Pharm chelation therapy Flashcards Preview

ABBEY MSII U6 > Pharm chelation therapy > Flashcards

Flashcards in Pharm chelation therapy Deck (46):
1

what is the mechanism of heavy metal toxicity?

-binds to sulfhydryl groups in various organ systems and enzymatic processes throughout the body
-affinity for organ system toxicity is a result of the characteristics of the heavy metal and its distribution sites

2

effects of acute heavy metal exposure on the cardiovascular system

tachycardia and in some cases dysrhthmias and cardiomyopathy

3

effects of acute heavy metal exposure on the CNS

altered mental status and peripheral neuropathy

4

effects of acute heavy metal exposure on the GI system

nausea, vomiting and diarrhea

5

effects of acute heavy metal exposure on the renal system

proteinuria, aminoaciduria and acute tubular necrosis

6

effects of chronic heavy metal exposure

more subtle findings - increased effects at organ sites that may be less accessible acutely (esp CNS and PNS, hematologic, renal, skin/skeleton/CT abnormalities, neoplasm)

7

how is heavy metals diagnosis made?

-routine PE
-question occupation and hobbies
-labs: CBC with peripheral smear, renal function, liver function, u/a, acid-base balance and radiograph anaylsis
-serum metal levels, whole blood metal levels, urine metal levels, hair analysis

8

what are the 4 most common heavy metal exposures?

lead, arsenic, mercury, thallium

9

what is done for acute toxicity of heavy metal toxicity?

-ABCs
-GI decontamination (activated charcoal, whole bowel irrigation)
-chelation therapy

10

what is done for chronic toxicity of heavy metals?

-removal from source!!
-chelation therapy

11

how does chelation work? (mechanism)

-chelating agent forms complexes with heavy metals and prevents or reverses the binding of metallic cations to reactive groups (ligands)

12

what are characteristics of ideal chelators?

-VD of the chelator greater than VD of chelate
-high water solubility
-ability to reach the site of where the metal is stored
-capacity to form nontoxic complexes
-stable at physiologic pH
-low affinity for trace elements

13

british anti-lewisite (BAL) class and mechanism

dithiol: forms stable chelate via electron pair donation and coordination with metal ion

14

BAL implication

mixed with peanut oil (peanut allergies)

15

BAL therapeutics

arsenic, lead, inorganic mercury poisoning

16

BAL side effects

renal toxicity (unless urine is alkalinized), pain at injection site (IM), nausea, vomiting, increases in BP and HR

17

what is done to prevent metal-induced renal toxicity? why must this be done?

urinary alkalinization because dissociation of BAL-metal chelate in acidic urine happens

18

2,3-dimercaptosuccin acid (DMSA) class and mechanism

dithiol: coordinate bonding to sulfur (arsenic and mercury) or sulfur and oxygen (lead and cadmium)

19

DMSA therapeutics

arsenic, lead, mercury, cadmium poisoning

20

DMSA side effects

mild ALT/AST elevation - otherwise well tolerated

21

when is DMSA most used?

lead poisoning in children

22

how is DMSA administered

orally - can be given outpatient

23

edetate calcium disodium (EDTA) mechanism

displacement of calcium by lead

24

EDTA therapeutics

lead poisoning

25

which version of EDTA used? which should not be used? why?

CaNa2EDTA - NOT Na2EDTA because it causes severe hypocalcemia

26

EDTA side effects

malaise, fever - renal toxicity

27

how is EDTA administered? when?

IV at hospital - esp given when there is encephalopathy due to lead poisoning

28

prussian blue mechanism

stays in gut and not absorbed until it grabs metal - goes into gut and is excreted that way

29

prussian blue therapeutics

thallium and radioactive cesium poisoning

30

prussian blue side effects

well tolerate - not absorbed after oral dosing into systemic circulation

31

normal role of iron

various intracellular processes (accepts and donates electrons), extracellular is bound to transferrin

32

when does iron toxicity occur?

free iron in circulation

33

what are the pharmacokinetics of iron?

peak serum concentrations occur 2-6 hours after ingestion (overwhelmed transferrin and increase in circulating free iron)

34

local toxicity of iron

direct corrosive effect to GI mucosa (leading to hematemesis, melena, periportal necrosis of liver and intetional ulceration and edema)
-resultant volume depletion

35

systemic toxicity of iron

-high anion gap metabolic acidosis
-uncoupler of oxidative phosphorylation!
-direct negative inotropic effect
-hypotension (vasodilator)

36

early clinical effects of iron toxicity

local tissue effects of GI tract (nausea and lots of vomiting) within 6 hours

37

intermediate clinical effects of iron toxicity

nausea and vomiting may temporarily decrease with an increase in development of metabolic acidosis and sequelae

38

late signs of iron toxicity

severe local and system effects - hepatotoxicity, ARDS, renal, gastric outlet obstruction

39

chelator for iron poisoning

deferoxamine

40

deferoxamine mechanism

chelates FREE iron and iron transported between transferrin and ferritin

41

deferoxamine side effects

rate-related hypotension, anaphylactoid reactions, yersinia enterocolitis (facilitates growth of unusual organisms), acute lung injury/ARDS
-can only treat for 24 hours before acute lung injury manifests

42

clinical pearls for lead poisoning in kids

colic, lower levels associated with IQ changes, think PICA

43

clinical pearls for lead poisoning in adults

hypertension, tolerate higher lead levels

44

clinical pearls for arsenic poisoning

rice-water diarrhea, prolonged QT, arsenical dermatitis, "rain drops on a dusty road"

45

clinical pearls for mercury poisoning

labile mood "mad as a hatter", intention tremor, mercury salts: caustic

46

clinical pearls for thallium

painful neuropathy, alopecia