Final Notes Patho PDF

Hernia S Congenital Diaphragmatic failure/malformation of posterior lateral portion of diaphragm prior to 8 weeks leaves opening btwn peritoneal + pleural pressures Treatment : int...

Hernia S Congenital Diaphragmatic failure/malformation of posterior lateral portion of diaphragm prior to 8 weeks leaves opening btwn peritoneal + pleural pressures Treatment : intubate immediately , Nitric oxide to ↓ pulmonary hypertension Tracheoesophageal Fistula Defect w/ atresia of upper esophagus w/ communication to trached Diagnosis inability to pass catheter into stomach : management ventilate Keep upright 30 to to aspiration frequent suctioning : , , Pierre-Robin Syndrome Defect w/ mandibular hypoplasia. Meconium Aspiration Big tongue small Chin , short jaw , combination of undigested amniotic fluid t management : prone position , nasotracheal tube , trach epithelial cells contained in fetal bowel Results in : obstruction Air leak+, Choanal Atresia Inflammation RDS, retanded CO2 ↑ PVR , Defect of a blockage/absence of have due to congenital malformation persistent pulm hypertension. obstruction may be unilateral or bilateral hypoxemia + hypercarbiat Acidosis Diagnosis inability to pass suction catheter down naves : CXR : coarse asymmetric pattern management : make neo cry oral airway intubate , persistent pulmonary Hypertension (PPHN) Tracheomalacia + Tracheal Stenosis from Failure ofa PVR to fall after birth cartilage is weak or stenotic section of trachea Pulm arterial press remains elevated.. causes ↓ radius on insp cause Stridor + dyspnea. R=L Shunt through ductus arterious + former viewed w/ bronchoscope ovale Echo-Gold Standard Transient Tachypnea of Newborn (TTNB) "Wet lung, Type It respiratory distress ↑ fluid in to ↓ ↑ deadspace lung causes compliance Ve , + Signs: Grunting + ↑ WOB , retractions , nasal flaring RR above 140 + ↑ + management : CPAP , Heated high Flow , prone positioning CBG-M lactate , + RDS/HMD (Hyaline Membrane Disease S due to prematurity + insufficient lung Surfactant - v/Qmismatch leads to : ↑ alveolar surface tension = collapse : Atelectasis = ↓ compliance = hypoxia + ↑PVR + acidosis alveolar management : Oz , PPV , CDAP surfactant replacement (BLES or MIST) , Permissive hypercaphed , HFO + iNO for Y PVR , Bronchopulmonary Dysplasia (BPD) Chronic Lung Disease (CLD) chronic lung disease in infants treated w/ mechanical ventilation for a primary lung disease can be considered CLD/BPD W/ demonstrated ventilation / O2 dependence of 2 weeks or more or Oz dependent & 28 days management : lowest fil possible , It 4-6 m//kg , permissive hypercaphia , avoid ↑ SpOz , Wean to CPAP , HFO, iNO + surfactant therapy Pneumonial pneumonitis usually bacterial , Strep B most common Bronchiolitis-sticky crackles leads to : Alveolar infection , filling , pus formation , RDs , inflammation inflammatory disease of bronchioles, most common cause RSV Cresp syncytial. Pulmonary Interstitial Emphysema (PIE) Virus) need 02 + hydration - Enterocolitis (NEC) leakage of air into perivascular tissues of the lung from overdistention Necrotizing leads to ↓ pulm perfusion. + ↑ PUR = REL Shunting necrosis of colon + ileum caused by "bubbling" near hilar region intestinal ischemia management : minimal vent. support (CPAP) , prone Brunchietasis pulmonary Hypoplasia irreversible dilation+ distortion bronchial tree lung development wy too few cells Alveoli , or airways hernia SIDS common diaphragmatic in risk factors: prone smoking,6months management CPAD : , brain abnormalities in brainstem , upper airway Hyperbilirubinemia infection - supine to sleep AKA Jaundice or icterus either when breakdown of is I'd a t'd excretion of bili t'd enzyme activity that prevents breakdown Hgb , or of bili 2 form bilirubin : Conjugated water soluble zutero unconjugated fat soluble ,  S Cystic Fibrosis recessive exocrine gland disorder by excessive viscid secretions-wet cough caused by mutations in gene that encodes , : Staph Aureous Haemophilus influenza, pseudomonas multifunctional protein (CFTR) common pathogens , L Aeruginosa Diagnosis : Sweet Chloride test ( 60 mmol/L) main culprit Epiglottitis - no supine ! inflammation of epiglottis-Acute bacterial infection , cherry red epiglottis primary cause: Haemophilus influenzae type B - signs : drooling , Stridor CXR : thumb sign Croup/Laryngotracheobrochitis-steeple sign subglottic inflammation obstruction most or , common pathogen : parainfluenza type I Adenovirus , , RSV , Onset-6 month to 3 years signs barking cough stridor hoarsness : , , Systemic corticosteroids : dexamethasone + Racemic epinephrine"causes vasoconstriction Congenital Heart Disease RS & early deformation of the a itself or vascular structures associated w it. ↑ workload on > - Acyanotic disease : I'd pulm blood flow oxygenated blood is shunted from LER side of - Generally associated. , Cyanotic disease : I'd pulm blood flow deoxygenated blood is shunted from REL side of a resulting in severe hypoxemia. , + cyanosis central ↳ usually requires ASD , USD + /or PDA for survival Acyanotic Defects I'd pulmn blood flow , LER Shunt : ↳ DDA : LER Shunt , failure of ductus arteriosus to functionally close due to ↑ POL's + ↓ prostaglandins, LIVSDI Ventricular Septal Defect : LER Shunt, a communication in ventricular wall or failure of wall to close s , sound-lub (HoloSystolic , murmur ↳ (ASD) Atrial septal defect : LeR Shunt communication buth R + L Atria I'd press on LSD Split S2 Dub sound , , af or below site of ductus arteriosus his flow out of Aorta-need PDA Or USD , ↳ Coarctation of Aorta : constriction of aorta just , ↳ systolic press murmur,. ↑ in upper extremities than lower extremities ↳ Aortic Stenosis : narrowing of aortic. obstructs flow out of LV-IV Hypertrophy , CHF + MI need PDA - ↳ PulmonaryStenosis: pulmonic value defect-need PDA  S Cyanotic Defects I'd pulmn blood flow REL Shunt & : , ↳Tetralogy of fallot most common CHD 4 concomitant defects: 1 Pulmonary Stenosis : ,. , 2 RV. hypertrophy, 3. USD , 4.. Overriding Aorta "boot" X-ray ↳Tricuspid Atresia : REL Shunt no tricuspid value no connection btwn Ratrium + R ventricle need Patent foramen ovale (PFO) or , = - ASD ↳ Hypoplastic Left & syndrome: no systemic flow underdeveloped LV + severe narrowing of ascending Sorta-need PDA , ↳ Total Anomalous pulmonary venous return (TAPVR) : pulmonary venous return routed to R atrium instead of LA-need ASD arteries from LV-need PDA/VSD/ASD ↳Transposition of the great Arteries (TGA) : Aorta arises from RV + pulm. ↳ severe black/blue hypercyanosis w/ refractory hypoxemia ↳(XR : "egg on string" ↳Truncus Arteriosis : Single artery arises from ventricles carrying both pulmn. t systemic blood flow Vent strategies for most a pts poz's pCO2 + : 40's PH : 7 40. SpO2 : 70-80 prevent Acidosis ↓ pressures +to volumes Influenza 4 of viruses : A , B,C types , Or D Influenza A most common can be Asymptomatic, may trigger GBS management hydration, rest+ acetaminophen : Anti-viral Drugs: TamifluCoseltamivir) Relenza (anamivir)+ of Sleep Stages Non-rapid eye movement (non-REM) sleep : 4 stages , Quiet or slow-wave sleep Rapid eye movement (REM) : Active or dreaming sleep stage of sleep determined by electrophysiological monitoring  S NREM sleep N1 N3 (has 2 levels Stages N2 4 : + , typically 1st stage of sleep , cycles of 60-90 mins-majority in N2 NI + N2 more chaotic , NB slower more regular interruption in these stages (typically N3) interfere wh norm growth, healing + immune response REM Sleep EEG activity, lasts 5-40 min signified by I'd contributes to psychological rest + long-term emotional well-being ; may baster the memory role in sleep disordered breathing Sleep related hypoventilation appea are frequent reduced response to hypoxia hypercaphia : t , t Sleep-Disordered Breathing (SDB) 3 types of sleep apnea (Hypophea , YARS) -upper airway resistance, Obstructive sleep appea + central sleep appea Snoring - Hypopned > mild - OSA - > Severe OSA Hypopnea ↓ in breathing wyout complete cessation Defined : 30% t in airflow w/ 4 % Of desaturation Upper Airway Resistance Syndrome ↑ 'd airway resistance results in extra effort to breath can cause arousals + ↑ in BP "Continuum" : Snoring-YARS-OSA Apnea cessation of breathing for 10 sec or longer , diagnosed when more than 5 apneas per hr overbhr period occur either in Non-REM or REM Sleep more frequent + severe in REM + in supine position  S Obstructive Sleep Apnea (OSA)I most common small or unstable pharyngeal airway Anatomical (Excessive soft tissue) obesity causes : , tonsillar hypertrophy + Neurological Ch muscle tone)pharyngeal tone lost Quiet I still while sleeping followed by an I'd effort to inhale shorting , signs : (Hallmark) excessive daytime sleepiness,insomnia , Hypertension, dry month or sore throat Risks : excessive weight large neck size, Hypertension, narrow upper airway, Chronic nasal congestion , , Smoking , Alcohol sedatives , or tranquilizers , =65 yr., more in male untreated OSA: , Cardiovascular HTN disease (S attacks+ stroke), Diabetes, Neurocognitive, Neuroaffective, cardiovascular pulmonary STOP BANG Questionnaire S: T : snoring tiredness O : Observed apneas/ gasping p: Pressure (as in BP B : BMI A: Age N: Neck circumference G: gender Central Sleep Apnea heterogenous group of disorders display periodic , breathing patterns-Cheyne-strokes often wy CHF respiratory centers of medulla fail to send signals to resp muscles. characterized by : cessation of airflowa w/absence of excursions nose + mouth diaphragmatic Mixed Sleep Apnea combination of Obstructive + central sleep apnea , usually begins as central sleep Apnea followed by Ventilatory efforts w/ out airflow-OSA clinically classified + treated as OSA  S Diagnosing Sleep Disordered Breathing narcolepsy My ex : Epworth Sleepiness scale , valid for OSA , 0-9 : norm , 10-24 : need for medical Advice , 16 : possibility of OSA Level 1 Sleep Study(pSG):polysomnography, 16 channels to gather: SpOz, Snoring, Airflow, EMG, resp efforts, limb movement, EOG ECGEEG. , Level 3 sleep Study Chome/bedside : 6 channels to SpOz, Shoring airflow, resp efforts , body position t HR : gather , , 4) if positive: pt has OSA , if negative : need pSG to rule out OSA Apnea-Hypopnea Index(AHI) : Ave # of apneas + hypopheas the pt. has per hr. of sleep norm :5 , mild : 5-15 moderate : 15-30 Severe : 30 - AHI Is , clinically significant , Respiratory Disturbance Index (RDI) : # of apheat hypophea t resp -efforts related arousal (RERA) / per - hr sleep > 15 clinically significant : Treatment of SDB Lifestyle modifications weight loss good sleep Avoidance of alcohol smoking cessation : , , , positive Airway pressure CPAP (used like peep to stent open airway) ApAplan to CPAD) ↓ fatigue rate "C flex : , - , to ↓ expiration to ease it BipAp-used w/ hypoventilation (pickwicken syndrome) Neuromuscular pts CSA + , , AvApS-volume targeted + minimal minute ventilation used w/ severe osA or a central component , Oral appliances typically used for Snoring YARS, mild-mod OSA tongue retaining device Cholds forward Mandibular advancement : + , device-cholds lower jaw forward , may be used w/ CPAP surgical interventions side positional therapy : Device used to encourage sleeping on the Hypertension Categories ending primary hypertension idiopathic : - Angl, "pril" ↳ Management : B-blockers (inhibit Symp. Nerv. Syst) , ACE inhibitors. (StopR-A-A cycle) Diuretics (lasix) calcium channel , , blockers Nitroglycerin/Nitroprusside secondary hypertension disease-responsible for majority 2 HTN, retention of salt + : renal ↳ Excessive Adrenocorticosteroids (ex cortisol)-seen in primary Hyperaldosteronism, Cushings syndrome. ↳Coarctation of the aorta : I'd blood flow to Kidneys t triggers RA-A System - H20 retention + HTN results ↳ pregnancy  S Renin-Angiotensin-Aldoster one System of causes hypertension ? Bleed , ↓H2 volume (dehydrated), ↓ sodium t BP renin released from Kidneys > factor > - Angiotensin I (from liver) - Angiotensin II (from lungsmain contributing to ↓BP) - release in Aldosterone reabsorbs NaCl or + vasoconstriction- > ↑BP H20 Malignant Hypertension pt w/ 20 HTN develops accelerated + potentially fatal form of the disease characterized by sudden elevation in BP w/ diastolic press > 120 mmHg ecocedem ↳ peripheral vascular : Development of atherosclerosis (plaque in arteries or veins ninfarction of are ↳ Renal : Stimulation of R-A-A System - Worsens HTN I'd risk intraocular press ↳ Retinal : damage to vasculature + resulting vision problems ,. can cause retinal separation Coronary Artery Disease Also ischemic & disease - narrowing of one or more coronary arteries due to build-up of fatty deposits w/in arterial wall -Thus atherosclerosis results in t'd blood flow, thus less O nutrients are delivered to a muscle fed by the affected arteries risk factors I'd : cholesterol Diabetes , HTN , , smoking Obesity + stress , Lumen narrowing: I'd blood flow to myocardium, resulting ischemia can result in chest pain, chronic ischemia leads myocardial fibrosis t'd to + ventricular wall compliance plaque Rupture: exposes lipid core - results in plaque adherence , clot development further narrows lumen t may result in a complete occlusion + MI  S CAD Exam findings Lab test : ↑ cholesterol levels , ↑ levels of protein (Both non-diagnostic C-reactive ECG : 12 lead tells us specific section may reveal ischemia , MI or rhythm disorder , Cardiac Stress test : ECG may exertional myocardial ischemia show of blood flow to myocardium of under exertion Thallium Stress test : combines nuclear imaging best I coronary Angiography (Gold Standard): uses catheter inserted into artery threaded up to aorta to openings of coronary arteries - should include angioplasty or CABG's (Coronary artery By-pass Grafts - - : CAD Treatment lungs B: 2 : medical asprin statins Nitroglycerin B-blockers calcium channel Non-invasive : Lifestyle changes , management : ↓ dose , , , , blockers , ACE inhibitors - "pril" ending Invasive : ↳ Angioplasty = (PTCA) percutaneous transluminal coronary angioplasty : balloon in blockage is inflated results in widening of artery+ plaque flattened against wall of artery ↳ Stenting: goal to prevent restenosis or lengthening time before it occurs , use of drug-impregnated stents reduce risk of restenosis of from vessel ↳ CABG : treat severe CAD that hasn't responded to medical therapy or PTCA , block parts artery are by-passed w/ graft radial artery used most commonly for grafting above + below blockage-saphenous vein, internal mammary artery or methods: traditional approach : full bypass used-prosi still , Cons:"pump time " sternotomy a stopped+ clung , "Off-pump" or "beating " full sternotomy but I not stopped no bypass required - MICABS/MICS : no sternotomy access through intercostal (rib) region-typically for front of , G vessels ; 1 or 2 vessels Myocardial Infarction - 13 are silent trocarnsubendraa area lack of blood supply ora demand , area of myocardium is deprived of ischemia then area of injury infarction oxygen leads to = , risks: Smoking illict drugs hyperlipidemia, Diabetes mellitus, poor controlled , HTN Classification of MI STEMI : St elevation on z or more contiguous leads - can be considered for re-perfusion therapy Non-STEMI : non elevated ST Segment , ECG alone doesn't confirm , must MI rely on serum markers  S 12 Lead ECG helps locate areas of ischemia , infarct or injury Lateral injury : lead I AvL US + v6 , , inferior injury: lead II I , AVF septal injury : v I + V 2 Anterior injury : Uz + V4 MI Management MONA acronym Nitrates (vasodilation) , morphine (paint vasodilator), B-blockers (NSNS Stimuli medical : Oxygen , Asprin , post MF↓ after load- contractility) , STEMI : have reperfusion + therapy (thrombolytics or angioplasty ( Reperfusion Therapy : ↓ mortality + limit infarct size Thrombolytics : Dissolve blood+ platelet count , best if used 60-90 mins of onset risk of bleeding PCI-percutaneous coronary intervention CABG Heart Failure inability of a to pump enough blood to meet body's metabolic needs may affect - LV , RV or both Left or Right sided cor pulmonale right a Failure classified as I output or t : + - output Left-sided-supplies body (systemic circulation) : Due to failure of LV to move blood from lungs to body results in blood backing up into pulmonary system Right-sided CJVD , Edema) : failure of Due to RV to pump returning venous blood out to lungs results in blood backing up into systemic circulation a Failure involves both Long-term High-output.vs Low-output. High output : uncommon , occur when theres a excessive need for cardiac output - functs "supranormal" Low-output : disorders that impair pumping ability ofI can be systolic or diastolic low-output systolic : impaired ejection of blood fromG during systole results from : impair contractility of 2 produce vol or press Overload on -results in ↓ stroke vol ,... + thus t ejection diastolic impaired relaxation of a diastole , caused by restrict diastolic filling,I ventricular thickness (thus to chamber size) low-output during + Delay diastolic relaxation (fibrosis). ↳ results in ↓ Stroke volume  S Left-side clinical manifestations Exertional dyspnea, orthopned, /A: Fine/coarse crackles "Cardiac" cough frothy , blood tinged Sputum , Cyanosis , wheezes , ↑ pawp Right-sided Clinical manifestations peripheral/dependent edema , fatigue JVD Hepatomegaly , Ascites cyanosis , , , + + Cup HeartFailure Etiology Direct causes : myocardial ischemia + myocardial infarction (most common) Arrhythmias, a valve , lesions , congenital malformations , pericarditis + cardiomyopathies Indirect causes : Fluid overload renal failure + Sepsis , Causing RHF (Cor pulmonale) : COPD , PE + pulmonary HTN bathophysiology I of Heart failure I. Inadequate cardiac output triggers compensatory mechanisms 2 compensatory mechanisms # Frank-starling : I preload = ↑ Stretch = force of contraction= ↑ stroke volume in a failure responsible for , maintaining norm CO in face of t end-diastolic volumes (reflected by the Y pAwp + Cup) ↑ 'd SNS Activity Stimulated bytrSV + co-leads to Systemic vasoconstriction stimuli ofS CHR ↑ contractility : : , + Disadvantage of mechanism:Y SVR that results leads toa afterload I further I myocardial demand , Renin-angiotensin mechanism: the t + Co result in to'd perfusion Kidneys- result Aldosterone cause Nat H2 retention : resulting inI'd blood volume Angiotensin It causes vasoconstriction , This mechanism I's blood vol-results ina end-diastolic vol attempting toa CO thru Frank starling mechanism , Myocardial Hypertrophy long-term : mechanism in response to I'd work demand,results inM of contractile fibers in myocardium This mechanism allows ventricles to do more work, results inI myocardial demand + myocardial O requirements Decompensated Heart Failure compensatory mechanisms only work for so long + eventually CO is further reduced I start to contribute to problem  S Heart Failure Exam findings CXR : cardiomegaly ↳ Left a failure : Diffuse bilateral infiltrates , pleural effusion Kerley Blines , Echocardiography : Useful to diagnose cause of a Failure ECG : may DX Cause (MI, arrhythmia a Failure : Acute Treatment preloadreductionpureNogyepesspreloadMorphinePRAAsyst) Inotropic Support Cuse wy cautions : milrinohe, Inamrinone,digoxin , dobutamine,Dopamine + norepinephrine - To contractility NIPPV : Pt ++ SOB Start w/ Bipap (1 Intrathoracic press.) If no WOB then CPAP OK. , ↳ FiOztYp mean will improve oxygenation Ejection fraction, best indicator  S Valvular Disorders can affect any one of the 4 G values of mechanical disruptions occur : 2 types Stenosis : that it doesn't open properly- obstructs blood flow , It's resistance ↳ narrowing of a value so ↳Incompetence : distortion of the value so that it doesn't close properly ; results in flow-backward flowregurgitant Result of Stenotic Valve + Regurgitant/incompetent values Stenotic value: Distension of the chamber that pumps the blood thru the diseased value (I'd press here. Impairs filling of the chamber that receives the blood (tid press here. Incompetence : backward flow thru value causes distention of the chamber prior to the diseased value (A press (. that places ↓ work demands on the chamber ↳ mild valvular disease disorders may only minimally impact the pressure seen-may only see o murmur · consider : Tricuspid , pulmonic mitral , or Aorta for stenosis or regurgitation Clinical manifestations Hx or newly developed murmur , Exertional dyspnea*, Orthopnea paroxysmal nocturnal dyspnea, + Effort-induced Fatigue Angina , 20 ischemia , palpations syncope, signs of1 Failure (sts depend on Lor R , a Failure Tests Diagnostic Auscultation G murmurs : ble of turbulent flow may be extra sounds heard Echocardiogram transesophageal : echo Types of Aortic Aneurysms hole in wall Management -+ blood balloon of stenotic values pours out surgery , percutaneous valvuloplasty-tx Aortic Aneurysms - Form where vessel wall are weakened Abnormal localized dilation of a blood vessel by 750%, can occur in arteries or veins more common in Aorta classified to area of occurrence : according ↳ Abdominal aortic aneurysm (AAA, triple A) most common 15 % of all aortic Aneurysms - , ↳ Thoracic aortic aneurysm (TAA) ↳Cerebral aneurysm ↳ peripheral aneurysm  S Risk factors of Aortic Aneurysms Atherosclerosis , HTN, inherited condition : pt w/ : relative W/ AAA are I'd risk marfans syndrome, , disorders , trauma collagen-vascular Signs/symptoms most ppl asymptomatic General : Strong palpable pulse in Abdomen area sensitive , to toucha area of aneurysm , chest abdominal back pain or lower coughing horsness or dysphagia , , , ist Rupture sign seen ↳ results in Hypotension (BP diff in each arm) , pale, t LOC, extreme pain , Dizziness/syncope , palpating Abdominal mass (30-50% of time) Cerebral Aneurysm looks like stroke Diagnosing x ray-calcification surrounding Aneurysm cannot detect rupture/leakage ultrasonography - CT Scan (Gold standard) MRI , Angiography-invasive Management Stable Aneurysm treat HTN (B-blockers) surgical repair : , Ruptured Aneurysm : treat shock supportive care (02 Vent Analgesia) surgical repair , , , , cardiomyopathies group of disorders that affect a muscle + diminishes cardiac performance , can develop as primary or secondary disorder main types : Dilated , restrictive Hypertrophic , or Congestive Dilated + Congestive Kinda same thing  S Causes Cardiomyopathies of primary IdiopathicCunknown) Genetic infectious or toxins : , , secondary ischemia, HTN valvular disorders, metabolic disorders vascular disease collagen : or , Dilated Cardiomyopathy causea to become enlarged myocardium become weak thin , + floppy-idopathic in origin mostly Affected ventricle is unable to pump the blood it receives : LV'- L Failure, RV - RS & failure Results in systolic dysfunction Hypertrophic cardiomyopathy Cardiac Arrest / leading cause in Sudden disorder disorganized proliferation of myocardial cells I caused by a genetic Effects LV , frequentlyin interventricle septal area results in both diastolic + systolic dysfunction RestrictiveCardiomyopathy-least common causes walls of ventricles to become stiff but not necessarily thickened often due , to infiltration by foreign materials doesn't imparesfillingofbloodasVentricle normally - failure RVRs fileas · relax , pericarditis inflammation of pericardium , can be acute or chronic inflammation can lead to accumulation of fluid in pericardial sac Characterizedbuichest pain ,pericardiarubserchangesestant (4 Ratrial press a sounds , hypotension possible Kussmall signs on insp + + JVD. on insp ).  S Constrictive pericarditis scarring of pericardium after one episodes of pericarditis , becomes thickened + stiff or more impaired of thea thus diastolic dysfunction Results in filling , Signs + symptoms similar to a failure-kussmauls sign often seen Diagnosing pericarditis lab studiesInfectious blood cultures Cardiac enzymes : : Etiology - WBC + , MI CXR may show pericardial effusion : ECG : 4 classic stages for pericarditis echocardiography : DX type of effusion CT : DX type of effusion Analysis of pericardial find 4 Classic ECG for stages pericarditis StageI : St elevation in all leads , PR depressed (end of p + beginning of QRS Stage 11 : preudonormalization inverted T-wave - T wave Flattening (1-3 weeks Stage III : normalization Stage Iv : Management pericardiocentesis pericardial window : remove small part of sact allows drainage of excess fluid + prevents recurrence of effusions pericardio desis : Fuse layers of pericardium by injecting sclerosant fcause local inflammation) used in cancer + hematologic , malignant disease pericardiectomy Excision of part : of the pericardium , Done for constrictive pericarditis or chronic recurring pericarditis Cardiac Tamponade intra-pericardial impairs diastole elevated pressures the filling of a during ↑ press results from an - , accumulation of fluid in the pericardial sack, results in SV + ↓ CO Severity of condition depends on amount of fluid present + rate which accumulated pericardial space normally contains 20-some of fluid  S Etiology Trauma (biggest reason), cardiac surgery , cardiac rupture 2 MI , pericarditis , Neoplasm clinically d on diagnosed these Signs + Symptoms - Becks triad(hypotension ↑ JVD + Diminished a , sounds) , tachycardias , pulsus paradoxus , PEA Treatment pericardio centesis : Acute subxiphoid percutaneous drainge w/ - 18 gauge needle) , less acute: finoroscopy/echo for tamponade effusions pericardial window pericardiodesis pericadectomy tx of underlying cause , recurring 20 : , , Disseminating IntravascularCoagulation (DIC stimulus causes hyperstimulation of clotting pathways resulting in formation of diffuse clots in microvasculature + depletion of clotting factors which can result in generalized bleeding not primary disease, occurs as a complication of widespread conditions Etiology infectious , shock (especially hypovolemic) , frauma , surgical problems other disease states , obstetric , conditions Hematologic conditions , Signs + Symptoms petechial (tiny bruises), Ecchymosis (bruise) ,bleeding (gums) , Sts of thrombosis+ resulting ischemia Lab Findings D-dimerelevated when clot in vessel), Abnormal ↓ platelet count , clotting times Anemia,↓ coagulationes , treatment management of primary disease replacement clotting components , , prevent further activation of clotting mechanisms heparin therapy controversial - Complications Death organ infarction, limb/ , digit ischemia  S Hypovolemic shock most due to hemorrhagic shock - ↑ Hbg + 4 Hct ↓ Bp caused bya blood volume - due to loss of blood or fluid, i'd lactate levels Cup :+, PAP : ↓ PAwp : N Bp : t , , , CO : N HRit SURit , , CardiogenicShock most often anterior MI ↓ BP caused by to pump blood forward , a ability ↑ Id lactate + ↓ cardiac enzymes if MI occurred pH ↑ , manage : ↓ preload + afterload , inotropic drugs Cup : 4 , PAP : 4 , PAWp :↑ , BP:N , COit HRit , SUR : , Norms hemodynamics CVp : 2-6 Distributive Shock PAP : 20-35/5-15 widespread vasodilation (SVR) results in relative hypovolemia powp : 5-10 can be : Co : 4-8 septic (most common) Cup : ↓ PAP : ↓ , PAwp :, BP : N CO : t HR : T SURit 14-18 : , , , , MHbg : Anaphylactici FHbg : 12-16 pap :, Pawp : N N Hrit , Surit neurogenic (bradycardial Cupit : , , Brit , Co : , obstructive shock ↓ Bp caused by Impedance of filling of theo or an obstruction to blood leaving the ex Cardiac tamponade (impedance) , PE tension pneumo, Diaphragmatic hernia, Aorta Stenosis : (emptying , Cup :↑, PAp : ↑ PAwp : N/t , Bir , CO : N , HRit SURit , , vasopressors Norepinephrine Ist in-line for sepsis , b , + A , but attract A , Chronotrope + Inotrope : Epinephrine : neb for upper airway, it infine for cardiac arrest vasopressin : Atrial smooth muscle Vasoconstrict , ADH milrinone : 1st in-line cardiogenic shock , isotrope I myocardial contractility , Phenylephrine : reverse hypotension , stimulates A , receptors potent I will ↓ Sur of expense for , organs  S Drowning wet near drowning browning glottis + H20 relaxes enters lungs non-cardiogenic pulmonary edema, ↓ surfactant Alveolar consolidation , , CNS damage-primary prolonged hypoxemia secondary reperfusion Injury cerebral edema,seizures : : , , arrhythmias eXR may be norm , cough w/ frothy white or pink sputum Dry-drowning involuntary laryngospasm liquid doesn't enter lungs , lungs are norm ist Burn Degree minimal depth in skin , superficial burn-outer layer epidermis reddened skin , Blisters not present , healing 6-10 days 2nd Burn Degreeto deep thickness of skin , extends thru epidermist into dermis , blisters Superficial present If secondary infection results, man be equivalent to so burn healing 7-21 days zrd Degree Burn full thickness of skin including tissue beneath , both epidermist dermis destroyed , tissue charred or coagulated , no cap refill healing may occur after 21 days or never w/out skin draft  Determination of Area-Surface But n Thermal Injury injury caused inhalation of not gases, usually confined to upper airway by Distal airways usually spared bic upper airway cools not gases reflex of larygospasm , + glottic closure Direct thermal injury usually don't occur below level of larynx - Smoke inhalation Injury tracheobronchial free + Alvedi inflammed , bronchospasm , excessive bronchial secretions + mucous plugging , ↓ mucocillary transport Atelectasis , resp. Akalosis 3 Stages : acute. non-cardiogenic ↳ Early Stage (0-24hr after inhalation) : Delay , onset inflammation, bronchospasm, y secretions pulm edema ,. ↳Intermediate (2-5 days after) : improvement/resolution Smoke Inhalation peak pneumonia ARDS , , , results in ↳ late (S or days after) : concern on infection Pneumonia , pe 20 to more , hypercoagulable state , restrictive + obstructive Acute resp Acidosis. disorders lactate ringers for fluid resuscitation Management Antibiotics , expectorants Analgesic , prophylactic , Tuberculosis infectious disease belong to mycobacteriaceae family-characterized by bacterial multiplication times of 18-24hr , - most important agent M. tuberculosis Spread through air droplet , need Nas mask , close contact at risk prevention : Bacille Calmette Guerin (BCG) humidity , temp ventilation affect droplet size t density , vaccine not recommended - initial lesions called Ghon nodules in pts W/ HIV  S TB Classification primary TB (primary infection stage) : Latent TB infection (post primary TB, dormant TBJ : no signs/symptoms , not active TB , will test positive Disseminated TB Cextrapulmonary TB miliary TBI, : most often in Oz rich organs (brain, Kidneys, longbones , genitalia , meninges) spread outside of lungs TB CXR findings ↑ 'd opacity Ghon nodules Ghon complex (tubercles + lymph nodes in hilar region) Cavity formation , , , , bronchiectasis , pleural effusion, calcification t fibrosis retraction of segments or lobe , RV enlargement , lung Diagnosing TB sputum sample : 3 % hypertonic saline Acid- fact bacillus (AFB test) useful in pts wy , smear negative or unable to produce sputum Quantiferon-TB (Gold Standard) : blood test , cannot distinguish btwn activevs. latent mantoux tuberculin skin test : injection of PPD , detect latent negative - ↳Wheal < 5mm : ↳ wheal 5-amm : Suspicious ↳ wheal 210mm : positive daily once per day TB treatment - < intensive phase (2 months) : Isoniazid , Rifampin , Ethambutol pyrazinamide , continuation phase (4 months) : isoniazid + Rifampin both once daily - Tumors Benign tumor: don't endanger life Slow growth, don't invade normal tissue I don't metastasize , malignant tumor : composed of embryonic , primitive or poorly differentiated cells, rapid growth disorganized manner, can lead to nutritional issues resulting in necrosis, cavitation t ulceration , can evolve to metastasize or invade tissue Lung Cancer (Bronchogenic carcinoma smoking I's risk (most common cause) COPD is a risk factor asbestos exposure (mesotheliomal risk factor radon and , , , leading cause exposure to chromium, arsenic beryllium, air pollutiona radiation to lungs + other inhaled chemicals/minerals , , chronic illness such pulmonary Fibrosis I risk of as lung cancer  S Lung Cancer tumor that originates in bronchial mucosa is bronchogenic carcinoma causes inflammation t edema when tumor enlarges mucous productioni's , hemoptysis occurs when tissue erodes , atelectasis alveolar consolidation Cavity formation , , secondary pleural effusion often accompanies lung cancer very common Lung Cancer Types chemo noteffective non-small cell lung carcinoma CNSCLC) think big Italian guy "SAL late METS ↳ squamous cellepidermoid) : Slow growth, commonin central bronchus or hila cavitation t necrosis , surgical resection preferred to 25-30 , 40 % Adenocarcinoma: from mucous glands of tracheobronch tree moderate growth,weakest association wy smokers small tumors , , , resemble glandular tissue, mucous production pathologic feature found in 10-15 lung periphery, cavitation + pleural effusion common , ↳ large cell carcinoma (undifferentiated): rapid growth, distort trached + large airways associated w/ chest wall pain , Pleural effusions , , hemoptysis + cavity formation early + widespread METS , Small cell lung carcinoma (SCLC) : starts w/ 's" think smoker ↳ small cell or oat cell carcinoma: Grow quickly , arises centrally Chilar large airways), almost exclusively in area + smokers , poorest Prognosis tiny tumors , (6-8um) small, round val, I finely granulated , responds well to radiation Chemo , + very early METS OTHER types : Lung Carcinoidtumor - neuroendocrine cell tumors , slow growth, exception small cell lung cancer screening + Diagnosing CXR most common , CT , PET scan , biopsy Glavage brushing , needle EBUSI , , thoracentesis, sputum cytology TNM Staging System T-size + extent of primary tumor N- # ofnearby lymph nodes M-extent of metastasis e My Spread to other lung M1b-spread to other , organs O-least advanced IV-most advanced X- can't be assessed/measured Treatment/management Surgery-wedgeresectionSegmetectomylobectomy bilobectomy , , , Pneumoneit is radiation-destroy or damage cells  S BUN-waste product from the breakdown The Kidney : Renal Disorders of proteins receives 20-25 % of cardiac output ↑ levels = dehydration, impaired Kidney funct Iprotein. intake cleans blood , maintain homeostasis Erythropoietin t renin/angiotensin levels are regulated by Kidneys creatinine. byproduct of muscle metabolism Vitamin D activation occurs here Renal Disorders classified as acute Kidney failure: acute impairment of renal function,often reversible ↳ Prerenal inadequate perfusion of Kidneys : Shock,a failure Hypotension , sepsis Atherosclerosis rhabdomyolysis : , , , ↳ Renal (intrinsic) : damage of nephrons-tubular necrosis lischemic or cytotoxic glomerulonephritis interstitial nephritis , , ↳ post renal : obstruction of urinary collecting system-Stone disease,tumors,stricture thrombosis, hematoma,enlarged , prostate. - ↑'d tubular press Its filtration. driving force chronic renal failure : disease lasting longer than 3 months, irreversible , commonly due to diabetes t HTN other causes : auto-immune disorders,multiple kidney infections inflammation , polycystic Kidney disease, , congenital disease , Drugs toxins + ↳ characterized by 5 stages : I live norm life , 2 , 3 , 4-dialysis starts , no coming back 5- same as , stage 4 Clinical Signs Acute Renal failure of oliguria, anuria, fluid overload pulmonary edema, electrolyte imbalances-weakness nausea + vomiting - , 'hypernatremia,hyperkalemia, hyperchloremia LAB Findings : I'd BUN creatinine sedimentation in urine WBCs + RBC + , , of Acute Renal Failure Management Dialysis , CRRT (continuous renal replacement therapy) hemodialysis-A-U Fistula "Shunt" access , ↳ loop diuretic Clasix :Furosemide) : inhibits Nat + c reabsorption in loop of henle Treat edema or hypervolemia. ↳ Potassium-Sparing Diuretic (Spironolactone/ aldactone): For a Failure,liver failure treat wy aldosterone ,. blocks receptor for aldosterone + reabsorption in late distal tubule t in collecting duct Nat ↳ Carbonic anhydrase inhibitor (diamox) : blocks carbonic anhydrase enzyme which block Nat + bicarbonate reabsorption in proximal tubule Treat metabolic alkalemia. ↳ thiazide diuretic Chydrochlorothiazide/microzide , end in "zide " ) : block Natt C reabsorption in distal tubule also inhibits carbonic anhydrase in proximal tubule Treat mild edematous states , HTN. ↳ Osmotic diuretic (mannitol very powerfull: freely filter at glomerulus but not reabsorbed , block reabsorption of H2 in proximal tubule + descending loop of nenle Controls ICP by reducing cerebral edema.  S Clinical Signs of Chronic Renal Failure tiredness poor appetite itching, I BUN creatinine , , levels, anemia, poor sleep/dyspnea, frequent vomiting Effects of PPV on Renal system reduces urinary output : glomerular filtration A renal blood flow , rate , nat t kt excretion + ↓ mean arterial press. marked affect on Nat + Hz retaininghormonal system ADH release is affectedby intrathoracic pressure- ppV enhances ADH release ↓ atrial natriuretic : ↓ atrial filling press causing↓ secretion of AND , activates RAA system which I Nat + Hz0 retention