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Pharmacology > Immunopharm - Eicosanoids/Inflammation/RA > Flashcards

Immunopharm - Eicosanoids/Inflammation/RA Flashcards

1
Q

Eicosanoids:

This is a family of _____ C20 ___ ___ that are metabolites of 5, 8, 11, and 14 eicosatetraenoic acid (_____ acid)

A

Eicosanoids:

This is a family of oxygenated C20 fatty acids that are metabolites of 5, 8, 11, and 14 eicosatetraenoic acid (arachadonic acid)

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2
Q

Eicosanoids:

What are the four major groups and their products?

A

Eicosanoids:

a. Cyclooxygenases: PGs, TX, and prostacyclin (PGI2)
b. Lipoxygenases: LTs, HPETEs, HETEs, and lipoxins
c. P450: HETEs, diHETEs, and EETs
d. Endocannabinoids

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3
Q

Steps in eicosanoid biosynthesis:

  1. What is the precursor? How is the precursor derived?
  2. What stimulates the formation of the precursor?
A

Steps in eicosanoid biosynthesis:

  1. Precuror is arachidonic acid generated from phospholipids by PLPA2
  2. PLPA2 is stimulated by mechanical trauma, cytokines, or growth factors
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4
Q

Cyclooxygenases:

  1. Where are the membrane proteins?
  2. What are the 3 isomers?
  3. Aspirin irreversibly inhibits by ___ of ___
A

Cyclooxygenases:

  1. Membrane proteins are in the ER
  2. 3 isomers: COX-1. COX-2, and COX-3
  3. Aspirin irreversibly inhibits by o-acetylation of Ser
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5
Q

Lipoxygenases:

  1. Where is 12 lipoxygenase found?
  2. What two have a lot of sequence homology?
  3. What do they require?
A

Lipoxygenases:

  1. 12 lipoxygenase: CNS
  2. Sequence homology: 5 and 15 lipoxygenases
  3. They all require Ca++, ATP, and hydroperoxy acid
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6
Q
  1. Eicosanoids are paracrine or ___ hormones that are not stored but?
  2. They act largely as ____ hormones though the activation of?
A
  1. Eicosanoids are paracrine or autocrine hormones that are not stored but synthesized on demand
  2. They act largely as local hormones through the activation of G-protein coupled receptors
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7
Q

Pharmacology of Prostaglandins:

Cardiovascular:

  1. Blood pressure: What causes it to increase? Decrease?
  2. What dilates coronary vessels?
  3. What constricts coronary vessels?
A

Pharmacology of Prostaglandins:

Cardiovascular:

  1. BP: increased by TXA2; decreased by PGE and PGI2
  2. Dilation: PGE and PGI2
  3. Constriction: TXA2
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8
Q

Pharmacology of Prostaglandins:

Cardiovascular:

  1. What stimulates platlet aggregation?
  2. What inhibits platlet aggregation?
A

Pharmacology of Prostaglandins:

Cardiovascular:

  1. Stimulates: TXA2
  2. Inhibits: PGI2
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9
Q

Pharmacology of Prostaglandins:

Cardiovascular:

  1. What can maintain the patency of the ductus arteriosus?
  2. Clinical function of Alprostadil? What is it?
A

Pharmacology of Prostaglandins:

Cardiovascular:

  1. Patency of ductus arteriosus: PGE2 and PGI2
  2. Alprostadil (PGE1) maintains maternal/fetal blood flow
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10
Q

Pharmacology of Prostaglandins:

Kidney:

Role of PGE and PGI2?

A

Pharmacology of Prostaglandins:

Kidney:

PGE and PGI2 cause vasodilation, natriuresis, diuresis, and renin release

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11
Q

Pharmacology of Prostaglandins:

Respiratory:

  1. What dilates bronchioles?
  2. What constricts bronchioles?
A

Pharmacology of Prostaglandins:

Respiratory:

  1. Dilation of bronchioles: PGE and PGI2
  2. Constriction of bronchioles: TXA2 and PGF2alpha
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12
Q

Pharmacology of Prostaglandins:

Respiratory:

  1. ___ can be used as aerosol in bronchial asthma
A

Pharmacology of Prostaglandins:

Respiratory:

  1. _PGE2 _can be used as aerosol in bronchial asthma
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13
Q

Pharmacology of Prostaglandins:

GI:

  1. Roles of PGE2 and PGI2?
  2. Misoprostrol: analog of? use?
A

Pharmacology of Prostaglandins:

GI:

  1. PGE2/I2: inhibit gastric acid/pepsin secretion and increase mucous secretions
  2. Misoprostrol: PGE1 analog to promote ulcer healing
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14
Q

Pharmacology of Prostaglandins:

Reproductive system:

  1. Role of PGE2?
  2. Role of PGF2alpha?
  3. PGE2alpha and PGF2alpha are used for?
A

Pharmacology of Prostaglandins:

Reproductive system:

  1. PGE2: relaxes non-pregnant but contracts pregnant uterus
  2. PGF2alpha: contracts both nonpregnant and pregnant uterus
  3. PGE2alpha/F2alph: used as contraceptive, to induce abortion and to control postpardum hemorrhage
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15
Q

Pharmacology of Prostaglandins:

Reproductive system:

  1. Drugs for parturition? Their analogs?
  2. What is alprostadil used for?
  3. What prostaglandin is responsible for facilitating labor? How?
A

Pharmacology of Prostaglandins:

Reproductive system:

  1. Carboprost tromethamine (PGF2alpha) and Dinoprostone (synthetic PGE2)
  2. Alprostadil - used for impotency
  3. PGE2 facilitates labor through dilation of the cervix
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16
Q

Pharmacology of Prostaglandins:

Pain and inflammation:

PGs produce ___ or ____ (increased sensitivity to painful stimuli)

Fever: central administration of PGs - especially into the ____ produces fever

A

Pharmacology of Prostaglandins:

Pain and inflammation:

PGs produce pain or hyperalgesia (increased sensitivity)

Fever: central admin, especially into the hypothalamus produces fever

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17
Q

Lipoxygenase Products:

Hydroperoxy-eicosatetraenoic acids (HPETE):

Role in:

  1. Blood vessels?
  2. Platelets?
  3. Inhibit ____ synthetase
A

Lipoxygenase Products:

Hydroperoxy-eicosatetraenoic acids (HPETE):

Role in:

  1. Contract blood vessels
  2. Promote platelet aggregation
  3. Inhibit prostacyclin synthetase
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18
Q

Lipoxygenase Products:

Hydroperoxy-eicosatetraenoic acids (HPETE):

  1. Cause ____
  2. Role in pain?
  3. May be __ ___ in cells
A

Lipoxygenase Products:

Hydroperoxy-eicosatetraenoic acids (HPETE):

  1. Cause chemotaxis
  2. May cause pain or hyperalgesia
  3. May be second messengers
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19
Q

Lipoxygenase Products:

Leukotrienes:

  1. Synthesized from ____ in ___ cells and ___.
  2. What is the predominant mediator of inflammation?
  3. What causes bronchoconstriction? Through activation of?
A

Lipoxygenase Products:

Leukotrienes:

  1. Synthesized from 5-HPETE in mast cells and neutrophils
  2. Predominant mediator of inflammation = LTB4
  3. Bronchoconstriction: LTC4 and LTD4 by activation of the cys-LT1 receptor
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20
Q

Lipoxygenase Products:

Leukotrienes:

  1. LTC4 and LTD4 are the slow reacting substance of ____
  2. Actions of LTC4/D4/#4 at cys-LT1 receptor are blocked by what two antagonists? What are these used in
A

Lipoxygenase Products:

Leukotrienes:

  1. LTC4 and LTD4 are the slow reacting substances of anaphylaxis
  2. cys-LT1 receptor is blocked by zafirlukast and montelukast in the treatment of asthma
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21
Q

NSAIDs:

  1. Inhibit the formation of ___ by blocking the actions of ______.
  2. Reduce symptoms associated with inflammatory disease but?
  3. NO _____ development
A

NSAIDs:

  1. Inhibit the formation of PGs by blocking the actions of cyclooxygenases
  2. Do not affect the underlying disease
  3. NO tolerance development
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22
Q

NSAIDs:

  1. Main therapeutic actions?
  2. Acetaminophen does not have one of the main actions: which?
  3. Aspirin is the only prophylactic drug to reduce risk of ____: why?
A

NSAIDs:

  1. Analgesic, Antipyretic, and anti-inflammatory
  2. Acetaminophen - is NOT anti-inflammatory
  3. Aspirin is the only prophylactic drug to reduce the risk of MI because it is the only drug that irreversibly blocks the pathway
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23
Q

NSAIDs:

Untoward effects:

  1. Stomach?
  2. Respiration?
  3. Coagulation?
  4. Gestation?
  5. Potential ___ damage and disturbance in ___/___ balance
A

NSAIDs:

Untoward effects:

  1. Gastric irritation
  2. Altered respiration
  3. Increased bleeding
  4. Increased gestation time
  5. Potential renal damage and disturbance in acid/base balance
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24
Q

Salicylates:

  1. Drug?
  2. Therapeutic action?
  3. Role of aspiring in MI? and other cardiac conditions?
  4. Topical for?
A

Salicylates:

  1. Acetylsalicylic acid
  2. Analgesia, antipyresis, anti-inflammatory
  3. Aspirin: reduces incidence of acute MI and death in patients with unstable angina and reduces frequency of ischemic attacks in patients with atherosclerosis
  4. Topical for keratolytic action (warts)
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25
Q

Salicylates:

Primary effects:

  1. CNS?
  2. GI?
  3. Respiration?
  4. ____thermia and _____
A

Salicylates:

Primary effects:

  1. CNS - tinnitis, confusion, decreased hearing
  2. GI - N/V
  3. Stimulates respiratory center
  4. hyperthermia and dehydration
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26
Q

Salicylates:

Primary effects:

  1. Uncoupling of ____ ___
  2. Inhibits ____ cycle
  3. Lipid metabolism?
A

Salicylates:

Primary effects:

  1. Uncoupling of oxidative phosphorylation
  2. Inhibits TCA cycle
  3. Stimulates lipid metabolism
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27
Q

Salicylates:

Therapeutic doses:

  1. ____ respiration secondary to ___ oxygen consumption and ____ CO2 production.
  2. Also directly ____ respiration
  3. Results in respiratory ____ (__ CO2 expelled due to ___ breathing) and increased renal excretion of ___ to compensate and return pH to normal
A

Salicylates:

Therapeutic doses:

  1. Stimulates respiration secondary to increased oxygen consumption and decreased CO2 production
  2. Also directly stimulates respiration
  3. Results in respiratory alkalosis (decreased CO2 expelled due to increased breathing) and increased renal excretion of HCO3- to compensate and return pH to normal
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28
Q

Salicylates:

Toxic doses:

  1. Respiration?
  2. Metabolic ____. Displacement of ____. Decreased renal excretion of organic ___. Increased ___ __ production secondary to increased carbohydrate metabolism
A

Salicylates:

Toxic doses:

  1. Decreased respiration –> increased CO2 (shifts towards H+ then)
  2. Metabolic acidosis. Displacement of HCO3-. Decreased renal excretion of organic acids. Increased lactic acid production secondary to increased carbohydrate metabolism
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29
Q

Salicylates:

Toxicity:

  1. Effects on GI?
  2. Effects on blood?
  3. Liver?
A

Salicylates:

Toxicity:

  1. GI: epigastric distress, N/V, gastric ulceration, hemorrhage, exacerbation of ulcers
  2. Blood: inhibit platelet aggregation and prolong bleeding
  3. Potential hepatotoxicity
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30
Q

Salicylates:

Toxicity:

  1. Acute ___ insufficiency in patients with underlying disease. What kind of patients would this be?
  2. ___ acid excretion. Low doses can worsen ___.
  3. And __/__ balance issues.
A

Salicylates:

Toxicity:

  1. Acute renal insufficiency; liver disease with ascites, CHF, or renal disease
  2. Uric acid excretion. Low doses can worsen gout
  3. Acid/base balance issues
31
Q

Salicylates:

Toxicity:

Can lead to Reye’s syndrome: what are the symptoms?

What is prognosis linked to?

A

Salicylates:

Toxicity:

Reyes: persistant/recurrent vomitting, listlessness, irritability, combativeness, disorientation or confusion, delirium, convulsions, and loss of consciousness

Prognosis is linked to the severity of brain swelling

32
Q

Salicylates:

Toxicity:

How do you treat poisoning?

A

Salicylates:

Toxicity:

Poisoning: charcoal, laxative, lavage (up to 1 hour after), IV fluids, alkaline diuresis, and/or hemodialysis

33
Q

Salicylates:

Contraindications:

Thinking of the side effects of toxicity and the things they cause, what kind of patients should not take salicylates?

A

Salicylates:

Contraindications:

a. Patients with ulcers or clotting disorders
b. Patients allergic to aspirin
c. Pregnant women
d. Gout (but only in high doses)
e. Viral infections in kids (increased risk of Reyes)

34
Q

Salicylic acid derivatives:

  1. Mesalamine = amino salicylate: treats?
  2. Sodium salicylate: function
A

Salicylic acid derivatives:

  1. Mesalamine: treats/prevents ulcerative colitis and mild to moderate chrons
  2. Sodium salicylate: replacement for those with salicylate sensitivity
35
Q

Acetaminophen:

In contrast to salicylates:

  1. Not a useful ______ agent with weak effects on ___.
  2. No alterations in ___ balance and thus no ____ effects.
  3. Minimal effects on?
A

Acetaminophen:

In contrast to salicylates:

  1. Not a useful anti-inflammatory agent with weak effects on platelets
  2. No alterations in pH balance and thus no uricosic effects
  3. Minimal effects on GI
36
Q

Acetaminophen:

In contrast to salicylates:

Because its weak on platelets, no pH alteration, minimal GI effects, no uricosuric effects its advantageous in:

  1. Patients with ___ ___ disease
  2. People who are ___ intolerant
  3. Patients on oral ____ or have ___ disorders
  4. Patients with ___ or infections suceptible to ___
A

Acetaminophen:

In contrast to salicylates:

Because its weak on platelets, no pH alteration, minimal GI effects, no uricosuric effects its advantageous in:

  1. Patients with peptic ulcer disease
  2. Patients who are aspirin intolerant
  3. Patients on oral anticoagulants or coagulation disorders
  4. Patients with gout or suceptibility to Reyes
37
Q

Acetaminophen:

Therapeutic uses?

A

Acetaminophen

Analgeia and antipyresis

38
Q

Acetaminophen:

Toxicity:

  1. Most serious potential problem?

Course: initially ___ symptoms followed by a period of recovery and then appearance of ______. A metabolite has been formed to exceed the availability of ___ to inactivate it before it causes cell ___ and necrosis. NAPQI - irreversibly conjugated with ____.

A

Acetaminophen:

Toxicity:

  1. Most serious: fatal hepatic necrosis with acute od

Course: initially GI symptoms followed by a period of recovery and then appearance of jaundice. A metabolite has been formed to exceed the availability of glutathione to inactivate it before it causes cell death and necrosis. NAPQI - irreversibly conjugated with glutathione

39
Q

Acetaminophen:

Toxicity:

2 treatment for poisons? Administration?

A

Acetaminophen:

Toxicity:

Poison: methionine (oral) and N-acytylcystine (NAC: precursor for glutathione: IV or Oral)

40
Q

Acetaminophen:

  1. Side effects?
  2. Rare but serious/fatal side effects?
A

Acetaminophen:

  1. SE: rash, mucosal lesions, and leukopenia
  2. Rare: steven johnson’s, toxic epidermal necrosis, or acute generalized exanthematous pustulosis
41
Q

Other NSAIDs:

  1. Indomethacin - why no longer first choice?
  2. Sulindac - prodrug used in what patients? Where does inactivation occur?
  3. Ibuprofen: lowest incidence of?
A

Other NSAIDs:

  1. Indomethacin - High GI toxicity
  2. Sulindac - prodrug used in patients with impaired renal function. Inactivation occurs in the kidney
  3. Ibuprofen: lowest incidence of GI side effects of all NSAIDs
42
Q

Other NSAIDs:

  1. Naproxin - lowest incidence risk of?
  2. Diclofenac - better ____
  3. Piroxicam is ____ acting
A

Other NSAIDs:

  1. Naproxin - lowest CV risk of all NSAIDs
  2. Diclofenac - better tolerated
  3. Piroxicam is long acting
43
Q

Other NSAIDs:

Name the other NSAID categories and the drug(s) associated.

A

Other NSAIDs:

a. Indole/Indene Acetic Acids - indomethacin and sulindac
b. Heteroaryl Acetic Acids - Ketorolac
c. Arylpropionic Acids - ibuprofen and neproxin
d. Phenyl Acetic Acid - Diclofenac
e. Enolic Acids - Piroxicam

44
Q

COX-2 inhibitors:

  1. Drug?
  2. Less ___ ___ compared to those that inhibit both COX-1 and COX-2.
  3. Contraindications?
  4. ___ onset of analgesia and thus not used for __ pain
A

COX-2 inhibitors:

  1. Celecoxib
  2. Less side effects
  3. Celecoxib - contra w. sulfa sensitivity
  4. Slow onset of analgesia and thus not used for acute pain
45
Q

COX-2 inhibitors:

  1. Some reports of?

Warnings:

  1. NEVER EVER?
  2. ___ plasma protein binding of NSAIDs and _____ (anti-diabetics)
  3. Increased risk of bleeds with NSAIDS + ___
A

COX-2 inhibitors:

  1. Some reports of GI bleeding/ulceration

Warnings:

  1. NEVER EVER use 2 NSAIDs concurrently
  2. High plasma protein binding of NSAIDs and sulfonylureas
  3. Increased risk of bleeds with NSAIDs + Warfarin
46
Q

Rheumatoid arthritis:

  1. Symptoms?
  2. Diagnosis?
  3. Key cytokine?
A

Rheumatoid Arthritis:

  1. Symptoms: swollen glands, morning stiffness, joint pain, swollen joints, decreased appetite and can have pleurisy, nodules under skin, and numbness/tingling/burning in hands or feet
  2. Diagnosis: anti-CCP antibody test, X-ray, MRI, ultrasound
  3. Key cytokine = TNF
47
Q

Rheumatoid Arthritis:

  1. These are all DMARDs: what does this stand for?
  2. What are the antineoplastic drugs and when are they used?
  3. Side effects of antineoplastic drugs?
A

Rheumatoid Arthritis:

  1. Disease Modifying Anti-Rheumatic Drugs
  2. Antineoplastic drugs: azathioprine, leflunomide, methotrexate, and penicillamine; used only in severe RA
  3. SE: fever, chillse, anorexia, N/V, hepatotoxicity, agranulocytosis, leukopenia, anemia, and thrombocytopenia
48
Q

Rheumatoid Arthritis:

Methotrexate:

  1. Uses?
  2. Analog of?
  3. Inhibits metabolism of ___ acid by inhibiting _____ ___.
A

Rheumatoid Arthritis:

Methotrexate:

  1. One of the most effective drugs for RA, also good for neoplasms, GVHD, and autoimmune disorders
  2. Analog of folic acid
  3. Inhibits metabolism of folic acid by inhibiting dihydrofolate reductase
49
Q

Rheumatoid Arthritis:

Methotrexate:

  1. Has ___ and anti-inflammatory activity.
  2. SE?
A

Rheumatoid Arthritis:

Methotrexate:

  1. Has cytotoxic activity
  2. SE: dyspnea, diarrhea, vomitting, blood in stool/urine, fever, chills, aches, and teratogenic
50
Q

Rheumatoid Arthritis:

Methotrexate:

MOA:

RA: inhibition of enzymes involved in ____ ____ –> accumulation of ___ or inhibition of __ cell activation

Cancer: competitive inhibition of ____ for _____ synthesis needed to make ___ –> this inhibits synthesis of?

A

Rheumatoid Arthritis:

Methotrexate:

MOA:

RA: inhibition of enzymes involved in purine metabolism –> accumulation of adenosine or inhibition of T cell activation

Cancer:competitive inhibition of DHFR for tetrahydrofolate synthesis needed to make thymidine –> inhibits synthesis of DNA, RNA, thymidylates, and proteins

51
Q

Rheumatoid Arthritis:

Methotrexate:

  1. The one main drug interaction?
A

Rheumatoid Arthritis:

Methotrexate:

  1. Penecillin: causes decreased elimination of methionine and thus increases the risk of toxicity
52
Q

Rheumatoid Arthritis:

  1. Etanercept: moa?
  2. Infliximab and Adalimumab: MOA?
  3. Anakinra: MOA?
A

Rheumatoid Arthritis:

  1. Etanercept: acts as a decoy and binds to TNFalpha receptor
  2. Infliximab and Adalimumab: antibodies to TNFalpha
  3. Anakinra: IL-1beta receptor antagonist
53
Q

Rheumatoid Arthritis:

Etanercept, Infliximab, Adalimumab, and Anakinra:

  1. Major side effects secondary to injection for Etanercept?
  2. Infusion reaction between ____ and anakinra: causes?
  3. Major SE of concern?
A

Rheumatoid Arthritis:

Etanercept, Infliximab, Adalimumab, and Anakinra:

  1. SE secondary to injection: pain, swelling, redness, and itch
  2. Infusion reaction between infliximab and anakinra: causes fever, chills, rash, and itch
  3. Major SE of concern is infection
54
Q

Rheumatoid Arthritis:

Etanercept, Infliximab, Adalimumab, and Anakinra:

  1. Other SE?
  2. Rarely, infliximab can cause?
  3. These are contraindicated in?
A

Rheumatoid Arthritis:

Etanercept, Infliximab, Adalimumab, and Anakinra:

  1. SE: nausea, HA, abdominal pain, and vomitting
  2. Infliximab: anaphylaxis, hypotension, or lupus-like syndrome
  3. Contraindicated in sepsis
55
Q

Rheumatoid Arthritis:

Abetacept:

MOA?

Function?

A

Rheumatoid Arthritis:

Abetacept:

MOA: Binds to B7 on APC and prevents delivery of costimulatory signal to T cells

Function: to render T cells inactive

56
Q

Traditional DMARDS:

Hydroxychloroquine:

  1. Type of drug? For?
  2. MOA? Result?
A

Traditional DMARDS:

Hydroxychloroquine:

  1. Antimalarial also for arthritis and lupus
  2. MOA: blocks TLR on dendritic cells –> decreases activation of dendritic cells and inflammatory processes
57
Q

Traditional DMARDS:

Leflunomide:

  1. Activities?
  2. MOA?
  3. T1/2?
A

Traditional DMARDS:

Leflunomide:

  1. Immunomodulator and anti-inflammatory
  2. MOA: inhibition of mitochondrial DHODH for pyrimadine ribonucleotide uridine monophosphate (rUMP); pyrimidine synthesis inhibitor
  3. Very long
58
Q

Gold compounds:

  1. Name 3 drugs?
  2. Uses?
  3. Can relieve ___ and ___ and for some may ___ progression but DO NOT ___ ___ that has already occured
A

Gold compounds:

  1. Auranofin, Aurothioglucose, and Gold sodium thiomalate
  2. Management of progressive RA that is unresponsive to traditional therapies
  3. Can relieve pain and symptoms and for some may arrest progression but DO NOT reverse damage that has already occured
59
Q

Gold compounds:

Side effects?

A

Gold compounds:

SE: metallic taste, stomatitis, diarrhea, cramping. Some develop a rash, dermatitis, thrombocytopenia, aplastic anemia, agranulocytosis, and acute tubular necrosis

60
Q

Rituximab:

  1. What is this? MOA?
  2. SE?
  3. Major SE?
  4. Contraindications?
A

Rituximab:

  1. Monoclonal Ab to CD20 on B cells - allowing a new population of healthy B cells to develop from lymphoid stem cells
  2. SE: pain/swelling/itching/fever/chills/rash, N/V, HA
  3. Major: infection
  4. Contraindication: sepsis
61
Q

Gout:

Acute gout:

  1. Where does this occur?
  2. Symptoms?
  3. Duration?
A

Gout:

Acute gout:

  1. It is monoarticular in the first metatarsophalangeal joint
  2. Symptoms: severe pain (allodynia), inflammation, limited range of motion
  3. Can resolve in a week or more even with no treatment
62
Q

Gout:

Chronic gout:

  1. Where?
  2. Associated with what in the elderly?
  3. Contains Tophi - what is this? Where?
  4. What can Tophi cause?
A

Gout:

Chronic gout:

  1. Polyarticular in joints in upper extremities
  2. Associated with diuretic use or renal insufficiency in old
  3. Tophi = deposit of monosodium urate crystals; in joins, cartilage, and bones
  4. Can cause deformities, tissue damage, and joint destruction
63
Q

Causes of Hyperuricemia: name 2?

A

Causes of hyperuricemia:

a. increased uric acid production or
b. decreased uric acid excretion

64
Q

Hyperuricemia:

Increased Uric acid production associated with:

  1. High ___ intake
  2. ___ disorders such as myeloproliferation or?
  3. Medications such as?
A

Hyperuricemia:

Increased Uric acid production associated with:

  1. High purine intake
  2. Hematologic disorders such as myeloproliferation or sickle cell anemia
  3. Cytotoxic medications
65
Q

Hyperuricemia:

Increased Uric acid production associated with:

  1. Genetic factors resulting in altered ____ metabolism
  2. What 4 other things?
A

Hyperuricemia:

Increased Uric acid production associated with:

  1. Genetic factors resulting in altered hypoxanthine metabolism
  2. diabetes, obesity, alcohol consumption, and excessive exercise
66
Q

Hyperuricemia:

Decreased uric acid excretion associated with:

  1. Use of what med?
  2. Disease factors affecting ___ function (hypertension)
  3. Genetic factors resulting in ___ ___ or excretion of urate
  4. What 2 other things?
A

Hyperuricemia:

Decreased uric acid excretion associated with:

  1. Use of diuretics
  2. Disease factors affecting renal function
  3. Genetic factors resulting in reduced clearance of urate
  4. Obesity and toxemia/pre-eclampsia in pregnancy
67
Q

4 ways to diagnose gout?

A

Gout diagnosis:

a. Synovial fluid analysis
b. Joint x-ray (may be normal)
c. Synovial biopsy
d. Uric acid in blood or urine

68
Q

Drug treatment of Gout:

Name 8 drugs or classes?

A

Drugs:

a. NSAIDs
b. Glucocorticoids
c. Cochicine
d. Probenecid and Sulfinpyrazone
e. Allopurinol and Febuxostat
f. Rasburicase

69
Q

Treatment of gout:

Cochicine:

  1. Use?
  2. Not _____
  3. Inhibits migration of ___ to inflammed area.
  4. SE? Long term?
A

Treatment of gout:

Cochicine:

  1. Acute attacks and prophylactic for actue attacts
  2. Not ucosuric
  3. Inhibits migration of granulocytes to inflamed area
  4. SE: GI distress, N/V, diarrhea, abdominal pain; Long term: blood dyscrasias
70
Q

Treatment of gout:

Probenecid and Sulfinpyrazone:

  1. Prevention of ____ by increasing renal clearance of ___ __ by ____ reabsorption
  2. Probenecid: no longer for elderly - why?
  3. Patient should dring lots of water and ___ the urine to prevent?
A

Treatment of gout:

Probenecid and Sulfinpyrazone:

  1. Prevention of hyperuricemia by increasing clearance of uric acid by decreasing reabsorption
  2. Probenecid: no longer for elderly due to decreased renal function
  3. Water and alkalanize to prevent precipitation of uric acid in renal tubules
71
Q

Treatment of gout:

Probenecid and Sulfinpyrazone:

  1. MOA: Prevent uric acid ___ in tubules by interfering with ___ ___ ___ which reclaims uric acid from ___ and returns it to ___
  2. SE?
  3. Caution in what patients? WHy?
A

Treatment of gout:

Probenecid and Sulfinpyrazone:

  1. MOA: Prevent uric acid crystals in tubules by interfering with organic anion transporter which reclaims uric acid from urine and returns it to plasma
  2. SE: rash and hypersensitivity
  3. Caution in patients with peptic ulcers bc it can cause GI irritation
72
Q

Treatment of gout:

Allopurinol and Febuxostat:

  1. Allopurinol is?
  2. Febuxostat is?
  3. How does it prevent hyperuricemia?
A

Treatment of gout:

Allopurinol and Febuxostat:

  1. Allopurinol is a purine analog
  2. Febuxostat is a non-purine inhibitor
  3. Prevents hyperuricemia by decreasing uric acid production
73
Q

Treatment of gout:

Allopurinol and Febuxostat:

  1. MOA: inibition of ___ ___ which is responsible for?
  2. SE?
A

Treatment of gout:

Allopurinol and Febuxostat:

  1. MOA: inhibition of xanthine oxidase which is responsible for the succesive oxidation of hypoxanthine and xanthine –> resulting in production of uric acid
  2. SE: rash and hypersensitivity; also maybe fever, malaise, muscle aches, and rarely leukopenia
74
Q

Treatment of gout:

Rasburicase:

  1. How does it prevent hyperuricemia?
  2. Recombinant version of?
  3. MOA: catalyzes the conversion of?
A

Treatment of gout:

Rasburicase:

  1. Prevents hyperuricemia by decreasing uric acid production
  2. Recombinant version of urate oxidase
  3. MOA: catalyzes the conversion of uric acid to allantoin which is an inactive metabolite of purine metabolism (renal excretion is then more effective)

Pharmacology (24 decks)

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