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HOW TO SURVIVE Pharmacology
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A SDSG PUBLICATION
TABLE OF CONTENTS Hey everyone!
So, you’ve survived through physiology, health care, and behavioral medicine. Now onwards to spring term, which is basically just a lot of memorization, and nothing but memorization. Sure, there’s some understanding involved, but that gets piled down under all the laundry lists you have to cram into your head! Before memorizing lots of microorganisms, though, you get to learn more than you ever thought possible about drugs. This guide comes with a disclaimer, though. You’ve probably heard a lot of bad things about this class. This guide has advice from different people, and each of us has a different opinion on the class. You’ll hear from some people that the class wasn’t bad, and from others that it’s the worst course ever in Sophie. Just to let you know, it’s definitely doable. From the class that took the course in spring 2007, only five people had to reassess. Considering other classes, where that number is often a lot more, this really isn’t that bad. So don’t let this intimidate you, don’t be scared. Pharm is definitely doable! After the main text of the survival guide, you’ll find some notes and review questions that may help with your study, if you choose to use them. Please excuse any errors that may exist there, they were not intentional. Good luck! Topic Introduction to Pharmacology How to Study Pharmacology Written Exams and Quizzes Textbooks Review Material (from Samuel Anandan) Exam 2 – High Yield Lecture Points Exam 3 – High Yield Lecture Points Toxicology and GI Decontamination Questions GI Pharmacology Questions Hormone Questions How to Survive: Pharmacology Samuel Anandan (5th year) Fang Zhou (5th year) Pages 2 3 4 5 6-31 6-12 13-16 17-20 21-27 28-31
Introduction to PHARMACOLOGY Pharmacology is the study of drugs. What you’ll learn this term is really only part of pharmacology. What Sophie did was take the study of pharmacology and sort of divide it up into three separate courses. You’ll learn drugs that you use on bacteria, viruses, and other microorganisms in HDIP (Step 8), and drugs used for your brain in neuropsychiatry in fifth year. That still leaves a good amount for this course, though, including drugs for the heart, endocrine system, autonomic nervous system, and more. What this course involves it largely memorization, but a lot of it also makes sense. For example, you learned about the autonomic nervous system in anatomy and physiology, so you know what the sympathetic and parasympathetic nervous systems do. In this course, you’ll learn drugs that either act on those systems, or block them. And by knowing what they do, you know what effect the drugs will cause, and some side effects that may accompany it.
That’s not to say that there’s no randomness involved at all. Sometimes some drugs will have side effects, like minoxidil causing hair growth, that have absolutely nothing to do with the mechanism. Overall, though, it’s not as much memorization as you may initially think. The course mainly involves, as usual, exams, as well as quizzes. The following sections will explain more on how to study and the exams. A good part of this course is that they’ll give you a good amount of time off. Like two days free before an exam, a privilege we don’t always have. Make use of that time wisely! Now, one thing you’ll realize right off the bat is that this course is very disorganized. I believe this is the biggest problem with the course, and basically it’s only problem. Lectures will switch around, course directors may be out near an exam, these kind of things are what gives this course the bad reputation it has. You’ll hear worse from some people, though, who will say that the lecturers were awful, the class was totally unfair, things like that. Don’t believe all that you hear, from us or anyone else. Go in with an open mind, and just know what you have to do to pass the class. That’s all we’ll say regarding this, just remember, don’t believe everything you hear. An additional note- you may notice that esims and your transcript will have this course listed as two separate ones, introduction to pharmacology and systemic pharmacology, or something along those lines. Please note that this is actually one single course. The reason it’s separated into two is because, two years ago, the class of 2007 took an intro to pharm course in fourth year, and systemic pharm in fifth year. However, the following year, it was all combined into one course. So you can’t fail one course and pass the other; it’s all the same course. Good luck!
HOW TO STUDY PHARMACOLOGY A lot of pharmacology is about cramming details into your head, and then spitting back out during an exam. However, these details are actually important, so it’s useful to find some way to memorize them. Although the department suggests the big Katzung book (see the textbook section), the smaller version is much more concise, and a much better read. Use little Katzung. Big Katzung is a great reference book, but it is of little use to the novice med student. Another great alternative is Lippincott’s, which gives you lots of nice colorful illustrations to make your studying more fun, but also provides all the necessary details. I used Lippincott’s more than small Katzung, and it worked just fine. If flash cards work for you, there’s a good set called PharmCards, which has tons of drugs and all the crucial information (and then some) that you have to know. One of the best ways to learn this material is through mnemonics. The books and cards mentioned above don’t give you mnemonics, so it’s kind of up to you to make them up. First Aid does have some good ones, but sometimes the best ones, the ones that stick in your head, are the ones you invented. Think of any silly way to memorize the drugs that you can. But first, try to find the logic in what you’re memorizing. If you can find some way to make it make sense, that’s less memorizing you have to do. For instance, a lot of drugs in the same class end the same way, like a lot of beta-blockers end in “-olol.” If you know that, it’ll make recognizing the class of a drug that much easier.
For lectures, follow each professor's style. Some (like Dr. Wang) are great. Others just sit tight. Dr. Banerjee = notes-intensive. Know his notes, even if it seems wrong (unless you feel like getting into an unprofessional argument with him). It's okay, as long as YOU know the truth! Don’t get intimidated by the volume of material you have to learn. It looks like a lot at first, but once you start categorizing the drugs in your mind in terms of what they do and so on, it’ll become a lot more manageable. And, on the plus side, you’ll know what all those drug commercials on TV are talking about!
WRITTEN EXAMS Ah, what are these courses if not filled with exams, right? This course derives the vast majority of its questions from the lecture notes. However, please note that some lecturers will nitpick heavily from lecture slides, the textbook, etc. These usually are only one or two questions, maybe a couple of more at most. It’s not really worth your time worrying about how to tackle the few nitpicky questions there will be, because you’ll waste too much time trying to do so, and still maybe get them wrong, because they’re kind of hard to tell where those questions come from. But by and large, the tests overall come straight from the notes, and are fair. Dr. Banarjee will go over the test after it is finished, in the class, and you can address questions and concerns to him. Now, you’ve taken neuro, and you know how this department works, so keep that in mind when taking this course. Just make sure you learn all the relevant material, and don’t rely solely on notes, be sure to also read another source of your choice. Do that, and you should be fine. And here’s some good news – the miniboard for this class is fifth year! So you won’t have to worry about keeping the pesky drugs in your head until eight months after you finish the course, so you can move right onwards to HDIP when this course is done.
TEXTBOOKS Textbook Name Lippincott’s Pharmacology Edition Price* 3rd $42.54 Description ISBN Great, colorful, comprehensive book on0781741181 pharmacology. If you liked Lippincott’s biochemistry book, expect more of the same quality here. This is the required textbook. It’s very0071451536 lengthy, and might be too much of a read to be worthwhile, but give it a try first. A more concise version of the bigger Katzung0071422900 textbook, offering a much more manageable read. Haven’t used it, so can’t comment on it’s0781780748 value, but as the quality of the BRS series fluctuates among courses, definitely check it out and see for yourself. Lots of cards, lots of drugs, and lots of detailed0781734010 information. If flash cards work for you, definitely check these out. And you’ll have to remember these drugs for the miniboard in fifth year, so these may come in handy when it’s review time. Also written by Trevor and Katzung, it’s a0071445811 much smaller book than the others listed above.
Katzung’s Basic and 10th Clinical Pharmacology Katzung and Trevor’s Pharmacology BRS Pharmacology 7th 4th
$59.95 $36.22 $31.95
PharmCards: Review Cards for Medical Students
Road Map Pharmacology
* Prices taken from www.amazon.com.
EXAM 2 – HIGH YIELD LECTURE POINTS Angina Lecture – Dr. Kashfi 1.) Beta blockers are eliminated faster from plasma but last longer on receptors 2.) CCBs (calcium channel blockers) are induced by CYP3A a. All are orally active CHF Lecture – Dr. Kashfi 1.) Left side heart failure à pulmonary edema (can treat with loop diuretics) and Na retention 2.) NSAIDs reduce diuretic efficacy because of fluid retention because of PG block 3.) Diuretic toxicity can cause increased BUN 4.) Spironolactone = primary benefit is because if blocks ald receptors in heart 5.) ACE inhibitor effects wears off over time 6.) So far, ACE = ARB in terms of efficacy 7.) CCBs not good for CHF but are good for CHF symptoms 8.) Amrinone and milrinone = phosphodiesterase inhibitors (mil safer than amrinone) 9.) Beta blockers = used for chronic HF, possible function is it stops downregulation of beta receptors due to increased catecholamines a. Counterintuitive
10.) a. b. c. d. e. f. g. h. i.
Digitalis Lactone ring has to be unsaturated OH group at position 14 is necessary Ouabain > Digoxin > Digitoxin in terms of # of OH groups Glycosides = cis rings; regular hormones = trans rings Low therapeutic index Reduces size of enlarged heart Not indicated for diastolic dysfunction (thickened muscle wall prevents relax.) Digitoxin = more enterohepatic circulation and hepatic degradation than digoxin Binds to same receptors as K
j. Decreases HR, TPR, venomotor tone (VMT) (inc. TPR and VMT in norm. heart) i. Increases HR by increasing vagal tone k. Thyroxine, bran, cholestyramine, anatacids dec. [digoxin] l. Erythromycin, omeprazole, tetracycline, cyclosporine and CCBs and ACEs inc. [digoxin] m. toxic effects = “Starry Night” painting, enhanced response to hypoxia n. Inc. PR interval, decreases QT, depressed S o. PVC, then VTach, than AV block p. Treat OD with phenytoin, lidocaine, and propranolol i. Also can use mad expensive Fab Anemias and Hematopoietic Growth Factors – Dr. Rich 1.) Most Fe stored in Hb 2.) Fe absorption inc. with inc. HCl and inc. Vit C 3.) Fe deficiency with low storage iron, low serum ferritin, low TIBC, low MCV, low MCHC, low Fe binding saturation 4.) Desferoxamine = chelates Fe and gets rid of it 5.) Phlebotomy is best treatment for hemochromatosis 6.) Pernicious anemia = lack of intrinsic factor b/c autoimmune to parietal cell 7.) Vitamin B necessary to produce myelin 8.) Glossitis= burning of tongue, sign of vitamin B deficiency 9.) Ataxia = abnormal gait, sign of vitamin B deficiency 10.) Macrocytic anemia = leucopenia, thrombocytopena b/c affects all cell lines 11.) Babinski’s response = sign of vitamin B deficiency 12.) Cobalt = part of vitamin B 13.) Vitamin B mainly stored in liver, mad storage (lasts for years) 14.) Transcobalamin I = storage; transcobalamin II = transport 15.) Folate trap = bypassed by folic acid; buildup of methylTHF, loss of THF 16.) Deoxyadenosylcobalamin loss causes dec. methionine causing abnormal myelin and neurological symptoms a. Not helped by folic acid
2+ 2+ 2+ 2+ 2+ 12 12 12 12 12 12
17.) Folic acid deficiency = most common cause = pregnancy a. Also vegetarian diet, chronic alcoholism, inadequate diet 18.) Methotrexate = used for MOPP regimen for Hodgkin’s disease, rheumatoid arthritis, and cancer 19.) Erythropoietin can only increase RBC production in healthy bone marrow 20.) Patients with chronic renal failure = good response to exogenous erythropoietin a. Inc. reticulocyte count in 10 days, hematocrit in 2 to 6 weeks b. Works best in patients with erythropoietin levels less than 100 IU/L c. Use erythropoietin after phlebotomies 21.) G-CSF activates progenitor cells already committed to the neutrophil line a. Used for stem cell transplantation 22.) Aplastic anemia = low RBC, WBC, and platelets
23.) G-CSF reduces duration of neutropenia after chemotherapy and febrile neutropenia 24.) PBSCs have almost replaced using bone marrow stem cells in autologous transplantation 25.) IL-11 = stimulates growth of many cells, inc. # of platelets and neutrophils, acts with GFs to stimulate growth of megakaryocytic progenitors a. Use it to increase platelets = main thing to know from little Katzung 26.) G-CSF = keyword is mobilize
Drugs Used to Lower Cholesterol – Dr. Kashfi 1.) Apoproteins a. Chylomicrons = E, C, B-48 b. Chylomicron remnants = E, B-48 c. VLDL = B-100, E, C d. IDL = E, B-100 e. LDL = B-100 f. HDL = A1, A2 2.) Hyperlipidemias a. Type I = sever chylomicronemia b/c lack of LPL Rs or something b. Type IIa = increased LDL (familial) c. Type IIb = inc. LDL and VLDL (combined) d. Type III = abnormal VLDL/LDL (dysbetalipoproteinemia) e. Type IV = inc. VLDL f. Type V = inc. VLDL, rare, in adults (mixed hyperlipemia) 3.) Statins competitively bind to the thing that HMG-CoA binds to 4.) Fibrates = second most useful anti-hyperlipidemic drugs a. Used in types II, IV, V b. PPRalpha thing 5.) Bile acid sequestrants = useful in IIa and IIb, positively charged Ns sequester bile 6.) Nicotinic acid = used in all forms except type I 7.) Ezetimbe = useful in all forms except type I 8.) Using statins can cause rebound LDL Rs by the liver a. Give at night 9.) Run from bar to bar to inc. HDL 10.) Values a. Total = less than 200 b. HDL = over 40 c. LDL = under 100 11.) Diet modification a. Limit total fat to <30% of total fat intake, saturated to <10% of caloric intake, and cholesterol to <300 mg/day 12.) Statins
a. Combine with niacin and resins to dec. serum cholesterol by 2/3 b. Mechanism = dec. LDL synthesis causes more LDL Rs on liver and dec. [LDL] c. Make sure to follow up with liver function test 13.) a. b. c. d. e. Resins Farting Combine with nicotinic acid to dec. serum cholesterol by 50% 15% LDL reduction on its own Steatorrhea is a side effect Blocks absorption of digitalis, warfarin, thiazides, provastatin, levastatin
14.) Nicotinic acid a. Risk of second MI in patients taking it b. Liver function tests are useful (like with statins) c. Gout 15.) Fibrins a. PPARalpha b. Reduces TGs c. Pancreatitis, rashes, gallstones, etc. 16.) Estrogen reduces LDL up to 25%, inc. HDL up to 15% 17.) Antioxidants effective in preventing heart attacks 18.) 3-omega FAs lower risk of heart attack 19.) Total cholesterol – (TG/5) – HDL = LDL 20.) Xanthomas = types I and III 21.) Type I seen in children, type V in adults a. Type V has creamy blood 22.) Artherogenic index à LDL/HDL < 4 23.) Phases 2 and 3 = decreases fat at expense of carbs Anticoagulants and Thrombolytics – Dr. Kashfi 1.) Heparin = uses activated favtors of II, VII, IX, X, XI, XII 2.) Hemostasis = blood clot 3.) Clotting phases a. Vascular = constriction, tissue factor activation b. Platelet = platelets adhere and release VPF, undergo viscous metamorphosis i. TXA from platelets, PGI from vessls ii. Thrombus in veins can become emboli c. Coagulation = intrinsic pathway is slower, uses aPTT (26 to 33s); extrinsic uses PTT (12 to 14s) d. Fibrinolytic phase
4.) Arterial thrombosis = associated with MI, stroke, ischemia 5.) Venous thrombosis = associated with CHF, cancer, surgery 6.) Proteins C and S = inhibit Va and VIIIa 7.) Heparin and warfarin = prevent VENOUS thrombosis a. Aspirin prevents arterial thrombosis
8.) Don’t inject heparin IM 9.) α antiprotease, α microglobulin, α antiplasmin, antithrombin = fibrin inhibition a. get DIC if you mess up fibrin inhibition
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10.) aminocaproic acid decreases fibrinolysis – lysine analog inhibits protease 11.) Warfarin is protein-bound a. Don’t use with pregnancy 12.) High dose of aspirin = no effect because inhibits prostacyclin synthesis and allows aggregation 13.) DO NOT give aspirin to patients with G6PD deficiency à hemolytic anemia 14.) Drugs that inc. warfarin activity a. Aspirin, sulfonamides = decreasing binding to albumin b. Cimetidine, disulfiram = inhibit degradation c. Antibiotics = decreasing clotting factor synthesis 15.) Promote bleeding a. Aspirin = b/c of platelet inhibition b. Heparin, anti-metabolites 16.) Drugs that decrease warfarin activity a. Barbiturates, phenytoin = induce CYP2C9 b. Vitamin K = induce clotting factor synthesis c. Cholestyramine, colestipol = reduced absorption 17.) SK = causes immune rxn, UK doesn’t, tPA is mad expensive
Drugs for Hypertension – Dr. Friedman 1.) ACE inihibitors = side effect is rash and hyperkalemia and renal failure 2.) Organic nitrates and sodium nitroprusside a. Short-acting for acute effort angina (for nitroglyceride and isosorbide dinitrate) b. Long-acting for angina prophylaxis (for nitroglyceride and isosorbide dinitrate) c. Sodium nitroprusside = IV only 3.) Be careful using organic nitrates with elevated intracranial pressure, sildenafil, etc. 4.) Amiodipine = use for Raynaud’s syndrome 5.) CCBs cause reflex tachycardia a. Can cause AV block (diltiazem and verapamil) i. Beta blockers can also cause AV block 6.) Beta blockers = can be used for thyrotoxicosis and essential tremor 7.) Hydralazine = lupus, mostly in slow acetylators, acts on veins only a. ACE acts on both 8.) ACE inhibitors good for diabetics a. Effect wears over time, but not for ARBs 9.) Can use beta blockers for pretty much all heart problems 10.) Don’t use ACE for angina
i. For ANGINA, use beta blockers, CCBs, vasodilators, antiplatelet agents, and K channel openers 11.) 12.) 13.) 14.) 15.) Heart Failure Diuretics Beta Blockers ACE Inhibitors CCBs Alpha Blockers AT R antagonists Ald Antagonist AT II is most potent vasoconstrictor Bretylium stops NE release, is a Class III antihypertensive ACE inhibitor causes edema (angioedema?) For HTN, first use thiazides Hydralazine and prazosin = long term use Angina Beta Blockers CCBs Ald Antagonist Vasodilators Antiplatelet Agents K channel openers
MI Beta Blockers ACE Inhibitors
Integrative CVS Pharmacology – Dr. Banarjee 1.) Pump-based HTN caused by inc. sensitivity to catecholamines and symp. NS 2.) Vascular cause of HTN = dec. NO, too many endothelins, impairment of ion channels 3.) Renal cause of HTN = GF impairment (low GFR causes renin secretion à HTN), mutation in Na channels (Liddle’s?), renal artery stenosis, embolic vasculocytis 4.) Neuroendocrine cause of HTN = mess up in central regulation of symp. NS, atypical stress responses, abnormal responses from baroreceptors and volume receptors 5.) Secondary HTN = pheochromocytoma, primary aldosteronism, hyperthyroidism 6.) Should use multiple therapy to block both the baroreceptor pathway and the renin-AT-ald pathway 7.) Coronary blood flow reserve (CBFR) = max. coronary blood flow (CBF) / resting CBF 8.) CAD = stable angina; ACS = unstable 9.) Subendocardial = no ST elevation 10.) Elevation of ST segment = Q wave transmural MI 11.) HTN crisis = TPR inc. and causes impedence to left ventricular ejection 12.) Distributive shock = dec. MAP, reduction of blood perfusion in different organs 13.) Arterial HTN causes pressure loading 14.) Systolic HF can be caused by mitral or aortic valve deficiencies
Diuretics 1.) Thiazides are given orally, loop by IV 2.) Sulfonamides = all diuretics except osmotic and K sparing 3.) Thiazides can be used for nephrogenic diabetes insipidus a. Can cause impotence
4.) Amiloride = used for Liddle’s syndrome 5.) Can cause GOUT
6.) DON’T USE THESE IN ANGINA or MI 7.) Osmotic diuretics a. Filtered into urinary lumen b. expel electrolytes c. cisplatin = causes renal failure, anti-cancer drug, give osmotic diuretic d. intoxication with barbiturates, bromides, etc. 8.) Carbonic Anhydrase Inhibitors (CAIs) a. Secreted into urinary lumen b. 30% of filtered load reabsorption prevented c. Used in wide-angle glaucoma d. CNS sedation e. Motion sickness treatment = because causes metabolic acidosis to counter respiratory alkalosis 9.) Loop Diuretics a. Secreted into urinary lumen b. 25% of Na reabsorption c. Used in acute or chronic renal failure, b/c that leads to Na and H O retention d. Inc. Mg secretion à hypomagnesemia
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10.) a. b. c. d. 11.) a. b. c. d. e.
Thiazide diuretics Secreted into urinary lumen 50% blockade of Na reabsorption Inc. Mg secretion à hypomagnesemia Use with ACE for synergistic effects
K -sparing diuretics Edlerenone, amiloride, triamterene, spironolactone Acts on principal cell Use with liver cirrhosis with ascites Use with nephritic syndrome Causes kidney stones and (hyperkalemic) metabolic acidosis
12.) Nephrotic syndrome = transfer of proteins into urine, causes dec. plasma oncotic pressure because of dec. albumin 13.) All the acidosis and alkalosis (metabolic) associated with diuretics are called hyper- or hypo-kalemic 14.) CAIs, thiazides, and osmotic are secreted; K -sparing enter from basolateral side; osmotic are filtered a. Therefore, the secreted ones DEPEND on proper renal function
Antiarryhthmic Agents – Dr. Josephson 1.) Phase 3 = delayed rectifier 2.) Phase 4 = inward rectifier 3.) Quinidine = shows REVERSE use-dependence 4.) Amiodarone doesn’t show use-dependence
5.) Lidocaine and CCBs binds to inactive and active states; IA bind to active (A for active); Amiodarone binds only to inactive (it smells so bad it makes everything inactive) 6.) Phases affected a. IA = inc. QT and inc. QRS (phase 0) = does AF, AFib, VTach b. IB = dec. QT (phase 3) = does VTach = still causes inc. refractory period c. IC = inc. QRS = does SVT d. II = inc. PR (phase 4) = does all e. III = inc. QT= amiodarone does all f. IV = inc. PR = does SVT g. Adenosine = PSVT, AV nodal block Miscellaneous 1.) HTN drug of choice = thiazides 2.) Alpha blockers NOT used for angina 3.) Nitrites à methemoglobinemia à treatment for CN toxicity 4.) Disopyramide = has mAChR activity (Diso’s the macker)
EXAM 3 – HIGH YIELD LECTURE POINTS Overview of Endocrine Pharmacology, Pharmacology of Anterior Pituitary, Diabetes Insipidus, Thyroid Disease – Dr. Banarjee 1.) Table TRH Decrease Somatostatin Synthesis Glucocorticoids CRH Atropine Hexamethonium NE Melatonin GABA 5-HT ACTH GH α-blockers dopamineantagonists 5-HT Dopamine β-blockers ADH α-blockers atropine
2.) Drugs to know a. Sermorelin = GHRH substitute b. Hexarelin = GHRH substitute c. Leuprolide = GnRH substitute d. Histerine = GnRH substitute e. Nafarelin = GnRH substitute f. Goserelin = GnRH substitute g. Flutamide = androgen antagonist h. Finasteride = inhibits DHT i. Haloperidol = atypical dopamine antagonist j. Chlorpromazine (CPZ) =atypical dopamine antagonist k. Bromocriptine = Dopamine agonist (D agonist) l. Somatotropin = synthetic GH (?) m. Somatonorm = synthetic GH n. Somatorem = synthetic GH
o. Cyproheptadine = 5-HT blocker p. Phentolamine = alpha blocker q. Octriotide = somatostatin analog r. Pitressin = aqueous vasopressin s. Desmopressin = synthetic vasopressin w/o vasoconstrictor effect t. Lypressin = synthetic vasopressin, less vasoconstrictor, not as good as desmopressin u. Vasopressin in tannat oil = longer duration of action for vasopressin v. Chlorfibrate = dec. release of ADH, used for Type II diabetes w. Chlorpropamide = same as chlorfibrate x. Hydrochlorthiazide = used for nephrogenic diabetes insipidus y. Perchlorate z. Thiocyanate aa. PTU bb. MMI cc. Colchicine dd. Iodides ee. Cytochalasin B ff. Lithium ion i. Can cause drug-induced hypothyroidism ii. Used to stop colloidal reabsorption in thyroid gland gg. Phenylbutazone i. Can cause drug-induced hypothroidism hh. Dinitrotyrosine ii. Synthroid = T , use in hypothyroidism jj. Liothyronin = T , use in hypothyroidism kk. Liotrix = T and T (trix gives you the best of both worlds = Locutus eating trix), use in hypothyroidism ll. Thyroglobulin = pulverized porcine thyroid gland, use in hypothyroidism
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3.) Stimulate synthesis – of what? a. Nicotine, morphine, barbiturates (Morph smoking on some barb wire) b. Vincristine, vinblastine, cyclophosphamide (Blast the Christian cycles) c. Clofibrate, chlorpropamide, anti-depressants (Prop the anti-depressant fibers) 4.) Decrease synthesis – of what? a. Morphine antagonists, EtOH, CPZ (Anti-Morph drinking on a CPZ) b. Reserpine, diphenylhyrdatoin (DPH) 5.) Types of vasopressin receptors a. V = inc. IP , involved in vasoconstrictionV = inc. IP , involved in ACTH releaseV = inc. cAMP, involved in H O reabsorption
1a 3 1b 3 2 2
6.) Drugs used in blocking steps of thyroid synthesis a. Entrance of I into gland = thiocyanate, perchlorate b. Iodination and Coupling = PTU, MMI (methimazole) c. Colloidal Reabsorption = colchinice, iodides, Li, cytochalasin B d. Thyroglobulin proteolysis = iodides e. Deiodination of MIT and DIT = dinitrotyrosine f. T à T conversion = β-blockers, glucocorticoids
7.) Iodides, PTU, MMI used most b/c dec. toxicity 8.) MMI is mad potent 9.) β-blockers and CCBs given in hyperthyroidism because it causes inc. sympathetic which affects the heart
Adrenal Disease- Dr. Banarjee
1.) a. O at position 3 = essential for biological activity b. OH at position 11 = necessary for anti-inflammatory activity i. Desoxycortosterone doesn’t have this, so it only has mineralocorticoid activity ii. Metyrapone blocks the hydroxylation here c. Double bond between C4 and C5 = dec. Na retention, inc. anti-inflammatory i. Like prednisalone d. Methyl on Ring B = inc. both Na retention and anti-inflammatory e. Add F at C9 = inc. anti-inflammatory, more selective for carb. Metabolism control f. Carbon 16 = add –OH or –CH group like in dexamethosone, you inc. glucocorticoid activity and dec. Na retention
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2.) Glucocorticoids (GCs) dec. lymphocyte and thymocyte count, therefore dec. hypersensitivity a. Called anti-mitotic actions 3.) Inc. BP (via vasoconstriction) and dec. permeability of capillary endothelium cells 4.) GCs suppress aldosterone release 5.) Congenital adrenal hyperplasia (CAH) caused b/c deficiency in enzyme that puts –OH on C11 a. Dec. GC (therefore inc. ACTH, which causes inc. androgens) b. Use prednisone to treat via dec. androgens
6.) Cushing’s syndrome = excessive activity of hypothalamic-pituitary-adrenal axis or adrenal adenoma (Tarkin’s got mad hormones) a. Can also be drug-induced b. Treat with stuff that blocks steroid production i. Ketoconazole, RU-486, aminoglutethamide, trilostane, metyrapone, mitotone, cyproheptadine (serotonin antagonist) 7.) Use GCs with…. a. Allergic stuff (b/c dec. hypersensitivity) i. Remember, hypersensitivity = allergies b. Skin, eye, kidney diseases c. Arthritis (can be given intra-articularly) d. Crohn’s and IBS e. Lymphocytic leukemia 8.) Mitotane = for Cushing’s syndrome, can cause anorexia, neurological symptoms, etc. Drugs for Diabetes Mellitus- Dr. Banarjee 1.) Oral glucose causes more insulin secretion, because the oral route activates digestive enzymes which themselves cause more insulin from pancreas a. Thus need more glucose orally to cause hyperglycemia as compared to IV 2.) α stops insulin release, β and mAChRs increases insulin release a. thus, atropine and β-blockers decrease insulin release 3.) Glucagon loves all, and somatostatin hates all a. Glucagon stimulates insulin and somatostatin; somatostatin inhibits both b. Insulin inhibits glucagon (think of biochem) 4.) GCs cause hyperglycemia and gluconeogenesis…. thus they can cause secondary DM 5.) GCs anatagonize vitD and therefore stop Ca absorption 6.) Insulin secretagogues a. Maglinitides i. Act by binding on sulfonurea site in pancreatic β–cells ii. Gout b. Sulfonureas i. Blocks K channels to increase insulin release from pancreas cells ii. Reduces serum glucagon iii. Allows insulin to bind to its target tissues and Rs better 7.) Insulin sensitizers a. TZDs i. PPAR-α binding ii. Lipogenesis iii. Rosiglitazone = inc. LDL and HDL, possible anemia 1. Rosi’s got no blood cells but loves to inc. DLs b. Biguanides (ex- metformin) 8.) Miglitol = glucosidase inhibitor, but miglitides are insulin secretagogues
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Mineral Homeostasis and Mineral Disorder- Dr. Wang 1.) Osteoblasts are involved in bone formation 2.) Osteoclasts = pac-man 3.) PTH binds to a GPCR 4.) Gallium nitrate = treats hypercalcemia, given IV
5.) 6.) 7.) 8.)
Paget’s disease = mad pac-man (uncontrolled bone resorption) Osteoporosis = bone mass loss, normal mineral/collagen ration GCs anatagonize vitD and therefore stop Ca absorption Alendronate = stops bone resorption a. Take on empty stomach b. 10% absorbed c. GI effects 9.) Calcium gluconate = IV for severe hypoglycemia
EXAM 3 - Toxicology and GI Decontamination Questions 1.) Who is the father of toxicology? a. Yoda b. Gandalf c. Paracelsus a. Morpheus b. Obi-Wan 2.) Diaphoresis is also known as a. Smelling b. Sweating a. Diarrhea b. Constipation c. Lacrimating 3.) Which of the following symptoms are consistent with antimuscarinic overdose? a. Increased pupil size b. Decreased peristalsis c. Decreased diaphoresis d. Increase pulse e. All of the above 4.) Benzodiazepines can be used if one is concerned about safety using physostigmine for a anticholinergic overdose. a. True a. False 5.) Tricyclic antidepressants are a contraindication for using physostigmine. a. True a. False 6.) Which of the following in consistent with a cholinergic toxidrome? a. No change in HR b. No change in pupil size c. Peristalsis increases d. Diaphoresis increases
e. Respiratory rate increases 7.) Atropine can be used to treat a cholinergic toxidrome, but pralidoxime cannot. a. True b. False (they can both be used) 8.) Atropine does not bind to the a. M b. M c. M d. M
1 2 3 5
e. Nicotinic 9.) Atropine use is contraindicated in all of the following except a. Narrow angle glaucoma b. Obstructive uropathy c. Myasthenia gravis d. Hypotension a. Hypertension 10.) Pralidoxime acts by a. Increasing synthesis of AChE b. Increasing synthesis of ACh c. Preventing aging from exposure to atropine-related compounds d. Preventing aging from exposure to organophosphorous compounds a. None of the above 11.) a. b. c. d. e. Which of the following is inconsistent with an opioid toxidrome? Decreased HR Decreased BP Decreased RR Decreased pupil size Increased peristalsis
Questions 12-17- Match the following opioid receptors with the appropriate effects A. B. C. D. E. F. 12.) D 13.) μ μ δ κ κ κ
1 2 1
Spinal analgesia and miosis Respiratory depression, GI dysmotility, pruritis (itching) B
14.) F 15.) 16.) 17.) E 18.) a. b. c. d. 19.)
Supraspinal analgesia Euphoria and supraspinal and peripheral analgesia Spinal analgesia and modulation of and μ dopamine Psychotomimesis, dysphoria Which of the following is most correct? Morphine is a pure opioid agonist Naloxone is a pure opioid antagonist Buprenorphine is a partial agonist on mu Rs, but antagonist on kappa Rs Pentzocine is an agonist on kappa Rs, but antagonist on mu Rs A C
e. All of the above Opioids decreases tidal volume before respiratory rate a. True a. False Ventilation and oxidation are more critical that naloxone in an opioid overdose a. True a. False Which of the following are consistent with an amphetamine overdose? Increased HR Increase BP Increased pupil size Increased peristalsis
21.) a. b. c. d.
e. All of the above (Mnemonic- Amphetamines inc. everything, opioids dec. basically everything) 22.) All of the following are true concerning MDMA except that it a. Is also known as ecstasy b. Is an indirect sympathomimetic c. Has both direct and indirect 5-HT agonism d. Is not an amphetamine a. Is an enactogen, because it releases 5-HT 23.) a. b. c. d. MDMA toxicity can cause SIADH 5-HT syndrome Dehydration Depression e. All of the above All of the following are true concerning antidotes for amphetamine overdose
24.) except a. Benzodiazepines can be used for sedation b. Nitrates, CCBs, and alpha blockers can be used for cardiovascular stimulation
c. Acidification of urine is essential a. Serial neurological evaluation is good b. None of the above 25.) Which of the following is not characteristic of a sedative-hypnotic toxidrome, such as that caused by benzodiazepines a. Decreased respiratory rate b. Decreased HR c. Decreased BP d. Increased peristalsis a. No effect on pupil size and diaphoresis 26.) Flumazenil can have life-threatening or fatal complications is used with overdose of all of the following except a. Benzodiazepines a. Tricyclic antidepressants b. Chloral hydrate c. Carbmazepine d. None of the above 27.) a. b. c. d. The following are important to consider when using flumazenil Use wisely and safely Works well with children Works well with iatrogenic causes (caused by physician) Exclude other toxins when using this
e. All of the above 28.) GHB can be used for benzodiazepine overdose and has dose related CNS depression a. True a. False 29.) Which of the following is uncharacteristic of sedative-hypnotic or ethanol withdrawal toxidrome? a. Increased HR b. Increased BP c. Increased RR d. Increased pupil size and peristalsis e. Decreased diaphoresis
EXAM 3 - GI Pharmacology Questions 1.) Bethanechol is characterized by all of the following excepta. Degraded rapidly by acetylcholinesterase a. Enhances amplitudes of contractions of LES b. Is a muscarinic receptor agonist c. Is orally active d. Does not increase the rate of gastric emptying 2.) Which of the following is characteristic of metoclopramide, a D antagonist? a. Acts as a direct ACh agonist b. Can be blocked by vagotomy
c. The only pro-kinetic drug that increases GI motility a. Decreases tension of LES and pyloric sphincter b. Decreases peristalsis 3.) Which is not a use for metoclopramide? a. Fast, complete stomach emptying b. Treatment for “lazy stomach,” aka diabetic gastric stasis c. GERD d. Anti-emesis
e. None of the above 4.) Atropine is added to lomotil® because a. It is required to absorb water and toxins from the GI tract b. It reduces the risk of attempted opiate abuse a. It is essential to decrease peristalsis b. It is the only anti-diarrhea drug to cross the blood-brain barrier c. All of the above (Mnemonic- Lomotil = “lo motor” = dec. peristalsis, so inc. H O and electrolyte reabs.) 5.) Pick the incorrect statement a. Pepto-bismol® is the drug of choice for travelers diarrhea because it inhibits the effects of E. coli b. Imodium® does not cross the BBB and should be avoided in patients with shigella or salmonella infections c. Lomotil® decreases peristalsis d. Kaopectate® is an OTC drug used to treat diarrhea
e. Zofran® is an OTC drug used to treat diarrhea 6.) Which of the following amino acids are NOT needed for somatostatin activity? a. Phenylalanine (Phe) b. Tryptophan (Trp) c. Lysine (Lys) d. Threonine (Thr) e. Asparagine (Arg) 7.) Octreotide is only used for treatment of diarrhea in patients with HIV infection. a. True a. False 8.) A decision regarding choice of laxative should involve a. Time to onset of action b. Adverse effects of drug c. Chronic or acute constipation d. A and B e. All of the above 9.) Pick the incorrect statement a. Adequate fluid intake is essential when taking bulk-forming laxatives b. Surfactants allow smoother bowel movements by decreasing H O tension c. Lubricants decrease vitamins A, D, E, and K absorption and can cause aspiration lipid pneumonia d. Saline is used for complete and rapid GI emptying, and work faster rectally
e. Stimulants are the drug of choice in constipated patients with CHF 10.) Emetic agents that affect the stomach activate vagal and sympathetic nerves, which act DIRECTLY on the a. Solitary tract nucleus b. Chemo-receptor trigger zone
c. Emetic center d. A and B a. All of the above 11.) A bulimic patient constantly gags herself to vomit. Which of the following centers is her gagging directly influencing? a. Solitary tract nucleus a. Chemo-receptor trigger zone b. Emetic center c. A and B d. All of the above 12.) H antagonists, antimuscarininc agents, and benzodiazephines are minimally effective as antiemetic agents a. True a. False
13.) a. b. c. d. 14.) a. b. c. d. 15.) a. b. c. d.
Which is true of cisapride? Is prokinetic and acts on a class of 5-HT receptors Increases absorption of diazepam and alcohol Should be given in smaller doses in those with hepatic insufficiency Used in disorders of gastric hypomotility e. All of the above Which is incorrect regarding domperidone? a. Rapidly crosses the BBB Causes hyperprolactinemia Can be used as a antiemetic May help in counteracting GI effects of L-dopa and bromocriptine Effects resemble those of metoclopramide The 5-HT antagonists are characterized by all of the following except Drugs with the suffix “-tron” Metabolized by the liver Anti-emesis induced by cisplatin Granisteron prevents nausea
e. Only eliminated in the urine 16.) Corticosteroids are beneficial because of all of the following EXCEPT a. They can augment the effect of antiemetic drugs b. They can reduce adverse effects of antiemetic drugs such as diarrhea, caused by metoclopramide c. Prevent hyperglycemia in diabetics a. A and B b. All of the above 17.) All of the following are uses for cannabinoids, found in pot, except
a. b. c. d.
Anti-emesis Analgeis Anticonvulsant Glaucoma treatment
e. Bronchoconstrictor 18.) Crohn’s Disease (CD) and Chronic Ulcerative Collitis (CUC) differ in that a. Events can be preceded by stress in CUC, but not in CD b. CUC is an inflammatory disease of the large bowel, while CD is a disease primarily of the small intestine c. CD has “skip areas” on a pathological section, while CUC does not d. B and C a. All of the above 19.) a. b. c. d. 20.) a. b. c. d. Which of the following is NOT true regarding treatment of IBD? 5-ASA is used, but cannot be taken orally Most drugs bind and release 5-ASA in the distal GI (colon, ileum) Sulfasalazine can inhibit folic acid absorption Antibiotics can be used e. Methotrexate is contraindicated Which of the following are major pathways for gastric secretion? Vagal stimulation Endocrine stimulation via antral G cells Histamine release from ECL cells A and C
e. All of the above 21.) Which of the following is responsible for release of H from the parietal cell? a. PGE b. PGI c. ACh
+ 2 2
d. A and C a. B and C 22.) a. b. c. d. Which of the following is responsible for mucous and HCO release?
PGE PGI ACh A and C
e. B and C 23.) Which of the following act via a Ca -dependent pathway? a. Gastrin b. Histamine c. ACh
d. A and C a. B and C 24.) Which of the following acts via a cAMP mechanism? a. Gastrin b. Histamine a. ACh b. A and C c. B and C 25.) a. b. c. d. Misoprostol is a a. Prostaglandin agonist Prostaglandin antagonist H receptor agonist H receptor antagonist ACh analog
Questions 26-30- Match the following (each choice can have more than one answer) A. B. C. D. E. Cimetidine Ranitidine Famotidine Nizatidine Zolentidine
26.) Imidazole replaced by a thizol C, D 27.) Retains the imidazole ring of histamine A 28.) Imidazole ring replaced by a furan B 29.) Reversible blockers of H receptors A, B, C, D, E 30.) Can cross the BBB E 31.) Which of the following is NOT true regarding H -receptor blockers? a. Inhibit basal and nocturnal acid secretion b. Inhibit gastric acid secretion in a dose-dependent manner c. Requires a dosage reduction in patients with renal impairment
d. Inhibit H receptors in vascular and bronchial smooth muscle a. Can be given in oral form
32.) Cimetidine and other H antagonists increase the concentration of ________ particularly in men by inhibiting its hydrolyzation via the Cyt P450 system a. Testosterone
b. Estradiol a. DHT b. Progesterone c. Cholesterol
33.) a. b. c. d. 34.) a. b. c. d. e. 35.) a. b. c. d.
Cimetidine can prolong the half-lives of Phenytoin Sulfonylureas Ca channel blockers N-acetyl procainamide
e. All of the above H -receptor blockers can be used for Peptic ulcers Duodenal ulcers Gastric ulcers Zollinger-Ellison syndrome GERD
All of the above Which is true regarding omeprazole? CYP2C19 metabolizes the R isomer more than the S isomer CYP3A4 metabolizes nexium CYP2C19 metabolizes nexium faster than CYP3A4 B and C
e. All of the above 36.) Pirenzipine is equivalent to cimetidine in preventing ulcer recurrence. a. True a. False 37.) a. b. c. d. 38.) a. b. c. d. Which is true regarding mAChR antagonists? a. They reduce basal secretion of gastic acid by about 50%, but stimulated secretion inhibition is much less Selective M blockers (ex- pirenzipine) are not as effective as atropine M blockers would be unsuccessful in blocking parietal cell activity Selective M blockers have greater side effects than atropine, like tachycardia They block nicotinic acetylcholine receptors
1 3 1
Which of the following are actions of sucrafate? Binds bile salts Adheres to base of ulcer craters Stimulates PG synthesis and production of EGF Adsorbs pepsin
e. All of the above 39.) Sucrafate can reduce the bioavailability of all of the following except a. Digoxin b. Tetracycline c. Carbenoxolone (this is another agent in the same category as sucrulfate) a. Ketoconazole b. Cimetidine
40.) Which is the major side effect of bismuth compounds (ex- Pepto-Bismol®?) a. Green tongue b. Black tongue a. Red tongue b. Blue tongue c. Purple tongue 41.) a. b. c. d. e. Bismuth compounds have been shown to reduce the availability of Subcitrate Subsalicylate Tetracyclines All of the above None of the above
42.) Misoprostol is best used for treatment of a. General gastric ulcers b. NSAID-induced gastric ulcers a. Peptic ulcers b. Duodenal ulcers c. Pregnant women Questions 43-46- Match the following drugs with their characteristic A. Can cause hypercalcemia B. Can cause constipation and hypophosphatemia C. Diarrhea D. Systemic alkalosis 43.) Magnesium hydroxide C 44.) Sodium bicarbonate D 45.) Calcium carbonate A 46.) Aluminum hydroxide B 47.) Antacids decrease the bioavailability of all the following except a. Atenolol b. Propranolol c. Metoprolol a. All of the above b. None of the above 48.) a. b. c. d. e. Antacids decrease the bioavailability of Quinolone antibiotics Iron Tetracycline Ketoconazole Theophylline f. All of the above
49.) Type I ulcers are characterized by characterized by . a. Impaired mucosal factors; acid hypersecretion a. Acid hypersecretion; impaired mucosal factors b. Increased histamine; decreased gastrin c. Decreased gastrin; increased histamine d. NSAID use; H. pylori infection
, while Type II ulcers are
50.) If a patient comes in with a NSAID-induced gastric ulcer, which of the following treatments, in the order presented, would be the best option? a. Aluminium hydroxide, cimetidine, sulcrafate b. Cimetidine, omeprazole, misoprostol c. Misoprostol, omeprazole, cimetidine a. High dose of cimetidine, omeprazole, and triple drug therapy (bismuth subsalicylate + amoxicillin + metronidazole) b. None of the above 51.) A 30-year-old accountant comes to your office, and you diagnose him with a refractory duodenal ulcer. Which course of action do you pursue, in this order? a. Aluminium hydroxide, cimetidine, sulcrafate b. Cimetidine, omeprazole, misoprostol c. Misoprostol, omeprazole, cimetidine d. High dose of cimetidine, omeprazole, and triple drug therapy (bismuth subsalicylate + amoxicillin + metronidazole) a. None of the above 52.) Gastric ulcers are best treated by which of the following sequentially organized treatments? a. Aluminium hydroxide, cimetidine, sulcrafate b. Cimetidine, omeprazole, misoprostol a. Misoprostol, omeprazole, cimetidine b. High dose of cimetidine, omeprazole, and triple drug therapy (bismuth subsalicylate + amoxicillin + metronidazole) c. None of the above 53.) Uncomplicated duodenal ulcers are best treated by which of the following sequentially organized treatments? a. Aluminium hydroxide, cimetidine, sulcrafate a. Cimetidine, omeprazole, misoprostol b. Misoprostol, omeprazole, cimetidine c. High dose of cimetidine, omeprazole, and triple drug therapy (bismuth subsalicylate + amoxicillin + metronidazole) d. None of the above
EXAM 3 - Pharmacology of Female Gonadal Hormones and Contraception; Menopause and Hormone Replacement Therapy; Pharmacology of Male Sex Hormones 1.) Which of the following is incorrect regarding estrogen and its actions? a. Has two receptor isoforms b. There are estrogen receptors in the skin c. Serum estradiol levels bind to SHBG d. Is subject to the first-pass effect e. None of the above 2.) The most common side effect of combined contraceptives is a. Bleeding irregularities a. Headache b. Breast tenderness c. Mood swings d. Weight gain 3.) Oral contraceptives (OC) have no effect on a. Myocardial infarction b. Gastrointestinal diseases c. Breast cancer risk a. Endrometrial hyperplasia b. Cardiovascular disease 4.) Which of the following are best used within 72 hours of coitus to prevent pregnancy? a. Prevens b. Copper IUD c. Plan B d. B and C e. All of the above 5.) Which of the following is NOT true of misopristone (RU-486)? a. It is a progesterone antagonist b. It is a progesterone agonist a. Used for medical termination of pregnancy b. Can be used as an emergency contraceptive c. Can be followed by misoprostol, a PG agonist 6.) Diethylstilbestrol (DES) is a synthetic estrogen
a. True a. False 7.) Which is the following is NOT true of tamoxifen? a. Can be used as a treatment for advances breast cancer b. Stabilizes bone loss c. Is an estradiol partial agonist inhibitor d. Is similar in class to clomiphene citrate e. Is a major cause of osteoporosis 8.) SERM is beneficial because a. It affects lipid, bone, breast, and endometrium b. It affects lipid and bone, but not breast and endometrium a. It affects breast and endometrium, but not lipid and bone b. It does not affect lipid, bone, breast, or endometrium c. It affects breast and bone, but not lipid and endometrium 9.) Which is true regarding the levels of various hormones at menopause? a. Increased FSH and LH b. Increased estrogens c. Same levels of testosterone d. A and C a. B and C Questions 10-13- Match the following A. B. C. Estradiol (E ) Estrone (E ) Estriol (E )
2 1 3
10.) Present in the fetal-placental unit (FPU) C 11.) Predominant estrogen before menopause A 12.) Second most prominent estrogen before menopause B 13.) Dominant estrogen after menopause B 14.) Oral conjugated equine estrogens (CEE), like premarin, can ____ HDL but ____ TGs when given orally a. Increase, increase a. Increase, decrease b. Decrease, increase c. Decrease, decrease d. None of the above 15.) Which route of CEE administration is preferred for women with high TGs? a. Vaginal b. Patch
a. IV b. IM c. Buccal 16.) Phytoestrogens, an alternative estrogen therapy derived from plants, are characterized by all of the following except a. Possible low incidence of breast cancer b. Used in treatment of hot flashes c. Include isoflavones d. Include lignans 17.) a. b. c. d. 18.) a. b. c. d. e. Very conclusive in scientific studies vs. placebo Risk factors for osteoporosis include White or Asian race Petite Heparin, progesterone, tamoxifen use Type I diabetes e. All of the above Which of the following is NOT true regarding testosterone? It is made from cholesterol in Leydig cells It is made from androstenedione in the adrenal gland LH controls its secretion Is a C19 steroid
e. None of the above 19.) Testosterone is bound 65% to albumin and 35% to SHBG a. True 20.) a. b. c. d. b. False (it’s the other way around) Which is true regarding the daily variations in testosterone levels? a. Peaks in AM, trough in PM Trough in AM, peaks in PM Equal in AM and PM None in AM None in PM
21.) All of the following are characteristic of DHT except a. Amplifies testosterone action in some tissues because DHT-receptor complexes are more stable b. Binds to same receptor as testosterone c. Binds to different receptor than testosterone a. Produce by 5-alpha reductase b. Responsible for prostate enlargement, hairline recession, and facial hair 22.) Male pseudohermaphrodites are caused by a. Type 1 5-alpha reductase defect
b. Type 2 5-alpha reductase defect a. Type A defect b. Type B defect c. I don’t know and I don’t care 23.) Prader-Willi Syndrome and Kallmann’s Syndrome can be a cause of a. Primary hypogonadism b. Secondary hypogonadism a. Primary midichlorianism b. All of the above c. None of the above 24.) a. b. c. d. 25.) a. b. c. d. 26.) a. b. c. d. All of the following are causes of secondary hypogonadism except Pituitary adenoma Respiratory disorders Inflammatory diseases, ex- Crohn’s disease Use of ketoconazole, glucocorticoids, spironolactone, etc. e. Congenital All of the following testosterone administration systems are effective except a. Oral (b/c of first pass effect) IM Transdermal patches Transdermal gel All of the above What are the disadvantages of IM testosterone injections? Can cause gynecomastia Can cause polycythemia Can cause supraphysiological fluctuations Requires healthcare professional for administration
e. Less frequent administration 27.) Oral testosterone replacement requires multiple daily dosing and can cause hepatotoxicity, while a transdermal patch a. Mimics circadian rhythm b. Can cause high incidence of skin irritation c. Is visible d. Has low patient compliance, compared to high compliance with transdermal gels e. All of the above 28.) Testosterone _____ bone quality, while hypogonadism _____ bone quality. a. Increases, increases b. Increases, decreases a. Decreases, increases b. Decreases, decreases c. None of the above
29.) Erectile dysfunction (ED) can be an early marker for cardiovascular disease, as arthersclerosis in penile arteries may manifest before other arteries a. True a. False 30.) PDE-5 inhibitors, used to treat ED, are used with caution with alpha blockers, because of a possible additive effect a. True a. False