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Nr341 study guide weekly, Lecture notes of Nursing

Chamberlain College of NursingNursing

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NR341 WEEK 7
INTRODUCTION TO COMPLEX GASTROINTESTINAL AND ENDOCRINE
ALTERATIONS
•The gastrointestinal and endocrine systems are responsible for a wide
variety of functions in the digestive process and beyond.
•The endocrine system secretes hormones that affect digestion.
•Because hormones have a wide range of action, problems with their
regulation are associated with homeostatic changes, some severe.
Adverse effects are related to perfusion and glucose metabolism and
cause difficulty regulating fluids, electrolytes, and temperature.
•Gastrointestinal problems, such as severe vomiting, diarrhea, or
bleeding, can also alter fluid, electrolyte, and acid-base balances.
Additionally, many critical illnesses affect the motility of the
gastrointestinal tract and metabolic function, leading to poor
outcomes.
•Secretion of many gastrointestinal hormones is disrupted in critical
illness, making it essential that nurses understand the process and
actions that can be taken to maintain homeostasis during these
difficult periods.
GASTROINTESTINAL BLEEDING
TYPES:
Stomach & Duodenal bleeding
- Peptic ulcers
Esophageal bleeding
Diagnostics:
Endoscopy
Labs:
- Occult
- Coagulation
- Liver enzymes
- H&H
- BUN
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NR341 WEEK 7

INTRODUCTION TO COMPLEX GASTROINTESTINAL AND ENDOCRINE

ALTERATIONS

  • The gastrointestinal and endocrine systems are responsible for a wide variety of functions in the digestive process and beyond.
  • The endocrine system secretes hormones that affect digestion.
  • Because hormones have a wide range of action, problems with their regulation are associated with homeostatic changes, some severe. Adverse effects are related to perfusion and glucose metabolism and cause difficulty regulating fluids, electrolytes, and temperature.
  • Gastrointestinal problems, such as severe vomiting, diarrhea, or bleeding, can also alter fluid, electrolyte, and acid-base balances. Additionally, many critical illnesses affect the motility of the gastrointestinal tract and metabolic function, leading to poor outcomes.
  • Secretion of many gastrointestinal hormones is disrupted in critical illness, making it essential that nurses understand the process and actions that can be taken to maintain homeostasis during these difficult periods. GASTROINTESTINAL BLEEDING TYPES: Stomach & Duodenal bleeding
  • Peptic ulcers Esophageal bleeding Diagnostics: Endoscopy Labs:
  • Occult
  • Coagulation
  • Liver enzymes
  • H&H
  • BUN
  • ABGs Stomach and Duodenal Bleeding Peptic ulcers due to infection or overuse of non-steroidal anti-inflammatory drugs (NSAIDs) are the most common cause of upper gastrointestinal bleeding. Stress-related mucosal disease (SRMD) most often occurs in critically ill clients due to bleeding gastric ulcers. SRMD is common in clients experiencing burns, trauma, or major surgery. Clients receiving continuous renal replacement therapy are also at high risk. Mallory-Weiss syndrome is characterized by a linear tear of the gastric mucosa found at the stomach and esophageal junction. It is caused by retching during vomiting. Benign and malignant tumors of the stomach can lead to gastrointestinal bleeding. Esophageal Bleeding Esophageal varices and esophagitis are the likely cause of bleeding from the esophagus. Esophagitis is common with gastroesophageal reflux disease (GERD), smoking, and alcohol use. Benign and malignant tumors of the esophagus can cause gastrointestinal bleeding. DIAGNOSIS OF GI BLEEDING: Massive gastrointestinal (GI) hemorrhage is classified as a loss of more than 500 mL (25% of intravascular volume). Endoscopy is the primary tool for diagnosing the source of upper gastrointestinal bleeding. Laboratory studies that must be closely monitored include: occult blood testing of all vomitus and stools coagulation studies (prothrombin time, partial thromboplastin time) liver enzymes hemoglobin and hematocrit

O

Surgery PPIs Isotonic fluids are needed for volume replacement. Whole blood, packed red blood cells, and fresh frozen plasma may also be used in massive hemorrhages. Supplemental oxygen may be needed to maintain adequate ventilation. Endoscopic stasis of a bleeding vessel is the first-line management for gastrointestinal bleeding. If this therapy fails, surgical intervention is necessary. During the acute phase of bleeding, proton pump inhibitors (PPI) can be used to decrease bleeding, decrease hydrochloric acid (HCl) secretion, and neutralize the HCl that is present. PPIs reduce acid secretion, which is necessary to prevent altered platelet function and clot stabilization. Later, antacids may be given to neutralize the pH of stomach contents. ESOPHAGEAL VARICES Dilated veins Cirrhosis Treatment:

  • Vasopressin, nitro
  • Endoscopic banding
  • Balloon tamponade
  • TIPS Esophageal varices are distended, engorged veins that are susceptible to hemorrhage. They occur from cirrhosis of the liver and portal hypertension due to chronic alcoholism. To reduce the pressure, the body creates collateral circulation. Rupture can cause life-threatening bleeding. Treatment focuses on reducing portal pressures. Medications to reduce portal pressures include:
  • vasopressin
  • octreotide acetate
  • beta-blockers
  • nitrates Treatment options:
  • Endoscopic ligation or banding involves the suctioning of a vein into the chamber of the endoscope, which is then tied up with a small band. The vein then loses its blood supply and, over time, thrombosis and fibrosis occur.
  • Sclerosis involves injecting an agent into the vein that causes thrombosis and hemostasis.
  • Balloon tamponade uses an inflated balloon to put pressure on the varices to stop esophageal blood flow. If these treatments do not work, surgical intervention is necessary. A shunt may be placed to divert blood flow and reduce portal pressures. ACUTE ADRENAL INSUFFICIENCY Addisonian Crisis – life threatening
  • Low cortisol Triggers
  • Stress, infection, surgery
  • Stopped taking meds Manifestations
  • Hypotension
  • Tachycardia
  • Dehydration
  • Fever
  • Weaknesses
  • Hypoglycemia
  • Low NA and high potassium
  • GI issues – N/V Adrenocortical insufficiency, hypofunction of the adrenal cortex, can lead to acute adrenal insufficiency, which is a life-threatening emergency. Otherwise known as an Addisonian crisis or adrenal crisis, this problem is caused by a sudden sharp decrease in adrenocortical hormones (glucocorticoids and mineralocorticoids). If not treated quickly, the prognosis is poor. Addisonian crisis is triggered by:

Cortisol replacement

  • High dose hydrocortisone Hypoglycemia
  • Glucagon High Potassium
  • Regular insulin
  • D5NS
  • Sodium polystyrene sulfonate
  • Loop diuretics Gastric stress ulcers
  • Famotidine or omeprazole Circulatory collapse associated with acute adrenal insufficiency is often unresponsive to vasopressors and fluid replacement. Treatment strategies include:
  • intravenous (IV) 0.9% normal saline (NS) to replace volume
  • IV high-dose hydrocortisone has both glucocorticoid and mineralocorticoid properties
  • IV glucagon treats hypoglycemia
  • IV regular insulin to treat hyperkalemia
  • IV dextrose 5% normal saline (D5NS) to move potassium back into the cells
  • sodium polystyrene sulfonate binds to potassium so it can be excreted
  • loop diuretics (furosemide) treat hyperkalemia
  • IV famotidine or omeprazole prevents gastric stress ulcers ACUTE THYROTOXICOSIS Thyrotoxicosis – life threatening
  • High T3 & T Triggers
  • Uncontrolled hyperthyroidism
  • Overmedication post thyroidectomy Manifestations
  • hypertension
  • tachycardia
  • high temperature
  • respiratory distress
  • anxiety
  • confusion Acute thyrotoxicosis refers to the physiologic effects of hypermetabolism resulting from a sudden surge of excess circulating T3 and T4 levels. It can be life-threatening and requires aggressive treatment. It is most commonly caused by uncontrolled hyperthyroidism or overmedication after a thyroidectomy. Clinical manifestations of acute thyrotoxicosis are severe hyperthermia up to 106 °F (41.1 °C), severe hypertension, vomiting, abdominal pain, tachycardia, chest pain, dyspnea, delirium, and heart palpitations. Severe cardiovascular involvement can lead to heart failure. TREATMENT OF THYROTOXICOSIS Medications or thyroid removal Medications to block thyroid hormone production and the sympathetic nervous system are needed.
  • Thionamides (methimazole, propylthiouracil) prevent the release of thyroid hormones.
  • Beta-blockers (propranolol) block the effects of sympathetic nervous system stimulation. INTRODUCTION TO NURSIN CARE: End Stage Liver Disease Chronic liver disease Slow progression Cirrhosis – alcohol abuse
  • vomiting
  • change in bowel pattern Impaired Bile Formation Clinical Manifestations
  • Decreased formation of bile salts leads to increased serum bilirubin.
  • Excess serum bilirubin causes jaundice. Impaired Detoxification The liver is key to detoxifying the body and neutralizing a range of internal and environmental chemicals. As it fails, the following functions are impaired.
  • Filtering blood to physically remove large toxins decreases.
  • Binding fat-soluble toxins to bile slows due to decreased bile formation.
  • Production enzymes that break down unwanted substances decrease, as liver cells become nonfunctional. Clinical manifestations
  • acne
  • skin rashes
  • allergies
  • blood sugar alterations
  • brain fog
  • depression
  • digestive issues
  • high cholesterol
  • fatigue
  • headaches
  • mood swings
  • joint pain
  • muscle pain
  • fetor hepaticus
  • a sweet, musty odor to the breath caused by increased serum toxins and glucose NURSING CARE: END STAGE LIVER DISEASE Promote rest Preventing transmission Monitor for complications Provide adequate nutrition END STAGE LIVER DISEASE: PORTAL HYPERTENSION Portal Hypertension Portal hypertension occurs when the failing liver shunts blood, causing increased cardiac output in the presence of vasodilation. This results in decreased perfusion to all organs in the presence of high cardiac output. Clinical Manifestations
  • Initial findings include:
  • systemic hypertension
  • flushed skin
  • bounding pulses
  • Later findings are those commonly associated with heart failure.
  • jugular venous distension
  • hypotension
  • cardiac dysrhythmias
  • crackles in lungs
  • decreased tissue perfusion to organs
  • Varices shown in the esophagus or stomach are caused by the increase in portal venous pressure.
  • monitor intake and output (to assess fluid balance)
  • monitor for bleeding (for early detection of blood loss)
  • Use bioartificial liver devices
  • includes bioartificial liver, molecular adsorbents recirculating system (MARS), and others
  • remove water- and protein-bound toxins
  • may clear cytokines from the liver END STAGE LIVER DISEASE: TESTS Albumin
  • protein Ammonia
  • neuro assessments
  • lactulose
  • care with protein Bile pigments
  • bilirubin Coagulation studies
  • bleeding
  • safety Liver enzymes
  • ALT, APT, AST COMPLICATIONS OF END STAGE LIVER DISEASE Ascites
  • Third spacing
  • Treatment is bed rest, low sodium/fluid and diuretics
  • Paracentesis or TIPS Hepatopulmonary syndrome
  • Dilated lung blood vessels
  • Liver transplant

Hepatorenal syndrome

  • Decreased urine output
  • Hemodialysis
  • End of life Portal system encephalopathy
  • Increased ammonia
  • Lactulose ASCITES: Ascites is the third-spacing of fluid in the peritoneum (abdomen) caused by portal hypertension and the retention of sodium and water. As the fluid in the peritoneum increases, pressure on nearby organs increases and may interfere with normal functions, particularly the lungs. General treatment of ascites includes bed rest, a low-sodium diet, fluid restriction, and diuretic therapy. Paracentesis (removal of fluid with a needle) or transjugular intrahepatic portosystemic shunting (TIPS) can be used to remove the fluid from the abdomen to decrease pressure and improve symptoms. Daily assessment of the abdominal girth at the umbilicus provides information on the effectiveness of treatment. Explore the effects on impacted body systems and potential therapeutic actions. PORTAL SYSTEM ENCEPHALOPATHY: Portal systemic (or hepatic) encephalopathy manifests as impairment of the central nervous system. Often associated with increased serum ammonia levels, the exact cause of portal systemic encephalopathy is not known. Manifestations are present in stages and reflect the severity of the condition. Treatment for portal system encephalopathy is aimed at lowering the serum ammonia level. Lactulose, given orally or via rectum, lowers the pH in the bowel, causing ammonia to leave the bloodstream and enter the bowel. Once trapped, the ammonia is excreted. Restriction of hepatotoxic medications is important. Collaboration with a clinical pharmacist to review all medications for potential impact on the liver is advised.

HHS/DKA: LABS COMPARISON

GOALS OF TREATMENT: HYPERGLYCEMIA EMERGENCIES

Short term goals:

  • Lower glycose 140-
  • Restore volume and perfusion
  • Correct electrolytes
  • Correct acidosis (if present)
  • Treat underlying cause Long term goals:
  • Prevent recurrence
  • Med adjustment as needed
  • Lifestyle modifications
  • Education
  • Behavior modification

Short-Term Goals –

  • Short-term treatment goals for clients experiencing diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS) are the same—lower the serum glucose to restore homeostasis (American Diabetes Association, 2021).
  • restoration of circulatory volume and tissue perfusion
  • resolution of hyperglycemia
    • target glucose 140–180 mg/dL
  • correction of electrolyte imbalance
  • correction of acidosis, if present
  • treatment of the underlying cause
    • sepsis, myocardial infarction, and stroke Long-Term Goals Long-term treatment goals for both DKA and HHS focus on understanding the cause of the hyperglycemic emergency to prevent recurrence through collaborative disease management (American Diabetes Association, 2021).
  • medication adjustment, as needed
  • lifestyle modification
  • dietary patterns
  • physical fitness
  • stress reduction
  • medication compliance
  • client education related to current health needs
  • behavior modification to increase compliance TREATMENT OF HYPERGLYCEMIC EMERGENCIES NURSING ACTIONS Monitor cardiac/VS IV access/fluids IV insulin Assess mental status