NURS 6202 Exam 1 Questions and Answers

NURS 6202 Exam 1 Questions and Answers UTI risk factors Pregnancy, menopause, habitual delay of urination, instrumentation, sexual intercourse UTI symptoms -Dysuria, frequency, urgency, suprapubic discomfort or pressure -elderly have more vague symptoms- confusion, falls UTI treatment trimethoprim-sulfonamide (TMP-SMX) or nitrofurantoin (Macrodantin) *Antibiotics UTI health promotion Teaching preventive measures- urinating frequently, water, wiping from front to back, urinating after intercourse Cystitis inflammation of the bladder -Sx: urgency, frequency, pain in the bladder/pelvis - Stress management techniques, tricyclic antidepressants and OTCs help with burning pain and urinary frequency; avoid clothing that creates suprapubic pressure Urethritis -inflammation of the urethra -most commonly from an STI -Sx: discharge, dysuria, urgency, and frequency -tx: underlying cause and symptomatic relief Pyelonephritis -inflammation of renal parenchyma and collecting system - most common cause is bacterial infection that begins in the lower urinary tract -Sx: mild fatigue to sudden onset of chills, fever, vomiting, malaise, flank pain, and the lower UTI characteristics -Tx: antibiotics and hydration - teaching: medication, follow up urine culture glomerulonephritis -inflammation of the glomeruli -results from antibody-induced injury -sx: hematuria, and urine excretion of RBC, WBC, proteins - will need extensive lab work -tx: supportive and symptomatic Acute poststreptococcal glomerulonephritis -develops 5 to 21 days after infection -manifestations: generalized body edema, hypertension, oliguria, hematuria with rusty appearance, proteinuria Urinary calculi - Various types: calcium phosphate, calcium oxalate, uric acid, cysteine, struvite -Diet needs: fluid intake, low sodium -Sx: severe abdominal or flank pain, hematuria, renal colic -tx: treating symptoms of pain, infection, or obstruction; lithotripsy stress incontinence -the inability to control the voiding of urine under physical stress such as running, sneezing, laughing, or coughing -mechanical problem -ligaments in pelvis and sphincters become weak -tx: surgical urge incontinence -involuntary leakage of urine with a sudden, strong desire to urinate - can be part psychological (I have to pee right when I get home) - Can go on oxybutynin, anticholinergicsto minimize bladder spasm - can be part of the aging process -tx: bladder training overflow incontinence Involuntary release of urine—due to a weak bladder muscle or to blockage—when the bladder becomes overly full, even though the person feels no urge to urinate Reflex incontinence -occurs when the bladder muscle contracts and urine leaks (often in large amounts) without any warning or urge. -This can happen as a result of damage to the nerves that normally warn the brain that the bladder is filling. Urinary Incontinence management -Adequate volume of fluids and reduction or elimination of bladder irritants from the diet -Voiding regimens, bladder retraining, pelvic floor muscle training -Drug therapy, devices, surgery Urinary retention -Inability to empty the bladder despite micturition -Acute urinary retention is a medical emergency that requires prompt recognition and bladder drainage -Chronic retention may be managed by behavioral methods, catheterization, surgery, or drugs -Scheduled toileting and double voiding benign prostatic hyperplasia (BPH) - prostate gland enlargement caused by hyperplasia of prostate cells -compresses the urethra BPH symptoms -Diminished size and force of urinary stream - difficulty initiating voiding -intermittency -dribbling BPH treatment - Prostate resection or ablation -Transurethral resection of the prostate (TURP) Transurethral resection of the prostate (TURP) -Removal of the prostate tissue using a resectoscope inserted through the urethra -gold standard of treatment continuous bladder irrigation -post op care -irrigating solution is constantly infused and drained from the bladder -urine drainage should be light pink without clots (may need to adjust flow rate) -Monitor for clots Image: continuous bladder irrigation Acute kidney injury causes Dehydration, hypotension, diuretic therapy, aminoglycoside therapy, prostatic hyperplasia, surgery, infection, and contrast media AKI populations at risk -Older adult is more susceptible than the younger adult -Decreased number of functioning nephrons AKI leading cause of death infection -- ascetic technique is critical Prerenal AKI factors (i.e. hypovolemia) that reduce blood flow to the kidney and lead to decreased glomerular perfusion and filtration Intrarenal AKI -conditions that cause direct damage to the renal tissue, resulting in impaired nephron function. -Acute tubular necrosis accounts for most cases of intrarenal failure Postrenal AKI involve mechanical obstruction of urinary outflow. Common causes are prostatic hyperplasia, prostate cancer, calculi, trauma, and extrarenal tumors Phases of AKI Oliguric, diuretic, recovery Oliguric phase -decrease in urine production -hyperkalemia, hyponatremia, hypocalcemia -elevated BUN and creatinine -metabolic acidosis, anemia, and platelet abnormalities Diuretic phase - gradual increase in urine production - nephrons still not fully functional -uremia may still be severe -elevated BUN and creatinine -persistent signs and symptoms Recovery phase -GFR increases -BUn and serum creatinine levels plateau and then decrease -renal function may take 12 months to stabilize Clinical manifestations of AKI -fluid volume overload -metabolic acidosis -elevated potassium with ECG changes -significant change in mental status -pericarditis, pericardial effusion, cardiac tamponade Dietary management of AKI - low K+ diet (40 mEq/day) - fluid restriction -moderate protein intake - low sodium - low phosphorous -dietary fat increased Stages of chronic kidney disease Stage 1: minimal Kidney damage with normal or increased GFR (GFR 90) Stage 2: mild Kidney damage with mild decrease in GFR (GFR 60-89) Stage 3: Moderate damage/decrease (GFR 30-59) Stage 4: Severe damage/decrease (GFR 15-29) Stage 5: kidney failure and End Stage Renal Disease (ESRD) (GFR 15= dialysis) Even though kidneys are failing they can still release renin (increases BP) stages 1-3 are not severe 4 and on needs dialysis Dietary management of CKD Low: Na, K, phosphate, and protein. Add folate supplement 1 mg. Fluid restriction for some patients Electrolyte changes in CKD High: Sodium, potassium, phosphorus Low: Calcium, Vitamin D hemodialysis (HD) -treatment for renal failure using artificial kidney machine to filter waste from blood - Complications: hypotension, muscle cramps, blood loss AV fistula Created mostly in the forearm with an anastomosis between an artery and a vein AV graft -Made of synthetic materials and for a "bridge" between the arterial and venous blood supplies -Grafts are placed under the skin and are surgically anastomosed between an artery and a vein Peritoneal dialysis -Indicated when there are vascular access problems or when a patient is intolerant of HD -Three phases: inflow, dwell, drain -Patient can dialyze at home: Self-management requires 3-7-day training -Complications: Exit site infection, Peritonitis, Hernias, Pain, Bleeding, Atelectasis, pneumonia, bronchitis Assessment of shock -Focuses on assessing responsiveness and ABCs -Further assessment focuses on the assessment of tissue perfusion: VS, peripheral pulses, LOC, cap refill, skin, urine output Stages of shock initial, compensatory, progressive, refractory (irreversible) Initial stage of sock -occurs at a cellular level and is usually not clinically apparent -elevated lactic acid Compensatory stage of shock -clinically apparent and involves neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis - decreased urine output -increased HR -Increased glucose Progressive stage of shock -begins as compensatory mechanisms fail and aggressive interventions are necessary to prevent the development of multiple organ disfunction -acidosis, irregular HB, pallor, cool and clammy skin, Altered LOC Refractory stage of shock -decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism - profound hypotension and hypoxemia, as well as organ failure -recovery is unlikely cardiogenic shock -Systolic or diastolic dysfunction of the pumping action of the heart results in reduced cardiac output Cardiogenic shock causes MI, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, myocardial depression Cardiogenic shock manifestations Tachycardia, hypotension, narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, diaphoresis, decreased capillary refill time, anxiety, confusion, and agitation Cardiogenic shock treatment -Thrombolytic therapy, angioplasty with stenting, emergency revascularization, and valve replacement -Hemodynamic monitoring, drug therapy (diuretics to reduce preload), and use of circulatory assist devices Hypovolemic shock -Occurs when there is a loss of intravascular volume -Absolute: Fluid is lost through hemorrhage, GI loss, fistula drainage, diabetes insipidus, diuresis -Relative: Fluid volume moves out of the vascular space into the extravascular space; Sepsis and burns Hypovolemic shock manifestations -Anxiety -increased HR -increased CO -increased RR and depth -decrease in stroke volume, pulmonary artery wedge pressure, and urine output Hypovolemic shock treatment Stopping the loss of fluids and restoring the circulatory volume Neurogenic shock hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in response to spinal anesthesia. Neurogenic shock clinical manifestations Hypotension, bradycardia, temperature dysregulation, dry skin, poikilothermia Neurogenic shock treatment -General measures to promote spinal stability -Vassopressors to treat hypotension -Atropine to treat bradycardia -Fluids administered cautiously -Monitor for hypothermia Anaphylactic shock -Acute and life-threatening hypersensitivity (allergic) reaction -Immediate reaction causes massive dilation, release of vasoactive mediators, and an increase in capillary permeability resulting in fluid leaks from the vascular space into the interstitial space Anaphylactic shock clinical manifestations Anxiety, confusion, dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, uticaria, angioedema Anaphylactic shock treatment -Drug of choice is epinephrine -Maintaining airway is critical -Aggressive fluid replacement Septic shock -Systemic inflammatory response to a documented or suspected infection -Three major pathological effects: vasodilation, maldistribution of blood flow, myocardial depression septic shock manifestations Hypotension, respiratory failure, alteration in neurological status, acute kidney injury with decreased urine output, GI dysfunction Septic shock treatment -Large amounts of fluid replacement -Vasopressor drug therapy -IV corticosteroids: when pt cannot maintain adequate BP with vasopressors -Antibiotics: Culture obtained within the first hour Obstructive shock Physical obstruction to blood flow occurs with a decreased CO Obstructive shock causes -Cardiac tamponade, tension pneumothorax, superior vena cava syndrome -Abdominal compartment syndrome -Pulmonary embolism and right ventricular thrombi Obstructive shock manifestations Decreased CO, increased preload, jugular venous distention, and pulsus paradoxus Obstructive shock treatment Early recognition and treatment to relieve or manage the obstruction General treatment guidelines for all types of shock - patent airway and O2 delivery - correction of decreased tissue perfusion: vasopressors or vasodilators - Early enteral nutrition hypoxemic respiratory failure -PaO2 less than or equal to 60 mm Hg when the patient is receiving an inspired O2 concentration greater than or equal to 60% -Interfere with O2 transfer into the blood Causes of hypoxemic respiratory failure Pneumonia, pulmonary edema, pulmonary emboli, heart failure, shock, and alveolar injury related to inhalation of toxic gasses and lung damage related to alveolar stress/ventilator-induced lung injury hypercapnic respiratory failure -PaCO2 greater than 45 mm Hg in combination with acidemia (arterial pH less than 7.35) -Compromised CO2 removal hypercapnic respiratory failure causes Drug overdoses with CNS depressants, neuromuscular diseases, acute asthma, COPD exacerbations, and trauma or diseases involving the spinal cord Clinical manifestations of acute respiratory failure -Changes in mental status (initial indication) -Other early signs: tachycardia, Tachypnea, and mild hypertension -Rapid, shallow breathing pattern or a respiratory rate that is slower than normal -muscle retractions and use of accessory muscles overall goals for ARF -normal ABG values or values within the patient's baseline -normal breath sounds or within the patient's baseline -no dyspnea or breathing patterns within the patient's baseline -independent maintenance of the airway -effective cough and ability to clear secretions Maintaining adequate oxygenation and ventilation in ARF -coughing, adequate hydration and humidification, chest physical therapy (chest physiotherapy), proper patient positioning, airway suctioning, and patient positioning -positive pressure ventilation (PPV) is provided invasively through orotracheal or nasotracheal intubation or noninvasively through a nasal or face mask -Noninvasive PPV ARF drug therapy -Short acting bronchodilators- bronchospasms -Corticosteroids- used with bronchodilators for bronchospasm and inflammation -Diuretics, nitroglycerin, and/or opioids - decrease pulmonary congestion caused by HF -calcium channel blockers and β-adrenergic blockers - if afib is present -IV antibiotics- infection -Sedation- decrease anxiety, agitation, and pain acute respiratory distress syndrome (ARDS) a form of the sudden onset of severe lung dysfunction affecting both lungs, making breathing extremely difficult Stages of ARDS Exudative Proliferative Fibrotic Exudative phase of ARDS -dyspnea, tachypnea, cough, restlessness - chest xray- normal or reveal fine, scattered crackles - 2-4 days after lung injury Proliferative phase of ARDS - 1-2 weeks after initial lung injury - lung becomes dense and fibrous - lung compliance continues to decrease - hypoxemia worsens - if phase persists- fibrosis results - if phase ends- lesions resolve Fibrotic stage of ARDS - linked with increased mortality and prolonged mechanical ventilation - lung tissue becomes fibrous making it more difficult to breathe