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Terms in this set (55)

Peritoneal Dialysis
o Peritoneum acts as the filter—for the patient this is a much gentler option although ver complicated for the HCP
o Involves siliconized rubber catheter placed into abdominal cavity for infusion of dialysate (goes into the peritoneum and dwells there, 3 hours or so, the exchange occurs through the peritoneum, and then there is a clamp released and a drain bag to collect the waste and remove it)
o Peritoneal dialysis exchange for control of fluids, electrolytes, nitrogenous wastes, blood pressure, and acid-base balance.
o For some people this is great because they can receive the fluid, let it dwell and go out, and then return to drain the fluids) and the fluid shifts aren't as severe
o Types:
o Continuous ambulatory (CAPD)
o Automated
o Intermittent
o Continuous-cycle
o Continuous Ambulatory Peritoneal Dialysis (CAPD)→→
o Automated Periotoneal Dialysis that keeps adding the dialysate and then draining the accumulated fluid—can occur while someone is sleeping and it continues to change and filter throughout the night
o Complications of a Peritoneal Dialysis
o Hypotension not as common here—infection is the worst complication—this is actually worse in the hospital because of all of the germs- at home its done with clean technique and less opportunity for infection
o ** main infection is Peritonitis
o Pain
o we don't want the urine to be cloudy, want it to look like urine (be straw colored)
o Exit site/tunnel infections—cath can develop infections, can have anatomical issues with flow, their inflow can be 3 liters into the belly which is a lot—want what you instill to be at least a bit more than what you input to monitor net outflow
o If they don't let out what was put in, it may be an anatomical problem, we might ask them to change position, they may have been dehydrated,
o The tonicity of the fluid can be a reason for this
o Be careful if not managed appropriately—can experience flash pulmonary edema
o Can become critical depending on the fluid—ie that story where she lost the drain and then they added more fluid and person had 6 Liters or more of fluid inside
o Poor dialysate flow
o Dialysate leakage
o Other complications
o Nursing care for Peritoneal Dialysis
o Before treatment—evaluate baseline vital signs, weight, laboratory tests
o Continually monitor patient for respiratory distress, pain, discomfort--
o Monitor prescribed dwell time, initiate outflow
o Observe outflow amount and pattern of fluid--** weight will always be the best way to tell
o Want to make sure output isn't cloudy, looks normal
Incontinent Urinary Diversion (Ileal Conduit)
o Ileal conduit (ileal loop), most common type: 6-8 inches of ileum are converted into a conduit for urinary diversion
o Take a piece of the ilium (small intestine) and then they create a pouch or conduit and drain the ureters into this, cannot be connected ot the urethra, will have to then void through the stoma and then that's brought out through the skin
o Incontinent ostomy—urine is always flowing into the bag, need to be careful about the skin around the stoma which can be impacted and may be infected by constant contact with the constantly flowing urine
o More difficult on account of the lack of the detruser muscle which really helps ocntrol urine flow
o Ureters are anastomosed into one end of the conduit, and other end of the bowel is brought out to the abdominal wall to form a stoma (sticking out of the belly, want it to be red and well perfused looking, don't want it to be dusty which might be an emergency, initially and always
o Urine flows continuously
o Requiring external collection device, requires frequent emptying
o Risk for infection
o With the stoma—want it to be pink and moist, if there are any signs of it not being well perfused, or herniated, want to let the HCPS know
o Later when pt goes home, they will have a bag covering the stoma site (an ostomy appliance)
o Teaching
o Care of stoma & appliance—the stoma can usually handle the free flowing urine but the skin around it cannot so the applicance and dressing need to be appropriately applied
o Increase fluid intake
o Signs and symptoms of infection
Hemothorax/Pneumothorax
o Pneumothorax
o Presence of air or gas in pleural space that causes lung collapse—bc the pressure system is altered. This collapse can be rated by how much air
o Tension pneumothorax
o Occurs when air enters pleural space during inspiration thru 1 way valve caused by blunt chest trauma & can't exit upon expiration
o ↑ pressure compresses blood vessels & ↓ venous return → ↓CO → death can occur quickly if untreated
o can be open or closed so broken rib could puncture the lung from a trauma, or a stabbing could provide a direct line , or a central line could puncture
o Hemothorax
o Accumulation of blood in pleural space
o Can also be hemo-neuro thorax with blood and loss of pressure in the system
o Common Risks
o Blunt chest trauma
o Penetrating chest wounds
o Closed/occluded chest tube
o Diagnostics
o ABG - specimen placed in heparinized syringe on ice
o CXR
o Thoracentesis - may be used to confirm hemothorax
o Assessment→their lung is on the way to being partially or fully collapsed, will obviously manifest in a lot of respiratory responses
o Pleuritic pain—loaded with nerve endings
o Respiratory distress
• ↑ RR, ↑ HR, hypoxia, cyanosis, dyspnea, use of accessory muscles
o Tracheal deviation to unaffected side (tension pneumo)—need immediate action to reduce the pressure
o ↓ or absent Breath sounds (affected side)
o Asymmetrical chest wall movement
o Anxiety
o Percussion
• Hyperresonance (pneumothorax)
• Dullness (hemothorax)
o Subcutaneous emphysema—air bubbles under the skin
o Will be diagnosed based on clinical manifestations plus an xray
o Interventions
o Assess & monitor respiratory status
o Monitor chest tube drainage
o Give meds as ordered
• Anxiolytics - lorazepam (Ativan) or midazolam (Versed)
• Analgesics - morphine or fentanyl
o Provide emotional support
o Put in a chest tube!! As there is air or blood which is messing up the negative pressure in the lungs, we want to use this to restore that!!
o The chest tube is not just about getting air inside to reinflate the lung, but about the drainage as well
Peripheral vascular disease (PVD), commonly referred to as peripheral artery disease (PAD) or peripheral artery occlusive disease (PAOD) or peripheral obliterative arteriopathy, refers to the obstruction of large arteries not within the coronary, aortic arch vasculature, or brain. PVD can result from atherosclerosis, inflammatory processes leading to stenosis, an embolism, or thrombus formation. It causes either acute or chronic ischemia (lack of blood supply). Often PVD is a term used to refer to atherosclerotic blockages found in the lower extremity.[1]
PVD also includes a subset of diseases classified as microvascular diseases resulting from episodal narrowing of the arteries (Raynaud's phenomenon), or widening thereof (erythromelalgia), i.e. vascular spasms.

Tx
Dependent on the severity of the disease, the following steps can be taken:[23]
Smoking cessation (cigarettes promote PVD and are a risk factor for cardiovascular disease).
Management of diabetes.
Management of hypertension.
Management of cholesterol, and medication with antiplatelet drugs. Medication with aspirin, clopidogrel and statins, which reduce clot formation and cholesterol levels, respectively, can help with disease progression and address the other cardiovascular risks that the patient is likely to have.
Regular exercise for those with claudication helps open up alternative small vessels (collateral flow) and the limitation in walking often improves. Treadmill exercise (35 to 50 minutes, 3 to 4 times per week[1]) has been reviewed as another treatment with a number of positive outcomes including reduction in cardiovascular events and improved quality of life.
Cilostazol[24] or pentoxifylline treatment to relieve symptoms of claudication.[1]
Treatment with other drugs or vitamins are unsupported by clinical evidence, "but trials evaluating the effect of folate and vitamin B-12 on hyperhomocysteinaemia, a putative vascular risk factor, are near completion".[23]
After a trial of the best medical treatment outline above, if symptoms remain unnacceptable, patients may be referred to a vascular or endovascular surgeon; however, "No convincing evidence supports the use of percutaneous balloon angioplasty or stenting in patients with intermittent claudication".[23]
Angioplasty (PTA or percutaneous transluminal angioplasty) can be done on solitary lesions in large arteries, such as the femoral artery, but angioplasty may not have sustained benefits.[25][26] Patency rates following angioplasty is highest for iliac Arteries, and decrease with artery towards toes.other criteria that affect out come following revascularization are length of the lesion, number of lesion.[27][28]
Plaque excision, in which the plaque is scraped off of the inside of the vessel wall.
Occasionally, bypass grafting is needed to circumvent a seriously stenosed area of the arterial vasculature. Generally, the saphenous vein is used, although artificial (Gore-Tex) material is often used for large tracts when the veins are of lesser quality.
Rarely, sympathectomy is used - removing the nerves that make arteries contract, effectively leading to vasodilatation.
When gangrene of the toes has set in, amputation is often a last resort to stop infected dying tissues from causing septicemia.
Arterial thrombosis or embolism has a dismal prognosis, but is occasionally treated successfully with thrombolysis.
o Menieres Disease
o Disorder of the inner ear
o Cause unknown—its an excess accumulation of endolymphatic fluid in membranous labyrinth
o Assessment—sudden severe attacks of whirling vertigo, roaring or tinnitus and fluctuating hearing loss and pallow, sweating, nausea, vomiting, H/A, exhaustion.
o Can be triggered by—increase in Na+ intake, stress, allergies, menstrual fluid retention
o Diagnosis—hearing testing (audiometic exam), Electronystagomograph (ENG), Xray &CT scan for abnormalities in ear structure
o Usually seen as a "tripod" of symptoms—Tinnitus (ear ringing), one side hearing loss and vertigo
o Interventions (directed mainly at preventing flairs and symptoms)
• Low Na+ diet and diuretics
• Avoid alchol, caffeine, nicotine
• Bedrest to control vertigo
• Medication treatment:
• Atropine (anticholinergic), diazepam (Valium) for n/v
• Vestibular suppressants: Meclizine (antivert) which tells the brain not to pay attention to abnormal pulses coming from the brain
• Surgical intervention
• Endolympathic decompression→ decrease pressure in labyrinth and creates shunt for fluid drainage
• Vestibular neurectomy→balance nerve is cut as it leaves inner ear
• Labyrinthectomy→ destruction of the membranous labyrinth (inner ear)
• Cochlear implant→ sensorineuronal hearing
o Client Education
• Priorities: to maintain safety and minimize vertigo (teach pt to recognize when or sense when an episode might occur)
• Restrict Na+, fluid, nicotine, alcohol
• Take medications
• Allergy follow up
• Learn signs of impending attack
• Quiet, darkened room during acute attack
• Avoid sudden movements, move head slowly
• Medic alert bracelet
Ulcerative Colitis
o ** chart in iggy helps to make distinctions between crohns and this, find it!!
o Widespread inflammatory process going on, mainly rectum & rectosigmoid colon—mainly in large intestine seen with this
o When body in state of inflammation—there is swelling, irritated state, WBCs are being activated, there is damage being done to the tissue which is the **ulcerative part of the disease which is important bc the eroisions can also see bleeding and bloody stools
o 10-20 liquid , bloody stools/day** during exacerbation period, can be bright red blood because the bleeding is occurring right at the end of the colon
o Periodic remissions (may just be smaller bleeding, but doesn't go away) & exacerbations
o Can range from mild to severe or fulminant
o Inflammation is usually only involved with the outer lining of the GI tract vs crohns which is the entire lining layers
o Ulcerative Colotis: Incidence
• Can occur any age, more late teens to early adult and then later
• 15-25 yr and 55-65yr
• Males & females equally affected
• More common in American Jewish of European decent
• Cause unknown
• Tends to run in families but no research yet to support genetic link
o Assessment:
• Family history--
• Obviously bloody stools are big signs—are they in flair or more remission period
• Treatment - are they on it
• Surgery
• Nutrition history—no direct relation between nutritional status and the inflammatory process—here nutritional abnormalities aren't seen as much bc this is happening in the large instestine and less responsibility for ingestin nutrients, more pts able to maintain normal weight vs crohns—ask about weight loss
• Bowel patterns—very important, want them to save stool sample for eval
• Timing of diarrhea
• Recent antibiotics
• Travel to tropical areas-- flairs can come more alongside infections, esp things that will irritate GI
• Recent NSAID use
• Extraintestinal symptoms
• Arthritis, mouth sores, vision or skin problems
• Psychosocial assessment
• Fever—
• Abdominal distention along colon—have to treat the pain, narcotics and then trying to reduce the inflammation
• Abdominal tenderness
• Signs & symptoms peritonitis—board like rigidity of colon/stomach area—need to act quickly bc can lead to sepsis/death
• Hgb, Hct, platelets, WBC, C-reactive protein, ESR, electrolytes (Na, K,) albumin (someones protein store status)—blood pressure, pulse, O2 sat
o Diagnostics
• Sigmoidoscopy or colonoscopy**gold standard - also need to be weary of colon cancer due to the long term irritation that's occurring - but can also remove colon and get rid of all risk—really hard to do during acute phase, may just treat and do this later
• CT scan
• Barium enema—radilogical procedure, have a rectal barium and then they can look at the inflammation patterns with opaque dye—this diease process tends to have more widespread inflammation we can see vs Crohsn with skip lesions - the dye can be very constipating so we need to be careful
o Drug Therapy—mention in broad strokes
• Aminosalicylates (5-ASA): anti-inflammatory drugs, e.g., sulfasalazine & oral formulations of mesalamine—taken long term to keep the inflammation at bay
• Corticosteroids: Prednisone & methylprednisolone PO or PR—short term use to manage exacerbations—don't want long term sue bc higher risk for infection (altered immune fxn) and puts them at risk for peptic ulcer diease/ bleedng, higher risk for osteoperosis and pathological fractures, pushing syndrome and altered glucose levels—cant abruptly stop, hve to be tapered off—only acute exacerbations**
• Immune modifiers: may use to ↓ steroid dosage (for autoimmune influence)—Methotrexate
• Antibiotics: metronidazole, ampicillin, ciprofloxacin, others—if a flaire thought to be related to a pathogen
• Biologic therapies: Infliximab (Remicade®) (alters tumor necrosis factor for autoimmune disorders) IV monthly- (newest) Monoclonal antibody → blocks tumor necrosis factor (TNF) & allows time for remission.—can be antidiarrheal but want to be careful to not mask other problems going on
Chest Tube Chambers
o Chamber 1: collects the fluid draining from the patient
o Chamber 2: water seal that prevents air from entering the patient's pleural space
o Chamber 3: suction control of the system
Clinical Guidelines for Care of Pt with Chest Tubes & Water Seal Drainage
o Review Iggy (7th ed) Chart 32-14 (p. 637)—this is the best info for us
o Avoid routinely stripping or milking tubes—this is shown to actually increase the pressure going in!
o in order to see what is coming out, there are small markers to show the last level of drainage which can tell you if later when you come back if there has not been a change and can tell you about the patency of the tube'
o always want to check pt, look for bubbling in the chambers, and call physican if concerned
o there will always be drainage—is the draining occluded or is the wound healing? Just change the tube vs milking
o avoid clamping bc if there is air present in the tube, that pressure can cause pneumothorax bc the air is kept in the closed system
o If CT becomes disconnected from the drainage system, what do you do?
o Potential complication will be pneumothorax into what we want to be a closed system with negative pressure and a water seal so we will place it in at least 2 inches of water (submerge it in 250 mL sterile bottle of water)
o If CT becomes dislodged from the patient, what do you do?
o Make sure that you have dry gauze to cover it—this allow for some air to come out but not really any to flow in, leave one flap untapped
o Want them to cough whats in there, then put the triangle
o Know agency policy and procedures re: chest tube management
o Also be careful bc bad placement can cause a tension pneumothorax, and the treatment for that is a chest tube!!
o

Chest Tubes: Notify MD or Rapid Response Team Immediately
o Tracheal deviation—extreme with tension pneumothorax, buildup of high tension air, everything getting compressed
o Sudden onset or ↑SOB
o O2 sat < 90%
o Drainage > 70 mL/hr—any kind of high flow drainage (form Iggy is this) can affect hemodynamic stability and possibly pulmonary edema
o Don't leave if pt is stressed in this emergency, call DR.
o CT falls out of chest
o 1st cover dry sterile dsg & tape 3 sides
o CT disconnects from drainage system
o 1st put end of tube in sterile H2O & keep below level of chest
o Drainage in tube stops within 1st 24 hours—or whenever it stops, make sure to get it checked out
o Dysrhythmia (abnormal cardiac rhythms)
o These are used as a diagnostic tool to figure out what is happening with the heart and prevent death
o Abnormal rhythms can have to do with rate, rhythm or both
o Rememebr that a:
• P Wave: is atrial repolarization
• The SA Node is the pacemaker of the heart, embedded in the atria and will be the impetus for every heart beat and that should be the first sign that comes through on the ECG
• QRS: coming form the left ventricle and demonstrating ventricular depolarization
• T wave: ventricular repolarization as the heart is getting ready again to restart the heartbeat
• Remember there is a certain automaticity of the heart so that if the SA node is not working for some reason, we can also see the AV node as the starting point of the heart beat** that will be a ventricular dysrhythmia
o The Cardiac Conduction System:
• Sinoatrial node: send electrical impulses at 60-110 bpm, and is the "P wave" on the ECG
• Atrioventricular junction or AV node: is the PR segement on the ECG and this contraction is known as the "atrial kick"
• The Bundle of His: is the right bundle branch system and left bundle branch system
o Electrocardiogram waveforms
o Each tiny little box will measure 0.04 seconds, and each of the larger group of boxes will be .2 seconds so when we have a strip of 15 of those bigger boxes, we should have 3 seconds but generally we want to look at a 6 second strip bc we can easily multiply that by 10 t give us /min heart rate

o Atrial Fibrillation→still a dysrhythmia coming from the SA node
o Is associated with atrial fibrosis and loss of muscle mass
o Common in heart disease such as hypertension, heart failure and CAD and aging→most common in our society
o Cardiac output can decrease by as much as 20-30%
o This is over firing of the atria and theyre not working effectively bc instead of contracting theyre quivering
o Although it is asymptomatic in the beginning, eventually their incorrect cardiac output will catch up to them
• It is characterized by total depolarization of atrial activity without effective contraction
• can be chronic or intermittent
• will usually occur with underlying heart disease such as RHD, CHF, cardiomyopathy, pericarditis, thyrotoxicosis, alcohol intox, valvular disease, caffeine use, electrolyte disturbance, cardiac surgery
o you can tell that the rhythm is irregular but you can still hear the 70 beats and atrial contractions
o considered "irregularly irregular" no pattern that can really be seen—when we identify that there are multiple P waves and at a regular rate it will be a-fib
o with the irregularity, there is a high risk for Emolic stroke due to clot formation!!
• Treatment:
o Will be patient centered collaborative care:
o There is risk for PE, VTE
o Antidysrhythmic drugs
• Amiodorone (to help bring the rhythm back to normal)—this is the drug of choice
o Cardioversion
o Percutaneous radiofrequency catheter ablation
o Bi-ventricular pacing
o Maze procedure
o Goals are decreased in ventricular response and conversion to sinus rhythm
o Drugs for rate control/conversion include:
• Digoxin
• Beta blockers
• Calcium channel blockers
• Amiodarone (Cordarone) - most effective in converting AF to NSR
• Dronedarone
o Anticoagulation therapy recommended for 3 to 4 weeks in AF > 48 hours before attempt at conversion to sinus rhythm—if they are not able to convert them or they aren't candidates for the other drugs
o Direct Current Cardioversion (DC) or Synchronized Cardioversion (other term used)
o Catheter Ablation—intervention with high frequency lazer to burn off an area of sa node that is misfiring
o Ventricular Dysrhythmias
o These are more life threatening than atrial dysrythmias
o left ventricle pumps oxygenated blood through the body to perfuse vital organs and tissues
o There are also what are called Premature ventricular Complexes which come up on ECGs and are not consistent
• It is the result of increased irritability of the ventricular cells—early ventricular complexes followed by a pause but it is missing the first atrial contraction
• Can be caused by hypoxia and a little ischemia, electrolyte imabalances (K+, Mg+), some drugs, maybe some things that cause tachycardia as well
• Can be unifocal or multi focal, just be weary that sometimes on strips you can see the PVC and we should be aware—and many people can experience these throughout life but if more frequent, can be a precursor to a more seirous condition
• If you have more than 3 PVCs in a row, or if you ahd a run of more than 3, then it will be a "non sustained ventricular tachycardia"
• Dyrrhythmias often have to do with someone who is in a hypoxic state so we can first put a patient on oxygen
• can use anti arythmic drugs
• There can also be Artifact or "not true waveforms" so always be looking at your patients as well to see how they are
Pathophysiology of Burns
• Skin changes resulting from burn injury
• Anatomic changes
• Functional changes
• Temperature

Priorities
• Health promotion/prevention
• Resp/oxygenation
• Shock prevenion—different degrees of burn injury—inflammation can be really bad and thes burns can cause massive fluid shifts in the body
• Pain
• Fluid status—much determined by skin, lots lost when our skin is breached
• Electrolytes--
• Pevent infection—as skin is our main barrier, when its lost, at greater risk for infection
• Wound care—pain management ,
• Psychosocial - can see alterations in body image, and these issues can be life long

Depth of Burn Injury
• Severity determined by how much body surface is involved ,as well as depth
• Differences in skin thickness in various parts of the body also a factor
• Plays a role in temperature regulation

Superficial Thickness
• Least damage; epidermis is only part of skin that is injured
• Desquamation (peeling of dead skin) occurs 2 to 3 days after burn

Partial Thickness
• Involves entire epidermis and dermis (varying depths), now the nerves in the dermis are being exposed and can be super painful


Full Thickness
• Destruction of entire epidermis and dermis
• Skin does NOT regrow
• They might cut up the skin to relieve some of the pressure that is being caused in response to the inflammation that is occurring

Resuscitation/Early Phase of Burn Injur
• Continues for about 24 to 48 hours
• Goals of management:
o Secure airway ie if burn is around the chest—may be hard to breath or
o Support circulation—fluid replacement
o Prevent infection
o Maintain body temperature
o Provide emotional support

Injuries to the Respiratory System
• Direct airway injury
• Carbon monoxide poisoning
• Thermal injury
• Smoke poisoning
• Pulmonary fluid overload
• External factors

Pulmonary Fluid Overload
• Occurs even when lung tissues have not been damaged directly
• Histamine, other inflammatory mediators cause capillaries to leak fluid into pulmonary tissue space

Cardiovascular Assessment
• Hypovolemic shock common cause of death in early phase in patients with serious injuries
• Vital signs
• Cardiac status, especially in cases of electrical burn injuries

Kidney/Urinary Assessment
• Changes related to cellular debris, decreased kidney blood flow
• Myoglobin released from damaged muscle, circulates to kidney
• Kidney function, BUN, serum creatinine, serum sodium levels.
• Urine color, odor, presence of particles/foam

Skin Assessment
• Size and depth of injury
• Percentage of total BSA affected
• "Rule of nines" using multiples of 9% of total BSA

Gastrointestinal Assessment
• Changes in GI function expected
• Decreased blood flow and sympathetic stimulation during early phase cause reduced GI motility, paralytic ileus (non mechanical obstruction, need to put NG tube in to help them with GI tract)
• GI bleeding
• At risk for a stress ulcer (r/t GI problems, part of the SNS when blood is being shunted, and that results in a stress ulcer)—might be on prophylactic Proton pump inhib


Vascular Changes resulting from Burn Injuries
• Fluid shift: Third spacing or capillary leak syndrome, usually occurs in first 12 hr, can continue 24 to 36 hr
• Profound imbalance of fluid, electrolyte, acid-base; hyperkalemia and hyponatremia levels; hemoconcentration
• Fluid remobilization after 24 hr, diuretic stage begins 48 to 72 hr after injury, hyponatremia and hypokalemia

Rehabilitative state can go on for the rest of their lives
Lupus is a chronic inflammatory disease that occurs when your body's immune system attacks your own tissues and organs. Inflammation caused by lupus can affect many different body systems — including your joints, skin, kidneys, blood cells, brain, heart and lungs.

Lupus can be difficult to diagnose because its signs and symptoms often mimic those of other ailments. The most distinctive sign of lupus — a facial rash that resembles the wings of a butterfly unfolding across both cheeks — occurs in many but not all cases of lupus.

Some people are born with a tendency toward developing lupus, which may be triggered by infections, certain drugs or even sunlight. While there's no cure for lupus, treatments can help control symptoms.

Tx
Nonsteroidal anti-inflammatory drugs (NSAIDs). Over-the-counter NSAIDs, such as naproxen (Aleve) and ibuprofen (Advil, Motrin, others), may be used to treat pain, swelling and fever associated with lupus. Stronger NSAIDs are available by prescription. Side effects of NSAIDs include stomach bleeding, kidney problems and an increased risk of heart problems.
Antimalarial drugs. Medications commonly used to treat malaria, such as hydroxychloroquine (Plaquenil), also can help control lupus. Side effects can include stomach upset and, very rarely, damage to the retina of the eye.
Corticosteroids. Prednisone and other types of corticosteroids can counter the inflammation of lupus, but often produce long-term side effects — including weight gain, easy bruising, thinning bones (osteoporosis), high blood pressure, diabetes and increased risk of infection. The risk of side effects increases with higher doses and longer term therapy.
Immune suppressants. Drugs that suppress the immune system may be helpful in serious cases of lupus. Examples include cyclophosphamide (Cytoxan), azathioprine (Imuran, Azasan), mycophenolate (Cellcept), leflunomide (Arava) and methotrexate (Trexall). Potential side effects may include an increased risk of infection, liver damage, decreased fertility and an increased risk of cancer. A newer medication, belimumab (Benlysta) also reduces lupus symptoms in some people. Side effects include nausea, diarrhea and fever.
Hepatitis A
• Mode of transmission primarily fecal - oral r/t to travel, sanitation, food borne, bad water systems
• Usually thru ingestion of contaminated foods/liquids
• Prevalent in underdeveloped countries, overcrowding, & poor sanitation
• Infected food handler can spread disease
• Can contract by consuming water or shellfish from contaminated water
• Commonly spread person to person, rarely by blood transfusion
• Worldwide - usually among children and young adults (ages 5 to 14 )
• Low mortality
• Continuum of sx, some can have severe or some can have non
• There is a vaccine—rec for people traveling abroad
• Can he sexual contact—more common through food/fecal oral
• Resolves itself
Diagnostic
• Hematology
• ↑ ALT, AST, alk phosphatase, LDH, bilirubin & ESR—Liver enzyme function test, tyring to overcompensate so will see higher values—increased WBCs bc of inflammation process
• good history and phsycal—checking for Tylenol 4 g/day, chemotherapy which can cause this
• alcohol use
• Prothrombin time prolonged
• Leukocytosis
• Bilirubin - Direct, indirect & total - ↑ in icteric phase
• Antibody testing (for specific viruses)

• Urine chemistry
• ↑ urobilinogin, mild proteinuria & mild bilirubinuria—there will be alterations in kidneys/urine as well bc they are now picking up the responsibilities that the liver failed to do
o Collaborative Management
• Monitoring level of activity
• Bed rest may be indicated when sx are severe with a gradual return to normal activity as sx subside—hard to diagnose
• Diet
• Small, frequent, palatable meals as tolerated
• May need parenteral & enteral feedings
• Na+ restrictions in presence of edema
• High calorie diet, moderate protein and fat
• All alcoholic beverages are strictly prohibited
• Vitamins
• Management of pruritis
• Alkaline soaps restricted, emollients & liquid creams prescribed
• Antihistamines & tranquilizers if used administer with caution as they are metabolized by the liver
• Although early studies indicate that a high protein, high calorie diet may be beneficial, advise pt not to force food and that fat intake should be restricted (Brunner & Suddarth, 2010, p.1141).
o Percutaneous Transluminal Coronary Angioplasty—This is the best way to go according to evidence based research for reperfusion therapy
o This is a type of Percutaneous Coronary Intervention
o In order to do this, it is necessary to have a cardiac cath lab—if one isn't available, that will be different and they may have to choose fibrinolytics instead
o Patients comordidities, what the patients situation, if theyre a candidate for what treatment, what kind of MI did they have etc needs to be considered but know that there is a decision making process for reperfusion and those will be Fibrinolytics and PCI
o Clopidogrel before procedure
o IV heparin after procedure
o IV or intracoronary nitroglycerin or diltiazem
o Possible IV GP IIb/IIIa inhibitors
o Long-term therapy, antiplatelet therapy, beta blocker, ACE inhibitor, or ARB
o Will use femoral vs brachial to avoid pneumothorax
o Nursing Interventions Post CC/PCI
o Frequent/continuous monitoring of V/S, ECG, SpO2 , coagulation profile, e.g., activated clotting time (ACT), PT/PTT
o Check puncture site (post artery puncture), distal pulses, skin color/temp, capillary refill, urine output, etc, make sure there is no hematoma (swelling or bruise), blood can pool under patient so making sure no blood gathering elsewhere in the bed, retroperitoneal bleed, leg has to be kept straight and we want the artery to stay still and heal in a flat way 4-6 hours after
o Watch for complications:
• Bleeding, hematoma, pseudoaneurysm, retroperitoneal bleed, compartment syndrome, reocclusion (will develop chest pain if it reoccludes—usually can be seen to happen within an hour), dysrhythmias, potential to bleed is high
o Check for clots, emboli, rupture, infection later, but it's a temporary fix and these can reocclude! They will give a stent to hold the occlusion open, but then you have to give meds to stop clots from forming
• Some stents also have meds that release anticoagulants as well
• It a patient has too many blockages, they will do a bypass later

If then patient is not eligible for a PCI or fibrinolytics bc the problem is too great...they can be a canditate for→
o This is the graphic of a Coronary Artery Bypass graft surgery—emergency Cabage
• They have to open the chest, put the heart on a pump while we do the procedure—can see a lot of side effects after the fact
o Preoperative care
• Standard for most surg procedure
• This patient is a ticking time bomb so they will be closely monitored, don't want them to over exert themselves or exacerbate the damage
• Think about where they are choosing the graft r/t the pts lifestyle
o Postoperative care
• Manage F&E balance
• Complications—hypotension, hypothermia, hypertension, bleeding, cardiac tamponade, change in level of consciousness
o Nursing Management: Pre-Op
o Interventions
• NPO
• Reinforce teaching
• Complete pre-op checklist
• Type & cross match blood products
• Labs (check for abnormal values), ECG, CXR, Echo, cath report, old medical record, etc
• Consent: Surgical, Anesthesia, Blood
• Skin prep: clip versus shave, betadine shower
• Medication "on call " to OR
• Pain relief/comfort measures, therapeutic environment
• Anxiolytic meds, integrative cardiac medicine, sleep meds
o Pre-op considerations: emergent vs. elective, choice of grafts (e.g. radial: non-dominant hand, job a factor)
o Immediate Post-Op Period—these are listed below the pic as well
o Potential for complications are high—understand the seriousness of this
o This pt also has 3 chest tubes in place
o Might have to go for cardiac rehab as well—they have to adjust to their new life restrictions
o So many more potential complications even outside of the huge
o Atelectasis, pneumonia,
o Plus the majority of these surgeries are performed in those over 65 so aging isusses as well need to be taken into account, pump head/cognitive impairment
GERD
o Most common upper GI disorder in the US
o No single identifiable cause--- can be called chronic heart burn,
o Relaxation of LES/Reflux of gastric contents into lower esophagus—allows the stuff to go back up
o Also need to pay attention to respiratory manifestations when gastric contents possibly coming back up into esophagus as well


o
o Clinical Manifestations
• Dyspepsia—indigestion/heart burn—may at first seem like angina/chest pain—may bring Maalox with them incase a heart attack turns into heart burn
• Regurgitation
• Belching (eructation)/Flatulence(gas)
• Chronic GERD—dysphagia (dfficulty swallowing/painful—apiration risk /aspiration pneumonia big here when chronic damage occurs
• Other
• Atypical chest pain-- angina
• Cough, Wheeze, Asthma—aspiration into trachea and see resp symptoms
o Diagnostic studies—this is such a prevalent disease, that pts will usually treat themselves at home first and then go to a doc and get a prescription (H2 blocker, proton pump inhib) and if sx go away then that's the diagnoses...if they really wanted to test they would do the things listed below
• ** Thinking about differential diagnoses--Risk factors to think about—hialtal hernia, obesity causes internal pressure that can make the esophagus hard to close, pregnancy, high fat/spicy foods/chocolate/caffeine/ciggs/some meds nitrate, estrogen , presence of NG tube can all impact the sphincter
• Diagnostic Studies—tretat it like worst case scenario such as MI--
• 24 hour esphogeal pH monitoring--)** gold standard, its troublesome for pt bc it's a nasogastric tube for 24 hours that measures pressure and pH , so not done too often

• Esophogogastroduodenoscopy (EGD)—done by escdoscopist, can go through all of these, can get samples along the way to test if barrets or carcinoma—pts have to be NPO to reduce risk for aspiration r/t numbing of back of throat
• Will do a quick check with water post surgery to see how they handle and can swallow
• Biopsy & cytologic specimens to differentiate carcinoma from Barrett's esophagus
• Chronic irritation can be bad and lead to metaplasia and cancer—encourage pts dealing with this to be aware and get checked out!!
o GERD: Collaborative Care
o Lifestyle modifications
• Nutritional therapy: Avoid milk products at night, late snacks or meals, caffeine, alcohol, citrus fruits, chocolate, & high-fat foods** done to avoid the GERD response from food
• Weight reduction
• Stress management??
• Sit upright when eating, put up pillows or blocks under bed, smaller more frequent meals/aovid heavy meals, avoid late night snacks** shouldn't do this at all
o Drug Therapy
• H2 receptor blockers, Proton pump inhibitors, Antacids
o Prevention
• Avoid factors that cause reflux
• HOB > 30 degrees
• Decrease intra-abdominal pressure
• Stay upright for 2 hrs after eating
• No eating 3 hrs before bed
• Drug therapy
o Complications: Ulcers, increase risk of esophageal cancers, strictures (after the years of having chronic GERD and the inflammatory process these can arise and lead to aspiration risk)
Epidural Hematoma
Occurs between the dura mater and the skull as a result of high impact to temporal areas of brain
Typically artery is source
Approximately 90% are associated with linear fracture, usually the temporal bone just above the ear
Classic presentation:
1. Brief loss of consciousness
2. Followed by AOx3
3. Loss of consciousness again

Subdural Hematoma
Accumulation of blood between dura and arachnoid layers
Typically venous injury
Types:
Acute subdural
Subacute subdural
Chronic subdural

Subarachnoid hematoma
Accumulation of blood between arachnoid layer of meninges and brain
Common in severe head injuries, such as brain aneurysm
Assessment finding: nuchal rigidity
Medical management:
Placement of IVC and monitor ICP
Nursing Management:
Neurological assessment
Monitor ICP
Quantity and color of CSF

Accumulation of blood in brain parenchyma
Result from uncontrolled HTN, ruptured aneurysm, or trauma
Assessment Findings:
H/A
Decreasing LOC
Dilation of one pupil
Hemiplegia
Medical management
Manage ICP

Complications of Closed Head Injury
Syndrome of Inappropriate Antidiuresis Hormone (SIADH)
Excess secretion of ADH
Classic diagnostic profile:
Urine output <400 mL/day (oliguria)
Specific gravity >1.020 (concentrated urine)
Decrease in serum NA
Increased ICP
Treatment:
Fluid restriction
Nursing Management
Monitor I/O
Neurological assessment
Enforce fluid restriction
Cerebral Salt Wasting (CSW)
State of hypovolemia with low serum sodium and urine osmolality
Must differentiate SIADH from CSW
Treatment
Na replacement (NS IV or oral salt tablets)
Herniation
Seizures
Alzheimer's Disease
o Most common neurodegenerative disorder
o Incurable dementia illness
o Chronic, progressive neurodegenerative illness
o Marked cognition dysfunction
o Onset 45-65 years old
o Affects 13 million Americans and 81 million individuals worldwide in next 40 to 50 years
o 10th most common cause of death in the United States
o Cost approx $100 billion annually to care for persons with AD in the United States—costs are increasing
o Possible factors
• Genetic predisposition
• Slow virus
o Pathophysiology (see picture in text, p. 339; in 7th ed: p. 327)
• Degeneration of cholinergic neuron & acetylcholine deficiency
• Neuritic plaques outside neurons & in cerebral cortex
• Apolipoprotein E4 promoting formation of neuritic plaques which binds beta-amyloid in the plaques—blocking the neuron communication and NTs in the brain
Acetylcholinesterase (AChE) Inhibitors
o These are used because there is a theory of ACh deficiency in Alzheimer's, so they want to block the enzymes that destroy the ACh
o Rationale for acetylcholinesterase inhibitors is acetylcholine deficiency in the brain in Alzheimer's Disease
o Acetylcholinesterase is enzyme responsible for breaking down Acetylcholine neurotransmitter
o Prototype: Donepezil (Aricept)
o May also see Tacrine (Cognex)

Donepezil (Aricept) /Tacrine (Cognex)
o Used to improve cognitive function in mild to moderate Alzheimer's
o Increases Acetylcholine at cholinergic synapses
o May slow disease process
o Effective response is limited
o Short-lasting
o Duration of Tacrine is 24-36 hrs while Aricept is up to 72 hours—would want to look for side effects over time, and signs of toxicity if drug is possibly building up
o
o Contraindications
o Liver & renal disease
o
o *Monitor closely for side effects & cumulative effect in elderly & pts with liver & renal dysfunction
o Side Effects
• Anorexia
• N/V
• Diarrhea
• Constipation
• Dizziness
• H/A
• Rhinitis
• Depression

• Life-threatening: Hepatoxicity


N-methyl-D-aspartate (NMDA) Inhibitor
o Glutaminate main excitatory neurotrasmitter in brain—it antagonizes the receptor for this in order to stop the over excitation which can cause to neurodegeneration
o Stimulates NMDA receptor
o Over-stimulation may lead to neurodegeneration
o Memantine (Namenda)
o NMDA receptor antagonist
o Associated with reduced rate of clinical deterioration in patients with moderate to severe
o Unclear whether due to disease-modifying or reducing excitotoxity from disease
Chronic Kidney Disease
o Progressive, irreversible kidney injury; kidney function does not recover—not reversible
o 2 leading causes—diabetes and hypertension (interesting bc can be a cause or can be a symptom/complication)
o End-stage kidney disease (ESKD)
o Azotemia (increased toxicity n the blood)
o Uremia (increase in ___ in the urine)
o Uremic syndrome
o Stages of CKD—cant reverse or cure, we can limit its progression, by fixing underlying causes ie if hypertension causing it, we can reduce it and (CKD --micorvascular complication of diabetes- we can control their blood sugar with Hemoglobin A1C)
o Want to test their creatinine clearance and GFR which will give us the best picture
o Reduced renal reserve
o Reduced GFR (when below 90, we can use that as baseline for whats normal, and this is when they will start to have sme symptoms)—will be called "renal insufficiency" when below 90—aim is to stop progression and treat symptoms
o ESKD—transplants or dialysis—their GFR has dropped so far where if we don't come up with a renal replacement therapy like transplant or dialysis they are going to die
o **here she showed the stages of kidney disease on kidney.org
o Kidney changes—changes in how it functions, GFR is doing
o Metabolic changes
o Urea and creatinine (telling us that the filtration and how were metabolizing protein)
o output andw aht their urine output is
o Electrolyte changes—happen at the later stages,
o Sodium -- depending upon where the patient is, if theyre oliguric (they could have hypernatremia, or if theyre fluid overloaded, could be dilutional hyponatremia)
o Potassium—its excreted from kidneys, and if not excreted and built up, we can see dysrythmias
o Acid-base imbalance—resp acidosis
o Calcium and phosphorus—Phosphorus will be elevated, and the inverse relationship will be that calcium is low—
o Looking at these will helps us to know what to look for
o Cardiac changes:
o Hypertension—damange to the rennin angio ssytem
o Hyperlipidemia—occurs in the later stages
o Heart failure—can occur when pt is in a state of volume overload and that will be in the early stages of kidney disease, but after living at a state of increased preload, the afterload will be impacted and left ventricle damage from being
o Pericarditis—inflammation of outer heart tissue due to the increase urea toxicity
o Hematologic changes—Erythropoetin- which make RBCs so alterations in kidneys can experience anemia, decreased hemoglobin—will see anemia, low energy, dyspnea
o GI changes—increase dnitro waste, can see n/v, anorexia, can flucturate between constipation and diarrhea bc of fluid status and uremic toxins
o Clinical Manifestations** be very comfortable, has manifestations within each body system—there will be more depending on the stage of disease
o Neurologic—altererd mental status, confusion, lethargy (EPO, low level hypoxia)—can see depression and grieving
o Cardiovascular—hypertension, pt can develop heart failure so left ventricular changes, dysrhythmias bc of anemia and electrolyte imbalances
o Respiratory—respiratory acidosis, kusmaul respirations can develop (LOOK UPIN IGGY TEXT QUESTIONS, SHE KEEPS TALKING ABUT THIS CHAPTERS QUESTIONS!!), pulmonary edema from volume overload
o Hematologic - alteration in platelets (unsure patho) but were worried about thrombocytopenia (and they can fall and have a bleed- we are worried)—can also be at increased risk for infection
o Gastrointestinal—anorexia, n/v, its hard - sometimes pts can have such high uremic levels that it goes through GI system nd can manifest as halitosis (bad breath)
o Skeletal - can have breakdown, living with the low level of calcium, breaking down bone
o Urinary—they may still be making urine - oliguric or aniuric )no urine)—they have renal stasis
o Skin—have crazy pruiritis bc of the altered chemicals (uremic toxin) and its coming out of the skin—have ot be careful about the treatment ie giving meds that have to be processed through the kidney—can use Benadryl but be careful—also increased phosphorus can come through the skin
o Can give anxiolytics - to calm them bc they can have yellowing or infection/cellulitis from scratching
o Uremic frost** (more at end stage) can come up and mix with your normal sweat and oils in the skin and make crystals that adhere to the skin
o Almost all fo these can be r/t electrolyte distrucbance, acid base balance, build up of nitrogenous waste or fluid build up
o Assessment
o Psychosocial
o Laboratory—elecrolutes, ABG (in emergency), creatinine, hemoglobin, WBCs, platelets, Albumin
o Imaging—diagnostic things but not common with this type of kidney disease
o want to identify baseline weight for fluid volume status
o
o Priority Nursing Care—from IGGY text
o Dietary restrictions—should be individualized, should refer to dieticians, or general it will be below 60g of protein a day, (should be invidivual based on weight, status)
o Phosphorus, sweet tea (high phosphorus), salt, protein, organ meat, chocolate, colas,
o Fluid restriction and overload—maintaingin like 500-700 mLs/day,
o Uremic frost—tepid bath can help, but want to decrease uric toxins
o Muscle strength, energy—the whole catabolic state that's happening, maybe include PT, low hemoglobin state
o Family members—think about someone on dialysis, so many issues, a dialysis schedule, its so hard to do alone so any family and management etc should be shared with the family (diet, support etc)
o Excess fluid volume—diuretic is usually a loop diuretic, thiazides can work as well, no pot sparing because could increase risk of hyperkalemia - at some point, kidneys so compromised that diuretics don't work
o Decreased cardiac output—they might be on ACE inhibitors and decrease in vasoconstriction
o Recombinant human erythropoietin—with compromised peeps, we can give these to help with hematological status/increased RBC countt—might be transfused, packed RVCs (colloids)—but it could put them into further fluid overload—might be done during dialysis so fluid overload not a problem
o For the anemia we might also give iron, vitamins, folic acid—vitamins are important in end stage kidney disease
o Remember dialysis—management and not cures , life sustaining treatments
o Interdisciplinary team—may need to deal with PT, cardiologist, endocrinologist, all together delivering patient centered care, families, nutritionist , energy issues and muscle breakdown so PT, and pharmacist (to work out altered kidney function), nephrologist


Radio opaque dye can be very toxic to kidneys, cause acute kidney injury!!—can experience these symptoms byt can be reversed if we fix it
Unlike emboli that arise from thrombi (blood clots), fat emboli are small and multiple, and thus have widespread effects.
Fat embolism syndrome (FES) is distinct from the presence of fat emboli. Symptoms usually occur 1-3 days after a traumatic injury and are predominantly pulmonary (shortness of breath, hypoxemia), neurological (agitation, delirium, or coma), dermatological (petechial rash), and haematological (anaemia, low platelets). The syndrome manifests more frequently in closed fractures of the pelvis or long bones. The petechial rash, which usually resolves in 5-7 days, is said to be pathognomonic for the syndrome, but only occurs in 20-50% of cases.
Fat emboli occur in almost 90% of all patients with severe injuries to bones, although only 10% of these are symptomatic. The risk of fat embolism syndrome is thought to be reduced by early immobilization of fractures and especially by early operative correction. There is also some evidence that steroid prophylaxis of high-risk patients reduces the incidence. The mortality rate of fat-embolism syndrome is approximately 10-20%.[1]
Fat emboli can be either traumatic (resulting from fracture of long bones, accidents, or trauma to soft tissue) or non-traumatic (resulting from burns or fatty liver).[

Clinical fat embolism syndrome presents with tachycardia, tachypnea, elevated temperature, hypoxemia, hypocapnia, thrombocytopenia, and occasionally mild neurological symptoms.

tx-The most effective prophylactic measure is to reduce long bone fractures as soon as possible after the injury.
Maintenance of intravascular volume is important because shock can exacerbate the lung injury caused by FES. Albumin has been recommended for volume resuscitation in addition to balanced electrolyte solution, because it not only restores blood volume but also binds fatty acids, and may decrease the extent of lung injury.[6]
o Urinary Tract Infection
o Most common health care aquired infection—hospitals, long term care facilities (pneumonia, cellulites)
• 75% according to CDC in hospitals are from urinary catheters, 25% of pts in the hospital get urinary catheter - do they all need it? Should only be really necessary
• those who really need it, kidney failure, I&Os, someone with urinary obstruction, post operative, incontinence is never an indication, bacteria can colonize in 24 hours, mobilization/very careful considerations for immobile people and whether to do it, have to balance : is the reason for the cath outweigh the risks of the bacterial infection
• understanding now that a UTI can also lead to septic shock and death
• if it really is necessary, start bringing on the aspects of maintenance, cleaning, perineal cleaning (to avoid cross contamination), if someone fecally incontinent, the E coli can pass up and get in
• worry about bactiuria with pts who use the "in and out" bladder cath
• neurogenic bladder, they might have a suprapubic catheter placed
• has to be a delicate balance between whether you put in a cath, or have constant moisture and possible skin breakdown
• advocate for the
o Most common cause of sepsis in hospitalized patient
o "Urosepsis"
o Most common organisms are from GI tract
o E. coli (most common)
o Common source of hospital-acquired UTI (CAUTI)
o UTI Classification→anywhere along the tract
o Can be complicated (person in the hospital, other comorbid conditions, indwelling cath etc or Diabetes)
o Upper tract: renal parenchyma, pelvis, ureters
• Signs and symptoms: fever, chills, flank pain
o Lower tract: lower urinary tract
• No usual systemic manifestations (localized symptoms)
o Sites of infection
o Pyelonephritis
o Cystitis
o Urethritis
o Older adult:
• Could be asymptomatic
• Non-localized abdominal discomfort rather than dysuria
• May have cognitive impairment
• Less likely to have fever
o Significant bacteriuria may have no symptoms or nonspecific symptoms like fatigue or anorexia
o Diagnostic Studies
o Urinalysis (clean-catch is preferred, or catheterization or suprapubic needle aspiration)—infection will be indicated by WBCs, bacteria, protein that shouldn't be there, nitrates—pay attention to abnormalities)
o Urine culture and sensitivity—if it's a more complicated case, then we do cultures—is it an infection or colonization (if below 100,000 could be bactiuria, may decide not to use antibiotics and use other intervention—some pts just live with bactiuria, might not be abnormal for them and would treat differently)
o Imaging studies in some cases
• IVP or abdominal CT when obstruction suspected
o Collaborative Care: Some UTI therapy—
o Trimethoprim-sulfamethoxazole or nitrofurantoin—just for simple tract infections diagnosed based off the classic symptoms and urinalysis results—in the hospital, will do something stronger than oral antibiotic, until they wait for the
• Used to treat empiric uncomplicated UTI )—oral and managed at home
o Pyridium
• OTC, provides soothing effect on urinary tract mucosa
• Stains urine reddish orange
• Urinary tract anesthetic, not doing anything for infection but helps treat symptoms—bright orange red color to stain and undergarments and skin
o Prophylactic or suppressive antibiotics
• Patients with repeated UTIs
• Prevent recurrence, or a single dose prior to events likely to cause UTI
Multiple Sclerosis
o Chronic, autoimmune disease affecting myelin sheath & conductive pathway of CNS
o One of leading causes of neurological disability in young adults
o Periods of exacerbations & remissions
• As severity & duration progresses, exacerbation > frequent
o Relapsing-remitting most common type
o Major concern → long time to diagnose
o Exact cause unknown
o Research on viral, immunologic, genetic, & environmental factors
o Tends to occur among family members
o Usually occurs between 20-40y/o
o Women affected twice as often than men
o Assessment—difficult to diagnose, no definitive test to tell
• Often presents like other neuro diseases
• Diagnosis difficult
• Early symptoms vague & nonspecific
• Vision, mobility, & sensory changes
• Ask if factors aggravate symptoms
• Fatigue, stress, overexertion, temp extremes, hot bath or shower
o Clinical Manifestations—pretty vague, will be vision, fatigue, -- may not jump first to a diagnosis of MS
• Fatigue & weakness
• Abnormal reflexes (absent or exaggerated)
• Visual disturbances—probs go to eye doctor first
o Impaired, diplopia, or nystagmus
• Motor dysfunction
o Weakness, tremors, incoordination—muscle weakness can key in a little more to MS
• Sensory dysfunction:
o Parasthesias, impaired vibration & position
• Impaired, slurred speech
• Urinary dysfunction:
o Hesitancy, frequency urgency, UTI
• Neurobehavioral symptoms:
o Depression, emotional lability
o Diagnostics
• No specific procedure diagnostic of MS
• Collective results of variety of tests—often times to rule out others things with similar manifestations
o Abnormal CSF
o Two attacks separated in time & space
o MRI consistent with MS
o Nursing Interventions—try to keep them healthy, avoid complications, promote function, working with PT also
• Promote Motor Function
o Muscle stretching
o Frequent rest periods, avoid sudden position changes
o Ambulation and activity with assistive devices
o Change positions
• Minimize Fatigue
o Brief rest periods in day
o Avoid overheating, overexertion
• Optimize Sensory Function
o Eye patch for double vision
o Orientation to environment, remove obstacles
• Maintain Urine Elimination
o Adequate intake, voiding schedule, helping to keep them continent when they lose innervation
• Normalize Family Processes
• Promoting Sexual Functioning
o Collaborative Care
• Acute Attacks -these meds can have a lot of side effects
o Corticosteroids
o Immunosuppressive agents - avoid kids, crowds, proper oral care, make sure pts understand meds and uses
• Chronic Symptom management
o Treatment of spasticity
o Control of fatigue
o Treatment of depression with antidepressants & counseling
o Bladder management with anticholinergics & intermittent catheterization
o Bowel management - stool softeners, bulk laxatives, suppositiories
o Multidisciplinary rehab approach
o Dystonia
Heart Failure: Diagnostic Studies
o Primary goal to determine underlying cause
o History & physical exam
o ABGs, serum chemistries
o Chest X ray
o 12-Lead ECG-- dyrhythmias
o Hemodynamic assessment/monitoring—want to check BP frequency, hypertensive as a compensatory mechanism and should be monitored
o Echocardiogram (determines LVEF)
o Stress testing—these (and the next 2) are looking at the underlying problems for heart failure
o Nuclear imaging studies
o Cardiac catheterization -will tell us/show us the underlying issue)
o Laboratory tests (underlying problems); CBC (want to see blood count, hemoglobin== can be whether or not enough oxygenation is occurring based on the amount of hemoglobin), BMP, HBA1C (to test for diabetes, there are big correlations between diabetes and CAD), Lipid profile, thyroid levels (can impact dysrhythmias), cardiac enzymes and B type natriuretic peptide level (BNP)

Acute Heart Failure: Management and Nursing Diagnoses
o Primary goal is to improve LV function/ symptoms by: (really need to understand patho bc it really is r/t treatment and tying it all together)
o ↓ intravascular volume (decrease pre and afterload) (ie with a diueretic)
o ↓ preload (venous return)
o ↓ afterload—ie with the use of Lasix diuretics and decreasing the blood flow/work load—this will usually be administered push so It doesn't have to go with any extra carrier fluid
o Improving gas exchange & oxygenation—patient might get a loop diuretic to decrease fluid volume/maybe help with pulmonary edema
o Improving cardiac function
o Reducing anxiety—they def will have it due to the alterations in all of the above
o Will insert a foley catheter to be able to measure I&O (time limited use—due to increased risk of infection)
o Will be in a IV D5W just to make sure we have a line, but want to limit fluids

Discharge Teathing ** So important, repeated twice bc of hospital responsibility—huge responsibility
o MAWDS
o Medications—lasix, ACE inhibitors, beta blockers, nitrates, antidysrhytmics
o Activity—balanced with rest
o Weight—really important, best indicator of someones fluid status, weigh every day at same time, same clothes, and weigh every day—insurance comp will send a scale—tell MD if you gained 2 lbs over night, or 5 lbs in a week , call!!
o Diet—prudent diet, low fat, low sodium - recmommends less than 2 grams, less than 1.5 grams of salt )1 teaspoon is 2300mg!! so underlying cardiac problems are at high risk, explain well!
o Symptoms
o Follow-up Appointment—pts have much better outcome when they are given a specific appt to come back and visit
o Important review info!!
o Ace and arbs—quality indicator, want all pts to be using at least one of these when discharged, or a clear reason for why not
o Diueretic—loops lke lasix (furosemide)—teach them to take it at a time when they will be close to a toilet for at least 6 hours (ie like 3pm)—think about a K+ and dysrhythmias
o Nitrates—longer acting nitrate, patch, door?
o Beta blockers as well—be weary of BP and pulse rate—preventing orthostatic hypotension (have them get up slowly, especially for their first dose, want them not to rise rapidly)
o Digoxin—no longer first line treatment but helps
o Also helps with atrial fibrillation
o Have them balance with rest, and if theyre developing new activity intolerance
o Want them to weigh, best indicator of fluid status!! 2lbs over night, 5 lbs in a week—HCP might say some in for eval or do further assessment (might have had salty food they didn't cook, recommend a diuretic for them for that day)
o Diet is big—low sodium , 1.5 and less than 2—website AHA is great
o Always be as culturally aware/competent as possible
o Fluid restriction—can be really hard, need to make it realistic—pt was on such (ejection fraction of 10%) strict fluid restriction of 500mL
o Symptoms, getting savy, thinking of clinical cues -SOB, dependent edema (pedal edema- shoes don't fit, legs are heavy—tell them to improve venous return,
o Looking for JVD as a symp, looking at ascites/abdominal girth
o **DNP value—hormone rlesease from left ventricle when its over stretched, and severity of health failure—but normal is less than 100 okay, 100-300 is midl, anything over
o Myocardial Infarction
o Is a risk in it of itself can cause dysrhythmias
o time =brain and time=muscle for MI
o Divided by ACC/AHA (American college cards/American heart association to provide evidence based research)
• Non-ST MI (NSTEMI)
• Has a better prognosis, and the ST heightened segment, and doesn't show full occlusion of a coronary artery and this classification has a better prognosis
• ST elevation MI (STEMI
o Types of MI→thinking about how far/deep the heart muscle damage goes
o There is the zone of infarction, zone of ischemia, and zone of injury—if we don't reperfuse, those are going to continue to grow
o Anterior wall MIs have the highest mortality
o Transmural MI
• Involves entire thickness of myocardium
o Subendocardial MI
• Damage has not penetrated thru entire thickness
o Described by area (wall) of occurrence
• Anterior, Inferior, Lateral, Septal, etc
• Anterior wall MI's have the highest mortality rate
o Laboratory Assessment
• Troponin T and troponin I (protein that is released when there is death of heart muscle—in those without ischemia or necrosis, this should not be present)
• These best help to tell if an MI has occurred, will arise 1-2 hours after
• Creatine kinase-MB (CK-MB) (enzyme relesed from heart muscle, but this is heart specific)
• More specific to heart muscle, but doesn't arise for 24 hours
• Myoglobin (enzyme when injury to muscle)—these are the 3 cardiac markers
• Rises quickly but not specific enough
• Imaging assessment—in acute phase, not likely to be used right away
• 12-lead electrocardiograms—can help show us dysrhythmias and immediately what is happening with the heart
• Cardiac catheterization—its an invasive assessment, a guidewire is inserted through an artery and the physician and interventional card specialist can visual any blockages in the arteries
• They can also perform coronary interventions to break them up as well
• ECG Lead placement→
o Acute MI Assessment:
o Pain—can be culturally dependent, use different words like discomfort or pressure—underlying patho is lack of O2—this is an ABC issue—this pain is different! Should not have any pain, not like regular pain
• Chest pain not relieved: hallmark of MI
• Diabetics—may have neuropathy and not feel as much pain as others
• Women—nausea/vomiting, but theres a lot of stress/reasons to be tired so they see a higher prevalence of negative outcomes bc theyre not recognized to be in cardiac distress
• Older Adults—flu like symptoms, overwhelming malaise, confusion, dyspnea
o Nausea & vomiting
o Fever
o CV symptoms—alterations in vital signs, BP could be elevated or decrease, tachy
o Sympathetic Nervous System Stimulation—fight or flight, will see blood shunted to vital organs and vasocontriction, skin might be cool and clammy, sweating
o Anxiety wise—high, fearing death, pt may be in denial, don't want to think about it, impending doom
o A lot of the time, may see GERD as the same kind of pain—bring Maalox as well
o Fever—its part of an inflammation process, as high as 102 (not great for older adults not as great at mounting fevers)
o Pain Management—relieve pain and ischemia
o Nitroglycerin—potent vasodilator, will want to make sure pt is in semi-fowlers or sitting, beware of BP, have a cuff to check
• Also pts who are using nitro make sure they know not to stand up when taking the med
• Can be used IV in the acute setting to relieve pain and as a spray as well
o Morphine sulfate—recommended med in the acute setting, is administered intravenously to reduce pain but it can also reduce respiratory rate (can be good or bad) but is mainly considered good and recommended for
• Want to monitor BP and RR
• "Start low go slow"
o Oxygen→immediate intervention for cardiac pain, to provide supplement in hypoxic state
o Position of comfort; semi-Fowler's position
o Quiet and calm environment
o MONA (morphin, Oxygen, Nitroglycerin and Aspirin)

Ineffective Tissue Perfusion (Cardiopulmonary) → know nitro, morphine and Beta blockers (post MI to reduce the workload of the heart as long as they are hemodynamically stable)!!
o Interventions:
o Drug therapy (aspirin (at home, should take 4 low dose aspirin (81mg) bc they help with antiplatelet action, thrombolytic agents)
o Restoration of perfusion to injured area limits amount of extension, improves left ventricular function→improves and limits the disability they will feel
o Complete sustained reperfusion of coronary arteries in first few hours after MI has decreased mortality
o Thromolytic Therapy:
o Fibrinolytics dissolve thrombi in coronary arteries, restore myocardial blood flow→layterm is "clot buster" that interfere with the coagulation path
• Tissue plasminogen activator
• Reteplase
• Tenecteplase
o There are also some contraindications ie if someone has a high tendancy to bleed, or someone with low platelet count where you might not want to give these meds bc it will be worse for them—there is a text box which shows these contraindications
o Other Drug Therpaies:
• Glycoprotein (GP) IIB/IIIa inhibitors→
• Once-a-day beta blockers
• ACE inhibitors or angiotensin receptor blockers—to deal with heart failure which is a major complication from MI
• Calcium channel blockers—reduce the workload of the heart
• Ranolazine (Ranexa)—antianginal
o We are those at the last delivery of care—we play a crucial role and we're the end point provider of medications—we need to know when to give med, when to hold, when to monitor/ what to look for—lots of responsibility


o Reperfusion Therapy
o Myocardial tissue can become increasingly ischemic and necrotic
o Thrombolytic therapy using fibrinolytics dissolves thrombi in the coronary arteries and restores myocardial blood flow
o Medical Management
o Pain relief and decreased myocardial oxygen requirements through preload and afterload reduction
o Drug therapy
o Intra-aortic balloon pump—a pump that can help improve perfusion to the heart
o Immediate reperfusion

Acute MI: Nursing Interventions
o Administration of oxygen, positioning→some pts might even be admitted due to such extreme dehydration or anemia
o Continuous ECG monitoring
o Frequent vital signs
o Pain relief (e.g. morphine), rest & comfort
o Anxiety→want to monitor the psychosocial issues that will arise
o Emotional & behavioral reactions→addressing the changes that will occur in their daily life
• Communicate with family
• Provide support
o Nursing measures to prevent complications &/or progression of MI
o Discharge Teaching & Home Care→talking about resumption of all physical activity
• Patient teaching
• Factors that precipitate angina
• Avoid exposure to extremes of weather
• Rehabilitation
• Cardiac rehab, physical exercise
• Resumption of sexual activity
• Emotional readiness
• Physical training

o After cardiac arrest, the hospitals have to have the protocol of putting the patient on ice to reduce the damage done to the brain
Factors that can cause a sickle cell crisis can be dehydration, infection, decreased blood volume, electrolyte imbalances, and excessive oxygen demands. As the majority of the pain and complications arise due to a depletion of oxygen, a circumstance where not enough oxygen is being delivered by the blood or the demand for O2 is higher than the body can handle, will lead to a sickling crisis.
Common complications are CVA, anemia, vasooclusive pain, pulmonary hypertension, retinopathy, hepatomegaly and splenomegaly, abdominal pain, and osteomyelitis.
Key points to include for the patient, as well as whoever may be caring for him or her, will mainly be related to noting signs of sickle cell crisis and methods to prevent one from occurring. These patients should be advised to seek medical help if he or she has a temperature 101.3 and over, should take penicillin as ordered, as well as recognize signs and symptoms of splenic sequestration and respiratory problems that can lead to hypoxia. Promotion of adequate hydration in order to delay the adhesion-stasis-thrombosis-ischemia cycle will also need to be included. Avoiding hot weather and dehydration, as well as close monitoring of urination or overwhelming thirst will be key in preventing these crises. Pain medications should also be given as needed considering that this is a frequent occurrence in these patients. What will be most important is treating this person or child normally, but being vigilant about rest, adequate hydration, and monitoring for infection to ensure that this patient avoids sickle crises.
Acute Kidney Injury—used to be called Acute renal failure
o Pathophysiology—comes on suddenly, potential reasons for AKI are in different stages or types listed below
o Types:→be familiar with what categories and patho go where
o Prerenal (shock, low perfusion low volume/dehydration, sickle cell?)
o Intrarenal (damage directly to the kidney, kidney stones, polycystic kidney disease, glomerulonephritis, drugs, nephrotoxic agents ( NSAIDS, antibiotics** main to appreciate)
o Postrenal (obstruction, kidney stones, BPH, balder cancer/tumor)
o Prerenal azotemia (increasing nitrogenous waste in the blood)
o Causes:
o Hypovolemic shock
o Heart failure (not enough perfusion (prerenal), excess fluid)
o Very complex—very different nuances, acid base/electrolyte balances, maintenance of many different types of
o Remember, if caught and the underlying issue is treated is reversible
o Phases of AKI—hopefully we can fix it if it comes on fast, related to pre or post renal issue—we hope they will go through the phases and get better—if not, AKI can lead to chronic kidney disease
o Rapid decrease in kidney function lead to collection of metabolic wastes in the body
o Phases:
o Onset—having the insult, maybe theyre takin nephrotoxic drugs
o Oliguric—small urine output, small injury to kidneyaffecting output,, if they start to improve, they will go on to start a diuresis (getting rid of fluid) to increase urination,
o Diuretic
o Recovery
o Acute syndrome may be reversible with prompt intervention
Parkinsons Disease
o Progressive, idiopathic neurologic disorder—can treat symptoms but not the
o Unknown etiology
o Caused by imbalance of neurotransmitters dopamine and acetylcholine
• Degeneration of neurons
• Motor tracts originate in substantia nigra of midbrain and terminate at the basal ganglia of the extrapyramidal motor tract
• Due to degeneration of neurons, the imbalance of dopamine arises and does not oppose Ach—interesting to relate to the parksinonism that you see as an EPS related to the blocking of the dopamine receptors by the typical antipsychotics***
o Combination of symptoms:
o Tremor at rest
• Usually starts with hands
• May include head & neck
o Bradykinesia
• Slow movement
o Rigidity
• ↑ muscle tone
o Postural instability
o Dimentia and depression can arise as well
o Symptoms
• Postural changes
• Chest and head thrust forward with knees and hips flexed
• Shuffling gait
• Involuntary tremors
• Mask-like facial expression
• Pill rolling motion of hands


Stages of Parkinsonism
o A, Flexion of affected arm. Patient leans toward the unaffected side. B, Slow shuffling gait.
o C, Patient has increased difficulty walking and looks for sources of support to prevent falls.
o D, Further progression of weakness. Patient requires assistance from another person for ambulation.
o E, Profound disability. Patient may be confined to a wheelchair because of increasing weakness.


Dopaminergic Drugs—Dopamine is what we give to restore this activity but there is a problem! There is an enzyme in the PNS that destroys or uses up most of the dopamine before it gets to cross the BBB so we give a synthethic form (Levodopa is destroyed as well)
o Goal is to restore dopaminergic activity with levodopa and dopamine agonists—they used to just give the levodopa in large amounts in an attempt to get more dopamine to the brain BUT there were a lot of side effects so along came...
o Prototype drug
• Carbidopa-Levodopa (Sinemet)
o Action
o In Parkinson's Dx, there is an imbalance of dopamine to acetylcholamine
o Goal for medication is to restore balance by increasing amount of dopamine in the brain
o The BBB admits levodopa but not dopamine; 99% of levodopa is converted to dopamine by enzyme dopa decarboxylase in the peripheral nervous system BEFORE it is admitted to the brain
o Carbidopa is added, therefore, to block the conversion of levodopa to dopamine in the peripheral nervous system
o allowing for more levadopa to enter the brain...there, it is then coverted to dopamine
Meningitis
o Pathphysiology
• Inflammation of the meninges—usually infectious in nature, parasite, meninges around brain and spinal cord
• Pathogenic organisms cross the blood brain barrier & enter CNS
• Viral usually self-limiting; bacterial may be life-threatening—niceria meningitis is common and now there is a vaccine—college freshman at high risks
• Seen with men meeting in anonysmouse sex locations and seeing an outbreak of bacterial meningitis—lot of them are dying before getting treatment
• Usually droplet spread—coughing, sneezing, need to be in close contact
o Clinical Manifestations
• Severe headache, fever, N/V
• Classic: nuchal rigidity (flex the neck), (+) Kernig's (flex pts hips, look for pain) & Brudzinski's (flex pts neck, causes them to flex hips up) signs—hallmark signs—wont ask on test--
• Photophobia, symptoms of ↑ICP
• ↓ LOC, seizures, rash (enterovirus)
• Lumbar puncture will be the way to get the cerebrospinal fluid to test for pathogen—in the mean time will isolate them and maybe give antibiotics to start—only need to be isolated for 24 horus and after 24 hours of treamtnent, they are okay
o Complications—can be severe
• Cranial nerve dysfunction
• Hemiparesis, dysphasia, hemianopsia
• Cerebral edema → seizures , bradycardia-- death
• Kernig's sign: Flexing the patient's hip 90 degrees then extending the patient's knee causes pain.
• Brudzinski's sign: Flexing the patient's neck causes flexion of the patient's hips and knees.
o Lab Assessment
• CSF analysis by lumbar puncture most significant
• Severe headache—can also be hemorrhagic stroke but also
• CT scan
• CBC with differential—lookin for increased WBCs
• Serum electrolytes—looking for alterations in their sodium level due to inappropriate administration of a diuretic
• May have dilutional ↓Na++ R/T SIADH
o Nursing Interventions
• Follow ABCs
• V/S, neuro checks (can be a tool, can be short, Glascow coma scale, have baseline and look for deviation) , lungs, skin
• Reduce fever - fever ↑ cerebral edema—look for changes in mental status, anything that indicates these changes—may require some rehab—may use osmotic diuretics
• Cooling blankets, Tylenol, sponge baths
• Manage fluid balance (I & O)
• Enhance Cerebral perfusion
• Reduce pain
• Optimal level of functioning
• Rehab—after some of the neuro or muscular problems seen
• Passive to active exercises
• Prevention: Meningococcal vaccine for at risk pts
Neurogenic Shock
o Vasodilation as a result of loss of balance between parasympathetic and sympathetic stimulation
o Mimics hypovolemia even though fluid volume is adequate
o Common causes are:
o Spinal cord injury
o Spinal anesthesia, medications
o Nervous system damage
o Signs and Symptoms:
o ↓ SVR (systemic venous resistance)
o ↓ BP
o Bradycardia—this is a diagnostic hallmark after experiencing some sort of neuro trauma**
o Syncope/fainting
o Dry, warm skin→ this is also different vs the cool skin in others bc the blood is stuck out in the periphery bc the symp and parasymp are in a middle state**
o Pharmacological Interventions
o Heparin or LMWH—given because these patients are at risk for clots
o Osmotic diuretics, glucose, LR, steroids


Nursing Diagnoses and Interventions→the worry here is hypoperfusion so monitoring for BP, fluids, neuro status first so see what the situation is
o Ineffective peripheral, cerebral & renal tissue perfusion re: ↓ circulating blood volume
o Neuro status
o Monitor B/P at frequent intervals for hypotension
• Readings > 20mmHg below normal range → indicate hypotension → dizziness, orthostatis
• BP must be > 80/60 for adequate coronary & renal perfusion
o √ Peripheral pulse perfusion
• Report coolness & pallor of extremities, delayed capillary refill
o √ ↓ Cardiac perfusion
o √ Urine output < 30mL with adequate intake
o Electrolytes - ↓ Na+, ↑ K+, √ s/sx
o Administer fluids - to ↑ volume
• Hypovolemic shock - amt lost is replaced
• Cardiogenic shock - fluids limited to prevent overload
• Septic Shock - LR, plasma & blood
o Impaired gas exchange re: altered oxygen supply→ in a hypoperfused state, always going to apply O2 to stablize the pt
o Ensure a patent airway
o Monitor respirations
o Monitor pulse oximetry
o Monitor mental status
o Encourage patient to breath slowly & deeply to promote oxygenation
o Administer O2
o Monitor ABG
• Be alert to hypoxemia → ↓O2 sat & ↓PaCO2
• Acidosis may be present
Beningn Prostatic Hyperplasia or hypertrophy (BPH)—DOES NOT PUT SOMEONE AT RISK FOR PROSTATE CANCER
o Glandular units in the prostate that undergo an increase in number of cells, resulting in enlargement of prostate gland
o Creates the seminal fluid that helps carry the semen along
o Androgen dependent—male sex hormones will impact
o 90% of men over age 80 will have some degree of this—can start to develop around Age 40
o when looking at where the tissue enlarges, you can think of it—the cancer cells will be readily palpated, will feel "rubbery" when doing a digital rectal exam
o The prostate gland said to look sort of like a donut that sits around the urethra—as the hypertrophy starts to progress, the pressure builds up and cause symptoms in the urinary system
o Symptoms
o Hyperirritable bladder but dribbling or inability to really make urine
o Urgency and frequency—pressing of the ureter
o Hypertrophied bladder wall muscles
o Cellules and diverticula
o Hydroureter
o Hydronephrosis
o Overflow urinary incontinence—may lead to psychosocial issues, people wont leave the house because they can urinate but then lose it—very distressing symptoms
o At higher risk for UTIs

Potential Complications
o As this is a post renal obstruction that can lead to renal failure—the picture shows hydonephrosis from BPH
o Not evacuating bladder—having urinary retention—risk for UTI

Surgical Procedures
o Transurethral resection of prostate (TURP)
o Prostatectomy
o Suprapubic
o Retropubic
o Perineal

Prostatectomy

Postoperative Care
o Urinary catheter with retention balloon placed into bladder
o Traction via taping to patient's abdomen or thigh
o Uncomfortable urge to void continuously

Collaborative Care—treatment largely done based on their symptoms and progression of the disease
o Diagnostic Studies:
o Men might not want to bring it up—past a certain age, its necessary to bring it up and ask them about urinary patterns and want them to be comfortable to talk about ti
o Digital rectal exam
o Urine analysis and culture—see if indices of infection,
o Serum creatinine and BUN—looking at kidney function
o PSA (Prostate Specific Antigen)—thought to be a specific way to tell risk factors for prostate cancer but is very controversial
o Urodynamic flow studies
o Cystourethroscopy
o
o Treatment Goals:
o Have less symptoms and no complications
o Restore bladder drainage
o Relieve symptoms
o Treat complications
o Drug Therapy:
o Hormonal manipulation (androgen)
o Proscar—can manipulate androgens—generally something given to a male patient to shrink prostate over a few months—can be hard with their symptoms continuing
o Alpha-adrenergic blockers—can have significant blood pressure issues ie. Hypotension—even though they are trying to open up urine ability
• Meant to decrease the amount of pressure being put on the urethra but affect BP
• Minipress, Cardura, Hytrin
• Side effects: orthostatic hypotension, dizziness—many pts will take this at night so don't get up
o
o Conservative therapy
o uroscopy—trying to open up the urethra
o Stents, prostatic balloon
o Foley catheters—not long term bc of infection risk
o
o Invasive therapy
o TURP (Transurethral resection of the prostate)—surg procedure with extensive symptoms—they access the prostate via the urethra and trying to resect the tissue and decrease its size—new methods that are being done, can be with laser instead
o Complications
o The biggest is the risk for bleeding
o Side effects relating to messing witht the prostate—and what it does—low chance that it can lead to ED and **retrograde ejaculation—which can have effects on reproduction
o Incontinence as well—but very rare