Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Chemistry > Nutrition & Trace Elements > Flashcards

Nutrition & Trace Elements Flashcards

1
Q

In what form in iron stored in the body?

A

Ferritin:
24 subunit protein – MW ~450 kD
Binds up to 4500 Fe3+ as hydroxyphosphate
Present in most cells, esp. liver, spleen, marrow
Readily mobilized as needed

Hemosiderin:
Insoluble complex derived from ferritin
Decreased apoferritin content
Releases iron less readily than ferritin

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

Iron is part of what 5 important things in the body?

A

1 Hemoglobin (2500 mg)
2 Myoglobin (130 mg)
3 Enzymes, cytochromes (8 mg)
4 Transferrin, plasma (3 mg)

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

In a typical diet 10-20 mg/day is available yet only 5-10% of that is absorbed. Where does iron absorption take place?

A

Absorbed in duodenum and jejunum only as Fe2+

Gastric reducing environment (e.g., vitamin C) helpful

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

How is iron transported within plasma and why?

A

Free unbound iron is toxic. So it is bound and transported very transferrin.

Transferrin:
ß-globulin glycoprotein
MW 79.5 kD
Two Fe3+ binding sites per molecule
Trf is in excess; Fe saturation 20-50% typically
—–Specific Trf receptor for tissue uptake

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

How is serum iron measured? What type of specimen can be used?

A

Specimen: serum or heparinized plasma
Principle:
Fe3+ is released from binding proteins by acidification
Fe3+—> Fe2+ by ascorbate or other reducing agent
Fe2+ binds to ferrozine, ferene, or bathophenanthroline and is measured with a spectrophotometer
Usually not affected by hemolysis
Heme iron not released in assay
Test should also include iron-binding capacity
Reference Interval:
Male 65-170 mcg/dL
Female 50-170 mcg/dL
Diurnal variation (high in am, low in pm)

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

How is transferrin measured?

A

Immunoassay (nephelometry or turbidimetry)

Reference interval 200-320 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is TIBC? How is it measured?

A

TIBC-Total Iron Binding Capacity (semi-automated):

Add excess Fe3+ to sample and equilibrate
Complex non-bound iron (e.g., MgCO3) and separate
Measure Trf-bound iron (as in total iron)
Reference interval: 175-400 mcg/dL (iron)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is UIBC? How is it measured?

A

UIBC-Unsaturated Iron Binding Capacity (automated)

Add excess Fe3+ to sample and equilibrate
Measure unbound iron only (no acidification)
TIBC = UIBC + serum iron
UIBC = Added iron-measured iron
Do not report UIBC results, only TIBC (& percent saturation)

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

How is Transferrin Saturation and Transferrin itself calculated?

A

Transferrin Saturation = Fe ÷ TIBC (or Trf)
—Usually expressed as a percent

Transferrin (mg/dL) ≈ 0.8 x TIBC (mcg Fe/dL)

TIBC reference interval: 175-400 mcg/dL
Trf Sat’n reference interval: 15-60% (TIBC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Serum ferritin is ______ to stored iron and will _____ as iron stores______.

A

directly proportional.
decrease.
deplete.

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

What are the tree stages of iron deficiency anemia?

A

Stage 1 : Iron DEPLETION
Depletion of iron stores marked by ferritin decrease
Normal serum iron and TIBC (ferritin maintains serum levels)
No anemia
Normal RBC morphology

Stage 2: Iron-deficient Erythropoiesis
Decreased iron available for erythropoiesis (stores depleted)
Decreased ferritin, serum iron, Trf sat’n; increase in TIBC (Trf)
No anemia; RBC slightly microcytic, no hypochromia, inc. RDW

Stage 3 : Iron DEFICIENCY ANEMIA
Decrease in ferritin, iron, Trf sat’n; increase in TIBC (Trf)
Decrease in hemoglobin, MCV, MCH, MCHC; inc. RDW
Microcytic, hypochromic anemia

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

Describe the pathogensis of anemia due to chronic disease.

A

Inflammatory cytokines induce hepcidin production by the liver
Hepcidin prevents iron release from enterocytes and macrophages
Low available iron interferes with bacterial growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What role does copper play in the body?

A

Enzyme cofactor – esp. redox enzymes

Bound to ceruloplasmin (α2-globulin)

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

Copper deficiency leads to…?

A

Deficiency:
Microcytic, hypochromic anemia
Neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Copper excess is called…?

A

Excess: Wilson’s disease
Copper deposition in tissues, esp. liver and brain
Decreased ceruloplasmin and serum Cu, plus elevated urine Cu

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

How is copper measured?

A

Measure Cu by atomic absorption, ceruloplasmin by immunoassay (nephelometry or turbidimetry)

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

What are the fat soluble vitamins?

A

A: carotene, retinol, retinal, retinoic acid
Vision
Epithelial cell stability

D: cholecalciferol
Ca2+ absorption

E: tocopherols
Antioxidant, free radical scavenger

K: phylloquinones, menaquinones
Synthesis of clotting factors II, VII, IX, X, C and S
Cofactor for enzymatic formation of γ-carboxyglutamate

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

Fat soluble vitamins are readily stored in the body and deficiency slowly develops. What can cause it?

A

Decreased dietary intake
Decreased absorption
Biliary deficiency
Intestinal malabsorption

19
Q

Which vitamin is commonly measured? How?

A

(Vitamin D) by HPLC
Vitamin D: LC-MS/MS or immunoassay

—-Immunoassay:
Must measure both D3 and D2 equally
Must displace from binding protein - (D3 bound tighter)
—–LC-MS/MS: preferred method but more expensive
Reference intervals controversial:
80->150 ng/mL seen)

20
Q

Vitamin D absorption/conversion can be inhibited by…?

A

Dec. by pigmented skin, low sun angle (high latitude, winter)

21
Q

Where is Vitamin D mostly found?

A

primarily in milk (added), cod liver oil, multi-vitamins, and supplements

22
Q

UV light converts 7-dehydrocholesterol to what?

A

vitamin D3—-cholecalciferol

23
Q

How is Vitamin D metabolized?

A

UV light + 7-dehydrocholesterol in skin——->Vitamin D3

Vitamin D3 to liver—–>25(OH) Vitamin D

In Kidney 25(OH)Vitamin D—->1,25(OH)2 Vitamin D (ACTIVE METABOLITE!!!)—–>Tissue specific Vitamin D response

24
Q

What is Vitamin D2

A

Ergocalciferol from ergosterol UV irradiation
Of plant origin (yeast and mushrooms)
Identical hydoxylations as D3 (1- and 25-)
1,25 diOH D2 has same action as D3
Possible shorter half-life
More common form of pharmaceutical vitamin D (in U.S.)
OTC supplements are usually D3

25
Q

Actions of Vitamin D?

A

Raise calcium levels:

  • –Increases GI (duodenal) Ca absorption
  • –Stimulates osteoclast precursors to become mature osteoclasts (break down bone)
  • –Stimulates osteoblasts to influence osteoclast bone resorption

Immune modulation, …?
—All cells have vitamin D receptors but few have calcium responses

26
Q

What is the best marker for vitamin D status?

A

Best marker of vitamin D status is 25-OH D (cf case)

—-Pts w/ renal disease may req. 1,25-diOH D measurement

27
Q

What is Vitamin B1?

A

Thiamine (B1)

  • –α-ketoacid deHase cofactor (Pyr, α-KG)
  • –Beriberi & Wernicke’s encephalopathy (alcoholics)
  • –Measure in whole blood, not plasma
  • —–Transketolase enzyme assay historical surrogate
28
Q

What is Vitamin B2?

A

Riboflavin (B2)

—-Dehydrogenase enzyme cofactor

29
Q

What is Vitamin B3?

A

Niacin (B3) – nicotinic acid

  • —Required for NAD+ and NADP+
  • —-Pellagra results from deficiency
30
Q

What is Vitamin B6?

A

Pyridoxine (B6)

  • Cofactor in >60 enzymes
  • Aminotransferases (ALT, AST)
  • —Provide glucogenic substrates
  • Tryptophan metabolism
  • Catecholamine synthesis

Excess can lead to peripheral neuropathy

31
Q

What is Vitamin B12?

A

Corrin ring w/ Co+ coordination atom
Involved in one carbon transfers
Thymidine synthesis (DNA)
Primary sources are meat and dairy (bacterial)
Absorption requires:
—-Low gastric pH to dissociate B12 from food
—–Intrinsic factor (IF, stomach) for ileal absorption
Transported in blood by transcobalamins

32
Q

How is Vitamin B12 measured?

A

Immunoassay or intrinsic factor binding assay
—–Use IF as binder in competitive assay
Reference interval: 180-900 pg/mL
-Definite deficiency

33
Q

What causes Vitamin B12 deficiency?

A

Decreased gastric acidity
——-Atrophy or proton pump inhibitors (e.g., Prilosec)
Decreased intrinsic factor
——-Anti-intrinsic factor antibodies (pernicious anemia)
Malabsorption
——–Pancreatic insufficiency, celiac dz, Crohn’s dz
Decreased intake (vegetarians)

34
Q

Vitamin B12 deficiency results in….?

A

Results in macrocytic anemia (reversible)
—-Macrocytosis, hypersegmented PMN nuclei
Irreversible neuropathy possible
Treat by IM injections (if PA)

35
Q

What is Folate?

A

A water soluble vitamin needed in the synthesis of DNA.

  • Primarily plant derived
  • Involved in one carbon transfers
  • Measure by immuno- or ligand-binding assay
  • Serum – may reflect recent diet, therefore reduced utility
  • Reference interval: >3.0 ng/mL, deficient 280 ng/mL, def.
36
Q

What is Heme?

A 
Fe-containing prosthetic group in:
Hemoglobin
Myoglobin
Cytochromes
Peroxidase
Catalase
37
Q

What color are porphyrinogens?

A

Colorless.

38
Q

In Heme synthesis what is the rate limiting step?

A

1) ALA Synthase, inhibited by heme

39
Q

Give an overview of heme synthesis.

A

Succinyl CoA—->ALA—->Porphobilinogen—–>Uro—->Copro————————>Proto—->heme

decreasing polarity of side chains—–>
Urine: ALA PBG URO COPRO
Stool: PROTO and COPRO (oxidation in urine and stool forms color)

40
Q

What are porphyrias?

A

Rare disorders of partial enzyme deficiencies

  • Genetic or acquired
  • Dec. heme production reduces inhibition of ALA synthase, precursors accumulate
Clinical manifestations:
Neurologic – usually acute presentation
---Abdominal pain, psychiatric
--------Early precursor (ALA, PBG) accumulation
Photosensitivity – usually more chronic
---Skin reactions, erythema, blistering
------Porphyrin(ogen) accumulation
41
Q

How are Porphyrias diagnosed?

A

Urinary PBG if acute, neurological symptoms

  • —Collect during an attack
  • —-If negative, acute porphyria unlikely
  • —-ALA dehydratase (PBG synthase) def. very rare (
42
Q

Macronutrition: What can we make and what must we get from diet?

A

We can make carbohydrate
We can make essential lipids (chol)
Essential amino acids must be in diet
We do not recycle nitrogen very well

43
Q

What does Nitrogen balance mean?

A

Relationship of nitrogen intake to excretion
Negative nitrogen balance – excretion exceeds intake
Indicates muscle catabolism is providing nitrogen needs

44
Q

What is enteral and parental feeding?

A 
Enteral feeding (“stomach tube)
---Preferred

Parenteral feeding (IV)

  • –Peripheral – usually short term
  • –Total (TPN) - central line, usually longer or more critical patient
  • –Solutions may be high in glucose (5-10%) & lipid
  • ——–Consider effect on blood samples drawn

Clinical Chemistry (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions