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FN 3344 > Lecture 8 - Anemia > Flashcards

Lecture 8 - Anemia Flashcards

1
Q

Which vitamins and mineral are involved in RBC synthesis?

A

Folate
B12
Protein

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2
Q

Which vitamins and mineral are involved in hemoglobin ?

A

B6
Fe
Glycine
Protein

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3
Q

Which vitamins and mineral are involved in the maintenance of RBCs?

A

Vitamin E

-prevents free radicals from impacting the cell wall

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4
Q

Which vitamins and mineral are involved in clotting function?

A

Vitamin K
Ca
Protein
Eicosanoids

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5
Q

Which vitamins and mineral are involved in oncotic pressure?

A

Proteins

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6
Q

What is PLP?

A

Pyridoxal Phosphate

-an essential cofactor for delta aminolevulinic acid synthase (ALAS)

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7
Q

Where does PLP and ALAS come from?

A

From Krebs cycle

-substrate for reaction includes succinylcholine CoA& glycine

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8
Q

What does a deficiency win B6 lead to?

A

B6 required in the 1st step of heme synthesis in all tissues
-rxn occurs in the mitochondria

Deficiency of B6 or malabsorption will inhibit heme synthesis
-if your body doesn’t have enough B6 the body won’t start this process

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9
Q

Where is hemoglobin synthesized?

A

Liver and bone marrow

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10
Q

Why is vitamin C important?

A

increases bioavailability of non-heme Fe
-acts as a reducing agent to turn Fe3 to Fe2 to be absorbed better in the body

-Chelate remains soluble in the small intestine intestine improving absorption `

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11
Q

What is the effect of Vitamin C related too?

A

It is dose related

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12
Q

Why is vitamin E important?

A

Is a strong antioxidant which stabilizes membranes to prevent oxidative damage

  • helps prolong RBC life
  • helps reduce platelet aggregation and platelet adhesion to collagen
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13
Q

What is erythropoiesis?

A

Hematopoietic tissue in bone marrow produce RBC (red bone marrow)

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14
Q

What do erythroblasts require during their differentiation?

A

Folate and B12 for proliferation

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15
Q

What are folate and B12 important for?

A

Involved in DNA and RNA synthesis

Helps RBCs to form and split

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16
Q

What does a deficiency in Folate or B12 result in?

A

Deficiency inhibits purine and Thymidylate synthesis

  • which causes cells to die early
  • causes erythroblast apoptosis
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17
Q

What is Fe required for?

A

Hemoglobin synthesis

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18
Q

What is a deficiency in Fe result in?

A

Inhibits heme synthesis and RBC contain reduced amount of hemoglobin (hypochromic)

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19
Q

where does most of the Fe in your body go too?

A

80% Fe transported to bone marrow for heme synthesis

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20
Q

At what stage of the RBC does the bone marrow release it into the body?

A

Reticulocyte phase

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21
Q

What are the different kind of nutritional anemias you can have?

A

Microcytic, hypochromic: low hemoglobin levels, heme requires Fe, B6 (Vt C to enhance Fe absorption), glycine

Macrocytic: Immature RBC, cellular differentiation requires folate and B12

Normocytic, Normochromic: Anemia due to chronic disease

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22
Q

What does it mean to have Fe Deficiency?

A

Hypochromic mycrocytic

-Missing hemoglobin if you font have enough Fe you don’t have the hemoglobin to give it the colour

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23
Q

What does it mean when you have an anemia of chronic disease?

A

Related to inflammation of the body due to chronic conditions (small but norma in colour)

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24
Q

What do RBC look like when you have macrocytic/megaloblastic anemia?

A

Big and red RBC

-due to lack of folate and or B12 deficiency which affects DNA synthesis

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25
Q

What are the lab results of someone with Macrocytic or megaloblastic anemia?

A

Erythrocytes

  • Increase mean cell hemoglobin (MCH)
  • Increase mean cell volume
  • Decrease RBC count

Decrease in Serum RBC[Folate], [B12], [Hgb], [Hct]

Increase Reticulocyte distribution widths (RDW)

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26
Q

What is RDW?

A

Reticulocyte distribution Width
Distribution of the size of the cells
-tells you that there is a variance in the RBC size
-doesnt say if its larger or smaller

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27
Q

What are scenarios when you have small or large RDW?

A

Small: cells are normal and are all the same size, there is little variance in size

Large:Micro/Macto anemia cause there is going to be different sized RBC

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28
Q

What does having microcytic or hypochromic anemia result in?

A

Fe deficiency

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29
Q

What do the labs look like for microcytic or hypochromic anemia?

A

Erythrocytes

  • Decrease (MCV)(MCH)
  • Increase RBC count

Decrease: Serum [Fe] [Ferritin][Hgb][Hct], Fe transferrin saturation

Increase: Serum [Transferrin] Total Fe binding Capacity, RDW

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30
Q

What is transferrin?

A

Transporter for Fe

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31
Q

What is the function of Fe?

A

Transport O2 as a component of Hgb or RBC
-also a component of myoglobin of muscles (stays in muscle)

Required for some runs involving energy formation

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32
Q

How many gs or Fe does out body have and where is it found within the body?

A

2-4g of elemental Fe

65% hemoglobin
10% Myoglobin
1-5% Enzymes
Remainder in blood/storage

-Bacteria love Fe so it has to be bound

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33
Q

How does Fe get transported and stored?

A

Transport= Transferrin

Storage= Ferritin

  • liver
  • bone marrow
  • spleen
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34
Q

What are the 2 forms of Fe?

A

Heme- Fe in the porphyrin ring structure
-high bioavailability

Non heme- bound to components of food and have to be hydrolyzed, digested or solubilized prior to absorption

  • mostly Fe3 (ferric)
  • less bioavailability
  • more subject to inhibitors
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35
Q

What are some inhibitors of non heme Fe absorption?

A 
Polyphenols (coffee and tea)
Oxalic Acid (spinach)
Phytates (legumes)
Ca
Zn
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36
Q

How it Heme Fe absorbed and transported?

A

-Hydrolyzeed from global portion
-Remains soluble and absorbed intact across brush border by hem protein 1
-Proximal small intestine
0Heme hydrolized within mucosal cell into Ferrous Fe and protoporphyrin

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37
Q

How its non heme Fe absorbed and transported/

A

Hydrolyzed from components of food (Hal proteases)

Mostly Ferric Fe- remains soluble if acidic

Transported into mucosal cell via divalent mineral transporters (DMT-1)
-Zn, Mn share same transporter

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38
Q

What does the transferring transporter saturation depend on?

A

Rate of uptake

  • binding serves to protect Fe from redox rxns
  • carries Ferric (Fe3)
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39
Q

Where is most Fe stored?

A

Spleen and liver 60% as ferritin and hemosiderin

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40
Q

What is the turnover for Fe like?

A

20% absorption for heme
8% Absorption for nonheme
-amount of Fe absorbed cannot meet daily Fe requirements of body
-body is really good at conserving and recycling Fe from RBC

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41
Q

How do you lose Fe?

A

Stools due to cells, bile and blood loss

Gut due to gastritis, aspirin, infection, parasites, ulcers, cancer, hemorrhoids

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42
Q

What characteristics does one have to be Moree susceptible to Fe deficiency?

A

Decreased stomach acidity
Impaired Fe absorption
Blood donation
Intestinal parasitic infection

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43
Q

Why are kids and infant susceptible to Fe deficiency?

A

Cow milk is a poor source of Fe (very filling too)

Periods

Adolescent growth spurts - high demand in growth increases demand for everything to match

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44
Q

Can drugs impact Fe absorption ?

A

Yes, oral contraceptives and HRT

-reduces blood loss

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45
Q

Which groups of people have inadequate intake of Fe?

A

Elderly (reduced Hal and meant consumption)

Alcoholics

Vegetarians

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46
Q

Does being extremelyy active affect your Fe intake?

A

Yes, due to high wear and teat and Fe being used to repairs the body constantly

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47
Q

How common is Fe deficiency?

A

5-10% of women

> 50% of women have inadequate Fe stores in USA

1/3 pregnant women who do not take supplants have IDA

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48
Q

What is Fe deficiency?

A

An anemia: microcytic, hypochromic, with diminished O2 transport

Decreased performance during physical exertion

Long term deficiency results in permanent effects on development in children (fatigue, psychomotor performance, brain development)

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49
Q

What is Fe deficiency anemia?

A

Impaired adaptations to cold

Reduced immune functions

Increased lead absorption

Can lead to low birth weigh and preterm delivery

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50
Q

What can Fe toxicity be due to?

A

Accidental Fe overload (excessive ingestion of Fe supplements

Genetic Disorder (HH)

Absorbed Fe progressively deposited within joints and tissues

2 mutation found on chromosome, HFE gene

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51
Q

What is HH?

A

Hereditary hemochromatosis

  • caucasian males ~20yo
  • have increased absorption, maximally absorbing all Fe in body and depositing it elsewhere in the body when stores are full
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52
Q

How do you treat Fe toxicity?

A

Blood work (donating blood) and low Fe diet

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53
Q

What is the risk of excess Fe in population?

A

More Fe in the body can lead to more mutations leading to an increase in cancer

Indication of inflammation

Avoid alcohol if you have HH

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54
Q

What is the 1 stage when assessing Fe deficiency status?

A

[Fe Depletion]
Depletion of Fe stores (body can’t replace)

Plasma ferritin <12microg/L associate with ID

Inflammation/infection serum ferritin concentration rise unrelated to Fe stores

Confounded by chronic disease states (infection, inflammation, neoplastic& liver disease)

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55
Q

What is the 2nd stage when asses for Fe deficiency status?

A 
[Fe deficiency]
Transport Fe decreases
Transferrin Saturation <16% (confounded)
Plasma transferring increases 4mmol/L
TIBC increases (confounded)
Serum Fe <9mmol/L
Increase erythrocyte protoporphyrin (precursor for hemoglobin molecules)
56
Q

What is the 3rd stage when we asses for Fe deficiency?

A

[Fe deficiency Anemia]
Functioinal Fe limited
Hemoglobin women, pregnant, men= <120, 110, 130g/L
Mematocrit women, pregnant, men= <37%, 33% 40%
Decrease in MCV
Increase RDW
*plus all markers in stage 2

57
Q

Do plant based milks have Fe?

A

Its voluntary Fe fortification but if they do they have to do it to the same concentration as cow milk

58
Q

How much Fe do we need?

A

For growth and UL 45mg

Men: 8mg

Women: 18mg

50+: 8mg

Pregnant: 27mg

59
Q

What is the major cause of Fe deficiency in women men and children in developing countries?

A

Women: Diet or excess menstrual losses

Men: Suspect other factors (Disease)

Children: When giving Fe supplement, beware of feeding parasites

60
Q

What are sources of folate?

A

Supplements and white wheat flour
(folic acid)

Legumes and leafy greens (naturally occurring, not stable, destroyed via cooking

61
Q

What are the roles of Folate in the Body?

A

One carbon metabolism

  • Universal methyl donor
  • Uracil resides in transfer RNA
  • deoxyuridylate to thymiidylate ini DNA synthesis

Amino acid synthesis

  • Methionine (homocysteine)
  • Serine/glycine interconversions

DNA/RNA synthesis
-Pyrimidines, purines

62
Q

When do you need more folate?

A

Increased anabolic activity/periods of growth

63
Q

If you are deficient in either Folate or B12 what is the result?

A

Megaloblastic anemia

64
Q

How do you get megaloblastic anemia from a B12 deficient?

A

Methylfloate trap

  • folate is metabolically unavailable for thymidylate formation
  • Folate accumulates as 5-methyl tetrahydrofolate (inactive form) in absence of B12
65
Q

What can not enough folate lead too?

A

Birth defects
Stroke
Anemia

66
Q

What can too much folate lead to?

A 
Masking B12 deficiency
Presence of circulating unmetabolized folic acid
Cognitive function
Drug efficacy
Epigenetic effects
67
Q

What influences the absorption of folate?

A

Alcohol
Chrons
Tropical sprue
Celiac

68
Q

Which groups are most at risk fro Folate deficiency?

A

Elderly (intake, lack of HCl)
Pregnant (Demand)
Alcoholics, smokers
Those taking the pill, anticonvulsants, depression meds

69
Q

What does your blood look like and characteristics you have when you have a folate deficiency?

A

Megaloblastic anemia

Decreased white cells and decreased platelets

INtestinal function altered due to abnormal turnover of intestinal villa cells

Fatigue, weak, pallor, irritable, diarrhea, sore tongue, forgetfulness

70
Q

What is the gestational risk of folate deficiency?

A 
NTD
Cleft lip/palate
Heart defect
LBW
Preterm birth
71
Q

What is the population risk of folate deficiency?

A

Stroke
Cancer
Megaloblastic anemia

72
Q

What are the most common types of neural tube defects?

A

Spina bifida

Anencephaly (top and back of head)
-due to which part of the neural tube didn’t form properly

73
Q

What are neural tube defects?

A

Congenital anomalies caused by failure of closure of the neural tube at 22-27 days after fertilization
1/1000or2000

-since fortification NTD declined 46% since 1998

74
Q

What increases with what deficiency to increase the risk of CVD and stroke?

A

Homocysteine increases in patients with folate or vitamin B12 deficiencies

75
Q

What studies showed an increase in CVD/stroke when you have a B12 or Folate deficiency?

A

Physicians Heart study

Framingham Heart study

NHANES II (2.9x increase in odds for stroke)

HOPE Study (Vitamin supplementation B6,12 and FA, decreased they but no evidence of reduced risk)
-Didnt reduce heard disease which is the relation with homocysteine
76
Q

What is a folate deficiency and its relation to cancer?

A

Deficiency leads to:

  • Increased uracil incorporation in DNA (makes it more susceptible to oxidation)
  • In vitro change suggestive of DNA & chromosomal damage
  • Excess folate (leads to the development in breast, prostate and colon cancer)
77
Q

What is the population strategy?

A

Mandatory food fortification effective 1998 for folate

  • enriched white flour and bread (100gflour has 0.15 folic acid)
  • Enriched pasta cornmeal (200mg FA/ 100g)
78
Q

How much does the population strategy increase someone’s overall FA intake/day?

A

100micrograms/day

79
Q

What is the risk of HIGH FA intake in the population?

A 
Masking B12 deficiency
Reduced response to Antifolate drug
Immune infection
Cognitive impairment
Cancer
80
Q

What is the risk of HIGH FA intake for the gestaition period?

A

Fetal programming :

  • respiratory
  • obesity
  • Insulin sensitivity
81
Q

What is the general intake of Folate in Canada?

A

Less than 1% had deficiency

40% showed [high]

22% women of child bearing age had concentrations below optimal for NTD risk reduciton

82
Q

How does high FA mask B12 deficiency?

A

Prevents the anemica that normally develop when you are deficient in B12
-Folate cant Evers the hematological response in B12 patients but fails to prevent irreversible neurological changes associated its B12

83
Q

How can you measure folate status?

A

Serum/Plasma Folate

  • most commonly performed test
  • Poor indicator of the degree of folate deficiency
  • Poor sensitivity (low plasma may reflect how dietary intake and provide little Information on tissue reserves
84
Q

What affects the specificity of the Serum/Plasma Folate test?

A

Affected by an:
-Increase: liver damage, hemolysis

-Decrease; Alcohol, oral contraceptives, pregnancy, smoking

85
Q

What is the limit off FA intake?

A
  • intakes of 1mg/day are not likely to mask B12

- No evidence exists that 0.4mg/day of folate4 increased risk of masking B12 deficiency

86
Q

What can high FA supplementation revers the effects off?

A

Anticonvulsant meds:

  • phenyton (dilatin)
  • Phenobarbital
  • Pyrimidine
87
Q

What is the Folate RBC test?

A

RBD [Folate] is more accurate and less variable than plasma folate as to the severity of folate deficiency

  • not affected by short term influx
  • $$$$
88
Q

Is the RBC[Folate] test easy to measure? What does it measure?

A

More difficult to measure and $$$
-microbiological assay (gold standard)

Folate incorporated during erythropoiesis

  • indicative of tissue folate stores
  • not influenced by dietary intake
89
Q

What is the sensitivity of the RBD [Folate] test?

A
  • Reduction in tissue folate stores is reflected by RBC folate
  • RBD [Folate] Reflects folate states at the time it was being synthesized
  • Decreases more slowly than serum/[plasma folate in deficiency
90
Q

What is the specificity in RBC [Folate]?

A

Not specific for folate deficiency - low values occur in B12 deficiency

Increases in Fe deficiency (magnitude and Etiology)

Elevated in liver disease and certain cancers

91
Q

What is plasma homocysteine?

A

tHCY in plasma can serve as a marker for folate, B12 and B6 inadequacies

  • High plasma tHCY almost always exists with B12/6 or Folate deficiency
  • In the absence of B12/6 deficiency [homocysteine] can serve as functional test for folate status
92
Q

What is the sensitivity and specificity of Homocysteine?

A

Sensitivity:
-more sensitive than fall in plasma folate to mark change in folate related physiology

Specificity:
-Mot specific for folate as affected by B12/6 also

93
Q

What is the Leukocyte lobe count?

A

Tells you that you have a nutrient deficiency related to blood cells but cant distinguish which one
-earlier hematological sign for folate deficiency (physical sign in blood smear)

94
Q

How many lobes do leukocytes have in general and how many makes it abnormal?

A

Usually have 3.2 lobes in a healthy individual

Greater than 3.5 lobes Is abnormal in later stages of folate deficiency

95
Q

What happens to leukocytes in folate deficiency?

A

Hypersegmentation occurs resulting in an increased in number of n nuclear lobes
-also increase with B12 deficiency, uraemia, certain types of leukaemia

Following hypersegmentaiton, next change is an increase in size of RBC (increased MCV)

96
Q

What is the sensitivity and specificity for leukocyte lobe count?

A

Sensitivity:
-no relationship between severity and degree of hypersegmentation

Specificity:
-Does not distinguish between folate and B12 deficiencies - occurs in other conditions

97
Q

What is a dU?

A

Deoxyuridine suppression test

  • folate status measurement
  • not common
  • Function indicator of folate status
98
Q

What do you test in a dU?

A

Testing of bone marrow incorporation of radioactive substrate into RBC

Identifies which nutrient is deficient (B12 or folate) by seeing the incorporation of iridium into DNA strands

99
Q

In folate deficiency what does it show the synthesis of in RBCs?

A

Megaloblasts

  • abnormal precursors of RBCs, showing abnormal erythropoietic process
  • reffered to as folate deficiency erythropoiesis
100
Q

What are the DRIs for folate?

A

M/F 400micrograms/day

Pregnant 600micrograms/day

101
Q

What is the upper limit for folic acid?

A

1000micrograms/day

-anything above that can mask B12 deficiency

102
Q

What is Cyanocobalamin Pernicious Anemia?

A

Deficiency in B12

  • megaloblastic anemia and nerve/brain damage
  • Actual cause was defective parietal cells or lack of intrinsic factor (IF)
103
Q

What are sources of B12?

A

B12 or cobalamin produced by micro organisms in plants

Animal products and meat alternatives

104
Q

What are the DRIs for B12?

A

RDA

  • Adults 2.4 micrograms/day
  • 2.8 during pregnancy
105
Q

What is the limiting factor for B12 absorption?

A

Intrinsic Factor

-we can only absorb so much

106
Q

What are the 2 forms of B12?

A

Methylcobalamin
-involved in carbon metabolism

5-Deoxyadenosylcobalamin
-MG pathway

Both contain cobalt

107
Q

What is the function of B12 in the body?

A

DNA synthesis
Folate absorption
Myelin Synthesis
Enzymatic Rxns

108
Q

What are the 3 rxns that B12 is involved in?

A

Homocysteine-> methionine
-methionine synthase where b12 is a cofactor

Methylmalonic Acid -> Succinyl CoA
-Energy pathway by methylmalonyl CoA mutase

Methyltetrahydrofolate-> tetrahydrofolate

109
Q

How is B12 absorbed and metabolized?

A

B12 binds intrinsic factor (glycoprotein-> B12 absorption limited by capacity of IF
-absorption on receptor sites in ileum

110
Q

How is B12 transported?

A

Trans cobalamin II

111
Q

Where is the storage of B12?

A

Stored in Liver in these forms:
Doxyadenosyl cobalamin 65-75%
Hydroxycobalamin 20-30%
Methylcobalamiine 1-5%

112
Q

How does one get B12 deficiency?

A

Genetic- polymorphism, deficiency in receptors
Pharmacological- H2 receptor inhibitor, PPIs
Infection and Parasites- H pylori, tropical sprue
Disease- Celiac, Chrones
Age (Lack HCl)
Social (Religion)
Dietary (vegetarian)
Lifestyle (Obesity, Chronic alcoholabuse)

113
Q

What are the clinical signs and symptoms of B12 deficiency?

A 
Fatigue
Generalized weakness
Indigestion
Pallow
Diarrhea
Smooth beefy red tongue (atrophic glossitis)
114
Q

What is a secondary effect of vitamin B12?

A

Demyelination affected Spinal cord, brain, optic nerve and peripheral nerves may all be affected

  • start to feel tingles in the feet and hands first
  • confounding cause diabetes causes numbness and tingling
115
Q

What are the cerebral signs of B12 deficiency affecting the nervous system?

A 
Irritability
Apathy
Marked Confusion
Depression
Memorry Loss
Psychosis
Optic neuropathy
116
Q

What are the ways in which to test for B12?

A

Serum B12
Leukocyte lobe count
Holo transcobalamin (transporter for B12)
Methylmalonic Acid (MMA)
(distinct molecule related to the energy pathway)
Schilling test (radioactive IF)
Serum Homocysteine

117
Q

What is the serum B12 test?

A

Serum B12 + CBC
-reflects B12 intake and body stores

Classical Findings: Megaloblastic anemia- identical to folate deficiency

118
Q

what is the sensitivity and specificity of B12?

A

Sensitivity: Stores only reflected when low

Specificity: B12 Levels measured are directly affected by serum binding proteins

119
Q

What does serum B12 have decreased levels in?

A 
Elderly
Pregnancy
Fe/Folate deficiency
Cancer
Medications
Malabsorption
Gastrectomy/ileum resection
120
Q

What is the holo transcobalamin II test?

A

Circulating transport protein delivers B12 tro receptors

Early and sensitive measure of B12 deficiency

  • short 1/2 life
  • Amount of B12 attached to holoTCII drops but no drop in serum B12
  • Decrease with deficiency

B12 rapidly depleted from holo transcobalamin II with low fit B status

121
Q

What is the specificity of holo transcobalamin II test?

A

More specific than tHYC

122
Q

What is the MMA test?

A

Serum of plasma methylmalonic acid (Functional test)
MMA may be an early indicator of deficiency

Useful to identify individuals with deficiency even if subclinical (only seeing reduced functions)
-elevated in B12 deficiency but not with folate or B6 deficiency

123
Q

When does myelin damage occur?

A

Doesn’t occur until we area talking about deficiency

124
Q

How sensitive if MMA test?

A

More sensitive and specific indicator of B12 deficiency than Serum B12

125
Q

What is the Shilling test?

A

Older test for B12

  • Newer tests to detect pernicious anemia
  • Newer is better and cheaper
126
Q

What does Serological assays measure?

A

B12 deficiency by measuring intrinsic factor using antibodies
-is presence of IF antibodies then you have pernicious anemia

127
Q

What does gastrin measure?

A

Endocrine regulatory. peptide secreted by stomach, attempt to increase Hal secretion by stomach
-if gastrin increases you have pernicious anemia

128
Q

How do you treat B12 deficiency?

A

Supplementation

-usually oral, then if it doesn’t start to correct in 3 months then injection

129
Q

What are the advantages of oral supplementation?

A

Save money
Avoid painful injection
Avoid repeated patients visits

130
Q

What dosage is required to correct neurological deficits?

A

1000microgram/day to help improve and correct neurological deficits

131
Q

After someone is on oral B12 supplements for 3 months, what should the checkup tests be?

A

Serum B12

CBC

132
Q

Is the masking of Vitamin B12 really something to worry about?

A

Prevalence of inadequacy under estimated due to erroneous belief that deficiency unlikely except among strict vegetarians or patient with pernicious anemia

  • adults: 5% severe, 14-16% marginal
  • 70+: 6% severe, >20% marginal
133
Q

Out of the different types of vegetarians, who ones have the most B12?

A

Omnivores
LOV+Fish
LOV
Vegan

134
Q

What % of Canadas population is B12 deficiency?

A

4.6%

20% marginal B12 status

94.9% had normal tHcy

135
Q

What are the B12 concentration in breast milk like?

A

B12 concentrations in breast milk DO reflect maternal status

136
Q

How much FA do prenatal supplements need to have?

A

More than 200 micrograms of FA

FN 3344 (13 decks)

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