Mastering Functional Blood Chem - 2 Flashcards
Key anemia markers
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%
Anemia pattern iron vs folic/B12
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
What is total iron
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
Primary sources of iron in food
Egg yolks, liver dark meats, leafy greens,
Good to combine with proetin
Total iron def causes
Decreased dietary intake
Hypochlohydria
Iron loss
Increased iron requirements (pregnanacy or vegans, PPIs)
Total iron labs
SRR: 40-160
Optimal: 85-130
Alarm <25 >200
Iron symptoms Decreased vs increased
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
Iron management
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!
Transferrin Labs
SRR: 188 - 370
Optimal 200-370
Alarm none
What is transferrin
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
Low transferrin cxs
All bound up too much circulating iron
Liver Dysfunction - Decreased transferrin production
Transferrin Decreased vs increased
Decreased :
Iron overload
Inflammation of infection
Liver disease
Malnutrition
Increased:
Hormonal changes (oral contraceptives)
Iron deficiency anemia
Transferrin management
Rule out Exogenous exposures: cookware, well water, supplements
Investigate inflammation
Sufficient dietary intake of protein, fats carbs and sufficient upper digestive function
Ferritin labs
SRR 10-32
Optimal 30-70
Alarm <8 >322
What ia ferritin
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
Ferritin overload
Increased ferritin = cardiovascular dx
Highly inflam
Can damage hepatocytes
- Silymarin and milke thistle
> 160 F
200 M
Ferritin inc vs dec
Decreased
Iron deficient anemia
Increased
Excess iron
Inflammation
Cardiovasculair dx
Liver Dysfunction
Liver supporting foods
Beets
Cruciferous veggies
Sulphur containing foods
TIBC labs
Total Iron binding capacity
SRR 240 - 425
Optimal 250 - 350
Alarm <175 >585
What is TIBC
Helps indicate type of anemia
Decreased:
Iron overload
Increased
Irom def anemia
Hypochlohydria
TIBC management
If drastically high - think hemochromatosis
UIBC
TiBC +serum iron
Unsaturated iron binding capacity
SRR 130 - 300
Optimal 130-300
Alarm none
% Transferrin Saturation labs
SRR 15-50%
Optimal 20-35%
Alarm 0 or >75%
What is %Transferrin Saturation
Calculated value, serum iron x100 /TIBC
Screen for hemochromatosis
Measures % of iron to transferrin
Decreased
Iron deficient anemia
Hypochlohydria
Increased
Iron overload
Iron overload effect in body
Oxidative
Stimulate free radicals
-damage cell membranes
- impacts proteins
- causes DNA mutations
-leads to apoptosis
Iron overload untreated
Metabolic syndrome
Cirrhosis
Neoplasm
DM
Alzheimers
Parkinson’s
CvD
Hemochromatosis
Hereditary = excess irom deposition
Ferritin > 1000
Serum iron > 220
TIBC <250
%Transferrin increased >60
ALT Elevated
Hemosiderosis
Non hereditary form of hemochromatosis
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
Liver triad
Zinc, copper, iron
Have to be in balance
Hemochromatosis lab pattern
Iron - Inc
Ferritin - inc
% sat - inc
TiBC - dec
Transferrin - dec
HCB - normal
Sideroblastic anemia lab pattern
Iron - inc
Ferritin - Inc
% sat - inc
TiBC - dec
Transferrin - dec
HCB - dec
Thalassemia lab patterns
Iron - inc
Ferritin - inc
% sat - inc
TiBC - dec
Transferrin - dec
HCB - dec
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
Iron deficient anemia lab pattern
Iron - dec
Ferritin - dec
% sat - dec
TiBC - inc
Transferrin - inc
HCB - dec
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
B12 labs
SRR 200-1100
Optimal 450 - 800
Alarm none
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
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
Reasons for high vit B12
Deficient because of increased B12 consumption
Or decreased intrinsic factor
Function of B12
Carb metabolism
Component of myelin sheath
Maintain nerve function
Required for conversion of homocysteine to methionine
Consequences of B12 def (3)
Irreversible neuro damage
Lack of intrinsic factor can be caused by Pernicious anemia = blocks B12 absorption
Signs B12 def (3)
Progressive peripheral neuropathy
Marked anemia
Swollen, red tongue
B12 food sources
Egg yolk
Liver
Sardines
Salmon
Beef
Cheese/diary
Clinical uses of B12 (4)
Reduction of wheezing
Acne
Depression
Neuropathies and neuralgias
Severe symptoms of B12 including labs
<200
Involuntary movements
Deep depression
Anxiety
Paranoia
Delusions
Memory loss
Incontinence
Loss of taste and smell
Vit B12 labs for deficiency (3)
Mild: 351 - 449
Moderate 200 - 350
Severe <200
B12 management (4)
Inquire dietary intake of animal proteins
Hypochlohydria or Malabsorption
Pancreatic insufficiency
Parasites/ intestinal issues
Link between SIBO and B12 (1)
B12 is absorbed in ilium, where SIBO lives.
MMA labs
Methylmalonic Acid
SRR 0-318
Optimal 0-216
Alarm none
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
MMA folate vs B12
High - B12
Low - folate
Cx for increased MMA (4)
Parietal cell insufficiency
B12 def
Impaired absorption of B12
Kidney insufficiency
High levels of B12 (2)
Support liver
Supoort kidney
Folate basics
B9
Coenzyme for methylation
B12 helps folate incorporate into cells
Folate labs
Double check!
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
Food sources Folate
Dark leafy greens
Avo
Asparagus
Nuts and seeds
Cauliflower
Broccoli
Beets
Oranges
Vit D labs
SRR 30-100
Optimal range 35-50
Alarm <30 or >70
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
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
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
Vit D on calcium
Vit D NB for calcium balance in body
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
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
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
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
Vit D recommended lab
50ng/ml
Consequences of vit D toxicity:
Stroke
Heart attack
Kidney stones
Headache
Osteoporosis
Nausea, diarrhea, vomiting
Anorexia
Weight loss
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
