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Increases capillary infiltration pressure Produces additional ul Liquid stools containing - - - bloody mucou Bleeding cause by damage of liver cells bleeds into liver debris and forms anchovy paste If infection persists f Predisposing factors Precipitating Factors Living in a developing/tropical country food meals prepared with poor sanitation water for drinking comes from a common tank of the entire town ingestion of E. histolytica cyst life cycle of E. histolytica continues and morphs into a metacystic trophozoite reaches and survives in the colon (especially the cecum) nausea and vomiting- - - - - attachement to cecal mucosae and penetration of epithelium by lytic digestion aided by ameboid movement-------loose stools, loss of appetite trphozoites burrow deeper reaches muscularis mucosae invades further into the mesentery towards portal venous system thrombos formation on branches of the portal vein due to lytic necrosis of ------- right upper quadrant pain portal vessel walls to generate pathway to lobules of liver phagocytes (Kupffer) in the liver attack the invading trphozoites trophozoite survivors of the attack continue to destroy neighboring liver cells more leukocytes are called to aid in the attack-------- increased WBC, fever, chills development of by products of the encounter: live and dead leukocytes liquefied liver cells and trophozoites Obstructs blood flow, portal outflow to vena cava Blood backs up and causes portal hypertension Fans out laterally and ulcerate having a flask shape Colon contraction squeezes colonies inside ulcers and are carried to lower portions of the colon

Amebic Hepatic Abscess

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Page 1: Amebic Hepatic Abscess

Increases capillary infiltration pressure

Produces additional ulcers in the colonLiquid stools containing - - - bloody mucous Bleeding cause by damage of liver cells bleeds into liver debris and forms anchovy paste

If infection persists for months or years there will be massive destruction of colonic mucosa

Peritonitis, hemorrhage, perforation

Predisposing factors Precipitating FactorsLiving in a developing/tropical country food meals prepared with poor sanitation

water for drinking comes from a common tank of the entire town

ingestion of E. histolytica cyst

life cycle of E. histolytica continues and morphs into a metacystic trophozoite reaches and survives in the colon (especially the cecum)

nausea and vomiting- - - - - attachement to cecal mucosae and penetration of epithelium by lytic digestion aided by ameboid movement-------loose stools, loss of appetite

trphozoites burrow deeper

reaches muscularis mucosae

invades further into the mesentery towards portal venous system

thrombos formation on branches of the portal vein due to lytic necrosis of ------- right upper quadrant painportal vessel walls to generate pathway to lobules of liver

phagocytes (Kupffer) in the liver attack the invading trphozoites

trophozoite survivors of the attack continue to destroy neighboring liver cells

more leukocytes are called to aid in the attack-------- increased WBC, fever, chills

development of by products of the encounter: live and dead leukocytesliquefied liver cells and trophozoites

walling off of inflamed area with its exudates to form an abscess

HEPATIC ABSCESS

Direct extension of abscess from liver to lungs passing through the diaphragm

Obstructs blood flow, portal outflow to vena cava

Blood backs up and causes portal hypertension

Fans out laterally and ulcerate having a flask shape

Colon contraction squeezes colonies inside ulcers and are carried to lower portions of the colon

Page 2: Amebic Hepatic Abscess

Hepatocytes decrease in ability to synthesize albumin

Decreases capillary osmotic pressure

Decreases effective plasma volume

Increase in rennin, stimulation of vasopressin, aldosterone and antidiuretic hormone --- increase in BP

abscess ruptures into pleural cavity

pleural effusion ------ sob, tachypnea, increase tactile fremitusdiminished breathsounds, egophony

Pushes fluids from vessels to extra vascular space

Acscites ---- rigid abdomen, bloating of abdomen

Hepatocellular damage or obstruction of bile canaliculi

Liver unable to conjugate and excrete bilirubin

Backs up to liver and reabsorbed into the blood circulation

Bilirubin is deposited in tissues ------- jaundice

Page 3: Amebic Hepatic Abscess

Increase renal reabsoprtion of Na and H20

Ascites, hemodilution, edema on distal extremeties