Study Guide-Final - Adult Health II

Prioritize nursing care for the patient during the acute phase of burn injury.

(wound healing) •The acute phase begins with the mobilization of extracellular fluid and subsequent diuresis. •The acute phase is concluded when the burned area is completely covered by skin grafts, or when the wounds are healed. --Hyponatremia, hypernatremia, hyperkalemia, hypokalemia Complications: infection, increased blood glucose, increased insulin production, decreased ROM, contractures, paralytic ileus, diarrhea, constipation, curling's ulcer. Nursing Care: Pain management PT and OT Relaxation Strategies Psychosocial care Nutritional therapy High protein, high carb diet Favorite foods from home Should be weighed regularly

Describe the role of the nurse in monitoring for and managing potentially life-threatening complications of cirrhosis.

-Portal hypertension and esophageal varices -Peripheral edema and ascites -Hepatic encephalopathy -Fetor hepaticus - characteristic liver breath—musty, sweet odor •Portal Hypertension: a persistent increase in pressure within the portal vein greater than 5 mm Hg, is a major complication of cirrhosis •It results from increased resistance to or obstruction (blockage) of the flow of blood through the portal vein and its branches. The blood meets resistance to flow and seeks collateral (alternative) venous channels around the high-pressure area. •Blood flow backs into the spleen, causing splenomegaly (spleen enlargement). Veins in the esophagus, stomach, intestines, abdomen, and rectum become dilated. •Portal hypertension can result in ascites (excessive abdominal [peritoneal] fluid), esophageal varices (distended veins), prominent abdominal veins (caput medusae), and hemorrhoids. Esophageal Varices: •Avoid alcohol, aspirin, and irritating foods •If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin) (BP support) •Management of Nausea and Vomiting. •Endoscopic sclerotherapy or ligation (inject a sclerotherapy or other type agent into the affected area to stop the bleeding) • Esophageal Bandings Hepatic encephalopathy •Liver damage causes blood to enter systemic circulation without liver detoxification •Increased levels of ammonia •Often terminal if untreated assess for changes in LOC - lethargy, etc •Goal: reduce NH3 formation •Protein restriction (0-40g/day) •Sterilization of GI tract with antibiotics (e.g., neomycin) --neomycin can lead to nephrotoxicity, ototoxicity, and cdiff related collitis •lactulose - traps NH3 in gut, decreases ammonia levels bc they diarrhea it out •Levodopa only if conventional treatment did NOT work Nursing Management: Ambulatory and Home Care -Symptoms of complications -When to seek medical attention -Hepatotoxic meds - tylenol, sedatives, barbituates, opiods, OTC -Abstinence from alcohol -Maintenance of normal body weight -Maintenance of skin integrity -Effective breathing pattern -No injury -No signs of infection Peripheral edema and ascites •Ascites is the collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension. •The collection of plasma protein in the peritoneal fluid reduces the amount of circulating plasma protein in the blood (Hypoalbuminemia). Normal Albumin level 3.5-5.0 g/dL •High carbohydrate, low protein, low Na+ diet ---low protein decreases ammonia levels ---low NA decreases fluid •Diuretics •Paracentesis (Chart 58-1) ---give IV albumin after paracentesis (paracentesis could lead to MI)

AIDS prevention

Abstinence! Condoms! Limit number of sexual partners Routine testing Do not share needles Avoid contact with other people's bodily fluids Be careful with blood transfusions, organ donations, etc

Compare the pathophysiology and causes of acute kidney injury (AKI) with those of chronic kidney disease (CKD).

AKI The loss of kidney function affects the ability to maintain normal processes of urinary elimination, fluid and electrolyte balance, and acid-base balance The causes of AKI are reduced perfusion to the kidneys, damage to kidney tissue, and obstruction. Types --Prerenal --Intrarenal --Postrenal Other Causes --Hypovolemic shock --Heart failure earlier you catch it the less damage there is Pre-renal - •Any condition that reduces blood flow to the kidneys ( upstream ) •Cardiac failure •Decreased cardiac output •Hypovolemia •Burns, dehydration, trauma, shock, diuretic overuse •Peripheral vasodilation •Antihypertensive medications •Renal artery stenosis or embolism lack of perfusion anaphylaxis can cause pre-renal failure pre-renal can progress to intrarenal failure Intrarenal - •Filtering structures of the kidneys are damaged •Usually from " acute tubular necrosis " •Ischemic damage to tubular cells •Nephrotoxic substances •Gentamycin, NSAID, Lead, Analgesics, Diuretics •Rhabdomyolysis: breakdown of muscle Þ myoglobin or fat embolism •Caused by major trauma or systemic infections •Acute glomerularnephritis: inflammation of the nephrons damage to nephron compromises kidney function glomerulonephritis, pyelonephritis, and infection Postrenal - •Results from obstructed outflow •Urolithiasis •Bladder obstruction •Infection, tumor, obstructed Foley catheter (FC) •Ureteral obstruction •Blood clots, calculi, accidental ligation, edema •Urethral obstruction •Prostatic hyperplasia or tumor •Strictures of the urethra --BPH - benign prosthetic hypertrophy Prostate cancer = cause can be stone or congenital narrowing etc PATHO •initiating phase - symptom onset •Oliguric Phase: less than 400mL / 24 hours •At risk for fluid volume excess •Azotemia: elevated BUN, Creatinine and Uric Acid •decreased level of consciousness •Electrolyte imbalance: hyperkalemia •Renal cells can regenerate if etiology is treated •Diuretic Phase: those who recover renal function •gradual increase in urine output •tubular transport is still hindered...urine is dilute •high urinary outputs places pt at risk for dehydration --lasts 1-3 weeks •Recovery Phase: gradual return to normal function •3 to 12 months or longer for recovery CKD •Progressive, irreversible kidney injury; kidney function does not recover •CKD will progress to End-stage kidney disease (ESKD) •Clinical manifestation •Azotemia (nitrogen in blood) •Uremia •Uremic syndrome (a condition of premature destruction of red blood cells caused by infection) --diabetes and HTN are 1st and 2nd causes of CKD --native americans and men are at risk of CKD --usually CKD is asymptomatic until it is advanced --may have uremia which is high levels of urea in the blood --GFR less than 60 = stage three CKD, stage 4 15-29, stage 5 (end stage) less than 15 Stages of CKD 1. Reduced renal reserve - may be a sign of a maladaptive repair or subclinical loss of renal mass. Thus, a reduction in RFR may represent the equivalent of renal frailty or susceptibility to insults. 2. Reduced glomerular filtration rate (GFR) - when gFR is below 60 for more than three months, this is moderate-to- severe chronic kidney disease. you may be referred to a nephrologist (kidney doctor) for evaluation and treatment. a gFR below 15 means kidney failure. if kidney failure occurs, dialysis or a kidney transplant will be needed to survive. 3. ESKD - the last stage of long-term (chronic) kidney disease. This is when your kidneys can no longer support your body's needs. End-stage kidney disease is also called end-stage renal disease (ESRD) •Kidney changes (reduces GFR and abnormal urine production) •Metabolic changes • Urea and creatinine - RISE • GFR decrease •Electrolyte changes •Sodium •Potassium - increases leading to metabolic acidosis •Acid-base imbalance •Calcium and phosphorus - elevated phosphorus, low calcium ----secondary hyperparathyroidism •Cardiac changes • Hypertension • Hyperlipidemia • Heart failure • Pericarditis •Hematologic changes --HIGH BP meds cannot be administered on dialysis days because you are moving around a lot of fluid so it may lead to pressure changes without it --pt should be on a statin to treat high fat level (ends in -for) •GI changes --decreased motility fluid and electrolytes and acid-base balances are severe lack of activated vitamin D

Compare and contrast the pathophysiology of acute and chronic pancreatitis.

Acute Pancreatitis • An acute inflammatory process of the pancreas can be mild or severe • It ranges from Mild edema to severe necrosis •Most common in middle-aged men and african american males • Can be life-threatening can lead to SIRS - systemic inflammatory response system which can lead to sepsis which is the same thing as SIRS but with an added infection Chronic Pancreatitis • Progressive destruction of the pancreas with fibrotic replacement of pancreatic tissue • Strictures and calcifications (can block duct and lead to acute pancreatitis) may also occur in the pancreas --scar tissue The crucial difference one can make to tell the difference is in the longevity of the pain. Acute pancreatitis starts with a sudden attack of pain that peters out after a few hours to days while chronic pancreatitis remains persistent for months. However, even then that symptom might not be as reliable as it seems.

Explain the relationship between hypertension and kidney disease.

As the vessels are compressed and blood flow to the kidneys decreases, the renin-angiotensin system is activated, raising blood pressure. Control of hypertension is a top priority because proper treatment can disrupt the process that leads to further kidney damage High blood pressure can constrict and narrow the blood vessels, which eventually damages and weakens them throughout the body, including in the kidneys. The narrowing reduces blood flow. If your kidneys' blood vessels are damaged, they may no longer work properly.

Define the Monro-Kellie doctrine

Brain tissue, CSF, and blood occupy a rigid space (the skull) When one component increases, the others must decrease to maintain equilibrium to prevent compression of brain tissue.

Identify different degrees of burn.

Chemical Burns: •Chemical should be quickly removed from the skin. •Clothing containing the chemical should be removed. •Tissue destruction may continue up to 72 hours after a chemical injury. contact w wet cement, hydrochloric acid, bleach, etc --acids can produce coagulation necrosis complications liquefaction necrosis denaturing of the protein irrigation/brushing off powder is very important in management of burns --this puts us at risk, so be careful to wear PPE severity related to pH of agent, how much is there, length of time of decontamination, is it powder, liquid, etc --Bases can cause liquefaction necrosis which denatures proteins and fats Smoke Inhalation Injuries -----Above the Glottis •Hot air, steam, smoke •Facial burns, singed nasal hairs •Hoarseness, painful swallowing •Black sputum, saliva •Burns of throat, mouth, larynx •Medical Emergency -Patent Airway soot around mouth or nasal passages are indicative of this ----Below the Glottis •Related to the length of exposure to smoke or toxic fumes - chemicals •Pulmonary edema may not appear until 12 to 24 hours after the burn •Acute Respiratory Distress Syndrome ----Cause damage to respiratory tract •Major predictor of mortality in burn victims •Need to be treated quickly Electrical Burns •Intense heat generated from an electric current •Burn damage internal •Cardiac dysthymias •Myoblobinuria •Severity depends on voltage, duration, and pathway of the current •Damage to vital organs (bones are more resistant to electric currents) worry about entrance and exit points (contact points) lineman are at most risk Burn Severity Classification is based on depth, extent (total body surface area), location, and patient risk factors. •Superficial partial-thickness burn •Involves the epidermis and part of dermis --blisters, can be wet, heal within 1-2 weeks with minimal to no scarring --caprefill decreased --hypersensitivity, erythema --Sunburn •Deep partial-thickness burn •Involves the dermis --most concerning, decrease in sensation, appear waxy, no blisters, light pink to cherry red in color --cap refill decreased or absent --Hypersensitive --may need surgery •Full-thickness burn •Involves fat, muscle, bone --appear dry, leathery, pale, white, brown, tan, black, charred in color --no or very limited pain due to damaged nerves, but very sensitive to pressure --will not heal without surgical intervention and grafting --no blisters are present --Surgery and grafting is required

•Cardiogenic :

Direct pump failure (fluid volume not affected). ---Examples: Myocardial infarction and Cardiac arrest •Actual heart muscle is unhealthy -----Pumping is directly impaired •Myocardial infarction most common cause Cardiogenic shock is characterized as inadequate pumping ability of the heart muscle, most typically the result of an acute myocardial infarction (AMI). Independent of fluid volume status, the inadequate pumping of the heart results in decreased cardiac output and poor perfusion at the tissue level.

who is at risk for shock

Hemorrhage Trauma/burns Decreased cardiac output Infection/anaphylaxis

What nursing interventions would be important with a patient with neutropenia?

Implement neutropenic precautions. This includes a private room with appropriate signage so staff is aware. Equipment may be left in the room, so it is only used by that patient to prevent the transmission of pathogens. Limit visitors. Patients with neutropenia are susceptible to infections and must be isolated accordingly. Limiting visitors reduces the risk of disease. Teach the patient proper handwashing techniques. Handwashing is an effective infection control method. Germs from unwashed hands can easily be transmitted from person to person. Administer medications as ordered. The granulocyte-colony stimulating factor is often given to help stimulate the bone marrow into producing more neutrophils. Maintain aseptic technique. The nurse and staff should maintain strict aseptic techniques when accessing IV lines or ports, cleaning catheters, or touching the patient.

Discuss the mechanisms of hemodialysis (HD) as renal replacement therapies

In hemodialysis, the wastes and excess water are removed by using an external filter called a dialyzer, which contains a semipermeable membrane. The separation of wastes is done by creating a counter-current flow gradient, where blood flow is in one direction and the fluid of the dialyzer is in the opposite direction. Only indicated if GFR is <15 •Patient selection •Dialysis settings •Procedure •Anticoagulation CRRT indicated for acutely ill patients, can manage acid-base balance, electrolyte, and fluid balance indicated for GFR less than 15!!

Impact of diuretics on electrolytes.

Loop diuretics (Lasix/furosemide) - risk for HYPO-natremia, -kalemia, -calcemia, and -magnesemia Thiazide diuretics (Hydrochlorothiazide) - risk for HYPO-natremia, -kalemia, and -magnesemia; risk for HYPERcalcemia Potassium-sparing diuretics (Spironolactone) - risk for HYPO-natremia, -magnesemia, and -calcemia; risk for HYPERkalemia

Assess ABG results for abnormalities and apply to pt. Situation

NORMAL LEVELS pH: 7.35-7.45 Low = acidosis High = alkalosis CO2: 35-45 Low = alkalosis High = acidosis HCO3: 22-26 Low = acidosis High = alkalosis

Explain the EKG findings in a NSTEMI vs a STEMI

NSTEMI (aka non ST segment elevation MI) - may or may not have s-t depression and T-wave inversion. May look normal on an EKG. - is a partial blockage of a major artery or a full blockage of a minor artery. - Damage is reversible -There may also be the presence of Q waves indicating past myocardial damage. STEMI (aka ST segment elevation MI) - Will have s-t elevation on an EKG, may have T inversion - Full blockage of a major artery. - Damage is NON-reversible -indicates ongoing acute myocardial damage.

Respiratory acidosis

Numbers pH < 7.35 CO2 > 45 Partially compensated: HCO3 > 26 Acute or chronic ( COPD) Caused by HYPOVENTILATION - retaining CO2 Pneumothorax Pulmonary embolism Myasthenia gravis Can be caused by hyperkalemia S/s HA Dysrhythmias Tachycardia Decreased response Confusion Respiratory distress Tx Bronchodilators Oxygen Kayexalate Antibiotics Removal of foreign object Chest tube Compensation: INCREASE in hydrogen secretion and bicarbonate reabsorption

Prioritize the nursing care for the patient with sepsis or septic shock

Patho •Inflammatory syndrome from severe infection ----Vasodilatation ----Increased WBCs ----Leakage of fluid from capillary beds ----Remote from the site of infection ----cytokines ----secondary prothrombotic state rt inflammation •Infection = invasion of normally sterile tissue by organisms •Bacteremia - Presence of viable bacteria in blood ----get specimen before starting antibiotics tachycardia, bounding pulses, flushed skin, fever, decreased urine output, pale skin, cool extremities, threaded pulses, hypotension, hypothermia In taking care of a patient with sepsis, it is imperative to re-assess hemodynamics, volume status and tissue perfusion regularly. Tip: Frequently re-assess blood pressure, heart rate, respiratory rate, temperature, urine output, and oxygen saturation

Explain the pathophys, causes, S/S, and treatment of Heart Failure

Pathophysiology - HF Is a response to cardiac dysfunction, a condition in which the heart cannot pump blood at a volume required to meet the body's needs. - Hypertension is the precursor - uncontrolled high BP is one of the biggest causes of heart failure especially in african americans -Heart failure can occur due to a variety of reasons that affect the heart's ability to pump effectively. The most common causes of heart failure include coronary artery disease, high blood pressure, valve disease, heart attack, and conditions that damage or weaken the heart muscle, such as infections, toxins, or genetic factors. Over time, these conditions can cause the heart to become enlarged, stiff, or weakened, making it harder for it to contract and pump blood effectively. risk factors 65 or older, African American, men are more at risk than women, high BP, diabetes, metabolic syndrome, central obesity, smoking preserved ejection fraction - diastolic heart failure usually 50% or more - tend to be older females an abnormality of the heart muscle that makes it unable to relax, stretch, or fill during diastole reduced ejection fraction - systolic heart failure usually 40% or less -- weakened contraction of the heart that decreases CO describes an abnormality of the heart muscle that markedly decreases contractility during systole (ejection) and lessens the quantity of blood that can be pumped out of the heart Left-Sided Heart Failure Clinical Manifestations •Weakness •Fatigue •Dizziness •Acute confusion (low flow) •Pulmonary congestion •Breathlessness •Cough •Oliguria •Crackles in lungs lung-related respiratory symptoms Right-Sided Heart Failure Clinical Manifestations •Jugular vein distention •Increased abdominal girth •Dependent edema •Hepatomegaly (liver enlargement) •Hepatojugular reflux •Ascites in abdomen •Weight most reliable indicator of fluid gain/loss ---take daily weights, if they gain more than 2.5 pounds day to day or more than 5 pounds in a week they need to call their provider problems with circulation or fluid overload •Nursing management •Optimizing cardiopulmonary function •Promoting comfort and emotional support •Monitoring the effects of pharmacologic therapy •Nutritional intake •Patient education •Daily weight •Fluid restriction •Medication management •Promoting oxygenation and gas exchange •Ventilation assistance •Monitor respiratory rate every 1-4 hr •Auscultate breath sounds every 4-8 hr •Position in high Fowler's if patient dyspneic •Maintain oxygen saturation of 90% - 93%-94% is ideal •Improve/increase cardiac pump effectiveness •Preload •Afterload •Contractility •Hemodynamic regulation MEDS Morphine sulfate ACE inhibitors Diuretics - Loop - Thiazide Cardiac glycoside (digoxin) Increases contractility Reduces heart rate (HR) Slows conduction through atrioventricular node Inhibits sympathetic activity - CPAP - CRT (Cardiac Resynchronization Therapy ( Pacmaker)) - slows heart rhythms - Gene therapy CPAP, Continuous positive airway pressure; CRT, cardiac resynchronization therapy.

Explain the pathophys of a primary injury vs. a secondary injury

Primary injury: -Initial mechanical disruption of axons as a result of stretch or laceration Secondary injury: -Ongoing, progressive damage that occurs after initial injury

Normal value for different blood products.

RBCs - volume 300 mL, indicated for symptomatic anemia and acute and chronic blood loss •Hemoglobin less than 8 •ABO compatibility and Rh factor Fresh Frozen Plasma - volume 200 mL, deficiency of plasma coagulation factors, massive transfusion in trauma, need for emergency reversal of elevated prothrombin time and international normalized ratio (PT/INR) that indicates increased risk of bleeding, disseminated intravascular coagulation (DIC) Platelets - volume 40-70 mL??, bleeding due to thrombocytopenia or platelet abnormalities ---infusion: Platelet counts below 10,000 Pooled from as many as 10 donors Contain 250 - 300 mL Platelets need to be transfused immediately over a 15 - 30 min period Platelet transfusion set and filter Take vital signs before, 15 min, and at end Granulocytes - volume 200-300 mL, neutropenia with infection, unresponsive to appropriate antibiotics Clotting factors Albumin - volume varies, volume expansion when crystalloid solutions are not adequate

NSR

Rate: 60-100 beats/min Rhythm: Regular P waves: Present, consistent configuration, one P wave before each QRS complex PR interval: 0.12-0.20 second and constant QRS duration: 0.04-0.10 second and constant this is the ONLY NORMAL RHYTHM

AFlutter

Rate: Atrial rate 250-350, Vent 150 common Rhythm: Atrial = Regular, Vent = Reg. or irreg P waves: Not identifiable; Uniform F waves present (sawtooth) PRI: not measurable QRS: 0.04 - 0.10 second - NORMAL

Describe and prioritize nursing interventions for acid-base imbalance

Respiratory acidosis interventions: Bronchodilators Supplemental oxygen Medications to treat hyperkalemia Antibiotics to treat infection Chest physiotherapy Removal of a foreign body from airway Chest tube insertion Respiratory alkalosis interventions: Discontinuation/removal of the causative agent Steps to reduce fever Eliminate the source of sepsis Oxygen therapy to treat acute hypoxemia Sedative or anxiolytic therapy to treat anxiety Metabolic acidosis interventions (depend on the cause): Use sodium bicarbonate IV Parenteral fluid replacement Rapid-acting insulin Antidiarrheals Dialysis Mechanical ventilation Metabolic alkalosis interventions (depend on the cause): Discontinuation of: Thiazide diuretics Nasogastric suctioning Antiemetic to treat nausea and vomiting Administer acetazolamide as prescribed

Recognize how the body compensates for acid-base imbalance

Respiratory compensation occurs in these conditions. Metabolic acidosis: increase in respiratory rate and depth Metabolic alkalosis: decrease in respiratory rate and depth Renal compensation occurs in these conditions. Respiratory acidosis: increase in hydrogen secretion and bicarbonate reabsorption Respiratory alkalosis: decrease in hydrogen secretion and bicarbonate reabsorption

Sinus Bradycardia

Same as normal sinus rhythm except heart rate is less than 60 bpm Rhythm: Regular P waves: Present, consistent configuration, one P wave before each QRS complex PR interval: 0.12-0.20 second and constant QRS duration: 0.04-0.10 second and constant Treatment (when symptomatic) - Atropine 0.5 mg IV, increase fluids and oxygen, may need a pacemaker - assessing the patient for symptoms of hypotension or decreased cardiac output, - administering oxygen - preparing to administer medications such as atropine or pacing if the patient is symptomatic.

Sinus Tachycardia

Same as normal sinus rhythm except heart rate is over 100 bpm Rhythm: Regular P waves: Present, consistent configuration, one P wave before each QRS complex PR interval: 0.12-0.20 second and constant QRS duration: 0.04-0.10 second and constant Treatment - use of carotid massage, vagal maneuvers (cough/bear down), valsalva maneuvers (plug nose and blow), and if heart rate is over 150, treat with beta blockers - assessing the patient for symptoms of decreased cardiac output - administering oxygen - treating the underlying cause of the tachycardia.

Hypocalcemia

Serum Ca < 9 mg/dl •Assessment Findings Fatigue, depression Numbness, tingling, hyperreflexia, muscle cramps, tetany, seizures Chvostek's sign, Trousseau's sign •Treatment Oral or IV supplements (IV Ca gluconate) Foods high in Ca

Hypercalcemia -

Serum Ca > 11 mg/dl thiazide diuretics can cause this as well as hyperparathyroidism taking too many vitamins can cause this too Assessment findings •Weakness, lethargy, confusion, coma •Decreased reflexes •Bone pain, fractures, kidney stones •ECG changes - ventricular problems Treatment •Diuretics - lasix •Hydration w oral fluids - isotonic IV fluids, drink 3,000 - 4,000 ml/daily •Calcitonin - lowers calcium levels •Weight bearing activity - prevent calcium from staying in bones, you want it in the blood stream

Hypernatremia -

Serum Na > 145 mEq/L want this to be rapidly corrected because it can lead to cerebral edema Causes •Loss of fluid - diarrhea, inadequate fluid intake, diuretics, DI, high fever •Gain of sodium - Hypertonic IV fluids, saltwater near drowning, IV Na bicarbonate --- might occur if patient received a solution that has sodium bicarbonate so it is important to stop administering this solution Assessment findings •Intense thirst, restlessness, agitation, seizures, coma, crackles, BP Treatment •Hypotonic IVs, oral fluids

What is the nurse's role in preventing HAP?

The nurse plays a crucial role in preventing HAP by implementing strategies to reduce the risk of infection. This may include practicing hand hygiene, ensuring proper sterile technique during procedures, using prophylactic antibiotics or antiseptic mouthwash, elevating the head of the bed, and promoting mobility and early ambulation

who is at risk for dehydration

athletes, older adults, and infants

Describe the relationship between pH and hydrogen ion level

it is an inverse relationship H+ goes up, pH goes down (becomes acidic) H+ goes down, pH goes up (becomes basic) meanwhile the relationship between bicarbonate and pH are the same so if bicarb goes up pH goes up (is basic) bi carb goes down pH goes down (is acidic)

Lactulose treatment for cirrhosis

lactulose - traps NH3 in gut

Explain the patho of Pneumonia and nursing priorities

•Excess fluid in lungs resulting from inflammatory process •Inflammation triggered by infectious organisms, inhalation of irritants Classification of Pneumonia(31-3) •Community-acquired infectious pneumonia •Nosocomial or hospital-acquired Pneumonia leads to: 1. Atelectasis (is the collapse or closure of a lung resulting in reduced or absent gas exchange) 3. Hypoxemia (abnormally low concentration of oxygen in the blood.) Nursing priorities for patients with pneumonia may include - administering antibiotics or antiviral medications - administering oxygen therapy, - providing respiratory treatments such as bronchodilators and nebulizers - managing symptoms such as fever and cough - preventing complications such as sepsis or respiratory failure. Encourage coughing and deep breathing and use of incentive spirometer. Position client in semi-Fowler position to facilitate breathing and lung expansion. Change client's position frequently and ambulate as tolerated to mobilize secretions Perform nasotracheal suctioning if the client is unable to clear secretions. Provide a high-calorie, high protein diet with small frequent meals. Encourage fluids up to 3 L a day to thin secretions unless contraindicated. Provide a balance of rest and activity, increasing activity gradually.

VFib

- Result of electrical chaos in ventricles, total unorganized multifocal rhythm, ventricles quiver, no cardiac output Treatment - CPR and defibrillate (followed by epinephrine) - administering oxygen

Indicate the symptoms of Unstable Angina vs. Acute MI

- Unstable angina is chest pain or discomfort that occurs at rest, with minimal exertion, or at an increasing frequency or intensity. The symptoms may be new, occur at rest, or become more severe and frequent over time. ---SOB, breaking out into a cold sweat, sudden fatigue, nausea, lightheadedness, general chest pain or pressure ---Woman may have different signs and symptoms than men - such as fatigue, SOB, indigestion, and anxiety - acute myocardial infarction (MI) presents with sudden, severe, and crushing chest pain that may radiate to the arm, neck, jaw, or back. ----Other symptoms may include sweating, nausea, shortness of breath, and lightheadedness. ----The symptoms are not relieved by rest or nitroglycerin, and prompt medical attention is necessary. Pain described as a heaviness, pressure, tightness, burning, constriction, or crushing. General discomfort, weakenss, or SOB may be the only symptoms sometimes Woman may have SOB and fatigue People with diabetes may be asymptomatic due to cardiac neuropathy, or they may have atypical symptoms like dyspnea Older adults may have alterations to their mental status, like confusion, or may have SOB, pulmonary edema, dizziness, or dysrhythmias Sympathetic nervous system stimulation - skin can be cool and clammy Cardiovascular symptoms - elevated BP and HR initially, when MI is prolonged may see a decrease in BP because of lowered CO Nausea and vomiting Fever

Use laboratory data and clinical manifestations to determine the effectiveness of therapy for shock.

----The patients begin to manifest the signs of poor perfusion, including cool skin, cool extremities, and delayed capillary refill (cold shock). In sepsis, symptoms may include decreased urine output and cyanosis (blueish discoloration of the lips and/or digits). ----Improvement of signs of perfusion ----Increased urine output ----Decreased WBC ----Conventional parameters such as restoration of normal blood pressure are not adequate to gauge the extent of shock or the success of resuscitation strategies. ----The initiation of compensatory mechanisms in the second stage of shock may temporarily restore homeostasis without fully repaying the oxygen debt, allowing continuing hypoperfusion at the tissue level. ----Physical assessment parameters to assess perfusion at the tissue level, such as level of consciousness, urine output, respiratory status, pulse quality, skin color and/or mottling, and temperature, are important to monitor. ----Hemodynamic monitoring and laboratory analyses of endpoints, such as lactate, base deficit, venous oxygen saturation, and blood gas analysis, are also essential parameters to consider when evaluating the extent of shock and success of resuscitation.

How would a patient with a hip fracture present in the ED?

----Top ten impairments for disability in people 50 and above ----Increase due to living longer ----90% result from a simple fall ----Consequences: loss of life, impaired functioning and quality of life ----Morbidity associated with DVT's, muscular deconditioning, post operative infection, pain, and loss of mobility They could present in the ED w: ----Inability to move immediately after a fall ----Severe pain in your hip or groin ----Inability to put weight on your leg on the side of your injured hip ----Stiffness, bruising and swelling in and around your hip area ----Shorter leg on the side of your injured hip ----Turning outward of your leg on the side of your injured hip Bucks traction, surgery, and positioning every 2 hours to avoid injured side are all interventions

Explain the causes, pathophysiology, and manifestations of acute glomerulonephritis.

-Glomerulonephritis is a group of diseases that injure the part of the kidney that filters blood (called glomeruli), kidneys cannot filter as well. -Predominantly affects children from ages 2 to 12 -Incubation period is 2 to 3 weeks Assessment: -Ask about health problems, including systemic diseases, kidney or urologic disorders, infectious diseases. -Identify the patient's voiding pattern. Ask whether the frequency of urine elimination has increased or the quantity of urine has decreased. -Ask about changes in urine color, odor, or clarity and whether dysuria or incontinence has occurred. Nocturia is a common manifestation Etiology: -Infectious -Streptococcal (assess for sore throat) -Non-Streptococcal post-infectious glomerulonephritis —Bacterial —Viral —Parasitic S/S: -Hematuria: dark brown or smoky urine -Oliguria: urine output is < 400 ml/day -Edema: starts in the eyelids and face then the lower and upper limbs then becomes generalized; may be migratory -Hypertension: usually mild to moderate -Proteinuria: protein in the urine

Define the principles of traction.

1. Free hanging weight 2. Splints and slings must be suspended without interference 3. Counter traction 4. Must be in opposite direction (the counter weight) 5. Rope must hang free 6. Precise amount of weight must be applied 7. pulling effect Skeletal traction - pins, tongs, screws, wire, hardware that are secured to the bone (most invasive traction) Skin traction - uses a harness or boot to secure extremity with 5 or 10 pound weight (least invasive) - preferred ---Bucks traction is common example ---Nurses should not mess with the weights in traction

What are the nursing priorities when administering a blood transfusion?

1. Nurse must knowledgeable of time limit placed on blood products outside of storage 2. Patient consent and an order for the administration of blood products need to be confirmed before the blood components is obtained from laboratory ----- The order should contain the type of blood component to be administered, the number of units or volume of the blood components to be infused, the flow rate or durations of the infusion, and other parameters for infusions 3. The nurse needs to condoms adequate IV access and that all supplies and equipment needed for the transfusion are available prior to the blood component being released from the lab 4. Once the component is obtained from lab then there needs to be verifications performed by two licensed staff members which includes matching the blood product to the order and matching the patients to the blood product, the ABO and Rh also needs to be confirmed 5. Expiration date, time the component was released from the lab and the date need to be confirmed 6. Then immediately before starting the blood transfusion a patient assessment needs to be performed (baseline vitals, and resp) 7. Then explain the procedure and confirm patient understanding and clinical manifestations to report Nursing priorities when administering a blood transfusion include ensuring that the correct blood product is selected and matched to the patient, monitoring vital signs and symptoms for any adverse reactions or transfusion-related complications, and maintaining the patency and integrity of the IV line.

Explain the role of the systemic inflammatory response syndrome (SIRS) in the manifestations and progression of sepsis and septic shock.

2 or more of the following abnormalities ----Temp ----HR ----RR ----WBC count Systemic Inflammatory Response Syndrome Identical to sepsis but without infection Noninfectious process as a cause Pancreatitis Autoimmune disease Vasculitis Thromboembolism Burns Surgery/trauma Pulmonary contusion

Hypomagnesemia

< 1.6 Caused by/pts at risk Malnutrition Excessive excretion of magnesium via the renal system May be present in pts with hypokalemia and hypocalcemia Chronic alcohol abuse Diarrhea Dehydration Laxative abuse S/s Primarily neuromuscular - HYPERACTIVE Weakness Cramping/tetany/tremors Hyperreflexia Chvostek's and Trousseau's Disorientation (could be psychosis) Vertigo Hypertension and tachycardia PVCs Seizures Tx Dietary increase in intake (whole grains, green leafy vegetables) Magnesium oxide or magnesium gluconate supplements ----May get magnesium sulfate IV in unable to tolerate PO intake - monitor for hypotension, rate/rhythm changes, and respiratory depression Cardiac monitoring Seizure and fall precautions

Hypermagnesemia

> 2.2 Caused by/pts at risk Over-replacement of magnesium Renal insufficiency/failure Lithium toxicity increases risk of developing (decreases renal excretion of magnesium) Rhabdomyolysis Burns and trauma Sepsis Tissue lysis syndrome Hypomotility in GI tract (narcotics, anticholinergics, chronic constipation, bowel obstruction) S/s Hypotension (d/t vasodilation) Bradycardia, A fib, widened QRS complex Drowsiness/lethargy → coma Weakness Hyporeflexia Paralysis Decreased respiratory rate Decreased platelet clumping (d/t delayed formation of thrombin) Tx Dependent on cause GI hypomotility → cathartics and enemas Cessation of Mg supplements Treat dysrhythmias Airway support Correction of hypotension with fluids Hemodialysis may be needed Calcium gluconate - antagonize the neuromuscular and cardiovascular effects Monitor vital signs and neuro assessment Education r/t magnesium-containing laxatives and antacids

How do you determine if a stroke is ischemic or hemorrhagic?

A brain CT scan can show if there is bleeding in the brain or damage to the brain cells from a stroke. Magnetic resonance imaging (MRI) uses magnets and radio waves to create pictures of your brain. An MRI may be used instead of—or in addition to—a CT scan to diagnose a stroke. If there is no ischemia at the time of MIR it was a TIA if there was ischemia it was a stroke Ischemic stroke will show normal on ct for the first 6 hours Hemorrhagic stroke will show white on the ct scan Ischemic stroke: Thrombosis: it all begins with a clot Damage to endothelial lining of the vessel Thrombolic- Think blood clot at the site caused by atherosclertic plaques ----Embolism: a clot on the move Embolic - Debris or clot originating from elsewhere in the body. Atherosclerosis - Most common embolus is plaque Chronic atrial fibrillation Mechanical prosthetic heart valves Bacterial and nonbacterial endocarditis can be source ----Presentation: Hemiparesis Loss of speech Hemisensory loss Slower onset, thrombosis as clot grows, common when sleeping Abrupt, embolus occurs suddenly and without warning Hemorrhagic stroke: Hemorrhage: blood where it isn't supposed to be Bleeding into brain tissue Rupture of "stressed" cerebral vessel Rupture of aneurysm or vascular malformation HTN primary cause High mortality, slowest recovery Outcome depends on volume of bleed -Presentation: ----Occur rapidly, usually during waking hours ----Severe headache, nuchal rigidity, Kernig sign, vertigo, syncope, epistaxis

Evaluate patient risk for acute kidney injury

AKI is the loss of kidney function affects the ability to maintain normal processes of urinary elimination, fluid and electrolyte balance, and acid-base balance The causes of AKI are reduced perfusion to the kidneys, damage to kidney tissue, and obstruction. Types --Prerenal --Intrarenal --Postrenal Other Causes --Hypovolemic shock --Heart failure earlier you catch it the less damage there is 1. AKI can be readily identified by close monitoring of routine serum creatinine, BUN and urine output results 2. AKI can be prevented by early recognition and treatment of the underlying cause, for example: -Early treatment of infections/sepsis -Early treatment/prevention of dehydration -Correcting hypovolaemia 3. AKI can also be prevented by: -Monitoring use of drugs such as NSAIDs and ACE inhibitors, especially if a patient is acutely unwell -Taking care with at-risk patients who need iodinated contrast agents with scans BUN: Blood Urea Nitrogen ( 10-20 mg/dL ) -Reflects excretion of " UREA " -Urea is an end product of protein metabolism -Is affected by volume status & protein intake -Rises when GFR decreases below 40-60% Creatinine: ( 0.6-1.2 mg/ dL ) -Product of muscle metabolism -Not affected by fluid status or diet creatinine is more specific to the kidneys than BUN Increased creatinine decreased kidney functions so higher potassium ---potassium will be higher Less than 400 ml of urine in 24 hours = scant urine output decrease the use of diuretics

What are the medication therapies associated with HIV/AIDS?

ART (Antiretroviral Therapy) Highly Active Antiretroviral Therapy (HAART) Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)- stall reproduction of HIV. They force the virus to use faulty versions of building blocks. alters DNA to make copies of cells Non-nucleoside RT inhibitors (NNRTIs)- bind to the RT protein. This disables it, preventing HIV from making copies of itself. Protease inhibitors (PI)- interfere with an enzyme that HIV uses to create infectious viral particles. Fusion inhibitors- help block HIV's entry into healthy cells. Entry inhibitors- help block HIV's entry into healthy cells. Integrase inhibitors- block insertion of viral DNA into the host cell DNA. HIV is very resistant to meds which is why it needs a multidrug regimen One type ... eventually becomes resistant... and more aggressive Focus on supportive measures Drug therapy Respiratory support and maintenance Comfort Rest and activity changes

Interpret common assessment findings associated with acute and chronic pancreatitis.

Acute • Low-grade fever • Leukocytosis • Hypotension - due to fluid loss from vomitting • Tachycardia • Jaundice • Flushing • Cyanosis • Edema • Nausea • Vomiting hiccups that don't resolve abdominal bloating guarding w pain, rebound tenderness ​​Abdominal pain Left UQ, radiates to back Mid-epigastric region Sudden onset Severe, deep, piercing, steady Aggravated by eating Not relieved by vomiting Chronic • Abdominal pain •Malabsorption with weight loss • Constipation • Mild jaundice with dark urine • Steatorrhea - fatty stools • Diabetes mellitus - might develop type 2 diabetes from chronic pancreatitis

What is the nurse's priority in assessing an extremity after a trauma?

Assessment, inspection, and palpation ----Note the 5 Ps - Pain, pulselessness, parasthesia, pallor, paralysis ----If one or more of the "Ps" are present it could mean there is neurovascular damage which could lead to compartment syndrome, hemmorhage, or infection. Look at patient's vital signs and frequently assess location of injury if one is present Run lab tests for things such as ----myoglobin because if this is present it could be indicative of rhabdomylysis ----CBC and metabolic panel - monitor for signs of blood loss ----Electrolytes - electrolytes imbalance could also lead to rhabdomylysis ----Assess urine - if tea colored = rhabdomylysis Intake and output ----it is important to monitor for ss of hypovolemic shock, decreased amounts of urine could indicate this ----It is also important to encourage fluids to the kidneys can be adequately flushed which prevents rhabdomylysis Administer analgesia, antibiotics, and anticoagulants as ordered Wound care/pin care/traction/splinting/immobilization RICE extremity ----Elevate above heart level UNLESS it is compartment syndrome, do not ice or elevate for compartment syndrome ROM and ambulation exercises Maintain pulmonary hygiene

Define basilar skull fracture and the main complication associated with skull fracture?

Basilar skull fracture - fracture at the base of the skull, involves bony structures at the level of the mid face Hemotympanum - presence of blood in the middle ear cavity and to ecchymosis of the tympanic membrane Battle's Sign - bruising over the mastoid process Raccoon Eyes - dark circles under the eyes, late sign of basilar fracture Rhinorrhea - Excess drainage, ranging from a clear fluid to thick mucus, from the nose and nasal passages Otorrhea - drainage of liquid from the ear - fluid from ear is hallmark sign that dura has been breached

Describe the characteristics of infected burn wounds and how to prevent it (Hint: using PPE).

Because the skin is a barrier against infection, patients with burn injuries are immune-compromised. It is important for the nurse to implement: Contact precautions Disposable equipment (such as blood pressure cuffs, stethoscopes, ecg leads) Antibiotic-coated urinary and central line catheters. Proper hand washing Prophylactic widespread antibiotics are not recommended because of the risk of antibiotic-resistant pathogens. Instead, antibiotics are given based on positive cultures

Nursing actions before starting blood transfusion.

Before transfusing blood, the nurse should perform a patient assessment, including taking a history of any past transfusion reactions, verifying the patient's identity, checking the blood product for compatibility, and ensuring the proper administration technique. The nurse should also monitor the patient for any adverse reactions during the transfusion. Vital signs should be assessed before, 15 minutes after start, and at the end for the bare minimum. watch for transfusion reactions Febrile - after multiple transfusions -Chills, tachycardia, fever, hypotension, tachypnea Hemolytic - ABO incompatibility -Fever and chills -Apprehension, headache -Chest pain, low back pain -Tachycardia, tachypnea, hypotension -Sense of impending doom

Explain brain herniation. What are the S/S?

Brain herniation: if increased ICP is left untreated, it can lead to cerebral herniation, which is the protrusion of a portion of the brain through an abnormal opening ----Emergency! ----Brain moves from area of high pressure to low pressure s/s: decreased LOC ----Sensorimotor: withdrawing, posturing, flaccidity, abnormal posturing ----Respiratory: cheyne stokes, central neurogenic hyperventilation, apneustic, cluster breathing ----Reflex testing: absent doll's eyes, ice water caloric test ----Status epilepticus: seizure activity of 30 minutes or more. Usually no return to consciousness. Supratentorial Herniation: ----Cingulate herniation Usually not life threatening Lateral shift or tissue, compressing the frontal lobes of the cerebrum ----Central or Transtentorial Herniation Downward shift of one or both cerebral hemisphere ----Uncal or Lateral Transtentorial Herniation Most common Usually in the temporal area ----Transclavarial Herniation Frequently occurs after a skull trauma or penetrating head injury with a fractured skull Protrusion of brain tissue through the cranium Infratentorial herniation: Tonsillar or downward cerebral herniation ----Downward shift through the foramen magnum ----Compresses the medullary and upper portion of the spinal cord ----Nuchal rigidity ----Ataxic respirations ----Eventual cardiac arrest due to brainstem compression Upward transtentorial herniation ----Nuchal rigidity ----Compression of CN III ----Obstruction of csf flow ----Distortion of third ventricle

Distinguish between CAP and HAP and risk factors for each:

CAP = community acquired pneumonia, pneumonia occurs in individuals who have not recently been hospitalized or are living outside of a healthcare/long-term care facility. ---Streptococcus pneumoniae is the most common causative organism ---Risk factors for CAP include age over 65, chronic lung disease, smoking, and weakened immune system. HAP = hospital acquired pneumonia, pneumonia develops in pts after 48 - 72 hours of admission ---Risk factors for HAP include mechanical ventilation, prolonged hospitalization, immune suppression, and invasive procedures.

Identify pathophysiology of COPD and Asthma

COPD Patho: •Includes: •Emphysema •Chronic bronchitis •Characterized by bronchospasm and dyspnea •Tissue damage not reversible; increases in severity, eventually leads to respiratory failure Approximately 80% to 90% of COPD deaths are caused by smoking. Asthma Patho: occurs intermittently due to inflammation of airway hyperresponsiveness leading to bronchoconstriction. This causes intermittent and reversible airflow obstruction affecting airways only, not alveoli. •Occurs in two ways: 1. Inflammation 2. Airway hyperresponsiveness leading to bronchoconstriction Status Asthmaticus: severe, life-threatening, acute episode of airway obstruction. It intensifies and does not respond to common therapy --give epi Asthma Attack: 1. Exposure to trigger 2. IgE antibodies bind to receptors on mast cells, causing degranulation and the release of inflammatory mediators, such as histamine and leukotrienes 3. Vasodilation and increased capillary permeability. 4. Edema of the airways and an increase in basophils, eosinophils, and neutrophils, which stimulate the production of mucus. 5. Mucus causes a thickening of the airways and bronchial hyperresponsiveness. 6. The release of histamine also causes constriction and spasm of the smooth muscles surrounding the bronchial tubes, causing bronchospasm of the bronchial tubes. 7. The bronchospasms cause further narrowing of the airways. 8. The bronchospasms, mucus production, and edema produce obstruction to the flow of air into and out of the lungs.

Identify risk factors and care of pts with COPD

COPD Risk Factors: - Women, caucasian, former smokers, history of asthma, live in the southwest or midwest, american indians, and alaskan natives Signs and Symptoms of COPD: Pink puffer - emphysema: red complexion, barrel chest, tripod position, "puffing" when breathing Blue Bloater - bronchitis: obese, cough, excess mucus, cyanotic, rhonchi, wheezing Signs of COPD Decompensation: hypoxemia, acidosis, resp infections, right sided heart failure, dysthymias. - Spontaneous pneumothorax: small collection of air between lung and outer surface - Cor pulmonale: ventricular enlargement Signs of COPD Exacerbation: Increase cough Increase shortness of breath Increase sputum COPD Treatments: - Beta-adrenergic agents - albuterol - Cholinergic antagonists - pressair, tudorza - Methylxanthines - theophylline - Corticosteroids - Pulmicort - NSAIDs - Mucolytics - Mucinex - Lung reduction surgery: considered in severe copd patients. Removes damaged lung tissue; improvement of respiratory muscle strength and mechanics - VATS: video assisted thoracic surgery - removal of diseased lung and lymph nodes oBullectomy and pneumothorax

Explain the cardiac blood flow and electrical system

Cardiac Blood Flow - Deoxygenated blood enters through the superior and inferior vena cavas into the right atrium. Blood travels through the tricuspid valve into the Right Ventricle. Blood is then pushed through the pulmonic valve into the pulmonary arteries and into the lungs. Oxygenated blood is then returned to the heart through the pulmonary veins and empty into the Left Atrium. Blood is then moved through the Mitral valve into the Left Ventricle. Then blood is pumped up and out of the heart through the aortic valve into the aorta and into the body. Electrical system- Electrical impulse travels from SA node (through L and R atria causing them to contract)→ AV node→ Bundle of His → Bundle Branches (in between the ventricles)→ Purkinje Fibers (outside the ventricles) → throughout the L and R ventricles expelling their blood into the rest of the body via the aorta

•Obstructive:

Cardiac function decreased by noncardiac factor (indirect pump failure). Total body fluid is not affected although central volume is decreased. ----Examples: Cardiac tamponade, Arterial stenosis, Pulmonary embolus - also severe bowel disease •Occurs when there is an Impaired ability of normal heart muscle to pump effectively •Generally caused by conditions outside the heart that prevent either adequate filling of heart or adequate contraction of healthy heart muscle •When blood in the interstitial tissue, these fluids are stagnant and cannot deliver oxygen or remove tissue waste products •Cardiac Tamponade is the most common cause for obstructive shock ---- pericardiocentesis to drain fluid could be caused by pulmomary embolism, administer thrombolytics if so Obstructive shock is caused by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload), causing decreased cardiac output. Examples of disorders resulting in impaired filling include cardiac tamponade and tension pneumothorax. An example of a disorder resulting in increased afterload is severe valvular disease.

What is the nurse's understanding and role in cardioversion and defibrillation?

Cardioversion is a procedure used to convert an irregular heart rhythm, such as atrial fibrillation, to a normal sinus rhythm using a low-energy shock. Defibrillation is a procedure used to terminate a life-threatening arrhythmia, such as ventricular fibrillation or pulseless ventricular tachycardia, using a high-energy shock. The nurse's role in cardioversion and defibrillation - preparing the patient for the procedure - ensuring proper sedation and pain management - applying the electrodes or paddles to the patient's chest - monitoring the patient's response to the procedure.

Compartment syndrome and how to asses for compartment syndrome.

Compartments are areas in the body in which muscles, blood vessels, and nerves are contained within fascia. Most compartments are located in the extremities. Acute compartment syndrome (ACS) is a serious condition in which increased pressure within one or more compartments reduces circulation to the area. Causes include: Decreased compartment size for example : dressings, casts, traction happens w rigid immobilization like a cast Increased compartment contents for example bleeding, edema, IV infiltration, snakebite Physical Exam Pain when the area is squeezed Extreme pain when you move the affected area (for example, a person with compartment syndrome in the foot or lower leg will have severe pain when moving the toes up and down) Swelling in the area To confirm the diagnosis, the doctor or nurse may need to directly measure the pressure in the compartment. This is done using a needle attached to a pressure meter, which is placed into the body area. The test must be done during and after an activity that causes pain. You can measure pressure with a striker device, normal pressure is 0-10mmHg Assessment Findings Ischemia occurs within 4 - 8 hours Paresthesia Pain not relieved by narcotics Pressure increases in compartment Positive Homan's sign (sign of deep vein thrombosis (DVT)) Pallor, coolness , loss of normal color Diminished or absent distal pulses Myoglobinemia - dark reddish brown urine can lead to AKI, which is caused by rhabdomylysis Collaborative Care Early diagnosis needed DO not elevate extremity.... Why ? Want to maintain arterial pressure and elevating it above heart level will cause more ischemia DO not apply ice....Why ? Vasoconstriction - do not want to decreae tissue perfusion Loosen bandages - bivalve cast Fasciotomy - surgery decompression

Plan prevention strategies for the complications of PD.

Complications of Peritoneal Dialysis •Peritonitis - could see cloudy fluid/pus in dialysis bag ---can treat w IV antibiotics •Pain •Exit site/tunnel infections infection = number one complication •Poor dialysate flow •Dialysate leakage •Other complications •hernia Nursing Care for Peritoneal Dialysis •Before treatment: Evaluate baseline vital signs, weight, laboratory tests •Continually monitor patient for respiratory distress, pain, discomfort •Monitor prescribed dwell time, initiate outflow •Observe outflow amount and pattern of fluid

Analyze the cardiac markers used to aid in diagnosis of an MI

Creatinine kinase - rise about 6 hours after MI, peak 18 hours after, and return to normal 24-36 hours after - These enzymes are fractionated into bands - CK-MB band is specific to myocardial cells and help to assess damage ****Troponin (THIS IS TEST OF CHOICE) - a myocardial muscle protein that is released into circulation after myocardial injury (levels rise with amount of injury) - There is troponin I and troponin T - they are highly specific indicators of MI. they increase 4-6 hours after MI, peak 10-24 hours after, and eventually return to baseline after 10-14 days Myoglobin - released into circulation 2 hours after MI and peaks 3-15 hours after - This is one of the first markers to appear after an MI, but it is not as specific as troponin - The kidneys extrete this rapidly in urine, and it returns back to normal after about 24 hours These markers are usually tested in a series of blood draws over several hours to help confirm the diagnosis of an MI.

Define cushing's triad

Cushing's triad: a late sign of increased intracranial pressure 1. Widened pulse pressure (180/50) Elevated systolic blood pressure 2. irregular respirations 3. Bradycardia **increased icp affecting the brainstem will reflect respiratory changes

How does the RN know what to delegate?

Delegation - transferring a task/activity to unlicensed assertive personnel (UAP) The nurse is accountable for the task and activity that is delegated Rules can vary from state to state 5 Rights of Delegation TPCCS 1. Right task - is it in the UAPs job description, policies, or procedures according to the nurse practice act 2. Right circumstances - patient needs to be stable 3. Right person - person you delegate to must have knowledge skills and abilities to do tasks 4. Right communication - person you delegate to should be asking you clarifying questions, they should understand the task at hand and not modify anything 5. Right supervision - delegation must be within your scope of practice, you must monitor activity and follow-up to ensure the activity is completed. the person you delegate to should communicate any significant patient information that occurred while giving that task, such as pain being reported. you must also ensure that you document this appropriately They should delegate things with predictable outcomes, and should consider patient safety Do delegate Turning, positioning, vitals, intake, output, feeding, ambulation, oral suctioning, etc Things that do not vary depending on patients needs - stuff that is pretty much the same for everyone/follow a sequence of steps Dont delegate Tasks that involve ongoing assessment, interpretation, or decision making -------LPNs can do ongoing assessments, UAPs cannot Any admission assessments, irrigations of NG tubes, hanging blood transfusions, etc

Address the nursing care priorities for patients with Diabetes, including DKA

Diabetes Monitor blood glucose levels regularly. Administer insulin as ordered. Encourage a healthy diet and exercise. Educate the patient on self-monitoring and management of their disease. Type 1 - insulin dependent ----Polyuria, polydipsia, polyphagia Type 2 - insulin resistance to insulin deficiency Microvascular complications Eye blood vessels - retinopathy, cataracts, glaucoma Nephropathy Peripheral neuropathy - foot wounds go unnoticed Macrovascular complications Increased risk of stroke High blood pressure Increased risk of CAD DKA Type 1 Rapid onset Glucose ~250+ Body can't produce enough/doesn't receive enough insulin Begins to breakdown fat as fuel instead Causes a buildup of acids (ketones) S/s Weight loss Confusion Abdominal pain Shock Dehydration Coma Fruity breath Kussmaul respirations Treatment Correction of electrolyte imbalances Specifically, hypokalemia BEFORE insulin admin Insulin IV Isotonic fluids Monitor acid-base imbalance Monitor for signs of cerebral edema and hypoglycemia

Discuss the mechanisms of peritoneal dialysis (PD) as renal replacement therapies.

During peritoneal dialysis, a cleansing fluid flows through a tube (catheter) into part of your abdomen. The lining of your abdomen (peritoneum) acts as a filter and removes waste products from your blood. After a set period of time, the fluid with the filtered waste products flows out of your abdomen and is discarded. •Involves siliconized rubber catheter placed into abdominal cavity for infusion of dialysate •Types •Continuous ambulatory (CAPD) •Automated •Intermittent •Continuous-cycle •Peritoneal dialysis exchange for control of fluids, electrolytes, nitrogenous wastes, blood pressure, and acid-base balance. Automated Peritoneal Dialysis - cyclar, multiple over night exchanges tailored to patients needs ----maybe 30 min cycles over night - leaves them dialysis free during the day ----3 phases complications: •Peritonitis - could see cloudy fluid/pus in dialysis bag ---can treat w IV antibiotics •Pain •Exit site/tunnel infections infection = number one complication •Poor dialysate flow •Dialysate leakage •Other complications •hernia Nursing Care •Before treatment: Evaluate baseline vital signs, weight, laboratory tests •Continually monitor patient for respiratory distress, pain, discomfort •Monitor prescribed dwell time, initiate outflow •Observe outflow amount and pattern of fluid

Explain the teaching a nurse does with a patient with low platelets.

Educate patient to avoid NSAIDs ----NSAIDs such as ibuprofen and aspirin can increase the risk of bleeding and should be avoided. If pain relief is necessary, recommend acetaminophen or non-pharmacological alternatives. Initiate bleeding precautions; use only electric razors, limit needlesticks, use soft toothbrush, provide safety devices to prevent injury (non-skid shoes/socks, etc.) Decreased platelet counts do not always indicate bleeding, but may lead to excessive bleeding if injury occurs. Nutrition and lifestyle education: Avoid activities that could cause injury (contact sports, martial arts, etc) Limit or avoid alcohol Avoid NSAIDs Increase intake of leafy greens

Differentiate between an epidural bleed and a subdural bleed

Epidural hematoma: bleed that develops between the dura of the skill that is mainly caused by a tear in the middle meningeal artery Talk & die syndrome because patients may be lucid, rapidly deteriorate, and die. Brain can compensate for a short time. Go to OR immediately to relieve pressure Subdural Hematoma: a venous bleed. Common in old people Might need to just let blood reabsorb

Explain the nursing care required of a patient with an external fixation device.

External fixation - rods and pins to area surrounding the fracture which makes a frame around the fracture for extensive soft tissue damage ----Surgeon must be able to cut them open in order to visualize the fracture ----The fracture is then realigned and secured w rods and screws and such ----For an external fixation - the rods and pins form an external frame outside the body which is utilized specifically when there is extensive soft tissue damage at the site of the fracture Care of a Patient with external fixation: ----Administer analgesics, antibiotics, anticoagulants ----RICE ----Wound care/pin care and checks Watch for ss of infection or inflammation - in the first 48-72 hours clear drainage is expected. The site should be assessed every 8-12 hours and if there is drainage, odor, color, or redness it could indicate infection which could lead to osteomylitis = bad ----ROM exercises ----Neuro assessment ----Pulmonary assessment ----Assess for complications

•Distributive :

Fluid shifted from central vascular space (total body fluid volume normal or increased). --due to massive vasodilation ---Examples : Neural induced (neurogenic shock, Pain, stress). Chemical induced (Anaphylaxis, Burns) •Blood volume distributed to interstitial tissues where it cannot circulate, deliver oxygen •Caused by loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, capillary leak •Neural-induced distributive shock ---- neuro induced could be from spinal cord injury --- neurogenic shock is the least common type of shock - ss are tachycardia, orthostatic hypotension, differentiating factor is PT MAY HAVE WARM DRY SKIN AND FLUSHED APPEARANCE RT VASODILATION •Chemical-induced distributive shock ----anaphylaxis is an example Chemical-Induced Distributive Shock •Anaphylaxis •Sepsis: Sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammatory responses throughout the body. This inflammation can trigger a cascade of changes that can damage multiple organ systems, causing them to fail. •Capillary leak syndrome: is the response of capillaries to the presence of body chemicals that enlarge capillary pores and allow fluid to shift from the capillaries into the interstitial tissues. anaphylaxis and sepsis are the two most common Distributive shock is the result of disease states such as sepsis, anaphylaxis, or neurogenic shock that cause poor vascular tone and vasodilation, resulting in increased vascular capacity and venous pooling. In this form of shock, a state of relative hypovolemia exists due to vasodilation without a concurrent increase in volume. Venous pooling results, causing a decreased venous return to the right heart.

The indication for using some medications, such as, heparin in treating NSTEMI

Heparin is used in treating NSTEMI to prevent blood clot formation in the coronary arteries, which can lead to a heart attack. Heparin works by preventing the formation of blood clots by inhibiting the activity of clotting factors.

Describe complications to body systems after a severe burn injury.

Infections - sepsis Wound infection Endocrine: increase blood glucose levels Increase insulin production Musculoskeletal: Decreased ROM contractures Gastrointestinal: Paralytic ileus Constipation Curlings Cardiac Dysrhythmias Respiratory Intubation ARDS Pulmonary edema Pneumonia Nephrology Kidney damage Shock hypovolemia

What factors influence ICP and what are the main signs and symptoms for increased ICP?

Intracranial volume → Monroe-Kellie Doctrine (explained below) Many conditions impact (increase) ICP Severe head injury Intraventricular hemorrhage Subdural hematoma Meningitis Hydrocephalus Encephalitis Brain tumor Aneurysm rupture Hypertensive brain hemorrhage Subarachnoid hemorrhage Status epilepticus Stroke Main signs and symptoms DECREASED LEVEL OF CONSCIOUSNESS ----Want to go beyond person, place, and time to determine baseline ----Establish specifics of place or location & specifics about pts current state/situation Sluggish pupils Early Blurred vision Diplopia Restlessness Headache Decreased orientation DECREASING GCS Decreased visual acuity Personality changes Vomiting Slurred/slow speech Decreased sensation Decreased grasps Later FURTHER DECREASE IN GCS CUSHING'S TRIAD 1. Wide pulse pressure (Hypertension) 2. Bradycardia 3. irregular respirations Posturing (decorticate or decerebrate) Absent speech Positive Babinski (fanning out) Loss of corneal and gag reflexes Fixed and dilated pupil(s)

What symptoms do you expect to see when a pt. has a stroke?

Ischemic stroke: Hemiparesis Loss of speech Hemisensory loss Slower onset, thrombosis as clot grows, common when sleeping Abrupt, embolus occurs suddenly and without warning Hemorrhagic stroke: Occur rapidly, usually during waking hours Severe headache, nuchal rigidity, Kernig sign, vertigo, syncope, epistaxis Sudden numbness/weakness of the face, arm, leg, especially on one side of your body Sudden confusion, trouble speaking or understanding Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance

Rule of nines

Lund-browder chart: more accurate, but takes a more in-depth assessment Rule of nines: consider accurate for initial assessment of adult patients

What assessment tool is used to help diagnosis a stroke?

MRI- used to confirm type of stroke CT- done first because it is quicker and can tell which type of stroke Visual assessment The National Institutes of Health Stroke Scale (NIHSS) is a valuable tool for both initial assessments of stroke severity and ongoing assessment to monitor for actionable changes in patient condition. ----This stroke scale may be used to identify the likelihood of a stroke, and can also estimate severity.

septic shock treatment

Manage Airway and correct Hypoxemia; Fluid resuscitation, Vasopressors, Treat infection w antibiotics epi and norepinephrine

What is autonomic Dyseflexia? What are the symptoms? Nursing priorities?

Massive uncompensated cardiovascular reaction mediated by sympathetic nervous system Occurs if reflexes return after spinal shock and injury level is T6 or above Most common precipitating factor - distended bladder or rectum ----A strong sensory input precipitates ----Causes widespread vasoconstriction Manifestations Hypertension Piloerection Blurred vision Flushing of skin above injury Throbbing headache (need to take BP) Spots in vision Diaphoresis above level of injury Nasal congestion Bradycardia Nausea Anxiety Nursing Care: ----Elevate HOB at least 45 degrees or sit patient upright ----Notify physician ----Determine cause ----Immediate catheterization ----Patient and family education about causes and symptoms Neurogenic bladder - any type of bladder dysfunction related to abnormal/absent bladder innervation ----Commonly experience urgency, frequency, and incontinence

Metabolic acidosis

Numbers pH < 7.35 HCO3 < 22 Partially compensated: CO2 < 35 Caused by Accumulation of metabolic wastes/acids DKA Starvation Hyperkalemia S/s Tx IV Na bicarbonate Rapid-acting insulin Antidiarrheals Dialysis Mechanical ventilation Compensation: INCREASE in respiratory rate and depth (HYPERVENTILATION - blow off CO2)

Respiratory alkalosis

Numbers pH > 7.45 CO2 < 35 Partially compensated: HCO3 < 22 Caused by HYPERVENTILATION - blowing off all the CO2 Panic attacks S/s Tx Remove cause Reduce fever Address sepsis Oxygen Anxiolytic Compensation: DECREASE in hydrogen secretion and bicarbonate reabsorption

Metabolic alkalosis

Numbers pH > 7.45 HCO3 > 26 Partially compensated: CO2 > 45 Caused by Increased loss of acid - mainly via GI tract NG suctioning Vomiting Excessive diuresis Hypokalemia S/s Tx Discontinue: thiazide diuretics and/or NG suctioning Antiemetics Acetazolamide - increases CO2 levels Compensation: DECREASE in respiratory rate and depth (HYPOVENTILATION - retain more CO2)

Coordinate the nursing care for the patient experiencing any stage of hypovolemic shock.

Nursing Interventions Assessments Neurological status ----A decreased level of consciousness occurs as a result of decreased cardiac output and carotid vasoconstriction that occurs as a result of hyperventilation and respiratory alkalosis. Vital signs ----Blood pressure may remain normal initially because of the stimulation of compensatory mechanisms. Tachycardia will be present as one of the compensatory mechanisms. Hypotension and bradycardia signal the end of effective compensation. Hemodynamic readings ----Decreased cardiac output occurs as a result of decreased filling pressures, as evidenced by decreased CVP and decreased PAOP. Increased systemic vascular resistance is evident as the sympathetic nervous system is stimulated, resulting in vasoconstriction to increase blood pressure and cardiac output. Urine output ----Decreased urine output occurs as a result of decreased cardiac output and stimulation of compensatory mechanisms that increase reabsorption of sodium and water. Skin color and temperature ----Cold and clammy skin may be a sign of decreasing peripheral perfusion and progressing shock. Laboratory Tests ABGs ----Initial ABGs may reflect a respiratory alkalosis due to hyperventilation. Later stages of shock reveal a metabolic acidosis due to anaerobic metabolism. Venous oxygen saturation; SvO2/ScvO2 ----Decreased oxygen saturation is an indicator of inadequate oxygen delivery. Hemoglobin and hematocrit ----Hemoglobin and hematocrit values may be decreased if the cause of hypovolemic shock is bleeding. Metabolic profile ----Renal failure and liver failure, as evidenced by increased BUN and creatinine levels and liver function test results, may become evident as a result of decreased organ perfusion. Lactate/base deficit ----Increased lactate level and negative base deficit are evidence of poor perfusion at the cellular level. Decreasing lactate level is an endpoint demonstrating adequate resuscitation. Actions Apply a 100% nonrebreather mask. ----Maximizing oxygenation is the number one priority. Anticipate and prepare for intubation. ----Intubation and mechanical ventilation may be required to improve oxygenation. Insert large-bore IV lines for fluid administration. ----Large-bore IV lines facilitate the rapid infusion of fluid necessary to reverse hypovolemic shock. Administer fluid replacement as prescribed: Normal saline Lactated Ringer's solution Blood products ----Fluid replacement is the foundation of treatment in hypovolemic shock. Teaching Instruct patient and family on the cause of hypovolemia. Depending on the cause of hypovolemia, patient and family understanding may help prevent a repeat occurrence. • Allow family members visitation during hospital treatment; provide frequent updates on condition and treatment. Family visitation and information can help to decrease a patient's and family's anxiety.

Identify the nursing priorities with a patient with chest pain and/or MI

Nursing priorities with a patient with chest pain and/or MI include: - assessing the patient's pain and vital signs - providing oxygen - initiating cardiac monitoring - administering aspirin and nitroglycerin as prescribed - activating the rapid response team or calling a code if the patient is unstable . Other priorities include obtaining an electrocardiogram (ECG), drawing cardiac biomarkers, administering heparin or other anticoagulants, and preparing the patient for possible cardiac catheterization or other interventions.

Explain the function of pO2 levels in stable and unstable CODP pts.

Over-oxygenation of a patient with COPD can lead to oxygen induced hypoventilation This means that patients with COPD lose their drive to breathe due to over oxygenation and high PaO2. This can lead to: Low PaO2 is the primary drive for breathing Hypercarbia: retention of Co2 Co2 narcosis: loss of sensitivity to high levels of co2 Normal PO2 is 80-100 mm Hg. COPD causes respiratory acidosis and a decrease in PO2 <80

Explain the pathophys, causes, S/S, and treatment of Pulmonary Edema

Patho ---a condition caused by excess fluid in the lungs. This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe. ---Pulmonary edema is caused by an increase in the pressure within the blood vessels of the lungs, which can be due to several factors. ---This can be due to heart failure, where the heart is unable to pump blood effectively, causing fluid to back up into the lungs. ---It can also be caused by damage to the lung tissue itself, such as acute respiratory distress syndrome (ARDS), or by a blockage in the pulmonary vasculature, such as a pulmonary embolism. Causes: Pulmonary edema can be caused by a variety of factors: - heart failure - a complication of congestive heart failure - heart attack - valve disease - arrhythmias - hypertension - lung infections - pneumonia - exposure to high altitudes -inhalation of toxic substances. Signs and Symptoms: The symptoms of pulmonary edema can develop suddenly or gradually and can include : - shortness of breath - coughing - wheezing - rapid breathing - difficulty breathing when lying down - Sweating - pale or bluish skin - anxiety. Severe cases of pulmonary edema can cause frothy sputum, confusion, or even loss of consciousness. coughing up PINK SPUTUM the alveoli are occupied by this fluid and you have decreased gas exchange Management Assess for early signs (for example, crackles in bases) ---Dyspnea at rest, disorientation, confusion ---High Fowler's position ---Oxygen therapy ---Nitroglycerin ---Rapid-acting diuretics ---IV morphine sulfate ---Continual assessment medications to reduce the workload on the heart: o ACE inhibitors o beta-blockers o nitroglycerin. In severe cases, mechanical ventilation or even extracorporeal membrane oxygenation (ECMO) may be necessary to support the patient's breathing. It is also important to identify and treat the underlying cause of the pulmonary edema, such as heart failure or pneumonia. Close monitoring and management of the patient's vital signs, electrolyte levels, and fluid balance are crucial in the treatment of pulmonary edema

Identify patients at risk for acid base imbalance

People with the following are at risk for respiratory acidosis: chest deformities or injuries chronic lung and airway diseases overuse of sedatives obesity The following puts you at risk for respiratory alkalosis: lack of oxygen high altitude fever lung disease liver disease salicylate poisoning The following put you at risk for metabolic acidosis: prolonged exercise lack of oxygen certain medications, including salicylates low blood sugar, or hypoglycemia alcohol seizures liver failure cancer kidney disease severe dehydration poisoning from consuming too much aspirin, ethylene glycol, and methanol The following can put you at risk for metabolic alkalosis: Prolonged vomiting nasogastric suctioning renal excretion

What are important medications and nursing interventions for TBI

Positioning the head of the bed greater than 30 degrees with the patients head in midline, and avoiding sharp hip flexion Management of CSF leak: if clear fluid is draining from the ear or nose, it should not be stopped; it should be collected using loosely applied gauze Avoid nasogastric tube placement in patients with a known basilar skull fracture or in patients where the base of the skull has not been visualized on radiographic injury Initiate enteral nutrition Maintain normothermic temperature (antipyretics and cooling devices as ordered) Implement seizure precautions Ensure venous thromboembolism prophylaxis with sequential compression devices, graduated compression stockings, and subcutaneous injections of an anticoagulant as prescribed Specific teaching regarding the patient's injury, coma, and increased ICP Orientation to the patients ICU room and monitoring equipment Medications: Hyperosmolar agents to decrease fluid in the brain Dexamethasone Antibiotics Pain medications

What principles guide patient education when receiving radiation?

Provide accurate information to help patients cope Skin care needs during radiation therapy Do not remove temporary ink markings(tattoo) Avoid skin irritation Follow radiation-oncology department's policy for skin care product use Nutritional support Care for xerostomia (dry mouth) increase the risk for tooth decay Teach about risk for fractures (for bone exposed to radiation)

AFib

Rate: Ventricular rate variable, up to 200 bpm Rhythm: Irregular, QUIVER P waves: No p waves Presence of fibrillatory (F) waves PR Interval: Unable to measure QRS duration: 0.04-0.10 second and constant - normal Treatment - amiodarone (may cause liver and lung damage), calcium channel blockers (diltiazem), Beta blockers (metoprolol), cardiac glycoside (digoxin), anticoagulation therapy (heparin and warfarin - with warfarin monitor INR and PTT), prepare for synchronized cardioversion - administering anticoagulants as prescribed - can lead to clots -preparing to administer medications such as beta-blockers or calcium channel blockers to slow the ventricular response.

Identify the roles of the nurse in emergency preparedness and response.

Role in the ED --Trauma nurses treat patients in a state of emergency, and handle urgent situations where the cause of injury or disease isn't yet known. They can work in hospital emergency rooms and other chaotic environments, and often need to coordinate with doctors, family members and other nurses --Patients have variety of heath care needs --Cultural considerations --Care of patients with mental illness --Disposition and discharge needs --Case management --Patient/family teaching Role in disaster preparedness --Policy development prior to disaster situation --Meet patient needs in collaboration with medical command --Personal emergency preparedness plan --Personal readiness supplies or "go bag" --Creativity and flexibility are essential

Use laboratory data and clinical assessment to determine the effectiveness of therapy for kidney dysfunction.

Serum creatine = 0.6-1.2 (normal), increase in this occurs once 50% of the kidneys function has been lost BUN = 8-21 (normal), decreased BUN indicates severe liver damage, malnutrition, consumption of a low protein diet, or fluid volume excess// elevated BUN = not a dx of renal dysfunction but indicates a possibility BUN-Creatine ratio = used to assess if the cause of elevated BUN is renal or nonrenal, normal is 10:1 or 20:1 Uric acid = 3.5 - 8 is normal range, values greater than 12 are critical and need immediate intervention because it can cause renal damage Bicarbonate = 22-26 (normal), decrease in these levels indicates renal failure Electrolytes Bedside urine dipstick Urinalysis Culture and senstivity Composite urine collection Creatine clearance Urine cytology Bedside sonography X-ray Intravenous urography Renal ultrasound CT MRI Cystogrpahy and urethrography Arteriography Renography Renal biopsy Cystoscopy

What is Spinal Shock? What are the symptoms? Nursing priorities?

Spinal shock ----Complete but temporary loss/depression of all/most spinal reflexes and sensory, motor, and autonomic function below the level of injury ----Occurs immediately after injury Characterized by: ----Decreased reflexes ----Loss of sensation ----Flaccid paralysis below ----Impaired proprioception, anhidrosis (no sweating), paralytic ileus, urinary and fecal retention ----Can have hypotension due to loss of sympathetic tone ----Lasts days to months

Explain the difference between stable and unstable MI

Stable myocardial infarction (MI) refers to a heart attack that has occurred in the past and has resulted in scar tissue formation in the heart. The symptoms may have resolved, and the patient may not have any current symptoms, but there is a risk of developing another heart attack. stable angina--(more common) - attacks have a trigger (such as stress or exercise) and stop within a few minutes of resting, it is usually predictable and can mimic previous episodes of chest pain Unstable MI refers to a heart attack that is currently occurring or is about to occur, and the symptoms are severe and unstable unstable angina-(more serious) - attacks are more unpredictable (they may not have a trigger) and can continue despite resting, ST segment elevation or depression may occur Stable angina can turn into unstable angina if the pattern of chest pain changes, or if it is brought on by less activity than normal/becomes unpredictable

Identify different assessment tools that helps with diagnosing GI problems.

Standard imaging tests for gastric conditions include upper gastrointestinal series (UGI), ultrasounds, MRIs, CT scans and X-rays. For an even clearer picture of the gastrointestinal tract, a barium swallow or barium enema may be used in conjunction with an X-ray.

What are the characteristics of superior vena cava syndrome? Tumor lysis syndrome?

Superior Vena Cava Syndrome: compression of the superior vena cava by lymph nodes and tumors s/s: engorgement of collateral veins of the thorax, head and neck; dyspnea, facial and periorbital edema, seizures, headache. Tx: goal is to decrease the size of the tumor obstruction to relieve pressure. It is based on the cause and type of cancer Lung cancer: chemo and radiation Lymphoma: chemotherapy with thrombus, fibrinolytic therapy Tumor Lysis Syndrome: an oncological emergency that is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into systemic circulation. ----Can cause renal failure, hyperuricemia, hyperphosphatemia, hyperkalemia, and hypocalcemia Tx: hydration, decrease uric acid

Explain the nursing interventions to lower a pt's ICP

The immediate goal is to reduce the size of the brain HOB up to at least 30 degrees Neck in a neutral position and minimal hip flexion Maintain the pts airway Bladder distention and bowel constipation ----Foley insertion & stool softeners Monitor for SIADH and DI Fluid restriction Dressing care for catheter/drain CALM ENVIRONMENT Neuro checks and vitals q1-2h Electrolytes, BUN, Cre, ABGs Glasgow coma scale

AKI

The loss of kidney function affects the ability to maintain normal processes of urinary elimination, fluid and electrolyte balance, and acid-base balance The causes of AKI are reduced perfusion to the kidneys, damage to kidney tissue, and obstruction. Types --Prerenal --Intrarenal --Postrenal Other Causes --Hypovolemic shock --Heart failure earlier you catch it the less damage there is Pre-renal - •Any condition that reduces blood flow to the kidneys ( upstream ) •Cardiac failure •Decreased cardiac output •Hypovolemia •Burns, dehydration, trauma, shock, diuretic overuse •Peripheral vasodilation •Antihypertensive medications •Renal artery stenosis or embolism lack of perfusion anaphylaxis can cause pre-renal failure pre-renal can progress to intrarenal failure Intrarenal - •Filtering structures of the kidneys are damaged •Usually from " acute tubular necrosis " •Ischemic damage to tubular cells •Nephrotoxic substances •Gentamycin, NSAID, Lead, Analgesics, Diuretics •Rhabdomyolysis: breakdown of muscle Þ myoglobin or fat embolism •Caused by major trauma or systemic infections •Acute glomerularnephritis: inflammation of the nephrons damage to nephron compromises kidney function glomerulonephritis, pyelonephritis, and infection Postrenal - •Results from obstructed outflow •Urolithiasis •Bladder obstruction •Infection, tumor, obstructed Foley catheter (FC) •Ureteral obstruction •Blood clots, calculi, accidental ligation, edema •Urethral obstruction •Prostatic hyperplasia or tumor •Strictures of the urethra --BPH - benign prosthetic hypertrophy Prostate cancer = cause can be stone or congenital narrowing etc PATHO •initiating phase - symptom onset •Oliguric Phase: less than 400mL / 24 hours •At risk for fluid volume excess •Azotemia: elevated BUN, Creatinine and Uric Acid •decreased level of consciousness •Electrolyte imbalance: hyperkalemia •Renal cells can regenerate if etiology is treated •Diuretic Phase: those who recover renal function •gradual increase in urine output •tubular transport is still hindered...urine is dilute •high urinary outputs places pt at risk for dehydration --lasts 1-3 weeks •Recovery Phase: gradual return to normal function •3 to 12 months or longer for recovery

How would you determine if drainage is CSF?

The most common symptom of a spinal CSF leak is a headache, while a cranial CSF leak causes symptoms such as clear fluid leaking from the nose or ear. test for BETA 2 TRANSFERRIN Some CSF leaks may heal with conservative treatments such as bed rest. Many CSF leaks need a blood patch to cover the hole or surgery to repair the leak. The nose and ear should not be packed if CSF leakage is suspected. --If the drainage contains blood, look for the halo sign: a ring formed when protein in the CSF migrates to the edge of the wet spot as the gauze dries. --If the drainage is clear, the nurse should check it for glucose.

VTach

Three or more premature ventricular contractions (PVCs) in a row - if its just 3 and then done, it is nonsustained Repetitive firing of irritable ventricular ectopic focus, usually at 140-180 beats/min No P waves QRS is wide/ bizarre (>.10) Rate: > 100 per minute Rhythm: Usually regular Extremely serious, May lead to lethal rhythms Treatment - VT with pulse(Stable) - Elective cardioversion, Monitor more closely, Prepare for Cardioversion (O2, lidocaine, treat cause) VT without pulse (Unstable) - Defibrillate and CPR (followed by epinephrine) - assessing the patient's level of consciousness - administering oxygen - preparing to administer medications such as amiodarone or lidocaine - preparing for cardioversion or defibrillation if the patient becomes unstable.

Differentiate between decererate and decorticate posturing.

Top - decorticate (arms flexed) (worse) Bottom - decerebrate (arms extended)

List the lab abnormalities expected with a HIV/AIDS pt.

Total lymphocyte count (decreases) CD4 (decreases) CD4-CD8 ratio (decrease) CD8 (remain the same) Viral load: the amount of virus in the blood, which indicates the level of viral replication and disease activity (want this to be undetectable) Complete blood count (CBC): may show anemia, neutropenia, and thrombocytopenia Liver function tests: may show abnormal liver enzymes due to medication toxicity or HIV-related liver disease Lipid panel: may show elevated triglycerides and cholesterol due to medication side effects Kidney function tests: may show abnormal kidney function due to HIV-related nephropathy or medication toxicity

Explain the use of drug therapy to lower a pt's ICP

Treatment of increased ICP is based on decreasing the volume of brain water, blood, CSF in the intracranial space. The initial approach is airway management and decreasing intracranial contents, such as osmotic diuretics and hyperventilation. Osmotic diuretics - mannitol Mannitol: increases the osmolarity in the blood to pull water from the interstitial space of the brain into the vascular space. --Mannitol can cause hypovolemia, so IV fluids should be administered to replace losses ----Only with serum osmolality < 315 ----Pulls water from interstitial space of brain into the vascular space Loop diuretics Steroids - prednisone Anticonvulsants - phenytoin or Keppra IV fluids - NOT LR or free water Barbiturate/medically induced coma - Decreases metabolic demands of the brain - Monitor brain waves - Common sedatives: -----Morphine -----Versed (midazolam) -----Fentanyl -----Propofol If hypoglycemic - 50% dextrose

Prioritize nursing care for the patient with abdominal trauma.

Two Types 1. Blunt •Falls, assaults, explosions •Motor vehicle accidents 2. Penetrating •Gunshot wounds •Knife Assessment findings •Hypovolemic shock •Open wounds, lacerations •Impaled object •Nausea and vomiting, hematemesis •Absent or decreased bowel sounds •Rigid, distended abdomen •Pain with palpation, rebound tenderness •Pain radiating to shoulder or back Diagnostic testing •CBC, chemistry, and urinalysis •ABG, PT, BUN, creatnine, type and crossmatch •Abdominal ultrasound - portable •Abdominal CT •Diagnostic Peritoneal Lavage (DPL) - check for blood, fecal contents, bile - immediate surgery Collaborative Management •Patent airway •Oxygen with non-rebreather mask •Direct pressure on external bleeding •Vital signs, oxygen sat, ECG monitoring •IV access - large bore - saline or lactated ringers •Stabilize impaled objects with bulky dressings - do not remove •Cover protruding organs with saline dressing •Foley catheter •NG tube •Anticipate surgery

Identify the different types of Hypersensitivity reactions?

Type I: immediate hypersensitivity, mediated by IgE antibodies, which results in anaphylaxis or allergic reactions. also known as immediate hypersensitivity reactions or allergic reactions. They occur within minutes to hours after exposure to an allergen. When an allergen enters the body, it triggers the production of immunoglobulin E (IgE) antibodies. These IgE antibodies bind to mast cells and basophils, triggering the release of histamine and other chemical mediators, which cause symptoms such as itching, hives, swelling, and difficulty breathing. Examples of type 1 hypersensitivity reactions include allergic rhinitis food allergies anaphylaxis Type II: antibody-mediated hypersensitivity, mediated by IgG or IgM antibodies, which results in cytotoxic reactions. Type 2 hypersensitivity reactions are also known as cytotoxic hypersensitivity reactions. They occur when antibodies produced by the immune system bind to antigens on the surface of cells, causing destruction of those cells. This can lead to a variety of conditions, such as hemolytic anemia autoimmune hemolytic anemia Goodpasture's syndrome Type III: immune complex-mediated hypersensitivity, mediated by immune complexes that form when antigens bind to antibodies, which results in inflammatory reactions. Type 3 hypersensitivity reactions are also known as immune complex-mediated hypersensitivity reactions. They occur when antigen-antibody complexes form in the bloodstream and are deposited in tissues throughout the body. This triggers an inflammatory response, leading to tissue damage and organ dysfunction. Examples of type 3 hypersensitivity reactions include systemic lupus erythematosus rheumatoid arthritis serum sickness Type IV: delayed hypersensitivity, mediated by T cells, which results in cell-mediated reactions such as contact dermatitis or graft rejection. Type 4 hypersensitivity reactions are also known as delayed hypersensitivity reactions. They occur 48-72 hours after exposure to an allergen or antigen. These reactions are mediated by T cells rather than antibodies. When T cells recognize an antigen, they release cytokines, causing inflammation and tissue damage. Examples of type 4 hypersensitivity reactions include contact dermatitis tuberculin skin tests graft rejection

How do we measure ICP?

Ventricular system (intraventricular catheter/ventriculostomy) GOLD STANDARD OF ICP MEASUREMENT Catheter inserted via burr hole Inserted onto anterior horn of lateral ventricle in non-dominant hemisphere Drains CSF in addition to pressure monitoring ----Ability to monitor pressure and drain CSF ----Considered "gold standard" for ICP measurement because of the location of the tip of the catheter in the lateral ventricle ----Can be inserted at the bedside or in the operating room (OR) Subarachnoid system Small, hollow bolt/screw placed in subarachnoid or subdural space via burr hole Pressure monitoring only Epidural system Sensor placed via burr hole into epidural space

Explain the viral load and it's importance.

Viral load is a measure of the amount of HIV virus in a person's blood. It is an important marker for disease progression and treatment response in HIV/AIDS patients. A higher viral load indicates a higher level of viral replication, which can lead to more rapid disease progression and increased risk of transmission to others. Monitoring viral load is an important part of HIV/AIDS management, and treatment goals aim to achieve and maintain an undetectable viral load.

Hyperkalemia -

above 5 •more likely to have peaked t wave •watch for ventricular fibrillation or ventricular standstill •high potassium can lead to cardiac arrest (normal is 3.5-5) - might get orders to hold ACEs and ARBs because those can increase potassium in blood, same with spironolactone Treatment: •Stop oral and IV replacement of K •Diuretics - Lasix (lower potassium) •Dialysis •Ion exchange resins - kayexalate (binds potassium in the colon in exchange for sodium - poop out potassium) --Gastrointestinal excretion is accomplished using sodium polystyrene sulfonate (Kayexalate), which binds potassium in the colon in exchange for sodium; •IV Ca gluconate •IV insulin/glucose- move K into cells

Prioritize nursing care for patients with acute pancreatitis and patients with chronic pancreatitis

acute pancreatitis • Conservative therapy Aggressive hydration - Plasma or plasma volume expanders - Lactated Ringers - may give fluid bolus to help w hypovolemia and decreased BP - Pain management - Hypotension - dopamine - Minimizing pancreatic stimulation - Prevent infections --IV antibiotics - Peritoneal lavage --used in diagnosis but has been replaced by CT scan, now it is not done as frequently - CT can show stuff that is wrong - can be put on dopamine in order to increase BP and increase contractions in the heart - stop drinking, AA • Surgical therapy - ERCP - if obstructive, can retreive gallstone or remove gallbladder - Laparoscopic cholecystectomy • Drug therapy - IV morphine - Nitroglycerin - promotes pancreatic drainage - Antispasmodics - dicyclamine, decreases volume of pancreatic secretion - Carbonic anhydrase inhibitor (Diamox) - Antacids - H2-receptor antagonists - pepcid, prevents gastric ulcers in patients chronic pancreatitis • Prevention of attacks - prevent acute pancreatitis from happening • Relief of pain • Control of pancreatic exocrine and endocrine insufficiency • Low-fat, high-carb, high-protein diet • Pancreatic enzyme replacement • Control of diabetes - blood sugar control • No alcohol • Acid-neutralizing and acid-inhibiting drugs (H2 receptor antagonists) • Surgery - Indicated when biliary disease is present or if obstruction or pseudocyst develops

Interpret laboratory test results associated with acute pancreatitis.

amylase (aids in digestion of carbs) is increased lipase (digests fats) increased ---MOST specific test for pancreatitis because it is only produced by the pancreas AST and ALT increased rt obstructibe pancreatitis ---AST - damaged liver cell ---ALT - indicates gallstone WBC elevated rt immune response and inflammation BUN increased due to decreased fluid volume or hypercatabolic state

What are the symptoms of FES? Treatment?

basically a clot of fat that can happen most frequently in long bone and pelvic fractures because these bones have bone marrow that contains a high level of fat. It can cause respiratory distress, confusion rt hypoxia, restlessness, and death. Signs and Symptoms ----Feeling of impending doom ----Symptoms similar to pulmonary embolism ----Altered mental status, memory loss, headache ----Petechiae rash - axilla, chest, chest wall, conjuctiva, eyes, buccal ----ARDS - chest pain, tachypnea, cyanosis, dyspnea ----Fat cells in urine, blood, sputum Treatment ----Prevention is best - immobilization of long bones, early fixation with plate and screw ----High Flow Oxygen ----Fluid replacement - albumin is recommended-Binds with the fatty acids and may thus decrease the extent of lung injury ----Mechanical ventilation with PEEP ----Medications, including steroids, heparin have been found to be ineffective ---------Heparin, warfarin, anticoagulants, thrombolytics, DO NOT WORK FOR THIS BC IT IS A HUNK OF FAT NOT BLOOD

Hypokalemia -

below 3.5 •Check urine output •Increase dietary intake •Potassium oral supplements •IV potassium -never IV push- Always Dilute! DO NOT PUSH --Should not exceed 60 mEq/liter --Best is 40 mEq/liter or less --Rate max is 10-20 mEq/hour --Pain at IV site hypokalemia can put pts at risk for digoxin toxicity - potassium binds to the same sites as digoxin so lower potassium leads to more binding sites open which allows digoxin to bind more than normal which leads to toxicity •Urine output should be at least .5 ml/kg of body weight

Identify S&S for anaphylaxis, treatment.

can see angioedema swelling of lips tongue or throat low BP hives confusion - d/t decreased cerebral perfusion due to vasodilation and decreased CO wheezing, stridor •Prevention is best Medical alert bracelet and carry epi pen Notify health care personnel about specific allergies Carry anaphylaxis kit or epinephrine injector Medical records should prominently display list of specific allergens Precautionary measures if drug or agent must be used despite history of allergic reaction premedication with corticosteroids, IV Solu medrol or dipenhydramine in someone pre CT for those with an allergy to dye Assess for : Feelings of uneasiness, apprehension, impending doom Generalized itching, urticaria Erythema, angioedema Wheals or hives Congestion, rhinorrhea, dyspnea, respiratory distress, SOB Interventions: Assess respiratory function Establish or stabilize airway Stay with patient Epinephrine Antihistamines Oxygen Beta-adrenergic agonist - agonist activates a receptor, these receptors are in lungs which epi connects to in order to relax smooth muscle, an example of the beta adrenergic agonist is albuterol Corticosteroids, oral steroids - IV Solu Medrol

Identify risk factors for hepatitis

fecal -oral contamination Alcohol abuse Autoimmune disease Statins Anabolic steroids Azathioprine Methotrexate Isoniazid Valproic acid Tetracyclines Phenytoin Acetaminophen Industrial toxins Carbon tetrachloride Phosphorus mushrooms

Interpret laboratory test findings commonly seen in patients with cirrhosis

jaundice - if liver cannot process RBCs as they break down ----bilirubin builds up causing jaundice esophageal varices ascites - buildup of fluid in the abdomen, accumulation of extravascular fluid, albumin levels are decreased ---treat w diuretics or pericentesis if those don't work Diagnostics •Liver function tests ---AST and ALT are elevated, albumin is low ---lactate dehydrogenate and AGG •Liver biopsy •Liver scan ---uses radioactive dye to look at liver •Liver ultrasound •Esophagogastroduodenoscopy (EGD) ---scope, endoscopy procedure • ERCP •Prothrombin time •Testing of stool for occult blood

Hyponatremia -

way more common than hypernatremia Serum Na less than 135 mEq/L Causes •Loss of Na - excessive sweating, GI, diuresis, vomitting, diarrhea, SIADH •Dilutional - salt free IVs (5%DW), polydipsia, renal disease, increased ADH ----D5W = causes hyponatremia because it doesnt have NaCl •chronic alcohol use Assessment findings •Muscle cramps, weakness, fatigue •Na < 125 - progressive neuro sympotms, seizures, coma Treatment - fluid restriction (which increases percentage of sodium), 3% NS IV, fluid replacement containing Na - give 3% NS Evolemic hyponatremia - water intoxication can be seen in someone with excessive thirst due to psychotic polydipsia hypervolemic - too much fluid relative to soidum

Identify emergency interventions for the patient with bleeding esophageal varices

•Avoid alcohol, aspirin, and irritating foods •If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin) (BP support) •Management of Nausea and Vomiting. •Endoscopic sclerotherapy or ligation (inject a sclerotherapy or other type agent into the affected area to stop the bleeding) • Esophageal Bandings

Identify risk factors for cirrhosis

•Chronic, progressive disease •> 50% of liver disease in the US is directly related to alcohol consumption •Growing number of cases related to chronic hepatitis C --nash can also cause it - nonalcoholic hepatitis •4th leading cause of death in people between 35 and 54 years of age •Cell necrosis occurs •Destroyed liver cells are replaced by scar tissue •Normal architecture becomes nodular •Four types of cirrhosis: •Alcoholic cirrhosis: Alcoholic liver cirrhosis is the most advanced form of liver disease that's related to drinking alcohol •Postnecrotic cirrhosis: necrosis involving whole lobules, with the collapse of the reticular framework to form large scars; it may follow viral or toxic necrosis, or develop as a result of dietary deficiencies •Biliary cirrhosis: is an autoimmune disease of the liver. It results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver. Further slow damage to the liver tissue can lead to scarring, fibrosis, and eventually cirrhosis. •Cardiac cirrhosis: Cardiac cirrhosis is the consequence of the hemodynamic rearrangements caused by a failing heart. For this, heart failure is the first event that precipitates hepatic congestion and liver injury. •Avoid alcohol, aspirin, and irritating food, they can cause esophageal varices

Define different types of shocks: anaphylactic, hypovolemic, cardiogenic. Compare the risk factors, causes, and manifestations of different types of shock.

•Hypovolemic : Total body fluid decreased (in all fluid compartments). ----Examples: Hemorrhage and Dehydration. •Cardiogenic : Direct pump failure (fluid volume not affected). ---Examples: Myocardial infarction and Cardiac arrest •Distributive :Fluid shifted from central vascular space (total body fluid volume normal or increased). --due to massive vasodilation ---Examples : Neural induced (neurogenic shock, Pain, stress). Chemical induced (Anaphylaxis, Burns) •Obstructive: Cardiac function decreased by noncardiac factor (indirect pump failure). Total body fluid is not affected although central volume is decreased. ----Examples: Cardiac tamponade, Arterial stenosis, Pulmonary embolus - also severe bowel disease

Chronic Bronchitis what is it affects what produces what what is deficient

•Inflammation of bronchi and bronchioles caused by chronic exposure to irritants, especially cigarette smoke •Inflammation, vasodilation, congestion, mucosal edema, bronchospasm •Affects only airways, not alveoli •Production of large amounts of thick mucus Enzyme-Alpha-Antitrypsin 1 deficiency

Emphysema what is it

•Loss of lung elasticity and hyperinflation of lung •Dyspnea; need for increased respiratory rate •Air trapping caused by loss of elastic recoil in alveolar walls, overstretching and enlargement of alveoli into bullae, collapse of small airways (bronchioles) His Notes Bullae are air-filled alveoli (air pockets) in the lungs or blisters.

•Hypovolemic :

•Low circulating blood volume ----Causes mean arterial pressure (MAP) decrease; inadequate total body oxygenation - hypoxia •Commonly caused by hemorrhage (external or internal), dehydration ex: gunshot wound results when there is a rapid fluid loss resulting in inadequate circulating volume. Most commonly, hypovolemic shock is secondary to blood loss from penetrating or blunt trauma or severe gastrointestinal (GI) bleeds. Examples of penetrating trauma include gunshot wounds and knife injuries. Blunt trauma examples include blood loss into the abdomen due to damage to the liver, trauma to the thoracic cavity resulting in a ruptured aorta, or long bone or femur fractures. Excessive fluid loss may be caused by severe vomiting or diarrhea. Extensive burns can also cause severe loss of fluids, resulting in hypovolemic shock.

Prioritize nursing care for the patient during the resuscitation phase of burn injury. (it is the emergent but listed them all)

•Prehospital care - EMS should stop the burn process and manage the airway 1. Prevent hypothermia 2. airway •Emergent (resuscitative fluid, prevent hypothermia) --Geared towards resolving any life-threatening injuries due to the burn --Usually lasts up to 72 hours --Primary concerns are hypovolemic shock and edema --prevent immediate life-threatening issues •Airway management*** PRIORITY •Early endotracheal intubation •Escharotomies of the chest wall - surgical division of nonviable eschar •Fiberoptic bronchoscopy - definitive diagnosis of amount of injury •Humidified air and 100% oxygen •Fluid therapy** SECOND PRIORITY •Two large-bore IV lines for >15% TBSA •Type of fluid replacement based on size/depth of burn, age, and individual considerations •Parkland (Baxter) formula for fluid replacement ---total body percentage burned x weight in kg x 2-4mLs (usually 4) - half of this is given in the first 8, then the other half is given over the following 16 •Lactated ringers •Colloidal solutions - albumin •Wound care delayed - until stable, put a sheet over before wound care is possible •Wound care •Cleansing - Can be done in a cart shower, shower, or bed •Debridement - May need to be done in the OR, loose necrotic skin is removed. •Hands and arms elevated on pillows or slings •Tetanus immunization •Pain Management •Morphine •Versed •Ativan •Dilaudid •Haldol DVT prophylaxis •Low-molecular-weight heparin or low-dose unfractionated heparin is started. •Those at high bleeding risk, with mechanical VTE prophylaxis with sequential compression devices •Nutritional therapy - hyper-metabolic state •Fluid replacement takes priority over nutritional needs. •Enteral feedings - started within first 24 hours •Acute (wound healing) •The acute phase begins with the mobilization of extracellular fluid and subsequent diuresis. •The acute phase is concluded when the burned area is completely covered by skin grafts, or when the wounds are healed. --Hyponatremia, hypernatremia, hyperkalemia, hypokalemia Complications: infection, increased blood glucose, increased insulin production, decreased ROM, contractures, paralytic ileus, diarrhea, constipation, curling's ulcer. Nursing Care: Pain management PT and OT Relaxation Strategies Psychosocial care Nutritional therapy High protein, high carb diet Favorite foods from home Should be weighed regularly •Rehabilitative (restorative) begins when pt is admitted!! •Burn wounds are healed •Patient is able to resume a level of self-care activity

CKD

•Progressive, irreversible kidney injury; kidney function does not recover •CKD will progress to End-stage kidney disease (ESKD) •Clinical manifestation •Azotemia (nitrogen in blood) •Uremia •Uremic syndrome (a condition of premature destruction of red blood cells caused by infection) --diabetes and HTN are 1st and 2nd causes of CKD --native americans and men are at risk of CKD --usually CKD is asymptomatic until it is advanced --may have uremia which is high levels of urea in the blood --GFR less than 60 = stage three CKD, stage 4 15-29, stage 5 (end stage) less than 15 Stages of CKD 1. Reduced renal reserve - may be a sign of a maladaptive repair or subclinical loss of renal mass. Thus, a reduction in RFR may represent the equivalent of renal frailty or susceptibility to insults. 2. Reduced glomerular filtration rate (GFR) - when gFR is below 60 for more than three months, this is moderate-to- severe chronic kidney disease. you may be referred to a nephrologist (kidney doctor) for evaluation and treatment. a gFR below 15 means kidney failure. if kidney failure occurs, dialysis or a kidney transplant will be needed to survive. 3. ESKD - the last stage of long-term (chronic) kidney disease. This is when your kidneys can no longer support your body's needs. End-stage kidney disease is also called end-stage renal disease (ESRD) •Kidney changes (reduces GFR and abnormal urine production) •Metabolic changes • Urea and creatinine - RISE • GFR decrease •Electrolyte changes •Sodium •Potassium - increases leading to metabolic acidosis •Acid-base imbalance •Calcium and phosphorus - elevated phosphorus, low calcium ----secondary hyperparathyroidism •Cardiac changes • Hypertension • Hyperlipidemia • Heart failure • Pericarditis •Hematologic changes --HIGH BP meds cannot be administered on dialysis days because you are moving around a lot of fluid so it may lead to pressure changes without it --pt should be on a statin to treat high fat level (ends in -for) •GI changes --decreased motility fluid and electrolytes and acid-base balances are severe lack of activated vitamin D

Triage patients in the ED to prioritize the order of care delivery (most serious)

•Red: Emergent (class I) - ex - tension pneumothorax, massive hemmorhage •Yellow: Can wait short time for care (class II) - ex - isolated simple femur fracture •Green: Non-urgent or "walking wounded" (class III) ---ex - ankle sprain •Black: Expected to die/are dead (class IV) - burns over 95% of body