Why MARA MOJA works like UMEME

Hornbill

New Lister
View attachment 31136

So Mara Moja packs the following ingredients: 200mg of Paracetamol, 400mg of Aspirin, & 50mg of caffeine, ok?

For context, the kawaida, normal Panadol contains 500mg of Paracetamol alongside a bunch of other smoll-smoll ingredients.
Now, this will surprise you but the EXAAAAACT mechanism of action of Paracetamol (PCM) isn't that well known.

Our resident pharmacists can go much deeper on this, but what we do know is that Paracetamol works on the brain pain pathways.
The downside of this is that it relieves PAIN but doesn't necessarily deal with the INFLAMMATION that is an important part of your pain.

Yaani, Paracetamol serves an analgesic role but not an anti-inflammatory one, you understand?
Say for example you have pain after busting your shoulder in the gym, yeah?

The reason you're in pain isn't because you're just "in pain"; it's cause the muscle tendons at your shoulder are inflamed/ "on fire".

So when you take PCM, it deals with the "pain" but doesn't really deal with the pain, y'know what I'm saying?
Now, in comes someone like DICLOFENAC.

Diclofenac is a non-steroidal, anti-inflammatory drug, NSAID for short.

it's primary role is to reduce inflammation, ok? to turn down the heat.

And let me tell you Maina, it does this role veeeeeeeery well.
View attachment 31137

However, Diclofenac only REDUCES the inflammation but doesn't deal with the pain pathway, you follow?
In comes MARA MOJA tablets;
"kicking in the door waving the 44,
all you heard was Mara Moja don't hit me no more!"


So Mara Moja comes in carrying that solid Paracetamol Power, that badass Aspirin Ability (Aspirin is also an NSAID, btw) (non-steroidal anti-inflammatory drug, ie), & to top it off, some of that good-good Caffeine Content.

Now, full disclosure, I didn't know much about the caffeine, but turns out it works by directly blocking the receptors (adenosine ones) that are found at the organ in pain.
that is, the Paracetamol works on brain pathways, Aspirin reduces inflammation, then caffeine tells the organ to stop feeling pain.

The pain is just zimwa'd like "shhh, it's okay"

Now, I'd end there but here's a disclaimer;

Because of the high Aspirin, this drug can be very crude on your gastrointestinal tract.
Gastric & duodenal ulcers are common in ppl who use them frequently.
Like for me, I've had issues with acidity so I go for other pain-relievers before going for this one.

Now here's an academic question for you to think about;

WHY does Paracetamol still exist if its role seems to be done "better" by other pain relievers?
Maybe it's cause of Big Pharma...

Maybe I'll answer that question in a future thread so that's why you should consider following me.

Maybe I also don't know the answer.

Tons of possibilities!!!

Another IMPORTANT disclaimer, btw, is that there's tons of fake drugs out there, especially for drugs that are well known to work well like this one.

That said, please be sure to purchase your medications from reliable pharmacies/chemists/shops.
If this was a sponsored thread I would have plugged those guys who are an online drugstore and I'd have said how their drugs are all original & said how they're affordable & reliable & koso-koso but behold, I will not...
Well explained. Thanks
 

Luther12

Elder Lister
View attachment 31136

So Mara Moja packs the following ingredients: 200mg of Paracetamol, 400mg of Aspirin, & 50mg of caffeine, ok?

For context, the kawaida, normal Panadol contains 500mg of Paracetamol alongside a bunch of other smoll-smoll ingredients.
Now, this will surprise you but the EXAAAAACT mechanism of action of Paracetamol (PCM) isn't that well known.

Our resident pharmacists can go much deeper on this, but what we do know is that Paracetamol works on the brain pain pathways.
The downside of this is that it relieves PAIN but doesn't necessarily deal with the INFLAMMATION that is an important part of your pain.

Yaani, Paracetamol serves an analgesic role but not an anti-inflammatory one, you understand?
Say for example you have pain after busting your shoulder in the gym, yeah?

The reason you're in pain isn't because you're just "in pain"; it's cause the muscle tendons at your shoulder are inflamed/ "on fire".

So when you take PCM, it deals with the "pain" but doesn't really deal with the pain, y'know what I'm saying?
Now, in comes someone like DICLOFENAC.

Diclofenac is a non-steroidal, anti-inflammatory drug, NSAID for short.

it's primary role is to reduce inflammation, ok? to turn down the heat.

And let me tell you Maina, it does this role veeeeeeeery well.
View attachment 31137

However, Diclofenac only REDUCES the inflammation but doesn't deal with the pain pathway, you follow?
In comes MARA MOJA tablets;
"kicking in the door waving the 44,
all you heard was Mara Moja don't hit me no more!"


So Mara Moja comes in carrying that solid Paracetamol Power, that badass Aspirin Ability (Aspirin is also an NSAID, btw) (non-steroidal anti-inflammatory drug, ie), & to top it off, some of that good-good Caffeine Content.

Now, full disclosure, I didn't know much about the caffeine, but turns out it works by directly blocking the receptors (adenosine ones) that are found at the organ in pain.
that is, the Paracetamol works on brain pathways, Aspirin reduces inflammation, then caffeine tells the organ to stop feeling pain.

The pain is just zimwa'd like "shhh, it's okay"

Now, I'd end there but here's a disclaimer;

Because of the high Aspirin, this drug can be very crude on your gastrointestinal tract.
Gastric & duodenal ulcers are common in ppl who use them frequently.
Like for me, I've had issues with acidity so I go for other pain-relievers before going for this one.

Now here's an academic question for you to think about;

WHY does Paracetamol still exist if its role seems to be done "better" by other pain relievers?
Maybe it's cause of Big Pharma...

Maybe I'll answer that question in a future thread so that's why you should consider following me.

Maybe I also don't know the answer.

Tons of possibilities!!!

Another IMPORTANT disclaimer, btw, is that there's tons of fake drugs out there, especially for drugs that are well known to work well like this one.

That said, please be sure to purchase your medications from reliable pharmacies/chemists/shops.
If this was a sponsored thread I would have plugged those guys who are an online drugstore and I'd have said how their drugs are all original & said how they're affordable & reliable & koso-koso but behold, I will not...

Hehehe...excellent narration skills. An addendum:


There's a class of painkillers called NSAIDs (Non-Steriodal Anti-Inflammatory Drugs), so called as to differentiate them from steroids anti-inflammatory molecules like Prednisolone, etc. NSAIDs are a broad class of drugs but some of the common examples include acetyl salicylic acid (aspirin; note it's an acid), ibuprofen (brufen), indomethacin (indocid), mefenamic acid (ponstan), diclofenac, meloxicam, piroxicam, etc.

NSAIDs broadly exhibit three main effects: antipyretic (pyrexia=fever), anti-inflammatory and analgesic (pain-killing) effects. They do this by stopping synthesis of prostaglandins from cell membrane phospholipids, via the so-called cyclo-oxygenase (COX) pathway. Paracetamol (aka Acetaminophen) is the outlier here since it exhibits excellent antipyretic effects with little to no anti-inflammatory effects.

In the body, prostaglandins perform different functions like uterine contractions, mediate pain, mucus lining production in the stomach, keep the ductus-arteriosus open, etc. This therefore explains some of the side-effects and contraindications we see with NSAIDS. For instance, NSAIDS will stop mucus production in the stomach hence predisposing one to gastric ulceration. In utero, the developing fetus does not have an active pulmonary (lungs) circulation and blood is shunted directly from the right to the left ventricle via a patent ductus artriosus. This 'hole in the heart' is supposed to close just before birth under the influence of PGs, hence the reason we don't recommend NSAIDS to expectant mothers especially in the third trimester. Their effect on the uterus explains their (ab)use in initiating labor.

In an attempt to minimize some of these side effects, further studies realized that there are two COX pathways, one in all cells (COX-1) and and one that only exists/ activates in inflammed/ injured cells (COX-2). This then led to development of selective COX-2 inhibitor NSAIDS like nimesulide, celecoxib, rofecoxib, valdecoxib, etc. Some of these were or have been withdrawn from the market due to other issues that arose from pharmacovigilance studies/ post-marketing surveillance.

The COX pathway also mediates release of Thromboxane A2 (Tx A2) that induces blood clotting. Thus COX inhibition by NSAIDs will lead to diminished Tx A2 production and hence minimize risk of blood clot formation in predisposed individuals. This explains the use of low dose aspirin (so called junior aspirin -JASA - that comes in 75mg or 80mg tablets) as a blood thinner in patients at risk of clot formation. Normal aspirin analgesic dose in adults is 300mg. Aspirin is contraindicated in kids due to the risk of Reye's syndrome.

Over time different NSAIDS have been observed to have unexpected but beneficial effects that we medically exploit, e.g. mefenamic acid will reduce blood loss over and above fighting pain so we often use it to manage excessive blood loss in menstruation, etc.

The membrane phospholipids that give us PGs are also precursors of chemicals called Leukotrienes (LTs) which are potent bronchoconstrictors. NSAIDS are therefore largely contraindicated in asthmatic patients due to the risk of precipitating asthmatic attacks. Blockage of COX pathway often causes the Lipoxygenase pathway that produces LTs to predominate. LT receptor antagonists (blockers) e.g. zafirlukast, montelukast, pranlukast are often used to manage asthma and other allergic reactions.

Finally, Pharmacovigilance. This is a branch of pharmacy that's concerned with documenting and studying adverse events/ reactions due to drugs, vaccines, medical devices and non-pharmaceutical commodities as well as documenting poor quality issues. The rationale is that during drug development, the drugs under study are tested on only a small number of people and therefore some of those rare adverse effects may be missed only to show up when the drugs come into widespread use. To that end, pharmacovigilance is a form of post-marketing surveillance. In Kenya, this is administered by the Pharmacy & Poisons Board (PPB) whose reporting portal is https://pv.pharmacyboardkenya.org.

Any time you have an adverse or allergic reaction to a particular drug, always get in touch with your pharmacist so that the same can be documented and reported. Those reports are what informs product recalls and withdrawals, changes in treatment guidelines, precautions in drug inserts, etc. This is going to be quite an important field especially with the ongoing rollout of covid vaccination.

~~THE END~~
 

Luther12

Elder Lister
For me Maramoja works. Paracetamol not at all. I recently discovered why as you have said up there, Aspirin. BTW what happened to the good old small tablets Aspirin,? and recently Betapyne were banned I cant get them in a chemist without @Luther12 Prescription Unless someone's knows me. Kama jana nilinyimwa kabisa even a Beautiful yellowish veiled in a long dress Wagithomo Girl (I don know why they all look similar like twins) who sold to me once refused completely.

Betapyn contains codeine, a narcotic analgesic as one of the ingredients.
Formulations containing narcotics cannot legally be dispensed without a prescription, which cannot be refilled i.e. a fresh prescription must be obtained every time.
Codeine is a relative of morphine. Other common narcotic analgesics include pethidine, (micro)fentanyl, tramadol, etc which all are potential drugs of abuse and addiction. All are controlled substances as stated in the Narcotics & Psychotropic Substances (Control) Act of the laws of kenya.
 

shocks

Elder Lister
Hehehe...excellent narration skills. An addendum:


There's a class of painkillers called NSAIDs (Non-Steriodal Anti-Inflammatory Drugs), so called as to differentiate them from steroids anti-inflammatory molecules like Prednisolone, etc. NSAIDs are a broad class of drugs but some of the common examples include acetyl salicylic acid (aspirin; note it's an acid), ibuprofen (brufen), indomethacin (indocid), mefenamic acid (ponstan), diclofenac, meloxicam, piroxicam, etc.

NSAIDs broadly exhibit three main effects: antipyretic (pyrexia=fever), anti-inflammatory and analgesic (pain-killing) effects. They do this by stopping synthesis of prostaglandins from cell membrane phospholipids, via the so-called cyclo-oxygenase (COX) pathway. Paracetamol (aka Acetaminophen) is the outlier here since it exhibits excellent antipyretic effects with little to no anti-inflammatory effects.

In the body, prostaglandins perform different functions like uterine contractions, mediate pain, mucus lining production in the stomach, keep the ductus-arteriosus open, etc. This therefore explains some of the side-effects and contraindications we see with NSAIDS. For instance, NSAIDS will stop mucus production in the stomach hence predisposing one to gastric ulceration. In utero, the developing fetus does not have an active pulmonary (lungs) circulation and blood is shunted directly from the right to the left ventricle via a patent ductus artriosus. This 'hole in the heart' is supposed to close just before birth under the influence of PGs, hence the reason we don't recommend NSAIDS to expectant mothers especially in the third trimester. Their effect on the uterus explains their (ab)use in initiating labor.

In an attempt to minimize some of these side effects, further studies realized that there are two COX pathways, one in all cells (COX-1) and and one that only exists/ activates in inflammed/ injured cells (COX-2). This then led to development of selective COX-2 inhibitor NSAIDS like nimesulide, celecoxib, rofecoxib, valdecoxib, etc. Some of these were or have been withdrawn from the market due to other issues that arose from pharmacovigilance studies/ post-marketing surveillance.

The COX pathway also mediates release of Thromboxane A2 (Tx A2) that induces blood clotting. Thus COX inhibition by NSAIDs will lead to diminished Tx A2 production and hence minimize risk of blood clot formation in predisposed individuals. This explains the use of low dose aspirin (so called junior aspirin -JASA - that comes in 75mg or 80mg tablets) as a blood thinner in patients at risk of clot formation. Normal aspirin analgesic dose in adults is 300mg. Aspirin is contraindicated in kids due to the risk of Reye's syndrome.

Over time different NSAIDS have been observed to have unexpected but beneficial effects that we medically exploit, e.g. mefenamic acid will reduce blood loss over and above fighting pain so we often use it to manage excessive blood loss in menstruation, etc.

The membrane phospholipids that give us PGs are also precursors of chemicals called Leukotrienes (LTs) which are potent bronchoconstrictors. NSAIDS are therefore largely contraindicated in asthmatic patients due to the risk of precipitating asthmatic attacks. Blockage of COX pathway often causes the Lipoxygenase pathway that produces LTs to predominate. LT receptor antagonists (blockers) e.g. zafirlukast, montelukast, pranlukast are often used to manage asthma and other allergic reactions.

Finally, Pharmacovigilance. This is a branch of pharmacy that's concerned with documenting and studying adverse events/ reactions due to drugs, vaccines, medical devices and non-pharmaceutical commodities as well as documenting poor quality issues. The rationale is that during drug development, the drugs under study are tested on only a small number of people and therefore some of those rare adverse effects may be missed only to show up when the drugs come into widespread use. To that end, pharmacovigilance is a form of post-marketing surveillance. In Kenya, this is administered by the Pharmacy & Poisons Board (PPB) whose reporting portal is https://pv.pharmacyboardkenya.org.

Any time you have an adverse or allergic reaction to a particular drug, always get in touch with your pharmacist so that the same can be documented and reported. Those reports are what informs product recalls and withdrawals, changes in treatment guidelines, precautions in drug inserts, etc. This is going to be quite an important field especially with the ongoing rollout of covid vaccination.

~~THE END~~
jeso, munene, you guys do this deep dive for all drugs, na kichwa inabaki sawa?
 

Kamau wa Kíríro

Elder Lister
Hehehe...excellent narration skills. An addendum:


There's a class of painkillers called NSAIDs (Non-Steriodal Anti-Inflammatory Drugs), so called as to differentiate them from steroids anti-inflammatory molecules like Prednisolone, etc. NSAIDs are a broad class of drugs but some of the common examples include acetyl salicylic acid (aspirin; note it's an acid), ibuprofen (brufen), indomethacin (indocid), mefenamic acid (ponstan), diclofenac, meloxicam, piroxicam, etc.

NSAIDs broadly exhibit three main effects: antipyretic (pyrexia=fever), anti-inflammatory and analgesic (pain-killing) effects. They do this by stopping synthesis of prostaglandins from cell membrane phospholipids, via the so-called cyclo-oxygenase (COX) pathway. Paracetamol (aka Acetaminophen) is the outlier here since it exhibits excellent antipyretic effects with little to no anti-inflammatory effects.

In the body, prostaglandins perform different functions like uterine contractions, mediate pain, mucus lining production in the stomach, keep the ductus-arteriosus open, etc. This therefore explains some of the side-effects and contraindications we see with NSAIDS. For instance, NSAIDS will stop mucus production in the stomach hence predisposing one to gastric ulceration. In utero, the developing fetus does not have an active pulmonary (lungs) circulation and blood is shunted directly from the right to the left ventricle via a patent ductus artriosus. This 'hole in the heart' is supposed to close just before birth under the influence of PGs, hence the reason we don't recommend NSAIDS to expectant mothers especially in the third trimester. Their effect on the uterus explains their (ab)use in initiating labor.

In an attempt to minimize some of these side effects, further studies realized that there are two COX pathways, one in all cells (COX-1) and and one that only exists/ activates in inflammed/ injured cells (COX-2). This then led to development of selective COX-2 inhibitor NSAIDS like nimesulide, celecoxib, rofecoxib, valdecoxib, etc. Some of these were or have been withdrawn from the market due to other issues that arose from pharmacovigilance studies/ post-marketing surveillance.

The COX pathway also mediates release of Thromboxane A2 (Tx A2) that induces blood clotting. Thus COX inhibition by NSAIDs will lead to diminished Tx A2 production and hence minimize risk of blood clot formation in predisposed individuals. This explains the use of low dose aspirin (so called junior aspirin -JASA - that comes in 75mg or 80mg tablets) as a blood thinner in patients at risk of clot formation. Normal aspirin analgesic dose in adults is 300mg. Aspirin is contraindicated in kids due to the risk of Reye's syndrome.

Over time different NSAIDS have been observed to have unexpected but beneficial effects that we medically exploit, e.g. mefenamic acid will reduce blood loss over and above fighting pain so we often use it to manage excessive blood loss in menstruation, etc.

The membrane phospholipids that give us PGs are also precursors of chemicals called Leukotrienes (LTs) which are potent bronchoconstrictors. NSAIDS are therefore largely contraindicated in asthmatic patients due to the risk of precipitating asthmatic attacks. Blockage of COX pathway often causes the Lipoxygenase pathway that produces LTs to predominate. LT receptor antagonists (blockers) e.g. zafirlukast, montelukast, pranlukast are often used to manage asthma and other allergic reactions.

Finally, Pharmacovigilance. This is a branch of pharmacy that's concerned with documenting and studying adverse events/ reactions due to drugs, vaccines, medical devices and non-pharmaceutical commodities as well as documenting poor quality issues. The rationale is that during drug development, the drugs under study are tested on only a small number of people and therefore some of those rare adverse effects may be missed only to show up when the drugs come into widespread use. To that end, pharmacovigilance is a form of post-marketing surveillance. In Kenya, this is administered by the Pharmacy & Poisons Board (PPB) whose reporting portal is https://pv.pharmacyboardkenya.org.

Any time you have an adverse or allergic reaction to a particular drug, always get in touch with your pharmacist so that the same can be documented and reported. Those reports are what informs product recalls and withdrawals, changes in treatment guidelines, precautions in drug inserts, etc. This is going to be quite an important field especially with the ongoing rollout of covid vaccination.

~~THE END~~
He he he....I thought Junior Aspirin ni ya watoto ala @Ngimanene na Muchere kwa hio thread ingine
 
Last edited:
Top