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Foundations Midterm Practice Exam 1. Which of the following is evidence for the existence of cell receptors? a. Extreme potency and efficacy of drugs b. Chemical selectivity (similar molecules produce similar effects c. Molecular cloning and reconstitution d. All of the above 2. What factors determine the affinity of a drug for a receptor? a. Shape, charge, atomic composition, temperature b. Shape, size charge c. Shape, size, charge, atomic composition d. Shape is the only thing that determines affinity 3. Which of the types of drugs has the highest affinity for a receptor? a. Agonist b. Antagonist c. Partial agonist d. All of these types could have the same level of affinity 4. Which of the types of drugs has the highest efficacy? a. Agonist b. Antagonist c. Partial agonist d. All of these types could have the same level of efficacy 5. How does binding of a ligand activate a G-protein in GPCRs? a. The exchange of ADP for ATP on the alpha subunit of the G-protein b. The exchange of GDP for GTP on the alpha subunit of the G-protein c. The exchange of ADP for ATP on the gamma subunit of the G-protein d. The exchange of GDP for GTP on the beta subunit of the G-protein 6. What is the difference between a competitive and noncompetitive antagonists? a. Noncompetitive antagonists bind either allosterically or irreversibly, so the antagonistic effect cannot be overcome with increased dose of agonist b. Noncompetitive antagonists can be overcome with increased dose of agonist while competitive antagonists cannot c. Competitive antagonists bind to a site that is not the ligand binding site d. Noncompetitive antagonists turn off endogenous activity of the receptor itself 7. Which G protein coupling pathway increases activity of cAMP and PKA and can indirectly alter ion channel function and gene transcription? a. Qs b. Qi
c. Qq d. PLA2 8. Beta adrenergic receptors in the heart regulate cardiac rate and contractile strength. Studies have indicated that about 90% of the beta receptors in the heart are spare receptors. Which of the following statements about spare receptors is most correct. a. Spare receptors, in the absence of drug, are sequestered in the cytoplasm b. Spare receptors may be detected by finding that the drug receptor interaction lasts longer than the intracellular effect c. Spare receptors activate the effector machinery of the cell without the need for a drug d. Spare receptors may be detected by the finding that the EC50 is smaller than the Kd for the agonist 9. Which of the following statements is NOT true about methotrexate? a. This drug can be used to treat certain types of cancer, severe psoriasis, and severe rheumatoid arthritis b. When taking methotrexate for extended periods of time, both blood tests and liver biopsies should be performed regularly c. Methotrexate should not be used if you are allergic to gluten d. Methotrexate should not be used if you are pregnant, trying to get pregnant, or nursing 10. A new drug is approved to treat hypertension (Thiazide X) that marketers are claiming to be 100 times “better” than the current standard treatment (Thiazide Y). Upon further investigation, you find that a 3mg dose of X provides the same effect as 300mg of Y, but the therapeutic index of X is 10 while that of Y is 100. What would you say to a patient who comes in asking about this new drug? a. Thiazide X has a higher efficacy than Thiazide Y, but it has a much smaller therapeutic index which means it is less safe than the current standard b. Thiazide X has a higher potency than Thiazide Y, but it has a much smaller therapeutic index which means it is less safe than the current standard c. Thiazide X has a lower potency and efficacy than Thiazide Y, but it has a much smaller therapeutic index which means it is safer than the current standard d. Thiazide X has a lower potency and efficacy than Thiazide Y, but it has a much smaller therapeutic index which means it is less safe than the current standard 11. Which of the following correctly pairs the adrenergic receptors with their correct GPCR pathway? a. Alpha1 receptors are Gq, Alpha2 receptors are Gi, Beta1 receptors are Gs, Beta2 receptors are Gs b. Alpha1 receptors are Gs, Alpha2 receptors are Gq, Beta1 receptors are Gi, Beta2 receptors are Gs c. Alpha1 receptors are Gi, Alpha2 receptors are Gi, Beta1 receptors are Gs, Beta2 receptors are Gq d. Alpha1 receptors are Gq, Alpha2 receptors are Gs, Beta1 receptors are Gi, Beta2 receptors are Gi 12. Which GPCR pathway cause smooth muscle contraction?
a. Qs b. Qi c. Qq d. PLA2 13. Which of the drugs represented on this dose-response curve has the highest efficacy? a. Green b. Blue c. Purple d. They have the same efficacy 14. Which of the drugs represented on this dose response curve is more potent? a. Blue (A) b. Green (B) c. They have the same potency 15. Which of the following factors are essential to normal embryological development? a. Growth factors b. Transcription factors c. Cell behaviors d. Apoptosis e. All of the above 16. A woman walks into your clinic complaining of abdominal cramping and a missed period. She claims that her period should have started two weeks ago. You collect a urine sample and the pregnancy test you ordered came back positive. Remembering from your thorough history that she had attended a total rager of a party and gotten
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blackout drunk the night before, you consider the possible effects of the alcohol on the baby. What type of effect might you expect to see (if any) in the baby’s development? a. A major malformation due to a numeric chromosomal abnormality b. A major disruption of development c. A minor deformation such as a clubbed foot d. Either miscarriage or no effect 17. A child presents with a great vessel septum defect. Which germ layer is responsible for this defect? a. Mesoderm b. Endoderm c. Ectoderm d. Electroderm 18. In the child from Q17, which subset of germ layer is responsible? a. Intermediate mesoderm b. Visceral lateral plate mesoderm c. Neural crest ectoderm d. Surface ectoderm 19. In development the ___ (germ layer) will give rise to the gut tube, while the ___ (germ layer) will give rise to the muscles and supporting tissue for the gut tube a. Endoderm, mesoderm b. Endoderm, endoderm c. Ectoderm, mesoderm c. Mesoderm, ectoderm 20. Which of the following birth defects is caused by insufficient regression of the primitive streak? a. Saccrococcygeal teratoma b. Laterality defect c. Skull defects d. Neurological defects 21. What structure forms from mesoderm, endoderm, and extra-embryonic mesoderm in week 3 of development to function in waste removal? a. Amnion b. Allantois c. Neural plate d. Visceral lateral plate
22. A woman is seen in your clinic who is pregnant with monozygotic twins. The embryo split into twins late in the blastocyst stage, after the amnion had formed. What type of twinning is this? a. Monochorionic monoamnionic b. Dichorionic monoamnionic c. Monochorionic diamnionic d. Dichorionic diamnionic 23. Which of these would NOT be a concern for the twins from Q22? a. Conjoining b. Twin-twin transfusion syndrome c. Twisted umbilical cord d. Strangulation 24. Which of the following features is NOT a characteristic of a reticulocyte? a. It is a precursor to erythrocytes b. It contains no nucleus c. It contains some ribosomes, making it stain slightly more basophilic than a normal erythrocyte d. It contains a nucleus and will become a mature erythrocyte when the nucleus is ejected 25. What function of normal erythrocytes would be affected in those with a defect in a gene that codes for the band 3 protein? a. Storage of oxygen in muscle fibers b. Cell membrane flexibility c. Anion exchange of HCO3- and Cl d. Binding of O2 to the heme molecule 26. Which of the following ranks these oxygen-binding molecules in order from HIGHEST to LOWEST affinity? I) myoglobin II) R-state hemoglobin III) T-state hemoglobin a. III > II > I b. II > I > III c. I > II > III d. III > I > II 27. What is the globin chain composition of the form of hemoglobin that predominates in a newborn? a. α2β2 b. α2γ2 c. α2δ2 d. α2ε2
28. The presence of which of the following molecules does NOT result in a right shift of the oxygen binding curve? a. H+ b. CO2 c. BPG d. O2 29. How does hemoglobin contribute to acid-base homeostasis? a. Conversion of CO2 to bicarbonate via carbonic anhydrase b. Binding basic metabolites for removal from the body c. The Bohr effect d. I am absolutely going to PASS this test! 30. How might kidney disease lead to anemia? a. Thrombopoietin production in the kidney would be inhibited b. It wouldn’t c. Erythropoietin production in the kidney would be inhibited d. Stem cells from the kidneys would not give rise to red blood cell precursors 31. During your exam you are anxiously flipping your scratch piece of paper over trying to find a blank spot to draw out ANOTHER 2x2 table when you get a paper cut on your finger (ouch!) and it bleeds a little bit before stopping. Which of the following is the first thing the damaged blood vessels do to respond to your injury? a. Vasoconstriction to reduce red blood cell leakage and increase platelet/vWF contact with exposed sub-endothelial collagen b. Vasodilation to increase number of white blood cells reaching the site of injury c. Exposed tissue factor and binding of FVII initiates coagulation d. FXII, FXI, FIX, and FVIII in the bloodstream react to thrombin to amplify coagulation 32. In the situation above, what is the function of thrombin in hemostasis as your paper cut heals? a. To initiate coagulation b. To regulate clot formation c. To convert fibrinogen to insoluble fibrin d. To bind to the phospholipid surface of platelets in formation of the platelet plug 33. Oh no! For some reason your paper cut just won’t stop bleeding! You’ve also noticed that you have had a lot of nosebleeds lately, but you’ve never had either of these problems in the past. Which of the following is the most likely explanation for this? a. You have Von WIllebrand Disease b. You have thrombocytopenia caused by a vitamin deficiency c. You are deficient in FVII
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d. You have Hemophilia A 34. In Hemophilia A, which laboratory test would you expect to have abnormal results caused by the disease? a. APTT b. PT-INR c. Fibrinogen d. AST/ALT 35. A patient presents to your clinic complaining of fatigue and shortness of breath during her daily walks. She claims to have a family history of anemia. She is jaundiced and you are able to palpate her spleen. You do a peripheral blood smear while waiting for the lab to return the CBC results. What do you expect to find in the CBC results based on the information provided? a. A high MCV b. A normal reticulocyte count c. A normal total bilirubin d. A high MCHC 36. If the answer you chose for Q35 does come back on the CBC, what diagnostic test would you run to confirm your suspected diagnosis? a. Sequencing of a globin gene b. No additional testing is needed c. Osmotic fragility or EMA binding test by flow cytometry d. Hemoglobin electrophoresis 37. What classification of anemia does your suspected diagnosis fall under? a. Normocytic hemolytic b. Macrocytic megaloblastic c. Microcytic d. Normocytic nonhemolytic 38. What type of cell is characteristic of beta thalassemia? a. Spherocytes b. Target cells
c. Teardrop cells d. Hypochromic cells 39. Why might an infant with Sickle Cell Disease be asymptomatic for several months (up to a year) after birth? a. This does not happen b. It takes this long for the sickle cells to build up and cause symptoms c. Elevated HbF type hemoglobin at birth is not replaced with HbS type until 6-9 months d. Sickle cell disease is asymptomatic and simply confers malaria resistance to carriers 40. You are a pathologist who reads peripheral blood smears sent from clinics in your area. You recognize schistocytes in the smear of a 72 year old man. What might you find in the medical history and lab findings for this patient that would most completely explain the presence of schistocytes in his blood? a. Anemia evidenced by his Hgb and Hct b. A very slight Vitamin D deficiency c. Past medical history of COPD d. A mechanical heart valve placed one year prior 41. A patient presents to your clinic with a blood pressure of 165/96 mmHg. What is one way that you might treat a case of stage 2 hypertension? a. Prescribe an alpha1 receptor agonist b. Prescribe an Angiotensin Converting Enzyme agonist c. Prescribe an Angiotensin Converting Enzyme inhibitor d. Prescribe a beta1 receptor agonist 42. What is one major side effect of the drug you prescribed in Q41? a. Dry cough b. Bradycardia c. Polyuria d. Tachycardia 43. If your patient quits taking the drug you prescribed in Q41 because of the side effect you named in Q42, what is another drug that you could try that would have the same effect without that side effect? a. Methotrexate b. Lisinopril c. Hydrochlorothiazide d. Gentamicin 44. A small change to which of the following determinants of total peripheral resistance would have the greatest effect on blood pressure?
a. Blood viscosity b. Vessel length c. Vessel radius d. All of these will affect blood pressure equally 45. Cardiac troponin is frequently tested for those presenting to the ER with chest pain. The test is repeated every few hours to monitor how the concentration of cardiac troponin is changing over time. A patient presents to your ER complaining of several hours of chest pain that is steadily worsening. His initial cardiac troponin level is 0.38 ng/mL (normal <0.05 ng/mL) and several hours later this level has risen to 0.73 ng/mL. What might this increased value indicate? a. The patient is having an active myocardial infarction that is continuing to worsen b. The patient was having a myocardial infarction but it is no longer worsening c. The patient has a pulmonary embolism d. The patient is absolutely going to die 46. What type of necrosis is recognizable by tissue that is bright pink and amorphous? a. Coagulation necrosis b. Liquefactive necrosis c. Caseous necrosis d. Fibrinoid necrosis 47. What type of necrosis is recognizable by cells that maintain their basic structure but appear hypereosinophilic? a. Coagulation necrosis b. Liquefactive necrosis c. Caseous necrosis d. Fibrinoid necrosis 48. Which of the following is NOT a molecular change that occurs in cells in response to hypoxia? a. Depletion of ATP stores b. Apoptosis c. Oxidative stress d. Loss of calcium homeostasis 49. What is the primary treatment of acetaminophen poisoning and why is it used? a. Glutathione because it protects cells from oxidative stress b. Nothing, acetaminophen poisoning will self-resolve over time c. N-acetylcysteine because it is a precursor of glutathione d. L-acetylcysteine because it is a precursor of cysteine
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50. You investigate two tissues under a microscope. Tissue A shows cellular swelling with broken cell membranes and an inflammatory response while Tissue B shows cellular condensation with intact cell membranes and no inflammatory response. What process of cell death did each tissue experience and what may have been the cause of cell death? a. Tissue A went through necrosis that may have been caused by hypoxia and Tissue B went through apoptosis that may have been caused by a neurodegenerative disorder b. Tissue A went through apoptosis that may have been caused by ischemic injury and Tissue B went through apoptosis that may have been caused by a neurodegenerative disorder c. Tissue A went through necrosis that may have been caused by bacterial infection and Tissue B went through necrosis that may have been caused by AIDS d. Tissue A went through apoptosis that may have been caused by a neurodegenerative disorder and Tissue B went through necrosis that may have been caused by hypoxia 51. What is the difference between a thrombus and an embolus? a. A thrombus is found in venous circulation while an embolus is found in arterial circulation b. A thrombus is found in arterial circulation while an embolus is found in venous circulation c. A thrombus is a piece of an embolus that has broken off and traveled elsewhere in the body d. An embolus is a piece of a thrombus that has broken off and traveled elsewhere in the body 52. You are a pathologist investigating a tissue sample from a patient that died suddenly. You see what appears to be clotted blood in your slide and need to determine whether this is a post-mortem clot or a true thrombus. What feature would you look for to conclude that what you are seeing is a true thrombus? a. No attachment to the vessel wall b. Tightly packed blood cells that do not appear to follow any rhyme or reason c. Lines of zahn d. Something that looks suspiciously like chicken fat 53. What puts individuals with the Factor V Leiden mutation at higher risk for thrombosis? a. Mutated FV is resistant to inactivation by activated Protein C b. Mutated FV promotes faster thrombosis c. The Factor V Leiden mutation reduces risk for thrombosis d. I’m going to pass this test with flying colors! 54. Which of these possible outcomes of pulmonary embolism is most common? a. Sudden death caused by right heart failure b. The PE is small and clinically silent c. Pulmonary hemorrhage with embolic obstruction of medium-sized pulmonary arteries d. Pulmonary hypertension
55. Where to white infarcts primarily occur? a. In organs with end-arterial circulation b. In organs with collateral circulation c. In loose tissues d. In the small intestine 56. How can tissue show signs of hemorrhage but still be infarcted? a. This is not possible b. The occluded vessel does not allow any blood to reach the tissue c. Nearby capillaries attempting to perfuse hypoxic tissue become leaky, allowing blood into the extracellular space d. Apoptosis of infarcted cells appear like hemorrhage 57. Which of the following is NOT a component of Virchow’s Triad? a. Abnormal flow b. Endothelial injury c. Hypercoagulable state d. Coagulation factor deficiency 58. A 56 year old woman presents to your emergency room complaining of sudden onset extreme pain in her right leg. Upon physical examination, you find that the leg is pale and cool to the touch. No popliteal, dorsals pedis, or posterior tibial pulse can be found. The leg is not swollen. What is your diagnosis? a. Deep vein thrombosis b. Deep vein embolism c. Atherosclerosis d. Arterial embolism