Gastrointestinal Flashcards
(122 cards)
1
Q
How long does it take for the stomach to empty?
A
15-90 minutes
2
Q
What are the two types of mucosa in the stomach?
A
Oxyntic gland mucosa (body+fundus) and pyloric gland mucosa
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
4
Q
What do enterochromaffin-like cells do?
A
Make histamine
5
Q
What do d-cells do?
A
make somatostatin to inhibit gastric secretions
6
Q
What do chief cells do?
A
Make pepsinogen. Make gastric lipase.
7
Q
What do parietal cells do?
A
Make HCL and intrinsic factor
8
Q
What do G cells do?
A
Secrete gastrin
9
Q
What does intrinsic factor do?
A
vitamin B12 absorption in the intestine
10
Q
How does the anion exchanger work in the parietal cell?
A
Secretes bicarb into blood in exchange for Cl- into the cell
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
12
Q
What stimulates gastrin release?
A
Antral distension, amino acids, food peptides, vagal stimulation, rise in pH above 4.0
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
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)
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).
16
Q
What are the 3 phases of gastric acid secretion?
A
Cephalic, gastric, intestinal
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.
18
Q
What stimulates pepsin?
A
Acetylcholine
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.
20
Q
The stomach absorbs very little. Name two substances it does.
A
Alcohol, aspirin.
21
Q
What’s a mallory-weiss tear?
A
Forceful coughing leads to ruptured esophagus
22
Q
Name a primary, secondary (drug), and genetic cause of peptic ulcer disease
A
H.pylori, NSAID, Zollinger Ellison syndrome (G cell hyperplasia)
23
Q
How do NSAIDs cause peptic ulcers?
A
Inhibits prostaglandin (from COX enzymes). Thus, epithelium loses its protection
24
Q
Name some three tests for h pylori.
A
Serology, urea breath test, stool antigen
25
What's H pylori?
gram-negative, spiral, flagellated bacterium
26
Who drank the H pylori for the experiments?
Barry J Marshall, in 1984
27
What are the 3 subtypes of h pylori infection?
duodenal ulcer, simple gastritis, gastric cancer.
28
How to treat peptic ulcer disease?
Decrease acid production, give prostaglandin analogues (e.g. misoprostol), give sucralfate
29
Will eradicating h pylori prevent peptic ulcer reoccurrence?
Yes
30
What do pancreatic acinar cells do?
Secrete pancreatic digestive enzymes. Stimulated by CCK (indirectly), and nerves (directly).
31
What do pancreatic duct cells do?
Secrete alkaline fluid (bicarb). Stimulated by secretin.
32
What's the acidic tide?
When acid is released into the blood (in exchange for Cl-) to allow for bicarb secretion into the ducts.
33
What are the 3 phases of pancreatic secretion?
Cephalic, gastric, intestinal (major)
34
How are acinar cells stimulated?
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
35
What secretes secretin?
S-cells, in response to gastric acid
36
What's the current hypothesis for chronic pancreatitis?
Zymogen and lysosome enzymes are being co-localized within the cell, causing auto-digestion
37
How do tight junctions differ in villus versus crypt cells?
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
38
What transporters are involved in chloride secretion?
NK2CCl channel, which brings Cl into the cell. The Cl- selective channel on the luminal side exports it into the feces.
39
In which sections of the intestine is Na absorbed?
Everywhere. Note that in the small intestine, Na is coupled with a co-transporter (e.g. glucose).
40
How is chloride absorbed in the intestinal sections?
Na coupler and bicarb exchanger in ileum and colon (can cause acidosis).
41
Describe K transport in the intestines
K passively absorbed in the smalls. Secreted in the colon.
42
How does cholera cause diarrhea?
Toxin stimulates the switch for chloride secretion and keeps it on. Constant chloride secretion, Na follows. Water follows. Diarrhea.
43
What are three mechanisms for diarrhea?
Secretary, osmotic, motility.
44
How does the secretary mechanism of diarrhea work? What's an example?
When enterocyte absorption is inhibited, or if fluids and electrolytes are secreted. Ex. cholera.
45
How does the osmotic mechanism of diarrhea work? Example?
Presence of osmotically active agents in lumen. Lactose malabsorption, magnesium hydroxide.
46
How does the motility mechanism of diarrhea work? Example?
Increased motility causing decreased contact time. E.g. irritable bowel syndrome.
47
What's the stool osmolality gap formula?
gap = 290 - 2x[Na+K] (of stool). if gap <50, then secretary diarrhea. if gap ≥50, then osmotic diarrhea.
48
Name some anti diarrheal drugs
Adsorbent (pectin, guar gum, bismuth)
Antimotility (codeine, loperamide, diphenoxylate)
Anti-secretary (clonidine, somatostatin)
49
What's the leading cause of death in children <5 worldwide?
Diarrhea
50
How many children does diarrhea kill every year?
1.3 million
51
What's in oral rehydrating solution?
glucose, sodium, chloride, potassium, citrate
52
When did oral rehydrating first start?
1980s (1979?)
53
How did reduced osmolality oral rehydration solution clinically improve upon the original ORS in 2002?
Less stool output, less vomiting, less unscheduled IV treatment
54
How does zinc clinically manage diarrhea?
Reduces duration, frequency, and risk of episodes. Reduces mortality.
55
How many people get/die from diarrhea in total each year?
4 billion cases a year, 2.2 million deaths
56
What's a major cause of diarrhea in the developing world?
Nematode infection, schistosomiasis
57
How many people use unimproved sources for drinking-water?
884 million (37% in sub saharan africa)
58
Which continents are not on track to meet MDG targets?
Africa and Asia
59
How well did rotavirus vaccines work?
Reduced hospitalization, ER and MD visits by 85-96%
60
What are the fat soluble vitamins?
ADEK
61
Which enzymes do the salivary glands secrete? Are they acid-sensitive?
Amylase and lipase. Amylase is acid-sensitive. Lipase is not.
62
What enzymes are produced in the stomach?
Pepsin and lipase.
63
What enzymes are produced in the pancrease?
Amylase, trypsin, pancreatic lipase
64
What enzymes are produced in the small intestine?
Enterokinase, Dissacharidases, Peptidases.
65
What does the stomach contribute to protein digestion?
Gastric acid, pepsinogen to pepsin, proteins to polypeptides
66
What does the pancreas contribute to protein digestion?
Proteolytic enzymes (e.g. trypsin) to further digest polypeptides. Carboxylpeptidases remove amino acids from ends of polypeptides.
67
How are proteins absorbed in the enterocyte?
Brush border has peptidases that break down into di/tripeptides and amino acids. It also has Na-AA cotransporters.
68
How are amino acids brought to the circulation?
Na-AA cotransporters also in the basolateral blood side to bring to liver. Also, H-AA exchangers.
69
How much of fat digestion happens in the mouth?
About 10% of triglycerides are broken down in the mouth
70
What from the pancreas helps in fat digestion?
Pancreatic lipase, colipase, bile salts
71
How do fats enter enterocytes?
They form micelles to penetrate the watery mucosal barrier, and then MG and FFA readily diffuse through the villi
72
In which organelle do the MG and FFA re-esterify into TG in enterocytes?
endoplasmic reticulum. TG then go to golgi apparati, and are packaged with apo B48 to make chylomicron
73
Apoproteins are required for fat exocytosis (not a question.
word
74
How does cystic fibrosis affect the pancreas?
Insufficiency; blocks the ducts of the pancreas. Leads to pancreatitis, poor fat absorption
75
What disaccharide does salivary amylase break starch into?
Maltose
76
How is glucose absorbed into enterocytes?
Na-glucose co-transporter. Can be solvent drag when the glucose is in high concentrations.
77
Where is iron and calcium absorbed in the intestines?
Duodenum
78
Where's cobalamin absorbed?
Ileum
79
Where's the myenteric plexus? What's another name for it?
Between the long and circ muscle layers of the GI tract. Auerbach's plexus.
80
Where's the submucosal plexus? What's another name for it?
Between the circ muscular layer and submucosa.
81
What's the interstitial cell of Cajal?
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
What's the excitatory neurotransmitter for the intestines?
Acetylcholine
83
What's the inhibitory neurotransmitter for the intestines?
Nitric oxide and vasoactive intestinal peptide
84
What are three types of peristalsis in the esophagus?
Primary: initiated by swallow.
Secondary: initiated by local distention.
Tertiary: spontaneous - for clearance.
85
Give examples of diseases that cause upper esophageal dysmotility
dementia, myositis, stroke, parkinson's
86
Give examples of diseases that cause middle esophageal dysmotility
esophageal spasm, achalasia, DM, scleroderma
87
Give examples of diseases that cause lower esophageal dysmotility
achalasia, GERD, DM, scleroderma
88
What's the functional difference between the right and left colons?
Right colon is for most water and lyte absorption. Left colon is mostly for feces storage; diarrhea vs constipation determined here.
89
What's the housekeeper phase for the MMC?
phase 3
90
Where does nausea originate in the brain?
Area postrema
91
What's the blood distribution to the liver?
80% portal vein, 20% hepatic artery
92
What's the immune cell of the liver called?
Kupffer cell
93
The liver produces primary bile acids. Where do secondary bile acids come from?
Bacterial metabolism of primary bile acids in the colon
94
What's the critical micellar concentration?
Min concentration of lipids to form micelles
95
What's the Krafft point
temp below which micelles composed of a particular BA will not form
96
What percentage of gallstones are cholesterol-based?
80-85%
97
What percentage of gallstones is not cholesterol-based?
15%. These are black (hemolysis and cirrhosis and bilirubin excretion) or brown (calcium bilirubinate)
98
How does the liver process bilirubin?
Take unconjugated bilirubin and conjugates it to albumin
99
What gives feces its reddish-brown pigment?
Stercobilinogen
100
Where are clotting factors made?
All factors (except VIII) are made in the liver
101
What are two enzymes that can be checked to assess liver function?
ALT (alanine aminotransferase) and AST (aspartate aminotransferase). Degree of abnormality has no direct correlation with liver function.
102
What's Wilson's disease?
Causes liver damage, due to copper overload
103
Which three liver enzymes go up in cholestatic liver disease?
Alkaline phosphatase, gamma-glutamyltransferase, 5' nucleotidase. Degree of abnormality has no direct correlation with liver function.
104
Which infiltrative diseases can cause cholestatic liver disease?
sarcoidosis, amyloidosis, TB, fungi, lymphoma, metastases
105
Which conditions can result from cholestatic liver disease?
primary biliary cirrhosis, primary sclerosing cholangitis, gall stones
106
Name the two patterns of abnormal liver biochemistry
Hepatocellular and Cholestatic
107
Which enzymes are upregulated in hepatocellular pattern abnormal liver biochemistry?
ALT, AST
108
Which enzymes are upregulated in cholestatic pattern abnormal liver biochemistry?
ALP, GGT, Bilirubin (not an enzyme), 5-nucleotidase
109
What are 3 liver function tests?
Bilirubin, INR (clotting time), albumin. Also glucose, but only in end-stage.
110
What's the rate-limiting step in liver bilirubin conjugation?
Excretion into the canniliculi as bile
111
Which clotting factor is the first to cause the clotting problems in acute liver failure?
Factor VII (has shortest half life)
112
What are three clinical consequences of liver dysfunction?
Impaired excretion of bilirubin, impaired metabolism of drugs, impaired control of energy metabolism (clotting, albumin, ammonia, glucose)
113
What's the hepatic vein pressure gradient formula?
(Wedged - free) hepatic vein pressure. If >5, may have clinical problems
114
How does cirrhosis affect peripheral vascular systems?
Cirrhosis causes release of NO, which dilates arteries
115
What classifications does the Child-Pugh-Turcotte score rank liver patients?
Compensated cirrhosis (A), decompensated cirrhosis (B), advanced decompensated cirrhosis (C)
116
Which three parameters does the MELD score for liver transplantation rankings take into account?
Creatinine, INR, Bilirubin
117
How many Canadian households experienced food security?
1.7 million (1/8 households)
118
How many children have felt food insecurity in Canada?
1 in 6
119
What are 3 big predictors of food insecurity?
Low income, single-mother families, aboriginal/black families
120
How much is welfare?
~20k for a couple with 2 children
121
How do people cope with food insecurity?
cut size of meal or skip meals
122
How many people in the world are chronically undernourished?
870 million
