Physiology Flashcards

1
Q

Where is the source of Gastrin production?

A

G cells in antrum of stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is the source of CCK production?

A

I cells in duodenum, jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is the source of secretin production?

A

S cells in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is the source of somatostatin production?

A

D cells in pancreatic islets and GI mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is the source of Glucose-dep insulinotropic peptide (GIP) production?

A

K cells in duodenum and jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is the source of Vasactive intestinal polypeptide (VIP) production?

A

parasympathetic ganglia in sphincters, gallbladder, small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is the source of Motilin production?

A

small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Actions of gastrin

A

increase gastric H+ secretion
increase growth of gastric mucosa
increase gastric motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Actions of CCK

A

increase pancreatic secretion
increase gallbladder contraction
increase sphincter of Oddi relaxation

decrease gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Actions of Secretin

A

increase pancreatic HCO3
increase bile secretion

decrease gastric secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Actions of somatostatin

A

decrease gastric acid & pepsinogen secretion
decrease pancreatic & small intestine fluid secretion
decrease gallbladder contraction
decrease insulin & glucagon secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Actions of GIP

A

Exocrine: decrease gastric H+ secretion

Endocrine: increase insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Actions of VIP

A

increase intestinal water & electrolyte secretion

increase relaxation of intestinal smooth muscle & sphincters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Actions of Nitric oxide

A

increase smooth muscle relaxation, including lower esophageal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Actions of motilin

A

produces MMCs to clears remaining from GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

regulation of gastrin

A

increased by stomach distention, alkalinization, amino acids, peptides, vagal stimulation;

decreased by stomach pH < 1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Amino acids that increase stimulation of gastrin

A

phenylalanine and tryptophan are potent stimulators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Chronic use of what drug lead to sustained increase in serum gastrin?

A

chronic PPI use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Recurrent peptic ulcers that do not respond due to very high levels of gastric is due to what?

A

Zollinger Ellison syndrome increases Gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes an increase in CCK production / regulation?

A

increase in fatty acids and amino acids in the duodenum and jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What GI hormone causes pancreatic secretion? How?

A

CCK acts on neural muscarinic pathways to cause pancreatic secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes an increase in secretin production / regulation?

A

increase in H+, fatty acids in lumen of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What GI hormone is necessary for pancreatic enzymes to function?

A

increase HCO3 neutralizes gastric acid in duodenum allows pancreatic enzymes to function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What regulates somatostatin release?

A

increase in acid production

decrease in vagal stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the primary role of somatostatin?

A

Inhibitory hormone that inhibits digestion and absorption of substances needed for growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes an increase in GIP?

A

increase by fatty acids, amino acids, oral glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does GIP affect glucose load?

A

oral glucose load is used more rapidly than IV glucose due to GIP secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What causes an increase in VIP?

A

VIP increased by distention and vagal stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What will lead to a decrease in VIP?

A

adrenergic input causes a decrease in VIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What produces VIP in very high amounts? what does it cause?

A
non-alpha and non-Beta islet cell pancreatic tumor (VIPoma);
presents w/ WDHA syndrome
Watery
Diarrhea
Hypokalemia
Achlorhydria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

If Nitric Oxide secretion is lost, what will this lead to in the esophagus?

A

lower esophageal tone of achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What will increase motilin?

A

increases in fasting state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is an antibiotic that will stimulate intestinal peristalsis?

A

Erythromycin => by binding to motilin agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the source and action of intrinsic factor?

A

parietal cells in body of stomach => Vit B12 binding protein required for uptake in terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

A patient w/ an autoimmune disease may be susceptible to what?

A

autoimmune destruction of parietal cells => chronic gastritis and pernicious anemia

36
Q

What is the source and action of gastric acid?

A

parietal cells in stomach => decreases stomach pH

37
Q

What will cause an increase in gastric acid?

A

increased by histamine, ACh, gastrin => leads to potentiation causing more to be produced

38
Q

What will cause a decrease in gastric acid?

A

somatostatin, GIP, prostaglandin, secretin

39
Q

What pathology / tumor will cause high acid secretion and ulcers?

A

gastrinoma

40
Q

What is the source and action of pepsin?

A

chief cells in stomach => protein digestion

41
Q

What regulates pepsin production?

A

increase w/ vagal stimulation and local acid

42
Q

An increase of pH in the stomach would cause a decrease in what enzyme?

A

pepsin that is cleaved from pepsinogen by H+

43
Q

What is the source and action of HCO3 in GI tract?

A

neutralizes acid from production from mucosal cells and Brunner’s glands

44
Q

Where are mucosal cells found in the GI tract that produce HCO3?

A

stomach, duodenum, salivary glands, pancreas

45
Q

Where are Brunner’s glands found?

A

duodenum

46
Q

What regulates HCO3 production?

A

increase by pancreatic and biliary secretion w/ secretin

47
Q

How is HCO3 used in the stomach?

A

trapped in mucus that covers gastric epithelium

48
Q

What causes saliva to be secreted? from where?

A

stimulated by SANS & PANS acting on the parotid, submandibular, and sublingual glands

49
Q

What secretory products are found in saliva and what is there purpose?

A

Amylase=> digests starch
HCO3 neutralizes bacterial acids
mucins=> lubricate food

50
Q

What type of solution is saliva excreted from its gland? what changes this?

A

normally hypotonic bc of absorption;

more isotonic w/ higher flow rates (less time for absorption)

51
Q

How does gastrin lead to increase of acid secretion?

A

primarily through effects on ECL cells leading to Histamine release moreso than direct effect on parietal cells

52
Q

What is the pathway that the Vagus nerve leads to stimulation of acid? What drug would block the this cascade?

A

releases ACh => ACh binds to M3 receptor => activates Gq pathway leading to activation of IP/Ca+ cascade => activation of H/K ATPase

Atropine blocks ACh binding to M3 receptor

53
Q

What is the pathway that gastrin leads to stimulation of acid? What drug would block the this cascade?

A

Vagus stimulates GRP release=> GRP activates G cells to release gastrin => gastrin binds to CCK-B receptor => activates Gq => activation of IP3/Ca+ => activation of H/K ATPase

No clinically useful inhibitor

54
Q

What is the pathway that histamine leads to stimulation of acid? What drug would block the this cascade?

A

Gastrin binds to ECL cells to release histamine => Histamine binds to H2 receptor => H2 receptor activates cAMP => increase cAMP activates H/K ATPase

H2 blockers

55
Q

What drug class will inhibit H/K ATPase?

A

proton pump inhibitors

56
Q

What causes a prevention of acid secretion into GI lumen? how?

A

prostaglandins / misoprostol; Somatostatin => bind to Gi to BLOCK cAMP increase thus blocking H/K ATPase

57
Q

After eating, what does the gastric parietal cell cause? how?

A

alkaline tide & acid secretion => H2O and CO2 are bound via carbonic anhydrase to make H2CO3 which is broken down to form H+ and HCO3- => H+ is used in H/K ATPase to promote acid along w/ Cl- secretion while HCO3- / Cl- exchange occurs w/ HCO3- going to blood (alkaline tide)

58
Q

Where are Brunner’s glands located and what is there function? when would hypertrophy of these cells occur?

A

duodenal submucosa and secretes alkaline mucus

hypertrophy in PUD

59
Q

What type of solution are pancreatic secretions? How does flow affect concentrations?

A

isotonic fluid
low flow => high Cl-
high flow => high HCO3-

60
Q

What pancreatic secretion is important in starch digestion?

A

alpha-amylase

61
Q

What pancreatic secretion is important in fat digestion?

A

lipase;
phospholipase A;
colipase

62
Q

What pancreatic secretion is secreted in active form?

A

alpha amylase

63
Q

What pancreatic secretions are secreted as proenzymes?

A

proteases for protein digestion => trypsin, chymotrypsin, elastase, carboxypeptidases

64
Q

What is the key to activation of pancreatic enzymes?

A

duodenal mucosa secretes enterokinase to convert trypsinogen to trypsin which activates other zymogens to create more trypsinogen => positive feedback loop

65
Q

What enzymes are associated w/ carbohydrate digestion?

A

salivary amylase;
pancreatic amylase;
oligosaccharide hydrolases

66
Q

How does salivary amylase promote carb digestion?

A

starts digestion=> hydrolyzes a-1,4 linkages to yield disaccharides (maltose and alpha-limit dextrins)

67
Q

How does pancreatic amylase promote carb digestion?

A

highest concentration in duodenal lumen => hydrolyzes starch to oligosaccharides and disaccharides

68
Q

How does oligosaccharide hydrolases promote carb digestion?

A

at brush border of intestine => RATE LIMITING STEP IN CARB DIGESTION => produces monosaccharides from oligo- and disaccharides

69
Q

After carb digestion, what is absorbed by enterocytes?

A

only monosaccharides => glucose, galactose, fructose

70
Q

Differentiate the mechanisms of absorption of carbohydrates

A

glucose and galactose are taken up by SGLT-1 => Na+ dependent

Fructose taken up by facilitated diffusion by
GLUT-5

71
Q

How are monosaccharides transported to blood?

A

GLUT-2

72
Q

If a patient presents w/ malabsorption, what is a test distinguishing GI mucosal damage?

A

D-xylose absorption test distinguishes GI mucosal damage from other causes of malabsorption

73
Q

Where is Iron absorbed?

A

Fe^2+ in duodenum

74
Q

Where is folate absorbed?

A

jejunum

75
Q

What is occurred in the terminal ileum?

A
Vit B12 (requires intrinsic factor);
Bile acids
76
Q

What are Peyer’s patches? what is their function?

A

unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum => contain specialized M cells that take up antigen

77
Q

How does the Peyer’s patch in the gut deal w/ intraluminal antigen?

A

B cells stimulated in germinal centers differentiate into IgA-secreting plasma cells that reside in lamina propria => IgA receives protective secretory component and transported across epithelium

IgA=> Intra-gut Antibody

78
Q

What does bile contain?

A

bile salts, phospholipids, cholesterol, bilirubin, water and ions

79
Q

What is necessary for bile salts to be in bile?

A

bile acids conjugated to glycine or taurine making them water soluble

80
Q

What is the rate limiting step in bile function?

A

cholesterol 7a-hydroxylase catalyzes rate limiting step

81
Q

What are the functions of bile?

A

1) digestion and absorption of lipids and fat-soluble vitamins
2) cholesterol excretion (body’s only means of eliminating cholesterol)
3) antimicrobial activity (via membrane disruption)

82
Q

How is the product of heme metabolism removed from blood?

A

bilirubin removed from blood by liver, conjugated w/ glucuronate and excreted in bile

83
Q

What is difference in direct vs indirect bilirubin?

A

direct=>conjugated w/ glucuronic acid; water soluble

indirect=> unconjugated; water insoluble

84
Q

In the breakdown of heme, what occurs in macrophages?

A

RBC=> Heme => unconjugated bilirubin which is indirect bilirubin (water insoluble)

85
Q

In the breakdown of heme, what occurs in bloodstream?

A

albumin binds to form unconjugated bilirubin-albumin complex

86
Q

In the breakdown of heme, what occurs in liver?

A

unconjugated bilirubin-albumin complex uses UDP-glucuronosyl-transferase to form conjugated bilirubin (direct bilirubin that is water soluble)

87
Q

In the breakdown of heme, what occurs in gut?

A

conjugated bilirubin is converted by gut bacteria to urobilinogen => 80% excreted in feces as stercobilin (stool color); 20% goes to gut and 10% to kidney for urobilin (urine color) and 90% enters enterohepatic circulation to liver