|
| A) | is the same thing as a phobia. | ||
| B) | does not prevent patients from seeking dental care. | ||
| C) | is associated with a more immediate and real stressor. | ||
| D) | is associated with a vague and general feeling of being powerless and unable to cope. |
It is difficult to estimate the prevalence of dental anxiety and dental phobia. These conditions are distinct from fear, which is defined as a feeling associated with a more immediate and real stressor, such as immediately prior to an injection of a local anesthetic. Anxiety, on the other hand, is a state in which an individual experiences a vague, generalized feeling of powerlessness and inability to cope with a real or imaginary stressor. This can lead to physical signs, such as sweating, trembling, and rapid breathing, and can culminate in a panic attack. A patient who has a dental appointment in the future may dwell upon this well in advance of the appointment date. Patients may imagine an exaggerated length or gauge of an anesthetic needle, be resigned that there will be intense pain upon the injection, or be unduly concerned that an untoward systemic reaction will occur upon injection of a local anesthetic. These are patients for whom anxiolytic medications and protocol are beneficial. For patients with anxiety about untoward events, preparing them for the possibility of short-term systemic effects (e.g., transient tachycardia) as a result of the inclusion of the vasoconstrictor epinephrine may help ease fears and prevent a panic attack.
| A) | are unaware that their fears are irrational. | ||
| B) | frequently skip or cancel dental appointments. | ||
| C) | do not usually experience insomnia before dental points. | ||
| D) | become more relaxed as their dental appointment date draws near. |
When severe anxiety is concentrated upon a singular concern, such as dental treatment, out of proportion with the real risks and dangers involved, this is called a phobic disorder or a phobia [1]. Patients with a dental phobia are aware that their fears may be irrational, but they lack the ability to change their reaction. These patients often exhibit classic avoidance behavior and will go to extremes to avoid dental appointments. Insomnia before dental appointments and an intense state of nervousness that increases as the appointment date draws near (especially while the patient is waiting in the reception area) can occur [2]. These difficulties often prompt patients to skip or cancel appointments, which can result in progressive dental deterioration. Patients with concomitant psychological problems, such as agoraphobia, behavior disorders, social phobias, and substance abuse problems, are more prone to a higher magnitude of dental anxiety that can evolve into dental phobia [3]. These patients generally require oral anxiolytic medications and possibly supplemental nitrous oxide oxygen inhalation for most dental treatment. Intramuscular or intravenous agents that produce deeper sedation or even general anesthesia may be required for surgical procedures or for more complex dental treatment. Clinicians and those who administer these medications must be prepared to treat adverse drug reactions, including allergic reactions, excessive respiratory depression, and cardiac arrest. Educational and preparatory requirements for the use of these medications vary by state. Any medication administered must be compatible with the patient's medical history.
| A) | The patient has witnessed a traumatic event. | ||
| B) | The patient has had a negative dental experience. | ||
| C) | The patient always has pre-existing psychiatric problems. | ||
| D) | The patient has heard of painful or unsatisfactory dental experiences from other dental patients. |
Cognition and perception, consciously or subconsciously, are the mental processes through which a traumatic dental event (real or anticipated) becomes a psychological and behavioral concern. A three-part model has been established to define the primary sources of dental fear. This model posits that patients are fearful of dental treatment because they have had a negative dental experience themselves, have heard accounts from other people who have had an unsatisfactory or painful dental experience, or have witnessed a traumatic event [4]. However, anxiety or phobia develops, these patients usually share one or more of these common concerns, which initiates and maintains the reaction.
| A) | Running behind schedule and keeping the patient waiting for a long time. | ||
| B) | Beginning treatment promptly when they are seated in the dental operatory. | ||
| C) | Taking the time to discuss the patient's concerns and fears about their treatment. | ||
| D) | Using properly maintained equipment that increases efficiency and decreases treatment time. |
The anxiety, fear, and phobias that affect dental patients can be considered significant sources of stress. These patients may have issues that have caused chronic stress, which can exacerbate to acute stress during dental appointments. As discussed, two of the most common dental appointment-related stressors are the sight of anesthetic needles or injection itself and the sight and sound of a high-speed hand piece. Simple techniques, such as keeping the anesthetic syringe from view, the use of topical anesthetics before injections, manual vibration of the tissue that is to be anesthetized, and a proficient injection technique, can contribute to the patient's ability to undergo injection procedures successfully. Because high-speed hand pieces are used for longer periods than anesthetic needles and the sounds cannot be avoided, different techniques must be employed to allay patients' concerns. Portable listening devices with headphones may be useful to mask the sounds of the high-speed hand piece. The hand piece that produces the least amount of sound should be selected. Proper maintenance and the use of new burs for each procedure increase operator efficiency and decrease length of the procedure.
Beyond the realm of instruments, time spent waiting in the reception area or in an operatory can be a significant stressor for patients who are anxious or fearful about dental treatment. Effective practice management techniques should be used to minimize the waiting time for patients. When patients are seated in the dental operatory, the dentist and assistant should begin treatment promptly rather than leaving the patient waiting alone. This initial time spent directly with the patient can do much to allay fears about dental treatment. The initial patient meeting should also feature a dialogue to identify any issues relative to dental treatment that the patient considers stressful. Some will require sedation or anxiolytic techniques.
| A) | should be used for pediatric patients only. | ||
| B) | compliments the patient for their cooperation during dental procedures. | ||
| C) | uses videos or models to demonstrate the procedure scheduled for the patient. | ||
| D) | does not allow the patient time to seek clarification about their scheduled treatment. |
The tell-show-do technique was initially developed for the treatment of pediatric patients; however, it can be used successfully for the treatment of fearful and anxious adult dental patients as well. The first step is to provide a verbal explanation of the proposed dental treatment in terms the patient can understand. Technical dental terms beyond the patient's comprehension will only serve to alienate the patient and perpetuate the fear and anxiety. The second step is to use a video or model to demonstrate the scheduled dental treatment. Clinicians should pause after each step to allow the patient ample opportunity to ask questions before proceeding. The final step is to perform the actual procedure [6].
| A) | gradual exposure to the stressor. | ||
| B) | slow breathing through the nose. | ||
| C) | distraction using music or television. | ||
| D) | the conscious tensing and relaxing of a specific group of muscles. |
Progressive muscle relaxation consists of the conscious tensing and subsequent relaxing of a specific group of muscles. This practice can involve all of the major muscle groups and is designed to create an awareness of the different feelings associated with muscles that are tensed and those that are relaxed. Fear, anxiety, or phobia about dental treatment often induces muscular tension, and the emotional reactions can be decreased when the patient makes a conscious effort to relax the muscles [9].
| A) | has a half-life of 40 to 48 hours. | ||
| B) | is safe to use for pregnant patients. | ||
| C) | does not produce any active metabolites. | ||
| D) | has 50% bioavailability after oral administration. |
Diazepam has anxiolytic, sedative, skeletal muscle relaxant, amnestic, and hypnotic properties, which make it a useful adjunct for the treatment of the anxious or fearful dental patient [12]. It has a rapid onset of action and more than 90% bioavailability after oral administration. Peak plasma levels occur within 15 to 150 minutes after oral administration [13]. It is available in 2-mg, 5-mg, and 10-mg tablets. When diazepam is used for anxiolytic purposes related to dental treatment, one tablet can be administered the evening before treatment and the second tablet administered one hour before the appointment. The use of diazepam the evening before an appointment can decrease the patient's anxiety and induce deeper and more restful sleep. Dosing will depend on the patient's medical history, weight, degree of anxiety, and the concurrent use of other medications.
As with the use of any medication, there are precautions and considerations when diazepam is used, even for the short-term relief of anxiety. Patients should be counseled to refrain from alcohol, other sedative agents, and narcotic analgesics while using diazepam, as these combinations can potentiate respiratory depression. Many medications can prolong the effect of diazepam by decreasing the rate at which it is eliminated systemically, including antifungal medications (e.g., ketoconazole, itraconazole) and the macrolide antibiotic erythromycin [14].
The half-life of oral diazepam can range from 40 to 48 hours in adults, and its metabolism produces an active metabolite known as desmethyldiazepam, which has a half-life of 100 hours [13]. The half-lives of each of these substances are prolonged in the elderly and those with impaired hepatic function. Because the half-life and subsequent sedative effect can vary, patients should refrain from driving or being in any situation in which sedation or drowsiness could place themselves or others in danger. Patients who have used diazepam for anxiolytic purposes should have a responsible adult drive them to and from the dental appointment.
Diazepam has been assigned pregnancy category D by the U.S. Food and Drug Administration, so its use is contraindicated in pregnant patients or those who are breastfeeding. Diazepam is excreted in human milk, and nursing infants can become sedated and lethargic. The American Academy of Pediatrics considers the effects of diazepam upon nursing infants unknown, but of possible concern [13].
| A) | It is not found in human milk. | ||
| B) | If an antibiotic is needed, erythromycin is the best choice. | ||
| C) | Its half-life is shortened in elderly patients and in those with impaired hepatic function. | ||
| D) | Antifungal medications such as ketoconazole and itraconazole should not be used concurrently. |
Diazepam has anxiolytic, sedative, skeletal muscle relaxant, amnestic, and hypnotic properties, which make it a useful adjunct for the treatment of the anxious or fearful dental patient [12]. It has a rapid onset of action and more than 90% bioavailability after oral administration. Peak plasma levels occur within 15 to 150 minutes after oral administration [13]. It is available in 2-mg, 5-mg, and 10-mg tablets. When diazepam is used for anxiolytic purposes related to dental treatment, one tablet can be administered the evening before treatment and the second tablet administered one hour before the appointment. The use of diazepam the evening before an appointment can decrease the patient's anxiety and induce deeper and more restful sleep. Dosing will depend on the patient's medical history, weight, degree of anxiety, and the concurrent use of other medications.
As with the use of any medication, there are precautions and considerations when diazepam is used, even for the short-term relief of anxiety. Patients should be counseled to refrain from alcohol, other sedative agents, and narcotic analgesics while using diazepam, as these combinations can potentiate respiratory depression. Many medications can prolong the effect of diazepam by decreasing the rate at which it is eliminated systemically, including antifungal medications (e.g., ketoconazole, itraconazole) and the macrolide antibiotic erythromycin [14].
The half-life of oral diazepam can range from 40 to 48 hours in adults, and its metabolism produces an active metabolite known as desmethyldiazepam, which has a half-life of 100 hours [13]. The half-lives of each of these substances are prolonged in the elderly and those with impaired hepatic function. Because the half-life and subsequent sedative effect can vary, patients should refrain from driving or being in any situation in which sedation or drowsiness could place themselves or others in danger. Patients who have used diazepam for anxiolytic purposes should have a responsible adult drive them to and from the dental appointment.
Diazepam has been assigned pregnancy category D by the U.S. Food and Drug Administration, so its use is contraindicated in pregnant patients or those who are breastfeeding. Diazepam is excreted in human milk, and nursing infants can become sedated and lethargic. The American Academy of Pediatrics considers the effects of diazepam upon nursing infants unknown, but of possible concern [13].
| A) | It has a slow onset of action. | ||
| B) | It produces active metabolites. | ||
| C) | It has a half-life of about 12 to 15 hours. | ||
| D) | Its use as dental preprocedure oral sedation is off-label. |
Triazolam is another benzodiazepine with anxiolytic, amnesic, sedative, and muscle relaxant qualities. Triazolam is approved for the treatment of insomnia, and its use as dental preprocedure oral sedation is off-label [13]. Unlike diazepam, triazolam does not generate active metabolites, so its half-life ranges from 1.5 to 5.5 hours [13]. When used to treat dental anxiety, a dose of 0.125–0.25 mg is taken the evening before and 0.125–0.25 mg is taken one hour before the appointment. It has a rapid onset of action (15 to 30 minutes), with a time to peak less than two hours and a duration of action of six to seven hours [13]. The short half-life of triazolam drastically reduces the duration of sedation as compared to the prolonged sedative effect of diazepam. However, patients still must have a responsible adult drive them to and from the appointment.
| A) | has a shorter half-life than triazolam. | ||
| B) | is metabolized into pharmacologically active metabolites. | ||
| C) | has a bioavailability of about 43% after oral administration. | ||
| D) | taken concurrently with alcoholic beverages can produce fatal respiratory depression. |
With a half-life of between 12 to 18 hours in adults, the sedative, anxiolytic, and amnestic effects of lorazepam, another benzodiazepine, are intermediate compared to diazepam and triazolam [13,19]. The dental dosage can range from 1 mg to 10 mg per day in two to three divided doses, and is dependent on the patient's medical history, weight, and simultaneous use of any other medications. It has a bioavailability of 90% after oral administration, and it is metabolized into pharmacologically inactive metabolites [13]. The peak effects of lorazepam occur approximately two hours after oral administration, so its use as a pretreatment anxiolytic medication should be timed accordingly [13]. The usual dose for preprocedural anxiety is 1–2 mg one hour before the procedure. The sedative effects of lorazepam will linger for several hours after the peak serum levels have been attained, so a responsible adult must transport this patient to and from the appointment.
Patients with alcohol dependency problems should not use this medication, as the combination of alcohol and lorazepam can lead to fatal respiratory depression. The simultaneous use of other sedative medications or narcotic analgesics with lorazepam can also cause respiratory depression. Lorazepam is assigned pregnancy category D, and its use should be avoided in pregnant or breastfeeding patients.
| A) | 30 seconds. | ||
| B) | 5 minutes or less. | ||
| C) | 30 minutes. | ||
| D) | 1 hour or more. |
The route of administration is inhalation via a mask secured to the patient's nose. The concentration of nitrous oxide for dental sedation and analgesia should be 25% to 50% nitrous oxide with oxygen [13,22]. Onset of action can occur in as quickly as 30 seconds, with the peak effects seen in five minutes or less. Unlike the benzodiazepine medications, nitrous oxide is not metabolized in the body. It is eliminated via respiration within minutes after 100% oxygen is inhaled at the conclusion of the dental procedure [25].
| A) | An anxious patient | ||
| B) | A patient with emphysema | ||
| C) | A patient with pneumothorax | ||
| D) | A patient with recent middle ear surgery |
Nitrous oxide is generally well tolerated; however, some patients may experience nausea, vomiting, or central nervous system depression. Absolute contraindications to the use of nitrous oxide include emphysema, pneumothorax, recent middle ear surgery, and the presence of an air embolus. Relative contraindications include pulmonary hypertension, first-trimester pregnancy, and a high risk of nausea or vomiting [26]. Long-term exposure to nitrous oxide can lead to neurotoxicity, female infertility, numbness, and decreased mental acuity. These issues are of more concern to the dental staff, who may regularly inhale trace amounts of nitrous oxide as it is exhaled. The appropriate use of scavenger systems can drastically reduce this occurrence. During procedures, patients should restrict speaking to that which is germane to the dental procedure. State regulations vary as to the degree of training required for dentists using nitrous oxide.
| A) | Deeply sedated patients may have difficulty in maintaining a patent airway. | ||
| B) | Lightly sedated patients can independently and continuously maintain a patent airway. | ||
| C) | Clinicians and their staff must be prepared to respond to emergencies caused by sedation. | ||
| D) | All of the above |
The combination of nitrous oxide and a benzodiazepine can produce varying levels of sedation (i.e., light, moderate, or deep) depending on the dose and clearance and can even ultimately produce a state of general anesthesia. Lightly sedated patients have a minimally depressed level of consciousness, can independently and continuously maintain their airway, and will respond in a normal fashion to verbal commands and tactile stimulation. Patients who are moderately sedated need more tactile stimulation or a higher level of verbal stimulation to respond but can still maintain a patent airway on their own. Finally, deep sedation is a state in which patients cannot easily be aroused and may begin to experience difficulty independently maintaining a patent airway [27].
Clinicians should only sedate dental patients to a degree in which airway maintenance is not compromised. If sedation produces an airway that is not patent, the clinician must be able to re-establish airway patency and provide immediate emergency care. Again, it is vital to consider one's level of expertise in the principles of sedation and ability to respond to respiratory compromise and cardiovascular collapse before attempting to administer sedation.
| A) | Women comprise about 90% to 95% of all cases. | ||
| B) | It is not associated with serious medical consequences. | ||
| C) | The teeth and oral mucosa are unaffected by this disease process. | ||
| D) | Patients with anorexia usually have a normal body weight and appearance. |
Patients with anorexia nervosa have an extreme obsession with their body weight and the restriction of food intake. Women comprise 90% to 95% of anorexia cases, and it is estimated that 1% of all women suffer from anorexia in their lifetime, with the onset usually occurring during the adolescent years [22,28]. Anorexic patients often view themselves as overweight even though most are 15% or more below ideal weight.
Patients with anorexia go to extreme measures to lose weight and prevent weight gain. The most common mechanism is restricting or halting eating. Other patients may exercise excessively. Some anorexic patients will use laxatives, enemas, or self-induced vomiting as a supplemental means to control their weight. These behaviors can lead to severe acute and chronic medical problems. Patients may appear emaciated but refuse to acknowledge the serious nature of the problem and do not consider the potential medical consequences of the disease.
Women who are anorexic often have irregular menstrual cycles. The skin can become dry and thin and at greater risk for traumatic injury. The restriction of caloric intake can stunt the physical and mental development of children and adolescents, and cognitive damage is possible in all patients. Problems with the cardiovascular system, including hypotension, bradycardia, and cardiac arrhythmias, are very common. Self-induced vomiting and use of laxatives can cause a severe disturbance in the body's mineral and electrolyte balance, and a drastic reduction of the minerals potassium, sodium, and calcium can interfere with the conduction of nerve impulses and the contraction of smooth, skeletal, and cardiac muscle. Failure of multiple organs and systems can lead to death. As part of the disease process, repeated episodes of self-induced vomiting can cause ulceration of the esophageal lining, with the subsequent development of esophageal varicosities and bleeding. Oral effects are generally limited to those caused by extreme starvation and malnutrition.
| A) | appears emaciated. | ||
| B) | has a recurrent practice of binge eating. | ||
| C) | has a body weight that is at least 15% below normal. | ||
| D) | has no risk of serious medical or dental consequences from this disease process. |
Patients with bulimia nervosa tend to lack the emaciated appearance of patients with anorexia nervosa; their body weight and appearance often appear normal. Bulimia nervosa features recurrent binge eating, in which a large quantity of food is consumed in a short time, followed by purging (e.g., self-induced vomiting, use of diuretics, laxatives, or enemas) to compensate for the excessive overeating. During binging episodes, the bulimic patient experiences a loss of control over the quantity and variety of food consumed [29]. The practice of binge eating and purging must continue at least twice a week for three months for a diagnosis of bulimia nervosa to be made [14].
The teeth and the oral mucosa of bulimic patients can undergo damage as the recurrent regurgitation of highly acidic gastric contents can induce pathologic change in both. In addition, the mucosa of the soft palate and the anterior pharyngeal area can be traumatized when fingers or objects are inserted to induce vomiting. Healing of these areas may be prolonged by the physical and chemical assault associated with this repetitious behavior. Ulcerated areas of the oral mucosa may lead to local or regional oral infections. The virulence of infections can be exacerbated when the altered nutritional status of these patients compromises their immune response.
| A) | is not seen in patients with bulimia nervosa. | ||
| B) | develops from repetitive tooth-to-tooth contact. | ||
| C) | is caused by an abrasive force such as overzealous tooth brushing. | ||
| D) | is caused by repeated contact of gastric hydrochloric acid with the teeth. |
Enamel is the hardest substance in the human body, but the repeated exposure to the hydrochloric acid in regurgitated gastric contents over an extended period of time can lead to a unique pattern of enamel erosion called perimylolysis (Image 1). Perimylolysis features the loss of enamel on the lingual, occlusal, and incisal surfaces of the teeth. As opposed to attrition, which is the loss of enamel from repetitive tooth-to-tooth contact or abrasion via an external source (e.g., excessive or overly forceful tooth brushing), the gradual dissolution of the enamel matrix in patients with bulimia nervosa leaves a glossy, smooth surface, most commonly on the lingual surfaces of the maxillary anterior teeth [31]. Any lost enamel cannot be regenerated. The underlying matrix of dentin is then exposed; it will wear faster than enamel and is more prone to caries. While enamel is devoid of any neural element, dentin contains dentinal tubules whose odontoblastic processes can perceive thermal stimuli as a source of pain. This can cause patients to neglect oral hygiene and increase the risk of caries and periodontal disease. The irreversible loss of enamel will also cause a change in the occlusion, decreasing the vertical dimension of occlusion. The loss of tooth structure requires that more complicated and expensive restorative options, such as crowns, be utilized. The loss of enamel support around composite or amalgam restorations can lead to their weakening and ultimate loss. The amount of time necessary for the enamel to be eroded in such fashion can range from six months to two years [32].
| A) | There is an increase in digestion. | ||
| B) | Glucose is released into the bloodstream. | ||
| C) | There is an increase in heart rate and cardiac output. | ||
| D) | There is an increase in the rate and depth of breathing. |
The human body has the biologic means to instantaneously and automatically respond to an acute life-threatening situation. The stress, or "fight-or-flight," response originates from the sympathetic division of the autonomic nervous system and provides the rapid dissemination of neural and hormonal messengers through which these rapid physiologic changes occur. The physiologic needs of a person at rest are vastly different than those of a person who is confronted with an emergency situation. For individuals who believe they are at risk, there is an increase in heart rate, cardiac output, respiratory rate and depth, and perspiration. Digestion is decreased as blood is diverted to the skeletal muscles and the brain. Glucose is released into the bloodstream to supply the enhanced metabolic needs of the major muscle groups and the brain. This stimulatory effect is induced by the hormones epinephrine, norepinephrine, and cortisol, the effect and secretion of which subsides after the stress-provoking situation is resolved. Epinephrine and norepinephrine are catecholamines produced by the chromaffin cells in the medulla of the adrenal gland. Epinephrine accounts for approximately 80% of catecholamine production, while the remaining 20% is norepinephrine [39]. These hormones are essential components for the stress response and have different effects upon their target tissues. Epinephrine exerts a profound effect upon metabolic activities, the dilation of the bronchioles, and increased perfusion of blood to skeletal and cardiac muscle. The primary metabolic effect of epinephrine is to elevate blood glucose levels to meet the body's increased metabolic demands. This is achieved by the conversion of glycogen stored in the liver and the muscles into glucose and the release of cortisol from the adrenal cortex, which causes a redistribution of glucose to the brain and major muscles [40]. Norepinephrine has a greater influence on peripheral vasoconstriction and blood pressure. Increased constriction of the smooth muscles in blood vessels raises the blood pressure.
| A) | decreases blood glucose levels. | ||
| B) | is produced by the chromaffin cells of the adrenal gland. | ||
| C) | accounts for approximately 20% of the catecholamine production. | ||
| D) | has a more profound effect on peripheral vasoconstriction than norepinephrine. |
The human body has the biologic means to instantaneously and automatically respond to an acute life-threatening situation. The stress, or "fight-or-flight," response originates from the sympathetic division of the autonomic nervous system and provides the rapid dissemination of neural and hormonal messengers through which these rapid physiologic changes occur. The physiologic needs of a person at rest are vastly different than those of a person who is confronted with an emergency situation. For individuals who believe they are at risk, there is an increase in heart rate, cardiac output, respiratory rate and depth, and perspiration. Digestion is decreased as blood is diverted to the skeletal muscles and the brain. Glucose is released into the bloodstream to supply the enhanced metabolic needs of the major muscle groups and the brain. This stimulatory effect is induced by the hormones epinephrine, norepinephrine, and cortisol, the effect and secretion of which subsides after the stress-provoking situation is resolved. Epinephrine and norepinephrine are catecholamines produced by the chromaffin cells in the medulla of the adrenal gland. Epinephrine accounts for approximately 80% of catecholamine production, while the remaining 20% is norepinephrine [39]. These hormones are essential components for the stress response and have different effects upon their target tissues. Epinephrine exerts a profound effect upon metabolic activities, the dilation of the bronchioles, and increased perfusion of blood to skeletal and cardiac muscle. The primary metabolic effect of epinephrine is to elevate blood glucose levels to meet the body's increased metabolic demands. This is achieved by the conversion of glycogen stored in the liver and the muscles into glucose and the release of cortisol from the adrenal cortex, which causes a redistribution of glucose to the brain and major muscles [40]. Norepinephrine has a greater influence on peripheral vasoconstriction and blood pressure. Increased constriction of the smooth muscles in blood vessels raises the blood pressure.
| A) | It is produced from the cortex of the adrenal gland. | ||
| B) | It does not have any affect upon blood glucose levels. | ||
| C) | It can stimulate the vasoconstricting actions of both epinephrine and norepinephrine. | ||
| D) | The release of cortisol is under control of the hypothalamus and the anterior pituitary gland. |
The secretion of cortisol is regulated by the release of corticotropin-releasing hormone (CRH) from the hypothalamus, which stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. Cortisol is released from the cortex of the adrenal gland via ACTH stimulation and influences the energy metabolism of most body cells by keeping the blood glucose levels relatively constant. It also assists in the maintenance of blood pressure by stimulating the vasoconstricting actions of both epinephrine and norepinephrine.
| A) | emotional responses such as depression and insomnia. | ||
| B) | cognitive signs such as impaired concentration and memory lapses. | ||
| C) | physical symptoms such as hypertension and chronic fatigue. | ||
| D) | All of the above |
People affected by chronic stress may experience emotional exhaustion and depersonalization, both of which are mental/emotional symptoms of burnout [20]. This problem reduces the ability of the affected individual to work at his or her ideal capacity. Other emotional responses to chronic stress include depression, anxiety, insomnia, irritability, and anhedonia. Cognitive signs can include impaired concentration, memory lapses, and negative thinking. Among the numerous physical responses to chronic stress are tension headaches, hypertension, cardiovascular problems, chronic fatigue, and immunosuppression [21]. Coping mechanisms for chronic stress (e.g., compulsive eating, drug and/or alcohol abuse, excessive gambling, withdrawal, extramarital affairs, suicide) can also lead to negative health effects. These self-destructive behaviors are ineffective in addressing the cause of stress and will compound the problem and delay a long-term resolution.