1
Q
pharmacology
A
The study of drugs and their interactions with living systems.
2
Q
toxicology
A
The study of harmful effects of chemicals on living organisms.
3
Q
drug agonist
A
A molecule that binds a receptor and activates it.
4
Q
competitive antagonist
A
Blocks receptor by competing with agonist at the same site; reversible with more agonist.
5
Q
non-competitive antagonist
A
Binds a different part of receptor and decreases max effect; cannot be overcome with more agonist.
6
Q
partial agonist
A
Produces a lower maximal response than a full agonist even at full receptor occupancy.
7
Q
inverse agonist
A
Reduces constitutive receptor activity below baseline.
8
Q
pharmacokinetics (PK)
A
What the body does to the drug (ADME).
9
Q
pharmacodynamics (PD)
A
What the drug does to the body (receptors, signaling, effect).
10
Q
pharmacogenomics
A
Study of genetic influences on drug response.
11
Q
ADME
A
Absorption, Distribution, Metabolism, Elimination.
12
Q
aqueous diffusion
A
Drug movement through water-filled pores down concentration gradient.
13
Q
lipid diffusion
A
Passive movement across lipid membrane depending on lipid solubility & pKa/pH.
14
Q
endocytosis/exocytosis
A
Vesicular drug transport into (endo) or out of (exo) the cell.
15
Q
volume of distribution (Vd)
A
Theoretical volume needed to contain total drug at plasma concentration.
16
Q
clearance
A
Volume of plasma cleared of drug per unit time.
17
Q
Zero-order elimination vs first order
A
Zero: constant amount cleared. First: constant fraction cleared.
18
Q
half-life
A
Time for plasma concentration to fall by 50%.
19
Q
steady-state
A
Drug intake = drug elimination; stable concentration.
20
Q
Loading dose purpose
A
Rapidly achieve target plasma concentration.
21
Q
Maintenance dose purpose
A
Maintain steady-state concentration.
22
Q
four major receptor/signaling types
A
Intracellular receptors, Enzyme-linked receptors (tyrosine kinase), Ligand-gated ion channels, GPCRs.
23
Q
GPCR structure highlight
A
7 transmembrane α-helices, heterotrimeric G-proteins (α, β, γ).
24
Q
Second messengers involved in GPCR signaling
A
cAMP, IP3, DAG, cGMP.
25
Major drug-efflux family
ABC transporters (P-gp etc.).
26
BBB excludes drugs mainly through what mechanism
Tight junctions + efflux transporters.
27
Phase I metabolism
Oxidation (CYP450), reduction, hydrolysis → more polar metabolites.
28
Phase II metabolism
Conjugation (glucuronidation, acetylation, sulfation) → highly polar, inactive.
29
CYP3A4 is responsible for what
Metabolism of ~50% of all drugs.
30
CYP induction effect
↓ drug levels if inactivated by metabolism; ↑ effects if drug is a prodrug.
31
CYP inhibition effect
↑ drug levels → toxicity risk.
32
EC50
Concentration producing 50% maximal response (potency).
33
Emax
Maximal achievable drug effect (efficacy).
34
Potency vs efficacy
Potency: how much drug needed. Efficacy: how well drug works once fully bound.
35
What are the three major parts of a neuron?
Dendrites, cell body, axon.
36
What type of cells myelinate the CNS?
Oligodendrocytes.
37
What type of cells myelinate the PNS?
Schwann cells.
38
What is the functional purpose of myelin?
Increases conduction velocity via saltatory conduction.
39
Name the major cholinergic neurotransmitter.
Acetylcholine.
40
Name the monoamine neurotransmitters.
Norepinephrine, dopamine, serotonin.
41
What are the major excitatory and inhibitory amino acid neurotransmitters?
Excitatory: glutamate. Inhibitory: GABA.
42
Are NO (nitric oxide) neurotransmitters stored?
No—synthesized on demand.
43
What is the “gut’s own nervous system”?
The enteric nervous system.
44
Length pattern of sympathetic fibers?
Short pre-ganglionic, long post-ganglionic.
45
Length pattern of parasympathetic fibers?
Long pre-ganglionic, short post-ganglionic.
46
Neurotransmitter at all preganglionic autonomic synapses?
Acetylcholine (nicotinic receptors).
47
Primary neurotransmitter at parasympathetic target organs?
Acetylcholine (muscarinic receptors).
48
Primary neurotransmitter at most sympathetic target organs?
Norepinephrine (α or β receptors).
49
Sympathetic effect on heart rate?
Increases HR (β1 receptors).
50
Parasympathetic effect on heart rate?
Decreases HR (M2 receptors).
51
Sympathetic effect on bronchi?
Bronchodilation (β2).
52
Parasympathetic effect on bronchi?
Bronchoconstriction (M3).
53
What second messengers does α1 receptor activation produce?
IP3 and DAG.
54
What receptor type are all adrenergic receptors?
GPCRs (G-protein coupled receptors).
55
β1 and β2 receptors primarily activate which G-protein pathway?
Gs → ↑cAMP.
56
α2 receptors activate which G-protein pathway?
Gi → ↓cAMP.
57
Effect of muscarinic agonists on the eye?
Miosis + ↑aqueous humor drainage.
58
Effect of muscarinic agonists on the heart?
↓HR (bradycardia).
59
Effect of muscarinic agonists on vasculature?
Vasodilation via NO (endothelial M3).
60
What are the major effects of cholinergic excess (SLUDGE-BM)?
Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis, Bronchospasm, Miosis.
61
What is the antidote for organophosphate poisoning?
Atropine + pralidoxime (2-PAM).
62
In muscarinic excess, what does the “M” in SLUDGE-BM stand for?
Miosis.
63
Direct cholinomimetic vs indirect cholinomimetic mechanism?
Direct: binds receptor. Indirect: inhibits acetylcholinesterase.
64
Alpha-1 receptor activation leads to what physiologic effect?
Smooth muscle contraction → ↑BP.
65
Which system has long preganglionic fibers?
Parasympathetic.
66
Which ANS division slows the heart?
Parasympathetic.
67
Parasympathetic receptors are of what type?
Muscarinic (M1–M5).
68
What receptor is located at ALL autonomic ganglia?
Nicotinic (Nn).
69
What receptor is located at the neuromuscular junction (NMJ)?
Nicotinic Nm.
70
What receptors does epinephrine activate?
α1, α2, β1, β2.
71
What receptors does norepinephrine activate?
α1, α2, β1 (minimal β2).
72
What receptors does isoproterenol activate?
β1, β2.
73
What receptors does dobutamine activate?
β1 > β2.
74
Receptor activity of dopamine?
Low dose: D1 Medium: β1 High: α1
75
β1 stimulation effect on the heart?
↑HR, ↑contractility, ↑CO.
76
β2 stimulation effect on vasculature?
Vasodilation → ↓PVR.
77
α1 stimulation effect on vasculature?
Vasoconstriction → ↑BP.
78
What is the mechanism of amphetamine?
Indirect release of NE from nerve terminals.
79
What is the mechanism of ephedrine?
Mixed: direct receptor stimulation + indirect NE release.
80
Direct β1 effects on cardiac output?
↑SV and ↑HR → ↑CO.
81
Effect of adrenergic agonists on peripheral resistance?
Depends—but β2 decreases, α1 increases.
82
Reversible alpha blockers examples?
Phentolamine, prazosin, tolazoline.
83
Irreversible alpha blocker example?
Phenoxybenzamine.
84
Clinical use of alpha blockers in pheochromocytoma?
Control hypertensive episodes.
85
Non-selective beta-blocker example?
Propranolol (β1 + β2).
86
β1-selective blockers?
Metoprolol, atenolol.
87
Why safer for asthma/COPD patients?
Less β2 blockade → less bronchoconstriction.
88
Esmolol highlight?
Ultra short-acting; used for acute arrhythmias.
89
Acute β-blockade effect on peripheral resistance?
Increases (loss of β2 vasodilation).
90
Chronic β-blockade effect on peripheral resistance?
Decreases (mechanism unclear).
91
Mechanism of direct-acting cholinomimetics?
Bind and activate muscarinic/nicotinic receptors.
92
Mechanism of indirect-acting cholinomimetics?
Inhibit AChE → ↑ACh levels at synapses.
93
Indirect cholinomimetic classes?
Alcohols (edrophonium), carbamates (neostigmine), organophosphates.
94
Muscarinic effects on the eye?
Miosis + ↑aqueous drainage (glaucoma therapy).
95
Cardiovascular muscarinic effects?
Vasodilation (M3 endothelial NO). Large doses: bradycardia (M2).
96
Pathophysiology of MG?
Autoimmune destruction of nicotinic ACh receptors at NMJ.
97
Mechanism of treatment (neostigmine/pyridostigmine)?
AChE inhibition → ↑ACh at NMJ.
98
Organophosphate poisoning symptoms acronym?
SLUDGE-BM.
99
SLUDGE-BM: what does “B” stand for?
Bronchospasm.
100
Treatment for organophosphate poisoning?
Atropine + pralidoxime.
101
Acronym for atropine overdose?
“BRAND”: Blind, Red, Absent bowel sounds, Nuts, Dry.
102
Treatment for atropine overdose?
Physostigmine.
103
Muscarinic excess vs nicotinic excess differences?
Muscarinic: SLUDGE-BM. Nicotinic: muscle fasciculations → paralysis.
104
What receptors does NE lack significant action on?
β2.
105
Beta-blockers reduce renin by blocking which receptor?
β1 on juxtaglomerular cells.
106
Why is atropine contraindicated in glaucoma?
Causes mydriasis → worsens angle closure.
107
Example of a ganglionic blocker?
Hexamethonium.
108
Organophosphates mechanism?
Irreversible AChE inhibition → excess ACh.
109
Why does pralidoxime need to be given early?
“Aging” process makes AChE inhibition irreversible.
110
What drug class causes reflex tachycardia?
Direct vasodilators, α1 blockers, nitrates.
111
Mechanism of nitrates/nitrites?
↑NO → activate guanylyl cyclase → ↑cGMP → smooth muscle relaxation.
112
Mechanism of β2 agonists in smooth muscle?
GPCR → ↑cAMP → relaxation (mainly respiratory).
113
Mechanism of sildenafil?
PDE-5 inhibitor → ↑cGMP.
114
Good hemodynamic effects of nitrates?
↑venous capacitance, ↓preload, ↓ventricular size, ↓CO demand.
115
Bad effects of nitrates?
Orthostatic hypotension, syncope, headache, reflex tachycardia.
116
What channels do CCBs block?
L-type Ca²⁺ channels in vasculature and heart.
117
Dihydropyridines act primarily where?
Peripheral vasculature → strong vasodilation.
118
Verapamil & diltiazem act primarily where?
Heart → ↓contractility, ↓SA/AV conduction.
119
Major CCB toxicities?
Bradycardia, AV block, CHF.
120
Why used in angina?
↓O₂ demand (↓HR, ↓BP, ↓contractility).
121
Why not vasodilators?
They do not dilate vessels directly.
122
Four anatomic control sites for BP regulation?
Arterioles, venules (capacitance), heart, kidneys.
123
Four antihypertensive classes?
Diuretics, sympathoplegics, direct vasodilators, anti-angiotensins.
124
Equation relating BP to cardiac output?
BP = CO × PVR.
125
CO equals…?
SV × HR.
126
Centrally acting α2 agonists?
Clonidine, methyldopa.
127
Their mechanism?
↓sympathetic outflow from brainstem.
128
Ganglion blocker example?
Hexamethonium.
129
Neuron blockers?
Guanethidine, reserpine.
130
Prazosin/Terazosin/Doxazosin mechanism?
α1 blockade → dilation of arterioles & venules.
131
When is BP more reduced with α1 blockers?
Upright posture (orthostatic effect).
132
Minoxidil mechanism?
Opens K⁺ channels → smooth muscle hyperpolarization → relaxation.
133
Hydralazine mechanism?
Increases NO → arteriolar dilation.
134
Nitroprusside mechanism?
Releases NO → ↑cGMP. Dilates arteries + veins.
135
Fenoldopam mechanism?
D1 agonist → peripheral arteriolar dilation.
136
ACE inhibitors example?
Captopril.
137
ARBs examples?
Losartan, valsartan.
138
Systolic vs diastolic failure?
Systolic: ↓contractility, ↓EF. Diastolic: impaired filling, normal EF.
139
Pulmonary edema cause in HF?
↑LVEDP → ↑pulmonary venous pressure.
140
What triggers Ca²⁺ release from SR?
Ca-induced Ca release (trigger Ca enters cell).
141
Mechanism of digoxin?
Inhibits Na⁺/K⁺ ATPase → ↑intracellular Ca²⁺ → positive inotropy.
142
Digoxin toxicity signs?
Arrhythmias, N/V, visual disturbances.
143
Milrinone mechanism?
PDE-3 inhibitor → ↑cAMP → ↑contractility + vasodilation.
144
SA node function?
Primary pacemaker ~75 bpm.
145
AV node function?
Delays conduction; backup pacemaker.
146
Purkinje fiber function?
Rapid conduction to ventricles.
147
Class I drugs mechanism?
Na⁺ channel blockade.
148
Class II drugs?
β-blockers.
149
Class III drugs?
Prolong AP via K⁺ channel effects (ex: amiodarone).
150
Class IV drugs?
CCBs (verapamil).
151
Carbonic anhydrase inhibitor?
Acetazolamide.
152
Loop diuretic?
Furosemide.
153
Thiazide diuretic?
Hydrochlorothiazide.
154
K⁺-sparing diuretics?
Spironolactone, conivaptan.
155
Osmotic diuretic?
Mannitol.
156
Plateau (Phase 2) of cardiac AP is due to what currents?
Ca²⁺ influx + K⁺ efflux.
157
How do diuretics reduce BP?
↓blood sodium → ↓blood volume.
158
Nitrates relax smooth muscle by which mechanism?
Activation of guanylyl cyclase (↑cGMP).
159
How many histamine receptors exist?
Four (H1, H2, H3, H4).
160
H1 receptor effects?
Bronchoconstriction, vasodilation, pain/itch signaling.
161
H1 antagonists are actually what?
Inverse agonists.
162
Example of a 1st-gen antihistamine?
Diphenhydramine (Benadryl).
163
Why do 1st-gen antihistamines cause sedation?
Cross BBB → central antimuscarinic effects.
164
Why are 2nd-gen antihistamines preferred?
Minimal sedation; less CNS penetration.
165
Short-acting inhaled β-agonists for asthma?
Epinephrine, isoproterenol, terbutaline.
166
Long-acting β2 agonists?
Formoterol, salmeterol.
167
Main toxicity of β-agonists?
Skeletal muscle tremor & arrhythmias.
168
Examples of methylxanthines?
Theophylline, theobromine, caffeine.
169
Theophylline mechanism?
PDE inhibition → ↑cAMP → bronchodilation.
170
Mechanism of ipratropium/tiotropium?
Block M3 receptors → prevent bronchoconstriction + mucus secretion.
171
Clinical use?
COPD (mainstay), adjunct in asthma.
172
5-lipoxygenase inhibitor?
Zileuton.
173
Leukotriene receptor blockers?
Zafirlukast, montelukast.
174
Mechanism of omalizumab?
Anti-IgE monoclonal antibody; prevents IgE from binding mast cells.
175
Benefit in asthma?
↓severity, ↓steroid need, ↓hospitalizations.
176
Serotonin functions?
Pain/itch modulation, platelet aggregation, GI motility, CNS mood effects.
177
Which serotonin receptor family mediates migraines (targeted by triptans)?
5-HT1B/1D.
178
Toxicity of triptans?
Recurrence of migraine; serotonin syndrome if combined with SSRIs/MAOIs.
179
5-HT3 antagonist used for nausea?
Ondansetron.
180
Three major classes of antidepressants?
MAOIs, TCAs, SSRIs.
181
TCA mechanism?
Inhibit NET + SERT; anticholinergic.
182
SSRI mechanism?
Selectively inhibit SERT (e.g., sertraline).
183
SNRI mechanism?
Inhibit SERT + NET.
184
Major universal warning for all antidepressants?
Suicidal ideation (especially early therapy).
185
What can trigger serotonin syndrome?
Anything ↑serotonin (SSRIs, MAOIs, SNRIs, triptans, MDMA).
186
Drugs used for tonic–clonic seizures?
Phenytoin, phenobarbital, carbamazepine.
187
Drug used for absence seizures?
Ethosuximide.
188
Broad-spectrum anticonvulsant covering multiple seizure types?
Valproic acid.
189
Benzodiazepines role in seizures?
Acute status epilepticus.
190
Status epilepticus unresponsive to phenytoin/phenobarbital — next step?
Benzodiazepines; consider intubation.
191
Why are 2nd-gen antihistamines preferred?
They don’t cause sedation.
192
Which drug is an SSRI?
Sertraline (Zoloft).
193
Three main components of thrombogenesis?
Vasoconstriction, platelet plug formation, coagulation cascade.
194
Platelet plug phases?
Adhesion → Aggregation → Secretion → Platelet cross-linking.
195
Intrinsic pathway trigger?
Collagen exposure + vWF.
196
Extrinsic pathway trigger?
Tissue factor (TF).
197
Final common pathway step?
Prothrombin → thrombin → fibrin.
198
Protein C + S function?
Inhibit factors Va and VIIIa.
199
DIC causes?
Massive tissue injury, malignancy, sepsis, abruptio placentae.
200
DIC treatment?
Plasma transfusion + treat underlying cause.
201
Mechanism of UFH (unfractionated heparin)?
Enhances antithrombin → ↓thrombin, ↓Xa.
202
Major UFH toxicity?
HIT (heparin-induced thrombocytopenia).
203
Antidote for heparin?
Protamine sulfate.
204
LMW heparin acts mainly on?
Factor Xa.
205
Fondaparinux action?
Selective factor Xa inhibitor.
206
Parenteral direct thrombin inhibitor examples?
Lepirudin, bivalirudin, argatroban.
207
Which DTIs bind both active + substrate recognition sites?
Hirudin derivatives.
208
Mechanism of warfarin?
Inhibits vitamin K recycling → ↓factors II, VII, IX, X.
209
Therapeutic monitoring tool?
INR (target 2–3).
210
Onset delay cause?
Must wait for existing clotting factors to degrade.
211
Mechanism of tPA?
Converts plasminogen → plasmin (preferentially on fibrin).
212
Streptokinase origin?
Streptococci.
213
Urokinase origin?
Kidney.
214
Aspirin mechanism?
Irreversible COX-1 inhibition → ↓TXA₂ → ↓platelet aggregation.
215
ADP receptor blockers?
Clopidogrel (Plavix), ticlopidine.
216
GP IIb/IIIa inhibitor?
Abciximab.
217
Vitamin K-dependent clotting factors?
II, VII, IX, X.
218
Aminocaproic acid mechanism?
Prevents plasmin formation (inhibits fibrinolysis).
219
Four types of diabetes?
Type I, Type II, Type III (secondary), Type IV (gestational).
220
Where is insulin produced?
Pancreatic β-cells.
221
Insulin receptor type?
Tyrosine kinase receptor.
222
Insulin effects?
↑GLUT translocation, ↑glycogen synthesis, ↑lipogenesis.
223
Rapid-acting insulins?
Lispro, aspart, glulisine.
224
Short acting (regular)?
Humulin R, Novolin R.
225
Intermediate insulins?
NPH, isophane.
226
Long-acting insulins?
Glargine, detemir.
227
Metformin mechanism?
↓hepatic glucose production.
228
Sulfonylureas mechanism?
Block K+ channels → ↑insulin release.
229
TZDs mechanism?
PPARγ activation → ↑insulin sensitivity.
230
α-glucosidase inhibitor example?
Acarbose.
231
SGLT2 inhibitors?
“-gliflozins” (prevent glucose reabsorption in PCT).
232
GLP1 agonists / DPP4 inhibitors purpose?
↑incretin effect → ↑insulin, ↓glucagon.
233
Amylin analog effect?
↓glucagon release.
234
Where are chylomicrons formed?
Intestine.
235
LDL function?
Delivers cholesterol to tissues.
236
HDL function?
Scavenges cholesterol from tissues.
237
Statin mechanism?
Inhibit HMG-CoA reductase → ↓cholesterol synthesis → ↑LDL receptors.
238
Major statin toxicities?
↑LFTs, myopathy, rhabdomyolysis.
239
Niacin effects?
↓VLDL, ↓LDL, ↑HDL.
240
Classic toxicity?
Cutaneous flushing (PG mediated).
241
Fibrate mechanism?
↑lipolysis in liver, ↓VLDL.
242
Key toxicity?
Arrhythmias, ↑LFTs, potentiates warfarin, myopathy.
243
Mechanism?
Bind bile acids → prevent reabsorption → ↑LDL clearance.
244
Ezetimibe effect?
Blocks intestinal cholesterol absorption.
245
Mechanism?
Prevent LDL receptor degradation → massively ↑LDLR → ↓LDL.
246
What structure do penicillins and cephalosporins share?
Beta-lactam ring.
247
Amoxicillin + beta-lactamase inhibitor?
Augmentin (clavulanic acid).
248
Vancomycin use?
MRSA, serious Gram+ infections.
249
Vancomycin toxicities?
Nephrotoxicity, ototoxicity, “Red Man Syndrome.”
250
Polymyxins mechanism?
Detergent action disrupting bacterial membranes (Gram– effective).
251
Tetracyclines toxicity?
GI upset, bone/teeth deposition.
252
Macrolide prototypes?
Erythromycin, clarithromycin, azithromycin.
253
Rifampin mechanism?
Inhibits mRNA synthesis (RNA polymerase).
254
Fluoroquinolone examples?
Ciprofloxacin, levofloxacin.
255
Fluoroquinolone mechanism?
Inhibit DNA gyrase (topoisomerase II).
256
Sulfonamide mechanism?
PABA analog → inhibits folate synthesis.
257
Trimethoprim-sulfamethoxazole effect?
Sequential folate blockade.
258
Why does acyclovir cause chain termination?
Missing 3’ hydroxyl group.
259
Indications for acyclovir?
HSV1, HSV2, VZV; safe in pregnancy.
260
Zidovudine (AZT) mechanism?
Reverse transcriptase inhibitor.
261
Lamivudine mechanism?
Inhibits HBV polymerase + HIV RT.
262
Tamiflu (oseltamivir) mechanism?
Neuraminidase inhibitor.
263
Zanamivir route?
Inhaled powder.
264
Xofluza (baloxavir) mechanism?
Polymerase acidic (PA) endonuclease inhibitor.
265
Paxlovid contains what?
Two antivirals; oral.
266
Remdesivir mechanism?
RNA chain terminator (IV).
267
What do monoclonal antibodies for COVID block?
Viral entry.
268
Which drug inhibits ADP-mediated platelet aggregation?
Clopidogrel.
269
Which drug class blocks PCSK9?
PCSK9 inhibitors.
270
Which antibiotic class always has a beta-lactam ring?
Penicillins + cephalosporins.
271
Classic Parkinson’s symptoms acronym?
TRAP — Tremor, Rigidity, Akinesia/bradykinesia, Postural instability.
272
Pathophysiology of Parkinson’s?
Degeneration of nigrostriatal dopamine pathway.
273
Brains of Parkinson patients contain what abnormal structure?
Lewy bodies (α-synuclein aggregates).
274
Why is levodopa given with carbidopa?
Carbidopa inhibits peripheral metabolism → ↑CNS delivery.
275
Levodopa long-term complications?
Dyskinesias, on/off fluctuations, hallucinations.
276
Dopamine agonists?
Pramipexole, ropinirole.
277
MAO-B inhibitors?
Selegiline, rasagiline.
278
COMT inhibitors?
Tolcapone.
279
Drug for sudden “off” periods?
Apomorphine.
280
Anticholinergic used in Parkinson’s?
Benztropine.
281
Illicit drug impurity destroying dopaminergic neurons (causing Parkinson-like symptoms)?
MPTP.
282
Huntington’s disease treatment?
Tetrabenazine.
283
Duchenne muscular dystrophy classic sign?
Gower’s sign.
284
Cerebral palsy spasticity treatment?
Baclofen, dantrolene.
285
Alzheimer’s drugs?
Tacrine, memantine.
286
What does aspirin inhibit?
COX-1 > COX-2; irreversible.
287
Aspirin platelet effects last how long?
8–10 days (platelet lifespan).
288
Aspirin daily dose for antiplatelet effect?
81–325 mg/day.
289
Side effects of NSAIDs?
GI ulcers, kidney injury, bleeding, bronchospasm.
290
Acute steroid effects?
Anti-inflammatory, mobilize glucose, alertness, ↑BP.
291
Chronic steroid toxicities?
Immunosuppression, diabetes, obesity, muscle wasting, HTN, depression.
292
Long-acting glucocorticoid example?
Dexamethasone.
293
What chemicals trigger pain from tissue injury?
Bradykinin, prostaglandins (AA cascade).
294
What channels generate action potentials in pain fibers?
Sodium channels.
295
What theory explains descending pain modulation?
Gate control theory.
296
Opioid MOA?
Bind mu receptors → ↓neurotransmitter release + hyperpolarization.
297
Morphine metabolism?
Phase II; M3G and M6G active metabolites.
298
Opioids are eliminated mainly via?
Kidneys.
299
Classic opioid triad?
Miosis, respiratory depression, coma.
300
Opioids effect on cough?
Suppress cough reflex.
301
Opioid effect on temperature?
Mu: hyperthermia; kappa: hypothermia.
302
Strong opioid agonists (phenanthrenes)?
Morphine, hydromorphone, heroin.
303
Strong opioid agonist (phenylpiperidine)?
Fentanyl.
304
Methadone key features?
Long half-life, treats chronic pain & opioid dependence.
305
Why is meperidine falling out of use?
Seizures + toxic metabolites; used only for post-op shivering.
306
Moderate agonists?
Codeine, oxycodone.
307
Opioid antagonists?
Naloxone, naltrexone.
308
Difference between proto-oncogenes & tumor suppressors?
Proto-oncogenes promote growth; tumor suppressors inhibit it.
309
Three major cancer treatments?
Surgery, radiation, chemotherapy.
310
Most commonly used alkylating agent?
Cyclophosphamide.
311
Nitrosoureas special feature?
Cross BBB.
312
Platinum compounds?
Cisplatin, carboplatin.
313
Cisplatin uses?
Testicular cancer, ovarian cancer, solid tumors.
314
Cisplatin toxicities?
Nephrotoxicity, ototoxicity, neuropathy.
315
Mechanism of methotrexate?
Inhibits DHFR → ↓DNA/RNA synthesis.
316
Toxicities of methotrexate?
Bone marrow suppression, mucosal ulcers, fetal toxicity.
317
Plant-based chemo examples?
Vincristine, paclitaxel.
318
Antitumor antibiotics?
Dactinomycin, doxorubicin, bleomycin.
319
Hormonal agents?
Tamoxifen, fulvestrant, corticosteroids.
320
Cytokine types?
ILs, interferons, growth factors, TNF, chemokines.
321
TNF source?
Macrophages and T-cells.
322
DiGeorge syndrome defect?
No thymus → no T cells.
323
Agammaglobulinemia defect?
No B cells.
324
SCID defect?
No B or T cells.
325
Autoimmune diseases from the slides?
SLE, MS, MG, Hashimoto’s, Grave’s, Addison’s, Type I DM.
326
Cyclosporine mechanism?
Inhibits calcineurin → ↓T-cell activation.
327
Cyclosporine toxicities?
Nephrotoxicity, HTN, hyperglycemia, seizures.
328
Tacrolimus mechanism?
Same pathway, macrolide structure.
329
Azathioprine mechanism?
Interferes with purine synthesis → suppresses B/T proliferation.
330
Azathioprine side effect?
Leukocytopenia (bone marrow suppression).
331
Cyclophosphamide use?
Autoimmune disorders, cancer.
332
Anti-CD3 antibody?
Muromonab.
333
Anti-TNF antibody?
Adalimumab.
334
Requirement for drug approval?
Must be “safe and effective.”
335
A dietary supplement must contain what?
Vitamins, minerals, herbs, botanicals, amino acids.
336
Supplements cannot legally claim what?
Disease treatment or prevention.
337
Three permitted claim types?
Nutrient content, structure/function, health.
338
Examples of questionable/ineffective supplements?
Milk thistle, saw palmetto; ineffective: colloidal silver, oleandrin.
339
Monoclonal antibody used for Rh-negative mothers?
RhoGAM.
340
Strong opioid agonist with phenylpiperidine structure?
Fentanyl.
pharm dr T
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