https:\/\/learnexams.com\/search\/study?query=<\/a><\/p>\n\n\n\nPatho 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<\/p>\n\n\n\n
Clinical Manifestations of PE
Dyspnea
Chest Pain
Anxiety, Fever, Tachycardia, Cough, Tachypnea<\/p>\n\n\n\n
Treatment Emergency PE
Oxygen Nasal
IV lines
ABG & SpO2 & ECG
IV Morphine or Sedative
Blood is drawn for serum electrolytes, complete blood count, and coagulation studies.<\/p>\n\n\n\n
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 therapy
Elevate Legs & Anti-embolism socks<\/p>\n\n\n\n
Prevention of PE
Ambulation & Active\/Passive Leg Exercises
“Pumping” legs to increase venous flow
Do 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.<\/p>\n\n\n\n
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<\/p>\n\n\n\n
Meds for Mechanical Ventilation
Sedatives that may be used are lorazepam (Ativan), midazolam (Versed), dexmedetomidine (Precedex), propofol (Diprivan), and short-acting barbiturates
neuromuscular 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<\/p>\n\n\n\n
Clinical Manifestations ARDS
Severe dyspnea with rapid onset that does not respond to supplemental oxygen<\/p>\n\n\n\n
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.<\/p>\n\n\n\n
Hepatitis B Tranmission
Blood, Sex, and Mom to Baby<\/p>\n\n\n\n
Prevention Hep A
A: hygiene, vaccination, safe food prep<\/p>\n\n\n\n
Prevention Hep B & C
Avoid dirty needles, vaccination, clean & sterilization of medical devices<\/p>\n\n\n\n
Nutrition Hepatitis
Avoid things that are toxic to liver (St. John Wort)
Enteral feedings may be necessary
Monitor fluid balance
No alcohol for at least 6 moths post infection
Small meals frequently<\/p>\n\n\n\n
Medication Induced Hepatitis
Medications that can lead to hepatitis include isoniazid (Nydrazid), halothane (Fluothane), acetaminophen, methyldopa (Aldomet), and certain antibiotics, antimetabolites, and anesthetic agents.<\/p>\n\n\n\n
Clinical Manifestations Acute Pancreatitis
Severe abdominal pain and back
24-48 hr after big meal or alcohol binge
Rigid boardlike abdomen
Ecchymosis on abdomen<\/p>\n\n\n\n
Treatment Acute Pancreatitis
NPO
Pain Management
Enteral nutrition
Semi-fowlers<\/p>\n\n\n\n
Complications Acute Pancreatitis
Fluid and electrolyte imbalances
Pancreatic Necrosis
Septic Shock<\/p>\n\n\n\n
Causes Chronic Pancreatitis
Malnutrition
Alcohol<\/p>\n\n\n\n
Clinical Manifestations Chronic Pancreatitis
recurring attacks of severe upper abdominal and back pain, accompanied by vomiting
The stools become frequent, frothy, and foul-smelling<\/p>\n\n\n\n
Treatment Chronic Pancreatitis
Endoscopic and laparoscopic procedures such as distal pancreatectomy, longitudinal decompression of the pancreatic duct, nerve denervation, and stenting
Pain Management<\/p>\n\n\n\n
Cirrhosis Patho
Nutritional deficiency with reduced protein intake
Excessive alcohol
Normal tissue is replaced with fibrosis scared tissue<\/p>\n\n\n\n
Cirrhosis Clinical Manifestations Compensated
Abdominal pain
Ankle edema
Firm, enlarged liver
Flatulent dyspepsia
Intermittent mild fever
Palmar erythema (reddened palms)
Splenomegaly
Unexplained epistaxis
Vague morning indigestion
Vascular spiders<\/p>\n\n\n\n
Cirrhosis Clinical Manifestations Decompensated
Ascites
Clubbing of fingers
Continuous mild fever
Epistaxis
Gonadal atrophy
Hypotension
Jaundice
Muscle wasting
Purpura (due to decreased platelet count)
Sparse body hair
Spontaneous bruising
Weakness
Weight loss
White nails<\/p>\n\n\n\n
Treatment Cirrhosis
Rest
Weight and I&O
Oxygen therapy
Mild exercise
H2
Antacids
Potassium Sparing Diuretics
Supplements
Angiotensin
Statins<\/p>\n\n\n\n
Pre Intra and Post Renal
Pre: Before kidney, cardiac
Intra:In kidney, nephrotoxic drugsPost:Blockage after kidney<\/p>\n\n\n\n
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<\/p>\n\n\n\n
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<\/p>\n\n\n\n
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<\/p>\n\n\n\n
Acute Renal Failure L
Loss: Persistent acute kidney injury with equals complete loss of kidney function in 4 hours<\/p>\n\n\n\n
Acute Renal Failure E
ESKD: Over 3 months<\/p>\n\n\n\n
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 fatigue
Integumentary: Coarse, thinning hair, Dry, flaky skin, Ecchymosis, Gray-bronze skin color, Pruritus, Purpura, Thin, brittle nails
Cardiovascular: 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 pneumonitis
Gastrointestinal: 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, Thrombocytopenia
Reproductive: Amenorrhea, Decreased libido, Infertility, Testicular atrophy
Musculoskeletal: Bone fractures, Bone pain, Footdrop, Loss of muscle strength, Muscle cramps, Renal osteodystrophy<\/p>\n\n\n\n
Chronic Renal Failure Diagnostics
GFR Decreases
BUN & Creatine Increase
Erythropoietin decreses
Phosphate Increases
Calcium Decreases<\/p>\n\n\n\n
Metabolic Acidosis<\/p>\n\n\n\n
Nutrition Chronic Renal Failure
Decrease protein
Decrease fluid
Decrease potassium
Watch sodium<\/p>\n\n\n\n
Respiratory Acidosis is
High CO2 level related to low respiratory rate
Low pH below 7.35
High CO2<\/p>\n\n\n\n
Causes of Respiratory Acidosis
Shallow breathing or not breathing
Surgery and anesthesia lowering RR
Narcotic use, causing lethargy and depressed RR
COPD, Obstructive Sleep Apnea
Muscular Dystrophy, MS, Myasthenia Gravis
Pneumonia & ARDS<\/p>\n\n\n\n
Clinical Manifestations of Respiratory Acidosis
Hypoventilation
Cyanosis
Low O2 Sat
Confused
Decreased LOC (Lethargic)
Tachycardia
Dysrhythmias (severe)
Hyperkalemia<\/p>\n\n\n\n
Chronic Respiratory Acidosis
COPD & Obstructive Sleep Apnea<\/p>\n\n\n\n
Treatment Respiratory Acidosis
Always find underlying cause
Improving Ventilation
Bronchodilator (asthma) or Antibiotics (pneumonia)
Increase Water
Pulmonary Hygiene (incentive spirometer, deep breath & cough)
Semi-fowlers<\/p>\n\n\n\n
Compensation Respiratory Acidosis
hold onto HCO3<\/p>\n\n\n\n
Compensation Respiratory Alkalosis
excrete HCO3<\/p>\n\n\n\n
Treatment Respiratory Alkalosis
treat underlying cause
Breath into paper bag<\/p>\n\n\n\n
Chronic Respiratory Alkalosis
Chronic Hypocapnia (low Co2)
Chronic Hepatic Insufficiency (bad liver)<\/p>\n\n\n\n
Respiraotry Alkosis Is
High pH over 7.45
Low CO2
Decreased CO2 level related to increased RR
Decrease of calcium levels<\/p>\n\n\n\n
Causes Respiratory Alkalosis
Always caused by Hyperventilating
Anxiety
Fever- increased metabolic demand, increase O2 demand, increase RR
Pain
Salicylate Intoxication (aspirin OD)<\/p>\n\n\n\n
Clinical Manifestations of Respiratory Alkalosis
Light headedness, dizziness
Pass out
Inability to concentrate
Tachycardia
Dysrhythmias
Hypokalemia
Hypocalcemia (muscle twitching)<\/p>\n\n\n\n
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 acid
Diabetes (+ acid)
Type 1 diabetes- no insulin production- breakdown of fats for energy- results in a byproduct ketone which are acids- DKA
Can’t eat because nauseous so they cant have insulin
Diarrhea (- base)
Lower GI secretions are rich in bases to neutralize acids from stomach. Rapid loss- ie diarrhea results in loss of bases
Lack of O2- anaerobic metabolism results in lactic acid<\/p>\n\n\n\n
Metabolic Acidosis Is
Low pH below 7.3
Low HCO3 below 22
Addition of an Acid (DKA, Lactic Acidosis, Renal Failure) or loss of a Base (Diarrhea)<\/p>\n\n\n\n
Clinical Manifestations of Metabolic Acidosis
Headache
Confusion Drowsiness
Nausea\/Vomiting
Severe hypotension
Cold, Clammy Skin
Dysrhythmias
Hyperkalemia (due to kidney failure)<\/p>\n\n\n\n
Chronic Metabolic Acidosis
Chronic Renal Failure
Low Calcium is usually with Chronic State<\/p>\n\n\n\n
Treatment Metabolic Acidosis
Calcium FIRST (when pH flips it can make calcium lower)<\/p>\n\n\n\n
Sodium Bicarbonate (usually IV)
Monitor Sodium Levels**<\/p>\n\n\n\n
Compensation Metabolic Acidosis
Increase breathing<\/p>\n\n\n\n
Compensation Metabolic Alkalosis
Decrease breathing<\/p>\n\n\n\n
Treatment Metabolic Alkalosis
Monitor I & O Carefully
Restore normal fluid volume loss (from puking, give IV)
Potassium Chloride (KCl) (also have chloride losses from vomiting)<\/p>\n\n\n\n
Chronic Metabolic Alkalosis
Long term diuretic use<\/p>\n\n\n\n
Clinical Manifestations Metabolic Alkalosis
Hypocalcemia (tingling in fingers and toes)
Hypokalemia (dysrhythmias)<\/p>\n\n\n\n
Causes Metabolic Alkalosis
Hypokalemia (diuretic use)
Upper GI secretion loss
Upper GI secretions are acidic- vomiting or NG tube suction can result in loss of acids
Antacid Overuse
Excess intake of bicarbonate<\/p>\n\n\n\n
Metabolic Alkalosis Is
pH over 7.45
HCO3 over 26
Loss of Acid or excess Bases
Decrease of calcium levels<\/p>\n\n\n\n
Long term use of diuretics can lead to
Metabolic Alkalosis<\/p>\n\n\n\n
Vecuronium class and use
Class: Neuromuscular Blocking Agent
Use:Intubating<\/p>\n\n\n\n
Vecuronium Side Effects and Adverse Effects
Side Effect: relaxes vocal chords and jaw muscles
Adverse Effect:patient unable to breathe on their own<\/p>\n\n\n\n
What electrolyte imbalance can be created by diuretics? Specifically, what class of diuretics?
Potassium<\/p>\n\n\n\n
What class is preferred for pulmonary edema
Loop Diuretics<\/p>\n\n\n\n
What class is preferred to treat hypokalemia?
Spirolactone (potassium sparing)<\/p>\n\n\n\n
What would you monitor in patients receiving Diuretics?
I & O
Daily Weights
Potassium & Electrolyte levels<\/p>\n\n\n\n
What acid base imbalance requires calcium and sodium bicarbonate
Metabolic Acidosis with Hyperkalemia<\/p>\n\n\n\n
When would you giev a ESKD patient calcium?
When their phosphate is high, opposite relationship<\/p>\n\n\n\n
What are S\/S of hypocalcemia
tingling of the fingers and toes, dizziness, and hypertonic muscles.<\/p>\n\n\n\n
Morphine Class and Use
Class: Opioids
Use:Severe Pain<\/p>\n\n\n\n
Morphine Routes with Time for Affect
IV- takes affect quickly, used when patient is nauseated
PO- takes 45-60 min to take affect
Topical- takes 24hrs to take full affect<\/p>\n\n\n\n
Side Effects of Morphine
respiratory depression, hypoxia<\/p>\n\n\n\n
Disease that uses morphine
Acute and Chronic Pancreatitis<\/p>\n\n\n\n
Heparin Class and Use
Class: Anticoagulant, Antithrombotic
Uses:Thrombosis prevention in MI, PE, open Heart Surgery, DVT<\/p>\n\n\n\n
Side Effects and Adverse Effects of Heparin
Side Effects: rash, fever, hyperkalemia<\/p>\n\n\n\n
Adverse Effects:Hemorrhage, Thrombocytopenia, anaphylaxis<\/p>\n\n\n\n
Nursing Considerations Heparin
Uses PTT to adjust dosing
PTT level
Normal 25-35 seconds
Therapeutic on Heparin: 45-70 seconds<\/p>\n\n\n\n
Antidote of Heparin
Protamine Sulfate: 1mg\/100mg of Heparin<\/p>\n\n\n\n
Milk Thistle What does it do?
Treats Jaundice
Healing and Regenerative Properties
Anti-inflammatory & Antioxidant<\/p>\n\n\n\n
Disease for Milk Thistle
End Stage Cirrhosis<\/p>\n\n\n\n
Sodium Polystyrene Sulfonate
(Kayexalate) What is it used for
Removes potassium from the body in stools
Used in renal failure patients<\/p>\n\n\n\n
How is Sodium Polystyrene Sulfonate
(Kayexalate) Administered?
Mix with water and drink<\/p>\n\n\n\n
How to know when Sodium Polystyrene Sulfonate
(Kayexalate) is working
Potassium levels normal<\/p>\n\n\n\n
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<\/p>\n\n\n\n
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<\/p>\n\n\n\n
What disease is Erythropoietin given for
ESKD
Renal<\/p>\n\n\n\n
Therapeutic Effect of Epogen
The nurse observes for increased RBCs, hemoglobin, and hematocrit; increased energy and exercise capacity; and improved quality of life<\/p>\n\n\n\n
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.<\/p>\n\n\n\n
What patients recieve Epogen?
Renal Patients with Hematocrit less than 30%
Hemoglobin below 10g\/dL<\/p>\n\n\n\n
\n- <\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"
Exam 2: NSG223\/ NSG 223 (Latest 2024\/ 2025 Update) Med Surg 2 Exam| Guide Questions and Verified Answers| 100% Correct| Grade A- Herzing Exam 2: NSG223\/ NSG 223 (Latest 2024\/2025 Update) Med Surg 2 Exam| GuideQuestions and Verified Answers| 100%Correct| Grade A- HerzingQ: Meds for Mechanical VentilationAnswer:Sedatives that may be used are lorazepam (Ativan), midazolam […]<\/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-131394","post","type-post","status-publish","format-standard","hentry","category-exams-certification"],"_links":{"self":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/131394","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=131394"}],"version-history":[{"count":0,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/131394\/revisions"}],"wp:attachment":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/media?parent=131394"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/categories?post=131394"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/tags?post=131394"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}