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Drugology, Shebin al-Kom (2025)

30/09/2023

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11/09/2023

♡Amiodarone...It's a pleasure to meet u..^^

=Hello amiodarone, can you tell us a little about you?

》Yes I was originally an antianginal agent but later I found that I have antiarrhythmic characteristics
Tell us about your pharmacokinetics properties?
I have slow and wide distribution to fats, muscles and highly perfused organs (brain, liver and kidney) so it takes me long loading periods to have rapid activity

^^I have lipophilic characteristics so it takes time to reach stable plasma levels .
I have incomplete absorbtion following oral administration ranges from (22-86%) and interindividual variations.

=How do you perform your action?

》It is a little bit confusing but I possess all Vaughan _Williams anti arrhythmic classes properties ....
1 ⇒ na channel blocking effect
2⇒anti adrenergic effects
3 ⇒inhibition of K outward channels
4 ⇒ca channel blocking effect

=That is tremendous! When can I use you?

♤Ventricular arrhythmia
Treatment or prevent recurrent VF and recurrent hemodynamically unstable VT that do not respond to other antiarrythmic drugs.

♤Supra ventricular tachy arrhythmia
of SVTS
of atrial fibrillation to sinus rhythm
of AVNRT and AVRT.

♤Angina
Chronic stable angina pectoris and prinzemtal variant angina but not a first line choices.

》I've two dosage forms;tablets &injection.

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Sources;Uptodate,AMBOSS

31/08/2023

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Source:ESC Guidelines

24/08/2023

Hello digoxin….

Plz introduce yourself...
》I am cardiotonic glycoside and belongs to the digitalis class,I used to treat various heart problems such as atrial flutter, atrial fibrillation, and heart failure with its associated symptoms

》I am a positive inotrope ….

inhibiting the activity of the myocardial Na-K ATPase pump (an enzyme that controls the movement of ions into the heart),increase in intracellular sodium that will drive an influx of calcium in the heart and cause an increase in contractility, Cardiac output increases with a subsequent decrease in ventricular filling pressures.

》I also have vagomimetic effects on the AV node, slows electrical conduction in the atrioventricular node, therefore, decreasing the heart rate.

Who needs you?

♡Pt with Heart failure with reduced ejection fraction (LVEF

08/08/2023

Cause we always look forward to The Best 👌 .....We will present a new coming drugs series،،
Titled.... ^^Drug Toxicity series ♥️👏

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♥️♥️♥️♥️

15/07/2023

السلام عليكم ورحمة الله ❤
الناس ال متابعه الصفحه، محتاجه حد يشتغل معايا ف السيرش وتجميع الداتا للناس ال عندها شغف لكدا، ولو حد عنده أفكار نقدر نقدم بيها المعلومه بشكل أفضل يقترح ياريت، ولو حد هنا يقدر يساعد ف اني اتعلم ازاي اعمل فيديوهات بفويس يقولي علي مصدر اتعلم منه يكون مشكور😃❤

25/03/2023

Upcoming Post!!!

Ramadan Mubarak ❤💞

17/03/2023

COPD EXACERBATION MANAGEMENT

GOLD 2022

02/10/2022

Upcoming post soon......
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18/09/2022

Has Empa,Dapagliflozin Role in HF ??!

There was a significant reduction in the second primary outcome (a composite of cardiovascular death or hospitalization for heart failure), primarily driven by a significant reduction in hospitalization for heart failure.

What's Empa,Dapagliflozin?!

They're Members of SGLT2 Inhibitor ...Antidiabetic Agent, May be used as an adjunctive agent or alternative monotherapy for patients in whom initial therapy with lifestyle intervention and metformin failed or those who cannot take metformin.
Role of SGLT2 Inhibitor in Heart failure !!!

The EMPEROR Reduced trial found that....

*patients with heart failure with reduced ejection fraction (HFrEF), with or without diabetes, empagliflozin has been shown to reduce cardiovascular mortality and worsening heart failure with reduced ejection fraction (HFrEF).

*Dapagliflozin — The DAPA-HF trial found that....

*In patients with or without diabetes, dapagliflozin has been shown to reduce all-cause mortality and worsening heart failure in adults with heart failure with reduced ejection fraction (HFrEF) with New York Heart Association functional class II, III, or IV .

How SGLT2 Inhibitor Can do this in HF?!
Empagliflozin also reduces sodium reabsorption and increases the delivery of sodium to the distal tubule, which may lower both pre- and afterload of the heart and downregulate sympathetic activity.

****Accumulating mechanistic insights suggest that SGLT‐2 inhibitors may be valuable in the treatment of HF regardless of diabetes mellitus status and EF. SGLT‐2 inhibitors may exert cardioprotective effects through several distinct mechanisms, including

(1) improvement in ventricular loading conditions secondary to reductions in preload (mediated by osmotic diuresis and natriuresis) and afterload (potentially occurring via lowering of arterial pressure and stiffness)
(2) provision of an alternative cardiac energy supply in the form of cardiac ketones (specifically β‐hydroxybutyrate)
(3) direct inhibition of the sodium/hydrogen (Na+/H) exchanger in the myocardium,leading to reduction in or reversing of cardiac injury, hypertrophy, fibrosis, remodeling, and systolic dysfunction
(4) reduction in left ventricular mass and improvement in diastolic function through inhibition of cardiac fibrosis (a feature of HF)
(5) improvement in endothelial dysfunction
(6) stimulation of increased glucagon secretion,potentially improving cardiac performance by either increasing cardiac index and fuel availability or decreasing peripheral vascular resistance.

****Empagliflozin causes significant natriuresis, particularly when combined with loop diuretics, resulting in an improvement in blood volume. However, off-target electrolyte wasting, renal dysfunction, and neurohormonal activation were not observed. This favorable diuretic profile may offer significant advantage in the management of volume status in patients with heart failure and may represent a mechanism contributing to the superior long-term heart failure outcomes observed with these agents.
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04/06/2022

Upcoming post soon

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08/03/2022

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~OFF-label USE OF ACETYLCYSTEINE...

=N-acetylcysteine (NAC) is the mainstay of therapy for acetaminophen toxicity. NAC has Federal and Drug Administration (FDA) approval for the treatment of potentially hepatotoxic doses of acetaminophen (APAP), and it is almost 100% effective if given within 8 hours post-ingestion.

*** NAC repletes glutathione reserves by providing cysteine, which is an essential precursor in glutathione production. NAC by itself also binds to the toxic metabolites and scavenges free radicals.

=Mucolytic Effect, NAC has been reported to reduce the viscosity of sputum in both cystic fibrosis and COPD, facilitating the removal of pulmonary secretions.

***The free sulfhydryl group confers NAC with the ability to reduce disulphide bonds, thus decreasing mucus viscosity and facilitating mucociliary clearance.

=acute hepatic failure(or Ischemic Hepatitis, IH)

***N-Acetylcysteine (NAC), a potent anti-oxidant, may prevent IH by improving tissue oxygen delivery and improving hepatic hypoxia.

=prevention of contrast-induced nephropathy.

***Since acetylcysteine is a vasodilator as well as an antioxidant, it may work in two distinct ways, by preventing reduction in renal blood flow (RBF) or contrast-induced oxidative damage.

=The NAC orally daily produced a greater improvement in s***m concentration, ej*****te volume, s***m motility and normal morphology for idiopathic infertile men, whereas no significant influence in serum hormones.

***NAC can also reduce the effect of ROS activity in s***matozoa, which was a factor of reducing s***m viscosity, Therefore, the decrease in viscosity may be the reason of the increase in semen volume.

=topical treatment of keratoconjunctivitis sicca.

***Owing to its potent antioxidant, anti-inflammatory and mucolytic properties, topical NAC has had extensive use in the treatment of ocular pathology.

=There is good evidence to show it is of benefits in acute exposures to cyclopeptide containing mushrooms and carbon tetrachloride.

***Antidote for amatoxin poisoning,
N-acetylcysteine (NAC) has been used for decades but its benefit is still unproven.

=There are animal and human tissue studies showing its use in decreasing cisplatin-induced nephrotoxicity, although clinical evidence is minimal.

=NAC may also have therapeutic application in chronic valproate hepatotoxicity and acute pennyroyal or clove oil ingestion-induced hepatotoxicity..

=NAC being used as an antineoplastic agent as well as for psychiatric conditions like schizophrenia, bipolar disorder, depression, gastrointestinal conditions like hepatorenal syndrome, Helicobacter pylori infections, necrotizing enterocolitis, critical care patients like lung injury, cardiac injury, multiorgan dysfunction, sepsis and hematological conditions like sickle cell disease(still in the experimental stage).

=There's a case reports of NAC helping with improving neurological status in patients comatose with carbon monoxide poisoning.
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08/03/2022

Upcoming post soon
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17/01/2022

☠️☠️☠️A FATAL INTERACTION BETWEEN THEOPHYLLINE AND CIPROFLOXACIN MUST BE AVOIDED?!

=Concurrent administration of theophylline along with ciprofloxacin can lead to a harmful sid effects to patient!

=This is a Serious, Major interaction.

=Concomitant use of theophylline and ciprofloxacin has decreased theophylline clearance and increased plasma levels and symptoms of toxicity.

=Ciprofloxacin will increase effect of theophylline by affecting hepatic/intestinal enzyme CYP3A4 metabolism.

= Serious and fatal reactions have included cardiac arrest, seizure, status epilepticus, and respiratory failure.

=So this interaction Should be avoided,but
If concomitant use cannot be avoided, monitor theophylline levels and adjust dosage as needed.
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08/01/2022

☠️Drugs contra_indicated in pregnancy!!!

1)chloramphenicol
=antibiotic can cause blood disorders And gray baby Syndrome.

2) Ciprofloxacin And Levofloxacin
=fluoroquinolone antibiotics that can cause problems with the baby's muscle and Skeletal growth as well as joint pain and potential nerve damage in the mother.
=Fluoroquinolones may also increase chances of having a miscarriage, acc. To a 2017 study.

=Fluoroquinolones can increase the risk of aortic tears or rupture, this can result in life threatening bleeding especially people with a history of aneurysm(occurs when an artery's wall Weakens and causes an abnormally large bluge) and certain heart diseases.

3)Primaquine (drug used to treat malaria)
=there is not a lot of data on humans who's taken this drug during pregnancy, but animal studies suggest it's harmful to developing fetus, it can damage blood cells in a fetus.

4)Sulfonamides(Sulfa drugs---antibiotics that used to kill germs and ttt of bacterial infections )
=can cause Jaundice in newborn, also may increase the risk of miscarriage.

5)Trimethoprime (primsol)
=a type of antibiotic When taken during pregnancy, can cause neural tube defects. These defects affect brain development in a developing baby.
6)Codeine
(drug used to relieve pain. In some states, codeine can be used as a cough medicine)
=The drug has the potential to become habit-forming. It can lead to withdrawal symptoms in newborns.
7)Ibuprofen
High doses can cause many serious problems, including:
miscarriage, delayed onset of labor, premature closing of the fetal ductus arteriosus,jaundice
hemorrhaging for both mother and baby, necrotizing enterocolitis, or damage to the lining of the intestines, oligohydramnios, or low levels of amniotic fluid, fetal kernicterus, a type of brain damage, abnormal vitamin K levels.
=Most experts agree that ibuprofen is probably safe to use in small to moderate doses in early pregnancy.

**It’s especially important to avoid ibuprofen during the third trimester of pregnancy, however. During this stage of pregnancy, ibuprofen is more likely to cause heart defects in a developing baby.

8)Warfarin
= It can cause birth defects.
*It should be avoided during pregnancy unless the risk of a blood clot is more dangerous than the risk of harm to the baby.

9)Clonazepam
= is used to prevent seizures and panic disorders. It’s sometimes prescribed to treat anxiety attacks or panic attacks.

**Taking clonazepam during pregnancy can lead to withdrawal symptoms in newborns.

10)lorazepam
=It's a common medication used for anxiety or other mental health disorders.
** It can cause birth defects or life-threatening withdrawal symptoms in a baby after birth.
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02/01/2022

NSAIDS ARE CONTRAINDICATED IN PATIENTS WITH HTN?!!!
patients with HTN should not take NSAIDS, this is because NSAIDS counteract antihypertensive drugs effect.

NSAIDS are non-selective COX inhibitor thus PG synthesis is inhibited!

In normal human subjects, NSAIDs do not have a significant influence on renal function. Nevertheless, prostaglandins are important mediators at the kidney level. They are involved in maintaining the volume control and electrolyte balance, they also control the release of renin and contribute to renal vasodilation. All NSAIDs can alter renal function by inhibiting COX‐1 (which regulates renal hemodynamics and glomerular filtration) and/or COX‐2 (which mediates salt and water excretion) expressed in the kidneys .

Usually, NSAIDs are associated with salt and water retention, due to the loss of PG‐induced action on ADH. This hydro‐saline retention has the potential of triggering arterial hypertension.

This occures with
-RAAS Blockers
-ACEI
-Beta blockers
-Diuretics (loop or thiazide)
*Calcium channel blocker are less affected by NSAIDS.

*Changes in blood pressure level determined after 4 months of continuous use of NSAIDS, in daily practical use this action is not observed.
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17/12/2021

Should people avoid grapefruit with statin?!!

=Only people who take atorvastatin, simvastatin or lovastatin should avoid taking it with grapefruit.
-This occurs only if those statin taken orall(This is because the interaction happens in your digestive tract)so if patient took his medicine as patch or direct in vein this decrease side effects that may occur.

-What grapefruit can do if taken with those statin?!
=This result in liver damage, rhabdomyolysis and this lead to kidney damage, also can causedigestive problemsincreased blood sugarneurological side effects

-The secret to the interaction is in furanocoumarins, This compound deactivates the CYP3A4 enzyme that the body uses to metabolize, or process, these particular statins. Grapefruit doesn’t affect other statins because they are metabolized by a different enzyme, CYP2C9

Furanocoumarins are organic chemical compounds present in many different plants, including grapefruit and also other plants as(Legume, Citrus families,and Carrot).
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Drugology

30/09/2023

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