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BMS 150 Midterm 2 > Crystal Arthropathies > Flashcards

Crystal Arthropathies Flashcards

1
Q

which base is N-containing single ring structure

A

pyrimindine

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2
Q

which base is N-containing double ring structure

A

purine

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3
Q

which nucleotides are purines

A

A and G

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4
Q

which nucleotides are pyrimidines

A

C, T, and U

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5
Q

difference in DNA and RNA for nucleotides

A

DNA has T and RNA has U

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6
Q

what are the two pathways to synthesize purines?

A

de novo synthesis pathway and salvage pathway

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7
Q

explain the de novo pathway to synthesize purines

A

Glutamine is used to transfer an N to PRPP, then a base is built on the N, the nucleotide product is inosine monophosphate (IMP)

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8
Q

what is used in the de novo synthesis pathway?

A

glutamine

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9
Q

what is the nucleotide product of the de novo synthesis pathway

A

inosine monophosphate (IMP)

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10
Q

IMP can then be used to make what?

A

AMP or GMP
ATP to make GMP
GTP to make AMP

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11
Q

why is reciprocal control in the de novo synthesis useful?

A

Helps ensure you are not making all of one type of purine and not enough of the other

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12
Q

what purine base is made from the de novo synthesis pathway?

A

hypoxanthine

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13
Q

what does the salvage pathway use?

A

Uses hypoxanthine, guanine, and adenine bases that already exist

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14
Q

what are the two enzymes used in the salvage pathway?

A
  • hypoxanthine-guanine phosphoribosyl transferase
  • adenine phosphoribosyltransferase
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15
Q

what does hypoxanthine-guanine phosphoribosyl transferase do?

A

catalyzes the addition of phosphoribose (sugar +P) from PRPP to:
- Hypoxanthine to make IMP
- guanine to make GMP

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16
Q

what does adenine phosphoribosyltransferase do?

A

catalyzes the addition of phosphoribose (sugar + P) from PRPP to:
adenine to make AMP

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17
Q

what is the pathway for pyrimidine nucleotide synthesis

A

de novo pathway

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18
Q

how is the de novo pathway different in pyrimidine than purine synthesis

A

in purimidine, it involves making an intermediate pyrimidine ring first, then attaching a ribose-5-P (via PRPP)

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19
Q

what are the substrates for the pyrimidine ring in pyrimidine synthesis

A
  • carbamoyl phosphate (made from glutamine, ATP, CO2)
  • aspartate
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20
Q

during the de novo pathway for pyrimidine, what is the nucleotide intermediate when the pyrimidine ring is attached to PRPP?

A

UMP

21
Q

how is CTP made from UMP

A

UMP is phosphorylated via kinases to make UTP, UTP is aminated to make CTP (glutamine provides the N)

22
Q

how to make dTMP from UMP

A

UMP is phosphorylated (kinase) to make UDP, then converted to dUMP, dUMP is methylated to dTMP using folate coenzyme

23
Q

what removes P’s from nucleotides to relase nucleosides

A

nucleotidases

24
Q

what happens when pyrimidine bases are degraded

A

cytosine to uracil and ultimately alanine

25
Q

what happens when purine bases are degraded

A

first to xanthine, then uric acid, and then excreted in urine

26
Q

what is the enzyme that converts hypoxanthine to xanthine, and xanthine to uric acid?

A

xanthine oxidase

27
Q

what leads to gout?

A

hyperuricemia

28
Q

what is hyperuricemia

A

underexcretion (most common) or overproduction (less common) of uric acid

29
Q

what is chronic tophaceous gout

A

Nodular masses of monosodium urate crystals (tophi) may be deposited in soft tissues

30
Q

what is the enzyme that is responsible for the degradation of uric acid?

A

uricase

31
Q

what is gout?

A

joint inflammation due to deposition of urate crystals

32
Q

what results in acute gouty arthritis?

A

monosodium urate crystal precipitation

33
Q

in a patient with acute gout, how does the joint become inflamed

A

Urate crystals are phagocytosed by macrophages, activating them, they then release chemokines that attract neutrophils into the joint, found within the synovial fluid, Neutrophils mediate joint inflammation

34
Q

people with acute gout tends to have pain in which joints

A

1st metatarsal-phalangeal joint, insteps, ankles, heels, knees, wrists, elbows, finger, Lower limbs are more often affected than upper

35
Q

Chronic gout leads to ?

A

chronic arthritis with joint erosion, chronic inflammation, development of pannus, and development of tophi

36
Q

what is the pathognomonic hallmark of gout

A

tophi

37
Q

what are tophi

A

uric acid crystals that accumulate in and around the affected joint

38
Q

how does Lesch-Nyhan Syndrome happen?

A

deficiency of HGPRT

39
Q

Lesch-Nyhan Syndrome can lead to?

A

hyperuricemia because increase in uric acid

40
Q

what is calcium pyrophosphate crystal deposition disease (CPPD) also known as ?

A

pseudogout

41
Q

most cases of pseudo gout are?

A

sporadic

42
Q

what causes pseudogout?

A

caused by the buildup of calcium pyrophosphate crystals in the joints, macrophages phagocytose the crystals, recruiting neutrophils and causing inflammation

43
Q

what is used to distinguish what type of arthritis a person has?

A

synovial fluid analysis

44
Q

what are the 3 C’s when doing the synovial fluid analysis

A

Crystals
Cells
Culture

45
Q

when the cells (seen in synovial fluid analysis) are super high, it’s usually what

A

septic arthritis

46
Q

what are some anti-gout agents

A
  • target the inflammation (corticosteriods and colchicine)
  • analgesics (NSAIDs)
  • decrease uric acid production
  • increase uric acid excretion
47
Q

how does colchine effect inflammation

A

Blocks the migration of leukocytes (most importantly neutrophils), thereby decreasing the inflammatory response

48
Q

what is the most serious adverse effect of colchine

A

bone marrow depression

BMS 150 Midterm 2 (30 decks)

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