Medical Concepts

 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