Pulmonary Pathology: COPD/COLD Flashcards
Bullae
-large dilated airspaces bulging from beneath pleura
Polycythemia
- increased RBC production
- more viscous
Obstructive
trouble getting air out
Primary problem center on obstruction to airflow
- increased resistance through decreased sized airways
- loss of elastic recoil
- tendency of airways to collapse
differences in obstructive
- cause of obstruction
- reversibility/prognosis of disease
- location of obstruction
common signs of obstructive lung diseases
- decr EFR
- incr residual volume
- incr WOB
- incr risk of DVT
- vent-perfusion mismatching
- polycythemia
- pulm HTN
- cor pulmonale (RVH)
- lung failure–>hypoxemia
- pump failure–>alveolar hypovent/hypercapnia
- expiratory Mm weakness
- Extrapulmonary effects
Common Prognosis of Obstructive Lung Disease
- increase loss lung tissue if don’t quit smoking
- chronic hypoxemia–>ishcemia in all organs
- most common cause of death=CHF, resp failure, pneumonia, bronchiolitis, PE
- LVRS in pt with emphysema=~5 year increase in benefits
Common Symptoms of Obstructive
- chronic cough
- productive cough
- abnormal/adventitious breath sounds
- dyspnea on exertion
Pediatric Obstructive Lung Diseases
- bronchopulmonary dysplasia
- cystic fibrosis
- asthma
- bronchiectasis
Adult Obstructive Lung Diseases
- chronic bronchitis
- emphysema
- asthma
- bronchiectasis
Asthma Etiology
- chronic inflam disease of airways
- heightened bronchial activivty to stimuli
- irritants cause bronchospasm–>wheezing
Asthma stimuli
- allergies
- Exercise
- infections
- stress
Intrinsic Asthma
- begins after age 35
- more severe
- year round
- related to viral infection
Extrinsic Asthma
- usually children, young adults
- hayfever, allergies
- fall/spring
- 1/2 grow out of it
Asthma Treatment
- bronchodilators
- avoid irritants
- pt/family edu
- exercise goals
BPD pathophysiology
-damage to alveoli by mechanical ventilator–>inflammation, pulmonary edema and fibrosis
BPD Prognosis
- death by 1 year in some
- survivors have longterm problems with resp infections, hyperinflated lungs & bronchospasm
- resp symptoms into childhood
- some: decreased growth and increased neurodevelopmental sequelae
BPD Etiology
-neonates who have been mechanically ventilated or treated with high O2 levels as result of RDS
Factors leading to BPD
- born <12,000 grams at birth
- ventilated with continuous positive pressure
- O2 given at 60% or higher FIO2
- 50+ hours on supplemental O2
- Birth mother is diabetic
BPD Treatment
- Bronchodilators
- Diuretics
- K+ supplement
- Nutritional Support
- Antibiotics
Emphysema
- abnormal permanent enlargement of air spaces distal to terminal bronchiole, w/ destruction of their walls
- “pink puffer”
2 Types of Emphysema
- centrilobar
- panlobar
Panlobar Emphysema
- –>enlargment of destruction of alveoli
- affects lower lobes (worse prognosis)
- Alpha1-Antitripsin deficiency
- affects alveoli more
Centrilobar Emphysema
- 20x more common than panlobar
- affects bronchioles more
- ->inflam, edema & thickening of bronchiole walls w/ destruction of respiratory bronchioles
- more affect upper segments and loves
- more common in men & pts with bronchitis
- rare in non-smokers
Emphysema Etiology
- destruction of alveolar walls & elastic tissue distal to terminal bronchioles
- ->abnormal permanent enlargement of gas exchange airways
- loss of elastin and cause collapse of airways
- due to imbalance between enzyme inhibitors and proteolytic enzymes
Emphysema Pathophysiology
- SMOKING
- smoke particles in lungs–>neutrophils & macrophages move in to remove smoke–>release enzymes to destroy smoke–>some enzymes (protease) attack alveolar walls & (elastase) destroy elastin
Emphysema:
Enzyme/Inhibitor Imbalance
- Proteolytic Enzymes: break down tissue
- Enzyme inhib: control enzymes
- Alpha1-Antitripsin Deficiency–>decreased proteolytic enzyme inhib
- Smokers have too many proteolytic enzymes
so lung tissue gets destroyed
Emphysema:
Alpha1-Antritripsin Deficiency
- inherited
- symptoms around age 40-55
- cause liver disease; children @ risk for hepatitis and cirrhosis
- ->inability to inhibit neutrophil elastase enqume and breaks down lung tissue
-Treatment: Alpha1-Antitripsin Injections
Emphysema Treatment
- irreversible
- stop smoking to stop further destruction
- no effective Tx
- PT
PT Management of Emphysema
-pursed lip breathing to increase lung efficiency and decrease collapse of airways
Bronchiectasis Pathology
- a reaction to having something else
- result of infection
- usually localized to a few segments
- airways become dilated, fibrotic, lined with hyperplastic nonciliated, mucus secreting cells
-decr cilia–>incr mucus accum–>infection risk incr
Bronchiectasis Prognosis
-with use of antibiotics as needed, can live into 70’s & 80’s
Bronchiectasis Etiology
- abnormal permanent dilation of medium-sized bronchi that extends distally
- areas filled with secretions are swollen/inflamed & can be ulcerated
Types of Bronchiectasis
- cylindrical/longitudinal
- varicose
- saccular/cystic
Cylindrical/Longitudinal Bronchiectasis
- most common
- uniform dilation of airways
Varicose Bronchiectasis
- greater dilation than cylindrical
- bronchial walls look like varicose veins & irregular
Saccular/Cystic Bronchiectasis
-balloon shaped
Bronchiectasis Treatment
- antibiotics
- pulmonary hygiene
- hydration
- immunizations to prevent flu & pneumonia
- surgical resections of segments
CF Etiology
- autosomal recessive gene disorder
- probs affect cystic fibrosis transmembrane regulator (protein channel for Cl- transport)
- unable to resorb Cl- in sweat glands=salty sweat
- progressive obstruction of exocrine glands by increase mucous secretions
CF Treatment
- chest PT
- Antibiotics
- Mucolytics (increase hydration)
- Bronchodilators
- Nutrition (pancreatic enzyme replacement)
- Single/double lung or heart transplant
CF Prognosis
- median survival 35 years
- cause of death usually respiratory
CF Vent-Perf Mismatching Causes
- arterial hypoxemia–>dyspnea
- Pulm HTN–>cor pulmonale–>R ventricle failure
- Increased CO2
- Respiratory Acidosis
CF:
Bacterial Infections
- pseudomonas aeruginosa most common
- staph aureus
- haemophilus influenza
- burkholderia cepacia
CF:
Obstructive Pulmonary Disease
- small airways inflam & infection–>
- incr mucus secretion–>
- incr infection–>
- neutrophils in airways–>
- accumulated micro-organisms destroy lung tissue–>
- fibrosis & vent-perf mismatching
CF:
Pancreatic Insufficiency
- destruction by mucous secretions–>
- enzymes trapped in ducts–>
- autodestruction pancreas–>
- decreased ability to absorb nutrients
CF:
Meconium Ileus
-obstruction of intestines by meconium stools due to lack of trypsin & other pancreatic enzymes
CF:
Salty Sweat
- Cl- imbalance & exocrine glands clogged by mucus
- excess Cl- can’t be reabsorbed in sweat ducts so goes out to skin
Chronic Bronchitis Pathology
- due to chronic inflam of tracheobronchial tree–>
- hyper-secretion of mucus–>
- damage to cilia–>
- mucus collects–>
- place for infection and inflam
chronic bronchitis etiology
- # 1 cause is smoking
- pollution
Chronic Bronchitis Diagnosis
- productive cough (>100 ml/day) for 3 months of the year for 2 consecutive years
- “blue bloaters”
Chronic Bronchitis Treatment
- quit smoking
- can improve if before blue and bloated stage & only has cough
- IV antibiotics if infection
- bronchodilators/O2
- chest PT
