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NUR 326 - GI and Endocrine > upper and lower GI > Flashcards

upper and lower GI Flashcards

1
Q

what organs are part of the upper GI?

A

esophagus
stomach
beginning of small intestines

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2
Q

what organs are part of the lower GI?

A

small intestines, colon, 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

A

gastritis
acute gastroenteritis
PUD

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5
Q

dysphagia

A

difficulty swallowing

begins with solids and processes to liquids

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6
Q

common causes of dysphagia

A

mechanical obstruction

neuromuscular dysfunction

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7
Q

what is a mechanical obstruction

A

stenosis or stricture
diverticula
tremors

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8
Q

what is a neuromuscular dysfunction

A

CVA ( intubation or trachs)

achalasia (lower esophageal sphincter cant open properly)

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9
Q

GERD

A

backflow of gastric acid from stomach to esophagus

occurs when LES doesn’t close properly

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10
Q

causes of GERD

A

anything that alters closure strength of LES or increases abdominal pressure
(fatty, spicy, acidic, tomato, citrus, caffeine, alcohol, smoking, sleep, obesity, pregnancy)

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11
Q

what symptoms can GERD cause in the mouth?

A

tooth decay
gingivitis
bad breath

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12
Q

what symptoms can GERD cause in the chest

A

chronic cough
worsening asthma
recurrent pneumonia

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13
Q

what symptoms can GERD cause in the abdomen

A

bloating

belching

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14
Q

what symptoms can GERD cause in the ears

A

earache

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15
Q

what symptoms can GERD cause in the throat

A 
hoarseness
chronic sore throat
throat clearing
laryngitis
lump in throat
post nasal drip
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16
Q

clinical manifestations of GERD

A 
heartburn (pyrosis)
dyspepsia
regurgitation
chest pain
dysphagia
pulmonary symptoms
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17
Q

complications of GERD

A

ulceration
scarring
strictures
barrettes esophagus

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18
Q

what are the risks with barrettes esophagus?

A

premalignant
three-fold increased risk of developing esophageal cancer
overall survival rate 17%

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19
Q

hiatal hernia

A

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

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20
Q

what are the 2 types of hiatal hernias?

A

sliding

paraoesophageal

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21
Q

sliding hernia

A

usually small
does not need tx
peritoneum stays intact

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22
Q

paraoesophageal hernia

A

part of stomach pushes through diaphragm and stays there, peritoneum thins and ruptures

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23
Q

risk factors for hiatal hernias

A

age
obesity
smoking

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24
Q

manifestations of hiatal hernia

A 
asymptomatic
belching
dysphagia
chest or epigastric pain
common for GERD and hiatal hernia to coexist
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25
Q

tx for hiatal hernia

A 
conservative
small frequent meals, avoid lying after meals
avoid tight clothes and abd supports
weight control
antacids
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26
Q

acute gastritis

A

temporary inflammation of stomach lining

lasts 2-10 days

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27
Q

aggregators of acute gastritis

A

alcohol
nsaids ( r/t decreased prostaglandins)
infectious agents (h. pylori)

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28
Q

chronic gastritis

A

progressive, chronic inflammation
lasts weeks to years
immune related/ non immune related

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29
Q

complications of chronic gastritis

A

PUD
bleeding ulcers
anemia
gastric cancers

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30
Q

2 main causes of chronic gastritis

A

autoimmune- attacks own cells

chronic h. pylori infections

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31
Q

h. pylori thrives in what kind of enviornment?

A

acidic

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32
Q

what is h. pylori

A

destructive pattern of persistent inflammation

can cause Chronic Gastritis, PUD, stomach cancer

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33
Q

how is H. Pylori transmitted?

A

person to person via saliva, fecal matter, or vomit

contaminated food or water

34
Q

symptoms of gastritis (acute or chronic)

A 
vomiting
stomach burning
upset stomach
loss of appetite
vomiting blood
black stool
postprandial discomfort
35
Q

acute gastroenteritis

A

inflammation of stomach and small intestine
usually lasts 1-3 days
caused by viral, bacterial, parasitic infections
let infections play out.. usually no abx

36
Q

manifestations of acute gastroenteritis

A

watery diarrhea (can be bloody is bacterial), abdominal pain, N/V, fever, malaise

37
Q

what is a complication of gastreoenteritis

A

fluid volume deficit

38
Q

What is PUD

A 
ulcerative disorder of upper GI tract
esophageal
stomach - gastric ulcers
duodenum- peptic ulcer
develops when GI tract exposed to acid and h. pylori
39
Q

aggressive factors of GI tract

A 
h. pylori
NSAIDS
acid
pepsin
smoking
40
Q

defensive factors or GI tract

A

mucus
bicarbonate
blood flow
prostaglandins

41
Q

causes of PUD

A 
H. pylori
nsaids
asa
alcohol
excessive secretion of acid
smoking 
family fx
stress
42
Q

risk factors for NSAID induced PUD

A 
age
high doses of NSAIDS
chronic corticosteroids
chronic anticoagulants
autoimmune disorders
h. pylori infection
43
Q

how does PUD develop?

A

mucosa damage
histamine secretion resulting in increased acid and pepsin production, vasodilation
if blood vessels are destroyed results in bleeding

44
Q

duodenal ulcer

A

most common type

can occur at any age

45
Q

gastric/peptic ulcer

A

peak at age 50-70

caused by increased of NSAIDs, corticosteroids, anticoagulants, more likely to have systemic illness

46
Q

clinical manifestations of PUD

A 
sometimes none unless bleeding
n/v, anorexia
wt loss
bleeding
burning pain in middle of abd, worse when stomach is empty
47
Q

gastric ulcer
Characteristics
location
timing

A

burning, cramping, gas like
epigastrium, back
1-2 hours after eating

48
Q

duodenal ulcer
characteristics
location
timing

A

burning, cramping, gas like
epigastrium, back
2-4 hours after eating

49
Q

complications of PUD “HOP”

A

hemorrhage
obstruction
perforation and peritonitis

50
Q

appendicitis

A

inflammation of appendix

caused is obstructed which leads to inflammation

51
Q

complications of appedicitis

A

gangrene
abscess formation
peritonitis

52
Q

key points of appendicits

A

RLQ pain, periumbilical area
rebound pain at McBurney’s point
sudden pain relief may indicate rupture/peritonitis

53
Q

manifestations of appendicitis

A 
age 10-12
starts as dull, steady pain in periumbilical area
progresses over 4-6 hours
RLQ
low grade fever
nausea
elevated WBC
54
Q

peritonitis

A

inflammation of peritoneum
fluids shift causing third spacing can lead to hypovolemic shock and sepsis
decreased peristalsis
can lead to paralytic ileus and intestinal obstruction

55
Q

causes of peritonitis

A 
think ruptured or perforated
perforated ulcer
ruptured gallbladder
pancreatitis
ruptured spleen
ruptured bladder
ruptured appendix
56
Q

clinical manifestations of peritonitis

A 
sudden and severe
abdominal pain (worst pain of life)
rigid board like abdomen
INCREASED HR
DECREASED BP
57
Q

IBS

A

changes in intestinal motility
can be IBSC or IBSD
symptoms vary by individual
intermittent abdominal pain relieved by deification
bowel urgency
intolerance to certain foods (sorbitol, lactose, gluten)
non-bloody mucous stool

58
Q

psychological stress and IBS

A

cause unknown, triggered by stress, food, hormone changes, GI infections, menses

59
Q

IBD

A

life changing chronic illness
2 types: crohns and UC
causes chronic inflammation, exacerbations and remission in intestines
autoimmune activated by infection

60
Q

IBD is more common in

A

women
Caucasians
Jewish descent
smokers

61
Q

crohns

A

lymph structures of GI tract are blocked, tissues become engorged and inflamed
deep linear fissures and ulcers
skip lesions
cobblestone appearance

62
Q

complications of crohns

A 
malnutrition
anemia
scar tissue and obstructions
fistulas
cancer
63
Q

GALS (crohns disease)

A

granulomas, all layers, skip lesions

64
Q

clinical manifestations of crohns

A 
crampy RLQ pain
watery diarrhea
weight loss
fatigue
no appetite 
malabsorption of nutrients
PALPABLE RLQ mass
mouth ulcers
65
Q

UC

A

inflammation of mucosa of rectum and colon

usually develops in third decade of life

66
Q

UC is more common in

A

white people of European descent, esp. Ashkenazi Jewish
occasionally in black/African
rare in Asians

67
Q

pathogenesis of UC

A

inflammation begins in rectum extends in CONTINUOUS segment that involves entire colon
inflammation leads to large ulcerations
necrosis of epithelial tissues
CRYPT ABSCESSES
damage repaired with new granulation tissue

68
Q

why is new granulation tissue a problem with IBD?

A

tissue is fragile and bleeds easily

69
Q

clinical manifestations of UC

A 
abdominal pain
bloody diarrhea (not seen with crohns)
wt loss
fatigue
no appetite
fever
70
Q

complications of UC

A 
hemorrhage
perforation
cancer
fissures
Crypt abscesses
toxic megacolon
increased risk of colo/rectal cancer
liver disease
fluid, electrolyte, and PH balances
increased risk of VTE and PE
71
Q

diverticulosis

A 
small pouches bulging outwards through weak spots
can be congenital or acquired
caused by low fiber diet
usually in descending colon
discovered accidentally
72
Q

diverticulitis

A 
inflammation
retained fecal matter
LLQ pain
increased WBC
acute passage of large frank blood
73
Q

complications of diveritculitis

A

perforation
peritonitis
obstruction

74
Q

g-cells

A

produce gastrin, facilitates production of HCl

75
Q

parietal cells

A

produce HCl to break down food

produce intrinsic factor to protect mucosa

76
Q

chief cells

A

secrete pepsin

77
Q

epithelial cells

A

secrete bicarbonate-rich solution to coat and protect stomach

78
Q

order of small intestine

A

duodenum
jejunum
illeum

79
Q

crypts of lieberkuhn

A

intestinal glands
secretes 2l fluid daily into lumen of intestine
Crypt abscesses in UC

80
Q

goblet and brunner cells

A

secrete mucus to protect small intestine from acidic gastric juices

81
Q

ileocecal sphincter

A

area where food passes from small to large intestine

82
Q

large intestine includes

A

appendix, ascending colon, transverse colon, descending colon, sigmoid colon and rectum

NUR 326 - GI and Endocrine (6 decks)

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