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48 Cards in this Set
- Front
- Back
what does CO bind?
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reversibly binds with O2 binding site of Hb (about 220 x more affinity than O2).
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how does carboxyhaemoglobin work? (2)
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1. can't transport O2
2. interferes w dissociation of O2 from remaining oxyHb |
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which organs are most affected by CO poisoning?
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brain
heart |
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what is normal concentration of CO in atmosphere? in heavy traffic? what is recommended thresshold? how many ppm would be required for a carboxyHb level of 50%
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N - 0.1ppm
traffic - >=100ppm thresshold - 25ppm would need 1000ppm (0.1% CO ) for carboxyHb level of 50% |
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what saturation of CO can be seen in smokers?
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5-10%
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what are the principal signs of CO intoxication due to and list them in order (5)
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hypoxia
1. psychomotor impairment 2. headache & tightness temporally 3. confusion & loss of visual acuity 4. tachycardia, tachypnoea, syncope & coma 5. deep coma, convusions, shock, resp failure |
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how can normal non smoking adults have a very small normal carboxyHb level?
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endogenous formation of CO from heme catabolism
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at what concentrations do most people start to have symptoms of CO poisoning?
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25%
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what is the treatment of CO poisoning
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remove from source
oxygen |
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what is elimination half time of CO at room air? at 100% O2? hyperbaric O2?
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320 min RA
80 min 100% O2 20 min hyperbaric |
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what are organophosphates based on?
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war gases
eg soman, sarin, tabun |
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when are organophosphates used in medicine?
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human/vet medicine as local or systemic antiparasitics
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how does the body absorb organophosphate?
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skin, respiratory & GI tract
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how do organophosphates work?
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inhibit ACh through phosphorylation of the esteratic site
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do organophosphates remain in the enviroment?
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no, they are unstable & break down from hydrolysis & photolysis
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what chemical process causes S&S of organophosphate poisoning?
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inhibition of enzyme -> accumulation of ACh
some also posess direct cholinergic activity |
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what are the general manifestations of organophosphate poisoning?
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altered neuro & cognitive funciton & psychological symptoms
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what other enzyme can organophosphates affect & what happens?
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neuropathy target esterase
-> progressive demyelination of the longest nerves -> paralysis & axonal degeneration |
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what kind of volume of distribution do organophosphates have?
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high - significant stores in body fat
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how are organophosphates metabolised (3)
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esterases
P450 conjugation |
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where do organophosphates have cellular actions? (3)
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autonomic ganglia
neuromuscular junction post ganglionic ACh fibres |
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what kind of onset does acute organophosphate poisoning have?
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rapid onset (5min) in severe intoxication esp inhalation
slow onset transdermal most will be symptomatic within 12 hours |
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what is intermediate syndrome in organophosphate poisoning? how many patients get it? what is the most serious side effect?
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delayed onset of muscular weakness 1-4 days post resolution of cholinergic signs
10-40% treated patients may feature respiratory paralysis requiring intubation |
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what can happen weeks after organophosphate poisoning?
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delayed neurotoxicity (2-3 wks) - associated with leaching from lipid sources
organophosphate induced delayed polyneuropathy (1-4 weeks) rare - distal degeneration of some axons -> weakness, numbness, quadriplegia if serious` |
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what is muddles in organophosphates?
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M - muscular paralysis/miosis
U - urination D - defaecation D - diaphoresis L - lacrimation E - excitation of muscles/fasciculation S - salivation/seizures |
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what is the general mechanism of neurotoxins that inhibit acetylcholinesterase?
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excess ACh at neuromuscular junction -> paralysis of muscles needed for breathing & stops beaing of heart
stimulation muscarinic receptors -> diarrhoea, salivation, urinary frequency stimulation nicotinic receptors -> generalised ganglionic activation -> hypertension + tachy/bradycardia; muscle twitching ~> weakness ~> resp muscle paralysis |
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what is the antidote to organophosphate poisoning? (2)
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atropine at muscarinic sites (nil effect nicotinic sites)
pralidoxime - can restore cholinesterase activity; muscarinic & nicotinic |
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how do we give pralidoxime for OP poisoning
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1g IV every 3-4 hours or constant infusion
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how do we give atropine of OP poisoning?
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1-2mg IV repeated until signs of atropinism occur (tachy, dilated pupils, ileus). end goal is decreased secretions
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draw the generalised features of autonomic & somatic motor nerves WRT Ach?
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katzung fig 6-1
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??? DO WE DO TESTING FOR ACH CLINICALLY ????
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....
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what is the toxic dose of paracetamol for adults? children?
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adults 7g total
children >150-200mg/kg |
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when does evidence of liver injury occur in paracetamol toxicity? how does it manifest
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24-36 hours after ingestion
elevated aminotransferase & hypoprothrombinaemia |
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what is the serum level of paracetamol indicating risk of injury? after what time?
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>150-200mg/L >4 hours post ingestion
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where is cyanide found in the world?
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chemical synthesis (eg rodenticides)
HCN in burning plastics/wool & other products cassava seeds (eg apple, peach, apricot) |
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what physiological mechanism does cyanide have?
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binds readily to iron in cytochrome oxidse (in electron transport chain of mitochondria) -> can't transport electrons to oxygen-> can't produce ATP -> cellular hypoxia & lactic acidosis
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what findings would suggest cyanide poisoning? (5)
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altered mental state
dilated pupils anion gap metabolic acidosis bitter almond odour retinal arteries & veins same colour & macula cherry red |
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what is the smell of HCN?
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bitter almond
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what defines a cyanide?
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any chemical compound with a C triple bonded to N
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are all cyanides poisonous?
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no, eg prussian blue which is an antidote to thallium & radioactive caesium poisoning
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how does acetylcysteine affect paracetamol toxicity?
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acts as a glutathione substitute, binding toxic metabolite as produced
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draw the basic steps in paracetamol metabolism?
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paracetamol
(glucuronidaton 65%) -> nontoxic glucuronide (sulfation 35%) -> non toxic sulfate (CYP2E1 or CYP3A4 conjugate w cysteine after other mechanisms overwhelmed) -> reactive toxic intermediate --> either (glutathione conjugation) -> mercapturic acid conjugate OR (protein-SH) -> liver cell death |
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who is at risk of lower level of paracetamol toxicity? how low can these levels be?
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alcoholics & those taking P450 enhancing drugs
100mg/L at 4 hours |
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how do we treat cyanide poisoning?
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dicobalt edetate IV asap
keep out of reach & sight of children |
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how does cyanide Rx work?
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cobalt salts chelate cyanide directly
greater affinity for cyanide than MetHb or cytochrome oxidase & forms stable compounds w less toxicity than MetHb with low Vd - only binds circulating cyanide T1/2 1 hr |
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what investigations can we do in organophosphate poisoning?
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ECG
RBC acetylcholinesterase amylase (mildly elevated in 50%) |
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what ECG changes can be seen in OP poisoning?
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QT prolongation 65%
ST elevation 25% sinus tachy 35% sinus brady 25% |