GERD (Gastroesophageal Reflux Disease)

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Brad Bass
ASN,RN
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Included In This Lesson

Study Tools For GERD (Gastroesophageal Reflux Disease)

GERD causes (Mnemonic)
GERD Pathochart (Cheatsheet)
Abdominal Pain – Assessment (Cheatsheet)
Patho of GERD (Image)
Gastroesophageal Reflux Disease (GERD) Assessment (Picmonic)
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Outline

Overview

  1. Backward movement of gastric contents into esophagus

Nursing Points

General

  1. Causes
    1. Relaxed or incompetent lower esophageal sphincter
    2. Pyloric stenosis
    3. Increased gastric volume
    4. Motility disorder
  2. Diagnosis
    1. pH test of regurgitation
    2. Esophagoscopy used to rule out malignancy

Assessment

  1. Heartburn
    1. Exacerbated by bending over, straining, or recumbent position
    2. Differentiate between heartburn and cardiac chest pain
  2. Regurgitation
  3. Hypersalivation
  4. Difficulty swallowing
  5. Dyspepsia (discomfort in upper abdomen)

Therapeutic Management

  1. Avoid medications that ↓ gastric emptying (anticholinergics)
  2. Medications
    1. Antacids
      1. Calcium carbonate
    2. H2 receptor antagonists
      1. Famotidine
    3. Proton pump inhibitor
      1. Omeprazole

Nursing Concepts

  1. Comfort
    1. Elevate HOB while sleeping
    2. Do not eat within 2 hours of bedtime
  2. Nutrition
    1. Avoid food that reduce lower esophageal sphincter tone
      1. peppermint
      2. chocolate
      3. carbonated beverages
      4. smoking
      5. fried and fatty foods
    2. Eat a low fat, high fiber diet

Patient Education

  1. Adhere to dietary instructions
  2. Take medications as prescribed

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Transcript

Hey guys, my name is Brad and welcome to nursing.com. And in today’s video, what we’re going to be doing is, we’re going to discuss gastroesophageal reflux disease. Also known as GERD. I’d like to discuss some of the pathophysiology behind it, some of the different causes, symptoms, as well as how we’re going to treat patients experiencing it. Let’s dive in. 

So in gastroesophageal reflux disease, what is occurring is essentially a disease that causes stomach acid to flow backwards, right? And the way that I like to think about this, is I like to think about the GI tract, like a GI factory, essentially broken up into four different departments, right? The first department of the GI factory is our food processing factory, right? This is where we actually take food in by mouth and we chew it up. We process the food, right? Now, this department is connected to the acid producing department, right? And it’s connected via the esophagus. So the way that I like to think about this, we chew food up in the processing department, it goes from, travels through the esophagus, to the acid producing department, right, which is our stomach. This is then connected to our nutrient extraction department, right? Think about the actual small intestine and large intestine. And then we actually have waste removal, okay. And you guys get the idea there. What we have, whenever we’re talking about GERD, is we have a breakdown, an issue with our acid factory, the acid producing factory in our body, which ends up causing acid to flow backwards instead of homeostatically moving forward. 

And so now whenever we’re talking about causes, right, whenever we’re talking about causes of GERD, it’s important to understand and to remember, like I said, this is something that causes stomach acid to flow backwards. And it’s a direct result of a breakdown in that acid producing department, right? So what we have here is the stomach, as we can see, also from this image on the right, we had the stomach. Now, remember the stomach actually produces hydrochloric acid, entire idea behind that being that hydrochloric acid is produced so that the food we intake can then be dissolved, broken down, so that once it passes into the nutrient extraction department, it’s able to be actually, you know, extracted. So nonetheless, what we have, think about it, going from our food processing department, down here into our acid producing department, down into the stomach, we have two doors. This is the way I think about it. This is a factory, connected, made up of four departments. We have two doors, right? Our first door is the door allowing us into the stomach. And our second is a door that allows us out of the stomach, right? Now, this door here that allows us entrance into the stomach itself is our esophageal sphincter. Also you may see it called a cardiac sphincter. Nonetheless, it’s our esophageal sphincter. This is a sphincter that essentially allows passage of the food that we consume to go down into the stomach. So the first cause of GERD can be a breakdown in that esophageal sphincter, right? Lower esophageal sphincter weakening. So basically think about it like a door that allows you access into the stomach. If this door starts to weaken and it allows stomach acid to backflow out of the stomach, back up into the esophagus, that causes acid reflux, that’s GERD.  

The second cause could be delayed gastric emptying, right? So think about delayed gastric emptying. As we have this food passing down into the small intestine, down into the large intestine, if we have delayed gastric emptying, which basically means that our acid in our stomach is delayed in exiting our stomach. That is going to cause more and more hydrochloric acid, still being produced at the same rate it was before, but the rate at which it’s exiting, the stomach is reduced. So it’s not flowing out of the stomach as quickly, but we’re still producing just as much, this causes more and more hydrochloric acid to be produced. And eventually backflows. Just like we said, before acid flows backwards. 

And the one other thing to understand that as a possible cause is pyloric stenosis. This door out of the stomach, that is your pyloric sphincter. Okay. We can have pyloric stenosis, just like aortic valve stenosis, any other kind of stenotic process. Think about it as a stiffening. That’s what stenosis means, stiff. So if we have a stiff pyloric sphincter, which is our door out, it’s our door out of the stomach. If it’s stiff, if it’s hard to get through, think about it like you’re just trying to bust through a door, but it’s like, you’re going through a brick wall. As this stomach acid is trying to push against a brick wall to exit the stomach, again, hydrochloric acid is still being produced at the same rate it was before, therefore acid is going to back up and backflow. 

So some of the common assessment findings that we’re going to see in patients experiencing GERD is burning in the throat or chest. You know, another word for this that a lot of you guys may know is heartburn, right? That’s what GERD causes a symptom of. It feels like burning, actually, in the throat and the chest as that stomach acid regurges and flows backwards. You may also see difficulty swallowing, a more loose esophageal tone. It may be more difficult for patients to actually get food down, food regurgitation. Again, if that entrance door into the acid factory, if that esophageal sphincter is loose, food and acid, both can regurgitate back up. This is going to cause nausea and an upset stomach. And all of this regurgitation back up into that sphincter is going to feel like a lump in the throat. These are all common assessment findings. 

So what are some different medications that we’re going to use to treat patients who are experiencing GERD, but one could be a simple antacid, right? Something like calcium carbonate. Okay. TUMS, right? These are medications that actually combine directly with hydrochloric acid and neutralize it. It immediately, instantaneously reduces the amount of hydrochloric acid in the stomach and therefore reduces symptoms of GERD. You can also see things such as H2 blockers, right? This could be something like famotidine, right? Thinking that it ends in -tidine. And these are medications that are used that actually affect cellular processes within the stomach itself. And an overall attempt to proactively reduce the amount of acid that we are producing in our stomach, as opposed to being reactive, such as using TUMS, and after the GERD has already occurred, trying to treat it then. These H2 blockers such as famotidine oare more of a proactive attempt, as are PPIs, such as omeprazole. These are medications that end in -prazole.  Another cellular attempt by actually disrupting the hydrogen and potassium pumps in the lining of the stomach itself in an overall attempt to decrease the amount of acid that’s being produced in the stomach and to therefore reduce the symptoms of GERD. 

So some of the education that we’re going to be mindful of whenever we’re taking care of patients who are experiencing GERD, we want to make sure that we’re telling them to avoid any kind of foods that may produce acid that may cause additional acid production in the stomach and worsen symptoms of GERD. Medications, or foods I should say, such as peppermint, such as chocolate, such as coffee, spicy foods, things that are going to cause more acid to be produced. We’re going to educate them on eating smaller portions and eating slowly, right? Again, remember a lot of the causes could be such as delayed gastric emptying or pyloric sphincter stenosis, right? We want to encourage smaller portions and to eat slower in an overall attempt to reduce the amount of food or volume of hydrochloric acid in that stomach at any one given time. Also elevating your head while sleeping, as again, remember GERD is that backwards flow of acid. So elevating the head while sleeping to try and prevent that acidic regurg.  Also educating on smoking cessation as well as weight loss, as obesity and smoking, both contribute to GERD and GERD like symptoms. 

And finally summarizing some of our key points related to gastroesophageal reflux disease is remembering that GERD causes stomach acid to flow backwards. Remember thinking about it or conceptualizing it like a GI factory and what we’re really looking at whenever we’re looking at causes of GERD are breakdowns in that door, into the stomach, as well as that door out of the stomach, right? That esophageal sphincter and that pyloric sphincter. Also remember that all of the assessment findings that you’re going to see in patients with GERD are all directly a result of that regurgitant backward flow of stomach acid back up into the esophagus. Also remember that a lot about therapeutic management, the pharmacological options that we’re going to use are either geared reactively at reducing the total volume of stomach acid in the tummy, such as calcium carbonate, or a more proactive measure using medications, such as H2 blockers or PPIs. And the patient education, which we just discussed. 

Guys, I hope that this helped bring a little bit of clarity to gastroesophageal reflux disease. And I hope that you have a more firm grasp on what the physiology is, as well as, how we’re going to treat it. I hope that you guys go out there and be your best selves today. And as always, happy nursing.

 

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Concepts Covered:

  • Basics of NCLEX
  • Test Taking Strategies
  • Prioritization
  • Studying
  • Fundamentals of Emergency Nursing
  • Developmental Considerations
  • Developmental Theories
  • Communication
  • Concepts of Mental Health
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  • Renal Disorders
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  • Prenatal and Neonatal Growth and Development
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  • Respiratory Disorders
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  • Disorders of Pancreas
  • Acute & Chronic Renal Disorders
  • Liver & Gallbladder Disorders
  • Hematologic Disorders
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  • Intraoperative Nursing
  • Lower GI Disorders
  • Gastrointestinal Disorders
  • Upper GI Disorders
  • Vascular Disorders
  • Sexually Transmitted Infections
  • Neurologic and Cognitive Disorders
  • Microbiology
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  • Disorders of the Adrenal Gland
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  • Disorders of the Thyroid & Parathyroid Glands
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Study Plan Lessons

Overview of the Nursing Process
Nursing Process – Assess
Nursing Process – Diagnose
Nursing Process – Plan
Nursing Process – Implement
Nursing Process – Evaluate
Critical Thinking
Thinking Like a Nurse
The Nurse Routine
Prioritization
Triage
Cultural Awareness and Influences on Development
Developmental Considerations for the Hospitalized Individual
Family Structure and Impact on Development
Kohlberg’s Theory of Moral Development
Erikson’s Theory of Psychosocial Development
Piaget’s Theory of Cognitive Development
Body Image Changes Throughout Development
Nurse-Patient Relationship
Therapeutic Communication
Defense Mechanisms
Self Concept
Patients with Communication Difficulties
Maslow’s Hierarchy of Needs in Nursing
Nutrition Assessments
Nutrition (Diet) in Disease
Specialty Diets (Nutrition)
Developmental Stages and Milestones
Cultural Awareness and Influences on Development
Environmental and Genetic Influences on Growth & Development
Growth & Development – Late Adulthood
Developmental Considerations for End of Life Care
Growth & Development -Transitioning to Adult Care
ABGs Nursing Normal Lab Values
ABG (Arterial Blood Gas) Interpretation-The Basics
ROME – ABG (Arterial Blood Gas) Interpretation
ABGs Tic-Tac-Toe interpretation Method
Respiratory Acidosis (interpretation and nursing interventions)
Respiratory Alkalosis
Metabolic Acidosis (interpretation and nursing diagnosis)
Metabolic Alkalosis
ABG (Arterial Blood Gas) Oxygenation
Lactic Acid
Base Excess & Deficit
Fluid & Electrolytes Course Introduction
Fluid Compartments
Fluid Pressures
Fluid Shifts (Ascites) (Pleural Effusion)
Isotonic Solutions (IV solutions)
Hypotonic Solutions (IV solutions)
Hypertonic Solutions (IV solutions)
Potassium-K (Hyperkalemia, Hypokalemia)
Sodium-Na (Hypernatremia, Hyponatremia)
Calcium-Ca (Hypercalcemia, Hypocalcemia)
Chloride-Cl (Hyperchloremia, Hypochloremia)
Magnesium-Mg (Hypomagnesemia, Hypermagnesemia)
Phosphorus-Phos
Calcium Acetate (PhosLo) Nursing Considerations
Epoetin (Epogen) Nursing Considerations
Enalapril (Vasotec) Nursing Considerations
Calcium Carbonate (Tums) Nursing Considerations
Epoetin Alfa
Acute Renal (Kidney) Module Intro
Nursing Care and Pathophysiology of Acute Kidney (Renal) Injury (AKI)
Nursing Care and Pathophysiology of Nephrotic Syndrome
Nursing Care and Pathophysiology of Glomerulonephritis
Nursing Care and Pathophysiology of Urinary Tract Infection (UTI)
Nursing Care and Pathophysiology of Renal Calculi (Kidney Stones)
Chronic Renal (Kidney) Module Intro
Nursing Care and Pathophysiology of Chronic Kidney (Renal) Disease (CKD)
Nursing Care and Pathophysiology of BPH (Benign Prostatic Hyperplasia)
Dialysis & Other Renal Points
Peritoneal Dialysis (PD)
Hemodialysis (Renal Dialysis)
Continuous Renal Replacement Therapy (CRRT, dialysis)
Anesthetic Agents
Anesthetic Agents
Epidural
Patient Controlled Analgesia (PCA)
Bismuth Subsalicylate (Pepto-Bismol) Nursing Considerations
Bisacodyl (Dulcolax) Nursing Considerations
Clindamycin (Cleocin) Nursing Considerations
Proton Pump Inhibitors
Atenolol (Tenormin) Nursing Considerations
Captopril (Capoten) Nursing Considerations
Amlodipine (Norvasc) Nursing Considerations
Azithromycin (Zithromax) Nursing Considerations
Cephalexin (Keflex) Nursing Considerations
Ampicillin (Omnipen) Nursing Considerations
Ciprofloxacin (Cipro) Nursing Considerations
Acyclovir (Zovirax) Nursing Considerations
Anti-Infective – Antivirals
Anti-Infective – Antifungals
Cefdinir (Omnicef) Nursing Considerations
Cefaclor (Ceclor) Nursing Considerations
Parasympatholytics (Anticholinergics) Nursing Considerations
Diuretics (Loop, Potassium Sparing, Thiazide, Furosemide/Lasix)
Hematology Module Intro
Thrombocytopenia
Ferrous Sulfate (Iron) Nursing Considerations
Nursing Care and Pathophysiology for Anemia
Nursing Care and Pathophysiology for Sickle Cell Anemia
Nursing Care and Pathophysiology for Disseminated Intravascular Coagulation (DIC)
Iron Deficiency Anemia
Hemophilia
Hemoglobin (Hbg) Lab Values
Hematocrit (Hct) Lab Values
Platelets (PLT) Lab Values
Diabetes Mellitus (DM) Module Intro
Nursing Care and Pathophysiology of Diabetes Mellitus (DM)
Diabetes Management
Nursing Care and Pathophysiology of Diabetic Ketoacidosis (DKA)
Hyperglycaemic Hyperosmolar Non-ketotic syndrome (HHNS)
Hypoglycemia
Addisons Disease
Nursing Care and Pathophysiology for Cushings Syndrome
Nursing Care and Pathophysiology for Diabetes Insipidus (DI)
Nursing Care and Pathophysiology for SIADH (Syndrome of Inappropriate antidiuretic Hormone Secretion)
Insulin Drips
Antidiabetic Agents
Thrombolytics
Iodine Nursing Considerations
Propylthiouracil (PTU) Nursing Considerations
Glucagon (GlucaGen) Nursing Considerations
Insulin – Mixtures (70/30)
Insulin – Intermediate Acting (NPH) Nursing Considerations
Insulin – Short Acting (Regular) Nursing Considerations
Insulin – Long Acting (Lantus) Nursing Considerations
Insulin – Rapid Acting (Novolog, Humalog) Nursing Considerations
Nursing Care and Pathophysiology for Cholecystitis
Nursing Care and Pathophysiology for Cirrhosis (Liver Disease, Hepatic encephalopathy, Portal Hypertension, Esophageal Varices)
Nursing Care and Pathophysiology for Hepatitis (Liver Disease)
Nursing Care and Pathophysiology for Pancreatitis
Nursing Care and Pathophysiology for Appendicitis
Hiatal Hernia
Nursing Care and Pathophysiology for Diverticulosis – Diverticulitis
GERD (Gastroesophageal Reflux Disease)
Gastritis
Bariatric Surgeries
Nursing Care and Pathophysiology for Peptic Ulcer Disease (PUD)
Nursing Care and Pathophysiology for Inflammatory Bowel Disease (IBD)
Nursing Care and Pathophysiology for Ulcerative Colitis(UC)
Nursing Care and Pathophysiology for Hemorrhoids
Nursing Care and Pathophysiology for Crohn’s Disease
Appendicitis
Pantoprazole (Protonix) Nursing Considerations
Omeprazole (Prilosec) Nursing Considerations
Pancrelipase (Pancreaze) Nursing Considerations
Ondansetron (Zofran) Nursing Considerations
Vasopressin
Proton Pump Inhibitors
Parasympatholytics (Anticholinergics) Nursing Considerations
Nursing Care and Pathophysiology for Multiple Sclerosis (MS)
Nursing Care and Pathophysiology for Myasthenia Gravis
Nursing Care and Pathophysiology for Parkinsons
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