Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FS V, Final > 4A. Arthritis and Gout > Flashcards

4A. Arthritis and Gout Flashcards

1
Q

Arthritis
____ of a joint, usually accompanied by pain, swelling, and stiffness, and resulting from infection,
trauma, degenerative changes, metabolic disturbances, or other causes.

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q 
Rheumatoid Arthritis (RA)
(the most \_\_\_\_ \_\_\_\_, \_\_\_\_ arthritis)
A

common
autoimmune
inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

RHEUMATOID ARTHRITIS DEFINITION

  1. Progressive, ____, inflammatory disorder
  2. Predominantly affecting ____ membranes of diarthrodial joints; ____
  3. ____ manifestations occur in most
  4. ____ etiology
  5. ____ predisposed host
A 
systemic
synovial
symmetric
extraarticular
unknown
genetically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

RHEUMATOID ARTHRITIS EPIDEMIOLOGY

  1. About ____% of total adult population affected by RA
  2. ____ distribution
  3. ____ ethnic groups
  4. Can occur at any ____
  5. Peak incidence ages ____
  6. Prevalence 2.5 x higher in ____
  7. ____ clusters
  8. Triggers: ____, periodontal disease?, others
A 
1
worldwide
all
age
30-50
women
familial
smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Joint anatomy

This diagram can represent a knee or finger joint, it is meant to represent any joint

  • at end of bones you find ____ cartilage
  • lining the joint capsule, which provides structural integrity to the joint), is the ____
  • thin membrane that lines capsule and extends across the bone that is within this ____ space
  • provides ____ to the joint and lubricating fluid
  • inflammation from RA sets in the ____
A 
articular
synovium
joint
lubrication
synovium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology Cartoon

this is a knee joint:

  • bones
  • ____ cartilage
  • joint capsule
  • synovium membrane lining the capsule
  • ____ (specific to the knee)

In RA there is chronic inflammation developing in ____
-hypertrophy
-hyperplasia
As the disease becomes more chronic, the synovium becomes larger and can be seen and felt in examination (called ____ At this stage)

Synovium continues bringing in inflammatory cells to the joint and can ____ the bone around it causing damage. It is ____ at this point so the objective is to prevent the dx from getting to this stage.

A 
articular
meniscus
synovium
pannus
erode
irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
Pathophysiology, Slide 1
genetically \_\_\_\_ host
->
? exogenous factors,
? breach in tolerance
->
synovial membrane hyperplasia, \_\_\_\_ infiltration (lymphocytes, macrophages)
->
\_\_\_\_ inflammation
A

predisposed
cellular
chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology Slide 2

chronic inflammation
->
____ production (TNF, IL1, IL6)
->
____ formation (synovial fibroblast hyperplasia)
->
structural damage of cartilage and ligaments; ____ of bone

A

cytokine
pannus
erosion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

RA affects ____ more often.

Ppl wake up feeling stiff for more than an hour (so more common in the ____)

In hands the ____ joints are most commonly affected (where the finger attaches to the hand).

Also the ____ joing in middle of the finger.

Other common joints: ____ (30% of pts), ____ spine (important for pts being anesthetized for surgery as they are at risk of spine damage due to inflammation). Rest of the joints are listed, RA doesn’t commonly affect ____.

A 
hands and feet
mornings
MCP
PIP
TMJ
cervical
lower or middle back
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Rheumatoid Arthritis: Early Joint Involvement

____ region swelling in digit 2, 3 and 5. Sparing (sp?) at digit 4 Some ____ seem swollen.

Distal interphalangeal joints don’t have much swelling (doesn’t clarify which ones those are)

It will be roughly ____ in other hand

A

MCP
PIP
symmetrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

RA: Late Disease

Late disease looks like this.

Prolonged inflammation around MCP joints causes ____ of the digits (fingers slide off and go in the ulnar wrist direction, known as ____)

Skin appears ____ and vessels are easily seen, which is common in RA

____ in PIP joints (doesn’t clarify what that means). Nodules of inflammation in subcutaneous tissue known as ____ usually on extensor surfaces of joints

Muscles appear less ____, wasting is common since fingers are no longer functional

A

subluxation
ulnar deviation

thin

nodules
rheumatoid nodules

developed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Erosions

Pannus can eat away at ____ as seen in this ____ stage radiograph

Another example of the bone degradation. Top bone in image looks fine but bottom has a ____ taken out of it. Typical sign of erosion

A

bones
late

bite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Extraarticular Manifestations of RA

Extraarticular manifestations:

  • skin ____
  • rheumatoid nodules
  • muscle wasting
  • ____ eyes and mouth
  • scleritis (inflammation of part of the eye)
  • ____(inflammation of lungs)
  • inflammations around heart
  • ____ enlargement
  • splenomegaly
  • ____ from chronic inflammation
A 
thinning
dry
pleural effusions
lymph node
anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Importance of Early Diagnosis

  1. RA is ____, not benign
  2. Structural damage occurs ____
  3. Slower progression of disease is linked to ____ treatment
  4. Advanced disease associated with ­increased morbidity and mortality
    – Life expectancy shortened ____ years
A

progressive
early
earlier
10-15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2002 ACR Treatment Algorithm for RA

this is an algorithm for treating RA -treat the disease ____

DMARD (diesase modifying anti-rheumatic drug): tx symptoms and slows down the ____
____ also used for tx disease
____ also used
Skips without reading anything else

A

early

progression
NSAIDs
corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Evolution of RA Treatment

Earl drugs include compounds with elemental ____ in them. Not used much anymore

Hydroxychloroquine (sp?) and corticosteroids initially synthesized around the 50s, sulfasalazine sp?), all still used
azathriapine is used not so much for RA but other conditions

D Penicilamin not used very frequently

____ is the standard of care for RA. Used aggressively in the 80s, only helped about ____% of pts

Biologic DMARDs (injectable and IV) target inflammatory cytokines and were developed in the 90s and 00s to supplement \_\_\_\_ DMARDs and MTX
More ppl go into remission now than in the past
A

gold
methotrexate
50
oral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Non-steroidal Anti-inflammatory Drugs (NSAID’s)

PRO’s

  • ____
  • analgesic
  • improve ____, Flexibility, ROM (range of motion)
  • improve quality of life

CON’s

  • no effect on disease ____
  • frequent ____ effects (liver, renal, gut, coagulation)
A

antiinflammatory
mobility
progression
side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NSAIDs and Cyclo-oxygenase: Arachidonic Acid Metabolism

Mechanism of Action: Inhibit ____ which breaks down arachidonic acid to prostanoids and thromboxane

____ are the main cuprit in causing inflammation

A

cyclooxygenase

prostanoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Prostanoids as Mediators of Inflammation

• Inflammatory pain (____)
– ____
– ____ (2)

• Redness (____)
– ____
– ____ (2)

• Heat (____)
– Local ____,
central Fever
– ____ (1)

• Swelling (____)
– ____, edema and leucocyte filtration and chemotaxis
– ____ (3)

A

dolor
nociception
PGE2 and PGI2

rubor
vasodilation
PGE2 and PGI2

calor
vasodilation
PGE2

tumor
vasodilation
PGI2, PGE2, and PGD2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

NSAID MOA and Biological Effects

Antiinflammatory MOA:
1. Primary: inhibition of
biosynthesis of ____

  1. Secondary (depends on NSAID):
    - inhibition of ____
    - down-regulation of IL-1
    production
    - decreased production of ____ and superoxide

Uses:

  1. ____
  2. Anti-inflammatory
  3. ____
  4. drug-specific indications
A 
prostanoids
chemotaxis
free radicals
analgesic
antipyretic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

NSAID General Side Effects (i.e. What happens when you interfere with COX function?)

  1. ____: dyspepsia, stomach or duodenal ulceration; increased liver enzymes
  2. ____: fluid and salt retention, edema, hypertension, acute renal failure
  3. blood: ____ bleeding time

Other: skin ____, heart failure, hyperkalemia, confusion, bronchospasm, rash

A

gastrointestinal
renal
increased
photosensitivity

22
Q

Acetylsalicylic Acid: Aspirin

General:

  1. ____ NSAID
  2. ____ inhibits COX
  3. ____ bleeding time which requires 8-10 days for return to normal (lifetime of platelet)
  4. Uses: pain relief; antipyretic; heart attack (MI) and stroke prevention; rheumatic fever …

Route: ____ (81 mg, 325 mg), ____ (per rectum)

Side Effects: similar to NSAID +
- Salicylism (overdose): ____, fever, vertigo, nausea, vomiting, and diarrhea; more severe intoxication can cause altered mental status, coma, noncardiac pulmonary edema, and death

  • Acid/Base Abnormalities (overdose): ____/metabolic acidosis (anion gap)
A 
acetylated
irreversibly
increases
PO
PR
tinnitus
respiratory alkalosis
23
Q

Non-Selective NSAIDs

Don’t memorize the table, just realize that there are different chemical classes of NSAIDs (6 different ones)

  • ____
  • ____
  • among others
A

salicylates

propionic acid

24
Q

Non-Selective NSAIDs

Mechanism of action for all is the same but diff ppl react diff to each class, so if someone is on ibuprofen and it isn’t working, you might switch them over to ____

A

etodolac

25
Q

COX-1 Vs COX-2

COX-1:
• \_\_\_\_ expressed in most cells
• Modestly \_\_\_\_ during inflammation
• Generates \_\_\_\_ for housekeeping functions
• \_\_\_\_ tissue distribution

COX-2:
• Constitutively expressed in ____ tissues (e.g. vasculature, kidney, brain)
• Massively induced by ____ stimuli (cytokines, growth factors, tumor promoters)
• Principle source of prostanoid formation in ____ and inflammation
• ____ tissue distribution.

A

constitutively
upregulated
prostanoids
broad

some
inflammatory
cancer
restricted

26
Q

COX-2 Selective Inhibitors

  1. Demonstrated ____ efficacy
  2. Reduced risk of gastric and duodenal ulcers ____, but not of GI intolerance
    - Can be used with ____ such as warfarin or heparin
  3. Side effects increased with exposure
    - ____
    - Renal insufficiency
    - Myocardial infarction, cerebrovascular accidents

Result: rofecoxib (Vioxx) and valdecoxib (Bextra) withdrawn ($$)

____ (Celebrex) only remaining COX2 selective drug 100, 200, 400 mg tabs given once or twice daily
max = 400 mg/day

A

analgesic
bleeding
anticoagulants

congestive heart failure

celecoxib

27
Q

COX-2 selectivity

NSAIDS are not solely selective for COX1 or COX2, there is a ____ of selectivity as shown in the slide

A

range

28
Q
  • The risk of ____ or stroke can occur as early as the first weeks of using an NSAID. The risk may increase with ____ use of the NSAID.
  • The risk appears greater at ____ doses
A

heart attack
longer
higher

29
Q

Naproxen Package Insert: GI Risks

“Studies have shown that patients with a prior history of ____ disease and/or gastrointestinal bleeding and who use NSAIDs, have a greater than ____-fold risk for developing a GI bleed than patients with neither of these risk factors…. several other co-therapies or co-morbid conditions that may increase the risk for GI bleeding such as: treatment with oral ____, treatment with anticoagulants, ____ duration of NSAID therapy, smoking, ____, older age, and poor general health status.”

A 
peptic ulcer
10
corticosteroids
longer
alcoholism
30
Q

Conclusions

  • NSAIDs have well known side-effects that influence their use (e.g. never give to patients with moderate or severe ____ disease)
  • If one NSAID doesn’t work, try another one (individual variation in ____)
  • Giving 2 or more NSAIDs to one patient will not ____ efficacy but will ____ side effects (____ side effects). It’s best to use a different ____ of analgesic for further pain control (such as acetaminophen or a narcotic).
  • COX-2 inhibitors do not affect ____ and are easier on the stomach. It’s okay to use celecoxib with warfarin, but non- selective NSAIDs are contraindicated with ____.
  • Non-selective NSAIDs and aspirin ____ the bleeding time; these drugs should be held prior to ____.
  • Given at ____ doses and PRN for pain. Given at ____ doses and on a fixed schedule for anti-inflammatory effect. Worry about side effects with ____ term use and generally not with short term use. VERY DIFFERENT SIDE EFFECT PROFILES DEPENDING UPON ____ OF DRUG!
A 
kidney
efficacy
improve
worsen
additive
class
platelets
warfarin
prolong
surgeries
lower
higher
long
use
31
Q

Corticosteroids

Pros

  • ____
  • immunosuppressive
  • used as a ____ to another therapy
  • ____ injections for joint flares

Cons

  • unclear effect on disease progression (i.e. ____)
  • tapering difficult
  • significant ____
A 
antiinflammatory
bridge
intraarticular
erosions
side effects
32
Q

Corticosteroids

  1. mimetics/derivatives of ____, a steroid hormone produced in the adrenal cortex
  2. glucocorticoids: corticosteroids with effects on ____; anti-inflammatory properties
    mineralocorticoids: corticosteroids involved in ____ regulation
  3. MOA: corticosteroids enter cells, bind to the steroid receptor and influence ____ of up to 20% of the cell’s genes
  4. Effects: Potent ____ agents
    i. Decrease in ____ margination, migration, and accumulation at
    inflammatory sites
    ii. inhibition of neutrophil and macrophage ____, enzyme release, and pro-inflammatory cytokine production
    iii. indirect decrease in ____ and leukotriene production
    iv. decrease in ____ proliferation and interleukin-2 (IL-2) synthesis and secretion
A 
cortisol
metabolism
salt
transcription
anti-inflammatory
neutrophil
phagocytosis
prostaglandin
T-cell
33
Q

Intracellular mechanism of action of the glucocorticoid receptor.

  • When they are circulating they are bound to ____
  • translocate to cell membrane and bind to glucocorticoid receptor, which can then disassociate after structural change from the hitchock (sp?) proteins and get into the nucleus to affect ____ and protein production.
  • steroids don’t work immediately since it takes a while to affect protein production (effects seen within ____ days)
A

corticosteroid binding globulin
transcription
2-3

34
Q

Effects of Glucocorticoids

• Metabolic
– ____
– Lipogenesis (insulin secretion)

• Catabolic
– \_\_\_\_ catabolism (muscle)
– Lipolysis (hormone sensitive lipase)
– Bone – \_\_\_\_
– Wasting other tissues
• lymphoid, connective tissue, skin

• Other
– ____ / fluid homeostasis, blood pressure
– Behavioral / mood effects

A

gluconeogenesis
protein
osteoporosis
Na+

35
Q

Effects of Glucocorticoids

• Anti-inflammatory
– Decrease in ____
– Inhibition of PLA2
– Decrease ____

• Immunosuppressive
– ____ immunity
– Reduced proliferation of ____, neutrophils and monocytes

A

cytokines
mRNA COX

cell mediated
lymphocytes

36
Q

Corticosteroid Side Effects and Administration

Short- to Medium-term: increased appetite, bone demineralization, glucose intolerance/diabetes, nervousness, insomnia, psychosis, fluid retention (depends on mineralocorticoid activity of drug), delayed ____ healing, acne

Medium- to Long-term: Short-term Side Effects + osteonecrosis (bone death), osteoporosis (severe bone demineralization), ____, hirsutism, muscle wasting, cataracts, glaucoma, depression, hyperpigmentation, fat redistribution (moon facies, buffalo hump), ____ insufficiency

Administration: ____, IV, intra-articular (IA), IM, topical for RA: typically PO and IA

Metabolism: generally ____

A 
wounded
infection
secondary adrenal
PO
liver
37
Q

Secondary Adrenal Insufficiency

  • cortisol is secreted in response to ____ (e.g. major surgery)
  • prolonged exogenous corticosteroid use leads to ____ ACTH levels and atrophy of cortisol-secreting cells in the adrenal gland.
  • Adrenal insufficiency: Inability of adrenal gland to synthesize sufficient ____ in response to stress
  • cortisol insufficiency can lead to:
    ____, shock, death, fever, nausea/vomiting, depressed mentation, fatigue, weakness, hypoglycemia
  • adrenal suppression seen after ____ 5mg daily for as few as 2 weeks
    -so, people on long-term steroids may need ____ steroids at the time of big stressors (e.g major surgery)
A 
stress
decreased
cortisol
hypotension
prednisone
more
38
Q

Synthetic Compounds

List of commercial ____

Point is to compare with ____ which is the endogenous steroid we make naturally

Prednisone or Prednisolone is used to treat ____ and it is x____ stronger as an antiinflammatory than cortisol while it’s mineralcorticoid properties are about a ____ (less likely to cause fluid retention)

A 
steroids
hydrocortisone (cortisol)
inflammation
4-5
1/3
39
Q

Disease Modifying Anti-Rheumatic Drugs (DMARDs)

Non-corticosteroid containing medications that suppress the ____ and/or delay disease progression in RA.

Goal: Get patients off of corticosteroid within ____ months and onto a ____.

A

immune ststem
6
DMARD

40
Q

methotrexate (Rheumatrex, Trexall)
– INDICATED FOR NEWLY ____ OR ESTABLISHED DISEASE
– STANDARD OF CARE
– 60-70% ____

Routes: ____: PO, SC (SC dosing gives levels ~30% > than equivalent PO dose)
Cancer: ____, IM, intrathecal

Dosage (Arthritis): 7.5-25 mg/week (2.5 mg tabs, 25 mg/mL solution)

Metabolism/Elimination: eliminated via ____ mostly (decreased elimination when patient on NSAIDs can lead to increased methotrexate toxicity)

MOA: At ____ doses (for arthritis treatment) the effect of methotrexate is thought to be the blockage of ____ biosynthesis at the step catalyzed by aminoimidazolecarboxamide (AICA) ribotide transformylase, indirectly resulting in elevated serum levels of ____, a T-lymphocyte toxin.

A

diagnosed
improvement
arthritis
IV

urine
low
purine
adenosine

41
Q

methotrexate (Rheumatrex, Trexall)

MOA continued: At ____ doses (for cancer treatment) methotrexate irreversibly binds to dihydrofolate reductase inhibiting the formation of reduced folates, and thymidylate synthetase, resulting in inhibition of purine and thymidylic acid synthesis (inhibits ____). Actively proliferating tissues such as malignant cells, bone marrow, fetal cells, buccal and intestinal mucosa, and cells of the urinary bladder are in general more sensitive to this effect of methotrexate.

Response: observed in ____ weeks

Adverse reactions: gastrointestinal, hematologic, pulmonary, hepatic, n/v,
____, malaise, ____

To minimize side effects: Give with ____ 1mg QD or leucovorin 5mg Q
week. No ____ use (additive ____ toxicity).

Monitor: ____, LFT’s, creatinine, albumin

A 
high
DNA synthesis and repair
4-6
stomatitis
teratogenic
folic acid
alcohol
liver
CBC
42
Q

Antimalarial: hydroxychloroquine (Plaquenil)

  • INDICATED FOR ____, MILD DISEASE
  • WAS FIRST DRUG OF CHOICE (US) IN THE PAST
  • ONSET ~ 3 MO IN 50%

Route: ____
Dosage: 200 mg PO 1 or 2 times a day (max 6.5 mg/kg/day)
Metabolism: Liver

MOA: ____; likely multiple; inhibits ____ of neutrophils and chemotaxis of eosinophils; impairs complement-dependent antigen-antibody reactions, (reduced activation of Toll Like Receptors 7 and 9 in dendritic cells)

Other: Benefit seen after 2-4 months

Adverse effects: myopathy, headache, aplastic anemia, seizures, retinopathy,
ototoxicity (also, ____ change)

Monitor: Need dilated ____ eye exam every 12 months

Other: firstline treatment for ____ (lupus)

A 
early
PO
unknown
locomotion
mucosal pigmentation
fundoscopic
SLE
43
Q

sulfasalazine (Azulfidine)
– INDICATED FOR EARLY, MILD, SERONEGATIVE DISEASE
– WAS FIRST DRUG OF CHOICE (EUROPE) IN THE PAST

Route: ____
Dosage: 1-3 g/day; start at 500 mg/day

Metabolism: colonic intestinal flora convert to ____ and 5-aminosalicylic acid (5-ASA); metabolites eliminated in urine

MOA: 5-ASA inhibits ____ synthesis + ? Effect of sulfapyridine

Other: Benefit seen after 1-2 months

Adverse reactions: Common: ____, headache, rash
Others: ____ syndrome, hepatitis, agranulocytosis, peripheral
neuropathy, reversible decrease in sperm count

Monitor: ____, kidney function, liver function

A 
PO
sulfapyridine
prostaglandin
nausea
stevens-johnson
CBC
44
Q

Leflunomide (Arava)

  • “new” traditional DMARD
  • similar efficacy to methotrexate

Route: ____
Dosage: 10-20mg PO every day
Metabolism: ____; excreted in urine and feces; long half-life (about 2 weeks). The drug can be measured in the ____ for > 2 years after the last dose. Rapid detoxification requires administration of ____ (8g PO TID for eleven days).

MOA: metabolite of leflunomide inhibits ____ which leads to inhibition of pyrimidine synthesis

Adverse Reactions: ____, alopecia, diarrhea, nausea, weight loss, rash, hepatotoxicity, teratogenicity

Monitor: ____, LFT’s, creatinine, albumin

A 
PO
hepatic metabolism
serum
cholestyramine
dihydroorotate dehydrogenase
myelosuppression
CBC
45
Q

azathioprine (Imuran, Azasan) - occasionally used for RA

Route: PO, IV (PO for arthritis)
Dosage: start at 50mg PO QD; Max: 3 mg/kg/day; increase by 25mg every 2
weeks to desired dose (typical dose 50-150 mg PO every day)

Metabolism/Elimination: Hepatic metabolism; clearance of metabolites in urine

MOA: active ____ leads to decreased synthesis of purine nucleotides (6-MP accumulates when patients given ____ - TOXICITY)

Other: Response seen in 2-3 months

Adverse Reactions: Common: ____, abdominal pain, rash, increased LFTs, myalgias, alopecia; Serious: ____, leukopenia, bone marrow suppression, hepatotoxicity, risk of neosplasm, hypersensitivity reaction, hepatic veno-occlusive disease

Monitor: ____, LFTs

A 
metabolite 6-mercaptopurine (6-MP)
allopurinol
diarrhea
pancreatitis
CBC
46
Q

cyclosporine-A (Gengraf, Neoral, Sandimmune)

  • rarely used for RA

Route: ____ (arthritis), IV, topical
Dosage: 1-4 mg/kg/day; (typically 1-2 mg/kg/day)
Metabolism: ____/feces

MOA: Inhibits T-helper cell release of ____; bind to cyclophillin which blocks effects of ____

Adverse Reactions: ____, renal toxicity, infection, cancers, ____ hyperplasia, neurologic toxicity, hyperlipidemias, ____, numerous others

Monitor: ____, kidney function; always looking for potential drug interactions which can potentiate renal damage

A 
PO
hepatic
IL2
calcineruin
hypertension
gingival
hyperglycemia
blood pressure
47
Q

Gold

  • rarely used for RA now
  1. ____ gold (auranofin; Ridaura)
    Dosage: 3 mg PO 1-2 times a day; max of 9 mg/day. Benefit seen 4-6 months after starting therapy
  2. ____ gold (aurothioglucose; Solganal)
    Dosage: 25-50 mg IM every 2-4 weeks. Benefit observed in 3-6 months

MOA: unknown; may inhibit phagocytosis by ____

Adverse Reactions: ____, rash, pruritus, abdominal pain, ____, nausea, confusion, conjunctivitis, ____ (taste changes), elevated LFTs, proteinuria
Serious: ____, ulcerative colitis, nephrotic syndrome, anemias, pulmonary fibrosis
Monitor: ____ and urinalysis (to look for proteinuria)

A 
oral
injectable
macrophages
diarrhea
stomatitis
parageusia
seizures
CBC
48
Q

penicillamine (Cuprimine, Depen)

  • rarely used for RA now

Route: ____
Dosage: 250-1000 mg PO every day; take 0.5-1 hrs before meals Metabolism/Excretion: metabolized by ____, excreted in urine

MOA: supresses ____ but not ____ activity; also chelates lead, copper, mercury

Other: maximal response seen after 3-6 months of therapy

Adverse reactions: ____, rash, n/v, nephropathy, taste changes, ____, hirsuitism, drug-induced lupus
Rare: ____, pancreatitis, thrombocytopenia

Monitor: ____ and urinalysis

A 
PO
liver
T-cell
B-cell
pruritus
stomatitis
aplastic anemia
CBC
49
Q

cyclophosphamide (Cytoxan)

  • generally reserved for ____ extraarticular manifestations of RA
  • chemotherapeutic agent
  • more commonly used in Rheumatology for vasculitis or certain forms of kidney disease associated with Systemic Lupus Erythematosus

Route: ____, IV
Dosage: Oral: 50-100 mg/m2/day as continuous therapy; I.V.: Single doses: 500-1000 mg/m2 (30-50 mg/kg) per treatment course (1-5 days) which can be repeated at 4-week intervals
Metabolism: Hepatic to ____ metabolites acrolein, 4-aldophosphamide, 4- hydroperoxycyclophosphamide, and nor-nitrogen mustard. Eliminated in urine.

MOA: Cyclophosphamide is an ____ agent that prevents cell division by cross-linking ____ strands and decreasing DNA synthesis. Cyclophosphamide is a prodrug that must be metabolized to ____ metabolites in the liver.

A 
PO
active
alkylating
DNA
active
50
Q

cyclophosphamide (Cytoxan)

Adverse Reactions:
>10%: ____: Alopecia (40% to 60%); ____: Fertility: May cause sterility; ____: Nausea and vomiting, usually beginning 6-10 hours after administration; anorexia, diarrhea, mucositis, and stomatitis are also seen; ____: Severe, potentially fatal acute hemorrhagic cystitis (7% to 40%); ____: Thrombocytopenia and anemia are less common than leukopenia
1-10%: headache, flushing, rash
<1%: multiple, including malignancy (e.g. ____ cancer), lung inflammation, heart dysfunction, liver toxicity

Monitor: ____, kidney function, liver function

A 
alopecia
endocrine
GI
GU
hematologic
bladder
CBC

FS V, Final (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions