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BMS150 Test 2 > Crystal Arthropathies - Gout, CPPD (Rheumatology 3 - Week 5) > Flashcards

Crystal Arthropathies - Gout, CPPD (Rheumatology 3 - Week 5) Flashcards

1
Q

How many rings do pyrimidine bases have?

A

1

Examples: C, T (DNA only), U (RNA only)

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2
Q

How many rings do purine bases have?

A

2

Examples: A, G

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3
Q

How many carbons make up the sugar component of DNA and RNA?

A

5

Note: for RNA, it’s a 5-C ribose and for DNA it’s a 5-C deoxyribose

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4
Q

What do we call a sugar and base together?

A

nucleoside

Example: adenosine (adenine + ribose sugar)

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5
Q

What do we call a nucleoside (base + sugar) and 1-3 phosphates?

A

nucleotide

Example: adenosine triphosphate (ATP)

Note: nucleotides are the building blocks used in DNA and RNA synthesis

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6
Q

What is the nucleoside name for cytosine?

A

cytidine

Note: notice the “ine” ending of the bases changing to “dine” endings for pyramidine nucleosides

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7
Q

What is the nucleoside name for thymine?

A

thymidine

Note: notice the “ine” ending of the bases changing to “dine” endings for pyramidine nucleosides

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8
Q

What is the nucleoside name for uracil?

A

uridine

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9
Q

What is the nucleoside name for adenine?

A

adenosine

Note: notice the “ine” ending of the bases changing to “sine” endings for purine nucleosides

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10
Q

What is the nucleoside name for guanine?

A

guanosine

Note: notice the “ine” ending of the bases changing to “sine” endings for purine nucleosides

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11
Q

What is the nucleoside name for xanthine?

A

xanthosine

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12
Q

What is the nucleoside name for hypoxanthine?

A

inosine

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13
Q

What are the two pathways for purine nucleotide biosynthesis?

A

1) de novo pathway
2) salvage pathway

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14
Q

Describe the de novo pathway for purine nucleotide biosynthesis

A

“Adding things onto an activated ribose (PRPP) to make a completely new base”

After we have that ribose and make that base, we have a nucleotide, because the phosphates are already attached (on the activated ribose)

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15
Q

Describe the salvage pathway for purine nucleotide biosynthesis

A

Again, you have the activated ribose with the phosphates (PRPP), but you also already have a pre-formed base in your body (can be from diet or products from cell turnover)

We put the PRPP and base together, and we get a nucleotide

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16
Q

What molecule is used to transfer an N (nitrogen) to PRPP in de novo synthesis?

A

glutamine

Recall: “amine” = nitrogen containing

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17
Q

True or False: Inosine monophosphate (IMP) can be used to make AMP or GMP

A

True

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18
Q

How do ATP and GTP levels influence GMP and AMP synthesis?

A
  • when ATP levels are high, you make GMP (ATP makes GMP)
  • when GTP levels are high, you make AMP (GTP makes AMP)

Note: we can refer to this as reciprocal control

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19
Q

What is a disadvantage of the de novo pathway?

A

It uses a lot of energy because we’re making bases from scratch.

Therefore, helpful that we also have the salvage pathway.

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20
Q

What are two important enzymes for the salvage pathway?

A

1) hypoxanthine-guanine phosphoribosyl transferase (HGPRT)

2) adenine phosphoribosyltransferase (APRT)

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21
Q

What reaction does HGPRT catalyze?

A

addition of phopsphoribose (sugar + P) from PRPP to:

  • hypoxanthine to make IMP
  • guanine to make GMP
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22
Q

What reaction does APRT catalyze?

A

addition of phosphoribose (sugar + P) from PRPP to:

  • adenine to make AMP
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23
Q

What is the pathway used for pyrimidine nucleotide synthesis?

A

1) de novo pathway

Remember: “de novo” means making from scratch (completely new)

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24
Q

Describe the de no pathway for pyrimidine nucleotide synthesis

A
  • make an intermediate pyrimidine ring first
  • then attaching a ribose-5-P (via PRPP)

Note: this is opposite to purines, where the ring is constructed directly onto the ribose-5-P

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25
What are the substrates used for the ring in the de novo pathway in pyrimidine nucleotide biosynthesis?
1) carbamoyl phosphate 2) aspartate Note: carbamoyl phosphate is made from glutamine + ATP + HCO3-
26
How do we make CTP?
- phosphorylate UMP to make UTP - UTP is aminated to CTP (N supplied by glutamine)
27
How do we make dTMP?
- phosphorylate UMP to make UDP - UDP converted to dUMP - dUMP is methylated to dTMP (via folate coenzyme/B9 coenzyme) recall: folate = vitamin B9
28
True or False: IMP, AMP, and GMP are examples of monophosphates
True
29
What do nucleotidases do?
Remove phosphates from nucleotides to release nucleosides Recall: nucleoside = sugar + base
30
What does cytosine get degraded into?
cytosine --> uracil --> alanine
31
What does thymine get degraded into?
thymine --> aminoisobutyrate
32
What do purines (guanine and adenine) get degraded into? Note: purine degradation is more relevant to today's lecture on gout (compared to pyrimidine degradation)
guanine/adenine --> xanthine --> uric acid Note: uric acid is eventually excreted in urine, and elevated levels (hyperuricemia) can lead to GOUT
33
What enzyme converts hypoxanthine to xanthine, and then xanthine to uric acid? ** POTENTIAL TEST QUESTION **
xanthine oxidase
34
What do we call the condition characterized by joint inflammation due to the deposition of urate crystals?
Gout
35
Gout can be due to ____________ (underexcretion/overexcretion) or ______________ (underproduction/overproduction) or uric acid, leading to hyperuricemia.
underexcretion or overproduction Note: underexcretion = more common
36
True or False: Hypouricemia can also lead to gout
False. Only hyperuricemia can lead to gout
37
In gout, immune cells mount an inflammatory response to what type of crystal deposited in the joints?
monosodium urate crystals
38
True or false: Gout is also known as gouty arthritis
True
39
What are tophi?
Nodular masses of monosodium urate crystals Other descriptors: - large, inflammatory bodies that surround areas of crystal deposition - form foreign-body giant cells - consist of macrophages and lymphocytes - occur in articular cartilage, ligaments, tendons, and bursae - can invade joint and surrounding soft tissues, kidney, earlobes, fingertips
40
Uric acid stones (aka "kidney stones") is referred to as what?
Urolithiasis (or sometimes nephrolithiasis, depending on location of stones)
41
Humans lack what enzyme that can degrade uric acid?
uricase Note: because we can't degrade it, we rely on excreting it (but sometimes this doesn't work as we want because uric acid is readily reabsorbed back into the body)
42
What are modifiable risk factors of gout?
- diets high in alcohol (beer has a lot of purines) - diets high in meat (especially organs) - high asparagus consumption
43
What are non-modifiable risk factors for gout?
- male sex - decreased renal excretion
44
What percent of the general population has gout?
1-4% Note: 10-20% of the population of the Western hemisphere has hyperuricemia, but not all develop gout
45
What might cause increased uric production?
- enzyme defects (i.e., xanthine oxidase) in metabolism of uric acid - cancers (i.e., leukemia)
46
What might cause decreased uric acid excretion?
- idiopathic (meaning we don't know why, it's just happening) - chronic kidney disease
47
_____________ phagocytose urate crystals and release chemokines that attract ____________
Macrophages, neutrophils
48
Complement activation via the ____________ pathway also contributes to neutrophil recruitment
alternative
49
Phagocytosis by macrophages results in the activation of what?
inflammasome Note: this leads to secretion of IL-1 and chemokines/other cytokines... all of which attracts more neutrophils
50
Spontaneous remission (of acute gout) can occur after how long?
Days to weeks
51
What are some characteristics of CHRONIC gout?
- chronic arthritis/chronic inflammation - development of tophi/urate crystals encrust the articular surface of the joint, forming deposits in the synovium - synovium becomes hyperplastic, fibrotic, and thickened with inflammatory cells (i.e.., pannus formation) - destruction of underlying cartilage leads to bone erosion - in severe cases, a fibrous or bony ankylosis can form, resulting in loss of joint function
52
What is the pathognomonic hallmark of gout?
tophi
53
90% of affected individuals experience acute attacks in what common locations?
- 1st metatarsal-phalangeal joint *** - insteps (top part of foot) ** - knees** - ankles - heels - wrists - elbows
54
True or False: lower limbs are more often affected than upper limbs
True
55
True or False: acute gout attacks are relatively pain-free
False Acute gout attacks may be excruciatingly painful as joints become inflamed (redness, swelling) If untreated, acute gouty arthritis may last for hours to weeks
56
True or False: In the absence of appropriate therapy, gout attacks recur at shorter intervals and frequently become polyarticular.
True
57
What is Lesch-Nyhan Syndrome?
A syndrome that can lead to hyperuricemia via: - deficiency of HGPRT (leading to accumulation of hypoxanthine and guanine, which ultimately break down into uric acid) - PRPP also accumulates and stimulates production of purine nucleotides, which ultimately break down into uric acid Hyperuricemia --> leads to urolithiasis and gouty arthritis usually presents with severe neurological problems
58
Calcium pyrophosphate crystal deposition disease (CPPD) is also known as what?
pseudogout
59
What is the prevalence of CPPD/pseudogout in those older than 85 years?
30-60% Note: prevalence of CPPD increases with age
60
True or False: Most cases of CPPD/pseudogout are sporadic
True However, other causes may include: - genetic component (autosomal dominant) - hyperparathyroidism - hemochromatosis - diabetes - hypothyroidism - some medications (not well defined)
61
Where do the calcium pyrophosphate crystals deposit?
in the matrix of the menisci & connective tissue of the joint
62
True or False: Similar to gout, in CPPD, macrophages phagocytose the crystals, neutrophils are recruited, and rupturing induces this inflammatory process to continue
True
63
How does CPPD/pseudogout present clinically?
- can be asymptomatic or can mimic osteoarthritis or rheumatoid arthritis - asymmetric - monoarticular or polyarticular - commonly affects KNEES - less common sites: wrists, shoulders, elbows, ankles - eventually, 50% patients have significant joint damage (therefore affecting mobility)
64
What is the standard treatment for CPPD/pseudogout?
no therapy is effective in preventing damage mostly symptomatic treatment (i.e., pain management)
65
Why do we do synovial fluid analysis?
- can let us know if we're dealing with septic arthritis (emergency), gout, pseudogout, hemarthroses, or rheumatic joint diseases Note: hemarthrosis and gout should also be managed "semi-urgently" - also distinguishes between an acute flare of gout or pseudogout and septic arthritis
66
When does a synovial fluid analysis have poor sensitivity and specificity?
When it's more difficult to visualize crystals (aka during the time in between flares)
67
When would you conduct a synovial fluid analysis?
Suspicion of: - infectious arthritis - flare of crystal arthritis - hemarthrosis (blood in the joint) - monoarthritis with or without a prior history of arthritis of other joints - trauma to a joint (with effusion)
68
What does a synovial fluid analysis analyze? (Hint: 3 C's)
1) CRYSTALS (what type?) 2) CELLS (if there's blood in the joint, we'll see more RBCs, whereas if there's inflammation there may be neutrophils/lymphocytes) 3) CULTURE (if there's microorganisms, would indicate that it's septic)
69
What would normal results be for a synovial fluid analysis?
Cells: less than 200ul (low) Crystals: Negative Culture: Negative
70
Synovial fluid analysis results for a patient with gout:
Cells: greater than 2000ul (high, but not as high as septic) Crystals: Birefringent, needle-shaped** Culture: Negative
71
Synovial fluid analysis results for a patient with pseudogout:
Cells: greater than 2000ul (high, but not as high as septic) Crystals: Birefringent, cuboidal** Culture: Negative
72
Synovial fluid analysis results for a patient with septic arthritis:
Cells: greater than 50, 000 (very high) Crystals: Negative Culture: Positive**
73
Synovial fluid analysis results for a patient with hemarthrosis:
Cells: lots of RBCs** Crystals: Negative Culture: Negative
74
What are some treatment options for gout?
- corticosteroids (to target inflammation; specific for gout = colchicine) - analgesics (pain relief; i.e., NSAIDs such as aspirin) - most common treatment - allupurinol (decrease uric acid production) - uricosurics, such as probenecid and sulfinpyrazone (increase uric acid excretion)
75
What is the mechanism of colchine (corticosteroid/anti-inflammatory) for gout?
Binds to tubulin and prevents microtubule polymerization Recall: microtubules are like "highways", so when we block these highways/prevent them from forming, you block the migration of leukocytes (mainly neutrophils), thereby decreasing inflammation Dosage to terminate an acute attack (just FYI): 1-1.2 mg every hour until attack abates or until diarrhea
76
True or False: Colchine cannot be used as a prophylactic
False Colchine, taken prophylactically, can reduce frequency of attacks Dose (FYI): 0.5mg/day for 3-4 days/week
77
What is the mechanism of allopurinol for treatment of gout?
it's a competitive inhibitor of xanthine oxidase (thereby decreasing production of uric acid) Note: CANNOT stop an acute attack, but can reduce frequency of attacks
78
What is the mechanism of uricosurics for treatment of gout?
Block tubular reabsorption of uric acid, thereby increasing excretion
79
Can allopurinol precipitate an attack of gout at the beginning of therapy?
Yes (because immune system is getting used to the change) aspirin typically given at beginning of allopurinol therapy
80
Can uricosurics precipitate an attack of gout at the beginning of therapy?
Yes (immune system is getting used to change)
81
True or false: uricosurics can be taken prophylatically
True

BMS150 Test 2 (10 decks)

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