1
Q
What causes slow waves in the GI tract?
A
Interstitial cells of Cajal induce slow waves that do not induce action potential
2
Q
What is the neural control of the GI tract?
A
- 2 plexuses
- Myenteric plexus
- Submucosal plexus
3
Q
Describe the layers of the myenteric plexus & Submucosal plexus
A
Outermost to Innermost
- Longitudinal smooth muscle
- Myenteric Plexus
- Circular Smooth muscle
- Submucosal smooth muscle
- Epithelium
4
Q
What PNS innervates the GI plexuses from the colon to anus?
A
Pelvic N coming off the PNS from S2-S4
5
Q
What are excitatory NT in the enteric NS?
A
Acetylcholilne
Substance P
Serotonin
6
Q
What are the inhibitory NT of the enteric NS?
A
VIP & NO
7
Q
What cells secrete Gastrin?
What stimulates its release?
What inhibits it?
A
- Gastrin is secreted from G cells
- Stimulated by: Ingestion of food, nervousness, physical distension, decaf & regular coffee, wine
- Inhibited by: Acidifcation of antrum
8
Q
What are some effects of gastric secretion?
A
- Stimulatory effect
- Growth of mucosa cells
9
Q
What cells secrete CCK?
What stimulates CCK?
A
- CCK released by I cells
- Stimulated by: Fat, Peptide, A.A. in chyme
10
Q
What are the downstream effects of CCK?
A
- Relax sphincter of Oddi allowing flow of bile and pancreatic enzymes into duodenum
- Contract gallbladder to release bile
- Increase pancreatic enzyme secretion
11
Q
________________ induces Zollinger-Ellison syndrome. Which is:
A
- Gastrinoma is a non B-cell tumor of the pancreas or G-cells tumor in duodenum
- Causing increase of epithelial cell layer
- Secretion of Gastrin which induces increase of mucosa cells
12
Q
_____________-___________ syndrome induced by gastrinoma causes the following symptoms: Duodenal ulcers, diarrhea, steatorrhea, hypokalemia, peptic ulcer. What causes the hypokalemia & steatorrhea?
A
- Steatorrhea: because there is increased gastrin released resulting in more HCl release = lower pH. The lower pH inactivates pancreatic lipase and bile salt precipitation. Thus fats are not broken down and are excreted
- Hypokalemia: because there is loss of gastric juices which have lots of K+
13
Q
What test is used for Gastrinoma/Zollinger-Ellison syndrome?
A
- Chirhostim test
- Use synthetic secretin to see if this inhibits the Gastrin
- Gastrin inhibition = normal function b/c secretion blocks gastrin
- If cont. secretion of Gastrin = tumor b/c tumor will not respond to negative feedback
14
Q
What cells secrete Secretin?
What stimulates its release?
A
- Secretin comes from S-cells
- Secretin inhibits Gastrin release which inhibits HCl = increased pH
- Stimulates liver & pancreas to release bicarb
- Tropic effect of pancreas
- Simulate pepsin release from stomach
15
Q
What cells release GIP/GLIP AKA Glucose dependent insulinotropic peptide?
A
- Released by K cells of duodenum & proximal jujenum
16
Q
What stimulates release of GIP & GLIP?
What are the downstream effects?
A
- Stimulated by ingestion of foods including oral glucose (not released if administered IV glucose)
- Effect: insulin release via feedforward control & inhibits gastric acid secretion
17
Q
GILP/GIP is a hormone classified as an enterogastrone. What is an enterogastrone?
A
Hormones released from intestine that acts on stomach to inhibit acid secretion
18
Q
What cells secrete Motilin?
A
- Released by M-cells of duodenum & proximal jujenum
19
Q
What stimulates the release of Motilin?
What are the downstream effects?
A
- Stimuli: Fasting
- Effects: upper GI motility & contributing to slow wave contractions
20
Q
Somatostatin and Histamine are both paracrine hormones meaning:
A
They are hormones that acts locally and do not enter blood stream
21
Q
What stimulates the release of Somatostain in the gut?
What are the effects?
A
- Stimuli: Acid & Acetylcholine
- Effects: Inhibit release of gut hormones, inhibit parietal acid secretion
22
Q
What stimulates the release of histamine in the GI?
What are the downstream effects?
A
- Stimuli: Gastrin & ACh
- Effects: Acid secretion
23
Q
Differentiate Intrinsic control of the GI tract vs Extrinsic control:
A
- Intrinsic: Enteric NS further specified as myenteric & submucosal plexus
- Extrinsic: ANS
24
Q
What is the location of the myenteric plexus & what is its purpose?
A
- Most outer plexus b/t longitudinal (outermost) & circular SM layers (innermost)
- Increase tonic contraction, increase frequency & intensity
- Inhibitory Influence: decrease sphincter tone
25
Where is the submucosal plexus found?
What is its function?
- Located b/t circular smooth muscle (outermost) and epithelium (innermost)
- Functioning in: secretion, absorption, and contraction of muscularis mucosa
26
Describe Parasympathetic innervation of the GI
- Upper half-Colon: Vagus N
- Colon to Anus: Pelvic N through sacral inn. S2-S4
- Post-ganglions synapse with ENS neurons
27
Describe the sympathetic innervation of GI
- Pre-ganglions emerge from T5-L2 to form to synapse in prevertebral ganglia
- Post-Ganglions originate from ganglia and innervate the entire gut. Terminate in the ENS
- Tend to inhibit/decrease activity in ENS
28
Describe sensory afferent neurons in the GI
- Dendrites at the epithelium receiving input
- Info can be sent to submucosal plexus or myenteric plexus or to brain/higher level
29
Describe Vasovagal reflex:
- Controls gastric motor and secretory activity w/afferent & efferent activity via vagus
30
The _______________________ do not induce action potential in GI, what does?
- Interstitial cells of Cajal don’t induce AP
- Induced by Voltage dependent Ca+2 channels
31
What induces peristalsis? What blocks it?
- Peristalsis can be induced by distention, PNS, or irritation of gut epithelium
- Can be blocked by atropine
- Atropine is a ACh blocker
32
What is Hirshsprung disease?
Missing myenteric plexus so no peristalsis can occur
33
What cells secrete α amylase & lipases?
Describe the saliva composition here
- Acinar cells at the distal end of salivary glands
- When secereted, this saliva is isotonic with the body.
- But as saliva moves towards release, it is modified
34
Describe the modification of saliva through the duct
- Distal to acinar cells and proximal to secretion, there is no movement of water
-Na+ & Cl- are reabsorbed in exchange for H+ and HCO-3 respectively
- K+ is secreted in exchange for H+ reabsorption
- With no water reabsorption, Saliva is now hypotonic
35
Describe how Acinar cells modify saliva
- Acinar cells have CFTR channels where in cAMP causes efflux of Cl- into saliva
- Na+ follows Cl- to balance charge
- H20 follows solute gradient
36
Aside from initiating digestion of starches and lipids, what are some other functions of saliva?
- Allowing tase molecules to dissolve
- Activate tase receptors
- Destroy bacteria, has IgA
37
Why is it important to brush your teeth in the morning?
- Saliva flow decreases during sleeping
- Since saliva kills bacteria, at night it can build up
38
What normally induces saliva secretion?
What else can induce saliva secretion?
1. PNS normally induces via M3 receptors and secretes watery alkaline saliva
2. When SNS induces saliva secretion b/c the person is stressed, the β1 & β2 receptors secrete a protein rich saliva making it feel drier
39
Cystic fibrosis is a mutation of: __________ channel. Inducing what changes to saliva?
- Mutation of CFTR channels which causes saliva have higher content of Ca+, Na+, and proteins
40
Describe receptive relaxation of stomach:
Swallowing center initiates relaxation of stomach smooth muscle to allow storage of food in the stomach
41
What is achalasia?
- Motility disorder of lower 2/3 esophagus due to dysfunction of myenteric plexus
- Inability of lower esophageal sphincter to relax & pressure is high
- Causes megaesophagus
42
What induces primary peristalsis?
Vagus N
43
What induces secondary peristalsis?
Enteric NS
44
Is contraction or relaxation occurring in the UES during swallowing? What about LES?
- Relax
45
What are three byproducts of electron transport chain?
NAD+
FAD+
H2O
46
The mitochondria is a double membrane structure, where are complexes?
- All complexes, **except** Cyt C are within the inner membrane
- Cytochrome C is located **within** the inner membrane space
47
Which layers of the mitochondria are permeable and which are not? Why is this important?
- The outer membrane of the mitochondria is more permeable to allow ions and small molecules in
- Inner membrane is impermeable to most small molecules
48
Aside from it's location, what is special about Cytochrome C?
It is closely associated with the inner membrane and _is water soluble_
49
What is special about Complex V in the ETC?
1. It is not part of the ETC!
2. AKA ATP synthase
50
What enters complex I in the ETC?
NADH
51
What enters complex II in the ETC?
FADH 2
52
Which complexes are associated with cytochromes? What do cytochromes do?
- Cytochromes are **heme containing** complexes that transfer electrons to its subsequent complex
53
List three places NADH can be generated to be sent to the ETC
1. Glycolysis
2. TCA cycle
3. β oxidation
54
List where FADH2 can be generation for the ETC
1. β oxidation
2. TCA cycle when succinate → fumerate
55
In NADH dehydrogenase, what is creating the energy to pump H+ ions from the ________________________ to the ________________________?
In ETC, the removal of electrons from NADH by NADH dehydrogenase generates the energy for H+ protons to be pump from the mitochondrial matrix into the inner membrane space
56
What is the purpose of CoQ in the ETC?
Coenzyme Q receives electrons from NADH dehydrogenase (Complex I) and succinate dehydrogenase (Complex II) to deliver the electrons to Complex III
- Does **not** pump H+ across the inner membrane of the mitochondria
57
Which complexes contribute directly to ATP production in the ETC?
- H+ proton pumping complexes including Complex I, Complex III, and Complex IV
58
Cytochromes are ________ containing proteins. How does this impact the ETC?
- Cytochromes are Heme containing proteins
- Their composition allow for differences in reduction potential along the ETC
- This means different heme have different affinity for electrons
59
Describe 4 defining features of Cytochrome C & where it is located
- Cytochrome C receives electrons from complex III and delivers them to Complex IV
- Heme-containing protein
- Water soluble
- Intermembrane space
- Donates electrons to Cu ions of Complex IV
60
What is the action of Complex IV in the ETC?
- Catalyzes transfer of electrons from Cyt C to O 2
- O 2 is the final electron acceptor in the ETC
- The energy derived from e- transfer from Cyt-C to O 2 to pump protons from the matrix to the intermemebrane space
61
Define oxidative phosphorylation
Coupling oxidation of High E molecules (removing electrons in ETC) with phosphorylation of ADP → ATP utilizing O 2
62
What creates the E potential of ADP phosphorylation in oxidative phosphorylation?
- The high [H+] in the inner membrane space flows down the gradient through F 0
- This creates E to push ADP through F 1 from the matrix into the inner membrane space where it is phosphorylated
- ATP flows into the matrix in exchange for ADP flowing into the inner membrane space
63
Describe the effects of inhibitors on oxygen uptake by mitochondria and ETC function
- If there is decreased O 2 then there is no final e- acceptor in the ETC
- This causes a build up of NADH & FADH
- Means there is no NAD+ to return to the glycolytic pathway and **decrease** in ATP production by oxidative phosphorylation
- Inc. NADH & FADH will also d/c the TCA which causes the build up of pyruvate and its conversion to lactic acid
64
What do Barbiturates and Rotenone inhibit in the ETC?
Inhibit Complex I
65
What does Malonate inhibit?
Complex II in the ETC
66
What does Doxorubicin inhibit?
CoQ inhibitor
67
What do Cyanide and carbon moxide inhibit in the ETC?
Complex IV
68
What do uncouplers cause in the ETC?
- Decrease ATP synthesis
- Increase O 2 consumption
- Decrease NADH concentration
69
What causes uncoupling in the ETC?
- Disrupted proton gradient like a proton leak
- Increase rate of O 2 consumption with no ATP synthesis
- Causes energy to be released as heat
70
What is a "natural" uncoupler of ETC & why?
Brown fat because it expresses Thermogenin that dissipates H+ gradient
- Energy used for generation of heat instead of ATP
71
Define Uncoupling in ETC
Uncoupling the electron transport system from the complex V ATP synthase by proton motive force generated in inner membrane space
72
What is the physiologic mechanism for fat burning in uncoupling of ETC
- The [H+] concentration gradient is lost so H+ flows **back into the matrix**
- This causes the complex pumps to move electrons very rapidly down the electron transport chain to try and restore the [H+] in the inner membrane space
- this uses a lot of energy and O2 with little production of ATP
73
How does brown fat generate heat?
- has lots of small lipid droplets where you can very rapidly metabolize lipids
- causes very rapidly flow electrons to the electron transport system
74
Name 2 synthetic uncouplers of the ETC
1. Aspirin
2. 2,4-Dinitrophenol
75
Describe an amino sugar
amino group at position 2
+ charge at physiologic pH
balanced with acetyl group
76
List types of monosaccharides
- Derived monosaccharides: Deoxy-sugars, amino-sugars, sugar alcohols, phosphorylated and sulfated sugars
77
Describe sugar alcohols & what they are
- Sugar alcohols are a type of derived monosaccharide
- Reduced carbonyl carbon (aldehyde or ketone group)
- Want to be associated with water
78
What is the most abundant monosaccharide in living cells?
Pentoses & hexoses
79
What links 2 monosaccharides?
- Diasaccharides are linked by a glycosidic bond
80
What is the linkage of lactose?
Galactose + glucose via β (1-4) glycosidic bond
81
What is the linkage of sucrose?
Glucose + fructose via α (1-2) glycosidic bond
82
What is the linkage of maltose?
Glucose + glucose via α (1-4) glycosidic bond
83
What is the basic defining feature of oligosaccharides?
3-10 monosaccharides linked by glycosidic bond
84
What are the two classes of oligosaccharides?
N-linked oligosaccharides & O-linked oligosaccharides
84
Describe the basic structure of an N-linked oligosaccharide
- Attached to polypeptide by an N-glycosidic bond with the side chain amide group of the amino acid asparagine
85
Describe the basic structure of an O-linked oligosaccharide
- Attached to the side chain hydroxyl group of amino acid serine or threonine in polypeptide chains or the hydroxyl group of membrane lipids
86
What is the purpose of polysaccharides?
- Storage forms of energy or structural materials
87
What are the two chief constituents of starch?
- Amylose
- Amylopectin
88
Compare the branching in amylopectin and amylose
- Amylose is non-branched and helical in structure
- Amylopectin is branched & composed of α (1-4) glycosidic bond & α (1-6) glycosidic bond
89
What are the bonds between monosaccharides in amylopectin?
What are the bonds at branch points in amylopectin?
α (1-4) glycosidic bond b/t monosaccharides
α (1-6) glycosidic bond at branch points
90
Compare the bonds between glycogen and amylopectin
α (1-4) glycosidic bond b/t monosaccharides
α (1-6) glycosidic bond at branch points
- Glycogen has more α (1-6) glycosidic bond b/c it has more branches!
91
What does cellulose do in humans? What is cellulose?
- Cellulose is a polysaccharide
- Has β (1-4) glycosidic bond glucose residues that cannot be digested by humans because we don't have enough hydrolase to break linkages
- Can help move things, like cholesterol, through the gut
92
A cyclic sugar can be opened where:
A cyclic sugar has the ability to open at the anomeric carbon (the carbonyl carbon in linear form)
93
All _______________ have reducing ability. What does this mean?
- All monosaccharides are reducing
- This means if the cyclic sugar can be opened then they can be used as a reducing agent such that they can give up electron or H+
94
What test can determine if a carbohydrate is reducible?
Benedicts reagent changes color in the presence of reducing sugars whether they be monosaccharides, disaccharides, etc
95
Describe how a disaccharide can be a reducible sugar?
- If at least one sugar has anomeric carbon with -OH group not linked to another compound by glycosidic bond
96
How do α amylases digest carbohydrates?
- Break down large carbs like starches and glycogen
- break down of α (1-4) glycosidic bond b/t monosaccharides to make shorter branch and unbranched oligosaccharides
- Optimal pH 7.0
97
How does pancreatic α amylase digest carbohydrates?
- Break down of α (1-4) glycosidic bonds only
98
What plasma level can indicate pancreatitis if increased?
- Plasma levels of either pancreatic amylase or total amylase are used as diagnostic marker for pancreatitis
99
Where are monosaccharides absorbed in the small intestine?
In duodenum and jejunem
100
What do sucrase/isomaltase do?
- Protease that cleaves α (1-2) glycosidic bonds in _sucrose_
- Also cleaves α (1-6) glycosidic bonds in isomaltase
- Works on luminal surface of the intestinal mucosal cells
101
What does maltase-glucoamylase (MGA) do?
- Protease that cleaves α (1-4) glycosidic bonds in maltose/maltotriose & α (1-4) glycosidic bonds in dextrins
- Works on luminal surface of the intestinal mucosal cells
102
What does Lactase do?
- Cleaves β (1-4) glycosidic bonds in lactose
- Works on luminal surface of the intestinal mucosal cells
103
What does Trehalase do?
- Works on luminal surface of the intestinal mucosal cells
- Cleaves α (1-1) in trehalose (mushrooms & fungi)
104
What three transporters are involved in the absorption of monosaccharides in the duodenum & upper jejunum?
- SGLT-1
- GLUT-5
- GLUT-2
105
Where and what is SGLT-1 transporter?
- Involved in **absorption** of monosaccharides in the jejunum and duodenum
- On the apical/lumenal surface
- Transports Glucose and galactose using active transport
106
Where and what is GLUT-5 transporter?
- On the apical/lumenal surface of brush border in the duodenum and upper jejunum
- Passively **absorbs** fructose
107
How do glucose, galactose and fructose get into circulation from the small intestine?
- Via absorption through GLUT-2 transport on the basal surface of cells of the duodenum & upper jejunum
108
If _________________ get into the large intestine they can cause diarrhea by what mechanism?
- If disaccharides reach the large intestine they can cause _diarrhea_ by increasing the osmotic gradient and drawing water into the lumen
- They are also substrates for intestinal microbiota that ferment them to 2 and 3 carbon compounds causing release of gases = cramping and bloating
109
What test can be used to determine if carbohydrates are not being absorbed by the body?
- Can measure H 2 gas in breath
110
What causes sucrose intolerance?
- Sucrase-isomaltase complex deficiency
- Autosomal recessive disorder
111
What does GLUT-1 do and where is it found?
- Found in most tissues
- Largely abundant in brain and RBC
- Basal uptake of glucose
112
What digests proteins in the stomach?
Pepsin
113
What digests proteins in the stomach?
Pepsin
114
What proteases are released from the pancreas?
- Trypsin
- Chymotrypsin
- Elastase
- Carboxypeptidases
115
What proteases are found in the small intestine?
Enteropeptidase
Aminopeptidase
Dipeptidase
Tripeptidase
116
What is the difference between endopeptidases & exopeptidases?
- **Endopeptidases**: break down peptide bonds of nonterminal amino acids
- **Exopeptidases**: catalyze cleavage of the terminal peptide bonds
117
Pepsinogen is:
- Pepsinogen is a zymogen
- Activated by acid or pepsin in the stomach for digestion of proteins
118
CCK is:
CCK is a hormone from the small intestine that works on the pancreas and gallbladder
- Pancreas: release digestive enzymes
- Gallbladder: causing contraction and release of bile
119
_________________ is produced by the S cells of the duodenum. Its purpose is:
- Secretin is produced by the S cells of the duodenum
- In the pancreas it causes a release of a solution rich in NaHCO3- to help neutralize incoming contents
- Also causes bile ducts to increase water and HCO3 secretion
120
Where is enteropeptidase & what does it do?
- Enteropeptidase is produced in the cells of the duodenum
- Cleaves trypsinogen from the pancreas into trypsin for proteolysis
121
Pancreatic insufficiency would cause a significant decrease in the:
Decrease in the digestion & subsequent absorption of proteins in the duodenum
122
If only free amino acids are found in the portal vein, why can free amino acids, _dipeptidases, and tripeptidases_ be absorbed by intestinal epithelial cells?
- Dipeptidases and tripeptidases are cleaved in the cytoplasm by dipeptidases and tripeptidases before they cross the basal surface for entry into the portal system as free amino acids
123
What is cystinuria?
- Most common inherited disease of amino acids transport
- Results from defective kidney transport for reabsorption of Cys, ornithine, Arg, and Lysine (COAL)
- Thus they are found in the urine and can cause precipitation of kidney stones
124
What is Hartnup disease?
- Inherited disorder with intestinal defects of nonpolar amino acids absorption and urinary wastage
- Sx. include Diarrhea, Dementia (hallucinations), dermatitis
125
Where are the main stores of glycogen found?
- Skeletal muscle
- Liver
126
What organ mainly supplies glycogen during fasting?
- Liver senses blood glucose level and maintains blood glucose during early fasting
127
T/F: Both skeletal muscle and liver contain glycogen stores that are broken down by Glucose-6-P but muscle uses the energy for itself while the liver contributes to blood glucose
True
128
What does glycogen have to do with weight?
- Glycogen storage is associated with significant amounts of water storage there for weight can vary significantly based on the amount of glycogen stored
129
Describe the structure of glycogen
- Branched polysaccharide made from α-D-glucose
- Primarily α (1,4) linage
- Has α (1,6) links after about 8-10 glucosyl residues for branching
130
Inside the organ, where does glycogen reside?
- Large molecules of glycogen exist as discrete cytoplasmic granules (β-particles)
131
Which kinase is in the liver for transformation of glucose to Glucose-6-phospate? Why?
- **Glucokinase** has a lower affinity for glucose so that the liver can contribute to blood glucose levels
132
After forming G-6-P, what is the second step for glycogenesis?
- Move the P group to the 1 position of glucose, makes G-1-P
- Then G-1-P + UPD = UDP-Glucose which uses energy to create but can now begin the synthesis of Glycogen
133
After the synthesis of Uridine-Glucose, what is the next step in glycogenesis?
- Need to make a primer for _Glycogen synthase_ to be able to start building molecule
- A primer can be: either Glycogenin + Tyr or already made glycogen
134
What is the importance of Glycogenin+Tyr?
- Significant in the process of glycogenesis
- Glycogenin is a protein that when attached to Tyrosine, can serve as an attachment point for UDP-glucose
- Glycogenin can catalyze the addition of Tyrosine **&** the attachment of a few UDP-glucose molecules via α (1,4) glycosidic bonds
135
What are 2 significant molecules in glycogenesis?
- Glycogen synthase
- Branching enzyme
136
After the initial building/priming of UDP-glucose, what continues to build the α (1,4) glycosidic bonds? Is this a significant step & why?
- The enzyme **glycogen synthase**
- Elongates the existing glycogen primers via the _non-reducing_ end of the primer by removing UDP from glucose. Then forming α (1,4) glycosidic bonds between C-1 of UPD-glucose on the existing chain and C-4 of the incoming primer
- Yes, this is significant because this enzyme and step is **rate limiting**
137
Describe the steps of how branching enzyme forms α (1,____) glycosidic bonds in glycogenesis
- Branching enzyme forms α (1,6) glycosidic bonds by removing a chain of 6-8 glucosyl residues from the end of the glycogen chain by breaking α (1,4) glycosidic bonds
- Then it attaches this to a _non-terminal_ glucosyl residue with a α (1,6) glycosidic bond
- After glycogen synthase can continue adding glycogen to this newly formed branch
138
What is the significance of the branching in glycogen?
- Increases the solubility of glycogen molecules
- Increases the number of nonreducing ends that allow for faster synthesis and degradation
139
List 3 important enzymes used in Glycogenolysis
- Debranching enzyme
- Glycogen phosphorylase (rate limiting)
- Glucose-6-phosphatase
140
Contrast glycogenolysis in skeletal muscle vs liver:
- Glycogen break down to form glucose
- Muscle is 3 step pathway and utilizes Glucose-6-P since it stays in the cell its is generated in
- Liver is a 4 step pathway to convert Glucose-6-P back into glucose so it may enter the blood stream
141
T/F: Glycogen breakdown begins by removing each chain from the molecule that can then be broken down further by glycogen phosphorylase
False, start by removing α (1,4) glycosidic bonds
142
What vitamin is Pyridoxal phosphate (_____) derived from?
Derived from B 6
143
This enzyme is the first step & rate limiting step in Glycogenolysis. It requires the cofactor __________________ _____________ which is a derivative of Vit B 6
- Glycogen phosphorylase is the first enzyme involved in glycogenolysis and is rate limiting
- It requires PLP/ Pyridoxal phosphate and is derived from Vitamin B 6
144
What specifically does glycogen phosphorylase do in glycogenolysis?
1. Cleaves α (1,4) glycosidic bonds from glycogen chains
- Does so by using inorganic P to cleave the bond and simultaneously attaches it to the glucose
- Yields: _Glucose-1-P_
145
After α (1,4) glycosidic bonds are largely removed from glycogen, how are branches removed in glycogenolysis?
2. Debranching enzyme will come when there are only about 4 residues left on a chain after
2a. Removes 3 of the 4 glycosyl residues at the end of a chain by breaking α (1,4) glycosidic bonds and will attach this set to the remaining branches
2b. The remaining 1 glycosyl residue with α (1,6) glycosidic bonds and will be a free glucose molecule
146
What are the two activities of debranching enzyme in ____________________________
Debranching enzyme acts in glycogenolysis
4:4 Transferase activity by moving 4 glucosyl residues to another chain
1:6 by removing the last/final glucosyl unit from a branch
147
What is the last step of glycogenolysis that occurs in both liver and skeletal muscle tissue?
- **Phosphoglucomutase** will transform Glucose-1-P into Glucose 6-P
- This is the last step of glycogenolysis in muscle
148
What is a cofactor of Phosphoglucomutase in Glycogenolysis?
- Glucose 1,6-bisphosphatase is an intermediate of Phosphoglucomutase and activates the enzyme
149
What enzyme transforms Glucose-6-P to Glucose so it can leave the liver in glycogenolysis?
Other than the liver, where else in the body is this enzyme found & why?
- Glucose-6-phosphatase
- Also found in the kidney cortex since the kidney weakly contributes to blood glucose homeostasis
- Even in some β-pancreatic cells
150
Epinephrine is released for _________________________, insulin is released for _________________.
Epinephrine is released to induce **glycogenolysis**
Insulin is released for glycogenesis
151
Which NT acts oppositely to insulin and glycogenesis that insulin induces?
Epinephrine since it induces glycogenolysis
&
Glucagon
152
Glycogen synthase:
Glycogen phosphorylase:
Regulation of these enzymes is maintained by two major mechanisms:
1.
2.
Glycogen synthase: glycogenesis
Glycogen phosphorylase: glycogenolysis
Regulation of these two enzymes is maintained by two major mechanisms:
1. Hormonal regulation
2. Allosteric regulation
153
Contrast the hormonal vs. Allosteric regulation of glycogen synthase in ____________________________.
- Glycogen synthase is Glycogenolysis
- In Hormonal: epinephrine & glucagon inhibit. While Insulin activates
- In allosteric: activated by Glucose 6-P
154
Contrast the hormonal vs. Allosteric regulation of glycogen phosphorylase in ____________________________.
- Glycogen phosphorylase is Glycogenolysis to make glucose
- In hormonal: activated by Epinephrine & Glucagon, inhibited by Insulin
- In allosteric: activated by AMP & Ca+2, inhibited by Glucose-6-P, Glycose & ATP
155
What enzyme is deficient in Von Gierke (__________________________________)
- Von Gierke is Glycogen Type I storage disease
- Deficient in Glucose-6-Phosphatse in the liver and kidneys
156
The following symptoms are indicative of:
- Severe fasting hypoglycemia
- Lactic acidosis
- Hepatomegaly
- Hyperlipidemia
- Hyperuricemia
- Short stature
Von Gierke/Type Ia glycogen storage disease
157
Contrast Type Ia vs. Type Ib glycogen storage disease
Type Ib is Glucose-6-phosphate translocase deficiency and is associated by neutropenia & recurrent infections in addition to all the symptoms associated with type Ia
158
Glycogen storage disease Type II: __________________________________. What is deficient?
- GSD Type II is AKA Pompe disease
- Deficient in Lysosomal alpha glucosidase
159
Pompe disease is ____________________________________________. Caused by a deficiency in Lysosomal alpha glucosidase which causes:
- Glycogen storage disease type II
- Excess glycogen concentrations in abnormal vacuoles of lysosomes
- Cardiomegaly
- Early death in infants
160
Glycogen storage disease Type III/________________________________ is caused by a deficiency of:
- GSD Type III: Cori disease
- Caused by a deficiency of Debranching enzyme
161
Cori disease aka ___________________________ is caused by a deficiency of debranching enzyme which causes:
- Cori disease AKA glycogen storage disease type III
- Causes mild hypoglycemia
- Liver enlargement due to accumulation of glycogen
162
Glycogen storage disease type IV aka ___________________________ is caused by a deficiency of:
- Glycogen storage disease type IV AKA Anderson disease
- Lack of branching enzyme
163
Anderson disease aka ____________________________ is very rare and due to deficiency of branching enzyme. Its associated symptoms are:
- Anderson disease aka Glycogen storage disease type III
- Associated symptoms: abnormal shaped glycogen
- Infantile hypotonia
- Cirrhosis since linear glycogen is less soluble = cell damage
- Early death to heart & liver complication
164
Type V glycogen storage disease aka ____________________________ is caused by deficiency of:
Type V glycogen storage disease aka McArdle Disease is a deficiency of muscle glycogen phosphorylase (muscle only!)
165
McArdle disease aka ___________________________________________ is caused by deficiency of glycogen phosphorylase in muscle only. Associated symptoms include:
- McArdle disease AKA Glycogen storage disease type V
- Muscle gramps and weakness on exercise
- Myoglobinuria because of destruction of muscle cells due to lack of ATP
- **NO** lactate build up
166
Glycogen storage disease type VI aka _______________________ is a deficiency of:
GSD TVI is aka Hers disease
- Caused by a deficiency of hepatic glycogen phosphorylase
167
Glycogen storage disease type VI is ______________________________________. Caused by a deficiency of Hepatic glycogen phosphorylase with associated symptoms:
- GSD VI is Hers disease
- Mild fasting hypoglycemia
- Hepatomegaly & cirrhosis
168
What is Lafora disease and why does it cause progressive myoclonic epilepsy?
- Lafora disease is a brain glycogen storage disorder
- There is accumulation of poorly branched glycogen
- Associated with Lafora bodies
- Laforin is a phosphatase that removes extra P group added by glycogen synthase
169
Other than muscle, kidney, and liver, where else can glycogen be found?
Lysosomes
About 1-3% of glycogen is here
170
Where does glycolysis occur?
Cytosol
171
What is the product of aerobic glycolysis?
What is the product of anaerobic glycolysis?
- All glycolysis is **anaerobic**, its what happens to pyruvate depends on the Oxygen status & mitochondrial availability
- **Aerobic**: NADH, ATP, & Pyruvate
- **Anaerobic**: Final product is pyruvate which is converted into Lactate
172
Glycolysis requires: NADH or NAD+?
- **anaerobic** glycolysis requires NAD+ and _generates_ NAHD to send to the ETC
173
Why is pyruvate converted to lactate in anaerobic ___________________________.
In anaerobic glycolysis, pyruvate is converted to lactate so that NAD+ can be regenerated to send back through glycolysis
174
What are the two states of glycolysis?
1st phase is energy _investment_
2nd phase is energy _generating phase_
175
Where does the energy investment phase begin in glycolysis & when does it end?
1. Starts with Glucose 6-P being converted into Fructose-6-P
2. Then Fructose-6-P will be converted into Fructose 1,6-bisphosphate and broken into G3P and DHAP *DHAP will also be converted into G3P
176
The steps below describe the energy _______________________ phase of ______________________:
1. Starts with Glucose 6-P being converted into Fructose-6-P
2. Then Fructose-6-P will be converted into Fructose 1,6-bisphosphate and broken into G3P and DHAP *DHAP will also be converted into G3P
What are the major enzymes at work here?
- This is glycolysis in the energy *investment phase*
- Important enzymes are **PFK-1** that converts Fructose 6-P into Fructose 1,6-bisphosphate
- Use 2 ATP (first one is for Hexokinase when it converts Glucose to G-6-P)
177
What step of glycolysis generates NADH?
When G3P is converted into Glycerate-1,3-Bisphosphate by **Glyceraldehyde-3-phosphate dehydrogenase** in the energy generating phase
178
What steps of glycolysis generate ATP?
- During second phase of Glycolysis
- When glucose-1,6-bisphosphate is broken down into G3P & When PEP is converted into Pyruvate
179
What are the major enzymes taking part in the second portion of glycolysis?
- Glyceraldehyde-3-phosphate dehydrogenase
- Pyruvate kinase
- Glyceraldehyde-3-phosphate dehydrogenase generates Glycerate 1,3-bisphosphatase to set up next reaction for the generation of ATP while also generating NADH
- Pyruvate kinase breaks Phosphoenolpyruvate into 2 pyruvate molecules
180
What is Hexokinase IV?
Hexokinase IV = Glucokinase which is present in the liver and pancreas and has lower affinity for glucose
181
Describe the V max & K m for Glucokinase
- High V max
- High K m
- This is because glucokinase is in the liver and has to contribute to blood glucose level as well as sense the glucose level
- Needs to have high efficiency but lower affinity so that glucose can be released
182
Where is glucokinase found? What is another name for it?
-Glucokinase is Hexokinase IV
- Found in β-pancreatic cells
183
What does low K m mean?
substrate concentration at which an enzyme reaches half of its maximum reaction rate (Vmax)
- thus if LOW K m then enzyme has HIGH affinity for its substrate
184
When Hexokinases have low V max what does this contribute to?
- Trapping glucose in the cell
- Hexokinase has high affinity and low efficiency & thus will trap the glucose in the cell regardless of systemic glucose levels
185
What inhibits Glucokinase?
- Nothing technically
- Indirectly **inhibited** by Fructose-6-phosphate
- Indirectly _stimulated_ by glucose
186
What is MODY?
- Maturity-onset diabetes of the young
- A mutation of Glucokinase induces diabetes *rare*
187
What is the committing step of glycolysis?
When PFK-1 transforms Fructose-6-phosphate into Fructose-1,6-bisphosphate
188
What are inhibitors of PFK-1? Why?
- APT & Citrate
- ATP-means the cell is already in a high energy state and does not need to make more
- Citrate is also an indicator of high energy state
189
What is a stimulator of PFK-1? Why?
- AMP
- Fructose-2,6 Bisphosphate which is a product of **PFK-2**
190
What is the significance of isomerization of dihydroacetone-P?
This is when DHAP is transformed into G3P so that glycolysis can continue
191
What does arsenic have to do with Glyceraldehyde-3-P dehydrogenase?
- In the glycolytic pathway, this is a NADH generating step of the energy generating portion of glycolysis
- Arsenic _inhibits_ Glyceraldehyde 3-P dehydrogenase by competing with P that will be attached to G3P
- The P instead forms a complex which spontaneously oxidizes and bypasses the next energy producing step
192
What is a modification of glycolysis pathway that is prevalent only in RBC?
- RBC's generate & Protect (through a side reaction) 2,3-BPG
193
Where in the glycolytic pathway does substrate level phosphorylation occur?
- When phosphoenolpyruvate is turned into pyruvate by **pyruvate kinase** and generates ATP in the process
194
Fructose 1,6 bisphosphate is an _____________________ ___________________ of pyruvate kinase & why?
Fructose 1,6-bisphosphate is an allosteric up-regulator of Pyruvate kinase because it informs the cell there is extra substrate available for glycolysis
195
What type of receptor does glucagon bind to?
G α s & thus phosphorylates things & can induce transcription
196
Glucagon binds to G α s. Explain how this effects pyruvate kinase in the glycolytic pathway during fasting:
- If glucagon phosphorylates enzymes downstream, then when someone is in the fasting state (glucagon = fasting) their enzymes will be phosphorylated
- Pyruvate kinase is **inactivated** in the phosphorylated state
197
What is the status of Pyruvate kinase when it is phosphorylated?
Inactive
198
What is the status of pyruvate kinase when it is dephosphorylated?
Active
199
What is the status of pyruvate kinase when there is insulin released in the body
Dephosphorylated so that the body can use the incoming glucose for energy
200
______________________ is only active in the liver in a well-fed state meaning there is high glucose availability
Pyruvate kinase is only active in the liver in the well-fed state when glucose levels are high
201
Deficiencies of pyruvate kinase affect _____________________ the most. Why?
- Deficiencies of pyruvate kinase affect RBCs the most
- This is because they rely on glycolysis for energy production and maintenance of shape
202
What are the two most common causes of hemolytic anemia?
1. Glucose-6-phosphate dehydrogenase w/Heinz body presence
2. Pyruvate kinase deficiency w/out Heinz body presence
203
What happens in pyruvate kinase deficiency?
- The RBCs become misshaped and damaged so they are lysed
- Hemolytic anemia
204
What is the fate of glycolysis products in the presence of oxygen and mitochondria?
- NADH will be sent to the ETC as a H+ donor and return to Glycolytic pathway for use as NAD+
- Pyruvate will be converted to Acetyl CoA for the TCA cycle
205
what is the fate of glycolysis products in anaerobic conditions?
- Pyruvate will be reduced to lactate by lactate dehydrogenase (**reversible step**)
206
What does pyruvate carboxylase generate when acting on pyruvate?
- Generates TCA cycle intermediates for use in gluconeogenesis
207
Where is lactate production normal?
- In RBC & exercising skeletal muscle
208
Cells can handle some generation of pyruvate, how?
What does excessive lactate buildup induce?
- Lactate can be released into plasma and taken up by other tissues for metabolism into pyruvate and shunted to other pathways
- When there is no oxygen for lactate to be turned back into pyruvate, there is lactate build up with lowers the intracellular pH → denaturing enzymes → inducing cell death and tissue necrosis
209
Describe the hormonal regulation of glycolysis
- The three key enzymes: PFK-1, Glyceraldehyde 3 dehydrogenase, & Pyruvate Kinase are all under transcriptional control in the liver
- Insulin stimulates transcription of the enzymes while glucagon inhibits their transcription
210
What are the three key steps in the TCA cycle?
Why are they the key steps?
1. Citrate synthase
2. Isocitrate dehydrogenase
3. α-ketoglutarate dehydrogenase
- They are key steps because they are not reversible
211
Where does the TCA cycle take place?
Mitochondrial matrix
212
What are two major purposes of the TCA cycle?
- The converging pathway where catabolism of carbs, amino acids, and fatty acids converges for their carbon skeletons to be converted into CO 2
- Large producer of NADH & FADH 2 that will be sent to the ETC and coupled to oxidative phosphorylation
213
How does pyruvate enter the TCA cycle?
Must be converted from Pyruvate to Acetyl CoA by **pyruvate dehydrogenase complex**
214
What happens in the PDH?
- Pyruvate Dehydrogenase Complex
- Pyruvate is transformed into 2 Acetyl Co-A with the generation of NADH & CO 2
-
215
What is the status of PDH (________________) when it is phosphorylated?
Pyruvate dehydrogenase complex is **inactive** when it is _phosphorylated_
216
What is the status of PDH (________________) when it is dephosphorylated?
When pyruvate dehydrogenase complex is _dephosphorylated_ it becomes **active**
217
Pyruvate dehydrogenase complex can be regulated by substrate activation & product inhibition. Discuss substrate activation
- Firstly, the enzymes, **PDH kinase and PDH phosphorylase control the regulation of PDH complex**
- When the cell is in a high energy status with lots of ATP, Acetyl CoA or NADH
- This activates PDH kinase to inactivate PDH
218
What is the significance of PDH kinase & PDH phosphatase?
- PDH kinase adds a P to Pyruvate dehydrogenase complex rendering it **inactive**
- PDH phosphorylase removes a P from Pyruvate dehydrogenase complex rendering it **Active**
219
WhatPyruvate dehydrogenase complex can be regulated by substrate activation & product inhibition. Discuss product inhibition
- Firstly, the enzymes, **PDH kinase and PDH phosphorylase control the regulation of PDH complex**
- When there is lots of Pyruvate (entering molecule) this inactivate PDH kinase rendering PDH complex _inactive_
- While the breakdown of Pyruvate into NADH and Acetyl Co-A will inhibit Pyruvate dehydrogenase _directly_
220
What stimulates PDH phosphatase & what does it do?
- When the cell is low in energy indicated by: NAD+, ADP, Ca+2 (muscle), present, this will activate pyruvate phosphatase to remove P from PDH complex
- When PDH complex is dephosphorylated, it is _active_ and can turn pyruvate into Acetyl Co A for the ETC
221
The PDH complex requires 5 cofactors. List the cofactor originator
1. Vitamin B1
2. Vitamin B5
3. Vitamin B2
4. Vitamin B3/niacin
5. Lipoamide
222
What is thamine?
Vitamin B1
223
Thiamine pyrophosphate, TPP is a derivative of:
It is important in:
TPP is a derivative of Vitamin B1
It is a cofactor of Pyruvate dehydrogenase complex
224
What is pantothenic acid?
Vitamin B5
225
What is the precursor of Coenzyme-A?
It is a cofactor of:
Pantothenic Acid/Vitamin B5
Coenzyme A is a cofactor of the PDH complex
226
What is riboflavin?
Vitamin B2
227
FAD is a cofactor of the pyruvate dehydrogenase complex. What is it derived from?
FAD is derived from Vitamin B2
228
NAD+ is a cofactor of the pyruvate dehydrogenase complex. What is it derived from?
Vitamin B3/niacin
229
Thiamine deficiency is commonly seen in 2 populations:
- Persons with alcoholism
- Dietary deficient due to malnutrition, prolonged IV therapy, GI Disorders)
230
What is the clinical presentation of Thiamine deficiency?
BeriBeri can be wet or dry type or infantile type
231
Beri Beri is a clinical presentation of ____________________________. What are the associated symptoms of wet Beri Beri
- Beri Beri is a TPP deficiency affecting the PDH complex system since TPP is a cofactor
- Wet: cardiovascular system problems
232
Beri Beri is a clinical presentation of ____________________________. What are the associated symptoms of dry Beri Beri
- Beri Beri is a TPP deficiency affecting the PDH complex system since TPP is a cofactor
- Dry type has neuro issues including peripheral neuropathy
233
Beri Beri is a clinical presentation of ____________________________. Discuss infantile Beri Beri.
- Can occur if baby is strictly breastfeeding & mom is deficient in thiamin & thus deficient in TPP
- Life threatening
- Beri Beri is a TPP deficiency affecting the PDH complex system since TPP is a cofactor
234
What is Wernicke-Korsakoff's syndrome?
- A clinical presentation of Thiamin deficiency & thus deficiency of TPP which is a cofactor of the PDH complex
- Required for glucose metabolism in nerve cells & regulation of neurotransmitters
- Unable to use tissues that have high glucose demand, like retina = ophthalmoplegia
235
PDH complex requires cofactor: ______________ which is derived from niacin/____________________. Deficiency of this cofactor results in:
PDH complex requires cofactor NAD+ which is derived from niacin/Vitamin B3. Deficiency of this cofactor results in the clinical disorder: Pellagra
236
What is Pellagra & what causes it?
- Pellagra is caused by a deficiency of niacin which makes NAD+ for the PDH complex
- Manifests in dermatitis, diarrhea, dementia, sores in the mouth & exposed skin
237
PDH complex requires this cofactor: ___________________ which is derived from Vitamin B2. Deficiency of this cofactor results in:
- FAD is made from Vitamin B2/Riboflavin
- Results clinical manifestations: Angular stomatitis, Cheilosis, Glossitis
238
What is the initial entering step of the TCA cycle:
- In the mitochondrial matrix the acetyl co a enters and rapidly joins oxaloacetate which is converted to **citrate** by **citrate synthetase**
239
Aconitase is an enzyme of the TCA cycle responsible for:
What are 2 unique things about it?
Aconitase is responsible for isomerization of citrate to isocitrate
- This enzyme is reversible
- It is a Fe-S protein
240
Fluoroacetate is a plant toxin that inhibits this enzyme: __________________________________ which is present in the TCA cycle & is responsible for:
- Fluoroacetate is a plant toxin responsible for the inhibition of the enzyme Aconitase that is present in the TCA cycle which generates isocitrate from citrate
- Results in citrate build up
241
The oxidative decarboxylation by _________________________________ to yield α-ketoglutarate from isocitrate also generates:
The oxidative decarboxylation by isocitrate dehydrogenase to yield α-ketoglutarate from isocitrate also generates NADH & CO 2
242
What is the significance of the enzyme isocitrate dehydrogenase in the TCA cycle?
- Is an irreversible and rate limiting step
- Regulated allosterically
243
Isocitrate dehydrogenase yields _________________________ from ____________________________. It is allosterically regulated by:
Isocitrate dehydrogenase yields α-ketoglutarate from isocitrate. It is allosterically regulated by: **ATP & NADH AS INHIBITORS**
- _ADP & Ca+2 as ACTIVATORS_
244
Oxidative decarboxylation of α-ketoglutarate is performed by what enzyme and yields _______________________ in the TCA cycle.
Oxidative decarboxylation of α-ketoglutarate is performed by the enzyme _α-ketoglutarate dehydrogenase_ and yields Succinyl CoA in the TCA cycle.
245
Oxidative decarboxylation of α-ketoglutarate is performed by the enzyme _α-ketoglutarate dehydrogenase_ and yields Succinyl CoA in the TCA cycle. What is significant about this step?
- Also produces CO 2 and an NADH
- Has coenzymes: TPP, Lipoic acid, FAD, NAD+, and CoA
246
Oxidative decarboxylation of α-ketoglutarate is performed by the enzyme _α-ketoglutarate dehydrogenase_ and yields Succinyl CoA in the TCA cycle. What are the regulators and cofactors of this enzyme?
- **inhibited by**: its products
- **activated by**: Ca+2
- Coenzymes: TPP, Lipoic acid, FAD, NAD+, CoA
247
Other than α-ketoglutarate dehydrogenase in the TCA yielding Succinyl CoA, where else can Succinyl CoA come from for entry into the TCA?
- Succinyl CoA can be derived from propionyl CoA which comes from Fatty acid synthesis
248
__________________ ______________________ forms a stable thiol with the -SH group in lipoic acid making it unavailable to serve as a coenzyme
Arsenic poisoning
249
Other than isocitrate dehydrogenase generating α-ketoglutarate from isocitrate, where else can α-ketoglutarate come from?
α-ketoglutarate can be generated from the metabolism of glutamate
250
Oxidative decarboxylation of α-ketoglutarate is performed by the enzyme _α-ketoglutarate dehydrogenase_ and yields Succinyl CoA in the TCA cycle. What are the additional products formed in this step?
- GTP which can be ready transformed into ATP
- CoA
251
Fumarate is formed in a reversible step of the TCA by the enzyme Fumerase. Fumarate is also produced in:
1. Urea cycle
2. Purine synthesis
3. Phe & Tyr Catabolism
252
The final step that regenerates Oxaloacetate has a +ΔG. The enzyme performing this action is:
What drives this reaction with the +ΔG?
- Malate Dehydrogenase makes Oxaloacetate from L-malate
- Because when Oxaloacetate joins Acetyl CoA so rapidly to form Citrate, this exergonic reaction drives the +ΔG reaction of producing OAA
253
What step of the TCA is the last generator of NADH?
- Malate Dehydrogenase makes Oxaloacetate from L-malate
254
In the TCA cycle, Malate Dehydrogenase makes Oxaloacetate from L-malate in a +ΔG driven by the following highly exergonic step. Where is another place oxaloacetate can come from?
Oxaloacetate can come from transamination of aspartic acid
255
Which has more energy, saturated or unsaturated Fatty Acids?
Saturated because each C has H with it which means more E if reduced
256
What causes the kinds in Fatty Acids?
- Unsaturated fatty acids with double bonds which are found about every 3 carbons
257
More double bonds in a fatty acid:
More double bonds in a fatty acid equates to less likely to be solid at room temperature and increased fluidity
258
Arachidonic acid is a ______________________________ fatty acid. Explain its structure
- Arachidonic acid is an omega-6 fatty acid becuase it has a double bond 6 Carbons _ahead_ of te terminal carbon
259
What determines what type of Omega Fatty acid will be?
The terminal methyl group carbon is call the omega-carbon
Wherever the last double bond ahead of the last carbon in the chain will determine what type of omega fatty acid it is
Like, If 20 carbon long and 6 Carbons ahead is double bond = Omega 6 FA
260
What type of FA is α-Linolenic acid 18:3 (9, 12, 15)?
The FA is 18 carbon long with 3 double bonds
The last double bond is at Carbon 15, meaning 3 C ahead of the terminal methyl carbon
- Omega-3 FA
261
What are the 2 most important FA & why?
Linoleic acid α-Linolenic acid are the most important because they are essential meaning they can only be obtained through diet.
They are found in plants
262
Linoleic acid and α-Linolenic acid are essential fatty acids, what happens if a person is deficient in Linoleic acid?
- Arachidonic acid becomes essential if linoleic acid is deficient in the diet
263
Linoleic acid is a precursor for:
Linoleic acids is a precursor for other shorter and longer omega-**6** fatty acids
264
_________________________________ for other shorter and longer omega-**6** fatty acids
Linoleic acids
265
Arachidonic acid is a substrate for:
Arachidonic acid is a substrate for prostaglandin synthesis
266
This fatty acid is a substrate for prostaglandin synthesis:
Arachidonic acid
267
α-Linolenic Acid is a precursor for:
α-Linolenic Acid is a precursor for omega-3 fatty acids which are important for growth and development
268
What constitutes a short-medium chain fatty acid?
4-10 carbons, generally anything less than 16 Carbons
269
The fatty acid, ________________________________ is a precursor for omega-3 fatty acids which are important for:
-α-Linolenic Acid is a precursor for omega-3 fatty acids which are important for growth and development
270
What constitutes a long chain fatty acid?
- 16-22 Carbons
271
What constitutes very long fatty acids?
More than 22 carbons
272
Where might one find very long chain fatty acids which are generally more than ________ carbons long
- Found in the brain
- Generally longer than 22 C chain
273
What type of fatty acids are commonly found in milk?
Short to medium chain fatty acids
274
What is the major difference between a free fatty acid and a fatty acyl ester?
- Free fatty acid is unesterified meaning it does not have a glycerol backbone
- Fatty acyl esters are esterified meaning they have a glycerol backbone
275
Where are two sources of free fatty acids in the body?
- From TAG in adipose
- From circulating lipoproteins
276
What types of tissues will take up free fatty acids?
Most tissues will consume free fatty acids
277
Free fatty acids can be oxidized, in what tissue particularly?
Free fatty acids are oxidized to provide energy particularly in the liver and muscle
278
Describe the levels of fatty acids in the body
1. Low concentration of free fatty acids in most tissues
2. High level concentration of fatty acids in blood serum **during fasting**
279
List 3 uses for Fatty Acids not including energy production by oxidation.
1. Structural component of cell membranes
2. Conjugation to proteins for membrane anchoring proteins
3. Precursors for hormone-like prostaglandins
280
Transport of _____________ chain fatty acids in the blood serum requires albumin
Transport of long chain fatty acids in the blood serum requires albumin
281
How are fatty acyl esters stored?
- Stored in adipose tissue as TAG
282
What is the significance of fatty acyl esters?
- Serve a major energy reserve for the body
283
What is the funciton of the myenteric plexus?
Control GI motility
284
What is the functions of the submucosal plexus?
Local control in secretion, absorption, contraction of muscularis mucosa
285
What is the effect of Gastrin?
What is the stimulus for release?
- Effect: stimulation of parietal cells to secrete H+ and ECL cells to secrete histamine
- Stimulus: Oligopeptides arriving in gastric antrum
286
What does CCK inhibit?
Where is it from?
- Inhibits gastric empyting and H+ secretion
- From duodenum in response to fatty acid and hydrolyzed protein arrival
287
What endocrine GI hormones stimulate insulin secretion? These cells also inhibit:
GIP & GDP induce insulin secretion and inhibit gastric acid secretion in response to fatty acids and glucose in the intestine
288
Describe a paraesophageal hiatial hernia
- Occurs when a pouch of peritoneum containing part of the funds extends through the esophageal hiatus
- Cardia remains in normal position
- **no regurgitation of of gastric contents**
289
Why does a paraesophageal hiatal hernia not result in regurgitation of gastric contents?
- Cardial orifice of the stoamch remains in place
- Only the funds extends
290
The majority of hiatal hernias are:
The majority of hiatal hernias are sliding
291
What portion of the stomach extends through the esophageal hiatus in a sliding hiatal hernia?
- Portion of the abdominal esophagus,Cardia & parts of the fundus
- Occurring especially when the person lies down or bends over
- Some regurgitation of stomach contents into the esophagus
292
What portion of the stomach extends through the esophageal hiatus in a sliding hiatal hernia?
- Portion of the abdominal esophagus,Cardia & parts of the fundus
- Occurring especially when the person lies down or bends over
- Some regurgitation of stomach contents into the esophagus
293
Much of the duodenum is considered __________________________
Retroperitoneal
294
Compare the vasa recta and arcades in jejunum & ileum
- Jejunum: long vasa recta, few arcades, Larger, site for absorption
- Ileum: shorter vasa recta, many short arcades, site for fluid and electrolyte reabsorption
295
What embryologic tissue gives rise to the epithelium and glands of the gut?
Endoderm of primordial gut gives rise to most of its epithelium and glands
296
What embryologic tissue gives rise to the muscular and connective tissues of the GI?
Splanchnic mesoderm (surrounding primordial gut)
297
What is formed from the midgut cranial embryologic tissue:
In the midgut, the cranial loop gives rise to _small intestine_
298
What arises from the caudal embryologic tissue in the midgut?
Caudal gives rise to large intestine
299
What is a double-bubble sign caused by?
- Dudodenal atresia in utero
- Transverse ultrasound shows 2 bubbles instead of connected stomach and duodenum
- Causes polyhydramnios
300
Accessory pancreatic tissue may be found in:
1. Stomach mucosa
2. Proximal duodenum
3. Jejunum
4. Pyloric antrum
5. Ileal diverticulum (of Meckel)
301
What does this embryologic defect cause:
Failure of rupture of the cloacal membrane and defective development of the urorectal septum
No anal opening
No passing of meconium at birth
302
An infant projectile nonbilious vomiting has a pronounced:
circular layer of pylorus smooth muscle
303
What does the general mesentery contain
Blood supply
Lymphatics
Nerves to viscera
304
The parietal peritoneum becomes inflammed, patients may interpret it in as visceral pain. What is innervation is actually inducing pain?
Dermatomes, somatic afferents
Like for appendix pain, T10 dermatome
305
The ascending and descending colon are:
Secondarily retroperitoneal
306
What structure marks the division of the supracolic and infracolic compartment?
Transverse colon
307
When patients are laying supine, what space of the superior abdomen can fluid accumulate if there is a perforation?
- Right subhepatic region
308
Gastric ulcer + duodenal ulcer = _____________. Gastric ulcers can perforate the posterior wall with accumulation:
- Parietal ulcer
- Accumulation of gas in lesser sac
309
In a paracentesis, what region is fluid drawn from?
Paracolic cutter
310
What is Fitz-Hugh-Curtis syndrome?
Organism from peritoneal cavity through uterine tube and can cause perihepatic inflammation
311
T/F: Aseptic peritonitis involves inflammation from bacteria
False, aseptic!
Can be cuased from bile, sterile materials causing inflammation
- Septic peritonitis is bacterial involvement
312
What are the boundaries of the Epiploic foramen?
Anterior: portal triad-heptic artery, bile duct, & portal vein
Posteriorly: IVC
313
What is a pancreatic pseudocyst?
Fluid collection in the lesser sac due to pancreatitis
314
What is Pringle maneuver?
Compression of the free edge of the lesser omentum to control bleeding from the liver
M1 Block 5
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