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Diseases in
Pregnancy
IGN BAGUS ARTANA
Outline
Introduction to respiratory system
Asthma
Acute bronchitis AECB
Pneumonia
Tuberculosis
RESPIRATION
Respiration refers to the processes involved in:
Oxygen transport from the atmosphere to the body tissue
Transportation of carbon dioxide produced in the tissue to
the atmosphere
Respiration components :
A Gas exchange system Lung
A Transport system Cardiovascular system
BASIC CONCEPTS:
Oxygen supply to body tissue is essential
The three key steps involved in gas
exchange :
Ventilation
Perfusion
Diffusion
VENTILATION
The movement of air
in/out of the respiratory
system
Determined by :
Respiratory rate (N: 12
20X/mnt)
Tidal volume (volume of each
breath)
Main mechanism :
pressure differences
Air flows from a highpressure area to a lowpressure area
VENTILATION
Inspiration :
Contraction of diaphragm
increasing intrathoracic
volume
External intercostal
muscles raise the rib cage
Results in a lowered
pressure within thoracic
cavity air flow into the
lungs
Expiration :
Passive, a result of elastic
VENTILATION
Impaired ventilation :
Obstructive disorders : narrowed airways and
increased resistance to airflow (Bronchial
Asthma, Chronic Obstructive Lung Diseases)
Restrictive disorders : impaired in lung
expansion so gaseous exchange is reduced
(Pleural Effusion, Atelectasis, Pneumothorax,
Interstitial Lung Diseases)
SPIROMETRY
PERFUSION
Alveoli contain a dense network
of capillaries
Capillaries blood air barrier
extremely thin
Gas exchange take place
Ventilation (V) / Perfusion (Q)
apprx 1 efficient gaseous
exchange
V/Q mismatched most
common cause of hypoxemia
(Pneumonia, Adult Respiratory
Distress Syndrome, Lung
DIFFUSION
Diffusion occurs across the
alveolar capillary membrane
depends on gasses (O2 or
CO2) partial pressure
gradients
Blood perfusing pulmonary
capillaries is mixed-venous
blood, so:
O2 diffuse from higher PO2
(environment of alveoli) into
the capillaries
CO2 diffuse from higher CO2
(blood in capillaries) into the
CLINICAL PRESENTATIONS:
Breathlessness, Cough,
Sputum, Haemoptysis, Wheeze,
CLINICAL
Chest pain, Hoarseness, Weigh
INVESTIGATIONS:
loss, Ankle sweeling
DIAGNOSIS:
Conginetal abnormalities, Pneumonia,
Tuberculosis, Asthma, COPD, Lung
cancer, Pleural Diseases .............
MANAGEMENT:
Pharmacological and Non-pharmacological
(Oxygen therapy, Asisted ventilation,
Physiotherapy, Surgery)
ASTHMA
Burden of Asthma
Definition of Asthma
Mechanisms: Asthma
Inflammation
Mucous
gland
hypertroph
y
Edema
Mucus
Thickening of
basement
membrane
Adapted from National Asthma Education and Prevention Program. Expert Panel
Report: Guidelines for the diagnosis and management of asthma. NHLBI, NIH. 1991.
Epitheli
al
damage
Airway
smooth
muscle
Inflammator
y cell
infiltration
Vascular
dilatation
Mekanisme Dasar
Faktor risiko asma
INFLAMASI
Obstruksi jalan nafas
Hiper-aktivitas
Jalan nafas
Faktor risiko
(Terjadi eksaserbasi)
Gejala
Klinis
Symptoms
Coughing and wheezing are the most common
symptoms of childhood Asthma
Breathlessness, chest tightness or pressure, and
chest pain also are reported
Poor school performance and fatigue may indicate
sleep deprivation from nocturnal symptoms
Cough
Nocturnal cough, recurring seasonal cough, or
cough in response to specific exposures
Although wheezing hallmark of asthma, cough is
often sole presenting complaint
Most common cause of chronic cough in children
older than 3 years is asthma
Wheeze
Wheezing is a high-pitched, expiratory sound
produced when air forced through narrow airways
Asthma wheeze tends to be polyphonic (varied in
pitch)
When airflow obstruction severe, can appreciate
wheeze with inspiration and expiration.
Asthma Diagnosis
Controlled
(All of the following)
Twice or less
per week
Partly controlled
(Any present in any week)
More than
twice per week
None
Any
Nocturnal symptoms
None
/ awakening
Any
Uncontrolled
Twice or less
per week
More than
twice per week
Normal
3 or more
features of
partly
controlled
asthma
present in
any week
TO STEP 3
TREATMENT, SELECT
ONE OR MORE:
TO STEP 4
TREATMENT, ADD
EITHER
Asthma Treatment
Controller
Medications
Reliever
Medications
Controller Medications
Inhaled glucocorticosteroids
Leukotriene modifiers
Long-acting inhaled 2-agonists in
combination with inhaled
glucocorticosteroids
Systemic glucocorticosteroids
Theophylline
Cromones
Anti-IgE
Reliever Medications
Rapid-acting inhaled 2agonists
Systemic
glucocorticosteroids
Anticholinergics
Theophylline
Short-acting oral 2-agonists
Asthma
Asthma Management
Management and
and Prevention
Prevention Program
Parameter
Mild
Moderate
Severe
Breathless
Walking
Can lie down
Talking
Infantsofter shorter
cry; difficulty feeding
Prefers sitting
At rest
Infantstops feeding
Hunched forward
Talks in
Phrases
Sentences
Words
Alertness
May be agitated
Usually agitated
Usually agitated
Respiratory rate
Increased
Increased
Often >30/min
Usually not
Usually
Usually
Paradoxical
thoracoabdominal
movement
Wheeze
Moderate, often
only end
expiratory
Loud
Usually loud
Absence of wheeze
Pulse/min
<100
100-120
>120
Bradycardia
Pulsus paradoxus
Absent <10 mm
Hg
Absence suggests
respiratory muscle
fatigue
Over 80%
Approximately 6080%
Normal
Test not usually
necessary
>60 mm Hg
<60 mm Hg
Possible cyanosis
PaCO2
<45 mm Hg
<45 mm Hg
>45 mm Hg:
Possible respiratory failure
>95%
91-95%
<90%
Respiratory arrest
imminen
Drowsy or confused
Asthma
Asthma Management
Management and
and Prevention
Prevention Program
Asthma
Asthma Management
Management and
and Prevention
Prevention Program
Acute Bronchitis
Acute Exacerbations of Chronic
Bronchitis
Etiology
Associated with respiratory viruses, including
rhinovirus, coronavirus, inuenza viruses, and
adenovirus.
Mycoplasma pneumoniae,Chlamydia
pneumoniae, and Bordetella pertussis may also
cause bronchitis.
Secondary invasion with bacteria such as
Haemophilus inuenzae and Streptococcus
pneumoniae may also play a role in acute
bronchitis
Acute bronchitis
Acute bronchitis is an inammation of the
tracheobronchial tree, usually in association with a
generalized respiratory infection
Etiology
Table 1. List Of Pathogen As The Etiology Of Several Lung Infection
Clinical Findings
Cough is the most prominent manifestation of acute
bronchitis. Initially, the cough is nonproductive, but later
mucoid sputum is produced
Symptoms of tracheal involvement include burning
substernal pain associated with respiration and a very
painful substernal sensation with coughing
Clinical Findings
There are no signs of consolidation and the chest
radiograph shows no opacity
Management
If there is a predominant microorganism seen in the presence of
more than 25 polymorphonuclear neutrophils and fewer than 10
squamous epithelial cells per low-power eld
antibiotic therapy directed against S. pneumoniae and H. inuenzae
should be instituted
Management
Comments
Influenza virus
Parainfluenzavirus
None available
Respiratory syncytial
virus
None available
Coronavirus
None available
Adenovirus
None available
Rhinovirus
None available
Table 3. Recognized Causes of Acute Bronchitis and Options for Therapy (cont)
Pathogen
(ATYPICAL)
Comments
Bordetella pertussis
Mycoplasma
pneumoniae
Chlamydophila
pneumoniae
Acute Exacerbation of
Chronic Bronchitis (AECB)
Microbial
colonization
Bacterial
products
Bacterial
products
Airway
inflammation
Pathogenesis of
Chronic Bronchitis
(Balter et al, 2003)
Cigarette smoke
Viral infection
Impaired local
defense
Tissue
damage
Loss of cilia
Damaged
epithelium
Altered mucus
Local IgA
breakdown
AECB: Etiology
Role of bacteria considered leading cause
Other causes: viruses, allergens, pollution, increased
smoking
AECB: Etiology
H. influenzae
S. pneumoniae
S. pneumoniae,
H. influenzae and
M. catarrhalis
account for ~80%
of bacterial isolates
18%
49%
Other
19%
14%
M. catarrhalis
AECB Stratification
(Anthonisen et al, 1987)
Increased dyspnea
Increased Sputum
Sputum purulence
Type I:
all three
symptoms
Type II:
two
symptoms
Treat
Probably
Treat if
include
Purulence
Type III:
one
symptom
No
treat
% Deterioration
35
30
25
P < .05
20
Placebo
15
Antibiotic
10
5
0
All
Type 1
Type 2
Type 3
Type of Exacerbation
Anthonisen NR et al. Ann Intern Med. 1987;106:196.
RISK FACTORS:
Number of AECBs
Comorbidity
FEV1
Steroid use
Recent antibiotics
>4 exacerbations/yr
As in group II
Cardiac disease
FEV1 <50%
Home O2
Chronic oral steroids
H. influenzae
H. Spp
M. catarrhalis
S. pneumoniae
Ab use in past 3 mo
Group I plus
Klebsiella spp +
Other gram-negatives
Increased -lactam
resistance
Group II plus
P. Aeruginosa &
Multi-resistant
Enterobacteriaceae
>4 exacerbations/yr
As in group II
Cardiac disease
FEV1 <50%
Home O2
Chronic oral steroids
Ab use in past 3 mo
Fluoroquinolone
-lactam/-lactamase
inhibitor
Tailor to pathogen
Ciprofloxacin
PNEUMONIA
Pneumonia Definition
An
Pneumonia
The
Pneumonia - Symptoms
Chills/Sweats
Fatigue
Headache
Diarrhea (Legionella)
URI, sinusitis (Mycoplasma)
Findings on Exam
Physical:
Vitals:
Fever or hypothermia
Lung Exam: Crackles, rhonchi, dullness to percussion or egophany.
Labs:
Elevated
WBC
Hyponatremia Legionella pneumonia
Positive Cold-Agglutinin Mycoplasma pneumonia
Chest X-ray
RUL
LUL
RUL
Lingula
LUL
RML
RLL
Lingula
LLL
RML
RLL
LLL
Types of Pneumonia
Community-Acquired (CAP)
Health-Care Associated Pneumonia (HCAP)
HCAP or HAP
Pseudomonas aeruginosa
Staphylococcus aureus
(Including MRSA)
Klebsiella pneumoniae
Serratia marcescens
Acinetobacter baumanii
Diagnosis of pathogen
Sputum
Culture
Blood
Cultures
Strep. pneumo urinary antigen
Legionella urinary antigen
HIV test?
safety at home
CURB-65 or PORT score
Clinical Judgement
Treatment of CAP
Outpatient:
Macrolide (Azithromycin)
Fluoroquinolone (Levofloxacine, Moxifloxacin)
Doxycycline
Inpatient:
Beta-Lactam + Macrolide
Ceftriaxone
+ Azithromycin
Fluoroquinolone
For
Special Cases!
HIV
Pneumocystis jirovecii
Mycobacterium tuberculosis
Cryptococcus
Histoplasmosis
Transplant Patients
Fungi (Aspergillosis, Cryptococcus, Histoplasmosis)
Nocardia
CMV
Neutropenic Patients
Fungi ( Aspergillosis)
Gram-negatives
Tuberkulosis paru
INTRODUCTION
CHARECTERISTICS OF M. TUBERCULOSIS
Strict aerobes
CAUSES
The high lipid content of this pathogen accounts for many of its unique
clinical characteristics.
RISK FACTORS OF
TUBERCULOSIS
Low
socioeconomic status
Crowded
living conditions
Diseases
Person
Health
care workers
Alcoholism
Recent
Silicosis
Prolonged
Other
Low
corticosteroid therapy
immunosuppressive therapy
Diabetes
mellitus
Residents
Patients
and employees of
with CRF
coughing,
sneezing,
shouting,
or any other way that will expel bacilli into the air
lung
renal cortex
reticuloendothelial system
Evaluation for
TB
1.HIV test
2.Medical history
3.Physical examination
4.Bacteriologic or histologic
exam
(Chest radiograph if
indicated)
Medical History
HIV
status
Symptoms
History
Past
of disease
TB treatment
Demographic
Other
Symptoms of
Pulmonary TB
Productive, prolonged
cough
(duration of 2-3 weeks)
Chest pain
Hemoptysis (bloody
sputum)
Signs may vary based on
HIV status
Specimen Collection
Procedure
Obtain 3 sputum specimens for
smear examination
and culture
Alur Diagnosis
TB Paru
Be
carefully
with the
imaging
interpreta
tion
Hasil pemeriksaan dahak 3 kali menunjukkan BTA negatif, gambaran klinis dan
kelainan radiologi menunjukkan TB aktif. Hasil pemeriksan dahak 3 kali
menunjukkan BTA negatif dan biakan M. TB positif.
Adalah pasien yang belum pernah mendapat pengobatan dengan OAT atau sudah
pernah mendapat OAT kurang dari satu bulan.
TB paru kambuh yang ditentukan oleh dokter spesialis yang berkompeten menangani kasus TB.
Adalah pasien yang telah menjalani pengobatan 1 bulan dan tidak mengambil
obat 2 bulan berturut-turut atau lebih sebelum masa pengobatan selesai.
Adalah pasien BTA positif yang masih tetap positif pad akhir bulan ke-5 atau akhir
pengobatan.
Kasus kronik.
Adalah pasien dengan hasil pemeriksaan BTA masih positif setelah selesai
pengobatan ulang dengan pengobatan kategori 2 dengan pengawasan yang baik.
Hasil pemeriksaan BTA negatif dan biakan juga negatif dan gambaran radiologi
paru menunjukkan lesi TB yang tidak aktif, atau foto serial menunjukkan gambaran
yang menetap. Riwayat pengobatan OAT adekuat akan lebih mendukung. Pada
kasus dengan gambaran radiologi meragukan dan telah mendapat pengobatan
OAT 2 bulan serta foto toraks ulang tidak ada gambaran radiologi.
TREATING TB DISEASE
(GENERAL PRINCIPLES)
MEDICAL MANAGEMENT
15mg/kg
Isoniazid
Rifampin
10 mg/kg
Pyrazinamide
15 30 mg/kg
Ethambutol(Myambutol)
MEDICAL MANAGEMENT
Second Line Medications .
Capreomycin
Ethionamide
12 -15 mg/kg
15mg/kg
Paraaminosalycilate
Cycloserine
Vitamin
15 mg/kg
MEDICAL MANAGEMENT
Third
Line Drugs
Other
Rifabutin
Macrolides:e.g.,clarithromycin
Linezolid(LZD)
Thioacetazone(T)
Thioridazine
Arginine
(CLR)
Kategori 2 (2HRZES/HRZE/5H3R3E3)
Paduan obat ini diberikan untuk pasien BTA positif yang telah diobati sebelumnya :
Pasien kambuh
Pasien gagal
Mode of action
3 x per week
5 (4-6)a
Bactericidal
Isoniazid (H)
Bactericidal
Rifampicin (R)
Bactericidal
Pyrazinamide (P)
Ethambutol (E)
Streptomycin (S)
Thioacetazone (T)
Bacteriostatic
Bactericidal
Bacteriostatic
10 (8-12)
10 (8-12)
10 (8-12)
25 (20-30)
35 (30-40)
15 (15-20)
30 (25-35)
15 (12-18)
15 (12-18)
2.5
Not applicable
Standar
Terapi
Standar
Terapi
Dosis Standar
(mg/kg)
Periksa BB pasien
Standar
Terapi
Dosis Standar
(mg/kg)
THANK YOU