Other metals 2 Flashcards

1
Q

Copper interactions, acute tox, chronic tox, factors influencing tox

A

Mo, Zn, Fe, sulphate;
Acute tox: irritation– cramps, vom, diarrhea
chronic tox– hemolysis of RBCs; liver necrosis, decrease glutathione; methemoglobin formation
factors: ingestion liver disease; mineral imbalance; genetics (Muenke’s disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is wilson’s disease, and what causes it?

A

Cu; Cu not excreted via biliary route due to autosomal recessive gene mutation; therefore Cu accumulates in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is menkes disease?

A

opposite of wilson’s disease–inability to store Cu–>bone problems–die at 2 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe Mo toxicity

A

Causes Cu deficiency–>strong interaction b/w Mo and Cu–>decreases abs of Cu and increases excretion of Cu
alters activity of xanthine oxidase and aldehyde oxidase, which are dependent on Cu
wherever Cu is stored, Mo is found–>liver, kidney, blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how is Mo excreted?

A

50% in urine

bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

biological effects of Mo?

A
  1. Interferes wth Cu storage
  2. Interferes with Cu enzymes–ceruloplasmin
  3. interferes with P abs
  4. Reduces phospholipid synth–>low P, membrane effects
  5. reduces ATP synth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

clinical manifestations of Mo?

A

anemia, poor growth, diarrhea, joint deformities, depigmentation of wool/hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

treatment of Mo poisoning?

A

Cu!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the forms of Se, and what are the ones which cause major problems?

A

Selenate– Se 6+
Selenite– 4+
Selenide – 2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Absorption of Se forms

A

Selenite (4+) – 90%

Selenide (2+) – 0%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Distribution of Selenite

A

liver, kidney, blood, brain, muscle

crosses placenta–teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Se metabolism?

A

methylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Se excretion

A
Urine-- 15-40%
Se-Met complex
Milk
Sweat as a dimethyl selenide (probably 2CH4 + Se4+ --> CH3--Se2+--CH3)--HAS GARLIC SMELL
lungs--breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the function of Se in our bodies?

A

important for GSH peroxidase–>has antioxidant activity again free rad, lipid perox, membrane damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acute tox of Se?

A

severe tissue destruction–lungs, breath problem

dyspnea, cyanosis, diarrhea (destroyed gut cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

subacute tox of Se?

A

wandering, weakness, blind, emaciation (gut membrane damage–destroys absorptive epithelial cells); CNS manifestations–>destroys myelin, etc

17
Q

chronic tox of Se?

A

hair loss–brittle hair and nails (hair has lots of S, which Se displaces)
skin lesions, blisters
numbness, convulsions, paralysis
simian B monkey virus looks like Se tox in monkeys

18
Q

Se also reduces fertility, is teratogenic, causes liver tumors but may act as an anticarcinogen

A

ya

19
Q

what does Se interact with?

A

Cd, Hg, As, Th (thorium), Cu, Vit E

20
Q

factors enhancing Fe tox?

A

Age
high iron stores
low vit E status–>Fe interacts with vit E heavily; Vit E is needed
low Se status–interacts, Se stabilizes membrane

21
Q

route of exposure of Fe?

A

oral, IP, inject (highest)

22
Q

how is Fe proposed to cause damage

A

is very redox-active, damages membrane

23
Q

Iron tox pathogenesis?

A
  1. CV collapse–increases perm of mem bc iron damages; fluid loss, and shock
    2 liver damage
  2. impaired clotting mechs–hemorrhage
    pathgenesis not fully understood
24
Q

iron tox peracute syndrome?

A
  1. anaphylactoid-LIKE rxn

shcok

25
Q

iron tox subacute syndrome

A

classic iron tox
CNS–drowsniess, coma, death wthin 4-5 hours
GIT–vomitting, diarrhea, blood in gut
liver– icterus, liver damage,
shock– pale skin, dyspnea, hemorr., acidoses

26
Q

chronic iron tox syndrome?

A

poor grwoth, rickets,

Fe interacts with PO34—>soft bones

27
Q

treatment of iron tox?

A
milk of magnesia--forms FeOH-->ppts out
fluids (for shock)
-- something to relieve acidosis
--VIT E BIG ONE
--chelators okay, NOT CA-EDTA