ATI MEDSURG PROCTORED UPDATED AND VERIFIED GUIDE TO 'A' GRADE

ATI MEDSURG PROCTORED UPDATED AND VERIFIED GUIDE TO 'A' GRADE 1. Understand the ABG’s and how to decide if a patient is in resp acidosis or resp alkalosis, metabolic acidosis, or metabolic alkalosis. 2. Understand the function of potassium, sodium, and calcium in the body- especially the heart and how to administer these electrolytes. Be able to correct the calcium using the calculation. - Sodium: Na - Normal value: 135-145 - Hyponatremia <135 - Common imbalance in the elderly caused by Na loss or water gain - Symptoms: decrease BP, poor skin turgor, headache, nausea, cramps - If seizure occurs: small infusion of 3%-5% NaCl SLOWLY - Hypernatremia >145 - Sodium gain or water loss - Problem with elderly/pts who can’t sense thirst or don’t meet fluid needs - Symptoms: increase in temp, dry swollen tongue, neuro symptoms/changes=FIRST sign usually - Potassium: K - Normal value: 3.5-5.0 - K+ necessary for normal cardiac rhythms, necessary for skeletal and smooth muscle contraction, K+ helps make glycogen deposit in the liver - K imbalances can be life threatening - Hyperkalemia >5.0 - Manifestations: cardiac changes & dysrhythmias, ECG shows tented T waves, arrhythmias, muscle weakness, GI cramps - Management: Give diuretics to excrete K+, 10 units regular insulin IV push with glucose (1 amp D50), Beta-2 agonist (albuterol MDI), Kayexalate (ion-exchange resin) - Hypokalemia <3.5 - Manifestations: fatigue, dysrhythmias, DTRs, constipations, muscle weakness, anorexia, ECG changes: flat T waves or inverted T waves or both, suggesting ischemia, and depressed ST segments - Med Management: increase PO of K+, give KCL supplements when patient is on loop or thiazide diuretics to prevent hypokalemia - KCl should be administered IV at rate of 10-20 mEq/L per hour → rapid infusion can cause CARDIAC ARREST - Hold KCl unless urine output is at least 0.5 ml/kg of body weight per hour - Calcium: Ca - Normal Value: 9-11 - Ca++ works as an enzyme co-factor for clotting and hormone secretion. Stored in parathyroid glands, maintains plasma membrane stability-particularly in the cardiac cell nerve receptors, aids in the transmission of nerve impulses and contraction of muscles - Corrected Calcium: - Measured total serum Ca++ level (mg/dl) = 0.8 x (4.0 – measured albumin level [g/dL]) = corrected total calcium concentration (mg/dL) - Pt’s serum calcium level is reported as 7.5 mg/dL and serum albumin is 2.5 g/dL. - 4.0 – 2.5 = 1.5 g/dL (albumin difference) - 1.5 x 0.8 = 1.2 - 1.2 + 7.5 = 8.7 mg/dL (corrected calcium) - Hypocalcemia: <9 - Manifestations: - Tetany- paresthesias of nose, ears, fingertips that progresses to painful muscle spasms and convulsions; Positive Chvostek’s sign- cheek twitch; Positive Trousseau’s sign- carpal spasm of hand- with BP cuff inflation; Hyperreflexia; Laryngospasm; Arrhythmias- VF, torsades de pointes, Long QT, ↓ Cardiac contractility and ↓ blood pressure, Hypomagnesemia - trousseau’s chvostek’s - Meds: Emergency Management: - Administer Calcium Gluconate or Calcium Chloride by slow IV push (0.5-1.0 ml/min) - Maximum rate for intermittent infusion is 200 mg/min. - For Non-Acute Hypocalcemia: - Give Calcium Carbonate PO with Vitamin D to help with absorption of Ca++ in the GI tract - May need to give Magnesium if serum levels are low - Hypercalcemia: >11 - Levels >12= coma ; <14=death - Causes: increase Vitamin D and A, hyperparathyroidism, metastatic cancer to bone - Manifestations: fatigue/weakness, constipation, dehydration, ECG changes= decreased heart rate, heart blocks, shortened QT interval and depressed T Wave; kidney stones - Med Management: IV fluids followed with loop diuretics (lasix) → increase hydration (IV fluids) to ml/day to flush Ca++ and to ↓ calculi formation, synthetic Calcitonin can be given to lower Ca++ levels, IV calcitonin-promotes renal excretion of Ca, antiemetics for nausea, IV biphosphates to reduce bone resorption - Magnesium: - Hypomagnesium Mg+ < 1.5 mEq/L - Causes: - Alcoholism - Hemodialysis - Poor dietary intake - Poor absorption of by GI tract - Excessive Mg+ loss from GI tract (diarrhea) - Kidney disease(primary aldosteronism, DKA, hyperparathyroidism) - Sepsis, burns, some wounds - S/Sx: - Neuromuscular: muscle weakness, respiratory muscle paralysis, hyperactive DTRs - CV: Complete heart block (EKG changes), tachycardia - CNS: Altered LOC, confusion, hallucinations - GI: Dysphagia, anorexia, nausea, vomiting - Tx: - Dietary replacement - Oral supplements - IM or IV supplementation—SLOWLY - Hypermagnesium Mg+ > 1.5 mEq/L - Causes: - Renal insufficiency - Continuous infusions of Mg+ as used with seizures, pregnancy-induced HTN, preterm labor - S/Sx: - Decreased muscle and nerve activity - Hypoactive DTRs - Generalized weakness, lethargy, flaccid, paralysis - Nausea & vomiting - Shallow, depressed respiratory system - Hypotension - Sedation - ECG changes - Cardiac arrest - Tx: - Fluids up, Mg+ level down - Increased fluid intake raises urine output to rid of excess Mg+ - Dialysis - Phosphorus: - Hypophosphatemia - - Hyperphosphatemia - → Functions of electrolytes in the heart: CONDUCTION ● Phase 4: resting membrane potential associated with diastole ● Phase 0: rapid depolarization; rapid influx of Na+ into cell through fast channels ● Phase 1: movement of K+ and Cl- ions out of cell ● Phase 2: movement of Ca++ into cell and movement of K+ out of cell ● Phase 3: rapid repolarization; electrolytes return to normal location either in or out of cell; membrane potential returns to normal ● 3. Know the differences between angina and an MI and what the interventions are for a patient who is positive for an MI. - Angina: myocardial ischemia - Reversible cell injury - ST depression - Relieved by rest, nitrates - No N/V - MI: myocardial death and necrosis - Non Reversible cell injury - ST elevation - Not relieved by rest, nitrates - N/V 4. What are the cardiac markers (labs) for a patient having an MI? - Lab Analysis of an MI - Cardiac markers: proteins are released into blood in large quantities from necrotic heart muscle - Myoglobin - CK – MB bands - Troponin T-myocardial muscle proteins - Troponin I-myocardial muscle proteins 5. What is the current standard of care for a patient having an MI? - Cardiac catheterization labs for reperfusion of blocked coronaries OR - Receive IV fibrinolytic therapy (Streptokinase, Urokinase) to dissolve the clot - Current standard of care is to reperfuse heart via percutaneous coronary intervention or PCI with/without stents 6. What are the signs and symptoms of decompensated heart failure? - Decompensated HF: when compensatory mechanisms fail to maintain CO, do not meet metabolic demands, and can’t maintain adequate tissue perfusion - S/Sx: - Fatigue - DOE - Orthopnea - Paroxysmal nocturnal dyspnea - Tachycardia - Poor activity intolerance - Fluid weight gain - Lower extremity edema - Pulmonary edema - Pulmonary crackles - Nocturia - Skin changes - Chest pain - Cough - Hepatomegaly - Anorexia - Nausea 7. What medications are given for heart failure management? (EX: Beta blockers, ace inhibitors, diuretics, nitrates, etc.) - GOAL - improve symptoms and quality of life, prevent morbidity, prolong survival. - ACE inhibitors - 1st line therapy in all stages of HF - Diuretics- Lasix, HCTZ - Inotropes- Digoxin - B-Adrenergic Blockers - Metoprolol - Calcium channel Blockers - Amlodipine - Vasodilators - Imdur - Antiarrhythmics- Amiodarone - Blood thinners, platelet inhibitors- ASA, Plavix, - Nitrates/ vasodilators - Morphine IV 8. Know the criteria for normal sinus rhythm, atrial fibrillation, ventricular tachycardia and ventricular fibrillation and the treatment for AF, VT, and VF. Recognize the rhythms. - Normal Sinus Rhythm: - There is a P wave in front of every QRS - Distance between P wave and QRS complex is the same in each complex - Distance between R-R waves is the same - Rate is between 60-100 BPM - Rate increases as metabolic demand increases with activity (ex. Exercise) - AFib - Most significant risk of arrhythmia is EMBOLIC STROKE - Longstanding uncontrolled HTN is the single most contributing factor in developing afib - No visible P wave, irregular R-R interval, irregular ventricular rate (110-180 BPM) - Treatment options: Rate VS Rhythm control - Rhythm control – medications to slow down ventricular rate plus anticoagulant med - Rate control – antiarrhythmic plus anticoagulation - BB: Metoprolol - CCB: Verapamil, Diltiazem - Other antiarrhythmics: Amiodarone, Sotalol, Rhythmol, Flecainide - VTach - Rapid, regular heart beat from a site in one of ventricles (wide QRS) - Frequently, the site is an area of scar tissue caused by damage from a heart attack - VT significantly impairs the hearts ability to pump blood - May degenerate to ventricular fib - During VT, HR is much faster 100-280 BPM, minimal CO - VT Symptoms: palpitations, chest tightness, dizziness, SOB, and/or LOC - When a pt loses consciousness, it is a life-threatening emergence and requires immediate cardioversion/defibrillator - 1st thing to do is to ASSESS PT - VFib - Chaotic quivering of the ventricles. Patient has no BP or HR. - Heart is unable to pump blood throughout the body. Cardio-pulmonary arrest! Heart can’t deliver blood to lungs, brain, and other vital organs – no perfusion anywhere - For the patient to be saved without brain damage, circulation must be restored to the vital organs within 6 minutes - When a MI involves the left main artery (widow maker), death by VF is often the result - Treatment: the only way to treat VF is to shock the heart back to normal rhythm with a defibrillator - Defibrillation (1st thing) is the only effective method of terminating VF, should occur within 15-20 seconds of onset of arrhythmia - This includes passage of direct current electrical shock that is sufficient to depolarize the cells of myocardium - The goal is for subsequent repolarization of the myocardial cells to allow the SA node to take over their role in conduction - Defibrillation is most effective when myocardial cells are NOT anoxic or acidotic - 1st recommended energy is 200J, 2nd shock is 300J, 3rd shock is 360J (max) - CPR, endotracheal intubation, airway support are performed - Emergency meds: Epinephrine, Amiodarone, Procainamide, Lidocaine, Atropine, may be used as needed 9. Know the indications for Coumadin therapy and the patient teaching and bleeding precautions that are associated with Coumadin therapy. - Vit K and fresh frozen plasma are given as an anecdote - Huge risk for bleeding and patient has to be screened if risks outweigh the benefits 10. What are the signs and symptoms of acute respiratory failure? - Tachypnea, dyspnea with prolonged expiratory phase - approximately 1:4. - Use of accessory muscles, intercostal retractions, and decreased breath sounds. - Decreased SpO2 < 80%. Patient pauses while speaking to breathe. - Respiratory or Metabolic acidosis per ABG analysis most common. 11. What is the criteria for a diagnosis of ARDS? - A clinical syndrome characterized by: - Sudden and progressive pulmonary edema - Increasing bilateral infiltrates on chest x-ray - Hypoxemia that is unresponsive to oxygen therapy - Reduced lung compliance (elasticity) - These signs occur in the absence of left-sided heart failure - 50-60 % mortality rate 12. What are the cardinal signs of a patient with COPD? How are they managed medically? - Narrowing occurs in the small peripheral airways due to chronic inflammation and the body attempts to repair it (causes scarring) - Airflow limitation is not reversible (progressive and consistent) - Comprised of chronic bronchitis and emphysema - Medical management: - Smoking cessation prevent further damage and slow progression) - Bronchodilators - Long term MDI or nebulizer - Corticosteroids - Inhales & systemic - not for continued use - Do not slow decline in lung function, but will improve symptoms - O2 long term therapy of continuous O2 (1-2L/min) - Increases quality of life and length of survival - BE CAREFUL with O2 therapy - Hypoxemia stimulates respiratory to retain CO2 - Increasing O2 flow to a high rate may rise pts O2 level and suppress resp drive and increase the CO2 - Signs of CO2 necrosis will occur and pt will stop breathing 13. Know the rule of nines in estimating burn percentages on a patient. 14. Know how to use the Parkland formula in determining the amount of fluid replacement a burned patient will need in the first 8 hours and the next 16 hours. - The Parkland Formula helps you calculate the fluid resuscitation for a burn patient or the first 24 hours, fluid replacement is based on the extent of the burn injury. - The Parkland Formula is used: - 4 ml Lactated Ringers x body weight (kg) x percent burn. - ½ total volume given in the first 8 hours - ½ the total volume given over the next 16 hours - Regulate the infusion rate and volume based on weight and response to treatment - Example: 15. Know the goals of cancer therapies (cure, control, palliation), and what to do if a patient has an implanted radiation device that suddenly becomes explanted. - Cure: can we remove it? - Control: can we limit spread? - Palliation: can we keep patient comfortable? - Use long handled forceps to pick up device if implant comes out and place in lead container - do not attempt to put back in patient 16. How is the radiation source handled and what 3 things does the nurse need to remember in dealing with a patient with a radiation implant (in terms of protecting herself)? Know the screening tests for different cancers and when they are given. - Nurse safety: TDS (time, distance, shielding) - Can be by pt 30 mins per shift, must stay 3-6 feet away from patient, lead apron → Screenings: - Breast cancer: - Beginning at age 20, routine monthly self-breast exams. - After age 40, yearly mammograms - Colon and Rectal Cancer: - After age 50: yearly fecal-occult blood test - Digital rectal exam and flexible sigmoidoscopy every 5 years - Colonoscopy every 10 years. (May require more frequently if + family history) - Prostate Cancer: - Beginning at age 50 yearly rectal digital exam - Beginning at age 50 yearly PSA blood test - Cervical/Uterine Cancer: - Yearly Pap smear and pelvic exam for sexually active females and/or over 18 - High risk women should have endometrial tissue biopsy at menopause 17. Know the CAUTION algorithm for warning signs of cancer. - Warning Signs: CAUTIONS C: change in bowel or bladder habits A: a sore that does not heal U: unusual bleeding or discharge T: thickening or lump in breast or elsewhere I: indigestion or difficulty in swallowing O: obvious change in mole or wart N: nagging cough or hoarseness S: sudden and unexplained weight loss 18. Know what the TNM staging for cancer means. - T: the extent of the tumor - N: absence or presence and extent of lymph node - M: absence or presence of metastasis 19. What is the 4 drug regimen for a patient having an anaphylactic reaction? - Epinephrine 1:1000 dilution injection subq with IV infusion of Epinephrine - Antihistamines: Diphenhydramine (Benadryl) 25-50mg IV push - Corticosteroids: Solucorfter or Solumedrol 150 mg IV push - H2 receptor blocker IV: Pepcid or Zantec to prevent stress ulcer 20. What are the signs and symptoms of a patient having an anaphylactic reaction? - Pruritus (itching), rhinitis (stuffy/runny nose), rash, redness, fever, urticaria (hives), localized edema, angioedema 21. How is HIV contracted? - Main route: sexual contact - 2nd direct route is through blood, needles, drug paraphernalia - Transmission in utero, during deliver, through breast milk - Occupational HIV (healthcare workers) – not common 22. What is the current HAART therapy for treating HIV? - 4 regimen drug combo (NRTI, NNRTI, integrase inhibitor, protease inhibitor) - HAART: highly active antiretroviral therapy - Current recommendation: 2 NNRTI’s, an integrase inhibitor and a protease inhibitor 23. What are the clinical manifestations and assessments for patients with the autoimmune diseases SLE and RA? SLE RA Musculoskeletal: 90% joint involvement, similar to RA but no RF and no joint destruction Integumentary: Rashes, “butterfly” rash on nose, cheeks; alopecia, sun sensitivity, mucous membrane lesions Cardiovascular: Pericarditis, ischemic heart disease Pulmonary: Pleural effusion, pneumonitis, PE Renal: Glomerulonephritis, nephrotic syndrome Neurological: 30-75%; vasculitis leads to CVA, seizures, depression, psychiatric complications Hematopoietic: Hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia, lymphadenopathy with lesions on head, scalp, neck Dx: ANA will be positive Tx: Corticosteroids Joint pain, redness and warmth with swollen effusions Lack of joint mobility and function bilaterally Joint instability, contractures Deformities of the hands and feet Fatigue, malaise, anorexia Elevated body temperature Subcutaneous nodules on joints Limited ROM, paresthesias of hands/feet Morning stiffness and crepitus Pericarditis (ask pt to hold breath, no inflammation sound, , sizzle sound), Leukopenia Splenomegaly, Enlarged lymph nodes Fever: low grade <101.5 F Weight loss Fatigue Anemia Lymph node enlargement Peripheral Neuropathy Raynaud’s phenomenon- cold and stress induced vasospasm of the hands and feet giving them a cyanotic (bluish) appearance Dx: positive for Rheumatoid factor 24. What labwork is diagnostic of SLE and RA? - RA Labs: - Serum rheumatoid factor is present in 80 % - Elevated erythrocyte sedimentation rate (ESR) indicates inflammation - C-reactive protein is positive (CRP) indicates inflammation - RBC’s decreased - C4 complement is decreased - Serum Antinuclear antibody (ANA) is positive - Synovial fluid may display a straw-colored fluid with fibrin flecks and the WBC count may be elevated. - X-rays may reveal bone demineralization and soft tissue swelling during early phases. Later may reveal narrowing of joint spaces, destruction of articular cartilage, erosion, and deformity. - SLE Labs: - SLE is an inflammatory disease affects all organs so you want to watch BUN and Cr labs 25. What is the medical and nursing management of SLE and RA? - Medical for RA: - NSAIDS & rest - 1st line - Low dose corticosteroids: Hydroxychloroquine for mild disease - For moderate, Methotrexate and Imuran is prescribed - For severe, biologic therapy is prescribed. Enbrel, Remicade, Kineret and Humira slow progression - Nursing for RA: - Achieve adequate pain control - Decrease fatigue - Promote restorative sleep - Increase mobility - Facilitate and encourage self-care - Improve body-image and coping - Monitor and manage potential complications - Promote home and community-based care/ resources - Balancing periods of activity with rest - Exercise to maintain joint function and mobility - Patient support related to chronic illness - Assistive devices for joint protection - Support groups and other information - Medical for SLE: - Corticosteroids: - Prednisone, low doses, high doses for exacerbations - Anti-malarial medications, for serious forms that don’t respond to conservative therapies - Nursing for SLE: - Decrease fatigue - Increase restorative sleep – important - Providing protection for impaired skin integrity - Sun and ultraviolet light exposure can increase disease activity or cause exacerbation - Facilitating self-care - Improving body-image and coping – because corticosteroid effects on body - Monitoring and managing potential complications- cardiac and renal involvement 26. What is the difference between DM type 1 and DM type 2? - Type I Diabetes: - Affects 5-10% of people with diabetes - Characterized by destruction of pancreatic beta cells - Genetic, immunologic, viral, and possible environmental factors are thought to contribute to beta cell destruction - Beta cell destruction results in: - Unchecked glucose production by the liver - Glucose derived from food cannot be stored in the liver so remains in the bloodstream - Glycosuria occurs when renal threshold (180 mg/dL) is reached - When excessive glucose is excreted in urine, F&E electrolytes will follow – this is called osmotic diuresis - Diabetic ketoacidosis ** - Type II Diabetes: - Decreased sensitivity to insulin (insulin resistance) and impaired beta cell function results in decreased insulin production - 90-95% of persons with diabetes, onset over age 30 years, increasing in children, obesity - Slow, progressive glucose intolerance - Treated initially with diets and exercises - Oral hypoglycemic agents initially may need to convert to insulin or use both 27. What are the clinical manifestations of hyper and hypoglycemia? - Hypoglycemia - More serious bc symptomatic in the CNS below 50-60 - Causes: - Too much insulin/oral hypoglycemic agent - Too little food - Excessive exercise - Symps: - Very confused and body shakes, irritability, lack of coordination - CNS adrenergic symptoms (sweat, tremor, tachycardia, palpitations, nervous, HA, hungry, double vision, drowsiness) - SEVERE: dirorient, seizures, LOC, death - TX: - Dextrose 50%, glucagon, juice - Hyperglycemia - Usually because of dehydration (dry mouth, freq urination, thirst) - Causes: - Lack of insulin= osmotic diuresis occurs! (loss of water, hyperNa, increased osmolarity) - Symptoms: - Hypotension, dehydration, tachycardia, change in mental status 28. What are the microvascular and macrovascular complications of patients with DM? - Macrovascular complications - Accelerated atherosclerotic changes, CAD, cerebrovascular disease, peripheral vascular disease - Microvascular complications - Diabetic retinopathy and neuropathy 29. What is DKA and HHNS? What are the similarities and differences between them and how are they both treated? - HHNS (hyperglycemic hyperosmolar nonketotic syndrome) - Hyperosmolality and hyperglycemia occur due to lack of effective insulin; ketosis: minimal or absent - Hyperglycemia causes osmotic diuresis with loss of water and electrolytes; hypernatremia and increased osmolality occur - Manifestations include hypotension, profound dehydration, tachycardia and variable neurological signs due to cerebral dehydration - Higher mortality than DKA - Treatment of HHNS - 1st – rehydration with IV fluids - Insulin administration - Monitor fluid volume and electrolyte status - Prevention: SMBG, diagnosis/management of diabetes, promote self-care - Diabetic Ketoacidosis (DKA) - Caused by an absence of inadequate amount of insulin resulting in abnormal metabolism of carbohydrate, protein, and fat (anaerobic) - Clinical Features: - Hyperglycemia, Severe Dehydration, Metabolic Acidosis - Manifestations: polyuria, polydipsia, blurred vision, weakness, headache, anorexia, abdominal pain, nausea, vomiting, acetone breath, hyperventilation with Kussmaul respirations, and mental status changes - Treatment of DKA - Rehydration with IV fluids 0.9% NS - IV continuous infusion of regular insulin - Reverse acidosis and restoration of electrolyte balance - Note: rehydration leads to increased plasma volume and decreased K+; insulin enhances the movement of K+ from extracellular fluid into the cells (don’t treat initial hyperkalemia) 30. What are the signs and symptoms of hypothyroidism and hyperthyroidism? - Hypothyroidism - Causes: autoimmune thyroiditis and Hashimoto’s disease (most common) - Manifestations: myxedema (non-pitting edema) may progress to coma, stupor, and death - Treatment: synthetic levothyroxine-replacement therapy: must be taken on an empty stomach and no food after 30 mins of taking the med - Hyperthyroidism - Causes: excessive output of thyroid hormone and Graves disease (most common) - Treatment: slice and dice (take out thyroid), radioactive therapy, Propylthiouracil and Methimazole, sodium and potassium iodine solutions, Dexamethasone, Beta Blockers, or surgery 31. What are the three types of acute renal failure and what causes them? - Prerenal: azotemia caused by hypoperfusion (can be caused by NSAIDs, hypotension, hypovolemia) of the kidney, most common reason patients go into ARF - Volume depletion as a result of: hemorrhage, renal losses: diuretics, osmotic diuresis, GI losses: suctioning - Impaired cardiac function due to: MI, HF, dysrhythmias, shock - Vasodilation resulting from: sepsis, anaphylaxis, vasodilatory medications (antihypertensive) - BP drops for 6 mins so GI, kidneys, livers, etc go into a state of shock - Intrarenal: inside, the renal parenchyma or nephron is damaged. Can be caused from nephrotoxic medications - Prolonged renal ischemia: most common cause is ATN (acute tubular necrosis) - Pigment nephropathy – breakdown of blood cells containing pigments that occluded kidney structures - Myoglobinuria – trauma, crash, injuries, burns - Hemoglobinuria – transfusion reaction, hemolytic anemia - Infectious processes – pyelonephritis, glomerulonephritis - Nephrotoxic agent such as: - Aminoglycosides antibiotics (-cin drugs) - Radiopaque contrast agents used in CAT scans and angiograms - Heavy metals like lead and mercury - Arsenic poisoning - NSAIDs, ACEI - Postrenal: urine outflow is obstructed. Can be by kidney stones which cause hydronephrosis (swelling in the kidney due to increased fluid volume). PBH (benign prostatic hypertrophy) is also a big obstruction in men. - Calculi – renal stones - Tumors - BPH - Urethral strictures - Obstructive blood clots - Renal and bladder tumors - #1 cause is smoking 32. What is the most common cause of chronic renal failure? - Longstanding, uncontrolled hypertension and DM 33. What are the two types of dialysis? - Peritoneal Dialysis: uses a peritoneal membrane - Can be done by patient independently at home. Patient can maintain a fairly normal lifestyle. PD can be done at night while sleeping or the patient can do cycles during the day (about every 4 hours) - 2 types: automated and continuous - Catheter is surgically implanted in abdomen - Peritoneal membrane is used as semipermeable membrane - 2L of dextrose: 1.5%, 2.5%, or 4.5% are infused into the abdominal cavity. Called fill cycle à dwells in cavity. Called dwell cycle à fluid is then drained and weighed to make the same amount is drained as was filled. Called drain cycle à abdomen filled with dialysate - Complications: peritonitis, infection caused by staph aureus or staph epidermidis - Hemodialysis: uses cellulose or synthetic material as semipermeable membrane - Done at a center or in hospital and is done three days a week and takes about 4 hours for each session - Two 14-16 gauge needles are inserted into fistula or graft for access à attached via tubing to dialysis lines using sterile technique à one needle pulls blood into dialyzer machine and other is to return clean blood to patients - A thrill can be felt by palpating the anastomosis and a bruit can be heard with a stethoscope - Strict following of dietary restrictions necessary for optimal management - 34. What are the criteria for a patient to receive a renal transplant? - Need to be exact blood match ** - Criteria to meet: End Stage disease in transplantable organ, Failure of conventional therapy, Absence of untreatable malignancy or irreversible infection, Absence of disease that would attack the transplanted tissue, Ability of patient to survive procedure, Psychosocial characteristics - Absolute contraindications: smoking, drinking, drug use, Age, Active infection, Acute pulmonary embolism, Bleeding disorders, AIDS, Psychopathology, Inability to comply with therapeutic regimen, Inability to understand risks involved, Recent malignancy, Severe damage in another organ - Relative contraindications: Cachexia (less than 80% IBW), HIV, Lack of functioning psychosocial support, Morbid obesity (over 140% IBW), Severe osteoporosis - Cannot be HTN or have any underlying mental conditions 35. What signs of rejection do you want a renal transplant patient to know and monitor themselves for after they go home? - Acute rejection: - Most commonly occurs days to months after transplantation. - Mediated by the recipient’s T cytotoxic lymphocytes which attack the foreign kidney. - Common to have at least one episode of rejection especially with cadaver kidneys. - Usually reversible with increased corticosteroid therapy, cyclosporine, and monoclonal antibodies. - Signs: - Elevated BUN and creatinine - Fever - Weight gain - Decreased urine output-oliguria - Increased blood pressure - Tenderness or swelling over the transplanted kidney - Elevated white blood cell count - Rejection is confirmed by renal biopsy 36. What are the long-term effects of corticosteroids? - Cushing’s disorder and those SE - Moon face, weight gain, buffalo hump, fluid retention (edema) - Glucocorticoids: group of corticosteroids; used with transplant patients - Adrenal Insufficiency - Metabolic: Increased ....................................................................................................................................................DOWNLOAD FOR MORE REVISION GUIDE....................................................................................................