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Physiology > Chapter 6 ( Gastrointestinal Physiology ) > Flashcards

Chapter 6 ( Gastrointestinal Physiology ) Flashcards

1
Q

Origin of preganglionic sympathetic cholinergic fibers to git and they synapse in which ganglia ?

A

Originates in the spinal cord between T8 and L2

Synapse in the prevertebral ganglia

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2
Q

Intrinsic innervation of git components and their functions ?

A

1- Myenteric plexus ( Auerbach plexus ) : controls the motility of git
2- Submucosal plexus ( Meissner plexus ) : controls secretion and blood flow of git

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3
Q

Actions of Gastrin ?

A

1- increases H+ secretion by gastric parietal cells

2- stimulate growth of gastric mucosa by stimulating synthesis of RNA and new proteins

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4
Q

Stimuli and inhibitors of gastrin secretion ?

A

1- stimuli :
Small peptides and amino acids
Distention of the stomach
Vagal stimulation ( mediated by GRP )

2- inhibitors :
H+ in the stomach
Somatostatin

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5
Q

Actions of CCK ?

A

1- contraction of gallbladder and relaxation of sphincter of Oddi
2- stimulates pancreatic enzyme secretion
3- enhance secretin effect of pancreatic HCO3 secretion
4- stimulates growth of exocrine pancreas
5- inhibits gastric emptying

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6
Q

Stimuli for release of CCK ?

A

Small peptides and amino acids

Fatty acids and monoglycerides

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7
Q

Actions of secretin ?

A

1- Stimulates pancreatic HCO3 secretion
2- increases growth of exocrine pancreas
3- stimulates HCO3 and H2O secretion by the liver and increases its bile production
4- inhibits H+ secretion

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8
Q

Stimuli for secretin secretion ?

A

H+ in the duodenum

Fatty acids in the duodenum

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9
Q

Actions of GIP ?

A

1- stimulates insulin secretion

2- inhibits H+ secretion by gastric parietal cells

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10
Q

Stimuli for release of GIP ?

A

Fatty acids
Amino acids
Glucose

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11
Q

Candidate hormones ?

A

Motilin
Pancreatic polypeptide
GLP-1

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12
Q

GIT paracrines ?

A

1- somatostatin : in response to H+ in the lumen and inhibited by vagal stimulation , inhibit the release of all gi hormones
2- histamine : increase gastric H+ secretion by potentiation of gastrin and vagal stimulation

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13
Q

GIT neurocrines ?

A

1- VIP : causes relaxation of GIT smooth muscles , stimulate pancreatic HCO3 secretion and inhibits gastric H+ secretion
2- GRP : stimulates gastrin release from G cells
3- Enkephalins : stimulates contraction og git smooth muscles , inhibits intestinal secretion of fluid and electrolytes

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14
Q

Site of satiety center ?

A

Ventromedial nucleus of hypothalamus

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15
Q

Site of feeding center ?

A

Lateral hypothalamic area of hypothalamus

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16
Q

Substance released by anorexigenic neurons to decrease appetite ?

A

POMC

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17
Q

Substance release by orexigenic neurons to stimulate appetite ?

A

Neuropeptide gamma

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18
Q

Hormones decreasing appetite ?

A

Leptin ( by fat cells )
Insulin
GLP-1

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19
Q

Hormone secreted by gastric cells that increase appetite ?

A

Ghrelin

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20
Q

Contractile tissue of the git that are striated muscles ?

A

Pharynx
Upper one third of the esophagus
External ana sphincter

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21
Q

Site of tonic contractions in the git ?

A

Lower esophageal sphincter
Orad stomach
Iliocecal sphincter
Internal anal sphincter

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22
Q

Pacemaker for gut smooth muscle and origin of slow waves ?

A

Interstitial cells of Cajal

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23
Q

Mechanism of slow wave production ?

A

Cyclic opening of Ca channels ( depolarization ) followed by opening of K channels ( repolarization )

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24
Q

Where is the swallowing reflex coordinated ?

A

The medulla

Fibers of vagus and glossopharyngeal nerve carry information between medulla and git

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25
Q

The nerve and the neurotransmitter responsible for lower esophageal sphincter relaxation during swallowing ?

A

Vagus

By VIP

26
Q

Migratory myoelectric complex def ? Hormone responsible for it ?

A

Propulsive movement initiated during fasting begins in the stomach and moves undigested material from stomach and smooth intestine to the colon , occurs every 90-120 mins
Hormone responsible : Motilin

27
Q

Gastroileal reflex mediated by what ? Its function ?

A

Mediated by : extrinsic ANS and possibly by gastrin
Its function : presence of food in the stomach triggers increased peristalsis in the ileum and relaxation of ileocecal sphincter , as a result the intestinal content are delivered to the large intestine

28
Q

Gastrocolic reflex ? Mediated by what ?

A

Presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements
Has rapid Parasympathetic component
And slower hormonal component by CCK and Gastrin

29
Q

Composition of saliva ?

A 
High volume 
High K , HCO3 
Low Na , Cl
Hypotonicity 
Alpha-amylase , lingual lipase , kallikrein
30
Q

Type of Cholinergic receptors in the salivary gland ? Second messenger ?

A

Muscarinic

Second messenger : iP3 , increased intracellular Ca

31
Q

Type of adrenergic receptors in the salivary gland ? Second messenger ?

A

Beta-adrenergic

Second messenger : cAMP

32
Q

Omeprazole mechanism ?

A

Inhibition of H-K ATPase pump in the parietal cells of stomach and blocks H+ secretion

33
Q

Mechanism of metabolic alkalosis in vomiting ?

A

Loss of H+ in the vomitus will lead to decreased H+ arriving in the small intestine , there is no stimulus for pancreatic HCO3 secretion leading to its excess in the blood and the arterial blood becomes alkaline

34
Q

Why atropin doesnot block H+ secretion completely ?

A

Because it does not inhibit the indirect pathway using the GLP as a neurotransmitter

35
Q

Which receptor does the gastrin interact with on the parietal cells ? Second messenger ?

A

CCK B

Second messenger : iP3 / Ca

36
Q

Which receptor does histamine interact with on the parietal cells ? Second messenger ?

A

H2 receptors

Second messenger : cAMP

37
Q

Inhibitors of H+ secretion ?

A

Somatostatin
Prostaglandins
By coupling with Gi protein

38
Q

Diagnostic test for H-pylori ?

A

Urea breath test : drinking a solution of 13C-urea which is converted to 13CO2 by urease of H-pylori and measured in breath

39
Q

Why is H-pylori is a major cause for duodenal ulcer ?

A

Because
1- it inhibits somatostatin secretion ( thus increases gastric H+ secretion )
2- inhibits intestinal HCO3 secretion

40
Q

Function of alpha-amylases ?

A

Hydrolyzes 1,4 glycosidic bonds in starch , yielding maltose , maltotriose and alpha-limit dextrins

41
Q

Absorption of carbohydrates from intestine ?

A

Glucose and Galactose : by Na dependent cotransport from intestinal lumen to cells and by facilitated diffusion by GLUT 2 from cells to blood

Fructose : by facilitated diffusion only

42
Q

How is the pepsinogen activated ?

A

By gastric H+ in pH : 1-3

43
Q

How is the trypsinogen activated ?

A

By the brush border enzyme : Enterokinase

44
Q

Pancreatic proteases ?

A

Trypsin
Chymotrypsin
Elastase
Carboxypeptidase A , B

45
Q

Absorption of proteins in intestine ?

A

1- free amino acids : by Na dependent amino acid cotransport from lumen to cells then by facilitated diffusion from cells to blood

2- dipeptides and tripeptides : by H dependent cotransport from lumen to cells where they are hydrolyzed by plasmic peptidase then transported by facilitated diffusion from cells to blood

46
Q

Where is the chemoreceptor trigger zone for vomiting ? Activators ?

A 
In the Fourth Ventricle 
Activated by : 
Emetics 
Radiation 
Vestibular stimulation
47
Q

Composition of pancreatic secretion ?

A 
Same Na and K concentrations as plasma 
Much higher HCO3 concentration than plasma 
Much lower Cl concentration than plasma 
Isotonic 
Pancreatic lipase , amylase , proteases
48
Q

Second messenger and site of action of secretin on the pancreas ?

A

Pancreatic ductal cells

cAMP

49
Q

Second messenger and site of action of CCK on the pancreas ?

A

Pancreatic acinar cells

IP3 and Ca

50
Q

Primary bile acids and secondary bile acids ?

A 
Primary : 
Cholic acid 
Chenodeoxycholic acid 
Secondary : 
Deoxycholic acid 
Lithocholic acid
51
Q

Bile salts ?

A

Bile acids conjugated with Glycine or Taurine

52
Q

Site and mechanism of recirculation of bile acids ?

A

Terminal ileum

By Na-Bile acid cotransporter ( secondary active transporter )

53
Q

Pancreatic lipases ?

A

Pancreatic lipase
Cholesterol ester hydrolase
Phospholipase A2

54
Q

Causes of steatorrhea ?

A 
Pancreatic disease ex: cystic fibrosis 
Hypersecretion of gastrin ex: zollinger ellison syndrome 
Ileal resection
Bacterial overgrowth 
Tropical sprue 
Abetalipoproteinemia
55
Q

Na absorption in small intestine and colon ?

A

1- In small intestine : by Na glucose cotranspor , Na amino acid cotransport , Na H exchange ( similar to renal proximal tubule

2- in colon : by passive diffusion through Na channels ( similar to those in renal distal tubule and also are stimulated by aldosterone )

56
Q

Site of active secretion of K in git ?

A

Colon and is stimulated by aldosterone like in distal tubule of kidney

57
Q

Site of secretory mechanisms and absorptive mechanisms in the intestine ?

A

Secretory : Crypts

Absorptive : villi

58
Q

Primary ion secreted in small intestine ?

A

Cl- which is regulated by cAMP

59
Q

Site of vit B12 absorption ?

A

Ileum

60
Q

Intestinal Ca binding protein ?

A

Calbindin D-28K

61
Q

Site of absorption of Divalent cations ?

A

Duodenum

Physiology (7 decks)

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