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PATHO/PHARM II > Conditions Effecting the Musculoskeletal System and PharmacotherapyPart Five: Inflammatory DX - Gout > Flashcards

Conditions Effecting the Musculoskeletal System and PharmacotherapyPart Five: Inflammatory DX - Gout Flashcards

Exam 4 (Final)

1
Q

Patho of Gout

Normal A&P
Purines: How are they found in the body?

A

Found naturally in body

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2
Q

Patho of Gout

Normal A&P
Purines: When does the body produce uric acid?

A

Body produces uric acid (UA) when it breaks down purines

Purines –> UA

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3
Q

Patho of Gout

Normal A&P
Purines: What kind of foods are they in?

A

Foods: Organ meats, shellfish, anchovies,
herring, asparagus, mushrooms, salmon, beer, high fructose sugar-sweetened beverages

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4
Q

Patho of Gout

Normal A&P
Purines: What kind of products are formed from the breakdown of purines?

A

Waste product formed from the breakdown of purines

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5
Q

Patho

Normal A&P:

What is UA formation dependent on?

A

UA formation is pH dependent

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6
Q

Patho

What is Gout?

A

Type of inflammatory arthritis

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7
Q

Patho

When does gout occur?

A

Occurs from deposits of urate crystals formed from high levels of uric acid in the blood, body or synovial fluids (hyperuricemia)

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8
Q

Patho

What two things must occur for gout to form?

A

Overproduction/Underexcretion of UA

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9
Q

Gout:

Elevated level of Uric Acid leads to what kind of deposits and where?

A

Elevated level of UA –> needle-shaped deposits of monosodium urate crystals in/around joints

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10
Q

Gout:

How does immune system react to uric acid crystals?

A

The immune system reacts to these crystals, causing intense inflammation and pain.

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11
Q

Gout:

What do leukocytes do?

A

Infiltration of leukocytes inside synovial cavity phagocytize crystals

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12
Q

Gout:

What does the breakdown of crystals lead to?

A

Crystals breakdown –> release of destructive enzymes

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13
Q

Gout:

What forms in affected joints from crystal deposition?

A

Large, gritty deposits (tophi) form in affected joint from crystal deposition in subcu tissues

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14
Q

Gout:

Large, gritty deposits (tophi) form in affected joint from crystal deposition in subcu tissues:

What situations does this happen?
How does it appear?

A

Happens in chronic gout

Appears as lumps, nodules

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15
Q

Gout:

Large, gritty deposits (tophi) form in affected joint from crystal deposition in subcu tissues:

What does it develop with?

A

Develops with long-standing hyperuricemia, recurrent gout attacks

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16
Q

Gout:

Large, gritty deposits (tophi) form in affected joint from crystal deposition in subcu tissues:

What can it cause?

A

Can cause joint damage, ulceration if skin over tophi breaks down

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17
Q

Prevalence:

What is the most common inflammatory arthritis in older adults?

A

Gout

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18
Q

Prevalence:
Gout
How are women affected compared to men?

A

Men affected three times as often as women

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19
Q

Prevalence:
Gout
What ethnicity are incidences higher in?

A

Incidences higher among African Americans

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20
Q

Prevalence:
Gout
What is the peak age to develop gout in men? How are incidences with age (men and women)

A

Men (age 40-50 peak age)

Increased age

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21
Q

Gout: Predisposing Factors (other factors beside hyperuricemia)

A

Genetic predisposition (deficiency of enzyme –> increase UA), fam hx

Obesity, kidney disease, DM, HF

High alcohol consumption

Low urinary pH

Diuretics

Dietary intake of purine-rich food (e.g., red meat, shellfish), alcohol, and sugary beverages

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22
Q

Complex series of events in Gout:

What triggers an inflammatory response?

A

Crystals trigger inflammatory response

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23
Q

Complex series of events in Gout:

When crystals trigger inflammatory response, what is activated?

A

Activation of cytokines, interleukins

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24
Q

Complex series of events in Gout:

When crystals trigger inflammatory response, what occurs next (having to do with neutrophils)?

A

Draws out neutrophils from circulation attracted to site of crystal deposition, phagocytizes the crystals

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25
Q

Complex series of events in Gout:

When crystals trigger inflammatory response, what kind of damage occur??

A

Tissue damage

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26
Q

Complex series of events in Gout

What is an acute gouty attack?

A

Acute Gouty Attack: The inflammatory response leads to sudden and severe pain, swelling, redness, and warmth in the affected joint.

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27
Q

Clinical Manifestations of Gouty Arthritis

What are signs and symptoms?

A

Warm to touch, red, swollen, stiff, and extremely painful joint

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28
Q

Clinical Manifestations of Gouty Arthritis

What formation occurs? Where? When does this formation occur?

A

Tophi formation, usually on the affected joint, great toe, the extensor surfaces, or the forearm, or in the pinnae of the ear; occurs a few years after the first attack

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29
Q

Clinical Manifestations of Gouty Arthritis

What causes the acute inflammatory response seen in gout?

A

Uric acid crystals and urate crystals in the joint synovia fluid causing an acute inflammatory response

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30
Q

Clinical Manifestations of Gouty Arthritis

What causes a local inflammatory response seen in gout?

A

Hard nodule(s) painless from urate crystals in soft tissue or bone causing a local inflammatory response

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31
Q

Clinical Manifestations of Gouty Arthritis

What are deposits of crystals surrounded by?

A

Accumulation of urate crystals

Deposits of crystals surrounded by inflammatory cells, collagen fibers, and sometimes calcium deposits.

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32
Q

Gout

Clinical Manifestations: What can happen to joints (other than uric crystal build up)?

A

Tophi in/around joints

Abrupt attacks in joint

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33
Q

Gout

Clinical Manifestations: What will reoccur?

A

Recurrent arthritic attacks

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34
Q

Gout

Clinical Manifestations: Where are the sites where abrupt attacks on joints occur?

A

Joint of great toe
Hot, red, tender, swollen
Stiff, aching

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35
Q

Gout

Clinical Manifestations: What are other symptoms?

A

Severe pain

Lymphagitis & systemic sx

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36
Q

Gout

Clinical Manifestations: When does severe pain occur?

A

Mostly at night

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37
Q

Gout

Clinical Manifestations: Lymphagitis & systemic sx include what?

A

Fever, leukocytosis

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38
Q

Gout

Clinical Manifestations:

When do Untreated attacks subside?
mild v severe. How are symptom resolution?

A

Subside several hours –> 1-2 days

Severe – days/weeks

Sx resolve upon recovery

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39
Q

Clinical Manifestations:

Evaluation and Treatment

What would you evaluate?

A

High uric acid levels

Elevation sedimentation rate (ESR)

BUN & Creat

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40
Q

Clinical Manifestations:

Evaluation and Treatment:

What is non-pharmacological treatment?

A

Ice

Monitor diet

Fluids to dilute UA in blood, reducing saturation, support kidney function, prevent stones

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41
Q

Clinical Manifestations:

Evaluation and Treatment:

Non-pharmacological treatment: What should be avoided?

A

Avoid weight-bearing on joint

Avoid etoh

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42
Q

3 phases of Gout

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis
  3. Tophaceous gout
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43
Q

3 phases of Gout

Asymptomatic hyperuricemia:
How do labs appear?

A

Elevated serum urate level

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44
Q

3 phases of Gout

Asymptomatic hyperuricemia: What is not present in this stage?

A

Arthritic sx, tophi, renal stones - not present

45
Q

3 phases of Gout

Asymptomatic hyperuricemia: How long does this stage persist?

A

This stage may persist throughout life

46
Q

3 phases of Gout

Acute gouty arthritis: How do attacks develop?

A

Attacks develop with increased serum urate concentrations

47
Q

3 phases of Gout

Acute gouty arthritis: How do attacks tend to occur?

A

Tends to occur with sudden or sustained increases of hyperuricemia

48
Q

3 phases of Gout

Acute gouty arthritis: What can trigger it?

A

Can be triggered by trauma, drugs, alcohol

49
Q

3 phases of Gout

Tophaceous gout: What kind of stage is it?

A

Chronic stage

50
Q

3 phases of Gout

Tophaceous gout: When does it begin?

A

Can begin anywhere from 3 to 40 years after initial attack of gouty arthritis

51
Q

3 phases of Gout

Tophaceous gout: What appears and why?

A

Progressive inability to excrete UA –> crystal deposits (tophi) appear in cartilage, synovial membranes, tendons, soft tissue

52
Q

Overview of Drug Therapy

What are the two groups of drugs?

A

Short-term to relieve symptoms of attack (Anti-inflammatory)

Long-term to lower blood levels of uric acid

53
Q

Overview of Drug Therapy

Short-term to relieve symptoms of attack (Anti-inflammatory)

What kind of flareups are they used for?

A

Infrequent flare-ups (fewer than 3 times/year)

54
Q

Overview of Drug Therapy

Short-term to relieve symptoms of attack (Anti-inflammatory)

What is the first line medication? What is it used for? When does relief occur?

A

NSAIDs: First-line agents to suppress inflammation – marked relief after 24h

55
Q

Overview of Drug Therapy

Short-term to relieve symptoms of attack (Anti-inflammatory)

What are other medications used? What is it used for? When does relief occur?

A

Glucocorticoids also used

Colchicine

56
Q

Overview of Drug Therapy

Short-term to relieve symptoms of attack (Anti-inflammatory)

How are meds tolerated?
When should meds be started?

A

Better tolerated
More predictable
Start ASAP after sx onset

57
Q

Overview of Drug Therapy

Long-term to lower blood levels of uric acid

What kind of drugs does this include?

A

Uricosuric drugs

Allopurinol

58
Q

Overview of Drug Therapy

Long-term to lower blood levels of uric acid

What does Uricosuric drugs do?

A

Uricosuric drugs to decrease UA production & increase UA excretion

59
Q

Overview of Drug Therapy

Long-term to lower blood levels of uric acid- what are they used for specifically?

A

Used for chronic gout, tophaceous gout, frequent attacks (3+ per yr)

60
Q

Overview of Drug Therapy

What is not recommended while taking Gout meds?

A

Breast-feeding is not recommended for other drugs taken for gout.

61
Q

Colchicine (anti-inflammatory):

What is it used to treat? What does this increase and lead to?

A

Treats acute gouty attack/flares (high dose) – increases joint movement, inflammation gone 2-3d

62
Q

Colchicine (anti-inflammatory):

What does this reduce?

A

Reduces incidences of attack

Decreases pain & inflammation

63
Q

Colchicine (anti-inflammatory):

What does this do to an impending attack?

A

Aborts an impending attack

64
Q

Colchicine (anti-inflammatory)

What is it used short term and long term for?

A

Short-term tx of gout flare & long-term to prevent (low dose) attacks from recurring

65
Q

Colchicine (anti-inflammatory)

MOA
Anti-Inflammatory Effects:
What does it inhibit?

A

Inhibits the migration of neutrophils to the site of inflammation & leukocyte infiltration.

66
Q

Colchicine (anti-inflammatory)

MOA
Anti-Inflammatory Effects:
What does it disrupt?

A

Disrupts microtubules

67
Q

Colchicine (anti-inflammatory)

MOA
Anti-Inflammatory Effects:
What are Microscopic hollow tubes required for?

A

Microscopic hollow tubes required for cell movement, cell division

68
Q

Colchicine (anti-inflammatory)

MOA
Anti-Inflammatory Effects: What plays a key role in inflammatory response in gout?

A

Neutrophils play a key role in the inflammatory response in gout.

69
Q

Colchicine (anti-inflammatory)

MOA
Anti-Inflammatory Effects: What does neutrophils do exactly?

A

They are attracted to the urate crystals in joints and release inflammatory mediators, causing pain and swelling.

70
Q

Colchicine (anti-inflammatory)

MOA
Anti-Inflammatory Effects: What does this drug do? What does this lead to?

A

By preventing the migration of neutrophils, colchicine reduces inflammation and the severity of gouty attacks.

71
Q

Colchicine

Pharmacokinetics: How is it absorbed?Metabolized? Excreted?

A

PKs: readily absorbed, with or without meals, met by liver, renal excretion

72
Q

Colchicine :

Adverse effects:

A

Severe GI ADE during tx of acute attacks ~ n/v/d, abdominal pain

Myelosuppression

Myopathy

73
Q

Colchicine :

Adverse effects: Severe GI ADE during tx of acute attacks ~ n/v/d, abdominal pain

What should be done if this occurs?

A

D/C regardless of joint pain!!!

74
Q

Colchicine :

Adverse effects: Severe GI ADE during tx of acute attacks ~ n/v/d, abdominal pain

Why does this occur?

A

Injury to rapidly proliferating cells of GI epithelium – toxic to any tissue with large % of proliferating cells

75
Q

Colchicine :

Myelosuppression

A

Injury to rapidly dividing cells

76
Q

Colchicine :

Myopathy: What occurs?

A

Rhabdomyolysis (muscle breakdown) with LT low dose tx

77
Q

Colchicine :

Myopathy: What should be monitored?

A

Monitor for sx of muscle injury (tenderness, pain, weakness)

78
Q

Colchicine :

Myopathy:

What should this medication be used cautiously with?

A

Caution with concurrent statins

79
Q

Hyperuricemia drug: Urate-lowering tx (ULT):

What is this used for?

A

ULT is for frequent gouty attacks

80
Q

Hyperuricemia drug: Urate-lowering tx (ULT):

What does it do?

A

Dissolves urate crystals

81
Q

Hyperuricemia drug: Urate-lowering tx (ULT):

What does it prevent?

A

Prevent new crystals & disease progression

82
Q

Hyperuricemia drug: Urate-lowering tx (ULT):

What does it prevent? What does it improve?

A

Reduce frequency of acute attacks

Improve quality of life

83
Q

Hyperuricemia drug: Urate-lowering tx (ULT):

What kind of effect does it not have? So what should it NOT be used for?

A

No anti-inflammatory effects

so ⍉ use against acute gouty attack or pain directly

84
Q

Hyperuricemia drug: Urate-lowering tx (ULT):

What is the prototype drug?

A

Prototype drug: Allopurinol

85
Q

Xanthine Oxidase Inhibitors:

What is the prototype?

A

Allopurinol

86
Q

Xanthine Oxidase Inhibitors:

Allopurinol: What is it used for specifically?

A

Use: chronic tophaceous gout

87
Q

Xanthine Oxidase Inhibitors:

Use: chronic tophaceous gout
How does it stop chronic tophaceous gout?

A

Prevents new tophi from forming

Lessens tophi that have already formed

88
Q

Xanthine Oxidase Inhibitors:

Use: chronic tophaceous gout
What does it do to joint function?

A

Better joint function

89
Q

Xanthine Oxidase Inhibitors:

Use: chronic tophaceous gout
What does it do to serum uric acid levels?

A

Lowers serum uric acid levels

90
Q

Xanthine Oxidase Inhibitors:

Use: chronic tophaceous gout
What does it prevent? What does it not do?

A

Prevents but does not relieve acute gout attack

91
Q

Xanthine Oxidase Inhibitors

MOA

A

Inhibits xanthine oxidase (XO), the enzyme required for UA formation from breakdown of DNA products

92
Q

Xanthine Oxidase Inhibitors

ADEs

A

Mild GI effects, drowsiness, metallic taste and exacerbation of gouty attacks

Paradox acute attack w/ initiation

Hypersensitivity syndrome

93
Q

Xanthine Oxidase Inhibitors

ADEs: What ADE occurs with initiation?

A

Paradox acute attack w/ initiation

94
Q

Xanthine Oxidase Inhibitors

Paradox acute attack w/ initiation: What may initial therapy elicit?

A

Initial therapy may elicit acute gouty attack from urate crystals being shed into the joint space

95
Q

Xanthine Oxidase Inhibitors

Paradox acute attack w/ initiation:
How could this be avoided?

A

Prevented by co-administration with colchicine or low-dose NSAID

96
Q

Xanthine Oxidase Inhibitors

Paradox acute attack w/ initiation: What should you tell patients?

A

Forewarn pts & educate not to stop med in an attack

97
Q

Xanthine Oxidase Inhibitors

Paradox acute attack w/ initiation: When should you not start this medication (XIO)?

A

Don’t start in attack

98
Q

Xanthine Oxidase Inhibitors

Who may it be given to?

A

May be given to children under 6 years old to treat hyperuricemia associated with cancer therapy

99
Q

Allopurinol:

ADEs: Hypersensitivity syndrome

How common is it? How is it seen?

A

Rare, but potentially fatal

100
Q

Allopurinol:

ADEs: Hypersensitivity syndrome

What kind of symptoms are seen?

A

Eosinophilia, hepatic & renal dysfunction, rash

101
Q

Allopurinol:

ADEs:

What is a situation in which this med should be dc’d?

A

D/C if (+) fever, 1st sign of rash

Rash ALL Over – ALLopurinol – could be deadly, even a mild rash

102
Q

Allopurinol:

ADEs:

What can a rash progress to?

A

Can progress to SJS, TENS

103
Q

Allopurinol:

ADEs:

What may be required for treatment for ADEs?

A

Some may require hemodialysis or GCs if ⍉ spontaneous recovery

104
Q

Allopurinol

Interactions

A

Can inhibit hepatic drug-metabolizing enzymes, delaying inactivation of other drugs

105
Q

Allopurinol

Interactions: Can inhibit hepatic drug-metabolizing enzymes, delaying inactivation of other drugs

So what must be monitored?

A

Monitor LFTs

106
Q

Allopurinol

Interactions: What drugs?

A

Warfarin

Ampicillin

107
Q

Allopurinol

Interactions: If warfarin is used, what should be done?

A

decrease dose is warranted

108
Q

Allopurinol

Interactions: If ampicillin is used, what could be occur? What should be done?

A

Combo TX ~ rash

D/c if occurs

PATHO/PHARM II (27 decks)

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