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Pulmonology > Chronic Obstructive Disorders > Flashcards

Chronic Obstructive Disorders Flashcards

1
Q

Chronic Obstructive Pulmonary Disease (COPD)

  • what is it characterized by?
  • what are the major disorders in this disease?
A
  • characterized by decreased airflow rate during expiration, often accompanied by elevated functional residual capacity resulting from trapped air
  • characterized by slow, progressive IRREVERSIBLE airway obstruction due to chronic bronchitis and/or emphysema

-Chronic bronchitis, emphysema, bronchiectasis

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2
Q

Define:
chronic bronchitis
emphysema
bronchiectasis

A

Chronic Bronchitis- a chronic productive cough for three months in each of two successive years in a pt in whom other causes of chronic cough have been excluded

Emphysema- abnormal and permanent enlargement of the airspaces that are distal to the terminal bronchioles, accompanied by destruction of the airspace walls WITHOUT obvious fibrosis

Bronchiectasis- shares many clinical features with COPD, including inflamed and easily collapsible airways and obstruction to airflow usually caused by infection

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3
Q

Is COPD a preventable disease?
Is it treatable?
Is it fully reversible?

A

preventable-YES!!

treatable- yes!

reversible- nooooo, airflow limitation is not fully reversible

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4
Q

COPD has periodic exacerbations with what sx?

A
  • increased dyspnea
  • increased sputum (usually colorless)
  • occasionally respiratory failure
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5
Q

What is the most common cause of COPD? other causes?

A

cigarette smoking!

other causes include alpha 1 antitrypsan deficiency, environmental/occupational dusts and gases

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6
Q

COPD pathophysiology

how does COPD affect RV, FRC (functional residual capacity), TLC, and VC?

A

Airways become irritated or poisoned from cigarettes and cause airway obstruction in the smaller conducting airways. This results in peripheral airway resistance due to:

  • destruction of alveolar support
  • loss of elastic recoil
  • structural narrowing due to inflammation

RV- increased
FRC- increased
TLC- may remain normal but is often increased
VC- reduced (due to air trapping and the decrease in lung elastic recoil)

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7
Q

Would you expect to see a V/Q mismatch in COPD? why or why not?

A

Yes, the loss of surface area along with bronchial obstruction and altered distribution of ventilated air results in V/Q mismatch

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8
Q

How does COPD create physiologic dead space?

A

COPD causes hyperinflation of the lungs (because of air trapping), in which alveolar pressure exceeds pulmonary artery pressure, stops perfusion and creates a physiologic dead space

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9
Q

Pathophysiology of Airflow Obstruction

A
  • structural changes increase the work of breathing
  • larger lung volumes put inspiratory muscles at a mechanical disadvantage
  • diaphragm is flattened, decreasing its ability to change intrathoracic volume
  • destruction of alveoli decreases surface area for gas exchange
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10
Q

How does Asthma differ from COPD?

A

asthma is reversible, COPD is not

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11
Q

Chronic bronchitis
aka and why
pathologic findings
classic sx

A

aka- Blue Bloaters, unable to maintain normal blood gases by increasing their breathing effort and therefore become hypoxic, hypercapic, cyanotic

findings-

  • goblet cell hyperplasia
  • mucous plugging, excess mucous secretion
  • fibrosis (not interstitial fibrosis)
  • narrowing of the airway lumen
  • excessive bronchial secretions and airway obstruction cause a V/Q mismatch

classic sx

  • dyspnea
  • chronic cough (productive)
  • mucous production (leading to frequent and recurrent pulmonary infections)
  • weight gain (early on because they cant breathe so they become couch potatoes)
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12
Q

Emphysema
aka and why
what is it
most common cause

A

aka- pink puffers, pursed lip breathing is helpful because: 1. it increases resistance to the outflow of air and 2. helps prevent airway collapse by increasing airway pressure

what is it- abnormal enlargement of the airspaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillary beds. The abnormal airspaces (Bullae) compress surrounding area of more normal lung

cause- cigarette smoking and alpha-1 antitrypsin deficiency

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13
Q

Emphysema patient presentation

A
  • long history of progressive dyspnea with late onset of nonproductive cough
  • initially, they are able to overventilate and maintain relatively normal blood gas levels until late in the disease
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14
Q

What are the two types of emphysema? Which one is most common? For each, what part of the lung is it most severe in?

A

Centrilobular emphysema (CLE) -most common type, most severe in upper lobes

Panlobular emphysema (PLE)- most severe in lower lung zones, generlly develops in pts with alpha-1 antitrypsin deficiency

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15
Q

What might you suspect in a 35 year old smoker patient with dyspnea?

A

alpha-1 antitrypsan deficiency

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16
Q

What is alpha-1 antitrypsin?

A

AAT is a protective protein that prevents alveolar wall destruction.

People with AAT deficiency do not release enough AAT from the liver, leading to progressive emphysema

17
Q

What testing might be done for emphysema?

A

lab
-serum AAT levels and phenotyping to confirm AAT deficiency

CXR
-AAT def produces a hyperlucent appearance because healthy tissue has been destroyed

Chest CT
-demonstrates widespread abnormally hypoattenuating areas resulting from a lack of lung tissue

18
Q

AAT-def tx

A

replace enzymes with Prolastin (weekly IV infusion)

19
Q

COPD

physical signs

A
  • increased AP chest diameter (barrel chest)
  • accessory muscle use
  • peripheral cyanosis
  • clubbing of the fingernails (hypoxia)
  • decreased breath sounds
  • hyperresonance on percussion
  • wheezing on expiration
  • prolonged expiratory phase
  • low, flat diaphragm

advanced

  • polycythemia
  • pulm HTN
  • RV hypertrophy
  • Cor Pulmonale
20
Q

Key indicators for COPD

A
  • chronic cough
  • chronic sputum production
  • dyspnea (progressive, persistent, worse during excersize and resp infections)
  • acute bronchitis
  • hx of exposure to risk factors
21
Q

What would you expect to see on a CXR of COPD?

A
  • hyperinflation
  • flattening of diaphragm
  • increased retrosternal air space
  • long narrow heart shadow
22
Q 
PFT's are the cornerstone of making COPD dx. what happens to:
FEV1
TLC
FVC
RV
CO2 diffusing capacity
A 
FEV1-decreased
TLC-increased
FVC-increased
RV-increased
CO2 diffusing capacity-decreased

AND NO REVERSIBILITY

23
Q

COPD complications

A
  • Cor Pulmonale (pulmonary HTN and right sided heart failure)
  • pneumonia (strep pneumoniae most common)
  • Pneumothorax (d/t weaken lung structure)
  • secondary polycythemia
  • end stage lung disease (resp failure, decline in lung function, rising levels of co2 in blood)
24
Q

COPD tx

A 
SMOKING CESSATION (has to happen before anything else)
pulmonary rehab
immunizations
medications
nutrition
whole body conditioning
25
Q

bronchodilators and steroids for stable COPD

A

Bronchodilators

  • SABA (albuterol)
  • LABA (salmeterol and formoterol)
  • Anticholinergics (ipratropium, tiotropium)
  • methylxanthines (theophylline)

Steriods

  • oral (prednisolone)
  • inhaled (fluticasone ((flovent)), budesonide)
26
Q

Pharmacotherapy steps for Stable COPD

A
  1. as needed short-acting inhaled bronchodilators (SABA, anticholinergics)
  2. give both bronchodilators together
  3. long-acting inhaled bronchodilators
  4. corticosteroids

combined therapy with LABA +ICS is better than not

mucolytics- mucomyst: leads to a small reduction in acute exacerbations, although not considered standard therapy

27
Q

What is the only tx that has been shown to prolong survival in COPD pts?

A

long term oxygen!

  • decreases risk of right sided heart failure, polycythemia, impaired mental status
  • PROLONGED SURVIVAL
  • O2 delivery must be a low of a dose as possible to maintain hemodynamic stability and to not suppress the drive to breathe
28
Q

Tx for severe COPD

A
  • lung reduction surgery for emphysema (decrease overall lung volume by removing diseased lung tissue, improve elasticity, reshape diaphragm)
  • -LVRS is not a cure but can improve quality of life

-lung transplant

  • guidelines for referral are the BODE index exceeding 5.
  • guidelines for transplantation are a BODE index of 7-10 and at least one of the following
  • -hx of hospitalization for exacerbation associated with acute hypercapnia
  • -pulm HTN or cor pulmonale or both
  • -FEV1 of less than 20% and either DLCO of less than 20% or homogeneous distribution of emphysema
29
Q

precipitating causes of acute exacerbation

A
  • bacterial infections (strep pneumo most common)
  • viral infections
  • no specific precipitant can be ID’ed
30
Q

Indications for ICU admission for COPD pt

A
  • severe dyspnea
  • mental status changes
  • persistent worsening hypoxemia
  • hypercapina
  • respiratory acidosis
31
Q

Discharge criteria for COPD pt

A
  • clinical and ABG stability for at least 12-24 hrs
  • use of inhaled bronchodilators less frequently than every 4 hours
  • acceptable ability to eat, sleep, ambulate
32
Q 
Bronchiectasis
causes
requires what two factors
what is the host response to these factors
result
A

causes:

  • congenital (50% are CF)
  • acquired (often from recurrent inflammation or infection of the airways)

requires:

  • infectious insult
  • impaired drainage, airway obstruction, or defect in host defense

host response:
-transmural inflammation, mucosal edema, ulceration, and neovascularization in the airways (pus collects within the bronchi and normal flow of o2 into the lungs and co2 out of the lungs is impaired)

result:
-permanant abnormal dilation and destruction of the major bronchi and bronchiole walls. Recurrent infection is common which leads to to further scarring, obstruction, distortion of the airways along with temporary or permanent damage to the lung parenchyma

33
Q

Bronchiectasis

sx

A
  • chronic cough with larde amounts of FOUL SMELLING SPUTUM PRODUCTION
  • hemoptysis
  • cough worsened by lying on one side
  • SOB
  • weight loss
  • fatigue
  • clubbing
  • wheezing
  • cyanosis
  • paleness
  • halitosis
34
Q

Bronchietasis work up and Dx

A

-may hear small clicking, bubbling, wheezing, rattling, or other sounds, usually in the lower lobes

work up

  • CXR
  • Chest CT
  • sputum culture
  • CBC
  • sweat test of other CF testing
35
Q

Bronchiectasis Tx

A

*Team effort (refer to pulmonologist)

  • resolve any underlying disorder and improve bronchial hygiene
  • Abx therapy (for acute exacerbations, prevent infection, or reduce bacterial burden)
  • removal of foreign object
  • mucolytics to help thin sputum
  • physiotherapy (percussion to help the lungs drain)
  • surgery
  • pneumococcal and influenza vaccine
  • ICS BID
  • NSAIDS (slowed progression of CF-bronchiectasis)
  • Pulmonary rehab improved exercise tolerance

Pulmonology (15 decks)

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