11.19: Pulm I Flashcards

1
Q

Which lung has three lobes?

A

Right

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2
Q

Which lung has the lingula?

A

Left

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3
Q

What does the trachea branch into?

A

Left and right bronchus

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4
Q

Which lung will items tend to get lodged in?

A
  • Right

- Right bronchus is in direct continuity with trachea where as the left bronchus branches off more

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5
Q

What lines the trachea?

A

Pseudo stratified Ciliated columnar epithelial cells

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6
Q

Is there cartilage in trachea?

A

Only on anterior side

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7
Q

What is difference between bronchus and bronchiole?

A
  • Bronchus has plates of cartilage and mucosal glands

- Bronchiole has neither

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8
Q

What does terminal bronchiole become?

A

Respiratory bronchiole > Alveolar duct > Alveolar sac made of alveoli

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9
Q

2 cell types in alveoli?

A

Type I cells: squamous pneumocytes conducting gas exchange
- Thin: good for exchange, 95% of surface
Type II cells: granular pneumocytes secreting surfactant

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10
Q

Where are blood vessels found?

A
  • In the alveolar septum
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11
Q

Which pneumocytes are not able to regenerate?

A
  • Type I

- Type II can regenerate if damaged and can become Type I cells in case of tissue damage

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12
Q

What changes in alveolar can lead to hypoxia?

A
  1. Reduction in alveolar surface area
  2. Increased distance to capillary
    3.
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13
Q

What is the mucociliary escalator?

A
  • Rhythmic beating of cilia pushing mucus from goblet cells up and out of airway
  • Cilia and goblet cells are present to the end of respiratory bronchioles
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14
Q

Where does the mucociliary escalator end?

A
  • Below the respiratory bronchioles
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15
Q

What is oligohydramnios?

A
  • Impairment of amniotic fluid in development usually form agenesis of kidney leading to failure of lung to develop properly
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16
Q

What happens in agenesis of diaphragm?

A

GI will bump into respiratory space giving lungs less room to develop

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17
Q

What is a bronchogenic cyst?

A
  • Foregut buds that become disconnected from bronchial tree and enlarge to form cysts
  • Can compress on structures causing SOB, cough
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18
Q

What is CCAM?

A

“Congenital cystic adenomatoid malformation”

  • Cysts lined with bronchial epithelium w/in lungs
  • Can obstruct breathing or cause infection
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19
Q

What is pulmonary sequestration?

A
  • Discrete mass of lung tissue w/o connection to airway
  • Has vascular supply but not connected to airways
  • Likely to get infected as mucus wont train as in normal escalator
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20
Q

What does atelectasis mean?

A

Collapse of lung

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21
Q

3 main types of adult atelectasis?

A
  1. Contraction: fibrosis
  2. Compression: effusion
  3. Resorption / obstruction
22
Q

What will obstruction of lung cause?

A
  • Air that was in alveoli absorbed into circulation and area of lung collapses as no air to keep it inflated
  • Mediastinum pulled towards compressed lung
23
Q

What happens in compression ?

A
  • Mediastinum shifts away from compressed lung

- Air, blood, pleural secondary to CHF

24
Q

Can contraction be fixed?

A
  • No, tissue is fibrotic
25
Q

What is pneumothorax?

A
  • Air in chest wall leading to respiratory distress via compression or collapse
  • TB, asthma, or emphysema often cause
  • Pushes mediastinum away from affected lung
26
Q

Where do aspirated items lodge?

A
  • Right lower lobe
27
Q

Causes of edema?

A
  1. Increased hydrostatic pressure
  2. Reduced osmotic pressure
  3. Lymphatic obstruction
  4. Na retention
  5. Inflammation
28
Q

What is edema?

A
  • Increased fluid in interstitial spaces
29
Q

What is most common cause of pulmonary edema?

A
  1. Left sided heart failure

2. Volume overload

30
Q

What does edema do to lung structure?

A
  • Makes them much heavier and distended
31
Q

What is acute lung injury?

A
  • Acute onset of dyspnea
  • Hypoxemia
  • Development of bilateral pulmonary infiltrate with absence of cardiac failure
  • Can progress to ARDS
32
Q

What is ARDS?

A

“Adult respiratory distress syndrome”

  • Rapid onset of deadly respiratory insufficiency
  • Cyanosis
  • Can lead to organ failure
  • Arterial hypoxia that does not respond to oxygen therapy
33
Q

Causes of ARDS?

A
"ARDS"
A - Aspiration, acute pancreatitis, air/amniotic embolism
R - Radiation
D - Drug overdose, DIC, Drowning
S - Shock, sepsis, smoke inhalation
34
Q

Symptoms of ARDS?

A
  • Tachypnea

- Dyspnea

35
Q

What is DAD?

A

“Diffuse alveolar damage”

- This is what ARDS results in

36
Q

How is ARDS different than acute, cardiogenic pulmonary edema?

A

Acute: increased hydrostatic pressure is the problem
ARDS: neutrophils move to alveoli causing epithelial injury causing proteins to leak into alveolar space

37
Q

What is hyaline membrane?

A
  • Thickening of septa between alveoli see in ARDS from proteins being released
  • Hyalinization blocks oxygenation
  • Diuretics cannot fix this as it can in pulmonary edema
38
Q

Characteristics of DAD?

A
  • Pneumocyte and endothelial cell necrosis
  • Edema that does not respond to diuretic
  • Hyaline membrane formation blocking exchange
  • Type II pneumocyte proliferation
39
Q

Fundamental abnormality in NRDS?

A

“Neonatal respiratory distress syndrome”

- Lack of surfactant resulting in failure of lungs to inflate at birth

40
Q

Causes of Neonatal RDS?

A
  1. Aspiration
  2. Cord compression
  3. Excessive sedation of mother
  4. Hyaline membrane disease
41
Q

Predisposing factors for NRDS?

A
  1. Prematurity
  2. C section
  3. Maternal diabetes
42
Q

Function of surfactant?

A
  • Stabilizes lung be reduces surface tension
  • Barrier for inhaled particles
  • Made by type II Pneumocytes
43
Q

Why is surfactant an issue in premature babies?

A
  • Surfactant is not secreted in sufficient amounts until 34 weeks old
  • Alveoli cannot stay inflated and will collapse
44
Q

Pathogenesis in NRDS?

A
  • Lack of surfactant leads to alveolar collapse
  • Blood travels to area that can’t be ventilated
  • Hypoxia and CO2 retention lead to acidosis leading to to vasoconstriction
  • Acidosis and hypoxia lead to cellular damage in lungs
45
Q

What can induce surfactant synthesis?

A

Glucocorticoids

46
Q

What can decrease surfactant production?

A

Insulin from diabetic mother

47
Q

How to control NRDS?

A
  • Delay labor as long as possible
  • Administer exogenous surfactant
  • Amniotic fluid analysis looking for lecithin:sphingomyelin ratio >2
48
Q

Complications of oxygen therapy in RRDS?

A
  1. Retinopathy

2. Bronchopulmonary dysplasia

49
Q

What causes ARDS?

A
  • Imbalance between pro and antiinflammatory mediators
50
Q

What is same findings as in DAD with no identifiable cause indicative of?

A
  • Acute interstitial pneumonia
51
Q

What is HMD?

A

“Hyaline membrane disease”

- Pathologic term for NRDS

52
Q

What does normal capillary wedge pressure rule out?

A

Pulmonary edema