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BMS150 Midterm 2 > Rheumatology 3 - Crystal Arthropathies > Flashcards

Rheumatology 3 - Crystal Arthropathies Flashcards

1
Q

Purines in DNA and RNA

A

Adenine (adenosine) and Guanine (guanosine)

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2
Q

Pyrimidines in DNA

A

Thymine (thymidine) and Cytosine (cytidine)

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3
Q

Pyrimidines in RNA

A

Uracil (uridine) and Cytosine (cytidine)

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4
Q

Sugar + Base

A

Nucleoside

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5
Q

Nucleoside + 1-3 phosphates

A

Nucleotide

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6
Q

Purine nucleotide biosynthesis pathways

A
  1. De novo pathway
  2. Salvage pathway
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7
Q

In purine de novo synthesis, what is used to transfer N to PRPP? What is the result?

A

Glutamine; phosphoribose with an added N

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8
Q

What atoms/molecules supply the C, H, O and N to make a nucleotide?

A

Other amino acids, CO2, folate (B9)

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9
Q

What is the nucleotide product of purine de novo synthesis?

A

inosine monophosphate (IMP)

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10
Q

IMP can be used to make ____ or _____

A

AMP or GMP; these pathways can also use GTP to make AMP, and ATP to make GMP

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11
Q

Why is reciprocal control in the de novo pathway of purines 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

Purine salvage pathway uses what molecules that already exist?

A

Hypoxanthine, guanine, and adenine bases

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13
Q

Where do the existing bases come from?

A

Diet or normal cell turnover

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14
Q

Enzyme that catalyzes addition of sugar+P to hypoxanthine or guanine? Products?

A

Hypoxanthine-guanine phosphoribosyl transferase
Hypoxanthine => IMP
Guanine => GMP

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15
Q

Enzyme that catalyzes addition of sugar+P to adenine? Product?

A

Adenine phosphoribosyl transferase
Adenine => AMP

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16
Q

De novo synthesis of Pyrimidines involves making what first? Then what?

A

Makes an intermediate pyrimidine ring first, then attaching the ribose-5-P

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17
Q

Substrates for pyrimidine ring are?

A

Carbamoyl phosphate and Aspartate

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18
Q

How to make CTP?

A

UMP phosphorylates => UTP
UTP aminated (glutamine) => CTP

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19
Q

How to make dTMP?

A

UMP phosphorylated => UDP
UDP converted => dUMP
dUMP methylated using B9 => dTMP

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20
Q

What does the “d” mean in dTMP?

A

deoxy- form (one less oxygen)

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21
Q

Enzyme that removes phosphates from nucleotides => nucleosides?

A

Nucleotidases

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22
Q

What are pyrimidine bases degraded to?

A

Cytosine and uracil then ultimately alanine

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23
Q

What are purine bases degraded to?

A

Xanthine and then uric acid, which is excreted in urine

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24
Q

Enzyme used to convert hypoxanthine to xanthine and xanthine to uric acid?

A

Xanthine Oxidase

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25
Q

What is gout commonly caused by? Less commonly caused by?

A

Commonly underexcretion of uric acid
Less commonly overproduction of uric acid

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26
Q

Deposition of monosodium urate crystals in the joints that triggers an inflammatory immune response?

A

Gout (gouty arthritis)

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27
Q

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

A

Chronic tophaceous gout

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28
Q

Uric acid crystals forming in the kidneys?

A

Kidney stones

29
Q

Enzyme that humans lack but other mammals have?

30
Q

Where is uric acid highly reabsorbed?

A

In the urine

31
Q

Major modifiable risk factors for gout?

A

Diet rich in alcohol, meat, and asparagus

32
Q

Non-modifiable risk factors for gout?

A

Male sex and decreased renal excretion

33
Q

Local anatomical factors that increase likelihood for arthritis?

A
  • Temperature
  • pH
  • trauma
  • joint hydration
34
Q

What activates urate crystals? What does activation attract?

A

Phagocytosis by macrophages activates them
Then they release chemokines that attract neutrophils

35
Q

What complement pathway is activated that contributes to neutrophil recruitment?

A

Alternative Pathway

36
Q

What happens when the inflammasome is activated?

A

Secretion of IL-1 => further accumulation of neutrophils and macrophages => further inflammation

37
Q

What happens after the first attack of gout?

A

Enter an inter-critical phase with a varying number of acute attacks (every few mo.)

38
Q

Chronic gout leads to?

A

Chronic arthritis

39
Q

In chronic cases, urate crystals encrust the _______ of the joint forming deposits in the ________.

A

Articular surface; synovium

40
Q

In chronic cases, synovium becomes ______, ______, and _______ with inflammatory cells (pannus).

A

Hyperplastic, fibrotic, and thickened

41
Q

In chronic cases, destruction of underlying cartilage leads to what?

A

Bone erosion

42
Q

Pathognomonic hallmark of gout?

A

Tophi = Large inflammatory bodies that surround areas of crystal deposition

43
Q

Where do most individuals experience acute gout attacks?

A
  • 1st MTP, insteps, ankles, heels
  • Knees, wrists, elbows
44
Q

Eventually, over the span of years, what develops following acute gout attacks?

A

Chronic tophaceous gout

45
Q

Syndrome characterized by deficiency in HGPRT leading to hyperuricemia?

A

Lesch-Nyhan Syndrome

46
Q

How does Lesch-Nyhan Syndrome lead to hyperuricemia?

A

PRPP accumulates and stimulates production of purine nucleotides => break down to uric acid

47
Q

Pseudogout?

A

Calcium Pyrophosphate Crystal Deposition Disease (CPPD)

48
Q

Epidemiology of Pseudogout?

A

Common, prevalence increases with age

49
Q

Etiology of pseudogout? (3)

A
  • genetic component (autosomal dom.)
  • hyperparathyroidism, hypothyroidism, diabetes, hemochromatosis
  • medication triggers (?)
50
Q

Pathology of Pseudogout?

A

Crystals deposit in matrix of menisci => Rupture and trigger immune response => recruitment of neutrophils = inflammatory damage

51
Q

What can Pseudogout mimic?

52
Q

Where does Pseudogout commonly affect?

53
Q

Synovial fluid analysis can help distinguish between what?

A

Septic arthritis, gout, pseudogout, hemarthrosis, and rheumatic joint disease

54
Q

When is synovial fluid analysis done?

A

Suspicion of infectious arthritis, flare of crystal arthritis, or hemarthrosis

55
Q

What do you analyze in synovial fluid analysis?

A

The 3 C’s:
- Crystals
- Cells
- Culture

56
Q

Synovial fluid analysis of Gout?

A
  • Cells high
  • Birefringent, needle-shaped crystals
57
Q

Synovial fluid analysis of Pseudogout?

A
  • Cells high
  • Non-birefringent, cuboidal crystals
58
Q

Synovial fluid analysis of Septic Arthritis?

A
  • Cells very high
  • Culture positive
59
Q

Synovial fluid analysis of Hemarthrosis?

A
  • Lots of RBC’s
60
Q

Anti-gout medication that targets inflammation?

A

Colchicine

61
Q

Colchicine mechanism of action?

A

Binds tubulin = prevents microtubule polymerization = blocks migration of leukocytes and therefore decreases inflammatory response

62
Q

Does colchicine act prophylactically? Acutely? Both?

A

Both
- Pro: reduce frequency
- Acute: can terminate attack if taken at first sign of inflammation

63
Q

Major adverse effect of colchicine?

A

Bone marrow depression since it blocks cell division

64
Q

Anti-gout medication that decreases uric acid production?

A

Allopurinol

65
Q

Allopurinol is a competitive inhibitor of what?

A

Xanthine oxidase

66
Q

Does Allopurinol act prophylactically? Acutely? Both?

A

Only Prophylactically = reduce frequency of attacks

67
Q

Anti-gout medications that increases uric acid excretion by blocking tubular reabsorption of uric acid?

A

Uricosurics

68
Q

Do Uricosurics act prophylactically? Acutely? Both?

A

Only Prophylactically = reduce frequency of attacks

BMS150 Midterm 2 (14 decks)

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