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Procedure of IV selection!

 IV DRUG THERAPY- SELECTION OF EQUIPMENTS AND INSERTION OF CATHETER Equipment: Canula selection: Select cannula based on purpose and duration of use and age of patient. Consider risk of infection and extravasation. Cannula made from polyurethanes are associated with decreased risk of phlebitis. Steel needles have higher risk of extravasation and should be avoided where tissue necrosis is likely if extravasation occurs.       2. Skin Prep: Antiseptic solution, use an aqueous based alternative if there is a known allergy to alcohol.       3. Other Equipment: Intravenous solution as ordered, torniquet, giving set, IV stand/pole, infusion pump, transparent occlusive dressing, tape or similar to secure cannula, gloves, paper bag.       4. Additional Equipment which may be required: Syring (5mL), sterile sodium chloride 0.9%, local anesthetics (in children), 3-way tap or triflow, short extension tube. Selection Of the Catheter Site: Generally speaking, the vein section with the straightest a

Intravenous Therapy!

 INTRAVENOUS THERAPY Definition: "Intravenous therapy or IV therapy is the giving of liquid substances into vein".  It can be intermittent or continuous; continuous administration called an Intravenous drip.  The word intravenous simply means "within vein" but is most commonly used to refer to IV therapy. Compared to other routes of administration, the intravenous route is the fastest way to deliver fluids and medications throughout the body. Some medications, as well as blood transfusions and lethal injections can only be given intravenously. The simplest form of intravenous access is a syringe with an attached hole in needle. The needle is inserted through the skin into a vein, and the contents of the syringe are injected through the needle into the bloodstream. This is easily done with an arm vein, especially one of the metacarpal veins. Usually, it is necessary to use a constricting band first to make the vein bulge; once needle is in place, it is common to dra

Drug-Induced Hepatotoxicity!

 DRUG-INDUCED HEPATOTOXICITY "Hepatotoxicity is the injury or liver damage caused by exposure to certain drugs, when taken in overdoses and sometimes when administered at therapeutic ranges, may injure the organ". Drug-induced hepatotoxicity is also referred to as the Drug-Induced Liver Injury (DILI). Physiological functions of liver: Formation and sensation of bile. Nutrient and vitamin metabolism (amino acid, lipid). Detoxification and inactivation of various substances (toxin drugs). Synthesis of plasma proteins (Albumin, clotting factors). Immune systems (Kupffer cells). Hepatotoxicity is most prevalent in older patients especially in those with pre-existing hepatic impairment. The few examples of drugs that cause hepatotoxicity are listed below: 1. ACE Inhibitors: Hepatic injury occurs occasionally with ACE-Inhibitors. Captopril and Enalapril are implicated in most reported cases, but others also have similar hepatotoxic potential. Most cases show cholestatic injury, b

Drug-Induced Oculotoxicity!

 DRUG-INDUCED OCULOTOXICITY Occasionally, non-specific blurred vision occurs with almost all the drugs. The drugs listed below are associated with a specific pattern of drug-induced oculotoxicity when administered systemically: 1. Allopurinol: Despite the discovery of Allopurinol in cataractous lenses taken from patients on long term (>2 years) therapy, there is no clinical evidence for an increased risk of cataracts in allopurinol-treated patients. 2. Beta-Adrenergic Blocking Agents: A reduction in tear production occurs, which can produce a hot, dry, gritty sensation in the eyes. This is rapidly reversible with drug discontinuation. 3. Contraceptives, (Oral): A variety of retinal vascular disorders have been occurred due to oral contraceptives, but the association remains unproved. Some oral contraceptives users cannot tolerate contact lenses, possibly because of ocular edema or dryness. However, a prospective study failed to show any difference in lens tolerance between oral cont

Anatomy and the Complications Associated with Liver Diseases!

  LIVER AND THE COMPLICATIONS ASSOCIATED WITH THE PROGRESSION OF DISEASE! Liver: The liver weighs up to 1.5kg in adults and is the 2nd largest organ in the body. Hepatocytes are the functioning unit of liver. Impairment of liver may lead to: Acute liver diseases Chronic liver diseases Liver cirrhosis Acute Liver Disease (ALD): ALD is a self-limiting episode of hepatocyte damage which in most cases spontaneously without clinical sequelae, but acute liver failure (ALF) may develop. This is a rare condition in which there is a rapid deterioration in liver function with associated encephalopathy and coagulopathy. ALF carries significant morbidity and mortality and may require emergency liver transplant. Chronic Liver Disease (CLD): CLD occurs when the longstanding cell damage causes permanent structural changes within the liver, with the loss of normal liver structure and functions. In many cases, this may lead to cirrhosis where fibrosis sears divide the liver cells into areas of regenera

PNEUMONIA- Its Etiology, Pathophysiology, Classification and Severity Assessment Method!

 PNEUMONIA Definition: "Pneumonia is an infection of pulmonary parenchyma". (Harrison)                                                    OR "Pneumonia is defined as an acute respiratory illness associated with recently developed radiological pulmonary shadowing which may be segmental, lobar or multilobar". (Davidson) Etiology: Microorganisms gain excess to the lower respiratory tract in several ways: Aspiration from the oropharynx (most common). Inhalation of contaminated droplets. Hematogenous spread. Contiguous extension. Pathophysiology of Pneumonia: Pneumonia results from proliferation of microbial pathogens at the alveolar level and the hosts response to these microorganisms.  Defensive Mechanisms against Pneumonia: The defensive mechanism against pneumonia involve: Branching architecture of tracheobronchial tree. Muco-ciliary clearance. Local antibacterial factors. Gag Reflex. Cough mechanism. Normal flora adhering to mucosal cells of oropharynx. Alveolar mac

Drug-Induced Nephrotoxicity!

 DRUG-INDUCED NEPHROTOXICITY Drug-Induced Nephrotoxicity is increasingly recognized as a significant contributor to kidney disease including Acute Kidney Injury (KI) and chronic kidney disease (CKD). Nephrotoxicity has a wide spectrum, reflecting damage to different nephron segments based upon individual drug-mechanisms. 1. ACE-INHIBITORS: ACE-Inhibitors are frequently associated with Proteinuria and Renal Insufficiency. The prevalence of Proteinuria in Captopril treated patient is estimated to be 1%. The risk of Renal Insufficiency is greater with long-acting ACE Inhibitors such as Lisinopril or Enalapril than with Captopril. Immune complex glomerulopathy is a major contribute to ACE Inhibitor nephrotoxicity. Predisposing factors include: Hyponatremia Diuretic therapy Pre-existing renal impairment Congestive Heart Failure (CHF) Diabetes Mellitus Recovery of renal function usually follows ACE-Inhibitor discontinuation. 2. CEPHLOSPORIN: The cephalosporin antibiotics are capable of pro

Drug-Induced Ototoxicity!

 DRUG-INDUCED OTOTOXICITY What is drug Induced Ototoxicity? Drug-Induced ototoxicity can affect hearing (auditory or cochlear function0, balance (vestibular function) depending on the drug. Drugs of almost every class have been reported to produce tinnitus (sounds in ear), as have placebos. The following agents are associated with measurable changes in hearing or vestibular defect when administered systemically. 1. AMINOGLYCOSIDES: Aminoglycosides antibiotics can cause cochlear or vestibular toxicities. Cochlear toxicity: occurs as progressive hear loss, starting with highest tones and advancing to lower tones. Thus, considerable damage can occur before the patient recognizes it. S ymptoms of Vestibular damage : include;  Dizziness Vertigo Ataxia Both forms of ototoxicity are bilateral and potentially reversible, but permanent damage is common and can progress even after discontinuation of aminoglycosides. Clinically detectable ototoxicity in as many as 5% patients. Most aminoglycosid

Ways of Gastrointestinal Decontamination After Poisoning!

 GASTROINTESTINAL DECONTAMINATION AFTER POISONING GI-decontamination can be achieved by the administration of: Activated Charcoal Gastric Lavage Ipecac-induced Emesis Whole-Bowel Irrigation Indication for GI-decontamination: Ingestion of a known toxic dose Ingestion of an unknown dose of a known toxic substance Ingestion of a substance of known toxicity * For all methods of GI-decontamination, the value of the procedure diminishes with time. Some investigators now question the usefulness of gastric lavage, or ipecac-induced emesis more than 1 hr after ingestion.* *In general, activated charcoal is the most useful agent for preventing absorption of ingested toxic substance. Other methods may be considered if the ingested substance is not adsorbed by activated charcoal or if circumstances do not permit its prompt  administration. * 1.Activated Charcoal: Activated charcoal is a non-specific absorbent that binds unabsorbed toxins within the GIT.  Activated charcoal is not effective for abs

Management of Medical Emergency-Poisoning!

MEDICAL EMERGENCY- POISONING Management of the poisoned patient involves procedures designed to prevent the absorption, minimize the toxicity, and hasten the elimination to the suspected toxin. The prompt employment of appropriate emergency management procedures often can prevent unnecessary morbidity and mortality. A Regional Poison Center is a practitioner's best source of definitive treatment information and should be consulted in all poisonings, regardless of the apparent simplicity of the case. In all cases, every attempt should be made to accurately identify the toxin, estimate the quantity involved, and determine the time that has passed since the exposure. These data, plus patient-specific parameters such as age, weight, sex, and underlying medical condition or drug-use will assist the person and the Regional Poison Center in designing an appropriate therapeutic plan for the patient. POISONING BY TOPICAL EXPOSURES: Immediately irrigate affected areas with a copious amount

Medical Emergency- Cardiac Arrest and Basic Life Support (BLS)!

  MEDICAL EMERGENCY- CARDIAC ARREST AND BASIC LIFE SUPPORT Definition: " Cardiac Arrest is a medical emergency requiring a systematic approach". Early recognition must be followed by prompt, effective application of Basic Life Support (BLS) techniques to sustain the patient until Advanced Life Support (ALS) capabilities are available. Management: The management of Cardiac Arrest is a 4-step approach: Recognition and Assessment BLS Advanced Cardiovascular Life Support (ACLS) Post-resuscitation Care 1. RECOGNITION AND ASSESMENT Verify that the respiration and circulation have ceased: Loss of consciousness Loss of functional ventilation (respiratory arrest or inadequate respiratory effort) Loss of functional perfusion (No pulse). 2. BASIC LIFE SUUPORT (BLS) The goal in cardiac arrest is the restoration of spontaneous circulation (ROSC). The first step towards achieving this ROSC goal is prompt initiation of BLS, where the goal is to rapidly and effectively perfuse the tissues wi

GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)!

MANAGEMENT OF GASTRO-ESOPHAGEAL REFLUX DISEASE  "GERD refers to the endoscopically determined esophagitis or endoscopy-negative reflux disease" . "GERD is the term used to describe any symptomatic clinical condition or histopathological alteration resulting from episodes of reflux of acid, pepsin and occasionally, bile into the esophagus from the stomach". Patients with uninvestigated "reflux-like" symptoms should be managed as patients with uninvestigated dyspepsia. There is currently no evidence that H.pylori should be investigated in patients with GERD. Symptoms: Heartburn is the characteristic symptom of GERD. Acid regurgitation Dysphagia Belching Upper abdominal discomfort Bloating and postprandial fullness Chest pain Hoarseness Cough Complications include: Esophageal ulceration Formation of specialized columnar-lined esophagus at the gastro-esophageal junction known as Barretts Esophagus . Mechanism of Acid Reflux: The mechanism of acid reflux is mu

Management of H.pylori and NSAID-associated ulcers Eradication!

MANAGEMENT FOR H.PYLORI ERADICATION It is known that H.pylori infection is associated with over 90% of duodenal ulcers and 80% of Gastric Ulcers. Antibiotics alone or acid-suppressing agents alone, do not eradicate H.pylori . Both therapies act synergistically as growth of the organism occurs at elevated pH and antibiotics efficacy is enhanced during growth. Additionally, increasing intragastric pH may enhance antibiotic absorption. High eradication rates are achieved by a short course of Triple Therapy consisting of:            1 .PPI                                         2. Clarithromycin                         3. Amoxicillin/Metronidazole          in a twice recommended simultaneous regimen. First-Line Therapy :  European Guidelines recommended 1 week of therapy, whereas the US Guidelines recommend 10-14 days of therapy and achieve 7-9% better eradication rates.     OCA : Omeprazole(20mg), Clarithromycin (500mg) and Amoxicillin (1g)                                         

Peptic Ulcer- Clinical Manifestations, Presenting Symptoms, Alarming features and Investigating Tests!

 PEPTIC ULCER Clinical Manifestations: Upper abdominal pain; occurring 1-3hour after meals and relieved by food or antacids in the classic symptom of peptic-ulcer disease. Anorexia Weight loss Nausea Vomiting Heartburn Hemorrhage Chronic-iron deficiency anemia Pyloric stenosis Perforations In the elderly, the presentation is more likely to be silent and gastro-intestinal bleeding may be the first clinical sign of disease. Patient Assessment: Presenting symptoms of dyspepsia require careful assessment to judge the risk of serious disease or to provide appropriate symptomatic treatment.      1.Reflux-like dyspepsia: Heartburn plus dyspepsia Acid regurgitation plus dyspepsia       2. Ulcer-like dyspepsia:  Localized epigastric  pain. Pain when hungry Pain relieved by  food. Pain relieved by antacids or acid-reducing  drugs. Pain that wakens the patient from sleep Pain with remission and relapse       3. Dysmotility-like Dyspepsia: Upper abdominal discomfort (pain not dominant) Early sati

Peptic Ulcer- Definition, Epidemiology, Etiology and Pathophysiology!

 PEPTIC ULCER Definition: "The term Peptic Ulcer describes a condition in which there is a discontinuity in the entire thickness of the gastric or duodenal mucosa, that persists as a result of acid and pepsin in the gastric juice." Esophageal ulceration due to acid reflux, is generally classified under GERD. Peptic ulcer disease often presents to clinicians as dyspepsia. However, not all patients with dyspepsia have peptic ulcer disease. " Dyspepsia " is defined as persistent or recurrent pain or discomfort centered in the upper abdomen.  The most common causes of dyspepsia include: non-ulcer or functional dyspepsia GERD Peptic ulcer Epidemiology: The incidence of duodenal ulcer is now declining, which follows the decline H.Pylori infection. However, hospital admission rates for gastro-intestinal bleeding associated with gastric and duodenal ulcers are rising. This is probably a consequence of increased prescription for low-dose aspirin, NSAIDs, Antiplatelets, anti

Myocardial Infarction- Etiology, Pathogenesis, Clinical Diagnosis and Management!

MYOCARDIAL INFARCTION Definition: Myocardial Infarction is defined as " a diseased condition which is caused by reduced blood flow to the coronary artery due to atherosclerosis and occlusion of artery by embolus or thrombus." Myocardial Infarction (or Heart attack) is the irreversible damage of myocardial tissue due to prolonged ischemia or hypoxia. Universally accepted definition of MI:  Evidence of myocardial necrosis in consistent with the myocardial ischemia, in which case any of the following meets the diagnosis of Myocardial Infarction. Evidence rises and/or fall of cardiac biomarkers (preferably troponin). ECG changes indicative of new ischemia (new ST-T changes or new left bundle branch block) Development of pathological Q waves. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. Etiology: Tobacco smoking Diabetes Mellitus Age Hypertension Obesity Gender Stress Drug abuse Alcohol consumption Family history of ischemic heart dise