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Block 3 Found Sci > 4-Pulmonary Diseases > Flashcards

4-Pulmonary Diseases Flashcards

1
Q

obstructive disorders caused by what generally

A

inc resistance to airflow from changes in
1. properties of airway wall
2. lung parenchyma
3. airway lumen

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2
Q

airway wall diseases

A

asthma, acute and chronic bronchitis
-chronic inflamm

will obstruct airway lumen from conditions of wall

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3
Q

lung parenchyma diseases

A

emphysema, COPD

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4
Q

airway lumen disesases

A

cystic fibrosis, acute tracheobronchial obstruction (foreign objects), epiglottitis, croup

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5
Q

pathway of damage for COPD

A
  1. smoke/chemicals/ROS
  2. inflammation = chronic inflamm
  3. neutrophils activate
  4. inactivate antiproteases
  5. inc elastase activity (break down)
  6. tissue destruction

also hereditary def in a-1 antitrypsin = inc elastase

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6
Q

why expiration limited in COPD

A

combo of inc airway resistance + reduced airway tethering so more prone to collapse
-alveolar not emptied sufficiently so lung over inflates (barrel chest) > dec inspiratory capacity too

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7
Q

asthma definition

A

diffuse airway inflamm + inc airway responsiveness to variety of triggering stimuli
-partial or complete reversible bronchoconstriction

dyspnea + cough/wheezing/anxiety

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8
Q

asthma triggers

A
  1. exercise
  2. exposure to known allergen (extrinsic)
  3. no identifiable reason (intrinsic)
  4. exposure to rapid change in temp and humidity of inspired air
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9
Q

results of asthma inflammation

A
  1. mucus hypersecretin
  2. vasodilation
  3. damage to airway epithelliu
  4. epithelial shedding and fibrosis
  5. activation of cholinergic reflex = bronchoconstrict
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10
Q

asthma treatments

A
  1. acute reliever agents for bronchodilation
  2. controller treats to modify asthmatic airway environment to dec need for rescue treats, treat the inflammation
  3. beta adrenergic agonists to stimulate on bronchial SM to dilate
  4. anticholinergics
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11
Q

long term inflammation treatments

asthma

A
  1. inhaled corticosteroids
  2. antileukotrienes
  3. long acting beta agonists
  4. theophylline
  5. systemic corticosteroids
  6. anti IgE treatment
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12
Q

restrictive disorders caused by what generally

A

dec ability to expand chest/lungs from changes in
1. lung parenchyma
2. pleura
3. chest wall
4. neuromuscular function

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13
Q

fibrotic interstitial lung dz

A

disorders of alveoli/ducs/respir bronchioles

  1. diffuse interstitial lung dz
  2. sarcoidosis
  3. hypersensitivity pneumonitis
  4. occupational lung dz

any long exposure to noxiuos agents

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14
Q

atelectatic disorders

A

disorders of alveoli/ducts/respir bronchioles
1. acute respir distress syndrome
2. infant respir distress syndrome

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15
Q

pleural effusion characteristics

A
  1. inc capillary hydrostatic P from heart failure
  2. dec plasma protein from kidney/liver dz
  3. inc vascular permeability from inflamm
  4. impaired lymphatic drainage from tumors
  5. fluid from ab cavity from diaphragm dysfxn

inc fluid in intrapleural space

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16
Q

pneumothorax

A

from blunt force trauma or spontaneous so air into intrapleural space

17
Q

neuromusclar disorders

A
  1. poliomyelitis
  2. amyotropic lateral sclerosis ALS
  3. muscular dystrophy
  4. guillain barre syndrome
  5. myasthenia gravis
18
Q

deformities/restrictions of thorax

A
  1. kyphoscholiosis
  2. pectus excavatum
  3. obesity or preg
19
Q

infections

A
  1. pneumonia
  2. pulmonary TB
  3. hypersensitivity pneumonitis
  4. flu
20
Q

inflammation of lung tissue

A

severe acute respir distress syndrome

21
Q

how to dx ARDS

A
  1. moderate/severe dyspnea
  2. relevant history (COVID)
  3. dec in PaO2 refractory/response to O2 therapy aka hypoxic even though receiving 100% O2
22
Q

causes of ARDS

A
  1. sepsis
  2. aspiration of gastric acid
  3. severe trauma
  4. infection
  5. exposure to toxins
  6. drowning
23
Q

key pathologic features of ARDS

A
  1. damage to alveolar/cap membrane
  2. noncardiogenic pulmonary edema from inc permeability of alveoli so widespread alveolar infiltrates
  3. atelectasis with lack of surfactant
  4. fibrosis with inflamm deposition of proteins (not all cases)
  5. dec perfusion and or thrombosis
24
Q

common clinical signs ARDS

A
  1. dec lung compliance/atelectasis from loss surfactant
  2. dec function residual capacity from dec lung vol
  3. severe hypoxemia from V/Q mismatch
  4. severe dyspnea from changes in complinace and inc drive to breathe from hypoxemia
  5. fluffy alveolar infiltrates ‘white out’ on x ray
25
Q

treating ARDS

A

enhance tissue oxygenation until inflamm resolves
1. maintain fluid/electrolyte balance
2. block infamm cells
3. supplemental oxygen but can be toxic
4. mechanical vent but requires heavy sedation
5. airway pressure release ventilation/ PEEP-a but may reduce CO
6. inhale vasodilator but not lasting effect

Block 3 Found Sci (60 decks)

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