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
tx for hiatal hernia
``` conservative small frequent meals, avoid lying after meals avoid tight clothes and abd supports weight control antacids ```
26
acute gastritis
temporary inflammation of stomach lining | lasts 2-10 days
27
aggregators of acute gastritis
alcohol nsaids ( r/t decreased prostaglandins) infectious agents (h. pylori)
28
chronic gastritis
progressive, chronic inflammation lasts weeks to years immune related/ non immune related
29
complications of chronic gastritis
PUD bleeding ulcers anemia gastric cancers
30
2 main causes of chronic gastritis
autoimmune- attacks own cells | chronic h. pylori infections
31
h. pylori thrives in what kind of enviornment?
acidic
32
what is h. pylori
destructive pattern of persistent inflammation | can cause Chronic Gastritis, PUD, stomach cancer
33
how is H. Pylori transmitted?
person to person via saliva, fecal matter, or vomit | contaminated food or water
34
symptoms of gastritis (acute or chronic)
``` vomiting stomach burning upset stomach loss of appetite vomiting blood black stool postprandial discomfort ```
35
acute gastroenteritis
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
manifestations of acute gastroenteritis
watery diarrhea (can be bloody is bacterial), abdominal pain, N/V, fever, malaise
37
what is a complication of gastreoenteritis
fluid volume deficit
38
What is PUD
``` ulcerative disorder of upper GI tract esophageal stomach - gastric ulcers duodenum- peptic ulcer develops when GI tract exposed to acid and h. pylori ```
39
aggressive factors of GI tract
``` h. pylori NSAIDS acid pepsin smoking ```
40
defensive factors or GI tract
mucus bicarbonate blood flow prostaglandins
41
causes of PUD
``` H. pylori nsaids asa alcohol excessive secretion of acid smoking family fx stress ```
42
risk factors for NSAID induced PUD
``` age high doses of NSAIDS chronic corticosteroids chronic anticoagulants autoimmune disorders h. pylori infection ```
43
how does PUD develop?
mucosa damage histamine secretion resulting in increased acid and pepsin production, vasodilation if blood vessels are destroyed results in bleeding
44
duodenal ulcer
most common type | can occur at any age
45
gastric/peptic ulcer
peak at age 50-70 | caused by increased of NSAIDs, corticosteroids, anticoagulants, more likely to have systemic illness
46
clinical manifestations of PUD
``` sometimes none unless bleeding n/v, anorexia wt loss bleeding burning pain in middle of abd, worse when stomach is empty ```
47
gastric ulcer Characteristics location timing
burning, cramping, gas like epigastrium, back 1-2 hours after eating
48
duodenal ulcer characteristics location timing
burning, cramping, gas like epigastrium, back 2-4 hours after eating
49
complications of PUD "HOP"
hemorrhage obstruction perforation and peritonitis
50
appendicitis
inflammation of appendix | caused is obstructed which leads to inflammation
51
complications of appedicitis
gangrene abscess formation peritonitis
52
key points of appendicits
RLQ pain, periumbilical area rebound pain at McBurney's point sudden pain relief may indicate rupture/peritonitis
53
manifestations of appendicitis
``` age 10-12 starts as dull, steady pain in periumbilical area progresses over 4-6 hours RLQ low grade fever nausea elevated WBC ```
54
peritonitis
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
causes of peritonitis
``` think ruptured or perforated perforated ulcer ruptured gallbladder pancreatitis ruptured spleen ruptured bladder ruptured appendix ```
56
clinical manifestations of peritonitis
``` sudden and severe abdominal pain (worst pain of life) rigid board like abdomen INCREASED HR DECREASED BP ```
57
IBS
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
psychological stress and IBS
cause unknown, triggered by stress, food, hormone changes, GI infections, menses
59
IBD
life changing chronic illness 2 types: crohns and UC causes chronic inflammation, exacerbations and remission in intestines autoimmune activated by infection
60
IBD is more common in
women Caucasians Jewish descent smokers
61
crohns
lymph structures of GI tract are blocked, tissues become engorged and inflamed deep linear fissures and ulcers skip lesions cobblestone appearance
62
complications of crohns
``` malnutrition anemia scar tissue and obstructions fistulas cancer ```
63
GALS (crohns disease)
granulomas, all layers, skip lesions
64
clinical manifestations of crohns
``` crampy RLQ pain watery diarrhea weight loss fatigue no appetite malabsorption of nutrients PALPABLE RLQ mass mouth ulcers ```
65
UC
inflammation of mucosa of rectum and colon | usually develops in third decade of life
66
UC is more common in
white people of European descent, esp. Ashkenazi Jewish occasionally in black/African rare in Asians
67
pathogenesis of UC
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
why is new granulation tissue a problem with IBD?
tissue is fragile and bleeds easily
69
clinical manifestations of UC
``` abdominal pain bloody diarrhea (not seen with crohns) wt loss fatigue no appetite fever ```
70
complications of UC
``` 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
diverticulosis
``` small pouches bulging outwards through weak spots can be congenital or acquired caused by low fiber diet usually in descending colon discovered accidentally ```
72
diverticulitis
``` inflammation retained fecal matter LLQ pain increased WBC acute passage of large frank blood ```
73
complications of diveritculitis
perforation peritonitis obstruction
74
g-cells
produce gastrin, facilitates production of HCl
75
parietal cells
produce HCl to break down food | produce intrinsic factor to protect mucosa
76
chief cells
secrete pepsin
77
epithelial cells
secrete bicarbonate-rich solution to coat and protect stomach
78
order of small intestine
duodenum jejunum illeum
79
crypts of lieberkuhn
intestinal glands secretes 2l fluid daily into lumen of intestine Crypt abscesses in UC
80
goblet and brunner cells
secrete mucus to protect small intestine from acidic gastric juices
81
ileocecal sphincter
area where food passes from small to large intestine
82
large intestine includes
appendix, ascending colon, transverse colon, descending colon, sigmoid colon and rectum