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My DEMS I > Pathophysiology of Pacreas > Flashcards

Pathophysiology of Pacreas Flashcards

1
Q

exocrine pancreas

A

Synthesis of enzymes needed for digestion of fats, proteins, and carbohydrates

Neutralizes gastric acid and chyme

80% of pancreatic cells are epithelial in origin and comprise acinar glands (form exocrine component)

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2
Q

endocrine pancreas

A

Synthesizes and secretes hormones (insulin, glucagon) that regulate glucose and lipid metabolism

pancreatic islet cells

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3
Q

Main proteases

A

trypsinogen
chymotrypsinogen
carboxypeptisases A/B

(most enz of panc are secreted in zymogen form, require activation in duodenum)

acinar cells secrete many diff proteins (proteases, lipases (sec in active form), amylase (sec in active form), nucleases, trypsin inhibitors (deactivates prematurely active typsin), etc)

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4
Q

What forms the bulk of pancreas juice volume?

A

bicarb and water secreted by acinar/ductal epi cells (keep zymogens inactive w/ high pH, also neutralize gastric acid in duod)

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5
Q

increased secretin

increased CCK

A

secretin: leads to panc bicarb secretion

CCK: gallbladder emptying, panc enzyme secretion

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6
Q

Enzyme activation

A

in duodenal lumen:

enterokinase converts trypsinogen into trypsin. Trypsin cleaves/activates other zymogens into active form

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7
Q

Acute pancreatitis

A

Acute inflammation
Acute abdominal pain
Elevated pancreatic enzymes in serum
Self-limited

Trypsinogen and other pro-enzymes are prematurely activated within the pancreas
Auto-digestion of gland
Leakage of enzymes around pancreas may lead to other complications
Inflammatory cascade may result in organ failure or death when severe and systemic

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8
Q

chronic pancreatitis

A

Chronic inflammation
Ductal obstruction
Chronic pain or malabsorption
Permanent loss of pancreatic function

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9
Q

Most common causes of acute pancreatitis

A

alcohol abuse

duct obstruction from gallstone (#1 in US)

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10
Q

How does alcohol cause acute pancreatitis

A

premature release and activation of zymogens
proteinacious plugs within pancreas duct

-direct toxic effect on panc acinar cells and ductal epithelium, causing premature release and activation of trypsinogen and stagnant flow of pancreas juice

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11
Q

How does ductal obstruction lead to acute pancreatitis?

A

Abrupt ductal obstruction (stone, trauma, etc)
bile reflux or retention of enzymes

stone lodges in distal common bile duct +/- ampulla, resulting in obstruction of ventral duct and or bile reflux into panc, reinforcing zymogen activation

stagnation of pancreas enzymes within the duct lumen and activation of the enzyme activation cascade

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12
Q

Other causes of acute pancreatitis

A
  • tumors blocking duct
  • procedures (ERCP)
  • congenital ductal abnorm (panc divisum, annular panc)
  • Sphincter of Oddi dysfunc types 2 or
  • severe hyperlipidemia
  • penetrating trauma
  • drugs
  • hypercalcemia
  • Mumps, Coxsackievirus
  • CF
  • idiopathic
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13
Q

Clues to dx Gallstone pancreatitis

A 
Risk factors for gallstones
Gallstones seen on imaging (in gallbladder or bile duct)
Elevated liver chemistries 
Dilated bile duct
Absence of other risk factors
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14
Q

Presenting features of acute pancreatitis

A 
abdominal pain
n/v
tachycardia
low grade fever
abdominal guarding
loss of bowel sounds
jaundice
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15
Q

Dx tests for acute pancreatitis

A

serum enzymes (enz elevated greater than 3x upper normal): amylase (rises and falls over 24-48 hours, less specific), *lipase (rises in 1-2 hrs, falls over a week)
U/S (best for stones)
CT (edema, calcifications, fluid collections)
CT w/ contrast: detects necrosis

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16
Q

Complications of acute pancreatitis

A

Ileus (paralysis of gut)
intra-abdominal hemorrhage
pseudocyst formation

Severe:
pancreatitic necrosis
bowel or bile duct obstruction
shock
resp or renal failure
Death
17
Q

Pancreatic pseudocyst

A

Collection of pancreatic fluid, debris surrounded by wall of granulation tissue - lacks epithelial lining

Results from ductal disruption, necrosis, or both

Develop in 10-30% of cases of acute pancreatitis

Majority (60-70%) will resolve with time, others may persist or lead to chronic pain, infection, or obstruction of viscera

May need cyst gastrostomy and stent placed leading to stomach

AP or CP

18
Q

Pancreatic necrosis

A

presence of one or more diffuse or focal areas
of nonviable pancreatic parenchyma

If necrotizing, infection and mortality are much higher rates than in interstitial acute panc

19
Q

ARDS

A

Adult resp distress syndrome
complication of acute panc

  • in severe pancreatitis
  • delayed onset
  • assoc w/ panc necrosis
  • assoc w/ hyperlipidemia
  • commonly leads to respiratory failure
  • Dx: hypoxemia, normal wedge pressure
  • potentially reversible
20
Q

Management of acute pancreatitis

A

Admit to hospital (usually)
NPO, then slow advancement in diet
IV narcotics for pain
Surgery consult if gallstones present
Consider ERCP for bile duct stone removal
Severe disease → feeding tube, IV nutrition, pancreatic debridement, pseudocyst drainage, etc..

21
Q

How does chronic pancreatitis develop?

A
  • develops after repeated bouts of acute pancreatitis
  • most commonly as a result of chronic alcohol abuse
  • panc tissue replaced by hard fibrous tissue; atrophy of gland
  • calcifications may develop in duct
  • Micro: scar tissue replaces lost lobular tissue, poss lymphocytes/plasma cells (sparing of islet cells)

Permanent destruction of pancreatic parenchyma with replacement by fibrosis (scar tissue)
May lead to ductal strictures, ductal or parenchymal calcifications (stones), or pseudocysts
May be associated with prior episodes of acute pancreatitis

22
Q

Most common cause of CP in western countries?

A

chronic alcohol abuse

  • smoking contributes to fibrosis
  • familial causes (CFTR gene mutations and/or cystic fibrosis; hypertriglyceridemia; tropical pancreatitis– idopathic variant)
  • hereditary pancreatitis
23
Q

ductal strictures/stones

A

pain, exocrine failure

CP

24
Q

panc pseudocysts

A

pain, n/v

CP

25
Q

acinar destruction

A

exocrine failure

CP

26
Q

Diabetes

A

endocrine failure (late)

CP

27
Q

Functional pancreas reserve

A

need to lose 85-90% of healthy pancreas b/f sx

fat malabs, then prot/carb malabs even later

28
Q

Clinical spectrum of CP

A

Abdominal pain: chronic epigastric pain, rad to back, worse after meals

Steatorrhea: oily stools, large volume, light colored, foul smelling

Hypo or hyperglycemia: brittle diabetes from loss of islets

29
Q

Sx of pancreatic insufficiency

A 
weight loss (fat malabs)
steatorrhea (")
bleeding problems (Vit K)
anemia (vit b12)
weakness/edema (protein)
watery diarrhea (CHO, protein)
30
Q

Mech of steatorrhea

A

decreased lipase and colipase in duodenum

-decreased duodenal pH (inactivation of pancreas enzymes,bile acid precipitation)

31
Q

Dx of chronic pancreatitis

A 
History, PE
Plain XR (calcification in pancreas)
CT (dilated duct, atrophy, calcifications, pseudocysts)
secretin test (given IV, bicarb of less than 80mEq/L suggest panc obstruction or failure) ERCP, or endoscopic ultrasound (more accurate but invasive)
32
Q

Tx of CP

A

ETOH avoidance
Pancreas enzyme replacement (pills) for steatorrhea
Treatment of duct obstruction - dilation, stent placement, or stone removal
Celiac nerve block for pain
Surgical resection if refractory and severe
Pancreatectomy with islet cell transplant
Young patients, refractory disease

33
Q

Pancreatic cancer

A

4th leading cancer death in US
ADENOCARCINOMA most common (mostly from ductal epithelial cells, others acinar cells)
-forms gland like structures, mucin+
-dx late: ~30% appear resectable by EUS; only 20% taken to OR are cured (Whipple)

Survival:
median: 18 mo
5 yr survival 5%

diagnoses ~ # deaths

34
Q

panc cancer presentation

A

Jaundice, dark urine, pruritus (Bile duct obstruction (tumors in head))
Abdominal or back pain - late (Capsular distension or nerve invasion)
Weight loss
Nausea/vomiting (late) –
(Duodenal or gastric obstruction)
Hormonal excess (neuroendocrine)
insulin, glucagon, gastrin, VIP

35
Q

Dx/treatment of panc cancer

A

CT/MRI
biopsy (EUS)
Tx:
Surgical resection - select few that are diagnosed early
ERCP with stent for palliation of cholestasis
Celiac nerve block for pain

36
Q

Pancreatic neuroendocrine tumor

A

Slow-growing, prognosis favorable
Islet cell origin
May present with symptoms of hormone excess
Insulin, glucagon, somatostatin, gastrin, VIP
Diagnosis, treatment same
Octreotide scan may be used to detect small NETs not seen on CT or EUS

Insulinomas cause recurrent hypoglycemia. Glucagonomas cause hyperglycemia/diabetes, weight loss, and diarrhea. Gastrinomas cause GERD or peptic ulcers, diarrhea, and fat malabsorption from deactivation of pancreatic enzymes. VIPomas produce severe, chronic, secretory-type diarrhea with hypokalemia and weight loss. Somatistatinomas are rare but cause weight loss, malabsorption, and acalculous cholecystitis by decreasing GI motility and exocrine secretion.

Surgical resection of all NETs if fit (except insulinoma)

37
Q

Autoimmune pancreatitis

A

Diffuse or focal enlargement of pancreatic parenchyma
Infiltration by IgG-4 + plasma cells and lymphocytes
Males, typically ages 40-70
Association with other autoimmune diseases – RA, Sjogren’s, IBD, SLE
May masquerade as pancreatic cancer!

38
Q

Sx/imaging/dx/tx of AIP

A

Symptoms: abdominal pain, jaundice, weight loss, (rarely) pancreatitis
may have sx of cholestasis (jaundice, dark urine, and/or itching)

Imaging: diffuse or focal enlargement of pancreas with narrowing of CBD +/- PD

Diagnosis: CT/MRI, serum IgG-4, EUS, ERCP, and occasionally FNA/biopsy

Treatment:
PO corticosteroids x 6 weeks
biliary stenting for symptom relief

39
Q

Metastatic NETs producing serotonin byproducts

A

carcinoid syndrome

My DEMS I (26 decks)

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