Drug interactions and adverse effects

Drug interactions and adverse effects US Medical PG Question 1: A student is reviewing the various effects that can be plotted on a dose-response curve. He has observed that certain drugs can work as an agonist and an antagonist at a particular site. He has plotted a particular graph (as shown below) and is checking for other responses that can be measured on the same graph. He learned that drug B is less potent than drug A. Drug B also reduces the potency of drug A when combined in the same solution; however, if additional drug A is added to the solution, the maximal efficacy (Emax) of drug A increases. He wishes to plot another curve for drug C. He learns that drug C works on the same molecules as drugs A and B, but drug C reduces the maximal efficacy (Emax) of drug A significantly when combined with drug A. Which of the following best describes drug C?

• A. Reversible antagonist
• B. Competitive antagonist
• C. Full agonist
• D. Inverse agonist
• E. Non-competitive antagonist (Correct Answer)

Drug interactions and adverse effects Explanation: ***Non-competitive antagonist*** - A non-competitive antagonist **reduces the maximal efficacy (Emax)** of an agonist, even at high agonist concentrations. This is because it binds to a site other than the active site or binds irreversibly to the active site, preventing the agonist from producing its full effect. - Unlike competitive antagonists, its effects cannot be overcome by simply increasing the concentration of the agonist. *Reversible antagonist* - This is a broad category; while some non-competitive antagonists can be reversible, the key characteristic for drug C is its impact on **maximal efficacy (Emax)**, which points more specifically to non-competitive antagonism. - A reversible antagonist's effect can be overcome by increasing the agonist concentration, which is not the defining feature described for drug C. *Competitive antagonist* - A competitive antagonist **reduces the potency** (shifts the dose-response curve to the right, meaning a higher concentration of agonist is needed for the same effect) but **does not reduce the maximal efficacy (Emax)** of an agonist. - Its effects can be fully overcome by adding more agonist, allowing the agonist to reach its original Emax. *Full agonist* - A full agonist **binds to a receptor and produces the maximal possible effect (Emax)**. - This drug C is described as reducing the Emax of drug A, which is the opposite effect of an agonist. *Inverse agonist* - An inverse agonist **binds to a receptor and produces an effect opposite to that of a full agonist**, by stabilizing the receptor in an inactive conformation. - While it modulates receptor activity, its primary action is not described as reducing the Emax of another agonist in the manner of an antagonist.

Drug interactions and adverse effects US Medical PG Question 2: A 61-year-old man with a history of type 1 diabetes mellitus and depression is brought to the emergency department because of increasing confusion and fever over the past 14 hours. Four days ago, he was prescribed metoclopramide by his physician for the treatment of diabetic gastroparesis. His other medications include insulin and paroxetine. His temperature is 39.9°C (103.8°F), pulse is 118/min, and blood pressure is 165/95 mm Hg. Physical examination shows profuse diaphoresis and flushed skin. There is generalized muscle rigidity and decreased deep tendon reflexes. His serum creatine kinase is 1250 U/L. Which of the following drugs is most likely to also cause this patient's current condition?

• A. Fluphenazine (Correct Answer)
• B. Tranylcypromine
• C. Desflurane
• D. Methamphetamine
• E. Nortriptyline

Drug interactions and adverse effects Explanation: **Fluphenazine** - The patient's symptoms (fever, confusion, muscle rigidity, elevated CK, autonomic instability like tachycardia and hypertension) after starting metoclopramide are highly suggestive of **neuroleptic malignant syndrome (NMS)**. Metoclopramide is a **D2 receptor antagonist** that can precipitate NMS. Fluphenazine is a **typical antipsychotic** that also blocks D2 receptors and is a classic cause of NMS. - The combination of **D2 receptor blockade** (by metoclopramide) and another potent D2 blocker like fluphenazine would significantly increase the risk of NMS. *Tranylcypromine* - This drug is a **monoamine oxidase inhibitor (MAOI)**. While it can cause **serotonin syndrome** when combined with serotonergic drugs like paroxetine, the clinical picture of NMS (marked rigidity, very high fever, elevated CK) is distinct from typical serotonin syndrome. - Serotonin syndrome typically involves **hyperreflexia** and **clonus**, whereas this patient presents with **decreased deep tendon reflexes** and generalized **muscle rigidity**, key features of NMS. *Desflurane* - Desflurane is an **inhaled anesthetic** that can trigger **malignant hyperthermia** in susceptible individuals. Malignant hyperthermia shares some features with NMS (hyperthermia, muscle rigidity) but is specifically triggered by inhaled anesthetics and succinylcholine, not D2 antagonists. - Malignant hyperthermia presents acutely during or immediately after anesthesia exposure, which is not consistent with the patient's presentation following metoclopramide initiation. *Methamphetamine* - Methamphetamine is a **stimulant** that can cause hyperthermia, tachycardia, and agitation. However, it does not typically cause the profound **muscle rigidity** and significantly elevated **creatine kinase** characteristic of NMS. - The mechanism of action for methamphetamine is primarily related to increased release of dopamine, norepinephrine, and serotonin, not D2 receptor blockade leading to NMS. *Nortriptyline* - Nortriptyline is a **tricyclic antidepressant (TCA)**. While TCAs can have anticholinergic effects and cause some autonomic instability, they are not typically associated with NMS or malignant hyperthermia. - Long-term use of TCAs can occasionally contribute to **serotonin syndrome** when combined with other serotonergic agents, but NMS is not a direct result.

Drug interactions and adverse effects US Medical PG Question 3: A 76-year-old man comes to the physician for a follow-up examination. One week ago, he was prescribed azithromycin for acute bacterial sinusitis. He has a history of atrial fibrillation treated with warfarin and metoprolol. Physical examination shows no abnormalities. Compared to one month ago, laboratory studies show a mild increase in INR. Which of the following best explains this patient's laboratory finding?

• A. Drug-induced hepatotoxicity
• B. Depletion of intestinal flora
• C. Inhibition of cytochrome p450 (Correct Answer)
• D. Increased gastrointestinal absorption of warfarin
• E. Increased non-protein bound warfarin fraction

Drug interactions and adverse effects Explanation: ***Inhibition of cytochrome p450*** - **Azithromycin**, while a weaker inhibitor compared to erythromycin and clarithromycin, **does inhibit CYP3A4 and other cytochrome P450 enzymes** to a clinically significant degree. - This inhibition **reduces warfarin metabolism**, leading to increased warfarin levels and **enhanced anticoagulant effect**, manifesting as an **increased INR**. - This pharmacokinetic interaction is well-documented and is the **primary mechanism** for azithromycin-warfarin interaction. *Depletion of intestinal flora* - The theory that antibiotics deplete **vitamin K-producing gut bacteria** leading to increased warfarin effect is a **common misconception**. - Humans obtain vitamin K primarily from **dietary sources** (leafy greens, vegetable oils), not from gut bacterial synthesis; intestinal bacteria contribute minimally to vitamin K stores. - This mechanism has been **debunked** in modern pharmacology literature and does not explain antibiotic-warfarin interactions. *Drug-induced hepatotoxicity* - While hepatotoxicity can impair **clotting factor synthesis** and increase INR, **azithromycin** rarely causes significant liver injury. - The presentation shows only a **mild INR increase** one week after starting therapy, without other signs of liver dysfunction. - This acute, mild change is more consistent with a **pharmacokinetic drug interaction** than hepatotoxicity. *Increased gastrointestinal absorption of warfarin* - **Warfarin** has high oral bioavailability (~100%) under normal conditions. - **Azithromycin** does not enhance the **gastrointestinal absorption** of warfarin. - This mechanism is not supported by pharmacological evidence for this drug interaction. *Increased non-protein bound warfarin fraction* - Displacement of warfarin from **plasma protein binding sites** can transiently increase free drug. - However, **azithromycin** does not significantly displace warfarin from **albumin**. - This mechanism does not explain the sustained INR elevation seen with azithromycin therapy.

Drug interactions and adverse effects US Medical PG Question 4: After being warned by the locals not to consume the freshwater, a group of American backpackers set off on a week-long hike into a region of the Ecuadorean Amazon forest known for large gold mines. The group of hikers stopped near a small stream and used the water they filtered from the stream to make dinner. Within the next half hour, the hikers began to experience headaches, vertigo, visual disturbances, confusion, tachycardia, and altered levels of consciousness. Which of the following enzymes was most likely inhibited in this group of hikers?

• A. NADH dehydrogenase
• B. ATP synthase
• C. Cytochrome c oxidase (Correct Answer)
• D. Cytochrome bc1 complex
• E. Succinate dehydrogenase

Drug interactions and adverse effects Explanation: ***Cytochrome c oxidase*** - The symptoms described (headaches, vertigo, visual disturbances, confusion, tachycardia, altered consciousness occurring within 30 minutes) are characteristic of **acute cyanide poisoning**. - **Cyanide** is commonly found in water near **gold mining operations**, where it is used in the gold extraction process and can contaminate local water sources. - **Cyanide** is a potent inhibitor of **cytochrome c oxidase** (Complex IV) in the electron transport chain, binding to the heme iron (Fe³⁺) and preventing oxygen utilization, leading to **histotoxic hypoxia**. - This results in cellular energy failure, particularly affecting high-energy-demand organs like the brain and heart, explaining the acute neurological and cardiovascular symptoms. *NADH dehydrogenase* - While NADH dehydrogenase (Complex I) is a component of the electron transport chain, it is not the primary target of **cyanide poisoning**. - Inhibitors of Complex I include rotenone and barbiturates, which cause different clinical presentations and do not produce the rapid onset of symptoms seen with cyanide. *ATP synthase* - **ATP synthase** (Complex V) synthesizes ATP using the proton gradient, but it is not directly inhibited by **cyanide**. - Inhibitors of ATP synthase, such as oligomycin, prevent ATP synthesis by blocking the enzyme directly, whereas cyanide acts upstream at Complex IV. *Cytochrome bc1 complex* - The **cytochrome bc1 complex** (Complex III) is involved in electron transfer and proton pumping, but it is not the primary enzyme inhibited by **cyanide**. - Inhibitors of Complex III include antimycin A, which would disrupt the electron transport chain but do not cause the characteristic rapid-onset symptoms of cyanide poisoning. *Succinate dehydrogenase* - **Succinate dehydrogenase** (Complex II) participates in both the citric acid cycle and the electron transport chain, but it is not targeted by **cyanide**. - Inhibitors of Complex II, such as malonate, competitively block succinate oxidation but do not produce the acute systemic toxicity characteristic of cyanide poisoning.

Drug interactions and adverse effects US Medical PG Question 5: A medical student is reviewing dose-response curves of various experimental drugs. She is specifically interested in the different factors that cause the curve to shift in different directions. From her study, she plots the following graph (see image). She marks the blue curve for drug A, which acts optimally on a receptor. After drawing the second (green) curve for drug B, she discovers that more of drug B is required to produce the same response as drug A, although drug B can still achieve the same maximum effect. Which of the following terms best describes the activity of drug B in comparison to drug A?

• A. Decreased efficacy
• B. Increased affinity
• C. Higher potency
• D. Higher efficacy
• E. Lower potency (Correct Answer)

Drug interactions and adverse effects Explanation: ***Lower potency*** - **Potency** refers to the amount of drug required to produce a given effect; if more of drug B is needed for the same response as drug A, it has lower potency. - On a dose-response curve, **lower potency** is indicated by a rightward shift of the curve, meaning a higher dose is required to achieve any given effect. *Decreased efficacy* - **Efficacy** is the maximum effect a drug can produce, regardless of the dose. - While drug B has a lower ability to produce a reaction (implying lower efficacy), the statement "more of the second drug B is required to produce the same response as the first one" specifically points to potency, not just the maximal effect. *Increased affinity* - **Affinity** describes how strongly a drug binds to its receptor. - Increased affinity would generally lead to greater potency (less drug needed for an effect), which contradicts the scenario where more drug B is required. *Higher potency* - **Higher potency** would mean that less of drug B is required to produce the same effect as drug A, which is the opposite of what is described in the question. - A drug with higher potency would cause the dose-response curve to shift to the left. *Higher efficacy* - **Higher efficacy** would mean drug B could produce a greater maximal effect than drug A, but the question states drug B has a "lower ability to produce a reaction" compared to drug A. - The peak of the dose-response curve for drug B would be higher than drug A, which is not suggested by the description.

Drug interactions and adverse effects US Medical PG Question 6: You are currently employed as a clinical researcher working on clinical trials of a new drug to be used for the treatment of Parkinson's disease. Currently, you have already determined the safe clinical dose of the drug in a healthy patient. You are in the phase of drug development where the drug is studied in patients with the target disease to determine its efficacy. Which of the following phases is this new drug currently in?

• A. Phase 4
• B. Phase 1
• C. Phase 2 (Correct Answer)
• D. Phase 0
• E. Phase 3

Drug interactions and adverse effects Explanation: ***Phase 2*** - **Phase 2 trials** involve studying the drug in patients with the target disease to assess its **efficacy** and further evaluate safety, typically involving a few hundred patients. - The question describes a stage after safe dosing in healthy patients (Phase 1) and before large-scale efficacy confirmation (Phase 3), focusing on efficacy in the target population. *Phase 4* - **Phase 4 trials** occur **after a drug has been approved** and marketed, monitoring long-term effects, optimal use, and rare side effects in a diverse patient population. - This phase is conducted post-market approval, whereas the question describes a drug still in development prior to approval. *Phase 1* - **Phase 1 trials** primarily focus on determining the **safety and dosage** of a new drug in a **small group of healthy volunteers** (or sometimes patients with advanced disease if the drug is highly toxic). - The question states that the safe clinical dose in a healthy patient has already been determined, indicating that Phase 1 has been completed. *Phase 0* - **Phase 0 trials** are exploratory, very early-stage studies designed to confirm that the drug reaches the target and acts as intended, typically involving a very small number of doses and participants. - These trials are conducted much earlier in the development process, preceding the determination of safe clinical doses and large-scale efficacy studies. *Phase 3* - **Phase 3 trials** are large-scale studies involving hundreds to thousands of patients to confirm **efficacy**, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug to be used safely. - While Phase 3 does assess efficacy, it follows Phase 2 and is typically conducted on a much larger scale before submitting for regulatory approval.

Drug interactions and adverse effects US Medical PG Question 7: A researcher is currently working on developing new cholinergic receptor agonist drugs. He has formulated 2 new drugs: drug A, which is a selective muscarinic receptor agonist and has equal affinity for M1, M2, M3, M4, and M5 muscarinic receptors, and drug B, which is a selective nicotinic receptor agonist and has equal affinity for NN and NM receptors. The chemical structure and mechanisms of action of both drugs mimic acetylcholine. However, drug A does not have any nicotinic receptor activity and drug B does not have any muscarinic receptor activity. Which of the following statements is most likely correct regarding these new drugs?

• A. Drug B may produce some of its effects by activating the IP3-DAG (inositol triphosphate-diacylglycerol) cascade
• B. Drug B acts by stimulating a receptor which is composed of 5 subunits (Correct Answer)
• C. Drug A acts by causing conformational changes in ligand-gated ion channels
• D. Drug A acts on receptors located at the neuromuscular junctions of skeletal muscle
• E. Drug A acts by stimulating a receptor which is composed of 6 segments

Drug interactions and adverse effects Explanation: ***Drug B acts by stimulating a receptor which is composed of 5 subunits*** - **Nicotinic acetylcholine receptors (nAChRs)**, which drug B agonizes, are **ligand-gated ion channels** composed of five subunits surrounding a central pore. - This pentameric structure is characteristic of all nAChRs, whether neuronal (NN) or muscle (NM) type. *Drug B may produce some of its effects by activating the IP3-DAG (inositol triphosphate-diacylglycerol) cascade* - The **IP3-DAG cascade** is a signal transduction pathway primarily associated with **G protein-coupled receptors**, specifically **M1, M3, and M5 muscarinic receptors**. - Drug B is a selective **nicotinic receptor agonist**, and nicotinic receptors are **ion channels**, not GPCRs that activate IP3-DAG. *Drug A acts by causing conformational changes in ligand-gated ion channels* - Drug A is a selective **muscarinic receptor agonist**. Muscarinic receptors are **G protein-coupled receptors (GPCRs)**, not ligand-gated ion channels. - Activation of GPCRs leads to intracellular signaling cascades, such as the **IP3-DAG or cAMP pathways**, rather than direct ion flow through a channel. *Drug A acts on receptors located at the neuromuscular junctions of skeletal muscle* - The **neuromuscular junction (NMJ)** contains **nicotinic (NM) receptors**, which mediate muscle contraction. Drug A is a selective **muscarinic receptor agonist**. - Therefore, drug A would **not act at the NMJ** to produce its effects. *Drug A acts by stimulating a receptor which is composed of 6 segments* - This statement inaccurately describes the structure of acetylcholine receptors. While some ion channels have multiple transmembrane segments, the primary classification relevant here is between **nicotinic receptors (pentameric ligand-gated ion channels)** and **muscarinic receptors (monomeric G protein-coupled receptors with 7 transmembrane domains)**, neither of which are described as being composed of "6 segments." - **Muscarinic receptors themselves are single polypeptide chains** that weave through the membrane seven times, so they are not "composed of 6 segments."

Drug interactions and adverse effects US Medical PG Question 8: A 28-year-old male presents to his primary care physician with complaints of intermittent abdominal pain and alternating bouts of constipation and diarrhea. His medical chart is not significant for any past medical problems or prior surgeries. He is not prescribed any current medications. Which of the following questions would be the most useful next question in eliciting further history from this patient?

• A. "Does the diarrhea typically precede the constipation, or vice-versa?"
• B. "Is the diarrhea foul-smelling?"
• C. "Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life"
• D. "Are the symptoms worse in the morning or at night?"
• E. "Can you tell me more about the symptoms you have been experiencing?" (Correct Answer)

Drug interactions and adverse effects Explanation: ***Can you tell me more about the symptoms you have been experiencing?*** - This **open-ended question** encourages the patient to provide a **comprehensive narrative** of their symptoms, including details about onset, frequency, duration, alleviating/aggravating factors, and associated symptoms, which is crucial for diagnosis. - In a patient presenting with vague, intermittent symptoms like alternating constipation and diarrhea, allowing them to elaborate freely can reveal important clues that might not be captured by more targeted questions. *Does the diarrhea typically precede the constipation, or vice-versa?* - While knowing the sequence of symptoms can be helpful in understanding the **pattern of bowel dysfunction**, it is a very specific question that might overlook other important aspects of the patient's experience. - It prematurely narrows the focus without first obtaining a broad understanding of the patient's overall symptomatic picture. *Is the diarrhea foul-smelling?* - Foul-smelling diarrhea can indicate **malabsorption** or **bacterial overgrowth**, which are important to consider in some gastrointestinal conditions. - However, this is a **specific symptom inquiry** that should follow a more general exploration of the patient's symptoms, as it may not be relevant if other crucial details are missed. *Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life* - Quantifying pain intensity is useful for assessing the **severity of discomfort** and monitoring changes over time. - However, for a patient with intermittent rather than acute, severe pain, understanding the **character, location, and triggers** of the pain is often more diagnostically valuable than just a numerical rating initially. *Are the symptoms worse in the morning or at night?* - Diurnal variation can be relevant in certain conditions, such as inflammatory bowel diseases where nocturnal symptoms might be more concerning, or functional disorders whose symptoms might be stress-related. - This is another **specific question** that should come after gathering a more complete initial picture of the patient's symptoms to ensure no key information is overlooked.

Drug interactions and adverse effects US Medical PG Question 9: A 78-year-old man receives chemotherapy for advanced hepatocellular carcinoma. Despite appropriate therapy, he dies 4 months later. Histopathological examination of the cancer cells shows the presence of a transmembrane efflux pump protein that is known to cause decreased intracellular concentrations of chemotherapeutic drugs. Which of the following best describes this membrane protein?

• A. G protein
• B. Cadherin
• C. P-glycoprotein (Correct Answer)
• D. Tyrosine receptor
• E. Channel protein

Drug interactions and adverse effects Explanation: **P-glycoprotein** - **P-glycoprotein** (also known as **MDR1**) is a well-known **efflux pump** that actively transports many chemotherapy drugs out of cancer cells, leading to **multidrug resistance**. - Its presence explains the **decreased intracellular concentrations** of chemotherapy drugs and the poor response to treatment in this patient. *G protein* - **G proteins** are intracellular signaling molecules that mediate responses to various extracellular stimuli, not primarily involved in drug efflux. - They are typically associated with **G protein-coupled receptors** and downstream signaling pathways, not direct drug transport. *Cadherin* - **Cadherins** are cell adhesion molecules that play a crucial role in cell-cell binding and maintaining tissue structure. - They are not involved in the active transport of drugs across the cell membrane. *Tyrosine receptor* - **Tyrosine kinase receptors** are transmembrane proteins that bind to growth factors and initiate intracellular signaling cascades, promoting cell growth and differentiation. - They are involved in signaling, not in the active transport of chemotherapy drugs out of the cell. *Channel protein* - **Channel proteins** facilitate the passive diffusion of ions or small molecules across the cell membrane, typically down their electrochemical gradient. - While they are transmembrane proteins, they do not actively pump drugs out against a concentration gradient, which is characteristic of multidrug resistance.

Drug interactions and adverse effects US Medical PG Question 10: A 63-year-old man with high blood pressure, dyslipidemia, and diabetes presents to the clinic for routine follow-up. He has no current complaints and has been compliant with his chronic medications. His blood pressure is 132/87 mm Hg and his pulse is 75/min and regular. On physical examination, you notice that he has xanthelasmas on both of his eyelids. He currently uses a statin to lower his LDL but has not reached the LDL goal you have set for him. You would like to add an additional medication for LDL control. Of the following, which statement regarding fibrates is true?

• A. Fibrates inhibit the rate-limiting step in cholesterol synthesis
• B. Fibrates can potentiate the risk of myositis when given with statins (Correct Answer)
• C. Fibrates can cause significant skin flushing and pruritus
• D. Fibrates can increase the risk of cataracts
• E. The primary effect of fibrates is to lower LDL

Drug interactions and adverse effects Explanation: ***Fibrates can potentiate the risk of myositis when given with statins*** - **Fibrates** and **statins** can both independently cause muscle toxicity (myopathy, rhabdomyolysis). - When used concomitantly, especially **gemfibrozil** with statins, there is an **increased risk of muscle adverse events** due to pharmacokinetic interactions that raise statin levels. - This combination requires careful monitoring and is often avoided; **fenofibrate** is preferred over gemfibrozil when combination therapy is needed. *Fibrates inhibit the rate-limiting step in cholesterol synthesis* - This statement describes the mechanism of action of **statins**, which inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis. - Fibrates, on the other hand, act primarily by activating **PPAR-alpha receptors**, leading to altered lipid metabolism (increased lipoprotein lipase activity, decreased VLDL synthesis). *Fibrates can cause significant skin flushing and pruritus* - **Niacin (nicotinic acid)** is the lipid-modifying agent most commonly associated with significant **skin flushing and pruritus**, mediated by prostaglandin release. - Fibrates do not cause significant flushing; their side effects include GI disturbances, gallstones, and potential muscle toxicity. *Fibrates can increase the risk of cataracts* - This is **not an established adverse effect** of the fibrate class. - While **clofibrate** (an older, largely discontinued fibrate) showed some association with cataracts in older studies, this is not a recognized risk with modern fibrates like **fenofibrate** and **gemfibrozil**. - Current fibrate therapy does not require routine ophthalmologic monitoring for cataracts. *The primary effect of fibrates is to lower LDL* - The primary effect of **fibrates** is to significantly **lower triglycerides** (by 30-50%) and **increase HDL cholesterol** levels (by 10-20%). - While they can cause a modest decrease in LDL cholesterol (10-15%), this is not their primary or most pronounced lipid-modifying effect. - Fibrates are primarily indicated for **hypertriglyceridemia** and mixed dyslipidemia.

Drug interactions and adverse effects Flashcard 1 of 10

Question: What is the most serious adverse effect associated with antipsychotics? _____

Answer: Neuroleptic malignant syndrome (NMS)

Drug interactions and adverse effects Flashcard 2 of 10

Question: Macrolides are _____ of CYP-450

Answer: inhibitors

Drug interactions and adverse effects Flashcard 3 of 10

Question: What drug class does bivalirudin belong to? _____

Answer: Direct thrombin inhibitor

Drug interactions and adverse effects Flashcard 4 of 10

Question: Examples of the beers criteria include drugs that increase the risk of _____ infections (PPI's)

Answer: C. difficile

Drug interactions and adverse effects Flashcard 5 of 10

Question: Warfarin is _____ by cytochrome P450 and thus has many drug interactions

Answer: metabolized

Drug interactions and adverse effects Flashcard 6 of 10

Question: Phase _____ of clinical trials assesses safety, toxicity, pharmacokinetics, and pharmacodynamics

Answer: I

Drug interactions and adverse effects Flashcard 7 of 10

Question: What drug class does abciximab belong to? _____

Answer: GPIIb/IIIa inhibitor

Drug interactions and adverse effects Flashcard 8 of 10

Question: Isoniazid _____ cytochrome p450 (induces or inhibits)

Answer: inhibits

Drug interactions and adverse effects Flashcard 9 of 10

Question: thalidomide

Answer: limb defects (flipper limbs)

Drug interactions and adverse effects Flashcard 10 of 10

Question: warfarin

Answer: bone deformities, fetal hemmorhage, abortion, ophthalmologic abnormalities