NO and Inhalation Anesthetics Flashcards
NO
-MOA-Activates guanylyl cyclase, increases cGMP synthesis, causes smooth muscle relaxation
-Use-Pulmonary hypertension, hypoxic respiratory failure
-Inhaled gas administered continuously
-Tox-Methemoglobinemia, conversion to nitrogen
dioxide (a pulmonary irritant)
L-NMMA
-MOA-Competitive nitric oxide synthase inhibitor
Superoxide Dismutase
- MOA-Protects NO from inactivaction from superoxide by scavenging superoxide anions
- Use-Enhance NO potency and prolonging its duration of action
Methyline blue
- MOA-prevents the action of NO by inhibiting the soluble guanyl cyclse
- Used to reverse pulmonary hypotension caused by NO
L-arginine
-Substrate by which eNOS, activated by calcium-calmodulin complex, makes NO
L-citrulline
-Produced from the use of NOS on arginine to produce NO and L-citrulline
Desflurane, Enflurane, Halothane, Isoflurane, Sevoflurane, methoxyflurane, Nitrous oxide
-MOA-Facilitate GABA-mediated inhibition, block brain
NMDA and ACh-N receptors
-Pharmakological effect-Increase cerebral blood flow
-enflurane and halothane decrease cardiac output.
-Others cause vasodilation-all decrease respiratory functions—lung irritation (desflurane)
-Rate of onset and recovery vary by blood:gas partition
coefficient, recovery mainly due to redistribution from brain to other tissues
*You recover from halothane and methoxyflurane faster because those are also partially metabolized by the liver.
-Toxicity: extensions of effects on brain, heart/
vasculature, lungs,
-Drug interactions: additive CNS depression with many agents, especially opioids and
sedative-hypnotics
Carbon Monoxide
- MOA-220 times the affinity for Hb than O2, clinical effects may be aggravated by heavy labor, high altitude and high ambient temperature. Interferes the dissociation of O2 from oxyhemoglobin, reducing the transger of O2 to tissues.
- ->psychomotor impairment, headaches tightness in the temporal area, confusion, loss of visual acuity, tachycardia, tachypnea, syncope, coma, convulsions, shock and respiratory failure.
Sulfur dioxide
- MOA-causes irritant effects on the eyes, mucous membranes and skin, absorbed in the upper respiratory tract, causes bronchoconstriction, PNS reflexes, and altered smooth muscle tone
- SO2 forms sulfurous acid upon contact with moist membranes
- ->irritation of the eyes, nose, and throat and reflex bronchoconstriction, severe exposure leads to deleyed onset pulmonary edema
Nitrogen oxides
- Brownich irritant gas associated with fires, cause of silo-filler’s disease.
- capable of producing pulmonary edema, at low conc. affects type I pneumocytes, but at higher conc. affects type II as well.
- ->irritation of the eyes and nose, cough, mucoud or frothy sputum production, dyspnea, and chest pain, pulmonary edema and fibrotic destruction of terminal bronchioles
- Tx w/bronchodilators, sedatives, and antibiotics
ozone
- bluish irritant gas, irritant of mucous membranes, mild exposure respiratory tract irritation, severe exposure is deep lung irritation, pulmonary edema
- forms free radicals in lower lung
- ->shallow rapid breathing, dec pulmonary compliance, inc sensitivity on the lung to bronchoconstrictors, dryness of throat, long term exposure can result in chronic bronchitis, bronchiolitis, fibrosis, emphysematous change
Aromatic hydrocarbons, benzene, toluene, and xylene
- benzene-found in inhaled fumes, causes aplastic anemia, leucopenia, pancytopenia, thrombocytopenia, and leukemia by targeting stem cells
- toluene-cns deppressant, skin and eye irritant, fatigue, ataxia, fetotoxic
- xylene-cns deppressant and skin irritant
Theophylline, aminophylline
- MOA-Methylxanthine derivative found in tea, Inhibits PDE, which increases cAMP and promotes bronchodilation; used in asthma.
- Uses-Bronchodilator, mild CNS stimulant.
- Tox: seizures.
Bosentan
- MOA-ETA and ETB receptor antagonist
- Use-Pulmonary hypertension
- Oral, Half-life: 5 h
- Tox-Hepatic impairment; possible teratogen
