Copper

Front 1

How is copper bound and eliminated

Back 1

Ceruloplasmin (>95% of plasma copper)

5-10% of serum copper is bound to albumin

Only elimination is biliary excretion

Front 2

Copper and redox

Back 2

Copper inhibits sulfydryl groups on enzymes
-GSH reductase

Generates oxidative stress
-Cu+ catalyzes formation of OH radical

Front 3

DMPS and Copper

Back 3

CMPS worsens Hemolysis

Front 4

Cu and Erythrocytes

Back 4

Cu++ is reduced to Cu+
Generates Hydroxyl radical
-Fe++ to Fe+++ methemoglobin
-RBC membrane: Hemolysis

Front 5

Cu and Liver

Back 5

Free intracellular Cu ions generate OH
-lipid peroxication
-mitochondrial damage
-DNA adducts
-Cetnrilobular necrosis

Front 6

Kidney and Cu

Back 6

Bioaccumulates Cu
-Oxidant stress
-ATN
-Hemoglobinuria (from hemolysis)

Front 7

Cu and CNS

Back 7

Carrier mediated albumin bound Cu

Wilson Disease

Front 8

Cu Salt (copper sulfate) GI

Back 8

Blue vomitus
Ulceration
Hemorrhage

Front 9

Copper Sulfate Hematologic

Back 9

Hemolysis (biphasic)
Methemoglobin

Front 10

Renal and copper sulfate

Back 10

ATN
Hemoglobinuria
Methemoglobinuria

Front 11

Copper Sulfate and Hepatotoxicity

Back 11

Jaundice
Centrolobular necrosis

Front 12

Copper sulfate and Skin

Back 12

Green skin with irritation
Green hue hair shafts

Front 13

Copper and Labs

Back 13

Methemoglobin
(copper salts radiolucent)
Serum Copper
-for confirmation or investigation

Front 14

serum [Cu]

Back 14

Whole blood matrix better correlation with clinical findings

There is relationship between whole blood Cu and severity of poisoning

Front 15

Cu Chelation

Back 15

BAL

Oral D-Peniciallamine
Concurrently or after BAL
(prevents hemolysis in Wilson disease)

Front 16

Metal Fume Fever and Cu

Back 16

Severe flu like illness
Self-limited, resolves within 24 hours

No long term sequellae

Front 17

Metal Fume Fever Labs

Back 17

Leukocytosis
Normal CXR

Front 18

Chronic Ocular Cu exposure

Back 18

Chalcosis Lentis
Brown discoloration of lens or cornea

Front 19

Vineyard Sprayers Lung

Back 19

Portugese vineyard workers applying Bordeaux solution

1-2% copper sulfate associated with hydrated lyme

Interstitial pulm fibrosis, histiocytic granulomas with Cu

Lung Adenocarcinomas, hepatic angiocarcinoma, micronodular cirrhosis

Front 20

Wilson Disease

Back 20

Cu Accumulation
Autosomal Recessive
Liver capacity for Cu storage exhausted

Front 21

Wilson CNS

Back 21

Cu not taken up by neurons

Increased extracellular Cu causes free radical production

Lenticular nucleus in Basal ganglia

Front 22

Wilson Disease clinical

Back 22

Liver disease most common presentation
8-18 yrs
Transaminasemia, hepatitis, FHF, cirrhosis

Chronic Liver disease may precede neurologic symptoms by years

Kayser Fleischer Rings
-Golden brown deposit at level of Descemet's membrane

Front 23

Wilson Disease Clinical Neuro Findings

Back 23

Dysarthria
Dyspraxia
Ataxia

Typical: Parkinson like extrapyramidal signs

Begins with mild tremor, speech, writing problems

Front 24

Wilson Disease Psychiatric

Back 24

Most common-depression
Labile mood
psychosis

Front 25

Wilson Lab

Back 25

Low serum ceruloplasmin

Front 26

Wilson MRI

Back 26

Lesions in 60% neuro symptomatic and 19% asymptomatic

Front 27

Wilson Disease Treatment

Back 27

Symptomatic- Penicillamine

Presymptomatic-
Penicillamine or trientine
Zn (competes with intestinal Cu absorption)

Front 28

Idiophathic Copper toxicosis

Back 28

Excessive dietary copper intake
-Cu contaminated water
-Brass vessels to store milk

Serum Cu and ceruloplasmin markedly increased

Front 29

Menkes "Kinky Hair" syndrome

Back 29

Genetic Defect in Cu absorption

Mental retardation
Thermoregulatory dysfunction
Hypopigmentation
connective tissue abnormalities
Pili torti (kinky hair)