SURGERY COURSE AUDIT- Stomach + Pancreas DR.

VEQUILLA – March 2020

-Increase aggressive factors: Hcl -Decreased defensive factors:

COME AT
acid secretion , alcohol use, mucosal bicarbonate secretion,
ME, Surg! smoking, NSAID use, H pylori mucus production, cell renewal
FEU-NRMF PGI
Batch 2019-2020 and blood flow impeded by cardiac
SURGERY COURSE AUDIT- Pancreas & Stomach problem.
-80-95% of H. pylori will cause duodenal ulcer, while 75% gastic ulcers ->
The
.
following are a set of notes from Dr. Vequilla before
Angels….errr COVID started trending big time & before we were all associated with H pylori
set in a Long-ass PGI vacation. For further & detailed notes, you can
check out Schwartz or Surgery Platinum. The ones with this: -H.pylori produce urease, local mucosal immune response, gastrin increased
are the ones he had mentioned mostly. acid secretion and D cell reduction (D cells secrete somatostatin which
reduces gastric secretion & emission of gastrointestinal hormones, such as
The ones with this: were taken from Surg Plat/elsewhere – but secretin and gastrin)
only a few. That doesn’t mean you shouldn’t read/check out Surg
-NSAID absorption-> COX inhibition-> prostaglandin synthesis decreased->
Plat or Schwartz! Happy Reading if ever!
mucosal protection failure. If nonselective-> can inhibit cox 1 and 2
COX 1: responsible for pain and inflammation
Most common cause of bowel obstruction: post-operative adhesions COX 2: defense barrier of stomach, for neutral pH

STOMACH: Chronic NSAID use-> peptic ulceration

A. Gross Anatomy
• The stomach is commonly found in the left upper quadrant of the
abdomen, surrounded by the
colon, liver, pancreas, spleen, and sometimes, the kidney
• It is a mango·shaped organ that begins just distal to the lower esophageal
sphincter and ends at the
pyloric orifice to open into the proximal duodenum
• The right border is the lesser curvature, and the longer left border is the
greater curvature
• It has an average capacity of approximately l liter in an adult. When
distended, the gastric rugae
flatten, so it can hold as much as 4 liters of food
A. Pathophysiology
• Focal defects in the gastric or duodenal mucosa which extends into the
submucosa or deeper
• Ultimately caused by an imbalance between the action of acid and mucosal
defense
• Classification based on anatomic location & pathophysiology:
• Types I and IV: associated with normal or low acid output
• Types II and Ill: associated with gastric acid hypersecretion
(similar to duodenal ulcers)
Gastric ucler: most ulcers consequence of H pylori: Johnson classification

Diagnosis of gastric disease

1.) EGD (Esophagogastroduodenoscopy) -> Mc dx test

->Especially for alarming symptoms that indicate need for upper endoscopy-
> weight lost, recurrent vomiting, dysphagia, bleeding, anemia

2.)X-rays: plain abdominal x-ray for gastric perforation->

pneumoperitoneum, or delayed gastric emptying

3.) Double contrast upper GI series-> better than EGD at elucidating gastric
diverticula, fistula, tortuosity, stricture location and size of hiatal hernia Clinical manifestation of ulceration:
Type 1: lesser curvature mid epigastric abdominal pain
4.)CT scan and MRI Type 2 and 3: acid hypersecretors Pain can be tolerable -> but gets worse
Know difference between the two: Perforation: typically sudden onset
5.) Endoscopic ultrasound->new**-> local staging of gastric adenocarcinoma
is accurate-> Can stage patient preoperatively

Stomach Gastric??Disease??-> clinical staging pre-op, and post op:

pathologic staging

6.) H. pylori Testing -> majority of problems-. 2ndary to h pylori

->Positive test, accurate of h pylori ( pag positive believe it), if negative,

don’t believe it as it is unreliable -> always manage patient as positive for h
pylori

Test for h pylori: histo exa of anthral mucosal biopsy-> gold standard->
biopsy of anthrum-> hy pylori

PEPTIC ULCER DISEASE (PUD)

MC symptoms —> pain, weight lost, early satiety, and anorexia -> some with
GERD->-> erosions that extend to muscularis mucosa
Risk Factors: aggressive factors & decreased defensive factors

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 SURGERY COURSE AUDIT- Stomach + Pancreas DR. VEQUILLA – March 2020

Duodenal: Gastric: Truncal vagotomy

-more common incidence Less common Selective vagotomy Truncal vagotomy and antrectomy-> to reduce
- first part of duodenum, and lesser curvagure of stomach Parietal vagotomy acid production
-can acute or chronic Chronic Truncal vagotomy: left anterior, and right posterior
-Rare malignancy Benign vs malginant Vagus Nerve:
-Relieved by food (So “kain ng kain” ) Worsened by food **left trunk of vagus nerve: seen in anterior of stomach
** Right trunk of vagus nerve: seen in posterior of stomach
Diagnosis: invasive and non-invasive Ulceration:
1.) Radiography: -> if ulceration on ->If duodenum, no more biopsy, just patch
- less expensive & 90% accurate stomach-> must have it; if duodenal ulcer
-If testing for accuracy: radiography BIOPSY then patch ->Trim down then patch
-Disadvantage is there’s no biopsy -> Stomach, why biopsy? ->In duodenum-> no biopsy coz chance of
-> can detect free abdominal air when perforation is suspected Because it may be -> coz chance of malignancy is low/rare in
2.) Flexible upper endoscopy: Most reliable method, visual diagnosis, can do secondary to cancer small intestine
biopsy of H. pylori -> If > 3cm perforation-> can resect
Non-Invasive Tests: Small intestine is alkaline & transit time very fast, free radicals have a
3.) Urea breath test: sensitivity -> 90% sensitivity/ Specificity-86-92 % -> difficult time to transform them , also, small intestine is sterile, and has lots
easily accessible of IgA coz of peyer’s patches
4.) Stool antigen-> sensitivity: 90% -> good dx tool -> most cost-effective
Duodenal-> may result to Gastric outlet obstruction 2ndary to ulcer
Treatment -> may show Acute inflammation of the duodenum
Type 1: wedge resection or gastrectomy without vagotomy, coz it’s not an ->Mechanical obstruction may delay gastric emptying & produce anorexia
acid hypersecretor
Types 2 and 3 Always with vagotomy -> excise ulcer! For perforated peptic ulcer disease: GRAHAM patch repair
Type 4 is too high , difficult to manage
Type 5, stop NSAIDs ; depending on how large ( maybe if >3 cm

-targeted against H. pylori -> reduce acid level Malignancy

Risk factor: gastric cancer (Surg Plat, same with what he said)
• Family history o Previous gastric surgery (for non
• Diet high in nitrates (e.g., cancerous conditions)
preserved, smoked, and cured • Atrophic gastritis
foods) and salt o Cigarette smoking
o Diet low in vitamins A and C o Adenomatous gastric polyps
• Familial polyposis and adenomas o Menetrier's disease
o Hereditary nonpolyposis colon o Pernicious anemia
cancer (HNPCC) o Type A blood
o Helicobacter pylori infection
-H pylori**-> major cause of stomach cancer
-Stomach cancer-> more common in men
-Aging-> sharp increase after age 50 ( that’s why screening at 50 yrs old)
-Ethnic: Asian/pacific islander-> raw food
-Obesity: overweight or obese-> cardia
-Previous stomach surgery:
-Pernicious anemia: risk fact: cells in stomach make intrinsic factor which is a
substance needed to absorb B12
-Inherited cancer syndrome

Manifestations: (From Surg Plat, similar to what he said)

Surgical treatment: Symptoms Signs
Intractable: parietal cell vagotomy =/- antral resection o Usually produces no specific symptoms when • Physical examination
superficial and potentially surgically curable is nonspecific
o Lack of early pathognomonic symptoms leads to a o Patients with
delay in diagnosis
advanced tumors may
Some symptoms:
present with a palpable
• Weight loss + anorexia + early satiety: most
abdominal mass,
common
cachexia, or bowel
• Abdominal pain, nausea, vomiting, bloating,
obstruction
abdominal mass
• UGIB (occult, anemia, hematemesis,
melena), dysphagia
• Paraneoplastic syndrome, Trosseau
syndrome, Acanthosis nigricans

Symptom’s: mc: weight loss-> also malnutrition

Signs: palpable abdominal mass

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 SURGERY COURSE AUDIT- Stomach + Pancreas DR. VEQUILLA – March 2020

If cancer spreads via lymphatics: B. Location

Diagnostics:
1.) Serologic markers: a lot but none are diagnostic for stomach
2.) Endoscopy: Gold standard (visualize + biopsy) -
3.)Barium studies: false negative in 50% not used anymore
4.)Endoscopic Ultrasound: MOST RELIABLE NON SURGICAL METHOD TO
DEPTH OF INVASION
->can see invasion of tumor in diff layers
->more acute than CT for T stage: If want to stage based on the T-> EUS is the
best option ( non surgical)
Staging **to determine Depth of invasion
5.) CT scan: for metastasis
6.)PET: more sensitive than CT for detection of distant metastases, for
detecting LNs but uber expensive
So you do it one by one! First, EGD with biopsy (So biopsy first!) -> once with
results, do CT SCAN
Biopsy, if with result, do ct scan,
• The pancreas is retroperitoneal, behind the stomach at the level of the L1-
L2 junction
• It is related to the omental bursa superiorly, the transverse mesocolon
anteriorly, and the greater sac inferiorly
ACUTE PANCREATITIS
-Initiated by several factors, 80-90% of time secondary to biliary tract
obstruction (gallstone), others are idiopathic
-Zymogens activated -> cascades of events
->A diagnosis of exclusion (usually when patient has epigastric pain-> hx & pe
+ imaging-> must exclude pancreatitis
A. Pathophysiology
Main patho: it EATS up itself because have activation of digestive zymogens,
but exact patho is still unknown.
• Acute inflammatory process of the pancreas with variable involvement of
other regional tissues or remote organ systems
• Regardless of the primary etiology, the final common event is activation of
pancreatic proenzymes into nascent enzymes within the pancreas itself
• Once pancreatic parenchymal damage occurs from auto digestion, acute
inflammatory cell infiltration begins and is accompanied by the release of
cytokines, further aggravating the inflammatory reaction
B. Clinical Manifestations
1. Signs and Symptoms of Acute Pancreatitis
Clinical presentation: Severe Epigastric Pain
Bowel sounds decreased or absent
Hemorrhagic pancreatitis-> cullen’s sign

Malignant neoplasm of stomach:

Adenocarcinoma - Majority ( -95%) of cancer in the stomach are
adenocarcinomas
linitis plastica: diffuse-type gastric cancer ( submucosa & muscularis ) ->
Entire region of stomach
->on barium studies, stomach does not expand Diagnostics:
Location of tumor: mc in stomach antrum, followed by body • Diagnosis is based on two or more of the following criteria:
Treatment o Severe abdominal pain
Stage 1 -3 curable o Serum amylase or lipase more than three times (3x) higher than the upper
4: palliative limit
Lymphadenectomy: If ever it will be asked: o Contrast-enhanced computed tomography (CECT) findings of acute
Do- remove less than all relevant N1 nodes pancreatitis
D1 : remove N1 nodes only
D2: removes all N1 & N2 Serum Markers:
D3: removes all N2 & N3 Nodes Serum Amylase-> Increases immediately ->remains elevated to 3-5 days
before returning to normal, not specific
Residual tumor class: If question is which rises up right away-> amylase
Ro: no demonstrable residual tumor But serum LIPASE is more specific
R1 :microscopically demonstrable residual tumor
R2: tumor removed but..some still remained-> macroscopically visible tumor Ultrasound: if gallstone is suspected-> this is requested
PANCREAS CT Scan with bolus IV contrast media: Gold standard for detecting and
SURGICAL ANATOMY: Pancreas assessing severity of pancreatitis
Gross Anatomy
• The pancreas is an endocrine and exocrine organ approximately 15-20 cm
long and weighs about 75
to 100 g in an adult
• Embryologically, it is formed by the fusion of a ventral bud and a larger,
dorsal bud, as a result of gut rotation
• Five parts: head, neck, uncinate process, body, and tail
How to assess severity? Will determine how we manage:
Ranson’s criteria ( 1974 ). Early identification On admission and at 48 hours
• Historical score in which parameters at hospital admission and at 48 hours
are used to define mortality
• Ranson severity score is an indication of severe acute pancreatitis

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 SURGERY COURSE AUDIT- Stomach + Pancreas DR. VEQUILLA – March 2020

• Disadvantage: can be read only at 48 hours

• Parameters at hospital • Parameters at 48 hours: Some briefly delay after 72 hrs
admission: o Fall in hematocrit of> 10% High risk patients: elderly-> ERCP first
o Age>55 years • Fluid sequestration >6 L
o WBC count >16,000/mm3 • Hypocalcemia Chronic Pancreatitis:
o Blood glucose level >200 mg/dL • PaO2 <60 mmHg MC Cause-> Alcoholism
• Serum LDH >350 IU/L • Increase in BUN by >5 mg/dL after Majority consume alcohol
• Serum AST >250 IU/L intravenous fluid hydration -> hard to manage
• Base deficit> 4 mmoi/L Pain is mc system- epigastric -> persist for hours or days
** in the boards they seldomly ask about interpretation. If panc exocrine capacity is <10%
<2 signs-> 0 % -diarrhea, steatorrhea
5 signs= 10-20% -Good appetite
>7 signs= >50% mortality
How managed? Majority medical therapy -> analgesic
Questions for Ransom is more of recall, Problem with this is you need 2
whole days to test all 11 signs, sometimes before 48hrs KO na patient. Anti-secretory therapy: somastatin-> chronic pancreatitis but very expensive
-> Others resort to surgery-> stents on pancreatic duct
That’s why they came up with APACHE II: used by IM
advantage: assess severity Pancreatic neoplasms
Common questions: what is more in predicting / assesses severity-> apache 2 • Pancreatic carcinoma: adenocarcinoma of the pancreas arising from the
• ICU-based scoring system to calculate morbidity and mortality duct cells (other types: cystadenocarcinoma, acinar cell carcinoma)
• APACHE severity score: 8 is an indication of severe acute pancreatitis • Pancreatic cancer ranks 13"' in incidence but 8'" as a cause of cancer death
• Cumbersome to use and very complex; however in comparison with the worldwide
Ranson's and Glasgow systems, it can be calculated and recalculated daily • It is the 11"' most common cause of new cancer deaths in 2010 for both
Parameters or chronic health points:APACHE II sexes (Philippine Cancer Facts
o Age >45 years and Estimate) representing 2% of all cancer deaths
• WBC count <3,000 or> 14,900 I mL • Males > females
o Rectal temperature <36°C or> 38.4°
o MAP <70 or >109 mmHg Etiology:
o HR <70 or >109 bpm • Cigarette smoking (contributes to the development of 20% to 30% of
• RR <12 or >24 per minute pancreatic cancers)
o pH <7.33 or >7.49 • Increased age (about 80% of cases occur between ages 60 and 80)
o Na concentration <130 or >149 mM o Chronic pancreatitis
- K concentration <3.5 or >5.4 mM • Increased saturated fat intake
o P02 <70 or >200 mmHg • Exposure to nonchlorinated solvents
• Creatinine <0.6/100 mL or >1.4 mg/100mL
• Hematocrit <30% or >45.9% 2x -3 x fam hx. ( parent or sibling)
o Low GCS Smoking inc the risk 2x
Diets high in fat and low in fiber fruits and veggies
Other Diagnostics:
Biochemical Markers: mild severe discrimination Most common pancreatic endocrine neoplasm
-> CRP marker of choice in clinical settings
90% insulinomas, -> majority benign, 10% malignant
Management: -> you don’t need to remove pancreas, enucleation is enough
-NPO
-Hospitalization for observation, imaging to assess severity: goals of admit,
NPO to rest GI tract to rest the GI tract, Gastrinoma: usually found at the pasarro’s triangle ( Boundaries: Cystic duct,
Replace fluid and electrolytes coz of third spacing border of 2nd and 3rd parts of duodenum, junction of neck and body of
-Assess CVP for severe acute pancreatitis pancreas)
-> address severe pain
STAGING:
-> severe acute pancreatitis: if with signs of infection-> give antibiotics Don’t focus too much on staging -> try to know the principles behind staging
Mild & moderate: antibiotics are not usually given especially on mild, Ex: small and large intestine, tumor size not based on the size of tumor
moderate (depend) Gastro intestinal tract, colon/rectum -> depth of invasion
-breast ca ex: size of the tumor
Treatment:
NGT-> to lessen gastric load Tumor Marker for malignancy: CA199
Antibiotic therapy not proven to have value -> mostly not given -Goal: before and after requested, prognosis -> #1 predictor ( pag sobrang
taas, you can actually predict that this is an aggressive type of tumor, or baka
Infection: abscess ( can be seen in CT scan ) stage 4 na siya, #2 prognosis ( baka metastatic na siya)
Drained surgically or percutaneously
Majority-> percutaneous

Biliary Pancreatitis: gallstone most common cause-> when admitted ->

gallstone-> immediate surgery 48-72 hrs. before pinapatagal patient-> cause
of problems so need to remove
Ex: mataas preoperative, and mataas pa rin after operation-> meron pang source
of pancreatic tumor

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 SURGERY COURSE AUDIT- Stomach + Pancreas DR. VEQUILLA – March 2020

Baka mali staging , baka early cancer, then stage 4 na pala siya or mali
management, after surgery-> it should go down , request again after
months-> you want focus on progression in the management

CA 19-9 -> mucin associated carbohydrate antigen that can be detected in

the serum of patients with panc cancer
-> elevated in 7% of patient with panc cancer
-> Also, elevated in 10% of patients with benign diseases of pancreas, liver
and bile ducts

CT with dynamic enhanced contrast -> diagnostic

MDCT (multidetector dynamic contrast enhanced CT scan) -> with contrast
enhanced to diagnose stage
-> dx and staging tests of choice for pancreatic cancer
-> accuracy of predicting unrespectable disease is 90-95%
Accuracy to predict unresectable disease

CT findings: that tumor is unresectable -> invasion of hepatic or superior

mesenteric artery, enlarged lymph node invasion and outside boundaries of
resection, ascites, and distant metastasis
SMV-> can be included in specimen; patent-> can be included in resection Surveillance:
Monitored with frequent pe and lab tests -> inc CA 19-9
Jaundice: pancreatic cancer: gastric outlset obstruction Ct scans are typically ordered after a course of chemotherapy is completed
or when a rising CA19-9 or new symptoms suggest recurrence
SMV/Portal Vein-> invasion of superior mesenteric vein or portal vein is not a
contraindication to resection as long as veins are patent -> okay to include in Pseudocyst-> most common complication of pancreatitis (chronic)
specimen Treatment for pseudocyst:
Infection suspected-> aspirated & not drained( coz patient may be more
Palliative surge and endoscopy septic ) by ct or us guided FNA, may also do Internal drainage: connect
pseudocyst with stomach -> cysto gastrostomy
3 clinical problem in advanced pancreatic that require palliation
1.) Pain
2.) Jaundice-> bile duct stent/ biliary bypass
3.) Duodenal obstruction -> enteric bypass

Chemotherapy:
Radiation> Gemcitabine-> survival is improved by 1 to 2 months

Surgical resection:
-> tissue dx before panc duodenectomy is not essential
-> wont know if malignant or benign; will only complicate management, coz
management will not differ
Ex: bukol sa pancreas, whether benign or malignant

If Stage iv with metastasis-> that is the time you need tissue biopsy

BALIKTAD siya.
If Pancreatic Cancer without metastasis, no need for biopsy
But if metastatic-> do biopsy

Surgical resection: pancreticoduodenectomy

** Findings contraindicating resection: liver metastasis, celiac lymph invasion

peritoneal implants, hepatic minor lymph node involvement

Findings not contraindicating resection :

-> invasion at duo or distal stomach ( they are actually removed during
operation)
->Involved peri pancreatic lymph nodes along portal-hepatic area

"Sometimes you need a little

wishful thinking just to keep on
living."-Misato Katsuragi
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