Treating allergy, acid, and asthma Flashcards
(23 cards)
What are the four main modes of cell signalling?
1 - Neurotransmissoin - Nerves release neurotransmitters onto effector tissues
2 - Endocrine signalling - Hormones circulate in the bloodstream and act on distant tissues
3 - Paracrine signalling - Local transmitters affect nearby cells
4 - Autocrine signalling - Cells release signals that act on themselves
Why must endocrine hormones be stable?
They need to remian intact while travelling through the bloodstream to distant tissues
What is histamine’s role in the body?
Acts locally in allergic responses, acid secretion, and bronchial smooth muscle contraction
Where are mast cells found?
In aerated tissues (lungs, skin, GI tract, stomach)
How does allergen exposure trigger histamine release?
1 - IgE antibodies bind mast cells
2 - Susequent allergen exposure dimerizes IgE, activating degranulation
3 - Histmaine release causes inflammatory responses
What enzymes metabolize histamine?
N-methyl transferase and monoamine oxidase
What are the effects of histamine bidning?
H1 receptors - Vasodilation, increased permeability, sensory nerve activation (itch/pain
H2 reeptors - Gastric acid secretion
H1 receptors in lung - Bronchial smooth muscle contraction (asthma trigger)
What stimulates acid secretion in the stomach?
Autonomic control (Vagus nerve, mescarinic receptors)
Hormonal control (Gastrin)
Histamine released by mast cells acts on H2 receptors on parietal cells
What are H2 antagonists and their effects?
Cimetidine, ranitidine -> Block H2 receptors, preventing acid secretion
How do proton pump inhibitors work?
Omeprazole irreversible inhibits the proton pump, stopping acid production
What do H1 antagonists do?
Block H1 receptors, reducing inflammation, swelling, and airway irritation
Why do some antihistamines cause drowsiness?
First-gen antihistamines cross the blood-brain barrier, affecting the CNS
What are common non-drowst antihistamines?
Loratadine
Acrivastine
What happens during an asthma attack?
Mast cell degranulation releases spasmogens (histamine, prostanoids, leukotrienes)
Smooth muscle contraction leads to bronchospasm
Inflammatory cells infiltrate airways, worsenning obstruction
What are the two phases of asthma?
1 - Early phase: Rapid onset bronchospasm due to spasmogens
2 - Late phase: Delayed inflammatory response cause airway hypersensitivity
What are bronchodilators used for asthma treatment?
Beta-2 adrenoreceptor agonists
Activate G[CR signalling via Gs -> Increases cAMP and PKA -> Bronchodilation
How is the late inflammatory phase treated??
Glucocorticoids (e.g., beclomethasone, betamethasone)
How are glucocorticoids regulated?
1 - Hypothalamus releases CRH
2 - CRH stimulates the anterior piruitary to release ACTH
3 - ACTH activates GPCRs on adrenal cortex -> Secretion of glucocorticoids
What are glucocorticoids used for?
Asthma
Arthritis
Autoimmune diseases
What effects do glucocorticoids have on immunity?
Supress inflammation (reduce microvascular permeability, T-cell proliferation)
Reuduce interleukin and cytokine production
How do glucocorticoids regulate gene transcripton?
Bind glucocorticoid response elements (GRE) in DNA promoter regions
Supress NF-kappa B and AP-1 transcription factors, reducing inflammation
What are novel asthma treatments beyond bronchodilators?
- Fostair (combined beta-2 agonist + glucocorticoid)
- Leukotriene receptor antagonists (CystLT inhibitors)
- Phosphodiesterase 4 inhibitors (prevent cAMP/cGMP breakdown)
- 5-lipoxygenase inhibitors (prevent leukotriene synthesis)
What is the standard clinical asthma treatment pathway?
1 - Short-acting beta agonist -> imdiate relief
2 - Long-acting beta agonist -> If symptoms perist
3 - Low-dose inhaled glucocorticoid -> If LABA alone is insufficient
4 - Add leukotriene receptor antagonist if further control needed
5 - Combination LABA + IHC for severe cases
