GI Flashcards
what is in the upper gi tract?
mouth, esophagus, stoamch
What are the four functions of the gi system?
ingestion, digestion, absorption, elimination
what is in the middle gi tract
small intestine
what is amylase
helps breakdown larger polysaccharides into smaller sugars and dextrins
secreted by the parotid gland
what is in the lower gi tract?
caecum, colon, rectum
peritoneum
one continuous thin membrane that lines the abdominal cavity
supports abdominal organs
highly vascularized
lots of lymphatics
parietal peritoneum
outer layer attached to abdominal wall
peritoneal cavity
serous
sterile
comes into contact with lymphatics and blood
visceral peritoneum
inner layer wrapped around organs
cells secrete fluid to help keep organs slide freely past one another
esophagus
posteriort o trachea
propel food into stomach
only part of upper gi tract where no enzymes are secreted
upper esophageal shpincter
prevent air from entering the esophagus
aspiration of gastic contents back into the mouth
lower esophageal sphincter
controls passage of food into stomach
prevents reflux of gastric contents
your patients medical history included GERD. What is the pathophysiological abnormality?
lower esophageal sphincter incompetence
risk of upper gi bleed
cancer of essophagus
ulcers
Serosa
part of the visceral peritoneum
secretes serous fluid
muscularis
longitudinal and circular
stomach additional layer
muscle layer that helps mix chyme and propel it forward
what are the four layers of the stomach from outer to inner
serosa
muscularis
submucosa
mucosa
submucosa
blood vessels
lymphatics
when erosion through the mucosa can lead to bleeds here
mucosa
tight epithelial junctions
barrier to bacteria and other molecules
layer right against food and gastric contents
when tight junctions loosen, there is erosion which can lead to ulcers
secrete mucous to help protect the wall from the acidity of the gi contents
ruggae
coarse folds that expand and contract to help digest foods without increasing pressure
secretes acid
what are the functions of the stomach
temporary storage and mixing of chyme regulated emptying of gastric contents hematostatin inhibits the release of gastrin secretes substances for digestion releases gastrin and somatostatin
gastric secretions
hydrochlorioc acid pepsin (helps break down protein) mucous (with bicarb to neutralize acid) intrinsic factor (for b12 absorption) gastrin(promotes growth gastric mucousa)
parts of the small intestine
duodenum (extends to ligament of treitz)
jejunum
ileum
primary function of small bowel
nutrient absorption
talk about how small intestine digests carbs, proteins, fats, vitamins, minerals and water
proteases from pancrease to break down proteins
carbs get further broken dow
bile helps break down fats (produced in liver, stored in gallbladder)
water soluble vitamins and minerals and water passively reabsorb
microvilli
mucosa and submucosa covered by a series of projectile like folds
drastically increases the absorptive digestive surface
which other organs facilitate absoprtion and digestion
pancrease
liver
gallbladder
peistalsis
contraction above with distal relaxation
sequential contraction
segmentation
rhythmic contraction to help propel food bolus forward
What are the two modes of gi motility
peristalsis
segmentation
hepatic flexure
ascending colon to transverse colon bend
splenic flexure
transverse colon to descending colon bend
primary function of large intestine
water reabsorption primary
but also lytes, glucose, urea
movement of fecal mass
elimination of fecal mass
liver
largest solid internal organ glissons capsule - connective tissue surrounds liver, contains blood vessels and lymphatics right lobe larger than left under diaphragm primary cell hepatocyte functional unit lobule in health, you cannot palpate the liver
liver lobule
surrounds a central vein
sinusoids - liver specific capillaries
kupfer cells - line sinusoids, macrophages to phagocytosis bacteria or toxins passing through capillaries
discuss blood flow of the liver
hepatic artery supplies one third of the blood to the liver. oxygenated
portal vein comes from the gi tract, is venous, but very nutrient rich, branches into sinusoids to transport blood to each lobule
capillaries drain into hepatic vein which then drains into the inferior vena cava
liver receives one third of CO
liver can cope with times of decreased perfusion because of multiple sources of blood supply
major functions of the liver
metabolizes and store essential elements - carbs, fat, proteins, fat soluble vitamins and minerals (a, e, d, k, b12, iron, copper)
bile synthesis and secretion
glucose metabolism, stores glucose in the form of glycogen
biotransformation of breakdown and detoxification of drugs
synthesize plasma proteins - albumin which has important roles for drug binding, and helps to maintain oncotic pressures
synthesize clotting factors
What is glucneogenesis?
creation of new glucose from non carbohydrate sources
What is glycogenolysis?
breakdown of glycogen into glucose
occurs during fight or flight response
bile
continuously formed in the lived
excreted into hepatic duct
transported to gall bladder via cystic duct
functions to emulsify fat, absorb fat soluble vitamins
bilirubin
primary bile pigment
conjugated (direct), unconjugated (indirect)
formed by the degradation of the heme portion of your hemoglobin, breakdown happens mostly by the kupffer cells in the liver although a small amount is broken down in the spleen and the liver
can help distinguish types of disease
before bilirubin can be secreted in bile, the liver must process it (conjugation)
what would high levels of conjugated or unconjugated bilirubin suggest?
high levels of unconjugated- hepatocellular dysfunction
high levels of conjugated - biliary tract obstruction, something post liver
gallbladder
pear shaped organ underside of liver collects concentrates bile up to 15-29x by removing water helps absorb fat
pancreas
endocrine and exocrine tissue
main divisions- head, body, tail
pancreatic duct - alcinar cells to secrete digestive enzymes
sphincter of oddi opens and closes bile duct to go into the duodenum
exocrine functions of the pancreas
produces secretions that pass through a duct before entering blood
acinar cells exocrine excretory units secrete pancreatic juice
enteric nervous system
GI tract has a nervous system all its own
functions for gi motility
two major plexuses - myenteric outer plexus, submucosal, inner plexus
myenteric nervous system
controls of motor activity of the gi tract
submucosal nervous system
controls gi secretion and local blood flow within each minute segment of gut
gi blood flow facts
receives about 25% of CO
when circulation is impaired it can compromise for short period of time because it doesn’t take a lot of oxygen
very minimal collateral circulation, so ischemia a huge risk
what are the general components of a gi assessment?
reason for admit history of gi disease medications that are harmful to gi tract malnourished? overweight? nausea vomiting distended abdomen hemodynamic stability diarrhea good oral cavity assessment
importance of mouthcare
saliva production reduced in icu patients
- change in gram negative to gram positive flora, increased protease levels (decrease in protective coating which acts as host defence mechanism), increased bacterial load, oropharyngeal suctioning important
thrush puts them at increased VAP risk
Why do we assess the abdomen from least invasive to most invasive?
because palpation could stir up false bowel sounds
components of abdominal inspection
contour symmetry colour scarring bruising ?intra peritoneal hemorrhage
What are some common gi lab work tests?
cbc electrolytes - malabsorption coagulation profile- liver dysfunction lactate stool specs
what is lactate and why is it important?
end product of anerobic metabolism hypoperfused or ischemic bowel liver failure pancreatitis gi perfusion often compromised in a shock state upper limit for lactate is 2.2
what are some common diagnostics?
abdominal xray - gas patterns, foreign bodies, bowel obstuction, perfs
abdominal ultrasound - biliary, liver, gallstones, hepatic, abscessed and hematomas
CT scan - useful in identifying pancreatic pseudocysts, abcessed, biliary obstuction, gi neoplasms, can be challenging for icu pts because they often want oral contrast
MRI - more information about smaller or vascular abnormalities, because they are more lengthly they aren’t common for icu pts
Angiography - highly invasive, nephrotoxicity, good for identifying mesenteric ischemic bowel, or active gi bleeds, but not suitable for unstable patients but they are the ones that need it
endoscopy
What is the rationale for lateral abdominal xray?
usually left side lying
looking for free air floating in the abdominal cavity verses free air in the stomach or intestines
if shows free air it is a medical emergency and pt needs emergent surgery
functions of the liver
metabolism of fat, protein, carbs, hormones, drugs
synthesis of plasma proteins, cholesterol, lipids, glucose, clotting factors
storage of fat soluble vitamins, minerals, glycogen
production bile salts
excretion of bacteria, degrated rbcs, bilirubin
key facts of acute liver failure
impaired hepatic function with coagulopathy and enecephalopathy in less than 3 months time
multiple complications
mortality rates 30% due to multiendorgan disfunction
what are some primary causes of acute liver failure
tylenol od
ischemia
idiopathic
what is the end result of acute liver failure
injury to hepatocytes causing cell damage or cell death
loss of kuppfer cell function that results in increased risk of infection
how does dysfunction of the liver affect the body?
disruption of:
coagulation
serum osmolality - seen as ascities, edema
acid/base imbalance - liver converts lactate into bicarb, so there could be a metabolic acidosis due to liver dysfunction
detoxifiaction of waste products including drugs and ammonia
decrased glucose regulation
portal hypertension - 2/3 of liver blood flow supplied by portal vein
how does bloodwork indicate liver disease?
ALP - increased with liver disease and bile duct obstruction
AST - specific to liver, increases with disease
LDH- found in all body tissues, released due to damage
CBC- elevated white count due to inflammation or infection
PTT INR- elevated
reduction in serum proteins
elevated creatinine - usually in end stage liver failure with a resulting kidney failure (hepatorenal syndrome - thought to be caused by increased portal htn, increased abd pressure, leading to decreased renal perfusion)
elevated albumin
Which diagnostic tests are used for the liver?
ultrasound ct mri ercp - scope to sphincter of oddi to look for biliary blockages, hepatic angiography liver biopsy
what are some common signs and symptoms of acute liver failure?
RUQ pain and tenderness nausea and vomiting edema confusion ascities irritability depression altered loc due to increased ammonia levels
what are the common treatments for acute liver failure
primarily supportive: airway protection, fluid resusitation and vasopressor support, treatment of coagulopathies (won’t correct unless actively bleeding or requiring an intervention), monitor and treat electrolyte changes, cautious pain control
curative: transplantation
What are some complications of acute liver failure?
encephalopathy due to rising ammonia levels
sepsis
cerebral edema due to change in oncotic pressure
hypoglycemia
gi bleed - esophageal varices due to portal htn
acute renal failure
coagulopathies
Describe management of encephalopathy
lowering ammonia levels
restrict dietary protein
12-47normal
cautious blood products (because they contain ammonia)
avoid hypokalemia
try to avoid acidosis but this is very difficult because they are no longer metabolizing lactate into bicarb
lactulose and metronidazole lowers ammonia levels
lactulose draws ammonia into the colon and facilitates excretion in the feces. preferred medication. holding lactulose not indicated when treating hepatic induced encephalopathy
metronidazole works in a similar way, but is metabolized by the liver so can easily accumulate toxic levels
What are some hepatotoxins?
ETOH, medications, acetaminophen, certain antibiotics, NSAIDS, MAOIS, viruses including hepatitis, pesticide exposure, poisonous foods such as mushrooms
important facts of acetaminophen overdose
two pathways (sulphation and gluconidation) for metabolism pathway, but saturate with od, harmful pathway (NAPQ1) picks up leading to hepatic cellular death and liver necrosis can manage 7-10g/ day
how is acetaminophen overdose treated?
acetylcystine increases abilites of positive liver pathways by increasing hepatic glutathione stores and decreases changes of using the harmful metabolite pathway
activated charcoal - bind to any tylenol that hasn’t been metabolized yet
liver transplant
supportive care
What are the phases of acetaminophen overdose?
1- 0-24 hours, asymptomatic, nausea, vomiting, malaise, ast and alt increase sharply
2- 18-72 hours, RUQ pain and tenderness, anorexia, nausea, vomiting, tachycardia and hypotension, shock, AST and ALT peak, full extentof damage has been done
3- 72-96hours, nausea and vomiting, tender hepatic edge, jaundice, coagulopathy, hypoglycemia, fluid and vasopressor support for shock state, high rish for multiorgan failure and death, hepatic encepthaolpathy, only cure is transplantation
4- 4 days to 3 weeks, if they survive with at least 25% function the liver will start to slowly regenerate to functioning level, but not normal healthy level, high risk of mortality because of infection risk
Describe pathoiphysiology of hypotensive acute liver failure.
prolonged hypotension
imbalance between hepatic oxygen supply and demand
diffuse hepatic injury
high risk patients have pre-existing liver disease, portal htn, passive congestion due to low cardiac output that causes backing up from the right side of the heart into the inferior
Describe the treatment of hypotensive acute liver failure
supportive
restore circulation
restore cardiac output
reversing underlying cause of hemodynamic instability
monitor closely for end organ hypoperfusion (decreased renal function)
What are the endocrine functions?
insulin, glucagon, somatostatin
What are the exocrine pancreatic secretions?
secretes digestive enzymes
discuss alcohol induced pancreatitis
common after 1-3 days binging
sphincter of oddi spasm
may obstruct flow of pancreatic secretions
damage to acinar cells
Discuss gallstone induced pancreatitis
impaired drainage of pancreatic secretions
increased intraductal pressure
extravasion of pancreatic juices
3-7% develop pancreatitis
What are some other classifications of acute pancreatitis?
postpartum pancreatitis,
necrotizing pancreatitis usually associated with intra-abdominal infections and pancreatic necrosis
idiopathic pancreatitis can be caused by ercp or elevated triglycerides
Stages of pancreatitis
1 premature activation of enzymes (trypsin-proteins, amylase-carbs, lipase-fats)
2 intrapancreatic inflammation - enzymes autodigest pancreas and peripancreatic tissues
3 systematic inflammation injury which could lead to ards
acute pancreatitis signs and symptoms
no correlation between severity of injury and intensity of symptoms signs and symptoms of shock cullens sign - bleeding at the umbilicus grey-turners sign - flank bleeding elevated lipase
how does lipase reflect pancreatitis
enzyme only found in the pancrease
starts increasing 4-8 hours after onset
peak 24 hours
levels decrease within 8-14 days
how does amylase relate to pancreatitis
rises 6-12 hours
peaks 12-72 hours
elevated 3-5 days
will show improvement before lipase levels
blood work abnormalities in acute pancreatitis
low hgb
elevated wbc showing infection
hyperglycemia due to islets of langerhans injury
elevated triglycerides
gallstone induced will have increased direct bilirubin
acute pancreatitis diagnostics
repeat in 72 hours to look for improvement
abdominal ultrasound
abdominal ct with contrast
mri
what consideration must you keep in mind when administering opiates for acute pancreatitis
opiates increases sphincter of oddi peristalsis and biliary pressure
what is the best method of nutrition for pts with acute pancreatitis
nj feeds
What is ercp?
endocopic retrograde cholangiopancrestography
small scope into sphincter oddi to look at state, extract stones, place stents
causes irritation to the sphincter and thus mild pancreatitis
pancreatitis complications
abcess, result from localized infection
pancreatic necrosis occurs from severe autodigestion without infection
psuedocysts, collections of encapsulated enzymes, necrotic tissue. when they burst can cause widespread digestion and hemorrhage
multiorgan failure
When is surgery indicated in acute pancreatitis?
percutaneous drainage of abcess collections
documented infected pseudocysts
removal of dead or damaged part of the pancreas for infection control
Discuss gallstone induced pancreatitis
impaired drainage of pancreatic secretions
increased intraductal pressure which causes injury to acinar cells
extravasion of pancreatic juice into tissues
emesis causes
serotonoin receptors dopamine receptor muscarinic receptors stimulation of the vomiting centre, higher centre (in response to drugs, anticipation, fear, memory) and lower vomiting sensory ( sight, smell, pain, motion sickness ) vestibular apparatus
Describe specific drugs responsible for antiemetics
anti emetics are more effective at preventing than suppressing serotonin- ondansetron dopamine blockers - metoclopramide histamine blockers - gravol, muscarinic - scopolamine
zofran and ctz serotonin receptors
sci patient and the bowel routine
unable to sense if they are constipated or having abdominal pain
skin breakdown
autonomic dysreflexia
requires daily bowel routine
manual disimpaction in consultation with the physician
why are stress ulcers important in icu?
at increased risk
can lead to gi bleed and mortality rate associated with bleeds due to stress ulcers is very high 48-87%
what are predisposing factors to stress ulcers?
resp failure coagulopathy hypotension sepsis hepatic/renal failure correlation between severity of illness and incidence of ulceration gi ischemia due to loosening of the tight junctions loss of defence factors loss of ability to product mucous
What are some pharmacological preventions for stress ulcers?
histamine receptor agonist - ranitidine, famotidine, inhibits the production of stomach acid, blocks production of histamine on the parietal cells of the stomach.
proton pump inhibitors - pantoprazole, lanzoprazole, reduces amount of acid produced in the stomach
usually in conjunction with enteral feeds. Early enteral feeding is the mainstay of prophylactic treatment
What is meant by the acute abdomen?
sudden, severe abdominal pain, tenderness, distension indicative of intra abdominal disease process of unknown etiology,
can be paralytic ileus, mesenteric ischemia, bowel obstruction, bowel perforation
what are the diagnostic challenges of the acute abdomen?
intubation,
altered mental state
opioid analgesia
previous antibiotic therapy
corticosteriod use decreases inflammatory response
delays in surgical evaluation and intervention are critical contributors to mortality rate in patients who develop acute abdomen complications
pathophysiology of the paralytic ileus
the peristaltic movement of the intestine is lost even though there is no evidence of obstruction
this lack of coordinated propulsive movement leads to the accumulation of both fluid and gas in the bowel
why is a paralytic ileus important?
Prohibits enteral feeding
promotes bacterial overgrowth and translocation
promotes endotoxin absorption
an untreated ileus may ultimately lead to distension of the colon, increasing the risk of colonic wall ischemia and perforation
What are some causes of paralytic ileus?
intra abdominal surgery
opiods
general anethetics
Describe the recovery time of the gi tract following abdominal surgery
small intestine 3-5 hours, stomach 24 hours, large intestine 72 hours
What is the critical care management of the paralytic ileus?
determine and try to treat cause, OG/NG IV fluids electrolytes bower rest supportivec are
pathophysiology of ischemic bowel
loss of blood flow to intestine
can lead to infarction and bowel necrosis
increased lactate - release of cellular contents from cell death, by product of anerobic metabolism
ischemic bowel loses proteins, electrolytes, and fluid into the bowel lumen and wall leading to third spacing and decreased intravascular volume
gradual occlusion allows for the development of collateral circulation, abrupt does not
vascular occlusion of the messenteric vessels is rare by catastrophic resulting in profound illness
pathophysiology of mesenteric ischemia
usually arterial
can be caused arterial embolis, arterial thrombosis, or non-occlusive from prolonged vasoconstriction
mortality high
describe critical care management of mesenteric ischemia
supportive care fluid resucitation antibiotics vasopressor surgical intervention as needed to reverse the cause pain management
large bowel obstruction pathophysiology
mechanical or functional obstruction of the large intestine
obstruction may be due to causes within the bowel lumen, within the wall of the bowel, or external to the bowel (compression, entrapment, or volvulus)
what are some causes of large bowel obstruction
neoplasms
hernias
inflammatory bowel disease
fecal impaction
large bowel perforation pathophysiology
complete penetration of the wall of the large bowel resulting in intestinal contents flowing into the abdominal cavity
results in potential for bacterial contamination of the abdominal cavity
as you go further away from the stomach, which is virtually sterile, bacterial numbers increase, so a large bowel perforation is particularly at risk for developing sepsis
causes of large bowel perforation
constipation
obstruction
ischemia
trauma
what are the diagnostics for large bowel perforation?
elevated wbc neutrophillia elevated lactate abg metabolic acidosis abd xray looking for free air ct abdomen- fluid collection, air and abscess formation laparotomy
management of large bowel perforation
bowel resection peritoneal lavage airway and hemodynamic supportive care abx pain control
pathophysiology of intra abd hypertension
high pressure within the abdominal cavity resulting from expansion or swelling of the intra-abdominal contents beyond the capacity of the abdominal cavity
IAH=IAP >12
chronic iah can be seen in morbidly obese, pregnant, and ascites patients. increased mortality with rapid changes
pathophysiology of abdominal compartment syndrome
elevated intraabdominal pressure may progress to abdominal compartment syndrome resulting in decreased blood flow to organs in the abdominal cavity and adversely affecting the functioning of multiple organs
ACP = >20
what are the acs systemic effects?
cns- elevated iap increases icp and reduces venous drainage from head
cvs- decreased venous return which leads to decreased intra-thoracic pressure
renal- decreased CO and compression of kidney cause oliguria andan uria
resp- elevated diaphragm increasing intra thoracic pressure, leads to decreased functional capactiry ,a telectasis, hypoxia, and hypercapnea
gi- decreased perfusion causes bowel ischemia, acidosis, bacterial translocation and sepsis. Decreased liver perfusion leads to hepatic impairment
What are some risk factors for abdominal compartment syndrome in the icu?
anything that decreases wall compliance- ards, surgery, trauma
increased intraluminal contents- gastroparesis, ileus, obstruction
increased abdominal contents- hemoperitoneum, pneumoperitoneum, ascites, liver failure
capillary leaks/fluid resuscitation- acidosis, hypotension, coagulopathy, massive fluid resuscitation, septics hock, pancreatitis
What is the IAH grading system?
grade 1 IAP 12-15
grade 2 IAP 16-20
grade 3 IAP 21-25
grade 4 IAP >25
What are some management options for IAH/ACS
surgical abdominal decompression OG/NG decompression prokinetic agents reduce or stop enteral feeds enemas optimize fluid administraion optimize systemic perfusion
Where is the anatomical division of upper and lower gi bleed?
ligament of trietz right below duodenum
hematemesis
upper gi bleed
bright red emesis
coffee ground meaning digested blood
melena
black tarry stools often related to upper gi bleeds but can be seen in upper lower bleeds
hematochezia
rectal bleed
pathophysiology of peptic ulcer disease
imbalance between the aggressive factors and the defensive mechanisms
patient presentation of peptic ulcer disease
hx of NASAID, ETHO, smoking’ previous treatment from h pylori/peptic ulcer disease
hematemesis- bright red or coffeeground
melena
pathophysiology of esophageal varices
engorged and distended blood vessels of the distal portion of thee sophagus that develop as a result of portal hypertension
varices vulnerable to damage from gastric secretions leads to rupture, leads to massive hemorrhage
What are some causes of portal hypertension?
pre-hepatic: thrombosis of portal vein
most common intra-hepatic: cirrhosis of liver
post-hepatic: inferior vena cava obstruction
l
long term portal hypertension leads to what?
varices
splenomegaly
ascited
hepatic encephalopathy
pathophysiology of the ruptured diverticulum
most common cause of gi bleed
outpocketings of the colonic mucosa and submucosa through weaknesses of muscle layers in the colon wall
submucosal layer contain blood vessels which if exposed lead to lowe gi bleed
diagnostics of gi bleed
cbc
coagualtion studies
urgent endoscopy- locating and cauterizing, or banding to stop esophageal varices from bleeding further
angiography
gi hemorrhage management
secure airway fluid resuscitation blood products large bore IV massive transfusion protocol rapid infuser interventions to stop the bleeding invasive hemodynamic monitoring correction of contributing factors NG/OG tube - use caution in upper GI bleed vasopressors
octreotide infusion
massive gi bleed or esophageal hemorrhage
inhibits gastric acid production, pancreatic and biliary secretion
decreased portal flow and intravascular pressures
stimulation of mucous production
pantoprazole
suppress production of gastric acid
shown to reduce the incidence of re-bleeding in acute gi bleed
what is a transjugular intrahepatic portosystemic shunt? tips
portal vein is connected to a hepatic vein via a shunt to drastically improve hepatic blood flow which decreases portal hypertension and esophageal varices can shrink over time. intraventional radiologist
supportive treatment but does nothing to treat the cause of the portal hypertension
indications of gastric tamponade
acute esophagogatric and or gastric hemorrhage that is unresponsive to medical therapy
when endoscopy is unavailable or fails
applies direct pressure against the bleeding vessels while decompressing the stomach.
CXR for confirmation of placement
What are the safety considerations for gastric tamponade?
must be intubated high risk of migration and airway compromise
scissors at bedside at all times to rapidly decompress a balloon port because they can hold 600mls of air
mark tube at lips - if migrates by >2 cm notify MD
supine HOB 30-45degrees in reverse trendelenberg, no hip flexing
paralytics
traction to be maintained at all times
