Lecture 18: Pancreatic Disorders

Question 1

pancreas is both ____ and ___ organ

Answer 1

endocrine; exocrine

Question 2

what does it do as exocrine organ?

Answer 2

produce enzymes and bicarbonate necessary for digestion

Question 3

what are some exocrine hormones?

Answer 3

trypsin, chymotrypsin, carboxypeptidase, ribonyclease, elastase, lipase, cholesterol esterase, alpha amylase

Question 4

what does it do as endocrine organ?

Answer 4

produce hormones central for substrate metabolism

Question 5

what are some endocrine hormones?

Answer 5

insulin, glucagon, somatostatin, pancreatic polypeptide

Question 6

valve that controls pancreatic juices is called:

Answer 6

sphincter of Oddi

Question 7

before activation, pancreatic enzymes called :

Answer 7

zymogens

Question 8

zymogens only activate when enter _____

Answer 8

small intestine

Question 9

first zymogen to activate is:

Answer 9

trypsinogen –> trypsin (activates other things)

Question 10

what are things that stim pancreatic secretion?

Answer 10

CCK, secretin, gastrin, VIP, cephalic phase of eating

Question 11

what are things that inhibit pancreatic secretion?

Answer 11

GLP1, PP, PYY, OXM

Question 12

pancreatitis is characterized by:

Answer 12

hemorrhage of pancreatic tissue,
edema,
autodigestion,
fat necrosis

Question 13

types of acute pancreatitis:

Answer 13

interstitial and hemorrhagic

Question 14

acute interstitial (80-85%) characterized by:

Answer 14

gland architecture preserved but edematous, inflamm cells prominent

Question 15

acute hemorrhagic (15-20%) characterized by:

Answer 15

marked necrosis, hemorrhage of tissue, fat necrosis, vascular inflamm and thrombosis

Question 16

signs and symptoms of acute pancreatitis?

Answer 16

ab pain, nausea/vomiting, low-moderate fever

Question 17

diagnostic markers for AP

Answer 17

^ pancreatic enzymes 3x greater than high end of normal (^ amylase and lipase)

Question 18

__% AP caused by gallstones, ___% by alcohol, and ___ % by hypertriglyceridemiea

Answer 18

40; 30;2-5

Question 19

what is MNT for mild AP?

Answer 19

pain limited analgesics, IVF, start progressive low fat oral diet, small meals (6x/d), eventually normal diet

Question 20

what is MNT for severe AP?

Answer 20

NPO for pancreatic rest, EN is preferred route (traditionally)

Question 21

for EN in severe AP, feed into where?

Answer 21

gastric (NG), if not tolerated then jejunal (NJ)

Question 22

feed NJ below the ligament of ___

Answer 22

Treitz

Question 23

when to start feeding for severe AP?

Answer 23

early EN indicated, anticipate NPO >5-7days

Question 24

rate (modality) of feed for severe AP?

Answer 24

continuous

Question 25

severe AP need ___ kcal/kg, protein ____ g/kg

Answer 25

25-35; 1.2-1.5

Question 26

EN preferred for SAP cuz:

Answer 26

v mortality, v septic complications, v surgical procedures, v hospital LOS, ^ trophic action on intestinal wall, prevent/reduce bacteria translocation

Question 27

when is PN warranted for SAP?

Answer 27

EN not tolerated or contraindicated for other reasons

Question 28

examples of irreversible morphological changes of CP?

Answer 28

fibrosis, calcifications/stones, loss of islet/acinar cells

Question 29

exocrine/endocrine insufficiency associated with:

Answer 29

steatorrhea, wt loss, malnutrition

Question 30

clinical manifestations of CP:

Answer 30

ab pain with/without exocrine/endocrine insufficiency, pain which is increased by fatty food and alcohol intake (result in anorexia)

Question 31

etiopathogenic risk factors for CP:

Answer 31

toxic metabolic (alcoholism, smoking, hypertriglyceridemia), genetic mutations, autoimmune pancreatitis, obstructive, idiopathic

Question 32

exocrine insufficiency is attributed to:

Answer 32

loss of acinar cell mass or pancreatic duct obstruction–>v digestive enzymes, v ductal bicarbonate secreted

Question 33

endocrine insufficiency is attributable to destruction of pancreatic _____ which results in loss of islet cells, or _____ diabetes

Answer 33

parenchyma; pancreatogenic (type 3c)

Question 34

nutr implications of exocrine insufficiency in CP?

Answer 34

fat maldigestion (steatorrhea), CHO and protein maldigestion (v amylase, v trypsin)

Question 35

steatorrhea occurs when pancreatic lipase secretion < ___% of normal, and is the primary cause of ____ in CP

Answer 35

10; weight loss

Question 36

steatorrhea = fecal fat excretion > __g/d

Answer 36

7

Question 37

v amylase secretion causes:

Answer 37

impaired CHO digestion, abdo distension, gas, loose stools

Question 38

vit ____ deficiencies most common

Answer 38

A and E

Question 39

clinical manifestations of deficiencies in fat sol vits?

Answer 39

vision, bone density

Question 40

average resting expenditure in CP is ___kcal/day > than average

Answer 40

200

Question 41

3 pronged approach to nutr management of CP:

Answer 41

1) pancreatic enzyme replacement therapy
2) assessment/correction of nutr deficiencies
3) maintain adequate diet intake and avoid alcohol

Question 42

enzymes in PERT usually combo of ____

Answer 42

lipase, protease, amylase

Question 43

example of PERT:

Answer 43

cotazyme (also used in EN feed tube clogged)

Question 44

if uncoated, use with ____ (eg. PPI)

Answer 44

gastric acid suppressant

Question 45

timing of PERT?

Answer 45

with/just before eating

Question 46

if on PERT, need to know these things:

Answer 46

adherence, dose, timing of doses

Question 47

nutr recommendations for CP?

Answer 47

high energy (35kcal/kg), high protein (1-1.5g/kg), fat restriction if steatorrhea persists (MCT oil?)

Question 48

v trypsin secretion means less ____ digestion

Answer 48

protein