GI Function 1&2 Flashcards
(302 cards)
1
Q
Consumes, digests, and eliminates food
A
Gastrointestinal System
2
Q
2 divisions of G.I tract
A
- Upper division
2. Lower division
3
Q
oral cavity, pharynx, esophagus, and stomach
A
Upper division of G.I tract
4
Q
small intestine, large intestine, and anus
A
Lower division of GI tract
5
Q
Mucosa, submucosa, muscle, and serosa (connective tissue)
A
Four layers of G.I tract
6
Q
Large serous membrane that lines the abdominal cavity, semi permeable, made of layers
A
Peritoneum:
7
Q
Parietal peritoneum:
A
Outer layer
8
Q
Visceral peritoneum:
A
Inner layer
9
Q
space between the two layers
A
Peritoneal cavity
10
Q
What happens if there is decreased blood supply to the G. I tract?
A
GI tract goes without good blood supply, no good intervention –> parelytic illeus: Intervention of blood supply to the gut is lacking so now food particles movement through gut is limited which can lead to sepsis and sever infection, obstruction
11
Q
Double-layer peritoneum containing blood vessels and nerves that supplies oxygen and nutrients to the intestinal wall
A
Mesentery
12
Q
Food enters through the mouth to begin chemical and mechanical digestion.
A
Upper GI Tract
13
Q
opening from stomach to the duodenum
A
pyloric sphincter
14
Q
______ is coordinated by the swallowing center in the medulla and cranial nerves 5 (trigeminial), 9 (glossopharyngeal), 10 (vagus), and 12 (hypoglossal nerve).
A
Swallowing
15
Q
- expansion of the stomach as food enters;
- contractions of the stomach to break food into smaller particles
- release of gastric acid required for food processing;
A
Vagus nerve (X)
16
Q
emptying of the stomach contents into the small intestine;
secretion of digestive pancreatic enzymes (amalayze, lipase, protease) that enable absorption of calories; and
controlling sensations of hunger, satisfaction and fullness.
A
Vagus Nerve (X)
17
Q
______ Duct: synthesizes bile, needs this to digest and absorb fat, travel to L/R hepatic duct.
A
Hepatic
18
Q
Where bile is stored
A
Gallbladder
19
Q
Enzymes backup to the pancreas and cause inflammation and that’s how we end up with ________
A
pancreatitis
20
Q
colytheciasis
A
has to do with gallstone collection in the gallbladder
21
Q
Metabolize carbohydrates, protein, and fats
Synthesize glucose, protein, cholesterol, triglycerides, and clotting factors
Store glucose, fats, and micronutrients and release when needed
A
Liver functions
22
Q
Detoxify blood of potentially harmful chemicals
Maintain intravascular fluid volume
Metabolize medications to prepare them for excretion
A
Liver function
23
Q
Produce bile
Inactivate and prepare hormones for excretion
Remove damaged or old erythrocytes to recycle iron and protein
Serve as a blood reservoir
Convert fatty acids to ketones
A
Liver function
24
Q
Bile is produced by the?
A
Liver
25
Produces enzymes, electrolytes, and water necessary for digestion (lipase, protease, amalyase)
--Secreted into duodenum to help digest those foods
Exocrine functions (Pancreas)
26
Produces hormones (insulin) to help regulate blood glucose
Endocrine function (Pancreas)
27
Continues digestion
Absorbs nutrients and water
Lower GI Tract
28
Atrophic gastritis
Achloryhdria
Decrease digestion
Liver experiences reduced blood flow, delayed drug clearance (bc not metabolized well), and diminished regeneration capacity
Changes in lactose, calcium, and iron metabolism and absorption
Decreased peristalsis
Greater risk for constipation
Changes associated with aging
29
Decreased/absence of hydrochloric acid, absent or diminished HCl in the stomach. More severe form of hypochlorhydria, deficiency of stomach acids
Without stomach acids, the
body won’t properly break
down protein
Achlorhydria B12 deficiency (?), deficiency of stomach acid, not able to digest proteins
Achlorhydria,
30
Patient with achlorhydria, what happens to the albumin levels?
Decrease
31
3.5-5.5
Normal albumin levels
32
______: These conditions include issues consuming, digesting, and absorbing food. Affected individuals are often underweight and vitamin deficient.
Altered nutrition
33
Disorders of the upper GI tract: congenital defects (cleft lip and palate and pyloric stenosis), dysphagia, vomiting, hiatal hernia, gastroesophageal reflux disease, gastritis, peptic ulcers, cholelithiasis
Altered nutrition
34
Disorders of the liver: hepatitis, cirrhosis
Disorders of the pancreas: pancreatitis
Altered nutrition
35
These conditions may be symptoms of another secondary condition, or the primary one. They may alter nutrition as well as impair elimination.
Impaired elimination
36
Disorders of the lower GI tract: diarrhea, constipation, intestinal obstruction, appendicitis, peritonitis, celiac disease, inflammatory bowel disease, irritable bowel syndrome, diverticular disease
Impaired elimination
37
Cancers: oral cancer, esophageal cancer, gastric cancer, liver cancer, pancreatic cancer, colorectal cancer
Impaired elimination
38
Common congenital defects of the mouth and face that are apparent at birth and vary in severity.
Cleft Lip and Palate
39
Develops between the fourth and ninth weeks of gestation
Cleft Lip and Palate
40
Associated with genetic mutations, drugs, toxins, viruses, vitamin deficiencies, and cigarette SMOKING.
Most frequent in American Indians, Hispanics, and Asians
Cleft Lip and Palate
41
Males are twice as likely as females to have a cleft lip.
True
42
Females are twice as likely as males to have a cleft palate.
True
43
Can affect one’s appearance and may lead to feeding issues, speech problems, ear infections, and hearing problems
Teeth and nose malformations may also be present.
Cleft Lip and Palate
44
results from failure of the maxillary processes and nasal elevations or upper lip to fuse during development.
Cleft lip
45
results from failure of the hard and soft palate to fuse in development, creating an opening between the oral and nasal cavity.
Cleft palate
46
history, physical examination, and prenatal ultrasound
Diagnosis of cleft lip and palate
47
temporary measures (e.g., special nipples or dental appliances), surgical repair, cosmetic plastic surgery, speech therapy, orthodontist consultation, and multidisciplinary case management
Treatment for cleft lip and palate
48
Most cases present at 3 weeks of life.
| Exact cause unknown; a combination of environmental and hereditary factors
Pyloric Stenosis
49
Exposure to macrolides in early infancy leads to increased pyloric stenosis risk.
Most common in Caucasians and males.
Pyloric Stenosis
50
appear within several weeks after birth: hard mass in the abdomen, regurgitation, projectile vomiting, wavelike stomach contractions, small and infrequent stools, failure to gain weight, dehydration, and irritability.
Pyloric Stenosis
51
Pyloric sphincter muscle fibers become thick and stiff, making it difficult for the stomach to empty food into the small intestine
Pyloric Stenosis
52
Known as infantile hypertrophic pyloric stenosis
Pyloric stenosis
53
history, physical examination, abdominal ultrasound, barium X-ray, endoscopy, arterial blood gases, and blood chemistry
Pyloric stenosis
54
surgical repair called pyloromyotomy or balloon dilation (to dilate sphincter)
Pyloric stenosis
55
operation to loosen the tight muscle causing the blockage between the stomach and small intestine.
Pyloric stenosis
56
Difficulty swallowing
Difficulty swallowing
57
congenital atresia, esophageal stenosis or stricture, esophageal diverticula, tumors, stroke, cerebral damage, achalasia, Parkinson’s disease, Alzheimer’s disease, muscular dystrophy, Huntington’s disease, cerebral palsy, multiple sclerosis, amyotrophic lateral sclerosis, and Guillain-Barré syndrome
Causes of dysphagia
58
A condition in which a body passage is closed or missing. It includes lack of the valve opening in the heart to allow blood flow (pulmonary atresia) and lack of an external ear canal (aural atresia). This is a cause of Dysphagia.
Dysphagia
59
Failure of lower esophageal sphincter (LES) to relax because of loss of innervations. This a cause of Dysphagia.
achalasia
60
a sensation of food being stuck in the throat, choking, coughing, “pocketing” food in the cheeks, difficulty forming a food bolus, delayed swallowing, and odynophagia
Dysphagia
61
Pain on swallowing food and fluids
Odynophagia (manifestation of dysphagia)
62
: history, physical examination, barium swallow, chest and neck X-ray, esophageal pH measurement, esophageal manometry, and esophagogastroduodenoscopy (EGD)
Diagnosis of dysphagia
63
specific for the causative condition but usually includes speech therapy
Treatment for dysphagia
64
Take in a solution and watch as they are swallowing the barium to see if there is any stenosis/occlusion
Barium sallow (dysphagia)
65
procedure during which a small flexible endoscope is introduced through the mouth (or, with smaller-caliber endoscopes, through the nose) and advanced through the pharynx, esophagus, stomach, and duodenum --- to see if there is anything
esophagogastroduodenoscopy (diagnosis for dysphagia)
66
A nurse teaches the family of a client with dysphagia about decreasing the risk of aspiration when the client eats. Which of the following strategies should the nurse include in the teaching plan? Select all that apply:
A. Maintain an upright position while eating
B. Restrict the diet to clear liquids until swallowing improves
– liquids make it worse,
separating the food
C. Introduce foods on the unaffected side of the mouth
D. Keep distractions to a minimum during meals
E. Cut food into large pieces of finger food
A. Maintain an upright position while eating
D. Keep distractions to a minimum during meals
67
A nurse plans care for a client who has dysphagia and has a new dietary prescription. Which of the following should the nurse include in the plan of care? Select all that apply:
A. Have suction equipment available for use
B. Use thickened liquids
C. Assign an assistive personnel (nursing assistant) to feed the client slowly
D. Teach the client to swallow with the neck flexed.
A. Have suction equipment available for use
B. Use thickened liquids
C. Assign an assistive personnel (nursing assistant) to feed the client slowly
D. Teach the client to swallow with the neck flexed.
68
Involuntary or voluntary forceful ejection of chyme from the stomach up through the esophagus and out the mouth
Vomiting
69
protection, reverse peristalsis, increased intracranial pressure, and severe pain
Causes of vomiting
70
Coordinated by the medulla
vomiting
71
Vomiting is not due to stomach contraction - stomach, esophagus and associated sphincters are relaxed
True
72
Vomiting is co-ordinated by the vomiting centre (VC) in the medulla oblongata of the brain stem
true
73
Vomiting is frequently preceded by profuse salivation, sweating, elevated HR, and the sensation of _____ or retcching
nausea
74
Recurrent vomiting can be exhausting and lead to fluid, electrolyte, and pH ______
Imbalances
75
Aspiration can cause serious damage and inflammation and can occur when supine, unconscious, or the vomiting or cough reflex is suppressed.
True (vomiting)
76
Vomiting = loss of hydrochloric acid, metabolic alkalosis, pH is high, and bicarbonate will be ____
elevated
77
blood in the vomitus
Hematemesis:
78
Has a characteristic “coffee grounds” appearance resulting from protein in the blood being partially digested.
Hematemesis
79
Blood is irritating to the gastric mucosa.
Can occur from any conditions that cause upper GI bleeding.
Hematemesis
80
Usually indicates the presence of bile
Can occur as a result of a GI tract obstruction
Yellow or green vomitus
81
May indicate content from the lower intestine
Frequently results from intestinal obstruction
Bleeding from lower GI tract
A deep brown vomitus
82
Caused by conditions that impair gastric emptying
segments of food, stomach has not had time to digest
Undigested food vomitus
83
history, physical examination,
| and blood chemistry
diagnosis of vomiting
84
in infants- a depressed anterior fontanel, dry mucous membranes, lethargy dark urine, sunken eyeballs, decreased skin turgor, tachycardia
Losing volume,
Symptoms of dehydration
85
Noticeable thirst
Muscle cramps
Weakness
Decreased performance
signs of dehydration
86
Nausea
Headache
Fatigue
Lightheaded feeling or dizziness
Difficulty paying attention
Signs of dehydration
87
Skin with decrease turgor remains elevated after being pulled up and released
Signs of dehydration
88
Sunken eyes, dark yellow urine, poor skin turgor, lack of tears, rapid heart rate, low BP, delayed capillary refill
Signs of dehydration
89
antiemetic medications,
oral or intravenous fluid replacement,
correct electrolyte imbalance (hypokalemia) ,
restore acid–base balance (vomiting leads to loss of gastric acid →metabolic alkalosis).
Treatment for vomiting
90
Monitor intake and output, daily weighs
Treatment for vomiting
91
A stomach section protrudes upward through an opening in the diaphragm toward the lung. Vary in severity depending on size
Hiatal Hernia
92
weakening of the diaphragm muscle, increased intrathoracic pressure or increased intra-abdominal pressure; abdominal straining , frequent heavy lifting, pregnancy, trauma; and congenital defects
Causes of hiatal hernia
93
advancing age and smoking, obesity
Risk factors for hiatal hernia
94
Include indigestion, heartburn, frequent belching, nausea, chest pain, strictures, dysphagia, and soft upper abdominal mass (protruding stomach pouch)
S/S hiatal hernia
95
Worsen with recumbent positioning, eating (especially after large meals), bending over, and coughing
s/s hiatal hernia
96
Any factor that increase intra-abdominal pressure, abdominal straining , frequent heavy lifting, pregnancy
s/s hiatal hernia
97
history, physical examination, barium swallow, upper GI tract X-rays, manometry, and esophagogastroduodenoscopy
diagnosis of hiatal hernia
98
eat small frequent meals (six small meals a day), avoid alcohol, assuming a high Fowler’s position after meals, sleep with the head of the bed elevated 6 inches, cease smoking, reduce stress (stress increases gastrointestinal ischemia), antacids, acid-reducing agents, mucosal barrier agents, and surgical repair (only if medical therapy, lifestyle modifications, & weight loss fail)
Treatment of hiatal hernia
99
Chyme periodically backs up from the stomach into the esophagus. Bile can also back up into the esophagus.
These gastric secretions irritate the esophageal mucosa.
Gastroesophageal
| Reflux Disease
100
certain foods (e.g., chocolate, caffeine, carbonated beverages, citrus fruit, tomatoes, spicy or fatty foods, and peppermint),
alcohol consumption, nicotine,
hiatal hernia, obesity, pregnancy,
certain medications (e.g., corticosteroids, beta blockers, calcium-channel blockers, and anticholinergics),
nasogastric intubation, and delayed gastric emptying
Causes of Gastroesophageal
| Reflux Disease
101
heartburn, epigastric pain (usually after a meal or when recombinant), dysphagia, dry cough, laryngitis, pharyngitis, regurgitation of food, and sensation of a lump in the throat
s/s GERD
102
Often confused with angina and may warrant ruling out cardiac disease
s/s GERD
103
esophagitis, strictures, ulcerations, esophageal cancer, and chronic pulmonary disease, aspiration
complications of GERD
104
history, physical, barium swallow, esophagogastroduodenoscopy, esophageal pH monitoring, and esophagus manometry
Diagnosis of GERD
105
is done to measure muscle pressure and movements in the esophagus in the evaluation of achalasia
esophagus manometry
106
avoid triggers, avoid clothing that is restrictive around the waist, eat small frequent meals
Treatment for GERD
107
high Fowler’s positioning 2–3 hours after meals, avoid all caffeine and milk products (caffeine ↓ pressure in lower esophageal sphincter; milk ↑ gastric acid secretion),
Treatment for GERD
108
weight loss, stress reduction,
elevate HOB approximately 6 inches when sleeping,
antacids, acid-reducing agents, mucosal barrier agents, herbal therapies (e.g., licorice, slippery elm, and chamomile), and surgery
Treatment for GERD
109
Inflammation of the stomach’s mucosal lining (may involve the entire stomach or a region)
Gastritis
110
Can be a mild, transient irritation, or it can be a severe ulceration with hemorrhage
Acute gastritis
111
Usually develops suddenly and is likely to be accompanied by nausea and epigastric pain**
Acute gastritis
112
Develops gradually.
May be asymptomatic, but usually accompanied by dull epigastric pain and sensation of fullness after minimal intake.
Chronic gastritis
113
Gastritis can be further categorized as erosive or non-erosive
True
114
Inflammation of the stomach and intestines, usually due to infection or allergic reaction
Gastroenteritis
115
_____ is the most common cause of GASTRITIIS embeds itself in the mucous layer, activating toxins and enzymes that cause inflammation
Helicobacter pylori
116
Genetic vulnerability and lifestyle behaviors (e.g., smoking and stress) may increase the susceptibility
Gastritis
117
organisms transmitted through food and water contamination,
long-term use of nonsteroidal anti-inflammatory drugs (Aspirin, ibeuprofen is really irritating which can lead to this and ulcers)
excessive alcohol use, severe
stress,
autoimmune conditions, and other chronic diseases
Causes of gastritis
118
Alcohol increases GI toxicity of NSAIDS
True
119
peptic ulcers, gastric cancer, and hemorrhage
Complications of chronic gastritis
120
indigestion, heartburn, epigastric pain, abdominal cramping, nausea, vomiting, anorexia, fever, and malaise.
S/S gastritis
121
Hematemesis and dark, tarry stools (MELENA) can indicate ulceration and bleeding
Gastritis
122
history, physical examination, upper GI tract X-ray, esophagogastroduodenoscopy, serum H. pylori antibodies levels, H. pylori breath test, and stool analysis (H. pylori and occult blood)
Diagnosis of gastritis
123
Patient states that they are dizzy, and you see there is hemorrhaging of the ulcer, what do you do?
Get him back in bed, check HR, BP, hb hematocrit then call the doctor with the info
124
Tachycardia, low bp
something has been perforated, hypovolemic shock
125
Client usually on the left side is the best position for procedure EGD for scope to migrate down
True
126
Monitor for indicators of stomach/esophageal perforation:
Elevated temperature
Epigastric pain
Hematemesis/monitor bleeding
**Drowsiness, sore throat are common
Post Esophagogastroduodenoscopy
127
rare but that scope can perforate the esophagus, can have weakening of the esophagus = a hole, not good. Look for signs of bleeding, tachycardia, hypotension, bad epigastric pain
Post EGD
128
Acute gastritis is often self-limiting and resolves within few days.
true
129
etiology-specific interventions, antacids, acid-reducing agents, and mucosal barrier agents
Treatment for chronic gastritis
130
Clear liquids followed by soft foods (bananas, rice, apple-sauce, toast)
Treatment for gastritis
131
banana, rice, apples sauce, toast
BRAT diet
132
How to stop diarrhea
settles GI tract
Good for peds
BRAT
133
Lesions affecting the lining of the stomach or duodenum
Peptic ulcer disease
134
being male, advancing age, nonsteroidal anti-inflammatory drug use, H. pylori infections, certain gastric tumors, and those for GERD (e.g., smoking and alcohol use)
Risk factor for peptic ulcer disease
135
Vary in severity from superficial erosions to complete penetration through the GI tract wall
Peptic ulcer disease
136
Develops because of an ______ between destructive forces and protective mechanisms (peptic ulcer disease)
imbalance
137
H. Pylori, NSAIDS, mental stress, smoking, alcohol consumption, genetics
Causes of peptic ulcer disease
138
Most commonly associated with excessive acid or H. pylori infections
**Typically present with epigastric pain that is relieved in the presence of food
Duodenal ulcers
139
Less frequent but more deadly.
Typically associated with malignancy and nonsteroidal anti-inflammatory drugs.
**Pain typically worsens with eating
Gastric ulcers
140
Develop because of a major physiological stressor on the body due to local tissue ischemia, tissue acidosis, bile salts entering the stomach, and decreased GI motility.
Stress ulcers
141
stress ulcers associated with burns
Curling’s ulcers
142
stress ulcers associated with head injuries. – can lead to hemorrhages
Cushing's ulcer
143
Most frequently develop in the stomach; multiple ulcers can form within hours of the precipitating event.
```
Often hemorrhage is the first indicator because the ulcer develops rapidly and tends to be masked by the primary problem.
-- Gastric acid reduction
medication
--Protocol make sure you
don’t got GERD
```
Stress ulcers
144
Epigastric or abdominal pain (after eating), cramping, heartburn, indigestion, N/V, weight loss, melena (dark, tar-like stool, evidence of digested blood)
Peptic ulcer disease
145
history, physical, upper GI tract X-ray, EGD, serum H. pylori antibody levels, H. pylori breath test, and stool analysis (H. pylori and occult blood)
Diagnosis of peptic ulcer disease
146
Prevention is crucial and may include prophylactic medications (e.g., acid-reducing agents) to persons at risk
Peptic ulcer disease
147
Zantac, omeprazole
Prophylactic meds for pepti c ulcer disease
148
Suspecting someone who has peptic ulcer disease and see their pain gets worse/severe = signs of _____
perforation
149
GI hemorrhage, obstruction, perforation, and peritonitis
Complications of peptic ulcer disease
150
board-like abdominal rigidity, extreme pain. Notify MD immediately = indication or rupture ulcer and are now bleeding
Signs of perforation (peptic ulcer disease)
151
Includes those for gastritis; Surgical repair may also be necessary for perforated or bleeding ulcers.
Treatment of peptic ulcer disease
152
Gallstones.
A common condition that affects both genders and all ethnic groups relatively equally.
Cholethiasis
153
advancing age, obesity, diet, rapid weight loss, pregnancy, hormone replacement, and long-term parenteral nutrition.
Risk factors for cholelithiasis
154
Fair, fat, forty
Cholelithiasis
155
Gallbladder w the stones, gallbladder goes into a portal called cystic duct, cystic duct comes down and joins pancreatic duct and then ends up in the common bile duct
true
156
Stone that migrated our of gall bladder and got stuck in common bile duct – its blocked so can you have cholelithiasis like yes you can (Chol = gallbladder), pancreatitis can also happen
True
157
inflammation or infection in the biliary system (cystic duct, common bile duct, pancreatic duct) caused by calculi
Cholecystitis
158
May obstruct bile flow and cause gallbladder rupture, fistula formation, gangrene, hepatitis, pancreatitis, and carcinoma
Cholelithiasis
159
Cystic duct, common bile duct, pancreatic duct
biliary system
160
biliary colic (spasm of cystic duct due to stone), abdominal distension, nausea, vomiting, jaundice (blockage of hepatic duct), fever, tenderness where gallbladder is and leukocytosis (↑ WBC), ↑cholesterol, ↑Bilirubin, hypertriglyceride
S/S cholelithiasis
161
history, physical examination, abdominal X-ray, gallbladder ultrasound, and laparoscopy
Diagnosis for cholelithiasis
162
Low-fat diet, medications to dissolve calculi
(Ursodiol/ursodeoxycholic acid is a bile acid that gradually dissolves cholesterol-based gall stones),
antibiotic therapy, nasogastric tube with intermittent suction, lithotripsy, choledochostomy (surgery to create an opening for drainage), and laparoscopic removal of calculi or gallbladder
Choleithiasis trwatment
163
What does the NG tube do after removal of gallbladder surgery?
Will allow draining of gastric acid AND decompress the stomach (take pressure off= air causes the pressure) and get air out of the stomach, and can suck out secretion,
164
Inflammation of the liver
Hepatitis
165
infections (usually viral), chronic alcohol intake, medications (e.g., acetaminophen [Tylenol], antiseizure agents, and antibiotics), or autoimmune disease
High liver enzymes and impairment not good idea idea to give with meds listed above
Causes of heptatitis
166
Can be acute, chronic, or fulminant
| Can be active or nonactive
Hepatitis
167
Contagious.
Usually recover in time with no residual damage.
Advancing age and comorbidity increase the likelihood that liver failure, liver cancer, orcirrhosis will develop.
Viral hepatitis
168
Can result in hepatic cell destruction, necrosis, autolysis, hyperplasia, and scarring
Hepatitis
169
transmitted by Fecal oral route, intake of contaminated food exposed to soil or fecal matter, enteric precaution
A&E viral hepatitis
170
Transmitted through blood, needles, paraphernalia, drugs, blood transfusions
B,C,D viral heptitis
171
Proceeds through four phases—an asymptomatic incubation phase and three symptomatic phases
Acute hepatitis
172
Characterized by continued hepatic disease (elevation of enzymes) lasting longer than 6 months.
Symptom severity and disease progression vary depending on degree of liver damage.
Can quickly deteriorate with declining liver integrity.
Chronic hepatitis
173
An uncommon, rapidly progressing form that can quickly lead to liver failure, hepatic encephalopathy (liver loses ability to metabolize and leads to toxic ammonia levels rise = extreme confusion, disorientation, tremors, handwriting illegible: asterixis) or death within 3 weeks
Fulminant hepatitis
174
history, physical examination, serum hepatitis profile, liver enzyme panel, clotting studies, liver biopsy, and abdominal ultrasound
Diagnosis of heptaitis
175
As liver cells become inflammed they rupture and release enzymes =common liver enzymes you wanna look at -> ALT (alanine transferase) and AST (aspartate transferase) so this will be elevated ALT&AST levels (liver enzymes)
True (hepatitis)
176
Vaccinations are cornerstone of prevention—available for hepatitis A and B.
Prevention also includes limiting exposure to the virus.
No method of destroying the virus.
Hepatitis A and E usually resolve with no treatment.
Other types of viral hepatitis can be treated with interferon injections (liver failure) and antiviral medications.
Additional strategies: rest, adequate nutrition, increased hydration, paracentesis, and liver transplant.
Treatment for heptatitis
177
for ascites, ______ to draw off fluid but not really effective bc tomorrow fluid will come back
paracentesis
178
Chronic, progressive, irreversible, diffuse damage to the liver resulting in decreased liver function
Cirrhosis
179
hepatitis and all those factors that can lead to hepatitis
Hepatitis C infection and chronic alcohol abuse are the most frequent causes of cirrhosis in the United States.
Cirrhosis
180
Leads to fibrosis, nodule formation, impaired blood flow, and bile obstruction that can result in liver failure
May take up to 40 years to develop
Can develop even with the removal of the underlying cause
Irreversible
Cirrhosis
181
Portal hypertension
Varicosities in the esophagus and abdomen
Enlargement of nearby organs (gallbladder, spleen, abdominal organs)
Bleed - either slow or severe, particularly in the esophagus (liver huge role in clotting factors, if liver not working = no clotting = bleed)***
S/S of Cirrhosis
182
back up of blood in veins (veins are not mean to withstand high pressure, should have less pressure than arteriole pressure)
Portal hypertension
183
Ascites
Changes in clotting factors
Muscle wasting: due to synthesis and production of albumin, albumin levels drop
Hyperlipidemia
Hyperglycemia or hypoglycemia
Can't maintain glucose
levels
Bile accumulation in the liver causes inflammation and necrosis
S/S cirrhosis
184
Fluid will move out of blood vessel, no oncotic pressure of albumin to hold on to fluid which contributes to ascites
(cirrhosis)
Low albumin
185
Veins are gathering the nutrients from stomach and duodenum and delivering particles to the liver by _____________. what will be happening now? Organ factory will be like “oh I believe something is in the burger I’m going to detoxify it and get rid of it”, vessel that carries the cleaned up blood to heart by way of inferior vena cava (hepatic vein carries to the inferior vena cava so you don’t have to worry about stuff)
Portal vein
186
Cirrhotic liver = not good filtration of blood going into the liver, high BP, esophageal varices which rupture and now we have a GI bleed, chronic long term alcoholics vomit blood
true
187
Jaundice
Intolerance to fat and fat-soluble vitamin deficiency
Clay-colored stools
Dark urine
Intense itching
Excessive estrogen leads to female characteristics in men and irregular menstruation in women
S/S Cirrhosis
188
Numerous toxins and waste products accumulate
Ulcers and GI bleeding
Ascites (fluid accumulation as portal hypertension pushes fluid back into the abdominal cavity; also damaged liver no longer produces ALBUMIN which is responsible for maintaining oncotic pressure:↓ALBUMIN = third spacing.
Spontaneous bacterial peritonitis
Neurologic impairment
Encephalopathy
S/S Cirrhosis
189
history, physical examination, liver biopsy, abdominal X-ray, liver enzyme panel, esophagogastroduodenoscopy, clotting studies, and stools examination (for occult blood)
S/S Cirrhosis
190
Complex and varies depending on the underlying cause. – multifactorial
Hepatitis-related cirrhosis will be treated with antiviral agents and interferon.
Avoid alcohol, drugs, and hepatotoxic medications.
Nutritional imbalances (usually treated with total parenteral nutrition [TPN]) and metabolic dysfunction are corrected
Bile acid–binding agents can aid bile excretion.
.
Cirrhosis Treatment
191
Bc don’t digest fat well
High levels of carb, protein, and fats
Monitor glucose levels
This typically goes into central vein, risk for infection is great so think about looking at hyperglycemia and infection
Taking them off TPN – we taper it, to give body time to deal w high glucose levels, if taken off abruptly-glucose levels will plummet
TPN for cirrhotic patients
192
Portal hypertension is treated with a surgically implanted shunt.(connecting portal vein to hepatic vein to improve flow of blood to alleviate prob of backing up and portal hypertension, decrease esophageal varices)
Fluid restriction, a low-sodium diet, diuretics, paracentesis, and shunts may be used to treat ascites.
```
Esophageal varices are treated with endoscopic bands (circular band around varices to prevent rupture of esophageal varices) shunts, or sclerotherapy.
To prevent blood flow to
varices --- circular band
around varices…
Antacids and acid-reducing agents.
```
Cirrhosis treatment
193
Encephalopathy
Lactulose
Antibiotics (can be given to suppress intestinal flora and decrease endogenous ammonia production)
Liver transplant
Cirrhosis treatment
194
sugary medicine draws water in bowel and produces diarrhea so get rid of high ammonia levels) can promote ammonia excretion in the stools.
To treat high ammonia
Lactulose
195
due to the high ammonia levels and toxins for cirrhotic state) is treated by eliminating the source of protein breakdown.
```
Some of the clients we will
make sure they do not have
excessive protein levels bc of
rapid onset of
encephalopathy so protein
restriction
```
Encephalopathy
196
Inflammation of the pancreas.
| Can be acute or chronic.
Pancreatitis
197
cholelithiasis (gall stone stuck at pancreatic duct-leads to this), alcohol abuse, biliary dysfunction, hepatotoxic drugs, metabolic disorders, trauma, renal failure, endocrine disorders, pancreatic tumors, and penetrating peptic ulcer.
Causes of pancreatitis
198
_____ injury causes pancreatic enzymes to leak into the pancreatic tissue and initiate autodigestion, resulting in edema, vascular damage, hemorrhage, and necrosis.
Pancreatic tissue is replaced by fibrosis, which causes exocrine and endocrine changes and dysfunction of the islets of Langerhans.
Pancreatic
199
Pancreatic enzymes get trapped, cant drained out through pancreatic/ampula duct cant move through duodenum, cant help with digestion of cars, fat, protein. There is back up of these pancreatic enzymes about lipase which is enzyme to break down fat, there is amylase which break down starch, protease to help with metabolism so if those enzymes get trapped in tissue of pancreas they begin to eat the pancreatic tissue itself called ________ which leads to edema, vascular damage, hemorrhage and necrosis of pancreas
autodigestion
200
Considered a medical emergency.
Mortality increases with advancing age and comorbidity.
Complications: acute respiratory distress syndrome (can’t breathe on their own), diabetes mellitus, infection, shock, disseminated intravascular coagulation, renal failure, malnutrition, pancreatic cancer, pseudocyst, and abscess
Acute pancreatitis
201
Swelling of the pancreas, movement of enzymes eating pancreatic tissue, excess fluid, abdominal pain, purulent drainage, fluids that move across diaphragm not only peritoneal effusion/ascites, fluids going into lungs so clients will develop ________________ (pancreatitis)
Acute respiratory distress syndrome
202
abrupt and painful
Upper abdominal pain that radiates to the side and back, worsens after eating, and is somewhat relieved by leaning forward or pulling the knees toward the chest, fetal position bc pain is so severe
Nausea and vomiting
Mild jaundice
Low-grade fever
Blood pressure and pulse changes (tachy)
S/S Acute pancreatitis
203
insidious: slower
Upper abdominal pain (stabbing)
Indigestion
Losing weight without trying
Steatorrhea: excess fat in stool bc lipase can’t absorb
Constipation
Flatulence
Pain can be intermittent or chronic
S/S Chronic pancreatitis
204
excess fat in stool bc lipase can’t absorb
Steaorrhea
205
If you have ______, your stools will be bulkier, pale, and foul-smelling. They tend to float because of higher gas content
Steaorrhea
206
history, physical examination, serum amylase and lipase levels, serum calcium levels, complete blood count, liver enzymes panel, serum bilirubin level, arterial blood gases, stool analysis (lipid and trypsin levels), abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, abdominal ultrasound, and endoscopic retrograde cholangiopancreatography
Diagnosis of pancreatitis
207
REST inflamed pancreas, decrease production and secretion of pancreatic enzymes by not putting anything in the GI tract, food triggers release of enzymes so we make them NPO. iv fluids, may places on IV TPN or admixture, start back on diet when get better
Treatment for pancreatitis
208
Close monitoring and aggressive management
Resting the pancreas by fasting, administering intravenous nutrition, and gradually advancing diet from clear liquids to soft foods as tolerated to low fat
Pancreatic enzyme supplements when diet is resumed
Maintaining hydration status with intravenous fluids
Nasogastric tube with intermittent suction to compress stomach to remove excess air and drainage, to not stimulate the contraction of pancreas and the release of those enzymes
Antiemetic agents
pancreatitis treatment
209
```
Pain management – major*
-Pain killers – refraining from
NSAIDS and morphine bc
opioid particularly morphine
may cause spamming of bile
and pancreatic duct which
makes It worse
-Demurral over morphine =
bias
```
Antacids and acid-reducing agents
Anticholinergic agents
Slow down peristalsis & slow
down GI tract
Antibiotic therapy = controversial some say no need
Insulin = due to high glucose levels
Identifying and treating complications early
Treatment for pancreatitis
210
Change in bowel pattern characterized by an increased frequency, amount, and water content of the stool
Results because of bacterial/viralinfection, increased fluid secretion, decreased fluid absorption, or an alteration in GI peristalsis
Diarrhea
211
Often caused by viral or bacterial infections or certain medications (e.g., antibiotics, antacids, and laxatives)
Usually self-limiting, depending on the cause
Acute diarrhea
212
Lasts longer than 4 weeks
Causes: inflammatory bowel diseases, malabsorption syndromes, endocrine disorders, chemotherapy, and radiation
Chronic diarrhea
213
Originating in the ____ intestine
Stools are large, loose, and provoked by eating.
Usually accompanied by pain in the right lower quadrant.
(Diarrhea s/s)
small
214
Originating in the ____intestine
Stools are small and frequent.
Frequently accompanied by pain and cramping in the left lower quadrant.
large
215
____ diarrhea is generally infectious and accompanied by cramping, fever, chills, nausea, and vomiting.
Acute
216
Blood (may be frank-red blood, occult-dark blood, or melena-tarry like thick stool), pus, or mucus may be present.
Bowel sounds may be hyperactive.
**Problem with diarrhea: Fluid (look at turgor, mucous membrane), electrolyte, and pH imbalances (acid base) – hypovolemic shock
Look at electrolytes
S/S diarrhea
217
history (including usual bowel pattern and completion of the Bristol Stool chart), physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, arterial blood gases, and abdominal ultrasound
Diagnosis of diarrhea
218
Antidiarrheal agents (lomodal, emodium) may or may not be used. But bacteria remains in the gut so may not use this for an infectious process
Antibiotics may be necessary.
Anticholinergics. = decrease peristalsis, may not wanna do this if infection
diarrhea treatment
219
Antispasmodic agents. = decrease spasms
When oral intake is recommended, a clear liquid diet is usually ordered until the diarrhea subsides.
Then the diet is advanced to a regular diet as tolerated.
Diarrhea treatment
220
Rest the gut = avoiding all food or at least stick to soft clear liquids until diarrhea leaves
True
221
Dietary fiber can be used to manage chronic diarrhea.
Maintaining hydration status and correcting electrolyte and pH imbalances.
Meticulous skin care in cases of bowel incontinence.
Diarrhea treatment
222
Change in bowel pattern characterized by infrequent passage of stool in reference to the individual’s typical bowel pattern.
Stool remains in the large intestine longer than usual, increasing the amount of water removed.
Constipation
223
low-fiber diet, inadequate physical activity, insufficient fluid intake, delaying the urge to defecate, laxative abuse, stress, travel, bowel diseases, certain medications, mental health problems, neurologic diseases, and colon cancer.
Common in children who are toilet training.
Causes of constipation
224
pain during the passage of a bowel movement, inability to pass stool after straining or pushing for more than 10 minutes, no bowel movements for more than 3 days, and hypoactive bowel sounds
S/S constipation
225
: anal bleeding, anal fissure, pH disturbances, hemorrhoids, diverticulitis, impaction, intestinal obstruction, and fistulas
Complication of constipation
226
don’t want them to become constipation bc straining of stool excess work on heart muscle = MI, hypertensive episodes
Cardiac patients
227
: history (including usual bowel pattern and completion of the Bristol Stool Chart), physical examination (may include a digital examination), abdominal X-ray, upper GI series, barium swallow, colonoscopy, and proctosigmoidoscopy
Diagnosis of constipation
228
increasing dietary fiber with concomitant increase in hydration, increasing physical activity, defecating when initial urge is sensed, taking stool softeners, limited use of laxatives and enemas, and digitally removing impaction
Treatment for constipation
229
Blockage of intestinal contents in the small intestine or large intestine –
Intestinal Obstruction
230
Mechanical obstructions: foreign bodies, tumors,
adhesions (scar tissues build up between one area of bowel to another, usually after scar tissues through to previous surgeries- coming together of 2 pieces of bowel bc of scar tissue)
hernias (Strangulate and cut off blood flow, outpatching of the intestine through muscle wall),
intussusception (part of bowel telescoping into another part), volvulus, strictures (twisted bowel),
Crohn’s disease, diverticulitis,
Hirschsprung’s disease, and fecal impaction
Causes of intestinal obstruction
231
```
Functional obstructions (also called paralytic ileuses):
neurologic impairment; intra-abdominal surgery complications; chemical, electrolyte, and mineral disturbances; intra-abdominal infections; abdominal blood supply impairment; renal and lung disease; and use of certain medications (e.g., narcotics)
```
Causes of intestinal obstruction
232
abdominal distention which may result in increase peristalsis (movement) = force content pass the obstruction causing colicky pain, severe vomiting, lose a quit of fluid & electrolytes, see narrowing of GI tract so nausea bc things can’t move forward
Increase in fluid and gas (intestinal obstruction)
233
causes more fluid to go the intestine, decrease BP & hypovolemic shock bc fluid shift into intestine and third space, continued pressure causes edema and end up with paralytic illeus = Not good flow to the bowel
Increased pressure on GI wall (intestinal obstruction)
234
Can develop either suddenly or gradually and can be either partial or complete.
Chyme and gas accumulate at the site of the blockage.
Saliva, gastric juices, bile, and pancreatic secretions begin to collect as the blockage lingers.
Serum electrolytes and protein increase, causing abdominal distension and pain.
Intestinal obstruction
235
Intestinal blood flow can become impaired, leading to strangulation and necrosis.**
Intestinal contents can seep into the abdomen as the pressure increases.**
Complications: perforation, pH imbalances, fluid disturbances, shock, and death.**
(intestinal obstruction)
True
236
abdominal distension, abdominal cramping, colicky pain, nausea, vomiting, constipation, diarrhea, borborygmi (rumbling or gurgling noise made by the movement of fluid and gas in the intestines), intestinal rushes, decreased or absent bowel sounds, restlessness, diaphoresis, tachycardia progressing to weakness, confusion, and shock
Manifestations of intestinal obstructions
237
history (including usual bowel pattern), physical examination, blood chemistry, arterial blood gases, complete blood gases, abdominal computed tomography, abdominal X-ray, abdominal ultrasound, sigmoidoscopy, and colonoscopy
Diagnosis of intestinal obstruction
238
Strategies depend on the underlying causes. - may solve on its own but it tumor or severe then surgically
Correcting fluid, electrolyte, and pH imbalances.
Before surgery: Nasogastric tube with intermittent suctioning. = to eliminate excess fluid in gas, NPO, TPN,
Fasting and total parenteral nutrition until bowel function is restored.
Ambulation.
Laxatives should be avoided in most cases until the obstruction is resolved.
Surgery.
Treatment of intestinal obstruction
239
Inflammation of the vermiform appendix.
Most often caused by an infection.
Triggers local tissue edema, which obstructs the small structure.
As fluid builds inside the appendix = microorganisms proliferate
Appendicitis
240
The appendix fills with purulent exudate and area blood vessels become compressed. – severe ___ quadrant pain
right
241
Ischemia and necrosis develop.
The pressure inside the appendix escalates, forcing bacteria and toxins out to surrounding structures.
Vary from asymptomatic to sudden and severe.
Urgent diagnosis and treatment are crucial
Appendicitis
242
abscesses, peritonitis, gangrene, and death
Complications of appendicitis
243
Sharp abdominal pain develops, gradually intensifies (over about 12–24 hours), and becomes localized to the lower right quadrant of the abdomen (**_____ point).
Pain may occur anywhere in abdomen.
McBurney
244
**Pain will temporarily subside if the appendix ruptures, and then the pain will return and escalate.
Not good
245
Nausea, vomiting, abdominal distension, decreased or absent bowel sounds and bowel pattern changes
Appendicitis
246
Indications of inflammation and infection (e.g., fever, chills, and______) - appendicitis
**leukocytosis
247
Indications of _____ (e.g., abdominal rigidity, tachycardia, and hypotension = shock like)
-Appendicitis
peritonitis
248
history, physical examination, complete blood count, abdominal ultrasound, abdominal X-ray, abdominal computed tomography, and laparoscopy.
Diagnosis of appendicits
249
Surgery, either laparoscopic or open, and may include extensive irrigation.
Drainage tubes.
Long-term antibiotic therapy.
Analgesics.
Avoid activities that increase intra-abdominal pressure (e.g., straining and coughing).
Treatment of appendicitis
250
Inflammation of the peritoneum
Peritonitis
251
: chemical irritation (e.g., ruptured gallbladder or spleen) or direct organism invasion (e.g., appendicitis and peritoneal dialysis)
Causes of periotnitis
252
Several protective mechanisms are activated
A thick, sticky exudate that bonds nearby structures and temporarily seals them off.
Abscesses may form in an attempt to wall off the infections.
Peristalsis may slow down in a response to the inflammation, decreasing the spread of toxins and bacteria.
Peritonitis
253
Usually sudden and severe
Classical manifestation = abdominal rigidity
Abdominal tenderness and pain
Large volumes of fluid leak into the peritoneal cavity
Nausea and vomiting
s/s peritonitis
254
Decreased peristalsis
Intestinal obstruction
Indicators of infection (e.g., fever, malaise, and leukocytosis)
Indications of sepsis and shock (e.g., tachycardia, hypotension, restlessness, and diaphoresis)
s/s peritonitis
255
Board like, distention, reflex contraction of abdominal muscles
Peritonitis
256
: history, physical examination, complete blood count, abdominal X-ray, abdominal ultrasound, abdominal computed tomography, paracentesis with peritoneal fluid analysis, and laparotomy
Diagnosis of peritonitis
257
surgical repair, long-term antibiotic therapy, correcting fluid and electrolyte imbalances, nasogastric tube insertion with intermittent suction, and total parenteral nutrition
Peritonitis treatment
258
Also known as celiac sprue or gluten-sensitive enteropathy* --(gut-pathy) – disease of gut due to gluten
Inherited, autoimmune, malabsorption disorder
Primarily a childhood disease, but can develop at any age
Results from a combination of the immune response to an environmental factor (gliadin) and genetic predisposition
Prevention: Gluten free diet
Most common in cacusaians and females
Celiac disease
259
_____ sprue is a related disorder that occurs in tropical regions and is thought to be caused by a bacterial, viral, parasitic, or amoebic infection.
Can be resolved with antibiotic therapy
(celiac disease)
Tropical
260
Results from a defect in the intestinal enzymes that prevents further digestion of _____ (a product of gluten digestion).
- celiac disease
gliadin
261
Gluten is an ingredient of some grains.
True
262
Intestinal villi atrophy and flatten, resulting in decreased enzyme production and making less surface area available for nutrient absorption. (celiac disease)
true
263
anemia, arthralgia (joint pain) , myalgia, bone disease, dental enamel defects and discoloration, intestinal cancers, depression, growth and development delays in children, hair loss, hypoglycemia, mouth ulcers, increased bleeding tendencies, neurologic disorders, skin disorders, vitamin or mineral deficiency, and endocrine disorders.
complications of celiac disease
264
In infants, generally appear as cereals are added to their diet (usually around 4–6 months of age)
Include abdominal pain, abdominal distension, bloating, gas, indigestion, constipation, diarrhea, changes in appetite, lactose intolerance, nausea, vomiting, steatorrhea, unexplained weight loss, irritability, lethargy, malaise, and behavioral changes**
s/s Celiac disease
265
history, physical examination, duodenal biopsy, and celiac blood panel (includes immunoglobulin A antibody–endomysium antibodies, immunoglobulin A antigliadin antibodies, deamidated gliadin peptide antibody, immunoglobulin A antitissue transglutaminase, lactose tolerance test, and D-xylose test)
Diagnosis of Celiac disease
266
gluten-free diet, periodic monitoring for cancer development, and long-term support**
gluten-free diet (avoid all grains, breads, pretzel, pasta), periodic monitoring for cancer development, and long-term support
Instruct clients to Read labels carefully as many food items use gluten as fillers, i.e. chocolate candy, hot dogs.
Celiac disease treatment
267
Chronic inflammation of the GI tract, usually the intestines
Inflammatory bowel disease
268
Chiefly seen in women, Caucasians, persons of Jewish descent, and smokers
Includes _____ disease and _______ colitis
Characterized by periods of exacerbations and remissions
Crohn's, ulcerative
269
Thought to be caused by a genetically associated autoimmune state that has been activated by an infection.**
Immune cells located in the intestinal mucosa are stimulated to release inflammatory mediators that alter the function and neural activity of the secretory and smooth muscle cells.**
Inflammatory bowel disease
270
Fluid, electrolyte, and pH imbalances develop.**
Can be painful, debilitating, and life-threatening.**
Inflammatory bowel disease
271
Insidious, slow-developing, progressive condition
Often develops in adolescence
Crohn's disease
272
Characterized by patchy areas of inflammation involving the full thickness of the intestinal wall and ulcerations (skip lesions)
Form fissures divided by nodules, giving the intestinal wall a cobblestone appearance
Painful & debilitative disorder
Crohn's disease
273
Life threatening due to loss of fluids and electrolytes (diarrhea) = can lead to hypovolemia
Crohn's disease
274
The entire wall becomes thick and rigid, and the intestinal lumen becomes narrowed and potentially obstructed.
Granulomas develop on the intestinal wall and nearby lymph nodes.
The damaged intestinal wall loses the ability to digest and absorb.**
The inflammation also stimulates intestinal motility (diarrhea), decreasing digestion and absorption.**
Crohn's disease
275
Difficulty digesting and absoribing their nutrients. Unable to get what they need from food.
(crohns)
true
276
Less than body requirements, alteration in nutrient, fluid
| electrolyte imbalance diagnosis
Crohns disease nursing diagnosis
277
malnutrition, anemia (especially iron deficiency), fistulas, adhesions, abscesses, intestinal obstruction, perforation, anal fissure, and delayed growth and development as well as fluid, electrolyte, and pH imbalances*
Complications of Crohn's disease
278
abdominal cramping and pain (typically in the right lower quadrant), diarrhea, steatorrhea, constipation, palpable abdominal mass, melena, anorexia, weight loss, and indications of inflammation (e.g., fever, fatigue, arthralgia, and malaise)*
s/s of Crohn's disease
279
history, physical, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, barium studies (swallow and enema), sigmoidoscopy, colonoscopy, and biopsy
Diagnosis of Crohn;s
280
low-residue, high-calorie, high-protein diet; oral nutritional supplements; multivitamin supplements; total parenteral nutrition; antidiarrheal agents; aminosalicylates (5-ASAs); glucocorticoids; immune modulators; biologic agents; analgesics; antibiotics; surgical intestine resection; stress management; and support; medications: HUMIRA
Treatment of Crohn's disease
281
Progressive condition of the rectum and colon mucosa. *
Usually develops in the second or third decade of life.*
Ulcerative colitis
282
Inflammation triggered by T-cell accumulation in the colon mucosa causes epithelium loss, surface erosion, and ulceration that begins in the rectum and extends to the entire colon.
Rarely affects the small intestine.**
Mucosa becomes inflamed, edematous, and frail.
Necrosis of the epithelial tissue can result in abscesses.
The ulcers merge, creating large areas of stripped mucosa that results in an inadequate surface area for absorption
Ulclerative colitis
283
diarrhea (usually frequent [as many as 20 daily], watery stools with blood and mucus), tenesmus (rectal pain, urge to defecate even if already had a bowel movement), proctitis, abdominal cramping, nausea, vomiting, weight loss, and indications of inflammation (e.g., fever, fatigue, arthralgia, and malaise)*
s/s ulcerative colitis
284
malnutrition, anemia, hemorrhage, perforation, strictures, fistulas, pseudopolyps, toxic megacolon, colorectal carcinoma, and liver disease,as well as fluid, electrolyte, and pH imbalances*
Complications of ulceritis colitis
285
history, physical, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, barium enema, colonoscopy, and biopsy
diagnosis of ulcerative colitis
286
high-fiber, high-calorie, high-protein diet (not during exacerbation); oral nutritional supplements; multivitamin supplements; total parenteral nutrition (during exacerbation); antidiarrheal agents; antispasmodics; anticholinergics; aminosalicylates (5-ASAs); glucocorticoids; immune modulators; biologic agents; analgesics; antibiotics; surgical intervention (e.g., ileostomy or colostomy); stress management; and support
Treatment for uclerative colitis
287
Chronic, non-inflammatory, GI condition characterized by exacerbations associated with stress
Includes alterations in bowel pattern and abdominal pain not explained by structural or biochemical abnormalities
Less serious than IBD, is non-inflammatory, and does NOT cause permanent intestinal damage
Irritable Bowel Syndrome
288
More common in women than in men
Thought to be an intensified response to stimuli with increased intestinal motility and contractions—may have a low tolerance for stretching and pain in the intestinal smooth muscle
Irritable bowel syndrome
289
Three theories of its etiology: altered GI motility, visceral hyperalgesia, and psychopathology
Irritable bowel syndrome
290
hemorrhoids, nutritional deficits, social issues, and sexual discomfort
Irritable Bowel Syndrome
291
Stress, mood disorders, food, and hormone changes often worsen symptoms.
Abdominal distension, fullness, flatus, and bloating.
Intermittent abdominal pain exacerbated by eating and relieved by defecation.
S/s irritable bowel syndrome
292
Chronic and frequent constipation or diarrhea, usually accompanied by pain
Nonbloody stool that may contain mucus
Bowel urgency
Intolerance to certain foods (usually gas-forming foods and those containing sorbitol, lactose, and gluten)
Emotional distress
Anorexia
s/s irritable bowel syndrome
293
history (including bowel pattern and Rome III criteria), stool analysis (including cultures and occult blood), celiac blood panel, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance, barium studies (swallow and enema), sigmoidoscopy, colonoscopy, and biopsy
diagnosis of irritable bowel syndrome
294
antidiarrheal agents, laxatives, antispasmodics, antidepressants, avoid triggers, maintain adequate fiber intake, stress management, and support
Irritable bowel syndrome treatment
295
Conditions related to the development of diverticula, outwardly bulging pouches of the intestinal wall that occur when mucosa sections or large intestine submucosa layers herniate through a weakened muscular layer. = may cause foods to be trapped in the pouch and lead to more difficulty(inflammation of dicertucla)
Diverticular disease
296
2 disease processes =diverticulosis and diverticulitis
True
297
May be congenital or acquired.
Thought to be caused by a low-fiber diet and poor bowel habits that result in chronic constipation.
The muscular wall can become weakened from the prolonged effort of moving hard stools.
More common in developed countries where processed foods and low-fiber diets are typical.
Diverticular disease
298
Asymptomatic diverticular disease, usually with multiple diverticula present (a lot of out patching areas in colon)
Encourge good fiber so good bowel contents move through and forward
Divertulosis
299
Diverticula have become inflamed, usually because of retained fecal matter
DON’T want high fiber in diet
Can result in potentially fatal obstructions, infection, abscess, perforation, peritonitis, hemorrhage, and shock
Often asymptomatic until the condition becomes serious
Diverticulitis
300
abdominal cramping followed by passing a large quantity of frank blood, low-grade fever, abdominal tenderness (usually left lower quadrant), abdominal distension, constipation, obstruction, nausea, vomiting, palpable abdominal mass, and leukocytosis
Diverticular disease manifestations
301
history, physical exam, stool analysis (including for occult blood), abdominal computed tomography, abdominal magnetic resonance imaging, colonoscopy, barium enema, and biopsy
Diagnosis for diverticular disease
302
high-fiber diet, omitting foods with seeds or popcorn that may be trapped in pouches which lead to inflammation = diverticulitis, decreased food intake when active bleeding is present, adequate hydration, proper bowel habits (e.g., defecating when urge is sensed and not straining), stool softeners, antibiotics, analgesics, colon resection, and blood transfusions, use steroids, anti-inflam drugs
Diverticular disease treatment
