Medical toxo (analgesic and antipyretic)DONE Flashcards

1
Q

ANALGESIC AND ANTIPYRETIC Drugs

A

Acetaminophen (paracetamol)
salicylates (Aspirin)

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2
Q

the remaining amount of acetamenphin is converted by ……….. to ………..

A

by cytochrome P450 to N-acetyl-p-benzoquinone imine (NAPQI).

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3
Q

NAPQI is converted by ………… to non toxic compound

A

glutathione

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4
Q

mechanism of toxicity of acetamenophen

A

active metabolite NAPQI lead to oxidant cell injury, hepatic failure and death.

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5
Q

the four clinical phases of parcetamol overdose

A

Phase 1 (first 24 hours): anorexia, nausea, vomiting, malaise and pallor.
Phase 2 (24-48):
* initial damage to the hepatocytes.
* right upper quadrant pain
* increases in liver transaminases serum bilirubin , prothrombin time.
Phase 3 (72-96):
* the peak of the hepatotoxic effects.
* metabolic acidosis,
* acute renal failure,
* acute pancreatitis,
* fulminant hepatic failure evidenced by jaundice, extensive coagulopathies, hypoglycemia, and hepatic encephalopathy.
Phase 4 ( 4-14 days): resolution

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6
Q

phase 1 of paracetamol toxicity

A

Phase 1 (first 24 hours): anorexia, nausea, vomiting, malaise and pallor.

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7
Q

phase 2 of paracetamol toxicity

A

Phase 2 (24-48):
* initial damage to the hepatocytes.
* right upper quadrant pain
* increases in liver transaminases serum bilirubin , prothrombin time.

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8
Q

phase 3 of paracetamol toxicity

A

Phase 3 (72-96):
* the peak of the hepatotoxic effects.
* metabolic acidosis,
* acute renal failure,
* acute pancreatitis,
* fulminant hepatic failure evidenced by jaundice, extensive coagulopathies, hypoglycemia, and hepatic encephalopathy.

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9
Q

right upper quadrant pain related to

A

phase 2 of paracetamol toxicity

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10
Q

causes acute pancreatitis

A

paracetamol phase 3

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11
Q

Investigations of paracetamol

A
  1. Routine investigation.
    Liver function tests, Renal function tests, ABG and Blood glucose level.
  2. Serum Paracetamol levels
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12
Q

causes hepatic encephalopathy

A

paracetamol phase 3

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13
Q

treatment of parcetamol toxicity

A
  • ABC
  • No GL, AC, Ipecac
  • specific antidote: N-acetyl cysteine
  • Hemodialysis may be indicated if renal failure, refractory acidosis, or fluid and electrolyte changes occur.
  • Symptomatic Treatment of hypoglycemia, hypotension, metabolic acidosis and hepatic encephalopathy.
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14
Q

ctivated charcoal is not recommended to be administered in Paracetamol toxicity due to

A

charcoal may adsorb NAC.

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14
Q

Ipecac is not recommended in paracetamol tox

A

it may interfere with oral NAC.

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15
Q

Gastric lavage not recommended in paracetamol tox

A

it is rapidly absorbed from the GIT.

16
Q

froms of NAC

A

Oral (Mucomyst)
Intravenous (Parvolex)

17
Q

Two situations in which IV NAC is undoubtedly preferable to oral:

A
  1. Fulminant hepatic failure (FHF)
  2. Inability to tolerate oral NAC.
18
Q

accidental intoxication of ………… may occur during treatment because pyrexia

A

salicylates (aspirin)

19
Q

NAC should be given after paracetamol ingestion.within

A

8 hours

20
Q

tinnitus related to

A

salicylates aspirin

21
Q

the only manifestations of salicylates that occur within the therapeutic range

A

tinnitus

22
Q

aspirin on CNS

A

Alterations in mental status, cerebral edema and seizures
Tinnitus

23
Q

aspirin on respiratory

A

acute lung injury
Non cardiogenic pulmonary edema

24
Q

causes acute lung injury

A

salicylates

25
Q

aspirin on CVS

A

sinus tachycardia
hypotension due to hypovolemia

26
Q

aspirin on acid base balance

A

respiratory alkalosis in adults due to hyperventilation
metabolic acidosis in children due to accumulation of lactic acids and ketoacids

27
Q

aspirin on urinary

A
  • Direct nephrotoxicity&raquo_space; renal tubular necrosis&raquo_space; renal failure.
  • Indirect effect due to:
    o Decreased renal flow caused by dehydration. .
    o Rhabdomyolysis.
28
Q

causes reyes syndrome in children

A

aspirin

29
Q

aspirin on blood

A

Bleeding tendencies is common in chronic intoxication due to inhibition of prothrombin synthesis & platelet aggregation.

30
Q

hyperthermia in aspirin due to

A

Uncoupling of oxidative phosphorylation with increase in cellular metabolic rate.
-Dehydration.

31
Q

bad prognostic sign of aspirin

A

hyperthermia

31
Q

causes angioneurotic edema.

A

aspirin

32
Q

Fluid and electrolyte disturbances due to aspirin

A

Dehydration due to:
-Hyperthermia (sweating).
-Vomiting.
-Hyperpnea.

33
Q

investigations of aspirin

A

1)Routine investigations.
-Renal function tests, Electrolytes, Blood glucose level and ABG
2) Coagulation profiles:
-Prothrombin time (PT), prothrombin concentration, PTT (partial thromboplastin time), bleeding time and INR (International Normalized ratio).
3) Serum salicylate levels (mg/dl):
4) Imaging studies.
-Abdominal X-Ray: radiopaque concretions of enteric coated aspirin.
-Chest X-Ray: pulmonary edema.
-Brain CT/MRI: cerebral edema.

34
Q

treatment of aspirin toxicity

A

ABC
the 4 GIT
no specific antidotes
Forced alkaline diuresis: Effective in moderate toxicity (>40mg/dL in acute toxicity).
Hemodialysis in serum salicylates levels >80

35
Q

hemodialysis in aspirin is indicated in

A

Serum salicylate levels > 80 mg/dL after acute overdose).
Seizures, coma & cerebral edema.
Pulmonary edema.
Refractory acidosis.
Renal failure.
Severe electrolytes disturbances