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Hurst Review NCLEX Study Guide
Fluid Volume Excess (hypervolemia) - ✔Too much fluid in the vascular space caused by: HF, RF, and High Na intake (meds, food, IVF with Na) and Hormones (aldosterone and ADH) How does HF cause FVE (Fluid Volume Excess)? - ✔bc the weak heart cant perfuse the the kids therefore decreased Urine out put. How does RF cause FVE? - ✔the kidneys are not functioning therefore no urine out put and fluid remains in vasc space Aldosterone - ✔created in adrenal glands on Kidneys, it is a steroid and mineralocosteroid; retains water and sodium. therefore increases BP AHD - ✔anti diuretic therefore RETAINS water only. found in pituitary therefore any head trauma, surgery, or increased ICP can lead to ADH issues. Dx name for it is Vasopressin or "Pressins" Too much ADH - ✔SIADH, therefore reatains water in vasc space. Urine is concentrated (increased serum spef) and blood is diluted (decreased Blood HCT). Too little ADH - ✔Diabetes insipidus; diuresis fluid leads to FVD (shock), Urine will be dilute (urine spef will decrease) and blood will be conc. (HCT will be increased). the three labs that concentration (increases) and dilution (decreases) - ✔Na, Hct, Urine spef FVE SS - ✔incresaed: BP, P, RR, CVP (2-6), DW, JVP wet lungs, polyuria, P is bounding and full 3rd spacing FVE trx - ✔low Na, fluid restriction I&O and DW Diuretics bed rest FVD (hypovolemia) - ✔not enough fluid in vasc space which can lead to shock and is casued by fluid loss, 3rd space, Disease with polyuria. FVD ss - ✔wt decreases, poor skin turg,
dry mm decreased Urine decrease BP & CVP, Tachy and weak/thready, cool clammy r/t vasocons increase urine spef. FVD trx - ✔prevent loss, replace fluid safety precs (falls r/t loc), Hypermagnesemis - ✔acts like a sedative and think of muscles; excreted by kidneys therefore: RF and antacids can be the problem. Hypermagnesemia ss - ✔vasodil--> warm/flushing; decreased DTRS, flaccid tone, decreased LOC/P/RR, and arrythmias (same as....hypo....) Hypermagnesemia trx - ✔ventilator, dialysis, Ca Gluc (antidote), safety precs (sedation) Hypercalcemia - ✔Sedative, think of the muscles; caused by hyperparatyroidism too much PTH therefore pulls from bones into blood; Thiazides retains Ca, and immobility Hypercalcemia SS - ✔bones and stones Decreased DTRs, flaccid, decrease: P, RR< LOC arrythmias Hypercalcemis Trx - ✔Mobility, increase fluids, inverse r/s with phos so admin phosphates and calcitonin, steroids, safety precs, Hypomagnesemia - ✔Not enough sedative; caused by diarrhea and alcoholism bc it suprresses ADH and it is a hypertonic solution and they dont eat. Hypomagnesemia & Hypocalcemia ss - ✔Convulsions. confusion (loc change) Arrythmias Tetany, DTRS increase, Sstridor, swallow prob (positive Stridor and chevotske)
SS: confusion, sleepy, coma and hypoxic TRX: fix the primary resp issue and give oxygen Resp Alkalosis - ✔Think excitable, too little CO2 r/t hyperventilation. Kidneys exrete bicarb and ratin H. Hysteria, acute ASA OD can cause this. SS: vasoconstriction therefore lightheaded, faint, periorbital numbness, tingling toes, and fingers. TRX: sedate, treat the cause and ABGs Metabolic acidosis - ✔too much H r/t DKA, Starvation, RF, severe diahrea. cells are starving b/c gluc not available therefore breakdown of fat creates keteone (an acid). SS: think lethargy and hyperK (MURDER- twitch, weak, flaccid, and arrythmia) Kussmaul (increased resp r/t DM). Metabolic alkalosis - ✔Too much bicar r/t to loss of upper GI or too many antacids. SS: hyperactive, and hypokalemia(CRAMPS and arrrythmia) TRX: replace K Burns - ✔Cap permeability puts the client at first for 24 hours. therefore cardiac output will decrease kidney perfusion. They will exprete EPI and NOreEPI furthur vasoconstricuting. ADH and Aldosterone are secreted too. Fluids are replaced within 24 hours of the burn contact and half of the fluid is given in 8 hours. Burn Trx - ✔1. cool water for 10 min
- Keep pt covered to promote warmth and decrease bacteria introduction
- Remove jewlery or constricting artificats DO NOT peal away skin. Inhalation burns - ✔Carbon monozide and hydrogen cyanide. treat with 100% oxygen and think of possible intubation. Burn Meds - ✔Albumin: increases vol. therefore monitor for FVE IV pain meds not IM b/c decreased circulation. Immunications: active (2-4 wks) or passsive (immediate-globulins) ABX: braods like Mycins (nephro/ototoxic). Silvers Enzymatic debriment - ✔ASES: eat dead tissues. Contraindicated: Face, Preg, large nerves and open body cavity. Hyddroptherapy debriment - ✔PAINFUL and at increased risk for cross contamination. Grafting - ✔Autograph-own skin and donor site left open; reharvest 12-14 days. No bubbles beneath graph.
Burn Nutrition - ✔increased calories with protein and Vit C Burn Complications: circulation - ✔monitor: Color, NVS pulses, refill, temp; prep for potential escharotomy or fasciotomy Burn Complications: Renal - ✔Renal vasoconstriction occurs d/t loss of intravascular fluid; kidneys stop producing urine and try to hang on - glomerular filtration is decreased, decreased renal plasma flow; may see hematuria - because RBC are burned and lysed - not a gross hematuria 48 hours post expect diuresis therfore monitor FVE r/t large water in vasc sys. Burn complication: Lytes - ✔increased K bb/c cells are lysed Burn Complications: GI - ✔Decreased perfusion therfore NPO bc parlytic ilieus may develop; Give prophylaxis my. carbonate or panto to prevent stress ulcer Burn complication: integumentary system - ✔Developments of contractures or fusions and infections. Chemical and electrical burns - ✔remove from the chemical and flush 5 to 30 min with cool or sterile water. if there are powders, brush off first. Cspine for electricals and find both entrance and exit (more severe) points. this pt must be monitored on a cardiac monitor for 24hrs bc of increased risk for Vfib, monitor for internal damage, and the myoglobin/hemoglobin increase bc of kid damage. Thyroid Hormones - ✔T4, T3, and Calcitonin; Iodine (diet) to make hormones. This gives energy Hyperthyroidism - ✔Graves Disease Too much Energy; increase T4 and Decreased TSH hyperthyroidism SS - ✔Increase: P and BP, warm/diaphoretics Decrease Focus Decrease Wt therefore increased GI and Appetite, Exophthalumus irritable/nervous DX Hyperthyroidism - ✔Labs (increased T4, and decreased TSH); Thyroid Scan (1 wk pre and 6 wk post no Iodine-Amiodarone med) and MRI, CT, US
Hypocalcemia SS (energetic cats). Hypoparathyroidism treatment - ✔IV Ca with Vit D, phosphate binding medications to help decrease the Phos. Adrenal Glands - ✔Two Parts: Adrenal Medulla and Adrenal Cortex. Medulla (think Meds- epi and nore epi AKA (catecholamines) Cortex: Think COR-steroid and EX- Sex Pheocromacytoma - ✔Is an adrenal problem where boluses of cateacholamine (EPI/Nore EPI) are bolused in the body. Begnign tumor therefore do not palpate the abdomen which may release another bolus. Familiail traits. Pheocromacytoma SS - ✔Increased: HR, BP, Palps Flushed/Diaphoretic extremeties HA Pheochromocytoma Dx - ✔catecholamine levels (Vanilymadelic and metanepi). 24 hr urine collection: first void discard, no losses, and decreased stress for 24 hrs. Adrenal Cortex - ✔COR: glucocorticosteroid and meneralocosteroid EX: Sex hormones Glucocorticoids - ✔1) changes mood, 2)immunosuppressants, 3)breaks down fat/protein, inhibits 4)insulin = hyperglycemia Mineralocorticoids - ✔Aldosterone- retains water and Na; losses potasium. Sex hormones - ✔Estrogen, progesterone, and testosterone. Adrenal Cortex Problems - ✔1) not enough steroid (addisons)
- shock
- hyperKalemia
- hypoglycemia Addison's disease - ✔Too little Aldosterone (gluco and sex) therefore water and sodium cant retain water. RISK for SHOCK,
Addisons SS - ✔Fatigue, NVD Anorexia/wt loss Hypotensive Confusion Decreased Na, Increased K, and HYPOGLYCEMIA Hyperpigmentation (bronzing) Vitiligo (patchy depigmented) Addisons trx - ✔give prednisolone (BID 2/3rd first and 1/3 last) Fludrocortisone (aldosterone), DW and BPs Increased Na intake. Cushings - ✔Too much glucocorticoids, mineralocorticoids and sex hormones Cushings Gluco SS - ✔growth arrest, thin extremities (lipolysis), infection risk, HYPERGLYCEMIA, psychosis to depression) Moon face, truncal obesity, buffalo hump Cushings Sex SS - ✔oily skin, acne, Women with male traits Cushings Mineralocorticoids SS - ✔High BP, CHF, Wt gain, FVE TOO much aldosterone therefore the K will be low. Cushing's Diet - ✔Increased Potassium, Decreased Sodium, Increased the protein, and increase Ca. (WHY?) Steroid Medications - ✔1) Increase glucose, 2)immunosuppresses,
- excretes Calcium from the GI therefore brittle bones/Osteoprosis Cushing's trx - ✔Adrenalectomy (uni or bilateral) Type 1 Diabetes - ✔No insulin, abrupt onset, presents with DKA, T1A: autoimmune, T1B: idopathic, often in childhood Type 1 SS - ✔Polyuria (hypertonic)
*not given with contrast dye d/t kidney fxn (await 48hr post). Rapid Insulin NovoRAPID and Humalog) - ✔Onset: 10-15min Peak: 60-90min Duration: 4-5hr SC infusion pumps Clear and bolus Rapid Insulin - ✔NovoRAPID and Humalog Regular (Humulin, Novolin) - ✔Onset: 30-60min Peak: 2-4 hrs Duration: 5-8hrs Clear BOlus IV Fluid Standard Intermediate (NPH, Humulin N) - ✔Onset: 1-3hr Peak: 5-8hr Duration: up to 18 hours. Cloudy Long Acting (Humulin U) - ✔Onset: 3-4 hours Peak: 8-15 hours Duration: 22-16 hours Do NOT MIX Clear NO IV Basal/Bolus - ✔Combination of Long acting given only once a day with rapid insulin BEFORE meals. do not need a snack with this method; However anytime you admin rapid insulin you give food. Hypoglycemia SS - ✔shakey, cool/clammy confusion nervous HA Nausea Increased P and hunger Hypoglycemia treatment - ✔15g simple carb NO FAT. 15 min retest 15g simple or complex carb depending on BGM
D50W - ✔IV for hypoglycemia once pt awakes give them something to eat. Glucagon - ✔IM for when there is no IV access. Hypoglycemia preventions - ✔Eat monitor BGM SS hypoglycemia Take insulin regularly DKA - ✔increased BGM r/t infection, illness, skipping insulin, First sign of type 1 DM No insulin=Increased BGM therefore 3 Ps Fat breaks down to ketones. Ketones lowers pH =kussmaul (acidotic) DKA trx - ✔find the cause, Q1Hr BGM and output, IV insulin and K, ECGs ABGs Fluids NS 9BGM 14-16.5) then D5W (prevent hypglycemia). HHS - ✔Think Diabetic 2, non acidotic, No fat breakdown therefore no Ketones. Nephropathy - ✔R/t DM complication and is Sexual impotence d/t decreased sensation, peripheral pain/ parasthesia/numbness, Neurogenic bladder (retention/incontinence), Gastroparsesis: delayes empty therefore increased risk ASP Mg - ✔1.8-2. Ca - ✔2.25-2. Dig Levels - ✔0.5-2 mg/L L.A - ✔0.6-2. BUN - ✔3.6-7. Crea - ✔44. CBC - ✔Men: 4.7-6. Women: 4.2-5.
decreased CO ss - ✔decreased LOC, CP, wet lungs &SOB, skin cool/clammy, Kidney decrease, PPweak Arrythmias that are cardiac output problem - ✔Vfib,Vtach, and asytole Coronary artery disease - ✔most common cardiovascular diasea, includes chronic and acute angina Chronic/stable angina - ✔decrease flow r/t exertion leads to ischemia; temporarly pain/pressure and relieve with rest Chronis stable angina trx: NITRO - ✔venous/artierial dialtion and of the coronary arteries therefore decreased preload/afterload, Kept in a cool/dark glass bottle and renewed Q6mon, and the spary Q2years. Will complain of HA Beta blockers - ✔decreases BP/P/contractivility therefore decrease workload=decreased CO. blocks catecholamines (epi and Nore epi). Decreases size Affects kidneys First line therapy for HR Treats: hyperthyroidism and stable angina Fatigue is a big side effect Stable angina CCB - ✔(nifedipine, verapril, amlodipine, diltiazem) will decrease BP d/t vasodil arterial/coronary arteries, decreases afterload and increase oxygen in the heart Stable Angina Education - ✔1) rest 2)Avoid: over eating, excess caffein or drugs increasing HR, extreme temps, stress
- wait 2 hours post eating to exercise,
- stop smoking, isometric exercise
- decrease wt, Cardiac Catherization: stable angina - ✔Preprocedure: allergy to shellfish/iodine, check kidney fxn d/t excretion, acetylcystein for kidney protection, it's a hot shot palpations are normal POST: VS assess fleeding at puncture site, 5Ps, bed rest with straight extremety 4-6 hrous, HOld metformin 48hr
Acute Coronary Syndrome - ✔(MI or unstable Angina) decreased blood flow->ischemia-> necrosis No trigger, rest does not relieve ACS SS - ✔CP withradiation Women are atypical: feeling full,fatigue, cant catch breath, achey jaw, NUMBER 1 SIGN (ELDERLY) SOB, cold/clammy decreased BP ECG changes, vomiting ACS labs - ✔CPK-MB, Trops, Myoglobin CPK-MG - ✔cardiac spef, increases with cardiac cell damage, increased within 3- hours and peaks 12-24 hours Trops - ✔less than 0.03 (0.10), most sensitive/specific, biomarker, elevates in 3- hours and remains elevated up to 3weeks Myoglobin - ✔Neg will rule out MI, but a positive increases within 1 hr and peaks 12 hrs ACS Major arrhythmias - ✔Pulseless V tack, VFIB, Asystole pts are at risk for sudden death. VFIB - ✔defib and CPR between. GIVE EPI first, then Amiodarone and Lidocaine are administered Amiodarone - ✔antiarrhytjmic used for pulessless VT; side effects are hypotension or can lead to asystole LIdocain - ✔to precent a secont VFIB or PVC, monitor for toxicity which will be Neuro changes MI Trx - ✔(MONA-out of order): Oxygen, ASA (CHEW), Nitro, and Morphine; Thrombolytics MI & ACS thrombolytics - ✔TPa, TNKase, dissolve clott and admin within 6-8 hours of symptoms. FIRST COMPLICATION: hemmorhage Thrombolytics comtaindications - ✔Bleeding history ie bleeds/surgery, Intracranial Neoplams/bleeds, suspected aortic dissection or internal bleeds. CANNOT: do IMS, ABGs, Labs are drawn of IV starts
Sensitive, if it is (+) but the CXR is (-) it still is positive for HF. If the client is on Nesiritirde remeber to stop for 2 hrs to draw. HF diagnostic CXR - ✔will indicate an enlarged Heart of pulmonary inflitrates HF ECG - ✔will look at pumpin action/ejection fraction of the heart. will also give info on backflow and valve disease ACE - ✔Supresses RAS, Prevvents Angio 1 converting to 2 (dilation and increases Stroke Vol.) Blocks Aldosterone (loss water/NA, increasesK) Drug of Choice for HF, used for: HTN, MI common brady cough Watch for Angioedema ARBi - ✔"artans" Stops Aldosteron (decreases NA/Water and increases K) e, decreases workload and afterload. Blocks Angio 2 receptors therefore decrease arterial resistance. Treatment of HF when ACES can't be used. and HTN watch for: hypoglycemia, hyperK, Renal dysfunction DIG - ✔Used for HF and Afib Contractions stronger and decrease rate of ventricals therefore increases OP and increases kid perfusion. Early DIg tox - ✔Anorexia, NV late digoxin toxicity - ✔vission change and arrythmias. Decreased K and Dig will lead to Toxicity IV inotrops for HF - ✔severe or acute decompensating HF are Milrionone and dobutamine Vasodilators HF - ✔when decomplensation of HF therefore use NITRO and neseritide HF diet - ✔decreased NA, monitor salt subs (contain increased K), no canned/processed foods Pacemakers - ✔Two types: demand and fixed. Used to increase HR with symptomatic Brady.
Demand: shocks/paces when needed Fixed: constant pacing therefore know set rate Set Rate is the min number if the HR is lower than Set rate theres something wrong Post Op pacer - ✔monitor incision (bleeding), for electrode displacement (common complication), Immbolize the arm, assist with Passive ROM (prevents shoulder freeze), DO NOT raise arm above shoulder Loss of caption - ✔no contraction after stiumlus is a pacer malfunction Failure to sense - ✔fires inapropriately, it is a pacer malfunction Pacer Malfunctions cause by - ✔Programmed incorrectly, electrodes dislodge, battery depletion Pacer Education - ✔1) pulse monitoring,
- ID/Bracelet #)aboid electromagnetics fields (cell phones/large engines) 4)battery depletion Pulmonary Edema - ✔at risk pts: fast fluid, very old/young, heart/kidney hx Pumonary Edema SS - ✔sudden onset, breathless,restless/anxious, seere hypozia, productive (pink frothy) sputum/cough Pulmonary Edema TRX: - ✔oxygen (90%<), diuretics (1-2min push otoxicity) Morphine-decrease anxiety and vasodilates Nesirited: less than 48hr use, vasodilates veins/arteiries; turn off 2 hrs prior to draw Pulmonary edema position - ✔upright and legs down (fluid in legs rather than lungs), imoves cardiac OP Cardiac tamponade - ✔fluid in pericardial sac compresses heart d/t MVA, Vent Biopsy, MI, pericarditiis, hemorrhage, post CABG Cardiac Tamponade SS - ✔decrease cardiac OP, (HALLMARK: increased CVP and decreased BP), muggled Heart sound, distended neck vein, schock (decreased CO), narrowed pulse pressure (small numbere sys/dys) Narrow pulse pressure - ✔think cardiac tamponade Widdened pulse PRessure - ✔Think ICP
communication (Neologism, word salad, echolalia, concrete, religiosity, delusion, hallucination) Schixo trx - ✔decreased stimuli, observe freq., re-orientate, conversations reality based, observe for hallucinations, warn prior to touching, dont refer to voices as "they", don't shar their perceptions, raise HOB, turn off TV, reassure Paranoid Personality Trx - ✔be reliable to build trust, be honest and consistent, brief/Freq visits, matter of fact, respect personal space, caution touch, dont mis meds,theyll want their own food, Paranoid personality SS - ✔suspicious with no reason, cant explain their delusions, pathologic jealousy, hypersensitive, cant relax, no humour, no emotion, abnoral agner and rages Anxiety diosrder ss - ✔universal emotion, dosorder when it interfers iwth daily fxn, mild: increases performances and does not require a nurse. Severe cases will decrease performance and require nurse assistance for step-bystep assistance Generalized anxiety disorder ss - ✔Chronis anxiety, worries daily, fatigue r/t to constant activity and muscle tension, seeks help Wernicke's encephalopathy - ✔A brain disorder caused by thiamine deficiency and characterized by visual disturbances, ataxia, somnolence, stupor, and , without thiamine replacement, death. Korskoff's Syndrome - ✔Caused by chronic alcoholism which severely impairs short- term memory Glomerulonephritis - ✔Inflammed glommerulus, antibodies in flomural causes damage therefore decreases Filtration caused by step, skin infection, mono, hepatits Glomerulonephritis SS - ✔flank pain, decreased urine, hematuria, proteinuria, periorbital edema, increased BP, FVE, Urine concentration, azotemia (increased BUN and Crea), malaise and HA (increased toxins). Glomerulonephritis treatment - ✔treat the causing infection, I&O, DW, diuretics, monitor BP, restrict fluids, balance rest/activity, Increase Carbs and decrease Na and Protein, Dialysis Glomerulonephritis education - ✔diures 1-3 weeks post injury, blood and protein in urine for months, signs and symptoms of RF: malaise, HA, anorexia, NV, decreased out put, and increased DW Nephrotic Syndrome - ✔inflammed response in glomerulus creates big holes allowing protein to escape therefore causing hypoalbumemia thus causing edema and FVD.
Now RAS produces aldosterone in attemts to retain water and Na therefure further fluid leaking into cells : ANASARCA!!!! a decrease in protein can lead to blood clots Nephrotic syndrom caused by - ✔idiopathic (unknown) thought to be caused by bacterial/viral infection, NSAIDS, CA, genes, systemic disease like lupus or DM Nephrotic syndrome ss - ✔massive proteinuria, hypoalbumenia anasarca hyperlipidemia Nephrotic syndrome trx - ✔diuretics, ACE (stop aldosterone) Prednisone (decrease inflammation) cyclophosphamide (chemo agent-supress immune system therefore decrease inflammation) Diet: increased Protein (1-2g/kg/day) and decrease Na Lipid lowering agent, anticoagulant dialysis AKI - ✔suddent onset and goal is to reverse or precent chronic kid injury Pre-renal - ✔blood cant get to kid d/t hypovoplemia, shock, dcreaesed HR. this is the most common cause for AKI INtra renal AKI - ✔injury/damage within the kidgney like glommerulonephritis, nephrotic sundrome, malignat HTN, DM, acute tubular nephritis (cant filter), Dyes, drugs (aminoglycosies) NSAIDS Post renal AKI - ✔urine cant get out r/t to enlarged prostate, stones, tumor, urethral obstruction, edematous stoma (ileal conduit) AKI phases - ✔intial- injury occured
- oliguric (OP less than 100ml/hr) 3)diuretic phase: fliod needs to be replaced according to labs.
- Recovery which can take 3-12 months and increase protein/calories during this time with resuming activity AKI ss - ✔Increased BUN/Crea, spef gravity. Spef grav can become fixed where you know the kidneys are no longer function to concentrate or dilute. FVE (HTN,HF), increased Toxins (HA, NV, anorexia, itching), increased phos=decreased Catherefore Ca pulls from bones (osteoathritis), anemia r/t decreased erythropoietin, increase K d/t no excretions=arrythmias and met. acidosis
