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Patho of Pulmonary Embolism Most commonly, PE is due to a blood clot or thrombus. However, there are other types of emboli: air, fat, amniotic fluid, and septic (from bacterial invasion of the thrombus). When a thrombus completely or partially obstructs a pulmonary artery or its branches, the alveolar dead space is increased
Clinical Manifestations of PE DyspneaChest PainAnxiety, Fever, Tachycardia, Cough, Tachypnea
Treatment Emergency PE Oxygen NasalIV linesABG & SpO2 & ECGIV Morphine or SedativeBlood is drawn for serum electrolytes, complete blood count, and coagulation studies.
Treatment Once Stable PE Treatment goal is to dissolve (lyse) the existing emboli and prevent new ones from forming.General measures to improve respiratory and vascular status, anticoagulation therapy, thrombolytic therapy, and surgical intervention.Measures are initiated to improve respiratory and vascular status. Oxygen therapyElevate Legs & Anti-embolism socks
Prevention of PE “Ambulation & Active\/Passive Leg Exercises””Pumping”” legs to increase venous flowDo not to sit or lie in bed for prolonged periods, not to cross the legs, and not to wear constrictive clothing.Legs should not be dangled or feet placed in a dependent position while the patient sits on the edge of the bed; instead, feet should rest on the floor or on a chair.”
Mechanical Ventilation Assessment Nursing assessment is important to identify problems with ventilation that may be causing the anxiety reaction: tube blockage by kinking or retained secretions, other acute respiratory problems (e.g., pneumothorax and pain), a sudden decrease in the oxygen level, the level of dyspnea, or ventilator malfunction. In some cases, sedation may be required to decrease the patient’s oxygen consumption, allow the ventilator to provide full support of ventilation, and decrease the patient’s anxiety
Meds for Mechanical Ventilation Sedatives that may be used are lorazepam (Ativan), midazolam (Versed), dexmedetomidine (Precedex), propofol (Diprivan), and short-acting barbituratesneuromuscular blocking agents (paralytic agents) may be given to paralyze the patient. Examples of these agents include pancuronium (Pavulon), vecuronium (Norcuron), atracurium (Tracrium), and rocuronium (Zemuron
Clinical Manifestations ARDS Severe dyspnea with rapid onset that does not respond to supplemental oxygen
Hepatitis A & E Tranmission Hepatitis A & E: fecal-oral route, HAV is transmitted primarily through the fecal-oral route, by the ingestion of food or liquids infected with the virus.
Hepatitis B Tranmission Blood, Sex, and Mom to Baby
Prevention Hep A A: hygiene, vaccination, safe food prep
Prevention Hep B & C Avoid dirty needles, vaccination, clean & sterilization of medical devices
Nutrition Hepatitis Avoid things that are toxic to liver (St. John Wort)Enteral feedings may be necessaryMonitor fluid balanceNo alcohol for at least 6 moths post infectionSmall meals frequently
Medication Induced Hepatitis Medications that can lead to hepatitis include isoniazid (Nydrazid), halothane (Fluothane), acetaminophen, methyldopa (Aldomet), and certain antibiotics, antimetabolites, and anesthetic agents.
Clinical Manifestations Acute Pancreatitis Severe abdominal pain and back24-48 hr after big meal or alcohol bingeRigid boardlike abdomenEcchymosis on abdomen
Treatment Acute Pancreatitis NPOPain ManagementEnteral nutritionSemi-fowlers
Complications Acute Pancreatitis Fluid and electrolyte imbalancesPancreatic NecrosisSeptic Shock
Causes Chronic Pancreatitis MalnutritionAlcohol
Clinical Manifestations Chronic Pancreatitis recurring attacks of severe upper abdominal and back pain, accompanied by vomitingThe stools become frequent, frothy, and foul-smelling
Treatment Chronic Pancreatitis Endoscopic and laparoscopic procedures such as distal pancreatectomy, longitudinal decompression of the pancreatic duct, nerve denervation, and stentingPain Management
Cirrhosis Patho Nutritional deficiency with reduced protein intakeExcessive alcoholNormal tissue is replaced with fibrosis scared tissue
Cirrhosis Clinical Manifestations Compensated Abdominal painAnkle edemaFirm, enlarged liverFlatulent dyspepsiaIntermittent mild feverPalmar erythema (reddened palms)SplenomegalyUnexplained epistaxisVague morning indigestionVascular spiders
Cirrhosis Clinical Manifestations Decompensated AscitesClubbing of fingersContinuous mild feverEpistaxisGonadal atrophyHypotensionJaundiceMuscle wastingPurpura (due to decreased platelet count)Sparse body hairSpontaneous bruisingWeaknessWeight lossWhite nails
Treatment Cirrhosis RestWeight and I&OOxygen therapyMild exerciseH2AntacidsPotassium Sparing DiureticsSupplementsAngiotensinStatins
Pre Intra and Post Renal Pre: Before kidney, cardiacIntra:In kidney, nephrotoxic drugsPost:Blockage after kidney
Acute Renal Failure R Risk: Increased serum creatine 1.5 times baseline or GFR decrease of more than 25%. Urinary Output of 0.5mL\/kg\/hr for 6 hours
Acute Renal Failure I Injury: Increased serum creatine 2 times baseline or GFR decrease more than 50%. Urinary Output of 0.5mL\/kg\/hr for 12 hours
Acute Renal Failure F Failure: Increased serum creatine 3 times baseline or GFR decrease over 75% or serum creatine of greater than 354 mmol\/L with acute rise of atleast 44 mmol\/L. Urinary Output of less than 0.3 mL\/kg\/hr for 24 hours or anuria for 12 hours
Acute Renal Failure L Loss: Persistent acute kidney injury with equals complete loss of kidney function in 4 hours
Acute Renal Failure E ESKD: Over 3 months
Chronic Renal Failure Clinical Manifestations “Neurologic: Asterixis, Behavior changes, Burning of soles of feet, Confusion, Disorientation, Inability to concentrate, Restlessness of legs, Seizures, Tremors, Weakness and fatigueIntegumentary: Coarse, thinning hair, Dry, flaky skin, Ecchymosis, Gray-bronze skin color, Pruritus, Purpura, Thin, brittle nailsCardiovascular: Engorged neck veins, Hyperkalemia, Hyperlipidemia, Hypertension, Pericardial effusion, Pericardial friction rub, Pericardial tamponade, Pericarditis, Periorbital edema, Pitting edema (feet, hands, sacrum)Pulmonary, Crackles, Depressed cough refle, Kussmaul-type respirations, Pleuritic pain, Shortness of breath, Tachypnea, Thick, tenacious sputum, Uremic pneumonitisGastrointestinal: Ammonia odor to breath (“”uremic fetor””), Anorexia, nausea, and vomitin, Bleeding from gastrointestinal tract, Constipation or diarrhea, Hiccup, Metallic taste, Mouth ulcerations and bleeding, Hematologic, Anemia, ThrombocytopeniaReproductive: Amenorrhea, Decreased libido, Infertility, Testicular atrophyMusculoskeletal: Bone fractures, Bone pain, Footdrop, Loss of muscle strength, Muscle cramps, Renal osteodystrophy”
Chronic Renal Failure Diagnostics GFR DecreasesBUN & Creatine IncreaseErythropoietin decresesPhosphate IncreasesCalcium DecreasesMetabolic Acidosis
Nutrition Chronic Renal Failure Decrease proteinDecrease fluidDecrease potassiumWatch sodium
Respiratory Acidosis is High CO2 level related to low respiratory rateLow pH below 7.35High CO2
Causes of Respiratory Acidosis Shallow breathing or not breathingSurgery and anesthesia lowering RRNarcotic use, causing lethargy and depressed RRCOPD, Obstructive Sleep ApneaMuscular Dystrophy, MS, Myasthenia GravisPneumonia & ARDS
Clinical Manifestations of Respiratory Acidosis HypoventilationCyanosisLow O2 SatConfusedDecreased LOC (Lethargic)TachycardiaDysrhythmias (severe)Hyperkalemia
Chronic Respiratory Acidosis COPD & Obstructive Sleep Apnea
Treatment Respiratory Acidosis Always find underlying causeImproving VentilationBronchodilator (asthma) or Antibiotics (pneumonia)Increase WaterPulmonary Hygiene (incentive spirometer, deep breath & cough)Semi-fowlers
Compensation Respiratory Acidosis hold onto HCO3
Compensation Respiratory Alkalosis excrete HCO3
Treatment Respiratory Alkalosis treat underlying causeBreath into paper bag
Chronic Respiratory Alkalosis Chronic Hypocapnia (low Co2)Chronic Hepatic Insufficiency (bad liver)
Respiraotry Alkosis Is High pH over 7.45Low CO2Decreased CO2 level related to increased RRDecrease of calcium levels
Causes Respiratory Alkalosis Always caused by HyperventilatingAnxietyFever- increased metabolic demand, increase O2 demand, increase RRPainSalicylate Intoxication (aspirin OD)
Clinical Manifestations of Respiratory Alkalosis Light headedness, dizzinessPass outInability to concentrateTachycardiaDysrhythmiasHypokalemiaHypocalcemia (muscle twitching)
Causes of Metabolic Acidosis Renal failure- (+ acid)Major function of kidneys is to excrete acid. In kidney failure they are unable to do this resulting in excess acidDiabetes (+ acid)Type 1 diabetes- no insulin production- breakdown of fats for energy- results in a byproduct ketone which are acids- DKACan’t eat because nauseous so they cant have insulinDiarrhea (- base)Lower GI secretions are rich in bases to neutralize acids from stomach. Rapid loss- ie diarrhea results in loss of basesLack of O2- anaerobic metabolism results in lactic acid
Metabolic Acidosis Is Low pH below 7.3Low HCO3 below 22Addition of an Acid (DKA, Lactic Acidosis, Renal Failure) or loss of a Base (Diarrhea)
Clinical Manifestations of Metabolic Acidosis HeadacheConfusion DrowsinessNausea\/VomitingSevere hypotensionCold, Clammy SkinDysrhythmiasHyperkalemia (due to kidney failure)
Chronic Metabolic Acidosis Chronic Renal FailureLow Calcium is usually with Chronic State
Treatment Metabolic Acidosis Calcium FIRST (when pH flips it can make calcium lower)Sodium Bicarbonate (usually IV)Monitor Sodium Levels**
Compensation Metabolic Acidosis Increase breathing
Compensation Metabolic Alkalosis Decrease breathing
Treatment Metabolic Alkalosis Monitor I & O CarefullyRestore normal fluid volume loss (from puking, give IV)Potassium Chloride (KCl) (also have chloride losses from vomiting)
Chronic Metabolic Alkalosis Long term diuretic use
Clinical Manifestations Metabolic Alkalosis Hypocalcemia (tingling in fingers and toes)Hypokalemia (dysrhythmias)
Causes Metabolic Alkalosis Hypokalemia (diuretic use)Upper GI secretion lossUpper GI secretions are acidic- vomiting or NG tube suction can result in loss of acidsAntacid OveruseExcess intake of bicarbonate
Metabolic Alkalosis Is pH over 7.45HCO3 over 26Loss of Acid or excess BasesDecrease of calcium levels
Long term use of diuretics can lead to Metabolic Alkalosis
Vecuronium class and use Class: Neuromuscular Blocking AgentUse:Intubating
Vecuronium Side Effects and Adverse Effects Side Effect: relaxes vocal chords and jaw musclesAdverse Effect:patient unable to breathe on their own
What electrolyte imbalance can be created by diuretics? Specifically, what class of diuretics? Potassium
What class is preferred for pulmonary edema Loop Diuretics
What class is preferred to treat hypokalemia? Spirolactone (potassium sparing)
What would you monitor in patients receiving Diuretics? I & ODaily WeightsPotassium & Electrolyte levels
What acid base imbalance requires calcium and sodium bicarbonate Metabolic Acidosis with Hyperkalemia
When would you giev a ESKD patient calcium? When their phosphate is high, opposite relationship
What are S\/S of hypocalcemia tingling of the fingers and toes, dizziness, and hypertonic muscles.
Morphine Class and Use Class: OpioidsUse:Severe Pain
Morphine Routes with Time for Affect IV- takes affect quickly, used when patient is nauseatedPO- takes 45-60 min to take affectTopical- takes 24hrs to take full affect
Side Effects of Morphine respiratory depression, hypoxia
Disease that uses morphine Acute and Chronic Pancreatitis
Heparin Class and Use Class: Anticoagulant, AntithromboticUses:Thrombosis prevention in MI, PE, open Heart Surgery, DVT
Side Effects and Adverse Effects of Heparin Side Effects: rash, fever, hyperkalemiaAdverse Effects:Hemorrhage, Thrombocytopenia, anaphylaxis
Nursing Considerations Heparin Uses PTT to adjust dosingPTT levelNormal 25-35 secondsTherapeutic on Heparin: 45-70 seconds
Antidote of Heparin Protamine Sulfate: 1mg\/100mg of Heparin
Milk Thistle What does it do? Treats JaundiceHealing and Regenerative PropertiesAnti-inflammatory & Antioxidant
Disease for Milk Thistle End Stage Cirrhosis
Sodium Polystyrene Sulfonate(Kayexalate) What is it used for Removes potassium from the body in stools Used in renal failure patients
How is Sodium Polystyrene Sulfonate(Kayexalate) Administered? Mix with water and drink
How to know when Sodium Polystyrene Sulfonate(Kayexalate) is working Potassium levels normal
How soon does Vecuronium start working and last? Maximum neuromuscular blockade with vecuronium occurs within 3 to 5 minutes, and the duration of action is 25 to 40 minutes. The onset and duration are dose-dependent. For example, larger doses result in faster onset and longer duration
How are you able to determine if Vecuronium is working? Anesthesia providers use a device called a peripheral nerve stimulator to monitor the level of paralysis. Using this as a guide, the anesthesia provider is better able to select the correct dosing regimen
What disease is Erythropoietin given for ESKDRenal
Therapeutic Effect of Epogen The nurse observes for increased RBCs, hemoglobin, and hematocrit; increased energy and exercise capacity; and improved quality of life
How is Epogen Administered? Epoetin alfa is administered IV or subcutaneously three times a week in ESKD.For patients with chronic kidney disease on hemodialysis, the nurse gives epoetin alfa by bolus injection at the end of dialysis.
What patients recieve Epogen? Renal Patients with Hematocrit less than 30%Hemoglobin below 10g\/dL<\/p>\n","protected":false},"excerpt":{"rendered":"Exam 2: NSG223\/ NSG 223 (New 2024\/ 2025 Update) Med Surg 2 Exam| Guide Questions and Verified Answers| 100% Correct| Graded A- Herzing Exam 2: NSG223\/ NSG 223 (New 2024\/ 2025Update) Med Surg 2 Exam| Guide Questionsand Verified Answers| 100% Correct|Graded A- HerzingQUESTIONCirrhosis PathoAnswer:Nutritional deficiency with reduced protein intakeExcessive alcoholNormal tissue is replaced with fibrosis […]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"site-sidebar-layout":"default","site-content-layout":"","ast-site-content-layout":"default","site-content-style":"default","site-sidebar-style":"default","ast-global-header-display":"","ast-banner-title-visibility":"","ast-main-header-display":"","ast-hfb-above-header-display":"","ast-hfb-below-header-display":"","ast-hfb-mobile-header-display":"","site-post-title":"","ast-breadcrumbs-content":"","ast-featured-img":"","footer-sml-layout":"","ast-disable-related-posts":"","theme-transparent-header-meta":"","adv-header-id-meta":"","stick-header-meta":"","header-above-stick-meta":"","header-main-stick-meta":"","header-below-stick-meta":"","astra-migrate-meta-layouts":"default","ast-page-background-enabled":"default","ast-page-background-meta":{"desktop":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"tablet":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"mobile":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""}},"ast-content-background-meta":{"desktop":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"tablet":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"mobile":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""}},"footnotes":""},"categories":[25],"tags":[],"class_list":["post-131863","post","type-post","status-publish","format-standard","hentry","category-exams-certification"],"_links":{"self":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/131863","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/comments?post=131863"}],"version-history":[{"count":0,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/131863\/revisions"}],"wp:attachment":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/media?parent=131863"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/categories?post=131863"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/tags?post=131863"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}