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RESP II Exam 1 > Lung Part 1 > Flashcards

Lung Part 1 Flashcards

1
Q

Cells in trachea/bronchus

A

Goblet cell
Seromucous gland
Cartilage

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2
Q

Cells in bronchiolus

A

Clara cell - exocrine cells

No cartilage, goblet cells or seromucous glands

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3
Q

Cells in alveolus

A

Type 1 pneumocyte (95%)

Type 2 pneumocyte (5%)

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4
Q

Lobule

A

Cluster of terminal bronchioles with attached acini

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5
Q

Acinus

A

Respiratory bronchiole and all attached alveolar ducts and alveolar sacs

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6
Q

Pulmonary hypoplasia

A

Common - 10% neonatal autopsy

Seen with fetal compression and with other anomalies

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7
Q

Tracheoesophageal Fistula

A

Most common form is blind ended proximal and distal end opening into trachea

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8
Q

Congenital foregut cysts

A

Mediastinal and hilar locations
Maldeveloped foregut, usually bronchogenic with respiratory epithelium
Not connected to the airways

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9
Q

Congenital Cystic Adenomatoid Malformation

A

CPAM
Hamartomatous lesion with abnormal bronchiolar tissue
Larger cysts have better prognosis because they aren’t associated with other congenital abnormalities

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10
Q

Bronchopulmonary Sequestrations

A

Areas of lung without normal connection to airways

Blood supply is from systemic arteries

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11
Q

Extralobar sequestrations

A

External to lung (thorax or mediastinum)

May have other congenital anomalies

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12
Q

Intralobar sequestrations

A

Within lung

Associated with recurrent local infection and/or bronchiectasis
Most likely an acquired lesion

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13
Q

Cause of respiratory distress in newborns

A 
Excessive maternal sedation
Fetal head injury
Blood or amniotic fluid aspiration
Intrauterine hypoxia from nuchal cord
**Hyaline membrane disease
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14
Q

NRDS - Hyaline Membrane Disease

A

Rate inversely proportional to gestational age
Immaturity of lungs
Deficiency of pulmonary surfactant
Associated with male sex, maternal diabetes mellitus, multiple gestation and C-section before onset of labor

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15
Q

How does insulin effect surfactant

A

Inhibits secretion

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16
Q

How do glucocorticoids and thyroxine effect surfactant

A

Increase secretion

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17
Q

Lungs 20 weeks gestation

A

Glandular

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18
Q

Lungs 30 weeks gestation

A

Saccular

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19
Q

Lungs at term

A

Alveolar

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20
Q

Surfactant

A

From type II pneumocytes
Made of phospholipids and glycoproteins

Methods:
***Thin layer chromatography
Flourescence polarization
Foam stability index
Lamellar body count
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21
Q

L/S ratio

A

Lung to surfactant ratio
>2 at term
1 at less than 32 weeks

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22
Q

Clinical presentation of RDS

A 
Preterm and AGA
Male sex, maternal DM, C-section
Low APGAR
May need resuscitation
Then may do well for short time (< 1 hour)
Become cyanotic
Fine pulmonary rales (crackles)
Reticulonodular/ground glass chest x-ray
Oxygen therapy needed
Death or recovery in 3 – 4 days

Not seen in still born

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23
Q

Clinical course of RDS

A

Administration of surfactant (<26-28 weeks)
Antenatal treatment with steroids (24-34 weeks)
Monitor amniotic fluid surfactant for lung maturity
Death now unusual
Recovery begins at about 4 days
Therapy with O2 carries risks:
Retinopathy of prematurity
Bronchopulmonary dysplasia

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24
Q

Bronchopulmonary Dysplasia

A

> 28 days of O2 therapy in infant > 36 weeks post-menstrual age

Alveolar hypoplasia and thickened walls

O2 decreases lung maturation
**Developmental arrest at saccular stage

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25
Q

Cystic fibrosis

A

Disorder in epithelial transport affecting fluid secretion in exocrine glands and the epithelial lining of the respiratory, gastrointestinal, and reproductive tracts

Viscid mucus
Autosomal recessive - cystic fibrosis transmembrane conductance regulator (CFTR) gene

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26
Q

Diagnostic criteria of CF

A

Phenotypic characteristics or family history or positive infant screen

AND

Increased NaCl in sweat or 2 CFTR mutations or abnormal nasal ion transport

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27
Q

Treatment of CF

A

Pancreatic insufficiency - oral pancrelipase
Vitamin deficiency - ADEK
Pulmonary disease - percussion, bronchodilators, mucolytic agents, antibiotics, hypertonic saline, ibuprofen
Liver transplants

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28
Q

Apparent Life Threatening Event

A

Infants resuscitated from ALTE are at increased risk of future respiratory death

Have prolonged apnea and diminished response to hypercarbia and hypoxia

Often premature or mechanical disorders

Not considered SIDS

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29
Q

Atelectasis in neonate

A

Collapsed lung

Incomplete expansion

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30
Q

Atelectasis in adult

A

Acquired collapsed lung
Resorption (obstruction) - Mediastinal shift toward involved lung
Compression (external pressure like tension pneumo) - Mediastinal shift away from involved lung
Contraction (secondary to fibrosis) - irreversible

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31
Q

Atelectasis at risk for

A

Infection

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32
Q

Hemodynamic pulmonary edema

A 
Most common
**Left sided heart failure
Basal lower lobes
**Heart failure cells
Secondary infections
Chronic leads to brown induration of lung (fibrosis)
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33
Q

Microvascular injury pulmonary edema

A

Increased permeability - infection (pneumonia), injury (direct or indirect)
**Can lead to ARDS

34
Q

Acute lung injury

A

Acute onset of dyspnea
Hypoxemia
Bilateral infiltrates
**Absence of Primary left-sided heart failure

35
Q

Cause of acute lung injury

A 
Numerous
Injuries include:
Congestion
Surfactant disruption
Atelectasis
Pulmonary edema

May progress to ARDS, DAD or AIP

36
Q

Acute ARDS

A 
Shock Lung = Acute Alveolar/Lung Injury
Patients with severe disease
Diffuse damage to alveolar capillary walls (inflammatory mediators -> neutrophil migration)
**Secondary loss of surfactant
Microthrombi
37
Q

Infectious cause of ARDS

A

Sepsis
Pulmonary infection
Gastric aspiration

38
Q

Physical injury cause of ARDS

A

Mechanical trauma/head injury

Contusions, drowning, burns, embolism, radiation

39
Q

Inhaled irritants causing ARDS

A

Oxygen, smoke, gas/chemicals

40
Q

Chemical injury causing ARDS

A

Paraquat

41
Q

Reperfusion injury after transplant

A

Can lead to ARDS

42
Q

50% of ARDS caused by

A

Sepsis
Pulmonary infection
Gastric aspiration
Trauma

43
Q

Clinical presentation of ARDS

A

Patients are already ill
Profound dyspnea, tachypnea, cyanosis and respiratory failure
Diffuse bilateral infiltrates on xray
High mortality - permanent damage

44
Q

Histology of ARDS

A

Collapsed alveoli

Hyaline membranes

45
Q

Histology of lung recovering from ARDS

A

Lots of inflammatory cells, fibroblasts and collagen

Atypical type II pneumocytes

46
Q

Acute interstitial pneumonia

A

Similar to ARDS but NO causative disorder

Acute respiratory failure following an illness

47
Q

Obstructive chronic lung disease

A

Limit rate of flow
FEV1/FVC ratio low
Due to resistance at any level:
Emphysema, chronic bronchitis, bronchiectasis, asthma

48
Q

Restrictive chronic lung disease

A

Low TLC and RV
Nearly normal flow rates
FEV1/FVC ratio low but levels are low
Chest wall disorders, obesity, ARDS, interstitial fibrosis, pneumoconioses

49
Q

Chronic bronchitis

A 
Bronchus
Gland hyperplasia and hypersecretion
Airway inflammation
Caused by inhaling irritants
Productive cough
50
Q

Bronchiectasis

A

Bronchus dilation and scarring
Persistant infections
Productive cough

51
Q

Asthma

A

Bronchus
Reversible obstruction
SM hyperplasia, extra mucus and inflammation
Episodic wheezing and cough

52
Q

Emphysema

A 
Acinus
Airspace enlargement and wall destruction
Overinflation
Smoking
Dyspnea
53
Q

Small-airway disease, bronchiolitis

A

Bronchiole inflammation and scarring
Caused by irritants
Cough and dyspnea

54
Q

Centriacinar/centrilobular emphysema

A

Caused by smoking!!
Most common
Upper lobes - bronchiole

55
Q

Panacinar/panlobular emphysema

A

Anti-trypsin or smoking

Lower lobes - alveolus and duct

56
Q

Distal acinar/paraseptal emphysema

A

May be bullous and cause spontaneous pneumothorax in young adults
Associated with previously damaged lung

57
Q

Irregular/paracicatrical emphysema

A

Common and focal

Asymptomatic with scarring

58
Q

Emphysema pathophysiology

A 
Proteolytic digestion of alveolar walls
**Neutrophil-secreted elastase
Free radicals inhibits the antiprotease
Associated with alpha-1 antitrypsin deficiency
**Made worse with smoking
59
Q

Clinical presentation of emphysema

A

Airspaces enlarge and then collapse - expiration is difficult
Barrel chest, dyspnea, wheezing
Low FEV1 (bronchiole collapse and fibrosis), high TLC and RV
**Pink puffer
**Bullous emphysema and pneumothorax
Acidosis

60
Q

Compensatory hyperinflation

A

Loss of adjacent tissue but no wall destruction

61
Q

Obstructive overinflation

A

Trapped air

1) object causing obstruction
2) collaterals feeding around obstruction -> life threatening
(pores of kohn, canals of Lambert)
3) congenital -> lack of cartilage

62
Q

Interstitial emphysema

A

Any air in the interstitium

63
Q

Chronic bronchitis

A

3 months of productive cough/year for 2 consecutive years
SMOKING
Hypersecretion
Increased Reid index
Bronchiolitis obliterans in small airways

Secondary infections, cor pulmonale, dyspnea on exertion
**Blue bloaters

64
Q

Reid index

A

Thickness of glands/thickness of wall

Increased - glands are enormous

65
Q

Asthma

A

Episodic, partially reversible bronchoconstriction
Recurrent wheezing/breathlessness/chest tightness and cough
**Can progress to acute severe asthma and death
Increasing incidence, cause not always found

66
Q

Atopic asthma

A

Type 1 hypersensitivity
Tendency to develop IgE antibodies
Bronchial SM constricts in reaction to inflammatory mediators

67
Q

Nonatopic asthma

A

Associated with infections and air pollutants

Infection lowers vagal response -> bronchospasm

68
Q

Common cause of drug induced asthma

A

Aspirin

Increase leukotriene production -> leukotrienes favor bronchoconstriction

69
Q

Asthma morphology

A 
Overinflated lungs
Airway remodeling:
Goblet cell hyperplasia
Subbasement membrane fibrosis
Eosinophilic inflammation
Muscle hypertrophy
70
Q

Charcot-Leyden Crystals

A

Asthma (or allergic diseases)

Eosinophilic

71
Q

Curschmann Spiral

A

Asthma

From shed epithelium

72
Q

Bronchiectasis

A

Permanent dilation
Tissue destruction secondary to infection
Dyspnea, orthopnea and rarely severe hemoptosis but foul smelling sputum
Associated with cystic fibrosis, obstruction, infections

Chronic inflammation, sequestration, transplant rejection, and aspergillus

73
Q

Chronic interstitial lung disease

A

X-ray reticulonodular or ground glass
Restrictive -> decreased TLC and RV
Dyspnea, tachypnea, cyanosis, end-inspiratory crackles
End stage -> honeycomb lung
Can lead to pulmonary HTN and cor pulmonale

74
Q

Fibrosing CILD

A 
Usual interstitial pneumonia
Nonspecific interstitial pneumonia
Crytogenic organizing pneumonia
CTD
Pneumoconiosis
Drugs
Radiation
75
Q

Granulomatous CILD

A

Sarcoidosis
Hypersensitivity
Eosinophilic pneumonias

76
Q

Other CILD

A

Pulmonary alveolar proteinosis
Pulmonary Langerhans cells histiocytosis
Lymphoid interstitial pneumonia

77
Q

Smoking related CILD

A

Desquamative

Bronchiolitis associated

78
Q

Idiopathic pulmonary fibrosis

A 
Usual interstitial pneumonia
Repeated injury to alveolar wall
Type 1 death
Type 2 hyperplasia
Inflammation with Th2

**Smoking

79
Q

Pathogenic mechanism leading to idiopathic fibrosis?

A

Increased signaling through the PI3K/AKT pathway -> activated fibroblasts

80
Q

Clinical presentation of idiopathic pulmonary fibrosis

A

Dyspnea, dry cough, hypoxemia with cyanosis, digital clubbing
Mean survival < 3 years

Only treat with transplant

81
Q

Pathology of idiopathic pulmonary fibrosis

A

Repeated cycles of alveolitis
Predominently subpleural/interlobar and lower lobe
Honeycomb lung

82
Q

Nonspecific interstitial pneumonia

A

Dyspnea and cough for several months

Better prognosis, not as sick as UIP

RESP II Exam 1 (2 decks)

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