GI Flashcards

1
Q

What causes stomatitis?

A

Poor oral hygiene, dietary protein insufficiency, poorly fitted dentures, burns from hot food, allergies, conditions affecting the whole body

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2
Q

Where can candida be found

A

Mouth + esophagus

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3
Q

What 2 things are needed for the LES to function properly?

A

Inner circular esophageal muscle Surrounded by a loop of diaphragmatic muscle

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4
Q

Why does the LES not work well when there is a Hiatal Hernia?

A

Because part of its function depends upon the diaphragm circling around it

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5
Q

What structure drains the foregut, midgut and hindgut?

A

Portal vein

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6
Q

Cirrhosis causes portal HTN, what is the significance of this condition?

A

 Blood cant get through the liver effectively, so it shunts it through the Azygous and Hemiazygous veins in order to get it back to the heart  Blood backs up into other structures like the esophageal veins, this causes esophageal varices

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7
Q

What drains the majority of the esophagus?

A

Hemiazygous and azygous v.v.

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8
Q

What drains the cervical region of the esophagus?

A

inferior Thyroid v

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9
Q

What happens in esophageal varices?

A

HTN from backed up portal vein flowing into azygous and hemiazygous v.v. These veins can rupture and bleed. 33% mortality; 50% recurrances

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10
Q

Tx for esophageal varices

A

*shunting *banding and sclerotherapy for mild cases 90% effectiveness *vasopressin

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11
Q

The Vagus nerve has been surgically cut (ligated) in the past before it’s function was fully understood. Why did we do this? 

A

The Vagus nerve releases Ach in the stomach, and the stomach in turn produces HCl

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12
Q

If someone had ulcers that could not be treated in any other way, the nerve would be cut…

A

stopping the release of Ach and thus stopping acid production

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13
Q

What is stomatitis?

A

Inflammation of any of the structures of the mouth, including the buccal mucosa, gums, tongue, throat, lips, or palate

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14
Q

Why do esophageal cancers metastasize so quickly? 

A

No serosa

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15
Q

The Vagus nerve has been surgically cut (ligated) in the past before it’s function was fully understood. Why did we do this? 

A

The Vagus nerve releases Ach in the stomach, and the stomach in turn produces HCl

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16
Q

Is the vagus primarily a sensory or motor nerve?

A

Sensory

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17
Q

What cell type normally lines the esophagus?

A

 Stratified Squamous epithelium

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18
Q

why are most esophageal cancers NOT SCC (squamous cell carcinoma)?

A

 Intestinal metaplasia occurring in invading columnar epithelium for the stomach causes Barrett’s esophagus and thus adenocarcinoma

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19
Q

How can having a hiatus hernia ultimately lead to cancer?

A

 Acid reflux leads to intestinal metaplasia (influx of columnar epithelium from the stomach)

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20
Q

What structure causes the plica circulares to form?

A

 Muscularis mucosa

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21
Q

What layer houses the glands?

A

Submucosa

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22
Q

What are 2 muscle layers in most of GI

A

Inner circular, outer longitudinal

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23
Q

What are the histo logical layers in most of GI? Lumen –> serosa

A

Mucosa *epithelium *lamina propria *muscularis mucosa Submucosa Muscularis Externis Serosa

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24
Q

What is the blood supply to the foregut, midgut and hindgut?

A

 Celiac, Superior Mesenteric, Inferior Mesenteric Arteries

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25
Q

Which Vagus nerve can be seen on the anterior surface of the stomach?

A

 Clockwise rotation makes the left branch of the Vagus anterior

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26
Q

Which divisions of the gut have both dorsal and ventral mesogastrium?

A

 Note that the foregut is the only place where the structures are tethered both dorsal and ventral by their respective mesogastrium

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27
Q

Why is the greater omentum important? 

A

Walls off inflammatory processes in the abdomen

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28
Q

What artery comes off the aorta cephalad to the pancreas? 

A

Celiac

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29
Q

What is the first major artery to come off caudad to the body of the pancreas from the aorta?

A

superior mesenteric artery

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30
Q

Why is the antrum of the stomach sometimes removed, and where is it located?

A

 Intractable peptic ulcer disease initial part of the pylorus

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31
Q

Where is the pylorus and what does it do? 

A

Valve separating the stomach from the duodenum

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32
Q

What do flattened rugae indicate? 

A

If the rugae, folds, are flattened, it may indicate stomach inflammation (gastritis)

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33
Q

Why do babies with pyloric stenosis have Non-bilious vomiting?

A

 Bile is released by the common bile duct in the duodenum, so the bile cannot get backwashed into the stomach, as the enlarged pylorus prevents this

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34
Q

pyloric stenosis

A

condition that causes non-bilious projectile vomiting in the first 2-6 weeks of life. more common in first born males. result of an olive shaped mass (congenital or hypertrophy) in middle upper or upper right quadrant that narrows the pyloric sphincter.

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35
Q

What is the classic metabolic disturbance in pyloric stenosis and why?

A

loss of HCl (along with K+) from persistent vomitting –> metabolic alkalosis hypokalemia hypochloremic

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36
Q

if you see an ulcer at location V, what location is this and what is associated with causing it?

A

 Body of the stomach  NSAIDs

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37
Q

Type I: Ulcer

A

along the body of the stomach Not associated with acid hyper secretion; associated w/ Type A blood

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38
Q

Type II: Ulcer

A

in the body in combination with duodenal ulcers. Associated with acid oversecretion.

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39
Q

Type III: ulcer

A

In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion

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40
Q

Type IV: ulcer

A

Proximal gastroesophageal ulcer

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41
Q

what ulcers are type O blood associated with?

A

II-IV

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42
Q

Where is iron absorbed?

A

duodenum

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43
Q

Where does the foregut end?

A

 The foregut ends after the first portion of the duodenum, a location when the bile and pancreatic ducts drain into the duodenum

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44
Q

Why do anterior duodenal ulcers perforate and posterior duodenal ulcers bleed?

A

Anterior ulcers perforate the diaphragm causing pneumoperotonium  The largest arterial supply generally comes from the posterior surface of a hollow viscus (intestines and stomach)  Gastroduodenal artery runs on the posterior surface of the duodenum

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45
Q

When does pancreatic adenocarcinoma occur in most people and what are the symptoms?

A

 50s-60s  Pain radiating to the spine

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46
Q

Why are most cases of pancreatic adenocarcinoma inoperable?

A

 The tumor has encased the SMA and SMV

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47
Q

What is the outlook for pancreatic adenocarcinoma?

A

20% 5 yr. Survival rate with resection  50% invade portal vein, SMV or retroperitoneum at time of diagnosis (unresectable disease)

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48
Q

What structure connects the GI capillary beds to the liver sinusoids?

A

Portal Vein

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49
Q

Major GI veins

A

splenic–spleen and stomach superior mesenteric—sm intestine, cecum, ascending colon, transverse colon inferior mesenteric–transverse and descending colon, rectum, anal canal

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50
Q

Why doesn’t a persons “gut’s” spill out onto the floor when they are attacked and eviscerated by a ninja?

A

 The midgut and hindgut are tethered by the dorsal mesogastrium AKA the Unlike with the stomach and 1st portion of mesentary the duodenum, these structures are not connected by a ventral mesogastrium

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51
Q

Mesentery

A

Portion of dorsal mesogastrium that spans between the posterior wall and the small and large intestines. Lack of a ventral portion permits intestines to move freely within abdominal cavity.

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52
Q

The midgut and hindgut leave the abdomen during what week of development?

A

5

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53
Q

The midgut and hindgut return the abdomen during what week of development?

A

10

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54
Q

Why do the midgut and hindgut leave the abdomen during development?

A

Gives the abdomen time to enlarge and allows them to move around so that they can rotate 270

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55
Q

Why is knowing the arterial branches of the midgut important?

A

 It tells the surgeon where to resect, as resection is done to include everything perfused by the artery and veins where the primary tumor is located (in order to get the LN (lymph nodes) that may be harboring cancer

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56
Q

ascending and transverse colon are supplied by what arteries

A

ileocolic, R & middle colic arteries

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57
Q

What is the fuel used by enterocytes?

A

glutamine

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58
Q

What is the fuel used by colonocytes?

A

Short-chained fatty acids

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59
Q

How does the vascular pattern differentiate the ilium from the jejunum?

A

ileum–branched or multiple vascular vascular arcades

jejunum–straight vascular arcades

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60
Q
A
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61
Q

What structures run in the mesentery?

A

Arteries, veins and lymphatic structures

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62
Q

 Where does the SMA insert?

A

 The posterior aspect of the hollow viscera

 (The Mesenteric Boarder)

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63
Q

What branches of the SMA supply the ascending and transverse colon?

A

iliocolic, right colic, and middle colic arteries

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64
Q

What allows the sm intestine to absorb so much food?

A

Plica–>villi–>microvilli

65
Q

microvilli

A

projections of enterocyte cell membranes into the lumen; also called the brush border.

66
Q

Why is it bad sometimes for lymphatic drainage if a person gets stabbed in the left neck?

A

Thoracic duct empties into the junction of the left subclavian and internal carotid vein

67
Q

What structure in a villi marks the beginning of the lymphatic collection system in the GI tract?

A

The Lacteal

68
Q

Thoracic Duct ascends along ??? & drains into the ???

A

ascends along vertebral column & drains into the junction of left internal jugular and subclavian vein

69
Q

Cisterna Chyli

A

diliated lymphatic vesslel taht receives lymph from several areas of the GI tract and abdomen

70
Q

 Intestinal Malrotation

A

This is what happens if the gut does not rotate 270 degrees

71
Q

what does intestinal malrotation cause?

A

bowel obstruction

72
Q

What is the clinical significance of Ladd’s Bands?

A

series of bands crossing the duodenum that can cause bowel obstruction

73
Q

bilious vomitting in babies can indicate

A

intestinal malrotation

74
Q

What happens if the Vitelline duct does not obliterate (3)

A

Meckel’s diverticula  Vitelline cyst
 ophalmocele

75
Q

Why does Meckel’s sometimes bleed

A

 Has gastric tissue in it that responds to circulating blood gastrin and subsequently produces HCl, which erodes the intestinal wall

76
Q

What is the most common

malformation of the GI tract?

A

 Meckel’s

77
Q

What are the characteristics of Meckel’s Diverticulum?

A

* small bulgein the sm intestine

*bleeing may only start in adulthood

*antimesenteric border of the small bowel

78
Q

Where is Meckel’s found?

A

The anterior or antimesenteric boarder

79
Q

What is the #1 cause of painless GI bleeding in children?

A

Meckel’s Diverticulum

80
Q

What 4 conditions can occur if the vitelline duct fails to completely close?

A

meckel’s diverticulum

viteline cyst

vitelline fistula

omphalocoele

81
Q

classic symptom is Currant jelly stools (from vascular congestion)

A

intussusception

82
Q

What is intussusception?

A

Telescoping of one segment of intestine into another

83
Q

What does it mean when it says that there is a “lead point” in intussusception ?

A

 Usually a swelling that leads the telescoping segment into the other

84
Q

in intussusception,

What is the most common lead point for a child?

 How about an adult?

A

 For children, the lead point is often a swollen lymph

node, for an adult it is often a tumor

85
Q

What is the most common cause of small bowel obstruction?

A

Intra-abdominal adhesions

86
Q

What is the most common cause of large bowel obstruction?

A

 Cancer

87
Q

What major vessel supplies the hindgut?

A

Inferior Messenteric Artery

88
Q

What are the minor branches of the IMA? What do they supply?

A

left colic–left colic flexure + some transverse colon

sigmoid branches–sigmoid colon

superior rectal–rectum

89
Q

What is the function or consequence of Tenia Coli?

A

 Being shorter than the underlying viscus, they create Haustra and attachment points for structures

90
Q

What are the divisions of the large intestine?

A

 Ascending colon, transverse colon, descending colon

 Sigmoid colon

 Rectum

 Anal canal

91
Q

Why is the sigmoid colon’s “floppiness” clinically important?

A

 The sigmoid colon is floppy, so diseases there can appear to be on the right side since it can flip over to that side even though the sigmoid is on the left

92
Q

What is the underlying problem that causes Hirschsprung’s disease?

A

the failure of the neural crest cells (ganglion cells) to progress in craniocaudal direction

93
Q

Hirschsprung’s disease symptoms

A

newborns

green or brown vomit

explosive stools after a doctor inserts a finger into the rectum

swelling of the belly, also known as the abdomen

lots of gas

bloody diarrhea

94
Q

What layers are missing in

“diverticular disease”?

A

 Muscular layers

95
Q

How do a true and false diverticula differ

A

 True has muscle layers and usually occurs on the right side of the colon, is congenital not acquired, and is more common in asians

96
Q

Diverticulitis

v.

 Diverticulosis

A

Diverticulitis in inflammation, usually from infection, occurring in a diverticula

 Diverticulosis is the presence of several diverticuli

97
Q

What structure is missing in the appendix?

A

 Villi

98
Q

What are the characteristics of Crohn’s disease?

A

skip lesions

can involve anus

fissures

bleeding absent ~30% of time

99
Q

What are the characteristics of Ulcerative colitis v. crohns?

A

 UC always has bloody diarrhea, Crohn’s about 70% of the time

100
Q

ulcerative colitis characteristics

A

bloody diarrhea

abdominal pain

fever

weight loss

involves mucosa and submucosa

fistulas and strictures rare

spares anus

mucosal involvement contiguous

101
Q

What plexus do hemorrhoids form in?

A

 Both the internal rectal venous plexus, and the inferior rectal venous plexus

102
Q

What plexus to suppositories take advantage of for absorption in hemorrhoid Tx?

A

 Internal rectal venous plexus

 (Not the inferior rectal venous plexus)

103
Q

merocrine secretion

A

products in membrane bound vescicles fuse with the cell membrane and secrete via exocytosis

104
Q

apocrine secretion

A

product plus some cytoplasm is released wrapped in cell membrane.

common in skin

*double check slide*

105
Q

holocrine secretions

A

whole cell undergoes apoptosis and secretes product and cell debris

(sebacous gland of skin)

106
Q

duct

A

cylinders of cells that convey saliva and secrete various proteins and electrolytes

107
Q

acinus

A

spherical structure of secretory mucus/serous cells

108
Q

serous cells secrete

A

digestive enzymes

109
Q

goblet cells secrete

A

mucin, from glycoproteins

110
Q

myoepithelial cells

A

surround and contract the acinar cells to promote salivary flow

111
Q

why can chronic stress cause cavities

A

a more active sympathetic system increases the protein to fluid ratio and decreases the alkalizing components of the saliva like bicarbonate.

There also MAY be less bactericidal agents in sympathetic secretions

112
Q

relative composition of different salivary gland products

A

parotid–watery saliva

sublinguial–mucin

submandibular–mixture

113
Q

Why do you salivate so much when you vomit?

A

nausea induces saliva in anticipation of neutralizing the stomach acid

114
Q

parietal cells secrete

A

HCl

intrinsic factor (increases Ca++ absorption)

115
Q

mucous neck cell secretes

A

mucus

bicarbonate

116
Q

enterochoraffin-like cell secretes

A

histamine to stimulate acid

117
Q

chief cells secrete

A

pepsinogen

gastric lipase

118
Q

g cell secretes

A

gastrin

119
Q

d cell secretes

A

somatostatin

120
Q

mucus cell secretes

A

mucus

121
Q

somatostatin

A

inhibits gastrin release

122
Q

gastrin

A

leads to the release of acid from pareital cells

123
Q

describe the digestion cascade

A

vagus n fires

release Ach

–>G cells

secrete gastrin

–>pareital cells

secrete HCl

cleaves pepsinogen

pepsin breaks down proteins

124
Q

how is the release of HCO3 triggered

A

when HCL is released,

the acidity causes goblet cells to release mucus

this leads to the release of bicarb

125
Q

describe the histamine cascade

A

HCl

g cells

gastrin

ECL cells

histamine

–> A. chief cells/pepsinogen

B. pareital cells/HCl

126
Q

what cells in the stomach have the most important protein pump?

A

pareital cells–necessary for facilitated transport of HCl release

127
Q

in para- or sympathetic state do cells “want” glucose

A

sympathetic

128
Q

glucose homeostasis should be b/w

A

70-110 units

129
Q

glucagon – blood glucose levels

A

raises

130
Q

insulin – blood glucose

A

lowers

131
Q

SST is a product of

A

product of D cells in antrum and Delta cells in pancreas

132
Q

what does pancreatic secretions of somatostatin do?

A

inhibits release of glucagon and insulin

133
Q

how does glucagon act on the liver to increase glucose secretion and production

A

glycenolysis

gluconeogenesis

134
Q

insulin function

A

primary regulator of carbohydrate and fat metabolism and storage

135
Q

multiple actions of the insulin receptor (4)

A
  1. glucose uptake into the cels
  2. protein, fat, and glycogen synthesis
  3. growth and gene expression
  4. satiety signal
136
Q

describe the facilitation of glucose uptake via GLUT-4 transporters

A

glucose enters adipose and muscle cells via GLUT-4 transporters

insulin receptors trigger the translocation of GLUT4 transporter into the cell membrane

137
Q

pancreatic alpha cells secrete

A

glucagon

138
Q

pancreatic beta cells secrete

A

insulin

139
Q

how does insulin promote glycogen storage?

A

activates glycogen synthase

inhibits glycogen phosphorylase

140
Q

how is insulin secretion regulated by glucose levels?

A

incoming glucose stimulates glycolysis

–>ATP

–>K+ channel closes

–>Ca++ released

–>stimulates release of insulin (via synaptic transmission)

141
Q

what stimulates glucagon release?

A

low glucose

AAs

ACh, Epi, NE

142
Q

what inhibits glucagon release?

A

high glucse

insulin

fatty acids

sommatostatin

143
Q

role of SST

A

paracrine release from delta cells

inhibits secretion of glucagon and insulin

prevents rapid nutrient exhaustion

144
Q

what stimulates pancreatic SST release?

A

hyperglycemia, glucagon, amino acids

145
Q

symptoms from Type I diabetes

A

hyperglycemia: excessive hunger, excessive thirst, frequent urination, weight loss, fatigue, weakness, irritability, blurry vision

146
Q

symptoms of Type II diabetes

A

symptoms: excessive hunger/thirst, increased urine volume, weight loss, fatigue, recurrent infections, changes in vision, tingling/prickling sensations in skin

147
Q

is a patient with DM I or II more likely to experience Diabetic ketoacidosis

A

II but I is more serious when it happens

148
Q

what inhibits insulin secretion

A

NE, epi

SST

149
Q

what stimulates insulin secretion

A

growth hormone and cortisol

certain AAs

ACh

endocrines secreted from the stomach–CCK, GLP-1, GOP

150
Q

Endopeptidase

A

is an enzyme that cleaves a molecule in the middle

151
Q

Enteropeptidase or enterokinase

A

is an endopeptidase that cleaves a short series of oligopeptides from trypsinogen which leads to activation

152
Q

Aminopeptidase

A
153
Q

Most proteins are denatured where

A
154
Q

GLUT 2

A

GLUT 2 help enterocytes, liver, and pancreas cells uptake glucose. It has a lower affinity but higher capacity which means that it will only uptake small amounts of glucose in normal situations BUT it is capable of storing glucose when there are small amounts present within the blood.

155
Q

Remember role of mothers passing on X to promote the growth of X in infants

A

oligosaccharides

Bifidobacterium

156
Q

If fibers produce a gel then things will be digested more [slowly/faster]?

A

slowly

157
Q

insulin doesn’t alter the rate at which glucose enters the brain because

A

the brain uses GLUT 1 transporters

158
Q
A