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Metabolism and Nutrition > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

How long does it take for the stomach to empty?

A

15-90 minutes

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2
Q

What are the two types of mucosa in the stomach?

A

Oxyntic gland mucosa (body+fundus) and pyloric gland mucosa

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3
Q

What are 6 kinds of cells in the oxyntic mucosa?

A 
Mucus surface cells
mucus neck cells
enterochromaffin-like cells
D-cells
chief cells
parietal cells
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4
Q

What do enterochromaffin-like cells do?

A

Make histamine

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5
Q

What do d-cells do?

A

make somatostatin to inhibit gastric secretions

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6
Q

What do chief cells do?

A

Make pepsinogen. Make gastric lipase.

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7
Q

What do parietal cells do?

A

Make HCL and intrinsic factor

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8
Q

What do G cells do?

A

Secrete gastrin

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9
Q

What does intrinsic factor do?

A

vitamin B12 absorption in the intestine

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10
Q

How does the anion exchanger work in the parietal cell?

A

Secretes bicarb into blood in exchange for Cl- into the cell

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11
Q

What neurotransmitters regulate HCl secretion?

A

Acetylcholine, histamine, gastrin directly upregulate the parietal cell. Gastrin and PCAP stimulate the enterochromaffin-like cells to make histamine to stimulate the parietal cell

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12
Q

What stimulates gastrin release?

A

Antral distension, amino acids, food peptides, vagal stimulation, rise in pH above 4.0

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13
Q

What inhibits gastrin (in the stomach)?

A

Indirectly pH < 3.0 and directly by somatostatin (from D cells), which binds to G cells and ECL cells

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14
Q

What’s the name of the receptor for histamine? What kinds of drugs block this receptor?

A

H2-receptors. Blocked by drugs ending in -tidine (e.g. cimetidine)

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15
Q

What inhibits gastrin (in the intestines)?

A

Secretin and CCK. Released from duodenum in response to acid and fat. CCK stimulates somatostatin release (D cell). Secretin inhibits gastrin release (G cell) and acid secretion (parietal cell).

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16
Q

What are the 3 phases of gastric acid secretion?

A

Cephalic, gastric, intestinal

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17
Q

What’s in mucus?

A

Mucus (mucin glycoproteins), and prostaglandins, which help for blood flow and epithelial lining repair. Alkaline fluid comes from epithelial cells.

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18
Q

What stimulates pepsin?

A

Acetylcholine

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19
Q

When does pepsinogen become activated to pepsin? When is pepsin inactivated?

A

Acidic, at pH < 4. Pepsin irreversibly inactivated at pH 7-8.

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20
Q

The stomach absorbs very little. Name two substances it does.

A

Alcohol, aspirin.

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21
Q

What’s a mallory-weiss tear?

A

Forceful coughing leads to ruptured esophagus

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22
Q

Name a primary, secondary (drug), and genetic cause of peptic ulcer disease

A

H.pylori, NSAID, Zollinger Ellison syndrome (G cell hyperplasia)

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23
Q

How do NSAIDs cause peptic ulcers?

A

Inhibits prostaglandin (from COX enzymes). Thus, epithelium loses its protection

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24
Q

Name some three tests for h pylori.

A

Serology, urea breath test, stool antigen

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25
Q

What’s H pylori?

A

gram-negative, spiral, flagellated bacterium

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26
Q

Who drank the H pylori for the experiments?

A

Barry J Marshall, in 1984

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27
Q

What are the 3 subtypes of h pylori infection?

A

duodenal ulcer, simple gastritis, gastric cancer.

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28
Q

How to treat peptic ulcer disease?

A

Decrease acid production, give prostaglandin analogues (e.g. misoprostol), give sucralfate

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29
Q

Will eradicating h pylori prevent peptic ulcer reoccurrence?

A

Yes

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30
Q

What do pancreatic acinar cells do?

A

Secrete pancreatic digestive enzymes. Stimulated by CCK (indirectly), and nerves (directly).

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31
Q

What do pancreatic duct cells do?

A

Secrete alkaline fluid (bicarb). Stimulated by secretin.

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32
Q

What’s the acidic tide?

A

When acid is released into the blood (in exchange for Cl-) to allow for bicarb secretion into the ducts.

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33
Q

What are the 3 phases of pancreatic secretion?

A

Cephalic, gastric, intestinal (major)

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34
Q

How are acinar cells stimulated?

A

CCK is released by I cells. CCK stimulates afferent vagal fibres, which stimulate efferent vagal fibres to release Ach (Vago-vagal), which binds to receptors on acinar cells

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35
Q

What secretes secretin?

A

S-cells, in response to gastric acid

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36
Q

What’s the current hypothesis for chronic pancreatitis?

A

Zymogen and lysosome enzymes are being co-localized within the cell, causing auto-digestion

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37
Q

How do tight junctions differ in villus versus crypt cells?

A

Crypt cells have looser tight junctions, which allows for more fluid leakage if exposed (e.g. when villi are damaged in gastroenteritis). Increased leakage can lead to diarrhea

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38
Q

What transporters are involved in chloride secretion?

A

NK2CCl channel, which brings Cl into the cell. The Cl- selective channel on the luminal side exports it into the feces.

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39
Q

In which sections of the intestine is Na absorbed?

A

Everywhere. Note that in the small intestine, Na is coupled with a co-transporter (e.g. glucose).

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40
Q

How is chloride absorbed in the intestinal sections?

A

Na coupler and bicarb exchanger in ileum and colon (can cause acidosis).

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41
Q

Describe K transport in the intestines

A

K passively absorbed in the smalls. Secreted in the colon.

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42
Q

How does cholera cause diarrhea?

A

Toxin stimulates the switch for chloride secretion and keeps it on. Constant chloride secretion, Na follows. Water follows. Diarrhea.

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43
Q

What are three mechanisms for diarrhea?

A

Secretary, osmotic, motility.

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44
Q

How does the secretary mechanism of diarrhea work? What’s an example?

A

When enterocyte absorption is inhibited, or if fluids and electrolytes are secreted. Ex. cholera.

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45
Q

How does the osmotic mechanism of diarrhea work? Example?

A

Presence of osmotically active agents in lumen. Lactose malabsorption, magnesium hydroxide.

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46
Q

How does the motility mechanism of diarrhea work? Example?

A

Increased motility causing decreased contact time. E.g. irritable bowel syndrome.

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47
Q

What’s the stool osmolality gap formula?

A

gap = 290 - 2x[Na+K] (of stool). if gap <50, then secretary diarrhea. if gap ≥50, then osmotic diarrhea.

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48
Q

Name some anti diarrheal drugs

A

Adsorbent (pectin, guar gum, bismuth)
Antimotility (codeine, loperamide, diphenoxylate)
Anti-secretary (clonidine, somatostatin)

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49
Q

What’s the leading cause of death in children <5 worldwide?

A

Diarrhea

50
Q

How many children does diarrhea kill every year?

A

1.3 million

51
Q

What’s in oral rehydrating solution?

A

glucose, sodium, chloride, potassium, citrate

52
Q

When did oral rehydrating first start?

A

1980s (1979?)

53
Q

How did reduced osmolality oral rehydration solution clinically improve upon the original ORS in 2002?

A

Less stool output, less vomiting, less unscheduled IV treatment

54
Q

How does zinc clinically manage diarrhea?

A

Reduces duration, frequency, and risk of episodes. Reduces mortality.

55
Q

How many people get/die from diarrhea in total each year?

A

4 billion cases a year, 2.2 million deaths

56
Q

What’s a major cause of diarrhea in the developing world?

A

Nematode infection, schistosomiasis

57
Q

How many people use unimproved sources for drinking-water?

A

884 million (37% in sub saharan africa)

58
Q

Which continents are not on track to meet MDG targets?

A

Africa and Asia

59
Q

How well did rotavirus vaccines work?

A

Reduced hospitalization, ER and MD visits by 85-96%

60
Q

What are the fat soluble vitamins?

A

ADEK

61
Q

Which enzymes do the salivary glands secrete? Are they acid-sensitive?

A

Amylase and lipase. Amylase is acid-sensitive. Lipase is not.

62
Q

What enzymes are produced in the stomach?

A

Pepsin and lipase.

63
Q

What enzymes are produced in the pancrease?

A

Amylase, trypsin, pancreatic lipase

64
Q

What enzymes are produced in the small intestine?

A

Enterokinase, Dissacharidases, Peptidases.

65
Q

What does the stomach contribute to protein digestion?

A

Gastric acid, pepsinogen to pepsin, proteins to polypeptides

66
Q

What does the pancreas contribute to protein digestion?

A

Proteolytic enzymes (e.g. trypsin) to further digest polypeptides. Carboxylpeptidases remove amino acids from ends of polypeptides.

67
Q

How are proteins absorbed in the enterocyte?

A

Brush border has peptidases that break down into di/tripeptides and amino acids. It also has Na-AA cotransporters.

68
Q

How are amino acids brought to the circulation?

A

Na-AA cotransporters also in the basolateral blood side to bring to liver. Also, H-AA exchangers.

69
Q

How much of fat digestion happens in the mouth?

A

About 10% of triglycerides are broken down in the mouth

70
Q

What from the pancreas helps in fat digestion?

A

Pancreatic lipase, colipase, bile salts

71
Q

How do fats enter enterocytes?

A

They form micelles to penetrate the watery mucosal barrier, and then MG and FFA readily diffuse through the villi

72
Q

In which organelle do the MG and FFA re-esterify into TG in enterocytes?

A

endoplasmic reticulum. TG then go to golgi apparati, and are packaged with apo B48 to make chylomicron

73
Q

Apoproteins are required for fat exocytosis (not a question.

A

word

74
Q

How does cystic fibrosis affect the pancreas?

A

Insufficiency; blocks the ducts of the pancreas. Leads to pancreatitis, poor fat absorption

75
Q

What disaccharide does salivary amylase break starch into?

A

Maltose

76
Q

How is glucose absorbed into enterocytes?

A

Na-glucose co-transporter. Can be solvent drag when the glucose is in high concentrations.

77
Q

Where is iron and calcium absorbed in the intestines?

A

Duodenum

78
Q

Where’s cobalamin absorbed?

A

Ileum

79
Q

Where’s the myenteric plexus? What’s another name for it?

A

Between the long and circ muscle layers of the GI tract. Auerbach’s plexus.

80
Q

Where’s the submucosal plexus? What’s another name for it?

A

Between the circ muscular layer and submucosa.

81
Q

What’s the interstitial cell of Cajal?

A

Initiates the basal electrical rhythm of the intestines (pacemaker). Is the communicating cell between neurons and smooth muscles. Present in myenteric plexus of SI, and submucosal plexus of colon.

82
Q

What’s the excitatory neurotransmitter for the intestines?

A

Acetylcholine

83
Q

What’s the inhibitory neurotransmitter for the intestines?

A

Nitric oxide and vasoactive intestinal peptide

84
Q

What are three types of peristalsis in the esophagus?

A

Primary: initiated by swallow.
Secondary: initiated by local distention.
Tertiary: spontaneous - for clearance.

85
Q

Give examples of diseases that cause upper esophageal dysmotility

A

dementia, myositis, stroke, parkinson’s

86
Q

Give examples of diseases that cause middle esophageal dysmotility

A

esophageal spasm, achalasia, DM, scleroderma

87
Q

Give examples of diseases that cause lower esophageal dysmotility

A

achalasia, GERD, DM, scleroderma

88
Q

What’s the functional difference between the right and left colons?

A

Right colon is for most water and lyte absorption. Left colon is mostly for feces storage; diarrhea vs constipation determined here.

89
Q

What’s the housekeeper phase for the MMC?

A

phase 3

90
Q

Where does nausea originate in the brain?

A

Area postrema

91
Q

What’s the blood distribution to the liver?

A

80% portal vein, 20% hepatic artery

92
Q

What’s the immune cell of the liver called?

A

Kupffer cell

93
Q

The liver produces primary bile acids. Where do secondary bile acids come from?

A

Bacterial metabolism of primary bile acids in the colon

94
Q

What’s the critical micellar concentration?

A

Min concentration of lipids to form micelles

95
Q

What’s the Krafft point

A

temp below which micelles composed of a particular BA will not form

96
Q

What percentage of gallstones are cholesterol-based?

A

80-85%

97
Q

What percentage of gallstones is not cholesterol-based?

A

15%. These are black (hemolysis and cirrhosis and bilirubin excretion) or brown (calcium bilirubinate)

98
Q

How does the liver process bilirubin?

A

Take unconjugated bilirubin and conjugates it to albumin

99
Q

What gives feces its reddish-brown pigment?

A

Stercobilinogen

100
Q

Where are clotting factors made?

A

All factors (except VIII) are made in the liver

101
Q

What are two enzymes that can be checked to assess liver function?

A

ALT (alanine aminotransferase) and AST (aspartate aminotransferase). Degree of abnormality has no direct correlation with liver function.

102
Q

What’s Wilson’s disease?

A

Causes liver damage, due to copper overload

103
Q

Which three liver enzymes go up in cholestatic liver disease?

A

Alkaline phosphatase, gamma-glutamyltransferase, 5’ nucleotidase. Degree of abnormality has no direct correlation with liver function.

104
Q

Which infiltrative diseases can cause cholestatic liver disease?

A

sarcoidosis, amyloidosis, TB, fungi, lymphoma, metastases

105
Q

Which conditions can result from cholestatic liver disease?

A

primary biliary cirrhosis, primary sclerosing cholangitis, gall stones

106
Q

Name the two patterns of abnormal liver biochemistry

A

Hepatocellular and Cholestatic

107
Q

Which enzymes are upregulated in hepatocellular pattern abnormal liver biochemistry?

A

ALT, AST

108
Q

Which enzymes are upregulated in cholestatic pattern abnormal liver biochemistry?

A

ALP, GGT, Bilirubin (not an enzyme), 5-nucleotidase

109
Q

What are 3 liver function tests?

A

Bilirubin, INR (clotting time), albumin. Also glucose, but only in end-stage.

110
Q

What’s the rate-limiting step in liver bilirubin conjugation?

A

Excretion into the canniliculi as bile

111
Q

Which clotting factor is the first to cause the clotting problems in acute liver failure?

A

Factor VII (has shortest half life)

112
Q

What are three clinical consequences of liver dysfunction?

A

Impaired excretion of bilirubin, impaired metabolism of drugs, impaired control of energy metabolism (clotting, albumin, ammonia, glucose)

113
Q

What’s the hepatic vein pressure gradient formula?

A

(Wedged - free) hepatic vein pressure. If >5, may have clinical problems

114
Q

How does cirrhosis affect peripheral vascular systems?

A

Cirrhosis causes release of NO, which dilates arteries

115
Q

What classifications does the Child-Pugh-Turcotte score rank liver patients?

A

Compensated cirrhosis (A), decompensated cirrhosis (B), advanced decompensated cirrhosis (C)

116
Q

Which three parameters does the MELD score for liver transplantation rankings take into account?

A

Creatinine, INR, Bilirubin

117
Q

How many Canadian households experienced food security?

A

1.7 million (1/8 households)

118
Q

How many children have felt food insecurity in Canada?

A

1 in 6

119
Q

What are 3 big predictors of food insecurity?

A

Low income, single-mother families, aboriginal/black families

120
Q

How much is welfare?

A

~20k for a couple with 2 children

121
Q

How do people cope with food insecurity?

A

cut size of meal or skip meals

122
Q

How many people in the world are chronically undernourished?

A

870 million

Metabolism and Nutrition (7 decks)

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