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Respiratory System Module > L20 COPD > Flashcards

L20 COPD Flashcards

1
Q

Goals of Health care

A

Preventative
Curative
Restorative (Chronic= non-curable)
Palliative (can no longer extend like –> help improve quality of life)

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2
Q

Effects of Disease

A
  1. Physiological Impairment (prior to symptoms. e.g. spirometry changes in COPD/asthma)
  2. Disability (breathlessness on rest/little exercise)
  3. Handicap
    (increased be social deprivation, (pshycosocial) mental illness)
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3
Q

Chronic disease management

A

Goals of Health care: Curative and Restorative
Effects of disease: Disability and Handicap
-Assessment of risk-clinical and social (peer support from patients with similar conditions)
-Diagnosis
-Clinical Advice
-Enhance patients ability to implement advice/self manage

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4
Q

Risk assessment Criteria

A
  • clinical medicine has limited ability to help someone with chronic disease (10-15 years)
  • social determinants become increasingly important
  • clinical and social determinants that effect people’s handicap
    1. Socio/economic profile
    2. Clinical Profile
    3. Environmental Factors
    4. Health Behaviours
    5. Living circumstances
    6. Health service related factors
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5
Q

Risk Assessment Criteria Personal Profile

A

Personal PRofile:

  • psychological issues heavily related to peoples ability to self manage
  • manefestations:
    1. Role models and norms inherent in cultural orientations
    2. Self-efficacy/self esteem
    3. Health locus of control
    4. Health literacy (understanding and being able to use the health system)
    5. Health beliefs/attitudes
  • so if there is a reasonably clear view of what should be done, how should it be delivered?
  • multidisciplinary team
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6
Q

If there is a reasonably clear view of what should be done, how should it be delivered?

A

-multidisciplinary team

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7
Q

Definition of COPD

A

COPD is a disease state characterised by airflow limitation that is not fully reversible
The airflow limitation is usually both progressive and associated with abnormal inflammatory response (neutrophil infiltration) of the lungs to noxious particles or gases (common cigarette smoke)

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8
Q

COPD spirometry

A

Volume/Time = maximal forced expiration
FEV1= Forced Expired volume in 1 second
Reduced FEV1 and
FEV1/FVC

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9
Q

COPD amplified inflammatory response

A

Macrophages, neutrophils, CD8+ T cells
Fibrosis of airways
Destruction of parenchyma (due to elastases released by neutrophils) –> emphysema

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10
Q

COPD Noxious particles and gases

A

cigarette smoke (often feel guilt/deserve)
-rest noxious particles often underestimated
coal dust
pollution
biomass fuels
(noxious particles create chemotaxis for neutrophil infiltration)

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11
Q

COPD history

A

productive cough
dyspnea
cigarette smoking

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12
Q

Flow volume curves in Obstructive lung disease

A

Concavity of expiratory loop= Flows falling as squeeze lung/airways collapsing due to:
1. Loss of elasticity
2. Reduced Airway Calibre: due to mucosal inflammation
RV hugely increased= expire and basal airways are closing. COPD patient closes airways much earlier than normal patients (hyperinflation)

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13
Q

Flow-volume curves in restrictive lung disase

A

Small lungs
FVC= about 3
Relatively Normal expired flow rates

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14
Q

Flow volumes

A

spirometers cannot measure lung volume as cannot measure residual volume

  • curves are superimposed
  • start at TLC
  • residual volume 1.5L. therefore vital capacity= 1.5–>6=4.5
  • Straight decline in flow as lung reduces with expiration
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15
Q

Hyperinflation in COPD

A

breath FRC towards the top of their lung volume (6L)

-harder to breathe high up, than compared to lower in lung volume

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16
Q

COPD pressure-volume curve

A 
Lung volume (up to TLC) vs Pressure
COPD= tidal breathing occurring at top of pressure volume curve (inspire and then try and tidal breath as well after that. very full)
-produce less change in volume for a given change in pressure
-breathing high up in lung volume increases the work of breathing (1. increased airways resistance 2. elastic forces(harder to breath high up))
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17
Q

COPD resusitation

A

try to reduce residual volume or degree at which a person is breathing at a high lung volume

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18
Q

Morbidity and Mortality Burden of COPD

A

COPD is a leading cause of morbidity and mortality world wide
results in an economic and social burden that is both substantial and increasing
-increasing rates in third world
-environmental pollution still an issue

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19
Q

Worldwide Burden of COPD

A

COPD prevalance, morbidity and mortality vary across countries and across different groups within countries

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20
Q

Timeline of COPD burden

A

The burden of COPD is projected to increase in the coming decades due to:

  1. continued exposure to COPD risk factors
  2. changing age structure of the world’s population
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21
Q

Differential Diagnosis b/w COPD and Asthma: COPD

A
  • Long smoking history (noxious particle/gas)
  • Symptoms slowly progressive
  • Dyspnoea during exercise
  • Onset in midlife (50-60 yrs)
  • Largely irreversible airflow limitation (10-15% response to bronchodilators)
22
Q

Differential Diagnosis b/w COPD and Asthma: Asthma

A

-Onset early in life (often childhood) (completely reversible)
-Symptoms vary from day to day
-Symptoms at night/early morning
-Allergy, rhinitis and/or eczema also present (assoc. with other forms of atopy)
-Family history of asthma
-Largely reversible airflow limitation
People with asthma develop COPD. asthma for 30yrs will have fibrorsis of airways)

23
Q

Asthma diagram

A 
Asthma:
Allergens -->
a) Ep cells --> CD4+ cells (Th2)
b) Mast cell --> Eosinophil (angiogenesis)
--> Bronchoconstriction AHR
--> Airflow limitation 
--> Reversible
24
Q

COPD diagram

A 
COPD
Cigarette smoke-->
a) Alv macrophage --> CD8+ cell (Tc1)
b) Ep cells --> Neutrophils
--> Small airways narrowing + alveolar destruction
--> Airflow limitation
--> Irreversible
25
Q

Asthma Eosinophil

A

Eosinophils are the dominant inflammatory cell in asthma

  • Reversible by steroids. (eosinophils very responsive to steroids)
  • inhaled steroids main part of asthma medication (not COPD)
26
Q

COPD medication

A

antibiotics
bronchodilators
B-agonists
anti-cholanergics

27
Q

COPD Exposure to (Noxious) Particles

A
  • Tobacco smoke
  • Occupational dusts, organic and inorganic
  • Indoor pollution from heating and cooking with biomass in poorly ventilated dwellings
  • Outdoor pollution
28
Q

Risk Factors for COPD

A
  1. Genes (COPD runs in families exp Emphysema)
  2. Exposure to (Noxious) Particles
  3. Lung growth and development (premature birth)
  4. Oxidative Stress
  5. Gender
  6. Age
  7. Respiratory infections
  8. Socioeconomic status
  9. Nutrition
  10. Co-morbidities (short of breath= do less= loss of muscle strength. Strengthening makes a large Distance. Heart failure and diabetes common)
29
Q

COPD-X Checklist

A 
Guidline for Diagnosis and Management of COPD
C- Confirm Diagnosis
O- Optimise management
P- Prevent Deterioration
D- Develop self-management plan
X- manage eXacerbations
30
Q

C- Confirm Diagnosis: COPD severity

A 
Post broncho-dilator FEV1%
-abitary definition based on spirometry
-% of normal (FEV1)
Mild COPD: 60-80%
Mod COPD: 40-59%
Severe COPD:
31
Q

O- Optimise Function

A 
(standard parts of care)
Check smoking status
Query optimal drug therapy
Check compliance
Review exercise status
Check current device in use
Nutrition
Consider Sleep apnoea
32
Q

Initial Treatment for Mild COPD

A 
FEV1= 60-80% 
Suggested Treatment:
Intermittent b/dilator
1. Salbutamol (200mcg) or
2. Ipratropium bromide (40 mcg) as needed
33
Q

Initial Treatment for Mod COPD

A 
FEV1= 40-59% 
Suggested Treatment:
Intermittent or regular b/dilator
1. Salbutamol (200-400mcg 4x daily) or
2. Ipratropium bromide (40 mcg 4x daily) or combined b/dilators
34
Q

Initial Treatment for Severe COPD

A

FEV1=

35
Q

Intermittent Bronchodilator

A

B- aggonist
Anti-cholanergic
-any combinations
Long acting: Ipratropium bromide and B aggonist. helpful advance

36
Q

P- Prevent Deterioration

A

Essential steps:
Level A: Annual influenza vaccination
Level B: Pneumococcal vaccination (re-vaccination 5 & 10 years)
Consider long-term home oxygen

37
Q

Hypoxia

A

Defined as a lack of oxygen regardless of cause or site
Tissue level effect
Acute hypoxia is characterised by:
-increased cardiac and respiratory rates
-mental deterioration
-sometime cyanosis (hypoxia may be present w/o cyanosis)

38
Q

Hypoxia vs Hypercapnoea

A

mmHg = kPa x 8
Hypoxia: PaO2 6.0 KpA
-dominant response to arterial hypoxia is to hyperventilate (to get rid of PCO2)
-therefore most common form of respiratory failure is hypoxia with hypercapnoea
-people who cannot maintain sufficient alveolar ventilation (hypercapnic respiratory failure)
Hypoxia and/or Hypercapnoea = Respiratory Failure
1kPa = 7.5 mmHg

39
Q

Oxygen cascade

A 
Oxygen passes from the atmosphere to the mitochondria down a partial pressure gradient termed the oxygen cascade
Normal values:
PIO2= 20kPa
PAO2= 13.3 kPa
PaO2= 12.9kPa
Tissue capillary PO2= 12.9-5.3 kPa
Intracellular PO2= low,
40
Q

PIO2 in Oxygen cascade

A

PIO2= 20kPa= 150mmHg(21%)
-influenced by F102 and atmosphere
-person coming off anaesthetic. too low PIO2= wrong mixture of anaesthetic gases.
Causes of Hypoxia:-top of everest/airplane that depressurises/house fire (producing CO and other oxides of nitrogen, diminishing environmental PO2)

41
Q

PAO2 in Oxygen cascade

A

PAO2= 13.3 kPa = 110mmHg
Influenced by alveolar ventilation and O2 consumption
-maintenance of alveolar ventilation to get rid of CO2
-CO2 production increases with exercise. need to be able to raise total (alveolar) ventilation to keep pace of increased production of CO2
-difficult with: people who have had large dose of morphine, obese (high work of breathing, raised PCO2 and hypercapnic respiratory failure)

42
Q

PaO2 in Oxygen cascade

A 
PaO2= 12.9kPa
Influenced by:
-venous admixture (V/Q and shunt)
-gas diffusion
-mixed venous O2 content
Lung causes of hypoxia:
-areas of lung that arent well ventilated but may still be well perfused. vice versa. V-Q mismatch. common in all lung diseases. (1. Pulmonary embolise (diminished blood flow) 2. Pneumonia (diminished alveolar ventilation. lots of blood going pass but not being full re-oxygenated= diminished PO2 in LVentricle))
43
Q

Tissue Capillary PO2 in Oxygen cascade

A

Influenced by oxygen delivery and local O2 consumption
-Normal PO2 in LV but blood and hence O2 distribution is inadequate (Poor delivery: peripheral artery embolise, stroke, myocardial infarction, LV dysfunction)
-Biggest example of poor delivery is: 1. myocardial infarction, 2. LV dysfunction
(peripheral perfusion is inadequate to maintain PO2)

44
Q

Intracellular PO2 in Oxygen cascade

A

-what reaches cells and mitochondria. are the mitochondria functioning or cellular poisoning with cyanide
-If intracellular PO2 is abnormally low, this will be due to one of the influenced mentioned
-Intracellular PO2 can be increased by increasing the driving pressure for the oxygen cascade e.g. increased P102
In practice, this means delivering Oxygen- enriched air to the patient (oxygen therapy)

45
Q

P -Prevent Deterioration

A

Risk Factor Reduction:

  • Check current smoking status
  • Advise the risks of smoking and benefits of stopping
  • Refer to Quit Programme if appropriate (Quitline 0800 778778)
  • Advise about pharmacological treatments for nicotine dependance
  • Assess occupation e.g. dusty conditions
  • Schedule follow up visit
46
Q

D- Develop Self management plan

A

Assist in the development of a self management plan (peer support group, sharing stories)
-check for psychosocial problems and suggest supportive strategies e.g. MAGIC, Green prescription
-Refer to pulmonary rehabilitation
-Refer to respiratory physician to:
Clarify diagnosis (diagnositc problems (multiple-morbidities eg. COPD + heart LV failure which is more important. muscular weakness inhibiting more than COPD))
Consider other therapies
Consider long-term home oxygen (chronically hypoxic. Low flow O2 used for 16 hrs day improves quality of life and reduces mortality/extends survival)
Facilitate pulmonary rehabilitation

47
Q

Pulmonary rehabilitation

A

Pulmonary rehabilitation reduces carer strain and increases patient knowledge

  • reduces dyspnoea, anxiety and depression, improves exercise capacity QOL and may reduce hospital admissions
  • multidisciplinary care plans and individual self-management plans may help prevent or manage crises
  • advanced care planning- end of life discussions- Concerto
48
Q

D Develop self-management plan

A

Refer to hospital if:

  • inadequate response to ambulatory management
  • inability to walk between rooms when previously mobile
  • inability to eat or sleep because of dyspnoea
  • altered mental status suggestive of hypercapnia
  • worsening hypoxaemia or cor pulmonale
  • newly occurring arrythmia
  • cannot manage at home
  • high risk co-morbidity condition
49
Q

X- Manage eXacerbations

A

Ensure understanding of exacerbations and importance of early action and treatment at home if possible
Consider need for controlled oxygen
Inhaled bronchodilators, oral glucocorticoids
Antibiotics are effective (Level B)
Review regularily

50
Q

What are the classic symptoms of COPD?

A

Upper resp tract infection
Sputum increased- changed to yellow/green
More breathless
Waking at night- common and early sign
Loss of energy/Lethargy
Unable to do things theyre normally able to do/breathless at rest

51
Q

Home visits

A
  • ask for medications
  • some people are non-adherent with treatment medications
  • never uses them but still pays for prescription (denial/doesnt want to disappoint the doctor)
  • many patients are unable to manage medicine

Respiratory System Module (25 decks)

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