Disorders of the Pancreas Flashcards
1
Q
3 main parts of the pancreas
A
head
body
tail
Lies transversely in the posterior part of the upper abdomen
2
Q
what enzymes of the pancreas are considered exocrine
A
- pancreatic protease - proteins: trypsin, chymotrypsin
- lipase - TG
- amylase - carbohydrates
3
Q
what are the endocrine hormones
A
- insulin
- glucagon
4
Q
multiple spherical groups of epithelial cells embedded as nodules in the endocrine pancreas which are surrounded by a rich capillary plexus. Most numerous in the tail and make up 2% of the pancreas.
A
Islets of Langerhans
5
Q
3 cells of the Islets of Langerhans
A
- Alpha (15-20%): secrete glucagon which raises blood glucose levels by accelerating conversion of liver glycogen into glucose.
- Beta (60-70%): secrete insulin which influences carbohydrate metabolism enabling glucose utilization
- Delta (5-10%): secrete somatostatin which inhibits insulin and glucagon secretion
6
Q
what secrete pancreatic enzymes into the pancreatic duct while epithelial cells lining the small pancreatic ducts secrete bicarbonate.
A
Acinar cells
proteases, lipase, amylase, bicarb
7
Q
what neutralizes acid coming into the small intestine from the stomach?
A
bicarb
8
Q
what is the leading cause of gastrointestinal-related hospitalization in the US
A
Acute Pancreatitis
9
Q
The peak age of incidence of acute pancreatitis occurs when?
A
in the 50s-60s; however, mortality increases with age.
10
Q
MC causes of acute pancreatitis
A
- gallstone (MCC)
- heavy alc intake - not binge
- other: HTG, Hypercalcemia, Trauma (Surgery or ERCP), Meds (sulfa drugs), Infections, Genetic Mutations
- 20% are “Idiopathic”
- Smoking, high dietary glycemic load, abdominal adiposity increase the risk pancreatitis, with older age and obesity increase the risk for a severe course
11
Q
what may reduce the risk of developing acute pancreatitis
A
Vegetable consumption, dietary fiber, using statins
12
Q
what could specifically reduce the risk of non biliary pancreatitis
A
coffee
13
Q
pathophys of acute pancreatitis
A
- Edema or obstruction at ampulla of Vater (CBD meets PD) - Reflux of bile in pancreatic duct
- Premature or overactivation of pancreatic enzymes
- Autodigestion - accepted pathogenic theory resulting when proteolytic enzymes are activated in the pancreas acinar cell compartment rather than the intestinal lumen.
14
Q
what are the phases od the pathophys theory of acute pancreatitis
A
-
Initial phase: intrapancreatic digestive enzyme activation and acinar cell injury.
- acinar cell injury is the consequence of trypsin activation. - second phase: activation, chemoattraction, and sequestration of leukocytes and macrophages in pancreas = enhanced intrapancreatic inflammatory reaction
-
third phase: effects of activated proteolytic enzymes and cytokines, released by the inflamed pancreas, on distant organs.
- Digestion of cellular membranes causing proteolysis, edema, interstitial hemorrhage, vascular damage, coagulation necrosis, fat necrosis, and cellular necrosis & death .
15
Q
Pathophysiology Of Gallstone Induced acute pancreatitis
A
- Early event is blockade of secretion of pancreatic enzymes while the synthesis of them continues
- autodigestive injury to the gland
- normal defenses of the pancreas are overwhelmed by pancreatic enzymes, particularly trypsin
- Continuing synthesis of trypsin = activation of other enzymes = pancreatic autodigestion and damaging of acinar cells -
Microcirculatory injury happens d/t pancreatic enzymes that damage the vascular endothelium
- vasoconstriction, capillary stasis, decreased oxygen sat, progressive ischemia
- changes lead to increased vascular permeability and swelling of gland
activated pancreatic enzymes + microcirculatory impairment + inflammatory mediators = rapid worsening of pancreatic damage and necrosis
16
Q
Pathophysiology in alcohol induced
A
- Alcohol increases synthesis of enzymes by pancreatic acinar cells to make digestive and lysosomal enzymes
- The exact mechanism is unknown
- genetic and environmental factors is unknown
- why only a small proportion of alcoholics develop pancreatitis are unclear
17
Q
- Epigastric abdominal pain that radiates to the bacK - Worsens with activity and lying supine; Improves with leaning forward
- N/V
- Weakness, sweating, anxiety
- Pain can persist several hours/days
this presentation is for what dx?
A
acute pancreatitis
18
Q
what historial features may a pt have that may be the cause of acute pancreatitis
A
- Hx of binge or heavy drinking just before sx.
- Hx of biliary colic if d/t gallstone obstruction - Reaches max. Intensity in gallstone pancreatitis in 10-20 min
- Hx of heavy fatty meal just prior to sx if due to “overactivation” of pancreatic enzymes.
19
Q
PE findings of acute pancreatitis
A
- Epigastric Tenderness
- Distended abdomen with absent bowel sounds if with ileus secondary to inflammation
- Fever
- Tachycardia
- Tachypnea
- Hypotension
- Pallor, cool clammy skin
- Jaundice - if ampulla of Vater blockage
- Mass palpable d/t inflamed pancreas
20
Q
ecchymotic discoloration observed in the periumbilical region
A
although nonspecific, suggest the presence of retroperitoneal bleeding
Cullen’s sign - acute pancreatitis
21
Q
ecchymotic discoloration observed along the flank
A
Grey-turner’s sign - although nonspecific, suggest the presence of retroperitoneal bleeding
22
Q
classifications for acute pancreatitis
A
-
Acute interstitial edematous pancreatitis
- Acute inflammation of pancreatic parenchyma and peripancreatic tissues, but W/O tissue necrosis -
Necrotizing acute pancreatitis
- Inflammation associated WITH pancreatic parenchymal necrosis and/or peripancreatic necrosis
23
Q
Labs for acute pancreatitis
A
- Serum amylase
- Rises w/n 6-12 h of the onset; nml w/n 3-5 d
- Elevation of 3x ULN -
Serum Lipase - Most sensitive
- Elevation of 3x nml
- Rises 4-8 h of onset of sx; normal w/n 8-14 d
- Elevations occur earlier and last longer compared with amylase - CBC - leukocytosis
- CMP - elevated glucose, lyte abnml (N/V), alkaline Phos and ALT/AST (biliary pancreatits)
- lipids - HTG (severe hyperlipidemia)
- UA - proteinuria, glycosuria
24
Q
which lab study is more sensitive as compared with amylase in patients with pancreatitis secondary to alcohol
A
serum lipase
25
imaging for acute pancreatitis
1. plain X-ray
- “**Sentinel Loop**” - Dilated air filled small intestine near the pancreas
- “**Colon Cut-Off Sign**” - Gas filled segment of transverse colon abruptly ending near pancreas due to functional spasm of descending colon secondary to pancreatic inflammation
- Possible Ileus
2. US - more helpful for stone in suspected biliary pancreatitis
3. CT - enlarged and inflammation; complications: pseudocysts and abscesses
26
abrupt onset of **deep epigastric pain, often radiation to back**
Hx of previous episodes, often related to alcohol
N/V, sweating, weakness
abd tenderness and distention and fever
leukocytosis, elevated serume amylase and lipase
what are you suspecting?
acute pancreatitis
27
how to dx acute pancreatitis
1. Has **characteristic abd pain** and elevation in **serum lipase/amylase 3x ULN** = No imaging required
2. Noncharacteristic abd pain, amylase/lipase <3x ULN, OR dx is uncertain = CT WITH contrast
- Also to r/o other causes of acute abd pain
28
assessments of severity for acute pancreatitis
* **_Ranson’s Criteria_**
* _APACHE II_ (Acute Physiology and Chronic Health Evaluation)
* _BISAP_ (Bedside Index for Severity in Acute Pancreatitis) - Simplest
29
what is the Ranson's criteria?
help predict the prognosis of acute pancreatitis.
_5 signs can be documented at admission_:
1. > 55 y/o
1. Blood glucose > 200 mg/dl
1. Serum LDH > 350 IU/L
1. AST > 250/UL
1. WBC count > 16,000
**3+ = severe**
_Rest of Ranson’s signs are determined within 48 hrs of admission_:
1. HCT decrease > 10%
1. BUN increases > 5 mg/dl
1. Serum Calcium < 8 mg/dl
1. PaO2 < 60mm Hg
1. Base deficit > 4 mEq/L
1. Estimated fluid sequestration > 6 L
0-2 = 1%
3-4 = 16%
5-6 = 40%
7-8 = 100%
30
what is BISAP
Simple 5 Point Scale - utilized during first 24 hrs
1. BUN > 25 mg/dL
1. Impaired mental status
1. Systemic Inflammatory Response Syndrome (SIRS)
1. Age > 60
1. Pleural effusion
3+ = increased mortality and increased risk of complications
31
complications of acute pancreatitis
1. Prerenal acute kidney failure - severe volume depletion; Inadequate hydration = Acute Tubular Necrosis (ATN)
2. Ileus - ?d/t retroperitoneal inflammation?
3. Necrotizing Pancreatitis
4. Pancreatic Abscess
5. SIRS
6. Pleural effusion
7. ARDS - 3-7 d after onset; in pts requiring large volumes of fluid to maintain blood pressure and volume status
8. Chronic Pancreatitis
9. abscess
10. Acute peripancreatic fluid collection
11. Pancreatic Pseudocyst
32
tx for mild acute pancreatitis
1. **Admit to hospital; “Rest” pancreas;** resolves in 3 d
- NPO (Complete bowel rest)
- NG tube w/ vomiting and/or abd distention
- **IV fluids**: early and aggressive - _esp 1st 12-24 hrs_
- **IV analgesia**: opioids (Hydromorphone, fentanyl), Meperidine (Demerol) - TOC Historically
- IV antiemetics and/or NG tube
- Bed Rest
2. Once sx resolve: **Clear liquids, then low fat diet** as tolerated; return of BS, largely pain-free
3. *gallstone* → _cholecystectomy once recovered_ - preferably during same visit
33
caution when using Morphine for mild disease of acute pancreatitis as it may cause ?
sphincter of Oddi spasm
34
tx for severe disease of acute pancreatitis
1. **Admit to ICU, same supportive measures as acute**
- ***large volume fluid resuscitation*** (6-8L/d)
- If patient can’t tolerate oral foods for 5 d = enteral feeding
2. Treat all associated complications: Hyperglycemia, Hypocalcemia, Hypomagnesia, Hypotension, Hypoxemia (with ARDS)
3. Surgical consult - for biliary pancreatitis, abscesses, necrotizing, or pseudocysts.
4. Abx ONLY if infection (abscess) - **Imipenem**
35
how would an abscess complication from acute pancreatitis present?
* Suppurative process characterized by rising fever, leukocytosis, and localized tenderness
* Epigastric mass usually +6 wks into course of acute pancreatitis
36
how would Acute peripancreatic fluid collection
from acute pancreatitis present?
* Fluid collection develops in early phase, no well defined wall
* Generally resolve spontaneously within 7-10 days
37
how would a Pancreatic Pseudocyst
from acute pancreatitis present?
* Encapsulated collection of **fluid with well defined inflammatory wall**
* Occur >4 wks after onset
* Fluid collections **outside of the pancreas**
* Observation if asx; drainage if sx
38
CT findings that are predictive of mortality of acute pancreatitis
* Normal CT or mild pancreatic edema = good prognosis
* Peripancreatic fluid - increase mortality 10% (increases likelihood of abscess and volume depletion)
* Necrotizing pancreatitis - increase mortality 30% (increase risk of multi-organ failure)
39
A syndrome involving inflammation, fibrosis, and loss of acinar and islet cells
Chronic Pancreatitis
pancreatic type abdominal pain, steatorrhea, derangements in pancreatic function and visible damage on imaging studies
40
causes of chronic pancreatitis
1. **Alcoholism - MC**
1. Smoking alone or synergistically with alcohol
1. Recurrent bouts of biliary pancreatitis
1. Severe Hypertriglyceridemia
1. Autoimmune
1. Genetic mutations - 15%
1. Idiopathic - 25%
1. Obesity
1. **CF (MC in Child)** - Thick mucus also clogs the pancreas and hinders the release of digestive enzymes. About 90% develop exocrine pancreatic insufficiency
41
pathophys of chronic pancreatitis
1. **Persistent inflammation = permanent structural damage**
- May have stricturing or dilatation of pancreatic duct
- Leads to decline in both exocrine and endocrine function
42
presentation of chronic pancreatitis
1. Chronic, steady or intermittent **epigastric, LUQ pain- radiates to back**; worse 15-20 min after eating
1. Anorexia, weight loss
1. N/V, Constipation, flatulence
1. **Pancreatic insufficiency**
- Exocrine - malabsorption symptoms and steatorrhea
- Endocrine - overt DM late in course
1. **Intermittent acute “attacks”**
- Attacks may last only a few hours or as long as 2 weeks
- Considered on a continuum with acute/relapsing pancreatitis/chronic
- Pain may eventually be continuous evolving from episodic
1. ~65% of pts have either osteopenia or osteoporosis
43
what is the most common reason for hospitalization in chronic pancreatitis
pain
A change in pattern or sudden worsening of pain should also prompt a search for a complication of chronic pancreatitis - pseudocyst, Duodenal or biliary obstruction, Secondary pancreatic carcinoma
44
The cause of pain in chronic pancreatitis is due to ?
increased pressure, ischemia, and inflammation of the pancreas
45
lab findings for chronic pancreatitis
1. Amylase, Lipase - slightly elevated or nml
- d/t focal disease and fibrosis resulting in decreased abundance
- Markedly elevated during attacks
2. LFT’s - Elevated if biliary cause
3. UA/serum glucose - Glycosuria
4. Genetic testing, autoimmune workup (ANA, IgG levels, specific antibodies)
46
imaging for chronic pancreatitis
1. Plain X-rays - Calcifications in 30% of pts
2. **DX: CT (MC)** - image entire pancreas and pancreatic duct (Pancreatic enlargement, pseudocysts, calcifications, atrophy, ductal dilation)
3. endoscopic US - Dilated ducts, “honeycombing”
4. _ERCP_ - analyze pancreatic duct, most sensitive
5. MRCP - Similar and less invasive than ERCP
47
complications of chronic pancreatitis
* Pseudocysts
* DM
* Exocrine deficiency (Malabsorption)
* Opioid addiction
* Disability and reduced life expectancy
* **Pancreatic Carcinoma (main cause of death)**
48
noninvasive tx/pharm for chronic pancreatitis
1. Low fat diet
1. Avoid alcohol
1. Pain management
- Caution with opioids (addiction)
- Combo with **NSAIDS, Tramadol, or Acetaminophen with TCA’s**
1. Pancreatic digestive enzymes
1. Insulin for associated DM
1. Treatment of any malabsorptive disorders
49
invasive tx for chronic pancreatitis
1. **ERCP w/ stone extraction +/- stent placement** - biliary cause
1. **ERCP w/ decompression of pancreatic duct** - dilated in alcoholic pancreatitis
1. **_Puestow procedure_** for dilated pancreatic duct - Effective pain relief
1. Resection of head or tail (**Whipple procedure**)
1. Surgical **drainage** of pseudocysts
1. Pain management procedures: **Celiac plexus block, Spinal Cord Stimulators**
50
what is the puestow procedure
1. creating a longitudinal incision along the pancreas while the main pancreatic duct is filleted open longitudinally from the head to its tail
1. The duct and pancreas are then attached to a loop of the small intestines (jejuneum)
51
d/t pain is difficult to treat in chronic pancreatitis, this often leads to ?
opioid addiction
52
carcinoma of the pancreas MC occurs in what location?
* 75% in pancreatic head
* 25% body and tail - Poorer prognosis
53
MC type of carcinoma of the pancreas
adenocarcinoma (85%, ductal)
54
RF for pancreas carcinoma
1. Advanced age (rare before age 45)
1. High fasting plasma glucose
1. **Tobacco use (greatest risk factor)**
1. Heavy alcohol use
1. Obesity
1. Chronic pancreatitis
1. Family history/genetics
1. New onset DM after the age of 45
1. Prior abdominal radiation
1. Certain breast cancer carriers (BRCA 2) have 7% risk of concurrent pancreatic cancer
_Any older pt with new onset DM_ = **pancreatic cancer is in the DDx!**
55
presentation of pancreas carcinoma
1. Vague epigastric pain with radiation to back (MC)
- gnawing, visceral with insidious onset
- for 1-2 months before presentation - Can be worse after eating or lying supine
2. Wt loss, anorexia, fatigue, N/D, hyperglycemia
3. Acute pancreatitis w/o identifiable cause
Often asx until metastasis occurs….esp with body and tail masses.
56
PE findings of pancreas carcinoma
1. **Painless Jaundice and Enlarged palpable gallbladder**
- d/t tumor of pancreatic head causing obstruction of common bile duct (**Courvoisier sign**)
- Nontender put palpable distended gallbladder right costal margin
2. Malabsorptive diarrhea
3. If in tail, **pain can be in LUQ**
4. advanced cases - a hard periumbilical nodule may be palpable (**Sister Mary Joseph’s node**)
57
lab studies for pancreas carcinoma
* Amylase, Lipase - normal to mildly elevated
* Glycosuria, Hyperglycemia
* Elevated LFT’s if CBD obstruction
* +/- CA 19-9 tumor marker
58
imaging for pancreas carcinoma
1. **CT - 1st line** (detects mass in 80%)
- Can do CT guided FNA for cytologic studes and tumor markers
- Identifies metastases, delineates extent of tumor
2. Endoscopic U/S, MRCP
3. _ERCP - confirmation if *inconclusive CT*_ (“double duct”)
- Simultaneous dilation of pancreatic and common bile duct
4. Open surgical exploration needed for bx if unable to get CT guided or ERCP guided bx.
59
staging for pancreas carcinoma
TNM classification
* **Tis**: carcinoma in situ;
* **T1**: limited to pancreas, **<=2 cm** in greatest dimension
* **T2**: limited to pancreas, **>2 cm** in greatest dimension
* **T3**: extends **beyond pancreas** but w/o involvement of the celiac axis or the superior mesenteric artery
* **T4**: involves **celiac axis** (celiac artery, with left gastric, splenic, and common hepatic artery) or the superior mesenteric artery (unresectable primary tumor)
* **N1**, regional **LN metastasis**; **M1**, **distant metastasis**.
60
tx for pancreas carcinoma
1. if localized - **Whipple Procedure** - Radical pancreaticoduodenal resection
2. Distal Pancreatectomy
3. Total Pancreatectomy
61
what is the whipple procedure
1. Removal **pancreatic head, duodenum, first 15cm of jejunum, CBD, gallbladder, and a partial gastrectomy**
1. 5 year survival rates in these patients: 25-30% (Only 10% in node positive patients)
1. Surgery carries 4% mortality rate
1. Often preceded by biliary stenting if with jaundice/CBD blockage
1. Often followed by _chemotherapy +/- chemoradiation_
62
how to determine suitability for surgery in pancreas carcinoma
staging laparoscopy before surgery
63
* Resection of tumor in body and tail.
* Always do staging laparoscopy first - Only 13% of body and tail tumors resectable
* Typically also combined with splenectomy
* Surgery carries higher postoperative mortality rates
what type of procedure is this?
Distal Pancreatectomy
64
what makes a pancreas carcinoma nonresectable?
* Liver, peritoneum, and omentum mets
* Encasement of superior mesenteric artery/vein
* Extension into IVC
65
tx for nonresectable pancreas carcinoma
* Biliary stents (if sx of obstruction)
* Chemo
* Palliative treatment
66
screening recommendation for pancreatic cancer?
* Patients with FHx (1st degree) w/ pancreatic cancer should have screening CT age 40-45 or 10 years before onset of cancer in family member.
* There is NO screening test for healthy adults for pancreatic cancer.
67
Education of pts on PREVENTION of pancreatic cancer
* **Don't smoke**. People who smoke are twice as likely to get pancreatic cancer as non-smokers.
* **Limit alcohol**. Heavy drinking can lead to pancreatitis, or chronic inflammation of the pancreas. Long-term pancreatitis increases the risk for pancreatic cancer.
* **Maintain a healthy weight**. Someone with a BMI, or body mass index, of 30 or higher is considered obese.
* **KNOW YOUR FAM HX** - Can get genetic testing if + first degree relative
* Be familiar with common s/sx: **Jaundice**, **Unexplained weight loss, Pain**
68
a procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas.
Endoscopic Retrograde Cholangiopancreatography
(ERCP)
69
uses magnetic resonance imaging to visualize the biliary and pancreatic ducts non-invasively. This procedure can be used to determine whether gallstones are lodged in any of the ducts surrounding the gallbladder.
Magnetic Resonance Cholangiopancreatography (MRCP)
