vitamins Flashcards

1
Q

kasimerz funk

A

credited with coining the name “Vitamin” in 1913

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2
Q

elmer McCollum

A

discovered the first vitamin (A) in june 1913

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3
Q

frederick hopkins

A

1912 accessory food factor

first to theorize vitamins

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4
Q

Umetaru Suzuki

A

1910 discovered aberic acid (B1 thiamine)

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5
Q

water soluble vitamins

A

B’s and C

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6
Q

Fat soluble vitamins

A

A, D, E, K

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7
Q

Vitamin B1 (thiamine)

A

Maintains neural membranes and nerve conduction, especially in peripheral
nerves 
- Most important source of B1 is the husks of grains (unpolished grain)

(extra info)
More likely to be deficient:
o Alcoholics -
 Alcohol competes with B1 in neural functions and in biochemical
reactions
 Alcoholics are also more likely to spend their money on alcohol
than good nutrition
o 1st trimester of pregnancy → Morning sickness (vomiting causes the
pregnant women to lose the vitamins and nutrition needed) o Fast-growing teens use it up faster

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8
Q

Vitamin B1 (thiamine) deficiency

A

o Discovered by Christiaan Eijkman (food consumption vs. deficiency) o Severe nervous system disorder -3 types:
1-Dry Beriberi
2-Wet Beriberi
3-Wernicke encephalopathy and Korsakoff’s psychosis

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9
Q

Dry Beriberi

A

– nervous system
- Characterized by Non-specific peripheral polyneuropathy
with myelin degeneration and disruption of all 3
neurological arcs: sensory, motor and reflex arcs 
-Manifestations:
—-wrist drop, foot drop, and toe drop
—-Paresthesia, numbness, loss of reflexes

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10
Q

Wet Beriberi

A

– heart

  • Characterized by damage to cardiovascular system 
  • Enlargement of the heart with thinning of the heart
    (muscle) wall  flabby myocardium 
  • Peripheral vasodilation 
  • Cardiac failure 
  • Peripheral edema (pitting)
  • Dyspnea and orthopnea – shortness of breath
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11
Q

Wernicke encephalopathy

o

A

-Affects mamillary bodies in the brain  atrophy
-Characterized by psychological problems:
 — Global confusion
 — Apathy
— Listlessness
— Disorientation
— Ophthalmoplegia - paralysis of one or more
eye muscles
—– Deep damage of CNS 
—– resulting in irregular eye
movements, not simultaneous 
—– patient is close to death when this is
seen

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12
Q

Korsakoff’s psychosis

A

3 Manifestations:
1- Anterograde amnesia – loss of memory of events after the cause of the amnesia
2- Inability to acquire new information
3- Confabulation – excessive talking

-(a patient may present with 1,2 or all 3 types)

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13
Q

Vitamin B2 – (Riboflavin)

A

Deficiency usually seen in people with chronic debilitating diseases, called
ariboflavinosis
[-osis → disease not associated w/ inflammation]
o Oncologic diseases o Renal diseases
o Cheilosis (non-inflammatory) – cracks in the corner of the mouth,
 Symptoms:
 may lead to infection and become cheilitis (with inflammation)
 chelilitis is a secondary infection
o Glossitis – inflamed tongue
 Red
 May lead to atrophy of tissue and loss of taste
o Superficial interstitial keratitis – hardening of the cornea
 Cornea is avascular and relies on intraocular fluid and tears for
nutrients and waste removal
 With a deficiency in B2, a capillary net forms around and
penetrates into the cornea resulting in inflammation and damage
to the cornea (ulceration)
 Ulceration is painful due to nociceptors in the cornea
 As the cornea begins to heal  fibrosis and loss of vision
o Dermatitis
 Inflammation seen in especially the nasolabial folds, behind the
ears, and groin

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14
Q

Vitamin B3

A

– Niacin (nicotinic acid, nicotinamide):
 Used as a medicine for its vasodilation ability (nitroglycerine treatment)
 Can be produced via normal gut flora from tryptophan
 In plants (ex. maize) B3 is bound and cannot be absorbed when eaten
 B3 leads to decreased production of lipoproteins (LDLs) → prevention of
 Deficiency result Pellagra – “pelle agro” = dry skin
arteriosclerosis
o Deficiency in B3 o The 4 Ds
 Dermatitis – develops on skin exposed to sun
 Casal’s necklace  Glove-and-stocking lesions  Atrophy of epithelial cells of intestinal mucosa with
involvement of submucosal layer  Degeneration of cortical neurons  Loss of function
 Diarrhea
 Dementia
 Death

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15
Q

Vitamin B6

A

– (pyridoxine):
 Found in all foods  Thermolabile – a small amount of heat will destroy it  Some medications compete with B6 in biochemical reactions and may lead to
deficiency
o Izoniazid – antituberculosis medication, thought probably not used as
often today o Estrogens – high production of estrogens or hormone treatment
 Estrogens have hyperplastic activity → promotes replication of cells especially in endometrium, which could lead to cancer
 Predisposes to breast and uterine cancers
o D-penicillamine – medicine used for the treatment of Wilson’s disease
and systemic sclerosis

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16
Q

Vitamin B6 (pyridoxine) deficiency

A

 Symptoms of deficiency o Glossitis
-Cheilosis/cheilitis
-Peripheral polyneuropathy
o Convulsions – especially in infants and children
- Increased sloughing of epithelial cells
- Nidus formation  urinary tract stones
- Seborrheic dermatitis
—-Dandruff
—- Scaly and greasy squamous epithelial cells

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17
Q

Nidus

A

= organic core of urinary stones

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18
Q

Vitamin B12 – (cyan)cobalamin (AKA extrinsic factor of Castle):

A
  • Cannot be found in plant foods, major source is animal foods 
  • Cannot be absorbed directly, requires assistance via proteins
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19
Q

Obtaining B12 from food

cyan)cobalamin (AKA extrinsic factor of Castle

A

-When food is eaten, salivary glands secrete R-binder
-R-binder binds to B12 and carries it from the stomach to the duodenum
where they dissociate
-Stomach parietal cells produce and secrete intrinsic factor (AKA intrinsic
factor of Castle) which then moves into the duodenum
-Once they are both in the duodenum, intrinsic factor and extrinsic factor
bind and move along to the ileum
-The ileum has receptors for intrinsic factor, where intrinsic factor (bound
to extrinsic factor) bind and then move intrinsic factor (with extrinsic
factor) into the blood circulation where intrinsic and extrinsic factor
dissociate

20
Q

Causes of B12 deficiency

cyan)cobalamin (AKA extrinsic factor of Castle

A

o May be diet – not enough in the food o May be autoimmune (idiopathic)
 Autoimmune chronic gastritis
 Immune system produces parietal canalicular antibodies
which destroy parietal cells in the stomach
 Results in no production of intrinsic factor and B12 cannot
be absorbed
 Bind to intrinsic factor, blocking the receptor for B12  B12 cannot bind to intrinsic factor
 Bind to receptors for intrinsic factor in the ileum
 Intrinsic factor (bound to extrinsic factor) cannot pass
through to the GI wall and enter the blood circulation
 Blocking antibodies
 Binding antibodies

21
Q

B12 deficiency leads to

A

– Pernicious anemia (AKA malignant anemia)
–Demyelination

22
Q

Megaloblastic Anemias

A
  1. vitamin B12 deficient anemia  pernicious anemia

2. folic acid deficient anemia

23
Q

Folic acid deficiency

A

does not affect the nervous system (except for a developing

fetus) but vitamin B12 does

24
Q

Vitamin C – (Ascorbic Acid):

A
  • Cannot be produced in the human body 

- Found in potatoes, citrus fruit, etc.; many sources

25
Q

Hydroxylation of procollagen

A
    • Procollagen is full of proline
    • Proline is hydroxylated by vitamin C to become hydroxyproline
    • Makes connective tissues:
  • —Strong
  • —Increased tensile strength
26
Q

Vitamin C Deficiency

A
  • causes scurvy
  • bleeding issues
  • skeletal changes
  • –bowing of legs
  • tooth loss
  • protruding ribs and sternum (pigeon chest)
  • delayed wound healing
27
Q

Excessive amount of Vitamin C

A
  • enhanced immune system

- could cause systemic elimination of Vitamin C and weaken immune system if TOO much

28
Q

Vitamin A:

A
  • Discovered by professor McCollum (June 1913) 
  • Several forms:
  • -retinol
  • -retinal
  • -retinoic acid
29
Q

Retinol

A

– storage and transport form; 90% stored in the liver and the
amount kept in storage is enough to supply the body for 6 months

30
Q

Retinal

A

– maintains normal vision in dim light

31
Q

Retinoic acid

A

– important in determining life span of epithelial cells

32
Q

Carotinoids

A

– natural precursors for retinal, ex. beta-carotene

33
Q

Retinoids

A

– synthetic/artificial, avoid these (teratogenic affect)

34
Q

Hypervitaminosis A

A

-More common and dangerous with synthetic vitamin A use

35
Q

-ACUTE hypervitaminosis A

A

— Sign and symptoms similar to that of a brain tumor or intracranial
pressure

36
Q

CHRONIC hypervitaminosis A

A
  • Weight loss
  • Nausea, vomiting
  • Dryness of mucosa of lips
  • Bone and joint pain
  • Hepatomegaly
  • Hyperostosis (aka DISH)
37
Q

Vitamin E – (α-tocopherol):

A
  • A collective name – 4 tocopherols and 4 tocotrienols 

- Antioxidants neutralize free radicals

38
Q

Vitamin E – (α-tocopherol) Deficiency:

A

-damage of neuron membranes,
-damage to RBC membrane
degeneration of axons
-loss of nerve cells in the DRG

39
Q

2 types of cell membranes most susceptible to vitamin E deficiency:

A
o  RBCs (however does not lead to anemia) 
o  neurons
40
Q

Hypervitaminosis E

A

o Decreased coagulative ability of blood due to interference with vitamin K
 decreased production of clotting factors
o Impairment of normal function

41
Q

Vitamin K:

A

 Coagulation of blood (German – Koagulation); without it, clotting cannot occur  Produced by gut flora  Any food usually animal product  Important in the production of clotting factors (produced in the liver):
o CF 2 prothrombin
 Also used in the production of proteins
o CF 7 proconvertin
o CF 9 Christmas Factor
o CF 10 Stuart-Prower Factor
-also used in the production of proteins such as Osteocalcin

42
Q

Vitamin K deficiency

A

Bleeding diathesis
– hemorrhagic disease of newborns → could result in Intracerebral
hemorrhage (stroke)

43
Q

Iron deficiency

A

Hypochromic microcytic anemia

44
Q

Iodine deficiency

A

o Hypothyroidism

o Goiter

45
Q

Selenium deficiency

A

o Kashan’s Disease

o Myopathy, Congestive cardiomyopathy

46
Q

copper deficiency

A

o Muscles weakness

o hypopigmentation

47
Q

zinc deficiency

A
o  Deficiency of  Zinc: Distinctive rash, acrodermatitis enteropathica 
o  Anorexia, diarrhea
o  Growth retardation 
o  Hypogonadism, infertility 
o  Impaired wound healing 
o  Impaired night vision 
o  Impaired immune function 
o  Depressed mental function