Pulmonary Patho Flashcards

1
Q

How common is asthma in children?

A

Leading cause of acute and chronic illness in children and most frequent admitting diagnosis

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2
Q

What is asthma?

A

Reversible obstructive airway disease

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3
Q

What are the 3 mechanisms of asthma?

A
  1. Bronchospasms (obstruction)
  2. Inflammation and edema (mucus)
  3. Reactivity to variety of stimuli
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4
Q

High risk populations for asthma

A
  • African Americans and Hispanics
  • Live in inner city
  • Premature, low birth weight
  • Family history
  • Allergies
  • Eczema
  • Low SES
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5
Q

Intrinsic/Non-Allergic Asthma

A
  • Usually adult onset
  • No history of allergies
  • Respiratory infection/psychological
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6
Q

Extrinsic/Allergic Asthma

A
  • More in peds

- Triggers: pollen, dust, dust mites, cockroach droppings, drugs, chemicals, foods, MSG

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7
Q

Exercise induced asthma

A
  • Don’t have asthma attack until you exercise
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8
Q

Status asthmaticus

A
  • Cannot stop asthma attack

- Ongoing and life-threatening

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9
Q

Asthma Pathophysiology: early response

A

INFLAMMATORY

  • Allergen binds to IgE on mast cells
  • Mast cells degranulate
  • Mediators released: histamine, leukotrienes, prostaglandins, TNF, IL-1
  • Vasodilation, increased permeability, bronchospasm and edema and mucus secretion
  • Ach: released and leads to smooth muscle constriction and adds extra mucus
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10
Q

Asthma Patho: late response

A
  • 4-8 hours later
  • Continued recruitment of inflammatory process
  • Synthesize leukotrienes: prolong smooth muscle contraction
  • Eosinophils: direct tissue injury impaired mucociliary function
  • Accumulation of mucus and cellular debris form plug in airways
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11
Q

Asthma Chronic changes

A
  • Airway remodeling: changes to bronchial wall due to chronic inflammation
  • Basement membrane thickens and results in smaller airway
  • More mucus glands
  • Smooth muscle hypertrophy
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12
Q

Most common asthma clinical manifestations

A
  • Wheezing (vibrations through narrow airways)
  • Cough: often at night
  • Feelings of chest tightness
  • Sputum
  • Tachycardia = hypoxemia
  • Tachypnea
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13
Q

Severe clinical manifestations

A
  • Cyanosis
  • Retractions, nasal flaring
  • Decreased breath sounds
  • Agitation
  • Cannot speak in complete sentences
  • Pulsus paradoxus: decrease in systolic during inspiration
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14
Q

Asthma diagnosis

A
  • History and physical

- Pulmonary function tests: measuring obstruction

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15
Q

Asthma treatment

A
  • Asthma action plan
  • Manage allergens: patient education
  • Use peak flow meter to guide treatment at home
  • Pharm: maintenance
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16
Q

What is bronchiolitis?

A
  • Inflammation of bronchioles: lower resp tract, usually secondary to infectious agents
  • Related to RSV, influenza, bacteria
  • Seasonal: november to april
17
Q

Bronchiolitis Patho

A
  • Viral attack leads to necrosis of bronchial epithelium
  • Mucus production and obstruction
  • Chemical mediators released
  • Fibrin plugs
18
Q

Bronchiolitis changes to breathing mechanisms

A
  • Air trapping = hyperinflation
  • Decreased compliance = atelectasis (collapsing of airways)
  • Increased work of breathing
19
Q

Bronchiolitis Clinical manifestations

A
  • Rhinorrhea and tight cough
  • Decreased appetite, lethargy, fever
  • Tachypnea and respiratory distress (retractions)
  • Abnormal breath sounds: wheezing, rhonchi
  • Xray, hyper-expanded lungs, infiltrates, atelectasis
20
Q

Bronchiolitis Evaluation

A
  • History and physical
  • Chest x-ray
  • Nasal washing: specimen taken from nose to test for RSV
21
Q

Bronchiolitis Treatment

A
  • Supplemental oxygen
  • Increased hydration
  • Inhaled hypertonic saline: YES bronchodilators, steroids not as much
22
Q

What is a pulmonary embolus

A
  • Undissolved detached material that occludes blood vessels of the pulmonary vasculature
  • 90% originate from DVT but could also be fat, air, amniotic fluid
  • Virchow’s Triad: vessel wall injury, circulatory stasis, hyper coagulable conditions
  • Impact depends on size, area of circulatory impairment, health status of patient
23
Q

Patho of PE

A
  • Virchow’s triad leads to thrombus
  • Thrombus dislocates and travels to lungs
  • Leads to hypoxic vasoconstriction, decreased surfactant, atelectasis, edema
24
Q

Clinical manifestations of PE

A
  • Restlessness, apprehension, anxiety
  • Dyspnea
  • Chest pain
  • Tachycardia, tachypnea
  • Hemoptysis (maybe)
  • Progress to heart failure, shock, resp arrest
25
Q

Diagnosis of PE

A
  • History and physical: evidence of DVT, pulse ox, Virchow’s triad
  • Chest xray
  • ABG: oxygenation, will see low PaO2, low PCO2, high pH
  • Elevated D-dimer
  • CT
26
Q

Treatment of PE

A
  • Prevention: ROM
  • Resp support
  • Thrombolytic therapy and heparin