Julie's Nursing School Blog

Med Sheet for all!

2008-02-23T19:17:00.000-08:00

This spreadsheet is like a database of all the meds that people have posted in their paperwork...I didn't collect everything, but this should allow us to save time by cutting and pasting what someone else already typed up. Enjoy.

http://spreadsheets.google.com/ccc?key=pa-GnAC_jJcNvAtggzAw1SQ&hl=en

Patho: Heart Failure Day

2008-02-19T11:16:00.001-08:00

Heart Day [with Deb]

Will test questions be patho questions like in 205 last semester? No, they will be scenarios w/ clients

Called “Heart failure”: No longer called “CHF” which is still overused.

Mr. Ames age 59, has been on your floor since yesterday am. He was admitted with right sided heart failure following an MI 3 months ago. He has an IV of NS at 200 ml/hr, a F/C draining cloudy amber urine and has had no energy or appetite since admission.

What causes R side heart failure (which is uncommon)? Rt side failure either means respiratory stuff or rt ventricular MI. Usually caused by respiratory problems: “increased pressures in the pulm vasculature,” such as pulm fibrosis, COPD. An MI causes failure b/c the tissue dies. COPD + Rt Heart failure is called: Cor Pulmonale

Rt side heart failure causes edema to the periphery, esp the sacrum. Also splenomegaly, hepatomegaly. You won’t hear crackles or wheezes, b/c the blood backs up into the systemic circuit, [instead of the lungs, as in left sided heart failure.]

Heart failure of any type can also be caused by issues of preload: putting blood into the atria and preparing to eject it. If you don’t have good volume, you can’t pump it out well—too much volume means the heart gets stretched out over too much time [Starling’s Law: cardiomegaly/pooped out rubberband theory]

When talking about Heart failure, we care about:

Preload [gets blood into heart]: “In cardiac physiology, preload is the pressure stretching the ventricle of the heart, after passive filling and atrial contraction. Preload is theoretically most accurately described as the initial stretching of a single cardiac myocyte prior to contraction.” (wikipedia)

Contractility [how well the heart pumps the volume]: “Myocardial Contractility is a term used in physiology to describe the performance of cardiac muscle. Contractility is often defined as the intrinsic ability of a cardiac muscle fibre to contract at a given fibre length.” (wikipedia

And afterload [the resistance that you have to pump against.]: In cardiac physiology, afterload is used to mean the tension produced by a chamber of the heart in order to contract. In the clinic, the term end-systolic pressure is usually more appropriate, although not equivalent. Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber. Everything else held equal, as afterload increases, cardiac output decreases. In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the peripheral blood pressure in order to open the aortic valve.

What matters is how much you get in [preload], how hard the pumping is [contractility], and how hard you have to push against to get it out of the heart. [afterload]

Effects on the heart, compensatory mechanisms:

Dehydration= low blood volume. Overhydration=too much volume

Contractility: if you have cardiomegaly, you get too much volume in the heart, but it doesn’t pump enough blood out.

Tach: the body compensates for the lack of blood making its way out of the heart by kicking up the heart rate. Also increased BP and contractility.

Pumping against tough pipes: afterload is effected by how hard your pipes are: your pipes are hardened by plaque [atherosclerosis.]

kidneys aren’t getting enough fluid, they respond by saving salt, and therefore secrete Aldosterone—which causes higher vascular volume, and the preload and afterload increase.

ANP and BNP [atrial and Brain Natriuretic [sodium wasting via urine] Peptides are released, which causes vasodilation.

Ventricular remodeling: initially makes more productive contractions, the ventricles dilate to allow the excess blood volume of the body. Ultimately, this turns into ventricular hypertrophy and the O2 needs of the heart increase, and pooped-out-rubberband disorder.

What do we want to know from report?

UTI? Meds?

Test/check renal function [BUN, serum Creatinine]. The body will defend the kidneys last, and protect the heart and brain. The kidneys will shut down, so renal failure and acidosis are next up. Hepatomegaly/increased pressure on liver can cause it damage.

What are pt VS? Chest pain, peripheral edema, lung assessment, O2 sats. SOB? Tach? This client should be on tele; and those sinus rhythms should be reported. Why no appetite? [easy: he feels like crap.] His blood is gorged in his spleen and liver. IV is too fast. Does he really need isotonic solution? NS may cause him to retain. He should probably be on fluid restriction.

We’re looking up recent labs. What do you want: CBC: look for infections [b/c he is highly at risk], weight, electrolytes [esp sodium, and K.] This guy might not need blood gases taken.

What’s the first thing we do when we go in the room? Vitals. Sacral and peripheral edema. Sacral edema is “dependent edema.” You want to check the F/C, the IV, the lungs—which should not be affected unless the L side of the heart is now involved. Does he have pink frothy sputum [indicating pulmonary edema].

Things that look bad: Weight: a few pounds of weight gained is a big problem—daily weight is critical, control for every piece of clothing, use the same scale, etc.

LABS: Diagnosed w/ ANP and BNP labs-- Atrial and Brain Natriuretic [sodium wasting]. BNP lab: Human natriuretic peptides. Released as heart muscle stretches-- Peptides are released, which causes vasodilation.. They classify HF based on this lab. 100+ is ‘mild.’ 300-600=mod. 600-900= severe.

Serum electrolytes: measure to detect fluid rentention

Kidney and liver function tests

Thyroid tests to see if thyroid is the source [hypo or hyper]

Chest x ray shows pulm congestion and cardio megaly

HF is usually side effect of something else: TOB, MI, HTN. The S&S will only get worse.

Meds: What do we want meds to do? Effect those 3 things: preload, contractility, afterload.

Preload: it’s about volume—effected by diuretics. Why to HF pts take diuretics? Why do we like Lasix? It’s cheap. Why is it bad: it’s not potassium sparing, and if you’re on Dig too, you’ll become Dig toxic. We like potassium sparing diuretics. These get rid of both sodium and water. So never give diuretics at nighttime, or past 5 pm. It’s not nice.

What takes care of contractility? Dig. Lowers HR, increases contractility; stronger and slower [pos ionotrope.] Therefore increased volume due to slower HR, and better afterload b/c of contractility. Also works as a diuretic b/c the blood makes it to the kidneys better.
How do I know dig tox: Bradycardia, seeing halos/auras.
Afterload: what causes vasodilation? Pick a beta blocker. HR slow, vasodilation. ACE inhibitors, ARB’s.

Once you have perfusion finally, people have some negative side effects: headaches b/c you finally have blood getting to the brain. The baroreceptors freak out and try to get the BP down quickly to counter the new perfusion that is ‘normal’ but seems ‘too high’ to the baroreceptors.

Teaching; pt takes their pulse at home for 60 sec. This is trickier than it looks. Tell them to hold Dig if HR is less than 60, AND call their doc.

If they are on lasix, they should be getting K+ supplement. The lower your K is this happier your dig is, and out you go in to bradycardia land. How to eat K pills: dissolve them, cut them in half, etc. Daily weight: ½ lb or more means call the doc. Low Na+ diet.

How do I know they are better: pale urine, no edema, pink skin, appetite,

Getting worse: weight gain, cyanotic, low BP, ascites [fluid in abd], splenomegaly or hepatomegaly. VS going south. I/O: a lot in, nothing out means bad.

Do daily weight for HF clients. You don’t need an MD order. Give people their meds, make sure they are on the right meds.

Prognosis of HF: always fatal. Terminal disease when treated. When this guy goes home, he’s not cured, it’s not reversible. He has 5-8 years. What about transplant? Yes it happened for lots of pts. Most pts are older and have complex Hx. And, if you’ve got the cash, you can have a new heart. DM pts have a lot of HF.

Ryan Sanchez age 20 has been admitted to your unit with a diagnosis of chest pain and heart failure. Four weeks ago he had a “cold” with a very sore throat. It was busy at his work and he was unable to take time off. During his cold he had a high fever, red rash on his chest and swelling of his knees. Currently he is scheduled for an echo, VS stable except for a murmur. The night nurse is not sure what kind because she is “not very good at hearing heart murmurs.”

Rheumatic Fever: Sequelae. This is why you treat strep every time without fail.

One sequelae: when the antibodies of the immune system bind to the bacteria, they create ‘immune complexes’ These can attack the renal system [glomerular nephritis], and the mitral/bicuspid valve [on the left side of the heart.] This creates vegetations on the edges of the AV valves, especially the mitral valve, called “aschoff bodies.” Aschcoff Bodies are necrotic tissue surrounded by immune cells. The pt had strep and is now being treated for rheumatic fever. Pt thought he had a cold: but he had redness on his chest, swelling of knees. Now in hosp for HF/rheumatic fever.

What else do I want to know: what kind of murmur? He has a ‘grade 2 systolic murmur.’ We expect to hear murmur at the “money/mitral” position. Grading of murmurs means how loud: the grade 2 is pretty obvious, grade 4 you can hear at Bedside w/o stethoscope. Grade 2 is a trademark of rheumatic fever.

Labs to confirm rheumatic fever:

an ASO titer [antistreptolysin]—shows body reactivity to strep,

These say you have an infection: A SED rate [erythro sedification rate] and positive ‘C reactive protein’; these lab values just check for inflammation.

There is no reason to do a rapid strep test, b/c that infection is over, but it will ikely show Group A strep.

Cardiac enzymes elevated in severe carditis

So why does this guy have HF at 20?

Rheumatic fever hit a lot of people when we didn’t have PCN, and they would have valve replacements.

Things we want to know: What kind of heart failure? What’s his Hx of chest pain: is it resting or during activity, how new is the symptom? I/O, VS, his weight. How long has he been so sick, his diet, general health status, where does he work?

First thing I do in the room: vitals, if he’s experiencing chest pain. Right now.

Never take chest pain lightly.

How to rule out the heart in chest pain: give them Maalox to r/o GI, take deep breaths b/c pain on inhalation might be more lung than heart, etc.

Mitral valve means L side, water backing up into lungs.

He’ll come back from echo w/ positive for Ashcoff’s bodies: and he’ll get a valve replacement. Pretty much the only treatment.

Risks of replacement: endocarditis, infection/rejection [prophylactic antibiotics], etc. Clot formation: so coumadin, etc.

Meds: 10 day course of PCN to drop the strep, plus IM injection of PCN prophylaxis over several years. Pain meds/ anti inflamatories.

Nursie does: teaching about sequelae, how to prevent strep. How to handle carditis [surgery.] Interventions, teaching for pain and activity intolerance for the meantime.

Mrs. Wayans arrives to the outpatient surgery center for her second cataract surgery. While starting her IV she complains of chest pain. She tells you she has a history of angina. What are your first assessments? Interventions?

Questions to ask: what quality of pain, when, 0/10. “Do you take nitro, do you have it with you?” If yes, tell her to eat one. Also give her oxygen. Oxygen is mainstay of treatment for chest pain. I care about her vital signs, b/c the NTG opens all her arteries, and her BP drops.

Angina: caused by too much schmoo in the he-arteries, or heart spasms. The pain is caused by tissue crying out for O2, and there’s not enough blood coming thru the heart-eries.

Call primary care: let them know what’s up.

There is a fine line that says you cannot prompt her to eat her PRN med—b/c that’s not our med to serve her—it’s not a med that the outpatient center has orders for.

Question is: can she have her surgery today? We won’t. She’s not worried about the pain, but we are.

We need to be sure that at home, she is having good results w/ her NTG.

People w/ stable angina can take up to 3 NTG, but first they have to sit down. If they have oxygen at home, they need to put it on. You need to decrease O2 demand of the heart by resting, and supplement O2. beta blockers and calcium channel blockers [vasodilators, HR slow] can help mellow the heart’s demands as well. Then they take a Nitro, wait 15 mins, take another PRN, wait another 15, take a 3^rd, if that doesn’t work, CALL. Anyone else w/ chest pain that isn’t stable angina should get to the ED.

We send her home, but she is still at risk for MI. So you still want to remind/teach her the S&S of MI, and how to decrease O2 demands at home.

Does diet matter? Yes: we don’t need any more schmoo in the arteries. Mild exercise.

Beta blockers lead to impotence. Sex is still important to grampa and grama, so it needs to be talked about. Ca+ channel blockers don’t cause impotence.

Patho: DM day notes

2008-02-19T11:15:00.000-08:00

Stuff about why we care about DM:

35-45% of hosp pts are DM. sometimes they are under the care of an ortho doc who doesn’t know their shit on DM. unfortunately Dr. Ortho writes the MAR instead of using the Rx’es from the pt’s home. Sometimes you have a smart hospitalist or dietitican to manage their insulin orders.
DM rates jumped 30% in the last some odd years.
People die daily from DM, either their mismanagement or our mismanagement. Type 2 is truly manageable. DM pts are doing their best managing their DM—don’t mislabel them as noncompliant.
How does insulin work normally? [AP review]: BS of 70-110. Insulin comes out of my pancreas when there’s lots of glucose in my blood after meals or after glucagon [which lets out stored sugar from my liver.] My blood sugar should always be between 70 and 110, whether I just ate or not!
What happens when I’ve got the flu [w/o DM] and I’m not eating, and I run out of sugar stores b/c I don’t want to eat? You break down fats next, and you build up ketones, which makes your breath smell like juicy fruit.
If you have a Diabetic’s diseased kidney, and you put it in a relatively healthy person, it will heal the tissue.
“I have never seen anything other than U100 insulin.”

Case: Mr. Bertucchi age 50, has just been transferred from the ED to MS. Hi FSBS [fingerstick bloodsugar] is 388 and the ED nurse reports insulin was given. His VS were 37.7-88-22 148/78. He is A & O times one. Skin warm and dry, says he needs some water [polydypsia] and is squirming around in bed. His daughter is at his bedside.

He has the following orders:

Sliding Scale insulin with Lispro ac and hs

Rocephin 1 Gm every 24 hours IVPF

Dressing change to foot BID

Culture to open wound ASAP

What’s missing: When was insulin given, what was the FSBS before that, how much insulin was given. Admitting Dx. What’s his K+ level? [normal would be= 3.5-5] Where’s his wound, and why did I have to look in the orders to find it? Why is he squirming? How old is this daughter and is it appropriate she’s here? What’s his normal mentation if he’s AOx1. How long has he had DM? How is his DM managed at home?

What’s his I/O, what kind of fluids is he on? [let’s hope it’s NS]

What’s up with him? HHS: Hyperosmotic Hyperglycemic State [non-ketotic]. Hyperglycemic meaning: too much glucose and no insulin, and no fat breakdown. The glucose is in the blood causing hyperosmotic [high solute; chunky] blood, which draws in fluid from tissue. So your body is dumping as much fluid into the veins as possible, and the sugar ain’t going no where. The kidney then recognizes too much fluid in the body, so that kidney secretes Aldosterone to diurese the body. Hence, polyuria, polydipsia, and polyphagia. The reason his LOC is down: b/c he has all this sugar but his brain is starving for sugar.

He doesn’t need insulin at home—he uses oral meds. [wait, how do I know that?] Type 1 DM means your beta cells are fried—you’ll never get insulin out of them—but this man does get some insulin.

How did he spike this sugar? The infection spiked his sugar over the edge. How: The body wants lots of food/fuel to fight the infection—the liver is spitting out glucose like nuts to fight the infection. The metabolic needs of the inflammatory response require all that sugar—but the body cannot produce quite enough insulin to manage a body thru that infection process. His oral meds also cannot deal with this much glucose overwhelm.

Moral of the story: type 2 non-insulin dependent DM pt got a bug, spiked his sugar levels and got HHS.

How bad is a BS of 388? 388 is that bad—‘175’ is “ok” for a diabetic. Don’t let pts or RN’s tell you that “300 is their normal”—that’s not ok. BS at that level over time causes all the nasty DM toe-cutting-off-stuff.

IV insulin: if it’s in an IV it had better be “regular”, and if anyone is on IV insulin, get them to the ICU. They need FSBS Q 1 hr, and that’s ICU type care.

Lispro: is appropriate for him. It’s fast acting. Like humalog.

Fast acting: Lispro, Humalog

Short Acting: Regular

Moderate: NPH

Long: Lantus

Things to know when giving insulin:

onset
peak
duration
Make a light sine wave in pts FSBS; keep their BS’s steady. DO NOT let a pt’s FSBS bounce from too low to too high: it causes major complications.
If giving fast acting insulin, make sure the tray is in their hands; too many things happen with trays.
If the tray isn’t there, get them graham crackers and milk instead of orange juice. Otherwise you spike their sugar. Deb doesn’t like the OJ, even when it’s ordered for low BS
Never mix with lantus. Other stuff can be mixed. It’s a good idea because you can moderate their effects over time and keep FSBS steady.
Sliding scales: MD’s like the “noah’s ark” routine w/ sliding scales: always multiples of 2. MD’s pick their ‘favorite flavor’ of sliding scale, instead of customizing it to the pt. You can always take a few extra FSBS to track their responses. Call the doc with a request for a better scale—make your proposal.
If the pt’s FSBS is off the scale: there is no order for what’s outside the range—you have to call the doc. If someone’s ass is out past 400, try to get that insulin in them via their MD order or the local hospitalist or whoever w/in 30 mins.
Don’t hold food: the secret w/ most health issues is consistency: same meals, same times, etc.
Post-prandial BS: after the insulin; only some doctors order this. They are a clever way to track body response to insulin, and whether or not the insulin orders are suitable.
Rescue remedies for low BS: glucose gel subling, D50 IV, injection of glucagon [like seizing], orange juice is often the order but Deb doesn’t like that much.
Why do HHS and DKA pts drop in K+. These crises, the K+ goes to where: it is diluted in the excess fluid volume, and it is peed out with the hyperosmolar state of the blood. Life threatening arrhythmias like V Tach can show up.

Case: Amy age16, has just been admitted to your unit for a full work-up. She has recently experienced weight loss, fatigue, poor grades and complains of constant hunger. Her symptoms began suddenly. Her FBS was 425 and her urine was positive for ketones. She has no family history of DM. Her mother is at her bedside.

What’s happening: She is Type 1 sudden onset, in ketoacidosis.

What else might you see: juicy fruit breath, low potassium [K+], low bicarbonate, high CO2; kussmal breathing to blow off CO2.

First step: get that blood sugar down; she has no insulin of her own.

How did she get it: either virus, auto immune, trauma, “idiopathic” [we dunno.]

When does onset occur: Deb has seen it as early as 8mo, usually before 30.

What does onset look like before it gets ugly; tiredness, etc.

How do we want to get her FSBS down; IV drip regular and put her in ICU. On drip insulin, there should be a finger stick Q 1 hr, insulin will be adjusted accordingly.

Tell mommy about DM, tell her about DM…when she’s stable. Under 20 yrs old, DM is forgiving; and she will not have complications yet.

Give her fluids for dehydration; NS: a bolus; like 2000 cc’s wide open.

Once her BS is down, start DM education—leave them alone until they are out of crisis.

Let’s imagine our girl is now at 40 FSBS: first step is: stop insulin. Now! Bolus of D50. Document, call the MD. LOC: probably not too good. Assess skin; might be diaphoretic. She might be in seizure: insulin shock/hypoglycemic shock—there’s no FSBS at which people start seizing: everyone’s brain conks out at different points. Seizure happens b/c the brain is starving. The low hurts more than the 400+ high! People can feel just dandy at 400 FSBS.

She is a candidate for insulin pump: why? She is Type 1, she is clever enough to use it and understand her diabetes. They are filled w/ lispro usually, they work like a PCA: a basal drip rate and an on demand button. Stays in place for about a week.

Just because you’re Type 1 DM doesn’t mean that you can’t eat sugar any more; you just have to increase the insulin and be vigilant.

Your type 2 DM pts need to be more cautious w/ food b/c: they have desensitized cells and their oral meds ain’t that hot.

Why Weight loss? Diabetes affects the way your body uses blood sugar. Even when you eat as much as usual, you may lose weight if your muscle tissues don't get enough glucose to generate growth and energy. This is especially true with type 1 diabetes, in which very little sugar gets into your cells. With uncontrolled diabetes, sugar lost in the urine may also contribute to weight loss.
Labs: The A1c test evaluates the average amount of glucose in the blood over the last 2 to 3 months. It does this by measuring the concentration of glycosylated hemoglobin. As glucose circulates in the blood, some of it spontaneously binds to hemoglobin A (the primary form of hemoglobin in adults). Hemoglobin is a red protein that carries oxygen in the red blood cells (RBCs)). Once the glucose is bound to the hemoglobin A, it remains there for the life of the red blood cell (about 120 days). The more glucose that is in the blood, the more that binds to hemoglobin A. This combination of glucose and hemoglobin A is called A1c (or hemoglobin A1c or glycohemoglobin). A1c levels do not change quickly but will shift as older RBCs die and younger ones take their place.

John Faust, age 57, is one day post THA [replacement]. John has been a Type II diabetic for 5 years well controlled with meds and diet. Last night and this morning his FSBS has been 330 and 278 respectively. John is very upset when you arrive with his insulin.

Why is he pissed? B/c he doesn’t take insulin at home…and if you’re given insulin it means you’re getting sicker. Why does he need the insulin? B/c of the stress of surg and stress of pain, etc.
What screwed up his blood sugars so much? The surgery, which puts stresson the body. Why does stress whack you out? Bc glucocorticoids are released during stress: they are ‘gluco’ therefore they jack up the FSBS.
He says, “ok, I won’t eat.” This will not help him b/c he needs the food to help his healing, and the glucocorticoids are still being made. He needs the insulin and the food.
What do we tell him? We need to give you insulin temporarily to get you thru this stress phase, your body is still producing glucocorticoids and we need to keep up with them.

Complications:

DM is top cause of Renal Failure

QOF is decreased with moderate compliance

Complications can still show up with high compliance and tightly reigned FSBS.

CAD, atherosclerosis, HTN, neuropathy, blindness, amputations. Amputation and blindness

Psych Exam Study Guide with my book notes

2008-02-19T11:13:00.000-08:00

Here it is: it is a work in progress. I will keep updating.

PMH study guide, Exam 1

Chapter 1

Significance of National Mental Health Act of 1946 to nursing: page 9

Consequence of WW2: men disqualified from service b/c of mental instability, men returning from war w/ nuttiness. 1946, Truman signs act. Act started the 6 member mental health advisory panel [now the NIMH], supported research, training, and devel of clinics and treatment centers. The money: Hill-Burton act for hosp building, and bigger psych wards. Clinics popped up everywhere. Also created grants for fellowships for specially trained psych nurses. First grad-level RN program at Rutgers, developed by H Peplau. There are still many grad programs in psych RNing.

PMH nursing’s unique influence on development of nursing in general: Peplau’s work developed concept of therapeutic relationship, the value of interpersonal relationships, RN’s self as a healing tool, and creating the RN as separate from the MD hierarchy.

Chapter 2

Mental disorders are classified as clusters of symptoms with many likely causes, not by their origins like pathophysiology.

DSM–IV-TR: the dictionary of classifying MI’s. Provides criteria for diagnosis but without perfect boundaries btwn disorders.

Drawbacks: Some people think that diagnosis leads to labeling and makes pts into their illness rather than a whole person with treatable diagnoses. This is bullshit: doctors of all sorts treat patients as their diseases and not as people; psych docs aren’t unique. The DSM-4 is also a list of western disorders, and does not contain other culture specific disorders.

Multiaxial Diagnosis: DSM4 Dx critera are based on 5 axes:

Clinical disorder: focus of psych clinical attention
Personality disorders and Mental Retardation
General medical conditions: physical conditions
PsychSoc/environmental problems
Overall functioning in social, psych, and professional areas. Uses the GAF [global assessment functioning] Scale. Scored from low [0-10] to high [90-100.]

Contribution of epidemiology to understanding MI: epidemiology meaning ‘how prevalent is the disorder.’ Examine associations of disorder with the region of study [Marin: highest breast cancer rates], rather than etiology. CDC tracks this data.

“Rate”: proportion of cases compared to the total pop.
“prevalence”: total # of people w/ disorder in pop
‘Point prevalence’: # of people in pop at a certain time.
‘Incidence’: rate of only new cases in a defined time period.

Contribution is: helps understand the distribution of an illness. Helps with EBP. Knowing how this book harps on stigma, epidemiology probably helps remind people that these diseases can happen to anyone. Don’t hate!

Characteristics of MI diagnoses

Is that a part of this chapter? Things I know about MI Dx’es: they are usually wrong, if you put 5 MD’s together on one case they claim 5 different diagnoses between them. Few patients actually present ‘textbook’ symptoms, therefore no patient quite fits the mold, and often pt’s have multiple diagnoses in order to cover ‘all the bases’ of the symptoms they present. Just because we have the diagnosis doesn’t mean the treatment fits perfectly either: it’s not like staph and antibiotics. Also, several diagnoses have the same ‘symptom lists’ so one person may fit well under several diagnoses. It’s not exactly science.

Chapter 4 (accidently left this chapter off the list of chapters for exam 1 in syllabus)

Tx options for those with MI:

· Continuum of care: various options for treatment, varied treatment levels

· Least restrictive enviro: avoids enabling, creates enviro for pt independence

· Coordination of Care: what a case manager might do: to refer pt to the best care facilities/treatments, to create individualized plan

· Case management: care coordinator or team, meets w/ patient and other providers, works as a ‘broker’

· RN as case mgr: this actually requires the RN to have a lot of training.

· Crisis intervention: 6 hour short term intervention to stabilize pt. Found in ER of hospitals or psych hospitals. RNs must be expert in these settings: meds are usually administered to ‘bring down’ the patient. RNs also make referrals to other care providers

Where pts go to get care:

· 23 hour observation: Admits pts to inpatient setting [hosp] for 23 hours for rapid stabilization, but not ‘acute care.’ The problem is a major deviation from normal that is expected to improve fast; like drug induced psychosis, acute trauma from rape, or psych pts that stop taking their meds.

· Crisis stabilization: where you go if 23 hour observation didn’t fix you. Less than 7 days of treatment for ‘symptom management,’ coordination of after-care.

· Acute inpatient care: most intensive, and most restrictive intervention. You have to be so sick that: you will harm self or others, unable to care for basic needs. Where; in psych hosp, in psych unit of hosp, or state mental hospital. Admit is voluntary or involuntary. LOS is usually 24 hrs to a couple days if involuntary, if voluntary they will keep you based on degrees of symptoms and ability to pay. You are discharged when: you are non violent and can manage your needs w/ help of willing/able family/friends.

· Partial hospitalization [PHP’s: partial hosp programs]: a response to better outcomes in terms of price/benefit of outpatient care. Day hosp service; you go home at night. Intensive therapy, highly structured. Who goes: you have acute symptoms and decline in self care, but not a threat to self or others. Provide therapy and training for ADL’s.

· Residential services: rehab and therapy for people w/ chronic and serious MI. Treatment lasts from 24 hours to 6 months to several years. Some have more staffing than others: ‘intensive residential services.’ Funding for these programs is very tricky. Serves education, psych therapy, and training in ADL’s.

· Respite residential care: gives the family who tend to an MI pt a vacation: for short-term care.

· In-Home MH care: best cost/benefit option is always to have MI pts live at home. This is the alternative if outpatient care doesn’t work out. Case mgr and RN care help avoid hospital time and increase pt independence. RN needs to assess and create plan of care, ensure med compliance and lab tests, coordination of services.

· Outpatient care: often the step down from inpatient care. You need less than in home care, or residential care. Offers med management, ADL training, therapy/counseling, case management.

· Intensive outpatient programs: pt goes back to normal life, this is in place to prevent relapse. Few hours per day, few days per week: focus on med and stress management rather than social skills.

· Supportive employment: getting people w/ chronic MI, especially retardation, jobs. Job coaches get the pt the job and teach them on-site.

· Outpatient detox: most drug/ETOH rehab is now outpatient, except for those pts with need for severe withdrawal treatment needs or complicated Hx [seizure, pregnancy, etc.] Initially a 24 hour bed may be provided, follwed by 4-5 day/week rehab program until fully rehabbed. Uses the 12 step model of AA.

· In home detox: RN visits for the first week sober to assess and ensure med compliance.

· Assertive community Tx [ACT]: 24 hour services to allow serious MI pts live in the community, and prevent costly hospital visits. Provide 24 hour emergency hotlines, mobile treatment, and other services to help re-integration of severly ill pts.

· Psych Rehab programs: put people back into workforce and community with access to therapy and training in ADL’s and social skills. Promote high function with minimal intervention.

· Clubhouse Model: Run by MI pts. Offer ‘membership’ and ‘belonging’ and daytime support and opportunities for paid work. Pts are voluntary members and are expected to contribute to the household. Not a place to sleep usually. People start with work training around the clubhouse and move on to connect with outside part-time employment, and then competitive employment.

· Relapse prevention after-care: prevents re-hospitalization. Teaches family and pt about illness, coping, warning symptoms, etc.

· Technology based care: talk to the psych RN through your phone or computer [telemedicine] because you live way out in the boonies where there are no care facilities.

Alternative housing: places for the homeless, 40% of whom have severe MI, and pts who cannot be cared for by willing/able family. RNs are usually not involved with these services, but may do referrals or visit these settings for in-home treatment:

· Personal Care Homes: 6-10 pts with 24 hour supervision, assistance with meals, meds, ADL’s, transportation.

· Board-and-Care-Homes: 24 hour supervision, assistance with meals, meds, not so much self-care/ADL skills. 50-150 pts. Shared rooms: 4-6 people per room.

· Therapeutic foster care: for children and adults. Placement in family situation, where family members are trained for MI situations. Family provides structure and supervision. Pt is an active member of the family, may attend outpatient care during the day.

· Supervised apartments: pts live in their own apartments alone or with 1 flatmate. Staff stop by as little or as much as needed to ensure med compliance, self-care, etc.

Chapter 6

2 – differences between the various major forms of psychosocial interventions

A “duh” question

Knowledge of basic Peplau theory

Knowledge of Carl Roger’s approach

Psychodynamic theories: study of unconscious

Psychoanalytic: Freud’s

Conscious vs unconscious
Personality made of: id [primitive/selfish], ego [contact w/ reality, cognition, defense], superego [manages looking good inside of culture]
Object relations: obsessions and imitations of mommy, daddy, etc.
Anxiety and ‘defense mechanisms’: protecting what our attachments and object relations
Sexuality: libido lives inside the id. Sexuality is the end product of devel into adulthood
Psychoanalysis: couch session to change personality
“transference:” projecting mommy/daddy onto therapist. “countertransference;” therapist projects onto patient.

Neo-Freudians:

Adler: freud’s student, theory: we avoid feeling inferior
Jung: analytical psych. Concepts of persona, and introvert/extroverted people
Karen Horney: intro to fem psych—women are not sad about their substandard genitalia; it’s not penis envy. Stated that women’s angst stemmed from submissive cultural position/male dominated culture.
Otto Rank: student of freud. Stated primary source of pain was from pain of birth, underscored devel as freedom from need of mother, then from society, and that “will” is the primary goal of human devel
Fromm: Sociological interaction focused. Bring harmony btwn indiv and society
Klein: play therapy to reveal early childhood fears and desires. “early identity: meaning early object relations.”
Harry Stack Sullivan: your health is derived from interpersonal relations; how well you play w/ others

Humanistic Theories: all about the goodness of the human, develop worth, positive outlook on life

Carl Rogers client-centered therapy, Gestalt, and Maslow

Rogers: empathy w/ client via indirect non judgemental questioning
Gestalt: modern world makes people nuts; remind them of their drives and needs via indiv and group actions like catharsis, etc
Maslow’s: used to prioritize and needs

Behavioral theories: forget why you act so weird, let’s define “normal behavior”

Pavlov: dog and food and bell. Classical conditioning
Watson and “behaviorists”: “frequency vs recency,” likelihood of responses is increased by how often [frequent] or how recently the stim is responded to. No separation btwn mind/body

Reinforcement Theories

Thorndike: Our problem solving/learning is through trial and error: we maintain the ‘winning formula’ after it works a few times.
BF Skinner: respondent vs operational: respondent is like Pavlov, operant is like Thorndike

Cognitive theories: getting into thinking processes

Al bandura: Social Cognitive Theory: we learn by mimicry, modeling. Disinhibition means changing one modeled behavior based on the model of another, new person.
Aaron Beck: distorted viewpoints are the basis for depression—poor cognition makes disappointment.

Developmental theories:

Erikson: 8 stages w/ different conflicts and resolutions to be ‘met:’
Stages Infancy • Childhood • Preadolescence • Adolescence • Adulthood - Early adulthood • Middle adulthood • Late adulthood

Erikson also contributed: theory of turbulent teenage-dom, identity formation, identity crisis.

Jean Piaget: Learning in children; cognition devel in children. Applied to psych RNing: you can identify what cognitive level a client is at, which cognitive skills, as defined by Piaget, the client can perform
Carol Gilligan: gender differentiation. Boys’ development cognitively and socially vs girls’. Points out that devel theories that underscore detachment as the highest goal leave feminine bonding tendencies out of the loop of ‘successful.’
Jean Baker Miller: connection/bonding patterns of females again.

Social theories

Family Dynamics: the psychology of each family member has its influence on the otehrs’--little research on these
Balance Theory and Social Distance [litwak]: about caregiving in social groups. “formal support systems:” hospitals, etc. “Informal support system”=fam, friends, neighbors. People w/o informal support are found to have more accidental deaths and suicides. Social distance means how different are the group’s values from the dominant culture’s values—how much ‘outsiders’ are they? [The notion includes all differences such as social class, race/ethnicity or sexuality, but also the fact that the different groups do not mix.-- wikipedia]

Role Theories:

“role” meaning a person’s position or function inside an environment. In psych, we’re talking about the person’s role being in conflict with the ‘self’ or the ‘id.’

Sociocultural Perspectives:

Margaret Mead: culture and gender: are gender behaviors ‘nature’ or ‘nuture’? She puts her money on ‘nuture.’
Madeline Leininger: Transcultural Nursing. Caring and thereby nursing care are different between cultures.

Nursing Theories:

Interpersonal models:

Hildegard Peplau: a nursing theorist who…emphasized the nurse-client relationship as the foundation of nursing practice. At the time, her research and emphasis on the give-and-take of nurse-client relationships was seen by many as revolutionary. Peplau went on to form an interpersonal model emphasizing the need for a partnership between nurse and client as opposed to the client passively receiving treatment. Empathic linkage=empathy, self-system=lends framework of anxiety
Ida Jean Orlando: dynamic-RN-pt-relationship. Focuses on the needs of the pt, the rxns of the RN, and any factor that is inhibiting the pts’ needs being met. Pt distress is about inability to have their needs met.

Existential and Humanistic Theories

Joyce Travelbee: RNs helping pts find ‘meaning’ in their situation. Defined concepts of ‘suffering’ and ‘hope’
Jean Watson: all about caring as the essence of Nursing.
Imogene King: defines RNing as caring for the pt, creating goals and navigating the challenges. Addresses systems theories.
Dorothea Orem: self-care focused: self-care, self-care-deficit. Meaning self-care in pts when healthy and the need for RNs when not so healthy.

Chapter 7

Basic psychoneuroimmunology

Neurotransmitter-related activity

Chapter 8

SE’s of benzos

2 - Physiological responses to drugs

3 - SE’s of antipsychotics

Implications for psychotropic use in elderly

Phases of drug therapy

Complications with lithium

2 - Complications with antidepressants

Chapter 9

5 - Therapeutic communication

Defense mechanisms

2 - Self awareness

Chapter 10

Phases of a therapeutic relationship

Communication to enhance assessment

Outcome indicators

Chapter 11

Cognitive triad

CBT

SFBT

bibliotherapy

Chapter 17

Suicide: successfully killing oneself. 11^th leading cause of death.
Suicidality: all suicide related behaviors and thoughts
Suicidal ideation: thinking about and planning one’s own death
Suicide attempt: well, it didn’t work. Women make 3x the attempts that men do. Estimated 5% of all US pop have attempted. 20% of men and 40% of women die by suicide within a year of their 1^st suicide attempt; it is one of the best predictors for suicide. Adolescents also make more attempts than adults.
Parasuicide: voluntary apparent attempt at suicide, in which the real aim is not death. “Faking it” for reasons of sending a message or numbing out for a time. More common in younger age groups.
Lethality: probability that the person will complete the suicide; a combo of the person’s commitment and the chosen method.

Assessing and intervening with suicidal ideation and intent

Assessing:

Goals: identify ideation, determine the severity of the intent, what the suicide plan is, and assess pt access to the means to the end.
Assess: related events that are risk factors [loss, divorce, etc], warning behaviors [recklessness, giving things away, getting affairs in order legally and interpersonally]. Assess ETOH and drug consumption recently.
Assess pt access to overdose-able drugs and firearms.
Once you know the pt plan, assess its lethality.

Document: this is the time to cover your ass. It also helps provide a trail of breadcrumbs in the ‘continuum of care.’

Intervention:

RN intervention: We no longer hospitalize patients; only if the patient is acute. Don’t leave the pt for a second, until the interventions are started. Later RN role is to coach patients with coping skills and find resources.
Meds: antidepressants are used to raise serotonin and avert suicide risk: prozac, Zoloft, Paxil, Wellbutrin, Effexor, Celexa, Lexapro.
ECT: for pts w/ severe depression and suicidality that cannot be treated otherwise.
Therapy: to reverse negative thinking about oneself
No-suicide contract: to not kill yourself, and to get help when you need it. Dismantling of the plan happens: guns and meds are locked away, etc. Not a decent intervention with high risk pts [previous attempts, etc.] Not as effective for isolated pts: they need to be with family or friends.
Commitment to treatment statement: like a no-suicide contract, but the pt commits to living and going through the treatment course. Getting access to guns, etc, away from the patient is a ‘priority commitment.’ Family needs to be involved in enforcing the course of treatment including meds.
Create a plan for what the pt will do when they start considering suicide again
Psychoeducation: the pt and family learn more about the underlying MI and the precipitating thoughts and behaviors.
Social skills training
Develop support networks: family, friends, and support groups need to be identified to support the pt through recovery, so that no one person is burdened. Choose a MH professional who the pt can call when things get too difficult.
Reduce feelings of stigma

Risk factors: MI, esp depression, is top of the list.

Vulnerability: close family member suicide, MI, previous attempt, Loss [deaths, job, divorce], chronic illness

Risk: white man, elderly man, adolescent man, LGB sexual orientation, access to gun

Intent: plan and means to execute it

Dis-inhibition: drugs/ETOH, impulsivity, isolation, psychotic thoughts

Antidepressants and suicide

Meds: antidepressants are used to raise serotonin and avert suicide risk: prozac, Zoloft, Paxil, Wellbutrin, Effexor, Celexa, Lexapro.

Advance directives

Also known as a: Commitment to treatment statement: like a no-suicide contract, but the pt commits to living and going through the treatment course. Getting access to guns, etc, away from the patient is a ‘priority commitment.’ Family needs to be involved in enforcing the course of treatment including meds.

Chapter 20

Interventions for clients with mania

Mania: abnormal and elevated, expansive, or irritable mood for at least 1 week.

Elevated mood: euphoria, or feeling “high.”

Expansive mood: poor control of emotions: inappropriately expressive, overly enthusiastic about all sorts of things, and thinking oneself is overly important.

Irritable mood: easily annoyed or angered, esp when they cannot get what they want

Lability of mood: a tendency of mania to oscillate between irritable and euphoric

Intervention:

Need interdisciplinary treatment
Safety for the pt: mania can cause recklessness and delusion. Both physical and fiscal safety.
Help out the family
Pt forgets their needs: food, water, rest.
Monitor and encourage adequate sleep cycles: pts need to report lack of sleep which can be a precursor to manic episode.
Meds: lithium, depakote, tegretol, zyprexa, risperdal are all ‘mood stabilizers.’

Acute phase: In acute illness these are combined with antipsychotics to bring down major symptoms, otherwise they are increased gradually.
Continuum phase: Therapy continues under close supervision, maintenance: then independently.
Discontinuation: Prophylaxis with mood stabilizers are recommended lifelong to prevent acute symptoms.

Pt ed with lithium: most used mood stabilizer. But not usually adequate alone—needs to be in a cocktail—especially during acute phase. Lots of side effects, and narrowest therapeutic range. Because it is a salt, it is sensitive to sodium levels in the body: the more sodium you have the worse the lithium works. Similarly, lithium effects/side effects increase without enough fluid volume. African Americans are more at risk for these sodium-related sensitivities. Start dose low and slow and increase slowly due to narrow therapeutic range. If signs of toxicity: get a blood sample, push fluids, call the MD. Moderate tox= 1.5-2.5, high tox= >2.5 mEq/L. Pt ed: no ETOH or drugs [CNS depressants]. Pregnancy/breastfeeding risks. Avoid driving. Do not abruptly discontinue.

2 -Timeline of and assessing antidepressant effectiveness

“Duh”

1 extra credit

Psych week 3 class notes

2008-02-19T11:11:00.002-08:00

This wasn't the most rewarding class:

Class notes week 3

Stepson who had turrets and other junk:

Turrets is a tick disorder that can be a word or a gesture: like pawing the ground with a foot, and whinnying like a horse. Had religious delusions, spoke in tongues, etc.

How to start with the client: give autonomy: “would this be a good time to talk?”

They say yes, you say:

“like shit”

“things always get worse before they get better” [stereotypical ]

“I’ve never known the cops to bring in someone just for raising their voice” [sounds accusatory, but it’s actually grounding the pt in accessing what really happened]

Confrontation: “I find you really offensive when you keep using the word bitch” [about the RN, also confrontational.]

How to deal if pt is asking personal questions: redirect to person, “we’re here to talk about you, so would you tell me a bit about your relationships?” Sometimes ok in the beginning to give a little information to build repore, but not after that.

Posture: open and attentive. Paranoid pts: don’t use direct eye contact with these pts. Be careful about intent conversations with some pts.

Neutral, caring tone of voice. Detached concern: don’t be absorbed by the suffering in the other. Soothing, calm rather than upbeat or jovial.

Schizoaffective: elements of mood disorders, and some elements of schizophrenia, less acute than schizophrenia alone.

Differences of Social and Therapeutic Convo:

Social Therapeutic

2 way 1 way

2 way focus 1 way focus

2 way goals 1 way goal.

Casual professional

Non-confidential confidential

Psych day 1 class notes

2008-02-19T11:11:00.001-08:00

Ways we respond to deviant behavior:

Want to comfort ourselves: joking around

Might become afraid we also have the disease

A lot of students jump into the counseling centers here on campus

Diagnoses help w:

Labels serve us to feel comfortable and like symptoms are explained. They allow us to make prognoses and treatment plans. Helps w/ research.

www.nami.org or www.mami.org

No where is stigma more obvious than in mental illness.

The new asylums: a film we get. In march. We’ve come back to the 13^th century in how we treat mental illness: we put people in jail b/c they get better treatment than they do in the community.

This is the #1 disability in western countries, but you don’t see a “bonkers fundraising marathon”

How diagnosis works: Axis format w/ a person.

5 routes/axes:

Axis 1: clinical disorder, mental illness groups

Axis 2: personality disorders, mental retardation

Diff btwn these 2: they are more ‘developmental’ apparent in early devel: usually seem to show up in childhood/be inborn. Axis 1 can be more treatable.

Axis 3: medical conditions

Axis 4: psych/soc and environmental. Stressors/events.

Axis 5: GAF: global assessment of functioning: and we mean ADL’s and stuff like Freeman’s clients being “high functioning” The other axes add up to these abilities

This is all subjective, on scale from 0 to 100.

Let’s say we have mild mental retardation. Lives in a group home, has a global function of 45. How are they functioning now?

Example; hypothyroidism, Mild MR, Bipolar 1; GAF last year 45; GAF today 15; Fighting w/ members of group home

So these sort out like this:

A1: Bipolar 1

A2: MMR

A3: Hypothyroid

A4: fighting w/ home

A5: GAF’s

Mental health nursing is a lot about empowering the client. No one gets change from therapy unless they’re into it—need buy in. Asking client to help plan care helps with buy in. Taking decisions away don’t motivate anyone.

You need to synthesize your knowledge. We teach psych early b/c we want people to be ready for hosp patients.

What to believe or not to believe from pts? If someone believes they are being followed by the mafia, its really true for them.

Top priorities:
Safety first. To be committed: danger to self, others or unable to meet basic needs.

Clinical will have outpatient hosp: these pts may be involuntarily committed. To be released from an acute psych setting: you have to do whatever the people there tell you do and they’ll let you go. TO be committed you have to be out of ADL’s not for some organic reason; like organic brain damage.

Health: if someone has aids

Water: sometimes pts get dry mouth from meds and overdrink water

Intrapersonal problems: addiction, impulsivity

Interpersonal problems: fights w/ group home members, prob at home, job, etc.

Anxiety is not allowed: hugging the charts and break rooms will be noticed. Don’t fear conversations, you won’t kill anyone. Notice your feelings, stereotyping, reactions. If you’re really nervous about what you’re going to say, don’t say it and start listening. You don’t have to be on stage. Pts want to be listened to.

What if someone wants to share a secret with you? “I’m glad you trust me and that you want to share, and I won’t be able to hold information from your staff.”

Pts have a right to refuse. They have a right to be angry. And tell you to fuck off. We don’t want to have people get so angry that they damage stuff.

Dwell on strengths, not deficits. Play on their strengths.

ACT: means “assertive community treatment”

RNs do most health management on a psych floor.

In long term care fac. do more education than therapy or med admin.

Nurses

psych 2-4 class notes

2008-02-19T11:09:00.001-08:00

Lecture Outline: 2/4/08

Psycho pharm is really important for the boards

Know neurotrasmitters how they work so you can know how the drugs intereact with them

Know the limbic system, the components of it, and what moderates it

The sameness of mental and physical health:

Limbic system: effects hypothalamus which releases NT’s, they come down and do effect the immune system. The pituitary gland effects the adrenals which effect the immune system.

Where does the mental stop and the physical start? The brain allows us to perceive the physical world.

Several genes are involved in a disease. MI’s are categories of symptoms, therefore there are many genes producing symptoms. The genes can be effected by the environment of the cell. Nature/nurture are therefore very close, since genes can be effected by chemical environment, which are changed in response to stimuli.

Population genetics.

Psychobiology

Nature and Nurture interactions in MI

The brain

What it does

Filter, choose reactions, receive and transmit info

Involvement with MI

Sensory distrubances: hallucinations can come in along all 5 senses.

Circadian rhythm disturbances-- SAD: seasonal affective disorder

Psychotropics

How they work?

Had meds since '55. We don't really know quite how they work. It is complex b/c NT's are tricky: there are several types of serotonin, of dopamine, etc.

Psychopharm: sub specialty. These meds do not cure, they only control symptoms. Psychotropics effect cognition, emotion, behavior. They cause side effects b/c they are not target specific to certain synapses.

Psychopharmacology is:

Primary psychotropic neurotransmitters

Primary NT's:

AcH

Serotonin

Epinephrine

Dopamine

histamine

These work either by agonizing or antagonizing--enhance or block.

Therapeutic Index

Therapeutic index: the lowest dose at which drug is effective to the highest dose, at which point the drug becomes toxic. Important for psych meds b/c of the suicide/overdose risk of taking the whole bottle.

Assessing effectiveness of psychotropic: what makes this difficult?

No specific tests to see how much less crazy pt is
polypharmacy
multiple sources of an illness
different sources of a behavior

“Noncompliance”

We don't like this word. We need to have compassion for the reason why people don't take their meds. Complex w/ psychotropic drugs why:

side effects are awful
stigma/shame--denial of the disease
feel better and stop taking meds
noncompliance is part of disease symptoms
confusion
homelessness/money/insurance
can’t combine w/ alcohol or recreational drugs, so you have to involve cutting out a person’s habits.

Question: we give freedom but we also take it away—the freedom of authentic expression is taken but the freedom of functioning is given.

Antipsychotics/neuroleptics

Conventional typicals: have more side effects:

Haldol, thorazine [thorazine shuffle-- first psych med we had], prolixin, stelazine, navane. We will still see haldol and prolixin.

Atypicals: We will see more of these: abilify, zyprexa

Abilify: ARIPIPRAZOLE

Classifications: psychotherapeutic; antipsychotic, atypical; dopamine system stabilizer; Therapeutic: atypical antipsychotic
Prototype: Clozapine

Long term injections: see these in ACT program. They have shot clinics. Can cut down on the compliance risks. 3 long acting injections:

decanoate [prolixin/fluphenazine or haldol]
Risperdol

Clozeril: first great anti psychotic drug we got to handle schizophrenia. However, it is dangerous and causes horrible blood dyscrasias, and pts have to get blood testing frequently.

Lots of SE’s (side effects)

Dry mouth
Weight gain
Breast enlargement in men/women, can cause lactation in women
Photosensitivity
Water intoxication [r/t drymouth]
Sexual dysfunction
DM is a risk factor with atypicals

EPSs:

· Oculogyric crisis

· Torticollis

· Dystonia

· Psedo-parkinsonism: shuffling, tremors

· Apathesia [constant movement]

Tardive dyskinesia

Mood Stablizers

Antidepressants

Classes:

SSRIs

SNRIs

NDRI

Alpha 2 Antagonists

SARI

TCA’s

MAOIs

SEs

Anxiolytics

January 31, 2008

Battle Concussions Tied to Stress Disorder

By BENEDICT CAREY

About one in six combat troops returning from Iraq have suffered at least one concussion in the war, injuries that, while temporary, could heighten their risk of developing post-traumatic stress disorder, researchers are reporting.

The study, in The New England Journal of Medicine, is the military’s first large-scale effort to gauge the effect of mild head injuries — concussions, many of them from roadside blasts — that some experts worry may be causing a host of undiagnosed neurological deficiencies.

The new report found that soldiers who had concussions were more likely than those with other injuries to report a variety of physical and mental symptoms in their first months back home, including headaches, poor sleep and balance problems. But they were also at higher risk for the stress disorder, or PTSD, and that accounted for most of the difference in complaints, the researchers concluded. Symptoms of the disorder include irritability, sleep problems and flashbacks.

Experts cautioned that the study had not been designed to detect subtle changes in mental performance, like slips in concentration or short-term memory, that might have developed in the wake of a concussion and might be unrelated to stress reactions. Many returning veterans are still struggling with those problems, which can linger for months.

The findings are in line with previous research linking concussions to post-traumatic stress disorder that develops after frightening events outside a military context, like car accidents; concussions from athletic collisions rarely lead to the disorder.

“This study is a very good first step, and an important one, but like any first step it should lead us to ask further questions about these injuries,” said Brian Levine, a neuropsychologist at the Rotman Research Institute and the University of Toronto, who was not involved in the study.

Now that the prevalence of combat concussions is better known, Dr. Levine said, the next step should be to assess troops’ cognitive functioning early on and track it over time, before and after combat.

In the study, military psychiatrists had 2,525 soldiers from two Army infantry brigades fill out questionnaires asking about missed workdays and dozens of kinds of physical and emotional difficulties, including symptoms of PTSD. The soldiers had been back home from Iraq for three to four months.

The questionnaires also asked about concussions and their severity. A concussion is an injury from a blow or shock to the head that causes temporary confusion or loss of consciousness, without any visible brain damage. The investigators found that 384 of the soldiers, or 15 percent, reported at least one concussion. One-third of that 15 percent had blacked out when injured.

The severity of the concussion was related to the risk of developing the stress disorder, the survey showed. Nearly 44 percent of the soldiers who had blacked out qualified for the diagnosis, about three times the rate found in soldiers with other injuries. Among soldiers who did not black out, the rate of PTSD was 27 percent, significantly higher than the 16 percent rate among veterans with other kinds of injuries.

“There’s a lot we don’t know about these injuries, but we do know that context is important,” said the lead author, Dr. Charles W. Hoge, director of the division of psychiatry and neuroscience at the Walter Reed Army Institute of Research. “Being in combat, you’re going to be in a physiologically heightened state already. Now imagine a blast that knocks you unconscious — an extremely close call on your own life, and maybe your buddy went down. So you’ve got the trauma, and maybe the effect of the concussion is to make it worse.”

In an editorial that accompanied the study, Richard A. Bryant, a psychologist at the University of New South Wales in Australia, emphasized that concussed troops “should not be led to believe that they have a brain injury that will result in permanent damage.”

On the contrary, Dr. Bryant and other experts say, the link to post-traumatic stress suggests that mild brain injuries have a significant psychological component, which can improve with treatment.

Paul Rieckhoff, executive director of Iraq and Afghanistan Veterans of America, said the study, and the interest of doctors and military officials in brain trauma, were long overdue.

Autobiography in Five Chapters

1) I walk down the street.  There is a deep hole in the sidewalk

I fall in.  I am lost…I am hopeless  It isn't my fault.  It takes forever to find a way out.

2) I walk down the same street.

There is a deep hole in the sidewalk.

I pretend I don't see it.  I fall in again.  I can't believe I'm in the same place.  Bit it isn't my fault.  I still takes a long time to get out.

3) I walk down the same street.  There is a deep hole in the sidewalk

I see it is there.  I still fall…it's a habit  My eyes are open.  I know where I am.  It is my fault.  I get out immediately

4) I walk down the same street.

There is a deep hole in the sidewalk.  I walk around it.

5) I walk down another street.

Portia Nelson

Julie's Exam 3 Prototype List

2007-12-05T15:42:00.000-08:00

My strategy for this exam is to group the adverse effects in such a way that I have less to memorize. For instance, all the anti-HIV drugs cause either convulsion or seizure, and the "bad bad" drugs all either cause hypoglycemia, bleeding, or MI. The antibiotics have a list of 5 adverse effects which overlap between the drugs, and I could find a form of anemia with all the anti-inflamatory drugs. So, on my list, the adverse in bold is the one I've picked to memorize, based on categorization.
I found even more differences between the pharma book and the RN drug guide in doing this, and have taken out certain of the adverse effects that Margi listed, I assume they come from the pharma book. We need to know:

Indication for use
Mechanism of action
One adverse effect

For each drug. And because our exam is 3 parts for 39 drugs, and a total of 25 questions, that means each wrong answer is only0.21 points. Yee Haw!

Exam: what’s on it: a list of the drugs, with generic and brand name

Indication for use, Mechanism of action, 1 adverse.

From nutrition and electrolytes: Micro K, potassium and Calcium Carbonate

Resp: benadryl, robitussin DM [x2], alupent, singulair, vanceril, nedocromil

Cancer: cytoxan, neupogen, procrit.

Anti inflame: asprin, motrin, celebrex, toradol, zyloprim, amoxicillin, ancef, zithromax, vibramycin, garamycin, levoquin, bactrim, INH, diflucan, acyclovere,

Anti virals AZT, sustiva, cholestra, varicella

Bad bad drugs: heparin, warfarin, potassium, insulin [each kind onset/peak/duration: 4 types Regular, NPH, novalog, lantis], morphine

NUTRITION AND ELECTROLYTES

Micro K

Use: Correct potassium deficit: strengthen cardiac and muscle contraction. Pts at risk for hypokalemia: People on potassium wasting diuretics, loops, thiazides, etc. [HTN and CHF’ers.] Vit K is also given as the antidote for coumadin overdose.

Action: Transmits and conducts nerve impulses, contracts all 3 muscle types

Adverse: life threatening: dysrhythmias, resp distress, cardiac arrest.

Calcium Carbonate

Use: Hyperacidity as in acid indigestion, calcium supplement

Adverse: Hypercalcemia with alkalosis, hyperkalemia, metastatic calcinosis, hypercalciuria,

RESPIRATORY AGENTS

Diphenhydramine (Benadryl)

Action: compete with histamine for H₁ receptor sites, prevent histamine (allergic) response.

Use: allergic rhinitis, itching, sleep aid, antitussive

Adverse effects: agranulocytosis, hemolytic anemia, thrombocytopenia [not for long term]

Antitussives [anti-cough]

Dextromethorphan Hydrobromide (Robitussin DM)

Action: suppress cough reflex by inhibiting cough control center in medulla; reduces viscosity of tenacious/stringy secretions.

Use: Temporary relief of cough spasms in nonproductive coughs due to colds, pertussis, and influenza.

Contraindications: COPD, chronic productive cough

Adverse effects: cardiovascular collapse, hallucinations, CNS depression with very large doses

Expectorants

Guaifenesin (Robitussin, Mucinex)

Action: Enhances reflex outflow of respiratory tract fluids by irritation of gastric mucosa. [yes, gastric mucosa] Comes from the Guiac tree which also is used for Stool Guiac Tests.

Use: loosen mucus: Aids in expectoration by reducing adhesiveness and surface tension of secretions.

Contraindications: Cough due to CHF, ACE inhibitor therapy, or tobacco smoking.

Adverse effects: none. Nausea and dizziness, the end.

Metaproterenol (Alupent)

Use: bronchodilator

Action: Stimulates adrenergic beta 2 receptors: causing bronchodilation, relaxation of smooth muscles of bronchi.

Adverse effects: tremors, tachycardia, dysrhythmias, cardiac arrest, paradoxical bronchoconstriction.

Montelukast ( Singulair)

Not for: acute asthma attack; used for prophylaxis and maintenance

Action: Leukotriene Receptor Antagonist; interrupts smooth muscle contraction/bronchoconstriction

adverse effects: none known!

Beclomethasone (Vanceril) inhaler

Type: glucocorticoid, long acting

Use: for Rx of asthma, COPD, allergies

Action: suppresses inflammation and adrenal function

Adverse: with excessive doses: symptoms of hypercorticism, hyperglycemia

Mast Cell Stabilizer

Nedocromil: inhaler

Use: Don’t use for acute asthma attack. prophylaxis of bronchial asthma; inhibits histamine release; maintenance.

Action: antiinflammatory; mast cell stabilizer: Inhibits activation of and mediators released from inflammatory cells (e.g., neutrophils, mast cells, monocytes).

Adverse: none

CANCER DRUGS

Alkylating agent prototype: Cyclophosphamide (Cytoxan): Nitrogen Mustard

Uses: breast, lung, ovarian cancers; Hodgkin’s disease; leukemias; lymphomas

Action: inhibits protein synthesis through interference with DNA replication

Adverse effects: bone marrow depression [leukopenia, anemia, thrombocytopenia] cardiotoxicity, sterility, hepatotoxicity. Causes tissue necrosis if it infiltrates. Immunosuppresant. toxic epidermal necrolysis, Stevens-Johnson syndrome

Filgrastim (Neupogen)

Action: increases neutrophils

Use: to prevent post-treatment infections

Life threatening Adverse effects: MI, thrombocytopenia. Adverse: Neutropenia, dyspnea, hematuria.

D. Epoeitin Alfa (Erythropoietin) (Procrit)

1. Action: stimulates RBC production in bone marrow

Life threatening adverse effects: MI, CVA, Adverse: Seizures, hyperkalemia, HTN

ANTI-INFLAMATORY DRUGS

B. Prototype: Aspirin:

Use: analgesic, antipyretic, prevention of platelet aggregation, and anti-inflammatory

Action: by inhibiting prostaglandin synthesis, inhibiting hypothalamic heat-regulating center

adverse reactions: hemolytic anemia, ulceration, thrombocytopenia; anaphylaxis if hypersensitive: bronchospasm

Ketoralac: [Toradol]

Use: Exhibits analgesic, antiinflammatory, and antipyretic activity. Effective in controlling acute post-operative pain, Short-term management of pain;

Action: It inhibits synthesis of prostaglandins by inhibiting both COX-1 and COX-2 enzymes

Adverse: hemorrhage, severe renal and hepatic impact; should only be used short term.

Prototype: Celebrex (Celecoxib)

Use; analgesic, nsaid; cyclooxygenase-2 (cox-2 but not cox-1) inhibitor; antiinflammatory;

Action: Although an NSAID, unlike ibuprofen celecoxib inhibits prostaglandin synthesis by inhibiting cyclooxygenase-2 (COX-2, not COX-1)

Adverse: Increased risk of cardiovascular events.

Ibuprofen (Motrin)

Class: NSAID, cox-1 and cox-2 inhibitor; analgesic, antipyretic

Action: reduce inflammation and fever by inhibiting prostaglandin synthesis

Adverse reactions: aplastic anemia, toxic hepatitis, nephrotoxicity, GI bleeding, blood dyscrasias, cardiac dysrhythmias,

Antigout Drug

Allopurinol (Zyloprim)

1. action: reduces uric acid synthesis

Use: Antigout

2. caution with renal and hepatic disease

3. adverse effects: bone marrow disorders, Hepatotoxicity, Agranulocytosis, aplastic anemia, [drug guide doesn’t cite eye disorders]

ANTI-INFECTIVE DRUGS

Penicillin Prototype: Amoxicillin (Amoxil)

Use: Good for both gram negative and gram positive infections. Who gets it: kids with ear infections, UTI’s, etc.

action: inhibits enzyme in cell wall synthesis, bactericidal

adverse reaction: blood dyscrasias, anaphylaxis/respiratory distress

Cephalosporins

Cezazolin (Ancef), 1st generation

Use: Preop prophylaxis, UTI, bone, joint, soft tissue infections, bacteremia.

Action: Inhibits cell wall synthesis, destroys cell

adverse reactions: seizure, anaphylaxis

A. Macrolides: azithromycin (Zithromax)

Use: gm-positive and some gm-negative, with clients allergic to PCN, respiratory infections, gonorrhea

Action: inhibits steps of protein synthesis, bactiostatic or cidal

Adverse reaction: hepatoxicity

Doxycycline (Vibramycin)

Use: treat infections by uncommon bacteria

Action: inhibits steps of protein synthesis, cidal or static

Adverse: blood dyscrasias, hepatoxicity, CNS toxicity

Aminoglycosides:

Gentamicin (Garamycin)

Action: inhibits bacterial synthesis, cidal effect

Use: serious infections from gram-negative bacteria, PID, MRSA

Adverse: nephrotoxicity, liver damage [hepatomegaly]

D. Fluoroquinolones: Levofloxacin (Levaquin)

Action: interferes with DNA enzyme, cidal effect

Use: lower respiratory tract, renal, bone, joint infections

Adverse: seizures, dysrhythmias, encephalopathy, [drug guide says ‘none’]

Sulfonamides: May potentiate sulfonylurea-induced hypoglycemia

Co-trimoxazole/tmp-smz (Bactrim): combination of sulfamethoxazole (SMZ), a sulfonamide, and trimethoprim (TMP)

Use: complex UTI, bronchitis, PCP [Pneumocystis carinii pneumonitis: most common death in AIDS patients], burns.

Action: inhibits protein synthesis, cidal effect

Adverse: renal failure, bone marrow disorders,

Anti-tubercular agents:

Isoniazid (INH)

Action: inhibits cell-wall synthesis

Use: TB treatment and prophylaxis

Adverse: blood dyscrasias, hepatoxicity

Antifungal Drugs

2. Prototype: Fluconazole (Diflucan)

Use: treat Candida infections and meningitis

Action: increases permeability of cell membrane

Adverse: No adverse [really.] Cautious use with renal/hepatic impaired pts or AIDS pts.

A. Non-HIV Anti-Viral Prototype: Acyclovir sodium (Zovirax)

Use: treat HSV-2 and HSV-2 [Herpes]

Action: interferes with viral DNA synthesis

Adverse: nephrotoxicity/acute renal failure, seizures, bone marrow depression

ANTIVIRAL DRUGS

Zidovudine (AZT) first HIV drug developed in the 80’s. Used for post-exposure prophylaxis and maintenance.

Use: HIV infected clients and prevention of maternal-fetal HIV transmission

Action: inhibits viral enzyme transcriptase: being incorporated into growing DNA chains by viral reverse transcriptase, thereby terminating viral replication.

Adverse: anemia, seizures, neutropenia [bone marrow impact] [Drug guide: Bone marrow depression, granulocytopenia, anemia]

Efavirenz (Sustiva)

use: treat HIV-1 infections with other anti-retroviral agents—used in a cocktail

action: binds to reverse transcriptase—halts RNA change to DNA, blocks enzyme activity and HIV-1 replication

adverse: [drug guide: Stevens-Johnson syndrome, toxic epidermal necrolysis] allergic, convulsions, liver failure, suicide

caution: history of mental illness, drug abuse

Protease Inhibitors: Lopinavir/Ritonavir (Kalestra)

Use: treatment of HIV-I infections with other agents

Action: inhibits protease, prevents production of mature HIV particles

Adverse: hyperglycemia, DM,[convulsions, paralysis, palpitations, tach]

C. Prototype: Varicella (Varivax)

Use: prevention of chickenpox

Action: stimulates active immunity against natural disease

Adverse: anaphylaxis, thrombocytopenia, Stevens-Johnson syndrome [skin rash]

BAD BAD DRUGS:

INSULINS

Humalog (Lispro): Rapid acting

Onset: <15>

Peak: 0.5-1hr

Duration: 3-4hr

Adverse: Hypoglycemic Coma

Regular:

Short acting, only insulin given IV

Onset: 0.5-1hr

Peak: 2-4hr

Duration: 5-7hr

Adverse: Hypoglycemic Coma

NPH: [Insulin Isophane]

Intermediate acting

Onset: 1-2hr

Peak: 4-12hr

Duration: 18-24hr

Adverse: Hypoglycemic Coma

Lantus: [Insulin Glargine]

Long duration

Onset: 3-4hr

Peak: Unknown

Duration: 10-24hr

Adverse: Hypoglycemia, hypokalemia.

Morphine Sulfate

Use: severe acute and chronic pain, pre-op med, support anesthesia, resp distress

Action: narcotic opiate agonist

Adverse: cardiac arrest, resp. depression

Potassium Chloride

Use: potassium replacement

Action: intracellular cation, important for cardiac rhythm regulation

Adverse: very narrow therapeutic range, easy to become hyperkalemic and have dysrhythmias or hypokalemic and have cardiac arrest

Heparin

Use: venous thrombosis, pulmonary embolism, thrombolitic complications

Action: inhibits fibrin formation, inactivates clotting factors

Adverse: spontaneous bleeding, bronchospasm, anaphylactoid reactions

Coumadin

Use: DVT, pulmonary embolism, TIA, prophylactic for cardiac valves

Action: inhibits hepatic synthesis of vitamin K, decreases clotting factors in veins

Adverse: bleeding, nothing fatal until overdosage

Ali's Exam 3 Drug list

2007-12-05T11:48:00.000-08:00

Below are links to Ali's drug list, both in Word and Excel.

Word File
http://docs.google.com/Doc?id=dgc7bfbt_18zm99xt

Excel File

http://spreadsheets.google.com/pub?key=pa-GnAC_jJcOU-bSjv25GUg

This is what Ali says:
Hi Everyone- here is a quick matrix I made for the drugs for mondays final - Its a draft- feel free to add or subtract if there are adverse effects that you remember more. I grabbed adv. effects for some off the drugs website as well as the Nurses Drug guide- some they may be different from the text. enjoy

Barbara's Exam 3 drugs

2007-12-05T11:34:00.000-08:00

Unfortunately, this document typically has much better formatting than Blogger is allowing. Thanks Barbara!

NUTRITION & ELECTROLYTES

Micro K Use: correct potassium deficit, strengthen cardiac muscle contraction
Action: transmits and conducts nerve impulses, contracts muscle
Adverse: dysrhythmia, respiratory distress, cardiac arrest

Calcium Use: treat tetany, spasms, convulsions
Carbonate Action: calcium supplement for hypo/hypercalcemia
Adverse: hypercalcemia

CANCER AGENTS

Cytoxan Use: breast, lung, ovarian cancers; Hodgkins disease; leukemias; lympohomas
Action: alkylating agent: inhibits protein synthesis through interference with DNA replication
Adverse: bone marrow depression, leucopenia, thrombocytopenia, cardiotoxicity, hepatotoxicity

Neupogen Use: decrease length of post-cancer neutropenia; permit delivery of higher doses of chemotherapy; prevent severe thrombocytopenia with chemotherapy
Action: stimulates growth and differentiation of bone marrow stem cells
Adverse: tachycardia, pallor, confusion, thrombocytopenia

Procrit Erythropoietin
Use: anemia
Action: stimulates RBC production in bone marrow
Adverse: HTN, chest pain, injection site reaction, CVA, MI

RESPIRATORY AGENTS

Benadryl Antihistamine (1st generation)
Use: allergic rhinitis, itching, sleep aid, antitussive
Action: prevents allergic response
Adverse: agranulocytosis, hemolytic anemia, thrombocytopenia

Robitussin Antitussive and expectorant
DM Use: temporary relief of non productive coughs
Action: suppresses cough reflex by inhibiting cough control center in medulla, reduces viscosity of tenacious/stringy secretions
Adverse: hallucinations, CNS depression with very large doses

Alupent Sympathomimetic - tablet or inhaler
Use: asthma, bronchitis, emphysema (COPD)
Action: beta 2 agonist, bronchodilator
Adverse: dysrhythmias, HTN, cardiac arrest, paradoxical bronchoconstriction

Singulaire Leukotriene receptor antagonist:
Use: prophylaxis and maintenance of asthma. Not for acute attacks.
Action: interrupts bronchoconstriction
Adverse: none

Vanceril Glucocorticoid, long acting steroid
Use: inhaler for acute asthma attack COPD, allergies.
Action: suppresses inflammation and
Adverse: symptoms of hypercortism with large doses, HTN, hyperglycemia

Nedrocromil Mast cell stabilizer, inhaler
Use: prophylaxis and maintenance of bronchial asthma
Action: inhibits inflammation (histamine release)
Adverse: none

ANTIINFLAMMATORY AGENTS (NSAIDS)

Aspirin Use: dull pain in headache, cramps; acts on PNS pain receptor sites
Action: analgesic, antipyretic, antiplatelet, anti-inflammatory. Inhibits prostaglandin synthesis, inhibits heat-regulating center es
Adverse: tinnitus, ulceration, agranulocytosis, bronchospasm, thrombocytopenia, GI upset and bleeding

Toradol Use: analgesic, anti-inflammatory, antipyretic. Controls acute post-op pain. 5x as strong as morphine, should only be used short term.
Action: peripherally acting analgesic, inhibits prostaglandin synthesis by acting on Cox-1 and Cox-2 enzymes
Adverse: hemorrhage

Celebrex: Use: analgesic, Cox-2 inhibitor, doesn’t act on Cox-1; anti-inflammatory
Action: inhibits prostaglandin synthesis by inhibiting Cox-2
Adverse: Increased risk of cardiovascular events

Motrin: Use: reduce inflammation and fever
Action: inhibits prostaglandin synthesis, inhibits both Cox-1 and Cox-2
Adverse: GI bleeding, blood dyscrasias, cardiac dysrhythmias, nephrotoxicity

ANTIGOUT AGENTS

Zyloprim Use: antigout
Action: reduces uric acid synthesis
Adverse: retinopathy, cataracts, bone marrow disorders

ANTIBACTERIALS

Amoxil Peniclillin
Use: gram- and gram+ infections; ear infections, UTIs, etc.
Action: inhibits cell wall synthesis, bacterialcidal
Adverse: superinfections, blood dyscrasias, respiratory distress

Ancef Cephalosporin
Use: preop prophylaxis, UTI, bone, joint, soft tissue infections, bacteremia
Action: inhibits cell wall synthesis, destroys cell
Adverse: superinfections, seizures, anaphylaxis

Zithromax Macrolide
Use: gram+ and some gram- ; patients allergic to PCN; respiratory infections, gonorrhea
Action: inhibits protein synthesis; bacteriostatic/cidal
Adverse: superinfections, hepatotoxicity

Vibramycin Tetracycline
Use: treat uncommon bacterial infections
Action: inhibits protein synthesis; bacteriostatic/cidal
Adverse: blood dyscrasias, hepatotoxicity, CNS toxicity

Garamycin Aminoglycoside
Use: serious infections from gram- bacteria, PID, MRSA
Action: inhibits bacterial synthesis; bacteriocidal
Adverse: oliguria, superinfection, ototoxicity, nephrotoxicity, liver damage

Levoquin Fluoroquinolone
Use: lower respiratory tract, renal, bone, joint infections
Action: interferes with DNA enzyme, bacteriocidal
Adverse: encephalopathy, seizures, dysrhythmias

Bactrim Sulfonamide
Use: complex UTI, bronchitis, PCP (pneumonitis, most common cause of death in AIDS patients), burns
Action: inhibits protein synthesis, bacteriocidal
Adverse: bone marrow disorders, renal failure

ANTITUBURCULAR AGENTS

INH Use: TB treatment and prophylaxis
Action: Inhibits cell wall synthesis
Adverse: blood dyscrasias, hepatotoxicity

ANTIFUNGAL AGENTS

Diflucan Use: treat candida infections and meningitis
Action: Increases permeability of cell membrane
Adverse: none

ANTIVIRAL NON-HIV DRUGS

Zovirax Acyclovir
Use: treat HSV-2 (herpes simplex virus)
Action: Interferes with viral DNA synthesis
Adverse: nephrotoxicity, bone marrow depression, renal failure

HIV DRUGS

AZT Use: HIV infected clients and prevention of maternal-fetal HIV
Action: inhibits viral enzyme transcription
Adverse: anemia, seizures and convulsions

Sustiva Use: non nucleoside to use w/other antiretroviral agents
Action: binds to reverse transcriptase, blocks enzyme activity
Adverse: allergic rxn, convulsions, liver failure

Kalestra Use: treatment with other agent
Action: protease inhibitor
Adverse: hyperglycemia

VACCINE

Varivax Use: prevention of chicken pox
Action: stimulates active immunity against natural disease
Adverse: anaphylaxis, thrombocytopenia

MEDICAL ERROR DRUGS

INSULIN Humalog (Lispro): Rapid acting
Onset: <15 min
Peak: 0.5-1hr
Duration: 3-4hr

Regular: Short acting, only insulin given IV
Onset: 0.5-1hr
Peak: 2-4hr
Duration: 5-7hr

NPH: Intermediate acting
Onset: 1-2hr
Peak: 4-12hr
Duration: 18-24hr

Lantus: long duration
Onset: 3-4hr
Duration: 10-24hr

MORPHINE SULFATE
Use: severe acute and chronic pain, pre-op med, support anesthesia, relief of dyspnea of acute L ventricular failure and pulmonary edema and pain of MI
Action: narcotic opiate agonist
Adverse: cardiac arrest, resp. depression

HEPARIN Use: venous thrombosis, pulmonary embolism, thrombolitic complications
Action: inhibits fibrin formation, inactivates clotting factors
Adverse: bleeding, hemorrhage, hypotension

COUMADIN Use: DVT, pulmonary embolism, TIA, prophylactic for cardiac valves
Action: inhibits hepatic synthesis of vitamin K, decreases clotting factors in veins
Adverse: bleeding

KCL Use: potassium replacement
Action: intracellular cation, important for cardiac rhythm regulation
Adverse: very narrow therapeutic range, easy to become hyperkalemic and have dysrhythmias or hypokalemic and have cardiac arrest

Immunologic agents

2007-12-04T09:15:00.001-08:00

Evaluate on 203 website after today

N203 IMMUNOLOGIC AGENTS

Objectives: Upon completion of this class, the student will be able to:

1. describe the life cycle of HIV;

2. list the four classifications of antiretroviral therapy;

3. discuss the prototypes of HIV and AIDS drugs

4. discuss post-exposure prophylaxis for health care workers;

5. describe a prototype vaccine administered to adults;

6. discuss how to apply the nursing process to safe administration of these drugs.

Immune response: Inflammation, Cell mediated response [T-Cells] à leukocytes, antibody mediated [B cells]. Innate vs acquired immunity. Acquired: antibody mediated, natural/artificial

What screws up our immune system; certain meds, age, malnutrition, stress, chronic illness. And HIV.

I. HIV, AIDS

A. Pathology:

B. Lab and diagnostic tests

C. HAART:

D. Life cycle of HIV:

CD4 receptors are on T helper cells and also macrophages.

II. Antiretroviral therapy

A. Goals:

1. Suppress viral replication to slow decline in number of CD4 cells

2. Suppress viral replication to undetectable levels

3. Reduce incidence and severity of opportunistic infections [keep your t cells around]

4. Minimize adverse effects of antiretroviral therapy [lots of people can’t tolerate AZT—too many side effects; like chemotherapy]

5. Improve quality of life

6. Improve survival and reduce morbidity

B. Classes

1. Nucleoside analogues: act by inhibiting HIV reverse transcriptase so reduce viral replication

2. Nonnucleoside analogues: act by inhibiting HIV reverse transcriptase so reduce viral replication

3. Protease inhibitors: block protease, so suppress production of infectious virions in infected cell populations

4. Fusion inhibitors: bind to viral particles and prevent adhesion to CD4 cells

5. HAART: standard of care to treat HIV infection [highly active antiretroviral therapy= means combination therapy with more than one drug]

These drugs are rough on the liver

Zidovudine (AZT) first HIV drug developed in the 80’s. Used for post-exposure prophylaxis and maintenance.

• use: HIV infected clients and prevention of maternal-fetal HIV transmission

• action: inhibits viral enzyme transcriptase: being incorporated into growing DNA chains by viral reverse transcriptase, thereby terminating viral replication.

• adverse: anemia, seizures, neutropenia [bone marrow impact] [Drug guide: Bone marrow depression, granulocytopenia, anemia]

Efavirenz (Sustiva)

• use: treat HIV-1 infections with other anti-retroviral agents—used in a cocktail

• action: binds to reverse transcriptase—halts RNA change to DNA, blocks enzyme activity and HIV-1 replication

• adverse: [drug guide: Stevens-Johnson syndrome, toxic epidermal necrolysis] allergic,

convulsions, liver failure, suicide

• caution: history of mental illness, drug abuse

Protease Inhibitors: Lopinavir/Ritonavir (Kalestra)

• use: treatment of HIV-I infections with other agents

• action: inhibits protease, prevents production of mature HIV particles

• adverse: hyperglycemia, DM,[convulsions, paralysis, palpitations, tach]

Protease inhibitors changed AIDS into a chronic, not fatal disease.

D. Nursing process

Assess: signs of infection, quality of GI function, T Cell count [on CBC], liver panel, adverse reactions, what Rx’es do they have, where are their meds, how to make the schedule work?

Nursing Diagnoses: risk for infection, altered nutrition, knowledge deficit, inadequate thermal regulation, interrupted family process, pain, anxiety, fear,

E. Postexposure prophylaxis

III. VACCINES

20 infectious diseases that are preventable with vaccines.

A. Immunity

1. active

2. passive

B. Immunizations

1. childhood

2. adult

3. travel

C. Prototype: Varicella (Varivax)

1. use: prevention of chickenpox

2. action: stimulates active immunity against natural disease

3. adverse: anaphylaxis, thrombocytopenia, Stevens-Johnson syndrome [skin rash]

D. Nursing process

Pharma Exam

2007-12-04T09:14:00.000-08:00

Exam: what’s on it: a list of the drugs, with generic and brand name

Indication for use, Mechanism of action, 1 adverse.

From nutrition and electrolytes: Micro K, potassium and Calcium Carbonate

Resp: benadryl, robitussin DM [x2], alupent, singulair, vanceril, nedocromil

Cancer: cytoxan, neupogen, procrit.

Anti inflame: asprin, motrin, celebrex, toradol, zyloprim, amoxicillin, ancef, zithromax, vibramycin, garamycin, levoquin, bactrim, INH, diflucan, acyclovere,

Anti virals AZT, sustiva, cholestra, varicella

Bad bad drugs: heparin, warfarin, potassium, insulin [each kind onset/peak/duration: 4 types Regular, NPH, novalog, lantis], morphine

Bad Bad Drugs

2007-11-26T20:27:00.000-08:00

Bad Bad Drugs: Drugs we love to make errors with:

Margi says these will show up on the final exam. Just because they are bad bad.

Heparin: comes in 1000, 5000, 100, 10000 units/ml.

Insulin: Several kinds and several patients on insulin. We need to know forever the onset, peak, and duration of the different insulins. It’s actually hard to kill people with insulin, but you can certainly harm people.

Morphine Sulfate: IV, PO, IM, SubQ.

KCl: this is a good way to kill people.

Coumadin: fussy and amplified with other protein bound drugs. Always always check PT/INR.

Nursing students make the most errors with Insulin.

Anti Inflammatory and Anti Infective Agents

2007-11-26T20:25:00.000-08:00

N203 ANTI-INFLAMMATORY AND ANTI-INFECTIVE

AGENTS

Objectives: Upon completion of this class, the student will be able to:

1. identify the five cardinal signs of inflammation;

2. describe the action, indication for use, and potential adverse effects of aspirin

and ibuprofen NSAIDs;

3. describe Gold as the prototype for anti-arthritis;

4. describe allopurinol as the prototype for antigout;

5. explain the mechanisms of action, general adverse effects of antibacterial

drugs;

6. describe the prototypes of each type of antibacterial agents;

7. describe the prototypes of antitubercular drugs, antifungal drugs, and

metronidazole;

8. describe the prototypes of antiviral drugs and urinary antiinfectives;

9. discuss the nursing process with safe administration of these agents.

I. INFLAMMATION

A. Characteristics: cardinal signs; what are they?

B. How can it be prevented?

Inflammation: [heat, redness, swelling, edema, pain, all lead to ‘loss of function’]. Response to tissue injury. Lead to removal of dead cells. Want to stop it when: inappropriate inflammation or chronic painful inflammation. Always means you’re suppressing the immune system: risk for infection.

Tissue damage: arachadonic acid is released from tissue cells, that wakes up the prostaglandins and leukotrienes, and those stimulate nociceptors.

II. ANTIINFLAMMATORY AGENTS

A. How do they work?

B. Prototype: Aspirin:

action: analgesic, antipyretic, prevention of platelet aggregation, and anti-inflammatory by inhibiting prostaglandin synthesis, inhibiting hypothalamic heat-regulating center

caution with renal or hepatic disorders

adverse reactions: tinnitus, ulceration, agranulocytosis, bronchospasm,

thrombocytopenia;

C. Nonnonarcotic Analgesics: NSAIDs: non-steroidal antiinflamatory drugs are things like OTC pain killers: Ibuprofen, naproxen, etc. Good for dull throbbing pain like inflam, headaches, cramps. Act on PNS at pain receptor sites.

NSAIDS: irritate GI, take on full stomach. Reduce inflammation

COX 1&2 inhibitors:

COX-2 inhibitors: “Cyclooxidase-2”. These block the 2 and not the 1—which means less GI upset and GI bleeding.

Ketoralac: [Toradol]

Non-steroid, but severe renal and hepatic impact; should only be used short term. This is about 5x as strong as morphine—it inhibits prostaglandins.

Action: It inhibits synthesis of prostaglandins by inhibiting both COX-1 and COX-2 enzymes. Is a peripherally acting analgesic.

Use: Exhibits analgesic, antiinflammatory, and antipyretic activity. Effective in controlling acute post-operative pain, Short-term management of pain;

Adverse: hemorrhage

Prototype: Celebrex (Celecoxib)

Use; analgesic, nsaid; cyclooxygenase-2 (cox-2 but not cox-1) inhibitor; antiinflammatory;

Action: Although an NSAID, unlike ibuprofen celecoxib inhibits prostaglandin synthesis by inhibiting cyclooxygenase-2 (COX-2)

Adverse: Increased risk of cardiovascular events.

2. Ibuprofen (Motrin)

Class: nsaid, cox-1 and cox-2 inhibitor; analgesic, antipyretic

Action: reduce inflammation and fever by inhibiting prostaglandin synthesis

Caution with bleeding disorders, early pregnancy, SLE

Adverse reactions: GI bleeding, blood dyscrasias, cardiac dysrhythmias,

nephrotoxicity

III. ANTIRHEUMATIC DRUGS

A. NSAIDs

B. Immunosuppressive agents

C. Immunomodulators

D. Chrysotherapy (heavy metal therapy)

2. No longer a prototype: Auranofin (Ridaura)

1. use/action: symptom relief, prevent deformities, depresses migration of

leukocytes, suppresses prostaglandin activity

Contraindication: patients with colitis, SLE, hemorrhagic conditions, renal or

hepatic disorders, HTN, CHF, DM, pregnancy

Adverse reactions: nephrotoxicity, hematuria, thrombocytopenia

IV. ANTIGOUT DRUG

Anti-Gout Drugs: gout is uric acid in the joints that causes burning sensation.

A. Prototype: allopurinol (Zyloprim)

1. action: reduces uric acid synthesis

Use: Antigout

2. caution with renal and hepatic disease

3. adverse effects: retinopathy, cataracts, bone marrow disorders

IV. ANTIBACTERIAL DRUGS

A. Mode of action

Either bacteriostatic [prevent multiplication] or bacteriocidal [destroy pathogenic cells]

1. inhibit bacterial cell wall synthesis

2. alter membrane permeability

3. inhibit protein synthesis

4. inhibit synthesis of bacterial RNA and DNA

5. interfere with metabolism within bacterial cell

Modes of action: need to know in general how these drugs work. Some are both types, depending on the dose.

B. Body defenses

1. nutrition

2. age

3. immunoglobulins

4. WBCs

5. organ function

6. circulation

C. Resistance to antibacterials

1. MRSA

2. VRE

D. General adverse reactions to antibacterials

1. allergic reactions

2. superinfections: esp fungal, and superinfections are likely when someone has been on antibiotics for more than 1 week.

3. organ toxicity

4. The worst adverse reaction: anaphylactic shock. Lots of people are allergic to penicillin, and that means they are likely to be allergic to cephalosporins. A lot of people are also allergic to sulphanomides.

5. Also heavy renal and hepatic impacts with these.

E. Nursing Responsibilities

Patients w/ infections: maintain skin integrity—when skin breakdown occurs, it is harder to repair in patients with infections.

We don’t culture people’s pneumonia too often any more: RBP says if someone got their illness in the community, it’s probably a gram positive, so we treat them one way until we get back a culture that says to switch meds.

V. PENICILLINS AND CEPHALOSPORINS

Penicillin has been around forever. Unfortunately they’ve been overused.

A. PCN prototype: amoxicillin (Amoxil)

1. contraindication: PCN allergy

Use: Good for both gram negative and gram positive infections. Who gets it: kids with ear infections, UTI’s, etc.

2. action: inhibits enzyme in cell wall synthesis, bactericidal

3. adverse reaction: superinfections, blood dyscrasias, respiratory distress

B. Cephalosporins

1. 1-4 generations: stronger and broader

2. prototype: cezazolin (Ancef), 1st generation

Use: Preop prophylaxis, UTI, bone, joint, soft tissue infections, bacteremia.

Action: Inhibits cell wall synthesis, destroys cell

caution: renal disease and PCN allergy

adverse reactions: superinfections, seizures, anaphylaxis

We prefer to use our ‘little guns’; our 1^st generation antibiotics, before we use our 4^th generation antibiotics.

VI. MACROLIDES, TETRACYCLINES, AMINOGLYCOSIDES,

FLUOROQUINOLONES

A. Macrolides: azithromycin (Zithromax)

1. indication for use: gm-positive and some gm-negative, with clients allergic to

PCN, respiratory infections, gonorrhea

2. action: inhibits steps of protein synthesis, bactiostatic or cidal

3. adverse reaction: superinfections, hepatoxicity

B. Tetracycline: Tetracyclines: Vibramycin: can have more adverse effects. Given when you need to step up the antibiotics b/c you have an uncommon bacteria or unresponsive strain.

Doxycycline (Vibramycin)

1. caution: with alcoholism, hypokalemia, bradycardia

2. action: inhibits steps of protein synthesis, cidal or static

3. use: treat infections by uncommon bacteria

4. adverse: blood dyscrasias, hepatoxicity, CNS toxicity

C. Aminoglycosides: Aminoglycosides: these are super nephrotoxic. Gentamycin. They are for super sepsis situations. There are protocols to check BUN and Creatinine, etc, the pharmacy manages it based on body weight, etc.

Gentamicin (Garamycin)

1. action: inhibits bacterial synthesis, cidal effect

2. use: serious infections from gram-negative bacteria, PID, MRSA

3. adverse: oliguria, superinfection, ototoxicty, nephrotoxicity, liver damage

D. Fluoroquinolones: Levofloxacin (Levaquin)

1. action: interferes with DNA enzyme, cidal effect

2. use: lower respiratory tract, renal, bone, joint infections

3. adverse: encephalopathy, seizures, dysrhythmias

VII. SULFONAMIDES: may potentiate sulfonylurea-induced hypoglycemia

Co-trimoxazole/tmp-smz (Bactrim): combination of sulfamethoxazole (SMZ), a sulfonamide, and trimethoprim (TMP)

A. action: inhibits protein synthesis, cidal effect

B. use: complex UTI, bronchitis, PCP [Pneumocystis carinii pneumonitis most common death in AIDS patients], burns.

C. adverse: bone marrow disorders, renal failure. If you have a diabetic, toxic epidermal necrolysis. hepatitis, stomatitis, crystalluria. megaloblastic anemia, hypoprothrombinemia, allergic myocarditis.

Drug: Coumadin interference: sulpha’s cause clotting

VIII. ANTITUBURCULAR & ANTIFUNGAL AGENTS

A. Anti-tuburcular agents:

1. TB: pathology & symptoms: Symptoms; coughing, hacking, night sweats.

Tuberculosis bacteria and illness is back on the rise due to cramped populations, Russian prisons, highly resistant strains, etc. Combination therapies for 6-24 months is the usual treatment. Not just a lung disease, although mostly a lung disease. Droplet/airborne spread

2. Prototype Isoniazid (INH)

action: inhibits cell-wall synthesis

use: TB treatment and prophylaxis

adverse: blood dyscrasias, hepatoxicity

Nursing Process

B. Antifungal Drugs

1. Causes of fungal infections: Usually fungal infections are super infections; can be focal or systemic.

2. Prototype: Fluconazole (Diflucan)

use: treat candida infections and meningitis

action: increases permeability of cell membrane

adverse: none known, No adverse [really?] but not for renal/hepatic impaired pts. N/V

IX. ANTIVIRAL NON-HIV DRUGS & UTI DRUGS

Viruses are tricky b/c: they’ve already invaded our cells, and don’t do their own metabolism, so they are difficult targets

A. Non-HIV Anti-Viral Prototype: Acyclovir sodium (Zovirax)

1. caution: electrolyte imbalance, children

2. use: treat HSV-2 and HSV-2

3. action: interferes with viral DNA synthesis

4. adverse: nephrotoxicity, bone marrow depression, renal failure

Acyclovere: HSV ½ [herpes] Serious adverse effects: renal, bone marrow, etc.

UTI drugs: UTI symptoms: fever, burning, frequency, discharge, etc. Elderly: confusion—oddly enough old people don’t have the burning sensation but they get altered LOC.

B. UTI Drugs: Nitrofurantoin (Furalan)

1. use: treat acute and chronic UTIs

2. action: inhibits bacterial enzymes and metabolism

3. adverse: superinfection, hepatotoxicity

C. Nursing Process

X. CASE SCENARIOS

A. Migrant laborer with chronic cough, night sweats

Community nursing: migrant worker w/ nightsweats and cough. Think: TB. Get an interpreter, figure out how to get the meds paid for. Test the family and give them prophylactic drugs.

B. 85 yo hospitalized female with MRSA in her sputum

85 yo F w/ MRSA in her sputum. Vancomycin or Gentomycin. Contact precautions, handwashing, etc. Don’t let your RN manager give you this pt and a post op pt in the same rotation.

C. 55 yo with pneumonia

55 yo with pneumonia: assess lung sounds, adequate hydration, sitting up, drugs are good. Supplemental O2.

Fluid in the pleural space: pleural effusion; why Margi couldn’t hear anything in the right base.

D. 74 yo with UTI admitted from SNF

74 yo w/ UTI admitted from a SNF. High risk, elderly, needs antibiotics.

Care Plans

2007-11-25T21:41:00.000-08:00

Spreadsheets for Clinical

2007-11-25T21:15:00.000-08:00

My spreadsheet I use to grab information off the MAR:
http://spreadsheets.google.com/pub?key=pa-GnAC_jJcOSJd8TJvDHEw&output=xls

My sheet for lab tests at clinical, which I never use:http://spreadsheets.google.com/pub?key=pa-GnAC_jJcOB44Mx-_BJGw&output=xls

These are both formatted to allow a 1/2 inch margin for printing; most printers can handle that.

Cancer agents and BRM's

2007-11-25T21:06:00.001-08:00

N203 CANCER AGENTS AND BIOLOGIC RESPONSE MODIFIERS

Upon completion of this class, the student will be able to:

1. Differentiate between cell-cycle specific and cell-cycle nonspecific drugs;

2. Identify general side effects and adverse reactions to chemotherapy agents;

3. State three ways the nurse can prevent absorption of chemotherapeutic agents;

4. Discuss the actions of the biologic response modifiers;

5. List adverse effects of interferons, colony-stimulating factors, and interleukin-2;

6. Describe the nursing process with safe administration of these agents.

I. Cancer

A. Influences on Cancer Development

1. environmental [chemicals, asbestos, radiation]

2. infective [viruses that cause tumors like Epstein Barr and Stomach ulcers, HPV, Herpes, Hep B and C]

3. diet [high fat]

4. genetic [BRCA 1 or BRCA 2 mutation]

“BRCA1 (breast cancer 1, early onset) is a human gene that belongs to a class of genes known as tumor suppressors, which maintains genomic integrity to prevent uncontrolled proliferation. The multifactorial BRCA1 protein product is involved in DNA damage repair, ubiquitination, transcriptional regulation as well as other functions. Variations in the gene have been implicated in a number of hereditary cancers, namely breast, ovarian and prostate. The BRCA1 gene is located on the long (q) arm of chromosome 17 at band 21….BRCA2 (Breast Cancer Type 2 susceptibility protein) is a human gene that is involved in the repair of chromosomal damage and belongs to a class of genes known as tumor suppressor genes. Tumor suppressor genes regulate the cycle of cell division by keeping cells from growing and dividing too rapidly or in an uncontrolled way. Although the structures of the BRCA1 and BRCA2 genes are very different, their functions appear to be similar. The proteins made by both genes are essential for repairing damaged DNA. The BRCA2 protein binds to and regulates the protein produced by the RAD51 gene to fix breaks in DNA. [wikipedia]”

B. Cancer causes: damage to DNA within cell; many mutations required

II. Cancer Drugs; ‘Chemotherapeutics’ aka ‘antineoplastics’

A. Cell-cycle Non Specific: don’t effect the cells during division: they are effective during the “G0” phase or resting phase between divisions…or they act at any time during the cell cycle.

B. Cell-cycle nonspecific: attack cancers when they are dividing, and during a specific phase of division.

C. Chemotherapy: most effective when able to kill cancer cells in all phases of cell cycle. Kills cancerous and normal cells.

1. systemic administration

2. used in conjunction with surgery and radiation

3. guided by protocols from research

4. length of treatment based on type and extent of malignancy, type of chemotherapy, expected side effects, and amount of time normal cells need to recover

5. combination therapy: combine drug types so that the cancer is attacked during all points of the cell cycle; so cycle specific and non-specific drugs are combined. This makes it likely that the effects are synergistic. This also avoids drug resistance by the tumors.

D. Adverse and side effects: hardest on quickly multiplying cells, esp. GI tract, vagina, and mucus membranes.

1. bone marrow suppression: resulting in low RBC, platelet, and WBC counts (anemia and neutropenia) Anemia: high BP, mental confusion/fatigue, high HR, high RR, and little peeing. Neutropenia: susceptible to infections. Thrombocytopenia: bruising, bleeding gums, etc.

2. GI disturbances: Anorexia, N/V, Diarrhea, Mucositis/Stomatitis. N/V caused by chemotherapies that trigger the CTZ, irritation to Gi, and radiation. Diarrhea caused by various effects and injury to the GI tract or infections. Mucositis is direct damage to the rapidly dividing tissues of the GI tract.

3. Alopecia: hair loss or thinning

4. Fatigue: due to stress, chemo, pain, infection, etc

5. Infertility: sometimes from severe radiation of the body—leaving sex cells useless.

E. Alkylating agent prototype: Cyclophosphamide (Cytoxan): Nitrogen Mustard

1. therapeutic uses: breast, lung, ovarian cancers; Hodgkin’s disease; leukemias; lymphomas

2. action: inhibits protein synthesis through interference with DNA replication

3. adverse effects: bone marrow depression [leukopenia, anemia, thrombocytopenia] cardiotoxicity, sterility, hepatotoxicity. Causes tissue necrosis if it infiltrates. Immunosuppresant.

F. Other types:

1. antimetabolites: disrupt metabolic processes and therefore enzyme synthesis. Treat head and neck, leukemia, breast, lung cancers, and non-hodgkin’s lymphoma. Need to give lots of “leukovorin calcium” to counteract effects on healthy cells.

2. antitumor antibiotics: certain antibiotics interfere with RNA and DNA production. Most of these are CCNS.

3. mitotic inhibitors: plant alkyloids that block division at the M cycle, so they are CCS. Made from periwinkle and yew. Periwinkle derivatives can be neurotoxic [they interfere w/ microtubules.] These can all cause common chemo adverse effects.

4. hormonal agents: corticosteroids [slow tumors and inflammation], androgens [testosterone to shink advanced breast cancers] and estrogen [slow the growth of hormone dependent tumors like prostatic and certain breast cancers,] antiestrogens [treats certain breast cancers,] antiandrogens [prostate cancer], etc.

5. liposomal chemotherapy: packages chemotherapeutic agents into synthetic fat globs called liposomes. The coating keeps the drug in the body longer and decreases side effects.

G. Nursing Process

Biologic Response Modifiers (BRMs)

A. Purpose: enhance body’s immune system. Immune proteins and chemicals produced w/ recombinant DNA tech and hybridoma tech [in which mice produce monoclonal antibodies.]

B. Interferons:

What I learned in micro: these are interesting because these are important in limiting virus replication, esp flu, hepatitis, herpes, colds, etc. We thought we could use them for all sorts of stuff, but they are deadly to the patient if over dosed/overused.

Interferons:

1. Use:

2: Action: has antiviral, antiproliferative, and immunomodulatory effects. Inhibits intracellular replication of viral DNA, tumor growth, and enhances natural killer cell activity.

2. Adverse effects: tachycardia, pallor, confusion, thrombocytopenia

C. Colony-stimulating Factors: These are ‘hematopoetic agents’ that manage/promote growth and differentiation of bone marrow stem cells—that create our RBCs, WBCs, etc. Therefore they do not attack tumors, but they do counteract those nasty chemo side effects, like prevent bone marrow suppression. That means greater doses of chemo can be given, aid in healing of suppressed marrow after chemo and transplant, promote immune cells to prevent infections.

1. Uses:

· decrease length of post-cancer treatment neutropenia

· permit delivery of higher doses of chemotherapy

· prevent severe thrombocytopenia with chemotherapy

2. Prototype: Filgrastim (Neupogen)

Action: increases neutrophils

Use: to prevent post-treatment infections

Life threatening Adverse effects: thrombocytopenia, MI

Adverse: Neutropenia, dyspnea, hematuria.

D. Epoeitin Alfa (Erythropoietin) (Procrit)

1. Action: stimulates RBC production in bone marrow

Life threatening adverse effects: CVA, MI

Adverse: Seizures, hyperkalemia, HTN

E. Nursing Process

Hot website: Rn Care Plans by NANDA Dx

2007-11-12T10:30:00.000-08:00

Oh why didn't I find it sooner: a gold mine for my post clinical haze;

http://www1.us.elsevierhealth.com/MERLIN/Gulanick/Constructor/index.cfm

See: big fat list of NANDA Diagnoses, followed by the care plan, and rationales. All done!

Julie Danger

Pharma: Respiratory Agents

2007-11-06T21:00:00.001-08:00

N203 RESPIRATORY AGENTS

Normal Pulmonary Function:

Co2 out, O2 in

Pressure changes, diffusion across membranes, pressure gradients. Compliance: alveoli and airways stretch. Naturally humidified to 100%. Surfactant; decreases surface tension between alveoli—who would rather collapse. Pons and respiratory centers [pons and medulla] in the brain, diaphragm innervated by the phrenic nerve, which respond to baro receptors and chemo receptors [that notice O2, CO2, H2 levels.] Peripheral chemoreceptors: carotid and aortic arch also check chemicals going by. These are responsive especially to O2. Volume: around 500mLs. People post op get atelectasis [collapsed alveoli], pneumonia, etc because it hurts to take a deep breath. Lungs love to get involved when pts come in for any pathology—being still in bed the lungs are likely to get pathological too. Pts lung sounds can change day to day. That’s the “outlier:” a pt who gets complications in the hospital and is there for 3 weeks instead of the 3 day stay for their surgery.

Concerns about using supplemental O2: low O2 is sensed by peripheral chemoreceptors [at aortic arch and carotids] and triggers increased ventilation. Putting a person on supplemental O2 can thereby have the opposite effect of depressing respiration.

Bronchial smooth muscles: are on bronchi and bronchioles, and respond to bronchoconstrictive PNS signals from the vagus nerve, and bronchodilate in response to SNS neurotransmitters [epinephrine.]

II. Drugs for Common Upper Respiratory Disorders

Runny nose: is rhinorrhea or rhinitis due to the common cold or to hayfever.

Pharm treatments for the common cold: antihistamine [H1] blockers, simpathomimetic decongestants, antitussives, and expectorants.

H1 versus H2: There’s H1 and H2—H2 are in the gastric, the H1 are in the upper respiratory. Histamine is an immune inflammatory agent released from the mast cells.

A. Antihistamines

2. Prototype: Diphenhydramine (Benadryl)

Action: compete with histamine for H₁ receptor sites, prevent histamine (allergic) response.

Indication: allergic rhinitis, itching, sleep aid, antitussive

Contraindication: acute asthmatic attack, severe liver disease

Adverse effects: agranulocytosis, hemolytic anemia, thrombocytopenia [so please don’t take this long term]

side effects: drowsiness, N & V, urinary retention, blurred vision, hypotension

patient teaching; avoid other CNS depressants, driving. Don’t take this long term.

Prototype: Loratadine: Claritin: has fewer side effects, it’s a second generation drug.

Action: compete with histamine for H₁ receptor sites, prevent histamine (allergic) response. Non-sedating b/c It has poor affinity to CNS H₁ receptors.

Use: Relief of symptoms of seasonal allergic rhinitis; idiopathic chronic urticaria [hives].

Adverse: Hypotension, hypertension, palpitations, syncope, tachycardia

Education: Avoid CNS depressants.

B. Decongestants

1. action: produce vascular constriction of nasal mucosal capillaries

2. administration: nasal spray or drops

3. caution; frequent use can lead to rebound nasal congestion from irritation of mucosa; use less than 5 days

4. adverse effect: HTN, hyperglycemia

Prototype: Sinex

Action: alpha-adrenergic agonist; mydriatic; decongestant. Potent, synthetic, direct-acting sympathomimetic with strong alpha-adrenergic and weak beta-adrenergic cardiac stimulant actions. Produces little or no CNS stimulation.

Use: Used topically for rhinitis of common cold, allergic rhinitis, and sinusitis. Also : Parenterally to maintain BP during anesthesia, to treat vascular failure in shock, mydriatic for ophthalmoscopic examination or surgery.

Adverse effect: HTN, tremor, sneezing, severe visceral or peripheral vasoconstriction

C. Antitussives [anti-cough]

Prototype: Dextromethorphan Hydrobromide (Robitussin DM)

Action: suppress cough reflex by inhibiting cough control center in medulla; reduces viscosity of tenacious/stringy secretions.

Use: Temporary relief of cough spasms in nonproductive coughs due to colds, pertussis, and influenza.

Contraindications: COPD, chronic productive cough

Adverse effects: hallucinations, CNS depression with very large doses

D. Expectorants

Best expectorant: adequate hydration. Expectorants loosen bronchial secretions so they can be expectorated

Prototype: Guaifenesin (Robitussin, Mucinex)

Action: Enhances reflex outflow of respiratory tract fluids by irritation of gastric mucosa.

Use: loosen mucus: Aids in expectoration by reducing adhesiveness and surface tension of secretions.

Contraindications: Cough due to CHF, ACE inhibitor therapy, or tobacco smoking.

Adverse effects: none. Nausea and dizziness, the end.

III. Drugs for Acute and Chronic Lower Respiratory Disorders

A. COPD

1. “Bronchial asthma is a COPD” [not included in Lemone/Burk book]

Asthma is bronchoconstriction set off by some stimulant—bronchial asthma is a chronic histamine reaction. “Clinically asthma is diagnosed when a patient has reversible airway obstruction." This is manifested by:

Bronchospasm - wheezing, dyspnea, cough
Mucous hypersecretion - mucus plugs, V/Q mismatch
Airway edema - decreases airway diameter
Airway inflammation - makes airway stiff (decreased compliance)
Hyperactive airway - irritants can precipitate acute bronchospasm

Mild asthma is generally a seasonal condition or occurs sporadically. Wheezing and breathlessness may be experienced when triggered by events such as exercise. The attacks are mild, with symptoms presenting themselves only during the attacks. Treatment: a bronchodilator and used only to alleviate symptoms when they occur.

Moderate asthma usually occurs a couple times per week. Symptoms may present at night, may be triggered by exercise. An asthma attack may require emergency care. Treatment: may include a beta-agonist to be used when symptoms occur. Preventative treatment, such as an inhaled steroid, may be prescribed for administration between asthma attacks.

Severe asthma: continuous symptoms and/or frequent asthma attacks. These asthmatics must change their lifestyle to accommodate the condition. Overall activity levels are affected, and hospitalization and emergency care may be frequently required. Severe asthma has many triggers. Treatment: preventative medications, as well as medications to treat attacks.

Brittle asthma: is rare, unpredictable; attacks are very severe and can be life threatening. Treatment: Preventative and episodic medication is prescribed--Nebulizers and bronchodilators, and steroid tablets are used for long-term asthma maintenance and control.

2. Emphysema: oft from smoking but also sometimes from bad working conditions, coal, asbestos, steel workers. Also some genetic component from mutation of the Alpha-1-antitrypsin protein that prevents alveoli breakdown.

3. Chronic bronchitis: usually from smoking—these guys cough and rattle every morning and hack up sputum.

4. Factors Leading To Bronchoconstriction

· environment: what are they? Pollen, air pollution, temp changes, humidity, work, stifling perfume, etc.

· pollutants: what are they?

· allergic substances: what are they? Dust, animals, etc.

· drugs: such as? Asprin and NSAIDS [why? I don’t get it…]

COPD’ers get pneumonia b/c they don’t move as much air, low gas exchange, stagnant fluid in the lungs, all COPD’ers are always immunosuppressed because of chronic pathology. ‘Exacerbation’ is a flare up of symptoms: like pneumonia

B. Sympathomimetics

Prototype: Metaproterenol (Alupent)

Action: Hit Beta 2 receptors: bronchodilation, relaxation of smooth muscles of bronchi. “Potent synthetic beta-adrenergic agonist that acts selectively on beta₂-adrenergic receptors to relax smooth muscle of bronchi, etc.

Drug-drug interaction: increased with other sympathomimetics; Epinephrine, other sympathomimetic bronchodilators may compound effects of metaproterenol; MAO inhibitors, tricyclic antidepressants potentiate action of metaproterenol on vascular system; decreased effect of beta blockers

Given: PRN, Inhaler, PO, etc. Patient may use tablets and aerosol concomitantly.

Adverse effects: tremors, tachycardia, dysrhythmias, HTN, cardiac dysrhythmias, cardiac arrest, paradoxical bronchoconstriction.

RN Assessment: Listen to lungs before and after inhaler treatment.

Dyspnea: sense of breathlessness. DOE: dyspnea on exertion

PEOPLE ON ANTIINFLAMATORIES ARE ALWAYS AT RISK FOR INFECTION—BECAUSE WE ARE BLOCKING THEIR IMMUNE SYSTEM.

Inhaled drugs have local effects, therefore fewer systemic effects

C. Methylxanthine (Xanthine) Derivatives

Prototype: theophylline

Action: relaxes smooth muscle by direct action, particularly of bronchi and pulmonary vessels, but also GI.

Stimulates medullary respiratory center with resulting increase in vital capacity.

Stimulates myocardium, thereby increasing force of contractions and cardiac output,

Stimulates all levels of CNS, but to a lesser degree than caffeine.

Bad bad: narrow therapeutic range, not as effective as other inhalers— These are not inhaled, they are IV or PO.

Adverse effects: tachycardia, convulsions/seizure, dysrhythmias, cardiac arrest, CNS reactions, resp arrest, circulatory failure

D. Leukotriene Receptor Antagonists

1. effects of leukotrienes: inflammation in lungs:

2. Not to be used with acute asthmatic attack; used for prophylaxis and maintenance

Prototype: Montelukast ( Singulair)

Not for: acute asthma attack; used for prophylaxis and maintenance

Action: Leukotriene Receptor Antagonist; interrupts smooth muscle contraction/bronchoconstriction

adverse effects: none known!

Bronchodilators and Steroids are for acute asthma attack

E. Glucocorticoids (Steroids) for acute attack:

1. MDI [inhaler]

2. IV

3. PO

Beclomethasone (Vanceril) inhaler

Type: glucocorticoid, long acting

Use: for Rx of asthma, COPD, allergies

2. Action: suppresses inflammation and adrenal function

Side effects: Candidal infection of oropharynx, Dry mouth, itchy nose, etc.

Adverse: with excessive doses: symptoms of hypercorticism.

If ‘steroid dependent COPD’er,’ that’s a serious disease. If we see that, we have to make sure a steroid is ordered for them in order to keep their airways open. Don’t let them be abruptly stopped.

Hyperglycemia and hypertension always go with gluco [sugar] corticoids]

Mast Cell Stabilizer

F. Nedocromil: inhaler

Action: antiinflammatory; mast cell stabilizer: Inhibits activation of and mediators released from inflammatory cells (e.g., neutrophils, mast cells, monocytes).

Use: Don’t use for acute asthma attack. prophylaxis of bronchial asthma; inhibits histamine release; maintenance.

Adverse: none

Mucolytics: These are basically expectorants: they thin the mucus by acting like detergents. You need to see what the thickness of mucus is. If someone’s got thick mucus, you need to get them hydrated. Tenacious mucus is stringy.

IV. Case Scenarios

A. Your roommate has a cold, coughing all night so you can’t sleep. What drug and nondrug interventions are indicated?

Anti tussives, have them sit up, get OOB, vapo-rub,

B. Your patient has COPD with pneumonia. What drug and nondrug interventions are indicated?

Oxygen first. Get their pulse ox, in case they are CO2 retainers. Be upright for max lung expansion, or be comfortable. Use an incentive spirometer for breathing exercise. There’s a good chance the patient is dehydrated. Sympathomimetics, antibiotics, need to know the hx, might need steroids, need RT involved, and humidification. Think worst case: pt deteriorates and ends up on a vent.

C. Your 8 yo son plays CYO basketball. Every game he gets an asthma attack. What interventions are indicated?

Inhaler.

Objectives: Upon completion of this class, the student will be able to:

1. Compare antihistamine [blocks inflammatory immune response], decongestant [like sympathomimetics—sinex], antitussive [robitussin that depresses CNS cough center], and expectorant drug groups [mucinex or robitussin that thin mucus and irritate bronchial walls to get lung butter out];

2. Describe the nursing process with these agents;

3. Differentiate the drug groups used to treat COPD and asthma and the desired effects of each; glucocorticoids, xanthine derivatives [these are bad], mucolytics, Leukotriene Receptor Antagonists, sympathomimetics, Mast Cell Stabilizer

4. Contrast the therapeutic effects of these meds for for COPD and asthma; Leukotriene antagonists [leukotriene causes bronchconstriction, so we block it], glucocorticoids [block inflammatory response], Nedocromil [chills out the Mast cells by blocking their activating chemicals], antihistamines [blocks H1 receptors to prevent allergic reaction/inflammation], and mucolytics [get the lung butter thinner and expectorated]

5. Describe the nursing process with safe use of these agents.

205 IV and HIV day; class notes

2007-11-06T19:57:00.000-08:00

N205 INTRAVENOUS THERAPY AND AIDS

Objectives: Upon completion of this class, the student will be able to:

1. Correlate the pathophysiologic alterations with the manifestations of HIV/AIDS infection;

2. Discuss normal regulation of fluids and electrolytes;

3. Describe the regulation of acid-base balance;

4. Discuss nursing responsibilities with IV therapy;

5. Describe nursing responsibilities with IV sites, IV tubing, and IV solutions;

6. Demonstrate correct technique for calculating drip rate of IV solutions.

I. AIDS: acquired immune deficiency syndrome

HIV: human immunodeficiency virus

From exposure to body fluid that’s infected/contaminated; vaginal secretion, breastmilk, blood, etc.

A. Pathology

1. Retrovirus infects cells with CD4 antigen [T–Helper cells and macrophages]

No longer a fatal disease but a chronic disease.

2. Enters cell and converts RNA to DNA with reverse transcriptase

3. HIV DNA integrated into host DNA

4. duplication of HIV during cell division

5. virus buds from cell surface, destroys host cell and spreads—you are left without enough surveillance in the body.

B. Manifestations

1. Primary HIV infection: flu like symptoms

2. Asymptomatic infection: no symptoms now but you become sero-positive—you’ve made antibodies that show up on a blood test.

3. Persistent generalized lymphadenopathy [lymph-gland-disease]

4. Acute symptoms: fever, weight loss, night sweats [like TB],

5. Opportunistic infections and cancer: as the CD4 cells die off, you’re up for all sorts of infections that are life threatening or not—cancers like Kaposi’s sarcomas.

Symptoms: stomatitis [sores in the mouth]

C. Diagnosis

1. CD4 T cell count

2. clinical symptoms

3. viral load

Nurse’s job: how do you know someone’s positive? It should be in their Hx, they should divulge it. It’s illegal to test for HIV w/o pt permission—whether a preop concern or a needlestick injury.

D. Interdisciplinary Care

1. Medications: reverse transcriptase inhibitors, protease inhibitors, HAART

2. Prevention

3. Assessment

4. Nursing Diagnoses: list four

Knowledge deficit r/t new diagnosis, community resources, AEB asking questions

Risk for infection r/t immunodeficiency

Anxiety r/t diagnosis, AEB frequent questions

Inbalanced nutrition r/t stomatitis, anorexia, nausea

Ineffective sexual patterns

Social isolation

5. Standard Precautions for healthcare provider safety

After today we hang piggyback’s and hang IV’s.

II. Body Fluids

Where is body fluid- interstitial and intracellular, somewhat extracellular, and we can’t really measure that.

How can you tell if someone is balanced or out of whack?

Assess:

Edema; fluid retention. Not as much output as input.

Capillary refill

I & O

A. Components

B. Movement

1. Osmosis

2. Diffusion

3. Filtration

C. Regulation: fill the tank or empty the tank

1. fluid intake

2. fluid output

3. maintaining homeostasis: who controls it? Kidneys, juxtaglomerular apparatus triggers the RAA, ADH, Aldosterone from hypothalamus/pituitary. Thirst center—people who don’t have thirst centers are low LOC people, and elders whose neurons are just old.

Normal potassium level should be around 3.5-5.0 , depending on the lab. Margi might test us on this.

What causes hyperkalemia? Supplements [micro K]

D. Regulation of Electrolytes

1. Why is this important?

2. What are they?

3. What do they do?

E. Acid Base Regulation: who does it? Look in the book at this, we will be tested on most normal blood gas abnormality [resp acidosis from hypoventilation] and on common lab values. The lungs and the kidneys.

1. Metabolic buffers

2. Respiratory Regulation

Lungs: blow off CO2 from cellular respiration:

CO2+H2O à H2CO2 à H+ à high H+

Hypoventilation means high CO2 holding which means high acid in the blood.

Cheyne-stokes respirations: a type of hyperventilation that blows off CO2

Blood gas values are covered in the book.

ABG’s: dissolved pressures of CO2 or O2 in arteries, not in veins. Normals:

pH: 7.35-7.45

pCO2: 35-45

pO2: 80-100

saO2: >95%

Bicarb: 22-26

3. Renal regulation

Kidneys: provide bicarbonate buffer system for the body. These take hours to days to make blood pH effects.

CBC tells us: WBC count. Check the electrolyte labs. CBC we really care about: BUN/Creatinine, H&H [hemoglobin and hematocrit]

F. Factors affecting body fluid, Electrolytes, Acid-base balance

1. Age: why?

2. Gender and body size-why?

3. Lifestyle-why?

4. Environmental temperature-why?

G. Fluid imbalances

1. Deficit

2. Third space syndrome

3. Excess

4. Edema

5. Dehydration

6. Overhydration

H. Electrolyte imbalances: Memorize the normal values for these, the symptoms of hypo and hyper’s

1. K

2. Na

3. Ca

4. Mg

5. Cl

6. PO4

Margi’s memorization of ABG’s: she memorizes the midpoint of all the ranges

7.4 [ph]

40 [CO2?]

100 [o2]

25 [bicarb]

100 [?]

I. Acid-base imbalances

1. Respiratory acidosis from hypoventilation (know this one)

2. Respiratory alkalosis from hyperventilation

3. Metabolic acidosis from excess body acids

4. Metabolic alkalosis from excess body bases

III. Nursing Management

A. Assessment:

1. History

2. PE

3. Daily weights

4. I & O

5. VS

6. Labs

B. Nursing Diagnoses: list four

C. Planning

D. Implementation

IV. IV Infusions

Who gets IV? Fluid managements, medications IV [esp antibiotics: by IVPB.]

Normal saline: 0.9%

Once I set up a piggyback bag: it needs to be labeled: pt, dose, time, date, my initials

A. Calculating Drip Factor

1. Nursing Responsibilities: calculate correct IV flow rate; regulate infusion; monitor client’s responses

Not all pts have IV machines hooked up—it drips w/o regulation. Ambulances don’t get these machines either. This is why you have to memorize how to calculate IV drip rate by hand. This will sometimes show up on entrance tests to hospitals.

You have to know the drip rate, and the drop factor on your bag. Drop factor is affected by the tubing diameter. So…the drop factor is the # of drops to deliver one mL of fluid in that particular tubing.

2. IV control device: know how to work it!!

3. Drip factor: drop factor: printed on package of IV tubing

· macrodrop: 10, 15 drops/ml

· microdrop: always 60 drops/ml

4. Calculate milliliters/hour

· divide total infusion volume by total infusion time in hours

· example: 1L over 8H. Divide 1000 ml by 8; equals 125 ml/hr

5. Calculate drops/minute:

a. Drops/min= total infusion x drop factor

total time of infusion in minutes

b. example: Infuse 1000 ml in 8 hours and the drip factor is 20 drops/ml

1000 ml x 20 = 41 drops/min

8 x 60 min (480 min)

6. . Factors affecting flow rate

· position of IV site

· position of tubing

· height of IV bag

· infiltration of IV solution or fluid leakage

B. Changing IV tubing or solution

1. Perform hand hygiene

2. set up necessary equipment

3. maintain sterile technique

4. flush new IV tubing with solution

5. attach to IV catheter

6. infuse at prescribed rate

IV’s are an RN function; LVN’s don’t typically do them.

If the machine is beeping; silence it while you problem solve.

The machine will freak out if there’s air in the line; it will tell you what’s going on and it will not run.

Hanging a piggy back bag: check the date of the tubing. make sure you have set the rollerclamp open on the IVPB, hang it higher than the IVF bag.

Primary vs secondary tubing.

Incompatibility issues: come up when 2 meds are in the same container. Not a problem running them sequentially in the same tubing. “Y site” incompatibility means don’t mix in the same tubes. Gentomycin is not compatible with anything.

Back flushing: to get air out of the tube. Do a little gravity thing—turn the tube upsidedown—this flushes from the Saline bag up to the piggy back. Back flush when hanging Gentomycin after Vancomycin and you want to re-use the tubing.

Why do docs order different fluids? Because they have their favorite flavors—its not about what the pt needs. Surgeons always order LR. Post op is often Dextrose which might be a good thing. We need to know why they are on which fluid.

Which fluid? Most people get isotonics. Sometimes people get a 3% NS, because their sodium is really low—or they want water out of the tissue for whatever reason. Colloids are hypertonic to pull water into the vessels in septic situations, etc. NS be cautious with CHF, perhaps.

Tubing can now be changed every 4 days, according to the CDC, some hospitals are different—some say 2 days. The CDC says 72 hours is the shortest amount of time b/c you’re interrupting the system and creating opportunity for infection. TPN: new bag, new tubing—b/c it’s like nutritional broth for bugs. Don’t put old tubing into a new site. If no label, assume its too old.

C. Nursing Responsibilities with IVs

1. Site patency

2. Correct IV solution and rate

3. client response to IV fluids

4. prevent complications

My job if pt has IV: I need to know the solution as MD ordered, if they still need that solution—is that solution the best for that pt with the current state. Make sure site is patent. Make sure rate etc are also appropriate. RN is still accountable for delivering an inappropriate order—even IVF. Make sure no infiltration—that it’s going iv, not intra tissue!

Site is sterile, inside of bags and tubes is sterile.

Do you need gloves on to hang IV? No.

D. Complications of IV Therapy

1. Phlebitis

2. Infiltration of solution

3. Extravasation of medication

4. Infection at site

Phenobarbaratol's Lovely list of Exam 2 drugs

2007-10-31T14:03:00.000-07:00

We don't 'need' to know this set of drugs anymore, but we do 'need to know them forever.' So here's another tidy list o' exam 2 drugs compliments of Barbara. Thanks Barb[ituate]!

ANTIEMETICS

Benadryl Antihistamine
Use: allergy, insomnia, motion sickness
Adverse: cardiovascular collapse, anaphylactic shock.

Phenergan Dopamine antagonist, anticholinergic, phenothiazine
Use: suppresses CTZ , CNS depressant
Adverse: resp. depression, agranulocytosis, apnea

Haldol Dopamine antagonist
Use: chemo pts, post-op, Tourettes
Adverse: laryngospasm, resp. depression

Reglan Dopamine antagonist
Use: enhance GI motility, nausea
Adverse: sedation, HTN crisis

Ativan GABA mediated, benzodiazepine
Use: anxiety, suppress REM sleep
Adverse: hyper/hypotension

Zofran Selective serotonin antagonist in CTZ and vagus nerve
Use: nausea
Adverse: diarrhea

Decadron Hormone, glucocorticoid
Use: anti-inflammatory, immunosuppressant, reduces capillary dilation
Adverse: edema, hyperglycemia, bowel perforation, impaired wound healing

Cannabinoids

ANTIDIARRHEAL

Lomotil Synthetic opiate agonist
Use: reduces GI motility
Adverse: constipation, paralytic ileus

Sandostatin Hormone, somatostatin analog
Use: stimulates fluid & electrolyte absorption from GI tract, prolongs intestinal
transit time
Adverse: hyper/hypoglycemia, constipation

Kaopectate OTC antidiarrheal
Use: coats muscosa, binds bacteria and toxins that cause diarrhea
Adverse: CNS depression, constipation

LAXATIVES

Lactulose Osmotic
Use: moves water from plasma to intestines, stimulates peristalsis
Adverse: diarrhea, hypernatremia

Dulcalax Contact irritant
Use: irritates nerve endings and induces peristalsis
Adverse: electrolyte disturbance, esp. Ca and K

Metamucil Bulk laxative (mucilloid)
Use: bulk producing, promotes natural elimination
Adverse: if not taken with enough water, have hard BMs and possible blockage

Colace Emollient
Use: prevention of constipation

ANTIULCER

Amphojel Antacid
Use: neutralizes stomach acid and reduces gastric activity
Adverse: constipation

Zantac Histamin 2 blocker
Use: GERD, block parietal cells from producing acid
Adverse: hepatotoxicity, toxicity w/Metroprolol, cardiac dysrythmias

Prevacid PPI
Use: suppress gastric acid production
Adverse: diarrhea, elevated liver enzymes

Carafate Mucosal protectant
Use: absorbs bile, inhibits pepsin, blocks diffusion of H+, protects mucosa

NEURO: SYMPATHOMIMETIC

Epinephrin Adrenergic agonist
Use: anaphylaxis, cardiac arrest, asthma, glaucoma
Adverse: acute MI, V fib, pulmonary edema

Albuterol Beta 2 agonist
Use: bronchospasm
Adverse: bradycardia, tachycardia, hyper/hypotension

Atenolol cardio-selective beta blocker
Use: Acute MI, hypertension, angina. Decreases symp. flow to periphery, decreases rennin activity
Adverse: hypotension, bradycardia, CHF

NEURO: PARASYMPATHOMIMETIC

Urecholine Cholinergic agonist
Use: increases parasympathetic response (rest and digest). Relaxes GI tract and bladder. Used for post-op and postpartum urinary retention, BPH
Adverse: transient complete heart block, asthma

Atropine Anticholoinergic
Use: increase heart rate and cardiac output, bronchodilator, decrease GI spasm
Adverse: V fib, paralytic ileus

CNS STIMULANTS

Ritalin Cerebral cortex stimulant
Use: ADHD, narcolepsy
Adverse: hepatotoxicity, exfoliative dermatitis

Imitrex Serotonin agonist
Use: migraine, vasoconstricts cranial vessels
Adverse: angina, HTN, MI, cardiac arrest, coronary artery vasospasm

CNS DEPRESSANTS

Seconal Barbituate
Use: insomnia, pre-op for general, spinal or local anesthesia
Adverse: dependency, decreased LOC, resp. depression

Xanax Benzodiazepine
Use: anxiety, panic, increases GABA
Adverse: resp. depression, REM rebound

NEURO: PAIN MANAGEMENT

Tylenol NSAID, nonnarcotic analgesic
Use: mild to moderate pain, lowers body temp with fever
Adverse: hepatotoxicity, acute renal failure, coma

Morphine Narcotic opiate agonist
Use: severe acute and chronic pain; relief of dyspnea of acute L ventricular failure and pulmonary edema and pain of MI.
Adverse: cardiac arrest, resp. depression

Demerol Synthetic Morphine, narcotic opiate agonist
Use: moderate to severe pain, pre-op med, support anesthesia
Adverse: resp. depression, cardiac arrest, bronchoconstriction, CNS toxicity and seizure

Dilaudid Synthetic narcotic opiate agonist
Use: 8-10 times more potent than morphine, moderate to severe pain, cough suppressant
Adverse: resp. depression

Narcan Narcotic antagonist
Use: overdose of opiates, resp. sedation and hypotension
Adverse: HTN, tachycardia, elevated PT

ANTICONVULSANTS

Dilantin Reduces voltage, frequency and spread of electrical charges in motor cortex.
Use: controls grand mal seizures, psychomotor and nonepileptic seizures
Adverse: cardiovascular collapse, aplastic anemia, agranulocytosis, exfoliative dermatitis, toxic epidermal necrosis

Valproate Increases bioavailability of GABA to brain, decreases neuronal discharge in CNS Use: management of absence (petit mal) and mixed seizures, mania, migraine
Adverse: liver failure, coma, bone marrow depression

Neurontin GABA analog, mechanism of action unknown
Use: promotes GABA release for treatment of partial seizures and neuropathic pain
Adverse: increased frequency of partial seizures

NEUROLOGICAL DISORDERS

Sinemet Anticholinergic
Use: makes more levodopa available to brain for management of Parkinson’s Disease symptoms.
Adverse: neuroleptic malignant syndrome, depression/suicidal ideation

Cognex Cholinergic / cholinesterase inhibitor
Use: elevates Ach levels in cerebral cortex, improves memory in early stage Alzheimer’s and dementia
Adverse: hepatotoxicity, diarrhea

PSYCHIATRIC AGENTS *anticholinergics inc. HR, dec GI, dilate pupils, inhibit sweating

Prolixin Dopamine antagonist, phenothiazine, anticholinergic
Use: antipsychotic, schizophrenia. Combined anticholinergic, thermoregulatory effects. Depresses PNS
Adverse: agranulocytosis, grand mal seizures, impaired thermoregulation

Haldol Dopamine antagonist, nonphenothiazine
Use: agitation of psychosis, Tourette’s, short term treatment for hyperactive children, severe behavior problems in children
Adverse: laryngospasm, agranulocytosis, tardive dyskinesia, neuroleptic malignant syndrome, resp. depression

Ativan GABA inhibitor, benzodiazepine
Use: anxiety, insomnia
Adverse: hyper/hypotension

Elavil Serotonin and norepinephrine blocker, tricyclic antidepressant (TCA)
Use: major depression, anxiety, bipolar disorder
Adverse: agranulocytosis, thrombocytopenia, seizures

Prozac Selective Serotonin Reuptake Inhibitor
Use: depression, OCD, bulimia, premenstrual dysphoric disorder
Adverse: sexual dysfunction, anxiety, insomnia, diarrhea

Buspar Dopamine agonist in brain, serotonin reuptake inhibitor
Use: anxiety
Adverse: interacts with grapefruit, causes toxicity

Lithium Competes with cations and affects body water, neurotransmitters. Inhibits neurotransmitters and decreases receptor activity to control manic phase of bipolar disorder
Adverse: peripheral circulatory collapse

ENDOCRINE AGENTS

THYROID DRUGS

Synthroid Thyroid replacement, increases metabolism, oxygen consumption, body growth
Use: treat myxedema, hypothyroidism
Adverse: tachycardia, HTN, thyroid crisis, angina, CV collapse

ADRENAL DRUGS

Prednisone Glucocorticoid, synthetic analog of cortisone, anti-inflammatory
Use: cancer therapy, dermatologic disorders, immunosuppressant, decrease inflammation
Adverse: delayed wound healing, infection, muscle wasting, hypokalemia, asceptic necrosis of bone

Vanceril Glucocorticoid, inhaled
Use: treat steroid dependent asthma, rhinitis
Adverse: immunosuppression

Solu-Medrol Corticosteroid
Use: intermediate acting anti-inflammatory for allergic rxn, short-term asthma therapy, cerebral edema
Adverse: immunosuppression

ANTIDIABETIC DRUGS

INSULIN (subcut) Use: Type 1 DM

Lispro Rapid acting, shorter duration than regular insulin
Onset: 5 min. (< 15 min)
Peak: 0.5 – 1h
Duration: 3-4h

Regular Humulin R
Short acting – only insulin given IV Clear, colorless
Onset: 0.5 – 1h
Peak: 2 – 4h
Duration: 5 – 7h

Humulin NPH Intermediate acting, cloudy suspension (zinc insulin crystals)
Onset: 1 -2h
Peak: 4 – 12h
Duration 18 – 24h

Lantus Long duration, usually given at bedtime
Onset: 3 -4h
Peak:
Duration: 10.4 – 24h

Adverse side effects of subcut insulin: hyperinsulinemia, coma, psychic disturbances with overdose, hypoglycemia.

INSULIN (oral) Use: Type 2 DM, adjunct to diet control of hyperglycemia

Glucotrol Sulfonylurea: stimulates beta cells to make insulin. Increases insulin binding at receptors. Inhibits hepatic glucose production.
Adverse: hypoglycemia, coma

Prandin Meglitinide: stimulates release of insulin by pancreatic islets
Adverse: hypoglycemia

Actos Glitizone: stimulates insulin secretion, increases insulin receptor sensitivity, decreases hepatic glucose output,
Adverse: hypoglycemia

Glucophage Fixed combination: glyburide-metformin, Stimulates release of insulin from pancreas. Metformin decreases cell resistance, decreases hepatic glucose production, increases glucose uptake.
Adverse: upper resp. infection, diarrhea, lactic acidosis

Glucovance Biguanide: (Metformin) decreases cell resistance, prevents liver breakdown of glycogen, stimulates release of insulin.
Adverse: upper resp. infection, diarrhea, lactic acidosis

Precose Alpha-glucosidase inhibitor: delays absorption of glucose in GI tract.
Adverse: hypoglycemia, anemia

205 Perioperative care class notes

2007-10-30T21:07:00.000-07:00

Perioperative Nursing
N205 Fall 2007

Learning Objectives:
Explains the various types of surgery according to degree of urgency, degree of risk, and purpose.
Describes the phases of the perioperative period.
Demonstrates essential aspects of preoperative teaching, including pain control, moving, leg exercises and coughing.
Identify essential aspects of preoperative assessment.
Identify nursing responsibilities in planning perioperative care.
Describes essential aspects of preparing a patient for surgery, including skin preparation.
Compares various types of anesthesia.
Identify nursing assessments and interventions during the immediate postanesthetic phase.
Summarize five postoperative complications, their prevention, and their management.
Describe anxiety in terms of etiologies and nursing process and applies content to the management of the anxious patient.

ANXIETY

State of mental apprehension or dread, often initiated by feeling a loss of control.
Can be experienced at many levels (conscious or subconscious). Most anxiety is subconscious—most people don’t have awareness of anxiety
Four levels of anxiety: mild, moderate, severe, and panic.
Behavioral signs: rapid speech, pacing, increased heart and resp rate. Fidgeting repetitive motion, hair, nails, asking same question repeatedly, inappropriate speech
Physiologic signs and symptoms: flight or fight response (sympathetic nervous system response) - heart rate, B/P and respiratory rate increase. Blood vessels constrict as blood is shunted away from skin, stomach and kidneys. Catecholamines increase BP—which is bad pre-surg b/c we want the strain on the heart to be lowered. Post op anxiety increases bleeding, sometimes people will pull out tubes, become combative, try to get up out of a gurney before they’ve come out of anesthesia. Some people hover pre-operatively over every little detail.
Emotional and defensive responses – withdrawal, anger, denial, agitation.
Anxiety and activity response – increased movement, impatience, decreased concentration, repetitive speech, constant talking, overstimulation, hypervigilance.
Environmental interventions: Decreasing anxiety pre-op: have to work w/ the environment you’re in: ask the pt to bring headphones for themselves for nice music, decrease noise level, stimulation.
Behavioral interventions. Post op-people’s brainstems are active, their frontal lobe doesn’t wake up for a while. Preop behavioral interventions: breathing deeply and slowly. Give people control: don’t tell them they have to take their panties off—the power struggle will escalate. Work with them—they’ll be knocked out soon enough anyway.
Pharmacologic interventions: ativan—more than valium which is longer acting; versed [resp depression risk…not used too often]
Set limits, give limited choices, be calm but assertive.
Anxiety as it relates to the perioperative experience.

Want to maintain normothermia post op, warmth calms patients, the veins constrict and makes it hard to start an IV, normothermia prevents all sorts of complications including infections.

PERIOPERATIVE NURSING
Concepts of surgery:
Multidisciplinary approach
Effective communication (timeout): Communication is regulated and standardized for surg b/c the risk of wrong pt, wrong surg etc. The comm. Format is called “time out:” in this case the whole team stops to review the patient, the surgery, etc.
High quality care: hospital ratings are based on care, esp in surg b/c the results are so measureable.
Patient and family advocacy: Role of the RN: pt and family advocacy, like when the pt doesn’t understand their surg, want to talk to the MD, won’t sign the form, etc. Pts have a right to know.
Cost containment: same day vs. inpatient: there’s a lot of trends toward outpatient surg, esp like laproscopic. Pts out of the hosp are better off b/c lower risk of infection.
Pre, intra, and postoperative periods.

Types of surgery:
Degree of urgency: emergency and elective. Emergent: appendectomy, pts who come to the ED first—very little planning or prep. A cardiac bypass w/ an MI would be an emergent surgery. Trauma post MVA. Trauma 1 vs Trauma 2 centers. Elective: plastic, joint replacements, mastectomy, colectomy, etc.
Degree of risk: major and minor: tonsillectomy, repair of torn meniscus, open reduction of a fracture…would all be lightweight. Major surg is open-heart, anything abdominal b/c of the risk rate of bleeding and heat loss, long recovery time.
Purposes: diagnostic, palliative [debulking a tumor to prolong life, decrease pain], ablative, reconstructive, constructive, transplant, and cosmetic (examples of each).
By surgical service – neuro, cardiac, orthopedic, general, vascular, gynecologic, plastic, etc. what type of doc is operating. Some hospitals have services organized by floor.

Phases of the perioperative period –preop (briefly describe) intraop (briefly describe) post-op- PACU to discharge.

Preoperative:
Assessment: ASA classification: for anesthesia, its about the degree of risk based on comorbidity. Goes from 1-6. This rate is about which patients can go to outpatient surgery sites. Anesthesiologists read H/P and decide the rating.
ASA I; normal healthy patient
ASA II mild systemic disease
ASA III severe systemic disease
ASA IV severe disease with threat to life
ASA V moribund patient
ASA VI brain dead patient, organ donation
Planned surgery: doctor, procedure explained, scheduled, preoperative tests ordered, preoperative nursing interview: likely when pts have been dealing w/ illness or injury for some time, planned w/ doc, pt chooses timing, it’s not emergent, etc.
Unplanned: phases abbreviated patients less prepared, preoperative testing done immediately, less teaching done. Knowledge deficit, anxiety
Health problems that increase surgical risk.

Preop nursing assessment:
Current health status, allergies, medications, NPO status, last void, baseline vital signs, smoking, language barriers, social/family resources (ride home, home care): go over this w/ client b/c some people think they don’t have any problems but they’re on 20 heart meds. Sometimes people are in for CABG and they think they’re healthy.
Driving: safe discharge: people often don’t know that they can’t drive themselves home—that’s our responsibility if they get in an accident driving themselves home.
Cultural and spiritual considerations: some people want to have a family reunion at the hospital when they have surgery. Sometimes the patriarch answers the questions for the patient and family.
Prophylactic antibiotic dose.
Check doctor’s orders.
Surgical consent must be signed: this is the nurse’s job—getting the signature. This is highly regulated—no abbreviations, perfect spelling, etc.

Preop teaching – educate about the phases (will be asked for name and date of birth many times), pain control, nausea, prevention of infection (antibiotics), DVT prevention, postop ambulation, coughing and deep breathing. Goal: patient knows what to expect. Make sure patient has a ride home. This is about anxiety, knowledge deficit. Tell people the basics before surg, don’t give them lots of info and details preop. Details happen way before cut day. Tell them about the funny stockings, the tubes, when their family can show up, etc. All surg pts get an IV.

Preparing patients for surgery:
Nutrition and fluids – don’t make patient NPO without starting IVF.Hygiene – preop shower
2. Medications these days patients can often take their own meds preop—this is up to the anesthesiologist; usually heart meds are ok b/c they reduce strain on the heart. No blood thinners allowed. most pts get antibiotics preop b/c we’re opening them up. Has to be given 1 hr b4 cut time. Sometimes anesthesiologist is the one to give it.
3. Special orders:
allergies: we have to ask about their allergies; often people don’t know the difference btwn ‘sensitivities’ and allegies that can cause anaphalactic shock—morph makes most people itch—it’s a side effect not an allergy.
Last time people voided: need to know b/c sometimes people can’t urinate and they get super high BP
Most people come in dehydrated: so I/O is super important.
Know peoples baseline: b/c we don’t want to give dopamine to someone whose BP is very low.
Smoking Hx: will they go thru withdrawals during their stay, O2 requirements, etc.
4. Skin prep; hair removal [electric clippers are used these days—so less infection and dermabrasion—studies show that shaving is way more dangerous than leaving all the hair there.] Chloraprep [chlorhexadine gluconate]
Also keep glucose levels up: the anxiety levels will cause the SNS response of extra glucose in the blood.
5. Safety protocols
6. Deep vein thrombosis prophylaxis:
Questions Preop: what have you eaten, what’s your name and DOB, what surg are you having, which side of the body? The pt or the RN marks with a pen the site of surgery

Intraoperative
Medications
Tourniquet time
Length of surgery
Personnel – surgeon [don’t keep pts alive, they make sure the surgical technique is good], anesthesiologist [keeps pt alive]. Surgical assistant, circulator [RN who’s not in the sterile field], scrub tech [hands scalpels, etc], Sometimes an extra tech is there; xray tech in orthoscopic
Types of anesthesia
general: inhaled; they’re paralyzed, no voluntary or involuntary movement; can’t breath for themselves. Also given IV pain meds
Monitored anesthesia care (MAC): anesthesiologists intubate pts, monitor vitals and sometimes stick an EKG on the head to monitor if pts are sedated enough—sometime pts aren’t deep enough and they are conscious but unable to move [scary!]
Regional or local
Conscious sedation

Post anesthesia care (PACU): airway is number one here. Want to assess VS, LOC, nueor type check. Pts itch, can’t pee, nauseous are cold, we give warm IV fluids, don’t release from PACU until they can move their legs a little b/c of fall risk.
a. Assessment: airway, respirations, 0² sat, HR, B/P, rhythm, LOC, protective reflexes, CSM, pulses, drains, surgical site, lines, orders, X-rays, labs, IV fluid, special monitoring, suction, etc.
b. Nursing interventions – elevate surgical site, comfort, ice chips, scratch, etc.
Potential postoperative complications- respiratory, circulatory, urinary, gastrointestinal, wound, psychologic.

Receiving a patient from surgery: get the room ready, equipment ready
Assess airway, do a head to toe assessment of patient. Have all equipment needed in the room (oxygen, suction, IV pump, etc.)
Vital signs every 15 minutes until stable, including oxygen saturation and pain. Docs order VS Q15 minutes for 1 hr, then Q30 minutes
What are the most common post-operative complications? Can’t pee, itchy, nauseous, etc.
Family-centered care.

Pharma: Nutrition and Electrolytes and Vitamins and Stuff

2007-10-29T18:05:00.000-07:00

Nutrition/sElectrolytes

1: Vitamin Supplements
Vitamin Supplements and replacements
inadequate absorbtion; who? IBD [inflame bowel disorder], infections, antibiotics, people w/ diarrhea [from TF, infections, c diff, meds, illness, etc]
inability to use vitamins, why? Liver disease, cirrhosis, renal disease, genetic factors apperently
increased vitamin losses: why? Hypermetabolic state, hyperthyroid, inc vit requirements, infections, diuretics can lose some of these
increased vit requirements: why?

B: fat-soluble vit’s: these are toxic in high doses because they are fat soluble, and are not flushed from the body. Toxicity is called “hypervitaminosis D, E, K, or A”
vit A: skin disorders, bone development, prevent night blindness, Vit A deficiency [pancreatic disease, colitis, cirrhosis, celiac’s.] Stored in liver for up to two years, excreted through kidneys and poop. Don’t eat polar bear liver b/c you’ll OD on Vitamin A and die.

vit D: needed for Calcium absorption from the intestines. Overdose can cause hypercalcemia. Secreted through bile.

Vit E: antioxidant, good for cell membranes. Studies show protection from MI, CAD, by protecting blood vessel walls from free radicals. Good for Skin. May increase PT [monitor w/ coumadin], don’t take with Iron—iron disrupts body use and absorption of Vit E. 75% lost thru bile.

Vit K: good for clotting factors: prothrombin, factors VII, IX, and X. This can be used to prevent hemorrhage anticoagulant overdose. Who is lacking clotting factors: liver makes clotting factors so this is needed for liver disease clients, alcoholics coming in with GI bleed. Aquamephyton: commercial K1 preparation.

C: Water-sol vit’s
Vit B: lots of these B vitamin complex thingies. Given for dermatitis, inflammation. Niacin is Vitamin B3, used to fight off thrush, hyperlipidemia (big doses for that.) Large doses cause vasodilation: flushing or ‘blushing’ sensation.
Vit C/ascorbic acid: green leafy veggies, citrus are not super available in hosp meal trays. Aids in absorption of iron and conversion of folic acid. High doses can cause diarrhea and GI upset. You can’t really overdose on it, but rapid decrease can cause ‘rebound deficiency.’ Treats scurvy [vit c deficiency], good for wound healing and burns. Preserves integrity of blood vessels.

D: RN’ing process
Assess: skin integrity, healing, I/O, diet types, can they advance their diet, lab values (like electrolytes, pre albumin, CBC, platelet counts)

E: Minerals
Iron: need larger amounts during pregnancy. Iron deficiency anemia, Iron is vital fcor hemoglobin regeneration: 60% of the iron in the body is in hemoglobin. Vit C increases iron absorption.

Copper: for formation of RBC’s, connective tissues, enzyme cofactor, neurotransmitter production. Not-enough-copper-syndrome: anemia, decrease in WBC’s, hair color changes, skin and blood abnormalities. Seeds, shellfish, legumes and cocoa are high in copper.

Zinc: Not sure what its good for—maybe the common cold. Don’t take at the same time as an antibiotic—wait a couple hours. Large doses can cause copper deficiency, low HDL, weak immunity.

Chromium: May normalize blood glucose by sensitizing cells to glucose. Interesting in TPN; cancer pts, other pts who can’t use their GI tract [I have no idea why Margi says that.]

Selenium: cofactor for antioxidant enzyme. Works w/ vit E. May have anticarcinogen effect. High doses: weakness, hair loss, dermatitis, GI upset, make you smell like garlic.

RNing process
Assess: nutritional state, dietician, make some calls, ensure they’re tolerating tube feeding, dehydration, loose stools, etc.

II: FLUID/ELECTROLYTE REPLACEMENT
A: Body fluids: only %5 of total body water is in our blood vessels, so if someone is hypovolemic it means they’ve lost interstitial fluid or they’ve got edema.
B: Fluid replacement
IV solutions
Why iv’s: they’re dehydrated, they can’t swallow water
Crystalloids: most are crystalloids, they have dextrose or electrolytes, they are clear.
i. D5W: dextrose [sugar] and water
ii. NS: 0.9% NaCL
iii. LR: Lactated Ringer’s
Colloids: big proteins, they are ‘volume expanders’. These pull water osmotically from the periphery to increase Blood Volume. Needed in septic shock, burn patients, etc. Also need to give IV fluids.
i. Dextran 40: can interfere w/ platelet.
ii. Hetastarch: can decrease platelets, hematocrit
iii. Plasmanate: used to replace body protein

Blood and blood products: why? Not producing enough, lost too much blood, septic, low blood volume. We don’t transfuse very often b/c of blood borne diseases, we killed some people w/ the wrong blood—anaphylactic reaction.
i. Packed RBC’s: whole blood, no plasma—good because less risk circulatory overload, rxns to antigens, risk of transmitting hepatitis. Elevates hematocrit.
ii. Whole Blood: Do not use to correct anemia except in severe cases. Elevates hemoglobin.
iii. Plasma:
iv. Albumin
Lipids: administered as fat emulsion solution, used when on IV for >3days. Balance nutritional needs; given every few days to clients on TPN.

Safe admin

C: Potassium: biggest baddest; it’s fussy. It mostly lives intracellular [20x higher level inside cells, serum level is very low] Stare at K+ levels on lab values first, b/c the heart is sensitive to K+. Renal pts: hyperkalemia: why don’t they have dysrhythmias? Because they are dialyzed, and the change in K is slow w/ renal failure. If you give diuretics and you shift the K+ quickly, the heart gets really pissed off.

Prototype: Micro K
Use: who gets it? Correct potassium deficit: strengthen cardiac and muscle contraction. P At risk for hypokalemia: People on potassium wasting diuretics, loops, thiazides, etc. [HTN and CHF’ers.]
Action: Transmits and conducts nerve impulses, contracts all 3 muscle types…except for the love muscle.
Adherence to regimen: The liquid tastes nasty and the pills are big.
Adverse: life threatening: dysrhythmias, resp distress, cardiac arrest.

hypokalemia: nausea, vomiting, dysrhythmias, soft flabby muscles
hyperkalemia: nausea, decreased urine output, tachycardia, then bradycardia, weak muscles

Don’t have to know this:
To Quickly drop K+ levels: Can adjust with a certain “K-exylate” enema that pulls K+ out. Insulin and 10% dextrose will also drop K+. Also Kayexulate will pull down super high levels of K.

D: Sodium:
Hypernatremia: flushed skin, elevated body, higher BP
Hyponatremia: lost Na+ with vomiting/diarrhea. Neurons don’t like this—confusion can occur. People who over drink water will lose Na+.

E: Calcium: lives in the bones largely. Need to assess Ca+ level. Calcium promotes normal nerve and muscle actions; prevents clotting, important for forming bone and teeth. Osteoporosis hits women hard, esp. postmenopausal. Free calcium is bound to proteins, the rest is unbound and can cause physiologic changes.
Hypocalcemia: calcium leaves the bone to balance body needs, risk for fractures. Causes: hypoparathyroidism, vit D deficiency, multiple blood transfusions. Symptoms; tetany, spasms, convulsions.
Hypercalcemia: from hyperparathyroidism, hypophosphatemia, bone cancer, thiazides, fractures.
Calcium Carbonate is “tums.” People get this when they are at risk for hypo or hyper calcemia

F: Magnesium: promotes transmit of neuromuscular activity, mediates NS transmission in CNS. Promotes cardiac muscle contractility [like K], activates enzymes for metabolism of carbs, protein.
Hypomagnesemia: often in combination with K or Ca deficits. Increases release of ACh, increasing neuromuscular excitability.
Hypermagnesemia: don’t know what happens

Our job forever and ever is to check electrolyte levels.

III: NUTRITIONAL SUPPORT:

Enteral vs parenteral
Our job w/ tube feedings: ensure it’s flowing, placement, residuals, assume nothing! Flush the lines: tube replacement is a pain, and it’s preventable.

1: Routes: Feeding tubes: G, J, NG. There are certain tube feedings specified for certain illnesses.

2: Solutions: vary based on the pt’s needs. The rates may vary based on tolerance, rate of output by the patient [think poop…], etc. Doc and dietician pick which solution.

3: Methods of delivery:
Bolus: not great. 200-400 mL at once delivered 6x/day via syringe or funnel. Not tolerated well w/ ill people, but it doesn’t require technology.
Intermittent Enteral feedings: 300-400mL of solution Q 3 or 6 hrs over 30-60 minutes by gravity drip or pump.
Continuous feedings: critical pts, pts receiving feeding direct to sm. Intestine. Little bits at a time: 50-125 mL/hr.
Cyclic feeding: delivered over 8-16 hours daily, during night or during the day depending on the client’s activity level during day or night [more activity is a good time to have tube feeding off.

4: Complications of enteral nutrition: Dehydration risk, diarrhea [liquid in, liquid out]

Enteral Meds: supplemental pancreatic enzymes must be given enterically [is that a real word?], PO meds can usually be given via feeding tubes once dissolved
1: Calculations of doses: doc over stock times vehicle, same as all the other conversions
2: Delivery: via the tube…right?

TPN: given via a central line. Usually high %dextrose [30-40] via a Central Venous Pressure, a PICC, etc.
PICC: peripherally inserted central catheter [straight to the heart]. For Chemo, long term I V therapy. You can’t give these high concentrations peripherally.

1: Ingredients: high dextrose solutions, probably some aminos, lipids…the book really doesn’t say.

2: Complications:
A: Catheter insertion: Bad things from catheter insertion: pleural poke [that’s your lung, that’s bad], damage or perforation of vein, infection
B: Infusion: Air bubbles from sloppy hanging of solution, hypervolemia from osmotic pull into the blood vessels. You care about blood sugars; TPN pts have high blood sugars, sometimes low blood sugars when TPN is stopped abruptly.

Case scenario: TBI pt w/ G Tube…don’t really need to check placement, but we have to flush it, check site for infection, change dressing, check residuals, esp right away at beginning of shift.

God I’m so glad I actually finished this…happy we’re done with another Pharma Exam Day!