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STEP 1 (4) > Biochemistry-Nutrition > Flashcards

Biochemistry-Nutrition Flashcards

1
Q

What vitamins are fat soluble?

A

ADEK (absorption dependent on the gut and pancreas)

Toxicity of these is more common than for water-soluble vitamines b/c fat soluble vitamins accumulate in fat

Malabsorption syndromes with steatorrhea such as cystic fibrosis and sprue or mineral oil intake can cause fat-soluble vitamin deficiencies

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2
Q

Notes about water soluble vitamins

A

all wash out easily from the body except B12 amd folate (stored in the liver)

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3
Q

B-complex deficiencies often result in what clinical triad:

A

dermatitis

glossitis

diarrhea

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4
Q

B1 (thiamine: TTP)

B2 (riboflavin: FAD, FMN)

B3 (niacin: NAD+)

B5 (pantothenic acid: CoA)

B6 (pyridoxine: PLP)

A

B7 (biotin)

B9 (folate)

B12 (cobalamin)

C (ascorbic acid)

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5
Q

What is the function of vitamin A?

A

antioxidant

constituent of visual pigments (retinal)

essential for normal differentiation of epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells)

prevents squamous metaplasia

used to tx measles and AML subtype M3 (retinol)

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6
Q

What foods contain a lot of vitamin A?

A

liver and leafy veggies

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7
Q

What does deficiency in vitA cause?

A

night blindness (nyctalopia)

scaly skin (xerosis cutis)

corneal degeneration (keratomalacia)

bitot spots on conjnctiva (below)

immunosuppression

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8
Q

How would a vitA OD present?

A

acute toxicity: N/V, vertigo, and blurred vision

chronic toxicity: alopecia, dry skin, hepatic toxicity and enlargment, arthralgias, and pseudotumor cerebri

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9
Q

vitA OD is teratogenic. How?

A

causes cleft palate, cardiac abnormalities (thus a neg pregnancy test is required before isotreinoin is prescribed for severe acne)

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10
Q

What is the function of vitB1 (thiamine)?

A

In thiamine pyrophosphate (TPP), a cofactor for several dehydrogenase rxns including:

pyruvate dehydrogenase (links glycolysis to TCA cycle)

a-ketoglutarate dehydrogenase (TCA cycle)

Branched-chain ketoacid dehydrogenase

transketolase (HMP shunt)

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11
Q

What does deficiency of thiamine cause?

A

impaired glucose breakdown leading to ATP depletion worsened by glucose infusion (highly aerobic tissues such as the brain and heart are affected first)

can cause Wernicke-Krsakff syndrome and beriberi

seen in alcoholism and malnutrition

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12
Q

How is the diagnosis of thiamine deficiency made?

A

increased in RBC transketolase activity following vitB1 administration

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13
Q

What is Wernicke-Korsakoff syndrome?

A

confusion, ophthalmoplegia, ataxia (classic triad)

+ confabultation, personality change, memory loss (permanent)

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14
Q

Wernicke-Korsakoff syndrome is marked by damage to what brain structures?

A

medial dorsal nucleus of the thalamus, and mamillary bodies

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15
Q

What is the difference between wet and dry beriberi?

A

Wet: high-ouput cardiac failure (dilated cardiomyopathy), edema

Dry: polyneuritis, symmetrical muscle wasting

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16
Q

What is the function of vitB2 (riboflavin)?

A

component of flavins FAD and FMN, used as cofactor in redox rxns (e.g. the succinate dehydrogenase rxn in the TCA cycle)

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17
Q

What does a deficiency of riboflavin cause?

A

cheliosis (inflammation of lipds, scaling, and corner fissues)

corneal vascularization

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18
Q

What is the function of vitB3 (niacin)?

A

constituent of NAD+, NADP+ (used in redox rxns)

derived from tryptophan (synthesis requires vitB2 and vitB6)

used to tx dyslipidemia (lowers levels of VLDL and raised levels of HDL)

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19
Q

What does deficiency of vitB3 (niacin) cause?

A

glossitis

severe deficiency leads to pellagra, which can be casued y Hartnup disease (decreased tryptophan absorption), malignant carcinoid syndrome (increased tryptophan metabolism) and isoniazid (decreased vitB6)

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20
Q

What are the symptoms of pellagra?

A

diarrhea, dementia (also hallucinations), and dermatitis (C3/C4 dermatome ‘broad collar’ rash, aka casal necklace), and hyperpigmentation of sun-exposed limbs

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21
Q

What does OD of niacin cause?

A

facial flushing (induced by prostaglandins, not histamine; can avoid by taking aspirin with niacin)

hyperglycemia, hyperuricemia

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22
Q

What is the function of vitB5 (pantothenic acid)?

A

essential component of CoA and fatty acid synthase

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23
Q

What would a vitB5 (pantothenic acid) deficiency cause?

A

dermatitis, enteritis, alopecia, and adrenal insufficiency

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24
Q

What is the function of vitB6 (pyridoxine)?

A

converted to pyridoxal phospahte (PLP), a cofactor used in transamination (e.g. ALT and AST) decarboxylation rxns, glycogen phosphorylase

synthesis of cystathionine, heme, niacin, histamine, and NTMs including serotonin, epi, nor, dopamine, and GABA

25
Q

What does deficiency of vitB6 (pyridoxine) cause?

A

convulsions, hyperirritability,

peripheral neuropathy (deficiency inducible by isoniazid and oral contraceptives)

sideroblastic anemia due to impared hemoglobin synthesis and iron excess

26
Q

What is the function of vitB7 (biotin)?

A

cofactor for carboxylation enzymes (which add 1C):

pyruvate carboxylase: pyruvate (3C) to oxaloacetate (4C)

acetyl-CoA carboxylase: acetyl-CoA (2C) to malonyl-CoA (3C)

Propionyl-CoA carboxylase: Propionyl-CoA (3C) to methylmalonyl-CoA (4C)

27
Q

How does deficiency of vitB7 (biotin) present?

A

relatively rare

dermatitis, alopecia, enteritis (caused by ABX use of excessive ingestion of raw egg whites)

28
Q

What is the function of vitB9 (folate)?

A

converted to tetrahydrofolic acid (THF), a coenzyme for 1C-transfer/methylayion rxns

important for the synthesis of nitrogenous bases in DNA/RNA

29
Q

What foods contain lots of vitB9 (folate)?

A

leafy green veggies (absorbed in the jejunum and a small reserve pool is stored in the liver)

30
Q

What does deficiency of vitB9 (folate) cause?

A

macocytic, megaloblastic anemia

hypersegmented PMNs

glossitis

NO neurological symptoms (unlike B12 deficiency)

31
Q

What labs confirm deficiency of vitB9 (folate)?

A

elevated homocysteine, normal methylmalonic acid levels

seen in alcoholism and pregnancy

32
Q

What drugs can cause deficiency of vitB9 (folate)?

A

phenytoin

sulfonamides

methotrexate

33
Q

What is the function of vitB12 (cobalamin)?

A

cofactor for homocyteine methyltransferase (transfers CH3 groups) and methylmalonyl-CoA mutase (converts methylmalonyl COA to succinyl CoA during heme production)

34
Q

Describe the methionine production pathway

A

homocysteine is converted to methionine by addition of a CH3 group from THF-CH3 using homocysteine methyltransferase and B12 as a cofactor

Methionine can then converted to SAM using ATP, which can then be reconverted to homocyteine via loss of a CH3 group

35
Q

What foods is vitB12 found in?

A

animal products

synthesized only by microorganisms and humans generally have very large pools that can last for months in the liver

36
Q

What usually causes vitB12 deficiency?

A

insufficient intake (e.g. veganism), malabsorption (e.g. sprue, enterits, Diphellobothrium latum infection), lack of intrinsic factor, or lack of terminal ileum

37
Q

How does vitB12 deficiency present?

A

macrocytic, megaloblastic anemia

hypersegmented PMNs

paresthesias and subacite combined degeneration (degen of the dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts) due to abnormal myelin

38
Q

How is vitB12 deficiency diagnosed?

A

elevated serum homocysteine and methylmalonic acid levels

39
Q

What is the function of vitC (ascorbic acid)?

A

antioxidant

facilitates iron absorption from the duodenum by reducing it to Fe2+ (ancillary tx for methemoglobinemia)

necessayr for hydroxylation of proline and lysine in collagen synthesis

needed for dopamine-B-hydroxylase, which converts dopamine to NE

40
Q

Where is vitC found?

A

fruits and veggies

41
Q

What vitC deficiency cause?

A

Scurvy- swollen gums, brusing, petechiae, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, “corkscrew” hair

results from collagen defects

42
Q

What does vitC OD cause?

A

N/V, fatigue

diarrhea

calcium oxalaye nephrolithiasis

increased risk of iron toxicity in those with transfusions, hereditary hemochromatosis

43
Q

What are the forms of vitD?

A

D2= erocalciferol- ingested from plants

D3= cholecalciferol- consumed in milk, formed in sun-exposed skin (stratum basale)

25-OH D3= storage form

1,25- (OH)2 D3 (calcitrol)= active form

44
Q

What are the functions of vitD?

A

increased intestional absorption of calcium and phosphate and increase bone mineralization

45
Q

What does deficiency of vitD cause?

A

rickets in children (bone pain and deformity)

osteomalacia in adults

46
Q

What is the function of vitE (tocopherol)?

A

antioxidants (protects RBCS and membranes from free radical damage)

can enhance the anticoagulant effects of warfarin

47
Q

What does deficiency of vitE (tocopherol) cause?

A

hemolytic anemia

acenthocytosis

muscle weakness

posterior columna and spinocerebellar tract demyelination

Note that the neurological presentation is similar to vitB12 deficiency, but without megaloblastic anemia, hypersegmented PMNs, or elevated serum methylmalonic acid levels

48
Q

What are the functions of vitK (phytomenadione, phylloquinone, phytonadione)?

A

cofactor for the y-carboxylation of glutamic acid residues on various proteins required for blood clotting (synthesized by intestinal flora)

needed for the maturation of clotting factors II, VII, IX, and X and proteins C/S

49
Q

What does deficiency of vitK cause (via ABX or warfarin, etc.)?

A

neonatal hemorrhage with elevated PT an aPTT but normal bleeding time (neonates have sterile intestines and are unable to synthesize vitK)

can also occur after ABX use

Note that vitK is NOT in breast milk and neonates need supplements

50
Q

What is the function of zinc?

A

mineral essential for the activity of 100+ enzymes and zinc fingers

51
Q

How might zinc deficiency present?

A

delayed wound healing, hypogonadism

decreased adult hair (axillary, facial, pubic)

dyseusia (a condition in which a foul, salty, rancid, or metallic taste sensation will persist in the mouth.)

anosmia

acrodermatitis enteropathica

may predispose to alcoholic cirrhosis

52
Q

What is Kwashiorkor?

A

protein malabsoprtion resulting in skin lesions, edema due to decreased plasma oncotic pressure, liver malfunction (fatty change due to decreased apolipoprotein synthesis)

53
Q

What is Marasmus?

A

total calorie malnutrition resulting in tissue and msucle wasting, loss of subQ fat, and variable edema

54
Q

How is ethanol metabolized?

A

ethanol is converted to acetaldehyde via alcohol dehydrogenase (using NAD+; zero-order kinetics) in the cytosol (or via catalse in the peroxisome or CYP2E1 in the microsome)

and then to acetate via acetaldehyde dehdyrogenase (using NAD+)

55
Q

What drugs blocks the action of alcohol dehdyrogenase?

A

fomeprizole (an antidote for emthanol or ethylene glycol poisoning)

56
Q

What drugs blocks the action of acetaldyhde dehdyrogenase?

A

disulfram (acetaldehyde accumulates, leading to hangover symptoms)

57
Q

Ethanol metabolism increased the NADH/NAD+ ratio in the liver leading to:

A

pyruvate conversion to lactate (lactic acidosis)

oxaloacetate conversion to malate (prevents gluconeogenesis causing a fasting hypoglycemia)

dihydroxyacetone phosphate conversion to glycerol-3-phosphate (combined with fatty acids to make TAGs leading to heptatosteatosis)

58
Q

Note also the an icnreased NADH/NAD+ ratio disfavors TCA production of NADH, resulting in increased utilization of acetyl-CoA for ketogenesis (leading to ketoacidosis) and lipogenesis (hepatosteatosis)

A

STEP 1 (4) (18 decks)

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