TY  - CHAP
M1  - Book, Section
TI  - Cirrhosis and Portal Hypertension
A1  - Wells, Barbara G.
A1  - DiPiro, Joseph T.
A1  - Schwinghammer, Terry L.
A1  - DiPiro, Cecily V.
PY  - 2017
T2  - Pharmacotherapy Quick Guide
AB  - Cirrhosis  is  a  diffuse  injury  to  the  liver  characterized  by  fibrosis  and  a  conversion  of  the  normal  hepatic  architecture  into  structurally  abnormal  nodules.  The  end  result  is  destruction  of  hepatocytes  and  their  replacement  by  fibrous  tissue.The  resulting  resistance  to  blood  flow  results  in  portal  hypertension  and  the  development  of  varices  and  ascites.  Hepatocyte  loss  and  intrahepatic  shunting  of  blood  result  in  diminished  metabolic  and  synthetic  function,  which  leads  to  hepatic  encephalopathy  (HE)  and  coagulopathy.Cirrhosis  has  many  causes  (Table  21–1).  In  the  United  States,  excessive  alcohol  intake  and  chronic  viral  hepatitis  (types  B  and  C)  are  the  most  common  causes.Cirrhosis  results  in  elevation  of  portal  blood  pressure  because  of  fibrotic  changes  within  the  hepatic  sinusoids,  changes  in  the  levels  of  vasodilatory  and  vasoconstrictor  mediators,  and  an  increase  in  blood  flow  to  the  splanchnic  vasculature.  The  pathophysiologic  abnormalities  that  cause  it  result  in  the  commonly  encountered  problems  of  ascites,  portal  hypertension  and  esophageal  varices,  HE,  and  coagulation  disorders.Portal  hypertension  is  noted  by  elevated  pressure  gradient  between  the  portal  and  central  venous  pressure  and  is  characterized  by  hypervolemia,  increased  cardiac  index,  hypotension,  and  decreased  systemic  vascular  resistance.Ascites  is  the  pathologic  accumulation  of  fluid  within  the  peritoneal  cavity.  It  is  one  of  the  earliest  and  most  common  presentations  of  cirrhosis.The  development  of  ascites  is  related  to  systemic  arterial  vasodilation  mediated  by  nitric  oxide  that  leads  to  the  activation  of  the  baroreceptors  in  the  kidney  and  an  activation  of  the  renin–angiotensin–aldosterone  system,  activation  of  the  sympathetic  nervous  system,  and  release  of  antidiuretic  hormone  in  response  to  the  arterial  hypotension.  These  changes  cause  sodium  and  water  retention.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/20
UR  - accesspharmacy.mhmedical.com/content.aspx?aid=1144734296
ER  -