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236 Cards in this Set
- Front
- Back
size and location of liver
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largest gland in body, located Upper Right Abdomen
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veins and arteries of the liver
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One exit the Hepatic Vein, 1 artery the Hepatic Artery rich in O2, and the Portal Vein, where the Liver gets the nutrients from the GI tract
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What are the functions of the liver per PP
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Carbohydrate Metabolism
Protein metabolism Lipid & Lipoprotein metabolism Bile acid synthesis & excretion bilirubin excretion Storage Biotransformation/detoxification and excretion of endogenous & exogenous compounds removal of pathogens steroid catabolism |
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what are the funcitons of the liver - brunners
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amonia conversion
protein, fat, glucose and drug metabolism Vitamin & iron storage Bile formation |
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glycogenolysis is
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glycogen into glucose
|
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gluconeogenesis is
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synthesis of glucose
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glycogenesis
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glycogen from glucose
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synthesis of plasma proteins includes
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albumin, alfa and beta globulins
(not gamma globuins) |
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formation of ketone bodies comes from
|
broken down fatty acids
|
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hepatotoxic mes include
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acetaminophen
ketoconazole (fungal) valproic acid |
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T or F
the majority of blood supply to the liver, which is poor in nutrients, comes from the portal vein |
False, the majority of blood supply to the liver which is rich in nutrients from the GI tract, comes from the portal vein
|
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Carbohydrate metabolism includes
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glycogenesis
glycogenolysis gluconeogenesis |
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Protein metabolism includes
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Synthesis amino acids
Synthesis plasma proteins Formation of urea |
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lipid & lipoprotein metabolism includes
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Synthesis lipoproteins
Breakdown of triglycerides Formation ketone bodies Synthesis of fatty acids Synthesis & breakdown of cholesterol |
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Bile acid synthesis & excretion includes
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Bile formation (containing bile salts, bile pigments (bilirubin, biliverdin), cholesterol
Bile excretion—about 1 liter/day |
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bilirubin excretion is
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(pigment from breakdown of hemoglobin)Destroyed & ingested by macrophage system of liver, spleen, marrow. Chemically changed & excreted in bile via duodenum.
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storage includes
|
Glucose (as glycogen)
Vitamins A,D,E,K??, B1, B2, B12, folic acid) Fatty acids Minerals (Fe, Cu) Amino acids (albumin, beta globulins) |
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Biotransformation, detoxification, excretion of endogenous & exogenous compounds includes
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Inactivation of drugs & excretion of breakdown products
Clearance of procoagulants, activated clotting factors, byproducts of coagulation |
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steroid catabolism includes
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Conjugation & excretion of gonadal steroids
Conjugation & excretion of adrenal steroids (cortisol, aldosterone) |
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gerontologic considerations of the liver are
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• Steady decrease in size and weight
• Decrease blood flow • Decrease repair • Reduced drug metabolism / clearance • Decreased clearance Hep B antigen • Increase progression Hep C, lower response to therapy |
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what is the scoop on Vit K and the liver
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Vit K is absorbed and needed for prothrombin and clotting factors
|
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what are the minerals stored in the liver
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iron and copper
|
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which type of steroids can be excreted conjugated or unconjugated
|
conjugated
|
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explain protein turning into urea
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use of amino acids from protein for gluconeogensis (glucose from liver) results in formation of ammonia, which turns into urea
|
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what are causes of Chronic Liver Dysfunction ( 9th leading cause of death)
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*Infectious agents—bacterial, viruses (Hepatitis B & C)
*Nutritional deficiencies— malnutrition, alcoholism *Anoxia *Toxins, medications |
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what are the different types of hepatic cirrhosis
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• Alcoholic cirrhosis (#1)
• Postnecrotic cirrhosis • Biliary cirrhosis |
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what is the path of cirrhosis
|
Chronic degeneration of liver tissues
Results in destruction of hepatic cells (hepatocytes) Formation of extensive dense fibrous scar tissue • Scarring causes compression of blood, lymph and bile channels • Hepatic insufficiency |
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Hepatic Cirrhosis can lead to
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• Infection and peritonitis
• Gastrointestinal varices • Edema • Vitamin deficiency and anemia |
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what is postnecrotic cirrhosis
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from previous bout of acute viral hepatitis and the broad bands of scar tissue
|
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what is the common make up of a person who gets hepatic cirrhosis
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Women, 40-60
|
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alcoholism plays a part of cirrhosis?
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major, though some nondrinkers can get it.
|
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explain the liver in the early stages of cirrhosis
|
large and loaded w/fat. firm w/sharp edge on palpation, ABD pain
|
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explain the liver in the late stages of cirrhosis
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decrease in size, scar tissue contracts liver, edge is palable but nondular
|
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Dx of Hepatic Disease includes what type of tests
|
PHYSICAL ASSESSMENT
Liver Function Tests Alakaline phosphatase (ALK. PHOS) LDH ALT (SGPT) AST (SGOT) SERUM BILIRUBIN 0-0.3 mg/dL SERUM CHOLESTEROL ELECTROLYTES Ammonia 40 mcg/dL Serum Albumin 4-5.5 g/dL DIAGNOSTIC PROCEDURES Ultrasound of Liver CT SCAN of Biliary Tract and Liver LIVER SPLEEN SCAN LIVER BIOPSY |
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ALP (ALK Phos) norm is
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42-128
|
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LDH norm is
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under a few hundred normally
|
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ALT (SGPT) norm is,
and a ALT of 45 is |
8-20
most definitive of Hepatitis and cirrhosis |
|
AST (SGOT) norm is
and is indicative of |
5-40
damage to other organs |
|
liver function test of ALP, ALT, AST, and LDH are called serum ......
|
serum aminotransferase
|
|
what 2 liver enzymes will initially elevate then return to normal when no longer able to create an inflammatory response
|
ALT and AST
|
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why does Alakaline phosphatase (Alk Phos) or ALP increase in cirrhosis
|
usually due to biliary obstruction
|
|
what is the most definitive diagnostic procedure for ID intensity of infection and
degree of tissue damage |
liver biopsy
|
|
what are nsg considerations for a liver biopsy
|
consent
lie on affected side after surgery monitor BP & HR to detect bleeding. Post op - place pt on R side with Pillow under costal margin for several hours Caution: bleeding and bile peritonits pot op |
|
CBCs for a pt with cirrhosis will be
|
will be decreased due to anemia
|
|
PT and INR in a pt with hepatic diseases will be
|
increased
liver's ability to synthesize fibrinogen and vitamin K–dependent clotting factors: factors II (prothrombin), V, VII, and X |
|
manifestations of liver dysfunction incldues
|
Jaundice
Elevated bilirubin in blood, greater than 2.5 mg/dL Hepatocellular: damaged liver cells unable to clear bilirubin Obstructive: occlusion of bile duct; extrahepatic or intrahepatic |
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Jaundice is _ and found ___
|
Jaundice - Yellow- or green-tinged body tissues; sclera and skin due to increased serum bilirubin levels.
|
|
what is the bilirubin in blood level suppose to be under
|
2.mg/dL
|
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what are the different types of Jaundice
|
Hemolytic, Hepatocellular, and Obstructive
Hereditary hyperbilirubineamia |
|
what are the s/s of hepatocellular Jaundice
|
May appear mildly or severely ill
Lack of appetite, nausea, weight loss Malaise, fatigue, weakness Headache chills and fever if infectious in origin |
|
how is hepatocellular Jaundice Dx and is it reversible
|
Elevated Serum bilirubin > 2.5
urine urobilinogen > 17 AST > 40 ALT > 20 May be reversible |
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what are the s/s of obstructive Jaundice
|
Dark orange-brown (foamy) urine and light clay-colored stools
Dyspepsia and intolerance of fats, impaired digestion Pruritis Dyspepsia Intolerance to fatty foods Bilirubin & Alk Phos elevated bile stains skin, mucous membranes and sclerae |
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where does obstructive jaundice go
|
reabsorbed into the blood, due to occulsion of bile duct
|
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what is hepatocellular jaundice from
|
inability to clear normal levels of bilirubin
|
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what is hemolytic Jaundice
|
increase in RBC destruction, so much the liver cant conjugate it fast enough
|
|
in obstructive jaundice which liver aminotransferases are elevated
|
Alk Phos is elevated along with bilirubin
(AST, ALT and GGT are not significant) |
|
what is Portal hypertension
|
Obstructed blood flow through the liver results in increased pressure throughout the portal venous system
|
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what are the 3 main effects of Portal hypertension
|
Ascites
Varices Splenomegaly |
|
what is Ascites due to
|
Portal HTN, decrease in albumin and obstruction of hepatic Lymph Flow
|
|
what is the pathology of ascites
|
• Increased capillary pressure, obstructed venous blood flow
• Vasodilation in splanchnic circulation • Aldosterone not metabolize then Na+ and water retention • Decreased albumin synthesis , fluid to peritoneal space |
|
what is the fluid that goes into the peritoneal cavity in Ascites
|
albumin (15L)
|
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s/s of Ascites
|
• Increased abd girth
• Rapid wt gain • SOB due to enlarged ABD • Striae and distended veins |
|
nsg considerations for Ascites
|
• Dx: fluid wave
• Monitor daily wt and girth Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave Monitor for potential fluid and electrolyte imbalances |
|
what is the medical management for Ascites
|
Dietary: low sodium
Diuretics: Spironolactone, furosemide Bedrest promotes sodium excretion Admin IV of salt-poor albumin Paracentesis Administration of salt-poor albumin Transjugular intrahepatic portosystemic shunt (TIPS) |
|
Paracentesis for Ascites is to....
is it a permanent fix? |
is to relieve ascites for those at risk of difficulty breathing due to pressure. It is a temporary fix due to RAAS and increase ADH
|
|
what is the diet for ascites
|
low sodium diet from 2 g to 500mg. increase Milk
no fluid restriction. |
|
Why is TIPS used in Ascities
|
good for those who will be getting a transplant
|
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what type of diuretic is used with the pt with ascites
|
Spironolactone (Aldactone).
|
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Tell whether the following statement is true or false.
Aldactone is most often the first therapy in patients with ascites from cirrhosis. |
True. - Rationale: Spironolactone (Aldactone), an aldosterone-blocking agent, is most often the first-line therapy in patients with ascites from cirrhosis.
|
|
what are some surgical procedures for diverting portal vein
|
• TIPS (TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT)
• PORTACAVAL SHUNT • H-GRAFT MESOCAVAL SHUNT • SPLENORENAL SHUNT |
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what is the normal pressure gradient between the portal vein and inferior vena cava
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< 12
|
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how do you know the portal vein has increased resistance by measurement
|
when it is > 12mmHg between the portal vein and inferior vena cava
DO THE MATH |
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What happens with Portal hypertension?
|
Venous collateral develop from high portal system pressure to systemic veins in esophageal plexus and retroperitoneal veins
|
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why do you get resistance to portal blood flow.
|
scarring, or fat deposits in liver
|
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what are esophageal varices
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Dilated, tortuous veins
Esophagus into stomach Caused by portal hypertension Contributing factors: increased pressure in esophagus, irritation, medications, alcohol |
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how serious are esophageal varices
|
first bleeding episode has a mortality of 30-50%
occurs in about 1/3 of pts with cirrhosis and varices |
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what are the manifestations from esophageal varices
|
Hematemesis
Melena General deterioration mental or physical Shock pts with cirrhosis should undergo screening endoscopy every 2 years |
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what is the Dx for esophageal varices
|
Diagnosis: endoscopy,
Portal hypertension measurements |
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where will you see abnormal varicoid vessels
|
above the liver
|
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what is the main nsg consideration for the endoscopy
|
no fluids until gag reflex
|
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what is the Pharmacologic Tx to control bleeding in for Varices
|
Vasopressin (pit) - not for Coronary Artery Disea pts, the vasoconstriction may create an MI!!
Propranolo - BB to decrease Portal Pressure Somatostatin - more effective the Pitessin. Lacks Vasoconstriction |
|
what are some non-pharmacologic Tx to control bleeding in Varices
|
Esophageal balloon tamponade
Injection sclerotherapy—endoscopy Variceal banding |
|
Can nitroglycerin be used for Varices
|
Yes with Vasopressin to reduce coronary vasoconstriction.
|
|
Is the following statement True or False?
Bleeding esophageal varices result in an increase in renal perfusion. |
False - Bleeding esophageal varices do not result in an increase in renal perfusion. Bleeding esophageal varices result in an decrease in renal perfusion.
|
|
Which of the following treatment modalities exert pressure directly to bleeding sites in the esophagus and stomach?
a. Injection sclerotherapy b. Portal-systemic shunt c. Pitressin d. Balloon tamponade |
d. Balloon tamponade
Rationale: Balloon tamponade exerts pressure directly to bleeding sites in the esophagus and stomach to treat bleeding esophageal varices. |
|
Nsg Management for Varices includes
|
Monitor for encephalopathy - emotional and cognitive status
Parenteral nutrition Gastric suctioning Oral care Vitamin K Blood transfusions Decrease anxiety |
|
what are things we should monitor for
|
Monitor patient condition frequently, including emotional responses and cognitive status.
Monitor for associated complications such as hepatic encephalopathy resulting form blood breakdown in the GI tract and delirium related to alcohol withdrawal. Monitor treatments including tube care and GI suction. |
|
what type of environment is good for pt.
|
Quiet clam environment and reassuring manner
Implement measures to reduce anxiety and agitation Teaching and support of patient and family |
|
Hepatic encephalopathy and coma occurs primary in pts with..... and .....
|
portal HTN and Portal Shunting
|
|
what is hepatic encephalopathy from
|
From Profound liver failure from accumulation of ammonia and toxic metobolites
Ammonia from bacterial digestion of dietary and blood proteins Possible generation of endogenous benzodiazepines or opiates |
|
what is the coma from
|
increased toxins, ammonia and
Advanced false or weak neurotransmitters may cause hepatic coma |
|
What are the early manifestations of encephalopathy
|
minor mental & motor changes, day sleeping & insomnia @ night, hyperactive deep tendon reflexes,
Fector hepaticus, may see Asterixis (liver flap), apraxia |
|
what are the late manifestations of encephalopathy
|
DTRs disappear, flaccid, may have seizures
|
|
what is fector hepaticus
|
liver breath, fruity or musty
|
|
what is liver flap
|
tremoors
|
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what is apraxia
|
flexion of the wrist, inability to draw connected stick figures/stars
|
|
what is pharmacological management of encephalopathy
|
Lactulose (Cephulac) - decreases colon pH by removing amonia (excreted into stool), bowel evacuation, changes fecal flora
IV glucose, vitamins, electrolytes Neomycin - antibiotic diruetics Flagyl (metronidazole) same as Neomycin |
|
what is Neomycin do
|
it is an antibiotic to reduce # of GI bacteria capable of converting urea to ammonia.
|
|
what is the objectives for tx of cirrhosis
|
• Control bleeding
• Improve nutrition • Prevent skin breakdown • Prevent encephalopathy • Control fluid retention |
|
what vitamins are for mgmt of encephalopathy
|
B comples, folic acid, iron
|
|
nsg care of encephalopathy
|
• Daily Weights
• Monitor Electrolytes, Ammonia Levels • Assess Bowel Sounds & Measure Abdominal Girth • Maintain Diet • High CHO, High Calorie,LOW PROTEIN!!!!, Low Fat, as low as 500 to 800 mg NA+, Soft Diet • Consents for Procedures, Teaching • Monitor for signs of hepatic encephalopathy • Routine care, including pre-op & post-op care for portal caval shunts • Meticulous skin care |
|
Is protein high or low in encephalopathy
|
low,
high CHO low fat Na is 500=800 |
|
what is a spider angioma
|
above the waist on the skin surface
|
|
Nsg considerations for assessment
|
Focus upon onset of symptoms and history of precipitating factors
Alcohol use/abuse Dietary intake and nutritional status Exposure to toxic agents and drugs Assess mental status Abilities to carry on ADL/IADLs, maintain a job, and maintain social relationships Monitor for signs and symptoms related to the disease including indicators for bleeding, fluid volume changes, and lab data |
|
nsg considerations for Diagnosis
|
Activity intolerance
Imbalanced nutrition Impaired skin integrity Risk for injury and bleeding Complications: Bleeding and hemorrhage Hepatic encephalopathy Fluid volume excess |
|
nsg considerations for Planning
|
Goals may include increased participation in activities, improvement of nutritional status, improvement of skin integrity, decreased potential for injury, improvement of mental status, and absence of complications.
|
|
nsg considerations for Activity Intolerance
|
Goals may include increased participation in activities, improvement of nutritional status, improvement of skin integrity, decreased potential for injury, improvement of mental status, and absence of complications.
|
|
nsg considerations for Imbalanced Nutrition
|
I&O
Encourage patient to eat Small frequent meals may be better tolerated Consider patient preferences Supplemental vitamins and minerals, especially B complex, provide water-soluble forms of fat-soluble vitamins if patient has steatorrhea High-calorie diet, sodium restriction for ascites Protein is modified to patient needs Protein is restricted if patient is at risk for encephalopathy |
|
other interventions, safety/skin
|
Impaired skin integrity
Frequent position changes Gentle skin care Measures to reduce scratching by the patient Risk for injury Measures to prevent falls Measures to prevent trauma related to risk for bleeding Careful evaluation of any injury related to potential for bleeding |
|
what are infectious causes of Hepatitis
|
Viral
Bacterial Fungal Rickettsial Protozoal |
|
what are noninfectious causes of hepatitis
|
Metastatic Cancer
Alcoholism Chemical or Drug Reaction Rheumatological (lupus) |
|
what is viral hepatitis
|
a systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical changes. A, B, C, D, E, Hepatitis G and GB virus-C
|
|
what is nonviral hepatitis
|
—toxic and drug induced
|
|
which hepatitis is considered infectious hepatitis
|
hepatitis A
|
|
which hepatitis is considered Serum hepatitis
|
HBV
|
|
which hepatitis is considered post transfusion hepatitis
|
HCV
|
|
which hepatitis is considered Delta virus
|
HDv
|
|
which hepatitis is considered enteric non-A, non-B
|
HEV
|
|
what is the incubation and lasting time for HAV
|
Incubation--one month
Illness lasts 1-2 weeks |
|
what is the incubation and lasting time for HBV
|
Long Incubation period 26 weeks (up to 6 months)
Early acute phase 2-3 weeks Chronic |
|
what is the incubation and lasting time for HCV
|
Incubation 2 weeks to 6 months
Communicable 1-2 weeks before symptoms Chronic |
|
what is the incubation and lasting time for HDV
|
Incubation: 2-26 weeks
chronic |
|
what is the incubation and lasting time for HEV
|
Incubation 15-65 days
self limiting - non chronic |
|
how is HAV contracted
|
Fecal–oral transmission
Spread primarily by poor hygiene; hand-to-mouth contact, close contact, or through food and fluids |
|
how is HBV contracted
|
• Blood
• Body fluids • Mother to baby/pregnancy & birth • IV drug needle sharing, tatoos • Dialysis • Broken skin |
|
how is HCV contracted
|
- The most common blood-borne infection
Transmission needle sticks blood transfusions IV drug use sexual contact |
|
how is HDV contracted
|
Only persons with hepatitis B are at risk for hepatitis D.
Transmission is through blood and sexual contact. |
|
how is HEV contracted
|
Transmission oral-fecal route
Resembles hepatitis A and is self-limited with an abrupt onset. No chronic form |
|
s/s of HAV
|
mild flu-like symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen
Anti-HAV antibody in serum after symptoms appear |
|
Dx of Hep A
|
Diagnosis
Positive anti-HAV IgM antibody Anti-HAV IgG Elevated liver function tests Stool specimen |
|
Tx of HAV
|
Bed rest, high protein, low fat diet
Immune globulin within 2 weeks of exposure |
|
Prevention of HAV
|
Good hand washing, safe water, and proper sewage disposal
Vaccine Immunoglobulin for contacts to provide passive immunity |
|
why is a pt with HAV on bed rest
|
to decrease metabolic demaind, will increase blood flow and regenerate liver cells
|
|
how does the dosing of the Vaccine for HAV work - how many doses
|
Hepatitis A vaccine: one dose protects exposed children, recommended to travelers to high-risk countries
|
|
what are the immunoglobulins for
|
passive immunity (not active like the vaccine). for family members prophylactic or those who are exposed within 2 weeks. Lasts 6-8 weeks only
|
|
what does anictertric mean
|
with out jaundice
|
|
when is the hep A antigen found in the stool
|
7-10 days before illness and 2-3 weeks after symptoms appear.
|
|
main consideration with HAV
|
HAND WASHING!!
|
|
Hep B may progress to
|
cirrhosis, chronic hepatitis, liver cancer, death
|
|
who is most likely to get HBV
|
Highest in young adults, homosexual men, heterosexuals with multiple sex partners, health care & public safety workers
300,000 cases/year 1 million carriers in U.S. |
|
the virus Hep B has antigenic particles that elicit specific antibody markers during different stages of the disease
what are they |
HBsAg (Hepatitis B Surface Antigen)--incubation or early acute phase. At 3 months, chronic or carrier state.
HBeAg (soluble antigen)--high infectivity, more likely to be chronic. Anti-HBs (antibody to surface component of B virus)--after symptoms gone & HBsAg gone). Anti-HBc IgM (antibody to core B antigen)--acute infection with B virus. Anti-HBc (antibody to core B antigen)--past infection. Not protective. |
|
if you have Anti-HBs antibody where are you in the disease
|
symptoms gone, and HBsAg is gone (1st one)
due to recovery of Hep B or to vaccine |
|
if you have HBc antibody to surface component of B virus, where are you in the disease
|
past infection - no longer protective
|
|
if you have HBeAg (soluble) antigen, where are
you in the disease |
hihly infective
|
|
if you have HBsAg surface antigen where are you in the disease process
|
incubation or early acute phase. At 3 months, chronic or carrier state.
|
|
if you have anti-HBc IgM antibody to core B antigen where are you in the infection
|
acute infection with B virus
|
|
how is HBV diagnosed
|
Elevated liver function tests:
Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Elevated Alkaline Phosphatase Total bilirubin |
|
s/s of HBV
|
are insidious and varible
|
|
Tx Meds for HBV
|
• Recombinant interferon
• alfa-2b (Intron-A) o 33% remission in chronic o 10% cured • HB immune globulin (HBIG) • Lamivudine (Epivir) - antiviral agent with adefovir (good for transplants) • Adefovir (Hepsera) Medications for chronic hepatitis type B include alpha interferon and antiviral agents:lamividine (Epivir), adefovir (Hepsera) |
|
non pharmacologic interventions for HBV
|
• Bedrest
• Low protein diet • Prevention: • HBV vaccine Vaccine: for persons at high risk, routine vaccination of infants. Passive immunization for those exposed. Standard precautions/infection control measures Screening of blood and blood products Condom use Standard precautions • Full Recovery: negative HBsAg test, Positive anti-HBs, Normal ALT (SGPT) |
|
which Hepatitis is least likely to have S/S
|
Hep C
chronic carrier state frequently occurs |
|
when is Hep C communicable
|
1-2 weeks before symptoms
|
|
how is Hep C transmitted
|
needle sticks
blood transfusions IV drug use sexual contact |
|
how is Hep C diagnosed
|
enzyme immunoassay (EIA) - assays confirm presence of antibodies
recombinant immunoblot assay |
|
Tx for HCV
|
supportive
protective barrier with sex steroids antiviral drugs (Ribavirin) Interferon (Intron-A) there is no benefit of bedrest, diet or Vit. Must have antiviral drugs and Interferon Intron-A alfa 2A |
|
what are good teaching measures for Hep C
|
Prevention
Screening of blood Prevention of needle sticks for health care workers Measures to reduce spread of infection as with hepatitis B Alcohol encourages the progression of the disease, so alcohol and medications that effect the liver should be avoided |
|
what is the contradiction of Hep C meds
|
Ribavirin is contraindicated with Pregnancy
Hemolytic anemia may happen - stop medication |
|
what med will help extend the interferon
|
+PEG will exend the interferon to taking it only once a week
|
|
what combination of meds is important in Hep C
|
Ribavirin an antiviral and
Interferon - Intron A alfa 2A |
|
does HDV have a high mortality
|
yes, seen in Italy, middle east, Africa, south America.
Incidence--epidemically & endemically in those high risk for HBV. |
|
Dx of HDV
|
anti-HDV (antibody to HDV) indicates past of present infection.
|
|
Tx of HDV
|
Supportive
Recombinant interferon alfa-2b Vaccination against HBV prevents |
|
transmission of HDV
|
Transmission is through blood and sexual contact.
Symptoms and treatment are similar to hepatitis B but more likely to develop fulminant liver failure and chronic active hepatitis and cirrhosis. |
|
Is the following statement True or False?
Only persons with hepatitis B are at risk for hepatitis D. |
T - Only persons with hepatitis B are at risk for hepatitis D
|
|
what antigen is required for HDV
|
HBsAg, surface antigen for replication
|
|
HDV may go on to develop
|
fulmiant hepatitis and then progress to chronic active hepatitis and cirrhosis.
|
|
how is HEV transmitted
|
Transmission oral-fecal route
Resembles hepatitis A and is self-limited with an abrupt onset. No chronic form. rare in US |
|
Dx of HEV
|
Diagnosis:
*No test *Diagnosis made if other types ruled out. *Research on Anti-HEV IgM and IgG |
|
Tx of HEV
|
*Supportive (as with HAV)
|
|
how is hepatitis G transmitted
|
Blood
|
|
risk group for Hep G
|
transfusion recipients - 50%
*IV drug users *frequent co-infection with HBV or HCV Associated with chronic liver disease |
|
what is Hep G
|
Positive-stranded RNA virus with nucleotide sequence almost identical to HCV.
|
|
Which of the following types of hepatitis is spread by poor sanitation?
a. Hepatitis C b. Hepatitis B c. Hepatitis A d. Hepatitis D c. Hepatitis A |
A
Rationale: The mode of transmission of hepatitis A is through the fecal-oral route, water, food, poor sanitation, and person-to-person contact |
|
Toxic hepatitis if from
|
hepatotoxins and drug induced hepatitis
Hepatotoxins carbon tetrachloride phosphorus chloroform gold compounds Drug-Induced Hepatitis isoniazid, halothane (use nitrous oxide instead for anesthesia), acetaminophen, anesthetic agents, methyldopa, antibiotics, antimetabolites |
|
toxic hepatitis s/s
|
elevated temperature
persistent vomiting clotting abnormalities hemorrhages (under skin) delirium, convulsions & coma resembles viral, |
|
Tx of toxic hepatitis
|
restore, maintain fluids & lytes
replace blood loss liver transplant rapid relief if ID early, no antidotes |
|
what isFulminant Hepatic Failure
|
is usually defined as the severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease.
|
|
Fulminant Hepatic Failure is caused by
|
viral hepatitis
|
|
s/s of fulminant hepatic failure
|
Signs & Symptoms: (60-85% mortality)
jaundice #1 anorexia coagulation defects renal failure electrolyte disturbances infection hypoglycemia encephalopathy, cerebral edema |
|
Jaundice in Fulminant Hepatic Failure has three stages Highly acute, acute and subacute. When does jaundice occur in each
|
0-7 days = hyperacute
8-28 days = acute 28-72 days = subacute |
|
Tx for heaptic Failure
|
• Bedrest
• Low protein diet • Neomycin • Lactulose • Watch for slower metabolism of narcotics, toxicity • Blood & plasma exchange • Charcoal hemoperfusion • Corticosteroids • Liver transplant • Isolation (Hepatitis A & E) |
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what are the stages of encephalopathy
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1 plamr erythemia, normal loc , night day sleep patterns, asterixis
2 increase drowsiness, 3 everything. arousal difficult, increase deep tendon reflexes, rigidity, marked EEG 4 increase ICP, comatose, flaccidity |
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antidote for acetaminophen
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N-acetylcysteine (NAC). It is most effective when given within 8 hours of ingesting acetaminophen.
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Hepatitis Vaccines - OSHA requires:
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OSHA requires employers to offer Hep. B vaccine to at-risk employees at no cost.
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Hepatitis vaccines - CDC requires
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CDC: Hep. B vaccine to infants & children entering elementary & middle school
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Hep A vaccine is how often
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Hepatitis A vaccine: one dose protects exposed children, recommended to travelers to high-risk countries
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Hep B vaccine is
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• Recombinant form (Engerix-B or Recombivax-B)
• Plasma-derived vaccine (Heptavax-B) |
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how often is hep b vaccine
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• 3 IM doses of 20 mcg. In deltoid for adults:
o Initial dose o 2nd dose in one month o 3rd dose in five months |
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titer for HB vaccine
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Assess titer >10 SN ratio
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if you have been exposed to hep b, what vaccine do you get
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With exposure—give vaccine & Hepatitis B immune globulin
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Health care workers protection includes
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Standard precautions
Wash hands after patient care Hepatitis B vaccine Hepatitis B immune globulin |
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patient protection of Hepatitis includes
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Patient Protection
Patient education Modes of transmission Handwashing after toileting Wash food Barriers from body fluids Vaccines Wash equipment between patients For those with hepatitis: Avoid alcohol (6-12 months) Rest periods are essential |
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which is active, the vaccine or the HBIG
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Vaccine!!!
HBIG is passive prepared from plasma w/high titers of antiBGs. |
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what is liver cancer from
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• Usually associated with hepatitis B and C, cig smoking, fungus (aspergillus )
• Hepatocellular carcinoma (HCC) |
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manifestations of live of cancer
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• Pain, a dull continuous ache in RUQ, epigastrium, or back!!!!!
• Weight loss, loss of strength, anorexia, anemia may occur • Jaundice if bile ducts occluded, ascites if obstructed portal veins |
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nonsurgical mgmt of liver cancer
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Underlying cirrhosis, which is prevalent in patients with liver cancer, increases risks of surgery
Major effect of nonsurgical therapy may be palliative Radiation therapy Chemotherapy Percutaneous biliary drainage (document blood total, color, debris) keep irrigated, don't aspirate |
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what markers are elevated with liver cancer
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alfa fetoprotein tumor marker AFP 30-40% elevation
CEA marker |
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surgical mgmt of liver cancer
|
Treatment of choice for HCC if confined to one lobe and liver function is adequate
Liver has regenerative capacity Types of surgery: Lobectomy Cryosurgery ( -196C) Liver transplant 10% glucose 1st 48 hrs |
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in a lobectomy what is the cut on the R side
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thoracabdominal incision
L - ABD incision |
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what do they use to prioritize ones level for transplant
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MELD score
Model of End-Stage Liver Disease: used to prioritize one’s level by medical need |
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what is Orthotopic Liver Transplantation
|
in the same atomical location
|
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surgical complications of transplantation
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Bleeding - lack of clotting factors
Infection Rejection |
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who isn't considered a candidate for transplant
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severe cardiac and resp disease
metastic malignant live CA Hx of alcohol/substance abuse |
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diet for Transplant
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increase calories, mod fat, decrease Na (ascites) or fluid restrictions if na is low
decrease protein if encephalopathy or elevated ammonia, vitamins |
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what might be cause of rejection
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GVHD - recipients bone marrow T cells attack liver
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s/s of rejection
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increase HR, U R flank Pain, jaundice, lab results
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teaching for transplant
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immunosuppressants - DO NO miss a dose
|
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what are some immunosuppresants
|
Cyclosporine
Tacrolimus Corticosteroids Azathioprine Mycophenolate mofetil Sirolimus (rapamycin) Anti-thymocyte globulin Muromonab-CD3 (OKT3) |
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adverse effects of cyclosporine
|
Nephrotoxicity
Hepatotoxicity Hypertension Hirsutism Gingival Hyperplasia Tremors Paresthesia Nausea/Vomiting Diarrhea |
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adverse effects of azathiprine (Imuran)
|
Bone Marrow Suppression with decreased WBC—leukopenia, thrombocytopenia, anemia, pancytopenia
Increased Risk of Infection Hair Loss Hepatotoxicity Increased Risk of Neoplasm |
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adverse effects of prednisone
|
Increased Risk of Infection
Increased Appetite GI Irritation and ulceration Delayed Wound Healing Increased Risk of Bleeding Cushingnoid Face Muscle Weakness Emotional Distress Cataracts |
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interventions for pt undergoing a liver transplantation
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Preoperative nursing interventions
Postoperative nursing interventions Patient teaching |
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What do the bile salts do to the skin
|
the synthesis and excretion of bile has bile salts that can cause puritis
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How much bile is excreted in 1 day
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1 liter/day
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what is digoxins normal levels and doses
|
levels 1.8 - 2.0
dose 0.15 - .25 geriatrics - loading dose should exceed .125 |
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what are some toxins that effect chronic liver dysfunction under etiology
|
mushrooms
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what is the normal dose of acetaminophen
|
326 - 650
|
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with lab values overall for Liver Disease, what is the normal range
|
under 50. If the lab is over 100 there is disease
|
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what does a low serum albumin (norm 4-5.5) mean for hepatic disease
|
if you have low seum albumin, then pt may get ascites
|
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what is the elevated bilirubin level at
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> 2.5mg/dL
|
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when you have hepatocellular Jaundice (due to damaged liver cells unable to clear bilirubin), what is the changes in the pts wt.
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wt loss initially, later increase due to edema.
|
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what does the urine of obstructive jaundice look like
|
deep orange and foamy
|
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some labs to remember:
Bilirubin liver enzymes |
2.5
<50 okay, > 100 bad! |
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why isn't aldosterone metabolized by the liver, and then what happens, what med do you give
|
aldosterone isn't metaboliszed because liver function is decreased (portal HTN with increased capillary pressure and obstruction of venous blood flow) This makes increase in Na and water leading to ascites along with the decreased albumin contributing to it
Spironolactone (aldactone) |
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where do you measure girth
|
at umbilicus
|
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what is melena
|
black tarry stools
|
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what is the balloon tamponade called
|
Blakemore tube
|
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when in emergencies, to control bleeding with varicies, what is used?
|
Esophageal balloon tamponade
|
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when using ____ as an antibiotic for hepatic encephalopathy, how is it taken
|
PO, 1-3g q 6 hrs for 5 days
|
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in a diet for hepatic encephalopathy, what does the diet contain (protein-wise)
|
low protein 1.5g/kg use vegetable (soy)
also Na low as 500-800, monitor electrolyte labs and call doctor on significant changes. |
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If a pt on Cephulac (lactulose), what do you do if ammonia is 96
|
norm levels 10-80
don't stop med, but call doctor! |
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what type of fluids will be given for encephalopathy
|
D50%, TPN with thiamine and vitamins will be given (Bs, folic acids, iron)
|
|
some other high risks for Hep B
|
tattoos, hemodialysis, blood transfusions, needle sticks, Splashes
|
|
Hep B and A vaccine is active or passive
|
active
|
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Immune Globulin is active or passive
|
passive
|
|
Hep vaccine should be taken if you have an allergy to
|
bakers yeast
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