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BMS150 - Post Test 2 > Pancreas Physiology and Pathology (Week 12) > Flashcards

Pancreas Physiology and Pathology (Week 12) Flashcards

1
Q

What are the major parts of the pancreas?

A
  • head and uncinate process
  • neck
  • body
  • tail
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2
Q

The main pancreatic duct joins the common bile duct at the ____________

A

Ampulla of Vater (hepatopancreatic ampulla)

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3
Q

The accessory pancreatic duct drains into the ___________

A

minor duodenal papilla

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4
Q

The pancreas is about ______ long

A

25 cm

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5
Q

True or False: The pancreas is a retroperitoneal structure

A

True

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6
Q

What artery supplies the head of the pancreas?

A
  • superior mesenteric artery*
  • gastroduodenal artery
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7
Q

What artery supplies the neck, body, and tail of the pancreas?

A

splenic artery (celiac trunk)

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8
Q

Which veins drain the pancreas?

A
  • splenic vein
  • superior mesenteric vein
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9
Q

The exocrine functions of the pancreas are carried out by the ______

A

acini

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10
Q

The compound tubulo-acinar gland system produces ________ mL/day of bicarbonate-rich fluid, containing digestives enzymes

A

1200 mL/day

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11
Q

How many acinar cells form a spherical acinus?

A

40-50 acinar cells

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12
Q

The ________ cells are surrounded by acinar cells and line the lumen of the acinus

A

centro-acinar

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13
Q

Intercalated ducts branch from the lumen of the acinus and merge into _________ ducts

A

interlobular

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14
Q

Centroacinar cells and intercalated duct cells can both secrete ___________ in response to secretin

A

bicarbonate

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15
Q

What is the function of acinar cells?

A
  • secretion of inactive pancreatic enzymes (zymogens)
  • rich RER, lots of granules (filled with zymogens)
  • CCK major stimulator
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16
Q

What is the function of centroacinar cells?

A
  • secretion of HCO3- (bicarbonate) rich fluid

Note: major stimulator = secretin

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17
Q

CO2 and H2O can combine to form ___________ which dissociates into bicarbonate (HCO3-) and H+

A

carbonic acid (H2CO3)

Note: this reaction is catalyzed by carbonic anhydrase

Note: The centroacinar cells produce carbonic acid, and when it dissociates, it pumps the bicarbonate into the pancreatic duct

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18
Q

_______ follows bicarbonate out of the pancreas and into the lumen of the pancreatic duct

A

Sodium (Na+)

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19
Q

What are the phases of pancreatic secretion?

A

1) cephalic phase
2) gastric phase
3) intestinal phase

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20
Q

This phase of pancreatic secretion is stimulated by sight, smell, taste, mastication, and even the thought of food; it is stimulated by the vagus nerve, which signals the pancreas to secrete enzymes such as lipase and amylase to prepare for food digestion; 20% of pancreatic secretion

A

cephalic phase

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21
Q

This phase of pancreatic secretion is triggered by food in the stomach (distension) and gastrin; it involves the vagal-cholinergic pathway (aka nervous stimulation) and stimulates the release of bicarbonate ions to neutralize stomach acids and enzymes; 5-10% of pancreatic secretion

A

gastric phase

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22
Q

This phase of pancreatic secretion occurs when chyme leaves the stomach and enters the small intestine; this leads to release of hormones secretin and CCK, which triggers the pancreas to secrete A LOT of bicarbonate and digestive enzymes; 50-80% (majority) of pancreatic secretions

A

intestinal phase

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23
Q

REVIEW: What secretes secretin?

A

S cells

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24
Q

REVIEW: What secretes CCK?

A

I cells

25
Q

True or False: Pancreatic secretion is controlled by the nervous system

A

False

It is under both neural AND hormonal control. Cephalic and gastric phases are mostly regulated under nervous system and intestinal phase is mostly under hormonal control.

26
Q

REVIEW: What stimulates secretin release?

A

acid entering duodenum

27
Q

REVIEW: What stimulates CCK release?

A

fats (mostly) and amino acids entering duodenum

28
Q

The pancreatic duct combines with the ________

A

common bile duct

29
Q

an enzyme that cleaves peptide bonds at certain amino acids in the middle of the peptide via hydrolysis

A

endopeptidases

Ex: pepsin, trypsin, chymotrypsin, elastase

30
Q

an enzyme that cleaves peptide bonds at the carboxyterminus via hydrolysis

A

exopeptidases

Ex: carboxypeptidases A + B

31
Q

How do we control trypsin and pancreatic auto-digestion?

A

trypsin inhibitor

When trypsin “runs out” of proteins to break down in the duodenum, it then hydrolyzes itself in a form of negative feedback

Note: trypsin inhibitor is usually packaged together with other pancreatic enzymes in zymogen granules

32
Q

REVIEW:

_________ hydrolyzes alpha 1-4 linkages in amylose (starch)

A

Pancreatic amylase

33
Q

REVIEW:

______________ needs fat emulsification (bile salts) and colipase in order to cleave triglycerides into 2-monoglyceride and FFAs

A

Pancreatic lipase

34
Q

REVIEW:

____________ is activated by trypsin, and digests phospholipids

A

Phospholipase A2

35
Q

True or False: The severity of acute pancreatitis ranges from life-threatening to a self-limited illness that causes mild to moderate abdominal pain

A

True

36
Q

What are the major risk factors for acute pancreatitis?

A
  • excessive alcohol consumption
  • cholelithiasis

Note: 80% of acute pancreatitis is due to these two factors

37
Q

True or False: Acute pancreatitis is irreversible

A

False

It is reversible

38
Q

What genetic factors might contribute to the development in acute pancreatitis?

A
  • mutations in trypsinogen (thus unable or more difficult for trypsin to chop itself up and cleave itself)
  • mutations in trypsin inhibitors (e.g., SPINK1)
39
Q

What is the role of trypsinogen activation in acute pancreatitis?

A

activation of trypsinogen = trypsin

trypsin is a digestive enzyme capable of activating other zymogens; this may lead to autodigestion of the pancreas

40
Q

How does alcohol ingestion lead to the development of acute pancreatitis?

A

leads to excessive protein in pancreatic secretions (“a dehydrated secretion that is protein-rich and less fluid”)

this plugs the ducts –> pressure builds up and swelling occurs

it is also toxic to acinar cells

causes contraction of the sphincter of Oddi (thus can’t send secretions into duodenum)

41
Q

How does biliary tract obstruction lead to the development of acute pancreatitis?

A

pancreatic secretions are stuck in the ducts, due to a gallstone or sludge blocking outflow

42
Q

Describe the pathophysiology of acute pancreatitis

A
  • more than just auto-digestion
  • release of pro-inflammatory cytokines (leads to inflammation and edema)
  • activation of complement and clotting cascades
  • elevated interstitial pressures leading to impairment of blood flow
  • systemic inflammatory response (resulting in leukocytosis, hemolysis, intravascular coagulation, and acute respiratory distress syndrome)
43
Q

In acute pancreatitis, what would you see under the microscope (pathological features)?

A

1) microvascular leakage causing edema (mild)
2) digestion of fat by lipolytic enzymes
3) acute inflammation
4) proteolytic destruction of pancreatic parenchyma
5) destruction of blood vessels and subsequent interstitial hemorrhage (severe)

44
Q

when fatty acids combine with extracellular calcium

A

saponification

(can be a sign of fat necrosis)

45
Q

What are the clinical features of acute pancreatitis?

A
  • abdominal pain* (constant, intense, epigastric and often referred to the upper back or shoulder
  • anorexia, nausea, vomiting that may accompany the pain
  • elevated pancreatic amylase and pancreatic lipase (bloodwork)
  • systemic effects of severe acute pancreatitis = inflammation, hemorrhage, fluid loss which can proceed to shock or kidney failure… medical emergency
46
Q

What are some complications of acute pancreatitis?

A
  • pseudocysts
  • chronic pancreatitis
  • infection of fluid collections and/or necrotic debris by bacteria
  • hemorrhage, shock (acute respiratory distress and kidney failure can complicate shock)
  • 5% with severe acute pancreatitis die from shock during the first week of illness
47
Q

inflammation of the pancreas characterized by destruction of exocrine parenchyma, fibrosis, and in the late stages, destruction of endocrine parenchyma

A

chronic pancreatitis

48
Q

True or False: Chronic pancreatitis is irreversible

A

True

49
Q

Chronic pancreatitis is usually caused by repeated bouts of _________

A

acute pancreatitis

(often due to alcohol abuse)

50
Q

What are some less common causes of chronic pancreatitis?

A
  • cystic fibrosis
  • hereditary pancreatic disease
  • tumours
51
Q

Describe the pathophysiology of chronic pancreatitis

A
  • ductal obstruction by concretions
    (due to increased protein concentrations in the pancreatic juice, forms plugs that can become calcified)
  • alcohol also has a toxic effect on acinar cells (oxidative stress on pancreatic cells may result in the activation of pancreatic enzymes and damage)
52
Q

What would you see under the microscope in chronic pancreatitis (pathological features)?

A
  • parenchymal fibrosis
  • reduced number and size of acini (Note: islets of Langerhans are often spared until end-stage disease)
  • variable dilation of the pancreatic ducts
  • chronic inflammatory infiltrate around lobules and ducts
53
Q

How does chronic pancreatitis present clinically?

A
  • repeated attacks of mild or moderate severity abdominal pain or back pain (may be silent until pancreatic insufficiency and diabetes mellitus develop)
  • 50% mortality after 25 years (usually linked to development of malabsorption and diabetes)
  • nutrient deficiencies (e.g., fat soluble vitamins A, D, E, and K)
54
Q

localized collections of necrotic-hemorrhagic material, rich in pancreatic enzymes; usually solitary (only one present at a time); usually located within the pancreas, but also can be located within the lesser omentum, retroperitoneum between stomach and transverse colon or between the stomach and liver

A

pseudocysts

55
Q

True or False: Pseudocysts and true cysts have epithelial linings.

A

False

Cysts have epithelial linings. Pseudocysts do not.

56
Q

How do pseudocysts form?

A

via the walling off of fat necrosis with fibrous tissue

57
Q

True or False: Pseudocysts can range from 2-30cm in diameter

A

True

58
Q

What are some clinical features of pseudocysts?

A
  • symptoms are those of underlying illness (i.e., chronic pancreatitis)
  • can become complicated by secondary infection or perforation (can cause peritonitis if they rupture; medical emergency)
  • larger pseudocysts can compress adjacent structures causing symptoms

BMS150 - Post Test 2 (9 decks)

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