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Nutrition And Metabolism > Nutrition Overview > Flashcards

Nutrition Overview Flashcards

1
Q

Nutrient definition

A

Chemical substance in food

Provides sometimes energy and body balance

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2
Q

Types of nutrients

A

Macronutrients : carbohydrates, fats and proteins (water)

Micronutrients : vitamins, minerals

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3
Q

Nutrients that provide energy

A

Carbohydrates, proteins, fats

Alcohol too even though not a nutrient

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4
Q

Variables affecting nutrients requirements

A 
Age 
Gender 
Activity level 
State of nutrition 
Climate (more nutrients when cold) 
Health
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5
Q

Recommended daily allowance of nutrients

A

70kg Man = 2900kcal/day

50kg woman = 2100 kcal/day

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6
Q

Energy requirements

A

Basal metabolism rate => energy needed to survive , taken in resting state

Specific dynamic action => energy used when digesting

Physical activity => patient lifestyle

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7
Q

Micronutrients categories

A

Vitamins (organic)
Minerals ( inorganic)
Designer vitamins

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8
Q

Are vitamins essential

A

Yes because not produced in body

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9
Q

Fat soluble vitamins

A

A
D
E
K

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10
Q

How are fat soluble vitamins transported in plasma

A

By transporters

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11
Q

Where are fat soluble vitamins stored

A

Adipose tissue and liver

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12
Q

Why are fat soluble vitamins not readily excreted in urine

A

Bound to plasma protein for transport so too big to be filtered

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13
Q

Vitamin A main compound

A

Retinol which can produce retinoic acid

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14
Q

Source of vitamin A

A

Yellow dark green vegetables with carotene

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15
Q

Uses of vitamin A

A

Helps in vision because found in opsin which is involved in night vision

Helps in growth ( bones , CNS )

Helps in reproduction by maintaining fœtus and promote spermatogenesis

Improve epithelium

Antioxidant- protect against reactive species

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16
Q

Diseases related to vit A deficiency

A

Night blindness ( lack of adaptation to darkness)

Xerophthalmia - lens keratization

Acne/psoriasis - lack of normal epitheliazation and thickening skin

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17
Q

Amount of vitamin A to reach toxicity

A

7.5mg/day

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18
Q

Symptoms of hypervitaminoses A

A

Dry itchy skin
Hepatomegaly
Increased intracranial pressure
Congenital malformation\

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19
Q

Form of vitamin A stored in liver

A

Retinyl ester

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20
Q

Main function of vit K

A

Posttranslational regulation of clotting blood factor

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21
Q

Functions of vit K

A

Helps in synthesis of prothrombin and blood clotting factor (II,VII, IX,X)

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22
Q

Source of vit K

A 
Cabbage 
Kale
Spinach 
Egg yolk
Liver 
Synthesis by bacteria in gut
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23
Q

Deficiency of vit K

A

Rare

Lead to bleeding tendency

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24
Q

Why should you give vit k as single shot prophylaxis to new born

A

Because they are born sterile with no bacteria in gut responsible for vit k synthesis. Need it while they get enough of vit k from breast feeding

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25
Q

Vitamin k toxicity

A

Hemolytic anemia

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26
Q

Vitamin E functions

A

Antioxidants especially for polyunsaturated FAs

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27
Q

Source of vit E

A

Vegetable oils

Liver eggs

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28
Q

Deficiency of vit E

A

Seen in premature infants or adult with defective lipid absorption and and transport

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29
Q

Vit E toxicity

A

Least toxic

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30
Q

Vitamin D sources

A

D2 found in plants
D3 found in animal tissues
Can be synthesized under light exposition

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31
Q

Vit D functions

A

Intestinal absorption of calcium And phosphate

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32
Q

Vit D deficiency

A

Nutritional ricket ( growing bone disease in children ) with soft pliable bone

Osteomalacia in adults ( lack of sunlight exposure)

Renal osteodystrophy: chronic renal failure leading to failure of activation of vit D

Hypoparathyroidism: hypocalcemia due to lack of of parathyroid hormones

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33
Q

Water soluble vitamins are mostly

A

Coenzymes

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34
Q

2 groups of vitamins soluble

A

Vit C

Vit B

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35
Q

Vit b1 molécule

A

Thiamine

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36
Q

Vit b1 act as coenzyme in

A

Transketolase

Oxidative decarboxylation of alpha keto acids

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37
Q

Thiamine deficiency

A

Leads to decreased ATP and therefore cellular impairment

Beriberi: tachycardia, vomiting , convulsion, death, progressive paralysis in adults

Wernicke korsakoff syndrome : seen in alcoholics with apathy, loss of memory, ataxia,

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38
Q

Vitamin b2 name

A

Riboflavin

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39
Q

Is vit b2 deficiency associated with disease ?

A

No major disease

Just cheilosis, glossitis

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40
Q

Vit b3 name

A

Niacin

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41
Q

Source of vit b3 niacin

A 
Grain
Cereal 
Milk
Lean meats 
Liver
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42
Q

Niacin deficiency

A

Pellagra - skin disease involving GIT And CNS => Dermatitis, Diarrhea, Dementia

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43
Q

Which vitamin can use in hyperlipideamia

A

Vit b3 niacin by inhibiting lipolysis

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44
Q

Vit B9 molécule

A

Folic acid

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45
Q

Main vitamin deficiency in the work

A

Vit B9 or B12 deficiency

46
Q

Cause of folate deficiency

A

Pregnancy
Lactation
Poor absorption at small intestine due toalcoholism o

47
Q

Folate deficiency consequences

A

Megaloblastic anemia

Neural tube defects

48
Q

Vitb12 molecule

A

Cobalamin

49
Q

Source of vitb12

A

Animals only

50
Q

Vit b12 deficiency

A

Megaloblastic anemia due to lack of tetrahydrofolate necessary for thymine synthesis

Pernicious anemia ( malabsorption of vitb12 die to lack of intrinsic factor ) presents as anemia with neuropsychiatric symptoms

51
Q

Vit c molécule

A

Ascorbic acid

52
Q

Vit c function

A

Normal connective tissue maintenance ( collagen)

Wound healing

Facilitate iron absorption

Antioxidants

53
Q

Vit c defiency

A

Scurvy : sponge and gums loose teeth’s, swollen joints and anemia

54
Q

Protein energy malnutrition epidemiology

A

Children in developing countries who lack food and clean water

55
Q

Precipitating factors of protein energy malnutrition

A

Famine
poverty
Inappropriate breastfeeding
Wrong concepts about nutrition

56
Q

Disease caused by protein energy malnutrition

A

Quest your car

57
Q

Causes of kwashiorkor

A

Sudden and Early Weaning of child ( due in general to successive pregnancy)

They metabolize proteins before adipose tissue

58
Q

Symptoms of kwashiorkor

A 
Psychomotor
Edema 
moon face
Hair changes 
Skin de pigmentation 
Anemia 
Thin legs
59
Q

Storage of iron

A

Ferritin and hemosiderin

60
Q

Lifespan of RBC

A

90-120 days

61
Q

Where is iron stored when in excess

A

Liver

62
Q

What does iron do in bone marrow

A

Helps produce erythroblasts to form RBC

63
Q

Transport of iron in plasma

A

Transferrin transport

64
Q

Haem iron

A

Ferrous ion - Fe2+

65
Q

Non haem iron

A

Ferric ion Fe3+

66
Q

Physiological loss of iron

A

Pregnancy
Lactation
Menstruation
Cell loss

67
Q

Pathological loss of iron

A 
Bleeding 
Peptic ulcers 
Menorrhagia 
surgery
Haematuria
68
Q

Iron overload management

A

Phlebotomy

Iron chelation

69
Q

Megaloblastic anemia underlying defect

A

Defect in DNA synthesis (nucleotide synthesis or DNA polymerization) usually caused by vit B12 or folate deficiency

70
Q

Vit B12 appearance

A

Red water soluble

71
Q

Vit B12 source

A

Meat
Liver
Seafood
Dairy products with no plant source

72
Q

Vit B12 aborsoption mechanism

A

R-binder-cubilin in saliva binds to food and get into stomach

HCl released from parietal cells and act on pepsinogen released by chief cells to form pepsin

Pepsin break down proteins and release vitB12

VitB12 protected from gastric environment of stomach by by binding R-binder

VitB12-R-binder complex gets into small intestine and vitB12 released from complex because no more acidic

VitB12 binds now intrinsic factors because they have ileum receptors for absorption. Vit b12 gets absorbed by forming this complex

73
Q

Source of folic acid

A 
Green vegetables 
Fruits 
Liver
Yeast 
Groundnut 
Beans
74
Q

Site of absorption of folic acid

A

Proximal jejunum and duodenum

75
Q

Functional form of folic acid

A

Tetrahydrofolate

76
Q

Why is vit b12 important for folic acid

A

Helps free tetrahydrofolate from methyl tetrahydrofolate for conjugation reactions which helps in DNA Synthesis

77
Q

Folate trap hypothesis

A

Deficiency of vit b12 can lead to interruption of folate inter conversion which will cause accumulation of methyl tetrahydrofolate

78
Q

Causes of megaloblastic anemia

A

Vit B12 deficiency
Vit B12 metabolism abnormality

Folate deficiency
Folate abnormal metabolism

Defects in DNA synthesis

79
Q

Causes of vit B12 deficiency

A

Inadequate diet (vegan, poverty imposed, breast fed children with pernicious anemia mothers)

Malabsorption in stomach (hypochlorydria which reduces HCl, chronic H pump inhibition, atrophic gastritis, pernicious anemia, partial or total gastrectomy, caustic mucosal destruction)

Intestinal malabsorption ( pancreatic insufficiency, zollinger Ellison syndrome, stasis syndromes, fish tapeworm, ileal resection, Crohn’s disease , cubilin receptor defect )

80
Q

Folate deficiency cause

A

Inadequate diet intake ( poverty, famine, slimming diets, cooking techniques)

Increased folate use ( pregnancy, hyperemesis, prematurity, growth spurt

Excess loss ( dialysis, congenital heart failure)

Malabsorption ( congenital, sprue, gluten enteropathy)

Drugs ( alcohol, methotrexate, anticonvulsants, sulfasalazine)

81
Q

Abnormalities in DNA synthesis

A

Lesch nyhan syndrome
Congenital dyserythropoietic anemia

Drugs
Erythroleukemia
Hydroxyurea
Mercaptopurine

82
Q

Past medical history of megaloblastic anemia

A 
Past abdominal surgery 
Autoimmune disease
Veganism
Alcoholism
Epilepsy treatment 
Hemolytic anemia
83
Q

Neurologic symptoms of megaloblastic anemia

A

Darkened hands and feet
In both legs ( tingling, burning , numbness , falling over in dark low strength, altered sensation )
Memory loss
Psychosis

84
Q

Physical examination of megaloblastic anemia

A 
Pallor 
Jaundice 
Feeding state 
Glossitis
Angular cheilosis
Hyperpigmentation 
Vitiligo 
Reduced sensation
Optic nerve neuropathy 
Dementia
85
Q

3 questions to ask for megaloblastic anemia

A

Is there megaloblastic anemia ?
Is it due to folate or b12 deficiency
What caused deficiencyl

86
Q

To see megaloblastic anemia in lab you should see :

A

Full blood count : low Hb and high MCV , thrombocytopenia, neutropenia

Peripheral film : oval macrocytes, hypersegmented neutrophil

Bone marrow: megaloblasts, giants metamyelocytes, giant band cells

87
Q

differential diagnosis of macrocytosis

A 
Alcohol
Liver disease
Hypothyroidism 
Myelodysplasia
Myeloma 
Aplastic anemia 
Pregnancy
Neonates 
Hemolytic anemia 
Zydovudine
Methotrexate
88
Q

B12 and folate assays

A

First line tests (Serum b12/Serum and red cell folate)

Second line tests (homocysteine and methylmalonic acid test )
Homocysteine high => folate deficiency or b12
MMA => b12 deficiency

89
Q

Treatment of folate deficiency

A

Folate replacement therapy

Can be used in b12 deficiency anemia but can allow neurological symptoms of b12 deficiency to continue

90
Q

B12 deficiency treatment

A

B12 replacement IM or SC for life

91
Q

Dietary factors that favors iron absorption

A

Increased haem iron
Increased animal foods
Ferrous iron salts

92
Q

Dietary factors that reduce iron absorption

A

Decreased haem iron
Increased non haem iron
Decreased animal food
Ferric iron salts

93
Q

Luminal factors that promote haem absorption

A

Low molecular weight soluble chelates (vit c , sugars)

Ligand in meat

94
Q

Luminal factors decreasing iron absorption

A

Alkaline substance (pancreatic secretion)

Insoluble iron complex

95
Q

Systemic factors increasing iron absorption

A 
Iron deficiency 
Increased erythropoiesis 
Ineffective erythropoiesis 
Pregnancy 
Hypoxia
96
Q

Systemic factors decreasing iron absorption

A

Iron overload
Decreased erythropoiesis
Inflammatory disorders

97
Q

Iron absorption metabolism explained

A

Haem iron ring bind to receptor on enterocyte
Haem iron penetrates cell
Haem oxygenase free the Fe2+

Fe3+ outside of cell becomes Fe2+ by ferric reductase
Fe2+ enter the cell by divalent métal transporter

All the Fe2+ get into labile iron pool
Some iron go for cell metabolism
Some iron get stored into enterocytes
Some iron get absorbed

To get into blood , iron goes through ferroportin channel.
Hephaestin associated to channel to transform Fe2+ to Fe3+ to allow absorption

Ceruloplasmin convert Fe2+ that escaped to Fe3+

Transferrin attaches Fe3+

98
Q

How is ferroportin regulated by hepcidin

A

When hepcidin low , ferroportin opens

When hepcidin high, ferroportin closes

99
Q

How can iron Anemia of chronic disease mimic iron deficiency anemia

A

In disease like cancer , cytokines increase hepcidin level which shuts down ferroportin Which decreases iron absorption

Blood iron low , but iron storage high

100
Q

Iron level investigation

A

Serum ion

Transferrin saturation to see how much they are occupied in blood

Total iron bound in to see free transporters

Ferritin amount

101
Q

Iron deficiency anemia lab findings

A

Serum ion low
Transferrin saturation low
Iron high
Ferritin low

Elevated transferrin
Hypochromia
Microcytosis
Aneamia

102
Q

Anemia of chronic disease lab findings

A

Serum iron low
Transferrin saturation low
Total iron high
Ferritin normal level or high

103
Q

Iron overload lab findings

A

Iron serum high
Transferrin high
Iron low
Ferritin high

104
Q

Cause of iron deficiency anemia

A

Increased iron usage ( pregnancy, infancy , adolescence)

Blood loss

Malabsorption

Dietary inadequacy

Combinations of above

105
Q

Most specific lab findings for iron deficiency anemia

A

Low ferritin levels

106
Q

Stages of iron deficiency anemia

A

Reduced iron store
Iron deficient erythropoiesis
Iron deficient anémia

107
Q

Clinical features of iron deficiency anemia

A

Koilonychia

Angular cheilosis

108
Q

Iron deficiency anemia management

A

Iron therapy

Parentéral or Irak

109
Q

Genetic haemochromatisis

A

Iron overload disease caused by increased iron absorption which can cause organ damage

110
Q

Gene affected in genetic haemochromatosis

A

HFE gene associated with low hepcidin

Type I

Nutrition And Metabolism (17 decks)

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