Download COPD - ISpatula

Chronic Obstructive Pulmonary Disease
(COPD) part 1
Lecture 5
(in The 2nd half of Wednesday March 5th lecture)
MINUTE 24:20 "THE START"
The latest guideline "GOLD: Global Initiative for the study of Obstructive lung
diseases" is from February 2014.
Same definition of GOLD 2013, COPD: a common preventable and treatable
disease, characterized by persistent airflow limitation that is usually progressive and
associated with an enhanced chronic inflammatory response in the airways and the
lung noxious particles or gases. Exacerbations and comorbidities contribute to the
overall severity in individual patients.
COPD is with higher mortality rate than in Asthma. It is progressive disease, non fully
reversible (might be reversible in very very mild cases).
There might be a confusion while diagnosing for the first time, between sever
Asthma and mild COPD case (keeping in mind that Asthma is a risk factor for
COPD (not the major one, which is smoking, but definitely a risk factor)).
Some clinical terms are used to refer to COPD as the same condition (which isn't
clinically accurate, therefore not preferred.) conditions like Chronic Bronchitis and
Emphysema, because simply the patient can be suffering from either and yet not be
COPD patient, so again it wouldn't be clinically accurate.
MINUTE 30:44
The FEV1/FVC ratio (also referred to as the FEV1%) is our determinant of
reversibility in this disease. If that ratio was at least 70% post bronchodilators, then
the case is reversible.
If the FEV1 was 80% predicted normal or more, diagnosis of COPD should only be
made in the presence of respiratory symptoms. (breathlessness or cough)
COPD is a leading cause for world morbidity and mortality, and considered the 4th
world wide leading cause for death by 2030.
COPD is already one of the top 10 mortality causers worldwide, because of the high
risks COPD patients are predisposed to like pneumonia, HF, Cardiac risks, thrombosis
(so generally speaking, COPD is a risk factor for many fatal complications).
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
Figure from slide 4/53. (in the figure, pts with Asthma are 20.9mil, while they're
14mil in COPD, with 5000 and 120000 death rates, respectively).
Multiple pathogenetic mechanisms, are likely to contribute to the development of
COPD (there's definitely a genetic factor, but it's not the only determinant of COPD).
Genetic defects, like inherited deficiency of α1-antitrypsin, and the activation of
matrix metalloprotein 12.
Those enzymes, like antitrypsin (with it's proteolytic action, facilitating remodelings
in the structure of the airways), and the matrix metalloprotein (proteins that are also
involved in carcinogenesis; new structures and new matrices encouragers, the thing
that might lead to development of COPD) can be main linking causes to COPD, in
rare conditions.
Despite the rare leadership of those genetic defects to the condition of COPD, if no
such genetic defects were found, it is assumed that there are genetic defecting
correlations that are not known, yet have to do with the etiology.(it's reasonable to
assume that there is always some genetic susceptibility, with the always bigger role of
the environmental factors in the development.)
So the previous genetic defect resulting in the remodeling effect, the antitrypsin
deficiency, leads to a histological remodeling called "Emphysema".
This remodeling differs than Asthma's in the causative kind of inflammation, and the
more permanent changes in the Emphysema's.
Figure from slide 7/53.
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
In COPD, the cells with the most critical roles are macrophages and neutrophills
(eosinophils and mast cells in Asthma).
Emphysema is defined histologically, and Chronic bronchitis is defined clinically.
In the bronchitis, there is excessive mucus secretion witnessed, and it's known for the
accompanied cough (cough reveals bronchitis, and even bronchilities (if it's in the
smaller airways)).
In COPD, bronchitis is definitely chronic. So Bronchitis is: persistent productive
cough, that is present on most days for three months or more during the year over at
least two consecutive years. (so, the patient must be observed with (minimum) 6
months of persistent productive cough (3 months a year, in 2 years6 months)).
MINUTE 40
The increased mucus is an excellent medium for increased recurrent bronchial
infections, resulting in further damage, and repeated infections cause inability to clear
mucus and mucus plugs, resulting in progressive narrowing airways.
Smaller airways are more commonly affected in Asthma. Permanent changes happen
when smooth muscles proliferate, which stabilizes the recent structural changes.
Chronic bronchitis (also called blue bloaters, indication for cyanosis due to the
obstruction hypoxemia) presentation:
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
Slide 9/53.
Emphysema (pink puffers) is: what results from anatomical defects of the lung
characterized by abnormal permanent enlargement of the air spaces distal to the
terminal bronchiole accompanied by destruction of alveolar walls, but without
obvious fibrosis. (or in simpler language, it's the condition in which the air sacs of the
lungs are damaged and enlarged, causing breathlessness; collapse of the alveoli)
That destruction of the walls decreases the surface area decreasing the efficiency of
the alveoli. Complications of infection would result of filling those spaces with pus,
making gas exchange more and more impossible.
The term pink pertaining to Emphysema, indicates perfusion (Oxygen), so our patient
can exert additional effort(forced breathing) to reach optimum oxygen level, an effort
that makes up for nothing in chronic bronchitis.
Slide 11/53.
MINUTE 50
Pursed lips breathing (from point 4), is the act of breathing through the mouth
rapidly due to the unbalanced air exchange with the entrapped oxygen in the lungs.
The genetic (like α1-antitrypsin) correlation is more likely with patients younger than
30 years old.
Pulmonary rehabilitation(breathing exercises for dyspnea control) is to be done for
exacerbative and respiratory failure patients.
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
A clinical diagnosis for clinical COPD should be considered; any patient with
dyspnea, chronic cough or history of exposure to risk factors to the disease,
spirometry is needed for confirming the diagnosis (symptoms are never enough to
diagnose) spirometry is needed for evaluating reversibility.
Indicators for diagnosis:
dyspnea
Chronic cough
Exposure to risk factors
Cigarette smoking (most important)
ABG(arterial blood gas) determinations are important for the general assessment for
patient, for the hypoxemia. COPD patient can reach a severe level when he wont be
able to live without oxygen supply.
No screening is done for COPD confirmation, only spirometry.
MINUTE 60
There's a small percentage of patients who don't have COPD (we might overestimate
those patients with COPD, which even then with the scheduled standard treatment, it's
benefits outweigh the risks) while there is no such specific test we'd use to diagnose
COPD, other than the spirometry test for assessing the reversibility.
Post bronchodilator test, "albuterol" commonly used 400Mcg or 150Mcg
"anticholinergic Ipratropium bromide" or both, with the beta1 agonist test is
performed 10-15 mins later, and 30-45mins after administration with the
anticholinergics.
Usually 3 tests are performed with no more variations in values than 5%(or 150mls)
to consider it a valid test (we don't only depend on one value, so it's a reproduceable
test of 3 trials).
Differential Diagnosis
One of the most important conditions to differentiate COPD from is Asthma.
Tests like X-ray test aren't used to establish diagnosis, but still used in exacerbation
cases to screen for pneumonia infections.
MINUTE 64:15 "THE END".
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
Chronic Obstructive Pulmonary Disease
(COPD) part 2
Lecture 6
Monday March 10th lecture
Goals of therapy are of two domains; reducing the symptoms; and reducing the risk
(exacerbations; which directly increase the mortality in COPD cases, not necessarily
Asthma).
Figure from slide 17/53.
There are four components of the management:
- Assess and monitor disease
- Reduce risk factors (risk factors for exacerbations in COPD patients; mainly
smoking).
-
Manage stable COPD (maintenance treatment, with its pharmacologic and
non pharmacologic managements taught to patient and his family.)
- Exacerbations management.
(Patient isn't left to decide and take up the process of smoking cessation
because they barely would make progress on their own, we as practitioners
should be part of that management).
MINUTE 10
He pointed to the fact that the heavier the smoker is the longer his treatment of
maintenance might be.
Then he added something about the nicotine vaccines (which are still under clinical
trial) role of binding to nicotine receptors as a reason for decreasing the pleasure of
smoking (the mechanism of action).
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
Comorbodities are common in the COPD that should be actively identified. There
are the extrapulmonary effects (systemic) including: weight loss, nutritional
abnormalities, and skeletal muscle dysfunction.
Reduce Risk Factors: (slide 19/53)
-Reduction of total personal exposure to tobacco smoke.
-Smoking cessation
Unless contraindicated, offer NRT; varenicline or bupropion, as appropriate to people
planning to stop smoking.(as first line treatments) and if they weren't available the 2nd
line therapy would be clonidine and nortriptinin (tricyclic antidepressants) that would
decrease the withdrawal symptoms.
(NRT: nicotine replacement therapy).
There are helping strategies like asking, assesing, assisting and arranging the progress
of the smoking cessation along with the willingness of the patient to stop smoking.
Note not to confuse between the severity of the disease (the severity of the COPD)
and the severity of the airway obstruction.
The severity of the airway obstruction is measured and identified by a spirometry test
(and this is one component to asses the overall severity of the disease, so spirometry is
important for the diagnosis of the disease, but alone doesn't determine the severity of
the disease).
So, for now according to the limitation in the airflow, patients are classified into 4
categories (the 4 GOLDs 1,2,3,4).
From FEV1/FVC ration of <0.7 for determining irreversibility, and from the fact that
FVC fixed value in obstructive disease, the vriable value here would be the FEV1's;
so FEV1 value is what determines the degree of limitation: (slide 20/53)
GOLD1: Mild limitation  FEV1 80% or more of predicted (of standard from
charts).
GOLD2: Moderate limitation  FEV1 50%-less than80%
GOLD3: Severe limitation  FEV1 30%-less than 50%
GOLD4: Very severe limitation  FEV1 less than 30%
There is a link between airflow limitation and mortality, meaning: that the more
advanced the class is the higher mortality risk there is.
The overall severity would depend on three factors, which based on, patients are
catgorized:
- Limitation of airflow(the GOLD 4 categories).
- The symptoms.
- Risk of complications and death (expressed as the number of exacerbations).
MINUTE 20
Concerning the symptoms, up until last year there 2 scales that symptoms were
classified accordingly which are: the CAT (COPD Assessment Test) and the The
mMRC(Modified British Medical Research Counceil).
The mMRC(Modified British Medical Research Counceil) on the other hand isn't the
appropriate tool to assess the overall symptoms, because it addresses symptoms of
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
airflow limitation, not every other symptom though, while CAT addresses both.
Comprehensive assessment is recommended for the assessment rather than just the
mMRC that indicates the breathlessness that results from the airway limitation.
A new tool of assessment was the CCQ(COPD Control Questionaire) that was
introduced this year and expected to replace the mMRC(that isn't enough to cover all
symptoms) for the next guideline.
(slide22/53)
The score of current values ranges from 0-40, if it was less than 10 (less symptoms),
and if it was 10 and above (more symptoms experienced by patient).
The CCQ is a 10 item self administered(advantage) questionnaire developed to
measure clinical control in patients with COPD.
CCQ is short and easy to administer, plus it's reliable and responsive and available in
a range of languages and has been validated.
And for a full symptom evaluation and comprehensive management, there's the
SGRQ system, which is not adopted official tool yet.
But for determining the severity of condition and patient's category, we don't need the
overall symptoms, the main symptoms that can be known through the
CAT(breathlessness measure) and the mMRC when they'll be enough.
Number of Hospitalizations might become part of the determining criteria of patients
categories in the 2014 guideline, not just number of exacerbations(not every
exacerbations would result in hospital admission), and it is due to the increased risk
with the hospitalized cases than the unhospitalized.
MINUTE 30
There are four patient categories (A,B,C,D): (slide 25/53)
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
The used measurments for the previous grouping were:
-Spirometric classification.
-Number of exacerbations.
-Symptoms.
If there were 2 measurements, each indicates to 2 different groups, we diagnose the
patient with the higher group.
Now this grouping system is to determine treatment plans, since each group its own
specific course of treatment.
There are new pharmacological treatment agents like Salmeterol, Formoterol,
Indacetrol DPI (long acting beta2 agonist), and the long acting anticholinergics
(Aclidinium, glycopyrronium), and combinations like glycopyrronium and Indacetrol,
and planterol and umeclidinium, are new additions in therapy.
There is also the Roflumilast ,that elicited a big fuzz in the market for it's very
significant reduction in the risk, therefore assigned for only severe cases use.(like
exacerbation for chronic bronchitis).
Corticosteriods do decrease the risk too.
As we know, our courses of treatment for each group, would be consisting of
recommended (preferred) treatments, and alternatives (if recommended weren't
available for some reason).
MINUTE 40
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
Slides 28,29,30/53.
The most effective bronchodilators in Asthma are SABA, but in COPD LABA's and
SABA's have just the same effect.
The anticholinergics play central role in the symptomatic management in the COPD
patients.
(Doctor revised with some comparisons between therapy choices between groups, and
between COPD and Asthma, and emphasized on the no proven benefits for
duplication of medications from the same therapeutic family).
MINUTE 53:31 "THE END".
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
Chronic Obstructive Pulmonary Disease
(COPD) part 3 (and the last)
Lecture 7
Wednesday March 12th
As we mentioned before:
The most effective bronchodilator in the COPD are the the long acting.
anticholinergics, which are a very essential step in the management of COPD.
SABA's are not for all COPD patients, and the combination for SABA's and LABA's
are usually not preferred treatments.
Long term treatment with ICS is for patients very severe COPD and frequent
exacerbations that are not adequately controlled by long acting broncodilators,
patients at high risk like these are to be given ICS, and Roflumilast for exacerbations
risks decreasment, in addition to the adequate maintenance treatment.
it's a common practice unfortunately for some COPD patients to be prescribed ICS,
regardless of the category, which is totally inappropriate.
The reason for ICS uncommeness in COPD therapy as much as it is in Asthma
regimens of therapy, is the difference in the pathophysiology of each disease; due to
the different 2 types of inflammations involved, where the inflammation that's
involved in Asthma is the more responsive one to the ICS.
It is still proven for oral CS to be more effective than ICS, so orals are left to be given
to the exacerbation cases.
Bronchodilators are usually prescribed as needed (PRN; for group A), and for further
groups, usually on a daily basis, because any imbalance in their concentration can
lead to imbalance in control.
Combinations in treatment can improve the efficacy.
Indacetrol unlike Formoterol and Salmeterol, it is once daily given in the form of
DPI (not MDI), and it's bronchodilator effect is more than Salmetrol and Formetrol's
and similar to the Tiotropium.
MINUTE 10
(The Dr. (again) emphasizes on the fact of the unbeneficiency of combining LABA's
and SABA's in COPD management, and still expects some of us to miss that in the
exam! (so expect at least one question on this on your next exam!)).
The most important effect in COPD patients of anticholinergic medications, such as
Ipratropium, Oxitropium (short acting's) and Tiotropium bromide, aclidinium and
glycopyrronium (long acting's), appear to block the acetylcholine's effect on the
muscarinic receptors, current acting drugs block M2 and M3 muscaranic receptors.
The long acting anticholinergic Tiotropium has a pharmacokinetic selectivity for the
M3 pulmonary receptors and M1 neuronal receptors. The bronchodilating effect of
short acting inhaled anticholinergics lasts longer than that of short acting beta2
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
agonists, with some bronchodilator effect egenrally apparent up to 8 hours after
administration.
Tiotropium reduces exacerbations and related hospitalizations.
Aclidinium and Glycopyrronium seem to have similar action on lung function and
breathlessness as Tiotropium,, whereas far less data for other outcomes; such as
hospitalizations and survival.
Theophylline provides no additional bronchodilator effect beyond that of beta
agonists or anticholinergics; making its role controversial. (slide37/53).
Antioxidant agents, in particular N-acetyl cystine (the antidote IV given for
acetaminophen overdose toxicity for liver protection) which in COPD
bronchodilatory effect it's inhaled, it is not a standard treatment, used as alternative in
the group D.
In case of chronic bronchitis and it's productive cough the use of Mucolytic's in these
patients won't be effective.
In case of exacerbations, for short term relief, there are medications like codeine to
relieve cough, when chronic treatments with cough suppressants and mucolytics are
not recommended.
MINUTE 20
Nedocromil and leukotriene modifiers, have a modest role, are not standard
treatment.
Montilucast was an alternative for ICS in Asthma, but would have no beneficial role.
The TNF-alpha antibody (Infliximab)(that's usually for inflammatory bowel diseases)
was tried to reduce COPD inflammations but it's risks seemed to outweigh its
benefits.
The phosphodiesterase-4-inhibitor (Roflumilast) has been approved for chronic
bronchitis and exacerbation patients.
Clenbuterol beta2 agonist is during clinical trials.
Exacerbations, are the severe episodes that won't be relieved via maintenance
treatments. Most common causes for exacerbations are infections, with one third of
the causes are unfined.
The maintenance treatments then are given after knowing the causatives to prevent
any further exacerbations.
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
To determine the severity of the exacerbations:
(Figures from slide 43/53).
Exacerbations are classified into: Mild, Moderate and Severe.
There is a term in COPD called The cadinal symptoms; which are the three
essentials, starting from the worsening of dyspnea, the increase
in sputum volume; and the increase sputum purulence (so any change in color would
mean there is a case of infection).
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
These are not mandatory measures, but pretty preferred ones:
MINUTE 30
The Dr. emphasized on the importance of recognizing the indications for ICU
admission, and said that he'll be questioning us on them (maybe in the upcoming
exam, again).
Goals of therapy:
-prevention of hospitalization
-prevention of acute respiratory failure and death
-resolution of exacerbation symptoms
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
(Slide 45/53.)
(Slide 47/53).
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM
(Slide 47/53).
Oxygen treatment:
Supplement of oxygen is given if the oxygen saturation doesn't reach the 90% to
elevate the oxygen pressure (PaO2>60mmHg), variatedly some supplements on
sessions, and some 24/7 continiously, depending on the severity of the case.
Immunization:
The Pneumococcal vaccine should be received by COPD patients, and the
Influenza vaccine should be annually given too. And these vaccines are to reduce
the clinical infection rates in elderly patients by about 70%.
(Slide 49/53).
MINUTE 37 "THE END OF COPD/ THE START OF AKI".
good luck!!
DONE BY MENAS ABU ALHALAWA
LECTURED BY DR ALA LAHAM