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Block 4 week 2 Dani > Duan: Pharm > Flashcards

Duan: Pharm Flashcards

1
Q

(blank) is a defense reaction against tissue injury or damage caused by physical injury, thermal injury, infectious agents, antigen-antibody interaction, ischemia, etc

A

inflammation

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2
Q

What are the three phases of inflammation?

A

acute
subacute
chronic proliferative

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3
Q

What phase of inflammation is this:

vasodilation and capillary permeability

A

acute

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4
Q

What phase of inflammation is this:

infiltration of leukocytes and phagocytes (effects of chemokines)

A

subacute or delayed

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5
Q

What phase of inflammation is this:

tissue degeneration and fibrosis

A

chronic proliferative

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6
Q

What causes the redness seen in inflammation?

A

vasodilation of capillaries increases blood flow

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7
Q

What causes the heat felt in inflammation?

A

vasodilation

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8
Q

What causes the pain felt in inflammation?

A

hyperalgesia, sensitization of nocicpetors

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9
Q

What causes the swelling in inflammation?

A

increased vascular permeability (microvascular structural changes and escape of plasma proteins from the bloodstream)

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10
Q

What are these:
osteoarthritis, rheumatoid arthritis, juvenile arthritis, gouty arthritis, ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome

A

different kinds of arthritis

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11
Q

What are arthritic disorders characterized by?

A

inflammatory changes and symptoms (pain, heat, redness, and swelling) and subsequent tissue damage with atrophy and rarefraction of bones

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12
Q

In late stage of arthritis what may develop?

A

deformity and ankylosis

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13
Q

TO block an inflammatory response, do you want to block COX 1 or COX2?

A

COX 2

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14
Q

THe underlying causes for many of the arthritic disorders are complex and usually cannoto be cured. The goal of treatment is to (blanK).

A

relieve inflammation, control pain, improve function, prevent further joint damage, improve quality of life

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15
Q

Which part of your immune system does an infection affect?

A

the adaptive and innate immune system

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16
Q

What part of the immune system reacts to a perceived threat?

A

adaptive immune system

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17
Q

What will tissue injury, adaptive immune system, and the innate immune system activate?

A

leukocytes and endothelial cells

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18
Q

What will leukocytes and enothelial cells activate?

A

biochemical inflammatory mediators

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19
Q

So please briefly describe the inflammatory cascade

A

threat, tissue injury, infection-> immune system-> leukocytes and endothelial cells activation-> biochemical inflammatory mediators-> inflammation symptoms

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20
Q

The symptoms of inflammation are caused by a series of (blank) including the metabolites of eicosanoids.

A

biochemical mediators

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21
Q

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):

A

biochemical mediators

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22
Q

What are some arachidonic acid metabolites (eicosanoids)?

A

thromboxane A2 (TXA2)
HETE (hydroxy-eicostatraenoic aid)
Leukotrienes (LTs)
Prostaglandins (PG mediated by cyclooxygenases COX)

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23
Q

What is this:

20 C fatty acid chains and produce prostanoids and leukotrienes and acts as an immune system modulators

A

arachidonic acids

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24
Q

What does COX do?

A

cause inflammation

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25
Q

What does LOX (lipoxygenase) do?

A

phagocyte mobilization and changes vascular permeability and causes inflammation

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26
Q

Where do arachidonic metabolites come from?

A

from phospholipids

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27
Q

How will diverse physical, chemical, inflammatory, and mitogenic stimuli affect arachidonic metabolism?

A

it will activate phospholipase A2 which will convert phospholipids into the things that will cause inflammation

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28
Q

What do the prostanoids cause (prostaglandins, prostacyclin, thromboxane)?

A

inflammation

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29
Q

How do you convert arachodinoc acid into EETs for reuse?

A

via cytochrome P450

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30
Q

What cox does this:
platelet function
GI mucosal integrity
renal function

A

COX 1 (induces constitutive physiological regulation)

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31
Q

What cox does this:
inflammation
pain fever

A

COX2 (induces inflammatory response)

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32
Q

WHat does aspirin inhibit?

A

both COX1 and COX2

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33
Q

(blank) directly sensitize pain fibers (Ad and unmyelinated C fibers) so they respond to normally innocuous stimuli (hyperalgesia)

A

prostaglandins

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34
Q

Subdural injetion of PGE1 (prostaglandin E 1) with small amounts of bradykinin and histamine causes (blank)

A

headache and pain

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35
Q

What causes a fever?

A

neutrophils release pyrogens (cytokines, TNF A, ILs)

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36
Q

(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.

A

Pyrogens

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37
Q

If you inhibit prostaglandin synthesis in the CNS, what will happen?

A

cutaneous dialtion

increased heat loss-> reduction in fever and symptoms of fever

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38
Q

What do corticosteroids (predinisone, dexamethasone) do?

A

inhibit leukocyte and endothelial cells activation by blocking Phospholipase A2 and COX

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39
Q

What do NSAIDS do?

A

inhibit inflammatory mediators by blocking COX

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40
Q

What do 5-LOX inhibitors and leukotriene receptor antagonists (Zafirlukast, zileuton) do?

A

inhibit inflammatory mediators by blocking COX

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41
Q

What do you use aspirin for with heart issues?

A

as a blood thinner for prevention of heart attacks

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42
Q

(blank) covalently and irreversibly modifies both COX 1 and COX 2 by acetylating serine 530 in the active site.

A

acetylsalicylate (ASA)

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43
Q

What does the acetylation of COX by ASA do?

A

it causes a steric block to prevent arachidonic acid from binding

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44
Q

Does acetylation of COX-2 allow it to retain the cox activity but produce a different product, such as 15-R-HETE?

A

YES!

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45
Q

(blank) irreversibly inhibits platelet COX-1 and COX-2 and, thereby inhibits thromboxane production (remember, thromboxane stimulates platelet aggregation)

A

Aspirin

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46
Q

Why dont you give someone aspirin when they are pregnant?

A

cuz they may induce postpartum hemorrhage

premature closure of the fetal ductus arteriosus (cuz prostaglandins keep it open :) )

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47
Q

At less than 300 mg /Day, what kind of effects with aspirin induce?

A

blocks platelet aggregation and has antithrombic effects

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48
Q

At doses between 300-2400 mg/day, what kind of effects does aspirin have (intermediate)?

A

antipyretic, analgesic effects

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49
Q

At doses between 2400-4000 mg/day. what kind of effects does aspirin have (high)?

A

anti-inflammatory

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50
Q

Aspirin is most commonly used in the clinics for the treatment of a number of conditions, including…..?

A 
fever
pain
rheumatic fever
inflammatory diseases
lower doses of aspirin
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51
Q

What can treat rheumatoid arthritis, pericarditis, and kawasaki disease?

A

aspirin, bitches

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52
Q

What kind of acids are salicylates?

A

weak organic acids

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53
Q

aspirin has a pKa of (blank).

A

3.5

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54
Q

Why is aspirin rapidly absorbed from the stomach as well as from the intestine?

A

cuz the low pH favors absorption

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55
Q

where do unmetabolized salicylates go?

A

they are excreted by the kidney

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56
Q

How do you treat an acid overdose?

A

you raise the urine pH to increase the clearance of it

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57
Q

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 (

A

salicylic acid
glycine
salicyluric acid

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58
Q

If you oxidize salicylate, what do you get?

A

gentisic acid

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59
Q

If you conjugate salicylate with glycine what do you get?

A

salicyluric acid

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60
Q

If you conjugate salicylate with glucronic acid what do you get?

A

ester and other glucuronides

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61
Q

Is asprin rapidly hydrolyzed?

What does this mean about the levels of aspirin in the plasma?

A

yes

they are low and rarely exceed 20 mg/ml at ordinary therapeutic doses

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62
Q

What is the plasma half-life for aspirin? What happens to this half-life as the dose of aspirin increases?

A

15 minutes

the half life increases as well

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63
Q

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?

A

3.1 to 3.2 hours
~5 hours
~9 hours
15-30 hours

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64
Q

At low and moderate doses of salicylate, how is the drug eliminated?

A

first order

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65
Q

At high doses of salicylate, how is the drug eliminated?

A

zero order

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66
Q

In high doses of asprin, or toxic overdose, the enzymes for glycine and glucuronide conjugation become (blank)

A

saturated

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67
Q

Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with heparin or oral anticoagulants?

A

result in hemorrhage!

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68
Q

Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with antacids?

A

reduced rate of aspirin absorption

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69
Q

Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with probenecid or sulfinpyrazone?

A

decreased urate excretion (contraindicated in patients with gout)

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70
Q

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?

A

result in increased plasma concentration leading to prolonged half-lives, therapeutic effects, and toxicity

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71
Q

What are the adverse effects of aspirin?

A 
GI symptoms
allergic reactions
CNS toxicity
Salicylate reaction (CNS reaction)
renal damage
hematologic effects
metabolic acidosis 
Reyes syndrome
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72
Q

Why should aspirin not be given to patients with asthma?

A

it causes contraction of the bronchioles-

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73
Q

What are the three most common adverse effects of aspirin?

A

salicylate reaction (CNS reaction)
hematologic effects
Reye’s syndrome

74
Q

What is reye’s syndrom?

A

it is found in kids who take too much aspirin and results in severe hepatic damage and encephalopathy

75
Q

How do you get salicylism (overdose or poisoning)?

A

a dose greater than 5 g/d of aspirin or salicylate

76
Q

In adults, what is the initial sign of salicylism toxicity?

A

tinnitus, hearing loss, vertigo

77
Q

In children, what is the intitial sign of salicylism toxicity?

A

acidosis and hyperventilation with accompanying lethargy

78
Q

How do you treat salicylate overdose?

A 
alkalize urine
correct acid-base disturbance
replace electrolytes and fluids
cooling
forced diuresis, hemodialysis
gastric lavage or emesis
79
Q 
What are these: 
strong antipyretics 
analgesics 
has anti-inflammatory effects
mild and short-lasting antiplatelet effect 
vasoconstriction properties
A

ibuprofen (NSAIDS)

80
Q 
What can you use in these cases:
Fever
Inflammation
Headache,
Menstrual pain
Toothache
Back pain
Arthritis, includingjuvenile arthritis
Minor injuries
A

NSAIDS

81
Q

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?

A

Naproxen (aleve)

82
Q

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)?

A

indomethacin

83
Q

What are some severe adverse effects of indomethacin?

A

bleeding, ulceration, headache

84
Q

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.

A

Piroxicam (feldene, fexicam)

85
Q

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.

A

meloxicam (mobic)

86
Q 
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
A

acetaminophen (tylenol, APAP)

87
Q

How come acetaminophen (tylenol) can cause liver toxicity?

A

the toxic metabolite gets inactivated by glutathione and at high doses, causes liver toxicity

88
Q

How do you treat acetaminophen toxicity?

A

give charcoal and N cysteine (to replenish glutathione stores)

89
Q

Which one has these has these effects, NSAIDs or Acetaminophen?
anti-inflammatory effect, analgesic effect, antipyretic effect

A

NSAIDs

90
Q

What are the 2 strongest effects of acetaminophen?

A

analgesic effect and antipyretic effect

91
Q

How do NSAIDS work to create anti-inflammatory effects?

A

inhibits enzymes that produce prostaglandin H synthase (COX)

92
Q

What does prostaglandin synthase do?

A

converts arachidoni acid to prostaglandins, TXA2 and prostacyclins

93
Q

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.

A

irreversibly

reversibly

94
Q

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)

A

analgesic effect

95
Q

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.

A

antipyretic effects

96
Q

What is the only NSAID that has antiplatelet effects?

A

aspirin

97
Q

(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,

A

NSAIDs

98
Q

NSAIDS have anti-inflammatory effects that may develop only after several (blank) of treatment

A

weeks

99
Q

How do NSAIDs affect rheumatic disease?

A

slows destruction of cartilage and bone and allows patients increased mobility and use of their joints

100
Q

T or F

The inflammation and pain of arthritis are relieved, but the progressive degeneration of the joints is not prevented.

A

T

101
Q

What are the effects of NSAIDs?

A

inhibits PGs and TxA1 synthesis by inhibiting COX

102
Q

What are the effects of glucocorticoids?

A

inhibition of PLA2

103
Q

What is the clinical usage for NSAIDs when it comes to anti-inflammation?

A

rheumatic, rheumatoid,

trauma

104
Q

What are the side effects of NSAIDs?

A

Gi issues

105
Q

What are the side effects of Glucocorticoids?

A

metabolism disturbance, damage of defenses

106
Q

What 2 drugs are readily used for anti-inflammation?

A

glucocorticoids and NSAIDS

107
Q

What 2 drugs are readily used for analgesia?

A

NSAIDS and Opioids

108
Q

How do opioids work, what are they used for and what are the side effects?

A

stimulate opioid receptors
various pain including severe pain
addiction

109
Q

What reasons might you use NSAIDS to treat analgesia?

A

headache, toothache, neuralgia, arthronalgia, courbature, menalgia

110
Q

Which are more effective against pain associated with integumental structures?

A

NSAIDS

111
Q

Do anti-pyresis drugs eliminate the cause of the fever?

A

no, just the symptoms

112
Q

Does acetaminophen have anti-inflammatory effects? So what should you use with inflammation?

A

nope

aspirin and other salicylates

113
Q

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).

A

Reye’s syndrome

114
Q

How do NSAIDs have an antipyresis effect, what are they clinically used for and what are the side effects?

A

inhibit PG synthesis and enhance thermolysis

used in fevers

GI reactions,no addiction

115
Q

How do chlorpromazine have an antipyresis effect, what are they clinically used for and what are the side effects?

A

inhibit thermotaxic center in hypothalamus

artificial hibernation, hypothermic anesthesia

extrapyramidal effects

116
Q

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.

A

prostaglandins (PG)

117
Q

Long-term therapy with nonspecific NSAIDs is frequently limited by their (blank), particularly those caused by erosion of gastric mucosal protection.

A

adverse effects

118
Q

What are the most common adverse effects of high-dose aspirin use (70% of patients)?

A 
nausea
vomiting
diarrhea or constipation
dyspepsia (impaired digestion)
epigastric pain
ulceration (primarily  gastric) or aggravate existing ulcers (particularly in the elderly patient) 
gastric bleeding
119
Q

Tell me about gastric bleeding and aspirin.

A

10 g of aspirin causes bleeding regardless, may result in anemia or shock if gastric bleeding is severe

120
Q

When shouldnt you give someone aspiring?

A

if they have ulcers, instead give them antacids and some prostaglandins

121
Q

Why does aspirin cause GI problems?

A

acid on cells
decrease in prostaglandin
HCl on cells
decreased blood flow

(use PGE2,misoprostol, and flurbiprophen helps decrease damage)

122
Q

How do you reduce the irritation to the GI tract?

A

substitution of enteric-coated or timed-release preparations
the use of nonacetylated salicylates
taken with food or after a meal

123
Q

How come COX-2 selective inhibitors dont access COX1 enzymes?

A

cuz they are too bulky so they make for the perfect drug :)

124
Q

What is celecoxib?

A

a cox 2 specific inhibitor

125
Q

What is celecoxib? Does it cause ulcers? Does it cause CV events? Does naproxen cause ulcers?

A

a cox 2 specific inhibitor
NO
NO
YES

126
Q

What does thromboxane do?

A

vasoconstricts and promotes platelet aggregation -> homeostasis and thrombosis

127
Q

What does prostacyclin do?

A

vasodilator, inhibitor of platelet aggregation

128
Q

Are rofecoxib (vioxx) and valdecoxib good drugs?

A

no, they have been removed because they increase heart attacks and strokes

129
Q

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?

A

celecoxib

130
Q

(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.

A

Celecoxib

131
Q

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.

A

hypersensitivity (intolerance)

132
Q

Hypersensitivity due to aspirin is highest in patients with ……?

A

asthma, nasal polyps, recurrent rhinitis, urticaria.

133
Q

(blank) is not associated with:
sodium salicylate or
magnesium salicylate.

A

Hypersensitivity

134
Q

(blank) may exist:
to other NSAIDs
to the yellow dye tartrazine, which is used in many pharmaceutical preparations.

A

Cross-hypersensitivity

135
Q

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.

A

papillary necrosis

secondary interstitial nephritis

136
Q

Do we need to worry about nephropathy in daily use of NSAIDS for prophylaxis of MI?

A

no

phenacetin has been linked to causing a problem here

137
Q

What are APCs (aspirin, phenacetin, caffeine) strongly associated with?

A

renal disease

138
Q

What are the four selective cox-2 inhibitors?

A

celecoxib
etoricoxib
meloxicab
piroxicam

139
Q

What is the clinical use of aspirin, dose wise?

A

low dose-> PA (platelet aggregation)
middle dose-> PF (pain and fever)
high dose-> RA (rheumatoid arthritis)

140
Q

What are the major side effects of aspirin?

A 
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
141
Q

What is the mneumonic for ibuprofen clinical use?

A

RIP

inflammation, patent ductus arteriosus in premature infants, rheumatoid disease

142
Q

What are the major side effects of ibuprofen?

A 
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
143
Q

What does celecoxib work on?

A

it is a cox B inhibitor

144
Q

What do you use celecoxib for and what are the major side effects (CELECoxib)?

A

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

145
Q

How does acetaminophen work, what do you use it for, what are the major side effects?

A

weak inhibitor of all COXs

minor pain and high fever in children

messes with liver and kidney, hepatotoxicity, nephrotoxicity

146
Q

How come acetaminophen causes liver problem? How can you fix this?

A

it depletes glutathione

give N-acetyl cysteine to replenish glutathione stores

147
Q

(blank) inhibit eicosanoid production

A

corticosteroids

148
Q

What does lipocortin do?

A

inhibits phospholipase A2 (i.e. keeps phospholipids from converting to LOX or COX)

149
Q

(blank) regulate gene transcription and inhibits expression of interferon, granulocyte macrophage colony-stimulating factor, interleukins, and TNF alpha.

A

corticosteroids

150
Q

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

A

corticosteroids

151
Q 
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
A

toxicity of chronic systemic glucocorticoids

152
Q

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

A

Pros of corticosteroids

153
Q

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

A

Cons of corticosteroids

154
Q

How do corticosteroids work?

A

the regulate genes by binding to nuclear glucocorticoid receptors that reduce gene transcription and expression which reduces inflammation and immunity

155
Q

What do probenecid and sulfinpyrazone do and how do they act?

A

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).

156
Q

What are the major side effects of corticosteroids?

A

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)

157
Q 
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.
A

gout

158
Q

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. ????

A

colchicine

159
Q

What sucks about colchicine?

A

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)

160
Q

How can we sort of alleviate the negative effects of colchicine?

A

via IV administration (reduces GI disturbance and provides faster relief (6-12h) but increases risk of sloughing skin and subcutaneous tissue

161
Q

What can high doses of colchicine do?

A

result in liver damage and blood dyscrasias

162
Q

What do probenecid and sulfinpyrazone do and how do they act?

A

they are organic acids that reduce urate levels in the kidneys to prevent reabsorption of uric acid. Used for gout.

163
Q

Probenecid and sulfinpyrazone undergo (blank) oral absorption.

A

rapid

164
Q

What does probenecid and sulfinpyrazone do to the kidneys?

A

they inhibit the excretion of other drugs that are actively secreted by renal tubules (such as penicillin, NSAIDS, cephalosporins and methotrexate)

165
Q

Increased urinary concentration of uric acid may result in the formation of (blank). This risk can be decreased how?

A 
urate stones (urolithiasis)
the ingestion of large volumes of fluid or alkalinization of urine with potassium citrate
166
Q

What are common adverse effects of probenecid and sulfinpyrazone?

A

GI disturbances and dermatitis and rarely these agents cause blood dyscrasias

167
Q

(blank) inhibits the synthesis of uric acid by inhibiting xanthine oxidase, an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid.

A

allopurinol

168
Q

What is nifty about the metabolism of allopurinol?

A

that it inhibits xanthine oxidase, AND when it gets metabolized to allozanthine, it also inhibits xanthine oxidase : )

169
Q

(blank) also inhibits de novo purine synthesis.

A

allopurinol

170
Q

(blank) commonly produces GI disturbances and dermatitis. This agent rarely causes hypersenstivity, including fever, hepatic dysfunction, and blood dyscrasias.

A

allopurinal

171
Q

When should you be cautious about giving allopurinol?

A

in patients with liver disease or bone marrow depression

172
Q

(blank) blocks the action of xanthine oxidase by substrate competition and is also metabolized by it to form alloxanthine which also inhibits xanthine oxidase

A

Allopurinol

173
Q

Why would you want to treat gout with NSAIDs rather than colchicine?

A

because colchicine causes diarrhea

174
Q

Chronic gout is treated with (blank) to increase the elimination of uric acid and allopurinol to inhibit uric acid production.

A

uricosuric agents

175
Q

What are these drugs called:

allopurinol, probenecid, sulfinpyrazone

A

maintenance drugs

176
Q

(blank) gout is treated with NSAIDS. (blank) gout is treated with uricosuric agents.

A

acute

chronic

177
Q

For treatment of gout, what do you need to do with fluids and your urine?

A

crush them with fluids

alkalize their urine (to prevent renal calculi)

178
Q

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?

A

DMARDS (disease modifying antiarthritic drugs)

they take a while to work and they have adverse side effects in long-term use

179
Q

What is azathioprine?

A

a purine synthesis inhibitor and DMARD

180
Q

What is ciclosporin?

A

calcineurin inhibtor and DMARD

181
Q

What is methotrexate?

A

a purine metabolism inhibitor and DMARD

182
Q

What is leflunomide?

A

pyrimidine synthesis inhibitor and DMARD

Block 4 week 2 Dani (8 decks)

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