Asthma/DVT/PE Flashcards
Symptoms of Asthma
Chronic cough, Dyspnea, Wheezes
diminished FEV/FVC ratio, improves with administration of beta-2 agonist (PEFR also increases)
Atopic Asthma
Excessive Th2 response
type 1 IgE-mediated hypersensitivity; evidence of allergen sensitization, often in a patient with a history of allergic rhinitis, eczema
Non-atopic Asthma
often adult-onset/more severe disease: triggers can be: aspirin/other drugs, exercise, cold air, stress, inhaled irritants
Diphenhydramine, chlorpheniramine
1st generation anti-histamines
block H1, muscarinic, cholinergic receptors
not recognized by P-glycoprotein efflux pump –> sedation
side effects from other receptors
Fexofenadine, cetirizine, loratidine
2nd generation anti-histamines
block H1 receptor
recognized by P-glycoprotein efflux pump –> no sedation or side effects from other receptors
Theophylline
mechanism not fully elucidated
PDE inhibitor –> results in increase in cAMP levels –> results in broncho dilation
Toxic side effects –> don’t use
Normal dilation pathway of broncho smooth muscle
Epi binds beta-2 receptors –> GPCR –> adenylyl cyclase –> increased cAMP –> bronchodilation
Cromolyn Sodium
anti-inflammatory and mast cell stabilizer
blocks release of histamine and SRS-A
Albuterol
SABA –> binds beta-2 receptors causing broncho dilation
Salmeterol, formoterol
LABA –> binds beta-2 receptors causing broncho dilation
NEVER use by themselves!!!
Zileuton
5-lipoxygenase inhibitor –> inhibits synthesis of LTB4
may decrease the need for beta agonists
require monitoring for hepatic toxicity
Monteleukast, Zafirleukast
reversible leukotriene receptor antagonists (LTD4 receptor and Cyst-LTR1)
Safe and once daily administration
Phenylephrine
potent, direct acting alpha agonist with no beta activity –> vasoconstriction –> nasal decongestion
Pseudoephedrine
Directly stimulates alpha-adrenergic receptors of respiratory mucosa causing vasoconstriction; directly stimulates beta-adrenergic receptors causing bronchial relaxation
Inhaled corticosteroids
bind steroid response element –> alter transcription –> decreased NF-kB, and other inflammatory cytokines and mediators
Nasal sprays: enhanced uptake in lungs, prolonged tissue binding in the lungs, nearly complete first pass inactivation
Omalizumab
- binds to free IgE in circulation → inhibits IgE binding to mast cells & basophils→ decreases mediator release→ decreases free IgE & down-regulates IgE receptors
- Given as injection sub-q, expensive
- Anti-IgE treatment might be recommended if you have allergic asthma and you keep experiencing persistent symptoms despite taking your controller medications.
Treatment of different severities of asthma
Step 1 - SABA as needed
Step 2 - Low dose ICS and SABA as needed
Step 3 - Low dose ICS and LABA/medium ICS w/ SABA as needed
Step 4 - Medium dose ICS and LABA
Step 5 - High dose ICS and LABA
Step 6 - High dose ICS, LABA, oral corticosteroid
Severity of Asthma symptoms
- Intermittent: infrequent symptoms (less than twice a week) use albuterol
- Persistent: more than twice a week - waking up with cough/ not able to breath, Treat these people with daily inhaled corticosteroids. If someone has persistent asthma you will use the least effective dose. When they have an exacerbation you still use the albuterol just like everyone else.
- Severe: add a long acting, increase the dose, add a leukotriene inhibitor, never use theophylline
- Super severe: daily oral steroids!!
Nonpharmacologic treatment of asthma
Allergen/environment control
Patient Education
Recognition of symptoms and measurements of lung function
Inverse Agonist
binds same receptor but induces pharmacological response opposite to that of agonist
Competitive Agonist
receptor antagonist that binds receptor but does not activate the receptor
Virchow’s Triad
Stasis
Hypercoaguability
Endothelial Damage
PE and V/Q mismatch?
V/Q ratio goes to infinity (essentially no perfusion)
D-dimer test
Good sensitivity but LOW specificity
Negative test –> NO CLOT
Positive test –> can’t say there is a clot
