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Cardio Pulm > Pulmonary Pathology: COPD/COLD > Flashcards

Pulmonary Pathology: COPD/COLD Flashcards

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

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

2 Types of Emphysema

A
  • centrilobar

- panlobar

23
Q

Panlobar Emphysema

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

Centrilobar Emphysema

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
Q

Emphysema Etiology

A
  • 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
Q

Emphysema Pathophysiology

A
  • 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
Q

Emphysema:

Enzyme/Inhibitor Imbalance

A
  • 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
Q

Emphysema:

Alpha1-Antritripsin Deficiency

A
  • 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
Q

Emphysema Treatment

A
  • irreversible
  • stop smoking to stop further destruction
  • no effective Tx
  • PT
30
Q

PT Management of Emphysema

A

-pursed lip breathing to increase lung efficiency and decrease collapse of airways

31
Q

Bronchiectasis Pathology

A
  • 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
Q

Bronchiectasis Prognosis

A

-with use of antibiotics as needed, can live into 70’s & 80’s

33
Q

Bronchiectasis Etiology

A
  • abnormal permanent dilation of medium-sized bronchi that extends distally
  • areas filled with secretions are swollen/inflamed & can be ulcerated
34
Q

Types of Bronchiectasis

A
  • cylindrical/longitudinal
  • varicose
  • saccular/cystic
35
Q

Cylindrical/Longitudinal Bronchiectasis

A
  • most common

- uniform dilation of airways

36
Q

Varicose Bronchiectasis

A
  • greater dilation than cylindrical

- bronchial walls look like varicose veins & irregular

37
Q

Saccular/Cystic Bronchiectasis

A

-balloon shaped

38
Q

Bronchiectasis Treatment

A
  • antibiotics
  • pulmonary hygiene
  • hydration
  • immunizations to prevent flu & pneumonia
  • surgical resections of segments
39
Q

CF Etiology

A
  • 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
Q

CF Treatment

A
  • chest PT
  • Antibiotics
  • Mucolytics (increase hydration)
  • Bronchodilators
  • Nutrition (pancreatic enzyme replacement)
  • Single/double lung or heart transplant
41
Q

CF Prognosis

A
  • median survival 35 years

- cause of death usually respiratory

42
Q

CF Vent-Perf Mismatching Causes

A
  • arterial hypoxemia–>dyspnea
  • Pulm HTN–>cor pulmonale–>R ventricle failure
  • Increased CO2
  • Respiratory Acidosis
43
Q

CF:

Bacterial Infections

A
  • pseudomonas aeruginosa most common
  • staph aureus
  • haemophilus influenza
  • burkholderia cepacia
44
Q

CF:

Obstructive Pulmonary Disease

A
  • small airways inflam & infection–>
  • incr mucus secretion–>
  • incr infection–>
  • neutrophils in airways–>
  • accumulated micro-organisms destroy lung tissue–>
  • fibrosis & vent-perf mismatching
45
Q

CF:

Pancreatic Insufficiency

A
  • destruction by mucous secretions–>
  • enzymes trapped in ducts–>
  • autodestruction pancreas–>
  • decreased ability to absorb nutrients
46
Q

CF:

Meconium Ileus

A

-obstruction of intestines by meconium stools due to lack of trypsin & other pancreatic enzymes

47
Q

CF:

Salty Sweat

A
  • Cl- imbalance & exocrine glands clogged by mucus

- excess Cl- can’t be reabsorbed in sweat ducts so goes out to skin

48
Q

Chronic Bronchitis Pathology

A
  • due to chronic inflam of tracheobronchial tree–>
  • hyper-secretion of mucus–>
  • damage to cilia–>
  • mucus collects–>
  • place for infection and inflam
49
Q

chronic bronchitis etiology

A
  • # 1 cause is smoking

- pollution

50
Q

Chronic Bronchitis Diagnosis

A
  • productive cough (>100 ml/day) for 3 months of the year for 2 consecutive years
  • “blue bloaters”
51
Q

Chronic Bronchitis Treatment

A
  • quit smoking
  • can improve if before blue and bloated stage & only has cough
  • IV antibiotics if infection
  • bronchodilators/O2
  • chest PT

Cardio Pulm (27 decks)

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