GI Physiology Flashcards

1
Q

The purpose of peristalsis is to _

A

The purpose of peristalsis is to propel contents along the GI tract
* A ring of contraction pushes the bolus forward, widened segment receives the bolus

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2
Q

Behind the bolus, _ muscle is contracted and _ muscle is relaxed

A

Behind the bolus, circular muscle is contracted and longitudinal muscle is relaxed
* GIT is narrow, elongated

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3
Q

In front of the bolus, _ is contracted and _ is relaxed

A

In front of the bolus, longitudinal muscle is contracted and circular muscle is relaxed
* GIT is wide and shortened

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4
Q

Segmentation is _

A

Segmentation is back and forth movement of chyme that allows mixing without forward movement
* Alternating motion of circular muscle

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5
Q

Parasympathetic nerves originate in _ regions while sympathetic nerves originate in _

A

Parasympathetic nerves originate in brain, sacral spinal cord regions while sympathetic nerves originate in thoracic, lumbar

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6
Q

_ are the cells responsible for generation of slow waves

A

Interstitial cells of Cajal are the cells responsible for generation of slow waves
* “Pacemaker cells”

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7
Q

Electrical activity spreads through the smooth muscle cells of the GIT via _

A

Electrical activity spreads through the smooth muscle cells of the GIT via gap junctions
* Interstitial cells of cajal are generating slow waves spontaneously

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8
Q

How do slow waves influence action potential firing?

A

If the depolarization caused by slow wave exceeds threshold, action potentials are triggered during slow wave peak
* Higher membrane potential –> greater frequency of action potentials –> stronger contraction

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9
Q

_ and _ are neurotransmitters from excitatory enteric nerves that depolarize the smooth muscle cell membrane

A

ACh and Substance P are neurotransmitters from excitatory enteric nerves that depolarize the smooth muscle cell membrane

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10
Q

_ and _ are inhibitory factors that hyperpolarize the smooth muscle cell membrane

A

NO and VIP are inhibitory factors that hyperpolarize the smooth muscle cell membrane

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11
Q

When we swallow, enteric neurons release VIP and NO to cause _ and _

A

When we swallow, enteric neurons release VIP and NO to cause hyperpolarization and relaxation
* The lower esophageal sphincter and proximal stomach relax

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12
Q

The _ region of the stomach regulates gastric emptying

A

The pylorus regulates the rate of gastric emptying

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13
Q

The _ offers feedback control of gastric emptying

A

The duodenum offers feedback control of gastric emptying

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14
Q

The _ and _ regions of the stomach are responsible for mixing and grinding

A

The distal body and antrum regions of the stomach are responsible for mixing and grinding
* The most vigorus peristalsis and mixing occur close to the pylorus

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15
Q

Explain retropulsion

A

Retropulsion is when the pyloric end of the stomach pumps small amounts of chyme into the duodenum, while simultaneously forcing most of its contents backward into the stomach

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16
Q

The rate of gastric emptying depends on _ , _ , and _

A

The rate of gastric emptying depends on volume , physical state , and composition of a meal

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17
Q

During the fed state, we have background _ movements occuring

A

During the fed state, we have alternating segmentation and peristalsis

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18
Q

During the fasting state, we have _ movement in the background

A

During the fasting state, we have migrating motor complex

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19
Q

How do segmentation and peristalsis promote digestion and absorption?

A

Alternating segmentation and peristalsis:
1. Mixes luminal contents with pancreatic, biliary, small intestinal secretions to enhance digestion
2. Allows luminal contents greater contact with the mucosa to promote absorption

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20
Q

_ are strong waves of contraction that sweep from the stomach to the ileum between meals

A

Migrating motor complex are strong waves of contraction that sweep from the stomach to the ileum between meals

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21
Q

MMC is initiated by release of the hormone _ which is released from cells in the _

A

MMC is initiated by release of the hormone motilin which is released from cells in the small intestine

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22
Q

_ is the name for segmentation in the colon

A

Haustral shuttling is the name for segmentation in the colon

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23
Q

_ is the name for peristalsis in the colon

A

Mass movements is the name for peristalsis in the colon

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24
Q

Haustral shuttling in the colon helps to allow _ and _

A

Haustral shuttling in the colon helps to allow water absorption and compaction

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25
Mass movements in the colon are stimulated by _
Mass movements in the colon are stimulated by **contents in the stomach and duodenum** * Gastrocolic reflex
26
What is the purpose of the gastrocolic reflex?
The **gastrocolic reflex** is the mass movement in the colon that allows the colon to empty when there is food coming in the stomach and duodenum; helps to make room for the next bolus
27
Brush boarder enzymes are made by _ to aid in digestion and absorption
Brush boarder enzymes are made by **enterocytes** to aid in digestion and absorption
28
Amino acids and sugars get absorbed into _
Amino acids and sugars get absorbed into **bloodstream**
29
Fatty acids and glycerol get absorbed into _
Fatty acids and glycerol get absorbed into **lymph**
30
The salivary enzyme _ begins carbohydrate digestion at the mouth
The salivary enzyme **alpha-amylase** begins carbohydrate digestion at the mouth * Salivary alpha amylase
31
The exocrine pancreas also secretes _ to aid in carbohydrate digestion
The exocrine pancreas also secretes **alpha-amylase** to aid in carbohydrate digestion * Pancreatic alpha amylase
32
_ , _ , _ are brush border enzymes that help to break down carbohydrates
**Maltase** , **sucrase** , **lactase** are brush border enzymes that help to break down carbohydrates * These break down maltose, sucrose, lactose --> glucose, galactose, fructose
33
Fructose is transported across the apical/luminal membrane via _
Fructose is transported across the apical/luminal membrane via **facilitated diffusion** through **GLUT-5**
34
Glucose and galactose are transported across the apical/luminal membrane via _
Glucose and galactose are transported across the apical/luminal membrane via **SGLT-1** * Secondary transport coupled to Na+
35
_ and _ travel via SGLT-1
**Glucose** and **galactose** travel via SGLT-1
36
Glucose, galactose, and fructose all travel across the basolateral membrane via the _ transporter
Glucose, galactose, and fructose all travel across the basolateral membrane via the **GLUT-2**
37
Protein digestion begins at the stomach with the enzyme _
Protein digestion begins at the stomach with the enzyme **pepsin** * Chief cells make pepsinogen --> HCl cleavage --> pepsin
38
Proteases are released from the _ and active in the _
Proteases are released from the **pancreas** and active in the **duodenum**
39
The brush border enzymes that break down proteins are called _
The brush border enzymes that break down proteins are called **peptidases** * Ex: enterokinase
40
Proteins must be in the form of _ or _ for absorption
Proteins must be in the form of **amino acids** or **di- and tripeptides** for absorption
41
Amino acids get absorbed across the apical membrane via _
Amino acids get absorbed across the apical membrane via **secondary active transport coupled to Na+**
42
Dipeptides and tripeptides get absorbed across the apical membrane via _
Dipeptides and tripeptides get absorbed across the apical membrane via **pepT1** * Secondary active transport coupled to H+
43
Amino acids travel across the basolateral membrane via _
Amino acids travel across the basolateral membrane via **facilitated diffusion**
44
Pancreatic proteases are secreted as _ and activated in the small intestine
Pancreatic proteases are secreted as **inactive zymogens** and activated in the small intestine
45
_ is a brush border enzyme that converts trypsinogen to active trypsin
**Enterokinase** is a brush border enzyme that converts trypsinogen to active trypsin
46
Why is enterokinase so important to protein digestion and absorption?
Enterokinase converts trypsinogen --> active trypsin * Trypsin converts the other pancreatic proteases to their active form
47
Digestion of lipids begins at the mouth with _
Digestion of lipids begins at the mouth with **lingual lipase**
48
Emulsification of fats involves _ organ
Emulsification of the fats involves **bile components**
49
Why must fats be in the form of micelles for absorption?
Lipase is hydrophilic and can only digest fat on the perimeter; **micelles help to increase surface area**
50
Fatty acids and monoglycerides move across the apical membrane via _
Fatty acids and monoglycerides move across the apical membrane via **simple diffusion** (lipophilic)
51
Triglycerol and fat-soluble substances get packaged into lipoproteins called _ that enter circulation via _
Triglycerol and fat-soluble substances get packaged into lipoproteins called **chylomicrons** that enter circulation via **lacteals**
52
Gastric and pancreatic _ break down lipids
Gastric and pancreatic **lipase** break down lipids
53
Carbohydrates, proteins, and fats all get absorbed in the _
Carbohydrates, proteins, and fats all get absorbed in the **small intestine** (enterocytes)
54
Iron, Copper, Zinc, Manganese get absorbed in the _
Iron, Copper, Zinc, Manganese get absorbed in the **duodenum**
55
The key transporter for Iron, Copper, Zinc, and Manganese absorption is _
The key transporter for Iron, Copper, Zinc, and Manganese absorption is **DMT1**
56
We have exocrine cells in the salivary glands secreting...
We have exocrine cells in the **salivary glands** secreting... * Amylase * Lingual lipase * Haptocorrin * Lysozyme * Lactoferrin * Peroxidase
57
Parietal cells in the stomach make _ and _
Parietal cells in the stomach make **HCl** and **intrinsic factor**
58
Chief cells in the stomach make _
Chief cells in the stomach make **pepsinogen**
59
Pancreatic exocrine cells make digestive enzymes _ , _ , and _
Pancreatic exocrine cells make digestive enzymes **amylase** , **proteases** , and **lipase**
60
Ductal cells of the pancreas make _
Ductal cells of the pancreas make **HCO3-**
61
Brunner glands in the small intestine make _
Brunner glands in the small intestine make **HCO3-**
62
Saliva is produced in a two step process; first we have secretions from _ cells; then we have modification by _ cells
Saliva is produced in a two step process; first we have secretions from **acinar cells**; then we have modification by **ductal cells**
63
Acinar cells first secrete an enzyme containing _
Acinar cells first secrete an enzyme containing **plasma-like solution**
64
Ductal cells then modify the saliva via _
Ductal cells then modify the saliva via **reabsorption of Na+ and Cl-** and **secretion of K+**
65
Slow flow saliva content is: (Low/High) Na+ (Low/High) Cl- (Low/High) HCO3- (Low/High) K+
Slow flow saliva content is: **Low** Na+ **Low** Cl- **Low** HCO3- **High** K+ *hypotonic to plasma* * Ductal cells have enough time to modify saliva, reabsorbing Na, Cl and secreting K+ and HCO3-
66
The reabsorption of Na,Cl and secretion of K+ by ductal cells is a basal function; _ secretion occurs upon stimulation
The reabsorption of Na,Cl and secretion of K+ by ductal cells is a basal function; **HCO3- secretion** occurs upon stimulation
67
Acid secretion is stimulated by:
Acid secretion is stimulated by: * Vagal stimulation --> **ACh** * G cells --> **gastrin** * ECL cells --> **histamine** * Vagal stimulation --> **GRP** (gastrin releasing peptide) *ACh, gastrin, histamine, GRP all upregulate the production of acid by parietal cells*
68
Acid secretion is inhibited by:
Acid secretion is inhibited by: * D cells --> **somatostatin**
69
Low pH (high H+) will stimulate _ cells to release _
Low pH (high H+) will stimulate **D cells** to release **somatostatin**
70
Somatostatin inhibits H+ secretion by (3):
Somatostatin inhibits H+ secretion by: 1. Directly inhibiting **parietal cells** 2. Inhibiting gastrin release from **G cells** 3. Inhibiting histamine release from **ECL cells**
71
G cells are stimulated by _ to release gastrin
G cells are stimulated by **distention and digestion products** to release gastrin
72
Gastrin stimulates _ and _ cells
Gastrin stimulates **parietal cells** to release H+ and **ECL cells** to release histamine * Histamine can stimulate parietal cells to release H+
73
I cells in the duodenum release _
**I cells** in the duodenum release **CCK**
74
CCK release is stimulated by _
CCK release is stimulated by **digestion products in the duodenum**
75
CCK release from I cells (inhibits/stimulates) gastric emptying
CCK release from I cells **inhibits** gastric emptying
76
CCK stimulates _ and _
CCK stimulates **pancreatic enzyme secretion** and **gallbladder contraction and sphincter of oddi relaxation**
77
_ gets released in response to H+ in the duodenum
**Secretin** gets released in response to H+ in the duodenum
78
Secretin is released by _ cells
Secretin is released by **S cells**
79
Secretin functions to _ and _
Secretin functions to **stimulate pancreatic HCO3- secretion** and **inhibit gastric H+ secretion**
80
GIP is known as _ or _
GIP is known as **glucose-dependent insulinotropic peptide** or **gastric inhibitory peptide**
81
GIP gets released in response to _
GIP gets released in response to **oral glucose and digestion products in the duodenum**
82
GIP stimulates _ cells to secrete _
GIP stimulates **beta cells** to secrete **insulin**
83
GIP inhibits _ secretion
GIP **inhibits gastric H+ secretion**
84
CCK slows gastric emptying and _ the sphincter of Oddi
CCK slows gastric emptying and **relaxes** the sphincter of Oddi
85
CCK promotes gallbladder (contraction/relaxation)
CCK promotes gallbladder **contraction**
86
Secretin inhibits gastric acid production via _
Secretin inhibits gastric acid production via **somatostatin**
87
Crypts contain cells that (absorb/secrete) NaCl which causes _ movement of water
Crypts contain cells that **secrete NaCl** which osmotically **pulls water into the lumen**
88
Villi contain cells that (absorb/secrete) NaCl which causes _ movement of water
Villi contain cells that **absorb NaCl** which osmotically **pulls water out of the lumen**
89
VIP stimulates NaCl and water (absorption/secretion)
VIP stimulates NaCl and water **secretion**, while preventing reabsorption
90
Luminal stimuli that act on the small intestine include _ , _ , _
Luminal stimuli that act on the small intestine include **pH** , **stretch** , **nutrients**
91
Autonomic stimuli that regulate the GIT include:
Autonomic stimuli that regulate the GIT include: * Hunger * Satiety * Stress/Anxiety * Smell/taste of food
92
(Macrominerals/ Trace minerals) are the major solutes of your intra and extracellular space
**Macrominerals** are the major solutes of your intra and extracellular space * Ex: sodium, potassium, chloride, calcium, phosphorus, magnesium, sulfur * The body needs large quantities of these things
93
The body needs (small/large) quantities of trace minerals
The body needs **small quantities** of trace minerals for various functions * Ex: Iron, copper, zinc, iodine, fluoride, molybdenum, selenium, chromium, manganese
94
(Water/fat) soluble vitamins are easily absorbed and excreted
**Water soluble vitamins** are easily absorbed and excreted
95
Examples of water soluble vitamins include vitamin _ and _
Examples of water soluble vitamins include vitamin **B** and **C**
96
(Water/Fat) soluble vitamins have long term storage in adipose tissue
**Fat soluble vitamins** have long term storage in adipose tissue
97
Fat soluble vitamins include:
Fat soluble vitamins include: **ADEK**
98
Water soluble vitamins get easily absorbed in the gut via _ and easily excreted via _
Water soluble vitamins get easily absorbed in the gut via **portal circulation** and easily excreted via the **kidneys**
99
In general, water soluble vitamins do not get stored by the body so we need regular/daily dietary intake; the exception is that we have some long term storage of vitamins _ and _
In general, water soluble vitamins do not get stored by the body so we need regular/daily dietary intake; the exception is that we have some long term storage of vitamins **B12** and **B9**
100
It is possible to get toxicity/ overload of (water/fat) soluble vitamins
It is possible to get toxicity/ overload of **fat soluble vitamins** since we have long term stores of these
101
Fat soluble vitamins are absorbed in a similar way to lipids; they are incorporated into _ and then absorbed into the _ circulation
Fat soluble vitamins are absorbed in a similar way to lipids; they are incorporated into **chylomicrons** and then absorbed into the **lymphatic circulation**
102
Fat solube vitamins are stored in adipose tissue and the _
Fat solube vitamins are stored in adipose tissue and the **liver**
103
B1 is called _
B1 is called **thiamin**
104
B2 is called _
B2 is called **riboflavin**
105
B3 is called _
B3 is called **niacin**
106
B5 is called _
B5 is called **pantothenic acid**
107
B6 is called _
B6 is called **pyridoxine**
108
B7 is called _
B7 is called **biotin**
109
B9 is called _
B9 is called **folate**
110
B12 is called _
B12 is called **cobalamin**
111
_ is a deficiency in B1 (thiamin)
**Beriberi** is a deficiency in B1 (thiamin) * Wet beriberi: resembles CHF * Dry beriberi: affects the central and peripheral nervous system
112
_ is a deficiency in B3 (niacin)
**Pellagra** is a deficiency in B3 (niacin)
113
Deficiencies in _ or _ can lead to megaloblastic anemia
Deficiencies in **B9** or **B12** can lead to megaloblastic anemia
114
A deficiency in _ can lead to megaloblastic anemia + neuropathy
A deficiency in **B12 (cobalamin)** can lead to megaloblastic anemia + neuropathy
115
A deficiency in vitamin C can manifest as _
A deficiency in vitamin C can manifest as **scurvy**
116
Vitamin _ is responsible for eye and skin health
**Vitamin A** is responsible for eye and skin health
117
Vitamin _ is responsible for bone health
**Vitamin D** is responsible for bone health
118
Vitamin _ has antioxidant function
**Vitamin E** has antioxidant function
119
Vitamin _ is responsible for clotting
**Vitamin K** is responsible for clotting
120
Both B9 and B12 deficiencies cause a macrocytic anemia with high _ levels
Both B9 and B12 deficiencies cause a macrocytic anemia with **high homocysteine levels** * Bith vitamins are cofactors in the homocysteine-methionine pathway
121
Only (B9/B12) deficiency results in high serum MMA levels
Only **B12** deficiency results in high serum MMA levels
122
_ cells produce intrinsic factor
**Parietal cells** produce intrinsic factor
123
Intrinsic factor is made in the _
Intrinsic factor is made in the **stomach**
124
After intrinsic factor is made in the stomach it binds _
After intrinsic factor is made in the stomach it binds **B12** *to move through the intestine*
125
B12 gets reabsorbed in _ region but only if _
B12 gets reabsorbed in the **terminal ileum** but only when bound to IF * The ileal mucosa has specialized receptors that can absorb B12-IF complex
126
Pernicious anemia is _
**Pernicious anemia** is caused by conditions that result in *poor production of IF* and hence cause a B12 deficiency * Ex: autoimmune attack on parietal cells
127
Iron deficiency is a common mineral deficiency that can occur one of (3) ways:
Iron deficiency is a common mineral deficiency that can occur one of (3) ways: 1. **Poor dietary intake** 2. **Poor absorption** 3. **Iron loss** (bleeding)
128
Iron is primarily absorbed in the _
Iron is primarily absorbed in the **duodenum** * Crohn's patients might have poor absorption of iron from extensive bowel surgery
129
Iron deficiency results in a hypochromic, _ (RBC size) anemia
Iron deficiency results in a **hypochromic, microcytic** anemia
130
Name some possible mechanisms of mineral deficiencies:
Name some possible mechanisms of mineral deficiencies: * Poor dietary intake * Renal losses * GI losses * Medications
131
Patients with alcohol use disorder are at high risk of vitamin and mineral deficiencies; _ is a very common mineral deficiency
Patients with alcohol use disorder are at high risk of vitamin and mineral deficiencies; **magnesium** is a very common mineral deficiency
132
Magnesium deficiency can present with _ signs
Magnesium deficiency can present with.. * Seizures * Nystagmus * Tremor * Cardiac arrhythmias
133
What causes scurvy?
Scury is caused by **long-term depletion of vitamin C** * Vitamin C is found in citrus fruits, cantaloupe, veggies
134
Signs of scurvy include:
Signs of scurvy include: * Scaly, dry skin * Corkscrew hairs * Poor wound healing * Bone pain, fractures * Gingivitis, gum bleeding * Anemia, infection, cardiac effects
135
Dry beriberi is a deficiency in _ which leads to _
Dry beriberi is a deficiency in **B1 (thiamin)** which leads to **neurologic issues** * Peripheral neuropathy * Wernicke-Korsakoff (memory loss, confabulation)
136
Wet beriberi is a deficiency in _ which leads to _
Wet beriberi is a deficiency in **B1 (thiamin)** which leads to **dilated cardiomyopathy with HF symptoms**
137
4 D's of Pellagra
4 D's of Pellagra: 1. **Dermatitis**: hyperpigmentation in sun exposed areas 2. **Dementia**: irritability, confusion, ataxia 3. **Diarrhea**: N/V 4. **Death**: coma and death if not treated
138
Treatment for pellagra includes _
Treatment for pellagra includes **high dose niacin (B3) supplementation**
139
A majority of our bile acids get reabsorbed in the _
A majority of our bile acids get reabsorbed in the **distal ileum** * Any disease that leads to damage of the ileum can lead to poor bile acid resorption
140
Bile acids get reabsorbed in the distal ileum and circle back to the _ to be reprocessed and reused
Bile acids get reabsorbed in the distal ileum and circle back to the **liver** to be reprocessed and reused * Enterohepatic circulation
141
Explain how bile acid malabsorption can cause diarrhea
Bile acids *end up in the colon* and cause an **osmotic diarrhea**
142
Impaired bile acid resorption can also lead to malabsorption of _
Impaired bile acid resorption can also lead to malabsorption of **fat soluble vitamins**
143
Name some of the major functions of the liver
144
The pentose phosphate pathway takes glucose-6-phosphate and makes _ for detoxification
The pentose phosphate pathway takes glucose-6-phosphate and makes **NADPH** for detoxification
145
During a fed state, what happens to glucose in the liver?
Glucose --> glycolysis, TCA --> ATP Fatty acid synthesis --> VLDL Cholesterol synthesis Excess gets stored as glycogen
146
During a fed state, what happens to amino acids in the liver?
* Amino acids are used to synthesize liver proteins * Can also be sent for protein synthesis in other tissues
147
Amino acids get deaminated, producing _ as a byproduct which is converted to _
Amino acids get deaminated, producing **ammonia** as a byproduct which is converted to **urea** *via urea cycle*
148
The liver produces many serum proteins like:
The liver produces many serum proteins like: * **Albumin** * **Fibrinogen** * **Clotting factors** * **Transferrin**
149
What biochemical reactions are occuring inside the liver during a fasting state?
**Goal is to supply glucose to the body** * Gluconeogenesis * PPP generates NADPH for detox * Urea cycle is active due to aa destruction * Fatty acid breakdown (beta-oxidation) to make acetyl coA --> TCA or ketone formation
150
(Phase 1/Phase 2) of detoxification is carried out by CYP450
**Phase 1** of detoxification is carried out by CYP450 * ROS intermediate causes oxidative stress and liver damage * We need NADPH to fuel CYP450
151
(Phase 1/ Phase 2) of detox involves conjugation with charged species to make the compound more water soluble and easier to excrete
**Phase 2** of detox involves conjugation with charged species to make the compound more water soluble and easier to excrete * Ex: addition of glucuronic acid, glutathione, sulfate * Excretion by kidneys or inclusion in bile
152
The composition of bile includes:
The composition of bile includes: * Water (major component) * Electrolytes * Bile salts * Phospholipids * Cholesterol * Bilirubin
153
Bile salts are made using _
Bile salts are made using **cholesterol**
154
Bile salts help to form _ to increase the surface area for digestive enzymes like lipases to break down free fatty acids
Bile salts help to form **emulsion droplets** to increase the surface area for digestive enzymes like lipases to break down free fatty acids
155
Bile salts later join the lipid digestion products again to form _
Bile salts later join the lipid digestion products again to form **micelles**
156
Bile is made in the hepatocytes and transported into the bile canaliculi using _
Bile is made in the hepatocytes and transported into the bile canaliculi using **bile salt export pump** --> makes its way through the hepatic bile ducts --> gallbladder
157
How does bile concentration occur in the gallbladder?
Gallbladder epithelial cells **absorb ions and water in an isosmotic fashion** using transporters * *Organic components of bile are not absorbed and become concentrated in the gallbladder*
158
Bilirubin moves around the blood bound to albumin until it gets taken up by hepatocytes for _
Bilirubin moves around the blood bound to albumin until it gets taken up by hepatocytes for **conjugation**
159
Most of our bile is recaptured via the enterohepatic recirculation; it is reabsorbed in the _
Most of our bile is recaptured via the enterohepatic recirculation; it is reabsorbed in the **ileum**