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GEMS > Minerals > Flashcards

Minerals Flashcards

1
Q

Calbindin-D

A

Ca++ absorption in the intestine involves a viatmin D-induced intracellular Ca++ binding protein

Binds Ca++ once in the cytosol – keep inside the cell at rock bottom levels– Maintain steep gradient

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2
Q

Calmodulin

A

Most common Ca++ binding proteins in our cells
1. binds four calcium ions
2. Calmodulin changes conformation, resulting in an active complex
3. Two globular “hands” of the complex wrap around a binding site on a target protein

Essential allosteric activator of other proteins

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3
Q

Absorption of Ca++ occurs primarily in …

A

the duodenum

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4
Q

What two ion channels are involved in the absorption?

A

TRPV5 (transient receptor potential 5) & TRPV6

TRPV6»>TRPV5

TRPV5 mostly Ca++ DCT/PCT tubules of the kidney

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5
Q

TRPV5 expression

A

Highly induced by vitamin D (as calcitriol active hormone)

Lack of expression when vitamin D is low –>forces body to draw upon bone reserves —> low vitamin D – weak bones

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6
Q

PMCA1b

A

Basolateral Ca++-ATPase protein (active transport)

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7
Q

NCX1

A

Antiporter – 3Na+ for each outgoing Ca++

Not active, depend on Na+ gradient established by Na+/K+-ATPase – secondary active transport

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8
Q

Albumin

A

Binds calcium in serum, can not pass through the kidneys

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9
Q

Calcitriol

A
  1. Active form of vitamin D
  2. Role –> increase Ca++ levels in the blood
  3. stim bone resorption
  4. Intestinal Ca++ absorption
  5. Renal Ca++ reabsorption
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10
Q

PTH

A
  1. Role –> increase serum Ca++ and decrease serum Pi
  2. Increase bone resorption
  3. Increase renal Ca++ reabsorption
  4. Decrease renal Pi reabsorption

NO EFFECT on INTESTINAL Ca++ absorption

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11
Q

Calcitonin

A
  1. Role –> decrease blood Ca++
  2. Inhibit bone resorption
  3. Renal Ca++ reabsorption
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12
Q

Hypocalcemia causes?

A

Hypoparathyroidism (Wilson disease, thyroidectomy, Primary PTH deficiency, autoimmune destruction of parathyroid)

Low vitamin D (insufficient sunlight, low dietary intake, malabsorption, kidney disease)

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13
Q

Hypercalcemia causes?

A

Primary Hyperparathyroidism (excess PTH)
Cancer (bone mets)
Vitamin D toxicity

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14
Q

Hypocalcemia presentation?

A
  1. Bone density disorders (rickets, osteomalacia, osteoporosis)
  2. Neuromuscular tetany, spasms, cramping
  3. Bronchospasms, laryngospasms
  4. Cardiomyopathy, prolonged QT interval
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15
Q

Hypercalcemia presentation

A
  1. Soft tissue calcification
  2. EKG abnormalities, chronic Ca++ overload can lead to permanent damage
  3. N/V, anorexia
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16
Q

What stimulates 1alpha-Hydroxylase

A

Hormonal regulation of serum calcium levels

Low blood Ca++ stimulates –> PTH–>activates 1alpha-hydroxylase in kidney

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17
Q

1alpha-Hydroxylase function

A

Enzyme converts inactive form of Vitamin D (Cholecalciferol) into the active form (Calcitriol)

More potent than PTH in increasing serum Ca++

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18
Q

Acrodermatitis Enteropathica

A

Zn malabsorption disorder resulting in deficiency of SLC39A4 (encoding the ZIP4 protein)

Sx: skin rashes, slowed growth/development, immune deficiencies

Vision problems are also possible because Zn is involved in Vitamin A metabolism

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19
Q

ATP7A

A

Cu-ATPase –> actively transports Cu1+ across the basolateral membrane

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20
Q

ATP7B

A

Cu-ATPase protein

Affected by Wilson’s Disease–> impairs efflux of Cu from cells

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21
Q

Calcium Roles

A

Divalent cation (Ca++) with high charge density

Signaling molecule (second messenger)

Regulates activity of Calmodulin

Cofactor of blood clotting enzymes – THROMBIN

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22
Q

Ceruloplasmin

A

An additional Ferroxidase

Secreted by the LIVER and circulates in the blood

Helps to oxidize Fe++ –> Fe+++ for efficient loading onto Transferrin for transport

Also carries COPPER

23
Q

Copper

A

Key component of several enzymes that play critical functions in body

Necessary for proper iron metabolism: Required cofactor for FERROXIDASE enzymes

24
Q

Copper Transporter-1 (Ctr1)

A

Transports Cu+1 into enterocytes

Cu2+ atoms will be reduced to Cu1+ by Dcytb at luminal membrane so it can transport Ctr1

25
Divalent Metal Transporter-1 (DMT-1)
Transporter protein takes up non-heme iron Can only recognize Fe++ so to take up Iron in gut Fe+++ must be reduced to Fe++ (Dcytb reduces)
26
Duoudenal Cytochrome b (Dcytb)
Cell surface enzyme responsible for reducing Fe+++ into Fe++ (aka Ferrireductase)
27
Fenton reaction
Fe++ can participate in this reaction to produce the highly damaging hydroxyl radical H2O2 + Fe++ --> Fe+++ + OH- OH*
28
Ferritin
Storage protein for excess Fe+++ iron Prevents excess iron so that it cannot cause damage to the cell
29
Ferroportin
Fe++ transport protein on the basolateral membrane of the cell (infants & adult)
30
Heme Carrier Protein (HCP)
Heme receptor for receptor-mediated endocytosis Intestinal lumen receptor
31
Heme Oxygenase
Enzyme that "releases Fe++ from heme ---> oxidizes Fe++ to Fe+++
32
Hepcidin
Protein that functions to protect pts from absorbing too much iron Binds to Ferroportin causing its internalization and destruction in lysosomes of intestinal cells Produces and secreted by LIVER Iron deficiency causes a suppression of HEPCIDIN expression in LIVER ---> less hepcidin present to inhibit ferroportin function
33
Hephaestin (Heph)
Ferroxidase enzymes Involved in oxidation of Fe++ to Fe+++ required for intracellular storage (Ferritin) and transport in the blood (Transferrin)
34
Lactoferrin (multiple roles) 1/2
Protein secreted in breast milk that enhances iron absorption in growing babies Complexes with Fe+++ taken up by enterocytes via receptor mediated endocytosis ALSO a transcription factor --> stim expression of growth hormone, cytokines and other molecules that help infant grow
35
Lactoferrin (multiple roles) 2/2
Transcription factor that controls genes involved in INNATE & ADAPTIVE immunity, affording infant a high degree of protection ALSO tight binding to IRON deprives bacteria/pathogens that they need to grow
36
Macrominerals
Required by adults in relatively amounts (>100 mg/day) ie. Calcium
37
Menkes Syndrome
Risk factor for Copper deficiency Caused by genetic deficiency of ATP7A. Impairs Cu absorption into body. Rare X-linked disease Sx: Kinky hair disease due to strange effect that Cu deficiency has on hair structure
38
Metallothionein
Binds to Cu tightly in enterocytes, preventing absorption into the body Metallothionein-bound Cu is eventually lost in stool once enterocytes are sloughed off
39
Microminerals
Required by adults in trace amounts (1-100 mg/day) ie. Copper
40
Phosphorous
Free phospate (Pi=HPO4 2-) most abundant intracellular anion in cells Highly diverse roles: DNA/RNA, ATP/GTP, Enzyme regulation (phosphorylation
41
Thymulin
Zn dependent hormone involved in T-cell differentiation and maturation (role of immune signaling pathway/cell differentiation)
42
Transferrin (Tf)
Major iron-transporting protein present in the blood Binds Fe+++>>>Fe++
43
Ultratrace Minerals
<1 mg/day ex: Moybdenum
44
Wilson's Disease
High copper levels damage the parathyroid ---> Hypoparathyroidism ---> Hypocalcemia Cu overload disease AR disorder Defects in Cu-ATPase protein ATP7B Results in impaired efflux of Cu from cells; causes Cu accumulation in liver (esp**), eyes, brain, kidney, skin Sx: Cog impairment, loss of motor function, liver failure Tx with Zinc supplementation & chelation therapy
45
Zinc roles
Structural role in Zinc finger-containing transcription factors -- bind DNA and regulate gene transcription ---NO SUBSTITUES Involved in storage and secretion of insulin by pan Beta-cells Immune signaling pathway & immune cell differentiation Hundreds of enzymes require Zn for their activities (ADH, Carbonic Anhydrase, Prophobilinogen synthase, Superoxide Dismutase)
46
ZIP4 (gene: SLC39A4)
Majority of Zn enters enterocytes through this transporter
47
ZIP5
Transport protein -- Zn exits enterocytes It ZIP5 out
47
SLC39A4 gene
Encodes ZIP
48
Zinc supplementation
Tx for managing Wilson's disease Zinc induces the production of protein called Metallothionein in intestinal cells Binds Cu tightly in enterocytes for excretion in stool
49
Zinc Deficiency
Proteins will not assume their normal structures -- compromising the regulation of numerous genes Insulin secretion is compromised
50
Alcohol dehydrogenase (ADH)
Enzymes, which oxidize ethanol to acetaldehyde in the liver and other tissues
51
Carbonic Anhydrase
Involved in the blood bicarbonate buffer system
52
Porphobilinogen Synthase
An enzyme of the heme biosynthesis pathway
53
Surperoxide Dismutase (SOD)
Non-mitochondiral isoform, involved in elimination of superoxide

GEMS (20 decks)

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