• What is the mechanism of action of paracetamol? How is it different from that of aspirin?

Paracetamol is a weak cyclo-oxygenase (cox) COX 1 and COX 2 inhibitor in the peripheral
tissue. This is why it does not show anti-inflammatory effects. Paracetamol also inhibits the
COX 3 enzyme located in the central nervous system. If the COX 3 is blocked, it will activate the decreasing serotonergic analgesic pathways. Paracetamol is also antipyretic because it works directly on the hypothalamic thermoregulation center and then lowers the fever. 
Aspirin is an irreversible, non-selective COX 1 and COX 2 blocker. It lowers prostaglandin,thromboxane and prostacyclin production in the body. Aspirin is then also used to lower 
platelet adhesion, it is also antipyretic, analgesic and then has hyo ok anti-inflammatory 
effects.

• Name the indications for paracetamol. In what circumstances is it a preferred remedy in the treatment of moderate pain and fever?

Although it is said that aspirin and paracetamol are the same, it is completely wrong. 
Paracetamol does not have anti-inflammatory or anti-platelet adhesion properties. 
Paracetamol is useful for use in mild to moderate pain such as headaches, postpartum 
pain and myalgia where aspirin is also an effective analgesic. Paracetamol is also 
recommended for use in moderate pain if the patient is allergic to aspirin. A patient with a peptic ulcer and someone who has aspirin tightened his chest will also need to use paracetamol for pain and fever, as well as a patient who tends to hemophilia.

• Name side effects that can occur with paracetamol use. Concentrate only on common side effects and not acute paracetamol overdose.

Nausea and vomiting, constipation and abdominal pain, skin rash and urticaria and acute 
liver failure and jaundice. Bloody, black stools and dark urine.

• Due to the readily available paracetamol availability and the general public perception that paracetamol is a very safe drug, paracetamol poisoning (accidental / intentional) is fairly common. Compile a report discussing acute paracetamol toxicity with emphasis on dose, signs and symptoms and treatment. In your textbook, as well as in the SAMF, there is valuable information you can use.

The liver enzymes catabolize conjugation of paracetamol. When the enzymes are saturated, toxic NAPQI forms. NAPQI is deactivated by glutathione BUT if glutathione levels are 
depleted it causes NAPQI necrosis.in the liver and kidney tubes. A fatal dose can be 10-15g per day.This is between 20 and 30 tablets. If a patient experiences a lot of pain and 
thinks that paracetamol is very safe, someone can very easily take so many pills for pain 
and not even realise how toxic it is. The normal adult dose is only 4g per day. 
Unfortunately, the symptoms of paracetamol poisoning take a long time and you can only 
experience nausea and vomiting, stomach pain, decreased appetite, fatigue and 
weakness within 1-2 days after the overdose. After 1-2 days the big trouble comes and 
you may experience symptoms like right subcostal pain, tender liver and jaundice. Then 
renal insufficiency can occur, then liver necrosis and then death. The treatment of acute 
toxicity should happen vining. The treatment for acute toxicity is poorly effective for the first10 hours after poisoning. Within the first hour after poisoning, you should try to induce 
vomiting, you can do a gastric lavage and one can use activated carbon as IV treatment, 
The patient needs immediate supplementation of the sulfhydryl group to produce 
glutathione in the liver fill to prevent liver cell necrosis - acetylcysteine ​​should be 
administered in IV within 8-12 hours. The initial dose is 150mg / kg in 200ml 5% glucose 
over 15 minutes, then 50mg / kg in 500ml 5% glucose over 4 hours and then 100mg / kg in1000ml 5% glucose over the next 16 hours. 
Oral treatment can also be administered by acetylcysteine ​​at 140mg / kg or carbocystine 
at 150mg / kg.