PARACETAMOL + PHENYLEPHRINE HCl + CHLORPHENAMINE MALEATE Flashcards

1
Q

APAP, N-Acetyl-p-aminophenol

A

Paracetamol

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2
Q

3-[(1R)-1-hydroxy-2-(methylamino)ethyl]
phenol;hydrochlorid

A

Phenylephrine HCl

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3
Q

(Z)-but-2-enedioic
acid;3-(4-chlorophenyl)-N,N-dimethyl-3-
pyridin-2-ylpropan-1-amine

A

Chlorphenamine Maleat

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4
Q

Paracetamol (PAR), phenylephrine
hydrochloride (PHE) and chlorpheniramine
maleate (CPM) are commonly used in
clinical practice as

A

antipyretic and analgesic

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5
Q

T/F: can Paracetamol (PAR), phenylephrine
hydrochloride (PHE) and chlorpheniramine
maleate (CPM) be used as combination?

A

True; as antipyretic and analgesic
drugs to ameliorate pain and fever in cold
and flu conditions

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6
Q

first choice in the
treatment of acute and chronic pain

A

Paracetamol

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7
Q

also used in the temporary reduction of
fever

A

Paracetamol

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8
Q

alpha-adrenergic agonist that can be used
as a decongestant agent

A

Phenylephrine Hydrochloride

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9
Q

first-generation histamine H1 antagonist used
to prevent the symptoms of allergic
conditions, such as rhinitis and urticaria

A

Chlorphenamine maleate

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10
Q

This
drug can also be used in upper respiratory
tract conditions, such as in the temporary
relief of symptoms associated with hay fever.

A

Chlorphenamine maleate

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11
Q

a toxic metabolite linked to
liver toxicity in cases of paracetamol
overdose, is a component of the drug’s
toxicokinetics

A

N-acetyl-p-benzoquinone
imine (NAPQI)

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12
Q

NAPQUI is rapidly detoxified at
standard therapeutic dosages by conjugation with

A

glutathione

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13
Q

NAPQI attaches to the
______________ proteins of the _______
cells in overdose scenarios where
glutathione is low, resulting in
oxidative stress and toxicity.

A

mitochondria; liver

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14
Q

Strong vasoconstrictor phenylephrine is
absorbed from the ____________ tract somewhat
slowly

A

digestive

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15
Q

peak plasma levels of Phenylephrine happen _________
hours after oral treatment

A

2.5–6

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16
Q

Peak levels of chlorphenamine maleate are
observed _____________ following oral dosage

A

2.5–6 hours

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17
Q

T/f: chlorphenamine maleate has a limited bioavailbility

A

True: due to first pass effect

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18
Q

main organ
where chlorphenamine and its metabolites
are eliminated

A

Urine

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19
Q

main mechanism by which paracetamol
overdose is unsafe.

A

generation of NAPQI

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20
Q

___________ converts a
portion of it into NAPQI, which is typically
eliminated by glutathione

21
Q

In Paracetamol toxicity

When there is an overdose, oxidative stress,
hepatocellular necrosis, and liver failure are
brought on by ______________ depletion and
NAPQI binding to liver proteins

A

glutathione

22
Q

In Paracetamol toxicity

acting as
an antidote to replenish glutathione and
support NAPQI detoxification.

A

N-acetylcysteine

23
Q

negative se of phenylephrine and chlorphenamine even at appropriate dosages

A

tachycardia, hypertension, and drowsiness

24
Q

Chlorpheniramine is well absorbed following
oral administration, with peak plasma
concentrations reached within _________ hours

25
Chlorpheniramine is extensively metabolized in the _____________, primarily by cytochrome P450 enzymes, and the metabolites are excreted in the __________
liver; urine
26
elimination half-life of chlorpheniramine is __________hours; can be prolonged with overdose
12-24
27
competitively inhibits the binding of acetylcholine to muscarinic receptors
Chlorpheniramine
28
In overdose, this can lead to anticholinergic toxicity which oral ingestion is the primary cause
Chlorpheniramine
29
It has poor oral bioavailability (38%) in people because of a significant first-pass effect and extensive metabolism by monoamine oxidases in the GI tract and liver
PHENYLEPHRINE HYDROCHLORIDE
30
The oral LD50 in rats and mice is 350 mg/kg and 120 mg/kg, respectively. The half-life is 2–3 hr.
PHENYLEPHRINE HYDROCHLORIDE
31
mainly as an alpha-1 adrenergic receptor agonist with minimal beta-adrenergic action at therapeutic doses
PHENYLEPHRINE HYDROCHLORIDE
32
are found in vascular smooth muscle; agonism causes vasoconstriction
alpha-1 receptors
33
Antidote for Paracetamol toxicity
ACETYLCYSTEINE
34
acts as a hepatoprotective agent by restoring hepatic glutathione
ACETYLCYSTEINE
35
serving as a glutathione substitute to prevent the binding of NAPQI to hepatic macromolecules, and enhancing the nontoxic sulfate conjugation of acetaminophen
ACETYLCYSTEINE
36
Indications for NAC include serum levels that fall in the toxic range according to the
Rumack-Matthew nomogram
37
Acetylcysteine is fully protective against liver toxicity if given within __________after ingestion and can be administered in oral and IV route
8 hours
38
Other management technique for paracetamol toxicity
Decontamination Procedures:
39
Decontamination Procedures for paracetamol toxicity in px presenting within 4 hrs of ingestion
gastric lavage and a single dose of activated charcoal
40
In paracetamol toxicity: If the patient presents with nausea and vomiting, initiate the use of
standard antiemetic agents (eg, metoclopramide, selective 5-HT3 receptor antagonists)
41
may be considered for the treatment of central and/or peripheral anticholinergic syndrome
Physostigmine
42
CHLORPHENAMINE MALEATE antidote
Physostigmine
43
CHLORPHENAMINE MALEATE toxicity management should also include _________ monitoring and initiation of _________ access
cardiac; IV
44
In CHLORPHENAMINE MALEATE toxicity, if the patient presents within ____________ of ingestion, consider gastric lavage and single-dose activated charcoal.
1 hour
45
PHENYLEPHRINE HCl antidote:
no specific antidote
46
PHENYLEPHRINE HCl toxicity treatment is mainly __________
supportive and dependent on symptoms
47
Can be given for Phenylephrine HCl toxicity and as mainstay of treatment for agitation, hypertension, tachycardia, and seizures
Benzodiazepines
48
T/F: Benefits of decontamination in Phenylephrine HCl toxicity are unlikely
True