chemical injury case presentation Flashcards

1
Q

what are the effects of acetominophin on blood?

A

coagulation factors synthesized in liver - so want CBC, PTT, PT, INR

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2
Q

what is ALT?

A

alanine aminotransferase levels
part of liver enzyme tests for LFT - when injury to liver, cells lysed and enzymes released
10-56 is normal

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3
Q

what is AST?

A

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

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4
Q

what are the pathways in coagulation?

A

intrinsic and extrinsic

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5
Q

what is PT? what is it used to detect?

A

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

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6
Q

what is PTT? how is it measured?

A

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

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7
Q

what are some causes of prolonged PTT?

A
vit K deficiency
liver disease
DIC
factor deficiency
antifactor antibodies
lupus anticoagulant
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8
Q

how long does acetaminophen take to be fully absorbed?

A

4 hours - so will see a peak at 4 hours and if only took one dose will see drop after that

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9
Q

when can you use the rumack-matthew normogram?

A

only for a single acute ingestion and if the approximate time of ingestion is known

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10
Q

how does acetaminophen cause toxicity?

A

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

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11
Q

how does NAC prevent liver failure due to acetaminophen?

A

can be glutathione substitute

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12
Q

what is NAC? how does it work?

A

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

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13
Q

what is direct bilirubin versus indirect bilirubin?

A

direct = conjugated bilirubin + delta bilirubin

bilirubin that is soluble in plasma

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14
Q

what is conjugated bilirubin?

A

glucuronide attached bilirubin - soluble

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14
Q

what is direct bilirubin versus indirect bilirubin?

A

direct = conjugated bilirubin + delta bilirubin

bilirubin that is soluble in plasma

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15
Q

what is conjugated bilirubin?

A

glucuronide attached bilirubin - soluble

16
Q

what is delta bilirubin?

A

bilirubin covalently attached to albumin - soluble

16
Q

what is delta bilirubin?

A

bilirubin covalently attached to albumin - soluble

17
Q

what is unconjugated bilirubin?

A

no glucuronide attached to bilirubin - very insoluble

19
Q

what is unconjugated bilirubin?

A

no glucuronide attached to bilirubin - very insoluble

21
Q

what is total billirubin?

A

conjugated + delta + unconjugated

requires detergent or accelerator so that the unconjugated will react with the diazo dye

22
Q

what is total billirubin?

A

conjugated + delta + unconjugated

requires detergent or accelerator so that the unconjugated will react with the diazo dye

23
Q

what is the reason to give a patient lactulose? how does it work

A

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

24
Q

what is the reason to give a patient lactulose? how does it work

A

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

25
why would you give a patient vitamin K?
prolonged prothrombin time | vit k will counteract - will cause coagulation to go back to normal
26
why would you give a patient vitamin K?
prolonged prothrombin time | vit k will counteract - will cause coagulation to go back to normal
27
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
28
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
29
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
30
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
31
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
32
why can acetominophen be more toxic in alcoholics?
alcohol induces CYP2E in liver
33
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
34
why can aspirin increase bleeding?
acetylates platelet cyclooxygenase | irreversibly blocks production of thromboxane A2 (activator of platelet aggregation)