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Surgery EOR > GI / Nutritional Part 3 (dyspepsia - melena/hematochezia) > Flashcards

GI / Nutritional Part 3 (dyspepsia - melena/hematochezia) Flashcards

1
Q

Define Dyspepsia

A

pain/discomfort centered in the upper abdomen (epigastric)

acute, chronic, or recurrent

may be associated w/ heartburn, nausea, postprandial fullness, or vomiting

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2
Q

What foods are often the culprit of Dyspepsia

A

Alcohol and coffee

also over-eating or eating food too quickly can cause Dyspepsia

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3
Q

What meds are often the culprit of Dyspepsia?

A

ASA
NSAIDs
metformin
ACE/ARBs
Psych meds
steroids
iron
opioids

lots of meds can cause stomache ache

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4
Q

What chronic conditions often lead to Dyspepsia?

A

DM
Thyroid disease
CKD

also GERD and PUD

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5
Q

What history finding is common in young adults with chronic functional Dyspepsia?

A

anxiety/depression

also often psych med use

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6
Q

When might you consider imaging for Dyspepsia and what is the imaging?

A

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

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7
Q

Treatment of H pylori

A

Triple or quad therapy

Triple therapy:
CPA (cure pain abd)
clarithromycin
PPI
amoxicillin

quad therapy
PMTB (please make tummy better)
PPI
metro
tetracycline
bismuth

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8
Q

Herbal therapies for dyspepsia that is not reactive to PPI

<60 yo

A

peppermint or caraway

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9
Q

medication trial for unresponsive dyspesia

refractory to PPI

A

low-dose TCAs (desipramine or nortriptyline)

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10
Q

What seperates an UGI bleed from a LGI bleed

UGI = upper GI bleed
LGI = lower GI bleed

A

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.

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11
Q

Characteristic findings of an UGI bleed VS LGI

A

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

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12
Q

Common etiologies of UGI bleed (5)

A

*PUD
*esophagitis
*portal HTN
*Mallory-Weiss tear
*angiodysplasia

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13
Q

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

A

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

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14
Q

What is considered mild/moderate hypovolemia 2ndary to UGI/LGI bleed and associated symptoms

A

< 15% volume

tachycardia and sometimes s/s of dehydration

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15
Q

Symptoms of >15% and > 40% volume loss 2ndary to UGI/LGI bleed

A

*≥15% volume loss:orthostatic hypotension
*≥40% volume loss: supine hypotension

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16
Q

What lab value is highly suggestive of UGI bleed?

A

BUN/Cr > 30:1

thought to be because of ingested blood protein leading to elevated urea

LGI bleed typically have a normal BUN/Cr!

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17
Q

Imaging for UGI bleed vs LGI bleed

A

UGI = upper endoscopy (makes sense)
LGI = colonscopy (makes sense)

for LGI bleed, +/- upper endoscopy to r/o UGIB

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18
Q

Initial management of UGI/LGI bleed that is Hemodynamically unstable

A

*IV access
*fluids
*transfusion

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19
Q

Which type of GI bleed do you use a PPI for?

A

UGI bleed

PPIs would not affect the colon as much? Why not used as much in LGI?

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20
Q

When is octerotide used for a GI bleed?

A

If it is an UGI bleed associated with esophageal varices or cirrhosis

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21
Q

After identifying the underlying cause of a GI bleed, what are the common therapies used?

typically surgeries

Applies for both UGI and LGI bleeds

A

*endoscopic thermal probe
*endoscopic clips
*endoscopic injection
*angiographic embolization
*endoscopic intravariceal cyanoacrylate injection
*band ligation

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22
Q

What are the characterstics of carcinoid tumors?
1) tumor type
2) arrise from these cells

A

rare, well-differentiated neuroendocrine tumor that arise from enterochromaffin cells

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23
Q

MC and 2nd MC location for carcinoid tumors

A

MC = GI tract

2nd MC = lungs

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24
Q

Likely pathophys of carcinoid tumors

A

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

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25
Q

What are the symptoms of carcinoid tumors?

A

Often none

otherwise carcinoid syndrome

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26
Q

Describe carcinoid syndrome

A

periodic episodes of
diarrhea (serotonin release)
flushing
tachycardia
bronchoconstriction (histamine release)
*hemodynamic instability (e.g., hypotension)

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27
Q

What lab test is often used for carcinoid tumors?

A

24hr urinary 5-hydroxyindoleacetic acid/5-HIAA excretion

the end product of serotonin metabolism

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28
Q

Treatment of carcinoid tumors

A

Resection

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29
Q

MC hernia type

A

Inguinal

Indirect is MC inguinal hernia as well

Two “I”s for MCC of hernia

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30
Q

This hernia is MC in women

A

femoral

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31
Q

Location of inguinal hernia relative to the inferior epigastric artery for
1) indirect
2) direct

A

1) indirect = lateral
2) direct = medial

DM

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32
Q

Where does an indirect inguinal hernia protrude through?

A

internal inguinal ring

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33
Q

Where does a direct inguinal hernia protrude through?

A

Hesselbach’s triangle

MC on right side

“RIP” rectus abdominis, inferior epigastric, poupart’s (inguinal) ligament

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34
Q

Difference between incarcerated and strangulated inguinal hernia

reducible?

A

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)

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35
Q

Management of asymptomatic hernia in females

A

ALL FEMALES NEED SURGERY

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36
Q

Management of asymptomatic inguinal hernia in males

A

+/- surgery

depends on RF and surgeon preference

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37
Q

When is emergent surgery required for an inguinal hernia?

A

Strangulation

Incarceration = urgent

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38
Q

What are the surgery options for inguinal hernias?

A

Open or laproscopic

lap is preferred, but based on surgeon preference

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39
Q

Location of a femoral hernia?

relative to the inguinal ligament

A

Protrusion of the contents of the abdominal cavity through the femoral canal (below the inguinal ligament)

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40
Q

Why are femoral hernias almost always treated?

A

Often become incarcerated or strangulated because femoral ring is smaller in women

call a surgeon

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41
Q

Location of umbilical hernia

A

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

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42
Q

Treatment of congenital vs acquired umbilical hernia

A

Congenital = observe (typically resolves @ 2 yo)
Acquired = surgery

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43
Q

MC characteristic and population for incisional hernias?

A

vertical incisions in obese pts

typically after abdominal surgery

stretching and compromise of abdominal wall post-op

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44
Q

Location of obturator hernia

A

Rare hernia through the pelvic floor in which abdominal/pelvic contents protrude through the obturator foramen

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45
Q

RF for obturator hernia (2)

A

Multiparity women or women with significant weight loss

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46
Q

Sign seen in obturator hernia

A

Howship-Romberg sign: inner thigh pain w/ internal rotation of the hip

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47
Q

Location of a hiatal hernia

A

Herniation of structures from the abdominal cavity through the esophageal hiatus of the diaphragm

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48
Q

Describe a type I vs type II hiatal hernia

which is MC?

A

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

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49
Q

What is the typical presentation of hiatal hernia?

A

Asymptomatic

may develop intermittent epigastric or substernal pain, postprandial fullness, retching, or nausea, chest pain, dysphagia

50
Q

Dx of hiatal hernia

A

barium upper GI series, upper endoscopy

51
Q

How does the overall management of Type I vs Type II hiatal hernia differ?

A

Type I = symptomatic relief (typically no surgery)
Type II = surgical repair

52
Q

What symptoms are you trying to relieve for type I hiatal hernia and what is the management?

A

GERD

PPIs + weight loss

53
Q

What are the two IBDs?

A

Chron’s and Ulcerative Colitis (UC)

54
Q

RF of IBD
1) ethnicity
2) age
3) diet
4) meds

A

1) ethnicity = Ashkenazi Jews
2) age = 15-35 yo
3) diet = western
4) meds = NSAIDs, OCPs/HRTs

55
Q

What are the Extra-Intestinal Manifestations seen in IBDs

seen in both UC and CD

A

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

56
Q

Which IBD is transmural

A

Crohn’s

with skip lesions/ cobblestone appearanc

57
Q

What’s interesting about smoking and IBD?

A

It is a major RF for Crohn’s but is protective for UC!

UC is MC in non-smokers and previous smokers

58
Q

Which IBD is MC in males? Females?

A

Males = UC
Crohn’s = Females

just a bit

59
Q

MC location of UC vs Crohn’s

A

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

60
Q

Characteristics of lesions involved with Crohn’s disease

A

mucosal inflammation, stricturing, fistula development, and abscess formation

skip lesions

61
Q

Characteristics of lesions involved with UC

A

friability, erosions, ulcers w/ bleeding

affects mucosa AND submucosa

62
Q

Complications of Crohn’s vs UC

A

Crohn’s = Perianal disease and malabsorption (B12/iron)
UC = toxic megacolon

63
Q

Characterstic finding on barium enema for UC vs Chrohn’s

A

UC = stovepipe/ lead pipe sign
Crohn’s = string sign

For Crohn’s, barium is only performed when CT/MR enterography unavailable

64
Q

Lab findings of UC

A

Hct, albumin (⇣), ESR/CRP, fecal calprotectin
POSITIVE P-ANCA

65
Q

Lab findings of Crohn’s

A

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

66
Q

Overall treatment method of low vs high risk Crohn’s

A

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

67
Q

Overall treatment method of low risk UC

A

low/mod =
1) induction: mesalamine or 5-ASA (steroids if no remission)
2) maintainence = continue w/ same agent that induced remission except for steroids

68
Q

Overall treatment method of high risk UC

A

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

69
Q

What is the MC congential anaomaly of the GI tract?

A

Meckel’s (Ileal) Diverticulum

70
Q

What is the “rule of 2s” for Meckel’s (Ileal) Diverticulum?

7 of them

A

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

71
Q

What is the MC type of ectopic tissue for Meckel’s (Ileal) Diverticulum?

A

gastric

72
Q

What is the pathophys of Meckel’s (Ileal) Diverticulum and what is the resulting characteristic symptom?

remember, only 2% symptomatic

A

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

73
Q

How do you diagnose and treat Meckel’s (Ileal) Diverticulum?

A

Meckel scan: looks for ectopic gastric tissue

Surgical excision if symptomatic

Mesenteric arteriography or abdominal exploration

74
Q

Why does skin/eyes/nails appear yellow with jaundice?

A

hyperbilirubinemia

bilirubin deposition

75
Q

First sign of jaundice

A

scleral icterus

76
Q

What lab value is considered a sign of jaundice disease?

not a disease itself though

A

Serum bilirubin >2.5mg/dL

77
Q

List seven overall mechanisms that may lead to jaundice

A

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

78
Q

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

A

prehepatic= Hemolysis, Gilbert’s disease, Crigler-Najjar Syndrome
Hepatic = Cirrhosis (both), hepatitis
Posthepatic = Gallstones

79
Q

Explain the resulting lab values of both direct and indirect bilirubin for the following types of jaundice:

prehepatic
hepatic
posthepatic

A

prehepatic = elevated indirect bilirubin
hepatic = elevated direct and indirect bilirubin
posthepatic = elevated direct bilirubin

indirect = unconjugated bilirubin; direct = conjugated bilirubin

if omitted = assume WNL

80
Q

stool color of direct vs indirect bilirubin elevation

A

direct = light gray or clay-colored
indirect = mustard yellow or darker

fact check this later

81
Q

Gilbert syndrome vs Crigler-Najjar Syndrome - how are they similar?
Which is more severe?

A

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

82
Q

How does Physiologic jaundice of the newborn differ from Gilbert syndrome and Crigler-Najjar Syndrome?

what is the treatment?

A

It is transient

also involves low UGT

phototherapy is the treatment

83
Q

How does Dubin-Johnson Syndrome differ from Gilbert syndrome and Crigler-Najjar Syndrome? Characterisitic finding?

A

It involves deficiency of bilirubin canaliculi transport protein which increases CB

the liver is pitch-dark

84
Q

How does rotor syndrome differ from Dubin-Johnson Syndrome?

A

Liver is not dark

85
Q

What labs do you order for jaundice?

A

*serum total & unconjugated bilirubin
*alk phos
*AST/ALT
*PT/INR
*albumin

86
Q

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

A

suggests biliary obstruction or intrahepatic cholestasis

87
Q

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

A

suggests jaundice is caused by intrinsic hepatocellular disease

88
Q

You order a “jaundice” panel (not really a thing) and see an elevated INR, what is in your differential?

A

an elevated INR that corrects w/ vitamin K admin suggests impaired intestinal absorption of fat-soluble vitamins & is compatible w/ obstructive jaundice

89
Q

What is the MC primary liver malignancy in adults?

A

Hepatocellular Carcinoma (HCC)

90
Q

What is the MCC of Hepatocellular Carcinoma (HCC)?

A

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!

91
Q

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?

A

▪︎weight loss, anorexia
▪︎hepatomegaly & RUQ tenderness
▪︎jaundice, ascites

92
Q

What marker signifies HCC?

A

α-fetoprotein (AFP)

93
Q

If your α-fetoprotein (AFP) is >= 20 ng/mL and there is a liver lesion, what is the next step

A

CT/MRI

probs HCC

94
Q

What are the findings of HCC upon CT w/ IV contrast?

A

arterial phase hyperenhancement
*nonperipheral washout: hypointense compared to
surrounding in portal venous or delayed phase
*enhancing capsule

95
Q

Definitive dx of HCC

A

Liver biopsy

96
Q

What is the screening modality for HCC?

A

US

97
Q

What are the screening indications for HCC

with an US

A

cirrhosis from any cause
*chronic HBV + either ⇢ active infection, family hx of HCC

98
Q

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

A

No lesion = repeat US in 6mo
Lesion < 10 mm = repeat US in 3-6mo
Lesion >= 10 mm = CT scan

99
Q

Management of early stage HCC

A

excision

liver transplant if they ever meet indications

100
Q

Management of intermediate stage HCC

A

locoregional therapy:

*transarterial chemoembolization (TACE)
*transarterial radioembolization (TARE)

liver transplant if they ever meet indications

101
Q

Management of advanced stage HCC

A

systemic chemotherapy
*atezolizumab/bevacizumab

liver transplant if they ever meet indications

102
Q

Which Hep(s) have fecal-oral transmission? What are the other transmissions?

A

Hep A and E = fecal-oral
BCD = blood

interestingly, if it is fecal-oral it is an ACUTE disease - while bloodborne = ACUTE and CHRONIC

103
Q

Which Hep has IVDU as a very common RF?

A

Hep C

104
Q

How does hepatitis present overall?

for Hep A-E

A

*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

105
Q

What serology suggests acute/active Hep A?

A

IgM anti-HAV

106
Q

What serology suggests past exposure to Hep A?

A

IgG HAV Ab

107
Q

What serologic marker is the first to elevate in Hep B?

A

HBsAG

suggests infection

108
Q

What serologic marker indicates time of highest viral replication and most infective time?

A

HBeAG

109
Q

What suggests Hep B immunity

A

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

110
Q

What is the most sensitive way to assess viral replication activity for Hep B infection?

A

HBV DNA

111
Q

Management of acute Hep B

A

supportive care

112
Q

Indications for antiviral therapy for Hep B

A

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)

113
Q

How do you screen for Hep C?

A

HCV AB

114
Q

What confirms an infection of Hep C?

A

HCV RNA

115
Q

What serology is seen for acute vs chronic Hep C?

A

HCV RNA (+): acute or chronic
Anti-HCV (+): chronic

116
Q

Treatment of Hep C

A

Direct-Acting antiviral therapy

*ledipasvir-sofosbuvir
*elbasvir-grazoprevir
*ombitasvir-paritaprevir-ritonavir + dasabuvir
*simeprevir + sofosbuvir
*daclatasvir + sofosbuvir

  • vir = suffix
117
Q

How do you prevent Hep D?

A

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.

118
Q

How to dx Hep D?

A

Presents of HBV
anti-HDV
HDV RNA

119
Q

What population is Hep E concerning in and why?

treatment?

A

Preggo patients

Supportive treatment - remember, it is NOT chronic either

Highest mortality in preggos due to fulminant hepatitis during pregnancy (3rd trimester?)

120
Q

What are the lab findings of alcoholic hepatitis and treatment?

A

AST:ALT >2

stop drinkning, reversible if no cirrhosis!

glucocorticoids if severe

121
Q

Treatement of NASH

Nonalcoholic Steatohepatitis

A

Weight loss, statins, vitamin E

AST:ALT < 2?

Surgery EOR (17 decks)

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