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Clin Med III > Exam 2 CM3 Pancreatic dz > Flashcards

Exam 2 CM3 Pancreatic dz Flashcards

1
Q

What is the basic anatomy and function of the Pancreas

A

Divisions: Head, neck, body, tail
Vascular Supply: Celiac axis, SMA
Innervation: ANS
Function: Exocrine (amylase, Lipase, Protease) and Endocrine (insuline, Glucagon)

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2
Q

How is the Pancreas an Exocrine gland? What stimulates pancreatic secretions?

A
  • Amylase, Lipase and Protease
  • Pancreatic juice that contains electrolytes, bicarb and digestive enzymes to neutralize gastric acid and provide basic environment for pancreatic enzymes
  • Stimulated by: Gastric acid, CCK, Vagal stimulation
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3
Q

How is the Pancreas and Endocrine gland

A

Insulin (response to blood glucose , increase perm of cell membrane to glu)
Glucagon (stimulate glycogenolysis and Gluconeogenesis)

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4
Q

What is Acute Pancreatitis and what causes it

A

Definition: Inflammatory disease characterized by autodigestion of the pancreas by proteolytic enzymes prematurely activated within the pancreas

Etiology: Alcohol, *gallstones** together comprise 75% cause;
Other:
Blunt trauma, ERCP,
Drugs/toxins: (thiazide diuretics, estrogen, sulf, valproate, 6-MP, anti HIV meds, scorpion venom, salicylates)
Metabolic: Hypertrig (>1000), HyperCa
Vascular: ischemia, vasculitis
Infections: Viral (mumps, CMV, EBV, HIV, Varicella0
Genetic
Idiopathic up to 30%

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5
Q

What is the OLDCARTS presentation of Acute pancreatitis (abdominal pain)

A 
Onset: acute, may be after eating
Location: midepigastric, radiates to back
Duration: Constant
Character: Steady, Boring
Aggravators: lying supine
Relievers: sitting and leaning forward (less pressure on retroperitoneal pancreas)
Tx: 
Sx: Anorexia, N/V, abdominal distension
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6
Q

Besides OLDCARTS, what are other presenting indications of acute pancreatitis?

A

Vitals: fever, tachycardia, Tachypnea (watch PO2)
Skin: Jaundice (biliary obstruction/cholestasis)
Abd: hypoactive or absent BW, significant midepigastric tenderness w or w/o guarding or rebound)
CULLENS SIGN (periumbilical ecchymosis)
GREY TURNER SIGN: flank ecchymosis

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7
Q

What are Cullens sign and Grey Turners sign and what do they suggest

A

Cullens: periumbilical ecchymosis (the U’s together)
Grey Turners sign: flank ecchymosis

Suggest Acute pancreatitis

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8
Q

Ddx of Acute Pancreatitis

A 
Perforated PUD
Acute Cholecystitis
Bowel Obstruction
Diverticulitis (usually sigmoid though)
Pneumonia (lower lobes), MI, AAA (leaking(, mesenteric ischemia
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9
Q

What lab findings are consistent with acute pancreatitis

A

Elevated amylase and lipase (>3x normal)
Leukocytosis, elevated HCT (hemoconcentration/dehydration)
Elevated Cr, mild elevated Glucose (insulin not working)
HypoCa
Transient LFT elevations ( ALT >150 and/or bilirubin suggests gallstone pancreatitis)
ABGs: O2 may be decreased (metabolic acidosis)

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10
Q

What imaging studies can help dx Acute pancreatitis

A

Plain films: Normal vs. ileus; limited role
UTZ: gallstones** initial TOC
CT: pancreatic edema or inflammation, calcifications, pseudocysts, necrosis, abscess
MRCP
EUS: Latest and greatest sensitivity

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11
Q

What might an abdominal plain film reveal in a pt with acute pancreatitis (what can it help r/o)

A

Limited role in dx, but may show sentinel loop of dilated bowel, or calcified gallstones in RUQ
R/o obstruction, ileus, perforation (free air)
*CXR likely beneficial to r/o pulmonary infiltrates of pleural effusions

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12
Q

What is a CT scan helpful for in dx acute pancreatitis

A

CT is used for dx: enlargement, heterogenous enhancement, blurring of fat planes and fat stranding

  • Identifies severity of dz
  • Identifies complications: necrosis, pseudocysts, abscess, hemorrhage
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13
Q

How might and MRI of MRCP help dx acute pancreatitis?

A

MRI/MRCP similar to CT, but some advantages including: lower risk nephrotoxicity, increased characterization of fluid collections, necrosis, abscess, pseudocysts, and better view of biliary and pancreatic ducts (helps if CBD sotne not seen on CT or UTZ but biliary pancreatitis is expected)

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14
Q

What are indications for ERCP re. Acute Pancreatitis

A

Visualization of biliary and pancreatic ductal anatomy
May obtain cytology or biopsy
May be therapeutic (stone removal, stent insertion, sphincterotomy)
Can see common bile duct stricture with dilation of hepatic ducts
Extrahepatic biliary obstruction most often due to: gallstones, pancreatitis, pancreatic CA)

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15
Q

Extrahepatic biliary obstruction is most often due to what

A

Gallstones, pancreatitis, pancreatic cancer

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16
Q

How do you manage/treat acute pancreatitis

A
  1. Almost all are admitted
  2. Tx underlying cause
  3. Diet: NPO (if prolonged NPO, enteral pref over Parenteral); can advance diet when no longer on IV narcotics (clear liquids full liquids low fat diet)
  4. Hydration – IV fluids are KEY!!
  5. Pain control: Meperidine (Demerol)
  6. +/- ABX: controversial but indicated when infected necrosis is concern: Imipenem (Primaxin) penetrates pancreas
  7. Identify complications early: decrease urine output/rising creatinine, respiratory failure, worsening condition (pain, fever, leukocytosis)
  8. Monitor lab values closely
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17
Q

What are some complications of Acute pancreatitis

A

Local:
Pseudocyst (collection of fluid & debri; no epithelial lining; fibrotic wall)
Pancreatic abscess: infected pseudocyst or necrotic area (suspect with fever, WBC, clinical deterioration)
Pancreatic Necrosis: area of non viable tissue
Hemorrhage
Ascites: from leaking duct or pseudocyst

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18
Q

What is pancreatic Pseudocyst

A
  • Occurs in 10% of pt with acute pancreatitis
  • May cause: abdominal pain, early satiety, N/V
  • Can spontaneously resolve or continue to enlarge
  • Complicated by rupture, hemorrhage or infection
  • Surgery vs drainage: indicated if sx or infected (abscess?)
19
Q

What systemic complications can arise from acute pancreatitis

A 
Pulmonary: resp failure/ARDS, pulm edema, pleural effusions, atelectasis
Renal: renal failure
Cardiac: HypoTN/shock
GI: Ileus
Metabolic: hyperglycemia, hypoCa
20
Q

How do you determine prognosis for acute pancreatitis

A 
Ranson’s criteria
*add initial signs and delayed (48h) signs together: mortality related to number of signs present
0-2 = <1% mortality
3-4 = 15%
5-6 = 40%
7-8 = 100%
* overall mortality is 10-15%
21
Q

What are the initial and delayed signs in Ransons criteria for determining acute pancreatitis prognosis

A 
INITIAL
Age >55
WBC >16,000
Glu > 200
AST >250
LDH >350
DELAYED
HCT drop >10%
BUN  >5 mg/dL
Ca <3.2
Fluid sequestration 4-5 L
22
Q

What is APACHE

A

Acute Physiology and Chronic Health Eval (APACHE)
*alt way to assess mortality with improved sensitivity and specificity
Markers: Temp, MAP, HR, RR, PO2, pH, Na, K, HCT, WBC, Cr
Age of Pt
Chronic health problems (HF, renal failure, cirrhosis)

23
Q

How do you prevent Acute pancreatitis from recurring

A 
Tx underlying cause
Biliary Pancreatitis – ERCP if CBD stone, elective CCY
Alcoholic pancreatitis – stop drinking
HyperTAG – diet and lipid lowering meds
Drug induced – dc offending med
24
Q

What is chronic pancreatitis and what does it cause

A

Repeated episodes of acute inflam leading to permanent structural damage and ductal obstruction
Gradual loss of pancreatic function leads to exocrine and endocrine insufficiency

25
Q

What causes Chronic pancreatitis

A 
Alcohol most common (70-80%)
Repeated episodes of acute pancreatitis (10% develop chronic)
Cystic Fibrosis
Hereditary
Idiopathic
26
Q

Presenting s/sx of chronic pancreatitis

A

Predominant: epigastric pain (80%)
Early: episodic similar to acute pancreatitis
Late: may become continuous
Aggravators: alcohol, high fat meals
Gradual loss of pancreatic function: exocrine and endocrine insuff - malabsorption

27
Q

In chronic pancreatitis, exocrine insufficiency leads to

A

MALABSORPTION
Steatorrhea
Weight loss (secondary to fear of eating and malabsorption)

28
Q

In chronic pancreatitis, endocrine insufficiency leads to ..

A

DM
Sx of diabetes (polys)
Typically Insulin dep
Brittle DM bc alpha and beta cells affected

29
Q

What is the classic triad for chronic pancreatitis

A
  1. DM (due to endocrine dysfunction)
  2. Steatorrhea (due to exocrine dysfunction)
  3. Pancreatic calcifications
30
Q

What are some dx studies for chronic pancreatitis

A

Normal or slightly elevated amylase and lipase
Bilirubin and alk phos may be mildly elevated
glucose
Secretin stimulation test: abnormal if 60% of exocrine function is lost (cumbersome, expensive, not used often)
Increase fecal fat testing (prefer 72 hr)

31
Q

What will plain films show in pt with chronic pancreatitis

A

Scattered calcifications (30% of pt)

32
Q

What is a CT scan helpful for in pt with chronic pancreatitis

A

Calcifications, ductal dilation, pseudocysts

33
Q

How is MRCP helpful in dx chronic pancreatitis

A

Good image of pancreatic and biliary ducts, used with increasing freq for eval and dx

34
Q

What is the gold standard for chronic pancreatitis dx and what will it show

A

ERCP is gold standard (but more invasive so used less often)
Will show “chain of lakes” beaded appearance

*EUS can also be used w/o risk of pancreatitis

35
Q

How should you help manage/tx Chronic pancreatitis

A
  1. Behavior (stop ETOH, small and low fat meals, smoking cessation)
  2. Early Identification of complications
  3. Mgmt of DM – insulin
  4. Tx of malabsorption (pancreatic enzyme supplements – Enteric coated CREON or non enteric coated Viokase that should be taken with PPI or H2 antagonist)
  5. Pain relief: start with enzymes, then consider amitriptyline (TCA) or SSRI; then if needed, Narcotics (long acting better ie MS contin v Fentanyl patch)
  6. Other pain relief options:
    - endoscopic procedures (ductal dilation, stenting)
    - Nerve blocks or celiac plexus (ethanol or steroids)
    - Lithotripsy?
    - Surgical resection: used when CA suspected or when other tx failed
36
Q

What are typical dx statistics of pancreatic carcinoma

A

4th leading cause of CA death
Majority Pt dx late in dz (so we should have low index of suspicion, only 15% are resectable lesions)
Majority of tumors are in HEAD of pancreas

Pathology: most are adenocarcinomas (>85%)
**IMPORTANT: 15% of cysts are neoplasms
Refer all pt with pancreatic lesion to GI/surgery

37
Q

What are risk factors for Pancreatic CA

A

M>F, increase incidence in Af Americans, risk age >45

Smoking, alcohol, chronic pancreatitis, DM, obesity, family hx

38
Q

Pancreatic CA presentation

A 
Vague and nonspecific sx (bloat)
Abdominal pain is most ommon presenting sx, gnawing epigastric pain radiating to the back
Early satiety/anorexia
Wt loss, jaundice
Pruritis, acholic stools, dark urine
Acute Pancreatitis
Steatorrhea
39
Q

Pancreatic Carcinoma PE findings

A

GEN: cachectic, bitemporal wasting
SKIN jaundice
EYES: icterus
LYMPH: left Supraclavicular (VIRCHOWS NODE)
ABD: ascities, palpable non tender gallbladder (courvoisier’s sign)

40
Q

Lab findings consistent with Pancreatic CA

A

Elevated Bilirubin and alk phos (obstructive jaundice)
Milde in amylase and lipase
Mild anemia
Glucose intolerance
CA-19-9 (normal <37) tumor marker for pancreas; 80-90% sensitive and specific (elevations relative to tumor size)

41
Q

Dx studies for Pancreatic CA

A

UTZ: dilated CBD, pancreatic head mass

CT scan/ helical CT: dx/detects over 80% of masses; TOC for staging dz and identifying eligibility for resection

MRCP: as sensitive as ERCP w/o complication risk but cant obtain tissue sample

ERCP: classically considered primary dx tool, look for double duct sign (stricture of both CBD and Pancreatic duct)

EUS (endoscopic UTZ): eval local tumor involvement, vascular involvement and best for tissue dx (FNA biopsy)

42
Q

How do you treat Pancreatic CA

A

Surgical resection – whipple procedure (Pancreaticoduodenectomy) is the only potential cure
*very difficult

43
Q

Palliation of sx re pancreatic CA

A 
Biliary Obstruction (most will have pruritis, biliary stent)
Wt Loss (Cachexia – possible exocrine insufficiency)
Pain (narcotics – chemo vs radiation)
44
Q

Prognosis of Pancreatic CA

A

Mortality 5yr survival <5%, poor prognosis esp if unresectable (die within year)

Clin Med III (5 decks)

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