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pharmacology unit 6 > heavy metal > Flashcards

heavy metal Flashcards

1
Q

how do metals cause toxicity

A

bind to sulfhydryl groups which inhibit function and cause multi-system organ toxicity.

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2
Q

GI metal toxicity

A

nausea, vomiting, diarrhea.

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3
Q

renal toxicity

A

proteinuria, aminoaciduria, ATN

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4
Q

cardiovascular toxicity

A

response to volume depletion

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5
Q

nervous system toxicity

A

altered mental status, peripheral neuropathy.

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6
Q

skin, hair, nails toxicity

A

changes occur days to weeks post exposure,

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7
Q

chronic toxicity

A

low level, chronic exposure includes all of acute, just less obvious.

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8
Q

chronic toxicity hematologic

A

anemias and cytopenias of various forms.

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9
Q

chronic toxicity renal

A

mild to severe insufficiency

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10
Q

chronic toxicity skin and skeleton

A

rashes, mees lines on nails and or gums (burton lines)

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11
Q

arsenic sources

A

inhalation of dust from occupation. insecticide/rodenticide/herbicide powders or sprays. arsenic trioxide for neoplasia, natural remedies and traditional medicines, well water.

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12
Q

what form of arsenic is the most toxic

A

trivalent is more than pentavalent. inorganic is more toxic than organic.

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13
Q

how is arsenic absorbed

A

complete GI. variable pulmonary

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14
Q

what is the half life of inorganic arsenic

A

10 hours

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15
Q

what is the half life of organic arsenic

A

30 hours

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16
Q

GI effects of arsenic

A

nausea, vomiting, diarrhea, bleeding

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17
Q

cardio effects of arsenic

A

shock, arrhythmia, prolonged QT (torsades)

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18
Q

CNS effects of arsenic

A

agitation, coma, seizures.

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19
Q

renal effects of arsenic

A

hematuria, proteinuria, ATN

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20
Q

other effects of arsenic

A

bonemarrow suppression, anemia, peripheral neuropathy, hyperkeratosis, erythroderma, mees lines.

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21
Q

chronic effects of inorganic arsenic

A

skin: dermatitis, hyperpigmentation, malignancy. neurologic: stocking-glove neuropathy, hepatoxcity

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22
Q

treatment for acute arsenic

A

supportive care: airway/breathing/circulation. GI decontamination. chelation therapy

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23
Q

what is the chelation therapy for arsenic poisoning

A

BAL. succimer and/or DMPS

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24
Q

what is the therapy for chronic exposure to arsenic

A

there is no chelation. remove the sourcee.

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25
source of elemental mercury exposure
mining or processing, paint and battery manufacturing, ceramics, jewelry.
26
sources of inorganic mercury salt
fireworks, dye and ink manufacturing. hide and felt processing, battery.
27
sources of organic mercury
farming and pesticides/fungicides, embalming fluids and wood preservatives.
28
acute elemental mercury toxicity
malaise, HA, fever, lung injury, metal fume fever, encephalopathy
29
chronic elemental mercury toxicity
stomatitis, intention tremor, insomnia, mood swings, memory loss, sensory motor neuropathy.
30
acute organic methyl/dimethyl mercury toxicity
sensory and motor neuropathy, dysarthria, ataxia, tremor, hearing deficits, psychological changes.
31
acute organic phenyl/methoxymethyl mercury toxicity
similar to inorganic mercury salt.
32
acute inorganic mercury salt toxicity
skin blistering, weakness, pallor, shock-like.
33
chronic inorganic mercury salt toxicity
similar to elemental as well as acrodinia and rash.
34
how must we measure the exposure to mercury
with whole blood measurements, since it accumulates in RBCs
35
what is a common cause of organic mercury level elevation
seafood consumption
36
what is troublesome about measuring the organic mercury level
24 urine collection may indicate the presence however it is not excreted in the urine and thus it is not diagnostic for organic mercury
37
what is a way to confirm organic mercury exposure
hair analysis
38
treatment for mercury
ABC. activated charcoal absorbs mercuric chloride and thus is useful for patients not vomiting. chelation therapy (BAL for acute elemental or inorganic). DMSA for organic mercury and as an additional for chronic exposure to elemental or inorganic
39
sources of thallium
manufacture of semiconductors, jewelry, optical lenses, and low temp thermometers. old rodenticide and insecticide.
40
toxicity for thallium
results for the salts, rarely elemental.
41
how is thallium ingested
GI and absorption in the skin.
42
how much thallium is lethal in adults
1 gm
43
clinical progression of toxicity of thallium
within hours: nausea, vomit, diarrhea, constipation, pleuritic chest pain. within hours to days: lethargy, coma, psychosis, seizures, respiratory failure, painful ascending neuropathy without motor involvement. tachycardia, HTN, diaphoresis, fever. myocardial necrosis, arrhythmia ARDS. alopecia.
44
how to diagnose thallium
abdominal radiograph maybe positive within hours. blood levels. urine, hair.
45
treatment of thallium
activated charcoal. whole bowel irrigation if the radiograph is positive. chelation therapy: prussian blue exchanges with and promotes elimination in the gut.
46
what chelation does NOT work for thallium
BAL, EDTA, succimer, penicillamine.
47
sources of lead
paint (pre-1978), house dust, water from plumbing, leaded gasoline, dietary supplements. toys not made in the US. occupational: lead welders, bridge painters, firing range, shot makers.
48
manifestations of severe lead in children
encephalopathy (coma, altered sensorium, seizures, bizarre behavior, ataxia, apathy, loss of developmental skills, papilledema, cranial nerve palsies. persistent vomiting, anemia/pallor,
49
manifestations of mild lead poisoning in children
hyperirritable behavior, intermittent lethargy, difficult child not interested in play. vomiting, abdominal pain, anorexia,
50
asymptomatic lead poisoning in children
impaired cognition, behavior, balance, fine-motor coordination. impaired learning and growth.
51
manifestations of severe lead in adults
encepholopathy (coma, seizures, obtundation, delirium, focal motor disturbances, HA, papilledema, opticneuritis, foot drop, wrist drop, alcoholic colic, pallor/anemia, nephropathy.
52
manifestations of moderate lead poisoning in adults
HA, memory loss, insomnia, decreased libido. neuropathy, metallic taste, abdominal pain, anorexia, constipation, arthritis, gout, mild anemia, arthalgia, weakness.
53
mild lead poisoning in adults
fatigue, somnolence, moodiness, lessened interests in leisure activity, cognition, reporduction, kidney, bone density, HTN, cardiovascular disease and increased risk for cancer.
54
how to assess lead in children
finger stick, age 1-2. if elevated obtain blood sample.
55
adult lead screening
performed more in occupational risk. urine not useful. whole blood are standard.
56
treatment of lead
removal of source, whole bowel irrigation, for encepholopathy use BAL, PLUS, CaNa2EDTA for 5 days. succimer for 20 days.
57
iron metabiolism
primarily regulated through absorption in the intestine. taken up into plasma or stored in the mucosal ferritin. transferrin mediates transfer. liver, spleen and marrow are the major sources of storage
58
iron toxicity
irritating and corrosive effect on GI, nausea, vomit, diarrhea, bleeding, volume depletion. free radical formation and tisue damage in the myocardium, vasodilation, negative inotropy, uncoupling of ETC and lactic acidosis
59
treatment for iron
IV fluids, supportive, bowel irrigation deferoxamine
60
deferoxamine
high affinity chelator removes iron from ferritin and transferrin. IV is faster
61
deferoxamine adverse
hypotension, anaphylactoid, high doses for long periods ARDS. yersinia enterocolitis

pharmacology unit 6 (45 decks)

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