Respiratory Intensive 2021 PDF

Respiratory Intensive 2021 Investigations of respiratory system: Measurement of ventilator capacity of lung is (spirometer). *Tidal Volume: its volume of air that is inspired & expired during rest. *Forced vital capacity (FVC): its volume of air that can be forcefully ex...

Respiratory Intensive 2021 Investigations of respiratory system: Measurement of ventilator capacity of lung is (spirometer). *Tidal Volume: its volume of air that is inspired & expired during rest. *Forced vital capacity (FVC): its volume of air that can be forcefully expired after full inspiration. *Residual volume: its volume of air which remains in the lung after full expiration (hyper-inflated chest) +PEFM *Total Lung Capacity: its (VC + RV). *Functional residual capacity: its volume of air which remains in the lung after normal expiration. *Forced expiratory volume in 1st second (FEV1): its volumes of air which you can forcibly expire in 1st second. MCQ Normaly FEV1 / FVC X 100= 70-80%. But if pts has caugh … wheeze … or dypsnea then the type of respiratory disease is either: 1- Obstructive FEV1 / FVC (Normal) x 100 = < 70%. Asthma – Bronchiectasis -COPD 2- Restrictive  FEV1 /FVC X 100= 70-80%. Empysema To differentiate between them we can use Resting Transfer Factor (DLCO)= Chronic bronchitis Any other cause its increased in: 1-Obesity 2- B asthma 3- polycythemia its decreased in : 1-Empysema 2- ILD 3- Pulmonary vasculitis 4-hypovolemia 5-PE ABG analysis : Normal Values of ABG: *PH: 7.35-7.45. *Po2: 80-100mmHg.. *PCO2: 35-45mmHg. *HCO3: 22-28mmol/L. Uses : 1- respiratory failure 2- acid base balance To convert from pKa to mmHg ( *7.5) Respiratory Failure: Def: inadequate to maintain metabolic requirements of body of O2 with or without increasing of CO2. R.F I (due to ventilation perfusion Mismatch) R.F II (due to hypoventilation) -Hypoxia (Mild). -Hypoxia (sever). -CO2 (normal Or low due to compensatory -CO2 (High) hypercapnea,. hyperventilation). - in chronic type II Hco3 is also high MCQ C/P: due to of hypoxia  irritability, confusion -due to hypoxia & corpulmonal Reflex tachycardia / Dyspnea & central cyanosis. -hypercapnea ICP  headache & papilledema. Hyper dynamic circulation pounding pulse. palmar erythema & warm hand. Causes: *Respiratory center depression : -Narcotics, CVA, Brain stem lesion. Any other respiratory disease *Neuromuscular skeletal disease: -G.B.S, M.G, Muscle fatigue in life threating MCQ asthma, skeletal deformity. *Airway obstruction: -Chronic bronchitis, Late bronchiectasis, T pneumothorax, sleep apnea syndrome. Acute Type 2 RF: Co2 high >50mmhg 1-life threating asthma O2 low 28mmole (compensated) Rx: high concentration O2 given via poly mask -Low concentration O2 (24-28%) given via venture mask. - mechanical ventilation if Co2 > 60 mmHg - Acute cause = high o2 ACID BASE BALANCE: Causes of respiratory Causes of Metabolic Causes of respiratory Causes of Metabolic acidosis: acidosis: alkalosis: alkalosis: Same as RF type 2 Causes of metabolic 1-stress ,panic attacks A. pts dehydrated acidosis: 2-psychosis 1-Diarrea Anion gap = (K+Na) – 3-high attitude 2- burns Rx: (Hco3+ CL) 4-pyrexia 3-drugs (diuretics , normal = 8-16 Same as RF type 2 5-salcylates Carbonic anhydrase A. Normal anion gap Rx: inhibitors ) 1- Gastrointestinal base Rebreathing inside a bag MCQ loss (diarrhea , fistula) B. pts is volume 2-Renal tubular acidosis overload (RTA) 1- Cushing syndrome 3- poisoning with NH4Cl, Note: patient may & acetazolamide 2- Conns syndrome present with tetany as 3-drugs (steroids) Note : B. Increased anion gap * if the case is result of hypocalcemia 4- massive blood 1-Diabetic ketoacidosis compensated it means transfusion 2-Starvation ketosis chronic cause 3- Lactic acidosis * If the case is Rx: 4-Renal failure uncompensated it means If dehydrated -------- IV acute cause 5-Aspirin poisoning, fluids Methanol poisoning , Ethylene glycol poisoning If volume over loaded --- ---- acetazolamide or Rx: if PH > 7 ----- treat dialysis if failed cause only If PH < 7 ----- treat cause & give NaHco3 Home Work: 2017: Q1 to Q16 1001: 112 – 116 – 124 – 139 – 142 – 151 – 154 – 155- 197- 202 – 216 – 223- 224 – 225 Obstructive airway disease Physiology: Anatomy of Bronchial tree: 1-Function of URT Conduction of air. 2-Function of LRT  Gas Exchange. MCQ 1)Chronic Obstruction airway diseases Def: chronic slowly progressive airway disease which is irreversible due to destruction of airway ( but 70yrs Definition  abnormal dilation of airway distal terminal bronchiole. MCQ Decrease in surfactant amount by damage of pneumocyte II & presented by pursed lips as a reflex to prevent a collapse. Due to of destruction of Elastic tissue  Active Exp (Dyspnea & w.t loss) become thin & as a reflex to avoid a dyspnea  Tripod position. R.F I Mild hypoxia Normal or low Co2 (washout). –Reflex 2ry polycythemia (malar rash) pink. C/P: pursed lips breathing, tripod position (dyspnic). MCQ + clinic Malar rash, thin & old pt. Dx: by High C.T scan resolution.  Patient with COPD has : 1/no clubbing. 2/no hemoptysis, if present (devolpe to Bronchiectasis or Bronchogenic CA ). KEY words in COPD: Chest Examination in COPD : 1- Smoker 1/ Inspection: 2- Productive cough *Lt thoracotomy, surgical removal of bleb (Emphysema). 3- Barrel shaped chest *deformity barrel chest 60 Emphysema. 4- Bilateral basal crepitation *chest movement restricted  air entry. 2/Percussion: hyper resonance = Hyperinflated chest  bilateral. 3/ palpation: chest expansion . TVF. 4/Auscultation: - Air entry  Diminished.. Breathing  Vesicular or (harsh vesicular in sever stage). Added sound: Ronchi Expiratory musical sound due to passage of air in narrow tube below carini angle. If there is Ins & Exp Ronchi at same time that mean its ER sever COPD. Q= Clinical examination, How determine if the case need admission? Harsh vesicular breathing – & Inspiratory & Expiratory Ronchi. Bilateral Coarse Crepitation = Its Early inspiratory. & disappears with cough. * Complication of COPD: 1/ Bulles Rupture  pneumothorax. 2/ Pulmonary HTN = R.t H.F. 3/ RFII. 4/ Recurrent Infection. 5/ Polycytemia *Prognosis according to BODE: 1/BMI. 2/Obstruction. 3/Dyspnea. 4/Exercise. 1/RFI  Emphysema. INV: ABG 2/RFII  ch.Bronchitis. WBC: infection, if low due to inf with staph aures b/c coagulase enzyme LAB destruction of WBC. HB: due to polycythemia. PFT Imaging MCQ *Chest X-ray: *FEV1/FVC 60% (>60-70%). Late, signs of hyper inflated chest.= Moderate 33-59% (40-59%). Sever FEV1 IF Asthma >15%. IF COPD add Theophylline, ( phosphodiesterase inhibiter  bronchodilator. (Theophylline is a pro arythmogenic drug). 3/ Long Term Domiciliary O2 Therapy (LTOT): its small O2 tank gives low concentration 2L/min by nasal cannula. Indications: 1-Sever hypoxia O2< 60 mmHg. 2-Sever hypercapnea > 60 mmHg. 3-Corpulmonale + 2ry polycythemia. 4/ Res infection Rx: (as soon as possible by Abs) if: 1-Increase in mucous amount. 2- Change of its colure. 3- Change smell. 4- Increase cosistancy NB. So Abs not always required ( given in selected cases) 5/ Mucolytic & Expectorant: - Advise physiotherapy. –Cough suppression (not used). 6/ Surgery to bullectomy. Home work: 2017: Q17 to Q23. 1001: Q119 – 131 – 137 – 191 – 195 – 226 – 227 2)Bronchial Asthma. Def: chronic reversible MCQ inflammatory characterized by hyper- responsiveness (HSVI disorder {IgE-Esinophils}) of air way stimuli  Obstruction.  Types of clinical bronchial asthma : MCQ Extrinsic Asthma. Intrinsic Asthma. Triggering Pollen – dust mite MCC- pits- Exercise-smoking Internally. factor: Infection-house mite-cold air. Age: Childhood. Age: Adult hood. *+ skin prick test. *No allergen. *SPT: -ve. * Atopy +ve (H/S).(Smoking during Pregnancy *Atopy-ve. increases risk) *All over the year. *Seasonal. *Attacks more severe *Attacks(less severe & frequent). *poor prognosis *Good prognosis Remission with Teens. Rx: Stop expose to allergen. Mast cell stabilizer (Na chromgylate).  Bronchospasm. Bronchospasm. Drug Induced Asthma: 1/ NSAIDS: Aspirine inhibation of (Cyclo oxygenase) pathway  P.G with increasing of leukotriene by (Lypo oxygenase)  Bronchospasm. Nasal Polyps *Sametr’s Triad *Widals Syndrome. Aspirin induced Asthma Sinusitis. MCQ 2/B-Blocker  block of B receptor  bronchospasm Rx: stop the drug. *Exercise Induced Asthma: Dryness of airway  Histamine  by Rupture of mast cell. Dx: FEV1 decreases after exercise by (>15%). Rx: -warming up. – short duration (salbutamol) -Leukotrein Antagonist (Zafir leukast - Monte leukast). –Swimming. - Corticosteroids can be used *Occupational Asthma : CP increases in weekend Rx: change work *Nocturnal Asthma: Rx:  long acting B-agonist (Salmetrol). C/P: Chronic Dry Cough. Cough variant asthma= patient only CP is cough Dyspnea. Wheeze. Nocturnal due to: Types of Asthma: 1-Mite. MCQ + clinic 1- Bronchial Asthma. 2- Cortisone level. 2-Gastric Asthma  GERD. 3- function of cilia. 4-cold air. 3-Cardiac Asthma  L.t H.F. Key words in Bronchial Asthma: 1- Cough ( dry) 2- Wheeze , dyspnea (intermittent) 3- Barrel shaped chest  4-Infectioues Asthma Whooping Cough & T.B. Examination: Same as COPD But there is No Crepitation. ABG 1/RFI  Mild Moderate & Sever. INV: 2/RFII  Life threating Asthma, due to fatigability. LAB PFT Imaging CXR: signs of hyper inflated chest during attack but not diagnostic. *FEV1/FVC 33%. Admission. crystalscrystals of Eosinophilia. Life Threating Asthma FEV1. *FEV1: --- oral pridinsilone (14 days ) – how much > FEV1IF Asthma >15% improvement. IF COPD 20 Clinical grading in Bronchial Asthma : GINA (Day). GINA (Night). PFT Mild Intermittent 2/months. Normal Moderate persistent Daily with affect activity. >1/week. 60-70% Sever persistent Interfere with daily activity. Frequent. 50-60 MCQ + clinic *Management of Chronic Bronchial Asthma: s/e= tremor, Before starting this step (5) YOU should 1- Salbutamol (Short muscle cramps , ask pt about: acting) B2 Agonist inhaler. hypokalemia - How does he use a drug?. 2- Salbutamol + Corticosteroid 400mg inhaler. - -make sure pharmaceutical company. -Do Bronchoscopy to exclude aspergillosis. Advise Pt to gurgling by mouth wash to fungal infection & vocal cord paralysis due to fibrosis. 3-A= Salbutamol + C.S 400mg + Salmetrol. B= Salbutamol + C.S 800mg + Salmetrol. 4-A= Salbutamol + C.S 800mg + Salmetrol + L.K Antagonist or Aminophylline B= Salbutamol + C.S 2000mg + Salmetrol + L.K Antagonist or Aminophylline 5-Salbutamol + C.S 2000mg + Salmetrol + L.K Antagonist or Aminophylline + oral Steroid. Acute severe Asthma & Life Threating Asthma MCQ + clinic Acute severe Asthma Life Threating Asthma PEFR 110 b/min. Bradycardia. Bp Pulses paradoxical. / C/P Unable complete a sentence. Drowsy & Cyanosed. Chest Rhonchi all over the chest. Silent. CO2 Normal. CO2 PH Normal. Acidosis. Home work: 2017: Q24 to Q33. 1001: Q113 – 123 – 126 – 130 – 134 – 136 – 153 – 161 – 189 – 203 – 208 – 215 – 217 – 229 – 230 – 231 3-Bronchiectasis Def: Abnormal dilatation of large air way due to destruction. Causes: MCQ Destruction Inflammation 1-suppurative pneumonia 2- measles or whopping cough All layers H/o of Pneumonia Infection hypogammaglobulinemia Mucous accumulation Cilliary Dysfunction. Air way Ex Bronchi: Intra Bronchi: 1/kartagener syndrome -T.B (Broc’s Syndrome) -F.B. 2/Youngs Syndrome - Br carcinoma. -Aspergellposis 3/Immotile cilia. 4/Cystic Fibrosis(AR defect in long arm of chromosome 7) Complications of cystic fibrosis 1- Infective exacerbations of bronchiectasis 2- Spontaneous pneumothorax 3- Haemoptysis 4- Nasal polyps 5- Respiratory failure C/P: Constitutional Symptoms Inflammation Destruction *(Fever – malaise – headache – *Massive Hemoptysis. Anorexia – Vomiting – loss of w.t). *Dry Bronchiectasis( Sica). *Pus formation Infection *Headache & convulsions. -Halitosis. Wheeze -Clubbing. -High Grade Fever. Mucous Accumulation -Amyloidosis. Productive cough Dyspnea MCQ *Cillary Dysfunction -Massive sputum. DD of hemoptysis -Thick purulent. Bronchial disease -Worse at morning. *Carcinoma -Coarse crepitation. *Bronchiectasis *Acute bronchitis - Related to posture. Bronchial adenoma FB+ Endotracheal intubation Clinical examination same as COPD Parenchymal disease *Tuberculosis Lung abscess & Infections Complications: MCQ Trauma 1-Pneumonia, Asbestosis (rare) 2-Lung Abscess, Lung vascular disease 3-metastatic brain abscess, *Pulmonary infarction 4-open pneumothorax, Goodpasture's syndrome 5- pleurtic chest pain, Idiopathic pulmonary 6-Empyema haemosiderosis + PAN 7-lung collapse A-V malformation 8- 2ry amyloidosis Cardiovascular disease *Acute left ventricular failure Mitral stenosis Aortic aneurysm Key words in Bronchiectasis : Blood disorders 1- Productive caugh ( Purulent, positional) Leukaemia 2- Hemoptysis Haemophilia 3- Clubbing Anticoagulants 4- Bilateral basal crepitation  CBC, ESR, CRP Sputum analysis To detect cause: Chest xray = Air bronchogram , dextrocardia Investigation: Sweat test RF 1 ABG positive perception of aspergillus niger PFT Imaging FEV1/FVC LAB Chest x ray or CT scan (honey 500 5-Oligimic lung field MCQ ECG: LAB 1- S.T, T wave abnormality, 2- sins tachycardia – common Imaging: 3- S1Q3T3 --- specific but not sensitive Any Exudate filling with 4- incomplete RT BBB Eosinophil’s  Pulmonary V/Q Scan Abnormal Ventilation perfusion Embolism. scan exclude Dx. C.T angiogram: Diagnostic of site of obstruction.  Management of pulmonary Embolism: MCQ + Clinic Do quick assessment to the pts. A: Maintain Air Way. Give Morphine & Metoclopramide. B: Breathing, give O2 (60%). C: insert 2 large cannulas. To Pain & Anxiety. CBC, CRP + D-dimer ABG C- X ray & ECG CT pulmonary angio Give immediately 10,000 unit of Heparin. ( Not safe in renal faliuer) Un- stable Maintenance: dose 18u/kg/hr. >90/60: - Rapid Colloid Effusion. stable -Thrombolytic. Give Warfarin 10mg /24hr. Note: in pregnancy DOC is LMW heparin *Identifiable *Non Identifiable -Continues 3months. -Continue for 6 months *Recurrence* - On warfarin & recurrence IVC & Filter Paper. -Continues for warfarin for a life. Home work: 2017: Q88 to Q96. 1001: Q45 – 111 – 120 – 135 – 150 – 170 – 172 – 190 – 207 – 211 – 233 Pleural Effusion. Def: Accumulation of fluid in the pleural space > 50ml. MCQ C/P: as short case Inspection: scar  chest tube scar (which indicate recurrence P.E d/t malignancy. Bulging in the lower part  chest movement. Palpation: -chest expansion. -TVF Percussion: - Dullness in the lower part  Stony Dullness  D/D: -Pleural effusion. –Lung Fibrosis. –Lung consolidation.. -Pleural Thickening. –Raised Hemi diaphragm. Key Words: Auscultation: 1- Dyspnea Diminished air entry. 2- Absent of pluritic rub 3- Stony dullness Vesicular Breathing which is very hard to heard at site of effusion, *bronchial breathing if you put a stethoscope at upper part of pleural effusion INV: ABG RFI. MCQ + Clinic *Mild Pleural Effusion: 50-200ml Lateral Decubitus X-Ray showing  LAB Obliteration of constophrenic angle, U/Sbest. PFT > 70%. Imaging *Moderate Pleural Effusion: 200- *Massive Pleural Effusion: >500ml 500ml Chest X-Ray showing  Chest X-Ray showing  Homogenous white Homogenous white opacity in lower zone opacity with obliteration of costo phrenic & Crescent shape (Meniscus Sign). cardio phrenic angle. Trachea is pushed. Q- Detect the underlying cause? -By Tab or Diagnostic Thoracocentesis 40ml. -Bacteriology: Gram stain – Ziehl neelsen stain.(not always isolated) –Biochemistry: (Pr – LDH – Amylase – Sugar & PH). –Cytology: Types of cells. –Immunology: * Rheumatoid factor ----> R.A. *ANA----> SLE. *Macroscopically Examination of pleural fluid: 1/ Red  Hemi thorax D/D (T.B, Infection, Trauma, Pneumonia, Malignancy). 2/Yellow  Empyema D/D (Infection, T.B, Sub diaphragmatic Abscess). 3/White  Chylothorax D/D (Nephrotic Syndrome, L.N obstruction, R.A, Liver Cirrhosis)  Transudate Transudate Exudate Exudate *CHD (LT + RT). Malnutrition TB Acute pancreatitis *Hypothyroidism Ma Malabsorption. Pneumonia= Malignancy. *Meigs syndrome Liv Liver cirrhosis. (Para pneumonic Uremia. *PE= 0.5 (Ex) 0.6 (Ex) 200 IU/L (Ex) 1018 (Ex). 60 (Ex). 110 TAG + 5 Disappear  Resolution & days  surgery if Re accumulation  Discharge. Recurrent  C.T. aspiration (6hr CXR)  multiple bullae do Pleurodesis. Home work: 2017: Q44 to Q45. 1001: Q143 – 147 – 162 – 182 – 196 Bronchogenic Carcinoma -Most common cause of death ( 17 – 18% ) M > F. MCQ *Causes: 1- Smoking (90%). Active or passive 2- Air pollution (5%). 3- Lung Fibrosis (ILD) Risk by 3 times 4- Occupational (Asbestosis, Arsenic, Cadium). *Types of Lung Cancer: 2) Small Cell CA: 20% 1) Sq.Cell.CA (Epidermoid cell carcinom): -Characterized by sudden onset, rapid -35%. –Slowly Progressive. progressive. -Excellent Response to chemotherapy early. –Centrally. –Solid or Caveating. -High Risk with smoking. - PTH like peptides  Ca+. MCQ -(+ve) F/H. – Good response to surgery. MCQ -Poor Prognosis. 2) Adenocarcinoma: 30% – peripherally. –By CXR  Solid. –common in non-smoker & Female. 3) Large Cell CA: -Periphrally. –CXR: caveating. C/P: (majority have advanced disease at clinical presentation) *General Manifestation: 1)Anorexia. 2)N&V. 3)Cachexia. 4)Fever & Sweating. *Local Invasion: 1) Alveoli & Alveolar duct  collapse  Pulmonary B.V Scanty Hemoptysis, if including Bronchiectasis (Massive Hemoptysis). 2) Pleura  Pleurisy  Pleural effusion. * Surrounding: -Trachea: Dyspnea & Stridor. -Esophagus: Dysphagia. -Left Recurrent Laryngeal Nerve: Hoarseness of voice. -Sympathetic Chain: Horner Syndrome (partial ptosis, meiosis & Anhydrosis enoptalmos). -Superior vena cava syndrome: -Brachial Plexus: Weakness of upper limb Muscles. –Diaphragm: Raised, phrenic nerve palsy. –Heart: Pericarditis  pericardial effusion. –Thoracic cage: Chest wall pain. *Metastasis: Distal organ involvement with evidence of malignant cell. -Lymph Node (80%) -Liver: Jaundice (45%). -Adrenal gland (35%) -Bone (35%). -renal (35%) -CNS : Meningitis & Convulsions (20%) *Para neoplastic Syndrome: ( non-metastatic ) Common with Sq. cell carcinoma Distal organ involvement with evidence of metastatic (Malignant Cells). 1/ Clubbing  stage V, Hyper trophic pulmonary osteoarthropathy. With tenderness at wrist & head of fibula. 2/ Nephrotic Syndrome. 3/ Poly myositis & Dermatomyositis. 4/ Hematological  Anemia. 5/ Neurological  Eaten lambert Syndrome -Myasthenia Grave’s -Cerebellar Degeneration. 6/ Endocrine -Adrenal Gland  ACTH Cushing Syndrome. –PTH like Peptides, Ca+( para neoplastic & metastatic). –SIADH secreation ( leads to hyponatremia). –Gynecomastia. –Hypoglycemia  CXR: MCQ INV: ABG RF I. LAB PFT Imaging Due to phrenic nerve palsy CBC, CRP, ESR: High than 100. Bronchoscopy: Central Tumors (INV of Choice). Sputum analysis & cytology Percutaneous Needle aspiration under C.T or U/S Guided  peripheral Tumors. C.T: for staging & Metastasis  Medstinoscopy & *Management: Thoracoscopy. 1) Radiotherapy (palliative): -Restriction of Tumor Size. - Pr Symptoms (Hemoptysis, Cough W& D, Dysphagia, Horner syndrome, upper limb weakness). MCQ 2) Chemotherapy (palliative & curative): -Killing of cell, not regular used in B.CA which is effective in small Cell CA. 3) Surgery (Curative): -Dissect with safe margin, most effective to B.CA all types except in: (Metastasis, Contralateral L.N, Pleural Effusion, Pericardial effusion, severe obstruction, and mediastinum structure). This is effective in a (Pleurisy without P.E, Pericarditis without Pericardial effusion, Diaphragm, Trachea above carina 2cm & Chest wall). *Prognosis: Depends on stage of tumor 20%-30% survive  1ry. 5% survive  5yrs Home work: 2017: Q53 – 65. 1001: 117 – 128 – 156 – 160 – 164 – 178 – 185 – 199 –206 – 212 – 219 – 238 Pneumonia - Def: inflammation of pulmonary parenchyma ass’ with Recently Developed X-ray changes (12- 18hr) to be changed. MCQ Classification to Pneumonia: -According to etiology: Infective  Bacterial (MCC), Fungal, Virus, Parasitic. Non-Infective  chemical, Aspiration, Collagen, Radiation. -According to Radiology: Lobar Pneumonia  Localized. Broncho Pneumonia  Diffused. -According to Clinical: *Community Acquired Pneumonia (CAP). *Hospital Acquired Pneumonia (HAP). *Aspiration Pneumonia. *Pneumonia of Chronic Illness. *Pathophysiology: Source of infection - Droplet inhalation (Internally)( Function of cilia  Smoking, Old Age, Alcohol, Corticosteroid.) OR as result of blood born of septic foci -Once arriving to air way  Ag-Presenting Cells ---> Stimulation of inflammation  C.K IL & other inflammatory materials  Death Tissue & Cells Pus Formation (End 1stday).= C/P: Malaise, Fatigue, Anorexia, Fever. -Compress on alveolar duct & sac’s = C/P: Early dry cough (painful), Wheeze, Dyspnea. -Continues inflammation to 2nd day; will accumulate more pus & more inflammatory process  erosion of B.V = (*Hemoptysis) & compress on it  back to R.t H.F = (cor pulmunale)  then erosion of alveoli  *Rupture  escaping f mucous  *productive cough  (end of 2nd day) & pleurisy (*pleurtic chest pain). -presence of pus  High grade fever, rigor & convulsions – blood spread = Bacteremia  Shock (Septic)  R.F.  Death  healing by Attraction Fibroblast  deposition  fibrous tissue & collagen  Consolidation. Note: -If the symptoms are mentioned above are showed is called = Typical Pneumonia. -If the symptoms were extra pulmonary is called = Atypical pneumonia. MCQ Examination: Inspection: - Chest movement at affected site restricted. Palpation: -Chest Expansion Decreased –increased TVF increased b/c of Consolidation. Percussion: - Dullness Auscultation: -Bronchial Breathing + MCQ (+ve Egophony test & Whispread test.) -Added Sound: Ronchi & Crepitation ( Early Fine Crepitation , Late Harsh Crepitation) Key words: 1- Bronchial breathing 2- Increase TVF or VR  Chest X ray:( takes weeks to months to resolve ) 1-Lobar or Broncho Pneumonia. 2-Pleural Effusion. INV: ABG  RFI MCQ 3 –Pneumothorax. 4–Lymphadenopathy. 5-cavity & Lung Abscess. LAB CT scan Bronchoscopy >70% PFT Imaging Radionuclide bone scan (to detect spread of CBC: -WBC N, decrease, increase infection to bone) ESR, CRP = Prognosis if than 300 indicates pus. Sputum or B.Culture & Serology 60% can isolated (Mycoplasma usually –ve) Rx: Bed Rest. According to clinical presentation & severity Specific I.V fluid. O2: due to hypoxia. Anti-pyritic *Mild  Moderate: Orally 7-10 Days. *Assessment of severity (According to CURB-65): *Severe: I.V 14 days. C= Confusion. U=Urea >80. R= RR >30. *Resistant: I.V 21 day (3wks). B= Bp Dyspnea. Wheeze. which may lead to clubbing -Mild compression  Lung Collapse (not markedly). -pressure on Bronchus  Bronchiectasis -Hypersensitivity  1- Kerato conjunctivitis. 2-Ductility’s, 3-Skin Tender Erythema  Slightly Pleura effusion due to A-B complex = pleurisy. -Blood Stream  invasion of other organs  Liver & Spleen (Miliary TB). Miliary T.B: Hematogenous spread of T.B if with -1ry Classical. -Post 1ryCryptogenic. 1ry-Classical T.B. Post 1ry-Cryptogenic. -Constitutional C/P. -Constitutional C/P. -Mild Hepatosplenomegaly. -Markedly H.S megally 50% not Dx by CXR. -Coroidal Tubrcle. MCQ -Confirmatory by Biopsy. -affect CNS  Meningitis, rare but Fetally, so BCG given to Childs a Vac against Miliary T.B. -Miliary seeds (Micro). Bilateral by CXR.  CXR: Mass (Ghons Focus) *INV: ABG RFI. -Seeds of M.Tb. -Pleural effusion. -Lung Collapse. LA -Consolidation. Restricting PFT. Imaging. CBC: WBC mostly Low. –Bone marrow suppression by pus formation.= (Hb & WBC & PLT  pancytopenia). –ESR 25  >100. ( ESR & CRP to monitor prognosis) *Sputum  1) Ziehl Neelsen (Acid Fast Bacilli) early morning  3 samples, at least 24hr apart if +ve ( red rods in blue media) sputum +ve T.b. (+ in more than 80%) MCQ 0r Auramin Stain, can also stain Acid fast T.b. 2) Media: Lowesten Jensen Media = 4-8wks (Solid). Or BACTEC media= 1-2wks (Liquid). 3) Biopsy by U/S guided or C.T scan  Abraham’s Needle. 4) PCR = Quantiferon test & interferon release assay 5) Tuberculin test (Mantox test) Anti Tb Drugs: ( LFT & RFT done before & during Therapy) 1/ Isoniazid: *S/E: –Tingling & parasthesia. (Peripheral neuropathy.)  Rx by B12. 2/ Rifampicin: *S/E–Orange body fluids. MCQ 3/ Pyrazinamide: *S/E: -Hyper uracemia  Gout 4/ Ethanbuotol: *S/E: -Retro bulbar neuritis. –Peripheral neuropathy. th 5/ Streptomycin: *S/E: 8 CN damage. BCG vaccine giving NB…… add + Orally Steroids if ass’ with Pleural Effusion. during birth to protect against Meningitis *Regime: 1- *Prophylactic……….*Family member. *Childs. *Medical Stuff.  3 months (Rifampicin + Isoniazid) or isoniazid /6months. 2- *Recently Dx T.b: ((Isoniazid + Rifampicin + Pyrazinamide & Ethambutol)) 2 Months. ((Isoniazid + Rifampicin))  4 Months. 3- *Relapsing T.b: ‫ أشر رجعت الحالة‬6 ‫عالج و بعد‬ ((Isoniazid + Rifampicin + Pyrazinamide + Ethambutol & streptomycin)) 2 Months. ((Isoniazid + Rifampicin + Pyrazinamide & Ethambutol))  1 Months. ((Isoniazid + Rifampicin))  5-6 Months. 4- *Miliary T.B: ((Isoniazid + Rifampicin + Pyrazinamide + Ethambutol & streptomycin)) 2 Months. ((Isoniazid + Rifampicin + Pyrazinamide & Ethambutol))  1 Months. ((Isoniazid + Rifampicin))  9 Months. 5- *Multidrug Resistance: (if reisistant to Isoniazid + Rifampicin) common in HIV Amoxicillin.  Ciprofloxacin. 2nd Line Drug for 2 yrs. Cyclosporine. Para Amino obnetric Acid. Home work: 2017: Q66 – 73 1001: 121 – 140 – 145 – 163 – 174 – 175 – 184 – 193 – 198 – 201 – 205 – 220 – 235 *Interstitial Lung Disease * -Progressive Disease affect parenchyma of lung between alveoli & capillary inflammation  fibrous tissue around filled with fluid  prevent alveolar expansion = (Cough & Dyspnea) & prevent Gas Exchange  R.FI. late = cor pulmonal *Causes: ( > 125 cause) but most important is -Sarcoidosis. -Cryptogenic fibrosing alveolitis.(Idiopathic pulmonary fibrosis) Hx: -Mostly middle age +(Cough, Dyspnea are progressive slowly & over years, wheeze rare & clinical picture of RT side HF. *Examination: 1) Inspection: - Chest movement bilaterally. 2) Palpation: - Chest expansion. –TVF, not affecting, late by fibrosis. 3) Percussion: -Dullness (late). 4) Auscultation: -Air entry. –Vesicular Breathing. -May ass’ with crepitation  Fine (late Inspiration). Reticular fibrosis = upper INV: ABG  RFI zone(Sarcoidosis) or lower zone (CFA) Broncho alveolar lavage. LAB >70%PFT Imaging: CXR but most accurate  C.T scan. Rx: Auto immune  Steroid + immunosuppressant.  MCQ Sarcoidosis Cryptogenic fibrosing alveolitis: male = Female (Middle Age) smoking (decrease risk) Male > female. (old Age) smoking (increase risk) Clinical picture Clinical picture Asymptomatic 30%. Accidently by CXRBHL. Symptomatic: Gradually Symptomatic: Gradually 1-Flue like symptoms. 1-Flue like symptoms. 2-Lung: 90% Dyspnea is progressive. 2-Lung: Caugh & Dyspnea is progressive. *BHL + Lung Fibrosis 20%. *Central Cyanosis + Clubbing 2/3 cases. *Fine Crepitation (rare). *Fine Crepitation (Common). 3-Skin: *Erythema nodosum + Symptomatic: Acute *Lupus pernio(violaceous plaque lesions). *Lofgren Syndrome: 4-Arthralgia: *Pharyngeal Cyst. (BHL+ Poly Arthritis + Erythema Nodosum). 5-Uveitis. 6-Superficial L.N (cervical). *Heerfordt Syndrome: 7-Parotid enlargement. (Uveitis + Parotitis + Facial palsy). 8- Ca+. *Mikulicz syndrome: 9–Diabetes insipidus. (Parotid Enlargement +Lacrimal Enlargement). 10- CNS: cranial nerve palsy 11- cardiac : arrhythmia ( H.B ) *INV: *INV: 1 -LAB  ACE 60%. + Ca + ESR 1 -LAB: R.F, ANA & LDH. 2-Broncho alveolar lavage  Lymphocyte. 2-Broncho alveolar lavage -Neutr & Eosinophil’s. 3-CXR 3-CXR: Bilateral basal Reticulonoduler shadow + -Stage 0: Normal. Honey comb. -Stage I: BHL. - C.T is Diagnost - Stage II: BHL & interstitial infiltrates. -Stage III: Diffuse pulmonary Shadow. -Stage IV: pulmonary fibrosis. 4- Biopsy ---- non caseating granuloma 4- Biopsy ---- if in doubt *Rx: *Rx: -Stage I &II  Resolution spontaneously. -Oral steroid & immunosuppressant. -Stage III & IV + Extrapulmonary  corticosteroid. -Response  < 50%. POOR PROGNOSIS. *Asbestosis = Clubbing + Cancer larynx + Adenocarcinoma lung & mesothelioma + Exudate pleural effusion + lower pulmonary infiltrate *Silicosis = upper pulmonary infiltrate + TB MCQ *Hypersensitivity pneumonitis (extrinsic allergic alveolitis)= organic antigens inhalation (farm worker's lung and bird fancier's lung) + (Fever, Dry cough + breathlessness + Cyanosis) Common + lower zone infiltration Home work: 2017: Q97 – 103. 1001: 118 – 138 – 157 – 159 – 171 – 210 – 218 – 239 – 240  ARDS (non-cardiogenic pulmonary edema) Cause inflammatory damage to alveoli vascular permeability edema Clinical picture: 1-sepsis 2-gastric aspiration Sudden onset of cough 3-fat embolism 4-burn Wheeze dyspnea MCQ 5- multiple blood transfusion 6-acute pancreatitis 7- near drowning Dx : RF type 1 + Ground glass appearance in chest x ray Rx: 1- treat underlying cause 2- PEEP Home work: 1001: Q: 148