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DT4- Exam 3 > Valentovic- Herbs and Metals (2)- Leah :) > Flashcards

Valentovic- Herbs and Metals (2)- Leah :) Flashcards

1
Q

Why are metals dangerous?
Are they acutely toxic?
How are they metabolized?

A
  • some metals have t/12 10-30 years, so they accumulate with small doses over a lifetime.
  • they aren’t metabolized/ biotransformed, instead they bind to S/O/N functional groups on proteins and stay in the body
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2
Q

What is the most common way to remove toxic metals from the body?

What are the requirements for this therapy? (6)

A 
chelators 
must be: 
-less toxic than the metal itself 
-enhance metal excretion 
-active at physiological pH 
-not metabolized/ biotransformed
-hydrophilic (like metals)
-more affinity for toxic metals than endogenous
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3
Q

Calcium Disodium EDTA:
How does it work?
How is it administered?
What metals does it bind? (2)

A
  • Ca in center of molecule is displaced by toxic molecule; molecule excreted in urine
  • INJECTED (IV, IM)
  • Lead or cadmium

“CAL”cium= “CA”dmium + “L”ead

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4
Q

Succimer/ DMSA:

  • How does it work ?
  • How is it administered?
  • Why is compliance poor?
  • What metal is it used to remove? (1)
A

-two sufhydryl groups that bind metals –> metal + chelator excreted in urine
-oral
-bad odor/ taste = N/V
(Succimer has a SUCKY taste.)
-lead
(SUCKS to eat Lead.)

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5
Q 
Dimercaprol/ British Anti-Lewisite (BAL):
How does it work?
How is it administered?
What toxins is it used to remove? (3) 
How is it excreted?
A
  • SH groups bind metal
  • IM with peanut oil
  • Lead, arsenic, INORGANIC mercury
  • 1/2 bile (CI in liver disease), 1/2 urine excretion

-Dimercaprol had a little LAMB (Lead, Arsenic, Mercury = BAL.) He followed her to school one day where the PEANUTS cannot goooo….. (Mary Had A Little Lamb, with a spin off.)

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6
Q

Contraindications to dimercaprol? (3)

A
  • peanut allergy (IM formula includes peanut oil)
  • liver** / renal disease (excreted in bile and urine)
  • acidosis (complex disassociates in acidic urine)
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7
Q

Penicillamine:

  • derived from?/ how does it work?
  • how is it excreted/ administered?
  • What toxins does it remove? (3)
  • Drug of choice in?***
A
  • penicillin derivate with sulfhydryl groups that bind metals
  • oral administration, urinary excretion
  • removes inorganic mercury (HgCl2), arsenic, copper
  • WILSON’S DISEASE!

(Penicillamine treats the big MAC – mercury, arsenic, copper)

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8
Q

Penicillamine major side effect?

If penicillamine is not tolerated, to which chelator do we switch?

A
  • Agranulocytosis; reason to STOP therapy in Wilson’s Disease
  • Switch to TRIENTINE

(When you’re TRIENG to treat Wilsons w/ penicillamine and it fails use TRIENtine)

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9
Q

Contraindication for Calcium Disodium EDTA, succimer, dimercaprol, and penicillamine use?

A
  • All have urinary excretion
  • Not good in RENAL DISEASE
    (100% for all except dimercaprol which is 1/2 biliary excretion)
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10
Q

Which chelators are oral?

Which are injected?

A

oral: succimer and penicillamine
(SUCcimer has a SUCKY TASTE and penicillamine has a COPPER TASTE)
injected: “D”imercaprol + E”D”TA require “D”AMN needles!!!

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11
Q

Which chelators have sulfhydryl groups?

A

all except calcium disodium EDTA

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12
Q

How is lead taken in by humans?

In what local area is lead poisoning a real problem?

A

-Inhaled or ingested–>
water, soil, paint chips, pottery, or breweries using radiators

-Ohio (sorry, Melissa tears) = 1 of top 4 states for lead
poisoning

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13
Q

Major source of lead in the 1940’s

A
  • Single chip was of paint was toxic (1 chip = 100 mg lead)

- Changed in the industry, still problem in old homes

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14
Q

How toxic is lead in children compared to adults?
Where does the lead acutely distribute (3)?
How do we measure lead levels?

A

-children absorb 5x more Pb than adults
-goes to liver, kidney, RBC (95% bound to Hb)
= measure BLOOD NOT PLASMA (Pb binds Hb RBC)

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15
Q

Long term, where does lead go in the body?
What is the result?
What is the t 1/2 for lead?

A

Goes to the BONE and the BRAIN:

  • Replaces calcium in bones = tertiary lead phosphate
  • Interferes w/ calcium mediated processes in the brain
  • t 1/2 ~ 10 years
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16
Q

Effects of lead poisoning in:

  • blood
  • GI
  • neuro

What is the most serious condition that dan result from lead poisoning?
Which system is MOST sensitive indicator of toxicity? (i.e. where do FIRST symptoms arise)

A

Blood:

  • Microcytic anemia + basophilic stippling = RNA precipitation (hemolysis if acute)
  • *MOST SENSITIVE INDICATOR OF TOXICITY; prevents heme synthesis

GI:
-Lead “colic” – GI spasm w/ chronic exposure

Neuro:

  • Peripheral neuropathy (foot drop/ lead poisoning) –> MY FOOT IS AS HEAVY AS LEAD SO IT DROPS.
  • Memory loss (adults)
  • MR + LEAD ENCEPHALOPATHY in kids (fatal, most serious problem)
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17
Q

What two heme synthesis reactions are inhibited by lead?
Where do these two reactions take place?
(I have had uworld q’s on these reactions AND their LOCATIONS!!!)

A
  • Delta-aminolevulinate –> prophobilinogen
    delta-ALA dehydratase in CYTOSOL
    (A young LAD named CYTO= ALAD in the CYTOSOL)
  • Protoporphyrin IX –> heme
    *ferrochelotase in the mitochondria
    (PROTO the MIGHTY FERRET! =protoporphyrin breakdown, in the mitochdonria, by ferrochelotase)
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18
Q

How is lead poisoning diagnosed (2)?

What must we sample?

A
  • ^^ levels of deltaaminolevulinic acid and coporphyrin II (precursor to protoporphyrin) in urine
  • WHOLE BLOOD lead levels
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19
Q

How do we treat asymptomatic lead tox?

Symptomatic?

A
  • oral succimer or penicillamine (off label) for asx patients
  • injected EDTA (IV) / dimercaprol (IM) for sx patients
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20
Q

What are the three mercury forms?

When is each toxic?

A
  • elemental (Hg): only toxic when inhaled, not ingested
  • inorganic mercury (Hg 2+): toxic if inhaled or ingested
  • organicmercurial (C-Hg): MOST TOXIC, ANY ROUTE
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21
Q

Cellular mechanism of mercury toxicity?

A

Binds sulfhydryl groups –> inactivates enzymes/ proteins

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22
Q

Which mercury was in thermometers?

What are its toxic effects?

A
  • elemental
  • crosses BBB if inhaled
  • Hg –> Hg 2+ by catalase in RBC of brain = mercury TRAPPED in brain (charged molecule doesnt cross BBB)
  • irreversible neuro (tremor, delirium) and respiratory changes
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23
Q

Inorganic Mercury:

  • effects of oral exposure (GI, renal, eyes/face)
  • Is this form of mercury neurotoxic?
  • one source of exposure?
A

GI:
- grey esophagus/ mouth/ vomiting/ hematochezia
Renal:
- proximal tubular necrosis. glomerular damage
Eyes/Face:
- photophobia, acrodynia (red face)

  • NO NEURO TOX (2+ charge cannot cross BBB)
  • CERTAIN FISH! NO FISH FOR PREGGOS!

Mercury the poor beta fish lives in the basement & never sees the light. He has a grey mouth, red face, and he never pees (because

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24
Q

Methyl-mercury/ Dimethyl-mercury:

  • what type of mercury are these?
  • which is most toxic?
  • which body system is its main target?
A

-organomercurials
-dimethyl more toxic (^^ carbons in chain = ^^ toxicity)
…. two drops on skin are LETHAL.
-No charge, enters skin –> BRAIN
= ataxia, tremor, blindness –> death

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25
Q

Minamata Disease:

-How did it occur?

A
  • INORGANIC mercury released to environment in Japan
  • algae converts inorganic –> METHYLMERCURY
  • algae eaten by fish –> humans eat fish and mercury
  • HUMANS GOT IRREVERSIBLE NEURO DAMAGE FROM METHYLMERCURY

-MiniMata (MM)= Methyl Mercury (MM)

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26
Q

How is asymptomatic/ symptomatic elemental or inorganic mercury toxicity diagnosed? treated?

A
  • measure organic + inorganic Hg in blood
  • asx-mild: penecillamine
  • symptomatic: dimercaprol
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27
Q

What is the only chelator that can be used for organomercurials?

A

moderate success with penecillamine; NO DIMERCAPROL BECAUSE CAUSES ^^^ BRAIN LEVELS

DIMERCAPROL MAKES YOU DIE IN THIS SITUATION!!!

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28
Q

Arsenic:

  • what are the four types that can cause toxicity?
  • how do they each induce toxicity?
  • which has no antidote?
A
  • As3+: binds sulfhydryls
  • As5+: replaces P in ATP –> uncouples oxphos
  • Arsine gas/ AsH3: spontaneous hemolysis
  • Organoarsenial: she didnt say (not this year either…)

-AsH3= no antidote

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29
Q 
ACUTE Arsenic Tox: 
How does it effect...
-cardio system
-skin
-GI 
-kidney 
-blood
A
  • Cardio: vasodilator/ arrhythmias
  • Skin: hyperkeratosis –> skin cancer
  • GI: ^^ capillary perm = RICE WATER diarrhea
  • Renal: proximal tubular/ glomerular damage
  • Blood: spontaneous hemolysis in AsH3 (GAS ONLY!!)

ARSENIC is a pain in my ARS:
A=arrhythmia, R= renal damage/ rice diarrhea, S= skin cancer/ spontaneous hemolysis

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30
Q

Where is arsenic found in high levels?

A
  • ^^ levels of arsenic in ground water –> well water
    (esp. common in western US)
  • **Recently in babies’ rice cereal!!!

RICE cereal –> WATERY RICE diarrhea comes right out of the baby’s diaper and onto the GROUND.
(Rice water diarrhea, rice cereal, ground water)

31
Q 
CHRONIC Arsenic Toxi:
 How does it effect....
-muscle
-skin/finger nails 
-cardio
-liver
-breath
A
  • muscle weakness
  • hyperkeratosis/ Mee’s lines on fingernails (horizontal)
  • arrhythmias
  • large liver
  • garlic odor to sweat and breath
32
Q

Options for arsenic tox treatment?

A
  • oral penicillamine
  • injected dimercaprol

-NO OPTION for arsine gas

33
Q

Cadium:

  • targets which organ if ingested?
  • targets which organs if inhaled?
  • how does it cause toxicity?
A
  • oral: kidney- proximal tubular damage
  • inhaled: same kidney damage + lung: pulm edema/ emphysema if chronic
  • induces metallothionein–> binds sulfhydryl groups
34
Q

Which metals are capable of inducing metallothionein?

Where does the Cd- Metallothionein complex accumulate?

A

-mercury/inorganic mercury
-cadmium
-arsenic
(THE BIG “MAC” except in this case C= CADMIUM, not COPPER.)

-liver and kidney –> high levels of metals in these organs

35
Q

Treatment for cadmium tox:
+WHAT SHOULDNT BE USED?

How can cadmium levels be measured?

A
  • EDTA
  • No dimercaprol/ BAL, or sulfhydryls, causes ^^ renal tox

CAlcium EDTA =CAdmium tx
-measure B2microglobulin in urine

36
Q

Itai Itai Disease:

  • cause?
  • result?
A

Means “ouch ouch!”

  1. Cadmium in food/ water
  2. Low calcium in diet
    - Promotes replacement of Ca with cadmium in bones
    - Premenopausal women + men got osteoporosis
37
Q

Wilson’s Disease:

  • What are the defect? (2)
  • What is the treatment (1st line)? Must monitor for?
  • 2nd line treatment?
A

-Defect in ATP7B –> no biliary copper excretion
(Wilson is “7 year old BOY –> 7B= ATP type)
-low ceruloplasmin –> copper not taken up into blood
-penicillamine, monitor for agranulocytosis
-trientine = alternative in the event of agranulocytosis

38
Q

Which antidotes are used to treat:

  • lead
  • mercury
  • arsenic
  • cadmium
  • copper
A
  • lead: any of the four chelators, choose oral if asx
  • mercury + arsenic: penicillamine –> dimercaprol depending on severity
  • cadmium: EDTA
  • copper: 1st line penicillamine, 2nd line trientine
39
Q

What do each of the following substances contain?

  • willow bark
  • fox glove
  • opium poppies
  • pacific yew
  • deep sea sponge
A

-willow bark: aspirin (ASPen willow bark)
-fox glove: digitalis (DIGITAL fox glove)
-opium poppies: morphine
-pacific yew: paclitaxel (PACLITAXEL YEW)
-deep sea sponge: eribuline for breast cx mets
(ERIB has SPONGY BREASTS)

40
Q

How does the FDA handle drugs vs herbs?

A
  • drugs assumed to be unsafe unless proven otherwise

- herbs assumed to be SAFE unless otherwise (treats herbs like food vs. meds)

41
Q

What marker on herb supplement labels guarantees the amount of herb/ capsule?

A

“NF” or “USP certified”
= STANDARDIZED for purity/ strength; guarantees there is “at least x amount” of herb in a capsule

(could be MORE than the amount guaranteed)

42
Q

Herbals cannot claim to _____?

Two examples?

A

Cannot claim to cure disease, can only “treat symptoms”
-i.e. ginkgo and bilboa:
“improves memory, not for treatment of alzheimers”
i.e. St. John’s Wart
“improves mood, not for treatment of depression”

43
Q

Describe the complexity of herbal compounds:
Are they uniform?
What is one factor that may cause active ingredients to change?
How do we determine the active ingredient?

A
  • not uniform
  • active ingredients vary with climate,
  • contain a “complex” of ingredients”

(Hard to isolate one “active” ingredient–dependent on ‘family’ of compounds)

44
Q

Garlic:

  • how common
  • what are its two touted effects?
  • what is the active ingredient?
  • why is this not effective when it is cooked?
A
  • one of the top 5 supplements in US, 20 million dollar market
  • lowers cholesterol and prevents MI
  • when chopped: garlic –> allicin via allinase
  • heat causes loss of sulfur compunds/ active ingredient

ALLINASE: IT ALLwilltASTE better with GARLIC.

45
Q

Garlic:

  • How effective is it at lowering cholesterol?
  • What is its mechanism of action to lower cholesterol
  • How effective is it at inhibiting platelets ?
  • Mechanism?
A

Cholesterol:
- 1 clove garlic lowers cholesterol ~12%
(comparable to cholestiramine!)
- Allicin + diallyl sulfides = HMG CoA reductase inhibition

Patelet inhibition:

  • More effective than cholesterol reduction
  • Allicin (ajoene) causes platelet COX inhibition –> DECREASE TXA2
46
Q

Garlic:

  • important drug-herb interaction
  • contraindication?
  • where should it be stored and why?
A
  • Shouldnt combine high dose garlic + antiplatelet drugs because ^^^ chance of bleeding
  • Shouldn’t take garlic before surgery = ^^ bleeding
  • Must store in the refrigerator, room temperature = clostridium infection when ingested
47
Q

Horse Chesnut:

  • marketed use
  • 2 active ingredients/ effects?
  • problem?
A

(mproves varicose veins + decrease leg pain
Active ingredients = saponins
- Escin (good for leg pain/ swelling)– good
- Aesculin (bleeding)–Danger!
-The two CANNOT be separated)
**ESCIN/AESCULIN kind of sound like “EQUESTRIAN” and are saponins –> think SAPPY EQUESTRIANS*

48
Q

MOA for:
escin-
aesculin-

A

Escin: Decreases venous vascular permeability = less leg edema

Aesculin: coumadin like; ^^ bleeding

49
Q

Contraindications for horse chesnut? (2)

A
  • Coadmin w anticoags/ NSAIDs
  • Pregnancy X/ breastfeeding

(THINK: shouldn’t ride “HORSES” when “PREGNANT”.)

50
Q

Ginkgo Bilboa:

  • marketed use?
  • how common?
A
  • ^^ peripheral and cerebral circulation = ^^ mental focus

- #5 best selling herb in US

51
Q

What are the proven effects of ginkgo bilboa?

Which two active ingredients are responsible for its effects?

A

^^ skin/ peripheral blood flow (but not proven in brain)

  • kaempferol: anti-oxidant, raises ATP levels
  • kaempferol and apigenin: weak MAO-A/Bi

Gingkgo helps you put on your thinking KAP.
K=aempferol; ap=apgenin

52
Q

Ginkgo:

  • ADRs with leaves? seeds?
  • Avoid with what drugs?
A

Leaves:
- bleeding can slightly ^^

Seeds:

  • DOUBLES bleeding time
  • anti- B6 effect (aa metabolism issues)
  • Seizures + DEATH with small amount of seeds (2/150 lb person)

-DO NOT take with ANY anticoagulants/ antiplatelets

53
Q

St. Johns Wart:

  • marketed for (3)?
  • active components (2)?
  • MOA?
A
  • mood, sleep, weight loss
  • hypericin and hyperforin

hyperforian= hyper-euforia

54
Q

Hyperforin MOAs?

A
  • Hyperforin: SSRI, MAO-i, ^ GABA
  • Hypericin: MAO-i, ^ GABA

SSRI effect stronger than MAO
^ GABA inhibited by flumazinil

55
Q

St. John’s Warts:

  • which formula has higher hypericin/ hyperforin amounts: water or alcohol extracts?
  • effective to treat?
A
  • alcohol extract ^^ dose

- helps with MILD depression, moderate –> severe should get the real drugs.

56
Q

ADRs for St Johns Warts?
Drug-herb interactions?
Is this a CYP inducer or inhibitor; which drugs are affected?
Stop before?

A
  • H/A and loss of appetite
  • DO NOT coadmin w/ MAO-i’s, SSRi’s
  • CYP3A4 inducer –> must ^^ doses of theophylline, OCPs, warfarin
  • stop before surgery

Be careful not to get TOWed on St. Johns Street.
(increase doses for Theophylline, OCPs, Warfarin)

57
Q 
Valerian:
used for?
three active ingredients? 
MOA 
Don't combine with?
A
  • insomnia
  • valtrate, valerenic acid, glutamine
  • Augments GABA, opens Cl- channel
  • can induce sedation, don’t combine with alcohol
58
Q

Echinacea:
-Use?
-alcohol or water extract more effective?
What are the three echinacea types; what part of the plant do they include?

A

-reduces cold/ flu symptoms
-alcohol extract = more effective
E. purpura: aerial part only (above root)
E. pallida: aerial + root
E angustigolia: root only

[*Purpura= VISIBLE problem, superficial; PALpable (pallida) things can be superficial OR DEEP; angustiGOLDia= always DEEP, have to DIG for gold]

59
Q

Two active ingredients in Echinacea?
What are their specific MOAs?
How effective is the formula at preventing colds? In what age groups was it most effective?

A
  • arabinogalactan: releases IL1 + TNFa
  • heteroxylan- stimulates PMNs–> ^^ phagocytosis

-Studies= no cold PREVENTION, did have slight improvement of symptoms in those OVER 12yoa

(….. no benefit in kids but my mom gave this to me all of the time when i was a kid… SAMESIES**)

60
Q

Side effects of echinacea?

Shouldnt combine with what drugs?

A
  • allergic rxn in those allergic to ragweed/ daises

- don’t combine with immunosuppressants (reverses their effects)

61
Q

Saw Palmetto?

  • effects ?
  • mechanism of action? (2)
A
  • improves prostate health + acts as diuretic
  • 5ARi (like finasteride), prevents testosterone –> DHT
  • prevents movement of androgen receptor to nucleus
62
Q

Saw Palmetto v Finasteride:

  • which is more effective?
  • which has more ADRs?
A
  • same decrease in symptoms (SOME studies)
  • Saw Palmetto = less ADRs (less diminished libido)

**Some studies say could be given in cases of mild BPH; jury still out.

63
Q

Ginseng:
Four marketed uses?
Most active ingredients?

A

-antioxidant
-anti-aging
-anticancer
-adaptogen
(miracle drug!!!?)

-ginsenosides

64
Q

4 Proven MOAs of Ginseng–what are the effects on:

Cholesterol? Platelets? Vasodilation? Stress mediation?

A
  • lowers LDL, raises HDL
  • inhibits platelet aggregation
  • stimulate NO production
  • lower cortisol and NTs during stress (adaptogen)
65
Q

ACTUAL Effect of ginseng on:

  • cancer (which types?)
  • immune system
  • diabetes
A
  • lowers stomach and colon cancer; stimulates apoptosis
  • stimulates IFN production + chemotaxis
  • lowers blood glucose levels 10%
66
Q

ADRs of ginseng?

Shouldn’t be combined with?

A

-nervousness and insomnia (like caffeine)
“ginseng abuse syndrome”– think of drinking six starbucks
Melissa every morning Aug-Dec MS1

-Don’t combine with caffeine

67
Q

Kava:
alternative to?
MOA?
Well documented ADRs (2)?

A
  • beverage– alcohol alternative (induces relaxation)
  • interacts w/ GABA receptors
  • assc with HEPATOTOXICITY!
  • yellows skin and nails (not jaundice)
68
Q

Feverfew:

  • 2 active ingredients
  • most common use?
  • how is it taken?
A
  • sesquiterpene lactones + parthenolide** (most active)
  • migraines
  • daily/ prophylactic (not AT headache onset)

Stops your brain from SEQUESTering a MIGRAINE PARTY forafew days.

Stops your brain from sequestering (sesquiterpine) a mirgaine party (parthenolide) forafew (feverfew) days.

69
Q

How do parthenolides in feverfew work to lower migraine incidence? (2)

A
  • PLA2 inhibitor–> Inhib PG, LT prodxn
  • Inhibit platelet serotonin release

**actual alternative to drug therapy, but not MORE effective

70
Q

Three ADRs assc with feverfew

A

-Post feverfew sydrome:
muscle aches/ insomnia when stopping the herb

  • Uterine Contractions = NOT FOR PREGNANT WOMEN
  • menstrual irregularities
71
Q

Five herbs to avoid prior to surgery:

A

-garlic, horse chesnut, ginko bilboa
(all three ^^ increase bleeding)

  • St Johns Wart CYP450 INDUCER–> DECREASE drugs admin during surgery
  • Feverfew altered PGs + CYP450 INHIBITOR–> INCREASE drugs admin during surgery
72
Q

What two herbs should be avoided when taking SSRIs or MAOi’s?

A
  • St Johns Warts

- Valerian

73
Q

What two herbs should you avoid when consuming alcohol?

A
  • Valerian

- Kava

74
Q

PRACTICE QUESTIONS:
Which herb could increase the clearance of indinavir?
Which ingredient in horse chesnut reduces leg pain?

A
  • St. John’s Wart (enzyme inducer)

- Escin

DT4- Exam 3 (14 decks)

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