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BMS150 test 2 > gout CPPD (wk5) > Flashcards

gout CPPD (wk5) Flashcards

1
Q

2 bases are?

A

pyrimidine (single ring) or purine (double ring)

pyrimidine= CUT
purine= :pure as gold” = AG

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2
Q

what are the bases in DNA vs RNA

A

ACTG vs ACGU

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3
Q

sugars

A

5 C ribose (RNA) or deoxyribose (DNA)

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4
Q

nucleoside vs nucleotide

A

nucloeside= sugar + base

nucleotide= nucleoside + 1-3 phosphates (i.e. ATP)

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5
Q

ine vs dine or sine endings

A

ine= bases

sine or dine = nucleoside

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6
Q

3 pyridines to know

A
  1. cytosine (cytidine)
  2. thymine (thymidine) (in DNA)
  3. uracil (uridine) (in RNA)

CUT ACRONYM!

Note “ine” (DNA bases) to “dine” endings (nucleosides)

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7
Q

4 purines to know

A

pure as gold = AG + 2 more (HX)

  1. adenine (adenosine)
  2. guanine (guanosine)
  3. xanthine (xanthosine)
  4. hypoxanthine (inosine)

Note “ine” (bases) to “sine” endings (nucleosides)

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8
Q

pathways for pyrimidine vs purine nucleotide synthesis

A

purine
1. de novo pathway
2. salvage pathway

pyrimidine
1. de novo pathway

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9
Q

what is activated ribose AKA

A

phosphoribosyl pyrophosphate PRPP

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10
Q

de novo pathway for purine nucleotide biosynthesis

A

activated ribose (PRPP) + amino acids + ATP +CO2

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11
Q

salvage pathway for purine nucleotide biosynthesis

A

activated ribose (PRPP) + base

the base comes from diet, cell turnover

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12
Q

3 main steps of de novo synthesis of purines

A

PRPP –> phosphoribose (via glutamine adding nitrogen) –> IMP

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13
Q

after IMP is made in de novo synthesis of purines what are the 2 next options

A

make AMP (via GTP)
or
make GMP (via ATP)

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14
Q

reciprocal control in purine de novo synthesis; when ATP is high you
make ??, when GTP is high is make ??

A

ATP is high you make GMP, when GTP is high is make AMP

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15
Q

why is salvage pathway for purine synthesis needed

A
  • Important to have, as de novo uses lots of energy
  • Uses hypoxanthine, guanine, and adenine bases that already exist
    –> via diet, cell turnover
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16
Q

what 2 enzymes could be needed in the purine salvage pathway

and what reaction do they catalyze

A

HGPRT or APRT

Hypoxanthine-guanine phosphoribosyl transferase
(HGPRT)

Adenine phosphoribosyltransferase (APRT)

useed to catalyze the addition of phosphoribose (sugar+P) from
PRPP to:… the prodcut

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17
Q

Hypoxanthine-guanine phosphoribosyl transferase
(HGPRT) is used to make 2 products in purine salvage pathway what are they

A

hypoxanthine = IMP
guanine = GMP

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18
Q

what are the 2 substrates for the ring in pyrimidine nucleotide synthesis

A

Carbamoyl phosphate (made from glutamine, ATP, CO2)

▪ Aspartate

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19
Q

Adenine phosphoribosyltransferase (APRT) is used to make 1 product in purine salvage pathway what is it

A

adenine to make AMP

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20
Q

what is the difference for pyrimidine vs purine nucleotide synthesis

A

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

▪ Opposite to purines, where the ring is constructed directly on the ribose-5-P

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21
Q

how to make CTP from UMP in pyrimidine nucleotide synthesis

A

UMP –> UTP via phosphorylating (2x)

UTP –> CTP via adding nitrogen (aminated) via glutamine

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22
Q

how to make dTMP from UMP in pyrimidine nucleotide synthesis

A

UMP –> UDP (phosphorylated via kinase)

UDP –> dUMP (deoxugenate)

dUMP –> dTMP (methylated vis folate coenzyme)

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23
Q

what removes phosphate from nucleotides to release nucleosides (catabolism)

A

nucleotidases

24
Q

what do pyrimidine bases degrade to

A

▪ Cytosine to uracil and ultimately alanine

(remove sugar to relaase base)

25
what do purine bases get degraded to
First to xanthine, then uric acid * Uric acid is eventually excreted in urine * Elevated levels can lead to hyperuricemia and gout ▪ Conversion of hypoxanthine to xanthine, and xanthine to uric acid, uses the enzyme xanthine oxidase
26
what enzyme for hypoxanthine --> xanthine --> uric acid
xanthine oxidase
27
what is gout
* Can be due to underexcretion (most common) or overproduction (less common) of uric acid→ hyperuricemia * Hyperuricemia can lead to gout joint inflammation due to deposition of urate crystals
28
what is gouty arthritis
▪ Deposition of monosodium urate crystals in the joints → immune cells mount an inflammatory response to crystals * Known as gout (gouty arthritis)
29
what is chronic topaceous gout
Nodular masses of monosodium urate crystals (tophi) may be deposited in soft tissues * Known as chronic tophaceous gout
30
what is urolithiasis
Uric acid stones can form in the kidneys seen in gout
31
what enzymes do humans lack that can lead to gout
uricase * Humans lack uricase, the enzyme responsible for the degradation of uric acid in other mammals ▪ Uric acid is also highly reabsorbed in the urine ▪ Major modifiable risk factors include diets rich in alcohol (beer has quite a few purines) and meat (especially organ meats), asparagus * Non-modifiable include male sex (much more common in guys) and decreased renal excretion
32
gout etiology
* Increased uric acid production: ▪ Enzyme defects in degradation of uric acid ▪ Rapidly-dividing cancers – i.e. leukemia * Decreased uric acid excretion (in the kidneys) ▪ Idiopathic ▪ Chronic kidney disease
33
how are urate crystals activated in gout
phagocytosed by macrophages Urate crystals are phagocytosed by macrophages, activating them ▪ They then release chemokines that attract neutrophils into the joint, found within the synovial fluid * Neutrophilsmediatejoint inflammation Complement activation via the alternative pathway also contributes to neutrophil recruitment.
34
which cytokine is released when inflammasome is activated
IL1 Phagocytosis by macrophages results in activation of the inflammasome ▪ Secretion of IL-1 ▪ Further promotes accumulation of neutrophils and macrophages within the joint * Release cytokines, free radicals, proteases, & arachidonic acid metabolites
35
what happens in chronic gout
Chronic gout leads to chronic arthritis with joint erosion, chronic inflammation, development of pannus, and 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 (ie. 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.
36
what is a pathognomic hallmark of gout
tophi * 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 or kidneys * Earlobes, fingertips
37
which joints does gout effect
1st MTP!!! * 1st metatarsal-phalangeal joint, insteps, ankles, heels * Knees, wrists, elbows * Fingers * Lower limbs are more often affected than upper --> become more polyarticular if chronic
38
how long to get chronic topahceous arthritis in gout
12 years
39
what enzyme is deficient in leech nyhan syndrome and what does this causes an accumulation of
HGPRT accumulation of hypoxanthine and guanine which break down into uric acid PRPP also accumulate and stimulates production of purine nucleotides which ultimately breakdown into uric acid
40
leech nyhan syndrome
hyperuricieamia deficient HGPRT Hyperuricemia frequently results in urolithiasis and gouty arthritis
41
psuedogout AKA calcium pyrophosphate crystal deposition disease (CPPD) causes
▪ Some have a genetic component (autosomal dominant) ▪ Can be caused by hyperparathyroidism, hemochromatosis, diabetes, hypothyroidism ▪ Some medications may trigger pseudogout – this is poorly-defined, though increased with age
42
what is the pathology of pseudo gout
▪ Crystals deposit in matrix of menisci, connective tissue of joint ▪ Rupture, eliciting inflammation as macrophages phagocytose the crystals ▪ Recruit neutrophils, which are thought to mediate inflammatory damage
43
what joint is most effected in psuedogout
knees
44
clinical presentation of gout
▪ Can be asymptomatic – can mimic osteoarthritis or rheumatoid arthritis ▪ Asymmetric, can be monoarticular or polyarticular ▪ Commonly affects knees, less common sites are wrists, shoulders, elbows, ankles ▪ Eventually 50% have significant joint damage (affects mobility)
45
synovial fluid analysis
to distinguish between septic arthritis, gout, pseudogout, hemarthroses and rheumatic joint diseases do if think have infectious arthritis, flare of crystal arthritis, or hemarthrosis, mono arthritis, trauma to joint with effusion * Septic arthritis must be managed urgently * Hemarthrosis and gout should also be managed (semi- urgently)
46
3 C's of synovial fluid analysis
▪ Crystals – seen under microscopy with gout and pseudogout ▪Cells–redbloodcells? Leukocytes(neutrophilsor lymphocytes) ▪ Culture – any microorganisms growing in there?
47
which disorder is the only one that is positive for a culture (of microorganisms)
septic arthritis
48
crystal shape in gout vs psuedogout
gout: birefringent, needle spa[ed psuedogout: biregringent, cuboidal
49
anti gout agents
▪ Target the inflammation * General: Corticosteriods (previous lecture) * Specific to gout: Colchicine ▪ Analgesics * NSAIDs (ex aspirin) (previous lecture) ▪ Most common treatment ▪ Decrease uric acid production * Allopurinol ▪ Increase uric acid excretion * Uricosurics (probenecid and sulfinpyrazone)
50
what is colchine
corticosteroid for gout
51
how does colchine drug work
Binds tubulin and prevents microtubule polymerization so that leukocytes (neutrophils) cant migrate; decrease inflammation can reduce frequency of attacks
52
53
adverse effects of colchine drug
bone marrow depression and vomit, ab pain, diarrhea
54
what does Allopurinol do
Decrease uric acid production
55
what does Uricosurics do
Increase uric acid excretion
56
what is allopurinol a competitive inhibitor of
xanthine oxidase Can precipitate an attack of gout at the beginning of therapy – why? * As uric acid concentrations go down, crystals start to dissolve and the immune system responds ▪ Typically give aspirin at beginning of allopurinol therapy to reduce pain
57
uricosurics action
Block tubular reabsorption of uric acid, increasing excretion

BMS150 test 2 (18 decks)

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