LABROCLUB.RU

КЛУБ ЛЮБИТЕЛЕЙ ПОРОДЫ ЛАБРАДОР РЕТРИВЕР, ГОЛДЕН РЕТРИВЕР

ЛАБРОКЛУБ - ОСТРОВОК ДОБРА И РАДОСТИ В ОКЕАНЕ СТРАСТЕЙ КИНОЛОГИИ

Вы здесь

the handbook of japanese adjectives and adverbs

the handbook of japanese adjectives and adverbs

LINK 1 ENTER SITE >>> Download PDF
LINK 2 ENTER SITE >>> Download PDF

File Name:the handbook of japanese adjectives and adverbs.pdf
Size: 3319 KB
Type: PDF, ePub, eBook

Category: Book
Uploaded: 2 May 2019, 15:27 PM
Rating: 4.6/5 from 743 votes.

Status: AVAILABLE

Last checked: 9 Minutes ago!

In order to read or download the handbook of japanese adjectives and adverbs ebook, you need to create a FREE account.

Download Now!

eBook includes PDF, ePub and Kindle version

✔ Register a free 1 month Trial Account.

✔ Download as many books as you like (Personal use)

✔ Cancel the membership at any time if not satisfied.

✔ Join Over 80000 Happy Readers

the handbook of japanese adjectives and adverbsDefinitive diagnosis is now made earlier as well as more correctly than in the past. The physician is faced with a host of tests and measurements which can be done on the patient?s blood, serum, plasma urine, stool, exudates, transudates, secretions, or other fluids. The problem is to choose those tests which will give the greatest amount of information in the most efficient manner and for the least possible cost. This guide book will be apply for the opinion of the department members to enrich it and rewrite it according to the requirements of the curriculum as a revision for medical students and for candidates taking the master degree in Health sciences.Clinical laboratory studies have immeasurably advanced the medical diagnostic process. Defin itive diagnosis is now made earlier as well as more correctly than in the past. The physician is faced with a host of tests and measurement s which can be done on the patient?s blood, serum, plasma urine, stool, ex udates, transudates, secretions, or other fluids. The problem is to choose those tests which will give the greatest amount of information in t he most efficient manner and for the least possible cost. This guide book will be apply for the opinion of the d epartment members to enrich it and rewrite it according to the requirements of the curriculum as a revision for medical students and for candidates taking the master d egree in Health sciences. I hope this proposal book will be accepted as helpful guide that t hrough ed ucation medical laboratories will be used in such a manner so a s to result in optimal care for all patients. G.A.H 20 12 Central Ner vous System Cerebrospinal Fluid 11. Articular S ystem 12. Infectioius Diseases 14 9 156 170 13. T umor Markers 14. Appendix I: Laboratory Abbreviations 1 80 189 Appendix II: Normal Reference Range 12. Bibliography 1 201 206 Clinical laboratory studies have immeasurably advanced the medical diagnostic process.http://www.visualmotion.nl/uploads/dell-xps-m1210-laptop-manual.xml

    Tags:
  • the handbook of japanese adjectives and adverbs pdf, the handbook of japanese adjectives and adverbs, the handbook of japanese adjectives and adverbs, the handbook of japanese adjectives and adverbs worksheets, the handbook of japanese adjectives and adverbs adjectives, the handbook of japanese adjectives and adverbs verbs, the handbook of japanese adjectives and adverbs examples.

Definitive di agnosis is now made earlier as well as more correctly than in the past. The problem is to choose those tests which will give the greatest amount of infor mation in the most efficient manner and for the least possible cost. This guide book will be apply for the opinion of the d epartment members to enrich it and rewrite it according to the requirements of the curriculum as a revision for medical students and for candidates ta king the master degree in Health sciences. I hope this proposal book will be accepted as helpful guide that t hrough education medical laboratories will be used in such a manner s o as to result in optimal care for all patients. G.A.H 2012 Va riation occurs not only in the use of the pathology and radiology facilities, but also in the use of specialist referral. Pathological and radiological investigations are executed by skilled personnel using complex techniques. Human and technical errors are inevitable, as in all branches of medicine. The practicability of a test va ries with the time, expense and skill involved in its perf ormance. The accuracy of a test is the nearness with which the result approaches the true result. The precision is the reproducibility of the result on t he same sample. Laboratories should be able to quote a “reference i nterval” for ea ch test performed. This is the range within which the result for that test would fall for 95 of a normal population. It follows that 5 of normal individuals will have a result outside that reference interval. If a large profile of tests is performed on one individual, on average 1 in 20 test results will be outside its reference interval. In to be confident that a result is abnormal or a change is clinically significant one needs to know: 1. The analytical error of the method used 2. The stability of the analyses in health ( i.e physiologic al variation) Errors of labeling and identification wi ll always occur and put at least two patients at risk.http://bajajsports.com/userfiles/dell-xps-desktop-computer-manual.xml They may happen at any of the several steps between taking the sample and interpreting the report. Samples must be put into co rrect prelabelled bottles and taken promptly to the laboratory. Samples are often taken by incorrect techniques. Blood is occasionally taken from an arm into which an infusion is running. Prolonged venous occlusion before venesection raises the concentration of proteins, cells a nd protein-bound constituents in the blood. Clenching the fist raises the concentration of pyruvate, lactate and creatine kinase. Phosphate, glucose and some hor mone levels vary with the time of day. If blood samples are left standing, potassium, phosphate and lactate dehydrogenase leak from red Hemolysis has a similar effect the concentrati on of serum proteins. Saliva is often sent to the la boratory instead of sputum. Urine collections are notoriously inaccurate, partly be cause of difficulties with bladder emptying and partly because of difficu lties patient s experience in complying with instructions. It must be clearly explained that the first urine is discarded in a timed collectio n but all other specimens including the last must be included. Interpretation of Tests There can be few tests which when positive indicate the presence of a disease and when negative indicate its certain absence. The dis criminatory ability of tests is described in terms of sensitivity, specificity and pr edictive value Sensitivity This indicates the percentage of people who actually have the disease in whom a particular test is positive. Ninety-five per cent sensitivity implies 5 false negatives. Increase in sensitivity may reduce specificity. Screening tests should be sensitive. Specificity This is the percentage of people without the disease w ho have a negative test. Ninety-five per cent specificity implies 5 false positi ve. Specificity is sometimes increased at the cost of sensitivity. Definitive test should be specific.http://schlammatlas.de/en/node/22257 Predictive value Predictive value (posttest probability) of a positive test: Probability of a disease being present if the test is positive. Positive value (posttest probability) of a negative test: proba bility of a disease being absent if the test is negative. Prevalence (pretest probability): the frequency of patients w ith a certain disease in the group being tested with the measurement. Diagnostic sensitivity: the percentage of true -positive results in healthy patients TABLE 1.1: PREDICTIVE VALUE No with positive test result No with negative test result Total No. FP: False positives; the number of subjects free of the disease who are misclassified by the test. TN: True negatives; the number of the subjects free of the disease who are correctly classified by the test. FN: False negatives; the number of sick subjects miscla ssified by the test. Theref ore only one in f orty will be higher and one in forty lower, so a sli ghtly abnor mal result. Also, a result near the ed ge of normal may be abno rmal for that individual. Narrowing of the normal range may be possible if the population gr oup is mo re clearly defined with regard to sex, age, ra ce and pregnancy. Serum urea levels are higher in the old and lower in pregnancy. With some tests, methods differ between laboratories and the local normal results will vary. Measured with a spectrophotometer. An end- point method can be used to measure the concentrat ion of a substrate (e.g. The technique hashigh sensitivityi.e.isable to m easure lowconcentrationsofAg (nM to pM range).The mean is the average of a set of measurements. The mode is the most frequently occurring value in a set of measure ments. Accuracy ca n be determined by compari ng the technic in use with another technic for perfor ming the same measurement. Agreement of the two measurements by diff ering technics suggests accuracy.https://laurenmitchellband.com/images/96-honda-accord-manual-transmission-for-sale.pdf In practice, automated and hand methods can be assessed against each other, newly introduced methods against older, esta blished methods and a method of one laboratory agai nst the same or different method of another laboratory. The latter often involves use of commercial standards. Testing for recovery of known amounts of dded material to the sample ana lyzed is another way of determining accuracy. Rapid and accurate diagnosis of cardiac problems is a routine requirement in emergency departments. In this chapter, we discuss the common emergency disorders e.g AMI, rheumatic fever, hypertension, congestive cardiac fa ilure and shock and the information about cardiac enzymes, lipid disorder s, Antistreptolysin O and C-reactive protein. CARDIAC ENZYNES LACTATE DEHYDROGENASE (LDH) AND ? -HYDROXYBUTRATE DEHYDROGENASE (HBDH) The enzyme LDH is found in the cells of many tissues especially the heart, liver, RBC, Kidney, Skletal muscle, brain and lung. Because LDH is widely distributed thr ough the body, the total LDH level is not a specific indicator of any one disease or indicative of injury to any one orga n. When disease or injury affects the cell s containing LDH, the cells lyse and LDH is spilled into the blood stream where it is identified in higher than normal levels. The LDH is a measure of total LDH. Actually five sepa rate fractions (isoenzymes) makes up the total LDH. LDH consist of 5 separ able proteins, each made of tetrameres of 2 types of subunits H and M. TABLE 2.1: THE FIVE ISOENZYMES OF LACTATE DEHY DROGENASE (LDH), THEIR STRUCTURE, RELATIVE DISTRIBU TION IN SERUM AND ACTIVITY Isoenzyme Structure activity in serum Causes Speed in el ectrophoresis LDH1 LDH2 LDH3 LDH4 LDH5 HHHH HHHM HHMM HMMM MMMM 30 40 20 3 7 Heart muscle, RBC, Renal Reticuloendothelial system and heart Lung and other tissues Kidney, placenta,pancreas Liver and striated muscle Fastest electrophoretic mobility Slowest electrophoretic mobility The 5 Isoenzymes can be distinguished by Kinetics, ele ctrophoresis, chromatography and immunologic characteristic. Indications Suspect of myocardial infarction Follow-up of myocardial infarction Suspect of pulmonary embolism Differential diagnosis of icterus Diagnosis of organic damage This method is quite simila r to the colorimetric method for LDH. HBDH activity was principally associated with fast mo ving of LDH1 characteristic of heart muscle. Lysi s of t hese c ells c auses t he LDH to po ur out int o the s pecimen blood a nd fal sely e levate the L DH lev el. Sternuo us exe rcise m ay ca use el evatio n of t otal L DH and speci ficall y LDH1, LDH2 an d LDH5. Drugs t hat may caus e incr eased l evels inclu de anes thetic s, aspi rin, clofibr ate, m ithram ycin, narco tics an d proc ainami de. Drugs t hat may caus e decr eased levels inclu de asc orbic acid. CLINIC AL PRIO RITIES 1. Becau se LDH is wi dely d istrib uted th rougho ut the body, the t otal L DH lev el is not a s pecifi c indi cator of an y diseas e or organ i njury. Isoe nzyme i s more specifi c and helpfu l diag nosti cally. 2. When LDH1 is gre ater th an LD H2 myoc ardial injury is strong ly sus pected. This m ay be r eferre d to a s a “f lipped LDH” 3. Isol ated el evatio n of L DH5 u sually indic ates he patoce llular injur y or di sease. Serum L DH Incr eased in 1. Myoc ardial infar ction: elevat ion o f LDH1 and to a les ser d egree L DH2. 2. Pulm onary emboli sm: in 60 of pati ents. LDH3 and LD H4 3. Live r dis ease: L DH5. 3. Skle tel mu scle d isease: LDH 5 Serum CK level s are eleva ted wh en thes e mus cles or nerve cells are in jured. CK levels can ri se wit hin 6 hours, afte r damag e. If damag e is n ot pers istent, the levels peak a t 18 h ours a fter injury and r eturn t o nor mal in 2 to 3 days. CK spli ts cre atine phosph ate in the p resenc e of AD P to y ield c reatin e and ATP. Skletel, hear t musc le and brai n are rich in th is en zyme. CK -ISOENZ YME MB -Isoen zyme of heart muscle incre ased i n acut e myoc ardial infarc tion and cardiac surge ry. MM ISO ENZYME is incre ased i n skle tel mu scle BB -ISOEN ZYME is iso enzyme of bra in, in crease in ma lignan t hype rthermi a, uremia, lung, cardi ac ons et wi th brai n anox ia and necro sis of large i ntes tine. MiMi-I SOENZYM E (mito chond rial is oenzym e), is incre ased in Myoc ardial infarct ion, R eye's syndro me, m alignan t tumo urs an d nec rotic l iver di seases. IM inj ection s can cause elevat ed CK l evels. ? Sterno us exe rcise and re cent s urgery may ca use in crease d leve ls. ? Early pregna ncy may produ ce dec rease d level s. ? Drugs may ca use inc reased leve ls: am photeri cin B, ampi cillin, some anesthe tics, antico agulan ts, as pirin, clofi brate, dexam ethas one, l asix, c aptopr il, colchi cine, alcoho l, lov astati n, lith ium, l idocai ne, Pr opran olol, Succiny lchol ine and mor phine. Hig h leve ls may indic ate th at sign ifican t inf arctio n has already occur red, t hus pr ecludi ng a b enefit from thromb olytic thera py. Hyp othyro idism. 13. Hyp okalem ia INCREAS E OF CK IN T ISSUE DISORD ER 1. Necr osis o f panc reas 2. Col on canc er 3. Acut e live r cell necro sis 4. Preg nancy a. Skle tel mu scle C K- MM b. Uter us mus cle CK - BB 5. Mali gnancy of or gans ( CK-MM, CK-BB and CK -MiMi) MYOGLO BIN Myoglo bin is a glob in com plex s imilar to hem oglob in but prese nt in muscle tissue. It is excr eted in the u rine by way of glo merul ar filt ratio n. Its excret ion increas es in circum stances inv olving any mu scle c ell da mage. In the presenc e of a norm al tota l CK concent ration, norm al serum a nd uri ne myo globi n level s, and elect ricardi ogram (ECG) findin gs lim ited to sho rt-live d ST a nd T w ave ch anges, MI ca n usua lly be ruled out in patie nts with u nstable angin a. Mo re frequen tly, a retu rn to n ormal takes at le ast 24 hours. Seru m myog lobin may appear interm ittent ly in the fi rst 6 to 18 hours after an MI, and s erial determi nation s may be ind icated. Myoglo bin in creases can a ppear in the urine withi n 3 ho urs af ter an MI. Levels may re turn t o hig h norm al in 3 0 hours; usu ally, h oweve r, retu rn to normal takes 72 hou rs or longer. MYOGLO BIN LEV ELS IN CREASED IN 1. Card iac mu scle d amage 2. Skle tal mu scle d amage, most freque ntly i n crus hing i njuri es 3. Fami lial m yoglo binuri a (Meyer -Betz diseas e) 4. High fever s, St ress (e.g hyp ertherm ia an d vigor ous ph ysical activ ity. I n suscept ible p ersons, feve r can cause muscle destru ction 5. Unco mmon occuran ces wi th diab etic acidos is, hyp okalem ia, or barbi turate poison ing Tropon on Cardiac Tropo nin T (cTnT) and c ardiac Tropo nin I (cTnT ) is a s ensiti ve te st during the fi rst 4 8 hours afte r AMI w ith 80 sens itive for up to 5- 7 days but no t sensit ive fro m 0-4 hours. Diag nostic effici ency i s sim ilar t o CK-MB in e arly AMI until fifth day. It is s ensiti ve mar ker fo r min or myo cardial injur y in u nstabl e angi na with out AMI. It is u seful in di agnosi s of pr eopera tive AMI whe n CK-MB may be incre ased b y skeleta l mus cle inj ury.T he enzymes are pres ent in high c oncentra tions in muscle, li ver and b rain. The re are two majo r isoenzym es, cyto plasmi c and mitoch ondrial. Both enzymes have been demonstrat ed in plasma following tissue damag e, but th eir di fferent iation has not b een s hown to be of much diagnos tic val ue.Drugs that may cause increased levels incl ude; anti hyperte nsive, cho linerg ic agents, coumarin type anti coagul ants, digital s, erythro mycin, INH, methyldopa, oral co ntracept ive, op iats, s alicyl ates, ve rapamil and hep atotoxi c medica tions. LIPID D ISORDE RS Unequi vocal e vidence has d emonst rated a n incre ased ri sk of coronary heart disease in persons younger than age 50 who have an elevated total cholestero l level. How ever, eviden ce for elevated trigl yceride levels, as an independent risk factor f or coro nary he art dis ease is inconc lusive. The major lipoprote in, can be classified accordin g to d ensity (weigh t per vo lume) o r to el ectrop horetic mobil ity. Decreas ed ser um cho lester ol in hyperth yroid ism, ma lnutr ition, chroni c anem ia, cortis one and ACTH therap y, Abet alipop rotein emia an d Tan gier d isease. SERUM HD L- CH OLES TEROL HDLs ar e carri ers o f chol estero l. They are produc ed in the li ver an d to a small er degree, in th e inte stine. The purpos e of HD Ls is believ ed to be rem oval o f the choles terol f rom th e peri pheral tissu es and trans port to the liver for ex cretio n. Also, H DLs m ay have a pro tective effec t by p revent ing c ellular uptak e of choles terol an d lip ids. T hese potent ial act ions m ay be the s ource o f the prote ctive cardio vascul ar char acteri stics associ ated w ith HD Ls (goo d cho lestero l) wit hin th e blood.Smoki ng and alcoho l inge stion decreas e HDL levels. Binge eating can al ter li popr otein values. HDL val ues a re age and s ex dep endent SERUM L DL -CHOLES TEROL LDLs ar e also chole sterol rich. Chol esterol carri ed by LDLs c an be deposit ed int o the per ipheral tiss ues an d is associa ted wi th an increa sed ri sk of arteri oscler otic heart a nd peri pheral vasc ular di sease. Ther efore h igh le vels of LDL (bad choles terol) are at heroge nic. LDL is ver y diff icult to iso late a nd meas ure. To a lesse r degr ee, VLD L, are also associ ated w ith an incr eased risk o f art eriosc lerotic occlu sive disease. CLINIC AL PRIO RITIES 1. Lipo protein s are consid ered t o be p redict ors of heart disea se. Bl ood le vels sh ould be coll ected after a 12 t o 14 h ours fast. 2. HDL i s ofte n call ed GOO D CHOLE STEROL becaus e it remove s chol esterol from the tis sues and tra nsports it to the liver for ex cretio n. Hi gh leve ls are associ ated with a decrea sed ris k of corona ry hea rt dis ease. 3. LDL i s ofte n call ed BAD CHOLES TEROL, becau se it carrie s chole ster ol tis sues. High levels are as socia ted wi th an i ncrea sed ri sk of C HD. The ASO tite r is a serolo gic p rocedur e demo nstrati ng th e react ion o f the body t o infecti on cau sed by group A bet a hemo lytic s trept ococci. The strept ococcus organis m prod uces an enzy me call ed st reptoly sin O, whic h has t he abi lity t o destroy (lyse ) red blood corpu sceles. Becau se str eptoly sin O is anti genic, the body re acts, by pro ducing ASO, a neut ralizi ng ant ibody. ASO a ppears in th e serum o ne week to 4 weeks after the on set of a str eptoco oal in fectio n; a h igh ti ter is not spcifi c for a cert ain ty pe of postst reptoco ccal diseas e (i.e GN, R F) but merely indica tes th at a st repto coccal infect ion is or h as bee n pres ent. When AS O elev ation is see n in a patie nt wit h glome rulon ephriti s or endocar ditis one can safel y assu me tha t the diseas e was caused by st reptoc occal infect ion. ASO is o f no value for di agnos ing acu te str eptoco ccal i nfecti on. Cu ltures for strepto cocci are re quired for that. The hig hest i nciden ce of posit ive re sults i s duri ng the thir d week after the on set of acut e symp toms o f the strept ococcal disea se. By 6 mo nths, o nly 30 of patient s have abnor mal ti ters. The upp er nor mal li mit in norm al pers ons o f ASO t itre i s 150-2 00 uni ts. ASO is n ecess ary in A. Dir ect dia gnosti c in s carle t fever, erys pieles, stre ptoco ccus ph aryngi tis an d tonsil litis. B. Indi rect d iagno stic in rh eumat ic feve r and glomer ulone phritis. Interfe ring f actor s. Increas ed be ta lip oprotei n neu tralize ASO a nd cau se fal se pos itive ASO ti ter. Drugs that c ause de creas ed ASO includ e anti biotic s and steroi d C. REAC TIVE P ROTEIN C polys acchar ide of the p neumo coccus is pro bably an alp ha glo bulin, perha ps bound t o seru m lipi d. It is fo und in the se rum of norm al indi vidual. Its product ion is stimu lated by bac terial infe ctions, vario us py ogenic agents or the product s of i njured tissu es. It is o ften f ound in the serum of pa tients with. Active bacte rial in fecti ons. Active rheum atic f ever. Acute m yocard ial in farct ion. Active rheum atic a rthriti s. Active TB The CRP test is a m ore se nsitiv e and r apidly resp onding indica tor th an the ESR. In an acut e infl ammato ry chan ge, CR P sho ws an earlier and more in tense increas e than ES R; wit h reco very, the di sappea rance o f CRP prece des the retur n of E SR to normal. The C RP als o disa ppears when t he inf lammat ory pro cess i s supp ressed by anti inflam matory agent s, sal icylat es or steroi ds. This t est is also u seful in eva luatin g pati ents w ith an acut e myoca rdial infarc tion. The lev el of CRP co rrelat es wi th peak level s of t he MB isoen zyme of creat ine Fail ure o f CRP to nor malize may indicat e ong oing d amage t o the heart tissue. Level s are not e levate d in-p atients with an gina. This t est als o may be use d pos toperati vely to det ect wo und in fection s. CRP level s increas e with in 4 t o 6 ho urs af ter sur gery and ge nerall y begi n to de crease after the third p ostope rative day. Failu re of t he lev els to fall is an indic ator o f compli cation s, such as in fecti on or p ulmon ary inf arction. Interfe ring F actor s. An int rauter ine dev ice m ay cau se pos itive t est b ecause of tis sue i nflamma tion. ? Oral co ntrac eptive s may c ause increa sed lev els. Salicy lates and st eroids and cause d ecreas ed lev els. ACUTE MY OCARDI AL IN FARCTIO N Ischem ic myo cardial necro sis is us ually resulti ng fro m abru pt red uction in coronar y bloo d flow to a segmen t of m yocard ium. It is ch aracter ized b y pericar dial p ain. F or amb ulato ry pati ents w ho are seen in th e emerg ency departm ent wi th cli nical findin gs of acute m yocardi al in farcti on (AM I), dec ide on hospit al adm ission by usi ng the histo ry, phy sical examin ation, and electro cardio gram ( ECG). 1. Signs and symptoms: The pain of MI, unli ke angina pectoris, usually occurs at rest. The pain is similar to angina in location and radiation but is m ore severe and builds up rapidly. Usually it is described a s a retrosternal tightness or squeezing sensation or sometimes a dull ache. Radiation to t he left shoulder is not uncommon. Other symptoms include sweating, wea kness, dizziness, nausea, vomiting, and abdominal discomfort. Abdominal disco mfort is especially common in inferior wall MIs. 2. ECG changes: The classical evolution of changes is from peaked (hyperacute) T wave, to ST segment elevation, to Q wave development, to T wa ve inversion. This sequence may occur over a few hours or may take several days.(Note): If ECG changes are not present, do not assume an MI has not occurr ed. If signs and symptoms suggest MI, it is an MI until proved other wise. 3. Confirmatory evidence: Evidence of infarction is c onfirmed by elevation of CK- MB fraction or Troponin 4. Other diagnostic procedures: S cintigraphic studies including technetium- 99 and thalium201 imaging and radionuclide angiography, a s well as echocardiography, may help document the extent of th e damage. Labora tory F inding A. Myocar dial E nzymes: The cardi ac enzy mes mo st ass ayed a re crea tine k inase (CK), s erum gl utami ne oxa loacet ate tr ansami nase ( SGOT) and l actate dehydro genase (LDH). Each enzym e has a parti cular time c ourse for re lease into the vas cular compar ment f rom i rrevers ible d amaged heart cells durin g acute myocard ial in farcti on. Fo r pati ent adm itted to the hosp ital wi th cli nical f inding s of A MI, r equest serial measure ments o f CK and C K isoen zyme. Serial measur ement s of LD H and LDH isoenzy mes ma y be h elpful. Seru m tran samins e measu remen ts are unnece ssary. CK -MB, t he myo cardi al comp onent of cre atine kinase, is fo und in blood within 5 hou rs of m yocardi al n ecrosis. CK -MB is highl y sensi tive, and th eir abs ences in the seru m virtu ally e xclude the diagnos is of acute infarc tion. Routin e measu rement of CK -MB on admis sion an d 6-8 h for t he fir st 24 h will confirm or re ject t he dia gnosis. Norm al CK-M B for 24 h v irtual ly rul es out MI. If the test results show a cha racteri stic rise an d subs equen t fall of CK and CK -MB in the contex t of appropr iate clinic al find ings, concl ude th at the diagno sis i s AMI 2. GOT: G OT sta rt to rise a bout 8- 12 hou rs aft er in farcti on and reach ed a pe ak in the fir st or secon d day. 3. LDH: is li berate d from hemo lysis of red cells and is there fore l ess sp ecific. It starts to ris e afte r 24 hours; reac hes a peak after 3-5 day s. It i s use ful wh en the diagnos is is in dou bt sev eral d ays af ter po ssible infar ct. The iso enzyme s of LD H tha t are i ncreas ed ar e LDH1 and L DH2. An elev ated LDH1:2 isoenzy me ra tios a re typ ical o f myoc ardial infar ction and we re 96 sensit ive an d 97 s pecifi c. TABLE 2. 4: TIME COURSE O F RELEA SE OF CAR DIAC ENZ YMES AND TROPON IN DURIN G ACUTE MYOCAR DIAL INF ARCTIO N Become elevat ed (HRS) PEAK (HRS) Return to normal Myoglo bin 3- 5h 12 24 - 30h CK 4- 6h 18h 2-3 days SGOT 8- 12 18 - 3 6h 3-4 days LDH 24 - 48 72 - 120 8- 14days Tropon in T 4-6 10 - 24 10 days If seri al mea sureme nts fo r seru m CK, C K-MB, and LD H are normal in a patient seen early after the o nset of clini cal fi ndings of A MI, exc lude A MI. There i s a re lation ship b etween the p eak ser um co ncentr ations of CK, CK-MB, and LDH and s ize of the A MI, wit h larg e inf arcts p roduci ng hi gher v alues. This relatio n is s trong er with CK an d CK-M B than with LDH. In pati ents w ith cl inical findi ngs o f AMI b egin t hrombo lytic therapy as e arly as possi ble w ithout waitin g for enzym e and i soenzy me res ults. Measu re a seri al level o f seru m CK-a nd CK- MB to m onitor therap y. Ideally, in i ndivi duals w ithou t cont raindi cations throm bolyt ic agen ts sho uld be used wi thin 2 to 3 hours of th e onse t of fi ndings. Wait ing m ore th an 4 ho urs is to o long. B: Prot eins c ontain ing su bstanc es: My oglobi n and tropo nin Increas e seru m myog lobin peaks and myo globi nuria o ften occur and ret urn to nor mal ear lier t han CK, usef ul for diagn osis w ithin 6 hour s of on set of sympto ms. N.B: Th rombol ytic ag ents (e.g S trepto kinase, uroki nase, tissu e plasm inogen activat or alt er the enzym e patt erns. Tropon in is a prote in com plex co nsist ing of three isoty pes (T,I and C). Tropon in T an d trop onin I have the po tenti al to b ecome better diagn ostic markers for a cute m yocardi al in farctio n tha n exist ing en zymes (such as CK- MB), because these cardi ac iso type a re dis tinctl y diff erent from s kletal isotyp es. Se rum tropon in appe ars ea rlier than C K but p resent s 4 ti mes la reger, diagn ostic effecie ncy si milar to CK- MB in early M I unt il 5 th. At the prese nt tim e trop onins are mai nly us ed in emerge ncy dep artmen t, wit h a ce nte r wher e the patien t can be mon itored for s everal h ours while a wait ing te st res ults. Then a decisi on can be ma de reg ardin g admi ssion to the cardia c care unit o r dischar ge to home. In pati ent wi th AMI the f ollow ing add ition al abno rmal blood test r esults may occur. Increas e Hem atocrit. ESR is inc reased usuall y by the sec ond or third day, peak r ate re ach in 4-5 th day and persi st fo r 2-6 m onths. Increas ed ESR some t imes is mo re sens itive than W BCs. Degree o f incr eased ESR does no t corr elate with t he se verity or pr ognosi s. ? Decre ased pH with metabo lic a cidosi s caus ed by t issue hypo xia. ? Decrea se art erial pressu re of oxygen (PO2) from c ardio pulmon ary even with out compli cation s. ? Increas e glu cose r elated to d iabetes melli tus as a pre dispos ing ri sk fac tor or simply secon dary to the st ress of the infar ct. ? In str ess hy pergly cemia. Hemog lobin A1C is no rmal. ? Increas e ure a nitr ogen a nd crea tinine relat ed to decrea sed re nal p erfusio n. ? Decrea se pot assium caused by e ither a high level of ci rculat ing ca techol amines or previou s diur etic t herapy.RHEUMA TIC FE VER Multisy stemic disea se of i nflam matory lesio n with affec ting t o conn ective tissue s, whic h invo lve pr edomi nantly: Joints, hear t and kidne y. It i s mos t common cause of acq uired heart diseas e. Clinic al Mani festat ion: D iagno sis dep endes on 1. Modif ied Jo nes cri teria “1992 ” MAJOR CR ITERIA MINOR C RITERI A. Pancar ditis ? Polya rthriti s ? Sydenh am?s c horea ? Eryth ema mar ginatum. Subcut aneous nodul es. Fever ? Arthral gia ? Previo us rhe umatic heart di sease o r rheumat ic fever. Increa sed ESR ? Increa sed C-rea ctive pr otein. Increa sed PR interva l “1 st degre e heart block” Diagnos is is d one by 2 major or 2 min or and 1 major criteri a Plus 2.