Mastering Functional Blood Chem - 2 Flashcards

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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primary sources of iron in food

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Total iron def causes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Total iron labs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Transferrin Labs

A

SRR: 188 - 370
Optimal 200-370
Alarm none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Low transferrin cxs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Transferrin Decreased vs increased

A

Decreased :
Iron overload
Inflammation of infection
Liver disease
Malnutrition

Increased:
Hormonal changes (oral contraceptives)
Iron deficiency anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ferritin labs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ferritin overload

A

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

> 160 F
200 M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Ferritin inc vs dec

A

Decreased
Iron deficient anemia

Increased
Excess iron
Inflammation
Cardiovasculair dx
Liver Dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Liver supporting foods

A

Beets
Cruciferous veggies
Sulphur containing foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TIBC labs

A

Total Iron binding capacity

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is TIBC

A

Helps indicate type of anemia

Decreased:
Iron overload

Increased
Irom def anemia
Hypochlohydria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

TIBC management

A

If drastically high - think hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

UIBC

A

TiBC +serum iron
Unsaturated iron binding capacity

SRR 130 - 300
Optimal 130-300
Alarm none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

% Transferrin Saturation labs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Iron overload effect in body

A

Oxidative
Stimulate free radicals
-damage cell membranes
- impacts proteins
- causes DNA mutations
-leads to apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Iron overload untreated

A

Metabolic syndrome
Cirrhosis
Neoplasm
DM
Alzheimers
Parkinson’s
CvD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hemochromatosis

A

Hereditary = excess irom deposition
Ferritin > 1000
Serum iron > 220
TIBC <250
%Transferrin increased >60
ALT Elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hemosiderosis

A

Non hereditary form of hemochromatosis

29
Q

Other reasons for excess iron

A

Iron conversion issues
Decreased RBC, HGB and HCT
May need B12, B6 or copper to convert iron to HGB

Excess irom consumption

30
Q

Liver triad

A

Zinc, copper, iron
Have to be in balance

31
Q

Hemochromatosis lab pattern

A

Iron - Inc
Ferritin - inc
% sat - inc
TiBC - dec
Transferrin - dec
HCB - normal

32
Q

Sideroblastic anemia lab pattern

A

Iron - inc
Ferritin - Inc
% sat - inc
TiBC - dec
Transferrin - dec
HCB - dec

33
Q

Thalassemia lab patterns

A

Iron - inc
Ferritin - inc
% sat - inc
TiBC - dec
Transferrin - dec
HCB - dec

34
Q

Anemia of chronic dx lab pattern

A

Iron - dec
Ferritin - inc or normal
% sat - Decreased or normal
TiBC - Decreased or normal
Transferrin - Decreased or normal
HCB - Decreased

35
Q

Iron deficient anemia lab pattern

A

Iron - dec
Ferritin - dec
% sat - dec
TiBC - inc
Transferrin - inc
HCB - dec

36
Q

Vit b12 def lab patterns

A

Iron - inc or normaal
Ferritin - inc or normal
% sat - inc or normal
TiBC - Decreased or normal
Transferrin - decreased or normal
HCB - dec

37
Q

B12 labs

A

SRR 200-1100
Optimal 450 - 800
Alarm none

38
Q

Basics about B12

A

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
Q

Relationship of protein to B12

A

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
Q

Reasons for high vit B12

A

Deficient because of increased B12 consumption
Or decreased intrinsic factor

41
Q

Function of B12

A

Carb metabolism
Component of myelin sheath
Maintain nerve function
Required for conversion of homocysteine to methionine

42
Q

Consequences of B12 def (3)

A

Irreversible neuro damage
Lack of intrinsic factor can be caused by Pernicious anemia = blocks B12 absorption

43
Q

Signs B12 def (3)

A

Progressive peripheral neuropathy
Marked anemia
Swollen, red tongue

44
Q

B12 food sources

A

Egg yolk
Liver
Sardines
Salmon
Beef
Cheese/diary

45
Q

Clinical uses of B12 (4)

A

Reduction of wheezing
Acne
Depression
Neuropathies and neuralgias

46
Q

Severe symptoms of B12 including labs

A

<200
Involuntary movements
Deep depression
Anxiety
Paranoia
Delusions
Memory loss
Incontinence
Loss of taste and smell

47
Q

Vit B12 labs for deficiency (3)

A

Mild: 351 - 449
Moderate 200 - 350
Severe <200

48
Q

B12 management (4)

A

Inquire dietary intake of animal proteins
Hypochlohydria or Malabsorption
Pancreatic insufficiency
Parasites/ intestinal issues

49
Q

Link between SIBO and B12 (1)

A

B12 is absorbed in ilium, where SIBO lives.

50
Q

MMA labs

A

Methylmalonic Acid

SRR 0-318
Optimal 0-216
Alarm none

51
Q

Basics MMA (4)

A

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
Q

MMA folate vs B12

A

High - B12
Low - folate

53
Q

Cx for increased MMA (4)

A

Parietal cell insufficiency
B12 def
Impaired absorption of B12
Kidney insufficiency

54
Q

High levels of B12 (2)

A

Support liver
Supoort kidney

55
Q

Folate basics

A

B9
Coenzyme for methylation
B12 helps folate incorporate into cells

56
Q

Folate labs

A

Double check!

57
Q

Folate NB for (3) +clinical uses (4)

A

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
Q

Food sources Folate

A

Dark leafy greens
Avo
Asparagus
Nuts and seeds
Cauliflower
Broccoli
Beets
Oranges

59
Q

Vit D labs

A

SRR 30-100
Optimal range 35-50
Alarm <30 or >70

60
Q

Vit D basics (5)

A

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
Q

Reduced Vit D seen in: (6)

A

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
Q

Vit D3 endocrine metabolism (3, 3)

A

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
Q

Vit D on calcium

A

Vit D NB for calcium balance in body

64
Q

Vit D intracellular metabolism (4)

A

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
Q

Calcitriol helps maintain (5)

A

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
Q

Effects of low D (8)

A

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
Q

Vit D toxicity

A

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
Q

Vit D recommended lab

A

50ng/ml

Consequences of vit D toxicity:
Stroke
Heart attack
Kidney stones
Headache
Osteoporosis
Nausea, diarrhea, vomiting
Anorexia
Weight loss

69
Q

Why careful with Vit D?

A

Inactive D 25-OH converted into active form which is the hormone. If there is too much free vit D then receptors become desensitized