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1
Q

potentiation synergism,

A

effects of the interacting agents are multiplied. Pyrethroids and piperonylbutoxid are an example of potentiation synergism. Piperonylbutoxid markedly potentiates the effect of pyrethroids, and in practise pyrethroids are used as insecticides potentiated by piperonylbutoxid

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2
Q

Antagonism

A

interaction of two or more agents that in combination have an overall effect which is less than the sum of their individual effects

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3
Q
  • Chemical antagonism
A

is exemplified by neutralization occurring when an acid combines with a base, or a combination of cation-active and anion-active tensides in water. The same principle of chemical antagonism is also used in chelate treatment of metal poisoning

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4
Q

Functinal antagonism

A

Methyl alcohol poisoning is treated by administration of ethyl alcohol. The alcohol dehydrogenase enzyme in the liver “prioritizes” ethyl alcohol oxidation, and the conversion rate of methyl alcohol to formaldehyde and formic acid is thus slowed down.

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5
Q

Methaldehyde

Mechanism of action:

A
  • Metaldehyde itself causes decrease in neurotransmitters, mainly in GABA, but exact mechanism of the decrease is not known yet. Partially decomposed to acetaldehyde, which causes metabolic acidosis – cardiovascular effects. Both are local irritants

Metaldehyde is metabolised also by liver cytochrome P450 and undergoes enterohepatic cycling

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6
Q

Theobromide, theopylline, caffein

Mechanism of action:

A

stimulate CNS, muscles and heart, increase diuresis, cause vasodilatation of coronary vessels (sport doping)

a) inhibition of adenosine receptors in CNS – stimulation, tachycardia, vasoconstriction in brain, diuresis
b) inhibition of phosphodiesterase – increased cAMP leads to increased contractility of myocardium, increased glycolysis and lipolysis
c) inhibition of Ca2+ resorption back into sarcoplasmatic reticulum – also increased myocardial and muscle contractility

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7
Q

Onion + garlic

A

Mechanism of action is oxidation of iron in haemoglobin and formation of methaemoglobin, then Heinz bodies formation, haemolysis, anaemia, renal damage

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8
Q

Ethhanol

Non-specific mechanism of action

A

– osmotic activity + dissolves lipids in membranes,

  • influences GABA and NMDA receptors),
  • disturbs thermoregulation

First excitation, then depression of CNS, causes hypoglycaemia

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9
Q

Nitite metHb LD

A

50% death

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10
Q

Inorganic mercury

HgCl, Hg(NO3)2

A

Mercury binds with covalent bond to -SH, -COOH
This influences function of many enzymes and cell processes
Water soluble salts moreover coagulate peptides and are corrosive
They damage GIT mucosa + kidney tubules
Absorption less than 40 %
Only traces excreted to milk(cross placenta)

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11
Q

Organic mercury

A

Methyl- and ethylmercury – firm bond, whole compound toxic, absorbed from GIT (> 90 %)
Bind with –SH groups, block enzymes, destroy haematoencephalic (blood-brain) barrier, increase its permeability
Don’t have corrosive effect on mucosas
In blood transported bound to erythrocytes
They have high affinity to neural tissue

Cross the placenta and have fetotoxic effect

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12
Q

Inorganic lead

MCA

A 
Mechanism of action:
Binds to –SH groups and inhibits many enzymatic functions
Inorganic lead (mainly): 
   - Disturbs saccharide metabolism, metabolism of haem - inhibits Ala-D (Delta-aminolevulinic acid dehydratase) – increased concentration of aminolevulinic acid in urine, and other enzymes involved in haem formation
   - The toxicity comes also from its ability to mimic other biologically important metals - calcium, iron and zinc, and replace them
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13
Q

Organic lead (mainly):

MCA

A
  • interferes with excitatory neurotransmission by glutamate
    • it is a potent inhibitor of the NMDA receptor, a protein playing an important role in brain development and cognition (also in development of schizophrenia)
    • doesn’t influence synthesis of haem much
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14
Q

Cadmium
Mechanism of action:
Does NOTgo to fetus and placenta

A

Inhibition of many enzymes – binds to –SH groups
Antagonist to many metals – Zn, Cu, Ca, Fe
Formation of complexes, which are cleaved in kidney – release of Cd = damage
Damage to kidneys = disturbance of cholecalciferol (vit. D) hydroxylation, thus influences Ca metabolism
Xenoestrogennic element

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15
Q

Copper

Mechanism of action:

A

Haematotrophic poison – directly toxic to erythrocytes
Hepatotoxic – directly toxic to hepatocytes
Probably due to oxidation potential - catalyzes the production of very reactive radical ions – oxidative stress (free Cu joins Fenton reaction)

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16
Q

Zink

Mechanism of action:

A

Probably competes with copper and iron in the organism – decreased serum copper (deficiency in breathing enzymes, haematopoesis) – decreased utilisation of oxygen, oxidative stress, anaemia
Decreased ceruloplasmin – antioxidant
Decreases glutathione levels – antioxidant, conjugation agent

17
Q

Selenium

Mechanism of action:

A

Substitutes sulphur in amino-acids (loss of disulfide bond, misfolding), inhibition of oxidation-reduction enzymes, decrease in reduced glutathione = oxidative stress

18
Q

Thallium

Mechanism of action:

A

Bond to –SH groups - inhibition of respiratory enzymes and oxidative phosphorylation, interference with porphyrine and collagen metabolism, inh. of keratin disulfide bonds – hair loss
Exchange with K+ in muscles, neurons, enzymes (e.g. inhibition of Na/K ATPase)

19
Q

Tin

Mechanism of action:

A

Bond to –SH groups of enzymes - increases permeability of mitochondria membranes for anions – mineral imbalance (Ca2+).
Also inhibition of Ala-D, but weaker then in lead
Disturbance in steroid hormone synthesis and absorption of Zn, Cu, Fe and Ca

20
Q

Arsenic

Mechanism of action:

A

Binds to –SH groups – block of many enzymes (oxidative phosphorylation, glycolysis)
Damage of mucosa, endothelium = increased permeability of vessels, decrease in blood pressure

21
Q

Biphyridil

Mechanism of toxic action

A
  • free oxygen radicals

- proteolytic enzymes formed by active neutrophilic leucocytes

22
Q

Zink phospide

Mechanism of action:

A
  • Inside of the cells it blocks oxidative phosphorylation and energy production, and increases free oxygen radicals which damage the cells

…

23
Q
  1. Which active substances and additives are found in Advantix spot-on?
A

There are two
Permethrin = synthetic pyrethroid. It is a neurotoxin. Block Na channels and inhibit
GABA
Imidacloprid. A neonicotinoid made to mimic nicotine, which is toxic to insects. Block
Na channels

24
Q

Tensides function

A

Used in soaps, washing agents, food industry, cosmetics, pharmaceuticals, textile, paper, metal, building materials – concrete industry, decrease of dustiness etc.

25
Q

Tensides

- Amphoteric

A

Dodecyl betaine, cocamidopropyl betaine, phospholipids

26
Q

Tensides

Non-ionic

A
  • poloxamers or poloxamines,
27
Q

Tensides

- Cationic (based on quaternary ammonium cations)

A

cetylpyridinium chloride, benzalkonium chloride,

28
Q

Tensides

Toxicity to animals:

A
  • Irritation of skin and mucosas, allergic reactions
  • Decrease of cell membrane surface tension
  • Frothing (foam) in stomach – risk of foam aspiration and death
  • Cocamide DEA and TEA release nitrosamines (carcinogens) - monoderivate MEA is more stable and less toxic
29
Q

Ethylene glucol

CS

A

Stage 1: (1-3h, EG itself)
- neurological symptoms, dizziness, headaches, confusion, ataxia, polyuria/polydipsia
Over time, the body metabolizes ethylene glycol into other toxins
Stage 2: (3-6h, glycoaldehyde, glycolic acid)
- result of accumulation of these metabolites - metabolic acidosis = tachycardia, hypertension, hyperventilation, sometimes coma. Oxalate crystals in urine (6-8h)! Hypocalcaemia may occur
Stage 3: (6-48h) glyoxylic acid, oxalic acid, calcium oxalate
- renal oedema + damage by crystals = oliguric kidney failure - uraemia, vomiting, oral ulceration, seizures, death

30
Q

Ammonia autointoxication

A

Also in fish
Happens when there are big changes in temperatures within a few minutes or hours
In decreased temperature – decreased metabolism and excretion (ATP is necessary for ammonia excretion)
If fish ate before – proteins decomposed to ammonia inside of body
Cummulation of ammonia inside, poisoning – congestion and oedema of gills, incoordination, seizures

31
Q

H2S-

A

Reacts with metaloenzymes, most important is bond to Fe3+ in cytochrome-oxidase – similarly to cyanides – inhibition of cell respiration

32
Q

Imidacloprid

A
  • is a neonicotinoid insecticide which is highly specific to the acetyl-choline-receptors
    of insects.
  • When it is applied topically to the skin of a pet, the imidacloprid sits in the lipid layer
    on the surface. When fleas/ticks pass along the surface the substance gets transferred
    to them and absorbed.
  • When it enters the flea,
33
Q

Permetrhin:

A
  • Lipophilic pyrethroid that is quickly absorbed through the skin into the blood.
  • Due to the lipophilic properties of the substance, it can easily go through the BBB,
    where it reversibly locks the neuronal sodium channels in an open position.
  • This leads to sodium having free inflow to the cell, causing prolonged stimulation
    Hyper-excitability.
  • It also affects the calcium-channels and GABA, leading to hyper-excitability,
    exhaustion, and finally, death.
34
Q

chlorinated pesticides

A
  • acute poisoning with high dose: neurotoxicity
  • chronic poisoning with higher doses: similar signs to acute poisoning, but longer
    and gradual coming; again not seen nowadays
  • ingestion of residues from food: deposition in fatty tissues and elimination to milk – mainly genotoxicity, immunotoxicity etc. are expected
35
Q

Dioxin MCA

A

In cell cytosol, bind to AhR, transported to nucleus and here causes higher gene expression for.ex cytochrome. Higher synthesis of cytochrome protein causes higher production of free oxigen radicals - disruption DNA,gen information protein synthesis and cancerogenic effect

36
Q

PRODROMAL

A
  • non-specific signs: fear, headache, anxiety, agression, vision impairment
37
Q

NICOTINIC

A
  • again follows and blends with the two previous stages. Prognosis unfortunately bad.
  • hyperactivity of muscles, begins on head and neck, pure clonic seizures, exitus due to
    exhaustions and respiration centre paralysis
38
Q

Strychnine

A

Inhibit gycine receptor - inhibit neurotranmittor in spine, medulla oblongata

Intence seizures - exhaustion - death

Toxicology (10 decks)

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