Medical Concepts

 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 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

 PORTAL HYPERTENSION Definition: "Portal Hyperension is present when the hepatic venous pressure gradient exceeds 10mmHg and risk of variceal bleeding increases beyond a gradient of 12mmHg." Classification: According to The Site of Action: 1. Pre-Hepatic, Pre-Sinusoidal:     Caused by;          Portal vein thrombosis due to sepsis          Abdominal trauma including surgery. 2. Intra-hepatic pre-sinusoidal:    Caused by;          Schistosomiasis         Congenital hepatic fibrosis         Drugs         Sarcoidosis 3. Sinusoidal:     Caused by;          Cirrhosis         Polycystic liver disease        Nodular regenerative hyperplasia        Metastatic malignant disease 4. Intrahepatic Post-sinusoidal:     Caused by;        Veno-occlusive disease 5. Post-hepatic post-sinusoidal:   Caused by;       Budd-Chiari syndrome Etiology: Cirrhosis Schistosomiasis Portal vein thrombosis Drugs Fibrosis Clinical Features: Variceal bleeding Congestive gastropathy Renal failure Iron deficien

 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

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 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

  MEDICAL EMERGENCY- ANAPHYLAXIS Definition: " Anaphylaxis is a systemic response to exposure to an allergen caused by rapid, IgE-mediatd release of histamine and other mediators from tissue mast cells and circulating basophils". Symptoms: Symptoms usually occur within a few seconds or minutes of exposure but can be delayed or recur many hours after apparent resolution (exposure). Causes: Upper airway obstruction Cardiovascular collapse are the most common causes of death in anaphylaxis. Treatment: The treatment of anaphylaxis is directed towards its three Major Presentations : Skin Manifestations: Angioedema, Urticaria Respiratory distress: Wheezing, Stridor, Dyspnea from laryngeal edema, laryngospasm and bronchospasm Hypotension All specific treatment measures should be accompanied by basic resuscitative measures including clear airway, supplemented oxygen and IV access. General Therapy and Skin Manifestations: 1. Epinephrine HCl, IM or SC, 0.3-0.5mg ; may repeat q(every)

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 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)                                         

  COMPLICATIONS OF PEPTIC ULCER DISEASE Bleeding peptic ulcer Pyloric stenosis Zollinger-Ellison Disease Stress Ulcers Bleeding peptic ulcer: Peptic ulcer is the most common cause of non-variceal upper gastro-intestinal bleeding. Most patients with bleeding peptic ulcer are clinically stable and stop bleeding without any intervention, whereas other outcomes include re-bleeding and mortality. Endoscopy allows identification of the severity of disease. Endoscopic hemostatic therapy which is successful in reducing mortality. A number of pharmacological agents have been used for endoscopic injection therapy such as 1:10000 adrenaline (epinephrine), human thrombin and fibrin glue. Mechanical endoscopic treatment options include Thermocoagulation using a heater probe or endoscopic clipping. Combination therapies are superior to monotherapy and a combination of adrenaline 1:10000 with either thermal or mechanical treatment is recommended (SIGN,2008). Pyloric Stenosis: Malignancy is the most c

 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: "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 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

  CHRONIC ABSTRUCTIVE PULMONARY DISEASE (COPD) Definition: COPD is defined as "a disease state characterized by airflow limitation that is not fully reversible and this airflow limitation is progressive associated with abnormal inflammatory response to the noxious or gaseous particles. According to Davidson , COPD is defined as " COPD is preventable and treatable disease characterized by airflow limitation that is usually progressive and is associated with enhanced chronic inflammatory response in the airways and lungs to the noxious particles. According to National Institute for Health and Clinical Excellence (NICE) , COPD is defined as "Airflow obstruction with reduced FEV1/FEVc is less than 0.7, if FEV1 is greater than or equal to80%; so, diagnosis of COPD should be made on the presence of symptoms". Signs and Symptoms: Shortness of breathing Cough Pink puffers and Blue Blotters or Smokers Cough (classical signs of COPD). *Pink puffer is the major sign of emphyse