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

(121 cards)

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
What are the symptoms of carcinoid tumors?
Often none ## Footnote otherwise carcinoid syndrome
26
Describe carcinoid syndrome
periodic episodes of **diarrhea** (serotonin release) **flushing** **tachycardia** **bronchoconstriction** (histamine release) ***hemodynamic instability** (e.g., hypotension)
27
What lab test is often used for carcinoid tumors?
24hr urinary 5-hydroxyindoleacetic acid/5-HIAA excretion ## Footnote the end product of serotonin metabolism
28
Treatment of carcinoid tumors
Resection
29
MC hernia type
Inguinal | Indirect is MC inguinal hernia as well ## Footnote Two "I"s for MCC of hernia
30
This hernia is MC in women
femoral
31
Location of inguinal hernia relative to the inferior epigastric artery for 1) indirect 2) direct
1) indirect = lateral 2) direct = medial ## Footnote DM
32
Where does an indirect inguinal hernia protrude through?
internal inguinal ring
33
Where does a direct inguinal hernia protrude through?
Hesselbach’s triangle | MC on right side ## Footnote “RIP” rectus abdominis, inferior epigastric, poupart’s (inguinal) ligament
34
Difference between incarcerated and strangulated inguinal hernia ## Footnote reducible?
**Incarcerated** = irreducible **Strangulated** = compromised blood supply (leading to ischemia, & necrosis, overlying skin changes ) ## Footnote reducible = asymptomatic bulge at the hernia site that comes on with increased abd pressure (cough for instance)
35
Management of asymptomatic hernia in females
ALL FEMALES NEED SURGERY
36
Management of asymptomatic inguinal hernia in males
+/- surgery ## Footnote depends on RF and surgeon preference
37
When is emergent surgery required for an inguinal hernia?
Strangulation ## Footnote Incarceration = urgent
38
What are the surgery options for inguinal hernias?
Open or laproscopic ## Footnote lap is preferred, but based on surgeon preference
39
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)
40
Why are femoral hernias almost always treated?
Often become incarcerated or strangulated because femoral ring is smaller in women ## Footnote call a surgeon
41
Location of umbilical hernia
Hernia through the umbilical fibromuscular ring | Congenital (failure of umbilical ring closure) ## Footnote usually due to loosening of the tissue around in the ring in adults
42
Treatment of congenital vs acquired umbilical hernia
Congenital = observe (typically resolves @ 2 yo) Acquired = surgery
43
MC characteristic and population for incisional hernias?
vertical incisions in obese pts | typically after abdominal surgery ## Footnote stretching and compromise of abdominal wall post-op
44
Location of obturator hernia
Rare hernia through the **pelvic floor** in which abdominal/pelvic contents protrude through the obturator foramen
45
RF for obturator hernia (2)
Multiparity women or women with significant weight loss
46
Sign seen in obturator hernia
**Howship-Romberg sign**: inner thigh pain w/ internal rotation of the hip
47
Location of a hiatal hernia
Herniation of structures from the abdominal cavity through the **esophageal hiatus of the diaphragm**
48
Describe a type I vs type II hiatal hernia ## Footnote which is MC?
Type I: Sliding (95%) Type II: Paraoesophageal (“rolling hernia”) ## Footnote 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
49
What is the typical presentation of hiatal hernia?
Asymptomatic ## Footnote may develop intermittent epigastric or substernal pain, postprandial fullness, retching, or nausea, chest pain, dysphagia
50
Dx of hiatal hernia
barium upper GI series, upper endoscopy
51
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**
52
What symptoms are you trying to relieve for type I hiatal hernia and what is the management?
GERD | PPIs + weight loss
53
What are the two IBDs?
Chron's and Ulcerative Colitis (UC)
54
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
55
What are the Extra-Intestinal Manifestations seen in IBDs ## Footnote 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 ## Footnote lots
56
Which IBD is transmural
Crohn's ## Footnote with skip lesions/ cobblestone appearanc
57
What's interesting about smoking and IBD?
It is a major RF for Crohn's but is protective for UC! ## Footnote UC is MC in non-smokers and previous smokers
58
Which IBD is MC in males? Females?
Males = UC Crohn's = Females ## Footnote just a bit
59
MC location of UC vs Crohn's
**UC** = **RECTUM** always involved **Crohn's** = any segment of GI tract, but **terminal ileum** MC ## Footnote in UC, only the colon is involved - CRC is more common in UC remember
60
Characteristics of lesions involved with Crohn's disease
mucosal inflammation, stricturing, fistula development, and abscess formation ## Footnote skip lesions
61
Characteristics of lesions involved with UC
friability, erosions, **ulcers w/ bleeding** ## Footnote affects mucosa AND submucosa
62
Complications of Crohn's vs UC
**Crohn's** = Perianal disease and malabsorption (B12/iron) **UC** = toxic megacolon
63
Characterstic finding on barium enema for UC vs Chrohn's
UC = stovepipe/ lead pipe sign Crohn's = string sign ## Footnote For Crohn's, barium is only performed when CT/MR enterography unavailable
64
Lab findings of UC
Hct, albumin (⇣), ESR/CRP, fecal calprotectin **POSITIVE P-ANCA**
65
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**
66
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 ## Footnote change card later to follow easier anti-TNF inhibitors = Infliximab Adalimumab Golimumab
67
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
68
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 ## Footnote anti-TNF inhibitors = Infliximab Adalimumab Golimumab
69
What is the MC congential anaomaly of the GI tract?
Meckel’s (Ileal) Diverticulum
70
What is the "rule of 2s" for Meckel’s (Ileal) Diverticulum? ## Footnote 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 ## Footnote often an incidental finding during abdominal surgery for other causes
71
What is the MC type of ectopic tissue for Meckel’s (Ileal) Diverticulum?
gastric
72
What is the pathophys of Meckel’s (Ileal) Diverticulum and what is the resulting characteristic symptom? ## Footnote remember, only 2% symptomatic
ectopic gastric or pancreatic tissue may secrete **digestive hormones**, **leading to painless rectal bleeding or ulceration** ## Footnote may cause intussusception, volvulus, or obstruction; may cause diverticulitis in adults
73
How do you diagnose and treat Meckel’s (Ileal) Diverticulum?
**Meckel scan**: looks for ectopic gastric tissue | Surgical excision if symptomatic ## Footnote Mesenteric arteriography or abdominal exploration
74
Why does skin/eyes/nails appear yellow with jaundice?
hyperbilirubinemia ## Footnote bilirubin deposition
75
First sign of jaundice
scleral icterus
76
What lab value is considered a sign of jaundice disease? | not a disease itself though
Serum bilirubin **>2.5mg/dL**
77
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
78
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
79
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 ## Footnote if omitted = assume WNL
80
stool color of direct vs indirect bilirubin elevation
direct = light gray or clay-colored indirect = mustard yellow or darker ## Footnote fact check this later
81
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**
82
How does Physiologic jaundice of the newborn differ from Gilbert syndrome and Crigler-Najjar Syndrome? ## Footnote what is the treatment?
It is transient | also involves low UGT ## Footnote phototherapy is the treatment
83
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**
84
How does rotor syndrome differ from Dubin-Johnson Syndrome?
Liver is not dark
85
What labs do you order for jaundice?
*serum total & unconjugated bilirubin *alk phos *AST/ALT *PT/INR *albumin
86
You order a "jaundice" panel (not really a thing) and see Predominant **alk phos elevation**, what is in your differential? ## Footnote "jaundice panel": *serum total & unconjugated bilirubin *alk phos *AST/ALT *PT/INR *albumin
suggests **biliary obstruction or intrahepatic cholestasis**
87
You order a "jaundice" panel (not really a thing) and see Predominant **aminotransferase elevation**, what is in your differential? ## Footnote "jaundice panel": *serum total & unconjugated bilirubin *alk phos *AST/ALT *PT/INR *albumin
suggests jaundice is caused by **intrinsic hepatocellular disease**
88
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**
89
What is the MC primary liver malignancy in adults?
Hepatocellular Carcinoma (HCC)
90
What is the MCC of Hepatocellular Carcinoma (HCC)?
Cirrhosis (80%) M > F | HBV and HCV, but not as much ## Footnote Get a liver transplant before if you can and please do not drink too much alcohol!
91
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
92
What marker signifies HCC?
α-fetoprotein (AFP)
93
If your α-fetoprotein (AFP) is >= 20 ng/mL and there is a liver lesion, what is the next step
CT/MRI ## Footnote probs HCC
94
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
95
Definitive dx of HCC
Liver biopsy
96
What is the screening modality for HCC?
US
97
What are the screening indications for HCC ## Footnote with an US
**cirrhosis** from any cause ***chronic HBV** + either ⇢ active infection, family hx of HCC
98
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
99
Management of early stage HCC
excision ## Footnote liver transplant if they ever meet indications
100
Management of intermediate stage HCC
**locoregional therapy**: *transarterial chemoembolization (TACE) *transarterial radioembolization (TARE) ## Footnote liver transplant if they ever meet indications
101
Management of advanced stage HCC
**systemic chemotherapy** *atezolizumab/bevacizumab ## Footnote liver transplant if they ever meet indications
102
Which Hep(s) have fecal-oral transmission? What are the other transmissions?
Hep A and E = fecal-oral BCD = blood ## Footnote interestingly, if it is fecal-oral it is an ACUTE disease - while bloodborne = ACUTE and CHRONIC
103
Which Hep has IVDU as a very common RF?
Hep C
104
How does hepatitis present overall? ## Footnote 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
105
What serology suggests acute/active Hep A?
IgM anti-HAV
106
What serology suggests past exposure to Hep A?
IgG HAV Ab
107
What serologic marker is the first to elevate in Hep B?
HBsAG ## Footnote suggests infection
108
What serologic marker indicates time of highest viral replication and most infective time?
HBeAG
109
What suggests Hep B immunity
Anti-HBs appearance with NO HBsAG | low infectious risk = HBeAb ## Footnote those who are vaccinated will only have Anti-HBs because they never had the infection
110
What is the most sensitive way to assess viral replication activity for Hep B infection?
HBV DNA
111
Management of acute Hep B
supportive care
112
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 ## Footnote first, nucleotide and nucleoside analogs - interferon 2nd (as long as no active infection)
113
How do you screen for Hep C?
HCV AB
114
What confirms an infection of Hep C?
HCV RNA
115
What serology is seen for acute vs chronic Hep C?
HCV RNA (+): acute or chronic Anti-HCV (+): chronic
116
Treatment of Hep C
Direct-Acting antiviral therapy *ledipasvir-sofosbuvir *elbasvir-grazoprevir *ombitasvir-paritaprevir-ritonavir + dasabuvir *simeprevir + sofosbuvir *daclatasvir + sofosbuvir - vir = suffix
117
How do you prevent Hep D?
Hep B vaccine | only way to get Hep D is with Hep B ## Footnote No FDA approved treatment, but interferon alpha may help with chronic disease. Liver transplant definitive.
118
How to dx Hep D?
Presents of HBV anti-HDV HDV RNA
119
What population is Hep E concerning in and why? | treatment?
Preggo patients | Supportive treatment - remember, it is NOT chronic either ## Footnote Highest mortality in preggos due to fulminant hepatitis during pregnancy (3rd trimester?)
120
What are the lab findings of alcoholic hepatitis and treatment?
AST:ALT >2 | stop drinkning, reversible if no cirrhosis! ## Footnote glucocorticoids if severe
121
Treatement of NASH ## Footnote Nonalcoholic Steatohepatitis
Weight loss, statins, vitamin E ## Footnote AST:ALT < 2?