Download Major Electrolytes

Major Electrolytes
Iron
Laboratory tests for investigation of iron
disorder
Serum Iron
Total Iron Binding Capacity (TIBC)
Unsaturated Iron Binding Capacity (UIBC)
Serum ferritin
transferrin
Three stages of Iron deficiency anemia
• Stage I depletion of serum ferritin (↓) with no
functional impairment
• Stage II deficient erythropoiesis, RBC
protoporphyrin ↑, transferrin ↑, UIBC ↑BUT
Hb normal)
• Stage III Iron deficiency anemia (serum iron↓)
→Hb↓→microcytic hypochromic anemia
(only in the late stage, low concentration of
serum iron can be observed)
Hemochromatosis
Calcium
Normal daily calcium balance
Hormonal regulation of plasma
calcium
Serum calcium and albumin
• Cause of hypocalcaemia
• Hypoparathyroidism (magnesium deficiency or
neck surgery)
• Vitamin D deficiency
• Renal failure (fail to synthesize vit D)
• Pseudohypoparathyroidism (lake of receptor)
• Clinical features
• Neurologic (tingling and tetany)
• Cardiovascular (abnormal ECG)
Case study
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Cause of hypercalcaemia
Hyperparathyroidism (adenoma)
Malignancy ( tumors secrete parathyroid hormone related protein(PTHrP)
Vitamin D overload
Familial hypocalciuric hypercalcemia
Thyrotoxicosis (bone resorption)
Immobilization especially Pajet’s disease)
Long-standing → Hyperparathyroidism
Calcium therapy
Antacid poisoning
Clinical features
Neurologic and psychiatric (lethargy, confusion, irritability and depression)
Cardiovascular (arrhythmias)
Renal ( thirst, polyuria, renal calculi)
Gastrointestinal (anorexia, nausea, vomiting and constipation)
Calcium measurement
Phosphate
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Cause of hyperphosphatemia
Impaired renal excretion (commonest cause)
hypoparathyroidism
Hemolysis
Clinical features
Deposition of calcium phosphate in soft tissues
Cause of hypophosphatemia
hyperparathyroidism
Genetic disorder of phosphate reabsorption
Antacid ingestion
Treatment of diabetes ketoacidosis which enter phosphate to the cell
Dietary deficiency
Clinical features
Muscle weakness and respiratory impairment
Phosphate measurement
(colorimetric)
Phosphate
measurement
(enzymatic)
In the presence of Pi, the substrate
2-amino-6-mercapto-7-methylpurine riboside (MESG) is
converted enzymatically by purine nucleoside phosphorylase
(PNP) to ribose 1-phosphate and 2-amino-6-mercapto-7methylpurine
Enzymatic conversion of MESG results in a
spectrophotometric shift in maximum absorbance from 330 nm
for the substrate to 360 nm for the product.
Magnesium
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Cause of hypermagnesaemia
renal failure
Antacid ingestion
Cause of hypomagnesaemia
Malabsorbtion, sever vomiting, diarrhea
Osmotic diuresis such as in diabetes
Diuretic therapy
Cisplatinum that impairs renal reabsorption
Clinical features
Very similar to hypocalcemia including; impaired
neuromuscular function such as tetany, hyperirritability,
tremor, convulsion, muscle weakness
Magnesium measurement
4. Enzymatic: Based on the specific requirement of glycerol kinase for
Mg+2. An enzyme linked reaction leads to formation of an intensely
colored (λmax = 450nm) product whose formation is proportional to
Mg+2 concentration.
Copper
Copper
• Biochemical role (as a cofactor for
metaloenzymes, ceruloplasmin, cytochrome c
oxidase, dopamine β-hydroxylase, superoxide
dismutase and tyrosinase
• Absorption: stomach and intestine
• Transport: to the liver by Alb and then
ceruloplasmin
• Distribution: liver, kidney, muscle and bone
• Excretion: bile and urine
Laboratory tests
• Serum copper (Under acid environment, copper present in
the sample reacts, with the chromogen Di-Br-PAESA forming a
colored blue complex. The intensity of the colored complex is
proportional to the copper concentration in the sample.)
• Ceruloplasmin (ELISA and emzymatic based on
oxidase activity of ceruloplasmin on synthetic
substrate .
• Urinary copper
• Copper deficiency (in infants and intestinal bypass
surgery or parenteral nutrition) signs:
• mental retardation, depigmentation, anemia, hypotonia and
scorbutic changes in bone, Iron-resistant microcytic
hypochromic anemia.
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Copper toxicity
By administration of copper sulfate solutions,
Renal tubular damage
Damage to tissues
Treatment
Penicillamine
Wilson’s disease
in response to rising concentrations of copper in the intestine, an enzyme
called ATP7A releases copper into the portal vein to the liver. In Liver cells
ATP7B links copper to ceruloplasmin and releases it into the
bloodstream, as well as removing excess copper by secreting it into bile.
Both functions of ATP7B are impaired in Wilson's disease. Copper
accumulates in the liver tissue; ceruloplasmin is still secreted, but in a
form that lacks copper (termed apoceruloplasmin) and is rapidly
degraded in the bloodstream. The liver also releases copper into the
bloodstream that is not bound to ceruloplasmin. This free copper
precipitates throughout the body but particularly in the kidneys, eyes and
brain.
Kayser–Fleischer ring
Menkes syndrome
• Low serum copper and seruloplasmin
• Mutations in the ATP7A gene
• The decreased supply of copper can reduce the activity of
numerous copper-containing enzymes that are necessary for
the structure and function of bone, skin, hair, blood vessels,
and the nervous system.
• Signs: kinky hair; failure to gain weight and grow at the
expected rate (failure to thrive); and deterioration of the
nervous system; weak muscle tone (hypotonia), seizures and
intellectual disability.
Zinc
• Zinc is a co-factor in DNA and protein synthesis and
cell division
• In plasma it is bound to albumin (90%) and α2macroglobulin
• Located mainly in muscle and bone
• Excretion: urine, bile, pancreatic fluid and milk in
lactating mothers
• Deficiency a result of low intake or cadmium
poisoning: hair loss, skin rash, wound breakdown and
delayed healing; Anorexia
Sodium
‫‪Hyponatremia‬‬
‫عرق زياد‪ ,‬استفراغ‪ ,‬اسهال‪ ,‬استفاده از ديورتيكها ‪ ،‬كمبود آلدوسترون و •‬
‫ديگر مينرالوكورتيكوئيدها ‪ ،‬پلياوري‪ ،‬اسيدوزمتابوليك(دفع كاتيونها به‬
‫همراه آنيونهاي آلي)‪ ،‬هيپوناترمي ثانويه (ادم‪ ,‬اختالل مزمن قلبي‪ ،‬سندرم‬
‫نفروتيك‪ ،‬سندرم ترشح نامناسب هورمون آنتي ديورتيك‬
‫‪• Pseudohyponatremia‬‬
‫اختالل آناليزي در نمونههاي ليپميك •‬
‫‪• Clinical features‬‬
‫اختالل عصبي ضعف‪ ,‬فلج •‬
‫‪Hypernatremia‬‬
‫تزریق محلول های سالين‬
‫انسولين درمانی‪،‬‬
‫هیپرآلدوسترونیسم‬
‫‪Hypernatriuria‬‬
‫هيپرناتری اورياي فيزيولوژيك در مواقع افزايش جذب و‬
‫پس از دیورز قاعدگي ديده ميشود‪.‬‬
‫‪Hyponatriuria‬‬
‫در نتيجه كاهش دريافت سدیم و يا احتباس آب و سدیم قبل از •‬
‫قاعدگي ايجاد ميگردد‪ ,‬هيپرآلدوسترونيسم وكاهش‪GFR‬‬
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Potassium
‫كاتيون عمده داخل سلولي •‬
‫بازجذب در توبولهای پروکسيمال می گردد و ترشح در •‬
‫ديستال‬
‫‪Hypokalemia‬‬
‫ورود پتاسيم خارج سلولي به داخل سلولي ‪،‬كاهش دريافت •‬
‫افزايش دفع مايعات‪ ،‬انسولين درماني •‬
‫آلكالوز (توقف آنتی پورت پتاسیم‪ -‬پروتون) •‬
‫استفراغ‪ ,‬اسهال •‬
‫اسيدوز توبولهاي كليه •‬
‫آلدوسترونيسم •‬
‫دفع پتاسیم از کلیه←خروج پتاسیم از سلول ← ورود پروتون به •‬
‫سلول ← آلکالوز‬
‫‪Hyperkalemia‬‬
‫افزايش خروج از سلول در حالتهاي دهيدراتاسيون‪ ,‬هيپوكس ي بافتي‪• ,‬‬
‫ً‬
‫هموليز‪ ,‬سوختگيهاي شديد‪ ,‬فعاليت شديد عضالني(كال صدمات‬
‫بافتي)‪ ,‬كتواسيدوز ديابتي‬
‫اختالل در دفع كليوي •‬
‫كمبود آلدوسترون •‬
Sampling
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‫هموليز شديد← اثر رقتي‬
• K
• Hemolysis
• Serum > plasma
‫اندازهگيري سديم‬
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ISE
Flame spectrophotometry
Internal standard
Calibration with low and high concentration of analyte
Enzymatic
Using galactosidase and (ONPG) O-nitrophenyl-β-Dgalactopyranoside as enzyme and substrate
• Chromogenic ionophore, chromolyte, cryptand
‫اندازهگيري پتاسيم‬
• ISE
• Flame spectrophotometry
• Enzymatic
• Chromogenic ionophore, chromolyte, cryptand
Chloride
‫بيشترين آنيون خارج سلولي •‬
‫جذب‪ :‬روده‬
‫دفع‪ :‬عرق ‪،‬کلیه‪ ،‬پروکسیمال بطور غير فعال با سدیم و در‬
‫هنله بطور فعال با سدیم‬
‫‪Hypochloremia‬‬
‫اسیدوز در اثر تولید اسیدهای آلی‪ ،‬اختالل در بازجذب کلیوی‪،‬‬
‫ترشح نابجای هورمون آنتی دیورتیک‪ ،‬استفراغ‬
‫‪Hyperchloremia‬‬
‫دهيدراتاسيون‪ ,‬ناتوانيكليوي‪ ,‬ديابت بيمزه‪ ,‬افزايش فعاليت قشر فوق‬
‫كليه‪ ،‬آلكالوز تنفس ي‪ ،‬هيپركلرميا اسيدوز‬
‫اندازهگيري كلرايد‬
‫در مدفوع‪ :‬در بیماری آلكالوز هيپوكلريك مادرزادي با •‬
‫‪hyperchlororrhea‬‬
‫در سرم‪ ,‬پالسما‪ ,‬ادرار و عرق ‪ .‬پس از خونگيري سلولها بايستي بسرعت از پالسما جدا شوند •‬
‫چرا كه وقتي خون در معرض هوا قرار گيرد بعلت از دست رفتن دی اکسید کربن توزيع کلر بين سلولهاي خوني و‬
‫پالسما تغيير ميكند‪.‬‬
‫متد های اندازهگيري كلرايد‬
• Coulometric – Amperometric titration
• with silver ions. In the chloride titrator, a constant
• direct current is passed between a pair of silver
electrodes, causing release of silver ions
• into the titration solution at a constant rate. The
silver ions react with chloride to
• precipitate (Ag+ + Cl - ===> AgCl).
• ISE