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SRNAAnatomy II > Pulmonary 3 > Flashcards

Pulmonary 3 Flashcards

1
Q

Environmental inhales diseases

A

CO (carbon monoxide)
• Sulfur Oxides
• Nitrogen Oxides
• Hydrocarbons

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2
Q

CO2 Binds to Hb with

– No change in PaO2

A

200x the affinity of O2

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3
Q

Increases O2 affinity of remaining Hb =

A

does not release O2 readily to the tissues – dissociation curve shifted to the Left

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4
Q

CO poisoning

A

– Oxygen saturation % PaO2 high despite impaired oxygen deliver

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5
Q

CO poisoning : Dx by

A

measuring carboxyhemoglobin levels

– index of suspicion

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6
Q

Treatment of Co poisoning

A

No cyanosis, no tachypnea

– Tx: 100% FiO2

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7
Q

Nitrogen oxides –

A

produced when fossil fuels
burned at high temp. - yellow haze of smog, irritant
= tracheitis, bronchitis, pulmonary edema

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8
Q

Sulfur oxides – corrosive/poisonous – produced by

A

burning burning sulfur containing containing fuels @ power stations stations = chronic bronchitis, pulmonary edema

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9
Q

Hydrocarbons – unburned fuels in exhaust, UV light

reacts

A

produces photochemical oxidants (ozone,
aldehydes) greeenhouse effect – inhibit convective
processes & trap pollution at street level (LA basin)

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10
Q

Cigarette Smokingg

A

Contains 4% CO – raises carboxyhemoglobin in smoker’s blood to 10%

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11
Q

• Nicotine – stimulates

A

SNS

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12
Q

Nicotine excess leads to

A

– Tachycardia
– HTN
– Sweatin

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13
Q

• Tar – increase risk of

A

bronchial carcinoma, laryngeal, oropharyngeal, esophageal, stomach, pancreatic, cervical, kidney, bladder, ovarian, colorectal cancer, chronic bronchitis, emphysema, & CAD

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14
Q

Cigarette smoking Impaction

A

– Largest particles strike mucus surfaces, become trapped

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15
Q

Sedimentation with cigarette smoking

A

Smoke particles settle in terminal & respiratory

bronchioles, unlike gases, cannot diffuse to alveolar wall

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16
Q

Deposition of Particle Inhalation

A

Inhaled particles deposited in airways, mechanism
based on particle size
• Impaction – large particles > 5 microns filtered by
nasopharynx

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17
Q

Deposition of Particle Inhalation• Sedimentation Sedimentation

A

– particles particles 1 to 5 microns, microns, deposit deposit in terminal & respiratory bronchioles as laminar flow ceases

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18
Q

Deposition of Particle Inhalation

Diffusion –

A

particles < 0.1 micron, behave almost

like gas. Most exhaled, but some deposits in alveo

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19
Q

Smokers have

A

Centraacinar disease.

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20
Q

Clearance of Deposited Particles

Two mechanisms:

A

• Particles deposited in conducting airways cleared by
MCE (mucocilliary escalator) & swallowed
• Particles deposited in gas exchange units cleared by
alveolar macrophages (“dust cells”)
• Inhibited by: pollution, tobacco, steroids, radiation

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21
Q

MCE

A

Seromucus glands & goblet cells secrete mucus 5-10

microns thick. (Gel more viscous), Contains IgA

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22
Q

MCE Cilia

A

sweeps mucus ~ 1mm/min in bronchioles;

2cm/min in trachea. Total clearance q 24 hrs

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23
Q

↑contaminants =

A

↑ cough & mucus production and clearance

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24
Q

Deficient MCE predisposes to

A

infection & inflammatory damage – Pollution – tobacco, sulfur & nitrogen oxides paralyze cilia – Inflammation = desquamation – ↑ mucus in CB; ↑ viscosity in CF also ↓ clearance

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25
Q

Alveolar Macrophages

• No MCE in

A

alveoli

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26
Q

• Macrophages ingest

A

contaminants in alveoli

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27
Q

Macrophages

A

• Move to bronchioles to be cleared by MCE

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28
Q

• If ↑↑↑ particulates or toxic particles, macrophages

tend to dump ingested particles into interstitium =

A

Pneumoconiosis

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29
Q

• Diapedesis through epithelium

A

cleared by lymphatics

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30
Q

Pneumoconiosis

• Coal Miner’s Lung –

A

coal dust overwhelms alveolar
macrophages in terminal & respiratory bronchioles
• Condition can be simple or progressive

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31
Q

Coal Miner’s Lung –• Simple –

A

minor respiratory changes w/ series

ventilation impairments = restrictive effect

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32
Q

Coal Miner’s Lung –

A

• Progressive – Massive Fibrosis = obstructive effect

– increasing dyspnea, RF

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33
Q

Pneumoconiosis caused by

•

A

inhalation of SiO2

during quarrying, mining, or sandblasting

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34
Q

Coal dust vs SiO2

A

Coal dust is inert vs. SiO2

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35
Q

• Silica particles are toxic – provoke

A

severe fibrosis

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36
Q

• Silica nodules nodules form – composed of concentric

A

wholrs of dense collagen fibers around silica – Found in respiratory bronchioles, alveoli and along
lymphatics
Restricve effect

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37
Q

Asbestos –

A

used in insulation, brake liners & building
materials – aerodynamic, long thin fibers penetrate far
into lung

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38
Q

Asbestosis =

A

diffuse interstitial disease – Restrictive Effect

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39
Q

Pleural disease may occur after only trivial exposure –

A

Plaques may develop, usually insignificant – Malignant Mesothelioma may develop decades after
exposure

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40
Q

Bronchogenic Carcinoma-

A

originates in epithelial layer of respiratory tract
– 31% of cancer deaths in men
– 25% of cancer deaths in women (leading cause)

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41
Q

Other Cancers Found in Lung-

A

sarcoma, lymphoma, blastoma, mesothelioma, & metastases

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42
Q

• Smoking →
• Other exposures- radon, radiation, air pollution, iron
mining, coal mining, silica, diesel exhaust, asbestos

A

20 × risk for lung cancer, second hand

smoke → 30% increased risk

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43
Q

Symptoms of lung CA

A

Unproductive cough or hemoptysis common early

symptom

44
Q

• Quitting smoking

A

decreases risk but risk never returns to baseline (non-smokers)

45
Q
  • 2 major categories:
  • – Squamous cell – Adenocarcinoma
  • Bronchioalveolar carcinoma (subtype) – Large cell
A

Small cell

Non-small cell lung cancers

46
Q

• 2 major categories:
• Small cell (“oat cell”) – Highly malignant, rapid dissemination
•

A

• Small cell (“oat cell”) – Highly malignant, rapid dissemination

47
Q

Non-small cell lung cancers –

A

Squamous cell – Adenocarcinoma

48
Q

Small Cell (oat cell)

A
  • ≈15% of lung CA
  • Strongest correlation with smoking
  • May secrete hormones→ paraneoplastic syndromes
49
Q

Small Cell (oat cell) arises from

A

Arise centrally, Rapid growth, Metastasize early &

widely

50
Q

Small cell prognosis

A

• Worst prognosis, median survival from diagnosis 1-3

months, 10% 2 year survival

51
Q

Small cell have Paraneoplastic Syndromes

A

often the first clinical manifestation of cancer – SIADH- most common (up to 40%) – Gastrin releasing peptide – Calcitonin – ACTH → Cushing’s syndrome

52
Q

Squamous Cell

A 
≈30% of lung CA
• Centrally located near hilum
• Protrude into bronchi
• Hemoptysis &amp; obstructive pneumonia are common
presenting symptoms
• Metastasize late to hilar nodes
53
Q

Anenocarcinoma

A

≈35-40% of lung CA
• Arise in peripheral lung- surgical resection possible
but metastasize early & widely
• Usually discovered on CXR
• Pain & dyspnea common with pleural invasion
• Bronchoalveolar cell carcinoma- slow growing,
weakest association with smoking

54
Q

Large Cell

A 
• 10-15% of lung CA
• Undifferentiated (anaplastic) cells
• Commonly begin peripherally but may grow to
distort the trachea or bronchi
• Metastasize early &amp; widely
55
Q

Bronchial Carcinoid Tumors- ≈1% of lung CA

A

– Arise in mainstem or segmental bronchi
– May secrete neuroendocrine hormones, carcinoid syndrome
(less likely than with GI carcinoids)
– Not related to smoking

56
Q

Adenocystic Carcinoma

A

– Rare bronchial gland tumors

57
Q

• Mesothelioma

A

– associated with asbestos exposure
– most are malignant
– 80% arise from pleural surface

58
Q

Autosomal recessive defect on chromosome 7 →

A

defective chloride channel (cystic fibrosis
transmembrane conductance regulator) in sweat
glands, pulmonary epithelium, bile ducts, &
pancreas

59
Q

• Viscous secreQons →

A

mucus plugging, defective

MCE (chronic inflammation & infections)

60
Q

Cystic Fibrosis • Neutrophil dominated inflammation →

A 
parenchymal damage (bronchiectasis) along with air
trapping from plugs → bullae
61
Q

Cystic Chronic infections –

A

S. aureus, P. aeruginosa colonize ≈75%

62
Q

Cystic Fibrosis

A

• Sweat test- sweat chloride > 60 meq/L – (normal < 39)

63
Q

Pneumonial Pathology, clinical features & treatment vary

significantly

A

with causative agent & pt. variables

64
Q

PNA is Infection in airways→

A

obstruction via inflammation

(edema, SM constriction, etc) cell debris, & exudate

65
Q

PNA lung damage is

A

• Lung damage from PMN enzymes or bacterial
virulence factors may occur
• Pleuritic pain, dyspnea, fever, malaise

66
Q

• Risk factors –Pneumonia

A

Advanced Age - highest incidence & mortality – Immunocompromise – Smoking – Immobility – Malnutrition – Intubation – Cardiac &/or Liver disease

67
Q

Pneumococcal pneumonia-organisms

→ edema, consolidaQon, infection spreads

A

S. pneumoniae, encapsulated organism

68
Q

PNA Immune response -

A

IGA binds, PMNs activated,

complement system activated, cytokines released

69
Q

Pneumonia Red Hepatization-

A

alveoli fill with blood, fibrin,

edema, & bacteria

70
Q

Pneumonia Grey Hepatization-

A

fibrin deposits & WBCs

71
Q

Staphylococcus pneumoniae

A

Suppurative pneumonia with abscess formation, empyema

72
Q

Tuberculosis- Mycobacterium tuberculosis –

A

Acid fast bacillus spread by airborne particle – High incidence in HIV, drug abuse, & homeless

73
Q

Bacilli tend to

• Often disseminate via lymphatics

A

lodge in the periphery of Apices, high

PO2 = favorable environment for bacillus

74
Q

TB Can survive in

A

macrophages, incite more inflammation -
inflammatory cells wall off bacteria in tubercle→
caseating granulomas

75
Q

TB disseminate via

A

• Often disseminate via lymphatics

76
Q

TB Often

A

asymptomatic or nonspecific symptoms
Cough lasting more than 3 wks, vague flu-like symptoms,
wgt. Loss, night sweats – Multi-drug resistant strains emerging

77
Q

Stages of TB:

A

– 1) exposure only – 2) latent infection – 3) clinically active – 4) Tuberculosis in remission – 5) Reactivation (secondary TB)

78
Q

RF considered when:

A

– PO2 < 60mmHg = Hypoxemia

– PCO2 > 50 mmHg = Hypercapnia

79
Q

Treatment of RF depends

A

on cause

80
Q

Four mechanisms of hypoxemia:

A

– Hypoventilation (Weakness from NMB, narcotic OD, etc)
– Diffusion impairment (Ex. Interstitial lung disease)
– VQ mismatch (ex. Chronic bronchitis)
– Shunt

81
Q

“Normal” PaO2 =Calculation

A

102 - 0.33 × age

82
Q

Signs/Symptoms: hypoxemia

A

↓ PaO2 – Cyanosis – Tachycardia – Mental confusion

83
Q

Tissue Hypoxia – vulnerability depends on tissue –

A

CNS & Myocardium most vulnerable –

•mage

84
Q

Cessation of blood flow to cerebral cortex:

• 4-6 sec.

A

= loss of function

85
Q

10-20 sec.

• 3-5 min.

A

= l.o.c

= irreversible damage

86
Q

CNS:

A

– HA, Somnolence, L.O.C., Retinal hemorrhages, brain

damage

87
Q

Cardiovascular:

A

Cardiovascular:
–1st (↑SNS)Tachycardia/HTN, 2ndBradycardia/Hypotension
– Angina/HF may occur if CAD present
– Renal impairment w/ Na+ retention & proteinuria
– Pulmonary HTN 2o to alveolar hypoxia

88
Q

Hypercapnia caused by

A

Caused by:
• Hypoventilation
• Muscular weakness - residual NMB, myasthenia gravis,
Guillain-Barre
• Sedation - decreases hypercapnic respiratory drive
• Mechanical failure of the chest wall – Ex. flail chest

89
Q

Hypercapnia

A

• ⇑Work of breathing
• CNS receptor desensitization, permissive
hypercapnia
• renal compensation ( for ↑ H2CO3 - )
• CNS desensitization from chronic hypercapnia →
dependency on hypoxic respiratory driv

90
Q

Hypercapnia treatment with

A

Treatment with O2 could suppress hypoxic drive
and increase CO2 retention/acidosis
• Answer is to give low concentration (24-48% O2)
and monitor ABGs frequently to determine
whether depression of ventilation is occurring.

91
Q

Diaphragm Fatigue

•

A

Hypercapnia impairs diaphragm contractility

• Hypoxemia accelerates onset of fatigue

92
Q

Diaphragm Fatigue limited by reducing work of breathing:

A

– Treat bronchospams
– Control infection
– Give O2 judiciously to relieve hypoxemia

93
Q

(Methylxanthines and diaphragm fatigue?

A

improve diaphragm contractility & relieves bronchoconstriction)

94
Q

ARDS is a

A

Multi-organ system disease (SIRS) resulting from: – major trauma, aspiration, inhalation injury, sepsis
(especially gram negative), and shock. ≈40% mortality

95
Q

ARDS Pathologic progression: – Type 1 alveolar

A

alveolar cells & capillary endothelium damaged =interstitial edema – Alveolar exudate & hemorrhage – ⇑Neutrophil & macrophage activity – Type 2 cells replace type 1- much thicker – Cellular infiltration in interstitium & fibrotic changes, consolidation

96
Q

Capillary Pathology:

•

A

• endothelial damage → ⇑ permeability & exudate
• Inflammatory response- neutrophils/macrophages
cause more injury, chemotactic factors, &
Inflammatory response- neutrophils/macrophages
cause more injury, chemotactic factors, &
inflammatory mediators
Endothelial damage → platelet & complement
activation, intravascular thrombosis

97
Q

ARDS

• Clinical Manifestations: –

A

Rapid, shallow breathing – Marked dyspnea – Restrictive & obstructive lung defects – ⇓FRC – Hypoxemia unresponsive to O2 therapy – Diffuse alveolar infiltrates on CXR & rales

98
Q

Clinical Progression of ARDS

A

• hypoxia → hyperventilation → respiratory alkalosis
→ progressive dyspnea
• ⇑WOB → metabolic acidosis → fatigue →
respiratory acidosis & worsening hypoxia →
pulmonary HTN, cardiac decompensation & death

99
Q

Infant Respiratory Distress Syndrome

• Chief cause:

A

↓ surfactant – Premature infant – inadequate production
• Transudate & cellular debris in alveoli
• Right-to-left shunt exaggerates exaggerates hypoxemia hypoxemia
• Hemorrhagic edema
• patchy atelectasis
• hyaline membranes
• Tx: – PEEP or CPAP frequently beneficial – exogenous surfactant via the trachea

100
Q

Oxygen Therapy

• For treatment of Hypoxemia

A

– Recall the 4 mechanisms: hypoventilation, diffusion
impairment, VQ mismatch, Shunt
– Chart represents a hypoxic pt. breathing air, or given
FiO2 100%
• Breathing air only
= PaO2 of 50 mmHg

101
Q

Oxygen Therapy

• Hypoventilation

A

– FiO2 100% increases PO2 > 600 mmHg

102
Q

• VQ mismatch

A

– Most common cause of hypoxemia
– FiO2 100% effective b/c eventually washes out nitrogen
from all ventilated areas – increases alveolar PO2> 600
mmHg

103
Q

Oxygen therapy • Diffusion impairment

A

– CO2 unaffected b/c diffuses 20x faster than O2
– Small increase of inspired oxygen of 30% raises alveolar
PO2 by 60 mmHg (remember air = 21%); PO2 > 600
mmHg

104
Q

Oxygen therapy Shunt

A

– Refractory to O2 therapy
– Only small increase in PaO2
– FiO2 100% raises alveolar PO2 to 600 mmHg – raises
dissolved oxygen in plasma from 0.3 to 1.8 ml of O2/100
ml of blood.

105
Q

⇑⇑FiO2

•

A

Alveolar epithelial damage → Type 2 cells replace
type 1
• Capillary endothelial damage → ⇑permeability,
interstitial edema
• Interstitial exudate → fibrosis
• Absorption Atelectasis with low V/Q ratio - ⇑PAO2
in under ventilated alveoli, O2 absorbed → alveoli
collapse = atelectasis

SRNAAnatomy II (16 decks)

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