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70 Cards in this Set
- Front
- Back
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Decontamination- 6 ways of limiting absorption of ingested toxin
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1. gastric lavage
2.gastrotomy 3. activated charcoal 4. cathartics 5. enemas |
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How do you limit distribution of systemic toxin
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chelating agent- eg EDTA for Pb
D-penicillamine- Zn, Cadmium, mercury |
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How can you increase the rate of elimination?
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Ion trapping
toxin needs to be a weak acid or base with appropriate pka non protein bound with primarily renal excretion urinary acidification- ammonium chloride urinary alkalination- sodium bicarb Forced diuresis IV fluds to increase GFR risks- low na, K, water intox, oedema |
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Types of antidotes
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Chemical- directly interact with the poison or toxin
OPs- 2-PAM heavy metals (EDTA) Physical- antagonise the physiological effect of the toxin warfarin- give vit K ethylene glycol- ehtanol |
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Vit K antagonist groups
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originate from coumarin
1st gen- warfarin half life 14.5 hours. some rodents have become resistant less potent than 2nd gen- larger meal needed 2nd gen- brodifacoum half life 6 days more potent, now more common 2nd and 3rd gen consideable more toxic/potent longer 1.2 life |
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how do antivitK rodenticides work?
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redice the amount of useful VIk K in the body. Inhibit the hepatic nzyme VitK1 epoxide reductase
oxidised Vit K cannot activate clotting factors- needs to be in reduced form-- no clotting factor activation- coagulopathy |
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CSs of rodenticide poisoning and how fast?
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typically a lag period- 1-5 days after ingestion
doesnt work straight away in the liver- there is still vit K available doesnt affect circulating clotting factors- quicker if there si a haemostatic challenge CSs: Coagulopathy Pale Mms anaemia weakness collapse weak irregular pulse +/_ bloody V epistaxis bloody f+ s/c haemorrhages, haematomas |
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dx rodenticide tox
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history of exposure/ CSs
increased clotting parameters (partial thromboplastin time (PTT) and prothrombin time (PT) Increased PIVKA (new test method- not sure if avail) response to VitK therapy detection of poisons in tissue |
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How does PIVKA work?
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When Vitamin K is low, precursor proteins of factors II, VII, IX, X build up and can be detected by the PIVKA test.
PIKVA increases with rodenticide toxicity PIVKA increase within 6 hours of poison ingestion, where as PT rises take 24- 48 hours |
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tx rodenticide
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-decontam if recent
no point inducing v+ if CS are present suportive tx fluids blood transfusion- o2 and clotting factors cage rest to minimise trauma and unnecessary bleeds decrease invasive medical intrusions- small needle! Antidote- VIt K 1st gen- 4-6 days tx 2nd gen- 2-4weeks, 6-8 if bad neds to be given with a fatty meal or not absorbed |
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Most common insecticide poisonings plus others
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OPs
Carbamates others organochlorines, DEET, pyrethrins |
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Epidemioogy of OP and carbomate poisoning
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Exposure through ingestions nad dermal absorption
very potent, rapid onset less common due to new insecticides many OPs are lipophilic- absorbed and stored |
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OPs carbomates mech of action
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competitive inhibition of acetylcholinesterase
binds to AchE ensyme- cant break down in synapse- prolonged cholinergic activity binds strongly- irreversible |
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cloinical signs OP and carbomate tox
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dose and time dependent
usually fairly rapid- minutes to hours- except some lipophilic ones 1. muscarinic signs- SLUD, bradycardia, abdo pain, miosis, dypsnoea 2. Nicotinic signs- peripheral effects at higher doses or prolonged- muscle twitching, stiffness, rigid extension, tetany, paresis, paralysis 3. CNS signs- parasymp and symp effects from ganglionic stim and CNS- tachydcardia. mydriasis, anxiety, hyperactivity, seizures, coma signs occur in the order mus->nic->CNS |
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OPIDN
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some OPs can inhibit neuroesterase--> condition known as OP inducedd delayed neurotoxicity
- peripheral nerve demyelination and axonal degenertion--> ataxia patients usally cage rested and recover over a few weeks |
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OPs carbamates dx
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1. hx exposure
2. compatible CSs 3. response to tx 4. detect cholinesterase activity- whole blood (live) , brain (PM) 5. stomach contents, hair, suspected baits- for OP or carbamate conc 6. blood for OP and carbamates- often disappointing- potent so testing not sensitive enough |
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Tx carbomate and OP
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DEcotnam
supportive Physiological antidote- muscarinic rec antagonist- atropine Chemical antidote 2-PAM- can reactivate esterases early in toxicosis. Over tie the enzyme undergoes change that renders it unreactivatable |
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Metaldehyde toxicity- consequences of exposure
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very potent neurotoxin
8g for 20kg dog- active ingredient 1-5 % so needs 500g clinical signs after 1-2hr\ contain bitrex to decrease palatability for dogs but still same amount of metaldehyde |
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metaldehyde mech of action
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unknown but decreased serotonin and gaba in CNS- overexcitation
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CSs Metaldehyde
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centrally mediated seizures and hyperthermia
within a few hours dog becomes apprehensive and restless- progresses to hypersalivsation, ataxia and tremors often bright green seen in saliva and vomit characteristic odour of gastric contents and urine MEASURE BLOOD CHOLINESTERASE TO RULE OUT OP |
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tx metaldehyde
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no antidote
1. decontamination 2. supportive tx 3. anticonvulsants 4. muscle relaxants (methocarbamol) |
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what is sodium monofluoroacetate (1080)
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predacide
white odourless tasteless water sol, HIGHLY toxic occurs naturally in some plants |
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Mech 1080
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inhibits the citric acid cycle
decreased energy prod, build up of metabolic products, metabolic acidosis build up of citrate and ca- hypercalcaemia |
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1080CS
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30m-4 hours post ing
CNS excitement, GIT hyperactivity anxiety, frenzied behaviour V+, D+ hypersal seizures, coma, resp failure, death |
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1080 tx
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no antidote
decontam and treat early supportive: GA, gastric lavage, activated charcoal. slow IV bicarb therapy |
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Onions mech
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oxidative damage to RBCs- haemolytic anaemia
Cats more sensitive |
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grapes/raisins CS
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acute renal failure in dogs- mech unknown
no clear dose response rel V, anorexia, lethargy, abdo pain |
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teflon tox in which species? and mech?
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birds
teflon- undergoes chemical change at over 260 degrees and releases fumes birds enormously sensitive acute dypsnoea and death |
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which animals at risk of lead poisoning?
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caged birds, livestock, wildlife, pets
companion animals- ;ead based paints, lead sinkers birds- new cage syndrome (solder) large animals- batteries, paint flakings from buildings |
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WHy are young more susc to pb poisoning
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absorbed more efficiently from zGIT as the calcium transporters will preferentially transport lead into circ
readily cross the palcenta into milk |
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Pb toxicokinetics
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absorbed by active transport on Ca++ carriers
transported bound to RBCs deposited intially in soft tissues then in bone interferes with intracellular calcium unctions- CNS damage and interference with neurotransmitter action |
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Pb tox CSs
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variable CSs
GIT- V, anorexia, abdo pain, constipation neuro- depression to hysteria, behavour changes, seizures- cerenral oedema and disruption to peripheral n myelination anaemia- prevents maturation- may be hyperchromic due to incorp of iron into haem disturved |
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Dx Pb tox
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- blood lead concentration- test WHOLE blood- low in plasma and serum
- haematology changes- anaemia, nucleated RBC, basophilic stipling - radiography- lead lines- deposited in areas of new growth and show radipoopaque lines |
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Pb tx
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- supportive therapy
- decontam- removal of source (wash patient to remove pain flakes, give salt or magnesium cathartic to remove small particles in GIT) - chelation- CaEDTA- also binds ca, iron. 5 days at a time. No longer becuase neprotoxic |
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DIffernt Pb chelators
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bind to form insoluble complexes which are expelled inurine- limitrs dist and increases elim
-EDTA- nephrotoxic -SUccimer- most comm in humans- excellent safety margins, can be given rectally, not yet avail in vet - D-penicillamine- oral admin, can indice V+ |
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CS acute cu toxicosis in sheep
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Jaundice
anaemia haemoglobinaemia haemoglobinurea |
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plants with high nitrate content
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sorghum, hay, oats, corn stalks, ryegrass- fibrous parts have highest concentration
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factors affecting nitrate in plants
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species differences
fertiliser use clinactic conditions- frost, drought, cloudy herbicides |
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sources of nitrate
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plants,
fertilisers contaminated water |
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mech of nitrite poisoning
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rumen flora convert nitrate to nitrite to aammonia
nitrites oxidise iron from fe++ in haemoglobin to Fe+++, methaemogobin does not bind or transport O2 |
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CS nitrite
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toxicoses- 4h post exposure
>20%methaemoglobin- clinical signs >80%metHB death muddy brown mm chocolate brown blood sudden death hypoxia anxiety tachypnoea, tchycardia weakness ataxia depression seizures abortion- anoxic fetus |
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tx nitrite toxicity
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injections of methylene blue can be attempted tx
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prevention
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provide hungry stock with hay
can test content with commercially avalable test strip pasture management |
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what is type 1 photosensitisation
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primary photosensitisation
preformed photodynamic agent is directly absorbed or ingested eg hypricin in st johns wart |
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what is type3 photosensitisation
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hepatogenous
aka sedondary most common normal metabolic products accumilate in tissue through fault in liver excreton normally conj in liver and excreted in bile overflow into tissues- activated by UV |
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Dx photosensitisation
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skin lesions- light skin only
shade seeking behaviour elevted serum bilirubin- heptic dysfxn examination o rumen contents |
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tx photosensitisation
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remove from affected pastures into shade
topical zinc oxide can help |
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Brunsfella toxicosis- mech
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evergreen common garden plant
toxic alkaloids in all parts of plants particularly berries |
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nature of brunsfella CSs
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dose related
appear 15-18hr post ingestion initially non spec- salivation, V, D may occur with CNS signs- seizures, ataxia, tremors berries in faeces ddx molluscide poisoning |
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Brunsfella tox tx
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decontam and supportive tx]
symptomatic treatment- anticonvulsants, fluids, prevention of aspiration pneumonia |
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what is a mycotoxin+ significance
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toxin or secondary metabolite produced by some fungi (toxigenic fungi). may result in obvious clinical signs- eg staggers
in most cases- insidious losses due to 1. ill thrift 2. poor reproductive performance 3. decreased production 4. decreased disease resistance |
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What are factors for mycotoxin production
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1. species
2. type of feedstuff/plant 3. plant damage 4. environmental conditions- humidity,"", temp, moisture, o2 |
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Why is dx of mycotoxin diffictul
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1. long ddx list
2. often vague non specific signs 3. latent period 4. few detection methods |
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prevention of mycotoxin dz
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1.avoiding
2. testing 3. diluting 4. drying 5. preventative organic acids |
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Zearalenone- what is it?
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oestrogenic mycotoxin associated with fuasrium spp.
found in grains- particularly stored grains pigs most susceptible tx- remove contam grain |
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zearalenone- effect
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mimics oestrogen
act with estrodial receptor but 4x less effective hyperoestrogenusm repro abnormalities |
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Clkinical signs of zearalenone in females
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swollen vulva
mammary hyperplasia repro abnormalities splay legged piglets |
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Clinical signs of zearalenone in males
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testicular atrophy
preputial hyperplasia dereased libido |
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Penitrem A and Roquefortine- what are they?
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mycotoxins associated with penicillum spp
temorgenic mycotoxins |
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Penitrem A and Roquefortine- source
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mouldy food- cheese, bread, nuts or decaying material. compost
DOGS affeted |
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Penitrem A and Roquefortine CSs dogs
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salivation
excittion hyperaesthesia tremors siezures |
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Penitrem A and Roquefortin tx
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symptomatic- control tremors/seizures
- diazepam, methocarbamol, GA - maintain euthermia - fluid/electrolyte/acid-base decontam if poss |
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cats- paracetamol poisoning- how would you treat it
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1. chemical reduction of methaemoglobin- VIt C injection
2. glutathione precursors-Acetylcystine - enable phase 2 3. prevention of phase 1- histamine2 antagonist- minimise metabolite formation 4. IVFT +/- blood transfusion 5. O2 |
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paracetamol poisoning signs
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swelling of face and paws
muddy mucous membranes hypoxia/ dypsnoea hypothermia lethargy V+ |
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Gastroprotectants
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-proton pump inhibitors decrease acid
- H2-receptor antagonists reduce gastric acid secretion - Sucralfate reacts with HCl- paste-like substance; coating the mucosa preventing back diffusion of H+ - |
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COX1 roles
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constituive prostaglandins
- mucus secretion - bicarb secretion - GFR - decresed acid prod |
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COX2
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- potentiation of pain
- proinflamm mediators - vasodilators |
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the perfect sedative
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1. sedation with analgesia
2. minimal cardio or respiratory side effects 3. rapid onset/offset 4. minimal stress on iver and kidneys 5. cheap 6. no drug interactions 7. inactive metabolites |
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uses of benzodiazepines
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1. muscle relaxation
2. status epilecticus 3. anxiolytics 4. sedation combos |
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GA process
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1. work up= PE and PAS
2. premedication 3. induction 4. maintenance 5. recovery |
