gastro Flashcards
vomiting center (3)
medulla
- reticular formation
- tractus solitarius
vomiting center stimulated by
serotonin –> medulla
diarrhea: osmotic
malabsorption (too much water in lumen)
diarrhea: secretory
C. diff
- spores cause inflammation
- cells burst and die
diarrhea: motility
ex: irritable bowel syndrome
- overstimulated sympathetic
- accelerated peristalsis/intestinal movement
abdominal pain: parietal
along perineum (more specific to location of origin)
abdominal pain: visceral
actual organ (distention or inflammation)
abdominal pain: referred
examples:
urologic (calculi, bladder cancer)
cardiac (MI)
heartburn
dysphagia x2
mechanical (tumor, stricture)
functional (muscular or neuro problem, ex: myasthenia gravis)
achalsia
esophagus doesn’t relax, needs stent
common in elderly
hiatal hernia
bit of stomach fundus moves up through gap in diaphragm into thoracic cavity
surgical emergency when strangulation
GERD
reflux d/t decreased resting tone of lower esophageal sphincter
peptic ulcer: gastric
often antrum
- H. pylori, stress, critical illness
- histamine release = acid production increase = disrupted mucosa
peptic ulcer: duodenul
most common
d/t acid & pepsin penetrating mucosa
tx: H2 or PPI
upper GI bleed x3
+ sx + d/t
esophagus, stomach, duodenum
bright red blood, emesis, coffee ground stool
d/t esophageal varices + malory weiss tears, intractable vom
lower GI bleed
+ d/t
jejunum, ileum, colon, rectum
d/t inflammatory disease, hemorrhoids, diverticula
pyloric obstruction
“gastric outlet obstruction”
between stomach & duodenum
results in distention/discomfort and typically requires surgical repair
intestinal obstruction and ileus: herniation
prolapse/pouch through wall
intestinal obstruction and ileus: adhesions
common post-surgical - scarring or abnormal interaction of tissues (stuck to each other)
intestinal obstruction and ileus: volvulus
twisting
- can result in ischemia or death of chunk of tract = emergency
colectomy may result
intestinal obstruction and ileus: intussusception
telescoping
intestinal obstruction and ileus: intervention
SURGICAL!
gastritis: acute
destruction of mucosal barrier
- meds (NSAIDS!), chemicals, H. pylori
gastritis: chronic
chronic fundal gastritis = most severe
- t cell & autoantibodies involved = prolonged inflammatory response
common in geriatric
ulcerative colitis
- continuous lesions
- not transmural
- inflammation leads to cytokines = VERY WATERY DIARRHEA (less absorptive area, decreased transit time)
- most severe: rectum, sigmoid
- remission/flare
- can lead to toxic megacolon, perforation, abscess
crohn’s disease
- idiopathic
- ANYWHERE along tract (mouth - anus)
- skip lesions
- bloody or MUCOID stools (mucommon)
- weight loss (poor absorption, slower motility)
CHRISTMAS
crohn’s CHRISTMAS
c obblestones (radiology) h igh temp r educed lumen (inflamm) i ntest fistula (desperexit) s kip lesions t ransmural (all layers, can ulcerate) m alabsorption a bdominal pain s ubmucosal fibrosis
diverticular disease
colonic mucosa herniates through smooth muscle layers = outpouching
can be asymptomatic, inflammatory, or ruptred
flares common, 50s-60s common
mgmt: diet, bowel rest, abx, surgical (rupture = emergency)
appendicitis
inflamed appendix
common 20-30s
medical emergency
s/s: n/v fever, periumbilical pain radiating to RLQ
tx: abx, appendectomy
appendicitis pain
periumbilical radiating to RLQ
irritable bowel syndrome
w/ c or d or BOTH
dx of exclusion
tx: diet, anti-spasmodics, etc
no specific pathology:
- visceral hypersensitivity
- abnormal GI permeability, mobility, secretion
- post-infectious
- overgrown intestinal flora
- food/allergy intolerance
- psychosocial
obesity BMI
> 30 kg/m2
obesity: adipokines
secreted by adipocytes,
assist in regulation of intake, lipid metab/storage, insulin sensitivity
visceral fat leads to adipokine dysfunction
leads to adipokine dysfunction
visceral fat
brain bit related to obesity and what it does
arcuate nucleus (hypothalamus)
balances energy intake and metabolism
refeeding syndrome
severely malnourished pts must have nutrition restarted slowly with close monitoring
starvation causes lyte shift out of cell into plasma, aggressive nutrition = insulin causes glucose + ions to move back into cell = profoundly low serum lyte concentrations
- PO4, K, Mg, Ca
20kcal/kg/day with lyte monitoring
leading cause of acute liver failure in the US
acetaminophen
acute liver failure: complications
portal htn esophageal varices splenomegaly hepatopulmonary syndrome ascites hepatic encephalopathy jaundice hepatorenal syndrome
hep B
autoimmune or viral
- vertical or horizontal, sex, parenteral (IV), needle stick
damaged hepatocytes
hep C
contaminated needles
- less common: sex, vertical transmission
hep B damaged hepatocytes x3 mechanisms
- HLA Class I restricted cytotoxic T-cell response intended for HBV-infected hepatocytes
- cytopathic effect of Hep B viral protein antigen (HBcAg) expression in affected hepatocytes
- over expression, ineffective secretion HbsAg (compensatory mechanism)
C = core
S = surface
both r/t protein
hep C mechanism of damage
direct cellular toxicity d/t release of cytokines intended to kill virus
cirrhosis
irreversible damage to liver d/t inflammation and fibrosis
leading causes: EtOH abuse, hepatitis
fibrotic lesions (d/t Kuppfer cells) alter biliary/blood flow = jaundice, portal htn
kuppfer cells
part of reticular endothelial cells (system) - stellate macrophages in liver
in cirrhosis, can promote deposition of fibrotic products by releasing inflammatory mediators & growth factors
non-alcoholic fatty liver disease (NAFLD)
occurs in absence of alcohol
most commonly associated with obesity, HLD, metabolic syndrome, DM2
most common chronic liver disease (US)
may progress to NASH
non-alcoholic steatohepatitis (NASH)
can result from NAFLD
may progress to cirrhosis, ESLD, hepatocellular carcinoma
biliary cirrhosis: primary
t lymp & ab-mediated destruction of intrahepatic bile ducts
- often accompanies other autoimmune diseases
dx: 2/3 -
1. biochem evidence of disease (min 6 mo)
- antimitrochondrial antibody (AMA) positivity
- histologic features of liver biopsy
biliary cirrhosis: secondary
d/t partial or complete obstruction of common bile duct (or branches)
can be d/t gallstones, tumors, strictures, chronic pancreatitis
alcoholic cirrhosis
d/t toxic effects on liver metabolism, immunologic changes, oxidative stress and malnutrition
cholelithiasis
formation of gallstones
cholesterol or pigmented
cholelithiasis: risk factors
obesity rapid weight loss middle age female gender oral contraceptives
cholelithiasis: cholesterol
form in bile that is supersaturated with cholesterol, forming crystals
cholelithiasis: pigmented
black: hard, associated with hyperbilirubinemia
brown: soft often d/t bacterial infection of bile ducts
cholecystitis
usually caused by gallstone in cystic duct leading to obstruction (distends & inflames gallbladder)
acute pancreatitis x4
1) obstruction of bile or pancreatic duct, preventing outflow or pancreas digestive juices
2) alcohol abuse
3) drugs
4) viral infection
digestive enzymes activated in pancreas = autodigestion = inflammation
chronic pancreatitis
repeated occurences, may be d/t gallstones (** especially), autoimmune disease, gene mutations, smoking, chemical exposure, obesity
third most common cause of cancer death in US both men & women
colon cancer
hepatocellular carcinoma
closely related to cirrhosis
HCV, HBV, cirrhosis lead to this d/t cellular proliferation, effects of growth factor, cytokine, oxidative stress
MELD score for transplant
pancreatic cancer
most arise from exocrine cells (secretory cells provide enzymes for digestion) but can from endocrine (alpha, beta)
ductal adenocarcinomas most common
WHIPPLE PROCEDURE - temporizes, not curative (digestive capabilities still lacking, malnutrition, poor healing, underlying cancer)
whipple procedure
temporizing surgical procedure for pancreatic cancer
not curative bc digestive capabilities still lacking, malnutrition, poor healing, underlying cancer
four layers of GI tract
mucosa (mucus membrane)
submucosa
smooth muscle (circular then longitudinal)
serosa (serous membrane)
GI smooth muscle electrical activity:
waves + responsible + result
SLOW
- interstitial cells of Cajal (pacemaker) stim by parasymp vs symp
- not action potential, pulsation resting membrane potential
SPIKE
- Ca/Na channel (slow open = prolonged action potential)
- Ca = contraction
- true action potential
enteric nervous system + 2 plexes & function
GI-specific nervous system
myenteric (outer, between longitudinal & circular)
- fxn: movement
vs
submucosal (inner)
- fxn: secretion & blood flow
myenteric plexus aka
Auerbach’s plexus
submucosal plexus aka
Meissner’s plexus
ANS neuron neurotransmitters working in conjunction with enteric neurons x2
parasympathetic: ACh
(excites - take ACh-tion!!)
sympathetic: Norepineprhine
(inhibits - NO action!)
cranial nerve of mastication
V
deglutition
voluntary swallowing (ex: oropharyngeal bit of esophagus)
prevents backflow of food from stomach into esophagus
lower esophageal sphincter
why anticholinergics cause constipation
depress myenteric plexus
GI movements x2
propulsive (peristalsis)
- must have active myenteric plexus
mixing (segmentation)
- chopping, violent
stomach: 3 parts
fundus, body, antrum
stomach: absorption
very little
exceptions: NSAIDS, alcohol, aspirin
x2 hormones stimulate gastric motility & what mediates them
gastrin & motilin
- PS mediated vagal nerve
inhibits gastric motility & how
secretin
- symp nerve mediated
gastric secretion: gastric glands
along mucosa, primary secretory units
gastric secretion: parietal cells
secretes what & stimulated by
aka oxyntic
secretes: HCl, IF, gastroferrin
stim by ACh & gastrin & histamine
- ACh released by vagus nerve, stims g & h
gastric secretion: chief cells
secretes: pepsinogen
pepsinogen
secreted by gastric chief cells, inactive precursor to PEPSIN
- protein to peptide
responsible for GERD & esophageal degradation
gastric secretion: enterochromaffin cells secrete what
histamine
H2 blockers work here
gastric secretion: D cells secrete what
somatostatin
gastric secretion: somatostatin
stimulated by & result
stimulated by: acid
result: inhibits acid, pepsinogen release
strongest stimulation for pepsin secretion
ACh
gastric secretion: gastrin
stimulates gastric glands to secrete HCl, pepsinogen
growth of mucosa
promotes motility
gastric secretion phases x3
cephalic (sensory responses to food)
- mediated by vagus/myenteric plexus
gastric (food enters stomach = distension)
- mediated by vagus/enteric plexus
intestinal (chyme enters duodenum, GI motility slows)
duodenum ends at
ligament of Treitz
duodenal villi composed of x3
columnar epithelial
goblet cells
enterocytes
small intestine countercurrent exchange
arterial and venous flow in villi opposite directions, blood often goes from art to ven directly without being carried into tip of villi
short gut syndrome
after large resected gut chunk
- blood shunted
- disrupted countercurrent exchange
- poor absorption
crypts of Lieberkuhn
between villi of small intestine (duod) - goblet + enterocytes reside here
Paneth cells
built in immunity in small intestine
Paneth like Janeth T, ID MD
hepcidin
iron buffer preventing iron trafficking
fat digestion/absorption phases x4
- emulsification/lipolysis
- micelle formation
- fat absorption
- resynthesis of trigs & phospholipids
main types of lipids & function x3
triglyceride - energy
phospholipid - membrane structure
cholesterol - not a lipid but has lipophilic head or something / membrane structure
where chylomicron is synthesized & what it does
made in small intestine by enterocytes
with VLDL, delivers TAG to cells
enterocytes remind you of: x2
chylomicron makers
live in the Crypts of Lieberkuhn (between duodenal villi)
on chylomicron cell surface
Apoprotein B so they can be suspended and not stick to shit
TAG - what and what happens to it
energy rich molecule delivered by chylomicron/VLDL to cells
broken down by lipoprotein lipase into fatty acids and monoglycerides so they can diffuse into cell to be oxidized
how is adipose tissue mobilized to be used as energy?
hydrolysis turns triglyercides into fatty acids and glycerol
what happens to free fatty acids that leave fat cells
immediately bind with albumin
hydrolysis stimulated by
inadequate glucose (primary energy means)
hormones (endocrine glands)
where are lipoproteins made and what do they NOT do
made in liver
DON’T transport free fatty acids
liver role in storage of lipids
degrade fatty acids into smaller units for energy use
desaturates triglycerides lowering their melting point = they can stay liquid and are easy to transport
uses little of fatty acids made and turns remainder into acetoacetic acid to be sent to cells
how to turn triglycerides into ATP x6
- hydrolysis
- fatty acids & glycerol oxidized
- glycerol enters glycolytic pathway
- fatty acids degraded in mitochondria
- beta oxidation into Acetyl CoA
- Acetyl CoA enters Kreb’s
- what does beta oxidation do to fats? *
turns into acetyl CoA
the story of acetoacetic acid
it is siamese Acetyl CoA forme din the liver
they go to tissues, get broken back into 2 Acetyl CoA to enter Kreb’s
if there’s tons of acetoacetic acid (higher than normal) = ketosis
ketosis
acetoacetic acid levels are higher than normal
acetoacetic acid + not enough carbs
not enough carbs = not enough oxaloacetic acid = Krebs is hindered
acetoacetic acid steps in and makes ketons
lack of insulin or TH - what effect does it have on lipids?
increases plasma concentration of cholesterol
atherosclerosis vs arteriosclerosis
athero: fatty lesions on inner surface of arterial walls (macrophage oxidize lipoproteins = foam cells = fatty streak)
arterio: thick/stiff vessels
deamination
removes an amino group from protein
it is breakdown of proteins into smaller molecules for energy purposes
activated by aminotransferases
releases ammonia which is turned into urea in the liver and removed through urine
activate deamination
aminotransferases
urea cycle
deamination releases ammonia
liver turns ammonia into urea
5 enzymes involved
urea excreted in urine
how are deaminated amino acids mobilized for energy
KETO ACID turned into substance that can enter Kreb’s Cycle
the substance is used for energy the same way Acetyl CoA is
ketogenesis
conversion of amino acids into keto or fatty acids
blood supply to large intestine
superior and inferior mesenteric arteries
divides liver into 2 lobes
falciform ligament
liver blood supply
hepatic artery (branches from celiac, 25% CO)
portal vein (75% liver blood supply)
functional unit of liver
lobules aka acini (50-100k total)
central vein
branch of hepatic artery that goes through the middle of the liver
empties into IVC
venus sinusoids lined with 3 cell types
hepatic endothelial reticuloendothelial (Kupffer)
reticuloendothelial cells
aka Kupffer cells
macrophages of the liver
spaces of disse
permeable and allow fluids and proteins into parasinusoidal space - connect liver to lymphatic system
drainage & immunity
sphincter of Oddi
the gatekeeper of the gallbladder! decides when to let bile out
contracted during interdigestive period, causes bile to flow into gallbladder (thanks to increased pressure in common bile duct)
open during digestive period thanks to CCK
sphincter of Oddi stimulated by (and result)
cholecystokinin! stimulates gallbladder contraction + relaxation of sphincter of Oddi
what breaks down old RBCs (+ 2 things RBCs are broken into)
spleen or Kupffer cells in liver
+ globin = aa
+ heme = biliverdin
unconjugated vs conjugated bilirubin
un: lipid soluble
conj: water soluble & excreted as bile
liver stores which vitamin the most?
A!
liver stores iron as
ferritin
ampulla of Vater
common bile duct meets duodenum
acinar cells & what they secrete (specific) + function
secrete digestive enzymes in pancreas
tripsin, chylotripsin
+ carboxypepsidase, elastase
function:
- alkaline and help neutralize chyme
- hydrolyze protein, carbs, fats
