Lecture 14 & Lecture 15 - Nutrition I & II (2 lectures) Flashcards

1
Q

What are the fuel sources during early fasting and after 5 week of semi-starvation?

A
  1. Fasting:
    - glucose for CNS and RBC/WBC
    - fatty acids & ketones for heart, kidney , and muscle
  2. 5-6 Weeks of Semi Starvation:
    - decreased use of glucose
    * * increase in ketone as fuel for CNS,
    - glucose fuel for RBC/WBC, fatty acids fuel for heart, kidney muscle
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2
Q

What are the signs and symptoms of PEM?

Which is chronic mild PEM and which is acute PEM ( Stunting or Underweight)?

What is the difference between Marasmus and Kwashiorkor?

A

Protein–energy malnutrition (PEM) or protein–calorie malnutrition refers to a form of malnutrition where there is inadequate calorie or protein intake.

  1. Stunting = chronic mild PEM
    * * mean height for age**
  2. Underweight = acute mild PEM

WASTING = acute, severe PEM ** WEIGHT FOR HEIGHT**

Marasmus: severe wasting with loss of subcutaneous fat & skeletal muscle

Kwashiorkor: wasting of fat and muscle WITH EDEMA and skin and hair color changes, fatty liver, and impaired renal function

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3
Q

State the structural differences and health consequences of saturated, monounsaturated, and polyunsaturated fatty acids.

  1. SFA
  2. MUFA
  3. PUFA
A
  1. SFA
    - NO DOUBLE BONDS (hence, saturated)
    - associated with increased risk of CVD
    = hypercholesterolemia (decreased catabolism of LDL)
  2. MUFA
    - SINGLE double bond (hence, mono unsaturated)
    - not associated with increased CVD
    - not associated with increased LDL or decreased HDL!
  3. PUFA
    - multiple double bonds
    - associated with LOWER LDL levels
    ex: linoleic (omega 6 –> 2 DB) and alpha-linolenic (omega 3 –> 3 DB)
    BUT CAN ALSO LOWER HDL!! (not good)
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4
Q

Identify the essential fatty acids and signs of EFA deficiency.

A
  1. Linoleic Acid - omega 6 fatty acid
  2. Linolenic Acid - omega 3 fatty acid

EFA deficiency: infertility, scaly dermititis

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5
Q

Describe the structure, function, and health consequences of trans fatty acids.

A
  1. Structure:
    - manufactured** changed the double bond from cis to trans (less rotation = solid at room temp)

HYDROGENATION REACTION!!

  1. Function:
    - increased viscosity of vegetable oils & stability of baked goods
  2. Health consequences:
    - found to increase LDL and lower HDL
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6
Q

Explain by which mechanisms dietary fiber may impact plasma cholesterol levels. (3)

A
  1. Sequester bile in gut, decreasing reabsorption
  2. Slow carb absorption and subsequent rise in plasma insulin levels (thereby slowing cholesterol synthesis)
  3. Stimulate SCFA synthesis thereby inhibiting cholesterol synthesis

** this is from SOLUBLE FIBERS** - pectins & gums (legumes & fruit associated with lowering cholesterol)

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7
Q

Describe the functions of the following FAT SOLUBLE vitamins:

  1. Vitamin A
  2. Vitamin D
  3. Vitamin E
  4. Vitamin K
A
  1. Vitamin A
    - required for optimal vision
    - retinoic acid essential for cellular growth and differentiation
    - also required for cell - mediated & antibody mediated immune responses
    - ** epidermal differentiation** –> allopecia
  2. Vitamin D
    maintain serum Calcium & phosphorous levels
  3. Vitamin E
    - antioxidant in cell membranes
  4. Vitamin K
    - cofactor for proteins involved in coagulation and some bone associated proteins
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8
Q

Define the symptoms of deficiency & excessive intake for the following:

  1. Vitamin A
  2. Vitamin D
  3. Vitamin E
  4. Vitamin K
A
  1. Vitamin A
    - night blindness, stages of xerophthalmia, immune dysfunction & poor growth

TOXICITY: nausea, vomiting, headache, & bright red gingiva

  1. Vitamin D
    - rickets, osteomalacia
    TOXICITY: kidney stones, dehydration, thirst
  2. Vitamin E
    - ataxia with progressive peripheral neuropathy
    TOXICITY: extremel rare
  3. Vitamin K
    - hemorrhagic disease of newborns
    TOXICITY: unreported
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9
Q

Explain the general mechanism by which retinoids regulate cellular differentiation.

A

Retinoid Acid binds to receptor on response element in promoter region of target genes resulting in activation of transcription

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10
Q

What are 3 ways that Vitamin D maintains plasma calcium levels?

A
  1. Increase intestinal absorption of Calcium
  2. Increase renal calcium reabsorption
  3. Increase calcium reSORPTION from bone (breakdown)
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11
Q

What is the mechanism by which Vitamin E protects cell membranes from oxidative damage?

A
  1. Acts as an antioxidant and peroxide scavenger particularly for cell membrane PUFAs and lipoproteins
  2. Breaks chain reaction of oxidation preventing propagation of free radical damage
  3. Regeneration to reduced Vitamin E by Vitamin C
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12
Q

Explain etiologic factors contributing to hemorrhagic DISEASE OF THE NEWBORN. (3)

A
  1. Placenta poorly transmits vitamin K
  2. Liver is immature regarding prothrombin synthesis
  3. Intestine is sterile at birth (synthesized by intestinal bacteria normally) and breast milk is low in vitamin K

** given prophylaxis of Vitamin K at birth to prevent this**

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13
Q

Describe the primary function of the following water soluble vitamins:

  1. Thiamin
  2. Niacin
  3. Folic acid
A
  1. Thiamin
    - coenzyme required for metabolism of carbs and branched chain amino acids
  2. Niacin
    - coenzyme for multiple redox reactions
    - ATP synthesis & ADP ribose transfer
    - significant amount of dietary tryptophan metabolized to NAD
  3. Folic acid
    - coenzyme in methyl group transfer reactions such as purine & pyrimidine synthesis and methylation of transfer RNA
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14
Q

Describe the primary function of the following water soluble vitamins:

  1. Vitamin B 12
  2. Vitamin C
A
  1. Vitamin B 12
    - coenzyme for 2 critical enzymes involved in methyl group transfer
  2. Vitamin C
    - coenzyme for some redox reactions
    - hydroxylation of collagen
    - water soluble antioxidant
    - neurotransmitter & neuropeptide synthesis
    - corticosteroid synthesis
    - seratonin synthesis
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15
Q

How much kcal/gram are contained in the following:

  1. Proteins
  2. Carbs
  3. Fats/lipids
  4. Ethanol
A
  1. Proteins - 4
  2. Carbs - 4
  3. Fats/lipids - 9
  4. Ethanol - 7

<1% trans fats)
~ 15% kcal from protein
55-60% kcal from carbohydrate

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16
Q

A male patient has been admitted with severe inflammatory bowel disease and significant weight loss. His nutritional requirements include an increase in protein intake to 2.5 g/kg body weight (current recommendation for adults is ~ 0.8 g/kg/day), and decrease in calories from fat to 20% of total intake. Patient current weight is 60 kg and energy intake prescription is 2400 kcal/day.

How many calories will be derived from protein? Proportion of total intake?

How many grams of fat will be provided?

How many grams of carbohydrate will be provided?

A

How many calories will be derived from protein? Proportion of total intake? 600g; 25%

How many grams of fat will be provided? 53.3 g

How many grams of carbohydrate will be provided?
330 g

17
Q

State which fat soluble vitamins are the following:

  1. Retinol
  2. Colicolciferol
  3. Phylloquinone
  4. Tocopherol
A
  1. Retinol - VITAMIN A
  2. Colicolciferol - VITAMIN D
  3. Phylloquinone - VITAMIN K
  4. Tocopherol - VITAMIN E
18
Q

What are the primary active forms of Vitamin A?

A
  1. Retinaldehyde
  2. Retinoid Acid
  • yielded by oxidative cleavage of Beta- Carotene
19
Q

What initiates the signal transduction and nerve impulse in the rod cells of the retina?

A

RETINALDEHYDE

20
Q

What initiates the early embryogenesis & limb development, heart, eyes, ears, epithelial cell differentiation & OVERALL CELL GROWTH?

A

Retinoic Acid

21
Q

What are the precursors to retinoids?

What is the clinical assessment of vitamin A deficiency?

A

Carotenoids

  • pigmented yellow to red
  • only in plants

Clinical Assessment of Vitamin A deficiency: check the conjuctiva for changes in epidermis of the eye

22
Q

What are the 3 stages of vitamin A deficiency disease Xerophthalmia?

A
  1. Early COnjuctival Xerosis
  2. Bitot’s Spots
  3. Keratomalacia
23
Q

What metabolite of cholesterol forms Vitamin D?

What is the active form?

Major Circulating form?

A

7-dehydrocholesterol

  1. 1,25- (OH) - D3
  2. 25-OH-D3
24
Q

What vitamin inhibits platelet aggregation and increases vasodilation?

A

Vitamin E

25
Q

Where is vitamin E found primarily?

A

PUFAs –> vegetable oils

  • only synthesized by plants
26
Q

What enzyme is critical in vitamin K synthesis?

A

Gamma - Glutamyl Carboxylase

  • asses vitamin K by prothrombin levels
    Made by intestinal bacteria, high in green leafy vegetables
27
Q

Which population of people is most deficient in THIAMIN (B1)?

A
  • breast fed infants of deficient mothers
  • adults with high carb intake
  • chronic ALCOHOLICS
  • gastric bypass surgery patients
28
Q

What enzyme complex is Thiamine Required for?

Why do you need to give a thiamin treatment before administering glucose to a possible alcoholic?

A

PDH
- converts pyruvate to Acetyl Co A for the Kreb’s cycle

    • If they are deficient in thiamin, the excess glucose could lead to hyperglycemia since the glucose cannot be taken through the Kreb’s cycle pathway
  • build up of pyruvate & lactic acid

GASTRIC BYPASS PATIENTS = THIAMIN DEFICIENT (thiamin is reabsorbed in the terminal ileum)

29
Q

What are the diseases associated with Thiamin deficiency?

A

BERIBERI

  1. Dry Beri Beri - neuropathy
  2. Wet Beri Beri - edema, tachycardia, CHF
  3. Cerebral Beri Beri or WIERNICKE - KORSAKOFF syndrome:
    - severe alcoholics where there is increased requirement for thiamin
    - mental confusion, aphonia, nystagmus –> progress to bilateral 6th nerve paralysis
  4. Wernicke’s Encephalopathy - degeneration in family body & loss of nerve cells
  5. Infantile Beri Beri - aphonia, polyneuropathy, Cardiac failure