Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NSG 322 Med Surge I > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what does chron’s involve that UC doesn’t and what does that contribute to?

A

it involves the small intestine, contributing to malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IBD

A

chronic, recurrent inflammation of the intestinal tract that has periods of remission and exacerbation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

types of IBD

A

UC and chron’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

is UC or chron’s autoimmune?

A

chron’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

clinical manifestations of IBD

A
  • diarrhea
  • bloody stool
  • weight loss
  • abdominal pain
  • fever
  • fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

complications of IBD

A

hemorrhage, strictures, perforation, fistulas, colonic dilation, colorectal cancer, liver failure, systemic problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pattern of inflammation in chron’s

A

it involves all layers of the bowel wall that can occur anywhere in the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where is chron’s most commonly found?

A

the terminal ileum and colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is good way to recognize chron’s during a scope?

A

it will look like cobblestones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

because inflammation in chron’s goes through the entire wall, what can happen?

A
  • abscesses can form and peritonitis can result
  • fistulas can develop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical manifestations of chron’s

A
  • diarrhea
  • crampy abdominal pain
  • weight loss when the small intestine is involved
  • rectal bleeding
  • fever or other systemic symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pattern of inflammation in UC

A

starts in rectum and moves up towards the cecum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what electrolyte is mostly lost when someone has diarrhea?

A

mostly potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

clinical manifestations of UC

A
  • bloody diarrhea
  • abdominal pain
  • fever
  • rapid weight loss
  • anemia
  • tachycardia
  • dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what would you expect in lab results with UC?

A

low H and H and increased WBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

goal of drug treatment in IBD

A

to induce and maintain remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what kind of ostomy is usually given with IBD?

A

ileostomy: going to be very dehydrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

gerontologic considerations with IBD

A
  • second peak of disease in 60s
  • diagnosis can be difficult ~ confused with c. diff
  • distal colon is usually involved in UC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

clinical manifestations of IBS

A
  • abdominal pain
  • diarrhea or constipation
  • abdominal distention
  • excessive flatulence
  • bloating
  • urgency
  • sensation of incomplete evacuation
  • fatigue
  • sleep disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is loperamide (imodium) and when would you not recommend this drug?

A

it is used to treat diarrhea and it decreases the intestinal tract. you do not want to use it if F/E are out of balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is a huge factor of IBS?

A

stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

gastritis

A

inflammation of gastric mucosa that results in the breakdown of gastric mucosal barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

in gastritis, what is the stomach tissue unprotected from?

A

autodigestion by HCl acid and pepsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

since the stomach is in LUQ, what can this be confused with?

A

heart problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what problem results from gastritis?

A

tissue edema and disruption of capillary walls that can cause hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what kind of drugs can cause gastritis?

A

NSAIDs, including aspirin and corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what diet contributes to gastritis?

A

alcohol or spicy foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what environmental factors contribute to gastritis?

A

radiation or smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how can an NG tube contribute to gastritis?

A

there is constant irritation on the stomach wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

autoimmune atrophic gastritis

A
  • affects fundus and body of stomach
  • associated with increased risk of gastric cancer
  • may be linked to presence of H. pylori and development of chronic gastritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

clinical manifestations of acute gastritis

A
  • anorexia
  • N/V
  • epigastric tenderness
  • feeling of fullness
  • hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

clinical manifestations of chronic gastritis

A
  • similar to acute
  • loss of intrinsic factor can occur when acid-secreting cells are lost or nonfunctioning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is diagnosis of gastritis based on?

A

history of drug and alcohol abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

why would we confirm presence of anemia with possible gastritis?

A

unfound anemia is almost always a GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what diagnostic studies can we do for gastritis?

A
  • CBC
  • occult blood test
  • serum antibody tests
  • tissue biopsy to rule out cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what might be needed in severe cases of gastritis?

A

an NG tube; observe for bleeding and lavage to flush precipitating agent from stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

most common manifestations of GI diseases

A

nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

chemoreceptor trigger zone (CTZ)

A
  • responds to chemical stimuli of drugs and toxins
  • located in the brainstem
  • site of action of drugs used to induce vomiting
  • plays a role in vomiting cause by labyrinthine stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

parasympathetic stimulation of N/V

A
  • relaxes lower esophageal sphincter
  • increases gastric motility and salivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what can vomiting result in?

A
  • metabolic alkalosis: from loss of gastric HCl
  • metabolic acidosis: from loss of bicarbonate if the contents from the small intestine are vomited
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what might indicate a lower intestinal obstruction in throw up?

A

fecal odor and bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what kind of complications would bright red blood in vomit indicate?

A
  • mallory-weiss tear
  • esophageal varices
  • gastric or duodenal ulcer or neoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what nutritional therapy would we start after N/V?

A
  • IV fluids to replace fluids and electrolytes, glucose
  • NG tube suction to decompress stomach
  • clear liquids started first
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why do we use gatorade and broth with caution after N/V

A

because of high salt intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how can we avoid overdistention of the stomach?

A

take fluids between meals instead of with

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

GERD

A
  • common problem
  • chronic manifestation of mucosal damage
  • caused by reflux of gastric contents
  • not a disease, but a syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

who are GI issues more common in?

A

males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

incompetent LES

A
  • primary factor in GERD
  • results in decreased pressure in distal portion of esophagus so gastric contents move from stomach to esophagus
  • can be due to certain foods (caffeine, chocolate) and drugs (anticholingergics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

clinical manifestations of GERD

A
  • heartburn (pyrosis): burning, tight sensation felt beneath the lower sternum and spreading upward to throat or jaw
  • dyspepsia: pain of discomfort centered in upper abdomen
  • regurgitation: hot, bitter, or sour liquid coming into throat or mouth
  • respiratory symptoms: wheezing, coughing, dyspnea, nocturnal coughing with loss of sleep
  • otolaryngologic symptoms: hoarseness, sore throat, lump in throat, choking
  • GERD-related chest pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what can esophagitis result in?

A

dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

barrett’s esophagus (esophageal metaplasia)

A
  • replacement of normal squamous epithelium with columnar epithelium
  • precancerous lesion
  • must be monitored every 2-3 years by endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what can GERD cause from acid reflux into mouth?

A

dental erosion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

nutritional therapy in GERD

A
  • decrease high-fat foods
  • take fluids between rather than with meals
  • avoid milk products at night
  • avoid late-night snacking or meals
  • avoid chocolate, peppermint, caffeine, tomato products, orange juice
  • weight reduction therapy
  • chewing gum and oral lozenges can increase saliva and help with mild symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

anytime we cut into GI tract, what is there a risk for?

A

a stricture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

nursing management for GERD

A
  • elevate HOB 30 degrees
  • not lying down for 2-3 hours after eating
  • avoid late night eating
  • evaluate effectiveness of medications
  • observe for side effects of medications
  • avoid factors that cause reflux: smoking, alcohol, caffeine, acidic foods
  • stress reduction techniques
  • weight reduction
  • small, frequent meals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

hiatal hernia

A
  • hernation of portion of stomach into esophagus through an opening or hiatus in diaphragm
  • more common in older adults and women
57
Q

two types of hiatal hernia

A
  1. sliding ~ most common
  2. paraesophageal or rolling
58
Q

what factors increase risk of a hiatal hernia?

A
  • weakening of muscles of diaphragm
  • increased intraabdominal pressure: obesity, pregnancy, heavy lifting
  • increasing age
  • trauma
  • poor nutrition
  • forced recumbent position
  • congenital weakness
59
Q

clinical manifestations of hiatal hernia

A
  • heartburn
  • dysphagia
60
Q

lifestyle modifications for hiatal hernia

A
  • eliminate alcohol
  • elevate HOB
  • stop smoking
  • avoid lifting/straining
  • reduce weight
  • use antisecretory agents (H2) and atacids
61
Q

eosinophilic esophagitis

A
  • swelling of esophagus cause by an infiltration of eosinophils
  • personal or family history of other allergic diseases
62
Q

most common food triggers in eosinophilic esophagitis

A

milk, egg, wheat, rye, and beef

63
Q

clinical manifestations of eosinophilic esophagitis

A
  • severe heartburn
  • difficulty swallowing
  • food impaction
  • N/V
  • weight loss
64
Q

three main areas of esophageal diverticula

A
  • zenker’s diverticulum: most common, above the upper esophageal sphincter
  • traction diverticulum: near esophageal midpoint
  • epiphrenic diverticulum: above the LES
65
Q

clinical manifestations of esophageal diverticula

A
  • dysphagia
  • regurgitation
  • chronic cough
  • aspiration
  • weight loss
66
Q

how can we get rid of esophageal diverticula?

A
  • apply pressure at a point on the neck to empty pocket of food
  • diet limited to foods that are blenderized
67
Q

most common cause of esophageal stricture

A

GERD

68
Q

achalasia

A
  • rare, chronic disorder
  • in lower two third of esophagus, peristalsis is absent
  • LES pressure increases
  • obstruction occurs at/near diaphragm
  • food and fluid accumulate in lower esophagus
69
Q

result of achalasia

A

dilation of lower esophagus

70
Q

clinical manifestations of achalasia

A
  • dysphagia
  • substernal chest pain
  • halitosis
  • inability to belch
  • GERD
  • regurgitation
  • weight loss
71
Q

types of peptic ulcers

A

acute and chronic

72
Q

when do ulcers develop?

A

in the presence of an acid environment

73
Q

the stomach is normally protected from autodigestion by what?

A

gastric mucosal barrier

74
Q

how often is the surface mucosa of the stomach renewed

A

about every 3 days

75
Q

what can pass through the gastric barrier?

A

water, electrolytes, and water-soluble substances

76
Q

if the mucosal barrier is impaired, what can occur?

A

back diffusion of acid and pepsin

77
Q

destroyers of mucosal barrier

A
  • H. pylori
  • aspirin and NSAIDs
  • corticosteroids
  • lifestyle factors
78
Q

gastric ulcers

A
  • occur in any portion of the stomach
  • less common than duodenal
  • prevalent in women, older adults
  • peak incidence >50 years
79
Q

duodenal ulcers

A
  • occur at any age in anyone: increases between ages 35-45
  • familial tendency
  • associated with increased HCl acid secretion: alcohol and cigarette smoking
  • H. pylori found in 90-95% of patients
80
Q

clinical manifestations of gastric ulcers

A
  • pain is high in epigastrium
  • occurs 1-2 hours after meal
  • “burning” or “gaseous”
  • gastric ulcer pain doesn’t radiate around
81
Q

clinical manifestations of duodenal ulcers

A
  • midepigastric region beneath xiphoid process
  • back pain if ulcer is located posteriorly
  • 2-5 hours after meals
  • “burning” or “cramplike”
  • tendency to occur, then disappear, then occur again
82
Q

three major complications of an ulcer

A
  • hemorrhage
  • perforation
  • gastric outlet obstruction
83
Q

most common complication of PUD

A

hemorrhage

84
Q

most lethal complication of PUD

A

perforation

85
Q

clinical manifestations of a perforation

A
  • sudden, dramatic onset
  • initial phase (0-2 hours after): severe upper abdominal pain that spreads, tachycardia, weak pulse, rigid boardlike abdominal muscles
  • shallow, rapid RR
  • bowel sounds absent, N/V
86
Q

what can occur from a perforation?

A

bacterial peritonitis may occur within 6-12 hours

87
Q

clinical manifestations of gastric outlet obstruction

A
  • pain worsens toward end of day as stomach fills
  • relief obtained by belching or vomiting
  • constipation
  • swelling: if stomach is grossly dilated, may be palpable
  • loud peristalsis
88
Q

what does medical regimen consist of with PUD

A
  • adequate rest
  • drug therapy
  • elimination of smoking and alcohol
  • dietary modification
  • long-term follow-up care
  • stress management
  • reduce degree of gastric acidity
89
Q

how long does ulcer healing take?

A

requires many weeks of therapy, pain disappears after 3-6 days

90
Q

nutritional therapy for PUD

A
  • bland diet
  • six small meals
91
Q

what is an acute exacerbation accompanied by?

A

bleeding, increased pain and discomfort, N/V

92
Q

focus of treating a perforation

A
  • stop spillage of gastric or duodenal contents into peritoneal cavity
  • restore blood volume
  • place NG tube on continuous suction
  • indwelling catheter inserted and monitored hourly
93
Q

what is done to treat a perforation?

A
  • broad-spectrum antibiotics
  • pain meds
  • repair
94
Q

with a perforation, what do you want to do until the HCP is notified?

A

stop all oral, NG feeds/drugs

95
Q

HAV

A
  • mild to acute liver failure
  • not chronic
  • incidence decreased with vaccination
  • RNA virus transmitted via fecal-oral route
  • contaminated food or drinking water
96
Q

HBV

A
  • acute or chronic disease
  • incidence decreases with vaccination
  • DNA virus transmitted perinataly, percutaneously, via mucosal exposure to blood, blood products, or other body fluids
97
Q

at risk populations for HBV

A
  • high-risk sexual activity
  • household contact of chronically infected
  • pts. undergoing hemodialysis
  • health care and public safety workers
  • transplant recipients
98
Q

how long can HBV live on a dry surface?

A

7 days

99
Q

HCV

A
  • acute: asymptomatic
  • chronic: liver damage
  • RNA virus transmitted percutaneously
  • it is curable
100
Q

HDV

A
  • cannot survive on its own
  • requires HBV to replication
  • transmitted percutaneously
  • no vaccine
101
Q

HEV

A
  • RNA virus transmitted via fecal-oral route
  • most common mode of transmission is drinking contaminated water
  • occurs primarily in developing countries
  • few cases in US
  • acts like A, but out of country
102
Q

acute infection of hepatitis

A
  • liver damage: lysis of infected cells
  • cholestasis
  • liver cells can regenerate in normal form after resolution of infection
103
Q

chronic infection of hepatitis

A

can cause fibrosis and progress to cirrhosis

104
Q

systemic manifestations of hepatitis

A
  • rash
  • angioedema
  • arthritis
  • fever
  • malaise
  • cryoglobulinemia
  • glomerulonephritis
  • vasculitis
105
Q

symptoms during incubation phase of hepatitis

A
  • malaise
  • anorexia
  • weight loss
  • fatigue
  • N/V
  • abdominal discomfort
  • distaste for cigarettes
  • dec. sense of smell
  • headache
  • low-grade fever
  • arthralgias
  • skin rashes
106
Q

if a pt. is icteric, how would that present?

A
  • dark urine
  • light or clay-colored stools
  • pruritus
107
Q

clinical manifestations of convalescent phase

A
  • begins as jaundice is disappearing
  • lasts weeks to months
  • major complaints are malaise and easy fatigability
  • hepatomegaly persists
  • splenomegaly subsides
108
Q

recovery phase of hepatitis

A
  • homologous immunity to HAV or HBV
  • pt. can be reinfected with other types of viral hepatitis, as well as different strains of HCV
  • most pts. recover completely with no complications
109
Q

complications of hepatitis

A
  • acute liver failure
  • chronic hepatitis (some HBV and majority HCV)
  • cirrhosis
  • hepatocellular carcinoma
110
Q

how do we screen for hepatitis

A

specific antigen and/or antibody for each type of viral hepatitis

111
Q

collaborative care of acute and chronic hepatitis

A
  • well-balanced diet (increased calorie and low fat if not tolerated_
  • vitamin supplements
  • rest
  • avoid alcohol intake and drugs detoxified by the liver
  • notify possible contacts and health dept.
112
Q

what drug therapy do we give with acute hepatitis C

A

pegylated interferon to reduce progression to chronic infection

113
Q

goal of chronic hepatitis B

A

to decrease viral load, liver enzyme levels, and rate of disease progression

114
Q

who should receive a hepatitis vaccine?

A
  • all children at 1 year of age
  • adults at risk
115
Q

is isolation required for hepatitis?

A

no, just infection control measures

116
Q

which hepatitis is there no vaccine?

A

HCV; do general measures to prevent transmission

117
Q

how do stones form in cholelithiasis?

A

through biliary sludge

118
Q

cholecystitis

A

most commonly associated with obstruction from stones or sludge

119
Q

what occurs from inflammation in cholecystitis?

A
  • it is confined to mucous lining or entire wall
  • gallbladder is edematous and hyperemic
  • maybe distended with bile pus
  • cystic duct may become occluded
  • scarring and fibrosis after attack
120
Q

clinical manifestations of cholecystitis

A
  • steady, excruciating pain
  • tachycardia, diaphoresis, prostration
  • may be referred to shoulder/scapula
  • residual tenderness in RUQ near liver
  • occur 3-6 hours after high-fat meal or when patient lies down
  • indigestion
  • fever
  • jaundice
  • N/V
  • restlessness
  • diaphoresis
121
Q

total obstruction symptoms

A
  • jaundice
  • dark amber urine
  • clay-colored stools
  • pruritus
  • intolerance of fatty foods
  • bleeding tendencies
  • steatorrhea
122
Q

complications of cholecystitis

A
  • gallbladder rupture that can lead to peritonitis
  • gangrenous cholecystitis
  • subphrenic abscess
  • pancreatitis
  • cholangitis
  • biliary cirrhosis
  • fistulas
  • choledocholithiasis
123
Q

what would lab tests show with gallbladder problems?

A
  • inc. WBC
  • inc. serum bilirubin level
  • inc. urinary bilirubin level
  • inc. liver enzyme levels
  • inc. serum amylase level
124
Q

collaborative care with cholecysitis

A
  • pain control
  • control infection
  • maintenance of F/E balance
125
Q

surgical therapy treatment of choice for cholecystitis

A

laparoscopic cholecystectomy

126
Q

what drug can be given for pruritus in cholecystitis?

A

cholestyramine (questran)

127
Q

after a laparoscopic cholecystectomy, what would the nurse do to maintain pt. comfort?

A
  • referred pain to shoulder from CO2
  • sims’ position
  • deep breathing, ambulation, analgesia
128
Q

most common complication of a pressure ulcer

A

recurrence

129
Q

inflammatory response

A
  • neutralizes and dilutes inflammatory agent
  • removes necrotic materials
  • establishes an environment suitable for healing and repair
130
Q

vascular response of inflammatory response

A

after cell injury, arterioles in area briefly undergo transient vasoconstriction - decrease bleeding

131
Q

what do vasodilation chemical mediators do?

A
  • endothelial cell retraction
  • increased capillary permeability
  • movement of fluid from capillaries into tissue spaces - causing edema
132
Q

chemotaxis

A

mechanism for accumulating neutrophils and monocytes at site of injury

133
Q

neutrophils

A
  • first leukocytes to arrive at site of injury (6-12 hours)
  • phagocytize bacteria, other foreign material, and damaged cells
  • short life span (24-48 hours)
    *high neutrophils = body thinks it’s infected
134
Q

monocytes

A
  • second type to migrate to site of injury
  • arrive within 3-7 days after onset of inflammation
  • on entering tissue space, monocytes transform into macrophages
  • assist in phagocytosis of inflam. debris
  • have long life span and can multiply
135
Q

macrophage

A
  • important in cleaning the area before healing can occur
  • may stay in damaged tissues for weeks
136
Q

lymphocytes

A
  • arrive later at the site of injury
  • primary role involves immunity
137
Q

major functions of cellular response

A
  • enhanced phagocytosis
  • increased vascular permeability
  • chemotaxis
  • cellular lysis
138
Q

what can chronic inflammation result from?

A

changes in immune system (like autoimmune disease)

NSG 322 Med Surge I (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions