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GIR Test 1 > B5.009 - Stomach and Small Intestine > Flashcards

B5.009 - Stomach and Small Intestine Flashcards

1
Q

what is the gold standard for evaluating gastric emptying

A

scintigraphy gamma radiation is captured by external detectors generating a 2D image

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2
Q

what is breath testing

A

time of appearance of CO2 in the breath following administration of C labeled octanoate

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3
Q

what is smart pill

A

sends signals to a receiver as it passes along the GI tract

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4
Q

what is EGG

A

non invasive means of recording human gastric electrical activity of slow waves from cutaneous leads placed over the stomach

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5
Q

what is noraml rhythm

A

3 cycles/minute

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6
Q

what is tachygastria

A

4-9 electricle cycles/minute

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7
Q

how does tachygastria occur

A

emergence of an ectopic pacemaker in the distal stomach with an abnormally high prequency of electrical activity. Can generate slow waves too fast for normal corpus pacemaker to drive. Thus slow waves from the ectopic site can spread in the oral direction and collide with slow waves propagating in normal direction.

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8
Q

what is gastroparesis

A

when gastric emptying is slowed due to disrupted contractions of the stomach

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9
Q

what is bradygastria

A

0-2.5 electrical cycles/minute

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10
Q

what causes bradygastria

A

during stimulation the maximal contractile frequency is decreased and ther is ad devrease in the number of antral contractions.

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11
Q

conditions associated with dysrhythmic gastric electrical activity

A

pregnancy

nausea

bloat

motion sickness

anorexia

gastroparesis

antral hypomotility

dyspepsia

abdominal malignancies

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12
Q

what is the most common motility disorder

A

delayed gastric emptying from

failure of peristaltic driving force

obstruction to outflow at pylorus

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13
Q

what are 3 mechanisms of altered gastric emptying

A

delayed gastric emptying

dudenal gastric reflux

increased gastric emptying

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14
Q

what are causes of increased gastric emptying

A

decreased fundic compliance

loss of pyloric resistance

failure of duodenal feedback

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15
Q

risk factors for gastroparesis

A

DM

scleroderma

medications that block certain nerve signals

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16
Q

symptoms of gastroparesis

A

abdominal distension

hypoglycemia

nausea

premature abdominal fullness

weight loss

vomiting

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17
Q

complications of gastroparesis

A

esophagitis

bezoar

mallory weiss tear

post prandial hypotension

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18
Q

causes of transient gastroparesis

A

drugs like L dopa, morphine etc

viral gastroenteritis

endocrine

electrolytes

herpes zoster

post op ileus

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19
Q

some causes of chronic gastroenteritis

A

DM

sceroderma

CNS diseases

spinal cord injury

HIV

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20
Q

decreased driving force causes

A

altered electromechanical coupling

altered muscle tone

loss of extrinsic innervation

damage to enteric nervous system

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21
Q

what cell type may be disrupted in diabetic gastroparesis

A

ICC cells, dysrhythmias may originate from here

disruption of ICC network can disorganize gastric electrical activity

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22
Q

what are different mechanisms of diabetic gastroparesis

A

extrinsic denervation can result in delayed emptying

loss of NO synthase in enteric nerves

loss of ICC - decreased smooth m contractility

smooth muscle atrophy

altered function of immune cells like type 2 macrophages

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23
Q

what are 2 causes of increased resistance leading to delayed gastric emptying

A

pyloric stenosis

diabetic pylorospasm

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24
Q

what is pyloric stenossi

A

narrowing of the pylorus due to thickening of pylorus muscles prevents gastric emptying

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25
Q

risk factors of pyloric stenosis

A

<6 mo

belching

constant hunger

failure to gain weight

wave like motion of abdomen after feeding

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26
Q

what can cause a pyloric obsturction

A

tumor

duodenal ulcer

ingestion of caustics

gallstone

bezoar

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27
Q

what is dumping syndrome

A

rapid gastric emptying

contents fo stomach are entering intestine prematurly

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28
Q

symptoms of dumping syndrome

A

nausea

cramps

diarrhea

satiation

vomiting

flushign

usually within 30 min of a meal

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29
Q

what is late dumping syndrome

A

dumping syndrome but 1-3 hours after a meal

late dumping is usually associated with excess sugar rapidly entering the small intestine causing a large insulin response and hypoglycemia

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30
Q

what is rapid dumping syndrome caused by

A

usually post op

drugs

zollinger ellison syndrome

cyclic vomiting syndrome

31
Q

neural pathways leading to initiation of vomiting

A

pharyngeal stimulation - glossopharyngeal nerve - NTS

drugs or irritants

pregnancy

vertigo - cerebellum

pain

all stimulate brainstem vomiting center

32
Q

what causes vomiting mechanically

A
  1. start of a retrograde giant contraction in proximal jejunum
  2. retropelled digsta reach duodenum and are forced across the widely opened pylorus into the antrum
  3. giant contraction proceeds to antrum, the chyme accumulates in gastric resivoir
33
Q

fucntions of small intestine

A

digest macromolecular nutrients

absorb digestion products

absorption of fluid and electrolites

retain nutrients in small bowel until max digestion

move chyme from duodenum to point of emptying at ileo colonic sphincter

34
Q

what are the major hormones for regulating pancreatic secretions

A

GLP1

CCK

VIP

PP

35
Q

what are enteroendocrine cells in GI tract

A

they are stmulated to release CCK that sends signals

36
Q

what cel type produces CCK

A

I cell in duodenum

37
Q

what happens with I cells in the fed state

A

CCK is secreted from lipid stimulation or other digestive products that sends signals to brain via vegas to induce release of pancreatic juices like trypsin

38
Q

describe vagus’ role in regulation of pancreatic secretions

A

ACh is sufficient to fully stimulate pancreatic secretion. Acts mailty during intestinal phase of a meal

Atropine blocks CCK stimulation of secretion suggesting that CCK also acts via stimulatino of PARA

39
Q

what do acinar cells in the pancreas do

A

secrete enzymes

nucleases

pancreatic lipase

amylase

elastase

gelatinase

typsinogen

chymotrypsinogen

carboxypeptidase

40
Q

what do duct cells do in the pancreas

A

release bicarb and fluid

41
Q

what activates the acinar cell and what does that do

A

VIP

secretin

GRP

ACh

CCK

stimulates cAMP or increases intracellular Ca++ to cause the phosphorylation of structural and regulatory proteins leading to enzyme release into dodenum

42
Q

what does secretin do

A

released in fed state by S cells in mucosal layer of small intestine

stimulated mainly by entry of acidic gastric juice into duodenum

must act in concert with CCK and ACh on duct cell to produce bicarb to neutralize acid in small intestine

a mechanism to take acidic chyme and make it more neutral

43
Q

what do duct cells release and what stimulate the release

A

bicarbonate and fluid

secretin

ACh

GRP

44
Q

what is peptide YY

A

induced by fat in distal SI

reduced bicarb and enzyme release

45
Q

what is glucagon

A

from pancreatic islet alpha cells reduces bicarb and enzyme release nd flow volume

46
Q

what is somatostatin

A

produced by D cells in SI as hormone reduces bicarb and enzyme release an dinhibits insulin production

47
Q

what is pancreatic polypeptide

A

from PP cell in pancreas

release is stimulated by vagus and PP inhibits pacreatic secretions

48
Q

what 4 molecules are involved in negative feedback for pancreatic secretions

A

Peptide YY

Glucagon

Somatostatin

PP

49
Q

describe lipid digestion generally

A

fat in the duodenum inbibits gastric emptying to allow for enought ime to emusify and absorption

digestion of lipids occrus in the stomach (lingual and gastric lipases) nad intestinal lumen. Pancreatic lipase with colipase digests TGs into fatty acids, glycerol, and monoglycerol

50
Q

what do bile salts do

A

facilitate absportion of lipid products

51
Q

why are bile salts needed

A

fats are largety water insoluble so they help emuslify and get through liquid environment

52
Q

what are micelles

A

water solube formed from bile salts from teh gallbladder with products of lipid digestion

they provide a mechanism for the lipid products to access villous epithelia cells for lipid absorption

53
Q

how much bile acids are reused

A

90%, 10% newly synthesized by liver

54
Q

how do conjugated and non conjugated bile salts differ

A

conjugated - are more water solube, taken up by Na+-bile acid symptorter

unconjucated - taken up by diffusion

55
Q

what cell type makes CCK

A

I cell in duodenum

56
Q

what does CCK trigger

A

gallbladder contraction

relaxation of sphincter of Iddi

pancreatic secretions

reduce gastric emptying

57
Q

what stimulates CCK release

A

fatty acids entering duodenum

58
Q

how does CCK affect the gall bladder

A

can stimulate vagal complex to send neural signal to contract gall bladder

59
Q

what are segmenting contractions

A

special contractions in small intestine that function to mix up all the chyme with the bile salts

think ballon

reduces particle size of food and expose surface epithelium to nutrients to promote absormption

60
Q

what muscle layer stimulates contractions in duodenum

A

circular

61
Q

what does longitudinal muscle in the small intestine do

A

promotes opening/widening of the lumen

62
Q

what parts of the small intestine absorb what nutritents

A

duodenum - iron, calcium, carbs, fats and proteins

jejunum - carbs, fats and proteins

ileum - bile salts, B12, fats and proteins

63
Q

describe the lengths of different parts of SI

A

duodenum - 20 cm

jejunum - 3 m

ileum - 4 m

64
Q

describe innervation of the small intestine

A

extrinsic innervation by vagus nerve and symptathetic fibers from celiac and superior mesenteric ganglia

65
Q

where do micelles diffuse to

A

among the microvilli and through the instirred layer at the brush border , products are readily absorbed by the gut enterocyte. As products are absorbed more lipids partition out of micelles

66
Q

once fat is absorbed into the enterocyte what happens

A

fatty acids and cholesterol get transported to the SER where free fatty acids get converted to TGs and etc.

chylomcycrons are formed and undergo exocytosis

67
Q

where do chylomicrons go

A

enter lacteals (lymphatic capillaries in villi of the small intestine) not the portal vein

68
Q

where do lacteals go

A

merge into lymphatic duct and chylomicrons get transported to venous circulation

69
Q

what happens with short and medium chian TGs

A
70
Q

what transporter allows cholesterol to ender enterocytes

A

NPC1L1 transporter

71
Q

what part of the small intestine returns bile to the liver

A

the ileum

72
Q

what helps digest protein

A

pepsin

73
Q

how do AAs get absorbed

A

via Na+ depnedent transporters in the apical membrane

small peptides are absorbed by PEPT-1 a H+ dependend transporter

both are secondary active transport as they use energy from the electrochemical gradient set up by the Na/K ATPase

GIR Test 1 (15 decks)

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