Exam 2: NURS 663/ NURS663 (2026/ 2027 Updated) Psychiatric Mental Health Diagnosis and Management II Review with Qs & As| 100% Correct| Grade A (Accurate Answers) - Maryville.

Exam 2: NURS 663/ NURS663 (2026/ 2027 Updated) Psychiatric Mental Health Diagnosis and Management II Review with Qs & As| 100% Correct| Grade A (Accurate Answers) - Maryville. Q. Barriers to adherence ANSWER chemotherapy not understanding the purpose of the exercise not understanding how to do the exercise feeling overwhelmed by info forgetting to do exercises pain and fatigue Q. Facilitators of adherence ANSWER Social support Prevention Developing skill in performing exercises (especially with biofeedback) Developing a routine and/or system of reminders Feedback on effectiveness so that EXPECTATIONS are SPECIFIC Q. Chin tuck is the ANSWER most common strategy recommended (also recommended by doctors, not just SLPs) Q. Although the chin tuck is designed to make the swallow better, it can ANSWER make it worse (watch on MBSS first!) Q. Chin tuck is intended to reduce ANSWER premature spillage into vallecula/pharynx by using gravity to keep bolus in oral cavity Q. Chin tuck widens the ANSWER vallecular space to hold more food/liquid before swallowing Q. Chin tuck is best for people with poor ANSWER oral control, especially of liquids Q. Chin tuck allows one to be _____ to swallow; have more _____ over swallow ANSWER ready control Q. Chin tuck narrows the ANSWER opening to the laryngeal vestibule Q. Chin tuck may be enough to ANSWER prevent aspiration Q. Chin tuck can reduce residue in the _________ due to ______ weakness or inability to articulate what with what? ANSWER vallecula BOT BOT and PW because the space between them is reduced and thus propulsion of the bolus is easier or possible Q. Head turn is used when residue in pharynx is observed ANSWER mainly or only on one side, such as in one pyriform sinus, due to greater weakness on one side Q. In the head turn, turn to the ANSWER WEAK SIDE (to open the strong side/don't cut off the strong side) Q. For the head turn, it is best to observe efficacy with the _____ test because... ANSWER FEES It can be difficult to view on the MBSS because you don't always get an anterior view/need to see both sides Q. You can perform the chin tuck with the ANSWER head turn for increased clearance of bolus and improved airway protection Q. Head turn can help because it increases the duration of ANSWER TVC closure via extrinsic pressure Q. Head turn promotes passage of the bolus via the ANSWER stronger side (theoretically, try both ways with biofeedback and see which works better) Q. Head turn can decrease the resting pressure of the _________ muscle by pulling the _____ further from the _____ and allowing the _____ to do what? ANSWER cricopharyngeus cricoid cartilage PW UES relaxes just enough for passage of the bolus Q. Head turn is often recommended for ANSWER Unilateral VF Paralysis or partial laryngectomies (anything with a hemiparesis) Q. Effortful swallow is one of the best compensatory strategies because ANSWER it is not noticeable, it is more like a normal swallow, and people understand it Q. Effortful swallow is the most effective because it has the ANSWER highest adherence rate and high therapeutic value Q. Effortful swallow promotes stronger ANSWER tongue to palate contact and BOT to PW contact Q. Effortful swallow hits ANSWER every stage of the swallow Q. Effortful swallow can be seen as both ANSWER compensatory and restorative because it strengthens the swallow and approximates normal movement Q. Supraglottic swallow is intended to increase ANSWER VF closure during swallow Step one to supraglottic swallow: Hold breath right after food in mouth Step two to supraglottic swallow: Continue to hold breath during swallow Step three to supraglottic swallow: Voluntarily cough immediately after swallow Step four to supraglottic swallow: Dry swallow to clear again (if necessary) Supraglottic swallow is for patients experiencing premature spillage/aspiration before the swallow Super supraglottic swallow is the 3 to 4 steps of the supraglottic swallow plus bearing down Super supraglottic swallow is good for people without an epiglottis Super supraglottic swallow means there is no _____________ because larynx closes ___________ penetration completely/no air space in larynx In the Super supraglottic swallow, all the doors to the airway are closed BEFORE the swallow even occurs Have patients do the Super supraglottic swallow before giving consistencies (then with consistencies if that goes well) Mendelsohn Maneuver is the voluntary prolongation of ___________________ to prolong the duration of the _________ laryngeal elevation UES opening Mendelsohn Maneuver must be practiced In the Mendelsohn Maneuver, the goal is to reach the highest hyolaryngeal elevation possible Mendelsohn Maneuver is used more often in therapy for secretion management Mendelsohn Maneuver is a strengthening exercise for the suprahyoid muscles Compensatory postures/maneuvers are intended to improve swallow protect airway When trying compensatory postures/maneuvers at first, look at them with MBSS (or FEES) to see if they work on different consistencies and to help teach If a strategy does not work, try combining it with another strategy before abandoning compensatory maneuvers Recommendations in therapy Posture/maneuver Diet modification Strengthening exercises Oral-Motor Exercises Thermal-Gustatory or Thermal-Tactile Stimulation Biofeedback IOPI is a type of biofeedback therapy (balloon and lights measuring intraoral pressure and force during swallow) Bedside evaluation benefits ICU/extremely ill patients can be tested Used as screener--don't have to take patients to instrumental testing if unwarranted Can be done on any sized person No radiation Bedside evaluation disadvantages Can only be used as a screener Can only OBSERVE signs of aspiration/cannot actually see details FEES evaluation benefits Can be done at bedside and on any sized person No radiation Can see bolus transport and airway protection Can check sensory functions Can clearly see the structures and an abnormalities with them Can see residue and signs of aspiration Can see paralysis and difference between right and left sides Can see pooling in pyriform sinuses/Signs of poor secretion management With blue dye test, can more clearly see residue, premature spillage, and other signs of aspiration Can see how compensatory strategies are working at pharyngeal phase FEES Evaluation Disadvantages Can only see before and after swallow, not during swallow due to white out Can only see the pharyngeal phase Can only see residue Cannot see WHY residue is left MBSS evaluation benefits Can see the physiology of the swallow from oral to pharyngeal phase, all the way down Can see WHY there is residue or other signs of aspiration Can SEE penetration and aspiration Can see how compensatory strategies are working at all phases of swallow MBSS evaluation disadvantages Radiation Does not fit all people Difficult for ICU or very ill Bolus Maintenance/Lip Seal: Phase Category Oral phase Bolus Maintenance/Lip Seal: Signs Drooling Bolus Maintenance/Lip Seal: Treatment strategy Practice puckering lips with or without wide mouth to pucker and pressing lips tightly together for 10-15 times, 2-3 times daily Bolus Maintenance/Control: Phase Category Oral phase Bolus Maintenance/Control: Signs Poor mastication/formation of and maintenance of bolus Poor posterior bolus propulsion Premature spillage Oral residue Bolus Maintenance/Control: If food collects in the sulci, external digital pressure can be used Bolus Maintenance/Control: Treatment strategies Increase TONGUE STRENGTH (lateralization with or without resistance, tongue tip elevation and de-elevation into the anterior sulci and buccal sulci) Press tongue depressor against hard palate Circle lips with tongue slowly Chin tuck to reduce premature spillage Sensation difficult to treat Posterior Bolus Propulsion: Phase category Oral transit phase Posterior Bolus Propulsion: Signs Tongue pumping with premature spillage (disorganization) Posterior Bolus Propulsion: Treatment strategies Instruct pt. to consciously try and reduce pumping action and initiate hard, deliberate posterior tongue movement while watching biofeedback sEMG is recommended most (could also try MBSS) Straw use Delayed Pharyngeal Swallow: Phase category Oral transit phase Delayed Pharyngeal Swallow: Signs Pooling of food/liquid in hypopharynx/pyriform sinuses Delayed Pharyngeal Swallow: Treatment strategies Thermal-Gustatory Stimulation Thermal-Tactile Stimulation Chin tuck to widen vallecular space and allow for more food/liquid to be held safely until swallow is triggered Thermal-Gustatory Stimulation therapy technique which adds the use of flavored ice to the thermal stimulation procedure Thermal Tactile Stimulation utilize a 00 laryngeal mirror to rub the faucial arches 4 or 5 times in rapid fashion with a cold/iced mirror, repeat 5-10xs each side have the patient attempt to swallow purpose: to increase sensory awareness & improve the trigger of the swallow reflex Vallecular Residue: Phase category Pharyngeal phase Vallecular Residue: Signs BOT weakness Vallecular Residue: Treatment strategies Effortful swallow Chin tuck Masako Maneuver Masako Maneuver place tongue between teeth while swallowing to allow pharyngeal wall to move anteriorly to base of tongue May also strengthen superior constrictor Weak Pharyngeal Contraction: Category phase Pharyngeal phase Weak Pharyngeal Contraction: Signs PPW residue Pyriform sinus residue Weak Pharyngeal Contraction: Treatment strategies Effortful swallow Masako Maneuver (may strengthen superior constrictor) sEMG biofeedback Head turn to weak side Laryngeal Penetration/Aspiration: Category phase Pharyngeal phase Laryngeal Penetration/Aspiration: Signs See on MBSS or FEES Laryngeal Penetration/Aspiration: Treatment strategies Chin tuck (+ Head Turn) Effortful swallow Repeat dry swallow Thermal-Gustatory or Thermal-Tactile Stimulation DURING MEALS Supraglottic swallow (+ Super) Cricopharyngeal Dysfunction: Category phase Pharyngeal phase Cricopharyngeal Dysfunction: Signs LPR, GERD Burning sensation See on MBSS Regurgitation Cricopharyngeal Dysfunction: Treatment strategies Botox injections Surgical myotomy Head turn to pull UES open Laryngeal elevation exercises to pull UES open Laryngeal elevation exercises to pull UES open Prolonged high-pitched /i/, Mendelsohn Maneuver, Shaker Exercise Mendelsohn Maneuver Increased laryngeal movement stretches/opens the CP; Prolonging hyolaryngeal elevation keeps the CP open longer. used for 1) Decreased range/duration hyolaryngeal elevation; (2) Decreased range/duration cricopharyngeal opening; (3) Decreased pharyngeal swallow coordination Shaker Exercise -lay flat on floor -lift head up from floor without lifting trunk/shoulders from the floor -repeat slowly 3x -rest for 1 minute -repeat head lifts rapidly 30x -repeat entire series 3 times a day for 6 weeks -increased anterior laryngeal excursion and upper esophageal sphincter opening during swallowing with healthy subjects The biggest component of Informed Consent is Education Informed consent components: Adequate ________________ of information disclosure Informed consent components: _____________ _________ of patient or client to understand the information and make an informed __________ cognitive capacity decision Informed consent components: A __________ __________ made without _______ voluntary choice coercion Informed consent components: _________ ____ __________ of choices made, such as aspiration pneumonia or possible death Appreciation of consequences Ethical principles: Autonomy the right to decide for oneself about one's own life Ethical principles: Beneficence actions done for the benefit of others/actions that produce good Ethical principles: Nonmaleficence actions that avoid harm or evil Ethical virtues: Integrity completeness, wholeness, a unity with moral character Ethical virtues: Compassion suffering with another Ethical virtues: Prudence engaging in practical wisdom Informed consent: we should provide ______ ________ for education multiple avenues Issues to consider when educating about informed consent: Preserving the ability to eat or speak Issues to consider when educating about informed consent: Can the patient's ________ _________ withstand aspiration? pulmonary status Issues to consider when educating about informed consent: Does patient fully understand ________ _________ of aspiration? the consequences Issues to consider when educating about informed consent: Does patient ______ to master swallowing techniques that still leave him ___ ____? want at risk Advanced Directive is a document that enables people to express their wishes about their health care in a form that will tell others how to care for them and make decisions for them if and when the time comes when they are unable Types of Advanced Directives a) Living Will - expresses client's wishes regarding medical treatment in the event the client becomes incapacitated and is facing end of life issues b) Durable Power of Attorney for Health Care- designates a health care proxy who is an individual authorized to make health care decisions for a client who is unable c) Provider's Orders - Unless a DNR (do not resuscitate) or AND (allow natural death) order is written, nurse initiates CPR when client has no pulse or respiration. Written order for DNR or AND must be placed in client's medical record. Advanced Directives replace Informed Consent when A patient cannot understand or is not cognitively alert or able to make their own decisions due to illness or disability Alternatives to Advanced Directives Substituted judgement (what would the patient want?) Best interest (what is best for the patient?) Decision-Making Capacity (DMC) competencies to stand trial to manage property to make medical decisions for oneself Decision-Making Capacity (DMC): Legal competence presumes that all adults are competent to decide for themselves what will be done with their person or property Decision-Making Capacity (DMC) comprehension a patient must understand what they were educated on in order to decide whether to accept or reject treatment Decision-Making Capacity (DMC) choice deliberation about alternatives is essential Decision-Making Capacity (DMC) questions with choice consistent with values possible to maintain a stable choice change mind for intended reasons Biofeedback for dysphagia: Instrument options sEMG FEES MBSS Biofeedback for dysphagia is a real-time visual representation of the swallow Biofeedback for dysphagia is non-pharmacological Biofeedback for dysphagia can lead to better self-regulation and monitoring of a learned skill Biofeedback for dysphagia's primary goal is self-regulation Biofeedback uses _________ _________ to measure and give feedback on _________ ________ to patients scientific instruments physiologic information Biofeedback makes ________ _________ perceptible to the ________, so that one can _________ them __________ bodily processes senses manipulate consciously FEES as biofeedback tool: allows view of real structures in real time FEES as biofeedback tool: allows for visualization of post swallow bolus residue FEES as biofeedback tool: postural compensatory techniques are easily observed FEES as biofeedback tool: very helpful for vocal fold adduction and airway protection training (such as the head turn, supraglottic and super supraglottic swallow techniques) FEES as biofeedback tool: facilitates training of VP closure sEMG as biofeedback tool: can see the muscle ________ via a(n) ____ _______ that the muscle emanates function electrical signal sEMG as biofeedback tool: CANNOT measure force, strength, amount of effort, or resting muscle sEMG as biofeedback tool: NOT a diagnostic tool sEMG as biofeedback tool: bio-electrical energy upon _______ ____________ is recorded with _____ _______ muscle contraction skin sensors sEMG as biofeedback tool: real-time visual representation of the swallow, allowing for conversion of an involuntary function into a conscious deliberate process (can use WITH ultrasound for even more improvement) sEMG as biofeedback tool: helps with _________, ________ treatment expectations and ______ delineation for the patient via an ________ measurement of _________ concrete, objective goal objective progress sEMG as biofeedback tool: proven to help ______________ treatment process accelerate sEMG as biofeedback tool: is _____-driven patient sEMG as biofeedback tool: based on ________ memory/______________ motor motor learning theory sEMG as biofeedback tool: DOES NOT TELL US what the pharynx is doing, when to proceed to PO, when the re-evaluate with diagnostic tools, when the patient is aspirating, SO it is NOT a diagnostic tool sEMG as biofeedback tool: Treatment candidates cortical-brainstem infarct oral-pharyngeal cancer cancer with partial resectioning and/or radiotherapy (XRT) General surgical patients with disuse atrophy Cerebral palsy Neurodegenerative diseases--especially for education Blue Dye Test is mostly for patient with tracheostomy tube Blue Dye Test: 1) ____ cuff, Take tube out, Place _______ ______ Deflate Pulse oximeter Blue Dye Test: Can do at bedside evaluation or with FEES Blue Dye Test: 2) Start with ________, wait, then let nurse... water suction lungs to see if colored water comes out Blue Dye Test: 3) Continue with ____ _________, wait _______ minutes and see if __________ material is collected ______ the cuff other consistencies 10-15 aspirated above Blue Dye Test: 4) If patient passes exam and is made PO, his/her food is often tinged for a few days after to verify safety What do compensatory strategies do? Improve oral transit Improve pharyngeal transit Improve airway protection Most common reason people don't adhere to strategies social consequences When giving recommendations, avoid ____________ language, acknowledge ________, give ___________ rationale controlling feelings meaningful Four Decisions when giving recommendations: 1) Decide whether PO or NPO Four Decisions when giving recommendations: 2) Determine certain ________ or _______ of PO or NPO restrictions; components Four Decisions when giving recommendations: 3) Determine need for further evaluation Four Decisions when giving recommendations: 4) Determine need for dysphagia therapy/treatment If PO: patient needs to be mentally competent or monitored at every meal If PO: Must determine diet consistencies If PO: Must acknowledge and give precautions to take when feeding/eating If PO: Must recommend whether or not further evaluations are needed (or instrumental testing if only bedside eval was done) If PO: Must include if patient needs to use compensatory strategies, postures, or maneuvers when eating If PO: Must determine if therapy is needed If PO: Must determine level of supervision needed during meals If NPO: There is no need to talk about diet or compensatory strategies If NPO: Must determine whether or not further instrumental testing is needed If NPO if refused... risks must be discussed with the patient and caregivers (informed consent/DMC) If NPO is agreed to then status is determined on how often and when to follow-up If NPO: Must determine if there is a need for therapy Medical treatments for dysphagia Widening/strengthening of UES/CP dilation Cutting of CP/CP Myotomy (Brainstem stroke) NGT/PEG VF Medialization (Unilateral VF Paralysis) Medications (e.g. for GERD) Downsides of CP myotomy May not be able to trigger swallow still May have reflux with tube feeds NGT/PEG Advantages Increased life span Increased ability to recover from illness Increased possibility of returning to useful functioning Improved QoL Improved psychological and physiological state Improved resistance to infection Improved healing of skin and wounds NGT/PEG Disadvantages Nutrition may not be fully absorbed through the gut Patients may still experience a failure to thrive (e.g. Alzheimer's) Physical pain Cannot help because underlying condition is hopeless (e.g. permanent unconsciousness) Causes discomfort and only prolongs dying (e.g. terminal patients) Spiritual and emotional and social pain/suffering Indignity Emotional and financial burden on the family Clinical Feeding: Determine whether to feed if pt is already PO, then ____ _____ unless you observe will feed significant deficits on the oral-facial exam and poor mental status/alertness Clinical Feeding: Determine whether to feed if pt is NPO, then you will probably ____ ___ if there was severe... not feed oral-facial deficits or mental status/alertness issues respiratory disease Clinical Feeding: If you decide not to feed, you will recommend NPO or MBSS Clinical Feeding: If someone is acutely ill (e.g. 1-2 days post-CVA) and recommend NPO and no MBSS, you must follow-up daily Clinical Feeding: It is important to remember as you begin this feeding trial that if a ________ _________ was noted previously, this DOES NOT ensure what? voluntary cough a reflexive cough is present Clinical Feeding: Daniels et al. (1998) showed that an abnormal voluntary cough and coughing during feeding predicted... aspiration (MBSS) in 78% of persons Clinical Feeding: Medical history that may predict aspiration Dysphonia Dysarthria Clinical Feeding: Bedside observations that may predict aspiration Abnormal gag Change in voice quality after swallowing Dysphonia, dysarthria, abnormal gag, and change in voice quality after swallowing were less accurate in predicting aspiration than abnormal volitional cough or coughing on trial swallows combination Clinical Feeding: Begin feeding with a tsp of water or small sip from a cup depending on what is easier for the patient Clinical Feeding with a tsp of water note: Lip closure presence of drooling Clinical Feeding with a tsp of water note: Any delay in the initiation of the swallow Clinical Feeding with a tsp of water note: any overt coughing or choking before/during/after the swallow Clinical Feeding with a tsp of water note: the strength of the ______ and any ______ _______ after swallow cough throat clearing Clinical Feeding with a tsp of water note: the extent of _____ ________ during the swallow laryngeal elevation Clinical Feeding with a tsp of water note: presence of ____ _______ voice quality after a swallow wet-gurgly Clinical Feeding with a tsp of water note: oral ________ after the swallow residue (check the oral cavity) Clinical Feeding: Coughing/throat clearing during or immediately after the swallow and/or wet vocal quality probably represent penetration or aspiration BUT their absence does not rule it out Clinical Feeding: Reflexive cough in a ________ _________ population may be diminished rather than _________, so this means what neurologically impaired absent it may take a greater amount of penetration or aspiration to elicit the cough than the very small amount it takes to elicit such a response in normals Clinical Feeding with a tsp of water note: If all goes well, do what? proceed with another trial of liquid Clinical Feeding: after second trial of a tsp of water, proceed to 2-3 tsps/sips to try serial swallows During clinical feeding, a straw will place the bolus more posteriorly and may bypass certain oral control/initiation issues but because it enters the hypopharynx sooner, it may be more difficult to tolerate if there is a delay Clinical feeding after 2-3 tsps serial trials with water, continue 1 tsp, then another, then serial swallows with thick liquids, puree, and solids Clinical Feeding note with solids check mastication look for pocketing In clinical feeding, because puree and solids may block the airway, if any coughing/choking/throat clearing is noted, do what? discontinue trial feed Scintigraphy is food/liquid impregnated with a radioisotope and then observed via a gamma camera to determine precisely the amount going into the lungs The FEES is placed transnasally FEES steps Observe dry swallows/clearing of secretions Give food/liquid (with blue dye) Consistency order for MBSS Thins Thick liquids Puree Soft solid Regular solid On MBSS, liquid and puree consistencies are usually given first in ___________ ________ amounts, then advancing to ____ ______ amounts; Example? abnormally small more typical 1/2-1 tsp = sips = serial sips/gulps = allowing pt to feed self A very small amount of liquid is usually started with because it is easiest to clear from the airway and any aspiration will be less (more of a screener on first sip) Premature spillage can be normal with solids/some normals MBSS oral stage note drooling bolus formation (gathering on tongue blade) bolus maintenance--spreading or spillage to sulci bolus transit/propulsion -- smooth? pumping? check for oral residue premature spillage ability to chew/masticate MBSS pharyngeal stage position of bolus when swallow is triggered (delay?) adequacy of timing of VP closure adequacy of BOT retraction adequacy of epiglottic inversion/retroflexion adequacy of hyoid movement and laryngeal elevation adequacy of contraction of pharyngeal constrictors adequacy of CP/UES relaxation/opening amount of laryngeal penetration amount of aspiration (if silent, can it be cleared with a voluntary cough?) amount of pharyngeal residue (cleared with another dry swallow?) MBSS trigger of swallow delay times up to 3 seconds = mild 3-5 seconds = moderate 5+ seconds = severe MBSS Esophageal Phase--lateral view portions of cervical esophagus are visible to varying degrees depending on individual may notice backflow of food/liquid from the esophagus or sticking in or clearing slowly MBSS Esophageal Phase A-P View: typically done __________ with _________ at end of study thin or thick liquid bolus MBSS Esophageal Phase A-P View: allows one to view ______ of bolus transit, residue, and to observe any symmetry anatomical variations/abnormalities not clearly defined on lateral view MBSS Esophageal Phase: SLPs usually _______ this stage for any significant abnormalities screen Other observations on MBSS: Structural integrity of Zencker's diverticulum Cervical osteophytes Other observations on MBSS for head and neck cancer patients: Structural integrity of resected structures lymph edema fistulas pseudovallelae As patients show improvement in either direct or indirect tx, the clinician should determine what when to re-assess when the advance the pt's diet Who has the ultimate responsibility for the pt., including making decisions about PO and diet statuses? Medical Doctor SLP is usually the lead member of the _______ _________ as s/he is responsible for _____ and ____ of the pt., and makes most of the recommendations that other professionals can... dysphagia team diagnosis treatment agree/disagree with, add to, modify Who else can do bedside evaluations or MBSS? OT Who performs the MBSS under the direction of the SLP and is important in contributing to the dx of the nature/extent of pt's dysphagia? Radiologist Biofeedback treatment always involves a therapist a patient monitoring instruments Biofeedback applications in speech pathology other than dysphagia stuttering voice dysarthria aphasia Biofeedback modalities (in order) in dysphagia rehab FEES, MBSS, sEMG Ultrasound Endoscopy Oxygen Saturation Auscultation High correlations have been noted between peak sEMG amplitude and maximal hyoid elevation during all bolus consistencies Two stages of motor learning Acquisition phase (exteroceptive signals supplement patient's inadequate proprioceptive signals) Transfer phase (less immediate or continuous external feedback is needed--recalibration) Current swallowing rehability view recovery of muscle function through a narrow lens: ______ ______; however, neuromuscular deficits can be classified into more than flaccidity or hypofunction - what are the others? muscle weakness spasticity or hyperfunction muscle dyscoordination or apraxia sEMG: Use caution with patients with unstable cardiac conditions sEMG: Transient __________ is not uncommon dysphonia sEMG: Dicourage biting/grinding of teeth sEMG: Use care in removing electrodes due to skin breakdown on neck (i.e. from radiation) Treatment Protocol for Biofeedback Education Relaxation Patterning of a motor response Muscle recruitment Artificial feeding (NGT/PEG) is considered a medical treatment Mortality associated with feeding tubes in people living where, with what, and at what age? in nursing homes/SNFs severe cognitive deficits (e.g. dementia) over 65 Medical history notes: any _________ conditions and when was their ______? neurological onset Medical history notes: Any relevant ______ procedures/dates such as... surgical glossectomy, thyroidectomy, cervical laminectomy, partial laryngectomy, laryngeal trauma, etc. Medical history notes: Recent __________ or _________ intubation tracheostomy Medical history notes: History of recurrent ___________, ___________ infections, _______ conditions, or frequent ______ ______________ pneumonias respiratory heart high temperatures Medical history notes: Signs of GERD (including history of hiatal hernia) Medical history notes: Any unplanned weight loss Medical history notes: Medications that may contribute to dysphagia Medical history notes: Patient report show include Description of symptoms (where does it stick?) Onset date Progressive? Frequency? Consistency of foods? Odynophagia (pain during swallow)? General behavioral observations alertness mental status (confusion, attention/memory) Medical history notes: Comorbidities including aphasia, apraxia, dysarthria, dysphonia Medical history notes: Overall physical status Data suggests that patients with decreased alertness or altered mental status and poor cough reflex are more at risk of ________ ______, even if on ______ _______ aspiration pneumonia tube feeds #1 principle in swallowing treatment use normal swallowing movements (at every single stage) A 26-year-old woman began treatment for a major depressive episode 8 months ago. Two months into her treatment she began to experience noticeable symptom improvement, and for the last 5 months, she has been mostly symptom-free, except for persistent cognitive dysfunction. Which of the following statements regarding cognitive dysfunction in depression is most accurate? A. Cognitive dysfunction is one of the most common residual symptoms following recovery B. Cognitive dysfunction can be treated with serotonergic modulation of glutamate transmission C. Both A and B C. Both A and B Cognitive dysfunction is one of the most common residual symptoms of major depressive disorder and can endure longer than mood symptoms following recovery. Moreover, cognitive dysfunction is strongly correlated with physical, mental, and functional disability. Pharmacotherapies used to treat depression that have action on glutamate signaling via serotonergic modulation also show pro-cognitive effects. The prime example is vortioxetine, which has agonist action at 5HT1A, weak partial agonist action at 5HT1B/D, and antagonist action at 5HT3, 5HT1D, 5HT7, and the serotonin transporter. Antagonism of 5HT3 disinhibits glutamate release, while antagonism of 5HT7 enhances release of glutamate release in the prefrontal cortex. In addition, agonism of 5HT1A (full) and 5HT1B (partial) may enhance or suppress glutamate transmission based on neuronal localization. Amir is a 19-year-old patient with depression. He requests treatment with a serotonin norepinephrine reuptake inhibitor (SNRI) because he heard they are more effective than selective serotonin reuptake inhibitors (SSRI). Theoretically, what is the therapeutic advantage of a SNRI over a SSRI? A. Increased norepinephrine via norepinephrine transporter inhibition B. Increased dopamine via norepinephrine transporter inhibition C. Increased norepinephrine and dopamine via norepinephrine transporter inhibition C. Increased norepinephrine and dopamine via noreepinephrine transporter inhibition In addition to boosting serotonin like SSRIs (via inhibition of serotonin reuptake by the serotonin transporter [SERT]), SNRIs can boost norepinephrine by inhibiting reuptake by the norepinephrine transporter (NET). Additionally, in the prefrontal cortex, SNRIs can boost dopamine levels. In prefrontal cortex, SERTs and NETs are present in abundance on serotonin and norepinephrine nerve terminals, respectively, but there are very few dopamine transporters (DATs) on dopamine nerve terminals. Therefore, dopamine action is terminated either by enzymatic degradation or NET. If NET is inhibited by an SNRI then it cannot terminate the action of dopamine and dopamine levels increase in this brain region. A 36-year-old man with major depressive disorder is having lab work done to assess his levels of inflammatory markers. Based on the current evidence regarding inflammation in depression, which of the following results would you most likely suspect for this patient? A. Elevated levels of tumor necrosis factor-alpha (TNF-alpha) B. Reduced levels of interleukin 6 (IL-6) C. Reduced C-reactive protein (CRP) D. Elevated interferon gamma (IFN?) A. Elevated levels of tumor necrosis factor-alpha (TNF-alpha) There is growing evidence that inflammation may play an important role in the pathophysiology of major depression. Clinical studies have shown that depressed patients have significantly higher concentrations of several inflammatory central and peripheral markers, including the pro-inflammatory cytokines TNF-alpha and interleukin-6. Patients with depression also have higher concentrations of C-reactive protein, which is synthesized by the liver in response to pro-inflammatory cytokines, and reduced interferon gamma, which is a proinflammatory cytokine. Furthermore, both cytokines and cytokine inducers can cause symptoms of depression. For example, as many as 50% of patients receiving chronic therapy with the cytokine interferon develop symptoms consistent with idiopathic depression. A 28-year-old man with moderate depression achieves remission after 16 weeks on a therapeutic dose of an antidepressant. According to the neurotrophic hypothesis of depression, which of the following is most likely true of his brain-derived neurotrophic (BDNF) expression before and after his successful treatment? A. BDNF expression was abnormally low while he was depressed, and increased during antidepressant treatment B. BDNF expression was abnormally high while he was depressed, and decreased during antidepressant treatment C. BDNF expression was normal while he was depressed, and was unaffected during antidepressant treatment A. BDNF expression was abnormally low while he was depressed, and increased during antidepressant treatment The neurotrophic hypothesis of depression posits that depression results from decreased neurotrophic support, leading to neuronal atrophy, decreased hippocampal neurogenesis, and that antidepressant treatment blocks or reverses this deficit, thereby reversing atrophy and cell loss. Several meta-analyses have reported deficient BDNF levels in patients with major depressive disorder and an elevation in BDNF following antidepressant treatment. Margaret is a 42-year-old patient with untreated depression. She is reluctant to begin antidepressant treatment due to concerns about treatment-induced weight gain. Which of the following antidepressant treatments is associated with the greatest risk of weight gain? A. Escitalopram B. Fluoxetine C. Mirtazapine D. Vilazodone C. Mirtazapine Meta-analysis has shown that mirtazapine, an alpha 2 antagonist, may cause both short- and long-term weight gain. This is consistent with its secondary pharmacologic properties: mirtazapine is an antagonist at both serotonin 2C and histamine 1 receptors, the combination of which has been proposed to cause weight gain. However, it should be noted that average weight gain with any antidepressant is small, and rather than a widespread effect it may instead be that a small number of individuals experience significant weight gain due to their genetic predispositions and other factors. A 52-year-old man presents to the emergency room with symptoms of hypertensive crisis after an evening dining out with friends. He is currently taking a monoamine oxidase inhibitor (MAOI). Which of the following foods must be avoided by patients taking MAOIs? A. Fresh fish B. Aged cheese C. Bananas D. Bottled beer B. Aged cheese Aged cheeses in general have high tyramine content and must be avoided when a patient is taking an MAOI. Tyramine content in food can instigate a hypertensive crisis in patients taking MAOIs. Meals considered to contain a high level of tyramine content generally include 40 mg of tyramine. Foods to AVOID* Dried, aged, smoked, fermented, spoiled, or improperly stored meat, poultry, and fish Broad bean pods Aged cheeses Tap and unpasteurized beer Marmite Soy products/tofu Banana peel Sauerkraut, kimchee Tyramine-containing nutritional supplements *Not necessary for 6-mg transdermal or low-dose oral selegiline Foods ALLOWED Fresh or processed meat, poultry, and fish All other vegetables Processed cheese slices, cottage cheese, ricotta cheese, cream cheese, yogurt Bottled or canned beer and alcohol Brewer's and baker's yeast Peanuts Bananas, avocados, raspberries A 48-year-old woman with a history of treatment-resistant depression is currently taking duloxetine 60 mg/day with partial response as well as trazodone 50 mg/day for insomnia. Despite reporting strict adherence to her medication dosages, she states that she feels empty and useless, and she admits to having thoughts of death. She states that she does not have plans to kill herself because it would harm her family and pets. Her clinician decides to try tranylcypromine, a monoamine oxidase inhibitor (MAOI) and one of the few agents that she has not yet tried. Which of the patient's current medications MUST you discontinue BEFORE initiating tranylcypromine? A. Duloxetine B. Trazodone C. Both duloxetine and trazodone D. Neither duloxetine nor trazodone A. Duloxetine Duloxetine is a serotonin norepinephrine reuptake inhibitor. Inhibition of the serotonin transporter leads to increased synaptic availability of serotonin. Similarly, inhibition of MAO leads to increased serotonin levels. In combination, these two mechanisms can cause excessive stimulation of postsynaptic serotonin receptors, which has the potential to cause a fatal "serotonin syndrome" or "serotonin toxicity. Because of the risk of serotonin toxicity, complete washout of duloxetine is necessary before starting an MAOI. Duloxetine must be down-titrated as tolerated, after which one must wait five half-lives of duloxetine (at least 3–4 days) before initiating the MAOI. A 56-year-old male patient with major depression is brought to the ER with cardiac arrhythmia and possible cardiac arrest. While at the hospital, he suffers a seizure. His wife states that he may have ingested an increased dose of his medication. Which of the following is most likely responsible for this apparent overdose reaction? A. Atomoxetine B. Clomipramine C. Fluvoxamine D. Venlafaxine B. Clomipramine Clomipramine, a tricyclic antidepressant (TCA), may be most likely to cause these effects in overdose. TCAs block voltage-sensitive sodium channels (VSSCs) in both the brain and the heart. This action is weak at therapeutic doses, but in overdose may lead to coma, seizures, and cardiac arrhythmia, and may even prove fatal. A 65-year-old patient on theophylline for chronic obstructive pulmonary disease (COPD) and fluvoxamine for recurring depressive episodes required a decreased dose of theophylline due to increased blood levels of the drug. Which of the following pharmacokinetic properties may be responsible for this? A. Inhibition of CYP450 1A2 by fluvoxamine B. Inhibition of CYP450 2D6 by fluvoxamine C. Inhibition of CYP450 3A4 by fluvoxamine A. Inhibition of CYP450 1A2 by fluvoxamine Fluvoxamine is a strong inhibitor of CYP450 1A2. Theophylline is metabolized in part by CYP450 1A2, and thus strong inhibition of this enzyme by fluvoxamine may require a dose reduction of theophylline if the two are given concomitantly, so as to avoid increased blood levels of the drug. Mike is a 31-year-old patient with major depressive disorder (MDD) who has experienced some response with the serotonin and norepinephrine reuptake inhibitor (SNRI) venlafaxine XR (150 mg/day). However, the patient acknowledges that he and his wife have been having relationship problems because of his poor libido. The patient experienced this problem prior to being diagnosed and treated for MDD, but he has found that the venlafaxine has worsened this troubling symptom despite the fact that his mood has improved. He asks if there is a way to both prevent worsening of his mood and avoid this side effect. Which of the following treatment strategies would you recommend for this patient? A. Decrease venlafaxine dose B. Switch to a norepinephrine and dopamine reuptake inhibitor (NDRI) C. Switch to a selective serotonin reuptake inhibitor (SSRI) D. Augment current venlafaxine dose with a phosphodiesterase-5 (e.g., sildenafil) B. Switch to a norepinephrine and dopamine reuptake inhibitor (NDRI) Pharmacological agents that increase dopaminergic neurotransmission and/or decrease serotonergic neurotransmission (e.g., serotonin 1A agonists or serotonin 2 antagonists) are often effective in ameliorating sexual dysfunction. Switching to an NDRI such as bupropion would be expected to increase dopaminergic neurotransmission and improve sexual function. Given that the patient experienced libido problems prior to treatment with the SNRI, and that the problem has worsened on treatment with the SNRI, it makes sense to switch to bupropion. Augmentation with bupropion to address sexual dysfunction, although commonly done in clinical practice, is not actually supported by randomized controlled studies. In addition to treating depressed mood, preclinical data indicate that serotonin 5HT3 receptor antagonists may have clinical utility as adjunct treatment for which symptoms? A. Cognitive symptoms B. Irritability C. Psychomotor retardation D. Sleep problems A. Cognitive symptoms Serotonergic neurons synapse with noradrenergic neurons, cholinergic neurons, and GABAergic interneurons, all of which contain serotonin 5HT3 receptors. When serotonin is released, it binds to 5HT3 receptors on GABAergic neurons, which release GABA onto noradrenergic, glutamatergic, and cholinergic neurons, thus reducing release of norepinephrine, glutamate, and acetylcholine, respectively. In addition, serotonin may bind to 5HT3 receptors on noradrenergic and cholinergic neurons, further reducing release of those neurotransmitters. This may theoretically contribute to symptoms of depressed mood and impaired cognition. Therefore, treatment with 5HT3 receptor antagonists improve depressed mood and cognitive problems. A 36-year-old patient has only partially responded to his second monotherapy with a first-line antidepressant. Which of the following has the best evidence of efficacy for augmenting antidepressants in patients with inadequate response? A. Adding an atypical antipsychotic B. Adding buspirone C. Adding a stimulant A. Adding an atypical antipsychotic Atypical antipsychotics have been studied as adjuncts to selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitor (SNRIs), with approvals for aripiprazole, brexpiprazole, quetiapine XR, and olanzapine (in combination with fluoxetine). Overall, most studies of atypical antipsychotics show a benefit of combination treatment over monotherapy, although effect sizes have been modest. Although atypical antipsychotics have the best evidence of efficacy for augmenting antidepressants in patients with inadequate response, their adverse event profiles may still put them later in the treatment algorithm. Miryam is a 24-year-old woman with a major depressive episode that is only partially responding to treatment with a selective serotonin reuptake inhibitor. In particular, she continues to display reduced positive affect. She is prescribed adjunctive bupropion to manage this symptom. Through which mechanism(s) does bupropion theoretically ameliorate reduced positive affect? A. Inhibition of the serotonin transporter B. Inhibition of the dopamine transporter C. Inhibition of the norepinephrine transporter D. A and B E. A and C F. B and C F. B and C (Inhibition of the dopamine and norepinephrine transporter) Bupropion has weak reuptake blocking properties for dopamine (dopamine transporter [DAT] inhibition), and for norepinephrine (norepinephrine transporter [NET] inhibition). Human positron emission tomography scans suggest that as little as 10–15% and perhaps no more than 20–30% of striatal DATs may be occupied at therapeutic doses of bupropion. NET occupancy would be expected to be in this same range. Wei is a 33-year-old patient with major depressive disorder beginning at age 17; his current depressive episode has persisted for 10 months. His treatment history includes fluoxetine, nefazodone, venlafaxine, mirtazapine, agomelatine, lithium augmentation, and electroconvulsive therapy. Each of these treatments produced moderate but transient response; therefore, he will begin ketamine infusions to treat his treatment-resistant depression. Which of the following statements about ketamine treatment is true? A. The strongest evidence for the efficacy of ketamine is in bipolar depression B. Repeated dosing extends the duration of ketamine effects C. High frequency ketamine administration is recommended D. A history of antidepressant treatment is not necessary to start ketamine treatment B. Repeated dosing extends the duration of ketamine effects Studies suggest that repeated dosing may extend the duration of ketamine effects. Ketamine administration of 2–3 times per week over 2–3 weeks, followed by a taper period and/or continued treatments may be most effective. A patient with depression is prescribed mirtazapine as adjunctive treatment to venlafaxine, a serotonin-norepinephrine reuptake inhibitor. Mirtazapine acts on alpha 2 receptors to produce what effect? A. Disinhibition of norepinephrine and serotonin release via alpha 2 agonism B. Disinhibition of norepinephrine and dopamine release via alpha 2 agonism C. Disinhibition of norepinephrine and serotonin release via alpha 2 antagonism D. Disinhibition of norepinephrine and dopamine release via alpha 2 antagonism C. Disinhibition of norepinephrine and serotonin release via alpha 2 antagonism Norepinephrine turns off its own release via alpha 2 presynaptic receptors; therefore, alpha 2 antagonism with mirtazapine facilitates disinhibition of norepinephrine. Furthermore, norepinephrine migrating from a norepinephrine terminal can also turn off serotonin release via alpha 2 presynaptic heteroreceptors on serotonin neurons. Therefore, alpha 2 antagonists like mirtazapine can have a dual effect on facilitating the release of both norepinephrine and serotonin. A 34-year-old man with depression characterized by depressed mood, sleep difficulties, and concentration problems has not responded well to a selective serotonin reuptake inhibitor (SSRI) or a serotonin norepinephrine reuptake inhibitor (SNRI). His clinician elects to switch him to vortioxetine, which has prominent 5HT7 antagonism. What may be a primary function of these receptors? A. Regulation of serotonin-acetylcholine interactions B. Regulation of serotonin-dopamine interactions C. Regulation of serotonin-glutamate interactions D. Regulation of serotonin-norepinephrine interactions C. Regulation of serotonin-glutamate interactions 5HT7 receptors are postsynaptic G protein-linked receptors. They are localized in the cortex, hippocampus, hypothalamus, thalamus, and brainstem raphe nuclei, where they regulate mood, circadian rhythms, sleep, learning, and memory. A major function of these receptors may be to regulate serotonin-glutamate interactions. A 32-year-old woman with major depressive disorder has been taking a selective serotonin reuptake inhibitor (SSRI) with good response for months. She presents now with complaints that she feels numb, and that even when she's sad she can't cry. Her clinician is considering reducing the dose of her SSRI in an effort to alleviate this problem. Is this a reasonable option? A. Yes, data suggest that SSRI-induced indifference is dose-dependent and can be alleviated by reducing the dose B. No, although data suggest that SSRI-induced indifference is dose-dependent, patients who develop this side effect generally require switch to a different medication C. No, SSRI-induced indifference is not dose-dependent and thus cannot be alleviated by reducing the dose A. Yes, data suggest that SSRI-induced indifference is dose-dependent and can be alleviated by reducing the dose Apathy and emotional blunting can be symptoms of depression, but they are also side effects associated with selective serotonin reuptake inhibitors (SSRIs). These symptoms—termed "SSRI-induced indifference"—are under-recognized but can be very distressing for patients. They are theoretically due to an increase in serotonin levels and a consequent reduction of dopamine release. The first recommended strategy for addressing SSRI-induced indifference is to lower the SSRI dose, if feasible. Additional options include adding an augmenting agent or switching to an antidepressant in another class. A 31-year-old woman is diagnosed with severe postpartum depression 3 weeks after giving birth. Treatment with brexanolone, a positive allosteric modulator of gamma amino butyric acid (GABA) at the GABA-A receptor, ameliorated her symptoms. GABA has more recently been implicated in the neurobiology of depression. Theoretically, individuals with depression may display a lack of normal GABAergic tonic inhibition via: A. Postsynaptic benzodiazepine-sensitive GABA-A receptors B. Extrasynaptic benzodiazepine-insensitive GABA-A receptor C. Both A and B B. Extrasynaptic benzodiazepine-insensitive GABA-A receptor Extrasynaptic benzodiazepine-insensitive GABA-A receptor subtypes are thought to mediate tonic inhibition. Tonic inhibition may be regulated by the ambient levels of extracellular GABA molecules that have escaped presynaptic reuptake and enzymatic destruction and persist between neurotransmissions and is boosted by allosteric modulation at these sites. Thus, tonic inhibition is thought to set the overall tone and excitability of the postsynaptic neuron, and to be important for certain regulatory events such as the frequency of neuronal discharge in response to excitatory inputs. Since neuroactive steroids have antidepressant properties, this has led to the proposal that some depressed patients may have a lack of normal tonic inhibition, and thus too much excitability in some brain circuits. Indeed, in the case of postpartum depression, it may be potentially explainable on the basis that pregnant women have high circulating and presumably brain levels of neuroactive steroids. When they deliver, there is a precipitous decline in circulating neuroactive steroid levels, hypothetically triggering the sudden onset of a major depressive episode when tonic inhibition is lost. Restoring neuroactive steroid levels—and tonic inhibition—via brexanolone may be enough for the patient to respond by reversing their depression and then having some additional time to accommodate to the lower levels of neuroactive steroids postpartum. A 27-year-old patient who has been taking a selective serotonin reuptake inhibitor (SSRI) for depression for the last 2 years has just found out that she is 12 weeks pregnant. Cumulative data for SSRI use in pregnancy have established a small but clinically significant increase in absolute risk of: A. Cardiovascular malformations B. Persistent pulmonary hypertension C. Autism spectrum disorder D. All of the above E. None of the above E. None of the above Large cohort and case-controlled studies, as well as meta-analyses indicate there is no meaningful association between SSRI use during early pregnancy and risk for cardiovascular malformation, persistent pulmonary hypertension, or autism spectrum disorder in offspring. Sasha is a 58-year-old patient with a history of depression who has been prescribed agomelatine. At present, she is relatively free of depressive symptoms, likely due in part to binding of agomelatine to what receptors in the suprachiasmatic nucleus? A. Melatonin receptors B. Serotonin 2C receptors C. Melatonin and serotonin 2C receptors C. Melatonin and serotonin 2C receptors Agomelatine is both a melatonin M1 and M2 receptor agonist and a serotonin 5HT2C receptor antagonist. This unique receptor profile gives agomelatine the ability to address impairments in neurotransmission as well as circadian rhythm dysfunction. First, agomelatine can modulate circadian rhythms through its agonist actions at melatonin receptors. Melatonin is normally released from the pineal gland in response to environmental cues. It then acts on the suprachiasmatic nucleus, the location of the master clock, to reset circadian rhythms. Thus, as an agonist at melatonin receptors, agomelatine likewise regulates the molecular clock and can resynchronize circadian rhythms that are disturbed in depression. Second, agomelatine affects neurotransmission by blocking 5HT2C receptors. Normally, serotonin excites GABA interneurons by stimulating 5HT2C receptors, which increases the release of the inhibitory neurotransmitter GABA. GABA can then bind to GABA-A receptors on noradrenergic and dopaminergic neurons. Since GABA is inhibitory, it will prevent these neurons from releasing norepinephrine and dopamine in the prefrontal cortex. As a 5HT2C receptor antagonist, agomelatine blocks serotonin from binding to GABA interneurons. This leads to disinhibition of monoaminergic neurons and increased norepinephrine and dopamine in the prefrontal cortex, which could potentially improve mood and cognition. A patient presents to a new clinician with a major depressive episode. In addition to taking the patient's history, the two most useful factors for determining if a current depressive episode is indicative of unipolar or bipolar depression are: A. Family history and input from someone close to the patient B. Input from someone close to the patient and specific symptoms of the current episode C. Specific symptoms of the current episode and patient insight D. Patient insight and family history A. Family history and input from someone close to the patient Family history of bipolar disorders is arguably the most robust and reliable risk factor for bipolar disorder. Although most patients with bipolar disorder do not have a family history of bipolar disorder, individuals with a first-degree relative with bipolar disorder are at an 8-10 times greater risk of developing bipolar disorder compared to the general population. Obtaining additional information from a close outside informant, such as a parent or spouse, is also quite useful, as patients tend to under-report their hypomanic symptoms. Under-reporting may be due to patients not recalling important details of their history with enough accuracy or not viewing (hypo)manic symptoms as being problematic. April is a 14-year-old patient recently diagnosed with moderate-to-severe major depressive disorder (MDD). She endorses passive suicidal ideation, but no specific plan or intention for suicide attempt. She denies any suicidal ideation or attempts prior to her current depressive episode. In addition to beginning cognitive behavioral therapy (CBT), which pharmacotherapy option would be best suited for treating her depressive episode? A. Imipramine B. Bupropion C. Fluoxetine D. No pharmacotherapy should be initiated C. Fluoxetine Fluoxetine, a selective serotonin reuptake inhibitor (SSRI), has a good evidence base for efficacy treating pediatric MDD and is one of only two antidepressants with FDA approval for pediatric MDD. Escitalopram, also an SSRI, is the second antidepressant approved for treating pediatric MDD. There is no strong evidence to suggest that any particular SSRI is more effective than any other for pediatric MDD. However, both the National Institute of Clinical Excellence (NICE) and the American Academy of Child and Adolescent Psychiatry (AACAP) recommend evidence-based psychotherapy, such as CBT, and/or fluoxetine to treat moderate-to-severe depression in adolescence. The hypothesis that the therapeutic effects of antidepressants are due to downstream changes in neuroplasticity is consistent with the fact that clinical improvement with antidepressants is typically delayed by several weeks. The downstream effects of monoamine antidepressants include: A. Decreased AMPA receptor expression, decreased NMDA receptor expression, decreased glutamate B. Increased AMPA receptor expression, decreased NMDA receptor expression, decreased glutamate C. Decreased AMPA receptor expression, increased NMDA receptor expression, decreased glutamate D. Increased AMPA receptor expression, decreased NMDA receptor expression, increased glutamate B. Increased AMPA receptor expression, decreased NMDA receptor expression, decreased glutamate There is increasing evidence, the underlying mechanism of antidepressant treatment may not be alterations in the levels of monoamines themselves, but rather changes in the downstream molecular events and neuroplasticity triggered by those monoamines. Monoaminergic antidepressants likely exert their therapeutic effects by influencing downstream signaling, such as increased a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, or AMPA receptor expression, decreased N-Methyl-D-aspartate, or NMDA receptor expression, and decreased glutamate, suggesting agents with direct activity at these downstream targets may lead to faster treatment response. Antidepressant treatments may modify the AMPA:NMDA receptor ratio, resulting in downregulated NMDA receptors, and increased AMPA receptors.