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BIOCHEMISTRY > BIOCHEMISTRY- Vitamins Videos > Flashcards

BIOCHEMISTRY- Vitamins Videos Flashcards

1
Q

Which vitamins are related to Biotin?

A

Pyruvate carboxylase
Acetyl CoA carboxylase
Propionyl CoA carboxylase

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2
Q

Which pathway is related with Biotin and Pyruvate carboxylase?

A

Gluconeogenesis

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3
Q

Which is the most common cause of Biotin deficiency?

A

(RARE) Excessive consumption of raw eggs which leads to hypoglicemia

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4
Q

In which pathway do we see Acetyl CoA carboxylase and Biotin?

A

Fatty Acid synthesis

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5
Q

In which pathway do we see Propionyl CoA carboxylase and Biotin?

A

VOMIT pathway
Odd carbon fatty acids
Val, Met, Ile, Thr

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6
Q

Clinical findings of Biotin deficiency

A

Alopecia, bowel inflammation, muscle pain

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7
Q

Which vitamin is Thiamine?

A

B1

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8
Q

Which enzymes ate related to Thiamine?

A

Dehydrogenases:
Pyruvate dehydrogenase
α ketoglutarate dehydrogenase

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9
Q

What is the function of dehydrogenases?

A

Tightly associated to energy production

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10
Q

In which pathway do we see pyruvate dehydrogenase?

A

PDH

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11
Q

Pathway related to α ketoglutarate dehydrogenase

A

TCA cycle or Krebs Cycle

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12
Q

What is the product of pyruvate?

A

Acetyl CoA

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13
Q

What is one of the main importance of Thyamine?

A

ATP production due to its relationship with enzymes

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14
Q

How is the pathogenesis of thiamine deficiency?

A

CNS with no energy→ Na+ pump fails → Na+ stays intracellularly → the cell starts swelling → cell ruptures and it starts Neurologic failure

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15
Q

In which patients is thiamine deficiency more common?

A

Alcoholism (alcohol interferes with absorption)

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16
Q

Pathology associated with vitamin B1 deficiency

A

Wernicke Korsakoff Syndrome

Beri beri disease

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17
Q

Characteristics of Wernicke Syndrome

A

Ataxia, nystagmus, ophtalmoplegia

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18
Q

Characteristics of Korsakoff Syndrome

A

Confabulation, psychosis

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19
Q

One of the main structures damage in Thiamine deficiency

A

Destroys mammilary bodies (part of the limbic system)- patients confabulate

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20
Q

In case of Vitamin B1 deficiency, what is the treatment?

A

Supplementation of thiamine and Glucose

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21
Q

What is Dry beri beri?

A

Wernicke Korsakoff Syndrome

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22
Q

When is just Thiamine alimentary deficiency (not related to alcohol abuse)? What is the probable disease?

A

Wet beri beri

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23
Q

How else is wet beri beri adquired?

A

By eating rice that has been husked (white rise)

Very unusual

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24
Q

What is affected in wet beri beri?

A

Heart, High output, cardiac failure

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25
Q

Pathogenesis of wet beri beri

A
  1. Thiamine deficiency
  2. Kreb cycle ATP ↓ (no energy)
  3. Cells start swelling
  4. Organomegally
  5. Dilated Cardiomyopathy → systolic failure (dropping ejection fraction → Congestive heart failure
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26
Q

Which other enzymes are related to Thiamine?

A

Transketolase

Branched chain ketoacid dehydrogenase

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27
Q

In which pathway is Transketolase related?

A

HMP shunt

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28
Q

Which is the only cofactor needed by transketolase?

A

Thiamine (vitamin B1)

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29
Q

Which is the lab test for Thiamine deficiency?

A

Transketolase activity (Because transketolase only requires Thiamine as a cofactor to work)

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30
Q

Which is the importance of Branched chain ketoacid dehydrogenase?

A

Metabolism of Valine, isoleucine and leucine

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31
Q

Which Pathology is associated with Branched chain ketoacid dehydrogenase?

A

Mapple Syrup Urine disease

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32
Q

Which vitamin is Niacin?

A

B3

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33
Q

What is made with Niacin?

A

NAD (H)

NAPD (H)

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34
Q

Enzymes related to vitamin B3?

A

Dehydrogenases

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35
Q

In which patients is Niacin deficiency seen?

A

In malnourish and eldery “tea and toast”

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36
Q

Vitamin deficient in Pellagra

A

Vitamin B3 (Niacin)

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37
Q

Clinical findings of Pellagraa

A

3 Ds: Diarrhea, Dementia, Dermatitis, and if not treated Death

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38
Q

When you run our of Niacin what happens?

A

Source of electrons, for electron Transport chain to make ATP

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39
Q

What else is related to Pellagra?

A

Deficiency of tryptophan

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40
Q

Which is the major dietary staple of Tryptophan?

A

Corn

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41
Q

What is Hartnup disease?

A

Deficiency of Decrease uptake of tryptophan by kydney

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42
Q

What other disease is associated with Hartnup disease? Why?

A

Mild Pellagra, because Tryptophan is requireed for Niacin formation and because Try is decreased, Niacin is also decreased

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43
Q

In which food is folic Acid Obtained?

A

Leafy type of vegetables

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44
Q

Which enzyme requires folic acid ?

A

Thymidilate synthase

Enzyme in purine synthesis

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45
Q

Active form of Folic acid

A

THF

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46
Q

Which is the function of Thymidilate synthase?

A

Conversion of Uracyl to Thymidine

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47
Q

What is the final result of Folic acid deficiency? Why?

A

↓ DNA formation, because of ↓ Thymine

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48
Q

What is made with THF?

A

Adenine and Guanine

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49
Q

What is the final result of the THF deficiency?

A

↓ DNA synthesis due to decrease of Adenine and Guanine

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50
Q

In which patients is folic acid deficiency more common?

A

Alcoholics and pregnancy

and when we grow to quickly

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51
Q

How long does the body stores folic acid?

A

Body stores depleted in 3 months

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52
Q

Findings of folic acid deficiency

A

Megaloblastic anemia

Homocystinemia

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53
Q

What is found in the blood with Megaloblastic anemia?

A

Hypersegmented neutrophils and Macroovalocites

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54
Q

What risk is increased with homocystinemia?

A

Deep vein thrombosis and atherosclerosis

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55
Q

Which vitamin deficiency can cause homocystenimia?

A

Folic acid

B12, B6

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56
Q

Alternative name for Vitamin B12

A

Cyanocobalamin

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57
Q

How much is Vitamin B12 associated with poor diet?

A

Poorly associated

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58
Q

For how long can we store vitamin B12?

A

For decades

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59
Q

Which enzymes are related to vitamin B12?

A

Homocysteine methyltransferase

Methylmalonyl CoA mutase

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60
Q

What is the function Homocystine methyltransferase?

A

Untraps folate from the storage form, and folate is inactive when is the storage form (Ns Methyl THF)

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61
Q

What is the result of homocytine methyltransferase deficiency cause by Vitamin B12 deficiency?

A

Megaloblastic Anemia, because traps folate in its inactive form

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62
Q

What pathway is related to methylmalonyl CoA mutase?

A

VOMIT pathway
Odd carbon fatty acids,
Val, Met, Ile, Thr (They accumulate)

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63
Q

Importance of Methylmalonyl CoA mutase

A

Source of Succinyl CoA require for Kreb cycle, so no ATP when vitamin B12 is deficient

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64
Q

What is the finding of failure of Methyl CoA mutase due to Vitamin B12 deficiency?

A

Progressive peripheral neuropathy

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65
Q

Type of neuropathy seen with vitamin B12 deficiency

A

Subacute combined Degeneration of the spinal cord (posterior and lateral column)

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66
Q

Type of Motor neuron damage seen in Neuropathy of Vitamin B12 deficiency

A

Upper motor neuron syndrome

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67
Q

In which situations is subacute combined degeneartion of the spinal cord seen?

A

Vitamin B12 deficiency
HIV
Friedrich Ataxia

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68
Q

Which is the most common cause of Vitamin B12 deficiency?

A

Pernicious anemia

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69
Q

What is Pernicious anemia?

A

Autoimmune disease of the stomach, antibodies bound to parietal cells and intrinsic factor (require for vitamin B12 absorption)

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70
Q

Other causes of Vitamin B12 deficiency

A 
Also in aging
Poor nutrition
Bacterial overgrowth of terminal ileum
Resection of terminal ileum
Secondary to Crohn disease
Chronic Pancreatitis
Rarely in vagus or infection with D. Latum
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71
Q

Alternative name for Vitamin B6

A

Pyridoxine

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72
Q

How is Vitamin B6 used?

A

As pyridoxal- P (PLP) by every single Aminotrasferases (transaminase): AST (GOT), ALT (GPT)

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73
Q

What is the function of Aminotransferases?

A

Detoxify ammonic

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74
Q

What is ammonia?

A

A strong base that can disolve lipids of membranes

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75
Q

How is ammonia detoxified?

A

By the liver

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76
Q

What happens when having liver injury, how is ammonia affected?

A

The liver start producing Amminotrasferases, making sure that ammonia isn’t free to damage further tissue and B6 is decreased as a result

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77
Q

How do liver enzynes affect vitamin B6?

A

↑ AST/ ALT chronically , leads to B6 deficiency

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78
Q

Most common cause of Vitamin B6 deficiency

A

Alcohol (hepatitis) —> Cirrhosis

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79
Q

Which is the drug that most common cause vitamin B6 deficiency?

A

Isoniazid therapy

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80
Q

What other use does Pyridoxine have?

A

Heme synthesis

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81
Q

Which enzyme use vitamin B6 as a cofactor for Heme synthesis?

A

δ Aminolevulinate synthase

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82
Q

Type of anemia in Pyridoxine deficiency

A

↓ Heme synthesis → ↓ Hv → Mycrocytic anemia → ↓Iron build up → Sideroblastic anemia

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83
Q

Other clinical findings of Vitamin B6 deficiency

A

Cheilosis or Stomatitis (cracking or scaling of lip borders and corners of the mouth)
Convulsions due to ammonia accummulation encephalopathy

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84
Q

Alternative name for Rivoflavin

A

Vitamin B2

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85
Q

What is made with vitamin B2?

A

FAD (H2)

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86
Q

What does FAD produces?

A

Electrons

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87
Q

Pathways where FAD is realted

A

Succinate DH (TCA cycle)
Fatty Acyl CoA dehydrogenase (P oxidation)
Glysol phosphate dehydrogenase shuttle

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88
Q

When do we commonly see Vitamin B malnutrition?

A

In parenteral nutrition

89
Q

Clinical findings of Rivoflavin Deficiency

A

Corneal neovascularization
Cheilosis or Stomatitis
Magenta colored tongue (due to glositis)

90
Q

When is Ascorbate deficiency seen?

A

Diet deficient in citrus fruits and green vegetables

91
Q

Alternative name for Vitamin C

A

Ascorbate

92
Q

Which enzymes depend on Vitamin C?

A

Prolyl and lysyl hydroxylases

Dopamine hydroxylase

93
Q

What is the function of Prolyl and lysyl hydroxylases?

A

To make stable collagen

94
Q

Clinical findings of Ascorbate deficiency related to deficient collagen synthesis

A

Easy bruising (perifollicular hemorrhage), bleeding gums, poor wound healing, increased bleeding time

95
Q

Which other vitamin deficiency is differential diagnosis of Vitamin K?

A

Vitamin C, but vitamin C has increased bleeding time due to defective aggregation of platelets

96
Q

What is the function of Dopamine hydroxylase?

A

Converts Dopamine to Norepinephrine

97
Q

Which vitamin deficiency affects catecholamine synthesis?

A

Ascorbate (vitamin C) due to Dopamine hydroxylase failure

98
Q

When Vitamin C deficiency affects Catecholamines synthesis, what is the result?

A

Autoimmune Nervous system specially sympathetic

and Central Nervous system causing depression

99
Q

What does Vitamin C have to do with Iron?

A

Allows tha absorption of Iron in GI tract

100
Q

In which form does Iron come from vegetables?

A

Fe3+

101
Q

Can we absob Fe3+?

A

No

102
Q

What is needed to absorb Fe3+?

A

Stomach H+ and vitamine C so it is converted to Fe2+

103
Q

Disease caused by Vitamin C deficiency

A

Scurvy

104
Q

Is panthothenic acid water soluble or fat soluble vitamin?

A

Water Soluble

105
Q

What is made with panthothenic acid?

A

CoA–> AcetylCoA

106
Q

Can you live without panthotenic Acid?

A

NO, because it makes Acetyl CoA, substrate needed for TCA cylce

107
Q

Which pathways require Panthotenic Acid?

A

Fatty acid metabolism
PDH
TCA cycle

108
Q

Which vitmain is needed for CoA synthesis?

A

Panthotenic Acid

109
Q

Alternative name for Vitamin D

A

Cholecalciferol

110
Q

Functions of Vitmain D

A

In response to hypocalcemia, helps normalize serum calcium levels
Phosphate homeostasis

111
Q

From where does Vitamin K come?

A

Menaquine, bacterias

Phytoquinone, plants

112
Q

Important functions of Vitamin K

A

Carboxylation of glutamic acid residues in many Ca2+ - binding proteins
Importantly coagulation factors II, VII, IX, X as well as protein C and S

113
Q

Alternative name for Vitamin E

A

α Tocopherol

114
Q

Functions of Vitamin E

A

Antioxidant in the lipid phase, protects membrane lipids from peroxidation

115
Q

What is the effect of 1,25 hydroxycholecalciferol?

A

Bone: Osteoclasts- Ca2+ mineralization or mobilization (with PTH)
Intestine: (Duodenum) increase calcium uptake from intestine
Kidney: Ca2+ Reabsorption, BUT increases retention of PO4 3- (Phosphate)

116
Q

What is the difference on effects of PTH compared to Calcitriol?

A

PTH increases phosphate excretion

Calcitriol increases phosphate phosphate reabsorption

117
Q

In which food is vitamin D3 found?

A

In salt water fish (salmon) and egg yolks

Added to milk and some fortified cereals

118
Q

Which pathologies may affect vitamin D?

A

Cirrhosis and liver failure may produce bone mineralization

End stage renal disease

119
Q

Main causes of cirrhosis

A

60% chronic alcoholism
20% hepatitis viruses
15% cholestatic issues (gallstones) fibrosis of billiary duct
5% Weird metabolic diseases like Wilson, etc

120
Q

What do patients with end stage renal disease develop?

A

Renal osteodystrophy, with vitamin D lack because 1 hydroxylation can’t be done, developing hypocalcemia and secondary hyperparathyroidism–> Loss of PO4 3-

121
Q

In case the patinet has either liver failure or renal failure how does Vitamin D should be administered?

A

Depending on the pathology it should be administer in its proper hydroxylated form

122
Q

In case of Renal failure, which is the the vitamin D from that should be administered?

A

In 1,25 hydrocholecalciferol form

123
Q

In liver failure or cirrhosis which is the form that vitamin D should be administered?

A

In 25 hydrocholecalciferol

124
Q

What is the effect of Vitamin D deficiency?

A

↓ Ca2+ → secondary ↑ PTH
Bone demineralization
Rickets (children)
Osteomalacia (adults)

125
Q

Causes of vitamin D deficiency

A

Insufficient sunlight
Inadequate fortified foods (milk)
End stage renal disease (renal osteodystrophy)
Liver failure or cirrhosis

126
Q

Which renal calcification is seen in renal osteodystrophy?

A

Metastatic calcification

127
Q

Finidngs on the bone when renal osteodystrophy

A

Brown cyst called von Recklinhausen of the bone

128
Q

When is Vitamin D dietary supplementation needed?

A

If inssuficient exposure to UV light

129
Q

Before getting to Cholecalciferol what is first?

A

7 Dehydrocholesterol

130
Q

What is needed from the conversion of 7 dehydrocholesterol to cholecalciferol?

A

UV light

131
Q

Alternative name for Vitmain D3

A

Cholecalciferol

132
Q

What is needd for cholecalciferol to be activated?

A

Hydroxylation

133
Q

Where is cholecalciferol found?

A

In the liver

134
Q

First enzyme needed for hydroxylating cholecalciferol?

A

25 hydroxylase

135
Q

What is the result of cholecalciferol hydroxylation?

A

25- hydroxycholecalciferol

136
Q

Where is 25- hydroxycholecalciferol found?

A

In kidney

137
Q

What is needed to make 25 hydroxylase?

A

Have a good liver

138
Q

Which enzyme is required for 25 hydrocholecalciferol in order to become active?

A

1 α hydroxylase

139
Q

Which is the active form of cholecalciferol?

A

1, 25 hydroxycholecalciferol

140
Q

Alternative name for 1, 25 hydroxycholecalciferol

A

Calcitriol, 1, 25 - DHCC

141
Q

What is the result of ↓ Ca2+?

A

PTH production

142
Q

Waht is the effect og PTH?

A

Bone resorption ↑ Ca2+

Kidney ↑ Ca2+ reabsorption to the expense of phosphate PO4 3- (pee)

143
Q

What induces action of 1 α hydroxylase?

A

PTH

144
Q

Why does PTH induce 1 α hydroxylase?

A

Because that is the way it controls indirectly Ca2+ regulation in the gut, because it doesn’t have receptor in there

145
Q

What is the result of vitamin D toxicity?

A

In hypecalcemia, but primarily which can impair renal function

146
Q

Early signs of Vitamin D toxicity

A

Polyuria, Polydipsia and nocturia

147
Q

What is the effect on the bone if taking too much vitamin D?

A

Its going to break the bone

148
Q

What is consider Vitamin D toxicity?

A

Taking 10-15 times of what FDA recommends

149
Q

Main functions of Vitamin A

A

Maintenance of healthy epithelium

Vision

150
Q

Which are the three structures of how Vitamin A may be presented?

A

Hydroxyl (retinol)
Carboxyl (retinoic acid)
Aldehyde (retinal)

151
Q

Which vitamin forms are required for the growth, differentiation and maintenance of epithelial cells?

A

Retinol and retinoic acid

152
Q

Which vitamin A form is important for vision/

A

Retinal

153
Q

Where do we store vitamin A?

A

In the liver in Stellate cells (Ito cells)

154
Q

What is the importance of Ito cells?

A

They behave as fibroblast in the liver, work in liver injury, the one thath result in cirrhosis
Store of vitamin A

155
Q

Which vitamin A form is lacking in night blindess?

A

Retinal deficiency

156
Q

In case of Retinol and retinoic acid deficiency, where can we find keratinuzed squamous epithelia?

A

In the lung

In the eyes, causing Xerophthalmia, Bitot Spots (opaque spots/ ulcers on sclera and cornea)

157
Q

What is Keratomalacia?

A

Destruction of the cornea

158
Q

Causes of Vitamin A deficiency

A

Fat malabsorption

Fat free diets

159
Q

Findings of Vitamin A toxicity

A

Excessive sweating, brittle nails and diarrhea

160
Q

What are Outter Rod cells?

A

Photoreceptors in the retina, neurons

161
Q

What do eye Neurons produce when stimulated?

A

Glutamate (excitatory)

162
Q

What do Rod cells excite?

A

Bipollar cells

163
Q

What does Bipollar cell produces?

A

GABA containing nuerons in optic nerve (inhibitory)

164
Q

What happens if ↑ GABA are produced?

A

Blindness, because it inhibits optic nerve

165
Q

What is necesary to see?

A

↓ Glutamate produced by Rod cells → ↓GABA → disinhibition of optic nerve → you can see

166
Q

In order to have night vision what is needed?

A

Shut down Rod cells

167
Q

Type of protein found in Rod cells that forms the receptor

A

Rhodopsin (light receptor) → senses photones of light

168
Q

What kind of receptor are Rod Cells?

A

Light receptor

169
Q

When does the Rhodopsin receptor work?

A

During night time only because thay only work when few photones

170
Q

What composes Rhodopsin?

A

Protein transmembrane and retinal

171
Q

Which are the two forms in which Retinal exist?

A

Trans

Cis

172
Q

Once Rhodopsin is exposed to photones what happens?

A

Trans is changed to cis and transmembrane protein activates Gt protein

173
Q

Type of transmembrane protein of Rhodopsin

A

7 domain

174
Q

Which enyme is activated by Gt protein after Rhodopsin is stimulated?

A

cGMP PDE (Phosphodiester)

175
Q

What is the function of cGMP in Rod cells?

A

It keeps open Na+ channel and Na+ keeps the cell depolarized (↑ Glutamate) → can’t see in darkness

176
Q

Who inactivates cGMP?

A

cGMP PDE

177
Q

What is the function of cGMP PDE?

A

Inhibits cGMP → Closses Na+ channels → Cells hyperpolatized (↓ Glutamate) → Night vision is possible

178
Q

Which gene translocation is seen in Vitamin A receptor on promyelocytes?

A

t (15; 17)

179
Q

Which is the basis of treating AML M3?

A

Administration of high dose vitamin A because work in t(15; 17) receptor on promyelocytes, making it myelocyte → metamyelocyte → band→ Neutrophil (PMN)

180
Q

At which point of differentiation does a prmyelocyte stop differentiating?

A

Myelocyte → Metamyelocyte

181
Q

For what is Vitamin K required?

A

To introduce Ca2+ binding sites on several calcium dependent proteins

182
Q

What are the modifications that vitamin K does to introduce Ca2+ binding site?

A

γ carboxylation of glutamyl residue(s) in these proteins, often identified the γ carboxylation of glutamic acid

183
Q

Which proteins undergo vitamin K dependent carboxylation?

A

Coagulation factors II (prothrombin), VII, IX, and X and anticoagulant C and S

184
Q

What do coagulation factors II, VII, IX, X and anticoagulant C and S require?

A

Require Ca2+ for ther function

185
Q

Where does γ carboxylation is done?

A

In hepatocytes, NOT in the blood

186
Q

Which enzyme is activated by vitamin K in order to make γ carboxylation?

A

By γ glutamyl carboxylase

187
Q

What does Carboxylation means by vitamin K?

A

Adding another Carboxyl group –> Add negative charges –> Add of Ca2+ (only adequate γ carboxylation)

188
Q

What is the effect of activated prothrombin?

A

Convertion of Fibrinogen to fibrin and make the thrombus

189
Q

What is associated to vitamin K deficiency?

A

With significant bleeding

190
Q

Which drugs look like vitamin K and block γ carboxylation of glutamate?

A

Warfarin

Dicumarol

191
Q

Symptoms found in Vitamin K and C deficiency

A

Easy bruising, bleeding

192
Q

Vitamin K or C deficiency …. Increased bleeding time

A

Vitamin C deficiency

193
Q

How is bleeding time in vitamin K deficiency?

A

Normal

194
Q

Vitamin K or C deficiency…. Increased PT

A

Vitamin K deficiency

195
Q

How is PT in vitamin C deficiency?

A

Normal

196
Q

What is the difference in clinical findings between vitamin K and Vitamin C deficiency?

A

In vitamin K deficiency we only see Hemorrhargic disease with no conective tissue problems

197
Q

What is associated with vitamin K deficiency?

A

Fat malabsorption
Long term antibiotic therapy
Breat fed new born
Infant whose mother was taking anticonvulsant therapy during pregnancy

198
Q

What does bleeding timer measures?

A

Appropiate platelet function

199
Q

How can you calculate increased bleeding time?

A

Blood in tube if it doesn’t coagulate in 2-9 minutes, it means long bleeding time

200
Q

Which drugs can cause fat malabsorption?

A

Cholestyramine

Cholestypol

201
Q

Which situations can cause fat malabsorption?

A

Drugs, Pancreatic insufficiency (CF)

Bad lipoprotein being made

202
Q

Why long term antibiotics can cause vitamin K deficiency?

A

Because they kill the bacterias and remember a good source of vitamin K comes from bacterias

203
Q

Why newborn can have vitamin K deficiency?

A

They don’t have gut flora, so they can not produce endogenous vitamin K

204
Q

Why breast fed newborn can have vitamin K deficiency?

A

As newborn no gut flora

And breast milk is poor in vitamin K

205
Q

Which vitamin is injected in newborn?

A

Vitamin K

206
Q

In which process do warfarin and dicumarol interfere with?

A

With cotranslational modification during synthesis of the precoagulation factor

207
Q

In which situations do warfarin and dicumarol prevent coagulation?

A

Only in vivo and cannot prevent coagulation of blood in vitro

208
Q

How much time does warfarin and dicumarol take after given to a patient to see their full anticoagulant activity?

A

2-3 days

209
Q

What is the benefit of Heparin compared to Warfarin in time?

A

Heparin is often given to provide short term anticoagulant activity

210
Q

What is the mechanism of action of Heparin?

A

Activator of Antithrombin III

211
Q

Coumarin, vitamin K analogs

A

Warfarin and Dicumarol

212
Q

What vitamin is α tocopherol?

A

Vitamin E

213
Q

How is vitamin E consider?

A

An antioxidant

214
Q

What is the function of Vitamin E?

A

As a lipid compound, it is especially important for protecting other lipids from oxidative damage
It prevents perioxidation of fatty acids in cell membranes helping to maintain their normal fluidity. Incluiding LDL

215
Q

What is the side effect of high blood levels of vitamin E?

A

Can cause hemorrhage in patient given warfarin

216
Q

Vitamin E is associated with this element

A

Selenium

217
Q

Symptoms of vitamin E deficiency

A

Hemolytic anemia
Acanthocytosis
CNS effects: Peripheral neuropathy, Ataxia
Retinitis pigmentosum –> blindess

218
Q

CNS sites affeted in vitamin E deficiency

A

Dorsal column of Spinal column: Vibration, propioception
Dorsal Root ganglia: sensory path, pain
Spinocerebellar

BIOCHEMISTRY (12 decks)

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