Nutrition Flashcards
Fat soluble vitamins
A,D,E,K
Toxicity is most common with fat or water soluble vitamins (why)
Fat soluble (accumulate in fat)
How does mineral oil influence influence fat soluble vitamins absorption
Mineral oil (laxative) can cause fat-soluble deficiencies
Which syndromes can cause fat soluble vitamin deficiencies
Examples
Malabsorption syndromes steatorrhe
Ex. Cystic fibrosis, sprue
Water soluble vitamins
B1, B2, B3, B5, B6, B7, B9, B12, C
B1-3, 5-7, 9, 12
C
B vitamins complex deficiencies often result in
- Dermatitis
- Glossitis
- Diarrhea
Which water soluble vitamins does not wash out easily from the body (explain)
B12 –> liver for 3-4 years
Folate –> liver for 3-4 months
(Stored in the liver)
Vitamin A ( retinol) function
- Antioxidant 2. Constituent of normal visual pigment (retinal) 3. Essential of normal epithelial cells into specialized tissue (pancr cells, mucus secreting cells) 4. Prevent squamous metaplasia
Water soluble vitamins and their name
B1 --> Thiamine B2 --> Riboflavin B3 --> niacin B5 --> pantothenic acid B6 --> pyridoxine B7 --> biotin B9 --> folate B12 --> cobolamin C --> ascorbic acid
Vitamin A (retinol) is founded to
Liver and leafy vegetables
Vitamin A (retinol) is used to
- Treat measles (all trans retinoic)
- Treat AML (M3) (all trans retinoic)
- Topically for wrinkles and acne (oral isotretinoin)
Deficiency of vitamin A (retinol)
- Night blindness (nyctalopia)
- Dry scaly skin (xerosis cutis)
- Bitot spots on conjunctiva
- Corneal degeneration (keratomalacia)
- Immune suppression
Before isotretinoin prescription for severe acne what is needed
(-) pregnancy test and reliable contraception
Vitamin A (retinol) excess
- arthralgias 2. Skin changes (scaliness) 3. Alopecia 4. Cerebral edema 5. Pseudo-tumor cerebri 6. Osteoporosis 7. Hepatic toxicity and enlargment
- Teratogenic (cleft palate, cardiac abnormalities)
if acute –> nausea, vomiting, vertigo, and blurred vision
Vitamine D forms
D2 - ergocalciferol
D3 - cholecalciferol
Vitamin D2 (ergocalciferol) - source
Is ingested from plants
Vitamin D3 (cholecalciferol) forms
- 25-OH D3 = storage form
2. 1,25-(OH) D3 (calcitriol) = active form
Vitamin D3 (cholecalciferol) - source
- Consumed in milk
2. Formed in sun - exposed skin (stratum basale)
Vitamin D defiency
- Rickets (children) - bone pain and deformity
- Osteomalacia (adults) - bone pain and muscle weakness)
- Hypocalcemia tetany
Vitamin D function
- Increases intestinal absorption of calcium and phosphate
- Increases bone mineralization (at low levels)
- increases bone resorption at higher levels
Breastfed infants - vit D
Breastfed infants should receive oral vit D
Breast milk has not enough vitamin D
Rickets symptoms
Bone pain and deformity in children
Vitamin D deficiency is exacerbated by (in infants)
- Low sun exposure
- Pigmented skin
- Prematurity
Osteomalacia symptoms
Bone pain and muscle weakness
Vitamin D Excess findings
- Hypercalcemia
- Hypercalciuria
- Loss of apettite
- Stupor
Excess vitamin D is seen in:
granoulomatosis (increased activation of vitamin D by epitheloid macrophages)
Ricktes on x rays
Legs in toddler show bowing of femurs (genu varum)
Vitamin E name
Tocopherol / tocotrienol
Vitamin E vs vitamin B12 deficiency
Neurologic presentation of vit E deficiency may appear similar to B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or increased serum methylmalonic acid
Vitamin E function
- Antioxidant (protect erythrocytes and membranes from free radicals damage
- Enhance anticoagulant effects of warfarin
Vitamin E deficiency
- Hemolytic anemia
- Acanthocytosis
- Muscle weakness
- Posterior column and spinocerebellar tract demyelination
Zinc function
- Essential for the activity of more than 100 enzymes
2. Important in the formation of sinc fingers (transcription factor motif)
Zinc deficiency
- Delayed wound healing
- Hypogonadism
- Decreased adult hair (axillary, facial, pubic)
- Dysgeusia
- Anosmia
- Acrodermatitis enteropathica
- Predispose to alcoholic cirrhosis
Vitamin K function
It is cofactor for the γ-carboxylation of glutamic acid residues on varies proteins required for blood clotting
Acrodermatitis enteropathica
Acrodermatitis enteropathica is a rare inherited form of zinc deficiency, characterized by periorificial and acral dermatitis, alopecia, and diarrhea.
How is vitamin K synthesized
By intestinal flora
For the activation of which blot clotting factors is vitamin K necessary
2, 7, 9, 10 protein C, protein S
Warfarin mechanism of action
Vitamin K antagonist
Vitamin k deficiency
Hemorrhage with increased PT and aPTT but normal bleeding time
Neonates-vit K
Not in breast milk. Neonates are given vitamin K injection at birth to prevent bleeding diathesis
Vitamin k deficiency can occur
- In neonatal (sterile intestine, not in breast milk)
2. After prolonged use of antibiotic broad spectrum antibiotics
Kwashiorkor clinical picture
Small child with swollen belly
Kwashiorkor mechanism (and result in)
Protein malnutrition resulting in skin lesions, edema, liver malfunction (fatty change due to decreased apolipoprotein synthesis)
Kwashiorkor results in
Mnemonic MEAL
- Malnutrition
- Edema (low plasma oncotic pressure)
- Anemia
- Liver (fatty) (low apolipoprotein synthesis)
Function of vitamin C (Ascorbic acid)
- Antioxidant
- It facilitates iron absorption by reducing it to Fe2+ state
- Necessary for hydroxylation of,proline and lysine in collagen synthesis
- Necessary for dopamine β-hydroxylase, which converts dopamine to NE
Marasmus (definition and results)
Total calorie malnutrition resulting in:
- emaciation (tissue and muscle wasting, loss of subcutaneous fat)
- +/- edema
vitamin C (Ascorbic acid) is found in
- Fruits
2. Vegetables
vitamin C (Ascorbic acid) is ancillary treatment for
Methemoglobinemia by reducing Fe3+ to fe2+
Vitamin C (ascorbic acid) deficiency
- Scurvy
2. Weakened immune response
Vitamin C excess
- Nausea 2. Vomiting 3. Diarrhea 4. Fatigue 5. Calcium oxalate nephrolithiasis 6. Can increase risk of iron toxicity in in predisposed individuals (transfusions, hereditary hemochromatosis)
Vitamine B5 is also called
Pantothenate
Scurvy - presentation
Swollen gums, bruising, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, corkscrew hair
Vitamin B5 (pantothenate) function
Essential component of coenzyme A (CoA, a cofactor for acyl transfers) and fatty synthase
Vitamin B5 deficiency
- Dermatitis
- Enteritis
- Alopecia
- Adrenal insufficiency
Fat soluble vitamins absorption depends on
- Gut
2. Pancreas
Vitamin B1 name
Thiamine
Vitamin B1 (thiamine) function
In thiamine pyrophosphate (TPP) a cofactor of several dehydrogenase enzyme reaction:
- Pyruvate dehydrogenase - Links glycolysis to TCA cycle
- α-ketoglutarate dehydrogenase - TCA cycle
- Transketolase - HMP shunt
- Branched chain ketoacid dehydrogenase
Thiamine (vit B1) deficiency
- Wernicke - korskakoff syndrome
- Dry beriberi
- Wet beriberi
Deficiency of vitamin B1 pathophysiology
Impaired glucose breakdown –> ATP depletion worsened by glucose infusion. Highly aerobic tissues (brain, heart) are affected first
Thiamine (vit b1) deficiency seen in
- Malnutrition
2. Alcoholism (2ry to malnutrition and malabsorption)
Vitamin B1 (thiamine) deficiency diagnosis is made by
Increased in RBC transketolase activity following vitamin B1 administration
Dry beriberi
- Polineuritis
2. Symmetrical muscle wasting
Wet beriberi
- Hight cardiac output failure (dilated cardiomyopathy)
2. Edema
Wernicke - korsakoff syndrome pathophysiology
Damage to medial dorsal nucleus of thalamus, mamillary bodies
Wernicke - korsakoff syndrome classic triad
Confusion, opthalmoplegia, ataxia
Wernicke - korsakoff syndrome - symptoms
- Classic triad (Confusion, opthalmoplegia, ataxia)
- Confabulation
- Personality changes
- Permanent memory loss
Vitamin B2 (riboflavin)
Compoments of flavins FAD, FMN, used as cofactor in redox reaction
Eg. The succinate dehydrogenase reaction in the TCA cycle
Vitamin B2
Riboflavin
Vitamin B2 deficiency
- Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth)
- Corneal vascularization
Vitamin B3 name
Niacin
Niacin is constituent of
NAD+ and NADP+ (used in redox)
Niacin is used to treat
Dyslipidemia
It lowers levels of VLDL and raises levels HDL
Niacin synthesis
Derived from tryptophan. It requires B2 and B6
Niacin is derived from
Tryptophan
Synthesis of niacin requires
B2 and B6
Niacin deficiency
- Glossitis
2. Pellagra (of severe deficiency)
Causes of pellagra
- Hartnup disease (Decreased tryptophan absorption)
- Malignant carcinoid syndrome (increased tryptophan metabolism)
- Isoniazid (low B6)
Pellagra symptoms
- Diarrhea
- Dementia (and hallucinations)
- Dermatitis (casal necklace (C3.4 dermotome) or hyperpigmentation of sun-exposed limbs)
Niacin excess
- Facial flushing (induce by prostaglandins, not histamine)
- Hyperglycemia
- Hyperuricemia
Dermatitis of pellagra
- Casal necklace (C3.4 dermotome)
2. Hyperpigmentation of sun-exposed limbs
Facial flushing of excess niacin
Induced by prostaglandins, not histamine
Vitamin B7
Biotin
Biotin (vit 7) function
Cofactor for carboxylation enzymes
Carboxylation enzymes function
Add a 1-carbon group
Carboxylation enzymes that biotin is cofactor
- Pyruvate carboxylase
- Acetyl-coa carboxylase
- Propionyl-Coa carboxylase
Pyruvate carboxylase
Pyrivate (3C) to oxaloacetate (4C)
Acetyl-coa carboxylase
Acetyl - coa (2C) to malonyl - coa
Propionyl-Coa carboxylase
Propionyl - coA (3C) to methylmalonic - coa
Biotin deficiency symptoms
Rare.
Dermatitis, alopecia, enteritis
Biotin deficiency caused by
Caused by antibiotic use or excessive ingestion of raw egg whites
Folic acid (vit 9) found
Leafy green vegetables
Vitamin B9 name
Folic acid
Folic acid absorption
Jejunum
Folic acid (vit9) storage
Small reverse poll stored primarily in the liver
Folic acid function
- Converted to tetrahydrofolate (THF), a coenzyme for 1-carbom transfer/methylation reactions
- important for the synthesis of nitrogenous bases in DNA and RNA
Folic acid vs B12 symptoms deficiency
Folic acid has no neurologic symptoms
Folic acid (vit9) deficiency symptoms
- Macrocytic, megaloblastic anemia
- Hypersegmented polymorphononuclear cells (PMN)
- Glossitis
Folic acid deficiency labs:
- Increased homocysteine
2. Normal methylmalonic acid
The most common vitamin deficiency in United States
Folic acid (vitamin B9)
Folic acid deficiency causes
- Alcoholism
- Pregnancy
- Drugs
Folic acid - early pregnancy
Supplemental maternal folic acid in early pregnancy decreases risk of neural tubu defects
Drugs that cause deficiency of folic acid
- Phenytoin
- Sulfonamides
- Methotrexate
Vitamin that can enhance the anticoagulant effect of warfarin
Vitamin E (tocopherol/tocotrienol)
Vitamin B12
Cobalamin
Cobolamin (vit 12) is founded in
Animal products
Cobalamin (vit12) is synthesized
Only by microorganims
Cobalamin pool
Very large reserve pool (several years) stored primary in the liver
Cobalamin deficiency symptoms
- Macrocytic, megaloblastic anemia
- Hypersegmented PMNs
- Paresthesias
- Sabacute combined degeneration due to abnormal myelin
- If prolonged deficiency –> irreversible nerve damage
Cobalamin function
Cofactor for:
- methionine synthase (tranfers CH3 groups as methycobslamin)
- Methylmalonyl - coa mutase
Cobalamin deficiency labs
Increased serum homocysteine and methylmalonic acid levels
Cobalamin deficiency - CNS symptoms
- Paresthesias
- Sabacute combined degeneration (dorsal columns, corticospinal tracts, spinocerebellar tracts) due to abnormal myelin
- If prolonged –> irreversible nerve damage
causes of Cobalamin deficiency
- Lack of intrinsic factor (Pernicious anemia, gastric bybass, surgery)
- Insufficient intake (veganism)
- Malabsorption (sprue, enteritis)
- Diphylobothrium latum
- Absence of terminal ileum (crohn)
Methionine to homocysteine
Methionine + ATP –> S-adenosyl methionine Pi + PPi
–> out one CH3 + adenisine–>homocysteine
Methylmalonyc - coa source
Fatty acids with odd number of C and branched - chain amino acids
Homocysteine to methionine
homocysteine + B12+THF-CH3
–> methinine + THF (methionine synthase)
Methylmalonic - coa to succinyl - coa
Merhylmalonyc - coa mutase + B12 (Methymanoyl-coa Mutase)
Succinyl - coa next step
- TCA
- Myelin synthesis
- Heme (pyridoxine)
Vitamin B6 name
Pyridoxine
Pyridoxine function
Converted to pyridoxal phosphate, a cofactor used in: 1. Transamination (e.g ALT , AST), 2.decarboxylation reactions 3.glycogen phosphorylase
Synthesis of cystathionine, HEME, NIACIN, histamine and neurotransmitters including seretonin, epinephrin, norepinephrine, dopamine, GABA
Pyridoxime is converted to
Pyridoxal phosphate
Pyridoxal phosphate is a cofactor used in:
- Trasnamination
- Decarboxylation
- Glycogen phosphorylase
Pyridoxine-synthesis of
Cystathionine, heme, niacin, histamine, neurotransmitters
Pyridoxine-neurotransmitters
Serotonin, epinephrin, norepinephrin, dopamine, GABA
Pyridoxine deficiency
- Convulsions
- Hyperirritability
- Peripheral neuropathy (deficiency inducible by isoniazid and oral contraceptive)
- Sideroblastic anemias due to impaired hemoglobin synthesis and iron excess
B complex deficiency often result in
Dermatitis, glossitis disrrhea
Ethanol to acetaldehyde reaction (and location
- CYTOSOL: Ethanol + (NAD+) –> acetaldehyde NADH (enzyme alcohol dehydrogenase)
- PEROXISOME: ethanol + H202 –> acetaldehyde + H20 (catalase)
- MICROSOME: ethanol + NADPH –> acetaldehyde + NADP+ + ROS
Acetaldehyde to acetate reaction
Acetaldehyde +(NAD+) –> acetate + NADH (enzyme acetaldehyde dehydrogenase)
Acetaldehyde to acetate reaction - LOCATION
mitochondria
The limiting reagent of ethanol metabolism
NAD+
Alcohol dehydrogenase rate
Zero order kinetics
Fomepizole - mechanism of action
Alcohol dehydrogenase inhibitor
Alcohol dehydrogenase inhibitor
Fomepizole
Fomepizole clinical uses
Antidote for
- Methanol
- Ethlylene glycol
Disulfiram mechanism of action
Inhibitor of acetaldehyde dehydrogenase (acetaldehyde accumulates, contributing to hangover)
Acetaldehyde dehydrogenase inhibitor
Disulfiram
Which rate is increased by ethanol metabolism
NADH/NAD+
Ethanol metabolism increased NADH/NAD+ ration in liver causing
- Pyruvate –> lactate (lactic acidosis)
- Oxaloacetate –> malate ( prevents gluconeogenesis –> fasting hypoglycemia)
- Dihydroxyacetone - 3 - phosphate –> glycerol - 3 - phosphate (combines with fatty acids to make triglycerides–> hepatosteatosis)
Additionally NADH/NAD increased ratio in alcoholics disfavors:
TCA production of NADH –> utilization of acetyl - coa for ketogenesis (ketoacidosis) and lipogenesis (hepatosteatosis)
Ethanol metabolism/oxaloacetate to malate –>
Prevents gluconeogenesis….fasting hypoglycemia
Hartnup disease - mode of inheritance
AR
Hartnup disease - manifestation
deficiency of neutral amino acid (eg. tryptophan transporters in proximal renal tubular cells and on enterocytes –> neutral aminoaciduria and decreased absorption from the gut –> decreased tryptophan for conversion to niacin –> pelagra like symptoms
Hartnup disease - treatment
- high protein diet
2. nicotinic acid (niacin)
B6 deficiency - peripheral neuropathy - deficiency inducible by
- isonizid
2. oral contraceptives