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Cardiorespiratory > Lecture 12:COPD/A1AT > Flashcards

Lecture 12:COPD/A1AT Flashcards

1
Q

wht is the COPD?

A
  • -Chronic Obstructive Pulmonary Disease (COPD) 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 (vs asthma). The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
  • -A lung disease caused by inflammation of the small airways. Includes chronic bronchitis (characterized by productive cough ≥ 3 months in 2 consecutive years) and emphysema (dilation of the air spaces distal to the terminal bronchioles). Most cases of COPD (~ 90%) are caused by smoking.
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2
Q

what are the subtypes of COPD?

A

1)Chronic Bronchitis
“Cough productive of sputum on most days for at least 3 months for at least 2 consecutive years with no other attributable cardiac or respiratory cause”
2)Emphysema
“Abnormal and permanent enlargement of the airways distal to the terminal bronchiole”

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3
Q

what is the epidemiology of COPD?

A
  • -200 million people worldwide
  • -4th leading cause of death worldwide
  • -Predicted to become the 3rd most common cause worldwide by 2030
  • -Prevalence of COPD varies throughout different countries ranging from as low as 4% to 20%
  • -Sex: 3:2 male/female ratio
  • -The third most common cause of death worldwide
  • -Prevalence:
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4
Q

what are the risk factors of COPD?

A

–Cigarette smoking
95% of cases
–Biomass fuel burning (Developing world)
–Cessation decreases respiratory symptoms and rate of decline in lung function
–Pipe, cigar smokers, marijuana have a higher risk for COPD than non-smokers
–Sulphur dioxide and particulates (PM10) associated with chronic bronchitis, COPD
–Occupational dust: coal, silica, quartz, cadmium welding fumes
–Chest infections in 1st year of life
–Adenovirus/HIV

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5
Q

what is the main risk factor of COPD?

A

Smoking is the main cause of COPD, but only one in five smokers is affected, so it is likely that a genetic predisposition also plays a role in development of the disease.

  • -Those who have quit ≥ 10 years ago are not at increased risk.
  • -Passive smoking: If precautions against smoke exposure not taken, those who live in close proximity to smokers (e.g., children, relatives) have a significantly higher risk of COPD. The risk of asthma progressing to COPD also increases with exposure to smoke.
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6
Q

what are the endogenous factors associated with COPD?

A
  • -α1-Antitrypsin deficiency
  • -Antibody deficiency syndrome (e.g., IgA deficiency)
  • -Primary ciliary dyskinesia (e.g., Kartagener syndrome)
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7
Q

what are the baseline symptoms of COPD?

A 
1)Cough
Initially intermittent
2)Sputum production
purulent with exacerbation
3)Dyspnoea
on exertion initially but becomes progressive
4)Wheeze/chest tightness
- Initially intermittent, eventually chronic
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8
Q

natural history in a patient with COPD?

A
  • -Smokers
  • -Increasing symptoms: days to weeks
  • -Presence of baseline symptoms
  • Age profile

***New onset symptoms / rapid deterioration: suggests an alternate dx

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9
Q

what are the general inspection signs in a patient with COPD?

A

1) Central cyanosis
2) Accessory muscles of respiration
3) Nature of breathing
- -pursed-lip
- -prolonged expiration
- -hyperinflation

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10
Q

what are the respiratory P/E signs in patient with COPD?

A
  • -Decreased
  • -Rhonchi/wheeze
  • -Prolonged expiratory time
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11
Q

what are the P/E signs in acute COPD?

A
  • -Vital signs: RR, SaO2
  • -Hands: warm, sweaty, dilated veins, asterixis
  • -Hyperinflation / Hoover’s sign
  • -Auscultation: breath sounds, prolonged expiration, wheeze
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12
Q

what are the differential diagnoses of COPD?

A
  • -Acute CHF (CXR)
  • -Acute MI/tachyarrhythmia (ECG)
  • -Acute PE (Normal CXR/ decreased pCO2/ increased-D dimers)
  • -Pneumonia (CXR)
  • -Asthma (Peak expiratory flow rate/PFTs w’ reversibility)
  • -Mucus plugging (CT thorax/bronchoscopy)
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13
Q

what investigations should be performed in acute exacerbation of COPD?

A
  • -Arterial blood gas (ABG)
  • -CXR
  • -FBC, U&E, CRP
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14
Q

what ar the goals of management of acute exacerbation of COPD?

A
  • -Adequate oxygenation
  • -pH homeostasis
  • -Relief of bronchospasm
  • -Treat concurrent infection
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15
Q

what are the oxygenation goals in acute exacerbation of COPD?

A
  • -pO2 >8.0 kPa
  • -SaO2 >90%
  • -Venturi face mask
  • -FiO2: 28% - 40% (starting)
  • *Do not hyper oxygenate
  • **Do not under oxygenate
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16
Q

pH homeostasis in acute COPD?

A
  • -Maintain pH >7.27
  • -Therapeutic options
    1) NIPPV with BiPaP (non invasive positive pressure ventilation with bi-level positive pressure)
    2) Invasive ventilation (may not be appropriate depending on stage of disease and predicted outcome)

**CPAP contraindicated

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17
Q

what are the medications used in acute exacerbation of COPD?

A
  • -Bronchodilators
  • -Steroids
  • -Antibiotics
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18
Q

what are the medications used for bronchodilation in the acute exacerbation of COPD?

A
  • -Nebulised
    1) Ipratropium Bromide (Atrovent)
    2) Salbutamol (Ventolin)
  • -Repeat until symptomatic relief
  • -Maintenance 4 – 6 hourly
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19
Q

what steroids are used for acute exacerbation of COPD?

A
  • -Hydrocortisone IV 6 hourly
  • -Switch to oral prednisolone (within 48 – 72 hours)
  • -Tapering dose of prednisolone on discharge
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20
Q

what s the gold standard for COPD diagnosis?

A

Spirometry

21
Q

what are the characteristics of COPD in PFT?

A

Obstructive pattern
FEV1/FVC ratio decreased <70%
Not reversible
i.e. < 12% reversibility after bronchodilator therapy

22
Q

what are the characteristics of COPD in CXR?

A
  • -Hyperexpanded lung
  • ->7 ribs seen anteriorly
  • -Flattened diaphragm
23
Q

what are the FEV1/FVC and FEV1(pred) in very severe COPD?

A

<70% and <30%

24
Q

what are the FEV1/FVC and FEV1(pred) in mild COPD?

A

<70% and >*0%

25
Q

what are the FEV1/FVC and FEV1(pred) in moderate COPD?

A

<70% and 50-80%

26
Q

what are the FEV1/FVC and FEV1(pred) in severe COPD?

A

<70% and 30-50%

27
Q

what is the mMRC dyspnea scale?

A
  • -Modified Medical Research Council Dyspnea Scale
  • -An assessment tool used to evaluate the extent of a patient’s functional disability caused by dyspnea (e.g., secondary to chronic obstructive pulmonary disease). Its scale ranges from 0 (dyspnea only with strenuous exercise) to 4 (too dyspneic to leave the house or breathless when dressing).
  • -Low risk = FEV1/FVC ratio ≤ 0.7, FEV1≥ 50% predicted, and 0–1 exacerbation in the last year
  • -High risk = FEV1/FVC ratio ≤ 0.7, FEV1 ≤ 50% predicted, and ≥ 2 exacerbations in the last year
28
Q

what is the outpatient management of COPD?

A
  • -Smoking cessation
  • -Inhaled bronchodilators
  • -Inhaled corticosteroids
  • -Antibiotics for infective exacerbations
  • -Oxygen therapy
  • -Vaccinations
  • -Pulmonary rehabilitation
  • -Alpha 1 anti-trypsin replacement (only in A1AT patients)
  • -Non-invasive positive pressure ventilation
29
Q

what is the cause of chronic inflammation in COPD?

A
  • -Caused by increased oxidative stress (most commonly due to cigarette smoke) as well as by increased release of reactive oxygen species by inflammatory cells
  • -Increased number of neutrophils, macrophages, and CD8+ T lymphocytes → release of cytokines → amplification of inflammation and structural changes of lung parenchyma (e.g., growth factor release): CD8+ T lymphocytes mediate inflammation in individuals with COPD. CD4+ T lymphocytes and eosinophils mediate inflammation in individuals with bronchial asthma.
  • -Promotes goblet cell proliferation, mucus hypersecretion, and impaired ciliary function → chronic productive cough
    1) Reid index: The ratio of the width of the mucus-secreting glands to the combined width of the epithelium and cartilage in the bronchial tree. > 0.5 is characteristic of chronic bronchitis.
    2) Overproduction of growth factor → peribronchiolar fibrosis → narrowing of airway → obliteration → emphysema (airflow limitation)
    3) Smooth muscle hyperplasia of the small airways and pulmonary vasculature (mainly due to hypoxic vasoconstriction) → pulmonary hypertension → cor pulmonale
30
Q

what is the cause of tissue destruction in COPD?

A

1) Bronchopulmonary inflammation ↑ proteases, and nicotine use (or other noxious stimuli) inactivates protease inhibitors (especially α1-antitrypsin) → imbalance of protease and antiprotease → ↑ elastase activity → loss of elastic tissue and lung parenchyma (via destruction of the alveolar walls), which causes:
- -Enlargement of airspaces → ↓ elastic recoil and ↑ compliance of the lung → ↓ tethering of small airways → expiratory airway collapse and obstruction → air trapping and hyperinflation → ↓ ventilation (due to air-trapping) and ↑ dead space → ↓ DLCO and ↑ ventilation-perfusion mismatch (Va/Q) → hypoxemia and hypercapnia
- -↓ Blood volume in pulmonary capillaries → ↑ dead space → ↓ DLCO and ↑ Va/Q → hypoxemia and hypercapnia
2) Imbalance of oxidants and anti-oxidants and an overabundance of free radicals → contributes to chronic inflammation and inactivation of anti-elastase → exacerbates breakdown of elastic tissue

31
Q

what is the Tx of mild COPD with <1 exacerbation per year

A

Any bronchodilator (SABA or LABA)

32
Q

what is the Tx of severe COPD with <1 exacerbation per year

A

Any long-acting bronchodilator (LABA or LAMA)

If severe dyspnea: LABA and LAMA

33
Q

what is the Tx of mild COPD with >2 exacerbation per year

A

LAMA (Long-acting muscarinic agonist)

34
Q

what is the Tx of severe COPD with >2 exacerbation per year

A

LAMA or
If highly symptomatic (CAT > 20): LAMA and LABA or
If eosinophil count is ≥ 300/μl: LABA and ICS

35
Q

what are the measures to help in smoking cessation?

A
  • -Smoking cessation classes and counselling
  • -Nicotine replacement
  • -Varenicline
  • -Bupropion
36
Q

what are the 3 groups of bronchodilator therapy?

A
  • -B-agonists (short or long acting)
  • -Anti-cholinergics (short or long acting)
  • -Methylxanthines
37
Q

what bronchodilators are preferred in COPD?

A
  • -For both beta agonists and anticholinergics long acting formulations preferred
  • -Combined use of beta agonists and anticholinergics may be considered
  • -Inhaled preferred to oral
  • -Theophylline not recommended unless other bronchodilators not available
38
Q

what is the use of inhaled corticosteroids in COPD?

A
  • -Long term inhaled corticosteroids for patients with severe and very severe airflow limitations and frequent exacerbations not controlled by LA bronchodilators
  • -Long term monotherapy with inhaled steroids not recommended because less effective than combination with LA beta agonists
  • -Long term oral steroids not recommended
39
Q

what vaccinations are used in COPD?

A
  • -Influenza vaccine once yearly
  • -Pneumonia vaccines
    1) All COPD > 65 once off pneumonia vaccine
    2) COPD under 65 with FEV1<40%predicted every 5 years
40
Q

what are the complications of COPD?

A
  • -Respiratory Failure
  • -Cor pulmonale
  • -Recurrent chest infections
  • -Death
41
Q

what are the indications for long term oxygen therapy

A
  • ->16 hrs per day to COPD patients with chronic respiratory failure
  • -PaO2 ≤7.3kPa (55mmHg) or SaO2 ≤88% +/- hypercapnoea confirmed twice over a three week period
  • -PaO2 between 7.3kPa and 8kPa (60mmHg) or SaO2 of 88% if evidence of pulmonary hypertension, cor-pulmonale or polycythaemia (hematocrit >55%)
42
Q

what are the surgical options in COPD?

A
  • -Reserved for severe cases
  • -Bullectomy
  • -Lung volume reduction
  • -Lung transplant
43
Q

what is the A1AD?

A

An autosomal codominant deficiency of α1-antitrypsin, a protease inhibitor that suppresses enzymes that break down proteins (e.g., elastase, trypsin). Presents with panacinar emphysema and cirrhosis.

44
Q

what is the mutation in A1AD?

A

1) mutations in SERPINA1 gene
- -M is the normal allele.
- -S mutation causes a moderate decrease in AAT production.
- -Z mutation causes a significant decrease in AAT production.
2) The severity of disease depends on the specific genotypic expression, which correlates with the amount of α1-antitrypsin protein synthesis
- -PiMM: two normal alleles;100% expression of normal protein and therefore normal serum levels of AAT
- -PiMS: 80% of normal serum levels of AAT
- -PiSS, PiMZ, PiSZ: 40–60% of normal serum levels of AAT
- -PiZZ: ∼ 10% of normal serum levels of AAT (severe AAT deficiency)
3) Inheritance: autosomal codominant

45
Q

what is the pathophysiology of A1AD?

A

1) Alpha-1 antitrypsin: a protease inhibitor that is synthesized in the liver and protects cells from breakdown by neutrophil elastase
2) Gene mutation induces a conformational change in the structure of AAT protein.
- -Effect on the liver: impaired secretion of AAT by hepatocytes → accumulation of AAT in hepatocellular ER → hepatocyte destruction → hepatitis and liver cirrhosis
- -effect on the lungs: lack of functional AAT → uninhibited neutrophil elastase activity in the lungs → destruction of the pulmonary architecture → panacinar emphysema

46
Q

what are the clinical features of A1AD?

A
  • -Severe form: prolonged neonatal jaundice, hepatitis, cirrhosis, barrel chest, diminished breath sounds, wheezing, and dyspnea
  • -Mild form: manifests in adolescence, primarily with pulmonary disease; hepatic symptoms may also be present
  • -Increased risk of hepatocellular carcinoma (HCC)
47
Q

how A1AD is diagnosed?

A
  • -Serum: decreased antitrypsin protein levels
  • -Electrophoresis: decreased alpha-1 peak
  • -Chest x-ray: low and flat diaphragm, widened intercostal spaces, hyperinflation and increased basilar radiolucency of both lungs with rarification of peripheral pulmonary vessels
  • -Chest CT: panacinar emphysema (in contrast to centriacinar emphysema in smoking-related emphysema), bronchiectasis, bullae [5]
  • -Liver biopsy
  • -PAS-positive, spherical inclusion bodies in periportal hepatocytes
  • -Signs of cirrhosis
48
Q

what is the treatment of A1AD?

A
  • -Avoid active and passive exposure to cigarette smoke.
  • -Symptomatic treatment: bronchodilators, pulmonary rehabilitation, preventive vaccination, nutritional support if necessary
  • -Antitrypsin replacement: patients with severe AAT deficiency (e.g., ATT < 57 mg/dL) and evidence of decreased airflow
  • -Liver transplantation: results in correction of AAT deficiency; considered for end-stage liver disease

Cardiorespiratory (24 decks)

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