GI / Nutritional Part 3 (dyspepsia - melena/hematochezia) Flashcards
Define Dyspepsia
pain/discomfort centered in the upper abdomen (epigastric)
acute, chronic, or recurrent
may be associated w/ heartburn, nausea, postprandial fullness, or vomiting
What foods are often the culprit of Dyspepsia
Alcohol and coffee
also over-eating or eating food too quickly can cause Dyspepsia
What meds are often the culprit of Dyspepsia?
ASA
NSAIDs
metformin
ACE/ARBs
Psych meds
steroids
iron
opioids
lots of meds can cause stomache ache
What chronic conditions often lead to Dyspepsia?
DM
Thyroid disease
CKD
also GERD and PUD
What history finding is common in young adults with chronic functional Dyspepsia?
anxiety/depression
also often psych med use
When might you consider imaging for Dyspepsia and what is the imaging?
Alarm symptoms
endoscopy or abdominal CT indicated
upper endoscopy for pt > 60 yo
weight ⇣, persistent vomiting, constant or severe pain, progressive dysphagia, hematemesis, melena, family hx of UGI cancer, abdominal mass
Treatment of H pylori
Triple or quad therapy
Triple therapy:
CPA (cure pain abd)
clarithromycin
PPI
amoxicillin
quad therapy
PMTB (please make tummy better)
PPI
metro
tetracycline
bismuth
Herbal therapies for dyspepsia that is not reactive to PPI
<60 yo
peppermint or caraway
medication trial for unresponsive dyspesia
refractory to PPI
low-dose TCAs (desipramine or nortriptyline)
What seperates an UGI bleed from a LGI bleed
UGI = upper GI bleed
LGI = lower GI bleed
Ligament of Treitz
Above = characteristic UGI findings
Below = characteristic LGI findings
a thin band of tissue (peritoneum) that connects and supports the end of the duodenum and beginning of the jejunum in the small intestine. It’s also called the suspensory muscle of duodenum.
Characteristic findings of an UGI bleed VS LGI
UGI = hematemesis + melena
Hematemesis – vomiting blood, “coffee-ground vomit”
*bloody: suggests moderate-severe bleeding
*coffee ground: suggests more limited bleeding
Melena = black tarry stool
___
LGI = Hematochezia – maroon/bright red blood, blood clots
Common etiologies of UGI bleed (5)
*PUD
*esophagitis
*portal HTN
*Mallory-Weiss tear
*angiodysplasia
Symptoms associated with the following etiologies of UGI bleeds:
1) PUD
2) Esophageal ulcer
3) Mallory-weiss tear
4) variceal hemorrhage or portal HTN gastropathy
5) malignancy
1) PUD = upper abdominal pain that relieves with meals
2) Esophageal ulcer = odynophagia, reflux, dysphagia
3) Mallory-weiss tear = emesis, retching, or cough prior to bleeding
4) variceal hemorrhage or portal HTN gastropathy = jaundice + ascities
5) malignancy = early satiety, dysphagia, weight loss, cachexia
What is considered mild/moderate hypovolemia 2ndary to UGI/LGI bleed and associated symptoms
< 15% volume
tachycardia and sometimes s/s of dehydration
Symptoms of >15% and > 40% volume loss 2ndary to UGI/LGI bleed
*≥15% volume loss:orthostatic hypotension
*≥40% volume loss: supine hypotension
What lab value is highly suggestive of UGI bleed?
BUN/Cr > 30:1
thought to be because of ingested blood protein leading to elevated urea
LGI bleed typically have a normal BUN/Cr!
Imaging for UGI bleed vs LGI bleed
UGI = upper endoscopy (makes sense)
LGI = colonscopy (makes sense)
for LGI bleed, +/- upper endoscopy to r/o UGIB
Initial management of UGI/LGI bleed that is Hemodynamically unstable
*IV access
*fluids
*transfusion
Which type of GI bleed do you use a PPI for?
UGI bleed
PPIs would not affect the colon as much? Why not used as much in LGI?
When is octerotide used for a GI bleed?
If it is an UGI bleed associated with esophageal varices or cirrhosis
After identifying the underlying cause of a GI bleed, what are the common therapies used?
typically surgeries
Applies for both UGI and LGI bleeds
*endoscopic thermal probe
*endoscopic clips
*endoscopic injection
*angiographic embolization
*endoscopic intravariceal cyanoacrylate injection
*band ligation
What are the characterstics of carcinoid tumors?
1) tumor type
2) arrise from these cells
rare, well-differentiated neuroendocrine tumor that arise from enterochromaffin cells
MC and 2nd MC location for carcinoid tumors
MC = GI tract
2nd MC = lungs
Likely pathophys of carcinoid tumors
carcinoid tumors are thought to arise from transformation of enterochromaffin-like cells (ECL cells, which are responsible for histamine secretion) due to chronic stimulation by gastrin; autoimmune atrophic gastritis is associated w/ hypergastinermia
What are the symptoms of carcinoid tumors?
Often none
otherwise carcinoid syndrome
Describe carcinoid syndrome
periodic episodes of
diarrhea (serotonin release)
flushing
tachycardia
bronchoconstriction (histamine release)
*hemodynamic instability (e.g., hypotension)
What lab test is often used for carcinoid tumors?
24hr urinary 5-hydroxyindoleacetic acid/5-HIAA excretion
the end product of serotonin metabolism
Treatment of carcinoid tumors
Resection
MC hernia type
Inguinal
Indirect is MC inguinal hernia as well
Two “I”s for MCC of hernia
This hernia is MC in women
femoral
Location of inguinal hernia relative to the inferior epigastric artery for
1) indirect
2) direct
1) indirect = lateral
2) direct = medial
DM
Where does an indirect inguinal hernia protrude through?
internal inguinal ring
Where does a direct inguinal hernia protrude through?
Hesselbach’s triangle
MC on right side
“RIP” rectus abdominis, inferior epigastric, poupart’s (inguinal) ligament
Difference between incarcerated and strangulated inguinal hernia
reducible?
Incarcerated = irreducible
Strangulated = compromised blood supply (leading to ischemia, & necrosis, overlying skin changes )
reducible = asymptomatic bulge at the hernia site that comes on with increased abd pressure (cough for instance)
Management of asymptomatic hernia in females
ALL FEMALES NEED SURGERY
Management of asymptomatic inguinal hernia in males
+/- surgery
depends on RF and surgeon preference
When is emergent surgery required for an inguinal hernia?
Strangulation
Incarceration = urgent
What are the surgery options for inguinal hernias?
Open or laproscopic
lap is preferred, but based on surgeon preference
Location of a femoral hernia?
relative to the inguinal ligament
Protrusion of the contents of the abdominal cavity through the femoral canal (below the inguinal ligament)
Why are femoral hernias almost always treated?
Often become incarcerated or strangulated because femoral ring is smaller in women
call a surgeon
Location of umbilical hernia
Hernia through the umbilical fibromuscular ring
Congenital (failure of umbilical ring closure)
usually due to loosening of the tissue around in the ring in adults
Treatment of congenital vs acquired umbilical hernia
Congenital = observe (typically resolves @ 2 yo)
Acquired = surgery
MC characteristic and population for incisional hernias?
vertical incisions in obese pts
typically after abdominal surgery
stretching and compromise of abdominal wall post-op
Location of obturator hernia
Rare hernia through the pelvic floor in which abdominal/pelvic contents protrude through the obturator foramen
RF for obturator hernia (2)
Multiparity women or women with significant weight loss
Sign seen in obturator hernia
Howship-Romberg sign: inner thigh pain w/ internal rotation of the hip
Location of a hiatal hernia
Herniation of structures from the abdominal cavity through the esophageal hiatus of the diaphragm
Describe a type I vs type II hiatal hernia
which is MC?
Type I: Sliding (95%)
Type II: Paraoesophageal (“rolling hernia”)
Type I: Sliding (95%)
*GE junction “slides” into the mediastinum (increases reflux)
Type II: Paraoesophageal (“rolling hernia”)
*fundus of stomach protrudes through diaphragm w/ the GE junction remaining its anatomic location
What is the typical presentation of hiatal hernia?
Asymptomatic
may develop intermittent epigastric or substernal pain, postprandial fullness, retching, or nausea, chest pain, dysphagia
Dx of hiatal hernia
barium upper GI series, upper endoscopy
How does the overall management of Type I vs Type II hiatal hernia differ?
Type I = symptomatic relief (typically no surgery)
Type II = surgical repair
What symptoms are you trying to relieve for type I hiatal hernia and what is the management?
GERD
PPIs + weight loss
What are the two IBDs?
Chron’s and Ulcerative Colitis (UC)
RF of IBD
1) ethnicity
2) age
3) diet
4) meds
1) ethnicity = Ashkenazi Jews
2) age = 15-35 yo
3) diet = western
4) meds = NSAIDs, OCPs/HRTs
What are the Extra-Intestinal Manifestations seen in IBDs
seen in both UC and CD
Rheumatologic: MSK pain, arthritis, ankylosing spondylitis, osteoporosis
Dermatologic: erythema nodosum, pyoderma gangrenosum
Ocular: conjunctivitis, anterior uveitis/iritis (ocular pain, HA, blurred vision), episcleritis (mild ocular burning)
Hepatobiliary: fatty liver, primary sclerosing cholangitis
Hematologic: B12/iron deficiency (esp. w/ CD), ↑ r/o thromboembolism
lots
Which IBD is transmural
Crohn’s
with skip lesions/ cobblestone appearanc
What’s interesting about smoking and IBD?
It is a major RF for Crohn’s but is protective for UC!
UC is MC in non-smokers and previous smokers
Which IBD is MC in males? Females?
Males = UC
Crohn’s = Females
just a bit
MC location of UC vs Crohn’s
UC = RECTUM always involved
Crohn’s = any segment of GI tract, but terminal ileum MC
in UC, only the colon is involved - CRC is more common in UC remember
Characteristics of lesions involved with Crohn’s disease
mucosal inflammation, stricturing, fistula development, and abscess formation
skip lesions
Characteristics of lesions involved with UC
friability, erosions, ulcers w/ bleeding
affects mucosa AND submucosa
Complications of Crohn’s vs UC
Crohn’s = Perianal disease and malabsorption (B12/iron)
UC = toxic megacolon
Characterstic finding on barium enema for UC vs Chrohn’s
UC = stovepipe/ lead pipe sign
Crohn’s = string sign
For Crohn’s, barium is only performed when CT/MR enterography unavailable
Lab findings of UC
Hct, albumin (⇣), ESR/CRP, fecal calprotectin
POSITIVE P-ANCA
Lab findings of Crohn’s
inflammatory markers – albumin, CRP, fecal calprotectin; CBC (anemia), C. diff testing
*⇣ albumin
*⇡ ESR/CRP during active inflammation
*⇡ fecal calprotectin correlates w/ active inflammation
POSITIVE ASCA
Overall treatment method of low vs high risk Crohn’s
low/mod = budesonide and sulfasalazine/mesalamine for induction followed by a steroid of taper or maintanence with sulfasalazine
mod/high = top down approach (big guns first)
induction via immunomodulator (Adalimumab preferred) or Azathioprine along with a TNF inhibtor with infliximab
Maintanence via continue anti-TNF & immunomodulator, taper steroid if used
change card later to follow easier
anti-TNF inhibitors =
Infliximab
Adalimumab
Golimumab
Overall treatment method of low risk UC
low/mod =
1) induction: mesalamine or 5-ASA (steroids if no remission)
2) maintainence = continue w/ same agent that induced remission except for steroids
Overall treatment method of high risk UC
mod/high:
1) induction: anti-TNF +/- immunomodulator
2) maintanence: continue w/ same agent that induced remission except for steroids
anti-TNF inhibitors =
Infliximab
Adalimumab
Golimumab
What is the MC congential anaomaly of the GI tract?
Meckel’s (Ileal) Diverticulum
What is the “rule of 2s” for Meckel’s (Ileal) Diverticulum?
7 of them
1) 2% of population
2) 2 feet proximal from ileocecal valve
3) 2% symptomatic
4) 2 inches in length
5) 2 types of ectopic tissue (gastric or pancreatic)
6) 2yrs MC age
7) 2x MC in males
often an incidental finding during abdominal surgery for other causes
What is the MC type of ectopic tissue for Meckel’s (Ileal) Diverticulum?
gastric
What is the pathophys of Meckel’s (Ileal) Diverticulum and what is the resulting characteristic symptom?
remember, only 2% symptomatic
ectopic gastric or pancreatic tissue may secrete digestive hormones, leading to painless rectal bleeding or ulceration
may cause intussusception, volvulus, or obstruction; may cause diverticulitis in adults
How do you diagnose and treat Meckel’s (Ileal) Diverticulum?
Meckel scan: looks for ectopic gastric tissue
Surgical excision if symptomatic
Mesenteric arteriography or abdominal exploration
Why does skin/eyes/nails appear yellow with jaundice?
hyperbilirubinemia
bilirubin deposition
First sign of jaundice
scleral icterus
What lab value is considered a sign of jaundice disease?
not a disease itself though
Serum bilirubin >2.5mg/dL
List seven overall mechanisms that may lead to jaundice
1) Extravascular hemolysis/ineffective erythropoiesis
2) Physiologic jaundice of the newborn
3) Gilbert Syndrome
4) Crigler-Najjar Syndrome
5) Dubin-Johnson Syndrome
6) Biliary tract obstruction (obstructive jaundice)
7) Viral hepatitis
Characterisize if the following diseases would result in pre, intra, or post hepatic jaundice:
gallstones
hemolysis
Gilbert’s disease
Acute hepatitis
Alcoholic/ primary biliary cirrhosis
Crigler-Najjar Syndrome
prehepatic= Hemolysis, Gilbert’s disease, Crigler-Najjar Syndrome
Hepatic = Cirrhosis (both), hepatitis
Posthepatic = Gallstones
Explain the resulting lab values of both direct and indirect bilirubin for the following types of jaundice:
prehepatic
hepatic
posthepatic
prehepatic = elevated indirect bilirubin
hepatic = elevated direct and indirect bilirubin
posthepatic = elevated direct bilirubin
indirect = unconjugated bilirubin; direct = conjugated bilirubin
if omitted = assume WNL
stool color of direct vs indirect bilirubin elevation
direct = light gray or clay-colored
indirect = mustard yellow or darker
fact check this later
Gilbert syndrome vs Crigler-Najjar Syndrome - how are they similar?
Which is more severe?
Both involve UGT (enzyme resposible for conjugating indrect to direct bilirubin)
Gilbert syndrome = low levels of UGT leading to high indirect bilirubin (resulting in jaundice during stress)
Crigler-Najjar Syndrome = NO UGT, leading to high indirect bilirubin all the time and jaundice all the time, leading to kernicterus which is usually fatal
How does Physiologic jaundice of the newborn differ from Gilbert syndrome and Crigler-Najjar Syndrome?
what is the treatment?
It is transient
also involves low UGT
phototherapy is the treatment
How does Dubin-Johnson Syndrome differ from Gilbert syndrome and Crigler-Najjar Syndrome? Characterisitic finding?
It involves deficiency of bilirubin canaliculi transport protein which increases CB
the liver is pitch-dark
How does rotor syndrome differ from Dubin-Johnson Syndrome?
Liver is not dark
What labs do you order for jaundice?
*serum total & unconjugated bilirubin
*alk phos
*AST/ALT
*PT/INR
*albumin
You order a “jaundice” panel (not really a thing) and see Predominant alk phos elevation, what is in your differential?
“jaundice panel”:
*serum total & unconjugated bilirubin
*alk phos
*AST/ALT
*PT/INR
*albumin
suggests biliary obstruction or intrahepatic cholestasis
You order a “jaundice” panel (not really a thing) and see Predominant aminotransferase elevation, what is in your differential?
“jaundice panel”:
*serum total & unconjugated bilirubin
*alk phos
*AST/ALT
*PT/INR
*albumin
suggests jaundice is caused by intrinsic hepatocellular disease
You order a “jaundice” panel (not really a thing) and see an elevated INR, what is in your differential?
an elevated INR that corrects w/ vitamin K admin suggests impaired intestinal absorption of fat-soluble vitamins & is compatible w/ obstructive jaundice
What is the MC primary liver malignancy in adults?
Hepatocellular Carcinoma (HCC)
What is the MCC of Hepatocellular Carcinoma (HCC)?
Cirrhosis (80%)
M > F
HBV and HCV, but not as much
Get a liver transplant before if you can and please do not drink too much alcohol!
HCC is often asymptomatic, but as the disease progresses, there can be symptoms from underlying cirrhosis/hepatitis.
What are the s/s of advanced HCC?
▪︎weight loss, anorexia
▪︎hepatomegaly & RUQ tenderness
▪︎jaundice, ascites
What marker signifies HCC?
α-fetoprotein (AFP)
If your α-fetoprotein (AFP) is >= 20 ng/mL and there is a liver lesion, what is the next step
CT/MRI
probs HCC
What are the findings of HCC upon CT w/ IV contrast?
arterial phase hyperenhancement
*nonperipheral washout: hypointense compared to
surrounding in portal venous or delayed phase
*enhancing capsule
Definitive dx of HCC
Liver biopsy
What is the screening modality for HCC?
US
What are the screening indications for HCC
with an US
cirrhosis from any cause
*chronic HBV + either ⇢ active infection, family hx of HCC
Your patient recently got screened for HCC because they either had cirrhosis or chronic HBV + an active infection or fam Hx of HCC. How would you manage them if the following findings were found on US?
No lesion
Lesion < 10 mm
Lesion >= 10 mm
No lesion = repeat US in 6mo
Lesion < 10 mm = repeat US in 3-6mo
Lesion >= 10 mm = CT scan
Management of early stage HCC
excision
liver transplant if they ever meet indications
Management of intermediate stage HCC
locoregional therapy:
*transarterial chemoembolization (TACE)
*transarterial radioembolization (TARE)
liver transplant if they ever meet indications
Management of advanced stage HCC
systemic chemotherapy
*atezolizumab/bevacizumab
liver transplant if they ever meet indications
Which Hep(s) have fecal-oral transmission? What are the other transmissions?
Hep A and E = fecal-oral
BCD = blood
interestingly, if it is fecal-oral it is an ACUTE disease - while bloodborne = ACUTE and CHRONIC
Which Hep has IVDU as a very common RF?
Hep C
How does hepatitis present overall?
for Hep A-E
*anorexia, N/V
*fatigue, malaise, arthralgias, myalgias
*HA, photophobia
*pharyngitis, cough, coryza
1-2wks later 🡪 jaundice, +/- RUQ pain
Dark urine, clay-colored stools – may appear 1-5d before onset of jaundice
What serology suggests acute/active Hep A?
IgM anti-HAV
What serology suggests past exposure to Hep A?
IgG HAV Ab
What serologic marker is the first to elevate in Hep B?
HBsAG
suggests infection
What serologic marker indicates time of highest viral replication and most infective time?
HBeAG
What suggests Hep B immunity
Anti-HBs appearance with NO HBsAG
low infectious risk = HBeAb
those who are vaccinated will only have Anti-HBs because they never had the infection
What is the most sensitive way to assess viral replication activity for Hep B infection?
HBV DNA
Management of acute Hep B
supportive care
Indications for antiviral therapy for Hep B
persistent, severe sxs, marked jaundice, (bilirubin >10), inflammation on liver bx, ↑ ALT or (+) HB envelope antigen present
basically severe
first, nucleotide and nucleoside analogs - interferon 2nd (as long as no active infection)
How do you screen for Hep C?
HCV AB
What confirms an infection of Hep C?
HCV RNA
What serology is seen for acute vs chronic Hep C?
HCV RNA (+): acute or chronic
Anti-HCV (+): chronic
Treatment of Hep C
Direct-Acting antiviral therapy
*ledipasvir-sofosbuvir
*elbasvir-grazoprevir
*ombitasvir-paritaprevir-ritonavir + dasabuvir
*simeprevir + sofosbuvir
*daclatasvir + sofosbuvir
- vir = suffix
How do you prevent Hep D?
Hep B vaccine
only way to get Hep D is with Hep B
No FDA approved treatment, but interferon alpha may help with chronic disease.
Liver transplant definitive.
How to dx Hep D?
Presents of HBV
anti-HDV
HDV RNA
What population is Hep E concerning in and why?
treatment?
Preggo patients
Supportive treatment - remember, it is NOT chronic either
Highest mortality in preggos due to fulminant hepatitis during pregnancy (3rd trimester?)
What are the lab findings of alcoholic hepatitis and treatment?
AST:ALT >2
stop drinkning, reversible if no cirrhosis!
glucocorticoids if severe
Treatement of NASH
Nonalcoholic Steatohepatitis
Weight loss, statins, vitamin E
AST:ALT < 2?
