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65 Cards in this Set

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What effects does Acetaminophen possess?


**no anti-inflammatory activity
Acetaminophen (Tylenol) T or F:
1. Affects platelets fxn
2. Does not affect uric acid levels
3. causes gastric irritation
4. should not be given to children
1. False
2. True
3. False
4. False
What is the most serious adverse effect of acute overdose of Acetaminophen?
Hepatic necrosis
There is some evidence that Acetaminophen exerts its action on _______ in the CNS
What CYP causes bioactivation of Acetaminophen?

What 2 things induces this CYP?

Acetaminophen can cause __1__, especially in __2__-sensitive individuals
1. acute hemolytic anemia

2. Primaquine
Acetaminophen-induced __1__ is synergistic with __2__
1. Hepatotoxicity

2. Alcohol consumption or Isoniazid
What are 3 rare adverse effects of Acetaminophen?
1. Neutropenia
2. Pancytopenia
3. Leukopenia
What are the 3 mechanisms of Acetaminophen metabolism that are safe?
1. Sulfation
2. Glucuronidation
3. Glutathione
What is the down-side of Sulfation and Glucuronidation in Acetaminophen metabolism?
They run at a relatively full capacity = co-substrates needed for the rxn run out relatively quickly
What is the antidote for Acetaminophen overdose?

Within what time period should the antidote be given to yield maximal effects?
N-acetlycysteine = regenerates Glutathione

8 hours
What are the first line drugs used in Rheumatoid Arthritis treatment?
Drugs that cause dramatic improvement in Rheumatoid arthritis; do not arrest the disease process itself; adverse effects limit their long-term use
RA drugs that have a slow onset of action (6 wks to 6 months) and their mechanism of action is not well understood
Disease Modifying Antirheumatic Drugs (DMARDs)
What are the 2 antimalarial drugs used for Rheumatoid Arthritis treatment?

Which antimalarial is used more commonly to treat RA and SLE?
What is the contraindication for Hydroxychloroquine/Chloroquine?
Psoriatic Arthritis b/c of possible development of Exfoliative Dermatitis
Antimalarial drugs can cause irreversible __1__ damage.

Which one causes this more?
1. Retinal

2. Chloroquine
What should gold compounds not be given with? Why?

B/c it chelates gold
What are 4 contraindications for Gold compounds?
1. Previous gold toxicity
2. Pregnancy
3. Liver or Kidney impairment
4. Blood dyscrasia
What are the 4 adverse effects of Gold Compounds?
1. Dermatitis and diarrhea
2. Eosinophelia & other blood disturbances
3. Proteinuria -> nephrotic syndrome
4. Aplastic anemia (rare but fatal)
What are 2 gold compuonds used in RA?
1. Aurothioglucose

2. Auranofin
Administered IM and is an adjunctive treatment of early active cases of adult and juvenile RA
Adverse effects of this DMARD are listed below:
1. Erythema
2. Exfoliative dermatitis
3. Kidney toxicity
4. Blood dyscrasias
This is the only gold compound available for Oral administration
What is Penicillamine's mechanism of action?
Oral chelating agent
What is Penicillamine used for? (3)
1. Wilson's disease = copper accumulation disease
2. Cystinuria = urinary stones
3. resistant cases of RA
What is Sulfasalazine used to treat? (3)
1. Rheumatoid arthritis
2. Ankylosing spondylitis
3. Ulcerative colitis
-Administration: __1__
-converted to an active metabolite that inhibits __2__, an enzyme involved in __3__
-leads to a translocation of __4__ to the nucleus
-stimulated cells are arrested in __5__ phase
1. Oral
2. Dihydroorotic acid dehydrogenase
3. Ribonucleotide synthesis
4. P53
5. G1
DMARD that is converted to an active metabolite that inhibits Dihydroorotic acid Dehydrogenase, an enzyme involved in ribonucleotide synthesis.

Inhibits autoimmune T cell proliferation and production of auto-antibodies by B cells
This was the 1st agent that was indicated for both symptomatic improvement and retardation of structural joint damage in RA
What are 3 possible adverse effects of Leflunomide?
1. Alopecia

2. Rash

3. Diarrhea
List the 3 Anti-TNF-alpha compounds used to treat RA
1. Infliximab = monoclonal Ab to TNF-alpha

2. Etanercept = recombinant form of TNF receptor that binds TNF-alpha

3. Adalimumab = monoclonal TNF-alpha Ab
IL-1 receptor antagonist that reduces the signs and symptoms and slows the progression of structural damage of moderate to severe active RA in patients who failed one or more DMARDS
How is Anakinra administered?
Subcutaneously once per day

**anaKINra = SKIN = Subcutaneously
This drug is a co-stimulatory or second-signal blocker of T cell activation
How is Abatacept administered?
IV infusion
- day 0, week 2, & week 4 followed by monthly injections
When is Abatacept used?
In patients who are unresponsive to DMARDs of TNF antagonists
What is there an increased risk of when using Abatacept?
What causes Gout?
increase in the amount of Uric Acid in the body
What are the primary causes of Gout?
Overproduction or under-excretion of Uric Acid
-Under excretion = diabetes and in starvation
-Over production = de novo synthesis
What could be a secondary cause of Gout?
Accumulation of Uric Acid due to Leukemia
-diseases with alot of Purine synthesis and degredation
List 6 drugs or groups of drugs that may cause under-excretion and/or accumulation of Uric Acid (hint)
1. Diuretics = Thiazides, Furosemide, Ethacrynic acid
2. Anti-TB drugs = Pyrazinamide, Ethambutol
3. Nicotinic acid
4. Ethanol
5. Cytotoxic drugs
6. Salicylates
Dr. Gouty takes Diuretics, has TB, Smokes and Drinks (which are Cytotoxic) and treats everything with Aspirin
What are the symptoms of Gout?
Inflammatory reaction mediated prostaglandins and immune cells due to phagocytosis by synoviocytes of uric acid crystals deposited in peripheral joints -> inflammation -> severe pain
List the pathway leading to Gout
Why are Diuretics and Low-dose Salicylates contraindicated in Gout?
they block tubular secretion of Uric Acid
List the pathway of Uric Acid synthesis?
Purines -> Hypoxanthine -> Xanthine -> Uric acid
3 drugs used in the treatment of Acute Gout
1. Colchicine
2. NSAIDs -> Indomethacin
3. Corticosteroids
Explain Colchicines method of action in treating acute attacks of gouty arthritis
Inhibits microtubule polymerization = inhibits Leukocyte migration and phagocytosis = anti-inflammatory
What are the adverse effects of Colchicine?

**Colchicine makes you feel bad in NeVaDa
What is the primary NSAID used to treat severe gout?
What other NSAIDs can be used to treat gout?

"I SIN" with Gout
What NSAID should not be used to treat gout? Why?
Aspirin b/c of its dual effect on the kidney
What makes Corticosteroids useful in treatment of gout?
Anti-inflammatory properties

Side effects associated are significant with prolonged use
What are the 2 prophylactic drugs used in Gout?
1. Uricosuric agents
- Probenicid
2. Allopurinol
What is the mechanism of action of the Uricosuric agents?
increase urinary excretion of Uric Acid by blocking the Active Reabsorption in proximal tubule
What should be maintained when using Uricosuric agents? Why?
Large urine volume to minimize possibility of stone formation
What may Sulfinpyrazone increase the serum concentration of?
1. Sulfonamides

2. Salicylates

**displaces them from plasma binding proteins
Oral uricosuric agent used to treat hyperuricemia associated with CHRONIC gout or secondary to other causes (drug-induced hyperuricemia)

*also inhibits secretion of Penicillin
Gout drug that should not be used for ACUTE attacks b/c it can aggravate inflammation if administered during initial stages
What is Allopurinol's mechanism of action?
Inhibits Xanthine oxidase and thus inhibits Uric Acid synthesis
When is Allopurinol used?
In both primary and secondary forms of gout
What are the side effects of Allopurinol?
1. Vasculitis
2. Agranulocytosis
3. Hypersensitivity rxns
Allopurinol inhibits the conversion of __1__ and __2__ to their inactive metabolites.

If allopurinol needs to be used with these 2 antimetabolites, their doses must be __3__
1. Mercaptopurine

2. Azathioprine

3. reduced
When should Uricosuric agents not be used?
if GFR < 50 mL/min