FETAL DIAGNOSIS

INTRODUCTION: Several procedures are currently available to determine certain kinds of abnormalities in a fetus or to monitor development.  We should once again remember that the human gestation age goes 40 weeks from the days of the last normal menstruations period.  And although for some people this period may be less or slightly more, the fetus is always monitored with non invasive procedures to make sure that it's life is not in danger and any concerns diagnosed are addressed right away.

ULTRASOUND (OR FETAL ULTRASONOGRAPHY): This is a non-invasive procedure; high-frequency sound waves are transmitted through the abdominal wall into the uterus. The reflected sound waves are converted into an image called a sonogram. This method is used to confirm multiple pregnancies, fetal age or position, or to detect fetal abnormalities such as heart defects or malformations of other organs. Ultrasound may also be used to determine the thickness of the fetal neck, which is an indicator of Down syndrome.

AMNIOCENTESIS: This procedure is usually performed at 16 to 18 weeks of gestation. A hypodermic needle is inserted through the wall of the abdomen into the amniotic sac, and about 10 to 20 mL of amniotic fluid is removed. Within this fluid are fetal cells, which can be cultured so that their chromosomes may be examined. Through such examination and biochemical tests, a number of genetic diseases or chromosome abnormalities may be detected. Because women over the age of 35 years are believed to have a greater chance of having a child with Down syndrome, amniocentesis is often recommended for this age group. A family history of certain genetic diseases is another reason a pregnant woman may wish to have this procedure.

CHORIONIC VILLUS SAMPLING (CVS): In this procedure, a biopsy catheter is inserted through the vagina and cervix to collect a small portion of the chorionic villi. These cells are derived from the fetus but are not part of the fetus itself. The information obtained is the same as that for amniocentesis, but CVS may be performed earlier in pregnancy, at about 8 weeks. Although there is a risk that the procedure may cause a miscarriage, CVS is considered comparable in safety to amniocentesis. It is important to remember that no invasive procedure is without risks.

MATERNAL BLOOD TESTS: Alpha-fetoprotein (AFP) is produced by the fetus and is found in maternal circulation. The level reaches a peak between 12 and 15 weeks of gestation, and should then decrease. If AFP is still high after 16 to 18 weeks, there is a 95% chance that the fetus has spina bifida or anencephaly, malformations of the central nervous system. Maternal blood levels of pregnancy-associated plasma protein A (PAPP-A) and beta hCG can be measured during the first trimester. These tests, in conjunction with ultrasound, can reliably detect Down syndrome.

RELATED;

1. DRUG USE AND PREGNANCY  

2. HEMMOLYTIC DISEASE OF THE NEW BORN

3.  NORMAL LABOR AND VARGINAL DELIVERY

REFERENCES

CATEGORIES OF DRUGS IN RELATION TO PREGNANCY

 

INTRODUCTION:  Drug use during pregnancy is one of the most important threats to worry about in order to ensure the safety of the mother and the baby.  In the first place although the mother may have less or no effect, our fear rotates around the growing fetus that may take in the drug via the placenta and develop fetal malformations.

1.  RISK CATEGORY A

INTERPRETATION: Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities to the fetus in any trimester of pregnancy.

EXAMPLE OF DRUGS: Prenatal multivitamins, insulin, thyroxine, folic acid.

2.  RISK CATEGORY B

INTERPRETATION: Animal studies have revealed no evidence of harm to the fetus; however, there are no adequate and well-controlled studies in pregnant women.

OR

Animal studies have shown an adverse effect, but adequate and well-controlled studies in pregnant women have failed to demonstrate risk to the fetus in any trimester.

EXAMPLE OF DRUGS: Penicillins, cephalosporins, azithromycin, acetaminophen, ibuprofen in the first and second trimesters.

3.  RISK CATEGORY C

INTERPRETATION: Animal studies have shown an adverse effect and there are no adequate and well controlled studies in pregnant women.

OR

No animal studies have been conducted and there are no adequate and well controlled studies in pregnant women.

EXAMPLE OF DRUGS: Most prescription medicines; antimicrobials such as clarithromycin, fluoroquinolones, and Bactrim; selective serotonin reuptake inhibitors (SSRIs); corticosteroids; and most antihypertensives.

4.  RISK CATEGORY D

INTERPRETATION: Adequate well-controlled or observational studies in pregnant women have demonstrated a risk to the fetus. However, the benefits of therapy may outweigh the potential risk. For example, the drug may be acceptable if needed in a life-threatening situation or serious disease for which safer drugs cannot be used or are ineffective.

EXAMPLE OF DRUGS: Alcohol, ACE inhibitors, angiotensin receptor blockers (ARBs) in the second and third trimesters, gentamicin, carbamazepine, cyclophosphamide, lithium carbonate, methimazole, mitomycin, nicotine, nonsteroidal antiinflammatory drugs (NSAIDs) in the third trimester, phenytoin, propylthiouracil, streptomycin, tetracyclines, valproic acid.

5.  RISK CATEGORY X

INTERPRETATION: Adequate well-controlled or observational studies in animals or pregnant women have demonstrated positive evidence of fetal abnormalities or risks. The use of the product is contraindicated in women who are or may become pregnant. There is no indication for use in pregnancy.

EXAMPLE OF DRUGS: Clomiphene, fluorouracil, isotretinoin, leuprolide, menotropins, methotrexate, misoprostol, nafarelin, oral contraceptives, raloxifene, ribavirin, statins, temazepam, testosterone and thalidomide, and warfarin.

RELATED;

1.  HEMORRHAGIC DISEASE OF THE NEW BORN  

2.  ENDOMETRIOSIS

3.  OBSTETRICS AND GYNECOLOGY

REFERENCES

JAUNDICE

 

Objectives this article:  By the end of this article, the learner will be able to; 

1.  understand the cause of the yellow color that appear in mucous membranes.

2.  Explain the role of the liver in elimination of bilirubin

INTRODUCTION: Jaundice is not a disease, but rather a sign caused by excessive accumulation of bilirubin in the blood. Because one of the liver’s many functions is the excretion of bilirubin, jaundice may be a sign of liver disease such as hepatitis or cirrhosis. Hepatitis

This may be called hepatic jaundice, because the problem is with the liver. Other types of jaundice are prehepatic jaundice and posthepatic jaundice: The name of each tells us where the problem is. Recall that bilirubin is the waste product formed from the heme portion of the hemoglobin of old RBCs. Hemoglobin: The human red blood cells

PATHOPHYSIOLOGY: Prehepatic jaundice means that the problem is “before” the liver; that is, hemolysis of RBCs is taking place at a more rapid rate. Rapid hemolysis is characteristic of sickle cell anemia, malaria, and Rh disease of the newborn; these are hemolytic anemias. Sickle cell anaemia: Rh disease of the newborn

As excessive numbers of RBCs are destroyed, bilirubin is formed at a faster rate than the liver can excrete it. The bilirubin that the liver cannot excrete remains in the blood and causes jaundice. Another name for this type is hemolytic jaundice.

Posthepatic jaundice means that the problem is “after” the liver. The liver excretes bilirubin into bile, which is stored in the gallbladder and then moved to the small intestine. If the bile ducts are obstructed, perhaps by gallstones or inflammation of the gallbladder, bile cannot pass to the small intestine and backs up in the liver. Bilirubin may then be reabsorbed back into the blood and cause jaundice. Another name for this type is obstructive jaundice.

RELATED;

1.  THE CYTOCHROME P450 ENZYME SYSTEM  

2.  CATALASE

3.  FUNCTIONS OF THE LIVER

4.  MEDICAL CONDITIONS

REFERENCES

EFFECTS OF ALCOHOL ON NUTRITION

INTRODUCTION: Alcohol also sometimes referred to as the demon drink is one of the most commonly consumed and abused drink in all nations.  It is thought that some moderate quantities of this monster drink poses beneficial effects on the body systems however, because of the potential for addiction and drug dependance, it is discouraged by many in our communities.  Continuous intake of alcohol on a daily basis and in large quantities lead to development of condition known and Chronic alcoholism that comes with various health concerns some of which, are deficiency in minerals and ions in the body. 

In this article, we are going to look at some of the mineral and ion deficiencies that affect people consuming large amounts of alcoholic beverages.  This is one of the series of discussions related to drug abuse and the human body.  Our discussion on alcohol started earlier and if you did not start with us, you can find more about the previous topics by clicking on the link below; Alcohol and the human body  Chronic alcoholics run considerable risk of nutritional deficiencies for most of the food nutrients. The most common problems are neurologic symptoms associated with thiamine or pyridoxine deficiencies and hematological problems associated with folate or pyridoxine deficiencies.

ORIGIN OF DEFICIENCIES: Although it is well known that chronic alcohol abusers tends to have reduced appetite, it should be noted that the deficiencies seen with alcoholics are not necessarily due to this effect and or poor diet alone, although it is often a strong contributing factor. Alcohol causes pathological alterations of the gastrointestinal tract that often directly interfere with absorption of certain nutrients and or impaired distribution of others as we are going to see.  It should always be remembered that long term consumption of alcohol leads to development of ulcerative intestinal conditions including but not limited to peptic ulcer disease and gastritis.  

The continued corrosion of the intestinal walls causes disruption of the nutrient absorbing surface area and disruption in the chemical environment that frequently leads to nausea and vomiting, all of which alters the metabolic processes.

INVOLVEMENT OF THE LIVER: So much we have discussed about the human liver and it's role in the human body plus, the conditions that affect it.  In case you have not been following me, you can use the links below to read more about the liver.  The liver is one of the most important sites of activation and storage of many vitamins.  In fact in the liver alone, there are are always thousands of chemical reactions going on whose effects control the body. 

The severe liver damage associated with chronic alcoholism appears to interfere directly with storage and activation of certain nutrients. Alcohol appears to interfere directly with folate absorption and alcoholic cirrhosis impairs storage of this nutrient.  To understand more about the way such processes are affected, you can read more about the functions of the liver from here.

It is also astonishing to know that alcohol induced hepatitis is one of the leading causes of death in chronic and heavy alcohol drinkers.

NEURONAL INVOLVEMENT: The most sounding and intended effects of alcohol from mild enjoyment to toxicity occurs in the Central nervous system and the brain mainly.  Some alcoholics also develop a peripheral neuropathy that responds to pyridoxine supplementation. This problem appears to result from impaired activation and increased degradation of pyridoxine.  Pyridoxine is simply vitamin B6 and it is involved in the normal functioning of the brain, spinal cord and peripheral nerves.  The toxic effects of alcohol on the central nervous system is not only seen in chronic alcoholism but also, several individuals intentionally tend to drink, perceiving it that alcohol cures some sort of pain.  This is why the drug is taken as one of the most common Over The Counter Medications.

The most dramatic nutritionally related neurological disorder is Wernicke–Korsakoff syndrome. This symptoms include mental disturbances, ataxia which is described as unsteady gait and lack of fine motor coordination, and uncoordinated eye movements.  This is especially true with acute intoxication of alcohol.

CARDIOVASCULAR INVOLVEMENT: Congestive heart failure similar to that seen with beriberi is also seen in a small number of these patients. While this syndrome may only account for a small percentage of alcohol related neurologic disorders, the response to supplemental thiamine is so dramatic that it is usually worth consideration.

CAUSES OF THIAMINE DEFICIENCY: The thiamine deficiency appears to arise primarily from impaired absorption, although alcoholic cirrhosis may also affect the storage of thiamine in the liver. While those are the most common nutritional deficiencies associated with alcoholism, deficiencies of almost any of the water soluble vitamins can occur and cases of alcoholic scurvy and pellagra are occasionally reported.

VITAMIN A DEFICIENCY: Chronic ethanol consumption causes an interesting redistribution of vitamin A stores in the body. Vitamin A stores in the liver are rapidly depleted while levels of vitamin A in the serum and other tissues may be normal or slightly elevated. Apparently, ethanol causes both increased mobilization of vitamin A from the liver and increased catabolism of liver vitamin A to inactive metabolites by the hepatic P450 enzyme system.

BONE AND CALCIUM DISTURBANCES: Alcoholic patients have decreased bone density and an increased incidence of osteoporosis. This probably relates to increased rate of metabolism of vitamin D to inactive products by an activated cytochrome P450 enzyme system. Dietary calcium intake is also often poor. In fact, alcoholics generally have decreased serum levels of zinc, calcium, and magnesium due to poor dietary intake and increased urinary losses.

ISSUES TO DO WITH IRON: Iron deficiency anemia is very rare unless there is gastrointestinal bleeding or chronic infection. In fact, excess iron is a more common problem with alcoholics. Many alcoholic beverages contain relatively high iron levels, and alcohol appears to enhance iron absorption.

SUMMERY:  In summery, chronic alcohol consumption is one of the leading causes of ion and mineral deficiencies.  The most common pathophysiology is that it impairs absorption of many minerals from the gastrointestinal tract and increases elimination of those absorbed via urine.

RELATED;

1.  Alcohol and the human body

2.  The human liver

3.  Functions of the human liver

4.  Vitamin A

5.  Osteoporosis

6.  Calcium and the human body

7.  Dynamics of drugs and the human body

8.  Drug addiction and dependency 

9.  Over the counter medications

REFERENCES

SULFONAMIDES

 

INTRODUCTION: Sulfonamides with varying physical, chemical, pharmacologic, and antibacterial properties are produced by attaching substituents to the amido group (–SO₂–NH–R) or the amino group (–NH₂ ) of the sulfanilamide nucleus. Sulfonamides tend to be much more soluble at alkaline than at acid pH. Most can be prepared as sodium salts, which are used for intravenous administration.

MECHANISM OF ACTION & ANTIMICROBIAL ACTIVITY: Sulfonamide-susceptible organisms, unlike mammals, cannot use exogenous folate but must synthesize it from PABA. This pathway is thus essential for production of purines and nucleic acid synthesis. Nucleic acids  As structural analogs of PABA, sulfonamides inhibit dihydropteroate synthase and thus folate production.

SPECTRUM OF ACTIVITY: Sulfonamides inhibit both gram-positive and gram-negative bacteria, Nocardia sp, Chlamydia trachomatis, and some protozoa. Some enteric bacteria, such as Escherichia coli, Klebsiella pneumoniae, Salmonella, Shigella, and Enterobacter sp are also inhibited. It is interesting to note however that rickettsiae are not inhibited by sulfonamides but are instead stimulated in their growth. The activity is poor against anaerobes. Pseudomonas aeruginosa is intrinsically resistant to sulfonamide antibiotics. Bacteriology: Antibiotics  Combination of a sulfonamide with an inhibitor of dihydrofolate reductase (trimethoprim or pyrimethamine) provides synergistic activity because of sequential inhibition of folate synthesis.

RESISTANCE: Mammalian cells and some bacterial cells lack the enzymes required for folate synthesis from PABA and depend on exogenous sources of folate; therefore, they are not susceptible to sulfonamides. Sulfonamide resistance may occur as a result of mutations that; (1) cause overproduction of PABA, (2) cause production of a folic acid-synthesizing enzyme that has low affinity for sulfonamides, or (3) impaired permeability to the sulfonamide.

CLINICAL USES: Sulfonamides are infrequently used as single agents. Many strains of formerly susceptible species, including meningococci, pneumococci, streptococci, staphylococci, and gonococci, are now resistant. Antimicrobial drug resistance  The fixed-drug combination of trimethoprim-sulfamethoxazole is the drug of choice for infections such as Pneumocystis jiroveci (formerly P. carinii) pneumonia, toxoplasmosis, nocardiosis, and occasionally other bacterial infections.

ORAL ABSORBABLE AGENTS: Sulfisoxazole and sulfamethoxazole are short- to medium-acting agents used almost exclusively to treat urinary tract infections. The usual adult dosage is 1 g of sulfisoxazole four times daily or 1 g of sulfamethoxazole two or three times daily. Sulfadiazine in combination with pyrimethamine is first-line therapy for treatment of acute toxoplasmosis. The combination of sulfadiazine with pyrimethamine, a potent inhibitor of dihydrofolate reductase, is synergistic because these drugs block sequential steps in the folate synthetic pathway blockade. The dosage of sulfadiazine is 1 g four times daily, with pyrimethamine given as a 75-mg loading dose followed by a 25-mg once-daily dose. Folinic acid, 10 mg orally each day, should also be administered to minimize bone marrow suppression. Sulfadoxine is the only long-acting sulfonamide currently available in many countries including sub Saharan Africa, and only as a combination formulation with pyrimethamine (Fansidar), a second-line agent in the treatment of malaria.

ORAL NONABSORBABLE AGENTS: Sulfasalazine (salicylazosulfapyridine) is widely used in ulcerative colitis, enteritis, and other inflammatory bowel disease.

TOPICAL AGENTS: Sodium sulfacetamide ophthalmic solution or ointment is effective in the treatment of bacterial conjunctivitis and as adjunctive therapy for trachoma. Another sulfonamide, mafenide acetate, is used topically but can be absorbed from burn sites. The drug and its primary metabolite inhibit carbonic anhydrase and can cause metabolic acidosis, a side effect that limits its usefulness. Silver sulfadiazine is a much less toxic topical sulfonamide and is preferred to mafenide for prevention of infection of burn wounds.

ADVERSE REACTIONS: All sulfonamides, including antimicrobial sulfas, diuretics, diazoxide, and the sulfonylurea hypoglycemic agents, have been considered to be partially cross-allergenic. The most common adverse effects are fever, skin rashes, exfoliative dermatitis, photosensitivity, urticaria, nausea, vomiting, diarrhea, and difficulties referable to the urinary tract. Other unwanted effects include stomatitis, conjunctivitis, arthritis, hematopoietic disturbances, hepatitis, and, rarely, polyarteritis nodosa and psychosis.

RELATED;

1.  Artemisinin and its derivatives

2.  Antibiotics

3.  Metronidazole

4.  Pharmacology and therapeutics

REFERENCES

ALLERGY

 

INTRODUCTION: An allergy is a hypersensitivity to a particular foreign antigen, called an allergen. Allergens include plant pollens, foods, chemicals in cosmetics, antibiotics such as penicillin, dust, and mold spores. Such allergens are not themselves harmful. Most people, for example, can inhale pollen, eat peanuts, or take penicillin with no ill effects.

HYPERSENSITIVITY: Hypersensitivity means that the immune system overresponds to the allergen, and produces tissue damage by doing so. Allergic responses are characterized by the production of IgE antibodies, which bond to mast cells. Mast cells are specialized connective tissue cells and are numerous in the connective tissue of the skin and mucous membranes.

INFLAMMATORY MEDIATORS: Chemicals in mast cells include histamine and leukotrienes, which are released by the bonding of IgE antibodies or when tissue damage occurs. These chemicals contribute to the process of inflammation by increasing the permeability of capillaries and venules. Tissue fluid collects and more WBCs are brought to the damaged area. In an allergic reaction, the effects of inflammatory chemicals create symptoms such as watery eyes and runny nose (hay fever) or the more serious wheezing and difficult breathing that characterize asthma. Several medications are available to counteract these effects.

ANAPHYLACTIC SHOCK: Anaphylactic shock is an extreme allergic response that may be elicited by exposure to penicillin or insect venoms. On the first exposure, the person becomes highly sensitized to the foreign antigen. On the second exposure, histamine is released from mast cells throughout the body and causes a drastic decrease in blood volume. The resulting drop in blood pressure may be fatal in only a few minutes. People who know they are allergic to bee stings, for example, may obtain a self-contained syringe of epinephrine to carry with them. Epinephrine can delay the progression of anaphylactic shock long enough for the person to seek medical attention.

RELATED;

1.  IMMUNOGLOBULINS  

2.  IMMUNISATION

3.  MEDICAL CONDITIONS

REFERENCES

ISONIAZID (INH)

 

Therapeutic Class: Antituberculosis drug

Pharmacologic Class: Mycolic acid inhibitor

Actions and uses: Isoniazid is a first-line drug for the treatment of M. tuberculosis because decades of experience have shown it to have a superior safety profile and to be the most effective, single drug for the infection. The drug acts by inhibiting the synthesis of mycolic acids, which are essential components of mycobacterial cell walls. It is bacteriocidal for actively growing organisms but bacteriostatic for dormant mycobacteria. It is selective for M. tuberculosis. Isoniazid may be used alone for chemoprophylaxis, or in combination with other antituberculosis drugs for treating active disease. Approximately 10% of patients will develop resistance to isoniazid during long-term therapy.

Administration alerts: Give on an empty stomach, 1 hour after or 2 hours before meals. For IM administration, administer deep IM, and rotate sites. The drug is pregnancy category C.

Adverse effects: The most common adverse effects of isoniazid are numbness of the hands and feet, rash, and fever. Neurotoxicity is a concern during therapy, and patients may exhibit paresthesia of the feet and hands, convulsions, optic neuritis, dizziness, coma, memory loss, and various psychoses.

Warning: Although rare, hepatotoxicity is a serious and sometimes fatal adverse effect; thus, the patient should be monitored carefully for jaundice, fatigue, elevated hepatic enzymes, or loss of appetite. Liver enzyme tests are usually performed monthly during therapy to identify early hepatotoxicity. Hepatotoxicity usually appears in the first 1 to 3 months of therapy but may occur at any time during treatment. Older adults and those with daily alcohol consumption are at greater risk of developing hepatotoxicity.

Contraindications: Isoniazid is contraindicated in patients with hypersensitivity to the drug and in patients with severe hepatic impairment.

Interactions: Drug–Drug: Aluminum-containing antacids should not be administered concurrently because they can decrease the absorption of isoniazid. When disulfiram is taken with INH, lack of coordination or psychotic reactions may result. Drinking alcohol with INH increases the risk of hepatotoxicity. Isoniazid may increase serum levels of phenytoin and carbamazepine.

Treatment of Overdose: Isoniazid overdose may be fatal. Treatment is mostly symptomatic. Pyridoxine (vitamin B6) may be infused in a dose equal to that of the isoniazid overdose to prevent seizures and to correct metabolic acidosis. The dose may be repeated several times until the patient regains consciousness

RELATED;

1. DRUG USE IN RELATION TO PREGNANCY  

2. TUBERCULOSIS

3.  ETHAMBUTOR

4.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

IMPETIGO

 

INTRODUCTION:  Impetigo is a superficial infection of the skin caused by staphylococci, streptococci, or multiple bacteria. Exposed areas of the body, face, hands, neck, and extremities are most frequently involved. Impetigo is contagious and may spread to other parts of the skin or to other members of the family who touch the patient or who use towels or combs that are soiled with the exudate of the lesion. Impetigo is seen in people of all ages. It is particularly common among children living in poor hygienic conditions. Chronic health problems, poor hygiene, and malnutrition may predispose adults to impetigo.

CLINICAL MANIFESTATIONS: Lesions begin as small, red macules that become discrete, thin-walled vesicles that rupture and become covered with a honey-yellow crust. These crusts, when removed, reveal smooth, red, moist surfaces on which new crusts develop. If the scalp is involved, the hair is matted, distinguishing the condition from ringworm.  Bullous impetigo, a deep-seated infection of the skin caused by Staphylococcus aureus, is characterized by the formation of bullae from original vesicles. The bullae rupture, leaving a raw, red area.

MEDICAL MANAGEMENT:  Pharmacologic Therapy: Systemic antibiotic therapy is the usual treatment for impetigo. It reduces contagious spread, treats deep infection, and prevents acute glomerulonephritis (kidney infection). Agents for nonbullous impetigo: benzathine penicillin, oral penicillin, or erythromycin. Topical antibacterial therapy is the usual treatment for disease that is limited to a small area. The topical preparation is applied to lesions several times daily for 1 week. Lesions are soaked or washed with soap solution to remove central site of bacterial growth and to give the topical antibiotic an opportunity to reach the infected site.

RELATED;

1.  STREPTOCOCCUS

2.  STAPHYLOCOCCUS

3.  SEBORRHEIC DERMATITIS

REFERENCES

HISTAMINE H2 RECEPTOR BLOCKERS

 

INTRODUCTION: Histamine has two types of receptors: H1 and H2. Activation of H1 receptors produces the classic symptoms of inflammation and allergy, whereas the H2 receptors are responsible for increasing acid secretion in the stomach. The H2-receptor antagonists are effective at suppressing the volume and acidity of parietal cell secretions. Duodenal ulcers usually heal in 6 to 8 weeks, and gastric ulcers may require up to 12 weeks of therapy. All of the H2-receptor antagonists are available OTC for the short-term (2 weeks) treatment of GERD.

Prototype Drug: Ranitidine

Therapeutic Class: Antiulcer drug

Pharmacologic Class: H2-receptor antagonist

ACTIONS AND USES: Ranitidine acts by blocking H2 receptors in the stomach to decrease acid production. It has a higher potency than cimetidine, which allows it to be administered once daily, usually at bedtime. Adequate healing of the ulcer takes approximately 4 to 8 weeks, although those at high risk for PUD may continue on drug maintenance for prolonged periods to prevent recurrence. Gastric ulcers require longer therapy for healing to occur. Intravenous (IV) and intramuscular (IM) forms are available for the treatment of acute, stress-induced bleeding ulcers. Ranitidine is available in a dissolving tablet form for treating GERD in children and infants older than 1 month of age. 

ADMINISTRATION ALERT: Administer after meals and monitor liver and renal function.

Pregnancy category B (Read about drug use in relation to pregnancy)

ADVERSE EFFECTS: Adverse effects are uncommon and mild. Ranitidine does not cross the blood–brain barrier to any appreciable extent, so it does not cause the confusion and

CNS depression observed with cimetidine. Although rare, severe reductions in the number of red and white blood cells and platelets are possible; thus, periodic blood counts may be performed. High doses may result in impotence or loss of libido in men.

Contraindications: Contraindications include hypersensitivity to H2-receptor antagonists, acute porphyria, and OTC administration in children less than 12years of age.

INTERACTIONS: Drug–Drug: Ranitidine has fewer drug–drug interactions than cimetidine. Ranitidine may reduce the absorption of cefpodoxime, ketoconazole, and itraconazole. Antacids should not be given within 1 hour of H2-receptor antagonists because the effectiveness may be decreased due to reduced absorption. Smoking decreases the effectiveness of ranitidine.

Lab Tests: Ranitidine may increase the values of serum creatinine, AST, ALT, LDH, alkaline phosphatase, and bilirubin. It may produce false positives for urine protein.

Herbal/Food: Absorption of vitamin B12 depends on an acidic environment; thus, deficiency may occur. Iron is also better absorbed in an acidic environment.

RELATED;

1. PROTON PUMP INHIBITORS  

2. ANTIBIOTICS  

3. PEPTIC ULCER DISEASE

4.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

CANDIDIASIS

INTRODUCTION:  This is a fungal infection that is common especially in immunocompromised patients.  Usually fungi microbes are not a big burden in immunocompetent individuals and if the do infect an individual, in most cases they will be asymptomatic.  The commonest of these fungal species is Candida albicans.  Other important species include; Candida tropicalis, C. pseudotropicalis, C. brumptii, C. parapsilosis, C. guilliermondii, C. krusei.  

MORPHOLOGY AND REPRODUCTION:  The thallus of Candida consists of yeast cells and pseudohyphae. They reproduce by budding, ferment a number of sugars and assimilate nitrogen.  Microscopic examination of pathological material shows round or oval yeast cells in the process of budding and often exhibiting pseudohyphae.

PATHOGENESIS:  Under normal conditions this fungus is not pathogenic. Many factors predispose to pathogenic effect and these include the following;

1.  Impaired immune defences,

2. Pregnancy

3. Spontaneous hormonal

4. Menopause changes

5. Premature birth

6. Use of Corticosteroids

7. Immunosuppression

8. Long-term antibiotic therapy

9. Oral contraceptives

10. Diabetes mellitus

11. Pre-existing lesions of skin

CLINICAL FEATURES:  A variety of infections are caused by Candida species though it is an opportunistic fungus.  In addition to general predisposing factors, following local conditions also predispose to this infection: Chemical, mechanical or biological irritants, Reduced salivation, Digestive disorders, Remnants of milk left fermenting in the mouth of infants.

LABORATORY DIAGNOSIS:  Collection of Infected Material Skin or nail scrapings, mucous patches from the mouth, vagina or anus, sputum, blood, CSF or faeces may be collected for diagnosis in the laboratory. The material should be collected in sterile containers or as smears on slides.

TREATMENT:  Predisposing factors should be eliminated. The affected area should be kept dry.  Topical application of nystatin and systemic treatment with Amphotericin B, oral ketoconazole and fluconazole is effective.

 

RELATED;

1.  INTRODUCTION TO FUNGI

2.  AMPHOTERICIN B

3.  OPPORTUNISTIC MYCOSES

REFERENCES

ANTIBACTERIAL PROPERTIES OF GOLDENSEAL

 

INTRODUCTION:  Goldenseal (Hydrastis canadensis) was once a common plant found in woods in the eastern and midwestern United States. Native Americans used the root for a variety of medicinal applications, including skin diseases, ulcers, and gonorrhea. Recent uses include the treatment of colds and other respiratory tract infections, infectious diarrhea, eye infections, vaginitis, wounds, canker sores, and cancer.

Goldenseal was once reported to mask the appearance of drugs in the urine of patients wanting to hide drug abuse but this claim has since been proved false. The roots and leaves of goldenseal are dried and are available as capsules, tablets, salves, and tinctures. Two of the active ingredients in goldenseal are berberine and hydrastine, which are reported to have antibacterial properties.

When used topically or locally, goldenseal is claimed to be of value in treating bacterial and fungal skin infections and oral conditions such as gingivitis and thrush. As an eyewash, it can soothe inflamed eyes. Considered safe for most people, it is contraindicated in pregnancy and hypertension. Hypertension: Pregnancy and drug use

RELATED;

1.  GINSENG FOR CARDIOVASCULAR DISEASE  

2.  GARLIC FOR CARDIOVASCUAR DISEASE

REFERENCES

THROMBOCYTOPENIA

 

INTRODUCTION: Thrombocytopenia which is a condition of low platelet count, is the most common cause of abnormal bleeding.

PATHOPHYSIOLOGY: Thrombocytopenia can result from decreased production of platelets within the bone marrow or from increased destruction or consumption of platelets.

CAUSES: Causes include failure of production as a result of hematologic malignancies, myelodysplastic syndromes, metastatic involvement of bone marrow from solid tumors, certain anemias, toxins, medications, infections, alcohol, and chemotherapy; increased destruction as a result of idiopathic thrombocytopenia purpura, lupus erythematosus, malignant lymphoma, chronic lymphocytic leukemia, medications, infections, and sequestration; and increased utilization, such as results from disseminated intravascular coagulopathy (DIC).

CLINICAL MANIFESTATIONS: With platelet count below 50,000/mm³ : bleeding and petechiae. With platelet count below 20,000/mm³ : petechiae, along with nasal and gingival bleeding, excessive menstrual bleeding, and excessive bleeding after surgery or dental extractions. With platelet count below 5,000/mm³: spontaneous, potentially fatal central nervous system hemorrhage or gastrointestinal hemorrhage.

ASSESSMENT AND DIAGNOSTIC FINDINGS: Bone marrow aspiration and biopsy, if platelet deficiency is secondary to decreased production. Increased megakaryocytes (the cells from which platelets originate) and normal or even increased platelet production in bone marrow, when platelet destruction is the cause.

MEDICAL MANAGEMENT: The management of secondary thrombocytopenia is usually treatment of the underlying disease. Platelet transfusions are used to raise platelet count and stop bleeding or prevent spontaneous hemorrhage if platelet production is impaired; if excessive platelet destruction is the cause, the patient is treated as indicated for idiopathic thrombocytopenia purpura.

For some patients a splenectomy can be therapeutic, although it may not be an option for other patients for example, patients in whom the enlarged spleen is due to portal hypertension related to cirrhosis.

RELATED;

1. BLOOD PLATELETS

2. THE COAGULATION CASCADE

3. BLEEDING DISORDERS

4.  MEDICAL CONDITIONS

REFERENCES

DRUG ABSORPTION

 

Introduction: Absorption is a process involving the movement of a substance from its site of administration, across body membranes, to circulating fluids. Drugs may be absorbed across the skin and associated mucous membranes, or they may move across membranes that line the gastrointestinal (GI) or respiratory tract. Most drugs, with the exception of a few topical medications, intestinal anti-infectives, and some radiologic contrast agents, must be absorbed to produce an effect. Absorption is the primary pharmacokinetic factor determining the length of time it takes a drug to produce its effect. Pharmacokinetics

In order for a drug to be absorbed it must dissolve. The rate of dissolution determines how quickly the drug disintegrates and disperses into simpler forms; therefore, drug formulation is an important factor of bioavailability. Bioavailability

In general, the more rapid the dissolution, the faster the drug absorption and the faster the onset of drug action. For example, famotidine administered as an orally disintegrating tablet dissolves within seconds and after being swallowed is delivered to the stomach where it blocks acid secretion from the stomach, thereby treating conditions of excessive acid secretion. Pepticulcer disease: Histamine H2 receptor blockers

At the other extreme some drugs have shown good clinical response as slowly dissolving drugs such as liothyronine sodium (T3) and thyroxine (T4) administered for resolution of hypothyroid symptoms. In some instances it is advantageous for a drug to disperse rapidly. In other cases, it is better for the drug to be released slowly where the effects are more prolonged for positive therapeutic benefit. Absorption is conditional on many factors. Drugs in elixir or syrup formulations are absorbed faster than tablets or capsules. Drugs administered in high doses are generally absorbed more quickly and have a more rapid onset of action than those given in low concentrations. The speed of digestive motility, surface area, pH, lipid solubility, exposure to enzymes in the digestive tract, and blood flow to the site of drug administration also affect absorption. Because drugs administered IV directly enter the bloodstream, absorption to the tissues after the infusion is very rapid. IM medications take longer to absorb. Drug distribution

Other factors that influence the absorption of medications include the following: Drug formulation and dose, Size of the drug molecule, Surface area of the absorptive site, Digestive motility or blood flow, Lipid solubility, Degree of ionization, Acidity or alkalinity (pH), Interactions with food and other medications. The degree of ionization of a drug also affects its absorption. A drug’s ability to become ionized depends on the surrounding pH. Aspirin provides an excellent example of the effects of ionization on absorption. In the acid environment of the stomach, aspirin is in its non-ionized form and thus readily absorbed and distributed by the bloodstream. As aspirin enters the alkaline environment of the small intestine, however, it becomes ionized. In its ionized form, aspirin is not as likely to be absorbed and distributed to target cells.

Unlike acidic drugs, medications that are weakly basic are in their nonionized form in an alkaline environment; therefore, basic drugs are absorbed and distributed better in alkaline environments such as in the small intestine. The pH of the local environment directly influences drug absorption through its ability to ionize the drug.

Drug–drug or food–drug interactions may influence absorption. Many examples of these interactions have been discovered. For example, administering tetracyclines with food or drugs containing calcium, iron, or magnesium can significantly delay absorption of the antibiotic.  High-fat meals can slow stomach motility significantly and delay the absorption of oral medications taken with the meal. Dietary supplements may also affect absorption.

RELATED;

1.  DRUG DISTRIBUTION  

2.  PHARMACOKINETICS

3.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES