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Toxicology > Venoms & Toxins > Flashcards

Venoms & Toxins Flashcards

1
Q

Venomous animals

A

Actively inject toxins into victim

Venom is used for hunting and defense

Example: brown recluse

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2
Q

Poisonous animals

A

Secrete poisons which are passive defense mechanisms

Example: poison dart frog

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3
Q

Three classes of venom compounds

A
  1. LMW substances
  2. Peptides
  3. Enzymes
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4
Q

What are LMW substances?

A

Substances that often cause pain, inflammation, and hypotension

Examples: Prostaglandins, histamine, epinephrine

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5
Q

What are toxic peptides?

A

Peptides that cause direct toxic effects and allergy

Examples: Melittin, bungarotoxin

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6
Q

What are toxic enzymes?

A

Eznymes that cause toxicity and allergy

Examples: hyaluronidase, collagenase, protease

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7
Q

Hymenoptera

A

Includes bees, wasps/hornets, and fire ants

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8
Q

Crazy Ants

A

Native to Africa
Very aggressive
Numbers growing in Florida

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9
Q

Mechanism of action of bee venom

A

Composed of

50% melittin: acts as detergent, is hemolytic, and causes pain and histamine release

12% phospholipase A2: destroys cell membranes

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10
Q

Mechanism of action of wasp/hornet venom

A

Contain neurotoxins, alarm pheremones (alert the swarm to the intruder), and kinins (the primary pain-inducing substances)

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11
Q

Mechanism of action of ant venom

A

Piperidine causes dermal necrosis
Formic acid causes burning sensation and pain
Both chemicals have cytotoxic, hemolytic, fungicidal, insecticidal, and bactericidal properties

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12
Q

Clinical signs of bee, wasp/hornet, ant stings

A

Site of sting: swollen, red plaques, edema, regional allergic reaction

Anaphylaxis (most common cause of death)

Systemic toxicity caused by delayed hypersensitivity (shock, hemolysis, rhabdomyolysis, hepatic and renal injury)

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13
Q

Treatment of bee, wasp/hornet, ant stings

A

Removal of stinger by scraping (not forceps!)

Cold compress

Antihistamines/corticosteroids

Monitor for anaphylaxis

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14
Q

Genus of ticks that can cause toxicity

A

Dermacentor

Ixodes

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15
Q

Mechanism of action of tick toxin

A

Holocyclotoxin causes impaired neuromuscular junction, causing weakness and paralysis

Also may act on Na+ channels

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16
Q

Clinical signs of tick holocyclotoxin toxicosis

A

Appear 6-14 days after attachment of tick

Loss of appetite and voice, incoordination, flaccid paralysis, excessive salivating, vomiting, respiratory distress, death

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17
Q

Diagnosis of tick holocyclotoxin toxicosis

A

No definitive diagnosis
History of tick infestation
Presence of ticks
Ascending paralysis and loss of voice

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18
Q

Treatment of tick holocyclotoxin toxicosis

A 
Supportive therapy
Atropine sulfate
Anti-emetics
Fluid replacement therapy
Oxygen

Prognosis is good if treated

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19
Q

Species of toad that cause poisoning

A

All species of Bufo secrete toxins for defense

B. Marinus in Florida, B. Alvarius (California/Arizona)

Eggs and tadpoles are also toxic

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20
Q

Cane Toad/Giant Toad (B. Marinus)

A

Found in Florida
Secrete potent compounds that can be fatal
Have few predators

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21
Q

Compounds and mechanism of action of toad poisons

A

Biogenic amines: cause vasoconstriction, hypotension, hallucination, GI effects

Bufogenins (bufotalin): inhibit Na/K ATPase and produce toxic arrhythimias

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22
Q

Clinical signs/diagnosis of toad poison toxicosis

A 
Hypersalivation, foaming at mouth, head shaking, vomiting
Hyperemic gums (brick red)
Arrhythmias
Convulsions, ataxia, hallucination
Severe hyperkalemia
Death can occur in 15 minutes
23
Q

Treatment of toad poison toxicosis

A

Immediate oral decontamination (water lavage)
Activated charcoal if no seizures
Diazepam/barbiturates for seizures
Propanolol, lidocaine, esmolol for arrhythmias
Fluid therapy
Digoxin for neuro signs/hyperkalemia

24
Q

What are Black Widow spiders (Lactrodectus mactans)?

A

Shiny black spider with red hourglass on bottom
Only females are toxic
Messy web

25
Q

Venom of black widow spider

A

Contains alpha-latrotoxin
Created pores in membranes allowing Ca++ entry and release of massive amounts of neurotransmitter
Causes sustained muscle spasms

26
Q

Clinical signs of black widow spider envenomation

A 
muscle cramping and spasms
Rapid weightloss
Abdominal rigidity 
Restlessness, writhing
Vocalization
Hypertension
Tachycardia, respiratory collapse

CATS MOST SENSITIVE BECAUSE THEY EAT SPIDERS

27
Q

Treatment of black widow spider envenomation

A

Anti-venom only proven treatment
Control muscle spasm and pain
Calcium gluconate for muscle camps
Supportive care, especially respiratory

28
Q

Characteristics of Brown Recluse spider (Loxosceles reclusa)

A

Nocturnal and non-aggressive
Animals bitten when they lay down on spider
Dogs are most susceptible
Venom contains several necrotizing enzymes

29
Q

Brown Recluse venom

A

Sphingomyelinase D binds to cell membranes and cleaves head off lipids
Causes tissue necrosis
Victim’s immune response determines severity of lesion

30
Q

Clinical signs of brown recluse envenomation

A

Initial bite causes little to no pain
3-8 hours after envenomation, site becomes red, swollen, tender, and forms a “bulls eye” and non-healing ulcer
Can cause hemolytic anemia, fever, weakness, leukocytosis

31
Q

Diagnosis of brown recluse envenomation

A

Difficult if bite is not witnessed

32
Q

Treatment of brown recluse envenomation

A

Dapsone to treat dermal lesion
Fluids, NSAIDs, glucocorticoids
Antibiotics
Analgesics

For necrotic lesions: clean with burrow’s solution (Aluminum acetate) or hydrogen peroxide, debridement of necrotic tissue, bandage

33
Q

Characteristics of snake envenomation

A

Venomous snakes - Elapidae or Crotalidae
Dogs and horses most common victims
Size of victim and amount of venom determines severity
Death due to respiratory paralysis

34
Q

Eastern Coral Snake (Micrurus fulvius fulvius)

A

Red, yellow, black alternating bands
Small fangs, small heads, round pupils
Shy, non-aggressive, and nocturnal

35
Q

Mechanism of action of coral snake envenomation

A

Venom is composed of polypeptides and enzymes
Neurotoxicity due to bungarotoxin
Acts by preventing binding of ACh causing paralysis
Local tissue necrosis, myoglobinuria in cats, and hemolysis in dogs

36
Q

Clinical signs of coral snake envenomation

A

Onset of clinical signs may be delayed up to 12h
Salivation, dyspnea, weakness, hyporeflexia, CNS depression, paralysis
No definitive diagnostic test

37
Q

Treatment of coral snake envenomation

A

If neurologic signs develop, administer anti-venom immediately
Respiratory function should be closely monitored
Broad-spectrum antibiotics and symptomatic wound care
Prognosis is good when prompt care received
Monitor for a minimum of 24 hours! Recovery can be up to 10 days

38
Q

Characteristics of pit vipers (Crotalids)

A

Copperhead, cottonmouth, rattlesnakes
Characterized by heat sensing pit and hinged, retractable fangs
Head is wider than body (triangular-shaped)
Elliptical/vertical pupil

Copperheads are responsible for majority of animal snake bites but rattlesnakes cause most deaths

39
Q

Examples of pit vipers in Florida

A

Cottonmouth
Timber Rattlesnake
Eastern Diamondback
Copperhead

40
Q

Clinical signs of pit viper envenomation

A 
Distinct fang marks
Immediate swelling and bruising
Hypotension, shock, tachycardia, tachypnea
Anticoagulation
Tissue necrosis

Cats often hide
Dogs seek human attention

41
Q

Treatment of pit viper envenomation

A

Every case is different!
Only proven therapy is anti-venom
Symptomatic and supportive care
Copperhead bites can be managed with antihistamines
Rattlesnake and moccasin bites often managed with fluids and corticosteroids for shock and glucocorticoids for inflammation

DON’T cut, ice, or tourniquet (these localize effects of toxin to one area so is harder for body to fight)

42
Q

Garbage/carrion toxicity

A

Usually from protein-rich foods during warm months
Enterotoxins and endotoxins
Can be due to bacteria or preformed toxins

43
Q

Mechanism of action of enterotoxins

A

Bacteria bind intestinal epithelium, increasing permeability, and causing fluid loss (diarrhea) and decreased absorption of nutrients

44
Q

Examples of enterotoxins

A

Salmonella, E. coli, bacillus, Strep, and C. Perfringens

45
Q

What are Endotoxins?

A

Lipopolysaccharide from gram negative cell walls

46
Q

Mechanism of action of endotoxins

A

Activates inflammatory processes and causes release of prostaglandins and histamine

47
Q

Clinical sign of endotoxin toxicity

A 
Shock
Pancreatitis
Activation of clotting cascade
Heart effects
Lethargy
Fever
Diarrhea, extremely bad smelling feces
Abdominal pain
48
Q

Treatment of endotoxin toxicosis

A

Emesis (if not already occurred)
Support cardiovascular function
Fluids
Antibiotics

49
Q

What is botulism?

A

Caused by clostridium botulinum

Extremel potent toxin

50
Q

Mechanism of action of botulism toxicosis

A

Prevents release of ACh, causes paralysis

51
Q

How to diagnose botulism?

A

Hard to diagnose

Often only circumstantial evidence (access to carrion, garbage, compost piles)

52
Q

Clinical signs of botulism

A 
Decreased tongue and tail tone
Dropping food from mouth, salivation
Weakness, weak vocalization, progressive paresis
Bradycardia
Constipation, urinary retention
53
Q

Differential diagnoses for botulism

A

Anticholinesterase
Ionophores
Lead
Nitrate poisoning

54
Q

Treatment of botulism

A 
Supportive therapy and IV fluids
Oxygen
Warm water enemas and bladder expression
Antibiotics
Antitoxin (not always effective- does not neutralize toxin already in neurons)

Poor prognosis

Toxicology (7 decks)

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