W3 Symptom Wheezing (Review By Sunday For Quiz Monday) Flashcards

1
Q

Wheezing
Acute
Emergent

Polyphonic wheezing in Pediatric population attributed to?
Monophonic wheezing causes?

A

Acute
Asthma and Bronchiolitis
Emergent
Pneumothorax
Esophageal perforation
Forgien body
Pulmonary embolism
Anaphylaxis

Wheeze:
—high-pitched, musical, whistling lung sound.
—Can be localized or diffuse, caused by airway narrowing, located from the larynx to small bronchi of the lungs.
—Narrowing of airway can be caused by bronchoconstriction, mucosal edema, partial obstruction or
external compression, tenacious secretions, forgien body or tumor.

Polyphonic wheezing in Pediatric population attributed to?
—viral bronchioloitis
—asthma
Monophonic wheezing causes?
—tracheomalacia
—bronchomalacia
—foreign body aspiration
—anatomical compression of airways

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2
Q

Acute wheezing, asthma
3 symptoms
Obstructive but is _________?

A

Definition:
—A chronic disease that affects the airways, involving variable airway obstruction, hyperresponsiveness and inflammation. Airways become inflamed, narrow and swollen, impairing breathing.

Chronic Airway inflammation — Bronchial hyperreactivity —🔑Reversible airway obstruction

Wheezing
Cough
SOB

Relaxation and contraction of the smooth muscles of the bronchi and bronchioles can change the diameter of the air passageways and so change the volume of air moving through them

Cellular elements include
—mast cells, Basophils, eosinophils, neutrophils, and macrophages also are responsible for extensive mediator release in the early and late stages of bronchial asthma.
—Stretch and irritant receptors reside in the airways, as do cholinergic motor nerves, which innervate the smooth muscle and glandular units.

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3
Q

Asthma
T2 high and low
What does Th2 produce?
And what do they have?
Which do asthmatics have more of?

A

Patho not completely understood
—allergic reactions mediated by IgE antibodies
These people are said to be atopic

Background
—Two types of helper T cells. Th1 and Th2
—Th1 = promote cell-mediated immune response, produce IL-2 and TNF-Beta
—Th2 produce IgE antibodies by producing IL-4 and 13.
—They act on B cells to promote IgE antibodies.
—IgE release local mediators that cause sneezing, coughing, diarrhoea to expel microbes.

asthmatic have a higher ratio of Th2 to Th1

The pathophysiology of asthma is heterogeneous
—division into T2-high and T2-low endotypes

T2-high
—allergic asthma falls into the T2-high endotype, as do
late-onset T2-high asthma and aspirin/NSAID-associated respiratory disease.
—most common type
—usually begins in childhood and is associated with other
allergic diseases such as eczema, allergic rhinitis, or
food allergy.

T2-low
—T2-low asthma phenotypes include non allergic
asthma, which tends to occur in adults and be
marked by neutrophilic inflammation and variable
response to standard therapies

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4
Q

Asthma
Etiologies — 5

A

● Asthma with persistent airflow limitation
—due to airway remodeling
● Asthma with obesity
—prominent respiratory symptoms in obese patients with little airway inflammation.
● Occupational asthma
—triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization
● Catamenial asthma
—affects women at predictable times during the menstrual cycle.
● Exercise-induced bronchoconstriction
—during exercise or within 3 minutes after its end, peaks
within 10–15 minutes, and then resolves by 60 minutes. Thought to be a consequence of the airways’ warming and humidifying an increased volume of expired air during exercise

see image for all the possible causes

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5
Q

Asthma
Symptoms — 3 big ones! ⭐️
Presentation
PE findings:
Nose, skin, percussion, auscultation

A

⭐️wheezing, shortness of breath, chest tightness, and cough. ⭐️
● Symptoms vary over time and in intensity and are often worse at night or in the early morning.
● Asthma symptoms may occur spontaneously or be precipitated or exacerbated by many different triggers, as discussed above

Physical Exam
Nasal mucosal swelling, increased secretions, and polyps are often seen in patients with allergic asthma.
Eczema, atopic dermatitis, or other allergic skin disorders may also be present.
● Chest examination may be normal between exacerbations in patients with mild asthma
hyperressonance to lung percussion
● severe asthma exacerbations, airflow may be too limited to produce wheezing, and the only diagnostic clue on auscultation may be globally reduced breath sounds with prolonged expiration.
difficulty breathing
cannot finish a sentence
● Hunched shoulders and use of accessory musclesof respiration suggest an increased work of breathing.

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6
Q

Asthma
Diagnostics — 3
What would you see on ABG
What is PEF and when is it used?
What is bronchoprovocation testing? What result is specific for asthma

A

Arterial blood gas (ABG) measurements
—may be normal during a mild asthma exacerbation, but respiratory alkalosis can be present.
—During severe exacerbations, hypoxemia develops and the PaCO2 returns to normal.
—The combination of an increased PCO2 and respiratory acidosis may indicate impending respiratory failure and the need for mechanical ventilation

Peak expiratory flow (PEF)
—is measured during a maximally forceful and rapid exhalation that immediately follows a maximal inhalation.
—An advantage is that small, portable devices can be used.
—PEF measurements are most often used to monitor patients with a known diagnosis of asthma or to assess the role of a particular occupational exposure or trigger, rather than as a tool for the primary diagnosis of asthma

Bronchoprovocation testing
if PFT results are normal and you suspect exercise or allergen induced asthma, this is the next step
inhaled histamine or methacholine
—A positive methacholine test is defined as a fall in the FEV1 of 20% or more at exposure to a methacholine concentration of less than or equal to 8 mg/mL.
—negative methacholine test has a negative predictive value for asthma of 95%.
—Exercise challenge testing may be useful in patients with symptoms of exercise-induced bronchospasm.

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7
Q

Asthma
PFT

A

Spirometry (forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and FEV1/FVC) before and after the administration of a short-acting bronchodilator. These
measurements help determine the presence and extent of airflow obstruction and whether it is immediately reversible.

Airflow obstruction is indicated by a reduced FEV1/FVC ratio, generally below 0.7.

Significant reversibility of airflow obstruction is defined by an increase of 12% or more and 200 mL in FEV1 or FVC after inhaling a short-acting bronchodilator.

A positive bronchodilator response strongly supports the diagnosis of asthma but a lack of responsiveness in the pulmonary function laboratory does not preclude success in a clinical trial of bronchodilator therapy. Severe airflow obstruction results in significant air trapping, with an
increase in residual volume and consequent reduction in FVC, resulting in a pattern that may mimic a restrictive ventilatory defect.

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8
Q

Asthma
Spirometry — which pattern, what will asthma show?

A

Both asthma and COPD will give an obstructive pattern , but asthma will show reversibility.

Reversibility means that the FEV1 (forced expiratory volume in 1 second) and FVC (forced vital capacity) will increase by at
least 12-15% after bronchodilator treatment

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9
Q

Asthma
Control — how to assess

A

Asthma symptoms are assessed by asking patients about their past 4 weeks including frequency of symptoms (days per week)

awakening from sleep

frequency of short-acting beta-agonist (SABA) reliever use for relief of symptom

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10
Q

Asthma — classifications
Intermittent
Mild

A

Intermittent Asthma
●Daytime asthma symptoms occurring two or fewer days per week
Two or fewer nocturnal awakenings per month
●Use of short-acting beta agonists (SABAs) to relieve symptoms two or fewer days per week
●No interference with normal activities between exacerbations
●FEV1 measurements between exacerbations that are consistently within the normal range (ie, ≥80 percent of predicted)
●FEV1/FVC ratio between exacerbations that is normal (based on age-adjusted values)
●One or no exacerbations requiring oral glucocorticoids per year

Mild persistent
●Symptoms more than twice weekly (although less than
daily)
●Approximately three to four nocturnal awakenings per
month due to asthma (but fewer than every week)
●Use of SABAs to relieve symptoms more than two days out of the week (but not daily)
●Minor interference with normal activities
●FEV1 measurements within normal range (≥80 percent
of predicted

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11
Q

Asthma — classifications
Moderate persistent
Severe persistent

A

Moderate persistent
●Daily symptoms of asthma
●Nocturnal awakenings as often as once per week
●Daily need for SABAs for symptom relief
●Some limitation in normal activity
●FEV1 ≥60 and <80 percent of predicted and FEV1/FVC below normal

Severe persistent
● asthma symptoms throughout the day
● nocturnal awakening due to asthma nightly
● reliever medication needed for symptoms several times/day
● activity limitation due to asthma

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12
Q

Asthma
4 steps
Intermittent
Mild persistent
Moderate persistent
Severe persistent

A

Step 1 for intermittent asthma is as follows:
● Controller medication not indicated
● Reliever medication is a short-acting beta-agonist (SABA) as needed for symptoms-Albuterol

Step 2 for mild persistent asthma is as follows:
● Preferred controller medication is a low-dose inhaled corticosteroid
● Alternatives include cromolyn, leukotriene receptor antagonist (LTRA), or theophylline

Step 3 for moderate persistent asthma is as follows:
● Preferred controller medication is either a low-dose inhaled corticosteroid (ICS) plus a long-acting beta-agonist (LABA) (combination medication is the preferred choice to improve compliance) or an inhaled medium-dose corticosteroid
● Alternatives include a low-dose ICS plus either an LTRA or theophylline

Step 4 for moderate-to-severe persistent asthma is as follows:
● Preferred controller medication is an inhaled medium-dose corticosteroid plus a LABA (combination therapy)
● Alternatives include an inhaled medium-dose corticosteroid plus either an LTRA or theophylline

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13
Q

Asthma
LT controller
Reliever meds
Add on therapies

A

long-term controller medications
→used long-term to reduce airway inflammation, symptoms, and risk of future exacerbations
—Inhaled corticosteroids are essential controller medications

reliever medications
→used on an as-needed basis to relieve breakthrough symptoms
—Beta-agonists are divided into SABAs and LABAs. SABAs, including agents such as albuterol, levalbuterol, bitolterol, pirbuterol, and terbutaline, are mainstays of reliever or rescue therapy for asthma patients.

••add-on therapies for severe asthma**.

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14
Q

Asthma
What are the goals of therapy 7

A
  1. Reduction in symptom frequency to ≤2 times/week
  2. Reduction of nighttime awakenings to ≤2 times/month
  3. Reduction of reliever use to ≤2 times a week (except before exercise)
  4. No more than 1 exacerbation/year
  5. Optimization of lung function
  6. Maintenance of normal daily activities
  7. Satisfaction with asthma care with minimal or no side effects of treatment
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15
Q

Asthma
SABA
LABA

A

Short-Acting β2-Agonists-SABA
—Albuterol (also known as salbutamol) is the most commonly used agent.
—Bronchodilation begins within 3–5 min of inhalation, and effects generally last 4–6 h.
—It is most commonly administered by metered-dose inhaler. Solutions for nebulization are also used, especially for relief of bronchospasm in children.
—Oral forms are available but are not commonly used.

Long-Acting β2-Agonists-LABA
—Salmeterol and formoterol are the two available LABAs.
—They have an ~12-h duration of action.
—Formoterol has a quick onset comparable to the short-acting β2-agonists.
—Salmeterol has a slower onset of action.
—These agents can be used for prophylaxis of exercise-induced bronchospasm.
—In contrast to their use in chronic obstructive pulmonary disease (COPD), these agents are not recommended for use as monotherapy in the treatment of asthma.

For asthma LABA always in combination with an ICS.

Ultra-Long-Acting β2-Agonists
—These agents (indacaterol, olodaterol, and vilanterol) have a 24-h effect. They are only used in combination with ICSs in the treatment of asthma.

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16
Q

Asthma
Corticosteroids, are the “______” of asthma therapy
They reduce?
Which combo med?
Use how often?

A

Cornerstone of asthma therapy
—Corticosteroids are particularly effective in reducing type 2 inflammation and airway hyperresponsiveness.
—Corticosteroids also, improve airway function, prevent exacerbations, and improve symptoms.
Corticosteroid use by inhalation (ICSs) minimizes systemic toxicity and represents a cornerstone of asthma treatment.

ICS and ICS/LABA (LABA-Salmeterol and formoterol)
ICSs are the cornerstone of asthma therapy and associated with decreased asthma mortality.
Combo from pharm: Budesonide (ICS) + formoterol (LABA) = symbicort

USE:twice a day as first-line therapy for all forms of persistent asthma.
—For increased Asthma severity doses can be increased and combined with LABA.
Combining them with LABAs permits effective control at lower ICS dose.
—Their effects can be noticeable in several days, but continued improvement may occur over months of therapy
—Not all patients respond to ICS.
—Evidence suggests that the most responsive patients are those with significant type 2–mediated asthma

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17
Q

Asthma
Anticholinergics
Theophylline

A

Anticholinergics
Cholinergic nerve–induced smooth-muscle constriction plays a role in asthmatic bronchospasm. Anticholinergic medications can produce smooth-muscle relaxation by
antagonizing this mechanism of airway narrowing.

The long-acting agents in this class are known as long-acting muscarinic antagonists (LAMAs).

Theophylline
—Theophylline, an oral compound that increases cyclic AMP levels by inhibiting phosphodiesterase, is now rarely used for asthma due to its narrow therapeutic window, drug-drug interactions, and reduced bronchodilation as compared to other agents.

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18
Q

Asthma
Leukotrienes modifiers — used when?
CystLT1 Antagonists — med name? used in which population, why?
5-lioxygenase inhibition

A

Agents that inhibit production of leukotrienes (zileuton, an inhibitor of 5-lipoxygenase) or the action of leukotrienes at the CysLT1 receptor (montelukast and zafirlukast) are moderately effective in asthma.

—improve airway function and reduce exacerbations but not to the same degree as bronchodilators or ICS, respectively.
—also effective in reducing symptoms of allergic rhinitis, can be used in patients with concomitant allergic rhinitis.
Montelukast, in particular, is frequently used in children with mild asthma due to concerns of ICS-related growth suppression.
—Leukotriene modifiers are effective in preventing exercise-induced bronchoconstriction without the tachyphylactic effects that occur with regular use of LABAs. effective in aspirin-exacerbated respiratory disease, which is characterized by significant leukotriene overproduction.
—They have also shown modest effect as add-on therapy in patients poorly controlled on high-dose ICS/LABA.

CysLT1 Antagonists
—**Montelukast and ** are administered orally once or twice daily, respectively. The onset of effect is rapid (hours), with the majority of chronic effectiveness seen within 1 month.

5-Lipoxygenase Inhibition
—Zileuton in its extended form is administered orally twice a day

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19
Q

Asthma Cromolyn sodium — helpful in which case? And which populations?
Anti-IgE — med name?

A

Cromolyn Sodium:
—Cromolyn sodium is an inhaled agent believed to stabilize mast cells.
—It is only available by nebulization and
must be administered two to four times a day.
—Mildly to moderately effective and appears to be helpful for exercise-induced bronchospasm.
—It is used primarily in pediatrics in those concerned about ICS side effects.

Anti-IgE
Omalizumab, a monoclonal antibody.
—Anti-IgE has been shown to increase interferon production in rhinovirus infections, decrease viral-induced asthma exacerbations, and reduce duration and peak viral
shedding.
—This effect is believed to be due to IgE’s ability to reduce interferon γ production in response to viral infections.
—It is generally used in patients not responsive to moderate- to high-dose ICS/LABA.
—It reduces exacerbations by 25–50% and can reduce asthma symptoms but has minimal effect on lung function.
Most effects are generally seen in 3–6 months

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20
Q

Asthma
IL-5 active drugs
Anti IL-4/13

A

IL-5–Active Drugs
Mepolizumab and reslizumab are monoclonal antibodies that bind to IL-5, and benralizumab binds to
the IL-5 receptor.
—They rapidly (within a day) reduce circulating eosinophils.
—For use In patients symptomatic on moderate- to high-dose ICS/LABA, generally with two or more exacerbations that require OCS per year and with an eosinophil count of ≥300/μL
—IL-5–active drugs reduce exacerbations by about half or more. Most clinical effects are usually seen within 3–6 months.

Anti–IL-4/13
—The IL-4 and IL-13 receptors are heterodimers that share a common subunit, IL-4 receptor α.
Dupilumabbinds to this subunit and, thus, blocks signaling through both receptors.Effective in patients that respond to anti-IL-5 therapies and poorly controlled on moderate- to high-dose ICS/LABA
—Dupilumab reduces exacerbations by ≥50%, decreases symptoms, and may produce more of an effect on FEV1 than anti–IL-5 drugs.
—It gradually reduces FeNO and IgE levels.
—Most effects are seen by 3–6 months of therapy

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21
Q

Acute wheeze — bronchioloitis
What is it?
What are the 6 groups?

A

—Bronchiolitis is an inflammatory processes that affect the
bronchioles.
—Bronchiolitis; affects the small airways <2mm in diameter.
—Associated disorders: post-infectious, Inhalation injury, organ transplant, connective tissue diseases, hypersensitivity pneumonitis.
—Divided into groups based on etiology: acute, constrictive, proliferative, COP, follicular and respiratory < most common
—Histopathological findings may be identical in different clinical syndromes.

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22
Q

Wheezing
Acute bronchiolitis
Seen in which population?
Causes/pathogen?
How long does it last?
Treatment?

A

—Seen after viral infections, more common in children (esp. neonates) <2 years old

Common viral causes
—RSV, rhinovirus,parainfluenza, coronavirus and adenovirus.

Path:
—Involves Neutrophilic and mononuclear infiltration.
—absence of fibroblast proliferation or collagen deposit).

S/S:
—Wheezing, abdominal breathing, apnea, grunting, high or low respiratory rate
—signs of respiratory distress: abdominal breathing, accessory muscle use, intercostal and subcostal recessions
—stridor > croup

Course
—coryza symptoms, 3-4 days worse
—lasts 7-10 days
—normal 2-3 weeks

Supportive Care
—Administer supplemental humidified oxygen, if necessary, to maintain a transcutaneous oxygen saturation higher than 90%.

Parenteral therapy
—May be necessary in those patients who are unable to take fluids by mouth or who have a respiratory rate higher than 70 breaths/min.
—Patients with apneic episodes should have access to IV hydration.
—Infants with bronchiolitis and recurrent apnea or increased work of breathing with respiratory failure occasionally require mechanical ventilation: high flow nasal cannula / CPAP > intubation and ventilation

23
Q

Wheezing
Constrictive bronchiolitis

AKA obliterative bronchiolitis or bronchiolitis obliterans or popcorn lung
Occurs with? 2
What is the pathological course?
S/S
PFT
CT
Tx?

A

Commonly occurs following
inhalation injury, ex. Vaping, Ammonia, welding fumes, heavy metals.
—Can also occur with Rheumatoid arthritis, medication reactions, ex busulfan, PCN (penicillamine and gold), chronic rejection post transplant.
—chronic patchy inflammation, concentric submucosal and peribronchiolar fibrosis and smooth muscle hypertrophy —> luminal obstruction (obliterans)
S/S : dry cough, wheezing, fatigue, progressive deteriorating clinical course
PFT/spirometry : airflow obstruction and trapping
CXR unremarkable
CT Scan air flow trapping and obstruction
TX corticosteroids or immunosuppressive agents

Progressive clinical course

24
Q

Wheezing
Proliferative Bronchiolitis:
What are the lipid-laden macrophages called?
What’s on CXR? 3
Tx?

A

Proliferative Bronchiolitis:
—Infection, Aspiration, Acute respiratory syndrome (ARDS),Hypersensitivity pneumonitis, connective tissue disorders, organ transplant.

Patho:
—organizing intraluminal exudate, made up of fibroblasts, lipid laden macrophages-”foamy, and cells obstructing the lumen.

Abnormal Chest X ray and CT Scan
—may show patchy consolidation “foamy cells!”
—ground-glass opacities
—peripheral nodular appearance

Treatment:
—Corticosteroids

25
Q

[SKILLS OSCE]
What is this?
What do you see?
How do you treat?

A

Chest X-Ray ARDS- after
tiger snake bite
Proliferative bronchiolitis
—lipid-laden macrophages = foamy
—patchy consolidation
—ground glass opacities
TZ: corticosteroids

26
Q

Wheezing

Cryptogenic organizing pneumonitis (COP)

Affects?

S/S:

Physical exam:
PFT:
Chest X Ray:
CT Chest:

**Treatment:

A

Proliferative pattern occurring when organizing intraluminal exudate extends through bronchiole into the alveolar space, with prominent intraluminal buds of fibroblasts embedded in immature collagen. Masson bodies (buds of loose connective tissue), and inflammatory cells fill alveoli and distal bronchioles.

—Affects men and women equally, betweens the ages 50-70
—Onset is sudden→weeks to months following a flu-like illness.

S/S:
—Dyspnea
—Dry cough
—may also have fatigue, fever and weight loss.

Physical exam: Crackles, Wheezing (⅓ patients)
PFT: restrictive ventilatory defect
Chest X Ray: interstitial and parenchymal disease with discrete, peripheral alveolar and ground-glass infiltrates. Nodular opacities are also commonly seen.
CT Chest: showing subpleural consolidation and bronchial wall thickening and dilation.

Treatment: Corticosteroids and cyclophosphamide

27
Q

[SKILLS OSCE]
What is this?

A

Cryptogenic organizing pneumonitis (COP) = interstitial and parenchymal disease

—discrete, peripheral alveolar and ground-glass infiltrates.
—Nodular opacities are also commonly seen

28
Q

Wheezing
Follicular bronchitis
Common with?
Patho?
CT shows?
Tx?

A

—common with connective tissue disorders, Rheumatoid arthritis and Sjogren syndrome or immunocompromised/HIV or AIDS patients.

Patho: chronic peribronchial inflammation and hyperplastic lymphoid follicles with reactive germinal centers arising from bronchus-associated lymphoid tissue (BALT)

—CT scan may show centrilobular and peribronchial nodules.

TX: steroids, immunosuppressants, sometimes macrolide abx

29
Q

Wheezing
Respiratory bronchiolitis

A

Respiratory Bronchiolitis
Affects small airways in smokers
—Most common cause of bronchiolitis in adults
—Typically no clinical symptoms or evidence of lung impairment
—Accumulation of pigments alveolar macrophages within respiratory bronchioles, associated with mild interstitial fibrosis and chronic inflammation
—Occasionally; patients with respiratory bronchiolitis causes diffuse parenchymal infiltrates→ referred to as Respiratory-Bronchiolitis- associated interstitial lung
disease(RB-ILD).
—Included in the spectrum of the smoking-related interstitial lung diseases

30
Q

Wheezing

Diffuse panbronchiolitis
Which country origin?
M/F?
Treatment?

A

Idiopathic disorder
Patho:
—Peribronchiolar mixed inflammatory cell infiltrates and accumulation of lipid laden macrophages within the
interstitium and alveolar spaces.
- Most frequently diagnosed in Japan.
- Men are more likely to be affected
- ⅓ are smokers
- Most patients have a history of chronic pansinusitis
- Dyspnea, cough, and sputum production
- Crackles and rhonchi present on chest exam
- PFTs= obstructive abnormalities
- CXR= pattern of diffuse, small,nodular shadows and hyperinflation

Treatment: Azithromycin

31
Q

Wheezing
What are the emergent situations? 5

A

-Pneumothorax
-Esophageal perforation
-Foreign body
-Pulmonary embolism
-Anaphylaxis

32
Q

Wheezing — Emergent: Pneumothorax

A

Pneumothorax:
presence of air or gas in the pleural cavity (ie, the potential
space between the visceral and parietal pleura of the lung)“Collapsed Lung”

—Pneumothorax can impair oxygenation and/or ventilation.
If the pneumothorax is significant, it can cause a shift of the mediastinum and compromise hemodynamic stability = Tension Pneumothorax
—Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura
—Until the late 1800s, tuberculosis was a primary cause of pneumothorax development.

Types
● Primary and secondary spontaneous pneumothorax
● Iatrogenic and traumatic pneumothorax
● Tension Pneumothorax
● Pneumomediastinum

33
Q

Wheezing — Emergent: Pneumothorax
Primary spontaneous
Patient demographic?
What symptoms if any?
Treatment if small?

A

—occurs in people without underlying lung disease and in the absence of trauma or event.
Typical ages 18-40 years, peak incidence age ~20, Rare over age 40
tall, thin, and, often, are smokers
● More common in males with a 6:1 ratio

S/S:
Primary pneumothorax- may not have symptoms, in bleb rupture
● Spontaneous pneumothorax:
—No clinical signs or symptoms in primary spontaneous pneumothorax until a bleb ruptures and causes pneumothorax; typically, the result is acute onset of chest pain and shortness of breath, particularly with secondary spontaneous pneumothorax
● Spontaneous and iatrogenic pneumothorax: Tachycardia most common finding; tachypnea and hypoxia may be present

Work-up:
ABG, Chest X Ray, CT Scan, Chest Ultrasound

Treatment:
Monitoring, usually with supplemental Oxygen

34
Q

Wheezing — Emergent: Pneumothorax
Secondary spontaneous
Most common cause?

A

Secondary spontaneous pneumothorax (SSP) occurs in people with a wide variety of parenchymal lung diseases.
● frequently in patients aged 60-65 years
● male-to-female ratio of age-adjusted rates is 3.2:1
(COPD) is a common cause of secondary spontaneous pneumothorax that carries an incidence of 26 cases per 100,000 persons.

35
Q

Wheezing — Emergent: Pneumothorax

Iatrogenic — most common sign?
and traumatic pneumothorax

A

Iatrogenic pneumothorax:
—Tachycardia most common finding; tachypnea and hypoxia may be present
—air introduced into the pleural space secondary to diagnostic or therapeutic medical intervention.

Traumatic
—Penetration of blunt force trauma
—Management steps for traumatic pneumothoraces are similar to those for other, nontraumatic causes. If hemodynamic or respiratory status is compromised or an
open (communicating to the atmosphere) and/or hemothorax are also present, tube thoracostomy is performed to evacuate air and allow re-expansion of the lung.

36
Q

Wheezing — Emergent: Pneumothorax
Tension pneumonthorax
What should you never do if you suspect a tension pneumothorax??

A

🆘 EMERGENCY→air can get in the pleural space, but cannot get out!
S/S:
—Hypotension, hypoxia, chest pain, dyspnea

Other findings:
—tachycardia; ipsilateral air entry on auscultation; breath sounds absent on affected hemithorax; trachea may deviate from affected side; thorax may be hyperresonant; jugular venous distention and/or abdominal distention may be present ipsilateral lung: hyperresonance, absent breath sounds, decreased vocal fremitus, and diminished chest wall
expansion

‼️Tx: IMMEDIATELY TREAT WITH DECOMPRESSION WITH OR WITHOUT RADIOGRAPHIC CONFIRMATION!!! DO NOT GET CHEST X RAY IF CLINICAL SUSPICION FOR TENSION PNEUMOTHORAX ‼️

37
Q

Wheezing — Emergent: Pneumothorax
Pneumomediastinum
predisposing factors? Gender/age?

A

Spontaneous pneumomediastinum
—occurs in healthy patients, with no preceding cause, however, there are predisposing factors including tobacco use or recreational drug use.
—More common in age group 20-40, slightly more common in males

S/S
—severe chest pain, labored breathing, voice distortion and subcutaneous emphysema of chest, neck and face.

DX
—Chest X Ray, CT Chest

TX
—observation, pain control, supplemental oxygen, manage reversible causes.
—If perforation of trachea or esophagus ->bronchoscopy/endoscopy→surgical intervention

See picture for causes

38
Q

[SKILLS OSCE]
What is this?

A

Pneumothorax-Pneumomediastinum

39
Q

Pneumonthorax — DDX

A

Myocardial Infarction
Pneumonia
PE
URI
Rib Fracture
Pericarditis
Mesothelioma

40
Q

Wheezing- Emergent: Esophageal perforation
Etiologies
S/S
DX
TX
Associated with?

A

pneumomediastinum = complication

41
Q

Wheezing- Emergent: Forgein Body

A
42
Q

Wheezing- Emergent: Pulmonary Embolism
Acute
Subacute
Chronic
Pathology
Risk factors
See page 49 in notebook

A
43
Q

Wheezing- Emergent: Pulmonary Embolism
S/S

A
44
Q

Wheezing- Emergent: Pulmonary Embolism- Diagnosis
What are the PE rule out criteria ? PERC
What is the Wells criteria to assess a PE?
What other diagnostic tests can you do?

A
45
Q

Wheezing- Emergent: Pulmonary Embolism-Diagnosis
Which test is gold standard?
Which is used in catheter directed?
What test if contrast is contraindicated in a patient?

A
46
Q

Wheezing- Emergent: Pulmonary Embolism-Treatment
What is mainstay?
How do you determine hemodynamically stable/unstable?

A
47
Q

Wheezing- Emergent: Pulmonary Embolism-Treatment
High risk or massive PE?
Tx for patients contraindicated for anticoagulation

A
48
Q

Wheezing - emergent: Anaphylaxis

A

Immunologic — IgE
Non-immunologic — exercise/cold for example

49
Q

Wheezing- Emergent: Anaphylaxis
S/S
Treatment

A

Only after EPI administration can these adjunct medications be considered:
—histamine H1 and H2 antagonists (diphenhydramine)
—corticosteroids
—beta2 agonists
—glucagon

monitor patient for biphasic reaction: recurrence of analphylaxis for 4-12hr

—develop emergency plan
—refer to allergist
—patient education on allergen avoidance
—appropriate use of epi-pen

50
Q

Asthma
What is Samter’s triad?
What is the atrophic triad?

A

Samter’s
—asthma
—nasal polyps
—ASA/NSAID sensitivity

atrophic
—asthma
—atrophic dermatitis (eczema)
—allergic rhinitis
genetic predisposition to certain allergens

51
Q

Asthma vs COPD

A

Asthma
—normal DLCO, lung volume and elastic recoil
—reversible!

COPD
—abnormal DLCO, hyperinflation and decreased elastic recoil

52
Q

[SKILLS OSCE]
What is this?

A

Constrictive bronchioloitis

53
Q

[SKILLS OSCE]
Wheezing — emergent
PE Westermark sign

A
54
Q

How is anaphylaxis distinguished from mild or moderate allergic reaction?

A