Med Sheet for all!

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

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

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:

1. onset
2. peak
3. duration
4. 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.
5. If giving fast acting insulin, make sure the tray is in their hands; too many things happen with trays.
6. 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
7. 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.
8. 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.
9. 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.
10. Don’t hold food: the secret w/ most health issues is consistency: same meals, same times, etc.
11. 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.
12. 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.
13. 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

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:

1. Clinical disorder: focus of psych clinical attention
2. Personality disorders and Mental Retardation
3. General medical conditions: physical conditions
4. PsychSoc/environmental problems
5. 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