Transcript COPD,Asthma,Rhinitis - KSU Faculty Member websites

Introduction
• The respiratory system is an organ system
which is used for gas exchange. The
respiratory system generally includes tubes,
such as bronchi, used to carry air to the
lungs, where gas exchange takes place. In
the lung the trachea (windpipe) divides into
two main bronchi, the left and the right. The
right main bronchus is winder, shorter, and
more vertical than the left main bronchus.
Anatomy and Physiology
The air-conducting passage that bring air into
the lung are the nose, pharynx, trachea
bronchi, and bronchioles. The respiratory tract
form the nose to the bronchioles is lined with
ciliated mucous membranes.
These three processes (filtered, warmed and
humidified) are primarily function of the
respiratory mucosa. Which consists of pseudo
stratified, ciliated, columnar epithelium and
goblet cells.
The epithelial surface is covered by a mucous
blanket, which is secreted by both the goblet
cells and the serous glands.
Bronchioles are not supported by cartilaginous
rings but are surrounded by smooth muscle,
which allows alteration in size. All the airway
down to the level of the terminal bronchioles are
called conducting airway because to the gas
exchanging areas of the lung.
The physiologic process of respiration by
which O2 is transferred from the air to the
tissues and CO2 is excreted in the expired air
maybe divided into three main stages, the first
stage is ventilation , which the flow of a mixture
of gases into and out of the lungs. The second
stage, diffusion, must be considered from
several aspects:
(1) The diffusion of gases between the alveolus and
pulmonary capillary and exchange of gases
between the systemic blood and tissue cells
(perfusion)
(2) The distribution of the blood in the pulmonary
circulation and its match with the distribution of
the air in the alveoli.
(3) The chemical and physical reactions of O2and
CO2with the blood.
Cell respiration, or internal respiration, is the final
stage of respiration, during which substrates are
oxidized to obtain energy and CO2is produced as
a waste product of cell metabolism and excreted
by the lungs.
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Clinical presentation:
“COPD” refers to chronic obstructive pulmonary
disease.
(Chronic) means long term .
(Obstructive) means there is a blockage to airway.
(Pulmonary) means to the lung.
Obstructive pulmonary encompasses several separate
and distinct sets of pathologic changes, including
asthma, chronic bronchitis and emphysema.
chronic obstructive pulmonary disease (COPD)
describes the presentation of chronic cough,
expectoration, and a significant and progressive
reduction in expiratory airflow. This airflow
obstruction may respond to varying therapeutic
options, but it is largely irreversible.
1-Asthma: is characterized by narrowing of the
airway as a result of bronchial hyper activity,
excessive bronchial secretions, and airway
inflammatory changes. The resulting airflow
obstructing is usually reversible.
2-chronic bronchitis: is condition of bronchial
inflammation & hyper secretion of mucus
manifested by cough, heavy septum production
&hypoventilation.
3- Emphysema: irreversible loss of alveolar wall
and abnormal enlargement of alveoli and
alveolar ducts ,therefore the airway tend to close
in expiration whenever outside pressure
exceeds that within. Patient suffer dyspnea &
wheezing with any increase respiratory efforts.
* The three disease mentioned before
are classified as:
** obstructive disorders: means air flow
is limited during expiration due to
bronchospasm, excessive amount
cause obstruction of air flow & edema.
** Restrictive disease : means air flow is
limited during inspiration duo to chest
deformity(kyphoscoliosis) & low of
elasticity of alveoli e.g,pneumonia.
Chronic bronchitis and emphysema are often
grouped together &indistinguishable on clinical
examination, and patient have overlapping
features due to pathogenic common
denominator, cigarette smoking.
With the onset of attacks infections of the nasal
sinuses or tracheobronchial tree. The attacks
become more frequent over time, and the
condition merges into chronic bronchitis and
sometimes emphysema.
Etiology:
Passive smoking has been identified as a
possible factor in COPD development, and other
environmental factors as pollution and
occupational exposures have been implicated.
Pathophysiology :
With obstructive pulmonary disease, air exchange
is impaired in several ways. Airway integrity is
compromised through smooth muscle
contraction, inflammation, edema, and
peribronchiolar fibrosis. Changes in pulmonary
vasculature result from hypoxia. Pulmonary
hypertension , pulmonary vascular resistance,
may develop. Cor pulmonale, or hypertrophy of
the right ventricular due to primary lung disease,
may then develop & progress to heart failure.
Physical obstruction of the airways due to
chronic or recurrent excessive mucus
secretion, accompanied with inflammation,
also interferes with normal mechanisms to
maintain airway integrity in chronic
bronchitis. This excessive mucus production
is the result of irritation of the airway by
smoke or other irritants. With chronic
irritation, the mucous glands increase in
number and size and their ducts dilate within
the bronchial mucosa destruction of alveoli
and further functional air exchange area
reduction occurs.
Clinical presentation:
Screening programs to identify patients at risk for COPD,
or in the earliest stages of the disease, are not
prevalent compared with programs for detection of
heart disease or cancer.
Significant overlap between the clinical presentation
of chronic bronchitis and emphysema exists. The
presentation of chronic bronchitis begins with
morning cough productive of sputum
1- cough
2- increased sputum production.
3-weight loss (sometimes profound) may be reported by
the patient with primary emphysema.
4-dyspnea •
5-Wheezes: may be heard
6-Increase in the anteroposterior diameter of the
chest
7-The chest X-ray
8-hypoxemia
9-Resparatory acidosis (hypoventilation)
10-Respiratory infections of bacterial, viral, and
mycoplasmal
Diagnosis:
No specific laboratory information is useful
in differentiating the various form a COPD,
the diagnosis test (alpha1 antitrypsin
deficiency )is made by a serum protein
electrophoretic study.
Pulmonary function test (spirometry) provide
the best information on degree of airway
obstruction.
.
• Complications :
Patient in whom chronic bronchitis predominates
may undergo repeated episodes of acute
respiratory failure. These patients may develop
cor pulmonale & right sided congestive heart
failure. The term blue bloater has been
associated with this type of COPD patients.
Hypoxemia & respiratory acidosis are common
finding. Acute respiratory failure is rare until the
end stage of emphysema. These patients are
termed “Pink puffers” because alveolar
ventilation is maintained until the terminal stages
of the disease . Respiratory infection of the
bacterial, viral & mycoplasmal etiology can
trigger an acute COPD exacerbation especially
in the patient with chronic bronchitis.
Bronchial asthma
Definition:
A chronic inflammatory
disorder of the
airways in which
many cells and
cellular elements play
a role in particular
mast cells, eosinophil,
T-lymphocytes,
macrophages,
neutrophils, and
epithelial cells
Asthma is a disease in which inflammation
of the airways causes airflow into and out
of the lung to be restricted. The muscle of
the bronchial tree become tight and the
lining of the air passage swells, reducing
airflow and producing the characteristic
wheezing sound. >>> this is known as (
Asthma attack ), or as a part of a complex
disease cycle which may include reaction
to stress or exercise >> ( chronic asthma).
In children, boys show a greater risk for
asthma than girls.
Etiology:
(1)-allergen e.g., mold, mites pollen ,
animal dander.
(2)- exercise (the increase in temperature
cause bronchoconstriction).
(3) Environmental irritant e.g., cigarette
smoking , pollutant , cold dry
(4) Medications e.g., Aspirin ,NSAID ,Bblockers.
(5) Viral respiratory tract infection .
Classes of asthma:
Classes of asthma according to the cause:
1- extrinsic ( allergic ) asthma.
Found in a minority of adult patient, is clearly
caused by a known allergen. This form generally
beings in childhood in a member of family with a
history of a topic disease.
Allergic asthma result from the sensitization of
such a person to an allergen, usually a protein,
animal dander, mold spores, feathers, dust, lint
or food like milk or chocolate.
exposure to the allergen, even in minute •
quantities, produces an asthmatic attack.
Allergen induced asthma is divided into:
A- immediate asthma: where air flow
limitation begins minutes after contact with
allergens.
B- dual asthmatic resonce: immediate
followed by late reaction.
C- late phase reaction : a more prolonged
and sustained attack of air flow limitation.
D- recurrent asthmatic reaction:
development of late phase reaction with
an increase in airway hyperactivity
2- intrinsic ( cryptogenic or idiopathic ) asthma.
Is characterized by the absence of clearly defined
precipitating factors. Non specific factors such as
the common cold, exercise or emotion may trigger
the asthmatic attack. The intrinsic type of asthma
is more apt to develop after age 40.
3- mixed asthma:
Which is composed of components of both extrinsic
& intrinsic asthma.
In children boys show a greater risk for asthma than
girls.
In children younger than 14 years, the prevalence is
twice as high in boys compared to girls.
Disease onset can occur in person of any age, but
often present in children younger than 6 years.
Classes of asthma according to the course:
Chronic asthma & acute asthma.
• 1) chronic asthma:
• Individuals have
intermittent attack of
dyspnea
• Wheezing & cough .
• 2) Acute sever
asthma( status
asthmaticus(
• Is compatible with
bronchial obstruction.
• Not easily revered
• Can be fatal & require
energetic treatment.
• Hospitalization may
be necessary.
• Clinical manifestation:
• Symptoms
• Dyspnea: abnormal
shortness of breath.
• Wheezing :is a high
pitched sound resulting
from turbulent gas flow in
the upper airway. It may
be inspiratory, expiratory
or present on both
inspiration and expiration
• Cough with or without
sputum production.
** Signs:
-Reduced airflow
-Increase airway resistance
-Reduce conductance
-Hyperinflation of the lung
-Bronchial hyper-responsiveness
*In acutely obstructed patients:
-Tachypnea: rapid breathing
-Tachycardia: rapid heart rate
-Retraction (pilling of the skin between the ribs
when breathing)
-Hypoxemia
-Cyanosis ( bluish color of lips and face)
• Pathophysiology:
• The Pathophysiology of bronchial asthma is a
complex process. Its pathogenesis involves a
number of cells, mediators, nerve & vascular
leakage. Involving three main components
(i) airway inflammation
(ii)bronchial hyper-responsiveness
(iii)intermittent airflow obstruction .
• There is a certain mechanism that causes
airway inflammation and by the way this
happens one can judge whether asthma is acute
,chronic or sub-acute. Other signs that help in
diagnosis here are the edema of the airway ,the
mucus hyper-secretion and the bronchial hyper
–reactivity ,all these are causes for airflow
obstruction.
• Upon further inspection, it can be found that
varying degrees of infiltration of eosinophil ,
hyper-secretion of mucus and desquamation of
the epithelium will be present.
• Bronchial Hyper responsiveness:
• Hyper responsiveness :is an exaggerated
bronchoconstrictive response to stimuli such as
cold air, exercise, allergens, viral, infection, and
certain chemicals. It is caused by interaction
between an asthmatic's baseline bronchial
responsiveness and airway changes caused by
inflammation. The greater number of
inflammatory cells (Eosinophill) in the air way,
the greater its hyper responsiveness, the
mechanism by which inflammatory cells and
their mediators promote airway hyper
responsiveness are not clear.
Airway inflammation :characterized by •
(1)acute bronchoconstriction :causes
include allergens, exercises aspirin ,
coldair,iritants.
(2)Airway edema: caused by increase
microvascular permeability and leakage
resulting in stiffer and narrow air way.
(3)chronicmucus plug formation: which
always present in sever asthma :
.(4)airwayremodeling:result from epithelial
fibrosis or collagen deposition.
• Airway inflammation:
• It is a complex interaction of various cells and
mediators that result in bronchial hyper
responsiveness and airway obstruction as well
as ongoing inflammation.
• Role of inflammatory cells:
• (a) Alveolar macrophage :( in the late state of
bronchial hyper responsiveness and airway
obstruction )
• Non granular, present in the lumen of small and
large airway flow. They produce mediators
involved in the initiation of inflammatory process
(leukotreines, eosinophil chiropractic factors),
act as antigen - presenting cells by preparing
antigen for presentation to T-lymphocyte, and
have some anti –inflammatory effect.
• (b) T-lymphocyte: play an important role in the
pathogenesis of asthma by coordinating the
inflammatory response .T-lymphocytes produce
cytokines, which promote inflammation.
• (c) Mast cells: known as acute response cell,
they increased in both the epithelium and
surface secretion of asthmatics .they release in
early stage immediate –acting mediators such
as histamine, leukotrienes, prostaglandins,
platelet-activating factor (PAF) that cause
immediate bronchoconstriction, and in the late
stage they release longer-acting mediators such
as eosinophil and neutrophil chemo tactic
factors and cytokines. It appears that other cell
such as important that mast cell in maintaining
the chronic airway inflammatory processes.
Further evidence of the importance of the mast
cell is the finding in large number.
• Eosinophiles: present in the peripheral blood,
bronchiol mucosa, and bronchoalveolar fluid of
patients with asthma .Their granule contain
major basic protein (MBP) and eosinophil
cationic protein (ECP) which are responsible of
airway epithelium damage . They release
mediator (cytokines) to regulate their own
function. The important of adhesion cell in
drawing eosinophil to the site of inflammation.
• Neutrophiles: are source of proteases and
oxygen radicals, which can cause tissue
damage , and lipid mediator , because
neutrophil can be produced in large amount by
bone marrow and have very short half- life .They
have a greater role in acute asthma than in
chronic asthma symptoms
• Mediators: The cells involved in inflammatory
processes present asthma produce and release
mediators responsible of the pathophysiologic
changes include epithelial damage ,smooth muscle
contraction, mucosal edema, inflammation and mucus
secretion .These mediators are rapidly produced by
cells after activation or stimulation and can removed
by inhibition or antagonism result in amelioration of
the asthmatic response .
• Types of inflammatory mediators:
• (1)Immediate acting mediators :( early attack),
characterized by bronchoconstriction. Such as,
histamine, leukotrienes.
• (2) Long acting mediators :( late attack)
• Characterized by inflammation, excess mucus
secretion and edema, e.g.:cytokines,neutrophile...
Mediators should have
the following
characters:
(1)it must be capable of
producing the pathologic
changes observed in
asthma or physiologic
changes that that define
asthma.
(2)it must be produced in the
lung during an asthmatic
episode and measurable in
body fluid .
(3)removable by specific
inhibition or antagonism
result in amelioration or
attenuation of the
asthmatic response
• Adhesion molecules: They are glycoprotein
expressed by cell membrane of endothelial
cells, platelets, WBCs, and epithelial cells.
• Function:
• -Adhesion of inflammatory cells to surface of
vasculature (an important early step in
inflammatory response)
• -promoting cell activation.
• -Cell-cell communication.
• -Allow WBC migration( the recruitment of WBC
from vascular lumen to tissue site ) & infiltration.
• Classification of adhesion molecules:
• Based on their chemical structure.
• Integrins, immunoglobulin family,
selectine, endothelial adhesion molecules
• Transcription factor: It is the production
of inflammatory proteins .e.g, cytokines,
adhesion molecules and enzyme can be
augmented by an increase the
transcription of selected target genes.
• Nuclear factor-KB (NF-KB): It is the
transcription factor that can be activated by
cytokines and oxidants to increase the production
of inflammatory cytokines, chemokines and
adhesion molecules.
• Corticosteroids: They are potent inhibitors of
the activity of NF-KB in airway inflammation.
• Nitric oxide: It is produced by endothelial and
neuronal nitric oxide synthase which regulate
vascular tone, platelet activation and
neurotransmission.
The amount of nitric oxide induced during
inflammation is much greater than that produced
normally and appears to have protective effects
such as relaxation of bronchia.
Neuronal mechanism: Neural regulation of the
airway is complex and involves:
parasympathetic, sympathetic, sensory system.
• It affects airway functioning by regulating
epithelial, vascular and glandular and smooth
muscle activity mechanism. This affected
through release of neurotransmitters and
neuropeptides.
• These affected are classified as:
• (1) Cholinergic (bronchconstriction) increase
secretion.
• (2) Adrenergic (bronchodilator) decrease
secretion.
• (3) Inhibitory non-adrenergic non- cholinergic
(bronchodilator).
• (4) Excitatory non-adrenergic noncholinergic (bronchoconstictor).
• (5) Sensory.
These results from the specific combination of
neurotransmitters and neuropeptides within
the sensory sympathetic and
parasympathetic system.
• (1) Parasympathetic contains ACH
vasoactive intestinal peptide which causes
bronchoconstriction and glandular
exudation.
•
• (2)Sensory nervous system: Present in human
airway contains neuropeptides such as
substance P and neurokinineA (collectively
called tachykinine).Tachykinine are
bronchoconstrictor to asthmatic patients and
cause increased vascular permeability, mucus
secretion and leukocyte Infiltration.
•
NeuronalEndopeptidase (NED): The enzyme
that degrades neuropeptide and NEP activity
is reduced by external factors. e.g, cigarette
smoke, viral infection, pollution and the
presence of these factors will inhibit the
activity of the enzyme and that will lead to
asthma.
**Investigations:
A- detailed history:( family history or child
medical history )
B- physical examination:
Listening to the lung with stethoscope,
examination of nasal passage.
C- laboratory & diagnostic tests:
blood test (presence of eosinophiles indicate
*asthma
* chest x-ray (may be done to exclude the
possibility of breathing problems being caused
by something other than asthma or obtained
when a patient of asthma needs to be
hospitalized)
.
pulmonary function tests ( spirometry): it is
breathing test which measure the amount &
rate of air passage through airways.
- Vital capacity (VC)
The maximum expiration after maximum
inspiration
)also called full expiration(
residual volume :amount of air left in the
lungs after a maximal exhalation
-functional residual capacity: volume
of air remaining after normal
expiration.
-total lung capacity (TLC)
The volume of gas contained in the
lung at the end of maximal inspiration.
The total volume of the lung.
Peak expiratory flow test: maximum
rate of air flow produced by forced
expiration
• Complications:
(1)Asthma and pregnancy
(2)pneumothorax.
(3)Repiratory fatigue .
(4)Adrenal insufficiency .
(5)Status asthmaticus :
sever acute disease that doesn’t respond to
drug therapy and may cause death from acute
respiratory insufficiency.
(6) Physiological problems such as depression.
Rhinitis
• Definition: Is an inflammatory
condition affecting the mucous
membrane of the nose and
upper respiratory system, and
it is the most common of all
allergic disease.
• nasal symptoms
characterized by:
1) rhinorrhea
2) Itching {pruritus} of the nasal
mucosa & throat.
3) Sneezing
4) Congestion
5) Postnasal drainage
6) Ears is often distressing
- These nasal symptoms can be accompanied
by ocular pruritus & conjunctival redness and
lacrimation, and can be exacerbated by the
development/presence of sinusitis. The
involved mucous membranes show dilation of
blood vessels (particularly venules) &
extensive edema with prominent eosinophils
in both tissue & secretions. All these features
including pruritus, can be duplicated by
applying histamine alone to the normal
mucosa.
• Etiology of allergic rhinitis:
• Both genetic factors and
environmental influences are
associated with the development of
allergic rhinitis.
• in patients with intermittent allergic
rhinitis, pollens and airborne mold
spores are the most common
allergens.
• Although the pollen season varies
with geographic location, grasses,
trees and weeds can be problematic
for many people during active
pollination.
• In patients with persistent allergic
rhinitis, the major allergens are house
dust mites, indoor molds, animal
danders, and cockroach antigen.
• Another common occupational
exposure, in which symptoms can be
precipitated by agent such as flour,
wood and detergents.
• Pathophysiology:
The primary pathophysiologic features in allergic
rhinitis are inflammation of mucous membrane of
the nose.
• Allergic rhinitis is characterized by
immunoglobulin [IgE]-mediated response that
involves three primary steps:
• sensitization, early phase event, late phase
event.
•
Sensitization:
In a topic patient the result of
initial exposure to allergens is
production of IgE. Following
initial exposure antigenpresenting cells of the
immune system react to
allergens disposition in the
nasal mucosa. This result in
helper T-lymphocyte
differentiation into Th2 cells
which are associated with
production of cytokines and
other mediators of
inflammation. As a result
memory cells programmed
for IgE production are
produced.
• Early response:
When a susceptible patient is exposed to
allergens previous sensitization has occurred,
an early-phase allergic response generally
occurs. This reaction is attributed largely to the
interaction between the allergen, IgE and the
sensitized mast cell resulting in mast cell
degranulation.
• Late response:
In this phase the nature of inflammation is even
more complex and nasal congestion is
prominent feature. Numerous cells and
mediators play important roles, including
T-lymphocytes, cytokines, eosinophiles,
neutrophiles, macrophages, mast cells and
leukotrienes.
• Classification:
• 1) Acute rhinitis:
• the causes of acute rhinitis are:
• a- viral or bacterial upper respiratory infection or the
common cold [the most common cause]
• b- Hormonal causes of acute vasomotor rhinitis [ usually
associated with a clear watery discharge without other
symptoms include hyporthyroidism and pregnancy.
• - Finally the development of rhinitis-like symptoms has
been attributed to some medications.
• c- Drugs like: angiotensin-converting enzyme inhibitor,
B-blockers, resrpine, non steroidal anti-inflammatory
drugs[NSAID], oral contraceptive and topical
decongestant all have been associated with these
effects.
• 2) Chronic rhinitis: chronic
rhinitis can be classified into:
• A- allergic: an inherited
tendency to develop a clinical
hypersensitivity condition. It has
been classified as:
•
1) - seasonal [intermittent]:
this is often called (hay fever).
There symptoms are:
• Nasal irritant-sneezing.
• Itching of the eyes and soft
palate and occasionally even
itching of the ears because of
the innervations of the
pharyngeal mucosa and ear.
• 2)- perennial [persistent]: its symptoms are: have
the affect the eyes or throat, sneezing, watery rhino
rhea, lose of sense of smell and taste.
• Can be divided into four main types:
• * Perennial non-allergic rhinitis with eosinophilia
(NARES)
• * Perennial allergic rhinitis.
• * Vasomotor rhinitis.
• * Nasal polyps.
• - The demonstration of specific IgE antibodies by
skin testing or in vitro testing can be important for
confirmation of sensitivity to specific allergens.
• Diagnosis & Assessment of Rhinitis:
• Because it is difficult to measure nasal function
in a completely satisfactory manner, the specific
cause of rhinitis is based on a carefully obtained
patient history, physical examination, and a
limited number of relevant laboratory
examinations. A thorough medication history can
also add insight into nasal function.
• Other diagnostic tests: sinus X-ray, computed
tomography, rhinomanometry, and spirometry
maybe useful
• Complications:
1- Sleep disorder.
2- Loss of appetite.
3- General weakness.
4- Fatigue
5- Mood disorder.
6- Decrease contraction.
7- Difficulty learning.
References:
• 1)-Text book of Pathophysiology.
• 2) - Applied therapeutics.
• 3) – clinical concepts of disease:
Thank You…
Done by :
Afnan Al-Addad
Nouf Al-Fadel
Refa’ah Al-Ajmi
Asma’a Al-Ruwaili
Supervised by :
Dr.Azza Azzo
Teach.Raniah