GI Flashcards
Management of gastroenteritis
Treatment is largely supportive
Give NS for nausea and LR for diarrhea
Replete electrolytes
Order Zofran for nausea
PO Challenge with bland drinks and foods
—BRAT diet: bananas, rice, apple sauce, toast
Don’t miss appendicitis or mesenteric ischemia in the elderly patient
Sugary drinks (gatorade) can worsen diarrhea
Do not give anti-diarrheal medications in patients whose diarrhea has lasted <72 hours
What is Zollinger-Eillison syndrome
Neuroendocrine tumor in the stomach that secretes gastrin
Small - can occur anywhere along the GI tract
Can cause coffee ground emesis, diarrhea, steatorrhea, severe esophageal pain and acachexia
Treatment includes PPI, H2 blocker or surgical excision
What causes hematemesis bright red blood, copious amounts?
variceal bleed or a Dieulafoy lesion
How do you get varices? What conditions are associated
A varix is an engorged blood vessel anywhere in the GI tract, although usually in the esophagus, which is caused by portal vein HTN.
Can be torn or irritated and then start bleeding briskly
Associated with cirrhosis (the cause of the portal vein HTN) - also platelets are low because of poor liver function.
Treatment of variceal bleeding
Need two large bore IVs and start with IVF and then switch to colloid to replace blood lost
Tamponade the bleeding if possible with a Minnesota or Blakemore tube tethered to a football helmet
Intubate and mechanically ventilate if needed
Start protonix ggt, sandostatin (reduces portal HTN) and vasopressin (moves blood from GI tract)
Could consider TIPS procedure (Transjugular intra-hepatic portal shunt)
—reduces portal venous pressure and shunts it to the IVC
How do Octreotide and vasopressin work for GI bleeds?
Octreotide inhibits gastrin secretion which causes vasoconstriction and therefore reduces portal venous pressure - only used for variceal bleeding
Vasopressin constricts blood vessels and reduces blood flow to the GI tract - splanchic blood flow
How to tell which type of hepatitis the patient has just by looking at the LFTs?
HAV: Elevated ALT (>1000), much higher than AST, elevated alk phos and bili
HBV: ALT:AST are 1:1, elevated bili
HCV: LFTs are not outrageously elevated, normal bili
In acute hepatic failure, how does coagulopathy happen?
Portal hypertension interferes with the transport of Vitamin K to the liver after it is synthesized by the gut flora.
The liver is also damaged and therefore not making thrombopoietin and therefore a decrease in platelets occurs. Hepatic vascular congestion also speeds platelet destruction in the spleen.
Disseminated Intravascular Coagulation develops when the liver stops producing enough clotting inhibitors.
–This triggers spontaneous clotting and the clotting cascade starts a chain reaction throughout the body.
—Clotting starts to interfere with organ function.
—Soon all the clotting factors are exhausted and then spontaneous bleeding begins.
Spontaneous Bacterial Peritonitis: Causes, Presentation and Treatment
Infection related to massive ascites
Ascitic fluid is a perfect bacterial media
Usually caused by translocation of gut flora into the peritoneal cavity due to low level mesenteric ischemia.
Presents just like septic shock but without a pathogen
Diagnostic paracentesis is performed to look for WBC in the fluid
Empirically treated with cetriaxone 2g IV every 24 hours or cefotaxime 2gm IV every 8 hours
What is choledocholithiasis?
gallstone pancreatitis when the gallstone becomes obstructed at the ampulla of Vater or at least distal to the common bile duct
Lipase will be elevated
Diagnostic testing and treatment of choledocholithiasis
Confirm diagnosis with RUQUS
Once stone gets into the common bile duct, it is a medical problem, no longer surgical. Needs ERCP.
If still in gall bladder, it is a surgical problem but often is asymptomatic - cholelithiasis
What is cholangitis
Infection of the gallbladder
This is an emergency!
Charcot’s Triad: Fever, RUQ pain and jaundice
Ranson’s Criteria
Helpful in determining the severity of pancreatitis
What do you draw initially and then what is assessed 48 hours later
On Admission:
George Washington Got Lazy After
–Greater than 55 years old
–WBC >16
–Glucose >200
–Lactate >3.5
–AST> 250
Initial 48 hours:
He Broke C-A-B-E
–HCT decrease >10%
–BUN increase >5
–Calcium <8
–Arterial O2 <60
–Base deficit >4
–Estimated Fluid Sequestration >6L
Less than 3, not serious
More than 6, 100% mortality
Treatment of pancreatitis
Aggressive IVF, often >12L in first 24 hours
Antiemetics, keep NPO
Vasopressors as needed
Generous IV pain medications
Consult GI for consideration of ERCP/MRCP
Antibiotic coverage with Zosyn, Flagyl
If you are worried about appendicitis, what test would you order?
CT A/P is the gold standard
Treatment of Infectious Colitis
-Check signs of clinical dehydration then check a careful hx to give a clue about exposure and the possible pathogen involved.
-Treat dehydration and correct lytes
-Check non-bloody stool for occult blood
-Stool culture only in the most at-risk pts
-Ova and parasite analysis is only needed in patient with strong clinical suspicion
-In general antibx are not indicated
— Treatment is hydration and BRAT diet
–If antibx are needed (fever, signs of systemic illness), fluoroquinolones (Cipro, levo) for 3-5 days
Treatment of C. Diff
Flagyl 500mg PO TID
Vancomycin 125mg PO QID
ALWAYS orally treated
Never give anti-motility agents because it will only help retain bacteria
Differences between Crohn’s and UC - Presentation
Crohn’s:
–Loose, non-bloody stools
–fevers are common during flares
–Weight loss and fistulae are common
–Can occur anywhere in the GI tract
Ulcerative Colitis:
–Mucoid, bloody stools
–Increased urgency
–Less likely fevers
–Rare weight loss or fistulae
–Only involves the colon
Differences between Crohn’s and UC - Pathophysiology and treatment
Crohn’s:
–Usually evident early in life and caused by T-cells that attack the colonic mucosa
–Can occur anywhere along the GI tract
–Mild cases often don’t need daily medicines, only need low dose steroids during flares.
–More severe cases can require chronic steroids
Ulcerative Colitis:
–Involves the rectum and colon only
–During remission, no sxs at all
–During flares, bloody, mucoid stools that are painful
–Flares treated with steroids - suppositories
–Hallmark is bloody diarrhea
–Complication is toxic megacolon
Risk factors for ischemic colitis and mesenteric ischemia
Ischemic colitis is usually caused by a low flow state caused by severe heart failure, shock or iatrogenic
Mesenteric ischemia is often caused by a superior mesenteric artery thrombus caused by A-fib or atherosclerosis.
Presentation and treatment of Ischemic colitis
Most common in the elderly with known atherosclerotic disease
Frequently pt’s present with severe and colicky abd pain and bloody diarrhea (dark blood)
Abd is diffusely tender
CT shows inflammation of descending colon and/or sigmoid
Treatment is to hydrate, consult GI and likely will require surgical intervention
Questionable utility of antibx
Diverticulitis Treatment
Uncomplicated:
-Bowel rest with strict liquid diet for 24-72 hours
-Cipro 500mg PO BID and Flagyl 500mg PO TID
Complicated:
-Zosyn 3.375gm IV every 6 hours or
- Cipro 400mg IV every 12 hours AND Flagyl 500mg IV every 8 hours
-Strict NPO, IV hydration and IV analgesics
Perforation will need surgical repair to avoid peritonitis (although if perf’ed they likely already have it)
Causes of small bowel obstruction
Adhesions from previous surgeries
Hernias containing bowel
Crohn’s disease causing adhesions or inflammatory strictures
Tumors
Volvulus - twisting of the intestine
Ischemia
Foreign body
Management of small bowel obstruction
Decompress the abdomen
NGT to continuous low suction
Foley catheter
NPO
IV hydration at higher than usual rates
Pain control but be careful because opiates decrease motility
Anti-emetics
If obstruction does not resolve in 48 hours then should consider surgery
What bacteria is most common cause of duodenal ulcers and gastric ulcers?
H. pylori
Present in >90% of duodenal ulcers and >75% of gastric ulcers
A younger patient (30-55) would most likely have which type of peptic ulcer, duodenal or gastric?
Duodenal
Duodenal ulcers occur between the ages of 30-55
Gastric ulcers occur between the ages of 55-65
As far as symptomatology, what is the difference between a duodenal and gastric ulcer? What are they relieved by?
Both have gnawing epigastric pain
Relief of pain with eating - duodenal
Pain worsens with eating - gastric
Treatment of H. pylori
Two antibiotics + PPI with or without bismuth for 10-14 days
For patients not allergic to PCN:
ECA: Esomeprazole BID, Clarithromycin BID, Amoxicillin BID
EBMT: Esomeprazole BID, Bismuth QID, Metronidazole QID, Doxycycline QID
ECAM: Esomeprazole BID, Clarithromycin BID, Amoxicillin BID, Metronidazole BID
For patients who are allergic to PCN:
ECM: Esomeprazole BID, Clarithromycin BID, Metronidazole TID
Then continue PPI for up to 3 months after
Symptoms and Physical findings of diverticulitis
Mild to moderate aching abd pain in LLQ
Constipation or loose stools
N/V
Physical findings:
Low grade fever
LLQ tenderness with palpation
What diagnostics would you order for diverticulitis?
CBC - mild to moderate leukocytosis
ESR - will be mildly elevated
Likely hem+ stool
**Plan abd films are obtained on all patients to look for evidence of free air (pneumoperitoneum - air under the diaphragm)
What is Murphy’s Sign and what does it suggest?
Deep pain on inspiration while fingers are placed under the right rib cage
Suggests Cholecystitis
Presentation of cholecystitis: Symptoms and diagnostics
Steady, severe pain in the epigastrium or RUQ - usually after a large, fatty meal
Physical findings: Positive Murphy’s Sign
RUQ tenderness to palpation
Muscle guarding and rebound pain
Fever
Diagnostics:
CBC - Leukocytosis
LFTs - Serum bilirubin elevated, AST, ALT, Alk phos all elevated
Amylase - elevated
RUQUS - GOLD STANDARD**
Endoscopic retrograde cholangiopancreatography (ERCP) - but ERCP can cause pancreatitis
ERCP: When is it used and what are the complications
Endoscopic retrograde cholangiopancreatography
Used to diagnose diseases of the gallbladder, bile system, pancreas and liver
Complications - Most common is pancreatitis
Perforation
Hemorrhage
Classic presentation of pancreatitis
Abrupt onset of steady, severe, epigastric pain worsened by walking and lying supine
Pain is improved by sitting and leaning forward
Pain usually radiates to the back
Nausea/vomiting
Weakness, sweating
Physical findings:
Upper abd tender to palpation, usually without guarding, rigidity or rebound
Distended abdomen
Absent or decreased bowel sounds
Fever
Tachycardia
Pallor, cool skin
Mild jaundice can be present
What are the two signs associated with hemorrhagic acute pancreatitis
Grey Turner’s Sign: Flank Discoloration
Cullen’s Sign: Umbilical discoloration
Gold standard for diagnosing acute pancreatitis
CT A/P
Symptoms or mesenteric infarct
Sudden onset of cramping, colicky abd pain
Pain out of proportion to physical exam findings
Nausea/vomiting
Fever
Abd guarding and tenderness
Peritoneal findings increase as state progresses
Can have shock
Physical findings with acute appendicitis
RLQ guarding with rebound tenderness
McBurney’s Point tenderness: One-third the distance from the anterior superior iliac spine to the umbilicus
Psoas Sign: Pain with right thigh extension
Obturator Sign: Pain with internal rotation of the flexed right thigh
Rovsing’s Sign: RLQ pain when pressure is applied to the LLQ
Low grade fever
