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Unit 4 GNA > LGS Week 5, 6, 7 > Flashcards

LGS Week 5, 6, 7 Flashcards

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1
Q

What are the counterregulatory hormones of insulin?

A

Glucagon, Epinephrine, Cortisol

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2
Q

Glucagon maintains blood glucose levels during the [a] state by activating [b]

A

a. Fasting

b. gluconeogenesis and glycogenolysis in liver, FA and glycerol release from adipose

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3
Q

Epinephrine mobilizes fuel during [a] by stimulating [b]

A

a. acute stress or exercise

b. glycogenolysis from muscle and liver, FA and glycerol release from adipose

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4
Q

Cortisol provides fuel during [a] by stimulating [b]

A

a. Stress, illness, trauma

b. AA mobilization and glucose uptake in muscle, gluconeogenesis in liver, FA and glycerol release from adipose, and inhibits insulin secretion from B cells, increases glucagon secretion by a-cells

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5
Q

Highly vascularized clusters of pancreatic endocrine cells

A

Islets of Langerhans

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6
Q

a-cells produce

A

Glucagon

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7
Q

B-cells produce

A

Insulin

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8
Q

The cluster of cells in the center is called [a] and the surrounding cells are [b]

A

a. Islet of Langerhans
b. Pancreatic acini

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9
Q

Preproglucagon is expressed as a long peptide which is eventually processed down into what smaller peptides

A

Glucagon
GRPP
IP1
Major Proglucagon fragment (GLP-1/2)

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10
Q

Glucagon secretion from a-cells is stimulated by

A
  1. Hypoglycemia
  2. Epinephrine/Cortisol
  3. Acetylcholine
  4. High AA
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11
Q

Glucagon secretion is inhibited by

A
  1. Hyperglycemia
  2. GLP1
  3. Insulin
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12
Q

Explain Glucagon’s MOA on glycogenolysis

A

Glucagon is stimulated by low blood sugar –> binds to GPCR (Gas) –> activation of Adenylate cyclase –> activation of cAMP –> stimulation of PKA –> activates Glycogen Phosphrylase –> stimulates conversion of glycogen to glucose through glycogenolysis

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13
Q

What effects does Glucagon have on hepatic metabolism?

A

Decreases: Glycolysis, Glycogenesis, and FA Biosynthesis – stops glucose from becoming anything other than glucose

Increases: Gluconeogenesis, Glycogenolysis, FA Oxidation – builds glucose from other molecules and builds FA to fuel the liver

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14
Q

What effects does Glucagon have on Adipocyte metabolism?

A

Decrease: Lipogenesis – stops glucose from becoming TG

Increase: Lipolysis - increased FA/glycerol release –> increased B-oxidation, ketogenesis, and gluconeogenesis in liver

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15
Q

What effects does Glucagon have on Skeletal muscle metabolism?

A

No effect

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16
Q

What is secreted with insulin that can be used as an index of secretory capacity of the endocrine pancreas?

A

C-peptide

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17
Q

Explain the MOA of insulin release

A

Hyperglycemia and increase of AA –> glucose and AA enter cell (glucose through GLUT4) –> go through TCA cycle to create ATP –> increase of ATP closes K+ channels –> K+ increases the RMP of cell –> stimulates opening of Ca2+ channels –> Ca2+ acts as second messenger –> binds Insulin granule to membrane for exocytosis –> Insult and C peptide released from cell

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18
Q

What is the biphasic insulin release?

A

Spike of insulin secretion from readily releasable pool for several minutes after eating

Then smaller, more prolonged spike of secretion from reserve pool sustained release over 1 hr

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19
Q

Outline the MOA of insulin and it’s overall effect

A

Insulin binds to TKR –> phosphorylated TK activates intracellular signaling proteins –> activates PI3K pathway which stimulates GLUT4 intra and extramembranous receptors, as well as PIP2 –> which stimulates PIP3 –> AKT pathway –>

Increased: glucose uptake, glycolysis, glycogen synthesis, lipogenesis, protein synthesis, cell survival and growth - do whatever it takes to get excess glucose out of the blood

Decreased: gluconeogenesis, lipolysis, proteolysis - stop anything from becoming more glucose

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20
Q

What effects does Insulin have on hepatic metabolism?

A

Increased: Glycolysis, Glycogenesis, FA synthesis, PPP - break down/convert glucose

Decreased: Gluconeogenesis, Glycogenolysis - avoid making more glucose

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21
Q

What effects does Insulin have on adipose metabolism?

A

Increased: Glycolysis, PPP, Pyruvate Oxidation, Lipogenesis

Decreased: Lipolysis

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22
Q

What effects does Insulin have on Skeletal muscle metabolism?

A

Increased: Glycolysis, Glycogenesis, protein synthesis

Decreased: Glycogenolysis

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23
Q

This illustrates the role of [a] in integration of metabolism

A

Glucagon

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24
Q

This illustrates the role of [a] in integration of metabolism

A

Insulin

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25
Q

The presence of food in the intestines induces the release of [a] from the intestines, which is a(n) [b].

A

a. GLP-1
b. Incretin - targets endocrine pancreas to produce and secrete insulin

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26
Q

During the fed state, liver becomes a (creator/consumer) of glucose

A

Consumer

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27
Q

List the metabolic changes in the liver during the fed state

A

Increase chylomicron and glucose uptake
Increase glycogenesis, PPP, glycolysis (Acetyl-CoA for FA synthesis and energy, DHAP for lipogensis)
Increase VLDL release
Increase AA release, AA catabolism, protein synthesis
Increase urea cycle

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28
Q

List the metabolic changes in adipose during the fed state

A

Increase LPL activity, FA uptake
Increase glucose uptake, glycolysis
Produces and secretes leptin

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29
Q

What is leptin and what is its function?

A

A hormone that acts on the hypothalamus to induce satiety

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30
Q

List the metabolic changes in skeletal muscle during the fed state

A

Increase glucose uptake, glycolysis, glycogenesis
Increase AA uptake and protein synthesis

Decrease LPL activity

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31
Q

What tissue solely takes up glucose independently of insulin?

A

the brain

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32
Q

What are the different fates of Glucose in the fed state?

A
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33
Q

What are the different fates of AA in the fed state?

A
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34
Q

What are the different fates of lipids in the fed state?

A
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35
Q

Label the glucose sources used during fasting

A
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36
Q

Label which illustration is during which state of fasting

A
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37
Q

When does the brain switch to ketone bodies as a fuel source? What does it use until then in the fasting state?

A

2nd week of fasting

Protein degradation

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38
Q

What is the body’s last attempt to create glucose?

A

Gluconeogenesis in the kidneys after 5-6 weeks of fasting

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39
Q

Differentiate Type I and Type II DM

A

Type 1: results from inability to produce insulin

Type 2: results from insulin resistance, inadequate insulin secretion and/or excessive glucagon secretion

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40
Q

A pt with acetone breath and low blood pH is indicative of

A

DKA - Diabetic Ketoacidosis

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41
Q

What antibody plays a key role in the pathogenesis of Type 1 Diabetes?

A

Anti-glutamic acid decarboxylase antibody

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42
Q

Which HLA serotype is most strongly associated with Type 1 Diabetes?

A

HLA-DR3

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43
Q

Outline the mechanism of Passive Chloride Channels found in the intestines

A

Located in the small and large intestines - Chloride ions are pushed in from the lumen into the cell, and from the cell through the basolateral side

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44
Q

Outline the mechanisms of Chloride/Bicarb Exchangers found in intestines

A

Located in small and large intestines
Exchanges Chloride for Bicarb by secreting Bicarb into the Lumen and bringing Chloride into the cell
Electroneutral because it exchanges a negative ion for another negative ion

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45
Q

Outline the mechanism of Chloride secretion in the small and large intestine

A

NKCC channel created negative gradient within the cell which drives chloride out of the cell into the lumen through the CFTR channel
Electrogenic bc only chloride is crossing the membrane –> pulls water and Na+ into lumen between cells

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46
Q

What regulates the CFTR channel?
What else can go through CFTR channels?

A

cAMP, cGMP, Ca2+

HCO3

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47
Q

Outline the mechanism of Sodium-Nutrient Cotransporter in small intestine

A

Glucose/Galactose follows Na+ into cell through SGLT1
AAs follow H+ into cell through PEPT1

Glucose leaves through diffusion on BL side once gradient builds
AA leaves through BL side once broken down into monomers

Na/K ATPase pushed Na out of cell on BL side, brings K in

Chloride and water move between cells by electrogenic force balancing Na+ being excreted to BL side

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48
Q

Outline mechanism of Sodium-Hydrogen Exchanger in the small and large intestine

A

Na is pulled into the cell while H+ is pushed out of the cell into the lumen
Found close by Cl/Bicarb exchanger

Helps regulate absorption in the fasted state

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49
Q

Outline the mechanism of Epithelial Sodium Channel in the large intestine

A

Na+ is pulled into the cell

Regulated by hormones - Gs stimulates, Gq inhibits

Gradient creates elecrtogenic cell –> pulls water and Cl- to BL side through cells

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50
Q

Malabsorptive diarrhea is caused by [a]
Secretory diarrhea is caused by [b]

A

a. nutrients not being absorbed keeping water in the lumen
b. upregulation of CFTR causing water to follow Cl into lumen

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51
Q

Which anti-diarrheals decrease motility

A

Loperamide
Alosetron
Dicyclomine

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52
Q

Which anti-diarrheals decrease secretions?

A

Octreotide
Colestripol
Alosetron
Loperamide
Clonidine
Polycarbophile
Bismuth subsalicylate

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53
Q

Explain the MOA of Enterotoxigenic coli-induced diarrhea

A

Two pathways:

Heat-stable toxin - binds to receptor guanalyl cyclase –> generates cGMP –> activates PKG II –> phosphorylation of CFTR –> increased Cl- secretions

Heat-labile toxin - binds to GPCR (Gs) –> activates adenylyl cyclase –> stimulates cAMP –> activates PKA –> phosphorylation of CFTR –> increased Cl- secretions

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54
Q

Explain how secretory diarrhea can lead to metabolic acidosis and low potassium

A

Upregulation of CFTR –> increased secretions of Cl- and HCO3 –> body becomes more acidic as it loses basic molecules –> metabolic acidosis –> hydrogen ions move into cells from blood in exchange for K+ ions –> reduce acidity but lower serum potassium

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55
Q

Explain how and why a Xylose test is used

A

Given to see if pt can breakdown monosaccharides and uptake them by SGLT1
Urine measured after 24 hrs, fecal measured after 72 hrs
If lower in urine and high in stool –> not being absorbed in small intestine
Can show if something is wrong with transporters or damage to intestinal lining

56
Q

What is the source of foul smelling food?

A

Undigested food in the small intestine

57
Q

List which macros and micros each part of the intestine takes up

A

Duodenum - Carbs, fats, proteins, iron, calcium
Jejunum - Carbs, fats, proteins
Ileum - Fats and proteins; bile salts and Vit B12 in distal ileum

58
Q

Explain how lower serum FGF19 and higher stool bile salt concentration can cause fatty stool and diarrhea

A

FGF19 is the transcription factor that regulates Bile Salt synthesis
When Bile Salts are taken up in the cell, FGF19 is activated –> inhibition of CYP7A1, the transcription factor for Bile Salt Synthesis.
FGF19 inhibits the synthesis of more Bile Salts bc its saying the body is reusing and they don’t need to make more.

If FGF19 is low, that means Bile Salts aren’t being taken up by the cells and recycled, and are being excreted. This leads to downregulation from FGF19 –> no longer inhibiting CYP7A1 –> activating transcription factors to synthesize Bile Salts –> increased Bile Concentration in stool but still not enough to breakdown all the fats without the bile salts that should have been recycled –> fatty stool

Too many Bile acids in the lumen –> upregulation of Cl- channels –> increase water secretion –> diarrhea

59
Q

What are some sources of malabsorptive diarrhea?

A

Lactose Intolerance
Pancreatic Insufficiency
Celiac disease
Bile Acid Malabsorption

60
Q

What are some sources of secretory diarrhea?

A

V. Cholerae
C. Difficile
E. Coli
Bile Acid Malabsorption

61
Q

Compare and Contrast the Visceral afferent innervation of the ascending colon vs the distal half of the sigmoid colon for reflex and pain sensations

A

Ascending Colon:
Pain - retrograde sympathetics - (DRG T10-T11)
Reflex - retrograde parasympathetics - (DRG S2-S4 through Pelvic Splanchnic n)

Sigmoid Colon:
Pain - retrograde parasympathetics - (DRG S2-S4 through Pelvic Splanchnic n)
Reflex - retrograde parasympathetics - (DRG S2-S4 through Pelvic Splanchnic n)

62
Q

Circular muscle and longitudinal muscle are responsible for what type of contraction?

A

Circular - segmentation
Longitudinal - Peristalsis

63
Q

What is the function of Interstitial Cells of Cajal?

A

Generate basoelectrical rhythm to keep the threshold of cells high for easy depolarization

64
Q

Explain the physiology of the small intestines during the fed state

A

Segmentation churns the food with back and forth motions to increase contact time for absorption
Duration depends on caloric contents
Regulated by ACh and NO/VIP

65
Q

Explain the physiology of large intestines during the fed state

A

Segmental propulsion creates Haustra (pouches) in large intestine, pushing stool from one to the next with forward and backward movement
High amplitude propulsions precede defecation (mass movement)

66
Q

What is the gastrocolic reflex?

A

The urge to defecate after eating stimulated by distention of the stomach

67
Q

Explain large intestine physiology during the fasted state

A

No caloric content in the small intestine stimulates MMC (migrating motility complex)
Excretes anything left in the colon
Keeps any contents from staying stagnant or traveling backwards - prevents bacterial overgrowth in small intestine

68
Q

Describe the Migrating Motility Complex

A

Phase 1 - quiescent
Phase 2 - intermittent action potentials
Phase 3 - max action potentials stimulated by Motilin

69
Q

What medication classes increase motility? (anti-constipation)

A

Dopamine antagonists
Macrolide antibiotics
AChE inhibitors
Opioid Receptor Antagonists
5-HT4 Receptor Agonists

70
Q

What medication classes decrease motility? (anti-diarrheal)

A

5-HT3 Receptor Antagonists
Opioid Receptor Agonists
Anticholinergics

71
Q

How does injury to the internal anal sphincter innervation lead to fecal incontinence?

A

Pressure of feces isn’t being regulated by the internal sphincter –> pt doesn’t know to contract external sphincter

72
Q

What medications increase H2O in the lumen?

A

Lubiprostone
Linilactide
Lactulose

73
Q

What medications increase H2O in the stool?

A

Psyllium
Docusate

74
Q

What medications increase smooth muscle contractions?

A

Methylnaltrexone
Prucalopride
Bisacodyl

75
Q

General sensation and taste of the posterior 1/3 of the tongue is supplied by

A

Lingual branch of glossopharyngeal n

76
Q

General sensation and taste of anterior 2/3 of the tongue is supplied by

A

Sensation: lingual n
Taste: facial n

Vallate Papillae: glossopharyngeal n

77
Q

The Lingual nerve contains which nerve fibers upon reaching the submandibular ganglion?

A

Pre-ganglionic Parasympathetic fibers (splitting off into SMG)
Taste sensation (chorda tympani)
General sensation (lingual)

78
Q

How would you differentiate Campylobacter jejuni and Shigella dysenteriae on diagnosis?

A

Campy - curved, motile, oxidase +
Shigella - rod, non-motile, oxidase -

79
Q

How would you differentiate E. Coli from other gram negative bacteria with similar clinical presentation?

A

Ferments lactose
Pink on MacConkey Agar
Green sheen on Eosin-methylane blue
Indole positive

80
Q

How would you differentiate Yersinia enterocolitica from Salmonella typhi?

A

Yersinia - Non H2S producing
Salmonella - Produces H2S

81
Q

How would you differentiate Yersinia enterocolitica from other gram negative bacteria?

A

Non H2S producing
Stains bipolar
Nonfermenting
Motile at 25, not motile at 37

82
Q

How do you differentiate Staph aureus, Bacillus cereus and Clostridium perfringens?

A

S. aureus - doesn’t produce spores
Bacillus - produces spores, motile
C. perf - produces spores, nonmotile

83
Q

What diarrheal causing bacteria can you treat with Macrolides?

A

Campylobacter jejuni, Shigella dysenteriae

84
Q

What diarrheal causing bacteria can you treat with Fluoroquinolones?

A

Shigella dysenteriae, Yersinia enterocolitica, Salmonella typhi

85
Q

What diarrheal causing bacteria can you treat with TMP-SMX?

A

Shigella dysenteriae, Yersinia enterocolitica

86
Q

What diarrheal causing bacteria can you treat with Ceftriaxone?

A

Shigella dysenteriae, Salmonella typhi

87
Q

What diarrheal causing bacteria do you treat with supportive care?

A

Staphylococcus aureus, Bacillus cereus, Clostridrium perfringens

88
Q

What are xenobiotics?

A

Foreign substances metabolized by the body for excretion

89
Q

What is the purpose of Phase I and Phase II metabolism?

A

Make xenobiotics more hydrophilic for excretion

90
Q

What four things are needed for Phase I metabolism to occur?

A

CP450
NADPH
O2
P450 Reductase

91
Q

Briefly explain the steps of Phase I metabolism

A

Step 1 - Fe3+/P450 binds with the Xenobiotic (RH)
Step 2 - NADPH donates an electron to Flavoprotein via P450 reductase which donates to Fe3+/P450-RH –> Fe2+/P450-RH
Step 3 - Fe2+/P450-RH binds to O2 and NADPH donates another electron to allow O2 to bind –> Fe2+/P450-O2-RH
Step 4 - O2 splits into H2O and Fe2+/P450-ROH –> ROH leaves and Fe2+/P450 turns back into Fe3+/P450

92
Q

What are some examples of inducers of CP450?

A

Cabamazepine
Phenobarbital
Phenytoin
Rifampin
Smoking
St. John’s Wort

93
Q

What are some examples of Inhibitors of CP450?

A

Azole antifungals
Cimetidine
Grapefruit Juice
Macrolides
Protease inhibitors
SSRIs

94
Q

How does the Ultrarapid Metabolizer polymorphism effect drug metabolism?

How is it different from prodrug metabolism?

A

URM in regular drugs:
Faster metabolism –> more drug broken down –> lower plasma concentration –> less drug response

URM in prodrugs:
Faster metabolism –> more drug created –> higher plasma concentration –> higher drug response

95
Q

How does the Poor Metabolizer polymorphism effect drug metabolism?

How is it different from prodrug metabolism?

A

PM in regular drugs:
Slower metabolism –> less drug broken down –> higher plasma concentration –> greater drug response

PM in prodrugs:
Slower metabolism –> less drug created –> lower plasma concentration –> less drug response

96
Q

What polymorphism can effect the metabolism of Warfarin? What issues can that cause?

A

2C9

Can cause bleeding or clotting complications

97
Q

Explain how an inducer can effect drug metabolism

A

A CP450 inducer increases the synthesis or decrease degradation of CP450
Increased speed of metabolism –> increased breakdown –> decreased drug response

98
Q

Explain how an inhibitor can effect drug metabolism

A

A CP450 inhibitor decreases the synthesis or decrease degradation of CP450
Decreased speed of metabolism –> decreased breakdown –> increased drug response

99
Q

What CP450 enzyme is responsible of the converstion of codeine –> morphine?

A

CP4502D6

100
Q

What CP450 enzyme is responsible for the breakdown of statins?

A

CP4503A4/5

101
Q

What are the major contributing enzymes of Phase I metabolism?

A

CP4503A4/5
CP4502D6
CP4502C9

102
Q

What are the major contributing enzymes of Phase II metabolism?

A

UGT

103
Q

What does the Hepatic Extraction Ratio tell us?

A

Ratio of what you give divided by what the liver takes out in first pass

104
Q

What does it mean to have a high hepatic extraction ratio?

Low extraction ratio?

A

High hepatic ratio = decreased bioavailability
Low hepatic ratio = increased bioavailability

105
Q

Where does Phase I and Phase II metabolism take place?

A

Phase I - SER
Phase II - cytoplasm

106
Q

What does a low insulin:glucagon ratio tell us?

A

Glucose is being made instead of used

107
Q

A diabetic patient with acetone breath and a low pH is likely having an episode of

A

Diabetic ketoacidosis

108
Q

Describe diabetic ketoacidosis and how it’s treated

A

Glucose is being made rather than used because glucose can’t be taken up –> fats broken down and made into ketone bodies –> acetone byproduct causes acetone breath, ketones low pKa lower blood pH

Treated with insulin to take up glucose from the blood

109
Q

Outline MOA and AE of Metformin

A

MOA: inhibits mitochondrial electron complex 1 –> less ATP, more AMP –> AMP stimulates AMPK –> stimulates phosphorylation of transcription factors –> decrease gluconeogenesis, shunts Pyruvate to Lactate pathway
Also increases glucose uptake in cells, glucose absorption to help with insulin sensitivity

AE: GI distress, Lactic acidosis (rare)

110
Q

Outline MOA and AE of Sulonylureas

A

Binds to pancreatic beta cell SUR1 receptor –> closes K+ channel –> influx of Ca2+ –> depolarization –> insulin release

AE: Hypoglycemia, weight gain, icnreased risk of MI (receptors on cardiomyocytes), B-cell exhaustion (stops working after a few years)

111
Q

Outline MOA and AE of TZDs

A

Binds to PPAR-y –> activates transcription involved in glucose and fat metabolism –> increased production of GLUT4

AE: Edema - can precipitate heart failure, increased risk of fractures (decreased production of osteoblasts)
CI in Stage 3+ HF, and bladder cancer

112
Q

Outline MOA and AE of GLP1 Receptor Agonists

A

MOA: works like endogenous GLP-1 –> stimulates insulin biosynthesis

AE: Increased risk of pancreatitis, weight loss, expensive
First line for pts with CVD
CI: thyroid cancer

113
Q

Describe the different types of insulin combinations

A

Prandial (before meal) always paired with basal (thoughout day)

Long acting (q24hrs) paired with rapid (injected 10-15 mins before eating)

Regular (1hr before eating) paired with NPH (intermediate - q12hrs)

114
Q

What are the biggest risks of using insulin

A

Hypoglycemia (most likely with prandial) if they don’t eat in time
Weight gain
Hypersensitivity reaction

115
Q

Identify the vitamin and mineral recommendations for children, pregnant women, and older adults

A

Children: Vit A & D; zinc
Pregnant women: Folate, Vit D; iron
Older adults: Vit D, Vit B12; calcium

116
Q

Identify the vitamin and mineral recommendations for age-related eye diseases, obesity and T2DM

A

Eye diseases: Vit A / Carotenoids
Obesity: Vit B6, C, D, E
T2DM: Vit A, C, E, thiamine, biotin, folate, B12

117
Q

What vitamins are fat-soluble?

A

Retinoids Vit A
Calciferol Vit D
a-Tocopherol Vit E
Vit K

118
Q

What vitamins are water-soluble?

A

Thiamin B1
Riboflavin B2
Niacin B3
Pantothenic Acid B5
Vit B6
Biotin B7
Folic Acid B9
Cobalamin B12
Choline
Ascorbic Acid Vit C

119
Q

Fill in the chart

A
120
Q

What diseases can B1 deficiency cause?

A

Beriberi - malnutrition
Wernicke-Korsakoff Syndrome - alcohol use disorder

121
Q

Outline Beriberi disease

A

Thiamin deficiency

Dry beriberi - peripheral neuropathy, muscle weakness/wasting, weight loss
Wet beriberi - heart enlargement/failure, peripheral vasodilation, edema

122
Q

Outline Wenick-Korsakoff syndrome

A

Thiamine deficiency from alcohol use disorder

Wernicke encephalopathy (acute) - delerium, ataxia, eye muscle paralysis
Korsakoff psychosis (chronic) - anterograde amnesia

123
Q

Outline Riboflavin deficiency disease

A

Ariboflavinosis - nutritional deficiency of Vit B2
Sore throat, cheilosis (cracking, crusting of mouth corners), glossitis (painful magenta tongue), seborrheic dermatitis, anemia

124
Q

Why is Vit B3 crucial to our diet, and how much do we need?

A

Vit B3 = Niacin –> part of NAD+ & NADP+
Need 14-16mg per day

125
Q

Outline the Vit B3 related diseases

A

Pellagra - 4 Ds - Diarrhea, Dermatitis (C3-4), Dementia, Death

Hartnup syndrome - decreased Trp –> decreased Niacin synthesis

Carcinoid syndrome - excess Trp utilization = decreased Niacin synthesis

Toxicity Diseases:
Niacin flush
N/V, liver damage, impaired glucose tolerance, gout

126
Q

Outline Vit B5 related diseases

A

Nutritional deficiencies rare

Pantothenate kinase-associated neurodegeneration (PKAN)
PANK2 mutation –> abnormal Fe accumulation –> parkinsonism, dystonia, dementia

127
Q

Outline Vit B6 related diseases

A

Nutritional deficiency from malnutrition, alcohol use disorder, etc –> dermatitis, sideroblastic anemia, depression, confusion, peripheral neuropathy

Toxicity diseases - depression, fatigue, irritability, headaches

128
Q

Outline Vit B7 related diseases

A

Biotinidase deficiency - BTD mutations –> encodes biotinidase (enzyme that releases biotin from proteins)
Infants: hypotonia, seizures, optic atrophy
Included in NBS

129
Q

How does the overconsumption of egg whites cause a Biotin deficiency

A

Egg whites contain avidin –> avidin binds to biotin that prevents absorption

130
Q

What are the functions of the different forms of Folic Acid B9

A

formyl-THF –> THF - purine biosynthesis
methylene-THF –> DHF –> THF - dTMP biosynthesis
THF <–> methylene-THF - Ser & Gly degradation and biosynthesis
methyl-THF –> THF - Vit B12-mediated Met recycling

131
Q

What symptoms would you see in Folic Acid Deficiency Diseases

A

Nutritional deficiency:
Megaloblastic anemia
Glossitis, fatigue, depression
Neural tube defects (ancephalopathy, spina bifida) if mother has Folate def.

Methylene-THF reductase deficiency - MTHFR mutation
Defect in enzyme involved in folic acid metabolism
High conc of homocysteine in blood, developmental delay, eye disorders, thrombosis

132
Q

What is the function of Cobalamin B12

A

Involved in coupled conversion of methyl-THF to THF
Involved in conversion of homocystine to Met
Propionyl-CoA metabolism

133
Q

Outline the absorption of Cobalamin

A

Cobalamin (B12) binds to R-binders in saliva and stomach –> protein-bound cobalamin must be released by protease digestion in stomach or small intestine –> binding to Intrinsic factor –> IF-B12 complex undergoes receptor-mediated endocytosis in terminal ileum –> In enterocytes, IF-B12 dissociates and B12 binds to transcobalamin II –> B12-TCII complex is released into blood

134
Q

Explain Cobalamin B12 deficiencies and findings

A

Nutritional deficiency:
Megaloblastic anemia
Fatigue, subacute degeneration of spinal cord, paralysis, anorexia

Methylmalonic acidemia & homocystinuria - MMACHC mutations
Encodes CblC - protein involved in cobalamin metabolism
Neurological symptoms, intrauterine growth retardation, microcephaly

135
Q

What can come from Choline deficiency?
What about Choline toxicity?

A

Deficiency - liver damage

Toxicity - Sweating, salivation, hypotension, liver damage

136
Q
A

Unit 4 GNA (6 decks)

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