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Pulmonary > Lectures6-10 > Flashcards

Lectures6-10 Flashcards

1
Q

Asthma is a chronic inflammatory disorder of the airways characterized by:

A

Paroxysmal symptoms of cough, wheezing, dyspnea and chest tightness, usually related to triggers
Airway narrowing that is partially or completely reversible

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2
Q

Why does asthma have increasing prevalence?

A

Improved hygiene, increased indoor air pollution, increased incidence of early-onset respiratory viral infections, survival or premature infants, increased awareness & recognition of asthma but pts and clinicians

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3
Q

What are some risk factors for asthma?

A

M>F, Low SES, urban dwellers, food allergies, family hx, atopy

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4
Q

What is atopy?

A

A genetic disposition to develop an allergic reaction and produce elevated levels of IgE upon exposure to an environmental antigen and especially one inhaled or ingested

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5
Q

What are some examples of atopy?

A

Atopic dermatitis, allergic rhinitis, asthma

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6
Q

Patho of asthma

A

Smooth muscle constriction around airways, airway wall edema, intra-luminal mucus accumulation, inflammatory cell infiltration of submucosa and basement membrane thickening

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7
Q

What immune cells are involved in asthma?

A

Eosinophils, activated helper T cells, mast cells, neutrophils

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8
Q

Fatal asthma

A

Severe collagen deposition of basement membrane, desquamation of epithelial lining with loss of ciliated cells, mucosal edema, airway smooth muscle hypertrophy, luminal plugging with inflammatory cells

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9
Q

What are the 3 main physiological consequences of asthma?

A
  1. Chronic airways inflammation
  2. Reversible or partially reversible bronchoconstriction
  3. Increased airways hyperresponsiveness to a variety of stimuli
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10
Q

What are the “classic’ sign and symptoms of asthma

A

Intermittent dyspnea, persistent cough, sudden onset or persistent wheezing

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11
Q

Additional features of asthma

A

Chest tightness, cold that take >10 days to resolve, apparent triggers, symptoms awake pt from sleep, exertional symptoms, seasonal, poor school performance and fatigue

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12
Q

The cough of asthma

A

Usually dry hacking, nocturnal, seasonal, response to specific exposures, lasts >3 weeks, frequently the sole complaint

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13
Q

What are some common asthma triggers?

A

Pollen, viral URIs, exercise, changes in air temp, perfumes, pets, molds, NSAIDs

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14
Q

What can be seen on PE for asthma?

A

Tachypnea, hypoxia if acute flare, cant speak full sentences without stopping to breath*, high-pitched musical wheeze

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15
Q

The wheeze of asthma

A

Initially with expiration but in severe cases also with inspiration

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16
Q

Critically severe asthma causes what?

A

Decreased breath sounds “silent chest/absent breath sounds”

Medical emergency: “the patient is very tight, not moving air”

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17
Q

Extrapulmonary PE findings associated with asthma

A

Pale, swollen nasal turbinates suggestive of allergic rhinitis, nasal polyps, atopic dermatitis

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18
Q

What diagnostic studies are used for asthma?

A

PFTs, spirometry with bronchodilator response testing, bronchoprovocation challenge, peak flow, CXR, allergy skin test

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19
Q

PFTs

A

Measurement of lung volumes, quantitation of diffusion capacity, measurement fo forced inspiratory and expiratory flow rates

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20
Q

What will PFTs show for an airway obstruction?

A

FEV1 decreased, FEV1/FVC ratio <70%

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21
Q

Vital capacity

A

Maximum amount of air a person can expel form the lungs after a maximum inhalation

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22
Q

What should you do if the baseline spirometry demonstrates an airway obstruction?

A

Administer albuterol 400mcg by MDI -> repeat spirometry 10 mins after

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23
Q

What suggests acute bronchodilator responsiveness?

A

Increase in FEV1 of >12%

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24
Q

What does the peak flow meter measure?

A

Peak expiratory flow

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25
Q

Peak flow meter

A

Effort dependent, useful for monitoring daily function during treatment of acute flare

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26
Q

What is needed to diagnose asthma?

A

Airflow obstruction symptoms, reversibility or obstruction, symptoms worse at night or early AM, prolonged expiration and wheezes on PE, limitation of airflow on PFT

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27
Q

Intermittent asthma severity

A

<2 days week symptoms and use of rescue inhaler

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28
Q

Mild persistent asthma

A

> 2 days/week symptoms and use of rescue inhaler (but not daily)

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29
Q

Moderate persistent asthma

A

Daily symptoms and use of rescue inhaler, some limitation to normal activity

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30
Q

Severe persistent asthma

A

throughout the day symptoms and use of rescue inhaler, extremely limited activity

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31
Q

What will the PFTs show for intermittent asthma?

A

Normal FEV1 between exacerbations, FEV1/FVC >.85

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32
Q

What will PFT show for mild persistent asthma?

A

FEV1 normal, FEV1/FVC >.8

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33
Q

What will PFT show for moderate persistent asthma?

A

FEV1 60-80%

FEV1/FVC 0.75-0.8

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34
Q

What will PFT show for severe persistent asthma?

A

FEV1 <60%

FEV1/FVC

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35
Q

What are the components of asthma management?

A

Routine monitoring of symptoms and lung fxn, patient education, controlling environmental triggers, pharmacological therapy

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36
Q

What is the treatment for intermittent asthma?

A

SABA prn

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37
Q

What is the treatment for persistent asthma (step 2)

A

Low dose ICS

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38
Q

What is step 3 treatment of asthma

A

either low dose ICS + LABA or med dose ICS + LABA

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39
Q

What is step 4 treatment of asthma

A

Med dose ICS + LABA

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40
Q

What is step 5 treatment of asthma

A

High dose ICS + LABA

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41
Q

What is step 6 for treatment of asthma?

A

High dose ICS +LABA + short course of oral systemic steroids

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42
Q

What is the treatment for acute asthma exacerbation?

A

02 between 90-96%, Methylprednisolone or prednisone, Albuterol (short acting bronchodilator), Magnesium IV

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43
Q

Can COPD and asthma co-exist?

A

Yes

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44
Q

What are some conditions that can exacerbate asthma?

A

Allergic rhinitis, GERD, cigarette smoking, obesity

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45
Q

COPD

A

A common preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases

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46
Q

What are 3 subtypes of COPD

A
  1. Emphysema
  2. Chronic bronchitis
  3. Chronic obstructive asthma
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47
Q

What is Emphysema?

A

Enlargement of air spaces and destruction of lung tissue

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48
Q

What is chronic bronchitis?

A

Obstruction of small airways

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49
Q

COPD differences from asthma

A

Usually from smoking, diagnosed at 50-60YO, obstruction is either irreversible or partially reversible with bronchodilator therapy

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50
Q

Asthma differences from COPD

A

Associated with atopy, diagnosed in childhood usually, reversible with bronchodilator therapy

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51
Q

Pathophys of COPD

A

Inflammation and fibrosis of bronchial wall, hypertrophy of submucosal glands, hypersecretion, loss of elastic fibers and alveolar tissue

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52
Q

What does COPD result in?

A

Airways obstruction, decreased surface area for gas exchange and mismatching of ventilation and perfusion

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53
Q

What does loss of elastic fibers cause in COPD?

A

Impairs expiratory flow, leads to air trapping, predisposes to alveolar collapse

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54
Q

What are common triggers of exacerbations for COPD?

A

Pulmonary infections

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55
Q

What are some risk factors for COPD?

A

Cigarette smoking*** airway hyperresponsiveness, biomass fuel exposure, 2nd hand smoke, ambient air pollution, genetics- alpha-1-anti-trypsin deficiency for COPD in young pts

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56
Q

Chronic bronchitis

A

Excessive secretion of bronchial mucus, chronic daily cough for 3mos

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57
Q

What may proceed or follow development of airflow limitation?

A

Chronic Bronchitis

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58
Q

What is an abnormal and permanent enlargement of the airspace’s that is accompanied by the destruction of the airspace walls & capillary beds?

A

Emphysema

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59
Q

Loss of elasticity

A

Emphysema

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60
Q

What are the two types of emphysema?

A
  1. Proximal acinar

2. Panacinar

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61
Q

Proximal acinar emphysema

A

Initial preservation of alveolar ducts and sacs

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62
Q

Panacinar emphysema involves what?

A

Involves both bronchioles and alveoli

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63
Q

What type of emphysema has an abnormal dilation or destruction of the respiratory bronchiole?

A

Proximal acinar (centrilobular)

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64
Q

What is proximal acinar emphysema commonly associated with?

A

Cigarette smoking

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65
Q

What can be seen in coal workers pneumoconiosis?

A

Proximal acinar emphysema

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66
Q

Which type of emphysema has enlargement or destruction of all parts of the acinus?

A

Panacinar emphysema

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67
Q

Panacinar emphysema is associated with that?

A

Alpha-1 antitrypsin deficiency

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68
Q

What can be seen on CXR for emphysema?

A

Hyperexpanded lungs, flattening of the diaphragm, volume is much longer looking

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69
Q

What else can be seen in CXR for emphysema that can lead to pneumothorax?

A

Blebs

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70
Q

What are some symptoms of COPD?

A

Chronic cough, sputum production, exertional dyspnea, wheezing, chest tightness, weight gain or weight loss

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71
Q

When do patients typically present with COPD symptoms?

A

5th or 6th decade of life, symptoms usually present at that point for around 10 years

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72
Q

PE findings for COPD

A

Prolonged expiratory phase, wheezing, barrel chest, enlarged lung volumes, respiratory distress in severe exacerbation, tripod position, pursed lips, cyanosis, weight loss, signs of RHF

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73
Q

Who are the pink puffers?

A

Emphysema

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74
Q

Who are the blue bloaters?

A

Chronic bronchitis

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75
Q

Pink puffer si/sxs

A

Dyspnea major complaint* scant clear mucus, thin, accessory muscle use, chest is quiet or soft-pitched wheeze

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76
Q

Blue bloater si/sxs

A

Chronic cough major complaint* mucopurulent sputum, frequent COPD exacerbations due to infections, mild dyspnea, noisy chest with Rhonchi and wheezing

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77
Q

What can be used to diagnose COPD?

A

Hx of SOB, cough, wheeze, smoking, labs: bicarb, CXR to rule out other causes, PFTs

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78
Q

What does serum bicarb identify for COPD pts?

A

Chronic hypercapnia in chronic disease

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79
Q

What else can be drawn for labs to test for COPD?

A

AAT deficiency, Hgb and BNP to rule out other causes of dyspnea

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80
Q

What PFTs should be used to diagnose COPD?

A

Spirometry, measurement of lung volumes, DLCO, forced inspiratory and expiratory flow rates

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81
Q

FEV1 measures what?

A

Forced expiratory volume in one second

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82
Q

FVC measures what?

A

Forced vital capacity

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83
Q

What is the vital capacity?

A

Maximum amount of air a person can expel from lungs after a max inhalation

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84
Q

What is the FRC?

A

Functional residual capacity, the volume of gas w/in the lungs at end of expiration during normal tidal breathing at rest

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85
Q

Conditions that decrease the DLCO

A

Anemia, emphysema, pulmonary HTN, recurrent PEs, interstitial lung disease

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86
Q

DLCO helps distinguish between when for obstructive lung diseases?

A

Between emphysema and chronic bronchitis or asthma

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87
Q

What will the PFTs show for obstructive lung disease?

A

FEV1 and FEV1/FVC ratio decreased, FVC normal, FEV1 improves with bronchodilators

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88
Q

What are the non-pharmacological treatments for COPD?

A

Stop smoking, reduce risk factors, vaccinations, oxygen therapy, pulm rehab

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89
Q

What is the 1st line treatment for newly diagnosed COPD?

A

Rescue inhaler! SABA: Albuterol or Levalbuterol, short acting anticholinergic: Ipratropium
Combo SABA + Ipratropium: Combivent**

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90
Q

What is most commonly prescribed for new diagnosis of COPD?

A

Combivent*** Combo of SABA + Ipratropium

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91
Q

What are the si/sx for an acute exacerbation of COPD

A

SOB, frequent cough with sputum, wheezing, associated with URI or pulm infection, minimal to no improvement with rescue inhaler

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92
Q

PE findings for COPD acute exacerbation

A

Respiratory distress, accessory muscle use, tripod position, pursed lips, hypoxia, tachypnea, wheezing, poor air movement, crackles if pneumonia

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93
Q

What is used to treat an acute COPD exacerbation?

A

O2 between 90-96, Prednisone PO or Methyprednisolone IV, Ipratropium and Albuterol nebulizer, Abx

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94
Q

What Abxs can be used for an acute exacerbation of COPD?

A

Levo and Azithromycin; want to cover atypicals

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95
Q

Who should be hospitalized for COPD flare?

A

Increased dyspnea, inability to eat or sleep, new cyanosis or hypoxia, acute respiratory distress, mental status change, insufficient home support, frequent exacerbations, high risk comorbidities

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96
Q

What can be seen when a pt is in acute respiratory distress?

A

Accessory muscle use, tachypnea, tripod position

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97
Q

Hospital admission for COPD

A

O2, Prednisone daily with a taper, Duoneb, Albuterol nebulizer, Levofloxacin or Azithromycin daily

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98
Q

When should you consider adding maintenance meds for COPD?

A

Frequent chronic symptoms, frequent exacerbations, disease progression

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99
Q

Which types of meds are used for maintenance for COPD?

A

LABA, LABA + ICS, LAMA, chronic steroids, chronic O2

100
Q

What LABA is used for maintenance for COPD?

A

Salmeterol inhaler

101
Q

What LABA + ICS is used for COPD maintenance?

A

Salmeterol/Fluticasone (Advair) inhaler

102
Q

What LAMA is used for COPD maintenance?

A

Triotropium (Spirivia)

103
Q

When are chronic steroids and oxygen used for COPD maintenance?

A

End stage disease

104
Q

What is 1st line treatment as “rescue inhaler” to manage COPD symptoms?

A

Short acting bronchodilators

105
Q

What is the most common cause of bronchiectasis?

A

Cystic fibrosis causes about 50% of cases

106
Q

What else can cause bronchiectasis?

A

Infections: TB, fungal, lung abscess, localized airway obstructions

107
Q

What is bronchiectasis?

A

Disorder of the large bronchi where there is permanent, abnormal dilation and destruction of the bronchial walls, localized or diffuse

108
Q

What disease does bronchiectasis share clinical features?

A

COPD

109
Q

What has a chronic daily cough and viscid sputum production?

A

Bronchiectasis

110
Q

What other clinical features are seen with bronchiectasis?

A

Bronchial wall thickening, luminal dilatation, frequent office visits and hospitalizations

111
Q

What is the pathophys belong bronchiectasis?

A

Infection -> host response -> transmural inflammation, mucosal edema, cratering, ulceration, neovascularization -> impaired drainage, permant dilatation and destruction of bronchi and walls

112
Q

Recurrent infections are common with bronchiectasis, leading to what?

A

Further damage of airways

113
Q

Which disease involves the abnormal transport of chloride and sodium across epithelium leading to thick, viscous secretions?

A

Cystic fibrosis

114
Q

What type of infections are most common for cystic fibrosis patients?

A

Pseudomonas aeruginosa infections

115
Q

How is cystic fibrosis diagnosed?

A

Sweat chloride test

116
Q

Clinical features of bronchiectasis

A

Cough, daily production or mucopurulent and tenacious sputum x mos-yrs, repeated respiratory tract infections

117
Q

Symptoms of bronchiectasis

A

Cough w/sputum, dyspnea, rhinosinusitis, hemoptysis, recurrent pleurisy, fatigue, urinary incontinence (stress incontinence)

118
Q

PE of bronchiectasis

A

Chronic pulmonary crackles, wheezing, rarely digital clubbing

119
Q

Lab tests utilized for bronchiectasis

A

CBCD, IgG, IgM, IgA to look for immunodeficiency, antibody tigers after pneumococcal vaccine, sputum gram stain and CX, sweat chloride testing

120
Q

Why are the antibody titers drawn after a pneumococcal vaccination?

A

To assess the immune response to vaccination

121
Q

What imaging studies are good for bronchiectasis?

A

CRX, CT

122
Q

What will CXR show for bronchiectasis?

A

Liner atelectasis, dilated, thickened airways, irregular peripheral opacities (mucopurulent plugs)

123
Q

What will be seen on chest CT for bronchiectasis?

A

Airway dilatation, bronchial wall thickening, mucopurulent plus, cysts of bronchial wall (destructive bronchiectasis)

124
Q

What will PFTs show for bronchiectasis?

A

Reduced FEV1/FVC, low FVC in advanced disease, 6 min walk test

125
Q

What is the treatment for bronchiectasis?

A

Treat underlying disease, pneumonia or other infection, HIV, prevent aspirations if possible, immunizations

126
Q

How do you treat an acute exacerbation of bronchiectasis?

A

Oral Abxs, nebulizer: hypertonic saline to thin secretions, chest physiotherapy, PEP device to loosen secretions, bronchodilators, pulm rehab

127
Q

What is the PEP device?

A

Oscillatory Positive expiratory pressure device used to loosen secretions for bronchiectasis

128
Q

What is virchow’s triad?

A
  1. Alterations in blood flow (stasis)
  2. Vascular endothelial injury
  3. Alterations in constituents of blood (inherited or acquired hypercoagulable states)
129
Q

What are the 3 classifications of pulmonary embolisms?

A

Acute, subacute, and chronic

130
Q

Acute pulmonary embolism

A

Signs and symptoms develop immediately after obstruction of pulmonary vessels prompting evaluation

131
Q

Subacute pulmonary embolisms

A

Patient present days or weeks following initial event

132
Q

Chronic pulmonary embolisms

A

Slowly develop symptoms of pulmonary HTN over many years

133
Q

What can a massive or submassive PE cause?

A

Hemodynamic instability, hypotension, severe RV failure, death

134
Q

What will a patient who is hemodynamically unstable need?

A

Fibrinolytic therapy (thrombolytic)

135
Q

What are the possible locations of pulmonary embolisms?

A

Saddle, Segmental, Subsegmental

136
Q

Saddle PE

A

In both right and left bronchi

137
Q

Segmental PE

A

Small branch effected

138
Q

Subsegmental PE

A

Small branch off of a branch is effected

139
Q

What are some common risk factors for PE?

A

Post op, sedentary state, malignancy, hx of VTE, pregnancy, oral contraceptives, obesity, smoking, HTN, hypercoagulable disorders

140
Q

What are some examples of inherited thrombophilia?

A

Factor V Leiden mutations, prothrombin gene mutation, deficiency of proteins C and S, amtithrombin 3 deficiency, anticardiolipin antibodies

141
Q

Venous thrombi dislodge and travel where?

A

To lungs, arterial system if there is a patent foramen ovals or atrial septal defect, can cause stroke or arterial embolization

142
Q

Symptoms of PE

A

Sudden SOB, pleuritic chest discomfort, heart palpitations

143
Q

PE findings for pulmonary embolism

A

DVT: unilateral swelling, erythema, calf tenderness, tachypnea, hypoxia, tachycardia

144
Q

What is used to determine the likelihood of a PE?

A

Wells Score

145
Q

What is your change of a PE if the Wells score is <2?

A

15%

146
Q

What is your change of PE if the Wells score is 2-5?

A

29%

147
Q

What is your chance of PE if your Wells score is >6?

A

59%

148
Q

Only use D-Dimer when?

A

For low probability patients when ruling out DVT and low to mod probability when ruling out PE

149
Q

What imaging modalities are used to diagnose PE?

A

Chest CTA with contrast* CXR, VQ scan, pulm angiography

150
Q

“Hampton’s Hump Sign”

A

Wedge shaped infarction from PE seen on CXR

151
Q

CTA advantages for diagnosing PE

A

Readily available, fast, minimally invasive, can detect alternative diagnosis

152
Q

CTA disadvantages

A

Expensive, radiation exposure, C/I️ in pts with renal failure, contrast allergies and pregnancy

153
Q

Who is a CTA C/I️ in?

A

Renal failure, contrast allergies and pregnancy

154
Q

Venous ultrasonography relies on what?

A

The loss of vein compressibility, occasionally the thrombus can be directly visualized

155
Q

EKD features associated with PE

A

sinus tachycardia, S1, Q3, T3, complete or incomplete RBBB, non-specific ST or T wave changes

156
Q

What can an echocardiogram show for a PE?

A

Evidence of right heart strain, RV enlargement or RV dysfunction

157
Q

Approach to treatment of venous thromboembolism

A

Primary therapy: clot dissolution with thrombolytic or removal by embolectomy
Secondary: anticoagulation or placement of IVC filter

158
Q

Who are high risk patients for PE?

A

Hemodynamic instability, RV dysfunction, RV enlargement, elevated troponin

159
Q

What is the anticoagulation treatment for VTE?

A

Parenteral drug, can bridge to warfarin

160
Q

Which anticoag should cancer patients stay on?

A

LMWH long term

161
Q

Provoked clot antiocagulation period

A

3-6 mos

162
Q

Unprovoked clot anticoagulation period?

A

Indefinite anticoagulation

163
Q

What are the indications for an IVC filter?

A

Active bleeding, recurrent venous thrombosis despite intensive anticoags, high risk pts who cannot have fibrinolytics

164
Q

What are the complications for IVC filters?

A

Caval thrombosis causing marked bilateral leg swelling, double DVT rate

165
Q

Prevention of VTE

A

Heparin or LMWH at lower doses for hospitalized pts, warfarin used peri-operatively

166
Q

What are some major adverse outcomes of a PE?

A

Recurrent thromboembolism, pulmonary HTN, death

167
Q

What is defined as the abnormal elevation in pulmonary artery pressure?

A

Pulmonary HTN

168
Q

What is the normal PAP (pulmonary artery pressure)

A

8-20 mmHg measured by R heart catheterization

169
Q

Pulmonary HTN =

A

MEan pulmonary artery pressure >25mmHg

170
Q

PAH is characterized by what?

A

Dyspnea, chest pain, syncope

171
Q

Pulmonary HTN can be caused by which 3 things?

A
  1. Increased pulmonary vascular resistance
  2. Elevated L arterial pressure
  3. Increased pulmonary blood flow
172
Q

What is the patho behind PAH?

A

Progressive increase in RV afterload results in RV hypertrophy -> eventually RV dilates resulting in decreased contractility, CO will fall

173
Q

What is the first study to order for PAH?

A

Transthoracic echocardiogram

174
Q

PH is likely if the PASP is estimated at what?

A

> 50mmHg and tricuspid regurg velocity is >3.4 sec

175
Q

PH is unlikely is PASP is estimated what?

A

<36mmHg and tricuspid regurg is <2.8 sec

176
Q

What is the gold standard and necessary to diagnose PH?

A

R heart catheterizaiton

177
Q

What is R heart catheterization?

A

Catheter guided to right side and passes into pulmonary artery, measure pressure

178
Q

What does the R heart catheter measure the pressures of?

A

R atria, R ventricle and pulmonary artery

179
Q

What is the pulmonary capillary wedge pressure? (PCWP)

A

Indirect measurements of L heart pressures by inflating a balloon in the pulmonary artery

180
Q

What is group 1 pulmonary HTN?

A

Secondary to diseases that localize to small pulmonary arteries/arterioles

181
Q

What is group 2 PH?

A

Secondary to L heart disease

182
Q

What is group 3 PH?

A

Secondary to lung disease or hypoxemia

183
Q

What is group 4 PH?

A

Secondary to thromboembolic disease

184
Q

What is group 5 PH?

A

Unclear multifactorial mechanisms

185
Q

What is WHO?

A

World Health Organization, functional classification for pulmonary HTN

186
Q

What is the WHO 1 classification for pulmonary HTN?

A

No limitations of physical activity. No fatigue or dyspnea, chest pain, or heart syncope

187
Q

What is the WHO 2 classification for pulmonary HTN?

A

Slight limitation of physical activity, comfortable at rest. Ordinary physical activity results in undue fatigue or dyspnea, chest pain, or heart syncope

188
Q

What is the WHO 3 classification for pulmonary HTN?

A

Marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes undue fatigue or dyspnea, chest pain, or heart syncope

189
Q

What is the WHO 4 classification for pulmonary HTN?

A

Inability to carry on any physical activity without symptoms, signs of RHF. Dyspnea and/or fatigue may be present even at rest.

190
Q

Group 1 characteristics

A

Abnormalities in pulmonary endothelial and smooth muscle cells: vasoconstriction, vascular proliferation, thrombosis, inflammation

191
Q

What type of dysfunction effects the layers of vascular wall in group 1PH?

A

Vasoconstriction, vascular proliferation, thrombosis, inflammation

192
Q

What criteria must be met for someone to be in PH group 1?

A

Mean PAP >25 mmHg at rest, mean pulmonary capillary wedge pressure <15mmHg, chronic lung disease is mild to absent, VTE disease is absent, other disorders absent

193
Q

Causes of group 1 PH

A

Idiopathic, hereditary, drugs or toxins, connective tissue diseases, HIV, portal HTN, congenital heart disease

194
Q

What types of drugs or toxins cause group 1 PH?

A

Appetite suppressants, cocaine, amphetamines, meds

195
Q

What type of connective tissue diseases cause group 1 PH?

A

Systemic sclerosis, narrowing arteries/arterioles, interstitial fibrosis

196
Q

Group 1 PH caused by what?

A

LH disease: L atrial HTN requires increased pulm artery systolic pressure to maintain adequate driving force across pulm vasculature

197
Q

Causes of PH group 3?

A

COPD, interstitial lung disease, obstructive sleep apnea, other causes of hypoxemia

198
Q

Group 4 PH causes

A

Chronic thromboembolic disease, multiple small PE, decrease in function or blood vessels

199
Q

Group 5 PH causes

A

Pulm HTN with unclear mechanisms: hematologist disorders, systemic disorders, metabolic disorders, miscellaneous

200
Q

What type of hematologic disorders can cause PH group 5?

A

Myeloproliferative disorders

201
Q

Which systemic disorder can cause PH group 5?

A

Sarcoidosis

202
Q

What metabolic disorder can cases PH group 5?

A

Glycogen storage disease

203
Q

What miscellaneous disease can cause PH group 5?

A

Sickle cell disease

204
Q

What is the definition of cor pumonale?

A

Altered structure and/or impaired function of the RV that results from pulmonary HTN

205
Q

What are some causes of cor pulmonale?

A

Pulm disease (COPD), vasculature (PAH),, upper airway (OSA), chest wall (kyphoscoliosis)

206
Q

What is the patho of cor pulmonale?

A

RH failure from longstanding pulmonary HTN, RV hypertrophy develops due to high pressure, eventually RV loses contractility

207
Q

What is the main cause of death in patients with PAH?

A

Circulatory collapse (existence in group 1 PAH is bad prognosis)

208
Q

Si/sx of pulmonary HTN

A

DOE, dyspnea at rest in advanced disease, fatigue

209
Q

Si/sx of right heart failure

A

Angina, exertional syncope, peripheral edema, abdominal discomfort due to hepatic congestion

210
Q

Why is angina a sign of right heart failure?

A

R heart requires more oxygen

211
Q

Why does exertional syncope happen with right hear failure?

A

Inability to increase cardiac output

212
Q

What are some PE findings for pulmonary HTN?

A

Increased intensity of S2 in pulmonic area, RV failure widens S2 split, S3, high pitched sytsolic murmur of tricuspid regurg, elevated JVP, hepatomegaly, peripheral edema, ascites

213
Q

What diagnostic tests are used for pulm HTN?

A

CXR, EKG, Echo, PFTs, overnight oximetry, polysomnography, V/Q scan

214
Q

What is assessed in the echo for pulmonary HTN?

A

Assess PASP, R heart size and assess for L to R shunts, can diagnose LV dysfunction

215
Q

What are some echo results that would point to pulmonary HTN?

A

Enlarged RV, small D-shaped LV, flattened septum

216
Q

Treatment for pulmonary HTN?

A

Early id and treatment ideal, assess disease severity, primary: directed at underlying cause
Advanced: direct at PH itself

217
Q

What is the treatment for group 1 PAH?

A

No effective primary therapy, advanced therapy often needed

218
Q

PAH treatment

A

Diuretics, anticoagulation, CCBs, endothelin receptor blockers, PDE-5 inhibitors, prostacyclin, lung transplant

219
Q

What is the primary treatment for group 2 PH?

A

HF treatment

220
Q

What is the primary treatment for group 3 PH?

A

Treat underlying cause of hypoxemia and correction of hypoxemia with supplemental O2

221
Q

What is the primary treatment for group 4 PH?

A

Anticoagulation, surgical thromboendarterectomy for selected pts

222
Q

What is the primary treatment for group 5 PH?

A

Target specific underlying cause

223
Q

What are some things to consider in all groups for PH?

A

Diuretics treat fluid retention, O2 can benefit all groups, exercise

224
Q

Which groups of PH can anticoagulation be used for?

A

IPAH, hereditary PAH, drug-induced PAH or group 4 PH

225
Q

Digoxin improves what?

A

RV EF of pts with group 3 PH and helps control HR in pts who have SVTs associated with RV dysfunction

226
Q

Who is advanced therapy for?

A

Persistent PH and WHP class 2 3 or 4, should be administered at specialized centers where clinicians are experienced

227
Q

Group 1 PAH advanced therapy

A

First line

228
Q

Group 2 PH advanced therapy

A

Possibly harmful, L heart unable to handle increased flow

229
Q

Advanced therapy group 3 PH

A

Not FDA approved, not recommended, occasionally considered

230
Q

Advanced therapy in group 4 PH

A

Can be considered

231
Q

Advanced therapy in group 5 PH

A

Favorable response in sarcoidosis

232
Q

What is the vasoreactivity test?

A

Administration of short-acting vasodilator, measure hemodynamic response using RH catheter

233
Q

What agents are commonly used for the vasoreactivity test?

A

Epoprostenol, Adenosine, and inhaled Nitric Oxide

234
Q

What is the vasoreactivity test done for?

A

Pts who are selected for advanced therapy to determine if they will benefit from CCBs

235
Q

What is the treatment if the vasoreactivity test is positive?

A

Trial of oral CCBs, they are less expensive and fewer side effects than other therapies

236
Q

What is the treatment if the vasoreactivity test is negative?

A

Prostanoid formulations, endothelin receptor antagonists, PDE-5 inhibitors

237
Q

What are the benefits of using CCBs?

A

Prolonged survival, sustained functional improvement, Hemodynamic improvement

238
Q

Epoprostenol benefits

A

Improves hemodynamics, functional capacity, and survival in IPAH

239
Q

What is the only therapy that has been shown to prolong survival?

A

Epoprostenol

240
Q

What are the prostanoid formulations?

A

Epoprostenol, Treprostinil, Iloprost

241
Q

Endothelin receptor antagonists

A

Endothelin is a potent vasoconstrictor found in high concentrations in lungs of pts with IPAH and other group 1 PAH

242
Q

What are the endothelin receptor antagonists?

A

Bosentan, Macitentan, Ambrisentan, and Sitaxsentan

243
Q

What are the benefits for endothelin receptor antagonists?

A

Improve exercise capacity, dyspnea, and Hemodynamic measures

244
Q

What are the PDE-5 inhibitors?

A

Sildenafil, Tadalafil

245
Q

What are the benefits of the PDE-5 inhibitors?

A

Prolong vasodilatory effect of nitric oxide, also used to treat ED, improves pulmonary hemodynamics and exercise capacity

246
Q

What is the function of the guanylate cyclase stimulant?

A

NO receptor stimulators, increase sensitivity of receptor to NO, directly stimulate the receptor to mimic action of NO

247
Q

What is the example of the Guanylate cyclase stimulant?

A

Riociguat

Pulmonary (3 decks)

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