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206 Cards in this Set

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  • Back

Where is most iron in the body?


Where can iron be functioning in the body other than hemoglobin?

myoglobin in muscles

When can iron be released in the body?

myoglobin, hemoglobin breakdown

Where is most iron storage in the body?

ferritin or hemosiderin

Where is ferritin and hemosiderin found and what do disease states do?

bone marrow, liver, spleen: disease states can cause them to release iron

How does iron get into RBCs?

binds to transferrin, binds to complex receptor on RBC, turn inward, iron stays in and transferrin goes back out

What is done with iron once in the RBC?

depending on the cell needs, it can be used for heme synthesis or converted to ferritin or hemosiderin

How does the body control iron intake?

GI absorption

What can GI diseases do?

cause iron deficiency or overload

How is iron absorbed and what is done to it?

absorbed in ferrous state and oxidized to ferric iron by the gut mucosal cells, must be converted to ferrous to bind to hemoglobin

What happens if ferric iron binds to hemoglobin?

methemoglobin is formed

Where is transferrin synthesized and what region is it in?

liver, beta

What is transferrin first secreted as?


What does transferrin do?

only iron transporting protein, each has 2 binding sites, 20-50% saturated is normal, most humans have 3-4 mg of plasma iron bound to transferrin

What does ferritin do?

major iron storage, can hold 4000 iron atoms, present in almost all cells

What is ferritin made of?

multi-unit apoferritin shell

Ferritin levels can accurately measure

iron storage

Normal ferritin levels

20-250 mg/L male

10-120 mg/L female

Iron levels in IDA

LOW ferritin

LOW serum iron

LOW transferrin saturation rates

What can cause an iron overload?

hemolytic events, blood transfusions, muscle deterioration

Iron levels in iron overload

HIGH ferritin

INCREASED iron serum

INCREAD transferrin saturation

What decreased first in IDA?


Iron levels in liver disease

INCREASED ferritin

What is hemosiderin made of?

complex derived form ferritin surface protein

How is hemosiderin different from ferritin?

higher iron:protein ratio, releases iron more slowly

How is hemosiderin stained?

prussian blue

Body distribution of iron

70% functional

30% storage

.1% transport

How much iron is present in humans?

4g in males, 2g in females

What can determine amount of iron in the body?

pregnancy, growing

How much iron is lost per dau?

1 mg, 2-3 mg for menstruating women

How much iron is in the diet and how much do you absorb?

10-30 mg per day, 5-10%

What can increase and decrease iron absorbtion?

increase: vitamin C, alcohol

decrease:dairy, coffee, tea

Why should calcium and iron not be taken together?

they are antagonistic

#1 cause of anemia

iron deficiency anemia

How many people have IDA and why?

15% of the world, malnutrition

Why does lead poisoning cause IDA?

competes for binding site in hemoglobin with iron

What can cause IDA?

lead poisoning, chrons disease, celiacs, gastric bypass surgery

What do RBCs look like in IDA and how are indices infected?

microcytic, hypochromic, MCV MCHC MCH ecreased

TIBC levels in IDA

increased, more capacity to bind iron

What can kids with IDA have?

growth impairment, impaired intellectual development

SYmptoms of IDA

GI abnormalities, tongue swelling, fatigue, pallor, no pink in eyelids, blue nails

WHy is iron overload bad?

iron is toxic

What is hemochromocytosis?

autosomal recessive genetic disease (but may not have even in homozygous) that increases dietary absorption of iron, up to 4mg extra per day, deposits in liver, spleen, under skin, in ferritin

WHat descent is hemochromocytosis more common in?

european, caucasian

WHen is hemochromocytosis diagnosed?


Are men or women more common to have hemochromocytosis?

men are 6x more likely to display symptoms, women may not see until menopause

What can hemochromacytosis lead to?

orangey skin, liver cirrhosis, pancreatitis, arthitic symptoms

Iron levels in hemochromocytosis

INCREASED ferritin


INCREASED iron saturation

How is hemochromocytosis diagnosed?

symptoms and iron tests

How is hemochromocytosis treated?

eat less iron, therapeutic phlebotomy


iron overload from repeated blood transfusions

Why do sickle cell patients need more blood transfusions?

sickle cells dont live as long and lack of O2 carrying can make them hypoxic

How much is a sickle cell patients life span shortened?

20-30 years

What can happen with multiple blood transfusions?

increased ferritin and hemosiderin, deposit in epithelial cells as granules

What can you give to help an iron overload?

mild chelator, but they may chelate calcium

Why is serum used to measure iron?

anticoagulants can bind iron

WHy must you test for iron around the same time each time?

diurnal variation

How is serum iron measured?

spectrophotometry method based on a colored complex after iron interacts with chromagen

1) dissociate iron bound to transferrin by adding acid reagent

2) convert ferric iron to ferrous iron to take chromagen better

3) add chromagen and measure on internal spec

normal serum iron

60-170 mg/dL

WHat is an indirect way to measure transferrin?


HOw do you measure TIBC?

1) give patient enough iron to fully saturate transferrin

2) remove access iron by giving magnesium carbonate

3) measure acces iron, subtract from total

NOrmal TIBC levels

250-425 mg/dL

When can you not measure TIBC?

if a patient is pregnant or on oral contraceptives, increased # of binding sites available

What may be decreased if TIBC is increased

serum iron

NOrmal transferrin % saturation

20-50% (around 30%)

Calculation for % transferrin saturation

serum iron/TIBC x 100

How is transferrin measured?

immunoassay techniques

What is the most common immunoassay method for transferrrin?

nephelometry: looks for scattering of light when Ag-Ab complex is formed

What can interfere with iron testing?

1) hemolyzed sample

2) ammonia: precipitates iron

3) diurnal variation

4) dairy, coffee, tea

5) antibiotics

What are porphyrias?

group of diseases that effect heme synthesis

WHy is it easy for heme synthesis to be disrupted?

long pathway with many enzymes

What happens if one heme enzyme is missing?

you will get a buildup of toxic precursors and wont get necessary heme production

WHat systems do porphyrias normally effect?

skin and nervous system

Why are some porphyrias life threatening and some asymptomatic?

unknown, some don't get diagnosed until 40s while some are as children

WHat triggers may turn on genes for a porphyria?

stress, toxic substances, medications

3 clinically significant porphyrin compounds

1) uroporphyrin

2) corpoporphyrin

3) protoporphyrin

Significant heme precursors

1) aminolevulinic acid (ALA)

2) porpobilinogen (PBG)

Porphyrin structure

4 pyrrole rings joined together, different side chains make different porphyrins

WHy can porphyrins absorb visible light and why is it significant?

alternating double bonds, when exposed to long wave UV light can give hemoglobin a reddish color, can use teeth or urine in light for diagnosis

Why can porphyrins chelate metal?

because of the nitrogen inside, why it chelates iron

Where does heme synthesis mainly take place?

bone marrow and liver

How many enzymes are involved in heme synthesis?


WHat is the first signal to make heme?

ALA synthase is turned on, ALA builds up to make amino levulinic acid

Are heme precursors usually increased or decreased in blood?

decreased because they are being used

POrphyrias can be tissue specific or symptoms specifc

if tissue specific, heme synthesis may only be defective in one area of the body

HOw can you get a porphyria?

autosomal recessive or dominant

How are porphyrias usually diagnosed?

excess porphyrins or precursors excreted

Where are uro/proto/corproporphyrins mainly excreted?

uro: urins

proto: feces

corpro: both

Where are ALA and PBG excreted?

mostly urine

What does excess of early heme precursors lead to?

neural problems: tachycardia, vomiting, hypertension, stomach ache, psychotic episodes

What does excess of later heme intermediates lead to?

cutaneous symptoms: photosensitivity, hyperpigmented

Can porphyrias be neurological and cutaneous?


What symptoms are present with neurological porphyrias?

abdominal pain, nausea, vomiting, tachycardia, vision loss, inappropriate secretion of anti-diuretic hormone

What does inappropriate secretion of anti-diuretic hormone do?

edema, hypertension, dilutional hypernatremia, psychotic episodes if sodium gets too low

NOrmal sodium


How can acute porphyria attacks be diagnosed?

ALA/PBG in urine

What can trigger a predisposition of porphyrias?

barbiturates, sulfa drugs, increased carbohydrates

WHat is the most common of neurological porphyrias?

acute intermittent porphyria, "swedish porphyria"

WHat is the problem in acute intermittent porphyria?

deficiency in PBG deaminase enzyme, causes a buildup in PBG and ALA that is excreted in the urine

HOw is acute intermittent porphyria diagnosed?

urine will turn red in UV light

What is there an excess of in cutaneous porphyrias?

precursors in skin tissue

Main characteristic of people with cutaneous porphyrias?

photosensitivity: extreme blistering, scarring, can't be in light

Why are ALA and PBG not in excess in cutaneous porphyrias?

the deficiency is later in the chain

What causes Porphyria Cutanea Tarda?

the gene for it and a trigger (alcohol, birth control, Hep C, iron overload)

What is the problem in Porphyria Cutanea tarda?

defect in enzyme uroporphyrinogen decarboxylase

What is in excess in Porphyria cutanea tarda?

uroporphyrins accumulate and are excreted in the urine?

Are ALA/PBG in excess in Porphyria Cutanea Tarda?

no, it is cutaneous

When are symptoms seen in Porphyria Cutanea Tarda?


Other names for Congenital Erythropoietic Porphyria

CEP, gunther's disease

When is Congenital Erythropoietic Porphyria seen?

as a baby, strictly genetic (autosomal recessive)

Is Congenital Erythropoietic Porphyria serious?

worse prognosis that other porphyrias

What causes Congenital Erythropoietic Porphyria?

uroporphrinogen cosynthase enzyme

Werewolf porphyria

Congenital Erythropoietic Porphyria


red teeth (Congenital Erythropoietic Porphyria)

Why is urine pink upon excretion in Congenital Erythropoietic Porphyria?

uroporphyrin and coproporphyrin

Why may blood fluoresce in Congenital Erythropoietic Porphyria?

RBCs have high amount of uroporphyrin and coproporphyrin

Why are people with porphyrias also anemic?

abnormal hemoglobin synthesis may lead to hemolytic anemia

Why are people with porphyrias prone to splenomegaly?

the spleen traps bad RBCs

Which porphyria is neurological and cutaneous?

Variegate Porphyria

What is the problem in Variegate Porphyria?

enzyme deficiency of protoporphyrin oxidase

Where is Variegate porphyria prevalent?

S. africa (traced to netherlands)

How do you get Variegate Porphyria?

autosomal dominant

What is elevated in Variegate Porphyria?

most precursors

What are secondary porphyrias?

not causes by genes but other life changes

What is the #1 cause of secondary porphyria?

lead poisoning

What two parts of the chain are effected in lead poisoning?

ALA dehydrase and lead chelates into Hgb instead of iron

What symptoms does lead poisoning lead to?

mental impairment

How long can lead damage the body after removal?

up to a year

What can lead poisoning lead to?

iron overload --> heart and liver damage

What is in excess in lead poisoning?

many heme precursors

How do you diagnose lead poisoning?

lead blood test

What is the Watson Schwartz test?

differentiating between urobilinogen and porphobilinogen in the urine

What is the Erhlich test?

seeing if urobilinogen or porphobilinogen are in the urine

How is the Watson Schwartz test done?

1) add 10 mL urine and Erhlichs reagent

2) if either Uro/Porpho are present it will turn cherry red (add sodium acetate if faint)

3) split into 2 tubes and add chloroform to one and butanol to one (B rises, C sinks)

4) Porpho is NOT soluble, so if it is present it will be on top of chloroform and below butanol

5) Uro IS soluble in both so if present, it will be in chloroform on bottom and in butanol on top

6) if both present, all will be red

What are vitamins needed for?

growth, bone formation, co-factors, antioxidants

Where do vitamins come from?

diet or bacterial enzymatic reactions

WHat vitamin do gut bacteria make?

vitamin K

WHen do vitamin requirements change?

pregnancy (more for baby), menopause (need vitamin D for calcium absorption), women need more than men

How are vitamins classifiied?

solubility in water

Which vitamins are water soluble?

B complex, niacin, folic acid, vitamin C

Which vitamins are fat soluble?


WHich vitamins can be toxic?

fat soluble: stored in liver and fat tissue so they are released more slowly. Water soluble vitamins will just be released by the kidney and peed out.

How are fat soluble vitamins transported?

bound to albumin

What group does vitamin A belong to?

retinoic acid

WHat is vitammin A important for?

eyesight in dark, cellular division and growth, immune function (t cells)

3 forms of vitamin A

1) retinol

2) retinal

3) retinoic acid

How do you get vitamin A?

foods with beta-carotene like carrots

What happens to vitamin A?

binds to transerythritin (prealbumin) and gets carried to eyes and is converted to a compound that aids in night vision

What can a vitmain A deficiency make you prone to?


WHo is prone to a vitamin A deficiency?

lipid storage disease, GI dirsorders

What can cause toxicity of vitamin A?

fish oil pills, can cause liver damage

What does vitamin D do?

helps calcium absorption and bone development

How do you get vitamin D?

sunlight and diet

Active forms of vitamin D?

1) D3(cholecalciferol): activated by sunlight, may get from diet

2) D4 (ergocalciferol): more from diet

3) D125 dihydroxyvitamin D3: kidneys

How does vitamin D helps calcium?

1) reabsorption

2) make bones release it

3) helps intestines absorb it

What hormone does vitamin D work with?

parathyroid hormone

WHat can be caused by a vitamin D deficiency?

1) ricketts

2) osteoporosis

3) hypoparathyroidism

4) liver disease

What can cause a vitamin D excess?

hyperparathyroidism (usually a tumor)

What is vitmain K essential for?

coag proteins

WHere is vitamin K made functional?


What happens to vitamin K with liver disease?

lower production of active vitamin K

What foods have vitamin k?

leafy veggies, cauliflower, broccoli, pork, soy beans, liver

what can cause a vitamin D deficiency?

poor diet, antibiotics (wipe out intestinal bacteria), no vitamin K in breast milk

What medications can be inhibited by vitamin k?

warfarin, heparin

WHat is vitamin E good for?

hair, skin, nails (keratin), antioxidant, cell membrane integrity, drug metabolism, neuromuscular function, decrease LDL

What is alpha tacoophenol?

biologically active vitamin E that is measured

What can vitmain E deficiencies lead to?

low birth rate babies, faster aging, disruption of cellular repair, hemolytic anemias, increase in platelet aggregation, alzheimers

What can an increase in vitamin E do?

interfere with absorption of vitamins D and K

Vitamins in B complex?


B2 (riboflavin)

B6 (pyridoxine)

B12 (cobalamin)

B3 (niacin)

Function of vitamin B1

cofactor in metabolic processes, especially in carb metabolism

Sources of vitamin b1


What can vitamin B1 deficiencies lead to?

nervous and cardiovascular problems


Functions of Vitamin B2

1) catalyzing oxidation-reduction processes

2) converts other B vitamins to active forms

WHy is it hard to get enough vitamin B2?

isnt sotred efficiently

Sources of vitamin B2

dairy, liver, meat, leafy veggies

What medications can interfere with absorption of vitamin B2?

antidepressants, oral contraceptives, antipsychotics

3 parts of pyridoxine

1) pyridoxal

2) pyridoxamine

3) pyridoxine

Sources of Vitamin B6

animal foods: pyridoxal

veggies: pyridoxamine, pyridoxine

FUnctions of vitamin B6

1) decrease pain and inflammation

2) promotes healing

3) aids in endocrine functions

WHen may vitamin B6 decrease?

pregnancy, oral conntraceptives

What are vitamin B6 deficiencies associated with?

sideroblastic anemia

SOurces of vitamin B12

animal products

Functions of VItamin B12

1) important coenzyme for DNA synthesis

2) myelin sheath maintenace

WHat may deficiencies in vitamin b12 lead to?

1) nerve disorders

2) pernicious anemia

3) megaloblastic anemia

4) hypersegmented neutrophils

What different things can cause pernicious anemia?

vitamin B12 deficiency, bad parietal cells, not enough intrinsic factor

Vitamin B12 absorption

parietal cells in the intestine secrete intrinsic factor which binds to vitamin b12 to be absorbed

How are people given vitamin B12 with a deficiency?


What is broked down to niacin?


Sources of tryptophan

turkey, onions

Functions of niacin (B3)

tissue respiration processes, lipid metabolism, glycolysis

Other terms for niacin

nicotinic acid, nicotanimide


deficiency of niacin

What can pellagria lead to?

4D syndrome: diarrhea, dermatitis, dementia, death

Why is niacin often prescribed?

can lower cholesterol by 25% and triglycerides by 45%, increased HDL and lowers LDL

WHat can megadoses of niacin cause?

hepatitis, gout, impaired glucose tolerance, skin flushing

*check liver enzymes before prescribing niacin

AScorbic acid

vitamin C

Functions of vitamin C

1) antioxidant

2) boosts immune system

3) metabolism of cholesterol

4) aids in iron metabolism

Deficiency of vitamin C

scurvy: bleeding gums, petechiae

Sources of vitamin C

oranges, tomatoes, lemons, leafy greens, green peppers

What can vitamin C megadoses lead to?

kidney stones

What is folate derived from?

folic acid

Functions of folate

1) cell division and health

2) protein synthesis

3) brain development of fetus

Why cant a folate specimen be hemolyzed?

stored in RBCs

#1 vitamin deficiency in the US


SOurces of folate

oranges and leafy veggies

FOlate deficiencies can lead to

1) neural tube defects

2) down syndrome

3) megaloblastic anemia and hypersegmentation