vitamins Flashcards
kasimerz funk
credited with coining the name “Vitamin” in 1913
elmer McCollum
discovered the first vitamin (A) in june 1913
frederick hopkins
1912 accessory food factor
first to theorize vitamins
Umetaru Suzuki
1910 discovered aberic acid (B1 thiamine)
water soluble vitamins
B’s and C
Fat soluble vitamins
A, D, E, K
Vitamin B1 (thiamine)
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
Vitamin B1 (thiamine) deficiency
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
Dry Beriberi
– 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
Wet Beriberi
– 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
Wernicke encephalopathy
o
-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
Korsakoff’s psychosis
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)
Vitamin B2 – (Riboflavin)
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
Vitamin B3
– 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
Vitamin B6
– (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
Vitamin B6 (pyridoxine) deficiency
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
Nidus
= organic core of urinary stones
Vitamin B12 – (cyan)cobalamin (AKA extrinsic factor of Castle):
- Cannot be found in plant foods, major source is animal foods
- Cannot be absorbed directly, requires assistance via proteins
Obtaining B12 from food
cyan)cobalamin (AKA extrinsic factor of Castle
-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
Causes of B12 deficiency
cyan)cobalamin (AKA extrinsic factor of Castle
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
B12 deficiency leads to
– Pernicious anemia (AKA malignant anemia)
–Demyelination
Megaloblastic Anemias
- vitamin B12 deficient anemia pernicious anemia
2. folic acid deficient anemia
Folic acid deficiency
does not affect the nervous system (except for a developing
fetus) but vitamin B12 does
Vitamin C – (Ascorbic Acid):
- Cannot be produced in the human body
- Found in potatoes, citrus fruit, etc.; many sources
Hydroxylation of procollagen
- Procollagen is full of proline
- Proline is hydroxylated by vitamin C to become hydroxyproline
- Makes connective tissues:
- —Strong
- —Increased tensile strength
Vitamin C Deficiency
- causes scurvy
- bleeding issues
- skeletal changes
- –bowing of legs
- tooth loss
- protruding ribs and sternum (pigeon chest)
- delayed wound healing
Excessive amount of Vitamin C
- enhanced immune system
- could cause systemic elimination of Vitamin C and weaken immune system if TOO much
Vitamin A:
- Discovered by professor McCollum (June 1913)
- Several forms:
- -retinol
- -retinal
- -retinoic acid
Retinol
– storage and transport form; 90% stored in the liver and the
amount kept in storage is enough to supply the body for 6 months
Retinal
– maintains normal vision in dim light
Retinoic acid
– important in determining life span of epithelial cells
Carotinoids
– natural precursors for retinal, ex. beta-carotene
Retinoids
– synthetic/artificial, avoid these (teratogenic affect)
Hypervitaminosis A
-More common and dangerous with synthetic vitamin A use
-ACUTE hypervitaminosis A
— Sign and symptoms similar to that of a brain tumor or intracranial
pressure
CHRONIC hypervitaminosis A
- Weight loss
- Nausea, vomiting
- Dryness of mucosa of lips
- Bone and joint pain
- Hepatomegaly
- Hyperostosis (aka DISH)
Vitamin E – (α-tocopherol):
- A collective name – 4 tocopherols and 4 tocotrienols
- Antioxidants neutralize free radicals
Vitamin E – (α-tocopherol) Deficiency:
-damage of neuron membranes,
-damage to RBC membrane
degeneration of axons
-loss of nerve cells in the DRG
2 types of cell membranes most susceptible to vitamin E deficiency:
o RBCs (however does not lead to anemia) o neurons
Hypervitaminosis E
o Decreased coagulative ability of blood due to interference with vitamin K
decreased production of clotting factors
o Impairment of normal function
Vitamin K:
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
Vitamin K deficiency
Bleeding diathesis
– hemorrhagic disease of newborns → could result in Intracerebral
hemorrhage (stroke)
Iron deficiency
Hypochromic microcytic anemia
Iodine deficiency
o Hypothyroidism
o Goiter
Selenium deficiency
o Kashan’s Disease
o Myopathy, Congestive cardiomyopathy
copper deficiency
o Muscles weakness
o hypopigmentation
zinc deficiency
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
