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NUR 326 Exam 3 > Patho of GI Diseases > Flashcards

Patho of GI Diseases Flashcards

1
Q

Components of Upper GI

A

–Esophagus
–Stomach
–Beginning of small intestines

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2
Q

Components of Lower GI

A

–small intestines
–colon (large intestines)
–rectum/anus

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3
Q

Esophageal disorders

A

–GERD
–Hiatal Hernia

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4
Q

Inflammatory disorders of the stomach (Upper GI)

A

–gastritis
–acute gastroenteritis
–PUD

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5
Q

dysphagia

A

difficulty swallowing

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6
Q

how does dysphagia progress?

A

begins with solids and progresses to liquids

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7
Q

common causes of dysphagia

A

–mechanical obstruction
–neuromuscular dysfunction
–intubation
–tracheostomy

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8
Q

examples of mechanical obstruction

A

–stenosis and stricture
–diverticula
–tumors

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9
Q

examples of neuromuscular dysfunction

A

–CVA
–achalasia

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10
Q

achalasia

A

lower esophageal sphincter can’t open properly

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11
Q

GERD

A

gastro esophageal reflux disease

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12
Q

GERD aka ________

A

heartburn

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13
Q

GERD definition

A

–backflow of gastric acid from stomach into esophagus
–occurs via LES

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14
Q

what triggers GERD?

A

–anything that alters closure strength of LES or increases abdominal pressure
–fatty foods
–spicy foods
–tomato based foods
–citrus foods
–caffeine
–large amounts of alcohol
–cigarettes
–sleep position
–obesity
–pregnancy
–pharm agents

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15
Q

clinical manifestations of GERD

A

–heartburn (pyrosis)
–dyspepsia
–regurgitation
–chest pain
–dysphagia
–pulmonary symptoms

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16
Q

complications of GERD

A

–ulceration
–scarring
–strictures
–Barrett’s esophagus

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17
Q

Barrett’s esophagus

A

development of abnormal metaplastic tissue–premalignant

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18
Q

treatment for Barrett’s esophagus

A

prevention, no treatment

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19
Q

risk associated with Barrett’s esophagus

A

three-fold increased risk of developing adenocarcinoma of the esophagus

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20
Q

Hiatal Hernia

A

a defect in the diaphragm that allows part of the stomach to pass into the thorax

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21
Q

two main types of hiatal hernias

A

–sliding hernia
–paraesophageal hernia

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22
Q

sliding hernia

A

usually small and often do not need treatment

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23
Q

paraesophageal hernia

A

part of the stomach pushes through the diaphragm and stays there

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24
Q

causes of hiatal hernia

A

–exact cause is unknown
–increased age
–injury or other damage may weaken the diaphragm muscle
–repeatedly putting too much pressure on the muscles around the stomach

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25
Q

examples of mechanisms that can cause a hiatal hernia

A

–severe coughing
–vomiting
–constipation and straining to have a bowel movement

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26
Q

clinical manifestations of hiatal hernias

A

–asymptomatic
–belching
–dysphagia
–chest or epigastric pain
–weaker LES

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27
Q

risk factors for hiatal hernias

A

–age
–obesity
–smoking

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28
Q

GERD and hiatal hernias

A

common for these to coexist

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29
Q

treatment of hiatal hernias

A

–conservative treatment
–surgery if conservative treatments don’t work
–antacids for the GERD/esophagitis syndrome

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30
Q

teaching for hiatal hernias

A

–small, frequent meals
–avoid lying down after eating
–avoid tight clothing and abdominal supports
–weight control for obese individuals

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31
Q

acute gastritis

A

temporary inflammation of the stomach lining only (intestines not affected)

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32
Q

duration of acute gastritis

A

generally lasts 2-10 days

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33
Q

etiology of acute gastritis

A

–irritating substances (alcohol)
–drugs (NSAIDs)
–infectious agents

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34
Q

infectious agent involved with acute gastritis

A

H. pylori

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35
Q

chronic gastritis

A

progressive disorder with chronic inflammation in the stomach

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36
Q

duration of chronic gastritis

A

can last weeks to years

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37
Q

complications of chronic gastritis

A

–PUD
–bleeding
–ulcers
–anemia
–gastric cancers

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38
Q

PUD

A

peptic ulcer disease

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39
Q

etiologies of chronic gastritis

A

–autoimmune (attacks parietal cells)
–H. pylori infection

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40
Q

H. pylori

A

helicobacter pylori bacterium

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41
Q

where does H. pylori thrive?

A

in acidic environments

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42
Q

how does H. pylori work?

A

destructive pattern of persistent inflammation

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43
Q

how is H. pylori transmitted?

A

–person to person via saliva, fecal matter, or vomit
–contaminated food or water

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44
Q

clinical manifestations of acute/chronic gastritis

A

–sometimes none
–anorexia
–N/V
–postprandial discomfort
–intestinal gas
–hematemesis
–tarry stools
–anemia

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45
Q

acute gastroenteritis

A

inflammation of stomach and small intestine

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46
Q

etiology of acute gastroenteritis

A

–viral infections: norovirus and rotavirus
–bacterial infections: E. coli, salmonella, campylobacter
–parasitic infections

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47
Q

duration of acute gastroenteritis

A

usually lasts 1-3 days, but many last as long as 10 days

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48
Q

clinical manifestations of acute gastroenteritis

A

–watery diarrhea (bloody if bacterial)
–abdominal pain
–N/V
–fever, malaise

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49
Q

complication of acute gastroenteritis

A

fluid volume deficits (dehydration)

50
Q

treatment for acute gastroenteritis

A

let virus run its course (>72 hours = see PCP)

51
Q

peptic ulcer disease (PUD)

A

ulcerative disorder of the upper GI tract

52
Q

body parts affected by PUD

A

–esophageal
–stomach
–duodenum

53
Q

PUD term in stomach

A

gastric ulcers

54
Q

PUD term in duodenum

A

peptic ulcer

55
Q

when does PUD develop?

A

when GI tract is exposed to acid and h. pylori

56
Q

aggressive factors for GI health

A

–H. pylori
–NSAIDs
–acid
–pepsin
–smoking

57
Q

defensive factors for GI health

A

–mucus
–bicarbonate
–blood flow
–prostaglandins

58
Q

PUD etiology

A

–H. pylori
–injury-causing substances
–NSAIDs, ASA, alcohol
–excess secretion of acid
–smoking
–family history
–stress

59
Q

how does stress affect PUD?

A

remember there is increased gastric acid secreted with the stress response

60
Q

risk factors for PUD

A

–age
–higher doses of NSAIDs
–hx of PUD
–use of corticosteroids and anticoags
–serious systemic disorders
–H. pylori infection

61
Q

pathogenesis of PUD

A

–mucosa is damaged
–histamine is secreted, resulting in (1) increase in acid and pepsin secretion - tissue damage, (2) vasodilation - causes edema
–bleeding if BV destroyed

62
Q

duodenal ulcer

A

–most common type
–age - any; early adulthood

63
Q

gastric/peptic ulcer age and causes

A

–age: peak 50-70
–increased use of NSAIDs, corticosteroids, anticoagulants, more likely to have serious systemic illnesses

64
Q

clinical manifestations of PUD

A

–sometimes none
–N/V, anorexia
–weight loss
–bleeding
–burning pain in middle of abdomen that is usually worse when stomach is empty

65
Q

symptomatic characteristics of gastric ulcer

A

–burning
–cramping
–gas-like

66
Q

location of gastric ulcer

A

epigastrium, back

67
Q

timing of gastric ulcer

A

1-2 hours after eating

68
Q

symptomatic characteristics of duodenal ulcer

A

burning, cramping, gas-like

69
Q

location of duodenal ulcer

A

epigastrium, back

70
Q

timing of duodenal ulcer

A

2-4 hours after eating

71
Q

PUD complications

A

H – hemorrhage
O – obstruction
P – perforation and peritonitis

72
Q

lower GI disorders

A

–appendicitis
–peritonitis
–IBS (Crohn’s, UC)
–IBD
–diverticulosis/diverticulitis

73
Q

etiology of appendicitis

A

–appendix is obstructed
–leads to inflammation

74
Q

complications of appendicitis

A

–gangrene
–abscess formation
–peritonitis

75
Q

types of pain with appendicitis

A

–classic pain (RLQ in periumbilical area)
–rebound pain
–sudden pain relief

76
Q

what might sudden pain relief indicate in appendicitis?

A

may indicate rupture – peritonitis

77
Q

peak incidence of appendicitis

A

10-12 years

78
Q

symptoms of appendicitis

A

–low grade fever
–nausea
–anorexia
–rebound pain or tenderness at McBurney’s point (RLQ)

79
Q

diagnosis of appendicitis

A

–clinical signs and symptoms
–increased WBC
–abdominal sonogram
–exploratory lap

80
Q

peritonitis

A

inflammation of peritoneum

81
Q

peritoneum

A

serous membrane that lines abdominal cavity and covers visceral organs

82
Q

what happens to the peritoneum in peritonitis?

A

–inflammation
–third spacing
–decreased peristalsis

83
Q

what can third spacing lead to?

A

can lead to hypovolemic shock and sepsis

84
Q

what can peritonitis lead to?

A

paralytic ileus and intestinal obstruction

85
Q

causes of peritonitis

A

–perforated ulcer
–ruptured gallbladder
–pancreatitis
–ruptured spleen
–ruptured bladder
–ruptured appendix

86
Q

s/s of peritonitis

A

–sudden and severe
–abdominal pain
–tenderness
–rigid “board-like” abdomen
–N/V
–fever
–elevated WBC
–HR increased
–BP decreased

87
Q

treatment of peritonitis

A

–antiinflammation
–treat the cause

88
Q

causes of increased HR and decreased BP in peritonitis

A

SNS activation from pain; fluid shifts

89
Q

lower GI problems

A

–inflammatory bowel syndrome
–inflammatory bowel disease

90
Q

irritable bowel syndrome

A

–chronic condition
–alterations in bowel pattern due to changes in intestinal motility

91
Q

types of irritable bowel syndrome

A

–chronic and frequent constipation (IBSC)
–chronic and frequent diarrhea (IBSD)

92
Q

symptoms of IBS

A

varies by individual

93
Q

potential symptoms of IBS

A

–abdominal distention, fullness, flatus, and bloating
–intermittent abdominal pain exacerbated by stress and relieved by defecation
–bowel urgency
–intolerance to certain foods
–non-bloody stool that may contain mucous

94
Q

psychosocial stress and IBS

A

–almost never the result of primarily psychological causes
–can be exacerbated by stress
–can cause stress and psych problems

95
Q

cause of IBS

A

unknown, but thought to be “triggered” by stress, food, hormone changes, GI infections, menses

96
Q

inflammatory bowel disease

A

(1) Crohn’s disease
(2) Ulcerative colitis

97
Q

what is IBD characterized by?

A

–chronic inflammation of the intestines
–exacerbation and remissions

98
Q

who is IBD most common in?

A

–women
–Caucasians
–Jewish people
–smokers

99
Q

etiology of IBD

A

genetically autoimmune; activated by an infection

100
Q

pathogenesis of Crohn’s disease

A

–lymph structures of GI tract are blocked
–tissue becomes engorged and inflamed
–deep linear fissures and ulcers develop in “patchy” pattern along the bowel wall (skip lesions, cobblestone)

101
Q

complications of Crohn’s disease

A

–malnutrition
–scar tissue and obstructions
–fistulas
–cancer

102
Q

clinical manifestations of Crohn’s disease

A

–crampy lower abdominal pain (RLQ)
–watery diarrhea
–systemic (weight loss, fatigue, no appetite, fever, malabsorption of nutrients)
–palpable abdominal mass (RLQ)
–mouth ulcers
–s/s of fistulas

103
Q

what are specific to Crohn’s disease?

A

–skip lesions
–granulomas

104
Q

complications of Crohn’s disease

A

VTE/DVT

105
Q

ulcerative colitis

A

inflammation of the mucosa of the rectum and colon

106
Q

development of UC

A

third decade of life

107
Q

who gets UC?

A

white people of European descent (Ashkenazi Jewish)
–occasionally in AA
–rare in Asians

108
Q

UC patho

A

–inflammation in rectum and extends in continuous segment that may involve the entire colon
–inflammation = large ulcerations
–colon and rectum try to repair the damage with new granulation tissue

109
Q

crypt abscesses

A

necrosis of the epithelial tissue can result in abscesses

110
Q

symptoms of UC

A

–abdominal pain
–bloody diarrhea
–systemic (weight loss, fatigue, no appetite, fever)

111
Q

complications of UC

A

–hemorrhage
–perforation
–cancer (colorectal carcinoma)
–malnutrition
–anemia
–strictures
–fissures
–abscesses
–toxic megacolon
–liver disease
–F/E, pH imbalances

112
Q

significance of bloody diarrhea

A

only happens with UC, not Crohn’s

113
Q

toxic megacolon

A

rapid dilation of large intestine that can be life-threatening

114
Q

diverticulosis

A

–development of diverticula
–may be congenital or acquired
–thought to be caused with low fiber diet with resulting chronic constipation

115
Q

usual location of diverticulosis

A

descending colon

116
Q

diverticula

A

small pouches in lining of colon that bulge outward through weak spots

117
Q

diverticulitis vs. diverticulosis

A

diverticulitis = with infection or inflammation
diverticulosis = without inflammation

118
Q

symptoms of diverticulosis

A

–asymptomatic
–discovered accidentally or with presentation of acute diverticulitis

119
Q

diverticulitis

A

inflammation of one or more of the pouches (usually from retained fecal matter)

120
Q

symptoms of diverticulitis

A

–abdominal pain (LLQ)
–fever
–WBCs increased
–constipation or diarrhea
–acute passage of large quantity of frank blood
–may resolve spontaneously

121
Q

complications of diverticulitis

A

–perforation
–peritonitis
–obstruction

NUR 326 Exam 3 (11 decks)

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