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CRP 2 KCP 1 & 2 > Drugs for asthma > Flashcards

Drugs for asthma Flashcards

1
Q

Pathophysiological features of asthma

A

mucosal edema
secretion of mucus
bronchoconstriction

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2
Q

Treatment for bronchial asthma

A

Bronchodilators
1. beta 2 adrenergic receptors agonists
-SABA: salbutamol
-LABA: salmeterol
2. antimuscarinic (M2/M3)
-SAMA: ipratropium bromide
-LAMA: tiotropium
3. PDE inhibitor
-theophylline
anti-inflammatory
1. corticosteroids
-inhaled corticosteroids: beclomethasone, fluticasone
-oral/IV corticosteroids: prednisolone
2. Anti-IgE antibodies: omalizumab
3. leukotriene pathway inhibitors
-receptor antagonists: montelukast, zafirlukast
-5-lipoxygentase inhibitor: zileuton

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3
Q

MOA of the most potent bronchodilators for treatment of asthma

A

beta 2 agonist (works like adrenaline)
SABA: salbutamol
LABA: salmeterol
MOA
+receptor activate adenylyl cyclase which turns ATP into cAMP. cAMP activates PKA which phosphorylate myosin light chain kinase (MLCK), resulting in relaxation of bronchial smooth muscle [bronchodilation] Besides, PKA also stimulates Ca-activated K channel to open, more potassium leaks out (hyperpolarisation) which causes relaxation

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4
Q

Differences of salbutamol and salmeterol

A

Salbutamol SABA
-hydrophilic
-short duration (cannot store in lipid)
-rapid onset
-seen in MDI & nebulizer
Salmeterol LABA
-lipophilic
-long duration
-slow onset
-seen in MDI

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5
Q

pharmacological effects of beta 2 adrenergic agonists like salbutamol and salmeterol

A

bronchodilator due to
a. Reduced Intracellular Calcium Levels: One of the primary effects of cAMP signaling is the inhibition of intracellular calcium release from intracellular stores (like the sarcoplasmic reticulum) in smooth muscle cells.
b. Inhibition of Calcium Entry: cAMP also reduces the influx of extracellular calcium ions (Ca2+) through voltage-gated calcium channels in the smooth muscle cell membrane. This decreased calcium entry is crucial for bronchodilation.
inhibition of inflammatory mediator release from mast cells and monocytes
enhance mucociliary clearance
expectoration of bronchial tract

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6
Q

beta 2 agonists (salbutamol and salmeterol) : adverse drug reactions

A

skeletal muscle tremors
nervousness
increased HR/reflex tachycardia due to vasodilation

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7
Q

MOA of bronchodilators: muscarinic antagonist (M2/M3) blocks muscarinic acetylcholine receptors=G protein-coupled receptors

A

SAMA: ipratropium bromide
LAMA: tiotropium
BLOCKS

M2 (cardiac, presynaptic autoreceptor) INHIBITORY
reduce cAMP
inhibit Ca channel, high K conductance
inhibit heart and presynaptic
inhibit respiratory ciliary activity
M3 ( resp tract, glandular) EXCITATORY
increase IP3, DAG
increase intracellular Ca
low K conductance=depolarization
bronchoconstriction
secrete glandular mucus
enhance mucociliary clearance

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8
Q

uses and adverse effects of muscarinic antagonists: Ipratropium and tiotropium

A

Ipratropium
non-selective muscarinic (M2 & M3)
acute, prophylaxis
treat COPD, CVS in elderly
Tiotropium
selective (M3)
longer duration of action
1st line therapy in COPD

Adverse effects
dry mouth
nausea
constipation
urinary retention
exacerbation of angle-closure glaucoma

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9
Q

MOA, pharmacological effects and uses of bronchodilators: methylcanthine (theophylline) PROTOTYPE

A

theophylline
MOA
inhibits PDE =increase cAMP [effects similar to beta agonist]

pharmacological effect
bronchodilation: stabilise mast cells, inhibit release of inflammatory mediators, increase mucocilliary function

*rarely used, not as effective as SABA
-uses/indications: bronchial asthma, prophylaxis for nocturnal asthma, bronchospasm + bronchitis (COPD)

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10
Q

pharmacokinetics of methyxanthines (theophylline)

A

metabolised by cytochrome P450 in liver=potential drug-drug interactions
rapidly absorbed from GIT
narrow therapeutic effect

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11
Q

adverse effects of methylxanthines (theophylline)

A

oral, slow IV ONLY
CNS (agitation, insomnia, nervousness, convulsions), CVS (tachycardia, arrhythmia), respiratory AE

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12
Q

Anti-inflammatory agents: corticosteroids aka glucocorticoids for asthma treatment

A

reduce inflammation
reduce hyperactivity
reduce responsiveness to stimulus
DOES NOT CAUSE BRONCHODILATION= does not help in asthma attack

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13
Q

prototype for corticosteroids aka glucocorticoids

A

prednisolone (oral)
hydrocortisone (IV)
beclomethasone (inhale) aka ICS

major mechanism:
effects on inflammatory mediators and cells

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14
Q

Corticosteroids aka glucocorticoids: Effects on inflammatory mediators

A

inflammatory stimuli acts on phospholipase A2, corticosteroids inhibit phospholipase A2 which inhibits Arachidonic acid

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15
Q

corticosteroids has gene repression effects

A

reduce cytokine (IL-1, 6, 10) and TNF alpha
reduce eosinophils
promote production & expression of IgE & its receptors

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16
Q

corticosteroids’ effects on inflammatory cells

A

inflammatory cells:
less cytokines
less mast cells, less eosinophil and T lymphocyte
less macrophage
less dendritic cell

structural cells:
less cytokines and mediators from epithelial cells
less endothelial leak
increase beta 2 receptors on airway smooth muscle
reduce mucus secretion

17
Q

systemic corticosteroids cannot be used for a long period of time due to its adverse effects

A

weight gain. drug-induced diabetes, easy bruising

18
Q

AE of inhalation of corticosteroids

A

low dose- local effects: oral candidiasis
high dose-long duration-systemic effects: cataract, glaucoma

side note:
**gargle and Rinsing the mouth after inhaling corticosteroids,
Preventing Oral Thrush: One of the potential side effects of inhaled corticosteroids is the development of oral thrush (oral candidiasis). This is a fungal infection caused by the yeast Candida albicans. Rinsing the mouth with water or brushing your teeth after inhaling corticosteroids helps remove any medication residue from the oral cavity, reducing the risk of oral thrush. This is particularly important for those who use high doses of inhaled corticosteroids or those who are more susceptible to fungal infections.

19
Q

interaction between corticosteroids and LABA(fixed dose)

A

corticosteroids: anti-inflammatory
LABA: bronchodilation

aka seretid
Seretide is a brand name medication that contains a combination of two active ingredients:

  1. Salmeterol: Salmeterol is a long-acting beta-2 agonist (LABA). It works by relaxing the muscles in the airways, which helps to open up the air passages and make it easier to breathe. LABAs are used to provide long-term control of asthma and chronic obstructive pulmonary disease (COPD) symptoms. They are not intended for rapid relief of acute symptoms but rather for ongoing management.
  2. Fluticasone Propionate: Fluticasone is an inhaled corticosteroid (ICS). It works by reducing inflammation in the airways, which is a key component of asthma and COPD. By decreasing inflammation, fluticasone helps to prevent and control symptoms such as wheezing, shortness of breath, and cough.

The combination of a LABA (salmeterol) and an ICS (fluticasone) in Seretide is commonly used for the management of asthma and COPD in individuals whose symptoms are not well-controlled by an ICS alone. It provides both bronchodilation (opening up of airways) and anti-inflammatory effects.

20
Q

MOA of leukotriene pathway inhibitor (STEP UP TREATMENT):

LOX inhibitor : zileuton

A

inhibit 5-lipoxygenase (LOX) , inhibit the formation of leukotriene

CAN relieve symptoms of bronchial asthma

21
Q

indications, pharmacokinetics and AE of leukotriene pathway inhibitor: zileuton

A

indications:
prophylaxis
chronic treatment in adults and kids over 12
cannot reverse bronchospasm in ACUTE asthma attack

pharmacokinetics: orally

AE: LIVER TOXICITY need to monitor liver function

22
Q

MOA, indications, pharmacokinetics and AE of leukotriene RECEPTOR inhibitors: zafirlukast, montelukast

A

MOA:
as the name goes

Indications:
prophylaxis
chronic treatment in adults and kids over 6

Pharmacokinetics: orally
AE: LIVER TOXICITY IN ZAFIRLUKAST hence less prescribed

23
Q

MOA of anti-IgE therapy: Omalizumab

A

recombinant humanised monoclonal antibody to IgE

+IgE via Fc
suppress mast cell response to allergens

24
Q

indications and AE of omalizumab

A

indications:
reduced in severity and freq of asthma attacks (high cost)

AE:
anaphylactic reaction
pain and inflammatory reaction at site of injection

25
Q

Cromolyn sodium (less commonly used)

A

MOA:
interferes with antigen-antibody reaction of mast cell

indications:
prophylaxis of chronic asthma

AE:
nasal stinging
nasal irritation

CRP 2 KCP 1 & 2 (8 decks)

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