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MHD2 > Block 7 (GI) - L14 to L15 > Flashcards

Block 7 (GI) - L14 to L15 Flashcards

1
Q

Describe the key anatomical features of the pancreas.

A
  1. Retroperitoneal organ
  2. Pancreatic tail located near the spleen
  3. Common bile duct passes through the pancreatic parenchyma
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2
Q

What are the regions of the pancreas?

A
  1. Tail
  2. Body
  3. Neck
  4. Head
  5. Uncinate
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3
Q

What are the three main tissues of the pancreas?

A
  1. Pancreatic acinar cells
  2. Islets of Langerhans
  3. Pancreatic ducts and ductules
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4
Q

The exocrine pancreas involves the acinar cells - what do they secrete?

A

Bicarbonate rich fluid containing digestive enzymes and pro-enzymes

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5
Q

Describe the appearance of acinar cells on histology

A

Pyramidally-shaped epithelial cells that are radially oriented around a central lumen; very pink eosinophilic cytoplasm, basal nuclei

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6
Q

Small interlobular pancreatic ducts secrete ___.

A

Water and sodium bicarbonate

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7
Q

Larger pancreatic ducts produce ___.

A

Mucin

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8
Q

The endocrine pancreas involves the Islets of Langerhans - what do they secrete?

A

Insulin, glucagon, somatostatin, PP, VIP, serotonin

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9
Q

How does the pancreas prevent self-digestion?

A
  1. Inactive proenzymes are synthesized
  2. Enzymes are contained in membrane-bound zymogen granules
  3. Activation of proenzymes requires activation of trypsinogen to trypsin (trypsin inhibitors are present + trypsin can inactivate itself)
  4. Resistance of acinar cells
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10
Q

Which pancreatic enzymes are not produced as pro-enzymes?

A

Amylase and lipase

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11
Q

What is acute pancreatitis?

A

Acute inflammatory process of the pancreas; usually associated with acinar cell injury and is usually non-progressive

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12
Q

What are the characteristics of acute pancreatitis?

A

Acute onset of abdominal pain resulting from enzymatic necrosis and inflammation of the pancreas

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13
Q

80% of cases of acute pancreatitis are associated with what 2 conditions? Are these more common in men or women?

A

Biliary tract disease (F>M)

Alcoholism (M>F)

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14
Q

What are the etiologic factors of acute pancreatitis?

A
  1. Obstruction of pancreatic ductal system (gallstones, periampullary neoplasms, others)
  2. Alcohol
  3. Drugs (azathioprine, estrogens, furosemide)
  4. Trauma
  5. Metabolic (hypertriglyceridemia, hyperparathyroidism/hypercalcemia)
  6. Vascular (ischemia due to shock, emboli, vasculitis - PAN)
  7. Infectious (mumps)
  8. Genetic (mutations in cationic trypsinogen and trypsin inhibitor gene)
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15
Q

Describe the pathogenesis of acute pancreatitis.

A

Autodigestion of pancreatic substance by inappropriately activated pancreatic enzymes

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16
Q

Once activated, what types of lesions are caused by enzymes, leading to acute pancreatitis?

A
  1. Interstitial inflammation and edema
  2. Proteolysis
  3. Fat necrosis
  4. Hemorrhage
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17
Q

What are some symptoms of acute pancreatitis?

A
  1. Abdominal pain
  2. ARDS
  3. Acute renal failure
  4. DIC
  5. Fluid sequestration
  6. Hypocalcemia (due to diffuse fat necrosis)
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18
Q

What is elevated in the blood acute pancreatitis?

A

Amylase and lipase

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19
Q

How is acute pancreatitis treated?

A

Supportive - analgesia, IV fluids, correct electrolyte abnormalities, oral intake when pain improves

Address underlying cause

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20
Q

What are the sequelae of acute pancreatitis?

A

Death (5%), pancreatic abscess, pancreatic pseudocyst, infected necrotic debris

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21
Q

What is chronic pancreatitis?

A

Progressive fibro-inflammatory process of the pancreas that result in permanent structural damage

Repeated bouts of mild to moderate pancreatic inflammation leads to continued loss of pancreatic parenchyma, replacement by fibrous tissue, and irreversible impairment of function (exocrine before endocrine)

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22
Q

What are predisposing factors for chronic pancreatitis?

A
  1. Long-term alcohol abuse
  2. Long-standing obstruction (biliary tract disease/calculi, pancreas divisum, neoplasms, pseudocysts)
  3. Tropical pancreatitis (Africa and Asia)
  4. Hereditary pancreatitis
  5. CFTR gene mutation
  6. Idiopathic (up to 40%)
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23
Q

What are proposed pathogenetic mechanisms of chronic pancreatitis?

A
  1. Hypersecretion of protein and insufficient ductal bicarbonate (proteinacious plugs form within ducts, obstruct, nidus for calcification, stone formation)
  2. Direct toxic effect
  3. Antioxidant imbalance (generation of free radicals in stressed acinar cells leads to injury)
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24
Q

What are the pathologies seen in chronic pancreatitis?

A
  1. Fibrosis
  2. Decreased number and size of acini
  3. Obstruction and dilation of pancreatic ducts (protein plugs)
  4. Late stage loss of endocrine pancreas
  5. Pseudocyst formation
  6. Calcified concretions
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25
Q

What are symptoms of chronic pancreatitis?

A
  1. Recurrent attacks of abdominal pain radiating to back; triggered by alcohol, overeating, and opiates
  2. Recurrent attacks of jaundice or vague indigestion
  3. Exocrine pancreatic insufficiency leading to steatorrhea
  4. Diabetes mellitus
  5. Pancreatic calcifications on imaging
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26
Q

What are pancreatic pseudocysts?

A

Localized collections of pancreatic secretions in the pancreatic interstitium as a result of damaged ducts; lacks a true epithelial lining

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27
Q

What are symptoms of pancreatic pseudocysts?

A

Abdominal mass, abdominal pain, may become infected/hemorrhage

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28
Q

What is another name for pancreatic carcinoma?

A

Infiltrating ductal adenocarcinoma of the pancreas

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29
Q

What are pathogenetic factors of pancreatic carcinoma?

A

Pancreatic intraepithelial neoplasia (PanIN), smoking, familial clustering, chronic pancreatitis, DM

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30
Q

Where are pancreatic carcinomas located most frequently and how do they appear grossly?

A

Head; gritty gray-white solid firm masses

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31
Q

Describe the histologic appearance of pancreatic carcinoma.

A

Adenocarcinoma - poorly formed infiltrating glands, majority of ductal origin

Dense stromal fibrosis (desmoplastic response)

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32
Q

Where does pancreatic carcinoma invade locally?

A
  1. Adjacent nerve
  2. Spleen, adrenals, transverse colon, stomach, vertebral column
  3. Regional lymph nodes
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33
Q

Where does pancreatic carcinoma metastasize to?

A

Liver, lungs, bones

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34
Q

What are symptoms of pancreatic carcinoma?

A

Clinically silent until tumor impinges on other structures, obstructive jaundice, pain (first symptom), weight loss, anorexia, malaise, weakness

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35
Q

What are tumor markers of pancreatic carcinoma?

A

Elevated CA19-9 and CEA in some cases

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36
Q

How does a pancreatic carcinoma in the head of the pancreas lead to obstructive jaundice?

A

Tumor obstructs ampullary region/common bile duct, which prevents conjugated bile from entering the duodenum. Pressure increases in the biliary tract and conjugated bile enters the vascular space. The biliary tree may also be distended.

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37
Q

What is the Trousseau sign?

A

Migratory thrombophlebitis (spontaneously appearing and disappearing venous thromboses) attributed to elaboration of platelet-aggregating factors and procoagulants from tumor

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38
Q

What is the prognosis for pancreatic carcinoma?

A

Brief, progressive course; less than 20% of tumors are resectable at time of diagnosis, <5% 5 year survival

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39
Q

What are the 3 pancreatic cystic neoplasms?

A
  1. Serous cystadenoma
  2. Mucinous cystic neoplasms
  3. Intraductal papillary mucinous neoplasms
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40
Q

Compare the behavior of the three types of pancreatic cystic neoplasms.

A

Serous cystadenoma: benign
Mucinous cystadenoma: benign
Mucinous cystadenocarcinoma: malignant
Intraductal papillary mucinous neoplasms: benign to malignant

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41
Q

Compare the gross morphology of the three types of pancreatic cystic neoplasms.

A

Serous: small cysts, clear, straw-colored fluid
Mucinous: cysts filled with thick mucin, not connected to main pancreatic duct
IPMN: arise in pancreatic duct or major branch

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42
Q

Compare the histopathology of the three types of pancreatic cystic neoplasms.

A

Serous: small cysts lined by cuboidal cells (glycogen rich)
Mucinous: cysts lined by columnar epithelium
IPMN: lined by columnar epithelium

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43
Q

Compare the clinical features of the three types of pancreatic cystic neoplasms.

A

Serous: F>M, 70 y/o, non-specific symtpoms
Mucinous: majority F, body/tail of pancreas, painless slow-growing masses
IPMN: M>F, head of pancreas

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44
Q

What are the 4 congenital anomalies of the pancreas?

A
  1. Agenesis
  2. Annular pancreas
  3. Pancreas divisum
  4. Ectopic pancreas
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45
Q

What is annular pancreas?

A

Ring of pancreatic tissue encircles the duodenum

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46
Q

What is pancreas divisum?

A

Failure of fetal duct system to fuse, leads to increased pancreatic pressure; may progress to chronic pancreatitis

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47
Q

What is ectopic pancreas?

A

Displaced pancreatic tissue (seen in stomach, duodenum, jejunum, Meckel diverticulum, ileum); asymptomatic or painful with mucosal bleeding

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48
Q

What are the associated glandular organs of the GI system?

A
  1. Salivary glands
  2. Pancreas
  3. Liver
  4. Gall bladder
  5. Endocrine glands/cells
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49
Q

What are the 6 sphincters of the GI system?

A
  1. Upper esophageal
  2. Lower esophageal
  3. Pyloric (pylorus to duodenum)
  4. Sphincter of Oddi (pancreas to duodenum)
  5. Ileocecal
  6. Internal and external anal
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50
Q

What are the 4 layers of the gut wall?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis externa
  4. Serosa
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51
Q

What are the layers of the mucosa?

A
  1. Epithelium
  2. Lamina propria
  3. Muscularis mucosae
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52
Q

What are the different cells contained in the epithelium of the GI tract?

A
  1. Absorptive enterocytes
  2. Enteroendocrine cells
  3. Gastric mucosal cells
  4. Mucin-producing cells
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53
Q

What do absorptive enterocytes do?

A

Digestion and absorption

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54
Q

What do enteroendocrine cells do?

A

Release regulatory peptides and amines to regulate GI function

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55
Q

What do gastric mucosal cells do?

A

Produce H+

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56
Q

What are the phases of digestion and absorption?

A
  1. Cephalic
  2. Oral
  3. Esophageal
  4. Intestinal
  5. Colonic
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57
Q

What are the two types of GI motility?

A
  1. Segmentation

2. Peristalsis

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58
Q

What are the steps in the formation of saliva?

A
  1. Acinar cells secrete initial saliva

2. Ductal cells modify initial saliva to produce final saliva

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59
Q

Describe the composition of initial saliva.

A

Isotonic (similar to plasma)

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60
Q

Describe the composition of final saliva.

A

Hypotonic

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61
Q

What are the three transporters of the luminal membrane of ductal cells?

A
  1. Na/H exchanger
  2. Cl/HCO3 exchanger
  3. H/K exchanger
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62
Q

Describe the production of final saliva.

A

Net absorption of Na/Cl and net secretion of K/HCO3; more NaCl is absorbed than KHCO3 is secreted, and ductal cells are fairly water-impermeable, so there is net absorption, leading to a hypotonic solution

63
Q

What are the three functions of saliva?

A
  1. Lubrication
  2. Protection (dilutes and buffers foods, buffers acid/pepsin during vomiting, washes away pathogenic bacteria)
  3. Initial digestion (of starches and lipids by salivary enzymes)
64
Q

What are the inorganic components of saliva?

A

Water, bicarbonate, Na, K, Ca2+, Mg2+, Cl, Fl

65
Q

What are the organic components of saliva?

A
  1. Salivary alpha-amylase (starch)
  2. Lingual lipase (lipid)
  3. Glycoprotein (mucin forms mucus when hydrated)
  4. Lysozyme
  5. Kallikrein (converts plasma protein into bradykinin)
66
Q

How is salivary secretion regulated?

A

Exclusively through neural pathways

67
Q

Salivary secretion is stimulated by both sympathetic and parasympathetic subdivisions of the ANS; which dominates?

A

Parasympathetic

68
Q

What are the three phases of swallowing?

A
  1. Oral
  2. Pharyngeal
  3. Esophageal
69
Q

Discuss the oral phase of swallowing.

A

Voluntary action, initiated when the tongue forces a bolus of food back toward the pharynx, activating stretch receptors, and initiating the pharyngeal phase

70
Q

Discuss the pharyngeal phase of swallowing.

A

Involuntary action (<1 second), soft palate is pulled upward and the palatopharyngeal fold moves inward, creating a narrow passage and preventing reflux into the nasopharynx. Food moves to the pharynx. The epiglottis covers the larynx and respiration is inhibited. The UES relaxes, the pharynx contracts, and peristalsis begins. After the bolus crosses the UES, the swallowing reflex closes the sphincter.

71
Q

Discuss the esophageal phase of swallowing.

A

Primary peristalsis occurs to propel food down the esophagus. Distention of the esophagus initiates another wave of secondary peristalsis to clear the esophagus. The LES relaxes and the orad region of the stomach relaxes.

72
Q

What mediates the primary and secondary peristalsis, and the opening of the LES?

A

Primary - swallowing reflex
Secondary - ENS
LES - VIP (from peptidergic fibers in the vagus nerve)

73
Q

Where are carbohydrates, proteins, and lipids absorbed?

A

Duodenum > Jejunum > Ileum

74
Q

Where are calcium, folate, and iron absorbed?

A

Duodenum (primarily); calcium is also absorbed in the jejunum and ileum

75
Q

Where is vitamin B12 absorbed?

A

Ileum

76
Q

List the 6 secretory cells contained in the fundus and antrum of the stomach.

A
  1. Parietal/oxyntic cells
  2. Mucous neck cells
  3. Peptic/chief cells
  4. Enterochromaffin-like (ECL) cells
  5. D cells
  6. G cells
77
Q

What is secreted by parietal/oxyntic cells?

A
  1. HCl

2. IF

78
Q

What is the role of HCl?

A

Kills bacteria, allows for activation of pepsin from pepsinogen

79
Q

What is the role of IF?

A

Essential factor that binds B12, making it absorbable by the ileum

80
Q

What is secreted by mucous neck cells?

A

Mucus

81
Q

What is the role of mucus?

A

Protection of gastric mucosa

82
Q

What is secreted by peptic/chief cells?

A

Pepsinogen

83
Q

What is the role of pepsinogen?

A

Pro-enzyme of pepsin, activated in acidic environment

84
Q

What is secreted by ECL cells?

A

Histamine

85
Q

What is the role of histamine?

A

Most powerful stimulator of HCl secretion

86
Q

What is secreted by D cells?

A

Somatostatin

87
Q

What is the role of somatostatin?

A

Powerful inhibitor of HCl secretion

88
Q

What is secreted by G cells?

A

Gastrin

89
Q

What is the role of gastrin?

A

Activates HCl secretion

90
Q

Describe the cellular mechanism of gastric acid secretion.

A
  1. In the lumen, H+ is secreted via the H/K ATPase exchanger. Cl- follows H+ through diffusion channels.
  2. In the basolateral membrane, HCO3- is absorbed via Cl/HCO3 exchanger.

Net secretion of HCl and net absorption of HCO3-

91
Q

What drug inhibits the H/K exchanger to reduce H+ secretion?

A

Omeprazole

92
Q

Describe the stimulation of gastric acid secretion by parietal cells.

A
  1. ACh from neurons act directly on the parietal cell to activate secretion.
  2. ACh from neurons act on ECL cells, which release histamine, which act on the parietal cell to activate secretion.
  3. GRP from neurons act on G cells, which release gastrin into the bloodstream. This can act on both ECL cells and parietal cells directly.
93
Q

Discuss inhibition of gastric acid secretion by parietal cells.

A
  1. Acidic chyme in the antrum of the stomach initiates a negative feedback loop.
  2. When the pH of the lumen is below 3, somatostatin is released, which inhibits via direct and indirect pathways.
    Direct: SS binds to receptors in parietal cells and inhibits histamine’s stimulatory effect
    Indirect: SS inhibits histamine release from ECL cells and gastrin release from G cells
  3. Prostaglandins also inhibit histamine
94
Q

What protects the surface of the stomach from H+ and pepsins?

A

Mucus and bicarbonate

95
Q

Describe the gastric mucosal barrier.

A

Protective mucus layer on the luminal side that contains alkaline secretions

96
Q

Why do gastric ulcers form, primarily?

A

Defects in the mucosal barrier, which allows H+ and pepsin to digest a portion of the mucosa

97
Q

What is a major causative agent of gastric ulcers?

A

H. pylori, which releases cytotoxins that destroys the protective barrier and cells underneath

98
Q

Which type of ulcer is more common?

A

Duodenal

99
Q

Why do duodenal ulcers form?

A

Higher H+ secretory rates - overpowers the buffering capacity of pancreatic bicarbonate

100
Q

What are the two major factors that contribute to inhibition or slowing of gastric emptying?

A
  1. Presence of fat in the duodenum

2. Presence of H+ (low pH) in the duodenum

101
Q

The effect of fat in the duodenum is mediated by ___, which is secreted when fatty acids are present.

A

Cholecystokinin (CCK)

102
Q

How does CCK work?

A

It slows gastric emptying (pyloric contraction) to ensure that there is adequate time for fat to be digested and absorbed. It also regulates gallbladder contraction, relaxation of the sphincter of Oddi, and pancreatic secretion.

103
Q

The exocrine pancreas secretes about 1L of fluid/day into the lumen of the duodenum. Describe its components.

A
  1. Aqueous component (high in bicarbonate)

2. Enzymatic component

104
Q

What secretes the bicarbonate for the aqueous component of pancreatic juice?

A

Centroacinar and ductal cells

105
Q

What secretes the enzymatic component of pancreatic juice?

A

Acinar cells

106
Q

How are pancreatic ductal secretions controlled?

A
  1. When luminal pH is <4.5, the S cells in the SI are triggered to release secretin.
  2. Secretin stimulates secretion of bicarbonate, which increases pH of intestinal lumen.
  3. Negative feedback to stop secretin release.
107
Q

Where is CCK released from in the SI?

A

I cells

108
Q

How is pancreatic acinar secretion controlled by CCK?

A
  1. CCK release is triggered by direct interaction of fatty acids or amino acids with I cells
  2. These components also bind to sensor paracrine cells that release CCK-RP
  3. Monitor peptide is released by pancreatic acinar cells, which stimulates I cells.
109
Q

Digestion of starch begins with ___.

A

Alpha-amylase

110
Q

Discuss the process of carbohydrate digestion.

A
  1. Salivary amylase starts the process but plays an insignificant role
  2. Pancreatic amylase digests internal a-1,4-bonds in starch, yielding a mixture of disaccharides (maltose), trisaccharides (maltotriose), and oligosaccharides (a-limit dextrins).
  3. Disaccharides are further digested to monosaccharides by intestinal brush border enzymes.
  4. Glucose is absorbed by the epithelial cells.
111
Q

What are the intestinal brush border enzymes that digest disaccharides?

A

A-dextrinase (isomaltase), maltase, and sucrase

112
Q

Lactase breaks lactose down into what two components?

A

Glucose and galactose

113
Q

Sucrase breaks sucrose down into what two components?

A

Glucose and fructose

114
Q

Trehalase breaks trehalose down into what component?

A

Glucose

115
Q

The symporter ___ transports glucose and galactose against their gradients by coupling transport with Na+. They are then extruded across the basolateral membrane by facilitated diffusion with ___.

A

SGLT1; GLUT2

116
Q

How is fructose transported?

A

GLUT5 (apical) - frutose specific
GLUT2 (basolateral)
Both facilitated diffusion

117
Q

What is lactose intolerance?

A

Lack or deficiency of lactase in the brush border; lactose is not digested; leads to osmotic diarrhea

118
Q

What is congenital lactose intolerance?

A

Lack of jejunal lactase - rare and very serious, must replace lactose with a sucrose or fructose diet

119
Q

Where does protein digestion begin?

A

Stomach

120
Q

Describe protein digestion.

A
  1. Pepsinogen is released in response to a meal by gastric chief cells and converted to pepsin at low pH
  2. Pepsin digests proteins into a mix of intact proteins, large peptides, and few free aa.
  3. Continues in the SI with combined actions of pancreatic and brush border proteases.
121
Q

True or false - pepsin is not essential for normal protein digestion.

A

True

122
Q

What are the 5 major pancreatic proteases secreted as inactive precursors.

A
  1. Trypsinogen
  2. Chymotrypsinogen
  3. Proelastase
  4. Procarboxypeptidase A
  5. Procarboxypeptidase B
123
Q

What are the steps in intestinal protein digestion?

A
  1. Activation of trypsinogen to trypsin by enterokinase (brush border enzyme)
  2. Trypsin catalyzes the conversion of all other inactive precursors to their active enzymes + autocatalyzes the remaining trypsinogen
124
Q

How are proteins absorbed?

A
  1. Symport into the cell with Na+ or H+
  2. Conversion to amino acids by cytosolic peptidases
  3. Exit the cell via facilitated diffusion
125
Q

There are some rare diseases of defective single amino acid absorption - how is this addressed?

A

Di- and tri-peptides are absorbed and hydrolyzed by enzymes in the cytoplasm of epithelial cells and released into the blood

126
Q

How is trypsinogen deficiency addressed?

A

Diet of partially hyrolyzed proteins

127
Q

What is cystinuria?

A

Transporter for dibasic amino acids is absent in SI and kidney, leading to low or no absortpion. The intestinal defect results in failure to absorb amino acids; the renal defect results in increased excretion (cystinuria).

128
Q

What are the major categories of lipid in the diet?

A
  1. Triglycerides
  2. Phospholipids
  3. Cholesterol
  4. Vitamins ADEK (not lipids, but are fat soluble)
129
Q

Where does lipid digestion begin?

A

Stomach

130
Q

Discuss the process of lipid digestion.

A
  1. Gastric lipase is released by gastric chief cells - hydrolyzes ~10% of dietary triglycerides (not essential)
  2. Stomach empties chyme slowly into the SI, allowing adequate time for pancreatic enzymatic action
  3. CCK is released when dietary lipids enter SI, reducing gastric empyting
  4. Bile acids + lysolecithin surround and emulsify dietary lipids
  5. Products are solubilized in the intestinal lumen in mixed micelles (excluding glycerol)
131
Q

What is emulsification?

A

Production of small lipid droplets dispersed in the aqueous solution of the intestinal lumen, which provides a large surface area for pancreatic enzymes

132
Q

What are the three important lipolytic enzymes contained in pancreatic juice that can work at a neutral pH?

A
  1. Pancreatic lipase
  2. Phopholipase A2
  3. Cholesterol ester hydrolase
133
Q

What are the products of lipid digestion?

A

Monoglycerides, fatty acids, cholesterol, lysolecithin

134
Q

Describe the structure of the mixed micelles formed during lipid digestion.

A

Core contains the productions of lipid digestion

Exterior is lined with amphipathic bile salts

135
Q

How are lipids absorbed?

A

Micelles diffuse to the apical membrane of brush border epithelium, where lipids are released at the apical membrane. They diffuse into the cells. Products are re-esterified inside the cell with free fatty acids on the smooth ER to form triglycerides, cholesterol ester, and phopholipids. These are packaged with apoproteins to form chylomicrons. These are packaged in secretory vehicles, migrate to the basolateral membrane, and are exocytosed. They are too large to enter the blood vessels and thus enter lymphatic capillaries, travel to the thoracic duct, and are emptied into the bloodstream.

136
Q

What is pancreatic insufficiency?

A

Diseases of exocrine pancreas (chronic pancreatitis, CF) lead to defects of pancreatic enzyme secretion; present with steatorrhea (abnormal lipid digestion/absorptin)

137
Q

What are two causes of abnormal acidic pH (leading to dysfunction of pancreatic enzymes0?

A
  1. Zollinger-Ellison syndrome (excessive H+ secretion by parietal cells)
  2. Pancreas doesn’t secrete enough HCO3- to neutralize acidic chyme
138
Q

What happens when there is a deficiency of bile salts?

A

No micelle formation, intereferes with lipid digestion/absorption

139
Q

What is abetalipoproteinemia?

A

Failure to synthesize ApoB - chylomicrons are either not formed or are unable to be transported into lymph

140
Q

REVIEW SLIDES 44 and 45.

A

Do it.

141
Q

What causes osmotic diarrhea?

A

Presence of non-absorbable solutes in the intestinal lumen

142
Q

What causes secretory diarrhea?

A

Excessive secretion of fluid by crypt cells (major cause is overgrowth of enterohepatic bacteria - V. cholerae or E. coli)

143
Q

Describe the process of calcium absorption.

A

Calcium is actively absorbed in the SI. It depends on the presence of the active form of vitamin D (1,25-OH)2-D3). Formation of this by the kidney depends on parathyroid hormone. 1,25 induces synthesis of vitamin D-dependent Ca2+ binding protein calbindin D-28K. Calcium diffuses into the cell down its graident, binds to calbindin D-28K, and is pumped across the basolateral membrane by a Ca2+ ATPase.

144
Q

Inadequate Ca2+ absorption causes ___ in children and ___ in adults.

A

Rickets; osteomalacia

145
Q

Describe absorption of vitamin B12 (cobalamin).

A

B12 is released from food by pepsin in the stomach. It binds to R proteins. In the duodenum, pancreatic proteases degrade R proteins. B12 is transferred to IF (secreted by parietal cells). This complex is absorbed in the ileum.

146
Q

Why can a gastrectomy lead to pernicious anemia?

A

Parietal cells are lost, IF is not released, B12 is not absorbed

147
Q

How is colonic function regulated?

A
  1. Enteroendocrine cells secrete peptide YY in response to lipid in the lumen of the terminal ileum and colon. It decreases gastric emptying and intestinal motility. It also reduces Cl- and fluid secretion by intestinal cells. Peptide YY ultimately reduces chyme propulsion to allow more time for digestion and absorption in the SI.
148
Q

What are the reflexes that regulate colonic function?

A
  1. Local - activated by the passage of a bolus of fecal material; stimulates short bursts of Cl- and fluid secretion
  2. Long reflex arcs -
    a. Gastrocolic - distention of the stomach increases colonic motility and mass movement of fecal material
    b. Orthocolic - activated on rising from bed
149
Q

What is the major role of colonic epithelium?

A

Absorb/secrete electrolytes and water (rather than nutrients)

150
Q

What nutrient is absorbed by the colon?

A

Short-chain fatty acids, which are salvaged from non-absorbed carbohydrates by colonic bacteria

151
Q

How are SCFAs absorbed?

A

Absorbed in the luminal side in a Na+ dependent fashion by symporters (sodium-monocarboyxlate transporters - SMCTs)

Driven by low intracellular Na+ established by basolateral ATPase

152
Q

Ejection of bile from the gall bladder begins within 30 minutes of meal ingestion. What is the major stimulus for bile secretion?

A

CCK, which causes contraction of gallbladder and relaxation of sphincter of Oddi

153
Q

Describe the enterohepatic circulation of bile acids.

A

Conjugated bile acids are unable to passively cross the intestinal epithelial lining. When chyme reaches the terminal ileum and lipid absorption is complete, conjugated bile acids are reabsorbed by a symporter (apical Na+ dependent bile acid transporter - asbt). A minor fraction enters the colon, is deconjugated, and is passively reabsorbed.

MHD2 (34 decks)

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