Final review Flashcards
Catecholamine metabolism
Epi/Norepi broken down by MAO to Dihydroxymandelic acid
Which is converted VIA COMT to VMA
Action of Nitric Oxide
Blockade of Ca into the cell and enhanced uptake into the SR:
Activation of Guanylate cyclase
Increased cGMP concentration
Activation of PKG
=Vasodilation
Prostacyclin pathway
Increased cAMP
Inhibitory effect on actin/myosin
=vasodilation
Endings for ace and aras
-pril
-sartan
Treatment for SNP toxicity
3% sodium nitrite
Sodium thiosulfate
Methylene blue
3 pathways for cyanide toxicity
Cyanomethemoglobin
Binding to tissue cytochrome oxidase- acute toxicity
Thiocyanate- long term
Pathophysiology of asthma main points
Reversible airway obstruction
Hyper reactivity to a variety of stimuli
Immunologic pathways- Th-2 and inflammatory
Describe inflammatory process in asthma
Liberation of cytokines-Interleukins
Mast cell activation (histamine release)
Neutrophil aggregation
Airway remodeling from chronic inflammation
6 types of asthma
Extrinsic (allergic)
Intrinsic (non-allergic)
Exercise induced
occupational
Drug induced-NSAIDS/Aspirin
Food additives
Excretion of albuterol
Unchanged in urine
Inhaled Anticholinergic main takeaways
Chronic COPD-ipratroprium
Mechanism- antagonism of airway M3= bronchodilation
-prevents gprotein signaling and calcium entry
Take 15-30 min onset
Anticholinergic effects-dry mouth, urinary retention, tachycardia
Inhaled corticosteroids takeaways
Mechanism-suppression of Th-2 activation and broad array of leukocytes
Stabilization of cell membranes-limiting formation of interstitial edema