Pulmonary 3 Flashcards
(105 cards)
1
Q
Environmental inhales diseases
A
CO (carbon monoxide)
• Sulfur Oxides
• Nitrogen Oxides
• Hydrocarbons
2
Q
CO2 Binds to Hb with
– No change in PaO2
A
200x the affinity of O2
3
Q
Increases O2 affinity of remaining Hb =
A
does not release O2 readily to the tissues – dissociation curve shifted to the Left
4
Q
CO poisoning
A
– Oxygen saturation % PaO2 high despite impaired oxygen deliver
5
Q
CO poisoning : Dx by
A
measuring carboxyhemoglobin levels
– index of suspicion
6
Q
Treatment of Co poisoning
A
No cyanosis, no tachypnea
– Tx: 100% FiO2
7
Q
Nitrogen oxides –
A
produced when fossil fuels
burned at high temp. - yellow haze of smog, irritant
= tracheitis, bronchitis, pulmonary edema
8
Q
Sulfur oxides – corrosive/poisonous – produced by
A
burning burning sulfur containing containing fuels @ power stations stations = chronic bronchitis, pulmonary edema
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)
10
Q
Cigarette Smokingg
A
Contains 4% CO – raises carboxyhemoglobin in smoker’s blood to 10%
11
Q
• Nicotine – stimulates
A
SNS
12
Q
Nicotine excess leads to
A
– Tachycardia
– HTN
– Sweatin
13
Q
• Tar – increase risk of
A
bronchial carcinoma, laryngeal, oropharyngeal, esophageal, stomach, pancreatic, cervical, kidney, bladder, ovarian, colorectal cancer, chronic bronchitis, emphysema, & CAD
14
Q
Cigarette smoking Impaction
A
– Largest particles strike mucus surfaces, become trapped
15
Q
Sedimentation with cigarette smoking
A
Smoke particles settle in terminal & respiratory
bronchioles, unlike gases, cannot diffuse to alveolar wall
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
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
18
Q
Deposition of Particle Inhalation
Diffusion –
A
particles < 0.1 micron, behave almost
like gas. Most exhaled, but some deposits in alveo
19
Q
Smokers have
A
Centraacinar disease.
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
21
Q
MCE
A
Seromucus glands & goblet cells secrete mucus 5-10
microns thick. (Gel more viscous), Contains IgA
22
Q
MCE Cilia
A
sweeps mucus ~ 1mm/min in bronchioles;
2cm/min in trachea. Total clearance q 24 hrs
23
Q
↑contaminants =
A
↑ cough & mucus production and clearance
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
25
Alveolar Macrophages
| • No MCE in
alveoli
26
• Macrophages ingest
contaminants in alveoli
27
Macrophages
• Move to bronchioles to be cleared by MCE
28
• If ↑↑↑ particulates or toxic particles, macrophages
| tend to dump ingested particles into interstitium =
Pneumoconiosis
29
• Diapedesis through epithelium
cleared by lymphatics
30
Pneumoconiosis
| • Coal Miner’s Lung –
coal dust overwhelms alveolar
macrophages in terminal & respiratory bronchioles
• Condition can be simple or progressive
31
Coal Miner’s Lung –• Simple –
minor respiratory changes w/ series
| ventilation impairments = restrictive effect
32
Coal Miner’s Lung –
• Progressive – Massive Fibrosis = obstructive effect
| – increasing dyspnea, RF
33
Pneumoconiosis caused by
| •
inhalation of SiO2
| during quarrying, mining, or sandblasting
34
Coal dust vs SiO2
Coal dust is inert vs. SiO2
35
• Silica particles are toxic – provoke
severe fibrosis
36
• Silica nodules nodules form – composed of concentric
wholrs of dense collagen fibers around silica – Found in respiratory bronchioles, alveoli and along
lymphatics
Restricve effect
37
Asbestos –
used in insulation, brake liners & building
materials – aerodynamic, long thin fibers penetrate far
into lung
38
Asbestosis =
diffuse interstitial disease – Restrictive Effect
39
Pleural disease may occur after only trivial exposure –
Plaques may develop, usually insignificant – Malignant Mesothelioma may develop decades after
exposure
40
Bronchogenic Carcinoma-
originates in epithelial layer of respiratory tract
– 31% of cancer deaths in men
– 25% of cancer deaths in women (leading cause)
41
Other Cancers Found in Lung-
sarcoma, lymphoma, blastoma, mesothelioma, & metastases
42
• Smoking →
• Other exposures- radon, radiation, air pollution, iron
mining, coal mining, silica, diesel exhaust, asbestos
20 × risk for lung cancer, second hand
| smoke → 30% increased risk
43
Symptoms of lung CA
Unproductive cough or hemoptysis common early
| symptom
44
• Quitting smoking
decreases risk but risk never returns to baseline (non-smokers)
45
* 2 major categories:
* – Squamous cell – Adenocarcinoma
* Bronchioalveolar carcinoma (subtype) – Large cell
Small cell
| Non-small cell lung cancers
46
• 2 major categories:
• Small cell (“oat cell”) – Highly malignant, rapid dissemination
•
• Small cell (“oat cell”) – Highly malignant, rapid dissemination
47
Non-small cell lung cancers –
Squamous cell – Adenocarcinoma
48
Small Cell (oat cell)
* ≈15% of lung CA
* Strongest correlation with smoking
* May secrete hormones→ paraneoplastic syndromes
49
Small Cell (oat cell) arises from
Arise centrally, Rapid growth, Metastasize early &
| widely
50
Small cell prognosis
• Worst prognosis, median survival from diagnosis 1-3
| months, 10% 2 year survival
51
Small cell have Paraneoplastic Syndromes
often the first clinical manifestation of cancer – SIADH- most common (up to 40%) – Gastrin releasing peptide – Calcitonin – ACTH → Cushing’s syndrome
52
Squamous Cell
```
≈30% of lung CA
• Centrally located near hilum
• Protrude into bronchi
• Hemoptysis & obstructive pneumonia are common
presenting symptoms
• Metastasize late to hilar nodes
```
53
Anenocarcinoma
≈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
Large Cell
```
• 10-15% of lung CA
• Undifferentiated (anaplastic) cells
• Commonly begin peripherally but may grow to
distort the trachea or bronchi
• Metastasize early & widely
```
55
Bronchial Carcinoid Tumors- ≈1% of lung CA
– Arise in mainstem or segmental bronchi
– May secrete neuroendocrine hormones, carcinoid syndrome
(less likely than with GI carcinoids)
– Not related to smoking
56
Adenocystic Carcinoma
– Rare bronchial gland tumors
57
• Mesothelioma
– associated with asbestos exposure
– most are malignant
– 80% arise from pleural surface
58
Autosomal recessive defect on chromosome 7 →
defective chloride channel (cystic fibrosis
transmembrane conductance regulator) in sweat
glands, pulmonary epithelium, bile ducts, &
pancreas
59
• Viscous secreQons →
mucus plugging, defective
| MCE (chronic inflammation & infections)
60
Cystic Fibrosis • Neutrophil dominated inflammation →
```
parenchymal damage (bronchiectasis) along with air
trapping from plugs → bullae
```
61
Cystic Chronic infections –
S. aureus, P. aeruginosa colonize ≈75%
62
Cystic Fibrosis
• Sweat test- sweat chloride > 60 meq/L – (normal < 39)
63
Pneumonial Pathology, clinical features & treatment vary
| significantly
with causative agent & pt. variables
64
PNA is Infection in airways→
obstruction via inflammation
| (edema, SM constriction, etc) cell debris, & exudate
65
PNA lung damage is
• Lung damage from PMN enzymes or bacterial
virulence factors may occur
• Pleuritic pain, dyspnea, fever, malaise
66
• Risk factors –Pneumonia
Advanced Age - highest incidence & mortality – Immunocompromise – Smoking – Immobility – Malnutrition – Intubation – Cardiac &/or Liver disease
67
Pneumococcal pneumonia-organisms
| → edema, consolidaQon, infection spreads
S. pneumoniae, encapsulated organism
68
PNA Immune response -
IGA binds, PMNs activated,
| complement system activated, cytokines released
69
Pneumonia Red Hepatization-
alveoli fill with blood, fibrin,
| edema, & bacteria
70
Pneumonia Grey Hepatization-
fibrin deposits & WBCs
71
Staphylococcus pneumoniae
Suppurative pneumonia with abscess formation, empyema
72
Tuberculosis- Mycobacterium tuberculosis –
Acid fast bacillus spread by airborne particle – High incidence in HIV, drug abuse, & homeless
73
Bacilli tend to
| • Often disseminate via lymphatics
lodge in the periphery of Apices, high
| PO2 = favorable environment for bacillus
74
TB Can survive in
macrophages, incite more inflammation -
inflammatory cells wall off bacteria in tubercle→
caseating granulomas
75
TB disseminate via
• Often disseminate via lymphatics
76
TB Often
asymptomatic or nonspecific symptoms
Cough lasting more than 3 wks, vague flu-like symptoms,
wgt. Loss, night sweats – Multi-drug resistant strains emerging
77
Stages of TB:
– 1) exposure only – 2) latent infection – 3) clinically active – 4) Tuberculosis in remission – 5) Reactivation (secondary TB)
78
RF considered when:
– PO2 < 60mmHg = Hypoxemia
| – PCO2 > 50 mmHg = Hypercapnia
79
Treatment of RF depends
on cause
80
Four mechanisms of hypoxemia:
– Hypoventilation (Weakness from NMB, narcotic OD, etc)
– Diffusion impairment (Ex. Interstitial lung disease)
– VQ mismatch (ex. Chronic bronchitis)
– Shunt
81
“Normal” PaO2 =Calculation
102 - 0.33 × age
82
Signs/Symptoms: hypoxemia
↓ PaO2 – Cyanosis – Tachycardia – Mental confusion
83
Tissue Hypoxia – vulnerability depends on tissue –
CNS & Myocardium most vulnerable –
| •mage
84
Cessation of blood flow to cerebral cortex:
| • 4-6 sec.
= loss of function
85
10-20 sec.
| • 3-5 min.
= l.o.c
| = irreversible damage
86
CNS:
– HA, Somnolence, L.O.C., Retinal hemorrhages, brain
| damage
87
Cardiovascular:
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
Hypercapnia caused by
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
Hypercapnia
• ⇑Work of breathing
• CNS receptor desensitization, permissive
hypercapnia
• renal compensation ( for ↑ H2CO3 - )
• CNS desensitization from chronic hypercapnia →
dependency on hypoxic respiratory driv
90
Hypercapnia treatment with
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
Diaphragm Fatigue
| •
Hypercapnia impairs diaphragm contractility
| • Hypoxemia accelerates onset of fatigue
92
Diaphragm Fatigue limited by reducing work of breathing:
– Treat bronchospams
– Control infection
– Give O2 judiciously to relieve hypoxemia
93
(Methylxanthines and diaphragm fatigue?
improve diaphragm contractility & relieves bronchoconstriction)
94
ARDS is a
Multi-organ system disease (SIRS) resulting from: – major trauma, aspiration, inhalation injury, sepsis
(especially gram negative), and shock. ≈40% mortality
95
ARDS Pathologic progression: – Type 1 alveolar
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
Capillary Pathology:
| •
• 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
ARDS
| • Clinical Manifestations: –
Rapid, shallow breathing – Marked dyspnea – Restrictive & obstructive lung defects – ⇓FRC – Hypoxemia unresponsive to O2 therapy – Diffuse alveolar infiltrates on CXR & rales
98
Clinical Progression of ARDS
• hypoxia → hyperventilation → respiratory alkalosis
→ progressive dyspnea
• ⇑WOB → metabolic acidosis → fatigue →
respiratory acidosis & worsening hypoxia →
pulmonary HTN, cardiac decompensation & death
99
Infant Respiratory Distress Syndrome
| • Chief cause:
↓ 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
Oxygen Therapy
| • For treatment of Hypoxemia
– 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
Oxygen Therapy
| • Hypoventilation
– FiO2 100% increases PO2 > 600 mmHg
102
• VQ mismatch
– Most common cause of hypoxemia
– FiO2 100% effective b/c eventually washes out nitrogen
from all ventilated areas – increases alveolar PO2> 600
mmHg
103
Oxygen therapy • Diffusion impairment
– 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
Oxygen therapy Shunt
– 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
⇑⇑FiO2
| •
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
