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BIOC34 disorders.docx

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University of Toronto Scarborough
Biological Sciences
Stephen Reid

Respiratory Disorders  Apnea= lack of breathing= occurs when upper airway muscles (that surround the trachea) are relaxed during sleep= these muscles are normally active and pull on the trachea to keep it open (patent= rigidity of trachea due to cartilage rings in contrast to collapsible esophagus) o Obstructive sleep apnea= caused by obesity where the excess weight pushes on the throat/neck and causes the trachea to collapse o Central sleep apnea= caused by abnormalities in the respiratory control centres in the brain  Dyspnea= difficult/labored breathing  Allergic reaction/chest constriction= difficulty breathing caused by constriction of smooth muscle around brochus/bronchioles  Pneumonia-induced buildup of fluid/pus + inflammation of alveoli= inhibit gas exchange (decrease in gas exchange efficiency)  Pleurisy= disorder of pleura when visceral and parietal membranes rub against each other and therefore become inflamed= severe chest pain with every breath  Pneumothorax= air leaks into chest wall so interpleural pressure is no longer negative= chest expansion + lung collapse= caused by an inflicted wound or the spontaneous rupture of a lung cyst (tall, thin middle aged men)= also could be side of effect of emphysema or heart disease= treated by placing a tube in interpleural space to remove the air and keep the lungs open until the wound is fixed o Tension pneumothorax= more serious pneumothorax= air enters chest wall but doesn’t exist because the wound creates a one-way valve= the increase in pressure with every breath compresses the heart and the non-collapses lung to one side= heart can’t fill properly and uncollapsed lung cannot expand properly= treated with a needle THORACOTOMY= needle in chest to remove pressure and tube implanted to remove air  Haemothorax= blood in the pleural space due to physical trauma= diagnosed by X-RAY or CT scan= treated with a chest tube to drain the blood  Pleural effusion= accumulation of fluid in lungs/pleural space/alveoli caused by pulmonary edema, or increase in blood vessel leakiness due to infection, or decrease in protein levels because of kidney/liver damage which results in a decrease in colloid osmotic pressure, or a blockage in the lymphatic system which usually drains fluid  Asbestosis= long term inhalation of small asbestos fibres which scar lung tissue= accumulate in pleural space/alveoli= chronic chest pain and breathing pain= can result in lung cancer or cancer of the pleura (mesotheloma)  Restrictive pulmonary disorder= interfere with lung expansion and therefore INSPIRATION= caused by damage to chest wall/lungs/pleura= for example. Pulmonary edema (expansion of alveoli inhibited by fluid in the lungs) OR pulmonary fibrosis= increase in FEV1/FVC ratio  Obstructive pulmonary disorder= hinders expiration= air doesn’t leave lungs efficiently so they over inflate= caused by damage to the alveoli= EX. ASTHMA or EMPHYSEMA= causes increase in FEV1/FVC ratio o expiration hindered= inefficient gas exchange= heart attempts to compensate by increasing blood flow to lungs= hypertrophy of RV= shift in mean electrical axis to the right  Sickle-cell anemia= genetic disorder caused by single-point mutation in haemoglobin beta chains so RBC’s are sickle shaped because heamoglobin beta chains adhere together in a distorted fashion= decrease efficiency of O2 transport + RBC’s viable for shorter periods of time + clogging of blood vessels= FATIGUE, LIMITS EXERCISE AND STRENUOUS ACTIVITY CARDIAC DISORDERS  Bradycardia= slow heart beat= less than 60 bpm o ECG= sinus bradychardia= impulse originates at SA, but space btwn beats is larger than normal= still evenly spaced just less than 60 bpm  Tachycardia= fast heart beat= more than 100 bpm o ECG= sinus tachycardia= impulses originate at SA node at rapid rate, all complexes normal and evenly spaced but less space between because rate is over 100 bpm  Arrhythmia= disrupted heart rhythm = ventricular arrhythmias are particularly dangerous as compared to superventricular ones (above them)= irregular/abnormal rhythms o Sinus arrhythmia= unevenly spaced QRS complex on ECG, irregular heart beat (but not extreme irregularity), P-waves and P-R distances will be the same (atrial origin)= disappears with exercise or holding breath o Wandering atrial pacemaker= P-waves aren’t uniform, and P-R distances change o Ventricular ectopic pacemaker= QRS complexes will be abnormally wide o Premature atrial contraction= mainly normal= normal QRS but occurs prematurely on some beats o Premature ventricular contraction= abnormal QRS appears occasionally as early beats  Heart block= slow/absent conduction of electrical activity from atria to ventricle o 1 degree= most part normal, but prolonged P-R distances= not normally dangerous= can occur in highly-trained athletes= can occur in people with enhanced vagal tone o 2 nddegree= electrical activity is only intermittently blocked= normal but occasionally P-waves are not followed by QRS complex, no longer 1:1 ratio of P:QRS o 3 degree= no transmission of electrical activity from atria to ventricles= there are P-waves but not followed by QRS (if they occur together it’s a coincidence= QRS complexes are wide and jagged because originate in ventricles (escape QRS complexes= QRS complexes generated in the ventricles= stable if originate above bundle of His but very dangerous if below that point)  right/left branch bundle block= conduction slowed in one of the branches= ECG lines are saw tooth or m shaped/ wide jagged QRS= ventricles no longer contract at the same time= blocked ventricle contracts later o RBBB= QRS complexes= saw tooth but still point up o LBBB= QRS complexes= saw tooth, some point down  flutter= common form of arrhythmia + fibrillation= both are caused by rapid rates of excitation/contraction= flutter is more benign than fibrillation o atrial flutter= rapid rate of electrical excitation= increased number of P-waves= but AV node and ventricles only activated by every second/third P-wave so ventricular function isn’t affected to a huge extent= can decrease/cause disappearance of T-P distance o atrial fibrillation=chaotic/rapid electrical excitation in atria= different parts of the atria depolarizing and contracting at different times= but heart function isn’t dependent upon the contration of atria so as long as QRS complex remains in tact, ventricles contract properly= heart rate however will be irregular o ventricular fibrillation= dangerous because uncoordinated + inefficient pumping= rapid/chaotic ventricular excitation due to recycling of electrical activity in the ventricular myocardium/muscle= circus waves created because refractory period of myocardial muscle that prevents recycling of electrical activity is altered (some cells emerge before others)= coordinated pumping impossible= fixed by padded defribillators that discharge all cells at one time and wipes out any re-entry circuits resetting the heart and allowing an endogenous pacemaker to establish a normal rhythm  rentry circuits= recycling of electrical activity due to uni directional block (which allows electrical activity to move in one way at a slow speed)  overall circus waves moving in circles through various regions of ventricular muscle through re-entry circus causing these regions to contract independently of other regions  Activation disorders= disruption in normal transit of electrical activity in the heart  Ischemia= decreased blood supply and therefore O2 to tissues  Hypertrophy= excess growth of heart over time due to overwork such as chronic
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