Fluid & Electrolyte-Nutrition Chart
Nutrient
Calcium
ECF-Mac
N:8.2-10.6mg/dl
C^: 10.6+, 12
C-: <8.2 mg/dl, 7
Phosphorus
ICF-Mac
N:2.5-4.5 mg/dl
C^: 4.5+
C<: <2.5
Sources
Functions
Absorbed from
foods
(intestines &
Vit.D)
-Dairy, dried
beans, leafy
greens, small
bony fish, &
dried peas.
-COAG & A.P
-Muscle contraction +
relaxation (NMJ+SF)
-Structural component
to bones
-IC function
Absorbed GI
Animal , based
products (meat,
eggs, dairy, poultry,
fish) bread, nuts
Acid/Base Balance. H+ Buffer
^Alkalinity
-Vital to several of the body’s
physiological processes. It helps
with bone growth, energy
storage, and nerve and muscle
production.
-Nucleic acid and Phospholipid
synthesis
Leafy greens,
nuts,
seafood,
whole grains,
mackerel, and
cocoa.
N:1.6-2.6 mg/dL
C^:2.6+, 6.1+
C<: <1.6, <1.2
Sodium
ECF
S & Sx of Excess
Losses
Regulation
Feces and urine
(kidney filtration)
Hypophosphatemia: can
cause breathing difficulties,
loss of appetite, confusion,
altered mental status,
muscle weakness and
rhabdomyolysis.
Alcoholism, <VitD,
Malnutrition,
hyperparathyroidism,
severe burns.
Hyperphosphatemia:
Tetany, anorexia, nausea,
Tachycardia,
phosphorus+calcium
deposits in arteries. DKA.
Hypocalcemia,
hypoparathyroidism
-Decreases concurrently as
Ca++, Mg, Al are ingested.
-Kidney Elimination
-2nd most abundant IC cation.
-Carb/Protein metabolism.
-NMJ/AP/Muscle relaxation.
-Vasodilator C
-Nucleic Acid Synthesis
-Needed for ADP ATP
conversion
HypomagnesemiaMuscle weakness,
tremors, tetany,
seizures, heart block,
mental status
change, DTR’s,
respiratory paralysis.
Hypermagnesemia
- Nausea, vomiting,
flushing, lethargy,
loss of DTR, resp
depress, coma, CA
-Urine & use of loop
diuretics
-Vomit and diarrhea
-Impaired absorption
-Renal failure/disease
-pancreatitis
-chronic alcoholism.
-Hyperaldosteronism
-Kidney elimination,
filtration, secretion,
and reabsorption.
-GI passively absorbs
-Bone serves as
reservoirPTH/Calcitonin ^/<
levels.
Mg, K, Ca,
Phosphate (PO4VitD) all go high or
low together.
Salt, Na
preservatives,
cured meats
1st abundant cation in ECF
-Maintains osmotic pressure
of ECF
- Regulates renal
retention/excretion of water.
-Stimulates NMJ and
maintains Sys BP
-A/B balance NaHCO3
Hyponatremia: < of
Na+: Confusion,
<BP, edema,
cramps/weakness,
dry skin.
Hypernatremia: <
of fluids: CNS
impairment 
restless,
delusional.
Hallucinating,
weakness
N-V-D (GI)
Sweat
Urination
-Na+/K pump ICF
to ECF
-RAAS
Excretion/Absorption
 Kidneys
-Na/H20 Intake
-Aldosterone
-ADH/Vasopressin
Assess I/OOverload/weight
Sources
Functions
S & Sx of
N:135-145 mEq/L
C^: >145; 160+
C<: <135; <120
Hypocalcemia
Numbness in
digits(F/T), mouth,
feet, tetanus,
cramps, seizures.
Primary- Absorbed
by mesenteric
capillaries leading
into systemic circuit.
-PTH-^Ca++
-Calcitonin- (-) Ca++
Lab Info
Hypercalcemia Can
be caused by cancer or
hyperparathyroidism.
Poor excretion (Kidney
X) -Nausea, vomiting,
constipation, CA,
confusion, ^urination,
slurred speech, bone
pain
pH
Magnesium
ICF-Mac
S & Sx of
Deficiency
-^Phosphate = (-)
Ca++
-(-)Phosphate = ^Ca+
+
-Mg controls
absorption
PTH
-Kidneys- Acid/Base
regulation
-Mg  controls
absorption
-^Phosphate = (-) Ca++
-(-)Phosphate = ^Ca++
Meds affecting the testantacids, ^VitD, IV glucose.
Meds that contain sodium
phosphate.
Vol.
Nutrient
S & Sx of Excess
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Losses
Regulation
Lab Info
Deficiency
Potassium
ICF-Mac
N: 3.5-5 mEq/L
C^: >5
C<: <2.5
Chloride
ECF-Mac
N:97-107 mEq/L
C^:>115
C<: <80
Vol.
Bicarbonate
ECF/ICF-Mac
N: 23 to 30 mEq/L
C^: 40+
C<: <10
-Avocado
-Banana
-Beans,
Potatoes
- Spinach
-Citrus Juice
-Fish
ICF osmolarity
-Enzyme regulator
-AP transmission
- A/B w/ H+
exchange.
-BPM regulator
-Protein/Carb
Synthesizer
component.
HypokalemiaN/V/D
-Loss of KCl
- alkalosis
-insufficient dietary
intake
-heart
failure/dysrhythmia
HyperkalemiaMetabolic acidosis,
-renal failure
-dehydration
-Tissue DamageBurns k+ exits
ICF
-CA
-Muscular Paralysis
-Kidneys
-N-v-d
-loss of KCl
-use of diuretics
(excluding K+
sparing)
-Aldosterone
-
-Aldosterone:
Na/H2O
retention K+
loss in urine
-K+^ = Cl-^
Transcellular
shifting between
cells.
-Coumadin/Warfarin:
Absorption of
NaCl intake.
-1st abundant anion in ECF
Hypochloremia^excitability in
muscles, tetany,
hyperactive DTR,
weakness and
cramps.
HyperchloremiaHTN, <CO,
Dysrhythmias,
comatose,
tachypnea,
lethargy, <cognitive
ability.
-Head injuries
Excreted/conserved
by kidneys
-Fecal
-Urine
-Sweat
-Aldosterone
-Loop Diuretics
Reabsorption
from the kidney
tubules.
Increase/decrease
proportionally with
Na+
-Not as essential to
measure in
comparison to K+
and Na+
-Reciprocal
relationship with
HCO3.
metabolic acidosis
<pH
- A wide range of
conditions, including
diarrhea, kidney
disease, and liver
failure, can cause
metabolic acidosis.
metabolic alkalosis: ^pH
Metabolic alkalosis can
happen from a loss of acid
from your body, such as
through vomiting and
dehydration. It may also be
related to conditions
including anorexia and
chronic obstructive
pulmonary disease.
-Kidney excretion.
Bicarbonate is
excreted and
reabsorbed by your
kidneys. This
regulates your body's
pH, or acid balance.
Bicarbonate also works
with sodium,
potassium, and
chloride, also called
electrolytes. These are
usually measured at the
same time as
bicarbonate.
Regulation
Lab Info
-seaweed,
rye,
tomatoes,
lettuce,
celery, and
olives.
-Metabolic
by product
-Over
ingestion of
acid
neutralizers.
-pH balance competes with
HCO3 for Na+
-W/ Na+; regulates water
balance & osmotic pressure.
-Gastric acid (HCl), pancreatic
juice, bile, saliva.
-Component of interstitial
fluid & Lymph.
pH balance
-Buffers lactic
acid (muscles)
-GI Buffer
<Gastric acid
-
Excretion from
peritubular
capillaries.
assess <K+
-NO IV PUSH Can
trigger cardiac
arrest/dysrhythmia
s
pH
Nutrient
Sources
Functions
S & Sx of
Deficiency
S & Sx of Excess
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Losses
Ingested;
dark leafy
greens, meat,
liver, seafood,
beans, nuts,
seeds,
concord
grapes, fruit
-Erythropoiesis
Iodine
Interstitial FluidMic
Thyroxine Levels
N:4.6-12 mcg/dL
C^:20+ mcg/dL
C<: <2 mcg/dL
Seaweed,
dairy, tuna,
shrimp and
eggs. +
Iodized table
salt.
Adsorbed in
the
duodenum
(partially).
Partially
absorbed
through skin
and lungs.
Essential component of
the thyroid hormones
thyroxine (T4) and
triiodothyronine (T3).
They are also required
for proper skeletal and
central nervous system
development in fetuses
and infants.
Nutrient
Sources
Iron
Mic
Varies*
Transferrin
N: 10-32 micromol/L
C^: 62.6+
C<: <10
-Hemoglobin
Synthesis
-O2 Affinity
-Catalyst in reactions.
-
Functions
- Excessive Blood
loss
-Dietary Deficiency
-Malabsorption
-Nephrosis <
erythropoietin
secreted.
-Pregnancy
-NSAIDs and
Antidiabetics +
others.
Iron in the body is
hoarded and recycled
by the
reticuloendothelial
system, which breaks
down aged red blood
cells.
Transferrin
saturation may
indicate iron
deficient
anemia.
Burning of the
mouth, throat, and
stomach, fever,
nausea, vomiting,
diarrhea, a weak
pulse, cyanosis, and
coma. Inflammation
of the thyroid gland.
May induce thyroid
cancer. Caused by
hyperthyroidism
(SLE, Cancer, thyroid
nodules) or Graves
Disease
(Autoimmune vs TSH
receptors)
Iodine enters the
circulation as
plasma inorganic
iodide, which is
cleared from
circulation by the
thyroid and kidney
80% stored as
-Assess Thyroxine
values to evaluate
and confirm
hypo/hyperthyroid
ism.
S & Sx of Excess
Losses
Fe-Deficient Anemia
dizziness, fatigue, or
lightheadedness,
fast heart rate or
palpitations, brittle
nails, pallor, or
shortness of breath
Iron Toxicity
Symptoms include
enlargement of the
thyroid gland
causing a bulge in
the neck (goiter)hypothyroidism.
Fatigue,
constipation, and
sensitivity to cold
temperatures may
also occur. Mental
status changes.
(Acute Delirium,
faint). Malaise.
S & Sx of
Deficiency
-Excessive intake
-Lead Toxicity
Displaces and releases
Fe
-Nephritis
-VitB6 <
-skin color changes
(ashen-bronze), fatigue,
pain, heart irregular
rhythm, CA/Heart
failure.
-^ Liver enzymes in
relation to liver failure
-There is no physiologic
regulatory mechanism
for excreting iron.
Deficiencies in uptake
 Fe overload
(Hemochromatosis)
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iodothyroglobulin
in the follicular
cells of the
thyroid gland.
(Colloid).
-Lab maybe
directed
specifically for
iodide levels, TSH,
or Thyroxine
(T3/T4). Iodide can
be tested via
blood, urine,
iodine patch.
Regulation
Lab Info
Folic Acid
Mic
N: 2.7-17 ng/ml
High: Not harmful
leads to B12 <
Deficient:<2.7* ng//ml
Vitamin C
(Ascorbic
Acid)
Mic
Vitamins and
fortified foods,
such as breads,
pastas and
cereals. Folate
is found
naturally in
foods such as
leafy green
vegetables,
oranges, and
beans.
Absorbed in
Duodenum and
jejunum
Necessary for RBC
production/function
, WBC function,
DNA replication, cell
division.
-helps the body
produce and
maintain new cells,
and also helps
prevent changes to
DNA that may lead
to cancer.
Persistent fatigue.
Weakness.
Lethargy.
Pale skin.
Shortness of breath.
Irritability.
Numbness/tingling in
hands & feet
Diarrhea
Reduced sense of
taste.
Maybe also be
related to B12 ^.
-Excessive intake
Citrus fruits,
broccoli,
green pepper,
strawberries,
greens, sweet
potatoes
Collagen formation,
antioxidant,
enhances iron
absorption.
Contributes to
immune system
function. Enhances
iron absorption.
Scurvy,
hemorrhaging.
Skin loses
elasticity and
becomes prone to
breakdown.
(+hypovolemia &
<Protein
intake) S/S:
fatigue,
depression, and
connective tissue
defects (eg,
gingivitis,
petechiae, rash,
internal bleeding,
impaired wound
healing).
Urination
Hot flashes,
headache,
nausea,
diarrhea.
Kidney stones
Accumulation in
the renal
tubules. Assess
iron toxicity
levels.
Sources
Functions
S & Sx of
Deficiency
N:0.6-1.9 mg/dL
High: Not harmful
acute S/S
C<: <0.3 mg/dL
Nutrient
-Pernicious Anemia
Related to <B12 levels due
impaired absorption
resulting in ^folate
circulation.
-B12 deficiency Impaired
absorption= inability to
metabolize folate= ^ folate
circulation.
> 1 mg daily might cause
abdominal cramps,
diarrhea, rash, sleep
disorders, irritability,
confusion, nausea,
stomach upset, behavior
changes, skin reactions,
seizures, gas, and
excitability.
S & Sx of Excess
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Sweat and
urination
Losses
-Produced by
bacteria in normal
flora.
-Stored in small
amounts in the
liver.
-Levels will always
drop when a
patient is
administered
antibiotics.
Absorbed from
the lumen of the
intestine and
renal tubules by,
respectively,
enterocytes and
renal epithelial
cells.
-Can be
converted from
glucose.
-Usually lost in
patients with
deficient fluid
volume.
Regulation
Lab Info
Thiamine (B1)
Mic
N: 2.5-7.5 μg/dL
C^:>12 mcg/dL
C<: <2.5 mcg/dL
Riboflavin (B2)
Mic
N: 4-24 mcg/dL
C^: Toxicity is rare
C<:1.2-1.4
mcg/dL
Nutrient
Whole grains,
meat, pork,
and fish.
Breads,
cereals, pasta,
and infant
formulas in
the United
States and
many other
countries are
fortified with
thiamin.
Coenzyme in key
reactions that
produce energy
from glucose.
Milk, organ
meats,
enriched
grains,
greens
Carbohydrate,
protein, and fat
metabolism.
Sources
Also plays a role in
muscle contraction
and conduction of
nerve signals.
Thiamin is essential
for the metabolism
of pyruvate
Helps convert
carbohydrates into
adenosine
triphosphate
(ATP).
Functions
Beriberi (weight
loss, emotional
disturbances,
impaired sensory
perception,
weakness and pain
in the limbs, and
periods of irregular
heart rate. Edema.
May ^ lactic acid
and pyruvic acid in
the blood.
May cause highoutput cardiac
failure and death.) ,
mental confusion,
fatigue.
None known.
Dermatitis, glossitis,
photophobia
None known.
-Ariboflavinosis =
riboflavin deficiency.
Rarely found in
isolation; occurs in
combination with
deficiencies of other
water-soluble vitamins.
Symptoms sore
throat, cheilosis/angular
stomatitis, magenta
tongue, and seborrheic
dermatitis.
S & Sx of
Deficiency
Urine
Can only be
stored for a short
time.
When thiamine is
given parenterally
 allergic
reactions, nausea,
lethargy, and
impaired
coordination.
Adults can store
approximately 30
mg of thiamine:
primarily in muscle
tissue, liver, and
kidneys.
Absorbed in the
jejunum and ileum
through an active
process at low
concentrations and
by passive diffusion
at high
concentrations.
Excess maybe
carcinogenic
(research in
progress)
S & Sx of Excess
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Continuously
excreted in the
urine of healthy
individuals, making
deficiency relatively
common when
dietary intake is
insufficient.
The endocrine
glands play an
important role in
the control of
various aspects
of riboflavin
metabolism. The
conversion of the
vitamin into its
active coenzyme
derivatives, FMN
and FAD, is
subject to
hormonal
regulation.
Losses
Regulation
-Assess for patients
who drink alcohol
heavily. (alcohol
reduces G.I
absorption)
-Assess in HIV/AIDS
patients
^deficiency
-Diabetics
Increased urinary
output = deficient
-Bariatric Surg
severe thiamin
deficiency due to
malabsorption
leads to
neurological
impairments.
Reference interval
reflects
flavinadeninedinucleotide
(FAD), that accounts for
approximately 90% of
the total riboflavin in
whole blood.
Assess labs in
patients with
hyperthyroidism 
B2 deficient
-history of chronic
alcohol use 
Deficient
-HIV/AIDS Triple
antibiotics for
secondary infections
cause deficiency.
Lab Info
Niacin (B3)
Mic
N:0.50-8.5 mcg/dL
C^: >10 mcg/dL
C<:<0.50 mcg/dL
Nutrient
Kidney,
grains, lean
meat, nuts
Red fish
(e.g., tuna,
salmon),
cereals,
legumes,
and seeds.
Sources
Carbohydrate,
protein, and fat
metabolism
Plays a role in
keeping the
nervous system
working properly.
Niacin also helps
the body make
sex- and stressrelated hormones
and improves
circulation and
cholesterol levels.
Functions
Pellagra,
dermatitis
Mild slow
metabolism,
causing decreased
tolerance to cold.
Flushing and
itching, nausea,
vomiting, liver
damage
Excess niacin is
methylated in the
liver to N1-methylnicotinamide,
which is excreted in
the urine.
Severe
Pellagra
diarrhea,
dermatitis, and
dementia, as well
as Casal's necklace
lesions on the
lower neck,
hyperpigmentation,
thickening of the
skin, inflammation
of the mouth and
tongue, digestive
disturbances,
amnesia, delirium,
and eventually
death, if left
untreated.
S & Sx of
Deficiency
S & Sx of Excess
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Losses
Niacin is
absorbed as
nicotinic acid, it
is transported
through the
intestines.
Nicotinic acid is
absorbed
through the
intestinal lining
and it is
described as
rapid.
Regulation
Assess levels in
chronic alcohol
users.
Assess levels with
isoniazid (TB
treatment)
Lab Info
B6
(Pyridoxine)
Yeast,
banana,
cantaloupe,
broccoli,
spinach.
Coenzyme in
protein, fat,
carbohydrate
metabolism.
Factor in RBC,
antibody, and
nucleic acid
production
N: 5-30 ng/mL
C^:
C<:
Electrolyte
balance
Enzyme activator
Vitamin A
Mic
Liver,
carrots, egg
yolk,
fortified milk
N: 30-120 mcg/dL
C^: 130+
C<: <25
Nutrient
Sources
Microcytic anemia,
CNS problems.
Usually caused by
pyridoxineinactivating drugs
(eg, isoniazid),
protein-energy
undernutrition,
malabsorption,
alcoholism, or
excessive loss.
S/S peripheral
neuropathy,
seborrheic
dermatitis,
glossitis, and
cheilosis, and, in
adults, depression,
confusion, and
seizures.
Difficulty walking,
numbness of feet
and hands.
Urinary excretion
The human
body absorbs
vitamin B6 in
the jejunum
Causes a sensory
neuronopathy
characterized by
poor
coordination,
numbness, and
decreased
sensation to
touch,
temperature, and
vibration.
Visual acuity in
dim light,
formation and
maintenance of
skin and mucous
membranes;
immune function,
supporting cell
growth, immune
function, fetal
development.
Night blindness,
rough skin, bone
growth ceases.
-Infertility and
Trouble
Conceiving.
-Delayed Growth.
-Throat and Chest
Infections.
-Poor Wound
Healing.
Acne and
Breakouts.
Hypervitaminosis
AAnorexia, loss
of hair, dry skin,
bone pain,
vomiting, birth
defects during
pregnancy, Liver
damage/failure,
Jaundice, Itchiness
Functions
S & Sx of
Deficiency
S & Sx of Excess
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Assess levels if
patient is taking
drug that induces
excessive loss.
-ES Renal
disease/renal
transplant
patientsoften
have low levels
-RA
Inflammatory
cytokines
accelerate B6
catabolism =
deficiency.
Feces and Urine
Absorbed in the
intestines and
liver.
Stored in the
hepatic stellate
cells (HSC) as
retinyl esters.
Losses
Regulation
Assess levels in
hypovolemia,
pregnant women,
breastfeeding
mothers, chronic
diarrhea/fluid loss.
Lab Info
Vitamin D
(Cholecalciferol,
ergosterol)
Mic
Sunlight,
fortified
milk, fish
liver oils,
cheese, egg
yolk
Retarded bone
growth, bone
malformation
-Rickets and
osteomalacia
Excessive
calcification of
bones, renal
calculi, nausea,
headache
Vitamin E (alpha- Vegetable
oils, wheat
tocopherol)
germ,
whole grain
products
Antioxidant,
protects vitamin
A, and heme
synthesis.
NSAIDs,
corticosteroids
cause storage
sites to release
contents.
Increased RBC
hemolysis and
macrocytic
anemia in
premature
infants
Relatively
nontoxic,
although large
doses can cause
fatigue,
diarrhea, and
enhance action
of anticoagulant
medications
The major route of
excretion is through
bile that is then
excreted in feces.
The second route is
in the urine after
vitamin E is chainshortened in a
process similar to
beta-oxidation to
make them more
water-soluble.
Sources
Functions
2 Active forms:
-25-Hydroxy
-1,25-diydroxy
(D1)
Inactive:
-Cholecalciferol
(D3)
-ergocalciferol
(D2).
-Assess elderly
Impaired skin
=Poor D3
formation.
-Assess obese
patients Poor
D3 circulation
The liver is the
master
regulator of the
body's vitamin
E levels in that
it not only
controls alphatocopherol
concentrations,
but also
appears to be
the major site
of vitamin E
metabolism
and excretion.
-Assess critical
Rarely found in
urine due to renal
reuptake via
peritubular
capillaries.
N: 5-18mg/L
C^: 25+
C<: <4
Nutrient
PTH and
Calcitonin
feedback loop
Vitamin D
metabolism
excreted into bile
 to feces.
-Neuromuscular
function
-Immune
modulator
-Antiinflammatory
mediator
N:30-100 ng/mL
C^: 150+
C<: <20 ng/mL
Mic
Calcium and
phosphorus
metabolism,
stimulates calcium
absorption (PTH
and calcitonin).
S & Sx of
Deficiency
S & Sx of Excess
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Losses
Regulation
high in:
Obstructive liver
disease; toxicity
-Assess lows:
Abetalipoproteinemia(<
fat metabolism
disorder= low fat
absorption)
-Hemolytic anemia
Lab Info
Vitamin K
(Phylloquinone,
phytonadione)
Mic
N: 0.13- 1.19 ng/mL
C^: 2+
C<: <0.1
Volume
Dark, green
leafy
vegetables;
only
vitamin
synthesized
in intestines
from gut
bacteria
Muscle
Synthesis of
certain proteins
necessary for
blood clotting
-Aids in calcium
absorption
(calcium binding
proteins)
-Role in Electron
Transport Chain
Maintenance
Hemorrhagic
disease of
newborn,
delayed blood
clotting
Hemolytic
anemia and liver
damage with
synthetic
vitamin K
-Bruises easily.
-small blood
clots underneath
their nails.
-Bleeding in
mucous
membranes that
line areas inside
the body.
-Produces stool
that looks dark
black (almost
like tar) and
contains some
blood.
-Vomiting
-Hyperbilirubinemia
-Albuminuria
-
CNS/PNS
Vol.
pH
Skeletal
Acid Base Balance
Thyroid
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Coagulation
Vitamin K is rapidly
metabolized and
excreted. Based on
phylloquinone
measurements, the
body retains only
about 30% to 40%
of an oral
physiological dose,
while about 20% is
excreted in the
urine and 40% to
50% in the feces via
bile
Antioxidant
Absorbed
through the
jejunum and
ileum in the
small intestine,
and like other
lipid-soluble
vitamins (A, D,
and E), vitamin
K is stored in
the fatty tissue
and liver.
Fat Soluble
-Assess values-
Anticoagulation
meds
-Kidney Disease
-Liver Disease
-Malabsorption
disorders
-Antibiotic
treatement
(<flora that
synthesize VitK)
-Hypoprothrombinemia
(low prothrombin =
maybe associated with
low VitK levels)
Function