Laboratory Interpretation

Laboratory Interpretation พญ . รพีพร โรจน์แสงเรือง โครงการจัดตั้งภาควิชาเวชศาสตร์ฉุกเฉิน คณะแพทยศาสตร์รพ . รามาธิบดี

Creatinine Creatine is synthesized in the liver. It is the chief source of high-energy phosphocreatine for muscle metabolism. It loses water to become creatinine, all of which is excreted. Use for renal function

case Male 60 years old came with fatigue BUN=40/Cr=2 This is renal failure –renal /prerenal?

Old man will lose muscle mass that makes low Cr. It might be prerenal or renal failure. You will ask for U/A to look for sp.Gr.

Urine hCG Normal pregnancy -secreted first by trophoblastic cells of conceptus and later by placenta positive as early as 4 days after expected date of menstruation it is >95% reliable by the 10th to the 14th day. Human chorionic gonadotropin (hCG) increases to a peak between the 60th and 70th days then decreases progressively.

Urine hCG False-Positive Result -Drugs, e.g., chlorpromazine, phenothiazines -Bacterial contamination -Protein or blood in urine False-Negative Result -Dilute urine -Missed abortion -Dead fetus syndrome

Hematuria <3% of normal persons ( ≥3 RBCs/HPF ) 18% of persons after very strenuous exercise. The source of microscopic hematuria remains obscure in ~70% of cases after workup .

Nonglomerular Hematuria Caused By Trauma Hemoglobinopathies Polycystic disease GU tract tumors, infections

Hematuria in Children Caused By -Glomerular Causes Acute postinfectious GN Membranoproliferative GN IgG-IgA nephropathy (Berger disease) Hereditary nephritis (Alport syndrome) SLE Renal infarction Henoch-Schönlein purpura -Nonglomerular Causes Polycystic kidneys Renal tumors Hydronephrosis GU tract infection, foreign body, calculi, etc.

Ketonuria is diagnosed when ketone bodies (acetone, beta-hydroxybutyric acid, acetoacetic acid) appear in urine. Use Screening for ketoacidosis, especially in diabetes mellitus when blood is not immediately available

case 30 year-old Female came with kussmual breathing and underlying DM Her BS= 500, Hco3=10,urine ketone-neg What is her diagnosis?

DKA Measure serum ketone or urine ketone cannot measure beta-hydroxybutyric acid ( measure esp.acetoacetate /acetone) DKA +lactic acidosis have high beta-hydroxybutyric acid

Ketonuria Metabolic conditions (e.g., diabetes mellitus, renal glycosuria) Dietary conditions (e.g., starvation, high-fat diets) Increased metabolic requirements (e.g., hyperthyroidism, fever, pregnancy and lactation)

Prerenal azotemia specific gravity >1.030 and Urine osmolality >500 mOsm/kg)

Proteinuria Transient(10%) high fever CHF HT Stress exposure to cold, strenuous exercise, seizures. Usually <2 g/d; disappears with recovery from precipitating cause.

Proteinuria PERSISTENT Glomerular Idiopathic (e.g., membranoproliferative GN, membranous glomerulopathy) Secondary Infection (e.g., poststreptococcal, hepatitis B, bacterial endocarditis, malaria) Vascular (e.g., renal artery stenosis) Drugs (e.g.NSAIDS, heroine, captopril, penicillamine) Autoimmune (e.g., SLE, RA, dermatomyositis, Henoch-Schönlein purpura, ulcerative colitis) Neoplasia

Microalbuminuria Microalbuminuria is defined as persistent proteinuria that is below detection by routine reagent strips but greater than normal.

Microalbuminuria patients with DM: microalbuminuria associated with longer duration of diabetes, poorer glycemic control, higher BP, advanced retinopathy and neuropathy, subsequent renal failure , and increased vascular damage and risk for cardiovascular disease.

Bence-Jones Proteinuria UseDetection of various gammopathies 80% of tests are true positive-Myeloma (70% ) False positive CNT (e.g., RA, SLE, scleroderma) Chronic renal insufficiency Lymphoma /leukemia Metastatic carcinoma of lung, gastrointestinal, or GU tracts

Anuria < 100 mL of urine in 24 hours. Caused By Bilateral complete urinary tract obstruction Acute cortical necrosis Necrotizing glomerulonephritis Certain causes of acute tubular necrosis

Oliguria is usually defined as excretion of less than 400 mL of urine in 24 hours(in children< 15 to 20 mL/kg/24 h) Caused By Prerenal causes (e.g., CHF, shock) Postrenal causes Renal causes

Polyuria urine volume > 2,000 mL / day. Caused By Osmotic diuresis( DM) Polydipsia(DI) Diuretic drugs Chronic renal failure Partial obstruction of urinary tract with impaired urinary concentration function acute tubular necrosis (aminoglycosides)

Acute rheumatic fever occurring 10 days to 6 weeks following an episode of group A Streptococcus infection. Diagnostic criteria confirmation of preceding group A Streptococcus infection by 1.Positive throat culture 2. Increased serologic titer of antistreptococcal antibodies

Acute rheumatic fever Symptom+2 major / 1 major + 2 minor Minor Criteria: High ESR or CRP, prolonged P-R interval, fever, arthralgia Major Criteria: Carditis, arthritis, Sydenham chorea, subcutaneous nodules, erythema marginatum

To determine clinical activity—follow ESR, CRP, and WBC. Return to normal should be seen in 6 to 12 weeks in 80% to 90% of patients it may take ≤6 months

Cor Pulmonale polycythemia Increased blood CO2 the primary lung disease (e.g., chronic bronchitis and emphysema

Blood lipid tests should not be performed during stress or acute illness (2 to 3 months after illness ) after a 12- to 13-hour fast

Myocardial Infarction Characteristics of Serum Markers for Myocardial Damage Early appearance : Myoglobin, CK isoforms High specificity : cTnI, cTnT, CK-MB, CK isoforms Wide diagnostic window : cTnT, cTnI, LD Risk stratification : cTnT, cTnI, CK-MB Predicts reperfusion : Myoglobin, cTnI, cTnT, CK isoforms Indicates reinfarction after 2–4 d : CK-MB

cTn cTn is as sensitive as CK-MB during the first 48 hours after AMI Specificity close to 100%. High sensitivity for 6 days. cTnT may remain increased for ≤14 days.

cTn cTnI is not increased by skeletal muscle injury, making it more highly specific for myocardial injury. cTnI/ cTnT may be detected in 10% to 30% of patients with CRF

CPK-MB Use in Detect reinfarction or extension of MI after 72 hours. Document reperfusion after thrombolytic therapy.

CK-MB usually is evident at 4 to 8 hours, peaks at 15 to 24 hours

Serum Myoglobin is an oxygen-carrying respiratory protein found only in skeletal and cardiac muscle. Earliest marker for AMI. Increased 1 to 3 hours in >85% of AMI patients peaks 8 to 12 hours becomes normal in about 24 to 36 hours or less;

B-type Natriuretic Peptide hormone secreted by myocytes in the ventricles in response to pressure overload/myocyte stretch use: BNP / N-terminal (NT) proBNP. Use in - screening and diagnosis of CHF -Prognostic tool for classes III and IV -Diagnosis of left ventricular dysfunction

B-type Natriuretic Peptide cutoff values : BNP: 80 to 100 pg/mL NT-proBNP: 125 pg/mL for age <75 Reading <100 pg/mL rules out CHF as cause of dyspnea. Reading >400 pg/mL indicates 95% likelihood of CHF

B-type Natriuretic Peptide Increase in BNP in right heart failure is less than in left ventricular dysfunction BNP and NT-proBNP can be increased in renal failure, especially if dialysis is needed

Secondary hypertension causes <10% of cases of hypertension. Many causes for secondary HT=?

Secondary hypertension Endocrine diseases Adrenal, e.g., pheochromocytoma, Cushing syndrome Pituitary disease, e.g., acromegaly Hyperthyroidism, hyperparathyroidism, etc. Renal diseases renal artery stenosis, nephrosclerosis, embolism Parenchymal, e.g., glomerulonephritis, polycystic kidneys Other, e.g., toxemia of pregnancy, polycythemia, acute porphyria Drugs, e.g., oral contraceptives, tricyclic antidepressants, licorice Toxic substances, e.g., poisoning by lead or cadmium

HT+ Hypo K Ought to think about many diseases?

HT+ Hypo K Primary aldosteronism Pseudoaldosteronism (caused by excessive ingestion of licorice) Secondary aldosteronism, e.g., malignant hypertension Hypokalemia caused by diuretic administration Potassium loss caused by renal disease Cushing syndrome

Infective endocarditis (IE) 2 major criteria 1 major plus 3 minor criteria 5 minor criteria pathologic findings (vegetation or intracardiac abscess confirmed histologically showing active endocarditis).

Major Criteria Typical organism in ≥2 blood cultures in absence of primary focus, or persistently positive blood cultures drawn >1 hour apart Involvement of endocardium by echocardiogram or valve regurgitation Positive serology for Coxiella burnetii (IgG >1:800) Bacterial or fungal DNA in blood or valve (including Bartonella sp., Tropheryma whipplei, other new or unusual organisms) S. aureus bacteremia, even if nosocomial or removable source of infection is present Positive echocardiogram (e.g., oscillating intracardiac mass)

Typical pathogen in IE Streptococcus viridans [~50% of cases] S. bovis Staphylococcus aureus HACEK [Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella]

Minor Criteria Risk factors: predisposing heart condition / IV drug abuse Fever >38°C (100.4°F) Vascular phenomena: septic pulmonary infarcts, major arterial emboli, Janeway lesions Immunologic phenomena: Osler nodes , Roth spots Microbiologic evidence: positive blood culture other than major criteria or positive serologic findings (Bartonella sp. or Chlamydia sp.) Clinical: newly diagnosed clubbing or splinter hemorrhages , microscopic hematuria Biochemical: CRP >100 mg/L or ESR >30 mm/h

Risk Factors Preexisting valve disease / congenital heart diseases Nosocomial: most are caused by enterococci and staphylococci. Case fatality >50%: IV lines; S. aureus in patients with central venous catheters, parenteral lines for feeding or chemotherapy Hemodialysis patients: >50% are caused by S. aureus S. bovis in patients with colon cancer causes 20% of cases Enterococcus faecalis in patients: genitourinary procedures, pelvic infections, prostate disease Blood culture is positive in 80% to 90% of patients:

Proper blood cultures require adequate volume of blood, at least five cultures taken during a period of several days with temperature 101°F or higher Beware of negative culture due to recent antibiotic therapy. based on ≥2 cultures that are positive for the same organism.

case Male 60 years old came with fever His H/C- strept. Bovis How to treat?

Treat with antibiotic Colonoscope finds CA colon

Prosthetic Heart Valves Early - caused by S. epidermidis, S. aureus; also gram-negative bacteria, fungi Late (>60 days postoperatively). Usually caused by streptococci., S. epidermidis Surgery is indicated if blood culture is still positive after 5 days of appropriate antimicrobial therapy or recurrent infection

Syphilitic Aortitis Syphilitic aortitis is an obliterative endarteritis of vasa vasorum of thoracic aorta that can lead to aneurysm formation. Aortitis is the most common expression of late syphilis A positive treponemal test is seen in ~90% of cases.

Behçet Syndrome is a systemic vasculitis -a triad of recurrent aphthous ulcers of mouth and genitalia, and relapsing panuveitis. No definitive laboratory tests are available.

Giant cell arteritis (GCA) is a systemic panarteritis of the large and medium arteries, especially the carotid arteries. affects the extracranial > the intracranial arteries. Biopsy of the involved segment of temporal artery is diagnostic

The classic triad of increased ESR (≥50 mm/h),anemia, and increased serum ALP is strongly suggestive of GCA Laboratory findings reflecting specific organ involvement (Kidney ,CNS,Heart)

Henoch-Schönlein Purpura is a hypersensitivity systemic vasculitis of the small vessels with IgA deposition. abdominal symptoms are predominant Diagnosis is made clinically there are no pathognomonic laboratory findings. Coagulation tests are normal. Renal or skin biopsy supports the diagnosis; it will show focal segmental necrotizing GN that with IgA and C3 deposition.

Kawasaki Syndrome (Mucocutaneous Lymph Node Syndrome) is a variant of childhood polyarteritis of unknown etiology, with a high incidence of coronary artery complications. Diagnosis is confirmed by histologic examination of the coronary artery (same as polyarteritis nodosa)+Laboratory changes due to AMI.

Takayasu syndrome is the term for granulomatous arteritis of the aorta. Diagnosis is established by characteristic arteriographic changes or histologic examination

Thromboangiitis Obliterans (Buerger Disease) is the vascular inflammation and occlusion of medium and small arteries and veins of limbs; it is related to smoking. Histology shows characteristic inflammatory and proliferative lesions

Wegener Granulomatosis (WG) is a rare autoimmune systemic necrotizing or granulomatous vasculitis most often affecting the respiratory tract and kidneys. c-ANCA is highly specific (>90%) for active WG.

Diarrhea -PMN Shigellosis,Salmonellosis,Campylobacter, Rotavirus,Invasive Escherichia coli colitis Ulcerative colitis Pseudomembranous colitis

Diarrhea –no cell Cholera Noninvasive E. coli diarrhea Other bacterial toxins (e.g., Staphylococcus, Clostridium perfringens) Viral diarrheas Parasitic infestations (e.g., G. lamblia, Entamoeba histolytica, Dientamoeba fragilis) Drug related

Plummer-Vinson Syndrome an iron-deficiency anemia associated with dysphagia, atrophic gastritis, glossitis, etc increased risk of cancer of the esophagus

Pseudomembranous colitis is an antibiotic-related diarrhea and colitis caused by C. difficile. Tissue culture assay is gold standard Character of stool-?

Enterocolitis, Necrotizing, in Infancy a syndrome of acute intestinal necrosis of unknown etiology; it is especially associated with prematurity and exchange transfusions. No specific laboratory tests are available. Persistent metabolic acidosis, severe hypoNa, and DIC are a common triad in infants.

Infarction of the Intestine Hematemesis, hematochezia, or melena are present in ~15% and occult blood in <50% of cases. Caused by Primary (idiopathic) Secondary (~75% of cases) to: Emboli (SBE), nonbacterial valve vegetations, left atrium or ventricle, atherosclerotic vascular disease,Venous thrombosis

Ascites blood-AF albumin gradient >1.1: portal HT • neutrophils count >250/µL is presumptive of bacterial peritonitis. Gram stain shows few bacteria in SBP Culture sensitivity = 50% for SBP and ~80% for secondary peritonitis • TB acid-fast stain sensitivity = 20% to 30% and TB culture sensitivity = 50% to 70%.

Chylous Ascites Triglyceride is 2-8 × serum level. Due to lymphatic obstruction (lymphoma or CA) inflammation or obstruction of small intestine trauma to chest or abdomen, filariasis; congenital lymphatic defects in pediatric

Abdominal Trauma Criteria to diagnose penetrating abdominal wounds by peritoneal lavage10,000 mL of normal saline 3 to 18 hours after injury : >10,000 RBC/µL (>5,000 RBC/µL for gunshot wounds) Bacteria, fecal or vegetable matter on Gram stain or bile

Occult Bleeding guaiac -detect blood losses of ~20 mL/d. Use of fecal sample obtained by digital rectal exam is not recommended Stools may appear grossly normal with GI bleeding of 100 mL/d. Consistent melena requires 150 to 200 mL blood in the stomach False positive in FBC, animal blood food

Croup or laryngotracheitis inflammation of the upper airway below the glottis. Caused by Group B Haemophilus influenzae causes >90% of cases of epiglottitis; other bacteria include β-hemolytic streptococci and pneumococci.

Pneumonia Prussian blue–nuclear red stain strongly positive indicates severe alveolar hemorrhage Pap smear- intranuclear inclusions of herpes or CMV Giemsa,GMS of sputum - PCP

Pleural fluid Light criteria-exudate/transudate 1.LDH in fluid > 2/3 normal serum LDH 2.Protein fluid/serum> 0.5 3.LDH fluid/serum> 0.6 4.Serum alb-fluid alb <1.2

Pleural fluid Nonpurulent fluid with positive Gram stain, positive blood culture, or low pH suggests that effusion will become or behave like empyema Streptococcus pneumoniae causes parapneumonic effusions in 50% of cases, especially with positive blood culture

case Male 25 years old came with dyspnea CXR-left pleural effusion Pleural tapping-WBC>50,000, high neutrophils Need ICD?

No ICD Indication for ICD 1.PH< 7 2.SUGAR<40 3.Frank pus 4.Gram stain /Culture +

pH <7.0 and glucose <40 mg/dL indicate need for ICD without grossly purulent fluid. pH of 7.0–7.2 is a questionable indication and should be repeated in 24 h, but ICD is favored if pleural fluid LD >1,000 IU/L. ICD is also indicated if there is grossly purulent fluid or positive Gram stain or culture.

hemothorax hematocrit (Hct) >50% of peripheral Hct indicates a hemothorax. Cytology establishes the diagnosis in approximately 50% of patients. Cytology plus biopsy is diagnostic in about 90% of cases

Exudative effusion Caused by Pneumonia, malignancy, pulmonary embolism, and gastrointestinal conditions (especially pancreatitis and abdominal surgery) cause 90% of all exudates

Pleural effusion Typically left-sided: Ruptured esophagus, acute pancreatitis, RA Typically right-sided or bilateral: Congestive heart failure (CHF) Typically right-sided: Rupture of amebic liver abscess.

Chylous Chylous (milky) is usually due to trauma or obstruction of duct PF triglycerides (TG) >110 mg/dL or TG PF:serum ratio >2 occurs only in chylous effusion

pseudochylous effusions Chylomicrons ≤50 mg/dL with cholesterol >250 mg/dL.

Amylase Increased PF:serum ratio >1.0 Acute pancreatitis—may be normal early with increase over time Also perforated esophageal rupture, peptic ulcer, necrosis of small intestine

TB pleura Large mesothelial cells >5% are said to rule out TB Acid-fast smears are positive in only <20% of TB pleurisy Sensitivity >50% in TB. Cultures from chest tubes culture combined with histologic examination establishes the diagnosis in 95% of cases Adenosine deaminase >70 IU/L

Malignancy effusion Cytology is positive in 60% of malignancies on first tap, 80% by third tap. Is more sensitive than needle biopsy Combined cytology and pleural biopsy give positive results in 90%.

Sputum exam Optimum specimen of sputum shows >25 PMNs and ≤5 squamous epithelial cells/LPF Sensitivity of sputum culture is estimated at 25% to 50%.

Carcinoma, Bronchogenic Cytologic examination of sputum for malignant cells -positive in 40% of patients on first sample -70% with three samples -85% with five samples. False-positive tests are <1%.

CA lung Classified as: Non-small cell lung carcinoma (NSCLC) in 70% to 75% of cases Squamous cell carcinoma (25%–30%) Adenocarcinoma (30%–35%) Large cell carcinoma (10%–15%) Small cell lung carcinoma (SCLC) in 20% to 25% of cases Combined pattern in 5% to 10% of cases

LE cells makes the diagnosis of SLE CHF is typically bilateral; ≤20% are right-sided and ≤9% are left-sided

Plasma D-dimer is a fibrin product generated by action of plasmin on cross-linked fibrin molecules indicating that a clot has formed At cutoff level of 500 µg/L

Total Serum Bilirubin Must exceed 2.5 mg/dL to produce clinical jaundice

Serum Bilirubin (Conjugated:total) <20% conjugated Constitutional (e.g., Gilbert disease, Crigler-Najjar syndrome) Hemolytic states 20% to 40% conjugated Favors hepatocellular disease rather than extrahepatic obstruction Disorders of bilirubin metabolism (e.g., Dubin-Johnson, Rotor syndromes) 40% to 60% conjugated: Occurs in either hepatocellular or extrahepatic type >50% conjugated: Favors extrahepatic obstruction rather than hepatocellular disease

AST Half-life of AST is 18 hours half-life of ALT is 48 hours. Thus, in early acute hepatitis, AST is usually higher initially, but by 48 hours, ALT is usually higher.

ALP Increased ALP in liver diseases (due to increased synthesis from proliferating bile duct epithelium) is the best indicator of biliary obstruction High values (>5× normal) favor obstruction Isolated increase of GGT is a sensitive screening and monitoring test for alcoholism

In cirrhosis with ascites, the kidney retains increased sodium and excessive water, causing dilutional hyponatremia Blood ammonia is increased in liver coma and cirrhosis and with portacaval shunting of blood.

WBC is usually normal with active cirrhosis; increased (<50,000/µL) with massive necrosis, hemorrhage, etc.; decreased with hypersplenism.

Hep. encephalopathy Blood ammonia is increased in 90% of patients but does not reflect the degree of coma. Normal level in comatose patient suggests another cause of coma. Not reliable for diagnosis but may be useful to follow individual

SBP Spontaneous bacterial peritonitis—in 10% to 30% of cirrhosis cases with ascites. 70% have positive blood culture; usually single organism, especially E. coli, pneumococcus, Klebsiella. ≥ 250 PMNs/µL is diagnostic.

AST:ALT ratio >1 associated with AST <300 U/L will identify 90% of patients with alcoholic liver disease; is particularly useful for differentiation from viral hepatitis, in which increase of AST and ALT are about the same. Anemia in >50% of patients may be macrocytic (folic acid or vitamin B12 deficiency), microcytic (iron deficiency), mixed, or hemolytic. In acute alcoholic hepatitis, GGT level is usually higher than AST level. GGT is often abnormal in alcoholics even with normal liver histology. Is more useful as index of occult alcoholism

hepatitis Hepatitis, Chronic ActiveProgressive hepatitis >6 months duration of unknown etiology affecting patients of all ages possibly due to an external agent Due To Viruses HBV (with or without HDV) HCV (with or without HGV) CMV, others

hepatitis Metabolic Wilson disease Alpha1-antitrypsin deficiency Hemochromatosis Primary biliary cirrhosis Sclerosing cholangitis

hepatitis Drugs (e.g., methyldopa, nitrofurantoin, isonizid, oxyphenacetin) and chemicals Nonalcoholic fatty liver Alcoholic hepatitis Autoimmune causes

Acute pancreatitis Serum Lipase Increases within 3 to 6 hours with peak at 24 hours and usually returns to normal over a period of 8 to 14 days. Is superior to amylase; increases to a greater extent and may remain elevated for up to 14 days after amylase returns to normal.

acute pancreatitis -In patients with signs of acute pancreatitis, pancreatitis is highly likely (clinical specificity = 85%) when lipase ≥5× URL, if values change significantly with time, and if amylase and lipase changes are concordant. -Lipase should always be determined whenever amylase is determined. New methodology improves clinical utility.

It has been suggested that a lipase:amylase ratio >3 (and especially >5) indicates alcoholic rather than nonalcoholic pancreatitis).

predisposing conditions of pancreatitis Alcohol abuse accounts ~36% of cases. Biliary tract disease accounts 17% of cases. Idiopathic accounts >36% of cases. Infections (especially viral such as mumps and coxsackie, CMV, AIDS) Trauma and postoperative accounts >8% of cases Drugs (e.g., steroids, thiazides) >5% of cases. Hypertriglyceridemia (Hyperlipidemia—Types V, I, IV) 7% of cases Hypercalcemia Tumors (pancreas, ampulla) Anatomic abnormalities of ampullary region causing obstruction Hereditary Renal failure; renal transplantation

Prognostic laboratory findings On admission WBC >16,000/µL Blood glucose >200 mg/dL Serum LD >350 U/L Serum AST >250 units/L Age >55 years Within 48 hours >10% decrease in HCT Serum calcium <8.0 mg/dL Decrease in Hct >10 points Increase in BUN >5 mg/dL Arterial pO2 <60 mmHg Metabolic acidosis with base deficit >4 mEq/L

prognosis Degree of amylase elevation has no prognostic significance CT scan, MRI, ultrasound are useful for confirming diagnosis or identifying causes or other conditions

CSF CSF -WBC may be corrected for presence of blood (e.g., traumatic tap, subarachnoid hemorrhage) by subtracting 1 WBC for each 700 RBCs/µL counted in CSF if the CBC is normal.

Neutrophilic leukocytes in CSF are found in: Bacteria (e.g., Nocardia, Actinomyces, Arachnia, Brucella) Fungal infections (Blastomyces, Coccidioides, Candida, Aspergillus, Zygomycetes, Cladosporium, Allescheria) Chemical meningitis Other conditions (e.g., SLE)

Lymphocytic cells in CSF are found in: Bacterial infections (e.g., Treponema pallidum, Leptospira,, Borrelia burgdorferi [Lyme disease], M. tuberculosis) Fungal infections (e.g., Cryptococcus neoformans, Candida species, Coccidioides immitis, Histoplasma capsulatum, Blastomyces dermatitides) Parasitic diseases (e.g., toxoplasmosis, cysticercosis) Viral infections (e.g., mumps, lymphocytic choriomeningitis). Atypical lymphocytes may be seen in EBV infection and less often in CMV or HSV infection. Parameningeal disorders (e.g., brain abscess) Noninfectious disorders (e.g., neoplasms, sarcoidosis, multiple sclerosis, granulomatous arteritis)

Eosinophils In CSF be found in: Lymphoma Helminth infection (e.g., angiostrongyliasis, cysticercosis) Rarely, other infections (e.g., TB, syphilis, Rocky Mountain spotted fever, coccidioidomycosis) Eo>5% may indicate malfunction or infection of a ventriculoperitoneal shunt

Multiple Sclerosis (MS) CSF changes are found in >90% of MS patients. Oligoclonal IgG bands or elevated IgG index are the 2 CSF findings recognized as positive.

Serum Enzymes in Diseases of Muscle Creatine kinase (CK) is the test of choice. It is more specific and sensitive than AST and LD and more discriminating than aldolase (ALD) but AST is more significantly associated with inflammatory myopathy and more useful in these cases Increased In Polymyositis Muscular dystrophy Myotonic dystrophy Some metabolic disorders Malignant hyperthermia Prolonged exercise; peak 24 hours after extreme exercise (e.g., marathon); smaller increases in well-conditioned athletes Wilms tumors with rhabdomyomatous features (CK-MB may also be increased

Hyperthyroidism Normal serum M.enzyme levels Increased urine creatine; decreased creatine tolerance Normal muscle biopsy findings Causes some cases of hypokalemic periodic paralysis

Malignant Hyperthermia Rare autosomal dominant hypermetabolic syndrome causing abnormally increased release of calcium from membrane of sarcoplasmic reticulum triggered by various inhalational [e.g., ether] and local anesthetic agents, muscle relaxants [e.g., succinylcholine, tubocurarine] causing hyperthermia, muscle rigidity, and 70% fatality Combined metabolic and respiratory acidosis is the most consistent abnormality and is diagnostic in the presence of muscle rigidity or rising temperature. pH is often <7.2, BE >-10, hypoxia, and arterial pCO2 of 70 to 120 torr. Immediate arterial blood gas analysis should be performed.

Myopathy Associated with Alcoholism Acute (necrotizing) Increased serum CK, AST, and other enzymes. Serum CK increased in 80% of patients; rises in 1 to 2 days; reaches peak in 4 to 5 days; lasts ~2 weeks. Gross myoglobinuria Acute renal failure

Myopathy Associated with Alcoholism Chronic : Increased serum CK in 60% of patients to average of 2× ULN Increased AST and other enzymes due to liver as well as muscle changes Increased urine creatine Diminished ability to increase blood lactic acid with ischemic exercise Abnormalities on muscle biopsy (support the diagnosis) Myoglobinuria

Infective Arthritis Bacterial In purulent arthritis, organism is recovered from joint in 90% of patients and from blood in 50% of patients. Most often due to S. aureus (60%) and Streptococcus species. Gram stain is positive in ~50% of patients; it is particularly useful for establishing diagnosis promptly and in cases in which cultures are negative. Culture may be negative because of prior administration of antibiotics. In children, most common organisms are H. influenzae type b, S. aureus, various streptococci, and gram-negative bacilli. In young adults, >50% of cases are due to Neisseria gonorrhoeae; rest are due to S. aureus, streptococci, or gram-negative bacilli.

TB arthritis Gram stain and bacterial cultures are negative but acid-fast stain, culture, and biopsy of synovia confirm the diagnosis

Myasthenia Gravis (MG) Acetylcholine Receptor (AChR) Binding Antibodies is the standard assay and should be ordered first: Negative in ≤34% of patients with MG Negative ≤50% of patients with ocular MG May be negative in first 6–12 months

Crystalline ArthropathyChondrocalcinosis (“Pseudogout”) Inflammatory mono- or polyarticular arthritis due to deposition of calcium pyrophosphate dehydrate crystals in joints Joint fluid contains crystals identified as calcium pyrophosphate dehydrate, inside and outside of WBCs, and macrophages that are differentiated from urate crystals under polarized light, which distinguishes them from gout. Crystals may also be identified by other means (e.g., chemical, x-ray diffraction).

Gout Group of disorders of purine metabolism characterized by monosodium urate crystal deposits in joints and soft tissues episodes of acute inflammatory arthritis [response to crystal deposits], and hyperuricemia. Most uric acid is synthesized in liver and intestinal mucosa. Two thirds excreted by kidney; one third excreted by bowel.

Gout Primary (i.e., inborn) (30% of patients) -Idiopathic -Increased purine biosynthesis (Lesch-Nyhan syndrome) Secondary (70% of patients) 1. Overproduction (10% of secondary cases); overexcreters: >750 to 1,000 mg/day of uric acid Neoplastic and hemolytic conditions 2.Increased breakdown of adenosine triphosphate Glycogen storage diseases (I, III, V, VII) Alcohol ingestion Myocardial infarction 3. Decreased renal function (90% of secondary cases); underexcreters: <700 mg/day of uric acid

Gout Diagnostic Criteria: -Presence of crystals of monosodium urate from tophi or joint fluid viewed microscopically under polarized light -strongly negative birefringent needle-shaped crystals both inside and outside PMNs or macrophages -differentiates it from pseudogout. (Found in synovial fluid in 75% of patients between attacks.)

Macrocytic anemias Macrocytic anemias (MCV >95 fL and often >110 fL; MCHC >30 g/dL) Megaloblastic anemias PA (vitamin B12 or folate deficiency) Sprue (e.g., steatorrhea, celiac disease, intestinal resection or fistula) Macrocytic anemia of pregnancy Alcoholism Liver disease Anemia of hypothyroidism Carcinoma of stomach, following total gastrectomy Drugs: Oral contraceptives Anticonvulsants (e.g., phenytoin, primidone, phenobarbital) Antitumor agents (e.g., methotrexate, hydroxyurea, cyclophosphamide) Antimicrobials (e.g., sulfamethoxazole, sulfasalazine, trimethoprim, zidovu-dine, pyrimethamine

Normocytic anemias Normocytic anemias (MCV = 80–94 fL; MCHC >30 g/dL) Following acute hemorrhage Some hemolytic anemias Some hemoglobinopathies Anemias due to inadequate blood formation

case 50 years old male came with pale BP นั่ง = 120/70, นอน 130/80 Hct=25, MCV=80 What is the cause of anemia?

Microcytic anemias Microcytic anemias (MCV <80 fL; MCHC <30 g/dL) Usually hypochromic Iron-deficiency anemia, e.g., Inadequate intake Poor absorption Excessive iron requirements Chronic blood loss Pyridoxine-responsive anemia Thalassemia Lead poisoning Anemia of chronic diseases Disorders of porphyrin synthesis

summary Kidney Cardio GI Respiration Hepatobiliary CNS musculoskeletal Hemato

Ferritin Ferritin is an acute-phase reactant and thus is increased in many patients with: various acute and chronic liver diseases alcoholism (declines during abstinence) malignancies (e.g., leukemia, Hodgkin disease) infection and inflammation hyperthyroidism Serum ferritin may not be decreased when iron deficiency coexists with these conditions; in such cases, bone marrow stain for iron may be the only way to detect the iron deficiency.

Iron overload Iron overload (e.g., hemosiderosis, idiopathic hemochromatosis). Can be used to monitor therapeutic removal of excess storage iron. Transferrin saturation is more sensitive to detect early iron overload in hemochromatosis serum ferritin is used to confirm diagnosis and as indication to proceed with liver biopsy. Ratio of serum ferritin (in ng/mL) to alanine aminotransferase (ALT) (in IU/L) >10 in iron-overloaded thalassemic patients but averages ≤2 in viral hepatitis; ratio decreases with successful iron chelation therapy.

TIBC Iron-Binding Capacity, Total SerumTIBC (in µmol/L) is obtained by the following equation: transferrin (mg/L) × 0.025. Unsaturated iron-binding capacity = TIBC minus serum iron (µg/dL). Use in 1.Differential diagnosis of anemias 2.Should always be performed whenever serum iron is done to calculate percent saturation (see Fig 11-2 ) for diagnosis of iron deficiency 3.Screening for iron overload Increased In -Iron deficiency -Acute and chronic blood loss -Acute liver damage -Late pregnancy Decreased In -Hemochromatosis -Cirrhosis of the liver -Thalassemia -Anemias of infection and chronic diseases (e.g., uremia, RA, some neoplasms

SerumTransferrin Transferrin, transports circulating Fe3 molecules. Normally only about 1/3 of iron-binding sites are occupied; the remainder is called unsaturated iron-binding capacity. Increased In -Iron-deficiency anemia; is inversely proportional to iron stores -Pregnancy, estrogen therapy, hyperestrogenism Decreased In -Hypochromic microcytic anemia of chronic disease -Acute inflammation -Protein deficiency or loss (e.g., burns, chronic infections, chronic diseases [e.g., various liver and kidney diseases, neoplasms]), nephrosis, malnutrition) -Genetic deficiency

Transferrin Saturation Serum transferrin saturation is obtained by serum iron / TIBC normal 20% to 50%. Use in Differential diagnosis of anemias/ Screening for hereditary hemochromatosis Increased In -Hemochromatosis -Hemosiderosis -Thalassemia -Birth control pills (≤75%) -Ingestion of iron (≤100%) -Iron dextran administration causes increase for several weeks (may be >100%)

Laboratory Interpretation

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Laboratory Interpretation