Gastrointestinal Disorders (Exam 2) Flashcards
diarrhea
passage of abnormally liquid or unformed stools at an increased frequency
causes of diarrhea
microbial infections
medications
food related
abrupt onset of chronic disease
functions of the GI system
assimilation of nutrients
excretion of waste products
endocrine, immune, barrier functions
control over multiple processes and organs is provided by
enteric nervous system
hormones
assimilation of nutrients includes
motility of food
secretion of fluid and enzymes for digestion
absorption of nutrients
transport of nutrients into circulatory system
layers of the GI from inside to outside
Mucosa
Submucosa
Muscularis externa
Serosa
mouth
chewing, mixing with saliva, bolus formation
stomach
1-4 hours transit time
mix, grind, dilute and dissolve food
exocrine secretions, gastric acid and intrinsic factor
level of absorption in the stomach
minor
gastric emptying
key control point for further delivery and indicating satiety
cells in the stomach
parietal cells
cheif cells
enteroendocrine cells
mucous neck cells
parietal cells
produce HCl and intrinsic factor
chief cells
produce pepsinogen
enteroendocrine cells
produce hormones
gastrin in stomach
peptide hormones in small intestine
mucous neck cells
produce thin, acidic mucus
small intestine
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
how much absorption occurs in the small intestine
90% (she works like a dog DAY AND NIGHT SIPPING FROM A POT NONE OF YOU WANT TO TOUCH!!!)
cells in small intestine
enterocytes
enteroendocrine cells
paneth cells
goblet cells
goblet cells
produce thick mucus
paneth cells
produce antimicrobial peptides
enterocytes
absorb water and nutrients
intestinal stem cells and migration of their progeny occurs from
crypt to villus
regenerates every 4-5 days
endocrine pancreas
regulating metabolism
produces and secretes hormones
what is secreted from endocrine pancreas and what do they do?
insulin - glucose uptake from blood
glucagon - breakdown glycogen to glucose
somatostatin - growth hormone inhibiting hormone; regulates endocrine system
exocrine pancreas
digesting food
produces and secretes enzymes
what is released from the exocrine pancreas?
proteases
lipase
amylase
enzymes are produced in the
inactive form (zymogen) and only activated when released
prevents self digestion of the pancreas
pancreas duct cells
produce and secrete bicarbonate
neutralize stomach acid
liver functions
prepares food for digestion in the SI
detoxifies blood from GI
regulates metabolism of biomolecules
produces plasma proteins
produces fats, lipids and cholesterol
gallbladder
stores and releases bile
large intestine
12-24 hrs transit time
water and electrolyte absorption
microflora process undigested food
storage of fecal waste
rectum and anus
elimination of fecal waste
1-3 days after meal ingestion
large intestines only have
crypts
NO VILLI!!!!
the small intestine has
both crypts and villi (because she does the hard work, needs more assistance)
what is the difference in cells in epithelium of the small and large intestines
large intestines do NOT have paneth cells
sphincters
help control over assimilation of nutrients
neural regulation
control over intestinal secretions and smooth muscle activity in intestinal wall and blood vessels
endocrine regulation
release of hormones into the bloodstream triggered by a meal
paracrine regulation
release of substances that alter nearby cells
neuronal signaling controls
digestion
fluid secretions and absorption
motility
blood flow
the enteric nervous system controls
every part of the GI tract
hormones in the GI coordinate
movement
secretions
digestion of food
absorption of nutrients
brain responses
peristalsis
propels contents orally to caudally
circular contraction behind contents
segmentation
forces the contents back and forth to mix
fluid and electrolyte balance
fluid ingested and secreted must equal fluid absorbed + fluid exerted
the ability to absorb 9.3 liters is due to the function of
several transport proteins
transport of Na across intestinal epithelium drives
simultaneous absorption of water into tissue by osmosis
transport of Cl across intestinal epithelium drives
simultaneous secretion of water into gut lumen by osmosis
mucosal immune system
recognizes pathogenic microbes, commensal microbes and foods
70% of immune system cells are in the GI tract
nausea
inclination to vomit or feeling in the throat alerting that vomiting is coming
vomiting
ejection/expulsion of gastric material through mouth, forcefully
regurgitation
gastric/esophageal contents rise to pharynx but no forceful ejection
symptoms of N&V
pallor, tachycardia, sweating
emetic
capable of inducing vomiting
Therapy induced causes of N&V include
antineoplastic agents (chemotherapy)
3 stages of emesis
- nausea
- retching
- vomiting
retching
labored movement of thoracic and abdominal muscles before vomiting
vomiting is coordinated
by the brainstem
vomiting requires
contractions of abdominal muscles, pyloric, antrum
raised gastric cardia
diminished lower esophageal sphincter pressure
esophageal dilation
mechanism of N&V
emetic compounds trigger vomiting by stimulating receptors in the 4 sensory centers of the vomiting center (nucleus of tracts solitarius)
4 sensory centers of vomiting center
cerebral cortex
vestibular system
GI tract and heart
CTZ
GERD
chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus
how much pyrosis frequency is required as criteria for GERD
2 times per week
if untreated, GERD can lead to
inflammation of the esophagus
or
erosion of the squamous epithelium of the esophagus
classifications of GERD
based on severity of erosions
based on presentation
baed on symptoms
Non erosive reflux disease vs Barrett esophagus
severity
NERD: most common, erosive
BE: most severe, least common
causes of GERD
motor abnormalities
impairment in the tone of the lower esophageal sphincter
transient LES relaxation
delayed gastric emptying
risk factors of GERD
obesity
alcohol abuse
smoking
excessive caffeine intake
respiratory diseases
mechanisms of Gerd
-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
decrease in LES pressure (GERD)
frequent transient LES relaxations not triggered by swallowing may occur, allowing reflux
can be atonic, permitting free reflux
stress reflux from bending over
hiatal hernia
protrusion of the stomach through the diaphragm into the chest
hiatal hernia role in GERD
-disrupts normal anatomic barrier between the stomach and esophagus
-allows stomach content to reflux into the esophagus
-hinder LES function
someone can have a hiatal hernia without
GERD symptoms
decreased clearance of stomach contents
acid spends too much time in contact with esophageal mucosa
issues with saliva production and decreased rates of swallowing -> decrease esophageal clearance
complications of GERD
esophagitis
erosions/ulceration of the esophageal mucosa
strictures of the esophagus
Barrett’s esophagus
esophageal adenocarcinoma
barretts esophagus
normal squamous epithelium in esophagus converts to columnar cell epithelium
can lead to cancetr
treatments for GERD
antacids
lifestyle modifications
prescription PPI
alarm symptoms –> endoscopy, antireflux surgery
peptic ulcer disease
areas of degeneration and necrosis of GI mucosa exposed to acid peptic secretions
acute PUD
result of severe trauma
rapid onset
regular borders
chronic PUD
affect stomach or duodenum
elevated borders with inflammation
common causes of PUD
H. pylori infection
long term NSAID use
does stress cause peptic ulcers?
NO!
risk factors of PUD
chronic obstructive lung disease
chronic renal insufficiency
coronary heart disease
tobacco use
alcohol use
H. pylori infection in PUD
gram negative bacillus
chronic –> cancer
flagella, urease, porins, adhesions, toxins are main problems that lead to infection
Pancreatitis
Inflammation of the pancreas
host factors that influence possibility of H. pylori infection
genetic susceptibility composition of microbiota
location/duration of exposure
nature/extent of inflammatory response
Acute Pancreatitis
Severe pain in upper abdomen and elevation of pancreatic enzymes
long term NSAID use in PUD
inhibit synthesis of prostaglandins which leads to mucosal injury
inhibit COX 1 and 2 genes
Chronic Pancreatitis
Long-standing inflammation that leads to loss of exocrine and endocrine functions
prostaglandins are essential for
maintaining mucosal integrity and repair
treatments for PUD
PPIs
histamine type 2 receptor antagonists
antacids
bismuth subsalicylate
antibiotics
reduce/discontinue NSAID use
What is the leading cause of GI disorders that require hospitilization?
Pancreatitis
Which type of pancreatitis is reversible?
Acute is reversible
Chronic is irreversible
mechanisms of diarrhea
secretory
altered intestinal transit
osmotic
inflammatory (exudative)
What are the causes of acute pancreatitis?
Gallstone disease
Alcohol misuse
Acute, gallstone mediated pancreatitis mechanism step 1
Gallstones block pancreatic duct causing back up of enzymes which increase pressure
secretory diarrhea
change in active ion transport by either decreased sodium absorption or increased chloride secretion
causes of secretory diarrhea
activation of cAMP
activation of cGMP
calcium dependent
Acute, gallstone mediated pancreatitis mechanism step 2
Increased pressure compresses blood vessels and activates inactive zymogens
in secretly diarrhea, bacterial toxins lead to
increased intracellular cAMP or Ca2+ in gut epithelial cells –> increased Cl- secretion via CFTR –> increased water secretion
Acute, gallstone mediated pancreatitis mechanism step 3
Activation of enzymes destroy pancreatic tissue and leak into surrounding tissue
altered intestinal transit diarrhea
increased intestinal motility causes a shorter transit time –> poor absorption of water and substances
causes of altered intestinal transit diarrhea
increased intestinal motility
decreased intestinal motility
bacterial infection
osmotic diarrhea
osmotically active, poorly absorbed substances in the lumen
inhibits normal electrolyte and water absorption
draws water into the lumen by osmosis
Acute, alcohol mediated pancreatitis mechanisms (5)
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
causes of osmotic diarrhea
malabsorption of water soluble nutrients
excessive intake of nonabsorbable solutes
excessive intake of carbonated beverages
inflammatory (exudative) diarrhea
damage to intestinal epithelial cells causes a loss of absorptive area
leaky tight junctions
release of inflammatory mediators and products from immune cells
causes of inflammatory diarrhea
celiac disease
toxigenic pathogen infection
intestinal inflammatory conditions
treatments for acute diarrhea
hydration
medications that slow down bowel movement
antibiotics
treatments for chronic diarrhea
antibiotics
probiotics
treatment for underlying condition
constipation
difficult and infrequent bowel movements
3 or fewer times per week
primary constipation
it is not a symptom
can be functional or chronic idiopathic
functional constipation
younger children
no structural/anatomic cause, other factors contribute
chronic idiopathic constipation
irregularity in dedication/difficulty passing stoll
no explination
causes of constipation
GI disorders
metabolic/endocrine disorders
pregnancy
cardiac disorders
lifestyle factors
neurological
psychogenic causes
mediations
Major takeaway of both types of acute pancreatitis
Activation of normally inactive enzymes lead to the pancreas digesting itself
constipation common contributors
reduced colonic motility
delayed transit of stool
impaired rectal sensation
ineffective coordination of pelvic floor muscles
constipation mechanism by effects of opioids (1)
decreased electrolyte and fluid secretion
(inhibition of Cl- secretion)
constipation mechanism by effects of opioids (2)
stimulation of circular muscle contraction and longitudinal muscle relaxation
(increased sphincter resting tone; decreased peristalsis)
Stages of Chronic Pancreatitis
- Preclinical inflammatory stage
- Acute attacks
- Abdominal pain
- Burnout stage
- effects of muscle (opioids –> constipation)
inhibition of Act and NO at the myenteric neural plexus
Chronic pancreatitis mechanism
Repeated acute inflammation and necrosis lead to scarring and fibrosis
Pain from increased pressure
Treatments of acute pancreatitis
No alcohol
Smoking cessation
Change diet
Removal of gallbladder
treatments for constipation
dietary modification
surgery
biofeedback
laxatives
inflammatory bowel disease
chronic episodes of GI tract inflammation caused by an exaggerated immune response to normal stimulus
types of IBD
crohns disease
ulcerative colitis
crohns disease
non continuous inflammation in any portion of the GI tract
entire bowel wall
ulcerative colitis
continuous inflammation of colonic mucousa (only top layer)
Treatments of chronic pancreatitis
NSAIDs
Digestive enzyme/vitamins
Chronic Liver Disease (CLD)
Progressive deterioration of liver functions for more than 6 months
mechanisms of IBD
intestinal immune system reaction to microbial flora
continued deterioration leads to further exposure of microbes and food causing even more inflammation
mechanism of ulcerative colitis
TH1 response to CD4 T cells activates macrophages and dendritic cells
pro inflammatory cytokine and IL-13 production
mechanism of Crohn’s disease
overactivation of NF-kB –> macrophages, dendritic cells, T cells,
overproduction of inflammatory cytokines
mutations in NOD2 gene
Clinical consequences of cirrhosis
(i have this extra highlighted ladies)
Increased intrahepatic resistance leads to
1. Portal hypertension
2. Varices
3. Ascites
4. Infection
5. Encephalopathy
6. Hepatocellular carcinoma
treatments of IBD
reduce intestinal inflammation of the colon
inhibit leukocyte adhesion and migration
suppress bacterial growth
remove damaged intestine
inflammatory bowel syndrome
abdominal pain or discomfort with altered bowel habits
diarrhea, constipation or both
mechanisms for IBS
results from altered gut-brain axis nerve signaling
environmental contributors such as early life stressors
intake of specific types of food
altered gut-brain axis nerve signaling leads to
motor dysfunction of the intestine to intestinal hypersensitivity
abnormal contractions in muscle layers in IBS cause
irregular spasms in the colon
food is moved too quickly or too slowly
emerging mechanisms of IBS
levels of 5-HT (serotonin) in the GI tract are increased after a meal in those diagnosed with diarrhea-predominant IBS
treatments for IBS
managing stress
changes in diet and lifestyle
fiber supplements
laxatives
anti-diarrheal
anticholinergic drugs
SSRI antidepressants
Stages of Liver Disease
Healthy –> Fatty –> Hepatic Fibrosis –> Cirrhosis –> Cancer
Primary cause of cirrhosis and liver disease
Alcoholic liver disease (ALD)
Causes of cirrhosis and liver disease
- ALD
- Non-alcoholic fatty lifer disease
- Chronic viral hepatitis
- Genetic causes
- Autoimmune conditions
Genetic Causes of cirrhosis and liver disease
Alpha-1 trypsin deficiency
Hereditary hemochromatosis
Wilson disease
Primary biliary cirrhosis (PBC)
Destruction of intrahepatic biliary channels
Primary sclerosing cholangitis (PSC)
associated with UC
Decrease in size of bile ducts because of inflammation and scarring
Autoimmune Hepatitis (AIH)
Chronic inflammatory hepatitis
Antibodies against nuclei and smooth muscle
