NUR 319 Final Exam

What are the phases of Peritoneal DIalysis?

Inflow (fill) • Solution infused through catheter over 10 minutes • After solution infused, inflow clamp closed to prevent air from entering tubing Dwell (equilibration) • Diffusion and osmosis occur between patient's blood and peritoneal cavity • Duration of time varies, depending on method Drain • Lasts 15 to 30 minutes • May be facilitated by gently massaging abdomen or changing position

What are the complications of Peritoneal dialysis?

Site infection Peritonitis Hernias Lower back problems Bleeding Pulmonary complications Protein loss

What is the procedure for Hemodialysis?

Two needles placed in fistula or graft First needle: placed to pull blood from the circulation to the HD machine Second needle: used to return the dialyzed blood to the patient Red catheter: attached to first needle Blue catheter: attached to second needle Dialyzer/blood lines primed with saline solution to eliminate air Terminated by flushing dialyzer with saline to remove all blood Needles removed and firm pressure applied

What is implantable cardioverter defibrillator (ICD)?

(if a person is a wake and in VT, give meds to relax them first) • Appropriate for patients who o Have survived SCD o Have spontaneous sustained VT o Have syncope with inducible ventricular tachycardia/fibrillation during EPS o Are at high risk for future life-threatening dysrhythmias • Decreases mortality • Artificial device that electrically stimulates the myocardium, depolarizes and starts contraction • Corrects conduction abnormality • Used in Brady-Tachy arrhythmias, AV Blocks • Generates and impulse from a power source and transmits an impulse to the heart muscle

What are the Grading of Heart Failure by NYHA

1. Class I: client exhibits no symptoms with activity 2. Class II: Client has symptoms with ordinary exertion 3. Class III: Client displays symptoms with minimal exertion 4. Class IV: Client has symptoms at rest

Medication calculations formulas

1. Use a streamlined equation where you only need 4 items: A. Ordered amount of drug B. Pt. weight (most of the time) C. Number of minutes in an hour (always the same!!) D. Dose/mL (calculated in #1) Ordered amount of drug x pt's weight x 60 (minutes/hr) Drug concentration 4. If the drug is not weight based, simply exclude the weight from the equation 2. Mg/Kg/D Convert pounds to kilograms 1 lb. = 2.2 kg Ex: 158 pounds = 71.8 Kg → 72 Kg What is the dosing schedule? and calculate base on the dosing schedule Calculate for highest and lowest range Infusion Formula for Drugs Ordered in mcg/minute Reduce the numbers in the standard solution to milligrams per milliliter. Change milligrams to micrograms. Divide by 60 to get micrograms per minute. Use either the formula, ratio, proportion, or dimensional analysis method to solve for milliliters per hour. Infusion Formula for Drugs Ordered in mcg/kg/minute To convert pounds to kilograms, divide by 2.2. Reduce the numbers in the standard solution to milligrams per milliliter. Change milligrams to micrograms. Divide by 60 to get micrograms per minute. Use either the formula, ratio, proportion, or dimensional analysis method to solve for milliliters per hour. IV infusion: Volumes to be infused (in ml) x drops per milliliters (gtt/mL - macro is 10,12,15, and 20, micro is 60 and blood is 10 gtt/mL) / (divided by) the time to be infused (in minutes) Conversion: 1 kg = 1000 g 1 g = 1000 mg 1 mg =1000 mcg 1 tsp =5 mL 1 tbsp = 15 mL 1 oz (or fl oz) =30 mL 1 pt =500 mL 1 qt =1 L or 1000 mL 2.2 lb =1 kg 1 inch =2.4 or 2.5 cm (centimeters) 1 m =1 gtt 1 dr =4 mL 1gr = 65 ot 60 mg 8 dr =1 oz or oz °C = (°F −32) ÷1.8 °F = (°C ×1.8) +32 Continuous regular insulin drip, 0.1 U/kg/hr Heparin 12 units/kg/hr Fluids for burn: 4 ml/kg/TBSA (follow the rule of nine)

What are the clinical manifestation of ADHF?

Early: increased pulmonary venous pressure Increase in the respiratory rate Decrease in Pao2 Later: interstitial edema Tachypnea Further progression: alveolar edema Respiratory acidemia Can manifest as pulmonary edema Life-threatening situation - alveoli fill with fluid Most commonly associated with left-sided HF

What is normal sinus rhythm

• Sinus node fires 60-100 beats/minute • Follows normal conduction pattern • Rhythm: regular • Rate: 60-100 beats/min • P Wave: round, smooth, upright • PRI: normal • QRS: normal • T Wave: normal • Q-T interval: normal • No ectopic beats

What is mixed heart failure?

Mixed systolic and diastolic failure Seen in disease states such as dilated cardiomyopathy (DCM) Poor EFs (<35%) High pulmonary pressures Biventricular failure Both ventricles may be dilated and have poor filling and emptying capacity • Disease states such as dilated cardiomyopathy (DCM) • Extremely low EF (less than 35%), high pulmonary pressures and biventricular failure (both ventricles are dilated and have poor fillings and emptying capacity)

What are the nursing management for HHS?

Monitor Blood glucose and urine output IV fluids Insulin therapy Lab: electrolytes Assess Neurological status Renal function Cardiac monitoring Pulmonary status

What are the surgical therapy for hyperthyroidism?

o Indications Large goiter causing tracheal compression Unresponsive to antithyroid therapy Thyroid cancer Not a candidate for RAI o More rapid reduction in T3 and T4 levels o Subtotal thyroidectomy Preferred surgical procedure Involves removal of 90% of thyroid Can be done endoscopically

What is ADHF?

Acute Decompensated Heart Failure Acute and life threatening Alveoli become filled with serosanguinous fluid Interstitial edema - tachypnea and patient becomes symptomatic Leading to alveolar edema Worsening arterial blood gas values Lower PaO2, possible increase of PaCO2 and progressive respiratory acidemia They cannot breathe and sounds like they are drowning They are panicking they need air There is an increase in the pulmonary venous pressure caused by decreased efficiency of the LV This results in engorgement of the pulmonary vascular system Lymphatic system increases it flow to help maintain a constant volume of pulmonary extravascular fluid Early stage associated with mild increase in respiratory rate and decrease in partial pressure of oxygen in arterial blood Lungs become less compliant and there is increased resistance in the small airways Put oxygen on them and turn it up! Get the order later You take vital signs anything change in the patient status

What are the nursing interventions for DI?

Adequate hydration Oral intake - limited IV: hypotonic saline or D5W Plasma expander - hypotonic saline IV hypotonic saline or dextrose 5% in water Monitor serum glucose levels due to hyperglycemia Hormone therapy Inadequate insulin product so the patient is at risk for hypoglycemia Monitor BG Looking at blood sugar Cardiovascular status Dysrhythmias Monitor for BP and heart rate Neurological status Due to the sodium levels, anything that affect sodium levels can affect the neuro status of the patient LOC Coma Seizure disorders Basis name and date of birth identification Scale for assessment is the Glasgow coma scale Monitor for dehydration Checking for dry mucus membranes Checking pulses Maintain I & O Placing a foley cath Need to measure it and report it to the healthcare provider May need to do a 24 hour urine collection Monitor vital signs and neurological and cardiovascular status. Provide a safe environment, particularly for the client with a change in level of consciousness or mental status. Monitor electrolyte values and for signs of dehydration. Monitor intake and output, weight, and specific gravity of urine. Maintain the intake of adequate fluids, and monitor for signs of dehydration. Instruct the client to avoid foods or liquids that produce diuresis. Administer chlorpropamide (Diabinese) if prescribed for mild diabetes insipidus. Administer vasopressin tannate (Pitressin) or desmopressin acetate (DDAVP,Stimate) as prescribed; these are used when the ADH deficiency is severe or chronic. Instruct the client in the administration of medications as prescribed (DDAVP may be administered by injection, intranasally, or orally). Instruct the client to wear a Medic-Alert bracelet. Biggest thing is to look at sodium levels, I&O, urine content and neurological status. Patient comes in with large amount of urine, what to do? Assessment, vital signs, IV and hypertonic solution, Lab works and foley cath, Use bladder scan

What is Angiopathy?

Angiopathy Damage to blood vessels related to chronic hyperglycemia Leading cause of death in diabetics Macrovascular and microvascular Tight glucose control helps prevent or minimize complications Macrovascular Angiopathy Diseases of large and medium-sized blood vessels Greater frequency and earlier onset in patients with diabetes Cerebrovascular disease Cardiovascular disease Peripheral vascular disease Decrease risk factors Obesity, sedentary lifestyle Smoking and HTN Microvascular Angiopathy Vessel membranes in capillaries and arterioles thicken Specific to diabetes and includes Retinopathy Nephropathy Dermopathy Usually appear 10 to 20 years after diagnosis

What are the chronic complications of DM?

Angiopathy, Retinopathy, Nephropathy, foot complications and skin complications

What is the nursing assessment for HF?

Ask about the number of pillows if trouble sleeping or ask about their sleep patterns Paroxysmal nocturnal dyspnea - they feel like they are suffocating and they wake up with the panic Insomnia - they are so afraid of dying that they don't go to sleep Chest pain or heaviness RUQ pain, abdominal discomfort enlarged liver Behavioral changes ask them what's wrong with them? Something is wrong Visual changes do a pupil check Skin: color, temperature, edema Respiratory Rate, sounds, administer O2 Sputum: frothy, blood-tinged Cardiovascular: HR and sounds GI: abdominal distention Neuro: changes in LOC When auscultating heart sounds, a S3 heart sound will occur (gallop) What is Chronic HF: Nursing Intervention? Semi-Fowler's position/High Fowler's position Hemodynamic status Daily weights I&O Administer prescribed drugs Alternate rest with activity Provide diversionary activities Monitor response to activity Collaborate with OT/PT Reduce anxiety Evaluate support system Patient teaching it starts when they walk in the door.

What are the nursing interventions for SIADH?

Assess for: Clinical manifestations of hyponatremia Low urine output with high specific gravity (dark yellow) Hint: Concentrated urine (dark yellow) and Diluted Serum! Sudden weight gain without edema Decreased serum sodium level Monitor I & O Be on alert for low urine output with high specific gravity Mild symptoms and Na >125mEq/L Fluid restriction: 800-1000mL/day - if the symptoms are mild and serum sodium is greater than 125 mEq/L Acute Care Setting Fluid restriction: includes IV medications No more than 1000 mL/day Daily weights HOB (head of bed) flat or slightly elevated 10 degrees enhance venous return to the heart and increase left atrial filling pressure and reducing the release of ADH Do frequent turning, positioning and range of motion however protect the patient due to there may be an altered mental status IV hypertonic saline (3%NSS) Patient is depleted of sodium In case of severe hyponatremia (less than 120 mEq/l) May give loop diuretic such as Lasix to promot diuresis but only if the sodium level is at least 125 mEq/l because it may promot further loss of sodium Be on the lookout for loss of K, Ca and Mg electrolytes Medications: tolvaptan It can cause diaphoresis (excess sweating) and increase urine output but it does not change the electrolyte balance Treat the underlying cause Medication that stimulate the release of ADH should be avoided or discontinued

What is acute (wound healing) phase of burn management?

Begins with the mobilization of extracellular fluid and subsequent diuresis o Concludes when Partial thickness wounds are healed and/or Full thickness burns are covered by skin grafts o Pathophysiology Diuresis from fluid mobilization occurs, and patient is less edematous Bowel sounds return Healing begins as WBCs surround burn wound and phagocytosis occurs Necrotic tissue begins to slough Granulation tissue forms Partial-thickness burn wounds heal from edges and from dermal bed Full-thickness burns must have eschar removed and skin grafts applied o Lab Values Sodium • Hyponatremia can develop from o Excessive GI suction o Diarrhea • Hypernatremia may develop from o Successful fluid replacement o Improper tube feedings o Inappropriate fluid administration • Water intoxication o Juices and nutritional supplements • Restrict sodium in IVs, oral feedings Hyperkalemia • Large amounts of potassium is released from damaged cells • May occur if patient has renal failure, adrenocortical insufficiency, or massive deep muscle injury • ECG changes, cardiac dysrhythmias and ventricular failure • Muscle weakness Hypokalemia can be caused by • Lengthy IV therapy without potassium • Vomiting, diarrhea • Prolonged gastrointestinal suction o Complications Infection • Localized inflammation, induration, and suppuration • Partial-thickness burns can become full-thickness wounds in the presence of infection • Watch for signs and symptoms o Hypothermia or hyperthermia o Increased heart and respiratory rate o Decreased BP o Decreased urine output Cardiovascular and respiratory systems • Complications are the same as in emergent phase Neurologic system • Severe hypoxia from respiratory injuries or complications from electrical injuries occur • Disorientated and combative • Hallucinations • Delirium Musculoskeletal system • Decreased ROM • Contractures Gastrointestinal system • Paralytic ileus • Diarrhea, constipation • Curling's ulcer (peptic ulcer) Endocrine system • Increased blood glucose levels • Increased insulin production • Hyperglycemia o Nursing Management Wound care • Assessment • Cleansing • Debridement: enzymatic debridement o Speeds up removal of dead tissue from healthy wound bed Dressing reapplication • Appropriate coverage of the graft • Gauze next to graft followed by middle and outer dressings • Unmeshed sheet grafts used for facial grafts Excision and grafting • Eschar is removed down to subcutaneous tissue or fascia • Graft is placed on clean, viable tissue • Wound is covered with autograft • Donor skin is taken with a dermatome • Choice of dressings varies • Grafts are attached with o Fibrin sealant o Sutures or staples o With early excision, function is restored, scar tissue minimized • Cultured epithelial autographs (CEAs) • Artificial skin Types of Grafts • Allograft or homograft skin o Usually from cadavers • Autograph • Biosynthetic • Temporary o Porcine o Biobrane Pain management • Continuous background pain o IV infusion of an opioid o Or slow-release, twice-a-day oral opioid • Treatment-induced pain o Analgesic o Anxiolytic (sedative and hypnotic) • Nonpharmacologic strategies o Relaxation breathing o Visualization, guided imagery Physical and occupational therapy • Good time for exercise is during wound cleaning • Passive and active ROM • Splints should be custom-fitted Nutritional therapy • Meeting daily caloric requirements is crucial • Caloric needs should be calculated by dietitian • High-protein, high-carbohydrate foods • Favorite foods from home • Patients should be weighed regularly

What are the depth of burn?

Burns have been defined by degrees (first, second, third, and fourth) • ABA advocates categorizing burn according to depth of skin destruction o Partial-thickness burn o Full-thickness burn • Superficial partial-thickness burn o First degree burns o Involves the epidermis o Heat flash • Deep partial-thickness burn o Second degree burns o Involves the dermis o Flash, scald, contact burns o Chemical and electrical current • Full-thickness burn o Third and fourth degree burns o Involves all skin elements, nerve endings, fat, muscle, bone o All skin elements and local nerve endings are destroyed o Necrosis develops o Surgical intervention

What are the risk factors for HF?

CAD including MI HTN including HTN crisis Rheumatic heart disease Congenital heart defects (ventricular septal defects) Pulmonary HTN Cardiomyopathy Hyperthyroidism Valvular disorders (mitral stenosis) Myocarditis diabetes, advanced age, tobacco use, obesity and high serum cholesterol

What is thermal burns?

Caused by flame, flash, scald, or contact with hot objects • Severity of injury depends on o Temperature of burning agent o Duration of contact time

What are the types of DI?

Central DI Interference with ADH synthesis, transport or release Brain tumor, head injury Nephrogenic DI Inadequate renal response to ADH despite the presence of adequate ADH Lithium, renal damage Primary DI Excessive water intake (water intoxication) Psychological disorder

What is the treatment for hypoglycemia?

Check blood glucose level If less than 70 mg/dL, begin treatment If more than 70 mg/dL, investigate further for cause of signs/symptoms If monitoring equipment not available, treatment should be initiated Treatment Rule of 15 Consume 15 g of a simple carbohydrate 4-6 oz of fruit juice or regular soft drink Do not give orange juice to a patient that have kidney problems due to the potassium levels. Give apple juice to a DM patient with kidney problems Also do not put sugar in the glass of orange juice or apple juice. You will spike their sugar level. Just give them the glass of orange juice. Recheck glucose level in 15 minutes Repeat if still less than 70 gm/dL Avoid foods with fat Decrease absorption of sugar Candy bars, cookies, and ice cream Give complex CHO after recovery 15 -20 grams of a simple carbohydrate - ( 4-6 oz of fruit juice or regular soda) (glucose tablets or gels) Check glucose in 15 minutes - still less than 70 ingest 15 more grams of carbohydrate recheck glucose in 15 minutes Then, meal or snack with complex carbohydrate and protein Glucagon IM or SC IV dextrose - 20 - 50 mL of 50% dextrose Life threatening Treat if glucose is below 70 15-20 grams of a simple carbohydrate = 4-6 oz of juice, soda, or 8 oz skim milk, 6-10 hard candies, 2-3 teaspoons of sugar or honey. There are several available commercial formulas to carry with patient After 15 minutes if still below 70-75 repeat If symptoms persist for longer than 10 minutes after treatment, repeat treatment no matter glucose level Medication Dextrose 50%: IV push Large amount of glucose and comes in prefilled syringes in 60 mL. Because it is a big syringe, it will take you several minutes to push in the medication Glucagon 1mg IM or subcutaneously After symptoms subside give Meal with protein and starch = peanut butter crackers, cheese, milk IV dextrose in acute care

What are the collaborative managements of ADHF?

Continuous monitoring and assessment VS, O2 saturation, urinary output High Fowler's position Supplemental oxygen Unstable Hemodynamic monitoring if unstable Mechanical ventilation Ultrafiltration (aquapheresis) for patients with volume overload and resistance to diuretics It will start to produce urine quickly to get the fluid off of the patient Circulatory assist devices for patients with deteriorating HF Intraaortic balloon pump (IABP) Ventricular assist devices (VADs) Treat any anxiety and/or depression Drug Therapy IV push rule of thumb is 1mL/min Diuretics Decrease volume overload (preload) Furosemide (Lasix), bumetanide (Bumex) Before you give it, check their potassium levels Lasix can produce a liter of urine in an hour. Patient is at risk for cardiac arrhythmia You need to place a foley. Tell your patient not to get up. Use the call button Also you need to measure how much fluid is coming out of the patient Vasodilators Reduce circulating blood volume and improve coronary artery circulation IV nitroglycerin Sodium nitroprusside (Nipride) Nesiritide (Natrecor) Morphine Reduces preload and afterload Relieves dyspnea and anxiety They are in pain and they feel like they are sufficating Positive inotropes B-adrenergic agonists: dopamine (Intropin), dobutamine (Dobutrex) - reduce the heart rate Phosphodiesterase inhibitors: inamrinone (Inocor), milrinone (Primacor) Digitalis - digoxin Digoxin helps to increase the force of contraction and trying to push as much as blood to the lv and as much as force to push the blood out of the body

What is diabetic nephropathy?

Damage to small blood vessels that supply the glomeruli of the kidney (renal failure) Leading cause of end-stage kidney disease Risk factors Hypertension Genetics Smoking Chronic hyperglycemia Annual screening Blood work done BUN, creatinine, CBC and all of our labs If albuminuria present, drugs to delay progression: ACE inhibitors Angiotensin II receptor antagonists Control HTN and tight blood glucose control

What are the infections complications?

Defect in mobilization of inflammatory cells and impaired phagocytosis Recurring or persistent infections Patient teaching for prevention Hand hygiene Flu and pneumonia vaccine

What is DIabetes Insipidus (DI)?

Deficiency of production or secretion of ADH or a decreased in renal response to ADH Underproduction or under secretion of ADH results in a condition called diabetes insipidus (DI) Kidney tubules fail to reabsorb water Decrease ADH Fluid and electrolyte imbalances Increased urine output Increased plasma osmolality

What is the clinical manifestation of DKA?

Dehydration Kussmaul respirations Fruity breath BG level: 250 mg/dL or higher pH less than 7.30 Bicarbonate (HCO3) less than 16 mEq/L Moderate to high ketones in blood and urine

What are the skin complications?

Diabetic dermopathy Most common Red-brown, round or oval patches Seen on patient shins Acanthosis nigricans Velvety light brown to black skin Necrobiosis lipoidica diabeticorum Red-yellow lesions Transparent, may see blood vessels under skin Can see right through it Skin prone to injury Infection Defect in mobilization of inflammatory cells and impaired phagocytosis Recurring or persistent infections Patient teaching for prevention Hand hygiene Flu and pneumonia vaccine

What is Emergent (resuscitative) burn management phase?

Emergent (resuscitative) phase is time required to resolve immediate problems resulting from injury o Up to 72 hours o Primary concerns Hypovolemic shock Edema o Pathophysiology Fluid and electrolyte shifts • Greatest threat is hypovolemic shock • Caused by a massive shift of fluids out of blood vessels as a result of increased capillary permeability • Colloidal osmotic pressure decreases • More fluid shifting out of the vascular space into interstitial spaces o Edema: second spacing o Decreased BP o Increased pulse • Na+ rapidly moves to interstitial spaces and remains until edema formation ceases • K+ shift develops because injured cells and hemolyzed RBCs release K+ into extracellular spaces Inflammation and healing • Neutrophils and monocytes accumulate at the site of injury • Fibroblasts and collagen fibrils begin wound repair within the first 6 to 12 hours after injury Immune system is challenged when burn injury occurs • Skin barrier is destroyed • Bone marrow is depressed • Circulating levels of immune globulins are decreased • WBCs develop defects o Clinical Manifestations Shock from hypovolemia Blisters Paralytic ileus Shivering Altered mental status o Complications Cardiovascular system • Impaired microcirculation and increased viscosity leads to sludging Respiratory system • Upper airway burns o Edema formation o Mechanical airway obstruction and asphyxia • Lower airway injury o Pneumonia o Pulmonary edema Urinary system • Decreased blood flow to kidneys causes renal ischemia • Acute tubular necrosis (ATN) o Nursing Management Airway management • Early endotracheal intubation • Escharotomies of the chest wall • Fiberoptic bronchoscopy • Humidified air and 100% oxygen Fluid therapy • 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 o 4 mL Lactated Ringers solution per Kg of bodyweight per percent of total body surface area (%TBSA) = total fluid requirements for first 24 hours. o ½ of total in first 8 hours o ¼ of total in second 8 hours o ¼ of total in third 8 hours Wound care • Delayed until a patent airway, adequate circulation, and fluid replacement have been established • Infection is most serious threat to further tissue injury 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 Open method • Burn is covered with topical antibiotic with no dressing over wound Multiple dressing changes or closed method • Sterilized gauze dressings are laid over topical antibiotic • Dressings may be changed from every 12 to 24 hours to once every 14 days o Drug Therapy Analgesics and sedatives • Morphine • Hydromorphone (Dilaudid) • Lorazepam (Ativan) Antimicrobial agents • Topical agents o Silver sulfadiazine (Silvadene) o Mafenide acetate (Sulfamylon) VTE prophylaxis • Heparin o Nutritional Therapy Hypermetabolic state • Resting metabolic expenditure may be increased by 50% to 100% above normal • Core temperature is elevated • Caloric needs are about 5000 kcal/day • Early, continuous enteral feeding promotes optimal conditions for wound healing • Supplemental vitamins and iron may be given

What are the nursing managements of burns?

Encourage both patient and caregiver to participate in care Skills for dressing changes Wound care Use water-based creams Reconstructive surgery is often needed following major burns The role of exercise cannot be overemphasized Constant encouragement and reassurance Emotional and psychological needs • Assess the circumstances of the burn • Burn survivors often experience guilt, concern, frustrations • New fears arise during recovery • Self-esteem may be adversely affected • Address spiritual and cultural needs • Family and patient support groups

What are the nursing interventions of DKA?

Ensure patent airway Establish IV access; begin fluid resuscitation NaCl: 0.45% or 0.9% Dextrose: 5% to 10% when BG level approaches 250 mg/dL Continuous regular insulin drip, 0.1 U/kg/hr - only one is IV Potassium replacement as needed

What are the clinical manifestations of heart failure?

Fatigue - earliest symptoms. Usually noticed after usual activities Decreased CO, impaired perfusion to vital organs, decreased oxygenation and Anemia Dyspnea - increased pulmonary pressures secondary to interstitial and alveolar edema. Can occur with mild exertion or at rest. Orthopnea often accompanies Paroxysmal nocturnal dyspnea (PND) - when a patient is asleep and can't breathe When lying flat, fluid is then moved all around, causing an increase pressure on the lungs and issues with breathing Patient awake in a panic and need to sleep sitting up (3 or 4 pillows rule) - They feel like they are drowning Patient may have a dry cough! Tachycardia First mechanism is to increase HR due to reduced CO and activation of SNS Edema Peripheral edema - may have pitting edema Sudden weight gain of more than 3 pounds in 2 days (seen in ADHF) Hepatomegaly Ascites (abdominal cavity) Lungs (pulmonary edema and pleural effusion) Nocturia - voiding frequently at night Impaired renal perfusion leading to decreased urine output - RAA system!!! When a person lies down at night, fluid is moved back from interstitial spaces back into circulatory system and cardiac output is decreased leading to increased Renal blood flow and diuresis Skin changes Skin may be blotchy Shiny and swollen Almost or no hair growth May be brown or brawny in areas of lower legs and ankles Behavioral Changes Cerebral circulation is reduced Unusual behavior such as restlessness, confusion, and decreased attention span or memory Panic level due to the feeling of drowning Chest Pain Angina due to ischemia Weight Changes Weight gain due to fluid retention may be from renal failure As it advances, patient may have cardiac cachexia (muscle wasting and fat loss) - may not be seen until edema subsides Weight loss due to abdominal fullness of the ascites and not eating

What are the characteristics of SIADH?

Fluid retention Serum hypoosomolality Dilutional hyponatremia Hypochloremia Concentrated urine In the presence of normal or increased intravascular volume and normal renal function

What are smoke inhalation injuries?

From inhalation of hot air or noxious chemicals • Cause damage to respiratory tract • Major predictor of mortality in burn victims • Need to be treated quickly • Three types o Metabolic asphyxiation o Upper airway injury o Lower airway injury • Metabolic asphyxiation o Carbon monoxide (CO) poisoning o CO is produced by the incomplete combustion of burning materials o Inhaled CO displaces oxygen Hypoxia Carboxyhemoglobinemia Death • Carbon monoxide (CO) poisoning o Hypoxia and ultimately death when CO levels are 20% or greater o Treat with 100% humidified oxygen o CO poisoning may occur in the absence of burn injury to the skin • Upper airway injury o Injury to mouth, oropharynx, and/or larynx o Thermally produced o Hot air, steam, or smoke o Swelling may be massive and onset rapid Eschar and edema may compromise breathing Swelling from scald burns can be lethal o Clinical Manifestations Presence of facial burns Singed nasal hair Hoarseness, painful swallowing Darkened oral and nasal membranes Clothing burns around chest and neck • Lower airway injury Injury to trachea, bronchioles, and alveoli Injury is related to length of exposure to smoke or toxic fumes Pulmonary edema may not appear until 12 to 24 hours after burn Manifests as acute respiratory distress syndrome (ARDS) o Clinical Manifestations Dyspnea, wheezing, altered mental status Carbonaceous sputum History of being burned in enclosed space

What are the diagnostic studies for HF?

History and physical examination Determination of underlying cause Chest x-ray 12-lead ECG Hemodynamic monitoring 2-dimensional echocardiogram Nuclear imaging studies Cardiac catheterization ECG stress test ABGs Echocardiography: ultrasound used to provide information about structure, anatomy, and physiology of the heart no ionizing radiation generated inexpensive quality of the image depends on the operator's skill, patient's body type, presence of barrel chesting and other chest wall anatomy diagnostic utility: assessing cardiac structure size and function LVH LV dysfunction: ischemia valves: morphology and mobility pericardium wall motion abnormalities: regional vs global Contractilities congenital abnormalities estimate ejection fraction very important post-MI assessing cardiac masses measuring RV and pulmonary pressures collapse of vena cava is normal and indicates normal central venous pressure won't collapse if pressures are high assessing murmurs: diastolic and cardiac evaluating syncope pre-op screening for clots before ablation of irritable foci causing arrhythmias assessing cardiac sources of emboli: looking for patent foramen ovale or atrial septal defect biggest risk in having a communication between sides of the heart is that you lose the filtering property of having all blood flow through the lungs, so that emboli are able to move from the right side of the heart to the left can use saline contrast to do a bubble study: + if bubbles seen in both sides of the heart assessing pericardial effusion, pulmonary embolism, pulmonary hypertension transthoracic echiocardiography: standard echo, done over chest wall transesophageal echiocardiography: more helpful in viewing posterior structures of the heart but more invasive quality not compromised by obesity or pulmonary disease helpful in assessing for suspected endocarditis and subsequent valvular damage improved visualization of vegetations, thrombi, masses, or left atrial appendage clot (most likely source of CVA/TIA) EKG many CHF patients will have LVH end stage CHF results in low voltage due to electricity going through greater muscle mass? evidence of ischemia or prior infarction (Q waves) Cardiac biomarkers if suspecting ischemic etiology CK/MB Troponin Cardiac cath in acute CHF with unstable angina or MI do left ventriculogram to evaluate LV function, calculate EF, assess wall motion, and to look for mitral regurgitation do an arch shot to assess for aortic regurgitation or aortic defects do coronary angiography to assess for blockages Chest X-ray with PA and lateral views look at size and shape of cardiac silhouette for cardiomegaly Kerley B lines: sharp, linear densities from interlobular interstitial edema pathognomonic for CHF! look for pleural effusions commonly caused by left sided CHF effusions will be transudative, small-med sized, and free-flowing BNP levels

What are the primary risk factors for HF?

Hypertension and CAD

What are the clinical manifestations of SIADH?

Hyponatremia Clinical manifestations Postural hypotension, Tachycardia Decreased urinary output, dry mucous membranes (chapped lips) Assess for turgor - if it stands up it means they are dehydrated Muscle cramps, weakness, Fatigue Nausea, vomiting Brain & CNS: most seriously affected - neurological status is altered Disorientation, confusion, lethargy, headache Gross motor weakness Depressed deep tendon reflexes Seizures, coma or death - patient get sleepy and if you try to wake them, they won't. Their sodium levels are down to the 120s. apprehension, anxiety, muscular, twitching, muscular weakness, headaches, tachycardia and hypotension Muscle cramping, pain, and weakness Low urine output Increased weight Na level below 120mEq/L Vomiting, abdominal cramps Muscle twitching Seizures Cerebral edema Initially the patient may displays thirst, DOE and fatigue

What is the pathophysiology of DKA?

Insufficient circulating insulin Ketones: acid by-products of fat metabolism Fat breaks down into ketones Kenonuria: ketones excreted in urine Impaired protein synthesis Insulin deficiency stimulates production of glucose from proteins in the liver Electrolyte imbalances Hypovolemia and shock Renal failure Comatose Untreated death

What is Hyperosmolar Hyperglycemic Syndrome (HHS)?

Life-threatening Type 2 diabetes Precipitating factors UTI, pneumonia, sepsis Acute illness Type 2 diabetes newly diagnosed Inadequate fluid intake Sufficient circulating insulin preventing ketoacidosis Fewer symptoms lead to higher glucose levels (>600 mg/dL) More severe neurologic manifestations because of increased serum osmolality Ketones absent or minimal in blood and urine Medical emergency Therapy IV insulin - regular insulin NaCl:0.45% or 0.9% Dextrose: 5% to 10% when BG level approaches 250 mg/dL More fluid replacement Monitor potassium Correct underlying cause

What are the medications used and treatment of HF?

Main treatment goals Treat the underlying cause and contributing factors Maximize CO Provide treatment to alleviate symptoms Improve ventricular function Improve quality of life Preserve target organ function - Especially the kidneys - will shut down Improve mortality and morbidity Patient needs to stick to their regimen! Oxygen therapy Relieves dyspnea and fatigue Physical and emotional rest Conserve energy and decrease oxygen needs Dependent on severity of HF Structured exercise program Biventricular pacing/cardiac resynchronization therapy (CRT) With implantable cardioverter-defibrillator (ICD) IABP and VADs as bridge or destination therapy Heart transplantation may occur so immunosuppression will be use for preparing for the surgery as well as lifelong - risk for infections Drug Therapy Diuretics Reduce edema, pulmonary venous pressure, and preload Promote sodium and water excretion Loop diuretics Thiazide diuretics Hydrochloric thiazide - not as much excretion of potassium as loop diuretics Monitor potassium levels (hypokalemia) Tell your patients to take the pill at 8 am or 2 pm, not at bed time RAAS inhibitors ACE inhibitors all patients need to be on an ACE inhibitor New drug on TV - Entresto is a combination of sacubitril (ACE inhibitor) and valsartan (angiotensin II receptor blockers) which is both an ACE inhibitor and Angiotensin II receptor blockers used for people with chronic heart failure Angiotensin II receptor blockers Aldosterone antagonists Monitor potassium levels (hyperkalemia) β-adrenergic blockers Bring the heart rate down Vasodilators Nitrates BiDil - contain a combination of isosorbide dinitrate (antianginal) and hydralazine (prevent the loss of the effects of isosorbide dinitrate) - work best with African Americans Positive inotropic agents Digitalis - Digoxin Increase the force of cardiac contraction Hold the medication is apical pulse is less than 60 beats/min. Must do apical pulse for a full minutes!!! Nutritional Therapy Low sodium diet Individualize recommendations and consider cultural background (www.nhlbi.nih.gov/health/index.htm#recipes) Recommend Dietary Approaches to Stop Hypertension (DASH) diet Sodium is usually restricted to 2 g/day Educate the patient about food that are with sodium such as in canned vegetables Fluid restriction Individualized <2L/day. Ice chips , gum, hard candy, ice pops (sugar free) Daily weights Same time, same clothing each day Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week Should be reported to health care provider

What are the causes of SIADH?

Malignancy: small cell lung cancer Head injury, brain tumor If head injury, it will subsided on its own Gullain-Barre Syndrome

What is the pathophysiology of HF?

May be caused by any inference with normal mechanisms of CO - Any changes lead to decreased ventricular function and HF which depends on Preload, Afterload, Myocardial contractility, Heart rate (HR)

What are the diagnostic Studies for SIADH?

Measurements of urine and serum osmolality Dilutional hyponatremia water excess in relation to the amount of sodium - the patient have too much water but sodium levels are still low Serum Na less than 134mEq/L Serum osmolality less than 280mOsm/Kg If the serum osmolality much lower than the urine osmolality it indicates the inappropriate excretion of concentrated urine in the presence of dilute serum Urine specific gravity greater than 1.025

What is Diabetic retinopathy?

Microvascular damage to retina Nonproliferative Partial occlusion of small blood vessels in retina causes microaneurysms Proliferative Involves retina and vitreous humor Neovascularization: new blood vessels formation, very fragile and bleed easily Can cause retinal detachment - medical emergency and is irreversible Glaucoma and cataracts Treatment Annual eye examinations Maintain glucose control Laser photocoagulation Most common Laser destroys ischemic areas of retina When patient is having an issue, they will have black and blue eyes Vitrectomy Aspiration of blood, membrane, and fibers inside the eye

What is diabetic neuropathy?

Nerve damage due to metabolic derangements of diabetes Reduced nerve conduction and demyelinization Sensory or autonomic Reduced nerve conduction and demyelinization Sensory neuropathy Loss of protective sensation (LOPS) in lower extremities Major risk for amputation Distal symmetric polyneuropathy Affects hands and/or feet bilaterally Loss of sensation, abnormal sensations, pain, and paresthesias Treatment for Sensory Neuropathy Tight blood glucose control Drug therapy Topical creams Tricyclic antidepressants Selective serotonin and norepinephrine reuptake inhibitors Antiseizure medications: gabapentin (Neurotin)-decrease the release of neurotransmitters that transmit pain Autonomic Neuropathy Can affect nearly all body systems Cardiovascular abnormalities Postural hypotension, resting tachycardia, painless MI Sexual function Erectile dysfunction Decreased libido Vaginal infections Neurogenic bladder Empty frequently Credé's maneuver - technique used to void urine from the bladder of an individual who, due to disease, cannot do so without aid. The Credé's maneuver is executed by exerting manual pressure on the abdomen at the location of the bladder, just below the navel Medications: bethanechol (Urecholine) Self-catheterization

What is hypoglycemic unawareness?

No warning signs/symptoms until glucose level critically low Caused by autonomic neuropathy and lack of counterregulatory hormones Patients at risk usually need to keep glucose levels slightly higher

What is the rehabilitation (restorative) phase of burn management?

Pathophysiologic Changes Burn wound heals either by spontaneous re-epithelialization or by skin grafting Keratinocytes begin to rebuild the tissue structure Collagen fibers add strength to weakened areas 4 to 6 weeks, the area becomes raised and hyperemic Mature healing is reached about 12 months Skin never completely regains its original color Discoloration of scar fades with time Pressure can help keep scar flat Newly healed areas can be hypersensitive or hyposensitive to cold, heat, and touch Healed areas must be protected from direct sunlight for 3 months Skin and joint contractures • Positioning, splinting, and exercise should be used to minimize contracture.

What is hypoglycemia?

Pathophysiology Too much insulin in proportion to glucose in the blood BG: less than 70 mg/dL Neuroendocrine hormones released Autonomic nervous system activated Clinical Manifestations Common Shakiness, nervousness Palpitations, anxiety Diaphoresis Neurological changes Difficulty speaking Visual changes Stupor Confusion LOC, seizures, coma, and death

What are clinical manifestations of DI?

Polydipsia and polyuria Excessive thirst and excretion of large amount of urine, these patient can urinate up to 15 to 20 liters a urine Excretion of large amounts of urine Drinking large amounts of water Urine output of more than 200 mL/hr with a specific gravity of less than 1.005 Poor skin turgor Dehydration Not enough circulating volume Hypotension, tachycardia Hypovolemic shock Central DI: Clinical Manifestations Acute with excessive fluid loss Intracranial surgery Acute phase: abrupt onset of polyuria Interphase: urine volume normalizes Permanent phase: 10-14 days postoperatively Triphasic pattern for intracranial surgery The acute phase with an abrupt onset of polyuria An interphase in which urine volume normalizes Third phase in which central DI is permanent 10 - 14 days post operatively Could be permanent

What are the assessments for DI?

Polyuria of 4 to 24 L per day Polydipsia Dehydration Decreased skin turgor, dry mucous membranes Inability to concentrate urine A low urinary specific gravity: 1.005 or less Fatigue Muscle pain and weakness Headache Postural hypotension that may progress to vascular collapse without rehydration Tachycardia

What is the etiology and pathophysiology of AKI?

Prerenal Causes: factors external to the kidneys that reduce renal blood flow • Severe dehydration, heart failure, decreased CO Decreases glomerular filtration rate Prerenal oliguria Autoregulatory mechanisms attempt to preserve blood flow o Intrarenal Causes: conditions that cause direct damage to kidney tissue • Prolonged ischemia • Nephrotoxins • Hemoglobin released from hemolyzed RBCs • Myoglobin released from necrotic muscle cells Acute tubular necrosis (ATN) o Postrenal Causes: mechanical obstruction in the outflow of urine. • Benign prostatic hyperplasia • Prostate cancer • Calculi • Trauma • Extrarenal tumors

What is Diabetes Ketoacidosis (DKA)?

Profound deficiency of insulin Characterized by Hyperglycemia Ketosis Acidosis Dehydration Occurs in type 1 diabetes Precipitating factors Illness Infection Inadequate insulin dosage Undiagnosed type 1 diabetes Poor self-management of DM There are the teenagers who want to be like everyone else. They don't want to take insulin like they are supposed to or take their blood sugar over and over again. They don't want to manage it.

What are the classification of aki?

RIFLE Classification o Risk (R) o Injury (I) o Failure (F) o Loss (L) o End-stage kidney disease (E)

What is acute kidney injury (AKI)?

Rapid loss of kidney function • Rise in serum creatinine level and/or a reduction in urine output • Develops over hours or days o Progressive elevations of BUN, creatinine, and potassium. o May or may not have a reduction in urine output. o Follows severe prolonged hypotension or hypovolemia

What is syndrome of Inappropriate Antidiuretic hormone (SIADH)?

Regulates OUTPUT Anti-diuretic hormone (ADH): retention of water in the blood and decreased urine output Synthesized by the hypothalamus from posterior pituitary ADH stimulated when hypothalamus is signaled by the osmoreceptors, and by baroreceptors in the large blood vessels Primary stimulus is an increase in osmolality Permits reabsorption of water from tubular fluid into the blood Abnormally high production or sustained secretion of ADH. Overproduction or over secretion of ADH resulting in SIADH A disorder of the posterior pituitary gland ADH is released despite normal or low plasma osmolarity.

What is the treatment for prehospital care?

Remove person from source of burn and stop burning process • Rescuer must be protected from becoming part of incident • Electrical injuries o Remove patient from contact with source • Chemical injuries o Brush solid particles off skin o Use water lavage • Small thermal burns o Cover with clean, cool, tap water—dampened towel • Large thermal burns o Airway, breathing, and circulation o Do not immerse in cool water or pack with ice o Remove burned clothing o Wrap in clean, dry sheet or blanket • Inhalation injury o Observe for signs of respiratory distress o Treat quickly and efficiently o 100% humidified oxygen if CO poisoning is suspected

What are electrical burns?

Result from coagulation necrosis caused by intense heat generated from an electric current • May result from direct damage to nerves and vessels, causing tissue anoxia and death • Severity of injury depends on o Amount of voltage o Tissue resistance o Current pathways o Surface area o Duration of the flow • Current that passes through vital organs will produce more life-threatening sequelae than current that passes through other tissue • Electrical sparks may ignite patient's clothing, causing a combination of thermal flash injury • Severity of injury can be difficult to assess, as most damage occurs beneath skin o "Iceberg effect" • Electrical current may cause muscle spasms strong enough to fracture bones • Patients are at risk for dysrhythmias or cardiac arrest, severe metabolic acidosis, and myoglobinuria • Myoglobin and hemoglobin from damaged RBCs travel to kidneys o Acute tubular necrosis (ATN) o Eventual acute kidney injury

What is chemical burns?

Result of contact with acids, alkalis, and organic compounds • Alkali burns are hard to manage o Cause protein hydrolysis and liquefaction o Damage continues after alkali is neutralized • Results in injuries to o Skin o Eyes o Respiratory system o Liver and kidney • Chemical should be quickly removed from the skin • Clothing containing the chemical should be removed • Tissue destruction may continue up to 72 hours after chemical injury

What is chronic SIADH and its management?

Self-management Fluid restriction: 800-1000mL/day Medication: demeclocycline (Declomycin) Blocks the effect of ADH on the renal tubules resulting in more dilute urine Preventing thirst Limit salt intake such as not having chips with salt Low sodium diet Ice chips Watch for exercising Keep themselves cool Sodium and potassium supplements Concentrated sodium salts Patient can swallow them Patient education Look at labs - BUN and creatinine

What are the foot complications?

Sensory neuropathy loss of protective sensation (LOPS), unawareness of injury Monofilament screening Peripheral artery disease Decreased blood flow Decreased wound healing Increased risk for infection Diabetic Foot Ulcer Patient teaching: prevent foot ulcers Proper footwear Avoidance of foot injury Skin and nail care The podiatrist If they are going to get their nails done, they need to take their own equipment Daily inspection of feet Prompt treatment of small problems Diligent wound care for foot ulcers Neuropathic arthropathy (Charcot's foot) It curves out and deforms

What are the lab values for HF?

Serum chemistries, cardiac markers, BNP or NT-proBNP level (see Table 32-6), liver function tests, thyroid function tests, CBC, lipid profile, kidney function tests, urinalysis B-Type Naturetic Peptide (BNP) Normal: 0-100 pg/mL Above 100 to 300 BNP - indicate heart failure Above 300 pg/ml - mild heart failure Above 600 pg/ml - moderate heart failure Above 900 pg/mL - severe heart failure

What are the compensatory mechanisms of HF?

Sympathetic nervous system (SNS) activation First mechanism triggered in low CO states Least effective compensatory mechanism - inadequate SV and CO Results in increased release of catecholamines (epinephrine and norepinephrine) Increase HR Initially it improves CO but over time its harmful because it increase the failing heat's workload and need for oxygen Increase myocardial contractility Peripheral vasoconstriction Vasoconstrictions causes immediate increase in preload cause an increase in CO. At the same time, an increase in venous return to heart which is volume overloaded and worsens ventricular performance Neurohormonal responses As CO falls, sensed by juxtaglomerular apparatus in the kidneys as the blood volume decrease - Initiate the RAA pathway RAA System: Renin converts angiotensinogen to angiotensin I then convert to angiotensin II (by converting enzyme made in lungs). Angiotensin II caused 1) adrenal to release aldosterone - retain sodium and water 2) peripheral vasoconstriction which increases BP Decrease Cerebral perfusion pressure Posterior pituitary gland secretes ADH (antidiuretic hormone, also known as vasopressin) Increase water reabsorption in kidneys causing water retention Blood volume is increase Production of endothelin - potent vasoconstrictor by vascular endothelial cells Stimulated by ADH, catecholamines and angiotensin II Increase cardiac contractility and hypertrophy and arterial vasoconstriction Inflammatory process Locally, cytokines are released by heart cells in response to cardiac injury Two cytokines, TNF and IL-1 depress heart function by causing hypertrophy, contractile dysfunction and cell death Later, systemic inflammatory response occurs All of these factors lead to increased cardiac workload, myocardial dysfunction and ventricular remodeling Hypertrophy of ventricular myocytes Large, abnormally shaped contractile cells Increased mass, increased wall tension, increased O2 consumption and impaired contractility Leading to less effective pumps Ventricular dilation Enlargement of chambers of heart Stretch in response to the volume of blood in the heart at the end of diastole Frank Starling Law - degree of stretch is directly related to the force of contraction (systole) Initially leads to increase CO, maintenance of BP and perfusion but becomes inadequate due to overstretching of muscle fibers and cannot contract effectively which leads to decreased CO Ventricular hypertrophy Increase in muscle mass and cardiac wall thickness Becomes poor contractility Requires more oxygen to work Has poor coronary artery circulation (ischemia) Dysrhythmias

What is Immune thrombocytopenia Purpura (ITP) ?

Thrombocytopenia • Autoimmune disease • Platelet count less than 150,000/mm • More common in women • Affects adults between ages 20 and 50 years

What are the causes of hypoglycemia?

Too much insulin or oral hypoglycemic agents Little food intake A delay in eating Extreme exercise Symptoms can also occur when high glucose level falls too rapidly

What are the diagnostic studies for TB?

Tuberculin Skin Test (TST) • Mantoux test • Purified protein derivative (PPD) injected intradermally • Assess for induration in 48 - 72 hours • Presence of induration (not redness) at injection site indicates development of antibodies secondary to exposure to TB. • A waning immune response can cause false negative results. • Repeating TST may boost reaction. • Two-step testing recommended for health care workers getting repeated testing and those with decreased response to allergens • Two-step testing ensures future positive results accurately interpreted Bacteriologic • Required for diagnosis • Sputum samples obtained (usually) on 2-3 consecutive days • Stained sputum smears examined for acid-fast bacilli • Culture results can take up to 8 weeks. • Can also examine samples from other suspected TB sites

What is the rule of nines?

Two commonly used guides for determining the total body surface area o Lund-Browder chart Considered more accurate o Rule of Nines (look in book) Used for initial assessment

What are the diagnostic studies for DI?

Very low specific gravity: less than 1.005 mOsm/Kg Urine osmolality: less than 100 mOsm/kg Serum osmolality is elevated: greater than 295 mOsm/Kg Looking at solutes per particles of volume of water Water deprivation test Patient is deprived of water for 8-12 hours Give desmopressin acetate (DDAVP) Patient's urine will start to concentrate and will see the yellow color. Then the waste products come out and less amount of urine - start to come down Patients with Central DI exhibits a dramatic increase in urine osmolality from 100 to 600 mOsm/kg and significant decrease in urine volume Patients with nephrogenic DI will not be able to increase urine osmolality to greater than 300 mOsm/kg

Type 1 Vs Type 2

You need to give them Dextrose when the blood glucose level gets below 250 because you don't want their sugar down too low. Just slowly bring down their sugar level but not too down due to cerebral issue if too low

What are the diagnostic studies and contraindicated diagnostic studies of AKI?

o History o Serum creatinine levels o Urinalysis o Kidney US o Renal scan o CT scan o Renal biopsy • Contraindicated: o Magnetic resonance imaging (MRI) o Magnetic resonance angiography (MRA) with gadolinium contrast medium Nephrogenic systemic fibrosis Contrast-induced nephropathy (CIN)

What are the nursing management of AKI?

o VS, I & O o Daily weights o Examine urine o Assess general appearance o Neurological assessment o Pulmonary assessment o Cardiovascular assessment o Laboratory and diagnostic tests o Assess dialysis access site o Patient education Protein and potassium intake Follow-up care

What is the nursing intervention for acute thyrotoxicosis?

o History and physical o Monitor lab values: T3 and T4 o Chest-X-Ray: enlarged heart o Medications to block thyroid hormone production and SNS o Monitor for dysrhythmias o Adequate oxygenation o Fluid and electrolyte replacement o Adequate rest Calm, quiet room Cool room Light bed coverings o If exophthalmos present Apply artificial tears to relieve eye discomfort Salt restriction and elevate head of bed Dark glasses Tape eyelids closed if needed for sleep ROM of intraocular muscles

What are the diagnostic studies of hypothyroidism?

o History and physical examination o TSH and free T4 TSH increased with primary hypothyroidism TSH decreased with secondary hypothyroidism o Thyroid antibodies Autoimmune origin o Increased Cholesterol o Increased Triglycerides o Increased Creatine kinase o Decreased RBCs (anemia)

What are the nursing intervention for pre-operative care?

o Administer medications to achieve euthyroidism o Administer iodine to decrease vascularization of the thyroid gland o Assess for signs of iodine toxicity o Patient teaching Comfort and safety measures Leg exercises, head support, neck ROM Routine postoperative care

What is the etiology and pathophysiology of Grave's Disease?

o Antibodies to TSH receptor stimulate release of triiodothyronine (T3), thyroxine (T4), or both Leads to clinical manifestations of thyrotoxicosis o Remissions and exacerbations o May progress to destruction of thyroid tissue o Autoimmune disease Diffuse thyroid enlargement Excessive thyroid hormone secretion o Precipitating factors interact with genetic factors o Cigarette smoking increases risk

What is hemodialysis Vascular access?

o Arteriovenous fistulas (AVFs) Anastomosis between an artery and vein Bruit and thrill o Arteriovenous grafts (AVGs) Synthetic material forms anastomosis between arterial and venous blood supplies Steal syndrome: shunted arterial blood o Temporary vascular access Long-termed cuff catheters Upper chest wall o Dialyzers Long plastic cartridges that contain thousands of parallel hollow tubes or fibers Fibers are semipermeable membranes Blood is pumped into the top of the cartridge and is dispersed into all of the fibers Dialysate is pumped into the bottom of the cartridge and washes the outside of the fibers with dialysis fluid.

What are the collaborative care and nursing intervention of Cirrhosis?

o Ascites Sodium restriction, diuretics, and fluid removal Diuretics: spironolactone (Aldactone) Paracentesis: needle aspiration o Hepatic encephalopathy Reduce ammonia levels Administer lactulose o Esophageal and gastric varices Bleeding: stabilize patient, manage airway Vasopressin: causes vasoconstriction of the splanchnic artery, decreasing portal blood flow and portal hypertension Balloon tamponade: mechanical compression of varices Sengstaken-Blakemore Tube Transjugular intrahepatic portosystemic shunt (TIPS) o Acute bleed Fresh frozen plasma Packed RBCs Vitamin K o Acute intervention Assess for jaundice Measures to relieve pruritus Monitor color of urine and stools Monitor lab values Monitor for bleeding from esophageal varices o Ambulatory and home care Supportive measures Proper diet Rest Avoid hepatotoxic OTC drugs No alcohol

What are the clinical manifestations of Cushing Syndrome?

o Centripetal (truncal)/generalized obesity o Moon facies with plethora o Purplish red striae o Hirsutism o Menstrual disorders o Hypertension o Hypokalemia o Excess glucocorticoids Weight gain from accumulation of adipose tissue Hyperglycemia related to glucose intolerance and increased gluconeogenesis Muscle wasting leading to weakness Loss of bone matrix leading to osteoporosis and back pain Loss of collagen → thin skin, easily bruises Delay in wound healing o Mineralocorticoid excess → hypertension o Adrenal androgen excess Severe acne Virilization in women: male characteristics in women Feminization in men: female characteristics in men

What are the collaborative care and Nursing Interventions for Addison's Disease?

o Correct underlying cause o Hormone therapy Hydrocortisone (most common) • Increase dose during periods of stress Fludrocortisone (Florinef) • Mineralocorticoid replacement • Administered daily o Increase dietary salt intake - saltines o Acute intervention Frequent assessment Vital signs Laboratory values: electrolyte imbalance Monitor mental status and weight Medication history Monitor for signs of Cushing syndrome Protect against infection Assist with daily hygiene Protect from extremes • Light • Noise • Temperature o Patient teaching Dosing • Glucocorticoids in divided doses • Mineralocorticoids once in the morning • Reflects normal circadian rhythm • Decreases side effects of corticosteroids o Signs and symptoms of corticosteroid deficiency and excess o Wear medical ID bracelet o Patient teaching o Emergency kit o How to administer IM hydrocortisone o Written instructions

What are the diagnostic studies of Addison's Disease?

o Decreased Serum and urinary cortisol o ACTH levels Increased in primary adrenal insufficiency Decreased in secondary adrenal insufficiency o ACTH stimulation test Distinguishes between primary and secondary disease o Decreased urinary cortisol and aldosterone o Increased potassium o Decreased Chloride, sodium, glucose o Anemia o Increased BUN/creat o ECG changes o CT scan, MRI - dysthymias

What are the diagnostic studies for Thyrotoxicosis?

o Decreased TSH and Increased free thyroxine (free T4) o Total T3 and T4 o Radioactive iodine uptake (RAIU) Differentiates Graves' disease from other forms of thyroiditis Treatment of choice in nonpregnant adults Damages or destroys thyroid tissue Delayed response of 2 to 3 months Treated with antithyroid drugs and β-blocker before and during first 3 months of RAI Given on outpatient basis Patient teaching Oral care Dryness and irritation of the mouth and throat. Radiation precautions Private toilet facilities Separate linens Food preparation Symptoms of hypothyroidism

What are the principles of DIalysis?

o Diffusion Solutes from an area of higher concentration to an area of lower concentration o Osmosis Fluid from an area of lower concentration of solutes to area of higher concentration o Ultrafiltration Water and fluid removal Results when there is an osmotic gradient across the membrane

What are the contraindications of kidney transplantation?

o Disseminated malignancies o Untreated cardiac disease o Chronic respiratory failure o Extensive vascular disease o Chronic infection o Unresolved psychosocial disorders

What are the collaborative and nursing interventions?

o Drug therapy Hyperkalemia • IV insulin • IV glucose to manage hypoglycemia • IV 10% calcium gluconate Sodium polystyrene sulfonate (Kayexalate) • Cation-exchange resin • Resin in bowel exchanges potassium for sodium o Manage HTN Antihypertensive drugs: diuretics, CCB, ACE inhibitors, ARBs o Diabetics BP: 130/80 mm HG o CKD BP: 125/75 mmHg o CKD-MBD Phosphate not restricted until patient requires RRT Phosphate intake restricted to less than 1000 mg/day • Phosphate binders o Calcium acetate (PhosLo): binds phosphate in bowel for excretion o Sevelamer hydrochloride (Renagel): lowers cholesterol and LDL levels o Anemia Decreased erythropoietin production Epoetin alfa (Epogen, Procrit) • Administered IV or subcutaneously • Increased in H/H in 2 to 3 weeks • Side effect: hypertension o Nutritional Therapy Protein restriction Phosphate restriction • Foods high in phosphate: meats, dairy Water restriction • Intake depends on daily urine output Sodium restriction • 2 to 4 g, depends on degree of edema & HTN • Salt substitutes: contain potassium Potassium restriction • Limit: 2 to 3 g, avoid high-potassium foods o Daily weight o Daily BPs o Monitor for hypernatremia hyperkalemia o Strict dietary adherence o Medication teaching o Self-care management

What are the collaborative care for AKI?

o Ensure adequate intravascular volume and cardiac output Loop diuretics: Lasix Osmotic diuretics: mannitol o Closely monitor fluid intake during oliguric phase Fluid restriction o Hyperkalemia Insulin Sodium bicarbonate Calcium gluconate Sodium polystyrene sulfonate (Kayexalate) o Renal replacement therapy (RRT) Peritoneal dialysis (PD) Hemodialysis (HD) Continuous renal replacement therapy (CRRT) o Nutritional therapy Adequate caloric intake Sodium restriction Increase dietary fat Enteral nutrition

What is the nutritional therapy for hyperthyroidism?

o High-calorie diet (4000 to 5000 cal/day) Six full meals/day with snacks in between Protein intake: 1 to 2 g/kg ideal body weight Increased carbohydrate intake o Avoid highly seasoned and high-fiber foods, and caffeine o Nutritional consult

What are the collaborative care and nursing interventions for hypothyroidism?

o Levothyroxine (Synthroid) Start with low dose Monitor for cardiovascular side effects (chest pain, dysrhythmias), weight loss, nervousness, tremors, insomnia Increase dose in 4- to 6-week intervals as needed Lifelong therapy • History and physical • VS, weight, I&O, edema • Myxedema coma necessitates acute care o Mechanical respiratory support o Cardiac monitoring o IV thyroid hormone replacement o Monitoring of core temperature • Skin care • Cardiovascular response to hormone • Energy level and mental alertness • Patient teaching o Need for lifelong therapy o Thyroid medicine in morning on empty stomach o Side effects of Synthroid Tremors Nervousness, irritability, insomnia Menstrual cycle changes Sensitivity to heat o S/S of hypothyroidism and hyperthyroidism • Patient Teaching o Regular follow-up care o Do not switch brands o Comfortable, warm environment o Measures to prevent skin breakdown o Emphasize need for warm environment

What is the nursing management?

o Live donor Care is similar to that for open or laparoscopic nephrectomy Close monitoring of renal function Close monitoring of hematocrit Donors have more pain than their recipients o Recipient Maintenance of fluid and electrolyte balance is first priority Large volumes of urine soon after transplanted kidney placed R/T: • New kidney's ability to filter BUN • Abundance of fluids during operation • Initial renal tubular dysfunction o Maintain ideal body weight o Acceptance of chronic disease o No infection o No edema o Monitor laboratory values Hematocrit, hemoglobin, and serum albumin levels • Immunosuppressive Therapy o Adequately suppress the immune response o Maintain sufficient immunity to prevent overwhelming infection

What are diagnostic studies for Cirrhosis?

o Liver enzyme tests Initially increase: Alkaline phosphatase, AST, ALT, and γ-glutamyl transpeptidase (GGT) They are released from damaged liver cells o Liver US: severity of cirrhosis. o Liver biopsy: liver cell changes \

What are the post-op care nursing interventions?

o Monitor for complications Hypocalcemia: inadvertent removal of parathyroid glands • Trousseau's and Chvostek's signs Hemorrhage Maintain patent airway • Monitor for laryngeal stridor: result of edema of the laryngeal nerve. • IV calcium for tetany Thyrotoxic crisis Infection o Assess every 2 hours during first 24 hours for signs of hemorrhage or tracheal compression o Semi-Fowler's position o Support head with pillows o Avoid neck flexion and tension on suture line o Patient teaching Monitor hormone levels Decrease caloric intake Adequate but not excessive iodine intake Regular exercise Avoid increased environmental temperatures Complete thyroidectomy • S/S of hypothyroidism • Lifelong hormone replacement

What are the complications of hypothyroidism?

o Myxedema coma Impaired consciousness Precipitated by infection, drugs, cold, trauma Subnormal temperature, hypotension, hypoventilation Cardiovascular collapse • Hypoventilation, hyponatremia, hypoglycemia, and lactic acidosis. Treat with IV thyroid hormone

What are the collaborative care and nursing interventions of Cushing syndrome?

o Normalize hormone secretion o Treatment depends on cause Surgical removal or irradiation of pituitary adenoma Adrenalectomy for adrenal tumors or hyperplasia Removal of ACTH-secreting tumors o If cause is iatrogenic Gradually discontinue therapy Decrease dose Convert to an alternate-day regimen o Dose must be tapered gradually Avoid adrenal insufficiency o History and physical o Laboratory values o Health promotion o Identify at risk patients o VS, daily weight o Glucose - risk for impaired wound healing o S/S of inflammation/infection o S/S of thromboembolism • Preoperative Care o Optimize physical condition o Control hypertension and hyperglycemia o Correct hypokalemia o High-protein diet to correct protein depletion o Dependent on surgery Hypophysectomy Adrenalectomy o What to expect after adrenalectomy NG tube Urinary catheter IV therapy Central venous pressure monitoring Leg sequential compression devices • Postoperative Care (fluids - crystalloid normal saline) o Increased risk of hemorrhage o Large release of hormones into circulation → instabilities in BP, fluid balance, and electrolyte levels o High doses of corticosteroids administered IV during and several days after surgery o Risk for hypertension and subsequent hemorrhage increased o Susceptibility to infection and delayed wound healing also increased o Report any significant changes in vital signs o Monitor fluid intake and output o Administer corticosteroids as ordered o Obtain morning urine samples for cortisol measurement o Monitor for acute adrenal insufficiency Vomiting, increased weakness Dehydration, hypotension Painful joints Pruritus Peeling skin Severe emotional disturbances o Bed rest until BP is stabilized after surgery o Monitoring for subtle signs of infection o Care to prevent infection o Patient teaching Home care referral Medic Alert bracelet Avoid extremes of temperature and stress Lifetime replacement therapy

What are the clinical manifestations of Addison's Disease?

o Not evident until 90% of adrenal cortex is destroyed o Insidious onset Progressive weakness Fatigue Weight loss Anorexia o Orthostatic hypotension o Hyponatremia: crave salt o Hyperkalemia o Nausea, vomiting, diarrhea o Irritability, depression o Addisonian crisis Life threatening, acute adrenal insufficiency Insufficient or sudden, sharp decrease in hormones Causes • Stress • Sudden withdrawal of hormone therapy • Adrenal surgery Shock management High-dose hydrocortisone replacement NaCl 0.9% and Dextrose 5%

What are the clinical manifestations of AKI?

o Oliguric phase Urinary changes • Urinary output less than 400 mL/day • Occurs within 1 to 7 days after injury • Lasts 10 to 14 days • Urinalysis may show casts, RBCs, WBCs Fluid volume • Hypovolemia may exacerbate AKI • With decreased urine output, fluid retention occurs o Neck veins distended, bounding pulse o Edema, hypertension Fluid overload: heart failure, pulmonary edema, and pericardial and pleural effusions Metabolic acidosis • Serum bicarbonate level decreases • Severe acidosis develops o Kussmaul respirations Sodium balance • Increased excretion of sodium • Hyponatremia can lead to cerebral edema Hyperkalemia • ECG changes Hematologic disorders • Leukocytosis Waste product accumulation • Elevated BUN and serum creatinine levels Neurologic disorders • Fatigue and difficulty concentrating • Seizures, stupor, coma o Diuretic phase Daily urine output is 1 to 3 liters May reach 5 L or more Monitor for hyponatremia, hypokalemia, and dehydration o Recovery phase Glomerular filtration rate (GFR) increases BUN and creatinine stabilize and return to normal May take up to 12 months

What are the clinical manifestations of cirrhosis?

o Onset is insidious o Fatigue may be an early symptom o Many patients have no symptoms until late o Later manifestations Jaundice, peripheral edema, ascites Skin, hematologic, endocrine, and neurologic disorders o Jaundice Functional derangement of liver cells Compression of bile ducts by overgrowth of connective tissue Decreased ability of liver cells to conjugate and excrete bilirubin o Spider angiomas: small dilated blood vessels with a red center

What is peritoneal dialysis?

o Peritoneal access: insertion of a catheter through the anterior abdominal wall o After insertion, sterile dressing applied Connected to sterile tubing system Secured to abdomen with tape o Use 7-14 days post placement o 2-4 weeks: site free from redness/ tenderness o May shower once site is healed

What is thyrotoxicosis (Thyrotoxic Crisis)?

o Physiologic effects/clinical syndrome of hypermetabolism o Results from increased circulating levels of T3, T4, or both • Hyperthyroidism and thyrotoxicosis usually occur together "A Thyroid Storm" • Excessive amounts hormones released • Life-threatening emergency • Death rare when treatment initiated • R/T stressors: infection, trauma, surgery • Thyroidectomy patients at risk o Manipulation of the hyperactive thyroid gland results in an increase in hormones released.

What are the diagnostic studies?

o Plasma cortisol measurement Increased levels in Cushings o 24-Hour urine collection for free cortisol o Low-dose dexamethasone suppression test o CT scan o MRI o Plasma ACTH levels High or normal with Cushing disease (pituitary etiology) Low or undetectable with Cushing syndrome o Hypokalemia and alkalosis With ectopic ACTH syndrome and adrenal carcinoma

What are the clinical manifestations of CKD?

o Polyuria Results from inability of kidneys to concentrate urine Specific gravity fixed: 1.010 o Oliguria Occurs as CKD worsens o Anuria Urine output lower than 40 mL/24 hours o Metabolic Disburbances Accumulation of waste products Decreased GFR, and increased BUN and increased creatinine Increased BUN level • Not only from kidney failure but also from protein intake, fever, corticosteroids, and catabolism • N/V, lethargy, fatigue, impaired thought processes, and headaches Altered carbohydrate metabolism • Impaired glucose metabolism o Cellular insensitivity to normal action of insulin Defective carbohydrate metabolism • Diabetics who develop uremia may require less insulin after onset of CKD • Excretion of insulin dependent on kidneys Elevated triglyceride levels • Hyperinsulinemia o Stimulates hepatic production of triglycerides • Altered lipid metabolism o Decreased levels of enzyme lipoprotein lipase Aid in the breakdown of lipoproteins o Electrolyte/Acid-Base Imbalances Potassium • Hyperkalemia: dysrhythmias Sodium • May be elevated, normal, or low • Impaired excretion, sodium is retained Metabolic acidosis • Inability of kidneys to excrete ammonia • Inability of kidneys to reabsorb and regenerate of bicarbonate o Hematologic System Anemia • Decreased production of erythropoietin • Decreased functioning of renal tubular cells Bleeding • Defect in platelet function Infection • Changes in WBC function • Altered immune response and function • Diminished inflammatory response o Cardiovascular HTN, HF, and LVH, peripheral edema, dysrhythmias o Respiratory Kussmaul respirations Dyspnea: R/T fluid overload, pulmonary edema, uremic pleuritis, respiratory infections o Gastrointestinal Mucosal ulcerations N/V, anorexia, and constipation o Neurologic System Attributed to: • Increased nitrogenous waste products • Electrolyte imbalances and metabolic acidosis • Atrophy and demyelination of nerve fibers Muscle twitching and irritability Inability to concentrate Peripheral neuropathy Seizures, coma

What is the Etiology and Pathophysiology of Addison's Disease?

o Primary Addison's disease Lack of glucocorticoids, mineralocorticoids, and androgens o Secondary Lack of pituitary ACTH Lack of glucocorticoids and androgens o Autoimmune response against adrenal cortex o Causes: TB, fungal infections, AIDS, metastatic cancer o Iatrogenic Medications: anticoagulation therapy, and chemotherapy Adrenalectomy

What are the complications of kidney transplantation?

o Rejection Acute or chronic o Infection Wound infections Fungal (Candida) and viral (CMV) o Cardiovascular disease Increased incidence of atherosclerotic vascular disease Immunosuppressants can worsen hypertension and hyperlipidemia o Malignancies Primary cause is immunosuppressive therapy Basal and squamous cell carcinoma of the skin

What are the clinical manifestations of Grave's Disease?

o Related to effect of thyroid hormone excess Increased metabolism Increased tissue sensitivity to stimulation by sympathetic nervous system o Goiter Inspection Auscultation: bruits o Ophthalmopathy Abnormal eye appearance or function o Exophthalmos Increased fat deposits and fluid Eyeballs forced outward o Cardiovascular system Systolic hypertension Bounding, rapid pulse, palpitations Dysrhythmias: atrial fibrillation • Respiratory system o Increased respiratory rate o Dyspnea on mild exertion • GI system o Increased appetite, thirst o Weight loss, diarrhea • Musculoskeletal system o Fatigue o Muscle weakness • Integumentary system o Skin: warm, smooth, moist o Nails: thin, brittle o Hair: fine, silky, premature graying o Clubbing of fingers o Diaphoresis o Vitiligo • Nervous system o Nervousness, fine tremors o Insomnia, exhaustion o Mood changes o Hyperreflexia of tendon reflexes o Inability to concentrate o Stupor, coma

What are the types of Dialysis?

o Renal Replacement Therapy (RRT) Peritoneal dialysis (PD): Peritoneal membrane acts as the semipermeable membrane Hemodialysis (HD): Artificial membrane is used as the semipermeable membrane and is in contact with the patient's blood https://youtu.be/M3lFgtcOml0

What are the stages of the CKD?

o Stage 1 Kidney damage with normal or elevated GFR o Stage 2 Kidney damage with mild decrease GFR o Stage 3 Moderate decrease GFR o Stage 4 Severe decrease GFR o Stage 5 Kidney failure

What are complications of Cirrhosis?

o Structural changes in the liver that cause compression and destruction of the veins o Portal Hypertension: increased venous pressure in the portal circulation Splenomegaly Collateral veins Ascites Gastric and esophageal varices o Esophageal varices Complex of tortuous veins at lower end of esophagus Very fragile Bleed easily; bleeding can be life-threatening o Ascites Accumulation of serous fluid in peritoneal or abdominal cavity Proteins shift from blood vessels to capillaries Abdominal distention with weight gain o Hepatic encephalopathy Neurotoxic effects of ammonia, abnormal neurotransmission, inflammatory cytokines o Liver unable to convert increased ammonia Ammonia crosses blood-brain barrier o Clinical manifestations Changes in neurologic and mental responsiveness Impaired consciousness and/or inappropriate behavior Sleep disturbances to lethargy to coma Asterixis

What are the clinical manifestations for hypothyroidism?

o Systemic effects characterized by slowing of body processes o Manifestations vary Depends on the severity and the duration of thyroid deficiency, and the patient's age at the onset of the deficiency. o Slow onset o Cardiovascular system Decreased cardiac contractility and CO Angina, MI Anemia, B12, iron, folate deficiencies Increased cholesterol and triglycerides o Respiratory system Low exercise tolerance DOE o Neurologic system Fatigue, lethargy, mood changes Impaired memory, slowed speech o Gastrointestinal system Decreased appetite, nausea & vomiting Weight gain, distended abdomen Constipation o Integumentary system Skin: dry, thick, cold, and pale Nails: thick, and brittle Hair: dry, sparse, coarse Puffy face o Musculoskeletal system Fatigue, weakness Muscle aches and pains

What are the clinical manifestations of Thyrotoxicosis?

o Tachycardia, HF o Shock o Hyperthermia o Restlessness, irritability o Delirium, seizures, coma

What are the diagnostic studies for CKD?

o Urinalysis o Dipstick evaluation of urine o Albumin-to-creatinine ratio o GFR o Renal US o CT scan o Renal biopsy

What are the treatment medication therapy for Thyrotoxicosis?

o Useful in treatment of thyrotoxic states o Not considered curative Antithyroid drugs • Propylthiouracil (PTU) and methimazole (Tapazole) o Inhibit synthesis of thyroid hormone o Improvement in 1 to 2 weeks o Good results in 4 to 8 weeks o Therapy for 6 to 15 months Iodine • Potassium iodine (SSKI) and Lugol's solution o Inhibit synthesis of T3 and T4 and block their release into circulation o Decreases vascularity of thyroid gland o Maximal effect within 1 to 2 weeks o Used before surgery and to treat crisis β-Adrenergic blockers • Propranolol (Inderal) and Atenolol (Tenormin) o Symptomatic relief of thyrotoxicosis o Block effects of sympathetic nervous stimulation o Treat by reducing circulating hormones o Supportive therapy Manage respiratory distress Reduce fever Replace fluids Eliminate or manage initiating stressor

What is hyperthyroidism?

• A sustained increase in synthesis and release of thyroid hormones by thyroid gland o Graves' Disease • Other causes o Goiter o Thyroiditis o Thyroid cancer

What are the clinical manifestations of chronic pancreatitis?

• Abdominal pain o Located in the same areas as in acute pancreatitis o Heavy, gnawing feeling; burning and cramp • Malabsorption with weight loss • Constipation, jaundice, steatorrhea, diabetes mellitus • Complications associated with o Pseudocyst o Bile duct or duodenal obstruction o Pancreatic ascites o Splenic vein thrombosis o Pseudoaneurysm o Pancreatic cancer

What are the clinical manifestation of acute pancreatitis?

• Abdominal pain o Left upper quadrant or midepigastrium o Radiates to the back o Sudden onset: deep, piercing, and continuous o Aggravated by eating, not relieved with vomiting o Starts when lying down • Abdominal tenderness with guarding • Decreased or absent bowel sounds • Crackles • Shock • Abdominal skin discoloration o Grey Turner's spots or sign: bluish flank discoloration o Cullen's sign: bluish periumbilical discoloration

What are the nursing intervention for thrombocytopenia?

• Acute Interventions o Monitor for bleeding Encourage patients to seek prompt treatment for any symptoms of bleeding. Prevent or control hemorrhage. Bleeding usually begins superficially. Any bleeding needs evaluation and treatment. o Avoid IM injections. o If subcutaneous injection is unavoidable, use small-gauge needles and application of pressure or ice packs after. o Teach self-care measures to reduce risks that could cause bleeding. • Lab values: platelet count, coagulation studies, Hgb, and Hct.

What are the collaborative care and nursing interventions for hepatitis?

• Acute and chronic o Well-balanced diet Increased calorie o Vitamin supplements o Rest: degree varies with severity o Avoid alcohol intake and drugs detoxified by the liver o Notification of possible contacts • Drug Therapy o Acute hepatitis A: no specific o Acute hepatitis B: only if severe o Acute hepatitis C Pegylated interferon to reduce progression to chronic infection o Support therapy Antiemetics • Health Promotion: Hepatitis A o Hand washing, sanitation o Vaccination All children at 1 year of age Adults at risk o Infection control measures: isolation not required o Postexposure prophylaxis with vaccine and immune globulin (IG) • Health Promotion: Hepatitis B o Hand washing o At risk populations: health care providers o Immunization Recombivax HB, Engerix-B Three IM injections All children and at-risk adults o Postexposure prophylaxis: vaccine and hepatitis B immune globulin (HBIG) • Health Promotion: Hepatitis C o No vaccine to prevent HCV o General measures to prevent HCV transmission Screening blood, tissue, and organ donors o No postexposure prophylaxis: baseline and follow-up testing • Assess for jaundice • Comfort measures • Adequate nutrition o Small, frequent meals o Measures to stimulate appetite o Adequate fluid intake • Ambulatory and home care o Regular follow-up for at least 1 year after diagnosis o No alcohol o Medication education How to administer interferon Side effects o No blood donation by HBsAg- or HCV-positive patients

What is the pathophysiology for Hepatitis?

• Acute infection o Liver damage: lysis of infected cells o Cholestasis: decrease in bile flow due to impaired secretion by hepatocytes o Liver cells can regenerate in normal form after resolution of infection • Chronic infection can cause fibrosis and progress to cirrhosis • Antigen-antibody complexes activate the immune system • Systemic manifestations o Rash o Angioedema o Arthritis o Fever o Malaise o Vasculitis

What are the complications of hepatitis?

• Acute liver failure • Chronic hepatitis o Some HBV and majority of HCV infections • Cirrhosis • Hepatocellular carcinoma

What is hepatitis B virus (HBV)?

• Acute or chronic disease • Incidence decreased with vaccination • DNA virus transmitted o Perinatally o Percutaneously o Via mucosal exposure to infectious blood, blood products, or other body fluids • At-risk populations o Household contact of chronically infected o Patients undergoing hemodialysis o Health care and public safety workers o Transplant recipients

What is hepatitis C virus (HCV)?

• Acute: asymptomatic • Chronic: liver damage • RNA virus transmitted percutaneously o IV drug use o High-risk sexual behaviors o Occupational exposure o Blood transfusions before 1992

What is the etiology of acute pancreatitis?

• Gallstones • Chronic alcohol intake • Smoking • Increased triglyceride levels o Biliary sludge: mix of cholesterol crystals and calcium salts • Less common causes o Drugs: corticosteroids, thiazide diuretics o Metabolic disorders: hyperparathyroidism, renal failure o Vascular diseases

What is kidney transplantation?

• Advantages of kidney transplantation over dialysis o Reverses many of the pathophysiologic changes associated with renal failure o Eliminates dependence on dialysis o Less expensive than dialysis after the first year • Candidate selection o By medical and psychosocial factors that vary among transplant centers • Preemptive transplantation (before dialysis is required) is possible if the recipient has a living donor

What is the drug therapy for TB Active Disease?

• Aggressive treatment • Two phases of treatment o Initial (8 weeks) o Continuation (18 weeks) • Four-drug regimen o Isoniazid (INH) o Rifampin (Rifadin) o Pyrazinamide (PZA) o Ethambutol

How to manage DIC?

• Alleviate underlying cause • Maintain organ perfusion and prevent end-organ damage • Administer IVFs, inotropic agents, PRBCs, FFP, platelets • Heparin • Recombinant activated protein C: acts as a anticoagulant

What is premature ventricular contractions (PVC)?

• Arise from ectopic focus from ventricle • Causes: stimulants, electrolyte imbalances, hypoxia, heart disease • Not harmful with normal heart but CO reduction, angina, and HF in diseased heart • Treatment o Treat the underlying cause o Antidysrhythmics

What is first degree AV block?

• Associated with MI and Ischemia • Drugs: Beta blockers, CCB • Typically not serious • Patients asymptomatic • No treatment • PR interval greater than .20

What is ventricular fibrillation?

• Associated with MI, ischemia, disease states, procedures • Unresponsive, pulseless, and apneic • If not treated rapidly, death will result • Treatment: o CPR and ACLS (advanced cardiovascular life support) o Defibrillation o Drug therapy: epinephrine (push IV), vasopressin

What is the health promotion of HIV?

• Avoid risky behaviors • Culturally sensitive, language- appropriate • Age-specific information • Behavior change counseling • Safe sex • Drug use • Perinatal transmission • Decreasing work related exposure Antiretroviral Therapy (ART) • ART can significantly slow disease progression • Individualized • Start therapy as soon as possible • To avoid burnout and nonadherence, treatment is recommended when immune suppression is great. • Nucleotide Reverse Transcriptase Inhibitors (NRTI) o Zidovudine (Retrovir, AZT): insert a piece of DNA into the developing HIV DNA chain, blocking further development of the chain • Protease inhibitors o Lopinavir with ritonavir (Kaletra): interfere with activity of enzyme protease

What is metabolic alkalosis?

• Base bicarbonate excess caused by • Prolonged vomiting or gastric suction (vomiting HCl (acid) all the base is left need to measure) • Gain of HCO3- • Compensatory mechanisms • Renal excretion of HCO3- • Decreased respiratory rate to increase plasma CO2 (limited) • Clinical manifestations • Dizziness • Light-headedness • Tachycardia • Tetany, tremors, tingling • Muscle cramps • Seizures • Hypoventilation

What is Anemia?

• Blood loss • Abnormal or inadequate production of RBCs • Destruction of RBCs • Acute anemia o Abrupt reduction of RBCs o Reduced production of erythropoietin

What is the clinical manifestations of symptomatic infection?

• CD4+ T cells drop to 200 to 500 cells/μL. o Viral load increases. • Symptoms become worse o Persistent fever o Frequent drenching night sweats o Chronic diarrhea o Recurrent headaches o Severe fatigue • Shingles • Persistent vaginal candidal infections • Herpes • Bacterial infections • Kaposi Sarcoma

What is respiratory alkalosis?

• Carbonic acid deficit caused by • Hypoxemia from acute pulmonary disorders • Hyperventilation: anxiety • Compensation • Rarely occurs when acute • Can buffer with bicarbonate shift • Renal compensation if chronic • Clinical Manifestations (assess pulse Ox before giving O2) • Dizziness • Light-headedness • Confusion • Tachycardia • Nausea, vomiting • Tetany, numbness, hyperreflexia • Hyperventilation (purse lip breathing)

What is respiratory acidosis?

• Carbonic acid excess caused by: • Hypoventilation (normal 12-20) • Respiratory failure • COPD • Compensation • Kidneys conserve HCO3- and secrete H+ into urine

What is the pathophysiology of acute pancreatitis?

• Caused by autodigestion of pancreas o Injury to pancreatic cells o Activation of pancreatic enzymes • Activation of trypsinogen to trypsin within the pancreas leads to bleeding

What is the etiology and pathophysiology of Cushing Syndrome?

• Caused by excess of corticosteroids • Iatrogenic administration of exogenous corticosteroids (Prednosine) • Adrenocorticotropic hormone (ACTH) secreting pituitary adenoma • Adrenal tumors • Ectopic ACTH production by tumors

What is synchronized cardioversion?

• Choice of therapy for ventricular (VT with a pulse) or supraventricular tachydysrhythmias • Synchronized circuit delivers a countershock on the R wave of the QRS complex • Procedure similar to defibrillation except sync button turned ON • If patient stable, sedate prior • Initial energy lower o 70-75 joules (biphasic) o 100 joules (monophasic) o If patient becomes pulseless, turn sync button off and defibrillate

What are the clinical manifestations for Hepatitis?

• Classified as acute and chronic phases • Many patients: asymptomatic • Symptoms intermittent or ongoing o Malaise o Fatigue o Myalgias (muscle pain) o Arthalgias (joint pain) o Hepatomegaly • Acute Phase o Lasts 1-4 months: patient is most infective o Symptoms during incubation Malaise Anorexia and weight loss Fatigue Nausea/vomiting Abdominal discomfort o Physical examination findings Hepatomegaly Lymphadenopathy Splenomegaly o Jaundice Dark urine Light or clay-colored stools Pruritus • Convalescent Phase o Begins as jaundice is disappearing o Last 2 to 4 months o Major complaints Malaise Fatigue o Hepatomegaly persists o Splenomegaly subsides • Recovery o Immunity to HAV or HBV o Patient can be re-infected with other types of viral hepatitis, as well as different strains of HCV o Most patients recover completely with no complications

What is sickle cell disease (SCD)?

• Group of inherited, autosomal recessive disorders o Characterized by the presence of an abnormal form of Hgb in the RBC o Genetic disorder usually identified in infancy or early childhood

What is HIV?

• HIV is a retrovirus that causes immunosuppression. • Transmitted through contact with body fluids o Blood, semen, vaginal secretions, and breast milk o Sexual contact with an infected partner

What are Pacemaker?

• Components o Pulse Generator: contains the o Pacemaker source and circuitry o Pacing Leads: wires o Electrode Tip: can be unipolar or bipolar o Can stimulate atrium, ventricle or both • For dual chamber the leads are placed in both chambers usually on the right side of the heart • Impulse is seen as a spike on the EKG • Depending on the position of the electrode the spike will appear in different locations • Atrium: spike followed by P Wave and the baseline QRS and T Wave. P Wave may look different from normal P Waves • Ventricle: Spike is followed by QRS and T Wave • Both: Spike than P Wave, Spike then QRS Transvenous Pacemakers • Vein-Subclavian or internal jugular, when inserted at bedside or non-surgical environment • Inserted under fluoroscopy suite or beside: lead wires are advanced through catheter into right ventricle or atrium and connected to pulse generator Epicardial Pacemakers • When undergoing cardiac surgery • Surgeon attaches the tips of the wires to surface of heart, then brings the wires through the chest wall and attaches to pulse generator and is removed several days after surgery Transcutaneous (External) Pacemakers • Non-invasive • One electrode is placed on the anterior chest wall and the other is placed on the back • External pulse generator emits pacing impulse through the skin to the heart muscle • Used in emergency until Transvenous (Inserted) or permanent pacer can be placed • Most alert patient can't tolerate the irritable sensation produced by prolonged pacing Pacemakers • ECG monitoring for malfunction • Failure to sense o Causes inappropriate firing o Firing at will, not sensing persons internal heart best • Failure to capture o Lack of pacing when needed leads to bradycardia or asystole o Pacemaker below 60 indicates something if wrong, notify doctor • ECG monitoring for malfunction • Failure to sense o Causes inappropriate firing • Failure to capture o Lack of pacing when needed leads to bradycardia or asystole

What is the collaborative and nursing care of acute pancreatitis?

• Conservative Therapy o Aggressive hydration o Pain management IV morphine o Management of metabolic complications Oxygen, glucose levels o Minimizing pancreatic stimulation NPO status, NG suction, decreased acid secretion, enteral nutrition if needed • Drug therapy o Antispasmodics: decrease vagal stimulation, motility, pancreatic outflow o Carbonic anhydrase inhibitors: decrease volume and bicarbonate concentration of pancreatic secretion o Antacids: neutralization of gastric hydrochloric (HCl) acid secretion o Proton pump inhibitors: decrease HCl acid secretion • Nutritional therapy o NPO status initially o Enteral versus parenteral nutrition o Monitor triglycerides if IV lipids given o Small, frequent feedings when able High-carbohydrate o No alcohol o Supplemental fat-soluble vitamins • Acute intervention o Monitor fluid and electrolyte balance o Chloride, sodium, and potassium o Hypocalcemia Tetany: calcium gluconate o Hypomagnesemia o Position for comfort with frequent position changes Flex trunk and draw knees to abdomen Side-lying with head of bed elevated 45 degrees o Frequent oral/nasal care o Proper administration of antacids • Ambulatory and home care o Dietary teaching Low-fat, high-carbohydrate No crash diets o Patient/family teaching Signs of infection, diabetes mellitus, steatorrhea Medications/diet

How is HIV transmitted?

• Contact with blood and blood products o IV drug-use o Blood products o Work-related: needle sticks • Perinatal transmission o During pregnancy, delivery, or breastfeeding • HIV-infected individuals can transmit HIV to others within a few days after becoming infected. • Include (1) duration and frequency of contact with the organism; (2) volume, virulence, and concentration of the organism; and (3) host immune status.

What is the etiology of chronic pancreatitis?

• Continuous, prolonged inflammatory, and fibrosing process of the pancreas o Alcohol, gallstones, tumor, pseudocysts, trauma, systemic disease o Acute pancreatitis o Idiopathic

What is the pathophysiology of DIC?

• Damage to the endothelium • Extrinsic pathway, release tissue factor • Intrinsic pathway leads to a secondary surge in thrombin formation • Excessive thrombin formation o Rapid consumption of coagulation factors and depletion of regulatory substances, protein C, Protein and antithrombin • Thrombin continue to form along damaged vessel walls

What is Disseminated Intravascular Coagulation (DIC)?

• Damage to the endothelium, resulting in activation of the coagulation mechanism • Characterized by bleeding and thrombosis, both which result from depletion of clotting factors, platelets and RBCs • Acute: acute illness • Chronic: malignancy

What is atrial fibrillation?

• Disorganization of atrial electrical activity • Rate: o Atrial: 350 to 600 o Ventricular: varies • P Waves: not discernible • PRI: not measurable • QRS: greater than 0.12 second • T Wave: none • Causes of Atrial Fibrillation o Mitral Regurgitation o Digoxin toxicity o Mitral Stenosis o Hyperthyroidism o Infection o CAD o Acute MI • Treatment of Atrial Fibrillation (controlled flutter 60-100, uncontrolled >101) o Drugs to control ventricular rate and/or convert to sinus rhythm Carzidem - calcium channel blocker, 1:1 concentration, slow push Amiodarone o Cardioversion - smaller amount of joules and electricity o Anticoagulation o Radiofrequency ablation o Maze procedure with cryoablation

What are the clinical manifestations of respiratory acidosis?

• Drowsiness • Confusion. Dizziness, seizures • Hypotension • Flushed skin • hypoventilation

What is Cirrhosis?

• Etiology and Pathophysiology o Progressive liver disease: degeneration and destruction of liver cells o Most common chronic hepatitis C and alcohol-induced liver disease Protein malnutrition Environmental factors Chronic inflammation and cell necrosis

How to interpret ABG?

• Evaluate pH (if pH is w/in normal limits its compensated, if it's not its uncompensated) • Analyze PaCO2 • Analyze HCO3- • Determine if CO2 or HCO3- matches the alteration • Decide if the body is attempting to compensate

What is metabolic acidosis?

• Excess carbonic acid or base bicarbonate deficit caused by • Diabetic ketoacidosis • Lactic acid accumulation (shock) • Severe diarrhea • Renal failure • Compensatory mechanisms • Increased CO2 excretion by lungs • Kussmaul respirations • Kidneys excrete acid • Anion gap (not tested on) • The difference between the cations and anions in ECF • Na+ - (Cl + HCO3) • Normal: 10-14 mmol/L • Increased with acid gain in metabolic acidosis • Normal if loss of bicarbonate • Clinical Manifestations • Drowsiness • Confusion • Dizziness • Hypotension • Nausea, vomiting, diarrhea • Deep rapid respirations

What is the clinical manifestations of acute infection?

• Flulike symptoms o Fever, swollen lymph glands, sore throat, headache, malaise, nausea, muscle and joint pain o Occurs about 2 to 4 weeks after infection o Lasts for 1 to 2 weeks

What are the diagnostic findings for DIC?

• Four basic characteristics of the syndrome o Increased coagulant activity Increased PT, aPTT, INR Decrease in platelet count and Fibrinogen o Increased fibrinolytic activity Levels of by-products increase D-dimer o Impaired regulatory function Decreased inhibitory factors: Protein C, factor V and antithrombin III o End-organ failure Results in occlusion of vessels and tissue ischemia

What is the donation process of kidney transplantation?

• Histocompatibility Studies o Human leukocyte antigen HLA-antigens o Purpose of testing is to identify the HLA antigens for both donors and potential recipients • Donor Sources o Deceased donors with compatible blood type o Blood relatives o Related living donors o Altruistic living donors o Paired organ donation • Live Donor Surgical Procedure o Nephrectomy Performed by a urologist or transplant surgeon Begins 1 or 2 hours before the recipient's surgery is started Rib may need to be removed for adequate view Takes about 3 hours o Laparoscopic donor nephrectomy Most common approach for live kidney procurement • Recipient o Before incision Urinary catheter placed into bladder Antibiotic solution instilled Distends the bladder Decreases risk of infection Crescent-shaped incision o Donor artery anastomosed to recipient internal/external iliac artery o Donor vein anastomosed to recipient external iliac vein o When anastomoses complete, clamps released and blood flow reestablished o Urine may begin to flow, or diuretic may be given o Surgery takes 3 to 4 hours

What is the nursing care for TB?

• History and physical o Productive cough, sputum collection o Night sweats o Weight loss o Pleuritic chest pain • Acute Intervention o Airborne isolation o Single-occupancy room with 6-12 airflow exchanges/hour o Health care workers wear high-efficiency particulate air (HEPA) masks o Immediate medical workup o Appropriate drug therapy • Teach patient to prevent spread. o Cover nose and mouth with tissue when coughing, sneezing, or producing sputum o Hand washing after handling sputum-soiled tissues • Patient wears mask if outside of negative-pressure room. • Identify and screen close contacts. • Ambulatory and Home Care o Can go home if cultures positive o Monthly sputum cultures o Teach patient how to minimize exposure to others o Ensure that patient can adhere to treatment o Notify health department o Teach symptoms of recurrence o Instruct about factors that could reactivate TB o Smoking cessation

What is the nursing care for HIV?

• History and physical • Medications: compliance • Functional health patterns: healthy lifestyle • Beneficial relationships • Spiritual well-being • Coping mechanisms

What are the collaborative care for TB?

• Hospitalization not necessary for most patients • Infectious for first 2 weeks after starting treatment if sputum + • Drug therapy used to prevent or treat active disease • Need to monitor compliance

What are the collaborative and nursing care for SCD?

• Hospitalized patients in sickle cell crisis o O2 for hypoxia and to control sickling o Vigilance for respiratory failure o Rest with DVT prophylaxis o Administration of fluids and electrolytes o Transfusion therapy Chelation therapy with repeat exacerbations Removal of iron • Patient and caregiver teaching and support are important. o How to avoid crises o Importance of prompt medical attention o Pain control o Resources for care and support Therapy Counseling & support groups

What are the complications of hemodialysis?

• Hypotension • Muscle cramps • Loss of blood

What is the clinical manifestation of Acquired Immunodeficiency Syndrome (AIDS)?

• Immune system severely compromised • Opportunistic infections o Cryptococcal meningitis o Cytomegalovirus retinitis o Tuberculosis • Malignancies • Wasting • Dementia

What is third degree AV heart block (Complete Heart Block)?

• Impulses from atria are completely blocked at the AV Node and can't be conducted to the ventricles • Rhythms: atrial and ventricular regular • Ventricle: regular rate can originate from either: o AV Node: heart rate 40-60 beats/min OR o Purkinjie Fibers: rate of 20-40 beats/min • P Waves: are independent over a strip of QRS complexes, atria maintains a constant beat • Causes: Anterior and Inferior Wall MI, • Results in decreased CO • Can lead to syncope, HF, shock • Medical emergency, HR in 20s can result in MI • Treat with pacemaker

What is diastolic heart failure?

• Inability of ventricles to relax and fill • HF with normal EF • Decreased filling of ventricles results in decreased stroke volume and CO • High filling pressures due to stiff ventricles • Results in venous engorgement in pulmonary and systemic vascular systems • LV hypertrophy • Part of left sided heart failure • Inadequate relaxation or stiffening of left ventricle Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO Heart failure with normal EF Result of left ventricular hypertrophy from hypertension, MI, valve disease, or cardiomyopathy

What are the complications for SCD?

• Infection is a major cause of morbidity and mortality. o The function of the spleen becomes compromised from sickled RBCs. Autosplenectomy is a result of scarring: spleen becomes small because of repeated scarring o Pneumococcal pneumonia most common o Severe infections can cause aplastic crisis. Can lead to shutdown of RBC production • Acute chest syndrome o Pulmonary complications that include pneumonia, tissue infarction, and fat embolism o Characterized by fever, chest pain, cough, pulmonary infiltrates, and dyspnea

What is hepatitis?

• Inflammation of the liver • Causes o Viral o Drugs (alcohol) o Chemicals o Autoimmune diseases o Metabolic abnormalities

What are the clinical manifestations of thrombocytopenia?

• Integumentary o Petechial hemorrhage of lower extremities, ecchymoses, gigival bleeding, spontaneous nose bleeds • Neurologic o Sudden severe HA, N&V, seizures, focal neurological deficits, decreased LOC • Renal o Hematuria • Gastrointestinal o Hematemesis (vomiting), melena, hematochezia (bright red colored stools) • Other o Heavy menses, retinal hemorrhage • Laboratory o Decreased platelet count, often <50,000mm3

What is the clinical manifestations of TB?

• LTBI - asymptomatic o Pulmonary TB o Takes 2-3 weeks to develop symptoms. o Initial dry cough that becomes productive o Fatigue, malaise, anorexia, weight loss, low-grade fever, night sweats o Dyspnea and hemoptysis late symptoms • Can also present more acutely o High fever o Chills, generalized flulike symptoms o Pleuritic pain o Productive cough o Adventitious breath sounds • Extrapulmonary TB manifestations dependent on organs infected

What is left sided heart failure?

• LV dysfunction • Blood back up into left atrium and pulmonary veins • Increase pulmonary pressure cause fluid leakage from pulmonary capillary bed into interstitial and alveoli • Pulmonary congestion and edema Most common form Results from left ventricular dysfunction Blood backs up into left atrium and pulmonary veins Increased pulmonary pressure causes fluid leakage → pulmonary congestion and edema - fluid in the lungs Patient feel like they are drowning - panic stricken

What is systolic heart failure?

• LV loses ability to generate enough pressure to eject blood • Inability to pump blood due to impaired contractile function, increased afterload, cardiomyopathy and mechanical abnormalities • LV is dilated and hypertrophied • Decrease in LV EF (ejection fraction) - less than 45% • Part of left sided heart failure Pulmonary and systemic congestion Inability to pump blood forward Caused by: Impaired contractile function Increased afterload Cardiomyopathy Mechanical abnormalities Decreased left ventricular ejection fraction (EF)

What is the diagnostic studies for acute pancreatitis?

• Laboratory tests o Liver panel: amylase and lipase o Triglyceride o Glucose o Bilirubin o Calcium • Abdominal ultrasonography • X-ray • Contrast-enhanced CT scan • Endoscopic retrograde cholangiopancreatography (ERCP) o Endoscope down the esophagus, through the stomach, and into the duodenal papilla (opening of the pancreatic duct)

What is the diagnostic studies for chronic pancreatitis?

• Laboratory tests o Serum amylase/lipase levels May be slightly increased or not at all o Increased serum bilirubin level o Increased alkaline phosphatase level o Mild leukocytosis o Increased sedimentation rate: monitors inflammation in the body • Endoscopic retrograde cholangiopancreatography (ERCP): treat problems of the bile and pancreatic ducts • CT, MRI • Stool samples for fat content • Glucose intolerance/diabetes • Secretin stimulation test

What are the drug therapies?

• Latent TB infection o Usually treated with INH for 6 to 9 months o HIV patients should take INH for 9 months. o Alternative: 3-month regimen of INH and rifapentine OR 4 months of rifampin • Vaccine o Bacille Calmette-Guérin (BCG) vaccine to prevent TB is currently in use in many parts of the world. o Can result in positive PPD reaction o Select individuals

What is second degree AV block Type 2 (Mobitz II)?

• Less common than Type I but more serious • When 2 or more atrial beats are blocked • P Waves: more than complexes • Decreased ventricular rate • Treatment: pacemaker

What is the clinical manifestations of asymptomatic infection?

• Median interval of 10 years between infection and diagnosis of AIDS o Fatigue, headache, low-grade fever, and night sweats o Most are not aware of their infection

What are the clinical manifestations of Anemia?

• Mild Anemia o Tachycardia, angina, dysrhythmias o Hypotension, orthostasis o DOE, tachypnea o Fatigue, weakness o Pallor, dusky nailbeds • Severe Anemia o Decreased oxygen delivery to tissues o Anaerobic metabolism o Lactate production o MI o Ischemic Stroke

What are the collaborative care for thrombocytopenia?

• Mild cases: corticosteroids • Lift-threatening hemorrhage o IV immunoglobulin: suppress platelet destroying antibody response o Methlyprednisolone (Solu-Medral): blocks inflammatory response • Platelet transfusion • Splenectomy: if patient do not respond to other treatments • Therapy initiated if platelets ↓ 30,000/μL • Corticosteroids o Suppress phagocytic response of splenic macrophages resulting in increased life span of the platelets. o Depress antibody formation. o Reduce capillary leakage. • High doses of IV immunoglobulin (IVIG) and anti-Rho(D) o Compete with antiplatelet antibodies for macrophage receptors in the spleen • Rituximab o Lyse activated B cells therapy o Reduces the immune recognition of platelets • Platelet transfusions o Used to increase platelet counts in life-threatening hemorrhage o Never used prophylactically because of antibody formation o Indicated for platelet count < 10,000/μL or if bleeding is anticipated before a procedure

What is the collaborative care for HIV?

• Monitor disease progression, immune function, and manage symptoms • Initiate and monitor ART • Prevent and/or treat opportunistic infections • Prevent further transmission of HIV

What is the nursing care of Acid-Base imbalance?

• Monitor for desired therapeutic effects • Monitor for adverse effects • CV and Respiratory assessment • Vital signs (always for change in status)* and time • Allen's test - occlude both wrist, change in color • Laboratory test • Electrolytes • Arterial blood gases

What is dialysis?

• Movement of fluid/molecules across a semipermeable membrane from one compartment to another • Indication: o Remove waste products o Fluid/electrolyte imbalances o Metabolic acidosis o Elevated BUN: >120mg/dL • Begun when patient's uremia can no longer be adequately managed conservatively o Initiated when GFR is less than 15 mL/min • ESKD treated with dialysis because: o Lack of donated organs o Physically or mentally unsuitability for transplant o Transplant refusal

What is directly observed therapy (DOT)?

• Noncompliance is major factor in multidrug resistance and treatment failures. • Requires watching patient swallow drugs • Preferred strategy to ensure adherence • May be administered by public health nurses at clinic site

What are the causes of thrombocytopenia?

• Occurs following a: o Viral infection o Pregnancy o Administration of certain medications Heparin, thiazide diuretics, chemotherapeutic agents o Malignancies o Splenomegaly o Blood transfusion o Alcoholism • Four mechanisms o Decreased platelet production o Increased platelet destruction o Splenic sequestration of platelets o Platelet dilution

What are the collaborative and nursing care for chronic pancreatitis?

• Pain medication: morphine • Diet o Bland, low-fat, small, frequent meals o Decrease pancreatic stimulation • No smoking • No alcohol or caffeine • Pancreatic enzyme replacement: replace the deficient pancreatic enzymes. • Bile salts: facilitate the absorption of the fat-soluble vitamins (A, D, E, and K) and prevent further fat loss. • Insulin or oral hypoglycemic agents • Acid-neutralizing and acid-inhibiting drugs • Antidepressants: reduce neuropathic pain • Surgery o Indicated when biliary disease is present or if obstruction or pseudocyst develops o Diverts bile flow or relieves ductal obstruction o Choledochojejunostomy o Roux-en-Y pancreatojejunostomy • Patient and family teaching o Dietary control o Pancreatic enzyme with meals/snack o Observe for steatorrhea o Antacids after meals and at bedtime o No alcohol

What is Sickle cell crisis?

• Severe, painful, acute exacerbation of sickling causes a vaso-occlusive crisis. • Severe capillary hypoxia eventually leads to tissue necrosis. • Life-threatening shock is a result of severe O2 depletion of the tissues and a reduction of the circulating fluid volume.

What is the pathophysiology and etiology of hypothyroidism?

• Pathophysiology o Deficiency of thyroid hormone o Primary hypothyroidism Caused by destruction of thyroid tissue or defective hormone synthesis o Secondary hypothyroidism Caused by pituitary or hypothalamic dysfunction • Decreased TSH or • Decreased thyrotropin-releasing hormone (TRH) • Etiology o Iodine deficiency o Atrophy of the gland: Graves disease o Treatment for hyperthyroidism o Cretinism if occurs in infancy Thyroid hormone deficiencies during fetal or early neonatal development

What are the diagnostic studies for SCD?

• Peripheral blood smear • Sickling test • Electrophoresis of hemoglobin: identify the different types of hemoglobin • Skeletal x-rays: bone and joint deformities deep vein thrombosis • Doppler studies: deep vein thrombosis

What is the pathophysiology of Thrombocytopenia?

• Platelets are coated with antibodies • Reach the spleen, and are recognized and a foreign body and are destroyed by macrophages. • Insufficient platelets result in disruption of normal coagulation pathway • Bleeding results

What is chronic kidney disease (CKD)?

• Progressive, irreversible loss of kidney function o Kidney damage o Pathologic abnormalities o Low glomerular filtration rate (GFR) <60 mL/min for 3 months or longer o Disease staging based on decrease in GFR Normal GFR: 125 mL/min • Reflected by urine creatinine clearance End-stage kidney disease (ESKD): • GFR <15 mL/min

What are the lab studies in DIC?

• Prothrombin time (PT) >12.5 sec • Platelets <50,000 mm3, or at least a 50% drop from baseline • Activated partial thromboplastin time (aPTT) >40 sec • D-dimer >250 mg/ml • Fibrin degradation products (FDP) >40ug/ml • Fibrinogen <100 mg/dl

What are the complications of acute pancreatitis?

• Pseudocyst o Fluid, enzyme, debris, and exudates surrounded by wall o Abdominal pain, palpable mass, nausea/vomiting, anorexia o Detected with imaging o Resolves spontaneously or may perforate and cause peritonitis o Surgical or endoscopic drainage • Pancreatic abscess o Collection of pus o Results from extensive necrosis of the pancreas o May perforate o Upper abdominal pain, mass, high fever, leukocytosis o Surgical drainage • Systemic complications o Respiratory Pleural effusion Atelectasis Pneumonia ARDS o Hypotension o Hypocalcemia: tetany

What is right sided heart failure?

• RV fail to contract • Backup fo blood into right atrium and then venous contraction • JVD • Heptomegal • Splenomegaly • Vascular congestion of GI (ascites) • Peripheral edema • Caused by LS-HR • Cor pulmonale (right ventricular dilation and hypertrophy caused by pulmonary disease) Inadequate right ventricle output and systemic venous congestion Right ventricular dysfunction Blood backs up into the right atrium and venous circulation Jugular venous distention Hepatomegaly, splenomegaly - ascites formation Vascular congestion of GI tract Peripheral edema Most commonly caused by left-sided HF

What is hepatitis A virus (HAV)?

• Ranges from mild to acute liver failure • Not a chronic infection • Incidence decreased with vaccination • RNA virus transmitted via fecal-oral route • Contaminated food or drinking water

What are the nursing care for anemia?

• Restore and maintain hemostasis o Blood administration remember that negative O is the universal donor! • Improve oxygen delivery o Supplemental oxygen • Identify and treat underlying disease states o Iron, vitamin deficiency • Minimize blood loss o Daily blood draws o Prophylactic ulcer medication

What is sinus tachycardia?

• Rhythm: regular • Rate: greater then 100 beats/min • P Wave: round, smooth, upright, may increase in amplitude or superimposed on the T Wave and difficulty to identify • PRI: normal • QRS: normal, increased amplitude • T Wave: normal • Q-T interval: shortened Causes of Sinus Tachycardia • Normal Response: exercise, pain, stress fever, fear anxiety • Cardiac: CHF, Cardiogenic Shock, pericarditis • Compensating: Shock, anemia, respiratory distress, PE, Sepsis • Drugs: caffeine, Epinephrine, Atropine, Amphetamines Sinus Tachycardia: Clinical Manifestations • Hypotension • Chest pain, palpitations • Fever • Exercise • Hypovolemia • Hypoxia • Nervousness and anxiety Treatment of Sinus Tachycardia • Asymptomatic: No treatment. • Treat underlying cause • Symptomatic: Prolonged-give meds to lower heart rate: • Beta Blockers: Lopressor, Tenormin (atenolol)

What is sinus bradycardia?

• Rhythm: regular • Rate: less than 60 beats/min • P Wave: round, smooth, upright • PRI: normal • QRS: normal • T Wave: normal • Q-T interval: normal Causes of Sinus Bradycardia • Vagal Stimulation: Decreased sympathetic stimulation, sleep, deep relaxation, Valsalva's Maneuver. • Cardiac Disease: SA Node disease, Cardiomyopathy, Myocarditis, MI, heart block • Drugs: Beta Blockers, Digitalis, Calcium Channel Blockers Sinus Bradycardia: Clinical Manifestations • Hypotension • Dizziness • Cool clammy skin • Altered mental status • Blurred vision • Angina • Syncope Treatment of Sinus Bradycardia • Asymptomatic: don't treat • Symptomatic: Atropine 0.5-1mg rapid IVP with a total of 3mg followed by flush normal saline in syringe • Dopamine • Epinephrine • Transcutaneous pacer • Chronic: permanent pacer

What are the clinical manifestations of DIC?

• S/S Related to Hemorrhage o Bleeding from gums, venipunctures &surgical sites o Hemoptysis o Hematuria o GI bleed, gastric ulcers o Subarachnoid hemorrhage • S/S related to Thrombi o Peripheral cyanosis, gangrene o Dysrhythmias, CP, Acute MI, PE, respiratory failure o Oliguria, acute tubular necrosis, renal failure o Diarrhea, constipation, bowel infarct o Altered LOC, ischemic stroke

What is atrial flutter?

• Sawtooth waves that originate from an ectopic area in the right atrium • Symptoms result from high ventricular rate and loss of atrial "kick" → decreased CO → heart failure • Characteristics o Atrial rate 200-350 beats/minute o Ventricular rate: 180 beats/minute • Rhythm Atrial and ventricle can be regular or irregular • P Waves: none, Flutter Waves • PRI: not measurable • QRS Complex: 0.10 second • T Wave: can't indentify • Treatment o Pharmacologic agent Calcium channel blockers Beta blockers o Electrical cardioversion o Radiofrequency ablation

What are the causes of DIC?

• Sepsis • Metabolic acidosis and hypoperfusion associated with shock syndromes • Tissue factor activation • Massive trauma or burns • Obstetric emergencies

What are the diagnostic studies for hepatitis?

• Specific antigen and/or antibody for each type of viral hepatitis • Liver function tests: elevated • Serum and urinary bilirubin: elevated • Liver biopsy • FibroScan: assess liver stiffness • FibroSure (FibroTest): biomarker that tests the degree of liver damage

What is the etiology and pathophysiology of Tuberculosis (TB)?

• Spread via airborne droplets • Can be suspended in air for minutes to hours • Transmission requires close, frequent, or prolonged exposure. • Not spread by touching, sharing food utensils, kissing, or other physical contact • Once inhaled, particles lodge in bronchiole and alveolus. • Local inflammatory reaction occurs. • Ghon focus: lesion that develops into granuloma • Infection walled off and further spread stopped Classification • Primary infection o When bacteria are inhaled • Latent TB infection (LTBI) o Infected but no active disease • Active TB disease o Primary TB o Reactivation TB (post-primary)

What are the complications of TB?

• TB pneumonia o Large amounts of bacilli discharged from granulomas into lung or lymph nodes o Manifests as bacterial pneumonia

What are sickling episodes?

• The major pathophysiologic event of this disease o Abnormal hemoglobin, HgbS, causes the RBC to stiffen and elongate (sickle shape) o Triggered by low oxygen tension in the blood o Infection is the most common precipitating factor. o Initially, sickling is reversible with re-oxygenation.

What is the pathophysiology of chronic pancreatitis?

• Two major types o Chronic obstructive pancreatitis Gallstones cause inflammation of sphincter of Oddi o Chronic nonobstructive pancreatitis Inflammation and sclerosis in head of pancreas and around duct

What is second degree AV block, Type 1 (Mobitz I, Wenckebach)

• Type I AV block is usually a result of myocardial ischemia or inferior MI. • Each successive impulse from the SA Node is delayed slightly longer than the previous one • Causes o CAD o Rheumatic fever o Vagal stimulation - bare down • Treat if symptomatic o Atropine o Pacemaker • If asymptomatic, monitor closely Saying is longer,longer,longer,drop, now you have a wenckebach

What are the clinical manifestations for SCD?

• Typical patient is asymptomatic except during sickling episodes. o Symptoms may include o Pain from tissue hypoxia and damage o Pallor of mucous membranes o Jaundice from hemolysis Prone to gallstones

What is ventricular tachycardia (start compression)?

• Ventricular rate is 150 to 250 beats/minute. • AV dissociation may be present, with P waves occurring independently of the QRS complex. • The QRS complex is distorted in appearance and wide (greater than 0.12 second in duration). • The T wave is in the opposite direction of the QRS complex. • Causes: heart disease, electrolyte imbalances, drugs, CNS disorder • Can be stable (patient has a pulse) or unstable (pulseless) • Sustained VT causes severe decrease in CO • Clinical Manifestations: o Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest • Precipitating causes must be identified and treated (e.g., hypoxia) • VT with pulse (stable) treated with antidysrhythmics or cardioversion • Pulseless VT treated with CPR and rapid defibrillation

What is the pathophysiology of HIV?

• Virus attaches to CD4 Receptor on T4-lymphocytes (Helper) • HIV proteins fuse with the receptor site and inputs its genetic material àsingle RNA strand • RNA converts to DNA by viral enzyme reverse transcriptase and incorporates itself into the host cell • Becomes a part of the genetic structure of the cell and replicates. • Leave host cell and enter the blood stream • Protease: viral enzyme slices some of the proteins of the helper cells • Virus infects other T4 lymphocytes • Immune problems start when CD4+ T-cell counts drop to < 500 cells/μL. o Severe problems develop when < 200 CD4+ T cells/μL. o Normal range is 800 to 1200 cells/μL. • Opportunistic infections

What are the arterial blood gas values?

• pH 7.35-7.45 • pCO2 35-45 • HCO3 22-26 • O2 95-100