2. RESPIRATORY SYSTEM
• The main functions of the respiratory system
are to obtain oxygen from the external
environment and supply it to the cells and to
remove from the body the carbon dioxide
produced by cellular metabolism.
• Hence, the respiratory system ensures
appropriate internal environment for cellular
metabolism and excretions of the unwanted
gases
3. 4 Basic Structures:
• The conducting airways ( conduction of the gases
from the external environment into the lungs and
contrariwise
• Lungs (Alveoli cells for gaseous exchange)
• The parts of the central nervous system
concerned with the control of the muscles of
respiration .
• The chest wall.
– the muscles of respiration—such as the diaphragm,
the intercostal muscles, and the abdominal muscles—
and
– the rib cage.
5. CNS Centers that control of
Respiration/breathing
• Medullary inspiratory center located in the
medulla oblongata is the part of CNS that
controls respiration
• Its main function is to send signals to the
muscles that control respiration ( diaphram
and intercostal muscles) to cause breathing to
occur.
6. • The pheumotaxic area, located in the pons,
inhibits the inspiratory center, limiting the
contraction of the inspiratory muscles, and
preventing the lungs from overinflating.
• The apneustic area, also located in the pons,
stimulates the inspiratory center, prolonging
the contraction of inspiratory muscles.
7. Oral cavity Vs respiratory System
• Direct spread of infection between oral infection
and respiratory system is not uncommon
• Oral cavity is contiguous with the upper
respiratory apparatus, hence infections of oral
cavity can affect the respiratory system the same
way the respiratory infection/pathologies can
affect the oral health..
• Most of the concern between oral cavity and
respiratory system is infection, but other
conditions has also been reported e.g tumour
seeding
8. Scientific reports in support of the
possible relationship
• Some respiratory diseases e.g Asthma have
been reported to have effects on orofacial
morphology or even on the dentition
• Antibiotic resistance may develop because of
the use of similar medication for both URTI
and odontogenic infections
9. • Another reported reason is possible aspiration
into the lung of oral pathogens capable of
causing pneumonia, colonization of dental
plaque by respiratory pathogens followed by
aspiration, or facilitation by periodontal
pathogens of colonization of the upper airway
by pulmonary pathogens.
10. DISEASES OF THE REPIRATORY SYSTEM
• UPPER RESPIRATORY
– Viral Upper Respiratory Infections
– Allergic Rhinitis and Conjunctivitis
– Otitis Media
– Sinusitis
– Laryngitis and Laryngotracheobronchitis
– Pharyngitis and Tonsillitis
• LOWER RESPIRATORY
– Acute Bronchitis
– Pneumonia
– Bronchiolitis
– Asthma
– Chronic Obstructive Pulmonary Disease
– Cystic Fibrosis
– Pulmonary Embolism
– Pulmonary Neoplasm
11. Viral Upper Respiratory Infections
• One of the common acute respiratory illness.
• Characterized by rhinorrhea, nasal congestion
and oropharyngeal irritation
• The viral agent is an RNA virus called Rhinovirus,
other implicated virus include: Coronavirus,
influenza virus, parainfluenza virus, adenovirus,
Enterovirus,coxsackievirus, and respiratory
syncytial virus
• Other associated symptoms include fever,
malaise, fatigue, headache, and myalgia
12. PATHOPHYSIOLOGY
• Following a successful transmission from the infected
persons (usually via droplet infection, contact e.t.c), the
virus lodge in the upper or lower respiratory tract
• The virus invade the respiratory epithelium and thereafter,
replications of the virus follows.
• Incubation period: 2-5 days
• The presence of the virus triggers the immune response
• This lead to inflammation of the tissue which results in
some of the patients’ complaints.
• Mechanism for viral clearance is also enhanced and this
include formation of secretion of mucous by the Goblet
cells.
13. MANAGEMENT
• Investigations to rule out co founders (MP, FBC e.t.c)
should be carried out
• Treatment is essentially symptomatic and most of the
time the infection is self limited
• Analgesic can be use to relieve pain from inflammation
in the throat(sorethroat), and myalgia. Antipyretics for
fever
• Anticholinergic can be used for reducing rhinorrhea.
Oral/topical decongestants such as sympathomimetics
can reduce decongestion
• Note that antibiotic have no role in the management if
there is no secondary infection
14. Oral manifestations
• The commonest sign is the presence of small,
round erythematous macular lesion on the
soft palate
• There may be enlargement of lingual tonsillar
tissue due to response of the lymphoid tissue
to the virus
15.
16.
17. Dental Aspects
• Use of decongestants may cause dry mouth
• Therefore necessary to include in our
treatment plan, a treatment for xerostomia so
as to avoid the complications of xerostomia
• It is an infectious disease, the attending
dentist should put appropriate infection
control measures in place
18. Allergic Rhinitis and Conjuctivitis
• Chronic recurrent inflammatory disorder of the nasal
mucosa/conjuctival, affecting 10-40% of population
• When they occur together called allergic rhinoconjuctivitis
• Common disease that pathology of which typical of Type 1
hypersentivity reaction
• Patients have genetically predetermine suceptibilty to
allergic hypersensitity reaction.
• Exposure of the allergen in a privioualy sentised patients
leads to interaction between IgE on the surface of mast cell
and the allergen, resulting in crosslinking, the cross linking
trigger the mast cell degranulation
19. • Symptoms include pruritus, lacrimation,
crusting, and burning.
• Nasal symptoms include sneezing, lear
rhinorrhea and nasal congestion. Others are
post nasal drainage, throat irritation, pruitus
of he palate and ear canal and fatigue
• Nasal mucosa is shows oedema, and pale blue
coloration of the turbinate
20. Treatment modalities
• Allergy complete avoidance: usually difficult and sometimes
impossible
• Pharmacotherapy
– Antihistamine second generation preferred: Loratidine and
fexofenadine
– steroid drugs, such as budesonide, tripedane and fluticasone, are
being used.
– Other topical drugs, such as cromolyn and ipratropium, are also
effective.
– Chromones are also used before exposure
– The use of decongestants should be limited to not more than 4 days.
Prolonged use does not have a place in the management of AR and
can be associated with side effects
• Supportive treatments
– Pcm
21. PNEUMONIA
• Defines as an infection and subsequent inflammation
of the lung parenchyma
• Caused by both virus and bacteria
• Two types: community acquired(CAP) and nosocomial
• Community-acquired infections can affect all persons
but are more commonly seen in otherwise healthy
individuals.
• The most common bacterial cause of community-
acquired pneumonia is Streptococcus
pneumoniae,followed by Haemophilus influenzae.
Staphylococcus aureus and gram-negativ bacteria are
common causes of nosocomial pneumonia
22. • A prodrome similar to that seen with acute
infections of the upper respiratory tract is
unusual
• Patients present with fever, pleuritic chest
pain coughing that produces purulent sputum
• Chills and rigors are common
• Findings on physical examination of the chest
are usually unremarkable, with only scattered
rhonchi
23. • Treatment is essentially with the use of drugs
• Empirical treatment for outpatient with CAP
amoxycilline-clavulanic acid, macrolide and
fluoroquinolones
24. Oral aspects
• If the predisposing factor of the pneumonia is
immunosuppression, then oral signs of
immunosuppression may be evident
• Oral microbials may be contributory to the lung disease
through direct aspiration
• Plaque bacterial has been implicated in pneumonia
• Px with periodontitis are at increased risk
• Chlohexidine mouth wash for patients in ICU to present
nosocomial infection
• Px with CAP coming for dental treatment should be
treated with less bearing the medical status in mind
25. Oral health care as a preventive
measure to developing pneumonia
• This is mostly applicable to both
inmunocompromised and elderly patients
• In one such study, the relative risk of developing
pneumonia increased 67% in the group without
access to oral health interventions, compared
with individuals who had access to oral care.
• This data support the benefit of increased
awareness and increased oral health
interventions in hospitalized and institutionalized
individuals
26. ASTHMA
• Asthma is a chronic inflammatory condition that causes
the airways to constrict and produce excess mucus,
making breathing difficult.
• It is characterized by recurrent and reversible airflow
limitation due to an underlying inflammatory process.
• This condition is reversible, either spontaneously or
can be controlled with the help of drugs
• The etiology of asthma is unknown, but allergic
sensitivity is seen in most patients with asthma.
• Genetic factors play a role, but no single gene or
combination of genes has yet been identified as
causative.
27. Signs
• The hallmark clinical features of asthma are recurrent
reversible airflow limitation and airway hyper-
responsiveness.
• These factors lead to the development of the signs and
symptoms of asthma, which include intermittent
wheezing, coughing, dyspnea, and chest tightness.
• Symptoms of asthma tend to worsen at night and in
the early morning hours
• Triggers include allergens, exercise, cold air, respiratory
irritants, emotional extremes, and infections
(especially viral infections)
28. Mgt
• The diagnosis is based on clinical evaluation and
functional demonstration of reversible airway
obstruction, either spontaneously or after medical
treatment
• Patients with mild-intermittent disease usually require
short-acting bronchodilators .
• These medications (such as albuterol) are preferably
administered by inhalation
• Preparations are available in metered-dose inhalers, in
dry-powder inhalers, and as solutions for a nebulizer.
• Patients with mild-persistent asthma require routine
therapy for control of underlying airway inflammation.
29. • Oral manifestations include candidiasis,
decreased salivary flow, increased calculus,
increased gingivitis, increased periodontal
disease, increased incidence of caries, and
adverse effects of orthodontic therapy
30. • prolonged use of ß-agonists may cause
reduced salivary flow, with a resulting increase
in cariogenic bacteria and caries and an
increased incidence of candidiasis
• The increased incidence of caries is further
accelerated by the use of cariogenic
carbohydrates and sugar-containing
antiasthmatic medications
33. Managing Ashma px
• Fluoride supplements should be instituted for all
asthmatic patients, particular those taking ß -agonists.
• The patient should be instructed to rinse his or her
mouth with water after using inhalers.
• Oral hygiene should be reinforced to reduce the
incidence of gingivitis and periodontitis.
• Antifungal medications should be administered as
needed, particularly in patients who are taking inhaled
corticosteroids.
• Steroid prophylaxis need to be used with patients who
are taking long-term systemic corticosteroids
34. DENTAL MANAGEMENTS
• Use stress-reducing techniques. Conscious
sedation should be performed with agents
that are not associated with
bronchoconstrictions, such as hydroxyzine.
• Barbiturates and narcotics should be avoided
due to their potential to cause bronchospasm
and reduce respiratory functions. Nitrous
oxide can be used for all but patients with
severe asthma as it may irritate the airways
35. • Avoid dental materials that may precipitate an
attack. Acrylic appliances should be cured
prior to insertion. Dental materials without
methyl methacrylate should be considered.
• Schedule these patients’ appointments for
late morning or later in the day, to minimize
the risk of an asthmatic attack.
• Have oxygen and bronchodilators available in
case of an exacerbation of asthma.
36. • There are no contraindications to the use of
local anesthetics containing epinephrine, but
preservatives such as sodium metabisulfite
may contribute to asthma exacerbation in
susceptible patients.
• Judicious use of rubber dams will prevent
reduced breathing capability.
37. • Care should be used in the positioning of
suction tips as they may elicit a cough reflex.
• Up to 10% of adult asthmatic patients have an
allergy to aspirin and other nonsteroidal anti-
inflammatory agents.
• A careful history concerning the use of these
type of drugs need to be elicited
38. • Sedatives are better avoided as even
benzodiazepines can precipitate respiratory
failure.
• GA is also best avoided,
• Prolonged steroid use may predispose to oral
candidiasis.
• Acute asthmatic attacks may be provoked by
anxiety. Handle patients with care and allay
fear and anxiety.
39. Tuberculosis
• Caused by Mycobacterium tuberculosis and
primarily a disease of the resp. system
• Usually transmitted by infected sputum and
currently affects about a third of the world
population and about 2 million die of TB every
year.
• HIV infection has contributed to the morbidity
and mortality from TB.
40. • The multidrug resistant and atypical variety is
becoming more common.
• It is a serious occupational risk to medical and
dental staffs.
• Risk of transmission in the dental setting
possible when there is a patient with active
disease and dental staffs with a compromised
immunity or HIV positive.
41. • Dental treatment must be deferred in patients
with active disease as they are highly
contagious.
• If they must be treated, minimize splatter and
aerosols use rubber dam and other barriers,
improve the ventilation and heat sterilize all
the instruments used.
• Relative analgesia and GA are contraindicated
due to impaired pulmonary function and risk
of contamination of equipment.
42. • Drug interactions with theophylline are
common. Macrolide antibiotics may increase
the level of theophylline whereas
phenobarbitals may reduce the level.
• Furthermore, drugs such as tetracycline have
been associated with more accentuated side
effects when given together with theophylline
43. • During an acute asthmatic attack, discontinue
the dental procedure, remove all intraoral
devices, place the patient in a comfortable
position, make sure the airway is opened, and
administer aß2-agonist and oxygen.
• If no improvement is noted, administer
epinephrine sub-cutaneously (1:1,000
concentration, 0.01 mg/kg of body weight, up
to a maximum of 0.3 mg) and alert emergency
medical assistance.
44. • Aminoglycosides such as streptomycin
enhance the activity of neuromuscular
blocking agents and may induce a myasthenic
syndrome.
• The clearance of diazepam and the
hepatotoxicity of acetaminophen is enhanced
by rifampicin.
• Isonaizid also enhances the hepatotoxcity of
acetaminophen.
• Azole antifungals, clarithromycin and
benzodiazepines interact with rifampicin.
45. • Rifampicin reduces the efficacy of antifungals,
corticosteroids and benzodiazepines.
• Chronic tongue ulcers are the most important
oral/ facial feature of TB and should arouse
suspicion.
• This is followed by cervical lymphadenopathy
which may sometimes suppurate (collar stud
abscess/scrofula
46. Chronic obstructive pulmonary disease
• Its a disease characterized by airflow
limitation
• Three processes:
– chronic inflammation throughout the airway
– Oxidative stress
– Imbalance of proteases and antiprotease
• This respiratory describes a chronic and largely
irreversible airway obstruction due to
inflammation of the lower airways.
• Chronic bronchitis is COPD due to chronic
bronchial inflammation
47. COPD=EMP+CB
• Chronic bronchitis is diagnosed on clinical
criteria and is defined as coughing and sputum
production for 3 or more months per year for
at least 2 consecutive years.
• Emphysema is diagnosed by histopathology
and is defined by enlarged air spaces and the
loss of alveolar tissue
48. • The hallmark features of COPD are dyspnea
and hypoxemia.
• Alveolar hypoventilation and diffusion
impairment causes hypercarbia, which may
result in pulmonary hypertension and cor
pulmonale
• Most patients display some degree of
progressive dyspnea, exercise intolerance, and
fatigue
49. • An increase in the production of often purulent sputum
is a sign of exacerbation due to respiratory infection.
Physical findings include diffuse wheezing, possibly
associated with signs of respiratory distress including
the use of accessory muscles of respiration
(retractions) and tachypnea.
• Liver enlargement due to congestion, ascites, and
peripheral edema can develop as the disease
progresses to pulmonary hypertension and
corpulmonale.
• This leads to the characteristic clinical patient
presentation termed the “blue bloater.”
50. Pathophysiology
• The primary defect in the CFTR gene results in a
defective chloride transport system in exocrine
glands.
• As a result, mucous production occurs without
sufficient water transport into the lumen. The
resultant mucus is dry, thick, and tenacious and
leads to inspissation in the affected glands and
organs.
• In the airways, the viscid secretions impair
mucociliary clearance and promote airway
obstruction and bacterial colonization. Bacterial
superinfection is common and can lead to
respiratory compromise.
51. Dental aspect
• Oral infections especially those caused by
Streptococcus viridans has been shown to be
the causative pathogen of exacerbation in 4%
of individuals with COPD.
• One prospective study suggested that oral
colonization with respiratory pathogens in
patients residing in a chronic care facility was
significantly associated with COPD.
52. • Drug interactions with theophylline may arise
(see above), and a change of medications by
the oral health care provider may be
appropriate
53. • Class discussions: SPIROMETRY
findings…implications
• TV 0.5L
• IRV 2.5L
• ERV 1.5