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
2
Q
What are the three phases of inflammation?
A
acute
subacute
chronic proliferative
3
Q
What phase of inflammation is this:
vasodilation and capillary permeability
A
acute
4
Q
What phase of inflammation is this:
infiltration of leukocytes and phagocytes (effects of chemokines)
A
subacute or delayed
5
Q
What phase of inflammation is this:
tissue degeneration and fibrosis
A
chronic proliferative
6
Q
What causes the redness seen in inflammation?
A
vasodilation of capillaries increases blood flow
7
Q
What causes the heat felt in inflammation?
A
vasodilation
8
Q
What causes the pain felt in inflammation?
A
hyperalgesia, sensitization of nocicpetors
9
Q
What causes the swelling in inflammation?
A
increased vascular permeability (microvascular structural changes and escape of plasma proteins from the bloodstream)
10
Q
What are these:
osteoarthritis, rheumatoid arthritis, juvenile arthritis, gouty arthritis, ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome
A
different kinds of arthritis
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
12
Q
In late stage of arthritis what may develop?
A
deformity and ankylosis
13
Q
TO block an inflammatory response, do you want to block COX 1 or COX2?
A
COX 2
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
15
Q
Which part of your immune system does an infection affect?
A
the adaptive and innate immune system
16
Q
What part of the immune system reacts to a perceived threat?
A
adaptive immune system
17
Q
What will tissue injury, adaptive immune system, and the innate immune system activate?
A
leukocytes and endothelial cells
18
Q
What will leukocytes and enothelial cells activate?
A
biochemical inflammatory mediators
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
20
Q
The symptoms of inflammation are caused by a series of (blank) including the metabolites of eicosanoids.
A
biochemical mediators
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
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)
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
24
Q
What does COX do?
A
cause inflammation
25
What does LOX (lipoxygenase) do?
phagocyte mobilization and changes vascular permeability and causes inflammation
26
Where do arachidonic metabolites come from?
from phospholipids
27
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
28
What do the prostanoids cause (prostaglandins, prostacyclin, thromboxane)?
inflammation
29
How do you convert arachodinoc acid into EETs for reuse?
via cytochrome P450
30
What cox does this:
platelet function
GI mucosal integrity
renal function
COX 1 (induces constitutive physiological regulation)
31
What cox does this:
inflammation
pain fever
COX2 (induces inflammatory response)
32
WHat does aspirin inhibit?
both COX1 and COX2
33
(blank) directly sensitize pain fibers (Ad and unmyelinated C fibers) so they respond to normally innocuous stimuli (hyperalgesia)
prostaglandins
34
Subdural injetion of PGE1 (prostaglandin E 1) with small amounts of bradykinin and histamine causes (blank)
headache and pain
35
What causes a fever?
neutrophils release pyrogens (cytokines, TNF A, ILs)
36
(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
37
If you inhibit prostaglandin synthesis in the CNS, what will happen?
cutaneous dialtion
| increased heat loss-> reduction in fever and symptoms of fever
38
What do corticosteroids (predinisone, dexamethasone) do?
inhibit leukocyte and endothelial cells activation by blocking Phospholipase A2 and COX
39
What do NSAIDS do?
inhibit inflammatory mediators by blocking COX
40
What do 5-LOX inhibitors and leukotriene receptor antagonists (Zafirlukast, zileuton) do?
inhibit inflammatory mediators by blocking COX
41
What do you use aspirin for with heart issues?
as a blood thinner for prevention of heart attacks
42
(blank) covalently and irreversibly modifies both COX 1 and COX 2 by acetylating serine 530 in the active site.
acetylsalicylate (ASA)
43
What does the acetylation of COX by ASA do?
it causes a steric block to prevent arachidonic acid from binding
44
Does acetylation of COX-2 allow it to retain the cox activity but produce a different product, such as 15-R-HETE?
YES!
45
(blank) irreversibly inhibits platelet COX-1 and COX-2 and, thereby inhibits thromboxane production (remember, thromboxane stimulates platelet aggregation)
Aspirin
46
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 :) )
47
At less than 300 mg /Day, what kind of effects with aspirin induce?
blocks platelet aggregation and has antithrombic effects
48
At doses between 300-2400 mg/day, what kind of effects does aspirin have (intermediate)?
antipyretic, analgesic effects
49
At doses between 2400-4000 mg/day. what kind of effects does aspirin have (high)?
anti-inflammatory
50
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
```
51
What can treat rheumatoid arthritis, pericarditis, and kawasaki disease?
aspirin, bitches
52
What kind of acids are salicylates?
weak organic acids
53
aspirin has a pKa of (blank).
3.5
54
Why is aspirin rapidly absorbed from the stomach as well as from the intestine?
cuz the low pH favors absorption
55
where do unmetabolized salicylates go?
they are excreted by the kidney
56
How do you treat an acid overdose?
you raise the urine pH to increase the clearance of it
57
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
58
If you oxidize salicylate, what do you get?
gentisic acid
59
If you conjugate salicylate with glycine what do you get?
salicyluric acid
60
If you conjugate salicylate with glucronic acid what do you get?
ester and other glucuronides
61
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
62
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
63
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
64
At low and moderate doses of salicylate, how is the drug eliminated?
first order
65
At high doses of salicylate, how is the drug eliminated?
zero order
66
In high doses of asprin, or toxic overdose, the enzymes for glycine and glucuronide conjugation become (blank)
saturated
67
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!
68
Drug-Drug interactions with salicylates leads to altered effects of drugs and metabolism. How will salicylate work with antacids?
reduced rate of aspirin absorption
69
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)
70
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
71
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
```
72
Why should aspirin not be given to patients with asthma?
it causes contraction of the bronchioles-
73
What are the three most common adverse effects of aspirin?
salicylate reaction (CNS reaction)
hematologic effects
Reye's syndrome
74
What is reye's syndrom?
it is found in kids who take too much aspirin and results in severe hepatic damage and encephalopathy
75
How do you get salicylism (overdose or poisoning)?
a dose greater than 5 g/d of aspirin or salicylate
76
In adults, what is the initial sign of salicylism toxicity?
tinnitus, hearing loss, vertigo
77
In children, what is the intitial sign of salicylism toxicity?
acidosis and hyperventilation with accompanying lethargy
78
How do you treat salicylate overdose?
```
alkalize urine
correct acid-base disturbance
replace electrolytes and fluids
cooling
forced diuresis, hemodialysis
gastric lavage or emesis
```
79
```
What are these:
strong antipyretics
analgesics
has anti-inflammatory effects
mild and short-lasting antiplatelet effect
vasoconstriction properties
```
ibuprofen (NSAIDS)
80
```
What can you use in these cases:
Fever
Inflammation
Headache,
Menstrual pain
Toothache
Back pain
Arthritis, including juvenile arthritis
Minor injuries
```
NSAIDS
81
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)
82
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
83
What are some severe adverse effects of indomethacin?
bleeding, ulceration, headache
84
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)
85
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)
86
```
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)
87
How come acetaminophen (tylenol) can cause liver toxicity?
the toxic metabolite gets inactivated by glutathione and at high doses, causes liver toxicity
88
How do you treat acetaminophen toxicity?
give charcoal and N cysteine (to replenish glutathione stores)
89
Which one has these has these effects, NSAIDs or Acetaminophen?
anti-inflammatory effect, analgesic effect, antipyretic effect
NSAIDs
90
What are the 2 strongest effects of acetaminophen?
analgesic effect and antipyretic effect
91
How do NSAIDS work to create anti-inflammatory effects?
inhibits enzymes that produce prostaglandin H synthase (COX)
92
What does prostaglandin synthase do?
converts arachidoni acid to prostaglandins, TXA2 and prostacyclins
93
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
94
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
95
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
96
What is the only NSAID that has antiplatelet effects?
aspirin
97
(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
98
NSAIDS have anti-inflammatory effects that may develop only after several (blank) of treatment
weeks
99
How do NSAIDs affect rheumatic disease?
slows destruction of cartilage and bone and allows patients increased mobility and use of their joints
100
T or F
| The inflammation and pain of arthritis are relieved, but the progressive degeneration of the joints is not prevented.
T
101
What are the effects of NSAIDs?
inhibits PGs and TxA1 synthesis by inhibiting COX
102
What are the effects of glucocorticoids?
inhibition of PLA2
103
What is the clinical usage for NSAIDs when it comes to anti-inflammation?
rheumatic, rheumatoid,
| trauma
104
What are the side effects of NSAIDs?
Gi issues
105
What are the side effects of Glucocorticoids?
metabolism disturbance, damage of defenses
106
What 2 drugs are readily used for anti-inflammation?
glucocorticoids and NSAIDS
107
What 2 drugs are readily used for analgesia?
NSAIDS and Opioids
108
How do opioids work, what are they used for and what are the side effects?
stimulate opioid receptors
various pain including severe pain
addiction
109
What reasons might you use NSAIDS to treat analgesia?
headache, toothache, neuralgia, arthronalgia, courbature, menalgia
110
Which are more effective against pain associated with integumental structures?
NSAIDS
111
Do anti-pyresis drugs eliminate the cause of the fever?
no, just the symptoms
112
Does acetaminophen have anti-inflammatory effects? So what should you use with inflammation?
nope
| aspirin and other salicylates
113
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
114
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
115
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
116
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)
117
Long-term therapy with nonspecific NSAIDs is frequently limited by their (blank), particularly those caused by erosion of gastric mucosal protection.
adverse effects
118
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
```
119
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
120
When shouldnt you give someone aspiring?
if they have ulcers, instead give them antacids and some prostaglandins
121
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)
122
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
123
How come COX-2 selective inhibitors dont access COX1 enzymes?
cuz they are too bulky so they make for the perfect drug :)
124
What is celecoxib?
a cox 2 specific inhibitor
125
What is celecoxib? Does it cause ulcers? Does it cause CV events? Does naproxen cause ulcers?
a cox 2 specific inhibitor
NO
NO
YES
126
What does thromboxane do?
vasoconstricts and promotes platelet aggregation -> homeostasis and thrombosis
127
What does prostacyclin do?
vasodilator, inhibitor of platelet aggregation
128
Are rofecoxib (vioxx) and valdecoxib good drugs?
no, they have been removed because they increase heart attacks and strokes
129
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
130
(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
131
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)
132
Hypersensitivity due to aspirin is highest in patients with ......?
asthma, nasal polyps, recurrent rhinitis, urticaria.
133
(blank) is not associated with:
sodium salicylate or
magnesium salicylate.
Hypersensitivity
134
(blank) may exist:
to other NSAIDs
to the yellow dye tartrazine, which is used in many pharmaceutical preparations.
Cross-hypersensitivity
135
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
136
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
137
What are APCs (aspirin, phenacetin, caffeine) strongly associated with?
renal disease
138
What are the four selective cox-2 inhibitors?
celecoxib
etoricoxib
meloxicab
piroxicam
139
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)
140
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
```
141
What is the mneumonic for ibuprofen clinical use?
RIP
| inflammation, patent ductus arteriosus in premature infants, rheumatoid disease
142
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
```
143
What does celecoxib work on?
it is a cox B inhibitor
144
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
145
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
146
How come acetaminophen causes liver problem? How can you fix this?
it depletes glutathione
give N-acetyl cysteine to replenish glutathione stores
147
(blank) inhibit eicosanoid production
corticosteroids
148
What does lipocortin do?
inhibits phospholipase A2 (i.e. keeps phospholipids from converting to LOX or COX)
149
(blank) regulate gene transcription and inhibits expression of interferon, granulocyte macrophage colony-stimulating factor, interleukins, and TNF alpha.
corticosteroids
150
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
151
```
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
152
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
153
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
154
How do corticosteroids work?
the regulate genes by binding to nuclear glucocorticoid receptors that reduce gene transcription and expression which reduces inflammation and immunity
155
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).
156
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)
157
```
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
158
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
159
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)
160
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
161
What can high doses of colchicine do?
result in liver damage and blood dyscrasias
162
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.
163
Probenecid and sulfinpyrazone undergo (blank) oral absorption.
rapid
164
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)
165
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
```
166
What are common adverse effects of probenecid and sulfinpyrazone?
GI disturbances and dermatitis and rarely these agents cause blood dyscrasias
167
(blank) inhibits the synthesis of uric acid by inhibiting xanthine oxidase, an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid.
allopurinol
168
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 : )
169
(blank) also inhibits de novo purine synthesis.
allopurinol
170
(blank) commonly produces GI disturbances and dermatitis. This agent rarely causes hypersenstivity, including fever, hepatic dysfunction, and blood dyscrasias.
allopurinal
171
When should you be cautious about giving allopurinol?
in patients with liver disease or bone marrow depression
172
(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
173
Why would you want to treat gout with NSAIDs rather than colchicine?
because colchicine causes diarrhea
174
Chronic gout is treated with (blank) to increase the elimination of uric acid and allopurinol to inhibit uric acid production.
uricosuric agents
175
What are these drugs called:
| allopurinol, probenecid, sulfinpyrazone
maintenance drugs
176
(blank) gout is treated with NSAIDS. (blank) gout is treated with uricosuric agents.
acute
| chronic
177
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)
178
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
179
What is azathioprine?
a purine synthesis inhibitor and DMARD
180
What is ciclosporin?
calcineurin inhibtor and DMARD
181
What is methotrexate?
a purine metabolism inhibitor and DMARD
182
What is leflunomide?
pyrimidine synthesis inhibitor and DMARD
