal (intracanial).


Pulmonary embolism18
PULMONARY EMBOLISM

TREATMENT

  • 1) ANTICOAGULATION.

  • Duration of treatment w/ warfarin may need to be longer than 6 months, possibly for life, in patients who have non-reversible risk factors for future clot development such as The Factor V (Leiden) mutation, Protein S or Protein C deficiency, or antiphospholipid syndrome, as compared to patients w/ a transient risk factor such as pelvic or orthopedic surgery.

  • For these patients, need to juggle the benefits of continued treatment vs. the risk of hemorrhage.


Pulmonary embolism19
PULMONARY EMBOLISM

TREATMENT

  • 2) THROMBOLYTIC THERAPY

  • W/ streptokinase, urokinase, and TPA.

  • No benefit for most patients.

  • Significant risk of hemorrhage

  • Reserved for patients at high risk of death in whom a more rapid resolution of the clot may be lifesaving. These patients are hemodynamically unstable and sick sick sick.


Pulmonary embolism20
PULMONARY EMBOLISM

TREATMENT

  • 3) OTHER

  • Placement of an inferior vena cava filter- a “basket”- for patients: a) with contraindications to anticoagulation, b) who continue to flip emboli despite anticoagulation, and c) chronic/recurring emboli.

  • Surgical embolectomy- procedure of last resort in patients who are critically ill and getting worse. Carries a high mortality rate.


Pulmonary embolism21
PULMONARY EMBOLISM

PROGNOSIS

  • 50,000 or 200,000 deaths per year, depending on which of these numbers you want to believe. Either way, it’s a bunch.

  • In most deaths, the PE is not recognized ante mortem or death occurs prior to initiation of specific therapy.

  • As such, need to target prevention.

  • Outlook for the survivors is good, and depends more on the underlying disease process (Factor V mutation, etc) rather than the clot itself.


Sleep apnea
SLEEP APNEA

  • See your text. Pg 310.

  • Central vs obstructive sleep apnea.

  • Obstructive way more common.

  • Association w/ obesity. Other causes: nasal polyps, deviated septum, congenital/traumatic defects.

  • Association w/: hypertension, cardiac disease, sudden death. Also fatigue, cognitive defects, etc

  • Lack of time spent in REM/Stage IV/ Delta wave sleep and its associated problems.


Sleep apnea1
SLEEP APNEA

  • Diagnosis: the “somnogram.” EEG combined w/ measurements of O2, CO2, O2 sat. ,etc. Documentation of apneic episodes.

    TREATMENT

  • Address the underlying problem.

  • Weight loss (you can at least try).

  • CPAP.

  • Surgical correction if the polyps, septum, etc.

  • Aggressive treatment is warranted due to the association between cardiovascular disease, sudden death.


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