• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/48

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

48 Cards in this Set

  • Front
  • Back
what does CO bind?
reversibly binds with O2 binding site of Hb (about 220 x more affinity than O2).
how does carboxyhaemoglobin work? (2)
1. can't transport O2
2. interferes w dissociation of O2 from remaining oxyHb
which organs are most affected by CO poisoning?
brain
heart
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%
N - 0.1ppm
traffic - >=100ppm
thresshold - 25ppm
would need 1000ppm (0.1% CO ) for carboxyHb level of 50%
what saturation of CO can be seen in smokers?
5-10%
what are the principal signs of CO intoxication due to and list them in order (5)
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
how can normal non smoking adults have a very small normal carboxyHb level?
endogenous formation of CO from heme catabolism
at what concentrations do most people start to have symptoms of CO poisoning?
25%
what is the treatment of CO poisoning
remove from source

oxygen
what is elimination half time of CO at room air? at 100% O2? hyperbaric O2?
320 min RA
80 min 100% O2
20 min hyperbaric
what are organophosphates based on?
war gases
eg soman, sarin, tabun
when are organophosphates used in medicine?
human/vet medicine as local or systemic antiparasitics
how does the body absorb organophosphate?
skin, respiratory & GI tract
how do organophosphates work?
inhibit ACh through phosphorylation of the esteratic site
do organophosphates remain in the enviroment?
no, they are unstable & break down from hydrolysis & photolysis
what chemical process causes S&S of organophosphate poisoning?
inhibition of enzyme -> accumulation of ACh

some also posess direct cholinergic activity
what are the general manifestations of organophosphate poisoning?
altered neuro & cognitive funciton & psychological symptoms
what other enzyme can organophosphates affect & what happens?
neuropathy target esterase

-> progressive demyelination of the longest nerves -> paralysis & axonal degeneration
what kind of volume of distribution do organophosphates have?
high - significant stores in body fat
how are organophosphates metabolised (3)
esterases
P450
conjugation
where do organophosphates have cellular actions? (3)
autonomic ganglia
neuromuscular junction
post ganglionic ACh fibres
what kind of onset does acute organophosphate poisoning have?
rapid onset (5min) in severe intoxication esp inhalation

slow onset transdermal

most will be symptomatic within 12 hours
what is intermediate syndrome in organophosphate poisoning? how many patients get it? what is the most serious side effect?
delayed onset of muscular weakness 1-4 days post resolution of cholinergic signs

10-40% treated patients

may feature respiratory paralysis requiring intubation
what can happen weeks after organophosphate poisoning?
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`
what is muddles in organophosphates?
M - muscular paralysis/miosis
U - urination
D - defaecation
D - diaphoresis
L - lacrimation
E - excitation of muscles/fasciculation
S - salivation/seizures
what is the general mechanism of neurotoxins that inhibit acetylcholinesterase?
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
what is the antidote to organophosphate poisoning? (2)
atropine at muscarinic sites (nil effect nicotinic sites)

pralidoxime - can restore cholinesterase activity; muscarinic & nicotinic
how do we give pralidoxime for OP poisoning
1g IV every 3-4 hours or constant infusion
how do we give atropine of OP poisoning?
1-2mg IV repeated until signs of atropinism occur (tachy, dilated pupils, ileus). end goal is decreased secretions
draw the generalised features of autonomic & somatic motor nerves WRT Ach?
katzung fig 6-1
??? DO WE DO TESTING FOR ACH CLINICALLY ????
....
what is the toxic dose of paracetamol for adults? children?
adults 7g total
children >150-200mg/kg
when does evidence of liver injury occur in paracetamol toxicity? how does it manifest
24-36 hours after ingestion

elevated aminotransferase & hypoprothrombinaemia
what is the serum level of paracetamol indicating risk of injury? after what time?
>150-200mg/L >4 hours post ingestion
where is cyanide found in the world?
chemical synthesis (eg rodenticides)
HCN in burning plastics/wool & other products
cassava
seeds (eg apple, peach, apricot)
what physiological mechanism does cyanide have?
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
what findings would suggest cyanide poisoning? (5)
altered mental state
dilated pupils
anion gap metabolic acidosis
bitter almond odour
retinal arteries & veins same colour & macula cherry red
what is the smell of HCN?
bitter almond
what defines a cyanide?
any chemical compound with a C triple bonded to N
are all cyanides poisonous?
no, eg prussian blue which is an antidote to thallium & radioactive caesium poisoning
how does acetylcysteine affect paracetamol toxicity?
acts as a glutathione substitute, binding toxic metabolite as produced
draw the basic steps in paracetamol metabolism?
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
who is at risk of lower level of paracetamol toxicity? how low can these levels be?
alcoholics & those taking P450 enhancing drugs

100mg/L at 4 hours
how do we treat cyanide poisoning?
dicobalt edetate IV asap
keep out of reach & sight of children
how does cyanide Rx work?
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
what investigations can we do in organophosphate poisoning?
ECG

RBC acetylcholinesterase

amylase (mildly elevated in 50%)
what ECG changes can be seen in OP poisoning?
QT prolongation 65%
ST elevation 25%

sinus tachy 35%
sinus brady 25%