pertussis - presentation slide
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PLENO PAKAR
25 NOVEMBER 2013
A3
2012/2013
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ANATOMY OF THE RESPIRATORY
SYSTEM
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HISTOLOGY OF THE RESPIRATORY
SYSTEM
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Nasal cavity Vestibulelined with keratinized stratified squamous epithelium. Hairs and sebaceous glands are
also present
Transition from vestibule to respiratory region (respiratory epithelium)stratified squamous ==
pseudostratified columnar == ciliated. Goblet cells also present in this epithelium.
Conchaebony projectionincrease surface area of the nasal cavity and create turbulence in the
stream of passing airfacilitates conditioning of the air.
Lamina propria supplements the secretion of goblet cells. Veins in the lamina propria form thin-
walled cavernous bodies.
Olfactory regiontissue on the superior conchae and nasal septum. Cilia in the epithelium of
olfactory region arise from olfactory cellsno dynein armsdeny motility.
Cell membrane covering the surface of the cilia respond to odorants. The axons of the olfactory cells
collect into bundles in the lamina propria. Supporting cells also present.
Basal cells == olfactory cells or supporting cells
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Pharnyx
Respiratory epithelium (nasopharynx or epipharynx)
Stratified squamous epithelium (oropharynx or meso- and hypo-phraynx)
Lymphocytes usually accumulate beneath the epithelium of the pharynxtonsils
Larynx
Vocal folds lined by stratified squamous epithelium.
Contains the muscle (striated, skeletal) and ligaments needed to control the vocal folds.
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Trachea Lined by respiratory epithelium.
Physical or chemical irritation increase goblet cell number. Prolonged intenseirritationtransformation to stratified squamous epithelium.
Also contains brush cells, endocrine cells, surfactant-producing cells, serouscells.
Mucosaepithelium and lamina propriaSubmucosaelastic membrane (lamina propria) borders mucosa andconnective tissue belows it. Submucosa glands supplement the secretion ofthe cells in the epithelium.
Tracheal cartilagedorsal ends : trachealis muscle and connective tissuefibres.
Annular ligamentsconnect individual cartilages.
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Bronchi Similar to those of the trachea and the main bronchi
Surrounded by a layer of smooth muscle, located between the cartilage andepithelium
Bronchioles Ciliated columnar epithelium
Glands and cartilage are absent
Smooth muscle layer relatively thicker
Alveoli Wallformed by a thin sheet of tissue separating neighbouring alveoli
epithelial cells and intervening connective tissue.
Between the connective tissue, we find dense, anastomosing network ofpulmonary capilaries.
Alveolar poresconnect neighbouring alveoli to each other.
o Alveolar type I cellsextremely flattened
o Alveolar type II cellsirregularly (sometimes cuboidal) shaped. Containcytosomes consisting of precursors to pulmonary surfactant.
Alveolar macrophagesremove particular matters inspired into the alveoli
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FISIOLOGI BATUK
Pada dasarnya mekanisme batuk dapat dibagi
menjadi empat fase yaitu :
I. FASE IRITASI
II. FASE INSPIRASI
III. FASE KOMPRESIIV. FASE EKSPIRASI
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Cough reflex
The bronchi and trachea are so sensitive to light touch that very slightamounts of foreign matter or other causes of irritation initiate the cough
reflex. The larynx and carina (the point where the trachea divides into thebronchi) are especially sensitive, and the terminal bronchioles and even thealveoli are sensitive to corrosive chemical stimuli such as sulfur dioxide gas orchlorine gas. Afferent nerve impulses pass from the respiratory passagesmainly through the vagus nerves to the medulla of the brain. There, anautomatic sequence of events is triggered by the neuronal circuits of the
medulla, causing the following effect.o First, up to 2.5 liters of air are rapidly inspired.
o Second, the epiglottis closes, and the vocal cords shut tightly to entrap the airwithin the lungs.
o Third, the abdominal muscles contract forcefully, pushing against thediaphragm while other expiratory muscles, such as the internal intercostals,
also contract forcefully. Consequently, the pressure in the lungs rises rapidly toas much as 100 mm Hg or more.
o Fourth, the vocal cords and the epiglottis suddenly open widely, so that airunder this high pressure in the lungs explodes outward.
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DD BATUK
Pneumonia : akut dan kronik
TBC Paru
Ca paru lokal Cystic Fibrosis
Abcess Paru
Bronchiektasis
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IMMUNIZATION
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NORMAL GROWTH AND
DEVELOPMENT OF A 7-YEAR-OLDCHILD
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Motor Development hand-eye coordination is well developed
has good balance
can execute simple gymnastic movements, such as somersaults Language and Thinking Development
uses a vocabulary of several thousand words
demonstrates a longer attention span
uses serious, logical thinking; is thoughtful and reflective
able to understand reasoning and make the right decisions
can tell time; knows the days, months, and seasons
can describe points of similarity between two objects
begins to grasp that letters represent the sounds that formwords
able to solve more complex problems
individual learning style becomes more clear-cut
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Social and Emotional Development
desires to be perfect and is quite self-critical
worries more; may have low self-confidence
tends to complain; has strong emotional reactions
understands the difference between right and
wrong takes direction well; needs punishment only rarely
avoids and withdraws from adults
is a better loser and less likely to place blame
waits for her turn in activities
starts to feel guilt and shame
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PERTUSSISETIOLOGY AND PATHOGENESIS
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Humans are the sole reservoir for B. pertussis and B. parapertussis. B.
pertussis, a gram-negative pleomorphic bacillus, is the main causative
organism for pertussis.
B. pertussis spreads by aerosolised droplets produced by the cough of
infected individuals, attaching to and damaging ciliated respiratory
epithelium.B. pertussis also multiplies in the respiratory epithelium,
starting in the nasopharynx and ending primarily in the bronchi.
Pertussis is highly contagious, developing in approx. 80-90% of susceptible
individuals who are exposed to it.
A mucupurulosanguineous exudate froms in the respiratory tract. This
exudate compromises the small airways (esp. those of infants) and
predisposes the affected individual to atelectasis, cough, cyanosis, and
pneumonia. The lung parenchyma and bloodstream are not invaded,
therefore, blood culture results are negative.
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Transmission of pertussis can occur through direct face-to-face contact,
through sharing of a confined space, or through contact with oral, nasal,
or respiratory secretions from an infected source.
Young infants, esp. those born prematurely, and patients with underlyingcardiac, pulmonary, neuromuscular, or neurologic disease are at high risk
for contracting the disease and for complications.
Risk factors :
Non-vaccination in children
Contact with an infected person
Epidemic exposure
Pregnancy
Transmission by contact with contaminated articles is rare. Patients are
usually not infectious after the third week of paroxysmal phase.
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PERTUSSIS
DIAGNOSIS
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The criterion standard for diagnosis of pertussis is isolation of B.
pertussis in culture. However, laboratory confirmation of pertussis is
difficult and delayed.Therefore, clinicians need to make the diagnosis of
pertussis presumptively in patients with a history of intense paroxysmal
coughing, with or without whooping, color changes, posttussive vomiting,incomplete or absent pertussis vaccination, and a finding of lymphocytosis
on a laboratory examination.
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Leukocytosis( 15.00050.000 /microlitre ) with absolute lymphocytosis
occurs during the late catarrhal and paroxysmal phases. It is a non-specificfinding but correlates with the severity of the disease.
Culture specimen should be obtained by using deep nasopharyngeal
aspiration or by holding a flexible swab (Dacron or calcium alginate) in the
patients posterior nasopharynx for 15-30 seconds or until a cough is
produced. The media preferred include Bordet-Gengou agar and modified Stainer-
Scholler media and should be promptly inoculated. B. pertussis usually
grows after 3-4 days. However, negative results can only be considered
until after 10 days.
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PERTUSSISCLINICAL FEATURES
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The incubation period averages 7-14 days (maximum of 3 weeks). B. pertussisinvades respiratory mucosa, increasing the secretion of mucus, which is initiallythin and later viscid and tenacious.
Uncomplicated disease lasts about 6-10 weeks and consists of :
- Catarrhal phase- Paroxysmal phase
- Convalescent phase
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The catarrhal stage begins insidiously, generally with sneezing,
lacrimation, or other signs of coryza; anorexia; listlessness; and a
troublesome, hacking nocturnal cough that gradually becomes diurnal.
Hoarseness may occur. Fever is rare.
Usually lasts for ca. 12 weeks.
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The paroxysmal phase begins with an increase in the severity and
frequency of the cough. Repeated bouts of 5 or more rapidly consecutive
forceful coughs occur during a single expiration and are followed by a
whoopa hurried, deep inspiration.
Copious viscid mucus may be expelled or bubble from the nares during orafter the paroxysms. Posttussive vomitting is characteristic.
In infants, choking spells (with or without cyanosis) may be more common
than whoops.
Usually lasts for 1-6 weeks, but may persists for up to 10 weeks.
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Symptoms diminish as the convalescent phase beginsrecovery is
gradual.
The cough becomes less paroxysmal and disappears in 2-3 weeks.
However, paroxysms often recur with subsequent respiratory infectionsfor many months after the onset of pertussis.
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PERTUSSIS
TREATMENT
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Supportive care
Erythromycin or azithromycin
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PERTUSSIS
PREVENTION
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Active immunization is part of standard childhood vaccination.Five doses
of vaccine are given (usually combined with diphtheria and tetanus [DTP
or DTaP]) at age 2, 4, and 6 mo; boosters are given at 15 to 18 mo and 4 to
6 yr. Significant adverse effects from the pertussis component of the
vaccine include encephalopathy within 7 days; seizure, with or without
fever, within 3 days; persistent, severe, inconsolable screaming or crying
for 3 h; collapse or shock within 48 h; fever 40.5 C within 48 h; and
immediate severe or anaphylactic reaction. These reactions
contraindicate further use of pertussis vaccine; combined diphtheria and
tetanus vaccine is available without the pertussis component.Theacellular vaccine (DTaP) is better tolerated.
Immunity after natural infection lasts about 20 yr. Passive immunization is
unreliable and is not recommended.
Close contacts < 7 yr who have had < 4 doses of vaccine should be
vaccinated. Contacts of all ages, whether vaccinated or not, should receive
a 10-day course of erythromycin 500 mg po qid or 10 to 12.5 mg/kg po
qid.
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CEREBRAL PALSY
PATHOGENESIS
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Cerebral Palsy (CP) ?
A group of disorders of the development of movement and posture
causing activity limitations that are attributed to non-progressive
disturbances that occurred in the developing fetal or infant brain.
The motor disorders of cerebral palsy are often accompanied by
disturbances of sensation, cognition, communication, perception, and/or
behaviour, and/or a seizure disorder.
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Major events in human brains development and their peak times of
occurrence include the following :
Primary neurulationweeks 3-4 of gestaion
Prosencephalic developmentmonths 2-3 of gestation
Neuronal proliferationmonths 3-4 of gestation
Neuronal migrationmonths 3-5 of gestation
Organisationmonth 5 of gestation to years postnatal
Myelinationbirth to years postnatal
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CEREBRAL PALSY
APPROACH CONSIDERATIONS
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TB MENINGITIS
COMPLICATIONS
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TBRM (Tuberculous radiculomyelitis) is a complication of TBM that has
been reported only rarely in the modern medical literature. It develops at
various intervals after TBM, even in adequately treated patients after
strerilization of the CSF.
The most common symptoms are subacute paraparesis, radicular pain,
bladder disturbance, and subsequent paralysis.
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TB MENINGITISPREVENTION
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BCG vaccination offers a protective effect (approx. 64%) against TBM.
Improvement in weight for age was associated with a decreased risk of the
disease.However, further studies are needed to evaluate the association,if any, between nutritional status and vaccine efficiency.