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

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

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

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