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Drugs Effecting Respiratory System (MSCN)
Drugs Effecting Respiratory System (MSCN)
respiratory system
Dr Arfa Azhar,
MBBS, Mphil, PhD Scholar
Senior Instructor,
Department of Biological and Biomedical Sciences,
Medical College, Pakistan
INTRODUCTION
Introduction
Asthma is a chronic inflammatory disorder of the airways
that is characterized:
Clinically by recurrent episodes of wheezing,
breathlessness, chest tightness, and cough, particularly at
night/early morning.
Physiologically by widespread, reversible narrowing of the
bronchial airways and a marked increase in bronchial
responsiveness.
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Classification
A heterogenous disorder.
Atopic /extrinsic /allergic ( 70%):
o Most common type
o Environmental agent: dust, pollen, food, animal
dander
o Family history - present
o Serum IgE levels - increased
o Skin test with offending agent –wheal flare
Classification
Non-atopic/ intrinsic /non-allergic( 30%)
Triggered by respiratory tract infection
Viruses - most common cause
Pathophysiology
I. Inflammation
Chronic inflammatory state
Involves respiratory mucosa from trachea to
terminal bronchioles, predominantly in the
bronchi.
Pathophysiology
I. Inflammation
Activation of mast cell , infiltration of
eosinophils & T-helper type 2 (Th2)
lymphocytes
Endogenous factors
Atopy
Genetic predisposition to IgE mediated type I
hypersensitivity
The major risk factor for asthma
Genetics
Pathophysiology
Pathophysiology
Clinical manifestations
Classification for asthma severity
Pulmonary function
tests:
Using Spirometry
estimate degree of
obstruction
↓FEV1, ↓FEV1/FVC,
↓PEF.
Laboratory diagnosis
CXR :
hyperinflation,emphysema
Arterial blood-gas analysis
hypoxia & hypocarbia
Skin hypersensitivity test
Sputum & blood eosinophilia
Elevated serum IgE levels
Status asthmaticus
Bronchodilators
Beta agonist e.g. salbutamol
Anticholinergics
Mast cell stabilizers, sodium chromoglycate, Ketotifen
Corticosteroids
Bronchodilators: β-Agonists
Mechanism of Action
Indications
Skin color
Baseline vital signs
Respirations (should be between 12 and 24 breaths/min)
Respiratory assessment, including PO2
Sputum production
Allergies
History of respiratory problems
Other medications
β-Agonists - Patient Education
Patients should be encouraged to have a good state of health
Check with their physician before taking any medication, including OTCs
Mechanism of Action
Acetylcholine (ACh) causes bronchial constriction and narrowing of the
airways
Anticholinergics bind to the ACh receptors, preventing ACh from
binding
Result:
bronchoconstriction is prevented
airways dilate
Adverse effects
2.Kitotifen :
It is absorbed orally.
Bioavailability is 50% due to first pass metabolism.
It is largely metabolized.
Plasma half life is 20-22 hours.
MAST CELL STABILIZERS
Mechanism of action
These drugs inhibit degranulation of mast cells.
Release of mediators like Histamine, LT<PAF<IL is inhibited.
This action may include delayed CI channel.
Chemo taxis of inflammatory cells is inhibited.
Bronchial hyperactivity is reduced.
Bronchospan due to various stimuli (allergens, irritants, cold air and ecercise)
is prevented.
It can’t be used to prevent attacks of asthma because it does not affect the
constrictor action of histamine.
Clinical Uses
Sodium cromoglycate :
Ketotifen :
Mechanism of Action
Pharyngeal irritation
Coughing
Dry mouth
Oral fungal infections
Systemic effects are rare because of the low doses used for inhalation therapy
Corticosteroids
Nursing Implications – Pt Education
Teach patients to gargle and rinse the mouth with lukewarm water
afterward to prevent the development of oral fungal infections
MODE OF TRANSMISSION
• It is spreaded through the air when people who have an active TB
infection cough, sneeze, or otherwise transmit respiratory fluids
through the air.
Types of tuberculosis
Macrophage
engulfing tubercle
bacilli
When infected person coughs or sneezes, the granulomas that may be present
in sputum comes in contact with air.
Cell death
Mechanism of resistance:
1. Mutation in KatG
2. Mutation of InhA
Pharmacokinetics:
1. Absorption: Readily absorbed through GIT.
2. Distribution: in all body fluids and tissues including CSF
3. Metabolism: Acetylation in liver
4. Excretion : renal route
Clinical use:
1. used in combination of other antitubercular agents
2. Also used as single agent in treatment of latent TB
Adverse Effects:
1. Fever, skin rash
2. Isoniazid induced hepatitis : jaundice, loss of apatite, nausea,
vomiting, pain stop isoniazid
3. Peripheral neuropathy due to pyridoxine deficiency
administer pyridoxine 10mg/day
4. Less common: CNS toxicity ( memory loss, seizures etc), GIT
discomfort, anemia
RIFAMPICIN
Active against slowly growing; both intracellular and extracellular;
bactericidal
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Pharmacokinetics
1. Absorption: well, absorbed from GIT
2. Distribution : all tissues, tubercular cavities, placenta, CSF
3. Metabolism: liver
4. Excretion: through liver into bile
Clinical Use
1. Atypical mycobacterium
2. Leprosy ( + dapsone)
Adverse Effects:
1. Hepatitis
2. Orange discoloration of urine, sweat, tears
3. Flu like symptoms: fever, chills, myalgia
4. Occasionally: rashes, GI disturbances, nephritis.
Drug-Drug interactions:
1. Potent enzyme inducer ( cytochrome p450)
2. Increases elimination of : anticonvulsants, anticoagulants,
OCPs, anti- HIV drugs replace with refabutin
Pyrazinamide
Pyrazinamidase
active
Mechanism of action
Arabinosyl transferase
Ethambutol inhibition
Polymerization of
arabinoglycan
Aminoglycoside
Against extracellular tubercular bacteria
Injectable
• This helps to ensure the right drugs are taken at the right
time for the full duration of treatment
• A Standardized recording and reporting is maintained by
health worker or medical professional. This helps to keep
track of each individual patient and to monitor overall
programme performance.