Pharmacology: Bronchodilators & Anti-inflammatory Medications Flashcards by Fatima Alz Dashti

Mention from ur drug list:

β2 agonists

there’s 2

Salbutamol (short acting)
Salmeterol (long acting)

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Mention from ur drug list:

Xanthine Derivative

there’s 1

Theophylline (aminophylline)

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Mention from ur drug list:

Muscarinic Antagonist

there’s 1

Ipratropium

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Mention from ur drug list:

Cyst-Leukotriene Receptor Antagonist

there’s 1

Zafirlukast

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Mention from ur drug list:

Leukotriene Synthesis Inhibitor

there’s 1

Zileuton

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Mention from ur drug list:

Corticosteroids

for ASTHMA there’s 3

Hydrocortisone (I.V, Systemic)
Prednisolone (oral, systemic)
Budenoside

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Mention from ur drug list:

Mast Cell Stabilizer

there’s 1

Cromolyn (disodium cromoglycate)

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What is the MOA of β2 agonists on bronchial smooth muscle?

a) Inhibition of adenylyl cyclase
b) Activation of adenylyl cyclase, leading to increased cAMP levels
c) Inhibition of cAMP-dependent protein kinase
d) Activation of myosin LC kinase

b) Activation of adenylyl cyclase, leading to increased cAMP levels

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Which enzyme is phosphorylated by cAMP-dependent protein kinase as a result of β2 agonist activation?

a) Adenylyl cyclase
b) Myosin light chain kinase
c) Protein phosphatase
d) G3P Phosphatase

b) Myosin light chain kinase

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Why is it important for β2 agonists to be highly selective to β2-adrenoceptors?

a) To increase heart rate
b) To avoid increasing heart rate by activating β1 receptors
c) To induce vasoconstriction
d) To enhance bronchoconstriction

b) To avoid increasing heart rate by activating β1 receptors

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Which β2 agonist is classified as short-acting and is also known as Ventolin?

a) Salbutamol
b) Salmeterol
c) Formoterol
d) Terbutaline

a) Salbutamol

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At high doses, what effect can β2-selective agonists have on β1-adrenoceptors?

a) Decrease heart rate
b) Decrease bronchodilation
c) Decrease blood pressure
d) Increase heart rate

d) Increase heart rate

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What phase of asthma does β2 agonists primarily target?

a) Phase II
b) Immediate phase (bronchoconstriction)
c) Late-phase
d) Chronic phase

b) Immediate phase (bronchoconstriction)

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What is the most common clinical use of β2 agonists?

a) Treatment of allergic rhinitis
b) Anti-asthma drugs
c) Treatment of peptic ulcers
d) Management of hypertension

b) Anti-asthma drugs

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Which type of β2 agonists is the drug of choice for acute asthma attacks?

a) Short-acting
b) Long-acting
c) Intermediate-acting
d) Ultra-long-acting

a) Short-acting

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How are β2 agonists typically administered?

a) Intravenously
b) Inhalation or orally
c) Topically
d) Subcutaneously

b) Inhalation or orally

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What is the duration of action for short-acting β2 agonists?

a) 24 hours
b) 3-5 hours
c) 8-12 hours
d) 30 minutes

b) 3-5 hours

(maximum effect occurs within 30 mins)

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When are long-acting β2 agonists given in the management of asthma?

a) As a first-line therapy
b) Only during acute attacks
c) Regularly twice daily as adjunctive therapy in patients whose asthma is inadequately controlled by glucocorticoids
d) Only in pediatric patients

c) Regularly twice daily as adjunctive therapy in patients whose asthma is inadequately controlled by glucocorticoids

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What is the duration of action for long-acting β2 agonists?

a) 3-5 hours
b) 8-12 hours
c) 24 hours
d) 8-12 hours

b) 8-12 hours

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Why are β-blockers contraindicated in asthmatics, including stable asthmatics?

a) They increase the bronchodilatory effect of adrenaline
b) They may precipitate asthma by blocking the bronchodilatory effect of circulating adrenaline
c) They enhance the anti-inflammatory effect of glucocorticoids
d) They reduce the risk of allergic reactions

b) They may precipitate asthma by blocking the bronchodilatory effect of circulating adrenaline

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Control of Airway Caliber:

Which of the following molecules is involved in bronchodilation?

a) Histamine
b) Leukotrienes
c) Acetylcholine
d) Adrenaline

d) Adrenaline

Bronchodilation (A PEN):
1. Adrenaline
2. PGE2
3. EpDRF
4. NO

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Which molecule is primarily responsible for bronchoconstriction?

a) Histamine
b) Adrenaline
c) Prostaglandin E2 (PGE2)
d) Nitric oxide (NO)

a) Histamine

Bronchoconstriction:
- Histamine
- Leukotrienes
- Acetylcholine
- Adenosine
- PGD2, etc

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What is the primary mechanism of action of adrenaline in controlling airway caliber?

a) Induction of leukotriene synthesis
b) Stimulation of acetylcholine release
c) Bronchodilation
d) Inhibition of nitric oxide production

c) Bronchodilation

Bronchodilation (A PEN):
1. Adrenaline
2. PGE2
3. EpDRF
4. NO

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Which of the following molecules is NOT involved in bronchoconstriction?
a) Leukotrienes
b) Acetylcholine
c) Adrenaline
d) Adenosine

c) Adrenaline

Bronchoconstriction:
- Histamine
- Leukotrienes
- Acetylcholine
- Adenosine
- PGD2, etc

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Which **xanthine derivative** is the most widely used drug in the treatment of **asthma**? a) Albuterol b) Theophylline c) Montelukast d) Beclomethasone

b) Theophylline ## Footnote *Theophylline (aminophylline)*

What is the **primary action of xanthine derivatives** in the treatment of respiratory conditions? a) Inhibition of leukotriene synthesis b) Bronchodilation c) Mast cell stabilization d) Suppression of cough reflex

b) Bronchodilation

How do xanthine derivatives exert their bronchodilator effect? a) Activation of histamine receptors b) Inhibition of acetylcholine release c) Inhibition of phosphodiesterases d) Activation of leukotriene receptors

c) Inhibition of phosphodiesterases

What **additional effect** do xanthine derivatives have **besides** bronchodilation? a) Hypotensive effect b) Sedative effect c) Anti-inflammatory effect d) Antihistamine effect

c) Anti-inflammatory effect

Which receptor do xanthine derivatives block to induce bronchodilation? a) β1-adrenoceptors b) Adenosine receptors c) Histamine receptors d) Muscarinic receptors

b) Adenosine receptors

Besides bronchodilation and anti-inflammatory effects, what other actions do xanthine derivatives have? a) Vasodilation b) Mild diuretic effect c) Stimulation of the heart and CNS d) All of the above

d) All of the above

Which beverage contains a xanthine derivative that is commonly consumed? a) Tea b) Orange juice c) Coffee d) Milk

c) Coffee

What is the primary mechanism of action by which xanthine derivatives exert their anti-inflammatory effect? a) Inhibition of leukotriene synthesis b) Activation of histone deacetylase to prevent transcription of inflammatory genes c) Inhibition of phosphodiesterases

b) Activation of histone deacetylase to prevent transcription of inflammatory genes ## Footnote *"exert their anti-inflammatory effect"*

Which of the following is **NOT** a common **side effect** of xanthine derivatives? a) Tremors b) Palpitations c) Diuresis d) Hypertension

d) Hypertension

What are the primary effects of **theophylline** in the treatment of asthma? a) Mast cell stabilization b) Bronchodilation and anti-inflammatory effects c) Leukotriene synthesis inhibition d) Mucus production inhibition

b) Bronchodilation and anti-inflammatory effects ## Footnote *xanthine derivative*

How is theophylline typically administered? a) Intramuscularly b) Orally or by slow intravenous infusion c) Inhalation d) Subcutaneously

b) Orally or by slow intravenous infusion ## Footnote *xanthine derivative*

Why is caution advised when using theophylline in patients with liver disease?

Theophylline is metabolized by the liver ## Footnote *xanthine derivative*

In patients with **liver diseas**e, which **xanthine derivative** is preferred due to its **different metabolism**? a) Theophylline b) Enprofylline c) Aminophylline d) Caffeine

b) Enprofylline

# 1. Why is caution advised when using theophylline in patients with heart disease? a) Theophylline causes vasodilation b) Theophylline inhibits heart rate c) Theophylline stimulates the heart d) Theophylline increases blood pressure

c) Theophylline stimulates the heart ## Footnote *xanthine derivative*

In which severity of asthma is **theophylline** commonly used? a) Mild intermittent b) Moderate to severe c) Severe persistent d) All severity levels

b) Moderate to severe ## Footnote *xanthine derivative*

Why is it important to **monitor blood levels of theophylline** during treatment? a) To adjust the dosage based on the patient's weight b) Due to its narrow therapeutic range c) To ensure adequate hydration d) To prevent allergic reactions

b) Due to its narrow therapeutic range ## Footnote *xanthine derivative*

Which of the following **adverse effects** is commonly associated with the therapeutic use of theophylline? a) Constipation b) Nausea and vomiting c) Hypotension d) Excessive salivation

b) Nausea and vomiting ## Footnote *xanthine derivative*

What **CNS**-related **adverse effect** is often observed with **theophylline** use? a) Sedation b) Memory loss c) Tremor d) Decreased alertness

c) Tremor ## Footnote *xanthine derivative*

Which adverse effect of theophylline is more likely to occur with rapid intravenous injection? a) Nausea b) Tremor c) Cardiac arrest d) Anorexia

c) Cardiac arrest

What type of drug interaction is commonly observed with **theophylline** due to its metabolism? a) Metabolism by CYP450 b) Inhibition of acetylcholinesterase c) Stimulation of histamine receptors d) Activation of adrenergic receptors

a) Metabolism by CYP450 | *xanthine derivative* ## Footnote *that's why it's contraindicated in p/x w/ liver disease*

How does enprofylline differ from theophylline in terms of side effects? a) Enprofylline causes more CNS stimulation b) Enprofylline has fewer CNS-related side effects c) Enprofylline causes more gastrointestinal disturbances d) Enprofylline has a higher risk of cardiac arrest

b) Enprofylline has fewer CNS-related side effects | *xanthine derivative*

What is the primary MOA of **ipratropium bromide** in the treatment of respiratory conditions? a) Stimulation of muscarinic receptors b) Blockade of muscarinic receptors on bronchial smooth muscle c) Inhibition of histamine release d) Activation of adrenergic receptors

b) Blockade of muscarinic receptors on bronchial smooth muscle | *muscarinic antagonist*

In addition to bronchodilation, what other effect does ipratropium bromide have? a) Increased mucus secretion b) Reduction of mucous secretion c) Stimulation of cough reflex d) Constriction of bronchial smooth muscle

b) Reduction of mucous secretion | *muscarinic antagonist*

In which phase of asthma is ipratropium bromide more effective? a) Immediate phase b) Late-phase c) Chronic phase d) Recovery phase

a) Immediate phase | *muscarinic antagonist*

In what form is ipratropium bromide given to patients? a) Tablet b) Liquid suspension c) Aerosol d) Injection

c) Aerosol | *muscarinic antagonist*

Why is **ipratropium bromide** considered safe and well-tolerated? a) It has systemic effects b) It causes significant sedation c) It is given by inhalation, resulting in no systemic absorption d) It has a long duration of action

c) It is given by inhalation, resulting in no systemic absorption | *muscarinic antagonist*

What is the primary effect of leukotrienes in asthma? a) Bronchoconstriction & inflammation b) Bronchodilation & anti-inflammation c) Mucus secretion inhibition d) Smooth muscle relaxation

a) Bronchoconstriction & inflammation

How are **leukotrienes synthesized** in the body? a) From histamine b) From acetylcholine c) From arachidonic acid via the 5-LOX pathway d) From adrenaline

c) From arachidonic acid via the 5-LOX pathway

Why is aspirin contraindicated in patients with aspirin-sensitive asthma? a) Aspirin induces bronchodilation b) Aspirin inhibits leukotriene synthesis c) Aspirin increases leukotriene production d) Aspirin blocks leukotriene receptors

c) Aspirin increases leukotriene production

What are the two types of drugs used to treat asthma by targeting leukotrienes? a) Antihistamines and beta-agonists b) Cysteinyl leukotriene receptor antagonists and leukotriene synthesis inhibitors c) Corticosteroids and mast cell stabilizers d) Cysteinyl leukotriene receptor agonist and leukotriene synthesis inducers

b) Cysteinyl leukotriene receptor **antagonists** and leukotriene **synthesis inhibitors** ## Footnote *we want to reduce the release of leukotrienes; they're pro inflammatory*

What is the primary mechanism of action of Zafirlukast in treating asthma? a) Inducing bronchodilation b) Blocking cyst-LT receptors c) Inhibiting leukotriene synthesis d) Stimulating mast cell degranulation

b) Blocking Cyst-LT receptors | *Cysteinyl leukotriene receptor antagonist*

Which of the following leukotrienes do **Cyst-LT receptor antagonists** commonly **block**? a) LTA4 b) LTB4 c) LTC4 d) LTD4 e) LTE4 f) LTF4 | there's more than 1

c) LTC4 d) LTD4 e) LTE4 | *Drug list E.g. Zafirlukast* ## Footnote *remember:* LT synthesis inhibitor: **B** LT receptor antagonist: **C, D, E**

How does the *bronchodilating* effect of **cyst-LT receptor antagonists** *compare* to **salbutamol**? a) It is more potent than salbutamol b) It is less potent than salbutamol c) It is equal to salbutamol d) It is unrelated to salbutamol

b) It is less potent than salbutamol ## Footnote Zafirlukast (cyst-LT receptor antagonist) Salbutamol (B2 Agonist)

What is the primary MOA of leukotriene synthesis inhibitors? a) Blocking leukotriene receptors b) Inducing leukotriene synthesis c) Inhibiting enzymes 5-LO or FLAP in LT synthesis d) Stimulating mast cell degranulation

c) Inhibiting enzymes 5-LO or FLAP in LT synthesis | *E.g. Zileutin*

Which leukotrienes are affected by leukotriene synthesis inhibitors? a) LTC4 and LTD4 b) LTD4 and LTE4 c) LTC4 and LTB4 d) Cyst-LT and LTB4

d) Cyst-LT and LTB4 | *E.g. Zileutin* ## Footnote *remember:* LT synthesis inhibitor: **B** LT receptor antagonist: **C, D, E**

Which drug blocks cyst-LT receptor? a) Montelukast b) Zafirlukast c) Zileutin d) Ipratropium bromide

b) Zafirlukast | *Cysteinyl leukotriene receptor antagonist*

What is the primary **MOA** of zileutin in treating asthma? a) Inducing bronchodilation b) Blocking cyst-LT receptors c) Inhibiting enzymes 5-LO or FLAP in LT synthesis d) Stimulating mast cell degranulation

c) Inhibiting enzymes 5-LO or FLAP in LT synthesis | *leukotriene synthesis inhibitor*

Which drug blocks cyst-LT receptors and is **less effective than salbutamol** in bronchodilation? a) Zafirlukast b) Zileutin c) Montelukast d) Ipratropium bromide

a) Zafirlukast | *Cysteinyl leukotriene receptor antagonist*

Which drug has **both** bronchodilating and anti-inflammatory effects? a) Montelukast b) Zafirlukast c) Zileutin d) Ipratropium bromide

c) Zileutin | *leukotriene synthesis inhibitor*

# TRUE OR FALSE Asthma comes in dual phases

True 1. **Bronchoconstriction** (Early/immediate phase) 2. **Inflammation** (Late phase) ## Footnote so we need drugs that target each.

Which of the following is a characteristic of corticosteroids in asthma treatment? a) They induce bronchodilation b) They have powerful anti-inflammatory and immunosuppressive actions c) They are used as first-line therapy in chronic asthma d) Their effects are immediate upon administration

b) They have powerful anti-inflammatory and immunosuppressive actions | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote corticosteroids have no effect on bronchodilation

**How long** does it typically take for the effects of **corticosteroids** to start in asthma treatment? a) 30 minutes b) 6 hours c) 24 hours d) 48 hours

b) 6 hours | *Budesonide, Prednisolone, Hydrocortisone*

Which of the following is **NOT** a corticosteroid commonly used in asthma treatment? a) Budesonide b) Prednisolone c) Salbutamol d) Hydrocortisone

c) Salbutamol | *this is a B2 Agonist*

What is the role of **corticosteroids** in the management of chronic asthma? a) They are the first-line therapy b) They are drugs of last resort c) They induce bronchodilation d) They stimulate mucus production

b) They are drugs of last resort | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote *no effect on bronchodilation therefore cannot be used as 1st line, cross out a & c*

What is the primary **MOA** of corticosteroids in asthma management? a) Inhibit the synthesis and/or release of inflammatory mediators b) Induce bronchodilation c) Stimulate mucus production d) Enhance histamine release

a) Inhibit the synthesis and/or release of inflammatory mediators | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote *remember that they're used as anti-inflammatory meds for asthma t/x*

What effect do **corticosteroids** have on the ability of inflammatory cells to respond to chemotactic and other stimuli? a) They block the ability b) They enhance the ability c) They have no effect on the ability d) They reduce the ability

a) They block the ability | *Budesonide, Prednisolone, Hydrocortisone*

Glucocorticoids in asthma primarily inhibit the synthesis of which pro-inflammatory agents? a) Leukotrienes b) Histamine c) Cytokines (IL-1, TNF-alpha, IL-5, IL-4, GM-CSF) d) Prostaglandins

c) Cytokines (IL-1, TNF-alpha, IL-5, IL-4, GM-CSF) | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote **Inhibition** of pro-inflammatory agents: - Cytokines (IL-1, TNF-alpha, IL-5,IL-4, GM-CSF) - Adhesion Molecules (ICAM-1, VCAM-1) - Enzymes (COX2, cPLA2, iNOS). **Induction** of anti-inflammatory agents: - Annexins (lipocortins) which inhibit PLA2

What effect do glucocorticoids have on adhesion molecules in asthma? a) They increase their expression b) They inhibit their expression (e.g., ICAM-1, VCAM-1) c) They have no effect on their expression d) They enhance their function

b) They inhibit their expression (e.g., ICAM-1, VCAM-1) | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote **Inhibition** of pro-inflammatory agents: - Cytokines (IL-1, TNF-alpha, IL-5,IL-4, GM-CSF) - Adhesion Molecules (ICAM-1, VCAM-1) - Enzymes (COX2, cPLA2, iNOS). **Induction** of anti-inflammatory agents: - Annexins (lipocortins) which inhibit PLA2

Which enzyme involved in the inflammatory process is inhibited by glucocorticoids in asthma? a) Cyclooxygenase-1 (COX-1) b) Cyclooxygenase-2 (COX-2) c) Lipoxygenase d) Phospholipase C

b) Cyclooxygenase-2 (COX-2) | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote **Inhibition** of pro-inflammatory agents: - Cytokines (IL-1, TNF-alpha, IL-5,IL-4, GM-CSF) - Adhesion Molecules (ICAM-1, VCAM-1) - Enzymes (COX2, cPLA2, iNOS). **Induction** of anti-inflammatory agents: - Annexins (lipocortins) which inhibit PLA2

Glucocorticoids induce the synthesis of which anti-inflammatory agents in asthma? a) Histamine b) Annexins (lipocortins) which inhibit PLA2 c) Leukotrienes d) Prostaglandins

b) Annexins (lipocortins) which inhibit PLA2 | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote **Inhibition** of pro-inflammatory agents: - Cytokines (IL-1, TNF-alpha, IL-5,IL-4, GM-CSF) - Adhesion Molecules (ICAM-1, VCAM-1) - Enzymes (COX2, cPLA2, iNOS). **Induction** of anti-inflammatory agents: - Annexins (lipocortins) which inhibit PLA2

What is the primary MOA of annexins in asthma management? a) Activation of inflammatory cells b) Inhibition of phospholipase A2 (PLA2) c) Stimulation of mucus production d) Enhancement of leukotriene synthesis

b) Inhibition of phospholipase A2 (PLA2) | *Corticosteroids: Budesonide, Prednisolone, Hydrocortisone* ## Footnote **Inhibition** of pro-inflammatory agents: - Cytokines (IL-1, TNF-alpha, IL-5,IL-4, GM-CSF) - Adhesion Molecules (ICAM-1, VCAM-1) - Enzymes (COX2, cPLA2, iNOS). **Induction** of anti-inflammatory agents: - Annexins (lipocortins) which inhibit PLA2

What is the preferred route of administration for steroids in asthma management? a) Intramuscular injection b) Inhalation c) Oral tablets d) Intravenous infusion

b) Inhalation | *Budesonide, Prednisolone, Hydrocortisone*

Steroids are often combined with which other class of medications in asthma management? a) Antihistamines b) Antibiotics c) Bronchodilators d) Leukotriene receptor antagonists

c) Bronchodilators | *Budesonide, Prednisolone, Hydrocortisone*

In what scenario are steroids given intravenously in asthma management? a) For long-term control b) As a first-line therapy c) In acute severe asthma d) In mild intermittent asthma

c) In acute severe asthma | *Budesonide, Prednisolone, Hydrocortisone*

Why is caution advised when using steroids in children with asthma? a) Due to their inability to reach therapeutic levels b) Due to the risk of adrenal suppression leading to growth retardation c) Due to increased susceptibility to bronchoconstriction d) Due to their potential to induce bronchodilation

b) Due to the risk of adrenal suppression leading to growth retardation | *Budesonide, Prednisolone, Hydrocortisone*

Which adverse effect is commonly associated with aerosolized steroid therapy in asthma management? a) Oropharyngeal candidiasis b) Dysphagia c) Laryngeal edema d) Pneumothorax

a) Oropharyngeal candidiasis | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote *Adverse Effects of Steroids by **Aerosol**: – Oropharyngeal candidiasis. – Dysphonia.*

What is a potential consequence of rapid withdrawal of systemic steroids in asthma management? a) Hypertension b) Adrenal insufficiency c) Hyperthyroidism d) Renal failure

b) Adrenal insufficiency | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote Adverse Effects of Steroids * **Systemic**: – Adrenal insufficiency (if withdrawn rapidly). – Osteoporosis. – Lowered resistance to infection. – Cushing’s syndrome. – Hyperglycemia.

Chronic use of systemic steroids in asthma management may lead to which of the following conditions? a) Hypoglycemia b) Osteoporosis c) Hyperthyroidism d) Peripheral neuropathy

b) Osteoporosis | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote Adverse Effects of Steroids * **Systemic**: – Adrenal insufficiency (if withdrawn rapidly). – Osteoporosis. – Lowered resistance to infection. – Cushing’s syndrome. – Hyperglycemia.

What effect does long-term systemic steroid therapy have on the body's resistance to infection? a) It enhances resistance b) It has no effect c) It lowers resistance to infection d) It leads to immune hyperactivity

c) It lowers resistance to infection | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote Adverse Effects of Steroids * **Systemic**: – Adrenal insufficiency (if withdrawn rapidly). – Osteoporosis. – Lowered resistance to infection. – Cushing’s syndrome. – Hyperglycemia.

Excessive and prolonged use of systemic steroids in asthma management may result in the development of which syndrome? a) Addison's disease b) Cushing's syndrome c) Graves' disease d) Myasthenia gravis

b) Cushing's syndrome | *Budesonide, Prednisolone, Hydrocortisone* ## Footnote Adverse Effects of Steroids * **Systemic**: – Adrenal insufficiency (if withdrawn rapidly). – Osteoporosis. – Lowered resistance to infection. – Cushing’s syndrome. – Hyperglycemia.

In asthma management, immunosuppressors are typically used: a) As first-line drugs b) At low doses for cases of steroid-resistant asthma c) As bronchodilators d) As adjuncts to antihistamines

b) At low doses for cases of steroid-resistant asthma | Not first-line drugs for treating asthma

Disodium cromoglycate (cromolyn) is primarily used in asthma management for: a) Bronchodilation b) Prophylaxis to prevent the development of asthma c) Immediate relief of asthma symptoms d) Long-term control of asthma symptoms

b) Prophylaxis to prevent the development of asthma | *weak & isn't used 1st line*

Disodium cromoglycate (cromolyn) is effective in reducing which responses in asthma? a) Bronchodilation b) Mucus production c) Immediate and late-phase asthmatic responses d) Coughing

c) Immediate and late-phase asthmatic responses

What is the primary **MOA** of disodium cromoglycate (cromolyn) in asthma management? a) Inhibition of leukotriene synthesis b) Stimulation of beta-adrenergic receptors c) Reduction of bronchial hyper-reactivity

c) Reduction of bronchial hyper-reactivity

Why is disodium cromoglycate (cromolyn) hardly used for all forms of asthma? a) Due to its bronchodilatory effects b) Due to its long duration of action c) Due to its weak effects and short duration of action d) Due to its adverse effects on the cardiovascular system

c) Due to its weak effects and short duration of action | *very short DOA + no bronchodilatory effect*

Disodium cromoglycate (cromolyn) is primarily administered via which route due to poor oral absorption? a) Intramuscular injection b) Inhalation c) Intravenous infusion d) Subcutaneous injection

b) Inhalation

Which Asthmatic drug works by **stabilizing mast cells?** a) Zileutan b) Hydrocortisone c) Salbutamol d) Cromolyn e) Theophylline

d) Cromolyn | *key word= stabilizing mast cells*

Which of the following statements about the **safety profile** of disodium cromoglycate (**cromolyn**) is **true**? a) It has numerous side effects, including gastrointestinal disturbances and cardiovascular effects b) It is associated with significant central nervous system effects, such as sedation and dizziness c) It is a very safe drug with minimal side effects, except for cough due to particle irritation d) It is contraindicated in children and pregnant women due to teratogenic effects

c) It is a very safe drug with minimal side effects, except for cough due to particle irritation

Which of the following is considered an important adjunctive therapy in the management of asthma? a) Antibiotics b) Antifungal medications c) Anticoagulants d) Oxygen

d) Oxygen | *so imp & obvious*

You get handed a case of Status Ashmaticus in the ER, how will you proceed to treat the P/X? ## Footnote *Status Ashmaticus: a medical emergency, an extreme form of asthma exacerbation characterized by hypoxemia, hypercarbia, and secondary respiratory failure*

I'll treat them with... 1. Oxygen 2. Inhalation β2 agonist (salbutamol) 3. I.V. steroid (hydrocortisone) 4. Followed by a course of oral steroid (prednisolone)

Pharmacology: Bronchodilators & Anti-inflammatory Medications Flashcards

(94 cards)