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Pharmacology & Medical Chemistry II > Exam 2: Lecture 5, DMARDs > Flashcards

Exam 2: Lecture 5, DMARDs Flashcards

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1
Q

DMARDs

A

Disease Modifying Slow-Acting Anti rheumatic Drugs

NSAIDS cannot reverse join damage, DMARDs are used for rheumatic disorders not responding to NSAIDs

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2
Q

Rheumatoid disease is…

A

a widespread chronic inflammatory condition

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3
Q

DMARDs info

A

operate in connective tissues

heterogeneous group of slow acting anti-inflame agents

all agents have very slow onset of effect, can take months

many do not respond to DMARDs (esp Gold Salts)

Controversy still about efficacy in arthritis

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4
Q

Gold Salts

A

Cytotoxic agent

most effective for rapidly progressive disease

cannot fix existing damage, prevent more

decrease O2 metabolites production

Suppress Phagocytosis, lysosomal enzyme activity, and histamine release

taken up by macrophages

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5
Q

Gold Salt Toxicity

A

observed in 1/3 pt, 1/10 have severe symptoms

skin rashes, occasionally severe
mouth ulcers
proteinuria
encephalopathy
peripheral neuropathy
Hepatitis
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6
Q

Methotrexate (rheumatrex)

A

First line

Anti-cancer med
cytotoxic immunosuppressant agent

reduce number of immune cells for inflammation response, actively dividing inflammatory cells vulnerable to effects of drug

inhibit enzyme essential for NA synth/cell rep

doses smaller than those for anticancer therapy, for sever rheumatoid arthritis

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7
Q

Methotrexate Toxicity

A 
Bone marrow suppresion
Leucopenia,thrombocytopenia,anemia
GI toxic
Hepatic toxicity
Pulmonary fibrosis
Renal Dysfunction
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8
Q

Sulfasalazine (Azulfidine)

A

Second line

Mechanism poorly understood, thought to be scavenger of free radicals

Drug is combo sulfonamide + salicylate, split not 2 In colon

used to treat RA. Ulcer colitis, Inflammatory Bowel disease

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9
Q

Sulfasalazine (Azulfidine) Toxicity

A

Gi Disturbance
Headache
Reversible drop in Sperm count
Possible anaphylaxis, dyscrasia (unspecified blood disorder)….this possible with other sulfonamides too

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10
Q

Penicillamine (Cuprimine, Depen)

A

A Chelating agent used in the treatment of poisoning by heavy metals

An analog of cysteine + substances that produced by penicillin hydrolysis

decrease progression of bone destruction

mechanism not clear, suggested the decrease of IL-1 formation and collagen synthesis

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11
Q

Penicillamine Toxicity

A 
Anorexia
Nausea
Rashes
Stomatitis
Bone-Marrow disorders

Chelator, so don’t give with gold compounds

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12
Q

Hydroxychloroquine (Plaquenil)

A

Antimalarial drug
Usually, Well tolerated
Used to treat RA

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13
Q

Hydroxychloroquine (Plaquenil) Mechanism

A

Depress activity of T-lymphocytes
Decrease leucocytes chemotaxis
Interferes with RNA/DNA synthesis

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14
Q

Hydroxychloroquine (Plaquenil) Toxicity

A 
Headache
Tinnitus
Arrhythmias
Nausea,Vomiting
Rashes
Possible retina damage = streaks/flashes
Eye swelling + color change
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15
Q

All DMARDs are related to….

A

Severe and Fatal Toxicities

Require monitoring

Danger of mixing DMARDs together, severe kidney damage.

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16
Q

Gold Salts severe toxicity

A

fatal dermatitis and bone marrow depression

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17
Q

Methotrexate severe toxicity

A

bone marrow depression and teratogenic fetal damage/abortion

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18
Q

D-Penicillamine severe toxicity

A

renal damage and aplastic anemia

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19
Q

Hydrochloroquine severe toxicity

A

dermatitis,bone marrow depression and RETINAL DEGENERATION

20
Q

Combo Therapy with DMARDs

A

high toxicity, but used to treat RA

plan is designed rationally,

use non-overlapping toxicities and pharmacokinetics

21
Q

Biological DMARDs

A

breakthrough in treatment

engineered recombinant antibodies and other proteins

hard + expensive to make

for patients that don’t respond to other DMARDs

admin with specialist supervision

22
Q

Immunoglobulin Structure

A

produced by specific activated B cell against particular antigen, 10^20 antibody molecules in individual

Heavy + Light Chain (H+L)
Antigen binding Frag (Fab)
Constant region (Fc)
N-terminal ends of H/L chain form Ag-binding site
Single antibody can bind 2 Ag
23
Q

Variable region Antibody

A

Top portion of the Y structure

24
Q

Constant region Antibody

A

Bottom portion of the Y structure

25
Q

Anakinra Dosing

A

Given daily

26
Q

Etanercept Dosing

A

Given once or twice per week.

27
Q

Abatacept and Golimumab Dosing

A

Given once monthly

28
Q

Adalimumab, Certolizumab, Infliximab, Rituximab Dosing

A

Given every two weeks.

29
Q

Biopharmaceuticals Therapy Limitations

A

only given to severely affected patients, when other therapy failed.

~30% don’t respond to them

Discontinued if no benefit seen 2/4 weeks

combo of drugs is more effective

30
Q

Biopharmaceutical Adverse effects

A

Precipitate latent infections (Tuberculosis/Hep B)
Encourage opportunistic infections
Provoke onset of psoriasis-like syndrome (Rare)
Hypersensitivity, injection site reactions and mild GI symptoms

31
Q

Gout is a

A

genetically determined metabolic disorder characterized by high conc of uric acid in the blood

32
Q

Chronic Gout causes

A

Genetic defect = increase purine synthesis

Renal Deficiency (genetic or caused by thiazides)

Lesch-Nyhan Syndrome (Excessive uric acid synthesis)

33
Q

Acute gout attacks can be provoked by…

A

Excessive Alcohol consumption, diet rich in purines or kidney disease

34
Q

Mechanism for Gout Attack

A

Purines -> Xanthine -> Uric Acid ->Uric Acid Crystals -> Phagocytosis by Neutrophils -> Inflammation Mediators Release -> Lysosomal Enzyme release ->Acute inflammation

35
Q

Gout Treatment Strategies

A

Reduce Inflammation (Indomethacin/ Colchicine)

reduce conversion of purines to uric acid (Allopurinol)

Increase uric acid excretion (Probenecid,Sulfinpyrazone)

36
Q

Colchicine (Colchrys)

A

Plant alkaloid, reserved for acute gout attacks

Mitotic Poison

can be used to treat Mediterranean fever

37
Q

Colchicine Mechanism

A

Selective inhibitor of microtubule assembly, bind to tubulin

Disrupts mobility of granulocytes into affected area

blocks cell division by binding mitotic spindles

reduces production of Leukotrienes (LTB4)/ Reduce inflammation

38
Q

Mediterranean fever

A

Fever, Hepatitis, peritonitis, arthritis

39
Q

Colchicine Toxicity

A

Nausea/Vomiting/Abdominal Pain/ Sever Diarrhea

Possible sever liver/kidney damage

  • Not to be used during pregnancy *

Fatal dose as little as 8mg in 24hrs, close monitoring

IV no longer approved

40
Q

Allopurinol (Zyloprim)

A

1st line agent for chronic gout treatment

not effective in acute attack

Purine Analog

41
Q

Allopurinol Mechanism

A

Competitive inhibits last two steps in uric acid biosynthesis

Inhibit Xanthine Oxidase

Decrease uric acid conc, precipitation of uric acid crystals in joints and tissues

  • Selective in humans but can severely impair purine metabolism in some protozoa*
42
Q

Allopurinol Toxicity

A

Well tolerated in most patients, oral admin

skin rashes in 3% of patients

Bone marrow depression
Hepatic Toxicity and Nephrotoxicity

** Rare peripheral neuritis/ vasculitis, very rare bind to lens resulting in cataracts **

43
Q

Uricosuric Agent

A

Reduce inflammation
Block proximal tubule reabsorption of uric acid
Uricosuric agents are organic acids - increase uric acid secretion

44
Q

Uricosuric Agents examples

A

Probenecid (Generic)

Sulfinpyrazone (Anturane)

45
Q

Uricosuric Agent Toxicity (of the 2 examples)

A

Both agents similar toxicity

rarely aplastic anemia

Gi irritation more active (sulfinpyrazone)
Nephrotic syndrome mostly (probenecid)

46
Q

Probenecid (Generic)

A

blocks kidney tubule secretion of penicillin

was developed to prolong penicillin level in blood

used occasionally to increase antibiotic conc

Pharmacology & Medical Chemistry II (43 decks)

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