Gastrointestinal Flashcards
List the structures of upper and lower GI tract:
Upper:
Mouth, esophagus, cardiac sphincter, stomach, pyloric sphincter, duodenum. Ligament of Treitz.
Lower:
Jejunum, ileum, caecum, ascending -> transverse -> descending -> sigmoid colon, rectum, anus.
Signs of ESLD:
Jaundice, ascites, spider angiomas (do not blanche), palmar erythema, asterixis, caput medusae, umbilical herniation.
When performing an abdominal exam, what does rebound tenderness signify?
That the peritoneum of the affected organ is also inflamed. This has a worse prognosis and indicates a progression of the pathology.
What are signs of pancreatitis?
"Sharp" postprandial, epigastric pain Lipase count > 3 x normal Cullen sign (discoloured umbilicus) Grey-turner sign (discoloured flanks) Hypo/hyperglycaemia *May also have elevated GGT/ALP
What is an “acute abdomen?”
A serious undifferentiated diagnosis indicating severe peritoneal inflammation that requires prompt surgical consult.
Patients will be unassessable due to significant abdominal tenderness.
How do you assess for appendicitis?
Pain on palpating at McBurney’s point (1/3 of the way between the right anterior iliac crest and the umbilicus).
Rovsing’s sign: Pain in the LRQ as the left abdomen is being firmly palpated.
Identify the difference between cirrhosis and hepatitis on radiological imaging:
Hepatitis will present with hepatomegaly while cirrhosis will be much smaller due to the scarring.
Costovertibral Angle (CVA) tenderness is indicative of what?
Pyelonephritis. Likely, from a severe bacterial infection of the kidneys.
What are your tranamynase enzymes and what do elevations in their count represent?
AST and ALT
They represent direct hepatocyte damage since they leak out of ischemic/damaged liver cells. In acute liver failure, levels might be normal if the patient has a long Hx of ESDL and the liver is no longer capable of producing enough of them.
*AST:ALT > 2:1 = EtOH
How do you tell if the liver failure is from an EtOH based etiology?
The AST will be at least twice as much as the ALT. Elevated GGT might also be present.
What do elevated levels of AST and ALT indicate?
Acute, undifferentiated hepatitis. Could be from toxins, trauma, infection or drugs.
What are cholestatic enzymes and what do they represent?
ALP and GGT
When downstream pressure in the bile duct backs up into biliary tree these endothelial enzymes are released into the circulation. They represent biliary obstruction.
What are the three most important liver function tests?
- Albumin
- INR (vitamin K dependant clotting factors of the extrinsic pathway)
- Bilirubin
- Lactate
Where is unconjugated bilirubin found?
In the pre-hepatic blood stream. An elevated level most often indicates hemolysis or liver failure.
What is the difference between amylase and lipase?
Lipase is produced only in the pancreas while amylase is also produced in the saliva.
*A pleural effusion with a positive amylase indicates esophageal rupture.
Will a GI bleed have a high or a low BUN?
High. Blood is reabsorbed, digested and the protein then elevates the BUN.
Signs of an upper GI bleed:
Hemoptysis
Coffee ground emesis
Melena
*Can also have bright, red rectal blood if it is brisk. These patients are unstable!
Variceal causes of UGIB:
Portal HTN
Portal vein thrombosis
Gastric varices
Non-variceal causes of UGIB:
- Peptic/duodenal ulcer (NSAIDs, prev PUD, H. Pylori, steroids)
- Boerhaave (+/- vomiting)
- Gastritis/esophagitis (EtOH)
Tx of non-variceal UGIB:
Transfuse, if necessary, and correct coagulopathies (PRBCs, FFP, Plex, Cryo, Vit K, Ca++)
PPI (80mg Pantaloc)
Antiemetics
TXA
Tx of variceal UGIB
Transfuse and correct coagulopathies Octreotide and/or vasopressin TXA ABx Blakemore or Minnesota
Discuss the insertion of a Blakemore:
- Lube it up and insert it approx 50cm
- Partially inflate it, pull back until resistance and check X-ray
- Fully inflate gastric balloon to tamponade vessels, apply 1kg traction
- If still bleeding, inflate esophageal balloon
- Consider using saline to inflate balloons for flight
Causes of LGIB:
- Colitis (radiation, infective [c-diff], inflammatory, ischemic)
- Diverticulitis
- Hemorrhoids
- Malignancy
Etiologies of ESDL
Drugs (acetaminophen, EtOH...) Viral hepatitis Ischemic liver Gall stones HELLP/preeclampsia
What is the “Thousands Club”
The following processes can cause liver enzymes to climb into the thousands:
- Viral (A, B) or autoimmune hepatitis
- Ischemic liver
- Acetaminophen overdose
- HELLP
How does acetaminophen (APAP) ruin your liver?
APAP is metabolized and excreted in 4 different ways. One of the pathways (glutathione) is used up which leaves the other pathways free to excrete unmetabolized toxins that directly attack hepatocytes.
Patients require an N-acetylcystine (NAC) infusion.
What do acetaminophen screens test for?
Exactly that. They cannot measure the amount of acetaminophen that’s already been metabolized into a toxin.
What is the scoring system that assesses for ESDL:
MELD
What are the major complications of ESDL?
- Hepatic encephalopathy
- Coagulopathies (hyper and hypo)
- Immunosupression
- Decreased plasma protein binding
- Decreased drug metabolism
- Fluid shift due to hypoalbumenia
- Hepatorenal syndrome
- Abnormalities with glucose, hormones and lipids
- Portal HTN -> varices and ascites -> ACS (shock), hepatorenal syndrome, splenomegaly -> thrombocytopenia
Discuss hepatic encephalopathy:
The liver is no longer able to clear osmolar, nitrogenous toxins. These toxins travel to the brain and cause direct cerebral dysfunction. Their osmolar property causes a fluid shift and cerebral edema formation. Treat with laxatives since stool is another source of nitrogenous waste removal.
Causes of pancreatitis:
Gall stones
EtOH
Drugs
Infection
Discuss pancreatitis:
Pancreatic dysfunction causes the very digestive enzymes it makes to turn on it and start eating it from the inside-out. They then run havoc on other organs and can cause distributive shock. Sick pancreatitis patients have a poor prognosis.
Tx for pancreatitis:
Analgesia
Hydration
Tx gall stones
No ABx
Complications of pancreatitis:
T2DM Hemorrhage Pleural effusion Pseudocysts-> aortoenteric fistulas Necrotic pancreas ACS
Define measurements of IAH and ACS:
IAH: IAP > 12mmHg
ACS: IAP > 20mmHg with end organ damage
How do you measure IAP?
Insert 30cc of warm saline into foley and clamp.
Put must be supine (MV and paralyzed preferred)
Measure once detrusor muscles relax and pt expires
Level at iliac crest
Etiologies for ACS:
Direct:
Ascites, colitis, bowel perforation, pancreatitis
Indirect: Over resuscitation (burns, sepsis, hemorrhage), retroperitoneal hematoma
Tx of ACS:
- OG/NG
- Lung protective mech vent w. permissive hypercapnia. Use esophageal ballon.
- Paracentis (use IV catheter if you have to)
- Enemas
- Sedation, analgesia and paralysis
If ACS patient has narrow IVC and high vent pressures, what should you think about?
Don’t fluid bolus. The IVC isn’t small because of hypovolemia. It’s just compressed.
Yeah, these patients are going to require high vent pressures since the FRC is compressed. Use permissive hypercapnia.
Discuss bowel obstruction:
Post prandial pain, N/V. Usually caused by post-operative adhesions (surgical scars). Can also be caused by CA, foreign body and IBD.
C-Diff is a contact precaution. Can you use alcohol to kill it?
No! Gotta soap and water that shit off. Take it seriously! C-Diff can fucking kill you!!!
Number one cause of acute liver failure
APAP ingestion
Considerations for ESDL
- APAP levels
- Blakemore (with lots of tube ties)
- Blood/FFP
- Octeotride
- Vasopressin
- DDAVP
- Pantaloc
- No lactulose for flight (it causes gas and shit)
Cullen’s sign (umbilicus) and Grey-Turner’s sign (flanks) are signs of pancreatitis or abdominal trauma. When do they usually appear?
12-24 hours following onset.
An increased unconjugated bilirubin indicates what?
There is a problem with the RBCs before they get to the liver. Usually a sign of hemolysis.
Will GI bleeds increase or decrease BUN levels?
Heme is a protein. When it is broken down and reabsorbed, as in the case of UGIB, it elevates BUN.qw
What level of lipase indicates pancreatitis?
3 x N.
How do vasopressin and Octeotride work?
Sphlancic vasoconstrictors that decrease portal venous pressure, and therefore, portal blood flow as well.
Generally describe hepatorenal syndrome (HRS):
- Liver sucks, so it releases vasodilators (NO, prostaglandins) to try and make it better.
- This causes mesenteric vasodilation and decreased pressures.
- Reduced renal blood flow from the low pressures is sensed by the kidney so it afferent arterioles constrict, reducing blood flow further.
- Kidneys shut down.
- Tx with vasopressin, levophed
Describe the difference between unconjugated and conjugated/total bilirubin:
Excessive unconjugated bilirubin can be caused by increased hemolysis or decreased liver function. This is more toxic. An increase in conjugated bilirubin is more a sign of bilary obstruction.
List some complications of liver failure:
- HRS
- Coagulopathies
- Hypoglycemia
- Varices
- Lactatemia
- Shock (distributive, then also cardiogenic)
- ALI
- Encephalopathy
What’s one sedative drug you want to stay the fuck away from when treating a patient with liver failure?
Midazolam. If you have to sedate them, use ketamine.
You’re intubating ruptured esophageal varices. What a fucking mess!! How are you going to do it?
Two tubes. One into the esophagus. Inflate and clamp the tube, then suction out the oropharynx. Once you have a clean view, go in with the second tube anteriorly.
Describe the relationship between lipase and amylase when differentiating between mesenteric ischemia (ACS) and pancreatitis:
Increased amylase is non-specific and could be either, while increased lipase alone, is likely to be pancreatitis.
When might the lactate in Ringer’s Lactate actually contribute to worsening lactate levels?
Severe liver failure. Otherwise, you can give liters and liters of it without it contributing to acidemia. Remember, lactate is not lactic acid.
Even if the patient is acidotic, ringer’s lactate may still be better for the patient than N/S because chloride pushes out bicarbonate.
