Week 5; Acute Care GI Flashcards
(122 cards)
1
Q
Normal fxn of liver
A
Filtration of blood from stomach, spleen, pancreas, intestine, manufactures & secretes bile, manufacture of fibrinogen, prothrombin, heparin, vitamin A, immunoglobulins, storage of vitamins, metabolism of carbohydrates, fats, proteins, drugs, alcohol, and hormones, aids in destruction of aging RBC, and regulation of blood volume by storing up to 400ml of blood.
2
Q
Cirrhosis
A
Characterized by widespread fibrotic (scarred) bands of connective tissue. This changes the liver’s normal makeup and its associated cellular regulation. Livers become nodular; blood and lymph flow are impaired. Inflammation destroys hepatocytes.
3
Q
Compensated cirrhosis
A
the liver is scarred and cellular regulation is impaired, but able to perform essential functions
4
Q
Decompensated cirrhosis
A
liver function is impaired and S/S of liver failure
5
Q
Common causes of cirrhosis
A
Alcoholic liver disease, hepatitis, steatohepatitis (from fatty liver), drugs and chemical toxins, gallbladder disease, metabolic/genetic causes, and cardiovascular disease
6
Q
Postnecrotic cirrhosis etiology
A
Hepatitis C—second leading cause in the United States, Hepatitis B and D—most common cause worldwide
NAFLD-non alcoholic fatty liver disease
7
Q
Alcoholic cirrhosis etiology
A
Alcohol use—excessive and prolonged
8
Q
Biliary cirrhosis etiology
A
Chronic biliary obstruction and infection.
9
Q
Non-alcoholic fatty liver disease (NAFLD)
A
Associated with diabetes, obesity, and metabolic syndrome. Can progress to liver cancer, cirrhosis, or liver failure. THE PNPLA3 gene identifies as a risk gene for the disease, hispanics have this gene more often than other ethnic groups. Most common cause of liver disease in the world.
10
Q
What is the leading cause of cirrhosis and liver failure in the US?
A
Hep C
11
Q
Assessing for liver disease
A
Assess for exposure to alcohol and drugs, herbs, chemicals, needlestick injury, tattoo placement, imprisonment, or employment as a healthcare worker, firefighter, or police officer. Assess sexual history and orientation. Inquire about family history. Collect previous medical history.
12
Q
Liver disease s/s
A
Fatigue, significant changes in weight, GI symptoms-anorexia and vomiting, alterations in abdominal area and liver tenderness, obvious yellowing of skin (jaundice) and sclerae, increased abdominal girth - ascites, dry skin, rashes, petechiae or ecchymosis, warm, bright red palms (palmar erythema), increased bleeding tendencies, dark urine, clay-colored stools, edema in extremities.
13
Q
Jaundice -
A
characterized by excessive circulating bilirubin levels. Liver cells cannot effectively secrete bilirubin and the skin and mucous membranes become characterized by a yellow discoloration,
14
Q
First sign of hepatic encephalopathy –
A
subtle changes in personality
15
Q
DX of liver disease
A
Laboratory assessment,
AST, ALT, LDH- elevated
Alkaline phosphatase-elevated
Serum protein-elevated, albumin-decreased
Serum total bilirubin-elevated
PT/INR prolonged liver because of decreased prothrombin.
Imaging assessment
Abdominal x-rays
CT, MRI
MR elastography
Other diagnostic assessment
Liver US, arteriography, EGD, ERCP
16
Q
Complications of cirrhosis
A
Bleeding, hypovolemia, edema, decreased albumin production in liver, massive ascites – renal vasoconstriction and sodium and water retention, coagulation defects, jaundice, splenomegaly, hepatorenal syndrome
17
Q
Hepatorenal syndrome
A
Prognosis for patient with liver failure poor; sudden decrease in urine output <500 mL/24hr, elevated BUN and creatinine levels. Often occurs after clinical deterioration from GI bleeding or onset of hepatic encephalopathy
18
Q
Spontaneous bacterial peritonitis
A
Those at risk have advanced liver disease.
Bacteria responsible typically from bowel and reach the ascitic fluid after migrating through bowel wall and transversing the lymphatics
Symptoms vary but fever, chills, pain and tenderness common. Can have worsening encephalopathy and increased jaundice without abdominal symptoms
19
Q
Portal hypertension
A
Major complication of cirrhosis. Persistent increase in pressure within the portal vein caused from resistance or obstruction of blood flow. Blood looks for alternative venous channels around the blockage. Blood backs up into the spleen, esophagus, stomach, intestines, abdomen and rectum.
20
Q
Varices
A
Thin vein walls distend from increased pressure.
Esophageal most common, hemorrhoids are another common area. Hypovolemic shock can occur.
21
Q
Esophageal varices
A
Are fragile and thin walled esophageal veins that become distended and tortuous from increased pressure. S/s include hematemesis and melena (black tarry stools)
22
Q
Bleeding esophageal varices
A
Life-threatening medical emergency resulting in hypovolemic shock
23
Q
Managing hemorrhage d/t esophageal varices
A
Endoscopic variceal ligation (banding)
Emergency rescue- esophagogastric balloon tamponade. Can cause life threatening complications such as aspiration, asphyxia and esophageal perforation. Patient usually intubated on mechanical ventilator to protect airway; only used if the patient can not have an endoscopy or TIPS procedure
24
Q
Hypovolemic shock review
A
Abnormally decreased volume of circulating fluid causing peripheral circulatory failure that endangers vital organs. The brain, heart, kidneys are particularly vulnerable. Tachycardia is an early sign of compensation for excessive blood loss. Tachycardia, tachypnea, BP normal initially, decrease or narrowing in pulse pressure (difference between systolic and diastolic), elevated BP can occur initially until compensatory mechanisms fail. Acidosis with vasodilation and decreased BP, increased bleeding, decreased circulating volume, and subsequent organ death.
25
Preventing or managing hemorrhage: pharmacological
Beta blocker, usually propranolol- decreases heart rate and hepatic venous pressure, resulting in decreased bleeding.
Vasoactive drug, usually vasopressin and octreotide-reduces blood flow resulting in decrease portal pressure.
Octreotide- suppresses secretion of gastrin, serotonin and intestinal peptides resulting in decrease blood flow and pressure in the varices. NG, platelets, fresh frozen plasma, albumin
26
Hepatic encephalopathy
AKA Portal-systemic encephalopathy
Complex cognitive syndrome from liver failure and cirrhosis. 4 stages and s/s progressively worsen
27
Factors leading to PSE
High-protein diet, infection, hypovolemia, hypokalemia, constipation, GI bleed, drugs
28
Hepatic encephalopathy signs and symptoms
Personality changes, behavior changes (agitation, belligerence), emotional lability (euphoria, depression), inability to concentrate, fatigue, drowsiness, slurred or slowed speech, sleep pattern disturbances, asterixis (hand flapping)
Last stage – the patient comatose and may experience seizures
29
Preventing or managing hepatic encephalopathy
Drugs are used sparingly- opioid analgesics, sedatives, and barbiturates (especially with encephalopathy)
Lactulose by mouth or NG to eliminate or reduce ammonia through the stool.
Need to watch potassium levels dehydration from excessive stools.
Neomycin or rifaximin(broad spectrum antibiotics) act as a intestinal antiseptic- decrease ammonia levels.
Assess for asterixis (coarse tremors) and fetor hepaticus (liver breath)- signs of worsening encephalopathy.
30
Ascites-
Collection of free fluid in the peritoneal cavity
Caused by portal HTN. Serum colloid osmotic pressure decreased in the circulatory system. A fluid shift from vascular to abdomen
31
Managing fluid volume
Monitor fluid/electrolyte balance, abdominal girth measurement, diuretic use, low sodium diet, paracentesis for severe ascites, transjugular intrahepatic portal-systemic shunt (TIP)
32
Paracentesis
A catheter or drain is inserted into the abdomen to drain fluid.
Procedure:
Obtain pre-procedure vital signs and wt
Ask patient to void before procedure
Position patient on bed with head elevated
Monitor vital signs per protocol
Measure drainage
Describe drainage
Label and send specimen to lab for analysis
Place a dressing at site after physician removes catheter
Maintain bedrest per protocol
Weigh patient after procedure
33
Cirrhosis nutritional support
Early stages- high protein & carbohydrates
Advanced stages- fiber, protein, fat and sodium restrictions.
Small, frequent feedings
34
Hep A transmission
fecal-oral
35
Hepatitis B transmission
Blood and body fluids, IV drug abuse, sexual contact maternal-fetal route, complications- cirrhosis and liver cancer
36
Hepatitis C transmission and complication
Contact with blood and body fluids
IV drug users
Contaminated blood transfusions
Complications- cirrhosis and liver cancer
37
Hepatitis D or Delta hepatitis transmission
Contact with Hep B, parenteral transmission, hepatitis E , oral-fecal, contaminated water, under-developed countries. Resembles Hep A
38
Hepatitis incidence
HAV and HBV are declining due to vaccination.
HCV most common—no vaccine, Higher incidence of cancer
39
Hepatitis health promotion and management
Vaccines for HAV and HBV
HAV-specific recommendations
Proper handwashing (especially after handling shellfish)
Avoid contaminated food or water.
40
Hepatitis assessment
Ask about exposure to someone with hepatitis. Ask about chemical exposure. Inquire about alcohol, drug, herbal use. Inquire about travel, sexual activities, needlestick exposure, drug (IV) use, military service. Assess for family history of liver disease.
41
Physical assessment/signs and symptoms of hepatitis
Abdominal pain, changes in skin or sclera (icterus), arthralgia (joint pain) or myalgia (muscle pain), diarrhea/constipation, changes in color of urine or stool, fever, lethargy, malaise, nausea/vomiting, pruritus (itching), weight loss due to complications associated with inflammation of the liver, fatigue due to decreased metabolic energy production, potential for infection related to state of immunocompromise
42
Dx of hepatitis
Liver enzymes, blood tests specific to hepatitis type- antibodies, liver biopsy
43
Care for hepatitis
HBV medications, post-exposure: Interferon
Low fat, high calorie, carbohydrates, and proteins
Addressing fatigue
Balance rest and activity periods
Reducing the potential for infection
HAV- enteric precautions
HBV, HCV- blood and body fluid precautions
Education regarding infection control is important.
Cannot give blood donation
Techniques to prevent spread
44
Fatty Liver – steatosis
Caused by accumulation of fats in and around hepatic cells caused by alcohol use or other factors.
Types of fatty liver disease:
Nonalcoholic fatty liver disease (NAFLD)
Nonalcoholic steatohepatitis (NASH)
45
Causes of fatty liver
diabetes, obesity, elevated lipids, genetics
46
Fatty liver disease interventions:
Teaching, weight loss, glucose control, lipid lowering agents, monitoring LFT
47
Fatty liver disease dx
Many patients are asymptomatic. Typical findings are elevated liver enzymes, elevated ALT or AST, MRI and ultrasound indicated or liver biopsy
48
A 59-year-old patient with a history of alcohol abuse spanning 15 years has been diagnosed with cirrhosis. The patient will be undergoing abdominal paracentesis today. Which assessment finding alerts the nurse that the paracentesis has been successful?
a. Decrease in post-procedure weight
b. No residual obtained during procedure
c. Substantial decrease in blood pressure
d. Immediate sensation of a need to urinate
Answer A
Weight should decrease as fluid is drained from the abdominal cavity.
A substantial decrease in blood pressure can indicate shock. Residual should be obtained during the procedure. The patient should not feel a sensation or need to urinate, because a primary safety measure is to have the patient void right before the procedure to avoid injury to the bladder during the procedure.
49
When a complete assessment of this patient is performed, what other signs and symptoms does the nurse expect? Think about signs severe chronic alcoholism with hepatoencephalopathy?
a. Dry skin with c/o itchy skin
b. Personality changes
c. Peripheral dependent edema
d. Ecchymosis, spider angiomas
e. Palmar erythema
Think about a patient with end severe cirrhosis? What will you find in your assessment?
Could be ALL OF THE ABOVE
50
The patient tells the nurse that once he is discharged to home, he has no intention to stop drinking alcohol. What is the appropriate nursing response?
a. “Let’s discuss the seriousness of your condition and the effect alcohol has on your situation.”
b. “It’s your choice to drink or not to drink.”
c. “Why won’t you consider quitting?”
d. “If you continue to drink, you are going to die.”
51
Liver transplant
Has become common procedure for person with end stage liver disease or acute liver failure who has not responded to conventional medical or surgical intervention. Cirrhosis is the most common reason
Patients not considered candidates: advanced cardiac disease, severe respiratory disease, metastatic tumors, or inability to follow instructions regarding therapy and self-management
Typically livers are from trauma patients
Living donors possible – usually close family member – liver resection. Recipient liver removed, implant done and Liver regenerates and grows.
52
Liver transplant rejection
Monitor for signs such as fever, tachycardia, pain in RUQ, decreased bile pigment and volume and increasing jaundice.
Labs: elevated serum bilirubin, rising ALT and AST, increase alkaline phosphatase, and increase Prothrombin Time
53
Cholecystitis
Inflammation of the gallbladder. Can be acute or chronic. Gallstones can obstruct the cystic duct, gallbladder neck or common bile duct. Trapped bile is reabsorbed and acts as a chemical irritant causing impaired circulation, edema and distention result. If gallbladder ruptures, can result in peritonitis.
54
Two types of acute cholecystitis:
calculous (from gallstones or Cholelithiasis) or acalculous (without gallstones)
55
Acalculous cholecystitis
Typically associated with biliary stasis caused by any condition that affects regular filling or emptying of the gallbladder. Decreased blood flow or anatomic problems such as twisting or kinking in the neck or ducts.
56
Chronic cholecystitis
results when repeated episodes of obstruction cause chronic inflammation
57
Cholecystitis risk factors
Women, aging, american indian, Mexican American, Caucasian, family history of gallstones, crohn’s disease, obesity, rapid weight loss, women on hormone therapy, gastric bypass, genetic factors
58
Cholecystitis s/s
Episodic or vague upper abdominal pain that can radiate to right shoulder, pain triggered by high fat or high volume meal, anorexia, N/V, dyspepsia, flatulence or belching, feeling of abdominal fullness, rebound tenderness, fever, jaundice, clay colored stools, dark urine, steatorrhea
59
Biliary colic
Severe pain produced by obstruction of the cystic duct of the gallbladder or movement of one or more stones. It can be so severe it occurs with tachycardia, pallor, diaphoresis, prostration. Assess patient for possible chock
Contact rapid response team
Stay with patient and keep head of bed flat
60
Cholecystitis assessment
R/o peptic ulcer, hepatitis, and pancreatitis – many symptoms are the same
Elevated liver enzymes
Direct and indirect serum bilirubin elevated
X-ray or ultrasound
HIDA scan (hepatobiliary scan)
ERCP – endoscopic retrograde cholangiopancreatography
61
Nursing care for cholecystitis
Nutrition and hydration, managing pain – typically an opioid, ketorolac for mild to moderate pain, oral bile acid dissolution or gallstone stabilizing agent. extracorporeal shock wave lithotripsy
Surgery: cholecystectomy
62
Cholecystitis teaching
Avoid fatty foods, fast foods
Medications – pain meds
Dietary consult if needed
Report complications post surgery
63
Normal function of pancreas
Contains the islets of Langerhans-produce insulin and glucagon. Manufacture and release pancreatic enzymes to aid in ingestion
Amylase- breaks down carbohydrates
Lipase- breaks down fats
Trypsin- breaks down protein
Produces and release insulin and glucagon into bloodstream
64
Amylase-
breaks down carbohydrates
65
Lipase-
breaks down fats
66
Trypsin-
breaks down protein
67
Pancreatitis
Inflammatory condition of the pancreatitis d/t premature activation of excessive pancreatic enzymes. Destroys ductal tissue and pancreatic cells, causes autodigestion, and leads to fibrosis of the pancreas.
68
Acute pancreatitis complications
Infection, hemorrhage, acute kidney failure, paralytic ileus, intervention-NG until patient is able to pass flatus or had a stool, hypovolemic or septic shock, vasodilation and release of protein-rich fluid, Pleural effusion, respiratory distress syndrome, pneumonia, multisystem organ failure- necrotizing hemorrhagic pancreatitis, disseminated intravascular coagulation-release of necrotic tissue and enzymes into bloodstream, diabetes mellitus
69
Pancreatitis s/s
Nausea and vomiting- may occur after heavy meals, fluid/electrolyte imbalance, abdominal and back pain- radiates to left flank or shoulder, increased with meals, fever, jaundice, hyperglycemia, weight loss, ascites, gray-blue discoloration of abdomen, decreased bowel sounds, elevated HR, decreased BP
70
Pancreatitis labs
amylase & lipase (amylase elevated first 12-24 hours)
Lipase may rise later and last up t0 2 weeks
Imaging Assessment- abd ultrasound
71
The priority collaborative problems for patients with acute pancreatitis include
acute pain due to pancreatic inflammation and enzyme leakage.
weight loss due to inability to ingest food and absorb nutrients.
72
Pancreatitis care
Manage Pain, IV Fluids, NPO, analgesics- Morphine or Dilaudid by PCA pump, histamine receptor antagonists- zantac, proton pump inhibitors- omeprazole, monitor for shock, renal failure, pleural effusions, hyperglycemia, NG, oral care, promote Nutrition- TPN early in acute phase, low-fat, bland diet, small frequent meals
73
Chronic pancreatitis
Progressive destructive disease of pancreas characterized by remissions and exacerbations
74
Chronic pancreatitis management
Drug therapy- H2 receptor blockers, proton pump inhibitors, analgesic administration, enzyme replacement- amylase, lipase and trypsin, insulin therapy, nutrition therapy, low fat, bland diet, 6 small meals a day
75
Pancreatic abscess
Most serious complication of pancreatitis. Always fatal if untreated
76
Pancreatic abscess s/s
High fever, blood cultures
77
Pancreatic abscess treatment
drainage via percutaneous method or laparoscopy, antibiotic treatment alone does not resolve abscess.
78
A 68-year-old patient presents to the ED the day after Thanksgiving, stating that he has “eaten and drunk quite a bit.” He states that about 1 hour ago he experienced a sudden onset of pain in the left upper quadrant that radiates to his left flank. He rates the pain as an 8 on a 0-to-10 scale. The patient is admitted with acute pancreatitis.
Which laboratory finding corroborates the diagnosis of acute pancreatitis?
Serum lipase, 150 U/L
Serum amylase, 200 U/L
Serum glucose, 80 mg/dL
White blood cells (WBCs), 6000 mcL
Which laboratory finding corroborates the diagnosis of acute pancreatitis?
Serum lipase, 150 U/L normal 0-60
Serum amylase, 200 U/L normal 100-300
Serum glucose, 80 mg/dL Fasting less than 100
White blood cells (WBCs), 6000 mcL Normal 4.5- 11.1
Correct answer is A
79
When the patient is asked about pain, he says that it is intense and continuous. He states that sometimes when he curls up in a fetal position the pain eases.
Which medication does the nurse recognize that will provide the most comprehensive pain relief at this time?
PCA morphine sulfate
IM fentanyl (Sublimaze)
PCA meperidine (Demerol)
Oral hydromorphone (Dilaudid)
PCA morphine sulfate Opioid via PCA is correct, first choice
IM fentanyl (Sublimaze) Possibility but Slow IV push or Patch preferred
PCA meperidine (Demerol) Can cause seizure in older adults
Oral hydromorphone (Dilaudid) Can be used but this is oral
Primary drug is opioid by PCA first
80
The patient has been NPO but is now tolerating food.
What education will the nurse provide regarding nutrition?
Small and frequent meals are best.
Use of alcohol and caffeine should be consumed in moderation.
Expect to experience nausea and vomiting as you begin to consume foods.
Low-carbohydrate, high-protein, and high-fat foods should be consumed.
ANS: A
Patients may experience nausea and vomiting but should not expect this to happen. High-carbohydrate, high-protein, and low-fat foods should be included in the diet. Alcohol and caffeine should be avoided.
81
The patient has been NPO but is now tolerating food. What education will the nurse provide regarding nutrition?
a. Small and frequent meals are best.
b. Use of alcohol and caffeine should be consumed in moderation.
c. Expect to experience nausea and vomiting as you begin to consume foods.
d. Low-carbohydrate, high-protein, and high-fat foods should be consumed.
Correct answer is A
82
The patient is being discharged to home. What patient teaching will the nurse provide regarding when the patient should notify the health care provider?
Bland diet, limit spices, diet (high carb, high protein, low fat), notify MD if pain, fever, n/v or diarrhea, jaundice, clay colored stools, darkened urine. These are possible indicators of complications
83
Appendicitis
Inflammation of the appendix. Most commonly occurring inflammatory lesion of the bowel and on of the most common reasons for surgery, More common in adolescents and young adults. Can become inflamed and pus filled and rupture. Perforation causes contents to flow into peritoneal space and cause peritonitis.
84
S/s of appendicitis
Fever, acute severe abdominal pain, abdominal distention, acute appendicitis Can result in death if not treated aggressively and rapidly, elevated White Count, might be Seen on ultrasound or x-ray or these can rule out other causes, RLQ tenderness with rebound tenderness is quite common
85
Appendicitis nursing consideration
Potential for Systemic Infection/Sepsis due to inadequate primary defenses occurring with the inflammatory process
86
Appendicitis treatment
Surgical removal, antibiotics, fluid resuscitation, supportive treatment to maintain vital signs, pain management
87
Celiac disease
Chronic immune-mediated disorder of small intestine causing impaired absorption of nutrients, fats, sensitivity to gliadin fraction of gluten. Severity depends on extent of mucosal involvement, duration of disease. Intestinal mucosa damaged by immunologic response
88
Celiac disease risk factors
Cause unknown. Genetic and immune factors play a role, caucasians of European descent most commonly affected, having a first-degree relative with celiac disease significantly increases risk
High-risk populations: iron deficiency anemia, osteopenic bone disease, insulin-dependent diabetes, Down syndrome, Turner syndrome
89
Celiac disease s/s
Abdominal bloating, cramps, diarrhea, steatorrhea, anemia, small stature, delayed maturity, signs of nutrient deficiency resolve when gluten removed from diet
90
Celiac disease dx
Enteroscopy with tissue biopsy, upper GI with small-bowel follow-through, serologic testing for antibodies, serum levels, hemoglobin, hematocrit, RBC
91
Celiac disease therapy
Vitamin, mineral supplements, iron, folic acid for anemia, vitamin K, corticosteroids
92
Celiac disease nutrition
Gluten-free diet high in calories, protein
Consultation with dietitian
Awareness of hidden sources of gluten
Restriction of fat, lactose
IV nutrition for refractory disease
93
Celiac disease nursing care
Improve bowel function, assess for fluid balance, weigh daily, monitor intake/output, assess skin, mucous membranes for dehydration, monitor perianal skin for breakdown, teaching about gluten free diet,
94
Lactose intolerance
Body unable to digest lactose (milk sugar)
Lactose is primary carbohydrate in milk
Must be broken down into monosaccharides by lactose
Lactose deficiency → lactose intolerance, manifestations of malabsorption
95
Lactose intolerance risk factors
Previous radiation therapy for abdominal cancer, history of celiac disease or Crohn disease, premature birth, increasing age, ethnicity, more common among Native Americans, Asians, Hispanics, and African Americans
96
S/s of lactose intolerance
Lactose deficiency often asymptomatic
Lactose intolerance: lower abdominal cramping, pain, diarrhea, diarrhea may be explosive
97
Lactose intolerance dx
Lactose breath test
Lactose tolerance test
98
Lactose intolerance therapy
Nonprescription lactose enzymes
Yogurt, calcium supplements
Vitamin D, riboflavin, protein supplements
99
Lactose intolerance nutrition management
Lactose-free or reduced-lactose diet, no milk, milk products for some patients, milk pretreated with lactose can be used
100
Lactose intolerance nursing care
Provide education, support, discuss sources of lactose, suggest trial of lactose-treated milk, lactose enzyme supplements, emphasize importance of obtaining proteins, calcium from other sources
101
Short bowel syndrome
May result from small bowel resection, tumors, infarction of mucosa, incarcerated hernias, crohn disease, trauma, enteropathy from radiation therapy, affects absorption of water, nutrients, vitamins, minerals, severity depends on amount of bowel resected, increased risk for kidney stones, gallstones
102
Short bowel syndrome s/s
Severity depends on total amount of bowel resected, which portions of bowel removed
103
Short bowel syndrome management
Management focuses on alleviating manifestations, multivitamins, mineral supplementation, antidiarrheal medications, proton pump inhibitor, frequent, small, high-kilocalorie, high-protein feedings, total parenteral nutrition (TPN) for severe manifestations, monitor
vital signs, input and output (I&O), daily weights, nutritional status , skin turgor, mucous membranes
104
Diarrhea nursing care
Document number, character of stools, limit lactose intake, provide skin care of perianal region
105
Short bowel syndrome teaching
Instruct about diet, medication regimen, stress adequate fluid intake, discuss need for frequent weight monitoring, reporting changes, refer to dietitian or counselor, patient manages disorder on day-to-day basis
106
Malabsorption disorders in infants and children: celiac disease
Irritability, behavioral issues, bloating, gas, diarrhea, vomiting, skin rashes
Decreased appetite, poor weight gain → failure to thrive, delayed growth/puberty, weak bones
Age-appropriate teaching important
107
Malabsorption disorders in infants and children: lactose intolerance
Primary lactose deficiency: rare hereditary condition, infants require special lactose-free formula
Secondary lactose deficiency: celiac or Crohn disease, GI tract infection. Resolves with treatment of causing disorder, dietary changes, supplements
108
Malabsorption disorders in infants and children: short bowel syndrome
Surgery for necrotizing colitis
Diarrhea, bloating, poor appetite, inability to gain weight
Prone to dehydration, vitamin, mineral, electrolyte imbalances
109
Malabsorption disorders in pregnant women: Celiac disease
Female infertility, amenorrhea
Poor pregnancy outcome, intrauterine growth restriction
Increased risk for miscarriage, stillbirth, perinatal morbidity
Testing at-risk patients, diet restrictions
110
Malabsorption disorders in pregnant women:
Lactose intolerance
Body’s ability to digest lactose may improve during pregnancy
If symptoms persist during pregnancy, focus on consuming other sources of protein
Calcium supplements, lactose-free products
111
Malabsorption disorders in older adults: Celiac disease
Underdiagnosed due to less severe symptoms, similarity of symptoms to other age-related changes
Increased risk of malnutrition, poor bone health
Gluten-free diet may be problematic
Resistance to dietary changes
Gluten in medications
112
Malabsorption disorders in older adults: lactose intolerance
Normal decline in lactose → increasing lactose intolerance
Dietary management
Calcium supplementatio
113
Malabsorption disorders in older adults: short bowel syndrome
Normal aging process may decrease GI function, increasing severity of syndrome
Medication may affect body’s ability to absorb nutrients, especially with short bowel syndrome
114
Pyloric stenosis
Narrowing of pyloric orifice that prevents food in stomach from passing into duodenum. Digestion and absorption impaired, causing dehydration, malnutrition. Affects newborns in first month, rare in adults
115
Pyloric stenosis risk factors
May have genetic factor, more common in males than females, antibiotics in late pregnancy or first few weeks of life
116
Pyloric stenosis s/s
Symptoms evident 3–6 weeks after birth
Projectile vomiting as stenosis worsens
Vomitus may contain blood
Persistent hunger
Peristaltic wave across abdomen
Leads to dehydration, malnutrition
Changes in stool
Failure to gain weight, may lose weight
117
Pyloric stenosis diagnostic tests
Abdominal ultrasound
Upper gastrointestinal (GI) study
Blood tests
118
Surgery for pyloric stenosis
Surgery is [erformed when fluid, electrolyte balance restored, open or laparoscopic pyloromyotomy, good prognosis
119
Pyloric stenosis in adults
Primary: no apparent cause
Secondary: result of other GI problems
Often long history of digestive disorders
Most common in middle-aged men
Individuals who had pyloric stenosis as infants may be at increased risk
120
Pyloric stenosis nursing care
Correcting electrolyte, acid–base imbalances, replacing lost fluids, minimizing parents’ anxiety
121
Pyloric stenosis assessment
Observe, auscultate, palpate abdomen
Health history
History of vomiting
Physical assessment
Vital signs, weight, nutritional status
Skin turgor, mucous membranes
Urinary output
122
Pyloric stenosis goals
maintain fluid and electrolytes, minimize weight loss, promote rest and comfort, prevent infection
