02-20 Pancreatits Clincal + Cases Flashcards

Question 1

Q

OBJECTIVE: Describe the anatomy and microanatomy of the pancreas. List the adjacent organs and structures to the pancreas

Answer

A

HEAD lies within the concavity of the duodenum; surrounds SMA, which emerges from it

—Blood supply = sup pancreaticoduodenal a. from gastroduodenal a. and inf pancreaticoduodenal a. from SMA

UNCINATE PROCESS emerges from the lower part of head, and lies deep to the superior mesenteric artery and vein. NECK is the constricted part between the head and the body. BODY lies behind the stomach. TAIL is on the left end of the pancreas

—Blood supply to NECK/BODY/TAIL = pancreatic branches of splenic a.

Question 2

Q

OBJECTIVE: Define the basic functional units of the pancreas, their cells types and products.

Answer

A

Endocrine panc is only 2%

<ul>
<li>Islets of Langerhans Produce:</li>
<li>insulin from B cells (50-80% of islet)</li>
<li>glucagon from A cells</li>
<li>somatostatin from D cells</li>
<li>panc. polypeptide from PP cells</li>
<li>amylin</li>
</ul>

Exocrine panc is 80%

<ul>
<li>acinar cells: proenzymes + enzymes
<ul>
<li>90% proteases</li>
<li>can see zymogen granules</li>
</ul>
</li>
<li>ductules: water + HCO3-</li>
</ul>

Question 3

Q

OBJECTIVE:Outline normal pancreatic physiology in terms of acinar cell secretion

<ul>
<li>Regulation</li>
</ul>

Answer

A

Acinar cells secrete pancreatic digestive enzymes

<ul>
<li>Endocrine regulation directly by secretin and CCK directly on CCK-R on acinar cells</li>
<li>Endocrine indirectly by CCK via vaso-vagal stim of ENS which releases neurocrine:
<ul>
<li>ACh</li>
<li>VIP</li>
<li>GRP</li>
<li>(Substance P)on slide not notes</li>
</ul>
</li>
<li>Above causes increased acinar secretion</li>
</ul>

Question 4

Q

OBJECTIVE: outline normal pancreatic physiology in terms of  ductule HCO3 secretion.

<ul>
<li>Importance of HCO3-</li>
</ul>

Answer

A

Ductule cell mainly secrete HCO3-

<ul>
<li>Regulated secretin (primarily; ↑s [cAMP]) and ACh (potentiates secretin)</li>
<li>Stomach acid → duod. "S" cells → secretin</li>
</ul>

Neutralization important b/c:

<ul>
<li>optimal digestion and absorption occur @ neutral pH</li>
<li>protects mucosa</li>
<li>↑ FFA and bile acid solubility</li>
<li>inactivates pepsin</li>
</ul>

Question 5

Q

Which two pancreatic enzymes are secreted in active form?

Answer

A

α-amylase and lipase

Question 6

Q

What bond does amylase split?

Answer

A

1 - 4 glucosidic bonds in starch

Question 7

Q

How are pancreatic zymogens activated?

Answer

A

Trypsinogen — enterokinase on brush border → trypsin

<ul>
<li>trypsin then activates all the other zymogens</li>
</ul>

Question 8

Q

OBJECTIVE: Describe the normal embryologic development of the pancreas and biliary system and the derivation of the most common pancreatic anatomic variant.

Answer

A

DEVELOPMENT
—The pancreas forms from two different outgrowths of the foregut: a ventral pancreatic bud (in the ventral mesentery, which is an outgrowth of the bile duct) and a dorsal pancreatic bud (in the dorsal mesentery), which is an outgrowth of the foregut. With the rotation of the duodenum, the ventral bud rotates dorsally behind the duodenum and fuses to the dorsal bud. It is also pressed against the dorsal body wall, and becomes secondarily retroperitoneal.
—In 10% of pts, the minor (Santorini) duct and the major duct do not fuse. ?Santorini duct becomes more important drainage

Question 9

Q

OBJECTIVE: Describe and contrast the clinical presentations of acute and chronic pancreatitis including historical features, physical exam findings, laboratory data and imaging studies

Answer

A

Acute

<ul>
<li>HPI:  mod to severe abd pain (usu upper abdomen, radiates to upper back).

<ul>
<li>pain sudden onset, similar to that of perf viscous or mesenteric infarction</li>
<li>steady and persists for hours w/o relief.</li>
<li>associated w/ n/v</li>
</ul>
</li>
<li>P.E. varies based on severity
<ul>
<li>all cases: tender in UQs > LQs
<ul>
<li>guarding to percussion</li>
<li>less rigid than peritonitis</li>
</ul>
</li>
<li>mild case: non-toxic</li>
<li>severe case: tachy, obtundation, hypotension, hypoxia, low gr fever</li>
<li>some cases:
<ul>
<li>loss of bowel sounds</li>
<li>ecchymosis one /both flanks (Grey-Turner sign)</li>
<li>or in the periumbilical region (Cullen sign)</li>
</ul>
</li>
</ul>
</li>
<li>Labs
<ul>
<li>↑ serum amylase (sens, but not spec)</li>
<li>
↑ serum lipase (^as sens, more spec)
</li>
<li>
↑ WBC
</li>
<li>
~↑ glucose
</li>
<li>
~↑ LFT, esp if 2° to gall stone
</li>
<li>
~↓ serum Ca
</li>
</ul>
</li>
<li>Imaging: supports dx and r/o ddx but not necessary to make dx
<ul>
<li>
Plain films exclude a perf viscous and obstruction
</li>
<li>
CT can show inflamed pancreas (dx)

<ul>
<li>
staging: shows extent of spread of inflam or presence of panc. necrosis
</li>
<li>
CT scan may be normal in 15-30% of pts w/ mild pancreatitis
</li>
</ul>
</li>
</ul>
</li>
</ul>

Chronic

<ul>
<li>HPI
<ul>
<li>Pain: UQs, periodic early → constant → anorexia/wt loss, malnutrition.

<ul>
<li>can be brought on by eating, is frequently nocturnal</li>
<li>often radiates to the back</li>
</ul>
</li>
<li>Malnutrition
<ul>
<li>no lipase → steatorrhea & ↓ A, D, E, K</li>
<li>no protease → azotorrhea/↓ prot</li>
</ul>
</li>
<li>Diabetes
<ul>
<li>occurs only after >80% panc lost</li>
<li>tricky, brittle DM b/c both insulin and glucagon gone</li>
</ul>
</li>
</ul>
</li>
<li>P.E. (not in notes)</li>
<li>Labs and Imaging
<ul>
<li>Structural Tests (commonly used)
<ul>
<li>EUS: best test, picks up things CT can't</li>
<li>CT: ductal abnormalities, pancreatic calcification, and pseudocysts</li>
<li>ERCP: duct ∆s, but risky</li>
<li>MRCP, non-invasive, \$\$</li>
<li>plain film: calcifications in late dz</li>
</ul>
</li>
<li>Functional Tests (not commonly used)
<ul>
<li>
secretin fxn test: measures output of panc enzymes, bicarb and water after secretion injection
</li>
<li>
new EUS secretin (Geisel profs)
</li>
</ul>
</li>
</ul>
</li>
</ul>

Question 10

Q

Organs besides panc that make amylase?

Answer

A

salivary gland, fallopian tube, ovary, prostate, lung, and possibly liver

Question 11

Q

OBJECTIVE: What are the etiologies of acute pacnreatitis?

<ul>
<li>Mnemonic</li>
</ul>

Answer

A

BADSHIT

<ul>
<li>B - Biliary (Gallstones) (40%)</li>
<li>A - Alcohol (40%)</li>
<li>D - Drugs (many, azathioprine HCTZ)/Doctors (ERCP)</li>
<li>S - Scorpion (other toxins)</li>
<li>H - Hereditary Pancreatitis/Hyper-TG/-Ca2+/-Parathyr.</li>
<li>I - Idiopathic (10-15%) (signif % may be 2° to biliary cholesterol crystals)</li>
<li>T - Trauma</li>
</ul>

Other Causes

<ul>
<li>Panc CA and ampullary CA</li>
<li>Infectious agents (predominantly viral)</li>
<li>Post-op</li>
<li>Pregnancy</li>
<li>Inherited
<ul>
<li>Trypsinogen Mutations</li>
<li>CFTR Mutations</li>
<li>Familial Hypertriglyceridemia</li>
</ul>
</li>
</ul>

Question 12

Q

OBJECTIVE: What are the etiologies of chronic pacnreatitis?

Answer

A

<ul>
<li>#1 cause in Global North = EtOH</li>
<li>10-30% idiopathic, 2 groups:
<ul>
<li>
younger (~19y/o) ♀s: present initially w/ severe pain. progresses slowly to panc exocrine and endocrine insuff.
</li>
<li>
older (~65 y/o), ♂ presents w/ milder pain, but eventual panc insuff
</li>
</ul>
</li>
<li>Hereditary (AD inheritance)
<ul>
<li>
 markedly ↑ panc CA risk (~40% by age 70)
</li>
<li>
several ID'ed mutations blcok trypsin inactivation
</li>
</ul>
</li>
<li>CFTR Mutations
<ul>
<li>malabsorption</li>
<li>maybe be presenting sx in mild cases of CF</li>
<li>usu. not assoc'd w/ painful attacks</li>
</ul>
</li>
<li>Auto-Immune
<ul>
<li>may or may not have sx</li>
<li>ductal narrowing and organomegaly</li>
<li>
↑ circulating IgG4
</li>
<li>assoc'd w/ other A-I d/o</li>
</ul>
</li>
<li>Ductal obstruction
<ul>
<li>many causes</li>
<li>
Pancreas divisum may cause chronic pancreatitis by producing a relative obstruction to outflow at the minor papilla.
</li>
</ul>
</li>
<li>Tropical pancreatitis
<ul>
<li>
Calcific pancreatitis of the tropics is a major cause of pancreatitis worldwide
</li>
<li>
etio unknown: ?micronutrient deficiency, ?mutation
</li>
</ul>
</li>
<li>Hyperparathyroidism
<ul>
<li>
<2% of cases of hyperparathyroidism
</li>
</ul>
</li>
<li>
Other

<ul>
<li>
abd rad therapy, Sjögren’s, 1° biliary cirrhosis, and SLE
</li>
</ul>
</li>
</ul>

Question 13

Q

OBJECTIVE: DDx of a patient presenting with acute pancreatitis

Answer

A

<ul>
<li>a.    Biliary colic</li>
<li>b.    Acute cholecystitis</li>
<li>c.    Acute cholangitis</li>
<li>d.    Perf (duodenal ulcer, bowel)</li>
<li>e.    Mesenteric ischemia</li>
<li>f.    Intestinal obstruction</li>
<li>g.    Inferior wall MI</li>
<li>h.    Aortic dissection</li>
<li>i.    Ruptured ectopic pregnancy</li>
<li>j.    Complication of Crohn’s</li>
</ul>

Question 14

Q

OBJECTIVE: DDx of a patient presenting with chronic pancreatitis

Answer

A

Not in notes, this is from DynaMed:

Causes of pancreatic insufficiency without inflammation:

<ul>
<li>
primary pancreatic insufficiency - pancreatic agenesis, congenital pancreatic hypoplasia, Shwachman-Diamond syndrome, Johanson-Blizzard syndrome, adult pancreatic lipomatosis, adult pancreatic atrophy, isolated lipase deficiency, pancreatic resection
</li>
<li>
secondary pancreatic insufficiency - mucosal small bowel dz (↓ CCK release), gastrinoma (intraluminal destruction of enzymes), Billroth II anastomosis (poor mixing or decreased hormone release), enterokinase deficiency, kwashiorkor (protein calorie malnutrition)

 
</li>
</ul>

Question 15

Q

OBJECTIVE: Define prognostic indicators for severity of acute pancreatitis

Answer

A

Ranson Score

On admission

<ul>
<li>Age >55 years</li>
<li>WBC count >16,000/mm3</li>
<li>Glucose >200 mg/dL</li>
<li>LDH >350 IU/L</li>
<li>AST >250 U/L</li>
</ul>

During initial 48 hours:

<ul>
<li>Hct decrease of >10mg/dL</li>
<li>BUN increase of >5 mg/dL</li>
<li>Calcium <8 mg/dL PaO2 <60 mmHg</li>
<li>Base deficit >4 mEq/L</li>
<li>Fluid sequestration >6L</li>
</ul>

Other scores: BISAP (bedside index of severity in acute pancreatitis), APACHE, Glasgow

Question 16

Q

OBJECTIVE:Describe the pathophysiologic mechanisms leading to acute pancreatitis and characterize theirpathologic features.

Answer

A

See image and path lecture

Question 17

Q

OBJECTIVE: Describe the pathophysiologic mechanisms leading to chronic pancreatitis and characterize their pathologic features.

Answer

A

See path lecture

Question 18

Q

OBJECTIVE: Describe both the systemic and local complications of acute pancreatitis.

Answer

A

Local

<ul>
<li>Necrosis (Microvasc hypoperfusion)→ superimposed infx</li>
<li>Pseudocyst → superimposed infx = abscess</li>
<li>necrotic obstruction/fistulization of adjacent bowel</li>
<li>GI hemorrhage (Stress ulceration, ischemia, varices 2° to splenic vein thrombosis)</li>
</ul>

Systemic

<ul>
<li>Shock (Sequestration of retroperitoneal fluid or hemorrhage, SIRS)</li>
<li>Coagulopathy (Circulating proteases)</li>
<li>Resp failure (ARDS)</li>
<li>ARF (hypotension and ATN)</li>
<li>Hyperglycemia (low insulin, hi glucagon)</li>
<li>HypoCa++ (hypoalbumin, peripanc fat necrosis sops up Ca)</li>
</ul>

Question 19

Q

OBJECTIVE: Describe both the systemic and local complications of chronic pancreatitis.

Answer

A

<ol>
<li>Chronic pain</li>
<li>steatorrhea/malnutrition/wt loss</li>
<li>DM</li>
<li>Panc. ascites or pleural effusion</li>
<li>Psuedocyst</li>
<li>Splenic vein thrombosis → varices</li>
<li>Duodenal obstruction</li>
<li>common bile duct obstruction</li>
</ol>

Question 20

Q

OBJECTIVE: Describe the management of acute pancreatitis

Answer

A

MILD

<ul>
<li>analgesia</li>
<li>NPO for a few days</li>
<li>slow re-feed</li>
<li>elective cholecystectomy after recovery if due to gallstones</li>
<li>
encourage EtOH abstinence if 2° to EtOH
</li>
</ul>

SEVERE

<ul>
<li>rapid fluid volume resusitation</li>
<li>narcotics</li>
<li>NPO for a few days → feeding tube into jejunum!</li>
<li>abx (only if infx b/c ↑ risk of fungal panc infx)</li>
<li>?ERCP to remove stones - debated</li>
<li>drain abscess, etc, via endoscopy PRN</li>
<li>tx underlying cause</li>
<li>
cholecystectomy after recovery if due to gallstones
</li>
<li>encourage EtOH abstinence if 2° to EtOH</li>
</ul>

Question 21

Q

OBJECTIVE: Describe the management of chronic pancreatitis

Answer

A

<ul>
<li>Pain Mgmt
<ul>
<li>(Non-narc for EtOH pts)</li>
<li>Sometimes: directly nerve block</li>
</ul>
</li>
<li>Exogenous enzymes ↓ demand on panc → improved absorption ?less pain</li>
<li>H2 blocker/PPI as panc is less able to secrete HCO3-</li>
<li>surgery/endo procedure: splenic vein thromboses, CBD or duodenal obstruction and pseudocysts</li>
</ul>

Brainscape's Knowledge GenomeTM

02-20 Pancreatits Clincal + Cases Flashcards

Brainscape's Knowledge Genome^TM