PMCOL 200 FINAL REVIEW QUESTIONS ANSWERED CORRECTLY LATEST UPDATE 2026

PMCOL 200 FINAL REVIEW QUESTIONS ANSWERED CORRECTLY LATEST UPDATE 2026 What is atherosclerosis? - Answers Formation of plaque within arteries; plaque can dislodge and damage distant organs. How is atherosclerosis different from arteriosclerosis? - Answers Atherosclerosis is plaque formation in arteries; arteriosclerosis is the broader idea of arterial stiffening. What coronary manifestation of atherosclerosis should you know? - Answers Myocardial infarction / heart attack. What carotid manifestation of atherosclerosis should you know? - Answers Stroke. What peripheral manifestation of atherosclerosis should you know? - Answers Intermittent claudication. What renal manifestation of atherosclerosis should you know? - Answers Chronic kidney disease. What mesenteric manifestation of atherosclerosis should you know? - Answers Abdominal pain. What three broad processes drive plaque development? - Answers Lipids, blood clots, and inflammation. What is the foundational pharmacologic approach for reducing ASCVD? - Answers Lower LDL-C. What are the four major lipoproteins emphasized? - Answers Chylomicrons, VLDL, LDL, and HDL. What does NPC1L1 do in lipid handling? - Answers Mediates dietary cholesterol uptake into enterocytes; it is inhibited by ezetimibe. What happens to VLDL in the endogenous pathway? - Answers It is cleaved by LPL to IDL and then LDL. What receptor clears LDL back into the liver? - Answers The LDL receptor. What receptor delivers HDL cholesterol back to the liver? - Answers SR-BI. What enzyme do statins inhibit? - Answers HMG-CoA reductase. What is the main result of lowering blood cholesterol with statins? - Answers Increased LDL receptor expression and increased LDL uptake from blood. How do PCSK9 inhibitors lower LDL? - Answers They block PCSK9-driven LDL receptor degradation, increasing LDL receptor availability. What enzyme does bempedoic acid inhibit? - Answers ATP-citrate lyase. What do fibrates activate? - Answers PPAR-alpha. How does aspirin reduce clotting risk in ASCVD? - Answers It inhibits platelet COX-1, lowering TXA2 and platelet aggregation. What is the basic blood pressure equation? - Answers Blood pressure = cardiac output x total peripheral resistance. What is the cardiac output equation? - Answers Cardiac output = stroke volume x heart rate. What is normal blood pressure? - Answers Less than 120/80 mmHg. What do baroreceptors sense? - Answers Stretch in the carotid artery and aorta. What happens to sympathetic tone when blood pressure falls? - Answers It increases. Which receptor on the SA node does norepinephrine stimulate to raise heart rate? - Answers Beta-1 receptors. Which receptor on vascular smooth muscle does norepinephrine stimulate to raise TPR? - Answers Alpha-1 receptors. What happens to renin release when blood pressure is low? - Answers Renin release increases, activating RAAS. What is pressure natriuresis? - Answers Sodium excretion in response to increased blood pressure. What blood pressure range is 'elevated'? - Answers SBP 120-129 with DBP less than 80. What defines stage 1 hypertension? - Answers SBP 130-139 or DBP 80-89. What defines stage 2 hypertension? - Answers SBP at least 140 or DBP at least 90. Name three bad outcomes of chronic hypertension. - Answers Stroke, dementia, vision loss, heart failure, heart attack, kidney disease/failure, sexual dysfunction. Name three dietary risk factors for hypertension. - Answers Higher sodium intake, lower potassium intake, lower calcium/magnesium intake, poor diet quality, alcohol intake. Why do drugs become necessary in chronic hypertension? - Answers Baroreceptors reset upward, RAAS is overactive, arteries stiffen, and pressure natriuresis shifts right. Which diuretic class is first line for HTN? - Answers Thiazides. Name the thiazides emphasized in lecture. - Answers Hydrochlorothiazide, chlorthalidone, indapamide. What are major thiazide adverse effects? - Answers Hyponatremia and hypokalemia. What does amiloride block? - Answers ENaC in the distal tubule. What does furosemide block? - Answers NKCC in the thick ascending limb. What is the main ACE inhibitor adverse effect pair? - Answers Dry cough and angioedema. Name three ARBs from lecture. - Answers Losartan, valsartan, telmisartan. What serious combination should never be used? - Answers ACE inhibitor plus ARB. What is a key adverse effect of spironolactone? - Answers Gynecomastia. Which calcium channel blocker subclass is first line for HTN? - Answers Dihydropyridines. Name two non-DHP calcium channel blockers. - Answers Verapamil and diltiazem. What is the main non-DHP adverse effect? - Answers Bradycardia. When are beta blockers especially useful in HTN? - Answers When the patient also has HFrEF. When are alpha-1 blockers particularly useful in HTN? - Answers When the patient also has BPH. Which antihypertensives are highlighted for pregnancy/preeclampsia? - Answers Methyldopa and hydralazine. Name three ways bacteria are classified in this lecture. - Answers By oxygen use, shape, and Gram cell wall type. What is a bacillus? - Answers A rod-shaped bacterium. What is a coccus? - Answers A spherical bacterium. What is a spirochete? - Answers A spiral-shaped bacterium. What major polymer makes the bacterial cell wall? - Answers Peptidoglycan. Which bacterial wall is thicker in peptidoglycan: Gram-positive or Gram-negative? - Answers Gram-positive. What additional structure surrounds Gram-negative bacteria? - Answers A second lipid membrane containing lipopolysaccharides and lipoproteins. What are the two alternating sugar residues in peptidoglycan? - Answers GlcNAc and MurNAc. What enzyme polymerizes glycan strands? - Answers Glycosyltransferase. What enzyme cross-links peptidoglycan strands? - Answers Transpeptidase / DD-transpeptidase / penicillin-binding protein. What is the strict definition of an antibiotic? - Answers A soluble compound produced and released by microorganisms that inhibits or kills other microorganisms. What is the difference between bactericidal and bacteriostatic? - Answers Bactericidal permanently removes replicative ability; bacteriostatic temporarily halts growth/replication. What does 'therapeutic index' mean? - Answers TD50/ED50, the ratio of adverse-effect concentration to effective concentration. Why are penicillins and cephalosporins called beta-lactams? - Answers They contain a four-membered beta-lactam ring. How do beta-lactams kill bacteria? - Answers They inhibit DD-transpeptidase/PBP, block cell wall cross-linking, create holes, and act bactericidally. What cell wall drug in the lecture is not a beta-lactam? - Answers Vancomycin. How do sulfonamides and trimethoprim work together? - Answers They mimic folate-pathway intermediates and block sequential steps in bacterial folic acid synthesis. What cell wall drug is not a beta-lactam? - Answers Vancomycin. Where do chloramphenicol and macrolides bind? - Answers The 50S ribosomal subunit. Where do tetracyclines bind and what do they block? - Answers They bind to the 30S subunit and block incoming tRNA binding. What are the three emphasized aminoglycoside actions? - Answers Misreading, inhibit translocation. Why don't these antibiotics usually stop human cytoplasmic protein synthesis? - Answers Because bacterial 70S ribosomes differ from mammalian 80S ribosomes. Name four resistance mechanisms. - Answers Drug inactivation, altered binding site, altered metabolic pathway, reduced drug accumulation/efflux. What is a virion? - Answers The extracellular virus particle outside an infected cell. What does 'obligate intracellular parasite' mean? - Answers A virus must use host cell machinery to reproduce. What is viral range? - Answers The group of cell types or species a virus can infect. What is a bacteriophage? - Answers A virus that infects bacteria. What is pathogenicity? - Answers The ability of a virus to cause disease. What is virulence? - Answers The degree of pathogenicity. What is latency? - Answers A dormant state in which the virus persists in the host. What is meant by a carrier? - Answers A chronically infected person who serves as a reservoir of virus. What are the three capsid morphologies highlighted? - Answers Helical, icosahedral, and complex. What are the four broad steps of the viral life cycle? - Answers Absorption, penetration, replication, and release. What is the major exception among DNA viruses mentioned? - Answers Poxviruses replicate in the cytoplasm and carry their own DNA-dependent RNA polymerase. What enzyme must double-stranded RNA viruses provide? - Answers RNA-dependent RNA polymerase. What unique direction of information flow defines retroviruses? - Answers RNA - DNA - mRNA - protein. What is the general principle of antiviral combination therapy? - Answers It can create synergism and delay resistance. Why are antiviral drugs described as virustatic? - Answers They work on replicating virus and do not eliminate latent virus. What kind of drug is acyclovir? - Answers A nucleoside analog that causes DNA chain termination. What virus enzyme gives acyclovir its selectivity? - Answers Viral thymidine kinase. Name one mechanism of acyclovir resistance. - Answers Loss of viral thymidine kinase, altered thymidine kinase specificity, or altered viral DNA polymerase. What receptor does maraviroc block? - Answers CCR5. What kind of HIV drug is lamivudine? - Answers An NRTI: nucleoside reverse transcriptase inhibitor. Why does lamivudine terminate viral DNA synthesis? - Answers It lacks the 3' hydroxyl group needed for the next nucleotide addition. What does raltegravir inhibit? - Answers HIV integrase. What does saquinavir inhibit? - Answers HIV protease. What are amantadine and zanamivir used for? - Answers Amantadine blocks influenza A uncoating; zanamivir blocks influenza A and B neuraminidase. What is metastasis? - Answers Spread of cancer to other parts of the body. What two broad sources of cancer causes were emphasized? - Answers Environmental and genetic factors. Name the phases of the cell cycle. - Answers G1, S, G2, M, and G0. What do tumor suppressor genes do? - Answers They repress the cell cycle, promote apoptosis, or support DNA repair. Name two tumor-suppressor examples from lecture. - Answers BRCA and p53. What is a proto-oncogene? - Answers A normal gene that helps regulate cell division or differentiation. What is an oncogene? - Answers A mutated proto-oncogene that is inappropriately activated and drives uncontrolled growth. Name four oncogene classes mentioned. - Answers Growth factors/receptors, signal transducers, transcription factors/nuclear transducers, apoptosis regulators. What does Knudson's multiple-hit hypothesis mean? - Answers Cancer usually requires accumulation of multiple genetic hits, not just one mutation. What is the log-kill principle in cancer therapy? - Answers A dose kills a constant fraction of tumor cells, not a constant number. Why is chemotherapy toxicity so common? - Answers Because many anti-cancer drugs also damage normal rapidly dividing cells. Name three normal tissues/processes commonly harmed by chemotherapy. - Answers Bone marrow, GI epithelium, hair follicles. What is primary drug resistance? - Answers Resistance already present before treatment begins. What is acquired drug resistance? - Answers Resistance that develops by adaptation or mutation during treatment. Which phase specificity is common for many anti-cancer drugs? - Answers S phase and M phase. What does cisplatin famously cause as a major toxicity? - Answers Severe nausea/vomiting and nephrotoxicity. What DNA base is especially susceptible to alkylating agents? - Answers The N7 of guanine. What does methotrexate inhibit overall? - Answers De novo nucleotide biosynthesis as an anti-folate. What are fluorouracil, cytosine arabinoside, and gemcitabine examples of? - Answers Pyrimidine analog antimetabolites. What are 6-mercaptopurine and 6-thioguanine examples of? - Answers Purine nucleobase analogues. What do vinca alkaloids do to microtubules? - Answers They inhibit tubulin polymerization. What does paclitaxel do to microtubules? - Answers It promotes assembly/stabilization and blocks mitosis by freezing microtubule dynamics. What do camptothecins target? - Answers Topoisomerase I complexes, preventing re-ligation and causing DNA breaks. Match the targeted/hormonal drugs: imatinib, cetuximab, tamoxifen. - Answers Imatinib - BCR-ABL tyrosine kinase; cetuximab - EGFR; tamoxifen - estrogen receptor antagonist. What are the three adrenal hormone groups emphasized? - Answers Glucocorticoids, mineralocorticoids, and adrenal androgens. What is the main endogenous glucocorticoid? - Answers Cortisol. What is the main endogenous mineralocorticoid? - Answers Aldosterone. What is the control axis for cortisol release? - Answers CRH - ACTH - cortisol. What mainly regulates aldosterone release? - Answers RAAS. What is the steroid precursor for adrenal steroids? - Answers Cholesterol. What is the rate-limiting first steroidogenic step mentioned? - Answers Cholesterol - pregnenolone in mitochondria. Why can't zona glomerulosa make glucocorticoids? - Answers It lacks 17alpha-hydroxylase. Name three metabolic effects of cortisol. - Answers Increases gluconeogenesis, increases protein breakdown, increases lipolysis. What protein does glucocorticoid-induced lipocortin-1 inhibit? - Answers Phospholipase A2. Which inflammatory transcription factors are transrepressed by glucocorticoids? - Answers NF-kB and AP-1. What plasma binding protein carries most cortisol? - Answers CBG, cortisol-binding globulin. Name three synthetic glucocorticoids from lecture. - Answers Hydrocortisone, prednisone/prednisolone, dexamethasone. Name three big glucocorticoid side effects from lecture. - Answers Hyperglycemia/diabetes, osteoporosis, infection risk. What are the three core renal/mineralocorticoid effects of aldosterone? - Answers Increased Na+ reabsorption, increased K+ excretion, increased H+ excretion. How does aldosterone increase Na+ reabsorption at the cell level? - Answers By increasing ENaC and Na/K-ATPase expression. Why doesn't cortisol strongly activate kidney mineralocorticoid receptors? - Answers 11beta-HSD2 converts cortisol to cortisone in the kidney. Name two synthetic mineralocorticoids. - Answers Fludrocortisone and desoxycorticosterone. What is the treatment for Addison disease? - Answers Hydrocortisone plus fludrocortisone. How are Cushing syndrome and primary aldosteronism treated? - Answers Cushing: surgery/radiation, ketoconazole, metyrapone; Primary aldosteronism: spironolactone/eplerenone. Which thyroid hormone is the active form? - Answers T3. What does TRH stimulate? - Answers TSH release from the pituitary. What does TSH stimulate? - Answers Thyroid hormone synthesis and release. What transporter brings iodide into thyroid cells? - Answers NIS. What enzyme oxidizes iodide and catalyzes iodination/coupling? - Answers Thyroid peroxidase (TPO). What do MIT and DIT stand for? - Answers Monoiodotyrosine and diiodotyrosine. Which coupling reaction makes T4? - Answers DIT + DIT. Which coupling reaction makes T3? - Answers DIT + MIT. Which enzyme converts T4 to T3 in peripheral tissues? - Answers 5'-deiodinase. What is reverse T3? - Answers The inactive form produced by D3 deiodination. What plasma protein binds most T3/T4? - Answers Thyroid-binding globulin (TBG).