Drugs and more drugs Flashcards
What receptors does Ephedrine act on?
α₁ + β₁+2 Agonist
Is Ephedrine a direct or indirect acting sympathomimetic?
1˚ Indirect Pressor for α₁ + β₁ stimulation; Direct β2 stim
Does Ephedrine have any effect on the GI system?
Yes. It has been known to lead to a decrease in gastric emptying.
What is the MOA for Ephedrine?
causes a release of Norepinephrine…. and ultimately stimulates calcium release by the sarcoplasmic reticulum leading to increased chronotropy/inotropy; in veins leads to constriction
What effects does Ephedrine have on the heart?
Increases Ca+ release from sarcoplasmic reticulum–> increase chronotropy/inotropy–> increase PVR, which leads to increase afterload and ultimately BP
What effect does Ephedrine have on renal perfusion and uterine blood flow?
A decrease in renal perfusion can be noted; no significant alteration is seen in uterine blood flow.
Is the vasopressor effect of Ephedrine primarily due to increased cardiac output or peripheral vasoconstriction?
Its vasopressor effect results largely from increased cardiac output and to a lesser extent from peripheral vasoconstriction.
What is tachyphylaxis and how does it relate to Ephedrine?
Tachyphylaxis is a decrease in drug effect after its administration that could be due to depletion of neurotransmitter stores. Ephedrine may deplete norepinephrine stores in sympathetic nerve endings, so that tachyphylaxis to cardiac and pressor effects of the drug may develop.
What effect does Ephedrine have on oxygen consumption and metabolic rate?
Ephedrine increases oxygen consumption and metabolic rate as a probable result of central stimulation.
How is Ephedrine metabolized?
Hepatic/Renal; slowly metabolized in the liver; renal excretion is dependent on urine pH… the more acidic the urine, the quicker the elimination
Ephedrine can be given as IV, IM, or SQ. What is the typical dose range for each of these?
IV= 2.5-10mg (peds 0.1mg/kg); SQ or IM= 10-50mg
What is the onset, peak, and duration of IV Ephedrine?
O: <1 minute, P: 2-5min, D: 10-60min; IM injection usually starts working within 10-20 min
What receptors do phenylephrine (Neosynephrine) act on?
α₁ Agonist; Anti-Hypotensive
What sympathetic adrenergic receptor does Ephedrine bind to and agonize?
Gs/q-receptors
What sympathetic adrenergic receptor does phenylephrine bind to and agonize?
Gq-receptors.
What is the MOA for phenylephrine?
binds to and agonizes sympathetic adrenergic G-q receptors, ultimately stimulating Ca++ release by the sarcoplasmic reticulum. In arteries and veins it leads to vasoconstriction.
What effect does phenylephrine have on chronotropy and inotropy?
Does not effect either. Strictly elevates BP without increasing HR or contractility.
Why is there a noted decrease in HR with administration of phenylephrine?
Due to reflex bradycardia from the increase in BP. This is useful in tachycardic patients or those with a cardiomyopathy. An increase in blood pressure can be caused by increased cardiac output, increased total peripheral resistance, or both. The baroreceptors in the carotid sinus sense this increase in blood pressure and relay the information to the cardiovascular centres in the brainstem. In order to maintain homeostasis, the cardiovascular centres activate the parasympathetic nervous system. Via the vagus nerve, the parasympathetic nervous system stimulates neurons that release the neurotransmitter acetylcholine (ACh) at synapses with cardiac muscle cells. Acetylcholine then binds to M2 muscarinic receptors, causing the decrease in heart rate that is referred to as reflex bradycardia.
What happens if phenylephrine is given through an infiltrated IV? What can be given?
Severe necrosis to surrounding tissues!! Damage may be prevented or mitigated by infiltrating the tissue with an alpha blocker like phentolamine by subcutaneous injection.
What is the dosage for phenylephrine when given as IV push or as a gtt?
IV push: 40-100mcg; 25-200 mcg/min
What is the onset, peak, and duration of phenylephrine?
O: <1min, P: 1min, D: 15-30min
What is the basic effect of Hydralazine (Apresoline) and is it direct or indirect acting?
a direct-acting smooth muscle relaxant used to treat hypertension by acting as a vasodilator primarily in arteries and arterioles. By relaxing vascular smooth muscle, vasodilators act to decrease peripheral resistance, thereby lowering blood pressure and decreasing afterload.
What is the specific hypothesized MOA of Hydralazine?
Precise MOA is not fully understood. Hydralazine increases cyclic guanosine monophosphate (cGMP) levels, increasing the activity of protein kinase G (PKG). Active PKG adds an inhibitory phosphate to myosin light-chain kinase (MLCK) – a protein involved in the activation of cross-bridge cycling (i.e. contraction) in smooth muscle. This results in blood vessel relaxation. It dilates arterioles more than veins.
Hydralazine requires the endothelium to provide NO (nitric oxide. ) thus only provides the effects of NO in vivo with functional endothelium. It will not work to vasodilate in vitro in an isolated blood vessel.
Hydralazine, by altering cellular calcium metabolism, interferes with the calcium movements within the vascular smooth muscle that are responsible for initiating or maintaining the contractile state.
Why is Hydralazine usually not used as a primary drug for treating hypertension?
Hydralazine is not used as a primary drug for treating hypertension because it elicits a reflex sympathetic stimulation of the heart (the baroreceptor reflex). The sympathetic stimulation may increase heart rate and cardiac output, and in patients with coronary artery disease may cause angina pectoris or myocardial infarction. Hydralazine may also increase plasma renin concentration, resulting in fluid retention. In order to prevent these undesirable side-effects, hydralazine is usually prescribed in combination with a beta-blocker (e.g., propranolol) and a diuretic.
