Pharmocology Week 9 Essay

Submitted By azkasaeed27
Words: 1195
Pages: 5

Respiratory

Asthma

Bronchoconstriction, higher inflammation, narrowing of airway, shortness of breath, difficulty moving air
Trigger: irritants to the respiratory tract

1. Beta 2 agonists bronchodilators, to terminate episodes, inhalers-topical delivery, tend to be little side effects because inhaled but if it gets orally absorbed orally in mouth then more systemic side effects- sympathetic responses, tachycardia, dysrhythmias, headaches
Interactions- beta blockers for hypertension, anticholinergic (more pronounced effect), contraindications- b2 agonists function in pancreas and release glucagon and increases blood sugar, concern for someone with diabetes, also maybe tachycardia so concern for existing dysrhythemia, narrowing of colon and benign prostate hyperplasia
Classifications:
ultra short –duration 2-3 hours - isoprotenol short- 5-6 hrs – salbutamol * most common intermediate -8 hrs - albuterol long -12 hrs, slower onset then the others, other three are rapid – salmeterol
2. Anticholinergic- termination , blocks muscarinic receptors in smooth muscle causing bronchodilator, SE- sympathetic-like, contra- dysthymias, NAG, BPH i.e. ipratropium bromide
3. Methyvanthines- similar in structure to caffeine, terminator- bronchodilator, SE-central nervous system stimulation, dysrhythmias- tachycardia, diuretic, contra- dysrhythmias primary concern, taking topically through inhaler i.e. theiothylline

Preventative Medication

4. Glucocorticoids anti-inflammatory, not going to terminate as occurring but helps prevent, giving through inhaler, systemic side effects- Cushing’s syndrome, increased blood sugar, increased risk for oral infections, contra- if you have an active infection it might suppress this, not be able to fight it, diabetes, hypertension and congestive heart failure i.e fluticasone, Flonase (trade name) interactions- bronchodilators
5. Mast cell stabilizers- when allergens interact with IE and they crosslink, calcium channels open and histamine is released, histamine causing vascular inflammation, mast cells stabilizers chelate calcium- neutralize them/mop them up/stick to them, no calcium available to enter mast cells and therefore no histamine release, decrease histamine release, decrease inflammation, side effects- irritate nasal mucosa, bitter taste, can cause bronchospasm and analphylaxis i.e. cromolyn, taking by inhaler or nasal
6. Omalizumab- monoclonal antibody, used against human IgE – binds to it, if all IgE receptors are sensitive to omalizumab and occupied than IgE can’t bind to allergens, therefore decrease inflammation in mast cells, last line of defense for asthma reaction
7. Leukotriene modifiers- arachidonic acid- produces prostaglandins, thromboxanes and *leukotrienes attached white blood cells to sites of inflammation, proimflammatory response, if you block leukotrienes production you will have less inflammation therefore less sensitive to allergies

Allergies- allergens- environmental—mast cells inhaled respiratory, rhinitis, dry irritant eyes, skin- itchy, hives, gi- sick, upset stomach

1. H1 Receptor Antagonics- block histamine receptors, H1- blood vessels, by blocking h1 receptors, no vasodilation –nose doesn’t dilate as much, produce less mucous, lower vascular response related to inflammation
A) first generation- diphenhydramine i.e. Benadryl Indications- allergic rhinitis, side effects- drowsiness, sympathetic, CNS stimulator, contraindicated- narcolepsy, dysrhythmias, NAG, BPH, pregnancy Interactions- alcohol-exaggerate drowsiness
B) second generation- i.e. fexofenadine, citirizine, lorahidine, SE- decreased anticholinergic effect, less drowsiness, contra- pregnancy, dysrhythmia
2. Glucocorticoids- slower onset, see asthma section
3. Adrenergic- mucous production is related to increased blood flow, use a vasoconstrictor- alpha 1 vasoconstrictor, alpha 1 agonist, promote vasoconstriction decrease mucous production SE- dry nose out/mucous membrane, stop suddenly- membrane…