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Pharmacology 2 Exam2
| Question | Answer |
|---|---|
| Describe the basic pathophysiology of Parkinson’s disease | The dopamine neurons in the extrapyramidal motor pathway are destroyed leading to too much acetylcholine and GABA stimulation-> slowed body movements, tremors, masked faces, pill rolling |
| T/F- Parknison’s is a syndrome not a disease because it it characterized by a cluster of symptoms. | True |
| What are some pharmacological treatments of Parkinson’s? | Anticholinergics- movement disorders, Dopamine agonists- increase dopamine to replace motor movements, MAOI-B and COMT inhibitors stop breakdown of dopamine when used earlier in disease |
| What is the drug Carbidopa-Levodopa (SInemet) used to treat? How does it work? | Used in Parkinsons, replaces dopamine, L converted to dopamine and C prevents L from converting until after it crosses BBB because dopamine doesn’t cross BBB. Must take high doses to work |
| What are some common and adverse reactions to Sinemet (Carbidopa-Levodopa)? | Used to treat Parkinson’s, may lead to anticholinergic effects, NV, hypotension, dizziness, dark urine. May also cause Rebound Parkinsonism, agranulocytosis, cardiac arrhythmias, and Neuroleptic Malignant Syndrome |
| You are the nurse teaching a patient about Carbidopa-Levodopa (Sinemet). What should you teach? Alcohol is ok in moderation, Take multivitamins daily, Take high protein diet, Take with meals. | Take with meals because NV is the most severe side effect because it stimulates the nausea center in brain, (Note- no alcohol, protein increases BUN which is bad) |
| T/F- Having too much OR too little Dopamine can worsen Parkinsonian symptoms | True |
| T/F- There are varied treatments for individuals presenting with psychosis so it is important to know the exact etiology (ie Schizophrenia, Depression, Intoxication, Traumatic Brain Injury, Dementia). | False, we treat people with psychotic symptoms similarly. |
| What is the Black Box Warning for antipsychotics? | Elderly Patients with Dementia-Related Psychosis who are treated with an antipsychotic have increased mortality rates. |
| What medications are used to treat schizophrenia spectrum disorders and psychoses? | |
| What are the expected effects of antipsychotics? When will the patient experience maximum relief? | Remove or significantly reduce the psychotic symptoms. Max relief after several weeks or months on medication, start to notice changes in first few doses. |
| How do traditional antipsychotics improve psychotic symptoms?- Inhibit enzymes at receptor sites, Block Post-synaptic dopamine receptor sites, Increase dopamine uptake at post-synaptic receptor sites, Decrease serotonin at post-synaptic receptor sites. | Block Post-Synaptic dopamine receptor sites which stops the positive symptoms |
| You have two patients on antipsychotics. One taking traditional antipsychotic, other is taking an atypical. You know that this patient is more likely to lead to peripheral side effects because it is nonselective and blocks ALL dopamine receptors. | Traditional |
| You have a patient with positive and negative symptoms of psychosis. You expect the order to be for a __________ antipsychotic. | Atypical, these were developed later and block some dopamine and also some serotonin which can lead to reduction of positive and negative symptoms |
| What are the 2 major categories of traditional antipsychotics? What differentiates them? | Phenothiazines- such as Thorazine and Fluphenazine block NE (leading to sedative and hypotension) Nonphenothiazines such as Haloperidol-Block Dopamine |
| Which type of traditional antipsychotic is more effective in treating psychotic symptoms, Low potency Phenothiazine, High Potency Phenothiazine or High Potency Non-Phenothiazine? | All have same efficacy, low potency meds require higher doses to be as effective. Have varied side effect profiles. |
| What is the mechanism of action of traditional antipsychotics? | Blocks the D2 receptor sites in mesolimbic pathway to stop positive symptoms, non-selective dopamine blockade can lead to other side effects such as EPSE, histamine antagonism, acetylcholine blockage, Parkinsonism, sedation, and orthostatic hypotension |
| Why do traditional antipsychotics like Haldol make patients sleepy? | Nonselectively binds to dopamine receptor sites which leads to histamine antagonism which leads to sedation |
| Extrapyramidal side effects associated with antipsychotic medications include acute dystonia. What is this? When does it develop? How to treat? | Severe muscle spasm develops within first days of medication, usually involves tongue, neck, face, back, and laryngeal muscles. Can be fatal when head/neck muscles involved. Need medical attention to reverse. Caused when too much dopamine is blocked. |
| What is antipsychotic induced Parkinsonism? When does it develop? Treatment? Symptoms? | An extrapyramidal side effect associated with too much dopamine blockage, develops within first month of taking antipsychotic, usually resolves on its own within a few months. Signs include akinesia, muscle rigidity, tremor, drooling, mask-like faces |
| Akathisia is an extrapyramidal side effect associated with antipsychotic medications. What is this? What cause it? Signs? When does it develop? Treatment? | Too much dopamine blockage can cause a profound sense of restlessness and anxiety. Develops within first 2 months. Major reason people stop taking antipsychotics. |
| Patients taking an antipsychotic should be warned about the potential for developing tardive dyskinesia. What is this? Treatment? How common is it? When does it start? | Involuntary twisting movements, begins with tongue and face and may progress to limbs and trunk. Can be IRREVERSIBLE (and often is). 15-30% of longer term users will develop it. It can happen at any time during the medication administration |
| Benztropine and Trihexyphenidyl are used to treat Parkinson’s disease and can also be used to treat parkinsonism side effects in patients taking antipsychotic medications. How do these work? | block the central cholinergic receptors (act as anticholinergic). When dopamine is suppressed (as with patients taking antipsychotics) the cholinergic effects are more pronounced (drooling, muscle spasms and movement etc… think PNS with acetylcholine) |
| Why would a patient who is taking antipsychotics also be prescribed diphenhydramine? | This histamine blocker is useful in treating extrapyramidal side effects by suppressing the central cholinergic activity and prolonging the action of dopamine by preventing its reuptake and storage |
| What are some of the signs of antipsychotic overdose? | Hypotension, CNS depression, extrapyramidal side effects, atropine psychosis, death (although it is rare) |
| What is atropine psychosis? Symptoms? | Psychotic delirium caused by excessive anticholinergic effects or by blocking too much acetylcholine, symptoms include agitation, confusion, dry flushed skin, tachycardia |
| Another adverse effect of antipsychotic medication is neuroleptic malignant syndrome. What is this caused by? Symptoms? Fatality? | Blocking too much dopamine >parasympathetic and sympathetic dysregulation. occurs within same day you take a dopamine blocker Symptoms include sudden high fever, sweating/drooling, rigidity/tremors, changes in LOC including seizures and death (10-20%) |
| T/F- Patients taking an atypical antipsychotic do not have to worry about neuroleptic malignant syndrome like patients taking a typical antipsychotic. | False, its caused by too much dopamine blockage so possible in both |
| Among the man adverse effects of antipsychotics, agranulocytosis is included. What is this? Symptoms? Fatality? | Characterized by severely decreased WBC count which puts patient at profound risk of infection and death from overwhelming infection. Suspect if develops sore throat, fever, or malaise during the first 2 months of medication initiation |
| What are some adverse effects of antipsychotics? | Hypotension, Sedation, Seizures, Arrythmias associated with sudden death, agranulocytosis, NMS, tardive dyskinesia, atropine psychosis, |
| A patient taking an antipsychotic medication may experience a variety of anticholinergic side effects including __________. Why? | Dry mouth, congestion, blurred vision, constipation, urinary retention. Antipsychotics block M-1-cholinergic receptors (although the aim is for them to only block the dopamine) |
| Do high or low potency antipsychotic medications do the following- (More anticholinergic effects, sedation and hypotension) and (less anticholinergic effects and more extrapyramidal side effects) | Low is More anticholinergic, High is less anticholinergic and more EPSEs. |
| T/F- Antipsychotic medication may cause dermatological side effects such as pruritic maculopapular rashes and short lived jaundice that usually goes away. | True! |
| A 25 year old female taking an antipsychotic tells you she hasn’t had a period in 4 months. You tell her… | Antipsychotics may cause amenorrhea but ovulation is still occurring (so you can still get pregnant). Medications that block dopamine cause amenorrhea because it regulates prolactin. It does NOT interfere with effectiveness of birth control. |
| List some common adverse effects in female clients taking antipsychotics. | Gynecomastia, Galactorrhea (inappropriate milk production r/t prolactin deregulation) Menstrual irregularities, Decreased libido, Impaired ability to achieve orgasm |
| What are some common adverse effects of antipsychotic medication specific to male clients? | Gynecomastia, decreased libido, erectile/ejaculatory dysfunction |
| T/F- Antipsychotic medications may lead to glucose dyscontrol and weight gain. | True. |
| Why are atypical antipsychotic medications good? | Treat positive and negative symptoms of schizophrenia, cause fewer extrapyramidal side effects r/t lesser dopamine affinity, lower risk of developing TD and less likely to elevate prolactin levels |
| Science assumes certain things about atypical antipsychotics and their effectiveness at treating negative symptoms. What are these? | We think negative symptoms are caused by hypodopaminergic processes in FRONTAL lobe. Selective subtypes of serotonin inhibit dopamine. Drugs that antagonize the serotonin subtypes will increase frontal lobe dopamine. |
| What is Metabolic Syndrome as associated with atypical antipsychotic use? | Insulin resistance, Hypertension, High serum lipids, Obesity, and Coagulation abnormalities. WARNING |
| Abilify or Aripiprazole is an atypical antipsychotic. It is special and different from most other antipsychotics in that it… | Is a serotonin and dopamine agonist and antagonist but is PRIMARILY a dopamine antagonist (potential for EPSE’s and parkinsoninism) and Serotonin agonist (CNS stimulation) |
| A patient is taking Clozapine (an atypical antipsychotic). Which lab value do you care about MOST? (Renal function study, Hepatic function study, WBC, Serum Clozapine levels) | WBC because agranulocytosis can lead to infection and death |
| Ziprasidone (Geodone) is known for what common adverse reaction? Clozapine is known to cause what significant adverse reactions? | Geodone- Cardiac events. Clozapine- Agranulocytosis and Seizures |
| When managing a patient with schizophrenia, how do you select a drug and doasage? How long until you see improvements? What do you monitor for? | Select based on PMH and treatments and family history. Start with divided doses, see symptom decline in 1-2 days and gradual improvement over months, Monitor for EPSEs |
| For a patient who is hospitalized and otherwise not diagnosed with any psychiatric illnesses but experiencing agitation and delirium, you expect to administer… | Haloperidol |
| T/F- Atypical antipsychotic medication come in a variety of preparations including PO, quick dissolve, and IM but never IV. | True |
| T/F- Traditional antipsychotic medications can be PO, IV, or IM including DEPOT. | True |
| Some of the traditional antipsychotics come in DEPOT preparations. What are these? Benefits? Drawbacks? | Long-acting injectable medications to treat schizophrenia, good for patients who are forgetful/noncompliant. Very expensive, IM injections every 2-4 weeks, may still require PRN medications. Cannot retrieve medication once administered. |
| There are many interactions with antipsychotic medications that a nurse should be aware of. List some. | CNS depressants. Anticholinergics. Antihypertensives (increase hypotension). Levodopa (counteract effects converted to dopamine in body). Smoking (increase metabolism antipsychotics but decrease medication induced parkinsonism) |
| How do you safely administer antipsychotics for the best outcomes while minimizing the adverse effects? | Give the lowest maintenance dose, treat the side effects, teach the patient, consider best formulation for patient, develop a therapeutic relationship |
| Whata re the expected and adverse effects of medications used to treat the neurocognitive disorder, Alzheimer’s Dementia? | |
| What neurotransmitter alterations are associated with Alzheimers type dementia? | Decreased acetylcholine leading to decreased acetyltransferase (interferes with cholinergic innervation in brain) Increased glutamate (results in overstimulation of NMDA, increased intracellular calcium, Neuron degeneration, and cellular death |
| What medication is currently being used to slow the progression of alzheimers type dementia? How does it work? Side effects? Interactions? | Rivastigmine (Exelon) is an acetylcholinesterase inhibitor that prevents the breakdown of acetylcholine. SE-NVD, dizziness, headache, cholinergic, bronchoconstriction. Interacts with traditional antipsychotics, TCAs and antihistamines |
| What is the function of the N-Methyl-D Aspartic (NMDA) antagonist Mematine (Namenda)? | used to improve symptoms of patients with alzheimers type dementia can be used alone or with the cholinesterase inhibitors. It inhibits glutamate and affects the NMDA receptors to regulate calcium. May cause dizziness, HA, confusion, and constipation |
| T/F- Estrogen increases the risk of developing Alzheimer’s type dementia. | True! |
| According to the biogenic amine theory of depression, depression is caused by… | A deficiency of monoamines (NE and Serotonin specifically) |
| According to the receptor sensitivity hypothesis of depression, depression is caused by… | Supersensitivity and up-regulation of the receptor sites on neurons. Basically, the post-synaptic neuron is trying to compensate for a lack of NE and serotonin stimulation by becoming extra sensitive. |
| What do MAOI’s do? Why are they used to treat depression? | they irreversibly block monoamine oxidase for 10-14 days, which inactivates monoamines (NE and Serotonin). So that there are increased amounts of NE and 5HT. |
| What is lag period? Why does it occur? | Time between starting a medication and experiencing full symptom relief. Believed to occur because of down regulation which reduces the stimulation at the post-synaptic site. |
| What patient education is important to deliver and understand in regards to using antidepressants? | Start at lowest dose and increase as needed, may have lag period, SE’s will usually occur within first 2 weeks. SUICIDE risk INCREASES with increasing ENERGY |
| When administering antidepressants to youth, you as the nurse know that there is a black box warning which says… | Antidepressants increase the risk of suicide in children and adolescents. Need close monitoring and observation for suicidality and manic behavior. Family needs education |
| How do tricyclic antidepressants work? | Inhibit the reuptake of norepinephrine and serotonin. Within the class, there is variation of SE profiles related to varying affinity for cholinergic, adrenergic, histamine and dopamine receptors. |
| Which of the following is NOT a common adverse effect of TCAs? (Cardiac arrhythmias, Hypotension, Hypertension, Sedation) | Hypertension |
| When educating a patient about the adverse effects of TCAs, you should include… | Hypotension, anticholinergic, sedation, diaphoresis, Cardiotoxicity, Seizures, Hypomania, Yawngasm (orgasm when yawning) |
| When educating a client aout things to avoid when taking at TCA, you include… | CNS depressants, Anticholinergics, Sympathomimetics, MAOI’s |
| You know that this class of antidepressants should NEVER be mixed with any other antidepressants or Anesthetics, Narcotics, Sympathomimetics, Cocaine, or antihyptertensives. | MAOIs |
| A client is taking a TCA. You suspect toxicity because… | Cardiac monitor reveals slowed conduction through heart and anticholinergic symptoms of agitation/confusion as well as seizures or coma. |
| T/F- Patients taking TCA’s need to have their plasma levels closely monitored. | False, focus on whether it is working and side effects, only take if worried about OD or not taking. You do need to titrate when stopping medication and have baseline ECG |
| Part of the education for a client taking an MAOI includes avoiding tyramine rich foods like aged cheese and other antidepressants. Why? | Tyramine is usually degraded by MAO, but if not degraded leads to increased BP and eventually hypertensive crisis. If you take an MAOI, you cant have a pepperoni pizza with a glass of wine or you will die of hypertensive crisis. |
| If a patient taking an MAOI calls in and reports suddenly high BP and headache or confusion, nausea, apprehension, stiff neck, fever, pallor, palpitations what do you tell them… | Take Nifedipine SL while someone calls 911 to get you to hospital, decrease BP as quickly as possible |
| When educating a client about their SSRI medication, you tell them it takes _____ to start seeing effects and __- to reach full effectiveness. | 2 weeks to notice and 4-6 weeks for full effects |
| SSRI’s like Prozac have specific pharmacokinetics that the nurse must understand for safe administration. Explain | Highly protein bound, Extensive hepatic metabolism, long half life |
| How do SSRIs work (Prozac)? How common is serotonin withdrawal? | Inhibit serotonin reuptake resulting in increase availability and intensified transmission to postsynaptic site. Serotonin withdrawal is more common with shorter half life medications. |
| When educating a client on the side effects and adverse effects of Prozac (an SSRI) you include… | Nervousness, insomnia, headache, nausea, weight change, SEXUAL DYSFUNCTION (70%), Bruxism, rashes, Risk for Hemorrhage (platelets may not coagulate properly) Hyponatremia, but many go away after first few weeks |
| What is serotonin reuptake inhibitor withdrawal? When does it occur? What does it cause? | More common when patient stops taking SSRI with shorter half life, occurs abruptly and lasts for 1-2 weeks, miserable, causes NVD, bloating, confusion, mania, flu like, agitation, depression. Treat by putting back on med |
| What is Central Serotonin syndrome? What causes it? When does it occur? | May occur within minutes up to 72 hours after starting a med that increases serotonin. Can causes mental (Restless, \/LOC, Coma), autonomic (Diaphoresis/^HR, HTN, Hyperthermia, Shock), and neuromuscular changes (Spasm, Rigidity, Tonic-Clonic seizures). |
| A patient taking an SSRI should avoid what other medications… | Antidepressants and NSAIDS and anticoagulants (increases risk of bleeding as Serotonin blockage may make platelets less effective) |
| The atypical antidepressant Effexor (Venlafaxine) does what… Side effects? | Serotonin-norepinephrine reuptake inhibitor. Does NOT block cholinergic, histaminergic, or alpha1 adrenergic receptors. May cause Headache, anorexia, insomnia, Serotonin syndrome, NMS, HTN, bleeding, mania |
| T/F- Atypical antipsychotics usually have fewer negative SEs than typical antidepressants because they are less selective. | False, they do have fewer SE’s but that’s because they are MORE selective |
| As a nurse, you know that many patients run into problems with their antidepressant treatment because… | Inadequate dosage, DC prior to full recovery, didn’t taper when DC, polypharmacy related to treatment resistance |
| When managing a client with depression, aside from antidepressants, you could expect a patient to be prescribed… | Benzodiazepines to decrease anxiety and agitation, Mood stabilizers to control labile mood, and Antipsychotics to decrease psychotic symptoms seen in severe depression |
| What are the expected functions of mood stabilizers? | Relieve labile mood symptoms in patients without bipolar. Relieve symptoms during mania/depression of BPAD, prevent recurrence of mania/depression in bipolar |
| What is the gold standard mood stabilizer? How does it work? What is it? | Lithium is an inorganic ion that alters the distribution of sodium and potassium to stabilize cell membrane, stabilizes electoral activity of neurons, and leads to decreased neuronal activity by decreasing glutamate |
| The nurse knows that a patient taking Lithium is at risk for becoming toxic if… | They become dehydrated as lithium interacts with Na and K |
| Lithium levels are dependent upon _______function. | Renal. Lithium is excreted unchanged via kidneys. Dehydration causes retention (Lithium and Na are interchangeable). When sodium is displaced, lithium takes its place and kidneys go to waste |
| What are the therapeutic plasma levels of lithium during the acute phase? During the stable phase? Toxic? | Acute- 0.8-1.4 mEq/L. Stable- 0.4-1.0 mEq/L. TOXIC >/= 1.5 |
| Teach the patient about the adverse effects of lithium. | Headache, muscle weakness, fatigue, confusion, tremor, renal toxicity, fetal effects, POLYURIA/POLYDIPSIA, do NOT breastfeed while taking Lithium, weight gain, ECG changes, decreased WBC |
| What assessments do you as the nurse expect to be ordered before starting a patient on lithium? | General health status, KIDNEY function, thyroid function, CBC, Electrolytes, Baseline ECG |
| You need to know the signs of lithium toxicity, both early and progressive as well as most common. | Early (polydipsia/polyuria, Lethargy, tremor, NVD) Progressive (Oliguria/anuria, Confusion, seizures, blurred vision, tinnitus, coma Death |
| How do you treat moderate lithium toxicity (1.5-2)? Severe? | Moderate- Hold, check levels, re-evaluate dosage. Severe- Stop med, increase excretion, renal dialysis |
| Lithium can be hard for patients to take properly due to frequent monitoring and dosing. What is common? | 300 mg TID/QID up to 1200 mg, yearly CBC, lytes, renal/thyroid function, |
| Another mood stabilizing medication is actually an anticonvulsant called Valproic acid or Depakote. This is a good choice fore rapid cyclers. How does it work? Concerns? Useful in what type of patients? | Suppresses sodium channels and calcium influx and augments GABA. REQUIRES frequent LFTs. Considered to be first line treatment for bipolar over lithium. |
| Benzodiazepines can be used to treat anxiety. How do they work? Expected outcome? | Binds to specific receptor sites to enhance actions of GABA leading to reduced anxiety. |
| This medication is a commonly used benzodiazepine with shorter half life than others. can cause CNS/respiratory depression, amnesia, Paradoxical psychological effects, Tolerance/Dependence, Schedule IV drug that readily crosses the placenta and breatmilk. | Alprazolam (Xanax). |
| What are the advantages of using a benzodiazepine to relieve anxiety? | Rapid onset, well tolerated, few drug interactions *Alcohol*, few CVS effects *when given PO, Generics are available, only activate existing GABA receptors |
| Buspirone (Buspar) is an antianxiety agent. How does it work? What are the side effects? | Binds with serotonin receptors/some dopamine. Take with food***. Peak at 3-6 weeks No euphoria like Benzos, doesn’t affect GABA, not controlled substance, takes 3-6 weeks to work, no risk for OD, used for GAD. Dizziness, nausea, headache, excitement |
| What’s the difference between the terminology of hormone replacement and hormone therapy? | Replacement is for males born male at birth. Therapy is for males born female at birth |
| What is the function of luteinizing hormone in males? | Stimulates the production of testosterone |
| What is the function of follicle-stimulating hormone in males? | Testicular growth and sperm maturation |
| What is hypogonadism? What does it cause? What causes it? | Diminished gonadal activity and diminished testosterone production. Primary c/b chemo, autoimmune, genetic, or infection. Central c/b poor nutrition, steroids, pituitary injury, alcohol, or other external causes. |
| What are the symptoms of hypogonadism? | Opposite of testosterone, loss of hair/muscle, gynecomastia, reduced growth of testicles/penis, ED, osteoporosis, low sex drive, infertility, fatigue, hot flashes, difficulty concentrating. |
| What is the expected function of Androgens Testosterone? Why would someone take it? How is it administered? | Replaces missing testosterone from natal males, contributes to skeletal muscle growth, helps maintain libido. Used for male hypogonadism, delayed puberty, hormone replacement. PO, Topical, IM |
| A male patient is taking androgen as hormone replacement therapy. Teach him about the adverse effects and other considerations. | Priapism, Premature epiphyseal closure, Gynecomastia, Acne, HDL/triglyceride elevation, Osteoporosis. Notify if errection lasting more than 4 hours, apply UNDER ARMS, not genitals. Maintain physical activity and monitor triglyerides. |
| How are anabolic androgenic steroids different from androgen testosterone. Risks associated with these? | abused in sports, used for building muscle tissue instead of skeletal muscular growth fat soluble can alter metabolic function of the cells whereas androgen testosterone water soluble NOT alter cellular function. LDL/HDL, acne, HTN. Liver. Heart |
| What do androgen antagonists do? Who would need this? What are some adverse effects? | Block the synthesis of androgens in people with BPH, Prostate cancer, Endometriosis, Male-Pattern bladness, Acne, or Hirsutism. Usually in male to female transition. May cause electrolyte problems, dehydration, gynecomastia and impotence. |
| Spironolactone (Aldactone) is used off label to treat a variety of hormonal conditions. Name some. What are some What are some adverse effects? | Acne, Polycystic ovary syndrome, Hirsutism, Male to Female transition, Prostate cancer or BPH. K sparing diuretic-> hyperkalemia, gynecomastia, impotence |
| What causes erectile dysfunction? | Impeded arterial/venous flow into corpus cavernosum, Stress and Performance anxiety, medications, pelvic trauma |
| How can you treat erectile dysfunction? | Phosphodiesterase inhibitors, Hormone, Injection, and Herbal therapy. Oral and topical meds and mechanical pumps |
| What would a patient taking a phosphodiesterase inhibitor be struggling with? What is the prototype of this? How do these drugs work? | Erectile dysfunction, -afil drugs such as Sildenafil (Viagra/Revatio). Enhance effect of nitric oxide leading to smooth muscle relaxation and increases arterial flow into corpus cavernosum by dilating blood vessels |
| What are the indications for Sildenafil? What are the pharmacokinetics? How is it administered? What are the adverse effects? | Erectile dysfunction, Pulmonary hypertension. Hepatic metabolism, excreted in feces and urine. Administered PO. May cause headache, Hypotension, Priapism |
| Penile implants may be appropriate for patients with erectile dysfunction. How do the different types work? | Non inflatable-2shafts, bend penis up for erection. 2 piece inflatable-pump in scrotum, pump fluid into reservoir. |
| A patient who has erectile dysfunction asks you about taking nitrates for chest pain. You say… | Use caution, may cause syncope if BP crashes |
| Explain the differences between premature, Inhibited, and Retrograde ejaculatory dysfunction. | Premature- too soon. Inhibited- too late. Retrograde- ejaculation flows backward into the bladder |
| A patient complains of premature ejaculation and asks what causes it and what they can do. You say… | Psychological factors (anxiety/stress/anticipation). Lidocaine cream to delay, Keegles, Pharm therapy, herbals? |
| A patient complains of inhibited ejaculation and asks what causes it and what can be done. You say…” | Physiological factors (age/structure/ NS pathology) Psychologic factors, Medications. Treat the underlying problem. Consider dopamine agonists and anti-serotonergic agents. |
| A patient has been told that he has retrograde ejaculation and is concerned. You tell him. | This is not harmful, it involves the backflow of semen into the bladder. It may cause infertility. Associated with BPH and blocked urethral passage |
| What does failure to detumescence or Ischemic Priapism mean? What causes it? Treatment? | Ischemic- blood trapped in penis can’t get out veins. May cause compartment syndrome, tissue doesn’t get oxygen, very painful. May be c/b penile trauma, vascular disease, neuroregulation. May be c/b AV fistula, . Facilitate venous drainage surgery/meds |
| What is nonichemic priapism? Cause? Treatment? | Prolonged erection. |
| How can you tell the difference between ischemic and nonischemic priapism? | Pain. Nonischemic is NOT painful and is NOT a medical emergency. |
| What is benign prostatic hypertrophy? What does it cause? Treatment? | Overgrowth of prostate treatment. Causes lower UT obstruction->fullness, hesitancy, frequency, nocturia, dribbling, treat symptoms with Tamsulosin (Flomax). |
| What is Tamsulosin (Flomax)? What is it used for? What are the adverse effects and nursing implications? | An alpha1 adrenergic blocker that relaxes smooth muscles in neck of bladder and prostate in patients with BPH. Can cause hypotension, orthostasis, dizziness. Don’t crush it (risk for profound hypotension) |
| What is gender dysphoria? When do most people experience this? | Strong feelings of identification with opposite gender, distress of assigned sex, dysphoria becomes worse with puberty (Tanner stage 2) |
| What is the goal of transgender treatment? | Ameliorate gender dysphoria, improve sexual function, achieve serum hormonal levels within the normal biologic range of born males or born females |
| When a transgender individual is taking hormone therapy drugs, what are the goals? | Induce secondary sex characteristics, virilization, diminish secondary natal sex characteristic, no RCTs to support proper dosages or formulations. Basically, get them to conform with desired gendered appearance. |
| What is included in Female to Male Hormone therapy? What are the legal and ethical initiation concerns? | Gonadotropin releasing hormone agonist (LH and FSH-> testosterone, Estrogen, Progesterone, Sperm…) Testosterone, Progestin. Hormone therapy may mean permanent changes, may start at 16 yo (tanner stage 2). |
| Adolescents may be transgender, experiencing gender dysphoria. What pharm therapy may they have? | Reversible-Gonadotropin releasing hormone analogues->suppresses puberty (reversible) to prevent full biological puberty and menses and diminish gender dysphoria |
| Why would an adolescent transgender take partial reversible therapy? | give testosterone> premature closure of growth plates and alter stature, indicated in individuals with strong gender dysphoria that is worsened with puberty. Taper doses of Testosterone up every 6 months until reaching adult dose of 75-100 mg |
| What is the target dosing for testosterone in the transgender population? What are the target outcomes? Serum levels? | 75-100 mg IM weekly and 200-250 mg q2weeks IM. Goal to suppress menses and virilize body/face and hair. Serum levels measured every 2-3 months goal range 320-1000 ng/dL with Estradiol <50pg/mL |
| How old must an adolescent be to undergo irreversible surgical reassignment? | 18 yo |
| An adult hormone therapy for transgender FtM may require the addition of daily progestin. Why? | used to halt menses or if estrodial levels are too high |
| T/F- Patients who want to transition from female to male can expect the same physical outcomes regardless of age initiated. | False- advanced age may mean that the physical changes are less appropriate to desired gender (shorter, wider hips, fat deposit locations) |
| What is involved in virilization? | Development of male characteristics. Facial/Body hair. Increased muscle mass. Deeper voice, Adam’s apple. Redistribution of fat. Cessation of menses. Increased libido. Male physical contours. |
| A patient has just started hormone therapy for female to male transition. For the first 6 months, what physical changes can he expect? | Acne, skin become more oily, fat is redistributed, menses stop, clitoris enlargement, vaginal atrophy. Maximum effect at 1-2 years. |
| A patient has just upped their hormone therapy for the Female to male transition and wants to know what to expect from 6-12 months. You tell them… | Facial and body hair growth, loss of scalp hair, increased muscle and strength, voice deepens. Maximum effect at 2-5 years. Also clitoromegaly, decreased breast tissue, and fertility |
| What are the risks of hormone therapy in transgender individuals that they should be made aware of? | increased risk ovarian/breast/vaginal/Lung/colon/ brain cancer. Too muc>polycythemia/erythrocytosis. Too little>bone demineralization. Continue ACOG recommendations for cancer screenings. Decreases HDL, increases triglycerides, may elevate liver enzymes |
| What are the contraindications for hormone therapy for transgender individuals? What screenings are required for individuals on hormone therapy? | Pregnancy. Unstable CAD. Untreated polycythemia. Clinic visits every 3 mos 1st year. 1-2 times a year after. Yearly blood work and cancer screenings |
| In order to be eligible for surgical treatment for transgenders, what are the requirements? | At least 18yo, taking cross-sex hormone for 12 mos, successful social transition for 12 mos. Compliant with clinic follow-up, knowledgeable of practical aspect of surgery |
| What are the surgical steps of female to male gender reassignment? | Mastectomy, Hysterectomy/Ovariectomy, Vaginectomy, Urethral reconstruction, Scrotoplasty/Penile reconstruction, Penile/testicular implants, Metodioplasty (microphallus for urination while standing) |
| There are several progestin-only contraception methods. Name some. | Depo-Provera, Mini-pills, IUDs and Nexplanon. |
| How is the progestin only mini-pill different from the combined mini-pill? | Each progestin only pill is worth 24 hours of protection. These must be taken at the EXACT same time each day. If more than 3 hours late, need a backup. Each pill has progestin in it so you have to take all. Not as effective. |
| The depo-provera is another progestin only contraception method. How is it administered? Frequency? Monitoring? Concerns? How does it work? | IM injection q12weeks, can cause weight and BP increase. Can lead to osteoporosis. Must be on calcium and vitamin D. Suppresses ovulation and changes the cervical mucus. |
| What is the mechanism of action for progesterone only contraception? Who are these recommended for? | Changes the endometrial and cervical mucus. Makes the uterus inhospitable. Good for women who can’t take combined methods, undiagnosed vaginal bleeding, hepatitis/cirrhosis. Breastfeeding, HTN, and women over 35 who smoke. |
| What are long-acting reversible contraceptives? | Progestin only methods of contraception such as Mirena and Skyla (IUDs) and Nexplanon. Also includes the non-hormonal method Paragard (IUD) |
| Whats the difference between mirena and Skyla? Same? | Both Progestin only Long acting reversible contraception made by same company. Sits at top of uterus. Immediate return to fertility after removal. Check strings monthly. Sklya 3 years, smaller, 14mcg/day. Mirena 5 years, 20 mcg/day |
| What is the mechanism of action for hormonal long-acting reversible contraceptives? | Thickens cervical mucus. Suppresses ovarian function. Inhibits sperm movement and thins the uterine lining. Basically makes uterus inhospitable as is expected with progestin only methods. |
| What is Nexplanon? How is it different from other long acting reversible progestin only contraceptives? Mechanism of action? | Implanted non-dominant arm3 years systemic b/c of placement. Common side effects include menstrual irregularities, weight gain, and headaches. Increased risk of blood clots. Etonorgestrel blocks LH surge to prevent ovulation and makes uterus inhospitable. |
| How are Mirena and Nexplanon similar? Different? | Mirena-5 years, in uterus, few contraindications. Nexplanon- 3 years, in arm, contraindicated in liver disease and venous thromboembolism. Both- irregular bleeding, don’t protect against STIs. |
| What makes paragard unique? Who is it good for? Side effects? | Similar to mirena in shape, Non hormonal long acting reversible contraception, good for women who can’t use hormonal methods. Used up to 10 years. May cause heavier bleeding and cramps. |
| Sometimes emergency contraception is necessary. What is it called? How do you take it? What does it do? | Plan-B is high dose progestin to prevent pregnancy for up to 3 days after unprotected sex. Take 1 pill ASAP and 1 pill 12 hours later or 1 pill within 72 hours. Stops ovulationbut won’t disturb an established pregnancy. |
| T/F- Plan B will stop an already established pregnancy if taken within 72 hours. | False, will only prevent wont disrupt a pregnancy. |
| What are the goals for caring for a transgender male to female client? | Suppress endogenous natal male hormones. Induce secondary sex characteristics of new sex, Achieve balance with hormonal medications and client desired outcomes. |
| What hormones are given to transgender women? Why? | Antiandrogens (Spironolactone)- block testosterone. Progestin-breast development. GnRH (expensive 2nd line)-Suppress testosterone production in testes. Estrogen-indirectly suppresses testosterone |
| What is the first line hormonal therapy for transgender women? Why? Second line? | Antiandrogen and estrogen for reduced side effects and decreased estrogen needs. Second-progestins to replace estrogen, GnRH in younger people to suppress puberty |
| For transgender people, GnRH is sometimes used. Why? | Used in younger transgender people to suppress puberty. Very expensive. |
| What are the goals for hormone therapy in transgender women? Monitoring? | Feminizing effects, serum testosterone WEL for women (30-100), Screen- lipids, adverse effects, prolactin/triglycerides, K+ if taking spironolactone, BMD for osteoporosis, breast/prostate cancer screening |
| Menopause sucks. It puts women at an increased risk for… Symptoms? | Stroke, heart disease, hip fractures, colorectal & endometrial cancer. Headache/hotflashes. Teeth loosen and gums recede. Thin hair, breasts droop/flatten, nipples shrink, skin drier. Vaginal dryness and shrinking, thicker body hair, osteoporosis. |
| What is menopause? | Permanent cessation of menses after 1 full year, ovaries stop functioning, median age 49-51. Moving from reproductive to non-reproductive years. |
| What happens during perimenopause? Menopause? Post menopause? | Peri2-8 years with decreased estrogen and progesterone->increased FSH. Meno-1 full year after end of menses. Post-body adapts. |
| What is the purpose of hormone replacement therapy in women? What does it involve? What is the difference in treatment for women depending on their uterus? | Temporarily relieving menopausal symptoms. Intact uterus- estrogen-progestin therapy (combo). Hysterectomy- Estrogen only |
| Premarin is an oral estrogen used to treat the symptoms of menopause. What is the expected outcome, SE, MOA, and risks? | Helps maintain female genital system to treat moderate to severe vasomotor symptoms (hot flashes). SE=NV, breast tender, fluid retention, cramps. First pass effect affects liver, increases hepatic production of triglycerides, HDL and clotting factors. |
| Transdermal estrogen, like Premarin, can be used to treat the symptoms of menopause. How is it different? Benefits? Risks? | Contains 17 beta estradiol. Patch applied once a week. Helps preserve bone density and treating symptoms, lower risk of DVT/stroke, and less effect on serum lipids. Perhaps a better choice with fewer side effects. |
| A patient complains of vaginal atrophy and asks what can be done. You teach her… | Vaginal rings may help but don’t treat other symptoms. Vaginal creams are good for vaginal complaints. Topicals are also available. |
| Combo Estrogen and Progesterone can be used to treat the symptoms of menopause. Who is this beneficial for? How long can it be used? What is the goal? How is it administered? | Used for women with an intact uterus for less than 5 years (more increases risk of breast cancer). Progestin (medroxyprogesterone acetate) decreases risk of hyperplasia. PO and patches. |
| Combo Estrogen and Testosterone can be used to treat the symptoms of menopause. Who? Why? Risks? | Only to treat severe vasomotor symptoms and libido loss. Short term use only. Hirsutism, voice changes, decrease in HDL. NV, Fluid retention, breast tenderness, leg cramps, breakthough bleeding, HA, mood, chloasma |
| Generally speaking, what are the risks and benefits of hormone replacement therapy for women experiencing menopause both combined and estrogen only? | Low risk for women in 40s-50s. Combined therapy-CHD, Stroke, DVT, breast cancer. Reduces fractures and colon cancer. Estrogen- Pulmonary embolism, Fractures. Decreased breast cancer, CHD, stroke, colorectal cancer, urinary symptoms. |
| Who should never take hormone replacement? | Pregnant, endometrial or breast cancer, thromboembolic disorders, liver impairment, gallbladder/pancreatic disease, CAD, vaginal bleeding, endometriosis. |
| Bioidentical hormone replacement therapy is a newer option. Benefits? Risks? | Uses estrogen derived from plants, custom made for patient based on blood/saliva. Can take PO or SL or implant. Limited evidence and high cost. |
| Why would a menopausal woman be taking an SSRI, Clonodine, or Gabapentin? | Can decrease number, amount, and severity of symptoms. |
| For patients interested in trying an alternative hormone replacement therapy such as Ginseng or Vitamin E, what advice can you give? | Takes 4-6 weeks to see any changes, limited evidence. May or may not work. |
| A patient is newly menopausal and is interested in hormone replacement therapy. You tell her that the recommended order of therapy is… | 1) Short term treatment of symptoms at lowest dose. 2) Increase estrogen dose if vasomotor symptoms persist. 3) If can’t uses HRT, use SSRI or alternative therapy. |
| What is osteoporosis? How can you prevent and treat it? | Progressive skeletal disease. Prevention is best, may use hormone replacement, increase calcium, vitamin D, and weight bearing exercise, and stop smoking. Treat with 1) Biphosphonates or Selective Estrogen Receptor Modulators if cant take. |
| Biphosphonates can be great, but come with risks and side effects. Name some | Ulcers, upper GI irritation, irregular heart beat, femur fracture, hypocalcemia, skin rash, muscle and joint pain, increased parathyroid hormone. |
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