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M1 Block 5 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What causes slow waves in the GI tract?

A

Interstitial cells of Cajal induce slow waves that do not induce action potential

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2
Q

What is the neural control of the GI tract?

A
  • 2 plexuses
  • Myenteric plexus
  • Submucosal plexus
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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

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4
Q

What PNS innervates the GI plexuses from the colon to anus?

A

Pelvic N coming off the PNS from S2-S4

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5
Q

What are excitatory NT in the enteric NS?

A

Acetylcholilne
Substance P
Serotonin

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6
Q

What are the inhibitory NT of the enteric NS?

A

VIP & NO

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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
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8
Q

What are some effects of gastric secretion?

A
  • Stimulatory effect
  • Growth of mucosa cells
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9
Q

What cells secrete CCK?
What stimulates CCK?

A
  • CCK released by I cells
  • Stimulated by: Fat, Peptide, A.A. in chyme
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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
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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
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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+
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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
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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
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15
Q

What cells release GIP/GLIP AKA Glucose dependent insulinotropic peptide?

A
  • Released by K cells of duodenum & proximal jujenum
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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
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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

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18
Q

What cells secrete Motilin?

A
  • Released by M-cells of duodenum & proximal jujenum
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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
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20
Q

Somatostatin and Histamine are both paracrine hormones meaning:

A

They are hormones that acts locally and do not enter blood stream

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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
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22
Q

What stimulates the release of histamine in the GI?
What are the downstream effects?

A
  • Stimuli: Gastrin & ACh
  • Effects: Acid secretion
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23
Q

Differentiate Intrinsic control of the GI tract vs Extrinsic control:

A
  • Intrinsic: Enteric NS further specified as myenteric & submucosal plexus
  • Extrinsic: ANS
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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
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25
Q

Where is the submucosal plexus found?
What is its function?

A
  • Located b/t circular smooth muscle (outermost) and epithelium (innermost)
  • Functioning in: secretion, absorption, and contraction of muscularis mucosa
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26
Q

Describe Parasympathetic innervation of the GI

A
  • Upper half-Colon: Vagus N
  • Colon to Anus: Pelvic N through sacral inn. S2-S4
  • Post-ganglions synapse with ENS neurons
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27
Q

Describe the sympathetic innervation of GI

A
  • 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
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28
Q

Describe sensory afferent neurons in the GI

A
  • Dendrites at the epithelium receiving input
  • Info can be sent to submucosal plexus or myenteric plexus or to brain/higher level
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29
Q

Describe Vasovagal reflex:

A
  • Controls gastric motor and secretory activity w/afferent & efferent activity via vagus
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30
Q

The _______________________ do not induce action potential in GI, what does?

A
  • Interstitial cells of Cajal don’t induce AP
  • Induced by Voltage dependent Ca+2 channels
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31
Q

What induces peristalsis? What blocks it?

A
  • Peristalsis can be induced by distention, PNS, or irritation of gut epithelium
  • Can be blocked by atropine
  • Atropine is a ACh blocker
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32
Q

What is Hirshsprung disease?

A

Missing myenteric plexus so no peristalsis can occur

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33
Q

What cells secrete α amylase & lipases?
Describe the saliva composition here

A
  • 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
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34
Q

Describe the modification of saliva through the duct

A
  • 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
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35
Q

Describe how Acinar cells modify saliva

A
  • Acinar cells have CFTR channels where in cAMP causes efflux of Cl- into saliva
  • Na+ follows Cl- to balance charge
  • H20 follows solute gradient
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36
Q

Aside from initiating digestion of starches and lipids, what are some other functions of saliva?

A
  • Allowing tase molecules to dissolve
  • Activate tase receptors
  • Destroy bacteria, has IgA
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37
Q

Why is it important to brush your teeth in the morning?

A
  • Saliva flow decreases during sleeping
  • Since saliva kills bacteria, at night it can build up
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38
Q

What normally induces saliva secretion?
What else can induce saliva secretion?

A
  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
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39
Q

Cystic fibrosis is a mutation of: __________ channel. Inducing what changes to saliva?

A
  • Mutation of CFTR channels which causes saliva have higher content of Ca+, Na+, and proteins
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40
Q

Describe receptive relaxation of stomach:

A

Swallowing center initiates relaxation of stomach smooth muscle to allow storage of food in the stomach

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41
Q

What is achalasia?

A
  • 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
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42
Q

What induces primary peristalsis?

A

Vagus N

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43
Q

What induces secondary peristalsis?

A

Enteric NS

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44
Q

Is contraction or relaxation occurring in the UES during swallowing? What about LES?

A
  • Relax
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45
Q

What are three byproducts of electron transport chain?

A

NAD+
FAD+
H2O

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46
Q

The mitochondria is a double membrane structure, where are complexes?

A
  • All complexes, except Cyt C are within the inner membrane
  • Cytochrome C is located within the inner membrane space
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47
Q

Which layers of the mitochondria are permeable and which are not? Why is this important?

A
  • The outer membrane of the mitochondria is more permeable to allow ions and small molecules in
  • Inner membrane is impermeable to most small molecules
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48
Q

Aside from it’s location, what is special about Cytochrome C?

A

It is closely associated with the inner membrane and is water soluble

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49
Q

What is special about Complex V in the ETC?

A
  1. It is not part of the ETC!
  2. AKA ATP synthase
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50
Q

What enters complex I in the ETC?

A

NADH

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51
Q

What enters complex II in the ETC?

A

FADH 2

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52
Q

Which complexes are associated with cytochromes? What do cytochromes do?

A
  • Cytochromes are heme containing complexes that transfer electrons to its subsequent complex
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53
Q

List three places NADH can be generated to be sent to the ETC

A
  1. Glycolysis
  2. TCA cycle
  3. β oxidation
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54
Q

List where FADH2 can be generation for the ETC

A
  1. β oxidation
  2. TCA cycle when succinate → fumerate
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55
Q

In NADH dehydrogenase, what is creating the energy to pump H+ ions from the ________________________ to the ________________________?

A

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

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56
Q

What is the purpose of CoQ in the ETC?

A

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

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57
Q

Which complexes contribute directly to ATP production in the ETC?

A
  • H+ proton pumping complexes including Complex I, Complex III, and Complex IV
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58
Q

Cytochromes are ________ containing proteins. How does this impact the ETC?

A
  • 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
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59
Q

Describe 4 defining features of Cytochrome C & where it is located

A
  • 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
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60
Q

What is the action of Complex IV in the ETC?

A
  • 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
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61
Q

Define oxidative phosphorylation

A

Coupling oxidation of High E molecules (removing electrons in ETC) with phosphorylation of ADP → ATP utilizing O 2

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62
Q

What creates the E potential of ADP phosphorylation in oxidative phosphorylation?

A
  • 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
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63
Q

Describe the effects of inhibitors on oxygen uptake by mitochondria and ETC function

A
  • 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
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64
Q

What do Barbiturates and Rotenone inhibit in the ETC?

A

Inhibit Complex I

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65
Q

What does Malonate inhibit?

A

Complex II in the ETC

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66
Q

What does Doxorubicin inhibit?

A

CoQ inhibitor

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67
Q

What do Cyanide and carbon moxide inhibit in the ETC?

A

Complex IV

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68
Q

What do uncouplers cause in the ETC?

A
  • Decrease ATP synthesis
  • Increase O 2 consumption
  • Decrease NADH concentration
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69
Q

What causes uncoupling in the ETC?

A
  • Disrupted proton gradient like a proton leak
  • Increase rate of O 2 consumption with no ATP synthesis
  • Causes energy to be released as heat
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70
Q

What is a “natural” uncoupler of ETC & why?

A

Brown fat because it expresses Thermogenin that dissipates H+ gradient
- Energy used for generation of heat instead of ATP

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71
Q

Define Uncoupling in ETC

A

Uncoupling the electron transport system from the complex V ATP synthase by proton motive force generated in inner membrane space

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72
Q

What is the physiologic mechanism for fat burning in uncoupling of ETC

A
  • 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
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73
Q

How does brown fat generate heat?

A
  • has lots of small lipid droplets where you can very rapidly metabolize lipids
  • causes very rapidly flow electrons to the electron transport system
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74
Q

Name 2 synthetic uncouplers of the ETC

A
  1. Aspirin
  2. 2,4-Dinitrophenol
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75
Q

Describe an amino sugar

A

amino group at position 2
+ charge at physiologic pH
balanced with acetyl group

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76
Q

List types of monosaccharides

A
  • Derived monosaccharides: Deoxy-sugars, amino-sugars, sugar alcohols, phosphorylated and sulfated sugars
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77
Q

Describe sugar alcohols & what they are

A
  • Sugar alcohols are a type of derived monosaccharide
  • Reduced carbonyl carbon (aldehyde or ketone group)
  • Want to be associated with water
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78
Q

What is the most abundant monosaccharide in living cells?

A

Pentoses & hexoses

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79
Q

What links 2 monosaccharides?

A
  • Diasaccharides are linked by a glycosidic bond
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80
Q

What is the linkage of lactose?

A

Galactose + glucose via β (1-4) glycosidic bond

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81
Q

What is the linkage of sucrose?

A

Glucose + fructose via α (1-2) glycosidic bond

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82
Q

What is the linkage of maltose?

A

Glucose + glucose via α (1-4) glycosidic bond

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83
Q

What is the basic defining feature of oligosaccharides?

A

3-10 monosaccharides linked by glycosidic bond

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84
Q

What are the two classes of oligosaccharides?

A

N-linked oligosaccharides & O-linked oligosaccharides

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84
Q

Describe the basic structure of an N-linked oligosaccharide

A
  • Attached to polypeptide by an N-glycosidic bond with the side chain amide group of the amino acid asparagine
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85
Q

Describe the basic structure of an O-linked oligosaccharide

A
  • Attached to the side chain hydroxyl group of amino acid serine or threonine in polypeptide chains or the hydroxyl group of membrane lipids
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86
Q

What is the purpose of polysaccharides?

A
  • Storage forms of energy or structural materials
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87
Q

What are the two chief constituents of starch?

A
  • Amylose
  • Amylopectin
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88
Q

Compare the branching in amylopectin and amylose

A
  • Amylose is non-branched and helical in structure
  • Amylopectin is branched & composed of α (1-4) glycosidic bond & α (1-6) glycosidic bond
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89
Q

What are the bonds between monosaccharides in amylopectin?
What are the bonds at branch points in amylopectin?

A

α (1-4) glycosidic bond b/t monosaccharides
α (1-6) glycosidic bond at branch points

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90
Q

Compare the bonds between glycogen and amylopectin

A

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!

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91
Q

What does cellulose do in humans? What is cellulose?

A
  • 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
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92
Q

A cyclic sugar can be opened where:

A

A cyclic sugar has the ability to open at the anomeric carbon (the carbonyl carbon in linear form)

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93
Q

All _______________ have reducing ability. What does this mean?

A
  • 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+
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94
Q

What test can determine if a carbohydrate is reducible?

A

Benedicts reagent changes color in the presence of reducing sugars whether they be monosaccharides, disaccharides, etc

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95
Q

Describe how a disaccharide can be a reducible sugar?

A
  • If at least one sugar has anomeric carbon with -OH group not linked to another compound by glycosidic bond
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96
Q

How do α amylases digest carbohydrates?

A
  • 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
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97
Q

How does pancreatic α amylase digest carbohydrates?

A
  • Break down of α (1-4) glycosidic bonds only
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98
Q

What plasma level can indicate pancreatitis if increased?

A
  • Plasma levels of either pancreatic amylase or total amylase are used as diagnostic marker for pancreatitis
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99
Q

Where are monosaccharides absorbed in the small intestine?

A

In duodenum and jejunem

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100
Q

What do sucrase/isomaltase do?

A
  • 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
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101
Q

What does maltase-glucoamylase (MGA) do?

A
  • 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
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102
Q

What does Lactase do?

A
  • Cleaves β (1-4) glycosidic bonds in lactose
  • Works on luminal surface of the intestinal mucosal cells
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103
Q

What does Trehalase do?

A
  • Works on luminal surface of the intestinal mucosal cells
  • Cleaves α (1-1) in trehalose (mushrooms & fungi)
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104
Q

What three transporters are involved in the absorption of monosaccharides in the duodenum & upper jejunum?

A
  • SGLT-1
  • GLUT-5
  • GLUT-2
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105
Q

Where and what is SGLT-1 transporter?

A
  • Involved in absorption of monosaccharides in the jejunum and duodenum
  • On the apical/lumenal surface
  • Transports Glucose and galactose using active transport
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106
Q

Where and what is GLUT-5 transporter?

A
  • On the apical/lumenal surface of brush border in the duodenum and upper jejunum
  • Passively absorbs fructose
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107
Q

How do glucose, galactose and fructose get into circulation from the small intestine?

A
  • Via absorption through GLUT-2 transport on the basal surface of cells of the duodenum & upper jejunum
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108
Q

If _________________ get into the large intestine they can cause diarrhea by what mechanism?

A
  • 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
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109
Q

What test can be used to determine if carbohydrates are not being absorbed by the body?

A
  • Can measure H 2 gas in breath
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110
Q

What causes sucrose intolerance?

A
  • Sucrase-isomaltase complex deficiency
  • Autosomal recessive disorder
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111
Q

What does GLUT-1 do and where is it found?

A
  • Found in most tissues
  • Largely abundant in brain and RBC
  • Basal uptake of glucose
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112
Q

What digests proteins in the stomach?

A

Pepsin

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113
Q

What digests proteins in the stomach?

A

Pepsin

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114
Q

What proteases are released from the pancreas?

A
  • Trypsin
  • Chymotrypsin
  • Elastase
  • Carboxypeptidases
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115
Q

What proteases are found in the small intestine?

A

Enteropeptidase
Aminopeptidase
Dipeptidase
Tripeptidase

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116
Q

What is the difference between endopeptidases & exopeptidases?

A
  • Endopeptidases: break down peptide bonds of nonterminal amino acids
  • Exopeptidases: catalyze cleavage of the terminal peptide bonds
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117
Q

Pepsinogen is:

A
  • Pepsinogen is a zymogen
  • Activated by acid or pepsin in the stomach for digestion of proteins
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118
Q

CCK is:

A

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

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119
Q

_________________ is produced by the S cells of the duodenum. Its purpose is:

A
  • 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
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120
Q

Where is enteropeptidase & what does it do?

A
  • Enteropeptidase is produced in the cells of the duodenum
  • Cleaves trypsinogen from the pancreas into trypsin for proteolysis
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121
Q

Pancreatic insufficiency would cause a significant decrease in the:

A

Decrease in the digestion & subsequent absorption of proteins in the duodenum

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122
Q

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?

A
  • 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
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123
Q

What is cystinuria?

A
  • 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
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124
Q

What is Hartnup disease?

A
  • Inherited disorder with intestinal defects of nonpolar amino acids absorption and urinary wastage
  • Sx. include Diarrhea, Dementia (hallucinations), dermatitis
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125
Q

Where are the main stores of glycogen found?

A
  • Skeletal muscle
  • Liver
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126
Q

What organ mainly supplies glycogen during fasting?

A
  • Liver senses blood glucose level and maintains blood glucose during early fasting
127
Q

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

128
Q

What does glycogen have to do with weight?

A
  • Glycogen storage is associated with significant amounts of water storage there for weight can vary significantly based on the amount of glycogen stored
129
Q

Describe the structure of glycogen

A
  • 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
Q

Inside the organ, where does glycogen reside?

A
  • Large molecules of glycogen exist as discrete cytoplasmic granules (β-particles)
131
Q

Which kinase is in the liver for transformation of glucose to Glucose-6-phospate? Why?

A
  • Glucokinase has a lower affinity for glucose so that the liver can contribute to blood glucose levels
132
Q

After forming G-6-P, what is the second step for glycogenesis?

A
  • 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
Q

After the synthesis of Uridine-Glucose, what is the next step in glycogenesis?

A
  • 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
Q

What is the importance of Glycogenin+Tyr?

A
  • 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
Q

What are 2 significant molecules in glycogenesis?

A
  • Glycogen synthase
  • Branching enzyme
136
Q

After the initial building/priming of UDP-glucose, what continues to build the α (1,4) glycosidic bonds? Is this a significant step & why?

A
  • 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
Q

Describe the steps of how branching enzyme forms α (1,____) glycosidic bonds in glycogenesis

A
  • 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
Q

What is the significance of the branching in glycogen?

A
  • Increases the solubility of glycogen molecules
  • Increases the number of nonreducing ends that allow for faster synthesis and degradation
139
Q

List 3 important enzymes used in Glycogenolysis

A
  • Debranching enzyme
  • Glycogen phosphorylase (rate limiting)
  • Glucose-6-phosphatase
140
Q

Contrast glycogenolysis in skeletal muscle vs liver:

A
  • 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
Q

T/F: Glycogen breakdown begins by removing each chain from the molecule that can then be broken down further by glycogen phosphorylase

A

False, start by removing α (1,4) glycosidic bonds

142
Q

What vitamin is Pyridoxal phosphate (_____) derived from?

A

Derived from B 6

143
Q

This enzyme is the first step & rate limiting step in Glycogenolysis. It requires the cofactor __________________ _____________ which is a derivative of Vit B 6

A
  • 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
Q

What specifically does glycogen phosphorylase do in glycogenolysis?

A
  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
Q

After α (1,4) glycosidic bonds are largely removed from glycogen, how are branches removed in glycogenolysis?

A
  1. 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
Q

What are the two activities of debranching enzyme in ____________________________

A

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
Q

What is the last step of glycogenolysis that occurs in both liver and skeletal muscle tissue?

A
  • Phosphoglucomutase will transform Glucose-1-P into Glucose 6-P
  • This is the last step of glycogenolysis in muscle
148
Q

What is a cofactor of Phosphoglucomutase in Glycogenolysis?

A
  • Glucose 1,6-bisphosphatase is an intermediate of Phosphoglucomutase and activates the enzyme
149
Q

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?

A
  • 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
Q

Epinephrine is released for _________________________, insulin is released for _________________.

A

Epinephrine is released to induce glycogenolysis
Insulin is released for glycogenesis

151
Q

Which NT acts oppositely to insulin and glycogenesis that insulin induces?

A

Epinephrine since it induces glycogenolysis
&
Glucagon

152
Q

Glycogen synthase:
Glycogen phosphorylase:
Regulation of these enzymes is maintained by two major mechanisms:
1.
2.

A

Glycogen synthase: glycogenesis
Glycogen phosphorylase: glycogenolysis
Regulation of these two enzymes is maintained by two major mechanisms:
1. Hormonal regulation
2. Allosteric regulation

153
Q

Contrast the hormonal vs. Allosteric regulation of glycogen synthase in ____________________________.

A
  • Glycogen synthase is Glycogenolysis
  • In Hormonal: epinephrine & glucagon inhibit. While Insulin activates
  • In allosteric: activated by Glucose 6-P
154
Q

Contrast the hormonal vs. Allosteric regulation of glycogen phosphorylase in ____________________________.

A
  • 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
Q

What enzyme is deficient in Von Gierke (__________________________________)

A
  • Von Gierke is Glycogen Type I storage disease
  • Deficient in Glucose-6-Phosphatse in the liver and kidneys
156
Q

The following symptoms are indicative of:
- Severe fasting hypoglycemia
- Lactic acidosis
- Hepatomegaly
- Hyperlipidemia
- Hyperuricemia
- Short stature

A

Von Gierke/Type Ia glycogen storage disease

157
Q

Contrast Type Ia vs. Type Ib glycogen storage disease

A

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
Q

Glycogen storage disease Type II: __________________________________. What is deficient?

A
  • GSD Type II is AKA Pompe disease
  • Deficient in Lysosomal alpha glucosidase
159
Q

Pompe disease is ____________________________________________. Caused by a deficiency in Lysosomal alpha glucosidase which causes:

A
  • Glycogen storage disease type II
  • Excess glycogen concentrations in abnormal vacuoles of lysosomes
  • Cardiomegaly
  • Early death in infants
160
Q

Glycogen storage disease Type III/________________________________ is caused by a deficiency of:

A
  • GSD Type III: Cori disease
  • Caused by a deficiency of Debranching enzyme
161
Q

Cori disease aka ___________________________ is caused by a deficiency of debranching enzyme which causes:

A
  • Cori disease AKA glycogen storage disease type III
  • Causes mild hypoglycemia
  • Liver enlargement due to accumulation of glycogen
162
Q

Glycogen storage disease type IV aka ___________________________ is caused by a deficiency of:

A
  • Glycogen storage disease type IV AKA Anderson disease
  • Lack of branching enzyme
163
Q

Anderson disease aka ____________________________ is very rare and due to deficiency of branching enzyme. Its associated symptoms are:

A
  • 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
Q

Type V glycogen storage disease aka ____________________________ is caused by deficiency of:

A

Type V glycogen storage disease aka McArdle Disease is a deficiency of muscle glycogen phosphorylase (muscle only!)

165
Q

McArdle disease aka ___________________________________________ is caused by deficiency of glycogen phosphorylase in muscle only. Associated symptoms include:

A
  • 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
Q

Glycogen storage disease type VI aka _______________________ is a deficiency of:

A

GSD TVI is aka Hers disease
- Caused by a deficiency of hepatic glycogen phosphorylase

167
Q

Glycogen storage disease type VI is ______________________________________. Caused by a deficiency of Hepatic glycogen phosphorylase with associated symptoms:

A
  • GSD VI is Hers disease
  • Mild fasting hypoglycemia
  • Hepatomegaly & cirrhosis
168
Q

What is Lafora disease and why does it cause progressive myoclonic epilepsy?

A
  • 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
Q

Other than muscle, kidney, and liver, where else can glycogen be found?

A

Lysosomes
About 1-3% of glycogen is here

170
Q

Where does glycolysis occur?

171
Q

What is the product of aerobic glycolysis?
What is the product of anaerobic glycolysis?

A
  • 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
Q

Glycolysis requires: NADH or NAD+?

A
  • anaerobic glycolysis requires NAD+ and generates NAHD to send to the ETC
173
Q

Why is pyruvate converted to lactate in anaerobic ___________________________.

A

In anaerobic glycolysis, pyruvate is converted to lactate so that NAD+ can be regenerated to send back through glycolysis

174
Q

What are the two states of glycolysis?

A

1st phase is energy investment
2nd phase is energy generating phase

175
Q

Where does the energy investment phase begin in glycolysis & when does it end?

A
  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
Q

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?

A
  • 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
Q

What step of glycolysis generates NADH?

A

When G3P is converted into Glycerate-1,3-Bisphosphate by Glyceraldehyde-3-phosphate dehydrogenase in the energy generating phase

178
Q

What steps of glycolysis generate ATP?

A
  • During second phase of Glycolysis
  • When glucose-1,6-bisphosphate is broken down into G3P & When PEP is converted into Pyruvate
179
Q

What are the major enzymes taking part in the second portion of glycolysis?

A
  • 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
Q

What is Hexokinase IV?

A

Hexokinase IV = Glucokinase which is present in the liver and pancreas and has lower affinity for glucose

181
Q

Describe the V max & K m for Glucokinase

A
  • 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
Q

Where is glucokinase found? What is another name for it?

A

-Glucokinase is Hexokinase IV
- Found in β-pancreatic cells

183
Q

What does low K m mean?

A

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
Q

When Hexokinases have low V max what does this contribute to?

A
  • 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
Q

What inhibits Glucokinase?

A
  • Nothing technically
  • Indirectly inhibited by Fructose-6-phosphate
  • Indirectly stimulated by glucose
186
Q

What is MODY?

A
  • Maturity-onset diabetes of the young
  • A mutation of Glucokinase induces diabetes rare
187
Q

What is the committing step of glycolysis?

A

When PFK-1 transforms Fructose-6-phosphate into Fructose-1,6-bisphosphate

188
Q

What are inhibitors of PFK-1? Why?

A
  • 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
Q

What is a stimulator of PFK-1? Why?

A
  • AMP
  • Fructose-2,6 Bisphosphate which is a product of PFK-2
190
Q

What is the significance of isomerization of dihydroacetone-P?

A

This is when DHAP is transformed into G3P so that glycolysis can continue

191
Q

What does arsenic have to do with Glyceraldehyde-3-P dehydrogenase?

A
  • 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
Q

What is a modification of glycolysis pathway that is prevalent only in RBC?

A
  • RBC’s generate & Protect (through a side reaction) 2,3-BPG
193
Q

Where in the glycolytic pathway does substrate level phosphorylation occur?

A
  • When phosphoenolpyruvate is turned into pyruvate by pyruvate kinase and generates ATP in the process
194
Q

Fructose 1,6 bisphosphate is an _____________________ ___________________ of pyruvate kinase & why?

A

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
Q

What type of receptor does glucagon bind to?

A

G α s & thus phosphorylates things & can induce transcription

196
Q

Glucagon binds to G α s. Explain how this effects pyruvate kinase in the glycolytic pathway during fasting:

A
  • 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
Q

What is the status of Pyruvate kinase when it is phosphorylated?

198
Q

What is the status of pyruvate kinase when it is dephosphorylated?

199
Q

What is the status of pyruvate kinase when there is insulin released in the body

A

Dephosphorylated so that the body can use the incoming glucose for energy

200
Q

______________________ is only active in the liver in a well-fed state meaning there is high glucose availability

A

Pyruvate kinase is only active in the liver in the well-fed state when glucose levels are high

201
Q

Deficiencies of pyruvate kinase affect _____________________ the most. Why?

A
  • Deficiencies of pyruvate kinase affect RBCs the most
  • This is because they rely on glycolysis for energy production and maintenance of shape
202
Q

What are the two most common causes of hemolytic anemia?

A
  1. Glucose-6-phosphate dehydrogenase w/Heinz body presence
  2. Pyruvate kinase deficiency w/out Heinz body presence
203
Q

What happens in pyruvate kinase deficiency?

A
  • The RBCs become misshaped and damaged so they are lysed
  • Hemolytic anemia
204
Q

What is the fate of glycolysis products in the presence of oxygen and mitochondria?

A
  • 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
Q

what is the fate of glycolysis products in anaerobic conditions?

A
  • Pyruvate will be reduced to lactate by lactate dehydrogenase (reversible step)
206
Q

What does pyruvate carboxylase generate when acting on pyruvate?

A
  • Generates TCA cycle intermediates for use in gluconeogenesis
207
Q

Where is lactate production normal?

A
  • In RBC & exercising skeletal muscle
208
Q

Cells can handle some generation of pyruvate, how?
What does excessive lactate buildup induce?

A
  • 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
Q

Describe the hormonal regulation of glycolysis

A
  • 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
Q

What are the three key steps in the TCA cycle?
Why are they the key steps?

A
  1. Citrate synthase
  2. Isocitrate dehydrogenase
  3. α-ketoglutarate dehydrogenase
    - They are key steps because they are not reversible
211
Q

Where does the TCA cycle take place?

A

Mitochondrial matrix

212
Q

What are two major purposes of the TCA cycle?

A
  • 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
Q

How does pyruvate enter the TCA cycle?

A

Must be converted from Pyruvate to Acetyl CoA by pyruvate dehydrogenase complex

214
Q

What happens in the PDH?

A
  • Pyruvate Dehydrogenase Complex
  • ## Pyruvate is transformed into 2 Acetyl Co-A with the generation of NADH & CO 2
215
Q

What is the status of PDH (________________) when it is phosphorylated?

A

Pyruvate dehydrogenase complex is inactive when it is phosphorylated

216
Q

What is the status of PDH (________________) when it is dephosphorylated?

A

When pyruvate dehydrogenase complex is dephosphorylated it becomes active

217
Q

Pyruvate dehydrogenase complex can be regulated by substrate activation & product inhibition. Discuss substrate activation

A
  • 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
Q

What is the significance of PDH kinase & PDH phosphatase?

A
  • 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
Q

WhatPyruvate dehydrogenase complex can be regulated by substrate activation & product inhibition. Discuss product inhibition

A
  • 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
Q

What stimulates PDH phosphatase & what does it do?

A
  • 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
Q

The PDH complex requires 5 cofactors. List the cofactor originator

A
  1. Vitamin B1
  2. Vitamin B5
  3. Vitamin B2
  4. Vitamin B3/niacin
  5. Lipoamide
222
Q

What is thamine?

A

Vitamin B1

223
Q

Thiamine pyrophosphate, TPP is a derivative of:
It is important in:

A

TPP is a derivative of Vitamin B1
It is a cofactor of Pyruvate dehydrogenase complex

224
Q

What is pantothenic acid?

A

Vitamin B5

225
Q

What is the precursor of Coenzyme-A?
It is a cofactor of:

A

Pantothenic Acid/Vitamin B5
Coenzyme A is a cofactor of the PDH complex

226
Q

What is riboflavin?

A

Vitamin B2

227
Q

FAD is a cofactor of the pyruvate dehydrogenase complex. What is it derived from?

A

FAD is derived from Vitamin B2

228
Q

NAD+ is a cofactor of the pyruvate dehydrogenase complex. What is it derived from?

A

Vitamin B3/niacin

229
Q

Thiamine deficiency is commonly seen in 2 populations:

A
  • Persons with alcoholism
  • Dietary deficient due to malnutrition, prolonged IV therapy, GI Disorders)
230
Q

What is the clinical presentation of Thiamine deficiency?

A

BeriBeri can be wet or dry type or infantile type

231
Q

Beri Beri is a clinical presentation of ____________________________. What are the associated symptoms of wet Beri Beri

A
  • Beri Beri is a TPP deficiency affecting the PDH complex system since TPP is a cofactor
  • Wet: cardiovascular system problems
232
Q

Beri Beri is a clinical presentation of ____________________________. What are the associated symptoms of dry Beri Beri

A
  • 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
Q

Beri Beri is a clinical presentation of ____________________________. Discuss infantile Beri Beri.

A
  • 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
Q

What is Wernicke-Korsakoff’s syndrome?

A
  • 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
Q

PDH complex requires cofactor: ______________ which is derived from niacin/____________________. Deficiency of this cofactor results in:

A

PDH complex requires cofactor NAD+ which is derived from niacin/Vitamin B3. Deficiency of this cofactor results in the clinical disorder: Pellagra

236
Q

What is Pellagra & what causes it?

A
  • 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
Q

PDH complex requires this cofactor: ___________________ which is derived from Vitamin B2. Deficiency of this cofactor results in:

A
  • FAD is made from Vitamin B2/Riboflavin
  • Results clinical manifestations: Angular stomatitis, Cheilosis, Glossitis
238
Q

What is the initial entering step of the TCA cycle:

A
  • In the mitochondrial matrix the acetyl co a enters and rapidly joins oxaloacetate which is converted to citrate by citrate synthetase
239
Q

Aconitase is an enzyme of the TCA cycle responsible for:
What are 2 unique things about it?

A

Aconitase is responsible for isomerization of citrate to isocitrate
- This enzyme is reversible
- It is a Fe-S protein

240
Q

Fluoroacetate is a plant toxin that inhibits this enzyme: __________________________________ which is present in the TCA cycle & is responsible for:

A
  • 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
Q

The oxidative decarboxylation by _________________________________ to yield α-ketoglutarate from isocitrate also generates:

A

The oxidative decarboxylation by isocitrate dehydrogenase to yield α-ketoglutarate from isocitrate also generates NADH & CO 2

242
Q

What is the significance of the enzyme isocitrate dehydrogenase in the TCA cycle?

A
  • Is an irreversible and rate limiting step
  • Regulated allosterically
243
Q

Isocitrate dehydrogenase yields _________________________ from ____________________________. It is allosterically regulated by:

A

Isocitrate dehydrogenase yields α-ketoglutarate from isocitrate. It is allosterically regulated by: ATP & NADH AS INHIBITORS
- ADP & Ca+2 as ACTIVATORS

244
Q

Oxidative decarboxylation of α-ketoglutarate is performed by what enzyme and yields _______________________ in the TCA cycle.

A

Oxidative decarboxylation of α-ketoglutarate is performed by the enzyme α-ketoglutarate dehydrogenase and yields Succinyl CoA in the TCA cycle.

245
Q

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?

A
  • Also produces CO 2 and an NADH
  • Has coenzymes: TPP, Lipoic acid, FAD, NAD+, and CoA
246
Q

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?

A
  • inhibited by: its products
  • activated by: Ca+2
  • Coenzymes: TPP, Lipoic acid, FAD, NAD+, CoA
247
Q

Other than α-ketoglutarate dehydrogenase in the TCA yielding Succinyl CoA, where else can Succinyl CoA come from for entry into the TCA?

A
  • Succinyl CoA can be derived from propionyl CoA which comes from Fatty acid synthesis
248
Q

__________________ ______________________ forms a stable thiol with the -SH group in lipoic acid making it unavailable to serve as a coenzyme

A

Arsenic poisoning

249
Q

Other than isocitrate dehydrogenase generating α-ketoglutarate from isocitrate, where else can α-ketoglutarate come from?

A

α-ketoglutarate can be generated from the metabolism of glutamate

250
Q

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?

A
  • GTP which can be ready transformed into ATP
  • CoA
251
Q

Fumarate is formed in a reversible step of the TCA by the enzyme Fumerase. Fumarate is also produced in:

A
  1. Urea cycle
  2. Purine synthesis
  3. Phe & Tyr Catabolism
252
Q

The final step that regenerates Oxaloacetate has a +ΔG. The enzyme performing this action is:
What drives this reaction with the +ΔG?

A
  • 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
Q

What step of the TCA is the last generator of NADH?

A
  • Malate Dehydrogenase makes Oxaloacetate from L-malate
254
Q

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?

A

Oxaloacetate can come from transamination of aspartic acid

255
Q

Which has more energy, saturated or unsaturated Fatty Acids?

A

Saturated because each C has H with it which means more E if reduced

256
Q

What causes the kinds in Fatty Acids?

A
  • Unsaturated fatty acids with double bonds which are found about every 3 carbons
257
Q

More double bonds in a fatty acid:

A

More double bonds in a fatty acid equates to less likely to be solid at room temperature and increased fluidity

258
Q

Arachidonic acid is a ______________________________ fatty acid. Explain its structure

A
  • Arachidonic acid is an omega-6 fatty acid becuase it has a double bond 6 Carbons ahead of te terminal carbon
259
Q

What determines what type of Omega Fatty acid will be?

A

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
Q

What type of FA is α-Linolenic acid 18:3 (9, 12, 15)?

A

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
Q

What are the 2 most important FA & why?

A

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
Q

Linoleic acid and α-Linolenic acid are essential fatty acids, what happens if a person is deficient in Linoleic acid?

A
  • Arachidonic acid becomes essential if linoleic acid is deficient in the diet
263
Q

Linoleic acid is a precursor for:

A

Linoleic acids is a precursor for other shorter and longer omega-6 fatty acids

264
Q

_________________________________ for other shorter and longer omega-6 fatty acids

A

Linoleic acids

265
Q

Arachidonic acid is a substrate for:

A

Arachidonic acid is a substrate for prostaglandin synthesis

266
Q

This fatty acid is a substrate for prostaglandin synthesis:

A

Arachidonic acid

267
Q

α-Linolenic Acid is a precursor for:

A

α-Linolenic Acid is a precursor for omega-3 fatty acids which are important for growth and development

268
Q

What constitutes a short-medium chain fatty acid?

A

4-10 carbons, generally anything less than 16 Carbons

269
Q

The fatty acid, ________________________________ is a precursor for omega-3 fatty acids which are important for:

A

-α-Linolenic Acid is a precursor for omega-3 fatty acids which are important for growth and development

270
Q

What constitutes a long chain fatty acid?

A
  • 16-22 Carbons
271
Q

What constitutes very long fatty acids?

A

More than 22 carbons

272
Q

Where might one find very long chain fatty acids which are generally more than ________ carbons long

A
  • Found in the brain
  • Generally longer than 22 C chain
273
Q

What type of fatty acids are commonly found in milk?

A

Short to medium chain fatty acids

274
Q

What is the major difference between a free fatty acid and a fatty acyl ester?

A
  • 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
Q

Where are two sources of free fatty acids in the body?

A
  • From TAG in adipose
  • From circulating lipoproteins
276
Q

What types of tissues will take up free fatty acids?

A

Most tissues will consume free fatty acids

277
Q

Free fatty acids can be oxidized, in what tissue particularly?

A

Free fatty acids are oxidized to provide energy particularly in the liver and muscle

278
Q

Describe the levels of fatty acids in the body

A
  1. Low concentration of free fatty acids in most tissues
  2. High level concentration of fatty acids in blood serum during fasting
279
Q

List 3 uses for Fatty Acids not including energy production by oxidation.

A
  1. Structural component of cell membranes
  2. Conjugation to proteins for membrane anchoring proteins
  3. Precursors for hormone-like prostaglandins
280
Q

Transport of _____________ chain fatty acids in the blood serum requires albumin

A

Transport of long chain fatty acids in the blood serum requires albumin

281
Q

How are fatty acyl esters stored?

A
  • Stored in adipose tissue as TAG
282
Q

What is the significance of fatty acyl esters?

A
  • Serve a major energy reserve for the body
283
Q

What is the funciton of the myenteric plexus?

A

Control GI motility

284
Q

What is the functions of the submucosal plexus?

A

Local control in secretion, absorption, contraction of muscularis mucosa

285
Q

What is the effect of Gastrin?
What is the stimulus for release?

A
  • Effect: stimulation of parietal cells to secrete H+ and ECL cells to secrete histamine
  • Stimulus: Oligopeptides arriving in gastric antrum
286
Q

What does CCK inhibit?
Where is it from?

A
  • Inhibits gastric empyting and H+ secretion
  • From duodenum in response to fatty acid and hydrolyzed protein arrival
287
Q

What endocrine GI hormones stimulate insulin secretion? These cells also inhibit:

A

GIP & GDP induce insulin secretion and inhibit gastric acid secretion in response to fatty acids and glucose in the intestine

288
Q

Describe a paraesophageal hiatial hernia

A
  • 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
Q

Why does a paraesophageal hiatal hernia not result in regurgitation of gastric contents?

A
  • Cardial orifice of the stoamch remains in place
  • Only the funds extends
290
Q

The majority of hiatal hernias are:

A

The majority of hiatal hernias are sliding

291
Q

What portion of the stomach extends through the esophageal hiatus in a sliding hiatal hernia?

A
  • 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
Q

What portion of the stomach extends through the esophageal hiatus in a sliding hiatal hernia?

A
  • 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
Q

Much of the duodenum is considered __________________________

A

Retroperitoneal

294
Q

Compare the vasa recta and arcades in jejunum & ileum

A
  • Jejunum: long vasa recta, few arcades, Larger, site for absorption
  • Ileum: shorter vasa recta, many short arcades, site for fluid and electrolyte reabsorption
295
Q

What embryologic tissue gives rise to the epithelium and glands of the gut?

A

Endoderm of primordial gut gives rise to most of its epithelium and glands

296
Q

What embryologic tissue gives rise to the muscular and connective tissues of the GI?

A

Splanchnic mesoderm (surrounding primordial gut)

297
Q

What is formed from the midgut cranial embryologic tissue:

A

In the midgut, the cranial loop gives rise to small intestine

298
Q

What arises from the caudal embryologic tissue in the midgut?

A

Caudal gives rise to large intestine

299
Q

What is a double-bubble sign caused by?

A
  • Dudodenal atresia in utero
  • Transverse ultrasound shows 2 bubbles instead of connected stomach and duodenum
  • Causes polyhydramnios
300
Q

Accessory pancreatic tissue may be found in:

A
  1. Stomach mucosa
  2. Proximal duodenum
  3. Jejunum
  4. Pyloric antrum
  5. Ileal diverticulum (of Meckel)
301
Q

What does this embryologic defect cause:
Failure of rupture of the cloacal membrane and defective development of the urorectal septum

A

No anal opening
No passing of meconium at birth

302
Q

An infant projectile nonbilious vomiting has a pronounced:

A

circular layer of pylorus smooth muscle

303
Q

What does the general mesentery contain

A

Blood supply
Lymphatics
Nerves to viscera

304
Q

The parietal peritoneum becomes inflammed, patients may interpret it in as visceral pain. What is innervation is actually inducing pain?

A

Dermatomes, somatic afferents
Like for appendix pain, T10 dermatome

305
Q

The ascending and descending colon are:

A

Secondarily retroperitoneal

306
Q

What structure marks the division of the supracolic and infracolic compartment?

A

Transverse colon

307
Q

When patients are laying supine, what space of the superior abdomen can fluid accumulate if there is a perforation?

A
  • Right subhepatic region
308
Q

Gastric ulcer + duodenal ulcer = _____________. Gastric ulcers can perforate the posterior wall with accumulation:

A
  • Parietal ulcer
  • Accumulation of gas in lesser sac
309
Q

In a paracentesis, what region is fluid drawn from?

A

Paracolic cutter

310
Q

What is Fitz-Hugh-Curtis syndrome?

A

Organism from peritoneal cavity through uterine tube and can cause perihepatic inflammation

311
Q

T/F: Aseptic peritonitis involves inflammation from bacteria

A

False, aseptic!
Can be cuased from bile, sterile materials causing inflammation
- Septic peritonitis is bacterial involvement

312
Q

What are the boundaries of the Epiploic foramen?

A

Anterior: portal triad-heptic artery, bile duct, & portal vein
Posteriorly: IVC

313
Q

What is a pancreatic pseudocyst?

A

Fluid collection in the lesser sac due to pancreatitis

314
Q

What is Pringle maneuver?

A

Compression of the free edge of the lesser omentum to control bleeding from the liver

M1 Block 5 (3 decks)

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