Nutrition Overview Flashcards
Nutrient definition
Chemical substance in food
Provides sometimes energy and body balance
Types of nutrients
Macronutrients : carbohydrates, fats and proteins (water)
Micronutrients : vitamins, minerals
Nutrients that provide energy
Carbohydrates, proteins, fats
Alcohol too even though not a nutrient
Variables affecting nutrients requirements
Age Gender Activity level State of nutrition Climate (more nutrients when cold) Health
Recommended daily allowance of nutrients
70kg Man = 2900kcal/day
50kg woman = 2100 kcal/day
Energy requirements
Basal metabolism rate => energy needed to survive , taken in resting state
Specific dynamic action => energy used when digesting
Physical activity => patient lifestyle
Micronutrients categories
Vitamins (organic)
Minerals ( inorganic)
Designer vitamins
Are vitamins essential
Yes because not produced in body
Fat soluble vitamins
A
D
E
K
How are fat soluble vitamins transported in plasma
By transporters
Where are fat soluble vitamins stored
Adipose tissue and liver
Why are fat soluble vitamins not readily excreted in urine
Bound to plasma protein for transport so too big to be filtered
Vitamin A main compound
Retinol which can produce retinoic acid
Source of vitamin A
Yellow dark green vegetables with carotene
Uses of vitamin 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
Diseases related to vit A deficiency
Night blindness ( lack of adaptation to darkness)
Xerophthalmia - lens keratization
Acne/psoriasis - lack of normal epitheliazation and thickening skin
Amount of vitamin A to reach toxicity
7.5mg/day
Symptoms of hypervitaminoses A
Dry itchy skin
Hepatomegaly
Increased intracranial pressure
Congenital malformation\
Form of vitamin A stored in liver
Retinyl ester
Main function of vit K
Posttranslational regulation of clotting blood factor
Functions of vit K
Helps in synthesis of prothrombin and blood clotting factor (II,VII, IX,X)
Source of vit K
Cabbage Kale Spinach Egg yolk Liver Synthesis by bacteria in gut
Deficiency of vit K
Rare
Lead to bleeding tendency
Why should you give vit k as single shot prophylaxis to new born
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
Vitamin k toxicity
Hemolytic anemia
Vitamin E functions
Antioxidants especially for polyunsaturated FAs
Source of vit E
Vegetable oils
Liver eggs
Deficiency of vit E
Seen in premature infants or adult with defective lipid absorption and and transport
Vit E toxicity
Least toxic
Vitamin D sources
D2 found in plants
D3 found in animal tissues
Can be synthesized under light exposition
Vit D functions
Intestinal absorption of calcium And phosphate
Vit D deficiency
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
Water soluble vitamins are mostly
Coenzymes
2 groups of vitamins soluble
Vit C
Vit B
Vit b1 molécule
Thiamine
Vit b1 act as coenzyme in
Transketolase
Oxidative decarboxylation of alpha keto acids
Thiamine deficiency
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,
Vitamin b2 name
Riboflavin
Is vit b2 deficiency associated with disease ?
No major disease
Just cheilosis, glossitis
Vit b3 name
Niacin
Source of vit b3 niacin
Grain Cereal Milk Lean meats Liver
Niacin deficiency
Pellagra - skin disease involving GIT And CNS => Dermatitis, Diarrhea, Dementia
Which vitamin can use in hyperlipideamia
Vit b3 niacin by inhibiting lipolysis
Vit B9 molécule
Folic acid
Main vitamin deficiency in the work
Vit B9 or B12 deficiency
Cause of folate deficiency
Pregnancy
Lactation
Poor absorption at small intestine due toalcoholism o
Folate deficiency consequences
Megaloblastic anemia
Neural tube defects
Vitb12 molecule
Cobalamin
Source of vitb12
Animals only
Vit b12 deficiency
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
Vit c molécule
Ascorbic acid
Vit c function
Normal connective tissue maintenance ( collagen)
Wound healing
Facilitate iron absorption
Antioxidants
Vit c defiency
Scurvy : sponge and gums loose teeth’s, swollen joints and anemia
Protein energy malnutrition epidemiology
Children in developing countries who lack food and clean water
Precipitating factors of protein energy malnutrition
Famine
poverty
Inappropriate breastfeeding
Wrong concepts about nutrition
Disease caused by protein energy malnutrition
Quest your car
Causes of kwashiorkor
Sudden and Early Weaning of child ( due in general to successive pregnancy)
They metabolize proteins before adipose tissue
Symptoms of kwashiorkor
Psychomotor Edema moon face Hair changes Skin de pigmentation Anemia Thin legs
Storage of iron
Ferritin and hemosiderin
Lifespan of RBC
90-120 days
Where is iron stored when in excess
Liver
What does iron do in bone marrow
Helps produce erythroblasts to form RBC
Transport of iron in plasma
Transferrin transport
Haem iron
Ferrous ion - Fe2+
Non haem iron
Ferric ion Fe3+
Physiological loss of iron
Pregnancy
Lactation
Menstruation
Cell loss
Pathological loss of iron
Bleeding Peptic ulcers Menorrhagia surgery Haematuria
Iron overload management
Phlebotomy
Iron chelation
Megaloblastic anemia underlying defect
Defect in DNA synthesis (nucleotide synthesis or DNA polymerization) usually caused by vit B12 or folate deficiency
Vit B12 appearance
Red water soluble
Vit B12 source
Meat
Liver
Seafood
Dairy products with no plant source
Vit B12 aborsoption mechanism
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
Source of folic acid
Green vegetables Fruits Liver Yeast Groundnut Beans
Site of absorption of folic acid
Proximal jejunum and duodenum
Functional form of folic acid
Tetrahydrofolate
Why is vit b12 important for folic acid
Helps free tetrahydrofolate from methyl tetrahydrofolate for conjugation reactions which helps in DNA Synthesis
Folate trap hypothesis
Deficiency of vit b12 can lead to interruption of folate inter conversion which will cause accumulation of methyl tetrahydrofolate
Causes of megaloblastic anemia
Vit B12 deficiency
Vit B12 metabolism abnormality
Folate deficiency
Folate abnormal metabolism
Defects in DNA synthesis
Causes of vit B12 deficiency
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 )
Folate deficiency cause
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)
Abnormalities in DNA synthesis
Lesch nyhan syndrome
Congenital dyserythropoietic anemia
Drugs
Erythroleukemia
Hydroxyurea
Mercaptopurine
Past medical history of megaloblastic anemia
Past abdominal surgery Autoimmune disease Veganism Alcoholism Epilepsy treatment Hemolytic anemia
Neurologic symptoms of megaloblastic anemia
Darkened hands and feet
In both legs ( tingling, burning , numbness , falling over in dark low strength, altered sensation )
Memory loss
Psychosis
Physical examination of megaloblastic anemia
Pallor Jaundice Feeding state Glossitis Angular cheilosis Hyperpigmentation Vitiligo Reduced sensation Optic nerve neuropathy Dementia
3 questions to ask for megaloblastic anemia
Is there megaloblastic anemia ?
Is it due to folate or b12 deficiency
What caused deficiencyl
To see megaloblastic anemia in lab you should see :
Full blood count : low Hb and high MCV , thrombocytopenia, neutropenia
Peripheral film : oval macrocytes, hypersegmented neutrophil
Bone marrow: megaloblasts, giants metamyelocytes, giant band cells
differential diagnosis of macrocytosis
Alcohol Liver disease Hypothyroidism Myelodysplasia Myeloma Aplastic anemia Pregnancy Neonates Hemolytic anemia Zydovudine Methotrexate
B12 and folate assays
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
Treatment of folate deficiency
Folate replacement therapy
Can be used in b12 deficiency anemia but can allow neurological symptoms of b12 deficiency to continue
B12 deficiency treatment
B12 replacement IM or SC for life
Dietary factors that favors iron absorption
Increased haem iron
Increased animal foods
Ferrous iron salts
Dietary factors that reduce iron absorption
Decreased haem iron
Increased non haem iron
Decreased animal food
Ferric iron salts
Luminal factors that promote haem absorption
Low molecular weight soluble chelates (vit c , sugars)
Ligand in meat
Luminal factors decreasing iron absorption
Alkaline substance (pancreatic secretion)
Insoluble iron complex
Systemic factors increasing iron absorption
Iron deficiency Increased erythropoiesis Ineffective erythropoiesis Pregnancy Hypoxia
Systemic factors decreasing iron absorption
Iron overload
Decreased erythropoiesis
Inflammatory disorders
Iron absorption metabolism explained
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+
How is ferroportin regulated by hepcidin
When hepcidin low , ferroportin opens
When hepcidin high, ferroportin closes
How can iron Anemia of chronic disease mimic iron deficiency anemia
In disease like cancer , cytokines increase hepcidin level which shuts down ferroportin Which decreases iron absorption
Blood iron low , but iron storage high
Iron level investigation
Serum ion
Transferrin saturation to see how much they are occupied in blood
Total iron bound in to see free transporters
Ferritin amount
Iron deficiency anemia lab findings
Serum ion low
Transferrin saturation low
Iron high
Ferritin low
Elevated transferrin
Hypochromia
Microcytosis
Aneamia
Anemia of chronic disease lab findings
Serum iron low
Transferrin saturation low
Total iron high
Ferritin normal level or high
Iron overload lab findings
Iron serum high
Transferrin high
Iron low
Ferritin high
Cause of iron deficiency anemia
Increased iron usage ( pregnancy, infancy , adolescence)
Blood loss
Malabsorption
Dietary inadequacy
Combinations of above
Most specific lab findings for iron deficiency anemia
Low ferritin levels
Stages of iron deficiency anemia
Reduced iron store
Iron deficient erythropoiesis
Iron deficient anémia
Clinical features of iron deficiency anemia
Koilonychia
Angular cheilosis
Iron deficiency anemia management
Iron therapy
Parentéral or Irak
Genetic haemochromatisis
Iron overload disease caused by increased iron absorption which can cause organ damage
Gene affected in genetic haemochromatosis
HFE gene associated with low hepcidin
Type I
