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VetMed Year 4- Term 2 > POS- Week 1 > Flashcards

POS- Week 1 Flashcards

1
Q

Toxicity associated with HRT/Oral contraceptives

A

Low toxicity along with powder flower food, silica gel, zinc oxide cremes

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2
Q

Why is Paracetamol toxic?

A

Toxicity occurs via saturation of metabolic pathways. Toxic metabolite conjugated by gluthione but this is promptly depleted. Leads to OXIDATION and the formation of NAPQI

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3
Q

CCWhy does NAPQI lead to cellular death

A

NAPQI is the result of oxidation of paracetamol and binds to essential amino acids and results in cellular death

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4
Q

Clinical manifestation of paracetamol toxicity a) <24 hrs c) days after

A

a) <4 hrs: Progressive cyanosis, brown/blue MM, weakness and lethargy
b) Facial/Paw Oedema, vomiting, depression, methhaemaglobin
c) Severe methaemaglobinaema, hepatic necrosis
Cyanosis DOES NOT RESPOND TO OXYGEN THERAPY

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5
Q

What colour is Methaemaglobin? Significance in toxicity

A

Methaemaglobin is brown (apparent from 4-24 hrs) and days ahead post paracetamol toxicity.
Toxic metabolite NAPQI

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6
Q

At what dose should ingestion of paracetamol be treated?

A

Cat: 20mg/kg (i.e. any ingestion)

DogL 150mg/kg

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7
Q

Treatment for Paracetamol toxicity

A

Emesis (within 2 hrs) Apomorphin or Xylazine
Antidote: Acetylcystiene (precursor of glutathione)
Also SAMe
Ascorbic acid

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8
Q

Antidote for Paracetamol; how does it work?

A

Acetylcystiene which is a precursor of gluthione (try to prevent pathway being saturated so oxidation pathway doesn’t happen = NAPQI)
Continue treatment until clinically well

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9
Q

How to induce emesis in a) cat b) dog

A

a) Cat: Xyazine

b) Dog: Apomorphine

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10
Q

NSAID’s toxicity is largely due to ___ inhibition

A

NSAIDs toxicity is largely due to COX-1 inhibition

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11
Q

Carprofen and meloxicam are examples of

A

COX-2 inhibitors. (Flunixn and Phenylbutazone are non-selective)

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12
Q

Early and Late clinical manifestations of NSAIDs toxicity

A

Early: Gastrointestinal erosion, ulceration and potentially perforation. Vomiting/Diarrhoea (bloody), rarely CNS signs
Late: Renal/ Hepatic failure

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13
Q

NSAIDs treatment

A

No specific Antidote.
Emesis (optimal within 3 hrs, apomorphine/xyalizine)
Activated charcoal
Prevention of gastric ulceration: H2 receptor antagonists, proton pump inhibitors. ulcer healing
Supplement prostaglandin, maintenance of renal function (fluid therapy)

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14
Q

Examples of a) H2 receptor antagonist b) proton pump inhibitor

A

a) h2 receptor antagonist: Cimetidine, Ranitidine

b) proton pump inhibitor: Omeprazole

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15
Q

Approx toxic dose of a) white chocolate b) milk chocolate

A

Theobromine is toxic component of chocolate

a) white chocolate: 2200g/kg!!!!!!
b) milk chocolate: 9g/kg
c) dark choc: 1.25 g/ kg

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16
Q

Clinical effects of Theobromine toxicity

A

Vomiting/Diarrhoea/ Polydipsea/ Salivation/ Dehydration
CNS / Myocardial stimulation - tremor convulsion/ tachycardia
Renal failure
Severe cases- severe convulsions/ circulatory failure

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17
Q

Management of Theobromine toxicity

A

Emesis- apomorphine/ activated charcoal/ adequate rehydration
ECG/ Benzodiazapine for CNS stim.
Treatment of arrthymia (lidocaine/ beta blocker)

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18
Q

Tremorgenic Mycotoxins

A

Mycotoxins are fungal metabolites produced by mould. Normally mouldy food waste. Penitrem A/ Roquefortine.

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19
Q

How does toxicity come about from Penitrem A

A

Penitrem A is a Tremorgenic Mycotoxin (mould).
Interfers with release of neutrotransmitters (glytamate, aspartic acid/ GABA)
- Within 3 hrs whole body muscle tremors, tachycardia, nystagmus, bleparospasm

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20
Q

Onset of effects of Penitrem A

A

Usually within 3 hours; vomiting/ataxia whole body muscle tremors, rigidity with hyperextension of exrememeties, tachycardia, tachypnoea, nystagmus

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21
Q

Management of Tremorgenic Mycotoxins

A

from mould e.g. Penitrem A.
Decontaimination (emesis/ apomorphine./ activated charcoal)
Anticonvulsants (benzodiapine, barbiturate)

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22
Q

Allium species includes…

Which part is toxic

A

Large group of plants (>600), mostly pereenial bulbous herbs inc LEEKS, ONIONS, SHALLOTS, SPRING ONIONS, GARLIC/ CHIVE.
Contain organosulphoxides

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23
Q

Toxic dose of Allium species

A

e.g. onions/leeks/shallots.
>0.5% of body weight (therefore 5 g/kg)
Leads to Heinz body formation and anaemia

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24
Q

Clinical effects of Allium species

A

Due to organosulphoxides, forms mixed sulphide bond between haemaglobin and gluthione resulting in formation of Heniz bodies = damaged erythrocytes removed from circulation

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25
Q

Onset of Allium species

A

Onset is variable (toxic dose = 0.5% of body weight)
Signs of haemolysis can be delayed for 1-5 days.
Heinz bodies can appear within 24 hrs.
Vomiting/ inappetance (onion breath..)
Heniz body anaemia (pale MM, tachycardia)
Haematuria/Haemaglobinurea are common
Urine smells of onions

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26
Q

Why would icterus be a (less common) effect of Allium species ingestion

A

Allium species = Heinz body formation and anaemia (Organosulphoxide)
More serve cases, icterus due to haemosiderin (high iron stores) in the liver.

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27
Q

Management of Allium poisoning

A

No antidote, supportive.
Emesis/ activated charcoal/ IV fluids
High protein diet may promote rsotration of gluthioone stores.

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28
Q

Anticoagulant poisoning halflife for a) warfarin and b) brodifacoum

A

a) Warfarin half life is 14 hrs
b) Brodifacum half life is 6 days.
Vit K essential for production of clotting factors (2, 7, 9 and 10)

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29
Q

Which coagulation test would be increased first in acute rodenticide poisoning

A

Factor VII has the shortest half life = Prolonged PT. (pro thrombin time)
Then will affect extrinsic and instrinsic pathway as factor 2, 7, 9 and 10 are all vit K dependent

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30
Q

Onset of effects for Rodenticide toxicity

A

Depends on half life of clotting factors.
VII 6.2 hors IX 13 hours
Onset of effects = 27-72 hours.
Bleeding from gums, nose, Gi tract and wounds

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31
Q

Treatment for Rodenticide toxicity

A

Not always required, monitor elevations in PT.
Vit K1 therapy if prolonged. Administer until PT normalises MULTIPLE INJECTION SITES.
Once PT is normalsed then oral K1 for 2-3 weeks gradually reduced dose.

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32
Q

What compound causes the most fatalities (as reported to VPIS)

A

Mollusicides. Contain Metaldehyde. Death normally due to respiratory depression. Common signs: Hypersalivation/ V&D/ Ataxia/ Convulsions

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33
Q

Mechanism of toxicity for Vipera berus?

A

Hypovolemia and local oedema result from increased vascular permeability due to released of mediated histamine.
Renal impairment possible due to Hypovolemic shock.

34
Q

Over the phone advice for suspected adder bite

A

reassure. high morbidity low mortality.
No tourniquets or ligatures (ischemia)
AVOID INTERFERENCE OF WOUND
Immobilise the affected limb. i.e. carry dog not walk)
Clip area and Look for puncture marks 5-10mm apart.
Necrosis is rare.

35
Q

Systemic effects of adder bite

A

shock, collapse and hypotension.
Pain, panting and hypersalivation, pale mm, tachypnoea.
Coagulopathy: anaemia, thrombocytopnea, leucocytosis, DIC, and haematuria.

36
Q

Monitoring and Treatment for adder bite

A 
Observation
IV fluids
Antivenom (zagreb)
BP, RR, HR, Temp
ECH (arrival, 12 hrs, 24 hrs)
BT (coagulopathy)
Renal/hepatic parameters
37
Q

Indications for use of antivenom *ZACREB)

A

Any animal with bite to facial region/ severe swelling.
Swelling beyound next major joint prox to bite
Hypotension unresponsive to IV fluid
Evidence of coagulopathy
Any ECG abnormality.
EXCESSIVE USE OF A/V = SEVERE REACTION. Previous use is not a contraindication.
Still indicated if systemic signs days after bite. If ONLY local signs NO value a/v after 24hrs.

38
Q

What analgesics are recommended for adder bite?

A

Opiods preferrerd over NSAIDs due to renal perfusion concern if hypovolemic.
Antibiotics routine use NOT recommended.
NO role for steroids unless anaphaylactic reactions to anti venom.

39
Q

Antidotes for a) Antifreze b) Benzodiapemine c) 5-HT

A

A) Anti-freeze: Ethanol

b) Benzodiazapine: Fluamezil
c) 5-HT - Cryptohepatidine

40
Q

Antidote for Organophosphate poisoning

A

Pralidoxime for OP poisoning

Naloxone for Opiod poisoning

41
Q

Lipid rescue therapy is useful for poisonings with____

A

Lipophillic drugs e.g. Moxidectin, Avermectin, Ivermectin

Thought that lipid component binds them so they cannot act as a toxin at their target receptor.

42
Q

Xylitol containing products and management (inc monitoring)

A

Some protein bars and CHEWING GUM (Wrigleys)
Nicorette gum, Strepsils,
AGGRESSIVE THERAPY - GASTRIC DECONTAIMINATION.
Rapid and potent stimulator of insulin release in dogs/ induces liver damage by unknown mechanisms.
Monitor glucose concentrations,. potassiu, phosphrous, total bilirubin, clotting tests

43
Q

Treatment of Xylitol

A

Hypoglycemia (ECG monitoring- hypokalamia-induced arrthymias)
Hepatotoxicty (consider immediate dextrose therapy)
Treat with IV saline, glucose and potassium supplements, and essential fatty acids

44
Q

Which breeds are more susceptible to Onion toxicity in dogs

A

Japanese (akitas) and Korean breeds.

Inhertied trait characterised by erythrocytes with high conc of gluthione.

45
Q

Once an idea of the likely therapeutic dose has been decided, safety studies will be undertaken at ))) times the therapeutic dose

A

3 to 5 times the therapeutic dose for up to 3 x the recommended dosing period. Up to 6 months if chronic dosing intended

46
Q

If a drug is for use in food producing animals how long is it tested

A

Life time safety studies in lab animals and 2 year safety studies in dogs. Carcinogenicity, embrotoxicicity and foetoxicity studies are also required.

47
Q

Example of Type A ADR

A

Augmented. PREDICTABLE e.g. beta blockers causing bradycardia. ACE inhibitors causing renal failure.

48
Q

In Neonates

a) gut motility
b) total body water
c) glomerular filtration

A

In Neonates, gut motility is decreased, neonates also have increased total body water (polar drugs have larger volume of distribution i.e. lower plasma concentration),
Neonates also have decreased glomerular filtration.

49
Q

Effect of decreased muscle mass on drug metabolism

A

Decreased lean muscle mass and decreased total bodt water in eldery lead to higher plasma drug concentrations (for polar drugs) e.g. Gentamycin.

50
Q

Endotoxin is only found in

A

Endotoxin is a lipopolysaccharide that is part of the outer membrane of gram NEGATIVES and never found in gram +ve.

51
Q

Endotoxin effects are thought to result from interaction of the _____ with a receptor on the macrophage membrane

A

Lipid A. This binding (Pattern regognition receptors) - this stimulates production and release of tumour necrosis factor, then interleukin (IL-1)
IL-1 acts on the hypothalamus to modulate temp.

52
Q

Exotins are produced by

A

gram positives and many gram negatives (cholera, e coli, pseudomonas, bordetella)

53
Q

Pathogenesis of Ergotism

A

Black ergots (fungal sclerotium) claviceps purpurea
Constriction of the arterioles in extremitis –> gangrene and lameness. Also convulsions.
Detection in food is relatively easy.

54
Q

Nociception pathway

A

Can have nociception without pain.

  1. Tranduction
  2. Transmission
  3. Modulation
  4. Projection
  5. Perception
55
Q

Define Allodynia

A

Non painful stimuli that is actually painful.

56
Q

Which spinal tract sends pain signals

A

Spinothalamic tract (transduction of nociception)

57
Q

Which fibres are involved in the Transmission phase of Nociception

A

Transmission phase
First order syndrome in dorsal horn
myelinated Aδ fibers$–first pain
unmyelinated fibres = visceral phase

58
Q

What happens in modulation

A

Peripheral sensory nerve impulses are amplified or surpressed in the spinal cord

59
Q

Visceral pain is

A

Unmyelinated fibres in transmission phase

60
Q

Projection occurs

A

Spinal cord/ white matter (NSAIDs work here)

61
Q

Which analgesics can be used as local anaesthetics?

A

Local anaesthetics, opiods and a2 agonists

62
Q

What is the difference between Buprenorphine and Butorphanol

A

buprenorphine is a partial u-agonist and butorphanol is a mixed agonist-antagonist.
Buprenorphine: Does not produce maximal effect, analgesia but not as profound as full agonistm mild to moderate pain

63
Q

Mechanism of action for NSAIDs

A

Phospholipids–>Arachidonic acid then cyclooxygenase pathway (COX1 and COX2) and Lipoxygenase Pathway

64
Q

COX-1 function

A

Production of prostaglandins important in the physiological modulation of function (gut mucosal barrier, intra rernal perfusion when reduced blood flow)

65
Q

Aside from the suppression of inflammation, pain and fever, what other benefits does COX-2 inhibition have?

A 
Alzheimers disease?
Some cancers (colon, pancreas, lung, transitional cell carcinoma, melanoma)
66
Q

Coxibs=

A

(100 x greater) inhibition of COX-2 receptors (inflamm, pain and fever)

67
Q

COX-1 Inhibition of clot induced___-

A

COX-1 inhibition of clot-induced thromboxane B2 production.

c.f. COX-2 activity = inhibition of lipopolysaccharide (LPS) induced prostaglandin E2.

68
Q

Therapeutic aim for NSAIDs (in terms of % inhibition)

A

> 80% Inhibition of COX-2

COX-1 Inhibition should be <10% (to avoid side effects of inhibiting clot induced thromboxane b2)

69
Q

Phenylbutazone and Asprin are examples of

A

Non selective COX inhibitors (Asprin, Phenybutzaone, Ketoprofen, Tolfenamic acid)

70
Q

Examples of some preferential inhibitors of COX-2 in the dog/cat

A

Meloxicam/ Carprofen.

Carprofen inhibits COX-1 receptors less than Meloxicam (i.e. should be less side effects?)

71
Q

Selective COX-2 inhibitors

A

Firocoxib/ Robenocoxib

72
Q

Tepoxalin

A

Inhibit LOX for short periods during day.

Non-selective inhibitor of COX-1 and COX-2

73
Q

Carprofen (dog, cat, horse)

A

Dog: COX-2 preferential
Cat: COX-2 preferential (LONGER HALF LIFE= NOT DAILY DOSING!)
Horse: Non-selective

74
Q

How do the pharmackinetics of Carprofen help

A

Readily absorbed from Stomach/ Small intestine after sc or im injec
Weak acid so readily penetrate inflammed tissue. Highly protein bound (accumulation of drug in protein rich exudate) therefore Duration may exceed apparent systemic half life
In cat much longer half life than dog!

75
Q

Licence of Carprofen in cats

A

Once only use (+++ half life in cats)

COX-2 preferential in cat (and dog) non selective in HORSE

76
Q

In general NSAIDs have a ____ half life in cats vs dogs

A

Generally NSAIDs have a longer half life in cats vs dogs i.e. asprin, carprofen (only licenced for one use in cats)

77
Q

How do PGE/ PGI2 normally protect the gastric mucosa

A

Inhibiting gastric acid secretion, maintaining mucosal blood flow, being involved in secretion/composition of healthy mucous, act as intracellular messengers for stiulus of mucosal cell turnover and migration
Cells that express COX-2 include - macrophages, neutrophils, myofibroblasts, endothelial cells

78
Q

Contraindications for use of NSAIDs

A

COX-2 rapidly expressed in response to GI injury and contributes to mucosal defense/repair.
Avoid NSAID use in patients with confirmed, presumed or potential GI inflammation (INC Pancreatitis)
Even highly selective COX-2 inhibitors GI ulceration reported occasionally.
Normal renal tissue has COX-1 and COX-2 receptors therefore CONTRAINDICATED in RENAL DISEASE

79
Q

Current opinion on the use of NSAIDs in the management of a patient in hypovolemic shock secondary to trauma

A

No rational basis and clinically insupportable, particularly when such drugs are used concurrently with corticosteroids.

80
Q

Which NSAIDs are given in renal disease

A

NO NSAIDS is completely renally safe when renal perfusion is reduced (e.g. retaining sodium in congestive heart failure). Preferential (carprofen/meloxiccam) have a LOWER RISK than non selective (ketoprofen, phenylbutazone, asprin)

81
Q

Why might animals on phenylbutzazone have increased risk of bleeding

A

Phenylbutzaone (asprin, ketoprofen) are non selective NSAIDs. Thromboxane is a potent vasoconstrictor and activator of platelet aggregation.
Inhibition of thromboxane can lead to increased risk of bleeding. Use with care if in breed with risk of VonWillebrand disease

82
Q

Why do you need to take care when using Diuretics and NSAIDs

A

COX-2 inhibition may attenuate effect of diuretc.

Also when using NSAIDs avoid high dose ACP as premed (and don’t use a2 as premed??)

VetMed Year 4- Term 2 (14 decks)

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