Medical Concepts

 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 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 "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 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

SUPPURATIVE PNEUMONIA (ASPIRATION PNEUMONIA) AND PNEUMONIA IN IMMUNOCOMPROMOISED PATIENTS  SUPPURATIVE PNEUMONIA Definition: "Suppurative pneumonia is characterized by destruction of the lung parenchyma by inflammatory process and although microabscessation formation is characteristic histological feature, pulmonary abscess" is usually taken to refer lesion which is a large, localized collection of pus or a cavity lined by chronic inflammatory tissue from which pus has escaped by rupture into bronchus". Etiology: Inhalation of septic material during operations on the nose, mouth, throat under general anesthesia Bulbar Vocal cord palsy Esophageal reflux Alcoholism Infecting Organism: Bacterioder melaninogenicus Anaerobic/microaerophilic cocci B. fragilis S. aureus (most common) K.pneumoniae S.pneumonia. *Leimerres Syndrome is a rare cause of pulmonary abscesses. Usually, causative agent is F.secrophorum . Illness signs include sore throat, painful swollen neck, fever, ri

 HOSPITAL ACQUIRED PNEUMONIA Definition: "HAP refers to a new episode of pneumonia occurring at least 2 days after the administration to hospital. It is the most common Hospital Acquired Infection (HAI) and leading cause of HAI-associated death". Predisposing factors: Aspiration of nasopharyngeal secretion Bacteria introduced into the lower GIT. Bacteriaemia Old age Mode of Spread:  Droplet infection Infecting agent: Bacteria: S.pneumonia , S.aureus , H.influenza Virus: Adenovirus, Corona virus, Herpes Simplex Clinical Features: Purulent sputum New radiological infiltrates Temperature > 38 degree Celsius Leukocytosis Investigations: Chest Pain:  to confirm the diagnosis and exclude complication. Pulse Oximetry : to monitor response to oxygen therapy, if SaO2 < 93% features of sever pneumonia, identify ventilatory failure or acidosis. Cell count:  ESR, Neutrophil leukocytosis Microbiological studies:  for severe CAP and those that do not respond to initial therapy (Gr

 COMMUNITY-ACQUIRED PNEUMONIA Definition: "It indicates pneumonia occurring in a person in a community (outside hospital)". Predisposing factors: Cigarette smoking Upper GIT infection Alcohol consumption Corticosteroid therapy Old age (pneumonia also called as Oldman's friend) Recent influenzae Indoor air pollution Mode of Spread: Droplet infection Infecting agents: S.pneumoniae S.aureus H.influenza Viruses - Influenza, Measles, Herpes simplex. Parainfluenza Clinical Features: Pulmonary symptoms such as : Breathlessness, cough (non-productive or productive with sputum), hemolysis, pleuritic chest pain, shortness of breath. Systemic symptoms such as : fever with chills, rigors, tachycardia, vomiting, Decreased appetite, headache, fatigue. In elderly: new onset/ progressive confusion In severely ill : Septic shock, organ failure, tachypnea, percussion note dull to flat, bronchial breathing with crackles. Investigations: Chest Pain: to confirm the diagnosis and exclude com

 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 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)