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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
Q

what do purine bases get degraded to

A

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
Q

what enzyme for hypoxanthine –> xanthine –> uric acid

A

xanthine oxidase

27
Q

what is gout

A
  • 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
Q

what is gouty arthritis

A

▪ Deposition of monosodium urate crystals in the joints → immune cells mount an inflammatory response to crystals
* Known as gout (gouty arthritis)

29
Q

what is chronic topaceous gout

A

Nodular masses of monosodium urate crystals (tophi) may be deposited in soft tissues
* Known as chronic tophaceous gout

30
Q

what is urolithiasis

A

Uric acid stones can form in the kidneys

seen in gout

31
Q

what enzymes do humans lack that can lead to gout

A

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
Q

gout etiology

A
  • 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
Q

how are urate crystals activated in gout

A

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
Q

which cytokine is released when inflammasome is activated

A

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
Q

what happens in chronic gout

A

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
Q

what is a pathognomic hallmark of gout

A

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
Q

which joints does gout effect

A

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
Q

how long to get chronic topahceous arthritis in gout

A

12 years

39
Q

what enzyme is deficient in leech nyhan syndrome

and what does this causes an accumulation of

A

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
Q

leech nyhan syndrome

A

hyperuricieamia

deficient HGPRT

Hyperuricemia frequently results in urolithiasis and gouty arthritis

41
Q

psuedogout AKA calcium pyrophosphate crystal deposition disease (CPPD) causes

A

▪ 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
Q

what is the pathology of pseudo gout

A

▪ 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
Q

what joint is most effected in psuedogout

A

knees

44
Q

clinical presentation of gout

A

▪ 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
Q

synovial fluid analysis

A

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
Q

3 C’s of synovial fluid analysis

A

▪ Crystals – seen under microscopy with gout and pseudogout
▪Cells–redbloodcells? Leukocytes(neutrophilsor lymphocytes)
▪ Culture – any microorganisms growing in there?

47
Q

which disorder is the only one that is positive for a culture (of microorganisms)

A

septic arthritis

48
Q

crystal shape in gout vs psuedogout

A

gout: birefringent, needle spa[ed

psuedogout: biregringent, cuboidal

49
Q

anti gout agents

A

▪ 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
Q

what is colchine

A

corticosteroid for gout

51
Q

how does colchine drug work

A

Binds tubulin and prevents microtubule polymerization

so that leukocytes (neutrophils) cant migrate; decrease inflammation

can reduce frequency of attacks

52
Q
A
53
Q

adverse effects of colchine drug

A

bone marrow depression

and vomit, ab pain, diarrhea

54
Q

what does Allopurinol do

A

Decrease uric acid production

55
Q

what does Uricosurics do

A

Increase uric acid excretion

56
Q

what is allopurinol a competitive inhibitor of

A

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
Q

uricosurics action

A

Block tubular reabsorption of uric acid, increasing excretion

BMS150 test 2 (18 decks)

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