Anti-Asthamtics Flashcards
Asthma is a (reversible or irreversible ?) (acute or chronic?) (obstructive or restrictive ?) disease of the _____ caused by _______ to various stimuli, characterized by episodic broncho______ and ________ of the airways.
reversible
chronic
obstructive
airway; hyperresponsiveness
constriction; inflammation
Upper Respiratory Tract consists of :
–______
–______
Nose
Pharynx
Pharynx:
___pharynx
___pharynx
_____pharynx
Naso
Oro
Laryngo
Components of Lower Respiratory Tract
–_______
–_________
————-
–______
Larynx
Trachea
Bronchus
Lungs
The Lungs consists of the
_______ and _______
• •
Bronchioles
Alveoli
ANATOMY: Tracheal
Also called _______
A ______ tube
Extends from the _____ to ______
Length of ______
Conduct air in and out of the respiratory tree
Windpipe
Cartilaginous
C6 to T4/T5
12cm
HISTOLOGY: Trachea
Made up of four layers of tissue
____,______,______,________
MUCOSA
SUBMUCOSA
CARTILAGE
MUSCLE
ANATOMY : Bronchus
______________ tube
Connects from the _____ to _______
Conduct air in and out of the respiratory tree
Musculo-cartilaginous
Trachea to Lungs
ANATOMY Bronchus
Divided into three parts
______ BRONCHUS
_______ BRONCHUS
_________ BRONCHUS
MAIN
LOBAR
SEGMENTAL
Histology: Bronchus
Made up of four layers of tissue
_____
_____
________
________
MUCOSA
SUBMUCOSA
CARTILAGE
MUSCLE
ANATOMY: LUNGS
Includes
______,________
Helps in the exchange of Oxygen and CO2
RIGHT LUNGS
LEFT LUNGS
HISTOLOGY Lungs
Composed of
_________
__________
BRONCHIOLES
ALVeoli
HISTOLOGY Lungs
Bronchioles is made up of
_______
_________
__________
MUCOSA
SUBMUCOSA
MUSCLE
HISTOLOGY Lungs
Alveoli is made up of _________
EPITHELIUM
REGULATORS OF RESPIRATION
_______ REGULATION
_________ REGULATION
NEURAL
CHEMICAL
ASTHMA
A (reversible or irreversible?) (acute or chronic?) ( obstructive or restrictive?) disease of the ________ caused by ______ to various stimuli, characterized by episodic _______ and ________ of the airways.
reversible
chronic
obstructive
tracheobronchial tree
hyperreactivity
bronchospasm and inflammation
Asthma result from a complex interaction between
–________ factors
–__________ factors
Genetic
Environmental
ASTHMA Aetiology: Genetic factor
– Many _______ or ______ have been
identified and this then to lead to
______________
– This involves abnormal ____________________ to wide range of environmental stimuli/allergens.
asthma genes or gene complexes
AIRWAY HYPER-REACTIVITY
sensitivity of the airways
Asthma: PATHOPHYSIOLOGY
Recurrent exposure of the airway to this Allergens triggers a ______________ reaction:
TYPE 1 HYPERSENSITIVITY
Asthma: PATHOPHYSIOLOGY
TYPE 1 HYPERSENSITIVITY reaction:
Allergens bind to _________ on Mast cell in the Airway
_________ ————
Release of —————- including ______,_______
IgE antibodies
Mast cell degranulates
inflammatory mediators
Histamine; Leukotriene
PATHOPHYSIOLOGY of Asthma
Histamine, leukotriene
These mediators target the ______ and ________ of the airway
Causing ________ and _______
Smooth muscle and Mucosa of the Airway
BRONCHOCONSTRICTION
INFLAMMATION
Asthma: Pathophysiology
Bronchoconstriction
–__________ of airway ________
– Airway ________
– Reduced (inspiration or expiration?) of air
Contraction
smooth muscles
narrowing
expiration of air
Asthma: Pathophysiology
Inflammation
– Vaso_________ of bronchial vessels
–____________ from vascular to interstitial space
– Mucosal _______
– Increase ____________________
– Airway _______
– Reduced expiration of air
dilatation
Extravasation of fluid
edema; mucus secretion and plugging
narrowing
Asthma: CLINICAL FEATURES
_________
Chest ________
_________
Rapid ________
_________
Shortness of breath
Tightness
Wheezing
respiration; Cough
Asthma: CLASSIFICATION
Based on Severity
–_________ or _________
–_________ Asthma
Acute Asthma or Status Asthmaticus
Chronic
CLASSIFICATION
Based on Severity
– Chronic Asthma
__________ Asthma
_____________ Asthma
____________ Asthma
______________ Asthma
Mild Intermittent
Mild Persistent
Moderate Persistent
Severe Persistent
Asthma: DIAGNOSIS
___________
___________
Peak-Flow meter
Spirometry
Asthma: management
Non-Pharmacological
–______________________________________
Pharmacological
–_____________
Identify and reduce exposure to Triggers
Anti-Asthmatics
The drugs used in the management of Asthma includes:
– ________________ AGENTS
–_______________
ANTI-INFLAMMATORY
BRONCHODILATORS
Anti-Asthmatics
ANTI- INFLAMMATORY AGENTS
__________
_________
____________
_________
Corticosteroids
Leukotriene antagonist
Mast cell stabilizers
Anti-IgE monoclonal antibody
Anti-Asthmatics
BRONCHODILATOR S
•_________
•_________
•_________
Beta 2 agonist
Anti-muscarinic
Methyl-Xanthine
Examples of short acting BETA 2 AGONIST
Albuterol
Salbutamol
Terbutaline
Levalbuterol
Pirbuterol
Epinephrine
Metoproterenol
Examples of long acting BETA 2 AGONIST
Formoterol
Clenbuterol
Arformoterol
Bambuterol
Salmeterol
MECHANISM OF ACTION of beta 2 agonist
Binds and stimulates BETA 2 ADRENERGIC RECEPTORS in the airway
Stimulation of βeta 2 receptors causes the activation of ____ and _______
This eventually results in ___________
Gs
increase in cAMP
BRONCHODILATION
ADVERSE EFFECTS of beta 2 agonists
Skeletal muscle _____.
_____ness
__________
__________ over dose
tremors
Nervous
Tolerance
Tachycardia
MUSCARINIC ANTAGONIST
EXAMPLES??
Tiotropium
Ipratropium
MUSCARINIC ANTAGONIST
MECHANISM OF ACTION
Binds and blocks MUSCARINIC CHOLINERGIC RECEPTORS in the airways
Blockade of Muscarinic receptors prevents the activity and effect of _____________
This inhibits Broncho_______ and _________
Thus leading to ____________
endogenous Acetylcholine
constriction
mucus secretion
BRONCHODILATION
MUSCARINIC ANTAGONIST
__________ skin
__________
_____________
______thermia
______cardia
Flushed skin
Constipation
Xerostomia
Hyper
Tachy
METHYL-XANTHINES
EXAMPLES??
Theophylline
Aminophylline
METHYL-XANTHINES : MECHANISM OF ACTION
Binds and blocks ________ ENZYME in the airway
This causes ________ and eventual accumulation of ______
This eventually results in __________
PHOSPHODIESTERASE
reduced breakdown ; cAMP
BRONCHODILATION
ANTI-INFLAMMATORY
Corticosteroids
EXAMPLE
Inhalational
– ________
–__________
–_____________
Budesonide
Fluticasone
Beclomethasone
ANTI-INFLAMMATORY
Corticosteroids
EXAMPLE
Oral
–________
–___________
Prednisone
Methyl prednisolone
ANTI-INFLAMMATORY
Corticosteroids
EXAMPLE
Intravenous
–_________
–____________
Hydrocortisone
Dexamethasone
CORTICOSTEROIDS
MECHANISM OF ACTION Binds and (blocks or stimulates?) __________
This (inhibits or stimulates?) the production of ___________
Lack of __________ leads to _________ of inflammatory mediators like ______ and ________
Thus eventually inhibiting _______
Blocks; PHOSPHOLIPASE A2
Inhibits; Arachidonic acid
Arachidonic acid ; reduced production
PROSTAGLANDIN; LEUKOTRIENE
INFLAMMATION
CORTICOSTEROIDS
Adverse effect: Inhaled Corticosteroids
______
Oropharyngeal ______ / Oral _____
_______/ Voice _________
_________ symptoms
Cough
candidiasis; Thrush
Dysphonia; hoarseness
Withdrawal
CORTICOSTEROIDS
ADVERSE EFFECT: Systemic Corticosteroids
Longgggggg
Cataract
Ulcers
Striae
Hypertension
Immunosuppression
Necrosis of the Head of Femur
Growth retardation
Obesity
Infection
Diabetes Mellitus
Myopathy
Adrenal suppression
Psychosis
LEUKOTRIENE MODIFIERS
Can be
___________ or _________
LEUKOTRIENE ANTAGONIST
LIPOXYGENASE INHIBITOR
Leukotriene Antagonist
List 3
Zafirlukast
Montelukast
Pranlukast
Lipo-oxygenase inhibitor
EXAMPLES
Zileuton
MECHANISM OF ACTION : Leukotriene Antagonist
(Reversibly or Irreversibly?) Binds and blocks LEUKOTRIENE
RECEPTORS (_______ receptors)
Prevent the action of Leukotrienes at its receptor site
Thus preventing ________
Reversibly
CysLT1
INFLAMMATION
MECHANISM OF ACTION: Lipo-oxygenase Inhibitors
Binds and blocks __________
Prevent ____________ to _________
Thus preventing __________
5-LIPOXYGENASE
the conversion of Arachidonic acid to Leukotrienes
INFLAMMATION
MAST CELL STABILIZERS
EXAMPLES
_________ / ________
____________
Cromolyn sodium
Cromoglycate
Nedocromil
MAST CELL STABILIZERS: MECHANISM OF ACTION
Binds and ______ the MAST CELLS ______
Inhibits ________________
Thus prevents __________
stabilize; MEMBRANE
Mast cell degranulation
INFLAMMATION
MAST CELL STABILIZERS: ADVERSE EFFECT
______ taste
_______ sensation
_________ congestion
Bitter
Burning
Nasal
IGE MONOCLONAL ANTIBODY
EXAMPLES
Omalizumab
IGE MONOCLONAL ANTIBODY: mechanism of action
Binds and blocks _________ on _____ cells
Prevents the _____________________
Thus prevents ______________ and ________
IGE ANTIBODY; Mast
crosslinking of Allergens to IgE
Mast cell degranulation
INFLAMMATION
OBSTRUCTIVE PULMONARY DISEASE
Characterized by airway obstruction that is worse with ______.
expiration
Most common obstructive diseases are ______,________, and _______
asthma, chronic bronchitis and emphysema.
Many people have both _______ and ________ ( chronic obstructive pulmonary disease – COPD).
chronic bronchitis and emphysema
Obstructive pulmonary disease
Major symptom of obstructive pulmonary disease is ______ and the unifying sign is ______.
dyspnoea
Wheezing
Individuals with OPD have _____eased work of breathing, V/Q _________, and a _____eased forced expiratory volume.
incr
mismatching
decr
ASTHMA
Factor that sets it apart from COPD is its ___________.
reversibility
ASTHMA
Occurs at _____ ages
approximately half of all cases develop during _______, and another 1/3 develop before age ______.
all
childhood
40
ASTHMA
Morbidity and mortality still low
T/F
F
Morbidity and mortality still high despite increased no. and availability of antiasthma medications
ASTHMA
Vaso——— and increased capillary permeability.
Chemotactic factors attract ____,______,______ to the area - _________
Smooth muscle spasm in _____ due to ___ effect on autonomic neurons – ACh.
Vascular _______
_______ formation
dilation
neutrophils, eosinophils and
lymphocytes ; bronchial infiltration.
bronchioles; IgE
congestion; Oedema
ASTHMA
Production of (thin or thick?) , tenacious mucus.
Impaired ______ function.
Thickening of _____
_____eased bronchial responsiveness.
Thick
mucociliary
airway walls.
Incr
ASTHMA
Untreated, this can lead to airway damage that is irreversible.
T/F
T
SYMPTOMS OF ASTHMA
During remission individual is ______ and pulmonary function tests are _____.
Dyspnoea
Severe cough
Wheezing exhalation
Attacks usually of _____ duration, but may be severe and continue for _______
If bronchospasm is not reversed by usual measures, the individual is considered to have ________ or ___________ which can be life threatening.
asymptomatic; normal
1-2 h; days or weeks.
severe bronchospasm or status asthmaticus
Lung function for :
Intermittent asthma
Mild persistent
Moderate persistent
Severe persistent
FEV1 >80%; FEV1/FVC is normal
FEV1 >80%; FEV1/FVC is normal
FEV1 60-80%%; FEV1/FVC is reduced by 5%
FEV1 <60 %; FEV1/FVC is reduced greater than 5%
MANAGEMENT OF ASTHMA
_____________
Patient ___________
Acute attacks - ________ and ________
Avoid triggers
education
corticosteroids and inhaled beta-agonists.
MANAGEMENT OF ASTHMA
Chronic management based on severity of asthma - regular use of inhaled anti-inflammatory drugs – _______,___________, or ____________
______ bronchodilators
Immunotherapy - ————-, etc.
corticosteroids, chromolyn sodium or leukotriene inhibitors.
Inhaled
allergy shots
MANAGEMENT OF ASTHMA
Bronchoconstriction may be a normal means of restricting airflow and intake of irritants and allergens.
T/F
T
Long term use of antiasthmatics may actually increase exposure to these factors and cause more pronounced and chronic symptoms.
T/F
T
MANAGEMENT OF ASTHMA
____________ agents have better long term effects.
Anti-inflammatory
β2 AGONISTS
Examples:
List, and mention the exceptions
Albuterol, Bitolterol, Fenoterol,,, Procaterol, Formoterol, Salmeterol .
Metaproterenol
Isoetharine.
Ritodrine.
Salbutamol
Terbutaline
β2 AGONISTS
Use with caution in patients with ___ disease (reduced by ____ administration)
minimal side effects → (short, long, or intermediate ?) acting.
CV
inhalational
intermediate
β2 AGONISTS
PPAs:
______ of bronchial smooth muscle
________ of uterine SM
_______ of other ____ after _____ administration.
Relaxation
relaxation
activation; β2Rs
systemic
β2 AGONISTS
PTUs:
_______ and __________
acute ______ (____________acting drugs)
premature labour ( _______)
prophylaxis (______ acting agents).
Asthma & chronic obstructive pulmonary disease
bronchospasm; short & intermediate
Ritodrine
long
β2 AGONISTS
AEs:
______ stimulation, headache, anxiety, nausea, muscle _____, nervousness, palpitations etc.
Cardiac
tremors
β2 AGONISTS
Cautious use in _____ and _____ disease.
Selective beta 2 agonists by ———- are drugs of choice.
____________ . in acute bronchoconstriction.
hypertension and cardiac
inhalation
Epinephrine subcutaneous
β2 AGONISTS
Rank order of potency:
β →______ >——. ≥ ____
α →_____ . ≥ ____ ≥ ________
.
Isoprenaline; Adr; NA
Adr; NA
Isoprenaline
β2 AGONISTS
Non-selective agonists:
Adr. (_________________)
NA (______________)
Isoprenaline (_________)
α1, α2, β1 , β2 , β3
α1, α2, β1»_space; β2
β1 + β2
Treatment of first choice to relieve acute asthma is ????
Use of beta 2 agonist short acting bronchodilator
Formoterol and Salmeterol are long acting beta 2 adrenergic agonists used only for __________.
prophylaxis
Salmeterol use in deteriorating asthma can be life- threatening.
T/F
T
Metaproterenol is (short, intermediate , or long?) acting useful in _____ induced asthma and treatment of _______
Intermediate
exercise
acute bronchospasm.
Indacaterol is ________-acting.
ultra-long
Terbutaline - selective beta 2 adrenergic agonist that is a ____-acting bronchodilator.
long
Terbutaline -
It loses selectivity when given __________.
subcutaneously
________ is Also used to decrease premature uterine contractions during pregnancy besides ritodrine
Terbutaline
MUSCARINIC ANTAGONISTS
________ administered via _______ for treatment of asthma and bronchitis.
Ipratropium
inhalation
MUSCARINIC ANTAGONISTS
Ipratropium/salbutamol is a formulation containing _______ and _________(______) used in the management of ___________
ipratropium bromide
salbutamol sulphate (albuterol sulphate)
COPD and asthma.
MUSCARINIC ANTAGONISTS
Ipratropium/salbutamol
Marketed as________ and _______
metered dose inhaler (MDI) and nebuliser preparations.
Ipratropium should be used with caution in ________ and ————-
BPH and narrow- angle glaucoma.
________ is another example.of a muscarinic antagonist besides ipratropoum
Tiotropium
MUSCARINIC ANTAGONISTS
________________________ is the main reason for the relative lack of unwanted systemic effects.
Direct delivery of antimuscarinic drugs to the lung
METHYLXANTHINES
Pharmacological actions include:
____ stimulation (including ———- stimulation)
diuresis
_________ of cardiac muscle
————- of smooth muscle especially ________ muscle.
CNS; respiratory
stimulation
relaxation; bronchial
METHYLXANTHINES
Theophylline attenuate reversible airflow ______, airway ——— and airway ______.
obstruction
hyperresponsiveness
inflammation
METHYLXANTHINES
Doses that facilitate high serum levels (toxic side effects may manifest), produce ____________ effects.
direct bronchodilatory
METHYLXANTHINES
Lower serum levels -
_________ effect but retains capacity as an _______________,______________,____________ drug.
weak bronchodilatory
immunomodulator, anti-inflammatory, and bronchoprotective
METHYLXANTHINES
Predominant role in asthma treatment is as a controller medication for _______,__________ disease.
chronic, persistent
METHYLXANTHINES
Administration - _____,______,_____,______ injection.
Oral, IV, inhalation and intramuscular
METHYLXANTHINES
Inhalation has (poor or well?) bioavailability and is (well or not well?) tolerated.
Intramuscular injection is (painful or painless?) and (recommended or not recommended?) .
Poor
Not well
Painful ; not recommended
METHYLXANTHINES
AEs: Have (wide or narrow?) therapeutic range, hence (low or high?) incidence of AEs.
Narrow
High
METHYLXANTHINES
Mild AEs: Precautions necessary in patients with _______ disease,_______ , ______ impairment, _______thyroidism, acute ______, peptic ulcer disease, seizure disorder and _________.
cardiovascular
cystic fibrosis
hepatic
Hypo or hyper
Gastritis
pregnancy
CORTICOSTEROIDS
Examples include
Mention 7
beclometasone dipropionate, budesonide, fluticasone propionate, hydrocortisone, prednisolone etc.
CORTICOSTEROIDS
Inhalation: mention 5
Systemic: mention 3
beclomethasone, budesonide, flunisolide, fluticasone, triamcinolone.
Prednisone, methylprednisolone, and hydrocortisone.
Most effective class of drug in the treatment of chronic asthma is ?????
CORTICOSTEROIDS
CORTICOSTEROIDS
.
No ______ effect, hence of no benefit in the _____ stages of an acute attack of asthma.
bronchodilator
initial
Corticosteroid are relatively ineffective in COPD.
T/F
T
CORTICOSTEROIDS
Inhibit transcription of genes coding for the ______ involved in _______.
Activate _________ genes and genes linked to _______ effects (high does).
cytokines; inflammation
anti-inflammatory ; glucocorticoid unwanted
CORTICOSTEROIDS
Reduce airway responsiveness to several bronchoconstrictor mediators
T/F
T
CORTICOSTEROIDS
Inhibit _____________ reactions to allergen with chronic therapy.
both the early and late
ANTI-INFLAMMATORY EFFECT OF CORTICOSTEROIDS
Reduced airway ______ and leucocyte recruitment by induction of ______ in vascular endothelial cells.
oedema
tight junctions
ANTI-INFLAMMATORY EFFECT OF CORTICOSTEROIDS
Reduced inflammatory cell activation (including macrophages, T-lymphocytes, eosinophils and airway epithelial cells) with reduced inflammatory cytokine, chemokine, adhesion molecule and inflammatory enzyme expression.
T/F
T
ANTI-INFLAMMATORY EFFECT OF CORTICOSTEROIDS
Reduced inflammatory cell recruitment to the airways (eosinophils, T-lymphocytes, mast cells etc.) through reduction in _______ and _______, and reduced cell survival (enhanced ________)
chemotactic mediators
adhesion molecules
apoptosis)
ANTI-INFLAMMATORY EFFECT OF CORTICOSTEROIDS
Decreased local generation of inflammatory prostaglandins and leukotrienes due to inhibition of ___________ by _______ ( ________ ) which reduces mucosal oedema.
phospholipase A2 by annexin 1
lipocortin
ANTI-INFLAMMATORY EFFECT OF CORTICOSTEROIDS
Suppression of the excess epithelial cell shedding and _______________ found in the bronchial epithelium in asthma etc.
goblet cell hyperplasia
CORTICOSTEROIDS
Pharmacokinetics:Given by ______ of an aerosol or dry powder in order to minimise systemic unwanted effects.
Can be used ____ or ____ . in severe asthma.
inhalation
IV or p.o
CORTICOSTEROIDS
Beclometasone dipropionate has (low or high?) rate of absorption across mucosal membranes but is (slowly or rapidly?) inactivated once it reaches the -_______ circulation.
IV or p.o
Low
Slowly
Systemic
CORTICOSTEROIDS
_______ budesonide (inactivated by _____________ in the liver following _____ absorption) or fluticasone (very _______ absorbed from the gut) may be preferred if (low or high?) doses of inhaled drug are needed or for the treatment of children in whom the systemic effects can be more problematic.
Inhaled
extensive first-pass metabolism; oral
poorly; high
CORTICOSTEROIDS
Unwanted effects: Inhaled corticosteroids
–________ ( ________ ), oral _______, unwanted effects with prolonged use - ____ suppression, osteoporosis and reduced ______ in children and increased risk of ______ in older people with COPD.
dysphonia; hoarseness
candidiasis
adrenal; growth velocity ; pneumonia
Ketotifen is a ????
Mast cell stabilizer
