Pshycology Test Essay Research Paper Physiology ExamDirections

Pshycology Test Essay, Research Paper Physiology Exam 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 one?s academic and clinical prowess.

Pshycology Test Essay, Research Paper

Physiology Exam

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 one?s 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. ABG?s are drawn, and the results are: pH – 7.3, PCO2 55, HCO3 24, PaO2 60.

1. Why is this gentleman?s PCO2 elevated?

a. Not enough total ventilation (CNS/Respiratory muscle weakness)

b.Too much total ventilation Dead Space (Rapid breathing)

c. a only

d. a and b are corect

(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 gentleman?s PaCO2 of concern to you clinically?

a. Increased PaCO2 (if no compensatory increase in HCO3) results in fall in pH

b. Increased PaCO2 results in a decrease in PaO2 unless FiO2 can increase enough to compensate

c. The higher the PaCO2, the less well defended this pt is against a further decrease in VA

d. a, b, and c are correct

e. His PaCO2 in this case is of little concern clinically

2. d – (a) This patient?s 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 patient?s 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.

4. Hyperventilation defined is

a. RR * 12-20/min

b. Ventilation * amount needed to maintain normal CO2

c. Exertional fatigue (result of cardiovascular, neuromuscular, or non-pulmonary disease)

d. Should be treated by placing a paper bag over a patient?s mouth and having them rebreath CO2

4. b – Hyperventilation is often misdefined, even among medical professionals. 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:

a. Grade I

b. Grade II

c. Grade III

d. Grade IV

e. Grade V

5. – d. Dyspnea (SOB) reflects an uncomfortable awareness of one?s 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 ABG?s. Grade IV is SOB @ rest with abnormal ABG?s. There is no Grade V based on Dr. Vaccihiano?s 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 ABG?s with ether an Increased PCO2 or decreased PO2, or (3) altered respiratory drive with normal respiratory system. Having shared the mechanisms

What are the proposed sources of breathlessness?

a. Mechanical receptors in chest wall and lungs

b. Chemoreceptors for PO2 and PCO2

c. The sense of respiratory effort (increased with increased WOB)

d. Imbalance between respiratory work, and ventilatory output

e. all of the above are proposed sources of breathlessness

6. 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 flow

b. Hemopneumothorax, pneumothorax, hemothorax, pneumocephalus

c. Diseases which increase in minute ventilation but decrease in alveolar ventilation

d. Dyspnea secondary to centrally medullary respiratory depression

7. – 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; and 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.

8. – PFT abnormalities are categorized into one of two patterns. They are:

a. Respiratory and Cardiac

b. Inspiratory and Expiratory

c. Obstructive and Restrictive

d. Smoking and non-smoking

e. Viral and Bacterial

8. c – Patterns of Pulmonary Functional Impairment are categorized into one of two patterns (1) Obstructive , such as asthma, COPD, chronic bronchitis (which increase lung volumes {air is “trapped and stacked” =* increased RV, TLC, and RV/TLC and decrease expiratory flow rates (decreased FEV1, FEV1/FVC, and MMFR) (2) Restrictive (decreased expiratory flow rates over time – decreased: TLC, VC, RV, and FRC. FEV1/FVC and MMFR are preserved)

An FEV1 * 80% is considered decreased. An FEV1/FVC ratio * 50% is significant, and these patients are likely going to be more difficult to wean from the ventilator

9. In regard to neural control of the airways, the vagus nerve (PSNS) carries afferent and effeerent nerve fibers with neurotransmitters which interact with specific protein macromolecular receptors to mediate airway responses. These responses take place at the goblet cell, blood vessels, submucosal glands, smooth muscle, and epithelial cells. When considering respiratory smooth muscle, it can be said that the neurotransmitter VIP has __________ properties, while the neurotransmitter acetylcholine possesses ___________ properties

a. Vasodilatory, Vasoconstrictive

b. Vasodilatrory, Vasodilatory

c. Vasoconstrictive, Vasodilatory

d. Vasoconstrictive, vasoconstrictive

9. e – VIP, a short chain amino acid or “small protein” mediates smooth muscle dilation to counter the vasoconstrictive properties of the neurotransmitter acetylcholine

10. You are leaving the ED after being paged for an “almost ready to be intubated” young asthmatic patient who subsequently responded well to your treatment of nebulized beta 2 agonists, and corticosteroids. You?ve been up all night writing exam questions, and as you drift off to sleep you are dreaming of hyperresponsive airways. Understanding the current hypothesis for pathology includes epithelial injury and airway inflammation??you consider the possibilities of airway hyperresponsiveness. You conclude that the possibilities of airway hyperresponsiveness incude:

a. Mediator release from inflammatory cells (luekotrines

b. Epithelial disruption which result in increased permeability of inhaled agents

c. Injury and inflammation after degradation of certain neuropeptides

d. A bronchial smooth muscle relaxant factor produced by the airway peithelium is decreased of absent

e. All of the above are possibilities of airway hyperresponsiveness.

10. e – all of the above. Mediator release form inflammatory cells can cause bronchoconstriction. Mediators such as leukotrines have positive effect on asthma, by modulating the degree of bronchoconstriction, without modulation, unopposed bronchoconstriction progresses. Without an epithelial barrier, submucosa of the airways are directly exposed to irritants, allergens and infections. Injury and inflammation to exposed submuxcosa may cause a release of tachykinins, which are now unopposed and cause bronchoconstriction.

11. The two branches of the immune system are:

a. Active and Passive

b. Focal and General

c. Adaptive (Specific) and Non adaptive (Non-Specific)

d. Adaptive and Maladaptive

11. c – the two branches of the immune system are adaptive (specific), and non-adaptive (non-specific)

Adaptive or specific consist of T-Cells, and B-Cells (lymphocytes), while nonadaptive are barriers which involve inflammatory responses, asd the part of the immune system which the body uses to recognize self from non-self. These cells emerge from their “home” in the bone into the “organ world” to mature. Lymphocytes which differentiate in the Thymus become T-Cells, lymphocytes which mature in bone marrow are B-Cells. The bone marrow and thymus are primary lymphoid organs.

12. Complete the following table, match the appropriate Blood Types with approriate antibodies and antigens. Which is the universal donor, and which is the universal recipient?

Blood TypeAntigenAntibody

a. A


c.A+B Antibodies

d. AB

12. Blood TypeAntigenAntibody

a. AA B

b. BBA

c. ONo AntigenA + B Antibodies (Universal Donor)

d. AB Antigens A + B No Antibodies (Universal Recipient)

13. A 24 y/o male is brought in for emergency appendectomy. In the emergency department he had an allergic reaction to his IV antibiotic. Which of the following immunoglobulins was most likely produced during this allergic reaction?

a. IgE

b. IgM

c. IgG

d. IgA

e. IgD

13. a – IgE is the subclass responsible for allergies; the IgD and IgM subclasses function as antigen receptors on lymphocytes; the IgG subclass comprises most of the antibodies in the blood; and the IgA subclass is found in external secretions.

Questions 14 and 15 are based on the following scenario:

Mrs. Jones is a 42 year old female who presented to the emergency department this evening for an acute onset of paliptations, chest pain, and shortness of breath. She has a known history of atrial fibrillation and mitral valve prolapse. Her current medications include Digoxin and hydrochlorthiazide. Currently, her ECG reflects atrial fibrillation with a rapid ventricular response at a rate of 220. He blood pressure is 90/palpation, she is cool, pale, and diaphoretic, and you are called to sedate her prior to sychronized cardioversion, While reviewing her chart, she becomes acutely hypotensive, and lethargic. She is cardioverted @ 100 joules, and converts to normal sinus rhythm, and her vital signs improve. 30 minutes later, Mrs. Jones? speech becomes slurred, and she complains of left facial paresthesias and droop, and left upper extremity paresis and paresthesias.

14. What is the most likely cause of Mrs. Jones? post-cardioversion symptoms?

a. Her brain has reperfused following management of her hypotension

b. Her sedation is making her “feel funny”

c. She is hyperventilating because of all of the excitement

d. A thrombus has cause and area of cerebral ischemia versus infarct

e. Both B and D are correct

14. d – Chronic atrial fibrillation is often due to hypertrophic atrial muscle through which conduction from sinus to AV node is disrupted, and asynchornous. The result is turbulent flow, and eddys of blood in the atrium which may fibrinolyze and become a clot. Once returned to Normal sinus rhythm, this clot likely was ejected and lodged in the microcirculation in the left side of her prain, causing her contralateralsensory and motor symptoms. She certainly has not perfused her brain (a), was cardioverted prior to sedation because of her acute hemodynamic instability (b), there is no respiratory history to determine c.

15. Mrs Jones BP rises to 160/100. The ED staff wishes to be aggressive in treating her hypertension with IV Nitrates. You are asked for your opinion. You recommend:

a. Hang the Nitrates Stat

b. With this MAP of 80, her cerebral perfusion pressure she should receive sublingual calcium channel blockers

c. Neurological insult has likely compromised her autoregulatry capabilities

d. Mrs Jones? hypertension is likely compensatory, and an acute decrease may further compromise cerebral perfusion.

e. Both c and d are correct.

15. e – both c and d are correct. Autoregulation via a myogenic reflex exists in the brain to maintain blood flow at 50-55 mL/100 g of brain tissue if pressure is between 50-60 mmHg and 150-160 mmHg. Autoregulation is an intrinsic effect in vascular smooth muscle (mediated by the myogenic reflex) which , in a sudden change in perfusion pressure, returns tissue flow back to normal by vasoactive responses (ie; vasodilation or vasoconstriction. In this case, while autoregulation may likely be compromised in the focal areas of the ischemic or infarcted brain, they are not completely destroyed. The brain retains some autoregulatory capabilities to maintain cerebral perfusion pressure. Hypertension is expected in ischemic events, ant the goal should be to maintain a mean arterial pressure close to her baseline, which we may assume is somewhat elevated in that she is prescribed hydrochlorothiazide, and antihypertensive medication. B is in incorrect ; MAP = 1SBP x 2DBP/3 =160 + 200/3 =120, and calcium channel blockers may decrease BP by blocking voltage-gated calcium channels, interrupting the physiological compensation attemping to maintain cerebral perfusion pressure (Cerebral perfusion pressure is defined as the difference between MAP and either ICP or CVP, whichever is higher). Nitrates (a) would decrease blood pressure, and ultimately cerebral perfusion pressure as well, essentially decompensation a physiological compensatory response. Whew!

16. Which of the following is not true regarding cerebral aneurysms?

a. Aneurysms are thought to reult from herniation of the intima through a fragmented internal elastic membrane

b. Factors which may contribute to a rupture include large size and sudden change in transmural pressure

c. Prodromal symptoms of intracranial aneurysms include severe headache, focal neurological signs

d. Expansion of an aneurysm may cause third nerve palsy with or without eye pain

e. all of the above are true

16. e – all of the above are true regarding cerebral aneurysms.

17. All of the following would be expected in a patient with Graves? disease EXCEPT

a. Increased sensitivity to heat and cold temperatures

b. weight loss

c. increased O2 consumption

d. increased cariac output

e. increased ventilation rate

17. a – Grave?s 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:

a. Increase Renal function

b. General anesthesia dececres BP, RBF, GFR, and increases renal vascular resitance,

c. Autoregulation is tightly maintained under general anesthesia

d. Drugs which are alpha-receptor antagonists cause the smallest changes in renal hemodynamics and function

18. 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?

a. Leads I and II

b. Lead II

c. ECG Leads I, II, and III

d. 12 lead ECG

e. Leads II and V5

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 surgeon?s history and physical as a complete risk assessment, after carefully 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 colleague?s 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 sympromatic 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)