Anti-Asthamtics Flashcards by Iseoluwa Ojo

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

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Upper Respiratory Tract consists of :

–______
–______

Nose

Pharynx

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Pharynx:

___pharynx
___pharynx
_____pharynx

Naso
Oro
Laryngo

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Components of Lower Respiratory Tract

–_______
–_________
————-
–______

Larynx

Trachea

Bronchus

Lungs

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The Lungs consists of the

_______ and _______
• •

Bronchioles

Alveoli

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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

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HISTOLOGY: Trachea

Made up of four layers of tissue

____,______,______,________

MUCOSA

SUBMUCOSA

CARTILAGE

MUSCLE

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ANATOMY : Bronchus

______________ tube

Connects from the _____ to _______

Conduct air in and out of the respiratory tree

Musculo-cartilaginous

Trachea to Lungs

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ANATOMY Bronchus

Divided into three parts

______ BRONCHUS
_______ BRONCHUS
_________ BRONCHUS

MAIN

LOBAR

SEGMENTAL

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Histology: Bronchus

Made up of four layers of tissue

_____
_____
________
________

MUCOSA

SUBMUCOSA

CARTILAGE

MUSCLE

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ANATOMY: LUNGS

Includes
______,________

Helps in the exchange of Oxygen and CO2

RIGHT LUNGS
LEFT LUNGS

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HISTOLOGY Lungs

Composed of

_________
__________

BRONCHIOLES

ALVeoli

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HISTOLOGY Lungs

Bronchioles is made up of

_______
_________
__________

MUCOSA
SUBMUCOSA
MUSCLE

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HISTOLOGY Lungs

Alveoli is made up of _________

EPITHELIUM

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REGULATORS OF RESPIRATION

_______ REGULATION

_________ REGULATION

NEURAL

CHEMICAL

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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

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Asthma result from a complex interaction between
–________ factors
–__________ factors

Genetic

Environmental

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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

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Asthma: PATHOPHYSIOLOGY

Recurrent exposure of the airway to this Allergens triggers a ______________ reaction:

TYPE 1 HYPERSENSITIVITY

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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

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PATHOPHYSIOLOGY of Asthma

Histamine, leukotriene

These mediators target the ______ and ________ of the airway

Causing ________ and _______

Smooth muscle and Mucosa of the Airway

BRONCHOCONSTRICTION

INFLAMMATION

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Asthma: Pathophysiology

Bronchoconstriction

–__________ of airway ________
– Airway ________
– Reduced (inspiration or expiration?) of air

Contraction

smooth muscles

narrowing

expiration of air

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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

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Asthma: CLINICAL FEATURES

_________
Chest ________
_________
Rapid ________
_________

Shortness of breath

Tightness

Wheezing

respiration; Cough

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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

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

Long term use of antiasthmatics may actually increase exposure to these factors and cause more pronounced and chronic symptoms. T/F

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 >> 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

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

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

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

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