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BMS 460 Unit 3 > Lecture #1 > Flashcards

Lecture #1 Flashcards

1
Q

What divides the GI tract into several functional units?

A

Muscular sphincters

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2
Q

Sphincters of the GI tract:

A
  1. esophageal sphincter.
  2. Rectal sphincter.
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3
Q

Which regions of the GI tract are there no sphincters?

A

Colon and small intestines.

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4
Q

Taeniae coli:

A

Discontinuous 3 distinct strips of outer longitudinal muscle.

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5
Q

Which cells of the GI tract are constantly replaced + have constant turnover:

A

Endothelial cells.

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6
Q

What are the 3 layers of the GI tube, from most internal to most external?

A
  1. Mucosal layer.
  2. Submucosal layer.
  3. Muscularis externa layer.
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7
Q

Components of the mucosal layer of the GI tube:

A
  1. Glandular epithelium that overlies the lamina propria.
  2. Lamina propria - made of loose connective tissue, resident chronic inflammatory cells.
  3. muscularis mucosa - seperates mucosa from submucosa.
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8
Q

Components of the submucosal layer of the GI tube:

A
  1. Adipose tissue, vessels, and nerves.
  2. Meissner’s plexus - a submucosal nerve plexus.
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9
Q

Components of muscularis externa layer of the GI tube:

A
  1. Two layers of smooth muscle - a circular muscle and a longitudinal muscle.
  2. Has inter-myenteric plexus - intrinsic nervous system plexus.
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10
Q

Which branch of the nervous system will control peristalsis via both the submucosal and intermyenteric plexus:

A

Intrinsic nervous.

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11
Q

The parasympathetic nervous system has a positive effect on:

A
  1. Motility.
  2. GI secretions.
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12
Q

The parasympathetic nervous system has a negative effect on:

A
  1. Sphinctor tone.
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13
Q

What effect does the parasympathetic nervous system have on vasoconstriction:

A

No effect.

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14
Q

The sympathetic nervous system has a positive effect on:

A
  1. Sphincter tone.
  2. Vasoconstriction.
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15
Q

The sympathetic nervous system has a negative effect on:

A
  1. GI glandular secretions.
  2. Motility.
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16
Q

________ reflex does brain-gut communication in the GI tract, allowing for receptive relaxation of the stomach. Has preganglionic fibers.

A

Vagovagel reflex.

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17
Q

_________ reflex does motility and secretions in the colon, also called the gastrocolic reflex. Has postganglionic fibers.

A

Local.

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18
Q

Four phases of secretion of gastric juices:

A
  1. Cephalic phase - mouth.
  2. Gastric phase - stomach.
  3. Intestinal phase - Intestines.
  4. Basal/interdigestive phase.
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19
Q

Which phase of gastric secretions will have a CNS reflex that is stimulated by thinking, seeing, tasting or smelling food:

A

Cephalic phase.

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20
Q

In which phase of gastric secretions do bile and pancreatic digestive enzymes get released into the duodenum?

A

The intestinal phase.

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21
Q

Basal/interdigestive phase:

A

Will excrete 50 g of slid waste and 100 ml of fluid as feces.

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22
Q

Fluid reabsorption primarily occurs in which phase of gastric secretions?

A

Intestinal phase.

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23
Q

What is the first enzyme that will help to break down carbohydrates - where is it released from?

A

Amylase from salivary glands.

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24
Q

Which enzyme will be released from the pancreas (via the small intestine lumen) to assist in carbohydrate breakdown?

A

Amylase from the pancreas.

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25
Q

What enzymes will be released from the small intestine mucosa to help break down carbohydrates into simple sugars?

A

Lactase, maltase, sucrase.

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26
Q

True or false: The breakdown of proteins into amino acids will begin in the mouth due to salivary enzymes.

A

FALSE: salivary enzymes do not work on proteins, they work on carbohydrates. The beginning protein breakdown happens in the stomach, where HCL directly works on proteins, and also HCL converts pepsinogen to pepsin - which also works on proteins.

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27
Q

What enzymes are created by the pancreas to help break down proteins into amino acids?

A

Ultimately causes the release of chemotrypsin and carboxypeptidases.

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28
Q

Explain the process of creating chymotrypsin and carboxy-peptidases:

A
  1. Trypsinogen in converted trypsin but usage of an enterokinase.
  2. Trypsin positively feedbacks, causing further conversion of trypsinogen to trypsin.
  3. Trypsin is a zymogen, but production of other zymogens will also occur.
  4. Zymogens are converted into chymotrypsin and carboxypeptidases
  5. Chemotrypsin and carboxypeptidase act on proteins to break them down to amino acids.
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29
Q

What enzymes are release by the brush border of the small intestine mucosa, to help break down proteins into amino acids?

A

Aminopeptidases.

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30
Q

Where does break down of fats into fatty acids begin?

A

In the small intestine lumen.

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31
Q

What enzyme released from the liver into the small intestine lumen, will help break down fats into fatty acids?

A

Bile.

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32
Q

Which enzyme released from the pancreas into the small intestine lumen, will help break down fats into fatty acids?

A

Lipase.

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33
Q

In digestion of chyme, fat products will diffuse into which vessel?

A

lacteals, of the lymphatic system.

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34
Q

In the digestion of chyme simple sugars and amino acids are absorbed into ______________ of the intestinal ________.

A
  1. Blood capillaries.
  2. Villi.
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35
Q

True or false: Chyle is the product formed when fat products diffuse into the lacteals, which ultimately will enter the venous blood.

A

TRUE!

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36
Q

Where is food converted into chyme?

A

In the stomach.

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37
Q

Water-soluble vitamins:

A

C + B

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38
Q

Fat-soluble vitamins:

A

A, D, E, and K vitamins.

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39
Q

What must vitamin B12 bind to, allowing it to be endocytosed into the ileum?

A

Intrinsic factor produced from gastric parietal cells.

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40
Q

True or false: iron (Fe) is primarily absorbed in the ileum and distal jejunum.

A

FALSE: Iron (Fe) is primarily absorbed in the duodenum and proximal jejunum.

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41
Q

When iron (Fe) is within the cell it is bound by ______________ and delivered to the ______________ membrane, where it forms a complex with ______________.

A
  1. Iron-binding proteins.
  2. basolateral membrane.
  3. Transferrin.
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42
Q

Iron is stored in the cells as:

A

ferritin.

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43
Q

Name two conditions that can result from iron deficiency or defect in iron transport/storage.

A
  1. Iron-deficient anemia.
  2. Anemia of chronic disease.
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44
Q

Deficiency of intrinsic factor or B12 will result in -

A

Pernicious anemia.

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45
Q

The three monosaccharide products - glucose, galactose, and fructose are absorbed by the:

A

Epithelial cells (enterocytes) of the small intestines, into the portal circulation.

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46
Q

Transporter found on apical membrane of enterocytes that transports glucose and galactose into the cell:

A

Sodium-glucose linked transporter, SGLT1

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47
Q

Transporter on the basolateral membrane of the enterocyte, that transports glucose, fructose, and galactose into the portal circulation.

A

GLUT 2.

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48
Q

Peptides + ____________, are co-transported into the enterocytes with _____.

A
  1. Peptides and amino acids.
  2. Na+
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49
Q

Two forms of proteins that can be absorbed into the enterocyte:

A
  1. Small peptides - major.
  2. Free amino acids - minor.
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50
Q

Absorption of digested lipids are absorbed as _______________________, and then reesterified back into _______________.

A
  1. Fatty acids and monoglycerides.
  2. Triglycerides.
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51
Q

Pathway of triglycerides:

A
  1. Triglycerides are packaged as chylomicrons.
  2. Chylomicrons are transported through intestinal lymphatics.
  3. Chylomicrons travel to the thoracic duct and into the left subclavian duct.
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52
Q

True or false: Chylomicrons travel through the portal venous system.

A

False: Chylomicrons travel through lymphatics, into the venous return via the thoracic duct.

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53
Q

Monosaccharide absorption is driven by gradients generated by:

A

Basolateral transporters.

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54
Q

How are bile salts returned to the liver?

A

Bile salts enter the intestinal tract in bile and are reabsorped in the ileum, where they travel back to the liver via the hepatic portal veins.

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55
Q

Splanchnic circulation:

A

Derived entirely from the celiac artery, the superior mesenteric artery, and the inferior mesenteric artery - which all branch directly off the aorta.

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56
Q

Hepatic portal circulation:

A

Venous blood from the intestines, stomach, pancreas, and spleen goes to the sinusoids of the kidneys via the portal vein.

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57
Q

Would would happen if there is disease of the distal ileum, impairing reabsorption of bile salts?

A
  1. Malabsorption of fats - steatorrhea.
  2. Impaired absorption of fat-soluble vitamins - vitamins A, D, E, K.
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58
Q

True or false: Bile salts are reabsorbed into the hepatic portal blood, by diffusion across the ileum.

A

FALSE - Bile salts have specific sodium-coupled transporters to help move them across the ileum and into the hepatic portal circulation.

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59
Q

The ________ nervous system enables the digestive tract to respond to both __________ stimuli, and input from the __________ nerves of the ANS.

A
  1. Enteric/intrinsic.
  2. Local.
  3. Extrinsic.
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60
Q

Where is the primary site of digestion in the GI tract?

A

Stomach and duodenum.

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61
Q

Where is the primary site of absorption in the GI tract?

A

first 1/2 of the small intestines.

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62
Q

Where is the primary site of secretion in the GI tract?

A

second 1/2 of the small intestines.

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63
Q

What regulates and controls peristaltic contractions of the muscularis of the GI tube?

A

Integrated extrinsic and enteric nervous networks.

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64
Q

When do segmenting contractions in the small intestines cease? What pattern will they be replaced by?

A
  1. When all the food is absorbed.
  2. Migrating myoelectirc complex (MMC)
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65
Q

What do we prevent by moving undigested food from the small intestines to the large intestines?

A

Bacterial multiplication in the small intestines.

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66
Q

A rise in which hormone will initiate the migrating myoelectric complex (MMC)?

A

Motilin.

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67
Q

Dysphagia:

A

Abnormal swallowing.

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68
Q

Dyspepsia:

A

Abnormal digestion.

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69
Q

Which intestinal structure acts as a barrier between the internal and external milieu?

A

Intestinal mucosa

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70
Q

The intestinal mucosa has abundant superficial blood vessels - What risk does this pose?

A

Makes the GI tract prone to hemorrhage or ischemia.

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71
Q

________ glands are composed of serous cells, and secrete a non-viscious saliva composed of water, electrolytes, and enzymes.

A

Serous glands.

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72
Q

_________ glands are composed of serous and mucous cells, and produce a vicious saliva that is rich in mucin glycoproteins.

A
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73
Q

What system regulates salivation?

A

The autonomic nervous system.

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74
Q

True or false: Both branches of the autonomic nervous system will stimulate salivation, but the parasympathetic branch is a much stronger stimulator than the sympathetic.

A

TRUE!

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75
Q

Symptoms of Mumps:

A
  1. Fever.
  2. headache.
  3. muscle aches.
  4. loss of appetite.
  5. swelling of salivary glands.
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76
Q

Which salivary gland is most frequently affected by Mumps?

A

parotid salivary glands.

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77
Q

Describe the inflammatory pattern of mumps:

A

causes inflammation of the brain (encephalitis) or miniges (meningitis), and can also cause inflammation to the testis (orchitis).

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78
Q

What is the most common cause of aseptic meningitis?

A

Mumps.

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79
Q

True or false: Mumps is a chronic viral illness that is caused by the mumps virus.

A

FALSE - Mumps is an ACUTE viral illness caused by the mumps virus.

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80
Q

_________ _______ is an adenolymphoma that is a benign tumor of the salivary glands - associated with smoking.

A

Warthin tumor.

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81
Q

Define Sjorgren’s syndrome:

A

An autoimmune disorder with lymphocytic infiltration of the exocrine glands, primarily affecting the salivary and lacrimal glands.

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82
Q

What is a major characterization of sjorgren’s syndrome?

A

Dry mouth (xerostomia) and dry eyes (keratoconjunctivitis).

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83
Q

Sjogren’s syndrome may also affect:

A

digestive organs, lungs, kidneys, joints, blood vessels, and nerves.

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84
Q

The vagus nerve stimulates the enterochromaffin-like cells (ECLs) to secrete -

A

histamine.

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85
Q

vagus nerve stimulates the enteroendocrine G cells (G-Cells) to secrete:

A

Gastrin.

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86
Q

The vagus nerve stimulates delta (D) cells to secrete:

A

somatostatin.

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87
Q

_________ stimulates the parietal cells to produce _____

A
  1. Gastrin.
  2. HCl.
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88
Q

______ stimulates chief cells to secrete ________ via pepsinogen.

A
  1. HCl.
  2. Pepsin.
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89
Q

Function of pepsin:

A

Pepsin cleaves proteins to amino acids, some of which stimulate G cells to release gastrin - further promoting HCl production.

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90
Q

Pepsin will specifically cleave 2 amino acids that will stimulate the g-cell production of gastrin. What are these two amino acids?

A
  1. Tryptophan.
  2. Phenylalanine.
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91
Q

What happens to gastric secretions when gastric pH drops below 3?

A

Secretion of gastrin stops.

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92
Q

What happens to gastric secretions when gastric pH drops below 2?

A

HCl production stops entirely.

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93
Q

What is the name of the inhibitory hormone that inhibits the secretion of gastrin, and sub sequentially, secretion of HCl from parietal cells.

A

Somatostatin.

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94
Q

Entry of food into the duodenum causes the release of:

A

Inhibitors of gastric secretions: secretin, cholecystokinin (CCK), somatostatin, and gastric inhibitory peptide (GIP).

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95
Q

Entry of chyme into the ileum leads to a release of:

A

release of peptide YY and cholecystokinin (CCK), which inhibit gastric emptying.

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96
Q

Function of histamine:

A

Stimulates acid secretion as it potentiates the response to acetylcholine (Ach).

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97
Q

___________ ___________, where many glands containing acid-secreting parietal cells are destroyed - Limiting gastric acidification causing __________

A
  1. atrophic gastritis.
  2. achlorhydria.
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98
Q

In atrophic gastritis, the lack of acid production will cause -

A
  1. A loss of feedback inhibition on gastrin secretion.
  2. Hypergastrinemia and ECL hyperplasia.
  3. Impaired protein digestion and iron absorption.
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99
Q

Pernicious anemia is caused by vitamin B12 deficiency. What is the cause of this?

A

Atrophic gastritis.

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100
Q

A deficiency of vitamins, such as seen in atrophic gastritis, will impair _____________________________, causing anemia, leukopenia, and thrombocytopenia.

A

maturation of hematopoietic cell precursors.

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101
Q

Pernicious anemia will show cells that are:

A
  1. Megaloblastic.
  2. Macrocytic.
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102
Q

Epithelial cells in the stomach wall will produce bicarbonate (HCO3-) and acid (H+), where will these two components go?

A
  1. Bicarbonate (HCO3-) diffuses into the plasma in exchange for chloride ions (Cl-).
  2. Acid (H+ ions) will be pumped into the stomach lumen, using the H/K-ATPase pump - Exchanging H+ for K+.
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103
Q

The H/K-ATPase pump moves H+ into the stomach lumen, what happens to K+?

A

K+ is pumped into the parietal epithelial cells, but due to K+ leak channels, it will leak back out into the stomach lumen.

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104
Q

How is bicarbonate and acid made in the parietal cell?

A

CO2, that is generated within or diffuses into the parietal cell will react to water to form HCO3- and H+ ions.

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105
Q

Parietal cells secrete ___________ into the fenestrated capillaries, while it also secretes __________ into the stomach lumen.

A
  1. Bicarbonate (HCO3-)
  2. Acid (H+)
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106
Q

Effects of excessive vomitting on acid and bicarbonate secretion:

A
  1. K+ depletion due to the leak channels.
  2. Metabolic acidosis due to loss of hydrogen ions.
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107
Q

What is the “alkaline tide” that occurs after a meal?

A

Caused by the bicarbonate entry into the circulation, making blood more alkaline. But doesn’t cause alkalosis because the pancreas secrete HCO3- into the stomach lumen to counteract gastric secretions.

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108
Q

What is the function of mucus in the gastric lumen?

A

Mucus gell provides pH neutralization, preventing the low acidic pH of the lumen from damaging the gastric epithelium.

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109
Q

Mucous suface cells produce:

A

Bicarbonate.

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110
Q

What stimulates mucus production?

A

Prostaglandins.

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111
Q

Mucosal blood flow is highly dependant on:

A

The local production of prostaglandins.

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112
Q

Prostaglandins are ___________ _____ derivatives, meaning their production can be inhibited by ____________ and _____ ___________ - such as ________.

A

Prostaglandins are arachidonic acid derivatives, meaning their production can be inhibited by corticosteroids and COX inhibtiors - such as NSAIDs.

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113
Q

What class of drugs can inhibit mucosal blood flow by inhibiting prostaglandin synthesis?

A

Anti-inflammatory drugs.

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114
Q

Inhibition of prostaglandin production will compromise what? Which can result in what?

A

This can compromise the protective actions of the gastric mucosa, and can cause irritation of the mucosa (gastritis) or ulceration (peptic ulcer disease)

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115
Q

______: Decreased ability of the lower esophageal sphincter to close, resulting in reflux that causes ulcerations.

A

GERD - Gastro-esophageal reflux disease.

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116
Q

What does the lower esophageal (LES) sphincter normally prevent?

A

Reflux of gastric juices into the esophagus.

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117
Q

Ulcerations of the esophagus in GERD are mediated by which gastric secretions?

A

Pepsin and HCl.

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118
Q

Symptoms of GERD:

A
  1. Heart burn.
  2. Esophagitis - inflammation of the esophagus.
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119
Q

Treatments for GERD:

A
  1. Lower esophageal repairing surgeries.
  2. Gastric acid inhibitors.
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120
Q

________ ________: A defect in the diaphragm that allows a portion of the stomach to pass through the esophageal hiatus, into the thorax.

A

Hiatal hernia.

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121
Q

Predisposing factors for hiatal hernia:

A

Increased intra-abdominal pressure - due to pregnancy, obesity, ascites, chronic straining, or chronic coughing.

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122
Q

Symptoms of hiatal hernia:

A

The same as the symptoms for GERD.
1. Heartburn.
2. Esophagitis - Inflammation of the esophagus.

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123
Q

Cardiac and esophageal pains may feel the same due to a shared ______ _______, from the __________ _________ sensory pain fibers.

A
  1. Nerve supply.
  2. Afferent visceral.
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124
Q

What is two unique things about the afferent visceral sensory pain nerve fibers that innervate the esophagus?

A
  1. They end without synapse in the 1st four segments of the thoracic spinal cord.
  2. Their pathway is shared with the heart innervation.
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124
Q

What is NON-GERD heartburn often related to?

A

Ischemis heart disease.

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125
Q

Antihistamines can be used to treat GERD, what is their mechanism?

A

Antihistamines block the binding of histamine to H2 receptors on the gastric parietal cell, which causes a downstream decrease in cAMP, which would normally stimulate H+K+ ATPase pump to H+ into the stomach lumen. These inhibit proton pump insertion.

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126
Q

Anticholinergic drugs can be used to treat GERD, what is their mechanism?

A

Anticholinergic drugs block ACh from binding to M3 receptors, causing a downstream decrease in IP3/Ca+, which would normally stimulate the H+K+ ATPase pump to pump H+ into the stomach lumen. These inhibit insertion of proton pump.

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127
Q

What is a common anticholinergic drug used to treat GERD?

A

Atropine.

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128
Q

What is a common antihistamine drug used to treat GERD?

A

The H2 blocker cimetidine.

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129
Q

Proton pump inhibitors can be used to treat GERD, what is their mechanism?

A

Proton pump inhibitors directly inhibit the H+K+ ATPase pump function, causing less H+ secretion. These inhibit inserted proton pumps.

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130
Q

True or false: Barret’s esophagus occurs when gastric mucosal epithelium go through metaplasia to act as esophageal mucosal epithelium.

A

FALSE: Barret’s esophagus occurs when ESOPHAGEAL mucosal epithelium go through metaplasia to act as gastric mucosal epithelium.

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131
Q

Barret’s esophagus is typically caused by:

A

Gastroesophageal reflux disease - GERD.

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132
Q

In Barret’s disease, stratified squamous epithelium transforms into _________________.

A

columnar epithelium.

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133
Q

True or false: Barrett’s esophagus will significantly increase the risk for esophageal adenocarcinoma.

A

TRUE!

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134
Q

What portion of the esophagusgus does esophageal adenocarcinoma typically occur in?

A

Distal 1/3 of the esophagus.

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135
Q

Squamous cell carcinoma of the esophagus will begin as an in situ lesion - causing ___________ __________.

A

Squamous dysplasia.

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136
Q

50% of esophageal squamous cell carcinomas will occur in which region of the esophagus?

A

Middle 1/3 of the esophagus.

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137
Q

An absence of serosa in the esophagus will contribute to what?

A

The ability for esophageal cancers to spread locally before detection.

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138
Q

Columnar metaplasia in the lower esophagus is called:

A

Barrett’s esophagus.

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139
Q

_______ ________: an erosion in the lining of the stomach or duodenum.

A

Peptic ulcer.

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140
Q
A
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141
Q

What gastric secretions are responsible for creating peptic ulcers?

A

HCl and Pepsin.

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142
Q

In peptic ulcer disease, HCl and pepsin will do what?

A

Cause breakdown of the epithelial barrier and slightly alkaline mucus.

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143
Q

Excess usage of what substances may cause peptic ulcers?

A

aspirin, NSAIDs, alcohol, and bile acids.

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144
Q

What kind of infection can occur in peptic ulcers, why does it?

A
  1. Helicobacter pylori infection.
  2. It thrives in acidic conditions, such as in peptic ulcers.
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145
Q

How does excess gastrin production result in peptic ulcers?

A

Increased basal activity of the vagus nerve will stimulate ECL cells to secrete histamine, which causes excess gastrin production, which will stimulate parietal cells to release excess HCL.

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146
Q

Consequences of G-ccell neoplasia:

A
  1. Hyperplasia of ECL cells, causing excessive histamine release.
  2. Excessive release of gastrin.
  3. Together, this will cause chronic stimulation of parietal cells to produce HCL - leading to peptic ulcers.
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147
Q

How are peptic ulcers named?

A

They are named based on their location - ie: duodenal ulcer or gastric ulcer.

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148
Q

What condition may mimic peptic ulcer disease?

A

malignant conditions - such as Zoellinger-Ellison Syndrome.

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149
Q

During endoscopy what does the presence of a duodenal ulcer indicate:

A
  1. A high probability of H pylori infection.
  2. A low probability of malignancy.
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150
Q

Which disease will show symptoms of peptic ulcer disease, with hypersecretion of gastric acid, and the presence of a gastrinoma. Due to a malignant tumor?

A

Zoellinger-Ellison Syndrome.

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151
Q

What type of tumor exists in Zoellinger-Ellison syndrome?

A

Malignant tumor of non-beta islet cells of pancreas or other tumors.

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152
Q

Multiple endocrine neoplasia-1 is seen in 20-30% of patients with _________________.

A

Zoellinger-Ellison Syndrome.

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153
Q

___________ of the _____________: A degenerative disease causing aperistalsis of the esophageal body and abnormal relaxation of the lower esophageal sphincter.

A

Achalasia of the esophagus.

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154
Q

Explain the cause of achalasia of the esophagus:

A

T-cell mediated destruction and fibrous replacement of the esophageal myenteric neural plexus.

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155
Q

What are the consequences of destruction of the myenteric plexus inn achalasia of the esophagus?

A
  1. Dysregulation of esophageal smooth muscle.
  2. Decreased or absent peristaltic activity in the distal esophagus.
  3. Impaired lower esophageal sphincter relaxation.
  4. Increased lower esophageal sphincter pressure.
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156
Q

In Achalasia of esophagus - Absent peristalsis, impaired LES relaxtion, and increased LES pressure will result in:

A
  1. Food cannot easily pass into the stomach.
  2. Difficulty swallowing - dysphagia.
  3. Chest pain from esophageal distention.
  4. Frequent pneumonia from aspiration of esophageal contents.
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157
Q

True or false: In achalasia of the esophagus, the neural function can be fully restored, therefore treatment is focussed on a complete restoration of esophageal function.

A

FALSE - Neural function cannot be restored. Therefore, treatment is focused on symptom control and preservation of the esophagus as a passive conduit.

Treatment targets lowering LES pressure and limiting the gastroesophageal sphincter.

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158
Q

Achalasia is most commonly idiopathic, but it can also be seen in __________ ________.

A

Chagas’ Disease.

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159
Q

__________: An infectious disease caused by the protozoan Trypanosoma Cruzi, and often manifests as Megaesophagus.

A

Chagas’ Disease.

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160
Q

True or false: Megacolon can be congenital or acquired.

A

TRUE!

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161
Q

Acquired megacolon may occur at any age as a result of:

A
  1. Chagas’ Disease.
  2. Obstruction by a neoplasm or inflammatory stricture.
  3. Toxic megacolon complicating ulcerative colitis.
  4. Visceral myopathy.
  5. Functional psychosomatic disorders.
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162
Q

What is the most common cause of megacolon?

A

Prolonged constipation.

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163
Q

Congenital megacolon is often associated with what disease?

A

Hirschsprung Disease.

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164
Q

_____________ ________: A congenital disorder of large intestines in which autonomic ganglia in the smooth muscle of the colon are absent or reduced.

A

Hirschsprung disease.

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165
Q

In Hirschsprung disease, which nervous plexuses are involved?

A

Both myenteric and submucosal plexuses are involved.

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166
Q

What is another name for Hirschsprung Disease?

A

Congenital Aganglionic Megacolon.

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167
Q

What causes Hirshsprung disease?

A

A premature end to normal migration of neural crest cells from the cecum to the rectum, or when ganglion cells undergo premature death.

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168
Q

Consequences of Hirshsprung Disease?

A
  1. No coordinated peristaltic contractions.
  2. Functional obstruction.
  3. Resulting dilation proximal to the affected segment.
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169
Q

Name 1 significant comorbidity of Hirschsprung Disease:

A

Down syndrome.

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170
Q

Heterozygous loss-of-function mutations in the proto-oncogene ____ encoding for a _________ _________ ________ is responsible for the majority of Hirschsprung Familial cases.

A
  1. RET.
  2. Tyrosine kinase receptor.
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171
Q

Mutations that may be involved in hirschsprung disease:

A
  1. RET protooncogene.
  2. RET ligand.
  3. Glial-derived neurotrophic factor, endothelin.
  4. Endothelin receptor.
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172
Q

True or false: Known mutation only accounts for 30% of Hirschsprung Disease, indicating that there are other etiological defects contributing.

A

TRUE.

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173
Q

Cells of the myenteric and submucosal plexuses originate primarily from which segment of the embryo? At what weeks of development do they form?

A
  1. Vagal segment.
  2. 12-16 weeks.
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174
Q

In Hirschsprung disease, the arrest of cell migration occurs in embryonic development. What happens as the arrest occurs earlier?

A

The earlier the arrest occurs, the longer the aganglionic section of the colon.

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175
Q

General info on Chagas’ Disease:

A
  1. Caused by Trypanosoma Cruzi protozoan.
  2. Will destroy the myenteric plexus of the colon, causing toxic megacolon.
  3. Can cause myocarditis - which often needs cardiac transplant.
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176
Q

Mechanism of T. Cruzi in Chagas’ Disease:

A
  1. T. Cruzi requires brief exposure to the acidic phagolysosome to stimulate the development of the intracellular stage of the parasite.
  2. Parasites reproduce in the cytoplasm of host cells and then develop flagella, lyse host cells, and enter the bloodstream.
  3. Via the bloodstream parasites will penetrate smooth, skeletal, and heart muscles.
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177
Q

What causes myocarditis in Chagas’ Disease?

A

Parasitization of scattered myofibers + inflammatory infiltrate of neutrophils, lymphocytes, macrophages, and occasional eosinophils.

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178
Q

What is a common treatment for myocarditis in Chagas’ Disease?

A

Heart transplantation.

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179
Q

T. Cruzi, the parasite associated with ___________ ___________, is spread by the ___________ ______.

A
  1. Chagas’ Disease.
  2. Kissing bug.
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180
Q

In Chagas’ Disease, damage to the myenteric plexus causes -

A

Dilation of the colon (megacolon) and esophagus.

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181
Q

In Chagas’ Disease, damage to the myocardial cells causes -

A

Dilated cardiomyopathy and cardiac arrhythmias.

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182
Q

_____________: Caused by toxins binding to membrane receptors of the intestinal cells, that increases secretions and causes a loss of fluids and electrolytes.

A

Gastroenteritis.

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183
Q

Acute gastroenteritis:

A

Is the result of direct infection of the GI tract lining by a virus or ingestion of the following:
1. Bacteria - Clostridium perfringes.
2. Preformed toxins - Staph aureus + vibrio cholerae.
3. Imbalance of normal flora.

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184
Q

Chronic gastroenteritis:

A

A result of another GI disorder - Such as ulcerative colitis.

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185
Q

Mechanism of gastroenteritis:

A
  1. Toxin binds to membrane receptors on intestinal cell.
  2. Activation of adenylate cyclase activation.
  3. Increased cAMP production.
  4. Increased secretion.
  5. Loss of fluids and electrolytes into the intestinal lumen.
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186
Q

True or false: Ulcerative colitis and Crohn’s Disease have very similar characteristics, but Crohn’s disease is much more common than ulcerative colitis.

A

FALSE - Ulcerative colitis is much more common than Crohn’s disease.

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187
Q

Similarities of ulcerative colitis and Crohn’s disease:

A
  1. Both diseases are multi-factorial and idiopathic.
  2. Both diseases are familial.
  3. The peak incidence of both diseases is 20-3o years old.
  4. Both diseases have the same extra-intestinal complications.
  5. The same drugs are used to treat bot diseases.
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188
Q

What distinguishes Crohn’s disease from ulcerative colitis?

A

Crohn’s disease will have transmural inflammation that mainly affects the terminal ileum and right side of the colon.

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189
Q

What distinguishes Ulcerative Colitis from Crohn’s disease?

A

Ulcerative colitis will have inflammation that is confined to the mucosa, and mostly involves the left side of the large intestines (the descending colon and rectum)

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190
Q

In ulcerative colitis and Crohn’s disease, there will be a decreased production of defensins (paneth cells), what will this cause?

A

Leads to uninhibited exposure to gut microbiota.

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191
Q

True or false: Irritable bowel syndrome has no proven etiology or definition, it is just a manifestation of altering diarrhea and constipation accompanied by cramping.

A

TRUE!

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192
Q

Ulcerative colitis and Crohn’s disease are both categorized as:

A

Inflammatory Bowel Disease.

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193
Q

What is the major difference between inflammatory bowel disease and irritable bowel syndrome?

A

Inflammatory bowel disease has an identifiable pathological process, while irritable bowel syndrome does not.

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194
Q

_________ disease is a chronic granulomatous disease of unknown origin.

A

Crohn’s Disease

195
Q

Which inflammatory bowel disease affects multiple portions of the colon, with intervening normal portions involving any part of the GI tract?

A

Crohn’s disease.

196
Q

Regional colitis and granulomatous colitis, are additional names for what condition?

A

Crohn’s disease.

197
Q

In a healthy state, how does the intestinal immune system work?

A
  1. Goblet cells will secrete a layer of mucus that limits exposure of intestinal cells to bacteria.
  2. Paneth cells secrete antimicrobial peptides to provide additional protection from luminal microbiota.
  3. Production of immunoglobulin A (IgA) provides additional protection from luminal microbiota.
198
Q

Innate microbial sensing is down by what cells in the intestinal immune system?

A

Epithelial cells, dendritic cells, and macrophages - Via toll-like receptors and nucleotide oligomerization domain (NOD) proteins.

199
Q

Dendritic cells present antigens to _______ ______ _______, in secondary lymphoid organs.

A

Naive CD4+ T-cells.

200
Q

Name two secondary lymphoid organs that have CD4+ T-cell maturation:

A
  1. Peyer’s patches.
  2. Mesenteric lymph nodes.
201
Q

What modulates the differentiation of CD4+ T-cell subgroups?

A
  1. Phenotype of the antigen-presenting cells.
  2. The cytokine milieu.
202
Q

Activated CD4+ T-cells, will circulate to the _________ ________ _________, where they carry out _________ functions.

A
  1. Intestinal lamina propria.
  2. Effector.
203
Q

What is the characteristic feature of Crohn’s disease?

A

It extends through all layers of the intestinal wall - Causing deep ulcers in the bowel wall which extend to adjacent organs.

204
Q

What is Crohn’s disease caused by?

A

Blockage of lymphoid and lymphatic structures in GI wall.

205
Q

Morphological hallmarks of Crohn’s disease:

A

Transmural inflammation with fibrosis of the muscularis propria (smooth muscle) and mesenteric adipose tissue.

206
Q

True or false: 3/4 of patients with Crohn’s disease also have extra-intestinal lesions - of the joints, skin, liver, or eyes.

A

FALSE: only 1/3 of patients with Crohn’s disease also have extra-intestinal lesions.

207
Q

Treatment for Crohn’s disease:

A

Colectomy for severe colitis - a colostomy bag is needed after.

208
Q

_________ _________: A relapsing inflammatory disease of the mucosa of the rectum and colon.

A

Ulcerative colitis.

209
Q

General info on ulcerative colitis:

A
  1. Frequently is co-morbid with autoimmune diseases.
  2. Is idiopathic.
  3. Changes are most severe in the rectum, but also extend into the colon.
  4. Begins at the base of crypts and causes large areas of ulceration.
  5. Has eventual invasion of WBC and abscess formation in the crypts.
210
Q

Symptoms of ulcerative colitis:

A

Abdominal pain and diarrhea.

211
Q

Treatment of ulcerative colitis:

A
  1. Corticosteroids - salicylate analogs.
  2. Immunomodulating agents. - azathiopurine, mercaptopurine.
212
Q

What causes the crypts to be destroyed in ulcerative colitis?

A

Peudopolyposis - accounting for the irregularity of the internal intestinal surface.

213
Q

In _________ _________ confluent areas of mucosal ulceration occur, leaving protruding islands of inflamed mucosa and submucosa-stimulating colonic polyps. (Pseudopolyps)

A

Ulcerative colitis.

214
Q

What disease is called non-tropical sprue?

A

Celiac disease.

214
Q

Mechanism of celiac disease:

A
  1. Gluten is digested by luminal and brush-border enzymes, into amino acids and peptides - including a-gliadin.
  2. a-gliadin is resistant to degradation by digestive enzymes.
  3. Gliadin peptides induce epithelial cells to express IL-15, triggering activation and proliferation of CD8+ intraepithelial lymphocytes.
  4. These cells are induced to express NKG2D - a natural killer cell marker.
  5. These CD8+ lymphocytes become cytotoxic and kill enterocytes that express MIC-A.
  6. MIC-A is a HLA protein in response to stress.
  7. Results in epithelial damage.
215
Q

Epithelial damage in celiac disease contributes to the process where other gliadin peptides cross the epithelium to be deaminated by ____________ ____________________.

A

Tissue transglutaminase.

216
Q

Deaminated gliadin peptides cross the __________ and interact with antigen-presenting cells (APC) and are presented to ________ ________.

A
  1. Epithelium.
  2. CD4+ T-cells.
217
Q

CD4+ T-cells produce cytokines that contribute to tissue damage and cause:

A

Charecteristic mucosal pathology and induce B-cells to produce antibodies against gliadin, and tissue transglutaminase.

218
Q

Define celiac disease:

A

An autoimmune disease triggered by exposure to gliadin in genetically predisposed people.

219
Q

In celiac disease, what is the main lesion:

A

Villous atrophy.

220
Q

Primary effects of celiac disease:

A

Gluten –> villus injury —> decreased villi surface area —> decreased absorption of nutrients + osmotic diarrhea —> malnutrition.

221
Q

Secondary effects of celiac disease:

A

Gluten –> mucosal damage —> decreased intestinal hormones —> decreased pancreatic function —> malnutrition.

222
Q

True or false: in celiac disease, withdrawal of gliadin from the diet will cause the mucosa to return to normal.

A

TRUE!

223
Q

Celiac disease is associated with a 10-15%b chance of developing __________.

A

Lymphoma.

224
Q

General info on tropical sprue:

A
  1. Unknown etiology - but may be associated to bacterial infections.
  2. Prevelant in equatorial countries.
  3. Main lesion is atrophy of the small intestine mucosa.
225
Q

Histopathology of celiac disease is characterized by:

A

Increased numbers of intraepithelial CD8+ T-lymphocytes (intraepithelial lymphocytosis), crypt hyperplasia, and villous atrophy, and dense plasma cells infiltrate in the lamina propria.

226
Q

Advances cases of celiac disease show -

A

Complete loss of villi, or villous atrophy.

227
Q

In the diagnosis of celiac disease, why do we take a biopsy of the second portion of the duodenum or proximal jejunum?

A

Because these are the areas that are exposed to the highest concentrations of dietary gluten.

228
Q

What is the most common cancer of the GI tract?

A

Colorectal carcinoma.

229
Q

Predisposing factors for colorectal cancer:

A

HEREDITARY SYNDROMES:
1. Familial adenomatous polyposis coli - mutation of APC tumor supressor gene.
2. Hereditary nonpolyposis colon cancer - mutation of DNA repair genes - MMR, mismatch repair genes.

230
Q

Mutation of APC tumor supressor gene is associated with:

A

Familial adenomatous polyposis coli.

231
Q

Mutation of DNA repair genes, AKA mismatch repair genes, are associated with:

A

Hereditary nonpolyposis colon cancer.

232
Q

Diagnostics for colorectal cancers:

A
  1. Test for occult blood in feces.
  2. Colonoscopy.
233
Q

Colorectal cancers produce carcinoembryonic antigen (CEA), but we cannot use test for thsi as a marker for colorectal cancer. Why not?

A

Because carcinoembryonic antigen (CEA) is produced in several other kinds of carcinomas. It cannot be used for diagnosis but can be used to monitor treatment.

234
Q

Persistently elevated carcinoembryonic antigen (CEA), is indicative of:

A

Residual cancer after resection, and is indicative of poor prognosis.

235
Q

After removing cancerous segments of colorectal carcinoma, there is an ____________ risk for developing _______________.

A
  1. Increased.
  2. Other carcinomas.
236
Q

Symptoms of colorectal cancer:

A
  1. Symptoms vary based on location of the tumor.
  2. Pencil like stools - due to narrowed colon lumen.
  3. Hematochezia - bloody stool. (why we test for occult in stool)
237
Q

Most colorectal cancers develop in the ____ or ______ _______ ______.

A

Proximal or distal large intestines.

238
Q

Define adenomatous polyposis coli (APC) -

A

APC is a tumor supressor protein - Germ line mutations of APC cause a spectrum of diseases under the broad category of familial adenomatous polyposis.

239
Q

In sporadic colorectal tumors, how many copies of the mutated APC gene are needed?

A

Both copies.

240
Q

Function of the APC gene product:

A

Indirectly regulates transcription of a number of critical cell proliferation genes, through its interaction with B-catenin.

241
Q

What is B-catenin:

A

It is a dual-function protein involved in the regulation + coordination of cell-cell adhesion and gene transcription.

242
Q

APC binding to B-catenin causes:

A

Ubiquitin-mediated B-catenin destruction.

243
Q

If B-catenin is unphosphorylated can cannot bind to APC, what will occur?

A
  1. Unphosphorylated B-catenin will accumulate in the cell.
  2. Excess of free B-catenin binds to Tcf3-Lef transcription factor complex, which translocates to the cell nucelus.
  3. Increased transcription fo B-catenin targets occurs.
  4. Colorectal tumorigenesis.
244
Q

In an abnormal APC binding pathway, what does accumulated B-catenin bind to - causing it to translocate to the cell nucleus?

A

Tcf3-Lef transcription factor complex.

245
Q

In normal APC pathway, B-catenin binding APC causes -

A

Ubiquitin mediated degradation of B-catenin

246
Q

Simple sugars and amino acids are absorbed into the -

A

Blood capillaries of the villi.

247
Q

Fat products diffuse into -

A

Lymphatic structures are called lacteals.

248
Q

The liver is connected to the digestive tract bu two links, what are they?

A
  1. The hepatic portal vein.
  2. The bile duct.
249
Q

Congestive heart failure effect on the liver:

A

an increase in central venous pressure causes an enlargement of the liver due to blood engorgement - because there are no valves in the vena cava or hepatic veins.

250
Q

Portal hypertension:

A

Obstruction of blood flow in the liver due to cirrhosis, together with failure of hepatocytes to produce plasma albumin, causes portal hypertension.

251
Q

Portal hypertension increases __________ pressure in the portal vein, and is aggravated by decreased __________ pressure due to a reduction in plasma albumin.

A
  1. Hydrostatic.
  2. Oncotic.
252
Q

In portal hypertension, increased hydrostatic pressure may result in -

A

Ascites - accumulation of fluid in the peritoneal cavity.

253
Q

Carcinoma of the pancreas:

A

A carcinoma of the head of the pancreas obstructs the liver, by compressing the outflow of bile through the ampullary region.

254
Q

The liver is essential for uptake, processing, and excretion of __________, that is released from aged RBCs.

A

Bilirubin.

255
Q

What is the most common manifestation of liver disease?

A

Hyperbilirubinemia.

256
Q

The liver is the major source of all plasma proteins, except for -

A

immunoglobulins.

257
Q

True or false: The liver can give rise to tumors, but it is often involved by tumor metastases.

A

TRUE. - Such as in hepatocellular carcinoma (hepatitis B)

258
Q

Causes of liver failure:

A
  1. Hepatitis - viral and non-viral.
  2. Cirrhosis.
  3. Liver cancer.
259
Q

Two conditions that occur in liver failure:

A
  1. Hepatorenal syndrome.
  2. Hepatic encephalopathy.
260
Q

The _______, is the largest gland in the human - consisting of four poorly defined lobes.

A

The liver.

261
Q

Which organ is surrounded by a collagen-elastic fiber-containing capsule - called the capsule of Glisson - and is lined by the peritoneum.

A

The liver.

262
Q

In the liver, the zone closest to the arterial center (zone 1) will have:

A

Highest oxygen saturation, nutrient levels, and metabolic activity. Hepatocytes heres are the first to undergo regeneration after damage or partial hepatectomy. These cells are also first to get hit by exposure to a direct toxicant.

263
Q

Example of a direct toxicant:

A

Phosphorus.

264
Q

In the liver, the zone farthest away from the arterial center (zone 3) will have:

A

Most susceptible region to ischemia, and is first to undergo necrosis in systemic hypoxia. Indirect toxicants mostly affect zone 3.

265
Q

Example of an indirect toxicant, that only becomes toxic after being metabolized:

A

Carbon tetrachloride.

266
Q

Signs of bile flow obstruction, are first see in ______, where bile will ultimately kill cells and cause the formation of ______ _______.

A
  1. Zone 3.
  2. Bile lakes.
267
Q

Three major cell types that line the liver sinusoids:

A
  1. Endothelial cells - Within the fenestrated cytoplasm.
  2. Kupffer cells - Large phagocytic cells.
  3. Stellate cells - Provide vitamin A storage and production of extracellular matrix + collagen.
268
Q

Function of Kupffer cells in the liver sinusoid:

A

Form part of the monocyte-macrophage defense system, with the spleen, do removal of spent RBCs and other debris in the circulation.

269
Q

Function of stellate cells in the liver sinusoid:

A

Dual function: Vitamin A storage and production of extracellular matrix and collagen.

270
Q

What is on the apical side of the hepatocyte membrane?

A

Biliary canaliculus.

271
Q

What is on the basolateral domain of the hepatocyte membrane?

A

Abuts the sinusoids.

272
Q

What do we call the space where chylomicron remnants (lipoproteins) get processed and cirrhotic changes occur?

A

Space fo Disse.

273
Q

Optimal absorption of weak acids and bases depends on -

A

The pH of the gastrointestinal tract or surrounding environment..

274
Q

First-pass effect in drug absorption:

A
  1. Major mechanism that determines the ultimate concentration of a drug in the plasma.
  2. Due to the anatomy, drugs absorbed beyond the oral cavity are transported to the liver via the portal vein.
  3. The combined effect of the metabolism of drugs by the liver and in the gut.
275
Q

Ways to avoid the first-pass mechanism of drug absorption:

A
  1. Orally administered and rectally administered drugs but avoid first-pass mechanism.
  2. Drugs that are absorbed into the lymphatic system (fats) also avoid first-pass.
276
Q

When to avoid giving drugs orally:

A
  1. If the drug causes nausea and vomiting.
  2. If the patient is currently vomiting.
  3. If the patient is unwilling or unable to swallow.
  4. If the drug is destroyed by digestive enzymes (insulin)
  5. If the drug is not absorbed through the gastric mucosa (aminoglycosides)
  6. If the drug is rapidly degraded (lidocaine).
277
Q

True or false: venous return from the oral cavity and anal cavity are both directed toward the liver for filtering of contents.

A

FALSE: Both venous return from the oral cavity and rectal cavity will go directly back into primary venous circulation.

278
Q

What do chylomicrons carry?

A

Chylomicrons carry diet-derived lipids to body cells. They can carry fats from the intestines to the liver via general circulation.

279
Q

What do VLDLs carry?

A

VLDLs carry lipids synthesized by the liver to the body cells.

280
Q

What do LDLs carry?

A

LDLs carry cholesterol around the body.

281
Q

What do HDLs carry?

A

HDLs carry cholesterol from the body, back to the liver for breakdown and secretion.

282
Q

What are the two mechanisms for the removal of LDL from plasma?

A
  1. LDL receptor-mediated.
  2. Recpetor for oxidized LDL mediated. (scavenger receptor).
283
Q

How does gastric bypass affect bile, sodium, and glucose transport?

A
  1. Decreasess the amount of sodium brought into the upper intestine with bile, due to bile deprivation.
  2. This impairs intestinal glucose uptake via sodium-glucose cotransporter.
  3. Decreases postprandial glucose response in humans.
284
Q

What is the primary consequence of bile deprivation in gastric bypass?

A

Impaired sodium-glucose co transport.

285
Q

How can we restore glucose transport in bile-deprivation?

A

Sodium supplementation.

286
Q

Roux-en-Y gastric bypass _________ postprandial ________ response in humans.

A
  1. Decreases.
  2. Glucose.
287
Q

___________: When liver cells secrete bile that contains bile salts, cholesterol, lecithin, bilirubin, electrolytes, and water.

A

Choleresis.

288
Q

Function of bile salts:

A

To emulsify fats.

289
Q

What are the two exocrine pancreatic enzymes that help break down fats?

A
  1. Colipase: Amiphipathic protein covers fat droplets with emulsifying agents accessible to water-soluble lipase
  2. Lipase: Breaks down triglycerides.
290
Q

For apoprotein A-1, what is its lipoprotein association, source, and biological role?

A
  1. Association: HDL, and Chylomicrons.
  2. Source: Liver + intestines.
  3. Role: Activates lecithin-cholesterol acyltransferase in HDL.
291
Q

For apoprotein B-48, what is its lipoprotein association, source, and biological role?

A
  1. Association: Chylomicrons.
  2. Source: Intestine.
  3. Role: Serves as a structural protein for chylomicrons.
292
Q

For apoprotein B-100, what is its lipoprotein association, source, and biological role?

A
  1. Association: VLDL, LDL.
  2. Source: Liver.
  3. Serves as a structural protein for VLDL and LDL.
293
Q

For apoprotein C-11, what is its lipoprotein association, source, and biological role?

A
  1. Association: HDL, VLDL, chylomicrons.
  2. Source: Liver.
  3. Role: Activates extrahepatic lipoprotein lipase.
294
Q

For apoprotein C-111, what is its lipoprotein association, source, and biological role?

A
  1. Association: VLDL.
  2. Source: Liver.
  3. Role: Inhibits lipoprotein lipase and hepatic lipase - inhibits catabolism of triglyceride-rich particles.
295
Q

For apoprotein E, what is its lipoprotein association, source, and biological role?

A

Association: VLDL + chylomicron remnants.
Source: Liver.
Role: Mediates uptake of chylomicron remnants by the liver.

296
Q

What mediates binding of lipoproteins to receptors in the tissues?

A

Apoproteins - also called apolipoproteins.

297
Q

What do apolipoproteins determine?

A
  1. Overall structures of lipoproteins.
    2, Interactions of lipoproteins with receptor molecules.
  2. Metabolism of lipoproteins in the liver and peripheral tissues.
298
Q

Lipoproteins are assembled in __________ + ___________, and constantly are _________ as the circulate.

A
  1. enterocytes and hepatocytes.
  2. Modified.
299
Q

Mechanism of lipoprotein lipase (LPL) delipidation of chylomicrons:

A
  1. With apolipoprotein C-11 as a co-factor, lipoprotein lipase hydrolyzes chylomicron triglycerides.
  2. Allows delivery of free fatty acids to muscle and adipose tissue.
  3. More triglyceride removal forms low-density lipoproteins (LDLs).
  4. Eventually, turns into chylomicron remnants with the help of more apolipoprotein’s - such as ApoE.
300
Q

True or false: In the liver, chylomicron remnants and LDL are resynthesized into high-density lipoproteins (HDL) + VLDL - and are put back into circulation

A

TRUE!

301
Q

What disease is caused by mutations in apolipoprotein E?

A

Familial dysbetalipoproteinemia - AKA remnant hyperlipidemia or remnant removal disease.

302
Q

Characterization of familial dysbetalipoproteinemia:

A
  1. Increased LDL, cholesterol, and triglyceride levels.
  2. Decreased HDL levels.
303
Q

What disease is caused by a genetic defect of the synthesis of apolipoproteins B-48 and B-100?

A

Abetalipoproteinemia - Lipids are not properly absorbed because chylomicrons cannot be formed and transported.

304
Q

If the size is appropriate to enter the space of disse, what will occur with chylomicron remnants in the blood?

A
  1. Chylomicron remnants are taken up by hepatocytes via LDL receptors.
    OR
  2. Acquire additional ApoE and be taken up LDL receptor-related proteins.
305
Q

VLDL assembly:

A

VLDL is assembled in the liver from triglycerides, cholesterol, and apolipoproteins.

306
Q

Nascent VLDL released from the liver contains what? As it circulates in the blood, what does it pick up?

A
  1. ApoB-100, ApoC-1, ApoE, cholesterol, cholesterol esters, and triglycerides.
  2. As it circulates in the blood, it picks up ApoC-11 and more ApoE, that are donated from HDL.
307
Q

What happens when a VLDL particle reaches the capillaries of adipose tissue or muscle?

A

It is cleaved by lipoprotein lipase using ApoC-11as a co-factor. This will extract most of the triglycerides into LDL. But will keep 2 of 3 apoproteins present in the parent VLDL - ApoB-100 + ApoE.

308
Q

What happens to 50% of newly formed plasma LDL?

A

It will be recycled by the liver to generate VLDL.

309
Q

What is a result of deficiency of LDL receptors?

A

Familial hypercholesterolemia.

310
Q

Which apolipoproteins are recognized fro binding to the LDL receptors?

A

ApoB-100 and ApoE.

311
Q

What is the function of the LDL receptor in the liver cells (hepatocytes)?

A

LDL binds to the receptor, causing the production of VLDL.

312
Q

What happens to VLDL in the circulation?

A

Lipoprotein lipase breaks VLDLs down into LDLs, via a process called lipolysis.

313
Q

What would happen with the loss of ApoC in VLDLs?

A

Termination of lipolysis of VLDLs in the circulation.

314
Q

ApoE is a moiety needed for rapid removal of fats from the hepatic cells, what would inhibit it’s function?

A

ApoE is inhibited by C apolipoproteins, primarily ApoC-1.

315
Q

Which drug helps to supress intracellular cholesterol synthesis by inhibiting HMG CoA reductase.

A

Statins.

316
Q

How does inhibition of HMG CoA reductase effect synthesis LDL receptors?

A

Allows for much more synthesis of LDL receptors, cause lowered cholesterol removes negative feedback on LDL receptor synthesis.

317
Q

Function of HMG CoA reductase:

A

Production of cholesterol.

318
Q

Define chylomicrons:

A

Chylomicrons from dietary fat absorption are taken up by the liver and resynthesized into VLDLs and HDLs and put back into circulation.

319
Q

Triglycerides are removed from VLDLs for tissue use, what does VLDL turn into?

A

IDL or LDL.

320
Q

LDL is taken up by the __________ ________ to obtain ___________.

A
  1. Peripheral tissues.
  2. Cholesterol.
321
Q

Function of HDL:

A

Circulates to peripheral tissues and takes up excess cholesterol for transport back to the liver. This is called reverse cholesterol transport.

322
Q

Nascent HDL is produced by the liver and small intestines, and is composed of ___________________, and the enzyme _____________________________.

A
  1. Apo A-1 + phospholipids.
  2. Lecithin-cholesterol acyltransferase (LCAT)
323
Q

What protein facilitates the efflux of cholesterol from extra-hepatic cells?

A

ATP-Binding Cassette (ABC) proteins.

324
Q

Cholesterol that effluxs out of extra-hepatic cells will be accepted by _________ _____.

A

Nascent HDL.

325
Q

What does HDL do to cholesterols?

A
  1. Esterifies them via lecithin-cholesterol acyltransferase, making cholesterol esters (CE).
  2. HDL transfers CEs to the liver via HDL receptor - Scavenger receptor B1.
  3. In the liver cholesterol esters are cleaved by hepatic hormone-sensitive lipase.
  4. Free cholesterol enters bile salt pathway or is secreted as cholesterol.
  5. HDL particles get recycled.
326
Q

What occurs due to mutations in Apo A-1:

A

Causes a complete absence of HDL, which gives rise to coronary heart disease and xanthomas.

327
Q

Explain infertility due to HDL receptor deficiency:

A

Scavenger receptor B type 1 (HDL receptor) is highly expressed in the adrenals and ovaries. If its gene SCARB1 gene is mutated, it will cause HDL receptor dysfunction and dysfunctional progesterone production in women.

328
Q

Mutations in Apolipoprotein A-1 causes:

A

Complete absence of HDL - Leading to coronary heart disease and xanthomas.

329
Q

Mutations in apolipoprotein B-48 or B-100 causes:

A

Abetalipoproteinemia or Bassen-Kornzweig syndrome - Interferes with normal absorption of fat and fat-soluble vitamins.

330
Q

Mutations in Apolipoprotein C-11 causes:

A

Familial hyperchylomicronemia syndrome - Pancreatitis, hepatosplenomegaly, lipemia retinalis, and xanthomas.

331
Q

Mutations in apolipoprotein C-111 causes:

A

Sequalae of excesses and deficiencies - Elevations of C-111 predispose to non-alcoholic fatty liver disease. Mutations of C-111 enhances break-down of triglycerides, causing lowered risk for heart attacks.

332
Q

Mutations in apolipoprotein E cause:

A

Familial dysbetalipoproteinemia - Accumulation of chylomicron contents (triglycerides, cholesterol, and LDL.) Causes xanthomas and premature atherosclerosis.

333
Q

What are other names for familial dysbetalipoproteinemia?

A
  1. Type III Hyperlipoproteinemia.
  2. Remnant hyperlipidemia.
  3. Broad beta disease.
  4. Remnant removal disease.
334
Q

_________ is a product of hemoglobin, that circulates in the plasma prior to undergoing hepatic conjugation and biliary excretion.

A

Bilirubin.

335
Q

The process by which bilirubin is formed:

A
  1. Senescent RBCs are taken up by phagocytic cells of the spleen and kupffer cells of the liver.
  2. Hemoglobin is degraded into heme and globin by these cells.
  3. Heme loses its iron and is transformed into bilirubin.
  4. Bilirubin formed in tissues circulates in the serum.
336
Q

Conjugation of bilirubin:

A

Unconjugated bilirubin is taken up by hepatocytes and conjugated by uridine diphosphate glucuronyl-transferase. (UDPGT) to become water-soluble bilirubin mono + di-glucuronides.

337
Q

Function of conjugated bilirubin:

A

It is excreted into the bile and participates in fat digestion in the intestines, and gets converted back to bilirubin and is reabsorbed by the terminal ileum and colon as urobilinogen.

338
Q

What gives urine its yellow color?

A

Urobilinogen in the plasma is filtered by the kidney, and is oxidized to urobilin which is what gives urine its color.

339
Q

Urobilinogen that remains in the colon does what?

A

Is converted to stercobilin - the main pigment of feces.

340
Q

A small fraction of urobilinogen is __________ from the colon, and ____________ by the kidneys and liver.

A
  1. Absorbed.
  2. re-excreted.
341
Q

In liver disease, what accounts for the rise in urinary urobilinogen?

A

The hepatic fraction decreases and the urinary fraction of urobilinogen increases.

342
Q

Under what conditions may the levels of urinary urobilinogen fall to zero?

A

With complete obstruction or bile flow or intestinal obstruction.

343
Q

___________: Bilirubin, both conjugated and un-conjugated, binds to connective tissue and stains it yellow; mucous membranes and skin will also get stained.

A

Jaundice.

344
Q

Unconjugated hyper-bilirubinemia has a ___________ origin.

A

Prehepatic origin.

345
Q

Conjugated hyper-bilirubinemia has a ___________ origin.

A

Posthepatic origin.

346
Q

Mixed unconjugated and conjugated hyperbilirubinemia has a __________ origin.

A

Hepatic.

347
Q

Define Gilbert Syndrome:

A
  1. Has unconjugated hyperbilirubinemia.
  2. Caused by a mutation in UGT1A1 gene - autosomal recessive.
  3. Usually recognized in childhood.
348
Q

_______ _________: A common infection of the liver, resulting in hepatic cell destruction, necrosis, and autolysis. Where edema of the interstitium, will cause collapse of capillaries and decreased blood flow, tissue hypoxia, and fibrosis.

A

Viral Hepatitis.

349
Q

Hepatitis type A:

A

Infectious or short-incubation hepatitis, due to contaminated food + water via fecal-oral route.

350
Q

Hepatitis type B:

A

Serum or long-incubation hepatitis; due to transfusion and needles.

351
Q

Hepatitis type C:

A

Accounts for 20% of all viral hepatitis and most transfusion cases - has a risk of hepatocellular carcinoma.

352
Q

Hepatitis type D:

A

Delta; requires the presence of type B, due to blood products and personal contact.

353
Q

Hepatitis type E:

A

Most common in developing countries, due to contaminated water.

354
Q

Prevention and treatment for hepatitis:

A
  1. Vaccination against hepatitis type A and B.
  2. Avoiding alcohol or other drugs, to prevent further hepatic damage.
355
Q

Hep A, C, D, and E are all _____ viruses.

A

RNA viruses.

356
Q

Hep B is a _____ virus.

A

DNA.

357
Q

_________ _________: Inflammation of the liver that usually results from exposure to certain chemicals or drugs.

A

Non-viral hepatitis.

358
Q

Which drug is the leading cause of acute liver failure?

A

Acetaminophen.

359
Q

Manifestations of non-viral hepatitis:

A
  1. Hepatic cellular necrosis, scarring, Kupffer cell hyperplasia, and infiltration by mononuclear phagocyte.
  2. Alcohol, anoxia, and pre-existing liver disease will worse the effects of some toxins.
360
Q

Direct effects of alcohol on the liver:

A

Increased fluidity of biological membranes, and disrupt cellular function.

361
Q

Indirect effects of alcohol on the liver:

A

Are a consequence of alcohol metabolism.

362
Q

In alcoholic fatty liver, how does alcohol produce fatty changes?

A
  1. Increased fatty acid synthesis.
  2. Decreased fatty acid oxidation (use of fat as an energy source)
  3. Decreased export of fats in the form of lipoproteins.
363
Q

Mechanism of hepatotoxic injury by ethanol in alcoholic fatty liver disease:

A
  1. Ethanol disorganizes the lipid portion of the cell membranes.
  2. Alters the capacity of liver cells to adapt.
  3. Oxidation of ethanol produces acetaldehyde, a toxic and reactive intermediate!!!!
364
Q

True or false: There are 3 different enzymes to convert alcohol to acetaldehyde, all three work by placing 2 OH groups onto the ethanol molecule.

A

FALSE: There are 3 different enzymes to convert alcohol to acetaldehyde, all three work by STRIPPING 2 H+ atoms from ethanol.

365
Q

Changes seen in chronic liver disease:

A
  1. Tumor necrosis factor-a (TNFa) causes a slowdown and arrest in flow of bile in bile ducts.
  2. Interleukin-6 released by Kupffer cells stimulates the synthesis of acute-phase proteins by hepatocytes.
  3. Transforming growth factor-b secreted by Kupffer cells and hepatocytes, stimulates the synthesis of type I collagen by hepatic stellate cells, causing fibrosis that compromises portal venous flow.
  4. Fat accumulates in hepatocytes. Steatosis is reversible if alcohol consumption stops.
366
Q

In portal hypertension, what are the effects of glucagon and adenosine?

A

They reduce vasoconstrictor sensitivity, causing further vasodilation of peripheral and splanchnic circulation.

367
Q

In portal hypertension, what provides collateral circulation?

A

Anastomoses from hepatic portal veins and systemic veins.

368
Q

Portal hypertension can manifest as:

A
  1. Varices.
  2. Hematemesis + melena.
  3. Ascites.
  4. Splenomegaly.
369
Q

Esophageal varices often cause ___________.

A

Hematemesis.

370
Q

Treatment for ascites:

A
  1. Diuretic and sodium restriction therapy.
  2. Removal of large volumes of peritoneal fluid - called paracentesis. - This may include shunting procedures, that direct peritoneal fluid to venous flow at the jugular vein. (Does not fix underlying issue)
371
Q

________ _________ __________: Scarring of bile ducts caused by inflammation. Resulting in narrowing and hardening of ducts, causing frequent infections of bile ducts and eventual liver failure.

A

Primary Sclerosing Cholangitis.

372
Q

Complications of primary sclerosing cholangitis:

A
  1. Portal hypertension.
  2. Bile duct cancer.
  3. Colon cancer - For people with PSC that is associated with inflammatory bowel disease.
373
Q

Primary sclerosing cholangitis is idiopathic, but what are the theorized etiologies?

A
  1. Immune system reaction to an infection or toxin.
  2. May be associated with inflammatory bowel disease - Crohn’s disease or ulcerative colitis.
374
Q

What is the only known cure for primary sclerosing cholangitis (PSC)?

A

Liver transplant.

375
Q

Alcohol can cause what to the liver?

A
  1. Fatty liver.
  2. Alcoholic hepatitis.
  3. Scarring.
    Overall causes cirrhosis of the liver.
376
Q

Viral infections can cause what to the liver? (viral hepatitis)

A
  1. Liver cell necrosis.
  2. Inflammation.
  3. Fibrosis.
    Overall causes cirrhosis of the liver.
377
Q

Clinical manifestations of cirrhosis of the liver:

A
  1. Collateral vein flow.
  2. Ascites.
  3. Splenomegaly.
  4. Jaundice.
  5. Muscle wasting.
378
Q

Badly smelling breath is called _____ _________, and is associated with ________.

A
  1. Fector hepaticus.
  2. Cirrhosis of the liver.
379
Q

_____________ _________: The onset of renal failure in individuals with severe chronic liver disease, who have no kidney dysfunctions contributing to renal failure.

A

Hepatorenal syndrome.

380
Q

Mechanism of hepatorenal syndrome:

A
  1. Hepatic portal hypertension increases hydrostatic pressure, and contributes to ascites.
  2. Decreased albumin production by the damaged liver will decrease oncotic pressure, contributing to ascites. \
  3. Decreased plasma volume triggers RAAS system to decrease renal perfusion and increase sodium and water retention.
  4. Reduced renal water excretion will further contribute to ascites.

Really nasty cycle that positively feedsback on itself.

381
Q

True or false: In hepatorenal syndrome, there is cellular dysfunction of both the liver and the kidney.

A

FALSE: In hepatorenal syndrome, the liver is damaged which effects the action of the kidney, but the kidney does not have any actual damage.

382
Q

_________ ______________: A disorder of the CNS and neuromuscular system, that is associated with elevated levels of false neurotransmitters and ammonia in the blood. - Causes neuro dysfunction and edema of the brain.

A

Hepatic encephalopathy.

383
Q

Manifestation of hepatic encephalopathy:

A

Behavioral changes, confusion, stupor, deep coma, or death.

384
Q

How does an increase in serum ammonia occur?

A

Due to a defective urea cycle that cannot metabolize ammonia.

385
Q

How do false neurotransmitters occur?

A

An increase in aromatic amino acids, which are converted to false neurotransmitters. Cirrhotic livers cannot detoxify false neurotransmitters or neurotoxins.

386
Q

Factors that precipitate hepatic encephalopathy:

A
  1. Increased protein - increases bacterial conversion of urea into ammonia.
  2. Alkalosis - Keeps ammonia in the NH3 state.
  3. Portosystemic shunts - Shunt ammonia away from the liver, which would normally metabolize ammonia in the urea cycle.
387
Q

______ _______ gallstones: Oxidized polymers of calcium salts of unconjugated bilirubin.

A

Black pigment gallstones.

388
Q

_____ ________ gallstones: Pure calcium salts of unconjugated bilirubin.

A

Brown pigment gallstones.

389
Q

Cholesterol gallstones:

A

Arise is exclusively in the gallbladder and are composed of cholesterol. Pure cholesterol stones are yellow, hard, and granular.

390
Q

Pigment gallstones:

A

Black pigment stones are found in the sterile gallbladder bile, while brown pigment stones are found in infected intrahepatic or extrahepatic ducts.

391
Q

Another word for gallstones:

A

Cholelithiasis.

392
Q

What causes the formation of gallstones?

A

Excess cholesterol or bile pigment accumulation alongside hypomotility of the gallbladder, leads to nucleation and aggregation of crystals. In part due to hypersecretion of mucus trapping nucleated crystals in the gallbladder.

393
Q

Phases of the pathogenesis of gallstone formation:

A
  1. Supersaturation.
  2. Nucleation.
  3. Stone growth.
394
Q

_________ _______: Pain in the abdomen, due to obstruction by stones in the cystic duct or common bile duct of the biliary tree. Pain resulting from contraction of the gallbladder following a meal.

A

Biliary colic.

395
Q

__________ may cause biliary colic due to a malignant condition due to genetic mutation, with a relevant inflammatory response. Often linked to over-expression of COX-2 (inflammation mediator)

A

Carcinoma of the gallbladder.

396
Q

____________: Formation of a cyst in the gallbladder or it’s duct system, that presents as biliary colic.

A

Cholecystitis.

397
Q

Acalculous cholecystitis:

A

Tends to occur after surgery, trauma, or critical illness. Has more serious implications than regular cholecystitis - can cause gangrene, perforation of the gallbladder wall, and empyema.

398
Q

True or false: Invasive carcinoma of the gallbladder is very slow forming and may take 30+ years to develop to tumor-specific stages.

A

TRUE!

399
Q

Types of malignant tumors of the hepatobiliary system:

A
  1. Hepatocellular carcinoma - most common malignant disease.
  2. Cholangiocellular carcinoma.
  3. Gallbladder carcinoma.
  4. Extrahepatic bile duct carcinoma.
  5. Kupffer cell sarcoma - extremely rare.
400
Q

Kupffer cell sarcoma is extremely rare, and is associated with:

A

Vinyl chloride exposure.

401
Q

Benign tumors of the hepatobiliary system:

A

Adenomas - 90% of them have been associated with oral contraceptives.

402
Q

Typical physical manifestations to the liver in metastatic cancer in the liver:

A

Nodules that have a depressed central area, with an umbilicated appearance.

403
Q

Long term usage of progestagen-only oral contraceptive is associated with increased risk of developing ___________.

A

Glioma.

404
Q

Cholecystokinin, a hormone released from small intestine mucosa will stimulate what?

A

The gallbladder to contract and release bile into the bile duct, and the pancreas exocrine cells to secrete digestive enzymes.

405
Q

Secretin, a hormone released from the small intestine mucosa, stimulates what?

A

Duct cells to secrete bicarbonate in the pancreas.

406
Q

_________ _________: A flat band of pancreatic tissue that completely encircles the second portion of the duodenum.

A

Annular pancreas.

407
Q

When does annular pancreas develop, and what symptoms does it show?

A
  1. The annular pancreas develops in embryologic development, causing the ventral and dorsal pancreas to become abnormally fused.
  2. Newborn symptoms: Projectile vomiting in the first few days of life.
  3. Adult symptoms: A very rare cause of chronic pancreatitis.
408
Q

What type of pancreatic secretions neutralize acidic chyme?

A

Ductal secretions.

409
Q

What type of pancreatic secretions provide the enzymes necessary for digestion?

A

Acinar secretions.

410
Q

What is a pancreatic complication in cystic fibrosis?

A

Thick secretions into the pancreatic duct may obstruct the duct and cause pancreatic insufficiency.

411
Q

There are over 100 hydrolytic enzymes present in pancreatic juice, what are two most important?

A

Trypsinogen and trypsin inhibitor (tightly bound to the active site of trypsin).

412
Q

What are the three isoforms of trypsinogen?

A
  1. Cationic.
  2. Anionic.
  3. Meso trypsinogen.
413
Q

Mutations in cationic trypsinogen can cause:

A

acute pancreatitis.

414
Q

General info on acute pancreatitis:

A
  1. Also known as acute hemorrhagic pancreatitis.
  2. Follows heavy meals or excessive alcohol abuse.
  3. Associated with gallstones and alcohol abuse.
  4. Diagnostic features: severe abdominal pain, nausea, vommitting, and rapid elevation of amylase and lipase in the blood serum.
415
Q

What is chronic pancreatitis causes by?

A
  1. Ischemia - an subsequent necrosis, fibrosis, or calcifications.
  2. Oxidative stress - Idiopathic.
416
Q

What is the most common form of pancreatic cancer?

A

Pancreatic ductal adenocarcinoma.

417
Q

Pancreatic carcinoma cells frequently spread to the ________, via the ____________.

A
  1. Liver.
  2. Portal vein.
418
Q

Why is surgery for pancreatic ductal adenocarcinoma typically ineffective?

A

The pancreas has close association with large blood vessels and extensive abdominal drainage to lymph nodes.

419
Q

What should we target in order to treat the tumor stroma in cancer?

A

CD40

420
Q

What are some defects that may lead to malabsorption in the GI tract?

A
  1. Deficient intraluminal digestion.
  2. Inadequate digestion on the luminal cell membrane of the enterocytes.
  3. Impaired transcellular transport in the enterocyte.
  4. Blocked passage of nutrients from enterocytes to lymphatics.
421
Q

Examples of clinical manifestations associated with GI defects:

A
  1. Achlorhydria (atrophic gastritis), steatorrhea (chronic pancreatic insufficiency, bile duct obstruction, and cirrhosis) - caused by deficient intraluminal digestion.
  2. Lactose intolerance (lactase deficiency) - Inadequate digestion on the luminal cell membrane.
  3. Defective chylomicron assembly (abeta-lipoproteinemia) - Impaired transport in the enterocytes.
  4. Lack of lipoproteins in circulation (amyloidosis or scleroderma) - Blocked passage from enterocytes to lymphatics.
422
Q

Malabsorption of carbohydrates and proteins will clinically present as:

A

Malnutrition and failure to thrive.

423
Q

Malabsorption of vitamin K will clinically present as:

A

Bleeding.

424
Q

Malabsorption of vitamin D will clinically present as:

A

Osteomalacia.

425
Q

Malabsorption can cause weight loss and steatorrhea, both of which can clinically manifest as:

A

Cachexia fatigue.

426
Q

Malabsorption of iron, vitamin B12, or folate, will clinically present as:

A

Anemia.

427
Q

Hepatobiliary disease that can cause malabsorption:

A
  1. Cirrhosis.
  2. Biliary tract obstruction.
428
Q

Gastric diseases that cause small intestine diseases, ultimately resulting in malabsorption:

A

Achlorhydria + gastrectomy.

429
Q

Pancreatic diseases that may cause malabsorption:

A

Chronic pancreatitis, pancreatic resection, and cystic fibrosis.

430
Q

What are the potential fates for carbohydrates, in an absorptive state?

A
  1. Immediately used to provide energy via aerobic pathways.
  2. Used for lipoprotein synthesis in the liver.
  3. Stored as glycogen in the liver and muscles.
  4. Excess carbs are converted to fat and stored in adipose tissue.
431
Q

What are the potential fates for proteins, in an absorptive state?

A
  1. Most amino acids go to tissues for protein synthesis.
  2. Amino acids can be used for energy in the liver - Under aerobic conditions.
  3. Excess proteins are converted to fat and stored in adipose tissue.
432
Q

Lipogenesis does what?

A

Turns carbohydrates into fat.

433
Q

Gluceoneogenesis:

A

Amino acids turn into glucose.

434
Q

Glycogenesis:

A

Glucose turns into glycogen stores.

435
Q

Lipolysis:

A

Fat stores are broken down into free fatty acids.

436
Q

Lipogenesis:

A

free fatty acids are turned into fat stores.

437
Q

Typically we keep a __________ store of _______ in the liver to provide energy under starvation conditions.

A
  1. 10-15 hour store.
  2. Glycogen.
438
Q

Explain glucose sparing:

A
  1. During fasting, both skeletal muscle and adipose tissue release gluconeogenic substrate directly into the blood stream.
  2. Indirectly these tissues release free fatty acids, which allow skeletal mucle and other tissues to consume less glucose.
  3. Release of free fatty acids and ketogenic amoni acids supports ketogenesis by the liver. Ketone bodies will be produced for ATP production mostly in the brain.
439
Q

Ketogenic amino acids are converted to ______ _____ via the process of ketogenesis.

A

Acetyl CoA.

440
Q

Glucogenic amino acids can be converted to glucose via ____________.

A

Gluconeogenesis.

441
Q

alpha cells of the pancreas secrete:

A

Glucagon - which increases blood glucose levels.

442
Q

beta cells in the pancreas secrete:

A

Insulin - which increases the transport of glucose into cells, such as a hepatocyte, skeletal, and cardiac muscle cells.

443
Q

Delta cells of the pancreas secrete:

A

Gastrin - which stimulates production of HCl by parietal cells in the lumen of the stomach and inhibits somatostatin - which inhibits the release of insulin, glucagon, and HCL.

444
Q

Delta 1 (D1) cells int he pancreas secrete:

A

Vasoactive intestinal polypeptide (VIP), which induces glycogenolysis and hyperglycemia - stimulating GI fluid secretions.

445
Q

What do PP cells in the pancreas produce?

A

Pancreatic polypeptide - which inhibits secretion of somatostatin and the cholecystokinin-stimulated secretion of pancreatic enzymes.

446
Q

True or false: Beta cells are coupled electrically to alpha cells in the pancreas.

A

FALSE: Beta cells are electrically coupled to other beta cells - but not to other cell types.

447
Q

_______ ___ _________: 2000-3000 cells surrounded by a network of fenestrated capillaries and supported by reticular fibers. These can do paracrine and autocrine communication with their neighbors.

A

Islet of langerhans.

448
Q

Islet cell tumors in the pancreas, with a hormonal syndrome, may present with:

A
  1. Hyperglycemia - Glucagon-secreting tumors.
  2. Hypoglycemia - Insulin-secreting tumors.
  3. Achlorhydria - somatostatin secreting tumors.
  4. Peptic ulcers - Gastrin-secreting tumor.
  5. Secretory diarrhea - due to malignant VIPoma inducing glycogenolysis and hyperglycemia - which stimulates GI fluid secretion.
449
Q

Islet cell tumors are also called:

A

pancreatic neuroendocrine tumors (NETs)

450
Q

NETs may be benign or malignant, malignant ones are called _________ _________ ________ or ________ _____ _________. Present with multiple metastatic tumor deposits in the liver.

A
  1. Pancreatic endocrine cancer.
  2. Islet cell carcinoma.
451
Q

Location and functionality of localized pancreatic islet tumors:

A
  1. Most islet cell tumors are nonfunctional and often reach a large size before being discovered.
  2. Most islet cell tumors develop in the tail of the pancreas and do not produce common duct obstruction and jaundice - as is common in ductal pancreatic adenocarcinomas.
452
Q

Treatment for metastatic tumors in islet cell cancer?

A

Octreotide - a somatostatin analog - may ameliorate hormonal symptoms but does not cure it.

453
Q

Synthesis of insulin gene transcripts codes for a precursor protein called:

A

pre-proinsulin

454
Q

How does plasma glucose concentration stimulate insulin release?

A
  1. Glucose enters beta cells via facilitated diffusion.
  2. Elevated intracellular glucose increased ATP/ADP ratio, resulting in blockage of the ATP-sensitive K+ channels - triggering depolarization.
  3. Depolarization opens voltage gated calcium channels - increasing free Ca++.
  4. Increased intracellular calcium triggers fusion of neurosecretory granules within the plasma membrane - causing exocytosis of insulin into the extracellular environment.
455
Q

Increased glucose uptake by beta cells will do what to extracellular insulin levels?

A

Increase them.

456
Q

What occurs due to insulin binding it’s receptor tyrosine kinase, which starts many protein activation cascades?

A
  1. translocation of Glut-4 transporter to the plasma membrane and influx of glucose.
  2. Glycogen synthesis.
  3. Glycolysis.
  4. Fatty acid synthesis.
457
Q

What is GLUT 4?

A

an insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle.

458
Q

Two types of glucose transporters:

A
  1. Glucose transporter proteins (GLUT) that transport glucose through facilitative diffusion.
  2. Sodium-dependant glucose transporters (SGLTs) that use an energy coupling mechanism (secondary active transport)
459
Q

True or false: All GLUT family glucose transporters are insulin-regulated.

A

FALSE: Only some are - such as GLUT 4

460
Q

What occurs in fed-state metabolism under the influence of insulin?

A

Promotion of glucose metabolism, and a decreased plasma glucose - that has a negative feedback on insulin release from Beta cells.

461
Q

What occurs in fasted state metabolism, under the influence of glucagon and insulin?

A

Increased plasma glucose via glycogenolysis, gluconeogenesis, and ketones (ketones only for brain) - that attempt to fix hypoglycemia. This will have a negative feed back on release of glucagon from alpha cells of the pancreas.

462
Q

______ Diabetes: Due to a lack of insulin because of destruction of B cells.

A

Type 1.

463
Q

In type 1 diabetes, B cells are damaged via _________ and _________ produced by inflammatory cells.

A
  1. Cytokines.
  2. Autoantibodies.
464
Q

________ diabetes: Insufficient insulin secretion relative to glucose levels. - Do not need exogenous insulin to sustain life, and a decrease in tissue response to insulin is often seen.

A

Type 2.

465
Q

Cystic fibrosis patients have a 5-10x higher risk of developing __________ ___________.

A

Colorectal cancer.

466
Q

What category of cystic fibrosis patients are most likely to develop colorectal cancer?

A

CF patients who have received a solid organ transplant.

467
Q

How does cystic fibrosis-related diabetes work?

A

Mucus from CF sticks to the pancreas, limiting the amount of insulin it can excrete.

468
Q

Treatments for cystic fibrosis-related diabetes:

A
  1. Blood glucose monitoring.
  2. Insulin injections.
  3. Proper diet.
469
Q

Cystic fibrosis will cause diabetes, via damage to what cell?

A

Either by Beta-cell dysfunction or beta-cell loss.

470
Q

___________ _____________: Is caused by the release of epinephrine - blocking any residual insulin actions and stimulating the release of glucagon.

A

Diabetic ketoacidosis - and hyperglycemia!

471
Q

What are two major signs that raise suspicion that a patient may have type 1 diabetes?

A
  1. Polyphagia - Excessive eating.
  2. Tissue lose - Weight loss.
472
Q

Dehydration in type 1 diabetes, will result in:

A
  1. Excessive thirst.
  2. Decreased blood pressure.
  3. Circulatory failure.
  4. Coma or death.
473
Q

Metabolic acidosis in type 1 diabetes will cause:

A
  1. Increased ventilation.
  2. Coma or death.
474
Q

Insulin deficiency stimulates ________ _______, which will cause breakdown of _________ _______. Oxidation of fatty acyl CoA molecules in the hepatic mitochondria will produce _______ ________. Ultimately this will cause systemic metabolic ketoacidosis.

A
  1. Lipoprotein lipase.
  2. Adipose store.
  3. Ketone bodies.
475
Q

Insulin deficiency coupled with glucagon excess will cause what effects?

A
  1. Decreased peripheral utilization of glucose while increasing gluconeogenesis - exacerbating hyperglycemia.
  2. Alteration to the insulin:glucagon ratio - activating ketogenic machinery.
476
Q

Release of _________ _____ _____ by protein catabolism, will aggrevate ketotic state.

A

Ketogenic amino acids.

477
Q

What factors contribute to diabetic coma?

A
  1. An absolute insulin deficiency, causing a catabolic
478
Q

Late complications from diabetes:

A
  1. Atherosclerosis.
  2. Arteriosclerosis.
  3. Gangrene - consequence of arteriosclerosis.
  4. Retinopathy - damage to the retina.
  5. Cataracts.
  6. Glaucoma.
  7. Glomerulosclerosis.
  8. Pyelonephritis.
479
Q

What is the kimmelstiel wilson lesion?

A

Diffuse thickening of the basal lamina of the glomerular capillaries, and proliferation of mesangial cells.

480
Q

What is the leading cause of legal blindness, peripheral neuropathy, chronic renal failure, and below-knee amputation.

A

Diabetes mellitus.

481
Q

__________ neuropathy: Affects the very ends of nerves first, starting with the longest nerves - feet and legs first, then hands and arms.

A

Peripheral neuropathy.

482
Q

___________ neuropathy: In the autonomic nervous system, that controls the heart, eyes, bladder, lungs, stomach, intestines, and sex organs.

A

Autonomic.

483
Q

_______________ neuropathy: Affects nerves closer to the hips or shoulders. More common is type two diabetes, and older adults.

A

Radiculoplexus neuropathy.

484
Q

_________ neuropathy: Damage to just one nerve, often comes on suddenly. Carpal tunnel syndrome is a common type of compression neuropathy.

A

Mononeuropathy or focal neuropathy.

485
Q

Diabetic neuropathy effects on histological aspects:

A

Causes loss of myelinated fibers and thickening of endoneurial vessel wall.

BMS 460 Unit 3 (1 decks)

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