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RESP II Exam 1 > Lung Part 1 > Flashcards

Lung Part 1 Flashcards

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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
Cystic fibrosis
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
26
Diagnostic criteria of CF
Phenotypic characteristics or family history or positive infant screen AND Increased NaCl in sweat or 2 CFTR mutations or abnormal nasal ion transport
27
Treatment of CF
Pancreatic insufficiency - oral pancrelipase Vitamin deficiency - ADEK Pulmonary disease - percussion, bronchodilators, mucolytic agents, antibiotics, hypertonic saline, ibuprofen Liver transplants
28
Apparent Life Threatening Event
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
29
Atelectasis in neonate
Collapsed lung | Incomplete expansion
30
Atelectasis in adult
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
31
Atelectasis at risk for
Infection
32
Hemodynamic pulmonary edema
``` Most common **Left sided heart failure Basal lower lobes **Heart failure cells Secondary infections Chronic leads to brown induration of lung (fibrosis) ```
33
Microvascular injury pulmonary edema
Increased permeability - infection (pneumonia), injury (direct or indirect) **Can lead to ARDS
34
Acute lung injury
Acute onset of dyspnea Hypoxemia Bilateral infiltrates **Absence of Primary left-sided heart failure
35
Cause of acute lung injury
``` Numerous Injuries include: Congestion Surfactant disruption Atelectasis Pulmonary edema ``` May progress to ARDS, DAD or AIP
36
Acute ARDS
``` 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
Infectious cause of ARDS
Sepsis Pulmonary infection Gastric aspiration
38
Physical injury cause of ARDS
Mechanical trauma/head injury Contusions, drowning, burns, embolism, radiation
39
Inhaled irritants causing ARDS
Oxygen, smoke, gas/chemicals
40
Chemical injury causing ARDS
Paraquat
41
Reperfusion injury after transplant
Can lead to ARDS
42
50% of ARDS caused by
Sepsis Pulmonary infection Gastric aspiration Trauma
43
Clinical presentation of ARDS
Patients are already ill Profound dyspnea, tachypnea, cyanosis and respiratory failure Diffuse bilateral infiltrates on xray High mortality - permanent damage
44
Histology of ARDS
Collapsed alveoli | Hyaline membranes
45
Histology of lung recovering from ARDS
Lots of inflammatory cells, fibroblasts and collagen | Atypical type II pneumocytes
46
Acute interstitial pneumonia
Similar to ARDS but NO causative disorder | Acute respiratory failure following an illness
47
Obstructive chronic lung disease
Limit rate of flow FEV1/FVC ratio low Due to resistance at any level: Emphysema, chronic bronchitis, bronchiectasis, asthma
48
Restrictive chronic lung disease
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
Chronic bronchitis
``` Bronchus Gland hyperplasia and hypersecretion Airway inflammation Caused by inhaling irritants Productive cough ```
50
Bronchiectasis
Bronchus dilation and scarring Persistant infections Productive cough
51
Asthma
Bronchus Reversible obstruction SM hyperplasia, extra mucus and inflammation Episodic wheezing and cough
52
Emphysema
``` Acinus Airspace enlargement and wall destruction Overinflation Smoking Dyspnea ```
53
Small-airway disease, bronchiolitis
Bronchiole inflammation and scarring Caused by irritants Cough and dyspnea
54
Centriacinar/centrilobular emphysema
Caused by smoking!! Most common Upper lobes - bronchiole
55
Panacinar/panlobular emphysema
Anti-trypsin or smoking | Lower lobes - alveolus and duct
56
Distal acinar/paraseptal emphysema
May be bullous and cause spontaneous pneumothorax in young adults Associated with previously damaged lung
57
Irregular/paracicatrical emphysema
Common and focal | Asymptomatic with scarring
58
Emphysema pathophysiology
``` Proteolytic digestion of alveolar walls **Neutrophil-secreted elastase Free radicals inhibits the antiprotease Associated with alpha-1 antitrypsin deficiency **Made worse with smoking ```
59
Clinical presentation of emphysema
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
Compensatory hyperinflation
Loss of adjacent tissue but no wall destruction
61
Obstructive overinflation
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
Interstitial emphysema
Any air in the interstitium
63
Chronic bronchitis
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
Reid index
Thickness of glands/thickness of wall | Increased - glands are enormous
65
Asthma
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
Atopic asthma
Type 1 hypersensitivity Tendency to develop IgE antibodies Bronchial SM constricts in reaction to inflammatory mediators
67
Nonatopic asthma
Associated with infections and air pollutants | Infection lowers vagal response -> bronchospasm
68
Common cause of drug induced asthma
Aspirin | Increase leukotriene production -> leukotrienes favor bronchoconstriction
69
Asthma morphology
``` Overinflated lungs Airway remodeling: Goblet cell hyperplasia Subbasement membrane fibrosis Eosinophilic inflammation Muscle hypertrophy ```
70
Charcot-Leyden Crystals
Asthma (or allergic diseases) | Eosinophilic
71
Curschmann Spiral
Asthma | From shed epithelium
72
Bronchiectasis
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
Chronic interstitial lung disease
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
Fibrosing CILD
``` Usual interstitial pneumonia Nonspecific interstitial pneumonia Crytogenic organizing pneumonia CTD Pneumoconiosis Drugs Radiation ```
75
Granulomatous CILD
Sarcoidosis Hypersensitivity Eosinophilic pneumonias
76
Other CILD
Pulmonary alveolar proteinosis Pulmonary Langerhans cells histiocytosis Lymphoid interstitial pneumonia
77
Smoking related CILD
Desquamative | Bronchiolitis associated
78
Idiopathic pulmonary fibrosis
``` Usual interstitial pneumonia Repeated injury to alveolar wall Type 1 death Type 2 hyperplasia Inflammation with Th2 ``` **Smoking
79
Pathogenic mechanism leading to idiopathic fibrosis?
Increased signaling through the PI3K/AKT pathway -> activated fibroblasts
80
Clinical presentation of idiopathic pulmonary fibrosis
Dyspnea, dry cough, hypoxemia with cyanosis, digital clubbing Mean survival < 3 years Only treat with transplant
81
Pathology of idiopathic pulmonary fibrosis
Repeated cycles of alveolitis Predominently subpleural/interlobar and lower lobe Honeycomb lung
82
Nonspecific interstitial pneumonia
Dyspnea and cough for several months | Better prognosis, not as sick as UIP

RESP II Exam 1 (2 decks)

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