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Clinical Medicine 2 > Lecture 3/4 (Pulm)-Exam 2 > Flashcards

Lecture 3/4 (Pulm)-Exam 2 Flashcards

1
Q

Approach to patients with pulmonary disorders: PHYSICAL EXAM

Observation/Inspection
* What is the normal rate and rhythm?
* What is the normal depth of breathing or tidal volume?
* What is the relative amount of time spent in inspiration and expiration?

A

rate and rhythm
* Normal 12-20 breaths per minute

depth of breathing or tidal volume
* 5ml/kg

relative amount of time spent in inspiration and expiration
* Ratio of 2:3 is normal

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2
Q

Physical Exam

  • What does the use of acessory muscles?
  • What are the different causes asymmetric chest expansion? (4)
A

use of accessory muscles
* Sign of significant pulmonary impairment
symmetric chest expansion
* Unilateral volume loss: atelectasis or pleural effusion
* Unilateral airway obstruction
* Asymmetric pulmonary or pleural fibrosis
* Splinting from chest pain.

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3
Q

Physical Exam

Palpation:
* Why do you palpate the trachea?
* Why do you palpate the posterior chest wall
* What does condsoliation cause?
* What does effusion cause?

A
  • trachea at the suprasternal notch, to detect shifts in the mediastinum
  • posterior chest wall, to gauge fremitus and the transmission through the lungs of vibrations of spoken words
  • Consolidation – increased tactile fremitus ⭐️
  • Effusion – decreased tactile fremitus ⭐️
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4
Q

Percussion
* What does dull and hyperresonant areas mean? ⭐️

A
  • Dull areas that correspond to lung consolidation or pleural effusion
  • Hyperresonant areas suggesting emphysema or pneumothorax
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5
Q

Physical Exam

Auscultation
* Normal breath sounds on periphery of lungs are what?

A

Normal breath sounds on periphery of lungs are vesicular
* gentle, rustling quality heard throughout inspiration that fades during expiration

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6
Q

Normal breath sounds over the suprasternal notch are called what?
* What is normal and abnormal?

A

tracheal or bronchial lung sounds
* louder, higher-pitched, and have a hollow quality that tends to be louder on expiration
* Bronchial breath sounds heard over periphery are abnormal and imply consolidation

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7
Q

What is predictive finding of significant airflow obstruction?

A

Globally diminished lung sounds are an important finding predictive of significant airflow obstruction

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8
Q
  • What is adventitious?
  • What are continuous lung sounds divided into what?
  • What are discontinuous are called what?
A
  • Adventitious = Unexpected or abnormal sounds
  • Continuous lung sounds are divided into wheezes and rhonchi
  • Discontinuous lung sounds are called crackles
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9
Q

Wheezes
* Manifestation of what?
* Wheezes occur in the setting of what? ⭐️ ⭐️ ⭐️

A
  • Manifestation of airway obstruction
  • Wheezes occur in the setting of bronchospasm, mucosal edema, or excessive secretions. In each case, the airway is narrowed to the point where adjacent airway walls flutter as airflow is limited
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10
Q

Rhonchi
* Rhonchi originate where? ⭐️
* Acute setting, manifestation of what?

A
  • Rhonchi originate in the larger airways when excessive secretions, obstruction of medium-sized airways, most often with secretions
  • Acute setting, manifestation of viral or bacterial bronchitis
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11
Q

Crackles (Rales)
* Commonly sign of what?
* Crackles in pulmonary edema are generally more prominent where? ⭐️
* What are other diseases that can result in crackles

A
  • Commonly sign of alveolar disease including pulmonary edema and pneumonia
  • Crackles in pulmonary edema are generally more prominent at the bases
  • Diseases that result in fibrosis of the interstitial (IPF) can result in crackles as well
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12
Q

What is egophony used to distinguish between? Explain⭐️ ⭐️ ⭐️

A

To distinguish between crackles associated with alveolar fluid and those of interstitial fibrosis
* Auscultation of the sound “Ah” instead of “EEE” when a patient phonates “EEE”
* Change in note is due to abnormal sound transmission through consolidated parenchyma and is present in pneumonia but not IPF

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13
Q

Lack or diminution of breath sounds can help determine etiology
* What does emphysema sound like?
* What does pneumothorax sound like?

A
  • Emphysema often have a quiet chest with diffusely decreased breath sounds
  • Pneumothorax or pleural effusion may present with an area of absent breath sounds
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14
Q

What is restrictive lung disease?

A

a decrease in the total volume of air that the lungs are able to hold, is often due to a decrease in the elasticity of the lungs themselves or caused by a problem related to the expansion of the chest wall during inhalation

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15
Q

What are the subcategories of obstructive (4) and restrictive (4) lung disease?

A
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16
Q

What are the two categories of restrictive lung disease?

A
  • Extrinsic or Extrapulmonary (occur outside the lung)
  • Intrinsic or Intrapulmonary (Interstitial) (occur within the lung itself)
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17
Q

Extrinsic or Extrapulmonary (occur outside
the lung)
* What does it include and why?
* Cause restrictive disease by what?

A
  • Includes Obesity, Kyphoscoliosis, neurodegenerative d/o ->weak chest wall/effort
  • Cause restrictive disease by externally impairing filling of the lung
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18
Q

Intrinsic or Intrapulmonary (Interstitial)(occur within the lung itself)
* What is acute and chronic?

A
  • Acute: Usually refers to acute respiratory distress syndrome (ARDS)
  • Chronic: Usually referred to as interstitial lung disease (ILD)
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19
Q

Intrapulmonary Restrictive Lung Disease
* What is the mechanism behind this?
* What does this cause to total lung volume? ⭐️ ⭐️⭐️⭐️

A
  • Healthy lung tissue is replaced by collagen fibers, process called fibrosis
  • Lung tissue is damaged, becomes stiff and can’t fill with as much air
  • Reduces/decreases the total lung volume
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20
Q

Interstitial Restrictive Lung Disease Classification
* Divided into what?
* What varys?
* What are the MC identifiable causes of ILD?

A
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21
Q

Interstitial Lung Disease (ILD):
* What is it? What is it characterized by?
* What is most common?

A
  • Chronic, nonmalignant, noninfectious intrapulmonary diseases of lower respiratory tract
  • Characterized by inflammation & derangement of alveolar walls leading to fibrosis
  • Most common – Idiopathic Pulmonary Fibrosis
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22
Q

Explain how interstitial lung disease is characterized by inflammation & derangement of alveolar walls leading to fibrosis?

A
  • Pathologic processes involves the ongoing repair process creating excess collagen, or scar tissue in the interstitial tissue of the lung
  • Leads to thickened interstitial layer, causing problems with ventilation, lungs stiff and hard for air to flow in and out
  • Leads to progressive loss of lung tissue
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23
Q

What are the different causes of ILD? (8)

A
  • Occupational or environmental inhalants; dusts; gases; fumes
  • Drugs (cytotoxic agents, amiodarone, nitrofurantoin, gold)
  • Radiation (CXR or cancer)
  • Infection (viral, bacterial, fungal, parasites)
  • Sarcoidosis
  • Pulmonary hemorrhage syndromes (Goodpasture’s, idiopathic hemosiderosis)
  • Idiopathic pulmonary fibrosis (IPF) – no cause
    * Bronchiolitis obliterans organizing pneumonia (BOOP) & Acute Interstitial Pneumonia (AIP)

only mentioned the bolded one

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24
Q

Explain the pathophysio of parenchymal lung disease?

A
  1. Injury from a specific exposure
    Asbestos, Amiodarone, Moldy hay, Auto-immune-mediated disorder (RA) or unknown (IPF)
  2. Immunopathologic response of lung to irritants causes an initial inflammation that heals by scar tissue formation
    -Lung responds by imperfect repairing with increased interstitial tissue replacing normal capillaries, alveoli, & healthy interstitium
  3. Extensive disruption of alveolar tissue, loss of functional alveoli
  4. If irritant/disease is persistent, a chronic phase of disorder is seen causing disruption of pulmonary function & gas exchange
  5. Larger airway can be involved in inflammatory process, leading to bronchiolitis obliterans & an organizing pneumonia (BOOP)
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25
Q

All Interstitial lung diseases can cause what?

A

All Interstitial lung diseases can cause fibrosis - scarring that causes stiffness of the lungs with progressive shortness of breath.

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26
Q

sxs of ILD
* What is progressively getting worst? ⭐️ ⭐️ ⭐️ ⭐️
* Gas exchange is impaired due to what?
* What is increased and why?

A

Progressively worsening exertional dyspnea(most common complaint) ⭐️ ⭐️ ⭐️ ⭐️
* Gas exchange is impaired due to ventilation/perfusion mismatching, R-to-L shunt, & decreased diffusion across abnormal interstitium
* Work of breathing markedly increased because of decreased lung compliance

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27
Q

What are the two other sxs of ILD?

A
  • Chronic nonproductive cough (second most common)
  • Crackles or rales heard on auscultation
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28
Q

ILD diagnostic testing:
* What is the best inital test? What does that show?
* What is the most accurate test?
* What does not yield specific diagnosis?

A
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29
Q

⭐️ ⭐️

Pulmonary function testing for ILD:
* What type of pattern?
* What is the FEV1, FVC, TLC and residual volume?

A

Decreased FEV1, FVC, TLC, and residual volume.
* The FEV1/FVC ratio is normal.
* Thus, if ratio of FEV1/FVC is normal in a person with a decreased FVC – restrictive lung pattern – they can not breathe in as deeply as normal
* In restrictive, both FEV1 and FVC are decreased, decline in FVC is more than FEV1 resulting in higher than 80% FEV1/FVC – so normal is restrictive, not obstructive.

  • FVC – amount of air that can be forcibly exhaled from your lungs after taking deep breath
  • TLC – maximum volume of air the lungs can hold
  • FEV1 – measure the progression of lung conditions such as chronic obstructive pulmonary disease or asthma, stands for forced expiratory volume, which is the air you can exhale in 1 second, low score means a breathing obstruction
  • FEV1/FVC represents the percentage of your lung capacity you can expel in one second. The higher the score, the larger your lung capacity and the healthier your lungs.
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30
Q

What is a common antibiotic that is used for UTI and what can that cause? (think xray and CT)

A
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31
Q

ILD managment:
* What is geared to?
* What is one viable therapeutic option?
* What can slow the decline of lung function?
* What about therpies?

A
  • Geared to cause, if known
  • Lung transplant is one viable therapeutic option
  • Antifibrotic therapy medications (pirfenidone) can slow decline of lung function
  • Physical therapy and supplemental oxygen->Can improve exercise tolerance and reduce chance of developing pulmonary hypertension
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32
Q

LY

ILD management:
* What is one type of med that can be used?
* What about if the patient cannot use that medication?

A
  • Corticosteroids
  • In patients who cannot tolerate corticosteroids or whose symptoms progress despite steroid treatment, options such as cyclophosphamide, azathioprine can be given in addition
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33
Q

prevention of ILD:
* What should you avoid? (4)
* What is there a strong association to?
* What is critical in evey geriatric patient?

A
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34
Q

Special Considerations of ILD
* Prognosis?
* What is utmost important?
* How is the trestment decision made?
* What can be done?
* These patients have a high prevalence of what?
* What can corticosterioid result in?
* Cardiac disease, sleep apnea, depression – higher percentage have what?

A
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35
Q

txt setting of ILD:
* Most are where?
* What are triggers for admission?
* What should be done for quality of life?
* What can extend survival and improve the quality of life?

A
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36
Q

Pulmonary Fibrosis (PF)
* What is the “typical” patient?
* What are the risk factors?
* What are teh causes?

A
  • Average age at presentation is 50-year-old, male smokers
  • Risk factors: Exposure to smoke, metal dust, farming dust, & hairdressing chemicals
  • Numerous causes – inhalation of toxins, infection, chronic inflammation – anything that damages lung tissue may lead to fibrosis
    * Idiopathic type is the most common interstitial lung disease (scar tissue within the lungs)
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37
Q

What are the sxs of pulmonary fibrosis?

A

dyspnea, non-productive cough, unintended weight loss, fatigue, clubbing of digits

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38
Q

Under slide 25

For pulmonary fibrosis, what type of predisposition is suspected? explain

A

Genetic predisposition suspected
* SFTPC, SFTPA2, TERT and TERC gene mutations
* Sporadic IPF, in absence of telomerase mutations, is often associated with telomere shortening.

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39
Q

What does this show?

A

pul fibrosis

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40
Q

What are the upper lobe causes of pul fibrosis?

A
  • S Silicosis, Sarcoidosis
  • C Coal miner’s pneumoconiosis – black lung
  • A Allergic alveolitis, aspergillosis
  • T Tuberculosis
  • O Other – drugs, berylliosis, eosinophilic granuloma
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41
Q

What are the lower lobe causes of pulmonary fibrosis?

A
  • R Rheumatoid arthritis
  • A Asbestosis
  • S Scleroderma
  • H Idiopathic Pulmonary Fibrosis
  • O Other – drugs, radiation
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42
Q

under slide 28

What does pulmonary fibrosis cause?

A

Pulmonary fibrosis causes reticular (net-like) shadowing of the lung peripheries which is typically more prominent towards the lung bases

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43
Q

Pulmonary Fibrosis
* What is shown on PE?
* Labs: What may be high? (2) What is common?

A
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44
Q

Pulmonary Fibrosis
* What does the PFT show? ⭐️
* What does the bronchoaveloar lavage show?

A
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45
Q

What is this in a 50 yo smoker?

A
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46
Q

What is the classic CT findings in pulmonary fibrosis? ⭐️ ⭐️ ⭐️ ⭐️

A
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47
Q

Pulmonary Fibrosis
* What is the txt?

A
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48
Q

Pulmonary fibrosis:
* What is the prognosis?
* What is the death timeline?
* What are the predictors of survival?

A
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49
Q

Pulmonary Hemorrhage Syndromes: Idiopathic Pulmonary Hemosiderosis
* What is it characterized by?
* May be what?
* Not associated with what/

A
  • Characterized by recurrent pulmonary hemorrhage (cough)
  • May be life threatening
  • Not associated with renal disease
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50
Q

Pulmonary Hemorrhage Syndromes: Goodpasture’s Syndrome
* What is it?
* Relapsing what?
* Who is mostly affected?

A
  • Rate autoimmune disorder that causes immune system to attack tissues in the lungs and kidneys
  • Relapsing pulmonary hemorrhage, anemia, & renal failure
  • Adult males most affected
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51
Q

What does goodpasture syndrome affect?

A
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52
Q

Sarcoidosis ⭐️
* What is the mechanism?
* What does it result in?

A
  • Inflammatory granulomatous disease of unknown etiology.Immune reaction to a trigger such as an infection or chemicals, alteration to the immune response after exposure to an environment, occupational, or infectious agents
  • Immunological disorder that results in lots of small nodules throughout the body
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53
Q

Sarcoidosis:
* What is the hallmark of the disease? 🌟
* What are the complications of advanced disease (3)?

A

The hallmark of the disease is non-caseating granulomas usually affecting the lungs (up to 90% of patients), however, any organ can be affected (except GI, that is rare)

Complications of advanced disease:
* Interstitial lung disease
* Pulmonary hypertension
* Venous thromboembolic disease

Everyone with sarcoidosis will eventually have pulmonary involvement.

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54
Q

Sarcoidosis

  • What are granulomas?
  • What do they represent? ⭐️ ⭐️ ⭐️
  • What is Non- caseating ”non-necrotizing” granuloma?
  • clusters of what?
A

  • May occur anywhere on body
  • May become calcified with time
  • Not cancer
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55
Q

What is this?

A

granulomas

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56
Q

Clinical Presentation of Sarcoidosis
* May be what?
* Sacroidosis will not cause what?
* What type of dyspnea?
* What type of cought?
* May have what?

A
  • May be asymptomatic
  • Sarcoidosis will NOT cause hemoptysis
  • Exertional dyspnea
  • Cough – dry, non-productive
  • May have chest pain, arrhythmias, restrictive cardiomyopathy
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57
Q

Clinical Presentation of Sarcoidosis
* What are the classic skin findings? ⭐️
* May have what? What is this?
* What will show on the lung+cardiac exam

A
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58
Q

Clinical Presentation of Sarcoidosis
* What is lofgren’s syndrome? ⭐️ ⭐️ ⭐️ ⭐️

A
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59
Q

What are these?

A

Skin Findings in Sarcoidosis
* Left side: Erythema Nodosum (painful nodules on the lower legs)
* Right side: Infiltrated, hyperpigmented, & slightly erythematous coalescent papules & plaques on upper arm.

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60
Q

What is lupus pernio?

A
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61
Q

What is the most common thracic finding in sarcoidosis?

A
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62
Q

What do the x-rays show in sarcoidosis?

A
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63
Q

What are the clinical staging based on cxr? (ly)

A
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64
Q

Sarcoidosis Diagnosis - Diagnostic Imaging

x-ray/ct
* staged according to what?
* Why is CT scan/ultrasound guided biopsy/fine-needle aspiration used?

A
  • Staged according to extent of lung involvement
  • CT scan/ultrasound guided biopsy/fine-needle aspiration of mediastinal lymph nodes
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65
Q

Sarcoidosis Diagnosis - Diagnostic Imaging

Pet scan:
* What is the lamba sign?
* What is the panda sign?
* What is specific for diagnosis?

A
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66
Q

What are the labs of sarcodiosis? ⭐️

A
  • High Ca2+ caused by dysreg calcium metabolism
  • High ACE from t cells-> corrlates with total granuloma load and can be used for monitoring txt and disease progression
  • Amyloid A serum marker ⭐️
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67
Q

Sarcoidosis Diagnosis - Diagnostic Imaging

  • What does the lung function test show?
A
  • Typically reveals restrictive pattern (reduced vital/total lung capacity)
  • Endobronchial sarcoid may lead to impairment of airflow, obstructive pattern
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68
Q

Sarcoidosis Diagnosis – Other Diagnostics

What does Diffusion of carbon dioxide (DLCO) MOST sensitive for? What does it measure? ⭐️

A
  • Most sen test for intersitial lung disease-lost of diffusion capacity of the lungs for CO2
  • Measure of how well oxygen and carbon dioxide are diffused between the lungs and the blood
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69
Q

Sarcoidosis Diagnosis – Other Diagnostics
* Bronchoscopy?
* Ophthalmological exam?
* ECG?

A
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70
Q

Sarcoidosis Diagnosis
* Requires both what?

A

Requires both compatible clinical features and pathologic findings
* Sarcoidosis remains elusive, diagnosis can not be made with 100% certainty
* Diagnosis can be made with reasonable certainty based on history and physical features along with laboratory and pathologic findings

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71
Q

Sarcoidosis Diagnosis
* Evaluation is usually based on what two scenarios? ⭐️

A
  • Patient may undergo a biopsy revealing a noncaseating granuloma in either a pulmonary or an extrapulmonary organ
  • If clinical presentation is consistent with sarcoidosis and there is no alternative cause for the granulomas that is identified, then sarcoidosis is felt to be the cause.
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72
Q

CT Findings of sarcoidosis? (4)

A
  • Ground glass opacification
  • Mosaic attenuation pattern
  • Thickening of the bronchovascular bundles and bronchial wall
  • Parenchymal nodules, cysts, cavities
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73
Q

Cardiac Sarcoid
* What is this?
* What is low yield?
* What is used?
* What is diagnostic?

A
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74
Q

What are the differential dx for sarcodiosis? (LY)

A
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75
Q

Prognosis of Sarcoidosis
* Chronic?
* Fatal?
* Prognosis worse if what?
* Vast majoiry will go into what?
* Major morbidity & mortality related to what?

A
  • Chronic ~ 30%
  • Fatal in < 5% (pulmonary fibrosis)
  • Prognosis worse if extrapulmonary sarcoidosis exists
  • Vast majority will go into sustained remission with treatment
  • Major morbidity & mortality related to progressive respiratory dysfunction in association with severe ILD
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76
Q

Prognosis of Sarcoidosis
* What is the most common extrapulmonary complication? What do you need to do?

A

Eye involvement (including blindness) is most common extrapulmonary complication -> so refer for routine exam exams (chronic macular edema and persistent ocular inflammation)

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77
Q

Treatment of Sarcoidosis
* Most people have what? ⭐️
* Resolve when? ⭐️
* Complete remission when?
* What is the decision to treat based on? (2)
* What is important indication to treat?

A
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78
Q

Treatment of Sarcoidosis
* Management of acute sarcoidosis is based on what?
* What do you do for acute disease?
* What do you do if Symptoms confined to only one organ?

A
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79
Q

Treatment of Sarcoidosis
* What is the txt for multiorgan disease or disease too extensive?

A

Multiorgan disease or disease too extensive for topical therapy
* Systemic therapy recommended
* Glucocorticoids (prednisone) remains drug of choice for this disease

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80
Q

Different Types of Treatment for Sarcoidosis
* Systemic therapies are usually what?
* What are effective for skin than pulmonary disease?
* What may be used for cutaneous sarcoidosis?

A
  • Systemic therapies are usually immunosuppressive, including glucocorticoids, cytotoxic, or biologics
  • Antimalarial drug hydroxychloroquine are effective for skin than pulmonary disease
  • Minocycline may be used for cutaneous sarcoidosis
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81
Q

Different Types of Treatment for Sarcoidosis
* What is Pulmonary or extrapulmonary disease?
* What is used to improve lung fxn?

A
  • Pulmonary or extrapulmonary disease, cytotoxic agents such as methotrexate has been used with success
  • Biologic anti-TNF agents have been success to improve lung function such as Infliximab
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82
Q

Environmental Lung Diseases
* What do you need to get from history?

A

Chronic intrapulmonary disease

Detailed workplace & work history
* Specific contaminants
* Availability & use of protective devices
* Ventilation
* Do coworkers have similar complaints?
* Ask about every job; short-term exposures may be significant

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83
Q

Environmental Lung Diseases
* What do you use for detacting and monitoring?
* What can be used to detect an acute bronchoconstrictive response? ⭐️

A
  • CXR is useful in detecting and monitoring the pulmonary
    response to mineral dusts, certain metals and organic dusts.
  • Measurement in change of force expiratory volume in 1 (one) second before and after a working shift can be used to detect an acute bronchoconstrictive response
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84
Q

Environmental Lung Disease-SX
* What is the most common presenting complaint?
* What else?
* If ILD is from a rheumatic source, a common complaint
may be what?
If pneumonia is present, what is major complaint?

A
  • Most common presenting complaint—developmentof progressive SOB, initially felt only with exertion, worsens as inflammatory process progresses.
  • Nonproductive, dry cough & fatigue
  • If ILD is from a rheumatic source, a common complaint may be pleuritic chest pain.
  • If pneumonia is present cough is a major complaint
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85
Q

Coal Worker’s Pneumoconiosis (CWP)
* What is this? What is most common? ⭐️

A

Inflammation commonly leading to fibrosis of lungs caused by inhalation of dust in various occupations
* Most common asbestos, silicosis, coal miners’ pneumoconiosis

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86
Q

Coal Worker’s Pneumoconiosis (CWP)
* What are the clincal findings?

A
  • Chest pain
  • Cough with little or no expectoration
  • Dyspnea
  • Reduced thoracic excursion
  • Possible cyanosis
  • Fatigue after slight exertion
  • Degree of disability depends on types of particles inhaled, as well as exposure level
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87
Q

Asbestosis
* Range os what?
* What is a key diagnostic feature? ⭐️ ⭐️ ⭐️ ⭐️ ⭐️

A
  • Range of respiratory diseases resulting from asbestos exposure
  • Key diagnostic feature – “pleural plaques” – areas of hyalinized collagen seen on x-ray
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88
Q

Asbestosis
* Who do you seen this in? (3)

A
  • Construction trades-pipefitting, boiler making
  • Manufacturing of safety garments, filler for plastic material & friction materials (brake & clutch linings)
  • Many houses / offices still contain building materials with asbestos, particularly insulation, so care must be taken when doing remodeling or reconstruction
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89
Q

Asbestosis
* Asbestosis disease burden is directly related to what?
* Usually develops when? ⭐️

A
  • Asbestosis disease burden is directly related to intensity and duration of exposure
  • Usually develops at least 10 years post exposure
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90
Q

Asbestosis
* What is seen on x-ray?

A
  • Irregular or linear opacities that usually are first noted in the 0 lower lung fields are the chest radiographic hallmark of asbestosis.
  • Indistinct heart border or a “ground-glass” appearance in the lung fields may be seen.
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91
Q

Time Frame for Disease Presentation- asbestosis
* Fibrosis?
* Cancer?
* Usually aren’t dx with asbestosis until when?
* What is more common?

A
  • Fibrosis – 10 - 30 years
  • Cancer – increased risk, typically at least 15-20 years post exposure
  • Usually aren’t dx with asbestosis until cancer symptoms appear
  • Bronchogenic carcinoma is more likely than mesothelioma
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92
Q

What does this show?

A

Pleural plaques-asbestosis

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93
Q

Fibrous Pleural Plaque
* Gross lesion typical for what?
* what does the picture show?

A
  • Gross lesion typical for pneumoconiosis, & asbestos in particular
  • Seen here on pleural side of diaphragmatic leaves are several tan-white pleural plaques.
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94
Q

Asbestosis clinical presentation:
* What does the pul function test show? ⭐️ ⭐️ ⭐️
* Evidence of what?
* What are the sxs?

A
  • Pulmonary function testing in asbestos reveals a restrictive pattern with a decrease in both lung volumes and diffusing capability
  • Evidence of mild airflow obstruction
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95
Q

What does asbestosis show on x-ray?

A
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96
Q

Asbestosis
* High frequency of what?
* More commonly predisposes to what?
* Smoking increases lung cancer risk by what?
* Smokers with a history of asbestos exposure have a risk of what?
* Smoking increases risk of lung CA after asbestos exposure but does not alter risk of what?

A
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97
Q

Mesothelioma
* What is it?
* What does it affect?
* Not associated with that?
* Relatively short-term asbestos exposures of less than what?
* What is the primary risk factor?

A
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98
Q

Silicosis
* What is the etiology?
* Acute silicosis can occur after what?
* Simple silicosis results from what?

A
  • Etiology – oldest known occupational pulmonary hazard, exposure to free silica – mining, stone cutting
  • Acute silicosis can occur after any heavy exposure, no matter the brevity (ONE TIME ONLY)
  • Simple silicosis results from long term exposure
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99
Q

Silicosis
* Clinical and pathological features of acute silicosis are what?
* Chest radiograph may show what?
* Chest CT scan can show what?
* What may provide symptomatic relief and show the progression?

A
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100
Q

What does the CT show with acute silicosis?

A
  • Characteristic chest CT pattern “crazy paving”
  • Crazy Paving is a scattered or diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines
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101
Q

pt CT after cutting stone for a long time, what is the dx?

A

silicosis

102
Q

What does simple silicosis show on x-ray?

A

Calcified lymph nodes – “eggshell” appearance and small round opacities in the upper lung fields

103
Q

What will silicosis progress to?

A

Progresses to Massive Fibrosis

104
Q

Chronic Silicosis
* When does this occur? Associated with what?
* What is fibrosis and what does it lead to? ⭐️
* Degree of exposure to silica & length of exposure determines what?

A
  • Longer-term, less intense exposures associated with upper lobe fibrosis & hilar adenopathy > 15 years after exposure
  • Fibrosisis nodular & may lead to pulmonary restriction on a pulmonary function test & airflow obstruction
  • Degree of exposure to silica & length of exposure determine amount of silicotic nodule formation & degree of restrictive lung disease
105
Q

Chronic Silicosis
* Associate with higher-than-normal risk for what? What warrant anti-tuberculosis txt?
* Silicosis increases risk for

A
  • Associate with higher-than-normal risk for TB (2- to 30- fold more often than coworkers without silicosis) & patients with chronic silicosis & positive PPD warrant anti-tuberculosis treatment
  • Silicosis increases risk for lung CA only about 2-fold (risk is increased when combined with exposure to tobacco smoke, diesel exhaust, or radon gas)
106
Q

Treatment of silicosis:
* Cure?
* Aim to do what?
* May need what?

A
  • No cure
  • No reversal
  • Aim to manage symptoms, slow progression and treat infections aggressively
  • May need cough suppressant, supplemental O2, bronchodilators
107
Q

Treatment of silicosis:
* What is indicated to monitor for occupational risks associated with coal mining?
* What is not recommended?

A
  • Spirometry is indicated to monitor for occupational risks associated with coal mining
  • Glucocorticoids not recommended
108
Q

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis
* What is pneumonitis? ⭐️
* Due to what?
* Response to what?

A
  • Pneumonitis – generalized lung inflammation
  • Due to foreign chemicals, molds, dusts, foreign
    proteins
  • Response to inhaled antigens that are small enough to deposit in distal airways and alveoli
109
Q

⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis
* What are the two distinct clinical manifestations (rapid/acute and intermittent/sub-acute)?
* What is the pathophysiology?

A

Symptoms

110
Q

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis
* sx of acute?

A
  • Fever, chills, malaise, cough, chest tightness, dyspnea,
    rash, headaches
  • Resolves in 12 hours to several days after cessation of exposure
111
Q

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis
* sx of sub-acute?

A
  • Productive cough, dyspnea, fatigue, anorexia, weight
    loss, pleurisy, mild hypoxemia
  • Lesser severity, longer duration
  • Resolves weeks after cessation of exposure
112
Q

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis
* sx of chronic?

A
  • Insidious onset cough, progressive dyspnea, fatigue,
    weight loss, clubbing, tachypnea, respiratory distress
  • Emphysematous component
  • May be irreversible component, even if antigen removed
113
Q

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis
* Dx depends on what?
* What does CXR (acute and sub-acute) show?
* What does the PFTs show?

A
114
Q

Hypersensitivity Pneumonitis (HP)/Extrinsic Allergic Alveolitis-DX
* What is preferred over CXR? why?
* What is the MOST sensitive tool to dectect alveolitis?
* What may be needed?

A
115
Q

⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️

Hypersensitivity Pneumonitis - Berylliosis
* Beryllium may produce what? What is far more commonly associated with what?
* Exposure to beryllium in what?
* What does the PFT show?
* How long of exposure? What does it depend on?

A
116
Q

⭐️ ⭐️ ⭐️ ⭐️

Hypersensitivity Pneumonitis - Berylliosis
* On open lung biopsy, what is present?

A

On open lung biopsy, granulomatous formation like sarcoidosis may make differentiation impossible unless tissue levels of beryllium are measured
* Finding evidence of a specific cell-mediated immune response (i.e., delayed hypersensitivity) to beryllium

117
Q

⭐️ ⭐️ ⭐️ ⭐️ ⭐️

Hypersensitivity Pneumonitis - Organic Dusts
* What is it caused by?
* Exposure occur in production of what?
* What happens first/
* In 10-25% of workers, disease may be progressive with what?
* After 10 years, recurrent symptoms are associated with what?
* What is txt?

A
118
Q

⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️

Hypersensitivity Pneumonitis- Silo Filler’s disease
* Acute chemical pneumonitis due to what?
* Who is at risk?
* sx of those of what?

A
  • Acute chemical pneumonitis due to toxic gases (Nitrogen Dioxide) released from fermenting silage into atmosphere inside silo
  • Farmers & grain elevator operators are at risk
  • Symptoms are those of cigarette smokers- cough, mucus production, wheezing & airway obstruction
119
Q

CXR: Hypersensitivity Pneumonitis
* What does it show?

A
120
Q

Treatment - Hypersensitivity Pneumonitis
* Mainstay of txt is what?
* What most be obtained and why? ⭐️

A
  • Mainstay of treatment is antigen avoidance
  • Exposure history must be obtained to attempt to identify the potential offending antigen and to identify the location where a patient is exposed
121
Q

txt of hypersensitivity pneumonitis
* Acute and chronic?

A

Subacute
* Role for glucocorticoid therapy – symptomatic disease, 10% decrease in lung capacity
* Prednisone therapy over a duration of 1-2 weeks, followed by a taper over next 2-6 weeks

Chronic
* Similar trial of corticosteroids although fibrotic disease may be irreversible
* With extensive fibrosis, lung transplantation may be necessary

122
Q

Radiation Pneumonitis
* Acute disease usually presents when?
* Late disease whe?
* Characterized as what?
* occurs in patients who are what?
* Resolution typically occurs when?

A
123
Q

Radiation Pneumonitis
* What are the sxs?
* What is common? (high)
* What does the CXR show?
* What does PFT show?

A
  • Symptoms: Fever, cough, dyspnea following XRT to chest/breast
  • Leukocytosis and elevated erythrocyte sedimentation rate (ESR) are common
  • Chest radiograph usually shows alveolar or nodular opacity limited to the irradiated area
  • PFT will show reduced lung volumes, lung compliance.
124
Q

Radiation Pneumonitis
* What is the txt?

A
  • ASA, cough suppression, and bed rest
  • Corticosteroid therapy not proven to be effective
  • If given, prednisone is usually used for one-week, higher doses for more critically sick followed by a taper
125
Q

Acute Respiratory Distress Syndrome (ARDS)
* A clinical syndrome of what?
* Lung injury may be direct, as occurs in what?
* ARDS is defined by what? (3)

A
126
Q

Clinical Disorders Commonly Associated with ARDS
* What are the direct lung injury?

A
127
Q

Clinical Disorders Commonly Associated with ARDS
* What is indirect lung injury?

A
128
Q

Causes of Diffuse Alveolar Damage->ARDS
* What are the four main causes?
* What are other causes (4)
* What is Acute interstitial pneumonitis?

A
129
Q

Acute Respiratory Distress Syndrome (ARDS)
* As a result from what?
* What develops?
* What becomes leaky?
* What gets injured and die? What are the two types and results? ⭐️

A

As a result of the inflammation that occurs from the initial insult
* More blood clots develop
* Endothelium becomes leaky

Pneumonocytes get injured and die
* Type I – leads to less gas exchange
* Type II – less surfactant which reduces the surface tension that keeps the alveoli open

130
Q

Acute Respiratory Distress Syndrome (ARDS)
* What is the result of Pneumonocytes getting injured and die?

A

Dead cells and protein-rich fluid will build up and forms a hyaline membrane which makes gas exchange more difficult

131
Q

ARDS – Exudative Phase – First 7-10 Days
* What is it?
* Ensues with what?
* What also occurs early?
* Alterations in alveolar spaces are exacerbated by what? What is mismatched?
* What developes?
* What does CXR show?

A
132
Q

ARDS – Proliferative Phase – 7-10 days
* Resolution of what?
* Patients recover when?
* Many may still experience what?
* Last how long?
* Some patients develop what?
* As part of reparative process, epithelial cells synthesize what?

A
133
Q

⭐️

ARDS – Fibrotic Phase
* Obliteration of what?
* Some recover lung function when? Some enter what?
* Fibroproliferation in the pulmonary microcirculation causes what?

A
134
Q

⭐️

ARDS – Fibrotic Phase
* Causes increase risk of what?
* What is sometimes obtained and why?

A
  • Causes increase risks of pneumothorax, reductions in lung compliance, and increased pulmonary dead space
  • Sometimes a lung biopsy is obtained for evidence of pulmonary fibrosis->Increased mortality risk if present
135
Q

What are all the different phases of ARDS? (picture)

A
136
Q

ARDS
* Mortality?
* Increases with disease serverity? (3)
* With survival, patients may develop fibrosis causing development of what? Which can lead to what?
* What is common among survivors; present usually for at least 5 years after, slow to improve?

A
137
Q

Clinical Features of ARDS
* Suspect ARDS if what?
* What are the PE findings (4)?
* What are the labs? (2)

A
138
Q

⭐️ ⭐️ ⭐️ ⭐️ ⭐️ ⭐️

Clinical Features of ARDS
* What does the ABG show?
* What is unusual and more likely from what?

A
139
Q

What is the 4 criteria of ARDS?

A
140
Q

Clinical Features of ARDS
* What does CXR show? What does CT scan?
* What do the labs?

A
141
Q

ARDS Imaging
* Between 12 and 24 hours:
* Between 24 and 48 hours:
* From 5 to 7days:
* More than 1 week:

A
142
Q

What does this show?

A
143
Q

ARDS CXR
* What does it show?

A
  • Extensive bilateral alveolar infiltrates
  • Air bronchograms (arrows)
  • Looks similar to pulmonary edema, heart size looks normal
  • Pleural effusions not typical, but can occur and very common in patients with acute pancreatitis (as here)
144
Q

What does this show?

A

Typical images of chest X-ray radiograph. The portable chest X-ray radiographs of a patient with ARDS resulted from pneumonia.
* a The baseline image within 24 h of patient admission, demonstrating bilateral infiltrates.
* b,c 5 and 9 days after the admission, showing the progression of the infiltration

145
Q

Other Testing for ARDS
* Individualized and dependent on the suspected condition that needs to be confirmed or excluded, the safety of testing, and the therapeutic and prognostic value of the test (risk vs benefit)-> TEE, Bronchoscopy, lung biopsy?

A
146
Q

Treatment of ARDS:
* Clinical management involves what?
* What are the supportive measutes? (5)

A
147
Q

Asthma
* Common or rate?
* Affects how many people?
* Increasing or decreasing in rate?
* How people are affected?

A
  • One of the most common chronic diseases globally
  • Affects approximately 300 million people worldwide, approximately 250,000 deaths annually.
  • Previously on the rise in affluent countries for the last 30 years, now has stabilized.
  • 10-12% of adults, 15% of children are affected.
148
Q

Asthma Background

  • What is increased?
  • What type of lung disease?
  • Can present at what age? (+gender preference)
A
149
Q

Asthma background:
* Why does asthma not vary?

A
  • Mild at onset, usually does not progress to
    severe
  • Severe asthma usually severe at onset
150
Q

Risk factors of asthma:
* What are endogenous risk factors?

A

Endogenous
* Genetic predisposition = Both parents have asthma will give the child 50% chance
* Atopy
* Airway hyperresponsiveness
* Gender
* Ethnicity
* Obesity
* Early viral infections

151
Q

Risk factors of asthma:
* What are environemental risk factors?

A

DUST is NUMBER ONE TRIGGER
* Indoor allergens dust
* Outdoor allergens
* Occupational sensitizers
* Passive smoking
* Respiratoryinfections
* Air pollution
* Diet
* Dampness and mold exposure
* Acetaminophen or ASA
* Exercise
* Cold Air
* Toxic fumes (paint)

152
Q

Asthma Types
* Allergic/endogenous asthma: In response to what? Will usually have what? What test is done?
* Idiosyncratic asthma: Typically develops after what? Usually worse with what?

A

Allergic/Endogenous Asthma
* In response to allergen exposure
* Will usually have Hx of urticaria or eczema
* Skin tests are allergen +

Idiosyncratic asthma (infection)
* Typically develops after a URI
* Usually is worse with exercise or cold air (rarely stress)

153
Q

Asthma Types:
* Toxin related: What are the drugs?
* Cough variant: Only presents as what?

A

Toxin related
* Cocaine or Aspirin (leukotriene synthesis leads to bronchiole constriction)

Cough Variant
* Only presents as chronic cough

154
Q

History-Asthma
* Pattern of respiratory symptoms that occur following what?
* What are the classic symptoms?
* Who has worse prognosis?

A
155
Q

Asthma Pathophysiology
* What is the pathophysiology?

A
  • Airway inflammation and airway structural changes accompanied by varying degrees of symptoms that can be influenced by exposure to triggers that can cause acute deterioration as well as chronic symptoms are believed to play fundamental role in airway hyperresponsiveness
    * Mast cells and eosinophils
  • Mucus from hypertrophied bronchial submucosal glands, bronchoconstriction, and dehydration contribute to the formation of mucus plugs that can block airways
156
Q

Clinical features of asthma:
* Can develop when?
* Common when?
* Adolescents and adults who present with “new” asthma symptoms may have a history of what?

A
  • Can develop at any age
  • Common in childhood, many children experience a remission of asthma symptoms
    around puberty, with potential recurrence years later.
  • Adolescents and adults who present with “new” asthma symptoms may have a history of childhood asthma or asthma symptoms
157
Q

Physical Exam-Asthma:
* What is does the respiratory exam display? (wheezing)

A

Widespread, high-pitched, musical wheezes
* Most heard on expiration; can occur during inspiration

Multiple different pitches, or “polyphonic”
* Differs from the monophasic wheezing of a local bronchial narrowing, aspirated foreign body or bronchogenic CA

158
Q

What are sxs of severe airflow of PE severe airflow obstruction?

A
  • Tachypnea
  • Tachycardia
  • Prolonged expiratory phase of respirations (decreased I:E ration)
  • Poor air movement, “quiet” chest
  • Tripoding position
  • Use of accessory muscles
  • Pulsus paradoxus (greater than 12 mmHg fall in SBP during inspiration)
  • Hyperinflation on CXR from air trapping in alveoli
159
Q

What is a poor predictor of severity of airflow obstruction? ⭐️

A
  • Presence or absence of wheezing is a poor predictor of the severity of airflow obstruction!
160
Q

Extrapulmonary Findings of asthma:
* What happens to the nasal cavities?
* What happens to the posterior pharyngeal wall?
* What happens with the skin?
* What is NOT typical of asthma?

A
161
Q

What is this?

A

Atopic dermatitis-asthma is associated to this

162
Q

Asthma Diagnosis
* What is the definition?
* What is the Classic sign?
* Can be difficult to do what?

A
  • Definition: classic presentation of intermittent cough, wheeze, and shortness of breath brought on by triggers and relieved by bronchodilating medications.
  • “Classic” signs: intermittent dyspnea, cough, and wheezing-> Always consider cough variant asthma
  • Can be difficult to distinguish asthma from other respiratory diseases since nonspecific and overlap
163
Q

Asthma Diagnosis
* Definitive diagnosis requires what?

A

Definitive diagnosis requires history or presence of respiratory symptoms consistent with asthma, combined with the demonstration of variable expiratory airflow obstruction.

164
Q

Pulmonary Function Testing
* What does it test?

A
  • Tests of airflow limitation are critical tools in the diagnosis of asthma
165
Q

What does Spirometry assess/determine

A
  • Determine if baseline airflow limitation (obstruction) is present
  • Assess reversibility of the obstruction
  • Characterize the severity of airflow limitation
166
Q

Spirometry
* Determine if baseline airflow limitation (obstruction) is present: What is the FEV1 and FVR ratio? What happens to RV and TLC?

A
  • reduced FEV1 and FVC ratio
  • residual volume (RV) and total lung capacity (TLC) increased during episodes of obstruction (can’t exhale)
167
Q

Spirometry
* Assess reversibility of the obstruction: What do you need to do? What will happen to the FEV1?
* Characterize the severity of airflow limitation: Based on what?

A

Assess reversibility of the obstruction
* Repeat spirometry after administration of a bronchodilator
* Reduction of FEV1 to < 25% predicted or < .75 L after administration of a bronchodilator indicates severe disease

Characterize the severity of airflow limitation
* Based on FEV1 as a percentage of the normal predicted value

168
Q

Dx of asthma:
* What is considered significant? ⭐️

A

Bronchodilator response = ([Post-bronchodilator value – Prebronchodilator value] x 100)/Predicted value, where “value” is either FEV1or FVC.

An increase of >10 percent is considered significant.

169
Q

asthma

accurate PFT/bronchodilator testing:
* What can be issues? (6)

A
  • Inadequate inhalation of the bronchodilator due to problems using the metered-dose inhaler correctly
  • Recent use of a quick-acting bronchodilator or other anti-asthmatic medications (eg, long-acting bronchodilators), resulting in near-maximal bronchodilation prior to testing
  • Minimal airflow obstruction at the time of testing (FEV1already close to 100 percent)
  • In some patients with asthma, the presence of irreversible airways obstruction due to chronic airways inflammation or scarring
  • Treatment with controller medications (eg, inhaled glucocorticoid or leukotriene receptor antagonist) that were not withheld prior to testing
  • Uncooperative patients leading to subjective test
170
Q

what happens if you need further testing passed PFT for asthma?

A

Bronchoprovocation Testing

171
Q

asthma

Bronchoprovocation Testing
* What type of patient needs this? (5)

A
172
Q

What is an important cause of unexplained chronic cough?

A

Asthma is one of the important causes of unexplained chronic cough; however, in the absence of bronchial hyperresponsiveness, a diagnosis other than asthma should be considered.

173
Q

asthma

Bronchoprovocation Testing:
* What is the provocative stimulus is used to stimulate bronchoconstriction?
* What happen in ppl with asthma?
* What can it predict?

A
  • (Methacholine, inhaled mannitol, exercise, or hyperventilation of dry air)
  • People with asthma are more sensitive (hyperresponsive) to such stimuli than those without asthma.
  • In addition, the percent improvement when bronchodilator is administered after bronchoconstriction may predict someone who is prone to exacerbations
174
Q

asthma

Methacholine Challenge
* What is performed to est baseline?
* How is methacholine administered? (2)
* How does the FEV1 get measured?

A
  • Spirometry performed to establish baseline
  • Methacholine is administered sequentially in increasing concentrations prepared in two to four-fold dilutions.
  • Methacholine is given via nebulization starting with the lowest (most diluted) concentration.
  • FEV1 gets measured at 30, then 90 seconds post aerosol inhalation.
175
Q

asthma

Methacholine Challenge
* What happens to the dose/concentration?
* When is the test considered positive? Negative?
* The results of the methacholine test are reported as what?

A
176
Q

asthma

Peak Expiratory Flow (PEF)
* Measures what?
* usually used to monitor what?

A
  • Measures a brief, forceful exhalation
  • Usually used to monitor patients with a known diagnosis of asthma or to assess the role
    of a particular occupational exposure or trigger.
177
Q

asthma

Peak Flow Monitoring
* important why?
* Warns of changes in what?
* Changes in peak flow will happen before what?

A
  • Daily evaluation with a peak flow meter is an important component of optimal asthma management
  • Warns of changes in disease states and allows for adjustments daily as needed
  • Changes in peak flow will occur prior to clinical symptoms
178
Q

Other tests of asthma:
* What test cannot determine the presence of presence or absence of asthma or gauge severity?
* What can you do to screen for eosinophilia? What can increase eosinophil be due to?

A

Blood tests cannot determine the presence or absence of asthma or gauge severity
* CBC with diff to screen for eosinophilia
* Eosinophil percentage >15% or counts >1500 eosinophils/microL may be due to allergic asthma

179
Q

Asthma

  • Tests for allergy are not useful for what? But what can it confirm?
  • What is almost always normal in patients with asthma?
  • ABG may help with what? What values are seen? What may be indicated?
A
180
Q

What does this show?

A

Hyperinflation

181
Q

⭐️ ⭐️

A
182
Q

Treatment of asthma:
* What is the goal?
* A person with well-controlled asthma should be able to do what?
* Avoid what?

A
  • Goal to optimize control of asthma symptoms and reduce the risk of exacerbations, while minimizing medication adverse effects.
  • A person with well-controlled asthma should be able to work, go to school, play, and sports without limitation due to breathing.
  • Avoid drying agents and stay hydrated (reduces mucus plug rates)
183
Q

What are the 4 essential components of asthma management?

A
  • Patient education
  • Control of asthma triggers
  • Monitoring for changes in symptoms or lung function
  • Pharmacologic therapy
184
Q

I dont think you need to know but still good for pharm

Available asthma medications
* What are the beta adrengic agonist? What do they do?

A
185
Q

besides Beta-Adrenergic Agonists, what else can you use for acute asthma?

A

Glucocorticoids (IV or PO, same time onset)
* Steroids in acute asthma requires 6 hours or more to have an effect
* Prednisone, Prednisolone, Triamcinolone, Methylprednisolone, Dexamethasone
* Very large doses of glucocorticoids have no advantage over more conventional doses

186
Q

Inhaled corticosteroid (ICS)
* adjunt to what?
* What are the types?

Cromolyn: What is it?

A

Inhaled corticosteroid (ICS)
* Adjunct to chronic therapy, have low yield of benefit in acute attacks
* Fluticasone (Flovent HFA, Arnuity Ellipta, others)
* Budesonide (Pulmicort Flexhaler)

Cromolyn
* Mast cell stabilizing agents, not really used in acute treatment of attack

187
Q

⭐️ ⭐️

Long-acting muscarinic antagonist (LAMA)
* What does it block? What does this prevent?
* She always be taken with what?

A
188
Q

Leukotriene receptor antagonist (LTRA)
* What is this/ how does it work?
* What are examples?

A

Leukotrienes are chemicals that are released when in contact with something you are allergic to - the chemicals cause classic allergy
symptoms including those found in asthma
* LTRA’s block this pathway and lessen symptoms of asthma
* Montelukast (Singulair®).
* Zafirlukast (Accolate

189
Q
A

If use of SABA greater than 2 days a week for symptom relief, there is evidence to step up treatment
Sometimes an additional step is added between 4 and 5 which includes a daily medium to high dose ICS-LABA-LAMA + SABA
* LAMA- long acting muscarinic antangonist

190
Q
A
191
Q

Under slide (seems like from book)

Anticholinergic drugs are used in asthma patients todo what?
* What is acetylocholine
* What can be used with this?

A
  • Anticholinergic drugs are used in asthma patients torelax and enlarge the airway, which makes breathing easier.
  • Acetylcholine is the predominant parasympathetic neurotransmitter in the airways and plays a key role in the pathophysiology of obstructive airway diseases, such as asthma, through bronchial smooth muscle contraction and mucus secretion
  • Anticholinergics are used along with short-acting beta2-agonists to treat severe asthma attacks or status asthmaticu
192
Q

Response to Therapy-asthma
* What is not there?
* Increased in what?
* What will require mechanical ventilation?

A
193
Q

Obstructive Lung Disease
* What are the major disorders?

A
194
Q

What are the two types of COPD?

A
195
Q

⭐️

A

Under slide:
* Blue bloater- hypoxic, cardiac sequalae, cor-pulmonale ->Cor pulmonale This occurs when low oxygen levels due to COPD cause arise in blood pressurein the arteries of the lungs, a condition known as pulmonary hypertension. This increase in pressure places excess strain on the heart’s right ventricle as it works to pump blood through the lungs. As a result, the heart muscle weakens and right-sided heart failure can occur.
* Pink puffer- short shallow breath- redness of cheeks

196
Q

How do the lungs look with chronic bronchitis and emphysema?

A
197
Q

What do these graphs show?

A

Representative spirograms (upper panel) and expiratory flow- volume curves (lower panel) for normal (A), obstructive (B), and restrictive (C) patterns.

198
Q

COPD Background
* What is it?
* Umbrella term for what?
* Reversible or not?

A
  • The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines COPD as a common, preventable, and treatable disease state characterized by persistent respiratory symptoms and airflow limitation due to airway and alveolar abnormalities usually caused by significant exposure to noxious particles or gases.
  • Umbrella term for chronic bronchitis and emphysema
  • Airflow limitation that is not fully reversible (<12% improvement after bronchodilator therapy)

  • COPD is a major cause of chronic morbidity and is the third leading cause of death worldwide and fourth leading cause of death in US.
  • Estimated to be present in 10% of adults over age 40
199
Q

COPD
* What is the leading cause of COPD?
* What are the other causes?
* What is a genetic component?

A
200
Q
  • What is the epidemiology of COPD (age, gender, poor what, hx of what, SES)
  • What are the sxs of COPD? Are they fast or slow?
A
201
Q

Emphysema
* What happens?

A
  • Permanent & destructive enlargement of airspaces distal to terminal bronchioles without obvious fibrosis
  • Gradual destruction of alveolar septae & pulmonary capillary bed, leading to decreased ability to oxygenate blood (dead space)
202
Q

Chronic Bronchitis
* Presence of what?
* Excessive production of what?
* What provides the obstructive component? What does that lead to?
* Relatively undamaged what?
* Later will develop what?

A
203
Q

What is the gold standard for dx COPD? ⭐️

A

Spirometry GOLD STANDARD for diagnosis and assessment of severity
* a post-bronchodilator FEV1/FVC <0.70 confirms the presence of persistent airflow limitation (poor reversibility with bronchodilators)
* Hemoptysis of unknown origin is a disqualifier for performing test

204
Q

⭐️

A
205
Q

COPD

Who Should have Spirometry?

A

All smokers & former smokers 35 years of age or older

  • Anyone of any age with 1 or more of the “cardinal” symptoms of COPD
  • Chronic cough
  • Excess sputum production
  • Dyspnea on mild exertion out of proportion to age
  • Wheeze
206
Q

Normal FEV1 essentially excludes what?

A

Normal FEV1 essentially excludes COPD
* Annual loss of FEV1 may range from 50-100ml per year in COPD patients

207
Q

What is the genetic screen for COPD?
* Who is recommended for that test?
* Typically done in patients with what?

A

Alpha-1 antitrypsin deficiency (AATD) screening (is an inherited disorder that may cause lung disease and liver disease)
* WHO recommends that all patients with dx of COPD should be screened, especially in areas with high AATD prevalence
* Typically done in patients with COPD <45 years old, no exposures, family history of COPD, unexplained liver disease

208
Q

⭐️

CXR for COPD
* What does it show?

A
  • Is usually normal early
  • Hyperinflation: flattened diaphragm and an increase in the volume of retrosternal airspace - “Tombstones”
  • Hyperlucency of the lungs
  • Rapid tapering of vascular markings
  • Enlargement of central pulmonary arteries in advanced disease with PAH
  • Respiratory infections are primary causes pf COPD exacerbations
209
Q

60 yo smoker of 20 years, what does this x-ray show?

A

Tombstones-emphysema
* Lungs are more radiolucent due to increased
* Air trapping

210
Q

70 yo smoker of 20 years, what does this show?

A

Bullae with Spontaneous Pneumothorax- Emphysema
* Can develop large bullae leading to pneumothorax

lose elastic tissue so cannot keep alevloi open

211
Q

When does bullous emphysema happen? What do they cause?

A

Bullous emphysema occurs when there’s damage to your alveolar walls, which stretch to form large pockets of air (bullae). These air pockets can measure larger than 1 centimeter (cm). Bullae affect how your lungs work. They make it more difficult for your alveoli to exchange oxygen and carbon dioxide

212
Q

CT for COPD
* Not routinely for? What does it detect?
* What will Emphysema show? Bronchitis?
* What will be enlarged?

A
  • Not routinely used for dx; used to detect bronchiectasis (bron-chi-ec-ta-sis) or screening lung CA in patients that meet criteria
  • Emphysema: tissue loss, blebs
  • Bronchitis: airway narrowing and wall thickening
  • Enlargement of central pulmonary arteries in advanced disease
213
Q

EKG for COPD
* What will it show?

A
  • P waves >3mm indicate cor pulmonale
  • Multifocal atrial tachycardia (different shapes of waves) seen in COPD
214
Q

Doppler Echo for COPD:
* Estimate of what?

A
  • estimate of pulmonary artery pressure
215
Q

ABGs for COPD
* What are the indications? ⭐️
* What are the findings? (2)?

A
216
Q

Low yield

Differentials of COPD (4)

A
217
Q

TREATMENT of COPD
* What is it based on?
* What are the goals?
* What is typically indicated?

A
218
Q

TREATMENT of COPD
* O2 when?

A

Oxygen (only when indicated!) – Goal is 88-92%
* Hypoxia is a respiratory stimulus and hence you
cannot just give O2 like to a non-COPD patient
* Oxygen has the greatest impact on survival

219
Q

Treatment of COPD
* What improves morality and sx? (stoping something and prevention measures)
* What can improve symptoms and QOL but not mortality?

A
220
Q

Combined COPD assessment
* What is this? What is it used for? ⭐️⭐️
* What does sprimetry determine?
* What does CAT assess?
* What do you need the hx of?

A
221
Q

COPD

Fill in and what is this scale called? ⭐️

A
  • Assessment of either dyspnea using mMRC or symptoms using CAT
222
Q

COPD

What is the cat assessment?

A

Assessment of either dyspnea using mMRC or symptoms using CAT

223
Q

Multidimensional assessment of COPD: fill in ⭐️

A
224
Q

⭐️⭐️⭐️⭐️

  • Group a COPD?
  • Group b COPD?
A
  • Group A: Minimally symptomatic, low risk of future exacerbations: mMRC grade 0 to 1 or CAT score <10; 0 to 1 exacerbation per year and no prior hospitalization for exacerbation
  • Group B: More symptomatic, low risk of future exacerbations: mMRC grade ≥2 or CAT score ≥10; 0 to 1 exacerbation per year and no prior hospitalization for exacerbation
225
Q

⭐️⭐️⭐️⭐️

  • Group c COPD?
  • Group d COPD?
A
  • Group C: Minimally symptomatic, high risk of future exacerbations: mMRC grade 0 to 1 or CAT score <10; ≥2 exacerbations per year or ≥1 hospitalization for exacerbation
  • Group D: More symptomatic, high risk of future exacerbations: mMRC grade ≥2 or CAT score ≥10; ≥2 exacerbations per year or ≥1 hospitalization for exacerbation
226
Q

COPD

What are the treatments for all the groups (a-d)

A
227
Q

COPD

What are the different types of inhaled bronchodilators?

A
  • SAMA (short-acting muscarinic antagonist)(anticholinergic)
  • SABA (Short-acting beta agonist)
  • Ipratroprium/Albuterol
  • LAMA
  • LABA
228
Q

COPD

  • SAMA (short-acting muscarinic antagonist)(anticholinergic): What is an exmaple?
  • SABA (Short-acting beta agonist): What are examples? When prescribed?
  • Ipratrorium/albuteral: What produces a greater response? What does it not alter?
A
229
Q

COPD

LAMA
* What is an example? ⭐️
* Improves what?
* Decreases what?
* May slow down what?

LABA: what are exmaples?

A
230
Q

COPD

Inhaled Bronchodilators
* Think about what?
* If acute exacerbation, what will happen?
* What can help with delivery for acute exacerbations?
* Where do capsules go?
* Only use in who?

A

  • Spacer helps medicine move past your mouth and throat and get deep into the lungs
  • Extends amount of time it takes for the medicine to enter the lungs.
231
Q

COPD

Inhaled Corticosteroids (ICS)/LABA
* LABA-ICS combinations have demonstrated reductions in what?
* improve what?
* ICS not not used how?
* Regular use in severe disease can increase risk of what?
* TRIPLE INHALED THERAPY of ICS/LAMA/LABA improves what? ⭐️

A
232
Q

I just placed it all together because I think it is low yield-COPD

Tobacco Cessation
* What are all the different components?

A
233
Q

COPD

Vaccinations
* What does it decrease the risk of?
* What are the different types?

A

Decrease risk of infections and subsequent COPD exacerbations
* Annual Flu
* 23-valent pneumococcal polysaccharide vaccine PPSV-23
* Once before 65/once after
* COVID

234
Q

COPD

Surgery
* What can be done with pts with upper lobe emphysema?
* What can be done with pts with advance emphysema?
* What can be done in select patients with large bulla?
* Consider what?

A
  • Lung volume reduction surgery in patients with upper lobe emphysema
  • Bronchoscopic lung reduction in select patients with advanced emphysema
  • Surgical bullectomy in select patients with large bulla
  • Severe COPD with other criteria, consider transplant
235
Q

Other measures for COPD
* _ rehab
* Long term non-invasive ventilation for what?
* What are the other 2?

A
  • Pulmonary rehab
  • Long term non-invasive ventilation for severe chronic hypercapnia and history of
    hospitalization for acute respiratory failure
  • Nutrition
  • Palliative care
236
Q

What are the complications in advanced COPD?

A
237
Q

Acute exacerbation of COPD:
* Commonly precipated by what?
* How does it present? (what increases?-3)

A
238
Q

⭐️ ⭐️⭐️⭐️

Acute exacerbation treatment
* What do you need to start? When?

A
  • Empiric antibiotic therapy is indicated for patients who are most likely to have a bacterial infection causing the exacerbation and for those who are most ill.
  • Empiric antibiotic treatment in patients with a moderate to severe COPD exacerbation (defined as having ≥2 of 3 cardinal symptoms: increased dyspnea, increased sputum volume/viscosity, or increased sputum purulence)ora COPD exacerbation requiring hospitalization and/or ventilatory support (either invasive or noninvasive).
239
Q

Acute exacerbation treatment
* When do you not initate antibiotic therapy?
* What can start?
* Systemic what?

A
240
Q

Acute exacerbation treatment:
* COPD should be considered in any patient who has what?
* What is required to make dx?
* What are the goals?
* Concomitant chronic diseases occur frequently in COPD patients, including what?

A
241
Q

Key points: Role of spirometry
* The gold guideline advise what?
* assessment of what?
* When do you need to do a follow up assessment?
* What does evidence emerge?

A
242
Q

Bronchiectasis
* What is it?
* This syndrome is typically the result of what?

A
  • Bronchiectasis is a clinical syndrome characterized by abnormal dilation and distortion of the bronchial tree, resulting in chronic obstructive lung disease with clinical manifestations of chronic cough, sputum production, and recurrent chest infections.
  • This syndrome is typically the result of a variety of pathophysiologic processes that cause the bronchi to have weak, distorted, and easily collapsible walls, with chronic inflammation, infection, and impaired mucociliary function and mucus plugging.

Under slide
* A condition in which the lungs’ airways become damaged, making it hard to clear mucus.
* Bronchiectasis may result from an infection or medical condition, such as pneumonia or cystic fibrosis. Mucus builds up and breeds bacteria, causing frequent infections.
* Symptoms include a daily cough that occurs over months or years and daily production of large amounts of phlegm.
* Treatment may include physical therapy and medications, such as antibiotics and drugs to help loosen mucus.

243
Q

Bronchiectasis
* Shares many characteritics of what? Explain?
* The diagnosis is established clinically based on what? What is shown on radiographs? ⭐️⭐️⭐️

A
244
Q

Bronchiectasis Epidemiology
* Who many have it?
* Increase prevalence in who?
* Increased freq in who?
* More common in who?
* Concomitant presence of COPD increases the use what?
* What is most common cause of bronchiectasis in children?

A
245
Q

Induction of bronchiectasis requires two factors, what are they? ⭐️

A
  • infectious insult
  • Impaired drainage, airway obstruction, or a defect in host defense
246
Q

Bronchiectasis Treatment
* Because only a few causes of bronchiectasis respond to direct treatment, treatment aimed at what?

A
  • Treating exacerbations
  • Controlling chronic infection
  • Reducing inflammation
  • Improving bronchial hygiene
  • Sometimes surgery
247
Q

Bronchiectasis-acute exacerbation
* Patients have high burden of what?
* Exacerbation determined based on what?

A
  • Patients have high burden of bacterial pathogens and inflammation, and exacerbations are associated with increase or change to the bacterial population.
  • Exacerbation determined based on symptoms rather than lab
248
Q

Bronchiectasis-acute exacerbation
* Deterioration in three or more of what sx lasting at least 48 hours?

A
  • Cough mn
  • Sputum volume and/or consistency
  • Sputum purulence
  • Breathlessness and/or exercise intolerance
  • Fatigue and/or malaise
  • Hemoptysis
249
Q

Acute Exacerbation of Bronchiectasis
* What does the PE show?

A
  • Focal or diffuse crackles
  • Sonorous wheezes/rhonchi
  • Mid-inspiratory squeaks
  • Sibilant wheezes
250
Q

Bronchiectasis Treatment
* What is the mainstay tx?
* Obtain what?
* What do you give if no culture information?
* Txt for how long?
* Change txt when?

A

Clinical Medicine 2 (16 decks)

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