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206 Cards in this Set
- Front
- Back
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Where is most iron in the body? |
hemoglobin |
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Where can iron be functioning in the body other than hemoglobin? |
myoglobin in muscles |
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When can iron be released in the body? |
myoglobin, hemoglobin breakdown |
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Where is most iron storage in the body? |
ferritin or hemosiderin |
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Where is ferritin and hemosiderin found and what do disease states do? |
bone marrow, liver, spleen: disease states can cause them to release iron |
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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 |
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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 |
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How does the body control iron intake? |
GI absorption |
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What can GI diseases do? |
cause iron deficiency or overload |
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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 |
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What happens if ferric iron binds to hemoglobin? |
methemoglobin is formed |
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Where is transferrin synthesized and what region is it in? |
liver, beta |
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What is transferrin first secreted as? |
apotransferrin |
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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 |
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What does ferritin do? |
major iron storage, can hold 4000 iron atoms, present in almost all cells |
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What is ferritin made of? |
multi-unit apoferritin shell |
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Ferritin levels can accurately measure |
iron storage
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Normal ferritin levels |
20-250 mg/L male 10-120 mg/L female |
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Iron levels in IDA |
LOW ferritin LOW serum iron LOW transferrin saturation rates |
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What can cause an iron overload? |
hemolytic events, blood transfusions, muscle deterioration |
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Iron levels in iron overload |
HIGH ferritin INCREASED iron serum INCREAD transferrin saturation |
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What decreased first in IDA? |
ferritin |
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Iron levels in liver disease |
INCREASED ferritin |
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What is hemosiderin made of? |
complex derived form ferritin surface protein |
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How is hemosiderin different from ferritin? |
higher iron:protein ratio, releases iron more slowly |
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How is hemosiderin stained? |
prussian blue |
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Body distribution of iron |
70% functional 30% storage .1% transport |
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How much iron is present in humans? |
4g in males, 2g in females |
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What can determine amount of iron in the body? |
pregnancy, growing |
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How much iron is lost per dau? |
1 mg, 2-3 mg for menstruating women |
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How much iron is in the diet and how much do you absorb? |
10-30 mg per day, 5-10% |
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What can increase and decrease iron absorbtion? |
increase: vitamin C, alcohol decrease:dairy, coffee, tea |
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Why should calcium and iron not be taken together? |
they are antagonistic |
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#1 cause of anemia |
iron deficiency anemia |
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How many people have IDA and why? |
15% of the world, malnutrition |
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Why does lead poisoning cause IDA? |
competes for binding site in hemoglobin with iron |
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What can cause IDA? |
lead poisoning, chrons disease, celiacs, gastric bypass surgery |
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What do RBCs look like in IDA and how are indices infected? |
microcytic, hypochromic, MCV MCHC MCH ecreased |
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TIBC levels in IDA |
increased, more capacity to bind iron |
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What can kids with IDA have? |
growth impairment, impaired intellectual development |
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SYmptoms of IDA |
GI abnormalities, tongue swelling, fatigue, pallor, no pink in eyelids, blue nails |
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WHy is iron overload bad? |
iron is toxic |
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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 |
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WHat descent is hemochromocytosis more common in? |
european, caucasian |
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WHen is hemochromocytosis diagnosed? |
30s/40s |
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Are men or women more common to have hemochromocytosis? |
men are 6x more likely to display symptoms, women may not see until menopause |
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What can hemochromacytosis lead to? |
orangey skin, liver cirrhosis, pancreatitis, arthitic symptoms |
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Iron levels in hemochromocytosis |
INCREASED ferritin DECREASED tibc INCREASED iron saturation |
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How is hemochromocytosis diagnosed? |
symptoms and iron tests |
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How is hemochromocytosis treated? |
eat less iron, therapeutic phlebotomy |
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Hemodiserosis |
iron overload from repeated blood transfusions |
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Why do sickle cell patients need more blood transfusions? |
sickle cells dont live as long and lack of O2 carrying can make them hypoxic |
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How much is a sickle cell patients life span shortened? |
20-30 years |
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What can happen with multiple blood transfusions? |
increased ferritin and hemosiderin, deposit in epithelial cells as granules |
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What can you give to help an iron overload? |
mild chelator, but they may chelate calcium |
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Why is serum used to measure iron? |
anticoagulants can bind iron |
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WHy must you test for iron around the same time each time? |
diurnal variation |
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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 |
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normal serum iron |
60-170 mg/dL |
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WHat is an indirect way to measure transferrin? |
TIBC |
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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 |
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NOrmal TIBC levels |
250-425 mg/dL |
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When can you not measure TIBC? |
if a patient is pregnant or on oral contraceptives, increased # of binding sites available |
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What may be decreased if TIBC is increased |
serum iron |
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NOrmal transferrin % saturation |
20-50% (around 30%) |
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Calculation for % transferrin saturation |
serum iron/TIBC x 100 |
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How is transferrin measured? |
immunoassay techniques |
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What is the most common immunoassay method for transferrrin? |
nephelometry: looks for scattering of light when Ag-Ab complex is formed |
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What can interfere with iron testing? |
1) hemolyzed sample 2) ammonia: precipitates iron 3) diurnal variation 4) dairy, coffee, tea 5) antibiotics |
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What are porphyrias? |
group of diseases that effect heme synthesis |
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WHy is it easy for heme synthesis to be disrupted? |
long pathway with many enzymes |
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What happens if one heme enzyme is missing? |
you will get a buildup of toxic precursors and wont get necessary heme production |
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WHat systems do porphyrias normally effect? |
skin and nervous system |
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Why are some porphyrias life threatening and some asymptomatic? |
unknown, some don't get diagnosed until 40s while some are as children |
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WHat triggers may turn on genes for a porphyria? |
stress, toxic substances, medications |
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3 clinically significant porphyrin compounds |
1) uroporphyrin 2) corpoporphyrin 3) protoporphyrin |
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Significant heme precursors |
1) aminolevulinic acid (ALA) 2) porpobilinogen (PBG) |
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Porphyrin structure |
4 pyrrole rings joined together, different side chains make different porphyrins |
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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 |
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Why can porphyrins chelate metal? |
because of the nitrogen inside, why it chelates iron |
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Where does heme synthesis mainly take place? |
bone marrow and liver |
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How many enzymes are involved in heme synthesis? |
8 |
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WHat is the first signal to make heme? |
ALA synthase is turned on, ALA builds up to make amino levulinic acid |
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Are heme precursors usually increased or decreased in blood? |
decreased because they are being used |
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POrphyrias can be tissue specific or symptoms specifc |
if tissue specific, heme synthesis may only be defective in one area of the body |
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HOw can you get a porphyria? |
autosomal recessive or dominant |
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How are porphyrias usually diagnosed? |
excess porphyrins or precursors excreted |
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Where are uro/proto/corproporphyrins mainly excreted? |
uro: urins proto: feces corpro: both |
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Where are ALA and PBG excreted? |
mostly urine |
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What does excess of early heme precursors lead to? |
neural problems: tachycardia, vomiting, hypertension, stomach ache, psychotic episodes |
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What does excess of later heme intermediates lead to? |
cutaneous symptoms: photosensitivity, hyperpigmented |
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Can porphyrias be neurological and cutaneous? |
yes |
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What symptoms are present with neurological porphyrias? |
abdominal pain, nausea, vomiting, tachycardia, vision loss, inappropriate secretion of anti-diuretic hormone |
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What does inappropriate secretion of anti-diuretic hormone do? |
edema, hypertension, dilutional hypernatremia, psychotic episodes if sodium gets too low |
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NOrmal sodium |
135-145 |
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How can acute porphyria attacks be diagnosed? |
ALA/PBG in urine |
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What can trigger a predisposition of porphyrias? |
barbiturates, sulfa drugs, increased carbohydrates |
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WHat is the most common of neurological porphyrias? |
acute intermittent porphyria, "swedish porphyria" |
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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 |
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HOw is acute intermittent porphyria diagnosed? |
urine will turn red in UV light |
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What is there an excess of in cutaneous porphyrias? |
precursors in skin tissue |
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Main characteristic of people with cutaneous porphyrias? |
photosensitivity: extreme blistering, scarring, can't be in light |
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Why are ALA and PBG not in excess in cutaneous porphyrias? |
the deficiency is later in the chain |
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What causes Porphyria Cutanea Tarda? |
the gene for it and a trigger (alcohol, birth control, Hep C, iron overload) |
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What is the problem in Porphyria Cutanea tarda? |
defect in enzyme uroporphyrinogen decarboxylase |
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What is in excess in Porphyria cutanea tarda? |
uroporphyrins accumulate and are excreted in the urine? |
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Are ALA/PBG in excess in Porphyria Cutanea Tarda? |
no, it is cutaneous |
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When are symptoms seen in Porphyria Cutanea Tarda? |
adulthood |
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Other names for Congenital Erythropoietic Porphyria |
CEP, gunther's disease |
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When is Congenital Erythropoietic Porphyria seen? |
as a baby, strictly genetic (autosomal recessive) |
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Is Congenital Erythropoietic Porphyria serious? |
worse prognosis that other porphyrias |
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What causes Congenital Erythropoietic Porphyria? |
uroporphrinogen cosynthase enzyme |
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Werewolf porphyria |
Congenital Erythropoietic Porphyria
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Erythrodentia |
red teeth (Congenital Erythropoietic Porphyria) |
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Why is urine pink upon excretion in Congenital Erythropoietic Porphyria? |
uroporphyrin and coproporphyrin |
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Why may blood fluoresce in Congenital Erythropoietic Porphyria? |
RBCs have high amount of uroporphyrin and coproporphyrin |
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Why are people with porphyrias also anemic? |
abnormal hemoglobin synthesis may lead to hemolytic anemia |
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Why are people with porphyrias prone to splenomegaly? |
the spleen traps bad RBCs |
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Which porphyria is neurological and cutaneous? |
Variegate Porphyria |
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What is the problem in Variegate Porphyria? |
enzyme deficiency of protoporphyrin oxidase |
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Where is Variegate porphyria prevalent? |
S. africa (traced to netherlands) |
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How do you get Variegate Porphyria? |
autosomal dominant |
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What is elevated in Variegate Porphyria? |
most precursors |
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What are secondary porphyrias? |
not causes by genes but other life changes |
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What is the #1 cause of secondary porphyria? |
lead poisoning |
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What two parts of the chain are effected in lead poisoning? |
ALA dehydrase and lead chelates into Hgb instead of iron |
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What symptoms does lead poisoning lead to? |
mental impairment |
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How long can lead damage the body after removal? |
up to a year |
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What can lead poisoning lead to? |
iron overload --> heart and liver damage |
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What is in excess in lead poisoning? |
many heme precursors |
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How do you diagnose lead poisoning? |
lead blood test |
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What is the Watson Schwartz test? |
differentiating between urobilinogen and porphobilinogen in the urine |
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What is the Erhlich test? |
seeing if urobilinogen or porphobilinogen are in the urine |
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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 |
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What are vitamins needed for? |
growth, bone formation, co-factors, antioxidants |
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Where do vitamins come from? |
diet or bacterial enzymatic reactions |
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WHat vitamin do gut bacteria make? |
vitamin K |
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WHen do vitamin requirements change? |
pregnancy (more for baby), menopause (need vitamin D for calcium absorption), women need more than men |
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How are vitamins classifiied? |
solubility in water |
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Which vitamins are water soluble? |
B complex, niacin, folic acid, vitamin C |
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Which vitamins are fat soluble? |
DAKE |
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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. |
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How are fat soluble vitamins transported? |
bound to albumin |
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What group does vitamin A belong to? |
retinoic acid |
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WHat is vitammin A important for? |
eyesight in dark, cellular division and growth, immune function (t cells)
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3 forms of vitamin A |
1) retinol 2) retinal 3) retinoic acid |
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How do you get vitamin A? |
foods with beta-carotene like carrots |
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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 |
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What can a vitmain A deficiency make you prone to? |
measles |
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WHo is prone to a vitamin A deficiency? |
lipid storage disease, GI dirsorders |
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What can cause toxicity of vitamin A? |
fish oil pills, can cause liver damage |
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What does vitamin D do? |
helps calcium absorption and bone development |
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How do you get vitamin D? |
sunlight and diet |
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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 |
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How does vitamin D helps calcium? |
1) reabsorption 2) make bones release it 3) helps intestines absorb it |
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What hormone does vitamin D work with? |
parathyroid hormone |
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WHat can be caused by a vitamin D deficiency? |
1) ricketts
2) osteoporosis 3) hypoparathyroidism 4) liver disease |
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What can cause a vitamin D excess?
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hyperparathyroidism (usually a tumor)
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What is vitmain K essential for? |
coag proteins
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WHere is vitamin K made functional?
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liver
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What happens to vitamin K with liver disease? |
lower production of active vitamin K |
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What foods have vitamin k? |
leafy veggies, cauliflower, broccoli, pork, soy beans, liver |
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what can cause a vitamin D deficiency? |
poor diet, antibiotics (wipe out intestinal bacteria), no vitamin K in breast milk |
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What medications can be inhibited by vitamin k? |
warfarin, heparin |
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WHat is vitamin E good for? |
hair, skin, nails (keratin), antioxidant, cell membrane integrity, drug metabolism, neuromuscular function, decrease LDL |
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What is alpha tacoophenol? |
biologically active vitamin E that is measured |
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What can vitmain E deficiencies lead to? |
low birth rate babies, faster aging, disruption of cellular repair, hemolytic anemias, increase in platelet aggregation, alzheimers |
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What can an increase in vitamin E do? |
interfere with absorption of vitamins D and K |
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Vitamins in B complex? |
B1(thiamin) B2 (riboflavin) B6 (pyridoxine) B12 (cobalamin) B3 (niacin) |
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Function of vitamin B1 |
cofactor in metabolic processes, especially in carb metabolism |
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Sources of vitamin b1 |
vegetables |
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What can vitamin B1 deficiencies lead to? |
nervous and cardiovascular problems BeriBeri |
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Functions of Vitamin B2 |
1) catalyzing oxidation-reduction processes 2) converts other B vitamins to active forms |
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WHy is it hard to get enough vitamin B2? |
isnt sotred efficiently |
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Sources of vitamin B2 |
dairy, liver, meat, leafy veggies |
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What medications can interfere with absorption of vitamin B2? |
antidepressants, oral contraceptives, antipsychotics |
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3 parts of pyridoxine |
1) pyridoxal 2) pyridoxamine 3) pyridoxine |
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Sources of Vitamin B6 |
animal foods: pyridoxal veggies: pyridoxamine, pyridoxine |
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FUnctions of vitamin B6 |
1) decrease pain and inflammation 2) promotes healing 3) aids in endocrine functions |
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WHen may vitamin B6 decrease? |
pregnancy, oral conntraceptives |
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What are vitamin B6 deficiencies associated with? |
sideroblastic anemia |
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SOurces of vitamin B12 |
animal products |
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Functions of VItamin B12 |
1) important coenzyme for DNA synthesis 2) myelin sheath maintenace |
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WHat may deficiencies in vitamin b12 lead to? |
1) nerve disorders 2) pernicious anemia 3) megaloblastic anemia 4) hypersegmented neutrophils |
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What different things can cause pernicious anemia? |
vitamin B12 deficiency, bad parietal cells, not enough intrinsic factor |
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Vitamin B12 absorption |
parietal cells in the intestine secrete intrinsic factor which binds to vitamin b12 to be absorbed |
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How are people given vitamin B12 with a deficiency? |
shots |
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What is broked down to niacin? |
tryptophan |
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Sources of tryptophan |
turkey, onions |
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Functions of niacin (B3) |
tissue respiration processes, lipid metabolism, glycolysis |
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Other terms for niacin |
nicotinic acid, nicotanimide |
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Pellagria |
deficiency of niacin |
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What can pellagria lead to? |
4D syndrome: diarrhea, dermatitis, dementia, death |
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Why is niacin often prescribed? |
can lower cholesterol by 25% and triglycerides by 45%, increased HDL and lowers LDL |
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WHat can megadoses of niacin cause? |
hepatitis, gout, impaired glucose tolerance, skin flushing *check liver enzymes before prescribing niacin |
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AScorbic acid |
vitamin C |
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Functions of vitamin C |
1) antioxidant 2) boosts immune system 3) metabolism of cholesterol 4) aids in iron metabolism |
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Deficiency of vitamin C |
scurvy: bleeding gums, petechiae |
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Sources of vitamin C |
oranges, tomatoes, lemons, leafy greens, green peppers |
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What can vitamin C megadoses lead to? |
kidney stones |
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What is folate derived from? |
folic acid |
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Functions of folate |
1) cell division and health 2) protein synthesis 3) brain development of fetus |
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Why cant a folate specimen be hemolyzed? |
stored in RBCs |
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#1 vitamin deficiency in the US |
folate |
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SOurces of folate |
oranges and leafy veggies |
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FOlate deficiencies can lead to |
1) neural tube defects 2) down syndrome 3) megaloblastic anemia and hypersegmentation |
