Cardio Pulm > Pulmonary Pathology: COPD/COLD > Flashcards

Pulmonary Pathology: COPD/COLD Flashcards

(51 cards)

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1
Q

Bullae

A

-large dilated airspaces bulging from beneath pleura

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2
Q

Polycythemia

A
  • increased RBC production

- more viscous

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3
Q

Obstructive

A

trouble getting air out

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4
Q

Primary problem center on obstruction to airflow

A
  • increased resistance through decreased sized airways
  • loss of elastic recoil
  • tendency of airways to collapse
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5
Q

differences in obstructive

A
  • cause of obstruction
  • reversibility/prognosis of disease
  • location of obstruction
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6
Q

common signs of obstructive lung diseases

A
  • 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
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7
Q

Common Prognosis of Obstructive Lung Disease

A
  • 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
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8
Q

Common Symptoms of Obstructive

A
  • chronic cough
  • productive cough
  • abnormal/adventitious breath sounds
  • dyspnea on exertion
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9
Q

Pediatric Obstructive Lung Diseases

A
  • bronchopulmonary dysplasia
  • cystic fibrosis
  • asthma
  • bronchiectasis
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10
Q

Adult Obstructive Lung Diseases

A
  • chronic bronchitis
  • emphysema
  • asthma
  • bronchiectasis
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11
Q

Asthma Etiology

A
  • chronic inflam disease of airways
  • heightened bronchial activivty to stimuli
  • irritants cause bronchospasm–>wheezing
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12
Q

Asthma stimuli

A
  • allergies
  • Exercise
  • infections
  • stress
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13
Q

Intrinsic Asthma

A
  • begins after age 35
  • more severe
  • year round
  • related to viral infection
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14
Q

Extrinsic Asthma

A
  • usually children, young adults
  • hayfever, allergies
  • fall/spring
  • 1/2 grow out of it
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15
Q

Asthma Treatment

A
  • bronchodilators
  • avoid irritants
  • pt/family edu
  • exercise goals
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16
Q

BPD pathophysiology

A

-damage to alveoli by mechanical ventilator–>inflammation, pulmonary edema and fibrosis

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17
Q

BPD Prognosis

A
  • 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
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18
Q

BPD Etiology

A

-neonates who have been mechanically ventilated or treated with high O2 levels as result of RDS

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19
Q

Factors leading to BPD

A
  • 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
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20
Q

BPD Treatment

A
  • Bronchodilators
  • Diuretics
  • K+ supplement
  • Nutritional Support
  • Antibiotics
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21
Q

Emphysema

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A
  • abnormal permanent enlargement of air spaces distal to terminal bronchiole, w/ destruction of their walls
  • “pink puffer”
22
Q

2 Types of Emphysema

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A
  • centrilobar

- panlobar

23
Q

Panlobar Emphysema

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A
  • –>enlargment of destruction of alveoli
  • affects lower lobes (worse prognosis)
  • Alpha1-Antitripsin deficiency
  • affects alveoli more
24
Q

Centrilobar Emphysema

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A
  • 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
25
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
26
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
27
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
28
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
29
Emphysema Treatment
- irreversible - stop smoking to stop further destruction - no effective Tx - PT
30
PT Management of Emphysema
-pursed lip breathing to increase lung efficiency and decrease collapse of airways
31
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
32
Bronchiectasis Prognosis
-with use of antibiotics as needed, can live into 70's & 80's
33
Bronchiectasis Etiology
- abnormal permanent dilation of medium-sized bronchi that extends distally - areas filled with secretions are swollen/inflamed & can be ulcerated
34
Types of Bronchiectasis
- cylindrical/longitudinal - varicose - saccular/cystic
35
Cylindrical/Longitudinal Bronchiectasis
- most common | - uniform dilation of airways
36
Varicose Bronchiectasis
- greater dilation than cylindrical | - bronchial walls look like varicose veins & irregular
37
Saccular/Cystic Bronchiectasis
-balloon shaped
38
Bronchiectasis Treatment
- antibiotics - pulmonary hygiene - hydration - immunizations to prevent flu & pneumonia - surgical resections of segments
39
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
40
CF Treatment
- chest PT - Antibiotics - Mucolytics (increase hydration) - Bronchodilators - Nutrition (pancreatic enzyme replacement) - Single/double lung or heart transplant
41
CF Prognosis
- median survival 35 years | - cause of death usually respiratory
42
CF Vent-Perf Mismatching Causes
- arterial hypoxemia-->dyspnea - Pulm HTN-->cor pulmonale-->R ventricle failure - Increased CO2 - Respiratory Acidosis
43
CF: | Bacterial Infections
- pseudomonas aeruginosa most common - staph aureus - haemophilus influenza - burkholderia cepacia
44
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
45
CF: | Pancreatic Insufficiency
- destruction by mucous secretions--> - enzymes trapped in ducts--> - autodestruction pancreas--> - decreased ability to absorb nutrients
46
CF: | Meconium Ileus
-obstruction of intestines by meconium stools due to lack of trypsin & other pancreatic enzymes
47
CF: | Salty Sweat
- Cl- imbalance & exocrine glands clogged by mucus | - excess Cl- can't be reabsorbed in sweat ducts so goes out to skin
48
Chronic Bronchitis Pathology
- due to chronic inflam of tracheobronchial tree--> - hyper-secretion of mucus--> - damage to cilia--> - mucus collects--> - place for infection and inflam
49
chronic bronchitis etiology
- #1 cause is smoking | - pollution
50
Chronic Bronchitis Diagnosis
- productive cough (>100 ml/day) for 3 months of the year for 2 consecutive years - "blue bloaters"
51
Chronic Bronchitis Treatment
- quit smoking - can improve if before blue and bloated stage & only has cough - IV antibiotics if infection - bronchodilators/O2 - chest PT
Cardio Pulm
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