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GIR Test 4 > B5.066 Exocrine Pancreas > Flashcards

B5.066 Exocrine Pancreas Flashcards

1
Q

general function of the exocrine pancreas

A

makes enzymes for digestion

enzymes flow through a small opening into your small intestine

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2
Q

2 primary cell types in exocrine pancreas

A

acinar cells

centriacinar (duct) cells

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3
Q

acinar cells

A

exocrine cells that produce and transport enzymes that are passed into the duodenum where they assist in the digestion of food

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4
Q

centriacinar (duct) cells

A

spindle shaped cells in the exocrine pancreas
extension of the intercalated duct cells into each pancreatic acinus
take bicarb to intralobular ducts which eventually converge to the main pancreatic duct

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5
Q

pancreatic secretion core concepts

A

secretes digestive enzymes, fluid, and bicarb in response to food ingestion

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6
Q

regulatory mechanisms of pancreatic secretions

A

neural reflexes, GI hormones, and absorbed nutrients
stimulatory and inhibitory influences that coordinate the delivery of digestive enzymes with food emptying into the intestine to assure adequate digestion of a meal

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7
Q

what happens in the absence of proper pancreatic secretion

A

maldigestion and malabsorption of nutrients

malnutrition and associated complications

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8
Q

how much does the pancreatic secrete per day

A

1.5-3 L

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9
Q

digestive enzymes produced by acinar cells

A

amylytic
lipolytic
proteolytic
ribonucleases

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10
Q

examples of zymogens

A

trypsinogen

chymptrypsinogen

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11
Q

examples of proenzymes

A

procarboxypeptidase

proelastase

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12
Q

function of amylase

A

carbs/starch into di- and trisaccharides to glucose

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13
Q

function of lipase

A

fats into fatty acids and cholesterol

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14
Q

sequence of pancreatic secretion cascade

A

chime contacts with intestinal mucosa and bile acids > contact enteropeptidase/ enterokinase on brush border of small intestine > enterokinase cleaves trypsinogen into trypsin > trypsin activates more of itself and other major enzymes > active enzymes contribute to digestion

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15
Q

purpose of proteolytic enzymes

A

continued breakdown of proteins that began in the stomach

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16
Q

prevention of premature enzyme activation/ autodigestion

A

prevented by 4 mechanisms:

  1. packaging of zymogen (inactive) granules
  2. intracellular calcium homeostasis keeps calcium levels low
  3. acid base balance prevents rise in pH (enzymes active in alkaline pH)
  4. protease inhibitors are secreted by acinar cells (SPINK1)
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17
Q

describe the sequence of events leading to premature trypsinogen activation

A

sustained global elevations in Ca2+ within acinar cells > triggers trypsin activation within the ZGs > digestion and destruction of ZG membranes > activated trypsin digests acinar cells and surrounding tissues > pain, fever, internal bleeding, organ failure, death

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18
Q

normal Ca2+ regulation of trypsinogen activation

A

stimulation results in release of Ca2+ from ER > ZG fusion with acinar cell membrane > ZGs release inactive trypsin into ducts > influx of extracellular Ca2+ to replace intracellular stores > enteropeptidase activates trypsin in small intestine

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19
Q

function of bicarb

A

neutralizes acidic chime coming from the stomach as well as prevent aggregation of digestive enzymes

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20
Q

contribution of pancreatic enzymes to carbohydrate digestion

A

starch and disaccharides > oligosaccharides and disaccharides

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21
Q

contribution of pancreatic enzymes to protein digestion

A

large polypeptides to small polypeptides/peptides

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22
Q

contribution of pancreatic enzymes to fat digestion

A

unemulsdified TGs to monoglycerides and fatty acids

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23
Q

contribution of pancreatic enzymes to nucleic acid digestion

A

nucleic acids to pentose sugars, N-containing bases, and phosphate ions

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24
Q

major activities of gastrin

A

stimulates gastric acid secretion and proliferation of gastric epithelium

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25
stimuli for release of gastrin
presence of peptides and amino acids in gastric lumen
26
major activities of CCK
stimulates secretion of pancreatic enzymes, contraction and emptying of the gallbladder, and delivery of bile to the small intestine
27
stimuli for release of CCK
presence of fatty acids and amino acids in the small intestine
28
major activities of secretin
stimulates secretion of water and bicarb from the pancreas and bile ducts, inhibits secretion of gastrin, stimulates bile production
29
stimuli for release of secretin
acidic pH in the lumen of the small intestine
30
major activities of GIP
inhibits gastrin secretion and motility and potentiates release of insulin from beta cells in response to elevated blood glucose concentration
31
stimuli for release of GIP
presence of fat and glucose in the small intestine
32
major activities of VIP
stimulates pancreatic bicarb and protein secretion
33
stimuli for release of VIP
released from pancreas, its release is coupled with bicarb secretion
34
major activities of PP
inhibits pancreatic bicarb and protein secretion
35
stimuli for release of PP
release from pancreas, stimulated by vagus
36
3 phases of pancreatic secretion
cephalic, gastric, intestinal
37
cephalic phase
1. thought, smell, taste of food stimulates medulla oblongata 2. vagus carries signals to stomach, activates enteric plexus neurons 3. postganglionic neurons stimulate parietal and chief cell sections, release of gastrin and histamine by endocrine cells 4. gastrin is carried through the circulation back to the stomach where, along w histamine, stimulates secretions
38
gastric phase
1. distension of stomach stimulates mechanoreceptors and activates parasym reflex (vagus to medulla oblongata) 2. medulla oblongata stimulates gastrin and histamine release 3. distension of stomach activates local reflexes which stimulates stomach secretions 4. gastrin is carried through circulation back to the stomach where, along w histamine, stimulates secretions
39
intestinal phase
1. chime in the duodenum inhibits gastric secretions: - duodenal chemoreceptors are stimulated by H+ or lipids, signal via vagus to medulla oblongata, inhibit parasym signaling, decreasing gastric secretions - local reflexes activated by H+ or lipids inhibit gastric secretions - secretin and CCK produced by duodenum decrease gastric secretions
40
causes of exocrine pancreatic insufficiency
1. impaired hormonal stimulation from the intestine due to untreated celiacs 2. obstruction of the main pancreatic duct by tumor 3. chronic pancreatitis 4. cystic fibrosis 5. loss of pancreatic parenchyma after pancreatic resection 6. DM1
41
most common cause of EPI
chronic pancreatitis
42
how does CF cause EPI
mutated CFTR gene leads to abnormal Na+ and Cl- transport; thick, sticky mucus blocks bile and pancreatic ducts
43
what is EPI
``` inability to break down and digest food properly characterized by: -frequent diarrhea -gas and bloating -stomach pain -steatorrhea -weight loss ```
44
treatment for EPI
pancreatic enzyme replacement therapy (PERT)
45
diagnosis of EPI
clinical suspicion > evaluation of serum nutritional markers and fecal elastase
46
fecal elastase values
< 15 high probability of EPI 15-200 check MPD calcifications on imaging (EPI if calcifications present) > 200 low probability of EPI
47
PERT supplements
porcine derived lipase, protease, and amylase take with each snack and meals track meals/ well being with dosage adjustments avoid calcium containing antacids as they can make steatorrhea worse
48
2 types of PERT supplements
enteric coated/ delayed release | non-enteric coated (must take with PPI or H2 blocker)
49
common side effects of PERT
``` blood sugar spike or decrease stomach pain frequent or abnormal BMs gas vomiting sore throat and cough joint pain/gout fibrosing colonopathy complication (due to excessive enzyme action on tissue structures) ```
50
enzyme ratios in PERT
1. 0 amylase 3. 2 protease 5. 0 amylase
51
contributing factors to chronic pancreatitis
hypoxia fibrosis oxidative stress
52
histo findings in acute to chronic pancreatitis
lymphocytic infiltration fibrosis hypertrophy/dystrophy of nerves
53
result of chronic pancreatitis
duct obstruction pancreatic ductal hypertension pain and complications
54
what is chronic pancreatitis?
``` long standing inflammation of the pancreas that alters normal structure and function irreversible damage (separate from reversible acute pancreatitis) ```
55
symptoms of chronic pancreatitis
``` nausea vomiting weight loss diarrhea steatorrhea pain? ```
56
pain associated with chronic pancreatitis
``` located in epigastrium and radiates to the back eased by patient leaning forward associated with nausea and vomiting gnawing not always painful ```
57
physical exam findings in chronic pancreatitis
epigastric tenderness | occasionally, a fullness or mass can be felt in the epigastrium (suggests presence of pseudocyst or inflammatory mass)
58
morphological distinction of acute vs chronic pancreatitis
chronic: patchy focal disease characterized by a mononuclear infiltrate and fibrosis acute: diffuse large portion of pancreas with neutrophilic inflammatory response
59
lab findings of acute vs chronic pancreatitis
serum amylase and lipase normal in chronic and elevated in acute
60
varied presentations of chronic pancreatitis
may be asymptomatic can present with fibrotic mass symptoms of pancreatic insufficiency without pain
61
pain associated with acute pancreatitis
upper abdominal pain that travels through back piercing aggravated by eating always painful, variable period of time
62
2 major cause of chronic pancreatitis
chronic alcohol abuse (>60%, smoking contributes) | idiopathic (10%)
63
minor causes of chronic pancreatitis
``` metabolic infection hereditary (CF) autoimmune (SLE) obstruction congenital ```
64
alcoholic chronic pancreatitis pathogenesis
1. site of initiation: acinar cell 2. ethanol increases expression of digestive enzymes, alters Ca2+ homeostasis, oxidative stress, perturbs lipid metabolism, destabilizes lysosomal and zymogen granule membranes 3. net result: trypsin activation, enzyme cascade activation, inflammation, necrosis 4. inflammation leads to fibrosis
65
2 forms of chronificationc pancreatitis
large duct | small duct
66
large duct disease
dilatation and dysfunction of the large pancreatic ducts visible on most diagnostic imaging pancreatic fluid changes composition and facilitates the deposition of precursors to calcium carbonate stones and causes diffuse pancreatic calcification more common in males
67
small duct disease
usually associated with normal imaging non dilated main pancreatic duct no pancreatic calification more common in females
68
lab testing associated with chronic pancreatitis
fecal elastase (low) hypercalcemia (hypo is acute) fecal fat (<10% normal) serum amylase/lipase RARELY elevated
69
why is there hypocalcemia in acute pancreatitis?
serum amylase levels are elevated and free digested fats may bind with serum calcium
70
abdominal USS
typically first line imaging in suspected chronic pancreatitis can show evidence of underlying causes and investigate for other pathology
71
CT abdomen-pelvis scan
follows US if required | demonstrates pancreatic calcification or pseudocyst formation
72
MRCP
identifies presence of biliary obstruction assess pancreatic duct cannot exclude pancreatitis
73
ERCP
more accurate way of eliciting the anatomy of the pancreatic duct and also has the advantage of being combined with intervention contrast required
74
MRCP/ERCP + IV secretin
can be combined with administration of IV secretin causes pancreas to produce bicarb rich fluid may reveal pancreatic duct stricture more accurate for detecting small duct disease
75
direct pancreatic function tests
secretin stimulation test CCK stimulation test secretin-CCK stimulation test stimulate pancreas w IV ^^ and aspirate duodenal contents to quantify production of bicarb and trypsin
76
long term complications of steatorrhea and malabsorption
patients are at risk of becoming deficient in the fat soluble vitamins regular clotting function and bone density checks hypocalcemia
77
complications of chronic pancreatitis
``` pseudocyst (10%) steatorrhea and malabsorption (25%) bile duct/duodenal obstruction (5-10%) pancreatic diabetes (30-50%) pancreatic ascites/ pleural effusion (15%) pancreatic malignancy ```
78
how does pancreatitis cause ascites or pleural effusions
disruption of main pancreatic duct leading to fistula formation in abdomen or chest rupture of pseudocyst
79
initial management of chronic pancreatitis
analgesia is the mainstay | PERT
80
definitive management of acute pancreatitis
avoidance of precipitating factor management of chronic pain PERT endoscopy/steroid management in select few patients steroids help with autoimmune etiology pancreatitis (initial high dose w low dose maintenance)
81
malabsorption management algorithm
PERT > low fat diet (50-75) > H2 receptor antagonist > PPI
82
chronic pancreatitis prognosis
significant morbidity and mortality reduced quality of life 1/3 die within 10 yrs autoimmune responds well

GIR Test 4 (20 decks)

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