Nursing Care and Pathophysiology for Peptic Ulcer Disease (PUD)

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Study Tools For Nursing Care and Pathophysiology for Peptic Ulcer Disease (PUD)

Peptic Ulcer Disease Pathochart (Cheatsheet)
Abdominal Pain – Assessment (Cheatsheet)
Peptic Ulcer Disease (Image)
EGD Image of Peptic Ulcer (Image)
Billroth I (Image)
Billroth II (Image)
Peptic Ulcer Disease Assessment (Picmonic)
Peptic Ulcer Disease Interventions (Picmonic)
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Outline

Pathophysiology:

Peptic ulcer disease (PUD) consists of open sores in the protective lining of the stomach and upper small intestine. Gastric ulcers occur on the inside of the stomach and duodenal ulcers occur on the inside of the upper portion of the small intestine (duodenum).

Overview

  1. Break in mucosal lining of stomach, pylorus, duodenum, or esophagus that come in contact with gastric secretions
  2. Irritation by gastric secretions may cause bleeding

Nursing Points

General

  1. Causes
    1. Helicobacter pylori
    2. Frequent use of NSAIDs, Aspirin
    3. Smoking
    4. Alcohol Use
  2. Diagnosis
    1. Upper GI Series x-rays
    2. EGD – Esophagogastroduodenoscopy

Assessment

  1. Nausea/Vomiting
  2. Abdominal Pain
    1. Usually upper abdominal pain
    2. Often burning or sharp pain
    3. Gastric Ulcer
      1. Gnawing, sharp 30-60 minutes after a meal
    4. Duodenal Ulcer
      1. 1.5 to 3 hours after eating
      2. Pain may be relieved by eating
  3. Hematemesis (gastric)
  4. Melena (duodenal)

Therapeutic Management

  1. Avoid aspirin and NSAIDs
  2. Monitor H&H and assess for bleeding
  3. Medications
    1. H2 receptor antagonists
    2. Proton pump inhibitors
    3. Antacids
    4. Sucralfate (Carafate) – take 30-60 minutes  before meals
  4. Surgical options
    1. Vagotomy
      1. Cut Vagus nerve
      2. ↓ Parasympathetic = ↓ gastric acid secretion
    2. Gastric resection / Gastrectomy
      1. Remove all or part of stomach to remove ulcerated tissue
    3. Billroth I, Billroth II
      1. Remove a portion of the stomach and reattach to duodenum (I) or jejunum (II)
    4. Post-Op:
      1. HOB 45°
      2. Clear Liquids x 3-7 days
      3. Assess Bowel sounds
      4. Risk for  Dumping Syndrome (rapid influx of gastric contents into small intestine)
        1. Avoid sugar or fatty foods
        2. Smaller meals
        3. No fluids with meal

Nursing Concepts

  1. Nutrition
    1. Avoid foods that cause irritation
      1. Coffee
      2. Soda
      3. Tea
      4. Chocolate
      5. High sodium
      6. Spicy foods
    2. Small, frequent meals
  2. Comfort
    1. Administer medications as ordered
    2. Encourage nutrition compliance

Patient Education

  1. Smoking Cessation
  2. Adhere to dietary restrictions
  3. 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 do is we’re going to be discussing peptic ulcer disease, some of the pathophysiology, as well as how we’re going to treat it. Without further ado. Let’s dive in. 

So regarding the pathophysiology of peptic ulcer disease, it’s important to understand that it’s like a chink in the armor, right? Whenever you’re looking at the stomach and you look at the inside lining of the stomach, right? What we actually have is this nice mucosal membrane, right? This mucosal lining on the inside of the stomach. And the entire purpose of this mucosal lining is to protect these sensitive submucosal and muscle layers. These delicate, sensitive tissues from that corrosive hydrochloric acid, right? Remember our stomach produces hydrochloric acid in an attempt to try and chew up and dissolve the food that we consume so that once it passes into the small intestine, we’re able to more effectively remove nutrients. 

Peptic ulcer disease is like a chink in that armor. It is a breakdown in an area of that mucosal lining that would then allow the spillage of hydrochloric acid into that mucosal membrane to then begin to chew away at these sensitive and delicate tissues. This is incredibly problematic, right? We think about hydrochloric acid. We think about acid in general as this liquid substance that’s capable of chewing. It’s being very corrosive and able to chew through anything, right? Well, imagine what would happen if you had a little breakdown, a chink in the armor of that mucosal lining, that’s supposed to protect those sensitive tissues. If you have that breakdown and you lose that protection, that stomach acid is now able to reach these more delicate tissues and it begins to chew away at it. And all of the symptoms that we’re going to see as well as the treatment modalities geared towards working on peptic ulcer disease are all related to that chink in the armor. 

So some of the different causes of peptic ulcer disease. What are some different things that would actually cause that chink in the armor, that disruption, in the mucosal lining that’s supposed to protect our stomach. One of the leading causes that’s important for you to know regarding peptic ulcer disease is H. pylori also known as Helicobacter pylori. And essentially not to get too technical, but what this is, is this an infection that ends up resulting in inflammation of that mucosal lining of the stomach, causing a breakdown in that mucosal lining, which then allows stomach acid to chew through that lining in the stomach, right? Peptic ulcer disease. So an actual infection, H. pylori, causes an inflammatory response in that mucosal lining, allowing hydrochloric acid to start to chew up those stomach tissues.  NSAIDs are another one, right? I’m not going to dive into this cellular process, but just know, or remember, or maybe research NSAIDs work on cyclooxygenase 1 (COX-1) as well as cyclooxygenase 2 (COX-2), right? One is responsible for reducing inflammation. That’s what NSAIDs are responsible for. But one of the other cyclooxygenases actually chews away that protective mucosal lining again, allowing hydrochloric acid to escape into those mucosal and submucosal tissues and start to chew away at our stomach lining. Also smoking as well as alcohol consumption, both also can directly lead to the development of peptic ulcer disease. But it’s important to know that the leading culprits are H. pylori as well as NSAIDs. 

So what are some of the assessment findings that we’re going to see in patients who are experiencing peptic ulcer disease? Well, one is going to be epigastric, stomach pain, right? Stomach pain in that upper abdomen. Again, we have an actual degradation in the lining of that stomach. We have hydrochloric acid, basically. We’re digesting ourselves, we’re digesting our own stomach. So that’s going to cause us epigastric pain. That’s going to cause nausea and vomiting, weight loss as your appetite is going to be greatly decreased. Every time you eat, you’re going to have increased hydrochloric acid production. More hydrochloric acid production, more chewing away at the lining of the stomach, right? It’s a very big problem. Abdominal fullness and hematemesis, right? You can actually have degradation in that lining to the point that you end up bleeding. You ended up producing a GI bleed. It’s not uncommon in peptic ulcer disease, right? 

And so some of the ways that we’re going to be able to diagnose whether a patient has a chink in the armor or not, is things such as an upper EGD, right? Where they actually would take a scope, feed it in through the mouth, down into the tummy and actually take a look at the stomach itself, actually visualize the mucosal lining of that stomach to see if there’s any chink in the armor. While they’re in there, right, this is kind of bleeding a little bit into therapeutic management or how we’re going to treat, but while they’re in there, they, if there is an active bleed in that lining that chink in the armor, they can also cauterize while they’re there. H. pylori testing. If we suspect that a patient may have peptic ulcer disease, we may very well undergo H. pylori testing. Remember that this is one of the leading causes of peptic ulcer disease, as well as a barium swallow, which is important. Should a patient be having this epigastric pain? Should they have evidence of peptic ulcer disease? A barium swallow is not uncommon. Also, as the patient swallows contrast, which is then highlighted through diagnostic imaging, which could be reflective and show whether we have hydrochloric acid actually spilling out of the stomach or not. Or if we have contrast spilling out of the stomach or not, basically a lot of different diagnostic indicators to tell us whether a patient has peptic ulcer disease or not. 

So what are some of the different things that we’re going to use in order to treat patients with peptic ulcer disease? But one is, of course we know H. pylori is one of the leading causes. So we’re going to treat H. pylori. usually through a combination of antibiotics, as well as PPI’s remember, these are Proton Pump Inhibitors, right? These are medications such as omeprazole, which end in -prazole, all right? These are medications that actually affect that hydrogen potassium pump in the stomach as a proactive means to try and reduce the amount of hydrochloric acid our stomach is producing.  Also H2 antagonist. Medications that again are a proactive attempt to reduce the overall hydrochloric acid produced. We’re going to discontinue NSAIDs as we know, these are common causes of a breakdown or a chink in the armor. Again, this is an actual ulceration, peptic ulcer diseases, an ulceration in that lining of the stomach, right? So what can happen is, you can have bleeding as we’ve already alluded to. It’s not uncommon to see blood transfusions occur as the patient’s hemoglobin is dropping. Something, I actually wasn’t aware of, is, there is a treatment modality called a vagotomy, which is an actual clipping of that vagus nerve. They actually clip the vagus nerve, which innervates the stomach and actually reduces the amount of hydrochloric acid produced. Very interesting, but has side effects, as you imagine, clipping a vagus nerve would. And then another possible treatment as a partial gastrectomy. If you have a patient who has recurrent peptic ulcers, they continue to occur, and as a result, you continue to have bleeding, it’s an actual problem. What may actually occur is they may actually take a portion of the stomach, surgically remove it to try and prevent that weakened chink in the armor to prevent those bleeds from continually reoccurring. 

Some of the patient education that we’re going to go over as well for patients with peptic ulcer disease, similar to patients experiencing GERD, right? But we know NSAIDs are one of the common causes of peptic ulcer disease. So making sure that we encourage them to stop using NSAIDs. We want to stop that breakdown in the cyclooxygenase process, so reducing that mucosal lining of the stomach and therefore continually causing ulceration in that stomach. Stopping smoking. We know that that also leads to peptic ulcer disease. Medication adherence, right? Those PPI’s, those H2 blockers. Anything that we’re prescribing to treat H. pylori. Medication adherence is paramount, as well as any kind of dietary adherence, right? Similar to GERD, reducing food intake is going to cause additional hydrochloric acid production within the stomach, citrus, chocolate, coffee, spicy foods, all of these things that lead to increased hydrochloric acid production. 

And so going over some of the key points surrounding peptic ulcer disease, remember it is like a chink in the armor. It is an actual degradation or break down in that mucosal lining of the stomach that’s supposed to protect our underlying tissues from that corrosive hydrochloric acid. We actually have digestion of our own stomach, basically. Remembering that a lot of the causes, primarily, H. pylori infections, but also overuse of NSAIDs breaking down that mucosal lining. Knowing that all of our assessment findings, again, are related to that hydrochloric acid, hitting that chink in the armor causing pain, causing possible bleeding, indigestion, nausea, vomiting, et cetera. And knowing that all of our therapeutic managements are directly geared at either treating an H. pylori infection or reducing the total amount of stomach acid in our tummy, or blood transfusions, things to actually treat that ulceration in the stomach. And all of the patient education that we just went over. 

Guys, that was peptic ulcer disease. I hope that that helped bring a little bit more understanding to the disease process. I hope that you guys go out there and be your best selves today. And as always, happy nursing.

 

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Study Plan Lessons

Nursing Care and Pathophysiology of COPD (Chronic Obstructive Pulmonary Disease)
Electrical A&P of the Heart
Cataracts
Electrolytes Involved in Cardiac (Heart) Conduction
Fluid Pressures
Nursing Care and Pathophysiology of Acute Kidney (Renal) Injury (AKI)
Alveoli & Atelectasis
Fluid Shifts (Ascites) (Pleural Effusion)
Hiatal Hernia
Macular Degeneration
Nursing Care and Pathophysiology for Cushings Syndrome
Nursing Care and Pathophysiology for Sickle Cell Anemia
Gas Exchange
Isotonic Solutions (IV solutions)
Nasal Disorders
Nursing Care and Pathophysiology for Diabetes Insipidus (DI)
Nursing Care and Pathophysiology for Disseminated Intravascular Coagulation (DIC)
Hearing Loss
Hypotonic Solutions (IV solutions)
Nursing Care and Pathophysiology for Peptic Ulcer Disease (PUD)
Fractures
Hypertonic Solutions (IV solutions)
Integumentary (Skin) Important Points
Meniere’s Disease
Casting & Splinting
The EKG (ECG) Graph
Drawing Blood
EKG (ECG) Waveforms
Levels of Consciousness (LOC)
Nursing Care and Pathophysiology of Chronic Kidney (Renal) Disease (CKD)
Sodium-Na (Hypernatremia, Hyponatremia)
Calcium-Ca (Hypercalcemia, Hypocalcemia)
Calculating Heart Rate
Diabetes Management
Dialysis & Other Renal Points
Nursing Care and Pathophysiology for Diverticulosis – Diverticulitis
Nursing Care and Pathophysiology of COPD (Chronic Obstructive Pulmonary Disease)
Routine Neuro Assessments
Adjunct Neuro Assessments
Chloride-Cl (Hyperchloremia, Hypochloremia)
Nursing Care and Pathophysiology of Diabetic Ketoacidosis (DKA)
Oncology Important Points
Restrictive Lung Diseases (Pulmonary Fibrosis, Neuromuscular Disorders)
Brain Death v. Comatose
Magnesium-Mg (Hypomagnesemia, Hypermagnesemia)
Nursing Care and Pathophysiology for Inflammatory Bowel Disease (IBD)
Nursing Care and Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)
Nursing Care and Pathophysiology for Ulcerative Colitis(UC)
Phosphorus-Phos
Cerebral Perfusion Pressure CPP
Immunizations (Vaccinations)
Cognitive Impairment Disorders
Normal Sinus Rhythm
Nursing Care and Pathophysiology of BPH (Benign Prostatic Hyperplasia)
Nursing Care and Pathophysiology for Acquired Immune Deficiency Syndrome (AIDS)
Nursing Care and Pathophysiology for Cholecystitis
Sinus Bradycardia
Nursing Care and Pathophysiology for Anaphylaxis
Sinus Tachycardia
Atrial Flutter
Nursing Care and Pathophysiology for Cirrhosis (Liver Disease, Hepatic encephalopathy, Portal Hypertension, Esophageal Varices)
Nursing Care and Pathophysiology for Parkinsons
Atrial Fibrillation (A Fib)
Brain Tumors
Premature Atrial Contraction (PAC)
Supraventricular Tachycardia (SVT)
Premature Ventricular Contraction (PVC)
Ventricular Tachycardia (V-tach)
Ventricular Fibrillation (V Fib)
1st Degree AV Heart Block
2nd Degree AV Heart Block Type 1 (Mobitz I, Wenckebach)
2nd Degree AV Heart Block Type 2 (Mobitz II)
3rd Degree AV Heart Block (Complete Heart Block)
Inserting an NG (Nasogastric) Tube
Hierarchy of O2 Delivery
NG (Nasogastric)Tube Management
Artificial Airways
NG Tube Med Administration (Nasogastric)
Nursing Care and Pathophysiology for Ischemic Stroke (CVA)
Airway Suctioning
Nursing Care and Pathophysiology for Menopause
Stroke Assessment (CVA)
Stroke Therapeutic Management (CVA)
Stroke Nursing Care (CVA)
Stoma Care (Colostomy bag)
Seizure Causes (Epilepsy, Generalized)
Seizure Assessment
Seizure Therapeutic Management
Chest Tube Management
Pain and Nonpharmacological Comfort Measures
Enteral & Parenteral Nutrition (Diet, TPN)
ABG (Arterial Blood Gas) Interpretation-The Basics
ABG (Arterial Blood Gas) Oxygenation
ABGs Nursing Normal Lab Values
ABGs Tic-Tac-Toe interpretation Method
Nursing Care and Pathophysiology of Acute Kidney (Renal) Injury (AKI)
Addisons Disease
Albumin Lab Values
Ammonia (NH3) Lab Values
Nursing Care and Pathophysiology for Anemia
AVPU Mnemonic (The AVPU Scale)
Base Excess & Deficit
Blood Urea Nitrogen (BUN) Lab Values
Bronchoscopy
Burn Injuries
Cardiac (Heart) Enzymes
Cardiac Anatomy
Chest Tube Management
Cholesterol (Chol) Lab Values
Nursing Care and Pathophysiology for Heart Failure (CHF)
Congestive Heart Failure (CHF) Labs
COPD (Chronic Obstructive Pulmonary Disease) Labs
Coronary Circulation
Creatinine (Cr) Lab Values
Nursing Care and Pathophysiology of Diabetes Mellitus (DM)
Dysrhythmias Labs
Neurological Fractures
Fractures
GERD (Gastroesophageal Reflux Disease)
Glaucoma
Glomerular Filtration Rate (GFR)
Heart (Cardiac) Failure Therapeutic Management
Heart (Cardiac) Sound Locations and Auscultation
Hemodynamics
Nursing Care and Pathophysiology for Hemorrhagic Stroke (CVA)
Hyperglycaemic Hyperosmolar Non-ketotic syndrome (HHNS)
Intracranial Pressure ICP
Ischemic (CVA) Stroke Labs
Lactic Acid
Leukemia
Liver Function Tests
Lung Sounds
Lymphoma
Metabolic Acidosis (interpretation and nursing diagnosis)
Metabolic Alkalosis
MI Surgical Intervention
Nursing Care and Pathophysiology of Myocardial Infarction (MI)
Nursing Care and Pathophysiology for Anemia
Nursing Care and Pathophysiology for Aortic Aneurysm
Nursing Care and Pathophysiology for Arterial Disorders
Nursing Care and Pathophysiology for Asthma
Nursing Care and Pathophysiology for Cardiogenic Shock
Nursing Care and Pathophysiology for Cardiomyopathy
Nursing Care and Pathophysiology for Crohn’s Disease
Nursing Care and Pathophysiology for Distributive Shock
Nursing Care and Pathophysiology for Gout
Nursing Care and Pathophysiology for Heart Failure (CHF)
Nursing Care and Pathophysiology for Hemorrhagic Stroke (CVA)
Nursing Care and Pathophysiology for Hepatitis (Liver Disease)
Nursing Care and Pathophysiology for Hyperthyroidism
Nursing Care and Pathophysiology for Hypothyroidism
Nursing Care and Pathophysiology for Hypovolemic Shock
Nursing Care and Pathophysiology for Influenza (Flu)
Nursing Care and Pathophysiology for Lyme Disease
Nursing Care and Pathophysiology for Meningitis
Nursing Care and Pathophysiology for Multiple Sclerosis (MS)
Nursing Care and Pathophysiology for Myasthenia Gravis
Nursing Care and Pathophysiology for Pancreatitis
Nursing Care and Pathophysiology for Pneumothorax & Hemothorax
Nursing Care and Pathophysiology for Rheumatoid Arthritis (RA)
Nursing Care and Pathophysiology for Seizure
Nursing Care and Pathophysiology for SIADH (Syndrome of Inappropriate antidiuretic Hormone Secretion)
Nursing Care and Pathophysiology for Thrombophlebitis (clot)
Nursing Care and Pathophysiology for Tuberculosis (TB)
Nursing Care and Pathophysiology for Valve Disorders
Nursing Care and Pathophysiology of Angina
Nursing Care and Pathophysiology of Diabetes Mellitus (DM)
Nursing Care and Pathophysiology of Endocarditis and Pericarditis
Nursing Care and Pathophysiology of Glomerulonephritis
Nursing Care and Pathophysiology of Hypertension (HTN)
Nursing Care and Pathophysiology of Myocardial Infarction (MI)
Nursing Care and Pathophysiology of Osteoarthritis (OA)
Nursing Care and Pathophysiology of Osteoporosis
Nursing Care and Pathophysiology of Pneumonia
Nursing Care and Pathophysiology of Renal Calculi (Kidney Stones)
Nursing Care and Pathophysiology of Urinary Tract Infection (UTI)
Pneumonia Labs
Potassium-K (Hyperkalemia, Hypokalemia)
Preload and Afterload
Pressure Ulcers/Pressure injuries (Braden scale)
Respiratory Acidosis (interpretation and nursing interventions)
Respiratory Alkalosis
ROME – ABG (Arterial Blood Gas) Interpretation
Skin Cancer
Spinal Cord Injury
Systemic Lupus Erythematosus (SLE)
Thoracentesis
Thrombocytopenia
Total Bilirubin (T. Billi) Lab Values
Troponin I (cTNL) Lab Values
Urinalysis (UA)
Vent Alarms