HEPATIC FAILURE

 

INTRODUCTION:  hepatic failure is the clinical syndrome of sudden and severely impaired liver function in a previously healthy person. It is characterized by the development of first symptoms or jaundice within 8 weeks of the onset of disease. Three categories are frequently cited: hyperacute, acute, and subacute. The hepatic lesion is potentially reversible, and survival rates are approximately 20% to 50%, depending greatly on the cause of liver failure. Those who do not survive die of massive hepatocellular injury and necrosis.

CAUSES OF LIVER FAILURE:  Viral hepatitis a common cause; other causes include toxic drugs and chemicals, metabolic disturbances, and structural changes.

CLINICAL MANIFESTATIONS:  Jaundice and profound anorexia.  Often accompanied by coagulation defects, renal failure and electrolyte disturbances, cardiovascular abnormalities, infection, hypoglycemia, encephalopathy, and cerebral edema.

MANAGEMENT:  Liver transplantation (treatment of choice).  Blood or plasma exchanges. Liver support systems, such as hepatocytes within synthetic fiber columns, extracorporeal liver assist devices, and bioartificial liver, until transplantation is possible.

 

RELATED;

1.  JAUNDICE

2. REAL FAILURE

3. HYPOGLYCEMIA

4. EDEMA

5.  ANATOMY AND PHYSIOLOGY OF THE HUMAN LIVER

6.  FUNCTIONS OF THE LIVER

REFERENCES

PARASYMPATHOLYTICS

 

INTRODUCTION:  Drugs that block the action of Acetylcholine are known by a number of names, including anticholinergics, cholinergic blockers, muscarinic antagonists, and parasympatholytics.  Although the term anticholinergic is most commonly used, the most accurate term for this class of drugs is muscarinic antagonists, because at therapeutic doses, these drugs are selective for Ach muscarinic receptors and thus have little effect on Ach nicotinic receptors.

PHARMACODYNAMICS:  Anticholinergics act by competing with Ach for binding muscarinic receptors. When anticholinergics occupy these receptors, no response is generated at the neuroeffector organs. Suppressing the effects of Ach causes symptoms of sympathetic nervous system activation to predominate. Most therapeutic uses of the anticholinergics are predictable extensions of their parasympathetic-blocking actions: dilation of the pupils, increase in heart rate, drying of secretions, and relaxation of the bronchi.

THERAPEUTIC USES:  1. GI disorders:  These agents decrease the secretion of gastric acid in peptic ulcer disease. They also slow intestinal motility and may be useful for reducing the cramping and diarrhea associated with irritable bowel syndrome. 

2. Ophthalmic procedures:  Anticholinergics may be used to cause mydriasis or cycloplegia during eye procedures.

3. Cardiac rhythm abnormalities:  Anticholinergics can be used to accelerate the heart rate in patients experiencing bradycardia.

4. Preanesthesia:  Combined with other agents, anticholinergics can decrease excessive respiratory secretions and reverse the bradycardia caused by general anesthetics.

5. Asthma:  A few agents, such as ipratropium, are useful in treating asthma, because of their ability to dilate the bronchi.

6. Overactive bladder:  Anticholinergics treat urinary retention and incontinence.

7. Degenerative nervous system application:  Anticholinergics are used to treat patients who have Parkinson’s disease and whose main symptom is tremor. The prototype drug, atropine, is used for several additional medical conditions due to its effective muscarinic receptor blockade. These applications include reversal of adverse muscarinic effects and treatment of cholinergic agent poisoning, including that caused by overdose of bethanechol, cholinesterase inhibitors, or accidental ingestion of certain types of mushrooms or organophosphate pesticides.

 

RELATED;

1.  ACETYLCHOLINE

2.  CHOLINOMIMETICS

3.  GENERATION OF A NERVE IMPULSE

4.  DIVISIONS OF THE CENTRAL NERVOUS SYSTEM

5.  ATROPINE

REFERENCES

ESOPHAGEAL VERICES

INTRODUCTION: Bleeding or hemorrhage from esophageal varices is one of the major causes of death in patients with cirrhosis. Esophageal varices are dilated veins usually found in the submucosa of the lower esophagus; they may develop higher in the esophagus or extend into the stomach. The condition is nearly always caused by portal hypertension.

RISK FACTORS FOR HEMORRHAGE: Risk factors for hemorrhage include muscular strain from heavy lifting; straining at stool; sneezing, coughing, or vomiting; esophagitis or irritation of vessels (rough food or irritating fluids); reflux of stomach contents (especially alcohol); and salicylates or any drug that erodes the esophageal mucosa.

CLINICAL MANIFESTATIONS: Hematemesis, melena, or general deterioration in mental or physical status; often a history of alcohol abuse. Signs and symptoms of shock including a cool clammy skin, hypotension, tachycardia and may be present.

ASSESSMENT AND DIAGNOSTIC METHODS: Endoscopy, barium swallow, ultrasonography, CT, and angiography.

Neurologic and portal hypertension assessment: Liver function tests including serum aminotransferases, bilirubin, alkaline phosphatase, and serum proteins. Splenoportography, hepatoportography, and celiac angiography.

MEDICAL MANAGEMENT: Aggressive medical care includes evaluation of extent of bleeding and continuous monitoring of vital signs when hematemesis and melena are present. Signs of potential hypovolemia are noted; blood volume is monitored with a central venous catheter or pulmonary artery catheter. Oxygen is administered to prevent hypoxia and to maintain adequate blood oxygenation, and IV fluids and volume expanders are administered to restore fluid volume and replace electrolytes. Transfusion of blood components may also be required. Nonsurgical treatment is preferred because of the high mortality associated with emergency surgery to control bleeding from esophageal varices and because of the poor physical condition of most of these patients.

Nonsurgical measures include: Pharmacologic therapy: vasopressin, vasopressin with nitroglycerin, somatostatin and octreotide, beta-blocking agents, and nitrates. Balloon tamponade, saline lavage, and endoscopic sclerotherapy. Esophageal banding therapy and variceal band ligation.

RELATED;

1.  NOSE BLEEDING

2.  PEPTIC ULCER DISEASE

3.  ULCERATIVE COLITIS

REFERENCES

METFORMIN

 

ACTIONS AND USES: Metformin is a preferred oral antidiabetic drug for managing type 2 DM because of its effectiveness and safety. It is used alone or in combination with other antidiabetic medications or insulin. It is approved for use in children age 10 or above. It is available as regular-release tablets, solution, and sustained-release forms. Metformin reduces fasting and postprandial glucose levels by decreasing the hepatic production of glucose by the process of gluconeogenesis and reducing insulin resistance. It does not promote insulin release from the pancreas. A major advantage of the drug is that it does not cause hypoglycemia. The drug's actions do not depend on stimulating insulin release, so it is able to lower glucose levels in patients who no longer secrete insulin. In addition to lowering blood glucose levels, it lowers triglyceride and total and low-density lipoprotein (LDL) cholesterol levels, and it promotes weight loss. Metformin reduces insulin resistance, which in turn lowers insulin and androgen levels, thus restoring normal menstrual cycles and ovulation.

ADMINISTRATION ALERTS: Sustained-release tablets must be swallowed whole and not crushed or chewed. Fasting blood glucose levels should be obtained every 3 months, and the dose adjusted accordingly. Discontinue the medication immediately if signs of acidosis are present. Pregnancy category B.

PHARMACOKINETICS: Onset Peak Duration Less than 1 h 1–3 h (regular release); 4–8 h (extended release) 12 h (regular release); 24 h (extended release)

ADVERSE EFFECTS: The most common adverse effects are GI related and include nausea, vomiting, abdominal discomfort, metallic taste, diarrhea, and anorexia. It may also cause headache, dizziness, agitation, and fatigue. Unlike the sulfonylureas, metformin rarely causes hypoglycemia or weight gain.

Warning: Lactic acidosis is a rare, though potentially fatal, adverse effect. The risk for lactic acidosis is increased in patients with renal insufficiency or any condition that puts them at risk for increased lactic acid production, such as liver disease, severe infection, excessive alcohol intake, shock, or hypoxemia.

RELATED;

1. DIABETES MELLITUS

2. INSULIN

3.  PATHOPHYSIOLOGY OF DIABETES

4.  PHARMACOLOGY AND THERAPEUTICS

MEGALOBLASTIC ANEMIA

 

INTRODUCTION: In the anemias caused by deficiencies of vitamin B12 or folic acid, identical bone marrow and peripheral blood changes occur because both vitamins are essential for normal DNA synthesis. DNA,the genetic material

PATHOPHYSIOLOGY:

Folic Acid Deficiency: Folic acid is stored as compounds referred to as folates. The folate stores in the body are much smaller than those of vitamin B12, and they are quickly depleted when the dietary intake of folate is deficient (within 4 months). Folate deficiency occurs in people who rarely eat uncooked vegetables. Alcohol increases folic acid requirements; folic acid requirements are also increased in patients with chronic hemolytic anemias and in women who are pregnant. Some patients with malabsorptive diseases of the small bowel may not absorb folic acid normally.

Vitamin B12 Deficiency: A deficiency of vitamin B12 can occur in several ways. Inadequate dietary intake is rare but can develop in strict vegetarians who consume no meat or dairy products. Faulty absorption from the GI tract is more common, as with conditions such as Crohn’s disease or after ileal resection or gastrectomy. Another cause is the absence of intrinsic factor. A deficiency may also occur if disease involving the ileum or pancreas impairs absorption. The body normally has large stores of vitamin B12, so years may pass before the deficiency results in anemia.

Clinical Manifestations: Symptoms of folic acid and vitamin B12 deficiencies are similar, and the two anemias may coexist. Symptoms are progressive, although the course of illness may be marked by spontaneous partial remissions and exacerbations. Gradual development of signs of anemia (weakness, listlessness, and fatigue). Possible development of a smooth, sore, red tongue and mild diarrhea (pernicious anemia). Mild jaundice, vitiligo, and premature graying. Confusion may occur; more often, paresthesias in the extremities and difficulty keeping balance; loss of position sense. Lack of neurologic manifestations with folic acid deficiency alone. Without treatment, patients die, usually as a result of heart failure secondary to anemia.

ASSESSMENT AND DIAGNOSTIC FINDINGS: Schilling test (primary diagnostic tool): Complete blood cell count (Hgb value as low as 4 to 5 g/dL, WBC count 2,000 to 3,000 mm3 , platelet count fewer than 50,000 mm3 ; very high MCV, usually exceeding 110 m3 ). Serum levels of folate and vitamin B12 (folic acid deficiency and deficient vitamin B12)

MEDICAL MANAGEMENT: Folic Acid Deficiency: Increase intake of folic acid in patient’s diet and administer 1 mg folic acid daily. Administer IM folic acid for malabsorption syndromes. Prescribe additional supplements as necessary, because the amount in multivitamins may be inadequate to fully replace deficient body stores. Prescribe folic acid for patients with alcoholism as long as they continue to consume alcohol.

MEDICAL MANAGEMENT: Vitamin B12 Deficiency: Provide vitamin B12 replacement: Vegetarians can prevent or treat deficiency with oral supplements with vitamins or fortified soy milk; when the deficiency is due to the more common defect in absorption or the absence of intrinsic factor, replacement is by monthly IM injections of vitamin B12. A small amount of an oral dose of vitamin B12 can be absorbed by passive diffusion, even in the absence of intrinsic factor, but large doses (2 mg/day) are required if vitamin B12 is to be replaced orally. To prevent recurrence of pernicious anemia, vitamin B12 therapy must be continued for life.

RELATED;

1.  CONDITIONS OF ANEMIA  

2.  COMPOSITION OF BLOOD

3.  MEDICAL CONDITIONS

REFERENCES

OPIOID ANALGESICS

 

Introduction: Successful treatment of pain is a challenging task that begins with careful attempts to assess the source and magnitude of the pain. The amount of pain experienced by the patient is often measured by means of a pain Numeric Rating Scale (NRS) or less frequently by marking a line on a Visual Analog Scale (VAS) with word descriptors ranging from no pain (0) to excruciating pain (10). In either case, values indicate the magnitude of pain as: mild (1–3), moderate (4–6), or severe (7–10).  For a patient in severe pain, the administration of an opioid analgesic is usually considered a primary part of the overall management plan. Determining the route of administration, duration of drug action, ceiling effect also known as maximal intrinsic activity, duration of therapy, potential for adverse effects, and the patient’s past experience with opioids all should be addressed.  Use of opioid drugs in acute situations may be contrasted with their use in chronic pain management, in which a multitude of other factors must be considered, including the development of tolerance to and physical dependence on opioid analgesics.

Clinical Use of Opioid Analgesics:  1)  Analgesia: Severe, constant pain is usually relieved with opioid analgesics with high intrinsic activity. This includes the pain associated with cancer and other terminal illnesses. Such conditions may require continuous use of potent opioid analgesics and are associated with some degree of tolerance and dependence. Opioid analgesics are also often used during obstetric labor. Because opioids cross the placental barrier and reach the fetus, however care must be taken to minimize neonatal depression. If it occurs, immediate injection of the antagonist naloxone will reverse the depression.  

2)  Acute Pulmonary Edema: The relief produced by intravenous morphine in dyspnea from pulmonary edema associated with left ventricular heart failure is remarkable. Proposed mechanisms include reduced anxiety and reduced cardiac preloa and afterload. However, if respiratory depression is a problem, furosemide may be preferred for the treatment of pulmonary edema. On the other hand, morphine can be particularly useful when treating painful myocardial ischemia with pulmonary edema.  

3) Cough: Suppression of cough can be obtained at doses lower than those needed for analgesia. However, in recent years the use of opioid analgesics to allay cough has diminished largely because a number of effective synthetic compounds have been developed that are neither analgesic nor addictive.  

4)  Diarrhea: Diarrhea from almost any cause can be controlled with the opioid analgesics, but if diarrhea is associated with infection such use must not substitute for appropriate chemotherapy. Crude opium preparations were used in the past to control diarrhea, but now synthetic surrogates with more selective gastrointestinal effects and few or no CNS effects, such as diphenoxylate or loperamide, are used.  

5)  Shivering: Although all opioid agonists have some propensity to reduce shivering, meperidine is reported to have the most pronounced anti-shivering properties. Meperidine apparently blocks shivering mainly through an action on subtypes of the α2 adrenoceptor.  

6)  Applications in Anesthesia: The opioids are frequently used as premedicant drugs before anesthesia and surgery because of their sedative, anxiolytic, and analgesic properties. They are also used intra-operatively both as adjuncts to other anesthetic agents and, in high doses, as a primary component of the anesthetic regimen . Opioids are most commonly used in cardiovascular surgery and other types of high-risk surgery in which a primary goal is to minimize cardiovascular depression. In such situations, mechanical respiratory assistance must be provided.

RELATED; 

1.  CORTICOSTEROIDS  

2.  CHRONIC INFLAMMATION

3.  MORPHINE

4.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

SPINAL CORD INJURIES

 

INTRODUCTION: Spinal cord injuries (SCIs) are a major health problem. Most SCIs result from motor vehicle crashes. Other causes include falls, violence especially primarily from gunshot wounds, and recreational sporting activities. Half of the victims are between 16 and 30 years of age; most are males. Another risk factor is substance abuse (alcohol and drugs). There is a high frequency of associated injuries and medical complications. The vertebrae most frequently involved in SCIs are the fifth, sixth, and seventh cervical vertebrae (C5–C7), the 12th thoracic vertebra (T12), and the first lumbar vertebra (L1). These vertebrae are the most susceptible because there is a greater range of mobility in the vertebral column in these areas. 

Damage to the spinal cord ranges from transient concussion (patient recovers fully), to contusion, laceration, and compression of the cord substance (either alone or in combination), to complete transection of the cord (paralysis below the level of injury). Injury can be categorized as primary (usually permanent) or secondary (nerve fibers swell and disintegrate as a result of ischemia, hypoxia, edema, and hemorrhagic lesions). Whereas a primary injury is permanent, a secondary injury may be reversible if treated within 4 to 6 hours of the initial injury. The type of injury refers to the extent of injury to the spinal cord itself. Incomplete spinal cord lesions are classified according to the area of spinal cord damage: central, lateral, anterior, or peripheral. A complete SCI can result in paraplegia (paralysis of the lower body) or tetraplegia (formerly quadriplegia— paralysis of all four extremities).

CLINICAL MANIFESTATIONS: The consequences of SCI depend on the type and level of injury of the cord.

Neurologic Level: The neurologic level refers to the lowest level at which sensory and motor functions are normal. Signs and symptoms include the following: Total sensory and motor paralysis below the neurologic level. Loss of bladder and bowel control (usually with urinary retention and bladder distention). Loss of sweating and vasomotor tone. Marked reduction of BP from loss of peripheral vascular resistance. If conscious, patient reports acute pain in back or neck; patient may speak of fear that the neck or back is broken.

Respiratory Problems: Related to compromised respiratory function; severity depends on level of injury. Acute respiratory failure is the leading cause of death in high cervical cord injury.

ASSESSMENT AND DIAGNOSTIC METHODS: Detailed neurologic examination, x-ray examinations (lateral cervical spine x-rays), computed tomography (CT), magnetic resonance imaging (MRI), and ECG (bradycardia and asystole are common in acute spinal injuries) are common assessment and diagnostic methods.

COMPLICATIONS: Spinal shock, a serious complication of SCI, is a sudden depression of reflex activity in the spinal cord (areflexia) below the level of injury. The muscles innervated by the part of the cord segment situated below the level of the lesion become completely paralyzed and flaccid, and the reflexes are absent. BP and heart rate fall as vital organs are affected. Parts of the body below the level of the cord lesion are paralyzed and without sensation.

EMERGENCY MANAGEMENT: Immediate patient management at the accident scene is crucial. Improper handling can cause further damage and loss of neurologic function. Consider any victim of a motor vehicle crash, a diving or contact sports injury, a fall, or any direct trauma to the head and neck as having an SCI until ruled out. Initial care includes rapid assessment, immobilization, extrication, stabilization or control of life-threatening injuries, and transportation to an appropriate medical facility. Maintain patient in an extended position (not sitting); no body part should be twisted or turned. The standard of care is referral to a regional spinal injury center or trauma center for treatment in first 24 hours.

MEDICAL MANAGEMENT: Acute Phase Goals of management are to prevent further SCI and to observe for symptoms of progressive neurologic deficits. The patient is resuscitated as necessary, and oxygenation and cardiovascular stability are maintained. High-dose corticosteroids (methylprednisolone) may be administered to counteract spinal cord edema. Oxygen is administered to maintain a high arterial PaO2. Extreme care is taken to avoid flexing or extending the neck if endotracheal intubation is necessary. Diaphragm pacing (electrical stimulation of the phrenic nerve) may be considered for patients with high cervical spine injuries. SCI requires immobilization, reduction of dislocations, and stabilization of the vertebral column. The cervical fracture is reduced and the cervical spine aligned with a form of skeletal traction (using skeletal tongs or calipers or the halo-vest technique). Weights are hung freely so as not to interfere with the traction. Early surgery reduces the need for traction. The goals of surgical treatment are to preserve neurologic function by removing pressure from the spinal cord and to provide stability.

MANAGEMENT OF COMPLICATIONS:

Spinal and Neurogenic Shock: Intestinal decompression is used to treat bowel distention and paralytic ileus caused by depression of reflexes. This loss of sympathetic innervation causes a variety of other clinical manifestations, including neurogenic shock signaled by decreased cardiac output, venous pooling in the extremities, and peripheral vasodilation. Patient who does not perspire on paralyzed portion of body requires close observation for early detection of an abrupt onset of fever. Body defenses are maintained and supported until the spinal shock abates and the system has recovered from the traumatic insult (up to 4 months).

RELATED;

1. THE CENTRAL NERVOUS SYSTEM  

2. THE ENTERIC NERVOUS SYSTEM  

3. ACTIVATION OF A NERVE IMPULSE

4.  BACK PAIN

REFERENCES

ARTEMISININ & ITS DERIVATIVES

INTRODUCTION: Artemisinin is a sesquiterpene lactone endoperoxide, the active component of an herbal medicine that has been used as an antipyretic in China for over 2000 years. Artemisinin is insoluble and can only be used orally. However, analogs have been synthesized to increase solubility and improve antimalarial efficacy. The most important of these analogs are artesunate which is water-soluble and is useful for oral, intravenous, intramuscular, and rectal administration. The other one is artemether which is lipid-soluble and useful for oral, intramuscular, and rectal administration, and dihydroartemisinin which is water-soluble and useful for oral administration.

CHEMISTRY & PHARMACOKINETICS: Artemisinin and its analogs are rapidly absorbed, with peak plasma levels occurring in 1–2 hours and half-lives of 1–3 hours after oral administration. Artemisinin, artesunate, and artemether are rapidly metabolized to the active metabolite dihydroartemisinin. Drug levels appear to decrease after a number of days of therapy.

Artemether-lumefantrine (Coartem, Lumartem, Combiat, Riamet): Co-formulated; first-line therapy in many countries; approved in the USA

Artesunate-amodiaquine (ASAQ, Arsucam, Coarsucam): Co-formulated; first-line therapy in many African countries

Artesunate-mefloquine: Co-formulated; first-line therapy in parts of Southeast Asia and South America.

Dihydroartemisinin-piperaquine (Artekin, Duocotecxin): Co-formulated; first-line therapy in some countries in Southeast Asia

Artesunate-sulfadoxine-pyrimethamine: First-line therapy in some countries, but efficacy lower than other regimens in most areas.

CLINICAL USES: Artemisinin-based combination therapy is now the standard for treatment of uncomplicated falciparum malaria in nearly all areas endemic for falciparum malaria. These regimens were developed because the short plasma half-lives of the artemisinins led to unacceptably high recrudescence rates after short-course therapy, which were reversed by inclusion of longer-acting drugs. Combination therapy also helps to protect against the selection of artemisinin resistance. However, with completion of dosing after 3 days, the artemisinin components are rapidly eliminated, and so selection of resistance to partner drugs is of concern. The WHO recommends five artemisinin-based combinations for the treatment of uncomplicated falciparum malaria. One of these, artesunate-sulfadoxine-pyrimethamine is not recommended in many areas owing to unacceptable levels of resistance to sulfadoxine-pyrimethamine, but it is the first-line therapy in some countries in Asia, South America, and North Africa. The other four recommended regimens are now all available as combination formulations, although manufacturing standards may vary. Artesunate-mefloquine is highly effective in Southeast Asia, where resistance to many antimalarials is common; it is the first-line therapy in some countries in Southeast Asia and South America. This regimen is less practical for other areas, particularly Africa, because of its relatively high cost and poor tolerability. Either artesunate-amodiaquine or artemether-lumefantrine is now the standard treatment for uncomplicated falciparum malaria in most countries in Africa and some additional endemic countries on other continents. Dihydroartemisinin-piperaquine is a newer regimen that has shown excellent efficacy; it is the first-line therapy for falciparum malaria in Vietnam. T he relative efficacy and safety of artemisinin-based combination therapies are now under active investigation. In general, the leading regimens are highly efficacious, safe, and well tolerated, and they are the new standard of care for the treatment of uncomplicated falciparum malaria. Artemisinins are also proving to have outstanding efficacy in the treatment of complicated falciparum malaria. Large randomized trials and meta-analyses have shown that intramuscular artemether has an efficacy equivalent to that of quinine and that intravenous artesunate is superior to intravenous quinine in terms of parasite clearance time and—most important—patient survival. Intravenous artesunate also has a superior side-effect profile compared with that of intravenous quinine or quinidine. Thus, intravenous artesunate will likely replace quinine as the standard of care for the treatment of severe falciparum malaria, although it is not yet widely available in most areas. Artesunate and artemether have also been effective in the treatment of severe malaria when administered rectally, offering a valuable treatment modality when parenteral therapy is not available.

ADVERSE EFFECTS & CAUTIONS: Artemisinins are generally very well tolerated. The most commonly reported adverse effects are nausea, vomiting, diarrhea, and dizziness, and these may often be due to underlying malaria rather than the medications. Rare serious toxicities include neutropenia, anemia, hemolysis, elevated liver enzymes, and allergic reactions. Irreversible neurotoxicity has been seen in animals, but only after doses much higher than those used to treat malaria. Artemisinins have been embryotoxic in animal studies, but rates of congenital abnormalities, stillbirths, and abortions were not elevated, compared with those of controls, in women who received artemisinins during pregnancy. Based on this information and the significant risk of malaria during pregnancy, the WHO recommends artemisininbased combination therapies for the treatment of uncomplicated falciparum malaria during the second and third trimesters of pregnancy, intravenous artesunate or quinine for the treatment of severe malaria during the first trimester, and intravenous artesunate for treatment of severe malaria during the second and third trimesters.

RELATED;

1.  PENICILLINS  

2.  AZITHROMYCIN

3.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

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