DAMS CRS Clinical Medicine-2020.pdf

DAMS COMPREHENSIVE REVIEW SERIES CLINICALS Medicine For PG Medical Entrance CONTENTS Chapter - 01: RESPIRATORY SYSTEM Chapter - 02: CARDIOVASCULAR SYSTEM Chapter - 03: NEPHROLOGY Chapter - 04: GASTROINESTINAL TRACT AND LIVER Chapter - 05: RHEUMATOLOGY Chapter - 06: ENDOCRINE SYSTEM Chapter - 07: CENTRAL NERVOUS SYSTEM Chapter - 08: INFECTIOUS DISEASE Chapter - 09: ELECTROLYTE AND ACID BASE IMBALANCE Chapter - 10: MULTIPLE CHOICE QUESTIONS PULMONARY FUNCTION TESTS LUNG VOLUMES – Tidal volume-Amount of air that moves into the lungs with each inspira on (or the amount that moves out with each expira on) during quiet breathing Expiratory reserve volume-Volume of air expelled by an ac ve expiratory eﬀort a er passive expira on Inspiratory capacity-Maximum amount of air inspired from the end- expiratory level Total lung capacity – Volume of gas contained in the lungs a er a maximal inspira on. Residual volume – Volume of gas remaining in the lungs a er a maximal expira on. Vital capacity – Maximum amount of air expired from the fully inﬂ ated lung SPIROMETRY – Recording of exhaled volume versus me. FEV1 (Forced expired volume in one second)–The maximum amount of air that can be exhaled in the ﬁrst second of expira on.Normally it is 70-80% of the FVC. FVC(Forced vital capacity) – Largest amount of air that can be expired a er a maximal inspiratory eﬀ ort FEV1 /FVC(as percentage)- The propor on of the total volume of air that can be expired in the ﬁrst second of expira on. FEF25 – 75% - Average expiratory ﬂow rate during middle 50% of the FVC. Also called maximal mid expiratory ﬂow rate.It is regarded as a more sensi ve measure of small airway narrowing than FEV1. PEFR(Peak expiratory ﬂow rate)-The maximal expiratory ﬂow rate achieved. STRENGTH OF RESPIRATORY MUSCLES – Maximal inspiratory pressure – When a pa ent exhales completely to RV and then tries to inspire maximally against an occluded airways, the pressure that can be generated is called MIP. Maximal expiratory pressure – When a pa ent inhales to TLC and then tries to expire maximally against an occluded airway, the pressure generated is called MEP. NORMAL VALUES – Lung volumes Male Female TLC 6.4 L 4.9 L FRC 2.2 L 2.6 L RV 1.5 L 1.2 L IC 4.8 L 3.7 L VC 1.7 L 1.4 L ERV 3.2 L 2.3 L Spirometry FEV1 3.8 L 2.8 L FEV1 % (FEV1/FEC) 76 % 77 % FEF25 – 75% 4.8 L/S 3.6 L/S FVC 4.8 L 3.3 L Resp. MS strength MIP > 90 CmH2O > 50 MEP > 150 CmH2O > 120 OBSTRUCTIVE PATTERN – Hallmark is decrease in expiratory ﬂow rates. RESTRICTIVE PATTERN – Hallmark is decrease in TLC. Pa ern TLC RV VC FEV1/FVC MIP MEP Obstruc ve Normal- increased decreased decreased normal normal increased Restric ve Parenchymal decreased decreased decreased normal - normal normal increased Extra- parenchymal decreased Normal- decreased normal Dec/norm normal Inspiratory decreased dec. decreased variable Dec/norm. Dec/norm. Ins+exp. increased CAUSES OF DIFFERENT PATTERN – OBSTRUCTIVE RESTIRICTIVE - PARENCHYMAL -EXTRAPARENCYMAL ASTHMA SARCOIDOSIS NEUROMUSCULAR COPD IDIOPATHIC PULM FIBROSIS Guillane-Barre syndrome BRONCHIECTASIS PNEUMOCONIOSIS Myasthenia Gravis CYSTIC FIBROSIS DRUGS Diaphragma c paralysis BRONCHIOLITIS RADIATION Cervical spine injury CHEST WALL Kyphosis Obesity Ankylosing Spondylosis Values b/w 80 – 120% of predicted values are normal. Mild obstruc ve (small airway) diseases have decrease FEF25 – 75% with normal FEV1/FVC. TLC, RV & ERC are measured using 1. Helium dilu on method 2. Body plethysmography INTERPRETATION OF SPIROMETRY BRONCHIAL ASTHMA Chronic inﬂammatory disease of airways with increased responsiveness of tracheobronchial tree to mul ple s muli. Pathologically – Wide spread narrowing of the airways which may be relieved spont. or as a result of therapy. Age & sex ra o – Can occur at all ages. Mainly occur in early life. Male : Female is 2 : 1 in childhood. Equalizes by age 30. Types – Extrinsic/ Allergic/ Intrinsic/ Exogenous nonallergic/ Endogenous Pathophysiology – Release of Induc on of vagal reﬂex bronoconstrictor substance via from mast cells sensi zed rec in mucosa. History – Onset. Childhood & Infancy & adult young adult Family h/o allergic Uncommon disorder Salicylate sensi vity Uncommon common Clinical course – Paroxysmal asthma Chronic asthma Status asthma cus- Frequent infrequent Sinus infec on / nasal Common polyp. Infrequent Favourable course Unfavourable course Pathology – IgE increase Normal Skin test posi ve Nega ve Treatment – Mast cell inhibitors Li le eﬀect PATHOGENESIS – State of persistent subacute inﬂamma on of the airways. Cells – Mast cells, eosinophils, lymphocytes & epithelial cells. Mediators – Histamine, brady kinin, LTC, D,E, PG E2, F2a, D2 & PAF, IL – 3, IL – 4, IL – 13. Response – Bronchoconstric on, vascular conges on, edema forma on, increase mucus produc on & impaired mucociliary func on. Reduc on in airway diameter is due to – Contrac on of smooth muscles Vascular conges on Edema of bronchial wall Thick secre ons Microscopically sputum consists of – Eosinophils Desquamated epithelium Curschmann spirals (whorled mucous plugs) Charcot Leyden crystals (crystalloid debris of easinophil membrane) Creda bodies (exfoliated cells due to disrup on of mucosal integrity) PPT. FACTORS – 1. Allergens – 2. Pharmacologic s muli – Aspirin, tartrazine, b - blockers, sulfa ng agent. 3. Air pollutants – Ozone, nitrogen dioxide, sulfur dioxide. 4. Occupa onal Factors – Metal salts – Pla num, chrome, nickel Wood /vegeta ve dust – oak, grain, ﬂour Dyes, biological enzymes, serum 5. Infec ons – viruses, RSV & Para inﬂuenza – children Rhinovirus & inﬂuenza – Adults Mechanism– Produc on of T. cell derived cytokines 6. Exercise – Mechanism – Thermally produced hyperemia & engorgement of microvasculature. No contrac on of smooth muscles 7. Emo onal stress – Mechanism– Vagal eﬀerent ac vity Endorphins CLINICAL FEATURES – Triad of dyspnea, cough & wheezing. Constric on in chest, non- produc ve cough Wheezing in both phases of respira on, prolonged expira on Tachypnea tachycardia, systolic HT Accessory muscles of respira on, pulsus paradoxus Life threatening features – Pt can’t speak, cyanosis, silent chest, altered sensorium, Po2 < 60mmHg, PCo2 > 45, pH < 7.35. DIFFERENTIAL DIAGNOSIS – Other disorders that can produce wheezing –COPD, LVF, ABPA, Carcinoid tumors, eosinophilic pneumonia, pulmonary embolism, systemic vasculi s, bronchiectasis. STATUS ASTHMATICUS (ACUTE SEVERE ASTHMA) Severe obstruc on persis ng for days to weeks and characterised by – Pulse > 120/m, RR > 30/m, Pulsus paradoxus swea ng, altered level of consc. , & I : E ≥ 1 : 3 NOCTURNAL ASTHMA Overnight fall of > 20% in FEV, or PEFR. GASTRIC ASTHMA Worsening of asthma a er meals and is due to GERD. INVESTIGATIONS – Chest X – ray – Normal or may show hyper inﬂa on Pulmonary func on test – It shows obstruc ve pa ern. In bronchial asthma there is reversibility, i.e., FEV, following 2 puﬀs of b - agonist shows an increase by 15% or more than the previous level ABG - Hypoxia, Hypocapnia, resp. alkalosis In severe obstruc on – Normocapnia/ Hypercapnia Metabolic acidosis MANAGEMENT Mild intermi ent Mild Mod. Persistent Severe Persistent Persistent Symptoms < 1 –2 /week > 1 –2 /week Daily Persistent Noct. < 2 / month > 2 /month > 1/week Frequent Symptoms Spirometry Normal Ab normal Ab normal Ab normal FEV1/PFER > 80% > 80% 60 – 80% < 60% PFER < 20% 20 – 30% >30% > 30% variability Treatment Short ac ng Low dose Low dose High dose inhaled inhaled inhaled inhaled b2 – agonist – SOS Steroids steroid + long steroid + long If needed > once a ac ng b2 – ac ng day agonist move to step II or High dose Bronchodil steroid and oral steroid STEP I STEP II STEP III STEP IV DRUGS – I. Used for preven on of asthma – Sodium cromoglycate – Useful in children with atopic asthma 5 – 10 mg 4 mes daily. Nedocromil sodium Keto fen II. Used to reverse bronchospasm – Catecholamines – epinephrine, isoproterenol Resorcinols – Terbutaline Saligenine – Salbutamol Long ac ng b2 agonist – Salmeterol, Formoterol, Bambuterol An – cholinergic – Ipratropium bromide Methyl xanthine – I.V. aminophylline, oral theophylline. III. An inﬂammatory – Steroids – Flu casone, Beclomethasone – Inhaled Prednisolone – oral LT antagonist – Montelukast, zaﬁrlukast Lipoxygenase inhibitor – Zileuton IV. Immunosuppressants – Methotrexate , Gold salt CHRONIC OBSTRUCTIVE PULMONARY DISEASE DEFINITION – Chronic and slowly progressive respiratory disorder characterized by reduced maximal expiratory ﬂow during forced exhala on. It includes chronic bronchi s & emphysema. CHRONIC BRONCHITIS – Cough with expectora on for at least 3 months a year for more than 2 consecu ve years and there is no other cause of expectora on. It is of 3 types 1. Simple chronic bronchi s – Mucoid sputum produc on 2. Chronic mucopurulent bronchi s – Persistent or recurrent purulent sputum produc on in the absence of local suppura ve disease. 3. Chronic bronchi s with obstruc on / chronic asthma c bronchi s – Severe dyspnea and wheezing in associa on with inhaled irritants or infec ons in the se ng of bronchi s EMPHYSEMA – Permanent and destruc ve enlargement of airspaces distal to the terminal bronchioles with out obvious ﬁbrosis and with loss of normal architecture. 3 types 1. Centriacinar – Central or proximal part of respiratory unit – acinus upper lobe involvement. Commonly seen in male smokers. 2. Panacinar – Uniform destruc on of acinus. Lower zone involvement. It is associated with a1 – AT deﬁciency. 3. Paraseptal – Involvement of distal acinus. It is found near the pleura and o en causes pneumothorax. Compensatory emphysema – Normal lung ssue undergoes hyperinﬂa on as a compensatory mechanism in response to the damage occuring in part of the same lung or opposite lung. Alveolar septa are preserved. REID INDEX – Ra o of the thickness of submucosal glands to that of the bronchial wall. Normal 0.44 ± 0.09 chronic bronchi s 0.52 ± 0.08 High Index is commonly associated with symptoms. RISK FACTORS – 1. Smoking – 15 – 20% of smokers develop COPD. 90% of COPD pa ent are smokers. Cigare e smoke produces oxygen free radicals. Source of Fe+2, releases Fe+2 from ferri n. Catalyzes the forma on of highly ac ve hydroxyl radicols from O2 -& H2O2 by eosinophils, neutrophils macrophy. Cigare e tar contains nitric oxide which is metabolised to cytotoxic peroxy nitrates. Inac vate a1 AT Chemoa ractant Increase Neutrophil transit me through pulm. Increase IL. 8 which recruit neutrophils, basophils, eosinophils, Tlymphocyte 2. Gene c - α1 AT deﬁciency 3 Air pollu on – SO2 4 Occupa on – Plas c plants, co on mills. 5 Infec on – Severe viral pneumonia in childhood. PATHOPHYSIOLOGY – Airﬂow limita on – loss of elas c recoil due to emphysema Increase resistance due to intrinsic narrowing of airways Increase collapsibility of small airways due to loss of radial trac on on airways. Hyperinﬂa on – Impaired gas exchange – Decrease in ven lla on of distal alveolar acini Pulmonary circula on – Decrease in total cross. Sec onal area of the pulm vascular bed due to Thickening of medium & large muscular pulm artery. Increase contrac on of vascular smooth ms. Destruc on of alveolar septa with loss of capillaries. Constric on of pulm vessels in response to alveolar hypoxia. Renal & hormonal changes – Increase NE, renin, aldosterone. Decrease RDH Cachexia – Increase TNF a Muscle dysfunc on – Proximal limb girdle ms. are usually aﬀected. Protein loss, malnutri on, glucocor coid use. Osteoporosis – CLINICAL FEATURES – Onset – 5th decade Morning smoker’s cough Episodes of exacerba on – ini ally intermi ent & less frequent later become more severe and more frequent Exacerba on – worsening of previously stable disease characterised by increased dyspnea, wheeze, cough, sputum volume, tenacity and purulence with variable degrees of water reten on and with worsening gas exchange and V/Q ra o. Exercise tolerance become progressively limited. CO2 reten on, cyanosis, erythrocytosis. Weight loss, cor pulmonale, amyloidosis. INVESTIGATIONS – Chest X – ray – Increase lucency of lungs Bullae (local radiolucencies > 1cm & surrounded by hairline shadows) Hyperinﬂa on Fla ened diaphragms Retrosternal airspace increase on lateral view. Sternal diaphragma c angle > 900 In PHT, Pulm arteries become enlarged Pulmonary func on test – MANAGEMENT – Smoking cessa on – Nico ne patches, gums, Bupropion Bronchodilators – Glucocor coids – Indica ons – Reversability is demonstrated Acute exacerba ons Severe COPD O2 therapy – Only treatment which decrease mortality in COPD Indica ons are ; – Sao2 ≤ 88% or Pao2 ≤ 55mmHg Sao2 ≥ 89% with Pao2 55 – 60 & Hct > 55% Cor pulmonale or Pulm HT Res ng awake Pao2 ≥ 60 with Sao2 ≥ 90% if they become hypoxic during exercise or sleep O2 should be given for minimum 15 hour/day at rate of 2 – 5 l/min. Surgery – Lung volume reduc on surgery – done in stage III Lung transplanta on – In pa ents who have FEV1 < 25% and with PHT/Cor pulm CI – Ac ve smoking Marked obesity/cachexia BRONCHIECTASIS DEFINITION – Persistent and irreversible dilata on and distor on of medium sized bronchi (5 – 9th genera on) by more than 2mm. It is due to bronchial disten on occuring as a result of chronic obstruc on & recurrent infec on PREDISPOSING FACTORS – Congenital – a) primary b) Secondary Kartagener’s syndrome Young’s Syndrome – idiopathic obstruc ve azoospermia Yellow nail syndrome – Cys c ﬁbrosis Alpha 1 AT deﬁciency Immunodeﬁciency syndrome Bronchomalacia – William – Campbell Syndrome Pulmonary sequestra on Acquired – a) Infec ons – measles, whooping cough, bronchi s b) Bronchial obstruc on – Foreign body, tumour, LN c) Ass. immune disorders – SLE, Sjogren’s RA ABPA, ulcera ve coli s. TYPES – Cylindrical Saccular/cys c Varicose/beaded CLINICAL FEATURES – Persistent, recurrent cough with large (> 60ml/d) quan ty of purulent sputum produc on, which is foul smelling Hemoptysis Clubbing Crepts/wheezing/BBS Bronchiectasis is common in le lower lobe because the lower lobe bronchus is longer & narrower. Middle lobe and lingual are next frequently involved. Upper lobe involvement is rare. But it is common in TB, cys c ﬁbrosis & ABPA. BRONCHIECTASIS SICCA/ DRY BRONCHIECTASIS – There is no sputum produc on only hemoptysis. Seen in upper lobe involvement in TB. MIDDLE LOBE BRONCHIECTASIS /BROCK’S SYNDROME – Recurrent atelectasis of the right middle lobe in the absence of endobronchial obstruc on. It is usually a sequde to primary pulmonary tuberculosis resul ng from obstruc on of middle lobe by TB LN. PSEUDO/REVERSIBLE BRONCHIECTASIS – It is a temporary bronchial dilata on occuring in an area of lung aﬀected by pneumonic consolida on, tracheobronchi s or lung collapse. COMPLICATIONS – Hemoptysis Metasta c abscess Pneumothorax Cor pulmonale Amyloidosis Recurrent pneumonia Lung abcess Hypoproteinemia, ms. was ng Ca lung INVESTIGATIONS – Assessment of ciliary func on – Pellet of saccharine placed in out chamber of nose, me taken to reach pharynx is noted. Normal 20 min. Sputum examina on – Classically 3 layered sputum is seen. Upper layer – Frothy & watery Middle layer – Turbid & mucopurulent. Lower layer – Purulent & opaque. Chest X – ray – Ring shadows, tram track sign, gloved ﬁnger appearance, Dextrocardia in Kartengener’s syndrome CT Scan – HRCT Scan Bronchography – Conﬁrming Δ & planning surgery. MANAGEMENT – Control of infec on by Ab. Chest physiotherapy Bronchodilators Correc on of underlying e ology. Treatment of complica ons Surgery – For localised disease & remaining lung is normal and no systemic disease. Lung transplanta on – If disease is extensive. CYSTIC FIBROSIS DEFINITION – CF is the most common autosomal recessive disorder with the basic defect in the gene located on the long arm of chromosome 7, which results in the deﬁciency of cys c ﬁbrosis transmembrane conductance regulato protein. (CFTR) PATHOPHYSIOLOGY – CFTR protein func on both as a CAMP. regulated Cl – channel and a regulator of other ion channels. Lungs – Increase Na+ absorp on due to absence of CFTR inhibitory eﬀect on Na+ channels Decrease Cl – permeability due to absence of CFTR Cl – channel This leads to decrease Salt & H2O content of mucus and deplete the volume of the perciliary liquid GIT – Decrease secre on of Na+ Hco3 – into pancrea c duct leading to reten on of enzymes in pancreas and destruc on of pancrea c ssue. Decrease Cl – and H2O secre on in intes nal epithelium fail to ﬂush secreted mucins leading to dessicated intraluminal contents and obstruc on of both small & large intes ne Sweat gland – Not able to absorb Nacl as it moves through duct. CLINICAL FEATURES – Respiratory – Bronchi s, bronchopneumonia, bronchiectasis, lung abcess ABPA (10%) Sinusi s, nasal polyposis Pneumothorax Hemoptysis, cor pulmonale, resp failure, PHT. Green coloured sputum H. inﬂuenza & staph aureus are common in newly Δed later Pseudomonas aeruginosa is most common Earliest X – ray change is hyperinﬂa on. RUL has the earliest & most severe changes Earliest lung func on abnormality – Increase RV/TLC ra o GIT – Intes nal – Meconium ileus Volvulus I leal atresia Rectal prolapse Intus suscep on Pneumatosis intes nalis Pancrea c Pancrea c insuﬃciency – Malabsorp on Steatorrhea Recurrent pancreali s Later DM Hepatobiliary Cholelithiasis Focal biliary cirrhosis Atrophic gall bladder Reproduc ve system Infer lity Late onset puberty Skeletal system Retarda on of bone age Demineraliza on Hypertrophic osteo arthropathy COMPLICATIONS – Recurrent respiratory Infec ons Pneumothorax Massive hemoptysis Respiratory failure Cor pulmonale ABPA DIAGNOSIS – Sweat Cl - > 70 mEq/L on 2 diﬃcult occasions. DNA analysis. TREATMENT – An bio cs – Pulse therapy of I.V. an bodies for 2 weeks at 3 month intervals -Inhaled tobramycin Human recombinant DNA ase – to decrease Sputum viscosity Uridine Tri phosphate (UTP) – Cl – channel ac vator. Amiloride inhaler – It is a Na+ channel blocker which inhibits Na+ reabsorp on into resp epithelial cells and decrease Sputum viscosity. Mucoly cs – N – acetylcysteine Gene therapy Treatment of complica ons. TUBERCULOSIS Caused by mycobacterium tuberculosis complex M. tuberculosis is acid fast. Other acid fast bacilli include – Nocardia, Rhodococcus, Legionella, Isospora, crytosporidium. TRANSMISSION – Droplet nuclei (3000 infec ous nuclei per cough) Skin, placenta Raw milk – M. bovis INFECTIVITY: Cavitary lesion, endobronchial/ laryngeal tuberculosis > smear nega ve > culture nega ve > extra pulmonary RISK FACTORS – Silicosis, lymphoma, leukemia, hemophilia, CRF, IDDM, immunosuppression, malnutri on, old ﬁbro c lesion. PATHOGENESIS – 2 – 4 weeks a er infec on two host response develop – Tissue damaging response – Result of delayed type hypersensi vity reac on to bacillary an gen. It destroys non ac vated macrophages that contain mul plying bacilli. Macrophage – ac va ng response – It results in the ac va on of macrophages that are capable of killing and diges ng tubercle bacilli. Ghon focus Subpleural focus usually at the lower border of upper lobe or upper border of lower lobe. Ghon’s Combina on of Ghon’s focus and the draining lymph nodes complex Ghon’s Calciﬁed parenckymal nodule on chest x- ray lesion Ranke’s Calciﬁed parenckymal nodule + calciﬁed hilar node complex Simon Focus Present in apical or post. segment of upper lobe Rich Focus Present in meninges CLINICAL FEATURES – Primary disease – First me infec on with tubercle bacilli, children up to 4 years Middle and lower lung zones In few pa ents, the ini al infec on progresses and manifests as – Rupture into pleural space causing pleural eﬀussion Extensive caseous pneumonia Enlargement of LN bronchial obstruc on Rupture of TB focus into a bronchus leading to endobronchial TB. Rupture into a pulmonary blood vessel causes hematogenous spread Mainfesta ons of hypersensi vity reac ons – erythema nodosum — Phlyctenular conjuc vi s Unilateral hilar lymphadenopathy as part of primary complex is characteris c feature of Primary TB Post Primary disease/Adult type/ reac va on/ Secondary – Apical and post segment of the upper lobe Superior segment of the lower lobes Caseous material contains 1 x 104 bacilli /gm Cavity contain 1 x 109 bacilli Pleural Eﬀusion- Primary Cavita on- Secondary Complica ons – Pleural eﬀusion Pneumothorax Empyema COPD like disease Resp failure Aspergilloma Poncet’s disease Po ’s disease Scar carcinoma Fibrosis Hemoptysis – causes Rupture of dilated vessel in a cavity (Rasmussen’s aneurysm) Erosion of vessel Aspergilloma forma on is an old cavity Hyponatremia due to SIADH TB aﬀec ng various organs Time taken a er primary infec on Miliary TB/TB meningi s with in 6 months Pleural eﬀusion with in 6 – 12 months Progressive primary with cavity with in 1 – 2 years Skeletal tuberculosis 1 – 5 years Genitourinary & skin tuberculosis 5 – 15 years MILIARY TUBERCULOSIS – This is produced by acute dissemina on of bacilli via blood resul ng in the appearance of discrete nodular shadows of size 2mm. HSM (+). Choroid tubercles on fundus examina on. Sputum nega ve in 80% of cases. Anemia, leukopenia CRYPTIC MILIARY TUBERCULOSIS – Seen in elderly, chronic course. No choroid tubercles. Tuberculin test nega ve. Chest x – ray normal (size of tubercles Radiologically old ﬁbro c lesion > 10 mm Posi ve FALSE NEGATIVE TUBERCULIN TEST – Infec ons – measles, mumps, chicken pox, typhoid, leprosy AIDS Hodgkin’s, NHL, Leukemia Sarcoidosis Protein malnutri on Miliary tuberculosis, TBM Immunosuppressive drugs Newborn & elderly Faulty storage or dilu on of PPD Live viral vaccina ons Errors of administra on & recording MANAGEMENT – First line – Drugs Dose Side eﬀects Hepa s, B6 deﬁciency, Neuropathy, pschycosis, INH 5 mg/kg agranulocytosis Hepa s, orange urine, ﬂu – like, inac vates oral Rifampicin 10 mg/kg contracep ves, thrombocytopenia. Ethambutol 15 – 25 mg/kg Op c neuri s, colour blindness Pyrazinamide 25 – 35 mg/kg Hepa s, arthralgias, hyperuricemia Streptomycin 15 mg/kg Renal toxicity, o c toxicity Second line - Newer drugs – Thiacetazone Rifabu ne Capreomycin Rifapantene PAS Vit D Ethionamide Amox/ clav combina on Kanamycin Oﬂoxacin Ciproﬂoxacin Clarithromycin Cycloserine Azithromycin Amikacin Clofazimine Drugs ac ng in acid medium – Pyrazinamide (Intracellular organisms Drugs ac ng in Alkaline medium – Streptomycin (Extracellular organisms) Drugs ac ng in both medium – INH, Rifampicin Drugs ac ng on persistors – Rifampicin Drugs crossing blood barrier – INH, Rifampicin, pyrazinamide It takes 3 weeks for sputum conversion if Rifampicin, 3 months if regimen without Rifampicin are used MULTIDRUG RESISTANT TUBERCULOSIS – When bacilli are resistant to at least INH & Rifampicin MDR-TB considered in- 1. Previous drug treatment for TB 2. Contact with case of known case of MDR-TB 3. HIV infec on 4. Failure of clinical response on treatment 5. Prolonged posi ve sputum smear (4 months) or culture (5 monhts) XDR- TUBERCULOSIS- MDR-TB + Resistance to ﬂuroquinolones and one or more injectables CORTICOSTEROIDS IN TB – TBM Addison’s crisis Seriously ill pt. before chemotherapy is eﬀec ve Pericardi s Genitourinary TB Choroid re ni s PYRIDOXINE IN TB – Alcoholics Malnutri on Pregnant /lacta ng mother CRF Diabetes HIV, AIDS CONTRAINDICATIONS IN SPECIFIC CONDITIONS 1. Pregnancy + TB S and Z 2. Jaundice + TB HRZ 3. CRF + TB S and Z (H half dose, E- ½ dose two mes a week) DURATION – Pregnant women 9 months Silico tuberculosis 8 months CNS TB 12 – 18 months MDR 3 + 18 months Skeletal TB 9 – 12 months SURGERY – Massive hemoptysis Empyema chest tube. MDR TB with localised disease Suspicion of malignancy. LUNG CANCER Leading cause of cancer death among males. PATHOLOGY – 4 major types 1) Squamous or epidermoid carcinoma 2) Small cell or oat cell carcinoma 3) Adeno carcinoma Most frequent, Non smoker. Male < 45 years 4) Large cell/ large cell anaplas c carcinoma Squamous cell and small cell Central mass with endobronchial growth Adenoca and large cell peripheral nodules / masses, pleural involvement Squamous cell and large cells Cavitory lesion. RISK FACTORS – Smoking Asbestos OCC Mining, arsenic, chromium, nickel, radon Vinyl chloride, synthe c rubber Air pollu on – SO2, carbonaceous par culate ma er Familial predisposi on H/o COPD, pulm ﬁbrosis, scleroderma, sarcoidosis Vitamin A deﬁciency Gene cally determined increase aryl hydrocarbon hydroxylase which convents hydrocarbons to more ac ve carcinogens. CLINICAL FEATURES – THORACIC MANIFESTATIONS – Cough, hemoptysis, dyspnea, pleuri c chest pain, recurrent and slowly resdving pneumonia, ﬁxed monophonic wheeze Pancoast tumor / Superior sulcus tumour – Pain in shoulder and arm, unilateral horner’s syndrome, small ms. was ng of hands. It is usually due to squamous cell ca. Symptoms due to SVC obstruc on. (Sq. cell ca) Recurrent laryngeal nerve palsy and dysphagia. Extrathoracic manifesta ons – Symptoms due to blood borne metastasis. Such as seizures, focal neurological deﬁcits, jaundice, Bone pains. PARANEOPLASTIC MANIFESTATIONS – Endocrine – SIADH – Small cell ca Ectopic ACTH – Small cell ca Hypercalcemia – Sq. cell ca Carcinoid syndrome Gynalcomas a Neurological – Myopathy, myosi s Neuropathy Cerebellar degenera on Eaton – Lambert Syndrome Demen a Others – Nephro c Syndrome Hypertrophic pulmonary osteoarthropathy Weight loss INVESTIGATIONS – Chest x – ray – Hilar enlargement, collapse, Pleural eﬀusion, rib erosion medias nal widening, elevated hemidiaphragm. Bronchoscopy – For central tumours to give histology and assess operability Sputum cytology – At least 5 samples. For metastasis – Liver func on tests Isotope bone scan USG Abd CT brain, Abdomen, thorax. 18FDG PET scan: to stage disease MANAGEMENT – SMALL CELL LUNG CANCER – Limited stage Chemotherapy + chest radiotherapy Extensive stage Chemotherapy Chemotherapy: Etoposide+ Cispla n/Carbopla n Limited Conﬁned to one hemithorax and regional LN (medias nal, contralateral hilar & ipsilat supraclavicular ) NON – SMALL CELL LUNG CANCER Stage I, II, IIIA Surgical resec on (+ chemotherapy for IIIA) Pancoast tumor Pre & post op RT also Stage IIIB RT + chemotherapy Stage IV RT to sympt. local sites Chemotherapy: Paclitaxel + Carbopla n/Cispla n PNEUMONIA Exuda ve solidiﬁca on of lung ssue. CLASSIFICATION – Primary/ community acquired pneumonia – Streptococcus pneumoniae H. inﬂuenzae Mycoplasma pneumoniae Chlamydia pnemoniae Legionella pneumophila Moraxella catarrhalis Staph aureus No cardia Oral anaerobes Virus – RSV, inﬂuenza, CMV, measles M. tuberculosis Fungi – Histoplasma, Coccidioides, Blastomyces Secondary pneumonia a) Nosocomial – Enteric aerobic gm nega ve bacilli Pseudomonas Staphylococcus aureus Oral anaerobes b) Aspira on pneumonia – Oral anaerobes c) HIV associated – Pneumocys s carinii M. tuberculosis S. pneumonial H. Inﬂuenzae PREDISPOSING FACTORS – Bronchopneumonia – Extreme of age Immunosuppression Lobar pneumonia – Disorders of Swallowing, coughing Fluid in alveoli – CHF, ARDS Impaired phagocytosis & decrease immunity SPECIFIC PATHOGENS – < 6 months RSV, Chlamydia trachoma s 6 months – 5 year H. inﬂuenzae Young adults M. pneumoniae, C. pneumoniae, hantavirus Elderly H. inﬂuenzae, M. catarrhalis Chronic lung disease Streptococcus pneumoniae, H. inﬂuenzae, M. catarrhalis Severe Streptococcus pneumonia, H. inﬂuenzae hypogammaglobulinemia Severe neutropenia Pseudomonas aeruginosa CD 4 + count < 500/ul M. tuberculosis < 200/ul P. carinii, H. capsulatum, cryptococcus < 50/ul MAI, CMV Long term glucocor coids M. tuberculosis, Nocardia SPECIFIC TYPES OF PNEUMONIA – Pneumococcal pneumonia – Rusty sputum Icterus Lobar pneumonia Staphylococcus pneumonia – Common in cys c ﬁbrosis Pneumatoceles Pneumothorax Klebsiella pneumonia – Brick red currant jelly sputum Upper lobe consolida on Bulging of horizontal ﬁssure Legionella pneumonia – Rela ve brady cardia, diarrhoea Mental confusion Renal and hepa c ab normal Hyponatremia Increase LDH & CK Mycoplasma pneumonia – Hemoly c anemia (Autoimmune) Erythema mul forme Bullous myringi s Enceophali s Transverse myeli s ANA posi ve VDRL posi ve Reynauld’s phen. GBS Chlamydia – Lower lobes VDRL posi ve ASS with CAD Hepatosplenomegaly Q fever – Thrombocytopenia B/L lower lobe Endrocardi s, hepa s with granuloma CMV – Commonest viral cause of pneumonia in immunocompromised pa ents LN HSM Anthrax – Haemorrhagic medias ni s CAVITORY LESIONS – Oral anaerobes, Gram nega ve bacilli, Pseudomonas Legionella, Staphylococcus aureus, Streptococcus pneumoniae (type IV) M. tuberculosis, Nocardia, H. capsulatum Coccidioides immi s, Blastomyces. H. inﬂuenzae, M. pneumoniae, virus, never cause cavity Chest x- ray normal in – P. carinii (30% cases) Agranulocytosis Dehydra on Early stages of an inﬁltra ve process Sputum adequecy - > 25 PMN /LPF < 10 epithelial cells/ LPF Complica on – Sep cemia (-) failure Parapneumonic eﬀusion Resp failure Metasta c infec on Lung abcess ARDS, MOF Pneumothorax Causes of recurrent pneumonia in the same segment Foreign body Sequestra on of lung Neoplasm Bronchiectasis TREATMENT Pen Amo/clav Tmp- SMZ Doxy Eryth Newer Fl. Str. pneum + + — + — + H. inﬂuenzae — + + + — + M. ca. — + + + + + Anaerobes — + — — — — Mycoplasma — — — + + + Chlamydia — — — + + + Legionella — — — — + + PLEURAL EFFUSION – DEFINITION – Accumula on of ﬂuid in pleural space. CAUSES Transuda ve- increased venous pressure or hypoproteinemia Exuda ve- increased leakage of pleural capillaries secondary to infec on, inﬂamma on or malignancy Transuda ve Exuda ve CHF Neoplas c disease Cirrhosis Infec ous disease Nephro c synd Plum embolus GI disease – Pancrea s, subphrenic abcess SVC obstruc on eosophageal perfec on, Liver abcess GN Heart disease – Dressler’s synd, Post CABG. Gynae disease – Meig’s synd, endometriosis collagen Myxedema vascular disease Drugs – Nitrofuran on, methylsergide amiodarone, Plum emboli methotrexate Sarcoidosis Hemothorax Hemothorax Hypoalbuminemia Chylothorax CLINICAL FEATURES – Symptoms – Pain – Pleuri c or dull aching in nature Due to inﬂamma on of parietal pleura Pt. has exuda ve pleural eﬀusion Referred pain Abdomen- peripheral diaphragma c pleura and p of shoulder – central diaphragma c pleura Cough – Dry cough Due to pleural inﬂamma on or Lung compression of ﬂuid bring opposing bronchial walls into contact. Dyspnea – As it is a space occupying process. Signs – Inspec on – Enlargement of hemithorax with bulging of intercostal spaces. Palpa on – Apex beat shi ed to opposite side ; Tac le fremitus decreased; Excep on – Obstruc on of major bronchus Percussion –stony dullness, shi ing dullness Ausculta on – BS decrease Bronchial BS over the superior border of the ﬂuid. Pleural rub Hydropneumothorax- horizontal ﬂuid level and succusion splash Aegophony/Bronchophony- INVESTIGATIONS – 1. Thoracocentesis – Done whenever, on lateral decubitus radiograph, the thickness of pleural ﬂuid > 10mm or whenever there is loculated pleural eﬀusion. Exuda ve pleural eﬀusion has at least one of the following criterias (Light’s criteria) Pleural ﬂuid protein/ serum protein > 0.5 Pleural ﬂuid LDH/ serum LDH > 0.6 Pleural ﬂuid LDH > 2/3 of upper limit of normal for serum LDH. Tests for diﬀeren a ng causes of exuda ve pleural eﬀusion Appearance of ﬂuid – RBC count – 5,000 – 10,000 RBC/mm3 imparts red colour to pleural ﬂuid or a leak of 1ml of blood Hemothorax – If hematocrit of pleural ﬂuid > 50% of peripheral hemotocrit. Causes Trauma, malignancy & Pulm embolis. WBC count - 1000/mm3 – Exuda ve Diﬀeren al WBC count – Neutrophils Pneumonia, early TB, pancrea s, pulmonary embolisa on, Subphrenic abcess Eosinophils Air in pleural space Blood in pleural space Asbestos related pleural eﬀusion Parasi c Drugs Churg Strauss syndrome Basophils Leukemic pleural eﬀusion Lymphocytes Tuberculosis, Malignancy, Post CABG Mesothelial Present normally ; D/D – Malignant cells cells No mesothelial cells are seen in TB (expect pa ent with AIDS) Glucose - < 60mg/dl seen in - Other rare causes – Parapneumonic eﬀusion Paragonimiasis Malignant disease Hemothorax Rheumatoid disease Churg strauss Tubercular eﬀusion Lupus pleuri s Amylase – Increase levels seen in – Pancrea s Malignant tumor Erophageal rupture LDH – Indicator of degree of pleural inﬂamma on Pa ents who meet the diagnos c criteria of exuda ve pleural eﬀusion with LDH but not with protein have Parapneumonic eﬀusion Malignant pleural disease pH – pH < 7.2 seen in Complicated parapneumonic eﬀusion Esophageal rupture Rheumatoid disease Tubercular pleuri s Malignancy Hemothorax SLE Tests for diagnosing tubercular pleural eﬀusion – Adenosine Deaminase (ADA) - >70U/L - Interferon Lysozyme Polymerase chain reac on CHYLOTHORAX – Thoracic duct is disrupted and chyle accumulates in pleural space When the lesion is above D5 level Le sided chylothorax occurs. When the lesion is below D5 level Right sided Causes – Trauma, Tumour – lymphoma, tuberculosis, LDM congenital absence of thoracic duct, yellow nail Syndrome Filariasis Chylous ﬂuid is milky and has a Triglyceride level >110mg/dl Pseudochylous – In chronic eﬀusion due to rheumatoid arthri s ﬂuid rich in cholesterol mimicking chyle accumulates. Treatment of choice for chylothorax Pleuroperitoneal shunt. Tube thoracostomy is contraindicated. HEMOTHORAX – Presence of blood in pleural cavity Causes – Trauma, Tumour, Recurrent pneumothorax PLEURAL EFFUSION IN AIDS – Causes Kaposi sarcoma Tuberculosis Lymphoma Parapneumonic eﬀusion Cryptococcosis CASES OF RIGHT SIDED EFFUSIONS – Fluid retaining states – CHF, CRF, Cirrhosis Amoebic liver abcess, subphrenic abcess Meig’s syndrome Thoracic duct involvement below D5 level. CUAES OF LEFT SIDED EFFUSIONS – Pancrea s Pericardial inﬂamma on Esophageal rupture. Le sided subdiaphragma c abcess Thoracic duct above D5 level CAUSES OF B/L EFFUSION – LHF, Pulmonary infarc on, Hypoalbuminemia, Malignancy HYPERSENSITIVITY PNEUMONITIS Disease An gen Source of an gen Bagassosis Thermophilic ac nomycetes “Moldy ‘ bagasse Bird fancier’s Parkeet, pigeon , chicken , (sugarcane) Breeder’s or handler’s turkey proteins Avian dropping or feathers lung Cephalosporium HP Contaminated basement (Sewage) Cephaosporium Cheese washer’s lung Penicillium casei Moldy cheese Chemical worker’s Isocyanates Polyurethane foam, Lung Varnishes , facquer Coﬀee worker’s lung Coﬀee bean dust Coﬀee beans Cornpost lung Aspergillus Compost Detergent worker’s Bacilius sub lis enzyme Detergent Disease (sub lisins) Familial HP Bacilius sub lis Contaminated wood dust in walls Farmer’s lung Thermophilic ac nomycetes “Moldy” hay, grain , silage a Fish food lung Unknown Fish food Fish meal wcrker’s lung Fish meal dust Fish meal Further lung Animal for dust Animal pelts Hot tub lung Clodosporium spp., Mold on ceiling mycobacterium ovium Contaminated water complex Humidiﬁer or air Aurebosidium pullulons, Contaminated water in Condi oner lung candida albicans, humidiﬁca on or forced air (ven la on Thermophilic air condi oning system pneumoni st) ac nomycetes, a mycobacterium spp., other Microgranism Japenese symmer-type Trichosporon cutaneum ; T. House dust bird HP Aschi and T. Cucoides Dropp rings Laboratory worker’s HP Male rat urine Laboratory rat Lycoperdonosis Lycoperdon pu alls Pu all spores Malt worker lung Aspergillus fumigates of A. Moldy barley Maple bark disease clavatus Maple bark Cryptostrome cor cale Metalworking ﬂuid lung Mycobacterium spp., Contaminated Miller’s lung pseudomomonas spp Metalworking ﬂuid Sitophilus granaries (wheat Infested wheat ﬂour Miscellaneous weevil) Medica on mecica on Amiodarone, bleomycin, efavirenz, gemcitabine, hydralazine hydroxyurea, isoriazid methotrexate pacilitaxel penicillin, Mushroom worker’s procarbazine, proparanolol , lung Mushroom compost ribuzole sirolimus Mushrooms Pituitary snuﬀ taker’s sulfasalazine lung Thermophilic ac nomycetes Heterologous pituitary snuﬀ a hypsizygus marmoreus bunoshimeji and other exo c mushrooms Animal protein Potato riddler’s lung Thermophilic ac nomycetes “Moldy” hay around , a Aspergillus potatoes Sauna taker’s lung Aureobasidium spp., other Sausage worker’s lung Penicillium nolgiovense Contaminated sauna water Dry sausage mold Sequuoiosis Aureobasidium graphium Redwood sawdust spp Streptomyces albus HP Streptomyces albus Contaminated fer lizer Suberosis Penicilium glabrum and Cork dust chrysonilia sitophila Tap water lung Mycobacteria spp. Contaminated tap water Thatched roof disease Saccharomonospora viridis Dried grasses and leaves Tobacco worker’s Aspergilius spp Mold on tobacco disease Winegrower’s lung Botry s cinerea Mold on grapes Wood trimmer’s disease Rhizopus spp , mucor spp Contaminated wood Trimmings Woodman’s disease Penicillium spp Oak and maple trees Woodworker’s lung Wood dust, altemaria Oak , cedar, pine , and maphogany dusts DIAGNOSTIC CRITERIA FOR ABPA Main diagnos c criteria Pulmonary inﬁltrates Peripheral eosinophillia (> 1000/ L) Immediate wheal – and ﬂare response to aspergilius fumfgatus Serum precipi ns to A. fumigates Elaveted serum IgE Central bronchiectasis Other diagnos c feature History of brownish plugs in serum Calculate of A fumigates from sputum Elevated IgE ( and IgC class an bodies speciﬁc for A fumigates SARCOIDOSIS Sarcoidosis is an inﬂammatory disease characterized by the presence of noncasea ng granulomas. The disease is o en mul system and requires the presence of involvement in two or more organs for a speciﬁc diagnosis. The ﬁnding of granulomas is not speciﬁc for sarcoidosis, and other condi ons known to cause granulomas must be ruled out. These condi ons include mycobacterial and fungal infec ons, malignancy, and environmental agents such as beryllium. While sarcoidosis can aﬀect virtually every organ of the body, the lung is most commonly aﬀected. Other organs commonly aﬀected are the liver, skin, and eye. Lung involvement occurs in >90% of sarcoidosis pa ents. The most commonly used method for detec ng lung disease is s ll the chest roentgenogram. The peribronchial thickening seen on CT scan seems to explain the high yield of granulomas from bronchial biopsies performed for diagnosis. While the CT scan is more sensi ve, the standard scoring system described by Scadding in 1961 for chest roentgenograms remains the preferred method of characterizing the chest involvement. Stage 1 is hilar adenopathy alone , o en with right paratracheal involvement. Stage 2 is a combina on of adenopathy plus inﬁltrates, Stage 3 reveals inﬁltrates alone. Stage 4 consists of ﬁbrosis. Usually the inﬁltrates in sarcoidosis are predominantly an upper lobe process. Only in a few noninfec ous diseases is an upper lobe predominance noted. In addi on to sarcoidosis, the diﬀeren al diagnosis of upper lobe disease includes hypersensi vity pneumoni s, silicosis, and Langerhans cell his ocytosis. For infec ous diseases, tuberculosis and Pneumocys s pneumonia can o en present as upper lobe diseases. The diﬀusion of carbon monoxide (DLCO) is the most sensi ve test for an inters al lung disease. Reduced lung volumes are a reﬂec on of the restric ve lung disease seen in sarcoidosis. Approximately one-half of sarcoidosis pa ents present with obstruc ve disease, reﬂected by a reduced ra o of forced vital capacity expired in one second (FEV1/FVC). Cough is a very common symptom. Airway involvement causing varying degrees of obstruc on underlies the cough in most sarcoidosis pa ents. Airway hyperreac vity as determined by methacholine challenge will be posi ve in some of these pa ents. A few pa ents with cough will respond to tradi onal bronchodilators as the only form of treatment. In some cases, high-dose inhaled glucocor coids alone are useful. Serum levels of angiotensin-conver ng enzyme (ACE) can be helpful in the diagnosis of sarcoidosis. However, the test has somewhat low sensi vity and speciﬁcity. Elevated levels of ACE are reported in 60% of pa ents with acute disease and only 20% of pa ents with chronic disease. Although there are several causes for mild eleva on of ACE, including diabetes, eleva ons of >50% of the upper limit of normal are seen in only a few condi ons including sarcoidosis, leprosy, Gaucher's disease, hyperthyroidism, and disseminated granulomatous infec ons such as miliary tuberculosis. CARDIOVASCULAR SYSTEM New York Heart Assoica on: Grading for dyspnea, palpita on, fa gue and angina in pa ents with cardiovascular disease. I. No symptoms with ordinary physical ac vity II. Symptoms with ordinary ac vity, slightly limita on of physical ac vity III. Symptoms with less than ordinary ac vity marked limita on IV. Symptoms with any physical ac vity or even at rest CYANOSIS: Bluish discolora on of skin and mucus membrane due to quan ty of reduced hemoglobin or hemoglobin deriva ves.The levels above which cyanosis becomes apparent are: Reduced Hb >5 gm % Methemoglobin > 1.5 gm % Sul emoglobin >0.5 gm % Intermi ent cyanosis is seen in Ebstein anomaly. Diﬀeren al cyanosis Cyanosis only Lower Limbs - PDA with PAH with reversal of shunt Cyanosis only Upper Limbs –PDA with PAH with TGA with reversal Cyanosis only L.U.L and B/L L.L. – Patent ductus opens proximal to origin of le subclavian artery with reversal of shunt. IMPORTANT ASPECTS OF BLOOD PRESSURE MEASUREMENT: Orthosta c hypotension is deﬁned as fall in systolic pressure more than 20mmHg or diastolic pressure more than 10mmHg in response to assump on of upright posture from a supine posi on within 3 minutes. ARTERIAL PULSE: Is a waveform felt by the ﬁnger, produced by cardiac systole, which traverses the arterial tree in a peripheral direc on at a rate much faster than that of the blood column. Rate: Normal pulse rate is 60-100 /min Bradycardia Tachycardia < 60/min >100/min Physiological -Athlete Infants Sleep Emo on,exer on Pathological - Hypothermia Tachyarrhythemia Sick sinus syndrome Anaemia, pyrexia Myxedema Beriberi, thyrotoxicosis Obstruc ve jaundice Ant wall MI ↑ ICT Hypotension b blockers, CCB Atropine, Salbutamol Inferior wall MI Rhythm: Best assessed in peripheral artery- Radial Regular irregular- Bigemini, trigemini Irregular irregular- Atrial/ ventricular ectopics, AF Volume: Best assessed in caro d artery, determined by pulse volume. (N) volume is 30-60 mm Hg pulse pressure. Character: Best assessed in caro d artery. a. Hypokine c pulse (low volume) * LVF, MS, Hypovolemia, AS b. Hyperkine c: Pulse (large volume and wide pulse pressure * Anaemia, beriberi, MR, VSD, AR c. Pulsus parvus et tardus : (slow rising and low peak) * Severe valvular AS d. Bisferiens : (2 peaks in sytole)- Radial/ brachial is assessed * severe AR, AR c AS, HOCM e. Dicro c: Pulse (1 peak in systole and other in diastole) * DCM, LVF f. Pulsus alternans: (regular alterna on of amplitude with regular rhythm) * Severe LVF, paroxysmal tachycardia, following premature beat g. Pulsus bigeminy : (regular alterna on of amplitude with irregular rhythm) * Digitalis toxicity h. Pulsus paradoxus: exaggerated reduc on in the strength of the arterial pulse during normal inspira on (N) is < 10 mm Hg systolic pressure. * Pericardial tamponade * Severe COPD/ Asthma * SVC obstruc on * Constric ve pericardi s (16 cm H2O) 8. Posi ve hepatojugular reﬂex 9. Circula on me ≥ 25 s 10. Weight loss ≥4.5 kg in 5d treatment Minor criteria: 1. Extremity edema 2. Night cough 3. Dyspnea on exer on 4. Hepatomegaly 5. Pleural eﬀusion 6. Vital capacity reduced by 1/32 from normal 7. Tachycardia (≥120 bpm) Clinical diagnosis of CHF is established when: 1. 2 major or 2. 1 major + 2 minor criteria are present Cardiogenic Pulmonary Non cardiogenic pulmonary edema edema Acute coronary event + - Cardiac output state Low ﬂow High ﬂow S3 gallop + - JVP (N) Crackles Wet Dry Underlying non-cardiac - + disease Ecg Ischaemia (N) CXR Perihilar Peripheral Cardiac enzymes (N) Pulmonary capillary > 18 mm 0.7 X-RAYS FINDING: (N) PVP < 10 mm Hg , (N) PAP < 15 mm Hg PAH when PAP > 50 mm Hg 10-15 mm Hg Early division (dilata on of upper lobe veins) 15-20 mm Hg Diversion (basal pulmonary veins narrowed and vein diameter > 3 mm in 1st intercostal space 20-25 mm Hg Diversion and inters al edema (kerley B and A lines) 25-35 mm Hg Intraalveolar edema (posi ve bronchogram) Treatment: 1. General therapeu c measure: a. Restrict salt intake to < 3 gm/d b. Recommend regular, moderate exercise c. Avoid an arrhythmic agents for asymptoma c arrhythmias d. Avoid NSAIDS as they are generally sodium salts. e. Provide inﬂuenzal and pneumococcal immuniza on 2. Diure cs: a. Administra on diure cs to all pa ents with heart failure and ﬂuid accumula on b. Weight daily to select / adjust dose c. Treat diure c resistance by: i. I/V administra on ii. Use diure cs in combina on (furosemide + metolazone) d. Administer short term dopamine to enhance renal blood ﬂow 3. ACE inhibitors: a. To be given to all pts c LV systolic failure and LV dysfunc on without heart failure: b. contra-indica ons of ACE inhibitors are: i. High output angioedema ii. Pregnancy iii. Hypotension iv. S crea nine > 3 mg/dl v. S. Potassium > 5.5 mmol/l vi. B/L renal artery stenosis 4. β adrenergic blockers: a. Administra on to all NYHA class II or III Pts with systolic HF, o en together with ACE I and diure cs b. Contra- indica ons: i. Broncho spas c disease ii. Symptoma c bradycardia or advanced heart block. iii. Mental Instability 5. Digoxin: Use in pts c LV systolic HF along with diure cs, aCEI, b blockers, esp useful in pts with AF and fast ventricular rate. 6. Other measures a. Spironolactone in pts with class IV symptoms b. ARB in pts who don’t tolerate ACEi c. Hydralazine- isosor de combina on in Pts who don’t tolerate ACEi. d. Avoid CCB for t/t of HF DRUGS TO DECREASE PRELOAD: Nitrates, Diure cs DRUGS TO INCREASE PUMPING: Digoxin DRUGS TO DECREASE AFTERLOAD: ACE inhibitors RHEUMATIC FEVER Acute, recurrent inﬂammatory disease. E ology agent is Group A b hemoly c streptococcus. (serotypes of b hemoly c streptococcus are M types- 1,3,5,6,14,18,24,27,29) 3% of individual with untreated group A streptococcus pharyngi s will develop rheuma c fever. Peak incidence is between 5-15 yrs but may occur as late as 4th decade. Recurrence of rheuma c fever in previous rheuma c fever is 50% Rheuma c fever has an average course of 6-12 wks. CRP tends to normalise earlier than ESR. Evidence of antecedent streptococcus infec on by history of recent a ack of scarlet fever is best clinical indica on of recent streptococcus infec on. Infec on of Pharynx and tonsils (not of the skin) An genic mimicry. a. Group speciﬁc carbohydrate of group A streptococcus and the glycoprotein of heart valves. b. Streptococcus cell membrane, streptococcal M protein sarcolemma and other moie es of human myocardial cell. 2002–2003 WORLD HEALTH ORGANIZATION CRITERIA FOR THE DIAGNOSIS OF RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE (BASED ON THE 1992 REVISED JONES CRITERIA) Diagnos c Categories Criteria Primary episode of rheuma c fever Two major or one major and two minor manifesta on plus evidence of preceding group A streptococcus infec on Recurrent a ack of rheuma c- fever in a pa ent Two major or one major and two without established rheuma c heart disease minor manifesta on plus evidence of preceding group A streptococcal infec on Recurrent a ack rheuma c fever in a pa ent Two minor manifesta on plus with established rheuma c heart disease evidence of preceding group A streptococcal infec on Rheuma c chorea insidious onset rheuma c Other major manifesta on or cardi sb evidence of group a streptococcal infec on not required Chronic valve lesion of rheuma c heart disease Do not require any other criteria (pa ents presen ng for the ﬁrst me with the to be diagnosed as having pure mitral stenosis or mixed mitral valve disease rheuma c heart disease and / or valve disease )d Major manifesta on Cardi s Polyarthri s Chorea Erythema marginatum Subcutaneous nodules Minor manifesta on Clinical fever , polyarthralgia Laboratory elevated erythrocyte sedimenta on Rate of leukocyte count e Electrocardiogram prolonged P-R interval Suppor ng evidence of a preceding Elevated or rising an - streptococcal infec on within the last 45 days streptolysin O or other streptococcal an body ,or A posi ve throat culture, or Rapid an gen test for group A streptococcus , or Rapid scarlet fevere 1. Cardi s: Pancardi s- Pericardium, myocardium & endocardium 40-60% cases Most speciﬁc criteria Characterized by any one or more: a. Sinus tachycardia b. Murmur of MR c. S3 gallop d. Pericardial fric on rub e. Cardiomegaly Develops within 2 wks of RHEUMATIC FEVER MV alone (40-50%), AV alone (15-20%), both valves (35-40%) MV, AV & TV in 2-3% cases involvement. Rheuma c pericardi s causes serous eﬀusion, ﬁbrin deposits and pericardial calciﬁca on but it doesn’t leads to constric ve pericardi s. 2. Migratory Polyarthri s: Most common criteria (75%) Large joints involved – ankle, wrist, knee, elbow No residual joint deformity In untreated case, it last for 4 wks Improves with in 48 hrs of star ng treatment OTHER CAUSES OF MIGRATORY POLYARTHRITIS: 1. Meningococcemia 2. Gonococcemia 3. Whipple’s disease 4. Hypercholesterolemia 5. Ulcera ve coli s 6. Sarcoidosis 3. Subcutaneous Nodules: Rare in ini al a ack Usually seen in long standing rheuma c heart disease (3-5%) Nodules are found over extensor surface of joints, skin, occiput and spine Non tender Pa ent having subcutaneous nodules always has cardi s 4. Sydenham’s chorea: Late manifesta on of RF Seem on < 10% pts Neurological disorder with rapid, involuntary, purposeless, non- repe ve movements Self limi ng over a period of 2-6 wks Females are most commonly aﬀected 5. Erythema Marginatum: Rare ( 240 Todds (adults) > 320 (children) 2. An DNAse B test is 2nd test to be done > 120 todds (adults) > 240 todds (children) 3. Streptozyme test, An hyaluronidase tests are also used. 4. Used three tests, 95% cases can be detected. FOR ESTABLISHING DIAGNOSIS: Two major criteria Essen al criteria + or 1 major + 2 minor criteria Excep ons to Jones criteria are; 1. Sydenham’s chorea 2. Indolent/ insidious/ late onset cardi s 3. Rheuma c recurrence Treatment – Primary: 1. An streptococcal an bio cs therapy a. Oral pencillin V 500 mg BD for 10 d, or b. Tab erythromycin 250 mg QID for 10 d, or c. Inj Benzathine penicillin 1.2 MV deep 1/m single dose ATD 2. Clinical manifesta ons of disease therapy a. Arthri s – Aspirin 75-100 mg/kg/d for 4-6 wks b. Severe cardi s (c CHF)- Prednisolone 30 mg QID then tapered. Secondary: Benzathine penicillin 1.2 MV deep 1/M every 3 wks or Oral penicillin V 250 mg BD or T. Sulfadiazine 1 gm/d or T. Erythromycin 250 mg / BD Category of pa ent Dura on of Prophylaxis Rheuma c fever without cardi s For 5 year a er the last a ack of 21 year of age (whichever is longer ) Rheuma c fever with cardi s but no For 10 year a er the last a ack or 21 year residual valvular disease age (whichever is longer ) Rheuma c fever with persistent For 10 year a er the last a ack, or 40 year valvular disease , evident clinically or of age (whichever is longer) some mes on echocardiography lifelong prophylaxis VALVULAR HEART DISEASE: MITRAL STENOSIS; (N) mitral valve (MV) size is 4-6 cm2 More common in females Causes: a. Rheuma c heart disease (RHD) b. Carcinoid, SLE, RA, fabry’s disease c. Congenital d. Methysergide, Amyloidosis e. Lutembacher syndrome ( congenital ASD+ acquired MS) PATHOPHYSIOLOGY MS : LA pressure pulmonary venous and pulmonary arterial wedge pressure increase pulmonary artery hypertension Causes of PAH: 1. Passive backward transmission of the elevated LA Pressure 2. Pulmonary arteriolar constric on due to LA and pulmonary venous hypertension i.e. reac ve pulmonary hypertension 3. Inters al edema in the walls of the small pulmonary vessels. 4. Organic oblitera ve changes in the pulmonary vascular beds Causes of LV dysfunc on: 1. Prolonged reduc on of preload 2. Extension of scarring from the valve into the adjacent myocardium CLINICAL FEATURES: Symptoms : a. Dyspnea: Due to pulmonary compliance Mitral valve area Symptoms < 2.5 cm2 None 1.5-2.5 cm2 Dyspnea on exer on 1-1.5 cm2 PND 15 mm Hg S1 in MS – Loud So in mild MS, calciﬁed valve, associated MR, AR, AF, CHF LAB INVESTIGATION ECG- P mitrale, AF, RAD, RVH CXR- Straightening of le heart border, double atrial shadow prominence of main pulmonary artery, features of CHF Echo- TTE/TEE to look for gradient, size, severity, leaﬂet thickness, mobility, calciﬁca on, suitability for BMV. TREATMENT: Medical : 1. Management of CHF (diet, diure cs, vasodilators, digitalis) 2. Managment of AF 3. Rheuma c fever prophylaxis 4. Infec ve endocardi s prophylaxis Surgical : 4 types of surgery 1. Percutaneous balloon valvuloplasty- criteria for valvuloplasty are: a. Isolated MS b. Signiﬁcant symptoms c. LA free of thrombus Inoue balloon is used for BMV. 2. Closed mitral valvotomy – when BMV unavailable 3. Open mitral valvotomy- In addi on to opening the valve commissaries, any subvalvular fusion of papillary muscles and chordae tendinae are loosened and calcium deposits are also removed. 4. Mitral valve replacement (MVR) in; a. Associated MR b. Valve is deformed by previous opera ve manipula ons c. Symptoma c –III, IV TYPES OF PROSTHETIC VALVES: a. Mechanical – Life long an coagula on is indicated in pt receiving mechanical prosthesis but its life is more than bioprosthe c valve. Preferred in young. b. Bioprosthesis- Older pts, where an coagula on C/I, pregnancy as risk of teratogenicity by an coagula on. APPROACH ADVANTAGES DISADVANTAGES Closed Inexpensive No direct visualiza on of valve surgical Rela vely simple Only feasible with ﬂexible valvotomy Good hemodynamic results in noncalciﬁed valves Contraindicated if selected pa ents MR > 2+ Good long- term outcome Surgical procedure with general anesthesia Open Visualiza on of valve allows Best results with ﬂexible, surgical direc ed valvotomy noncalciﬁed valves valvotomy Concurrent annuloplasty for Surgical procedure with general MR is feasible anesthesia Valve Feasible in all pa ents Surgical procedure with general replacement regardless of extent of valve anesthesia Eﬀect of loss of annular calciﬁca on of severity of MR papillary muscle con nuity on LV func on Prosthe c valve Chronic an coagula on Balloon Percutaneous approach No direct visualiza on of valve only mitral Local anesthesia feasible with ﬂexible noncalciﬁed valvotomy Good hemodynamic result in valves contraindica on if MR > 2 + selected pa ents Good long term outcome MITRAL REGURGITATION: More common in males Causes: Acute MR Chronic MR IE Rheuma c Ac. MI Congenital Trauma IHD, MVP Ac. RF Degenera ve Myocardial abscess CMP LA myxoma Amyolidosis CTD- Marfan, SLE, RA PATHOPHYSIOLOGY: Acute MR:- There is normal/ reduced compliance of LA leading to marked in a LA pressure pulmonary edema. Chronic MR: Increase in LA compliance normal/only slightly elevated LA pressure Co. CLINICAL FEATURES: Symptoms: Dyspnea on exer on, orthopnea, PND in acute MR, fa gue, exhau on, exer onal dyspnea in chronic MR Signs: (N) pulse c sharp upstroke JVP – (N) large a in PAH Prominent V in TR Apex beat- out & hyperdynamic PSH +VE S1 so , P2 loud S2 wide variable split Systolic thrill +ve S3 in severe MR, S4 in acute MR PSM at apex in MR, blowing in character, radia ng to axilla Damage to anterior leaﬂet- murmur radiates posteriorly. Damage to posterior leaﬂet- murmur radiates anteriorly. SEVERITY BY a. Systolic thrill, PSH b. Displaced apex c. Presence of s3, widely split s–2 d. Flow MDM across non-steno c MV LAB INVESTIGATIONS: ECG – P mitrale, LVH, AF CXR- Cardiomegaly (LV type), CHF Echo- Doppler shows regurgita on, LA size COMPLICATIONS: 1. AF: More common in MS than in MR. 2. IE: More common in MR than in MS SURGICAL TREATMENT: 1. Mitral valvuloplasty and/or mitral annuloplasty in: a. Severe annular dilata on b. Flail leaﬂets c. IE d. MVP e. Ruptured chorda 2. Mitral valve replacement; a. Severe, symptoma c MR b. Asymptoma c MR c LV dysfunc on LVEF < 60% AORTIC STENOSIS (N) aor c valve area in 3-4 cm2 More common in males CAUSES: Congenital AS Supravalvular Valvular – biscupid (most common) Subvalvular Rheuma c AS Degenera ve/ senile/ sclerocalciﬁc AS- M.C. in America Atherosclero c AS PATHOPHYSIOLOGY: Obstruc on to LV ou low LVH (concentric) C.O. rises at rest but fails to rise normally during exercise LVH O2 demand & CBF ischaemia Calciﬁc aor c stenosis is seen in: a. Paget’s disease b. End stage renal disease c. Rheumatoid involvement d. Ochronosis with alkaptonuria CLINICAL FEATURES Natural History of AS Angina – O2 demand, compression of coronary arteries, coronary embolisa on. (5 yrs) Syncope- ﬁxed C.O., fall in C.O. during arrhythmia, CBF (3 yrs) Cardiac failure - C.O (2 yrs) Signs 1. Pulsus parvus et tardus 2. (N) BP, SBP > 200 mm – excludes AS 3. JVP- a wave prominent when LVH + 4. Heaving apex beat 5. Caro d thrill 6. Paradoxical S2 split 7. S4 +ve (LVH) 8. S3 in late stages (when LV dilates) 9. Ejec on systolic murmur- in 2nd RICS, transmi ed to caro d artery and or apex Severity of AS 1. Reverse spli ng of S2 2. Valve area 50 mm Hg Silent AS in a. CCF b. MS c AS LAB INVESTIGATION ECG- LVH, LBBB CXR- Post steno c dila on of ascending aorta in valvular AS calciﬁca on of AV COMPLICATIONS – LVF, CHB, arrhythmia, IE TREATMENT Medical- Mx of CHF, RF, IE, angina Surgical: 1. Valve replacement; Severe as (systolic gradient >50 mm) LV dysfn 2. Percutaneous balloon aor c valvuloplasty- in children a. Young adults c congenital nn calciﬁc As b. Poor surgical risk pts- as a bridge to opera on 3. Simple commissural incision- under direct vision is done in children/adolescent c non calciﬁc congenital AS AORTIC REGURGITATION: Pure AR – males, associated with MV – females Causes: Aor c valve disease Aor c root disease Rheuma c Degenera ve I.E. Cys c medial necrosis Trauma Marfan Congenitally- bicuspid Aor c dissec on Large VSD Osteogenesis imperfecta Associated c RA, AS Syphili c aro s whipple, crohn Takayasu’s disease PATHOPHYSIOLOGY: Total stroke volume (eﬀec ve SV + volume regurgitate) such that eﬀec ve forward C.O. is normal LV dilata on LV dysfunc on C.O. ini ally on exer on and later at rest LV, LA pressure RV pressure. Myocardial ischaemia due to myocardial O2 demand as a result of both LV dilata on and elevated LV systolic tension and also because of marked in diastolic blood pressure when major por on of coronary blood ﬂow occurs. CLINICAL FEATURES Symptoms – Asymptoma c for long dura on 10-15 yrs 1. Palpita ons- earliest symptoms 2. Exer onal dyspnea- Next symptom – 1st symptom of diminished cardiac reserve. 3. PND, Orthopnea 4. Angina – nocturnal, reduc on in diastolic pressure at night accumula on SIGNS: signs of wide pulse pressure: Lighthouse sign: Alternate ﬂushing and blanching of forehead Landolﬁ’s sign: Change in papillary size c cardiac cycle Becker’s sign: Re nal artery pulsa ons (fundus) Muller’s sign: Pulsa ons of uvula De musset’s sign: Head pulsa on Corrigans’s sign: Dancing caro ds Quincke’s sign: Capllary pulsa ons on nail bed/lips Locomotor branchi: Muscle knock Collapsing pulse: Water hammer pulse Bisferiens pulse: Traube sign: Pistol shot heard in femoral A Duroziez sign: Systolic murmur heard over femoral A. when it is compressed proximally and diastolic murmur when compressed distally. Duroziez murmur: Diastolic murmur of femoral A Hill sign: Diﬀerence of SBP b/w UL/LL Mild AR 20-40 mm Hg Moderate AR 40-60 mmHg Severe AR > 60 mmHg Rosenthal sign: Pulsa on of liver Gerhardt’s sign: Pulsa on of enlarged spleen. Apical impulse is displaced laterally and hyperdynamic Diastolic thrill at apex + Systolic thrill at caro d A + S1 so A2 absent S3 S4 +ve Early diastolic murmur – high pitched blowing, 3rd ICS along le sternal border, best heard in forward bending posi on. Mid systolic ejec on murmur heard best at base of heart and transmi ed along caro d Vs. it is because of func onal AS. Aus n ﬂint murmur is so , low pitched, mid diastolic murmur heard at apex. Produced by the displacement of anterior leaﬂet of mitral valve by AR stream. Severity 1. Dura on of diastolic murmur 2. Bisferiens pulse 3. Hill sign (> 60 mm) 4. Apical impulse displacement 5. Marked peripheral signs 6. S1 so , S2 single, S3– LAB INVESTIGATIONS ECG- LVH CXR- Cardiomegaly (LV type) – Cor bovium TREATMENT: Medical – Mx of CHF, AF, RF, IE Surgical A er onset of LV dysfunc on –55/55 rule LVEF < 55% LV end systolic volume > 55 ml/m2, then Valve replacement is indicated. Valve repair in case of perfora on of leaﬂet by Infec ve endocardi s process. INFECTIVE ENDOCARDITIS Deﬁni on: Infec ve Endocardi s is a microbial infec on of the endothelial surface of the heart. The characteris c lesion, vegeta on, is a variably sized amorphous mass of platelets and ﬁbrin in which abundant micro organisms and scant inﬂammatory cells are enmeshed. SITES OF INFECTIVE ENDOCARDITIS: 1. Heart valves (MC) 2. Septal defect 3. On chordae tendineae 4. Mural endocardium 5. Intracardiac devices ENDARTERITIS: Infec on of arteriovenous shunts, arterioarterial shunts (Patent ductus arteriosus) or coarcta on of aorta is known as endarteri s. It is clinically & pathologically similar to Infec ve Endocardi s. TYPES: Acute: a. Pt more toxic, febrile b. Involving (N) valve c. Rapidly damages cardiac structures d. Hematogenous spread to extracardiac sites more common –metasta c infec on e. Caused by virulent organisms – Staphyloccus aureus Subacute: a. Indolent course b. Involves already damaged valve c. Metastas c infec on – uncommon d. Caused by less virulent organism – Streptococcus viridans, enterococci, coagulase –ve staphylococcus ETIOLOGY: Na ve valve endocardi s 1. Streptococci a. Viridans : 30-40 % b. Enterococci: 10-15% c. Other: 20-25 % 2. Staphylococci a. Aureus : 9-27% b. Coagulase –ve: 1-3% 3. Gram-ve bacilli 4. Haemophilus total 3-8% 5. Anaerobes HACEK organism (Haemophilus, ac nobacillus, cardiobacterium, Eickenella and kingella) also caused SABE with large vegeta ons Prosthe c valve endocardi s: Within 2 months – Coagulase –ve staphylococcus A er 2 months – streptococci 1. Predominantly males over 60 yrs 2. Aor c valve more commonly involved 3. Suture line involved Endocardi s in intravenous drug absusers: Right side (MC)site 1. Staph aureus(MC) 2. Pseudomonas 3. Candida 4. Polymicrobial infec on Culture –ve endocardi s: 1. Prior an bio c use 2. Pyridoxal required streptococci (Abiotrophia) 3. HACEK group of organisms 4. Bartonella 5. Tropheryma whippeli (Whipple’s disease) 6. Libmann sack Endocardi s 7. Maran c Endocardi s Predisposing condi ons: RHD- Rheuma c heart disease CHD- Congenital heart disease MVP- Mitral Valve Prolapse DHD- Degenera ve heart disease Parenteral drug abuse Clinical features: Symptoms Signs Fever 50-85% Fever 80-90% Chills 42-75% Murmur 80-85% Sweats 25% Changing/new murmur 10-45% Anorexia 25-55% Neurological abnormality 30-40% Weight loss 25-35% Embolic event 20-40% Malasie 25-40% Spleenomegaly 15-50% Dyspnea 20-40% Clubbing 10-20% Cough 20% Osler nodes 7-10% Stroke 13-20% Splinter hemorrhage 5-15% Headache 15-40% Petechiae 10-40% Nausea/ vomi ng 15-205 Janeway lesions 6-10% Chest pain 8-35% Roth spots 4-10% Confusion 10-20% PERIPHERAL SIGNS in Infec ve Endocardi s. Osler nodes: Small tender nodules over ﬁnger, toe pads, soles Janeway lesions: 1-4 mm non tender erythematous macules over palms, soles Petechiae : Over conjunc vae, palate, buccal mucosa & upper extremi es Clubbing: Seen in long standing cases Roth spots: Oval re nal haemorrhage c pale centre. Also seen in CTD, aneamia Splinter haemorrhages: Subungal, linear, dark streaks that may appear in endocardi s. Criteria for diagnosis of Infec ve Endocardi s: MAJOR CRITERIA MINOR CRITERIA DEFINITE INFECTIVE ENDOCARDITIS: Two major criteria, or 1 major + 3 minor criteria or ﬁve minor criteria TREATMENT: An bio c treatment for Infec ve Endocardi s caused by common organisms Organism Drug, Dose, Comments Dura on Streptococci Penicillin G 2-3 Avoid penicillin plus gentamicin if risk of Penicillin – million units IV aminoglycoside toxicity are increased or suscep ble q4h for 4 weeks case is complicated streptococci, s.bovis Penicillin G 2-3 Can use ce riaxone in pa ents with million units IV nonimmediate penicillin allergy q4th plus gentamycin Use vancomycin in pa ents with severe 1mg/kg IM or IV or immediate b lactam allergy q8h, both for 2 weeks Ce riaxone 2 g/d IV as single dose for 4 weeks Vancomycin 15mg/kg IV q 12 h for 4 weeks Rela vely penicillin- Penicillin G 3 Preferred for treatment of prosthe c resistant streptococci million units IV valve endocardi s caused by penicillin- q4th for 4-6 wks suscep ble streptococci; con nue plus gentamicin penicillin for 6 wks in this se ng 1mg/kg IV q8th for 2 wks Penicillin- Penicillin G 3-4 Can use streptomycin 7.5 mg/kg q 12h resistant/streptococci million units IV in lieu of gentamicin is not hight - leval pyridoxal – requirring q4h plus resistance to streptomycin streptococci gentamicin one (abiotrophia spp) mg/kg IV q8h, Do not use cephalosoporins or Enterococci both for 4-6 weeks carbapenems for treatment of enterococcal endocardits Penicillin G3-4 million units IV Use vancomycin plus gentamic for q4th plus penicillinallergic pa ents or desensi ze gentamicin one to penicilin mg/kg IV q8h, both for 4-6 weeks Ampicillin 2g IV q4h plus gentamicin 1 mg/kg IV q8th both for 4-6 weeks Vancomycin 15mg/kg IV q12th plus gentamicin 1 mg/kg IV q8h both for 4-6 weeks staphylococci Nafcillin or May use 3-4 million units q 6h if isolate Methicillin – oxacillin 2 g q4h is penicillin suscep ble (does not suscep ble infec ng for 4-6 weeks plus produce b- lactamase) na ve valves (no (op onal) foreign device) gentamicin 1 mg Can use cefazlion regimen for pa ents /kg IM or IV q8h with ninim medicate penicillin allergy for 3-5 days Use vancomycin for pa ent with Cefazolin 2 g IV q immediate (ur carial) or severe 8h for 4-6 weeks penicillin allergy plus gentamicinc 1 mg/kg IM or IV q 8h for 3-5 days Vancomycin 15 mg /kg IV q 12 h for 4- 6 weeks Methicillin- resistant Vancomycin 15 mg No role for rou ne use of rifampin infec ng na ve / kg IV q 12 for 4-6 valves(no foregin days device) Methicillin- Nacillin or oxacillin Use gentamicin in tal 2 weeks ; suscep ble, infec ng 2 g IV q 4 h for 6-8 determine suspec blity to gentamicin prosthe c valves weeks plus before ini a ng rifampin; if pa ent is gentamicin 1 mg highly allergic to penicillin ,use regimen /kg or IV q8h for for methicillin –resident staphy lococci; 2weeks plus if b- lactam allergy is of the minor, rifampin 300 mg nomidiate type., can subs tue efazolin po q8h for 6-8 for oxcillin /nafcillin weeks Methicillin resistant , Vancomycin 15 Use gentamicin during ini al 2 weeks infec ng prosthe c mg/ kg IV q 12 h 6- determine gentamicin susecp bilty valves 8 weeks plus before ini a ng rifampin gentamicin 1 mg/kg IM or IV q 8h for 2 weeks plus rifampin 300 mg PO q8h for 6-8 weeks INDICATIONS OF SURGERY: 1. Moderate to severe CHF (III or IV) due to valve dysfunc on 2. Unstable prosthesis 3. Uncontrolled infec on despite op mal an microbial therapy 4. Unavailable eﬀec ve an microbial treatment like in: a. Fungi b. Bruncellae c. Pseudomonas aeruginosa 5. Staphylococcus aureus prosthe c valve endocardi s 6. Large (> 10 mm diameter) hypermobile vegeta on 7. Culture nega ve NVE or PVE with persistent fever (≥ 10 d) PROPHYLAXIS: Cardiac condi ons when Infec ve Endocardi s prophylaxis not Recommended 1. ASD 2. CABG 3. MVP without MR 4. Cardiac pacemakers, implanted deﬁbrillators Other condi ons when Infec ve Endocardi s prophylaxis not recommended: 1. Dental procedures not causing bleeding 2. Et inser on 3. Bronchoscopy, UGIE (ﬂexible) 4. TEE 5. Caesarian sec on 6. Vaginal hysterectomy While: 1. Most dental procedures 2. Tonsillectomy 3. Bronchoscopy / UGIE( rigid) 4. Sclerotherapy 5. ERCP 6. Esophageal dilata on 7. Gall bladder surgery 8. Cystoscopy Infec ve Endocardi s prophylaxis by: Ampicillin 2mg i/v + Gentamycin 1.5 mg/kg within 30 min of procedure, repeat ampicillin 1gm i/v or give amoxicillin 1 gm PO 6 hrs later. CARDIOMYOPATHY Dilated Dila on and impaired contrac on of the le ventricle or both cardiomyopathy ventricles Caused by familyical-gene c viral immune alcoholic-toxic,or unknown factors or is associated with recognized cardiovascular disease Hypertrophic Le and/or right ventricular hypertrophy.o en asymmetric cardiomyopatyhy which usually involves the onterventricular septum Muta ons in sarcoplasmic proteins cause the disease in many pa ents Restric ve Res ctedd ﬁlling and reduced diastolic size of either ventricle cardiomyopathy or both ventricles with normal or near-normal systolic func on. Ldiopathic or associated with other disease (e.g.amyloidosis, endomycardial disease) Arrhythmogenic Progessive ﬁbrofa y replacement of theright.and to some right ventricular degreed the le.. ventricular myocardium cardiomyopathy Familial disease is common Unclassiﬁed Diseases that do not ﬁt reasily into any category examples cardiomyopathy include systolic dysfunc on with minimal dila on mitochondrial disease and ﬁbroelastosis. SPECIFIC CARDIOMYOPATHIES Ischemic Arises as dilated cardiomyopathy with depressed ventricular cardiomyopathy func on not explained Valvular Aries as ventricular dysfunc on that is out of propora on to the Cardiomyopathy abnormal loading condi ons producted by the valvular stenosis and/or regurgi on. Hypertensive Aries with le ventricular hypertrophy with features of cardiac Cardiomyopathy failure related to systolic or diastolic dysfunc on Inﬂammatory Cardiac dysfunc on as a consequence of myocardi s. Cardiomyopathy Matabolic Includes a wide variety of causes including endocrine Cardiomyopathy abnormali es glycogen disease deﬁciencies (such as hypokalemia) and nutri onal disorders. General Includes Duchenne, Becket-type and myotonic dystrophies systemic disease Mascular Includes duchenne Backer ype and myotonic dystrophies dystrophies Neuromuscular Includes friedreich ataxia Noonan syndrome and len ginosis discovered Sensi vity and Includes reac ons to alcohol catecholamines anthracyclines toxic reac ons irradia on and others Peripartum First becomes manifested in the peripartum period, but it is cardiomyopathy probably a heterogeneous group DILATED CARDIOMYOPATHY Cardiac enlargement & impaired systolic func on of one or both ventricles Reversible causes of DCM: a. Hypophosphatemia b. Hypocalcemia c. Uremia d. Hypothyroidism e. Hyperthyroidism f. Hemochromatosis g. Alcohol h. Arryhythmogenic i. HIV j. Pregnancy E ology: Familial gene c, viral, immune, alcohol, toxic T/t: as CHF 4 drugs (Digoxin, vasodilators, diure cs, diet) Surgical: Mitral annuloplasty Replacement of regurgitant valves Dynamic cardiomyopathy: Surgical transloca on of the la ssiumus dorsi muscle to wrap around heart. ALCOHOLIC CARDIOMYOPATHY: E ology: a. Direct toxic eﬀect of alcohol b. Nutri onal def- Thiamine Beri beri c. Toxins in alcohol -cobalt (foam stabilizer) Beri beri diﬀerent from Alcoholic CMP: 1. Peripheral vasodila on 2. High output C.F. right sided Holiday heart syndrome: Atrial Fibrilla on seen in pts (chronic alcoholic a er a binge) present as palpita ons, syncope, chest discomfort Hypokalemia may play a role. Arrhythmogenic right ven cular cardiomyopathy: Myocardial cell loss with par al or total replacement of RV muscles by adipose / ﬁbrous ssue; of apotosis. Associated c reentrant ven cular tachyarrhythmias of RV origin (predominantly LBBB) & of sudden death Treatment of arrhythmia – Sotalol / Amiodarone HYPERTROPHIC CARDIOMYOPATHY: In appropriate hypertrophy that occurred in the absence of an obvious cause of hypertrophy (AS/ HTN) Diastolic dysfunc on LVEDP Pulmonary conges on & dyspnea Dynamic ou low obstruc on : a. SAM: Systolic anterior mo on of MV b. ASH: Asymmetric septal hypertrophy Clinical features a. Dyspnea b. Angina c. Syncope d. Sudden death Causes of Angina in HOCM Despite (N) epicardial coronary artery 1. muscle mass 2. inadequate capillary density 3. diastolic ﬁlling pressure 4. Ab (N) intramural coronary A 5. Impaired vasodilatory reserve 6. Systolic compression 7. demand of Co2 HCM is harsh, crescendo decrecendo HCM AS Caro d pulse Brisk upstroke Pulsus parvus et tardus Murmur C valsolva (II, III) c Squa ng Thrill 4 IcS – L side 2 ICS – R side Murmur radia on to caro ds - + Echo: 1. Septum 1.3-1.5 X posterior wall in diastole 2. Narrowing of LV ou low tract Management : Treatment done generally of high risk group High risk group Sudden death, sustained VT Age < 30 yrs Massive LVH Adverse genotype Mul ple familial SD Presence of NSVT (non sustained VT) Treatment: 1. β Blockers 2. CCB 3. Amiodarone 4. Ethanol injec on– spetum 5. ICD 6. Morrow procedure - septal excision thransaro c root 7. MV Replacement Drugs avoided Digitalis Diure cs Nitrates Vasodilators β Adr. Agonists RESTRICTIVE CMP: Characterized by abnormal diastolic func on Causes: Amyloid, hemochromatosis, glycogen deposi on, endomyocardial ﬁbosis, sarcoidosis, Fabry’s disease, eosinophilias, scleroderma Clinical features: Exercise intolerance & dyspnea are most common (.. of inability of the ventricles to ﬁll limits cardiac output and raises ﬁlling pressures) Kussmaul sign is characteris c: Heart sounds: distant S3-S4 common Mitral regurgita on is common LAB INVESTIGATIONS: ECG: Low voltage, Av conduc on defects CXR: No pericardial calciﬁca on (seen in C.P) Echo: Symmetrically thickened le ventricular walls and normal or slightly reduced ventricular volumes and systolic func on. Characteris c granular sparkling texture on Echo in pts with amyloidosis TREATMENT: 1. Alkyla ng agents 2. Pacemaker 3. Anatolgons SCT- in primary (AC) amyloidosis 4. Cardiac / heart liver transplanta on Avoid: Digitalis, Nifedepine, Diure cs, Vasodilators. DILATED RESTRICTIVE HYPERTROPHIC 1. Symptoms CHF – le sided Dyspnea, fa gue Dyspnea, angina, Fa gue, Fa gue & weakness CHF-Right S/S of syncope, palpita ons systemic/pulmonary systemic dis emboli Amyloidosis, iron storage 2. C/E Moderate-severe Mild- moderate Mild cardiomegaly apical cardiomegaly s3/s4 cardiomegaly systolic thrill & haeve, Av (Mitral) s3/s4 kussmaul + brisk caro d upstroke s4 regurgita on (inspiratory in common systolic M on JVP) valsalva 3. CXR Cardiomegaly-Le Mild Mild PVH PVH LAE 4. ECG Sinus tachycardia Low voltage LVH A/v arrhythmia Intraventricular ST/T ab(N) ST/T ab(N) condi on defects Ab(N) q waves Av cond defects 5. Echo LV dilata on & LV thickness a. Asymmetrical septal dyspnea Ab(N) small LV cavity (N) hypertrophy(ASH) diastolic MV mo on sys fn. Diastolic b. Narrow ASH le vent. systolic dyspnea dysn. Ou low tract c. Systolic ant. Mo on (SAM) of mitral valve 6. Cardiac LV enlargement/ LV compliance LV compliance catheteriza on M/T regurgita on “Square root MR Lt/Rt sided ﬁlling sign” Vigourous sys. Fn pressure (N) sys. Fn Dysnamic LV ou low C.O Lf/Rt pressure Gradient MYOCARDITIS Cardiac inﬂamma on Caused by Microorganisms: a. Direct b. Toxins c. Immunologically mediated Viral (Most Common) Adenovirus Coxsackievirus, enterovirus Cytomegalovirus Parvovirus B19 Hepa s C virus Inﬂuenza virus Human immunodeﬁciency virus Herpesvirus Epstein-Barr virus Mixed infec ons Bacterical Mycobacterial species Chlamydia pneumonia Streptococcal species Mycoplasma pneumonia Treponema pallidum Fungal Aspergillus Candida Coccidioides Cryptococcus Histoplasma Protozoal Trypanosoma cruzi Parasi c Schistosomiasis Larva migrans Toxins Anthracyclines Cocaine Hypersensi vity Clozapine Sulfonamides Cephalosporins Penicillins Tricyclic an depressants Autoiommune Ac va on Smallpox vassina on Giaant cell myocardi s Churg-Stauss syndrome Sj?gren syndrome Infalmmatory bowel disease Celiac Disease Sarcoidosis Systemic lupus erythematosus Takayasu arteri s Wegener granulomatosis CLINICAL FEATURES: 1. Asymptoma c limited and focal fulminant CHF ie varied manifesta ons 2. Fa gue, dyspnea, palpita ons, precordial discomfort (& not pain) 3. Features of CHF - HR, S3,Apical systolic murmur(MR) LAB INVESTIGATION ECG – Tachycardia. ST, T changes, conductors blocks Echo:- LV dysfn (regional ), eﬀusion Radionuclide scanning – Gallium 67, Techne um –99 m pyrophosphate Endomyocardial biopsy: MANAGEMENT: 1. Bed rest 2. Mx of CHF- unusually sensi ve to digitalis 3. Cor costeroids are controverssial 4. High dose immunoglobulin- Rapid resolu on HIV Myocardi s: 1. MC ﬁnding LV dysfunc on 2. Causes: a. Inﬁltra on of myocardium by HIV itself b. Opportunis c infec on – Toxoplasmosis c. Cardiac metastases – kaposi sarcoma Bacterial myocardi s: 1. Staphylococcus, enterococci 2. Myocardial abscess may occur 3. Diphtheria myocardi s – may develop in pts of diphtheria (20%) – serious complica on- death secondary to CHF CHAGAS DISEASE: 1. Trypanosoma Cruzi- Causa ve organism 2. Reduviid bugs- vector 3. Most commn cause of heart disease in central & south america 4. Acute form – myocardi s 5. Chronic form- dilata on of chambers, ﬁbrous, thinning of ventricular wall, aneurysm forma on 6. ECG- RBBB, LAHB 7. Cause of death- CHF or arrhythmia 8. Emboli also occur ATHEROSCLEROSIS Involves both large & medium sized arteries Focal involvement Mechanism of atherosclerosis: 1. Accumula on of lipoprotein in in ma oxida on & glyca on 2. Adhesion of leucocytes 3. Penetra on of leucocytes- Monocyte chemoa ractant protein 1 (MCP- 1) 4. MCP-1 Scavanger receptors uptake of oxidized LDL macrocytes tranform into foam cells 5. Forma on of the ﬁbrous cap and lipid core Arteriosclerosis: 1. Concentric lesion 2. No lipid core 3. Diﬀuse narrowing Seen in: a. Restenosis a er PCI b. Accelerated atherosclerosis a er transplanta on Infec ons: Causing atherosclerosis: 1. CMV 2. C. Pneumoniae Novel atherosclerosis risk factors: 1. Homocysteine – Premature atherosclerosis, young MI, CRF 2. Lp(a) – Young MI 3. Fibrinogen 4. Markers of ﬁbrinoly c system- PAI-1, t-PA, clot lysis, D-dimer 5. Markers of inﬂamma on – hs CRP, ICAM-1, IL-6 hs CRP: (high sensi vity CRP) is single best predictor of future vascular thrombosis Risk Factors Dyslipidemia: a. 1°(Primary- gene c) b. 2°(Secondary)- causes like: * Hormonal Hypothyroidism : LDL, TG Estrogen : HDL, TG Androgen : TG GH : HDL, LDL (but not used therapeu cally) * Metabolic DM TG, HDL * Renal CRF TG, HDL GN, NS LDL * Liver PBC LPX (xanthoma forma on) Drugs: HIV therapy: Hypertriglyceridemia pancrea s & Atherosclerosis β blockers, thiazides, Cor costeroids LDL = Total Cholesterol – (TG/5 + HDL) (if TG < 400) TREATMENT: 1. Resins: Cholestyramine 9 g 2-6 mes/ d with meals Choles pol 5 g Cholesterol S/E – Gastrointes nal & TG 2. Sta ns: cholesterol S/E – Hepato toxicity, Myos s 3. Fibric A deriva ves: Gemﬁbrozil (600 mg BD) Finoﬁbrate, Ciproﬁbrate, Bezaﬁbrate TG 2° Prev. of CAD in pts c low HDL S/E – GI, cutaneous, Plasma homocysteine 4. Nico nic A: HDL, TG 300 mg/d S/E – Flushing, hyperuricemia, hyperglycemia, hepatotoxicity, acanthosis nigricans, gastri s Aspirin Niacin induced ﬂushing 5. Fish Oils: TG Monitoring 1. Smoking : risk of CAD, Anerurysmal form; PVD, Sudden death, Ischeamic stroke. CA-Lung, pancreas, stomach 2. HTN 3. D.M 4. Exercise 5. Obesity: BMI, waist/hip ra o 6. Mental stress 7. Estrogen status – HERS study showed no diﬀerence when estrogens were given postmenopausal. Risk Factors: Modiﬁable: a. Dyslipidemia b. HTN c. Smoking d. DM/insulin resistance e. Alcohol f. Obesity Non-modiﬁable: a. Age b. Sex c. Family H/O CAD d. male< 45 y e. female< 55 y MYOCARDIAL INFARCTION: Coronary plaques prone to rupture are those with a rich lipid core and a thin ﬁbrous cap. Causes: of MI in absence of coronary atherosclerosis 1. Arteri s – Leu c, TB, Takayasu, PAN, SLE, RA, AS 2. Congenital anomalies 3. Embolism, spasm 4. Trauma 5. AR, AS, CO poisoning 6. Hematological 7. Cocaine abuse Clinical Features of MI 1. Chest pain: Levine sign- pa ent depicts retrosternal chest pain by making a ﬁst. Pain of AMI may radiate as high as occipital area but not below umbilicus Painless AMI- in DM, Elderly 2. Sudden onset breathlessness. 3. Sudden loss of conciousness 4. Confusion 5. Profound weakness 6. Arrhythmia 7. Evidence of peripheral embolism 8. Unexplained drop in B.P Signs: Anterior MI- Symphathe c over ac vity Inferior MI- Parasympathe c over ac vity S4, S3 intensity of heart sounds, paradoxical spli ng of S2, Midsystolic murmur, pericardial fric on rub JVP, Temp upto 38°c Lab Δ Rise (hr) Peak (N) H FABP 1.5 5-10 hr 24 Myoglobin 1-4 6-7 hr 24 Myosin light chain 6-12 2-4 d 6-12 d Tn I 3-12 24h 5-10 d Tn T 3-12 12h-2d 5-14 d MB –ck 3-12 24h 48-72 h Enolase 6-10 24 h 48 h LDH 10 24-48 h 10-14 d Myolin heavy chain 48 5-6 d 14 d H FABP= Human fa y acid binding protein. CK- MB/CK > 2.5 (rela ve index ) speciﬁc CK- MB2/CK MB 1 > 2.5 (rela ve index ) speciﬁc & early iden ﬁca on CK- MB > 1.0 u/l ECG : leads helpful in diagnosing MI Anterior : V1-v6 Anterolateral : V5-6, I, aVL Anteroseptal : V3-4 Inferior : II, III, aVF Posterior : V7-V9 R.V. extension : RV4 (most speciﬁc), V1, RV2 STEMI: ST eleva on in 2 consecu ve leads NSTEMI: ST depression Recurrent ischemic discomfort is checked by ck-MB, myoglobin. Non-speciﬁc reac on to MI is by: 1. Leucocytosis 2. ESR Cardiac imaging – Echo TC 99m sestamibi scan Reveals a cold spot to an infarcted area MANAGEMENT: STEMI: Aspirin, b blockade, An thrombin therapy a. ≤ 12 hrs Eligible for thromboly c therapy * Thrombolysis a. Primary PCI- Gp II b/III a * Correct metabolic & electrolyte disorders, ACE i., nitrates b. ≥ 12 hrs Persistent symptoms Consider reperfusion therapy i.e. Aspirin, Sorbitrate, O2, Morphine, STK, Metoprolol, NTG, ± Heparin, Seda ve, laxa ve, An hypertensives Dose of ﬁbrinoly cs: STK : 1.5 MU/60 min Tpa : 100 mg/ 90 min 15 mg stat 50 mg in 30 min & then 35 mg in next 60 min rPA (reteplase) 2 *10 MU bolus, 30 min apart TNK – tpa (Tenecteplase) 0.5 mg/kg SAK- 20 -30 mg/ 30 min Choice of agent: 1. With in 4 hrs – Tenecteplase/ reteplase 2. 4-12 hrs (elderly) – STK 3. > 12 hrs in < 65 yrs – Thrombolysis 4. > 12 hrs in > 65 yrs- Primary PTCA 5. any me with shock – Primary PTCA Indica ons of diﬀerent drugs: 1. O2 – CHF, O2 sat < 90%, Rou ne to all (2-3 hrs) 2. I/v NTG- HTN, CHF, Ischaemia, Anterior MI (large) recurrent angina, persistent CHF 3. Aspirin – All 160-325 mg chew C/I – Clopidogrel 75 mg stat 4. Atropine: Sinus bradycardia, Ac inf. MI c type I, II block, if N,V a er Morphine, if hypotension a er NTG, ventricular asystole 5. Thromboly cs: ST eleva on (> 0.1 mv, 2 leads) < 12 hrs, < 75 yrs BBB + history s/o MI 6. Primary PTCA: Alterna ve to thromoly cs if done < 12 hrs onset ( in 90 min of admission) a. Within 36 hrs, who have cardiogenic shock b. C/I of thromboly c 7. CABG: a. Failed PTCA b. AMI refractory to medical therapy c. VSD/MR c MI d. Cardiogenic shock 8. GpIIb/IIIa: a. with primary PTCA b. NSTEM I c high risk and /or refractory ischaemia 9. Heparin ; a. PTCA/ CABG b. All NSTEMI c. In STEMI when thromboly cs not used d. In STEMI when alteplase used e. In STEMI when STK used associated c high risk (large, ant MI, AF, previous emboli, LV thrombus) 10. b blocker: a. All MI unless C/I: - HR < 60 - BP < 100

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