Copper

Front 1

What does Metallothionein do?

Back 1

While in the enterocyte, it binds copper and sequesters it into the cell where it remains until it is sloughed off

Front 2

Cerruplasmin roles are..

Back 2

copper transport (from liver to body). ferro-oxidase activity. superoxidase dimutase-like activity. regulation of acute inflammatory response.

Front 3

Where is hctr1 expressed?

Back 3

highly expressed in liver, pancreas, and heart.

intermediate expression in the intestines.

low expression in brain and muscle.

Front 4

What is the transporter that helps copper get absorbed in the small intestine and stomach?

Back 4

Divalent Cation Transporter 1
(DCT-1)

Front 5

What factors increase Copper bioavailability?

Back 5

need, amino acids, organic acids.

Front 6

What factors decrease copper
bioavailability?

Back 6

Vitamin C and other divalent cations

Front 7

What causes Menkes disease?

Back 7

a mutation in the ATP7a protein

Front 8

What does Metallothionein preferentially bind?

Back 8

copper over zinc.

Front 9

Where is copper absorbed?

Back 9

small intestine and stomach

Front 10

How many copper atoms bind to ceruloplasmin?

Back 10

6

Front 11

Name some intracellular proteins that bind copper:

Back 11

hctr1
ATP7A, ATP7B,
Metallothioneins

Front 12

Name 4 ways copper is transported?

Back 12

ceruloplasmin, histidine, albumin, transcuperin

Front 13

Copper Food sources?

Back 13

organ meat,nuts, seafood, seeds.

Front 14

What is the copper transport protein?

Back 14

hCTR1

Front 15

Human Copper Metabolism

Back 15

ingest it...goes into intestines...40-60 percent goes to portal vein, where it goes into the cerum copper pool. From here it goes to the liver or to tissue copper proteins, or to kidney to be peed out. From the liver, it goes into Bile and pooped out.

Front 16

Role of Metallothionein

Back 16

when there is elevated copper, MT synthesis is increased. IT binds copper (blocks it), and the copper absorption is decreased.

Metallothionein binds zinc and copper, but copper is the higher affinity binder.

Front 17

Intracellular transport storage proteins for Copper

Back 17

Metallothioneins, Ctr 1, ATP7A, ATP7B, CCS, C0x17, Atox 1

Front 18

Plasma Transport Proteins for Copper

Back 18

Ceruloplasmin, Albumin, transcuprein

Front 19

What does ceruloplasmin do?

Back 19

it carries copper in the blood.

Front 20

acquired copper deficiency

Back 20

malabsorption syndrome.
increased losses: diarrhea
decreased copper stores: low birth weight
low dietary copper
higher requirement: due to increased growth.

Front 21

Major causes of Copper Deficiency

Back 21

short bowel syndrome. oral zinc therapy. premature infants. prolonged total parenteral nutrition.

Front 22

Copper deficiency clinical manifestation

Back 22

anemia, neutropenia, bone abnormalities

Front 23

Copper Deficiency: Bone Abnormal

Back 23

osteoporosis. fractures of long bones and ribs.

Front 24

Copper deficiency: other manifestations

Back 24

impaired growth, cholesterol and heart problems. infections. lack of color in hair.

Front 25

Menkes disease Symptoms.

Back 25

seizures. hair abnormalities: kinky, short. white. arterial degeneration. neurological disturbances. eye problems
abnormal faces

Front 26

Medical Care in Menkes Disease

Back 26

care: mainly supportive.
copper supplementation sometimes work.
clinical features dont go away.

Front 27

Copper Toxicity
Problems and sources

Back 27

sources: pipes and fumes
Problems: Anemia. Liver, kidney, eye and brain problems.

Front 28

Wilsons Disease
What is it? What causes it?

Back 28

disorder where you absorb and retain a lot excessive amounts of copper.
Caused by a mutation ATP7B gene.

Front 29

Wilsons disease affects what body parts

Back 29

Red Blood Cell, Liver, Kidney, Eye, Brain Problems

Front 30

What is Wilson's disease diagnosis based on?

Back 30

a decreased ceruloplasmin level
an increase in the urine copper excretion.
presence of corneal kayser-fleischer ring.
large amounts of copper deposited in the liver.

Front 31

How can you tell if somebody has Wilson's disease with Kayser-Fleischer ring versus other diseases?

Back 31

Only in Wilson's disease are subnormal levels of ceruloplasmin present with Kayser-Fleischer rings.

Front 32

Wilson's Disease Treatment

Back 32

D-penicillamine (PA)
Trienthylene tetramine
Tetrethiomolybdate
zinc administration, diet maintenance, liver transplantation

Front 33

Manganese biological forms

Back 33

divalent: resistant to oxidation in acidic/neutral solutions

trivalent: transported by transferrin and for present in MnSOD

Front 34

Manganese uses:

Back 34

steel, alloy, batteries, fertilizers

Front 35

Modulators of Mn Absorption

Back 35

dietary fatty acids, chelation, organic acids and polyphenolics, fiber and phytates, pH, and interaction with other metals

Front 36

Manganese Plasma Binding Proteins

Back 36

transferrin (mostly), alpha2-macroglobulin, albumin

Front 37

Manganese Intracellular Binding Proteins

Back 37

manganoenzymes, specific and non-specific manganese activated enzymes

Front 38

Specific Mn-activated enzymes

Back 38

PEP carboxykinase, Glycosyl Transferases, Glutamine synthetase, farnesyl PP synthetase, prolidase

Front 39

Manganoenzymes

Back 39

arginase, pyruvate carboxylase, manganese-superoxide dismutase

Front 40

Arginase

Back 40

urea production. when you have a Mn deficiency, you have increased plasma NH3 and decrease urea production.

Front 41

What downregulates NIS?

Back 41

Iodine, T3 and T4, estrogen

Front 42

Effects of iodine Excess on thyroid

Back 42

inhibits NIS symporter,inhibits cAMP formation, inhibits thyroid, inihibits H202 generation.

Front 43

Thyroid Hormone Target Tissues

Back 43

heart, fat, brain, bone, muscle

Front 44

What is the function of iron

Back 44

iron is a binding site for gases. Iron regulates the activity of enzymes, including ribonuclease reductase which synthesizes DNA. iron regulates approx. 50 genes by transcriptional and post-transcriptional mechanisms,

Front 45

What are the food sources of magnesium?

Back 45

green vegetables. whole grains, fish and seafood. nuts.

Front 46

What increases Hepcidin?

Back 46

Iron load, hemochromatosis, inflammation

Front 47

What decreases Hepcidin?

Back 47

Iron Depletion, Anemia, Hypoxia

Front 48

Hypoxia Shuts what off?

Back 48

Hepcidin.

Front 49

Hypoxia shuts what on?

Back 49

HCP-1, BCRP

Front 50

What evidence that hepcidin really regulates iron balance?

Back 50

Hepcidin redistributes ferroportin, Hepcidin sends ferroportin to the lysosome, and it directly binds to ferroportin.

Front 51

Which iron is soluble?

Back 51

Fe2+

Front 52

Which iron is not soluble?

Back 52

Fe 3+

Front 53

What does DMT 1 do?

Back 53

DMT1 ("divalent metal transporter 1") is a transporter involved in human iron metabolism. It is located on the apical membrane of duodenal enterocytes and transports Fe2+ from the intestinal lumen to the cytosol.
Dietary iron must be reduced from Fe3+ to Fe2+ before being transported by DMT1.

Front 54

DCYTb

Back 54

reductase enzyme which catalyzes the reduction of Fe3+ to Fe2+ in the process of iron absorption in the duodenum of mammals

Front 55

Who has the highest bioavailability for iron?

Back 55

Heme-Fe.

Front 56

Where is Heme Fe absorbed?

Back 56

duodenum

Front 57

the pathway for the production of thyroid hormones.

Back 57

TRH in the hypothalamus to TSH in the pituitary to T4 in the thyroid to liver to T3 by TPO to fat, heart, brain, bone, muscle

Front 58

what are goitrogen?

Back 58

they are antithyroid compounds. rutabagas, turnips, brussel sprouts.

Front 59

Factors for enlarged thyroid:

Back 59

iodine deficient diets. increased TSH. decreased T4 to T3.

Front 60

What is a goiter?

Back 60

an enlarged thyroid.

Front 61

Sources of Selenium

Back 61

garlic, turnips, whole grains, brazil nuts, tuna, oysters.

Front 62

What is the oxidation state of organic selenium?

Back 62

-2

Front 63

What are the organic forms of selenium?

Back 63

selenocysteine, selenomethionine, selenoisothiocyanates

Front 64

Selenium deficiency clinical manifestations

Back 64

weight loss, alopecia, muscle wasting, hepatic generation

Front 65

Keshan Disease

Back 65

a congestive cardiomyopathy caused by dietary deficiency in the mineral selenium.

Front 66

Kaschin-Beck's Disease

Back 66

osteoarthrosis deformans. dwarfism.
from a deficiency in selenium.

Front 67

Hypothyroid cretinism

Back 67

due to congenital lack of thyroid hormone, from a selenium deficiency.

Front 68

Selenium Toxicity

Back 68

acute selonois...garlic breath
subacute selenois...blind staggers
chronic selnosis...hair loss and liver cirrhosis

Front 69

Selenium are located in cells rich in what?

Back 69

glutathione peroxidase

Front 70

Selenium is transported in the plasma by?

Back 70

globulins/apoproteins of VLDL/LDL

Front 71

Name 2 selenoproteins

Back 71

glutathione peroxidases, and iodothyronine deiodinases (T3 inactivation)

Front 72

Where is the primary site of regulation of copper?

Back 72

gut and liver. absorption in gut. excretion in liver.

Front 73

In wilson's disease, what organ cant eliminate Cu?

Back 73

liver

Front 74

What regulates homeostasis?

Back 74

excretion rather than absorption.

Front 75

How much manganese is in the body?

Back 75

200 to 400 umol

Front 76

What is a substrate for both arginase and NOS?

Back 76

arginine

Front 77

Mn tightly bound to ??? that translocate ???? fragments among macromolecules.

Back 77

transferases, glycosyl

Front 78

Where are MnSOD located?

Back 78

mitochondria

Front 79

What are inducers of MnSOD?

Back 79

alcohol. ozone. interleukin01, TNF-alpha

Front 80

What are inhibitors of MNSOD?

Back 80

elevated Fe. diabetes (high glucose, glycosylation), Mn deficiency

Front 81

Why would Mn possible cause diabetes?

Back 81

Mn deficiency impairs glucose metabolism and reduced insulin production.

Front 82

What are symptoms of Mn deficiency?

Back 82

skeletal deformities, ataxia, seizures, hearing loss, fainting

Front 83

Children with what 2 diesease exhibit low Mn?

Back 83

PKU and MSUD

Front 84

Low Mn contributes to which diseases?

Back 84

osteoporosis, diabetes, epilepsy

Front 85

Mn Toxicity...how do you get exposed to it?

Back 85

mining, dirty water, working on the railroad, working with cool or steel or pesticides

Front 86

what does Mn toxicity do to the body?

Back 86

neural damage, reproductive dysfunction, immune dysfunction, kidney, liver, and pancreas damage

Front 87

Stages of manganism

Back 87

1) lethargic,
2) mental problems
3) loss of facial expression, tremors,

Front 88

Treatment of manganism

Back 88

only successful at early phase. withdrawal of exposure.

Front 89

Whats the difference between Parkinson;s disease and Mn-induced Parkinsonism?

Back 89

Parkinsons experience a resting trmor and Manganism experience tremors with intention.

Front 90

What is magnesium essential for?

Back 90

cellular phosphate and energy transfer (NaK ATPase).
calcium atpase pump and proton pump
influences glucose and fat metabolism.
protein and nucleic acid synthesis
muscle contraction
membrane transport

Front 91

whats the excretion ratio between feces and pee? for Magnesium

Back 91

60 percent feces. 40 percent kidneys

Front 92

Daily requirement of Magnesium

Back 92

300-350mg

Front 93

What enhances Absorption of magnesium?

Back 93

acidic media.diets rich in animal proteins, unsaturated fatty acids, sodium, lactose, vitamin D and B6. diets that enhance secretion of insulin, PTH, VIP, CEP

Front 94

What diminishes the absorption of magnesium?

Back 94

alkaline environment
sigrid's diet of veggies, alcohol, fiber, saturated fats.

Front 95

What hormone regulates the magnesium excretion?

Back 95

adolsterone

Front 96

What increases the excretion of magnesium

Back 96

diuretics and alcohol

Front 97

hypomagnesia is defined as what?

Back 97

less than 1.5 mEq/L

Front 98

What drives Mg in and out of bones?

Back 98

PTH drives Mg out. CT drives Mg in

Front 99

What drives Mg in and out of soft tissues?

Back 99

Epinephrine drives Mg out. Insulin drives Mg in.

Front 100

Magnesium functions

Back 100

neuromuscular activity, heart muscle, cellular activities, energy production,synthesis of essential molecules, structural roles for bone, ion transport across cell membranes, cell signaling, cell migration

Front 101

Causes of hypomagnesemia

Back 101

redistribution, renal losses, dietary deficiencies, alcohol ingestion

Front 102

Refeeding syndrome can cause what diseases?

Back 102

hypomagnesemia, hypokalemia, hypophosphatemia

Front 103

Acute Manifestation of Mg deficiency

Back 103

neuromuscular and mental problems. renal and electrolyte disturbances.

Front 104

Chronic manifestation of mg deficiency

Back 104

heart and bone and kidney problems. and teeth problems

Front 105

Benefits of Mg

Back 105

migraines,hypertension, prevention, insomnia, depression

Front 106

hypermagnesemia does what?

Back 106

causes relaxation of heart and muscles.

Front 107

Gay Guy And Chicks Bang dicks

Back 107

gluconeogensis, glycoprotein synthesis, ammonia metabolism, cholesterol biosyntehsis, dipeptidase

Front 108

Men Pee-Poop Gross Fat Globs

Back 108

manganese PEP carboxylase, Prolidase, Glycosyl Transferases, Farnesyl PP Synthetase, Glutamine synthetase

Front 109

Pam likes Manganoenyzmes

Back 109

Pyruvate carboxylase, Arginase, MnSOD