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Gastroenterology > Stomach Disorders > Flashcards

Stomach Disorders Flashcards

1
Q

erosive and hemorrhagic gastritis causes

A

-medications (NSAIDs/ASA)
-EtOH
-stress (illness)
-portal hypertension
-caustic ingestion (rare)
-radiation (rare)- cancer

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2
Q

erosive and hemorrhagic gastritis S&S

A

-none or some
-dyspepsia- indigestion
-epigastric pain
-nausea and vomiting
-UGI bleed most common yet insignificant - small bleed
-poor correlation- insignificant exam with many symptoms (vice versa)

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3
Q

dx of gastritis

A

-endoscopy- lesions:
-superficial, vary in size/number, diffuse vs focal
-subepithelial hemorrhages
-petechiae
-erosion
-labs- normal vs anemia (long term blood loss)

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4
Q

specific causes and tx of erosive and hemorrhagic gastritis: stress

A

-develop within 72 hrs of critical illness
-HUGE TRAUMA- vent, trauma, burn, shock, organ failure
-higher mortality rate
-want gastric pH > 4
-prophylaxis- H2 blocker to prevent
-treatment- high dose PPI

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5
Q

specific causes and tx of erosive and hemorrhagic gastritis: NSAID

A

-25-50% gastritis
-direct irritant
-symptoms in only 5% (poor correlation)
-alarm symptoms- anemia, blood in stool -> endoscopy
-pts that dont require EGD: d/c agent, take with meals, lowest dose
-treatment- PPI

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6
Q

specific causes and tx of erosive and hemorrhagic gastritis: alcohol

A

-dyspepsia
-nausea
-vomiting
-hematemesis
-tx- PPI

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7
Q

portal hypertensive gastropathy

A

-congestion of capillaries and venules of gastric mucosa and submucosa
-correlates with severity of liver disease
-often asymptomatic but may present as chronic bleed or rarely significant hematemesis
-tx- beta blocker or portal decompressive procedures

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8
Q

esophageal varices tx

A

beta blocker

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9
Q

nonerosive nonspecific gastritis

A

-dx is based on histologic assessment of bx at endoscopy
-H. pylori infection
-pernicious anemia

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10
Q

H. pylori gastritis

A

-spiral gram negative rod
-gastritis and ulcers
-resides below gastric mucus layer adjacent to gastric epithelial cells
-causes gastric mucosal inflammation with PMNs and lymphocytes
-WBC invasion
-increased in nonwhites and immigrants
-transmission is person to person ?, fecal-oral

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11
Q

acute vs chronic H. pylori gastritis

A

ACUTE
-nausea and abdominal pain
-may last days
-acute histologic gastritis with PMNS
CHRONIC:
-diffuse, mucosal inflammation (PNMs, lymphocytes)
-majority are asymptomatic and without sequelae

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12
Q

complications of H. pylori

A

-15% develop PUD (peptic ulcer disease)
-increase cancer risk- carcinogen
-increased rate of gastric adenocarcinoma
-increased rate of low grade B cell gastric lymphoma
-never really dx its very common and not symptomatic - pts dont come in for it

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13
Q

screening for H. pylori

A

-gastric marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma)
-Active peptic ulcer disease or past history of peptic ulcer if cure of H. pylori infection has not been documented
-Early gastric cancer
-Screening isn’t indicated in general population

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14
Q

diagnosis and treatment for H. pylori

A

-Noninvasive tests: Fecal antigen tests and Urea breath tests > 95% sensitive and specific
-Invasive testing: Endoscopy with bx of antrum and body is gold standard but expensive
-Treatment: Antibiotics and PPI (see PUD Slides)
-Conformation of eradication
-treating h pylori can improve lymphoma if causing

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15
Q

pernicious anemia

A

-Hereditary autoimmune disorder involving the fundic glands
-Achlorohydria and vitamin B12 malabsorption
-Inflammation and destruction of parietal cells that secrete intrinsic factor -> B12 cannot be absorbed without intrinsic factor
-Histologic features:
-Severe gland atrophy
-Intestinal metaplasia caused by autoimmune destruction of gastric fundic mucosa
-intestinal metaplasia- cancer risk

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16
Q

pernicious anemia labs dx and tx

A

-Low B 12
-B12 deficiency develops over time- means there is a long term issue
-low B12 for vegans as well- B12 comes from animals
-Parietal cell Ab are present in 90%
-Intrinsic factor Ab present
-Hypergastrinemia- gastrin tries to promote parietal cells - but it cant and keeps in increasing
-Adenocarcinoma is increased 3 fold
-Tx: B12 injections

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17
Q

peptic ulcer disease

A

-h pylori
-Break in gastric or duodenal mucosa
-Mucosal defense impaired or overwhelmed by aggressive luminal factors (acid, pepsin)
-Ulcer= 5mm diameter + through muscularis mucosa
-Duodenum > stomach
-Men > women
-Duodenum 30-55 yo
-Stomach 55-70 yo

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18
Q

ulcers risk factor and causes of ulcers

A

-smoking
-NSAIDs
-H. pylori
-zollinger-ellison syndrome- gastrin secreting tumors
-uncommon causes- CMV, crohn’s, lymphoma, meds (bisphosphonates)

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19
Q

duodenal ulcers

A

-most bacteria in gastric antrum
-more common
-increased HCL production and decreased duodenal mucosal bicarbonate production
-hypothesized that increased acid secretion gives rise to small islands of gastric metaplasia in duodenal bulb

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20
Q

gastric ulcers

A

-H. pylori association with gastric ulcers is less
-Forms at junction of body and antrum
-Hypothesized that chronic inflammation (gastritis) overwhelms mucosal defense mechanisms

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21
Q

NSAID use and peptic ulcer disease

A

-10-20% -gastric
-2-5% -duodenal
-3x more likely to have complications from ulcers -> Risk of complications varies
-ASA (aspirin) the worst- uncoated on empty stomach

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22
Q

peptic ulcer disease signs and symptoms

A

-Epigastric pain (hallmark) 80% - “gnawing, dull ache, hunger like”
-20% with complications (ie bleeding) are asymptomatic
-50% report relief with food (esp DU) and recurrence of pain 2-4hrs after eating
-Nocturnal pain- 2/3 DU, 1/3 GU
-Radiation of pain may reflect penetration or perforation

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23
Q

peptic ulcer disease physical exam and labs

A

-normal
-+/- mild localized epigastric tenderness on deep palpation
-+/- heme positive stool
-labs are normal in uncomplicated disease
-other labs:
-anemia
-serum gastrin high (Zolumger Elison)
-penetration or perforation -> leukocytosis (penetration or perf) and increased amylase

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24
Q

peptic ulcer disease differential dx

A

-dyspepsia
-atypical GERD
-biliary tract disease- cholecystitis, choledocholithiasis
perforated pts:
-esophageal rupture
-gastric volvulus
-rupture AAA

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25
Q

peptic ulcer dx

A

-Endoscopy is procedure of choice
* 5% of benign appearing GU are malignant
* Must show documented healing with f/u
endoscopy
* Duodenal ulcers are virtually never
malignant
* Bx for H. pylori and cancer until healed

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26
Q

peptic ulcer disease tx**** know this

A

-PPI- duodenal ulcer (4 weeks) and gastric ulcer (8 weeks)
-h. pylori eradication therapy 85% effective:
-PPI (omeprazole) 2x day, clarithromycin 500mg bid, amoxicillin 1g BID
-treat for 14 days and continue PPI x 4/8 weeks (8 weeks for gastric)
-d/c aspirin, NSAIDs if possible

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27
Q

diagnosis of peptic ulcer disease

A

-endoscopy- procedure of choice
-5% of benign appearing gastric ulcer are malignant- must show documented healing with f/u endoscopy
-duodenal ulcers are virtually nerve malignant
-dx for H. pylori

28
Q

zollinger-ellison syndrome

A

-caused by gastrin secreting gut neuroendocrine tumors (gastrinomas)
-hypergastrinemia and increased acid secretion
-rare <1% of PUD
-primary gastrinomas arise in pancreas (25%), duodenal wall (45%) or lymph node (5-15%) other locations or unknown primary (20%)
-80% arise within gastrinoma triangle: porta hepatis, neck of pancreas, and 3rd portion of duodenum
-Most are solitary or multifocal nodules that are potentially resectable
-2/3 are malignant
-1/3 have metastasized to liver at initial presentation
-25% are assoc with MEN 1 and difficult to resect

29
Q

zollinger-ellison syndrome

A

-90% have PUD with similar symptoms
-GERD common
-Diarrhea in 1/3, steatorrhea, wt loss
-ulcers dont usually cause diarrhea**
-Ulcers are usually solitary in duodenum, may be multiple
-Isolated GU do not occur-always multiple
-gastrinnnn

30
Q

who is screened with fasting gastrin?

A

-ULCERS
-Refractory ulcers, neg H pylori, or no NSAID use
-Giant ulcers (>2cm)
-Distal to duodenal bulb
-Multiple duodenal ulcers
-Freq recurrences
-Assoc with diarrhea
-Ulcers after ulcer surgery
-Ulcer complications
-Hypercalcemia, fam hx suggesting MEN1

31
Q

labs with zollinger-ellison syndrome

A

-Fasting gastrin > 150 pg/ml
-Median level is 500-700 pg/ml, 60%> 1000pg/ml
-Gastrin>1000 and acid hypersecretion is diagnostic -> For others can do a secretin stimulation test
-All patients must have PTH, prolactin, LH-FSH, GH to exclude MEN 1

32
Q

hypergastrinemia

A

-MUST measure gastric pH in pts with hypergastrinemia
-hypochlorhydria with increased gastric pH is more common cause of hypergastrinemia than gastrinoma so must measure gastric pH in pt with hypergastrinemia
-gastric pH > 3 implies hypochlorhydria

33
Q

diff dx for pernicious anemia and ZE syndrome

A

-ZE- high gastric and low pH- acidic
-pernicious anemia- high gastric- normal pH (partital cells dont work)
-pH is differential

34
Q

image and tx with zollinger-ellison syndrome

A

-somatostatin receptor scintigraphy with SPECT scan > 80% sensitive
-if neg EUS to detect small tumors
-tx-
-metastatic disease- control hypersecretion with PPI, resect liver metastasis, cryoblation, 30% > 10 year survival
-localized disease- resect before liver metastasis, 15 year survival > 95%

35
Q

complications of PUD

A

-GI hemorrhage
-ulcer perforation
-ulcer penetration
-gastric outlet obstruction- from inflammation

36
Q

GI hemorrhage

A

-50% UGI bleed from PUD
-80% resolve on own
-10% significant bleeding
-Signs and symptoms
-Melena (500cc), hematemesis (1000CC), hematochezia
-Nasogastric lavage shows “coffee grounds” or red blood -> If neg doesn’t r/o duodenal ulcer
-if you get bile from duodenum from NG lavage -> good sign there is no bleed (no coffee grounds or blood)

37
Q

GI hemorrhage labs and tx

A

-decreased HCT, increased BUN
-tx-
-IV PPI
-blood, platelets
-endoscopy- dx and therapeutic procedure -> cautery, epi, endoclip
-octreotide- reduces splanchnic blood flow and gastric secretions, efficiency unclear

38
Q

ulcer perforation

A

-5% of ulcer patients- Anterior wall of stomach or duodenum
-Consider ZE
-Sudden, severe abdominal pain
-Causes a chemical peritonitis- Appear ill, rigid abdomen, no bowel sounds, rebound tenderness
-labs- leukocytosis
-films- upright or decubitus films-free air in 75%
-CT of abdomen

39
Q

ulcer perforation tx

A

-40% seal on own with omentum or adjacent organs
-surgery
-H. pylori tx - fluids, IV PPI, abx

40
Q

ulcer penetration

A

-Posterior wall of duodenum or stomach may penetrate into pancreas, liver or biliary tree
-Change in pattern/intensity of their pain - Severe constant pain, radiates to back, unresponsive to antacids
-Physical + labs nonspecific, increased amylase (if affect pancreas)
-Endoscopy confirm ulcer but not diagnostic of actual penetration
-IV PPI, no improvement surgical tx

41
Q

gastric outlet obstruction

A

-rare
-pyloric outlet obstructed from so much inflammation
-2% of ulcer pts
-edema or narrowing of pylorus or duodenal bulb
-Most with known history of ulcers
-Symptoms- Fullness and heaviness with meals progresses to early satiety, VOMITING, wt loss
-physical- succession splash may be heard in epigastrum
-dx:
-nasogastric aspiration > 200cc foul smelling fluid is diagnostic
-more subtle obstruction is diagnosed with a saline load test or nuclear gastric emptying study

42
Q

gastric outlet obstruction treatment

A

-correct fluid and electrolytes
-IV PPI - oral after
-nasogastric decompression of stomach
-endoscopy in 24-72 hrs to define nature of obstruction, r/o gastric cancer, dilation of obstruction

43
Q

benign tumors of stomach

A

-epithelial polyps
-fundic gland or hyperplastic polyps (a lot of them) -> of no consequence
-epithelial polys can be caused by long term PPI
-adenomatous polyps 10-20%: not many
-rarely ulcerate
-premalignant potential
-must remove

44
Q

malignant tumors of stomach

A

-adenocarcinoma
-lymphoma

45
Q

adenocarcinoma

A

-most common gastric cancer
-mean age 63 year old, uncommon <40 years
-men > women
-> incidence in latinos, african americans, asian americnas
-antrum MC
-polypoid or fungating intraluminal masses
-ulcerating masses
-diffusely spreading through submucosa (poor prognosis)
-superficially spreading confined to mucosa or sub mucosa +/- lymph node (excellent prognosis)

46
Q

risk factors of gastric adenocarcinoma and physical exam

A

-H. pylori, diet (nitrates)
-pernicious anemia
-h/o partial gastric resection > 15 yo
PHYSICAL EXAM:
-rarely helpful- rarely palpate gastric mass
-+/- heme + stool

47
Q

gastric adenocarcinoma signs and symptoms

A

-asymptomatic till advanced and nonspecific
-dyspepsia
-epigastric pain
-anorexia, early satiety, wt loss
-GI bleed vomiting
-dysphagia

48
Q

signs of metastatic spread of gastric adenocarcinoma

A

-virchow’s node- left supraclavicular node
-sister mary joseph nodule- umbilical nodule
-blumer’s shelf- rigid rectal shelf (peritoneal cul de sac)
-krukenberg tumor- ovarian metastasis

49
Q

gastric adenocarcinoma dx findings

A

-lab- Fe deficiency anemia or anemia of chronic disease and increased LFTs (if spread to liver)
-endoscopy:
->50% yo with new onset dyspepsia or fail short term PPI therapy
-highly sensitive
-no screening program in US

50
Q

gastric adenocarcinoma differential dx and staging

A

-is it cancer or an ulcer?
-ulcerating gastric adenocarcinoma vs benign gastric ulcers
-repeat endoscopy done for all gastric ulcers to confirm healing
-staging- PET-CT- distant metastasis and invasion of adjacent structures
-EUS- superior to CT in determining depth of invasion and metastasis
-staging- TNM (tumor size, lymph node size, metastasis)

51
Q

gastric adenocarcinoma treatment (details not on exam)

A

-curative surgical resection:
-localized to distal 2/3 of stomach- subtotal distal gastrectomy
-proximal gastric cancer or diffusely infiltration disease -> total gastrectomy is done
-+/- chemo for micro metastasis

52
Q

gastric adenocarcinoma treatment (noncurative)

A

-palliative modalities: peritoneal, distant, metastasis, or local invasion of other organs
-palliative resection for bleeding or obstruction
-laser, stenting, embolization
-chemo- epirubicin, oxaliplatin and capecitabine (controversial)

53
Q

prognosis for gastric adenocarcinoma

A

-Overall 5-year survival 35%
-5-year relative survival rates for stomach cancer, according to SEER stages.
-Localized: 74.7 percent
-Regional: 34.6 percent
-Distant: 6.6 percent

54
Q

gastric lymphoma (dont need to know details)

A

-2nd most common gastric malignancy**
-> 95% are Non Hodgkins B cell lymphoma
-primary- originating in stomach or*
-nodal lymphoma- MC*
-Primary or a metastasis from nodal lymphoma- Distinguish for tx and prognosis
-60% of primary gastric lymphomas arise from mucosa associated lymphoid tissue (MALT)
-H. pylori infection may be an important risk factor especially for MALT lymphomas

55
Q

conditions that predispose to gastric lymphoma

A

-Helicobacter pylori-associated chronic gastritis
-Autoimmune diseases
-Immunodeficiency syndromes (eg, AIDS)
-Long-standing immunosuppressive therapy (ie, post-transplantation)

56
Q

signs and symptoms of gastric lymphoma

A

-Abdominal pain, wt loss, early satiety
-Bleeding (occult)
-Night sweats ABSENT in primary gastric lymphoma*

57
Q

gasric lymphoma dx

A

-PE- Often normal, +/- Palpable mass, Peripheral lymphadenopathy (advanced disease)
-labs- tend to be normal at presentation -> anemia, high ESR
-endoscopy:
-ulcer, mass, or difficulty infiltration lesion
-bx to confirm dx
-PET-CT (abdomen and chest) for staging
-EUS most sensitive for perigastric lymphadenopathy

58
Q

staging of gastric lymphoma (dont need to know details)

A

-not staged with TNM*
-use diaphragm as landmark*
-IE: limited to the stomach
-IIE1: stomach and contiguous lymph nodes
-IIE2: stomach and noncontiguous subdiaphragmatic lymph nodes
-III: stomach and lymph nodes on both sides of diaphragm
-IV : Hematogenous spread (stomach and one or more extra lymphatic organs or tissues)
-Prognosis of Primary Gastric Lymphoma
-> Long-term survival -> Stage I >85%, and Stage II 35-65%

59
Q

gastric lymphoma treatment

A

-Secondary nodal lymphomas-advanced and seldom curable
-Primary low grade gastric lymphomas are usually localized to stomach wall (stage IE) or adjacent ln (stage IIE) -> Excellent prognosis
-Test for H pylori in those with MALT-lymphoma and tx if + -> Complete regression in 75% of stage IE low grade lymphoma after tx H. pylori -> Neg for H pylori or fail tx : radiation
-Failures, recurrence, advanced stage disease (ie, stage III or IV disease), and those with diffuse large B-cell lymphoma -> Multiagent chemotherapy

60
Q

acute upper GI bleeding

A

-250,000 hospitalization/year
-above ligament of trietz
-mortality rate 7-10%
-> 50% over 60 year old -> ulcers caused by NSAIDs
-die from complications of underlying disease not exsanguination
-self limited in 80%
-presentation:
-hematemesis
-melena - dark stool
-hematochezia (10% cases) - rushing through

61
Q

acute upper GI bleeding causes

A

-in order of frequency- many can cause acute or chronic bleed
-PUD- 50% of bleeds, incidence declining
-portal HTN- 10-20%, bleeding varices (esophageal most common), hypertensive gastropathy, if untreated -> 50% varices rebleed
-mallory-weiss tear- 5-10%, associated with alcohol and retching (less than 10% have continued or recurrent bleeding)- self limiting
-vascular anomalies (vascular ectasias, angiodysplasias)- 7%; throughout GI tract
-gastric neoplasms- 1%
-erosive gastritis- typically superficial, more commonly associated with chronic bleed
-erosive esophagitis- rare

62
Q

initial treatment of acute upper GI bleed

A

-Stabilization: Assess hemodymamics = severity of blood loss
-IV- Two 18 gauge IVs in patients with significant bleed
-collect labs- CBC, INR (bleeding/clotting time), creatinine, LFTs, cross-matching
-NG Tube placement: confirmation of bleed with coffee grounds or bright red blood -> neg in 10% especially if duodenal source
-cant rule out duodenal source with NG tube

63
Q

acute upper GI bleed: blood

A

-Amount is based on vitals, labs, aspirate
-Maintain HCT 25-30%
-Transfuse if actively bleeding
-May give platelets
-<50,000 or if on aspirin or clopidogrel regardless of count
-May give FFP (fresh frozen plasma) if coagulopathy

64
Q

clinical predictors of rebleeding and death: acute upper GI bleed

A

-> 60yo
-Comorbid illness
-Systolic BP <100mm Hg
-Pulse >100 beats/min
-Bright red blood on aspiration or rectal exam- huge sign

65
Q

low risk acute upper GI bleed

A

-Reliable patients without comorbidities
-Normal hemodynamics
-No hematemesis or melena within 48hrs
-Negative NG lavage
-Normal labs
-Do not admit and evaluate as outpatient
-Low to Moderate Risk: those that arnt high risk, Admitted to medical floor, Endoscopy in 12-24 hrs

66
Q

acute upper GI bleed high risk

A

-Active bleeders
-Hematemesis or bright red blood on NG aspirate
-Shock
-Poor response to fluids
-Serious comorbidities
-Advanced liver disease
-Admit to ICU
-Endoscopy within 12 hours

67
Q

post acute upper GI bleed

A

-Subsequent Evaluation and Treatment:
-Upper Endoscopy:
-All patients have endoscopy within 24 hrs
-Identifies source
-Risk of rebleeding
-Therapy-if needed- Cautery, injection, endoclips, Meds
-pharm therapy-
-IV PPI
-octreotide- decrease splanchnic blood flow and portal pressures -> given until liver disease and increased portal pressure ruled out
-other tx- intra arterial embolization (rare) and/or TIPS - hepatic vein portal vein shunt

Gastroenterology (20 decks)

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