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Dr Rhonda Nelson - Blood Chemistry > Mastering Functional Blood Chem - 2 > Flashcards

Mastering Functional Blood Chem - 2 Flashcards

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1
Q

Key anemia markers

A

RBC
Male: SRR 4.2-5.8 ; optimal 4.2-4.9
Female : 3.8 - 5.1 : optimal 3.9 - 4.5

HGB
Male: SRR 13.2 - 17.1 ; optimal 14.0 - 15.0
Female : 11.7 - 15.5 : optimal 13.5 - 14.5

HCT
Male: SRR 38.5% - 50%; optimal 40 - 48%
Female : 35 - 45%: optimal 37 - 44%

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2
Q

Anemia pattern iron vs folic/B12

A

Both: RBC, HGB and hematocrit: Decreased!

MCV, MCH, MCHC:
Iron anemia: Decreased
Folic/B12: increased

RDW: both increased

Ferritin
Iron Decreased
Folic/B12 Increased

%saturation
Iron decreased
Folic increased

TIBC
Iron increased
Folic Decreased

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3
Q

What is total iron

A

Measures dissolved iron in blood
Ferric form - reduced to ferrous iron
Only 10 % of dietary iron is absorbed
- occurs in duodenum and jejunum
Majority is bound to transferrin (30% saturated at any give time)
Other binding proteins: ferritin, hemosiderin and hemoglobin

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4
Q

Primary sources of iron in food

A

Egg yolks, liver dark meats, leafy greens,
Good to combine with proetin

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5
Q

Total iron def causes

A

Decreased dietary intake
Hypochlohydria
Iron loss
Increased iron requirements (pregnanacy or vegans, PPIs)

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6
Q

Total iron labs

A

SRR: 40-160
Optimal: 85-130
Alarm <25 >200

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7
Q

Iron symptoms Decreased vs increased

A

Decreased:
-iron deficient anemia
- Hypochlohydria
-internal bleeding
-chronic illness
-bacterial infection

Increased :
-liver Dysfunction (insufficient binding protein)
-excess consumption (cast iron pans, well water)
-viral infection
-hemochromatosis or hemosiderosis
-thalassemia
-hemolytic or sideroblastic anemia

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8
Q

Iron management

A

Iron rich foods - dark meats combined with plant protein. (heam and non heam together)
Meat with fat, fat helps iron absorption
Sufficient hydrochloric acid and pepsin. Pepsin is made from HCL and pepsinogen
Possible infxns
High iron - liver Dysfunction
Greater than 200 - REFER!

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9
Q

Transferrin Labs

A

SRR: 188 - 370
Optimal 200-370
Alarm none

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10
Q

What is transferrin

A

Produced in liver
Fxn - bind to iron and transport to liver, spleen and marrow
1/3 will be saturated with iron - healthy
When iron dec, production increases to try and pick up as much iron as possible
Associated with TIBC marker
Levels <100 = protein deficiency

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11
Q

Low transferrin cxs

A

All bound up too much circulating iron
Liver Dysfunction - Decreased transferrin production

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12
Q

Transferrin Decreased vs increased

A

Decreased :
Iron overload
Inflammation of infection
Liver disease
Malnutrition

Increased:
Hormonal changes (oral contraceptives)
Iron deficiency anemia

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13
Q

Transferrin management

A

Rule out Exogenous exposures: cookware, well water, supplements
Investigate inflammation
Sufficient dietary intake of protein, fats carbs and sufficient upper digestive function

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14
Q

Ferritin labs

A

SRR 10-32
Optimal 30-70
Alarm <8 >322

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15
Q

What ia ferritin

A

Storage form of iron
Most sensitive for iron def anemia
Ferritin is iron savings account, if body is low, draws iron out of ferritin = low ferritin

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16
Q

Ferritin overload

A

Increased ferritin = cardiovascular dx
Highly inflam
Can damage hepatocytes
- Silymarin and milke thistle

> 160 F
200 M

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17
Q

Ferritin inc vs dec

A

Decreased
Iron deficient anemia

Increased
Excess iron
Inflammation
Cardiovasculair dx
Liver Dysfunction

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18
Q

Liver supporting foods

A

Beets
Cruciferous veggies
Sulphur containing foods

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19
Q

TIBC labs

A

Total Iron binding capacity

SRR 240 - 425
Optimal 250 - 350
Alarm <175 >585

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20
Q

What is TIBC

A

Helps indicate type of anemia

Decreased:
Iron overload

Increased
Irom def anemia
Hypochlohydria

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21
Q

TIBC management

A

If drastically high - think hemochromatosis

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22
Q

UIBC

A

TiBC +serum iron
Unsaturated iron binding capacity

SRR 130 - 300
Optimal 130-300
Alarm none

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23
Q

% Transferrin Saturation labs

A

SRR 15-50%
Optimal 20-35%
Alarm 0 or >75%

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24
Q

What is %Transferrin Saturation

A

Calculated value, serum iron x100 /TIBC
Screen for hemochromatosis
Measures % of iron to transferrin

Decreased
Iron deficient anemia
Hypochlohydria

Increased
Iron overload

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25
Iron overload effect in body
Oxidative Stimulate free radicals -damage cell membranes - impacts proteins - causes DNA mutations -leads to apoptosis
26
Iron overload untreated
Metabolic syndrome Cirrhosis Neoplasm DM Alzheimers Parkinson's CvD
27
Hemochromatosis
Hereditary = excess irom deposition Ferritin > 1000 Serum iron > 220 TIBC <250 %Transferrin increased >60 ALT Elevated
28
Hemosiderosis
Non hereditary form of hemochromatosis
29
Other reasons for excess iron
Iron conversion issues Decreased RBC, HGB and HCT May need B12, B6 or copper to convert iron to HGB Excess irom consumption
30
Liver triad
Zinc, copper, iron Have to be in balance
31
Hemochromatosis lab pattern
Iron - Inc Ferritin - inc % sat - inc TiBC - dec Transferrin - dec HCB - normal
32
Sideroblastic anemia lab pattern
Iron - inc Ferritin - Inc % sat - inc TiBC - dec Transferrin - dec HCB - dec
33
Thalassemia lab patterns
Iron - inc Ferritin - inc % sat - inc TiBC - dec Transferrin - dec HCB - dec
34
Anemia of chronic dx lab pattern
Iron - dec Ferritin - inc or normal % sat - Decreased or normal TiBC - Decreased or normal Transferrin - Decreased or normal HCB - Decreased
35
Iron deficient anemia lab pattern
Iron - dec Ferritin - dec % sat - dec TiBC - inc Transferrin - inc HCB - dec
36
Vit b12 def lab patterns
Iron - inc or normaal Ferritin - inc or normal % sat - inc or normal TiBC - Decreased or normal Transferrin - decreased or normal HCB - dec
37
B12 labs
SRR 200-1100 Optimal 450 - 800 Alarm none
38
Basics about B12
Majority from animal sources Bound to protein carriers Needs HCL + pepsinogen to break from B12 carrier Requires intrinsic factor from periatal cells Therefore if periatal cells are not making HCL probably not making intrinsic factor Absorbed in ilium (NB for SIBO patients) Transcobalamin proteins transport to blood B12 stored 3 years in liver
39
Relationship of protein to B12
Protein hits stomach, activates periatal cells and release of HCL and intrinsic factor. Travels to ilium where Transcobalamin protein transport to blood by binding it to intrinsic factor
40
Reasons for high vit B12
Deficient because of increased B12 consumption Or decreased intrinsic factor
41
Function of B12
Carb metabolism Component of myelin sheath Maintain nerve function Required for conversion of homocysteine to methionine
42
Consequences of B12 def (3)
Irreversible neuro damage Lack of intrinsic factor can be caused by Pernicious anemia = blocks B12 absorption
43
Signs B12 def (3)
Progressive peripheral neuropathy Marked anemia Swollen, red tongue
44
B12 food sources
Egg yolk Liver Sardines Salmon Beef Cheese/diary
45
Clinical uses of B12 (4)
Reduction of wheezing Acne Depression Neuropathies and neuralgias
46
Severe symptoms of B12 including labs
<200 Involuntary movements Deep depression Anxiety Paranoia Delusions Memory loss Incontinence Loss of taste and smell
47
Vit B12 labs for deficiency (3)
Mild: 351 - 449 Moderate 200 - 350 Severe <200
48
B12 management (4)
Inquire dietary intake of animal proteins Hypochlohydria or Malabsorption Pancreatic insufficiency Parasites/ intestinal issues
49
Link between SIBO and B12 (1)
B12 is absorbed in ilium, where SIBO lives.
50
MMA labs
Methylmalonic Acid SRR 0-318 Optimal 0-216 Alarm none
51
Basics MMA (4)
1) Methylmalonic Acid 2) byproduct of metabolism of certain fatty acids and amino acids 3) requires B12 to metabolize 4) differentiate between folate and B12 def - will be INC B12 def
52
MMA folate vs B12
High - B12 Low - folate
53
Cx for increased MMA (4)
Parietal cell insufficiency B12 def Impaired absorption of B12 Kidney insufficiency
54
High levels of B12 (2)
Support liver Supoort kidney
55
Folate basics
B9 Coenzyme for methylation B12 helps folate incorporate into cells
56
Folate labs
Double check!
57
Folate NB for (3) +clinical uses (4)
NB nervous system development, esp 1st trimester of pregnancy Converts histidine to Glutamine Absorbed in small intestine, stored in liver Restless leg syndrome Cervical dysplasia Malabsorption and GI inflammation Reduction of homocysteine
58
Food sources Folate
Dark leafy greens Avo Asparagus Nuts and seeds Cauliflower Broccoli Beets Oranges
59
Vit D labs
SRR 30-100 Optimal range 35-50 Alarm <30 or >70
60
Vit D basics (5)
Fat soluble vitamin synthesized from cholesterol Activated in the skin when exposed to UVB light Two pathways for metabolism: 1) endocrine metabolism 2) intercellular metabolism Skin needs calcium and fatty acids to synthesis vit D
61
Reduced Vit D seen in: (6)
Obesity (decreased endocrine and cellular metabolism) Elderly population Sunscreen use Lack of sunlight Darker skin colour Frank deficiency isn't common, look at missing ci factors like polyunsaturated fats
62
Vit D3 endocrine metabolism (3, 3)
Vit D3 (cholecalciferol) is formed in the skin when exposed to sunlight (NB adequate choles/fat in skin) Converted into 25 hydroxtly vit D in liver Then converted into 1,25 calcitriol in kidney Increases absorption of calcium and phosphorus for SI Increased reabsorption of calcium from kidneys Stimulates release of calcium from bones
63
Vit D on calcium
Vit D NB for calcium balance in body
64
Vit D intracellular metabolism (4)
1)Synthesis of calcitriol within certain cells 2) certain cells take 25-OH D (inactive form of vit D) from circulation -breast, prostate, lung, lymph, colon, pancreas, adrenal medulla, brain 3) these cells are able to synthesize thier own calcitriol and don't need internal hormone pool 4)receptors also found in -Monocytes -T and B Lymphocytes -neurons -prostatic and ovarian cells -pituitary
65
Calcitriol helps maintain (5)
1) Modulation and transcription of genes that affect proliferation and differentiation 2) healthy neurotransmitter function and depression 3) immune function and reduction of inflammation, AI reactions, risk of cancer and infection 4)healthy glucose metabolism and insulin levels 5) normal lipids, reducing peroxidation
66
Effects of low D (8)
1) increased oxidative stress 2) fat-soluble nutrient deficiencies 3) AI Dxs 4) infections 5) decreased immunity 6) calcium and or phosphorus imbalance 7) EFA deficiency 8) reduced cognitive function
67
Vit D toxicity
1)Excess Vit D intake = elevated serum calcium 2) = calcification of arteries, kidneys and lungs 3) important to provide EFAs and calcium 4) promote adequate HCL levels 5) support liver and kidney function
68
Vit D recommended lab
50ng/ml Consequences of vit D toxicity: Stroke Heart attack Kidney stones Headache Osteoporosis Nausea, diarrhea, vomiting Anorexia Weight loss
69
Why careful with Vit D?
Inactive D 25-OH converted into active form which is the hormone. If there is too much free vit D then receptors become desensitized

Dr Rhonda Nelson - Blood Chemistry (3 decks)

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