respiratory dis. presentation1 for gen path.pptx
TRANSCRIPT
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RESPIRATORYDISEASE
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Major Determinants of
Disease Diseases of one lung compartment tend to affect
the others
The lungs are open to the environment, exposingthem to infectious agents, allergens, irritants, &carcinogens
Most lung disease is caused by inhalation ofmaterial; the most common exception isautoimmune lung disease
Lost pulmonary membrane is not recoverable
Smoking is a major cause of lung disease The heart & lungs are a functional unit; lungdisease usually affects the heart; & heart diseaseusually affects the lungs
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Common Approach Affecting
The airways The interstitium
The pulmonary vascular system
Chronic obstructive pulmonary disease(COPD)
Acute lung injury
Pulmonary infections Diffuse interstitial (restrictive, infiltrative)
lung diseases
Lung tumors
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Chronic Obstructive Pulmonary
Diseases (COPD)
Chronic bronchitis Emphysema
Bronchiectasis
Asthma
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Chronic B ronchi tis
Chronic bronchitis is defined clinically. It is
present in any patient who has persistent cough
with sputum production for at least 3 months in
at least 2 consecutive years, in the absence ofany other identifiable cause.
(1) Progress to chronic obstructive airway
disease (2) Lead to cor-pulmonale and heart failure
(3) Cause atypical metaplasia and dysplasia of
the respiratory epithelium
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Pathogenesis
Tobacco smoke
90% of patients are smokers.
Grain, cotton, and silica dust Air pollution
Infection
Bacterial and viral infections are important
intriggering acute exacerbation of the disease.
Others
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Morphology Grossly
Hyperemic and swollen Mucinous or mucopurulent secretions
Histologically
Chronic inflammation of the airways (predominantly
lymphocytes) Enlargement of the mucus-secreting glands in the
trachea and larger bronchi
Inflammatory cells, largely mononuclear but
sometimes admixed with neutrophils Goblet cell metaplasia, mucus plugging, inflammation,
and fibrosis (small airway disease, (bronchiolitis
obliterans)
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Chronic bronchitis. The lumen of the bronchus is above. Note the markedthickening of the mucous
gland layer (approximately twice normal) and squamous metaplasia of lung
epithelium. (From the teaching collection of the Department of Pathology,
University of Texas, Southwestern Medical School,
Dallas, Texas.)
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Clinical Course
Prominent cough
Production of sputum
Hypercapnia, hypoxemia, and cyanosis
Pulmonary hypertension and cardiac failure Recurrent infections and respiratory failure
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Complications
Emphysema
Cor pulmonale
Bronchiectasis
Bronchopneumonia
Bronchogenic carcinoma of lung
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Emphysema
Definition
Emphysema is a condition of the lungcharacterized by abnormal permanent
enlargement of the airspaces distal to the
terminal bronchiole, accompanied bydestruction of their walls and without
obvious fibrosis.
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Pathogenesis
The genesis of emphysema is not
completely understood.
A consequence of two critical imbalances
The protease-antiprotease imbalance
Oxidant-antioxidant imbalance
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Protease-An tip ro tease Imbalance
Hypothesis
Genetic deficiency of the antiprotease1- antitrypsin
The effect of cigarette smoking in the
development of emphysema Increased elastase availability and
decreased
antielastase activity occur in smokers. Smoking enhances elastase activity in
macrophages
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Oxidant-Ant ioxidant Imbalance
Tobacco smoke contains abundant
reactive oxygen species (free radicals),
which deplete these antioxidant
mechanisms, thereby inciting tissue
damage.
Tissue breakdown is enhanced as a
consequence of inactivation of protective
antiproteases by reactive oxygen species
in cigarette smoke.
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Pathogenesis of emphysema. The protease-antiprotease
imbalance andoxidant-antioxidant imbalance are additive in their effects and
contribute to
tissue damage.1-antitrypsin (1-AT) deficiency can be either
congenital or
"functional" as a result of oxidative inactivation.
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Types of Emphysema
According to its anatomic distribution within
the lobule
Four major types
CentriacinarPanacinar
Paraseptal
Irregular Only the first two cause clinically significant
airflow obstruction.
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en tr iac inar (Centr i lobu lar)
Emphysema
The central or proximal parts of the acini,
formed by respiratory bronchioles, are affected,
whereas distal alveoli are spared. The lesions are more common and severe in
the upper lobes, particularly in the apical
segments. Centriacinar emphysema occurs
predominantly in heavy smokers, often in
association with chronic bronchitis.
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Panacinar (Panlobular)
Emphysema
The acini are uniformly enlarged from the
level of the respiratory bronchiole to the
terminal blind alveoli. Tends to occur more commonly in the lower
zones and in the anterior margins of the lung,
and it is usually most severe at the bases. This type of emphysema is associated with
1- antitrypsin (1-AT) deficiency.
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A, Centriacinar emphysema. Central areas show
marked emphysematous damage (E), surrounded byrelatively spared alveolar spaces.
B, Panacinar
emphysema involving the entire pulmonary
architecture.
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Distal Ac inar (Paraseptal)
Emphysema
The proximal portion of the acinus is normal,
but the distal part is predominantly involved.
The characteristic findings are of multiple,continuous, enlarged airspaces from less than
0.5 cm to more than 2.0 cm in diameter,
sometimes forming cystlike structures. This type of emphysema probably underlies
many of the cases of spontaneous
pneumothorax in young adults.
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A irspace Enlargement w ith Fibros is
(Irregular Emphysema)
The most common form of emphysema
Autopsy shows one or more scars from
a healed inflammatory process.
In most instances, these foci of irregular
emphysema are asymptomatic and
clinically insignificant.
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In ters t i t ial Emphysema
The entrance of air into the connective
tissue stroma of the lung, mediastinum,
orsubcutaneous tissue.
Wound of the chest
Children with whooping cough andbronchitis,
Patients with obstruction to the airways
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Compensatory Hyper inf lat ion
(Emphysema)
Surgical removal of a diseased lung or
lobe.
Designate dilation of alveoli but not
destruction of septal walls.
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Bullous Emphysema
Produces large subpleural blebs or
bullae (spaces more than 1 cm in
diameter in the distended state) Most often subpleural, and occur near
the apex
Pneumothorax
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Bullous emphysema with large subpleural
bullae (upper left).
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Morphology
The diagnosis and classification of emphysemadepend largely on the macroscopic appearance
of the lung.
Panacinar emphysema Produces pale, voluminous lungs that often obscure
the heart when the anterior chest wall is removed at
autopsy.
Centriacinar emphysema
The upper two-thirds of the lungs is more severely
affected than the lower lungs.
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Morphology
DistalAcinar (Paraseptal) Emphysema
Adjacent to the pleurabullae
Spontaneous pneumothorax
Irregular Emphysema
The acinus is irregularly involved, is
almost invariably associated with scarring
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Microscopy
Thinning and destruction of alveolar
walls
Adjacent alveoli become confluent,creating large airspaces
Loss of elastic tissue in the surrounding
alveolar septa The number of alveolar capillaries is
diminished.
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Microscopically at high magnification, the loss of
alveolar walls with emphysema is demonstrated.
Remaining airspaces are dilated.
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Clinical Course
Dyspnea is usually the first symptom
Steadily progressive Cough and wheezing
Weight loss
Pulmonary function tests The ratio of FEV1 to FVC is reduced
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Complications
Cor pulmonale
Pneumothorax
Respiratory failure
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Anatomic distribution of pure chronic bronchitis and pure emphysema. In
chronic bronchitis the small-airway disease (chronic bronchiolitis) results in
airflow obstruction, while the large-airway disease is primarily responsible for
the mucus hypersecretion.
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Bronchiectasis
The permanent dilation of bronchi and
bronchioles caused by destruction of the
muscle and elastic supporting tissue. Resulting from or associated with
chronic necrotizing infections.
Cough and expectoration of copiousamounts of purulent sputum
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Pathogenesis
Obstruct ion
Chronic pers istent in fect ion
Damage to bronchial walls, leading to
weakening and dilation.
Obstructive secretions, inflammationthroughout the wall
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Morphology
Affects the lower lobes bilaterally The airways dilated
Histologically
Intense acute and chronic inflammatoryexudate within the walls of the bronchi and
bronchioles
The desquamation of lining epitheliumcause extensive areas of ulceration
Fibrosis of the bronchial and bronchiolar
walls and peribronchiolar fibrosis
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This is the microscopic appearance of bronchiectasis.
Bronchiectasis is not a specific disease, but a
consequence of another disease process that destroys
airways.
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Clinical Course
Severe, persistent cough with expectoration
of mucopurulent
Fetid, sputum.
The sputum may contain flecks of blood
Hypoxemia, hypercapnia, pulmonary
hypertension, and (rarely) cor pulmonale.
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Complications
Lung abscess
Pyemia--metastatic abscesses
Pulmonary fibrosis
Cor pulmonale
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Asthma
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Pathophysiology
Asthma trigger
- Inflammation & edema of the mucousmembranes.
- Accumulation of tenacious secretionsfrom mucous glands.
- Spasm of the smooth muscle of thebronchi & bronchioles decreasesthe caliber of the bronchioles.
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Clinical manifestations
A) General manifestations:
1. The classical manifestations are: dyspnea,wheezing, & cough.
2. The episode of asthma is usually beginswith the child feeling irritable &
increasingly restless. Asthmatic child
may complain headache, feeling tired, &
chest tightness.
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Clinical manifestations:
B) Respiratory symptoms:
- Hacking, paroxysmal, irritating and nonproductive cough due to bronchial edema.
Accumulation of secretion stimulate cough thatbecomes rattling & productive (frothy, clear,gelatinous sputum).
- Shortness of breath, prolonged expiration,wheezy chest, cyanosed nail beds, & dark redcolor lips that may progress by time to blue.
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C) On chest examination:
- Inspection reveals major changes in the form ofsupraclavicular, intercostals, subcostal, &
sternal retractions due to the frequent use of
accessory muscles of respiration.
With repeated episodes: chest shape is changed
to barrel chest, & elevated shoulder.
- Auscultation reveals loud breath sounds in theform of course crackle, grunting, wheezes
throughout the lung region.
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Diagnostic evaluation:
1. Clinical manifestations,history, physical examination,
& Lab tests.
2. Radiographic examination.
3. Pulmonary function tests
provide an objective method
of evaluating the degree of
lung disease.
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Coughing
Wheezing, a whistlingsound
Shortness of breath
Chest tightness
Sneezing & runny
nose
Itchy and inflamed
eyes
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Asthma
Therapeutic
management
- Allergic control
to preventattacks.
Drug therapy:
B- adrenergic,
Theophyllin, &
corticosteroids
preparations + chest
physiotherapy (onlyin between attacks).
Clinical
T
Anatomic
Sit
Major
P th l i
Etiology Signs/
S t
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Term Site Pathologic
Changes
Symptoms
Chronic
bronchitisBronchus Mucous gland
hyperplasia,
hypersecretion
Tobacco
smoke, air
pollutants
Cough,
sputum
production
Bronchiectasis Bronchus Airway dilation
and scarring
Persistent or
severe
infections
Cough,
purulent
sputum, fever
Emphysema Acinus Airspace
enlargement;
wall
destruction
Tobacco
smoke
Dyspnea
Asthma Bronchus Smooth
muscle
hyperplasia,
excess mucus,
inflammation
Immunologic
or undefined
causes
Episodic
wheezing,
cough,
dyspnea
Lower Respiratory Tract
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Lower Respiratory Tract
Infections: Bronchiolitis (RSV
Infection) 2-12 month Caused by syncytial virus Transmitted by oral droplet Predisposing factors (asthma, smoking) Causes necrosis and inflammation of small bronchi and
bronchioles
Signs Wheezing and dyspnea Rapid, shallow respirations Cough
Rales
Chest retractions Fever
Treatment Supportive and symptomatic
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Pulmonary Infections
Pneumonia can result
whenever these defense
mechanisms are impaired
or whenever theresistance of the host in
general is lowered.
Most deadly infectious disease in the U.S.
6th leading cause of death
P i
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Pneumonia
Etiological classification
Bacterial pneumonia
Viral pneumonia
Fungal pneumoniaetc.
Anatomical classification
Lobar pneumoniaLobular pneumonia
Interstitial pneumonia
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Pulmonary Infections or
Pneumonia
Pneumonia can be very broadly definedas any infection in the lung. It may
present as acute, fulminant clinical
disease or as chronic disease with amore protracted course.
Pathogenesis
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Pathogenesis
Streptoco ccus Pneumon iaeThe most common cause of acute pneumonia.
Exam inat ion o f Gram -stained sputum is an important step
in the diagnosis o f acute pneumon ia.
Pneumococcal pneumonias respond readily to penicillin
treatment, but there are increasing numbers of
penicillinresistant
strains of pneumococci.
Haemoph i lus Inf luenzae A major cause of life-threatening acute lower respiratory
tract
infections and meningitis in young children.
Moraxella Catarrhal is
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Streptococcal pneumon iae,pneumococcal
Infection localized in 1 or morelobes
Congestion
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Inflammation andvascular congestion in
alveolar wall
Exudate forms in alveoli Interferes with oxygen
diffusion
Consolidation
Neutrophils, RBCs, fibrinaccum in exudate Form solid mass
RBCs break down,infection resolves
Macrophages break downexudate
Expectorated or resorbed
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Pleurae typically involved Infection in pleural cavity Emphysema
Adhesions betweenmembranes
Manifestations Sudden onset Systemic signs: high fever,
chills, fatigue
Dyspnea, tachycardia Pleuritic pain Rales Productive cough
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Lung cancer
Lung cancer is currently the mostfrequently diagnosed major cancer in the
world and the most common cause of
cancer mortality worldwide. Cancer of the lung occurs most often
between ages 40 and 70 years, with a
peak incidence in the fifties or sixties.
The 5-year rate for all stages combined is
only 15%.
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Cigarette smoking
Passive smokingincreases the risk of
developing lung cancer to
approximately twicethat of nonsmokers.
Industrial Hazards
Air Pollution
Molecular Genetics
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Squamous dysplasia
and carcinoma in situ
Atypical adenomatous
hyperplasia
Diffuse idiopathic
pulmonary
neuroendocrine cellhyperplasia
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Squamous cell
carcinoma (25% to
40%)
Adenocarcinoma
(25% to 40%)
Small cell carcinoma
(20% to 25%) Large cell carcinoma
(10% to 15%)
I idi
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Insidious onset Normally metastized
before diagnosis 4 possible categoriesof signs of lung cancer
Direct effects oftumorSystemic effects ofcancer
Paraneoplasticsyndromes
Metastizes at othersites
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Persistent, productivecough, dyspnea,
wheezing Detection on chest X-ray Hemoptysis
Pleural involvement Chest pain Hoarseness
Facial, arm edema;headaches Dysphagia
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Systemic signsWt. loss, anemia,
fatigue
Paraneoplasticsyndrome
Signs of endocrinedisorder
Depends on hormonebeing secreted
Signs of metastasisdepends on site
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Chest X-rays Bronchoscopy Pulmonary function tests
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Surgery on localizedlesions Chemotherapy and
radiation
Poor prognosis unlesstumor in early stages
of development
Wh t i t b l i (TB)?
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What is tuberculosis (TB)?
Tuberculosis (TB) is a disease caused bybacteria called Mycobacterium tuberculosis.
The TB bacteria can affect any part of the
body, but usually affects the lungs. If not treated properly, a person who has TB
infection can develop TB disease.
If a person develops TB disease and does
not get appropriate medical treatment he/she
can die.
H d t TB?
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How do you get TB?
TB is generally spread through the airwhen a person who has TB diseasefrequently sneezes, coughs, speaks or
sings near others for a long period of time.Persons who breathe in air containingTB germs can become infected with TB.Typically, only close contacts of a
person who has TB disease areconsidered to be at risk.
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Mycobacterium tuberculosis
Chronic granulomatous inflammation with
caseous necros
Pathogenesis
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Pathogenesis
How is TB infection different
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How is TB infection different
from TB disease?
People with TB infection have a positive
TB skin test but they: are not sick, do not
have symptoms, cannot spread TB to others,can develop TB disease if not treated for
TB infection.
When TB infection is treated it greatlyreduces the chance that you will ever develop
TB disease.
How do I get tested for TB?
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How do I get tested for TB?
A TB skin test is performed byinjecting a small amount of fluid in the skin on the
lower part of the arm. You will need to return within
48-72 hours to have a trained health care worker see if
the skin test is positive or negative. You can get a skin test at your local health
department or at your healthcare providers office.
If you have a positive reaction to the skin test (TB
infection), your healthcare provider may do other
tests to see if you have developed TB disease.
Wh t th t f TB?
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What are the symptoms of TB?
Symptoms of TB disease include:feelings of sickness or weakness,
weight loss, fever, and night sweats.
When TB disease affects the lungs,additional symptoms may include: a bad
cough that lasts longer than 2 weeks,
shortness of breath, pain in the chest andcoughing up blood.
Remember
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Remember
TB infection occurs when a person hasbreathed in the TB germ, but the person is not
sick.
TB disease can develop in a person withTB infection if they do not get medical
treatment.
A person with TB disease is sick and mayhave several symptoms of the disease.
If left untreated, persons with TB disease
can die from TB.
How is TB treated?
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How is TB treated?
TB disease can usually be curedby taking several medicines for 6-12 months. It is very important that people who have TBdisease take the medication exactly as
prescribed. If you stop taking the medication too soon,you can become sick again. Also, if you do not take the medicationcorrectly, the germs may become resistant tothose medications and become more difficult totreat.
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An inflammation of the larynx.
It causes hoarse voice or the
complete loss of the voicebecause of irritation to thevocal folds.
Bronchitis
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BronchitisBronchitis is an inflammation of the main airpassages to the lungs
Most prevalent in winter
Generally part of an acute URIIt may develop after a common cold orother viral infection of the nasopharynx,
throat, or bronchi
Often with secondary bacterial infection
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1.Malaise
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. a a se2.Chilliness
3.Slight fever4.Back and muscle pain
5.Sore throat6.Onset of a distressingcough usually signals
onset of bronchitis7.Cough starts off dry and
later produces mucous.
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Tonsillitis
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Tonsillitis
What is tonsillitis?
Tonsillitis is a viral or bacterial infection inthe throat that causes inflammation of the
tonsils. Tonsils are small glands (lymphoid
tissue) in the pharyngeal cavity.
In the first six months of life tonsilsprovide a useful defense against
infections. Tonsillitis is one of the mostcommon ailments in pre-school children,
but it can also occur at any age.
Tonsillitis
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Tonsillitis
Palatinetonsils
(Visible duringoralexamination)
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Tonsillitis: Children are most often
affected from around the
age of three or four, when
they start nursery or
school and come intocontact with many new
infections.
A child may have tonsillitis ifhe/she has a sore throat, a fever
and is off food.
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Tonsillitis is caused by a variety of
contagious viral and bacterial
infections. It is spread by close
contact with other individuals and
occurs more during winter
periods. The most common
bacterium causing tonsillitis is
streptococcus.
Otitis media
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Otitis media
Background:
Otitis media (OM) is the second most
common disease of childhood, after upper
respiratory infection (URI).
Definition:
Otitis media is an inflammation of the middleear.
Otitis media:
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Otitis media:
Otitis media can be classified into many
variants on the basis of etiology,duration, symptomatology, and physical
findings as the following:
Acute Otitis media: implies rapid onsetof disease associated with 1 or more ofthe following symptoms:
Otalgia, Fever, Otorrhea, Recent onset ofanorexia, Irritability, Vomiting, &
Diarrhea
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Acute Otitis media (AOM):These symptoms are
accompanied by abnormal
otoscopic findings of the
tympanic membrane (TM),
which may include thefollowing:
- Opacity
- Bulging
- Erythema
- Middle ear effusion (MEE)
http://www.emedicine.com/ped/images/Large/1784NEWNormal_TM_2.jpg -
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Healthy Tympanic
Membrane
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1.Administration ofantibiotic
(Ampicillin or
Amoxicillin) & anti-inflammatory
(analgesic &
antipyretic).
Croup Syndrome:
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Croup Syndrome:Acute infection of the
larynx characterized by severe
involvement of voice & breathing appears
in the following clinical pictures:hoarseness of voice, resonant cough, &
varying degrees of respiratory distress.
Croup syndromes are usually describedaccording to primary anatomic area
affected e.g., laryngitis,
laryngotracheobronchitis (LTB).
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- Therapeutic management:1. Hospitalization for
continuous observation &
for possible tracheostomy
or endotracheal intubation.
2. Provide cool mist oxygen.3. Patients may respond to
corticosteroid therapy.
The disease is usually selflimited.
Home care:
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Home care:1. Encourage bed rest.2. Provide warm, high humidity
atmosphere, especially
during periods of coughing &
during sleep.3. Encourage inhalation of
warm steam to prevent
recurrence.
4. Keep the child calm most oftime (avoid crying, &
excessive talking).
Bronchiolitis:B hi liti i ill
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Bronchiolitis is a common illness
of the respiratory tract usually
caused by viral infection. Itaffects the tiny airways, called
the bronchioles, that lead to the
lungs. As these airways become
inflamed, they swell and fill withmucus, making breathing
difficult.
The variable degrees of
obstruction produced in airpassage by these changes lead
to hyperpnoea & progressive
emphysema.
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Normal lungs
& alveoli
Bronchiolitis:- Incidence:
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- Incidence:
- Typically occurs during the first 2years of life, with peak occurrence
at about 3 to 6 months of age.
- Is more common in males,
children who have not beenbreastfed, and those who live in
crowded conditions.
-Day-care attendance and
exposure to cigarette smoke also
can increase the likelihood that an
infant will develop bronchiolitis.
Bronchiolitis:
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Bronchiolitis:- Nursing Assessment (S &
S):
The first symptoms of bronchiolitis
are usually the same as those of
a common cold:
-Stuffiness runny nose, mild
cough, &mild fever
These symptoms last a day or two
and are followed by worsening of
the cough and the appearance of
wheezes (high-pitched whistling
noises when exhaling).
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Bronchiolitis: Diagnostic evaluation:
- Chest X-ray.
- Culture from respiratory
secretions.
Therapeutic management:
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Therapeutic management:
Fortunately, most cases of
bronchiolitis are mild andrequire no specific treatment.
Antibiotics aren't useful
because bronchiolitis
is caused by a viral infection.
Medication may sometimes be
given to help open a child's
airways e.g., bronchodilators,corticosteroids.
Cough suppressants.
Encourage bed rest.
Secondary bacterialinfection
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infection Obstruct drainage in 1 or
more paranasal sinuses
Common causativeorganisms Pneumococci Streptococci Haemophilus influenzae
Exudate accumulates Signs Nasal congestion, fever,
sore throat
Diagnosis confirmed byradiograph, transillumination
Decongestants, analgesics Antibiotics
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Naso-pharyngitis: =
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Naso-pharyngitis: =Common cold.
Def:
Viral infection of the nose& throat.
Assessment (S &S):
1.
Younger childFever, sneezing, irritability,
vomiting & diarrhea
2. Olderchild
Dryness & irritation of nose &throat, sneezing, &muscular aches.
Complications of
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Complications of
nasopharyngitis:
- Otitis media- Lower respiratory tractinfection
- Older child may developsinusitis
Medication:Acetaminophen
Pharyngitis:=Sore
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y g
throat including tonsils.
- Uncommon in childrenunder 1 yr. The peak
incidence occurring
between 4 & 7 yrs of age.
- Causative organism:virusesorbacterial (group A beta-hemolytic streptococcus).
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Assessment (S &S)
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of pharyngitis:
1.
Younger child
Fever, anorexia, general malaise, &
dysphage
2. Older
child
Fever (40 c), anorexia, abdominal
pain, vomiting, & dysphagea.
Complications ofpharyngitis:
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pharyngitis:
- Retro pharyngeal abscess.- Otitis media.- Lower respiratory tract
infection.
- Complications of GABHSInfection: Peritonsillarabscess; occurs in fewer
than 1% of patients treated
with antibiotics that leads to
rheumatic fever, oracute
glomerulonephritis.
Symptoms of influenza
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Symptoms of influenzainfection:
Headache
Fever, chills Muscle aches Nasal discharge Unproductive cough Sore throat
Influenza infection can causemarked inflammation of therespiratory epithelium and a loss ofciliated cells that protect therespiratory passages from otherorganisms.
As a result, influenza infection may
lead to co-infection of the respiratorypassages with bacteria. It is also possible for the influenza
virus to infect the tissues of the lungitself to cause a viral pneumonia.
Treatment of influenza: Bed rest, fluids, warmth
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, ,
Antiviral drugs
Influenza vaccine :
Provides protection against certainA and B influenza strains that areexpected to be prevalent in acertain year.
The vaccine must be updated andadministered yearly to be effectivebut will not be effective againstinfluenza strains not included in thevaccine.
The influenza vaccine is advisedfor elderly people, in individualsweakened by other disease and inhealth-care workers
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Carcinoma of theL
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Larynx
Common Mostly in malesmokers over 40
Alcohol abuseincreases the risk Presents with
hoarseness pain cough dysphagia hemoptysis
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Restrictive LungDi
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Disease
Chronic inflammationmaking lungs stiff &inelastic
Affects diffusion Scar tissue accumulates
in the interstitium Mostly cause is
unknown
Equal decline in FEV1 &FVC
Usually presents withshortness of breath Can lead to pulmonary
HTN
Interstitial Fibrosis withoutGranulomatous Inflammation
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G a u o atous a at o
Usually middle-agedmen at time ofdiagnosis
Shortness of breath;may progress to corpulmonale, hypoxia
Pneumoconioses black lung disease silicosis
most commonchronicoccupationaldisease
asbestosis mesothelioma
Interstitial Fibrosis with
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Interstitial Fibrosis with
Granulomatous Inflammation
Sarcoidosis
cause unknown
affects many tissues butmostly lungs
present with shortness of
breath, cough, chest pain,hemoptysis
Pulmonary Edema
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Pulmonary Edema
Fluid in alveoli Increased BP in lung normal is 25/8 mmHg
with average at 15 mmHg
Microvascular injury due to
toxic fumes hot gases septicemia IV drug abuse
Main symptom is SOB
PulmonaryThromboembolism
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Thromboembolism
About 50,000 deaths annually Mostly from DVT Inflammation predisposes you to
it
Promoted by
CHF pregnancy birth control pills prolonged bed rest metastatic cancer
genetics Most associated with nosymptoms but some cause lung infarcts chest pain & dyspnea death
Pulmonary Hypertension
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y yp Sustained systolic pressure over 30
mmHg or average in excess of 25mmHg
Vicious cycle Most common cause is increased
pulmonary vascular resistance
Usually secondary to
COPD heart disease collagen vascular diseases recurrent pulmonary
thromboemboli
With R heart failure is cor pulmonale Thickening of arteriolar walls SOB
chest pain fatigue
Adult Respiratory Distress Syndrome
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ARDS Alveolar or pulmonary capillary damage Pathogenesis
injury to endothelium or alveoli neutrophils infiltrate protein-rich fluid exudes into alveolar space SOB occurs with rapid breathing which dries the fluid into a thick
membrane stiffens lungs limits airflow & interferes with diffusion hypoxia 50% fatality
Causes sepsis smoke inhalation near drowning
O2 toxicity burns DIC fat embolism endotoxic shock
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Lung Abscess
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Purulentinflammation withtissue necrosis &liquefaction
Usually haveseveral types ofbacteria withanaerobic
Most commonly dueto aspiration ofgastric contents
Foul-smellingsputum
Mostly due to
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y
metastasis
Bronchogeniccarcinoma is the most
common
most common of allcancers#1 cancer death
about 90% arecigarette smokers
Bronchogenic Carcinoma
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Bronchogenic Carcinoma
Mostly caused by cigarettes Direct relationship between incidence of
cancer & number of cigarettes smoked
Direct relationship between precancerous
changes in bronchial mucosa & number of
cigarettes smoked
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