GI / Nutritional Part 1 (Abdominal pain - Cholelithiasis/choledocholithiasis) Flashcards
What are some causes of RUQ pain?
Think organ location
- Gallbladder issues
- Liver issues
- biliary colic, cholecystitis/angiitis
- hepatitis, thrombosis
What are some of the causes of LUQ pain?
Think organ location
Spleen issues
Splenomegaly
Splenic infarct
Splenic Abscess
Rupture
What are some of the causes of epigastric pain? (6)
- MI
- Pancreatitis (acute/chronic)
- PUD
- GERD
- Gastritis/opathy/paresis
- Dyspepsia
Classic cause of RLQ pain vs LLQ pain
RLQ = Appendicitis
LLQ = diverticulitis
What are some GI causes of anorexia?
- Gastric/duodenal ulcers
- Gastric/GI cancers
- Hematochezia
What is Cholelithiasis specifically?
Merely Gallstones in the biliary tract (usually in the gallbladder) w/o inflammation
MC type of gallstone?
cholesterol
others are black stones (hemolysis), brown stones in infections and Asian pop
RF for Cholelithiasis
remember, just gallstones
5 Fs and Native Americans
fat, fair, female, forty, fertile
also OCPs
What does Cholelithiasis feel like?
Nothing typically
sometimes biliary colic ( episodic, abrupt RUQ or epigastric pain, resolves slowly, lasting 30min-hrs; may be associated w/ nausea & precipitated by fatty foods or large meals)
What is the diagnostic test of choice for:
1. Cholelithiasis
2. Acute Cholecystitis
3. Choledocholithiasis
4. Acute Ascending Cholangitis
5. Primary Sclerosing Cholangitis
- Cholelithiasis = US
- Acute Cholecystitis = HIDA scan if US not dx
- Choledocholithiasis = ERCP diagnostic and theraputic
- Acute Ascending Cholangitis = cholangiography
- Primary Sclerosing Cholangitis = MRCP/ERCP
Typically start with US for all of these though?
MCC of Acute Cholecystitis
E coli
also klebsiella, other gram-neg enteric organisms
If you have Chronic Cholecystitis, you can bet you have ____
gallstones
Describe the pain of Acute Cholecystitis
1. Location
2. Precipitating factors
Continuous RUQ or epigastric pain – may be precipitated by fatty foods or large meals
may be associated w/ nausea, guarding, anorexia
PE of Acute Cholecystitis and classic finding
fever (often low-grade); enlarged, palpable gallbladder
MURPHY’S SIGN: RUQ pain or inspiratory arrest w/ palpation of the gallbladder
Apart from Murphy’s sign, what is another PE sign that is sometimes seen in Acute Cholecystitis and what causes it?
Boas sign: referred pain to the right shoulder or subscapular area (phrenic nerve irritation)
Upon first-line imaging of Acute Cholecystitis, you will see ____ of the gallbladder and sometimes a ____ sign
1) Thickening of the gallbladder wall
2) Sonographic Murphy’s sign
remember, HIDA scan is most accurate scan though and it is used when the GB cannot be visualized
Overall management of Acute Cholecystitis
NPO (prep for surg)
IV fluids
ABX followed by:
Cholecystectomy
What are the ABX used pre-Cholecystectomy?
rocephin + metronidazole
MR
If a pt cannot have a Cholecystectomy, what is another treatment option for Acute Cholecystitis?
Cholecystostomy (percutaneous drainage) if nonoperative
Cholesterolosis presentation and treatment
fat deposits on GB
“strawberry GB”
tx is cholecystectomy (only if symptoms)
How does Choledocholithiasis differ anatomically from Cholelithiasis and why is it a concern?
Gallstones in the common bile duct (can lead to cholestasis due to blockage)
CBD is formed from the merging of the cystic and hepatic ducts, meaning that drainaige from the liver is blocked as well
Presentation of Choledocholithiasis
Prolonged biliary colic: RUQ or epigastric pain, N/V – pain usually more prolonged due to the presence of the stone blocking the bile duct
PE: RUQ or epigastric tenderness, jaundice
Lab findings of Choledocholithiasis
↑ AST/ALT, alk phos, & GGT
cholestasis
Management of Choledocholithiasis
Typically US first, but:
ERCP stone extraction preferred over laparoscopic choledocholithotomy
ERCP: dx TOC – diagnostic + therapeutic
What differs Acute Ascending Cholangitis from
1) Cholecystitis
2) Choledocholithiasis
Sorta a combo of the two:
1) different from Cholecystitis in that the infection is a result from blockage of the CBD rather than just the cystic duct
2) Different from Choledocholithiasis in that there is a presence of infection in addition to blocking the CBD
MCC of Acute Ascending Cholangitis
E coli
same as Cholecystitis, EZ!
What is the classic triad of Acute Ascending Cholangitis?
Charcot’s Triad: fever + RUQ pain + jaundice
Reynold’s Pentad: charcots + shock or AMS
What are the lab findings of Acute Ascending Cholangitis and why does this make sense?
- Leukocytosis
- ↑ alk phos & GGT
↑ bilirubin > increased ALT/AST
Again, labs suggest a hybrid of Cholecystitis and Cholangitis
You start with an US and are sus of Acute Ascending Cholangitis, so you use ____
Cholangiography via ERCP: gold standard
Treatment of Acute Ascending Cholangitis
remember, infectious process and stones are present
Zosyn OR
Metro + ceph OR
Metro + cipro
ERCP removal
Eventually elective cholecystectomy
ZAC MC (zosyn acute cholangitis or metro + ceph/cipro)
Apart from Acute Ascending Cholangitis, what condition can present with Charcot’s Triad?
however, it does not classically present with all three
Primary Sclerosing Cholangitis
it CAN but not characteristic of the condition
What is Primary Sclerosing Cholangitis?
Autoimmune, progressive cholestasis leading to diffuse fibrosis of intra/extrahepatic biliary ducts
Your patient has Primary Sclerosing Cholangitis, what else do they likely have?
IBD (specifically ulcerative colitis)
90% association
also likely a 20-40 yo male
What symptom can help you differ Primary Sclerosing Cholangitis and from Acute Ascending Cholangitis?
Pruritis
also see fatigue and hepatosplenomegaly
What conditions have ↑ alk phos & GGT, ↑ AST/ALT (3)
uniting feature?
- Choledocholithiasis
- Acute Ascending Cholangitis
- Primary Sclerosing Cholangitis
all involve the CBD or hepatic duct (for PSC)
What key lab findings are seen in Primary Sclerosing Cholangitis?
IgM
P-ANCA
With this most accurate test, you will see ____ for Primary Sclerosing Cholangitis
MRCP, ERCP – most accurate test: beaded appearance of biliary ducts (narrowing, strictures)
beaded appearance due to chronic sclerosis and tissue healing?
liver bx rarely used for dx - but remember that the hepatic ducts are affected
Management of Primary Sclerosing Cholangitis
1) symptomatic relief
2) pruritits
3) definitive
1) symptomatic relief = stricture dilation (allowing emptying)
2) pruritits = cholestyramine (bile sequestrant reducing bile acids)
3) definitive = liver transplant (affects hepatic/bile ducts, remember?)
MCC of acute vs chronic pancreatitis
acute = gallstones
chronic= alcohol
2nd MCC of acute = alcohol
what specific cells are injured in pancreatitis and what is the normal function of these cells?
acinar cells, which secrete exocrine enzymes
exocrine enzymes (amylase, lipase, and protease)
Meds that can lead to acute pancreatitis (4)
Thiazides
Protease inhibitors
exanitide
valproic acid
PRO vet
Protease inhibitors
Valproic acid
Exantide
Thiazides
Classic presentation of acute pancreatitis
Epigastric pain radiates to back
exacerbated if supine, relieved leaning forward
N/V and fever
Classic PE findings of severe acute pancreatitis
Cullen’s sign (periumbilical)
Grey Turner sign (flank)
suggests necrotizing hemorrhage
Most useful lab for acute pancreatitis
also, what electrolyte abnormality is sometimes seen?
Lipase
3x UNL
can also see HYPOcalcemia
Imaging for acute pancreatitis
NOT NEEDED
only use if patient does not have classic symptoms OR lipase is < 3x ULN
CT w/ contrast is imaging of choice
What might an abd xray show for acute pancreatitis? (2)
1) sentinel loop = localized ileus of small bowel segment in LUQ
2) colon cutoff sign: abrupt collapse of colon near pancreas
Dx of acute pancreatitis
Ranson’s criteria
Admission:
(1) glucose >200mg/dL
(2) age >55yrs
(3) LDH >350IU/L
(4) AST >250IU/dL
(5) WBC >16,000/µL
Within 48hrs:
(6) calcium <8mg/dL
(7) hematocrit fall >10%
(8) PO2 <60mmHg
(9) BUN >5mg/dL
(10) base deficit >4mEq/L
(11) sequestration of fluid >6L
Interpretation:
≥3 🡪 severe pancreatitis likely
<3 🡪 severe pancreatitis unlikely
Tx of acute pancreatitis
Rest the pancreas
NPO
*high-volume IVF (LR preferred)
*analgesia (Meperidine)
Antibiotics:
*indicated only if >30% necrosis seen
Triad of Chronic Pancreatitis
calcification + steatorrhea (fatty stool) + DM
seen only in 1/3 of pts: think inhibited abs d/t problem with pancreas
also see weight loss from poor abs
How do labs differ from acute vs chronic pancreatitis
Chronic has normal amylase/lipase
What might a CT scan show for chronic pancreatitis?
calcifications
Most sensitive and specific test for chronic pancreatitis
fecal elastase most sensitive & specific; pancreatic stimulation w/ secretin & CCK
not usually done
Management of chronic pancreatitis
Lifestyle
ETOH abstinence, pain control, low fat diet, vitamin supplementation
Oral pancreatic enzyme replacement
Pancreatectomy only if retractable pain despite medical therapy
Describe the pathophys of achalasia?
what plexus is involved?
Loss of peristalsis & failure of relaxation of the LES
PATHO: idiopathic proximal degeneration of myenteric/Auerbach’s plexus leads to increased LES pressure & impaired LES relaxation
MC presents <50yrs of age
What will a patient with achalasia complain of?
dysphagia to both solids & liquids
can’t keep food down and will often cough it up - even can have chest pain
Diagnosis of choice and classic finding for achalasia
Barium esophagram:
”bird’s beak” appearance of the LES
Treatment of choice for achalasia and definitive
Pneumatic dilation of LES
Esophagomyomectomy is definitive
MC site of anal fissure
Linear, longitudinal tear in the posterior midline
skin tags are seen in chronic
bright red blood is seen in toilet
pain, straining
Initial treatment of anal fissure
Supportive
sitz baths
high fiber and increased H2O to minimize straining
consider surg if refractory, but can lead to fecal incontinence
MC location of Perianal Abscess and Fistulas
posterior rectal wall
What does a fistula allow if a patient has a Perianal Abscess?
connects an abscess w/ skin or adjacent organs
Symptoms of Perianal Abscess and Fistula and how this differs from just an abscess
- SEVERE pain paired with fever and malaise
- If there is a fistula, it is a more chronic, non-healing abscess - leading to purulent drainaige that is itchy and malodorous
How to diagnose Perianal Abscess and Fistulas
Abscess = clinical
Fistula = MRI & endosonography
You can not feel a fistula on PE alone?
Treatment of Abscess and Fistulas
I&D, Antibiotics; sitz baths, high fiber
*Augmentin, cipro + metronidazole
Fistula requires surgical treatment
Cure My Abscess
(cipro + metro) augmentin
Stage 1-4 hemorrhoids
I: Does not prolapse (confined to anal canal); may bleed w/ defecation
II: Prolapses w/ defecation or straining but spontaneously reduce
III: Prolapses w/ defecation or straining, requires manual reduction
IV: Irreducible & may strangulate
What are the veins involved with internal vs external hemorrhoids?
Internal = superior hemorrhoid vein; above dentate line
External = inferior hemorrhoid vein; below dentate line
How do symptoms differ between internal vs external hemorrhoids?
Internal = painless bleed
External = painful non-bleeding
opposites
Dx of hemorrhoids
DRE with fecal occult blood testing
sometimes anoscopy or proctosigmoidoscopy or colonoscopy if worried of other etiologies
Intial Tx of hemorrhoids
Same as anal fissures pretty much
high fiber diet, increased fluids; warm sitz baths; topical rectal corticosteroids
Procedures for failed conservative treatment of hemorrhoids
rubber band ligation
What is Zollinger-Ellison Syndrome?
gastric-secreting neuroendocrine tumor leading to severe PUD & diarrhea
gastrinoma
ZES reminds me of zombies - which are associated with your brain (neuroendocrine)
MC site of gastrinomas for ZES
Zollinger-Ellison Syndrome
duodenal wall, pancreas, lymph nodes, other sites
ZED (d = duodenum)
Presentation of ZES
Zollinger-Ellison Syndrome
severe, recurrent, multiple, or refractory ulcers + diarrhea
Severe PUD:
*multiple peptic ulcers
*refractory ulcers
*abdominal pain
Diarrhea
increased acidity inactivated the pancreatic enzymes, leading to malabsorption
increased acidicty d/t PUD?
What imaging is used for ZES and why?
Zollinger-Ellison Syndrome
endoscopy – confirm presence of ulcer
remember, ZES is associated with PUD and the diagnosis of choice for PUD is endoscopy + biopsy to confirm ulcer
Lab findings seen in ZES
Zollinger-Ellison Syndrome
elevated basal or stimulated gastrin levels
secreted by the gastrinoma!
You want to screen a patient for ZES, what do you do?
Zollinger-Ellison Syndrome
Check fasting gastrin levels and gastric pH
gastrin should not be elevated while fasting as it is secreted w/ meals?
elevated fasting gastrin levels
*>1000pg/mL + gastric pH <2 = likely diagnosis
How to confirm ZES
Zollinger-Ellison Syndrome
Secretin test w/ persistant gastrin elevation
persistent gastrin elevations upon trial of secretin confirms diagnosis
Secretin SHOULD inhibit gastrin release in a healthy GI tract, but gastrin release in gastrinomas are not impacted by secretin
MC location of METS for ZES
Zollinger-Ellison Syndrome
Liver and lung lymph nodes
pLants vs ZES
Treatment of ZES and treatment if it METS
Zollinger-Ellison Syndrome
Tumor resection
lifelong high dose PPIs if METS (to raise pH and manage symptoms?)
MCC of appendicitis
fecalith
preop ABX for appendicitis
cephalosporins + metronidazole
or zosyn
What is Paralytic Ileus?
temporary functional impairment of peristalsis
NOT a physical barrier
Meds that can cause Paralytic Ileus
Opioids and anticholinergics
Can’t see, can’t poop
Electrolyte abnormality that can cause Paralytic Ileus
HYPOkalemia
MCC of SBO vs LBO
small bowel vs large bowel
SBO = post abd surgical adhesions
LBO = adenocarcinoma > scarring secondary to diverticulitis > volvulus
What is volvulus?
torsion of bowel on its axis ⇢ closed loop obstruction
torsion of mesenteric vascular pedicle ⇢ occlusion/thrombosis of mesenteric vessels ⇢ bowel strangulation, ischemia, & gangrene
MC location of volvulus
Sigmoid colon
sigmoid makes the letter “S”, which is more susceptible to be twisted?
Explain the evolution of abd sounds in a SBO/LBO
Peristalsis intially increases greatly early on followed by abscence of bowel sounds in later course
hyperactive followed by hypoactive bowel sounds
Which bowel obstruction type is emesis more common in?
SBO or LBO?
SBO
more proximal, so it makes sense
3/6/9 rule of bowel obstruction
small bowel >3cm
large bowel >6cm
cecum >9cm
Classic sign seen in sigmoid volvulus
coffee bean sign
Classic finding of volvulus on CT
whirl sign = pathognomonic
remember, it winds on itself leading to blood flow compromise
Initial Tx of SBO
- NG Tube for gastric decompression (1)
- Fluids prior to surg if strangulation sus
(1) NG tube helps prevent aspiration and relieves gastric distension by removing gastric fluids + gas
Tx of SBO if 24 hours w/out improvement
I’m assuming without improvement w/ NG tube and whatnot?
- laparotomy
- Lysis of adhesions
- resect nonviable intestine followed by primary anastomsis of resected segments
Overall Tx of LBO
Surgery (in nearly all cases)
goals ⇢ resection of necrotic bowel &
decompression of obstructed segment
Surgery options for LBO (3)
1) *resection + primary anastomosis
2) *resection + diversion, diversion alone
3) *endoscopic stent placement
Treatment of cecal volvulus
ileocecal resection or R colectomy w/ ileocolic anastomosis
quick refresher; order of small intestine/ large intestine flow:
duodenum, jejunum, ileum, cecum, ascending colon, hepatic flexure (right colic flexure), transverse colon, splenic flexure (left colic flexure), descending colon, sigmoid colon, rectum, anus
Treatment of sigmoid volvulus w/OUT signs of peritonitis
sigmoidoscopy w/ rectal tube insertion for decompression, detorsion, & reduction
surgery if all else fails
Treatment of sigmoid volvulus WITH signs of peritonitis
sigmoid colectomy & primary anastomosis
Apart from BMI, in order to be a candidate for bariatric surgery, what do you need to do?
Fail a dietary program
Proof of failure typically required
BMI guidelines for bariatric surg
35+ if comorbidities (HTN, DM)
40+ otherwise
Goals of restrictive bariatric surgeries
Limit coloric intake by limiting the stomach’s resivoir capacity
2 restrictive bariatric surgeries
- Sleeve gastrectomy
- Laproscopic adjustable band
Sleeve gastrectomy involves _____
resection of greater curvature of stomach
restrictive + hormonal change = less hunger and better insulin control
reduces the size of the stomach and leads to a 60% weight loss @ 2 years
Which bariatric surgery is strictly restrictive
LAGB
Laparoscopic Adjustable Gastric Banding
not used much anymore
Roux-en-Y Gastric Bypass (RYGB)
▪︎small stomach pouch created & connected directly to small intestine ▪︎70% weight loss @2y
Dumping syndrome
what is this often seen in?
nausea, weakness, sweating, faintness, & possibly diarrhea soon after
eating within first few years after surgery ⇢ symptoms intensify w/ high-sugar foods
seen in Roux-en-Y Gastric Bypass (RYGB)
Which bariatric surgery involves removing the LESSER curvature of the stomach
One-Anastomosis Gastric Bypass (OAGB): “mini-gastric bypass”
Gastroparesis vs Ileus
for constipation
Gastroparesis: condition that affects the stomach muscles & prevents proper stomach emptying
Ileus = hypomobility of the GI tract in the absence of mechanical bowel obstruction
Gastro = specifically stomach
Ileus = GI tract
MCC of Gastroparesis
DM
chronic damage to nerves of GI tract (autonomic neuropathy)
s/s of gastroparesis vs ileus
- Gastroparesis = nausea, full feeling after little food is eaten, constipation
- Ileus = diminished bowel sounds and constipation
both constipation
treatment of gastroparesis and ileus
Underlying cause + treat constipation
Overall meds for constipation
- Fiber
- Bulk forming laxatives
- Osmotic laxactives
- Stimulant laxatives
MOA of fiber
retains water & improves GI transit
increases bulk of stool
What are the bulk forming laxatives?
- Psyllium
- Methylcellulose
- Polycarbophil
- Wheat dextran
notice how the names of these are related to carbs:
cellulose
carbophil
wheat
(then psyllium)
MOA of bulk forming laxatives
absorbs water & increases fecal mass; increases the frequency & softens the consistency of stool w/ minimal effects
*dietary fiber + bulk forming laxatives most physiologic & effective approach
What are the osmotic laxatives? (3) Specifically saline laxatives? (2)
- Sorbitol
- Polyethylene glycol (PEG)
- Lactulose
Saline = milk of magnesia, mag citrate (basically mg)
MOA of osmotic/saline laxatives
causes water retention in stool (osmotic effect pulls water into gut)
What are the SE of saline laxatives?
hypomagnesemia
idk why? fact check?
What are the stimulant laxatives? (2)
Bisacodyl
Senna
MOA of stimulant laxatives
increases acetylcholine-regulated GI motility (peristalsis) & alters electrolyte transport in the mucosa
All of the treatments for constipation (fiber + laxatives) have a SE of bloating except
stimulant laxatives
diarrhea, abdominal pain
