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BMS 300 > Digestive system > Flashcards

Digestive system Flashcards

1
Q

what is mastication

A

chewing

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2
Q

what moves to cause mastication

A

dental arches

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3
Q

what does mastication require function of

A

the entire brain

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4
Q

what does chewing increase

A

surface area/volume

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5
Q

what causes the enhancing of digestive enzymes

A

surface area/volume ratio

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6
Q

what is bolus

A

chewed food + saliva

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7
Q

what does bolus first compress against during swallowing

A

hard palate

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8
Q

what causes bolus to move into the oropharynx

A

tongue retracts

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9
Q

what does the bolus elevate

A

soft palate

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10
Q

what is the result of the soft palate being elevated

A

nasopharynx is blocked off

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11
Q

when do reflexes of swallowing occur

A

when bolus enter oropharynx

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12
Q

what happens to keep the bolus from entering the trachea

A

epiglottis folds

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13
Q

what causes bolus to enter the esophagus

A

pharyngeal muscles contract and force it through

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14
Q

what causes bolus to move into the stomach

A

lower esophageal sphincter opens

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15
Q

what pushes bolus further down the esophagus

A

peristaltic wave

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16
Q

what is the peristaltic wave

A

involuntary contraction/relaxation wave to push bolus

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17
Q

what causes PSNS vagus nerve stimulation

A

sight, smell, taste, or thoughts of food

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18
Q

what does the stomach release in response to vagus nerve stimulation

A

mucus, HCL, pepsinogen, ghrelin, gastrin (my hoe perfers grated garlic)

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19
Q

what causes pepsinogen to convert to pepsin

A

HCL

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20
Q

when does the gastric phase begin

A

when food reaches the stomach

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21
Q

what happens in the gastric phase

A

stretch receptors are activated, gastrin released, gastric lipase released, intrinsic factor

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22
Q

what enhances gastrin secretions

A

stretch receptors

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23
Q

what type of stimuli is stretch receptors

A

neural

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24
Q

what happens when gastrin is released into the bloodstream

A

protein digestion, mixing waves, gastric mobility

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25
Q

what is gastric mobility

A

stomach contents being moved into the small intestine

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26
Q

what does gastric lipase do

A

digests fat

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27
Q

what is the intrinsic factor

A

B12 absorption

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28
Q

what are the main functions of HCL

A

create an acidic environment, kills microorganisms, unfolds proteins, inactivates enzymes, breaks down cell walls and CT

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29
Q

what is the purpose of an acidic environment

A

so HCL can secrete pepsingoen

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30
Q

what does HCL inactivate

A

enzymes in food and salivary amylase

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31
Q

what does HCL break down

A

plant cell walls and CT in meat

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32
Q

where does bolus move to in gastric emptying

A

from the stomach to the small intestine

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33
Q

what is the only factor that increases gastric emptying

A

volume

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34
Q

how does volume increase gastric emptying

A

it increases stretch receptors which increases pressure

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35
Q

how does osmolarity decrease gastric emptying

A

water has to offset the osmolarity and it takes time

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36
Q

how does carbohydrate nutrient density decrease gastric emptying

A

duodenum has osmoreceptors that detect CHO and water is drawn in to offset it, but it takes time

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37
Q

how does fat and protein nutrient density decrease gastric emptying

A

release of cholecystokinin causes constriction of pyloric sphincter

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38
Q

what is the pyloric sphincter

A

tube below the duodenum

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39
Q

how does particle size decrease gastric emptying

A

the heavier particles are sifted and collect at the bottom of the stomach, and they take longer to empty

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40
Q

how does viscosity decrease gastric emptying

A

makes content thicker, and harder to move out

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41
Q

why does soluble fiber take a long time to gastrically empty

A

requires water to thin out viscosity which takes time

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42
Q

how are appetite suppressants activated

A

increase in viscosity

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43
Q

what is dietary fiber

A

carbs our body can’t digest

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44
Q

where is fiber found

A

in plant products only, not meat

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45
Q

where is insoluble fiber found

A

skin of plants

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46
Q

what happens to insoluble fiber in water

A

it swells like a sponge, but doesn’t dissolve

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47
Q

what happens to soluble fiber in water

A

it gets thicker, and dissolves

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48
Q

where is soluble fiber found

A

inner flesh of fruit

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49
Q

what are 2 functions of insoluble fibers

A

treats constipation and short-chain fatty acids produced

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50
Q

how does insoluble fiber treat constipation

A

increases the bulk of stool and promotes movement

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51
Q

how does insoluble fiber promote movement

A

swelling trigger peristalsis

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52
Q

what produces short-chain fatty acids

A

gut bacteria

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53
Q

how does short-chain fatty acids decrease risk for cancer

A

dilutes carcinogens

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54
Q

what are 4 functions of soluble fiber

A

increase viscosity, decrease constipation, help with diabetes, decrease cholesterol levels

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55
Q

how does viscosity increase satiety (soluble fiber)

A

decreases gastric emptying

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56
Q

how does soluble fiber decrease constipation

A

stools are softer

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57
Q

how does soluble fiber decrease cholesterol

A

body uses cholesterol to make more bile that has been lost in feces

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58
Q

how does soluble fiber help diabetes

A

traps sugar and inhibits amylase

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59
Q

what causes vomiting to occur

A

irritation in upper GI tract

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60
Q

where is signal sent if irritation is sensed in GI tract

A

vomit center of the brain

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61
Q

what happens when the vomit center of the brain is alerted

A

pyloric sphincter relaxes

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62
Q

what happens when pyloric sphincter relaxes when vomiting is gonna occur

A

contents move from duodenum to stomach via peristaltic waves

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63
Q

what happens once stomach contents are moved to the stomach from the duodenum when vomiting is gonna occur

A

lower esophageal sphincter relaxes

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64
Q

what happens when lower esophageal sphincter relaxes when vomiting is gonna occur

A

stomach content moves to esophagus, pharynx, and mouth

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65
Q

what are 4 consequences of constant purging

A

esophageal lesions, tooth decay, cardiac irregularities, and death

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66
Q

what happens when the esophagus gets lesions

A

scar tissue builds up which affects peristalsis

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67
Q

how do gastric ulcers come about

A

stomach acid damages digestive tract lining

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68
Q

what are two commons causes of gastric ulcers

A

pain reliever overuse and helicobacter pylori (bacteria)

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69
Q

how do you treat gastric ulcers

A

antibiotics

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70
Q

when does the intestinal phase begin

A

chyme enters duodenum

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71
Q

what does distention of the duodenum cause

A

inhibits gastrin production and gastric contractions, and stimulates pyloric sphincter contraction

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72
Q

what is secreted during the intestinal phase

A

alkaline mucus, cholecystokinin (CCK), GIP, secretin (always clean gutter shit)

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73
Q

what is alkaline mucus triggered by

A

vagus nerve stimulation

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74
Q

what CCK triggered by

A

protein and fat in chyme

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75
Q

what is GIP triggered by

A

carbs in chyme

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76
Q

what is secretin triggered by

A

decrease in pH

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77
Q

what does pancreatic amylase breakdown

A

carbs and starches

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78
Q

what does proteases breakdown

A

proteins into amino acids

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79
Q

what does pancreatic lipase breakdown and release

A

lipids and releases fatty acids

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80
Q

what does nucleases breakdown

A

RNA and DNA

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81
Q

what is the main purpose of the duodenum

A

secrete hormones

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82
Q

what is the main function of the jejunum

A

chemical digestion and nutrient absorption

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83
Q

what is the main function of the ileum

A

absorb bile acid and B12 and immune functions

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84
Q

what activates the immune functions in the ileum

A

Peyer’s patches

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85
Q

what is the main component of the small intestine

A

vili

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86
Q

what is vili

A

finger like projections

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87
Q

what is inside the vili

A

lymphatic vessels, nerves, and blood vessels

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88
Q

what makes up vili (on the outside)

A

epithelial cells

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89
Q

what do the epithelial cells on the vili contain

A

microvilli

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90
Q

what is the purpose of vili and microvilli

A

increase surface area

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91
Q

what is a characteristic of the epithelial cells in the small intestine

A

high turnover rate

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92
Q

what do the epithelial cells in the small intestine contain

A

digestive enzymes

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93
Q

what is celiac disease

A

reaction to gluten

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94
Q

what does celiac disease do to the digestive tract

A

destroys vili

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95
Q

what does celiac disease cause (if you eat gluten)

A

diarrhea, constipation, bloating, lactose intolerance, and fatigue

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96
Q

how does celiac disease cause diarrhea

A

water has to offset osmotic pressure of the carbs in the large intestine which causes watery stool

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97
Q

how does celiac disease cause constipation

A

impairs peristalsis

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98
Q

how does celiac disease cause bloating

A

when carbs that can’t be digested are moved to the large intestine, the bacteria that breaks it down produces gas

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99
Q

how does celiac disease cause lactose intolerance

A

microvilli is damaged which has digestive enzymes

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100
Q

how does celiac disease cause fatigue

A

nutrient deficiency

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101
Q

why do parts of the world have different rates of lactose intolerance

A

some parts have more access to dairy which means the people there produce more lactase

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102
Q

what is the mesentery

A

membrane that connects the intestine to the abdominal wall

103
Q

what does the mesentery contain a lot of

A

blood vessels

104
Q

what do the blood vessels in the mesentery aid in

A

fat storage

105
Q

what does the large intestine absorb

A

water, vitamins, and electrolytes

106
Q

what does the large intestine do in terms of digestion

A

form feces and send it to the rectum

107
Q

what is constipation defined by

A

less than 3 bowel movements a week

108
Q

what is constipation caused by

A

lack of fiber and exercise

109
Q

how does exercise affect constipation

A

SNS is activated during exercise and PSNS is activated after exercise

110
Q

does water affect constipation

A

no, fiber does

111
Q

what does amylase break down

A

starch

112
Q

what is starch broken down into

A

disaccharides

113
Q

what are the 3 main enzymes that break down disaccharides

A

sucrase, maltase, lactase

114
Q

what does sucrase break down

A

sucrose –> fructose and glucose

115
Q

what does maltase break down

A

maltose –> glucose and glucose

116
Q

what does lactase break down

A

lactose –> galactose and glucose

117
Q

what is glucose

A

a monosaccharide

118
Q

how is glucose taken to liver

A

portal vein

119
Q

what happens after glucose is sent to liver

A

used for energy, stored as glycogen or fat, makes amino acids, released into blood

120
Q

what 3 things does insulin act on

A

liver, muscles, adipose tissue

121
Q

what does insulin bind to in muscles and adipose tissue

A

insulin receptors (IR)

122
Q

what does insulin sensitivity depend on in muscles

A

movement

123
Q

what does insulin sensitivity depend on in adipose tissue

A

adipose cell size

124
Q

what does binding of insulin to IR trigger in muscles

A

glucose and fatty/amino acids move into cell

125
Q

what does binding of insulin to IR trigger in adipose tissue

A

glucose and fatty acids move into cell

126
Q

what happens once glucose moves into cells (in muscle)

A

it’s stored as glucose

127
Q

what happens once amino acids moves into cells (in muscle)

A

they become proteins

128
Q

what happens to glucose levels in muscles when exercising

A

they drop

129
Q

why do glucose levels drop when exercising

A

passive glucose uptake

130
Q

what causes passive glucose uptake

A

concentration gradient

131
Q

what is glucose stored as in the liver

A

glycogen and triglyercirides

132
Q

what happens to glucose synthesis in the liver

A

it decreases

133
Q

what cells are in the liver that release insulin

A

islet of langerhans beta cells

134
Q

what does the pancreas release insulin in response to

A

glucose levels

135
Q

what hormone causes the pancreas to release insulin

A

GIP

136
Q

what does glucose disregulation cause

A

diabetes

137
Q

how does a healthy person regulate glucose

A

pancreas releases insulin which binds to IR, causing glucose to enter the cell and lower BG levels

138
Q

what is the problem with glucose regulation in type 1 diabetics

A

the pancreas doesn’t release insulin so glucose doesn’t move into the cell and BG levels increase

139
Q

what is the problem with glucose regulation in type 2 diabetics

A

pancreas releases insulin but can’t bind to IR because the cell is to large and the sensitivity to IR is affected

140
Q

what does placental hormones do that cause gestational diabetes

A

they block IR from binding to insulin

141
Q

what does gestational diabetes cause

A

macrosomia

142
Q

what is macrosomia and what causes it

A

big baby; caused by increase in nutrients

143
Q

what is the Maillard reaction

A

sugar and proteins reacting

144
Q

what does the Maillard reaction lead to

A

advanced glycation end (AGE)

145
Q

what is advanced glycation end

A

products bind to collagen in the arteries, clogging them

146
Q

how does clogged arteries affect blood flow

A

decreases it

147
Q

what is the main cause of cataracts

A

AGE builds up

148
Q

what is the metabolic rate like for the eye lens

A

it’s high

149
Q

what does it mean for the lens to have a high metabolic rate

A

needs high turnover rates

150
Q

what does AGE build up cause to happen to the lens

A

decreases blood flow –> little regeneration –> debris clumps up

151
Q

what is the main cause of glaucoma

A

pressure buildup

152
Q

what causes pressure buildup in the eye

A

sorbitol and fructose can’t leave the eye

153
Q

what creates sorbitol and fructose

A

glucose converting

154
Q

how does diabetes impact peripheral nerves

A

fructose and sorbitol accumulate in nerves

155
Q

what happens when fructose and sorbitol accumulate in nerves

A

affects osmolarity

156
Q

what happens when osmolarity is impacted in peripheral nerves

A

water is drawn in which affects membrane potential

157
Q

what happens when membrane potential is affected in peripheral nerves

A

signal can’t get sent to the brain

158
Q

how is nerve damage caused

A

lack of signals being sent to brain –> failure to notice trauma

159
Q

how does increasing glucose levels impact immunity

A

decrease in neutrophil development and increase in bacterial growth

160
Q

how does fructose and sorbitol impact the kidneys

A

causes damaged nephrons

161
Q

how does AGE accumulation impact the kidneys

A

damages vasculature

162
Q

how does AGE damage vasculature

A

affects the re-absorptive process which means that kidneys can’t clean the blood

163
Q

what are 3 symptoms of diabetes

A

kidneys don’t absorb glucose, fructose and sorbitol production, and poor glucose uptake

164
Q

what is the result of kidneys not being able to absorb glucose

A

increase in osmotic pressure which leads to dehydration

165
Q

how does an increase in osmotic pressure lead to dehydration

A

there is an increase in water in take which leads to drinking more water which leads to more peeing –> dehydration

166
Q

why is there poor glucose uptake when it comes to diabetes

A

cells are using fat for fuel

167
Q

what do ketone bodies do

A

decrease pH

168
Q

what is diabetes insipidus

A

chronic dehydration

169
Q

what does the antidiuretic hormone cause

A

dehydration

170
Q

what type of diabetes results in tasteless urine

A

diabetes insipidus

171
Q

in regards to treating diabetes with lifestyle changes, what is the main goal

A

decrease blood sugar spikes

172
Q

what are 3 ways to decrease BG spikes

A

small, frequent meals; foods with low glycemic index; and insoluble fiber

173
Q

how does increasing insoluble fiber decrease BG spikes

A

slows down gastric emptying, entraps sugar, and decreases amylase

174
Q

what are lifestyle changes you can make to treat type 2 diabetes

A

weight loss and exercise

175
Q

how does weight loss help with diabetes

A

reduces the size of the fat cells

176
Q

how do you medicinally treat type 1 diabetes

A

insulin pump

177
Q

how do you medicinally treat type 2 diabetes

A

metformin and sulfonylurea

178
Q

what does metformin do

A

decrease glucose production in liver

179
Q

what does sulfonylurea do

A

increases sensitivity for beta cells which increases insulin production

180
Q

what do alpha cells in the pancreas produce

A

glucagon

181
Q

what does glucagon act on

A

the liver

182
Q

what does glucagon acting on the liver cause

A

breakdown of glycogen

183
Q

what does the breakdown of glycogen in the liver result in

A

increase in BG

184
Q

what hormone does the hypothalamus produce

A

corticotropic releasing hormone

185
Q

what does the medulla produce to send to liver

A

epinephrine

186
Q

what happens when epinephrine acts on the liver

A

breakdown of amino acids to make glucose

187
Q

what is gluconeogenesis

A

breakdown of amino acids to make glucose

188
Q

what does the medulla activate

A

hormone sensitive lipase

189
Q

what does the activation of fat cells via the medulla cause

A

hormone sensitive lipase to be secreted

190
Q

what does the secretion of hormone sensitive lipase to breakdown in the fat cells

A

triglycerides into fatty acids

191
Q

where are fatty acids from the fat cells sent to

A

muscle

192
Q

what do fatty acids do in the muscle

A

make ATP

193
Q

what hormone does the pituitary gland release

A

ACTH which acts on the adrenal cortex

194
Q

what do glucocorticoids act on

A

muscle

195
Q

what does glucocorticoids acting on the muscle result in

A

breakdown of amino acids

196
Q

what happens when amino acids are broken down in the muscle

A

glucose is made (gluconeogenesis)

197
Q

what is the main function of mucus

A

protect stomach from acidic environment

198
Q

what is the main function of pepsinogen

A

cleave off protein once activated

199
Q

what causes fasting hypoglycemia

A

not eating

200
Q

what happens during fasting hypoglycemia

A

glycogen isn’t broken down

201
Q

what cells cause glycogen to not be broken down in fasting hypoglycemia

A

hypoactive alpha cells

202
Q

what causes reactive hypoglycemia

A

eating a meal

203
Q

what happens during reactive hypoglycemia

A

insulin reaches peak levels

204
Q

what cells cause glycogen to not be broken down in reactive hypoglycemia

A

hypersensitive beta cells

205
Q

what else can cause hypoglycemia

A

tumors

206
Q

where does lipid metabolism start

A

in the mouth

207
Q

what does lipase breakdown

A

triglycerides into fatty acids

208
Q

what do fatty acids stimulate to make bile

A

CCK

209
Q

where do fatty acids send bile once they secrete it

A

to the gallbladder

210
Q

what does bile acid interact with in the gallbladder

A

fat, to emulsify it

211
Q

what causes fatty acids to be absorbed into intestinal cells

A

micelles

212
Q

where do fatty acids go after they exit intestinal cells

A

chylomicrons

213
Q

what happens to fatty acids when they enter chylomicrons

A

they convert to triglycerides

214
Q

what happens after fatty acids convert to triglycerides

A

VLDL

215
Q

where are chylomicrons located

A

epithelial cells

216
Q

where do chylomicrons move fat cells to

A

the liver

217
Q

what happens to fat in the liver

A

breaks down in to VLDL

218
Q

what does VLDL do

A

transport fat from the liver to muscles and adipose tissue

219
Q

what is VLDL broken down by

A

lipoprotein lipase

220
Q

how is IDL formed

A

removal of triglycerides from VLDL

221
Q

how is LDL formed

A

VLDL and IDL

222
Q

what does LDL do

A

fixes injured arteries

223
Q

what does HDL do

A

reverse cholesterol transport from tissues to the liver

224
Q

what does lipoprotein lipase do

A

breaks down triglycerides into fatty acids to enter the cell

225
Q

what is the order of lipid metabolism

A

VLDL to IDL to LDL to immune system to calcium to vessels

226
Q

what does calcium do in the blood vessels

A

forms plaque

227
Q

what causes vessel diameter to decrease

A

RBC build up

228
Q

what are two things you can take to treat atherosclerosis

A

statins and unsaturated fats

229
Q

what do statins do

A

increase sensitivity to LDL receptors

230
Q

what do unsaturated fats do for atherosclerosis

A

increase sensitivity to LDL and IDL receptors

231
Q

what does reducing calories do for atherosclerosis

A

decrease LDL

232
Q

what does reducing stress do for atherosclerosis

A

decreases VLDL

233
Q

how does nicotine impact atherosclerosis

A

increases LDL and decreases HDL

234
Q

what does omega 3/6 and baby aspirin do

A

decreases inflammation

235
Q

what is the first step in protein metabolism

A

HCL unfold proteins and pepsin breaks down amino acids

236
Q

what happens after protein is unfolded in protein metabolism

A

CCK triggers the release of pancreatic proteases

237
Q

what happens to the amino acids once they’ve been broken down in protein metabolism

A

they’re absorbed into the vili of the small intestine

238
Q

what happens to the amino group

A

can’t provide energy so it’s excreted in urea

239
Q

what happens to protein when the energy balance of the body is positive

A

protein is converted to fat

240
Q

what does lack of dietary protein cause

A

kwashiorkor and edema

241
Q

what characterizes kwashiorkor

A

impaired growth, increased rate of infection, pot belly, fatty liver, edema, and decreased cognition

242
Q

what causes impaired growth

A

decrease in anabolic reactions because of incomplete proteins

243
Q

what causes and increase in rate of infection

A

decrease in antibodies

244
Q

what causes pot belly

A

worms

245
Q

what causes fatty liver

A

decrease in VLDL

246
Q

what happens when VLDL levels are decreased and how does it cause fatty liver

A

fat isn’t transported away from liver

247
Q

what is the relationship of osmotic and blood pressure to cause an edema

A

osmotic pressure is lower than blood pressure

248
Q

how does edema work

A

the protein that cause osmotic levels to increase, moving water from tissue, back to blood, are decreased, so the water stays in the tissue and causes swelling

249
Q

what causes water to move from arterial blood to surrounding tissues

A

increased blood pressure

250
Q

what causes water to go back into the venous blood

A

osmotic pressure exerted by proteins in the blood

251
Q

what is the function of ghrelin

A

appetite

252
Q

what is the function of leptin

A

suppress hunger

253
Q

what is the function of pepsin

A

protein digestion

BMS 300 (14 decks)

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