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Stack #38928
RRC Maintenance - Hepatic conditions
| question | answer |
|---|---|
| what is hepatitis | widespread inflammation of liver |
| hepatitis A | fecal-oral route |
| hepatitis B | spread via body fluid transmission (saliva, tears, semen, CSF, ascitic fluid, breast milk, synovial fluid, gastric fluid, pleural fluid) |
| hepatitis C | spread via transfusion of blood and blood product |
| hepatitis D | defective RNA virus that requires co-infection with HBV in order for replication to occur |
| hepatitis E | fecal-oral route, commonly seen after catastrophic events that contaminate water supply in developing countries |
| cirrhosis | chronic progressive disease characterized by excessive degeneration and destruction of liver parechymal cells |
| alcoholic or Laennec's cirrhosis | associated with ETOH abuse...accumulation of fat in liver that can be reversible if stops consuming ETOH...if not, widespread scar formation occurs throughout liver |
| postnecrotic cirrhosis | complication of viral, toxic or idiopathic hepatitis where broad bands of scar tissue form within the liver |
| biliary cirrhosis | associated with chronic biliary obstruction and infection...there is diffuse fibrosis of liver with jaundice as main feature |
| cardiac cirrhosis | results from long-standing right-sided HF in clients with cor pulmonale, constrictive pericarditis and tricuspid insufficiency |
| s+sx of hepatitis | prodromal period = anorexia, N+V, fatigue, aethalgia myalgia, headache, photophobia...jaundice follows in about 2 weeks with alteration in taste/smell, pyrexia, tea-colored urine/clay coloured stool, weight loss, hepato/splenomegaly |
| Which takes longer to recover? Blood-borne or food-borne hepatitis viruses? | blood borne --> B, C, D |
| s+sx of ETOH cirrhosis | anorexia, cachexia, reduction in muscle mass, severe weakness/fatigue, spider angiomas on face/trunk, easy bruising, gynecomastia/testicular atrophy in men, anemia, gastritis, immunosuppression, splenomegaly, hypoglycemia, hypoalbuminemia, increase NH3 |
| s+sx of biliary cirrhosis | palmar pruritis, fatigue, jaundice, facial hyperpigmentation, steatorrhea, easy bruising, osteomalacia, problems with night vision, fatty deposits around eyes (xanthomas) |
| Kupffer cell dysfunction | complication where the phagocytic action of cells is reduced in liver disease...bacterial organisms coming from the gut are not phagocytized which means that pathogens gain access to the systemic circulation and results in an increased risk for sepsis |
| spontaneous bacterial peritonitis | pathogens migrate to ascitic fluid when there is Kupffer cell dysfunction |
| jaundice | yellow-green discoloration of epithelial tissue dur to accumulation of bile r/t impaired synthesis/excretion of bile |
| portal hypertension | created when the pressure increases due to obstruction of the portal vein or sinusoid dysfunction (fibrotic tissue formation in cirrhosis); body attempt to ameloriate uneven pressure gradient by creating collateral vessels - esophageal varices/hemorrhoids |
| esophageal varices | develop due to portal hypertension and results in vessel engorgement in small vessels not well designed to manage large blood flow, therefore increased risk of hemorrhage |
| Why are bleeding varices considered a medical emergency? | presents as painless hematemesis, exsanguination can occur and develop hypovolemic shock |
| Why does ascites develop in someone with hepatic failure? | portal hypertension raises the hydrostatic pressure in splanchnic capillary bed and intra-hepatically and lack of synthesis of albumin result in reduction of colloid osmotic pressure...therefore fluid is pulled into peritoneal space from the vasculature |
| What are assessment findings r/t ascites? | flank fullness, abdominal distention, fluid wave, umbilical eversion, SOB if fluid impinging on pulmonary system |
| treatment for ascites? | bedrest (to deactivate renin-angiotensin mechanism), restrict dietary Na+ to decrease fluid retention, diuretic to decrease fluid volume, paracentesis |
| hepatic encephalopathy | ammonia crosses the blood-brain barrier and is deposited in the brain tissue. NH3 is toxic to the body |
| pharmacological treatment of hepatic encephalopathy | neomycin, lactulose |
| What is the purpose of neomycin? | acts on ammonia-producing bacteria in the GI system to decrease production of NH3 |
| What is purpose of lactulose? | degrades enteric bacteria and lowers colonic pH...increase in H+ occuring due to shift in ammonia conversion to ammonium which can be excreted by feces |
| Why is an individual with hepatic failure put on protein restriction diet? | to reduce the creation of serum ammonia which is a by-product of protein synthesis |
| How many BMs should your patient with hepatic failure have to help prevent hepatic encephalopathy? | 3-4BMs/day |
| vitamin K injection | given in patients with prolonged prothrombin time to shorted bleeding time |
| propanolol | given to reduce portal hypertension to aid in control esophageal/gastric varices |
| why do we give a laxative/stool softener to someone with hepatic failure | to prevent straining and rupturing varices |
Created by:
bella83
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