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Pathophysiology > Gastrointestinal Disorders (Exam 2) > Flashcards

Gastrointestinal Disorders (Exam 2) Flashcards

1
Q

diarrhea

A

passage of abnormally liquid or unformed stools at an increased frequency

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2
Q

causes of diarrhea

A

microbial infections
medications
food related
abrupt onset of chronic disease

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3
Q

functions of the GI system

A

assimilation of nutrients
excretion of waste products
endocrine, immune, barrier functions

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4
Q

control over multiple processes and organs is provided by

A

enteric nervous system
hormones

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5
Q

assimilation of nutrients includes

A

motility of food
secretion of fluid and enzymes for digestion
absorption of nutrients
transport of nutrients into circulatory system

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6
Q

layers of the GI from inside to outside

A

Mucosa
Submucosa
Muscularis externa
Serosa

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7
Q

mouth

A

chewing, mixing with saliva, bolus formation

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8
Q

stomach

A

1-4 hours transit time
mix, grind, dilute and dissolve food
exocrine secretions, gastric acid and intrinsic factor

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9
Q

level of absorption in the stomach

A

minor

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10
Q

gastric emptying

A

key control point for further delivery and indicating satiety

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11
Q

cells in the stomach

A

parietal cells
cheif cells
enteroendocrine cells
mucous neck cells

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12
Q

parietal cells

A

produce HCl and intrinsic factor

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13
Q

chief cells

A

produce pepsinogen

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14
Q

enteroendocrine cells

A

produce hormones
gastrin in stomach
peptide hormones in small intestine

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15
Q

mucous neck cells

A

produce thin, acidic mucus

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16
Q

small intestine

A

7-10 hours transit time
continues digestion of proteins, fats and carbohydrates
receives digestive secretions from the liver and pancreas
produces enzymes, alkaline mucus
produces hormones

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17
Q

how much absorption occurs in the small intestine

A

90% (she works like a dog DAY AND NIGHT SIPPING FROM A POT NONE OF YOU WANT TO TOUCH!!!)

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18
Q

cells in small intestine

A

enterocytes
enteroendocrine cells
paneth cells
goblet cells

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19
Q

goblet cells

A

produce thick mucus

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20
Q

paneth cells

A

produce antimicrobial peptides

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21
Q

enterocytes

A

absorb water and nutrients

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22
Q

intestinal stem cells and migration of their progeny occurs from

A

crypt to villus
regenerates every 4-5 days

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23
Q

endocrine pancreas

A

regulating metabolism
produces and secretes hormones

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24
Q

what is secreted from endocrine pancreas and what do they do?

A

insulin - glucose uptake from blood
glucagon - breakdown glycogen to glucose
somatostatin - growth hormone inhibiting hormone; regulates endocrine system

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25
Q

exocrine pancreas

A

digesting food
produces and secretes enzymes

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26
Q

what is released from the exocrine pancreas?

A

proteases
lipase
amylase

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27
Q

enzymes are produced in the

A

inactive form (zymogen) and only activated when released
prevents self digestion of the pancreas

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28
Q

pancreas duct cells

A

produce and secrete bicarbonate
neutralize stomach acid

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29
Q

liver functions

A

prepares food for digestion in the SI
detoxifies blood from GI
regulates metabolism of biomolecules
produces plasma proteins
produces fats, lipids and cholesterol

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30
Q

gallbladder

A

stores and releases bile

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31
Q

large intestine

A

12-24 hrs transit time
water and electrolyte absorption
microflora process undigested food
storage of fecal waste

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32
Q

rectum and anus

A

elimination of fecal waste
1-3 days after meal ingestion

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33
Q

large intestines only have

A

crypts
NO VILLI!!!!

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34
Q

the small intestine has

A

both crypts and villi (because she does the hard work, needs more assistance)

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35
Q

what is the difference in cells in epithelium of the small and large intestines

A

large intestines do NOT have paneth cells

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36
Q

sphincters

A

help control over assimilation of nutrients

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37
Q

neural regulation

A

control over intestinal secretions and smooth muscle activity in intestinal wall and blood vessels

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38
Q

endocrine regulation

A

release of hormones into the bloodstream triggered by a meal

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39
Q

paracrine regulation

A

release of substances that alter nearby cells

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40
Q

neuronal signaling controls

A

digestion
fluid secretions and absorption
motility
blood flow

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41
Q

the enteric nervous system controls

A

every part of the GI tract

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42
Q

hormones in the GI coordinate

A

movement
secretions
digestion of food
absorption of nutrients
brain responses

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43
Q

peristalsis

A

propels contents orally to caudally
circular contraction behind contents

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44
Q

segmentation

A

forces the contents back and forth to mix

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45
Q

fluid and electrolyte balance

A

fluid ingested and secreted must equal fluid absorbed + fluid exerted

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46
Q

the ability to absorb 9.3 liters is due to the function of

A

several transport proteins

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47
Q

transport of Na across intestinal epithelium drives

A

simultaneous absorption of water into tissue by osmosis

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48
Q

transport of Cl across intestinal epithelium drives

A

simultaneous secretion of water into gut lumen by osmosis

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49
Q

mucosal immune system

A

recognizes pathogenic microbes, commensal microbes and foods
70% of immune system cells are in the GI tract

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50
Q

nausea

A

inclination to vomit or feeling in the throat alerting that vomiting is coming

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51
Q

vomiting

A

ejection/expulsion of gastric material through mouth, forcefully

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52
Q

regurgitation

A

gastric/esophageal contents rise to pharynx but no forceful ejection

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53
Q

symptoms of N&V

A

pallor, tachycardia, sweating

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54
Q

emetic

A

capable of inducing vomiting

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55
Q

Therapy induced causes of N&V include

A

antineoplastic agents (chemotherapy)

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56
Q

3 stages of emesis

A
  1. nausea
  2. retching
  3. vomiting
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57
Q

retching

A

labored movement of thoracic and abdominal muscles before vomiting

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58
Q

vomiting is coordinated

A

by the brainstem

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59
Q

vomiting requires

A

contractions of abdominal muscles, pyloric, antrum
raised gastric cardia
diminished lower esophageal sphincter pressure
esophageal dilation

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60
Q

mechanism of N&V

A

emetic compounds trigger vomiting by stimulating receptors in the 4 sensory centers of the vomiting center (nucleus of tracts solitarius)

61
Q

4 sensory centers of vomiting center

A

cerebral cortex
vestibular system
GI tract and heart
CTZ

62
Q

GERD

A

chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus

63
Q

how much pyrosis frequency is required as criteria for GERD

A

2 times per week

64
Q

if untreated, GERD can lead to

A

inflammation of the esophagus
or
erosion of the squamous epithelium of the esophagus

65
Q

classifications of GERD

A

based on severity of erosions
based on presentation
baed on symptoms

66
Q

Non erosive reflux disease vs Barrett esophagus

A

severity
NERD: most common, erosive
BE: most severe, least common

67
Q

causes of GERD

A

motor abnormalities
impairment in the tone of the lower esophageal sphincter
transient LES relaxation
delayed gastric emptying

68
Q

risk factors of GERD

A

obesity
alcohol abuse
smoking
excessive caffeine intake
respiratory diseases

69
Q

mechanisms of Gerd

A

-decrease in LES pressure
-hiatal hernia
-dec clearance of gastric contents from esophagus
-decreased mucosal resistance in esophagus
-composition of reflux contents extra acidic”
-decreased gastric emptying

70
Q

decrease in LES pressure (GERD)

A

frequent transient LES relaxations not triggered by swallowing may occur, allowing reflux
can be atonic, permitting free reflux
stress reflux from bending over

71
Q

hiatal hernia

A

protrusion of the stomach through the diaphragm into the chest

72
Q

hiatal hernia role in GERD

A

-disrupts normal anatomic barrier between the stomach and esophagus
-allows stomach content to reflux into the esophagus
-hinder LES function

73
Q

someone can have a hiatal hernia without

A

GERD symptoms

74
Q

decreased clearance of stomach contents

A

acid spends too much time in contact with esophageal mucosa
issues with saliva production and decreased rates of swallowing -> decrease esophageal clearance

75
Q

complications of GERD

A

esophagitis
erosions/ulceration of the esophageal mucosa
strictures of the esophagus
Barrett’s esophagus
esophageal adenocarcinoma

76
Q

barretts esophagus

A

normal squamous epithelium in esophagus converts to columnar cell epithelium
can lead to cancetr

77
Q

treatments for GERD

A

antacids
lifestyle modifications
prescription PPI
alarm symptoms –> endoscopy, antireflux surgery

78
Q

peptic ulcer disease

A

areas of degeneration and necrosis of GI mucosa exposed to acid peptic secretions

79
Q

acute PUD

A

result of severe trauma
rapid onset
regular borders

80
Q

chronic PUD

A

affect stomach or duodenum
elevated borders with inflammation

81
Q

common causes of PUD

A

H. pylori infection
long term NSAID use

82
Q

does stress cause peptic ulcers?

A

NO!

83
Q

risk factors of PUD

A

chronic obstructive lung disease
chronic renal insufficiency
coronary heart disease
tobacco use
alcohol use

84
Q

H. pylori infection in PUD

A

gram negative bacillus
chronic –> cancer
flagella, urease, porins, adhesions, toxins are main problems that lead to infection

85
Q

Pancreatitis

A

Inflammation of the pancreas

86
Q

host factors that influence possibility of H. pylori infection

A

genetic susceptibility composition of microbiota
location/duration of exposure
nature/extent of inflammatory response

87
Q

Acute Pancreatitis

A

Severe pain in upper abdomen and elevation of pancreatic enzymes

88
Q

long term NSAID use in PUD

A

inhibit synthesis of prostaglandins which leads to mucosal injury
inhibit COX 1 and 2 genes

89
Q

Chronic Pancreatitis

A

Long-standing inflammation that leads to loss of exocrine and endocrine functions

90
Q

prostaglandins are essential for

A

maintaining mucosal integrity and repair

91
Q

treatments for PUD

A

PPIs
histamine type 2 receptor antagonists
antacids
bismuth subsalicylate
antibiotics
reduce/discontinue NSAID use

92
Q

What is the leading cause of GI disorders that require hospitilization?

A

Pancreatitis

93
Q

Which type of pancreatitis is reversible?

A

Acute is reversible
Chronic is irreversible

94
Q

mechanisms of diarrhea

A

secretory
altered intestinal transit
osmotic
inflammatory (exudative)

95
Q

What are the causes of acute pancreatitis?

A

Gallstone disease
Alcohol misuse

96
Q

Acute, gallstone mediated pancreatitis mechanism step 1

A

Gallstones block pancreatic duct causing back up of enzymes which increase pressure

97
Q

secretory diarrhea

A

change in active ion transport by either decreased sodium absorption or increased chloride secretion

98
Q

causes of secretory diarrhea

A

activation of cAMP
activation of cGMP
calcium dependent

99
Q

Acute, gallstone mediated pancreatitis mechanism step 2

A

Increased pressure compresses blood vessels and activates inactive zymogens

100
Q

in secretly diarrhea, bacterial toxins lead to

A

increased intracellular cAMP or Ca2+ in gut epithelial cells –> increased Cl- secretion via CFTR –> increased water secretion

101
Q

Acute, gallstone mediated pancreatitis mechanism step 3

A

Activation of enzymes destroy pancreatic tissue and leak into surrounding tissue

102
Q

altered intestinal transit diarrhea

A

increased intestinal motility causes a shorter transit time –> poor absorption of water and substances

103
Q

causes of altered intestinal transit diarrhea

A

increased intestinal motility
decreased intestinal motility
bacterial infection

104
Q

osmotic diarrhea

A

osmotically active, poorly absorbed substances in the lumen
inhibits normal electrolyte and water absorption
draws water into the lumen by osmosis

105
Q

Acute, alcohol mediated pancreatitis mechanisms (5)

A

Products of alcohol metabolism can:
1. Destabilize lysosomes
2. Increase digestive enzyme synthesis + suppress secretion
3. Induce inflammatory cytokine production
4. Increase cytoplasmic Ca2+
5. Damage mitochondria

106
Q

causes of osmotic diarrhea

A

malabsorption of water soluble nutrients
excessive intake of nonabsorbable solutes
excessive intake of carbonated beverages

107
Q

inflammatory (exudative) diarrhea

A

damage to intestinal epithelial cells causes a loss of absorptive area
leaky tight junctions
release of inflammatory mediators and products from immune cells

108
Q

causes of inflammatory diarrhea

A

celiac disease
toxigenic pathogen infection
intestinal inflammatory conditions

109
Q

treatments for acute diarrhea

A

hydration
medications that slow down bowel movement
antibiotics

110
Q

treatments for chronic diarrhea

A

antibiotics
probiotics
treatment for underlying condition

111
Q

constipation

A

difficult and infrequent bowel movements
3 or fewer times per week

112
Q

primary constipation

A

it is not a symptom
can be functional or chronic idiopathic

113
Q

functional constipation

A

younger children
no structural/anatomic cause, other factors contribute

114
Q

chronic idiopathic constipation

A

irregularity in dedication/difficulty passing stoll
no explination

115
Q

causes of constipation

A

GI disorders
metabolic/endocrine disorders
pregnancy
cardiac disorders
lifestyle factors
neurological
psychogenic causes
mediations

116
Q

Major takeaway of both types of acute pancreatitis

A

Activation of normally inactive enzymes lead to the pancreas digesting itself

117
Q

constipation common contributors

A

reduced colonic motility
delayed transit of stool
impaired rectal sensation
ineffective coordination of pelvic floor muscles

118
Q

constipation mechanism by effects of opioids (1)

A

decreased electrolyte and fluid secretion
(inhibition of Cl- secretion)

119
Q

constipation mechanism by effects of opioids (2)

A

stimulation of circular muscle contraction and longitudinal muscle relaxation
(increased sphincter resting tone; decreased peristalsis)

120
Q

Stages of Chronic Pancreatitis

A
  1. Preclinical inflammatory stage
  2. Acute attacks
  3. Abdominal pain
  4. Burnout stage
121
Q
  1. effects of muscle (opioids –> constipation)
A

inhibition of Act and NO at the myenteric neural plexus

122
Q

Chronic pancreatitis mechanism

A

Repeated acute inflammation and necrosis lead to scarring and fibrosis
Pain from increased pressure

123
Q

Treatments of acute pancreatitis

A

No alcohol
Smoking cessation
Change diet
Removal of gallbladder

124
Q

treatments for constipation

A

dietary modification
surgery
biofeedback
laxatives

125
Q

inflammatory bowel disease

A

chronic episodes of GI tract inflammation caused by an exaggerated immune response to normal stimulus

126
Q

types of IBD

A

crohns disease
ulcerative colitis

127
Q

crohns disease

A

non continuous inflammation in any portion of the GI tract
entire bowel wall

128
Q

ulcerative colitis

A

continuous inflammation of colonic mucousa (only top layer)

129
Q

Treatments of chronic pancreatitis

A

NSAIDs
Digestive enzyme/vitamins

130
Q

Chronic Liver Disease (CLD)

A

Progressive deterioration of liver functions for more than 6 months

131
Q

mechanisms of IBD

A

intestinal immune system reaction to microbial flora
continued deterioration leads to further exposure of microbes and food causing even more inflammation

132
Q

mechanism of ulcerative colitis

A

TH1 response to CD4 T cells activates macrophages and dendritic cells
pro inflammatory cytokine and IL-13 production

133
Q

mechanism of Crohn’s disease

A

overactivation of NF-kB –> macrophages, dendritic cells, T cells,
overproduction of inflammatory cytokines
mutations in NOD2 gene

134
Q

Clinical consequences of cirrhosis
(i have this extra highlighted ladies)

A

Increased intrahepatic resistance leads to
1. Portal hypertension
2. Varices
3. Ascites
4. Infection
5. Encephalopathy
6. Hepatocellular carcinoma

135
Q

treatments of IBD

A

reduce intestinal inflammation of the colon
inhibit leukocyte adhesion and migration
suppress bacterial growth
remove damaged intestine

136
Q

inflammatory bowel syndrome

A

abdominal pain or discomfort with altered bowel habits
diarrhea, constipation or both

137
Q

mechanisms for IBS

A

results from altered gut-brain axis nerve signaling
environmental contributors such as early life stressors
intake of specific types of food

138
Q

altered gut-brain axis nerve signaling leads to

A

motor dysfunction of the intestine to intestinal hypersensitivity

139
Q

abnormal contractions in muscle layers in IBS cause

A

irregular spasms in the colon
food is moved too quickly or too slowly

140
Q

emerging mechanisms of IBS

A

levels of 5-HT (serotonin) in the GI tract are increased after a meal in those diagnosed with diarrhea-predominant IBS

141
Q

treatments for IBS

A

managing stress
changes in diet and lifestyle
fiber supplements
laxatives
anti-diarrheal
anticholinergic drugs
SSRI antidepressants

142
Q

Stages of Liver Disease

A

Healthy –> Fatty –> Hepatic Fibrosis –> Cirrhosis –> Cancer

143
Q

Primary cause of cirrhosis and liver disease

A

Alcoholic liver disease (ALD)

144
Q

Causes of cirrhosis and liver disease

A
  1. ALD
  2. Non-alcoholic fatty lifer disease
  3. Chronic viral hepatitis
  4. Genetic causes
  5. Autoimmune conditions
145
Q

Genetic Causes of cirrhosis and liver disease

A

Alpha-1 trypsin deficiency
Hereditary hemochromatosis
Wilson disease

146
Q

Primary biliary cirrhosis (PBC)

A

Destruction of intrahepatic biliary channels

147
Q

Primary sclerosing cholangitis (PSC)

A

associated with UC
Decrease in size of bile ducts because of inflammation and scarring

148
Q

Autoimmune Hepatitis (AIH)

A

Chronic inflammatory hepatitis
Antibodies against nuclei and smooth muscle

Pathophysiology (15 decks)

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