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UWorld - Biochemistry > Biochem - Nutrition > Flashcards

Biochem - Nutrition Flashcards

1
Q

How many calories per gram does the following yield:

  1. Protein
  2. Carbohydrates
  3. Fats
  4. Ethanol
A
  1. Protein = 4 cal/g
  2. Carbs = 4 cal/g
  3. Fats = 9 cal/g
  4. Ethanol = 7 cal/g
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2
Q

What are the fat soluble vitamins?

A

A (retinol)

D

E

K

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3
Q

What are the water soluble vitamins?

A

B1 (Thiamine - TPP) B12 (cobalamin)

B2 (riboflavin - FAD,FMN) C (ascorbic acid)

B3 (niacin - NAD+)

B5 (pantothenic acid - CoA)

B6 (pyridoxine)

B7 (biotin)

B9 (folate)

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4
Q

What are the functions of Vitamin A? (4)

A
  1. Antioxidant
  2. Constituent of visual pigments
  3. Differentiation of epithelial cells into specialized tissue
  4. Treatment of measles and acute promyelocytic leukemia (APL)
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5
Q

What are the symptoms of Vitamin A deficiency?

A
  • Night blindness (nyctalopia)
  • Dry, scaly skin (xerosis cutis)
  • Keratomalacia: corneal degeneration
  • Bitot Spots: foamy spots on conjunctiva
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6
Q

What are the symptoms of excess vitamin A

a. Acute Toxicity
b. Chronic Toxicity

A

a. nausea, vomitting, vertigo and blurred vision
b. alopecia (bald spots), dry skin, hepatic toxicity, arthralgias, pseudomtumor cerebri

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7
Q

Is Vitamin A safe to give to pregnant woman?

A

No, it is Teratogenic

Can result in cleft palate and cardiac abnormalities

(A negative pregnancy test and 2 forms of contraception are required before isotretinoin (vitA derivative) can be perscribed)

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8
Q

What is the function of Vitamin B1 (thiamine)

A

Thiamine Pyrophosphate (TPP) is a cofactor for several dehydrogenase enzyme reactions

  • Alpha-ketoglutarate dehydrogenase (TCA cycle)
  • Transketolase (PP pathyway)
  • Pyruvate dehydrogenase (links glycolysis & TCA cycle)
  • Branched-chain ketoacid dehydrogenase
  • “ATP for B1”*
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9
Q

What is the major consequence of vitamin B1 deficiency?

In who does this normally occur?

How is it diagnosed?

A

Impaired glucose breakdown/utilization due to lack of cofactors.

Most commonly seen in alcoholics and malnourished patients

Diagnosis is made by an increase in RBC transketolase activity after B1 administration.

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10
Q

Wernicke-Korsakoff Syndrome

  1. Occurs due to a deficiency of what?
  2. How does it present?
  3. How can it be prevented?
A
  1. Vitamin B1 (thiamine deficiency)

2.

Confusion, Opthalmoplegia, ataxia, memory loss

Hemorrhage/necrosis of mamillary bodies and grey matter

  1. In alcoholics/malnourished patients give thiamine before dextrose
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11
Q

Beriberi

  1. Occurs due to deficiency of what vitamin?
  2. How does it present?
A
  1. Deficiency of Vitamin B1 (thiamine)
  2. Peripheral neuropathy and heart failure
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12
Q

Vitamin B2 (riboflavin)

  1. What is it used to form?
  2. What is its function?
A
  1. FAD and FMN
  2. FAD & FMN are used as cofactors in redox reactions

(succinate dehydrogenase reaction in TCA cycle)

(succinate –> fumarate)

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13
Q

What are the symptoms of riboflavin (B2) deficiency?

A

Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth)

Corneal Vascularization

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14
Q

Vitamin B3 (niacin)

  1. What is it derived from?
  2. What does it make up?
  3. What is its function?
A
  1. Tryptophan
  2. NAD+ and NADP+
  3. Used to treat dyslipidemia

(lowers VLDL and raises HDL)

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15
Q

What does severe deficiency of Niacin (B3) lead to and how does it present?

A

Pellegra

- Diarrhea

- Dementia

- Dermatitis

(broad collar rash and hyperpigmentation of sun exposed limbs)

“The 3 Ds of B3 defiency/pellegra”

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16
Q

Hartnup Disease

  1. What is it?
  2. How does it present?
  3. How is it treated?
A
  1. AR diease that results in a defiency of tryptophan
  2. Presents with Pellegra-like symptoms

(Diarrhea, dementia, dermatitis)

  1. High protein diet and nicotinic acid
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17
Q

How does excess niacin/vit.B3 present?

A

Facial flushing (due to prostaglandins)

Hyperglycemia

Hyperuricemia

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18
Q

What is the function of Vitamin B5 (Pantothenic acid)?

A

It an essential component of CoA and Fatty Acid Synthase

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19
Q

What is the main function of Vitamin B6 (pyridoxine)? (3)

A

It gets converted to pyridoxal phosphate (PLP)

PLP is used as a cofactor for

1. Transamination (needed for amino acid synthesis)

2. decarboxylation reactions

3. glycogen phosphorylase

20
Q

How does Vitamin B6 deficiency present? (4)

A
  • cheilosis (fissures at corner of mouth)
  • glossitis
  • dermatitis

Can also result in Sideroblastic anemia

21
Q

What is the function of vitamin B7 (biotin)?

A

It is a cofactor for carboxylation enzymes (add 1C)

  • Pyruvate carboxylase
  • Acetyl-CoA carboxylase
  • Propionyl-CoA carboxylase
22
Q

How does B7 (biotin) deficiency most commonly occur? (2)

A
  1. antibiotic use
  2. Excessive consumption of raw egg whites

(they contain avidin, which avidly binds biotin)

23
Q

Vitamin B9 (folate)

  1. What is its function?
  2. Where is it absorbed?
  3. How large are our reserves?
A
  1. Gets converted to Tetrahydrofolic Acid (THF)

Important for DNA and RNA synthesis

  1. Absorbed in jejunum
  2. Small (lasts weeks to months)
24
Q

Folate Deficiency

  1. How does it present
  2. Labs (homocysteine, methylmalonic acid)
A
  1. Macrocytic Megaloblastic Anemia

Hypersegmented polymorphonuclear cells

Glossitis

NO neurological symptoms

  1. increased homocysteine, normal methylmalonic acid
25
Q

Should folate be given to pregnant woman?

A

YES

It is given during early pregnancy and 1 month prior to conception

It decreases the risk of neural tube defects

26
Q

Vitamin B12 (cobalamin)

  1. What are its main functions?
  2. Where is it absorbed?
  3. How large are our reserves?
A
  1. Methionine and DNA synthesis
  2. Terminal illeum
  3. Large (Can last years)
27
Q

Cobalamin Deficiency

  1. How does it present
  2. Labs (homocysteine, methylmalonic acid)
A
  1. Macrocytic Megaloblastic Anemia

Hypersegmented polymorphonuclear cells

Glossitis

Neurological symptoms

  1. increased homocysteine, increased methylmalonic acid
28
Q

What is the main function of Vitamin C?

A

1. Hydroxylation of proline and lysine in collagen synthesis

  1. Necessary for dopamine b-hydroxylase

(converts dopamine to norepinephrine)

  1. Faciliated iron absorption by converting it to ferrous state (Fe2+)
29
Q

What are the effects of Vitamin C on iron absorption?

How would it impart someone with:

a. methemoglobinemia
b. Hemochromatosis

A

It faciliates iron absorption by reducing it to Fe2+

a. It can be used to treat methemoglbinemia

(when there is too much Fe3+)

b. Increased iron toxicity in someone with hemochromatosis

(They already have too much iron and they dont need more)

30
Q

What occurs as a result of Vitamin C deficiency? How does it present?

A

Scurvy

  • swollen gums
  • bruising
  • petechiae
  • anemia
  • poor would healing
  • hemarthrosis
31
Q

What can occur due to excess vitamin C?

A

Calcium Oxalate Nephrothialisis

Nausea, vomitting, diarrhea

32
Q

What are the following forms of vitamin D:

1. D2 (ergocalciferol)

2. D3 (cholecalciferol)

3. 25-OH D3

4. 1,25-(OH)2 D3

A
  1. D2 (ergocalciferol) –> from ingestion of plants, fungi, yeast
  2. D3 (cholecalciferol) –> from sun, fish, milk
  3. 25-OH D3 –> storage form in liver
  4. 1,25-(OH)2 D3 –> active form in kidney
33
Q

What is the function of vitamin D?

A
  1. Increased intestinal absorption of Ca2+ and PO43-
  2. At LOW levels: increased bone mineralization/building
  3. At HIGH levels: increased bone resorption
34
Q

What is the consequence of Vitamin D deficiency in:

a. Children
b. Adults

A

a. Rickets

(bone deformities such as genu varum “bow legs”)

b. Osteomalacia

(bone pain and muscle weakness)

35
Q

Vitamin E

  1. What are the names of the 2 main types
  2. What is its function?
A
  1. Tocopherol and Tocotrienol
  2. Protects RBCs and membranes from free radical damage
36
Q

How does Vitamin E deficiency present?

A

Hemolytic Anemia

Acanthocytosis (acanthocytes)

Muscle Weakness

Ataxia, impaired proprioception and vibratory sensation

(due to posterior column & spinocerebellar degeneration)

(Similar to B12 but with no megalobastic anemia, increased methylmalonic acid and hypersegmented neutrophils)

37
Q

What is the function of Vitamin K?

How is it activated?

A

Cofactor for y-carboxylation of glutamic acid on proteins required for blood clotting

(clotting factors II, VII, IX, X and proteins C & S)

Activated by epoxide reductase

38
Q

Should vitamin K be given to neonates?

A

Yes, in order to prevent hemorrhagic disease of the newborn

39
Q

How does zinc deficiency present?

A
  • delayed wound healing
  • supressed immunity
  • hypogonadism
  • decreased adult hair (Axillary, facial, pubic)
40
Q

Kwashiorkor Malnutrition

  1. What is the classic presentation?
  2. Why does it occur?
A
  1. Child with swollen abdomen, edema, anemia, fattly liver and skin lesions)
  2. Occurs due protein malnutrition due to protein deficient meals
    * “Kwashiorkor occurs due to Protein deficient MEALS:*

_M_alnutrition, _E_dema, _A_nemia, _L_iver fat, _S_kin lesions”

41
Q

Marasmus Malnutrition

  1. What is it?
  2. How does it present?
A
  1. Malnutrition due to a diet deficient in calories but not nutrients
  2. Presents as muscle wasting and extreme skinniness
    * “Marasmus results in Muscle wasting”*
42
Q

Ethanol Metabolism

Ethanol —(?)—-> ?????? —(?)—-> ?????

A

Ethanol —(Alcohol Dehydrogenase)—>

Acetaldehyde —(acetaldehyde dehydrogenase)—>

Acetate

43
Q

Fomepizole

What does it inhibit?

What is it used for?

A

Inhibits alcohol dehydrogenase

(ethanol –> acetaldehyde)

Used as an antidote for overdoses of

  • methanol (regular alcohol)
  • ethylene glycol (antifreeze)
44
Q

Disulfiram

What does it inhibit?

What effects does it cause?

A

Inhibits acetaldehyde dehydrogenase

(acetaldehyde –> acetate)

It causes the symptoms of a hangover to discourage drinking

45
Q

What effects does ethanol metabolism have on the NADH/NAD+ ratio?

What are the consequences of this effect?

A

It increases the NADH/NAD+ ratio

(each step in ethanol metabolism requires NAD+ to NADH)

This results in:

  • Lactic acidosis (pyruvate to lactate)
  • Fasting hypoglycemia (prevents gluconeogenesis)
  • Hepatosteatosis (fatty liver)

UWorld - Biochemistry (5 decks)

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