Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_208_библиотеки_им_акад_М_И_Перельмана
.pdf
382 Laboratory Medicine in Psychiatry and Behavioral Science
Diabetes insipidus (DI) (continued)
Refardt J, Winzeler B, Christ-Crain M: Diabetes insipidus: an update. Endocrinol Metab Clin North Am
49(3):517–531, 2020
Schernthaner-Reiter MH, Stratakis CA, Luger A: Genetics of diabetes insipidus.Endocrinol Metab Clin
North Am 46(2):305–334, 2017
Yuen KCJ, Sharf V, Smith E, et al: Sodium and water perturbations in patients who had an acute stroke: clinical
relevance and management strategies for the neurologist. Stroke Vasc Neurol 7(3):258–266, 2022
https://t.me/med1917
383 Diseases and Conditions
Diabetes mellitus (DM)
Clinical findings DM refers to several metabolic disorders characterized by persistent
hyperglycemia arising from impaired insulin secretion, insulin resis
-
tance, or both. DM is classified as type 1 (absolute insulin deficiency),
type 2 (insulin resistance/decreased insulin response with relative
insulin deficiency), gestational, and other (which includes a variety of
conditions such as pancreatitis and drug-induced diabetes). Histori
-
cally, type 1 DM was thought to occur only in children and type 2 only
in adults, but it is now recognized that either type can occur at any age;
thus, terms such as adult-onset diabetes and non-insulin-dependent diabetes
have fallen out of use. The term latent autoimmune diabetes of adulthood
(LADA) is in current use and refers to an adult-onset form of type 1 DM.
Obesity is the primary risk factor for type 2 DM. Patients with type 2 DM
who are not overweight may show a redistribution of body fat to the
abdominal area. Other risk factors include increasing age, sedentary life
-
style, hypertension, dyslipidemia, positive family history of type 2 DM,
and ethnicity (higher risk for those of Black, American Indian, His
-
panic/Latino, or Asian race/ethnicity). The presence of depression or
sleep disturbance presents additional risk. A quick screening measure
for risk factors is available from the CDC at
www.cdc.gov/prediabetes/
takethetest.
Undiagnosed and untreated DM is a major public health problem.
Whereas type 1 DM usually presents with recognizable signs of hyper-
glycemia (polyuria, polydipsia, polyphagia, ketoacidosis), type 2 DM
can remain silent for years because hyperglycemia develops only grad
-
ually as insulin secretion becomes insufficient to overcome insulin resis-
tance. When hyperglycemia has developed, however, patients with
either form of DM can develop the same complications: neuropathy, ret
-
inopathy, vasculopathy, sexual dysfunction, kidney disease, and cogni-
tive impairment from cerebral small vessel disease.
Links between DM and psychiatric disease or psychological factors are
many and complex. Mounting evidence suggests a shared pathogenesis
of depression and type 2 DM involving overactivation of innate immu
-
nity with a cytokine-mediated inflammatory response, and possibly
HPA axis dysregulation. The presence of DM doubles the risk of depres
-
sion, and depression is associated with treatment nonadherence, poor
glycemic control, and diabetic complications. Anxiety disorders are also
associated with poor glycemic control. Eating disorders present a
un iq ue risk of compli cation s of DM w hen insul in is withheld by pati ents
as a means to lose weight. Minor and major neurocognitive disorders
may result from a variety of DM-related brain insults, including vascu
-
lar disease, oxidative stress, neuroinflammation, apoptosis, reduction of
neurotrophic factors, and mitochondrial dysfunction, among others.
Laboratory testing American Diabetes Association (ADA) guidelines suggest screening for
DM in adults age ≥45 years and in individuals with multiple risk factors
regardless of age. The same tests are used for screening and diagnosis.
Testing for diabetes/prediabetes in asymptomatic adults should be
considered for those who are overweight or obese (BMI ≥25 kg/m
2
, or
≥23 kg/m
2
in those of Asian ethnicity) who have one or more of the
following risk factors:
• First-degree relative with DM
• High-risk race/ethnicity (Black, American Indian, Hispanic/
Latino, or Asian)
https://t.me/med1917
384 Laboratory Medicine in Psychiatry and Behavioral Science
Diabetes mellitus (DM) (continued)
Laboratory testing
(continued)
• History of cardiovascular disease
•Hypertension (≥140/90 or on treatment)
• High-density lipoprotein cholesterol <35 mg/dL and/or triglycer-
ide level >250 mg/dL
• Female with polycystic ovary syndrome
•Sedentary lifestyle
• Other conditions associated with insulin resistance (e.g., acantho-
sis nigricans)
For asymptomatic patients with a normal test result, testing should be
repeated every 3 years. This interval can be shortened in those with
obesity or other risks. Patients with prediabetes should be tested an
-
nually. Females with a history of gestational DM should have lifelong
testing at least every 3 years. Patients with HIV should be tested before
antiretroviral treatment, 1–3 months after starting treatment, and ev
-
ery 6–12 months thereafter.
Test results used in the ADA diagnostic criteria for type 2 DM include
any the following:
• Fasting plasma glucose (FPG) ≥ 126 mg/dL
• 2-hour plasma glucose level ≥200 mg/dL during a 75-g oral glu-
cose tolerance test (OGTT)
• Random plasma glucose level ≥200 mg/dL in a patient with symp-
toms of hyperglycemia or hyperglycemic crisis
•HbA1c level ≥6.5%
Regardless of the test used, diagnosis requires two abnormal results,
either from same blood sample or a different sample. An FPG test re
-
quires fasting for 8 hours. The 2-hour OGTT is a standard test for ges-
tational diabetes at 24–28 weeks of pregnancy.
The HbA1c test is used to assess glycemic control, with the result re-
flecting average glucose values over preceding 3 months. The test is
not as sensitive as FPG or OGTT in detecting DM. The HbA1c test
should be performed at initial assessment and every 3 months there
-
after until the glycemic target has been attained. At that point, testing
should be done at least every 6 months in those with good control and
every 3 months otherwise.
The diagnosis of type 1 DM differs from that of type 2 in the early
stages of type 1 disease (involving autoantibodies), but the two algo
-
rithms converge when abnormal glucose levels are seen. The persis-
tence of two or more autoantibodies predicts the onset of clinical
diabetes. FPG rather than HbA1c testing is used to diagnose acute
onset of t
ype 1 DM.
Further testing for complications of DM includes the following:
• Screening for diabetic kidney disease: urine albumin and GFR at
least annually in patients with type 1 DM for ≥5 years or type 2 DM
and hypertension
• Eye exam (dilated retinal exam) every 1–2 years to evaluate reti-
nopathy
• Screening for hypogonadism with a morning serum testosterone
measurement in males with symptoms such as reduced libido or
erectile dysfunction
https://t.me/med1917
385 Diseases and Conditions
Diabetes mellitus (DM) (continued)
Laboratory testing • Attention to liver function, with further testing (e.g., with elastog-
(continued) raphy) as indicated
• Regular screening for psychiatric disorders such as depression and
anxiety
American Diabetes Association: Classification and diagnosis of diabetes: standards of medical care in di-
abetes—2021. Diabetes Care 44(Suppl 1):S15–S33, 2021
ARUP Consult: Diabetes mellitus, in ARUP Consult: The Physician's Guide to Laboratory Test Selection
and Interpretation.
Salt Lake City, UT, ARUP Laboratories, 2022. Available at: https://
arupconsult.com/content/diabetes-mellitus. Accessed April 2022.
Garrett C, Doherty A: Diabetes and mental health. Clin Med (Lond) 14(6):669–672, 2014
Hamed SA: Brain injury with diabetes mellitus: evidence, mechanisms and treatment implications.Ex-
pert Rev Clin Pharmacol 10(4):409–428, 2017
Holingue C, Wennberg A, Berger S, et al: Disturbed sleep and diabetes: a potential nexus of dementia
risk. Metabolism 84:85–93, 2018
Moulton CD, Pickup JC, Ismail K: The link between depression and diabetes: the search for shared mech-
anisms.Lancet Diabetes Endocrinol 3(6):461–471, 2015
Park M, Reynolds CF III: Depression among older adults with diabetes mellitus.Clin Geriatr Med
31(1):117–137, 2015
Petersmann A, Müller-Wieland D, Müller UA, et al: Definition, classification and diagnosis of diabetes
mellitus.Exp Clin Endocrinol Diabetes 127(Suppl 1):S1–S7, 2019
Tang Q, Li S, Yang Z, et al: A narrative review of multimodal imaging of white matter lesions in type-2
diabetes mellitus.Ann Palliat Med 10(12):12867–12876, 2021
https://t.me/med1917
386 Laboratory Medicine in Psychiatry and Behavioral Science
Down syndrome (DS)
Clinical findings DS is a common genetic disorder caused by abnormal cell division re-
sulting in an extra copy of chromosome 21 (trisomy 21). Mosaicism and
partial trisomy 21 also occur. DS is associated with varying degrees of
intellectual disability, characteristic physical findings, and a range of
cardiovascular, neuropsychiatric, endocrine, autoimmune, and muscu
-
loskeletal disorders. The most important risk factor for DS is advanced
maternal age. The life expectancy of affected individuals is ~60 years.
Many of the physical features of DS are recognizable at birth, such as
upslanted palpebral fissures, flat nasal bridge, nuchal folds, single pal-
mar flexion crease, clinodactyly of the fifth finger, and muscular hypo
-
tonia. The phenotype also includes short stature and, in some cases,
atlantoaxial instability.
Medical conditions affecting individuals with DS more often than the
general population include the following:
• Congenital heart disease—particularly ventricular septal defect and
atrioventricular septal defect
• Pulmonary hypertension—attributable in part to congenital heart
disease and upper airway obstruction
• Obstructive sleep apnea
• Endocrine disorders—obesity, hypogonadism (with or without in-
fertility), accelerated bone loss with aging
• Hematological/oncological disorders—myeloid leukemia, acute
lymphoblastic leukemia, and transient abnormal myelopoiesis (in
newborns)
• Autoimmune disease—thyroid dysfunction, celiac disease, juvenile
arthritis, type 1 diabetes mellitus, Addison’s disease, hemolytic ane
-
mia, dermatomyositis, alopecia, vitiligo
• Immune dysregulation—involving both innate and adaptive immu-
nity; infection is common, particularly respiratory (increased risk for
COVID-19 infection)
• Hearing and vision problems
• Neurological—dysphagia, seizures, Alzheimer’s disease (AD)
(early onset), moyamoya disease, cerebellar hypoplasia (causing hy
-
potonia, motor incoordination)
• Psychiatric—autism, anxiety disorders, depression, OCD, ADHD,
eating disorders, catatonia, psychosis, Down syndrome disintegra-
tive disorder (DSDD)
Trisomy at chromosome 21 results in the overproduction and early brain
deposition of amyloid-β protein. Patients with DS show histopatholog-
ical features of AD starting around age 40 years. Many remain asymp-
tomatic, however, with noticeable cognitive decline starting decades
later. Dementia may be more likely to develop in patients with seizures.
DSDD is a developmental regression characterized by a loss of previ-
ously acquired adaptive, cognitive, and social functions. Onset is sub-
acute, with symptoms including mutism, catatonia, dementia,
depression, and autistic features. The disorder may enter a chronic
phase in which the individual does not return to baseline functioning.
The cause of DSDD is not known; autoimmune mechanisms, neuroin-
flammation, psychiatric disease, and psychological stress have been
implicated.
https://t.me/med1917
387 Diseases and Conditions
Down syndrome (DS) (continued)
Laboratory testing Cell-free DNA screening has replaced other screening tests for prenatal
diagnosis of DS. In this test, a sample of the mother’s blood is drawn
after 10 weeks of pregnancy, and fetal DNA is measured to determine
whether DNA from chromosome 21 is overrepresented. Results nor-
mally take 1–2 weeks to return. A positive test can be followed up with
more invasive procedures of chorionic villus sampling or amniocente
-
sis, which provide definitive diagnosis.
If DS is suspected in an undiagnosed child, fluorescence in situ hybrid-
ization (FISH) of chromosome 21 can be performed to diagnose trisomy.
This can be followed up by a karyotype to determine the specific ge
-
netic cause (translocation or nondisjunction), which is needed for ge-
netic counseling.
The numerous medical conditions associated with DS require diagnos-
tic workup based on clinical signs and symptoms, such that practi-
tioners must not only maintain a high index of suspicion but also have
a thorough understanding of comorbidities. For example, if symptoms
of celiac disease are present, testing of levels of IgA antibodies to tissue
transglutaminase 2 is recommended. EEG is recommended if there is
any suspicion of seizure. Hearing and vision should be tested regularly,
and TSH blood testing performed annually.
Antonarakis SE, Skotko BG, Rafii MS, et al: Down syndrome.Nat Rev Dis Primers 6(1):9, 2020
Arumugam A, Raja K, Venugopalan M, et al: Down syndrome: a narrative review with a focus on ana-
tomical features. Clin Anat 29(5):568–577, 2016
Ballard C, Mobley W, Hardy J, et al: Dementia in Down’s syndrome. Lancet Neurol 15(6):622–636, 2016
Bull MJ: Down syndrome. N Engl J Med 382(24):2344–2352, 2020
Dard R, Janel N, Vialard F: COVID-19 and Down’s syndrome: are we heading for a disaster? Eur J Hum
Genet 28(11):1477–1478, 2020
Rosso M, Fremion E, Santoro SL, et al: Down syndrome disintegrative disorder: a clinical regression syn-
drome of increasing importance. Pediatrics 145(6):e20192939, 2020
Santoro JD, Pagarkar D, Chu DT, et al: Neurologic complications of Down syndrome: a systematic re-
view. J Neurol 268(12):4495–4509, 2021
Whooten R, Schmitt J, Schwartz A: Endocrine manifestations of Down syndrome. Curr Opin Endocrinol
Diabetes Obes 25(1):61–66, 2018
https://t.me/med1917
388 Laboratory Medicine in Psychiatry and Behavioral Science
DRESS syndrome
Clinical findings The DRESS syndrome—drug reaction with eosinophilia and systemic
symptoms—is a severe drug rash associated with fever, lymphadenop
-
athy, internal organ involvement, and hematological abnormalities. In-
ternal organs affected include the liver, kidneys, lungs, heart, and
pancreas. Encephalitis and meningitis may be seen. The syndrome has
a 10% or greater mortality rate, even with early recognition and treat
-
ment. DRESS has been underrecognized in psychiatry, even though
many of the implicated drugs are psychotropics. The pathogenesis of
DRESS is not known but may involve an interaction of genetics, viral
reactivation (herpesvirus, Epstein-Barr virus, cytomegalovirus), and
medication.
Psychotropic drugs commonly implicated in DRESS include carba-
mazepine, lamotrigine, phenytoin, valproate, and phenobarbital. Less
commonly, bupropion, mirtazapine, amitriptyline, oxcarbazepine,
gabapentin, benzodiazepines, clomipramine, quetiapine, clozapine,
olanzapine, aripiprazole, and certain antiretroviral drugs have been
reported. Retrospective reviews have demonstrated that DRESS is
grossly underreported with psychotropics.
The DRESS rash typically appears 2–8 weeks after the drug is initiated,
with earlier presentations seen with drug rechallenge. Classically de
-
scribed as morbilliform, the rash is now known to have various presen-
tations, including urticarial, targetoid (erythema multiforme–like),
pustular, and others. The rash spreads rapidly to involve more than
50% of the skin. In about one-third of cases, gross facial edema accom
-
panies the rash. Lymphadenopathy typically involves more than one
node, with enlargement often ≥ 1 cm.
The internal organ most affected in DRESS is the liver, with presenting
features of hepatitis, jaundice, or asymptomatic transaminitis. The pat
-
tern of injury can be hepatocellular, cholestatic, or mixed. Kidney in-
volvement takes the form of acute interstitial nephritis with
proteinuria, hematuria, and sterile pyuria. Pulmonary manifestations
include pneumonia, effusions, nodules, and acute respiratory distress.
Myocarditis associated with DRESS may develop in association with
the rash or as a late manifestation, up to 4 months after first symptoms.
Myocarditis may be asymptomatic, requiring a high index of suspicion
in patients with other elements of the syndrome. Pancreatic involve-
ment can be acute or late-appearing and may involve endocrine more
than exocrine functions. Hematological signs include eosinophilia, leu-
kocytosis, lymphocytopenia, and atypical lymphocytes.
Several autoimmune conditions are late-appearing sequelae of DRESS.
The most common is autoimmune thyroiditis, which may manifest at
any time from several weeks to 3 years after initial symptoms. Other
syndromes include SLE, diabetes mellitus type 1, and autoimmune he-
molytic anemia.
The scoring system developed by the European Registry of Severe Cu-
taneous Adverse Reactions (RegiSCAR) has been used for the formal
diagnosis of DRESS. It should be noted that formes frustes of DRESS can
be seen. The RegiSCAR with scoring is reproduced in the paper by Cho
et al. (2017) in the reference list below.
https://t.me/med1917
389 Diseases and Conditions
DRESS syndrome (continued)
Clinical findings Key criteria are as follows:
(continued)
• Acute skin rash
• Fever ≥ 38.5ºC
•Lymphadenopathy (≥ 1 cm) in at least two sites
• Internal organ involvement (one or more organs)
• Hematological abnormalities (lymphocytes, eosinophils, platelets)
Laboratory testing For laboratory confirmation of the diagnosis of DRESS, the following
tests are recommended:
• CBC with differential and platelets (including search for atypical
lymphocytes)
•CRP
•LFTs
• Creatinine, glucose, calcium
• Urinalysis for protein, cells
• Creatine kinase, troponin
•ECG
Other tests are recommended by different specialists, mainly to evalu-
ate internal organ involvement. These include thyroid function tests,
echocardiogram, lipase, PTH, serum ferritin, triglycerides, blood cul-
tures, chest X-ray, head CT or brain MRI, and CSF analysis. In addition,
PCR testing for herpesvirus 6, herpesvirus 7, cytomegalovirus, and
Epstein-Barr virus may be suggested.
Bommersbach TJ, Lapid MI, Leung JG, et al: Management of psychotropic drug–induced DRESS syn-
drome: a systematic review. Mayo Clin Proc 91(6):787–801, 2016
Cardones AR: Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome.Clin Derma-
tol 38(6):702–711, 2020
Cho YT, Yang CW, Chu CY: Drug reaction with eosinophilia and systemic symptoms (DRESS): an inter-
play among drugs, viruses, and immune system.Int J Mol Sci 18(6):1243, 2017
de Filippis R, Soldevila-Matías P, De Fazio P, et al: Clozapine-related drug reaction with eosinophilia and
systemic symptoms (DRESS) syndrome: a systematic review. Expert Rev Clin Pharmacol 13(8):875–
883, 2020
de Filippis R, Soldevila-Matías P, Guinart D, et al: Unravelling cases of clozapine-related drug reaction
with eosinophilia and systemic symptoms (DRESS) in patients reported otherwise: a systematic re-
view. J Psychopharmacol 35(9):1062–1073, 2021
Isaacs M, Cardones AR, Rahnama-Moghadam S: DRESS syndrome: clinical myths and pearls. Cutis
102(5):322–326, 2018
Jevtic D, Dumic I, Nordin T, et al: Less known gastrointestinal manifestations of drug reaction with eo-
sinophilia and systemic symptoms (DRESS) syndrome: a systematic review of the literature.J Clin
Med 10(18):4287, 2021
Taleb S, Zgueb Y, Ouali U, et al: Drug reaction with eosinophilia and systemic symptoms syndrome re-
lated to aripiprazole therapy.J Clin Psychopharmacol 39(6):691–693, 2019
https://t.me/med1917
390 Laboratory Medicine in Psychiatry and Behavioral Science
Drug abuse
Clinical findings Testing rates for drugs of abuse declined precipitously during the
COVID-19 pandemic, and although some testing programs are now
back on track, available evidence suggests that positivity rates for her
-
oin, non-prescribed fentanyl, and combinations of these drugs with
stimulants and sedative-hypnotics have all increased significantly. Not
surprisingly, the extreme stressors of the pandemic have been linked to
the rise in abuse and to disruption of treatment for those with preexist
-
ing substance-related diagnoses.
Cannabis use is also on the rise worldwide, and in the United States this
trend is fueled by state-level legalization. Neither harms predicted by
opponents of legalization nor benefits predicted by advocates have
materialized in any substantial way, except that tax revenues have
exceeded expectations.
This section provides a list of clinical findings linked to classes of com-
monly abused drugs. More information on laboratory testing can be
found in the Urine Drug Screen entry in the Laboratory Tests chapter.
Amphetamines
With mild to moderate intoxication, symptoms include talkativeness,
grandiosity, vigilance, suspiciousness, mydriasis, elevated blood pres
-
sure (both systolic and diastolic), tachycardia or reflex bradycardia, and
hyperreflexia. With severe intoxication, symptoms include agitation,
bizarre behavior, auditory and tactile hallucinations, delusions, brux
-
ism, choreoathetosis, dystonia, fever, diaphoresis, nausea, vomiting, di-
arrhea, abdominal cramping, delirium, and assaultive behavior.
Among high-dose users, psychosis may develop that takes days to
weeks to resolve despite abstinence, and even low-dose use can cause
recurrence of psychotic symptoms because of sensitization. On the
other hand, tolerance to euphoric effects is common, causing dosage
escalation in chronic users.
Withdrawal symptoms include dysphoria, fatigue, irritability, agita-
tion, insomnia or hypersomnia, and suicidal ideation. Medical com-
plications of amphetamine abuse include seizures, hypertensive
encephalopathy, cardiac dysrhythmias, MI, cardiomyopathy, hemor
-
rhagic and ischemic stroke, and rhabdomyolysis. Methamphetamine
abusers may develop a subcortical dementia that persists even with
long abstinence.
Cannabis (marijuana and derivatives)
With intoxication, the following signs and symptoms may be observed:
silly affect, depersonalization, derealization, sensory distortions, mem-
ory impairment, carbohydrate craving, injected sclerae, mild ataxia,
tachycardia, elevated supine blood pressure, and orthostatic hypoten
-
sion. Panic symptoms commonly occur. Psychosis is much less com-
mon; when present, symptoms include persecutory delusions and
auditory and visual hallucinations. Psychotic symptoms may take sev-
eral days to resolve with abstinence.
Cocaine
With usual doses, signs and symptoms include hyperactivity, talkative-
ness, vigilance, grandiosity, anorexia, insomnia, increased libido, tachy-
cardia, mydriasis, and hypertension.
https://t.me/med1917
391 Diseases and Conditions
Drug abuse (continued)
Clinical findings
(continued)
With higher doses (usually from smoking or IV administration), signs
and symptoms include agitation, hallucinations (visual and tactile), im
-
potence, nausea, vomiting, choreoathetosis, and delirium with high
risk of aggressive and assaultive behaviors. With abstinence, symptoms
of fatigue, depression, irritability, and anxiety are seen. With prolonged
use, psychosis can occur during intoxication, with persecutory delu
-
sions and auditory hallucinations. Comorbid alcohol or opioid abuse is
common. Medical complications are the same as with amphetamines,
except for the additional complication of necrosis of the nasal septum
among users who ingest cocaine intranasally.
Hallucinogens
With intoxication, psychosis with delusions, visual illusions, and hallu-
cinations occurs in the context of a clear sensorium. The patient reports
synesthetic experiences, depersonalization, and derealization. With 3,4
-
methylenedioxymethamphetamine (MDMA, Ecstasy), the patient ex-
hibits signs of emotionality and increased empathic experience. With
any hallucinogen, anxiety, panic, and dysphoric delusions can occur.
Signs include mild elevation of temperature, tachycardia, hyperten
-
sion, mydriasis, fine tremor, incoordination, and hyperreflexia. With
MDMA, bruxism is also seen.
Inhalants
Inhalant abuse usually begins in childhood or adolescence, more often
in males. Products inhaled include glue, paint thinner, gasoline, clean
-
ing products (some containing methanol), aerosol propellants (e.g.,
contained in canned whipped cream), fingernail polish or polish
remover, and typewriter correction fluid. A rag saturated with the
product is held over the mouth and nose or placed in a bag for inhala
-
tion. Common signs of inhalant abuse include scleral injection, rhinor-
rhea, chemical odor on the breath, paint or stains on clothing, and sores
around the mouth. Signs of intoxication include drunken appearance,
drowsiness, dizziness, ataxia, dysarthria, diplopia, nystagmus, confu
-
sion, visual hallucinations, and delusions. With continued use, agita-
tion, irritability, and impulsivity may be seen. In severe intoxication,
coma can occur. Medical complications such as ventricular arrhyth
-
mias, bronchospasm, and seizures can occur. With long-term use,
dementia may develop with amnesia, frontal lobe dysfunction, and cer-
ebellar signs. Atrophy and white matter changes consistent with
demyelination may be seen on brain MRI.
Opioids
With intoxication, signs and symptoms include drowsiness, inatten-
tion, elation, dysarthria, miosis, absent bowel sounds, constipation, uri-
nary retention, and pruritus. With overdose, most patients are lethargic
or comatose. Miosis may be noted, giving way to mydriasis if respira
-
tory depression worsens and cerebral anoxia develops. Seizures may
occur, and death by respiratory arrest is a common outcome. Individu-
als who survive an episode of anoxia may have postanoxic leukoen-
cephalopathy with residual cognitive impairment. With regular use,
tolerance develops to all symptoms of intoxication except miosis and
constipation.
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана