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Fall 2 > Metals in Medicine I - III > Flashcards

Metals in Medicine I - III Flashcards

1
Q

What is a transition metal?

A

in groups 3-12 in periodic table

presence of d orbitals

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2
Q

What is paramagnetism?

A

is defined as the phenomenon whereby some materials show magnetic properties only once they are exposed to a magnetic field. Outside this magnetic field, no magnetic properties are seen. This is in contrast to ferromagnets, which show magnetic properties independent of the environment.

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3
Q

Define Coordination complexes?

A

are defined as chemical structures that consist of a central atom or metal ion, and the surrounding molecules or anions called the ligands

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4
Q

Why use transition metals in medicine? (4)

A
  1. DNA deformation
  2. Photodynamic Therapy (PDT)
  3. Magnetic Resonance Imaging (MRI)
  4. Radiopharmaceuticals for Imaging and Therapy
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5
Q

What group are the coinage metals and what are their features?

A

Group 11
Relatively inert, corrosion-resistant metals
excellent conductors of heat and electricity

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6
Q

How is Copper involved in a medical context?

A

Copper and the human body
Wilson disease
Wound healing

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7
Q

What can copper do in the body in excessive amounts?

A 
Absorbed (50%) in GI tract
Processed in liver 
transported to peripheral tissue
Binding to glyco-proteines and albumin
Excessive copper excreted via bile and faeces
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8
Q

Define cuproenzymes and some examples

A

Copper–dependant enzymes
e.g.
Lysyl oxidase: cross-linking collagen and elastin (formation of blood vessels and heart)
Ceruloplasim: oxidation of ferrous to ferric ion
Cytochrome c
Superoxide dismutase

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9
Q

What forms of copper are present in the body?

A

Cupric (Cu2+) dominant form in human body compared to cuprous form (Cu+)

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10
Q

What is Wilson Disease?

A

Genetic, inherited

excessive copper built in body

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11
Q

What is the treatment for wilson disease?

A

Chelation therapy: BAL, D-penicillamine
Zinc supplementation
Liver transplant

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12
Q

What is the role of Glycyl-L-histidyl-L-lysine - Cu(II)?

A

GHK-Cu(II):
Anti-inflammatory: protects tissue from oxidative injury after damage
Activator for wound healing as activates tissue remodelling

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13
Q

Where is GHK secreted from?

A

Tripeptide- Secreted by mast cells in the skin

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14
Q

What is Silver used for in a medical context? (3)

A
  1. Water disinfectant
  2. Silver nitrate (AgNO3) – wart treatment
  3. Silver(I) sulfadiazine- antiseptic
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15
Q

What % silver nitrate does wart treatment contain?

A

40%

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16
Q

What are warts caused by?

A

Papilomavirus

17
Q

What type of burns is silver (I) sulfadiazine used on? What does it do?

A

2nd and 3rd degree burns

It prevents the growth of a wide array of bacteria, as well as yeast, on the damaged skin.

18
Q

What is the proposed mode of action for silver based compounds?

A

Oliogodynamic effect:

Ag damages irreversibly key enzymes (lactate dehydrogenase and glutathione peroxidase) in the cell membranes of pathogens
Enzymes precipitation / inactivation (bacteria but not viruses)

19
Q

What is the mode of action of silver dressing?

A

Silver ions bind to the DNA of bacteria and bacterial spores, thus reducing their ability to replicate

20
Q

How are Ag+ ions released from the dressing?

A

released from the dressing through oxidation when the silver atoms come into contact with fluid.

21
Q

What causes Argyria?

A

Caused by a build up of colloidal silver in the body.

bluish-gray discolouration of the skin

22
Q

What is the electron configuration of Gold?

A

5d106s1

23
Q

Whats the medical use of Gold?

A

Historic use

Treatment of rheumatoid arthritis

24
Q

What is Chrysotherapy?

A

The treatment of certain diseases, especially rheumatoid arthritis, with gold compounds

25
Q

What are the TWO types of groups used in Chrysotherapy?

A
  1. Au(I)thiolates

Solganol

(Di)sodium aurothiomalate

Aurothiopropanolsulphonate

Sodium gold 4-amino-2-mercaptobenzoic acid

  1. Auranofin
26
Q

What is the main toxicity concern with sodium aurothiomalate?

A

Myelosuppression (bone marrow suppression)

27
Q

What monitoring is required with sodium aurothiomalate?

A

with full blood counts (FBC) and urine tests before each dose!

28
Q

What is the dose regimen with sodium aurothiomalate?

A

Start therapy with 10mg test dose to exclude hypersensitivity

Follow with 50mg IM weekly injections until response occurs

Benefit not expected until patient receives 300-500mg (6-10 weeks)

Once disease is controlled, interval between doses can be lengthened gradually to monthly injections and continue for up to 5 years of complete remission

29
Q

At what dose should treatment with sodium aurothiomalate be discontinued if there is no response?

A

1g

30
Q

Summary Au(I)thiolates?

A

Linear
Mostly two coordinated
Au compounds are water soluble => intramuscular injection as preferred way of administration (50 mg/week).
Disadvantage: required frequent visit to the doctor.
3 - 6 months before gold injections have an effect on RA symptoms.
Side effects: accumulation in organs (kidneys, liver), resulting in nephrotoxicity.

31
Q

What are the side effects of gold injections? (6)

A

Discoloration of skin.
Nausea and vomiting.
Metallic taste
Gold injections cause mouth sores in about a third of patients
Itching and rash (can be severe in some patients).
Kidney damage and decreased white blood cell count (rare) – bone marrow damage.

32
Q

What is Auranofin?

A

2nd gen drug

Lipophilic => administered orally (doses 3-6 mg/d

33
Q

What is the dose regimen of Auranofin?

A

Less effective than sodium aurothiomalate
Given as 6mg/day in two doses initially, then one dose if tolerated, for 6 months
If no response, increase after 3 months to 9mg/day in three doses for a further 3 months

34
Q

If there is no response with Auranofin when should it be discontinued?

A

After 6 months

35
Q

When should gold therapy be discontinued?

A

in case of presence of blood disorders (sudden and fatal), GI bleeding or unexplained proteinuria (>300mg/litre)

36
Q

What is the mode of action of Gold? Poorly understood (4 steps)

A

1) In the blood stream, Au-drugs form a complex with albumin
2) Au(I)/albumin complex arrive at the site of action => synovial cavity

3) Au(I) may enter the cell via (second) thiol exchange reaction with membrane transport proteins.
Auranofin: taken up rapidly –>Thiol-Shuttle Model:

4) Once absorbed in the cell, Au(I) might interact with mitochondria inducing cell apoptosis.

Fall 2 (33 decks)

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