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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 ā€œdā€ 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
What is gout commonly caused by? Less commonly caused by?
Commonly underexcretion of uric acid Less commonly overproduction of uric acid
26
Deposition of monosodium urate crystals in the joints that triggers an inflammatory immune response?
Gout (gouty arthritis)
27
Nodular masses of monosodium urate crystals (tophi) may be deposited in soft tissue?
Chronic tophaceous gout
28
Uric acid crystals forming in the kidneys?
Kidney stones
29
Enzyme that humans lack but other mammals have?
Uricase
30
Where is uric acid highly reabsorbed?
In the urine
31
Major modifiable risk factors for gout?
Diet rich in alcohol, meat, and asparagus
32
Non-modifiable risk factors for gout?
Male sex and decreased renal excretion
33
Local anatomical factors that increase likelihood for arthritis?
- Temperature - pH - trauma - joint hydration
34
What activates urate crystals? What does activation attract?
Phagocytosis by macrophages activates them Then they release chemokines that attract neutrophils
35
What complement pathway is activated that contributes to neutrophil recruitment?
Alternative Pathway
36
What happens when the inflammasome is activated?
Secretion of IL-1 => further accumulation of neutrophils and macrophages => further inflammation
37
What happens after the first attack of gout?
Enter an inter-critical phase with a varying number of acute attacks (every few mo.)
38
Chronic gout leads to?
Chronic arthritis
39
In chronic cases, urate crystals encrust the _______ of the joint forming deposits in the ________.
Articular surface; synovium
40
In chronic cases, synovium becomes ______, ______, and _______ with inflammatory cells (pannus).
Hyperplastic, fibrotic, and thickened
41
In chronic cases, destruction of underlying cartilage leads to what?
Bone erosion
42
Pathognomonic hallmark of gout?
Tophi = Large inflammatory bodies that surround areas of crystal deposition
43
Where do most individuals experience acute gout attacks?
- 1st MTP, insteps, ankles, heels - Knees, wrists, elbows
44
Eventually, over the span of years, what develops following acute gout attacks?
Chronic tophaceous gout
45
Syndrome characterized by deficiency in HGPRT leading to hyperuricemia?
Lesch-Nyhan Syndrome
46
How does Lesch-Nyhan Syndrome lead to hyperuricemia?
PRPP accumulates and stimulates production of purine nucleotides => break down to uric acid
47
Pseudogout?
Calcium Pyrophosphate Crystal Deposition Disease (CPPD)
48
Epidemiology of Pseudogout?
Common, prevalence increases with age
49
Etiology of pseudogout? (3)
- genetic component (autosomal dom.) - hyperparathyroidism, hypothyroidism, diabetes, hemochromatosis - medication triggers (?)
50
Pathology of Pseudogout?
Crystals deposit in matrix of menisci => Rupture and trigger immune response => recruitment of neutrophils = inflammatory damage
51
What can Pseudogout mimic?
OA or RA
52
Where does Pseudogout commonly affect?
Knees
53
Synovial fluid analysis can help distinguish between what?
Septic arthritis, gout, pseudogout, hemarthrosis, and rheumatic joint disease
54
When is synovial fluid analysis done?
Suspicion of infectious arthritis, flare of crystal arthritis, or hemarthrosis
55
What do you analyze in synovial fluid analysis?
The 3 C's: - Crystals - Cells - Culture
56
Synovial fluid analysis of Gout?
- Cells high - Birefringent, needle-shaped crystals
57
Synovial fluid analysis of Pseudogout?
- Cells high - Non-birefringent, cuboidal crystals
58
Synovial fluid analysis of Septic Arthritis?
- Cells very high - Culture positive
59
Synovial fluid analysis of Hemarthrosis?
- Lots of RBC's
60
Anti-gout medication that targets inflammation?
Colchicine
61
Colchicine mechanism of action?
Binds tubulin = prevents microtubule polymerization = blocks migration of leukocytes and therefore decreases inflammatory response
62
Does colchicine act prophylactically? Acutely? Both?
Both - Pro: reduce frequency - Acute: can terminate attack if taken at first sign of inflammation
63
Major adverse effect of colchicine?
Bone marrow depression since it blocks cell division
64
Anti-gout medication that decreases uric acid production?
Allopurinol
65
Allopurinol is a competitive inhibitor of what?
Xanthine oxidase
66
Does Allopurinol act prophylactically? Acutely? Both?
Only Prophylactically = reduce frequency of attacks
67
Anti-gout medications that increases uric acid excretion by blocking tubular reabsorption of uric acid?
Uricosurics
68
Do Uricosurics act prophylactically? Acutely? Both?
Only Prophylactically = reduce frequency of attacks

BMS150 Midterm 2 (14 decks)

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