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causes of upper GI bleeding
tarry/dark blood, can look like coffee grounds
duodenal ulcer
esophageal or gastric varices
gastric ucler
mallory-weiss tear
causes of lower GI bleeding
bright red/maroon blood (hematochezia)
cancer
diverticulosis
hemorrhoids
inflammatory disease
polyps
vascular ectasias
biggest risk factor of peptic ulcer
alcohol consumption!!
H.pylori
NSAIDS
smoking
h.pylori infection
elevates levels of gastrin and pepsinogen and releases toxins and enzymes that promote ulceration and inflammation
melena
shiny, black, foul-smelling stool that results from the degradation of blood by stomach acids or intenstinal bacteria
causes of esophageal varices
most common is liver cirrhosis » leading to portal HTN
hepatitis B or C, or fatty liver disease
Blood clots in the portal or splenic vein
S/S of esophgeal varices
Varices usually cause no symptoms until they bleed. Vein walls are thin » rupture » bleeding can be severe and life-threatening
Vomiting blood (bright red or like coffee grounds)
Black, tarry, or bloody stools
Lightheadedness, fainting, rapid heartbeat
Pale skin
guaiac testing
GI blood is occult (not visible) and is tested w a chemical reagant
When blood is present in the stool, the heme in blood triggers a chemical reaction when a developer solution is added, and the spot turns blue (+)
pt signs of blood loss from upper GI tract
boody emesis (hematemesis)
hematochezia or melena
↑ bowel sounds
patho of upper GI bleed

diagnostic of upper GI issues
endoscopy: procedure can be done @ bedside, pt must be hemo stable, pt sedated
preferred for suspected ulcers, GI bleeding, Barrett’s esophagus, cancer, and esophageal varice
stress ulcer prophylaxis
High-risk patients given H2 blockers or PPIs
Mechanical ventilation for more than about 48 hours
A coagulopathy (impaired clotting), such as from liver disease, low platelets, or anticoagulants
H. pylori treatement
PPI (esomeprazole, lansoprazole, omeprazole, pantoprazole) plus two ABX (amoxicillin & clarithromycin)
vasopressin therapy
lowers portal vein pressure by constricting splanchic arteriolar bed (often given w NTG)
somatostatin or octreotide: reduce splanchnic blood flow by a different mechanism and have a much better safety profile than vasopressin
MOST COMMON cause of acute pancreatitis
alcohol ingestion and biliary disease
pancreatitis labs

S/S of acute pancreatitis
abdominal guarding/distension
cullen’s sign
dehydration
fever
grey turner’s sign (ecchymosis in flanks)
N/V
pain
patho of acute pancreatitis
Trigger: Acinar cell injury lets pancreatic enzymes (trypsin, chymotrypsin, elastase) leak into pancreatic tissue.
Autodigestion: causing edema, vascular damage, hemorrhage, necrosis, and fibrosis.
Systemic spread: Enzymes and inflammatory mediators enter the blood and injure distant organs
Immune response: Local inflammation is followed by CARS → too much CARS → ↑ infection risk
common hepatotoxic meds
APAP
ABX
NSAIDS
MAOIs
antiepileptics
statins
common cause of liver failure
hepatitis
treatment/prophylaxis of chronic liver disease
Avoid alcohol and unnecessary hepatotoxic medications (including excess acetaminophen)
Adequate nutrition and hydration
Monitoring liver enzymes and for chronic cases, screening for cirrhosis and liver cancer
S/S of acute liver failure
• Chills
• Convulsions
• ↓ LOC, coma
• Hyperexcitability
• Insomnia
• Irritability
• Jaundice
• Lethargy
• Nausea and vomiting
• Sudden onset of high fever
liver disease categories
portal HTN
impaired liver metabolic process
impaired bile formation and flow
high-output failure or hyperdynamic circulation
liver cell destruction » shunting of blood and ↑ CO + vasodilation » decreased perfusion to organs despite ↑ CO
s/s related to those of HF, JVD, & pulmonary crackles
causes of fatty liver
long-term alcohol abuse
obesity
types of liver cirrhosis (scarring)
alcoholic
biliary (obstruction of bile ducts)
cardiac (long term RHF)
postnecrotic (exposure to hepatotoxins or chemicals)
ascites
a complication of liver failure
acculumation of fluid in the peritoneum
assoc w/ low albumin levels
Na + H2O retention + portal HTN » ascites
ascites treatment
bed rest, low Na diet, fluid restriction, diuretic therapy
paracentesis (percutaneous needle aspiration)
why is ammonia high in liver failure?
The liver is the body’s main ammonia-detoxifying organ, and when it fails, ammonia builds up in the blood
Normally, hepatocytes convert ammonia into urea through the urea cycle, and the kidneys excrete the urea in urine
hepatic encephalopathy
Excess ammonia crosses into the brain, where astrocytes convert it to glutamine. Glutamine draws water into the cells, causing swelling, and disrupts neurotransmission. The result ranges from sleep reversal and mild confusion to asterixis (flapping tremor), stupor, and coma. In acute liver failure, the swelling can cause dangerous brain edema and raised intracranial pressure.
treatment of hepatic encephalopathy
lactulose (acts as a laxative + converts ammonia » ammonium)