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HOW TO SURVIVE
Pharmacology
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 Pages
Introduction to Pharmacology 2
How to Study Pharmacology 3
Written Exams and Quizzes 4
Textbooks 5
Review Material (from Samuel Anandan) 6-31
Exam 2 – High Yield Lecture Points 6-12
Exam 3 – High Yield Lecture Points 13-16
Toxicology and GI Decontamination Questions 17-20
GI Pharmacology Questions 21-27
Hormone Questions 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!
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
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.) Digitalis
a. Lactone ring has to be unsaturated
b. OH group at position 14 is necessary
c. Ouabain > Digoxin > Digitoxin in terms of # of OH groups
d. Glycosides = cis rings; regular hormones = trans rings
e. Low therapeutic index
f. Reduces size of enlarged heart
g. Not indicated for diastolic dysfunction (thickened muscle wall prevents relax.)
h. Digitoxin = more enterohepatic circulation and hepatic degradation than digoxin
i. 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
3.) Fe deficiency with low storage iron, low serum ferritin, low TIBC, low MCV, low MCHC,
2+
10.) Macrocytic anemia = leucopenia, thrombocytopena b/c affects all cell lines
11.) Babinski’s response = sign of vitamin B deficiency 12
13.) Vitamin B mainly stored in liver, mad storage (lasts for years)
12
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
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)
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
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.) Resins
a. Farting
b. Combine with nicotinic acid to dec. serum cholesterol by 50%
c. 15% LDL reduction on its own
d. Steatorrhea is a side effect
e. Blocks absorption of digitalis, warfarin, thiazides, provastatin, levastatin
15.) Fibrins
a. PPARalpha
b. Reduces TGs
c. Pancreatitis, rashes, gallstones, etc.
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
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
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
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
+
c. Used in acute or chronic renal failure, b/c that leads to Na and H O retention
+
2
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;
+
Miscellaneous
1.) HTN drug of choice = thiazides
2.) Alpha blockers NOT used for angina
3.) Nitrites à methemoglobinemia à treatment for CN toxicity
-
1.) Table
TRH CRH GH ADH
Decrease Somatostatin Atropine α-blockers α-blockers
Synthesis Glucocorticoids Hexamethonium dopamine- atropine
NE antagonists
Melatonin
GABA
Increase Estrogen 5-HT 5-HT mAChRs
Synthesis ACTH Dopamine β-agonists
β-blockers
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)
2
kk. Liotrix = T and T (trix gives you the best of both worlds = Locutus eating trix), use in
3 4
hypothyroidism
ll. Thyroglobulin = pulverized porcine thyroid gland, use in hypothyroidism
1.)
i. Like prednisalone
d. Methyl on Ring B = inc. both Na retention and anti-inflammatory
+
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)
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
2 2
c. Paracelsus
a. Morpheus
b. Obi-Wan
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
b. M 2
c. M 3
d. M 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
Questions 12-17- Match the following opioid receptors with the appropriate effects
A. μ 1
B. μ 2
C. δ
D. κ 1
E. κ 2
F. κ 3
20.) Ventilation and oxidation are more critical that naloxone in an opioid overdose
a. True
a. False
d. Is not an amphetamine
a. Is an enactogen, because it releases 5-HT
d. Increased peristalsis
a. No effect on pupil size and diaphoresis
e. Decreased diaphoresis
EXAM 3 - GI Pharmacology Questions
(Mnemonic- Lomotil = “lo motor” = dec. peristalsis, so inc. H O and electrolyte reabs.)
2
e. Asparagine (Arg)
7.) Octreotide is only used for treatment of diarrhea in patients with HIV infection.
a. True
a. False
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
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
15.) The 5-HT antagonists are characterized by all of the following except
3
17.) All of the following are uses for cannabinoids, found in pot, except
a. Anti-emesis
b. Analgeis
c. Anticonvulsant
d. 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
e. Methotrexate is contraindicated
20.) Which of the following are major pathways for gastric secretion?
a. Vagal stimulation
b. Endocrine stimulation via antral G cells
c. Histamine release from ECL cells
d. A and C
a. PGE 2
b. PGI 2
c. ACh
d. A and C
a. B and C
22.) Which of the following is responsible for mucous and HCO release?
3
-
a. PGE 2
b. PGI2
c. ACh
d. A and C
e. B and C
23.) Which of the following act via a Ca -dependent pathway?
2+
a. Gastrin
b. Histamine
c. ACh
d. A and C
a. B and C
b. Histamine
a. ACh
b. A and C
c. B and C
25.) Misoprostol is a
a. Prostaglandin agonist
a. Prostaglandin antagonist
b. H receptor agonist
2
c. H receptor antagonist
2
d. ACh analog
Questions 26-30- Match the following (each choice can have more than one answer)
A. Cimetidine
B. Ranitidine
C. Famotidine
D. Nizatidine
E. Zolentidine
particularly in men by inhibiting its hydrolyzation via the Cyt P450 system
a. Testosterone
b. Estradiol
a. DHT
b. Progesterone
c. Cholesterol
33.) Cimetidine can prolong the half-lives of
a. Phenytoin
b. Sulfonylureas
c. Ca channel blockers
2+
d. N-acetyl procainamide
a. Peptic ulcers
b. Duodenal ulcers
c. Gastric ulcers
d. Zollinger-Ellison syndrome
e. GERD
c. Selective M blockers have greater side effects than atropine, like tachycardia
1
b. Black tongue
a. Red tongue
b. Blue tongue
c. Purple tongue
c. Metoprolol
a. All of the above
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
52.) Gastric ulcers are best treated by which of the following sequentially organized
treatments?
a. Aluminium hydroxide, cimetidine, sulcrafate
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
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
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
d. A and C
a. B and C
A. Estradiol (E ) 2
B. Estrone (E ) 1
C. Estriol (E )
3
15.) Which route of CEE administration is preferred for women with high TGs?
a. Vaginal
b. Patch
a. IV
b. IM
c. Buccal
b. Secondary hypogonadism
a. Primary midichlorianism
b. All of the above
c. None of the above
e. Congenital
25.) All of the following testosterone administration systems are effective except
a. Oral (b/c of first pass effect)
a. IM
b. Transdermal patches
c. Transdermal gel
d. All of the above
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