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GI II Exam II AP > Abdominal Pain and Pancreatic Disease (Darrow) > Flashcards

Abdominal Pain and Pancreatic Disease (Darrow) Flashcards

1
Q

A 62 year old morbidly obese diabetic female presents with acute epigastric pain and mental confusion. She takes thiazides for hypertension. Pulse is 110 bpm with respirations of 30. She drinks alcohol occasionally. Result of ultrasound are equivocal related to the obesity. Serum triglycerides are 600 mg/dL. Amylase is 1500 U/dL (50-150) with lipase of 1200 U/L (10-140). WBC is 19,000 with elevated LDH and AST. ALT is 175 IU/L (8-32). Glucose is 350 mg/dL. BUN is 25 mg/dL with creatinine of 1.8 mg/dL. Most likely cause of pancreatitis in this patient would be:

CMV.
autoimmune. 
lipids.
thiazide.
alcohol.
gallstones.
pancreas divisum.
obesity.

The next day the BUN has increased from 25 to 35 mg/dL, the C-RP is 250 mg/dL*, creatinine is 2.2 mg/dL, and the hemoglobin has dropped from 12 to 8 grams. The abdomen is shown. The patient now has:

A. heparin induced thrombocytopenia
B. Cullen’s and Grey Turner’s sign (may be erythema only)
C. paniculitis
D. ruptured aortic aneurysm
E. Nikolsky’s sign

What facts and markers of this case point to a poor prognosis?

A

obesity adds a large complication to pancreatitis and also produces hypoxia by limiting respiration (BMI >30 = poor prognosis)

The patient now has B. Cullen’s and Grey Turner’s sign (may be erythema only)

What facts and markers of this case point to a poor prognosis?

If you have to pick one test to follow pancreatitis –> BUN- if this keeps increasing then you have a problem

patients are hemoconcentrated when they come in

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2
Q

What is the definition of acute Pancreatitis?

need 2 of 3 criteria

A

Characteristic Abdominal pain- epigastric going to the back, relieved my maintaing a supine position or leaning forward and not moving

Amylase or lipase > 3 times normal

Characteristic findings on CT

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3
Q

What is the significance of obesity in pancreatic disease?

A

Central obesity is a metabolically active organ associated with Barret’s epithelium, adenocarcinoma of the esophagus and, especially in diabetics, pancreatic cancer.

Obesity also makes acute pancreatitis worse by causing local circulatory changes in peripancreatic fat and produces hypoxia by limiting respiration.

So BMI > 30 kg/m2 = poor prognosis

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4
Q

What else can elevate the amylase?

A 
Amylase:
     Bowel problems (obstruction, perforation or infarction)
 Ectopic production

 Lung, fallopian tube and salivary gland secretion(mumps)

 Macroamylasemia (low urinary amylase b/c its too big to get through the kidneys) (normal serum lipase)

 Renal insufficiency

 Trauma (ERCP)
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5
Q

what are the labs used to diagnose acute pancreatitis

A

lipase- this is the best to use!
amylase
ALT
urine for trypsinogen activation peptide (TAP)

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6
Q

What causes acute pancreatitis?

A

Obesity

Obstructive cause- gallstones

Drugs and toxins- alcohol (raises AST >ALT) , sulfa drugs, tetracycline, metronidazole

Metabolic - hyperlipidemia, hypercalcemia

Infectious- EBV, CMV, MAC mumps

Genetic

  • hereditary pancreatitis (PRSS1) (SPINK1)
  • CF

Vascular- shock

Autoimmune - IgG4***, PSC, ANA, Celiac

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7
Q

what is the PRSS1 gene pancreatitis pathophysiology

A

Activating mutations in PRSS1 or inactivating mutations in CASR may result in elevated trypsin levels, and ethanol may act as a trigger to pancreatitis by elevating calcium levels.

The cystic fibrosis transmembrane conductance regulator (encoded by the gene CFTR) eliminates trypsin
by flushing the pancreatic duct. Inflammation caused by excess trypsin leads to up-regulation of the serine protease inhibitor Kazal type 1
(encoded by the gene SPINK1), which blocks trypsin, prevents further activation of trypsinogen, and limits further tissue injury

see slide 8

increased calcium drives the system- leading to pancreatitis

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8
Q

Ranson Criteria

what is a bad criteria

A

(score of 3 or more = bad!) and predicts a severe course complicated by pancreatic necrosis

At admission - 
Age (over 55)
WBC (>16x10^3)
Glucose (>200)
LDH (>350)
AST (>250)

At 48 hours, development of other findings indicates a worsening prognosis

  • BUN >5 (among other things)
  • arterial PO2 <60
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9
Q

APACHE II

A
  • (score of 8 or more = bad!) used to access severity;

Rectal temp, mean arterial pressure, HR, RR, FiO2, arterial pH, Na, K, Cr, Hct, WBC.

Score of 8 = necrosis.

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10
Q

BISAP***

A

BUN > 25 mg/dL

Impaired mental status *disorientation, lethargy, somnolence, coma or stupor

> 2 SIRS criteria- how do we know a pt has this? Pulse is over 110, resp over 30, WBC 19,000

Age > 60

Pleural effusion present or not

score of 3 or more = bad sign. (Obesity should also be considered as a point - BISOAP.)

Dr. darrow likes this one

it is a criteria used for pancreatitis

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11
Q

CRP in pancreatitis

A

Other markers

C-reactive protein (at 48 hrs) > 150 mg/dL – marker for pancreatic necrosis. (PMN elastase peaks at day 1).

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12
Q

Creatinine in pancreatitis

A

Creatinine > 1.8 mg/dL at 48 hours – marker for necrosis.

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13
Q

hematocrit in pancreatitis

A

Hemacrit > 44% at admission and 24 hours – necrosis.

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14
Q

HAPS score

A

the Harmless Acute Pancreatitis Score score

absence of rebound tenderness

normal hemacrit

normal creatinine

*** predicts a nonsevere course.

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15
Q

calcium in pancreatitis

A

Calcium - decreased with albumin extravasation or saponification.

hypercalcemia CAUSES pancreatitis

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16
Q

AMYLASE - what does this stand for in terms of clinical presentation of acute pancreatitis

A

Acute abdominal pain to the back

Mid-abdominal staining (Cullen’s and Grey Turner signs)

Yellow (jaundice –stones or cancer)

Lipase, Left sided pleural effusion or atelectasis (left side b/c the pancreas is on the left)

Amylase (>1000) (poor test compared to lipase)

Sentinel loop and colon cut off signs

Emesis and nausea

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17
Q

what needs to be done by the 4th day of acute pancreatitis

A

CT!
On the 4th day, after adequate hydration, CT scan reports gallstones in the GB along with pancreatic necrosis

wait to do CT by 3rd or 4th day (at least in a mild case)

*The first test for suspected gall stone pancreatitis should be US

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18
Q

What is the CT severity index?

A

CT severity index – better than
RANSOM and APACHE II for
severity and mortality!

Contrast CT
No necrosis            0 pts
Up to 30%              2
30-50%                   4
> 50%                      6

Noncontrast CT:
Normal pancreas 0
Pancreatic enlargement 1
Pancreatic inflammation and/or peripancreatic fat 2
single acute peripancreatic fluid collection 3

Two or more acute peripancreatic fluid collections or retroperitoneal air 4

19
Q

What is the significance of pancreatic necrosis and what does it indicate?

how do you measure multi-organ dysfunction

A

Necrotizing pancreatitis – indicates a 50% chance of infection (abscess) and 30% chance of mortality from MOF.

Complications of Acute Pancreatitis and Prediction of Severity.

  1. RANSOM (> 3) and APACHE II (> 8) scores.
  2. MOD (lipotoxicity and GI bacterial products) – BP < 90, pO2 < 60 (ARDS), Cr > 2 (ATN), GI bleed
20
Q

What complications may ensue with acute pancreatitis ?

A

Multiorgan dysfunction (lungs, kidneys, GI, heart/lungs)

  1. Systemic complications:
    DIC (Platelets < 100,000, Fibrinogen < 1g/L, FSP > 80 ug/mL),

hypocalcemia with Ca < 7.5 mg/dL (muscle spasms).

  1. Local complications:
    a. Infected fluid collections or pancreatic necrosis within 1-3 weeks(abscess) – often
    complicated by splenic vein thrombosis (gastric varices) and left pleural effusions.b. Pseudocyst – more than 4-6 weeks - if over 6 cm = surgery? Watch for pain,
    rupture, hemorrhage or abscess.c. Ascites.
    d. Chronic Pancreatitis.
21
Q

what do you do if there is evidence of progression of acute pancreatitis

A

Fine needle aspiration and drainage for C and S and institution of antibiotics (Imipenem)? Prophylactic – if > 30% necrosis and no more than 14 days of administration.

ERCP with endoscopic sphincterotomy? especially if there are gallstones

If there is evidence of progression, the patient should be placed on a standard enteral** formula through a feeding tube placed 60 cm below the ligament of Trietz. This may improve the integrity of the bowel and decreases chance of infection due to translocation of bacteria.- but don’t start within the first 3 days

Antibiotics prophylactically- not protocol but darrow does this

22
Q

what are the complications of acute pancreatitis

A
  1. ATN (usually 24 hours)
  2. Necrotizing pancreatitis – indicates a 50% chance of infection and 30% chance of mortality from MOF – so needs fine needle aspiration and surgical drainage if infected
  3. ARDS – usually in 3-7 days
  4. SIRS eventuating in organ dysfunction (lipotoxicity and GI bacterial products) or MOF
  5. Hypocalcemia
  6. Infected pancreatic necrosis (abscess) - often complicated by splenic vein thrombosis (gastric varices) and left pleural effusions
  7. Pseudocyst – more than 6 weeks - if over 6 cm = surgery? No epithelial lining.
  8. Ascites
  9. Chronic Pancreatitis
23
Q

how do you treat mild pancreatitis

A

NPO
NG suction for ileus
Low fat diet

24
Q

how do you treat severe pancreatitis

A

IV fluids
Calcium gluconate

FFP, albumin?

ERCP with sphincterotomy for stones
Enteral feedings after 3 days
Imipenem for infected necrosis
Necrosectomy  for infected necrosis (step up approach – percutaneous followed by retroperitoneal drainage).
Drainage of pseudocysts (when needed)
25
Q

A 35 year old male alcoholic presents with a history of 3 bouts of
pancreatitis. He complains of epigastric pain, weight loss and bulky
stools over the past 5 weeks. A random glucose is found to be
250mg/dL with no prior history of diabetes. You send the patient
for an abdominal xray expecting to find a (an):

“colon cut off sign”.
“sentinal loop”.
air in the biliary tree.
calcified pancreas.
left sided pleural effusion.
A

calcified pancreas.

26
Q

what are the causes of chronic pancreatitis

A

Alcohol ***and smoking

Surgery, radiation, vagotomy

Hyperparathyroidism

Obstructive

Autoimmune – Increases IgG4, ANA, antibodies to lactoferrin – associated with Sjögrens, PSC, IBD, Celiac disease

Cystic fibrosis(genetic) - transmembrane regulator gene mutations.

Hereditary types – SPINK1, PRSS1, etc.

27
Q

Chronic pancreatitis presentation:

A

Presentation:

 1. Calcification, Cancer
 2. Pain
 3. Steatorrhea and osmotic diarrhea
 4. Weight loss
 5. Vitamin deficiency (maldigestion of proteins 
      and fat)
 6. Diabetes (may be brittle with loss of insulin 
     and glucagon)
28
Q

how do you diagnose chronic pancreatitis

A
  1. Xray – diffuse speckled calcification
    2. US or CT – ductal dilation, calcification and cystic lesions
    3. ERCP – most sensitive and specific***
    4. MRI with cholangiopancreatography
    1. 24 hour fecal fat > 10 g/day = + test.
    2. Secretin/cholecystokinin secretion test (with tube in distal
      duodenum and assay for HCO3, trypsin, lipase, etc.)- not common
    3. Decreased fecal chymotrypsin or elastase.
    4. Elevated ANA, IgG4, antibodies to lactoferrin.
    5. Trial of pancreatic enzymes.
29
Q

How does one differentiate pancreatic from intestional steatorrhea?

A 
small intestine
-D-xylose (<4gm in urine) = + for intestinal cause
Schilling test
Breath tests
-small bowel Xray and biopsy
pancreas 
-secretin test
-fecal elastase*** 
-Abdominal X-ray
Ultrasonogram
CT scan
ERCP
30
Q

what is the d-xylose test and what do the results mean

A

25 gm of D-xylose is taken by mouth.
If less than 4 gm shows
up in a 5 hr urine collection, this indicates mucosal malabsorption
(xylose not absorbed) OR bacterial overgrowth (xylose fermented or
“eaten” by the bugs, so none absorbed).

In pancreatic insufficiency, d- xylose absorption (which requires no enzyme activity) is not effected, so that the urine shows adequate d-Xylose to be present.

31
Q

how do you treat chronic pancreatitis

A

Pain- drug addiction

Low fat diet

36,000 units of lipase/meal with H2 blocker (pancrelipase/Creon)

Surgical ductal decompression for pain relief prednisone or azathioprine

Watch for cancer

32
Q

A 65 y/o female presents with severe periumbilical pain with only mild tenderness upon palpation. She reports a history of postprandial periumbilical pains. She has sitophobia and has had significant weight loss. She also reports dyspnea, paroxysmal nocturnal dyspnea, nausea, vomiting, and mild hematemesis. She has had two prior MIs and recurrent CHF.
Physical exam also shows abdominal bloating with decreased bowel sounds. She has carotid and femoral bruits. WBC is 18,500 mm3. HCO3 is 18 meq/L.

What is the most likely diagnosis?

A

ischemic bowel disease

superior mesenteric stenosis

33
Q

what are the benign causes of pneumatosis intestinalis

A

Pulmonary: COPD, Asthma, Bronchitis, CF
Systemic disease: Scleroderma, SLE
Intestinal causes: Crohns, Celiac disease, Enteritis, PUD, Ileus, Diverticulitis
Iatrogenic: Postsurgical anastomosis, Endoscopy
Medications: Corticosteroids, Chemotherapeutic agents, Lactulose
Organ transplantation
Primary pneumatosis: Idiopathic, Pneumatosis cystoides intestinalis

34
Q

life threatening causes of pneumatosis intestinalis

A

Intestinal ischemia

Mesenteric vascular ischemia***

Intestinal obstruction
Colitis
Toxic megacolon
Trauma

you end up with air b/c bacteria take over and form gas!

35
Q

what is the presentation of abdominal or intestinal angina

A

Older age.
Diffuse arteriosclerosis of splanchnic vessels with abdominal bruit.
Seen on doppler ultrasound.
Episodic midabdominal pain 30 minutes after a meal – may last for up to 3 hours.

May have sitophobia* (fear of food), nausea, diarrhea, bloating, steatorrhea, and villous atrophy.

36
Q

what is SIRS

A

Temp >38 C (100.4)

Heart rate >90

RR >20

WBC >12,000

37
Q

how does necrotic tissue of a pancreas show up on CT

A

looks darker compared to viable pancreatic tissue

38
Q

any person who is over age 50 who develops diabetes with no family history or risk factors, especially if slender, should be evaluated for cancer of what?

A

pancreas

39
Q

what is pneumatosis intestinalis

A

Pneumatosis intestinalis is a radiological sign which is highly suggestive for necrotizing enterocolitis. Pneumatosis intestinalis refers to gas cysts in the bowel wall.[1]

40
Q

how does acute mesenteric ischemia differ from ischemic colitis ?

A

Acute mesenteric ischemia

  • pt is toxic (confused, fever, abd distention)
  • severe pain *(out of proportion to PE findings), less tenderness
  • bleeding is uncommon until late
  • Angiography or CT angiogram or MRA
  • usually associated with heart disease, embolic
  • immediate surgery
  • thumbprinting

Ischemic colitis

  • pt is NOT toxic
  • mild abd pain, tenderness
  • bloody diarrhea
  • colonoscopy
  • associated with arteriosclerosis
  • conservative treatment
41
Q

what are bacteriodes associated with

A

thrombophlebitis (mesenteric venous thrombosis)

42
Q

what causes acute intermittent prophyria

-young woman, acute peripheral or CNS dysfunction, recurrent psych issues, hyponatremia

porphobillinogen in the urine

A

deficiency of phophobilinogen deaminase

43
Q

A 16 y/o Armenian male presents to the ER with fever and abdominal pain. He had an appendectomy one year ago, at which time a normal appendix was removed. PE shows a pleural rub over the right posterior chest. The scrotum is tender and there is a rash on both ankles. WBC and sed rate are increased. This patient has:

A

Familial mediterranean fever- autosomal recessive

pt’s lack a protease in serosal fluids that normally inactivates IL-I, IL-8, and chemotactic complement factor 5A.

symptoms typically present before age of 20

peritoneal attacks occur with sudden onset of fever, abdominal pain, abd tenderness with guarding or rebound.

arthritis, pleuritis, peritonitis

The function of “pyrin” has not been completely elucidated, but it appears to be a suppressor of the activation of caspase 1, the enzyme that stimulates production of interleukin 1β. Thus bad pyrin = Inc IL beta = amyloid AA. Likewise increased Il 8 = WBC mobbing tissues!

many pt’s die of chronic amyloid production and deposition in their kidneys!! renal failure

GI II Exam II AP (4 decks)

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