Brainscape's Knowledge GenomeTM

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


See full index

biochem > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q

What are the two types of vitamins?

A

water soluble (precursors for coenzymes) and lipid soluble

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

What is the enzyme, pathway and deficiency of Biotin?

A

coenzyme=biotin-lysine

main pathway it activates: carboxylation

**alopecia

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

What is the enzyme, pathway and deficiency of thiamine (B1)?

A

coenzyme=thiamine PP

main action: decarboxylation

ophthalamoplegia: eyes can’t follow beam of light

Dry beri-beri: polyneuritis; occurs first, neurologic problems

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

What is the enzyme, pathway and deficiency of niacin (B3)?

A

coenzyme: NAD(H), NADP(H)

main action: oxidation/reduction

pellagra: nutritional problem

Tryptophan–>niacin

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

What is the enzyme, pathway and deficiency of folic acid?

A

coenzyme: THF (tetrahydrofolate)

main action: 1 carbon carrier; donor

megaloblastic anemia: large nucleated red cells in the marrow

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

What is the enzyme, pathway and deficiency of cyanocobalamin (B12)?

A

coenzyme: methyl-cobalamin and deoxyadenosyl-cobalamin
pathway: VOMIT

**megaloblastic anemia

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

What is the enzyme, pathway and deficiency of pyridoxine (B6)?

A

coenzyme: pyridoxal P (PLP)

main action: transamination

delta aminolevulinate synthase: need b6 (no poryphin so heme not made properly)

isoniazid therapy: treat Tb; binds B6 so can’t be absorbed

sideroblatsic anemiaa: Fe stays in the mitochondria becuase heme not formed properly

Heme: red because porphyrin

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

What is the enzyme, pathway and deficiency of riboflavin (B2)

A

coenzyme: FAD(H2)

–when it absorbs light, it degrades; consider with children using phototherapy

main action: oxidation/reduction

**cheilosis or stomatosis

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

What is the enzyme, pathway and deficiency of ascorbate (C)?

A

only water soluble vitamin without coenzyme

main action: antioxidant**scurby: ecchymoses, hyperelastic skin, loose teeth

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

What is the enzyme, pathway and deficiency of pantothenic acid

A

coenzyme: CoA

main action: carrier of fatty acid, HMG, acetate

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

Describe scurvy in an infant.

A

Swelling, bruising

2-10 months old

bottle fed with formula that is overheated for pasteurization and not supplemented with Vitamin C

–Vitamin C is destroyed by excessie heat

gum bleeding doesn’t occur unless erupted teeth

vitamin C: cofactor for proline and lysine hydroxylases in collagen syntehsis

–vitamin C deficiency–> collagen fibers less stable than normal

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

What are the other roles of vitamin C?

A

antioxidant

reducing iron in intestine to enhanble iron absorption

hepatic synthesis of bile acids

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

What are the four lipid soluble vitamins?

A

A, D, E, and K

A, D: work through enhancer mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the important functions of vitamin D?

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

What are the important functions of vitamin A?

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

What are the important functions of vitamin K?

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

What are the important functions of vitamin E?

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

How does vitamin D regulate calcium homeostasis?

A

hypocalcemia–>PTH release–>bind to receptor on renal proximal tubules–>coupled through cAMP to activate 1 alpha hydroxylase

–enzyme converts vitamin D to 1,25 DHCC (calcitriol)—lipid soluble hormone

–1,25 DHCC acts on duodenal epithelial cells

–intracellular receptor=Zn finger protein

–bind to response elements on enhancer regions of DNA to induce synthesis of Ca binding proteins which stimulate Ca2+ uptake from GI tract

–1,25 DHCC also causes Ca2+ reabsorption in the kidney

–1,25 DHCC mobilizes Ca2+ from the bone when PTH is present

BRINGS CALCIUM LEVELS BACK TO NORMAL

25 hydroxycholecalciferol: storage form of vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the action of calcitonin?

A

bind to receptors on osteoclasts and prevent demineralization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the action of bisphosphates?

A

treatment of osteoporosis

inhibit osteoclast action and resorption of bone

modest increase in bone mineral density (BMD), leading to strengthening of bone and decrease in fractures

Boniva (ibandronate), actonel (risedronate) and Fosamax (alendronate)

21
Q

What are the symptoms and causes of vitamin D deficiency?

A
22
Q

What are the symptoms and causes of vitamin A deficiency?

A
23
Q

What are the symptoms and causes of vitamin E deficiency?

A
24
Q

How is 1,25 Dihydroxycholecalciferol (calcitriol) synthesized?

A

*7 dehydrocholesterol derived from cholesterol in liver

*activation of 7-dehydrocholesterol by UV light in skin->cholecalciferol (vitamin D3)

–insufficient in people in cold, cloudy climates; vitamin D3 supplementation necessary

*25 hydroxylation in liver

–patients with severe liver disease may need to be given 25-DHCC or 1,25 DHCC

*1 alpha hydroxylation in the proximal renal tubule cells in response to PTH

–genetic deficiencies or patients with end stage renal disease develop renal osterodystrophy because of insufficiency of 1,25 DHCC –require 1,25 DHCC or drug analog not metabolized in kidney

patients includ: end stage renal disease secondary to diabetes mellitus; fanconi renal syndrome (renal proximal tubule defect), genetic deficiency of 1 alpha hydroxylase (vitamin D resistant rickets)

25
Q

What is vitamin D toxicity?

A

results in hypercalcemia

unlike water soluble vitamins, vitamin D not excreted, instead stored in liver as 25, hydroxycholecalciferol

excess vitamin D promotes intestinal absorption of calcium and phosphate

large amount of vitamin D can contribute to osteoporosis

hypercalcemia can impair renal function

early signs: polyuria, poplydipsia, nocturia

prolonged hypercalcemia: calcium deposition in soft tissue, including kidney leading to irreversible kidney damage

26
Q

Why do osteoporosis pateints take calcium and vitamin D?

A

take extra Calcium to be on high end of normal so parathyroid gland doesn’t secrete PTH

–without PTH, osteoblasts increase Ca2+

27
Q

What occurs in vitamin D deficiency?

A

childhood: rickets

–deformity of legs, muscle weakness

adult (after epiphyseal fusion): osteomalacia, less deformity, bone pain, muscle weakness

28
Q

What is isotretinoin?

A

form of retinoic acid

used in treatment of acne

teratogenic: malformations of craniofacial, cardiac, thymic and CNS structures

contraindicated in pregnant women

29
Q

What is the action of vitamin A?

A

maintenance of healthy epithelium and vision

30
Q

What are the three vitamin A structures?

A

based on functional group on C-1

* retinol: hydroxyl

*retinoic acid: carboxyl

*retinal: aldehyde

31
Q

What is the action of retinol and retinoic acid?

A

required for growth, differentiation and maintenance of epithelial cells

bind to intracellular receptors (Zn-finger proteins) and regulate transcription through specific response elements

32
Q

What is the action of vitamin A in vision?

A

retinal formed in trans form–not active

trans retinal converted to active cis-retinal in pigmented epithelial cells

cis-retinal transferred to opsin in rod cells and forms light receptor rhodopsin (functions similarly in rods and cones)

33
Q

What are the steps of the vitamin A pathway in vision?

A

rhodopsin is 7 pass recpetor coupled to trimeric G protein transducin (Gt)

pathway activates cGMP phosphodiesterase, lowers cGMP in response to light

rhodopsin and transducin are embedded in disk membranes in outer rod segment

cGMP gated Na channels in cell membrane of outer rod segment reponse to decrease in cGMP by closing and hyperpolarizing membrane

rod cell is unusual becaus membrane is partially depolarized (-30 mV) at rest (in darkness) and hyperpolarizes on stimulation

34
Q

How is vision signal sent to brain?

A

membrane is partially depolarized in dark so NT glutamate is continuously released

glutamate inhibits optic nerve bipolar cells –with which rods synapse

by hyperpolarizing the rod cell membrane, light stops release of glutamate, reducing inhibition of optic nerve bipolar cell and initiating signal to brain

35
Q

What are causes and symptoms of vitamin A deficiency?

A

clinical manifestations don’t arise until many months of extreme lack of dietary vitamin A because liver can store vitamin A

most common cause of blindness

3-5 years of age

most often due to fat malabsorption or liver cirrhosis

night blindness (rod cells responsible for vision in low light), metaplasia of corneal epithelium, xerothalmia (dry eyes), bronchitis, pneumonia, and follicular hyperkeratosis

Bitot spots on eyes

vitamin A important for immune cell differentiation so deficiency can cause frequent infection

36
Q

What is the use of beta carotene?

A

found in yams, carrots, yellow squash and potatoes

cleaved to form retinal by intestinal enzymes

37
Q

What is vitamin A toxicity?

A

excessive sweating, brittle nails and diarrhea

no beta carotene toxicity

38
Q

Why is vitamin K important?

A

required to introduce Ca2_ binding sites of calcium dependent proteins

–gamma carboxylation of glutamyl residues on proteins introduces Ca2+ binding sites

*gamma glutamyl carboxylase requires vitamin K

*usually on glutamic acid

*k dependent carboxylation is cotranslation modifcation occuring as proteins are synthesized on ribosome in RER during translation

39
Q

What proteins undergo vitamin K dependent carboxylation?

A

coagulation factors II (prothrombin), VII, IX and X

anticoagulation proteins C and S

40
Q

What are the symptoms of vitamin K deficiency?

A

prolonged bleeding, easy bruising, potentially fatal hemorhhagic disease

41
Q

What conditions predispose someone for a vitamin K deficiency?

A

fat malabsorption (bile duct occlusion)

prolonged treatment with broad spectrum antibiotics (eliminate intestinal bacteria that suply vitamin K)

breast fed newborns (little intestinal flora, breast milk very low in vitamin K), especially in home birht where postnatal injection of vitamin K may not have been given

infants whose mothers have been treated with certain anticonvulsants during pregnancy such as phenytoin (Dilantin)

42
Q

What are signs of vitamin K deficiency?

A

poor nutrition and malnourishment, lack of medication, occult blood in stool, prolonged PT, normal LFTs

43
Q

What is the difference between vitamin C and vitamin K deficiencies?

A

*platelets attracted by exposed collagen (increased bleeding time)

44
Q

What are anticoagulants and how do they work?

A

warfarin and dicumarol

competitive inhibitors

interfere with cotranslation modification during synthesis of precoagulation factors

anatgonize gamma carboxylation activity of vitamin K

**prevent coagulation in vivo not in vitro

**2-3 days to see full anticoagulant acitivity

herparin: short term anticoagulant activity; activator of antithrombin III

45
Q

What is the function of vitamin E (alpha tocopherol)?

A

antioxidant

lipid soluble

protects lipids from oxidative damage

prevents peroxidation of fatty acids in cell membrance, maintaining fluidity

46
Q

What occurs in vitamin E deficiency?

A

hemolysis, neurologic problems, retinitis pigmentosa

47
Q

What occurs in vitamin E toxicity?

A

hemorrhage in patients given warfarin

looks like vitamin K in excess

48
Q

What are antioxidants?

A
  1. catalase: destroys H2O2
  2. vitamin C: water soluble, acts in cytoplasm
  3. beta carotene: lipid soluble
  4. glutathione

biochem (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions