Pshycology test Essay Example For Students

Pshycology test Essay Directions: The following exam consists of various types of questions designed to test the critical reasoning skills of the examinee. Answers are found on the following page, with rationales. This is a Twenty question test, with an allotted time of 45 minutes to indulge ones academic and clinical prowess. Questions 1-4 are based on the following scenario:A 55 year old male, medium body build of 90 Kg presents complaining of acute shortness of breath. He has a history of CHF and acute respiratory failure, he is agitated and disoriented. He has been placed on a ventilator two times during the past year. His medications include HCTZ, captopril, digoxin, and lasix. Paramedics have placed him in 100% O2 via Non-rebreathing mask, established an IV and administered 40 mg of Lasix IV enroute. He is cold, pale, and diaphoretic, with a BP of 200/110, HR 120, RR 48, rales are audible througout. ABGs are drawn, and the results are: pH 7.3, PCO2 55, HCO3 24, PaO2 60. 1. Why is this gentlemans PC O2 elevated? a. Not enough total ventilation (CNS/Respiratory muscle weakness)b.Too much total ventilation Dead Space (Rapid breathing)(1) d The only reason for elevated PCO2 is an inadequate level of alveolar ventilation for the amount of CO2 produced and delivered to the lungs. Hypercapnea in this case is a combination of both. Since he is tachypneic his respiratory muscles are tiring, he is displaying mental status changes do to hypercarbia effects on the CNS. Because his RR is 48 he much of his VT ends up as alveolar dead space. 2. Why is this gentlemans PaCO2 of concern to you clinically?a. Increased PaCO2 (if no compensatory increase in HCO3) results in fall in pHb. Increased PaCO2 results in a decrease in PaO2 unless FiO2 can increase enough to compensatec. The higher the PaCO2, the less well defended this pt is against a further decrease in VAe. His PaCO2 in this case is of little concern clinically2. d (a) This patients PaCO2 has resulted in a fall in pH. It is important to remeber that a small change in pH in one direction means a large change in the other direction.a Ph of 7.30 = a 50 nM/L (25%) increase in H+.(b and c) Despite the fact that this pt is on 100% O2, his PaO2 is only 60. As his PCO2 is 55 his VA is further decreased. Letter E is just bad. 3. How would this patients decrease in inspired O2 and increase in CO2 affect the O2-Hgb dissociation curve response as opposed to an increase in CO2 alone?3. The effects are additive, and the response will be amplified (Oxygen will be unloaded from the hmeoglobin protein molecule) . Increased PCO2 shifts the curve to the right (Bohr effect). Increased H+ (even independent of PCO2 shifts the curve to the right. Should this patient be chronically hypoxemic, that would trigger 2,3 DPG synthesis which would further shift the curve to the right. These factors are compensatory, since the reduced affinity makes unloading of O2 in the tissues easier, therby faclicitating end-organ perfusion. b. Ventilation * amount needed to maintain normal CO2c. Exertional fatigue (result of cardiovascular, neuromuscular, or non-pulmonary disease)d. Should be treated by placing a paper bag over a patients mouth and having them rebreath CO24. b Hyperventilation is often misdefined, even among medical prof essionals. It is concisely defined as ventilation greater than that amount needed to maintain normal CO2. A RR * 12-20/min is tachypnea, which as we saw in our scenario does not neccessarily lead to a ventilation * amount needed to maintain normal CO2. Exertional fatigue may present with tachypnea, but still present with elevated PCO2. Treating patients with a paper bag a treatment of the past. Underlying pathology must always be ruled out when a patient presents with respiratory symptoms. 5. During preop examination, you patient is SOB at rest with an abnormal ABG. You you grade this patient:5. d. Dyspnea (SOB) reflects an uncomfortable awareness of ones own breathing. Significance depends heavily on the stimulus or amount of activity required to partcipate it. Grade I, pt can walk a distance, but slowly, Grade II, can walk a limited distance before becoming SOB, Grade III, Becomes SOB walking ino a room and may or may not have abnormal ABGs. Grade IV is SOB @ rest with abnormal ABGs. There is no Grade V based on Dr. Vaccihianos criteria. 6.The proposed mechanisms of dyspnea/SOB share no common link they are: (1) increased WOB due to Increased Raw, stiff lungs, (2) abnormal ABGs with ether an Increased PCO2 or decreased PO2, or (3) altered respiratory drive with normal respiratory system. Having shared the mechanismsWhat are the proposed sources of breathlessness?a. Mechanical receptors in chest wall and lungsc. The sense of respiratory effort (increased with increas ed WOB)d. Imbalance between respiratory work, and ventilatory outpute. all of the above are proposed sources of breathlessness6. e all of the above are proposed sources of breathlessness. It is important to note that despite decades of work to elucidate the underlying mechanisms of dyspnea, no satisfactory explanation yet exisits. 7. Respiratory diseases leading to dyspnea as presented in class can be primarily be categorized into which of the following areas? a. Airway disease, Parenchymal Disease, Pulmonary Vascular Disease, Pleural Disease, and Disease affecting expansion and blood flowb. Hemopneumothorax, pneumothorax, hemothorax, pneumocephalusc. Diseases which increase in minute ventilation but decrease in alveolar ventilation d. Dyspnea secondary to centrally medullary respiratory depression7. a. Diseases that lead to dyspnea most commonly are attributed to airway disease (obstruction, edema, tumor, foreign body); parenchymal disease (scarring of the lung, which when severe enough may become fibrous and a diffusion barrier. Pulmonary infiltrates may also be considered in this category); pulmonary vascular disease (due to blockage or loss of vessels as in pulmonary emboli, which can cause V/Q mismatch); Pleural disease (air or liquid in the pleural space such as with pneumothorax or pleural effusion; an d diseases affecting expansion and blood flow diseases (primary disease of the respiratory muscles, nerve supply, or neuromuscular interaction examples here may include paralysis @ or below C-4 which would cause diaphragmatic paralysis, myesthesnia gravis, Eaton-Lambert syndrome, or kyphoscoliosis). Answers b, c, and d are incorrect. Walter Lippman Essay17. All of the following would be expected in a patient with Graves disease EXCEPTa. Increased sensitivity to heat and cold temperatures17. a Graves disease (hyperthyroidsims) is caused by overstimulation of the thyroid gland by circulating antibodies to the TSH receptor (which then increases production of thyroid hormone just as TSH would). T3 increases O2 consumption by target tissues and, accordingly, increases cardiac output and ventilation rate to match the increased O2 consumption. Thyroid hormones cause increased heat production as a result of increased aerobic metabolism. Indiction agents such as Ketamine should be avoided in thses patients beacuise of symapthomimietioc properties of this drug. 18. Effects of anesthestic agents on renal function include all of the following EXCEPT:b. General anesthesia dececres BP, RBF, GFR, and increases renal vascular resitance,c. Autoregulation is tightly maintained under general anesthesiad. Drugs which are alpha-re ceptor antagonists cause the smallest changes in renal hemodynamics and function18. a General anesthesia temporarily depresses renal finction as measured by urinary output, GFR, RBF, and electrolyte excretion. Rebnal impairmaent is usually short- lived and completely reversible. Maintainance of systemic blood pressure and especially preopeartive hyfration lessen the effect on renal function.. Spinal and epidural anestheisia, but not to the same extent as general anesthesia. In this setting, decrements in renal function parallell the magnitude of symaptheitc blockade. Agents that produce myocardial depression (such as volatile anesthesic on renal autoregulation are conflicting, but their indirect effects on renal hemodybnamics are probably of greater significance (Duke and Rosenberg, 1996) ed, as evinced by decreases in GFR, RBF and increased renal vascular resistance. D is also a correct response. 19. How should a patient with suspected coronary artery disease be monitored via ECG intraoperatively?19. e The most important modality for monitoring this patient intraoperatively is a multiple lead ECG system. Up to 89% of ECG changes that are due to myocardial ischemia that are present on 12-lead ECG will be detected by a V5 precordial lead alone. Limb lead II and precordial lead V have been recommended for simultaneous monitoring to detace intraoperative myocardial ischemia. This combination should detect more than 98% of ischemic episodes. In addition, leads II (inferior) and V5 ( apical, anterolateral) monitor the distribution of the RCA and LCA. 20. All of the following are considered essentials of preoperative cardiac evaluation EXCEPT:a. History ( CAD, Ventricular function, arrhythmias, valvular disease)b. Physical Exam (VS, Heart sounds)c. Laboratry Eval (CXR, ECG, others as indicated)d. Considering the surgeons history and physical as a complete risk assessment, after car efully noting his documentation. 20. d While History, physical examination and laboratory studies are a firm foundation on which to build an anesthesic plan of care, deferrential trusting in a colleagues assessment while valuable, but should never be considered complete. Disciplines outside anesthesia may share the mutual goal of an optimal patient outcome, but the focal areas of concern for respective disciplines are by neceiisty different. Entrusted with the care of patients demands precsion, diligence, and attention to detail. This begins with the preoperative cardiac evaluation. Preoperative cardaic assessment includes a history, physical examination and labortayru resulkts, as well as historical information should asses the presence, severity and reversibility of corinary aretert disease risk factors for coronary artery disease, anginal patterns, and history of myocardial infarction: The left and right ventricular function (exercise caacity, pulmonary edema, plumonary hypertension; and the prescene of symproma tic dysrhythmsias (palpitations, syncopal or presyncopal episodes. Patients with valvular heart disease may be symptomatic for emobolic events. On physical examination, particular attention should be paid to VS, HR, BP, and PP (determinants of myocardial O2 consumption and delivery) , JVD, peripheral edema, pulmonary edema, or an S3 gallup and the presence of murmurs. Baseline labs include CXR, and ECG. Further evaluation may be determined based on results (Reich and Jaffee)Bibliography: