Chapter 42: Substance Use Disorders III: Nicotine

Welcome to Last Minute Lecture.

This free chapter overview is designed to help students review and understand key concepts.

These summaries supplement not replaced the original textbook and may not be redistributed or resold.

For complete coverage, always consult the official text.

Here are the key conventions to employ.

Disfluencies.

Fillers.

Use words like um uh you know i mean like actually and write naturally to pad sentences example it's uh it's actually really common to see that you know in the er false starts and self -corrections people often sort of thought pause and rephrase it mid -sentence example if they take if they swallow the pill too fast it causes nausea back channeling and active listening listeners rarely stay completely silent they interject with brief acknowledgments to show they are following along example expert speaker the blood pressure spikes almost instantly host speaker wow okay expert speaker and that constant strain causes long -term damage overlapping and interrupting in enthusiastic or fast -paced conversations seekers often finish each other's sentences or jump in before the other person has fully stopped speaking use m dashes to show sudden cut -offs or interruptions never use ellipses example host speaker so you're saying the heart has to work expert speaker work twice exactly it's running a marathon colloquialisms and informal phrasing use contractions aggressively there it's gonna wanna and conversational phrasing rather than textbook english example you're basically looking at a totally wrecked system instead of one observes a severely compromised system short turns break up long explanations if one person is explaining a complex mechanism the other should interject to clarify agree or ask a follow -up question every sentences short terms national notes usually um when you look at a medical issue there's this expectation of precision you know like engineering right like a broken arm or something exactly you break your arm the x -ray shows that jagged white line and the doctor just points and says there it is yeah it's right there in black and white but you step into the world of substance use disorders specifically nicotine dependence and suddenly that x -ray machine is totally useless completely useless you're dealing with an invisible systemic takeover and it's one that kills what one out of every five people in the u .s.

yeah four hundred and eighty thousand adults every single year i mean it doesn't leave a clean fracture on a scan but it strips 13 to 14 years off a patient's life wow 13 years and it drains 170 billion dollars in direct medical costs annually so welcome to this special last minute lecture edition of the deep dive right and our mission today is to completely unpack chapter 42 of lenz pharmacology for nursing care we're translating all that dense drug data into actionable bedside nursing knowledge for you because um while traditional adult cigarette smoking might have dipped slightly to around 13 .7 percent a few years back we're facing a massive new physiological challenge on the floor the vaping explosion i mean we are seeing middle schoolers like 18 percent of those who use e -cigarettes vaping 20 or more days a month it's staggering this isn't just an adult chronic illness problem anymore it is an acute pediatric and young adult crisis so if you're a nursing student getting ready for pharmacology exams or clinicals you need to map out exactly what nicotine is doing the moment it enters the body let's start with the basic pharmacology here because nicotine has a really bizarre dose dependent paradox right because most drugs have a linear relationship right more drug equals a stronger version of the same effect exactly but nicotine acts on nicotinic receptors differently depending on the volume low doses like the amount you get from taking a drag off a standard cigarette they actually activate those receptors but if you blast the system with incredibly high toxic doses it does the exact opposite it blocks them entirely that blockade is what makes acute toxicity so which we'll get into when we cover acute poisoning but in the day -to -day life of a typical smoker they're perpetually in that low dose activation state and the delivery system is just optimized for terrifying speed when nicotine from cigarette smoke is absorbed in the lungs it travels to the brain in just 10 seconds 10 seconds that's faster than iv delivery in some cases oh yeah it's a pharmacological bullet train it completely bypasses the liver's first pass metabolism and the body's normal defensive checkpoints but the catch is it's half -life right it's incredibly short super short only one to two hours before the liver metabolizes it into inactive products and it gets excreted by the kidneys so if i'm a nursing student looking at this pharmacokinetic profile i'm just seeing a relentless behavioral loop precisely the drug hits the brain almost instantly but it leaves just as fast so the patient is basically forced to dose themselves continuously throughout the day just to avoid crashing into withdrawal and we really need to look at what that continuous dosing does to the major organ systems the cardiovascular system has to take the absolute brunt of it right it does because nicotine throws the body into sympathetic overdrive it activates nicotinic receptors in the sympathetic ganglia and the adrenal medulla okay so that triggers a massive systemic release of norepinephrine from the sympathetic nerves yeah and epinephrine from the adrenals to classic fight or flight flood so physiologically we are looking at instant vasoconstriction the blood vessel is just rapidly narrow and at the exact same time the heart rate accelerates and the force of ventricular contractions increases so the heart is suddenly forced to pump significantly harder to push blood through a highly constricted vascular system it's like a plumbing system where you're completely maxing out the water pressure while simultaneously pinching the hoses closed that sounds exhausting so that constant daily mechanical strain is the underlying mechanism for those staggering cardiovascular mortality rates you mentioned absolutely and here is a critical nursing assessment point patients do not build a tolerance to this specific effect wait i want to pause on that because that goes against common intuition you always hear about smokers building tolerance right like a teenager smoking their first cigarette gets dizzy pale nauseous yeah but a veteran chain smoker doesn't feel any of that true but they only build tolerance to the central nervous system side effects the nausea the dizziness oh wow so tolerance structurally fails to develop in the cardiovascular system it never develops yeah even after 30 years of smoking every single time that patient lights a cigarette their blood vessels constrict their blood pressure spikes and their cardiac workload increases just as severely as it did on day one that is wild the receptors driving that sympathetic release just do not down regulate the way others do nope so the wear and tear is totally relentless that completely changes how you view a chronic smoker on the floor their heart is essentially running a marathon every time they take a smoke break and it's not just the sympathetic side either nicotine is also firing up the parasympathetic ganglia specifically in the gastrointestinal tract which increases gastric acid secretion and ramps up the tone and motility of gi smooth muscle yeah it also triggers vomiting by directly hitting receptors in the aortic arch the carotid sinus and the central nervous system which brings us to the central nervous system effects this is what chemically locks the patient into the habit right because nicotine is a cns stimulant it increases alertness facilitates memory improves cognition and suppresses appetite but the biological anchor of the dependency sits deep in the mesolimbic area of the brain right yes nicotine promotes the release of dopamine in this specific pleasure circuit it's hijacking the exact same reward system as cocaine amphetamines and opioids exactly it's not just a bad habit it is a fundamental recalibration of the brain's dopamine thermostat so the smoker isn't chasing a high their biological baseline has been moved so far that they need the nicotine just to feel what a non -smoker considers normal you nailed it and when you understand how deeply nicotine integrates into the bloodstream to reach the brain its devastating impact on fetal development makes a lot more sense let's talk about that smoking is the largest modifiable risk factor for pregnancy related morbidity ectopic pregnancy placental abruption preterm birth sudden infant death syndrome those risks just skyrocket and the reproductive toxicity stems from three distinct culprits in tobacco smoke right not just the nicotine alone right let's map out the mechanisms for those three because it's rarely just the drug acting alone first you have the nicotine itself which as we established causes systemic vasoconstriction so for a fetus entirely dependent on maternal blood flow through the placenta narrowed vessels mean severely reduced perfusion it starves them plus nicotine also carries direct neurotoxic effects that delay fetal brain development and stunt the maturation of pulmonary cells okay so that's culprit one what's the second carbon monoxide it binds the hemoglobin with a much higher affinity than oxygen does so it physically evicts oxygen from both the maternal and fetal red blood cells it's literally suffocating the developing tissues yeah and at high levels it is intensely neuro -toradogenic finally you have the oxidizing agents in the combustible smoke i imagine those are causing severe endothelial damage to the blood vessels they do they increase the risk for thrombotic events blood clots and they decrease the availability of nitric oxide and nitric oxide is a crucial smooth muscle relaxant so without enough of it you get even more placental vasoconstriction which starves the fetus even further and can easily trigger preterm labor so you have constricted vessels blood totally starved of oxygen and a high risk of clotting it's a triple threat it really is which brings up a massive clinical decision point for a nurse let's say you have a pregnant patient who is severely addicted quitting cold turkey is failing do we put them on nicotine replacement therapy like a patch or gum it feels totally counterintuitive right to give a pregnant woman a drug we just said causes fetal vasoconstriction and neurotoxicity exactly what do the guidelines say the american college of obstetrics and gynecology provides a clear risk benefit framework the absolute first line is intensive psychosocial intervention but if behavioral interventions fail then nrt is considered much safer than continuing to smoke yes you are still exposing the fetus to nicotine but you are entirely eliminating the carbon monoxide and the oxidizing agents you're removing thousands of combustible chemicals it's purely harm reduction at that point right and practically speaking pregnancy actually increases the metabolic clearance of nicotine so standard nrt doses might actually be too low for some pregnant patients that's a great clinical pearl what about the non -nicotine medications like gopropion is an option if behavioral methods fail primarily because it entirely lacks nicotine's adverse cardiovascular effect but there's a catch right there is but propion works partly by suppressing appetite for a pregnant patient who needs to maintain a healthy caloric intake for fetal growth appetite suppression is a significant clinical drawback that makes total sense all right let's pivot from chronic maternal exposure to immediate life -threatening acute toxicity i found this absolutely terrifying the chapter the fatal dose of nicotine is roughly 40 milligrams just 40 milligrams that is a minuscule amount of liquid we see this acutely when toddlers accidentally ingest tobacco products or agricultural workers mishandle nicotine containing insecticides and increasingly with highly concentrated e -liquids from vaping the clinical presentation of acute poisoning is violent and rapid very the patient will present with profound nausea heavy salivation vomiting diarrhea and cold sweats they might experience disturbed vision and hearing and their pulse will be rapid but very weak and the terminal event is respiratory paralysis let's explain exactly why that happens going back to that dose -dependent paradox we talked about earlier right low doses activate nicotinic receptors but massive toxic doses cause a depolarizing blockade it slugs the nicotinic receptors at neuromuscular junctions specifically the diaphragm and the intercostal muscles used for breathing the receptors chemically lock up so the brain is screaming at the lungs to breathe but the electrical signal cannot cross the junction the respiratory muscles are completely paralyzed and as a nurse your intervention window is incredibly tight because there is no pharmacological antidote for nicotine poisoning no reversal agent none your priority is stopping absorption by administering activated charcoal which binds to the nicotine in the gi tract so it can't enter the blood and more importantly because the respiratory muscles are paralyzed you must initiate mechanical ventilatory support immediately the silver lining of that short one to two hour half -life is that if you can keep the patient oxygenated on a ventilator the liver will metabolize the drug the blockade will lift and they can recover within hours exactly which brings to the elephant in the room regarding concentrated liquid nicotine vaping yeah let's dive into box 42 .1 back in 2006 e -cigarettes were heavily marketed as the safe alternative harmless water vapor but the pharmacology tells a very different story largely because of the intense chemistry involved in heating these liquids the base of most e -liquids is propylene glycol or vegetable glycerin pg and vg now these are used in food and cosmetics and they're labeled generally recognized as safe by the fda for oral ingestion but the delicate tissues of the lungs are not the stomach when you take pg and vg and run them through a superheated metal coil you fundamentally alter their molecular structure through thermal degradation yeah you aren't just boiling them into a vapor you are breaking their chemical bonds that harmless vegetable glycerin degrades into entirely new highly toxic carbonyl compounds it creates acryline which causes severe mucosal and formaldehyde which is a potent known carcinogen the heat essentially cooks safe food additives into lung poison furthermore these liquids contain hidden flavoring chemicals right like diacetyl diacetyl is safe to eat as artificial butter flavor in microwave popcorn but inhaling it vaporized causes bronchiolitis obliterans commonly known as popcorn lung it creates irreversible fibrous scarring in the tiny airways of the lungs add to that the heavy metals tin nickel lid leaching off the cheap heating coils directly into the aerosol and all of this chemistry culminated in a massive public health crisis by early 2020 evaly e -cigarette or vaping use associated lung injury we saw over 2800 hospitalizations and 68 deaths mostly young people between 25 and 34 years old evaly presents aggressively it looks like severe pneumonia with profound damage to the alveoli the clinical investigation found a strong link 82 percent of evaly patients had vaped products containing thc and the main chemical culprit identified was vitamin e acetate yeah it's being used as a cheap liquid thickening agent in black market thc cartridges and inhaling vaporized oil like vitamin e acetate poats the inside of the lungs it completely prevents gas exchange and triggers a massive destructive inflammatory immune response if i'm icu nurse looking at an evaly patient i know standard asthma bronchial dilators aren't going to fix oil -coated physically scarred alveoli we are looking at purely supportive care high dose corticosteroids to try and shut down the immune inflammation and antibiotics if secondary bacterial pneumonia sets in with all this physiological devastation from chronic cardiovascular wear and tear to acute lung scarring the most critical role a nurse plays is managing the exit strategy quitting cold turkey has an abysmal success rate only four to seven percent of people stay abstinent long term but if you combine structured counseling with specific pharmacological tools that success rate jumps to 25 percent the nursing framework for this is the five a's model ask all patients about tobacco use advise them to quit assess their willingness to try assist with medications and counseling and arrange follow -up contacts within the first week we need to be experts in that assist phase let's map out the medication toolkit starting with over -the -counter nicotine replacement therapy the gum and the lozenges the pharmacology of the gum like nicorette involves nicotine bound to an ion exchange resin called palack relax the nicotine is absorbed directly across the oral mucosa but the dosing requires a specific clinical assessment we call the 30 -minute rule which gauges the physical severity of the dependence i love this because it translates a complex addiction into a very practical question you ask the patient when do you smoke your first cigarette of the day if it's within 30 minutes of waking up their brains dopamine receptors are screaming for a baseline meaning they are highly dependent so they get the higher four milligram dose if they can comfortably wait longer than 30 minutes they start with the two milligram dose patient education here is paramount if a patient choose nicotine gum rapidly like a piece of regular bubble gum they will chemically dump the entire dose of nicotine into their saliva at once the oral mucosa can't absorb it that fast so they swallow it it hits the stomach causing intense nausea hiccups and throat irritation you have to teach them the chew and park method chew it slowly to release a little peppery taste then park it between the cheek and gum to let it absorb across the membrane then repeat for about 30 minutes and no coffee juice or acidic drinks for 15 minutes before or during because altering the ph of the mouth blocks the mucosal absorption the lozenge works on the exact same mucosal principle don't chew it don't swallow it just let it dissolve over 20 to 30 minutes what about patients who want a steady baseline without the act of chewing for them we use transdermal patches the nicotine slowly seeps through the skin into the bloodstream but nurses must understand the difference in product design some patches like nicoderm cq are designed for 24 -hour continuous wear others like nicorette patches are applied in the morning and taken off 16 hours later at bedtime simulating the actual waking cycle of a smoker so they aren't getting flooded with nicotine while they sleep exactly a major adverse effect of the 24 -hour patches is vivid sometimes deeply unpleasant dreams caused by nocturnal central nervous system stimulation if a patient complains of sleep disturbances the nursing intervention is simple have them switch to a 16 -hour patch or just instruct them to take the 24 -hour patch off before going to bed also localized skin irritation is very common so they must rotate the application site daily and avoid reusing the same spot for at least a week what if the patient is struggling specifically with the physical habit of smoking the ingrained hand -to -mouth muscle memory that's where the

puffing draws air over a nicotine plug and the vapor is absorbed in the mouth not the lungs it even contains menthol to simulate that harsh familiar throat hit but since drawing on it can cause mild bronchospasm and coughing it's generally contraindicated for patients with severe asthma the other prescription option is the nicotine nasal spray this is pharmacokinetically fascinating the nasal mucosa is highly vascularized so the blood levels of nicotine rise almost instantly closely mimicking the rapid massive peak of smoking a real cigarette it provides a fraction of that subjective pleasure which is why it boasts a very high abstinence rate about 27 at one year but there is a serious clinical trap there because the kinetic curve is so fast and spiky much like combustible tobacco patients frequently become dependent on the nasal spray itself they just trade one rapid delivery addiction for another plus the initial side

severe rhinitis coughing sneezing and watering eyes it is strictly off limits for anyone with sinus issues or allergies that leaves us with our primary non -nicotine option but propion er an atypical antidepressant also prescribed under the brand name wellbutrin we know it blocks the reuptake of norepinephrine and dopamine in the brain by inhibiting that reuptake it acts like a dam keeping those neurotransmitters artificially elevated and active in the synapses this reduces the biochemical urge to smoke and blunts withdrawal symptoms like anxiety and irritability now let's put our vigilant nursing hats on i'm looking at a chart and the provider just ordered the propion er for a patient trying to quit smoking what are my absolute red flags because bupropion has a known mechanism of lowering the seizure threshold meaning a seizure is much more easily triggered it is strictly contraindicated for anyone with a history of seizures previous head trauma too an anorexia nervosa which alters electrolytes and seizure risks or patients currently undergoing alcohol withdrawal you also have to heavily scrutinize their current medication list it cannot be combined with a monoamine oxidase inhibitor and maoi and you must verify they aren't already taking wellbutrin for depression it is the exact same chemical and doubling the dose could easily breach that seizure threshold expect to monitor for dry mouth insomnia and loss due to appetite suppression so stepping back and looking at the whole picture nicotine is a master manipulator it recalibrates the dopamine reward pathway forces the cardiovascular system to run a marathon every time a cigarette is lit and relentlessly crosses placental barriers to stunt fetal growth but you are not powerless against it by deeply understanding the pharmacokinetics the receptor dynamics and the specific contraindications of the cessation tools you can actively manage withdrawal and choose the safest most effective intervention you are interrupting a fatal physiological cycle but as we reflect on this consider how rapidly nicotine delivery has evolved we went from combustible leaves to highly concentrated synthetic e -liquids causing entirely new pathologies like evil eye it makes you wonder how will pharmacology and your specific nursing interventions have to adapt in the next decade to treat the next generation synthetic nicotine dependence it's a huge challenge but that is the kind of critical thinking that takes you from passing a test to saving a life nicotine dependence is a murky systemic web but with the pharmacological tools we've mapped out today you have the light to navigate through that fog and guide your patients out on behalf of the entire last minute lecture team thank you so much for joining us we wish you the absolute best of luck on your upcoming pharmacology exams and out there on your clinical rotations you've got this