quiz

Question 1

what causes acute gout attacks and how do we treat it

Answer 1

excessive alcohol consumption, a diet rich in purines, and kidney
disease.

 NSAIDs, corticosteroids, or colchicine are effective alternatives for the
management of acute gouty arthritis

Question 2

what are the drugs of choice for acute gout

Answer 2

Indomethacin

Intraarticular administration of corticosteroids (when only one or two
joints are affected) is also appropriate in the acute setting, with systemic
corticosteroid therapy for more widespread joint involvement

Question 3

what are xanthine oxidase inhibitors

Answer 3

Xanthine oxidase inhibitors (allopurinol, febuxostat) are first-line urate-lowering agents

xanthine oxidase inhibitors to ↓
synthesis of uric acid

Question 4

what are uricosuric agents

Answer 4

probenecid) may be used in patients who are
intolerant to xanthine oxidase inhibitors or fail to achieve adequate
response with those agents.

uricosuric drugs to ↑ its excretion of uric acid

Question 5

Medications for the prevention of an acute gout attack (low-dose
colchicine, NSAIDs, or corticosteroids) should be initiated with uratelowering therapy and continued for at least 6 months

Answer 5

ok

Question 6

what is Colchicine

Answer 6

Colchicine, a plant alkaloid, is used for the treatment of acute gouty
attacks.
 It is neither a uricosuric nor an analgesic agent, although it relieves pain
in acute attacks of gout

. Mechanism of action:
 Colchicine binds to tubulin, a microtubular protein, causing its
depolymerization. This disrupts cellular functions, such as the mobility of
granulocytes, thus decreasing their migration into the affected area.
Furthermore, colchicine blocks cell division by binding to mitotic
spindles

NSAIDs have largely replaced colchicine in the treatment of acute gouty
attacks for safety reasons.
 Colchicine is also used as a prophylactic agent to prevent acute attacks
of gout in patients initiating urate-lowering therapy

4. Adverse effects:
    Colchicine may cause nausea, vomiting, abdominal pain, and diarrhea

 Chronic administration may lead to myopathy, neutropenia, aplastic
anemia, and alopecia
The drug should NOT be used in pregnancy, and it should be used with
caution in patients with hepatic, renal, or cardiovascular disease.
 Dosage adjustments are required in patients taking CYP3A4 inhibitors,
like clarithromycin, itraconazole, and protease inhibitors.
 For patients with severe renal impairment, the dose should be reduced.

Question 7

what is Allopurinol

Answer 7

It ↓ the production of uric acid by competitively inhibiting the last two
steps in uric acid biosynthesis that are catalyzed by XO

Question 8

what is Febuxostat

Answer 8

Febuxostat, a XO inhibitor, is structurally unrelated to allopurinol;
however, it has the same indications.
 In addition, the same drug interactions with 6-mercaptopurine,
azathioprine, and theophylline apply.
 Its adverse effect profile is similar to that of allopurinol, although the risk
for rash and hypersensitivity reactions may be reduced.
 Febuxostat does not have the same degree of renal elimination as
allopurinol and thus requires less adjustment in those with reduced
renal function.

Question 9

what us probenecid

Answer 9

Probenecid is a uricosuric drug. It is a weak organic acid that promotes
renal clearance of uric acid by inhibiting the urate anion exchanger in the
prminoximal tubule that mediates urate reabsorption.
 At therapeutic doses, it blocks proximal tubular reabsorption of uric acid.
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Question 10

what us pegloticase

Answer 10

 Pegloticase is a recombinant form of the enzyme urate oxidase or
uricase.
 It acts by converting uric acid to allantoin, a water-soluble nontoxic
metabolite that is excreted primarily by the kidneys.
 Pegloticase is indicated for patients with gout who fail treatment with
standard therapies such as XO inhibitors.
 It is administered as an IV infusion/2 weeks

Question 11

what drugs causes CINV

Answer 11

severe: cisplatin, dacarbazine, streptozocin

moderate: cyclophosphamide, doxorubicin

low: fluorouracil, methotrexate, vincritine

Question 12

what are phenothiazine

Answer 12

✓ The first group of drugs shown to be effective antiemetic agents,
phenothiazines, such as prochlorperazine, act by blocking dopamine
receptors
Prochlorperazine is effective against low or moderately emetogenic
chemotherapeutic agents

Although increasing the dose improves antiemetic activity, side effects
are dose limiting

Question 13

what are 5-ht3 receptor blockers (setron)

Answer 13

The 5-HT3 receptor antagonists include ondansetron, granisetron,
palonosetron, and dolasetron. These agents selectively block 5-HT3
receptors in the periphery (visceral vagal afferent fibers) and in the
brain (CTZ)

This class of agents is important in treating emesis linked with
chemotherapy, largely because of their longer duration of action and
superior efficacy.
✓ These drugs can be administered as a single dose prior to
chemotherapy (intravenously or orally) and are efficacious against all
grades of emetogenic therapy.
✓ Ondansetron and granisetron prevent emesis in 50% to 60% of
cisplatin-treated patients. These agents are also useful in the
management of postoperative nausea and vomiting. 5-HT3 antagonists
are extensively metabolized by the liver; however, only ondansetron
requires dosage adjustments in hepatic insufficiency. Elimination is
through the urine. Electrocardiographic changes, such as a prolonged
QTc interval, can occur with dolasetron and high doses of ondansetron.
For this reason, dolasetron is no longer approved for CINV prophylaxis.

Question 14

what are substituted benzamides (metoclopramide)

Answer 14

✓ One of several substituted benzamides with antiemetic activity,
metoclopramide is effective at high doses against the emetogenic
cisplatin, preventing emesis in 30% to 40% of patients and reducing
emesis in the majority of patients.
✓ Metoclopramide accomplishes this through inhibition of dopamine in
the CTZ.
✓ Antidopaminergic side effects, including extrapyramidal symptoms,
limit long-term high-dose use.
✓ Metoclopramide was previously used as a prokinetic drug for the
treatment of GERD. However, due to the adverse effect profile and the
availability of more effective drugs, such as PPIs, it should be reserved
for patients with documented gastrop

Question 15

what are butyrophenones (Droperidol and haloperidol)

Answer 15

Droperidol and haloperidol act by blocking dopamine receptors.
✓ The butyrophenones are moderately effective antiemetics.
✓ Droperidol had been used most often for sedation in endoscopy and
surgery, usually in combination with opioids or benzodiazepines.
However, it may prolong the QTc interval and should be reserved for
patients with inadequate response to other agents.
✓ High-dose haloperidol was found to be nearly as effective as high-dose
metoclopramide in preventing cisplatin-induced emesis.

Question 16

corticosterids for CINV

Answer 16

Dexamethasone and methylprednisolone, used alone, are effective
against mildly to moderately emetogenic chemotherapy.
✓ Most frequently, however, they are used in combination with other
agents.
✓ Their antiemetic mechanism is not known, but it may involve blockade
of prostaglandins

Question 17

benzodiazepines in antiemetic drugs

Answer 17

✓ The antiemetic potency of lorazepam and alprazolam is low.
✓ Their beneficial effects may be due to their sedative, anxiolytic, and
amnesic properties.
✓ These same properties make benzodiazepines useful in treating
anticipatory vomiting.
✓ Concomitant use of alcohol should be avoided due to additive CNS
depressant effects.

Question 18

what are Substance P/neurokinin-1 receptor blocker (Aprepitant )

Answer 18

✓ Aprepitant targets the neurokinin receptor in the brain and blocks the
actions of the natural substance.
✓ Aprepitant is indicated only for highly or moderately emetogenic
chemotherapy regimens.
✓ It is usually administered orally with dexamethasone and a 5-HT3
antagonist.
✓ It undergoes extensive metabolism, primaril by CYP3A4, and it may
affect the metabolism of other drugs that are metabolized by this
enzyme, such as warfarin and oral contraceptives.

Question 19

what are mycobacteria

Answer 19

• Slender, rod-shaped aerobic bacteria
• Slow multiplication
• Cell wall contain mycolic acids which
are long fatty acids
• Acid-fast: lipid-rich cell walls lead to
poor gram stain, no decolorized by
acidified organic solvents
• Intracellular: form slow growing
granulomatous lesions

Question 20

the treatment of TB

Answer 20

• Difficult
• The organism grows
slowly,(requires treatment for
months to years)and it is difficult
to culture (to test for sensitivity)
• Resistance to the drugs is
common (some bacteria are
resistant to 7 drugs)
• Treatment takes 6 to 24 months
with combination of drugs
• (at least two drugs a time)

Question 21

what are the first line in TB drugs

Answer 21

• Isoniazid (most important)
• Rifampicin(most important)
• Ethambutol
• Pyrazinamide
• Preferred because of their:
• efficacy
• acceptable incidence of toxicity
• The multidrug regimen is continued well beyond the
disappearance of clinical disease to eradicate any
persistent organisms

Question 22

what is isoniazid INH

Answer 22

Most potent of the antitubercular drugs
• Should be used in combination

Bactericidal to rapidly dividing mycobacteria, but
is bacteriostatic if the mycobacteria are slow-growing
• Used also as prophylaxis for all household members
and very close contacts of patients with tuberculosis

Question 23

what is INH MOA

Answer 23

INH is a prodrug activated by a mycobacterial
catalase-peroxidase (KatG)
• Binds and inhibits the enzymes:
• acyl carrier protein reductase (InhA)
• & β-ketoacyl-ACP synthetase ( KasA)
• Which are essential for synthesis of mycolic acid, an
important component of mycobacteria cell wall
• Leading to a disruption in the bacterial cell wall
• Antibacterial spectrum:
• INH is specific for TB
• INH is particularly effective against rapidly growing
bacilli and against intracellular organism

Question 24

how does the resistance to INH happens

Answer 24

• 1) Mutation or deletion of KatG (producing
mutants incapable of prodrug activation)
• 2) Varying mutations of the acyl carrier proteins,
• 3) or over expression of the target enzyme InhA.
• Cross-resistance does not occur between
isoniazid and other antitubercular drugs ( except
with ethionamide 2nd line drugs)

Question 25

what are the kinetics for INH

Answer 25

• Rapid oral absorption, impaired iif taken with food, mainly high fat
foods
• Diffuses into all body fluids, cells, and caseous material (necrotic
tissue resembling cheese that is produced in TB).
• Drug levels in the cerebrospinal fluid (CSF) are about the same as
those in the serum.
• The drug readily penetrates host cells and is effective against
bacilli growing intracellularly. Infected tissue tends to retain the
drug longer.
• Elimination:
• INH undergoes N-acetylation and hydrolysis to inactive products
• INH acetylation is genetically regulated:
• Fast acetylators serum T1/2 90 minutes
• Slow acetylators serum T1/2 3-4 hours figure (32.4)
Chronic liver disease (as in chronic alcoholism)
decreases metabolism, and doses must be
reduced to decrease toxicity.
• Excretion is through glomerular filtration,
predominantly as metabolites.
• Slow acetylators excrete more of the parent
compound.
• Severely depressed renal function results in
accumulation of the drug, primarily in slow
acetylators.

Question 26

what are the sideeffects of INH

Answer 26

Hepatitis:
• The most serious AE, can be fatal if unrecognized and INH
treatment is continued
• Its incidence increases with:
• Age >35 yrs
• Patients who take rifampin
• Those who drink alcohol
• Peripheral neuropathy:
• Associated with paresthesia of hands and feet
• May be due to relative pyridoxine deficiency and can be avoided
by daily supplementation of pyridoxine (B6)
• CNS:
• Convulsions in patients prone to seizures
• Hypersensitivity: skin rash and fever