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Showing posts with the label Anatomy

Hospital Acquired Pneumonia- Definition, Predisposing Factors, Clinical Features and Management!

 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

CAP-Community Acquired Pneumonia-Definition, Etiology and Its Management Protocols!

 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

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-Anaphylaxis!

  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)

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

Complications of Peptic Ulcer Disease!

  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, 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