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COPD:
-Definition:
It is a preventable and treatable disease with some significant extra-pulmonary effects that
may contribute to the severity in individual patients. Its pulmonary component is characterized by
airflow limitation that is not fully reversible. The limitation is usually progressive and associated
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-Epidemiology:
Age: more in middle age and old age.
Sex: Males > Females (due to smoking, exposure to pollution)
Area: Urban areas > Rural areas
Seasonal variation: more in winter
Social class and occupation: more in low states (nutrition, pollution,
crowd, tobacco use)
-Risk Factors:
Exposures to:
o Smoking: in cigarette > cigar and pipe, normally FEV1 declines
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Host factors:
o Genes: (α1 anti-trypsin deficiency) it’s a glycoprotein
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Others:
o Socio-economic status
o Nutrition
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-Pathogenesis:
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*Notes:
Normal peripheral bronchial drainage is in left atrium, while central one
is drained in right atrium.
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Intrathoracic
- Chronic obstructive pulmonary disease
- Bronchial asthma
- Central bronchial carcinoma
- Endobronchial tuberculosis
- Bronchiectasis
- Left heart failure
- Interstitial lung disease
- Cystic fibrosis
Extrathoracic
- Postnasal drip
- Gastroesophageal reflux
- Drug therapy (e.g., ACE inhibitors)
-Signs of COPD:
General:
oPuffiness of lower eyelids (by chronic cough)
oCentral cyanosis
oOf hypoxia
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Local:
o Inspection: Hyperinflated chest Inc. A-P diameter (barrel)
Prominent sternal angle
Horizontal ribs
Wide sub-costal angle
Kyphosis
Hoover’s sign (decrease expansion of lower ribs,
later become paradoxical to pull the low flat diaphragm)
Trill’s sign
Short distance between cricothyroid &
supra-sternal notch (normal >3fingers)
Indrawing of spaces due to low Intrathoracic pr.
oPercussion: ± hyper-resonance
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Severity of symptoms
Severity of air flow limitation
Frequency and severity of exacerbations
Presence of respiratory failure
Presence of co-morbid conditions
General health status
No. of medications needed to manage
Presence of one or more complications:
o Pulmonary infections
o Corpulmonale RVF
o LVF
-D.D.:
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-Investigations:
[A] Laboratory investigations:
Leucocytosis in acute exacerbations
Polycythemia (HCT > 47% in females, > 52% in males) degree is
related to amount of carboxy-Hb with smoke
1-globulin by electrophoresis is dec. in AATD (qualitative test)
Radial immuno-diffusion and Assessment of trypsin inhibiting
capacity are quantitative tests for AATD (=mg of trypsin
inhibited by ml of serum) in ZZ (diseased) <0.4mg/ml
in MZ (diseased) 0.4-0.8mg/ml
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in MM (normal) 0.8-1.4mg/ml
(also decreases in BAL with high neutrophil elastase in BAL)
[B] Sputum analysis: (not a routine because organisms are well known)
.Neuraminic acid is increased in purulent sputum
- Signs of hyperinflation
Voluminous lungs
Hyper-translucency
Low flat diaphragm
Transverse ribs
Ribbon shaped heart
Posterior portion of 11-12th ribs may be visible
Bullae or tension cysts as fine hair like margins with
no vascular shadow (with infection they decrease in size
and may disappear)
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[E] ECG:
Clockwise rotation of the heart (rt. axis deviation, rt. BBB, RS
pattern in chest leads and V5-6, Poor R-wave progression, RS
pattern in AVL with QR pattern in AVF)
-Management of COPD:
[A] Assess and Monitor the disease: history, C/P, investigations.
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Yes No Yes No
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o Follow UP: within a week of quitting day then after a month (the
more the follow up the more the cessation rate).
*Smoking effects:
-Respiratory system:
a. Nicotine high alertness, mental concentration (stimulate
synaptic transmission in brain)
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Pharmacological ttt:
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• Long-acting inhaled bronchodilators are more effective and convenient.
• Combining BDs may improve efficacy and decrease the risk of side effects compared to
increasing the dose of a single bronchodilator.
*Steroids: -The effects of oral and inhaled steroids in COPD are much less dramatic than
in BA, & their role in the management of stable COPD is limited to specific indications.
-Based on the lack of evidence of benefit, and the large body of evidence on
side effects, long-term treatment with oral glucocorticosteroids is not recommended in
COPD, they are only used in exacerbations for 7-10 days.
*Others: Vaccines: .Influenza vaccines can reduce serious illness, pneumonias and
death in COPD patients by about 50%.
.Vaccines containing killed or live, inactivated viruses are
recommended as they are more effective in elderly patients.
Antibiotics: no current evidence that their use, other than for treating
infectious exacerbations of COPD and other bacterial infections, is helpful.
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Narcotics (morphine): Oral and parenteral opioids are effective for treating
dyspnea in COPD patients with advanced disease.
Non-pharmacological ttt:
a) Rehabilitation:
o The Cycle of Physical, Social, & Psychosocial Consequences:
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- Exercise training:
.Exercise tolerance can be assessed by:
Bicycle ergometry or treadmill exercise with the
measurement of a number of physiological variables,
including maximum oxygen consumption, maximum
heart rate, and maximum work performed (aerobic)
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b) O2 therapy:
o Aim:
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o Used in:
- Air travel hypoxia: to give 1.2 liters more to keep PO2 >70
o Advantages:
c) Ventilatory support:
NIMV (NPV/NIPPV) IMV
Indications -Moderate to severe dyspnea -Severe dyspnea with accessory
with use of accessory Ms & Ms use & paradoxical
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abdominal motion.
-Severe acidosis (PH < 7.30,
PCO2 > 60)
-RR > 35 b/m
paradoxical abdominal -PO2 < 40, PO2/FIO2 <200
motion. -Respiratory arrest
-Moderate to severe acidosis -NIPPV failure or contraindic.
(PH> 7.30, PCO2 >45) -Cardiovascular complication.
-RR >25 b/m -Somnolence, impaired mental
status.
-Metabolic abnormality, sepsis,
pneumonia, PE, barotrauma,
massive pleural effusion.
-Long-term NIPPV can’t be recommended for the routine ttt of
patients with chronic RF due to COPD, the combination of
NIPPV with LTOT in some patients, particularly in those with
Contra-ind. daytime hypercapnia.
(For non- -Resp. arrest, CV instability (MI, arrhythmia, hypotension).
invasive) -High aspiration risk, somnolence, impaired mental status.
-Recent facial or GE surgery.
-Cranio-facial trauma, fixed nasopharyngeal abnormality.
-Burns, extreme obesity
d) Surgical intervention:
o Bullectomy: when bullae >50% of hemi thorax causing
displacement of the adjacent lung.
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Causes of exacerbation:
o Bacterial: (more than 50%) H. influenza, Strept. Pneumonae,
Moraxella Catarrhalis, Mycoplasma Pneumonae.
- Severity of FEV1
- Duration of worsening or new symptoms
- Comordibities
o Signs of Severity:
- Hemodynamic instability
- Reduced alertness
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o PFT:
o ABG:
- PO2 < 60, PCO2 > 50, SO2 < 90 life threatening if:
- PO2 < 50, PCO2 > 70, PH < 7.30
Home management:
Initiate or increase BD + Antibiotic re-assess in hrs
Hospital management:
The risk of dying from an exacerbation of COPD is closely related
to the development of respiratory acidosis, the presence of significant
comorbidities, and the need for ventilatory support.
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Bronchodilators:
– Increase doses and/or frequency
– Combine B2-agonists and anticholinergics
– Use spacers or air-driven nebulizers
– Consider adding intravenous mehylxanthines, if needed
Add oral or intravenous glucocorticosteroids
Consider antibiotics (oral or IV) when signs of bacterial infection
Consider noninvasive mechanical ventilation
At all times:
– Monitor fluid balance and nutrition
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-B-lactam (Penicillin,
Ampicillin/Amoxicillin)
-Tetracycline OR OR
-Trimethoprim/
Sulfamethoxazole -Fluoro-quinolones
OR (alternative) (Gemifloxacin, -B-lactam with
-B-lactam/B-lactamase Levofloxacin, P.aeruginosa
inhib. (Co-amoxiclav) Moxifloxacin) activity
-New Macrolides
-Cephalosporin(2nd, 3rd)
-Ketolide
(Telithromycin)
*Antibiotic must be given with BDs, and steroids.
*Cardinal symptoms are increased dyspnea, sputum volume, and
sputum purulence.
*Diuretic therapy for corpulmonale can worsen RF due to metabolic
alkalosis which depresses RC (no effect of digitalis in RVF).
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- Need for LTOT +/- home nebulizer (for patients with Stage IV)
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Definition:
It’s a large air containing space within the lung parenchyma
resulting from destruction, dilatation and confluence of airspaces distal to
terminal bronchioles (>1cm)
Pathology:
- With emphysema pan-acinar (1ry or with chronic bronchitis)
para-septal (acinar)
- Infantile lobar emphysema
- Scar emphysema (traction on normal alveoli)
- Drug IV use
- Vanishing lung syndrome or 1ry emphysema (in end stages of
fibrotic sarcoid, pneumoconiosis, EAA) die of RF without
cough or infections.
C/P: Asymptomatic
Progressive dyspnea can be marked if (spontaneous
pneumothorax, or sudden increase in size with air trapping)
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D.D.:
Bulla Bleb Cyst
Epithelium lined
Accumulation of air
cavities that
Definition See before between layers of
resemble bullae
visceral pleura
radiologically
Lung parenchyma
Site With 2ry lobule In visceral pleura
or mediastinum
Size 1 cm 1-2 cm 2-10 cm
Connective tissue Elastic lamina of
Lining Epithelium
septa pleura
Spontaneous Respiratory
Association 2ry Pneumothorax
pneumothorax infections
Reid classification:
- Type 1 (narrow necked): with pedicle attached to the lung and
protruding outwards.
- Type 2 (superficial broad based): pleura limiting its outside
lining and emphysematous lung lining from inside.
- Type 3 (deep broad based): as type 2 but with greater depth can
extend to hilum (any lobe can be affected).
Investigations:
- Laboratory: leucocytosis (rare)
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Ttt: Surgery
- Excision, Plication, Lung Resection if large and
symptomatizing show improvement of FEV1 from 50-200%
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