Wednesday, October 31, 2007
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
Zofran Selective serotonin antagonist in CTZ and vagus nerve
Decadron Hormone, glucocorticoid
Use: anti-inflammatory, immunosuppressant, reduces capillary dilation
Adverse: edema, hyperglycemia, bowel perforation, impaired wound healing
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
Adverse: hyper/hypoglycemia, constipation
Kaopectate OTC antidiarrheal
Use: coats muscosa, binds bacteria and toxins that cause diarrhea
Adverse: CNS depression, constipation
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
Use: prevention of constipation
Use: neutralizes stomach acid and reduces gastric activity
Zantac Histamin 2 blocker
Use: GERD, block parietal cells from producing acid
Adverse: hepatotoxicity, toxicity w/Metroprolol, cardiac dysrythmias
Use: suppress gastric acid production
Adverse: diarrhea, elevated liver enzymes
Carafate Mucosal protectant
Use: absorbs bile, inhibits pepsin, blocks diffusion of H+, protects mucosa
Epinephrin Adrenergic agonist
Use: anaphylaxis, cardiac arrest, asthma, glaucoma
Adverse: acute MI, V fib, pulmonary edema
Albuterol Beta 2 agonist
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
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
Use: increase heart rate and cardiac output, bronchodilator, decrease GI spasm
Adverse: V fib, paralytic ileus
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
Use: insomnia, pre-op for general, spinal or local anesthesia
Adverse: dependency, decreased LOC, resp. depression
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
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
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
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
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
Synthroid Thyroid replacement, increases metabolism, oxygen consumption, body growth
Use: treat myxedema, hypothyroidism
Adverse: tachycardia, HTN, thyroid crisis, angina, CV collapse
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
Use: intermediate acting anti-inflammatory for allergic rxn, short-term asthma therapy, cerebral edema
INSULIN (subcut) Use: Type 1 DM
Lispro Rapid acting, shorter duration than regular insulin
Onset: 5 min. (< 15 min)
Peak: 0.5 – 1h
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
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
Actos Glitizone: stimulates insulin secretion, increases insulin receptor sensitivity, decreases hepatic glucose output,
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
Tuesday, October 30, 2007
N205 Fall 2007
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.
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.
Concepts of surgery:
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.
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
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
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.
Monday, October 29, 2007
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)
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.
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
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.
Lipids: administered as fat emulsion solution, used when on IV for >3days. Balance nutritional needs; given every few days to clients on TPN.
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.
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.
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!
Sunday, October 28, 2007
Exam 2: 6 questions per class, 25 questions, no scantrons. Less testing on patho more on the drugs.
Hormones and the hypothalamus:
ADH: works on kidney
AcTH: act on adrenals, which release corticosteroids
TSH: effects thyroid gland
A. Thyroid gland
1. Secretion of hormones T3 & T4 regulated by feedback mechanisms
feedback means: negative feedback, once a state is reached a chemical is released to prevent more stimulation.
2. Hypothyroidism: primary or secondary cause; myxedema: that’s severe hypothyroidism—odd syndrome. Hypothyroid: fatigue, obesity.
B. Thyroid Replacement:
C. Hyperthyroidism: Grave’s disease. Hypertrophy of the thyroid, could be autoimmune. This is the big bulging eye thing
D. Nursing Process
assess: vital signs, metabolic rate, body weight
RN Dx: fatigue r/t hypothyroidism, malaise etc. Activity intolerance.
Education re: drugs, compliance
E. Mrs. X takes Synthroid 0.05 mg daily. Pharmacy sends Synthroid 25 mcg tablets. How many tablets should she receive?
A. Addison’s Disease: adrenal insufficiency
B. Cushing’s Syndrome: adrenal hypersecretion
ADRENAL DRUGS we’ll give them a lot, there are quite a few. NCLEX likes Cushing’s and Addison’s questions. There are lots of corticosteroids. They decrease inflammation, therefore they decrease the immune system; TBI patients with swelling in the brain, decrease the systemic inflammation and shock from sepsis with an infection.
Glucocorticoids are influenced by Acth, from the pituitary. Effect carb, fat, protein metabolism. They act like mineralocorticoids.
C. Glucocorticoid Prototype:
D. Other glucocorticoid Prototypes
1. Inhaled Steroid:
E. Mineralocorticoids: secrete aldosterone; for Rx of adrenocortical insufficiency with Addison’s Disease. Aldosterone is a water/salt saver. We don’t give these that often.
F. Mr. P 68 had a severe allergic reaction to shellfish. He was taken to the ED and given dexamethasone 100 mg IV. Why? What patient education is needed before goes home? They gave this to reverse the inflammatory response. This patient needs to learn not to eat shellfish.
Hyperglycemia triggers insulin
Hypoglycemia triggers glucagon to release glycogen/glucose from the liver cells
1. Def: chronic disease from deficient glucose metabolism, resulting from insufficient insulin secretion from beta cells, causing hyperglycemia; Types 1 & 2, gestational, secondary from medications-such as?
Type 1: beta cells in the pancreas ain’t makin no insulin ever the end.
Type 2: insulin resistance
There’s an epidemic of both types of diabetes right now—we don’t know why, it’s our society probably.
Want to manage blood sugars b/c morbidity and mortality soar when sugars aren’t kept close to normal all the time
2. Sx: polyphagia, polyuria, polythirtya, blurred vision, frequent infections, poor wound healing, micro and macro vascular disease
DKA [diabetic ketoacidosis; the body starts breaking down fats and proteins b/c the cells are hungry, you lose a lot of water so you’re hypovolemic, ketones in the blood create acidosis, and it smells like fruit, sometimes we think it’s alcohol] When this person comes into the er: you give them insulin stat, IV. They need blood sugar tests Q hour. IV fluids for dehydration, check electrolyte levels. We bring the blood sugar up slowly to prevent weird fluid shifts in the body/brain. There’s usually a DKA protocol for an ER.
HHNS: Hyperosmolar something something.
Complications: High sugar is bad for nephrons, eyes, peripheral neuropathy, O2 delivery, MI’s, coronary syndrome [b/c insulin is also about fat metabolism.] Lose feet, lose kidneys, have an MI. If you keep blood sugars in rein, these complications are decreased 60-70%.
Normal fasting: 80-120
After a meal: 120-140
Prevent diabetes: we can redirect patients when filling out their menus.
Indicators: frequent vaginal infections/yeast infections, poor wound healing, blurred vision
Stuff that controls insulin levels: insulin, glucagon, adrenalines [they want the cells to have more sugar in the blood], cortisol/steroids, growth hormone
Sliding scale means Type 2.
1. Types: Know onset of action, peak effect, duration of action
3.Action: promote use of glucose by body cells
4. Adverse effects: shock, tachycardia, hypoglycemic reaction, rebound hyperglycemia (somogyi effect-happens when insulin peaks, esp overnight, blood sugar goes down, than the body reacts and releases sugar, and they wake up w/ high blood sugar. They need less HS insulin or an HS snack)
5. Administration: Sub cut, or inhaled
6. Sliding Scale coverage: Regular or Humalog prn blood glucose values q6h or ac & hs
7. Client education
8. Insulin pump
9. Herbal antidiabetic agents
C. Oral hypoglycemic agents: know action, adverse effects
First protocol for managing T2 DM: diet and exercise.
Next step: 1 oral agent
Next: 2nd oral agent or higher dose
D. Nursing Process
1. Assessment: Hemoglobin A1C [every three months to check hemoglobin to see how much sugar is attached to it], daily blood glucose values and trends [before and after meals], trends, patient education, complications
2. Nursing diagnoses: altered nutrition, knowledge deficit, risk for impaired tissue integrity
3. Planning: check blood sugars, vision, Hx, chest pain if Hx of MI or coronary disease.
E. Case Scenarios
1. Your patient is a 78 yo admitted with CHF and DM. What nursing interventions are indicated?
Check AC and HS blood sugars. Education: see what they know. Help w/ menu. Offer the new pamphlets w/ the newest research. Check their meds, get them ontime. If NPO for a procedure, make sure their blood sugar is ok. For the CHF: check vitals, lung sounds, listen for crackles in the bases.
2. Your patient is a 24 yo male admitted with DKA. His admit BS was 880. What interventions are indicated?
So this is lifethreatening: DKA protocol, IV insulin, IV fluids, get baseline lab values, O2 to get his metabolic O2 availability up. Education, prevention.
Objectives: Upon completion of this class, the student will be able to:
Describe thyroid replacement drugs in terms of action and adverse effects;
Describe the use of specific glucocorticoids in terms of action and adverse effects;
Discuss the pathology of Types 1 & 2 diabetes;
Describe pharmacological management of diabetes including insulin and oral agents;
Discuss patient education regarding effective management of diabetes.
Saturday, October 27, 2007
Oct. 15: NEUROLOGICAL AGENTS; PART 2
Categories of pain:
- Acute: mild, moderate, or severe, lasts the length of the tissue injury.
· Mild: use nonnarcs
· Mod: use narcs and non narcs [like acetaminophen w/ codeine]
· Severe: use narcs
- Cancer: r/t pressure or blockage of tissues. Use NSAIDs and Narcs
- Chronic: persistent pain. Use nonnarcs, unless risk is fully assessed for using narcs
- Somatic: from muscles, bones, joints. NSAIDS are better.
- Superficial: from mucous membranes or integumentary damage
· Mild: use nonnarcs
· Mod: use narcs and non narcs [like acetaminophen w/ codeine]
· Severe: use narcs
- Vascular pain: from vascular or perivascular conditions: nonnarcs
- Visceral pain: body-organ related pain: nonnarcs
Post op pts: narcs and maybe NSAIDs to prevent prostaglandins
Cancer pts: narcs, and as much as they need. They do develop a tolerance. Also anxiety comes along with pain mgmt, because more pain means more metastasis
BKA amputation pt: [below knee] from diabetes usually, trauma secondly.
Phantom limb pain: nerves are still firing; so you’d give them TCA’s, antidepressant drugs, gabapentin, which is funny. Neurontin is coming up in this way…if your client is on antidepressants w/o hx, pain mgmt is probably why.
Anyone suddenly stopping seizure meds is at risk for status epilepticus
Chronic pain is usually also nerve pain: so you’re using those TCA’s, Gabapentin, etc.
Nociceptors in viscera respond more to stretching, pressure, inflammation
Tissue damage causes release of prostaglandins, bradykinin, serotonin—nociceptors respond to these and send pain signals to the brain.
Pain and vital signs: HR increases, BP decreases
Nondrug: relaxation, visualization, comfortable positioning, time manage so that you’re doing everything at once and then leave the pt alone. Shut up at the nursing station, quiet the beeping equipment.
Pain: has to be assessed. CNA’s can gather data about pain, although they can’t assess pain.
I. PAIN MANAGEMENT
A. 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.
Not an NSAID or Narc: Acetaminophen (Tylenol); use, action; adverse effects:
Contra: severe hepatic or renal disease, ETOHism
Decrease pain and fevers
Inhibits prostaglandin synthesis, inhibits hypothalamic heat-regulator center [thermostat]
Adverse: hypoglycemia, oliguria, urticaria, hemorrhage, hemolytic anemia, thrombocytopenia
Liver toxic. Don’t try to kill yourself with Tylenol, you’ll just die slowly of liver toxicity. GI upset w/ all NSAIDS. Take them with some food in the stomach.
If your pt has pain meds PRN Q3 hrs, you should be assessing pain Q3hrs.
All these narcotics are lipophilic and readily cross the BBB.
PCA: best thing ever. Pts get instant relief. These pts need to be alert, educated about this medication system. Often there’s also a basal rate of small continuous dosing. These clients are still at risk for Resp and CNS depression, so these clients still need a lot of assessing.
B. Narcotic Analgesics: AKA narcotic agonists. Act largely on CNS, not PNS. Anti tussive [anti-cough] and anti-diarrheal.
1. Prototype: morphine sulfate ; use, action; adverse effects
Isolated from opium in 1803. Opium was made prescription only in 1914.
Use: acute pain, preop
Action: Depress CNS, depression of pain impulses by binding to the opiate receptor in CNS
Adverse: resp depression, seizures, increased intracranial pressure, miosis [pinned pupils], constipation, urinary retention
Always think of giving morph; it’s the gold standard narc.
All narcotics are likely to cause respiratory depression, slow GI tract. If you’ve got a patient on narcotics, you’d better know their last BM and what the laxative is to counteract it. Nurses are stingy w/ narcotics because they’ve seen someone go into resp depression.
2. Meperidine (Demerol): caution. Shorter action than morph. No anti-tussive.
Use: Not for long term use—usually 72 hours or less. In L&D it is preferred b/c it does not slow uterine contrxns. Less constipation and urine retention.
Contraindicated: Elders, cancer pts have developed neurotoxicity. Not for hepatic dysfunction, sickle cell, CAD, seizure hx, dysrhythmias. Metabolized in liver, therefore dyshepatic pts should have smaller dose.
Adverse: Don’t take it w/ other dope: CNS, resp depression risk. Long term use risk for CNS tox and seizures. Decreased BP.
3. Hydromorphone (Dilaudid): use, action, adverse effects: 6x more potent than morph—faster onset and ride. Less GI interactions, hypnotic effects. We’re using this more and more.
Use: relief of mod to severe pain
Action: like morph, depression of pain impulses by binding to the opiate receptor in CNS
Risk: CNS depression w/ other dope, ETOH
Adverse: bradycardia, tachycardia, respiratory depression [life threatening]
C. Narcotic antagonist: naloxone (Narcan): use, action, adverse effects
Use: Antidotes for overdoses of narcotics. Reverses CNS and resp depression
Action: have higher affinity to binding sites and kick the narcotics out.
Adverse: if client is in opioid withdrawal. High doses create hepatotox.
Good: approved in neonates of junkie moms.
Education: don’t quit taking the drugs suddenly, call if side effects show up.
Many of these drugs are teratogenic; if you want to get pregnant you’ve got to check in with some smart MD’s.
What’s w/ seizures: generalized [clonic tonic] vs partial. Generalized= all parts of the brain. These fire too spontaneously. Partial/Focal means one hemisphere. Grand mal=big bad. Absent= down LOC, can look like spacing out. Unfortunately you can only sort of blame your parents, high fevers as a child, drug withdrawals. People with chronic seizure activity are on drugs for life. Post period [posteptal] has low LOC, may need airway mgmt, rolled onto side in case of barfing.
Epilepsy: seizure disorder, 1% of pop. Abnormal electric discharges from cerebral neurons, causing loss or altered consciousness, and sometimes convulsions.
50% of epilepsy cases are thought to be primary, or of unknown origin, and the other 50% are r/t trauma, anoxia, stroke, or infection.
Grand mal: big bad, clonic tonic type.
Clonic means dysrhthmic muscle contraction, tonic means sustained muscle contraction
Petit mal: tiny bad, ‘absence’ type. Means brief loss of consciousness.
Psychomotor: complex symptoms: repetitive behaviors, motor seizure, behavioral changes
Status epilepticus: emergency seizures in rapid succession: a continuous seizure that will not stop without intervention. Pregnancy eclampsia, meningitis, or toxic stuff. Or withdrawal from anti-convulsants.
A. Hydantoins; Prototype: phenytoin (dilantin); Anti convulsant
Use: grand mal, partial complex seizures
Action: reducing motor cortex activity by altering transport of ions.
Adverse: least toxic effects. Aplastic anemia, Thrombocytopenia, ventricular fib. Bleeding disorders from not enough platelets, H&H. Teratogenic.
B. Barbituates: now used more for ‘status epilepticus:’ when there’s a long seizure that’s emergent.
C. Benzodiazepines now used more for ‘status epilepticus:’ when there’s a long seizure that’s emergent.
D. Valproate: Valproic acid: Rxed for various types of seizures. Hepatotoxic.
Action: was made to mimic GABA, but it doesn’t work that way. Its exact mechanism of action is unknown, but its therapeutic action on neuropathic pain is thought to involve voltage-gated N-type calcium ion channels. Book says “promotes GABA release”
Adverse: nothing too exciting. Best eaten with food.
E. Case Scenarios
A. Parkinsonism: serious disease. Involuntary tremors, movements, cerebral function is the same; don’t assume they have altered cognitive function. Imbalance of acetylcholine [short term memory, muscles, PNS] and dopamine. Acetylcholine is excitatory or activating NT, dopamine is an inhibitory NT. Lack of dopamine at pre-synaptic muscle receptors. Advanced stages can create confusion. Degradation of the dopamine secreting neurons in the substantia nigra
Prototype; carbidopa-levodopa (Sinemet): helps balance out lack of dopamine
Use: anti-parkinson; tremors and rigidity
Action: levodopa turns to Dopamine in the brain. Carbidopa inhibits levodopa from turning to dopamine in the rest of the body.
Adverse: palpitations, psychosis, hallucinations, depressions
Life threatening: hemolytic anemia, agranulocytosis, dysrhthmias
B. Alzheimer’s Disease: really prevalent pathophysiological syndrome. Stanford just came up with a pre-Alzheimer’s blood test; which can be helpful in terms of planning and prophylactic medication.
1. Pathology: Lack of acetylcholine. Caused by malformed neural microtubules, crumbling cells. Genetic predisposition. It’s just one type of dementia; forgetfulness; these guys can tell you all about WW2 but not remember breakfast. Incontinence and fall risks also increase b/c motor skills decrease. Wandering happens too. Exercise and mental activity help prevent Alzheimer’s by taking blood to brain.
Acetylcholinesterase inhibitors: block the enzyme from breaking down acetylcholine [which you need]
2. prototype: tacrine Cognex.
Use: alzheimers, memory loss, Myasthenia Gravis
Action: elevates Ach by blocking the Ach breaker-downer enzyme
Adverse: depression, hepatotox
A. Myasthenia Gravis: autoimmune, effects young women, lack of acetylcholine, lack of nerve impulses are myoneural junction; the nerves want to talk but they lost their cell phone [Ach]. Use Acetylcholinesterase inhibitors for this too.
B. Multiple Sclerosis: demyelination of neurons in CNS and PNS, also effects young white girls. Use muscle relaxants for this.
Lots and lots of drugs.
Depression is the most common chronic illness second to HTN [most common psych disorder: anxiety.]
Schizophrenia: disorganized thoughts and behaviors.
Just because you don’t want to be a psych nurse doesn’t mean psych patients won’t end up on your floor sick or getting surgery.
A. Antispychotics: there’s a laundry list of these drugs
1. Phenothiazines: fluphenazine (Prolixin): use, action, adverse effects increase the longer people are on the drugs, EPS symptoms, dyskinesia
Use: psychosis, schizophrenia
Action: blocks dopamine receptors in brain
Adverse: Agranulocytosis, EPS [parkinson’s-esque], tachycardia
NCLEX and quiz question: Phenothizazines have anticholinergic [pro SNS] effects:
2. Nonphenothiazines: haloperidol (Haldol): use, action, adverse effects
Use: neuroleptic that stabilizes thinking processes for confusion and psychosis, Tourette’s
Action: Book says it changes how dopamine acts on CNS. Margi says: blocks dopamine receptors in CNS. Resp depression.
Adverse: laryngospasm, resp depression, dysrhthymias, neuromalignant syndrome
B. Anxiolytics: anti-anxiety, some people have such acute anxiety they can’t leave the house.
1. Benzodiazepines: lorazepam (Ativan): Benzos are great: are used for panic attacks, severe or prolonged anxiety, depression, insomnia, seizures, ETOH withdrawal, skeletal muscle spasm, pre-op meds. Fewer side effects than barbs. Risky long term
use: anti-anxiety, anti-emetic, preop, status epilepticus
action: potentiate GABA effects by binding to specific GABA/benzo receptors; The main pharmacological effects of lorazepam are the enhancement of GABA at the GABAA receptor. I think the book might have eaten some ativan when they wrote out the drug action—it doesn’t sound right.
Adverse effects : fewer than other benzos. These cause amnesia when the drug is on board. Tolerance can be developed. CNS depression, resp depression, hypotension esp when hypovolemic.
2. Buspirone hydrochloride (BuSpar): use, action, adverse effects: better long term than ativan. effective after 1-2 weeks, fewer side effects.
Use: generalized anxiety
Action: It is thought to act by interfering with the function of the neurotransmitter serotonin in the brain, particularly by serving as a 5-HT1A receptor partial agonist. Additionally, it acts as a mixed agonist/antagonist on postsynaptic dopamine receptor
Side effects; less withdrawal than benzos.
All can cause suicidal tendencies
A. Depression: #2 most common chronic condition.
Reactive depression: after grieving, after major events. Usually need pharma until the NTs recover on their own.
If you have a pt w/ Hx of depression: what are their meds, do they treat with therapies, assess if they are feeling depressed, the chaplains are great non-denominational listeners
People don’t rehab or get well when they’re depressed.
Major depression: lack of motivation, interest
Bipolar: Manic and then Depressed
1. TCAs: amitriptyline (Elavil):
use: depression, bipolar, migraines,
action: serotonin and norepinephrine increased in nerve cells by blocking nerve fibers
adverse effects: seizures, agranulocytosis, thrombocytopenia
2. SSRIs: fluoxetine (Prozac): serotonin synaptic reuptake inhibitors
use: depression, bipolar, migraines
action: serotonin is increased in neurons by blocking reuptake: These don’t let them go back to the house on the pre-synaptic neuron, so it’s in the synapse longer. People w/ chronic depression often have serotonin-not-enough-syndrome
adverse effects :. Seizures
3. MAOIs: these are bad bad. High risk of interactions. Amino-amine-oxidase inhibitors, that break down epi and nor epi. HTN crisis. These interact w/ everything including cheese and wine. Old anti-depressants.
C. Mood Stabilizer: Lithium for bipolar disorder; use, action, adverse effects
Use; manic episodes, bipolar.
Action: ion transport in muscle and nerve cells, increased receptor sensitivity to serotonin
Adverse: dysrhthymias, circulatory collapse
At the completion of this class, the student will be able to:
1. Distinguish between nonnarcotic and narcotic analgesia and state indications for both;
2. discuss actions, uses, and adverse effects of specific opioids;
3. distinguish between the types of seizures;
4. describe use, action, and adverse effects of anticonvulsant drugs;
5. describe the actions and adverse effects of antiparkinson and Alzheimer’s disease drugs;
6. explain treatment strategies for multiple sclerosis and myasthenia gravis;
7. describe use, action, and adverse effects of antipsychotics and anxiolytics;
8. discuss use, action, and adverse effects of antidepressants;
9. discuss key patient teaching with safe use of these drugs.