•  Introduction.
•  Symptoms.
•  Infection.
•  complications.
•  Treatment and drugs.
•  Prevention.

 

 

Introduction:-

• Shingles is a viral infection that causes a painful rash on one side of the body. Often appears as a band of blisters that wraps between 2-3 weeks.
• Shingles is caused by the varicella-zoster virus (the same virus that causes chickenpox). After you've had chickenpox, the virus lies inactive in nerve tissue near your spinal cord and brain. Years later, the virus may reactivate as shingles.
• Causes of reactivation are unknown but mostly due to decreased immunity (more occurrence>50 years) and stress. 
• While it isn't a life-threatening condition, shingles can be very painful.

 

Symptoms:-

 

• Pain, burning, numbness or tingling.
• A red rash that begins a few days after the pain.
• Fluid-filled blisters that break open and crust over.
• Itching.

• Fever and chills.
• General achiness.
• Headache.
• Fatigue.

• The pain and rash occur near your eyes. If left untreated, this infection can lead to permanent eye damage.
• You or someone in your family has a weakened immune system (due to cancer, medications or chronic illness).
• The rash is widespread and painful.

• You can't catch shingles from someone else who has shingles. But a person with a shingles rash can spread chickenpox to another person who hasn't had chickenpox and who hasn't gotten the chickenpox vaccine. 
• If you have shingles, you are contagious especially the open sores of the shingles rash so avoid direct contact with people (especially newborns, pregnant women, any one has a weak immune system) until shingles blisters scab over. 
• Having had chickenpox can develop shingles.

 

Complications:- 

• Most people who get shingles will get better and will not get it again.

• Complications from shingles can range from a mild to severe, ranging from minor skin infections to post herpetic neuralgia (damaged nerve fibers with exaggerated pain).
• Other problems may be Vision loss, Encephalitis, an inflammation of the brain, Hearing or balance problems, Facial paralysis.
• If shingles blisters aren't properly treated, bacterial skin infections may develop.

• An episode of shingles usually heals on its own within a few weeks, but prompt treatment can ease pain, speed healing and reduce your risk of complications.
• There is no cure for shingles, but treatment may help you get well sooner and prevent other problems.

• Acyclovir (Zovirax), Valacyclovir (Valtrex), Famciclovir (Famvir).
• Drugs for the pain such as: Narcotics (e.g. oxycodone).
• Tricyclic antidepressants, such as amitriptyline
• Anticonvulsants, such as gabapentin (Neurontin).
• Numbing agents, such as lidocaine, delivered via a cream, gel, spray or skin patch.

• Anti-itch cream or calamine lotion.
• Oral antihistamines, such as diphenhydramine (Benadryl, others).

Prevention:-

 

• Two vaccines may help prevent shingles :  the chickenpox (varicella) vaccine and the shingles (varicella-zoster) vaccine.

• Varicella-zoster is part of a group of viruses called herpes viruses, which includes the viruses that cause cold sores and genital herpes. Because of this, shingles is also known as herpes zoster. But the virus that causes chickenpox and shingles is not the same virus responsible for cold sores or genital herpes, a sexually transmitted disease.

- Prepared by: Dr. Mustafa Abdel Tawab (pharmacist). - Resources:  -  mayoclinic.com  -  webmd.com.   -  Wikipedia.com. - Copyrights: All rights are reserved for pharmacist development group 2009 - 2011.

•  Introduction.
•  Signs and symptoms.
•  Diagnosis.
•  Prevention.
•  Treatment.
•  Transmission.
•  Some hygiene information to protect yourself.

Introduction:

• Hepatitis A(infectious hepatitis) is acute infectious disease of the liver caused by hepatitis a virus.
• The incidence of the infection is high in the developing countries and in regions with poor hygiene standards and the illness is contracted in early childhood.
• The incubation period (time between the infection and the appearance of symptoms) is between 2 to 6 weeks {average 28 days}.
• Hepatitis a doesn't have chronic stages, isn’t progressive, and doesn’t cause permanent liver damage.
• HA infection causes no clinical signs and symptoms in over 90% of the infected children and the infection confers life long immunity as following the infection, AB are formed that confers immunity against further infection.

Signs and symptoms:

• Symptoms may be mistaken for influenza (fever ,fatigue,abdominal pain , diarrhea, appetite loss, itching, nausea, jaundice, urine of dark color, stool of light color)
• The color of urine is due to the excretion of bile in it and the color of feces is due to lack of bilirubin.
• Symptoms can return over the 6-9 months
• Mortality is less than 0.5%

Diagnosis:

• IgM antibody is only present in the blood following an acute hepatitis A infection (detectable from 1-2 weeks after the infection and persists for up to 14 weeks.
• the presence of IgG antibody in the blood mean that acute stage is past and the person is immune to further infection
• IgG is also found in the blood after vaccination and tests for immunity to the virus are based on the detection of this Ab.

Prevention:

• Hepatitis A can be prevented by (vaccination,good hygiene and sanitation).
• The vaccine is given by injection into the muscle of the upper arm.
• The vaccines, (e.g. Havrix and VAQTA)contain no live virus and are very safe.
• Initial dose provides protection for 2-4 weeks after vaccination and the second dose(booster dose) is given 6-12 months later, provides protection up to 20 years.
• N.B. vaccine is given before the infection as it doesn't work after the exposure.
• Vaccine isn't recommended for children younger than 2 years as it's ineffective for them.
• If you have been exposed to person who is infected with HAV, there is treatment that may prevent you from becoming infected, it’s called immune globulin and is more likely to be effective when given 2 weeks of exposure.
• [Immune globulin is a preparation of Ab that can fight the virus in the body] given safely in children younger than 2 years, pregnant women and breast feeding.
• some samples taken to study ocean water quality was found to have HAV specially after rains so it's advisable not to go to oceans in coastal areas in this time.

Treatment:

• There is no specific treatment for hepatitis A, but symptomatic treatment (rest, well balanced diet, stay hydrated)and avoid fatty foods and alcohols.
• N.B. avoid taking medicine or any substance can cause harm to the liver e.g. acetaminophen.
• The low % of death scour usually in older ages (>50 years) and in those suffering another form of viral hepatitis (C or B).

Transmission:

• By fecal-oral route, poor sanitation, overcrowding,ingestion of shellfish cultivated in polluted water and by blood transfusion but this is very rare.
• Fecal-oral route mean that when a person put something in his mouth that has been contaminated with faeces of an affected person.
• N.B. people who don't have symptoms can still spread the virus.

Some hygiene information to protect yourself:

• Wash your hands thoroughly every time you use the bathroom,before touching or preparing food, and before touching others. Wash carefully with soap and warm water and dry thoroughly.
• Contaminated surfaces should be cleaned with household bleach to kill the virus. Heat food or water to 185°F or85°C to kill the virus. 

- Prepared by: Dr. Mustafa Abdel Tawab (pharmacist). - Resources:  -  Color atlas of pharmacology.  -  Drugs.com.  -  Master of Egyptian drugs. -  Wikipedia.   -  Master of Saudi drugs. - Copyrights: All rights are reserved for pharmacist development group 2009 - 2011.

•  Introduction.
•  Muscle relaxants.
•  Non-depolarizing muscle relaxants.
•  D-tubocurarin.
•  Pancuronium.
•  Depolaring muscle muscle relaxants.

Introduction:-

• Acetylcholine is a major neurotransmitter in the autonomic nervous system. In the peripheral nervous system, acetylcholine activates muscles .
• The enzyme acetylcholinesterase converts acetylcholine into the inactive metabolites choline and acetate .
• Acetylcholinestrase enzyme is abundant in the synaptic cleft, and its role in rapidly clearing free acetylcholine from the synapse is essential for proper muscle function .
• Acetylcholine receptor agonists and antagonists can either have an effect diretly on the receptors or exert their effects indirectly, e.g., by affecting the enzyme acetylcholinesterase, which degrades the receptor ligand. Agonists increase the level of receptor activation. antagonists reduce it.
• Certain neurotoxins work by inhibiting acetylcholinesterase, thus leading to excess acetylcholine at the neuromuscular junction, thus causing paralysis of the muscles needed for breathing and stopping the beating of the heart.

Muscle relaxants:-
 

• Muscle relaxants Used as adjuncts to general anesthesia, to ensure that surgical procedures aren't distributed by muscle contraction of the patient.
• Two types of those muscle relaxants used with anesthesia :

Non-depolarizing muscle relaxants:-

a- (d-tubocurarin) : it is given intravenously as it is not absorbed in GIT .

• Its effect start within 4 minutes & continues for 30 minutes
• The duration of action of d-tubocurarin can be shortened by administrating its antidote neostigmine (ACH esterase inhibitor) so inhibit ACH breakdown .
• Unwanted side effects result from non immune mediated release of histamine from mast cell leading to hypotension ,urticaria & bronchospasm .

b- Pancuronium (pavulon) : is a synthetic compound now frequently used .

• It's 5 fold more potent than d-tubocurarin & with somewhat longer duration & not likely to cause histamine release .
• Side effects : increase heart rate & blood pressure due to M2 cholinoceptor blockade &this effect not shared by newer congeners like vecuronium & pibecuronium .

Depolarizing muscle muscle relaxants:-

• This class contain only succinylcholines (succinyldicholine & suxamethonium) .
• Its structure has double ACH molecule. it is not hydrolyzed by acetylcholinestrase but by butyrylcholinesterase, (a plasma cholinesterase). This hydrolysis by butyrylcholinesterase is much slower than that of acetylcholine by acetylcholinesterase.
• Its effect start within seconds & continues for 10 minutes so used at the start of the anesthesia to facilitate intubation.
• Side effects :
  • histamine release (scoline apnea).
  • hyperkalemia which may lead to cardiac arrhythmia .
  • bradycardia .
• Care must be taken during eye surgery ,as increasing in intraocular pressure may occur.

- Prepared by: Dr. Mustafa Abdel Tawab (pharmacist). - Resources:  -  Color atlas of pharmacology.  -  Drugs.com.  -  Master of Egyptian drugs. -  Wikipedia.   -  Master of Saudi drugs. - Copyrights: All rights are reserved for pharmacist development group 2009 - 2011.

•  How gallstones are formed.
•  Types.
•  Causes.
•  Risk factors.
•  Symptoms.
•  Diagnosis.
•  Treatment.

How gallstones are formed:-

• Gallstones are of 2 types :

1. cholesterol stones 80% .
2. pigment stones (of bilirubin).

• Causes of gallstone formation:

1. too much cholesterol or bilirubin .
2. not enough bile salts .
3. gallbladder doesn't empty completely often enough .

• People at risk for gallstones include :-
• women—especially women who are pregnant, use hormone replacement therapy, or take birth control pills .
• people over age 60 .
• overweight or obese men and women .
• people who fast or lose a lot of weight quickly .
• people with a family history of gallstones .
• people with diabetes .
• people who take cholesterol-lowering drugs .

• Symptoms: (start to appear when stone become more than 8mm)

1. Steady pain in the upper abdomen .
2. pain in the right shoulder.
3. nausea .
4. fever.
5. jaundice .

• The symptoms appear suddenly so ,it's called gallbladder attack & usually follow fatty meals & may be during night .
• Silent stones: with no symptoms & no need for treatment.

• All stones are of mixed content to some extent (cholesterol 30-70%) + ca salts . so because of their calcium content they can be diagnosed radiologically. (ultrasound & ct) .
• blood test also needed to look for infection, obstruction & pancrititis.

- Prepared by: Dr. Mustafa Abdel Tawab (pharmacist). - Resources:  -  Color atlas of pharmacology.  -  Drugs.com.  -  Master of Egyptian drugs. -  Wikipedia.   -  Master of Saudi drugs. - Copyrights: All rights are reserved for pharmacist development group 2009 - 2011.

•  Introduction.
•  Statins.
•  Fibrates.
•  Nicotinic acid.
•  Cholesteramine and colestipol.
•  Omega - 3.
•  Probucol.

Introduction:-

Triglycerides:

• Main constituent of vegetable oil & animal fat.
• High triglycerides (normal range 150mg/dl) lead to atherogenesis.
• It's used by the body as energy store except for the brain.

 Cholesterol:

• Used as building block of biological membrane & precursor for most steroid hormones.
• Rate limiting enzyme in cholesterol synthesis in the liver is HMGCA reductase enzyme.
• Liver use cholesterol in the synthesis of bile acids & VLDL.
• 85% of the blood cholesterol is produced in the body.

Main Lipid lowering agents

1- Statins (atorvastatin, fluvastatin, rosuvastatin, simvastatin).

• Mechanism of action: statins are inhibitors of HMGcoA reductase (hydroxyl methyl glutaryl coA enzyme) so they inhibit cholesterol synthesis. In addition to that, they increase expression of LDL receptor.
• Statins may occur naturally in some foods like mushroom & red yeast rice.
• Cholesterol synthesis appears to occur mostly at night so short acting statin e.g. simvastatin (zocor) must be taken at night to maximize its effect but long acting statin e.g. atorvastatin (lipitor) may be taken at any time.
• The most potent statin [atorvastatin, rosuvastatin (crestor)].
• The least potent statin {fluvastatin (lescol)}.
• The result of statin therapy appears rapidly may be after one week.
• Side effects: rarely [skeletal musculature damage, liver enzymes become high].

2-Fibrates (bezofibrate, etofibrate, gemfibrozil, fenofibrate)

• Used as accessory therapy in many forms of hypercholesterolemia usually in combination with statins specially fenofibrate (tricor) and gemfibrozil (lopid600) because using of them with statin will increase muscle toxicity by decreasing statin metabolisms.
• It's indicated solely for patient no tolerant to statin.
• Mechanism of action:- activate PPAR (peroxisome proliferators activated receptor) which induce transcription of number of genes that facilitate lipid metabolism, also it decrease VLDL and increase HDL.
• When triglycerides increase more than 1000mg/dl lead to pancreatitis with abdominal pain & as fibrates decrease triglycerides they decrease pancreatitis.
• Side effects: high risk of gallstones (use over several years) myopathy, myalgia and rhabdomyolysis.
• Usage of statins with fibrates may increase the likelihood of rhabdomyolysis & liver failure.

3-Nicotinic acid [niacin or vit b3 & its derivatives]

• Mechanism of action: stimulate endothelial lipoprotein lipase so decrease triglyceride.
• At the first of the therapy PG mediated vasodilatation occur leading to 2 side effects {flushing and hypotension}.
• To overcome these 2 side effects 325mg of ASA can be taken 30 min prior to nicotinic acid (niaspan). also the extended release dosage decrease flushing.
• Flushing which occurs as side effect of nicotinic acid may make nicotinic acid to be used for male impotence.
• Deficiency of vit b3 may lead to pellagra disease (3 diseases: diarrhea, dementia & dermatitis).

 4-Cholesteramine & colestipol:

• They are bile acid sequestrants which bind bile acid in the GIT & prevent its reabsorbtion. As bile acid decrease, liver convert cholesterol into bile acid so cholesterol decrease.
• Side effects of cholesteran (questran) & colestipol (colestid) : 

1. Diverse GIT disturbance (constipation, diarrhea). 
2. Decrease the absorption of lipid soluble vitamins (A, D, E, and K). 
3. Decrease absorption of vit K antagonist, digitoxin and diuretics.

• If used with any other drug (statin or other) must be taken 1hour after the drug or the other drug taken 4 hour after it as they bind statin in the intestin & decrease its absorption.

5-Omega-3 (polyunsaturated fatty acid [eicosapentanoate-docosahexapentaneoate]

• Decrease each of (triglycerides, synthesis of VLDL lipoprotein B and remnant particles).
• Although it doesn't decrease LDL or total cholesterol, with increasing some dietary supplements as fish-leafy green vegetables-nuts-hummus-eggs- linseed-flaxseed this decrease Congestive heart disease.

6-Probucol:

•  Decrease HDL more than LDL nonetheless decreases atherogenesis and that may be due to decreasing LDL oxidation.

- Prepared by: Dr. Mustafa Abdel Tawab (pharmacist). - Resources:  -  Color atlas of pharmacology.  -  Drugs.com.  -  Master of Egyptian drugs. -  Wikipedia.   -  Master of Saudi drugs. - Copyrights: All rights are reserved for pharmacist development group 2009 - 2011.