This document discusses systemic inflammation and comorbidities in COPD. It notes that COPD is associated with various important comorbidities beyond the lungs, and inflammation is seen systemically, not just in the lungs. Common comorbidities discussed include cardiovascular diseases like heart disease, hypertension, and stroke. It also mentions increased risk of osteoporosis, diabetes, lung cancer, and other conditions. The systemic inflammation in COPD can be caused by factors like smoking and hypoxia and may contribute to the development and severity of these comorbid conditions.
New technology called Electromagnetic Navigation Bronchoscopy® (ENB) that uses virtual bronchoscopy and real time 3-dimensional CT images that enable me to localize these peripheral lung nodules for diagnosis and treatment. This outpatient procedure is minimally invasive and therefore has a small risk of pneumothorax (2-3%) and its published diagnostic yield rates range from 67% - 86%
New technology called Electromagnetic Navigation Bronchoscopy® (ENB) that uses virtual bronchoscopy and real time 3-dimensional CT images that enable me to localize these peripheral lung nodules for diagnosis and treatment. This outpatient procedure is minimally invasive and therefore has a small risk of pneumothorax (2-3%) and its published diagnostic yield rates range from 67% - 86%
Chronic Obstructive Pulmonary Disease BY
Dr Akram Yousuf
Resident Internal Medicine
Liaquat University of Medical Health and Sciences Jamshoro Pakistan
Pre operative pulmonary evaluation 2019Parthiv Mehta
Comprehensive over view of identification of risk factors and its assessment. understanding basics and specialized investigations, its interpretation and methodical use of algorithm.targeted to enhance identification of risks and prevention of complications
Napcon 2014 presentation abstract Page 14 - Presentation28
High Dose Rate Endobronchial Brachytherapy for Palliative Treatment of Lung Cancer – A Case Report Muhammed Aslam N K , Rajeev Ram , Achuthan V , Manoj D K ,Rajani M Pariyaram medical colleg , kannur
Chronic Obstructive Pulmonary Disease BY
Dr Akram Yousuf
Resident Internal Medicine
Liaquat University of Medical Health and Sciences Jamshoro Pakistan
Pre operative pulmonary evaluation 2019Parthiv Mehta
Comprehensive over view of identification of risk factors and its assessment. understanding basics and specialized investigations, its interpretation and methodical use of algorithm.targeted to enhance identification of risks and prevention of complications
Napcon 2014 presentation abstract Page 14 - Presentation28
High Dose Rate Endobronchial Brachytherapy for Palliative Treatment of Lung Cancer – A Case Report Muhammed Aslam N K , Rajeev Ram , Achuthan V , Manoj D K ,Rajani M Pariyaram medical colleg , kannur
Zahida Chaudhary, MD leads the discussion on Obesity amongst children and adults.
Want an audio version? Subscribe to our Podcast on iTunes! (Search "S'eclairer Chatterbox!")
Want to join us for the live discussion? Check out our Social Media in the noon hour every Monday as we sit down on Google Hangout OnAir! Follow us on Twitter (@seclairerlife), Facebook, or Google+ to get updated with the link when we start!
Obstructive Sleep Apnoea and the Metabolic SyndromeDr.Aslam calicut
Introduction
OSA and the Metabolic Syndrome
OSA and Obesity
OSA and Hypertension
OSA and Insulin Resistance
OSA and Dyslipidemia
Pathogenesis
Effect of Treatment
Conclusion
The latest guidelines on the management of a COPD patient ( Stable COPD, patient with an exacerbation of COPD), latest modalities of treatment of a COPD patient
Obstructive sleep apnea (osa)The relationship of airway obstruction and dento...奇卿 黃
Airway obstruction, coupled with loss of lingual and palatal pressure of the tongue, produces alterations in the maxilla. The positioning of the tongue also plays an important role in mandibular development. The tongue displaced downward can lead to a retrognathic mandible; and an interposed tongue can lead to anterior occlusal anomalies.
Assessing COPD comorbidities and linking the underlying mechanism of their occurrence with COPD and finding the prober stratification , clusterization and management of COPD comorbidities.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Gold update 2015
“ COPD a common preventable and treatable
disease, is characterized by persistent airflow
limitation that is usually progressive and associated
with an enhanced chronic inflammatory response in
the airways and the lung to noxious particles or
gases.
Exacerbations and comorbidities contribute to the
overall severity in individual patients.
3. Introduction
Over the last two decades, it has gradually been
recognised that:
1. Chronic Obstructive Pulmonary Disease (COPD) is
associated with various important co-morbidities
2. Inflammation in COPD is not confined to the lung
alone but is also seen systemically.
4. Currently, the “GOLD” definition of COPD includes
the words “some significant extrapulmonary effects
that may contribute to the severity in individual
patients”.
It has even been suggested that COPD should be
renamed a “chronic systemic inflammatory
syndrome” (Fabbri and Rabe).
5. Systemic Inflammation in COPD
The presence of systemic inflammation in COPD is
undeniable.
Several studies have shown that markers of systemic
inflammation are increased in subjects with stable
COPD, they appear early in COPD and increase with
increasing COPD severity
6. The markers of systemic inflammation that are
consistently increased are
hs C-Reactive Protein (hsCRP),
fibrinogen,
ferritin,
total leucocyte count,
Reactive Oxygen Species,
Interleukins and other cytokines
Transforming Growth Factor Beta1 (TGF b 1)
Tumor Necrosis Factor-a (TNF-a) receptor
polymorphisms.
7. Two explanations for the systemic inflammation of
COPD have been described:
1. Spillover of inflammation from the pulmonary into
the systemic compartment.
2. A pro-inflammatory phenotype, where systemic
inflammation occurs independent of the pulmonary
inflammation.
8. Discordance between TNF-α and IL-8 values in
induced sputum and plasma suggests that systemic
inflammation in COPD is independent of pulmonary
inflammation
9.
10. Causes of the Systemic
Inflammation
Smoking, a factor common to COPD and several of its
comorbidities may trigger systemic inflammation by
inducing oxidative stress, as well as by producing
peripheral vascular endothelial dysfunction.
These processes occur even in smokers of only a few
pack-years and in passive smokers
11. Inflammatory markers in COPD
In COPD ↑ levels of inflammatory cytokines, acute
phase proteins, and markers of oxidant stress (Oudijk
EJ, et al. Eur Respir J Suppl 2003;46:5s–13s)
Cytokines in COPD include TNF-α, TGF-β, interferon-
γ, and ILs- 6 and 8 (Wouters EF et al.Proc AmThorac
Soc 2005;:26–33)
COPD with lowest FEV1 have the highest levels of CRP,
fibrinogen, and other systemic inflammatory markers,
while those with the highest FEV1 have the lowest
values (Circulation 2003; 107:1514–1519)
12. ↑cytokines and CRP are associated with heart disease,
and atherosclerosis in patients with COPD (van Eeden
SF, et al. Proc Am Thorac Soc 2005;:61–7)
CRP and fibrinogen, are elevated in smokers, and ↑
fibrinogen levels in smokers are associated with ↓ lung
function and ↑ risk for COPD (Dahl M,et al. AJRCCM
2001;164(6):1008–11)
↑ CRP is an independent risk factor for CAD,
myocardial infarction and stroke (PRIME Study. 2003;
23: 1255–61)
13. Another trigger is hypoxia of severe COPD.
Hypoxia-inducible factor (HIF)-1 may signal the
presence of hypoxia to the gene-transcriptional
machinery in various tissues, and the need for adaptive
responses to this hypoxia.
HIF-1 activates a number of target genes involved in
angiogenesis, energy metabolism, erythropoiesis,
inflammation, cell proliferation, vascular remodeling,
and vasomotor responses.
14. Several HIF-1 target genes maybe involved in these
processes.
TNF-α levels were significantly correlated with the
severity of arterial hypoxaemia.
Improved survival in patients receiving domiciliary
oxygen therapy (LTOT), might be due to decreased
systemic inflammation
15. Adipokines may represent the link between COPD
and its co-morbidities.
Circulating leptin may promote systemic
inflammation in stable COPD.
Anti-elastin antibodies have been demonstrated in
COPD.
Auto-immunity may play a role, and explain why
COPD processes persist even after quitting smoking.
16. Accelerated lung ageing may underlie the systemic
inflammationof COPD.
Telomeres, “ protective caps” on the ends of
chromosomes, get progressively shorter as cells divide
and this is accelerated with oxidative stress.
COPD, which is characterized by oxidative stress, may
therefore be a disease of accelerated ageing of both the
lung and other systems.
17.
18. COPD is a complex disease
On the one hand, the latter could be the consequence
of the former, the socalled “systemic effects” of
COPD . On the other hand, they may represent the
cooccurrence of highly prevalent diseases
(cardiovascular, metabolic, muscular, and bone
disorders) in aged patients (comorbidities)
19. Consequences of Systemic
Inflammation
Several systemic manifestations and chronic complex
co-morbidities of COPD have been described
Skeletal muscle wasting
Cachexia: loss of fat-free mass
Lung cancer (small cell, non-small cell)
Pulmonary hypertension
Ischaemic heart disease: endothelial dysfunction
Congestive cardiac failure
Osteoporosis
Normocytic anaemia
Diabetes mellitus/ Metabolic syndrome
Obstructive sleep apnoea
Depression
20. ACCORDING TO Georgios Hillas, Fotis Perlikos,Ioanna
Tsiligianni2, Nikolaos Tzanakis
International Journal of COPD ON 2015 JAN
Respiratory comorbidities
Asthma
Lung cancer
Pulmonary fibrosis
Cardiovascular comorbidities
Hypertension
Congestive heart failure
Coronary heart disease
Atrial fibrillation
Pulmonary artery hypertension and subsequent right
heart failure
21. Venous thromboembolism
Stroke
Metabolic comorbidities
Diabetes and metabolic syndrome
Osteoporosis
Cachexia and myopathy
Mental comorbidities
Other comorbidities
Obstructive sleep apnea syndrome
Gastroesophageal reflux disease
Chronic renal failure
22.
23. Gold 2015
COPD patients are at increased risk for:
• Cardiovascular diseases
• Osteoporosis
• Respiratory infections
• Anxiety and Depression
• Diabetes
• Lung cancer
• Bronchiectasis
These comorbid conditions may influence mortality and
hospitalizations and should be looked for routinely, and
treated appropriately.
28. COPD and the Heart
COPD and CAD are closely linked, with often a failure
to recognize one in the presence of the other.
Cardiovascular mortality -14%- 42 % of the overall
observed mortality in COPD, compared with 14% -61
% due to COPD.
29.
30.
31. Data from the TORCH study also showed that
cardiovascular causes accounted for about 27% of the
overall mortality.
Data from the large Saskatchewan data base suggest
that patients with COPD had more deaths and
hospitalisations for cardiovascular causes than from
COPD itself.
32. Poor lung function is a risk factor for
Atrial fibrillation,
ventricular dysrhythmias, and left ventricular diastolic
dysfunction.
When stratified according to FEV1, there is a linear
increase in mortality (CVS and all-cause)among COPD
subjects, comparable with hypercholesterolemia
Every 10% decline in FEV1, cardiovascular mortality
increases by 28% showing a clear relation between
overall cardiovascular death and low lung function
33. Participants in the National Health and Nutrition
Examination Survey (NHANES) Epidemiologic
Follow-up Study with the lowest levels of FEV1 showed
5 times higher risk of death by ischemic heart
disease.
vital capacity index correlates inversely with CVS
mortality and all-cause mortality, across age and
gender, becoming even stronger with increasing age
and in women
34. Recent evidence suggests that beta-blocker co-
prescription improves cardio-vascular outcomes and
survival in patients with COPD.
Long-term cardioselective beta-blockade in patients
with COPD was shown to be safe and well-tolerated in
a Cochrane data base meta-analysis of 20 randomized,
controlled, crossover trials of cardioselective beta1
blockers in patients with COPD (without CHF).
35. Unrecognized heart failure in COPD causes confusion,
worsens outcomes and complicates management.
Almost 50% of patients in one study of heart failure with
preserved systolic function met the criteria for airflow
obstruction (FEV1/FVC% < 0.7).
In heart failure, the electrolyte derangements seem to
increase bronchial hyperresponsiveness,.
36. Endothelial dysfunction and COPD
The systemic inflammation in COPD ,key determinant
for the development of pulmonary and systemic
endothelial dysfunction.
Other factors could be involved in maintaining
endothelial integrity, such as circulating endothelial
progenitor cells (CEPCs).
The number of CEPCs appears to be reduced in the
systemic circulation and increased in the pulmonary
circulation of patients with COPD
37. Coagulopathy and COPD
The systemic inflammation present in COPD appears to
induce a ‘‘pro-coagulant’’ state.
In the basal state, COPD patients exhibit abnormally high
levels of tissue factor (tissue factor pro-coagulant activity)
and Factor VIIa , and their fibrin clots are resistant to lysis .
It was recently discovered that coagulation is altered in
patients with COPD.
An electron microscopy study showed that fibrin clots
isolated from the plasma of COPD patients are denser
and more resistant to lysis than those from control
subjects with an equivalent circulating fibrinogen
concentration(Kaczmarek P, Sladek K, Stepien E, et al.)
38. Systemic venous thromboembolism and COPD
The three factors of Virchow’s triad are observed in
COPD (systemic venous endothelial dysfunction,
coagulopathy and venous stasis due to a physical
inactivity), which explains their predisposition to
venous thromboembolism (VTE).
During COPD exacerbations, VTE is found in 3–29%
of cases
39. There are no specific clinical, biological or radiological
signs indicative of VTE.
It should be suspected during COPD exacerbation -chest
pain or syncope, or a fall in arterial carbon dioxide tension
in a patient who is usually hypercapnic.
VTE during a COPD exacerbation prolongs hospitalisation
by 4.4 days and increases the 1-year mortality rate by 30%
(Sidney S, Sorel M,).
Failure to diagnose VTE and to institute suitable
anticoagulant therapy increases the death rate by 25%
during hospitalisation.
40. Anemia
Anemia has been described with variable frequency in
the COPD population, from 3.3% in NHANES to 6.2%
among COPD outpatients, and up to 17% among
COPD inpatients.
It has been hypothesized that anemia in COPD shares
mechanisms with other anemias of chronic disease
with persistently elevated interleukins (especially IL-1)
interfering with the response to erythropoietin.
A recent cross-sectional study found higher levels of
erythropoietin in COPD patients with anemia,
compared with those with normal hemoglobin.
41. Different COPD outcomes, including poor functional
status,frequent exacerbations and increased health
care-related direct and indirect costs have been
associated with the presence of anemia.
Cohort studies suggest that survival also seems to be
affected by the hemoglobin level, being lower in those
with anemia than in those with a normal level or
polycythemia.
No specific treatment recommendations for coexistent
anemia in COPD are currently available
42.
43. COPD and Osteoporosis
Both osteopenia and osteoporosis are increased among
patients with COPD, with the severity of COPD related
to the prevalence of osteoporosis
This is at least partly independent of the effects of
steroids, being seen even in the absence of steroid use.
44. Osteoporosis may be related to elevated TNF-a and
Interleukin-1, which stimulate the differentiation of
macrophages into osteoclasts via mesenchymal cells
releasing receptor activator of nuclear factor-k B
ligand, a member of the TNF-a superfamily.
45. This suggests that COPD associated osteoporosis is
also due to systemic inflammation, and therefore a
systemic Consequence
Age, limited physical activity, low Body Mass Index
(BMI), smoking, decreased gonadal function (due to
both age and smoking) and malnutrition are also
contributing factors.
46. COPD and Body Weight
Skeletal muscle wasting is a typical co-morbidity of
COPD.
Skeletal muscle itself can contribute to systemic
inflammation.
Wasting is commonly seen in patients with COPD,
increasing in prevalence from 20% in early, stable
COPD to 35% in patients in severe COPD patients
enrolled for pulmonary rehabilitation.
The loss of body mass appears to mainly occur in fat-
free mass (FFM), typically skeletal muscle, while fat
mass is relatively preserved
47. The mechanism of weight loss appears to be related to
1. Increased levels of IL-6 in particular, and systemic
inflammation in general.
2. Decreased intake, though this is mainly during acute
exacerbations.
3. Hypoxia
4. Endocrine changes, including Growth Hormone
resistance, reduced Insulin-like Growth Factor- 1
(IGF-1) gene expression and low-levels of IGF-1
binding proteins, and reduced testosterone levels
48. The loss of muscle will have an adverse impact on
respiratory and peripheral muscle function, exercise
capacity, and health status.
Weight loss has been shown to be an important
negative predictor for survival in COPD.
BMI is one of the four parameters used in calculating
the BODE index, a validated prognostic score of
mortality in COPD
49. COPD and Diabetes
Systemic inflammation also explains the association
between COPD and diabetes.
prevalence of diabetes, quoted at only 2.9% is
probably an underestimated value
It is heavily influenced by the study of Sidney et al
which had the largest numbers (45066 subjects) and
the lowest prevalence (2%)
50. A much higher prevalence of diabetes in COPD was
reported by Mapel et al (12% of 200 subjects), and
Walsh and Thomashow (16% of 3000 subjects)
Overall, the consensus, is that there is a truly increased
prevalence of Type 2 Diabetes mellitus in COPD.
51. The presence of inflammation and of markers of inflammation
(fibrinogen, circulating white blood cell count and lower serum
albumin) predicts the development of diabetes and metabolic
syndrome.
Patients with Type 2 diabetes mellitus have increased circulating
levels of TNF-a, interleukin(IL)-6 and CRP -also risk factors for
cardiovascular events.
Diabetes is independently associated with reduced lung
function, and, with obesity could further worsen COPD severity.
It appears that there is a fairly complex interaction between
smoking, diabetes/ metabolic syndrome, COPD, cardiovascular
disease and obesity leads to the development of co-morbidities.
52. Some COPD patients may show features only of the
metabolic syndrome.
Metabolic syndrome is characterized by abdominal
obesity, elevated triglycerides, atherogenic
dyslipidaemia, elevated blood pressure, high blood
glucose, and underlying insulin resistance.
It is also associated with a pro-thrombotic and a pro-
inflammatory state with increases in plasminogen
activator inhibitor, CRP and fibrinogen.
Some part of the association is independent of steroid
treatment and decreased physical activity
53. COPD and lung cancer
COPD is not only a risk factor for lung cancer, but also
for death from lung cancer
The presence of moderate or severe airflow
obstruction is a significant predictor of incident lung
cancer
(Mannino DM et al. Arch Intern Med 2003;113:1475-1480 )
Hypoxia-inducible transcription factors (HIF) may
promote angiogenesis and involved in both ischemic
diseases and cancer
(Constans A et al The Scientist 2004;18:20-21)
54. Patients with COPD at the time of lung cancer diagnosis
have a poorer prognosis .
3-year survival in the COPD-lung cancer group was 15%
versus 26% in the lung cancer without COPD group
Very recently, genome analyses of patients with COPD and
lung cancer have shown susceptibility loci common to both
diseases on several chromosomes (e.g. 15q25, 4q31 and
6p21) .
Role for epigenetic changes common to the development of
lung cancer and COPD has also been suggested.
55.
56. Gastroesophageal Reflux Disease
Consistently higher prevalence of the disease
among those with COPD than in the general population.
Identification of GERD frequently among COPD
individuals with predominantly bronchitis phenotypes
(33.6% compared to 27.6% in those without chronic
bronchitis).
The role of mechanical factors such as persistent cough,
changes in thoracic and abdominal pressures and the
development of hiatal hernias (present in 13% of COPD
individuals) as explanations for the COPD-GERD
association.
57.
58. COPD and Depression
About 40% of patients with COPD are found to have
depression, compared to a prevalence of about 15-20 %
in the general population
Loss of independence with increasing disability in
COPD can cause, or aggravate, depression. A
predisposition to depression may increase the risk of
smoking, as nicotine has a mood-elevating effect
59. Obstructive Sleep Apnea
Population-based studies have identified sleep apnea
among COPD patients with a frequency similar or just
slightly higher than the general population: between
8% and 14%
Overlap syndrome is the increase in mortality for those
with untreated sleep apnea
Clinical findings that should prompt an evaluation of
sleep apnea include pulmonary hypertension or right
heart failure unexplained by or out of proportion to
the degree of obstruction.
60. Chronic renal failure
Renal complications of COPD are common, especially
in patients with hypoxemia and hypercapnea.
The arterial rigidity and endothelial dysfunction
caused by COPD lead to a decreased normal renal
functional reserve.
Impairment of renal functional reserve in COPD
patients is correlated with more severe airway
obstruction and inflammation
COPD have approximately twice the incidence of acute
renal failure, and three times the prevalence of
diagnosed chronic renal failure.
61. Chronic renal failure often goes undiagnosed, and is a
particular concern in elderly COPD patients and in
COPD patients with cachexia
Among COPD patients over 64 years of age, 25% may
have chronic renal failure even with normal serum
creatinine values.(Paz-Diaz H, Montes de Oca M,
Lopez JM, Celli BR et al)
62. Comorbidity Clusters in COPD
Phenotypes
The improving definition of COPD phenotypes
continues to enhance our understanding of COPD-
related comorbidities.
64. Summary of Evidence Regarding the Frequency, Impact,
Phenotypic Associations and Areas of
Uncertainty Around the Reviewed COPD Comorbidities
65. How is this Relevant to Our Clinical Practice?
Increasing recognition of systemic inflammation and
co-morbidities in COPD, and the understanding of its
molecular mechanisms, will hopefully offer new
strategies to improve survival and quality of life in
patients with COPD.
66. Treatment and management
The cornerstone of management for COPD and
comorbidities is guideline-based treatment.
The management and treatment of COPD is usually based
on GOLD guidelines
There is little specific guideline guidance for administering
cardiovascular regimens to patients with comorbid COPD.
As a result, β-blockers are frequently underused in
patients with COPD.
Awareness is needed for patients with congestive heart
failure and COPD not to be denied β-blocker treatment.
Cardioselective β-blockers improve the prognosis without
impairing lung function.
67. Caution is needed because cardioselectivity decreases
as the dosage escalates.
Patients with coronary heart disease should also not be
denied the protective effects of β-blockers.
GOLD guidelines recommend the use of the general
coronary disease guidelines, and especially note the
use of selective β1 -blockers even in patients with
severe COPD.
The use of angiotensin-converting enzyme (ACE)
inhibitors by smokers may protect against a rapid
decline in lung function and progression to COPD
68. Treatment of OSAS does not differ between patients
with COPD and those without.
Treatment of COPD patients with OSAS is based on
the treatment of constituent diseases (for COPD
bronchodilators, inhaled steroids when indicated,
rehabilitation, nutrition, domiciliary oxygen when
indicated, and for OSA weight loss and application of
continuous positive airway pressure [CPAP]).
The goal of treatment is to maintain adequate
oxygenation at all times and to prevent sleep-
disordered breathing.
69. chronic kidney failure in COPD patients, especially the
elderly, indicates that awareness is needed for
monitoring and addressing adverse effects caused
mainly by hydrosoluble drugs, which are cleared by the
kidney.
Special attention is warranted for drugs like thiazides
or digoxin, used in the treatment of cardiovascular
comorbidities, but also antibiotics commonly used in
acute exacerbations of COPD
70. Nonpharmacological treatment of COPD patients
includes smoking cessation (counseling plus
pharmacotherapy), influenza and pneumococcal
vaccination, and pulmonary rehabilitation.
Pulmonary rehabilitation, has the potential to affect a
number of comorbidities
Physical activity and regular exercise are proven to be
beneficial for multiple comorbidities, including
cardiovascular disease, diabetes, or musculoskeletal
diseases
71. Management of COPD needs a systemic holistic
approach.
Holistic approach includes COPD management based
on pharmacological and nonpharmacological
treatment, guideline-based management for specific
comorbidities, and modification of the risk factors for
COPD and comorbidities
Some researchers have started to advocate for an
integrated care approach to the management of
patients with COPD.
There is a need for a chronic care model approach to
the management of COPD, including automatic
screening for common comorbidities.
76. Search for co-morbidities in a patient with COPD, and
conversely, for COPD in a patient with recognized co-
morbidities, must head the list of changes in
management of patients with COPD
Early recognition and early intervention should
improve outcomes.
Preventive interventions, primary or secondary, may
be useful, and deserve further study.
The benefits of smoking prevention/ cessation,
interventions to reach a healthy weight range, diet and
exercise and rehabilitation (pulmonary and cardiac)
77. Pharmacologic interventions are still unclear, but
beta-blockers, anti-oxidants and inhaled cortico-
steroids are promising.
Statins evoke the greatest interest, with at least one
randomized controlled trial and several observational
studies suggesting benefits from their use.
Benefits described have included reductions in
mortality (COPD and all-cause), myocardial
infarctions, COPD exacerbations and hospitalisations
and intubations during exacerbations, as well as
slowing lung function decline.
78. Statin use and exacerbations in individuals with
chronic obstructive pulmonary disease.
Ingebrigtsen TS, Marott JL, Nordestgaard BG, Lange P, Hallas J, Vestbo J.
2015 THORAX JAN
Statin use was associated with reduced odds of
exacerbations in individuals with COPD from the
general population,
This was not apparent in those with the most severe
COPD without cardiovascular comorbidity.
Statins may thus only associate with reduced risk of
exacerbations in patients with COPD with coexisting
cardiovascular disease.
79. Conclusions
COPD is a disease characterized by systemic inflammation,
systemic consequences, and many chronic and complex co-
morbidities.
All patients with COPD should be examined and investigated for
co-morbidities, and conversely, patients with any of the known
co-morbidities should be screened for COPD.
If present these should be treated. Where not present, lifestyle
interventions such as smoking prevention and cessation, and
interventions such as diet control and exercise should be
advised.
The role of pharmacological interventions, including statins,
deserves further studies.
Greater efforts should be made at educating physicians and
patients about the existence of co-morbidities in COPD and the
need for screening and early intervention.