FP-C #8 Flashcards
Sedative-hypnotic agents
depresses the CNS and also provides some anesthesia –> relaxes muscle and brain
Antiarrhythmic class I medications
blocks sodium channels–> reduces myocardial conduction and automaticity–> slows HR and conduction
Anxiolytics
depresses the CNS–> calming and sedates - lowers BP and HR
Calcium
improves contractions and stabilizes heart cells
5- hydroxytriptamine receptor antagonist antiemetics
selectively blocks serotonin receptors in the medulla–> reduces nausea/vomiting
Direct vasodilator medications
causes direct dilation of arterial smooth muscle–> lowers BP and reduces SVR
Magnesium sulfate
calms muscle cells and slows SA conduction–> corrects convulsions in eclampsia, corrects torsades, corrects hypomagnesemia
Phenothiazine antiemetics
blocks dopamine in the cerebral medulla–> suppresses the vomiting center - also has some antihistamine action
Ultra short-acting nonbarbituate hypnotic agents: etomidate type
depresses the CNS –> relaxes muscles and brain
Nitrates
arterial and venous smooth muscle relaxant–> vasodilates–> lowers BP and increases coronary blood flow
Barbituates
depresses the sensory cortex–> prevents Sz and sedates - lowers BP and HR
Alpha-adrenergic antagonists
blocks alpha receptors–> prevents vasoconstriction–> BP lowers
ACE inhibitors
prevents angiotensin -aldosterone system–> lowers BP
Benzodiazepines
depresses the CNS through GABA inhibition –> relaxes muscles and brain- lowers BP and HR
Antiarrhythmic class II medications
blocks beta I receptors–> slows HR
Histamine-2 blocker
blocks histamine 2 receptors–> reduces gastric acids
Ultra short-acting nonbarbituate hypnotic agents: ketamine type
depresses the CNS and releases small amounts of chatecholamines –> relaxes muscles and brain without hemodynamic drop
Corticosterioids
reduces inflammation –> returns bronchial wall to more normal size –> improves airflow
NSAIDs
inhibits prostaglandin synthesis–> reducing pain
Antisecretory medications
reduces intestinal secretions and motility–> palliates esophageal varices
Non-depolarizing neuromuscular blocker
paralysis WITHOUT stimulation of the neuromuscular junction
Anticoagulants
impair platelet aggregation or activation ability–> prevents clots
Opioids
stimulates opioid receptor–> reduces the sensation of pain, lowers mental status, BP, HR and RR
Glucagon
causes release of blood sugar into liver and reverses beta blocker/calcium channel blocker tox
Beta-agonists
cause a sympathetic response –> raises HR and bronchodilates- can be selective
Histamine-1 blocker
blocks histamine 1 receptors–> prevents/corrects bronchospasm, allergy, or analphylaxis - potentiates opioids
Thrombolytics (fibrinolytics)
converts plasminogen to plasmin–> breaks apart clots
Anticholinergic medications
block acetylcholine receptors–> increases HR, BP, bronchodilation
Sodium bicarbonate
alkalizing agent–> increases urinary and serum pH–> corrects acidosis
Depolarizing neuromuscular blocker
paralysis from stimulation of the neuromuscular junction
Antiarrhythmic class III medications
blocks potassium channels–> delays repolarization and increases refractory period–> prepares heart for a safe ‘next’ beat
Potassium chloride
replaces lost potassium
Prostaglandin E
causes direct relaxation of the ductus arteriosis and vascular smooth muscle–> corrects some congenital heart conditions of a newborn
Antiarrhythmic class IV medications
blocks calcium channels—> slows HR and lowers BP
Hydantoin anticonvulsants
decreases cellular sodium in the CNS–> relaxes the brain and reduces the possibility of seizures
Catecholamines
mimics fight or flight response–> increases HR, BP, bronchodilation
Anticholinergic bronchodilators
blocks acetylcholine at bronchial smooth muscle receptor sites –> opens airways
Diuretic medications
prevents renal absorbtion of water–> reduces pulmonary/peripheral edema and SVR
Theophylline derivitives
blocks phosphodiesterase –> sympathetic response –> raises HR and bronchodilates
Opioid antagonist
blocks the opioid receptor–> corrects AMS from opioid OD
