1When the liver is compromised in hepatic enceph., what clinical management strategies will you do?
recognition and treatment of the immediate ramifications of the disease
2This is known as deteriorating neurological functions in prolonged or extreme disease
hepatic encephalopathy
3Identidy the 3 consistent precipitating factors in hepatic enceph
1. GI bleeding 2. Increased dietary protein 3. electrolyte disturbances
4What are the other potential contributors to hepatic enceph.
1. superimposed acute viral hepatitis 2. extrahepatic bile duct obstruction. 3. surgery in a pt with cirrhosis
5In the cellular level, what is the pathophysiology of hepatic enceph.?
Excess of nitrogenous wastes within the body and the inability of the liver to clear these and other waste products
6What is the primary result of protein degradation
Nitrogenous wastes from within the body
7Small amounts of ______ a nitrogenous product are produced normally by the what organs?
Ammonia, liver and kidneys
8What are the primary sources of ammonia?
1. Protein digestion within the small intestine 2. Metabolism of urea in the colon
9In cellular level of hepatic enceph., what is the effect of bacteria within the intestine?
It will facilitate the deamination of AA and proteins, releasing ammonia
10What is the effect of protein to nitrogen production
Increase
11What is the relationship between protein and nitrogen production?
Directly
12What organ is responsible for the conversion of ammonia into excretable urea?
Liver
13T or F: Nitrogenous wastes are not detoxified by the liver
True
14T or F: A problem arises when when the increased protein uptake and/or ammonia production is greater than the liver can tolerate
True
15What is the primary agent implicated in hepatic encephalopathy?
Ammonia production and accumulation
16This is another potential cause of increased ammonia production
Hypokalemia
17Effect of systemic alkalosis to the ratio of NH3-NH4
Increase
18Effect of alkalosis to the renal production of ammonia
Increase
19This the only uncharged ammonia that is gaseous and able to cross the blood-brain barrier(BBB)
NH3
20What is the preferred environment does ammonia move?
Acidotic environment
21Once in the brain, NH3 is metabolized into _______?
Glutamine
22This is an inactive substance and a precursor for several neurotransmitters?
Glutamine
23What are the theories regarding Glutamine in terms of mentation?
Either competes for neurtransmitter receptors or Increases development of inhibitory neurotransmitters which leads to DIMINISHED MENTATION.
24T or F: Almost all pts w/ hepatic enceph have increased serum NH3 levels
True
25T or F: Almost all pts recovering from hepatic enceph have decreased serum NH3 levels
True
26what is the relationship of amount of glutamine found in the CSF and degree of enceph.
Directly or have Good correlation
27What is the role of GABA in cellular level of hepatic enceph.
GABA is important in the developement of hepatic enceph.
28Relationship of GABA and LOC
Inversely
29What is the MOA of GABA
It is responsible for the inhibitory action of benzodiazepines (Valium)
30Relationship of GABA and benzodiazepines
Directly
31What will happen if there is an increased level of GABA in the CNS?
the liver's inability to clear out the amino acids or increased permeability of the BBB to those same AA
32T or F: GABA disturb the balance of inhibitory and excitatory neurotransmitters in the brain?
True
33In terms of gross pathogenesis, what is the risk of developing hepatic enceph?
pts with large-scale GI bleeding in the presence of liver disease
34T or F: Blood within the GI tract ( GI bleeding) is protein-laden
True
35Another precipitator of hepatic enceph?
Electrolyte and acid-base disturbances
36What are the most common causes of imbalances that create alkalotic envi.?
1. Injudicious use of diuretics. 2. vigorous paracentensis. 3. vomiting
37This also been identified as possible causative agent of hepatic enceph in terms of gross pathogenesis.
Acute Infections
38Why acute infections is considered as a possible causative agent of hepatic enceph in terms of gross pathogenesis?
increased catabolic activity that may result in protein breakdown and ammonia production
39What are the decisive factors of hepatic enceph?
1. degree pf hepatic compromise. 2. the amount of nitrogenous substances circulating. 3. shunting of blood past the liver
40What is the common finding in the pt with hepatic enceph?
Cerebral edema
41The most unique classic sign of hepatic enceph?
Asterixis
42When asterixis is found in conjuction with liver disease, it is known as_____
Liver flap
43This is an abnormal muscle tremors that create haphazard and involuntary jerking movements, especially in hands.
Asterixis
44What is the best measurement of asterixis
have the pt hold his/her arms out with hands dorsiflexed
45This is an unusual musty odor of the breath and urine of the pt with hepatic enceph.
Fetor hepaticus
46What is the best indicator of hepatic enceph?
measurement of serum ammonia concentrations
47Summary guidelines in diagnosing hepatic enceph?
1. Acute or chronic hepatocellular disease or extensive portal-systemic shunts. 2. Disturbances of mentation and awareness. 3. Shifting combinations of neurologic symptoms. 4. Nonspecific symmetric, high voltage, slow wave EEG findings
48What is the 1st step in caring for the pt with hepatic enceph?
identification of the precipitating event
49What will happen if you aggresively feed the pt above requirements
Protein imbalance
50This is a broad-spectrum antibiotic that destroys the normal bacterial flora of the bowel responsible for the breakdown of protein into NH3
Neomycin
51What Lab study should you judiciously monitor when administering neomycin
BUN and creatinine
52Another drug used to reduce NH3 levels and is a synthetic disaccharide
Lactulose
53This synthetic disaccharide is converted in the what organ to ______ and _______, which decreases the pH of the bowel.
Lactulose, colon, lactic and acetic acid
54What are the by-products of lactulose?
lactic and acetic acid
55What is the effect of lactic and acetic acid to pH of the bowel?
decrease
56This is an osmotic cathartic, which facilitates excretion of the NH3-laden stool.
Lactulose
57What are the functions of Lactulose?
1. Decrease the pH of the bowel thus reduces NH3 levels 2. facilitates excretion of the NH3-laden stool or osmotic cathartic. 3. metabolism of sugar in the lower intestinal tract. 4. increases water content in stool
58What will you do in order for the oral dose of lactulose to be tolerable?
mix it with fruit juices
59What is the therapeutic goal of oral dose of lactulose?
2-3 soft, acidic stools/day
60This drug suggest that elimination of relapsing encephalopathy is feasible
Flumazenil
61What will you do if hypokalemic alkalosis is a precipitating factor?
careful repletion of K+
62What is the function of K+ hepatic enceph.
Normalization of K+ may restore intracellular and extracellular balances of NH3.
63This is one of the most avoidable precipitators of hepatic enceph.
injudicious use of narcotics and other hepatotoxic drugs
64Hypercapnia theoritically assists in 2 ways:
1. it causes shift in the acid-base balance of the serum. 2. it stimulates the utilization of CO2 to facilitate NH4 production.
65If such mechanims are not successful in reducing ammonia load, what is the alternative mechanism?
Hemodialysis
66What are the nursing responsibilities/management/intervention of the heptic enceph?
1. recognition of the disease process. 2. prevention of complications. 3. facilitate of removal of NH3. 4. protection of compromised pts.
67These are recognized as indices od hepatic enceph
Ammonia (serum) and glutamine (CSF)
68Effect of neomycin
1. aminoglycosides. 2. antibiotic. 3. bacteriocide
69What is cause of hepatic failure in the US
acetaminophen overdose
70What is the non-alcoholic cause of chronic liver failure
Laennec's Cirrhosis
71What are the stages of Laennec's cirrhosis
stage 1: fatty liver. stage 2: cirrhosis. stage 3: cancer
72What is the antidote of acetaminophen toxicity?
N-acetylcysteine
73What is the definitivw treatmenf in liver failure
liver transplantation
74What is the important nursing management in hepatic failure?
elevate the head of the bed
75How does lactulose produce NH3?
increase peristalsis or bowel movement then it will increase absorption
76Diet of pt with hepatic enceph
low protein, high calorie
77Treatment of alcohol intoxication and is an aldehyde dehydrogenase inhibitor
Disulfiram
78What is effect of aldehyde dehydrogenase
metabolizes the alcohol to make it into polar compound for excretion
79How does liver metabolizes the alcohol
Alcohol is primarily metabolized in the liver by ALCOHOL DEHYDROGENASE to ACETYLDEHYDE then it will be converted into POLAR COMPOUND so that itis ready for excretion.
80What problem is this if you have thiamine (B1) deficiency and is associated with alcoholism?
Wernicke-Korsakoff Syndrome
81Wernicke-Korsakoff Syndrome often occur after alcohol intoxication, so what drug will you give to prevent it?
Vitamin B Complex
82What condition is this secondary to repeated vomiting due alcohol intake, which cause irritation to the esophageal lining and this condition is already a pre-cancerous stage?
Barrett's Esophagus
83What specifically vitamin B meds should you give to pt who have alcohol intoxication?
VIT B1( thiamine) & VIT B2(riboflavin)
84What vitamin B that is most depleted by your alcohol in acute alcoholic intoxication?
Vit B1 ( thiamine)
85What is the leading cause of hepatic failure?
Acetaminophen toxicity
86What drug that promotes the conversion of NH3-NH4 because of its ability to degrade an acidic pH
Lactulose
87What drug should you administer to prevent GI hemorrhage since hepatic pts often have elevated INR levels which increases the risk of abnormal bleeding?
Vit K (Phytonadione)
88T or F: Gastric metabolism of ethanol is decreased in women.
True
89What is the primary site of action in acute alcohol toxicity?
CNS
90With chronic alcohol use, the number of GABA receptors increased. This is a phenomenon known______ or _______
tolerance or mellanby effect
91What is the primary excitatory neurotransmitter in the CNS and this neurotransmitter is inhibited by the alcohol?
Glutamate
92How does alcohol intoxication occurs?
Alcohol intoxication occurs when ethanol enters the bloodstream faster than the liver can metabolize it into non-intoxicating byproducts
93This is a selective CNS depressants at low doses and a general depressants at high doses
Ethanol Alcohol
94What is BAC level or blood alcohol level of alcohol coma?
BAC of 0.35-0.45
95What nursing management should you give to pts with alcoholic intoxication?
Administer 50% glucose IV and Vit B complex
96This is defined by alcohol dependence, w/c is the body's physical inability to stop drinking and the presence of alcohol cravings.
Alcoholism
97This is the major inhibitory neurotransmitter and acts as "off" switch that restricts brain activity
GABA
98This is a GABA agonist
Ethanol
99What is the most severe form of ethanol withdrawal, manifested by global confusion and autonomic hyperactivity
Delirium Tremens
100When you combine negative reinforcement and positive reinforcement it will lead to what?
Alcohol addiction or Alcohol Use Disorder
101This is the most specific serum biomarker of heavy alcohol consumption
Carbohydrate-deficient transferrin
102This measures commonly to see if a person has been drinking recently, this can find alcohol in your blood, and shows amount of alcohol that you drank
Blood alcohol Concentration (BAC)
103What is the most effective treatment for alcoholism
a combination of individual and group therapy (motivational interviewing, cognitive behavioral therapy, peer support program)
104What are the clinical manifestations of GI bleeding
Occult blood, hematemesis, melena, & hematochezia
105Vomiting of bright red blood or blood
Hematemesis
106black, tarry, foul-smelling stools passed after a GI bleed
Melena
107bright red blood or maroon stool from the rectum
Hematochezia
108What condition that usually accompanies GI emergencies
Abdominal pain
109What is the prime risk factor of liver cirrhosis?
Age
110How to prevent acute alcohol intoxication
1. eat first before drinking alcohol 2. drink alcohol slowly
111When administering Aspirin, what should you monitor?
GI Bleeding
112Effect of intoxication with activated charcoal
Decrease
113What is/are the MOA of AZATHIOPRINE
1. Purine antagonists 2. Antimetabolite 3. Immunosuppressive agent