Clin Chem Revision　２

8/10/2019 Clin Chem Revision

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Pancreas

Endocrine: Insulin (beta), glucagon (alpha)

Exocrine: Enzyme: Amylase, Lipase, Trypsin, Chymotrypsin, Elastase

Pancreatic Disease:

Acute/Chronic pancreatitisCarcinoma

Congenital/Structural disease

Directly Measures by Hormonal stimulants: CCK, secretin

Indirectly by Exocrine insufficiency, faecal fat, feacal chymotrypsin, elastase

Acute pancreatitis: Mild/Severe APACHE II (mild >=8)

Complications of AP: Multi-organ failure, necrotizing pancreatitis, pseudocyst,

abscess, obstructive jaundice, bleeding adjacent organ

Diagnosis:

Biochemistry: Plasma amylase (also increased in renal failure, DKA,

macroamylasemeasure urine amylase as macroamylase cant pass through

glomerulusAmylase-to-Creatinine Ratio ACCR), plasma lipase


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Imaging: Ultrasound abdomen, AXR, Contrast enhanced CT, MRI

Plasma amylase (drop faster)

-Rise within 6-12 h, elevate 3-5 days

Plasma lipase-Rise within 4-8 hours of onset, sustained 8-14 days

Treatment: ERCP

Renal function: Urea, Creatinine (Higher than ref intervalRenal failure)

Lipase (not normally detected in urine)

Upon attack of pancreatitisincreases within 4-8 hours, peaked at 24hours,

decreases with 8-14 days (longer than amylase)

Measure by Titrimetry, Turbidimetry, Spectrometry, Enzymatic reaction rate

Diabetes (Plasma glucose >5.6)

Type 1: Autoimmune destruction of beta cellsketosis, polyuria, weight loss

Type 2: Genetic, old age, insulin resistancesubsequent beta cell failureGestational Diabetes (not diabetic before pregnancy)Increased insulin

resistance/fetal hyperinsulinism

Defects in diabetes

Uncontrolled LipolysisKetosis

Proteolysis

HyperglycemiaGlycosuriaOsmotic diuresisPolyuria, Thirst,

Dehydration, Hypotension

Diabetic microangiopathy

NephopathyRenal failure

Retinopathy & CataractsBlindness

NeuropathyPeipheral neuropathy & Autonomic

Atherosclerosis

Lab test for diabetics:

1. HbA1c (>6.5%--> Diabetes)& plasma glucose >11.1mmol/L

2.

OGTT

3. Ketones (Beta-hydroxybutyrate[bld], Acetoacetate[urine], Acetone)


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4.

NGSP(National Glycohemoglobin Standardization Program) certified assays

Urate and Gout

High UrateCAD & renal disease

Urate (Increase in gout; excrete via kidney/lost in GI)

Major product of catabolism of purine nucleosides (A&G)XanthineUric acid

Weak acid

Measurement of Urate( in prechilled 4C herparinzed tubes, analyzed in 4h)

Spectrophotometric/Enzymatic/HPLC

Not visible in X-ray, Calcium visible

Enzymatic colorimetric: Uricase & Peroxidase (red color)

Negative interference: Ascorbic acid, bilirubin, rasburicase

Specimen: herparinzed plasma/EDTA/serum at cool temperature

No refrigeration & acidifiedprecipitationAdd NaOH to urine samples to alkaline it to prevent ppt

Gouty arthritisIdentify uric acid crystal in synovial fluid but not quantitatively

Disorders of purine metabolismHyper or HypouricemiaTest serum uric

acid; urinary uric acid clearance inversely correlated to insulin resistance

Elevate uric acid level

Insulinmodify kidneys uric acid handlinghyperuricemia

Hyperuricemia-Overproduction

Primary: Inherited enzyme defectsOver-production of purine

Secondary: Blood disease, Malignancies, Psoriasis, Drugs/Alcohol

Under-excretion

Renal insufficiency, DKA, Obesity, Endocrine, Drugs


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Gout: Monosodium urate crystal deposition

Hyperuricemia*

Three clinical stages

1.

Acute gout arthritis (Asymptomatic hyperuricaemia)Severe pain, redness, swelling, disability;

2. Intercritical/Interval gout

3. Chronic recurrent and tophaceous gout

Characterized biochemicallyExtracellular fluid urate saturation

Clinical manifestations of 1 or more: Recurrent acute inflame arthritis attack,

chronic arthropathy, accumulation of urate crystal in tophaceous deposits, uric

acid nephrolithiasis, chronic nephopathy

Criteria for clinical diagnosis of gout

-History of one or more episodes of monoarticular arthritis

-Maximum inflame within 24 h

-Unilateral first metatarsophalangeal (MTP) joint attack

-Visible/Palpable lesionTophus

-Hyperuricemia, obesity, hypertension, hyperlipidemia

Pseudogout=Calcium Pyrophosphate dihydrate (CPPD)

Hypothyroidism

Hypouricemia: Reduced production of purine (liver disease), Increased excretion

Clinical test

Fraction Excretion of Urate (FEua)

24h urine urate

FEua=(UUa x PCr) / (PUa x UCr) x 100% [Normal ~7-10%]

HighHypouricaemia

Ratio between urate clearance & creatinine or insulin clearance

Hereditary Renal Hypouricemia (renal tubular defect in urea reabsorption)

URAT1/SLC22A12 mutation identifiedUrate anion exchangerRegulate

blood urate levels


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Gastric

Disorders: Peptic ulcer-Gastric & Duodenal ulcer

By H. pylori; caused/worsen by drugs as aspirin, NSAIDS..etc

Detected by invasive/non-invasive: urea breath test/IgG against H.pyloriUrea breath testing for H. pylori (produce urease that converts urea to NH3)

13C breath test, 14C breath test, Basal gastric output test for gastrin

(Zollinger-Ellison syndrome)

Determine gastric juice by titration with NaOH

Inflammation: Gastritis

Gastroesophageal reflux disease (GERD)

Tumour: gastric cancer

DiarrhoeaK/Cl depletion, acid-base abnormalities

Test: Stool culture, examination

Absorption >>> Secretion

Stool weight > 200g/day

Acute 4 weeks

-Secretory (deranged fluid & electrolyte transport across mucosa, no

malabsorbed solute, persist with fasting)

-Osmotic (poorly absorbable, nonabsorbable CHO, ceases with fasting)

-Steatorrhoea-Pancreatic/Intestinal

(fat malabsorption associated w/ weight loss; osmotic effect of fatty acid)

Foul smelling, gray, sticky

-Dysmotile cause (rapid transit of GI contents, hyperthyroidism

-Inflammatory (Exudation, Fat malabsorption, disrupted fluid/electrolyte

absorption, hypersecretion by inflammatory mediators with pain, fever,


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bleeding)

Tests: Hormonal profile, urine laxative screen, radiological studies

Malabsorption: loss of cells for absorption

GI tract cant take up dietarycompound

Maldigestion: lacking important digestive enzyme/tissue (genetic/injury)

Symptoms: Failure to thrive, diarrhea, cramping, Flatulence frequent bulky stools,

bloating, abdominal distension

Crohns disease-Inflammatory Bowel Disease

Test: serum, whole blood, urine, feces, breath, sweat, biopsy

Baseline test

GI function; Absorption test should not depend on liver function (bile

salts/pancreatic function: amylase, lipase, proteolytic enzyme)

Never MRIGI motility

Clinical application Appropriate investigation

Diarrhea Breath Hydrogen, urine laxative screen, fecal osmotic gap

Pancreatic function Fecal elastase

Coeliac disease Anti-gliadin Ab, anti-tissue transglutaminase Ab

CHO Oral sugar tolerance testmucosal dysfunction, Xylose

absorption test(absorbed rapidly from small intestine,

excrete in urine, test for small intestinal mucosal function

replace by Small intestine mucosal bopsy endoscopy),

Breath Hydrogen

Small intestine bacterial growth Breath testbesteradicate bacteriadisappear

symptoms

Gold standards: Quantitative culture of jejunal aspirate

Fat malabsorption (fecal) Fecal microscopy, fecal fat, 14C triolein absorption, 14CO2

breath

Qualitative examination of stool (24h not accurate, do 3 or 5

days)

B12

Pernicious anemia

Chronic pancreatitis

Schilling test

1) Gastric mucosa secrete IF [O/N fasttake radioactive

cobalamin B12flush nonradioactive to saturate body


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Achlorhydria

Bacterial overgrowth syndrome

Ileal disease

storescollect urinemeasure radioactivity]

2) Terminal ileum absorb Vit B12 [Taken 3 days after part I,

O/N fastRadioactive B12 + IFflush B12collect

urine & measure radioactivity]

Part I Normal Part II -Normal

Low NormalPernicious Anemia

Low LowIntestinal malabsorption

Others Fecal Alpha1-antitrypsin for PLE

Xylose: not normally present in blood, no digestion, absorbed in upper small

intestine, not metabolized by body, filtered by glomerulus

Pancreatic dysfunction, intestinal disease, altered bacterial flora, biliary

obstruction, local disease/surgery, gastric atrophy, disaccharidase deficiency,

protein-losing enteropathy, IEM

Biochemical consequence of Generalized malabsorption

-Steatorrhoea, Fat-sol VIt & Cal Malabsorption, Protein malabsorption, CHO

malabsorption

Biochem: Anemia, Decrease VitB12/Folate/Fe, Ca, PO4, total protein & albumin

Increase plasma ALP, prolong PT, abnormal TFT


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Serum protein- part of liver function test

-Total protein

Biuret method-color proportional to protein concentration in sample

Kjeldahl titrationPhenol

Folin-Lowry

Ninhydrin

Cause of hyperproteinaemia: Dehydration, prolonged tourniquet application

-Albumin

-Globulin

Hypergammaglobulinaemia

Polyclonal, monoclonal

Hyperglobulinaemia: serum protein electrophoresis

Urinary bence-jones proteins (BJP): light chain secreted excessively by myeloma

plasma cells

Hypoproteinaemia e.g. pregnancyHypoalbuminaemiasynthesized usually by hepatic parenchymal cells

-Haemodilution

-Decreased production: malnutrition, liver disease, APR, analbuminaemia

-Altered distribution: infection, inflammation, malignancy

-Loss from body

-Increased catabolism: malignancy, APR

Function of albumin: maintain colloidal osmotic pressure in both vascular and

extravascular spaces, transport protein, buffer

Measures by Bromcresol purple (BCP), BCG, methylorange

Hypogammaglobulinaemia: transient, primary, secondary, protein loss,

pregnancy

Alpha-1 anti-trypsin (AAT)protein inhibitor, Pi ZZ genotypeemphysema

-APR, synthesized in liver

Measure by immunonephelometrylight scattering


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Transferrin-iron transporting protein; transport from absorption site to bone

marrow for erythropoiesis

Measure by TIBC

Soluble transferrin receptor: correlates with erythroid precursorsdifferentiate iron deficiency anemia from anemia of chronic disease

sTfR/log ferritin

Increased: erythroid proliferation: hemolysis, beta-thal, decreased Fe store

Decreased: chronic renal failure, aplastic anaemia, post bone marrow trannsplant

Ceruloplasmin; age dependent

Synthesized in hepatocytes, secreted into circulation is holoceruloplasmin

Apoceruloplasmindevoid of copper, degraded intracellularly

Disease: Wilson disease

Tested by immunonephelometry

C-reactive Protein (HsCRP) predicts MI, stroke, peripheral arterial disease,

sudden cardiac death; correlates with LDL-cholesterol

Synthesized in liver; induced by IL-6

Stable in circulation, no circardian levels

Predicts CVD risk/MI

Method: immunonephelometry


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synthesize

d

Disease Measured

C reactive

protein

Liver Stable level CVD/MI Immunonephelometr

yCeruloplasmi

n

Hepatocyte

s

Wilsons Immunonephelometr

y

Soluble

transferrin

receptor

Erythroid

precursors

Predicts

iron

deficiency

& anemia

of chronic

disease

Transferrin Fe transport

protein for

erythropoesi

s

TIBC

Alpha1

anti-trypsin

Liver Protein

inhibitor

Emphysem

a

Immunonephelometr

y

Factors affecting migration of electrophoresis

-Net charge of molecule in solution

-Size & shape of molecule

-electric field strength

-frictional co-efficient

-properties of support medium (non-restrictive/restrictive e.g. PAGE)

-buffer composition (pH determines charge, ionic strength, calactate increase

beta region resolution)

-temperature

-volume of sample

-diffusion

-adsorption

-electroendosmosis

Fixation

-Dry

-PPT protein


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-Immunoppt

-Freeze

Detectionat 280nm, natural florescence, enzyme coupled reactions,

immunochemical labeled antibody, autoradiographyStains

Quantitation: elution, densitometry, absorbance at 214nm

Immunofixation: Immunoppt with specific anti-sera after PE

Wash non-ppt protein from gel after incubation

Applications of PE:

-Serum/urine PE as general screen

-Investigation of an elevated globulin fraction

Polyclonal gammopathy, Monoclonal gammopathy, Oligoclonal gammopathy

-Detection of oligoclonal bands in CSF (run Serum & CSF sample tgt)

-Phenotype specific proteins

Multiple myeloma:

single clone of plasma cell proliferation produces monoclonal antibodyBone pain, height reduction by several inches, weakness & fatigue, weightloss

Bone disease of multiple myeloma; hypercalcemiafree light chain assay

Non-secretory myeloma

Light Chain Myeloma

Cryoglobulins: serum protein ppt at temp < body temperature

Positive screeningQuantitation of total protein & IgG

Complements

C3 level decreasedincrease infection risk


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Therapeutic drug monitoring

Indications for TDM

Limitation of standard drug dosingiSerum concentration & clinical response?

Narrow therapeutic index

Long term therapy

Wide interindividual and intraindividual variability in pharmacokinetics

Absence of biomarker w/ therapeutic outcome

Administer w/ other, potentially interacting compounds (drug drug interaction)

Potential patient compliance

Therapeutic group: Anticonvulsants, Cardiovascular(Anti-hypertensives,

anti-arrhythmics), Endocrine

Pharmacodynamics: what drug does to body

Pharmacokinetics: what body does to drug: ADME

Absorption: first pass effect, enterohepatic circulation

Affected by food/co-administered drugBioavailability: fractional extent a dose reach site or action

Distribution: affected molecular weight, pKa, lipid solubility

Binding to blood components, receptor, pass membrane, hydrophobicity

Only free drug available for transport across membrane

Affected by abnormal protein status

Weakly bound drug displaced by those w/ high affinity or endogenous FFA

cytotoxicity

Metabolism: convert non-polar to polar water soluble form

Phase 1: functionalization reactions: oxidation, reduction, hydrolysis @ hepatic

cytochrome P450; genetic variation; reaction involve transform prodrugactive

Phase 2: Conjugates drug, increase water solubility

Elimination: renal/biliary, intestinal, pulmonary; assessed by creatinine & GFR

Half-life of drug: time required for drug to decline half

Affected by organ failure, intoxicate


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Pharmacokinetics

Therapeutic ranges Between MTC and MEC

Peak Level < Minimum Toxic Concentration

Trough > Minimum Effective Concentration [Therapeutic Range]~5 half lifvessteady state

Pharmacogenomics: genetic variation on drug response

Info required for serum drug conc:

Patient ID, time blood taken from last dose (trough vs peak), drug dosage,

Mode of administration, co-med, why take drug, what to monitor, clinical status

Specimen: blood/saliva/urine/sweat/hair

Analysis: IA, Chromatogram HPLC

Special drug group

Anti-convulsants:

Phenyltoin (90% protein bound, easily saturated)

Acute overdose: cerebellar, vestibular effectsChronic: + behavioral change, increase seizure freq

Assess Toxicity: near peak 4-5 hours after dose

Adequate therapy: trough lv b4 next dose

Phenobarbital: metabolized by liver, 70-100h half life

Side effect: sedation

Valproic acid: absence seizure, highly protein bound

Toxicity: GI, Hyperammonaemia, CNS, teratogenicity

Theophylline: bronchial muscle relaxant; caffeine as metabolite of theophylline

Antibiotics

Aminoglycosides: form complex w/ heparin

Vancomycin: excreted by kidney, auditory nerve toxicity

Cyclosporine: toxic at hepatic, renal, neuro, infective

Area under curvebetter estimates risk of acute rejection & toxicity

Pre-dose/Trough monitoring


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C2: 2 hours post dose

Immunosuppressants

Mood stablizers/antipsychotics

Lithium: treat bipolar illness

Digoxin: Cardiac glycosides, inhibits Na/K ATPase

Toxicity: cardiac failure, cross react digoxin analog endo: uremia, pregnancy; exo:

Chin med, digibindGI, neuro, heart, worsen with hypokalemia,

hypomagnesaemia, hypercalcaemia

Measure at least 6-8h after dose, prefer trough

Methotrexate: antimetabolite, interfere w/ DNA synthesis

Thyroid function

Hypothalamus produces TRHPituitary produces TSHat Thyroid gland

binds follicle cell receptorthyroglobulin at colloid space

+ IodineIodinated tyrosine residuesjoin tgtTriidothyronine (T3) &

Thyroxine (T4)increase T3, T4 in bloodHomeostasis negative fdbk to

pituitary, TRH receptor, hypothalamus

Peroxidase oxidize iodine to iodineIf no iodine available, thyroid hormone still maintained

Thyroglobulin

Thyroid hormones

Synthesis of T4 and T3 in thyroid gland

1. Thyroglobulin internalize by endocytosis back in follicle cell

2. Joins with LysosomeEnzyme cleave T3 and T4 from thyroglobulin

3. T3 & T4 released tgt in extracellular space by diffusion

4. Thyroid gland secrete T4:T3 in ratio of 10:1

T3 greater activity than T4; T4mono-deiodination at outerT3; inner

inactive reverse T3 rT3.

10% T4 & T3 produced dailysecrete in bile

Small amountsUrine


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Total thyroid hormone (T3,T4) affected by binding proteins (+/-)

Mostly bound to serum protein Thyroxine Binding Globulin TBG (inactive)

-Increased upon pregnancy & estrogen, decrease upon liver disease,malnutrition, glucocorticoids, nephrotic syndrome, hereditary TBG deficiency

few are free hormones (physiologically active); concentration regulated by

hypothalamus-pituitary-thyroid axis

Thyroid hormones function

Cardiac

-increase heart rate, cardiac contractions, stroke volume, cardiac output

Muscle

-rate & force of skeletal muscle contraction

Stimualtes BMR

-Increase activity of adrenal medulla (sympathetic, glucose production)

-Increase intestinal glucose reabsorption

-Increase mitochondrial oxidative phosphorylation (energy)

-Increase heat production

Investigation

Total thyroid hormone assay-estimation of TBG

T-uptake and Free thyroxine index (FTI): resin uptake method; resin used to

separate unbound labeled thyroid hormone(resin bound) from bound to TBG

Amount of resin bound hormone inversely proportional to unsaturated

binding sites of TBG

FTI only correlates well w/ free T4 only patient w/ mild TBG abnormalities

FT4,FT3: ref method for free thyroid hormones for equilibrium dialysis

Estimated by Immunoassays, unit in pmol/L

TSH inversely proportional to plasma T3,T4 level

Initial treatment of Hyperthyroidismlook at FT4

Thyroid antibodies: Graves disease

TSH receptor autoantibodies: like TSH that binds to TSH receptor


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overproduction of thyroid hormones=Hyperthyroidism; detection/exclusion of

Graves disease

Anti-thyroid peroxidase antibody, Anti-thyroglobulin antibody

-Confirmation/exclusion of autoimmune thyroiditisTRH stimunlation test: determine TSH at 0,30,60,120 minutes

HyperthyroidismResponse is flat

Differentiate secondary and tertiary hypothyroidism

Pituitary hypothyroidismFlat response

Hypothalamic hypothyroidismDelayed positive response

Red cell zinc: low in hyperthyroidism

Tumor markers: Thyroglobulin: correlates w/ size of thyroid gland

Increased in inflammation of thyroid gland; increased in most differentiated

thyroid cancers

Calcitonin: produced by C cells of thyroid gland; diagnosis & monitor marker of

medullary thyroid cancer

TSH assay-third generation: differentiate mildly subnormal TSH from highly

suppressed TSH levels; identify sick euthyroid syndromeFree T4

Solid phase competitive enzyme immunoassay

-Highly specific T4 polyclonal antibody bound to polystyrene well

Test Sample + T4 enzyme conjugate add to each antibody coated well

Incubate 60 minsT4 in patient sera competes with T4 enzyme-conjugate for

binding sites on coated wells

Amount of T4 in patient sample inversely proportional to amount of T4

enzyme conjugate to well

Free T3

-2 steps IA detect free T3 in sample using Chemiluminescent Microparticle

Immunoassay

Sample + Anti-T3 coated paramagnetic microparticles combined

Free T3 in sample binds to anti-T3 coated microparticles

T3 acridinium labeled conjugate added

Reverse relationship between free T3 in sample & Relative Lights Unit


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TSH assay: 2 step IA: determine presence of thyroid stimulating hormone in

human serum & plasma using Chemiluminescent Microparticle Immunoassay

Technology

1.

Anti-beta TSH antibody coated paramagnetic microparticles + TSH assaydiluent

2. TSH in sample binds anti-TSH antibody coated microparticles

3. After washing, anti-alpha TSH acridinium labeled conjugate

4. Pretrigger & Trigger solution add to reaction mixturemeasure RLU

5. Directrelationship b/w TSH in sample & RLU

Hyperthyroidism:excess thyroid hormone levels

Symptoms: nervousness, goiter

Cause: most commonly Graves disease (Female >>Male)

Lab results: Suppressed TSH, Raised FT3, FT4.

T3 toxicosis: normal FT4, raised FT3.

Subclinical hyperthyroidism: suppressed TSH w/normal thyroid hormones

Transient hyperthyroidism in pregnant women w/ severe vomiting: Thyroid

hormone normalizes in 2 and 3 trimester

hCG-Mild Thyroid stimulating activityPeripheral resistance to thyroid hormones: patient is euthyroid

Increase FT4 to a lesser degree FT3

TSH normal/slightly increased/not completely suppressed

Absence of usual symptoms & metabolic consequences of increase in thyroid

hormone

Hypothyroidism: decrease level of thyroid hormones: slow speech, cold

Deficiency of thyroid hormone during developmentshort stature, mental

deficits

Adult onset (myxedema)Severe hypothyroidism

Lab results: decreased FT4, FT3, increased TSH; (FT4 better analysis than FT3)

Cause: Hashimoto thyroiditis (Female >>> Male); present w/ goiter

Iodine deficiency also goitrous

Subclinical hypothyroidism:lownormal serum thyroid hormones, mildly

raised TSH


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Sick euthyoid syndrome: abnormalities in thyroid function in patient w/ serious

illness not caused by primary thyroid/pituitary dysfunction

Low T3 level w/ increased rT3 & low normal TSH, T4 levels

Iron

-O2 transport

-energy metabolism

-Hb 67%

-storage iron 27%, myoglobin 3.5%, tissue iron 0.2%, transport iron 0.08%

Iron deficiency: intake less, loss more (bleed)

Iron overload:

Hemosiderosis (no tissue injury),

Hemachromatosis (tissue injury)

-Bronzing of skin

-Cirrhosis

-Diabetes-Endocrinopathies

-Cardiomyopathies

-Arrhythmias

-Arthopathies

Detection: Chromogenic

Measure after release from transferrin (Fe3+ only)

Ferritin: protein shell surrounding iron core

=Fe store in body

Transferrin

Measure as Unsaturated Iron Binding Capacity

Saturate Fe3+ binding of transferrinRemove Fe3+Check saturation %

Lab assessment: Historical, Hematological, Biochemical

Biochemical: Serum ferritin, iron concentration, TIBC, Transferrin %


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tage Plasma Fe

Negative

APR

50%

lower in

pm

TIBC Transfer

rin

saturatio

n(Fe/TIB

C)

Negative

APR

Tells

how

much Fe

actually

bound

Ferritin

(sensitive and specific

marker for Fe deficiency in

metabolically stable patient)Positive APR

Cut off 225pmol not deficiency

Plasma

soluble

transferrin

receptor

Reflects

cellular Fe

status

Not affected

by chronic

disease/APR

Depletion of Fe stores Normal Normal Normal Low Normal

I: Functional Fe deficiency Low High Low Low High when

increased

effective or

ineffective

erythropoiesi

s

II: Fe deficiency anemia

With low Hb

Low High Low Low High

ron deficiency + anemia of

hronic disease

Low Low or

normal

Low or

normal


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Porphyria: Enzyme related disease: IEM

PBG: Porphobillinogen

Acute Prophyria

-suspected acute attack

Measure: Urine PBG (10X high), fecal porphyrin, fractionated fecal porphyrins,

plasma fluorescence emission spectroscopy

ALA dehydratase deficiency porphyria

Acute Intermittent Porphyria (PBG elevate for weeks or even months after

attack): when normal total fecal porphyrin

Congenital Erythropoietic Porphyria

Porphyria Cutanea Tards

Hereditary Coproporphyria (PBG returns to normal once resolve)

Abnormal total fecal porphyrin

Increased coproporphyrin III upon Fractionated fecal porphyrins

Variegate Porphyria(PBG returns to normal once resolve)

High PBG

Abnormal total fecal porphyrinCharacteristic peak at 624-628nm

Increased portoporphyrin IX

Erythropoietic Protoporphyria

Clin Chem Revision　２

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