Only $2.99/month

Strathmann Pharm Exam 1 Review NURS615

Terms in this set (59)

The first step is to define the patient's problem to generate a clear indication for treatment. It is in essence a summary of the diagnostic part of the consultation including complaints, symptoms, and/or diagnosis and relevant patient characteristics like co-morbidities, co-medication, pregnancy, and drug allergy. This step forms the basis for choosing and prescribing the correct treatment during the next steps.

The second step is to specify therapeutic objective, which is essentially not only for determining the right treatment but also for monitoring the effective treatment later on. Without clearly specified therapeutic objectives, preferably expressed in measurable parameters, it is not possible to adequately monitor treatment which could result in incorrect conclusions and further actions.

The third step is to choose which drug or treatment is needed. One of the key principles of the WHO approach is to divide step 3 into 2 parts.

First, selection of the so-called p-drug or the prescribers personal drug of first choice for the indication step 3A and then confirmation of its suitability for the patient in question step 3B.

Graduate nursing students should define their own p-drugs and are encouraged to develop a personal formulary on such drugs during their clinical attachments. These so-called standard treatments should be preferably evidence based. Verifying the suitability of a p-drug for individual patient requires thoroughly checking for potential contraindications and for interactions if the patient has co-morbidity, is taking other medications, is pregnant, or is allergic to certain drugs.

Once an appropriate drug has been chosen for the patient in question it needs to be administered correctly; this involves writing the prescription and starting treatment, which is step 4.

Giving the patient information instructions for and warning about the treatment is step 5.

Monitor the treatment is step 6.
The latter step includes decisions about whether to continue, adjust, or stop the treatment.
Beta-blockers are a class of drugs that are particularly used for the management of cardiac arrhythmias, protecting the heart from a second attack after first heart attack, which is called secondary prevention.

They have been used in hypertension but no longer our treatment of first choice.

Beta-blockers block the action of endogenous catecholamines, epinephrine, and norepinephrine on adrenergic beta receptors of the sympathetic nervous system, which mediates the flight or fight response. Some block all activation of beta adrenergic receptors and others are selective.

The three types of beta receptors are known designated beta-1, beta-2, and beta-3 receptors.

Beta-1 adrenergic receptors are located mainly in the heart and kidneys. Beta-2 are located in the lungs, GI tract, liver, uterus, vascular smooth muscle and skeletal muscle. Beta-3 adrenergic receptors are located in fat cells.

Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses especially when they are simulated by epinephrine. Beta 1 receptors effect chronotropy, inotropy, dromotropy, renin release and lypolysis.

Beta-blockers interfere with binding of the receptor to epinephrine and other stress hormones and weaken the effects of stress hormones.
There are two types of beta-blockers; there are non-selective agents, which we show combined to both beta-1 and beta-2 receptors, those include propranolol and carvedilol, although carvedilol has additional alpha blocking activity which can cause vasodilation of the peripheral vasculature, and labetalol as well. Beta 1 selective agents, also known as cardio selective, they have ionotropic effects as well as reducing with muscle tone these include atenolol, esmolol, and metoprolol. BB: tx of cardiac D/Os, HF, anxiety, migraine, tachy r/y hyperthyroidism. Work by latching on the BB rec. site and prevent those sites from the catecholamines being able to latch onto those sites
An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and peripheral nervous system. Anticholinergics inhibit parasympathetic nerve impulses by selectively blocking the binding of neurotransmitter acetylcholine to its receptor and nerve cells. The nerve fibers in the parasympathetic system are responsible for the involuntary movement of smooth muscles present in the GI tract, urinary tract, and lungs. Anticholinergics are divided into three categories in accordance with their specific target in the central and/or peripheral nervous system, this includes antimuscarinic agents, ganglionic blockers, and neuromuscular blockers. Anticholinergic drugs are used to treat a variety of conditions, GI disorders like gastritis, diarrhea, pylorospasm, diverticulitis, ulcerative colitis, nausea and vomiting; genitourinary disorders cystitis, urethritis, prostatitis; respiratory disorders like asthma, chronic bronchitis, COPD, sinus bradycardia due to hypersensitive vagus nerve, insomnia although usually only for a short term basis, dizziness including vertigo, motion sickness related symptoms. Anticholinergics decrease saliva production and most produce some level of sedation, both being advantageous for surgery procedures. For many of these effects cholinergic analogues produce the opposite effect so it would be helpful for you to go through and note make another chart with the cholinergic receptors and what happens when you block them and you simulate them and all the different organ systems. Anticholinergics produce muscarinic blockade against acetylcholine. Muscarinic receptors are all over the body. The goal of admin is to compete with acetylcholine at those receptor sites to keep acetylcholine from acting on them (gets in the way).

Side effects: can't pee, can't see, can't spit, can't shit