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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
Q

stimuli for release of gastrin

A

presence of peptides and amino acids in gastric lumen

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26
Q

major activities of CCK

A

stimulates secretion of pancreatic enzymes, contraction and emptying of the gallbladder, and delivery of bile to the small intestine

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27
Q

stimuli for release of CCK

A

presence of fatty acids and amino acids in the small intestine

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28
Q

major activities of secretin

A

stimulates secretion of water and bicarb from the pancreas and bile ducts, inhibits secretion of gastrin, stimulates bile production

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29
Q

stimuli for release of secretin

A

acidic pH in the lumen of the small intestine

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30
Q

major activities of GIP

A

inhibits gastrin secretion and motility and potentiates release of insulin from beta cells in response to elevated blood glucose concentration

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31
Q

stimuli for release of GIP

A

presence of fat and glucose in the small intestine

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32
Q

major activities of VIP

A

stimulates pancreatic bicarb and protein secretion

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33
Q

stimuli for release of VIP

A

released from pancreas, its release is coupled with bicarb secretion

34
Q

major activities of PP

A

inhibits pancreatic bicarb and protein secretion

35
Q

stimuli for release of PP

A

release from pancreas, stimulated by vagus

36
Q

3 phases of pancreatic secretion

A

cephalic, gastric, intestinal

37
Q

cephalic phase

A
  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
Q

gastric phase

A
  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
Q

intestinal phase

A
  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
Q

causes of exocrine pancreatic insufficiency

A
  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
Q

most common cause of EPI

A

chronic pancreatitis

42
Q

how does CF cause EPI

A

mutated CFTR gene leads to abnormal Na+ and Cl- transport; thick, sticky mucus blocks bile and pancreatic ducts

43
Q

what is EPI

A 
inability to break down and digest food properly
characterized by:
-frequent diarrhea
-gas and bloating
-stomach pain
-steatorrhea
-weight loss
44
Q

treatment for EPI

A

pancreatic enzyme replacement therapy (PERT)

45
Q

diagnosis of EPI

A

clinical suspicion > evaluation of serum nutritional markers and fecal elastase

46
Q

fecal elastase values

A

< 15 high probability of EPI
15-200 check MPD calcifications on imaging (EPI if calcifications present)
> 200 low probability of EPI

47
Q

PERT supplements

A

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
Q

2 types of PERT supplements

A

enteric coated/ delayed release

non-enteric coated (must take with PPI or H2 blocker)

49
Q

common side effects of PERT

A 
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
Q

enzyme ratios in PERT

A
  1. 0 amylase
  2. 2 protease
  3. 0 amylase
51
Q

contributing factors to chronic pancreatitis

A

hypoxia
fibrosis
oxidative stress

52
Q

histo findings in acute to chronic pancreatitis

A

lymphocytic infiltration
fibrosis
hypertrophy/dystrophy of nerves

53
Q

result of chronic pancreatitis

A

duct obstruction
pancreatic ductal hypertension
pain and complications

54
Q

what is chronic pancreatitis?

A 
long standing inflammation of the pancreas that alters normal structure and function
irreversible damage (separate from reversible acute pancreatitis)
55
Q

symptoms of chronic pancreatitis

A 
nausea
vomiting
weight loss
diarrhea
steatorrhea
pain?
56
Q

pain associated with chronic pancreatitis

A 
located in epigastrium and radiates to the back
eased  by patient leaning forward
associated with nausea and vomiting
gnawing
not always painful
57
Q

physical exam findings in chronic pancreatitis

A

epigastric tenderness

occasionally, a fullness or mass can be felt in the epigastrium (suggests presence of pseudocyst or inflammatory mass)

58
Q

morphological distinction of acute vs chronic pancreatitis

A

chronic: patchy focal disease characterized by a mononuclear infiltrate and fibrosis
acute: diffuse large portion of pancreas with neutrophilic inflammatory response

59
Q

lab findings of acute vs chronic pancreatitis

A

serum amylase and lipase normal in chronic and elevated in acute

60
Q

varied presentations of chronic pancreatitis

A

may be asymptomatic
can present with fibrotic mass
symptoms of pancreatic insufficiency without pain

61
Q

pain associated with acute pancreatitis

A

upper abdominal pain that travels through back
piercing
aggravated by eating
always painful, variable period of time

62
Q

2 major cause of chronic pancreatitis

A

chronic alcohol abuse (>60%, smoking contributes)

idiopathic (10%)

63
Q

minor causes of chronic pancreatitis

A 
metabolic
infection
hereditary (CF)
autoimmune (SLE)
obstruction
congenital
64
Q

alcoholic chronic pancreatitis pathogenesis

A
  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
Q

2 forms of chronificationc pancreatitis

A

large duct

small duct

66
Q

large duct disease

A

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
Q

small duct disease

A

usually associated with normal imaging
non dilated main pancreatic duct
no pancreatic calification
more common in females

68
Q

lab testing associated with chronic pancreatitis

A

fecal elastase (low)
hypercalcemia (hypo is acute)
fecal fat (<10% normal)
serum amylase/lipase RARELY elevated

69
Q

why is there hypocalcemia in acute pancreatitis?

A

serum amylase levels are elevated and free digested fats may bind with serum calcium

70
Q

abdominal USS

A

typically first line imaging in suspected chronic pancreatitis
can show evidence of underlying causes and investigate for other pathology

71
Q

CT abdomen-pelvis scan

A

follows US if required

demonstrates pancreatic calcification or pseudocyst formation

72
Q

MRCP

A

identifies presence of biliary obstruction
assess pancreatic duct
cannot exclude pancreatitis

73
Q

ERCP

A

more accurate way of eliciting the anatomy of the pancreatic duct and also has the advantage of being combined with intervention
contrast required

74
Q

MRCP/ERCP + IV secretin

A

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
Q

direct pancreatic function tests

A

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
Q

long term complications of steatorrhea and malabsorption

A

patients are at risk of becoming deficient in the fat soluble vitamins
regular clotting function and bone density checks
hypocalcemia

77
Q

complications of chronic pancreatitis

A 
pseudocyst (10%)
steatorrhea and malabsorption (25%)
bile duct/duodenal obstruction (5-10%)
pancreatic diabetes (30-50%)
pancreatic ascites/ pleural effusion (15%)
pancreatic malignancy
78
Q

how does pancreatitis cause ascites or pleural effusions

A

disruption of main pancreatic duct leading to fistula formation in abdomen or chest
rupture of pseudocyst

79
Q

initial management of chronic pancreatitis

A

analgesia is the mainstay

PERT

80
Q

definitive management of acute pancreatitis

A

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
Q

malabsorption management algorithm

A

PERT > low fat diet (50-75) > H2 receptor antagonist > PPI

82
Q

chronic pancreatitis prognosis

A

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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