STUDY - Technical - New Dacian's Medicine
Anorexia
Nervosa and Bulimia Nervosa (2)
Translation Draft
So, let's continue with the clinical picture! Anorexia nervosa usually occurs before or immediately after puberty, but can also occur later (around the age of 25). Many patients were overweight as children. The emaciation is similar to that found in victims in concentration camps during World War II. Despite the immense weight loss, patients deny feeling hungry, weak and tired. They are often physically active, and ritual exercises are common.
Frenetic rhythmic gymnastics and running can be practiced after eating. There is concern for food and sophisticated meals can often be prepared for others. If circumstances force them to eat more than usual, they cause vomit as quickly as they can, often in public toilets. Constipation is common. Amenorrhea accompanies any weight loss or occurs immediately after it, but may also occur before any physical change. Cold intolerance is probably due to a deficiency in regulating thermogenesis, secondary to a hypothalamic dysfunction.
In advanced cases, bradycardia, hypothermia and hypotension occur. Body fat is no longer even noticeable, and bones proemin through the skin (breast tissue is often preserved). The skin can also be dry with crusts and often yellow due to carotenemia (especially visible in the palms). Body hair often grows, is usually smooth and silky, similar to lanugo, but clear manifestations of hirsutism can also occur.
Parotid glands can be enlarged, as with other forms of starvation. The prolapse of the mitral valves is due to the mismatch of the ventricular valve-volume, as a result of the decrease in volume of the left ventricle, caused by starvation. Edema occurring in the absence of hypoalbuminemia is probably due to the inability of extracellular fluid to decrease proportionally with body mass during weight loss. Due to edema of the feet and enlarged parotid glands, which give roundness to the face, the actual state of emaciation can be masked when the patient is dressed.
Laboratory abnormalities include anemia and leukopenia (with bone marrow hypocellularity), hypocalcemia and hypoalbuminemia. Serum betacarotene levels tend to increase. If significant amounts of laxatives are used and/ or if a lot of vomiting is vomited, prerenal nitrogenemia may occur and the urea nitrogen in the blood may reach values of 21 to 25 mmol/ l. Renal concentration is impaired, probably due to partial reaction to vasopressin as a reaction to an osmotic stimulus. Cholesterol in plasma is occasionally increased, but triglyceride levels are not high. Glucose tolerance is abnormal, as in other forms of starvation.
Other manifest abnormalities include low levels of IgG, IgM and a variety of complement proteins. Despite these findings, immune function is generally maintained and serious infections are rare. Iron and ceruloplasmin levels in plasma are normal, but iron binding capacity is diminished. Zinc and plasma copper are low, but their concentrations are normal in the hair.
Serum amylase can be increased in the absence of pancreatic. The basic levels of luteinizing hormone (LH) and folliculic stimulation (FSH) are low when weight loss is severe and LH response to LHRH (luteinizing hormone release hormone) is also affected. FSH response to LHRH is normal, although the time for reaching the maximum level of growth may be delayed. Studies of the 24-hour circadian model of LH secretion show a delay in the stage of maturity in the model characteristic of girls in puberty or the prepubertary stage (for example, episodic release of LH is missing or is present only during sleep). These findings explain, at least in part, the presence of amenorrhea.
Menstruation occurs again with weight gain, although the weight required to re-install menstruation may be higher (approximately 10%) than that which was originally required for the first period. Ovulatory menstruation can be induced in patients suffering from anorexia nervosa by appropriate treatment with LHRH agonists, indicating that the release of gonadotropics by hypophysis is impaired due to hypothalamic dysfunction. Prolactin levels are normal. Estradiol levels in plasma are low, but plasma testosterone is normal in women. Testosterone levels are low in men suffering from anorexia nervosa.
Growth hormone (GH), in the basic state, may be normal or increased. An increase in GH occurs after injection of the erythrotropin release hormone (THR), as in other states with high basic LEVELS of GH, such as: acromegaly, uremia and protein-calorie malnutrition. Insulin-like growth factor I concentrations are low and may help raise growth hormone levels through negative feedback through cortisol. Suppression of plasma cortisol by dexamethasone and simulation of GH release by dexamethasone are abnormal in many patients. The levels of thyroxine (T4) and T4 in the free state are normal.
Triiodothyronine concentrations are low (T3) in reverse levels T3 (rT3) are increased. Basic levels of thyroid stimulating hormone (TSH) are normal and the TSH and THR response is intact. The primary defect in thyroid hormone metabolism is the low activity of 5'-deiodinase, which converts T4 to T3, and rT3 into diiodothyronine in nonthyroid tissues (these changes are characteristic of starvation and emaciation disease and are not specific to anorexia nervosa). Bone density decreases, the mechanism is suspected to be related to estrogen deficiency, but substitute therapy does not restore bone density. Excess cortisol may also have a role in bone loss. Excess cortisol may also have a role in bone loss. Norepinephrine levels are low.
Bulimia or "bull hunger" consists of the episodic, compulsive ingestion of large amounts of food (the patient is aware that this hunger is pathological, is afraid that he will not be able to stop voluntarily and after eating presents a depressive state). Bulimics have a morbid fear of obesity. While temporary increase in appetite may occur in multiple psychiatric conditions, many patients frequently have a history of anorexia nervosa (expressed or cryptic), suggesting that bulimia may be a different response to the same factors that lead to anorexia nervosa.
Episodes of appetite exacerbation are followed by vomiting caused, with or without subsequent ingestion of laxatives. Initially, vomiting is caused mechanically by irritation of the pharynx with the toothbrush or with the fingers, or by ingestion with the ipeca, but then most patients begin to vomit reflexively. Increased appetite is present daily (in one study, the weekly average of bulimia episodes was 12, with variations between 1 and 46). The duration of food intake was on average 1.2 hours, but there were cases where it lasted 8 hours.
The amount of food ingested can be impressive, reaching a total energy value of 50,000 kcal. It is usually preferred foods high in carbohydrates, at a meal consuming several kinds. In one statistic, the most common foods consumed were, in descending order, ice cream, bread, sweets, doughnuts, soft drinks. Dietary chaos is the most appropriate term for defining the diet of bulimics. Due to the increased carbohydrate content of ingested foods, tooth decay is a common pathological entity.
The secret that envelops alternative episodes of food-vomiting ingestion is characteristic, so family and friends are not aware of the facts. Bulimics often steal food most frequently. Among those affected, the rate of alcohol and drug use is high. Self-mutilation is not unusual and can be a manifestation of obsessive-compulsive disorders. Depression tends to be more serious than that associated with anorexia nervosa, so the tendency to suicide is a definite risk. You can encounter hysterical behavior. In the families of bulimic patients, the incidence of psychiatric disorders, alcoholism and drug use is higher than in patients with anorexia nervosa. Despite the close relationship with anorexia nervosa, there may be some differences.
Although many bulimic patients are weak, there is no emaciation (generally, the weight varies by 15% from the average limit. Frequently, there are cyclical fluctuations of it in a positive or negative sense). Some patients are slightly over-burdened. Unlike anorexia nervosa, many patients continue to have menstrual cycles and may become pregnant. Keeping menstruation probably reflects the fact that weight loss is not extreme. Sexual activity is more intense in bulimics than in anorexics.
The objective examination provides little useful information, although in cases where weight loss is significant one can observe some of the changes that occur in anorexia nervosa. The most common paraclinically revealed change is secondary hypokalemia to vomiting and laxative consumption. Metabolic alkalose may occur if potassium loss is significant. Endocrine abnormalities are less evident than in anorexia nervosa, and may be absent.
Serotonin and cholecystochinin secretion is deficient in some patients (the significance of these changes is not known). Dexamethasone suppression is frequently abnormal. Unlike patients with anorexia nervosa, some women with bulimia have low basal levels of prolactin and an exaggerated response to stimulation of prolactin through THR. Serum amylase can be increased in both bulimia and anorexia, without this signifying the presence of pancreatitis.
Patients with anorexia nervosa are susceptible to ventricular tachyarrhythmias that can lead to sudden death. Electrocardiograms revealed prolonged QT intervals. The risk of death becomes increased when the weight decreases is 35% of the ideal, probably due to protein deficiency. complications of bulimia consist of aspirations, oesophageal or gastric rupture, pneumomediastin, hypopotasemia accompanied by cardiac arrhythmias, pancreatitis and/ or ipeca-induced cardiomyopapathies.
From the point of view of prognosis, the evolution of anorexia nervosa is variable. In long-term monitoring, about half of patients reached normal weight, 20% gained weight but remained underweight, 20% remained anorexic, 5% became obese and 6% died. Even when there is weight gain, swallowing, vomiting and laxative use are still present in 2/3 of patients.
Death usually occurs through inaniation (mainly cardiac arrhythmias) or suicide. Signs in favor of a bad prognosis include advanced age at onset, long duration of the disease, history of bulimia or vomiting, extreme weight loss and the presence of significant depressive syndrome. Few long-term studies are available for bulimics. Because psychiatric disorders tend to be more severe (suicide has a higher frequency) and because the medical risks of excessive food consumption are higher, the prognosis of bulimia is more severe than that of anorexia. Approximately 40% of patients receiving treatment remained bulimic after 18 months of therapy.
There is no specific treatment in anorexia nervosa or bulimia. The failure of therapy is due to the fear of gaining weight, associated with the misperception of body sizes, in an overweight sense. The benefits of psychiatric therapy are minimal, as are those of the behavior modification technique or group or intra-family psychotherapy. Sustained support from the attending physician can lead to the same results as formal psychotherapy. The patient should be examined regularly for changes in weight, diet and exercise.
It is useful to establish an explicit "mutual contract" agreed by both parties (for example, if the patient is 30 kg and the ideal weight is 52 kg, in the first stage the target will be set to achieve the weight of 40 kg). At each meeting the patient should be assured by the doctor that "he will be helped so that he does not gain gain any fat". A calm but realistic review of the dangers that accompany inanimation, including sudden death, must be carried out, accompanied by statements such as "my duty is to help you fight this disease so that you enjoy a normal life expectancy and a reasonable quality of life".
The doctor should be regarded not as an enemy or as a surrogate of the parents, but as an advisor and as a partner in battle. A similar approach must be made in the case of bulimias. Even if you cannot interrupt the overeating-regurgitation cycle, the minimum goals of limiting food intake (to minimize the risk of aspiration and gastric rupture) and reducing the frequency of bulimia episodes can be achieved. Due to the fact that depression and antisocial behavior are more common in bulimia, psychiatric therapy is necessary. In anorexia nervosa, hospitalization may be the only means of saving patients' lives. As mentioned above, sudden death can occur when the weight is more than 35% below ideal, especially if the weight loss was rapid.
Hypopotasemia, hypotension and prerenal nitrogenemia due to volume deplation are indications of admission. It may be necessary to install a nasogastric probe, but it is preferable to convince the patient to eat. During admission, the patient should never be allowed to eat alone. Total parenteral nutrition is rarely indicated. It may be useful to include in the treatment plan lectures on nutrition, occupational therapy, group psychotherapy with family co-opting and individual psychotherapy. The "safety" in eating and repeated assurances that obesity will not occur must be repeated at all times. Some doctors argue that admission at the onset of the disease benefits all patients with serious impairment, but this opinion is not widely shared. Typically, admission of bulimic patients is done only in the presence of medical complications (e.g. aspiration). Treatment of anorexia-bulimia syndrome is long-term, can be doomed to failure and requires perseverance on the part of the patient, family and doctor.
I've presented enough... Next time I'll move on to diet therapy.
So, let's continue with the clinical picture! Anorexia nervosa usually occurs before or immediately after puberty, but can also occur later (around the age of 25). Many patients were overweight as children. The emaciation is similar to that found in victims in concentration camps during World War II. Despite the immense weight loss, patients deny feeling hungry, weak and tired. They are often physically active, and ritual exercises are common.
Frenetic rhythmic gymnastics and running can be practiced after eating. There is concern for food and sophisticated meals can often be prepared for others. If circumstances force them to eat more than usual, they cause vomit as quickly as they can, often in public toilets. Constipation is common. Amenorrhea accompanies any weight loss or occurs immediately after it, but may also occur before any physical change. Cold intolerance is probably due to a deficiency in regulating thermogenesis, secondary to a hypothalamic dysfunction.
In advanced cases, bradycardia, hypothermia and hypotension occur. Body fat is no longer even noticeable, and bones proemin through the skin (breast tissue is often preserved). The skin can also be dry with crusts and often yellow due to carotenemia (especially visible in the palms). Body hair often grows, is usually smooth and silky, similar to lanugo, but clear manifestations of hirsutism can also occur.
Parotid glands can be enlarged, as with other forms of starvation. The prolapse of the mitral valves is due to the mismatch of the ventricular valve-volume, as a result of the decrease in volume of the left ventricle, caused by starvation. Edema occurring in the absence of hypoalbuminemia is probably due to the inability of extracellular fluid to decrease proportionally with body mass during weight loss. Due to edema of the feet and enlarged parotid glands, which give roundness to the face, the actual state of emaciation can be masked when the patient is dressed.
Laboratory abnormalities include anemia and leukopenia (with bone marrow hypocellularity), hypocalcemia and hypoalbuminemia. Serum betacarotene levels tend to increase. If significant amounts of laxatives are used and/ or if a lot of vomiting is vomited, prerenal nitrogenemia may occur and the urea nitrogen in the blood may reach values of 21 to 25 mmol/ l. Renal concentration is impaired, probably due to partial reaction to vasopressin as a reaction to an osmotic stimulus. Cholesterol in plasma is occasionally increased, but triglyceride levels are not high. Glucose tolerance is abnormal, as in other forms of starvation.
Other manifest abnormalities include low levels of IgG, IgM and a variety of complement proteins. Despite these findings, immune function is generally maintained and serious infections are rare. Iron and ceruloplasmin levels in plasma are normal, but iron binding capacity is diminished. Zinc and plasma copper are low, but their concentrations are normal in the hair.
Serum amylase can be increased in the absence of pancreatic. The basic levels of luteinizing hormone (LH) and folliculic stimulation (FSH) are low when weight loss is severe and LH response to LHRH (luteinizing hormone release hormone) is also affected. FSH response to LHRH is normal, although the time for reaching the maximum level of growth may be delayed. Studies of the 24-hour circadian model of LH secretion show a delay in the stage of maturity in the model characteristic of girls in puberty or the prepubertary stage (for example, episodic release of LH is missing or is present only during sleep). These findings explain, at least in part, the presence of amenorrhea.
Menstruation occurs again with weight gain, although the weight required to re-install menstruation may be higher (approximately 10%) than that which was originally required for the first period. Ovulatory menstruation can be induced in patients suffering from anorexia nervosa by appropriate treatment with LHRH agonists, indicating that the release of gonadotropics by hypophysis is impaired due to hypothalamic dysfunction. Prolactin levels are normal. Estradiol levels in plasma are low, but plasma testosterone is normal in women. Testosterone levels are low in men suffering from anorexia nervosa.
Growth hormone (GH), in the basic state, may be normal or increased. An increase in GH occurs after injection of the erythrotropin release hormone (THR), as in other states with high basic LEVELS of GH, such as: acromegaly, uremia and protein-calorie malnutrition. Insulin-like growth factor I concentrations are low and may help raise growth hormone levels through negative feedback through cortisol. Suppression of plasma cortisol by dexamethasone and simulation of GH release by dexamethasone are abnormal in many patients. The levels of thyroxine (T4) and T4 in the free state are normal.
Triiodothyronine concentrations are low (T3) in reverse levels T3 (rT3) are increased. Basic levels of thyroid stimulating hormone (TSH) are normal and the TSH and THR response is intact. The primary defect in thyroid hormone metabolism is the low activity of 5'-deiodinase, which converts T4 to T3, and rT3 into diiodothyronine in nonthyroid tissues (these changes are characteristic of starvation and emaciation disease and are not specific to anorexia nervosa). Bone density decreases, the mechanism is suspected to be related to estrogen deficiency, but substitute therapy does not restore bone density. Excess cortisol may also have a role in bone loss. Excess cortisol may also have a role in bone loss. Norepinephrine levels are low.
Bulimia or "bull hunger" consists of the episodic, compulsive ingestion of large amounts of food (the patient is aware that this hunger is pathological, is afraid that he will not be able to stop voluntarily and after eating presents a depressive state). Bulimics have a morbid fear of obesity. While temporary increase in appetite may occur in multiple psychiatric conditions, many patients frequently have a history of anorexia nervosa (expressed or cryptic), suggesting that bulimia may be a different response to the same factors that lead to anorexia nervosa.
Episodes of appetite exacerbation are followed by vomiting caused, with or without subsequent ingestion of laxatives. Initially, vomiting is caused mechanically by irritation of the pharynx with the toothbrush or with the fingers, or by ingestion with the ipeca, but then most patients begin to vomit reflexively. Increased appetite is present daily (in one study, the weekly average of bulimia episodes was 12, with variations between 1 and 46). The duration of food intake was on average 1.2 hours, but there were cases where it lasted 8 hours.
The amount of food ingested can be impressive, reaching a total energy value of 50,000 kcal. It is usually preferred foods high in carbohydrates, at a meal consuming several kinds. In one statistic, the most common foods consumed were, in descending order, ice cream, bread, sweets, doughnuts, soft drinks. Dietary chaos is the most appropriate term for defining the diet of bulimics. Due to the increased carbohydrate content of ingested foods, tooth decay is a common pathological entity.
The secret that envelops alternative episodes of food-vomiting ingestion is characteristic, so family and friends are not aware of the facts. Bulimics often steal food most frequently. Among those affected, the rate of alcohol and drug use is high. Self-mutilation is not unusual and can be a manifestation of obsessive-compulsive disorders. Depression tends to be more serious than that associated with anorexia nervosa, so the tendency to suicide is a definite risk. You can encounter hysterical behavior. In the families of bulimic patients, the incidence of psychiatric disorders, alcoholism and drug use is higher than in patients with anorexia nervosa. Despite the close relationship with anorexia nervosa, there may be some differences.
Although many bulimic patients are weak, there is no emaciation (generally, the weight varies by 15% from the average limit. Frequently, there are cyclical fluctuations of it in a positive or negative sense). Some patients are slightly over-burdened. Unlike anorexia nervosa, many patients continue to have menstrual cycles and may become pregnant. Keeping menstruation probably reflects the fact that weight loss is not extreme. Sexual activity is more intense in bulimics than in anorexics.
The objective examination provides little useful information, although in cases where weight loss is significant one can observe some of the changes that occur in anorexia nervosa. The most common paraclinically revealed change is secondary hypokalemia to vomiting and laxative consumption. Metabolic alkalose may occur if potassium loss is significant. Endocrine abnormalities are less evident than in anorexia nervosa, and may be absent.
Serotonin and cholecystochinin secretion is deficient in some patients (the significance of these changes is not known). Dexamethasone suppression is frequently abnormal. Unlike patients with anorexia nervosa, some women with bulimia have low basal levels of prolactin and an exaggerated response to stimulation of prolactin through THR. Serum amylase can be increased in both bulimia and anorexia, without this signifying the presence of pancreatitis.
Patients with anorexia nervosa are susceptible to ventricular tachyarrhythmias that can lead to sudden death. Electrocardiograms revealed prolonged QT intervals. The risk of death becomes increased when the weight decreases is 35% of the ideal, probably due to protein deficiency. complications of bulimia consist of aspirations, oesophageal or gastric rupture, pneumomediastin, hypopotasemia accompanied by cardiac arrhythmias, pancreatitis and/ or ipeca-induced cardiomyopapathies.
From the point of view of prognosis, the evolution of anorexia nervosa is variable. In long-term monitoring, about half of patients reached normal weight, 20% gained weight but remained underweight, 20% remained anorexic, 5% became obese and 6% died. Even when there is weight gain, swallowing, vomiting and laxative use are still present in 2/3 of patients.
Death usually occurs through inaniation (mainly cardiac arrhythmias) or suicide. Signs in favor of a bad prognosis include advanced age at onset, long duration of the disease, history of bulimia or vomiting, extreme weight loss and the presence of significant depressive syndrome. Few long-term studies are available for bulimics. Because psychiatric disorders tend to be more severe (suicide has a higher frequency) and because the medical risks of excessive food consumption are higher, the prognosis of bulimia is more severe than that of anorexia. Approximately 40% of patients receiving treatment remained bulimic after 18 months of therapy.
There is no specific treatment in anorexia nervosa or bulimia. The failure of therapy is due to the fear of gaining weight, associated with the misperception of body sizes, in an overweight sense. The benefits of psychiatric therapy are minimal, as are those of the behavior modification technique or group or intra-family psychotherapy. Sustained support from the attending physician can lead to the same results as formal psychotherapy. The patient should be examined regularly for changes in weight, diet and exercise.
It is useful to establish an explicit "mutual contract" agreed by both parties (for example, if the patient is 30 kg and the ideal weight is 52 kg, in the first stage the target will be set to achieve the weight of 40 kg). At each meeting the patient should be assured by the doctor that "he will be helped so that he does not gain gain any fat". A calm but realistic review of the dangers that accompany inanimation, including sudden death, must be carried out, accompanied by statements such as "my duty is to help you fight this disease so that you enjoy a normal life expectancy and a reasonable quality of life".
The doctor should be regarded not as an enemy or as a surrogate of the parents, but as an advisor and as a partner in battle. A similar approach must be made in the case of bulimias. Even if you cannot interrupt the overeating-regurgitation cycle, the minimum goals of limiting food intake (to minimize the risk of aspiration and gastric rupture) and reducing the frequency of bulimia episodes can be achieved. Due to the fact that depression and antisocial behavior are more common in bulimia, psychiatric therapy is necessary. In anorexia nervosa, hospitalization may be the only means of saving patients' lives. As mentioned above, sudden death can occur when the weight is more than 35% below ideal, especially if the weight loss was rapid.
Hypopotasemia, hypotension and prerenal nitrogenemia due to volume deplation are indications of admission. It may be necessary to install a nasogastric probe, but it is preferable to convince the patient to eat. During admission, the patient should never be allowed to eat alone. Total parenteral nutrition is rarely indicated. It may be useful to include in the treatment plan lectures on nutrition, occupational therapy, group psychotherapy with family co-opting and individual psychotherapy. The "safety" in eating and repeated assurances that obesity will not occur must be repeated at all times. Some doctors argue that admission at the onset of the disease benefits all patients with serious impairment, but this opinion is not widely shared. Typically, admission of bulimic patients is done only in the presence of medical complications (e.g. aspiration). Treatment of anorexia-bulimia syndrome is long-term, can be doomed to failure and requires perseverance on the part of the patient, family and doctor.
I've presented enough... Next time I'll move on to diet therapy.
Understanding, love and
gratitude (Energy = Love x Gratitude square)...
(Warning, Fear = -Love, so
the energy that arises from this will be negative and anyway, in
the case of Fear, Gratitude is almost always 0, unless you have
problems with something like Stockholm syndrome, or things
related to heroism in crisis situations).
Dorin, Merticaru