MIME-Version: 1.0 Content-Type: multipart/related; boundary="----=_NextPart_01CA5F17.4738C5F0" Tento dokument je webová stránka tvořená jedním souborem, rovněž nazývaná soubor webového archivu. Zobrazí-li se tato zpráva, znamená to, že prohlížeč nebo editor nepodporuje soubory webových archivů. Stáhněte si prohlížeč, který podporuje webový archiv, například aplikaci Windows® Internet Explorer®. ------=_NextPart_01CA5F17.4738C5F0 Content-Location: file:///C:/228A91F9/mineraly.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Minerální hospodářství

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Miner<= b>áln<= b>í hospodářství
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BxIsaPAgwoQKFzJs6PAhxIgSJ1KsaPEixowaN3Ls6PEjyJAiR5IsafIkypQqV7Js6fIlzJgyZ9Ks afMmzpw6d/KU6eAn0KBChxItavQo0qRKlzJt6vQp1KhSp1KtavUq1qxat3LtOvQB2LBix5Ita/Ys 2rRq17Jt6/Yt3Lhy59Kta/cu3rx69/Lt6/cv4MCCByoTLmz4MOLEihczbuz4MeTIkidTrmz5MubM mjdz7uz5M+jQokeTLm0acUAAO0== ------=_NextPart_01CA5F17.4738C5F0 Content-Location: file:///C:/228A91F9/mineraly_soubory/slide0002.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii" Minerální hospodářství
Osmolalita
Je dána celkovým p= očtem částic rozpuštěných ve = vodní fázi, bez ohledu na jejich absolutní velikost. Relativně nejspolehliv= ější vzorec pro vý= ;počet osmolality v séru
2x Na+ + urea + glykémie = ;
Hlavním činitelem v sé= ru je tedy Na+, jehož změny koncentrace jsou = spojen= y s přesuny vody do buněk a z nich.
Regulační systémy udržují osmolalit= u v úzkých mezích (sekrece ADH je stimulována při hodnotě 287 mosmo= l/kg= H20 a inhibována při hodnotě 283) =
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Celková a efektivn&iacut= e; osmolalita
Celk= ová a efektivní osmolalita: na celkové osmolalitě se podílejí například urea a ethylalkohol, protože však pronikají do buněk pasivně podle koncentračních gradientů, nevykonávají žádný osmotický tlak na membránách.
Proto např. p= ři hyponatrémii kombinované s vysokou moč= ovinou naměříme normální nebo vyšš&iacut= e; osmolalitu, ale efektivní osmolalita je nízk&aacut= e;.
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Osmolalita
osmolalita v sé= ;ru 275 - 295 mosm/kg H20 =
osmolalita v moči - široké rozmezí
Skutečná osmolalita se můž= ;e lišit od vypočítané= až o 25 mosm/kg, při acidémii jsou častější vyšší hodnoty měření než výpočtu, v alkalémii byly naopak výpočty vyšší= ; než měř= ;ení (souvislo= st se změnami disociací v iontových systémech).= Rozdíl mezi měř= ;ením o výpočtem se rovněž= ; zvyšuje při intoxikacích látkami o malé molekule.
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Hyperosmolarita
P&ia= cute;iny&= #13;
<= span style=3D'font-size:88%'>ztráta prosté vody
<= span style=3D'font-size:88%'>akutní hyperkatabolismus
<= span style=3D'font-size:88%'>diabetické koma, hyperosmolámí koma bez acidózy
<= span style=3D'font-size:88%'>popáleniny
<= span style=3D'font-size:88%'>nesprávná TPV
<= span style=3D'font-size:88%'>akutní intoxikace látkami o malé molek= ule
<= span style=3D'font-size:88%'>diabetes insipidus
P&ia= cute;znaky =
    = žízeň, bolesti hlavy, malátnost, halucinace, koma
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Hypoosmolalita
Příčiny
   metabolická odpověď na trauma
   nadbytek celkové vody  
   úhrada ztrát izotonické tekutiny v= odou
   chronický katabolismus
Příznaky=
slabost, nevolnost, apatie, křeče, koma
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Osmolalita v moči
•<= /span>důležité jsou denní odpady
•<= /span>nemocní v tě= 82;kém katabolismu mají ztráty až 1200 - 1400 mosmol (výjimečně 2000 - 3000 mmol), k vylouení této nálože je zapotřebí množství vody, zejména jsou-li zároveň poškozeny tubulámí funkce (u nemocných v kritick<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman"'>ém stavu velmi často)
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Sodík - Na+ 
denní příjem Na potravou se pohybuje okolo 140 - 260 mmol/l
•<= /span>vylučován je především močí (90 % denního obratu)
dále stolicí a potem
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Fyziologické pozná= ;mky
Na+ = je hlavním kationtem extracelulární tekutiny (ECT), kde se vyskytuje v koncentr= aci 137-147 mmol/l &#= 13;
<= span style=3D'font-size:75%'>Koncentrace v intracelulárn&= iacute; tekutině - ICT je podstatně nižší = ;
     <= /span>5-30 mmol/l podle druhu tkáně
Celkový obsah Na+ = intracelulárně je však vyšší= ; než celkový obsah v ECT. V akutn= ích stavech se však mění především obsah a koncentrace v ECT. =
Z klinického hlediska je běžné stanovení koncentrace Na+ v s&= eacute;ru, vyšetřování obsahu Na+ v organismu se prakticky = neprovád&iacu= te;
Změna koncentrace Na+ v ECT můž= ;e být vyvolána změnou = obsahu Na+, ale i změnou obsahu vody = ;
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Hypernatrémie=
R= 26;Vzestup koncentrace Na+ v CT nad re= ferenn&ia= cute; mez  (klinicky z&aa= cute;van&ya= cute; je vzestup nad 150  mmol/l)
R= 26;Zvýšen&i= acute; zásob Na+ obvykle nevede k hypernatr<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:75%'>émii, neboť dojde ke stimulaci tvorby antidiuretického hormonu, retenci vody a k aktivaci dal<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:75%'>ších regulačních mechanism<= span style=3D'mso-bidi-font-family:"Times New Roman";font-size:75%'>ů =
Pří= činy hypernatrémie:
       dehydratace
        diabetes insipidus <= /span>    
        ztráta hypotonických tekutin z GIT
       snížený p<= span style=3D'mso-bidi-font-family:"Times New Roman";font-size:75%'>říjem tekutin
       hyperaldosteronismus
        iatrogenní vlivy - pod<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:75%'>ání konc. roztok= ů NaCI, TPV, hem= odialýza
Klinický obra= z závisí na rychlosti rozvoje stavu a na příčině
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Hlav= n&ia= cute; kli= nick&ea= cute; p&ia= cute;znaky hypernatrémie : <= /span>
- žízeň (můž= ;e chybět u poruch CNS nebo = ve stáří)
- snížený turgor ko= ž
- zvýšení tepové frekvence, orthostatická hypotenze
- bolesti hlavy, křeče, koma <= /div>
R= 26;Pro diagnózu stavu je nutné stanovení koncentrace Na+ v ECT (v séru) a stanovení osmolality, důležité jsou rovněž= ; nálezy Na+ a osmolality = v moči - zpravidla b&yacu= te;vá hyperosmolární moč, výjimkou je diabetes insipidus
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= 226;     Hype= rnatrémie + snížení objemu ECT= - stav provázen sníženým turgorem kožním
R= 26;     Hypernatrémie = + zvýšen&ia= cute; objemu ECT (obsah <= /span>natria v ECT je zvý<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman"'>šen ještě více než obsah vody) - stav je provázen zpravidla periferními edémy, ale i projevy stázy na plicích, zvýšenou náplní krčních žil
= Léčba: terapie příčiny, podání <= /span>hypoosmolálních roztoků= m diuretika pouze při současné expansi ECT
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Hyponatrém= ie
   snížení koncentra= ce Na+ v ECT<= span style=3D'mso-spacerun:yes'>     
= 226;   je-li deficit natria spojen se současným deficitem vody -při vyšetřen&= iacute; tuto změnu nezachytím= e     
Příčiny stavu:
         <= /span>sn<= /span>ížený p<= span style=3D'mso-bidi-font-family:"Times New Roman";font-size:88%'>říjem nebo zvýšená ztráta Na+ 
       ztráty mohou být extrarenáln&= iacute; (kůž= ;í, krvácením)         = ;            &n= bsp;            = ;            &n= bsp;         = renální (při osmotické diuréze)
= 226;endokrinní příčiny aha aha aha        
Klinicky= : únavnost, slabost, bolesti hlavy a z&= aacute;vratě křeče, = delirantní st= avy a koma
Klinické nálezy: snížený turgor ko= žní, such&eacu= te; sliznice
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Dif. dg. jsou hyponatrémie trojího typu
1.s de= ficitem (v obsahu) Na+ (současně obvykle deficit ECT) příčinou jsou obvykle extrarenální ztráty
2.s no= rmálním obsahem natria a mírným nadbytkem ECT - p= říčiny - deficit kortik= oidů, hypothyreoidismus, t= ěž= ;ký stres s SIADH
3.hyp= onatrémie se zvýšeným obsahem Na+. <= /span>V těchto <= span style=3D'position:absolute;top:61.75%;left:6.74%;width:99.25%;height:8.25%= '>případech je nadbytek E= CT ještě vyšší= ; než nadbytek natria a vzniká relativní hyponatrémie (příčiny - = akutní nebo chronické renální selhání, nefrotický syndrom, jaterní cirrhóza, kardiální dekompenzace)
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= 226;Pro proveden<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:88%'>í dif. dg. nutno vyšetřovat CVT, koncentrac= i albuminu v sé= ru, hematokrit, osmolalitu, koncentraci chloridů a kalia v sé= ru a parametry ABR.
Pseudoh= yponatrémie
= 226;    = Sérum obsahuje 93 % vo= dy a 7 % pevných součástí Při zvýšení koncentrace protein= ů nebo lipidů (HLP) dochází k poklesu procentuáln&= iacute;ho zastoupen<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:88%'>í vody v plasm= ě a tím i k pokle= su zastoupení natria. Při vyšetření natria = plamenovou fotometrií najdeme hyponatrémii, která nevede ke sn<= span style=3D'mso-ascii-font-family:"Times New Roman";font-size:88%'>íž= ení osmolality s= éra (v důsledku přepočtu výsledku na celkový objem vzorku). Skutečná aktivita iontu na membránách je však normální (i stanovení ISE). =
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Kalium - K+ 
Denní příjem draslíku potravou je 40 - 90 mmol. V ECT je kalium v koncentraci 3.8 - 5.1 mmol/l. =
V ICT je koncetrace = řádově vyšš&iacu= te; podle druhu tk&= aacute;ně v rozmezí 90-160 mml/l
Vylučování draslíku: ledvinami 90 %, zbylých<= span style=3D'mso-spacerun:yes'>   10 % je vylučováno stolicí. V ledvinách se K+ volně filtruje do primární moče, v proximálním tubulu se ze 2/3 resorbuje a do definitiv= ní moče j= e vylučovan&= eacute; v distálním tubulu.
Kalemie v séru neodráží stav zásob kalia v organismu
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Hyperkalémie:=
<= span style=3D'font-size:75%'>vz&= aacute;cně z nadměrného příjmu (je-li normální funkce ledvin)
<= span style=3D'font-size:75%'>zpravidla při poruše funkce ledvin (zejména poruchy v oblas= ti
<= span style=3D'font-size:75%'>distálního tubulu)=
<= span style=3D'font-size:75%'>Addisonova choroba a hypoaldosteronismus
<= span style=3D'font-size:75%'>distribučn&= iacute; hyperkalémie (při přesunu K z ICT do ECT= při acidóze, &#= 13;
     <= /span>hyperosmolalitě, deficitu insulinu
R= 26;        = ;  Klinicky: změny funkce převodního systému myokardu, cha= rakteristické změny na EKG (vysoké ostré vlny T, prodloužení PQ) parestézie, křeče
R= 26;Opět je nutné vyšetřovat ABR a zm= ěny koncentrace kalia= a = osmolality v moči.
R= 26;        = ;  Terapie: glukóza s insulinem, hydrogenkarbonát sodný - při acidóze, iontoměniče (vážou v GIT draslík a neresorbují se), hemodialýza
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Hypokalémie:<= /div>
= 226;   Příčinou můž= ;e být deficit= K+ v organismu n= ebo porucha v distribuci kalia
= 226;        = ;         Píčiny hypokalémie: vzácně nedostatečpříjem kalia (u gerontů) častěji nadměrné ztráty - zejména při poruše ledvin (renální tubulární acidóza, polyurická fáze ren.selhání, chronická renáln&iacu= te; insufficience sal= uretika, masivn&= iacute; průjmy, ztráty <= /span>tekutin z dolních částí GIT, diabetick&aacu= te; ketoacidóza hyperkorticismus
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Klinický obraz hypokalémie:
•<= /span>převodní poruchy v myokardu, zvýšená citlivost na digoxin
•<= /span>svalová slabost, k&#= 345;eče, obleně<= /span>ná činnost střev - paralytický i1eus = ;
•<= /span>snížení koncentra= 69;ní schopnosti ledvin a následná polyurie (kaliopenická nefropatie)
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Vztah mezi K+ a acidobasickou rovnováhou
Při akutní metabolické acidóze,charakterizovan&eacut= e; hromaděním iontů H+ v ECT, přecház&= iacute; část těchto <= span style=3D'position:absolute;top:40.0%;left:8.05%;width:94.38%;height:8.25%'= >kationtů do buněk a výměnou za ně část kationtů K+ přechází= z ECT do ICT
     - v d= ůsledku tohoto děje stoupá kalémie.
<= span style=3D'mso-special-format:nobullet;display:none'>• Platí, že pokles pH o 0.1 se projeví vzestupem koncentrace K+ v ECT 0.4 - 0.6 mmol/1. Naopak = alkalóza způsobuje hypokalémii
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Chloridy – Cl- 
Příjem potravou v dosp<= /span>ělosti je 140-260 mmol chloridů denně= . &= #13;
téměř= ; stejné množství se vyloučí močí, malá část <= /span>potem (10 mmol denn<= /span>ě) a stolicí &= #13;
Dynamika změn koncentrace chlori= dů je podobná <= /span>změnám koncentra= ce Na+, které obvyk= le doprováz&iacu= te;. Nacházíme-li u pacienta změny koncentrace chlorid<= /span>ů beze změn koncentrace natria, jde velmi pr= avděpodobně o poruchu ABR se změnami koncentrace ost= atních iontů.
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Hyperchlorémi= e:
provází hypernatrémii a má obdobné příčiny
R= 26;hyperchloremick&aacu= te; metabolická acidóza (renální = tubulárn&iacu= te; acidóza)
  nedostatečný příjem (spolu s nedosta= tečným p<= span style=3D'mso-bidi-font-family:"Times New Roman";font-size:88%'>říjmem Na+)
  hypochloremie ze ztr= át (zvracení žaludečního obsahu) = nebo renální ztráty
Hypoch= lorémie:
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Celková bílkovina, albumin
<= span style=3D'font-size:75%'>S- TP 65 - 80 g/l, albumin 32 - 45 g/l <= /div>
Stanovené hod= noty informují o tom, za jakých podmínek je = udržována náplň cévního řečiště. Při poklesu klesá koloidně osmotický tla= k.
K poklesu plasmatických bílkovin a zejména albuminu dochází zejména po traumatu (únik albuminu do intersticia je součást&= iacute; metabolické odpovědi na trauma, plasmaexpandery - způsobí přesun vody z buněk do ECT - naředění. V této situaci není vyšetření celkových bílkovin, ale ani albuminu dostatečnou informac<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:75%'>í o koloidně osmotickém t= laku plasmy.
Proto je výhodné měř= ;it onkotický tlak, norm. hodnota 3.33 - 3.52 kPa
Jeho sledování má význam prognostický quoad vitam, jednak v predikci plicního edému
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Magnézium
S-Mg+, 0.= 7 - 0.9 mmol/l, moč 1.2 - 12.0 mmol/den
Celková zásoba v těle je 800 - 1150 mmo= l, z tohoto množství je 60 % vázáno v kostech, zbytek v měkkých tkáních, v játrech, příčně pruhovaných svalech. Mg+ je aktivátorem mnoha enzymových sy= stémů (oxidativní fosforylace, stabilizuje makromolekulámí struktury, m&aacu= te; význam při syntéze bílkovin, zlep<= span style=3D'font-family:"Times New Roman";mso-bidi-font-family:"Times New Rom= an"; mso-hansi-font-family:"Times New Roman";font-size:88%'>šuje průtok = koronám&iacut= e;mi arteriemi).
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Hypomagnesémie:
P&ia= cute;iny<= /b> - malnutrice, TPV bez magnesia, poruchy GIT, dekomp. DM, hyperaldosteronismus, cirrhosa jater, akutní pancreatitis, polyurická fáze renálního selhání
<= span style=3D'font-size:75%;color:yellow'>Klinick&ea= cute; p&ia= cute;znaky
R= 26;     <= /span>Objevují se při poklesu pod 0.5 mmol/l, je to nausea, zvracení, sklon k tetani&iacut= e;m, karpopedální spasmy, svalové fascikulace, tremor, spasticita, slabost, ataxie, deprese, psychotické chování= ;. Na EKG je deprese S-T a inverze vln T
Deficit= Mg+ = má vliv na metabolismus kalcia, kalia a fosforu: kalcium - pokles ztráty močí a pozitivní bilance, stoupá vylučování kaIia ledvinami, zvyšují se ztráty fosforu ledvinami
Terapie: př= i křeč= ích intenzivní léč= ba MgSO4 až= 16 mmol bě= hem 10 minut.  Dalš&iac= ute; supplementace je pomalejší,= vě= tšinou parenterálně.
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Hypermagnesémie
Příčiny: renální selhání, po úrazu se zhmožděním svalstva
Příznaky: nauzea, zvracení, hypotenze, na EKG známky poruchy převodního systému, prodloužení QT intervalu, A -V blok
Terapie: přechodné zlepšení= ; po Ca-glukonátu, jinak dialyzační léčba
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Kalcium
S-Ca2+,  2.25 - 2.65,  ion. 1.0 - 1.4, moč - ztráta 1 mmol na 10 kg tě= lesné hmotnosti
Celková zásoba je 30 mol (1= 200 g), 75 % je součástí stavebního materiálu kostry.
<= span style=3D'font-size:88%'> Kalcium v séru je ve třech formách
= vázané= na bílkoviny - 40 - 45 %
= ionizované 50= %
<= span style=3D'font-family:"Times New Roman";mso-ascii-font-family:"Times New Ro= man"; mso-bidi-font-family:"Times New Roman";font-size:88%'>vázané= v komplexech s anionty kyselin (5 - 10 %)
Pouze ionizovaná forma má základní význam pro kardiáln&iacu= te; a neuromuskulámí funkci
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Hypokalcémie
P&ia= cute;iny:= nekrotizujíc&= iacute; pancreatitis, pokles proteinémie (bývá bez příznaků, protože ionizované Ca2+ je v normě), hypoparathyreoidismus, osteoma1acie, deficit vitaminu D, osteoblastické tumory
P&ia= cute;iny poklesu ionizovaného Ca+: alkalózy a = masivní transfúze (citrát)
<= span style=3D'font-size:88%;color:yellow'>Klinick&ea= cute; p&ia= cute;znaky
R= 26;     <= /span>parestezie, zvýšené šlachové reflexy, dušnost, = vzácně stridor, abdominální koliky, epileptiformní = křeče,
Pi posuzování kalcémie je nutno vždy sou<= /span>asn = hodnotit proteinémii a pH
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Hyperkalcémie
P&ia= cute;iny:= metastázy tumorů do kostí, hyperproteinémie, hyperparathyreoidismus, hypervitaminózy D, = immobilizace
Klin= ick&ea= cute; p&ia= cute;znaky: slabost, letargie, únava, deprese, zmatenost, nechutenství, zvracení, polyurie, žízeň, tachykardie, na EKG zkrácení QT a zvýšení citlivosti na digitalis
Hype= rkalcemická krize (nad 4 mmol) - rychlé zhoršení celkového stavu a smrt, zastavení srdce v sys= tole
L&ea= cute;en&i= acute;: rychlé zavodnění a diuretik= a, alkalizace, nitrožilně fosfáty (tvoří vazbu s Ca2+),steroidy (vazba kalcia na mitochondr= ie v buňkách), thyreokalcitonin
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Fosfor
<= span style=3D'font-size:88%'>S-P, 0.7-1.5 mmol/l, odpa= dy do moči = 15 - 90 mmol/den
Celková zásoba v těle je 19.3 - 25.8 mol (600 - 800 g), 80 % je v kostech a zubech, 9 % ve svalech
Hypo= fosforémie: metabolická alkalóza (stimulace glykolýzy, zvýšen&= iacute; fosforylací a přesun P do bun= ěk), chronická ter= apie antacidy (vazba P), malabsorpčstavy, zvýšení clearance fosfátů (hyperparathyreoidis= mus, deficit vitaminu D, Fanconiho syndrom, vrozené renální tubulámí poruchy), alkoholismus.
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Klinické příznaky hypofosforémie:
objevují se při poklesu sérové koncentrace pod 0.3 mmol/l ­třes a slabost svalstva končetin, vázne <= /span>artikulace, parestes= ie kolem úst, nevýbavné šlachové reflexy. Nespecifické patologie na EKG. Vzniká deplece ATP v thrombocytech a erythrocytech - snížen&= iacute; přežívání elementů =
Terapie: Při hypofosforé= mii dávky 30 - 40 mmol P/den, po 3 dnech snížení dá= vek
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Hyperfosforémie
<= span style=3D'font-size:88%'>m&= aacute;lo častá
P&ia= cute;iny:= oligurické f= ormy renálního selhání, hojení rozsáhlých fraktur, hypoparathyreóza
&#= 8226;Tekutiny ve třetím prostoru    &nb= sp; – vyskytují se jen za patologických situací (nahromadě<= span style=3D'font-family:"Times New Roman";mso-ascii-font-family:"Times New Ro= man"; color:yellow'>ní v lumen stř<= span style=3D'font-family:"Times New Roman";mso-ascii-font-family:"Times New Ro= man"; color:yellow'>ev, traumatický ed= ém, ascitická tekutina)
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return 0 } var MHTMLPrefix =3D CalculateMHTMLPrefix(); function CalculateMHTMLPrefix() { if ( document.location.protocol =3D=3D 'mhtml:') { href=3Dnew String(document.location.href) Start=3Dhref.indexOf('!')+1 End=3Dhref.lastIndexOf('/')+1 if (End < Start) return href.substring(0, Start) else return href.substring(0, End) } return ''; } function GetTags(base,tag) { if(g_supportsPPTHTML) return base.all.tags(tag); else return base.getElementsByTagName(tag); } function UpdNtsPane(){ if(frames["PPTNts"]) PPTNts.location.replace( MHTMLP= refix+GetHrefObj( gCurSld ).mNtsHref ) } function UpdNavPane( sldIndex ){ if(gNavLoaded) PPTNav.UpdNav() } function UpdOtNavPane(){ if(gOtlNavLoaded) PPTOtlNav.UpdOtlNav() } function UpdOtlPane(){ if(gOtlLoaded) PPTOtl.UpdOtl() } function SetHasNts( fVal ) { if( gHasNts !=3D fVal ) { gHasNts=3DfVal UpdNavPane() } } function ToggleOtlText() { gOtlTxtExp=3D!gOtlTxtExp UpdOtlPane() } function ClearMedia() { if (PPTSld.pptSound) PPTSld.pptSound.loop =3D 0; } function FullScreen() { if ( PPTSld.g_animUseRuntime ) PPTSld.document.body.pause(); ClearMedia(); var href =3D ( document.location.protocol =3D=3D 'mhtml:') ? FULLSCR_HREF = : FULLSCR_HREF+"#"+GetHrefObj(gCurSld).mSldHref; if(PPTNav.event.ctrlKey) { var w =3D (window.screen.availWidth * 1.0) / 2.0 var h =3D w * (PPTSld.g_origH * 1.0) / PPTSld.g_origW win =3D window.open( MHTMLPrefix+href,null,"toolbar=3D0,resizable=3D1,top= =3D0,left=3D0," + "width=3D"+ w + ",height=3D" + h ); if( win.document.body && PPTSld.g_animUseRuntime ) win.document.body.PPTSldFrameset=3Dwindow; } else { win =3D window.open( MHTMLPrefix+href,null,"fullscreen=3Dyes" ); if( win.document.body && PPTSld.g_animUseRuntime ) win.document.body.PPTSldFrameset=3Dwindow; } } function ToggleVNarration() { rObj=3DPPTSld.document.all("NSPlay") if( rObj && !PPTSld.g_animUseRuntime ) { if( (rObj.playState =3D=3D 1)||(rObj.playState =3D=3D 0) ) rObj.Play() else if( rObj.playState =3D=3D 2 ) rObj.Pause() else return; } else if( PPTSld.g_animUseRuntime ) { narObj =3D PPTSld.document.all("narrationID") if( narObj ) narObj.togglePause() } } function GetCurSldNum() { obj=3DGetHrefObj(gCurSld) if( obj.mOrigVis =3D=3D 1 ) return obj.mSldIdx else return gCurSld } function GetNumSlds() { if( GetHrefObj(gCurSld).mOrigVis =3D=3D 1 ) return GetSldList().mNumVisSlds; else return GetSldList().mList.length } function GetSldNum( href ) { for(ii=3D0; ii 1 ) PopSldList(); else if( !IsFramesMode() ) { if( gLoopCont ) GoToFirst() else EndShow() } } function GoToPrevSld() { ii=3DgCurSld-1 if( ii > 0 ) { obj=3DGetHrefObj(ii) while ( obj && ( obj.mVis =3D=3D 0 ) && ( ii>0 ) ) obj=3DGetHrefObj(--ii) if( ii =3D=3D 0 ) ii=3D1 GoToSldNum(ii) } } function GoToFirst(){ GoToSld( GetHrefObj(1).mSldHref ) } function GoToLast() { ii=3DGetSldList().mList.length if( ii !=3D gCurSld ) GoToSld( GetHrefObj(ii).mSldHref ) } function GoToSldNum( num ) { if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue obj =3D GetHrefObj( num ) obj.mVis=3D1 gPrevSld=3DgCurSld gCurSld =3D num; PPTSld.location.replace(MHTMLPrefix+obj.mSldHref) if( IsFramesMode() ) { UpdNavPane(); UpdOtlPane(); UpdNtsPane() } } function GoToSld( href ) { if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue GetHrefObj( GetSldNum(href) ).mVis=3D1 PPTSld.location.replace(MHTMLPrefix+href) } function SldUpdated( id ) { if( id =3D=3D GetHrefObj(gCurSld).mSldHref ) return gPrevSld=3DgCurSld gCurSld=3DGetSldNum(id) if( IsFramesMode() ) { UpdNavPane(); UpdOtlPane(); UpdNtsPane() } } function PrevSldViewed(){ GoToSld( GetHrefObj(gPrevSld).mSldHref ) } function HasPrevSld() { return ( gIsEndShow || ( gCurSld !=3D 1 && GetHrefO= bj( gCurSld-1 ).mVis =3D=3D 1 )||( GetCurSldNum() > 1 ) ) } function HasNextSld() { return (GetCurSldNum() !=3D GetNumSlds()) } function CloseWindow() { if( HideMenu() ) return; var event =3D PPTSld.event; if( !IsFramesMode() && event && (event.keyCode=3D=3D27 || event.keyCode=3D= =3D32 || event.type=3D=3D"click" ) ) window.close( self ); CatchNumKeys( self, event ); } function Unload() { gIsEndShow=3D0; } function SetupEndShow() { gIsEndShow=3D1; PPTSld.document.body.scroll=3D"no"; PPTSld.document.onkeypress=3DCloseWindow; PPTSld.document.onclick=3DCloseWindow; PPTSld.document.oncontextmenu=3D_CM; } function EndShow() { if( IsFramesMode() ) return if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue doc=3DPPTSld.document var dir =3D doc.body.dir if( dir !=3D "rtl" ) dir =3D "ltr"; doc.open() doc.writeln('


' + ENDSHOW_MESG + '

') doc.close() } function SetSldVisited(){ GetSldList().mList[gCurSld-1].mVisited=3Dtrue } function IsSldVisited(){ return GetSldList().mList[gCurSld-1].mVisited } function hrefList( sldHref, visible, advDelay, advClk ) { this.mSldHref=3D this.mNtsHref =3D sldHref this.mOrigVis=3D this.mVis =3D visible this.mVisited=3D false this.mAdvDelay=3D advDelay this.mAdvOnClk=3D advClk } function SldList(arr,curSld,fEnd) { this.mCurSld =3D curSld; this.mList =3D new Array(); var idx =3D 1; for(ii=3D0;ii 0) { PushSldList(sldList,fEnd); gCurSld =3D 1; } else if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue } function PushSldList(arr,fEnd) { var ii =3D gSldStack.length; gSldStack[ii] =3D new SldList(arr,gCurSld,fEnd); GoToSld( gSldStack[ii].mList[0].mSldHref ); } function PopSldList() { if (gSldStack[gSldStack.length-1].fEndShow) EndShow() else { gCurSld =3D gSldStack[gSldStack.length-1].mCurSld; gSldStack[gSldStack.length-1] =3D null; gSldStack.length--; var sldList =3D gSldStack[gSldStack.length-1]; GoToSld( sldList.mList[gCurSld - 1].mSldHref ); } } var custShowList=3Dnew Array(); function ImgBtn( oId,bId,w,action ) { var t=3Dthis t.Perform =3D _IBP t.SetActive =3D _IBSetA t.SetInactive=3D _IBSetI t.SetPressed =3D _IBSetP t.SetDisabled=3D _IBSetD t.Enabled =3D _IBSetE t.ChangeIcon =3D null t.UserAction =3D action t.ChgState =3D _IBUI t.mObjId =3D oId t.mBorderId=3D bId t.mWidth =3D w t.mIsOn =3D t.mCurState =3D 0 } function _IBSetA() { if( this.mIsOn ) { obj=3Dthis.ChgState( gHiliteClr,gShadowClr,2 ) obj.style.posTop=3D0 } } function _IBSetI() { if( this.mIsOn ) { obj=3Dthis.ChgState( gFaceClr,gFaceClr,1 ) obj.style.posTop=3D0 } } function _IBSetP() { if( this.mIsOn ) { obj=3Dthis.ChgState( gShadowClr,gHiliteClr,2 ) obj.style.posLeft+=3D1; obj.style.posTop+=3D1 } } function _IBSetD() { obj=3Dthis.ChgState( gFaceClr,gFaceClr,0 ) obj.style.posTop=3D0 } function _IBSetE( state ) { var t=3Dthis GetObj( t.mBorderId ).style.visibility=3D"visible" if( state !=3D t.mIsOn ) { t.mIsOn=3Dstate if( state ) t.SetInactive() else t.SetDisabled() } } function _IBP() { var t=3Dthis if( t.mIsOn ) { if( t.UserAction !=3D null ) t.UserAction() if( t.ChangeIcon ) { obj=3DGetObj(t.mObjId) if( t.ChangeIcon() ) obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-4)*t.mWidth else obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-0)*t.mWidth } t.SetActive() } } function _IBUI( clr1,clr2,nextState ) { var t=3Dthis SetBorder( GetObj( t.mBorderId ),clr1,clr2 ) obj=3DGetObj( t.mObjId ) obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-nextState)*t.mWidth-obj= .style.posTop t.mCurState=3DnextState return obj } function TxtBtn( oId,oeId,action,chkState ) { var t=3Dthis t.Perform =3D _TBP t.SetActive =3D _TBSetA t.SetInactive=3D _TBSetI t.SetPressed =3D _TBSetP t.SetDisabled=3D _TBSetD t.SetEnabled =3D _TBSetE t.GetState =3D chkState t.UserAction =3D action t.ChgState =3D _TBUI t.mObjId =3D oId t.m_elementsId=3D oeId t.mIsOn =3D 1 } function _TBSetA() { var t=3Dthis if( t.mIsOn && !t.GetState() ) t.ChgState( gHiliteClr,gShadowClr,0,0 ) } function _TBSetI() { var t=3Dthis if( t.mIsOn && !t.GetState() ) t.ChgState( gFaceClr,gFaceClr,0,0 ) } function _TBSetP() { if( this.mIsOn ) this.ChgState( gShadowClr,gHiliteClr,1,1 ) } function _TBSetD() { this.ChgState( gFaceClr,gFaceClr,0,0 ) this.mIsOn =3D 0 } function _TBSetE() { var t=3Dthis if( !t.GetState() ) t.ChgState( gFaceClr,gFaceClr,0,0 ) else t.ChgState( gShadowClr,gHiliteClr,1,1 ) t.mIsOn =3D 1 } function _TBP() { var t=3Dthis if( t.mIsOn ) { if( t.UserAction !=3D null ) t.UserAction() if( !t.GetState ) return if( t.GetState() ) t.SetPressed() else t.SetActive() } } function _TBUI( clr1,clr2,lOffset,tOffset ) { SetBorder( GetObj( this.mObjId ),clr1,clr2 ) Offset( GetObj( this.m_elementsId ),lOffset,tOffset ) } function Offset( obj, top, left ){ obj.style.top=3Dtop; obj.style.left=3Dle= ft } function SetBorder( obj, upperLeft, lowerRight ) { s=3Dobj.style; s.borderStyle =3D "solid" s.borderWidth =3D 1 s.borderLeftColor =3D s.borderTopColor =3D upperLeft s.borderBottomColor=3D s.borderRightColor =3D lowerRight } function GetBtnObj(){ return gBtnArr[window.event.srcElement.id] } function BtnOnOver(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetActive() } function BtnOnDown(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetPressed() } function BtnOnOut(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetInactive() } function BtnOnUp() { b=3DGetBtnObj() if( b !=3D null ) b.Perform() else Upd() } function GetNtsState(){ return parent.gNtsOpen } function GetOtlState(){ return parent.gOtlOpen } function GetOtlTxtState(){ return parent.gOtlTxtExp } function NtsBtnSetFlag( fVal ) { s=3Ddocument.all.item( this.m_flagId ).style s.display=3D"none" if( fVal ) s.display=3D"" else s.display=3D"none" } function _BSetA_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S= etActive() } function _BSetI_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S= etInactive() } function _BSetP_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S= etPressed() } function _BSetA_BorderImg() { b =3D gBtnArr[this.mBorderId] if( b !=3D null && this.mIsOn && !b.GetState() ) { obj=3Dthis.ChgState( gHiliteClr,gShadowClr,2 ) obj.style.posTop=3D0 } } function _BSetI_BorderImg() { b =3D gBtnArr[this.mBorderId] if( b !=3D null && this.mIsOn && !b.GetState() ) { obj=3Dthis.ChgState( gFaceClr,gFaceClr,1 ) obj.style.posTop=3D0 } } var gHiliteClr=3D"THREEDHIGHLIGHT",gShadowClr=3D"THREEDSHADOW",gFaceClr=3D"= THREEDFACE" var gBtnArr =3D new Array() gBtnArr["nb_otl"] =3D new TxtBtn( "nb_otl","nb_otlElem",parent.ToggleOtlPan= e,GetOtlState ) gBtnArr["nb_otlElem"] =3D new TxtBtn( "nb_otl","nb_otlElem",parent.ToggleOt= lPane,GetOtlState ) gBtnArr["nb_nts"] =3D new ImgBtn( "nb_nts","nb_ntsBorder",10,parent.ToggleN= tsPane ) gBtnArr["nb_nts"].SetActive =3D _BSetA_BorderImg; gBtnArr["nb_nts"].SetInactive =3D _BSetI_BorderImg; gBtnArr["nb_ntsBorder"] =3D new TxtBtn( "nb_ntsBorder","nb_ntsElem",parent.= ToggleNtsPane,GetNtsState ) gBtnArr["nb_ntsElem"] =3D new TxtBtn( "nb_ntsBorder","nb_ntsElem",parent.To= ggleNtsPane,GetNtsState ) gBtnArr["nb_prevBorder"] =3D gBtnArr["nb_prev"]=3D new ImgBtn( "nb_prev","n= b_prevBorder",30,parent.GoToPrevSld ) gBtnArr["nb_nextBorder"] =3D gBtnArr["nb_next"]=3D new ImgBtn( "nb_next","n= b_nextBorder",30,parent.GoToNextSld ) gBtnArr["nb_sldshw"]=3D new ImgBtn( "nb_sldshw","nb_sldshwBorder",18,parent= .FullScreen ) gBtnArr["nb_sldshwBorder"] =3D new TxtBtn( "nb_sldshw","nb_sldshwBorder",pa= rent.FullScreen,null ) gBtnArr["nb_sldshwBorder"].SetActive =3D _BSetA_Border; gBtnArr["nb_sldshwBorder"].SetInactive =3D _BSetI_Border; gBtnArr["nb_sldshwText"] =3D new TxtBtn( "nb_sldshw","nb_sldshwText",parent= .FullScreen,null ) gBtnArr["nb_sldshwText"].SetActive =3D _BSetA_Border; gBtnArr["nb_sldshwText"].SetInactive =3D _BSetI_Border; gBtnArr["nb_voice"] =3D gBtnArr["nb_voiceBorder"] =3D new ImgBtn( "nb_voice= ","nb_voiceBorder",18,parent.ToggleVNarration ) gBtnArr["nb_otlTxtBorder"] =3D gBtnArr["nb_otlTxt"]=3D new ImgBtn( "nb_otlT= xt","nb_otlTxtBorder",23,parent.ToggleOtlText ) gBtnArr["nb_ntsBorder"].m_flagId=3D "nb_nts" gBtnArr["nb_ntsBorder"].SetFlag =3D NtsBtnSetFlag gBtnArr["nb_otlTxt"].ChangeIcon=3D GetOtlTxtState var sNext=3D"Další",sPrev=3D"Předchozí",sEnd=3D"Kon= ec prezentace",sFont=3D"Arial",sArrow=3D"Šipka",sFreeform=3D"Voln&yacu= te; tvar",sRect=3D"Obdélník",sOval=3D"Ovál" function ShowMenu() { BuildMenu(); var doc=3DPPTSld.document.body,x=3DPPTSld.event.clientX+doc.scrollLeft,y= =3DPPTSld.event.clientY+doc.scrollTop m =3D PPTSld.document.all.item("ctxtmenu") m.style.pixelLeft=3Dx if( (x+m.scrollWidth > doc.clientWidth)&&(x-m.scrollWidth > 0) ) m.style.pixelLeft=3Dx-m.scrollWidth m.style.pixelTop=3Dy if( (y+m.scrollHeight > doc.clientHeight)&&(y-m.scrollHeight > 0) ) m.style.pixelTop=3Dy-m.scrollHeight m.style.display=3D"" } function _CM() { if( !parent.IsFullScrMode() ) return; if(!PPTSld.event.ctrlKey) { ShowMenu() return false } else HideMenu() } function BuildMenu() { if( PPTSld.document.all.item("ctxtmenu") ) return var mObj=3DCreateItem( PPTSld.document.body ) mObj.id=3D"ctxtmenu" mObj.style.visibility=3D"hidden" var s=3DmObj.style s.position=3D"absolute" s.cursor=3D"default" s.width=3D"120px" SetCMBorder(mObj,"menu","black") var iObj=3DCreateItem( mObj ) SetCMBorder( iObj, "threedhighlight","threedshadow" ) iObj.style.padding=3D2 CreateMenuItem( iObj,sNext,M_GoNextSld,M_True ) CreateMenuItem( iObj,sPrev,M_GoPrevSld,M_HasPrevSld ) CreateSeparator( iObj ) CreateMenuItem( iObj,sEnd,M_End,M_True ) mObj.style.visibility=3D"visible" } function Cancel() { window.event.cancelBubble=3Dtrue; window.event.returnVa= lue=3Dfalse } function Highlight() { ChangeClr("activecaption","threedhighlight") } function Deselect() { ChangeClr("threedface","menutext") } function Perform() { e=3DPPTSld.event.srcElement if( e.type=3D=3D"menuitem" && e.IsActive() ) e.Action() else PPTSld.event.cancelBubble=3Dtrue } function ChangeClr( bg,clr ) { e=3DPPTSld.event.srcElement if( e.type=3D=3D"menuitem" && e.IsActive() ) { e.style.backgroundColor=3Dbg e.style.color=3Dclr } } function M_HasPrevSld() { return( parent.HasPrevSld() ) } function M_GoNextSld() { if( gIsEndShow ) M_End(); 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charset="us-ascii" Minerální hospodářství ------=_NextPart_01CA5F17.4738C5F0 Content-Location: file:///C:/228A91F9/mineraly_soubory/outline.htm Content-Transfer-Encoding: quoted-printable Content-Type: text/html; charset="us-ascii"
 Po= známky
Prezentac= e
Osnova
= =
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