Pharmacology: Bronchodilators & Anti-inflammatory Medications Flashcards

1
Q

Mention from ur drug list:

β2 agonists

there’s 2

A

Salbutamol (short acting)
Salmeterol (long acting)

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2
Q

Mention from ur drug list:

Xanthine Derivative

there’s 1

A

Theophylline (aminophylline)

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3
Q

Mention from ur drug list:

Muscarinic Antagonist

there’s 1

A

Ipratropium

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4
Q

Mention from ur drug list:

Cyst-Leukotriene Receptor Antagonist

there’s 1

A

Zafirlukast

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5
Q

Mention from ur drug list:

Leukotriene Synthesis Inhibitor

there’s 1

A

Zileuton

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6
Q

Mention from ur drug list:

Corticosteroids

for ASTHMA there’s 3

A
  1. Hydrocortisone (I.V, Systemic)
  2. Prednisolone (oral, systemic)
  3. Budenoside
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7
Q

Mention from ur drug list:

Mast Cell Stabilizer

there’s 1

A

Cromolyn (disodium cromoglycate)

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8
Q

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

A

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

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9
Q

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

A

b) Myosin light chain kinase

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10
Q

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

A

b) To avoid increasing heart rate by activating β1 receptors

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11
Q

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

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

A

a) Salbutamol

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12
Q

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

A

d) Increase heart rate

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13
Q

What phase of asthma does β2 agonists primarily target?

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

A

b) Immediate phase (bronchoconstriction)

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14
Q

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

A

b) Anti-asthma drugs

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15
Q

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

a) Short-acting

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16
Q

How are β2 agonists typically administered?

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

A

b) Inhalation or orally

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17
Q

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

A

b) 3-5 hours

(maximum effect occurs within 30 mins)

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18
Q

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

A

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

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19
Q

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

A

b) 8-12 hours

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20
Q

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

A

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

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21
Q

Control of Airway Caliber:

Which of the following molecules is involved in bronchodilation?

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

A

d) Adrenaline

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

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22
Q

Which molecule is primarily responsible for bronchoconstriction?

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

A

a) Histamine

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

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23
Q

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

A

c) Bronchodilation

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

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24
Q

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

A

c) Adrenaline

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

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25
Q

Which xanthine derivative is the most widely used drug in the treatment of asthma?

a) Albuterol
b) Theophylline
c) Montelukast
d) Beclomethasone

A

b) Theophylline

Theophylline (aminophylline)

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26
Q

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

A

b) Bronchodilation

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27
Q

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

A

c) Inhibition of phosphodiesterases

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28
Q

What additional effect do xanthine derivatives have besides bronchodilation?

a) Hypotensive effect
b) Sedative effect
c) Anti-inflammatory effect
d) Antihistamine effect

A

c) Anti-inflammatory effect

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29
Q

Which receptor do xanthine derivatives block to induce bronchodilation?

a) β1-adrenoceptors
b) Adenosine receptors
c) Histamine receptors
d) Muscarinic receptors

A

b) Adenosine receptors

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30
Q

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

A

d) All of the above

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31
Q

Which beverage contains a xanthine derivative that is commonly consumed?

a) Tea
b) Orange juice
c) Coffee
d) Milk

A

c) Coffee

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32
Q

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

A

b) Activation of histone deacetylase to prevent transcription of inflammatory genes

“exert their anti-inflammatory effect”

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33
Q

Which of the following is NOT a common side effect of xanthine derivatives?

a) Tremors
b) Palpitations
c) Diuresis
d) Hypertension

A

d) Hypertension

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34
Q

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

A

b) Bronchodilation and anti-inflammatory effects

xanthine derivative

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35
Q

How is theophylline typically administered?

a) Intramuscularly
b) Orally or by slow intravenous infusion
c) Inhalation
d) Subcutaneously

A

b) Orally or by slow intravenous infusion

xanthine derivative

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36
Q

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

A

Theophylline is metabolized by the liver

xanthine derivative

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37
Q

In patients with liver disease, which xanthine derivative is preferred due to its different metabolism?

a) Theophylline
b) Enprofylline
c) Aminophylline
d) Caffeine

A

b) Enprofylline

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38
Q

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

A

c) Theophylline stimulates the heart

xanthine derivative

39
Q

In which severity of asthma is theophylline commonly used?

a) Mild intermittent
b) Moderate to severe
c) Severe persistent
d) All severity levels

A

b) Moderate to severe

xanthine derivative

40
Q

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

A

b) Due to its narrow therapeutic range

xanthine derivative

41
Q

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

A

b) Nausea and vomiting

xanthine derivative

42
Q

What CNS-related adverse effect is often observed with theophylline use?

a) Sedation
b) Memory loss
c) Tremor
d) Decreased alertness

A

c) Tremor

xanthine derivative

43
Q

Which adverse effect of theophylline is more likely to occur with rapid intravenous injection?

a) Nausea
b) Tremor
c) Cardiac arrest
d) Anorexia

A

c) Cardiac arrest

44
Q

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

a) Metabolism by CYP450

xanthine derivative

that’s why it’s contraindicated in p/x w/ liver disease

45
Q

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

A

b) Enprofylline has fewer CNS-related side effects

xanthine derivative

46
Q

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

A

b) Blockade of muscarinic receptors on bronchial smooth muscle

muscarinic antagonist

47
Q

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

A

b) Reduction of mucous secretion

muscarinic antagonist

48
Q

In which phase of asthma is ipratropium bromide more effective?

a) Immediate phase
b) Late-phase
c) Chronic phase
d) Recovery phase

A

a) Immediate phase

muscarinic antagonist

49
Q

In what form is ipratropium bromide given to patients?

a) Tablet
b) Liquid suspension
c) Aerosol
d) Injection

A

c) Aerosol

muscarinic antagonist

50
Q

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

A

c) It is given by inhalation, resulting in no systemic absorption

muscarinic antagonist

51
Q

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

a) Bronchoconstriction & inflammation

52
Q

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

A

c) From arachidonic acid via the 5-LOX pathway

53
Q

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

A

c) Aspirin increases leukotriene production

54
Q

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

A

b) Cysteinyl leukotriene receptor antagonists and leukotriene synthesis inhibitors

we want to reduce the release of leukotrienes; they’re pro inflammatory

55
Q

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

A

b) Blocking Cyst-LT receptors

Cysteinyl leukotriene receptor antagonist

56
Q

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

A

c) LTC4
d) LTD4
e) LTE4

Drug list E.g. Zafirlukast

remember:
LT synthesis inhibitor: B
LT receptor antagonist: C, D, E

57
Q

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

A

b) It is less potent than salbutamol

Zafirlukast (cyst-LT receptor antagonist)
Salbutamol (B2 Agonist)

58
Q

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

A

c) Inhibiting enzymes 5-LO or FLAP in LT synthesis

E.g. Zileutin

59
Q

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

A

d) Cyst-LT and LTB4

E.g. Zileutin

remember:
LT synthesis inhibitor: B
LT receptor antagonist: C, D, E

60
Q

Which drug blocks cyst-LT receptor?

a) Montelukast
b) Zafirlukast
c) Zileutin
d) Ipratropium bromide

A

b) Zafirlukast

Cysteinyl leukotriene receptor antagonist

61
Q

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

A

c) Inhibiting enzymes 5-LO or FLAP in LT synthesis

leukotriene synthesis inhibitor

62
Q

Which drug blocks cyst-LT receptors and is less effective than salbutamol in bronchodilation?

a) Zafirlukast
b) Zileutin
c) Montelukast
d) Ipratropium bromide

A

a) Zafirlukast

Cysteinyl leukotriene receptor antagonist

63
Q

Which drug has both bronchodilating and anti-inflammatory effects?

a) Montelukast
b) Zafirlukast
c) Zileutin
d) Ipratropium bromide

A

c) Zileutin

leukotriene synthesis inhibitor

64
Q

TRUE OR FALSE

Asthma comes in dual phases

A

True

  1. Bronchoconstriction (Early/immediate phase)
  2. Inflammation (Late phase)

so we need drugs that target each.

65
Q

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

A

b) They have powerful anti-inflammatory and immunosuppressive actions

Budesonide, Prednisolone, Hydrocortisone

corticosteroids have no effect on bronchodilation

66
Q

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

A

b) 6 hours

Budesonide, Prednisolone, Hydrocortisone

67
Q

Which of the following is NOT a corticosteroid commonly used in asthma treatment?

a) Budesonide
b) Prednisolone
c) Salbutamol
d) Hydrocortisone

A

c) Salbutamol

this is a B2 Agonist

68
Q

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

A

b) They are drugs of last resort

Budesonide, Prednisolone, Hydrocortisone

no effect on bronchodilation therefore cannot be used as 1st line, cross out a & c

69
Q

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

a) Inhibit the synthesis and/or release of inflammatory mediators

Budesonide, Prednisolone, Hydrocortisone

remember that they’re used as anti-inflammatory meds for asthma t/x

70
Q

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

a) They block the ability

Budesonide, Prednisolone, Hydrocortisone

71
Q

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

A

c) Cytokines (IL-1, TNF-alpha, IL-5, IL-4, GM-CSF)

Budesonide, Prednisolone, Hydrocortisone

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

72
Q

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

A

b) They inhibit their expression (e.g., ICAM-1, VCAM-1)

Budesonide, Prednisolone, Hydrocortisone

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

73
Q

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

A

b) Cyclooxygenase-2 (COX-2)

Budesonide, Prednisolone, Hydrocortisone

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

74
Q

Glucocorticoids induce the synthesis of which anti-inflammatory agents in asthma?

a) Histamine
b) Annexins (lipocortins) which inhibit PLA2
c) Leukotrienes
d) Prostaglandins

A

b) Annexins (lipocortins) which inhibit PLA2

Budesonide, Prednisolone, Hydrocortisone

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

75
Q

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

A

b) Inhibition of phospholipase A2 (PLA2)

Corticosteroids: Budesonide, Prednisolone, Hydrocortisone

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

76
Q

What is the preferred route of administration for steroids in asthma management?

a) Intramuscular injection
b) Inhalation
c) Oral tablets
d) Intravenous infusion

A

b) Inhalation

Budesonide, Prednisolone, Hydrocortisone

77
Q

Steroids are often combined with which other class of medications in asthma management?

a) Antihistamines
b) Antibiotics
c) Bronchodilators
d) Leukotriene receptor antagonists

A

c) Bronchodilators

Budesonide, Prednisolone, Hydrocortisone

78
Q

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

A

c) In acute severe asthma

Budesonide, Prednisolone, Hydrocortisone

79
Q

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

A

b) Due to the risk of adrenal suppression leading to growth retardation

Budesonide, Prednisolone, Hydrocortisone

80
Q

Which adverse effect is commonly associated with aerosolized steroid therapy in asthma management?

a) Oropharyngeal candidiasis
b) Dysphagia
c) Laryngeal edema
d) Pneumothorax

A

a) Oropharyngeal candidiasis

Budesonide, Prednisolone, Hydrocortisone

Adverse Effects of Steroids by Aerosol:
– Oropharyngeal candidiasis.
– Dysphonia.

81
Q

What is a potential consequence of rapid withdrawal of systemic steroids in asthma management?

a) Hypertension
b) Adrenal insufficiency
c) Hyperthyroidism
d) Renal failure

A

b) Adrenal insufficiency

Budesonide, Prednisolone, Hydrocortisone

Adverse Effects of Steroids

  • Systemic:
    – Adrenal insufficiency (if withdrawn rapidly).
    – Osteoporosis.
    – Lowered resistance to infection.
    – Cushing’s syndrome.
    – Hyperglycemia.
82
Q

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

A

b) Osteoporosis

Budesonide, Prednisolone, Hydrocortisone

Adverse Effects of Steroids

  • Systemic:
    – Adrenal insufficiency (if withdrawn rapidly).
    – Osteoporosis.
    – Lowered resistance to infection.
    – Cushing’s syndrome.
    – Hyperglycemia.
83
Q

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

A

c) It lowers resistance to infection

Budesonide, Prednisolone, Hydrocortisone

Adverse Effects of Steroids

  • Systemic:
    – Adrenal insufficiency (if withdrawn rapidly).
    – Osteoporosis.
    – Lowered resistance to infection.
    – Cushing’s syndrome.
    – Hyperglycemia.
84
Q

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

A

b) Cushing’s syndrome

Budesonide, Prednisolone, Hydrocortisone

Adverse Effects of Steroids

  • Systemic:
    – Adrenal insufficiency (if withdrawn rapidly).
    – Osteoporosis.
    – Lowered resistance to infection.
    – Cushing’s syndrome.
    – Hyperglycemia.
85
Q

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

A

b) At low doses for cases of steroid-resistant asthma

Not first-line drugs for treating asthma

86
Q

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

A

b) Prophylaxis to prevent the development of asthma

weak & isn’t used 1st line

87
Q

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

A

c) Immediate and late-phase asthmatic responses

88
Q

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

A

c) Reduction of bronchial hyper-reactivity

89
Q

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

A

c) Due to its weak effects and short duration of action

very short DOA + no bronchodilatory effect

90
Q

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

A

b) Inhalation

91
Q

Which Asthmatic drug works by stabilizing mast cells?

a) Zileutan
b) Hydrocortisone
c) Salbutamol
d) Cromolyn
e) Theophylline

A

d) Cromolyn

key word= stabilizing mast cells

92
Q

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

A

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

93
Q

Which of the following is considered an important adjunctive therapy in the management of asthma?

a) Antibiotics
b) Antifungal medications
c) Anticoagulants
d) Oxygen

A

d) Oxygen

so imp & obvious

94
Q

You get handed a case of Status Ashmaticus in the ER, how will you proceed to treat the P/X?

Status Ashmaticus: a medical emergency, an extreme form of asthma exacerbation characterized by hypoxemia, hypercarbia, and secondary respiratory failure

A

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)