chemical injury case presentation Flashcards
what are the effects of acetominophin on blood?
coagulation factors synthesized in liver - so want CBC, PTT, PT, INR
what is ALT?
alanine aminotransferase levels
part of liver enzyme tests for LFT - when injury to liver, cells lysed and enzymes released
10-56 is normal
what is AST?
aspartate transaminase
in heart and liver
part of liver enzyme tests for LFT - when injury to liver, cells lysed and enzymes released
normal is 8-45
what are the pathways in coagulation?
intrinsic and extrinsic
what is PT? what is it used to detect?
prothrombin time
measures intrinsic pathway of coagulation
used to screen for hemostatic dysfunction involving extrinsic pathway due to liver disease, vit K deficiency, factors deficiency, or disseminated intravascular coagulation
what is PTT? how is it measured?
partial thromboplastin time
will be prolonged if there’s a deficiency in clotting factors in both intrinsic pathway and common pathway - so measure of all clotting factors except factor 7
platelet-poor plasma is incubated with phospholipid and surface activator - after activation, Ca is added and time to clot formation is measured
what are some causes of prolonged PTT?
vit K deficiency liver disease DIC factor deficiency antifactor antibodies lupus anticoagulant
how long does acetaminophen take to be fully absorbed?
4 hours - so will see a peak at 4 hours and if only took one dose will see drop after that
when can you use the rumack-matthew normogram?
only for a single acute ingestion and if the approximate time of ingestion is known
how does acetaminophen cause toxicity?
60% of the time, attached to glucouronide and becomes water soluble and can be cleared
35% gets sulfonated, also water soluble so can be cleared
but 5% of the time uses cytochrome P450 to convert it to NAPQI = toxic
normally this will be cleared by conjugating it to glucothione and it can then be conjugated to cysteine or mercaptate and cleared
but if there’s a lot the enzymes needed to add glutathione (CSH) will be overloaded and so the NAPQI will form bonds with AA in proteins and enzymes - these will attack the liver and cause cell death
how does NAC prevent liver failure due to acetaminophen?
can be glutathione substitute
what is NAC? how does it work?
n-acetyl cysteine
exogenous glutathione does not penetrate hepatocytes unless given in massive doses
thiol-containing compound that is hydrolyzed to cysteine
cysteine is then used intracellularly along with glut and glycine to form glutathione (cysteine is the rate-limiting step in this)
glutathione depletion to cytotoxic damage and cell death
glutathione is a protective molecule against many stressors serving as a conjugant, reducing agent and antioxidant
so NAC is a substitute for glutathione - prevents liver damage because gets around the problem of overloading the system
what is direct bilirubin versus indirect bilirubin?
direct = conjugated bilirubin + delta bilirubin
bilirubin that is soluble in plasma
what is conjugated bilirubin?
glucuronide attached bilirubin - soluble
what is direct bilirubin versus indirect bilirubin?
direct = conjugated bilirubin + delta bilirubin
bilirubin that is soluble in plasma
what is conjugated bilirubin?
glucuronide attached bilirubin - soluble
what is delta bilirubin?
bilirubin covalently attached to albumin - soluble
what is delta bilirubin?
bilirubin covalently attached to albumin - soluble
what is unconjugated bilirubin?
no glucuronide attached to bilirubin - very insoluble
what is unconjugated bilirubin?
no glucuronide attached to bilirubin - very insoluble
what is total billirubin?
conjugated + delta + unconjugated
requires detergent or accelerator so that the unconjugated will react with the diazo dye
what is total billirubin?
conjugated + delta + unconjugated
requires detergent or accelerator so that the unconjugated will react with the diazo dye
what is the reason to give a patient lactulose? how does it work
high ammonium levels - ammonia can cross BBB and cause encelopathy - can be charged and uncharged - can clear charged molecules in the urine but can’t clear uncharged molecules - these can cross the BBB
lactulose is metabolized by bacteria in the colon and releases lactic, acetic and other organic acids
=> acidfication of colon contents and favors trapping of ammonium ions in the lumen and prevention of absorption
what is the reason to give a patient lactulose? how does it work
high ammonium levels - ammonia can cross BBB and cause encelopathy - can be charged and uncharged - can clear charged molecules in the urine but can’t clear uncharged molecules - these can cross the BBB
lactulose is metabolized by bacteria in the colon and releases lactic, acetic and other organic acids
=> acidfication of colon contents and favors trapping of ammonium ions in the lumen and prevention of absorption
why would you give a patient vitamin K?
prolonged prothrombin time
vit k will counteract - will cause coagulation to go back to normal
why would you give a patient vitamin K?
prolonged prothrombin time
vit k will counteract - will cause coagulation to go back to normal
where does alpha-amylase come from?
pancreas or salivary glands
most cleared by kidney by glomerular filtration
in acute pancreatitis, amylase levels will be very high
where does alpha-amylase come from?
pancreas or salivary glands
most cleared by kidney by glomerular filtration
in acute pancreatitis, amylase levels will be very high
what is disseminated intravascular coagulation (DIC)?
get both bleeding and thrombosis
liver damaged so depletion of platelets and coagulation factors => bleeding
also get intravascular deposition of fibrin in the small vessels => thrombosis of small and midsize vessels and organ failure
what is disseminated intravascular coagulation (DIC)?
get both bleeding and thrombosis
liver damaged so depletion of platelets and coagulation factors => bleeding
also get intravascular deposition of fibrin in the small vessels => thrombosis of small and midsize vessels and organ failure
what are the mechanisms by which NAPQI causes toxicity?
covalent binding to hepatic proteins => damage to cellular membranes and mitochondrial dysfunction
depletion of FSH => hepatocytes more susceptible to reactive O2 species-induced injury
why can acetominophen be more toxic in alcoholics?
alcohol induces CYP2E in liver
what is the consequence of aspirin overdose?
alkalosis due to stimulation of respiratory center in medulla => metabolic acidosis => accumulation of pyruvate and lactate due to uncoupling of oxidative phosp and inhibition of krebs
metabolic acidosis enhances formation of nonionized forms of salicylates - diffuse to brain => nausea to coma
why can aspirin increase bleeding?
acetylates platelet cyclooxygenase
irreversibly blocks production of thromboxane A2 (activator of platelet aggregation)
