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ALL YOU NEED TO KNOW ABOUT ACE INHIBITORS (ANIMATED)
 
04:06
Angiotensin II is a very potent chemical produced by the body that primarily circulates in the blood. It causes the muscles surrounding blood vessels to contract, thereby narrowing the vessels. The narrowing of the vessels increases the pressure within the vessels causing increases in blood pressure (hypertension). Angiotensin II is formed from angiotensin I in the blood by the enzyme angiotensin converting enzyme (ACE). (Angiotensin I in the blood is itself formed from angiotensinogen, a protein produced by the liver and released into the blood.) Angiotensin converting enzyme inhibitors (ACE inhibitors) are medications that slow (inhibit) the activity of the enzyme ACE, which decreases the production of angiotensin II. As a result, blood vessels enlarge or dilate, and blood pressure is reduced. This lower blood pressure makes it easier for the heart to pump blood and can improve the function of a failing heart. In addition, the progression of kidney disease due to high blood pressure or diabetes is slowed. benazepril (Lotensin) captopril (Capoten) enalapril (Vasotec, Epaned) fosinopril (Monopril) lisinopril (Prinivil, Zestril) moexipril (Univasc) perindopril (Aceon) quinapril (Accupril) ramipril (Altace)
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CALCIUM CHANNEL BLOCKERS SIMPLIFIED
 
03:35
Calcium channel blockers are usually well absorbed through the git which means that they go through first pass metabolism . However once entered into the blood stream calcium channel blockers are highly bound to plasma proteins, after doing their action calcium channel blockers are then metabolized by the liver and excreted renally.
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METFORMIN MECHANISM OF ACTION MADE SIMPLE *ANIMATED*
 
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Metformin is a biguanide medication used to treat type 2 diabetes in obese people, it works by three methods the first being that it decrease the gluconeogenisis from the liver , decreasing the glucose absorption by the intestines, and it improves insulin sensitivity. instagram: https://www.instagram.com/pill_whiteboard/
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Drug Metabolism Made Simple *ANIMATED*
 
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metabolism is the protective biochemical process by which our bodies alter xenobiotics either enzymatically or nonenzymatically. generally, drug metabolism begins with hydrophobic drug and converts it to a more hydrophilic metabolite to facilitate its elimination. an understanding of the drug metabolism process and the potential outcomes is critical for developing safe and useful pharmaceuticals. drug metabolism can result in one of two products, an inactive metabolite and an active metabolite. inactive metabolites of the drugs basically have no pharmacological activity of the original drug. an example of that would be the hydrolysis of procaine into para aminobenzoic acid and diethylethanolamine which results in the loss of the anesthetic activity of procaine. on the other hand, an active metabolite can mean that a metabolite can retain the same activity of the parent drug, that's apparent when codeine is demthylated to a more active drug which is morphine. however, in some cases we notice a result known as bioactivation where the parent drug is inactive and the metabolite would have a pharmacological activity, in this case the inactive parent drug is called a prodrug. an example of a prodrug is enalapril which has no activity as an antihypertensive, but upon hydrolysis it becomes enalaprilat which is a potent antihypertensive drug. bioactivation of a drug can also lead to toxic metabolites, the widely used acetaminophen has a metabolite that is called n-acetyl-p-benzoquinone imine which is hepatoxic, I explained the mechanism of the toxicity and the antidote in my previous video which I linked in the description below. The liver has the highest concentration of drug-metabolizing enzymes, because of it’s location between the gastrointestinal tract and the systemic circulation. Based on the reactions involved in the metabolism process we can classify the metabolic pathways into phase I metabolism and phase II. Phase I metabolism is characterized as a functionalization reaction, where they add or reveal a functional group by oxidation, reduction, or hydrolysis, hence, leading to increase in overall polarity of the drug which facilitates its excretion in the urine Oxidation is the most common phase I reaction, Cytochrome p450 is a superfamily of oxidases that are responsible for the majority of oxidation reactions, it’s found in very high concentrations in the liver. Oxidation can also happen through alcohol dehydrogenase which is an enzyme that oxidizes alcohols into aldehydes from primary alcohols and to ketones from secondary. Aldehydes can be oxidized from to carboxylic acid by the enzyme aldehyde dehydrogenase. We can see that in the example of the conversion of acetaldehyde to acetic acid in the metabolism of ethanol. Another phase I reaction is the reduction reaction, there are several reductase enzymes common reduction reactions include the reduction of disulfide bonds, in which the disulfides would be reduced to free sulfhydryls. Another reduction reaction is done by the aldo-keto reductases which reduce carbonyl containing compounds back to alcohol in a process opposite to the oxidation done by alcohol dehydrogenase. The last type of phase I metabolism reaction is hydrolysis, hydrolysis is basically the addition of water across a bond resulting in a more water-soluble metabolite. A great example of hydrolysis is ester hydrolysis which is performed by the enzyme esterase found throughout the body, esterase is responsible for the hydrolysis of an ester into a more soluble alcohol or carboxylic acid. Phase II Phase II reactions are commonly called conjugation reaction owing to the fact they add a functional group on the drug for the purpose of increasing its polarity. The conjugation process requires an enzyme generally termed as transferase, that transfers the large polar molecule called a co-factor onto the drug, Examples of phase II reactions: glucuronidation is the most common phase II reaction, glucuronosyltransferase is the enzyme that uses UDP-GA as the cofactor to transfer glucuronic acid to several functional groups like hydroxyl groups, carboxylic acid ,and hydroxylamines. The glucuronic acid adds a significant amount of hydrophilicity to the molecules facilitating it’s excretion process. Another popular reaction is glutathione conjugation which results from the addition of glutathione molecule to an electrophilic substrate. Being a nucleophile glutathione generally acts to detoxify electrophiles. Glutathione-s-transferase is the enzyme responsible for the reaction of glutathione with electrophiles like epoxides and halides. After the conjugation, the product is excreted as mercapturic acid in the urine. Paracetamol antidote video: https://www.youtube.com/watch?v=hg_gpWjWsRM
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Statins Mechanism Of Action *Animated*
 
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STATINS ARE A GROUP OF MEDICATIONS THAT REDUCE CHOLESTEROL LEVELS, THEY WERE DISCOVERED BY AKIRA ENDO IN 1971 A JAPANESE BIOCHEMIST. THERE ARE SEVERAL STATINS IN THE MARKET CURRENTLY WHICH ARE EASY TO REMEMBER BECAUSE THEY ALL END WITH THE SUFFIX STATIN. CHOLESTEROL IS PRODUCED BY THE LIVER AND TRANSPORTED BY LIPOPROTEINS WHICH CONSIST OF TWO TYPES, LOW DENSITY LIPOPROTEIN LDL WHICH IS KNOWN AS THE BAD FAT, IT'S MAIN FUNCTION IS TO TRANSPORT CHOLESTEROL THROUGHOUT THE BODY, THE OTHER TYPE IS HIGH DENSITY LIPOPROTEIN ALSO KNOWN AS GOOD FAT, THIS TYPE OF LIPOPROTEIN REMOVES EXCESS CHOLESTEROL AND CARRIES IT BACK TO THE LIVER FOR DEGRADATION. HOW DOES IT WORK? STATINS WORK BY COMPETITIVELY INHIBIT HMG COENZYME A REDUCTASE THIS ENZYME CATALYZES THE REDUCTION OF HMG COENZYME TO MEVALONATE. WHICH IS THE RATE LIMITING STEP IN HEPATIC CHOLESTEROL BIOSYNTHESIS, INHIBITION OF THIS ENZYME DECREASES CHOLESTEROL SYNTHESIS LEADING TO AN UPREGULATION IN LDL RECEPTORS IN THE LIVER, THIS INCREASES LDL UPTAKE BY THE HEPATOCYTS DECREASING THE AMOUNT OF LDL CHOLESTEROL IN THE BLOOD. WHO SHOULD STATINS BE GIVEN FOR? ACCORDING TO THE AMERICAN COLLEGE OF CARDIOLOGY, STATINS ARE GIVEN AS A PREVENTION OF CARDIOVASCULAR DISEASE IN PATIENTS WITH LDL CHOLESTEROL MORE THAN 190 MG/DL. ON AVERAGE STATINS CAN LOWER BLOOD LDL BY 70 MG/DL WHICH TRANSLATES INTO AN ESTIMATED 60% DECREASE IN THE NUMBER OF CARDIAC EVENTS LIKE HEART ATTACKS OR SUDDEN CARDIAC DEATHS. CONTRAINDICATIONS OF STATINS, BEING DRUGS THAT ARE METABOLISED AND EXCRETED BY THE LIVER, STATINS ARE CONTRAINDICATED IN CASES OF CHRONIC LIVER DISEASE, OR ELEVATION OF SERUM TRANSAMINASES. STATINS ARE ALSO NOT GIVEN IN PREGNANCY OR LACTATION AS THEY IN CATEGORY X. LIFESTYLE MODIFICATION IS STRONGLY ADVISED TO PATIENTS ON STATINS THESE MODIFICATIONS INCLUDE, LESS CALORIC INTAKE, LOW ANIMAL FAT DIET, AND PHYSICAL EXCERCISE. MONITORING CREATINE KINASE IS IMPORTANT IN PATIENTS TAKING STATIN AS MYOPATHY IS ONE OF THE MOST COMMON AND DANGEROUS ADVERSE EFFECT OF THIS CLASS OF MEDICATIONS
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SULFONYLUREAS MECHANISM OF ACTION EXPLAINED *ANIMATED*
 
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In this video i explain the mechanism of action of sulfonylureas witch are a very popular class of treatment for type II diabetes. sulfonylureas main mechanism of action is blocking the ATP sensitive potassium channels which are located on the cell membrane of the beta cells in the pancreas, blocking these channels will subsequently lead to depolarization of the cell witch in terms will open another type of channels on the cell membrane which are calcium channels, voltage sensitive calcium channels open up after the depolarization happens witch allows the exocytosis of insulin from beta cells into the blood stream. sulfonylureas consist of 3 generations Diabetes and Insulin video: https://www.youtube.com/watch?v=SgVVGs7nqZA&t=78s
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Thiazides Mechanism Of Action *ANIMATED*
 
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THIAZIDES ARE THE MOST WIDELY USED CLASS OF DIURETICS. THIAZIDES ARE CALLED THAT BECAUSE THEY CONTAIN SULFURE AND ARE SULFONAMIDE DERVIATIVES, THEY ARE KNOWN TO BE MODERATELY POTENT DIURETICS. THIAZIDES ARE MAINLY USED IN HYPERTENSION TREATMENT, THEY'RE EITHER USED ALONE OR IN COMBINATION WITH ACE INHIBITORS. THEY'RE USED IN HYPERCALCIURIA AS THEY REDUCE CALCIUM IONS EXCRETION BENEFITING PATIENTS WITH CALCIUM OXALATE STONES IN THE URINARY TRACT. HOW DO THEY WORK? THIAZIDES REDUCE WATER REABSORPTION IN THE NEPHRON BY INHIBITING THE SODIUM CHLORIDE SYMPORTER IN THE DISTAL CONVOLUTED TUBULE, NORMALLY SODIUM AND CHLORIDE ENTER THE DISTAL CONVOLUTED TUBULE CELL THROUGH THE SYMPORTER THEN THEY GET REABSORBED BACK INTO THE BLOOD STREAM THROUGH SODIUM POTASSIUM ATPASE CHANNEL AND CHLRIDE CHANNEL, THIAZIDES BLOCK THIS SYMPORTER CAUSEING THE SODIUM AND SUBSEQUENTLY WATER TO GET FILTERED INTO THE URINE. ALTHOUGH THE DIURETIC EFFECT OF THIAZIDES IS WEAK, THIAZIDES CAUSE VASODIALATION THAT HELPS REDUSING BLOOD PRESSURE AS WELL, UNFORTUNATLY THE MECHANISM OF THE VASODIALATION IS YET TO BE UNDERSTOOD. CHLOROTHIAZIDE IS THE FIRST ORALLY AVAILABLE THIAZIDE DIURETICS, HOWEVER RECENTLY, NEW THIAZIDE LIKE DIURETICS HAVE BEEN INTRODUCED LIKE CHLORTHALIDONE WHICH IS A NONTHIAZIDE THAT BEHAVES PHARMACOLOGICALLY LIKE HYDROCHLOROTHIAZIDE WIHT AN ADVANTAGE OF LONG DURATION OF ACTION, METOLAZONE IS ANOTHER THIAZIDE LIKE DRUG THAT IS MORE POTENT AND UNLIKE THIZAIDES CAUSES SODIUM EXCRETION IN ADVANCED RENAL FAILURE. THE MOST SIDE EFFECTS OF THIAZIDES ARE CAUSED BY ELECTROLYTE DEPLETION RESULTING FROM PROLONGED USE, LIKE HYPOKALEMIA, HYPOCLOREMIA, HYPONATERMIA AND DEHYDRATION. SINCE THIAZIDE IS NOT METABILISED AND EXCRETED UNCHANGED IN THE URINE, THEY CANNOT BE GIVEN IN PATIENTS WITH RENAL DISEASE. THIAZIDES ARE CONTRAINDICATED WITH DIGOXIN, AS A RESULT OF HYPOKALEMIA THE DRUG INTERATION CAN RESULT IN CARDIAC ARRYTHMIA, FURTHUREMORE, THIAZIDES ARE CONTRAINDICATED WITH DRUGS THAT CAUSE FLUID RETENTION SUCH AS CORTICOSTEROIDS AND NSAIDS.
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FLUOROQUINOLONES MADE SIMPLE (ANIMATED)
 
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FLUOROQUINOLONES
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5 ANTIDOTES EVERY PHARMACIST MUST KNOW (ANIMATED)
 
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As humans we are exposed to a huge amounts of harmful chemicals however our bodies are equipped with amazing mechanisms by which it's able to defend itself. In rare occasions people might over-dose on some medications or forget that they have taken a medicine, and sometimes they would be exposed to large amounts of the same toxin which doesn't give the body the chance to excrete all the toxins. this video discusses the different and most important and live saving antidotes in the medical practice. 1) Acetylcysteine 2) Penicillinamine 3) Vitamin K 4) Naloxone 5) Sodium nitrate check out my instagram: https://www.instagram.com/pill_whiteboard/?hl=en
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Diabetes and Insulin Made Simple
 
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In this video I explain diabetes type 1 and type 2 type 1 is caused by by an autoimmune reaction , that leads to the destruction of beta cells in the pancreas, wheres type 2 diabetes is caused mainly by insulin resistance , and it's treated by many medication
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