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BMS150 Post-MT2 > Physiology and Pathology: The Pancreas > Flashcards

Physiology and Pathology: The Pancreas Flashcards

1
Q

Four parts of the pancreas?

A
  • Head and uncinate process
  • Neck
  • Body
  • Tail
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2
Q

________ joins ________ at the hepatopancreatic ampulla (ampulla of vater)

A

Main pancreatic duct joins the common bile duct

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3
Q

Accessory pancreatic duct drains to what?

A

The minor duodenal papilla

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4
Q

Is the pancreas a retro-peritoneal structure?

A

yes

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5
Q

Arterial supply of pancreas head?

A
  • Pancreaticoduodenal branches of the gastroduodenal artery
  • Superior mesenteric artery
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6
Q

Arterial supply of pancreas neck, body, tail?

A
  • Branches of splenic artery (celiac trunk)
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7
Q

Venous supply of the pancreas?

A
  • Splenic vein
  • Superior mesenteric vein
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8
Q

The exocrine functions of the pancreas are carried out by what?

A

The acini

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9
Q

What type of gland system is the exocrine pancreas?

A

Compound tubulo-acinar

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10
Q

The compound tubulo-acinar gland system produces ______ rich fluid containing digestive enzymes

A

Bicarbonate

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11
Q

Acinar cells surround _______ cells - which function to line what?

A

Centro-acinar cells - line the lumen of the acinus = beginning of intercalated ducts

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12
Q

Intercalated ducts branch from the lumen of the acinus and merge into what?

A

Interlobular ducts

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13
Q

General functions of acinar cells? (3)

A
  • Secretion of inactive pancreatic enzymes (zymogens)
  • Rich RER, lots of granules
  • CCK major stimulator
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14
Q

General function of centroacinar cells? (2)

A
  • Secretion of bicarb-rich fluid
  • Secretin major stimulator
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15
Q

What two cell types secrete bicarbonate in response to secretin?

A
  • Centro-acinar cells
  • Intercalated duct cells
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16
Q

_____ diffuses from blood in to cell to combine with water to form ______

A

CO2 + H2O => Carbonic acid

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17
Q

Carbonic acid dissociates to form what?

A

HCO3- and H+

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18
Q

HCO3- is actively transported into the duct and what follows?

A

Na+

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19
Q

Movement of HCO3- and Na+ into the ducts creates what? Causes what?

A

Osmotic pressure causing osmosis of H2O into duct

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20
Q

Three phases of pancreatic secretion?

A
  1. Cephalic
  2. Gastric
  3. Intestinal
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21
Q

Cephalic phase stimulants?

A

Sight, smell, taste, mastication

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22
Q

Cephalic regulatory pathway?

A

Vagal pathway

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23
Q

Percentage of maximum enzyme secretion of cephalic phase?

A

20%

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24
Q

Gastric phase stimulants?

A

Distention, Gastrin (?)

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25
Q

Cephalic regulatory pathway?

A

Vagal-cholinergic pathway

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26
Q

Percentage of maximum enzyme secretion of gastric phase?

A

10-20%

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27
Q

Intestinal phase stimulants?

A

Amino acids, FAs, H+ (after chyme leaves stomach)

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28
Q

Intestinal regulatory pathway?

A

CCK and Secretin (most), Enteropancreatic reflexes

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29
Q

Percentage of maximum enzyme secretion of intestinal phase?

A

50-80%

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30
Q

Regulation of pancreatic secretetion has both ______ and ______ control

A

Neural and hormonal

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31
Q

What phases are mostly regulated through nervous system?

A

Cephalic and gastric phases

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32
Q

What phase is mostly under hormonal control?

A

Intestinal phase

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33
Q

What is the source of secretin and what is its stimulus?

A

Source = S cells lining duodenum
Stim = Acid entering duodenum

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34
Q

What is the source of CCK and what is its stimulus?

A

Source = I cells in duodenum
Stim = Fat and aa’s entering duodenum

35
Q

What do Secretin and CCK stimulate in the pancreas?

A

Secretin = fluid secretion (HCO3-)
CCK = Enzyme secretion

36
Q

What do Secretin and CCK stimulate in the gall bladder?

A

Secretin = nothing
CCK = contraction of GB, relaxation of sphincter of Oddi

37
Q

The 2 secretions combine and then flow through what?

A

The long pancreatic duct

38
Q

The long pancreatic duct joins _____ and releases the secretions where?

A

Common bile duct; releases secretions into ampulla of Vater

39
Q

Secretions empties into the duodenum through what? What is this surrounded by?

A

Major duodenal papilla - surrounded by Sphincter of Oddi

40
Q

Enzyme that through hydrolysis, cleave peptide bonds at certain amino acids?

A

Endopeptidase

41
Q

Examples of endopeptidases? (4)

A
  • Pepsin
  • Trypsin
  • Chymotrypsin
  • Elastase
42
Q

Enzyme that through hydrolysis, cleave peptide bonds at the carboxyterminus?

A

Exopeptidases

43
Q

Example of exopeptidase?

A

Carboxypeptidases (A + B)

44
Q

What do trypsin inhibitors do?

A

Prevent pancreatic auto-digestion

45
Q

What are trypsin inhibitors secreted from? What does this do?

A

Secreted from acinar cells = prevents activation of trypsin inside secretory cell and in ducts of pancreas

46
Q

What happens when trypsin runs out of proteins to break down in the duodenum?

A

Hydrolyzes itself in a form of negative feedback loop

47
Q

What does pancreatic amylase do?

A

Hydrolyzes alpha 1-4 linkages in amylose (starch)

48
Q

Enzyme activated by trypsin that digests phospholipids?

A

Phospholipase A2

49
Q

What are pancreatic lipase and colipase for?

A

Pancreatic lipase needs fat emulsification and colipase to cleave triglycerides

50
Q

Acute pancreatitis severity?

A

Ranges from life-threatening to a self-limited illness

51
Q

Major risk factors for acute pancreatitis?

A
  • Excessive alcohol intake
  • Cholelithiasis
52
Q

Acute pancreatitis is acute, reversible pancreatic injury associated with what?

A

Inflammation

53
Q

Metabolic etiologies of acute pancreatitis? (4)

A
  • Alcoholism
  • Hyperlipoproteinemia
  • Hypercalcemia
  • Drugs (eg azathioprine)
54
Q

Genetic etiologies of acute pancreatitis?

A
  • Mutations in the cationic trypsinogen and trypsin inhibitor genes PRSS1 and SPINK1
55
Q

Mechanical etiologies of acute pancreatitis? (3)

A
  • Gallstones
  • Trauma
  • Operative injury
56
Q

Vascular etiologies of acute pancreatitis? (3)

A
  • Shock
  • Atheroembolism
  • Vasculitis
57
Q

What is the tole of trypsinogen activation in acute pancreatitis?

A

Its a digestive enzyme (trypsin) capable of activating other zymogens

58
Q

What does alcohol ingestion cause regarding acute pancreatitis? (3)

A
  • Excessive protein in pancreatic duct
  • Directly toxic to acinar cells
  • Causes contraction of sphincter of Oddi
59
Q

What does biliary tract obstruction cause regarding acute pancreatitis?

A

Pancreatic secretions get stuck in the ducts

60
Q

Common factor regarding pathophysiology of acute pancreatitis>

A

Blockage of ducts

61
Q

As ducts become obstructed, pressure begins to build in the interstitia causing what?

A

Interstitial edema and impaired blood flow

62
Q

What do injured tissues, aeriacinar myofibroblasts and leukocytes release?

A

Pro-inflammatory cytokines: IL-1 beta, IL-6, TNF, platelet-activating factor, and substance P

63
Q

Activation of complement and clotting cascade leads to what?

A

Impairment of blood flow

64
Q

The systemic inflammatory response of acute pancreatitis can lead to? (4)

A
  • Leukocytosis
  • Hemolysis
  • Disseminated intravascular coagulation
  • Acute respiratory distress syndrome
65
Q

Pathological features of acute pancreatitis? (5)

A
  • Microvascular leakage = edema
  • Digestion of fat
  • Acute inflammation
  • Proteolytic destruction of parenchyma
  • Destruction of blood vessels
66
Q

What can be seen at any stage?

A

Fat necrosis

67
Q

What happens when free pancreatic lipases cleave triglycerides in the abdominal cavity?

A

Saponification - FAs combine with extracellular Ca2+

68
Q

What can saponification lead to?

A

Hypercalcemia

69
Q

Cardinal manifestation of acute pancreatitis?

A

Abdominal Pain

70
Q

Sx in acute pancreatitis?

A
  • Constant, intense, epigastric pain
  • Anorexia, nausea, and vomiting
71
Q

Systemic effects of severe acute pancreatitis? (3)

A
  • Systemic inflammation
  • Hemorrhage
  • Fluid loss into the abdomen
72
Q

Complications of acute pancreatitis? (5)

A
  • Pseudocysts
  • Chronic pancreatitis
  • Infection
  • Hemorrhage or shock
  • Death
73
Q

Inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis, and, in the late stages, the destruction of endocrine parenchyma?

A

Chronic Pancreatitis

74
Q

What usually causes chronic pancreatitis? (2)

A
  • Repeated bouts of acute pancreatitis
  • Long-term alcohol abuse
75
Q

What do you tend to see in chronic pancreatitis?

A

Irreversible/chronic ductal obstruction by concretions = calcified plugs

76
Q

Pathology of chronic pancreatitis? (4)

A
  • Parenchymal fibrosis
  • Reduced # and size of acini
  • Variable dilation of pancreatic ducts
  • Chronic inflammatory infiltrate around lobules and ducts
77
Q

What cells are usually spared until end-stage chronic pancreatitis?

A

Islets of Langerhans

78
Q

Clinical findings of chronic pancreatitis?

A

Repeated attacks of acute pancreatitis

79
Q

chronic pancreatitis may be entirely silent until when?

A

Pancreatic insufficiency (malabsorption) and diabetes develop

80
Q

What are localized collections of necrotic-hemorrhagic material rich in pancreatic enzymes?

A

Pseudocysts

81
Q

What do pseudocysts lack?

A

Epithelial lining

82
Q

When do pseudocysts usually arise?

A

After an episode of acute pancreatitis or in chronic pancreatitis

83
Q

Locations of pseudocysts? (4)

A
  • Within pancreas
  • Lesser omentum
  • Retro-peritoneum
  • Sub-diaphragmatic (rarely)
84
Q

What are pseudocysts formed by?

A

Walling off of fat necrosis with fibrous tissue

BMS150 Post-MT2 (17 decks)

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