Glossary of Block VII, WeekIII
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- what is the dual blood supply to the liver?
- 1. hepatic artery
2. portal vein
- describe how blood exits the liver
- central veins to hepatic vein to IVC
- which zone of the liver gets more blood and nutrients: the periportal or the centrolobular?
- periportal (peripheral)
(centrolobular is the most susceptible to anoxia)
- what lies at the center of an acinus?
- portal triad
- describe the three zones of the liver and their respective blood supply
- 1. Zone 1 - surrounding portal triad
2. Zone 2 - middle portion
3. Zone 3 - periphery, recieves blood that is poorest in oxygen and nutrients
- liver plates run between ? and ?
- run between central veins and portal areas
- Sinusoids are lined by?
- endothelial cells and Kupffer cells
- What is found in the space of Disse?
- stellate cells (aka. cells of Ito)
- define limiting plate
- the layer of hepatocytes closest to portal areas
- what is the most sensitive test for acute hepatocellular injury?
- which enzyme is elevated in cholestasis?
- Alkaline phosphatase
- which enzyme is a sensitive detector of chronic alcohol consumption?
- Gamma glutamyl transpeptidase
(also a sensitive indicator of hepatobilary disease)
- what does ceruloplasmin measure?
- transport and maintenance levels of copper
- describe copper levels in Wilson's disease
- What is alpha-fetoprotein?
- a tumor marker for hepatocellular carcinoma (also for germ cell tumors of ovary/testis)
- what is the enzyme called that conjugates bilirubin in the liver?
- what happens to conjugated bilirubin once it is excreted into bile?
- it is decongugated by bacteria in the intestine and degraded to urobilin. 20% is reabsorbed, 80% is excreted
- which type of bilirubin does the van den Bergh reaction measure?
- direct (conjugated) bilirubin
(then alcohol is added and total bilirubin can be measured)
- why does physiologic neonatal hyperbilirubinemia occur?
- caused by:
- functional immaturity in bilirubin clearance
- increased bilirubin production
- intestinal absorption of unconjugated bilirubin
- when do bilirubin levels peak in physiologic neonatal hyperbilirubinemia?
- day 5
- why is hyperbilirubinemia associated with breastfeeding?
How is this differentiated from physiologic neonatal hyperbilirubinemia?
- breast milk contains an inhibitor of bilirubin conjugation.
here bilirubin levels peak at 10-20 days
- what goes on in transient familial neonatal hyperbilirubinemia?
- - inhibitor of bilirubin conjugation present in maternal serum
- peak bilirubin level w/i 4 days, may cause kernicterus
- which two types of inherited disorders of bilirubin metabolism result in unconjugated hyperbilirubinemia?
- 1. Crigler-Najar syndromes I and II
2. Gilbert syndrome
- which two inherited disorders of bilirubin metabolism result in conjugated hyperbilirubinemia?
- 1. Dubin-Johnson syndrome
2. Rotor syndrome
- three classes of causes of conjugated hyperbilirubinemia?
- 1. biliary obstruction
2. parenchymal liver disease/cholestasis
3. metabolic disorders
- describe the morphology of cholestasis (5)
- - accumulation of bile pigment within hepatic parenchyma
- dilated bile canaliculi with bile plug
- feathery degeneration of hepatocytes
- bile lobes/infarcts
- portal tract fibrosis
- lab test characteristic of cholestasis vs. hepatitis
(ALP, AST, ALT)
- 1. marked elevation of Alkaline Phosphatase
2. milder elevations of AST, ALT
(hepatitis has marked elevations of AST, ALT, rather than Alk. phos.)
- extrahepatic causes of cholestatic liver disease (6)
- 1. gallstone in common bile duct
3. bile duct stricture
4. sclerosing cholangitis (fibrosis of bile ducts)
5. carcinoma of ampulla of Vater
6. carcinoma of head of pancreas
- intrahepatic causes of cholestatic liver disease?
- 1. hepatitis
3. primary biliary cirrhosis
- causes of hepatitis other than viral? (3)
- 1. alcohol, drugs or both
2. metabolic liver disease (hemochromatosis, alpha-1 antitrypsin deficiency, wilson's disease)
- what are the three major pathological mechanisms underlying cirrhosis?
- 1. cell death
- Top 3 causes of cirrhosis?
- 1. alcoholic liver disease
2. viral hepatitis
3. biliary disease
- stimuli for stellate cell activation? (4)
- 1. Chronic inflammation (TNF, IL-1)
2. Cytokine production (TGF-B, PDGF)
3. disruption of cellular matrix
- 3 types of portal hypertension?
- 1. prehepatic
- Prehepatic causes of portal hypertension?
- 1. portal vein thrombosis
2. portal vein stenosis
- Posthepatic causes of portal hypertension?
- 1. R sided heart failure
2. constrictive pericarditis
3. hepatic vein obstruction
- intrahepatic causes of portal hypertension? (6)
- 1. cirrhosis
3. granulomatous disease
5. miliary TB
- clinical consequences of portal hypertension? (4)
- 1. ascites
2. postsystemic venous shunts
3. congestive splenomegaly
4. hepatic encephalopathy
- three theories behind the pathogenesis of ascites? (3)
- 1. cirrhosis causes vascular obstruction, which causes increased hydrostatic pressure in sinusoids, which leads to ascites
2. cirrhosis leads to decreased albumin in blood. this leads to decreased plasma oncotic pressure, leads to ascites
3. leakage from liver surface
- in portal hypertension: thrombocytopenia and anemia suggest?
- congestive splenomegaly
- mortality of acute liver failure?
- what types of viral hepatitis may cause acute liver failure?
- Hep A,B,C,D,E
- which drug is notorious for causing acute liver failure?
- toxins causing acute liver failure (3)?
- 1. CCl4
2. Amanita phalloides
- vascular causes of acute liver failure?
- 1. ischemia
3. malignant infiltration
4. Budd-Chiari syndrome
- three miscellaneous causes of acute liver failure?
- 1. Wilson's disease
2. autoimmune hepatitis
3. acute fatty liver of pregnancy (AFLP)
- what is hepatorenal syndrome?
- kidney failure in patients with severely compromised liver function (w/o any other known causes of renal failure)
- what is hepatopulmonary syndrome?
- intrapulmonary microdilation (with liver disease or portal hypertension)
tx. - liver transplant
- what causes hepatic encephalopathy?
- portal blood enters the systemic circulation without being processed by the liver. appears to be associated with high ammonia levels
- what are the three clinical phases of viral hepatitis?
- 1. prodrome
2. icteric phase (jaundiced, ill)
3. convalescent phase
- what are some s/s of decompensated cirrhosis brought about by viral hepatitis?
- portal HTN
fulminant liver failure
- lab indications of acute viral hepatitis?
- extremely high levels of:
- describe the hepatic histological characteristics of acute viral hepatitis
- 1. hepatocyte injury or death
2. balloned hepatocytes
3. inflammatory infiltrate
4. bridging necrosis
5. Kupffer cell hyperplasia
6. portal tracts infiltrated with inflammation
7. may have cholestasis
- describe the hepatic morphology in severe chronic viral hepatitis (5)
- 1. increased inflammation in portal areas
2. bile duct damage
3. bridging necrosis
4. fibrous tissue deposition
5. regenerative hepatic nodules
- what is the predominant mode of transmission of HepA?
- where does the HepA virus replicate?
- jejunum (before it is transported to the liver)
- how is the HepA virus shed in the feces?
- liver -> excreted in bile -> feces
(shedding occurs during the prodrome phase, before it is clinically apparent)
- what is unique about a HepA infection?
- no carrier state
does not lead to chronic disease
- how long can relapsing HAV last?
- what type of virion is HepB
- HepB belongs to which family of viruses?
- mode of transmission of HepB?
- HepB is associated with increased risk of what cancer?
- hepatocellular carcinoma
- what is the incubation period of HepB?
- is there a correlation between the severity of an acute HepB attack and the progression to chronicity?
- the more severe the acute attack - the least likely to progess to chronicity
- which HepB serum antigen reflects the core protein?
- which HepB serum protein reflects the envelope glycoprotien?
- what is the function of protein X in HepB?
- virus replication
- describe the appearance of HBsAG (levels throughout the infection)
- *appears in serum weeks before clinical sx
*persists for a total of 3-4 months
- HBsAg levels present for >6 months denotes?
- carrier state
- what is the significance of antibodies to HBsAg appearing?
- indicates recovery as well as immunity
(appear a few weeks after the dissapearance of the antigen)
- which antibody is a marker of hepB infection in the "window period" between the dissapearance of HBsAg and the appearance of anti-HBsAg?
- in a HepB infection: which viral marker is closely correlated with viral infectivity?
- which type of Hepatitis can only be seen in conjunction with a HepB infection?
- type of genome of HDV?
- RNA virion
- why must HepD be associated with HepB?
- HDV cannot replicate on its own - genome incomplete
- clinical s/s of a patient with a HepB and HepD infection?
- *severe course
*suspect in a patient with a worsening case of HBV
- HepC belongs to which viral family?
- structure of HepC genome?
- HepC is associated with what cancer?
- hepatocellular carcinoma
- why is HepC often diagnosed when a person has been a chronic carrier for a while?
often find incidentally
- a chronic carrier of HCV often develops?
- cirrhosis or HCC
- transmission of HepE?
- can hepE become chronic?
- when is hepE unusually fatal?
- during pregnancy (20%)
- HGV belongs to which family of viruses?
- transmission mode of HGV?
(seen frequently in blood donors)
- can HGV become a chronic infection?
- yes, but not associated with mortality or HCC
- hepatocellular carcinoma is almost always seen after?
- cirrhosis of any kind
- besides hepatitis viruses, what are three other viruses associated with hepatitis?
- 1. EBV
2. Yellow fever
- bacteria known for causing hepatitis?
- Salmonella typhi
- what is the most common form of liver disease in the US?
- Alcoholic liver disease
- ETOH is metabolized into what intermediate?
- effect of excess acetaldehyde?
- produces excess NADH in liver mitochondria
*interferes with lipid metabolism, get fatty change
- what would the ALT/AST ratio be in alcoholic liver disease?
- lab results of the following in alcoholic liver disease?
- 1. decreased
- 4 CBC abnormalities seen in alcoholic liver disease?
(WBC, platelet #s, RBC size etc)
- 1. leukocytosis
3. mild anemia
4. increased MCV
- levels of the following in alcoholic liver disease?
2. uric acid
- 1. hypertrigliceridemia
- consequences of a thiamine deficiency in an alcoholic?
- Wernicke syndrome
- effects of alcoholism on the following:
- 1. cardiomyopathy
2. chronic and acute pancreatitis, acute gastritis
3. testicular atrophy, increased spontaneous abortions
- alcoholism is associated with a risk in what 4 GI/liver related cancers?
- is fatty change reversible?
(with no more alcohol consumption)
- alcoholic hepatitis is associated with accumulation of intracytoplasmic eosiniphilic hyaline inclusions known as?
- Mallory bodies
- is alcoholic cirrhosis reversible?
- microscopic characteristics of alcoholic cirrhosis? (4)
- 1. fibrous septae
2. regenerative micronodules or pseudonodules
3. Mallory bodies
- what is the difference between the following hepatotoxic agents?
- 1. predictable or true hepatotoxins
2. non-predictable toxicity (only toxic in a small proportion of people)
- at which hepatic zone are the following drugs toxic:
- 1. zone 3
2. zone 3
3. zone 2
4. zone 3 (or massive)
- tetracycline, phosphorous and ETOH are know to cause what kind of liver damage?
- which 2 drugs are notorious for causing hepatic vein thrombosis?
- oral contraceptives
- oral contraceptives also are known to cause what liver cancers?
- thorotrast is known to cause what sorts of liver cancer?
- how is autoimmune hepatitis clinically diagnosed?
anti-smooth muscle antibodies
(clinical s/s identical to other forms of chronic hepatitis so hard to distinguish)
- what is primary biliary cirrhosis?
- autoimmune liver disease
- which sex is primary biliary cirrhosis more common in?
- pathogenesis of primary biliary cirrhosis?
- destruction of bile ducts by T lymphocytes
- which type of antibodies are a key feature of primary biliary cirrhosis?
- antimitochondrial antibodies (AMA)
- what are some clinical s/s of primary biliary cirrhosis?
- lab tests used to diagnose primary biliary cirrhosis?
- *cholestatic liver function tests
- four histological stages of primary biliary cirrhosis?
- 1. damage to intrahepatic ducts
2. ductal proliferation
- what is primary sclerosing cholangitis?
- chronic inflammatory disease of the biliary tree - causes scarring which narrows and obstructs bile ducts
- is primary sclerosing cholangitis more common in males or females?
- primary sclerosing cholangitis is associated with what other disease?
- ulcerative colitis
- clinical progression of primary sclerosing cholangitis?
- pruritis -> cholangitis -> cirrhosis -> liver failure
- what is a radiographic hallmark of primary sclerosing cholangitis?
- "beading" of barium column in intrahepatic and extrahepatic bile ducts
- two antibodies we can look for in the lab to help diagnose primary sclerosing cholangitis?
- 1. ANA
- which type of hyperplasia is associated with portal HTN?
- nodular regenerative hyperplasia
- which hepatic tumor is associated with OC and anabolic steroid use?
- Hepatocellular adenoma
- what is a rare malignant vascular hepatic tumor that is associated with toxic exposure vinyl chloride, thorotrast and arsenic?
- prognosis of angiosarcomas?
- metastasize widely
death w/i 1yr of diagnosis
- what is the most frequent liver tumor in children?
- gross manifestations of hepatoblastoma?
- single mass
- what is the MC primary hepatic malignancy?
- hepatocellular carcinoma (HCC)
- what are some predisposing factors to HCC?
- 1. viral infections (HBV,HCV)
2. chronic alcoholism (cirrhosis)
3. food contaminants (aflatoxins)
- connection between X protien and HCC?
- X protein (found in HBV) may disrupt normal cell growth
(may activate proto oncogenes and disrupt the normal cell cycle)
- laboratory studies that help us diagnose HCC?
- increased alpha fetoprotein
- which has a better prognosis - classic HCC or fibrolamellar HCC?
- fibrolamellar HCC
- cancer that arises from the biliary epithelium anywhere in the biliary tree is called?
(bile duct carcinoma)
- where are some common places in the biliary tree for cholangiosarcoma to arise?
- *convergence of L and R hepatic ducts
*small bile ductules at periphery of hepatic lobule
- types of cancer that like to metastasize to the liver?
- risk factor for gallstones?
- 1. increased age
3. high estrogen levels (obesity, multiparous, OCs)
- pigment stones are the result of?
- precipitation of excess insoluble unconjugated bilirubin
(can be associated wtih bacterial infection or hemoytic anemia)
- what makes up 96% of all cases of acute cholecystitis?
- obstruction of the cystic duct by gallstones
- what are some causes for acute acalculous cholecystitis?
- major non-biliary surgery
multiple injury states
severe burns, sepsis
- effect of opiates on acute cholecystitis?
- increase the tone in the sphincter of Oddi - make it worse
- one of the complications of gallstones is an empyema. what is it?
- "pus filled gallbladder"
(usually see following an infection)
- what are three gas forming bacteria that are known to cause an emphysematous gallbladder?
- 1. E.coli
2. Clostridium welchii
3. anaerobic streptococcus
- what is the most common type of clinical gallbladder disease?
- chronic cholecystitis (calculous)
- are most tumors of the gallbladder benign or malignant?
(benign are rare)
- what makes up the majority of gall bladder carcinomas?
- neoplasms of the gall bladder are more common in which race?
- Native Americans
- prognosis for gall bladder cancer?
- Poor -- mean survival time is 6mo from diagnosis
(most have metastasized by the time they are diagnosed)
- what is a Klatskin tumor?
- a cholangiocarcinoma that arises from the bifurcation of the main hepatic ducts
(may mimic biliary cirrhosis and obstructive jaundice)
- are thromboses more common in the hepatic artery or portal vein?
- portal vein
- events that could cause a portal vein thrombosis?
- what is Budd-Chiari syndrome?
- hepatic vein thrombosis/IVC thrombosis
- clinical s/s of Budd/Chiari?
- Budd/Chiari syndrome is MC associated with what other disorders? (4)
- 1. polycythemia vera
3. other abdominal neoplasms
4. complication of pregnancy
- what condition causes a nutmeg liver?
- right sided CHF
- what genetic mutation is associated with alpha-1-antitrypsin deficiency?
- hepatic manifestations of a homozygous P1ZZ mutation?
- defective secretion of alpha-1-antitrypsin from the liver
(it's stuck in ER of hepatocyte, causes liver injury)
- function of normal working alpha-1-antitrypsin?
- inhibits neutrophil protease and elastase
- manifestations of an alpha-1-antitrypsin deficiency in:
- 1. emphysema
2. liver disease (cirrhosis)
- clinical features of alpha-1-antitrypsin deficiency in newborns?
- *persistent neonatal jaundice
*may present with portal HTN, esophageal bleeding, hypersplenism
*progresses to acute fulminant liver failure
- hepatic clinical features of alpha-1-antitrypsin deficiency in adults?
- chronic hepatitis
- lab values that assist in diagnosis of alpha-1-antitrypsin deficiency?
- what is the classic histological hallmark of alpha-1-antitrypsin deficiency?
- PAS positive (represents retained alpha-1-antitrypsin in hepatocytes)
- what is the most severe form of alpha-1-antitrypsin deficiency?
(there is a Z-, but it is incompatible with life)
- what is the mildest form of alpha-1-antitrypsin deficiency?
- what is Wilson's disease?
- impaired copper excretion by liver
(followed by copper deposition in other organs)
- where is the site of the biochemical defect seen in Wilson's disease?
- liver membrane
(mutation in ATP7B on chrom.13)
- when are most diagnoses of Wilson's disease made?
- after 5yrs old
(Copper needs time to accumulate)
- inheritance pattern of Wilson's disease?
- autosomal recessive
- what are the serum ceruloplasmin levels in a patient with Wilson's disease?
(ceruloplasmin is a copper binding protein-decreased levels mean it is all bound to copper)
- where does excess copper accumulate?
- Kayser-Fleischer rings are deposits of copper in?
- Descemet's membrane circumscribing the cornea
- treatment for wilsons disease?
- chelation of copper
- what stain can be used to see the copper deposits in the liver?
- Rhodamine stain
- what is hemochromatosis?
- iron storage disease
(1/3 of stored iron is in the liver)
- where in the GI is iron absorbed?
- duodenum and proximal jejunum
- when iron cannot be absorbed where does it accumulate?
(end result is cirrhosis and/or HCC)
- mutation of which protein leads to hemochromatosis?
(results in impaired transferrin)
- what is the "classic triad" seen in iron storage diseases?
- 1. pigment cirrhosis with hepatomegaly
2. skin pigmentation
3. diabetes mellitus
- in which population is iron storage diseases most prevalent?
- people of northern european ancestry
- diagnostic tests used to look for iron storage diseases?
- 1. transferritin saturation
2. unsaturated iron binding capacity
3. serum ferritin
4. liver biopsy
5. hepatic iron concentration/index
- which mutation would be looked for in genetic testing for hemochromatosis?
- C282Y mutation for HFE
- what is choledocholithiasis?
- presence of stones within the bile ducts of the biliary tree (stones migrated from gallbladder)
- where do stones tend to impact in choledocholithiasis?
- ampulla of Vater
- complications of choledocholithiasis? (4)
- 1. pancreatitis
3. hepatic abscess
4. biliary cirrhosis
- clinical s/s of choledocholithiasis? (3)
- 1. fever
3. acute jaundice
- what is cholangitis?
- inflammation of the bile ducts resulting from any obstruction of bile flow
(commonly from an ascending bacterial infection of the bile ducts)
- common infecting bacteria causing cholangitis? (5)
- 1. E.coli
5. enteric gram neg. anaerobes
- what are the 2 forms of extrahepatic biliary atresia?
- 1. embryonic (fetal) type
2. perinatal form (most)
*manifests 4-8 wks following a jaundice free period*
- what is the location of the following types of biliary atresia?
1. type 1
2. type 2
3. type 3
- 1. common bile duct
2. hepatic bile ducts
3. above porta hepatis
- what two things control (exocrine) pancreatic secretions?
- 4 major enzymes released by exocrine pancreas?
- 1. amylase (CHO)
2. lipase (TAGs)
- which lab value is followed to diagnose acute pancreatitis?
- serum amylase
(95% specificity first 24hrs)
- what are the causes of death in acute severe pancreatitis? (4)
- 1. shock
4. septic pancreatic abscesses
- why is hypocalcemia seen in acute pancreatitis?
- circulating Ca++ is precipitated into calcium-fatty acid soaps
- two MC predisposing conditions for pancreatitis?
- excessive alcohol intake
- what characterizes chronic pancreatitis?
- progressive parenchymal FIBROSIS and CALCIFICATION
- MC cause of chronic pancreatitis?
- are pancreatic pseudocysts associated with acute or chronic pancreatitis?
- what is the difference between a pancreatic cyst and a pancreatic pseudocyst?
- pseudocyst - lacks epithelial lining, solitary
cyst - anomaly of pancreatic duct
- 4 risk factors for pancreatic cancer?
- 1. smoking (2-3x)
2. chemical carcinogens (nitrosamines, polycycline hydrocarbons)
3. hi-fat diet
- MC pancreatic cancer?
- where do most pancreatic carcinomas arise?
- head of pancreas
(cause obstructive jaundice)
- which cells do most pancreatic carcinomas arise from?
- ductal cells (99%)
- prognosis for pancreatic carcinoma?
- usually results in death within 1 yr
(diagnosis is very late)
- where is ETOH absorbed?
- stomach (20%)
- which enzyme metabolizes 90% of alcohol in the liver and GI?
- alcohol dehydrogenase
- what type of kinetics does alcohol metabolism have?
- zero order kinetics
(always at a rate of 1drink/hr)
*drink any more than that - goes to serum*
- which would have a greater intoxication effect:
4 drinks in 1 hr
4 drinks over 4 hrs
- 4 drinks in one hour
- when would the MEOS kick in ?
- when the BAC >0.1
- what is one possible reason for the increased tolerance to ETOH?
- Induction of the MEOS can occur
- ETOH is metabolized by either alcohol dehydrogenase or MEOS into?
- what happens to acetaldehyde?
- aldehyde dehydrogenase converts it to acetic acid, then to acetyl CoA, then to CO2 and H2O
- ETOH has what effect on the CNS?
- the first part of the CNS to be affected by alcohol is?
then what is affected by higher doses?
- highly integrated functions
higher doses affect motor function
- ETOH and dopamine together have what effect?
- ETOH increases DA mediated pleasurable effects
- effect of ETOH increasing the release of NE?
- contributes to enlivening and activating "party" effects of alcohol
- effect of ETOH on GABA activity?
- potentiates GABA activity through the GABA A receptor
(amnesia and sedation effects)
- effect of ETOH on glutamate receptors?
- blocks excitatory NMDA receptor
(amnesia and other cerebral depressant effects)
- what antidepressant drug is associated with N/V when taken with alcohol?
- Serotonin stimulation
- which effect is responsible for the warm, flushed feeling experienced with alcohol intake?
(loss of central vasomotor control)
- cardiac manifestations of alcoholism? (2)
- effects of ETOH on gastric secretions?
- increased with low BAC
decreased with high BAC
- effect of ETOH on sphincter of oddi? significance?
- increased secretion and spasm - causes pancreatitis
- chronic alcoholism results in induction of which enzyme (responsible for some of the tolerance effects)
- excessive alcohol intake inhibits gluconeogenesis. consequences?
- mechanism of acetaldehyde causing hepatotoxicity?
- acetaldehyde precipitates oxidative stress (ROS) which leads to tissue damage
- Renal effects of ETOH?
- diuresis due to reduction of ADH
- what is the significance of less total body water in women vs. men?
- women have a higher BAC because of this
- describe the effects at the following BACs
- 1. feel relaxed, light feeling of exhileration
2. warmth and relaxation; decrease of fine motor skills
3. reaction time slowed, muscle control poor, speech slurred, legs wobbly
- describe the effects at the following BACs:
- 1. judgement clouded, inhibitions lessened, impaired reason and logical decision making
2. behavior impaired, difficult to stay awake
3. semi stupor or deep sleep
4. coma and danger of death; breathing center paralyzed
- what would the interaction of ETOH be with other drugs that utilize the CYP 450 system? (ie. clearance rates of the drugs)
- increases clearance of these drugs
- where does disulfiram act?
- inhibits aldehyde dehydrogenase
- besides disulfiram, what are some other inhibitors of aldehyde dehydrogenase?
- in ETOH withdrawal, when is the onset of symptoms?
- 6-8 hrs after d/c alcohol
- In ETOH w/d: when are peak syptoms experienced?
- 24-36 hrs after d/c
- what is the significance of having increased excitatory NMDA (glutamate) receptor levels at the time of stopping alcohol?
- causes large intracellular Ca++ influx, hyperexcitability and cell death. this results in a sudden decrease in ETOH mediated inhibitory actions via GABA - "excitatory overdrive"
- which neurotransmitter mediates the "excitatory overdrive"?
- what is the most serious stage of alcohol withdrawal syndrome?
- Delerium Tremens (DT)
- untreated, DT has a mortality of?
- up to 15%
- 4 drugs used to treat ETOH withdrawal (not DTs)
- 1. benzodiazapenes
4. B-Blockers or clinidine
- give some examples of benzodiazapenes used to treat ETOH w/d
- 1. chlordiazepoxide
- would anticonvulsants be used prophylactically?
only use if prolonged or frequent seizures occur
- why are beta blockers beneficial in treating ETOH w/d
- block sympathetic nervous system activity
- what is normally administered to treat DTs?
- large doses of benzodiazapenes
*if not controlled, use pentobarbital or propofol*
- which two benzodiazapenes are "long duration of action" agents?
- which benzodiazapene is considered a short action of duration agent and is therefore "safer" in elderly or liver disease?
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