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hptr 6: pplitin Prblms

The most common is called jaundice nadpechenochnaya increased destruction of red blood cells - both mature cells and their precursors. Destruction of mature cells may be the result of hemolysis or effect of utilization of blood after internal bleeding, such as damaged soft tissues. Ineffective Erythropoiesis occurs in pernicious anemia (a violation of maturation of red blood cells) or thalassemia (abnormal hemoglobin structure). Hyperbilirubinemia in nadpechenochnoy jaundice caused by the accumulation of unconjugated bilirubin, which is not excreted by the kidneys. This increases the flow of bilirubin from the liver into the intestine. Produced a large amount of urobilinogen, whose level in the urine increases.

Hepatocellular jaundice.

Inborn errors of bilirubin transport lead to jaundice due to imperfect absorption, decreased conjugation or impaired excretion of bilirubin. Generalized hepatocellular dysfunction may occur in hepatitis and decompensated liver cirrhosis. Pathogenesis of jaundice in these cases is complicated, your contribution is violation of the capture, intracellular transport, decreased conjugation of bilirubin. Drugs can cause hepatocellular injury in connection with its dose-related hepatotoxicity (eg, acetaminophen) or idiosyncratic sensitivity (eg, isoniazid). If hyperbilirubinemia is caused by a violation of conjugation, bilirubin is not conjugated, and there is no increased flow of bilirubin in the liver. The consequence is that absent bilurubinuriya and the level of urobilinogen in the urine is not increased. In the presence of a generalized dysfunction of the liver reduces the capture of bilirubin and, therefore, more quantitative it is excreted by the kidneys. In serum bilirubin may be conjugated and unconjugated, as may be defective UDP-glyukoroniltransferaza and intracellular transport of bilirubin. If the rate of conjugation exceeds excretory capacity, increases in blood levels of conjugated bilirubin and it can be excreted in the urine. This sometimes happens during convalescence after viral hepatitis.

Cholestatic jaundice.

Cholestatic jaundice may be the result of an outflow obstruction of bile from the hepatocytes in dvenadtsetiperstnuyu intestine. It can be caused by lesions in the liver (intrahepatic cholestasis) or in the bile ducts and pancreas head (extrahepatic cholestasis).

Intra-and can be differentiated vnepechenochnyyholestaz ultrasound or a biopsy of the liver, but not evaluative tests of liver function.

Vnutripechenochnyyholestaz often the result of generalized hepatocellular dysfunction, which develops, such as hepatitis or cirrhosis dekomnesirovannom. This condition is also a symptom of primary biliary cirrhosis. Biliary tree branch block may malignancies. Some medications such as anabolic streroidy, phenothiazines, and sulfonylurea may pprivodit to intrahepatic cholestasis.

Extrahepatic obstruction is often the result of major biliary tract tumors, tumors of the head of the pancreas and lymph nodes at the gate of the liver. To obstruction of bile ducts can also cause gallstones or sclerosing cholangitis.

Jaundice is caused by a violation of excretion and accumulation of conjugated bilirubin, filtered by the glomerulus and appears in the urine. However, bilirubin in urine may not be detected, possibly because changes in the processes of conjugation leads to the formation of less soluble bilirubin bound to albumin. When complete obstruction of bilirubin did not reach the intestine, urobilinogen is formed and not detected in the urine and feces may be of a color.


Jaundice newborns.

Hemolytic disease of newborn

Reasons. Incompatibility blood of mother and fetus in the group or Rh factor. The accumulation of hydrophobic forms of bilirubin in the blubber causes yellowness of the skin. But the real danger is the accumulation of bilirubin in the gray matter of nervous tissue and stem nuclei to the development of "kernicterus" (kernicterus).

Physiological (transient) neonatal jaundice


relative decrease in activity of UDP-glucuronyl transferase in the first days of life associated with increased degradation of fetal hemoglobin,

Nonhemolytic neonatal hyperbilirubinemia caused by breast milk.

It occurs in 1% of breastfed infants.

Reasons. Suppression UDP-glucuronyl transferase activity, presumably estrogens breast milk.

Laboratory diagnosis. Increase in the concentration of free bilirubin in the serum.

Liver disease.

In 5% of healthy people may experience a slight elevation in liver enzymes without any signs of liver damage. A practical approach to screening patients with isolated increased aminotransferase is a repetition of the test and further evaluation is only 2-fold excess of the norm or the identification of risk factors for liver disease. These enzymes exist not only the presence in the liver, but the AC T in cardiac muscle, skeletal muscle, kidney, brain, pancreas, lung, leukocytes and erythrocytes; A L T in skeletal and cardiac muscle (although much smaller than A C T amounts) of LDH in virtually all cells and body fluids, to the liver are more common isozymes LDG5 iLDG4.

Aminotransferase levels did not correlate with the outcome of liver disease, since acute hepatitis B with the increase in enzyme levels in more than 20 times as often ends in complete recovery, whereas alcoholic hepatitis with a much lower elevation of liver failure can be completed.



hptr 6: pplitin Prblms

  1. Yu r slf-mplyd untnt wh spilizs in tx prprtin srvis. Thr r mny mptitrs in yur industry wh ffr similr srvi but qulity f srvi vris mng mptitrs. ntry int this industry is rltivly sy. Yur mpny's dily dmnd urv nd st funtins, inluding yur wn pprtunity sts, r urrntly (with Q bing numbr f tx rturns prssd pr dy):

Dmnd: P= 100 - 4Q
Ttl Fixd sts: TF = 60
Ttl Vribl sts: TV = (8.5)Q2
Mrginl sts: M = 17Q

. Slv fr yur mpny's prfit mximizing utput nd pri.

b. lult th lvl f ttl prfit r lss pr prid tht wuld ru t th firm undr th utput nd pri dtrmind in ().

. Giv njtur but wht might hppn t yur prfits vr tim, givn th hrtristis f yur mrkt dsribd bv.

  1. uld mnply firm vr inur n nmi lss? xplin.
  2. nsidr n industry whr hmgnus prdut is sld by tw firms, with mrkt dmnd f P = 100 - Q. h firm hs idntil nstnt sts f T = M = $40.

. If th sllrs llud illglly t st pri nd utput, wht is th rsulting pri, utput, nd prfit pr firm?

b. Slv fr th urnt utput nd rsulting pri nd prfit, nd mpr t ).

. Slv fr th Brtrnd pri nd rsulting utput nd prfit, nd mpr t ) nd b).

  1. QulPrd nd KGd r th nly prdurs f diffrntitd prduts in thir mrkt sgmnts. Thy r stting thir pris fr thir prduts. Fr simpliity h firm is hsing btwn high pri nd lw pri strtgy. QulPrd hs suprir qulity tht yilds sm diffrntils tht r rfltd in th rsulting ttl prfit (pyff) figurs in th tbl blw:

. Find th Nsh quilibrium priing strtgis if bth mpnis slt thir pris nn-prtivly nd simultnusly in n-sht gm. xplin rfully.

b. xplin th bnfits s wll s prblms frm lluding t st pris high.

  1. sftwr firm is ttmpting t mrkt nw gnrl-purps sttistis pkg in mptitiv mrkt. Th mpny hs gd rputtin, nd mrkting hs just mpltd survy f th pris f th prduts f tn hif mptitrs. Thy hv didd t hrg pri f $170, whih is th mdin f th mptitrs' pris. Thir nsidrbl xprin in mrkting nd priing similr dvis nvins thm tht thy will b bl t sll prtty nrly s muh s thir pity will prmit.

Frm pst studis in lking t th st f prduing this prdut, thy hv stimtd ttl st t b:

whr Q = numbr prdud. Bsd n th priing nd mrkt infrmtin, th rvnu funtin is:

. Us sprdsht prgrm t rt nd mplt th fllwing tbl:

b. Bsd n th sprdsht rsults, wht is th prfit-mximizing lvl f prdutin? Wht is th prfit t this lvl f prdutin?

. Lking t th sprdsht rsults, dtrmin wht prdutin lvl(s) will llw th mpny t brk vn.

d. t wht prdutin lvl is vrg st minimum? (Us th sprdsht rsults.)

. ssuming thr firms hv this st strutur, wht shuld this sftwr firm xpt t b hrging fr its sftwr in th lng run quilibrium fr this mrkt? xplin.


Date: 2014-12-21; view: 102

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