Duan: Pharm Flashcards
(blank) is a defense reaction against tissue injury or damage caused by physical injury, thermal injury, infectious agents, antigen-antibody interaction, ischemia, etc
inflammation
What are the three phases of inflammation?
acute
subacute
chronic proliferative
What phase of inflammation is this:
vasodilation and capillary permeability
acute
What phase of inflammation is this:
infiltration of leukocytes and phagocytes (effects of chemokines)
subacute or delayed
What phase of inflammation is this:
tissue degeneration and fibrosis
chronic proliferative
What causes the redness seen in inflammation?
vasodilation of capillaries increases blood flow
What causes the heat felt in inflammation?
vasodilation
What causes the pain felt in inflammation?
hyperalgesia, sensitization of nocicpetors
What causes the swelling in inflammation?
increased vascular permeability (microvascular structural changes and escape of plasma proteins from the bloodstream)
What are these:
osteoarthritis, rheumatoid arthritis, juvenile arthritis, gouty arthritis, ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome
different kinds of arthritis
What are arthritic disorders characterized by?
inflammatory changes and symptoms (pain, heat, redness, and swelling) and subsequent tissue damage with atrophy and rarefraction of bones
In late stage of arthritis what may develop?
deformity and ankylosis
TO block an inflammatory response, do you want to block COX 1 or COX2?
COX 2
THe underlying causes for many of the arthritic disorders are complex and usually cannoto be cured. The goal of treatment is to (blanK).
relieve inflammation, control pain, improve function, prevent further joint damage, improve quality of life
Which part of your immune system does an infection affect?
the adaptive and innate immune system
What part of the immune system reacts to a perceived threat?
adaptive immune system
What will tissue injury, adaptive immune system, and the innate immune system activate?
leukocytes and endothelial cells
What will leukocytes and enothelial cells activate?
biochemical inflammatory mediators
So please briefly describe the inflammatory cascade
threat, tissue injury, infection-> immune system-> leukocytes and endothelial cells activation-> biochemical inflammatory mediators-> inflammation symptoms
The symptoms of inflammation are caused by a series of (blank) including the metabolites of eicosanoids.
biochemical mediators
What are these:
1) Vasoactive amines (Histamine, Serotonin)
2) Platelet activating factor (PAF)
3) Complement system
4) Kinin system
5) Cytokines
6) Nitric oxide
7) Adhesion Molecules
8) Arachidonic acid metabolites (eicosanoids):
biochemical mediators
What are some arachidonic acid metabolites (eicosanoids)?
thromboxane A2 (TXA2)
HETE (hydroxy-eicostatraenoic aid)
Leukotrienes (LTs)
Prostaglandins (PG mediated by cyclooxygenases COX)
What is this:
20 C fatty acid chains and produce prostanoids and leukotrienes and acts as an immune system modulators
arachidonic acids
What does COX do?
cause inflammation
What does LOX (lipoxygenase) do?
phagocyte mobilization and changes vascular permeability and causes inflammation
Where do arachidonic metabolites come from?
from phospholipids
How will diverse physical, chemical, inflammatory, and mitogenic stimuli affect arachidonic metabolism?
it will activate phospholipase A2 which will convert phospholipids into the things that will cause inflammation
What do the prostanoids cause (prostaglandins, prostacyclin, thromboxane)?
inflammation
How do you convert arachodinoc acid into EETs for reuse?
via cytochrome P450
What cox does this:
platelet function
GI mucosal integrity
renal function
COX 1 (induces constitutive physiological regulation)
What cox does this:
inflammation
pain fever
COX2 (induces inflammatory response)
WHat does aspirin inhibit?
both COX1 and COX2
(blank) directly sensitize pain fibers (Ad and unmyelinated C fibers) so they respond to normally innocuous stimuli (hyperalgesia)
prostaglandins
Subdural injetion of PGE1 (prostaglandin E 1) with small amounts of bradykinin and histamine causes (blank)
headache and pain
What causes a fever?
neutrophils release pyrogens (cytokines, TNF A, ILs)
(blank) are thought to cause release of prostaglandins in the preoptic area of the hypothalamus. The net effect is an imbalance in heat production and leading to fever.
Pyrogens
If you inhibit prostaglandin synthesis in the CNS, what will happen?
cutaneous dialtion
increased heat loss-> reduction in fever and symptoms of fever
What do corticosteroids (predinisone, dexamethasone) do?
inhibit leukocyte and endothelial cells activation by blocking Phospholipase A2 and COX
What do NSAIDS do?
inhibit inflammatory mediators by blocking COX
What do 5-LOX inhibitors and leukotriene receptor antagonists (Zafirlukast, zileuton) do?
inhibit inflammatory mediators by blocking COX
What do you use aspirin for with heart issues?
as a blood thinner for prevention of heart attacks
(blank) covalently and irreversibly modifies both COX 1 and COX 2 by acetylating serine 530 in the active site.
acetylsalicylate (ASA)
What does the acetylation of COX by ASA do?
it causes a steric block to prevent arachidonic acid from binding
Does acetylation of COX-2 allow it to retain the cox activity but produce a different product, such as 15-R-HETE?
YES!
(blank) irreversibly inhibits platelet COX-1 and COX-2 and, thereby inhibits thromboxane production (remember, thromboxane stimulates platelet aggregation)
Aspirin
Why dont you give someone aspirin when they are pregnant?
cuz they may induce postpartum hemorrhage
premature closure of the fetal ductus arteriosus (cuz prostaglandins keep it open :) )
At less than 300 mg /Day, what kind of effects with aspirin induce?
blocks platelet aggregation and has antithrombic effects
At doses between 300-2400 mg/day, what kind of effects does aspirin have (intermediate)?
antipyretic, analgesic effects
At doses between 2400-4000 mg/day. what kind of effects does aspirin have (high)?
anti-inflammatory
Aspirin is most commonly used in the clinics for the treatment of a number of conditions, including…..?
fever pain rheumatic fever inflammatory diseases lower doses of aspirin
What can treat rheumatoid arthritis, pericarditis, and kawasaki disease?
aspirin, bitches
What kind of acids are salicylates?
weak organic acids
aspirin has a pKa of (blank).
3.5
Why is aspirin rapidly absorbed from the stomach as well as from the intestine?
cuz the low pH favors absorption
where do unmetabolized salicylates go?
they are excreted by the kidney
How do you treat an acid overdose?
you raise the urine pH to increase the clearance of it
Aspirin (acetylsalicylic acid) is rapidly hydrolyzed primarily in the liver to (blank), which is conjugated with (blank) forming salicyluric acid and glucuronic acid and excreted largely in the urine as free salicylic acid (10%), (blank) (75%), salicylic phenolic (10%) and acyl (5%) glucuronides and gentisic acid (
salicylic acid
glycine
salicyluric acid
If you oxidize salicylate, what do you get?
gentisic acid
If you conjugate salicylate with glycine what do you get?
salicyluric acid
If you conjugate salicylate with glucronic acid what do you get?
ester and other glucuronides
Is asprin rapidly hydrolyzed?
What does this mean about the levels of aspirin in the plasma?
yes
they are low and rarely exceed 20 mg/ml at ordinary therapeutic doses
What is the plasma half-life for aspirin? What happens to this half-life as the dose of aspirin increases?
15 minutes
the half life increases as well
What is the half life of aspirin if you have 300mg to 650 mg?
What is the half life of aspirin if you have 1 gram?
What is the half life of aspirin if you have 2 grams?
what about greater than 3.5 grams?
3.1 to 3.2 hours
~5 hours
~9 hours
15-30 hours
At low and moderate doses of salicylate, how is the drug eliminated?
first order
At high doses of salicylate, how is the drug eliminated?
zero order
In high doses of asprin, or toxic overdose, the enzymes for glycine and glucuronide conjugation become (blank)
saturated
Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with heparin or oral anticoagulants?
result in hemorrhage!
Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with antacids?
reduced rate of aspirin absorption
Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with probenecid or sulfinpyrazone?
decreased urate excretion (contraindicated in patients with gout)
Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with bilirubin, phenytoin, naproxen, sulfinpyrazone, thlopental, thyroxine, triiodothyronine?
result in increased plasma concentration leading to prolonged half-lives, therapeutic effects, and toxicity
What are the adverse effects of aspirin?
GI symptoms allergic reactions CNS toxicity Salicylate reaction (CNS reaction) renal damage hematologic effects metabolic acidosis Reyes syndrome
Why should aspirin not be given to patients with asthma?
it causes contraction of the bronchioles-
What are the three most common adverse effects of aspirin?
salicylate reaction (CNS reaction)
hematologic effects
Reye’s syndrome
What is reye’s syndrom?
it is found in kids who take too much aspirin and results in severe hepatic damage and encephalopathy
How do you get salicylism (overdose or poisoning)?
a dose greater than 5 g/d of aspirin or salicylate
In adults, what is the initial sign of salicylism toxicity?
tinnitus, hearing loss, vertigo
In children, what is the intitial sign of salicylism toxicity?
acidosis and hyperventilation with accompanying lethargy
How do you treat salicylate overdose?
alkalize urine correct acid-base disturbance replace electrolytes and fluids cooling forced diuresis, hemodialysis gastric lavage or emesis
What are these: strong antipyretics analgesics has anti-inflammatory effects mild and short-lasting antiplatelet effect vasoconstriction properties
ibuprofen (NSAIDS)
What can you use in these cases: Fever Inflammation Headache, Menstrual pain Toothache Back pain Arthritis, includingjuvenile arthritis Minor injuries
NSAIDS
What is an awesome NSAID that attacks some viruses, and can be used to treat pain, fever, inflammation, stiffness, migraine, osteoarthritis, gout, rheumatoid arthritis, psoriatic arthritis, kidneys stones, ankylosing spondyliis menstrual cramps, tenditinitis, and bursitis and primary dysmenorrhea?
Naproxen (aleve)
What is used to treat acute gouty arthritis, not recommended as a simple analgesic or antipyretic, used to speed closure of patent ductus arteriosus in premature infants, can have severe adverse effects and is not used in children (except for the ones in need of ductus arteriosus closure)?
indomethacin
What are some severe adverse effects of indomethacin?
bleeding, ulceration, headache
What is an oxicam derivate of enolic acid with a t1/2 of 45 hours, it is a long acting anti-inflammatory and analgesic agent. Like aspirin and indomethacin, bleeding and ulceration are more common than other NSAIDS. Long term uses induces hemorrhage and ulcers in GI tract.
Piroxicam (feldene, fexicam)
What drug is this:
selectively inhibits COX 2 (especially at low doses)
has higher concentration in synovial fluid due to the lower albumin content in synovial fluid as compared to plasma. Works well for the treatment of arthritis.
meloxicam (mobic)
What drug is this: equal to ASA in analgesic, antipyretic effects Lack of anti-inflammatory effects (not generally classified as NSAIDS) no gastric irritation (pKa 9.5) no platelet function inteference half life 2-3 hrs weak inhibitor of cox1, Cox2, cox3 can use it even if you have asthma not associated with reye's syndrome can cause liver toxicity
acetaminophen (tylenol, APAP)
How come acetaminophen (tylenol) can cause liver toxicity?
the toxic metabolite gets inactivated by glutathione and at high doses, causes liver toxicity
How do you treat acetaminophen toxicity?
give charcoal and N cysteine (to replenish glutathione stores)
Which one has these has these effects, NSAIDs or Acetaminophen?
anti-inflammatory effect, analgesic effect, antipyretic effect
NSAIDs
What are the 2 strongest effects of acetaminophen?
analgesic effect and antipyretic effect
How do NSAIDS work to create anti-inflammatory effects?
inhibits enzymes that produce prostaglandin H synthase (COX)
What does prostaglandin synthase do?
converts arachidoni acid to prostaglandins, TXA2 and prostacyclins
Aspirin (blank) inactivates COX-1 and COX-2 by acetylation of a specific serine residue. This distinguishes it from other NSAIDS, which (blank) inhibit COX-1 and COX-2.
irreversibly
reversibly
NSAIDs have a lot of different effects. What kind of effect do these create?
peripheral inhibition of prostaglandin production
inhibition of pain stimuli at a subcortical site. NSAIDs prevent the potentiating action of prostaglandins on endogenous mediators of peripheral nerve stimulation (e.g. bradykinin)
analgesic effect
NSAIDs have a lot of different effects. What kind of effect do these create?
Inhibition of production of prostaglandins induced by interluekin-1 (IL-1) and interleukin-6 (IL-6) in the hypothalamus. “resetting” of the thermoregulatory system, leading to vasodilation and increased heat loss.
antipyretic effects
What is the only NSAID that has antiplatelet effects?
aspirin
(blank) are first-line drugs used to arrest inflammation and the accompanying pain of rheumatic and nonrheumatic diseases, including rheumatoid arthritis, juvenile arthritis, osteoarthritis, psoriatic arthritis, ankylosing spondylitis, Reiter syndrome, and dysmenorrhea, hyperuricemia (acute gout,
NSAIDs
NSAIDS have anti-inflammatory effects that may develop only after several (blank) of treatment
weeks
How do NSAIDs affect rheumatic disease?
slows destruction of cartilage and bone and allows patients increased mobility and use of their joints
T or F
The inflammation and pain of arthritis are relieved, but the progressive degeneration of the joints is not prevented.
T
What are the effects of NSAIDs?
inhibits PGs and TxA1 synthesis by inhibiting COX
What are the effects of glucocorticoids?
inhibition of PLA2
What is the clinical usage for NSAIDs when it comes to anti-inflammation?
rheumatic, rheumatoid,
trauma
What are the side effects of NSAIDs?
Gi issues
What are the side effects of Glucocorticoids?
metabolism disturbance, damage of defenses
What 2 drugs are readily used for anti-inflammation?
glucocorticoids and NSAIDS
What 2 drugs are readily used for analgesia?
NSAIDS and Opioids
How do opioids work, what are they used for and what are the side effects?
stimulate opioid receptors
various pain including severe pain
addiction
What reasons might you use NSAIDS to treat analgesia?
headache, toothache, neuralgia, arthronalgia, courbature, menalgia
Which are more effective against pain associated with integumental structures?
NSAIDS
Do anti-pyresis drugs eliminate the cause of the fever?
no, just the symptoms
Does acetaminophen have anti-inflammatory effects? So what should you use with inflammation?
nope
aspirin and other salicylates
The use of aspirin and other salicylates to control fever during viral infections (influenza and chickenpox) in children and adolescents is associated with an increased incidence of (blank) (an illness characterized by vomiting, hepatic disturbances, and encephalopathy that has a 35% mortality rate).
Reye’s syndrome
How do NSAIDs have an antipyresis effect, what are they clinically used for and what are the side effects?
inhibit PG synthesis and enhance thermolysis
used in fevers
GI reactions,no addiction
How do chlorpromazine have an antipyresis effect, what are they clinically used for and what are the side effects?
inhibit thermotaxic center in hypothalamus
artificial hibernation, hypothermic anesthesia
extrapyramidal effects
NSAIDs inhibit production of (blank) and alleviate most of the pathologic effects associated with inflammation, but they also interfere with the physiologic role of PGs.
prostaglandins (PG)
Long-term therapy with nonspecific NSAIDs is frequently limited by their (blank), particularly those caused by erosion of gastric mucosal protection.
adverse effects
What are the most common adverse effects of high-dose aspirin use (70% of patients)?
nausea vomiting diarrhea or constipation dyspepsia (impaired digestion) epigastric pain ulceration (primarily gastric) or aggravate existing ulcers (particularly in the elderly patient) gastric bleeding
Tell me about gastric bleeding and aspirin.
10 g of aspirin causes bleeding regardless, may result in anemia or shock if gastric bleeding is severe
When shouldnt you give someone aspiring?
if they have ulcers, instead give them antacids and some prostaglandins
Why does aspirin cause GI problems?
acid on cells
decrease in prostaglandin
HCl on cells
decreased blood flow
(use PGE2,misoprostol, and flurbiprophen helps decrease damage)
How do you reduce the irritation to the GI tract?
substitution of enteric-coated or timed-release preparations
the use of nonacetylated salicylates
taken with food or after a meal
How come COX-2 selective inhibitors dont access COX1 enzymes?
cuz they are too bulky so they make for the perfect drug :)
What is celecoxib?
a cox 2 specific inhibitor
What is celecoxib? Does it cause ulcers? Does it cause CV events? Does naproxen cause ulcers?
a cox 2 specific inhibitor
NO
NO
YES
What does thromboxane do?
vasoconstricts and promotes platelet aggregation -> homeostasis and thrombosis
What does prostacyclin do?
vasodilator, inhibitor of platelet aggregation
Are rofecoxib (vioxx) and valdecoxib good drugs?
no, they have been removed because they increase heart attacks and strokes
What is the only selective cox 2 inhibitor available in the US and is approved for osteoarthritis, rheumatoid arthritis, pain (bone pain, dental pain, headache) and ankylosing spondylitis?
celecoxib
(blank) includes a boxed warning, highlighting the potential for increased risk of cardiovascular events and the well described, serious, potential life-threatening gastrointestinal bleeding associated with their use.
Celecoxib
What is relatively uncommon with the use of aspirin but results in rash, bronchospasm, rhinitis, edema, or an anaphylactic reaction with shock, which may be life threatening.
hypersensitivity (intolerance)
Hypersensitivity due to aspirin is highest in patients with ……?
asthma, nasal polyps, recurrent rhinitis, urticaria.
(blank) is not associated with:
sodium salicylate or
magnesium salicylate.
Hypersensitivity
(blank) may exist:
to other NSAIDs
to the yellow dye tartrazine, which is used in many pharmaceutical preparations.
Cross-hypersensitivity
Prostaglandins are involved in regulating renal blood flow. Chronic users of NSAID analgesics disrupt this regulatory function, which may lead to (blank) and (blank). The damage may progress to irreversible renal insufficiency.
papillary necrosis
secondary interstitial nephritis
Do we need to worry about nephropathy in daily use of NSAIDS for prophylaxis of MI?
no
phenacetin has been linked to causing a problem here
What are APCs (aspirin, phenacetin, caffeine) strongly associated with?
renal disease
What are the four selective cox-2 inhibitors?
celecoxib
etoricoxib
meloxicab
piroxicam
What is the clinical use of aspirin, dose wise?
low dose-> PA (platelet aggregation)
middle dose-> PF (pain and fever)
high dose-> RA (rheumatoid arthritis)
What are the major side effects of aspirin?
Major side effects: (the HUMBle ASPIRIN) Hepatotoxicity, Uric acid in serum increase if used in low doses, Metabolic acidosis, Bleeding GI. Asthma, Salicylism, Peptic ulcers, Irritation of GI tract, Reye’s syndrome, and Respiratory changes Intolerance to glucose Nephrotoxicity
What is the mneumonic for ibuprofen clinical use?
RIP
inflammation, patent ductus arteriosus in premature infants, rheumatoid disease
What are the major side effects of ibuprofen?
AA worsens GI IBUPROFEN Aseptic meningitis Asthma worsens GI Irritation of GI tract Bleeding Ulceration Pruritus Rush Ototoxicity, leading to tinnitus, dizziness Fluid retention Eye disturbances (blurred vision) Nephrotoxicity
What does celecoxib work on?
it is a cox B inhibitor
What do you use celecoxib for and what are the major side effects (CELECoxib)?
inflammation
Major side effects: (CELECoxib).
Cardiovascular thrombotic events following long term use,
Edema
Less GI irritation, bleeding, and ulcer than other NSAIDs
Elevated blood pressure
Caution: as a sulfonamide derivative may cause allergic reaction
How does acetaminophen work, what do you use it for, what are the major side effects?
weak inhibitor of all COXs
minor pain and high fever in children
messes with liver and kidney, hepatotoxicity, nephrotoxicity
How come acetaminophen causes liver problem? How can you fix this?
it depletes glutathione
give N-acetyl cysteine to replenish glutathione stores
(blank) inhibit eicosanoid production
corticosteroids
What does lipocortin do?
inhibits phospholipase A2 (i.e. keeps phospholipids from converting to LOX or COX)
(blank) regulate gene transcription and inhibits expression of interferon, granulocyte macrophage colony-stimulating factor, interleukins, and TNF alpha.
corticosteroids
What is this:
Physiological modulators of the immune system, profoundly inhibit the immune system at multiple sites and Impact virtually all tissues, protect the organism against life-threatening consequences of a full-blown inflammatory response
Slow onset of effect
Most effective anti-inflammatory drugs available, can be used to bridge gap between initiation of DMARD therapy
The worst drug for adverse effects
corticosteroids
What are these symptoms of: euphoria buffalo hump hypertension thinning of skin cataracts moon face increased abdominal fat avascular necrosis easy bruising poor wound healing fat redistribution glucose intolerance osteoporosis (prevent w/ bisphosphonates) gastric ulcers (prevent w/ omeprazole, misoprostol) increased susceptibility to infection growth inhibition in children
toxicity of chronic systemic glucocorticoids
What are these:
Anti-inflammatory and immunosuppressive effects
Can be used to bridge gap between initiation of DMARD therapy and onset of action
Intra-articluar injections can be used for individual joint flares and this is the major benefit in rheumatic arthritis
Pros of corticosteroids
What are these:
Does not conclusively affect disease progression
Tapering and discontinuation of use often unsuccessful
Low doses result in skin thinning, ecchymoses, and Cushingoid appearance
Significant cause of steroid-induced osteopenia
Cons of corticosteroids
How do corticosteroids work?
the regulate genes by binding to nuclear glucocorticoid receptors that reduce gene transcription and expression which reduces inflammation and immunity
What do probenecid and sulfinpyrazone do and how do they act?
they are organic acids that reduce urate levels in the kidneys to prevent reabsorption of uric acid. Used for chronic gout (often in combo with colchicine).
What are the major side effects of corticosteroids?
I’M 4 HOPEs
Infections Iatrogenic Cushing’s syndrome, Myopathy
Hyperglycemia, Hypertension, Hypokalemia, Hypomania
Osteoporosis Osteonecrosis (aseptic necrosis of the hip)
Peptic ulcers Pancreatitis, Edema, Eye disorder (cataracts)
What is this: a familial disease characterized by: recurrent hyperuricemia arthritis severe pain caused by deposition of uric acid xtals in the joint space with hyperuricemia, resulting in an inflammatory reaction. Granulocytes phagacytose the xtals. Since lactate production is fairly high in synovium, the acidic environment promotes further xtalization. Symptoms are typically seen in the distal phalangial joints.
gout
What is the go to drug to treat acute attacks of gout. This alkaloid drug reduces pain within 12-24 hours of taking it. Thought to prevent polymerization of tubulin into microtubules and inhibits leukocyte migration and phagocytosis, and inhibits cell mitosis. ????
colchicine
What sucks about colchicine?
80% of patients get nausea, vomiting, abdominal pain, and particullary diarrhea. (cuz the dose necessary to treat gout is very close to where adverse effects occur)
How can we sort of alleviate the negative effects of colchicine?
via IV administration (reduces GI disturbance and provides faster relief (6-12h) but increases risk of sloughing skin and subcutaneous tissue
What can high doses of colchicine do?
result in liver damage and blood dyscrasias
What do probenecid and sulfinpyrazone do and how do they act?
they are organic acids that reduce urate levels in the kidneys to prevent reabsorption of uric acid. Used for gout.
Probenecid and sulfinpyrazone undergo (blank) oral absorption.
rapid
What does probenecid and sulfinpyrazone do to the kidneys?
they inhibit the excretion of other drugs that are actively secreted by renal tubules (such as penicillin, NSAIDS, cephalosporins and methotrexate)
Increased urinary concentration of uric acid may result in the formation of (blank). This risk can be decreased how?
urate stones (urolithiasis) the ingestion of large volumes of fluid or alkalinization of urine with potassium citrate
What are common adverse effects of probenecid and sulfinpyrazone?
GI disturbances and dermatitis and rarely these agents cause blood dyscrasias
(blank) inhibits the synthesis of uric acid by inhibiting xanthine oxidase, an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid.
allopurinol
What is nifty about the metabolism of allopurinol?
that it inhibits xanthine oxidase, AND when it gets metabolized to allozanthine, it also inhibits xanthine oxidase : )
(blank) also inhibits de novo purine synthesis.
allopurinol
(blank) commonly produces GI disturbances and dermatitis. This agent rarely causes hypersenstivity, including fever, hepatic dysfunction, and blood dyscrasias.
allopurinal
When should you be cautious about giving allopurinol?
in patients with liver disease or bone marrow depression
(blank) blocks the action of xanthine oxidase by substrate competition and is also metabolized by it to form alloxanthine which also inhibits xanthine oxidase
Allopurinol
Why would you want to treat gout with NSAIDs rather than colchicine?
because colchicine causes diarrhea
Chronic gout is treated with (blank) to increase the elimination of uric acid and allopurinol to inhibit uric acid production.
uricosuric agents
What are these drugs called:
allopurinol, probenecid, sulfinpyrazone
maintenance drugs
(blank) gout is treated with NSAIDS. (blank) gout is treated with uricosuric agents.
acute
chronic
For treatment of gout, what do you need to do with fluids and your urine?
crush them with fluids
alkalize their urine (to prevent renal calculi)
what is a category of otherwise unrelated drugs defined by their use in rheumatoid arthritis to slow down disease progression?
What sucks about these drugs?
DMARDS (disease modifying antiarthritic drugs)
they take a while to work and they have adverse side effects in long-term use
What is azathioprine?
a purine synthesis inhibitor and DMARD
What is ciclosporin?
calcineurin inhibtor and DMARD
What is methotrexate?
a purine metabolism inhibitor and DMARD
What is leflunomide?
pyrimidine synthesis inhibitor and DMARD
