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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

specific causes and tx of erosive and hemorrhagic gastritis: alcohol

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

esophageal varices tx

A

beta blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

nonerosive nonspecific gastritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

peptic ulcer disease differential dx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
peptic ulcer dx
-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
26
peptic ulcer disease tx****** know this
-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
27
diagnosis of peptic ulcer disease
-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
zollinger-ellison syndrome
-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
zollinger-ellison syndrome
-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
who is screened with fasting gastrin?
-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
labs with zollinger-ellison syndrome
-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
hypergastrinemia
-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
diff dx for pernicious anemia and ZE syndrome
-ZE- high gastric and low pH- acidic -pernicious anemia- high gastric- normal pH (partital cells dont work) -pH is differential
34
image and tx with zollinger-ellison syndrome
-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
complications of PUD
-GI hemorrhage -ulcer perforation -ulcer penetration -gastric outlet obstruction- from inflammation
36
GI hemorrhage
-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
GI hemorrhage labs and tx
-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
ulcer perforation
-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
ulcer perforation tx
-40% seal on own with omentum or adjacent organs -surgery -H. pylori tx - fluids, IV PPI, abx
40
ulcer penetration
-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
gastric outlet obstruction
-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
gastric outlet obstruction treatment
-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
benign tumors of stomach
-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
malignant tumors of stomach
-adenocarcinoma -lymphoma
45
adenocarcinoma
-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
risk factors of gastric adenocarcinoma and physical exam
-H. pylori, diet (nitrates) -pernicious anemia -h/o partial gastric resection > 15 yo PHYSICAL EXAM: -rarely helpful- rarely palpate gastric mass -+/- heme + stool
47
gastric adenocarcinoma signs and symptoms
-asymptomatic till advanced and nonspecific -dyspepsia -epigastric pain -anorexia, early satiety, wt loss -GI bleed vomiting -dysphagia
48
signs of metastatic spread of gastric adenocarcinoma
-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
gastric adenocarcinoma dx findings
-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
gastric adenocarcinoma differential dx and staging
-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
gastric adenocarcinoma treatment (details not on exam)
-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
gastric adenocarcinoma treatment (noncurative)
-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
prognosis for gastric adenocarcinoma
-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
gastric lymphoma (dont need to know details)
-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
conditions that predispose to gastric lymphoma
-Helicobacter pylori-associated chronic gastritis -Autoimmune diseases -Immunodeficiency syndromes (eg, AIDS) -Long-standing immunosuppressive therapy (ie, post-transplantation)
56
signs and symptoms of gastric lymphoma
-Abdominal pain, wt loss, early satiety -Bleeding (occult) -Night sweats ABSENT in primary gastric lymphoma*
57
gasric lymphoma dx
-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
staging of gastric lymphoma (dont need to know details)
-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
gastric lymphoma treatment
-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
acute upper GI bleeding
-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
acute upper GI bleeding causes
-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
initial treatment of acute upper GI bleed
-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
acute upper GI bleed: blood
-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
clinical predictors of rebleeding and death: acute upper GI bleed
-> 60yo -Comorbid illness -Systolic BP <100mm Hg -Pulse >100 beats/min -Bright red blood on aspiration or rectal exam- huge sign
65
low risk acute upper GI bleed
-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
acute upper GI bleed high risk
-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
post acute upper GI bleed
-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