Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Friedman > Micro - Exam 1 > Flashcards

Micro - Exam 1 Flashcards

1
Q

ZnT

A

Transports zinc out of cytosol (into ECF, organelles, vesicles)

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

ZIP

A

Transports zinc into cytoplasm (from ECF, organelles, vesicles)

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

Metallothionein (MT)

A
  • Zinc storage protein
  • Accept and donate zinc
  • Binds other metals
  • Redox function
  • Regulated by MTF-1 (Zn binds MTF1 which up-regulates genes producing MT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Zinc pools and why they are necessary

A
  • MT
  • Intracellular organelles
  • Endosomes and lysosomes

Because minerals may react with ROS, may have unintended consequences (deregulating genes, etc), and for osmotic purposes

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

Zinc sensing (response to high intracellular zinc)

A
  • Under high intracellular Zn, Zn binds MTF-1 (a transcription factor) which up-regulates genes to produce more proteins (MTs) for zinc storage
  • ZIP4 ubiquitination and degradation; up-regulation of ZnT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Zinc sources

A

Food (complexed with proteins and nucleic acids), supplements, and endogenous (bile secretions are reabsorbed – enterohepatic circulation)

Foods: meat, dairy, beans, nuts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Zinc absorption (3 ways)

A
  1. Carrier mediated (ZIP4, DMT1)
  2. Chelation by amino acids
  3. Paracellular diffusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Low/high zinc in diet and absorption bioavailability

A

Low: transport through specific transporter is efficient (bioavailability is high)

High: low bioavailability due to saturated transporters

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

Zinc absorption inhibitors

A

Phytate: zinc forms insoluble complexes with phytate

Oxalate

Large supplemental doses of iron and calcium (why?)

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

Zinc absorption enhancers

A
  • Gastric acid (digest food matrixes and reduce minerals to necessary oxidation state)
  • Chelation with amino acids and other organic acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Zinc sensing (response to low intracellular zinc)

A
  • Free (unbound to Zinc) KLF-4 transcription up-regulates ZIP4 gene transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Zinc functions

A
  • Used in proteins for structure

- Used in zinc fingers for gene regulation

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

Assessment of Zinc status

A
  • Plasma/serum concentration
  • Hair/nails
  • Urinary excretion
  • MTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Copper sources

A
  • Food (widely distributed), gastrointestinal secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Copper absorption

A
  • Transported through CTR1 and DMT1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ATP7A defects

A

Copper-transporting ATPase transports intracellular copper in the enterocyte to golgi for export into circulation
- defects cause Menkes disease – build up of copper in enterocyte and copper deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Copper excretion

A
  • Excreted through bile

- Urine, hair, nails, semen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Copper functions

A
  • Iron redox
  • Antioxidant
  • Electron transport
  • Gene expression
  • Enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of copper deficiency

A
  • Zinc supplementation
  • Gastrointestinal surgery
  • DMT1 competition
  • Malabsorption
  • Menkes disease (ATP7A defect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do zinc supplements cause copper deficiency?

A
  • Zinc up-regulates MT
  • MT has higher affinity for Copper
  • Enterocyte gets sloughed off
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chromium deficiency

A
  • Impaired glucose tolerance because chromium is used to increase insulin response
  • Chromium is widely available in foods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Flouride

A
  • Stimulates osteoblast proliferation

- Increases tooth enamel resistance to demineralization by acid

23
Q

Iodine basics

A
  • Used in synthesis of thyroid hormone

- Concentrations in food reflective of soil levels

24
Q

Iodine deficiency

A

With low iodine, TSH is not suppressed, so build up of thyroglobulin occurs and thyroid gets larger –> hypothyroidism

25
Q

Iron functions

A
  • oxygen transport (hemeoglobin/myoglobin)
  • electron transport (cytochrome) going from reduced to oxidized forms
  • antioxidant
26
Q

Heme iron (basics and absorption)

A
  • From flesh sources

- Transported into enterocyte as heme

27
Q

Non-heme iron (basics and absorption)

A
  • From flesh AND plant sources
  • Must be reduced from Fe3+ to Fe2+ by brush border reductases (DCYTB1)
  • DMT1 co-transport with protons into enterocyte
28
Q

Non-heme iron enhancers

A
  • Acids (reduction, chelation, substrate for DCYTB1)

- Meat factor (cysteine is iron ligand?)

29
Q

Inhibitors of non-heme iron

A

(reduce solubility and prevent reduction)

  • Phytate (but iron liberated when fermented)
  • Oxilates
  • Polyphenols
30
Q

Iron in the enterocyte

A
  • Bound to chaperone protein, organic molecules

- Bound to ferritin (storage protein)

31
Q

Iron assessment

A
  • Ferritin (storage protein)
  • Hemoglobin or hematocrit
  • %transferrin saturation
  • Dietary intake/forms
32
Q

Iron LOSSES

A
  • No physiology excretion mechanism
  • Lost via sweat, urine, skin cells, shedding of epithelia
  • Menstruation
  • Bleeding and blood donation
33
Q

Iron transport out of enterocyte

A
  • Fe2+ gets transported via ferroportin
  • Bound to transferrin (for transport in plasma)
  • Ferroportin regulated by hepcidin
34
Q

Hepcidin

A
  • Protein made in liver to regulate iron absorption
  • Hepcidin causes ferroportin to be internalized by enterocyte and sloughed up
  • Up-regulated with adequate iron stores (saturated transferrin)
  • Down-regulated with low iron stores
35
Q

Ferritin vs Transferrin

A 
Ferritin = iron storage protein
Transferrin = binds iron for transport in the blood
36
Q

heme oxygenase

A
  • degrades heme and liberates iron
37
Q

Active vitamin D

A
  • 1,25(OH)2 D3

- Tightly regulated, poor biomarker for assessment

38
Q

Metabolic pathway of Vit D

A
  • Vitamin D3 from skin/diet enter body
  • Gets converted to 25(OH)2D3 by 25-OHase
  • 25(OH)D3 gets converted to 1,25(OH)2D3
39
Q

Activators/inhibitors of production of 1,25(OH)2D3

A

Activator: low calcium, PTH
Inhibitors: 1,25(OH)2D3

40
Q

Main function of Vitamin D (calcium absorption)

A

Increase absorption of calcium!
- 1,25(OH)2D3 binds VDR and increases expression of a calcium channel and increases expression of calbindin (which mediates transport of calcium from luminal to basolateral side of enterocyte)

41
Q

Why do you not get Vit D toxicity from sunlight?

A
  • Many regulatory steps

- UVB converts substrate into various inactive form

42
Q

Storage form of Vitamin D

A

25(OH)D3 found mostly in liver and fat – great for status assessment

43
Q

Calcium sensing

A
  • Calcium sending receptor (CasR)
  • Located all over body but most importantly in parathyroid gland
  • Calcium sensing inhibits PTH secretion
44
Q

PTH and Calcium

A

PTH increases plasma calcium

45
Q

Effect of low vitamin D (and low Ca) on PTH

A

Plasma Ca is low, so CasR does not inhibit PTH. PTH is produced and secreted and increases plasma Calcium through variety of mechanisms

46
Q

How does PTH increase plasma Ca? (two main ways)

A
  1. Liberates Ca from bone

2. Increases Ca absorption through stimulating Vitamin D into active form

47
Q

Calcium absorption (transporters, factors influencing)

A
  • Through calcium channel
  • Calbindin mediates transport of calcium from luminal to basolateral side of enterocyte
  • Dose, matrix, inhibitors (phytate/oxalate), other divalent cations, gastric acid
48
Q

Calcitonin

A

Tones down calcium by slowing down bone resorption (inhibits osteoclasts)

49
Q

Refeeding syndrome

A

Malnourished -> cells are intracellularly depleted of phosphorous -> given glucose -> insulin -> drives glucose and other stuff into cells -> start to make ATP -> phosphorous levels in blood go dangerously low -> fatality

50
Q

Magnesium absorption

A

Mostly paracellular absorption!

51
Q

Vitamin D binding protein (DBP)

A
  • In blood, Vit D is picked up by DBP

- Free vitamin D is more bioavailable than bound

52
Q

Magnesium basics

A
  • Related to diabetes
  • Related to hypertension (relaxes vascular smooth muscle)
  • Necessary for metabolism and generation of ATP
53
Q

ATP7B and defect

A
  • Copper transporter in liver cells export copper to golgi for packaging on ceruloplasmin for secretion to serum and into bile for excretion (under high levels)
  • defect causes Wilson’s disease, a condition with reduced ceruloplasmin and biliary copper secretion
54
Q

Se assessment

A
  • Gpx activity - function

- sel P - status

Friedman (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions