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76 Cards in this Set
- Front
- Back
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When we draw blood for a blood glucose reading is this blood from the ECF or ICF
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ECF
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Osmotic Diuresis
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Fluid LEAVES the cell to balance the "levels"
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Type I or Type II that is genetic
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Type I is not
Type II is genetic |
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Fasting blood sugar (FBS)norms
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70-120
-higher that 126 on two seperate occations is diabetic |
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GTT or Glucose Tolerance Test
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Fasting BS followed by ingestion of a high concentration of glucose, then hourly BS drawn at 1,2,3, and sometimes 4 hours
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Post-prandial blood sugar or "feasting" blood sugar
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BS drawn 2 hours after ingestion of lunch or dinner. Increasingly used to understand individual tolerance to ingestion of food (esp. carbs).
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Symptoms of diabetes
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-FBS > 126 on 2 seperate occasions, or repeat BS if initial reading is >200
-2 Hr GTT > 200 (with 75g loading dose of glucose) -gestational DM is based on results on a 100g oral drop during pregnancy -C-peptide is produced in an amount equal to insulin |
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C-peptide
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A diagnostic tool. Amino acid chain that is converted from proinsulin to insulin. It's produced in = amounts to insulin. It's level provides info about the rate that beta cells secrete insulin
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Glycosylated hemoglobin or better known as Hb A1C or A1C
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Measures degree of glucose control during previous 3 months (life span of hemoglobin molecule)
Normal is 4-6% |
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How does the Pancreas work to aid in digestion
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In the pancreas the beta cells of the Islets of Langerhans are the cells that secrete insulin
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Glucose
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Carbohydrate is formed into sugar or glucose as we take in and then we use it for energy. This is the bodies preferred source of fuel because its easy to metabolize.
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Glycogen
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The storage form of glucose. Stored as glycogen in the liver and muscle and as triglyceride in fat cells Storage is facilitated by insulin and cortisol
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Glucagon
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a hormone secreted by the pancreas that increases blood glucose levels. It is a "counterregulatory" hormone that has actions Opposite action of insulin. Causes the release of glucose from cell storage sites whenever blood glucose levels are low
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Glycogenesis
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The production of glycogen in the body
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Ketogensis
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Conversion of fats to acids
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Insulin
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Transporter...regulator. Produced by beta cells of pancreas. Moves glucose across the cell membrane
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Glycogenolysis
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Conversion of glycogen back into glucose
-"liver glucose" |
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Gluconeogensis
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Changing amino acids and proteins into glucose
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Lipolysis
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Breakdown of fat (when liver glucose is unavailable)
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Preteolysis
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Break down of proteins
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In a normal person...When the body's storage of glycogen decreases what happens?
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Gluconeogenesis...this takes 8-12 hours without food.
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In a diabetic what happens when glycogen changes to glucose
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this happens in large amounts because there is no insulin to regulate it
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Insulin Functions
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-transports glucose across cell membrane
-promotes conversion of glucose to glycogen -regulates conversion of glycogen back into glucose -promotes storage of fats and proteins -inhibits the converting of fats and proteins into glucose |
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The "see-saw" effect of glucagon and insulin
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When one goes up in the blood the other goes down.
The body secretes 40-60 units/day |
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Hormones that increase your blood sugar
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-growth hormone
-epi and norepi (fight/flight) -Thyroxin (thyroid) -Glucocorticoids (cortisol, corticosterone (adrenergic effect)) |
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Type I pathophysiology
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-progressive destruction of beta cells of pancreas from autoimmune (viral)
-beta cells cannot produce insulin -patient requires exogenous insulin (from outside of body) -Rapid onset of symptoms |
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Pathophysiology of Type II
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-pancreas produces some endogenous insulin
-not enough insulin produced or it is poorly utilized by the tissues (insulin resistance-the glucose can't get into the cells) |
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Secondary Diabetes
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occurs from another medical condition...pancretitis, TPN, Cushing's Syndrom, hyperthyroidism, etc.
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Medications that can cause DM can include
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corticosteroids
Dilantin antipsychotic |
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Type II symptoms
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irritability, itching, poor wound healing, chronic infections, visual problems, drowsiness, +labs
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Insuline Resistance Syndrome
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-body issues do not respond to the action of insulin. Receptors are resistant to insulin or insufficient in number
-abnormalities associated with an increased risk of cardiac disease -elevated insulin levels, high triglycerides, decreased HdL, increased LDL, and HTN -obesity, sedentary, polycystic ovary syndrome, genetic, |
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Metabolic abnormalities leading to development of Type II DM
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-insuline resistance
-impaired glucose tolerance (prediabetes) -inappropriate glucose production by liver |
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-HHNS/HHNKS
Hyperglycemic Hyperosmolar NONKETONIC Syndrome |
-found in Type II
-profound hyperglycemia causes OSMOTIC DIURESIS, water shifts from ICF to ECF -The excess water is eliminated by the kidneys -The urine contains glucose and electrolytes |
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Outcomes of HHNS
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Profound dehydration, hypernatremia secondary to hyperosmolarity of blood (blood is thick and more concentrated than normal due to large amount of water excreted by the kidneys following the shift of fluid from ICF to ECF) occur.
-most common in older adults with mild Type II or sometimes no history of DM -leaves the ECF very concentrated, with increased amounts of Na+ |
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Diabetic Ketoacidosis - DKA
"diabetic coma" "diabetic acidosis" |
-Complication of Type I can be in Type II
-circulating supply of insulin is insufficient -glucose cannot be used for cells' energy -body breaks down fat stores as a 2ndary source of fuel -ketones are acidic, the by products of fat metabolism, build up in the blood -acidosis occurs -ketones excrete in the urine -because of lack "good" blood to kidneys they can fail which causes you to retain the Keatones you get metabolic acidosis |
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Cations
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-have a +charge
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Which electrolytes have cations
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Na+
K+ |
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Anions
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-have a - charge
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What is an example of an anion?
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Ketones
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How does the body keep and electrical neutrality in the blood
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excretes a lot of cations, which happen to be elctrolytes (K+ & Na+) along with the anaionic ketones
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What does the excessive urination in DKA lead to in hyperglycemia?
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Loss of K+....sometimes of course it can elevate K+ in DKA because of K+ shifts from inside cells to the blood
-keatones (-), K+, Na+ -acidosis can cause severe depletion of Cl, Mg, & P |
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Signs of DKA
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-poop skin turgor
-dry mucous membranes -tachycardia -orthostatic hypotension -lethargy -weakness -eyeballs sunken -abdominal pain -anorexia and vomiting -Kussmaul's respirations (deep rapid ) -Acetone breath |
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Labs associated with DKA
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-BS>250
-pH <7.35 -HCO3- <5 mEq/l -keatones in blood and urine |
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Treatment of DKA
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-fluid, insulin, check BS
-lower BS slowly so no rebound -treat underlying cause (fever, N/V/D, infection) |
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DKA vs HHNS
-Cause -onset -BS level |
DKA
-cause is omission of insulin/stressor -onset is rapid <24 hrs -BS >250 HHNS -cause is physiologic stress -onset is several days -BS >600mg/dl |
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DKA vs HHNS
-arterial pH -ketones -serum osmolality -plasma bicarb |
DKA
-arterial pH <7.3 -ketones present in serum/urine -serum osmolality 300-350 -plasma bicarb <15mEq/l HHNS -arterial pH WNL -ketones not present -serum osmolality >350 -plasma bicarb normal |
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DKA vs HHNS
BUN and Cr mortality rate |
DKA
-BUN/Cr elevated -mortality rate <5% HHNS BUN/Cr is elevated mortality rate is 10-40% |
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Hypoglycemia
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BS < 70mg/dl
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Treatment of hypoglycemia
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10-15 g of simple CHo, such as apple juice, regular soft drink, or 8 oz of low-fat milk
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Follow-up treatment of low BS
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-check BS 15 minutes after giving the glucose
-repeat tx of BS is <70 -Check again in 45 minutes -retreat with 10-15 g of CHo 2-3 times...then go to glucagon |
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Studies show about Type I
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-tight control is needed to manage it.
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Studies show about Type II
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-Exercise, it increases the # of receptor sites
-weight reduction decreases the demand for insulin -increase fiber-slows absorption of glucose |
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Self Glucose Monitoring
Type I Type II |
Type I- 4 x daily until stable then 2xdaily, PRN while ill q 3-4hrs
Type II 4xdaily initially, then 2xdaily, then 2-3 x weekly, more while ill Gestational DM 4-8xdaily -good control crcial, prevents complications |
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Ketone urine test....when do you do this?
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-begin when BS 240-250
-when ill -type I should know how |
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Macrovascular is associated with and what does it lead to and why?
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Type II
leads to -atherosclerosis -CAD -CVA -MI -PVD Because Macrovascular disease |
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Microvascular is associated with and what does it lead to and why?
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Type I
leads to -nephropathy -retinopathy -neuropath -reproductive (males) -infections and periodontal (type 1 & 2) Becuase its Microvascular disease |
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Prevention of Macroangiopathies
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-weight control
-BP control - med lifestyle -tight BS & lipid control -no smoking -annual EKG -regular exercise |
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PVD in Diabetics
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-occur in lower legs
-earlier age -progress rapidly -involves both feet |
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Symptoms/Interventions for PVD
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-good BS control
-avoid heat/cold -GOOD foot care -meds -no smoking -DP PT pulses |
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Microangiopathies of Type I
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-nephropathy-kidneys
-neuropathy-small nerve fibers -retinopathy-eyes |
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Micro =
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-KIDNEYS
-EYES -NERVES |
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MACRO=
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BRAIN
HEART FEET |
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Nephropathy cause
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stressed kiney filtering system
-protein leaks into urin (albuminuria) |
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Tests to perform yearly on kidneys for Type I include
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-urine for microalbuminuria
-BUN -Creatinine |
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Types of neuropathies
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-peripheral
-autonomic -GI system |
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Autonomic neuropathies
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-can be macro or micro
-fixed tachycardia -+orthostatic -painless MI |
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GI tract neuropathy what is it? Treatment?
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-Gastroparesis
-delayed stomach emptying and decreased peristaisis -anorexia, bloating, hearburn, N/V -insulin has trouble getting into bloodstream before the food -treatment w/ Reglan cause it increases motility or low-fat diet |
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Neuropathy in urinary tract what is it? Treatment?
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neurogenic bladder w/ urinary retention
-inner wall of bladder loses ability to sense pressure Treatment - Urecholine, manual pressure "Crede" |
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Treatment of peripheral neuropathy
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-frequent foot checks
-meds-non narcotic, antidepressants, neurontin -nerve blocks - |
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Ocular complications
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-retinopathy-good control in first 5 years of the disease decrease the risk of blindness
-cataracts -glaucoma -lens change -extraocular muscle palsy |
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Per the ADA what is the desired food intake %
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-CHO - 50-60%
-FAT - 20-30% -Proteins - 10-20% |
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Glycemic Index is measured how?
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The index of 100 refers to the response of 50g of glucose in a person without DM
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Alcohol consumption in a diabetic
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-must be calculated into meal plan, 1/day is ok.
-absorbed before other nutrients and does not require insulin for absorption -large amounts can be converted to fats, which increases risk for DKA -inhibitory effect on glucose production by the liver |
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Normal sodium Na+ range
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136-145
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Normal Potassium K+ range
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3.5-5.0
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-Normal Cacium range
-Ca2+ -Chloride Cl- -Magnesium Mg2+ -Phosphorus (P) |
-Ca2+ 9.0-10.5mg/dl
-Cl-98-106 -Mg2+ 1.3-2.1 -P - 3.0-4.5 |
