Asthma Drugs Flashcards
Brief overview of Asthma pathophysiology
Allergen
T Cell, TH2,
IL4 IL13 - B cell proliferation - IgE
IL5 - Eosinophils
IgE on Mast Cells;
Allergen 2
Cross-link IgE
Mast Cell degranulation - Histamine, PGs;
Eosinophil releases Leukotrienes too// Leukotrienes released by WBC
Bronchoconstriction, spasm
Mucous production
Vagal tone, Ach, bronchoconstriction
Name all controls [3] + mAbs [3]
Inhaled Corticosteroids - ICS - Fluticasone
Leukotriene Receptor Antagonist - LTRA - Montelukast
- LK stimulates receptors on Mast Cells, Eosinophils
Mast Cell Stabilizer - Na Cromoglycate
anti IL4 mAB - block IL4 AND IL13
anti IL5/5r mAB
anti IgE mAB - bind to Fc region AND decrease FcR1 expression hence downstream all blocked;
Explain MOA of all controls
ICS - Fluticasone
- immune suppression, anti-inflammatory
- Reduce expression of enzymes: PLA2, COXII, 5-LOX
- Decrease mucous production
- INCREASE b2 receptors (used w b2 agonist)
LTRA - Montelukast
- prophylaxis and treatment
Sodium Cromoglycate
- block degranulation of Mast cells
- block inflammatory mediators from ENM cells
Name all Relivers [3] + MOA of F
b agonists
muscarinic antagonists
Theophylline
- inhibit Phosphodiesterase enzyme, which depletes cAMP to 5 AMP (cAMP activates PKA, which then inhibits MLCK, less phosphorylation of myosin LC, hence relaxation)
- antagonist for Adenosine receptor, decrease bronchoconstriction by adenosine
- First line asthma maintenance
- PRN reliver therapy
- why first line is mixed?
Combined ICS w LABA
- Salmeterol + Fluticasone
- b agonists downregulates b2 receptors hence potential death; while CS upregulates b2 receptors
Relive of Salbutamol SABA PRN
b agonist name [4] + side effects [3] + MOA
Salbutamol SABA Salmeterol LABA Formoterol LABA Indacaterol LABA COPD
- all are b2 selective!
AE: tremors, peripheral (muscle, liver, uterine) vasodilation, TC/palpitations
MOA:
- beta 2 GPCR
- adenylyl cyclase, increase cAMP
- cAMP decrease MLCK function; decrease [Ca] concentration, open potassium channels, hyperpolarize cells
- Airway smooth muscle relaxation
m antagonists MOA (vs b agonists) + 2 names
which one better for COPD
m antagonists blocks when Ach causes asthma pathophysiology; if other CAUSES then no work, worse than BA
- blocks M3 receptors at lungs
- more bronchodilator effect during COPD, as COPD more vagus tone!
- SAMA: Ipratropium Bromide
- LAMA: Tiotropium Bromide
Name all Muscarinic Blockers you know [3] + Functions
Atropine (non-selective)
- used w diphenoxylate opioid for diarrhea
- used for nerve gas poisoning too; + pralidoxime
Scopolamine/ Hyoscine
- for M1 blocker for N&V
Ipratropium Bromide
Tiotropium Bromide
- non-selective
- blocks Ach mediated Bronchoconstriction in COPD/Asthma
- Ipratropium Bromide also functions as Mucous Regulator in Cough and Cold
Name all beta agonists and beta blockers you know
+ Functions
[2 main each]
Agonists SABA: Salbutamol (PRN) - b2 LABA: Salmeterol (first line + ICS Fluticasone) -b2 Formoterol LABA Indacaterol LABA COPD -- COPD/Asthma -- also used as Mucokinetic
Blockers
Propranolol:
- CVS, non specific, not for heart failure
- Propranolol is the preferred agent for β-blockade in hyperthyroidism and thyroid storm due to its additional effect of blocking the peripheral conversion of inactive T4 to active form T3.
Atenolol: b1 specific
Betaxolol: b1 specific - eye drops
Sotalol (beta)
Timolol (beta) - eye drops
Propranolol
Adenosine
- function as Class V anti-arrhythmic drug
- relation to Asthma Reliver drug
Adenosine
- opens K+ (Kach) channel, hence closes Ca2+ Channel
- suppresses AV conduction - AV block
- used for Supraventricular arrhythmia
Asthma Reliver
- adenosine leads to airway muscle CONTRACTION
- Theophylline antagonizes Adenosine receptor
- also inhibits PDE, which converts cAMP away to 5AMP
- – inhibited PDE accumulates cAMP - allowing for MLCK phosphorylation; MLC dephosphorylation
- – Airway muscle relaxation :)
