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Cardiovascular > Unit 3 Day 7 (Wed 4/29) > Flashcards

Unit 3 Day 7 (Wed 4/29) Flashcards

1
Q

Two Major Causes of Airflow Obstruction

A
  • intrinsic airway narrowing

- floppy airways

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2
Q

Two Major Causes of Airflow Obstruction

A
  • intrinsic airway narrowing

- floppy airways

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3
Q

How does airflow obstruction increase lung volumes?

A

Incomplete emptying of alveoli (breath stacking, gas trapping)

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4
Q

Anatomy Obstructed in Upper Airway Obstruction

A

-trachea

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5
Q

Anatomy Obstructed in Bronchitis

A

-bronchi

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6
Q

Anatomy Obstructed in Asthma and Bronchiectasis

A

-bronchioles

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7
Q

Anatomy Obstructed in Bronchiolitis

A

-respiratory bronchioles

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8
Q

Anatomy Obstructed in Emphysema

A

-alveolar sacs

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9
Q

Asthma Definition and Features

A

• Chronic inflammatory disorder of the airways
• Airway hyper responsiveness
– recurrent episodes of wheezing
– chest tightness
– coughing particularly at night or in the early morning.
• Episodes associated with airflow obstruction
• Reversible spontaneously or with treatment.
• Exacerbations with exposure to:
– Exercise
– Cold air
– Allergens
– Air pollution
– Infection
• normal to increased DLCO
• Bronchoprovocation demonstrates hyperreactivity

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10
Q

PV Curve in Acute Asthma

A

-PV curve slightly elevated and left, normal shape

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11
Q

Intermittent Class of Asthma

A
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12
Q

Mild Persistent Class of Asthma

A

> 2 sx per week, 2 night sx per month

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13
Q

Moderate Persistent Class of Asthma

A

-daily sx, multiple exacerbations per week

> once per week night sx

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14
Q

How does airflow obstruction increase lung volumes?

A

Incomplete emptying of alveoli (breath stacking, gas trapping)

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15
Q

Anatomy Obstructed in Upper Airway Obstruction

A

-trachea

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16
Q

Chronic Bronchitis- Basics

A

• Productive cough at least 3 months over the past 2 years without other cause”
• Increased airways resistance due to changes in airway structure (edema, mucus, fibrosis)”
– May have overlapping features with asthma”
• Impaired ventilation
-minimally reversible

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17
Q

Anatomy Obstructed in Asthma and Bronchiectasis

A

-bronchioles

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18
Q

Anatomy Obstructed in Bronchiolitis

A

-respiratory bronchioles

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19
Q

Anatomy Obstructed in Emphysema

A

-alveolar sacs

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20
Q

Asthma Definition and Features

A

• Chronic inflammatory disorder of the airways
• Airway hyper responsiveness
– recurrent episodes of wheezing
– chest tightness
– coughing particularly at night or in the early morning.
• Episodes associated with airflow obstruction
• Reversible spontaneously or with treatment.
• Exacerbations with exposure to:
– Exercise
– Cold air
– Allergens
– Air pollution
– Infection
• normal to increased DLCO
• Bronchoprovocation demonstrates hyperreactivity

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21
Q

PV Curve in Acute Asthma

A

-PV curve slightly elevated and left, normal shape

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22
Q

Intermittent Class of Asthma

A
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23
Q

Mild Persistent Class of Asthma

A

> 2 sx per week, 2 night sx per month

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24
Q

Moderate Persistent Class of Asthma

A

-daily sx, multiple exacerbations per week

> once per week night sx

25
Q

Severe Persistent Class of Asthma

A
  • continual sx, constant limitation of activity, frequent exacerbations
  • frequent night sx
26
Q

Vocal Cord Dysfunction- All Info

A

• Inappropriate vocal cord motion results in airflow obstruction”
• Variable extrathoracic obstructive pattern due to adduction of vocal cords during inspiration”
• Symptoms mimic asthma” – Shares similar triggers”
• Stridor mistaken for wheezes”
• Often coexists with asthma”
• Flow-volume loop suggestive
• Diagnosed by fiberoptic laryngoscopy”
• Bronchoprovocation studies can exacerbate VCD.”
– VCD may worsen with bronchoprovocation, but will not change FEV1 or PC20 “
• Acute treatment is anxiolytics, helium-oxygen mixture”
• Long term treatment is speech therapy, underlying triggers”
• Avoid over treating asthma”

27
Q

COPD Basics

A
  • COPD is defined by fixed airflow limitation”

* FEV1/FVC

28
Q

Chronic Bronchitis- Basics

A

• Productive cough at least 3 months over the past 2 years without other cause”
• Increased airways resistance due to changes in airway structure (edema, mucus, fibrosis)”
– May have overlapping features with asthma”
• Impaired ventilation

29
Q

Chronic Bronchitis PV Curve

A
  • a little up and left of normal curve

- normal shape

30
Q

Emphysema Pathogenesis

A

• Loss of normal alveolar spaces with enlargement of distal airspaces (acini)
• Increased compliance of the lung”
– Decreased elastic tissue”
– Loss of balance between proteases and anti-proteases in lung (alpha-1-antitrypsin deficiency)”
– Increased apoptosis of alveolar cells”
– Impaired repair mechanisms”
• Impaired gas exchange”

31
Q

Allergen Immunotherapy

A
  • potential therapy to modify disease by inducing specific allergen tolerance; tends to be more effective in managing allergic rhinitis and conjunctivitis than asthma
  • requires parenteral (sub Q) administration
32
Q

Chronic Bronchitis Physical Exam

A 
–  Cough"
–  Rhonchi" 
–  Wheezing"
–  Prolonged expiratory phase" 
–  Pursed-lip breathing"
–  Tri-pod position"
33
Q

Sustained Release Theophylline

A

-limited use due to adverse effect profile
• administered by the oral or intravenous
route
• onset of action: 30 - 60 minutes
• metabolism: half-life 7 hours; hepatic
metabolism
• duration of action: 12 - 24 hours after
single dose
• mechanism of action: inhibition of
phosphodiesterase
• beneficial effect: bronchodilator effect
and some anti-inflammatory activity
• adverse effect:
caffeine-like effects such as irritability,
gastrointestinal distress.
very narrow therapeutic range and requires
blood level monitoring to individualize dose. Significant adverse effects can include
seizures and irreversible neurologic damage. Multiple DDIs

34
Q

Acute Exacerbation of COPD

A
  • Increased cough”
  • Sputum volume and purulence”
  • Increased wheezing”
  • Worsening obstruction on PFT s”
  • UnchangedCXR”
  • Precipitated by infection, pollution, PE, unknown factors”
  • Increased work of breathing due to hyperinflation, increased airway resistance”
  • Treated with bronchodilators, steroids, antibiotics”
35
Q

Causes of Death From COPD

A
  • Respiratory failure”
  • Right ventricular failure”
  • Pneumonia”
  • Spontaneous pneumothorax” • Pulmonary embolism”
36
Q

Bronchiectasis Presentation

A
  • Cough productive of purulent sputum”
  • Sputum volume often copious—especially during an exacerbation”
  • Wheezing, hemoptysis “
  • May be either localized or diffuse”
  • Mucociliary escalator stops working…”
37
Q

Pathophysiology of Bronchiectasis

A

• Requires a combination of:”
– An infectious or inflammatory insult”
– Impaired drainage, obstruction or immunodeficiency”
• Loss of airway wall integrity with dilation”
• May be due to congenital structural anomalies “
• Recurrent infections worsen bronchiectasis”
• Dilated, collapsible airways result in
obstruction”
• May be compounded by inflammation”

38
Q

Management of Bronchiectasis

A
  • Airway clearance – to promote clearance of secretions”
  • Antibiotics – may be intermittent, chronic, or rotating courses.”
  • Treat reactive airways disease” – Bronchodilators, corticosteroids”
39
Q

Long Term Control Asthma Medications

A
  • inhaled glucocorticoids
  • long acting inhaled beta 2 agonists
  • leukotriene modifiers
  • omalizumab (anti-IgE)
40
Q

Inhaled Glucocorticoids

A

-prefferred long term control medication for treatment for persistent asthma

41
Q

Long Acting Inhaled Beta 2 Agonists

A

-preferred supplementary long term control agents for use with inhaled glucocorticoids

42
Q

Omalizumab

A

-biologic response modifier

43
Q

Allergen Immunotherapy

A

-potential therapy to modify disease by inducing specific allergen tolerance; tends to be more effective in managing allergic rhinitis and conjunctivitis than asthma

44
Q

Tiotropium

A

-long acting anticholinergic approved for COPD but not asthma

45
Q

Sustained Release Theophylline

A

-limited use due to adverse effect profile

46
Q

Quick Relievers in Asthma

A
  • short acting beta 2 agonists
  • anticholinergics
  • systemic glucocorticoids
47
Q

Short Acting Beta 2 Agonists

A

-preferred tx to relieve sx and prevent exercise induced asthma

48
Q

Anticholinergics

A
  • approved for use in COPD but not asthma

- used as secondary reliever for significant asthma exacerbations

49
Q

Systemic Glucocorticoids

A

-used to manage severe acute asthma exacerbations and occasionally for continued use in managing severe asthma

50
Q

Beta Adrenergic Agonists

A

• Clinical pharmacology: albuterol, terbutaline, salmeterol, formoterol. Used to treat asthma
and COPD.
– administered by the inhaled, injectable, and oral route
– rapid onset of action: minutes for albuterol and formoterol (slightly longer for salmeterol)
– duration of action:
• quick relievers: 4 - 6 hours (albuterol)
• long-term controllers: long acting ß-agonists last
approximately 12 hours (salmeterol, formoterol); used to prevent asthma symptoms.
• mechanism of action: ß-adrenergic receptor stimulation
• beneficial effect: bronchodilation via smooth muscle relaxation; inhibits production of respiratory secretions

51
Q

Anticholinergics

A

• Clinical pharmacology: atropine, ipratropium,
tiotropium; approved for use in COPD but not in
asthma
– administered by the inhaled route
– rapid onset of action: minutes
• duration of action:
– Quick relievers: up to 6 hours (ipratropium)
– Long-term controllers: up to 12 hours (tiotropium)
• mechanism of action: cholinergic receptor inhibition
• beneficial effect - bronchodilation via
smooth muscle relaxation
– inhibits production of respiratory secretions

52
Q

Systemic Glucocorticoids

A

Clinical pharmacology: hydrocortisone, prednisone, prednisolone, methylprednisolone. Used to treat acute exacerbations of asthma.
• administered by the oral or parenteral route
• onset of action: 30 - 60 minutes
• metabolism: half-life 2 -3 hours
• peak of action: approximately 8 hours
• duration of action:
– hydrocortisone - 12-24 hours
– prednisolone, methylprednisolone - 36-48
hours
• mechanism of action: phospholipase inhibition;
inhibition of cytokine synthesis
• beneficial effect :
– anti-inflammatory - reduces cellular infiltration, particularly eosinophils, mast cells, lymphocytes
– vasoconstrictor - reduces edema

53
Q

Inhaled Glucocorticoids

A

• Used as the preferred long-acting control agent to treat asthma and for the treatment of COPD, if repeated COPD exacerbations noted.
• administered by the inhaled route
• onset of action: 30 - 60 minutes
• metabolism: half-life 2 -3 hours for most except fluticasone (7 hours)
• peak of action: approximately 8 hours for single dose; approximately 4 weeks for continued administration.
• duration of action: requires once to twice daily administration to maintain effect
• mechanism of action: phospholipase inhibition; inhibition of cytokine synthesis
• beneficial effect
– anti-inflammatory - reduces cellular infiltration,
particularly eosinophils, mast cells,
lymphocytes;
– vasoconstrictor - reduces edema

54
Q

Long Acting Beta Adrenergic Agonists (LABA)

A

– Salmeterol and formoterol - Clinical pharmacology
– administered by the inhaled route
– onset of action: 15 minutes
– duration of action: 8 -12 hours after single
dose
– mechanism of action: ß-adrenergic
receptor stimulation
• beneficial effect- bronchodilator effect
• Black Box warning due to an observed
increase in asthma-related deaths noted in a post-marketing study.
Should not be used as monotherapy for asthma since long-acting ß-adrenergic agonists (LABA) do not reduce inflammation. LABA should be combined with an inhaled corticosteroid to control the inflammation component

55
Q

Particle Size For Inhaled Medications

A

1-5 um in size allows particles to reach lung

56
Q

Leukotriene Modifiers

A 
•  administered by the oral route
•  onset of action: 30 - 60 minutes
•  metabolism: half-life 6 hours; hepatic metabolism
•  duration of action: 12-24 hours
• mechanism of action:
leukotriene D4 antagonist – montelukast,
zafirlukast
5-lipoxygenase inhibition – zileuton
• beneficial effect
bronchodilator effect
anti-inflammatory effect due to leukotriene
blocking effect
attenuates exercise-induced asthma
57
Q

Cromolyn / Nedocromil

A

• administered by the inhaled route
• half-life: 20 minutes; excreted unchanged
• mechanism of action: inhibition of mast cell mediator release
• beneficial effect
preventative therapy for exercise-induced asthma can prevent allergen-induced pulmonary response

58
Q

Classification of COPD

A
  • GOLD 1: mild, FEV > 80% predicted
  • GOLD 2: moderate, FEV1 > 50% predicted
  • GOLD 3: severe, FEV2 > 30% predicted
  • GOLD 4: very severe. FEV1
59
Q

COPD Tx

A

§ Smoking cessation has the greatest capacity to influence the natural history of COPD. Health care providers should encourage all patients who smoke to quit.
§ Pharmacotherapy and nicotine replacement reliably increase long-term smoking abstinence rates.
§ All COPD patients benefit from regular physical activity and should repeatedly be encouraged to remain active.

Cardiovascular (29 decks)

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