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Clinical Chemistry > Iron, Porphyrin, and Hemoglobin > Flashcards

Iron, Porphyrin, and Hemoglobin Flashcards

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1
Q

iron metabolism

A

is the set of chemical reactions maintaining homeostasis of iron. The control of this necessary since excess or deficiency is significant to health and disease states.

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2
Q

State of Iron in Diet

A

Ferric (Fe3+)

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3
Q

State of Iron Absorbed

A

Ferretin (Fe2+)

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4
Q

How is Iron Stored?

A

Ferretin (Fe2+) is oxidized back to Ferric

(Fe3+)2(Fe3+) Ferric bound to apoferritin

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5
Q

How is Iron Transported?

A

Ferretin (Fe2+) is oxidized back to Ferric (Fe3+)

2(FE3+) Ferric bound to transferrin

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6
Q

Form of Iron bound to Heme

A

Ferretin (Fe2+)

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7
Q

Role of Ferritin (Fe2+):

A

molecule for intestinal absorption

incorporation with Heme Molecule

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8
Q

Role of Ferric (Fe3+)

A

molecule for transportation and storage

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9
Q

Role of Transferrin

A

binds to 2 ferric molecules for transportation

prevents loss through kidney

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10
Q

Define TIBC

A

Total Iron Binding Capacity (TIBC):

The theoretical amount of iron that could be bound if transferrin and other minor iron binding proteins present in the serum or plasma sample were fully saturated.

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11
Q

Transferrin Saturation Calculation

A

= Iron Concentration / TIBC

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12
Q

Low Transferrin Saturation:

A

Low Iron / High TIBC

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13
Q

High Transferrin Saturation

A

High Iron / Low TIBC

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14
Q

Reference Range: Iron (Fe)

A

65 – 175 ug/dl

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15
Q

Reference Range: TIBC

A

240 – 420 ug/dl

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16
Q

Reference Range: Transferrin

A

180 – 400 mg/dl

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17
Q

Reference Range: Ferretin (Fe2+)

A

Male 25 – 300 ng/ml
Female 10 – 130 ng/ml (menstruating)
Female 25 – 300 ng/ml (post-menopause)

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18
Q

%Fe Saturation

A

25 – 40 %

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19
Q

Decreased Total Iron (causes/symptoms)

A 
↑ Demand (Pregnancy)		
↑ Loss (blood loss)
↓ Release of stored Fe (infection impairs release)
↓ Absorption
↓ Dietary Intake	(Fe Deficient anemia)
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20
Q

Increased Total Iron (causes/symptoms)

A

↑ release of Fe (hemolysis)
↓ Utilization of Fe (lead poisoning)
↑ Absorbance (hemochromatosis or hemsosiderosis)
Defective Storage

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21
Q

Increased Ferretin (Fe2+)

A 
Iron Overdose
Liver Disease	
Chronic Renal Failure
Malignancy
Infection/Inflammation
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22
Q

Decreased ferretin (Fe2+)

A

Malnutrition
earliest indicator of deficiency
diagnostic of iron deficiency

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23
Q

Increased Transferrin

A

Iron Deficient anemia ↑Transferrin ↓ Ferretin

Iron Deficiency (inverse to ferritin)

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24
Q

Decreased Transferrin

A

Chronic Infection
Malnutrition
iron Overdose

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25
Q

Role of Haptoglobin

A

produced by liver “Heme scavenger”

Transports free hemoglobin that is extracellular to be removed by liver

  1. Hemolysis causes increase of extracellular hemoglobin
  2. Haptoglobin binds to free hemoglobin for transportation
  3. Haptoglobin brings free hemoglobin to liver for processing

Prevents loss of hemoglobin

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26
Q

significance of and situations in which changes in haptoglobin con¬centration occur

A

Decrease Caused by:

Hemolysis (hemolytic anemia, HDN, transfusion rxn) all haptoglobin bound

Liver Disease (liver not producing Haptoglobin)

Nephrotic syndrome

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27
Q

Haptoglobin Reference Range

A

Haptoglobin Normal: 35 – 200 mg/dl

28
Q

Iron (Fe) Measurement

A
  1. Create acidic pH
  2. Releases Iron from transferrin
  3. Reduce Ferriic (Fe3+) to Ferriton (Fe2+)
  4. Form color complex to Ferriton (Fe2+)
  5. Read spectrophotometrically
29
Q

Iron Measurment Interference

A

hemolysis
EDTA
citrate
oxalate

30
Q

TIBC Measurement

A
  1. 500ug excess Ferric iron added (Fe3+) pH 7.5
  2. All available transferrin sites are bound
  3. Supernatant analyzed for Ferric Iron (Fe3+) TIBC
  4. TIBC = TOTAL Fe + UIBC
    UIBC: Unbound Iron Binding Capacity
31
Q

TIBC Calculation

A

TIBC = TOTAL Fe + UIBC

UIBC: Unbound Iron Binding Capacity

32
Q

Transferrin Measurement (Indirect)

A

indirectly measure using TIBC

Transferrin = TIBC X 0.70

33
Q

Transferrin Measurement (Direct)

A

TURBIDOMETRIC

Transferrin + Anti-transferrin Antibody forms antigen/antibody complex

Change in the absorbance measured at 340 nm

34
Q

Porphyrin:

A

chelate metals to form the functional groups that participate in oxidative metabolism

Not biologically active but a intermediate for hemoglobin and myoglobin synthesis

35
Q

three clinically significant porphyrins

A
  1. Uroporphyrin (urine excretion)
  2. Coproporphyrin (urine or feces excretion) 3. Protoporphyrin (feces excretion)

Porphyrin Indicates abnormal heme synthesis when in excess

36
Q

effect of U.V. light on porphyrins

A

Porphyrins absorb visible light causing itchy skin, fluid accumulation, blisters, swelling

Extremely photosensitive causing severe reaction upon exposure to sunlight (UV)

37
Q

List and describe the components of heme and heme synthesis

A

1 .The first step in heme synthesis takes place in the mitochondrion, with the condensation of succinyl CoA and glycine by ALA synthase to form 5-aminolevulic acid (ALA).

  1. ALA is transported to the cytosol where a series of reactions produce a ring structure called coproporphyrinogen III.
  2. Coproporphyrinogen III returns to the mitochondrion where an addition reaction produces protoporhyrin IX.
  3. The enzyme ferrochelatase inserts iron into the ring structure of protoporphyrin IX to produce heme
38
Q

Makeup of Heme

A

Porphyrin + Iron

39
Q

significance of ALA synthetase in the regulation of heme synthesis

A

ALA synthase is an enzyme that catalyzes condensation of glycine and Succinyl CO A

MAIN REGULATOR of porphyrin synthesis (precursor to heme

Rapid response to negative feedback
↓ HEME = ↑ ALA Synthase Production

40
Q

factors which affect the activity of ALA syn¬thetase

A

Hereditary Defect/deficiency (enzyme)
x-linked sideroblastic anemia microcytic,hypochromic (small and low heme)
Fe overload
Siderblasts found in the bone marrow

ALA Synthase requires coenzyme (coenzyme doesn’t work/ALA doesn’t work)  Impaired Heme synthesis

41
Q

Porphyria

A

accumulation of porphyrins and their precursors

healthy individual has trace amounts of porphyrins since all porphyrins get converted to heme

42
Q

PORPHYRIA CLASSIFICATION

ORGAN INVOLVEMENT:

A

Erythropoietic Porphyria
- accumulation of excess porphyrins in blood producing tissues (bone marrow)

Hepatic Porphyria
- accumulation of excess porphyrins in liver

43
Q

PORPHYRIA CLASSIFICATION

ACQUISITION:

A

Inherited:
-genetic defect causing excess cells

Acquireed:
-liver disease, toxic metals, drugs causing excess in urine

44
Q

PORPHYRIA CLASSIFICATION

SYMPTOMS:

A

Cutaneous:
-skin manifestations, photosensitivity

Neurologic:
-abdominal pain, psychological disorders

45
Q

Differentiate porphyrinuria vs. porphyria.

A

Porphyria: excess porphyrins or its precursors (indicates disruption in heme synthesis)

Porphyrinurea: secondary porphyria
Mild to moderate increase in the excretion of urinary porphyrins is seen

Caused by of non-inherited defect in heme synthesis but rather drug or toxin interference

46
Q

Cutaneous Symptoms:

A

-skin manifestations, photosensitivity, skin lesions, discolored teeth, solar eczema, Itchy skin, fluid accumulation, blisters, swelling, disfiguring

Excess porphyrin production and excretion:
Uroporphyrin
Coproporphyrin
Protoporphyrin

47
Q

Cutaneous Porphyrias

A

PCT: Porphyria Cutanea Tardia (hepatic #1)

EP: Erythropoietic Porphyria

CEP: Congenital Erythropoietic Porphyria

48
Q

Neurologic Porphyria Symptoms:

A

-abdominal pain (constipation vomiting), psychological disorders (confusion, anxiety, depression, schizophrenia)

Excess of early precursors – ALA and PBG

49
Q

Types of Neurologic Porphyrias:

A

AIP: Acute Intermittant Porphyria (hepatic #2)

VP: Variegate Porphyria

HCP: Hereditary Coproporphyria

50
Q

Drugs and Chemicals Causing Porphyrias:

A 
Drugs				Chemicals	
Sedatives			       Alcohol
Anticonvulsants			Lead
Steroid Hormones		Insecticides
Sulfonamides
51
Q

Samples for porphyria testing

A

Random Urine (fresh morning collection)
24 Hour Urine (sodium bicarbonate preservative)
1 gram Feces

(store frozen & protected from light)

52
Q

Screening Method for Porphyria

A

Watson-Schwartz Test

53
Q

Sample for Watson-Schwartz test

A

First Morning Spot Urine

54
Q

Reagent for Watson-Schwartz

A

Erhlich’s Reagent

55
Q

Interference for Watson-Scwartz

A

urobilinogen, indole

56
Q

Confirmation for Watson-Scwartz

A

Extract with chloroform or butanal

Hoesch Test

No Interference

57
Q

Quantitative Test for Porphyrias

A

PBG isolated using ion-exchange column (removes urobilinogen)
Eluted, condensed, Erlich’s reagent added
Measured via spectrophotometry
Sample: 24 hour Urine

58
Q

mechanisms by which lead poisoning inter¬feres in heme synthesis

A

lead inhibits enzymes in the porphyrin pathway resulting in increases of substrates, which are subsequently eliminated and can be measured in urine. Cannot complete pathway to synthesize heme.

  1. Delta-ALA-Dehydrase
  2. Coproporphyrinogen Oxide
  3. Ferrochelatase
59
Q

Order of bands for Electrophorisis of hemoglobin on Cellulose citrate.

A

A F S C

60
Q

Cellulose Acetate

A

Alkaline pH, Moves way from application point to anode

61
Q

Citrate Gel

A

Acid ph, Moves in both directions away from application to anode and cathode (more separation of bands)

62
Q

Define Hemoglobinopathy

A

Defect in structure of hemoglobin

63
Q

Symptoms of Hemoglobinopathy

A 
Asymptomatic Initially	
nfections
Aseptic necrosis of bone
Retinopathy (clots in eye)
Renal Concentrating Defects
Cerebral Thombosis
Delayed Growth and Sexual maturation
64
Q

Define Thalassemia.

A

Normal structure of hemoglobin but a defect in quantity of hemoglobin

Decreased synthesis of globin gains alpha or beta

Lab Results: ↓ ferretin (Fe2), %SAT,
↑ transferrin, TIBC

65
Q

Differentiate myoglobin from hemoglobin

A

Hemogobin:
Heme protein carried on RBCs
Structure: 3% heme and 97% globulin gains (alpha, beta, gamma, delta)
4 hemes + 4 globulins
Function: transport oxygen to tissues and CO2 back to lungs
Buffering system

Myoglobin:
Heme protein in skeletal and cardiac muslces
Structure: 1 heme + 1 globin (1/4th the size of Hgb)
Function: transport oxygen to muscle cells

66
Q

conditions in which you would see increased myoglobin.

A 
Heart Attack (MI)	releases myoglobin
Skeletal Muscle Injury	releases myoglobin

(cannot differentiate between skeletal and cardiac myoglobin)

Clinical Chemistry (5 decks)

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