Pleural Pulmonary

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What is pleural effusion?: Pleural effusion is an abnormal accummulation of fluid in the pleural space.
Is pleural effusion detectable on a plain chest film?: Yes, pleural effusion is often detectable on a plain chest film.
What reabsorbs the aqueous phase of pleural fluid?: The visceral pleural capillaries.
What reabsorbs the protein phase of pleural fluid?: The parietal pleural lymphatics.
What is the rate of formation of pleural fluid on the parietal pleural surface?: 0.1 ml/kg/hr
What are the 5 major types of pleural effusion?: 1. exudate
2. transudate
3. empyema
4. hemothorax
5. chylothorax
What are the 3 possible features of exudate (must have 1)?: 1. > 1/2 the protein content of the patient's serum

2. > 6/10 the lactate dehydrogenase (LDH) content of the patient's serum

3. LDH content > 2/3 the upper limit of "normal" serum
What are the two most common causes of exudate?: Cancer and pneumonia.

Also:
various infections
TB
fungus/parasite
PE
uremia
Is exudate a passive or active metabolic/cellular process?: Exudate is an active process.
Is transudate pleural effusion an active or passive process?: It is a passive movement of fluid.
What are the 3 physiologic phenomena that result in transudate?: 1. increased vascular hydrostatic pressure
2. decreased plasma oncotic pressure (osmotic pressure/suction re protein)

3. increased negative intrapleural pressure
Name 5 causes of transudate.: 1. CHF congestive heart failure
2. nephrotic syndrome
3. constrictive pericarditis
4. acute atelectasis
5. pulmonary embolism
What is the most common cause of transudate?: CHF (syndrome) causes 90% cases. LVF causes ressure to increase in the pulmonary vessels --> increased hydrostatic pressure
How does nephrotic syndrome cause transudate?: It causes decreased plasma oncotic pressure
How does constrictive percarditis cause transudate?: noncompliant pericardium restricts ventricular filling and mimics CHF.
How does acute atelectasis cause transudate?: It causes increased negative intrapleural pressure. Some alveoli collapse, showing up as whitish area.
How does pulmonary embolism cause transudate?: It causes increased pulmonary vascular resistance which causes increased hydrostatic pressure.
Where does fluid start to collect and when does it show?: In the costal-phrenic angle. It starts to show up when 200 ml has collected
Is empyema a form of exudate or transudate?: Empyema is a form of exudate.
Why is empyema fluid turbid or purulent?: Because of infection in the pleural space.
What is hemothorax?: Hemothorax is gross blood in the pleural space.
What is the main cause of a hemothorax?: Hemothorax is usually due to chest trauma.
What is chylothorax?: It is the leakage of lymphatic fluid (cholesterol) into the pleural space.
What are 2 common causes of chylothorax?: 1. Tuberculous pleuritis

2. Rheumatoid ??
What kind of effusion is indicated by pleuritic chest pain (pain w/breathing NOT due to fractured rib)?: Effusion is usually exudative.
What are the signs/symptoms of small effusions?: Usually asymptomatic. No physical findings if < 200 ml.
What are the signs/symptoms of large effusions?: - dyspnea
- lung compression
- dullness to percussion
- displacement of trachea (if massive effusion)
- increased fremitus
What is fremitus?: Palpable vibration.
What do you see on an x-ray of pleural effusion?: - blunting of costophrenic sulcus (angle) due to fluid accumulation

- thickening of interlobal and/or interlobular lung fissures

- loculated fluid (white shadow w/broad base toward the chest wall and point toward the lung

- crescentic line or meniscus (white opacification; if not all the way to apex, upper edge is curved)
What test to you use to confirm pleural effusion?: Thoracentesis.
What is thoracentesis?: Aspiration of fluid w/syringe and needle.

Should be done below the level of the effusion and immediately above the rib.
What is the treatment for transudative PE?: Treat the underlying condition unless the PE is compressing the lung or causing tracheal/mediastinal shift -- then place chest tube for drainage.
How many primary bronchi are there?: 2
What branches are bronchioles?: 12th - 16th
What branches are terminal bronchioles?: 17th - 24th
Where are the alveolar ducts, sacs, and alveoli found?: At the ends of the terminal bronchioles
How far down is the respiratory "dead space"?: Down to the 16th branch
What is respiratory dead space?: Air in the passageways that is not being exchanged.

Approx. 150 ml of every breath.
Where does the diffusion of oxygen take place?: From the terminal bronchi to the alveoli
What is the acinus?: It is everything distal to the terminal bronchioles
How are capillaries arranged in the lungs?: They run in sheets between and among the alveoli
What nerve innervates the diaphragm?: The phrenic nerve, C4.
What is the primary respiratory muscle?: The diaphragm
How do the external intercostal muscles aid in respiration?: They cause elevation of the ribcage for inspiration
What are the accessory inspiratory muscles?: - scalenes: hook onto ribs 1 & 2; orig from transverse processes of the cervical region; innervated by cerv plexus (C1-4)

- SCM: pulls on sternum and middle 3rd of clavicle; orig on mastoid process
When are the accessory inspiratory muscles used?: During very labored breathing and to turn the head.
What muscles are used for expiration?: - diaphragm (relaxes)

- abdominal muscles: pull lower ribs down

- internal intercostals: pull down ribs and compress thorax
What is a thoracostomy?: It is an incision made for drainage (when patient has pneumothorax or fluid in pleural space)

Should be just above upper surface of rib so as not to cut nerve, veins just underneath
What instrument is used to measure lung volumes?: Spirometer
What is resting tidal volume?: TV; amount of air inhaled/exhaled when breathing normally

approx. 500 ml
What is Inspiratory Reserve Volume?: IRV: amount of air that can be taken in in addition to normal breath
What is Expiratory Reserve Volume?: ERV: amount of air that can be expelled after inhaling all the way

approx 1L
What is Residual Volume?: RV: amount of air left in lungs after expelling as much air as possible

approx 1000ml ??
What is Functional Residual Capacity?: FRC: = ERV + RV
What is Vital Capacity?: VC: The maximal amount of air that can be moved

= IRV + TV + ERV
What is Forced Vital Capacity?: FVC: the maximum volume of air which can be forcibly expelled after inhaling as deeply as possible
Is slow VC (vital capacity) greater or less than FVC (forced vital capacity)?: Slow VC is often greater than FVC.
What is an obstructive disease?: Patients have difficulty getting air out due to loss of collagen & elastin from bronchioles, and their lungs collapse during exhalation. Passages also narrowed by excess mucus.
Does excess mucus secretion (asthma, chronic bronchitis) cause difficulty breathing in or out?: It causes difficulty breathing in.
What are signs of OBSTRUCTIVE lung diseases?: - small and terminal bronchioles collapse

- FVC often decreased (> 6 sec)
Are emphysema, asthma, chronic bronchitis restrictive or obstructive diseases?: They are obstructive.
What is a RESTRICTIVE lung disease?: Patient has difficulty getting air in due to DECREASED LUNG COMPLIANCE and INCREASED, FOOTBALL-LIKE elasticity

- lung becomes fibrosed

- VC is smaller
Are chest x-rays usually taken as inspiratory or expiratory films? Why?: Inspiratory.

To accurately assess heart size.
Is pressure in intrapleural "space" positive or negative? Why?: Negative pressure.

Chest wall pulls outward; lungs pull inward (recoil)
What two elements are responsible for LUNG RECOIL?: 1. collective surface tension w/in all alveoli

2. elasticity of lung
At FRC, Functional Residual Capacity, how much is the chest expanded (%)?: 60%
What is surface tension?: Collection of molecular forces that occurs wherever a gas/fluid interface exists.
What is surfactant?: - Fluid that decreases surface tension to keep lungs from collapsing

- Dipalmitoylecithin
What cells produce surfactant?: Type 2 epithelial cells w/in the alveoli
What is the Law of LaPlace?: P = 2T / r

Pressure (in bubble/alveolus) = 2 x tension of fluid / radius of bubble
Why is air pressure greater in smaller alveoli?: Law of LaPlace - Surface tension of fluid in alveolus shrinks the alveolus and is greater in the smaller alv. Thus, air pressure P in smaller alv is greater.

Smaller the alveolus, greater the surface tension, greater the wall tension, harder to inflate when one inhales

W/o surfactant, small alveoli would inflate much less than large ones during normal inspiration
What is the effect of surfactant on surface tension T of alveoli?: Surfactant decreases T better, the smaller the alveolus. This tends to even out T in all alveoli so they inflate more equally.
What is lung compliance?: Change in volume vs. change in pressure
What is the cause of PRIMARY pulmonary hypertension?: The cause is unknown.
Who is most likely candidate for the rare primary pulmonary HTN?: Young to middle-aged women.
What are syptoms of primary pulmonary hypertension?: - progressive dyspnea

- narrowing of pulm arteries
What are common causes of secondary pulmonary hypertension?: - vasoconstriction (chronic hypoxia)

- loss of pulmonary vessels

- vascular obstruction

- increased pulmonary venous pressure

- increased blood viscosity - from polycythemia
What are the symptoms/signs of pulmonary HTN?: - dyspnea
- fatigue
- chest pain on exertion
- syncope on exertion
What is syncope?: Brief lapse in consciousness caused by transient cerebral hypoxia. Fainting.
What are the heart sounds associated with pulmonary hypertension?: Narrow splitting of S2 with a loud P2 -- instead of the normal A2-P2, inspiratory or physiologic splitting.
What are the lab findings for pulmonary HTN?: - hypoxemia (deficiency in [O2] in arterial blood.

- polycythemia in many cases

- ECG:
- right atrial enlargement
- right ventricular strain
- right ventricular hypertrophy
What will a V/Q scan show for pulmonary HTN?: May show unmatched defects if HTN is due to recurrent pulmonary emboli
What will show up on PFT's for pulmonary HTN?: Nothing unusual
What is the treatment for pulmonary?: - no effective treatment

- periodic phlebotomy if polycythemia and hematocrit > 60%

- prostacyclin (Epoprostenol) - a potent pulmonary vasodilator
What is phlebotomy?: Incision of vein for the letting of blood. Chief treatment for polycythemia vera.
What is polycythemia?: Increase in # of erythrocytes in the blood that may be primary or secondary to pulmonary disease, heart disease, or prolonged exposure to high altitudes. May be idiopathic.
What are the characteristics of asthma?: Inflammatory lung disease:

- airway inflammation w/o infection

- incrsd airway reactivity (bronchospasm, mucus) to variety of stimuli

- airway obstruction & acute dyspnea due to bronchospasm & mucus production
What is dyspnea?: Distressful sensation of uncomfortable breathing
What is the treatment for exudative pleural effusion?: Tube thoracostomy (chest tube), typically in 5th or 6th interspace at midaxillary line
If exudative pleural effusion is purulent and left untreated, what can result?: Progression to fibropurulent, organized stage. Formation of a peel which can encase part of the lung.
What is a peel?: Fibroblasts migrate into the pleural space from both the visceral and parietal pleura and organize the pleural loculations into a thick, inelastic membrane called a pleural peel.
What are the signs/symptoms of an asthma attack?: Airway narrowing and acute dyspnea due to:

- bronchial edema
- incrsd bronchial mucus
- bronchospasms
What are the 2 major categories of asthma?: 1. extrinsic (allergy/immune rxn)

2. instrinsic, aka cryptogenic asthma (non-immune/allergic)
What are the 3 types of extrinsic asthma?: 1. atopic (allergic)
2. occupational
3. allergic bronchopulmonary aspergillosis
Which is the most common type of extrinsic asthma? Describe: Atopic. Often associated w/other atopic manifestations (rhinitis, exzema, urticaria). Incrsd serum IgE and glood eosinophil count
What causes allergic bronchopulmonary aspergillosis?: Allergic response to colonies of aspergillus fungus in airways; incrsd serum IgE.
What is cryptogenic (asthma)?: Cryptogenic = "hidden"; pertaining to a disease of unknown cause
What are some stimuli that trigger intrinsic/cryptogenic asthma bronchospasms?: - exercise
- stress
- cold exposure
- inhaled irritants
- aspirin
- pul infxn, esp. viral
Why is it often difficult to distinguish betwn intrinsic and extrinsic asthma?: Patients w/allergic (extrinsic) asthma are often susceptible to attacks due to intrinsic triggers
What is the pathogenesis of asthma?: exaggerated bronchoconstrictor response, i.e., incrsd airway reactivity
How can exaggerated bronchoconstrictor response in asthma be demonstrated?: By a patient's response to inhalation of histamine or methacholine (FEV1 goes down by 20%)
What is the histologic substrate of asthmatic hyper-reactivity?: Episodic or persistent bronchial inflammation
In allergic asthma, how is persistent inflammation manifested in the bronchial tissue?: By inflammatory cells:
eosinophils
mast cells
lymphocytes
What type of hypersensitivity rxn causes the inflammation of allergic (extrins) asthma?: Type 1 Hypersensitivity reaction: mast cell degranulation & activation --> release of 1° and 2° chemical mediators of inflammation
What are suggested causes of intrinsic asthma bronchial inflammation?: - viral URI's

- common air pollutants, e.g., SO2 and NO2
What are common signs & symptoms of asthma?: - mild coughing & wheezing
- nocturnal cough in kids (1st clue)
- later punctuated by asthma "attack"
Describe basic asthma attack.: - respiratory distress w/accessory muscle use
- tachypnea & tachycardia
- audible wheeze on expiration or insp & exp
- possible coarse rhonchi
- prolonged exp phase
- dry, tight sounding cough
Describe severe asthma attack.: - wheeze may disappear
- can speak only few words at time
- central cyanosis (blue lips, tongue, buccal mucosa
- possible confusion/lethargy --> respiratory failure w/CO2 narcosis
Rhonchi?: Abnormal sound heard on auscultation of an airway obstructed by thick secretions, muscular spasm, neoplasm, or external pressure. Continuous rumbling.
CO2 narcosis?: Depression of CNS, including respiratory center, due to excessive CO2.
How do you reliably assess asthma attack severity?: - degree of dyspnea
- use of accessory muscles
- difficulty speaking
- cyanosis
Describe hyperventilation during asthma attack.: From hypoxemia, due to dcrsd V/Q ratio caused by airway obstruction. Dcrsd pCO2 early in attack.
Describe air-trapping in asthma attack.: - incrsd residual volume --> hyperinflation of lungs, worse hypoxemia (dcrsd pO2)
- incrsd pCO2 --> resp acidosis
- FVC and FEV1 decrease progressively
Describe chest x-ray of asthma attack.: Show hyperinflation (like emphysema)
How does the degree of eosinophilia relate to severity of asthma attack?: Eosinophilia correlates to severity.
How does the presence, absence, or prominence of wheezing correlate w/severity of asthma attack?: Wheezing does not correlate well.
What does eosinophilia in a patient indicate?: - atopy (allergy), including allergic asthma

- infection by parasite(s)
What is PEF?: peak expiratory flow - maximum flow generated during expiration performed with maximal force and started after a full inspiration; it is not effort-dependent
How is asthma treated?: - inhaled steroids to block inflammation
- oral steroids to block inflam during exacerbations
- leukotriene antagonists
- mast cell stabilizers to block histamine component of inflam
What are 3 bronchodilators used for asthma and when are they used?: 1. inhaled beta2 adrenergic agonists - resuce from symptoms

2. inhaled anticholinergics - rescue

3. oral xanthines - maintenance (opens airways)
What controls how much blood goes to the lungs?: ANS autonomic nervous system, symp and parasymp, and hypoxia
How do local pulmonary arterioles react to hypoxemia due to underventilated aveoli?: They constrict. Opposite of skeletal muscle arteries that dilate when muscles lack O2.
What is hypoxia?: Inadequate O2 tension at the cellular level. Area of lung not well ventilated.
What is hypoxemia?: An abnormal deficiency in the [O2] in arterial blood.
What is the most important control of pulmonary vascular resistance?: Hypoxia
What is the consequence of chronic hypoxia?: Under ventilation -> continuous local arteriole constriction -> incrs in total pulm vascular resistance -> RV has to work harder to push blood thru lungs
How does hypoxia affect V/Q Ventilation/Perfusion ratio?: Hypoxia causes vasoconstriction in local area, maintaining good V/Q ratio
What is atelectasis?: Collapse of the alveoli in a lung segment
What are the 4 main categories of atelectasis?: 1. resorption
2. compression
3. contraction
4. diffuse microatelectasis
How does resorption atelectasis work?: Obstruction in airway -> no ventilation -> air in alveoli get absorbed.

Typical obstructions: mucus, mucopurulent plug, FB, tumor, enlarged lymph nodes (TB)
What happens in compression atelectasis?: Something pushes lung tissue out of normal place:

pleural effusion, tumor, emphysematous bullae, cardiomegaly, elevated diaphragm in patients (bedridden or w/ascites)
What causes contraction atelectasis?: Local or generalized fibrosis in lung or pleura.
What is another name for cicatrization atelectasis?: Contraction atelectasis
What is diffuse microatelectasis?: Generalized loss of lung expansion due to inadequate surfactant
What causes diffuse microatelectasis?: - O2 toxicity - breathing high % O2 too long - wears out surfactant

- neonatal or adult resp distress syndrome

- infection, which may cause adult resp distress syndrome
What is bronchiectasis?: Form of obstruct. disease. Pathologic expansion of bronchi and/or bronchioles resulting from chronic necrotizing infections caused by various consitions which destroy bronchial smooth muscle and elastic tissue. Not 1° disease, but 2° to infx or other condition.
What are signs/symptoms of bronchiectasis?: - Cough

- expectoration of copious purulent, sometime fetid sputum

- flecks of blood in sputum, if not frank hemoptysis
What are 4 conditions that dispose to bronchiectasis?: 1. bronchial obstruction - tumor, FB, mucus impaction

2. cystic fibrosis

3. HIV or other immunodeficiency states (immunoglobin deficiencies

4. pneumonia, bacterial, incompletely unresolved
How does bronchial obstruction lead to bronchiectasis?: Obstruction -> infx -> bronchiectasis local to affected lung segment.

Also complication of asthma and chronic bronchitis, recurrent infx.
What is CF, cystic fibrosis?: Inherited disorder of exocrine glands, esp resp and GI tracts.

Causes viscid mucus -> recurrent infx -> severe bronchiectasis.
What TRIAD of conditions does CF cause?: 1. COPD (bronchiectasis)
2. exocrine pancreatic insufficiency
3. high sweat chloride content BOARD
What are the 2 critical factors in pathogenesis of bronchiectasis?: 1. obstruction -> dcrsd NL clearance mech -> 2° infx

2. chronic or recurrent infx -> obstr secretion -> worse infx/inflam
What part of lungs does bronchiectasis most affect?: Lower lobes, vertical airways
How much to bronchiectasis affected airways expand?: 4 x normal diameter
What flora can be cultured from bronchiectasis?: MIXED flora: staph, strep, pneumococci, H. flu, Pseudomonas
Can bronchiectasis lead to lung abscesses?: Yes, it often leads to lung abcesses eventually.
What does CT scan show for bronchiectasis?: Dilated airways
What does CXR show for bronchiectasis?: Incrsd bronchovascular markings from 1) peribronchial fibrosis and 2) intrabronchial secretions
What do labs cause suspicion of CF?: - CXR abnormalities mostly apical or upper lobe

- sweat chloride test
What diseases/disorders cause finger clubbing?: bronchiectasis, smoking, lung CA, acute bacterial endocarditis
How does bronchiectasis lead to cor pulmonale?: Severe, widespread bronchiectasis -> obstrctv ventilatory defects -> hypercapnia/hypoxemia -> pul HTN -> cor pulmonale
What is treatment for bronchiectasis?: - antibiotics ABX to control infx

- beta 2 agonists to max ventilation in non-bronchiectatic airways

- O2 therapy
What is cor pulmonale?: Enlargement of heart's right ventricle caused by primary lung disease
What is COPD, chronic obstructive pulmonary disease?: Denotes 2 conditions:

1. emphysema
2. chronic bronchitis
Why do emphysema and chronic bronchitis often co-exist?: 80% of COPD due to
- tobacco smoke, irritant chemical -> chronic cough & mucus secretions, CHRONIC BRONCHITIS

AND

- destruct of acinar walls, perm enlargement of acinar airspaces, EMPHYSEMA
What is emphysema?: perm enlargement of airspaces distal to term bronchioles (acinus) due to inflam-induced destruction of the walls of
- resp bronchioles
- alveolar ducts
- alveoli
Is emphysema always symptomatic?: No. 1/2 time Asymptomatic
Is emphysema associated w/smoking.: Yes
What structures comprise an acinus?: - resp bronchioles
- alveolar ducts
- alveoli
How many acini comprise a lobule?: 3 or more acini = lobule
What are the 3 histological types of emphysema?: 1. centriacinar

2. panacina

3. distal acinar
Describe centriacinar emphysema.: - enlarged bronchioles
- distal alveoli spared
- more common at lung apex
- due to smoking
Describe panacinar emphysema.: - entire acinus enlarged
- more common at lung base
- due to genetic alpha-1 antitypsinase deficiency
- rare
Describe distal acinar emphysema.: - far periph acini, close to lung pleura, are enlarged
What is thought to cause spontaneous pneumothorax in young, tall, thin adult smokers?: Distal acinar emphysema
What is the mechanism for emphysema-induced pneumothorax?: Enlarged acini burst, release air, cause separation of visceral from parietal pleura - + gravity -> pneumothorax. In tall, thin person, little abdom fat pushing abdom viscera up agnst diaphragm/lungs -> more downward gravity traction on lung
Are histological divs of emphysema clinically important?: No. They all amount to deterioration of lung function as COPD.
What are signs/symptoms of emphysema?: - progressive dyspnea

- airway obstructn -> long exp phase; pursed lip breathing (Pink Puffer)

- airway obtructn -> chng in chest A/P ratio; dcrsd diaphragmatic excursion; dcrsd vesicular breath sounds; distant heart sounds

- loss of alveolar capillaries -> incrsd pul vasc resist -> right heart failure
What is diaphragmatic excursion?: How far the diaphragm moves
What are weight changes associated w/emphysema and chronic bronchitis?: emphysema - weight LOSS

chronic bronchitis - weight GAIN
In emphysema, what enzyme activity leads to acinar wall destruction?: excess lung protease and/or elastase activity, unopposed by anti-protease activity
In emphysema, how does acinar wall destruction lead to hyperinflation of lungs? AIRSPACE ENLARGEMENT: 1. acinar wall destruct ->
dcrsd surface area for gas exchg

loss of struct integrity of acinar walls ->
obstructive collapse on exhale ->
air trapping & CO2 retention ->
lung hyperinflation
In emphysema, how does acinar wall destruction lead to hyperinflation of lungs? LOSS of ALVEOLI: loss of alveoli ->
incrsd lung compliance & dcrsd lung recoil ->
hyperinflation of lungs
What disorder causes acinar wall destruction: - airspace enlargement &loss of alveoli leading to lung hyperinflation - loss of alveolar capillaries?: Emphysema
What do labs indicate for emphysema?: - dcrsd FEV1, nr NL slow FVC (FEV1/FVC ration < 75%)

- dcrsd FEF 25-75%

- incrsd arterial pCO2 (above 50 mmHg)
What is clinical course of emphysema?: - progressive dyspnea (1st exertion, later resting

- severe weight loss

- chronic hypoxemia -> constrct of pul arterioles -> pul HTN -> RV fail (Cor Pulmonale) NOT due to LV fail

- death from pul fail: hypoxemia, resp acidosis, coma
What are 4 treatments for emphysema?: 1. stop smoking

2. bronchodilators: anticholinergic and beta-2 agonist inhalers

3. inhaled steroids - more for concurrent episodic asthma, URI, etc.

4. O2 supplementation in severe COPD to achieve certain arterial pO2, but not too much, to MAINTAIN HYPOXIC DRIVE
What is hypoxic drive?: Stimulation of respiration by low PaO2, mediated thru carotid and aortic bodies
What conditions define chronic bronchitis?: - mucus-producing cough most days

- cough 3 mos/yr for 2 successive yrs w/o other underlying disease to explain cough -> "Blue Bloater"

- inflam - scarred lining of bronch tubes - excess mucus - thick bronchial tube lining - irritating cough - hampered air flow - scarred lungs - infx breeding place

- dyspnea
What are treatments for chronic bronchitis?: - stop smoking

- avoid air pollution

- inhaled bronchodilator
What are signs/symptoms of atelectasis?: - dyspnea, cyanosis
- tracheal deviation
- uneven chest expansion
- dcrsd breath sounds
- dullness to percussion (vs. pneumothorax causes hyperresonance or tympany)
What is prophylaxis for atelectasis?: - surgery

- encourage ventilation by incentive spirometry, coughing, early ambulation
What is pneumothorax?: Separation of the visceral and arietal pleurae by a volume of air. Affected lung segment collapses under surface tension-induced recoil of its collective alveoli.
What are the 4 major categories of pneumothorax?: 1° spontaneous PTX: absence of underlying lung disease

2° spontaneous PTX: complication of lung disease (emphysema, asthma)

traumatic PTX: blunt or penetrating trauma, iatrogenic causes

tension PTX: air inhaled in thorax, can't exit; positive interpleural press > ambient press; due to trauma, CPR, mech ventilation
What are the symptoms of essential of diagnosis?: Acute onset of ipsilateral chest pain & dyspnea
What are the objective finding of diagnosis?: - in mild cases, minimal
- severe:
unilateral chest expansion
trach & mediastinal shift toward opposite side
dcrsd breath sounds & fremitus
percussion hyperresonance or tympany
CXR shows visceral-pleural line or area w/marked absence of pul vasculature
Describe 1° PTX.: - often tall, thin boys, young men

- maybe due to rupture of subpleural apical blebs due to high neg pleural pressure

- smoking increases risk
What is a bleb?: An accumulation of fluid under the skin.
Describe 2° PTX.: - assoc w/other lung diseases, e.g., pneumonia, TB, CF, asthma, COPD

- catamenial PTX
What is catamenial PTX?: a 2° PTX associated w/onset of menses and with intrthoracic endometriosis
What is pulmonary barotrauma and what does it cause?: Important contemp cause of PTX in patient on mech ventilation.

Often seen in ARDS patients w/hi pos inspir press or PEEP
What is PEEP?: positive end-expiratory pressure
What are general signs/symptoms of PTX: - chest pain, min-to-severe, on affected side
- dyspnea
- possibly mild tachycardia
- if large, dcrsd breath sounds and fremitus; asymmetric chest expansion
- hyperresonance or tympany
What are more specific signs/symptoms of TENSION PTX?: - severe dyspnea & marked tachycardia

- trach or mediastinal shift (?chest trauma open to ambient air

- widespread percussion hyperresonance or tympany
What do labs show for PTX?: - ABG show hypoxemia (low pO2) & acute resp alkalosis from hyperventilation

- CXR:
- see visceral pleural line on expiratory film
- pleural effusion, i.e., blunting of costophrenic angle
- shift of trach TOWARD NL PTX
- shift of trach away from TENSION PTX
What is ddx, differential diagnosis, for PTX?: Given acute onset of dyspnea and/or chest pain:

- pneumonia
- AMI
- PE
What are possible complications of PTX?: - subcutaneous emphysema

- pneumomediastinum on CXR: suspect rupture of esophagus or bronchus as cause of PTX
What is pneumomediastinum?: Gas or air in mediastinal tissues.
What is the treatment for a small PTX?: - observe, may self resolve
- O2 supplement may incr rate of air reabsorption
- aspiration
- thoracostomy (chest tube), small bore
- serial CXR's q24 hr to follow progress
What is the treatment for a large PTX?: - admit to hospital
- thoracostomy until lung expands on serial CXR's
What is average recurrence rate of PTX? Recurrence rate for smokers?: 30% for average

50% for smokers
What is restrictive lung disease?: Characterized by dcrsd lung compliance -> incrsd inspiratory effort and smaller static and dynamic lung volumes
What are the 2 major categories of restrictive lung disease?: 1. extrapulmonary causes

2. parenchymal diseases
What are the extrapulmonary cause of rest lung disease?: - conditions that cause chest wall deformities, e.g., MD, kyphoscoliosis

- obesity hypoventilation syndrome, pickwickian
What is another name for parenchymal restrictive lung disease?: Interstitial lung disease.
What are the 5 subdivisions of parenchymal disease?: 1. primary pulmonary disease - idiopathic pulmonary fibrosis
2. systemic disease
3. environmental & occupational
4. infections
5. drug induced
What are systemic diseases that may cause restrictive lung disease?: - hyaline membrane disease (kids)
- ARDS adult resp distress syn
- sarcoidosis, amyloidosis
- autoimmune: rheumatoid, SLE, systemic sclerosis, dermato/polymyositis
- pulmonary edema & pulmonary venous hypertension
What is a "blue bloater"?: COPD patients suffering primarily from chronic bronchitis. Derived from bluish color of lips and skin
What are environmental and occupational causes of parenchymal disease (RLD)?: - pneumonconioses (non-neoplastic lung reactions to inhaled inorganic dusts, e.g., asbestos, silica

- organic dusts
- toxic gases
- ionizing radiation
What are infectious causes of parenchymal disease (RLD)?: Fungi

Pneumocystis carinii - most frequently seen in AIDS patients

Viruses
Parenchymal restrictive lung disease:: 1.injury
2. affects alveolar epith cells or alveolar cap endothelium
3. affects interstitium
4a. interstitial fibrosis -> more damage to alveoli, caps -> hypoxia -> pul HTN -> cor pulmonale = RVH & RVF due to lung disease which causes pul HTN - not pul HTN for LVF
4b. intersitial fluid -> stiff lung -> incrsd effort-dyspnea
Parenchymal restrictive lung disease: Idiopathic pulmonary fibrosis: Findings similar to RLD cause by other etiologies which must be ruled out first.

Unknown antigen -> injury to type 1 alveolar cells and activation of fibroblasts > fibrosis of alveolar septa and arteriolar intima
What is the clinical course of idiopathic pulmonary fibrosis (parenchymal RLD)?: - fibrosis & pul edema >
decrsd ventilation >
hypoxemia

- dcrsd vent and pul arteriolar fibrosis >
pul arteriolar vasoconstriction >
pul HTN >
cor pulmonale & death

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