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23 spring: pharm > Test 4: 57-58 heavy metals > Flashcards

Test 4: 57-58 heavy metals Flashcards

1
Q

Inverse relationship between dietary protein content and — toxicity

A

cadmium and lead

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2
Q

Vitamin C increases — absorption while decreasing absorption of —

A

ferrous iron

lead and cadmium

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3
Q

metal binding proteins may be a target of toxicity (especially enzymes) or play a protective
role (—)

A

metallothioneins

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4
Q

— are low molecular weight proteins that enable high-affinity binding with cadmium, copper, mercury, silver, and zinc

A

Metallothioneins

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5
Q

Transferrin binds most — in plasma

A

ferric iron

Ferric transferrin is transported across cell membranes by receptor-mediated endocytosis

  • Transferrin also transports Al3+ and Mn2+
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6
Q

Ferritin stores iron in reticuloendothelial cells of —

A

liver, spleen, and bone

Also binds cadmium, zinc, beryllium, and aluminum

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7
Q

— is a copper-containing glycoprotein oxidase that converts
ferrous (Fe2+) to ferric (Fe3+) iron
in plasma so it can then bind to —

A

Ceruloplasmin

transferrin

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8
Q

— is the formation of a metal ion complex in which the metal ion is associated with a charged or uncharged electron donor ligand

A

Complexation

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9
Q

is the formation of ring structures consisting of the metal ion and 2 ligand atoms

A

chelation

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10
Q

ideal chelating agents should

A
  • Be water-soluble
  • Be resistant to biotransformation
  • Be able to reach sites of metal storage
  • Be capable of forming nontoxic metal complexes
  • Be capable of being excreted
  • Have a low affinity for essential metals, especially calcium and zinc
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11
Q

BAL is used to chelate

A

lead, inorganic mercury, antimony, bismuth, chromium, cobalt, gold, and nickel

adjunct treatment of lead
encephalopathy- removed lead from RBC and brain

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12
Q

BAL toxicosis

A

vomiting, hypertension, tachycardia, tremors, convulsions, and coma, culminating in death

Potentially nephrotoxic

BAL: adjunct treatment of lead
encephalopathy: chelate lead, inorganic mercury, antimony, bismuth, chromium, cobalt, gold, and nickel

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13
Q

sodium EDTA will do what to calcium levels

A

binds to calcium and will cause ↓calcium tetany

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14
Q

calcium EDTA is different from BAL because

A

BAL can chealte lead in brain

EDTA can not get into brain

drugs can be combined together

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15
Q

DMSA

A

used to chelate lead (not effective in brain)

can be given orally, not nephrotoxic

also effective in dogs exposed to methyl mercury and lead, and mice, rats, and rabbits exposed to arsenic

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16
Q

deferoxamine binds to —

A

ferric (Fe3+) iron

Competes for iron contained in ferritin and hemosiderin, but not transferrin, hemoglobin, or heme-containing enzymes

will change urine to vin rose when working

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17
Q

toxic effects of deferoxamine

A

nausea, vomiting, depression, hypotension, skin rashes, and possibly cataracts

used to bind to ferric iron

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18
Q

penicillamine is used to remove

A

copper, lead, mercury, and iron

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19
Q

— should not be used in pts with penicillin allergy

A

penicillamine: used for removal of copper, lead, mercury, and iron

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20
Q

N-Acetylcysteine is used to remove

A

mercury, methyl mercury and other metals

Free radical scavenger and precursor to glutathione

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21
Q

— is a free radical scavenger and precursor to glutathione that is used to remove mercury

A

N- Acetylcysteine

Orally administered, low toxicity, and widely available

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22
Q

— arsenicals inhibit cellular respiration

A

trivalent

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23
Q

trivalent arsenic affect what type of cells

A

inhibit cellular respiration:
Actively dividing cells of the intestinal epithelium, epidermis,
kidney, liver, skin, and lung

Trivalent arsenic also affects capillary integrity in GI tract

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24
Q

trivalent or pentavalent forms of arsenic are more toxic

A

trivalent: inhibit cellular respiration and affect capillary integrity in GI tract

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25
Q

how does pentavalent arsenic work

A

substitute for
phosphate in oxidative phosphorylation

causes ↓ATP, does NOT cause ↑temp

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26
Q

The hydride gas of arsenic, AsH3, can combine with hemoglobin and be oxidized to a —

A

hemolytic metabolite

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27
Q

clinical signs of arsenic posioning

A

Vomiting, intense abdominal pain,
weakness, staggering, ataxia, recumbency, and weak, rapid pulses with signs of shock are common

dog-sitting position with appetite and cognition remaining normal

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28
Q

— toxicity can present with animals assume a dog-sitting position with appetite and cognition remaining normal

A

arsenic

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29
Q

treatment for arsenic

A

Emergency and supportive care consist of treatment for shock, acidosis, and dehydration
* Dimercaprol (British anti-Lewisite, or BAL) is the classic antidote, but is largely ineffective unless
given before clinical signs begin
* Succimer is currently the preferred antidote
* Convalescent animals should be fed bland diets with vitamin supplementation and reduced amounts of high-quality protein

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30
Q

More than 90% of absorbed lead is bound to —

A

RBCs

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31
Q

lead toxicity works by

A

Lead binds sulfhydryl groups, resulting in the inactivation of enzymes involved in heme synthesis, causing RBC abnormalities

  • Damage to membrane-associated enzymes such as sodium-potassium pumps results in RBC fragility and renal tubular injury
  • Shortened RBC lifespan and decreased replacement both contribute to the anemia seen
    with chronic lead toxicosis
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32
Q

Lead toxicity
— will have CNS signs

A

ruminants

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33
Q

Lead toxicity
— will have peripheral neuropathies signs

A

horses

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34
Q

dogs and cats with lead toxicity will present with

A

neuro and GI signs

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35
Q

parrots with lead toxicity will present with

A

nonspecific GI, neurologic,
renal, and hematologic
abnormalities

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36
Q

Basophilic stippling can be normal in —, though may be more
diagnostic of — toxicity in dogs and horses

A

ruminants
lead

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37
Q

Large numbers of — without evidence of severe anemia can be suggestive of lead toxicosis in small animals

A

nucleated RBCs

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38
Q

treatment of lead toxicity

A
  • Stabilization
  • Elimination of lead from the GI tract
  • Chelation: Succimer(DMSA) or CaEDTA +/- BAL and/or thiamine
  • General supportive care
  • Elimination of lead from the animal’s environment
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39
Q

— mercury is excreted primarily in urine and causes direct tissue necrosis and renal tubular necrosis

A

Inorganic mercury

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40
Q

— mercurials are excreted mainly in bile and feces

A

Organic

41
Q

clinical signs of mercury toxicosis

A

stomatitis, pharyngitis, vomiting, diarrhea, dehydration, and shock

◼ Early signs: erythema of the skin, conjunctivitis, lacrimation, stomatitis ◼ Intermediate signs: depression, ataxia, incoordination, paresis, blindness
◼ Dermatitis, pustules, and epithelial ulcers increase
during the course of the disease
◼ Anemia can result because of hematuria and melena
◼ Advanced signs: proprioceptive defects, abnormal postures, complete blindness, anorexia, paralysis, slowed respiration, coma, death

42
Q

In acute exposure to elemental mercury or mercuric salts, — may be administered to bind ingested mercury; oral sodium thiosulfate also binds mercury

A

egg white or activated charcoal

43
Q

treatment of mercury

A

egg white or activated charcoal
cathartic or sorbitol
penicillamine
DMSA (succimer)
Supplemental selenium and vitamin E are somewhat protective against mercury toxicosis

44
Q

Domestic livestock and companion animals may become intoxicated with — after parenteral overdose

A

selenium

45
Q

Selenium-containing compounds have biological importance as an —

A

essential dietary constituent

46
Q

Intoxication can result from excess selenium supplementation of — rations

A

livestock

47
Q

The — is the primary site of selenium absorption, with little or no absorption occurring from the —

A

duodenum

rumen or abomasum

48
Q

Porcine focal symmetrical poliomyelomalacia (PFSP) results from an induced deficiency of nicotinamide as well as from — intoxication, suggesting the involvement of oxidative metabolic failure in the pathogenesis of the lesion

A

selenium

49
Q

Acute selenium intoxication usually manifests as

A

depression, weakness, dyspnea, and a garlicky odor to the breath

50
Q

Subchronic selenium intoxication in pigs manifests as a

A

CNS disorder characterized by initial hindlimb ataxia progressing to posterior paralysis, then
tetraparesis to paralysis
* Affected pigs remain alert and attempt to walk while dragging their hindlimbs
* Hoof separation at the coronary band also occurs

51
Q

what caused the hair to break

A

too much selenium

52
Q

Chronic intoxication, or “alkali disease,” results from chronic
consumption of —grasses and crops

A

seleniferous

53
Q

selenium will cause lesion in the —

A

heart

54
Q

Dietary — deficiency can result in excessive absorption and storage of copper

A

molybdenum

55
Q

Feeding calf or horse rations to — is a common source of excessive dietary copper

A

sheep

56
Q

Copper is actively transported through the enterocytes, then loosely binds to —, ceruloplasmin, and transcuprein before being distributed to the — for storage

A

albumin
liver, kidney, and brain

57
Q

Excess liver copper levels can cause liver necrosis and release of the copper into the bloodstream, resulting in — in the serum

A

erythrolysis, hemoglobinuria, and elevated copper levels

(copper levels can be transient)

58
Q
A

copper
gun metal kidney

excess copper accumulates in the kidney

59
Q

sheep with copper toxicity will show — clinical signs

A

when stressed

  • Intravascular hemolysis results in hemoglobinuria, icterus, anoxia, and death
  • Urine is dark red with a “port wine” appearance due to the presence of hemoglobin
60
Q

what kind of dogs can have hereditary copper hepatitis

A

bedlington terriers
labs
dobermanns
west highland white terriers
dalmatian

61
Q

— has a three-way interaction with copper and sulfur

A

Molybdenum

62
Q

Molybdenum is required for metalloenzymes, including —, xanthine dehydrogenase, aldehyde oxidase, and sulfite oxidase

A

xanthine
oxidase

63
Q

Diets high in sulfur — copper absorption and — susceptibility to molybdenum

A

decrease

increase

64
Q

Diets high in molybdenum may — absorption of zinc

A

decrease

65
Q

clinical signs of molybdenum

A

chronic diarrhea

A relative copper deficiency causes abnormalities in connective tissue formation and bone

  • Abnormal bone growth and parostosis

In addition to copper deficiency, abortions have been observed in pregnant mares

66
Q

clinical signs of fluoride

A

Fluorides replace hydroxyapatite,
delaying and altering mineralization of bone

  • Erupting incisors and molars are weaker than normal teeth and wear rapidly
  • Oxidation of organic material in damaged portions of the teeth causes brown or black discoloration
  • bones remodel and deform → subperiosteal hyperostosis with thickened and irregular long bone surfaces
67
Q

clinical signs of acute fluoride toxicosis

A

excitation, seizures, urinary and fecal incontinence, vomiting, weakness, hypersalivation, depression, cardiac failure, and death

68
Q

Aluminum sulfate, aluminum chloride, calcium aluminate, and calcium carbonate can be used to reduce absorption of — in the diet

A

fluorides

69
Q

Iron toxicosis is usually due to excessive injections in — or the ingestion of large amounts of iron-containing products in other species

A

baby pigs

70
Q

Iron is most toxic when given —

A

intravenously

71
Q

how is iron absorbed

A

First, ferrous ions are absorbed from the intestinal lumen into the mucosal cells (energy dependent carrier: transferrin-like protein moves ferrous iron into mucosal cells

The second step is the transfer of iron to ferritin or into circulation bound to transferrin proteins
* Complexed with transferrin, iron is distributed to other storage locations in the body

72
Q

Iron must be in — state for absorption

A

an ionized

73
Q

In acute overdoses, iron seems to be absorbed in a — fashion

A

passive, concentration-dependent

usually needs energy dependent carrier (transferrin-like protein

74
Q

70% of iron is in the — form when bound to normal hemoglobin and myoglobin

A

ferrous (Fe2+)

75
Q

Most of the remaining iron not bound to hemoglobin and myoglobin is found in the body as the — form, stored in hemosiderin, ferritin, and transferrin

A

ferric (Fe3+)

76
Q

Most iron is stored in the —

A

liver, spleen, and bone marrow

77
Q

at a cellular level, excess free iron causes

A

increased lipid peroxidation with resulting membrane damage to mitochondria, microsomes, and other cellular organelles

78
Q

what does excess iron do to the heart

A

fatty necrosis of the myocardium, postarteriolar dilation, increased capillary permeability, and reduced cardiac output

also interferes with clotting mechanisms and causes metabolic acidosis

79
Q

There is not a mechanism for excretion of —, so toxicity depends on the amount already present in the body

A

iron

80
Q

what level of iron is lethal for dog

A

less than 20- nontoxic
20-60: mild clinical signs
↑60: serious signs
100-200: deadly

81
Q

if a 10 kg dog eats 200 mg of ferric pyrophosphate
FP is 30% elemental iron

Toxic?

A

200 mg ( 0.3)= 60 mg elemental iron

60 mg/10 kg dog= 6 mg/kg elemental iron
less than 20- nontoxic

less than 20- nontoxic
20-60: mild clinical signs
↑60: serious signs
100-200: deadly

82
Q

is pathologic tissue accumulation of iron

A

Hemochromatosis

83
Q

is non-pathologic accumulation of iron

A

Hemosiderosis

84
Q

four clinical phases of iron toxicosis

what is 1 and 2

A

First stage: occurs between 0 and 6 hours post-exposure
* Vomiting, diarrhea, and GI bleeding
* Most animals with mild to moderate iron toxicosis do not progress beyond this stage

Second stage: occurs 6-24 hours post- exposure
* Transient latent period

85
Q

four clinical phases of iron toxicosis

what is 3rd and 4th

A

Third stage: occurs about 12-96 hours after clinical signs develop
* Lethargy, recurrence of GI signs, metabolic acidosis, shock, hypotension, tachycardia, cardiovascular collapse, coagulation deficits, and hepatic necrosis
* Death may occur

Fourth stage: occurs 2-6 weeks later in animals that develop GI ulcerations
* As ulcerations heal, scarring and strictures may develop

86
Q

peracute syndrome in pigs is characterized by sudden death is caused by excess —

A

iron (injection given IV?)

87
Q

Serum iron levels are the best method to confirm iron poisoning, and it is also beneficial to measure the —

A

total iron- binding capacity (TIBC)

When serum iron exceeds the TIBC,
severe systemic effects can be expected

88
Q

how to treat acute iron toxicity

A

acute: GI decontamination, activated charcoal does not work, can use sodium phosphate, sodium bicarbonate, or magnesium hydroxide instead

GI protectants: sucralfate
supportive: fluids

89
Q

how to treat severe iron toxicosis

A

chelation: Deferoxamine (Desferal)

90
Q

indirect vs direct sodium toxicosis

A

direct: eating too much salt

indirect: not enough water

91
Q

Hypernatremia occurs when the sodium content of the extracellular fluid (ECF) increases in relation to — or — from the ECF without a compensatory decrease in sodium

A

its free water content

free water is lost

92
Q

excess sodium can passively diffuse into the

A

CSF

93
Q

what happens to CNS with excess salts

A

the brain cells shrink from dehydration, tearing blood vessels that lead to hemorrhage, brain infarcts, and cerebral edema

94
Q

Although sodium — enters the CSF, it is — transported back out into serum

A

passively

actively

95
Q

if sodium is trapped in brain cause it can not be actively transported back and you give unlimited water, what will happen?

A

water will move into brain to try to balance salt

cerebral edema

96
Q

with excess sodium, Organic solutes called — increase to maximum levels within 48-72hours and a similar amount of time is required for their decline as a hypernatremic crisis is resolved

A

idiogenic osmoles

97
Q

in swine early clinical signs of excess sodium are

A
  • restlessness, thirst, pruritus, constipation, and vomiting, aimless wandering, blindness, head pressing, and circling
  • Muscle twitches start at the snout then spread to the head
  • As tremors progress, pigs assume a dog-sitting position before falling over into lateral recumbency
    with seizures and opisthotonos followed by death
98
Q

how to diagnosis excess salt

A

serum and CSF sodium levels

postmortem: eye fluids and brain tissue

99
Q

how to treat excess salt

A

slowly rehydrate to prevent cerebral edema

0.5% body weight of water every hour

Cerebral edema may require treatment with mannitol or glycerin

50% die

23 spring: pharm (46 decks)

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